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  • 1. Emergency Vascular SurgeryA Practical Guide
  • 2. Eric Wahlberg Pär Olofsson Jerry GoldstoneEmergencyVascular SurgeryA Practical GuideWith 68 Figures and 39 Tables
  • 3. Eric Wahlberg, MD, PhDAssociate ProfessorKarolinska Institute and University HospitalDepartment of Vascular Surgery17176 StockholmSwedenPär Olofsson, MD, PhDAssociate ProfessorKarolinska Institute and University HospitalDepartment of Vascular Surgery17176 StockholmSwedenProfessor Jerry Goldstone, MDUniversity Hospital of ClevelandCase Western ReserveDivision of Vascular SurgeryCleveland, Ohio 44106USAISBN 978-3-540-44393-3 Springer Berlin Heidelberg New YorkLibrary of Congress Control Number: 2006936731This work is subject to copyright. All rights are reserved, whether the whole or part of thematerial is concerned, specifically the rights of translation, reprinting, reuse of illustrations,recitation, broadcasting, reproduction on microfilm or in any other way, and storage in databanks. Duplication of this publication or parts thereof is permitted only under the provisionsof the German Copyright Law of September 9, 1965, in its current version, and permis-sions for use must always be obtained from Springer. Violations are liable for prosecutionunder the German Copyright Law.Springer is a part of Springer Science + Business© Springer-Verlag Berlin Heidelberg 2007The use of general descriptive names, registered names, trademarks, etc. in this publica-tion does not imply, even in the absence of a specific statement, that such names are exemptfrom the relevant protective laws and regulations and therefore free for general use.Product liability: The publishers cannot guarantee the accuracy of any information aboutdosage and application contained in this book. In every individual case the user must checksuch information by consulting the relevant literature.Editor: Gabriele M. Schröder, Heidelberg, GermanyDesk Editor: Stephanie Benko, Heidelberg, GermanyProduction: LE-TeX Jelonek, Schmidt & Vöckler GbR, Leipzig, GermanyDrawings: Medical Art, Gudrun and Adrian Cornford, Reinheim, GermanyTypesetting: am-productions GmbH, Wiesloch, GermanyCover design: Frido Steinen-Broo, eStudio Calamar, SpainPrinted on acid-free paper 24/3180 YL – 5 4 3 2 1 0
  • 4. PrefaceEmergency Vascular Surgery – A Practical Guide provides a concise guide tomanaging patients with all kinds of emergent vascular problems. It is not in-tended to be a “classic” textbook, so the background information given is veryconcise. The focus is instead on management and treatment, especially opensurgical strategies. The text is written for newcomers to the vascular surgical field, for surgicaltrainees, and for all doctors who treat emergent vascular surgical patients inthe emergency department. We believe the hands-on approach and the practi-cal tips will be appreciated by these readers in the clinical situation, and wehope the book may also serve as a quick review before a physician takes care ofa case. Medical students during surgical clerkships might find parts of thebook valuable, as will experienced vascular surgeons. The book is organized into two sections: specific body areas and generalconcepts. The former covers the body from head to toe and includes separatechapters for injuries and for nontraumatic disease. In the second part, somegeneral principles related to emergency vascular surgical practice are dis-cussed. Management of complications is difficult to cover in a book of thisscope, so the principles given in the chapter pertaining to this area are not verydetailed. The final chapter gives general vascular surgical guidelines for theinexperienced surgeon. All chapters are organized the same way. They start with a brief backgroundthat aims to motivate the reader and give an idea of incidence and pathophysi-ology. The rest of the chapter follows the patient’s course through the hospital:The clinical presentation is followed by suggestions for work-up and diagnosis,and the next part concerns management and treatment – emergency treat-ment, selection of patients for emergency surgery, and ways to perform com-mon vascular surgical procedures. Technical tips on complicated proceduresare also provided. Finally, the chapters end with a brief summary on manage-ment after treatment, with some examples of outcome and results. Most chap-ters also contain illustrations to facilitate the technical description of the surgi-cal procedures and notes to highlight particularly important aspects. A fewreferences for further reading are also suggested; they have been selected togive a better understanding of the issues and do not necessarily refer to infor-mation given in the text. The authors would like to acknowledge and thank a number of people in-volved in the writing of this book. First, we are grateful to the initial authors ofthe Swedish book from 1998 that gave us the idea to expand its contents andwrite an English version of it. Thank you all for letting us continue in thisdirection. We are also very grateful to all the residents, vascular trainees, andvascular surgeons who have read chapters and given us valuable suggestions on
  • 5. how to improve the content and structure. Last but not least, we acknowledgethe secretaries Annika Johansson and Synnove Nordstrom for all of their helpwith this project. Eric Wahlberg Pär Olofsson Jerry Goldstone Stockholm and Cleveland 2007
  • 6. ContentsPart A Specific Body AreasChapter 1 Vascular Injuries to the Neck 1Chapter 2 Vascular Injuries to the Thoracic Outlet Area 15Chapter 3 Vascular Injuries in the Arm 31Chapter 4 Acute Upper Extremity Ischemia 41Chapter 5 Abdominal Vascular Injuries 45Chapter 6 Acute Intestinal Ischemia 65Chapter 7 Abdominal Aortic Aneurysms 75Chapter 8 Aortic Dissection 91Chapter 9 Vascular Injuries in the Leg 101Chapter 10 Acute Leg Ischemia 119Part B General ConceptsChapter 11 Vascular Access in Trauma 135Chapter 12 Complications in Vascular Surgery 141Chapter 13 Acute Venous Problems 159Chapter 14 Acute Problems with Vascular Dialysis Access 167Chapter 15 General Principles of Vascular Surgical Technique 179 Subject Index 191
  • 7. Specific Areas PART A
  • 8. Vascular Injuries to the Neck 1CONTENTS 1.1 Summary1.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Severe vascular injury after blunt neck1.2 Background . . . . . . . . . . . . . . . . . . . . . . . . . 3 trauma can be present even in the absence1.2.1 Causes and Mechanism . . . . . . . . . . . . . 4 of clinical signs. Penetrating Trauma . . . . . . . . . . . . . . . . . 4 Be liberal with duplex or angiography after1.2.1.2 Blunt Trauma . . . . . . . . . . . . . . . . . . . . . . . . 4 blunt trauma when cervical vessel injuries1.3 Clinical Presentation . . . . . . . . . . . . . . . 4 cannot be ruled out.1.3.1 Medical History . . . . . . . . . . . . . . . . . . . . . . 5 Associated injuries on the cervical spine,1.3.2 Clinical Signs . . . . . . . . . . . . . . . . . . . . . . . . 6 airway, and digestive tract must always be considered.1.4 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . 6 Always stabilize the neck of patients in all1.4.1 Penetrating Trauma . . . . . . . . . . . . . . . . . 6 types of severe cervical trauma until the14.4.2 Blunt Trauma . . . . . . . . . . . . . . . . . . . . . . . . 7 entire spectrum of injuries is known.1.5 Management and Treatment . . . . . . 8 If the patient is stable angiography should1.5.1 Management Before Treatment . . . . . 8 always be performed in penetrating inju- Management in the Emergency ries to zones I and III. Department . . . . . . . . . . . . . . . . . . . . . . . . . 8 If available, duplex or angiography is rec- Airway Obstruction . . . . . . . . . . . . . . . . . 8 ommended in zone II injuries in order to1.5.1.3 Immediate Operation select between conservative and surgical or Further Diagnostic Work-up? . . . . . 9 management. Which Patients Can Be Safely Transported? . . . . . . . . . . . . . . . . . 91.5.2 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . . Preoperative Preparation 1.2 Background and Proximal Control . . . . . . . . . . . . . . . . Exposure and Repair . . . . . . . . . . . . . . . . 11 Traumatic injuries to the cervical vessels are rela- Exploration of Minor Injuries tively uncommon and constitute only about 5–10% and Hematomas . . . . . . . . . . . . . . . . . . . . . 12 of all vascular injuries. In about 25% of patients1.5.2.4 Injuries to the Vertebral Artery . . . . . . 12 with blunt head and neck trauma, the cervical ves- Venous Injury . . . . . . . . . . . . . . . . . . . . . . . . 12 sels are involved. The most common mechanism1.5.2.6 Endovascular Treatment . . . . . . . . . . . . 12 is penetrating injuries, but the incidence of blunt1.5.3 Management After Treatment . . . . . . 12 vascular trauma is probably underestimated be-1.5.4 Results and Outcome . . . . . . . . . . . . . . . 13 cause related symptoms are often vague and not Further Reading . . . . . . . . . . . . . . . . . . . . . 13 recognized. The patients are mostly young, and despite the low incidence, mortality and morbidity are very high. Mortality is, in most series, between 5% and 40%, and persistent neurological conse- quences are reported in up to 80% of patients. Mortality is not only caused by massive bleeding
  • 9. 4 Chapter 1 Vascular Injuries to the Neck and cerebral ischemia due to embolization or The internal carotid artery is involved in more thrombotic occlusion associated with the vascular than 90% of these injuries, most commonly its injury, but also secondary damage to the aerodi- distal parts. Three to ten percent of all carotid gestive tract (e.g., airway compression from a large injuries are caused by blunt trauma. The true inci- expanding hematoma). dence is unknown, but a few reports cite figures The anatomical location and the often complex in the range of 0.1–1.1% of all blunt head and neck associated injuries make traumatic cervical vascu- injuries. The variation is related to the type of lar injuries extremely challenging. study performed and methodology used; some studies are retrospective, while others use screen- ing with angiography or computed tomography 1.2.1 Causes and Mechanism (CT). Blunt carotid injuries occur in motor vehi- cle, industrial accidents or after assaults. Injuries Penetrating Trauma to the vertebral artery are less common because The most common mechanism for cervical vascu- they are well protected by osseous structures. In- lar injuries is penetrating trauma. As shown in juries to the vertebral arteries are most commonly Table 1.1, the common carotid is the most fre- caused by intraoral trauma dislocated fractures or quently injured major artery. The type of penetrat- penetrating trauma. The mechanisms are the same ing trauma is most often stab wounds by knives, as in the internal carotid artery. but other mechanisms are high- or low-velocity The mechanism of injury is either a direct projectile and gunshot wounds, and bone frag- blow or hyperextension and rotation of the neck. ments from fractures. High-velocity penetrating In the latter type, the internal carotid artery is trauma can also cause secondary “blunt” injuries stretched over the body of the C2 vertebra and by a shock wave. the transverse process of C3, which causes an inti- mal flap with subsequent risk for embolism or dis- Blunt Trauma section and thrombotic occlusion. Other conse- Blunt trauma to the cervical vessels is thought to quences are development of a pseudoaneurysm be less than 0.5% of all blunt traumas to the body, or, in rare cases, even complete disruption of the but recent reports indicate that many blunt vascu- internal carotid at the base of the skull. In some lar injuries go undetected. reports, up to 50% of patients are reported to have bilateral vascular injuries after blunt trauma to the neck. Carotid dissection is also reported to occur after minor head and neck trauma, and to be associated with activities such as unaccustomed Table 1.1. Frequency of vessel and associated organ physical exercise; “heading” a soccer ball and injuries in penetrating injuries to the neck childbirth. Site of injury Major vessels 1.3 Clinical Presentation Arteries Common carotid artery 73% (10–15%) Internal carotid artery 22% External carotid artery 5% Common to all neck trauma is that many patients with severe vascular or other injuries present with Veins External jugular 50% (15–25%) Internal jugular 50% a clinical picture deceptively lacking obvious symptoms and signs of their injuries. Further- Other organs more, significant associated intracranial lesions, Digestive tract 5–15% multiple organ injuries, and alcohol or drug in- Airway 4–12% toxication often confuse the clinical picture. The Major nerves 3–8% history and clinical examination must be per- No involvement 40% formed with a high level of suspicion in order to of important structures achieve a good platform for the diagnostic evalua- tion and management.
  • 10. 1.3 Clinical Presentation 5 1.3.1 Medical History hours or days from the injury to the appearance of neurological symptoms is common after bluntKnowing the mechanism of injury can provide carotid trauma. A frequent type of symptom is aimportant clues to the type of and potential vascu- typical transient ischemic attack but completelar injury. Information about the type and extent stroke or amaurosis fugax also occurs.of trauma should be obtained from the patient, Because the carotid is the most common in-paramedics, or relatives. In penetrating injuries, jured artery, it is essential to assess the patient’sinformation about external bleeding is important: mental status, including possible alterations dur-the magnitude and volume (brisk and pulsating or ing transport as well as transient, progressive, oroozing), the color (dark venous or bright arterial), permanent focal neurological changes. It is alsoand the duration (initial but stopped or ongoing). important to inquire about symptoms related toIn cases of brisk bleeding, injuries to the carotid associated cranial nerve injuries (see Table 1.2).artery or larger veins are likely. Symptoms of hy- Difficulties or pain with swallowing suggestpovolemia or shock during the course from inci- an esophageal injury and should increase the sus-dent to admission indicate significant blood loss. picion for associated vascular injuries. In bluntRespiratory problems indicates the presence of a carotid injuries, headache and/or cervical painlarge hematoma compressing the airway, which are the most common symptoms, followed bycould require immediate attention and manage- symptoms indicating cerebral or retinal ischemiament. A history of a symptom-free interval of (see Table 1.3). Neck wounds or bleeding from theTable 1.2. Examples of findings and symptoms in neck injuries Injury type Signs Symptoms Vascular penetration Artery or vein Bleeding, hematoma, swelling Bleeding, pain Carotid or vertebral Horner’s syndromea Hanging eye lid, headache Bleeding with tracheal Stridor, supraclavicular Dyspnea compression and intercostal retractions Embolization Hemiplegia/hemiparesis Weakness, numbness Arteriovenous fistula Bruit or thrill Swelling Cranial nerves Glossopharyngeal nerve IX Pharyngeal paresis, soft palate Difficulty swallowing hanging down Vagal nerve X Vocal cord paresis Hoarseness Accessory nerve XI Unable to shrug the shoulders Weakness Hypoglossal nerve XII Tongue deviation toward Difficulty swallowing the injured side Aerodigestive tract Subcutaneous emphysema Shortness of breath. Difficulty or pain with swallowing Hemoptysis Mandibular fracture Tenderness Pain, difficulty speakinga Caused by disruption of the blood supply (vasa vasorum) to the superior cervical ganglion or by direct injury to the sympathetic nerve plexus
  • 11. 6 Chapter 1 Vascular Injuries to the Neck Table 1.3. Consequences of blunt injuries to the carotid artery Type of injury Mechanism Consequences Symptoms/signs Direct blow Rupture Hematoma Swelling and respiratory problems Pseudoaneurysms Bruit, swelling Intimal tear Thrombosis Stroke, focal neurology Rotation-extension Intimal tear Dissection Stroke, focal neurology Thrombosis Stroke, focal neurology mouth, nose, or ears after severe blunt cervical vascular injury are tenderness over the carotid trauma may be associated with injuries to the ver- artery and in the scalp. The most common associ- tebral artery. ated injury is fracture of the mandible. NOTE 1.3.2 Clinical Signs The physical examination can be negative despite severe vascular injury after blunt A penetrating injury is usually obvious at inspec- cervical trauma. tion of an open wound with signs of recent or on- going bleeding. A “sucking wound” suggesting a connection with the aerodigestive tract indicates 1.4 Diagnostics an increased risk for “proximity” injuries to the major cervical arteries (i.e., the vertebral arteries). 1.4.1 Penetrating Trauma Even minor external signs of penetrating trauma can be associated with a severe underlying vascu- The location of penetrating cervical injuries are lar injury. One example is the expanding hemato- generally divided into three different zones that ma. The reverse however, is also possible – a large are helpful for planning the diagnostic work-up hematoma compressing adjacent structures har- and management (Fig. 1.1). It is therefore impor- bored by the stiff fascial layers of the neck but tant to classify the localization of the injury into undetectable at inspection. Sometimes signs of zones according to this subdivision. The rationale airway obstruction reveal such injuries. Signs and for this lies in difficulties achieving proximal con- symptoms of penetrating cervical vascular trauma trol in zone I injuries and distal control in zone III. are summarized in Table 1.2. Exploration and the possibility of obtaining con- Half of the patients with significant blunt vas- trol are much easier in zone II injuries. cular injuries to the neck lack symptoms at admis- Patients with “hard signs” of major vessel inju- sion but develop symptoms and signs within 24 h. ry – shock, active brisk bleeding, rapidly expand- In blunt trauma, it is therefore important to per- ing hematoma (for discussion about the definition form a careful neurological examination at admis- of “expanding hematoma,” see Chapter 12, p. 149) sion to obtain a baseline for later comparisons at – and those with neurological deficit or severe the mandatory repeated examinations. The neu- airway obstruction should be transported to the rological evaluation should seek signs of central as operating room for immediate exploration and well as peripheral nerve injuries – alertness, motor treatment. and sensory function, reflexes in the extremities Patients with “soft signs” of major vessel injury – as well as signs of cranial nerve dysfunction (Ta- – history of bleeding, stable hematoma, and/or ble 1.2). It is important to thoroughly inspect for cranial nerve injury – usually need further work- signs of contusion, asymmetry, or deformity that up. This is also true for patients who don’t have indicate underlying hematomas and to note the signs, but who have an injury in proximity to ma- hematoma size for later estimation of possible jor vessels. This group constitutes the majority of expansion. Other physical findings indicating a penetrating neck injuries. The following recom-
  • 12. 1.4 Diagnostics 7 tomas. Altered flow patterns indicating high resis- tance or abnormal turbulence can be associated with a lesion distally in the internal carotid artery. The developing experience of the duplex technique has prompted a policy change in some hospitals, and duplex ultrasound is used as the primary diagnostic tool for all injuries in stable patients. This examination is performed prior to the deci- sion about angiography or surgical exploration and irrespective of anatomic zone. In some cen- ters, therapeutic decisions are based on thin-slice high-speed CT scans instead. Gunshot wounds deserve special comment. All patients with such injuries should be screened with angiography or duplex ultrasound. Because associated injuries are common, CT scanning of the head, surgical spine, and aerodigestive tract should also be included in the diagnostic work- up.Fig. 1.1. Division of the neck into three zones aids in NOTEthe management of penetrating cervical vascular inju- Injuries not penetrating the platysmaries (Monson DO, Saletta JD, Freeark RJ. Carotid-verte- need no further vascular evaluation.bral trauma. J Trauma 1969; 9:987–999). Zone I extendsinferiorly from 1 cm above the manubrium to includethe thoracic outlet; zone II extends from the upper limitof zone I to the angle of the mandible; and zone III is 1.4.2 Blunt Traumabetween the angle of the mandible and the base of theskull The diagnosis of vascular injuries after blunt trau- ma is much more challenging. As previously not- ed, clinical signs and symptoms are frequently subtle or absent, and initial transient or late neu-mendations have been generally accepted in these rological deficits are common. The most com-cases: monly injured vascular segment is the distal inter- Zones I and III: With the exception of unstable nal carotid artery. Dissection, with varying de-patients, angiography is always indicated. The grees of luminal narrowing, is the most commongoals are detecting injury, planning an operation injury. Other types are pseudoaneurysm or evenpossibly requiring special exposures (e.g., intra- total transection of the artery with free extravasa-thoracic clamping), and excluding indications for tion. If an expert ultrasonographer is available,operation. duplex ultrasound can be considered as a primary Zone II: Injuries penetrating the platysma in screening method, but a negative study cannot bethis zone require surgical exploration to identify relied upon to exclude the presence of a clinicallyand treat vascular injuries as well as injuries to the significant injury. For all other patients, the rec-aerodigestive tract unless the patient is asymp- ommendation is angiography as the first option,tomatic and angiography, duplex ultrasound, and as it is still the gold standard.CT have ruled out such injuries. In all patients with basilar skull fractures, un- Duplex ultrasound in the hands of an experi- stable cervical spine fractures, Horner’s syndrome,enced examiner has been shown to be consistent or LeFort-II or-III facial fractures, recent studieswith angiography findings in more than 90% of advocate a more aggressive attitude with angio-cases. It can reveal dissections, thrombotic occlu- graphic screening for blunt carotid injuries. Extra-sion, intimal flaps, pseudoaneurysms, and hema- cranial carotid injuries are also reported to be
  • 13. 8 Chapter 1 Vascular Injuries to the Neck NOTE A patient with neck trauma and a possible vascular injury who is stable, has stabi- lized after resuscitation, or has a trans- cervical gunshot injury should undergo a selective aortic arch angiography. 1.5 Management and Treatment 1.5.1 Management Before Treatment Management in the Emergency Department As with other major trauma, the Advanced Trau- ma Life Support guidelines should be followed for severe cervical vascular injuries. Consequently, airway and respiration have first priority, followed by control of bleeding. Control of bleeding is best achieved by external finger or manual compres- sion applied directly to the bleeding site. Blindly applied clamps should not be attempted because of the risk of iatrogenic injuries to blood vessels as Fig. 1.2. Angiography showing a dissection of the well as to other organs. internal carotid artery resulting in a narrowing of the lumen with the typical “string sign” appearance (ar- Resuscitation to hemodynamic stability is im- rows) portant. Hypertension may increase bleeding and also induce progress of a dissection, while hypo- tension will increase the risk for thrombosis and more common in patients with a Glasgow coma cerebral malperfusion. scale of 8 or less and thoracic injury. A typical finding at angiography in caroid dissection is a Airway Obstruction stenosis, irregular and often tapered, beginning Patients with neck trauma and airway obstruction 2 or 3-cm distal to the bifurcation and often ex- require meticulous management and close co- tending up to the base of the skull, above which it operation with the anesthesiologist. Intubation is abruptly reconstituted with a normal lumen. should be performed in an anesthetized patient to Occasionally a typical “string sign” can be seen in avoid gagging, which might discharge clots and the stenosed segment (Fig. 1.2). thus cause profuse bleeding or embolization. Cau- CT is not reliable for diagnosing blunt cervical tion should also be taken when the patient’s neck vascular injuries. CT angiography is under devel- is flexed at the intubation because of the risk of opment and is likely to play a greater role in the associated cervical vertebral fractures. There is an future. It has the advantage of short examination obvious risk for dislocation and spinal injury. The times and concurrent diagnosis of other injuries, intubation might also be technically challenging such as brain injuries and skull or facial fractures. because a large hematoma might cause total com- Magnetic resonance imaging (MRI) has a high pression of the trachea. Emergency tracheotomy sensitivity and specificity in relation to angiogra- or coniotomy is then the only alternative, but it phy (95% and 99%, respectively) for detecting may also be complicated by the deranged anatomy blunt carotid injuries, as does MR angiography and risk of bleeding. The risk of profuse uncon- (84% and 99%), but both are time-consuming and trolled bleeding is greatest if the hematoma is complicate monitoring and resuscitation of the located on the anterior aspect of the neck because critically injured patient. the tamponade will be immediately lost when the
  • 14. 1.5 Management and Treatment 9pretracheal fascia is incised. By using liberal intu- employed. Anticoagulation therapy, antiplateletbation early on and under controlled conditions, therapy, or both should also be initiated.such situations could be avoided. Management of significant carotid artery in- jury existing with major neurological deficit and Immediate Operation coma is controversial. Some surgeons suggest only or Further Diagnostic Work-up? observation and palliation, especially in patientsThe surgeon has to decide in the emergency de- with CT-verified cerebral infarction, because ofpartment whether the patient requires immediate the poor prognosis. Others advocate repair. Thisoperation, further diagnostic examination, or standpoint is based on the difficulties of decidingcontinued observation. whether the vascular trauma, cerebral contusion, It is important to emphasize that although or drugs caused the coma. Some reports, however,standard teaching has been that exploration is re- indicate a possibility of better outcome after ex-quired for all zone-II injuries that penetrate the ploration and repair.platysma, as well as for gunshot wounds that cross When the carotid artery is occluded and therethe midline, the availability of better diagnostic are no neurological symptoms, observation andmodalities has permitted the use of selective ex- anticoagulation with heparin followed by 3 toploration protocols. 6-months of coumadin is a general treatment The following recommendations are given for irrespective of the type of trauma. In patientsthis initial selection: with major neurological symptoms and a verified1. Immediate operation is indicated for unstable infarction on CT, anticoagulation is associated patients with active bleeding not responsive to with a considerable risk for bleeding. The patients vigorous resuscitation or with rapidly expand- prognosis is then poor, and palliation is recom- ing hematoma or airway obstruction, irrespec- mended. tive of anatomical zone. In blunt trauma, indications for exploration2. Injuries in zone II not penetrating the platysma and open repair are rarer due to the mostly distal need no further examination. location of injuries to the internal carotid artery.3. All others require further diagnostic evalua- For asymptomatic injuries, including dissection, tion with angiography, duplex ultrasound, and anticoagulation is usually the only treatment need- CT to determine whether critical structures ed and is indicated to prevent thrombosis of the have been injured. If angiography or high-qual- injured segment and/or embolization from it. Only ity duplex ultrasound is not available, injuries injuries that after angiography appear to be easily in zone II need to be surgically explored. accessible during surgery and are symptomatic should be considered for repair. This is particu-Depending on the results of these diagnostic stud- larly important when there appears to be a highies, the following general recommendations can be risk for embolization. In patients with decreasedgiven regarding management of vascular injuries. consciousness having an occluded internal carotid Repair is recommended in all patients with artery after blunt trauma and with no, or with se-penetrating carotid injuries when there is still evi- vere, neurological symptoms, most reports advo-dence of prograde flow and the patient has no ma- cate only observation without surgical exploration.jor neurological symptoms. For minor injuries to As already mentioned, however, some do recom-the carotid artery, including those with small but mend a more aggressive approach. This strategyadherent intimal flaps, defects, or pseudoaneu- requires extensive experience in carotid surgery.rysms <5 mm in size, repair is recommended insymptomatic patients. If the patient is asymptom- Which Patients Can Be Safelyatic and there is no ongoing active bleeding, a con- Transported?servative approach has proven to be a safe alter- Because cervical vascular injuries often require annative. The patient needs to be followed on an experienced vascular surgeon, a thoracic surgeon,inpatient basis for a couple of days to monitor for an endovascular specialist, and frequently also athe appearance of neurological symptoms. Liberal specialist in head and neck surgery, some patientsindications for repeated duplex examination are would benefit from being transported to a hospital
  • 15. 10 Chapter 1 Vascular Injuries to the Neck where such expertise is available. A stable patient bectomy catheters is not recommended because of can be transported to another hospital after intu- the risks of mechanical disruption of the throm- bation, or with readiness for emergency intubation bus and bringing fragments up into the circle of in the ambulance, with no major risks. An unsta- Willis. Clamping of the external carotid artery is, ble patient should, of course, remain where he or on the other hand, almost always safe and can be she is. used more liberally. TECHNICAL TIPS 1.5.2 Operation Surgical Exposure of the Carotid Arteries Preoperative Preparation and Proximal Control An incision anterior and parallel to the anterior The management of patients with major external border of the sternocleidomastoid muscle is bleeding is mostly related to penetrating injuries recommended (Fig. 1.3). The incision can be ex- to the carotid artery. Surgical exposure of this tended dorsal to the ear and down to the sternal artery is described in the Technical Tips box. It is notch. As previously noted, preparations need important to prepare and drape the patient for to have been made to allow elongation of the possible median sternotomy, which might be nec- incision into a median sternotomy in order to essary to obtain proximal control. Bleeding can obtain proximal control of, for instance, the bra- usually be controlled by external compression by a chiocephalic trunk on the right side or the com- gloved finger during the preparation and until the mon carotid on the left. After the skin has been complete surgical team is at hand. In the rare and incised, subcutaneous fat is divided and, if need- challenging circumstance in which this is impos- ed, the external jugular vein ligated and divided. sible, a nonspecialist surgeon might be forced to The sternocleidomastoid muscle is retracted attempt exposure and control of the artery proxi- posteriorly, and a dissection plane anterior to mal to the injury through a separate incision with the muscle is identified. The next structure to continued external finger compression over the identify is usually the facial vein and its conflu- lesion by an assistant. During control by direct ence to the internal jugular vein. The former is finger compression of the artery, care must be suture-ligated and divided and is usually a very taken to minimize manipulation because of the good landmark because it is located just above risk of thrombus fragmentation and embolization. the carotid bifurcation. Dividing this vein allows Compression also needs to be balanced with the posterior retraction of the internal jugular vein desire to maintain flow in the artery. Clamping and exposure of the common carotid and its the common or internal carotid artery for control bifurcation. When preparing the carotid arteries, might be necessary but should be avoided unless extreme care must be taken to avoid squeezing the patient’s condition is life-threatening. The rea- of the vessel, and other types of operative ma- son for this is the risk of embolization and cerebral nipulation or trauma because of the risk of em- ischemia due to interrupted flow. Inserting a shunt bolization to the brain. Vessel loops are applied, may be the only way to avoid a major stroke; the and the most cranial clamp is applied first to risk of major stroke in this patient category after avoid embolization when the more proximal carotid clamping may be as high as 50%. Shunting parts are clamped. Important structures to pro- usually requires proximal and distal control, tect are the hypoglossal and vagus nerves. The arteriotomy, and possibly also extraction of the former usually crosses over the internal carotid thrombus before inserting the shunt. Extracting a artery 2–3 cm cranial to the bifurcation and is thrombus requires a delicate technique and spe- best exposed after cranial retraction of the di- cial consideration because it can easily be frag- gastric muscle. The latter runs parallel and dorsal mented and dislodged as embolic masses. The to the common carotid artery. The cervical ansa, safest way is to use traction with forceps and/or often located obliquely over the carotid bifur- suction. If the extraction is followed by brisk back- cation, can be divided to facilitate exposure. flow, the result is satisfactory. The use of throm-
  • 16. 1.5 Management and Treatment 11Fig. 1.3 a Recommended incision for exposure of the dorsal to the ear. b The normal anatomy and relationscarotid arteries, anterior and parallel to the anterior between major arteries, veins, and important nerveborder of the sternocleidomastoid muscle. The incision structures at exposure of the carotid and jugular ves-can be extended into a median sternotomy or cranially sels Exposure and Repair Resection with end-to-end anastomosis: This isFor larger arterial injuries, proximal and distal possible in limited injuries requiring minor re-control is mandatory. This always requires an in- sections, allowing an anastomosis without anydirect assessment of the cerebral perfusion by tension.checking the backflow from the internal carotid Resection with an interposition graft: Whenartery. Measuring the stump pressure in the inter- larger segments must be excised because of thenal carotid artery is recommended if there is injury, continuity might be restored with an au-sufficient time. This is obtained by first clamping tologous vein graft harvested from the greaterthe common and external carotid arteries and saphenous vein or with prosthetic grafts for un-then puncturing the internal carotid artery with contaminated wounds.a small-caliber injection needle connected to a Transposition of external to internal carotidcatheter filled with saline and a pressure trans- artery: This is a good alternative in special cas-ducer. If the backflow is poor or the mean stump es in which vein grafts are unavailable.pressure is <50 mmHg, shunting is probably nec- Ligation or balloon occlusion: Ligation shouldessary. be reserved for inaccessible injuries that are im- Different repair techniques include the follow- possible to repair. In cases with very distal inju-ing: ries to the internal carotid artery, even ligation Simple suture: Simple sutures are mostly suffi- might be difficult. An occluding balloon cath- cient in minor penetrating injuries or small eter can then be inserted into the artery at the pseudoaneurysms. base of the skull and insufflated until bleeding Patch: A patch can be used for a minor wall de- stops. The balloon catheter can be left in place fect or to compensate for diameter loss after for 1 to 2 days or more and then be deflated and arteriotomy and intimal repair. removed.
  • 17. 12 Chapter 1 Vascular Injuries to the Neck Exploration of Minor Injuries Endovascular Treatment and Hematomas As already described in sections and, A patient with an injury penetrating the platysma endovascular technique is an alternative to con- in anatomical zone II without a history of bleeding sider in some cervical vascular injuries. Endovas- may be explored by extending the traumatic skin cular treatment is the first option in injuries to the wound to allow inspection of the injured area, vertebral artery due to its location and surgical in- including vessels, trachea, and esophagus. If, how- accessibility. The application of detachable bal- ever, duplex ultrasound or angiography excludes loons, coils, stents, or hemostatic agents is usually a major vascular injury, there is no vascular indi- successful for managing bleeding, aneurysms, and cation for exploration. Patients with a history of fistulas. Endovascular techniques have also been significant bleeding as well as those with large reported to be successful for managing some ca- hematomas should be treated according to what rotid artery injuries (such as traumatic lacera- has been described above for proximal control, tions), pseudoaneurysms, and injuries in some before exploring the wound and evacuating the noncritical and small terminal branches. If endo- hematoma. vascular occlusion of an internal carotid artery is considered in severe traumatic injuries, the neuro- Injuries to the Vertebral Artery logic effect of a temporary occlusion should be Due to its relatively inaccessible location, injuries evaluated prior to occlusion. It is reasonable to be- to the vertebral artery in the cervical region are lieve that the endovascular treatment option will usually best treated by modern endovascular become even more useful in the near future. techniques. The options are intraluminal covered stents or endovascular embolization with coil. Be- sides bleeding and hematomas, pseudoaneurysms 1.5.3 Management After Treatment and arteriovenous fistulas can occur after verte- bral artery trauma and also be successfully treated As in elective carotid surgery, monitoring and cor- by transcatheter embolization. In unstable pa- recting blood pressure is important to minimize tients with life-threatening bleeding, immediate risks for bleeding and cerebral complications. intervention with proximal and distal ligation Most common are thrombosis and reperfusion might be necessary. problems. Acceptable postoperative systolic blood pressure limits are 100–180 mmHg. Venous Injury The patient should be checked for clinical signs Major venous injuries in the neck are almost ex- and symptoms of embolization, and if emboliza- clusively seen after penetrating trauma. The most tion is suspected, the operated artery should be commonly injured veins are the external and in- checked with ultrasound for complications that ternal jugular. Due to the low pressure in veins, might need urgent repair. many such injuries are never recognized. Isolated Antiplatelet and/or anticoagulation therapy venous injuries consequently rarely need explora- should be considered to maintain patency in re- tion or repair. Venous injuries encountered during constructed arteries and to avoid thrombosis in exploration of a neck injury can be treated either bluntly injured but still patent vessels. by repair using simple or running sutures or by Traumatic and surgical wounds should be ligation. In bilateral injuries to the internal jugular checked for signs of a developing hematoma and veins, however, reconstruction of one of the sides infection. The latter is particularly important in is indicated to avoid severe venous hypertension. contaminated wounds and when repair has in- As in all other types of venous surgery, gentle and cluded the use of prosthetic material. Antibiotic meticulous technique must be applied and caution treatment should be given liberally to avoid the taken not to extend the injuries to the veins by a development of severe deep infections in penetrat- traumatic technique. (See Chapter 15 on vascular ing cervical injuries. For the same reason, meticu- surgical technique.) lous wound care is important.
  • 18. 1.5 Management and Treatment 13Table 1.4. Stroke and mortality rates after different grades of blunt carotid and vertebral artery injuries. (FromBiffl et al. Ann Surg 2002; 235: 699–707) Injury grade/description Carotid artery injury Vertebral artery injury Stroke Death Stroke Death I Luminal irregularity 3% 11% 19% 31% or dissection, <25% narrowing II Dissection or intramural 11% 11% 40% 0 hematoma, >25% narrowing or intraluminal thrombus or raised intimal flap III Pseudoaneurysm 33% 11% 13% 13% IV Occlusion 44% 22% 33% 11% V Transection and free extravasation 100% 100% – – nation of other major injuries. Mortality directly 1.5.4 Results and Outcome related to vertebral artery injuries has been report- ed to be as low as 4%.Several authors report better results after repair ofpenetrating injuries to the carotid artery com-pared with ligation, with regard to neurological Further Readingoutcome (44% vs. 16% neurologically intact) andmortality (5% vs. 11%). Baumgartner RW, Arnold M, Baumgartner I, et al. Ca- The results of conservative treatment of carotid rotid dissection with and without ischemic events;dissection, the most common type of injury after local symptoms and cerebral artery findings. Neu- rology 2001; 57:827–832blunt trauma, are generally good with duplex-veri- Biffl WL, Ray CE, Moore EE, et al. Treatment relatedfied resorption of intramural hematoma within outcomes from blunt cerebrovascular injuries. Ann3 months of anticoagulation. The key to this is Surg 2002; 235:699–707early detection, preferably before the onset of Demetriades D, Theodorou D, Ascentio J. Managementsymptoms, and institution of a heparin infu- options in vertebral artery injuries. Br J Surg 1996;sion followed by oral anticoagulation for at least 83:83–863 months. Table 1.4 above summarizes the experi- Demetriades D, Theodoru D, Cornwell E, et al. Evalua- tion of penetrating injuries to the neck: prospectiveence of Biffl and colleagues at Brown Medical study of 223 patients. World J Surg 1997; 21:41–48School (Rhode Island Hospital, Providence, RI, Gomez CR, May K, Terry J B, et al. Endovascular thera-USA) from 109-patients with carotid injuries. py of traumatic injuries of the extracranial cerebral Recent series report good results in managing arteries. Crit Care Clin 1999; 15:789–809cervical vascular injuries, irrespective of zone, Kreker C, Mosso M, Georgiadis D, et al. Carotid dissec-with only careful physical examination, but the tion with permanent and transient occlusion or se-general impression is that it is too early to elimi- vere stenosis: long term outcome. Neurology 2003;nate angiography and duplex ultrasound from the 28:271–275 Mwipatayi BP, Jeffery P, Beningfield SJ, et al. Manage-work-up. ment of extra-cranial vertebral artery injuries. Eur J As seen, there is a correlation between the inci- Vasc Endovasc Surg 2004; 27:157–162dence of stroke and mortality in carotid injuries Navsaria P, Omoshoro-Jones J. An analysis of 32 surgi-that is not found in injuries to the vertebral artery cally managed penetrating carotid artery injuries.and the posterior circulation. Overall mortality Eur J Vasc Endovasc Surg 2002; 24:349–355after vertebral artery injuries seems to be around Reid J, Weigfelt J. Forty-three cases of vertebral artery20%, but this is usually in patients with a combi- trauma. J Trauma 1988; 28:1007–1012
  • 19. 14 Chapter 1 Vascular Injuries to the Neck Romily RC, Newell DW, Grady MS, et al. Gunshot Singh RR, Barry MC, Ireland A, et al. Current diagnosis wounds of the internal carotid artery at the skull and management of blunt internal carotid artery in- base: management with vein bypass grafts and a jury. Eur J Vasc Endovasc Surg 2004; 27:577–584 review of the literature. J Vasc Surg 2001; 33:1001– 1007 Sekharan J, Dennis JW, Veldenz H, et al. Continued ex- perience with physical examination alone for evalu- ation of penetrating zone 2 neck injuries; result of 145 cases. J Vasc Surg 2000; 32:483
  • 20. Vascular Injuries to the Thoracic Outlet Area 2CONTENTS 2.1 Summary2.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Always exclude injuries to the great2.2 Background . . . . . . . . . . . . . . . . . . . . . . . . . 15 thoracic aortic branches after injury to the2.2.1 Magnitude of the Problem . . . . . . . . . . 16 cervical, clavikular and thoracic regions2.2.2 Etiology and Pathophysiology . . . . . . 16 One third of patients who survive thoracic2.2.2.1 Penetrating Trauma . . . . . . . . . . . . . . . . . 16 vascular trauma has minor or lack external2.2.2.2 Blunt Trauma . . . . . . . . . . . . . . . . . . . . . . . . 16 signs of thoracic injury.2.3 Clinical Presentation . . . . . . . . . . . . . . . 17 A plain chest X-ray shall be performed2.3.1 Medical History . . . . . . . . . . . . . . . . . . . . . . 17 in all patients with thoracic injuries2.3.2 Clinical Signs . . . . . . . . . . . . . . . . . . . . . . . . 17 Moderate restoration of BP to 100– Physical Examination . . . . . . . . . . . . . . . . 18 120 mmHg is advisable to avoid rebleed- ing2.4 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . 18 Be liberal with insertion of a chest tube2.5 Management and Treatment . . . . . . 19 in patients with moderate or severe hemo-2.5.1 Management Before Treatment . . . . . 19 thorax2.5.1.1 Management in the Emergency Department . . . . . . . . . . . . . . . . . . . . . . . . . Patients in Extreme Shock . . . . . . . . . . . Unstable Patients . . . . . . . . . . . . . . . . . . . 22 2.2 Background2.5.1.4 Control of Bleeding . . . . . . . . . . . . . . . . . Stable Patients . . . . . . . . . . . . . . . . . . . . . . 23 This chapter is focused on injuries to the intratho- Nonsurgical Management . . . . . . . . . . 24 racic parts of the great aortic branches, from their2.5.2 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 origin in the aortic arch to the thoracic outlet. It2.5.2.1 Preoperative Preparation also includes the retroclavicular vessels – the dis- and Proximal Control . . . . . . . . . . . . . . . . 24 tal subclavian and the proximal axillary arteries. Exposure and Repair . . . . . . . . . . . . . . . . 25 These injuries are often difficult to diagnose and2.5.2.3 Endovascular Repair and Control . . . 27 distinguish from aortic arch injuries (i.e., injuries2.5.3 Management After Treatment . . . . . . 28 to the aorta, the pulmonary vessels, and the heart2.6 Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29 itself). Because cardiothoracic surgeons and not vascular surgeons usually manage the latter, they Further Reading . . . . . . . . . . . . . . . . . . . . 29 will not be covered here. A vascular injury to this region of the body is less common but is associated with high mortality. Many patients die at the scene of the accident or are in extremely bad condition at arrival in the emergency department. Accordingly, they regu- larly require immediate thoracotomy, but many patients are stable and possible to work up and can be treated without surgery. Most hospitals do not
  • 21. 16 Chapter 2 Vascular Injuries to the Thoracic Outlet Area have a thoracic surgeon on call; therefore, these juries often remain unrecognized. Arteriograms patients are often initially managed by general in patients with a widened mediastinum on plain surgeons with limited experience in thoracic or x-ray after thoracic trauma have been found to be vascular surgical procedures. Basic information negative for arterial injuries in 85%; this suggests about exposure and access routes and ways to that the mediastinal enlargement was caused achieve proximal and distal control of intratho- mainly by venous injury. racic great vessels is important not only in this situation but also to obtain proximal control of NOTE bleeding vessels in cervical and proximal upper Injuries to subclavian and axillary arteries extremity vascular injuries (these areas are dis- are most common after penetrating cussed in Chapters 1 and 3). Good anatomical trauma. knowledge, including that of common variations, is critical, especially for the difficult exposures of the subclavian and axillary vessels, such as when 2.2.2 Etiology and Pathophysiology the right subclavian artery originates directly from the aortic arch or has a common trunk with the right carotid artery. Penetrating Trauma Knife stabbings or missiles from firearms cause a NOTE majority of injuries to the great vessels. In this Anatomical aortic arch and branch type of penetrating trauma, all intrathoracic ves- variations can be expected in 25–35% sels are at risk of being injured. The extent of inju- of cases. ries is related to aspects of the weapon, such as the length of a knife or the velocity (high vs. low) and caliber (small vs. large) of a gun. The innominate 2.2.1 Magnitude of the Problem artery is injured mostly by bullets from firearms. Stab wounds by knives directed inferiorly into the The number of thoracic injuries (all types includ- right clavicular region may also damage the in- ed) is steadily increasing in the United States and nominate artery. The same mechanisms are com- is estimated to be 12 per million inhabitants per mon for injuries to the subclavian and proximal year. In penetrating neck and chest injuries, 3% axillary arteries. Stab wounds are associated with are associated with injuries to the subclavian and a better chance of survival than are injuries from axillary arteries, and in 20% of those injuries, firearms, particularly shotguns. Blood loss after a veins are also injured. In a meta-analysis of 2,642 knife injury is often limited by a sealing mecha- civilian cases of penetrating thoracic trauma, the nism in the wound channel. Furthermore, if the incidence of great vessel injuries was 1% innomi- vascular injury is small, the adventitia also limits nate artery, 5% subclavian, and 6% axillary artery the bleeding. injuries. But because many patients die at the The development of hypotension is another scene, particularly after penetrating trauma, these factor contributing to limited blood loss. Injuries numbers are uncertain. Irrespective of the type of to the major blood vessels in the thoracic outlet are injuries, trauma to the thoracic great vessels is always challenging because they are rare and tech- associated with a high mortality: 80–90% die at nically difficult to expose and control. This is re- the scene. The mortality among patients who flected in the high mortality reported in the litera- survive transport to the hospital is also high. ture. Patients with injuries in the distal parts of the intrathoracic arteries have a better chance of sur- Blunt Trauma vival because these vessels are covered with soft Blunt trauma to the intrathoracic vessels occurs in tissue, providing better prerequisites for sponta- motor vehicle and industrial accidents and in falls neous tamponade. from heights. If it leads to total disruption of the More proximal injuries increase the risk for ex- vessel, the patient will exsanguinate at the scene. sanguination into the pleural cavities. Venous in- When the adventitia remains intact, the possibility
  • 22. 2.3 Clinical Presentation 17of survival is better. The mechanism is shear motor vehicle, use of a safety belt, or the height ofcaused by acceleration/deceleration or compres- a fall can indicate the risk for intrathoracic vascu-sion forces. Deceleration forces are associated with lar injuries.injuries to the aorta but may also cause injuries to When deciding whether immediate thoracoto-the innominate artery. The innominate and com- my is needed, the course of transport and timemon carotid artery might be exposed to shear elapsed from injury to admission is always offorces at their origin from compression of the an- potential importance.terior chest wall. The subclavian and axillary ar-teries can also be injured by blunt trauma, andthen mostly in association with clavicle or 1st-rib 2.3.2 Clinical Signsfractures. Other possible mechanisms are hyper-extension combined with neck rotation, causing As in other vascular injuries, the following “hardtension and stretching of the contralateral subcla- signs” strongly indicate severe vascular injury:vian vessels. Alternative mechanisms include Severe bleedingstretching over the clavicle. Blunt injuries to the Shock or severe anemiasubclavian artery after deceleration trauma are Expanding hematomarare. There are, however, some controversies re- Absent or weak peripheral pulsesgarding the association between 1st-rib fractures Bruitsand injuries to the subclavian vessels. Two series of49 and 55 patients, respectively, reported an inci- “Soft signs” that also indicate vascular injuries in-dence of 14% and 5% of vascular injuries in asso- clude the following:ciation with rib fractures. On the other hand, in a Local and stable hematomalarge cohort of 466 patients only 0.4% was found. Minor continuous bleeding Mild hypotensionNOTE Proximity to large vessels Injuries to large veins in the thoracic Any periclavicular trauma outlet region are associated with a risk of air embolism and if this occurs, Injuries to the large vessels in the thorax are it significantly increases mortality. frequently associated with injuries to the aero- digestive tract. The following signs and symptoms should alert the responsible surgeon to exclude 2.3 Clinical Presentation underlying severe vascular injuries: Air bubbles in the wound 2.3.1 Medical History Respiratory distress Subcutaneous emphysemaThe diagnosis is obvious in most cases of penetrat- Hoarsenessing vascular trauma, but the following informa- Hemoptysistion is important for management. In injuries Hematemesiscaused by a firearm, the type of weapon used(shotgun, hand weapon, high or low velocity, small NOTEor large caliber) and the distance from where it Patients with periclavicular trauma shouldwas fired are relevant. For knife stabbings, the always be suspected to have intrathoracicblade length and size are important, as well as the great vessel injuries.angle and direction in which it struck the body.Stabbings directed inferiorly in the clavicular re- Intrathoracic injuries to the subclavian and axil-gion or at the base of the neck are associated with lary arteries are associated with high increased risk for injuries to the innominate or Like injuries to the thoracic aorta, the presenta-subclavian arteries. tion varies widely, from a fairly stable to a more In blunt trauma, information about the direc- extreme situation with massive bleeding and ex-tion and localization of force, the velocity of the sanguination and death at the scene or during
  • 23. 18 Chapter 2 Vascular Injuries to the Thoracic Outlet Area transport. The latter is more common after blunt bruits. A systolic bruit over the back and upper trauma that causes avulsion of great vessels and chest usually indicates a false aneurysm in any of penetrating trauma to the subclavian artery or the great intrathoracic vessels. A continuous bruit vein. The consequence of subclavian vessel injury indicates the presence of an arteriovenous fistula. is bleeding into the pleural cavity with or without Peripheral pulses, including axillary, brachial, air embolization. At arrival in the emergency de- and radial, should always be examined. They are partment, a patient with a penetrating intratho- normal in about half of cases with significant racic vascular injury is typically hemodynamically vessel injury. Absence of a radial pulse indicates a unstable, whereas a blunt vessel injury is not injury to the axillary, subclavian, or innominate always immediately apparent. arteries, causing occlusion, dissection, or emboli- Blunt injuries to the innominate artery are rela- zation. The latter is occasionally caused by an em- tively rare, and 75% are combined with other inju- bolizing bullet. ries such as rib fractures, flail chest, hemothorax A thorough neurological evaluation is also rel- or pneumothorax, extremity or facial fractures, or evant when considering the possibility of com- head or abdominal injuries in multitrauma cases. bined brachial plexus and vascular injuries. The Because there are no typical clinical signs or symp- absence of a radial pulse in combination with toms, diagnosis is difficult. The only frequent clin- Horner’s syndrome is suspicious for injury to the ical finding is that 50–70% of such patients have a subclavian artery. weak radial or brachial pulse. Distal extremity Coma or major neurological deficits can also ischemia is uncommon, however, due to good col- occur as a consequence of injuries to the innomi- lateral circulation in the shoulder region. This ex- nate and common carotid arteries leading to plains the possibility of having a palpable distal occlusion or embolization and different levels of pulse despite a severe proximal arterial injury. cerebral ischemia. Therefore, it is important to The subclavian artery is usually injured by evaluate the patient’s mental status upon admis- direct trauma associated with first-rib or clavicu- sion. The result influences the decision about if lar fractures that cause occlusion of the artery. and when to perform emergency surgical repair. About half of the patients have a combined injury This evaluation may also be important during the to the brachial plexus. Accordingly, clinical signs course of management as a baseline for later re- and symptoms indicating such neurological inju- evaluations. ries (see Chapter 3, p. 33) should increase the sus- The management and diagnostic work-up in picion of injuries associated with the subclavian the emergency department are strongly related to artery. the condition in which the patient arrives. In these types of injuries, the patient is often in an extreme Physical Examination condition, requiring immediate transfer to the The entire thorax should be inspected for stab operating room for an emergency thoracotomy wounds. It is important not to forget skin folds, or other surgical repair. Thoracotomy may even the axilla, or areas with thick hair. A penetrating be indicated in the emergency department for a trauma to this region is always obvious at arrival dying patient. in the emergency department. It is also important to remember that one-third of patients who sur- NOTE vive blunt trauma and are taken to the emergency One-third of patients who survive blunt department have minor or even no external signs thoracic vascular trauma have minor or of thoracic injury. no external signs of thoracic injury. A pulsatile mass or hematoma at the base of the neck, with or without a bruit, indicates an injury to the subclavian artery with leakage through the 2.4 Diagnostics vessel wall. At physical examination, auscultation can re- At arrival, most patients are in a condition that veal signs of hemothorax or pneumothorax. The necessitates immediate transfer to the operating entire chest and back should be auscultated for room for surgical exploration and treatment. In
  • 24. 2.5 Management and Treatment 19the remaining patients, the diagnostic work-up intrathoracic vessels, why it is important that thedepends on the type of trauma and the patient’s angiography visualizes the entire thoracic aortacondition. In a stable patient, such examinations and its branches. The endovascular treatment ofcan provide information of great importance for these injuries is discussed later in this chapter.the management strategy. A good rule is not to Chest tube placement should have liberal indi-start time-consuming examinations while the cations for diagnostic as well as therapeutic pur-patient is still hemodynamically unstable. poses, as a chest tube can reveal the presence of In a stable patient, plain neck and chest x-rays hemothorax or pneumothorax. The technique isshould always be done to see whether he or she has described in detail in the section on managementany of the following: below. Hemothorax or pneumothorax Widened mediastinum NOTE Irregular outline of the descending aorta A plain chest x-ray should be performed Tracheal dislocation in all patients with thoracic trauma. Blurring of the aortic knob Dilatation of the aortic bulb Presence of bullets or fracture fragments 2.5 Management and Treatment Fractures in cervical vertebrae, clavicles, or ribs 2.5.1 Management Before TreatmentDuplex examination has its limitations for detect-ing injuries to the innominate and subclavian ar- Management in theteries because of their deep intrathoracic location, Emergency Departmentparticularly in obese patients. It is also examiner- Management of these often severely injured pa-dependent, but nowadays a first choice in many tients in shock follows the usual Advanced Trau-centers. Transesophageal echocardiography may ma Life Support principles of trauma resuscita-be valuable for diagnosing aortic injuries, but less tion. The first priority is always airway controlso in injuries to the aortic branches. and resuscitation for hypovolemia. Injuries to the Spiral computed tomography (CT) with intra- great vessels in the thoracic outlet frequently re-venous contrast is mostly used to obtain informa- sult in expanding mediastinal hematoma, causingtion about a missile’s direction and trajectory tracheal compression and requiring emergencythrough the body. The trajectory’s vicinity to great endotracheal intubation.vessels is important when selecting patients for 1. Clear and maintain the airway.angiography. The modern multislice CT angio- 2. Secure ventilation by endotracheal intubationgraphy has the potential to become an important and 100% oxygen.diagnostic tool for providing more detailed de- 3. Consider chest tube insertion.scription of thoracic vascular injuries. 4. Place two or three intravenous lines, preferably Angiography can be diagnostic as well as thera- in the legs and/or the opposite arm.peutic. It reveals the presence and localization of 5. Support adequate circulation by rapid volumeocclusions, bleeding, leakage, or pseudoaneu- replacement with 2.000–3.000 ml of a warmrysms as well as intimal tears. To detect potential balanced electrolyte solution and blood prod-tears and other injuries in the innominate artery, ucts.aortography should be performed with posterior 6. Control bleeding. (See below.)oblique projections. A bulbous dilatation at or just 7. Consider putting the patient in Trendelenburgdistal to its origin and the visualization of an inti- position to avoid air embolism when majormal flap in the lumen indicate a tear injury to the venous injuries cannot be excluded.artery. 8. Insert a Foley catheter. In subclavian injuries, a pseudoaneurysm orocclusion can be found. It is important to remem- As in patients with a ruptured abdominal aorticber that 10% of patients with innominate or sub- aneurysm, resuscitation aims at keeping bloodclavian injuries also have other injuries to great pressure around 100–120-mmHg because of the
  • 25. 20 Chapter 2 Vascular Injuries to the Thoracic Outlet Area risk of sudden massive rebleeding if the blood within minutes) and systolic blood pressure pressure gets too high. Another event posing risk <50 mmHg, and those who experience cardiac ar- for new bleeding during resuscitation is gagging rest in the emergency department. These patients during endotracheal intubation or the insertion of are candidates for thoracotomy in the emergency an esophageal tube. department, aiming at controlling bleeding by If possible, obtain written consent from the pa- manual compression, tamponade, or clamping. tient or his or her family in case emergency sur- This allows more effective resuscitation and is a gery is necessary. The surgical procedure that may last lifesaving effort to improve these patients’ be required often includes clamping of central ar- vital functions enough to allow transfer to the teries, the aorta, or the common carotids, with a operating room for immediate surgery. great risk for severe cerebral and spinal complica- In such an extreme situation, surgeons with no tions. Therefore, it is advisable to alert an experi- or only limited experience in thoracotomy can be enced thoracic and/or vascular surgeon for early forced to choose between the two ultimate alterna- help with management. tives: to open the patient’s chest or to let him or her die. The prognosis for such a patient is, irrespec- NOTE tive of who is performing the thoracotomy, poor, Moderate restoration of blood pressure and the survival rate is only around 5%. This to 100–120 mmHg is advisable to avoid should be weighed against the alternative, which is rebleeding. 100% mortality. More than 20% of patients with injuries to subclavian and axillary vessels are in an Patients in Extreme Shock extreme condition with no vital signs or with im- In this category are patients who, most commonly minent cardiac rest upon arrival to the emergency after penetrating thoracic trauma, have lost con- department. These patients have a very poor prog- sciousness and present with no vital signs despite nosis. resuscitation during the transport but who still show activity on electrocardiography. Other pa- NOTE tients in this category are those with acute thera- Do not hesitate to perform a thoracotomy py-resistant deterioration, those with severe and in the emergency department on a patient persistent shock despite very rapid and aggressive with persistent electrocardiographic volume resuscitation (2.000–3.000 ml of fluids activity but with no detectable vital signs.
  • 26. 2.5 Management and Treatment 21 TECHNICAL TIPS Chest Tube Insertion Start by determining the desired site of insertion. clamp and then expand it with a gloved finger. The recommended site is the 4th or 5th intercostal This is to take precautions against iatrogenic space, landmark the nipple level just anterior to injury to the lung (Fig. 2.1 c, d). the midaxillary line, which is good for draining air Insert a catheter (32-French or 36-French) with as well as blood. Scrub and drape the predeter- the curved clamp and guide it with a finger. To mined area. Anesthetize the skin, intercostal mus- drain blood, it is best to direct it posterolaterally, cles, pleura, and rib periosteum locally (Fig. 2.1 a). and to remove air, an apical position is preferred. Make a 3 to 4 cm long skin incision over the Correct intrapleural position is indicated by intercostal space, parallel to the ribs (Fig. 2.1 b). “fogging” in the catheter during respiration and Bluntly dissect the subcutaneous tissue over the when the first side hole is 1 to 2 cm inside the cranial aspect of the rib to avoid the intercostal chest wall. Connect the tube to a water-suction vessels. Continue dissection down to the pleura, device. Secure the tube with a separate suture, preferably with a curved clamp or a finger. Then and suture the skin. puncture the parietal pleura with the tip of aFig. 2.1. Steps for chest tube insertion
  • 27. 22 Chapter 2 Vascular Injuries to the Thoracic Outlet Area TECHNICAL TIPS Emergency Anterolateral 5th-Interspace Thoracotomy for Control of the Aorta The patient must be intubated and ventilated. Incise the skin from the sternum to the axillary line along the upper border of the 5th rib on the left side. In women, the submamillary groove is a landmark. Continue cutting the muscles with scissors or a scalpel all the way down to the pleu- ra. Open the pleural sheath with a pair of scis- sors. The opening should be as large as the hand. One or two costal cartilages can be cut to obtain better access through the thoracotomy. Follow the aortic arch, pass the left subclavian artery Fig. 2.2. Incision for emergency anterolateral thora- and pulmonary artery, and mobilize the heart cotomy slightly to the right. Press the descending aorta manually or with an aortic occluder against the spine and try to achieve the best possible occlu- Unstable Patients sion. This occlusion is maintained under contin- Patients with blood pressure <50 mmHg and in uous fluid resuscitation and while the patient is severe shock are candidates for immediate sur- transferred to the operating room. Alternatively, gery. A rapid infusion of 2–3 l of a balanced elec- place a Satinsky clamp just distal to the origin of trolyte solution over 10–15 min should be given, the left subclavian artery. The proximal blood aiming to keep blood pressure between 70 and pressure must be kept <180 mmHg after clamp 90 mmHg. It is probably important to keep this placement, and it should be removed as soon level of blood pressure to avoid the risk of in- as possible. creased bleeding associated with a higher blood The left subclavian artery is, in contrast to the pressure. If the patient does not respond to this right, an intrapleural structure and can in most volume replacement, he or she should be taken to cases be visualized relatively easy and directly the operating room for immediate surgery. compressed with a finger, clamped, or packed. A Antibiotics covering staphylococci and strepto- left-sided thoracotomy can be extended over to cocci should be administered according to the the right, aiming at a higher interstitium. If, how- local protocols. One suggestion is cephalosporins. ever, it is obvious that the injury is on the right Analgesics, morphine 10 mg intravenously, and, side, the thoracotomy should be performed on in penetrating injuries, prophylaxis against teta- that side. Severe right-sided intrathoracic bleed- nus should also be administered. ing is best controlled by finger compression and packing a tamponade in the apex of the right Control of Bleeding pleural cavity, combined with heavy manual In penetrating injuries with continued external compression in the right supraclavicular fossa. bleeding, control is achieved by finger compres- If resuscitation fails despite adequate fluid sion over the wound. A gloved finger can also be substitution and successful control of bleeding, inserted into the wound to compress the bleeding air embolism should be suspected if there are and stop the outflow of blood. Another recom- injuries to large veins. Puncture and aspiration in mended method is to insert a 24-French Foley the right ventricle is diagnostic as well as thera- catheter into the wound tract and fill the balloon peutic. with water or saline (Fig. 2.3). The catheter is clamped after insufflation of the balloon, and if
  • 28. 2.5 Management and Treatment 23 >300 ml blood drained through the tube within an hour Deterioration of vital signs when the drain is opened Even in initially unstable patients, this strategy with evacuation of hemothorax and volume re- placement is often successful. It may allow enough time to let the patient undergo emergency work-up under close surveillance. Information obtained from CT scanning and/or angiography facilitates decisions regarding optimal positioning and routes for exposure of the injury at final surgical treatment (see section 2.5.2, p. 25–27). As de- scribed below, in many situations this type of management stabilizes the patient enough to allow continued nonsurgical management. NOTE Be liberal with chest tube insertionFig. 2.3. Temporary balloon tamponade of bleeding in patients with moderate or severeafter penetrating injury to a major subclavian vessel. hemothorax.A Foley catheter is gently inserted to the bottom ofthe wound tract. After the balloon is filled with saline,gentle traction is applied to the catheter, causing com- Stable Patientspression of the vessels against the clavicle Initial management is the same as described above for unstable patients or patients in extreme shock, as summarized in Table 2.1.the wound penetrates into the pleural cavity, it is Diagnostic examinations in stable patients in-gently pulled so the balloon tamponades the pleu- clude repeat plain chest x-ray, angiography or du-ral entrance. If external bleeding persists after this plex ultrasound under close surveillance. Also inmaneuver, a second balloon can be inserted into stable patients chest tubes should be placed on lib-the wound and insufflated to stop external bleed- eral indications for evacuation and monitoring ofing from the wound tract. By applying some trac- bleeding. The following indicate continued bleed-tion to the catheters, the balloon can also compress ing and the possible need for surgical treatment:injured vessels against the clavicle or the ribs. Deterioration of vital signs (i.e., hypotensive If there are clinical indications or radiological reaction) when the drain is startedsigns of moderate or large hemothorax, a chest 1.500–2.000 ml of blood within the first 4–8 htube should be inserted for its evacuation. The ra- Drainage of blood exceeding 300 ml/h for moretionale is that a hemothorax can contribute to con- than 4 htinued intrathoracic bleeding and restrict ventila- More than half of pleural cavity filled withtion and venous return. Depending on the results blood on x-ray despite a well functioning chestwhen the pleural cavity is drained, different ac- tubetions can be taken. In an unstable patient, the fol-lowing are considered strong indicators for emer- All of these factors may indicate thoracotomygency thoracotomy: and should alert the surgeon to consider operation 1.500 ml of blood drained directly after inser- and contact with a cardiothoracic surgeon when tion of the tube needed.
  • 29. 24 Chapter 2 Vascular Injuries to the Thoracic Outlet Area Table 2.1. Initial work-up and treatment of patients with thoracic outlet vascular injuries of different severity (US ultrasound, CT computed tomography, ED emergency department, OR operating room) Patient’s condition Responds US CT Angiography Treatment to resuscitation Extreme shock No No No No Emergency thoracotomy in the ED Unstable No No No No Emergency thoracotomy in the OR or ED Yes Maybe Maybe Yes As above or continued non-op management if only moderate injuries Stable Yes Maybe Maybe Yes Operative or nonoperative management depending on findings Deteriorates No No Maybe Emergency operation after opening in the OR chest drain Nonsurgical Management 2.5.2 Operation An initially unstable patient who responds well to resuscitation and becomes stable, as well as stable Preoperative Preparation patients with a continued stable course, and with and Proximal Control no major vascular injury necessitating surgery The patient is scrubbed and draped to allow inci- revealed at the work-up can often be managed by sions from the neck down to at least the knee. In blood transfusions, fluid replacement, and a chest an emergency situation without knowledge about tube to drain a hemothorax. the exact injury site, the patient is best positioned The management of patients with major neuro- supine with the arms abducted 30°. logical deficits or coma is a matter of debate. Many The aim of emergency thoracotomy in an un- physicians argue that these patients are never stable patient is primarily to control bleeding. This candidates for surgical intervention due to their can be achieved by surgeons without experience severe brain injury and poor prognosis. Others ar- in cardiothoracic surgery. Once control is accom- gue that vascular injuries should be repaired in all plished, the repair can wait to allow time for fur- of these cases because it is impossible to exclude ther resuscitation and for experienced assistance that the unconsciousness is related to some injury to arrive. Most experienced trauma surgeons to- other than a vascular one. day recommend a median sternotomy because it is considered the most versatile approach. Such an incision can easily be extended up along the ster- nocleidomastoid muscle on either side or laterally over the clavicle as needed. This approach is there- fore recommended when localization of the injury is uncertain (Fig. 2.4).
  • 30. 2.5 Management and Treatment 25 only a partially occluding clamp on the aorta. A total exposure of the proximal aorta and the innominate bifurcation is, however, frequently needed for proximal and distal control before opening the hematoma. In minor penetrating in- juries, simple sutures may occasionally be suffi- cient (Fig. 2.5). The need for shunting to prevent cerebral isch- emia during innominate artery clamping is con- troversial. Some argue that it is not needed if (1) clamping is caudal to the origin of the common carotid artery, (2) blood pressure and cardiac out- put are normal, and (3) the contralateral carotid artery is open. Others believe it is preferable to always measure stump pressure in the common carotid artery distal to the innominate clamp. Shunting is recommended if the mean pressure is <50 mmHg or not measurable.Fig. 2.4. Median sternotomy with possible extensionsfor proximal and distal control in vascular injuries in the Injuries to the common carotid arteries are ex-thoracic outlet region posed and managed according to the same guide- lines as for innominate injuries. Proximal injuries can be repaired by a prosthetic bypass or simple Exposure and Repair suture. In cases with occlusion also involving theFor innominate artery injuries, the median ster- internal carotid artery, ligation is the safest meth-notomy is extended along the anterior border of od. This applies for neurologically intact patientsthe sternocleidomastoid muscle to the right. The as well as those who are in deep coma.overlying innominate vein, which is often also in- The subclavian arteries, in particular the retro-jured, has to be divided to achieve exposure. If the clavicular portion of the left artery, are difficult toinjury is located at the base of the artery, which is expose and manage. Before approaching the in-common in blunt trauma, a reconstruction with jured area it is extremely important to have a strat-an 8–10-mm prosthetic graft end-to-side from egy for how to obtain proximal control in thesethe ascending aorta to the divided innominate is injuries; otherwise, severe uncontrollable bleedingfrequently employed. This can be performed with may occur. The subclavian arteries can be exposed Fig. 2.5. Repair of a penetrating injury to the innominate artery. a Clamp occlusion at the origin from the aorta. b Final repair with suture a b
  • 31. 26 Chapter 2 Vascular Injuries to the Thoracic Outlet Area On the left side, an alternative for proximal Fig. 2.7. In unstable patients and when rapid bleeding control is a high thoracotomy in the 3rd intercos- control is needed, some prefer an anterior 3rd-inter- tal space combined with a supraclavicular incision space thoracotomy in combination with a supraclavic- for distal control (Fig. 2.7). ular incision for distal control of the subclavian artery A thoracotomy is not necessary in injuries to the distal subclavian and proximal axillary artery. The recommended approach for control in these sternotomy. By placing a longitudinal pillow be- cases is a clavicular incision, starting at the sterno- tween the shoulders of the patient, the shoulder clavicular joint, extending over the medial portion can be pushed dorsally to further facilitate expo- of the clavicle to curve down into the deltopectoral sure (Fig. 2.8). groove. The exposure of the retroclavicular por- Principles of repair of the subclavian and axil- tion of the subclavian artery sometimes requires lary arteries usually involve resection and inter- division of the major pectoral and subclavian position grafting. Autogenous vein graft is the muscles, the sternoclavicular joint, and the clavi- first choice, but polytetrafluoroethylene (PTFE) cle. After these procedures, the medial portion or polyester grafts are alternatives. Resection and of the clavicle can be resected or rotated laterally. end-to-end anastomosis are rarely possible, and Clavicular resection in combination can also these vessels are particularly fragile, thus increas- be employed with a laterally extended median ing the risk for tension in the anastomosis.
  • 32. 2.5 Management and Treatment 27Fig. 2.8. Exposure of the distal subclavian and proxi- c The clavicle is divided and its medial portion resectedmal axillary artery. a A clavicular incision is used. b The or retracted. If necessary, the pectoralis minor musclesternocleidomastoid, pectoralis major, and subclavian is dividedmuscles are stripped of the medial half of the clavicle. Endovascular Repair imal left subclavian artery for temporary proximal and Control control. This minimally invasive endovascular al-The use of endovascular methods in trauma man- ternative, when applicable, is particularly attrac-agement is increasing. So far, insertion of covered tive in multiply injured patients by allowing timestents has been used successfully to seal leaks and for managing other major injuries.pseudoaneurysms (Fig. 2.9). The vascular segments of the thoracic outlet re- Coils are useful for occluding bleeding branch- gion can be catheterized by puncturing the com-es. Another evolving management technique is to mon femoral artery of either side or the contralat-place balloon catheters in the innominate or prox- eral brachial artery.
  • 33. 28 Chapter 2 Vascular Injuries to the Thoracic Outlet Area 2.5.3 Management After Treatment The proximity of the great vessels and trachea gives high priority to respiration and airways in the early postoperative period. Intubation is usu- ally required. Many patients with injuries to the aortic arch branches require chest tubes for drain- ing the thorax. Close monitoring of the chest tube for signs of bleeding is important because this is the most common postoperative complication. More than 300 ml of blood drained per hour is usually considered a clear indication for reex- ploration to exclude or repair surgical causes of the bleeding. Dilutional thrombocytopenia and hypothermia are other possible causes of post- operative bleeding problems. The recommenda- tion is to remove the chest tube within 24 h or as soon as the risk of bleeding is considered to be under control. a Associated neurological symptoms caused by the initial trauma or the repair are common. Ex- amples are injuries to the phrenic and vagal nerves. Secondary ischemic cerebral injuries also occur, and if aggravated during the postoperative course, this indicates embolization or thrombotic occlu- sion of a repaired or traumatized arterial seg- ment. 2.6 Results In textbooks the results are generally considered poor for patients with thoracic outlet injuries, but case series give some hope, at least for patients who reach the hospital alive. A large series of 228 patients from South Africa with penetrating thoracic outlet vascular trauma reported that 60% of the patients were dead on admission. The operative mortality was 15% for b the remaining patients, giving a total mortality of 66%. In a report from Los Angeles, the corre- Fig. 2.9. a Penetrating injury to the left subclavian sponding figures were a 34% total mortality and artery after a knife stabbing with extravasation of con- 15% operative mortality. trast into a pseudoaneurysm (arrows) at angiography. b No leakage after sealing the injury with a covered stent
  • 34. 2.6 Results 29 The results, however, vary greatly between Further Readingdifferent studies. In a study from 1989 30 patientswith blunt thoracic vascular trauma, substantially Abouljoud MS, Obeid FN, Horst HM. Arterial injury tobetter results were reported; the operative mortal- the thoracic outlet – a ten year experience. Am Surgity was 6.7%, and overall graft patency was 90% 1993; 59:590–595 Axisa BM, Loftus IM, Fishwick G, et al. Endovascularafter 5 years of follow-up. Another report from the repair of an innominate artery false aneurysm fol-same year had a similar mortality rate of 6.5%. lowing blunt trauma. J Endovasc Ther 2000; 7:245–It included 46 patients with 51 intrathoracic arte- 250rial injuries, 42 of which were penetrating injuries. Cox CS, Allen GS, Fischer RP, et al. Blunt versus pen-The incidence of neurological consequences in etrating subclavian artery injury: Presentation, in-the different series was relatively low, 5–29%. jury pattern, and outcome. J Trauma 1999; 46:445–Combined arterial and venous injuries or venous 449 Demetriades D, Chahwan S, Gomez H, et al. Penetrat-injuries are associated with a significantly higher ing injury to the subclavian and axillary vessels.mortality, up to 50% and higher. This is blamed J Am Coll Surg 1999; 188:290–295the risk for air embolization and more severe blood Hajarizadeh H, Rohrer MJ, Cutler BS. Surgical exposureloss due to less contractility of the veins. of the left subclavian artery by median sternotomy In summary, it seems that most patients die at and left supraclavicular extension. J Trauma 1996;the scene or during transport, but if the patient 41:136–139arrives alive in the emergency department, the Hoff SJ, Reilly MK, Merrill WH, et al. Analysis of bluntresults seem to be fair. and penetrating injury of the innominate and sub- clavian arteries. Am Surg 1994; 60:151–154 Pate JW, Cole FH, Walker WA, et al. Penetrating injury of the aortic arch and its branches. Am Thor Surg 1993; 55:586–589 Miles EJ, Buche A, Thompson W, et al. Endovascular re- pair of acute innominate artery injury due to blunt trauma. Am Surg 2003; 69(2):155–159 Weiman DS, McCoy DW, Haan CK, et al. Blunt in- jury of the brachiocephalic artery. Am Surg 1998; 64(5):383–387
  • 35. Vascular Injuries in the Arm 3CONTENTS 3.1 Summary3.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31 Suspect vascular injuries in patients with3.2 Background . . . . . . . . . . . . . . . . . . . . . . . . . 31 shoulder or elbow dislocation.3.2.1 Background . . . . . . . . . . . . . . . . . . . . . . . . . . 31 When blood pressures in the arms differ,3.2.2 Etiology and Pathophysiology . . . . . . 32 exclude vascular injuries in proximal ar-3.3 Clinical Presentation . . . . . . . . . . . . . . . 33 teries.3.3.1 Medical History . . . . . . . . . . . . . . . . . . . . . . 33 It is the nerve injury that determines the3.3.2 Clinical Signs and Symptoms . . . . . . . . 33 functional outcome of arm injuries. Evaluate the brachial plexus and the me-3.4 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . 33 dian nerve function before and during3.5 Management and Treatment . . . . . . 34 vascular exploration.3.5.1 Management Before Treatment . . . . . 34 Repair of vascular injuries in the upper3.5.1.1 Severely Injured limb is wise even when ischemia appears to and Unstable Patients . . . . . . . . . . . . . . . 34 be limited. Less Severe Injuries . . . . . . . . . . . . . . . . . . 343.5.1.3 Amputation . . . . . . . . . . . . . . . . . . . . . . . . . 353.5.2 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . . 363.5.2.1 Preoperative Preparation . . . . . . . . . . . 36 3.2 Background3.5.2.2 Proximal Control . . . . . . . . . . . . . . . . . . . . 363.5.2.3 Exploration and Repair . . . . . . . . . . . . . . 36 3.2.1 Background3.5.2.4 Finishing the Operation . . . . . . . . . . . . . 383.5.2.5 Endovascular Treatment . . . . . . . . . . . . 39 Arteries and veins in the arms are the second most3.5.3 Management After Treatment . . . . . . 39 common location for vessel injuries in the body3.6 Results and Outcome . . . . . . . . . . . . . . . 39 and constitute almost half of all peripheral vascu- lar injuries. Much more often than in the legs they3.7 Iatrogenic Vascular Injuries . . . . . . . . 39 occur together with neurological and skeletal Further Reading . . . . . . . . . . . . . . . . . . . . 40 injuries. Although vascular injuries in the arms rarely lead to fatal or serious bleeding, ischemic consequences are common. The extensive collat- eral network around the elbow makes clinical signs variable and often minute. On the other hand, if the brachial artery is obstructed proximal to the origin of the deep brachial artery, the risk for amputation is substantial: up to 50% of such patients lose the arm if the vessel is not repaired. While the vascular injury per se often can be man- aged easily, it is the damaged nerves that cause the main functional disturbances in the long run.
  • 36. 32 Chapter 3 Vascular Injuries in the Arm Because arm vessel trauma is common and sometimes appear without signs and symptoms, missed injuries cause considerable morbidity in trauma patients. Awareness and optimal manage- ment may reduce this morbidity. The arteries supplying blood to the arms – the subclavian and axillary arteries – are located in the thorax or thoracic outlet, and if these vessels are traumatized, the consequences are often more serious. This “intrathoracic part of the arm” is covered in Chapter 2 on vascular injuries in the thoracic outlet area. 3.2.2 Etiology and Pathophysiology Injury mechanisms are the same in the arms and legs, and the brachial, radial, and ulnar arteries can be damaged by both penetrating and blunt trauma. Knives and gunshots usually cause pene- trating injuries (most often to the brachial artery), but lacerations secondary to fractures occur regu- larly. Sharp fragments commonly penetrate vessel walls (Fig. 3.1). Blunt injuries occur in road traffic accidents because of fractures and joint dis- locations. The most frequent orthopedic arm inju- ries associated with vessel damage are listed in Fig. 3.1. Angiography showing an occluded brachial artery severed by the sharp ends of a shaft fracture of Table 3.1. the humerus There are also types of trauma specific for arm vessel injuries. A large number of upper limb vas- cular trauma are caused by industrial and domes- tic accidents. Splintered glass as well as self-in- Table 3.1. Most common sites for combined orthope- flicted wounds regularly damage vessels below the dic and vascular injury elbow. The popularity of using the brachial artery Orthopedic injury Vascular injury as a site for vascular access for endovascular pro- cedures has caused an increase in iatrogenic cath- Fractured clavicle Subclavian artery eter-related injuries to the brachial artery in prox- Shoulder dislocation Axillary artery imity to the elbow. Pseudoaneurysms are often Supracondylar fracture Brachial artery caused by radial artery punctures for arterial of the humerus blood samples. Elbow dislocation Brachial artery As in all traumatized vessels, transection or laceration may cause bleeding, thrombosis, or both. Transections, intimal tears, and contusions are more frequent after blunt trauma. The mecha- nisms are described in more detail in Chapter 9 bidity long term. Such injuries are equally com- (p. 102). Tissue in the distal parts of the arm is as mon after penetrating and blunt trauma. In the susceptible to ischemia as in the legs, and the time literature, 35–60% of arterial injuries in the upper limit of 6–8 h before irreversible damage occurs arm are associated with nerve injuries, and over is also valid for arm injuries. Concomitant nerve 75% are associated with nerve, bone, or venous injuries, as mentioned, are the main cause of mor- damage.
  • 37. 3.4 Diagnostics 33 3.3 Clinical Presentation panding hematoma. It is common for a dimin- ished radial pulse or an abnormal brachial blood 3.3.1 Medical History pressure to be the only sign of vascular obstruc- tion. Because pulse wave propagation through aPatients with vascular injuries in the arms arrive thrombus is possible, a palpable radial pulse doesat the emergency department after accidents, knife not completely exclude arterial obstruction; there-or shooting assaults, or car crashes causing multi- fore, a high suspicion of arterial injury is neces-ple injuries. As with all injuries, it is important to sary even when a palpable pulse is found. As ainterview the rescue personnel and accompanying guideline, a difference of more than 20 mmHg inpersons about the type of injury and the type of blood pressure between the arms should make thebleeding. The exact time of the injury should be examiner suspect a vascular injury. Inability toestablished to facilitate planning of repair. Because move the fingers, hands, and arms as well as dis-orthopedic injuries are associated with arterial turbances in sensation are frequently associateddamage, it is also essential to ask whether joint with vascular injury. The sensory and motor func-dislocations or fractures were noted or reduced. tions must therefore be carefully examined andComplaints of pain from areas around a joint indi- evaluated to disclose any nerve damage that shouldcate a possible luxation. Even more important is to be repaired. A list of what this examination shouldask for symptoms of nerve damage, including per- cover is given in Table 3.2. In unconscious pa-manent or transient numbness and impaired mo- tients, this examination is the only way to revealtor function in any part of the arm. indications of arterial damage.NOTE It is essential to evaluate nerve function 3.4 Diagnostics before taking the patient to the operating room. Investigations beyond the physical examination of the patient should be done only in stable patients. Accordingly, most patients with distal arm inju- 3.3.2 Clinical Signs and Symptoms ries can undergo angiography or duplex scanning provided that these investigations do not delayBoth the “hard” and the “soft” signs of vascular treatment. Arteriography is indicated when arte-trauma occur after upper extremity vascular inju- rial involvement not is obvious. For example, pa-ries. Examples, in descending frequency of occur- tients with trauma in the elbow region – blunt orrence, include diminished or absent radial pulse, penetrating – with clear ischemia and no radialmotor deficit, sensory loss, hemorrhage, and ex- pulse do not need arteriography before surgery.Table 3.2. Evaluation of nerve function in the arm Injured nerve (s) Symptom Findings Brachial plexus Inability to move the arm; limb hangs with Unable to discriminate sensation extended elbow and forearm pronated on the neck Axillary nerve Inability to abduct the arm Unable to discriminate sensation on the dorsal side of the shoulder Ulnar nerve Numbness and inability Unable to discriminate sensation to move the 5th finger in the pulp of the 5th finger Median nerve Inability to flex the hand and numbness Unable to discriminate sensation in the three middle fingers in the pulp of the index finger Radial nerve Numbness and inability Unable to discriminate sensation to move the thumb in the web between the thumb and index finger
  • 38. 34 Chapter 3 Vascular Injuries in the Arm If the patient has multiple injuries, shotgun in- ter analgesics (5–10 mg of an opiate IV) and, when juries, or suspected proximal arterial involvement, indicated, antibiotics and tetanus prophylaxis. arteriography is recommended to determine the Multiply injured patients with signs of arm exact site of injury. Arteriography should also be ischemia should be treated according to the hospi- done when there are indistinct signs of ischemia tal’s general trauma management protocol, and and arterial injury is only suspected. Included in the vascular injury is usually evaluated during the this indication for arteriography is the so-called second survey. Serious ongoing bleeding has high proximity injury, referring to injury in patients priority, but arm ischemia should be managed without signs of distal ischemia but with trauma after resuscitation and treatment of life-threaten- in close proximity to a major artery. Of patients ing injuries but before orthopedic repair in most undergoing arteriography for this indication, circumstances. When the patient has stabilized, 10–20% are reported to have arterial lesions. If arteriography can be performed if indicated (see the arteriogram reveals injury to the subclavian or above). axillary artery, endovascular treatment can pro- ceed right away. Less Severe Injuries Duplex scanning has replaced arteriography in Most patients with arm injuries arrive in the emer- some hospitals and is probably just as accurate in gency department in a stable condition without experienced hands. Intimal flaps and small areas ongoing bleeding but with signs of hand ischemia. of vascular wall thrombosis may be difficult to For these patients, careful examination of the arm identify with duplex scanning under some cir- including assessment of nerve function, is essen- cumstances, but such small lesions in the arm can, tial. Dislocated fractures or luxations should be on the other hand, usually be treated without reduced under proper analgesia. After reduction, exploration. examination of vascular function should be re- Computed tomography (CT) angiography is an peated. If the radial pulse and distal perfusion important modality for diagnosing proximal arte- return, the position should be stabilized and fixed. rial injuries in particular. It is reported to be at Repeated examinations during the following 4 h least as accurate as arteriography in this area. The are mandatory to ensure that the returned perfu- use of CT angiography is likely to increase in the sion is persistent. near future because it is quicker than angiography, If the vessel injury is definite – an absent radial and most trauma centers have rapid access to pulse and reduced hand perfusion – and the site of good-quality CT. vascular injury is apparent, the patient can be transferred to the operating room without further diagnostic measures. Patients with findings indi- 3.5 Management and Treatment cating vascular injury at examination, and those with obvious arterial disruption but with arms so 3.5.1 Management Before traumatized that the site of arterial injury cannot Treatment be determined, should undergo arteriography or duplex scanning. Expediency of repair is required Severely Injured for all locations of arterial injuries in the arm. The and Unstable Patients proposed time limits indicating a low risk for per- Patients arriving to the emergency department manent tissue damage range from 4 h for brachial with active serious bleeding after a single injury to artery injuries and up to 12 h for forearm injuries. an arm are rare. When this does occur, manual di- The risk limit for irreversible ischemia following rect pressure over the wound can control the forearm injuries is valid for patients with an in- bleeding while general resuscitation measures ac- complete palmar arch. The frequency of this ana- cording to Advanced Trauma Life Support princi- tomical variation is 20% in most Western popula- ples are undertaken: oxygen, monitoring of vital tions. signs, placement of intravenous (IV) lines, and in- Suspected injuries to the radial and ulnar ar- fusion of fluids (see also Chapter 9, p. 105, for sug- tery should be treated according to the general gestions). It is important not to forget to adminis- principles discussed above. Even cases with nor-
  • 39. 3.5 Management and Treatment 35Table 3.3. Allen test dons, and muscles is difficult. As a general princi- ple, arms with multiple fractures, nerve disrup- 1. Elevate the arm over the head tion, ischemia-time longer than 6 h, and extensive 2. Occlude the radial and ulnar arteries at the wrist crush injuries involving muscle and skin will nev- 4. Lower the arm er regain function and should be amputated. An- 5. Release blood flow through the ulnar artery other principle is that when four out of the five 6. Inspect and time the return of perfusion components of the arm are injured – skin, bone, muscles, and vessels – but there is only minor 7. Repeat, and release blood flow through nerve injury, an attempt to save the arm is reason- the radial artery instead. able. One must keep in mind, however, that the 8. A return of perfusion >5 s is considered arm needs at least some protective sensation in or- a positive Allen test, and the artery is suspected der to be functional. Children have a greater to be inadequate chance of regaining a functional arm than adults do, and a generous attitude to surgical repair in children is recommended.mal perfusion in the hand but without a radialpulse should be explored and repaired if reason- NOTEably simple. When forearm arterial injury is un- The surgeon should not try to save anclear, the Allen test (Table 3.3) can be added to the arm when it only has a small chance ofexamination procedure. A positive Allen test to- being functional and when repair can begether with a history of trauma to an area in close accomplished only at considerable risk.proximity indicate that the radial or ulnar arteryis indeed affected. The wound should then be ex- The mangled extremity severity score (MESS) is aplored and the traumatized artery inspected and grading system designed to aid the decision pro-mended. Patients with multiple severe injuries and cess for managing massive upper and lower ex-high-risk patients should not be explored if perfu- tremity trauma. A score of 7 or more has been pro-sion to the hand is rendered sufficient. For those posed as a cut-off value for indicating when ampu-circumstances, repeat examinations every hour tation cannot be avoided and should be performedare mandatory to make sure that perfusion is ade- as the primary procedure. In some studies, a scorequate and stable. 7 predicted an eventual amputation with 100% ac- curacy. The basis of the MESS scoring system is Amputation given in Table 3.4.Some arms with vascular injuries are so extensive- As shown in Table 3.4, a crush injury is regard-ly damaged that amputation is a treatment option. ed as particularly unfavorable. The duration ofThe decision of when to perform a primary ampu- ischemia is also a significant factor taken intotation versus trying to repair vessels, nerves, ten- account in the MESS system.
  • 40. 36 Chapter 3 Vascular Injuries in the Arm Table 3.4. MESS: Mangled Extremity Severity Score (BP blood pressure) Types Injury characteristics Points Low energy Stab wounds, simple closed fractures, small-caliber gunshot wounds 1 Medium energy Open fractures, multiple fractures, dislocations, small crush injuries 2 High energy Shotgun blasts, high-velocity gunshot wounds 3 Massive crush Logging, railroad accidents 4 No shock (BP normal) BP stable at the site and at the hospital 1 Transient hypotension BP unstable at the site but normalizes after fluid substitution 2 Prolonged hypotension BP <90 mmHg 3 No distal ischemia Distal pulses, no signs of ischemia 1 Mild ischemia Absent or diminished pulses, no signs of ischemia 2a Moderate ischemia No signals by continuous-wave Doppler, signs of distal ischemia 3a Severe ischemia No pulse; cool, paralyzed limb; no capillary refill 4a <30 years old patient 1 >30 years old patient 2 >50 years old patient 3 a Points are doubled if ischemia lasts longer than 6 h. 3.5.2 Operation Proximal Control For distal vessel injury, proximal control can be Preoperative Preparation achieved by inflating the previously placed tourni- Hemodynamically stable patients are placed on quet to a pressure around 50 mmHg above systolic their back with the arm abducted 90º on an arm pressure. The cuff should be inflated with the arm surgery table. The forearm and hand should be in elevated to minimize bleeding by venous conges- supination. Peripheral or central IV lines should tion. After inflation, the wound is explored direct- not be inserted on the injured side. Any continu- ly at the site of injury. ing bleeding is controlled manually directly over For more proximal injuries, control is achieved the wound. If the site of injury is the brachial ar- by exposing a normal vessel segment above the tery or distal to it, a tourniquet can be used to wounded area. The most common sites for proxi- achieve proximal control. It is then placed before mal control in the arm are the axillary artery be- draping and should be padded to avoid direct skin low the clavicle, and the brachial artery (which is contact with the cuff. This minimizes the risk for what the artery is called distal to the teres major skin problems during inflation. The arm is washed muscle) somewhere in the upper arm. Some com- so the skin over the appropriate artery can be in- mon exposures are described in the Technical Tips cised without difficulty. The draping should allow box. palpation of the radial pulse and inspection of fin- ger pulp perfusion. One leg is also prepared in case Exploration and Repair vein harvest is needed. Distal control is achieved by exploring the wound. The position of the arm is the same for more Sometimes this requires additional skin incisions. proximal injuries. Proximal control of high bra- The most common site for vascular damage in the chial and axillary artery trauma may involve ex- arm is the brachial artery at the elbow level. These posure and skin incisions in the vicinity of the injuries occurs, for example, because of supracon- clavicle and the neck, so for proximal injuries the dylar fractures in children and adults. In such draping must also allow incisions at this level. cases, exposure and repair of the brachial artery through an incision in the elbow crease is appro- priate. The anatomy is shown in Fig. 3.1, and a brief description of the technique is given in the Technical Tips box. Hematomas should be evacu- ated to allow inspection of nerves and tendons.
  • 41. 3.5 Management and Treatment 37 TECHNICAL TIPS Exposure for Proximal Control of Arteries in the Arm Axillary Artery Below the Clavicle median nerve and the medial cutaneous nerve An 8-cm horizontal incision is made 3 cm below that surrounds it. the clavicle (Fig. 3.2). The pectoralis major muscle fibers are split parallel to the skin incision. The Brachial Artery at the Elbow pectoralis minor muscle is divided close to its The incision is placed 2 cm below the elbow crease insertion. The nerve crossing the pectoralis minor and should continue up on the medial side along muscle can also be divided without subsequent the artery. If possible, veins transversing the morbidity. The axillary artery lies immediately wound should be preserved, but they can be di- below the fascia together with the vein inferiorly, vided if necessary for exposure. The medial inser- and the lateral cord of the brachial plexus is tion of the biceps tendon is divided entirely, and located above the artery. the artery lies immediately beneath it. By follow- ing the wound proximally, more of the artery can Brachial Artery in the Upper Arm be exposed (Fig. 3.3). If the origins of the radial The incision is made along the posterior border of and ulnar artery need to be assessed, the wound the biceps muscle; a length of 6–8 cm is usually can be elongated distally on the ulnar side of the enough (Fig. 3.3). The muscles are retracted medi- volar aspect of the arm. The median nerve lies ally and laterally, and the artery lies in the neuro- close to the brachial artery, and it is important to vascular bundle immediately below the muscles. avoid injuring it. The sheath is incised and the artery freed from theFor supracondylar fractures, the brachial artery,the median nerve, and the musculocutaneousnerves must sometimes be pulled out of the frac-ture site. Before the artery is clamped, the patientis given 50 units of heparin/kg body weight IV. Re-pair should also be preceeded by testing inflowand backflow from the distal vascular bed by tem-porary tourniquet or clamp release. It is often alsowise to pass a #2 Fogarty catheter distally to ensurethat no clots have formed. Occasionally, inflow isquestionable, and proximal obstruction must beruled out. This can be done intraoperatively by re-trograde arteriography as described in Chapter 4(p. 44) or by duplex scanning. As a general principle, all vascular injuries inthe arms should be repaired, except when revascu-larization may jeopardize the patient’s life. Arte-rial ligation should be performed only when am-putation is planned. Postoperative arm amputa- Fig. 3.2. The most proximal part of the axillary ar-tion rates are reported to be 43% if the axillary tery can be exposed through an incision parallel to and just below the clavicle. Exposure of the brachialartery is ligated and 30% at the brachial artery artery is through an incision in the medial aspect oflevel. Another exception is forearm injuries. When the upper arm. This incision can be elongated and con-perfusion to the hand is rendered adequate – as nected with the clavicular incision to allow exposureassessed by pulse palpation and the Allen test – and repair of the entire axillary and brachial artery seg-one of these two arteries can be ligated without ments
  • 42. 38 Chapter 3 Vascular Injuries in the Arm radial and ulnar arteries. Before suturing the anas- tomoses, all damaged parts of the artery must be excised to reduce the risk of postoperative throm- bosis. Rarely, primary suture with and without patching can be used to repair minor lacerations. Shunting of an arterial injury to permit osteo- synthesis is rarely needed in the arm. Vascular in- terposition grafting can usually be done with an appropriate graft length before final orthopedic repair. Also, extremity shortening due to fractures is less of a problem in the arms (in contrast to the legs), and orthopedic treatment without osteo- synthesis is common especially in older patients. Nevertheless, for some arm injuries shunting is a practical technique that allows time for fracture fixation, thus avoiding the risks of redisplacement and repeated vessel injury. One example is injuries to the axillary or brachial artery caused by a proxi- mal humeral fracture, where the fragment needs to be fixed in order to prevent such injuries. Another example is humeral shaft fracture, which needs to be rigidly fixed to abolish the instability that may otherwise endanger the vascular graft. For more details about shunting, see Chapter 9 (p. 111). Veins should also be repaired if reasonably sim- ple. If the vein injury is caused by a single wound with limited tissue damage, concomitant veins to the distal brachial artery can be ligated. For more extensive injuries where the superficial large veins are likely to be ruined, it is wise to try to repair the Fig. 3.3. Transverse incision in the elbow for exposing deep veins. For very proximal injuries in the shoul- the brachial artery and with possible elongations (dot- der region, vein repair is important to avoid long- ted lines) when access to the ulnar and radial branches as well as to more proximal parts of the brachial artery term problems with arm swelling. It is also impor- is needed tant to cover the mended vessel segment with soft tissue to minimize the risk for infection that may involve the arteries. morbidity. In a substantial number of patients with differing vessel anatomy, however, ligation of Finishing the Operation either the ulnar or radial artery may lead to hand When the repaired artery or graft’s function is amputation. If both arteries are damaged, the ul- doubtful and when the surgeon suspects distal nar artery should be prioritized because it is usu- clotting, intraoperative arteriography should be ally responsible for the main part of the perfusion performed. The technique is described in Chap- to the hand. ter 10 (p. 128). After completion, all devitalized For most arterial injuries, vein interposition is tissue should be excised and the wound cleaned. necessary for repair. Veins are harvested from the For penetrating wounds, damaged tendons and same arm, from parts of the cephalic or basilic transected nerves should also be sutured. This is vein if the trauma is limited, or from the leg. The not worthwhile for most blunt injuries. Fascioto- saphenous vein in the thigh is suitable for axillary my should also be considered before finishing the and brachial artery repair, while distal ankle vein operation. As in the leg, long ischemia times and pieces can be used for interposition grafts to the successful repair increase the risk of reperfusion
  • 43. 3.7 Iatrogenic Vascular Injuries 39and compartment syndrome, but the overall risk problems with hematoma formation around thefor compartment syndrome is reported to be wound. Early mobilization of the fingers facilitateless in the arm than in the leg. For a description of blood flow to the arm and should be encouraged.arm fasciotomy techniques, we recommend con-sulting orthopedic textbooks. After the woundsare dressed, a fractured arm is put into a plaster 3.6 Results and Outcomesplint for stabilization. The patency of arterial repair in the arm is often Endovascular Treatment excellent, but unfortunately, this appears to haveIn contrast to proximal arm vessel trauma, there little impact on the eventual arm function. Forare few instances in distal injuries when endovas- most patients in whom vessel trauma is associatedcular treatment is a feasible treatment option. Be- with nerve and soft tissue injury, it is the nervecause the brachial artery and the forearm vessels function that determines the outcome. Outcomeare easy to expose with little morbidity, open re- data after arterial repair in upper extremity inju-pair during exploration of the wound is usually ries have been reported in observational studiesthe best option. Possible exceptions to this are and case series. One example is a review from thetreatment of the late consequences of vascular United States of 101 patients with penetratingtrauma, such as arteriovenous fistulas and pseu- trauma, including 13 axillary or subclavian cases.doaneurysms. Half of the patients had nerve injuries as well. At Especially in the shoulder region, including the follow-up the limb salvage rate was 99%, and allaxilla, primary endovascular treatment is often patients who needed only vascular repair had ex-the best treatment option. Another circumstance cellent functional outcomes. Among arms that re-when endovascular treatment is favorable is bleed- quired nerve repair, 64% had severe impairment ofing from axillary artery branches – such as the arm function. The corresponding figure for mus-circumflex humeral artery – due to penetrating culoskeletal repair only was 25%.trauma. Active bleeding from branches, but not A report from the United Kingdom included 28from the main trunk, observed during arteriogra- cases of brachial artery injuries, of which six werephy is preferably treated by coiling. The bleeding blunt. In this study, half of the patients had con-branches are then selectively cannulated with a comitant nerve injury and underwent immediateguidewire and coiled, using spring coils or injec- nerve repair. All vascular repairs were successful,tions of thrombin to occlude the bleeding artery. but the majority of patients undergoing nerve re- pair appear to have had some functional deficit at follow-up. 3.5.3 Management After Treatment Fortunately, it seems that function improves over time in many patients. The risk factors forPostoperative monitoring of hand perfusion and poor outcome are similar to the ones used for theradial pulse is recommended at least every 30 min MESS score – severity of the fracture and soft tis-for the first 6 h. When deteriorated function of the sue damage, length of the ischemic period, severityrepaired artery is suspected, duplex scanning can of neurological involvement, and presence ofverify or exclude postoperative problems. Appar- associated injuries.ent occlusions should be treated by reoperation assoon as possible. Compartment syndrome in thelower arm may also evolve over time, and swelling, 3.7 Iatrogenic Vascular Injuriesmuscle tenderness, and rigidity must also be mon-itored during the initial days. For most patients, The brachial artery is increasingly being used fortreatment with low molecular weight heparin is cannulation, both for vascular access and for en-continued postoperatively. A common dose is dovascular procedures. The latter requires large5,000 units subcutaneously twice daily. introducer sheaths, and it is likely that we will ex- Keeping the hand elevated as much as possible perience an increase in the number of problemsmay reduce swelling of the hand and arm as well as related to this. Associated injuries are bleeding
  • 44. 40 Chapter 3 Vascular Injuries in the Arm and thrombosis. (Both of these issues are dis- Further Reading cussed in Chapter 12.) Management of bleeding is fairly straightforward. Bleeding is usually easy to Fields CE, Latifi R, Ivatury RR. Brachial and fore- control by manual compression; exposure is sim- arm vessel injuries. Surg Clin North Am 2002; ple; and repair is often accomplished by a few 82(1):105–114 McCready RA. Upper-extremity vascular injuries. Surg simple sutures. Thrombosis is much less common Clin North Am 1988; 68(4):725–740 but is more complicated to handle. Management Myers SI, Harward TR, Maher DP, et al. Complex upper should follow the guidelines given in Chapter 4. extremity vascular trauma in an urban population. Another problem that may be encountered is J Vasc Surg 1990; 12(3):305–309 related to arterial blood sampling from the radial Nichols JS, Lillehei KO. Nerve injury associated with artery. Occasionally, thrombosis of this artery will acute vascular trauma. Surg Clin North Am 1988; cause severe arm ischemia. This should then be 68(4):837–852 Ohki T, Veith FJ, Kraas C, et al. Endovascular ther- resolved by embolectomy and patch closure of the apy for upper extremity injury. Semin Vasc Surg injured vessel segment. Sporadically, vein graft in- 1998;11(2):106–115 terposition is needed. Bleeding or an expanding Pillai L, Luchette FA, Romano KS, et al. Upper-extrem- hematoma due to arterial puncture rarely occurs, ity arterial injury. Am Surg 1997; 63(3):224–227 but pseudoaneurysm formation is not so infre- Shaw AD, Milne AA, Christie J, et al. Vascular trauma quent. Such problems should be handled by sur- of the upper limb and associated nerve injuries. In- gery, including proximal control and patch closure jury 1995; 26(8):515–518 of the injured vessel. Stein JS, Strauss E. Gunshot wounds to the upper ex- tremity. Evaluation and management of vascular The radial artery is sometimes used as a graft injuries. Orthop Clin North Am 1995; 26(1):29–35 for coronary bypass procedures. This appears to Thompson PN, Chang BB, Shah DM, et al. Outcome fol- work extremely well, with little late morbidity in lowing blunt vascular trauma of the upper extrem- the arm where the artery was harvested. We have ity. Cardiovasc Surg 1993; 1(3):248–250 encountered occasional patients with mild hand ischemia immediately after surgery, but only a few cases who eventually needed revascularization. For these rare patients, a vein bypass from the bra- chial artery to the site where the ligature was placed at harvest is the recommended treatment.
  • 45. Acute Upper Extremity Ischemia 4CONTENTS plaques or an aneurysm in the subclavian or axil- lary arteries is the primary source of emboli.4.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Embolization to the right arm is more common4.2 Background and Pathogenesis . . . . 41 than to the left due to the vascular anatomy.4.3 Clinical Presentation . . . . . . . . . . . . . . . 41 For the 10% of patients with atherosclerosis and acute thrombosis as the main cause for their arm4.4 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . 42 ischemia, the primary lesions are located in the4.5 Management and Treatment . . . . . . 42 brachiocephalic trunk or in the subclavian artery.4.5.1 Management Before Treatment . . . . . 42 Such pathologies are usually asymptomatic due to4.5.2 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 well-developed collaterals around the shoulder4.5.2.1 Embolectomy . . . . . . . . . . . . . . . . . . . . . . . 42 joint until thrombosis occurs, and they cause4.5.2.2 Endovascular Treatment . . . . . . . . . . . . 43 either micro- or macroembolization.4.5.3 Management After Treatment . . . . . . 43 Other less frequent causes of acute upper ex-4.6 Results and Outcome . . . . . . . . . . . . . . . 43 tremity ischemia are listed in Table 4.1. Further Reading . . . . . . . . . . . . . . . . . . . . 44 4.3 Clinical Presentation 4.1 Summary Acute arm ischemia is usually apparent on the basis of the physical examination. The symptoms History and physical examination are suf- are often relatively discreet, especially early after ficient for the diagnosis. onset. The explanation for this is the well devel- Few patients need angiography. oped collateral system circumventing the brachial Embolectomy should be performed in most artery around the elbow, which is the most com- patients. mon site for embolic obstruction. The “six Ps” – It is important to search for the embolic pain, pallor, paresthesia, paralysis, pulselessness, source. Table 4.1. Less common causes of acute upper ex- tremity ischemia 4.2 Background and Pathogenesis Cause CharacteristicsAcute ischemia in the upper extremity constitutes Arteritis Lesions in distal10–15% of all acute extremity ischemia. The etiol- and proximal arteriesogy is emboli in 90% of the patients. The reason Buerger’s disease Digital ischemia in youngfor this higher rate compared with the leg is that heavy smokersatherosclerosis is less common in arm arteries. Coagulation disorders GeneralizedEmboli have the same origins as in the lower or distal thrombosisextremity (see Chapter 10, p. 120) and usually end Raynaud’s disease Digital ischemiaup obstructing the brachial artery. Sometimes
  • 46. 42 Chapter 4 Acute Upper Extremity Ischemia Table 4.2. Frequency of signs and symptoms in pa- almost always preferable. It has been suggested tients with acute arm ischemia that in patients with a lower-arm blood pressure Presentation Percentage >60 mmHg embolectomy can be omitted, but such a strategy has not to our knowledge been evaluated Pulselessness 96 systematically. In a patient series of nearly symp- Coldness 94 tomless acute arm ischemia, which was left to re- Pain 85 solve spontaneously or with anticoagulation as the Paresthesia 45 only treatment, late symptoms developed in up to 45% of the cases. Surgical treatment is also fairly Dysfunction 45 straightforward. It can be performed using local anesthesia and is associated with few complica- tions. poikilothermia – are applicable also for acute Very often an embolus is a manifestation of arm ischemia, but coldness and color changes are severe cardiac disease, so the patient’s cardiopul- more prominent than for the legs. Accordingly, monary function should be assessed and opti- the most common findings in the physical exami- mized as soon as possible. Preoperative prepara- nation are a cold arm with diminished strength tions include an electrocardiogram (ECG) and and disturbed hand and finger motor functions. laboratory tests to guide anticoagulation treat- Tingling and numbness are also frequent. The ra- ment (see also Chapter 10, p. 25). Heparin treat- dial pulse is usually absent but is pounding in the ment is started perioperatively and continued upper arm proximal to the obstruction. postoperatively in most patients. Gangrene and rest pain appear only when the obstruction is distal to the elbow and affects both NOTE of the paired arteries in a finger or in the lower Embolectomy is the treatment of choice arm. Ischemic signs or symptoms suggesting acute for almost all patients with diagnosis of digital artery occlusion in only one or two fingers, acute arm ischemia, regardless of the imply microembolization. severity of ischemia. 4.4 Diagnostics 4.5.2 Operation Only the few patients with uncertain diagnosis, Embolectomy and those with a history and physical findings that As mentioned previously, the most common site indicates thrombosis, need additional work-up. for embolic obstruction is the brachial artery. Em- Examples include patients with a history of chron- bolectomy of these clots is performed by expos- ic arm ischemia (arm fatigue, muscle atrophy, and ing the brachial artery as described in Chapter 3 microembolization) and bruits over proximal ar- (p. 37). The arm is placed on an arm table. We pre- teries. Angiography should then be performed to fer to perform embolectomy using local anesthe- reveal the site of the causing lesion. Duplex ultra- sia. Often a transverse incision placed over the sound is rarely needed to diagnose acute arm isch- palpable brachial pulse can be used. If proximal emia but may occasionally be helpful. extension of the incision is required, this should be done in parallel with and dorsal to the dorsal aspect of the biceps muscle. It has to be kept in 4.5 Management and Treatment mind that 10–20% of patients may have a different brachial artery anatomy. The most common varia- 4.5.1 Management Before Treatment tion is a high bifurcation of the radial and ulnar arteries, and next in frequency is a doubled bra- Even though symptoms and examination findings chial artery. The procedure is described in the may be so subtle that conservative treatment is Technical Tips box. tempting, surgical removal of the obstruction is
  • 47. 4.6 Results and Outcome 43 An alternative location for embolectomy in the Endovascular Treatmentarm is to expose the brachial artery in the bicipi- Thrombolysis is as feasible for acute upper extrem-tal groove. A longitudinal incision starting 10 cm ity ischemia as it is in the leg. The limited ischemiaabove the elbow that is extended proximally is that often occurs after most embolic events be-then used. cause of the collateral network around the elbow also allows the time needed for planning and mov- TECHNICAL TIPS ing the patient to the angiosuite. The technique Embolectomy via the Brachial Artery involves cannulation in the groin with a 7-French sheath. Long guide wires and catheters are re- Exposure of this vessel is described in Chapter 3. quired to reach the occluded site and makes iden- A transverse arteriotomy in the brachial artery tification of proximal lesions possible. A new arte- is made as close as possible to the bifurcation rial puncture in the brachial artery may be neces- of the ulnar and radial arteries. The embolecto- sary for thrombolysis of distal occlusions. my is performed in proximal and distal direc- It can be argued that thrombolysis in spite of tions with #2 and #3 Fogarty catheters. Separate acceptable results, rarely is needed for treating this embolectomy in each branch should be done disease because open embolectomy can be per- if technically simple. The Fogarty catheter other- formed under local anesthesia with good results wise slips down into the larger and straighter and little surgical morbidity. The advantages with ulnar artery. The route of the catheter can be endovascular treatment are indeed limited. For checked by palpation at the wrist level when patients in whom suspicion of thrombosis is strong the inflated balloon passes. On the other hand, or when proximal lesions are likely, it should be restored flow in one of the arteries is usually attempted first. However, case series indicates that enough for a result that is sufficient for adequate results of thrombolysis are inferior for forearm hand perfusion. The arteriotomy is closed occlusions. In summary, thrombolysis is an alter- with interrupted 6-0 sutures, and distal pulses native but has little to offer in reducing risk or and the perfusion in the hand are evaluated. improving outcome compared with embolectomy If the result is inadequate – poor backflow after for most patients. embolectomy, absence of pulse, a weak continu- ous-wave Doppler signal, and questionable hand perfusion – the arteriotomy should be 4.5.3 Management After Treatment reopened and intraoperative angiography per- formed (Table 4.3 and Chapter 10, p. 128). Patients usually regain full function of their hands immediately after the procedure, and postopera- tive regimens consist of anticoagulation and aIf it is hard to achieve a good inflow, a proximal search for the embolic source. Heparin or lowlesion may cause the embolization or thrombosis. molecular weight heparin is administered as de-More complicated vascular procedures are then scribed in Chapter 10 (p. 129), usually followed byrequired to reestablish flow. The embolectomy coumadin. The search for cardiac sources mayattempt is then discontinued and the patient taken advocate repeated ECGs, echocardiography, andto the angiography suite for a complete examina- duplex ultrasound of proximal arteries.tion. If practically feasible, an alternative is toobtain the angiogram in the operating room. Fre-quently, however, the preferred treatment is endo- 4.6 Results and Outcomevascular, and this is better done in the angiographysuite. Occasionally the films will reveal a proximal The number of salvaged arms after surgical inter-obstruction that needs open repair. Examples of vention is very high, 90–95%, and arm functionsuch are carotid-subclavian, subclavian-axillary, is usually fully recovered. The remaining 5–10%and axillary-brachial bypasses. represents patients with extensive thrombosis involving many vascular segments and most branches of the distal arteries. The postoperative
  • 48. 44 Chapter 4 Acute Upper Extremity Ischemia Table 4.3. Technique for retrograde intraoperative an- giography Further Reading 1. Control proximal to arteriotomy is achieved Baguneid M, Dodd D, Fulford P, et al. Management of by finger compression and/or vessel loop acute nontraumatic upper limb ischemia. Angiol- ogy 1999; 50(9):715–720 2. Insert an angiography catheter or a small caliber Eyers P, Earnshaw JJ. Acute non-traumatic arm isch- baby feeding tube through the arteriotomy in aemia. Br J Surg 1998; 85(10):1340–1346 retrograde direction Pentti J, Salenius JP, Kuukasjarvi P, et al. Outcome of 3. Place the tip of the catheter proximal to the surgical treatment in acute upper limb ischaemia. suspected obstructing lesion Ann Chir Gynaecol 1995; 84(1):25–28 4. Inject contrast under simultaneous fluoroscopy Ricotta JJ, Scudder PA, McAndrew JA, et al. Manage- in lateral projection with a C-arm ment of acute ischemia of the upper extremity. Am J Surg 1983; 145(5):661–666 Whelan TJ Jr. Management of vascular disease of the upper extremity. Surg Clin North Am 1982; mortality is around 10–40% in most patient series, 62(3):373–389 reflecting that embolization often is a consequence of severe cardiac disease. Postoperative mortality is similar for thrombolysis to treat acute arm isch- emia, while early technical success is slightly lower or similar. Less favorable results with thromboly- sis are achieved when the distal arteries also are obstructed.
  • 49. Abdominal Vascular Injuries 5CONTENTS 5.7.3 Iliac Artery Injuries During Endovascular Procedures . . . 625.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45 5.7.4 Iatrogenic Injuries5.2 Background . . . . . . . . . . . . . . . . . . . . . . . . . 46 During Orthopedic Procedures . . . . . 625.2.1 Background . . . . . . . . . . . . . . . . . . . . . . . . . . 46 Further Reading . . . . . . . . . . . . . . . . . . . . 635.2.2 Magnitude of the Problem . . . . . . . . . . 465.2.3 Etiology and Pathophysiology . . . . . . 465.2.3.1 Penetrating Injury . . . . . . . . . . . . . . . . . . . 465.2.3.2 Blunt Injury . . . . . . . . . . . . . . . . . . . . . . . . . . 465.2.3.3 Pathophysiology . . . . . . . . . . . . . . . . . . . . 465.2.3.4 Associated Injuries . . . . . . . . . . . . . . . . . . 475.3 Clinical Presentation . . . . . . . . . . . . . . . 47 5.1 Summary5.3.1 Medical History . . . . . . . . . . . . . . . . . . . . . . 475.3.2 Clinical Signs and Symptoms . . . . . . . . 48 Up to 25% of patients with abdominal trauma may have major vascular injury.5.4 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . 48 Shock out of proportion to the extent of ex-5.5 Management and Treatment . . . . . . 50 ternal injury suggests abdominal vascular5.5.1 Management Before Treatment . . . . . 50 injury. Treatment and Management Isolated abdominal injury in patients with in the Emergency Department . . . . . . 50 shock suggests major vascular injury that5.5.1.2 Unstable Patients . . . . . . . . . . . . . . . . . . . 50 requires emergency laparotomy for con- Stable Patients . . . . . . . . . . . . . . . . . . . . . . 51 trol. Laparotomy or Not?. . . . . . . . . . . . . . . . . . 51 After the abdomen is entered, immediate5.5.1.5 Renal Artery Injuries . . . . . . . . . . . . . . . . . 51 control of the supraceliac aorta should be5.5.2 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . . 52 considered before continuing the opera- Preoperative Preparation . . . . . . . . . . . . 52 tion. Exploration . . . . . . . . . . . . . . . . . . . . . . . . . . 52 Retroperitoneal hematomas should not be5.5.2.4 Vessel Repair . . . . . . . . . . . . . . . . . . . . . . . . 57 explored right away unless they are actively5.5.2.5 Finishing the Operation . . . . . . . . . . . . . 60 bleeding.5.5.3 Endovascular Treatment . . . . . . . . . . . . 60 Stopping the procedure after the initial ex-5.5.4 Management After Treatment . . . . . . 60 ploration for damage control to allow time5.6 Results and Outcome . . . . . . . . . . . . . . . 61 for resuscitation in the intensive care unit5.7 Iatrogenic Vascular Injuries is often a reasonable initial treatment. in the Abdomen . . . . . . . . . . . . . . . . . . . . 61 If the patient’s condition allows and if en-5.7.1 Laparoscopic Injuries . . . . . . . . . . . . . . . . 61 dovascular methods are available, consider5.7.2 Iliac Arteries and Veins placing an aortic balloon from the left bra- During Surgery for Malignancies chial artery for temporary occlusion. in the Pelvis . . . . . . . . . . . . . . . . . . . . . . . . . 62
  • 50. 46 Chapter 5 Abdominal Vascular Injuries 5.2 Background 5.2.3 Etiology and Pathophysiology 5.2.1 Background Penetrating Injury Penetrating injury creates the types of damage Abdominal vascular trauma is fairly common in that are common for most arteries – transection, modern civilian life and is a highly lethal injury, laceration, intimal dissection, and thrombosis, as with overall mortality around 40% in some well as false aneurysms and arteriovenous fistula reported series. The main cause for this high formation. The first two are more common after mortality relates to problems transporting injured stab wounds. Gunshot wounds inflict more wide- patients to the hospital fast enough to prevent ex- spread damage to the vessel wall, depending on sanguination. Furthermore, abdominal vascular the bullet’s velocity. For example, high-velocity injuries are rarely isolated, and other organs are missiles at speeds >700 m/sec cause up to 20 times often severely damaged as well. These factors more damage than low-velocity projectiles. An make it essential to resuscitate promptly and es- artery located within 10–15 cm of the trajectory tablish a rapid diagnosis. regularly thromboses after a high-velocity gun- The surgeon managing patients with major ab- shot injury. dominal injuries must be experienced with vascu- lar surgical techniques and be able to expose the Blunt Injury aorta and its main branches, as well as the vena Typically, blunt injury to abdominal vessels occurs cava. Dissection and the extensive organ mobili- after road traffic accidents or falls from heights. zation required for control and repair are often Most commonly damaged are upper abdominal difficult. It is therefore important to develop a arteries and veins such as the infrarenal aorta. The routine that can be employed during exploration mechanism is compression of the aorta against the and control. lumbar spine by the steering wheel, especially when seat belts are not used. This causes intimal tears and thrombosis of the aorta. Full-blown rup- 5.2.2 Magnitude of the Problem ture has also been reported. Vessel injuries are much less frequent when seat belts are used. Avul- Major abdominal vascular injury is seen in up to sion of branches is also common and there is a 25% of patients admitted with vascular trauma. high incidence of associated injury to the small Blunt trauma is more common than penetrating arteries. Veins are usually not affected by blunt trauma in most European countries, while the op- trauma, except for the left renal vein. Major ab- posite is reported in areas where gunshot wounds dominal injuries may cause avulsion of arteries; in are more frequent. Abdominal injury represents descending order of occurrence the vessels injured 10–20% of all traumas to the body caused by road are the left renal vein, the renal arteries, the supe- traffic accidents. Major vascular injury is estimat- rior mesenteric artery (SMA), and the abdominal ed to occur in about 10% of cases of penetrating aorta just distal to the renal arteries. stab wounds in the abdomen and in about 25% of gunshot wounds. Blunt abdominal trauma affects Pathophysiology major vessels less frequently, estimates of below When an artery is perforated, blood extravasates 5% is common in the literature. into surrounding tissues, causing a hematoma that counteracts the blood pressure and facilitates NOTE spontaneous closure of the hole in the vessel. Major vascular injury is rather common When a vein is damaged, tamponade of the bleed- after abdominal trauma. ing often occurs, especially if retroperitoneal, un- less the peritoneum is torn or is entered during laparotomy. If vein damage is caused by a pelvic fracture a cavity is created around the fragments, preventing effective tamponade, and the bleeding continues. Venous and arterial bleeding within
  • 51. 5.3 Clinical Presentation 47the mesentery is also enhanced by the same mech- 5.3 Clinical Presentationanism. The high blood flow through major arter-ies in the abdomen makes spontaneous cessation 5.3.1 Medical Historyof bleeding less likely. Even the aorta, however, hasbeen reported to seal spontaneously after pene- In patients who arrive to the emergency depart-trating trauma when it is completely transected. If ment in shock with signs of penetrating or bluntan artery is partially lacerated, the severed ends abdominal injury, the medical history does notcannot contract; the hole is held open, and blood add much to the management, although informa-flows more easily into the abdominal cavity. Pa- tion about the mechanism of trauma is usefultients rarely survive for long in this circumstance. when estimating the risk of associated injuries There are two principle mechanisms of vascu- (Table 5.1). Knowing exactly when the injury oc-lar injury in blunt abdominal trauma: compres- curred and when the patient became unconscioussion and deceleration forces. The former may cause may assist in predicting outcome.crush injuries and intramural hematoma or lacer- Stable patients allows more time to gather in-ations. The latter cause stretching that creates ten- formation, and it is possible to ask direct questionssion between fixed and movable organs, leading to about the injury. This may provide importantavulsion or intimal disruption and thrombosis. clues about the possibility for major vascular injury. For example, patients with contained he- Associated Injuries matomas are either stable or have a history of aAny and all organs within the abdomen may be transient hypotensive period. This information isinjured in association with a major vessel injury. A easy to get from Emergency medical personnel.general rule is that for every major vascular injury, Patients complaining of increasing abdominalthree to four other organs are damaged as well. pain after either penetrating or blunt traumaThe rate depends on the etiology of the trauma, should be suspected of bleeding intraabdominally,the location on the abdominal wall where the im- especially if the blood pressure is decreasing.pact or wound is located, and the direction of the Shoulder pain and pain when breathing indicatetraumatic force. Table 5.1 gives an estimation of referred pain from blood irritating the diaphragm.the likelihood of injury to individual organs in Patients should be asked about leg pain as an indi-association with major vascular injury. cation of arterial occlusion or embolization; this In general, blunt injury is more commonly as- is particularly important after blunt trauma. Asociated with injury to many other organs, while history of hematuria indicates renal or bladderthis is slightly less likely for penetrating trauma. trauma.The small bowel is often injured by blunt trauma,and the kidneys and spleen are frequently dam-aged in both trauma types.Table 5.1. Probability of organ injury together with major arterial injury in the abdomen (compiled from sevencase series) Stabbing Gunshot Blunt trauma Liver + ++ +++ Pancreas ++ + ++ Stomach + ++ ++ Kidney +++ ++ ++ Spleen ++ + +++ Duodenum + + – Small bowel + ++ ++ Colon ++ ++ +
  • 52. 48 Chapter 5 Abdominal Vascular Injuries 5.3.2 Clinical Signs and Symptoms tration. Signs of a pelvic fracture should lead to a high suspicion for iliac vessel damage. The patient who presents with shock a short time Distal ischemia should also be excluded, and after injury to the abdomen should be presumed palpation of pulses in the groins and distally is to have a major vascular injury, with bleeding obligatory after any major trauma. Particularly directly into the peritoneal cavity. Increasing ab- after blunt trauma, distal ischemia may be the dominal distension or persistent hypotension de- only sign suggesting vessel damage. Unfortunate- spite aggressive resuscitation are other signs sug- ly, 25% of patients who experience blunt trauma gestive of continuing bleeding from an injured causing some degree of arterial obstruction have vessel, liver, or spleen. Shock out of proportion to normal femoral pulses. Physical examination the extent of external injuries, including fractures, should also include an assessment of the “six Ps” suggests abdominal vascular injury as the cause of (see Chapter 10, p. 121). In hemodynamically sta- the bleeding. The finding of a mass during palpa- ble patients with abnormal pulse examination, the tion, which is sometimes enlarging and pulsating, ankle–brachial index (ABI) should be measured strongly suggests major vessel damage. The ana- to aid in assessing limb ischemia. An ABI <0.9 – tomical location gives some hint about the specific especially unilaterally – implies some degree of vessel injured. vessel obstruction. In general, trauma patients tend to be young and therefore do not have sig- NOTE nificant atherosclerosis, so an asymmetrical ABI Abdominal distension and shock out of could be the only clue to an occult vascular injury. proportion to the extent of external Penetrating injury together with absent pulses injuries indicate major vascular trauma. strongly indicates trauma to a major axial artery. In stable patients, assessment should include the location of the wounds to assess the likelihood for 5.4 Diagnostics intraabdominal injury. As a general rule, all pen- etrating wounds between the nipple line and the In some circumstances, patients are so unstable groin should be presumed to have penetrated the that they must be taken to the operating room for abdominal wall. Penetrating wounds in the mid- laparotomy without diagnostic procedures. In line carry a substantial risk for aortic and vena ca- stable multitrauma patients in whom laparotomy val injury, but lateral wounds can also cause injury is not indicated for other reasons, additional to these structures. Wounds around the umbilicus diagnostic measures may identify major vascular indicates that the bifurcation of these vessels is injury, determine the extent of damage to other likely to be affected. Entrance wounds located be- organs, and facilitate treatment planning. low the umbilicus suggest iliac vessel injury. A tra- Ultrasonography can and should be performed jectory of a gunshot wound that passes the midline in most patients with abdominal trauma, regard- also indicated major vascular trauma. It has to be less of their condition. The abdomen can be remembered, however, that it is notoriously diffi- scanned in the emergency department without cult to assess trajectories, and bone and even the moving the patient and often takes less than 10 min muscle fascia may deflect bullets. The victim’s to perform. Its main objective is to detect hemo- body position at the time of injury can also influ- peritoneum as a possible source of hypotension. It ence which structures are damaged. Intraabdomi- may also detect large hematomas and pseudoaneu- nal injuries may also be a result of wounds to the rysms, but often misses retroperitoneal hemor- back and buttocks. rhage. Ultrasound also has low sensitivity for de- Large hematomas tend to cause abdominal dis- tecting and excluding injuries to other organs such tension and tenderness in conscious patients. Ten- as the intestines, liver, spleen, and kidneys. derness may also be a result of peritonitis due to Computed tomography (CT) has become a contamination by perforated bowel or bowel isch- valuable and widely used tool for evaluating most emia. Blood in the urine, rectum, vagina, or a na- stable patients with abdominal trauma. The CT sogastric tube also indicates intraperitoneal pene- scan provides detailed information about the ret-
  • 53. 5.4 Diagnostics 49 dence of arterial damage. The arteriogram is then the initial step in an endovascular procedure for definite treatment. Examples are arteriovenous fistulas, pseudoaneurysm, active bleeding from branch vessels, liver and spleen injuries, and pelvic fractures. Other indications for angiography are to diagnose suspected minor arterial lesions after blunt trauma and to assess patients with signs of organ or distal ischemia. Examples include aortic and renal artery intimal tears and thrombosis. A plain x-ray may be indicated in patients with gunshot wounds in order to locate the bullet, to facilitate estimation of the trajectory after apply- ing markers at the entry and exit sites. If the bulletFig. 5.1. An example of computed tomography show- is suspected to have passed through regions whereing retroperitoneal bleeding caused by blunt abdomi- major vessels are located, angiography may benal trauma indicated. Plain x-ray can also identify gas in the abdominal cavity. Most of this information can also be gained from CT. Diagnostic peritoneal lavage (DPL) was theroperitoneal space, presence of hemoperitoneum, standard way to diagnose intraabdominal bleed-active bleeding, false aneurysms, and damage to ing before the CT era. Because of its invasivenessother organs. The main limitation is its inability to and the very high sensitivity in detecting evenidentify intestinal perforation, diaphragmatic in- minute intraabdominal bleedings that often doesjuries, and mesenteric tears. For blunt trauma it not need surgical repair, it is much less often per-gives information about the extent of damage to formed today. Furthermore, it may not detect eventhe liver and spleen and thereby often identifies significant retroperitoneal bleeding. DPL is indi-patients who do not need laparotomy and those cated in unstable patients when it is vital to deter-who should undergo arteriography. Because CT is mine the source of bleeding and when ultrasoundunreliable in diagnosing intestinal perforation, it is inconclusive and CT not possible to perform. Ithas not been as valuable after penetrating trauma. may also be considered in stable patients when CTThe use of contemporary spiral CT with intrave- and ultrasound are not available or in multitrau-nous contrast has made it possible to detect active ma patients who require neurological or orthope-bleeding, missile paths, and visceral perforation in dic operations and therefore will be inaccessibleboth blunt and penetrating trauma. For most ab- for evaluation for long time periods. Technicaldominal vascular injuries in stable patients, it is an details about DPL are beyond the scope of thisexcellent screening tool, and when enhanced by text, so for descriptions on how to carry out DPL,contrast, bleeding and vessel thrombosis can also we recommend textbooks on abdominal diagnosed. Examples include detection of renal Intravenous pyelography (IVP) is a tool for di-and visceral artery injuries, as seen in Fig. 5.1. agnosing renal vascular injury that largely has Some authors have recently suggested that CT been replaced by CT. It may still have a place in theshould be performed even in unstable patients in operating room because it can be used during sur-order to reduce the number of unnecessary lapa- gery. The sign of renal vascular injury is lack of therotomies. This concept depends in part on the appearance of contrast in one of the kidneys. Itsavailability of CT, its location in the hospital and main limitation is low sensitivity, and up to a thirdon a strict management protocol. of patients with vascular injury have normal IVPs Angiography is rarely used today to diagnose Laparoscopy has yet to find its place for evalu-arterial injury after abdominal trauma. Excep- ating patients with suspected abdominal vasculartions are stable patients with no signs of peritonitis injury. It requires an operating suite and generalfor whom a CT scan has given some indirect evi- anesthesia, it cannot easily evaluate the retroperi-
  • 54. 50 Chapter 5 Abdominal Vascular Injuries toneal space, and even small amounts of intraab- Unstable Patients dominal bleeding may disturb visualization. Its The management of unstable patients is summa- main advantage is reported to be diagnosis of dia- rized in Table 5.2. Patients in shock with isolated phragmatic injuries in stable patients. abdominal injury should undergo emergency lap- arotomy. An abdominal ultrasound scan is needed in multiply injured patients with injuries in the 5.5 Management and Treatment thorax, head, or extremities. Unstable patients with multiple injuries and a negative ultrasound 5.5.1 Management Before Treatment scan are a specific diagnostic problem. It may be worthwhile to pursue the evaluation to rule out Treatment and Management abdominal bleeding as a possible cause of hypo- in the Emergency Department tension in these patients. If they are in severe The early management should follow the ABCs of shock, DPL may be indicated to rule out intra- trauma resuscitation. Patients in shock should be abdominal origin of the bleeding. CT may also intubated and ventilated with 100% oxygen, and at be an option in “less” unstable patients, especially least two large intravenous (IV) lines should be if there is improvement with resuscitation and CT inserted, preferably in the upper extremity. Fluid is readily available. replacement through vascular access in the lower extremities may extravasate and not reach the NOTE heart if pelvic veins or the vena cava are injured. Unstable patients with a negative ultra- The strategy and technique for obtaining rapid ve- sound scan pose a particular diagnostic nous access in trauma are described in Chapter 11, problem when trying to exclude a major p. 137. When the lines are in place blood should be vascular abdominal injury. drawn for routine analysis and blood typing and cross-matching. Laboratory studies follow stan- If DPL is negative, the cause of bleeding is likely to dard trauma management and should also include be outside the abdomen, but false negatives can acid-base balance, serum amylase, and urineanal- occur. DPL may miss a serious retroperitoneal ysis. Fluid resuscitation with warm lactated Ring- bleeding. The ultimate management will then be a er’s solution is continued or started. If the patient matter of clinical judgment regarding whether the has obvious severe blood loss, blood and plasma patient will tolerate a CT scan or must be moved to are added as soon as possible. Platelet substitution the operating room for emergency laparotomy. should also be considered. A Foley catheter and a The boxes in Table 5.2 indicating “maybe” repre- nasogastric tube should be inserted in all patients sent circumstances in which clinical judgment is with abdominal trauma. Hypothermia must be especially important for the management. prevented by all means. If the patient is severely unstable and probably Physical examination should be done during not tolerates examination with CT, DPL could the second survey, and the findings lead the man- possibly rule out intraperitoneal hemorrhage. A agement. For some patients, further diagnostic positive DPL is an indication for surgery, while a procedures will determine whether they require negative DPL points to the need for continued surgery or nonsurgical treatment. Ultrasound, for evaluation as discussed above. More resuscitation, instance, performed in the emergency department for example, may be attempted followed by a CT can rule out or verify intraabdominal bleeding. scan under close surveillance. Patients with associated thoracic injury should undergo chest x-ray to detect hemothorax and Emergency Thoracotomy other thoracic injuries as possible sources of Patients with penetrating abdominal injury who bleeding. However, as outlined below, CT is now are unconscious and have prolonged severe hypo- the most important diagnostic modality for stable tension (<70 mmHg) but no other apparent inju- patients. ries causing the shock may occasionally be saved by immediate proximal control of the aorta in the emergency/operating room. Cross-clamping
  • 55. 5.5 Management and Treatment 51Table 5.2. Management of abdominal injuries when vascular damage is suspected Patient’s Other Ultrasonography Computed Diagnostic Surgery condition injuries tomography peritoneal lavage Finding Finding Finding Unstable No No No No Yes (Yesa) Yes Yes Positive No No Yes Negative Maybe Maybe Positive Yes Negative Maybe Stable Yes/no No Yes Positive No Maybe Negative No Observationa After blunt trauma, all patients should undergo ultrasonography.of the descending thoracic aorta through a thora- Stable patients undergoing CT must be super-cotomy in the 4th or 5th interspace may then be vised at all times because they may become un-attempted if the patient is believed to have a realis- stable quickly. Personnel must therefore be skilledtic chance of survival (e.g., became moribund in in assessing vital signs and the abdomen through-the emergency department or lost measurable out the examination.blood pressure during the last part of the trans-port to the hospital). The technique is briefly sum- Laparotomy or Not?marized in Chapter 2 (p. 22). Aortic clamping be- Unnecessary laparotomy is performed in up tofore laparotomy can facilitate perfusion through 25% of patients with abdominal trauma and is as-the coronary and carotid arteries and prevent fur- sociated with considerable morbidity and cost.ther bleeding during laparotomy. Deterioration is Nonoperative treatment has therefore grown incommon in these severely ill patients when the ab- popularity but has to be balanced against the pricedominal wall is incised and the tamponade it of missed injuries. This approach has increasedmaintains is released. It is disappointing, however, the need for additional diagnostic procedures tohow seldom this maneuver leads to the patient’s aid the decision process. Table 5.2 summarizessurvival. these diagnostic modalities and how they can be used for managing the patients. Stable Patients Nonoperative treatment is particularly appeal-Stable patients with clinical signs of peritonitis af- ing in stable and multitrauma patients. Examplester penetrating trauma should undergo laparoto- of injuries that may be treated nonoperatively aremy without delay for diagnostic procedures. All some liver, spleen, and renal injuries. For detailedothers – with either blunt or penetrating trauma discussion on this subject, we recommend text-– should be evaluated with CT to reveal the extent books on trauma. Vascular injuries may be treatedof injury (Table 5.2). If ultrasonography in the without open surgery using endovascular meth-emergency department is performed routinely in ods. One example is embolization of bleeding pel-all trauma patients, it can be added to the diagnos- vic vessels caused by pelvic fractures; another istic process, but most stable patients admitted after renal artery injuries.blunt trauma will need CT scanning regardless ofultrasound findings. For example, surgery is indi- Renal Artery Injuriescated for patients with ongoing active bleeding, The most common type of renal vascular injuryaortic thrombosis, or large hematomas caused by after blunt trauma is thrombosis. This is usuallyorgan injury. For other injuries, such as branch diagnosed by CT. For most blunt injuries, non-vessel bleeding, renal or SMA thrombosis, and operative treatment is appropriate if there are nopelvic arterial injuries, angiography followed by other indications for operative intervention, suchendovascular treatment is often the best option. as when the diagnosis is made more than 12 h after
  • 56. 52 Chapter 5 Abdominal Vascular Injuries the trauma occurred. Reconstruction attempts by compressing it against the spine with an aortic after renal ischemia of over 10–12 h are usually occluder. To perform this maneuver it is some- futile, and the kidney will not regain its function times necessary to mobilize the left lobe of the if this time limit is passed; however, successful liver to the right, as described in Chapter 7 (pp. 83, revascularization has been performed after 24 h of 84). If the hematoma is located above the trans- ischemia. Exceptions when salvage may be tried verse mesocolon and aortic compression does not after longer ischemia times, are bilateral renal rise the blood pressure, supraceliac or juxtaceliac ischemia, and patients with retrograde blood flow bleeding should be suspected. Extension of the in- as observed on an arteriogram indicating some cision into the thoracic area to obtain occlusion of collateral supply. the descending thoracic aorta is then recommend- Renal artery thrombosis following trauma can ed. This can be accomplished by dividing the usually be treated by angioplasty and stenting, diaphragmatic crura and rarely requires median provided that rapid access to the angiosuite is pos- sternotomy. sible. Also, minor lesions such as intimal flaps in The aortic compression or occlusion is main- the renal arteries do not always need surgical tained while evacuating blood and blood clots. Re- treatment. Such minor lesions should be treated by member that blood clots tend to accumulate close observation. This includes patients with segmen- to the bleeding site. Next, all sites where active tal parenchymal ischemia. Accordingly, surgical bleeding is noticed or suspected are packed with reconstruction is saved for patients with active laparotomy pads. Such pads usually stop even bleeding and for situations when the diagnosis is quite substantial bleeding from the liver and made during laparotomy. spleen as well as all venous bleedings, including bleeding from the vena cava. Bleeding from the aorta, iliac, celiac axis, SMA, and renal arteries, on 5.5.2 Operation the other hand, will usually continue despite pack- ing if the aortic occlusion is released and the pa- Preoperative Preparation tient not is hypotensive. Visual large arterial hem- The following section describes the recommended orrage may be handled without further dissection, procedure for a patient with active intraabdomi- by ligature but one must be careful not to interrupt nal bleeding. It is also applicable for stable patients the proximal SMA, aorta, or the renal arteries. in whom more time is initially available. Regard- Temporary shunting may be a solution for these less, the patient should be prepped from the chin vessels. to the knees so thoracic and groin vessel access So far the whole procedure should take less is possible if required. The saphenous vein must than 10–20 min. also be accessible for harvest. After the patient is prepped and draped and the surgeon is dressed NOTE and ready, the patient is quickly anesthetized fol- For patients in shock, the peritoneum is lowed by the start of the operation. left intact until the fascia is opened in its entire length to preserve the peritoneal Exploration tamponade as long as possible. Exploration At this point, bleeding sources and their serious- A midline incision from the xiphoid process to the ness are assessed. If the patient is hypothermic pubic bone is best for most situations. It is impor- and has coagulopathy, the best decision could be tant to divide fat and fascia for the entire length of to stop the procedure, to temporarily close the ab- the wound before the peritoneum is incised. The domen and continue resuscitation in the intensive peritoneum is then opened rapidly – particularly care unit. This option, or “damage control” break, if the blood pressure drops after the abdomen is may be considered even with some continuing ac- entered – and the lesser omentum is opened and tive bleeding. Damaged bowel segments are ligated widened using fingers. The aorta is palpated with and injured ureters externalized before temporary the index finger and can be occluded manually or closure of the skin. The other option is to continue
  • 57. 5.5 Management and Treatment 53the operation by focusing on definite control of technique is further described in Chapter 7 (p. 84).the most severe bleeding sites. While the exposure also gives satisfactory proxi- mal control to repair infrarenal aortic injuries,NOTE the clamp should be moved to an infrarenal site as Aortic compression at the supraceliac soon as possible. If the patient’s condition allows level is often a good way to achieve and endovascular methods are available, the place- temporary proximal control while ment of an aortic balloon through a left brachial assessing the damage. or femoral artery access, is of great potential value. This is best performed in the operating room. It Exposure and Control makes temporary occlusion of the aorta at differ-Before the operation for definitive control contin- ent levels possible in case of uncontrollable bleed-ues, packing is reinforced by adding more pads. ing during dissection. The technique is also de-Those packs should reapproximate disrupted tis- scribed in Chapter 7 (p. 83).sue planes if possible. Minor bleeding sites should The technique for vascular exposure and finalbe left for later, unless they disturb the surgical control of other bleeding sites is described in thefield. If the main bleeding appears to come from Technical Tips box. Active bleeding from arteriesthe aorta at the suprarenal or juxtarenal level, the and veins around the liver hilus can be controlledmanual supraceliac aortic occlusion is changed to by using the “Pringle maneuver” – digital occlu-a clamp. During the time needed for the initial ex- sion of the hepatoduodenal ligament – followed byploration described before, resuscitation can often careful dissection of the separate vessels.improve the patient’s condition enough to allowtemporary release of the aortic occlusion. If not, it NOTEis often wise to wait a while before trying to clamp Stopping the procedure after the initialthe supraceliac aorta more permanently. The aorta exploration of damage control to allowis freed by finger dissection, sporadically aided by time for resuscitation in the intensivecutting the muscle fibers from the diaphragmatic care unit is often a reasonable initialcrus with a long-bladed pair of scissors. This treatment.exposure is necessary for clamp placement. The TECHNICAL TIPS Exposure of Different Intraabdominal Vascular Segments Suprarenal Aorta and its Branches practical for repairing most injuries. On the other The best way to expose the suprarenal aorta, the hand, including the left kidney with the rotated origin of the SMA, the celiac axis, and the left renal viscera gives access to the posterior wall of the artery is to perform a “left medial visceral rota- aorta. When performed, little additional dissec- tion.” Divide the peritoneal reflection of the de- tion enables proximal control using a Satinsky scending colon, release the splenic flexure, and clamp. The clamp is placed as distal as possible on cut the attachments between the spleen and the the aorta but sufficiently above the wounded area diaphragm. Rotate the table slightly to the right to permit repair. Distal control is achieved by and move all viscera, including the colon, small clamps, balloons, or a Foley catheter. bowel, spleen, and the gastric fundus, to the right Injuries to the portal vein are exposed and con- side of the abdomen and cover all organs in large, trolled by dividing the head of the pancreas be- moist lap pads. This maneuver can be employed tween clamps or staplers to control the superior either in a plane dorsal to the left kidney – which mesenteric and splenic veins. Sometimes the gas- will include the kidney with the viscera rotated to troduodenal artery must be divided to facilitate the right – or ventral to the kidney. It is slightly exposure. (See Fig. 5.2.) more difficult to find the appropriate dissection plane for the latter approach, but this is more
  • 58. 54 Chapter 5 Abdominal Vascular Injuries TECHNICAL TIPS Exposure of Different Intraabdominal Vascular Segments (continued) Vena Cava and Right Renal Vein the omentum minus as described in the main text. and Artery The recommendation is to clamp the aorta if the Exposure of the infrahepatic vena cava and the blood pressure falls to 60 mmHg or less. If possi- right side of aorta, including the portal vein and ble, infrarenal cross-clamping is employed, espe- the distal part of the SMA, is initiated by dividing cially if clamping is required for a long time to the attachments of the ascending colon, including achieve vascular repair. The fourth step is to mobi- the hepatic flexure. Mobilize the colon, duode- lize the liver by dividing all hepatic ligaments – the num, and the head of pancreas medially – perform falciform, teres, and right and left triangular liga- a full “Kocher maneuver” by dividing the lateral, ments – and clamp the suprarenal cava. This must superior, and inferior attachments of the duode- be done with care so the bleeding does not in- num – and cover the organs in lap pads and place crease. Control of the proximal vena cava can be them under retractors. When the dissection is con- achieved below the diaphragm by continuing the tinued through the hematoma, the renal vein is blunt and sharp dissection through the falciform encountered first. To enable mobilization upward ligament. At this level the vena cava is freed cir- and downward, it is banded and freed from sur- cumferentially to permit clamping well above the rounding tissue. The renal artery is usually located hepatic veins. Sometimes supradiaphragmatic ex- below or somewhat cranially to the vein. Proximal posure is necessary. A right anterolateral incision control of the renal artery is accomplished either is then made in the diaphragm, and the dissection on the left side of the vena cava or below the renal is continued by opening the dorsal pericardial vein. A DeBakey clamp is used unless the injury is fold until the suprahepatic vena cava is reached. located close to the arterial origin; then partial Finally, the liver is mobilized upward from the aortic occlusion with a larger clamp is necessary. right and left to expose as much as possible of the As shown in Fig. 5.2, venous control is accom- retrohepatic vena cava. plished by digital or sponge-stick compression of the vena cava distal and proximal to the wounded Infrarenal Aorta area. Another option for control during vena cava The aorta is exposed as for elective aortic proce- repair is to insert a Foley catheter into the injured dures. Wrap the small bowel in moist lap pads and vessel and inflate the balloon in the hole. Dorsal move it to the right side of the abdomen. Incise cava injuries at the level of the renal vein some- the peritoneal reflection over the distal portions times necessitate mobilization and medial rota- of the duodenum and mobilize it to the right and tion of the right kidney to expose the wounded cephalad. Open the peritoneum directly over the area. This approach is also the best way to expose infrarenal aorta and free it from surrounding tis- the portal vein within the head of the pancreas. sue so that a clamp can be placed proximal to the The reason why it works is that it is the most dorsal injury. Another clamp distally or a Foley catheter structure in the portal triad (Fig. 5.3). inserted in the hole is used for distal control. If the injury is in one of the common iliac arteries or is Retrohepatic Vena Cava close to the bifurcation, the iliac arteries must be First, the inflow to the liver – the hepatic artery controlled distally. Dissection and clamping of and portal vein – is clamped together with the particularly the right common iliac artery must be bile duct. Use a small angled vascular clamp. Sec- done with care so the iliac vein located under- ond, the infrahepatic vena cava is freed as de- neath not is damaged. If the iliac veins are injured, scribed above and carefully cross-clamped proxi- exposure sometimes necessitates temporary divi- mal to the renal veins. Third, the proximal aorta sion of the iliac artery to reach the injured vein. is exposed to be ready for cross-clamping if the Control is obtained by manual compression. patient becomes hypotensive due to the cava disruption. This exploration is performed through
  • 59. 5.5 Management and Treatment 55 Iliac Arteries and Veins after mobilizing the sigmoid colon to the right The iliac arteries on the right side are found after and incising the peritoneum. The arteries and mobilizing the small bowel to the left and the ce- veins are usually quite easy to separate and con- cum proximally. The left-sided arteries are found trol at this level. Fig. 5.3. Peritoneal incision for a “Kocher maneuver” to mobilize the duodenum, small intestine, and right colon for a “right medial visceral rotation.” This allows exposure of the entire inferior vena cava, right renal, and iliac vesselsFig. 5.2. Medial rightward rotation of the left viscera,exposing the aorta from the diaphragm and all theway down to the iliac arteries (“left medial visceral rota-tion”)
  • 60. 56 Chapter 5 Abdominal Vascular Injuries It is necessary to have previous experience in liver necrosis and possibly death. “Medial visceral rota- surgery to successfully accomplish “total” control tion” or “high” infrarenal aortic exposure provides of liver injuries, and the medial visceral rotation access to the first 3–4 cm of the SMA, but the next for suprarenal aortic and cava exposure may also part of the vessel is incorporated in the pancreas. be very difficult without experience. Surgical hematomas in this area make the dissec- tion even more difficult. Therefore, it has been Retrohepatic Injuries. Particularly cumbersome suggested that the pancreas shall be divided to is control of injuries to the retrohepatic vena cava. expose SMA injuries. Another option is to leave This type of exposure is difficult because the liver the injured area and perform a bypass from the covers the entire anterior surface of the vena cava. aorta to a distal part of the SMA and ligate it at its The low number of patients surviving long enough origin. When a large hematoma around the head to arrive at the hospital with this type of injury of the pancreas is encountered and the bowel is also makes it hard for most surgeons to gather ischemic, the middle part of the SMA is probably experience with it. The special problems encoun- injured, and such a bypass can be attempted for tered concern the difficult access (because, as maintaining bowel perfusion. stated, the liver covers the vena cava) and the re- duced blood volume returning to the heart when NOTE the vena cava is clamped. The aorta, the renal arteries, and the A number of methods have been suggested for proximal part of the SMA should not control. One example is atriocaval shunting by in- be ligated for control during damage serting a large tube into the vena cava through a control surgery. hole in right atrium’s appendage. In the Technical Tips box, the technique for total clamping and control directly without adjunctive measures is Retroperitoneal Hematomas described because we feel this may occasionally be Particularly after blunt trauma, intact retroperito- a practical approach for controlling unmanageable neal hematomas are a common finding during bleeding from this area. For immediate control laparotomy. If such hematomas are not bleeding during the exploratory procedure for total control actively or expanding, they should not be explored (clamping the aorta, the infrarenal vena cava, and right away. Other injuries can be treated first if the suprahepatic vena cava and doing the Pringle needed and if sufficient time is available, addition- maneuver), the liver is compressed dorsally against al diagnostic work-up pursued. Hematomas with the spine manually and by using lap pads. Control signs of active bleeding and those that appear to be of bleeding by direct pressure is facilitated by di- expanding rapidly should be left intact until prox- viding the falciform ligament and tilting the liver imal and distal control is achieved. downward. However, it is reasonable to refrain Even small hematomas can harbor significant from attempting to repair injuries to the retrohe- vessel injuries. patic vena cava and instead, as the only measure When the surgeon is selecting the approach taken, pack the liver to reduce the bleeding. for vascular exposure and control, the location of the hematoma should be considered. A midline NOTE hematoma superior to the transverse mesocolon It is rarely sensible to try to repair retro- indicates injury to the suprarenal aorta or its hepatic vena cava injuries in unstable branches. If combined with ischemic bowel signs, patients. injury to the SMA should be suspected. Blood in the area of the portal triad suggests hepatic artery Superior Mesenteric Artery Injuries. SMA in- or portal vein injury. A midline infrarenal aortic juries can also be quite difficult to expose and or vena cava injury is suspected when the hemato- control. The importance of the SMA for perfusing ma is located below the mesocolon. Lateral perito- the intestine makes SMA injuries particularly neal hematomas occur after renal vessel and pa- cumbersome to manage. Delaying restoration of renchymal injuries. A pelvic hematoma indicate flow more than 4–6 h inevitably leads to bowel iliac vessel damage.
  • 61. 5.5 Management and Treatment 57 Because of their propensity to contain major Arterial Injuriesvessel damage, it is recommended to explore most In the suprarenal aortic area, the celiac axis can behematomas in the midline. As mentioned in the ligated for bleeding control and better exposure ofsection on management (page 51), contained kid- the aorta if injured. Although collateral supply toney and renal vessel injuries after blunt trauma the intestine is usually excellent in most traumacan often be treated nonsurgically. Therefore, lat- patients, there is a substantial risk for gallbladdereral hematomas found after blunt injury should be necrosis. Therefore, celiac axis ligation is recom-left intact. A common opinion is that, after pene- mended primarily in multitrauma high-risk pa-trating injury, lateral hematomas should be ex- tients in whom portal blood flow is intact. Aorticplored because they are more often associated with injuries at this level are repaired by 3-0 or 4-0 su-major vessel damage. Our recommendation, how- tures. The first 3–4 cm of SMA accessible throughever, is to leave all nonexpanding lateral hemato- suprarenal exposure must be repaired if injured.mas, regardless of trauma mechanism. Instead, the The middle portion can be ligated provided thatpatient should undergo CT, IVP, or angiography to blood flow through the celiac axis and inferiorrule out major vessel injury and urinary leaks. mesenteric artery is intact. Accordingly, ligating The most common cause of pelvic hematomas both the celiac axis and the SMA leads to extensiveafter blunt trauma is pelvic fracture. Hematomas necrosis and should not be done. A bypass fromin this area should not be explored routinely. Even the infrarenal aorta using saphenous vein to theif the pelvic hematoma is expanding, it is often distal SMA is a good option if feasible. The left re-better to pack the pelvic area and continue the nal artery should also be mended if possible; 5-0work-up with arteriography. For penetrating trau- sutures are often suitable, and patches are usedma, on the other hand, it is usually wise to explore liberally for both renal artery and SMA repair. Ifpelvic hematomas after securing proximal control the left renal artery is severely damaged, nephrec-to exclude vessel damage. tomy is an option to consider when the right kid- ney is functioning properly. Vessel Repair The right renal artery is encountered during ex-The principles of repair are similar to those for all posure of the right infrarenal vena cava. As for theother vascular injuries in the body. Lacerations left renal artery, repair is advisable. Injuries to thecan be sutured directly, using polypropylene su- distal SMA can be treated by ligature if repair isture appropriate to the vessel size. For larger holes not easy.a patch is used to avoid vessel narrowing. Vein is Repair of the infrarenal aorta is accomplishedthe preferred material. Complete transections can by suture or graft interposition. For thrombosisoccasionally be sutured end to end, but interposi- occurring after blunt trauma, it is important to re-tion grafting by using a saphenous vein is usually member to ensure that the vessel wall is in goodneeded. For renal, SMA, and celiac axis arterial condition before suturing the anastomosis. Ifrepair, the saphenous vein can be used as it is, but injured, the inferior mesenteric artery is ligated asfor aortic injuries larger sizes are required. Then, close to the aorta as possible. Common iliac arter-and if the abdomen is contaminated by perforated ies should be repaired using 5-0 sutures or graftbowel, a vein graft – which is more infection interposition. If either one of these vessels is ligat-resistant – is manufactured by suturing several ed, amputation rates up to 50% have been report-vein pieces together as described on Chapter 15, ed. Also, the external iliac arteries should be re-p. 189. Otherwise, expanded polytetrafluoroethyl- paired, but the internal iliac arteries can be ligated.ene (ePTFE) or polyester grafts can be used. Se- Interrupting blood flow through one of the exter-verely damaged vessels must be debrided to pro- nal iliac arteries leads to almost the same amputa-vide intact vessel walls before the anastomoses are tion rate as ligating the common iliac arteries.sutured. Vein lacerations and transection are Proximal ligature followed by a femorofemoraltreated in exactly the same way as arteries. Some bypass is a good alternative for repairing unilat-vessels in the abdomen can also be ligated without eral iliac artery injuries.significant morbidity. This is discussed below, Injuries to the common hepatic artery in thelisted in the same order as the areas described in portal triad do not need to be repaired if portalthe previous section on exploration and control. vein flow is adequate and there is no apparent liver
  • 62. 58 Chapter 5 Abdominal Vascular Injuries damage. If the proper hepatic artery is ligated, the postoperative period but is usually well tolerated. gallbladder may become gangrenous and should No effort should be spared to repair the right renal be excised liberally. If possible, lacerations in the vein if injured because, in contrast to the left side, proper hepatic artery should be sutured, but the collateral venous outflow is essentially lacking. If artery must be separated from the portal vein and the vein must be ligated in difficult situations, the common bile duct to avoid injuries to these right-sided nephrectomy is warranted. Also, the structures. Splenic and gastric arteries can be distal parts of the superficial mesenteric vein ligated without morbidity. should be repaired if straightforward. Portal vein injuries are taken care of by venoraphy or graft Venous Injuries interposition using 5-0 sutures if reasonably easy. In general, venous injuries are more difficult to Portacaval shunts have also been constructed to manage than arterial ones. There are several rea- repair injuries to the portal vein. It the patient is sons for this. It is more difficult to expose and re- hypotensive and hypothermic with extensive pair vein injuries due to their thin and fragile injuries, it is wise to ligate the portal vein. In most walls. Distal control is also more difficult to patient series, this maneuver is reported to be achieve. While arterial backbleeding often is associated with survival and low postoperative sparse when the patient is in shock, distal bleeding portal hypertension rates. from injured veins increases after proximal con- trol. For surgeons without experience in venous NOTE surgery, the consequence is that it is difficult to re- Repair of the right renal vein is important pair major venous injuries. Fortunately, many to save renal function on this side. veins can be ligated in difficult situations. The left renal vein encountered during suprare- Suspected injuries to the retrohepatic vena cava nal aortic exposure can be ligated, preferably as area should be packed, and this is often sufficient close to vena cava as possible to allow alternative for permanent bleeding control. Repair of injuries outflow through collaterals. Injured veins around to the vena cava behind the liver and the few cen- the celiac axis can also be ligated. If possible, the timeters of the right and left hepatic veins outside proximal superior mesenteric vein should be re- it requires total vascular control as described pre- paired. This vein lies in close connection to the viously. A few successful cases have been reported SMA. Control is achieved by manual or rubber- in the literature. To facilitate repair, one branch band occlusion while suturing the defect. If repair from the hepatic vein can be ligated without mor- is not possible, ligation leads to venous congestion bidity. If the total venous outflow is compromised of the intestine. In general, this is quite well toler- by interruption of the entire hepatic vein, lobec- ated, and the patient usually survives. However, if tomy may be necessary. Clips can control caudate the patient becomes hypotensive in the postopera- veins behind the liver. Anecdotally, retrohepatic tive period, it may be fatal. caval injuries have been repaired through a liver Infrahepatic vena cava injuries should be re- injury separating the lobes. Final access to the paired if possible. Interrupted 4-0 sutures can be cava may then be achieved by separating parts of used for most lacerations. For stab wounds pene- any remaining liver tissue using the “finger frac- trating both the ventral and dorsal part of the vein, ture” technique. access for repair includes extending the anterior Damaged common iliac veins and the first parts opening to be able to close the hole on the dorsal of the vena cava are difficult to expose for repair. side from the inside. Alternatively, the vena cava is The aortic bifurcation and the common iliac ar- dissected free and the lumbar branches secured teries must be freed entirely to allow mobilization and rolled over to expose the wound for suturing. and control of the veins. This includes division of (See Fig. 5.4.) lumbar arteries and the sacral artery. As men- Small dorsal vena cava injuries not actively tioned, temporary division of the left iliac artery is bleeding can be observed. In multiply injured pa- often required to provide exposure of the left iliac tients in bad condition, ligation rather than repair vein. Polypropylene suture, 5-0, is appropriate for may be preferable. This leads to leg swelling in the repair. A good option for multiply injured patients
  • 63. 5.5 Management and Treatment 59Fig. 5.4. a Manual control of bleeding from an injury lar clamps are used for bleeding control. c Repair of ain the ventral wall of vena cava. b Repair of the dor- dorsal injury after separation and rotation of the venasal injury of the vena cava through an anterior injury cavaafter stabbing through both walls. Note that no vascu-in shock is ligation of the distal vena cava or the thermia, coagulopathy, or acidosis and is morecommon iliac vein. stable. He or she is then returned to the operating Distal iliac vein injuries should be repaired. Li- room for final repair of vascular and other inju-gation of the internal iliac vein often facilitates re- ries. When arterial injury is suspected at the pri-lease of the external iliac vein and provides better mary operation, angiography should be performedexposure of the injured site. In high-risk patients if first to identify and provide information beforerepair is not feasible, a good option is ligation. Un- repair. This can take place any time between a fewfortunately, distal control of internal iliac veins is hours to 10 days after the primary operation. Thedifficult. Often the best way is to use compression second operation consists of meticulous explora-with a sponge-stick for distal control while sutur- tion of injured areas still bleeding, including he-ing the lacerations. It is important to reduce bleed- matomas and cavities. Any recurrent bleeding ising by closing the hole even if narrowing or ob- controlled and repaired as outlined previously.struction of the vein is the final result. Shunted vessel segments must also be controlled and repaired. It is difficult to give well-founded Final Vascular Repair advice regarding final repair of previously ligated After “Damage Control” vessels. A suggestion is to consider the hepatic ar-With any luck the patient will have improved he- tery and the SMA for secondary repair. It is usu-modynamically after a period of resuscitation in ally not worthwhile to try to mend ligated veins.the intensive care unit and does not have hypo- After final repair of organ and intestinal injuries,
  • 64. 60 Chapter 5 Abdominal Vascular Injuries the packs are removed and the abdomen closed. It thrombosis of a renal artery after blunt trauma di- is not uncommon that renewed hemorrhage ne- agnosed during early management is preferably cessitates repacking and a second period in the treated by angioplasty and stenting, providing that intensive care unit. It the literature this is reported angiography facilities are available and that such to happen in up to 10% of patients. management does not delay final treatment. Blunt abdominal trauma causing splenic injury Finishing the Operation can also be treated by endovascular embolization. After vascular repair, other injuries are taken care In most published patient series, CT has been in- of. For a detailed description, we recommend sufficient for selecting patients for endovascular trauma textbooks. If the peritoneal cavity is con- therapy, and diagnostic angiography is recom- taminated, careful cleansing using warmed fluids mended to rule out this possibility. High-quality is recommended. If possible, vascular anastomo- CT angiography, however, readily identifies such ses should be covered with tissue. If the SMA and lesions. Observed patients who continue to require proximal aorta are injured, it is important to as- fluids and blood because of the organ injury sess the viability of the intestine before closing the should undergo arteriography to rule out treatable abdomen. Sites of vessel repair should also be injuries. Examples are intraperitoneal or intrapa- checked one more time. Minor – and even quite renchymal contrast extravasation and vessel trun- substantial – bleeding from such areas can be cation, which are all amenable to embolization. managed by hemostatic adjuvant therapy, such as Treatment then consists of selective catheteriza- local application of fibrin glue or gel (page 189). tion and injection of microcoils. The late consequences of abdominal vascular injuries – pseudoaneurysm and arteriovenous fis- 5.5.3 Endovascular Treatment tula – can also be treated by endovascular meth- ods in most locations. To our knowledge, there are Endoluminal aortic stent-graft repair has become no reports of successful endovascular treatment of a possible option for blunt aortic injuries missed venous injuries in the abdomen. during initial exploration, especially in the tho- racic part of the aorta. In some of cases reported in the literature, the injured aortic site causing dis- 5.5.4 Management After Treatment section was treated by fenestration and stent place- ment. Other patients had stable hematomas that It is obvious that patients with abdominal vascular were examined with CT and found to involve par- injuries have a high risk for developing serious tial aortic occlusion. Also, injuries in the common complications in the postoperative period. Hypo- iliac artery caused by pelvic fracture have been tension due to continued blood loss is common, treated by stent-grafts. In one series, a few patients and reoperation should be employed liberally. Vis- had iliac artery occlusions that were passed with a ceral and leg ischemia may also occur due to li- guide wire and then successfully treated with a gated or thrombosed repaired vessel segments. covered stent. This approach may be particularly The abdominal appearance and leg perfusion must tempting when conventional repair is not possible therefore be monitored meticulously in the post- due to associated injuries and pelvic hematoma. operative period. Examination should, besides ab- Angiography and subsequent embolization of dominal palpation, consist of a rectal examination branches from the internal iliac artery for bleed- and inspection of the nasogastric tube to check for ing due to pelvic fracture is successful in many blood. Renal artery thrombosis may manifest as instances. One should remember that in up to 5% flank pain and a temporary rise in serum creati- of patients, gluteal muscle necrosis occurs after nine. Occasionally, emergency nephrectomy is such branch embolization. necessary in the postoperative period due to pain Blunt and penetrating renal trauma can also be or a very high blood pressure. managed by endovascular methods. Selective em- As mentioned before, it is extremely important bolization of bleeding renal artery branches is of- to keep the blood pressure at adequate levels if the ten successful. Isolated dissection and subsequent intestinal blood supply is compromised by a delib-
  • 65. 5.7 Iatrogenic Vascular Injuries in the Abdomen 61erate ligation during exploration. Extra careful tality to range from 30% for hepatic artery to 80%cardiac monitoring, fluid resuscitation, and phar- for aortic injuries. The mortality for renal, iliac,macological blood pressure adjustment are war- and SMA injuries was around 50–60%.ranted. If intestinal ischemia is suspected, imme- Abdominal venous trauma is also associateddiate relaparotomy is indicated. with high mortality due to exsanguination. Over- Swelling after vein ligation or thrombosis of a all, mortality ranges from 30–70%. The worst re-repaired major vein segment is also a common sults come from patient series of retrohepatic venaproblem. The measures recommended to mini- cava injuries, reporting a mortality of over 90%.mize this problem are supplying the patient with Also, portal vein and superior mesenteric vein in-compression stockings and infusing dextran to juries lead to substantial mortality. In one study,optimize the rheology of the blood. Furthermore, 30% died after lateral repair of the portal vein andas soon as the patient is hemodynamically stable, 78% after ligation of this vessel. The latter proce-standardized heparinization should be initiated. dure, however, was performed in more severelyPatients with repaired injuries in the portal vein injured patients with more associated injuries.and the superior mesenteric vein may also develop Another study reported only 20% mortality afterportal hypertension and hepatic failure. portal vein ligation. In patients with only venous Antibiotics should be continued postopera- injuries or in combination with other venous trau-tively. Patients arriving in shock are prone to ma, the mortality rates were 75% for inferior venainfection, especially if intestinal perforation is cava injury, 72% for portal vein injury, 56% forpart of the trauma spectrum. Careful monitoring renal vein injury, and 44% for iliac vein injury.of infection signs is necessary, and CT examina-tion is indicated if intraabdominal infection issuspected. 5.7 Iatrogenic Vascular Injuries in the Abdomen 5.6 Results and Outcome It is not uncommon that vessels are injured during abdominal surgery for malignancy or other proce-Outcome after abdominal vascular trauma is dures. Some procedures are particularly prone tostrongly related to whether shock is present at ar- cause injury to abdominal vessels. A discussion onrival. The time elapsing from the trauma to the some of these follows below. The principles ofpatient’s arrival at the hospital is important. For repair are essentially the same as for traumaticexample, few patients survived penetrating ab- injury caused by accidents or violence.dominal vascular trauma during World War II,whereas 42% did during the Vietnam War. In se-ries from civilian life looking at survival of pa- 5.7.1 Laparoscopic Injuriestients with aortic or vena cava injuries arrivingalive to the hospital, around half have been report- Trocars used for laparoscopic access frequentlyed to survive. Besides shock, free bleeding in the cause injury to major blood vessels in the abdo-peritoneal cavity and suprarenal location of the men. When the aorta or vena cava is injured, out-injury are risk factors for poor outcome. Survival come may even be fatal. The insufflation needlerates after blunt trauma are around 75% in the may also cause severe injuries. Injury is more com-literature. Observational studies including 200 pa- mon in thin patients who have previously under-tients or more list suprarenal or juxtarenal aortic gone abdominal operations and in patients ininjuries, retrohepatic and hepatic vein injuries, whom a blind technique for inserting the trocar isand portal vein injuries as associated with the used. When blood returns through the trocar orhighest mortality. needle, a severe injury should be suspected. An- It is more difficult to find data on survival rates other situation indicating vascular injury occursfor isolated injuries to a specific vessel. One report when the patient becomes hypotensive or whenof isolated arterial injuries or those combined with the abdomen swells rapidly before the gas is insuf-other arterial injuries in the abdomen found mor- flated. If the aorta or iliac arteries are injured con-
  • 66. 62 Chapter 5 Abdominal Vascular Injuries version to an open operation by a midline incision In an ultimate situation the bleeding pelvic area to achieve proximal control is necessary to save can be packed with an intestinal bag filled with a the patient. Lateral repair or, occasionally, graft number of swabs tied together. The abdominal interposition is usually possible for final repair. wall is closed allowing the opening of the plastic Vascular injury may also occur during the pro- bag with the end of the swabs to protrude. The cedure itself, during dissection by careless han- patient is then brought to the ICU for “damage dling of the instruments and occasionally by re- control” and the swabs and the plastic bag sub- tractors. Because visualization is hampered by the sequently removed one or two days later. bleeding, open repair is always recommended. 5.7.3 Iliac Artery Injuries During 5.7.2 Iliac Arteries and Veins During Endovascular Procedures Surgery for Malignancies in the Pelvis Perforation and dissection of the common and external iliac arteries are common during endo- Distortion of the pelvic anatomy is common in vascular procedures, but this rarely leads to severe malignant disease. Therefore, the surgical proce- bleeding. Most of the time, complications can be dures for tumor removal are often difficult, and managed by immediate stenting or stent-graft re- injuries, especially to veins, are sometimes un- pair. Occasionally the bleeding will continue or is avoidable to make radical excision possible. The not discovered during the procedure, and the pa- injury becomes obvious by the bleeding, and be- tient displays symptoms a few hours after the pro- cause it is usually veins that are injured, control is cedure. Often, he or she complains of severe ab- accomplished by compression. Definitive repair dominal pain in the flank of the injured side. The is often more difficult. If major veins such as the abdomen is positive for tenderness, and the pa- iliacs are damaged, suturing of the hole is possible tient’s general condition shows signs of ongoing during inflow and outflow control, either manu- bleeding. If one is in doubt, a CT can confirm the ally or by sponge-sticks. It is necessary to reduce diagnosis, but the diagnosis is usually obvious. bleeding sufficiently so that the hole can be visual- Most patients are unstable and should be taken to ized adequately for repair. Often, however, it is the the operating room for immediate repair. A mid- internal iliac or, rather, branches from this vein line incision is then recommended because it en- that bleed. Sufficient control for repair is then al- ables proximal control of the distal aorta if neces- most impossible to achieve, and attempts to apply sary. The hematoma makes it difficult to identify “blind” sutures often make the bleeding worse. the injury site, and a bypass followed by ligation of When the bleeding is moderate, simple compres- the common iliac artery is the best way to treat it. sion sometimes permanently stops it. If not, fibrin Besides an iliofemoral bypass, one good option is glue should be applied, followed by another period to perform a femorofemoral bypass. If the artery is of manual compression. If surgical repair is im- stented all the way up to the aortic bifurcation, it is possible and compression and local therapies have almost impossible to ligate it or to find a spot for been tried unsuccessfully, the only way to reduce inflow of a bypass. Therefore, the procedure oc- the bleeding might be to ligate the internal iliac casionally requires a bypass from the aorta and arteries. Before this measure, the surgeon must division of the iliac artery. check that the patient’s coagulation status is as op- timal as possible. The risk that this will cause glu- teal muscle necrosis is considerable, but it may oc- 5.7.4 Iatrogenic Injuries During casionally be indicated. If the patient’s condition is Orthopedic Procedures stable enough and the operating room is equipped for combined surgical and endovascular proce- Lumbar disc surgery is reported to cause aortic or dures, allowing angiography to identify the bleed- common iliac artery injury in 1–5 out of 10,000 ing site and selective coiling bleeding vessel operations. The mechanism is laceration caused branches, this risk can be reduced considerably. by the special instruments used for excising the
  • 67. Further Reading 63herniated disc. This injury generally presents as a Further Readingsubstantial bleeding in the wound, with an associ-ated systemic hypotension. Occasionally, the diag- Baker WE, Wassermann J. Unsuspected vascular trau-nosis becomes apparent after the procedure when ma: blunt arterial injuries. Emerg Med Clin Northsigns of shock develop during the first postopera- Am 2004; 22(4):1081–1098 Brown CV, Velmahos GC, Neville AL, et al. Hemody-tive hours. Even more common is that an arterio- namically “stable” patients with peritonitis aftervenous fistula or pseudoaneurysm is found, which penetrating abdominal trauma: identifying thoseis diagnosed any time from a few hours after the who are bleeding. Arch Surg. 2005; 140(8):767–772procedure to several years postoperatively. Find- Fuller J, Ashar BS, Carey-Corrado J. Trocar-associ-ings suggesting such injuries are, in descending ated injuries and fatalities: an analysis of 1399 re-order of frequency, bruits, heart failure, abdomi- ports to the FDA. J Minim Invasive Gynecol 2005;nal pain, and hypotension. The disc level where 12(4):302–307 Gupta N, Solomon H, Fairchild R, et al. Manage-the surgery is performed determines which vessel ment and outcome of patients with combined bilebecomes injured. At the L4–L5 and L5–S1 levels, duct and hepatic artery injuries. Arch Surg 1998;the common iliac artery and vein are injured. 133(2):176–181Higher up, the aorta and vena cava are at risk. Lee JT, Bongard FS. Iliac vessel injuries. Surg Clin North For emergency repair, a midline incision for ex- Am 2002; 82(1):21–48posure is needed, and the same principles are ap- Malhotra AK, Latifi R, Fabian TC, et al. Multiplicity ofplicable as for other types of trauma: lateral repair, solid organ injury: influence on management andpatching, or graft insertion. Arteriovenous fistu- outcomes after blunt abdominal trauma. J Trauma 2003; 54(5):925–929las and pseudoaneurysms may also be treated Nicholas JM, Rix EP, Easley KA, et al. Changing pat-using endovascular methods. terns in the management of penetrating abdominal During hip arthroplasty, the external iliac ves- trauma: the more things change, the more they staysels or the common femoral artery may be injured. the same. J Trauma 2003; 55(6):1095–1108; discus-While uncommon at primary procedures, it hap- sion 1108–110pens more often during revisions because of the Parks RW, Chrysos E, Diamond T. Management of liverneed to remove previous prosthetic material and trauma. Br J Surg 1999; 86(9):1121–1135 Smith SR. Traumatic retroperitoneal venous haemor-the anatomical alterations caused by previous rhage. Br J Surg 1988; 75(7):632–636surgery. The left side is more often injured. The Sugrue M, D’Amours SK, Joshipura M. Damage controlmechanism is sometimes direct lacerations by ac- surgery and the abdomen. Injury 2004; 35(7):642–etabular screws, dissection, or traction injury, but 648more common is cement destruction of the ves- Weber S, Murphy MM, Pitzer ME, et al. Managementsels. Arterial repair is performed after obtaining of retrohepatic venous injuries with atrial cavalproximal control of the common iliac artery. shunts. AORN J 199664(3):376–377, 380–382Usually, a “hockey-stick” incision is sufficient toobtain exposure. Destroyed vessel segments bycement need graft interposition or a bypass.
  • 68. Acute Intestinal Ischemia 6CONTENTS 6.1 Summary6.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 Triad of symptoms6.2 Background . . . . . . . . . . . . . . . . . . . . . . . . . 65 1. History of embolization6.2.1 Magnitude of the Problem 2. Pain out of proportion and Patient Characteristics . . . . . . . . . . 66 3. Intestinal emptying6.3 Pathophysiology . . . . . . . . . . . . . . . . . . . 66 Urgent management is essential: rehydra- tion, angiography and laparotomy6.4 Clinical Presentation . . . . . . . . . . . . . . . 67 If arterial obstruction – aggressive surgical6.4.1 Medical History . . . . . . . . . . . . . . . . . . . . . . 67 treatment6.4.1.1 Embolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67 If venous obstruction – restrictive with6.4.1.2 Thrombosis . . . . . . . . . . . . . . . . . . . . . . . . . . 67 surgical treatment6.4.2 Physical Examination . . . . . . . . . . . . . . . . 68 Embolectomy if jejunum is normal6.5 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . 686.5.1 Laboratory Tests . . . . . . . . . . . . . . . . . . . . 686.5.2 Angiography . . . . . . . . . . . . . . . . . . . . . . . . 696.5.3 Other Options . . . . . . . . . . . . . . . . . . . . . . . 70 6.2 Background6.5.4 Diagnostic Pitfalls . . . . . . . . . . . . . . . . . . . 706.6 Management and Treatment . . . . . . 70 Acute intestinal ischemia is often a fatal disease,6.6.1 Management Before Treatment . . . . . 70 and many patients with this disorder will die re- In the Emergency Department . . . . . . 70 gardless of treatment. Increased awareness and6.6.2 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . . 71 rapid management can improve this pessimistic6.6.2.1 Embolic Occlusion . . . . . . . . . . . . . . . . . . 71 course. Using wide definition acute intestinal6.6.2.2 Arterial Thrombosis . . . . . . . . . . . . . . . . . 71 ischemia is hypoxia of the small intestinal wall6.6.2.3 Venous Thrombosis and NOMI . . . . . . 72 due to a sudden decrease of perfusion caused by6.6.2.4 Endovascular Treatment . . . . . . . . . . . . 73 emboli or arterial or venous thrombosis. The6.6.3 Management After Treatment . . . . . . 73 symptoms are not specific, and the diagnosis is regularly established at laparotomy late in the6.7 Results and Outcome . . . . . . . . . . . . . . . 73 course when peritonitis has developed. With rapid Further Reading . . . . . . . . . . . . . . . . . . . . 74 and efficient management, including an aggres- sive diagnostic work-up, the number of successful embolectomies can increase and the need for ex- tensive intestinal resections can be diminished. The diagnosis must be established early in the course of the disease. A high level of clinical suspi- cion when evaluating acute abdominal pain, prompt management in the emergency depart- ment, and early angiography or laparotomy is required to achieve this.
  • 69. 66 Chapter 6 Acute Intestinal Ischemia 6.2.1 Magnitude of the Problem unusual and is further discussed in Chapter 12 on and Patient Characteristics complications in vascular surgery. The rest of this chapter will deal with acute ischemia of the small Even if patients with acute intestinal ischemia are intestine. usually admitted and treated by general surgeons, cooperation with a vascular surgeon may be a NOTE possible way to improve treatment results. Vascu- Occlusion of the SMA has devastat- lar surgeons contribute with their experience of ing effects on the perfusion of the angiography as well as with operations in the area intestine. around the superior mesenteric artery (SMA). The disease is relatively uncommon. Among all Because almost the entire small intestine gets its patients arriving in the emergency department be- blood supply from one single artery, a sudden oc- cause of abdominal pain, 0.5 % have acute intesti- clusion of this vessel has major consequences. The nal ischemia. The true incidence is probably high- initial response is spasm and vigorous contrac- er because patients can be suspected to die from tion. Because of its high metabolic activity 80% of intestinal ischemia without an established diagno- the blood supply to the intestine is consumed by sis. The relatively low incidence in combination the mucosa. This explains why the mucosa is dam- with the imprecise symptoms and moderate find- aged before the rest of the intestinal wall is. The ings at physical examination early in the course of cells at the tip of the villi are most sensitive and die the disease contribute to the bad prognosis. In ob- first. Under the microscope, ischemic changes can servational studies the 30-day mortality is 60–85% be seen in the mucosa within 30 min after occlu- for patients who are not treated surgically with the sion. Patients with SMA occlusion will, very early diagnosis established by angiography or physical after onset, vomit and have diarrhea and abdomi- examination. One more factor contributing to the nal pain. Occasionally they have blood in their poor prognosis is that this category of patients stools. Granulocytes are also activated early, and consists of elderly who have complicating diseases oxidants and proteolytic enzymes affect the intes- such as chronic obstructive pulmonary disease tine. Hypotension develops as the next step in the and generalized arteriosclerosis, including coro- course of the disease and contributes to further nary disease. In most studies, the mean patient age ischemic damage of the intestinal wall. This is is around 70 years. Two-thirds of the patients are followed by diffuse necrosis in the mucosa that female. spreads to the submucosal layer and finally ex- Intestinal ischemia secondary to mesenteric ve- tends through the entire intestinal wall. The nous thrombosis is associated with another group result is transmural infarction and local peritoni- of patients and has a significantly better progno- tis. The intestine then may perforate, and the sis. The 30-day mortality is around 30%. Five to patient develops general peritonitis. Metabolic 15% of all cases presenting with intestinal isch- acidosis, dehydration, anuria, and multiple organ emia are caused by venous thrombosis. failure could be the end result. The main etiology of acute intestinal ischemia is embolization or thrombosis of the SMA, both 6.3 Pathophysiology being equally common. In general, an embolus oc- cludes a relatively healthy artery with immediate The main blood supply to the small intestine dramatic consequences as described above, where- comes from the SMA, which also perfuses the first as a thrombotic occlusion is preceded by a steno- half of the colon. The inferior mesenteric artery sis, allowing collaterals to develop. The artery may and branches from the internal iliac arteries sup- then occlude without causing symptoms or isch- ply the distal part of colon and rectum. This dou- emic damage to the intestine. ble blood supply and an extensive collateral net- A less common cause is venous thrombosis. work explain why occlusion of the inferior mesen- This frequently affects younger patients and typi- teric artery seldom causes severe ischemia in the cally is secondary to trauma, inflammation, and distal colon. Primary ischemia of the colon is other diseases in which hypercoagulation is com-
  • 70. 6.4 Clinical Presentation 67mon. It may also be a consequence of congenital Table 6.1. Percentage of patients with symptoms andcoagulation disorders. laboratory findings at the time of admission to the hos- Other more unusual causes for acute intestinal pital, where the diagnosis acute intestinal ischemia due to arterial occlusion was established laterischemia, which are not within the scope ofthis book, are embolic or thrombotic occlusion of Symptoms/finding Frequencythe celiac trunk and the low-flow state nonocclu- Abdominal pain 100%sive intestinal ischemia (NOMI), a result of severecardiac dysfunction. Diarrhea or vomiting 84% Previous embolization/ 33% source of emboli 6.4 Clinical Presentation Blood in stools 25% Elevated lactate in plasma 90% 6.4.1 Medical History Leukocytosis 65% Metabolic acidosis 60%In many patients the initial clinical presentationof SMA obstruction is vague, making diagnosisdifficult. A triad of symptoms in the patients’medical history should make the surgeon suspi-cious for acute intestinal ischemia caused byocclusion of the SMA: these patients have a history of previous cardiac1. Severe periumbilical pain (“pain out of propor- disease, and 30% have had earlier episodes of em- tion”) bolization to other vascular systems (Table 6.1).2. Vomiting and/or diarrhea (“gut-emptying”) Embolization is common after acute myocardial3. Possible source of an embolus, or a previous infarction, debut of arterial fibrillation, and as a embolization in the medical history. complication of angiography and endovascular treatment.NOTE It is important to remember the triad of Thrombosis symptoms associated with occlusion Thrombosis of the SMA occurs in patients with of SMA. general arteriosclerosis and a history remarkable for previous manifestations of cardiac and periph- Embolism eral vascular disease. Sometimes symptoms ofFor a typical patient with embolic occlusion of chronic intestinal ischemia also are present. Thethe SMA, the symptoms include all three elements onset of symptoms after acute thrombotic occlu-of the triad. These are then sufficient for deter- sion is more insidious than for embolic disease.mining the diagnosis, as well as for differentiating The pain is usually constant and progressive overit from other causes of acute abdominal pain several hours but is otherwise similar to what hasand thrombosis of the same artery. The pain, been described for embolism. (See Table 6.2.)which often precedes vomiting or diarrhea, is the For thrombosis of the mesenteric vein, the du-key symptom. It has a dramatic precipitous onset ration of symptoms is commonly several days andand is localized in the paraumbilical region. The the symptoms are even more imprecise than forpain is usually severe and colicky. The expression arterial occlusion. The pain is less pronounced“pain out of proportion” indicates that there is a but is present to some degree in 90% of patients.discrepancy between the findings in the physical Fever is also a common sign. Eighty-five percent ofexamination of the abdomen and the pain inten- patients have a history of hypercoagulation disor-sity. The pain disappears when the intestine ders such as deep venous thrombosis or have hadbecomes necrotic, which may create a pain-free other diseases or risk factors predisposing them tointerval that frequently is misinterpreted as if thrombosis. Examples include pregnancy, oralthe patient has improved. The pain returns when contraceptive use, malignancy, inflammatory dis-the intestine perforates. Ninety-five percent of eases, portal hypertension, and trauma.
  • 71. 68 Chapter 6 Acute Intestinal Ischemia Table 6.2. Differentiation between causes of intestinal ischemia (DVT deep vein thrombosis) Arterial embolism Arterial thrombosis Venous thrombosis Older + + – Younger – – + Previous symptoms – + – of chronic intestinal ischemia Previous DVT – – + Possible source emboli + – – Sudden onset + – – Insidious onset – + + 6.4.2 Physical Examination ment. The only radiologic examination that is warranted, besides computed tomography (CT) Findings at physical examination in acute intesti- for diagnosing suspected venous thrombosis, is nal ischemia can be vague and difficult to inter- angiography and perhaps plain x-ray. The resourc- pret. It is still, however, very important to care- es and expertise available in the hospital should fully examine the patient. The examination reveals also influence the decision of whether any further signs of arteriosclerosis – carotid bruits, heart investigations or tests are performed. murmur, and so on – as well as sources of embolus. Abdominal examination findings are the basis for emergency management. For instance, without 6.5.1 Laboratory Tests signs of peritonitis, a patient should not undergo laparotomy when venous thrombosis is the sus- The leukocyte count is elevated early in the dis- pected diagnosis. A patient with arterial occlusion, ease course. Together with the clinical triad, a leu- however, needs surgery before peritonitis evolves. kocyte count higher than 15 109/l is pathogno- The abdominal findings vary with the time monic for acute intestinal ischemia. Values above point during the course of the illness when the pa- normal for serum lactate and D-dimer have also tient is examined. Anything from normal findings been suggested as prognostic markers for patients to general peritonitis may be found. In early stag- who need surgery. A lactate concentration exceed- es, a slight tenderness and amplified bowel sounds ing 2.6 mmol/l is considered to have a high sensi- are common findings, but when peritonitis is es- tivity (90–100%) for acute mesenteric ischemia, tablished, tenderness with muscular guarding and meaning that only one patient in 10 with intestinal a lack of bowel sounds due to paralysis are found. ischemia has a value <2.6 mmol/l and is at risk to Abdominal distension is a very late sign in the be missed by this test. The specificity with this course of the disease. The examination should cut-off value, however, is rather low (around 40%). also assess the patient’s general condition, includ- Overall, provided that shock, diabetes, severe re- ing possible dehydration. nal insufficiency, and pancreatitis have been ruled out, an elevated plasma lactate indicates that the patient has a disease very likely to be acute intesti- 6.5 Diagnostics nal ischemia, and that the patient definitely has a disease that needs surgery. More pronounced leu- For the majority of patients with the triad of symp- kocytosis and elevated hemoglobin and hemato- toms described the need for further diagnostic crit values are secondary to plasma losses in the work-up is limited and immediate laparotomy is injured intestine. Later, when the intestinal wall indicated. Laboratory tests can support the diag- becomes necrotic and blood leaks into the intesti- nosis but should not delay management and treat- nal lumen, hemoglobin and hematocrit decrease.
  • 72. 6.5 Diagnostics 69Metabolic acidosis also occurs late in the course of The surgeon is responsible for making sure thatthe disease, and as a diagnostic test it has no value. angiography will not cause an unacceptable delayThe acid-base balance, however, needs to be moni- in the management process. It should be per-tored and corrected continuously during the formed with close observation of the patient,course of treatment as a general measure. including continuous monitoring of vital signs and abdominal status. In hospitals without avail- able angiography, management has to be based on 6.5.2 Angiography clinical findings only. If this investigation resource is available, however, and the department hasIn hospitals where angiography is available 24 h a experience with emergency angiography, it is rec-day and can be performed rapidly, it is recom- ommended.mended before laparotomy for most patients sus-pected of having this disease. Exceptions are pa- TECHNICAL TIPStients with peritonitis. Angiography can possibly The technique for angiographybe preceded by a plain x-ray to exclude free gas in in acute mesenteric ischemiathe abdomen. Besides establishing the diagnosis,angiography is also helpful for separating the dif- 1. Scrub and dress for groin puncture.ferent etiologies for acute intestinal ischemia: 2. Shoot one plain frontal and one lateral x-ray1. Embolization to the SMA: Typically, this ap- (to exclude free gas). pears as a “meniscus” occlusion located 5–7 cm 3. Puncture the femoral artery. Insert a guide out in the SMA, which has its first branches wire and any angiography catheter. Place the open and filled with contrast. Such emboli are tip at the level of the first lumbar vertebra. usually possible to extract by simple embolec- 4. Withdraw the guide wire and rapidly inject by tomy. hand 10 ml of x-ray contrast. Images are first2. Arterial thrombosis in previously atheroscle- obtained in the frontal plane to visualize em- rotic arteries: On the films an occlusion of the bolization to the SMA. SMA is found approximately 1–2 cm from its 5. Repeat with the lateral projection (this is al- origin and no distal branches are filled with ways necessary to diagnose thrombosis when contrast. Sometimes the patient can then be the SMA is occluded at the origin). reconstructed with a bypass from the aorta. In 6. Consider injecting papaverine (1–2 ml of many circumstances, however, it is wise to 40 mg/ml) through the catheter, preferably avoid laparotomy if the contrast does not reach after its tip has been placed selectively into any part of the SMA. Total SMA thrombosis is the SMA. rarely curable by reconstructive vascular sur- 7. Pull the catheter and control the puncture gery. Thrombolysis may then be an option if a site by digital compression. guide wire can be inserted into the artery.3. Venous thrombosis or NOMI: If the branches from the SMA can be followed some distance out in the mesentery – more than 10 cm from 6.5.3 Other Options the origin – and the contrast is moving slowly, the finding indicates a state of threatening in- Ultrasound, including determination of flow ve- farction without arterial occlusion. This can be locity and color coding (duplex), is often techni- due to either venous thrombosis or NOMI. cally difficult to perform because of obscuring in- Laparotomy is not indicated in such patients. testinal gas and is not recommended for diagnos- ing acute intestinal ischemia. There are occasionalNOTE reports in the literature, however, about successful Emergency angiography is often helpful visualization of an occluded SMA that has been for diagnosing and managing acute helpful for diagnosis. Another possible benefit of intestinal ischemia. an ultrasound examination is to exclude other
  • 73. 70 Chapter 6 Acute Intestinal Ischemia causes of the patient’s symptoms such as renal or 6.6 Management and Treatment gall bladder diseases. When there is a strong suspicion of venous 6.6.1 Management Before Treatment thrombosis – for example in young patients with a history of hypercoagulation who have mild pro- In the Emergency Department longed symptoms without peritonitis on physical Most patients admitted to the emergency depart- examination – a CT scan with contrast should be ment with the described typical combination of performed to establish the diagnosis. The findings physical findings and medical history should un- on the CT scan that indicate thrombosis are dergo immediate angiography and laparotomy. thrombus in the superior mesenteric vein and Although patients with only segmental and not occasionally in the portal and splenic veins to- transmural ischemia may improve spontaneously gether with splenomegaly. Gas bubbles in these because of sufficient collateral blood flow, this is veins may also be found. difficult to identify preoperatively. As soon as the operating room has been notified, the following measures can be taken: 6.5.4 Diagnostic Pitfalls 1. Place at least one large-bore intravenous (IV) line. The three main difficulties in diagnosing and 2. Start infusion of fluids. Ringer’s acetate is the managing patients with acute mesenteric ischemia first option, but dextran is an alternative, espe- are (1) to suspect the diagnosis, (2) to make the cially if venous thrombosis is suspected. diagnosis fast enough, and (3) to differentiate 3. Obtain an electrocardiogram. between thrombotic and embolic etiologies. 4. Draw blood for hemoglobin and hematocrit, Patients with ruptured abdominal aortic aneu- prothrombin time, partial thromboplastin rysms, a ruptured urinary bladder, hemorrhagic time, complete blood count, creatinine, sodi- pancreatitis, or a perforated ulcer may also have um, and potassium as well as a sample for blood “pain out of proportion.” But their medical history type and cross-match. Consider ordering a and physical findings are usually sufficient to D-dimer as well. differentiate between these alternative diagnoses 5. Draw arterial blood for acid-base balance, and acute intestinal ischemia. Moreover, for all including lactate. patients with these diseases, except for pancreati- 6. Obtain informed consent. tis, emergency laparotomy is indicated, and a 7. Consider administering analgesics (5–10 mg wrong preoperative diagnosis is not so harmful. If opiate IV). not earlier the correct diagnosis can then be estab- lished during surgery. Overall, a high level of Early involvement of the anesthesiologist to dis- suspicion and early laparotomy will probably save cuss the patient’s condition and optimization of lives. organ function is wise. If time allows, this work- While an early diagnosis is essential, the delay up can be done in the intensive care unit. Any caused by performing angiography is often worth acidosis should be corrected, and blood and the time. Besides establishing the diagnosis and plasma infusions are often required. Administra- avoiding unnecessary laparotomies, it will also tion of drugs that reduce blood flow to the in- support management decisions during surgery. testine should be stopped as soon as possible. The relatively low complication rate of angiogra- Such drugs include digitalis, calcium channel phy also motivates liberal use. It will not negative- blockers, diuretics, and nonsteroidal anti-inflam- ly affect the management of the few patients matory drugs. When the decision to operate is suspected to have acute intestinal ischemia who made the patient should receive analgesics; a later turn out to have other diseases. Thrombolysis suggestion is an opiate 5–20 mg IV. Antibiotics may also be a reasonable treatment option for directed against intestinal bacteria, such as a acute mesenteric ischemia, further supporting an cephalosporin and metronidazole, should also be aggressive preoperative diagnostic work-up that given preoperatively. includes angiography.
  • 74. 6.6 Management and Treatment 71 Fig. 6.1. Acute intestinal ischemia with gangrene. a The entire intes- tine is affected, indicating arterial thrombosis. Surgical treatment pos- sibilities are limited. b Ischemic in- testinal gangrene but with a viable jejunum and left colon. This typical appearance suggests embolization to the superior mesenteric artery. Embolectomy should be attempted 6.6.2 Operation Arterial Thrombosis If the entire small intestine and colon are isch-The best access is achieved through a long midline emic, the cause is probably arterial thrombosisincision. The entire intestine should be examined (Fig. 6.1a). Embolectomy will then not be success-carefully to assess viability (Fig. 6.1). The basic ful and may even be harmful. If the entire intes-principle is that only parts with transmural necro- tine including the right colon is necrotic, the sur-sis should be resected. It is better to plan for a sec- geon should consider giving up surgery as treat-ond-look operation within 24 h than to be very ment and closing the incision. Findings in theliberal with resection margins. The intestine may preoperative angiography will facilitate this deci-appear quite normal at a quick glance, but careful sion.examination often reveals segments with a grayish At least one meter of small intestine is neededcolor and a dull surface, indicating severe isch- for survival. An emergency bypass between theemia. Viable segments often have pulsations in the aorta and the SMA is a surgical treatment optiondistal parts of the mesentery and preserved peri- for arterial thrombosis. It requires sufficient run-stalsis. In addition, a Doppler probe can be helpful off – often achieved by distal embolectomy andin this examination by detecting the presence or local thrombolysis – verified by intraoperativeabsence of arterial flow signals. Healthy segments angiography. The result of such emergency aorto-will have maintained the pink color of a healthy mesenteric reconstructions is meager but mayintestine. For a segmental injury, a wedge-shaped nevertheless save a few patients. The technique forexcision of the mesentery and the necrotic intesti- this is the same as for chronic disease. It is not cov-nal segment may be curative and all that is needed ered by this book and we recommend more gen-for treatment. eral vascular surgical manuals for a description. Embolic OcclusionIf the first part of the jejunum (Fig. 6.1b) looksnormal and there are pulsations in the first arte-rial arcade after the origin of the SMA, emboliza-tion is the most probable diagnosis. Under thesecircumstances embolectomy should be performedbefore intestinal resection (Technical Tips Boxand Fig. 6.2).
  • 75. 72 Chapter 6 Acute Intestinal Ischemia TECHNICAL TIPS Embolectomy of the Superior Mesenteric Artery Move the transverse colon cranially and identify it is important to not cause unnecessary bleeding. the SMA by using the fingers to palpate the area Continue distally towards the intestine with same ventral to the pancreas behind the superior mes- catheter. A #3 catheter is occasionally needed to enteric vein. This is facilitated by holding the mes- reach all the way out to the periphery. If the diag- enteric root between the thumb and the fingers. nosis is correct, an embolus with a secondary Expose the artery by incising the dorsal peritone- thrombus is extracted, and the backflow is brisk. If um longitudinally just over the area where the not, try a second time with the catheter directed pulse is lost (Fig. 6.2). manually into the branches. Inject 2–4 ml of pa- This sometimes requires partial division of the paverine through a catheter into the SMA. If the ligament of Treitz as well as inferior mobilization backbleeding is inadequate, try to instill the same of the 4th portion of the duodenum. Apply vessel amount of rtPA into the distal branches. Close the loops above and below the site of the intended artery with interrupted 6-0 prolene sutures. Place arteriotomy. At least 4–5 cm needs to be exposed. the intestine in its normal position and check the Administer 5,000 units of heparin IV, clamp the ar- final result by palpating distal pulses and inspect- tery as close to the aorta as possible, and make ing the intestine. If the viability of the intestine is a transverse arteriotomy distal to the clamp. uncertain, wait 20–30 min before deciding on Perform embolectomy with a #4 Fogarty cathe- what parts to remove. Finish the operation by re- ter. Start proximally while controlling bleeding secting nonviable parts as needed and close the through the arteriotomy using the vessel loop abdomen. and a finger. Inflow is usually quite vigorous, and If the intestine not is totally necrotic, it is sensible to wait for 30 min to see whether some segments of the intestine improve so that only a limited resection can be performed. Venous Thrombosis and NOMI The entire intestine can also be affected in venous thrombosis and NOMI. At laparotomy (which should be avoided if possible), the intestine affect- ed by venous thrombosis will look hyperemic and swollen and may have petechial bleedings in the serosa. If these are found, the operation should be stopped, the abdominal wall closed, and a second- look operation planned. Systemic anticoagulation is the best treatment. At the second-look opera- tion, segments with petechial bleeding might be hard to differentiate from gangrene. Such seg- ments need to be carefully examined to avoid un- necessary resections. Devitalized intestine in seg- mental venous thromboses, however, should be resected with safe margins. This is different from what is recommended for intestinal ischemia with arterial causes. Venous thrombectomy and throm- Fig. 6.2. Exposure of the superior mesenteric artery bolysis have anecdotally been reported, but there for embolectomy through an incision in the posterior is not much evidence that this is beneficial for the peritoneum patient.
  • 76. 6.7 Results and Outcome 73 Patients with NOMI may also not be discovered zation and as general prophylaxis against throm-before laparotomy. The intestine then displays the bosis, but it probably does not diminish furthersame appearance as for embolic and especially development of a thrombus in the intestine itself.thrombotic obstruction of the main artery. Intra- Because the damaged intestine is prone to bleed,operative diagnosis relies on pulse palpation and anticoagulation treatment also needs to be moni-insonation of the distal vascular bed with continu- tored carefully.ous-wave Doppler. Patients with NOMI have pre- Reperfusion after a successful embolectomyserved pulses and flow signals – monophasic and contributes, as in acute leg ischemia, to morbiditythrobbing – quite far out distally in the mesentery. and mortality. The primary damage caused byThese findings together with a typical medical hypoxia of the intestinal wall is followed by a sec-history should be enough to stop the attempt to ondary reperfusion injury. Therefore, patientsrevascularize the intestine surgically, and the pa- with acute intestinal ischemia who have been re-tient needs optimization of cardiac function. The vascularized are possible candidates for adjuvantdistinction from other arterial causes is difficult, pharmaceutical treatment to diminish the nega-however, and many patients with NOMI are likely tive effects on the central organs. The possibleto undergo embolectomy by mistake. substances are often called “scavengers,” and ex- amples include superoxide-dismutase, allopuri- Endovascular Treatment nol, and mannitol. Although all three of these doAt present only limited experience of thrombo- decrease mortality in animal models, there arelytic therapy for acute mesenteric ischemia is presently no clinical trials to support their use inavailable. Until 2003 about 50 cases had been re- patients.ported in the literature. But the results are promis-ing and the technique may evolve as a primarychoice in the future because it fits well with the 6.7 Results and Outcomeaggressive work-up required. The technique for thrombolysis involves groin As mentioned earlier, the mortality associatedaccess and diagnostic angiography as described, with acute intestinal ischemia is reported to bepreferably with selective catheterization of the very high. Intestinal resection as the only treat-SMA and introduction of a guide wire into the ment will result in a 30-day mortality of 85–100%.thrombus. An end-hole or side-hole catheter is If combined with embolectomy or vascular recon-then advanced into the clot and the infusion start- struction, mortality can be reduced to 55%. In twoed by a bolus injection. The catheter is then pulled studies with very positive results, it was proposedback somewhat and the continued infusion initi- that mortality could be reduced to less than 45% ifated. The preferable agent is rtPA. patients are managed very aggressively, with angi- ography in all patients (except for those with gen- eral peritonitis), followed by immediate laparoto- 6.6.3 Management After Treatment my. Ninety percent of the patients who survived in these two studies lost no or less than 30 cm ofWhile waiting for the second-look operation, the intestine. The most successful results were ob-patient should, if possible, be monitored in the in- served if the patient reached the operating roomtensive care unit. Besides continued fluid losses within 12 h after the onset of symptoms. Throm-from the injured intestine, toxic metabolites and bolysis in case series is reported to have excellentproteolytic enzymes are released, which negatively results, although the case mix was not comparableinfluence heart and lung function. There is also a to open surgery series, and only a few patientsrisk for septicemia because of bacterial transloca- had embolus as the etiology. It is likely that throm-tion. Therefore, rehydration, administration of bolysis should be attempted as the first optionplasma and blood, and antibiotic treatment are for thrombosis and that this will improve patientrecommended in the early postoperative period. survival considerably. Accordingly, the resultsAnticoagulation with heparin should be contin- from most studies favor management and treat-ued or begun in order to prevent further emboli- ment as outlined in this chapter: aggressive diag-
  • 77. 74 Chapter 6 Acute Intestinal Ischemia nostic work-up, liberal indications for laparatomy, Oldenburg WA, Lau LL, Rodenberg TJ, et al. Acute mes- embolectomy, and reconstructive vascular sur- enteric ischemia: a clinical review. Arch Intern Med gery. 2004; 164(10):1054–1062 Schoots IG, Levi MM, Reekers JA, et al. Thrombolytic therapy for acute superior mesenteric artery occlu- sion. J Vasc Interv Radiol 2005; 16(3):317–329 Further Reading Williams LF Jr. Mesenteric ischemia. Surg Clin North Am 1988; 68(2):331–353 Angelelli G, Scardapane A, Memeo M, et al. Acute Ward D, Vernava AM, Kaminski DL, et al. Improved bowel ischemia: CT findings. Eur J Radiol 2004; outcome by identification of high-risk nonocclusive 50(1):37–47 mesenteric ischemia, aggressive reexploration, and Burns BJ, Brandt LJ. Intestinal ischemia. Gastroenterol delayed anastomosis. Am J Surg 1995; 170(6):577– Clin North Am 2003; 32(4):1127–1143 580
  • 78. Abdominal Aortic Aneurysms 7CONTENTS 7.1 Summary7.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75 Abdominal aortic aneurysm rupture7.2 Background . . . . . . . . . . . . . . . . . . . . . . . . . 75 should always be suspected in men older7.2.1 Magnitude of the Problem. . . . . . . . . . . 75 than 60 years with acute abdominal pain.7.2.2 Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . 76 Patients who present with the triad of cir-7.3 Clinical Presentation . . . . . . . . . . . . . . . 76 culatory shock, abdominal or back pain,7.3.1 Medical History . . . . . . . . . . . . . . . . . . . . . . 76 and a positive examination for a pulsating7.3.2 Examination . . . . . . . . . . . . . . . . . . . . . . . . . 76 mass in the abdomen should immediately7.3.3 Differential Diagnosis . . . . . . . . . . . . . . . 77 be transferred to the operating room for7.3.4 Clinical Diagnosis . . . . . . . . . . . . . . . . . . . 77 emergency laparotomy. Urgent surgery should not be delayed7.4 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . 77 by unnecessary computed tomography or7.5 Management and Treatment . . . . . . 78 ultrasound scans.7.5.1 Management Before Treatment . . . . . 787.5.1.1 Ruptured AAA . . . . . . . . . . . . . . . . . . . . . . . 787.5.1.2 Suspected Rupture . . . . . . . . . . . . . . . . . . 797.5.1.3 Possible Rupture . . . . . . . . . . . . . . . . . . . . 79 7.2 Background7.5.1.4 Rupture Unlikely . . . . . . . . . . . . . . . . . . . . 807.5.2 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . . 80 7.2.1 Magnitude of the Problem7.5.2.1 Starting the Operation . . . . . . . . . . . . . . . 807.5.2.2 Exposure and Proximal Control . . . . . 80 Abdominal aortic aneurysm (AAA) is common. Other Options In men older than 60 years the prevalence is 5– for Proximal Control . . . . . . . . . . . . . . . . . 81 10%, which is four times the prevalence in women7.5.2.4 Continuing the Operation . . . . . . . . . . . 83 (Table 7.1). Not more than 1% of men over 60 years7.5.2.5 What to do While Waiting for Help . . 86 of age, however, have an AAA with a diameter7.5.2.6 Endovascular Treatment . . . . . . . . . . . . 86 around 5 cm, which is the limit at which the risk of7.5.3 Management After Treatment . . . . . . 87 rupture is considered motivation for elective op-7.6 Results and Outcome . . . . . . . . . . . . . . . 87 eration. The rupture incidence is reported to be 3–15% per 100,000 individuals per year. This7.7 Unusual Types means that every surgeon on call as well as emer- of Aortic Aneurysms . . . . . . . . . . . . . . . . 87 gency department physicians will most likely7.7.1 Inflammatory Aneurysm . . . . . . . . . . . . . 87 manage several patients with a ruptured AAA7.7.2 Aortocaval Fistula . . . . . . . . . . . . . . . . . . . 88 each year. It is possible that the number of patients7.7.3 Thoracoabdominal Aneurysm . . . . . . 88 with ruptured AAAs will decrease in the future7.7.4 Mycotic Aneurysm . . . . . . . . . . . . . . . . . . 89 because of screening programs. Presently, how-7.8 Ethical Considerations . . . . . . . . . . . . . 89 ever, it is still a very common patient type in many Further Reading . . . . . . . . . . . . . . . . . . . . 90 countries.
  • 79. 76 Chapter 7 Abdominal Aortic Aneurysms Table 7.1. Prevalence of asymptomatic abdominal aortic aneurysms (>3 cm) in different populations, as deter- mined by ultrasound Country Year N Population Prevalence United Kingdom 1993 Men, 65–75 years 8.4% United States 1997 73,451 50–79 years 4.7% (men) 1.3% (women) Netherlands 1998 2,419 Men, 60–80 years 8.1% Sweden 2001 505 65–75 years 16.9% (men) 3.5% (women) 7.2.2 Pathogenesis 7.3.1 Medical History AAA is a dilatation of the aorta caused by degen- The classic case of a ruptured AAA is brought to eration of the elastic components of the arterial the emergency department by ambulance. Often wall. The risk for developing AAA is related to the patient is a man who experienced immediate atherosclerosis, hypertension, and a genetic pre- onset of severe pain in the upper abdomen with disposition, but its etiology and the pathologic radiation to the back and flanks a few hours earli- process leading to AAA are unclear. Aneurysms er. The patient often describes an episode of un- usually originate below the renal arteries and ex- consciousness, dizziness, or sweating when the tend down to the aortic bifurcation. The natural pain started. Sometimes the family knows that the course is a gradually increasing dilatation leading patient has been previously diagnosed to have an to a progressively thinner wall that might end with asymptomatic AAA. rupture. The risk of rupture starts to increase ex- ponentially when the aneurysm diameter exceeds 5 cm, but aneurysms of smaller sizes can also rup- 7.3.2 Examination ture. The mortality from a ruptured AAA left un- treated is close to 100%, but the length of the pro- The patient may be circulatory-stable but with cess that leads to exsanguination and death varies positive signs of impending hypovolemic shock: from minutes to several days. The longer time pe- affected consciousness, tachycardia, sweating, and riod involves circumstances when the bleeding is hypotension. A pulsating tender mass is usually contained within the retroperitoneal space. found in the epigastrium above the umbilicus. Be- cause the aorta is a dorsal structure in the abdo- men, a mass is easy to miss in obese patients. It is 7.3 Clinical Presentation also difficult to palpate a pulsating mass when the blood pressure is low because of shock. Accord- When patients seek medical attention for abdomi- ingly, a pale patient with an increased heart rate nal or back pain, it is extremely important to and blood pressure <90 mmHg but negative for a always keep the diagnosis of a ruptured AAA in pulsating mass may have a ruptured AAA. A dis- mind. tinct local tenderness over the aneurysm is also a common finding. The pain is caused by the retro- NOTE peritoneal bleeding surrounding the aneurysm. An early correct diagnosis is crucial While almost all incipient and already ruptured because the prognosis for patients who AAAs are tender, the specificity of this sign is are not yet in shock is much better than low. for those in whom shock has already developed.
  • 80. 7.4 Diagnostics 77 7.3.3 Differential Diagnosis 7.3.4 Clinical DiagnosisPatients with a ruptured AAA who are not in A summary of different clinical presentations ofshock present with signs that are similar to a vari- AAA is presented in Table 7.2. These different sce-ety of other acute diseases in the abdomen or back. narios can be used in determining the risk for theTo avoid misdiagnosis with conditions that do not presence of a ruptured AAA.require emergency laparotomy, careful examina-tion of the abdominal aorta is important. NOTE Ruptured AAA, or symptomatic aneurysms The presentation of a patient with awith incipient rupture, should be included in the ruptured AAA varies, but in most casesdiscussion about differential diagnosis in all ab- a classic triad is found:dominal emergencies, particular in elderly men. – Abdominal painKidney stones located in the ureter, diverticulitis, – Circulatory instabilityconstipation, intestinal obstruction, pancreatitis, – Tender pulsating massgastric or intestinal perforation, intestinal isch- This combination of symptoms andemia, vertebral body compression, and even acute clinical findings should always be regard-myocardial infarction are all primary diagnoses ed as a ruptured AAA until the oppositethat can be mixed up with a ruptured AAA. Of is proven.course, there is a potential risk of sending a patienthome believing that, for example, a ureteral stone The purpose of Table 7.2 is to facilitate patienthas caused the trouble when AAA rupture is the management, and the remaining part of this chap-true diagnosis. A significant risk is also related to ter is largely based on this table. It should be re-performing a major operation because of a sus- membered, however, that patients might presentpected ruptured AAA in a patient who actually is with a clinical picture that lies in between the cat-suffering from an acute myocardial infarction. egories.The only way to avoid this is to keep the AAA di-agnosis in mind and to carefully examine thepatient. 7.4 Diagnostics Another important differential diagnosis isaortic dissection. It is common that a patient will When an aid in detecting AAA is needed, a com-initially have been treated at a smaller healthcare puted tomography (CT) scan is the first choice forunit or in the emergency department where an all categories used in Table 7.2. When the suspi-ultrasound was performed and misinterpreted as cion is strong and the risk for sudden deterioration“dissection in an aortic aneurysm.” This misun- is considered high, the scan should be performedderstanding is caused by the thrombus within the quickly. The responsible surgeon should superviseAAA, which can be interpreted as a doubled aortic the procedure so that it can be stopped if neces-lumen. There is, however, a clear distinction be- sary and the patient transferred to the operatingtween rupture and dissection. Rupture is a true room immediately. The CT scan should be per-burst of the aortic wall with bleeding out from the formed with contrast. The primary questions thevessel. Dissection starts with a tear in the inner scan should answer are as follows: Is there anlayer of the vascular wall through which the blood AAA? Are there signs of rupture? What size is thepasses and cause a longitudinal separation of the AAA, and how far proximally and distally does itlayers, causing a double lumen. Rupture is com- extend?mon in AAA, but dissection is rare (see the infor-mation on aortic dissection in Chapter 8). NOTE In the classic case of a ruptured AAA, no diagnostic tools except the physical examination are needed.
  • 81. 78 Chapter 7 Abdominal Aortic Aneurysms Table 7.2. Clinical findings and management of ruptured aortic aneurysms (AAA abdominal aortic aneurysm, OR operating room, CT computed tomography) Pain Hemodynamic Pulsating Clinical diagnosis Measures instability mass Yes Yes Yes Ruptured AAA Immediate transfer to OR (classic triad) Yes Yes No Rupture suspected If history of AAA or signs peritonitis, (lack of mass may be due to transfer to OR; obesity or low blood pressure) Perform ultrasound scan in the OR or CT scan with the surgeon present Yes No Yes Rupture possible Perform CT scan and consider urgent (may have an incipient rupture surgery if diagnosis of AAA is made or an inflammatory aneurysm) Yes No No Rupture unlikely Perform CT or ultrasound scan (may have a contained rupture if the patient obese or difficult to palpate) influences the indication for surgery. It is impor- tant to remember that a patient with a diagnosed AAA and pain but with a CT scan showing no signs of rupture needs to be managed as if the pa- tient has impending rupture. Pain may precede rupture, and the scan only answers the question of whether a rupture is already present at the exami- nation. Unfortunately, no signs can predict wheth- er an AAA is going to rupture soon. There is rarely a place for ultrasound when try- ing to diagnose a ruptured AAA. Performed in the operating room, it might occasionally be helpful to exclude or verify the presence of an AAA. Fig. 7.1. Typical appearance on computed tomog- When the patient is hemodynamically stable or raphy of a ruptured abdominal aortic aneurysm with when the suspicion of rupture is low, the use of ad- contrast in lumen, thrombus, calcifications in the wall, ditional diagnostic tests to exclude other illnesses and a large retroperitoneal hematoma is encouraged. Examples of such diseases are pan- creatitis and myocardial infarction. These can be verified by electrocardiogram (ECG), a plain ab- To look for anything other than what is mentioned dominal x-ray, a CT scan, ultrasound, or urogra- above is unnecessary in an emergency work-up of phy as well as by blood tests. a patient with a suspected ruptured AAA. The di- agnosis made by CT is easy, and typical findings are demonstrated in Fig. 7.1. 7.5 Management and Treatment Signs of rupture on the scan include a hemato- ma and contrast that is visible outside the aortic 7.5.1 Management Before Treatment wall retroperitoneally. An early sign of rupture is the presence of contrast in the thrombus and a Ruptured AAA very thin aortic wall overlying it. The location of If the triad is present the patient needs to be oper- the aneurysm in relation to the renal arteries is ated without delay caused by preoperative exami- important for planning an operation but rarely nations or tests. The time available for making the
  • 82. 7.5 Management and Treatment 79correct decision regarding patient management is AAA procedures is available, consider contactingusually limited. The following measures should another hospital and presenting the case to therapidly be done in the emergency department: vascular surgeon there. The patient may then be 1. Obtain vital signs, medical history, and physi- referred to that hospital or the vascular surgeon cal examination. could come and perform the procedure if the pa- 2. Administer oxygen. tient’s condition does not allow transport. Even 3. Monitor vital signs (heart rate, blood pressure, stable patients might start to rebleed at any mo- respiration, SPO2). ment and should therefore not be transported too 4. Obtain informed consent. liberally. If the patient is hemodynamically stable, 5. Place two large-bore intravenous (IV) lines. the start of operation should be delayed until an Insertion of central lines is time-consuming, experienced surgeon is available. However, if there and to avoid delays it is better done in the are signs of hemodynamic instability or manifest operating room after surgery has started. shock despite treatment, the operation should be 6. Start infusion of fluids. initiated. The aim then is to achieve control of the 7. Obtain blood for hemoglobin, hematocrit, bleeding. prothrombin time, partial thromboplastin time, complete blood count, creatinine, blood Suspected Rupture urea nitrogen, sodium, and potassium, as well The checklist described before is, by and large, as a sample for blood type and cross-match. also valid when rupture is only suspected. 8. Catheterize the urinary bladder (this often has This category of patients is the most challeng- to be done in the operating room to gain time) ing, and generally applicable advice is difficult to and start recording urine output. give. This category includes patients with a rup- 9. Administer analgesics, such as 2–3 mg mor- tured aneurysm but without a palpable pulsating phine sulphate IV up to 15 mg, depending on mass due to obesity and severe hypotension. There the patient’s vital signs, severity of pain, and are also many other life-threatening conditions body weight. that should not be treated with surgery in this10. Order eight units of packed red blood cells and group. One such condition is acute myocardial in- four of plasma. farction, which also may start with thoracic and abdominal pain and hypotension. Therefore, theThe list suggested above may vary among different surgeon must rapidly decide whether to performhospitals. Remember to include pulses, including an emergency operation or order diagnostic ex-femoral, popliteal, and pedal, in the physical ex- aminations to verify the diagnosis. In the case ofamination. This is important as a baseline test in an actual rupture, it is evident that examinationscase of thromboembolic complications to the legs that delay the start of the operation are associatedduring surgery. It is also important to be cautious with severe risk. Therefore, every such step shouldabout rehydration and administration of inotropic be performed simultaneously with other preoper-drugs. The latter should be used only when the pa- ative measures if possible. For example, ECG istient is in shock and when the low blood pressure helpful in the diagnosis of myocardial infarction,threatens to affect cardiac or renal function. The and ultrasound can verify or exclude the presenceaim should not be to restore the patient’s normal of an AAA.blood pressure; a pressure of around 100 mmHg issatisfactory if the patient’s vital functions are in- Possible Rupturetact. Hypotension may be an important factor A tender pulsating mass supports the suspicion ofminimizing the bleeding and keeping it contained rupture. In a circulatory-stable patient with pos-within the retroperitoneal space. Too intense vol- sible rupture, the following is done in the emer-ume replacement and increased blood pressure gency department:may initiate rebleeding. 1. Place an IV line and start a slow infusion of As soon as possible, the patient should be taken Ringer’s the operating room and a vascular surgeon con- 2. Order an emergency CT scan, with the patienttacted. If no surgeon with experience performing monitored by a nurse.
  • 83. 80 Chapter 7 Abdominal Aortic Aneurysms If the CT scan shows an AAA >5 cm in diameter start the operation before the patient is anesthe- without signs of rupture and the patient has not tized and intubated. The procedure starts with a displayed hemodynamic instability, the diagnosis long midline incision from the xiphoid process to impending rupture should be considered. The the pubis. This allows fast and good access to the patient then needs surgery within 24 h. The abdomen. Proximal control of the aorta above the timing of the operation is based on the patient’s aneurysm is of highest priority. The rest of the op- condition and the hospital’s available resources. eration includes reconstructing the aorta with a While awaiting surgery, patients who need medi- straight aortic tube graft or an aortoiliac or aorto- cal treatment to improve cardiac or pulmonary femoral bypass graft. The use of autotransfusion function should receive it. In this category they are of blood, a “cell saver,” is recommended. Resusci- also possible candidates for transfer to other hos- tation and anesthesia must be monitored closely. pitals if necessary. The goal is to achieve optimal hemodynamics, If the patient already has a known aneurysm at with a balance between infused volume and actu- admission, the management is also as described al, as well as expected, bleeding. The surgeon must above. However, if this known aneurysm has a di- realize that it is sometimes necessary to stop the ameter <4 cm, rupture is unlikely. In such patients procedure and maintain temporary bleeding con- the sign of a pulsating mass is also probably lack- trol by tamponade or manual compression in or- ing. A patient with a known small aneurysm who der to allow time for the anesthesiologist to com- is in shock should be resuscitated followed by a CT pensate for blood and fluid losses. Close contact scan. The possibility of cardiogenic shock due to with the anesthesiologist is important during the an acute myocardial infarction is a possibility that entire operation. has to be considered. If cardiac causes have been excluded and the shock is refractory to treatment, Exposure and Proximal Control laparotomy is advised. The conventional technique for exposure and proximal control with a long midline incision and Rupture Unlikely incision of the dorsal peritoneum is recommend- This category of patients should be evaluated with ed. The exposure must sometimes be modified regard to all possible differential diagnoses and because of bleeding or presence of a hematoma. managed as any case of “acute abdomen.” To rule Infiltration of blood in the tissue surrounding the out or verify AAA a CT scan or ultrasound is per- aneurysm makes it difficult to identify structures formed. The risk for rupture is substantially less such as the mesenteric, renal, and lumbar veins. for an AAA <5 cm in diameter than for larger On the other hand, it often facilitates dissection of aneurysms. The patient should be admitted for the proximal neck by loosening the fibrous tissue observation and worked up considering any other adjacent to the aorta. causes of pain, such as kidney stone, pancreatitis, In a hemodynamically stable patient it is rec- gallstone, perforated duodenal ulcer, perforated ommended to apply a self-retaining retractor after intestine, acute myocardial infarction, or vertebral entering the abdomen. Preferably, a type that is body compression. If the patient does not improve fixed to the table (such as the OmniTractm) is used. and no other reasonable cause for the pain can be This facilitates dissection by reducing protruding identified, operation of the aneurysm should be organs. After incision of the dorsal peritoneum considered if it is large. and mobilization of the duodenum to the right, sharp and blunt dissection is used to carefully ap- proach the anterior aspect of the aneurysmal neck 7.5.2 Operation (Fig. 7.2). The correct plane of dissection is reached when Starting the Operation the white and smooth surface of the aorta is visu- Elevated blood pressure in association with anes- alized. An important guide during the dissection thesia induction can accentuate the retroperito- through the hematoma is the aortic pulse. Accord- neal bleeding. The patient should therefore be ingly, a weak pulse due to hypotension makes the scrubbed and draped and the surgeon ready to dissection more difficult. Exposure of the aneu-
  • 84. 7.5 Management and Treatment 81 Fig. 7.2. Incision in the posterior peritoneum for exposure of the infrarenal aorta and the neck of an abdominal aortic aneurysm. The incision is placed in the angle between the duodenum and the inferior mesenteric vein, which occasionally has to be divided for good access. A 1–2-cm edge of the peritoneum is left on the duode- num to facilitate restoration of the anatomy at closurerysmal neck is usually facilitated by the dissection damage to the left renal vein, its gonadal branches,of tissue around the anterior aorta caused by the and the lumbar veins. Bleeding during this part ofhematoma. Blunt dissection with a finger behind the dissection usually emanates from any of thesethe aorta in the “friendly triangle” can therefore veins and is controlled by ligature, suture, or aoften be the easiest way to achieve control of the local tamponade. Another common source foraorta (Fig. 7.3). venous bleeding is the inferior mesenteric vein. It When a finger can be pushed behind the aorta, can also be ligated. If profuse bleeding from theapplication of the aortic clamp is possible. In this ruptured aorta occurs during dissection controlsituation an angled Satinsky clamp is suitable. can be obtained by several different strategies.When it is difficult to circumferentially free theaorta, a straight clamp can be applied in an an- Other Optionsteroposterior position just inferior to the renal ar- for Proximal Controlteries, leaving the aorta adherent dorsally. This There are ways to achieve proximal control of theoften works well, but suturing the anastomosis aorta that fit most situations. The recommenda-can be more difficult. The dissection behind the tions listed below are ordered according to theaorta should be performed with great care to avoid probability that they might be needed.
  • 85. 82 Chapter 7 Abdominal Aortic Aneurysms 2. Occlusion with balloon catheter A Foley catheter, size 24-French or larger, is inserted through the hole and the tip is placed proximal to the aneurysmal neck. The balloon is filled with saline until the bleeding dimin- ishes; usually 15–20 ml is sufficient. The re- maining bleeding is caused by backbleeding from the distal vascular bed. If it is significant, it has to be controlled before proceeding with dissection of the aneurysmal neck. With this technique the aorta is usually occluded at a su- prarenal level and occasionally even higher. When this method is used, the operation should be continued as quickly as possible with expo- sure of the neck of the aneurysm to allow an aortic clamp to be applied in an infrarenal posi- tion. The balloon should then be removed im- mediately before the clamp is applied. Specially designed balloon catheters for aortic occlusion are also available to facilitate this method of control. 3. Straight aortic clamp on the neck of the anu- erysm – anterior approach If the patient is in severe shock and rapid aortic control is necessary, there is little time for circumferential dissection and exposure. A straight clamp can then be applied as soon as the dorsal peritoneum is divided and the duo- denum retracted to the right. It is placed from the ventral portion at the level of the neck. The Fig. 7.3. When an abdominal aortic aneurysm is pres- clamp is positioned by blunt dissection and ent the anatomy is often changed. The first centimeters guided in place by the fingers. The surgeon of the infrarenal aorta (the neck of the aneurysm) are must be aware of the risk of damaging the vena usually angulated ventrally. The triangular space be- cava and should also check that the clamp bite tween the spine, the aneurysm, and its neck is called the “friendly triangle” because its tissue usually allows includes the entire aortic wall. blunt dissection easily 4. Manual compression of the subdiaphragmat- ic aorta If the rupture is located on the anterior aspect of the aneurysm and there is ongoing signifi- 1. Manual local compression or “a thumb in the cant bleeding within the peritoneal sac, an as- hole” sistant can achieve temporary proximal control Apply local compression over the rupture with by manual compression of the subdiaphrag- one or several swabs, or try to seal it by putting matic aorta. This is performed by simply plac- a finger or thumb into the hole in the aneu- ing the fist against the lesser omentum high up rysm. This method is convenient when the an- under the xiphoid process and pushing down- eurysm ruptures suddenly during dissection of ward and cranially, thereby compressing the the neck. It can often be followed by option aorta against the vertebral column. This gives number two below. the surgeon an opportunity to visualize and find the hole, followed by insertion of an oc- clusive balloon as previously described.
  • 86. 7.5 Management and Treatment 835. Straight clamp on subdiaphragmatic aorta dominal, retroperitoneal, or pelvic vessels, it through the lesser omentum can be advantageous to start the procedure by Better control can be achieved by placing an percutaneously inserting an intraluminal bal- aortic clamp in the subdiaphragmatic position loon for proximal aortic control (Fig. 7.5). De- (Fig. 7.4 a–d). The technique is not so easy but is pending on the location of the injury, this can useful when there is a very large hematoma sur- be done from the groin through the femoral ar- rounding the neck of the aneurysm, indicating tery or from the arm through the brachial ar- that the rupture is located in that area. In such tery. In the former situation, a supporting long a case there is considerable risk for uncontrol- introducer left in place is often needed to pre- lable bleeding through the rupture when the vent dislocation by the bloodstream. This pro- dorsal peritoneum is opened to expose the cedure requires the surgeon to have experience aneurysmal neck. To achieve subdiaphragmatic in endovascular methods or an interventional control, the lesser omentum is incised, the aor- radiologist to be available for assistance. Briefly tic hiatus at the diaphragmatic crus is exposed, the technique is as follows. The brachial artery and the aorta is clamped. The triangular liga- is punctured with a 12-French introducer. A ment must be divided to allow retraction of the guide wire is inserted under fluoroscopy with left liver lobe to the right. To avoid damage to its tip then in the proximal aorta. A 100-cm the ventricle and esophagus, these organs need long catheter with a 46-mm compliant balloon to be retracted to the left. Thereafter the muscle is inserted over the guide wire and connected to fibers in the diaphragmatic crus are divided to a syringe with saline for insufflation. If the pa- allow the straight clamp to be applied in an an- tient is in shock the balloon is immediately teroposterior position. A straight clamp, how- insufflated by the surgeon for resuscitation. ever, has a tendency to slip off the aorta and Once positioned such an intraaortic balloon cause rebleeding, and repositioning of it is of- can be temporarily insufflated when needed. ten necessary. This risk is increased if the mus- This might be a salvaging procedure in many cle fibers in the diaphragmatic crus are not cut cases of extensive vascular injuries because it sufficiently. Great care must be taken to avoid controls hemorrhage while allowing dissection damaging the esophagus and vena cava. As of the injured segment. Subsequent application soon as possible, any supraceliac aortic occlu- of ordinary vascular clamps can then provide sion is replaced by one in an infrarenal posi- better control. Aortic balloon occlusion can tion. also be valuable in extensive venous injuries in6. Clamping of the thoracic aorta the abdomen or pelvic area because the stopped Transthoracic control of the aorta can be used aortic inflow secondarily leads to diminished in extreme situations. It is performed through a venous bleeding. low left-sided thoracotomy in the 5th–6th in- tercostal space. The incision starts in the mid- Continuing the Operation clavicular line and is extended dorsally as far as Proximal aortic control usually stabilizes the pa- possible. After the pleura is incised, the lung is tient and the operation can proceed as in elective retracted anteriorly and caudally, after which operations for AAA. The iliac arteries are exposed. exposure of the thoracic aorta is relatively easy. The aorta and the iliac arteries are clamped, the There are few disturbing surrounding struc- aneurysm incised, and the thrombus extracted. tures. This technique, however, is associated If there are firm adhesions between the iliac artery with increased postoperative morbidity and is and the vein, dissection may be dangerous, poten- rarely necessary in the management of rup- tially causing severe bleeding by injuries to the tured abdominal aortic aneurysms. iliac vein. This can be avoided by using balloon7. Proximal endovascular aortic control occlusion of the iliac arteries from inside the an- In potentially technically challenging and se- eurysm once it has been opened. If there is back- vere cases of ruptured aortic or iliac aneurysms bleeding from lumbar arteries, the inferior mesen- in obese patients or in those with a “hostile” ab- teric artery, or the median sacral artery, their ori- domen or traumatic injuries to large intraab- gins are controlled with 2-0 suture from the inside
  • 87. 84 Chapter 7 Abdominal Aortic Aneurysms Fig. 7.4. a The left triangular ligament is divided to straight clamp, the posterior peritoneum is divided facilitate exposure of aorta at its diaphragmatic hilus. and the neck of the aneurysm is palpated and digitally b The gastrohepatic omentum is divided longitudi- dissected, as previously described, through the hema- nally, the lesser omental sac entered, and the aorta toma. d A second clamp is then placed on the neck of digitally mobilized at the diaphragmatic crus. c After the aneurysm and the subdiaphragmatic clamp slowly proximal subdiaphragmatic control is achieved by a released
  • 88. 7.5 Management and Treatment 85 Fig. 7.5. A balloon catheter occlud- ing the aorta at a desired level is in- serted through the brachial artery. An alternative is to use a femoral approach with a 16 French 55 cm introducer, supporting the balloon from belowof the aneurysm. Ligature of the inferior mesen- over it. Abdominal drains are never used becauseteric artery outside the aneurysm should be avoid- even significant postoperative bleeding cannot beed because this is associated with a certain risk for drained. More about bleeding complications afterocclusion of arcade arteries that sometimes are aortic surgery can be found in Chapter 12 (pageimportant collaterals in the intestinal circulation. 149). The most common causes for postoperativeA straight tube graft or an aortobiiliac bypass bleeding are lumbar arteries not being securedgraft is used for the aortic reconstruction. A col- during the procedure, anastomotic leakage, orlagen-coated woven Dacron graft is recommend- veins that were not ligated but being temporarilyed; these types of grafts are presealed with albu- contracted during the operation and later dilated.min and do not need preclotting. A tube graft is Because of the increased risk of bleeding, sys-used if aorta is soft and not dilated at its bifur- temic heparin should not be given to all patientscation. If the dilation continues down into any of with ruptured aneurysms. Those hemodynami-the common iliac arteries or if there are extensible cally stable and with little operative bleedingcalcifications in the bifurcation, a tube graft should be given heparin IV. A recommendation isshould not be used. If the iliac arteries are calcified to use half the dose used for elective procedures.or dilated extension of the graft limbs to the com- Local heparinization should be administered bymon femoral arteries may be necessary. This is infusing heparinized saline into the iliac arteries.combined with ligation of the common iliac arter- Liberal use of Fogarty catheters to remove clotsies. The proximal anastomosis is usually sewn and emboli dislodged to the leg arteries from thewith nonresorbable monofilic 3-0 or 4-0 suture. thrombus during dissection is also advocated. IfWhen the graft is anastomosed to the iliac or fem- there is no backbleeding from either one of theoral arteries a 5-0 suture is used. common iliac arteries, thrombectomy is manda- After the reconstruction is complete, the anas- tory.tomoses are checked for leakage and possible ob- Antibiotic prophylaxis should be administeredstruction. Finally, the aneurysmal sac is wrapped according to local protocols for operations involv-around the graft and the dorsal peritoneum closed ing synthetic vascular grafts. One suggestion is 2 g
  • 89. 86 Chapter 7 Abdominal Aortic Aneurysms cloxacillin given at the start of the operation, with the dose repeated after 4 h in prolonged proce- dures. Besides general perioperative IV fluids, mannitol is recommended to maintain urinary output. What to do While Waiting for Help For surgeons without experience in AAA surgery it is generally a good idea to wait for a more expe- rienced colleague if the patient is reasonably stable. While the surgeon is waiting for help the patient should be prepared up to the point of anesthesia induction. The surgeon scrubs and the patient is also scrubbed and draped while the an- esthesiologist closely monitors the patient’s vital functions and hemodynamics. If the patient’s blood pressure drops and cannot be maintained at an acceptable level, the patient is anesthetized and laparotomy is initiated without experienced help. The goal is then to achieve control of the bleeding. Besides the previously described techniques to gain proximal control of the aorta, tamponade with lots of swabs and compression with the fist over the bleeding area is usually enough in this situation. These simple measures combined with IV fluids and inotropic drugs is often sufficient to stabilize the patient until help arrives. Endovascular Treatment In recent years more than 300 patients with rup- Fig. 7.6. One alternative way to treat a ruptured AAA with endovascular technique. A unilateral aortoiliac en- tured AAA or incipient rupture have been treated dovascular graft decompresses the aortic aneurysm. A with endovascular techniques. The results pre- coil in the right internal iliac artery and an occluder in sented are observational studies and show that the left common iliac artery eliminate pressure caused endovascular repair of rupture is feasible. A large by backflow, the latter deployed to allow retrograde percentage of the patients in these early series were flow to the internal iliac artery from the groin. A femo- not in severe shock and the mortality rate aver- rofemoral bypass restores perfusion of the left leg aged around 10%. Furthermore, reduced post- operative morbidity rates compared with conven- The problems related to endovascular repair tional open repair have been suggested. include the availability and storage of suitable One major benefit of endovascular treatment is grafts as well as logistical problems getting the pa- the possibility of obtaining rapid proximal control tients worked up rapidly. Pretreatment evaluation by inserting an inflatable balloon from the groin with CT angiography or digital subtraction arteri- or through the brachial artery that occludes aorta. ography is necessary to evaluate the possibility This technique makes it possible to delay final for endovascular repair and to plan the procedure. treatment until the patient is stabilized. Another The number of different grafts needed to meet in- potential advantage may be that high-risk patients dividual requirements is minimized if a unilateral can also be treated. Particularly favorable is the aortoiliac tube graft is used in combination with possibility of using only local anesthesia and seda- an occluder of the contralateral iliac system and a tion for repair. femorofemoral crossover, as shown in Fig. 7.6.
  • 90. 7.7 Unusual Types of Aortic Aneurysms 87 The technique involves the following steps: The vere stress during preoperative shock and aorticpatient is prepped and draped as for an elective clamping and declamping. Deterioration of cardi-AAA procedure. The common femoral arteries ac function with secondary hypotension that re-are surgically exposed if a bifurcated graft is quires inotropic treatment is common. Renalinserted or if unilateral aortoiliac tube grafts in function is also often impaired and occasionallycombination with a femorofemoral crossover the patient requires dialysis. Almost all patientsbypass are used. For tube grafts access of only one have increased creatinine and blood urea nitrogencommon femoral artery is enough. One of the elevations after operation for ruptured AAA.femoral arteries is punctured and an introducer is These increases are also due to preoperative hypo-put in place, often a size 7 to 9-French. A guide tension and the stress of the operation. If the pa-wire is inserted, an aortogram obtained, and land- tient develops renal insufficiency with low urinarymarks, either radiolucent (placed preoperatively) output, dialysis should be considered at an earlyor external (such as clamps), are used to assess the stage.length of the AAA. After systemic heparinization, The greatest risk for developing ischemic colitisthe sheath with the graft is introduced over the is in patients with a ruptured aneurysm and wire to a level just below the renal arteries. The severity of ischemic colitis varies from onlyThe sheath is then withdrawn somewhat to allow discharge of the mucosa to transmural necrosis.proximal release of the graft. After final adjust- Registration of pH at the wall of the sigmoid withment of the proximal fixation level the system is a tonometer can be used to determine the risk forsecured by angioplasty. The distal end of the endo- developing ischemic colitis. This condition is fur-luminal graft is deployed in the common, external ther discussed in Chapter 12 on complications iniliac, or common femoral artery with angioplasty vascular surgery (page 145).of stents. Depending on the conditions a hand-sewn anastomosis is another option. An occluderof the common iliac is inserted from the contralat- 7.6 Results and Outcomeeral femoral artery. If a bifurcated endoluminalgraft is used, the contralateral graft limb is insert- The 30-day mortality after surgery for ruptureded through the same route. Finally, a completion AAA averages from 30% to 50%, the variabilityangiogram is performed after withdrawal of the depending on whether the patient developed shockentire sheath. and whether concomitant diseases were present. A bifurcated aortobiiliac endoluminal prosthe- For patients without shock, it is 20–25%, whichsis as a primary alternative in rupture is also grow- can be compared to 60–70% for those in popularity. The procedure requires a com- The long-term results and prognosis for patientspliant large-diameter balloon for aortic occlusion, who survive the initial postoperative period is5 and 12-French introducers, Amplatz guide wires, good. Outcome is even better than for patientshigh-resolution fluoroscopy, and an assortment of who have undergone elective aneurysm repair.endoluminal aortic stent grafts with a body diam- The reason for this is probably selection – the sick-eters ranging from 22 to 34 mm and limb diame- est patients die of rupture, and the survivors whoters of 12 to 24 mm. reach the hospital have fewer risk factors. 7.5.3 Management After Treatment 7.7 Unusual Types of Aortic AneurysmsThe patient is treated in the intensive care unit un-til circulatory, respiratory, and renal functions are 7.7.1 Inflammatory Aneurysmstable. This usually takes at least a couple of days.The most common early postoperative complica- An AAA can be symptomatic and cause paintions are congestive heart failure, renal failure, without actual or imminent rupture. The mostand ischemic colitis. The patient, often with con- common cause for this pain is an inflammatorycomitant coronary heart disease, is exposed to se- reaction in and around the wall – an inflammato-
  • 91. 88 Chapter 7 Abdominal Aortic Aneurysms 7.7.2 Aortocaval Fistula A special form of AAA rupture occurs when the bloodstream penetrates into the vena cava causing an aortocaval fistula (Fig. 7.8). The patient typi- cally develops sudden cardiac failure and cyanosis of the lower extremities. The cardiac failure is due to the large shunt and the discoloration of the legs occurs because of venous stasis in combination with the heart failure. At physical examination the patient is positive for a bruit and a palpable aneu- rysm in the abdomen. Treatment for an aortocaval fistula is an emergency operation, but in most cas- es some time for preoperative preparation is avail- Fig. 7.7. Typical appearance on computed tomogra- able. The operation follows the strategy for other phy of an inflammatory abdominal aortic aneurysm aneurysms as outlined previously and the fistula is with its thick wall usually closed by suture from inside the aneurysm while vena cava is controlled by manual compres- sion proximally and distally. ry AAA. CT, which then shows a thickened aneu- rysm wall, verifies the presence of such a condi- 7.7.3 Thoracoabdominal Aneurysm tion (Fig. 7.7). It could be presumed that the thick wall prevents rupture, but rupture of inflamma- A small number of aortic aneurysms engage the tory AAAs is not uncommon. Because inflamma- suprarenal or thoracoabdominal parts of the aorta tory AAAs often are painful, separating them including the orifices of the renal arteries, the from ruptured AAAs is a real diagnostic problem. superior mesenteric artery, and the celiac trunk. Elevated erythrocyte sedimentation rate (ESR) or They originate in the thoracic part of the aorta or C-reactive protein (CRP) supports the diagnosis, anywhere below the level of the diaphragm. Man- but CT is the only way to exclude it. agement of rupture in such aneurysms is challeng- Fig. 7.8. Computed tomography of a patient with an abdominal aortic aneurysm and a fistula into the inferior vena cava
  • 92. 7.8 Ethical Considerations 89 sion and subsequently rupture. Treatment is the same as for other AAAs with the addition of long- term antibiotics. 7.8 Ethical Considerations Difficult and delicate ethical considerations often arise when managing patients with ruptured AAA. Accordingly, it has to be emphasized that the ad- vice given above often needs to be modified in very old patients, patients with dementia, and patients with other serious medical conditions implying only a short expected survival time. On the other hand, patients who previously were de- termined not suitable for elective repair because of high risk should sometimes be considered for repair of a ruptured AAA. When rupture has already occurred the risk/benefit situation is com- pletely different. The patient has little to lose by undergoing an emergency operation.Fig. 7.9. Angiographic appearance of a typical mycotic Rupture of an AAA often occurs in elderlyaneurysm, with its saccular shape caused by local ero- patients and a complete medical history and infor-sion of the aortic wall and subsequent leakage of bloodinto an aneurysmal sac consisting of a fibrous capsule mation about their present quality of life is fre-(not a true vascular wall) quently missing when they are admitted. Because nonsurgical management is associated with 100% mortality, a policy of accepting every patient foring, and if its extension is known prior to the surgical treatment is advocated in many hospitals.operation someone with experience should be A certain selectivity, however, is often wise. It iscontacted before surgery begins. If such an aneu- obvious that a patient who had cardiac arrest inrysm is achieved during surgery for rupture, prox- the ambulance and remains unconscious at ad-imal control is sought by one of the techniques mission, is anuric, and has ECG signs of myocar-described previously. Endovascular repair is also dial ischemia is extremely unlikely to survive sur-an option that needs to be considered. gery. If the patient is 80 years old and also is known to have dementia, difficulties ambulating, and need for geriatric care, it is reasonable to avoid 7.7.4 Mycotic Aneurysm surgery and instead give the patient terminal care of high quality. Unfortunately, there are no reli-Another special type of AAA is caused by a local able prognostic factors for treatment outcome forinfection in an atherosclerotic and degenerated the individual patient, but many studies reportaortic wall, known as mycotic or septic aneurysm. relationships between presence of different riskDifferent from ordinary AAAs that are fusiform, factors and survival.mycotic aneurysms are usually saccular (Fig. 7.9). A common conclusion in the literature, how-Patients with this type of AAA frequently have a ever, is that age should never be considered as amedical history that includes fever and malaise. contraindication to surgery. It is always the sur-Elevated ESR, CRP, and other inflammatory pa- geon, the patient and relatives and their individualrameters are also common. The most common judgment that finally decide whether to operate orbacteria found in mycotic aneurysms and in the not. If one is in doubt, a good general rule is to bepatient’s blood are of the Salmonella species. It is liberal with repair attempts. It is always possible,the infectious process in the wall that causes ero- but difficult, to change such a strategy later during
  • 93. 90 Chapter 7 Abdominal Aortic Aneurysms the course when more information is available. Harris LM, Faggioli GL, Fiedler R et al. Ruptured ab- Accordingly, stopping the support of vital func- dominal aortic aneurysms: factors affecting mortal- tions and taking the patient to the floor for pallia- ity rates. J Vasc Surg 1991; 14:812–820 Johansson G, Swedenborg J. Ruptured abdominal aortic tion is a viable option. Some factors in the postop- aneurysms: a study of incidence and mortality. Br J erative course – large bleedings and cardiac, renal, Surg 1986; 73:101–103 respiratory, and infectious complications – are Johnston KW. Ruptured abdominal aortic aneurysms: considered to be associated with a worse prognosis six-year follow-up of a multicenter prospective and thus might indicate a suitable point at which study. J Vasc Surg 1994; 19:888–900 to make such a decision. Ouriel K, Geary K, Green RM, et al. Factors determin- ing survival after ruptured aortic aneurysm: the hospital, the surgeon, and the patient. J Vasc Surg 1990; 12:28–33 Further Reading Ohki T, Veith FJ. Endovascular grafts and other im- age-guided catheter-based adjuncts to improve the Bengtsson H, Bergquist D. Ruptured abdominal aortic treatment of ruptured aortoiliac aneurysms. Ann aneurysm: a population-based study. J Vasc Surg Surg 2000; 232(4):466–479 1993; 18:74–80
  • 94. Aortic Dissection 8CONTENTS 8.1 Summary8.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91 Aortic dissection is one of the “great mas-8.2 Background . . . . . . . . . . . . . . . . . . . . . . . . . 91 queraders,” so always suspect this diagno-8.2.1 Magnitude of the Problem . . . . . . . . . . 91 sis in any acute painful illness with a pulse8.2.2 Classification and Definition . . . . . . . . 92 deficit.8.2.3 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92 A practical classification in the emergency8.2.4 Pathophysiology . . . . . . . . . . . . . . . . . . . . 93 situation is type A, involving the ascend-8.3 Clinical Presentation . . . . . . . . . . . . . . . 94 ing thoracic aorta and the arch and type B8.3.1 Signs and Symptoms . . . . . . . . . . . . . . . . 94 involving the aorta distal to the left subcla-8.3.2 Medical History . . . . . . . . . . . . . . . . . . . . . . 94 vian artery.8.3.3 Physical Examination . . . . . . . . . . . . . . . . 96 Treatment of type A dissection is always surgical.8.4 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . 96 Treatment of type B dissection is medical8.5 Management . . . . . . . . . . . . . . . . . . . . . . . 97 in most cases and surgical if there is com-8.5.1 Treatment in the Emergency plicating organ ischemia or bleeding. Department. . . . . . . . . . . . . . . . . . . . . . . . . . 97 Alert the attending thoracic or vascular8.5.2 Emergency Surgery . . . . . . . . . . . . . . . . . 98 surgeon on call early during management,8.5.3 Type B dissection . . . . . . . . . . . . . . . . . . . . 98 especially in type A dissections.8.5.4 Endovascular Treatment . . . . . . . . . . . . 988.6 Results and Outcome . . . . . . . . . . . . . . . 99 Further Reading . . . . . . . . . . . . . . . . . . . 100 8.2 Background Dissection of the thoracic aorta represents a major clinical problem that is extremely demanding to manage even for experienced surgeons. Once it is diagnosed this condition is usually managed by an experienced specialist in thoracic or vascular surgery. The responsibility for the diagnosis and its primary management, however, mostly belongs to the surgical or medical emergency physicians. 8.2.1 Magnitude of the Problem The true prevalence and incidence of aortic dis- section are unknown, but it has been reported to have an annual occurrence of 5–10 cases per
  • 95. 92 Chapter 8 Aortic Dissection million and to affect between 10,000 and 25,000 patients annually in the United States. Autopsy studies in the United States and Denmark report dissections in 0.2–0.8% and 0.2% of cases, respec- tively. An age-adjusted mortality rate from aortic dissections of 0.5–2.7% per 100,000 inhabitants was calculated from 1950 to 1981. The overall inci- dence of aortic dissections consequently is in the same range or possibly up to two to three times greater than that for ruptured abdominal aortic aneurysm. It is two to five times more common in men than in women, and maximum occurrence is in the 5th decade of life. Still, in our era of modern diagnostic methods, a majority of patients proba- bly die with this disease undetected. Aortic dissec- tion is a dramatic and dangerous condition with a very high mortality: 20–50% of patients die within the first 24–48 h, and up to 75% within the first 2 weeks. It is considered as one of the “great mas- Fig. 8.1. Classification of aortic dissection in types A queraders,” with a wide range of presenting symp- and B, according to Daily (Stanford) toms. Because the diagnosis is difficult, awareness of aortic dissection in the differential diagnosis is essential, as is rapid and correct management. within 14 days of presentation, and chronic if more than 14 days have elapsed. 8.2.2 Classification and Definition NOTE The most practical classification in the Aortic dissection is characterized by two or more emergency situation is communicating flow channels originating from a – Type A: involving the ascending proximal intimal tear, with propagation of the thoracic aorta and the arch bloodstream within the medial layer. It should – Type B: involving the aorta distal be distinguished from an intramural hematoma, to the left subclavian artery which is a hemorrhage into the medial layer of the aortic wall without an intimal tear. Intramural he- matomas have a natural history similar to aortic 8.2.3 Etiology dissection and are treated similarly. The most useful classification of aortic dis- Aortic dissection is usually related to some kind of sections in the acute situation is the one proposed degenerative changes in the aortic wall, in partic- by Daily (Stanford classification), as shown in ular the media. Even if a dissection primarily Fig. 8.1. starts with a tear in the intima, its propagation Other classic classifications are by DeBakey within the media varies considerably from almost and Crawford (thoracoabdominal aneurysms and none to rapid progression along the entire length chronic dissections). The information in this chap- of the aorta. The variation is related to the condi- ter is based on the Stanford classification because it tion of the medial layer. Some congenital connec- simplifies the acute management. A type-A dissec- tive tissue defects are known to cause such degen- tion always involves the ascending aorta, regard- eration, including Marfan’s syndrome, Turner less of the distal extension. A type-B dissection syndrome, and Ehlers–Danlos’ syndrome. Cystic does not involve the ascending aorta. There is con- media necrosis is another predisposing condition. sensus in the literature that an aortic dissection is The role of arteriosclerosis is often discussed. It is considered acute if the onset of symptoms occurred present in older patients with hypertension pre-
  • 96. 8.2 Background 93senting with dissection and might constitute a ing aorta. The dissection is usually directed ante-rare mechanism by penetration of atherosclerotic gradely, but retrograde extension is also relativelyulcers extending through the intima into the me- common. A primary entry in the ascending aortadia. This is, however, mostly considered coinci- is associated with a great risk for bleeding into thedental rather than causative, and some authors pericardium, causing cardiac tamponade.even argue that atherosclerotic changes within the Type B dissection usually starts with a primaryaortic wall might be a barrier to the extension of a intimal tear in the descending thoracic aorta justdissection. distal to the origin of left subclavian artery. This Arterial hypertension is the most important type constitutes approximately 25% of all aorticpredisposing factor. It is noteworthy that the sud- dissections. A patient with a type-B dissection isden extreme hypertension associated with severe typically older, in the 6th–7th decade of life, andphysical exercise may cause aortic dissection in has thoracic aortic degeneration and hyperten-younger persons. Also, pregnancy with its hyper- sion.circulation and hormonal changes affecting con- Other possible but less common sites of the pri-nective tissue, is a certain risk factor particularly mary tear are the aortic arch, occurring in approx-during the last trimester and during labor. Fortu- imately 10% of cases, and the abdominal aorta,nately, aortic dissections in women are rare, but occurring in only 2%. As already mentioned, the50% of dissections occurring in women younger dissection in the aortic media can travel in a retro-than 40 years old do occur during pregnancy. grade as well as an antegrade direction, causing Iatrogenic injuries during coronary diagnostic two flow channels with a false and a true lumen.and therapeutic procedures with catheter manip- Secondary tears and reentries usually occur dis-ulations can also cause aortic dissection. Blunt tally, allowing flow from the false into the truechest trauma in otherwise healthy persons may lumen.cause aortic dissection, but such dissections are Rupture is the most common cause of death inusually very limited due to the minimal degenera- patients with aortic dissection and is mostly lo-tion in these structurally normal aortas. cated near the site of the primary intimal tear. Consequently, a type-A dissection usually rup-NOTE tures into the pericardial sac, causing cardiac A degenerative process causing weaken- tamponade, or an aortic arch rupture that bleeds ing of the aortic wall in combination with into the mediastinum. In addition, the close rela- hypertension is the most important tion to the aortic valve commisures can result in etiologic factor. acute valve regurgitation due to prolapse of the commissural attachments. Dissection into the aortic root may also involve the coronary arteries, 8.2.4 Pathophysiology leading to myocardial ischemia or infarction. A type-B descending aortic dissection typically rup-Type A dissection, constituting 60–70% of all aor- tures into the left pleural cavity, and less frequent-tic dissections, is mostly seen in younger patients ly into the right.with some elastic and connective tissue abnormal- As the dissection extends along the aorta itity. It characteristically starts with a primary inti- will subsequently engage major important cere-mal tear just distal to the sinotubular ridge in bral and visceral branches, possibly resulting inthe ascending aorta. This location is in the vicinity threatening end-organ ischemia. The mechanismsof the cephalad extension of the aortic valve com- behind this are compression of the true lumen bymissures. The tear is commonly transverse and the false lumen or shearing of the branch by thehas a length corresponding to 50–60% of the dissection process. A third possibility is disrup-aortic circumference. The dissection process starts tion of an important dissection membrane, caus-in the intimal tear and its extension and direction ing an intimal flap covering the orifice of a branch.vary, as does the speed with which it propagates. Such peripheral vascular complications occur in Typically, a type A dissection affects the right 25–30% of patients with aortic dissection and canlateral wall of the greater curvature of the ascend- critically affect cerebral, renal, visceral, and lower
  • 97. 94 Chapter 8 Aortic Dissection presenting with symptoms indicating acute arte- rial occlusion and an acute illness that seems to involve unrelated organ systems. 8.3.2 Medical History The most dominant symptom is severe pain, which is migrating or nonmigrating and experienced by more than 90% of patients. When analyzing the pain its typical characteristics are evaluated; if it is: sudden, severe, new, ripping or tearing, and constant. The pain is typically related to the loca- tion of the dissection and its propagation distally into different aortic segments. In proximal dissec- tion, the most common pain location is the ante- rior chest. The pain frequently radiates into the neck and jaws and can be associated with swallow- ing difficulties. As the dissection propagates dis- tally, the pain migrates to an interscapular loca- tion followed by pain in the midback, lumbar, and groin regions (Fig. 8.3). Abdominal pain might be severe in patients suffering from visceral or renal ischemia. As pre- Fig. 8.2. Mechanisms of branch occlusion and organ viously mentioned, the left renal artery is more malperfusion in aortic dissection. a False lumen expan- likely to be compromised, which may explain why sion causes compression of a side branch. b The orifice severe left flank pain mimicking ureteral colic is of a side branch is disrupted by dissection, and its inner often included in the reported history. One should layers are impacted distally always include questions about hypertension, car- diac disease, peripheral vascular disease, connec- extremity perfusion. Because the dissection in the tive tissue abnormalities (such as Marfan’s, Turner, descending aorta mainly engages its left perimeter, and Ehlers–Danlos’ syndromes), cystic media ne- the left renal and left iliac arteries are at higher risk than the right ones. Table 8.1. Differential diagnoses in aortic dissection Possible differential diagnoses NOTE Peripheral vascular complications occur Coronary ischemia in 25–30% of cases of dissection of the Myocardial infarction aorta. Aortic regurgitation without dissection Aortic aneurysm with dissection Musculoskeletal pain 8.3 Clinical Presentation Mediastinal tumors or cysts 8.3.1 Signs and Symptoms Pericarditis Gall bladder disease Acute aortic dissection patients can display a Pulmonary embolism variety of symptoms, and affected individuals Stroke can develop symptoms mimicking those of almost Visceral or lower extremity ischemia any other acute medical or surgical condition. without dissection Aortic dissection must be considered in patients
  • 98. 8.3 Clinical Presentation 95 Fig. 8.3. a Radiation of pain in type A dissection. The pain is usually referred to the neck, anterior chest, and interscapular area. b Radiation of pain in type B dissection. Pain is primarily interscapular, but with distal progression of dissection, pain is often referred to the lower back and groincrosis, diagnostic or therapeutic catheter manipu- Visceral ischemia: severe abdominal painlations, or intense exercise. (for further details of typical symptoms, see Secondary effects of aortic dissection with or- Chapter 6, p. 67)gan malperfusion necessitate a thorough and com- Lower-extremity ischemia: loss of pulse, loss ofplete history to include previous, present, and un- sensory or/and motor function, severe pain anddulating symptoms of the following: coldness (see Chapter 10, p. 122) Cerebral ischemia: stroke, loss of conscious- Cardiac malperfusion: angina pectoris or ness, focal neurological symptoms symptoms of acute congestive heart failure Spinal ischemia: paraplegia or parapareses Renal ischemia: flank pain, hematuria, dimin- Possible differential diagnoses are listed in Table ished urinary output 8.1.
  • 99. 96 Chapter 8 Aortic Dissection NOTE A complete and repeated neurological exami- Be aware of aortic dissection as an nation is mandatory. Horner’s syndrome, loss of important differential diagnosis in any consciousness, loss of sensory or motor function, acute case presenting with sudden painful paraparesis, paralysis, or paraplegia might be pres- illness, in particular if it is associated with ent. Acute cerebral vascular occlusion is for obvi- symptoms or signs of organ ischemia. ous anatomic reasons, more common in proximal dissection, but fortunately neurological deficits occur in only about 20% of those patients. 8.3.3 Physical Examination Lower extremity paralysis in the examina- tion is caused by shearing off or compression of Complete and repeated physical examinations are major arteries feeding the spinal cord (intercos- of paramount importance in diagnosing and man- tal-T8–L1). Another possible explanation is occlu- aging patients with suspected or verified acute sion of the thoracic or abdominal aorta, causing aortic dissection since this condition can affect so ischemia of the lower body including peripheral many different organ systems and has a dynamic nerves. The clinical distinction is important be- course. cause spinal cord ischemia has a poor prognosis, The typical patient presents with paradoxical while a peripheral nerve ischemia has a better physical findings. He or she is frequently pale, prognosis if treated. This distinction can be made restless, and in preshock or shock, and has an ap- by examining peripheral pulses. The latter condi- pearance indicating poor peripheral perfusion but tion is usually combined with loss of pulses in the with a paradoxically high blood pressure. Eighty groins and distally in the affected lower extremi- percent of the patients have arterial hypertension ties. at admission. The high blood pressure is second- Repeated examination of peripheral pulses as ary to underlying essential hypertension, elevated well as blood pressures in the arms and ankles are catecholamine levels due to severe pain, or occlu- important indicators of the extension of a dissec- sion of the renal arteries or even the thoracic or tion and its consequences of organ malperfusion. abdominal aorta. Repeated examinations are important in order to Twenty percent of the patients have a low blood follow the development. A peripheral pulse may pressure instead. This is usually secondary to car- disappear, or a pulse deficit may be dynamic and diac tamponade or rupture, or to acute congestive resolve spontaneously, which is reported to occur heart failure secondary to acute aortic insuffi- in one-third of the patients. Such a dynamic course ciency. Another possible explanation is pseudo- is probably related to redirection of flow from the hypotension secondary to mechanical obstruction false into the true lumen after spontaneous fenes- from the dissection of one or both subclavian tration of the aortic septum known as the reentry arteries. phenomenon. Auscultation of the chest is of vital importance. A new pulse deficit is found in approximately A cardiac murmur indicates aortic regurgitation. 60% of the patients. The first heart sound is diminished or absent due to elevated end diastolic ventricular pressure. There might be an S3 gallop rhythm. A continu- 8.4 Diagnostics ous murmur usually indicates rupture into the right atrium. A pericardial friction rub indicates An electrocardiogram (ECG) should be obtained leakage into the pericardial sac. Auscultation of in the emergency department. Low voltage might the lungs might reveal signs of pulmonary edema. indicate pericardial tamponade, and ST–T wave Loss of alveolar breath sounds can be found after changes could indicate myocardial ischemia. leakage or rupture into one or both of the pleural The following blood tests should be ordered: cavities. Jugular venous distension is also a com- complete blood cell count, arterial blood gases, mon finding. protrombin and thromboplastin times, serum electrolytes, creatinine, blood urea nitrogen, liver enzymes and lactate.
  • 100. 8.5 Management 97 As with the physical examination, repeated tunately often not available – diagnostic modali-blood tests according to the patient’s clinical ties.course might be of great diagnostic value during Aortography is the old gold standard and isthe acute stage of the disease. Mild anemia is com- highly accurate in diagnosing aortic dissection,mon, while severe anemia indicates rupture and but it can fail to recognize a thrombosed false lu-bleeding. Hemolysis with elevated bilirubin or lac- men. It also provides better information than CTtic acid concentrations can also be found. A leuko- or MRI about the condition and involvement ofcytosis with a count of 10,000–15,000 is common. the aortic branches. Furthermore, aortographyBlood gases might reveal a metabolic acidosis can be combined with therapeutic endovasculardue to anaerobic metabolism in ischemic tissue. management. However, the modern CT scannersUrinary tests showing hematuria indicates renal with up to 64 detectors can produce extremelyinvolvement. detailed images and, when available, should be the A plain chest x-ray in standard anteroposterior first imaging study after the chest x-ray.and lateral projections is rarely diagnostic, but thefollowing findings indicates the presence of aorticdissection: 8.5 Management Abnormal shadow adjacent to the descending thoracic aorta 8.5.1 Treatment in the Deformity of the aortic knob Emergency Department Density adjacent to the brachiocephalic trunk Enlarged cardiac shadow As soon as aortic dissection is clinically suspected, Displaced esophagus, trachea, or bronchus aggressive medical treatment must be started im- Abnormal mediastinum mediately. The goals are to (1) stabilize dissection, Irregular aortic contour (2) prevent rupture, and (3) prevent organ isch- Loss of sharpness of the aortic shadow emia. Pleural effusion These goals can be achieved by diminishing the Expanded aortic diameter stress on the aortic wall. Consequently, the thera- peutic cornerstone is to reduce blood pressure inHelical CT is accurate for determining the pres- order to minimize the force of the left ventricularence of an aortic dissection and provides informa- ejection (dP/dT). The reduction in blood pressuretion for classification. The identification of an must, however, be balanced against what is neededintimal tear is, however, difficult and motion for adequate cerebral, coronary, renal, and visceralartifacts of the ascending aorta are sometimes perfusion. A useful guideline is that the systolicmisinterpreted as dissection. MRI is highly accu- arterial blood pressure should be kept aroundrate and gives valuable information about the 100–110 mmHg and mean arterial pressure be-pathoanatomy. Unfortunately it cannot be per- tween 60 and 75 mmHg, provided that urinaryformed in hemodynamically unstable patients output and neurology are unaffected.who are on ventilator support. In the emergency department the following TEE (Transesophageal echocardiography) is measures can be employed:often considered as one of the most valuable diag- 1. Insert one or two large-bore intravenous (IV)nostic tools, making it possible to determine the lines for administering antihypertensive drugstype and extent of the aortic dissection, especially and fluids.distally. It has limitations in visualization of the 2. Obtain an ECG.distal ascending aorta and the arch. TTE (Trans- 3. Order blood tests as stated above.thoracic echocardiography) is, on the other hand, 4. Obtain a plain chest x-ray.superior for evaluating involvement of the proxi- 5. Administer oxygen by maskmal part of the descending aorta in the dissection. 6. Consider injection of a strong analgesic IV,Together, TEE and TTE yield a sensitivity and such as morphine 5–10-mg.specificity approaching 100% for diagnosing dis- 7. Insert an arterial catheter for blood pressuresection and are thus probably the best – but unfor- monitoring.
  • 101. 98 Chapter 8 Aortic Dissection 8. Start administration of a beta-blocker as de- pass. In type A dissection with persistent organ scribed below. ischemia despite open surgical repair and replace- ment of the ascending aorta, endovascular treat- The recommended agents for medical manage- ment of the rest of the dissection is often a success- ment of acute aortic dissection are direct vaso- ful complement. dilators, beta-blockers, nitroglycerin and calcium channel blockers if beta blockers cannot be used. Beta-blockers orally are recommended for all 8.5.3 Type B dissection patients. Contraindications for beta-blockers are heart failure, bradyarrhythmias, atrioventricular The management of acute distal aortic dissection blocks, and bronchospastic disease. is initially always medical because this results in Suggested emergency medical treatment (local lower morbidity and mortality than emergent sur- variations in drug choices are of course common) gical repair. Consequently, the continued regimen is as follows: for these patients follows the previously given rec- Start propranolol treatment, 1 mg IV, every ommendations regarding beta blockade and vaso- 3–5 min until achieving a systolic blood pressure dilators started in the emergency department. around 100 mmHg and a heart rate of 60–80 beats/ The medical treatment must be combined with min (maximum dose, up to 0.15 mg/kg). Continue careful observation for complications. Surgical or thereafter with 2–6 mg IV every 4–6 h. In patients endovascular intervention should be considered with severe hypertension an IV infusion of nitro- for the following situations: glycerin is started and the dose titrated after blood Aortic rupture pressure and heart rate. Increasing periaortic or intrapleural fluid (sug- gesting aneurysmal leakage) NOTE Rapidly expanding aortic diameter The main objective of the medical Uncontrolled hypertension treatment is to lower the blood pressure Persistent pain despite adequate medical the- to a level of 100–110 mmHg. It is manda- rapy tory to check the patient for the develop- Organ malperfusion – ischemia of brain, spinal ment of new complications of the dissec- cord, abdominal viscera, or limbs tion during medical treatment. The goal of surgical repair in a type B dissection is, as with all other treatment options, to prevent rup- 8.5.2 Emergency Surgery ture and restore visceral and limb perfusion. Be- cause a common site of rupture is associated with Emergency surgery should be considered in type A the site of primary dissection, at least the upper dissections involving the intrapericardial ascend- half of the descending thoracic aorta needs to be ing aorta and the aortic arch. A distal type B dis- replaced in most cases. Graft replacement in the section with retrograde dissection involving the acute setting should be limited and replacement of aortic arch is also a case for acute operation. A the entire thoracic aorta avoided if possible. An double aortic lumen in the pericardial portion of abdominal fenestration procedure is sometimes the ascending aorta is an absolute indication for necessary to restore flow to the lower extremities. emergency operation. Depending on the patient’s Extraanatomical by pass is another possible way to general condition prior to the dissection there are, reestablish flow to the legs. as usual, exceptions from these basic rules. Con- traindications include very advanced age and se- vere debilitating or terminal illnesses. 8.5.4 Endovascular Treatment Surgical repair of the condition requires tho- racic surgical expertise and includes replacing the In patients with peripheral vascular complications ascending aorta and resecting the primary intimal due to extension of the dissection into a branch, tear. The operation involves cardiopulmonary by causing compression and obstruction of its true
  • 102. 8.6 Results and Outcome 99 lumen, as well as in patients with central aortic true lumen collapse, the endovascular option should be considered. Provided, of course, that the institution has technically skilled physicians, the necessary equipment and back-up support. It is possible to create a fenestration through the inti- mal flap from the false into the true lumen with endovascular techniques. As shown in Fig. 8.2 a, stenting of the entry site to occlude flow into the false lumen will probably be successful in restor- ing flow into a branch with its orifice obstructed by the false lumen and the dissection membrane. If there is an avulsion of the intima of that branch as in Fig. 8.2 b, this is not an option. a Endovascular management is developing as an attractive alternative to surgical repair. Patients with an acute type B dissection who are not good candidates for surgery can be considered for endovascular management. Stenting has also been reported to give successful results in aortic collapse with severe ischemia of the lower part of the body. An endovascular approach can also be used as the initial treatment by performing aortic fenes- tration and stenting. Most centers prefer to delay either surgical or endovascular repair until after the patient has recovered from the acute phase of malperfusion, whereas others advocate early pro- phylactic stenting and coverage of the intimal tear to occlude the false lumen and prevent further dis- section (Fig. 8.4). 8.6 Results and Outcome b A recent article from 12 international centersFig. 8.4. a Computed tomography showing a type B covering 464 patients with aortic dissection re-dissection and its entry in the first part of the descend- ported, in-hospital mortality rates for type-A dis-ing aorta in a patient with a previous reconstruction of sections treated surgically of 28%, and medicallythe arch and the brachiocephalic trunk after a type Adissection. The true anterior aortic lumen is severely of 58%. The corresponding figures for type B werecompressed causing obstruction of the main visceral 31% and 10%, respectively.branches and leading to visceral ischemia. b Flow into Successful closure of the intimal tear with en-the true aortic lumen and all branches is restored after dovascular stent grafts and subsequent thrombo-deploying a covered stent over the entry site in the de- sis of the false lumen is reported in up to 75% ofscending aorta patients. Branch occlusions with ischemic symp- toms were relieved in 75–95% of the cases. Sur- vival after 30 days was 75–85 %, and long-term results are good, with <1% related deaths and veri- fied thrombosis of the false lumen in 100% of the survivors. No thromboembolic complications oc-
  • 103. 100 Chapter 8 Aortic Dissection cured. In general, survival is lower for patients Daily PO, Trueblood HW, Stinson EB, et al. Manage- with paraplegia or visceral or renal ischemia. In ment of acute aortic dissections. Ann Thorac Surg cases with type B dissections and indications for 1970; 10:237 De Bakey ME, McCollum CH, Crawford ES, et al. Dis- surgical intervention, the results of endovascular section and dissecting aneurysms of the aorta: intervention seem more favorable compared with twenty year follow up of five hundred twenty-seven conventional surgical repair, but the number of patients treated surgically. Surgery 1982; 92:1118 reported cases from any single center is still low. Hagan PG, Nienaber CA, Isselbacher EM, et al. The In all cases, long-term follow-up regarding devel- International Registry of Acute Aortic Dissection opment of aneurysms and continued antihyper- – new insights into an old disease. JAMA 2000; tensive medication is essential. 283(7):897903 Lilienfeld DE, Gundersson PD, Sprafka JM, et al. Epi- demiology of aortic aneurysms. Mortality trends in the United States, 1951–1981. Arteriosclerosis 1987; Further Reading 7:637 Slonim SM, Miller DC, Mitchell RS, et al. Percutaneous Cambria RP, Brewster DC, Gertler, et al. Vascular com- Balloon fenestration and stenting for life threaten- plications associated with spontaneous aortic dis- ing ischemic complications in patients with acute section. J Vasc Surg 1988; 7:199–209 aortic dissection. J Thorac Cardiovasc Surg 1999; Cigarroa JE, Isselbacher EM, DeSanctis RW, et al. Diag- 117(6):1118–1126 nostic imaging in the evaluation of suspected aor- Williams DM, Lee DY, Hamilton BH, et al. The dis- tic dissections: Old standards and new directions. sected aorta: Percutaneous treatment of ischemic N Engl J Med 1993; 328:35–43 complications principles and results. J Vasc Interv Radiol 1997; 8:605-625
  • 104. Vascular Injuries in the Leg 9CONTENTS 9.1 Summary9.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . 101 Major bleeding is controlled by manual9.2 Background . . . . . . . . . . . . . . . . . . . . . . . . 101 compression.9.2.1 Background . . . . . . . . . . . . . . . . . . . . . . . . . 101 Vascular injuries should always be sus-9.2.2 Magnitude of the Problem . . . . . . . . . 102 pected in extremities with fractures.9.2.3 Etiology and Pathophysiology . . . . . 102 Most vascular injuries are revealed by care- Penetrating Injury . . . . . . . . . . . . . . . . . . 102 ful and repeated clinical examination. Blunt Injury . . . . . . . . . . . . . . . . . . . . . . . . . 102 Obtain proximal control before exploring9.2.3.3 Pathophysiology . . . . . . . . . . . . . . . . . . . 102 a wound in a patient with a history of sub-9.3 Clinical Presentation . . . . . . . . . . . . . . 103 stantial bleeding.9.3.1 Medical History . . . . . . . . . . . . . . . . . . . . . 1039.3.2 Clinical Signs and Symptoms . . . . . . . 1039.4 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . 104 9.2 Background9.4.1 Angiography . . . . . . . . . . . . . . . . . . . . . . . 1049.4.2 Duplex Ultrasound . . . . . . . . . . . . . . . . . 104 9.2.1 Background9.5 Management and Treatment . . . . . . 1059.5.1 Management Before Treatment . . . . 105 Vascular trauma to extremity vessels is caused by9.5.1.2 Severe Vessel Injury . . . . . . . . . . . . . . . . . 105 violent behavior or accidents. Because of the rise9.5.1.2 Less Severe Injuries . . . . . . . . . . . . . . . . . 105 in the number of endovascular procedures, iatro- Angiography Findings . . . . . . . . . . . . . 105 genic injuries have also become an increasing9.5.1.4 Primary Amputation . . . . . . . . . . . . . . . 106 part of vascular trauma. Vascular injuries may9.5.2 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . 106 cause life-threatening major bleeding, but distal9.5.2.1 Preoperative Preparation . . . . . . . . . . 106 ischemia is more common. Ischemia occurs after9.5.2.2 Proximal Control . . . . . . . . . . . . . . . . . . . 106 both blunt and penetrating trauma. The vascular9.5.2.3 Distal Control and Exploration . . . . . 109 injury is often one of many injuries in multiply9.5.2.4 Shunting . . . . . . . . . . . . . . . . . . . . . . . . . . . 110 traumatized patients that make the recognition9.5.2.5 Vessel Repair . . . . . . . . . . . . . . . . . . . . . . . 112 of signs of vascular injury – which can be blurred9.5.2.6 Finishing the Operation . . . . . . . . . . . . 113 by more apparent problems – and the diagnosis9.5.3 Endovascular Treatment . . . . . . . . . . . 113 difficult. Table 9.1 lists common locations of com-9.5.4 Management After Treatment . . . . . 114 bined orthopedic and vascular injury. Multiple9.6 Results and Outcome . . . . . . . . . . . . . . 114 injuries also bring problems regarding priority.9.7 Fasciotomy . . . . . . . . . . . . . . . . . . . . . . . . . 1159.8 Iatrogenic Vascular Injuries to the Legs . . . . . . . . . . . . . . . . . . . . . . . . . 117 Further Reading . . . . . . . . . . . . . . . . . . . 117
  • 105. 102 Chapter 9 Vascular Injuries in the Leg Table 9.1. Most common locations for combined or- NOTE thopedic and vascular injury Penetrating injuries can cause both major Orthopedic injury Vascular injury bleeding and ischemia. Femoral shaft fracture Superficial femoral artery Blunt Injury Knee dislocation Popliteal artery Blunt vascular injuries are usually caused by mo- Fractured clavicle Subclavian artery tor vehicle and other accidents. The consequences Shoulder dislocation Axillary artery are thrombosis and ischemia distal to the injured vessel. The media and the intimal layers of the ves- Supracondylar fracture Brachial artery of the humerus sel wall are easily separated, and subsequent dis- Elbow dislocation section by the bloodstream between the layers may lead to lumen obstruction. Blunt injuries also in- duce thrombosis. This type of vessel injury is par- ticularly common when the artery is hyperextend- 9.2.2 Magnitude of the Problem ed as in knee joint luxations and upper arm frac- tures. Contusion of the vessel may also cause Data on the true incidence of vascular injuries to bleeding in the vessel wall. Thrombosis and isch- the legs is hard to gather. The incidence of vascu- emia by this mechanism can occur several hours lar trauma varies among countries and also be- after the traumatic situation. Narrowing of the ar- tween rural and urban areas. It is usually higher terial lumen following blunt trauma is rarely caused where gunshot wounds are common. There is an by spasm and it can be disregarded as etiology. equal share of blunt and penetrating injury in most studies from Europe, whereas penetrating Pathophysiology injury is slightly more common in the United The main pathophysiological issue after vascular States. Approximately 75% of all vascular injuries injuries to the extremities is ischemia. The process are localized to the extremities and more than is identical to what happens during acute leg isch- 50% to the legs. The true incidence of iatrogenic emia due to embolization (see Chapter 10, p. 120). trauma is unknown. Irreversible damage to the distal parts of the legs is not infrequent and the diagnosis is more difficult to determine than for other types of leg ischemia. 9.2.3 Etiology and Pathophysiology The reason is the multiple manifestations of the trauma. It must be kept in mind that the time lim- Penetrating Injury it for acute leg ischemia – 4–6 h before permanent Penetrating vascular injury is caused by stab and changes occur – is also valid for trauma. cutting injuries, gunshots, and fractures, the latter when sharp bone fragments penetrate the vascular NOTE wall. Gunshots cause major bleeding by direct ar- Irreversible tissue damage may occur if tery trauma, while high-velocity bullets create a more than 6 h passes before blood flow cavitation effect with massive soft tissue destruc- to the leg is restored. tion and secondary arterial damage. In fact, after all types of penetrating trauma both bleeding and A vascular injury missed during the initial exami- indirect blunt arterial injury with ischemia may nation may develop into a pseudoaneurysm or an occur. Bleeding is more often exsanguinating after arteriovenous fistula. A pseudoaneurysm is a he- sharp injury and partial vessel transection. Com- matoma with persistent blood flow within it that plete avulsion, especially when caused by blunt may enlarge over time and cause local symptoms trauma, makes the vessel more prone to retrac- and sometimes even rupture. When both an ar- tion, spasm, and thrombosis. This diminishes tery and an adjacent vein are injured simultane- the risk for major bleeding. Iatrogenic injuries can ously an arteriovenous fistula may develop. These be caused by catheterization and during surgical can become quite large with time and even cause dissection. cardiac failure due to increased cardiac output.
  • 106. 9.3 Clinical Presentation 103 9.3 Clinical Presentation pain may vanish with time as a consequence of ischemic nerve damage. Even a major internal 9.3.1 Medical History hemorrhage may be present without being clini- cally obvious after a very recent injury.Most patients with major vascular injury present Information about complicating diseases andwith any or several of the “hard signs” of vessel medication is also helpful. For instance, beta-injury (Table 9.2) and the diagnosis is obvious. blockers may abolish the tachycardia in hypovole-Penetrating injury patients who arrive in the mia.emergency department without active hemor-rhage are usually not in shock because the bleed-ing was controlled at the trauma scene. Shock in 9.3.2 Clinical Signs and Symptomspatients with penetrating injury usually meansthat the bleeding is ongoing. Still, information The physical examination is performed after theabout the trauma mechanism is often needed to primary and secondary surveys of a multitraumaestimate the likelihood for vessel injury and to patient and should focus on identifying major ves-facilitate the management process. sel injury. The examination should be thorough, Besides interviewing the patient, additional especially regarding signs of distal ischemia. Itbackground information may be available from should include examination and auscultation ofmedical personnel and accompanying persons. the injured area, palpation of pulses in both legs,The few minutes required to establish a picture of and assessment of skin temperature, motor func-the trauma situation are usually worthwhile. For tion, and sensibility. The presence of one or moreexample, a history of a large amount of bright red of the classic hard signs of vascular injury listed inpulsating bleeding after penetrating trauma sug- Table 9.2 suggests that a major vessel is damagedgests a severe arterial injury. Venous bleedings are and that immediate repair is warranted. Findingsoften described as a steady flow of dark red blood. of “soft” signs should bring the examiner’s atten-In high-impact accidents the risk for a severe vas- tion to the fact that a major vessel may be injuredcular injury is increased. but that the definite diagnosis requires additional Besides being helpful when assessing the risk work-up. As noted in Table 9.2, the hard sign offor a major injury estimation of the blood loss is distal ischemia as suggested by the “six Ps” (seealso important for later volume replacement. Chapter 10, p. 121) suggests vascular injury. Knowledge of the exact time when the injuryhappened is helpful for determining the available NOTEtime before irreversible damage occurs from isch- Measurement of ankle pressure shouldemia. The duration of ischemia also influences the always be included in the priority in multitrauma patients,and the time elapsed affects the presentation of the The principles of the vascular examination sug-ischemic symptoms. For example, an initial severe gested for acute leg ischemia are also valid for vascular injuries, but certain details need to beTable 9.2. Signs of vascular injury emphasized. Vascular trauma in the legs usually strikes young persons, so it should be assumed Hard signs Soft signs that the patient had a normal vascular status Active hemorrhage History of significant before the injury. A palpable pulse does not ex- bleeding clude vascular injury; 25% of patients with arterial Hematoma (large, Small hematoma injuries that require surgical treatment have a pulsating, expanding) palpable pulse initially. This is due to propagation of the pulse wave through soft thrombus. Pulses Distal ischemia (“six Ps”) Adjacent nerve injury may be palpated initially in spite of an intimal flap Bruit Proximity of wound or minor vessel wall narrowing and can later cause to vessel location Unexplained shock thrombosis and occlude the vessel. Ankle pressure measurements and calculation of the ankle bra-
  • 107. 104 Chapter 9 Vascular Injuries in the Leg chial index (ABI) should therefore supplement blunt trauma. It may occasionally be helpful to palpation of pulses. If the ABI is ≤0.9, arterial inju- perform angiography even when injury is evident ries should be suspected. in order to exactly locate the injured vessel. An Findings in the physical examination of a pa- option is to perform it intraoperatively. The tech- tient in shock are particularly difficult to inter- nique is described in Chapter 10, p. 128. Contra- pret. In several aspects findings of distal ischemia lateral puncture is important when the injury is caused by vascular injury are similar to vasocon- close to the groin. striction of the skin vessels in the foot. Differences The purpose of the arteriography is to identify in pallor, the presence of pulses, and skin tempera- and locate lesions such as occlusions, narrowing, ture between the injured and uninjured leg there- and intimal flaps. Contrast leakage outside the fore should be interpreted as the possible presence vessel can be visualized, and it also serves to pro- of vascular injury. Ankle pressure measurements vide a road map before surgery. It has, however, are also valuable during such circumstances. been argued that it is unnecessary to search for It is important to remember to listen for bruits minimal lesions; some studies have shown that it and thrills over the wounded area to reveal a pos- is safe and effective to manage such lesions nonop- sible arteriovenous fistula. eratively. On the other hand, angiography may be the first step in the final treatment of such small lesions by stenting. 9.4 Diagnostics When the injury is caused by a shotgun blast, angiography should always be performed because Recommendations for management of suspected multiple vascular injuries are common. It is then vascular injuries in the leg have evolved from indicated regardless of the clinical signs and symp- mandatory exploration of all suspected injuries toms. The risk for complications after angiogra- (a common practice during past wars), to routine phy is very low, but the risk of complications is angiography for most patients, to a more selective higher when the punctured artery is small. Chil- approach today. Regarding exploration and subse- dren therefore have a rather high rate of complica- quent angiography, it was found that negative tions. A contributing factor is that their very vaso- explorations and arteriograms were obtained in active arteries are prone to temporary spasm. over 80% of the patients. The associated risk for Overall, as described above, the risk for complica- complications and morbidity after these invasive tions after angiography does not warrant avoiding procedures is the rationale for a more selective it when indicated. approach. Rapid transportation, clinical exa- Occasionally it is worthwhile to order veno- mination, ankle pressure measurements, careful graphy. It may be indicated in patients not sub- monitoring, and duplex examination leave angi- jected to exploration because arterial injury was ography for some of the patients and urgent explo- ruled out but in whom a major venous injury is ration for a few. suspected. As an example, 5–10% of all popliteal venous injuries are reported to occur without arte- rial damage. 9.4.1 Angiography Angiography is unnecessary when a vascular in- 9.4.2 Duplex Ultrasound jury is obvious after the examination. The two most common indications for excluding vascular Despite the usefulness of duplex scanning in gen- injury are (1) when there are no hard signs at the eral for vascular diagnosis, it has not been univer- examination, and (2) when clinical findings are sally accepted for diagnosis of vascular trauma imprecise but the ABI is <0.9. despite the fact that it is noninvasive. It is operator Angiography is more often indicated after blunt dependent and vessels may be difficult to assess trauma than penetrating. The reason for this is the in multiply injured patients, legs with skeletal de- more difficult clinical examination because of the formities, large hematomas, and through splints more extensive soft tissue and nerve damage after and dressings. In some hospitals with expertise in
  • 108. 9.5 Management and Treatment 105duplex assessment and round-the-clock access to 7. Consider administering antibiotics and tetanusskilled examiners, duplex has replaced angiogra- prophylaxis.phy to a large extent. The indications proposed are 8. Consider administering analgesics (5–10 mgthen the same as for angiography. opiate IV). Duplex is also the method of choice for diagno-sis of most of the late consequences of vascular in- Less Severe Injuriesjuries to the legs – arteriovenous fistulas, pseudo- ABI must be measured when vascular injury isaneurysms, and hematomas. suspected. Patients with soft signs of vascular in- jury and an ABI <0.9 usually need arteriography to rule out or verify vascular damage. This is per- 9.5 Management and Treatment formed as soon as possible. Before the patient is sent to the angiosuite other injuries need to be 9.5.1 Management Before Treatment taken into account and the priority of manage- ment discussed. Ischemic legs should be given Severe Vessel Injury higher priority than, for example, skeletal and softMajor external bleeding not adequately stopped tissue injury, and temporary restoration of bloodwhen the patient arrives to the emergency depart- flow can be achieved by shunting.ment should immediately be controlled with digi- Patients with an ABI >0.9 and a normal physi-tal pressure or bandages. No other measures to cal examination (little suspicion of vascular inju-control bleeding are taken in the emergency de- ry) can be monitored in the ward. Repeated ex-partment and attempts to clamp vessels are saved aminations of the patient’s clinical status are im-for the operating room. portant and hourly assessment of pulses and ABI The patient is surveyed according to the trauma the first 4–6 h are warranted. If the ABI deterio-principles used in the hospital. For most patients rates to a value <0.9 or if pulses disappear, angiog-without obvious vascular injuries to the leg ves- raphy should be carried out.sels, more careful vascular assessment takes placeafter the secondary survey. If the vascular injury is Angiography Findingsone of many in a multitrauma patient, general Operative treatment and restoration of blood flowtrauma principles for trauma care are applied. are done as soon as possible if the angiographyTreatment of the vascular problem is then initiated shows arterial occlusion in the femoral, popliteal,as soon as possible when the patient’s condition or at least two calf arteries in proximity to theallows it. traumatized area. It should be kept in mind that Patients with hard signs of vascular injury but occlusion of the popliteal artery is detrimental forwithout other problems should be transferred im- distal perfusion and is associated with a high riskmediately to the operating room. Before transfer for amputation due to a long ischemia time. Pa-the following can be done: tients with popliteal occlusion should therefore be1. Give the patient oxygen. taken immediately to the operating room. Debate2. Initiate monitoring of vital signs (heart rate, is ongoing whether one patent calf artery in an in- blood pressure, respirations, SpO2). jured leg is sufficient to allow nonoperative treat-3. Place at least one large-bore intravenous (IV) ment. Some reports have found that as long as one line. of the tibial vessels is intact, there is no difference4. Start infusion of fluids. Dextran preceded by in limb loss or foot problems during follow-up be- 20 ml Promiten is advised especially if the pa- tween operative and nonoperative treatment. Our tient has distal ischemia. recommendation, however, is to try to restore per-5. Draw blood for hemoglobin and hematocrit, fusion if more than one of the calf arteries is prothrombin time, partial thromboplastin obstructed. time, complete blood count, creatinine, sodi- If combined with ischemic symptoms or signs um, and potassium as well as a sample for blood of embolization, angiography findings of intimal type and cross-match. flaps, minor narrowing of an artery, or minor6. Obtain informed consent. pseudoanuerysm (<5 mm in diameter) should also
  • 109. 106 Chapter 9 Vascular Injuries in the Leg be treated. Endovascular stenting is then a good ered with soft tissue. When the patient has other alternative to operative treatment. Expectancy injuries that motivate urgent treatment, or has could be favorable for asymptomatic patients with fractures in the leg that need to be surgically re- normal ABI. Such occult arterial injuries appear paired, this last step can be delayed while perfu- to have an uneventful course and late occlusion is sion to the distal leg is maintained by a shunt tem- extremely rare. The occasional pseudoaneurysm porarily bypassing the injured area. that will enlarge with time appears to benefit from later repair. Preoperative Preparation The patient is placed on a surgical table that allows Primary Amputation x-ray penetration. If not administered previously, In most circumstances, but not always, it is rea- infection prophylaxis treatment is started. The en- sonable to repair injured vessels. For a few patients, tire injured extremity is scrubbed with the foot however, primary amputation is a better option. draped in a transparent plastic bag. A very good This is often a difficult decision. Primary amputa- marginal of the sterile field is essential because in- tion is favorable for the patient if the leg is massa- cisions need to be placed much more proximal cred or if the duration of ischemia is very long than the wound to achieve proximal control. The (>12 h) and appears to be irreversible in the clini- contralateral leg should also be scrubbed and cal examination (Chapter 10, p. 123). Primary draped to allow harvest of veins for grafts. The ve- amputation may also be considered for certain pa- nous system in the injured leg should be kept in- tients: multitrauma patients, patients with severe tact if possible. If a patient is in shock and the comorbid disease, and those in whom the leg was bleeding is difficult to control, it is recommended already paralyzed at the time of injury. Extensive to delay inducing the anesthesia until just before nerve damage, lack of soft tissue to cover the the operation begins in order to avoid increased wound, and duration of ischemia >6 h support bleeding and an accentuated drop in systemic primary amputation for these patient groups. blood pressure due to loss of adrenergic activity. There are scoring systems, such as the Mangled Extremity Severity Score (MESS), to aid in making NOTE the decision to amputate a leg or an arm. For ex- It is usually wise to achieve proximal ample, a patient over 50 years old with persistent control through a separate incision before hypotension and a cool paralyzed distal leg after exploring the wounded area. high-energy trauma should have the leg amputat- ed according to MESS. It must be stressed, how- Proximal Control ever, that repair of both venous and arterial inju- In patients with injuries proximal to the femoral ries is superior for most patients. The MESS score vessels, control is achieved through an incision is described in Chapter 3 (p. 36). in the abdominal fossa. The common or external iliac artery can then be exposed retroperitoneally and secured. Proximal control for injuries in the 9.5.2 Operation thigh, proximal to the poplital fossa, is usually obtained by exposing the common femoral artery Surgical treatment of vascular injuries in the leg and its branches in the groin. Popliteal vessel trau- usually proceeds in a particular order common for ma can be controlled by exposing the distal super- most patients. First the patient is scrubbed, anes- ficial femoral artery or the proximal popliteal ar- thetized, and prepared for surgery. The next step tery through a medial incision above the knee. is to achieve proximal control. Occasionally, con- This is not too difficult, and the principles follow trol of the bleeding by manual compression with a the outline given in the Technical Tips box. Inflow gloved hand needs to be maintained throughout control for calf vessel injuries is reached by expos- these first two steps. Proximal control is followed ing the popliteal artery below the knee. by measures to achieve distal control, often ac- complished during exploration of the wound. Fi- nally, the vessels are repaired and the wound cov-
  • 110. 9.5 Management and Treatment 107 If there is no ongoing bleeding when the artery around the leg well above the wounded area beforeis exposed a vessel-loop is applied. Clamping scrubbing and draping. In the thigh a 20-cm wideshould be postponed until later. If bleeding is brisk cuff is often suitable. It is important to have at leastand continuous, however, the clamp is placed right 10 cm from the lower edge of the cuff to the woundaway. Clamping should be attempted even if the to allow prolongation of incisions if necessary. Thebleeding appears to be mainly venous in origin. cuff is inflated if bleeding starts during explora-Arterial clamping often diminishes such bleed- tion. For distal injuries this often works well andings substantially. may spare the patient one surgical wound. An alternative way to achieve proximal controlof distal femoral, popliteal, and calf vessels is to NOTEuse a cuff. A padded cuff, the width in accordance Tourniquet occlusion is a good option forwith the leg circumference, is then wrapped proximal control of distal injuries. TECHNICAL TIPS Exposure of Different Vessel Segments in the Leg Common or External Iliac Arteries, c At this stage the anatomy is often unclear Fig. 9.1 regarding the relation of branches to the common a A skin incision 5 cm above and parallel to the femoral artery. Encircle the exposed artery with a inguinal ligament is used. This incision allows ex- vessel-loop as described in Chapter 15, and gently posure of all vascular segments from the external lift the artery. Continue dissection until the bifur- iliac up to the aortic bifurcation. cation into superficial and deep femoral artery is b The muscles are split in the direction of the identified. Its location varies from high up under fibers. Dissection is totally retroperitoneal, with the inguinal ligament up to 10 cm further down. attention to the ureter crossing the vessels in this At this stage, the surgeon must decide whether region. Be careful with the iliac vein, which is sep- exposure and clamping of the common femoral arated from the artery by only a thin tissue layer. are enough. This is usually the case for proximal Exposure of the proximal common iliac artery and control in trauma distally in the leg. In acute isch- the aortic bifurcation is facilitated by a table-fixed emia it is more common that the entire bifurca- self-retaining retractor (i.e., Martin arm). tion needs to be exposed. During the continued dissection, attention Femoral Artery in the Groin, Fig. 9.2 must be given to important branches that should a A longitudinal skin incision starting 1–2 cm cra- be controlled and protected from iatrogenic inju- nial to the inguinal skin fold and continued lateral ries. These are, in particular, the circumflex iliac to the artery is used to avoid the inguinal lymph artery on the dorsal aspect of the common femo- nodes. A common mistake is to place the incision ral artery and the deep femoral vein crossing over too far caudally, which usually means the dissec- the anterior aspect of the deep femoral artery just tion is taking place distal to the deep femoral. after its bifurcation. To provide a safe and good b The dissection is continued sharply with the exposure of the deep femoral to a level below its knife straight down to the fascia lateral to the first bifurcation, this vein must be divided and su- lymph nodes and is then angulated 90° medially ture-ligated. Partial division of the inguinal liga- to reach the area over the artery. It should then be ment is occasionally needed for satisfactory expo- palpable. Lymph nodes should be avoided to min- sure. imize the risk for infection and development of seroma. The fascia is incised, and the anterior and lateral surfaces of the artery are approached.
  • 111. 108 Chapter 9 Vascular Injuries in the Leg TECHNICAL TIPS Exposure of Different Vessel Segments in the Leg (continued) Superficial Femoral Artery, Fig. 9.3 a The popliteal artery and adjacent veins and A skin incision is made along the dorsal aspect of nerve are then, without further division of mus- the sartorius muscle at a midthigh level. It is im- cles, easily found and separated in the anterior portant to avoid injuries to the greater saphenous aspect of the fossa. vein, which usually is located in the posterior flap of the incision. The incision can be elongated as Popliteal Artery Below the Knee, needed. After the deep fascia is opened and the Fig. 9.5 sartorius muscle is retracted anteriorly, the femo- a A sterile pillow or pad is placed under the distal ral artery is found and can be mobilized. Division femur. The incision is placed 1 or 2 cm posterior to of the adductor tendon is sometimes required for the medial border of the tibia, starting at the tibial exposure. tuberosity and extending 10–12 cm distally. Sub- cutaneous fat and fascia are sharply divided, with Popliteal Artery Above the Knee, caution to the greater saphenous vein. Fig. 9.4 b The popliteal fossa is reached by retracting a The knee is supported on a sterile, draped the gastrocnemius muscle dorsally. The deep fas- pillow. The skin incision is started at the medial cia is divided and the artery usually easier to iden- aspect of the femoral condyle and follows the tifiy. Occasionally, pes anserinus must be divided anterior border of the sartorius muscle 10–15 cm for adequate exposure. The popliteal artery is in a proximal direction. Protect the greater sa- often located just anterior to the nerve and in phenous vein and the saphenous nerve during close contact with the popliteal vein and crossing dissection down to the fascia. After dividing the branches from concomitant veins. If it is necessary fascia longitudinally, continue the dissection in to expose the more distal parts of the popliteal the groove between the sartorius and gracilis artery, the soleus muscle has to be divided and muscles, which leads to the fat in the popliteal partly separated from the posterior border of the fossa. tibia. Fig. 9.1. Exposure of common or external iliac arteries. Note the ureter crossing the arteries anteriorly
  • 112. 9.5 Management and Treatment 109Fig. 9.2. Exposure of femoral artery in the groin Distal Control and Exploration Distal control is achieved by distal elongation of the incision used to explore the site of injury. Through this incision careful dissection in intact tissue distal to the injured area usually reveals the injured artery. When it is identified and found to be not completely transected, a vessel-loop is posi- tioned around it. If the artery is cut, a vascularFig. 9.3. Incision for exposure of the superficial femo- clamp is applied on the stump. It is also possible toral artery gain distal control during the exploration of the injured area, but dissection may be tricky because of hematoma, edema, and distorted anatomy. Usu- ally the backbleeding from the distal artery is minimal and does not disturb visualization dur- ing dissection. Simultaneous venous bleeding that emerges from major veins must also be controlled. This can be done by balloon occlusion or clamps. The latter should be used with caution and closed as little as possible.
  • 113. 110 Chapter 9 Vascular Injuries in the Leg Fig. 9.4. Exposure of popliteal artery above the knee Fig. 9.5. Exposure of popliteal artery below the knee When control is obtained the wound is explored Finally, other parts of the wound are explored and the site of vessel injury identified. The best and all devitalized skin and muscle tissue is ex- way is to follow the artery proximally from where cised. Injured small adjacent veins should be li- the artery was exposed for distal control. Of gated and all larger veins, such as the femoral veins course, any foreign materials encountered need to and the popliteal vein, must be repaired. be removed. The injured artery should be explored in both directions until a normal arterial wall is Shunting reached. Several centimeters of free vessels are Insertion of a temporary shunt to restore distal needed. Side branches are controlled using a perfusion is sensible if the vascular injury appears double loop of suture with a hanging mosquito to require more extensive repair than a simple su- or by small vascular clamps (see Chapter 15, ture or an end-to-end anastomsis. Shunting pro- p. 181). Thrombosed arteries usually have a hema- vides the time needed to either perform a vascular toma in the vessel wall giving it a dark blue color. reconstruction, including harvesting of a vein Such parts need to be cut out and the vessel edges graft from the uninjured leg, or to wait for help. trimmed before shunting or repair. For penetrat- Shunting can also be valuable when patients have ing injuries all parts of the vascular wall that are other injuries that need attention or when leg frac- lacerated must be excised to ensure that the intima tures must be repositioned to give the appropriate will be enclosed in the suture line during repair. vascular graft length. In patients with fractures After this procedure the vessel can be shunted or shunting allows both repositioning and fixation repaired. without increasing the risk of ischemic damage.
  • 114. 9.5 Management and Treatment 111 Fig. 9.6. A special catheter for shunting (Pruitt–Inahara shunt). The shunt has a larger balloon in one end aimed for the proximal inflow vessel and a smaller one for placement in the outflow vessel. The occluding balloons are con- trolled by injecting saline through separate channels with stopcocks. The shunt can also be flushed through a third channel Fig. 9.7. Example of shunting in a severe artery and vein injury. The artery is shunted with a Pruitt–Ina- hara shunt and its balloons secured with vessel-loops. For shunting of the vein a piece of ordinary rubber tubing is used. It is also secured with vessel-loops and with a sutureA novel vascular reconstruction seldom tolerates The principles of vascular shunting are simple.the forces required for reposition of fractures. Specially designed shunts can be used if available;When perfusion is restored by a shunt the surgeon examples are Pruitt–Inhara and Javid. Most havehas plenty of time to carefully explore the wound inflatable balloons in both ends for occlusion andand other injuries. When a shunt is used for distal side channels with stopcocks through which theperfusion while other procedures are performed, function of the shunt can be tested (Figs. 9.6, 9.7).it is important to check its function at least every The side holes also enable infusion of a heparin-30 min. ized solution and contrast for fluoroscopy. The
  • 115. 112 Chapter 9 Vascular Injuries in the Leg extra channels can be used to draw blood during Table 9.3. Amputation frequencies after ligature of the operation. It is not, however, necessary to use different arteries manufactured shunts. Any kind of sterile plastic Vessel ligated Amputation rate or rubber tubing is sufficient. It is then important to use dimensions of the tube in accordance with Common iliac artery 54% the artery’s inner diameter. The tube is cut into External iliac artery 47% suitable lengths and the edges carefully trimmed Common femoral artery 81% with scalpel and scissors to avoid damage when Superficial femoral artery 55% inserted. The tube is positioned and secured with Popliteal artery 73% vessel loops that abolish the space between the artery and tube to manage bleeding. A loosely applied suture around the middle part of the shunt can be used to secure it. It is advantageous to possible to leave two interrupted, provided the simultaneously shunt concomitant vein injuries – remaining vessel is not the peroneal artery. at least the femoral and popliteal veins – to avoid Before definitive repair the surgeon must be swelling and to facilitate distal flow. sure that the inflow and outflow vascular beds re- main open and are free of clots. Liberal use of Fog- Vessel Repair arty catheters is therefore wise. The technique is While we advocate repairing both the artery and described in Chapter 10 (p. 126). If the backbleed- the vein, we do not favor reconstructing the in- ing is questionable, intraoperative angiography jured vein before the artery. If both can be mended should be performed to make sure the outflow within a reasonable timeframe we recommend tract is free of clots. Local heparinization, de- that the most difficult reconstruction is performed scribed in Chapter 15 (p. 181), is always indicated. first. If, however, the artery is shunted it may Systemic heparinization can be used for selected be advantageous to start with the vein to achieve patients without other injuries considered to have optimal outflow as soon as possible. Some vas- a low risk for continued bleeding from the wound cular surgeons favor vein ligature as a general after debridement. If the foot’s appearance or in- principle because of the potential risk for emboli- traoperative angiography suggests microemboli- zation from vein segments that thrombose after zation, local thrombolysis can be tried as described repair. in Chapter 10 (p. 127). The goal for repair is to permanently restore NOTE continuity of the artery without stenosis or ten- Popliteal occlusions should be managed sion. The type of injury determines the choice quickly because of the high risk of of technique. It varies from a couple of vascular amputation in case of delayed treatment. sutures to reconstruction with a patch, interposi- tion, or a bypass grafting. Lateral suture for repair Arterial Injuries of minor lesions, including patching, is described In general, all injured arteries should be repaired. in Chapter 15 (p. 183). Bypass techniques are be- Sometimes, when necessary in order to save the yond the scope of this book, and detailed descrip- patient’s life or when interruption of an artery tions can be found in other vascular surgery text- does not influence blood flow to the leg, the in- books. jured vessel may be ligated. The former is extreme- A graft is usually needed, and only occasionally ly uncommon, but the decision is difficult when it can an end-to-end anastomosis be performed arises. As an aid we have listed in Table 9.3 the am- without tension. It is always better to use an inter- putation rates, as obtained from the literature, fol- position graft or a bypass to avoid what is even lowing ligation of vessels. Among proximal ves- perceived as insignificant tension because anasto- sels, only branches from the deep femoral artery, motic rupture and graft necrosis may occur when but not the main branch, can be ligated without leg swelling and movements pull the arterial ends morbidity. Distally, we recommend repair of at further apart postoperatively. The major bleeding least two calf arteries to be on the safe side, but it is that can result from this may even be fatal.
  • 116. 9.5 Management and Treatment 113 An autologous vein is always the preferred graft their size. An autologous vein is preferred overmaterial. Vein is more infection resistant than synthetic materials.synthetic materials and is more flexible. It allowsboth elongation and vasodilatation to adjust varia- Finishing the Operationtions in flow requirements. The great saphenous After the vascular reconstruction is finished thevein from the contralateral leg is the primary resulting improvement in distal perfusion shouldchoice for a graft. It is a serious mistake to use the be checked. This is indicated as well-perfused skingreat saphenous vein from the traumatized leg if in the foot and palpable pulses. If there is anythe deep vein is also injured or if injury is suspect- doubt about the result control angiography shoulded. Interruption of the saphenous vein with ob- be performed. Preferably, it is done from the prox-structed concomitant deep veins will rapidly cause imal control site to enable visualization of all anas-severe distal swelling of the leg and graft occlusion tomoses. If problems are revealed the reconstruc-within days. The vein can be harvested at a level in tion must be redone and distal clots extractedthe leg where the saphenous vein diameter fits the as previously described. While vascular spasm isartery that needs to be repaired. A graft slightly rare and should not be regarded as the main expla-larger than the artery should be obtained if possi- nation for lack of distal blood flow, injection ofble. For common femoral artery lesions, two pieces 1–2 ml papaverine into the graft can also be tried.of saphenous vein, both open longitudinally and After vascular repair all devitalized tissue andthen sutured together, might be required. An op- foreign material should be removed to reduce thetion is to use arm veins as graft material. If veins risk of postoperative infection. Grafts and vesselsnot are available expanded polytetrafluoroethyl- should be covered with healthy tissue by looselyene (ePTFE) is the second choice. The main rea- adapting it with interrupted absorbable sutures.sons not to use it are the slightly higher risks for For injuries with massive tissue loss it may be im-postoperative graft occlusion and infection. possible to cover the graft. This increases the risk for postoperative anastomotic necrosis and rup- Venous injuries ture. Split or partial skin grafts or biological dress-Most venous injuries are exposed when the wound ings can be used to prevent this. Occasionally itis explored. While vein ligature may lead to leg may be better to perform a bypass through healthyswelling, it rarely causes ischemia or amputation. tissue, thus avoiding the traumatized area, to min-On the other hand, the only benefit of vein liga- imize graft infection and postoperative complica-ture is rapid bleeding control and a reduced oper- tions.ating time. Major veins can therefore be ligated tosave the life of an unstable patient. If possible,however, most veins should be repaired, especially 9.5.3 Endovascular Treatmentthe popliteal and the common femoral veins. Calfveins can be ligated without morbidity. In patients Endovascular treatment of vascular injuries to legwith combined injuries, both the vein and the ar- vessels is attractive because it provides a way totery should be repaired to enhance the function of achieve proximal control, reduce ischemia time,the arterial reconstruction. Control of bleedings and simplify complex procedures. There is not acan be achieved by fingers or a “strawberry” or lot of experience – at least not reported in the lit-“peanut” to compress the vein proximal and distal erature – with endovascular treatment. Some cen-to the injured site, or by using gentle vascular ters have reported successful semielective treat-clamps. A continuous running suture, almost ment of pseudoaneurysms and arteriovenous fis-without traction in the suture line, is often suffi- tulas in the groin. Small patient series have beencient to close a stab wound. When the vein is more published on embolization of bleeding branches toextensively damaged, a patch or an interposition the deep femoral artery and stent graft control ofgraft may be needed for repair. As with arteries, it small lacerations in the femoral arteries. We haveis important to match the caliber of the interposi- only treated occasional patients this way so far.tion graft and the injured vein. Veins without Endovascular treatment will probably be anblood are collapsed, so it is easy to underestimate option for many patients with soft signs of vascu-
  • 117. 114 Chapter 9 Vascular Injuries in the Leg lar injury, who will undergo angiography and then Table 9.4. Medical history and clinical findings sug- will be found to have a minor bleeding, a pseudoa- gesting that fasciotomy may be needed neurysm, a fistula, or an intimal flap. The possi- Severe ischemia lasting longer than 4–6 h bilities of considering endovascular repair for pa- Preoperative shock tients with hard signs of vascular injury to the legs will depend on logistics and the organization of a Firm/hard muscle compartment when palpated hospital’s endovascular team. With around-the- Decreased sensibility and/or motor function clock availability, patients with less severe distal Compartmental pressure >30 mmHg ischemia may be subjected to angiography with Pain out of proportion localized distal possibilities for endovascular treatment in mind. to the vascular injury Patients with penetrating injuries that are actively bleeding may undergo balloon occlusion of a proximal artery to accomplish control and then be transferred to the operating room for repair. In portant for patients with both venous and arterial other hospitals where an endovascular team is not reconstruction. Patients who have been subjected available during weekends, angiography is skipped to venous ligation need extra attention and mea- in some patients with soft signs, and they are sures against limb swelling. Antibiotic treatment treated with an open procedure and intraoperative started preoperatively or intraoperatively is usu- angiography instead. But it is likely that endovas- ally continued after the operation. We use a com- cular treatment will be the treatment of choice for bination of benzylpenicillin and isoxazolyl peni- a significant proportion of patients in the near cillin to cover streptococci, clostridia, and staphy- future. lococci. 9.5.4 Management After Treatment 9.6 Results and Outcome As for most vascular procedures, the risk for bleed- Mortality after isolated vascular injuries in the ing and graft thrombosis of the reconstructed legs is very low, ranging from 0% to 3% in most artery is higher during the first 24 h after the op- series. The few deaths reported were due to infec- eration. Postoperative monitoring of limb perfu- tion and sepsis, underscoring the importance of sion, including inspection of foot skin and wounds careful tissue debridement and graft coverage. For and palpation of pulses, is necessary at least every solitary vascular injuries, amputation rates are 30 min for the first 6 h. If pulses are difficult to also low. It has to be remembered that important ascertain, ankle pressure should be measured. nerves are located adjacent to the vessels and often Loss of pulses or an abrupt drop in pressure indi- are simultaneously severely damaged. This con- cate that reoperation may be required, even when tributes to long-term disability. In most studies, the graft appears to be patent either clinically or arterial patency is very high, while venous recon- on duplex scanning. As for acute leg ischemia structions tend to thrombose at a much higher fre- caused by thrombosis, there is also a substantial quency. Although some authors have argued that risk for compartment syndrome. Particularly venous repair is therefore unnecessary, we believe when the ischemia duration has been long, this it improves patency of the arterial graft. Fractures, risk is considerable, and it is important to examine especially open ones, in combination with arterial calf muscles for signs of compartment syndrome. injury have less encouraging long-term results. In This assessment includes motor function, tender- most reports the incidence of primary as well as ness, and palpation of the muscle compartments secondary amputation is higher when fractures in the calf. Findings that may suggest fasciotomy are combined with vascular and nerve injuries. In are listed in Table 9.4 one study the primary and secondary amputation For most patients administration of dextran or rates were 20% and 52%, respectively, during a fol- low molecular weight heparin is indicated to avoid low-up of 5.6 years. There was a 30% long-term postoperative thrombosis. This is especially im- disability rate for salvaged limbs in the same study,
  • 118. 9.7 Fasciotomy 115all related to poor recovery of neurological func- 9.7 Fasciotomytion. Although it is clear that popliteal injuries,combined injuries with femoral fractures, delayed When the compartment pressure is clearly in-repair >6 h, and injuries treated in patients in creased or when there is a risk of developing in-shock have a much higher amputation rate, the creased pressure, fasciotomy of muscular com-results may be less pessimistic than the results in partments distal to a vascular injury should bethe literature. For multitrauma patients outcomes performed in association with the vascular repair.of vascular injury in the leg are hard to come by. Factors suggesting an increased pressure are listed in Table 9.4. The technique for decompression of the four compartments in the lower leg is described in the Technical Tips box. TECHNICAL TIPS Fasciotomy of the Calf Compartments (Two Incisions) Medial Incision A 15–20-cm-long skin incision, starting slightly below the midpoint of the calf and downwards parallel to and 2–3 cm dorsally of the medial border of the tibia, is used to decompress the deep and superficial posterior muscle compart- ments (Fig. 9.8). It is important to avoid injury to the great saphenous vein. Sharp division of skin and subcutaneous fat reaches the fascia. The skin and subcutaneous fat is mobilized en bloc anteriorly and posteriorly to expose it enough to provide access to the compartments. The fascia is then opened in a proximal direction and dis- tally down toward the malleolus under the sole- us muscle. At this level, the soleus muscle has no attachments to the tibia, and the deep posterior compartment is more superficial and easier to access. Through the same skin incision, the fas- cia of the superficial posterior muscle compart- ment is cleaved 2–3 cm dorsally and parallel to the former. A long straight pair of scissors with blunt points is used to cut the fascia using a dis- tinct continuous movement in the distal direc- tion, down to a level of 5 cm above the malleoli and proximally along the entire fascia.Fig. 9.8. Incision and exposure for fasciotomy of pos-terior compartments. The posterior dotted line indicatesfasciotomy incision for the superficial compartmentand the anterior dotted line for the deep compartment
  • 119. 116 Chapter 9 Vascular Injuries in the Leg TECHNICAL TIPS Fasciotomy of the Calf Compartments (Two Incisions) (continued) Lateral Incision The skin incision for fasciotomy of the lateral and anterior muscle compartments is oriented ante- rior to and in parallel with the fibula. The dorsal position of the lateral compartment, however, often requires more extensive mobilization of the subcutaneous fat to reach it. The superficial peroneal nerve is located anteriorly under the fascia and exits the compartment through the anterior aspect of the fascia distally in the calf. To preserve this nerve, direct the scissors dorsally when making the fasciotomy in both directions. (See Fig. 9.9.) Unless the swelling is very extensive, 2-0 prolene intradermal suture is loosely placed to enable wound closure later (Fig. 9.10). It is impor- tant to leave long suture ends at both sides to allow wound edge separation the first postop- erative days. The skin incisions are left open with moist dressings. Fig. 9.9. Incision for fasciotomy of anterior and lateral compartments. Through the demonstrated skin inci- sion, long incisions are made along the dotted lines in the fascia. Caution must be taken with the peroneal nerve Fig. 9.10. Cross-section demonstrating the principles for decompression of all four muscle compartments in the calf through a medial and a lateral incision. The location of major nerve bundles in the different com- partments is indicated
  • 120. 9.8 Iatrogenic Vascular Injuries to the Legs 117 9.8 Iatrogenic Vascular Injuries The technique used for vascular repair is the to the Legs same as for all other vascular injuries. While main- taining compression, proximal and distal controlIatrogenic vascular injuries occur either in con- is created by careful dissection of the vesselsnection with other surgical procedures or as a around the suspected injury site. The vessel is thencomplication to groin catheterization for angiog- clamped or controlled by finger or swab compres-raphy, percutaneous coronary intervention, and sion. The traumatized vessel is then repaired. Forother endovascular procedures. The latter consti- iatrogenic injuries this often means just a few su-tutes the main part. In this book, bleeding and tures; only rarely is more complex repair needed.pseudoaneurysms that occur after angiography There are also specially designed instrumentsare covered in Chapter 14. for controlling vessels – especially veins – enough Vascular injury during surgery is also quite to allow suturing without needing extensive expo-common. The risk for vessel trauma during opera- sure to achieve control. One consists of a ring 2–tions varies with the type of procedure. Certain 3 cm in diameter welded at a 75° angle to a handle.procedures are also more prone to cause vascular The ring is placed around the injured vein andinjury (Table 9.5), and vascular procedures are the held in place, thereby controlling the bleeding.ones most frequently associated with vascular in- This device is particularly helpful for iliac veinjury. Suspicious signs of vascular injury during bleedings that occur during gynecologic, urologic,surgery are sudden bleeding that fills the operative and rectal cancer operations. Multiple vessel inju-field and problems maintaining the systemic blood ries are not uncommon and perseverance is oftenpressure. This is exemplified by major bleeding needed to repair all vessels before the originaloccurring behind retractors or in a field previ- operation can proceed.ously dissected during abdominal aortic aneu-rysm surgery. When the bleeding area is identi-fied, it is controlled by manual compression. It is Further Readingwise to always call for help when major bleeding issuspected. More hands facilitate repair, and real- Dennis JW, Frykberg ER, Veldenz HC, et al.Validationizing that one has caused a severe vascular injury of nonoperative management of occult vascular in-may generate stress and distract the surgeon from juries and accuracy of physical examination alone in penetrating extremity trauma: 5- to 10-year fol-accomplishing vascular repair. low-up. J Trauma 1998; 44(2):243–252 Hafez HM, Woolgar J, Robbs JV. Lower extremity arte- rial injury: results of 550 cases and review of risk factors associated with limb loss. J Vasc Surg 2001; 33(6):1212–1219Table 9.5. Examples of procedures associated with Hood DB, Weaver FA, Yellin AE. Changing perspec-iatrogenic vascular injury (PCI percutaneous coronary tives in the diagnosis of peripheral vascular trauma.intervention) Semin Vasc Surg 1998; 11(4):255–260 Modrall JG, Weaver FA, Yellin AE. Vascular consider- Procedure Vessel injured ations in extremity trauma. Orthop Clin North Am PCI/angiography Common femoral, 1993; 24(3):557–563 external iliac, Nair R, Abdool-Carrim AT, Robbs JV. Gunshot injuries deep femoral arteries of the popliteal artery. Br J Surg 2000; 87(5):602 Rich NM. Management of venous trauma. Surg Clin Knee arthroplasty Popliteal artery and vein North Am 1988; 68(4):809–821 Hip arthroplasty Common femoral Rowe VL, Salim A, Lipham J, et al. Shank vessel injuries. Stripping Common femoral vein Surg Clin North Am 2002; 82(1):91–104 of saphenous vein (groin arteries) Snyder WH 3rd. Popliteal and shank arterial injury. Surg Clin North Am 1988; 68(4):787–807
  • 121. Acute Leg Ischemia 10CONTENTS 10.7.2 Acute Ischemia After Previous Vascular Reconstruction . . . . . . . . . . . . 13110.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . 119 10.7.3 Blue Toe Syndrome . . . . . . . . . . . . . . . . . 13110.2 Background . . . . . . . . . . . . . . . . . . . . . . . . 119 10.7.4 Popliteal Aneurysms . . . . . . . . . . . . . . . 13210.2.1 Background . . . . . . . . . . . . . . . . . . . . . . . . . 119 Further Reading . . . . . . . . . . . . . . . . . . . 13310.2.2 Magnitude of the Problem . . . . . . . . . 12010.2.3 Pathogenesis and Etiology . . . . . . . . . 12010.2.3.1 Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . 12010.2.3.2 Embolus and Thrombosis . . . . . . . . . . 120 10.1 Summary10.3 Clinical Presentation . . . . . . . . . . . . . . 12110.3.1 Medical History . . . . . . . . . . . . . . . . . . . . . 121 It is important to evaluate the severity of10.3.2 Clinical Signs and Symptoms . . . . . . . 121 ischemia.10.3.3 Evaluation of Severity If the leg is immediately threatened, opera- of Ischemia . . . . . . . . . . . . . . . . . . . . . . . . . 122 tion cannot be delayed. Classification . . . . . . . . . . . . . . . . . . . . . . . . 122 If the leg is viable, there is no benefit of an10.3.3.2 Viable Leg . . . . . . . . . . . . . . . . . . . . . . . . . . 123 emergency operation. Threatened Leg . . . . . . . . . . . . . . . . . . . . 123 Before the operation it is vital to consider10.3.3.4 Management Strategy . . . . . . . . . . . . . 123 the etiology of the occlusion, to be pre- pared to perform a distal vascular recon-10.4 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . 123 struction, and to treat heart and pulmo-10.5 Management and Treatment . . . . . 124 nary failure if present.10.5.1 Management Before Treatment . . . . 12410.5.1.1 Viable Leg . . . . . . . . . . . . . . . . . . . . . . . . . . 12410.5.1.2 Threatened Leg . . . . . . . . . . . . . . . . . . . . 12510.5.2 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . 125 10.2 Background10.5.2.1 Embolectomy . . . . . . . . . . . . . . . . . . . . . . . 12510.5.2.2 Thrombosis . . . . . . . . . . . . . . . . . . . . . . . . . 127 10.2.1 Background10.5.2.3 Intraoperative angiography . . . . . . . . 12710.5.3 Thrombolysis . . . . . . . . . . . . . . . . . . . . . . . 128 Acute leg ischemia is associated with a great risk10.5.4 Management After Treatment . . . . . 129 for amputation and death. The age of the patients10.5.4.1 Anticoagulation . . . . . . . . . . . . . . . . . . . . 129 is high, and to some extent acute leg ischemia10.5.4.2 Reperfusion Syndrome . . . . . . . . . . . . . 129 can be considered an end-of-life disease. Patients’ Compartment Syndrome . . . . . . . . . . . 130 symptoms and the clinical signs of the afflicted leg10.6 Results and Outcome . . . . . . . . . . . . . . 130 vary. Sometimes grave ischemia immediately threatens limb viability, such as after a large em-10.7 Conditions Associated bolization to a healthy vascular bed. Other times with Acute Leg Ischemia . . . . . . . . . . 131 the symptoms are less dramatic, appearing as on-10.7.1 Chronic Ischemia set of rest pain in a patient with claudication. This of the Lower Extremity . . . . . . . . . . . . . 131 is usually due to thrombosis of a previously ste- nosed artery.
  • 122. 120 Chapter 10 Acute Leg Ischemia Table 10.1. Incidence of acute leg ischemia Country Year Surveyed popu- Population Yearly incidence lation size per 100,000 inhabitants Sweden 1965–1983 1.5 million All treated or amputated, 125 (men) >70 years old 150 (women) USA 2000 All hospitalized 95 Sweden 1990–1994 2.0 million All treated 60 (men) 77 (Women) United Kingdom 1995 0.5 million All diagnosed 14–16 It is the severity of ischemia that determines dration predispose the blood for thrombosis and management and treatment. To minimize the risk make the tissue more vulnerable to decreased per- for amputation or persistent dysfunction it is im- fusion. Besides the fact that a healthy leg is more portant to rapidly restore perfusion if an extremity vulnerable than one accustomed to low perfusion, is immediately threatened. When the leg shows it is unknown what determines the viability of the signs of severe ischemia but is clearly viable, it is tissue. The most important factor is probably the equally important to thoroughly evaluate and op- duration of ischemia. The type of tissue affected timize the patient before any intervention is initi- also influences viability. In the leg, the skin is ated. These basic management principles are gen- more ischemia-tolerant than skeletal muscle. erally applicable. Accordingly, we recommend “management by severity” rather than “manage- Embolus and Thrombosis ment by etiology” (thrombosis versus embolus) The etiology of the occlusion is not what deter- but recognize that the latter can also be an effec- mines the management process. It is, however, of tive strategy. importance when choosing therapy. Embolus is usually best treated by embolectomy, whereas ar- terial thrombosis is preferably resolved by throm- 10.2.2 Magnitude of the Problem bolysis, percutaneous transluminal angioplasty (PTA), or a vascular reconstruction. The reason It is difficult to find accurate incidence figures on for this difference is that emboli often obstruct a acute leg ischemia. Data from some reports are relatively healthy vascular bed, whereas thrombo- given in Table 10.1. The numbers listed do not in- sis occurs in an already diseased atherosclerotic clude conservatively treated patients or those artery. Consequently, emboli more often cause whose legs were amputated as a primary proce- immediate threatening ischemia and require ur- dure. The incidence increases with age and is gent restoration of blood flow. Thrombosis, on the seen with equal frequency in men and women. other hand, occurs in a leg with previous arterial Regardless, the frequency indicates that it is a very insufficiency with well-developed collaterals. In common problem. the latter case it is important not only to solve the acute thrombosis but also to get rid of the cause. It must be kept in mind that emboli can be lodged in 10.2.3 Pathogenesis and Etiology atherosclerotic arteries as well, which then makes embolectomy more difficult. Pathogenesis Table 10.2 summarizes typical findings in the Acute leg ischemia is caused by a sudden deterio- medical history and physical examination that ration of perfusion to the distal parts of the leg. suggest thrombosis or embolism. Many risk fac- While the abrupt inhibition of blood flow causes tors, such as cardiac disease, are common for both the ischemia, its consequences are variable be- embolization and thrombosis. Atrial fibrillation cause acute leg ischemia is multifactorial in origin. and a recent (less than 4 weeks) myocardial infarc- Hypercoagulable states, cardiac failure, and dehy- tion with intramural thrombus are the two domi-
  • 123. 10.3 Clinical Presentation 121Table 10.2. History and clinical findings differentiat- It is important to obtain a detailed medicaling the etiology of acute ischemia history to reveal any underlying conditions or Thrombosis Embolism lesions that may have caused the ischemia. More- over, identifying and treating comorbidities may Previous claudication No previous symptoms improve the outcome after surgery or thrombo- of arterial insufficiency lysis. No source of emboli Obvious source of emboli (arterial fibrillation, myocardial infarction) 10.3.2 Clinical Signs and Symptoms Long history Sudden onset (days to weeks) (hours to days) The symptoms and signs of acute ischemia are Less severe ischemia Severe ischemia often summarized as the “five Ps”: pain, pallor, Lack of pulses in the Normal pulses pulselessness, paresthesia, and paralysis. Besides contralateral leg in the contralateral leg being helpful for establishing diagnosis, careful Positive signs No signs of chronic evaluation of the five Ps is useful for assessing the of chronic ischemia ischemia severity of ischemia. Sometimes a sixth P’s is used – poikolothermia, meaning a low skin tempera- ture that does not vary with the environment. Pain: For the typical patient, as the one de-nating sources for emboli (80–90%). Other possi- scribed above, the pain is severe, continuous, andble origins are aneurysms and atherosclerotic localized in the foot and toes. Its intensity is unre-plaques located proximal to the occluded vessel. lated to the severity of ischemia. For instance, it isThe latter are often associated with microemboli- less pronounced when the ischemia is so severezation (discussed later) but may also cause larger that the nerve fibers transmitting the sensation ofemboli. pain are damaged. Patients with diabetes often Plaque rupture, immobilization, and hyperco- have neuropathy and a decreased sensation ofagulability are the main causes of acute thrombo- pain.sis. Severe cardiac failure, dehydration, and bleed- Pallor: The ischemic leg is pale or white initially,ing are less common causes. Hypoperfusion due to but when ischemia aggravates the color turns tosuch conditions can easily turn an extremity with cyanotic blue. This cyanosis is caused by vessellongstanding slightly compromised perfusion into dilatation and desaturation of hemoglobin in theacute ischemia. skin and is induced by acidic metabolites in combi- nation with stagnant blood flow. Consequently, cyanosis is a graver sign of ischemia than pallor. 10.3 Clinical Presentation Pulselessness: A palpable pulse in a peripheral artery means that the flow in the vessel is suffi- 10.3.1 Medical History cient to give a pulse that is synchronous with ves- sel dilatation, which can be palpated with the fin-The typical patient with acute leg ischemia is old gers. In general, palpable pulses in the foot there-and has had a recent myocardial infarction. He or fore exclude severe leg ischemia. When there is ashe describes a sudden onset of symptoms – a few fresh thrombus, pulses can be felt in spite of anhours of pain, coldness, loss of sensation, and poor occlusion, so this general principle must be ap-mobility in the foot and calf. Accordingly, all signs plied with caution. Palpation of pulses can be usedof threatened leg viability are displayed. The event to identify the level of obstruction and is facilitat-is most likely an embolization, and the patient ed by comparing the presence of pulses at the sameneeds urgent surgery. Unfortunately, such patients level in the contralateral leg.are unusual among those who are admitted for When the examiner is not convinced that pal-acute leg ischemia. The history is often variable, pable pulses are present, distal blood pressuresand sometimes it is difficult to decide even the must be measured. It is prudent to always measuretime of onset of symptoms. the ankle blood pressure. This is a simple way to
  • 124. 122 Chapter 10 Acute Leg Ischemia verify ischemia and the measurement can be used Paralysis: Loss of motor function in the leg is to grade the severity and serve as a baseline for initially caused by ischemic destruction of motor comparison with repeated examinations during nerve fibers and at later stages the ischemia direct- the course of treatment. (This will be discussed ly affects muscle tissue. When palpated, ischemic further later.) The continuous-wave (CW) Dop- muscles are tender and have a spongy feeling. Ac- pler instrument does not give information about cordingly, the entire leg can become paretic after the magnitude of flow because it registers only proximal severe ischemia and misinterpreted as a flow velocities in the vessel. Therefore, an audible consequence of stroke. Usually paralysis is more signal with a CW Doppler is not equivalent to a obscure, however, presenting as a decreased palpable pulse, and a severely ischemic leg can strength and mobility in the most distal parts of have audible Doppler signals. the leg where the ischemia is most severe. The most sensitive test of motor function is to ask the NOTE patient to try to move and spread the toes. This In acute leg ischemia, the principle use gives information about muscular function in the of CW Doppler is to measure ankle blood foot and calf. Bending the knee joint or lifting the pressure. whole leg is accomplished by large muscle groups in the thigh that remain intact for a long time after Paresthesia: The thin nerve fibers conducting ischemic damage in the calf muscle and foot has impulses from light touch are very sensitive to become irreversible. ischemia and are damaged soon after perfusion is interrupted. Pain fibers are less ischemia-sensi- tive. Accordingly, the most precise test of sensibil- 10.3.3 Evaluation of Severity ity is to lightly touch the skin with the fingertips, of Ischemia alternating between the affected and the healthy leg. It is a common mistake to believe that the skin Classification has been touched too gently when the patient actu- When a patient has been diagnosed to have acute ally has impaired sensitivity. The examiner then leg ischemia, it is extremely important to evaluate may proceed to pinching and poking the skin its grade. Ischemic severity is the most important with a needle. Such tests of pain fibers evaluate a factor for selecting a management strategy, and it much later stage of ischemic damage. The anatom- also affects treatment outcome. Classification ac- ic localization of impaired sensation is sometimes cording to severity must be done before the patient related to which nerves are involved. Frequently, is moved to the floor or sent to the radiology de- however, it does not follow nerve distribution areas partment. We have found that the simple classifi- and is circumferential and most severe distally. cation suggested by the Society for Vascular Sur- Numbness and tingling are other symptoms of gery ad hoc committee (1997) is helpful for grad- ischemic disturbance of nerve function. ing. It is displayed in Table 10.3. Table 10.3. Categories of acute ischemia Sensibility Motor function Arterial Venous Doppler signal Doppler signal I Viable Normal Normal Audible Audible (>30 mmHg) IIa Marginally Decreased or Normal Not audible Audible threatened normal in the toes IIb Immediately Decreased, Mildly to Not audible Audible threatened not only in the toes moderately affected IV Irreversibly Extensive Paralysis and rigor Not audible Not audible damaged anesthesia
  • 125. 10.3 Clinical Presentation 123 Fig. 10.1. Simplified algorithm to support the management of acute leg ischemia Viable Leg is more time-consuming and recommended forAs indicated in Figure 10.1, a viable ischemic leg is the marginally threatened leg. The immediatelynot cyanotic, the toes can be moved voluntarily, threatened leg must be treated as soon as possible,and the ankle pressure is measurable. The ratio- usually with embolectomy or a vascular recon-nale for choosing these parameters is that cyanosis struction. Irreversible ischemia is quite unusualand impaired motor function are of high prognos- but implies that the patient’s leg cannot be saved.tic value for outcome. Figure 10.1 is intended to show a simplified algo- The limit of 30 mmHg for the ankle pressure rithm to further support the management of acute(Table 10.3, Fig. 10.1) is not important per se but is leg ischemia.a practical limit useful to make sure that it is thearterial, and not a venous, pressure that has been NOTEmeasured. The dorsalis pedis, posterior tibial ar- Loss of motor function in the calfteries, or branches from the peroneal artery can be and foot muscles warrants emergencyinsonated. The latter can be found just ventral to surgical treatment.the lateral malleolus. If no audible signal is identi-fied in any of these arteries or if there only is aweak signal that disappears immediately when the 10.4 Diagnosticstourniquet is inflated, the ankle blood pressureshould be recorded as zero. It is important to rely A well-conducted physical examination is enoughon the obtained results and not assume that there to confirm the diagnosis of acute leg ischemia,is a signal somewhere that is missed due to inexpe- determine the level of obstruction, and evaluaterience. Qualitative analysis of the Doppler signal is the severity of ischemia. When the leg is immedi-seldom useful when evaluating acute leg ischemia. ately threatened, further radiologic examinations or vascular laboratory tests should not under any Threatened Leg circumstances delay surgical treatment. When theAs shown in Table 10.3, the threatened leg differs extremity is viable or marginally threatened, angi-from the viable one in that the sensibility is im- ography should be performed. Duplex ultrasoundpaired and there is no measurable ankle blood is of limited value for evaluating acute leg ischemiapressure. The threatened limb is further separated and angiography is recommended for almost allinto marginally threatened and immediately patients in these two groups. If angiography is notthreatened by the presence or absence of normal available or if examination of the patient has veri-motor function. The threatened leg differs from fied that emboli is the cause and probably is bestthe irreversibly damaged leg by the quality of the treated by embolectomy, angiography can be omit-venous Doppler signal. In the irreversibly dam- ted. This situation is rare, however.aged leg, venous blood flow is stagnant and inau- The arteriogram provides an anatomical mapdible. of the vascular bed and is very helpful in discrimi- nating embolus and thrombosis. The former is Management Strategy essential for planning the surgical procedure, andA viable leg does not require immediate action the latter may be of importance for selecting theand can be observed in the ward. A threatened leg treatment strategy.needs urgent operation or thrombolysis. The latter
  • 126. 124 Chapter 10 Acute Leg Ischemia Fig. 10.2. Embolus lodged at the origins of the calf vessels (arrow). Angiograms display films before and after thrombolysis An arteriogram representing an embolus is The groin of the contralateral leg is the pre- shown in Fig. 10.2. ferred puncture site for diagnostic angiography. Angiographic signs of embolism are an abrupt, A second antegrade puncture can be done in convex start of the occlusion and lack of collater- the ischemic extremity if thrombolysis is feasible. als. Thrombosis is likely when the arteriogram shows well-developed collaterals and atheroscle- rotic changes in other vascular segments. 10.5 Management and Treatment For most patients with viable and margin- ally threatened legs the diagnostic angiography 10.5.1 Management Before Treatment is followed by therapeutic thrombolysis right away. Viable Leg Angiography can be performed during daytime If the leg is viable the patient is admitted for obser- when qualified radiology staff is available. The vation. A checklist of what needs to be done in the patient should be optimized according to the emergency department follows below: recommendations given in the next section. Be- 1. Place an intravenous (IV) line. fore angiography it is important to keep the 2. Start infusion of fluids. Because dehydration is patient well hydrated and to stop administration often a part of the pathogenic process, Ringer’s of metformin to reduce the risk of renal failure. acetate is usually preferred. Dextran is anoth- Disturbances in coagulation parameters may er option that also is beneficial for blood interfere with arterial puncture and must also be rheology. checked before the investigation. The information 3. Draw blood for hemoglobin and hematocrit, is also important as baseline values in case of later prothrombin time, partial thromboplastin thrombolysis. time, complete blood count, creatinine, blood
  • 127. 10.5 Management and Treatment 125 urea nitrogen, fibrinogen, and antithrombin. poxemia, anemia, arrhythmia, and hypotension Consider the need to type and cross-match worsen ischemia and should be abolished if possi- blood. ble. A cardiology consult is often needed.4. Order an electrocardiogram (ECG). The above-mentioned treatment regime of re-5. Administer analgesics according to pain inten- hydration, anticoagulation, and optimization of sity. Opiates are usually required (morphine cardiopulmonary function often improves the 2.5–10 mg IV). ischemic leg substantially. Frequently this is6. Consider heparinization, especially if only enough to sufficiently restore perfusion in the Ringer’s acetate is given. Heparin treatment viable ischemic leg, and no other treatments are should be postponed until after surgery if epi- needed. If no improvement occurs, angiography dural anesthesia is likely. can be performed during the daytime, followed by thrombolysis, PTA, or vascular reconstruction.Repeated assessments of the patient’s clinical sta-tus are mandatory in the intensive care unit and Threatened Legwhen the patient has been moved to the ward. The If the leg is immediately threatened, the patient istime interval depends on the severity of ischemia prepared for operation right away. This includesand the medical history. This examination in- the steps listed above for the viable leg, includingcludes evaluating skin color, sensibility, and motor contact with an anesthesiologist. When there isfunction as well as asking the patient about pain no cyanosis and motor function is normal – thatintensity. is, the extremity is only marginally threatened – Dextran is administered throughout the obser- there is time for immediate angiography followedvation period. The risk for deterioration of heart by thrombolysis or operation. An option is cau-failure due to dextran treatment is substantial and tious monitoring and angiography as soon as pos-for patients at risk the volume load must be related the treatment’s expected possible benefits. For Before starting the operation, the surgeonsuch patients it is wise to reduce the normal dose needs to consider the risk for having to perform aof 500 ml in 12 h to 250 ml. Another option is to complete vascular reconstruction. It is probableprolong the infusion time to 24 h. that a bypass to the popliteal artery or a calf artery Heparin only or in combination with dextran is will be needed to restore circulation. If thrombosisrecommended when patients do have an embolic is the likely cause and the obstruction is distal (asource or a coagulation disorder. There are two palpable pulse is felt in the groin but not distally),ways to administer heparin. The first is the stan- a bypass may also be required even when emboli-dard method, consisting of a bolus dose of 5,000 zation is suspected.units IV followed by infusion of heparin solution(100 units/ml) with a drop counter. The dose at thestart of infusion should be 500 units of heparin 10.5.2 Operationper kilogram of body weight per 24 h. The doseis then adjusted according to activated partial Embolectomythromboplastin time (APTT) values obtained It is beyond the scope of this book to cover theevery 4 h. The APTT value should be 2–2.5 times technique for vascular reconstructions. But be-the baseline value. cause embolectomy from the groin with balloon Low molecular weight heparin administered catheters (known as Fogarty catheters) is one ofsubcutaneously twice daily is the other option. A the most common emergency vascular operationscommon dose is 10,000 units/day but it should be in a general surgical clinic and may be perform-adjusted according to the patient’s weight. ed by surgeons not so familiar with vascular sur- It is important to optimize cardiac and pulmo- gery, this is described in the Technical Tips boxnary function while monitoring the patient. Hy- below.
  • 128. 126 Chapter 10 Acute Leg Ischemia TECHNICAL TIPS Embolectomy Use an operating table that allows x-ray penetra- gives a good idea of what is happening inside the tion. Local anesthesia is used if embolus is likely artery. Wet the connection piece for the syringe to and the obstruction seems to be in the upper get a tight connection. It is smart to get external thigh or in pelvic vessels (no pulse in the groin). markers of the relationship between the catheter Make a longitudinal incision in the skin, and iden- length and important anatomical structures; for tify and expose the common, superficial, and example, the aortic bifurcation (located at the deep femoral arteries (Chapter 9, p. 107). If the umbilicus level), the trifurcation level (located common femoral artery is soft-walled and free approximately 10 cm below the knee joint), as well from arteriosclerosis – especially if a pounding as the ankle level. The catheters have centimeter pulse is felt proximal to the origin of the deep grading, which simplifies the orientation. femoral artery – an embolus located in its bifurca- It is common for the embolus to already be tion is likely. Make a short transverse arteriotomy protruding when the arteriotomy is done and a including almost half the circumference. Place the single pull with the catheter starting with the tip arteriotomy only a few mm proximal to the origin in the iliac artery is enough to ensure adequate of the profunda artery so it can be inspected and inflow. This means that a strong pulse can be cannulated with ease. In most other cases, a longi- found above the arteriotomy, and a pulsatile tudinal arteriotomy is preferable because it allows heavy blood flow comes through the nole. For elongation and can be used as the site for the in- distal clot extraction, a #3 or #4 catheter is recom- flow anastomosis of a bypass. For proximal embo- mended. A slight bending of the catheter tip lectomy, a #5 catheter is used. between the thumb and index finger might, in Before the catheter is used the balloon should combination with rotation of the catheter, make it be checked by insufflation of a suitable volume easier to pass down the different arterial branches of saline. Check the position of the lever of the (Fig. 10.3). syringe when the balloon is starting to fill, which Fig. 10.3. Use of Fogarty catheter for embolectomy. Note that withdrawal is parallel to the artery When the catheter is inserted into the artery and be located in one of the calf arteries, most probably while the surgeon is working with it, hemostasis of the posterior tibial artery or the peroneal artery. the arteriotomy is achieved by a vessel-loop or by a The balloon is insufflated simultaneously as the thumb–index finger grip over the artery and the catheter is slowly withdrawn, which makes it easi- catheter. In a typical case, an embolus, including a er to get a feeling for the dynamics and to not possible secondary thrombus, can be passed rela- apply too much pressure against the vascular wall. tively easily or with only slight resistance. If a ma- A feeling of “touch” is preferable, but a feeling of jor part of the catheter can be inserted the tip will “pull” against the vascular wall should be avoided.
  • 129. 10.5 Management and Treatment 127To get the right feeling the same person needs to Finally, the arteriotomy is closed. If necessary ahold the catheter, pull it, and insufflate the bal- patch of vein or synthetic material is used to avoidloon at the same time. To avoid damage in the narrowing of the lumen.arteriotomy, the direction of withdrawal should As mentioned before, the embolectomy proce-be parallel with the artery (Fig. 10.3). dure includes intraoperative angiography. If this When the catheter is withdrawn it moves into examination indicates significant amounts of em-larger segments of the artery and has to be succes- boli remaining in the embolectomized arteries orsively insufflated until it reaches the arteriotomy. if the foot still appears as being inadequately per-The reverse is, of course, valid when the embolec- fused after the arteriotomy is closed, other mea-tomy is done in a proximal direction. The throm- sures need to be taken. If there are remaining em-boembolic masses can be suctioned or pulled out boli in the superficial femoral or popliteal arteries,with forceps, and the arteriotomy should be in- another embolectomy attempt from the arterioto-spected to be clean from remaining materials my in the groin can be made. Clots, if seen in allbefore the catheter is reinserted. The maneuver the calf arteries, need to be removed through ashould be repeated until the catheter has been second arteriotomy in the popliteal artery. This ispassed at least once without any exchange of done by a medial incision below the knee; notethromboembolic materials and until there is an that local anesthesia is not sufficient for this. It isacceptable backflow from the distal vascular bed. usually necessary to restore flow in two, or occa-Depending on the degree of ischemia and collater- sionally in only one, of the calf arteries.als, the backflow is, however, not always brisk. Embolectomy at the popliteal level is the first If a catheter runs into early and hard resistance, treatment step when ischemia is limited to the dis-this might be due to previously occluded segment tal calf and foot and when there is a palpable pulsethat forced the catheter into a branch. It should in the groin or in the popliteal fossa.then be withdrawn and reinserted, using greatcaution to avoid perforation. If the resistance can- NOTEnot be passed and if acute ischemia is present, an- Do not forget to consider fasciotomygiography should always be considered to examine in patients with severe ischemia.the possibility of a vascular reconstruction. Besides performing embolectomy in the super- Thrombosisficial femoral, popliteal, and calf arteries, the deep The preliminary diagnosis of embolus must be re-femoral artery must be checked for an obstructing considered if the exposed femoral artery in theembolus or clot that needs to be extracted. Sepa- groin is hard and calcified. In most situations, clotrate declamping of the superficial femoral and removal with Fogarty catheters will then fail. It isdeep femoral arteries to check the backflow is the usually difficult or even impossible to pass thebest way to do this. Remember the possibility that catheter distally, indicating the presence of steno-backflow from the distal vascular bed after embo- ses or occlusions. Even if the embolectomy appearslectomy might emanate from collaterals located successful, early reocclusion is common. Such sec-proximal to distally located clots. Back flow does ondary thrombosis is usually more extensive andnot always assure that the peripheral vascular bed will aggravate the ischemia. Accordingly, angiog-is free from further embolic masses. A basic rule is raphy should be considered as the first step if thethat every operation should be completed with in- femoral artery is grossly arteriosclerotic and if it istraoperative angiography (see the technical tips hard to pass the catheter down to the calf level. Itbox in the next page and Fig. 10.4) to ensure good will confirm the etiology and reveal whether a by-outflow and to rule out remaining emboli and sec- pass is required and feasible. Vascular reconstruc-ondary thrombus. To dissolve small amounts of tion in acute leg ischemia is often rather difficultremaining thrombus local infusion of 2–4 cc re- and experience in vascular surgery is required.combinant tissue plasminogen activator (rtPA)can be administered before the angiography cath-eter is pulled out.
  • 130. 128 Chapter 10 Acute Leg Ischemia Intraoperative angiography TECHNICAL TIPS Intraoperative angiography With the proximal clamp in position a 5 or 8 French If the patient is suspected to have renal failure, baby-feeding catheter is inserted into the arteri- the amount of contrast used is kept at a minimum. otomy. The tip of the catheter is placed 5 cm into Angled projections can be obtained without the superficial femoral artery and distal control moving the C-arm by rotating the patient’s foot. around it is achieved with a vessel-loop. Contrast The use of contrast in the Fogarty catheter bal- for intravasal use containing 140–300 mg iodine/ loon during fluoroscopy allows the calf vessel ml is infused with a 20 cc syringe connected to into which the catheter slides to be identified. a three-way valve. Heparinized Ringer’s or saline The technique for intraoperative angiography is (10 units/ml heparin) is flushed through the also a prerequisite for interoperative use of endo- catheter before and after contrast injection to vascular treatment options such as angioplasty prevent thrombosis in the occluded vascular bed. (Fig. 10.4). Fig. 10.4. Intraoperative angiography 10.5.3 Thrombolysis Table 10.4. Some contraindications to thrombolysis Absolute Relative Thrombolysis is performed in the angiosuite. A consultation with a specialist in coagulation dis- Cerebrovascular Major surgery orders or a specialist in vascular medicine is some- incident <2 months or trauma <10 days times needed to discuss possible problems related Active bleeding diathesis Uncontrolled hypertension to coagulation before the procedure. Contraindi- (>180 systolic) cations to thrombolysis are listed in Table 10.4. Gastrointestinal bleeding Hepatic failure Treatment is usually directed toward resolving <10 days a fresh, thrombotic occlusion, but emboli and Pregnancy thrombi several weeks old can also be successfully Severe renal failure lysed. The procedure starts with a diagnostic angi- Diabetic retinopathy ography via contralateral or antegrade ipsilateral arterial punctures. If thrombolytic treatment is decided the procedure continues right away, and mary choices for lytic agent are recombinant tis- the tip of a pulse-spray catheter is placed in the sue plasminogen activator (rtPA) or urokinase. thrombus. The lytic agent is then forcefully inject- Because of the risk of allergic reactions, streptoki- ed directly into it to cause fragmentation. The pri- nase should be avoided. Intermittent injections of
  • 131. 10.5 Management and Treatment 1291 ml every 5–10 min to a total dose of 10–20 ml bleeding complications have to be weighed againstrtPA over 1–3 h is followed by angiographic con- the benefits. If the source of the emboli is not clear,trol of the result. If the thrombus is completely it should be investigated. Findings of atrial fibril-lysed any underlying lesion is treated. If thrombus lation and heart thrombus can then be treated. Ifstill remains, the rtPA infusion is continued slowly the ECG is normal, echocardiography is orderedover 6–12 h with 1 mg/h. If the initial thromboly- to search for thrombus and valve deficiencies. Ifsis fails, a variety of mechanical catheters can be the left atrium is a likely embolic source, trans-used to try to further dissolve and aspirate the esophageal echocardiography may be indicated.thrombus. Examples include the AngioJet and the When the etiology of leg ischemia is uncertainAmplatz. it is difficult to give general advice. There is no Because of the risk of bleeding and systemic scientific evidence that long-term postoperativecomplications, and also because the ischemic leg anticoagulation reduces the risk of reocclusion ormay deteriorate, careful monitoring during con- influences patient survival. Continued treatmenttinued thrombolysis is necessary. This is best done with dextran or low molecular weight heparin isin an intensive care or step-down unit. The patient recommended at least during hospitalization.should be kept supine in bed throughout the pro- If hypercoagulable states are suspected the pa-cedure. During this time the other measures sug- tient needs to be worked up during the postopera-gested for optimizing coagulation and central cir- tive period to reduce the risk of reocclusion. Ex-culation are continued. It is also necessary to check amples are patients with hyperhomocysteinemia,fibrinogen concentration to make sure the value who may be treated with folates, and patients withdoes not decline to <1.0 mg/ml. Below this level antiphospholipid antibodies, who need coumadinsurgical hemostasis is insufficient and the infu- and salicylic acid.sion should be stopped. Angiographic control ofthe result is performed afterwards, usually the fol- Reperfusion Syndromelowing morning, and occasionally during the slow Patients treated for severe acute leg ischemia areinfusion to check the effect and allow reposition- at risk of developing reperfusion syndrome. Thising of the catheter. The part of the thrombus sur- occurs when ischemic muscles are reperfusedrounding the catheter is lysed first, which is why it and metabolites from damaged and disintegratedoften is beneficial to advance the catheter further muscle cells are spread systemically. A part of thisinto the thrombus after a few hours. process consists of leakage of myoglobin; it may be Finally, the lesion that caused the thrombosis is nephrotoxic and colors the urine red. The metabo-treated with angioplasty. To avoid unnecessary lites also affect central circulation and may causebleeding from the puncture site, the fibrinogen con- arrhythmia and heart failure. The risk for reperfu-centration is checked again before the sheath is with- sion syndrome is higher when occlusions are prox-drawn to ensure that the level exceeds 1.0 mg/ml. imal and the affected muscle mass is large. One example is saddle emboli located in the iliac bifur- cation. The risk is also higher when the ischemia 10.5.4 Management After Treatment time is longer than 4–6 h. The elevated mortality associated with severe Anticoagulation acute leg ischemia may be due to reperfusion syn-Patients with embolic disease caused by cardiac drome. Survival may therefore be improved byarrhythmia or from other cardiac sources proven avoiding reperfusion and a lower mortality hasby ECG, medical history, or clinical signs should been reported from hospitals where primary am-be anticoagulated postoperatively. Treatment regi- putation is favored. It has also been suggested thatmens described previously (page 125) are em- thrombolysis saves lives by restoring perfusionployed, followed by treatment with coumadin. An- gradually. For a threatened leg this is seldom anticoagulation has no proven positive effect for the option because rapid restoration of perfusion isprognosis of the ischemic leg but is administered necessary to save reduce the risk of new emboli. The patient’s The best treatment for reperfusion syndromeabilities to comply with treatment and the risk for is prevention by expeditious restoration of flow.
  • 132. 130 Chapter 10 Acute Leg Ischemia There are no clinically proven effective drugs but perform fasciotomy right after the vascular proce- many have been successful in animal models, dure when the ischemia is severe and has lasted including heparin, mannitol, and prostaglandins. over 4–6 h. To open all four compartments, we Because heparin and mannitol also have other recommend using two long incisions, one placed potential benefits and few side effects they are laterally and one medially in the calf. The tech- recommended during the postoperative period. nique is described and illustrated in Chapter 9 Obviously, acidosis and hyperkalemia must be (p. 115–116). corrected, and the patient needs to be well hydrat- ed and have good urine output. For patients with suspected reperfusion syn- 10.6 Results and Outcome drome – urine acidosis and high serum myo- globin levels – alkalinization of the urine is often The outlook for patients with acute leg ischemia recommended in order to avoid renal failure has generally been poor. The 30-day mortality despite weak support in the literature. If the urine when an embolus is the etiology varies between is red, the urine pH <7.0, and serum myoglobin 10% and 40%. Survival is better when arterial >10,000 mg/ml, 100 ml sodium bicarbonate is thrombosis is the cause, around 90%. When con- given IV. The dose is repeated until the pH is sidering the amputation rate after surgical treat- normalized. ment the figures are reversed – lower for embolic disease, at 10–30%, than for thrombosis, which of- Compartment Syndrome ten has an early amputation rate of around 40%. The acute inflammation in the muscle after rees- A substantial number of the patients die or tablishing perfusion leads to swelling and a risk require amputation after 30 days. This is due to a for compartment syndrome. The available space combined effect of the patients’ advanced age and for the muscles is limited in the leg and when the comorbidities. In studies not differentiating be- increased pressure in the compartments reduces tween etiologies, only 30–40% of the patients were capillary perfusion below the level necessary for alive 5 years after surgery, and among those, 40– tissue viability, nerve injury and muscle necrosis 50% had had amputations. occur. Because the gradual release of ischemia is The essential clinical feature of compartment thought to reduce the risk for reperfusion syn- syndrome is pain – often very strong and “out of drome and thereby the negative effects on the proportion,” which is accentuated by passive ex- heart and kidneys mortality after thrombolysis is tension. The muscle is hard and tender when pal- thought to be lower. It is difficult, however, to find pated. Unfortunately, nerves within the compart- data on thrombolytic therapy comparable to sur- ments are also affected, causing disturbance of gical results. A majority of patients will undergo sensibility and motor function. This makes diag- surgery when thrombolysis is not technically pos- nosis more difficult. Moreover, the patient is often sible, leaving a selected group to follow up. In the not fully awake or disoriented, but early diagnosis few randomized controlled trials that compare is still important to save the muscle tissue. For that surgery and thrombolysis the short-term and long- reason measurement of intracompartmental pres- term amputation rates are alike. Survival is also sure is performed for diagnosis in some hospitals. similar, but in one study it was lower after throm- There are no precise limits that advocate fascioto- bolytic therapy at 1 year, 80%, compared with sur- my, but 30 mmHg has been proposed. The speci- gically treated patients, of whom only 60% were ficity for a correct diagnosis using this limit is alive at that time. high, but the sensitivity is much lower. To notice signs of compartment syndrome after operation or thrombolysis for acute ischemia, frequent physical examinations are vital. Fascioto- my should be performed immediately following the procedure if any suspicion of compartment syndrome exists. Common advice is to always
  • 133. 10.7 Conditions Associated with Acute Leg Ischemia 131 10.7 Conditions Associated 10.7.2 Acute Ischemia After Previous with Acute Leg Ischemia Vascular Reconstruction 10.7.1 Chronic Ischemia A substantial number of patients have chronic leg of the Lower Extremity ischemia and have undergone vascular recon- structions, so there is a high likelihood that emer-It is sometimes difficult to differentiate between gency department physicians will have to take careacute leg ischemia, deterioration of chronic leg of problems with postoperative acute leg ischemiaischemia, and just severe end-stage chronic disease in the operated leg. The clinical presentation ofin general. Periods of pain escalation bring pa- graft failure or occlusion is variable. An abrupttients with chronic ischemia to the emergency de- change in leg function and skin temperature ac-partment. Accentuated pain in these patients has a companied by the onset of pain can occur anywide range of origins. Decreased foot perfusion time after surgery, but especially within the first 6can be due to dehydration or lowered systemic months. Several years after the reconstruction it ispressure as a consequence of heart failure or a slightly more common for progressive deteriora-change in medication. Ulcers are frequently pain- tion to occur and an eventual graft occlusion toful, especially when complicated by infection or pass unnoticed.when dressings are changed. History and examina- As discussed previously in this chapter thetion of vital functions and the leg usually disclose management principles are roughly the same assuch conditions and can also sufficiently rule out for primary acute leg ischemia. It is the status ofacute leg ischemia that needs urgent treatment. the leg and the severity of ischemia that lead work- Patients with chronic ischemia benefit from up and management. Most patients will undergocareful planning of their treatment and should not angiography to establish diagnosis and to provide– with few exceptions – be expeditiously treated. information about possibilities to restore bloodElective therapy includes weighing risk factors flow. Thrombolysis is often the best treatment op-against the outcome of the proposed treatment tion because it exposes the underlying lesions thatand all the work-up that is needed to get this infor- may have caused the occlusion. As for patientsmation. (It is beyond this book’s purpose to de- with acute ischemia, those with an immediatelyscribe the management of chronic ischemia.) In threatened leg after a reconstruction should bethe emergency department it is sensible to identify taken to the operating room and treated as fast asand directly treat the patients with true acute leg possible. Management of acute ischemia after aischemia and schedule treatment of patients with previous vascular reconstruction is further dis-chronic disease for later. Examples of findings cussed in Chapter 12 on complications in vascularin medical history and physical examination are surgery.listed in Table 10.5 10.7.3 Blue Toe SyndromeTable 10.5. Medical history and physical examinationfindings suggesting chronic leg ischemia A toe that suddenly becomes cool, painful, and History Examination cyanotic, while pulses can be palpated in the foot, characterizes the classic presentation of blue toe Coronary artery disease Lack of palpable pulses and stroke in both legs syndrome. This has occasionally led to the as- sumption that the discoloration of the toe is not of Smoking Ankle pressure 15–50 mmHg vascular origin, and patients have been sent home without proper vascular assessment. Although co- Claudication, rest pain, Ulcers agulation disorders or vasculitis may contribute, and ischemic ulcers such an assumption is dangerous. Atheroembo- Previous vascular Hyperemic foot skin lism is the main cause for blue toe syndrome and surgery or amputation while dependent atheromatous plaques in the iliac or femoral arter- Lack of sudden onset ies or thrombi in abdominal or popliteal aneu- of pain rysms are the main sources. Blue toe syndrome
  • 134. 132 Chapter 10 Acute Leg Ischemia can also present without palpable foot pulses. The popliteal aneurysm is the reason for the obstruc- presentation may then be less dramatic. tion. It is common that the patient does not notice Popliteal aneurysms are frequent in men but the initial insult and wait to seek medical care un- rare in women. They are often bilateral – more til after several weeks. Ischemic ulceration at the than 50% – and associated with the presence of tip of the toe may then be found in the examina- other aneurysms. For instance, 40% of patients tion. During the foot examination more signs of with popliteal aneurysms also have an aneurysm microembolization are usually found, including in the abdominal aorta. blue spots or patchy discoloration of the sole and Most popliteal aneurysms are identified during heel. When both feet are affected it suggests an angiography performed as part of the manage- embolic source above the aortic bifurcation. The ment process for acute leg ischemia. When an clinical examination should include assessing the aneurysm is suspected during angiography or aorta and all peripheral arteries, including pulses examination, duplex ultrasound is performed to and auscultation for bruits. When pulses in the verify the finding and estimate the aneurysm’s foot are not palpable, ankle blood pressure needs diameter. to be measured. In the search for aneurysms If the severity of ischemia corresponds to the and stenoses patients need to be investigated with “immediately threatened” stage described earlier, duplex ultrasound to verify examination findings. the patient needs urgent surgery. The revascular- To prevent future embolization episodes lesions ization procedure is then often quite difficult. Ex- or aneurysms found should be treated as soon as posure of the popliteal artery below the knee, in- possible. cluding the origins of the calf arteries, should be Occasionally the pain is transient and the blue followed by intraoperative angiography and an color will disappear within a few weeks. More attempt to remove the thrombus. It is hoped that common, however, is an extremely intense pain in angiography can identify a spared calf artery dis- the toe that is continuous and difficult to treat. tally. The calf arteries are sometimes slightly Unfortunately, the pain often lasts several months dilated in this patient group and can serve as a until the toe is either amputated or healed. good distal landing site for a bypass excluding the The pain is best treated with oral opiates, and aneurysm. Often, however, it is impossible to open quite high doses are often required to ease the up the distal vascular bed due to old embolic oc- pain. A tricyclic antidepressant drug may be add- clusions and the prognosis for the leg is poor. In ed to the regimen if analgesics are not enough. such situations every possible alternative solution While waiting for diagnostic studies and final should be considered, including local thromboly- treatment of the lesions, the patient is put on aspi- sis, systemic prostaglandin infusion, and pro- rin therapy. There is no scientific evidence for us- fundaplasty. ing other medications such as coumadin, steroids, If the ischemia is less severe, thrombolysis or dipyramidole. Still, if suspicion for a popliteal may be considered following the angiography aneurysm is high we recommend anticoagulation before surgical exclusion of the aneurysm. While with low molecular weight heparin until the aneu- thrombolysis previously has been considered rysm is corrected. questionable because of the risk for further frag- mentation of thrombus within the popliteal aneu- rysm, this strategy may prove very favorable. Over 10.7.4 Popliteal Aneurysms the last few years several studies reporting restored calf vessels by thrombolysis have been published. A common reason for acute leg ischemia is throm- This may lead to more successful bypasses and bosis of a popliteal aneurysm. Such aneurysms are improved limb salvage. Once the bypass is ac- also one of the main sources for embolization to complished good long-term results are probable. the digits in the foot and blue toe syndrome. Be- Interestingly, vein grafts used for bypasses in sides the clinical signs of acute ischemia discussed patients with popliteal aneurysms appear to be previously, a prominent wide popliteal pulse or a wider and stay patent longer than for other patient mass in the popliteal fossa is often palpated when groups.
  • 135. Further Reading 133 Further Reading Galland RB. Popliteal aneurysms: controversies in their management. Am J Surg 2005; 190(2):314–318Berridge DC, Kessel D, Robertson I. Surgery versus O’Donnell TF Jr. Arterial diagnosis and management of thrombolysis for acute limb ischaemia: initial man- acute thrombosis of the lower extremity. Can J Surg agement. Cochrane Database Syst Rev 2002; (3): 1993; 36(4):349–353 CD002784 Ouriel K. Endovascular techniques in the treatment ofDormandy J, Heeck L, Vig S. Acute limb ischemia. acute limb ischemia: thrombolytic agents, trials, Semin Vasc Surg 1999; 12(2):148153 and percutaneous mechanical thrombectomy tech-Henke PK, Stanley JC. The treatment of acute embolic niques. Semin Vasc Surg 2003; 16(4):270–279 lower limb ischemia. Adv Surg 2004; 38:281–291
  • 136. General Concepts PART B
  • 137. Vascular Access in Trauma 11CONTENTS eral (sometimes central) IV lines are needed. In bleeding shock with collapsed and empty veins,11.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . 137 inserting peripheral IV lines are difficult. For11.2 Background . . . . . . . . . . . . . . . . . . . . . . . . 137 these reasons some techniques for alternative ac-11.3 Management . . . . . . . . . . . . . . . . . . . . . . 137 cess should be included in the armamentarium of11.3.1 In the Emergency Department . . . . . 137 all physicians who take part in the management of11.3.1.1 Management Guidelines trauma cases. In many hospitals the general sur- in Acute Vascular Access . . . . . . . . . . . 138 geon on call is in charge of the trauma care and is11.3.1.2 Which Route is Recommended thus responsible for providing adequate vascular for Acute Vascular Access? . . . . . . . . . . 138 access. Technique in Acute Vascular Access . . . . . . . . . . . . . . . . . . . . . 139 11.3 Management Further Reading . . . . . . . . . . . . . . . . . . . 140 11.3.1 In the Emergency Department 11.1 Summary Today most trauma patients admitted to emergen- cy departments already have one or two peripheral Make sure you are familiar with the tech- IV cannulas that were inserted by the paramed- niques for vascular access before the trau- ics. ma case arrives. After securing airways and respiration, the sur- Use the technique for vascular access in geon on call checks the patient for possible ongo- which you are most experienced. ing and previous bleeding and estimates the blood Do not hesitate to start simultaneous expo- losses. Besides being part of trauma management, sure of several different veins. this information is also necessary for planning the Do not forget the cubital fossa as a possible need for vascular access. According to our rou- site for vein exposure. tines all trauma cases are subjected to immediate infusion of 2 l of Ringer’s acetate. If this volume has a positive effect on tachycardia and the pa- tient’s general condition, and the patient is not ob- 11.2 Background viously bleeding externally, the total possible blood loss will usually not exceed 15–20% of theOptimal management of a trauma case includes total blood volume. For these patients two large-fast resuscitation, diagnosis, and immediate start bore IV cannulas (2 mm in diameter) are almostof treatment. In most injured patients, two large always enough for the initial volume replacement.peripheral intravenous (IV) lines are sufficient to The order in which the volume replacement shouldprovide adequate initial treatment and volume be done and in what proportion the Ringer’s,replacement. In rare cases of greater trauma and blood, plasma, packed cells, or dextran should bein unclear cases this might be insufficient and sev- given varies between hospitals and should, of
  • 138. 138 Chapter 11 Vascular Access in Trauma course, be in accordance with local prescriptions below the diaphragm to ensure that adminis- and routines. tered fluid reaches the central circulation and is not lost on the way because of vascular inju- Management Guidelines ries. in Acute Vascular Access Always start by checking that the patient has two Another possibility for acute access is an interos- functioning IV cannulas. If they are functioning seous cannula. This, however, is not described in but are too small in caliber – <1 mm in diameter this chapter. – a guide wire can be used to replace them with larger ones. Insert the guide wire in the thin can- Which Route is Recommended nula, pull it out over the guide wire, leave the guide for Acute Vascular Access? wire in the vein, and insert a new wider IV can- Some 20 years ago surgical cutdown was the meth- nula over the guide wire. Occasionally the skin od of choice in trauma because most surgeons perforation is too small and needs to be dilated. used this method electively. At that time it was The cannula replacement should be performed routine and surgeons could generally insert and simultaneously with another person’s attempt to fixate a large-bore IV line within just a couple of place IV cannulas in other sites. Patients with minutes. Today this experience is generally lack- greater ongoing bleeding, such as a patient who is ing and trauma care according to Advanced Trau- bleeding through a fresh wound dressing within a ma Life Support, for example, recommends the minute, as well as those with a history that indi- second alternative listed above, catheterization of cates larger blood losses, almost uniformly require the femoral vein. The reason is probably that cath- several IV cannulas. Short and large-bore cannu- eterization of the femoral vein is technically easier las permit the highest possible volume flow and if to perform for someone surgically inexperienced there is space available on the arms and neck more than surgical cutdown or central catheterization. peripheral cannulas are warranted. Make simulta- In many countries, including the United States, neous attempts at several different sites – for ex- catheterization of the jugular and subclavian veins ample, in the external jugular vein and in the veins is more widespread, in particular among anesthe- on the hands. If this is not successful there are siologists. three alternatives: If cutdown is chosen, most textbooks recom- 1. Surgical exposure of veins in the cubital fossa mend the greater saphenous vein at the level of or on the leg the median malleolus as the best, most easily ac- 2. Percutaneous catheterization of the femoral cessible, vein. This technique is identical with the vein one used in stripping a varicosed greater saphe- 3. Central venous catheterization in the subclavi- nous vein. The disadvantage is that it is rarely an vein or external and internal jugular vein possible to draw blood from the greater saphenous vein at the level of the ankle joint even if the The best choice of these three alternatives is not catheter has an intravasal position. This is due always obvious and should be based on factors to the vein valves and also to the fact that periph- such as the part of the patient’s body that is in- eral veins are often collapsed. The patients are jured, the responsible trauma surgeon’s experi- frequently in shock as a consequence of severe ence, the urgency and the type of fluid that needs bleeding. With longer catheters placed in the to be infused. The following general advice might greater saphenous vein drawing of blood samples be helpful irrespective of the technique chosen: is sometimes possible thanks to confluent vein Never place an IV cannula in extremities in- branches. The function is tested by rapid injection jured by crush or burn. of 10–20 cc of saline. Avoid extremities with fractures. If the patient has pelvic injuries or the best If larger vascular injuries are suspected, includ- veins have been consumed in previous varicose ing pelvic fractures, which are frequently asso- vein surgery or bypass operations, the cubital fossa ciated with extensive venous damage in the pel- is a very good alternative. These veins are also lo- vis, IV lines should be placed above as well as cated closer to the heart. In some cases, branches
  • 139. 11.3 Management 139to the greater saphenous in the groin can also be TECHNICAL TIPSused, especially if the surgeon is experienced in Vascular Access in Traumasurgical exposures in this area. Technique for exposing Technique in Acute the greater saphenous veina) Vascular Access 1. Scrub and drape a 10 10 cm large area ante-The cutdown technique is described in the Tech- rior to the medial malleolus.nical Tips box and displayed in Fig. 11.1. Note that 2. If the patient is awake, infiltrate a local anes-the technique is identical to that used for implant- permanent venous infusion ports and other 3. Make a 3 cm-long transverse incision anteri-central venous catheters. A surgeon experienced or to the medial such procedure can perform a cutdown and 4. Expose the greater saphenous vein by bluntcatheterization rapidly and effectively. For the dissection on a length of 2 cm, and protectsame reason, cutdown is probably an underesti- the saphenous nerve.mated and underused alternative. 5. Pull two absorbable 2-0 sutures under theCentral catheterization is performed in Scandina- exposed vein with a clamp.via mostly by anesthesiologists and with great 6. Ligate the vein as far distally as possible withskill. This alternative for access in trauma has the a distal suture. Do not cut the ends of thedisadvantage of long catheters with a relatively suture.small caliber, making rapid infusion of large vol- 7. Place a knot in the proximal suture but doumes difficult. Direct puncture in the neck region not tie it.can be difficult and even dangerous in an anxious 8. Make a transverse cut in the vein with an eyeand hypoxic patient. In a patient wearing a stiff scissor. Do not make it too small. Dilate theneck collar it is almost impossible. A central ve- venotomy with the tip of a small clamp (mos-nous catheter allows objective measurement of quito).central venous pressure (CVP), but its value in 9. Insert a catheter a few centimeters whilemanaging acute trauma is hard to appreciate, and applying slight traction on the distal su-CVP rarely needs to be measured in the emergen- ture. Tie the proximal suture around thecy situation. The recommendation is therefore to catheter for fixation. If tunnelation is consid-save central catheterization until the most impor- ered, make a second separate incision a fewtant emergency care is over. centimeters distally and pull the catheter For catheterizing the femoral vein, a Seldinger under the skin before inserting it into thetechnique is used. Make sure that suitable sets for vein (Fig. 11.1).catheterization and different catheters are at hand. 10. Connect the infusion system and close thePreviously described problems during cannula- wound with a nonresorbable single suture.tion in the lower extremities are, of course, also Do not forget to fix the catheter with a suturevalid for this technique. to the skin. In summary, surgeons managing trauma casesought to be familiar with one or several different a) An identical technique can be used to expose andtechniques for acute vascular access. This should cannulate the cubital practiced beforehand, prior to the arrival of thetrauma case in the emergency department.
  • 140. 140 Chapter 11 Vascular Access in Trauma Further Reading Klofas E. A quicker saphenous vein cutdown and a bet- ter way to teach it. J Trauma 1997; 43:985–987 Waisman M, Waisman D. Bone marrow infusion in adults. J Trauma 1997; 42:288–293 Fig. 11.1. Cutdown and exposure of a vein in the cubi- tal fossa for acute venous access
  • 141. Complications in Vascular Surgery 12CONTENTS 12.5 Infections . . . . . . . . . . . . . . . . . . . . . . . . . . 151 12.5.1 Pathophysiology . . . . . . . . . . . . . . . . . . . . 15112.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . 142 Types of Infection . . . . . . . . . . . . . . . . . . 15112.2 Background . . . . . . . . . . . . . . . . . . . . . . . . 142 Microbiology . . . . . . . . . . . . . . . . . . . . . . . 15212.2.1 Magnitude of the Problem . . . . . . . . . 142 Pathophysiology . . . . . . . . . . . . . . . . . . . 152 12.5.2 Clinical Presentation . . . . . . . . . . . . . . . 15212.3 Ischemic Complications . . . . . . . . . . . 142 Medical History . . . . . . . . . . . . . . . . . . . . . 15212.3.1 Pathophysiology . . . . . . . . . . . . . . . . . . . 142 Physical Examination . . . . . . . . . . . . . . . 15212.3.2 Clinical Presentation . . . . . . . . . . . . . . . 144 Laboratory Tests . . . . . . . . . . . . . . . . . . . 15312.3.2.1 Graft Occlusion in the Leg . . . . . . . . . . 144 12.5.3 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . 15312.3.2.2 Ischemia After Aneurysm Aortic Graft Infection . . . . . . . . . . . . . . . 153 Operations and Endovascular 12.5.4 Management and Treatment . . . . . . . 154 Procedures . . . . . . . . . . . . . . . . . . . . . . . . . 144 In the Emergency Department . . . . . 15412.3.3 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . 145 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . 15512.3.3.1 Leg Ischemia . . . . . . . . . . . . . . . . . . . . . . . . 145 Management After Treatment . . . . . 15512.3.3.2 Visceral Ischemia . . . . . . . . . . . . . . . . . . . 145 12.5.5 Results and Outcome . . . . . . . . . . . . . . 15612.3.4 Management and Treatment . . . . . . . 14612.3.4.1 Management in the Emergency 12.6 Local Complications . . . . . . . . . . . . . . . 156 Department, ICU, and the Ward . . . . 146 12.6.1 Lymphocele and Seroma . . . . . . . . . . . 15612.3.4.2 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . 147 Background and Causes . . . . . . . . . . . . 15612.3.4.3 Management After the Operation 147 Clinical Presentation . . . . . . . . . . . . . . . 15612.3.5 Results and Outcome . . . . . . . . . . . . . . 147 Management and Treatment . . . . . . . 15612.3.5.1 Graft Occlusion . . . . . . . . . . . . . . . . . . . . . 147 12.6.2 Postoperative Leg Swelling . . . . . . . . 15712.3.5.2 Ischemia After AAA Surgery Background and Causes . . . . . . . . . . . . 157 and Endovascular Procedures . . . . . . 148 Clinical Presentation . . . . . . . . . . . . . . . 157 Management and Treatment . . . . . . . 15712.4 Bleeding Complications . . . . . . . . . . . 148 12.6.3 Wound Edge Necrosis . . . . . . . . . . . . . . 15712.4.1 Causes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148 Background and Causes . . . . . . . . . . . . 15712.4.2 Clinical Presentation . . . . . . . . . . . . . . . 148 Clinical Presentation . . . . . . . . . . . . . . . . 15712.4.2.1 Medical History . . . . . . . . . . . . . . . . . . . . . 148 Management and Treatment . . . . . . . 15712.4.2.2 Physical Examination . . . . . . . . . . . . . . . 149 12.6.4 Local Nerve Injuries . . . . . . . . . . . . . . . . 15712.4.3 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . 149 Background and Causes . . . . . . . . . . . . 15712.4.4 Management and Treatment . . . . . . . 149 Clinical Presentation . . . . . . . . . . . . . . . 15812.4.4.1 In the Emergency Department, Management and Treatment . . . . . . . 158 ICU, or Surgical Ward . . . . . . . . . . . . . . . 14912.4.4.2 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . 150 Further Reading . . . . . . . . . . . . . . . . . . . 15812.4.4.3 Management After Treatment . . . . . 151
  • 142. 142 Chapter 12 Complications in Vascular Surgery 12.1 Summary 12.2.1 Magnitude of the Problem Wound infections may cause life-threaten- The number of complications is related to the ing bleeding by eroding an anastomosis. number of vascular surgical procedures per- An infected surgical wound overlying a formed. In Sweden, for instance, the number of vascular reconstruction should not be de- operations increased from approximately 500 per brided in the emergency department. million inhabitants per year in 1982 to almost A patient with an aortic graft admitted for 1,200 per million in 1995. A similar pattern is gastrointestinal bleeding should be treated common for most Western countries. The number as having an aortoduodenal fistula. of procedures, especially endovascular, has con- Vascular graft infection should be suspect- tinued to rise, and one-third of registered proce- ed in a patient with unspecific symptoms dures are classified as reoperations. The latter cov- and a previously implanted aortic graft. ers revisions of anastomotic problems, angioplasty Leg ischemia following thrombotic occlu- of restenosis and graft stenosis, operations for sion of a previous vascular reconstruction acute bleeding, and extirpation of infected grafts. requires careful consideration before a de- The incidence of postoperative complications cision to operate, unless the extremity is can be estimated from these Swedish data. If ap- immediately threatened. proximately 12,000 operations are performed Suspected extremity or visceral ischemic yearly and the risk of complications requiring a complications after aortic procedures visit to the clinic is estimated to be 20%, 2,400 pa- should be managed in close cooperation tients will seek medical attention for a complica- with an experienced vascular surgeon. tion following a vascular procedure (Table 12.1). In Sweden this corresponds to six or seven patients daily. Most doctors on call will meet such patients and manage their initial work-up and treatment. 12.2 Background The most common complications of vascular sur- 12.3 Ischemic Complications gery – myocardial infarction, aggravated angina, renal insufficiency, and pulmonary problems – 12.3.1 Pathophysiology will not be dealt with in this chapter. Such system- ic complications are consequences of the medical Ischemic complications after vascular operations background of vascular surgical patients. In fact, are common and influence several organ systems. most patients have general manifestations of arte- Examples of such complications are listed in Table riosclerosis, diabetes, and chronic obstructive pul- 12.2. There are many different causes and some- monary disease. These risk factors also contribute times several factors contribute simultaneously. to the higher incidence of specific complications The consequence is ischemic symptoms in the in this patient group after vascular as well as gen- affected organ. eral surgical procedures. The specific complica- Vascular reconstructions for chronic leg isch- tions of vascular surgical procedures can be cate- emia have a high risk for developing graft occlu- gorized into four groups: sion, especially in the first years after the primary 1. Ischemic, caused by thrombosis, embolization, operation. Up to half of the grafts will eventually dissection, and occlusion of vessels occlude. The causes for occlusion vary depending 2. Bleeding on when it occurs. Early (within 30 postoperative 3. Infection in wounds and grafts days), technical causes dominate, such as a badly 4. Local complications in the surgical field. sutured anastomosis, intimal tear, and intact valve cusps in an in situ bypass. Other examples are In this chapter complications will be discussed poor vein graft quality and extensive arteriosclero- under headings corresponding to these catego- sis in run-off arteries. Late graft occlusion is sec- ries. ondary to intimal hyperplasia in the graft or the
  • 143. 12.3 Ischemic Complications 143Table 12.1. Frequency of complications after vascular procedures Category Type of initial Complication rate Comment procedure/location of all interventions Ischemia Suprainguinal 15% Includes endovascular as well as open procedures Infrainguinal 20–60% Graft occlusions only (varies with the level of the distal anastomosis – more distal = higher risk) Diagnostic 0.5% Includes symptomatic embolization angiography Aortic surgery 4–5% Renal insufficiency only (higher risk after operations for rupture) Aortic surgery 1% Intestinal ischemia only after elective surgery (after surgery for rupture, up to 8%) Bleeding All types of proce- 1–3% Bleeding requiring reoperation dures Infection Wound 8–20% After inguinal incisions with antibiotic prophylaxis Aortic graft 1–3% After surgery for aneurysms as well as occlusive disease Femoropopliteal 2–5% Synthetic grafts only. Considerably lower bypass for vein graftsTable 12.2. Ischemic complications after vascular interventions (PTA percutaneous transluminal angioplasty,AAA abdominal aortic aneurysm) Symptomatic organ Original procedure Mechanism Time when Main cause it occurs Leg and foot Bypass Graft occlusion Early and late Technical errors, intimal hyperplasia Leg and foot, Aneurysms, PTA Embolization Early Dislodged thrombus intestine, kidneys Kidneys AAA (ruptured) Clamping, Early Impaired renal perfusion hypovolemia Colon AAA (ruptured) Clamping Early (late) Ligation of inferior mesenteric artery Leg and foot, intestine PTA, all vascular Dissection Early Intimal dissection causes operations vascular occlusionanastomotic area. Early graft occlusions are gener- orous manipulation of the aneurysm during sur-ally easier to treat and have a better prognosis. gery for abdominal aortic aneurysms (AAAs) Embolization and dissection complicates mainly might also cause embolization. This may result inpercutaneous transluminal angioplasty (PTA) and “trash foot,” a specific type of acute leg ischemiaangiography. The catheters can dislodge a throm- affecting the foot rather than the entire leg. Thebus located in the abdominal or thoracic aorta that name comes from the consequence – that the footfollows the bloodstream to the mesenteric or renal will end up as “trash.” It is caused by numerousarteries or down into lower extremity vessels. Vig- small emboli occluding distal foot arteries.
  • 144. 144 Chapter 12 Complications in Vascular Surgery Dissection, as a complication of angiography or The physical examination aims to establish the angioplasty, may also cause ischemia. This might graft occlusion, determining the severity of isch- happen anywhere an artery was catheterized, but emia and the level of occlusion. This is accom- usually in the aorta. The bloodstream then sepa- plished by inspecting the foot and leg and by pulse rates the layers in the vascular wall, creating two palpation. Furthermore, the ankle-brachial index separate lumina with blood flow. Most damage (ABI) is measured to objectively grade the isch- occurs when the orifices of the intestinal and renal emia. Palpation of pulses along the graft is also arteries are occluded by the dissection and these helpful to elucidate whether the graft is patent, but organs become ischemic. This is further described interpretation is sometimes difficult. An in situ in Chapter 8. graft may have pulsations in its proximal parts but Another type of ischemic complication is mul- be occluded distally with outflow into a residual tifactorial and follows aortic surgery, usually vein branch. The graft can also be patent despite after emergency operations in which hypovolemic occlusion of the recipient artery when blood flows shock is common. Arterial clamping, poor perfu- in the outflow artery in a retrograde direction. sion due to hypovolemia, and hypotension may Some grafts are difficult to palpate because they cause renal failure and ischemic colitis of the sig- are tunneled deep along the occluded artery. Syn- moid colon. Reperfusion injury after declamping thetic grafts are also hard to examine, and a pen makes the ischemic consequences worse. Renal in- Doppler can then identify the graft for palpation. sufficiency evolves within 1 week of the operation, The Doppler signal must also be interpreted with but a decrease in urine production is seen imme- care. The signal may emanate from flow in veins diately after the procedure. Intestinal ischemia or smaller arteries, so its presence does not guar- usually has an early onset because of postoperative antee graft patency. hemodynamic problems but might also be delayed. Generally, the medical history and physical ex- As soon as the intestinal perfusion is below the amination are sufficient to diagnose the ischemia critical limit damage will occur. and if there are no pulses along the graft this sug- gests occlusion or obstruction. When the examin- er is in doubt a duplex examination is performed. 12.3.2 Clinical Presentation Ischemia After Aneurysm Graft Occlusion in the Leg Operations and Endovascular Reappearance of preoperative symptoms is the Procedures main reason why patients seek help. Often this These complications are discovered in the post- is worsened claudication, rest pain, or new ulcer- operative period. A patient in the ward who has ations, and the patient describes a sudden onset undergone endovascular treatment and suddenly of symptoms that have deteriorated rapidly. The starts to complain of abdominal pain, a cold pain- time of onset coincides with the moment when the ful leg, or more unspecific symptoms should be graft occludes. It is important to note the time suspected to be suffering from embolization. The when a venous graft occludes because the endo- symptoms vary with the vascular segment that has thelium is destroyed within 8–10 h. First appear- been obstructed. If the superior mesenteric artery ance of severe problems is regularly preceded by a is affected, symptoms are similar to those of acute period of some deterioration, which is caused by a intestinal ischemia (Chapter 6, p. 67). Abdominal developing stenosis. pain may also be caused by renal infarction. If a It is important to gather as much information large artery to a lower extremity is occluded, the as possible about the original operation, the way symptoms are the ones described in Chapter 10 on the graft was tunneled, problems that occurred acute leg ischemia (page 121). during the operation (such as poor quality of the The medical history obtained should include vein graft, iatrogenic injuries, problems with in- information about the procedure, including flow), and the result of follow-up examinations. whether any problems occurred. For AAA proce- General risk factors also need to be considered if dures it is important to know if the AAA treated reoperation or thrombolysis is probable. involved the suprarenal or juxtarenal area, if it
  • 145. 12.3 Ischemic Complications 145contained large amounts of thrombus, if it was thrombolysis not is an alternative. This is the caselarge, and if it extended into the iliac arteries. The when more than 72 h have passed since the occlu-physical examination should cover signs of isch- sion occurred or when the patient has recentlyemia and embolization. An example of the latter is undergone a surgical or percutaneous petechiae in the artery’s distribution area. For other patients a duplex examination is the bestThe patient’s back and gluteal regions must be ex- way to verify graft occlusion as well as occlusion ofamined in addition to the skin of the feet and legs. previously patent native vascular segments in thePatients with “trash foot” or “blue toe syndrome” leg. It is also the first choice in patients with acuteoften have palpable ankle pulses. complications after endovascular procedures and After aneurysm operations the patients are aortic surgery. Angiography or other radiologicoften treated in the intensive care unit (ICU) for examinations are rarely needed, but they are, ofat least 24 h, and all organ functions are meticu- course, required prior to thrombolysis.lously monitored. After emergency aortic surgerythe risk for complications is greater and patients Visceral Ischemiaremain in the ICU for several days. Impaired or- Patients with peritonitis and suspected intestinalgan perfusion and embolization are common in ischemia do not need work-up and should be takenthis group and the nursing staff frequently suspect to the operation room immediately for diagnosticcomplications and will alert the doctor on call de- and therapeutic laparotomy. Those with suspectedspite the patient’s being under sedation. The pri- renal or mesenteric artery occlusion, on the othermary aim when examining the patient is to diag- hand, require angiography for an accurate diagno-nose complications requiring immediate surgical sis. In these segments duplex is obscured by in-treatment, such as intestinal ischemia and large testinal gas. A very good alternative is CT angio-major embolization to the kidneys and legs. Ab- graphy, which enables identification of renal in-dominal pain and diarrhea during the first post- farction as well as vascular segments filled withoperative day, especially if there is blood in the thrombus.stools, strongly indicates intestinal ischemia. Sev- Colon ischemia complicating aortic surgery isenty-five percent of patients with ischemic colitis sometimes difficult to rule out. The extent of isch-have diarrhea the first days after surgery. Physical emia ranges from a minor mucosal necrosis toexamination findings are a distended abdomen transmural intestinal gangrene, and diagnosis iswith signs of intestinal paralysis, tenderness in the hardest to make early when the changes are min-left lower quadrant, and blood on rectal examina- ute. Early diagnosis is important to save intestinetion. Patients also have general findings, including and to avoid multiple organ failure. The first diag-fever, acidosis, and oliguria. nostic option is coloscopy. Early ischemic signs are Examination of suspected embolization to the a pale mucosa with areas of petechial bleedings.legs is more clearcut, with typical findings such as When the mucosa is dark blue or black and partlyall of the common ones in distal ischemia, as well disintegrated immediate laparotomy is absent pulses. Suspicion for renal or intestinal If a tonometer is available for monitoring mucosalinfarction is hard to verify during clinical exami- pH in the sigmoid colon it should be placednation and further investigations with computed immediately postoperatively. A pH <7.1 for moretomography (CT) scanning and endoscopy are than 2 h is considered a strong prognostic sign forusually necessary. the development of intestinal ischemia. The speci- ficity is 90% and the sensitivity 100% if these val- ues are used. A normal CT scan does not exclude 12.3.3 Diagnostics ischemic colitis and pathologic CT findings are seen in only one-third of the patients with this Leg Ischemia diagnosis. Other, but less specific, parameters ofNo further diagnostic work-up is needed when it possible value are clinical signs of septicemia, in-is obvious that the patient needs an emergency creasing lactate concentration in blood, an elevat-operation. Examples are immediately threatening ed white blood cell count, and consumption ofleg ischemia and clear vein graft occlusions when platelets.
  • 146. 146 Chapter 12 Complications in Vascular Surgery Fig. 12.1. Weighing factors for and against reoperation in graft occlusion 12.3.4 Management and Treatment known poor run-off. A poor general condition of the patient is also a factor that opposes continued Management in the Emergency active surgical treatment. If the graft occlusion oc- Department, ICU, curred early after the primary operation, throm- and the Ward bectomy alone could possibly be successful. We prefer to perform angiography as soon as Leg Ischemia possible regardless of the type of primary opera- What previously has been written regarding treat- tion, duration of graft occlusion, or time of day. ment of acute leg ischemia (Chapter 10) is also Angiography is the first step in thrombolysis and valid for leg ischemia as a complication. Patients sometimes reveals the reason for the occlusion. If with an immediately threatened leg – disturbed it is impossible for some reason and the leg is motor function, no ankle pressure, paralysis – threatened, operation is performed right away. require urgent operation. When a vein graft has The information needed to make a decision to occluded treatment should be started as soon as operate or not is obtained from the medical chart, possible even if the leg is not immediately threat- patient interview and physical examination, and ened, as the graft can be destroyed within a few angiography findings. hours. It is, however, wise to carefully consider the decision to perform a reoperation. The decision Ischemia After Aneurysm Surgery to operate is more difficult than at the primary and Endovascular Procedures operation. Necessary information to facilitate the The work-up and treatment for suspected emboli- decision includes the reason for occlusion, the zation and dissection are difficult but very impor- indication for the primary operation, risk factors, tant because of the fatal consequences that might and available graft material. These factors should occur. Patients with postoperative embolization to be weighed against the expected outcome of the most arteries in the legs and those with confirmed reoperation (Fig. 12.1). For instance, a situation ischemic colitis and peritonitis, should all be reop- of the initial procedure being leg-saving with an erated. The timing depends on the patient’s gen- anticipated poor outcome stands against reopera- eral condition. Frequently it is necessary to opti- tion, as does a bypass to a distal calf artery with a mize the patient medically. When embolization to
  • 147. 12.3 Ischemic Complications 147the intestines is suspected liberal indications forrelaparotomy are warranted. For dissections, low- heparin is administered. If acceptable inflow andering of blood pressure and endovascular treat- outflow are accomplished, the graft is occludedment with stents are the first treatments choices. with a rubber-covered vascular clamp and the incision is closed with interrupted prolene su- Operation tures. If backflow is doubtful and the amount ofEmbolectomy of the arteries in the legs and intes- clot removal is scant, angiography is performed.tine has been previously described (Chapters 6 If the inflow is poor the operation must proceedand 10). If examination or angiography indicates by exposing the proximal anastomosis. A previ-that embolizations have occluded distal vessels, ously unknown proximal stenosis in the inflowclot removal is performed from the popliteal ar- artery or more proximal in the graft is anothertery or via separate exposure for the tibial arteries. possible explanation that might require repair.Embolectomy procedures for vascular segments The result of the thrombectomy is controlledother than those two above require experience either by angiography, continuous-wave Dop-from vascular surgery. The surgical treatment of pler, or palpation.ischemic colitis is usually colon resection (oftenthe sigmoid colon), colostomy, and Hartman clo-sure of the rectum. The difficult part of the opera-tion is to judge whether the colon is ischemic or Managementnot. This has also been discussed previously in After the OperationChapter 6 and should, of course, comply with pre- Patients who have undergone thrombectomy suc-vailing local routines and methods. The principles cessfully should receive heparin or low molecularfor thrombolysis are described in Chapter 10. The weight heparin according to local protocols. If theonly surgical procedure that may have to be per- reason for graft occlusion is not identified duringformed by someone without much experience in surgery, the postoperative period is used for work-vascular surgery is thrombectomy in a vein or syn- up. Duplex is the first choice for identification ofthetic graft; this is briefly described in the Techni- graft problems at this time. In particular, it shouldcal Tips box. look for a stenosed anastomosis or a stenosis in the graft. If thrombosis is unlikely, sources for emboli TECHNICAL TIPS must be sought. Patients with embolic ischemic Thrombectomy in a Graft complications after aortic surgery or an endovas- cular procedure who require surgical treatment Antibiotic prophylaxis should be given, and the usually need extensive care in the ICU. type of anesthesia chosen must allow extensive reconstruction. The distal anastomosis is the most common site for restenosis. A longitudinal 12.3.5 Results and Outcome incision in the proximal part of the previous inci- sion is used. The advantage with an incision over Graft Occlusion the anastomosis is that the operation can pro- Results of bypass operations in the legs are usually ceed with revision of the anastomosis if needed. reported as the share of patent grafts, or the share If it has already been decided that the operation of salvaged legs, of the total number operated. is aiming at thrombectomy only, irrespective of Accordingly, reoperation or thrombolysis of graft the result, the incision is placed where the graft occlusions is so common that it already is consid- can be palpated easiest. Four to five cm of the ered when results of the primary operation are graft is exposed first and a vessel loop is applied. reported. Outcomes are usually presented as life A transverse incision is made in the graft without table curves, where the secondary and sometimes clamping. Thrombectomy is performed with a the tertiary patency is reported. The data pre- suitable Fogarty catheter after intravenous (IV) sented are consequently the number of patent grafts after further treatment with thrombectomy, thrombolysis, and/or revision indicated by graft
  • 148. 148 Chapter 12 Complications in Vascular Surgery failure or occlusion, and are defined as secondary 12.4 Bleeding Complications patency or primary assisted patency. The differ- ence between primary and secondary patency is, 12.4.1 Causes in most reports, 10–15%. Bleeding usually happens within 24 h after the Thrombolysis Versus Thrombectomy primary procedure, but it can occur several years There are no randomized studies of graft occlu- postoperatively. A slipping suture or a leaking sion treatment options. It can be assumed that the anastomosis are the main explanations for peri- results of thrombolysis or thrombectomy are simi- operative bleedings. Sometimes the condition is lar, providing that the compared groups are strati- accentuated by an increased general tendency for fied according to the cause of graft occlusion. bleeding or by ongoing anticoagulation treatment. Thrombolysis has the advantage of minimizing Problems with ligatures on vein branches of an in the extent of the procedure. In graft occlusion situ infrainguinal vein graft are relatively com- during the immediate postoperative period (2– mon. Such ligatures have to resist much stronger 4 weeks), thrombolysis is associated with an in- forces than normal vein pressure. Late bleeding is creased risk for bleeding and thrombectomy is caused by infectious erosion of the vascular wall safer. Furthermore, several studies report that sur- or an anastomosis. gical thrombectomy has the best results when used The patient often bleeds considerably before to treat late occlusions of synthetic grafts, with the and during acute vascular operations. This results distal anastomosis above the knee. Reoperation in in increased fibrinolysis and consumption of co- theses cases often requires thrombectomy and agulation factors, which may lead to secondary revision of a stenosed anastomosis with a patch. hemostasis problems. Prolonged bleeding time as a Above the knee, 52% of the grafts are patent after consequence of antiplatelet medication is also com- 3 years and 15% after thrombolysis. The results are mon. A previously undetected hemophilia can, of better for synthetic grafts compared with vein course, also cause postoperative hemorrhage, as grafts. It is important, however, to repair the un- can overly generous perioperative anticoagulation. derlying reason for graft occlusion also during thrombolysis. If the reason for occlusion is un- known and not treated, only 10% of grafts are 12.4.2 Clinical Presentation patent 1 year after thrombolytic treatment. The presentation of bleeding is usually obvious. Ischemia After AAA Surgery and Endovascular Procedures Medical History Ischemic colitis requiring laparotomy has a 30 day An important part of the medical history is mortality of 50–60% if. If a total colectomy or found in the operation note. It describes techni- hemicolectomy was needed the mortality increas- cal difficulties, iatrogenic vascular injuries, and es to 80%. Interestingly, there doesn’t seem to be other problems. Information about preoperative an increased risk for graft infection after colecto- bleeding, substitution, and systemic anticoagula- my because of colitis despite the contamination of tion is found in anesthesia notes. A history of a the abdomen. Extensive embolization to the legs previous tendency to bleed (for instance, diffi- or “trash-foot” after aortic surgery is associated culties stopping bleeding after minor wounds, a with a 30% mortality within 30 days. Some data in tendency to bruise easily, or bleeding during the literature suggest that distal embolectomy tooth brushing) and bleeding complications in from the popliteal or tibial arteries reduces the previous surgery can be revealed if the patient is amputation rate. If the embolization leads to am- awake. Information about current medication putation, mortality increases to 40%. Multiple or- with aspirin or clopidogrel is important, along gan failure is associated with an increased risk for with the most recent INR and ACT values and all types of complications as well as increased platelet count. mortality.
  • 149. 12.4 Bleeding Complications 149 Physical Examination 12.4.4 Management and TreatmentEarly postoperative bleeding is noted as a subcuta-neous hematoma under the skin incision. Often it In the Emergency Depart-rapidly increases in size. Marking the limits of the ment, ICU, or Surgical Wardhematoma with a permanent marker pen is a goodway to facilitate estimating such expansion. Bleed- Emergency Measuresing from incisions is another common presenta- Profuse bleeding from a wound can be temporar-tion and is often revealed when nurses need to ily controlled by finger compression while the pa-change dressings frequently or when more than tient is being transported to the operating room.50 ml/h of blood is emptied from a drain. Bleeding Additionally, in large hemorrhages causing hypo-occurring after the first postoperative days is usu- volemia, packed cells and fresh-frozen plasma areally associated with signs of infection at physical given to the patient. Fresh-frozen plasma containsexamination. The patient can often inform the coagulation factors that are consumed duringphysician about infection and bleeding problems bleeding, and it decreases the risk for a disturbedin the surgical wound (Table 12.3). hemostasis. If overly generous preoperative or in- Postoperative bleeding in the abdomen after traoperative administration of heparin is suspect-major surgical procedures, such as aortic surgery, ed to be a contributing factor to the bleeding, itsis difficult to diagnose. Medical history, signs of effect could be reversed by protamine. Such treat-hypovolemia, and laboratory tests are helpful but ment should be avoided if possible, and heparin’simprecise (Table 12.3). Dilated intestines, which effects are probably overestimated as a cause fornormally are seen after aortic surgery, make ex- bleedings; the effect of heparin in plasma is de-amination of the abdomen difficult. In obese pa- creased by 50% within 90 min. Three hours post-tients it is almost impossible to interpret findings. operatively, only 25% remains to affect the coagu-Intestinal bleeding after aortic surgery is a sign of lation system. Too rapid infusion of protaminea intestinal ischemia and has already been dis- can induce hypotension because of diminishedcussed above. cardiac function. Furthermore, a slight overdose might cause thrombosis of small-caliber grafts.Table 12.3. Factors suggesting hemorrhage that re- If bleeding persists and there are no good alterna-quires reoperation after aortic surgery. tive treatment options, 10 mg of protamine dis- solved in 15 ml of saline can be administered over Tachycardia (>100/min for 15 min) 10 min. Hypotension (<90 mmHg for 15 min) Increasing abdominal circumference Which Patients Should be Reoperated? Acute or complicated primary operation A basic principle is that patients who are bleeding Hemoglobin concentration not rising despite and display some signs of hypovolemia, such transfusion of red blood cells as tachycardia and a blood pressure less than 100 mmHg for a while, shall be re-operated emer- gently. This is also true for hematomas that dou- bled its size within 30 minutes as well as drain bleedings exceeding 50–70 ml/h. These guidelines, 12.4.3 Diagnostics however, are not generally valid and each patient has to be individually evaluated.Postoperative bleeding does not require diagnos- The rationale for reoperation and evacuation oftic work-up. The only exception is intestinal bleed- hematomas is the risk for graft compression anding after aortic surgery; this situation has already postoperative infection. Other indications forbeen discussed. evacuating a hematoma are severe pain due to compression of nerves and extensively distended skin with risk for perforation. Evacuation opera- tions should always be performed under sterile conditions in an operating room. This is particu-
  • 150. 150 Chapter 12 Complications in Vascular Surgery larly important for bleeding with a coexisting agulation activity is required to obtain normal infection. A new dose of antibiotic prophylaxis values. A better measure of platelet function is should be given to all patients needing reoperation the number of platelets or the bleeding time. A for bleeding. prolonged bleeding time supports the use of des- mopressin. If a disturbed hemostasis without ob- Bleeding After Aortic Surgery vious causes is found, consultation with a coagula- Patients with signs of hypovolemia after aortic tion specialist is recommended. A platelet count operations should be reoperated with wide indi- <50 109/l is considered insufficient for hemosta- cations (Table 12.3). Such reoperations might be- sis and is an indication for platelet transfusion in come difficult and experienced assistance is often case of bleeding. At reoperations platelets should valuable. Besides being difficult to diagnose, the be administered immediately before the start of bleeding site is also often hard to identify, get the operation to give the best possible effect. access to, and repair during the reoperation. Substantial hemorrhage during the primary Operation operation can cause a deficiency in coagulation factors. Before starting the reoperation, it is rec- Control of Bleeding ommended to check if the patient has received Profuse bleeding sometimes needs compression packed cells. If the amount administered exceeded over the bleeding site while the patient is being four to six units, at least two units of fresh frozen scrubbed and draped for surgery. Compression plasma should be given right away. If more than must be applied proximal to the bleeding site to eight units of red blood cells had been given, a allow scrubbing if it is in the groin. For more distal thrombocytopenia may contribute to the bleed- incisional bleedings, a tourniquet achieves con- ing. trol. After opening the skin, an assistant com- presses the inflow artery with a “peanut” or Bleeding During Thrombolysis “strawberry” and keeps the wound free from blood The treatment of bleeding from a puncture site with suction to facilitate exposure. In bleeding after angiography or thrombolysis follows the episodes after endovascular procedures, proximal principles outlined above. After thrombolysis is control is best obtained cranial to the puncture completed, the introducer is usually left in place site, which mostly is in the groin, to avoid dissec- until the thrombolytic agent’s activity has dimin- tion through blood-embedded tissue. The tech- ished. nique has been described in Chapters 9 (p. 107) An oozing bleeding around the introducer dur- and 15 (p. 180). ing thrombolysis requires special attention. In Bleeding from or in the vicinity of the proximal most cases local compression around the catheter anastomosis of aortic surgery is sometimes chal- is sufficient to stop the bleeding and to allow lenging. In general, clamping the aorta is neces- continued thrombolysis. A prerequisite is that the sary to obtain control. If the reason for the bleed- fibrinogen concentration systemically is >1 g/l. If ing is a soft and weak posterior wall of the aorta fibrinogen levels are lower, and also if bleeding there is a substantial risk that even a slight pull on occurs in other locations, infusion of the throm- the graft will disrupt the suture line. If there is bolytic agent should be stopped. major bleeding from this region temporary sub- diaphragmatic aortic control should be obtained Medical Treatment and Observation Only before attempting to repair the suture row (see Minor bleeding from surgical wounds and small also Chapter 7). Other possible sites for arterial hematomas is observed with applied compression bleeding after AAA surgery are the anastomosis over the area. For prolonged minor bleeding, he- of the lumbar arteries in the aneurysmal sac and moglobin, INR and ACT values, and platelet count the inferior mesenteric artery. Anastomoses are are checked, and medications affecting the coagu- also possible bleeding sites. Venous bleeding after lation system are discontinued. These blood sam- aortic aneurysm surgery comes from the iliac ples have a low sensitivity as a screening test for veins or lumbar veins at the level of the proximal hemostasic function and only 30% of normal co- anastomosis.
  • 151. 12.5 Infections 151 Repair of Bleeding Sites treated in the ICU. They also suffer an increasedAnastomotic bleedings and minor puncture bleed- risk of developing ischemic colitis.ings in grafts or arteries are best controlled bysimple sutures. It is important to avoid applyingbites and stitches that are too large because that 12.5 Infectionsmay cause tears and reduce the vessel lumen. Plac-ing the sutures and tying them with the artery 12.5.1 Pathophysiologyclamped decrease the risk for tears. Bleeding froma vein graft branch caused by a slipped ligature Types of Infectionshould be repaired with prolene suturing rather The most common postoperative infection com-than another attempt with ligation. Vascular plicating vascular surgery is wound infection. It isclamps that are too strong may cause perforation benign, local, has few systemic effects, and re-of the graft wall. It is better to use rubber-rein- sponds well to local treatment and antibiotics. Theforced clamps or vessel loops. most common localization is in groin incisions, When major hemorrhage is under control the followed by thigh and calf. If left untreated, woundentire operating field is searched for minor bleed- infections can spread and engage subcutaneousings. Every single bleeding site should be con- tissue. Eventually the graft may be involved, whichtrolled by electrocautery. Hematomas are also is a serious complication. Graft infections mightevacuated. Continued bleeding from the wound occur any time postoperatively and have been re-edges suggests a disturbed coagulation system; if it ported as late as 15 years after the primary proce-occurs, coagulation tests and platelet counts are dure. A combination of surgical and antibioticrechecked. Administration of more fresh frozen treatment is sometimes successful. The surgicalplasma might be indicated. treatment includes total extirpation of the graft, In some circumstances hemostasis can be fa- and in many cases the distal perfusion has to becilitated by local measures. Examples are cellulose restored by extraanatomical reconstructions rout-sheets (Surgiceltm), which after contact with blood ed away from the infected area. The most fearedswells and produces a gelatinous substance and and challenging infectious complication occursthat mechanically facilitates coagulation. Another when an aortic graft is engaged. Aortic graft infec-alternative is sheets of collagen (Avitenetm and tion is a major diagnostic problem, and the 30-dayLyostypttm), which enhance local adhesion of mortality is as high as 50%.platelets. Another effective but rather expensivepossibility is to use fibrin glue (Tisseltm) or prepa-rations of thrombin (FlowSealtm) to cover the rawsurface and thereby seal bleeding minor vessels. Bleeding associated with infection should betreated by ligature of the graft. Synthetic grafts Table 12.4. Risk factors for development of vascularshould be removed entirely, with vein patching to graft infectioncover remaining defects in the artery. General Systemic Management After Treatment Emergency operation DiabetesPatients who have undergone reoperations for Reoperation Cortisone treatmentbleeding should, of course, be monitored post- Inadequate sterile Malignancyoperatively for continued bleeding. This is of great techniqueimportance if the cause it has not been identified. Long operating time LeukopeniaHemoglobin concentration and platelet counts are Simultaneous gastro- Malnutritionchecked every 4th hour, and after major bleeding intestinal operationreplacement with packed cells and fresh frozen Postoperative wound Chemotherapyplasma is continued. Patients requiring reopera- infectiontion because of bleeding after aortic surgery are at Remote infection Chronic renal insufficiencyrisk of developing multiple organ failure and are
  • 152. 152 Chapter 12 Complications in Vascular Surgery Microbiology fistula is established, sooner or later a massive and The vascular graft and the surgical wound become often lethal hemorrhage occurs. An alternative contaminated with bacteria systemically or by explanation for the pathophysiology of aortoduo- direct contact during the operation. Hematoma denal fistula infections is mechanical tear. The and leakage of lymph and other wound secretions, main argument for this is that the aortic pulsa- especially in diabetic patients, are all perfect me- tions cause movements between the anastomosis dia for bacterial growth. The virulence of the bac- and the duodenum that erode the intestinal wall teria and the patient’s general condition determine until it perforates and contaminates the graft. the course of the infection and its severity. There is also a possible correlation between bacterial viru- lence and the time when the infection occurs. 12.5.2 Clinical Presentation Early infections, within 30 days of the primary surgery, tend to be more serious and are often Wound infections are easy to recognize. Accord- caused by more virulent organisms such as Staph- ingly, it is aortic graft infections that will be the ylococcus aureus and Gram-negative bacteria. main subject of the following paragraphs. A high Late infections are caused by coagulase-negative level of suspicion is needed to even consider aortic staphylococci of low virulence. There is an ongo- graft infection because the clinical presentation is ing debate about the significance of these bacteria. diffuse and general. It should be suspected in pa- Some argue that they rarely are responsible for tients who have atypical symptoms. The diagnosis graft infections, that this a common contamina- is most difficult in a low-virulent graft infection. tion of the wound, and that the unspecific symp- toms and findings typical for these “low-virulence” Medical History infections instead represent an inflammatory re- Besides information about the primary operation, action to the graft material. This concept is sup- the patient should be asked about unspecific gen- ported by the fact that less aggressive treatment eral symptoms such as fatigue, loss of appetite, usually is more effective in coagulase-negative weight loss, nausea, and low-grade fever. The cir- staphylococci infections compared with those cumstances around the primary operation are im- caused by a more virulent bacteria. Wound infec- portant, and operations that were long in duration, tions are mostly caused by Staphylococcus aureus. complicated, and done as an emergency, support the suspicion of graft infection. A superficial Pathophysiology wound infection immediately after the primary Besides constituting a risk for septicemia and a operation should also alert the examiner. Symp- threat to graft function, infections also imply a toms of gastrointestinal bleeding are an alarming risk for bleeding by erosion of arterial and graft sign in patients who have undergone aortic recon- walls, including the anastomosis. Such erosions structions and the diagnosis of aortoduodenal fis- can, even if they are small, lead to life-threatening tula should always be suspected until disproved. hemorrhage and to the development of pseudo- The patient should also be asked about tender- aneurysms. If such bleeding occurs in the proxi- ness, delayed healing of surgical wounds, and the mal anastomosis of an aortic reconstruction it will presence of swelling or masses in the operation most likely be profuse and lethal. A special type of area. The latter can be the sign of a pseudoaneu- erosion-related bleeding is seen when an aortodu- rysm or abscess. It is also important to ask about odenal fistula develops. It results from an erosion secretions from the scars. that creates a communication between the aorta and the duodenum. It presents as gastrointestinal Physical Examination bleeding, and blood cultures are often positive for In addition to a general physical examination, intestinal bacteria. The bleeding usually starts as a including graft function, the operation wound is minor, deceptively innocent hematemesis or rectal examined with special emphasis on infection signs bleeding, followed by several days without symp- and secretions (Fig. 12.2). Also, the areas around toms. This “herald bleeding” is probably second- the scars need to be investigated for fistulas, pul- ary to the erosion of the duodenal wall. When the sating masses, and tender swellings. If an infected
  • 153. 12.5 Infections 153Fig. 12.2. Clinical signs of graft infection followinginfrainguinal bypass surgerysurgical wound is open due to dehiscence or de-bridement it is important to examine whether thegraft is visible. A visible graft often necessitatesgraft removal. Laboratory TestsIn wound infections and local infections engagingsmaller grafts, laboratory tests are not needed toestablish the diagnosis. Fig. 12.3. An example of a positive leukocyte scinti- gram. Arrows point toward areas with suspected infec- In aortic graft infections laboratory tests usu- tionally suggest a pronounced systemic infection withleukocyte counts >15 109/l and high C-reactiveprotein values. The amount of increase, how-ever, varies with the grade of infection. When pre-sentation is vague, additional laboratory tests such Aortic Graft Infectionas differential count or electrophoresis can occa- The first investigation done to reveal signs of aor-sionally facilitate differentiation from other dis- tic graft infection is CT. The question to be an-eases. Test results can be normal during infections swered is whether there is fluid or gas around thecaused by coagulase-negative staphylococci. Pa- graft and inside the aneurysm sac. The normaltients often also have a slight anemia and low albu- postoperative course is that fluid and gas shouldmin levels in serum. Stools should be checked for be absorbed within 3–6 weeks. Accordingly, gasthe presence of blood when aortic graft infections bubbles around the graft after 20 days postopera-are suspected. The value of this can, however, be tively suggest that infection is a possible diagnosis.debated because the specificity in diagnoses of oc- Unfortunately, it is not always easy to differentiatecult bleeding from aortoduodenal fistulas is low. from intestinal gas. Magnetic resonance imaging (MRI) is an alternative for the work-up. It is better for differentiating between fluid collections, old 12.5.3 Diagnostics thrombi, and inflammatory changes in tissue. Un- less the diagnosis is obvious after the initial inves-Ultrasound can reveal the presence of fluid collec- tigation, most patients with suspected aortic grafttions close to the graft or anastomosis and differ- infections are examined with both CT and MRI.entiate hematomas from aneurysms. A special Our recommendation is that CT is ordered firstproblem is deciding how much fluid can be con- when aortoduodenal fistula is suspected, and MRIsidered normal around grafts recently implanted. is ordered for all other patients. Other methodsThe fluid should be absorbed within 3–6 weeks, such as a leukocyte scintigram can be helpfulbut before that time, fluid collections can be con- when CT and MRI are unable to establish thesidered normal findings. diagnosis (Fig. 12.3).
  • 154. 154 Chapter 12 Complications in Vascular Surgery Table 12.5. Diagnostic methods used for aortic graft infections Method Sensitivity Specificity Comment Computed tomography 57–94% 85–100% Best results in aortoduodenal fistula Magnetic resonance imaging 85% 100% For primary graft infections Leukocyte scintigram 80–100% 50–85% For primary graft infections and aortoduodenal fistulas Patients with a history of gastrointestinal bleed- started after samples for microbiological cultures ing should be examined with endoscopy. It is im- are obtained. Because Staphylococcus aureus is portant to view the entire duodenum all the way the most common bacteria, oral cloxacillin is down to the distal part, which usually is located given. If the patient has diabetes or if the wound is close to the anastomotic area in the aorta and suspected to be contaminated with intestinal bac- where blood clots or ongoing bleeding are most teria, antibiotics with a broader efficacy spectrum likely to be found. An examination that fails to in- are recommended. clude this part of the duodenum is incomplete. For deeper infections, especially if a graft is in- Occasionally, graft material can be seen through a volved, the patient needs surgery as soon as possi- defect in the mucosa. A normal examination, on ble. If the patient is septic and has impaired circu- the other hand, does not exclude aortoduodenal lation, immediate surgery is indicated irrespective fistula. Unfortunately, none of the diagnostic of the time of day. The first dose of antibiotics methods mentioned above can exclude the diag- should be administered intravenously in the emer- nosis of graft infection (Table 12.4). gency department. When deciding if it is enough When the patient presents with mild symptoms to drain an abscess or if graft extirpation is neces- a lot of time is available for further diagnostic sary, a duplex examination can reveal whether an work-up, such as technetium or leukocyte scinti- infected hematoma is connected to the graft. Graft grams (Table 12.5). When the patient has groin extirpation is usually indicated when a synthetic sinus and fistula, a fistulogram can be done by in- graft is visible in a ruptured surgical wound. An jecting contrast. This can map the sinus system exposed vein graft must be ligated to prevent and disclose whether it connects with the graft. bleeding. In cases with deeper infections involv- Angiography does not add any information for es- ing autologous or synthetic grafts the patient is tablishing the diagnosis but is sometimes needed admitted to the ward and treated with antibiotics for planning the reconstruction after removal of even if he or she has mild symptoms. If a patient an infected graft. with a synthetic graft infection still has fever and signs of remaining infection in laboratory tests after 2–3 days of treatment, extirpation of the graft 12.5.4 Management and Treatment is also indicated. This is valid even with dimin- ished signs of local infection. In the Emergency Department Suspected Aortoduodenal Fistula Wound and subcutaneous Patients with a previous aortic procedure, a recent graft infections history of gastrointestinal bleeding, and an im- Patients with wound infections should be admit- paired general condition should be suspected to ted to the ward for observation because of the risk have an aortic graft infection. Accordingly, they for graft involvement and bleeding. Only very are candidates for observation and treatment in mild and superficial infections can be treated in the ICU. There is a risk for massive acute bleeding the outpatient clinic. Wound debridement should and careful monitoring of cardiac and renal func- never be performed in the outpatient clinic or tion is necessary. For such patients it is essential to emergency department. Antibiotic treatment is have IV lines inserted and packed red cells avail-
  • 155. 12.5 Infections 155able for transfusion if bleeding occurs. Blood cul- nor omentum (Chapter 7, p. 83). Control can alsotures and other cultures should be obtained before be achieved by balloon insertion from the groin orantibiotic therapy is started. If the patient’s condi- brachial artery (page 83). Once proximal controltion allows, investigations with endoscopy, duplex has been achieved resuscitation is continued whileor CT scanning are performed. If such a patient waiting for the arrival of experienced assistance.has ongoing significant bleeding and shows signsof prolonged hypovolemia, he or she must imme- Continued Operationdiately be transported to the operating room. It is Irrespective of strategy the continued operationalso important to call for assistance. Aortic graft usually requires experience in vascular surgeryinfection hemorrhage is one of the major chal- with the possible exception of vein graft ligation.lenges in vascular surgery and vast experience is Easiest is to divide the graft between two vascularnecessary to have some chance to save the patient. clamps proximal to the infected area and suture-Fortunately this complication is very rare, occur- ligate both ends with prolene sutures. Such liga-ring after only 0.1–0.2% of all aortic reconstruc- tures should preferably be placed in fresh, not in-tions. fected, tissue. Synthetic grafts should be totally extirpated and the defects in the native arteries Other Aortic Graft Infections covered with patches of autologous vein. It is usu-Patients with suspected graft infection in the ally necessary to restore the circulation in the ex-abdomen and mild symptoms are admitted to tremity. In graft infections in the lower extremi-the ward for daytime work-up. If the suspicion is ties it is common to try to delay immediate recon-strong, such as in cases with purulent secretion struction and wait until the infection has healed,from the groin, antibiotic therapy should be start- but this often increases the risk for amputation.ed immediately. Investigations include CT or MRI The continued operation in aortic graft infec-to verify the diagnosis to reveal if the graft is tions is complicated and requires vascular surgicalengaged and to plan an upcoming surgical proce- expertise. Several alternatives are possible and thedure. The surgical strategy often includes compli- type of infection, its extension, and the availabilitycated procedures even in cases of less dramatic of new graft material from the patient determinesinfections. The most common is an axillobifemo- the choice. In many cases the old graft has to beral bypass to ensure circulation to the lower ex- totally extirpated; the aortic, iliac, and femoraltremities, followed by a second procedure during stumps oversewn; and the circulation of the lowerwhich the entire aortic graft is removed. extremity restored extraanatomically, usually by an axillobifemoral bypass. Other cases can be re- Operation constructed in situ with vein grafts, thrombecto- mized arteries, or homologous or synthetic grafts. Control In infections of seemingly low virulence, onlyIn graft infections in the extremities, proximal partial excision of grafts can be considered. Localand distal control is obtained by separate incisions antibiotic treatment is then common as part of thethrough unaffected tissue. Synthetic grafts, for in- management.stance, must be controlled by exposure and band- Samples for aerobic as well as anaerobic micro-ing of inflow as well as outflow vessels, including biological cultures should be obtained from theall branches. This is easy when the graft is sur- operation field as well as from excised grafts. Therounded by pus but difficult if the dissection must wound should never be left open for secondarybe performed through scar tissue. healing with an exposed vascular graft. All seg- Control of the aorta during graft infection sur- ments of patent grafts must be covered with softgery is very difficult. Because of the risk for mas- tissue.sive bleeding it should not be attempted – unlessabsolutely necessary – if experience is limited. It Management After Treatmentinvolves a long mid line incision and clamping of Antibiotic treatment should be continued post-the aorta subdiaphragmatically, either manually operatively even if the infected graft has been re-or with a straight clamp applied through the mi- moved. Open wounds need daily control and
  • 156. 156 Chapter 12 Complications in Vascular Surgery dressing changes to avoid spreading or persisting lymph vessels or glands are damaged during dis- infection. Patients operated for aortic graft infec- section and the lymph collections are built up – a tion are treated in the ICU postoperatively. They lymphocele. Both types have the potential to spon- require careful monitoring of all vital organs, in- taneously be absorbed or drained through the in- cluding perfusion of the extremities. cision. In the latter case a lymph fistula is created and drainage of lymph will go on intermittently for several weeks. Lymphocele is reported to occur 12.5.5 Results and Outcome in 1–6% of all groin incisions. Both of these com- plications can transform into manifest infection Reported results of treatment of graft infections and are therefore associated with an increased risk clearly demonstrate that such infections are dan- for postoperative wound and graft infection. gerous and complicated to treat. Thirty-day mor- tality after surgery for graft infections in the ex- Clinical Presentation tremities is reported to be in the range of 10–17%, Seroma and lymphocele can be difficult to differ- with an amputation rate of 40%. The variability of entiate from early wound infection. A fluctuating the results depends on the choice of treatment mass that is easy to delineate by palpation is a method. If only a ligature of an infected graft is typical finding. The area around the incision is done, the risk of a new infection and postoperative swollen but not tender and red. A clear fluid might bleedings is low, approximately 5%. But at least ooze from the incision. The amount of drained 25% of patients have amputations within 30 days. fluid is generally considerable and the patient If, on the other hand, graft excision and a new often states that the dressing has to be changed vascular reconstruction are performed in situ af- several times a day to keep the area dry and clean. ter local treatment with antibiotics, a new infec- Ultrasound is sometimes required to differentiate tion and serious bleeding will occur in about 30% hematoma from lymphocele. of patients. The amputation risk is only 6% and is substantially less than with graft ligation. Management and Treatment Early mortality in primary aortic graft infec- Surveillance is the best management for most tions is 25% after the surgical treatment, and 20% cases of fluid collections. A majority are absorbed of patients will lose at least one leg. The mortality spontaneously and also when fistulation occurs. for patients with aortoduodenal fistulas is almost Much patience is needed in cases with lymph leak- 50%. Extraanatomical bypass construction before age because the healing process may take several graft excision appears to improve the results con- months. siderably compared with simultaneous extirpation Because seromas and lymphoceles are likely and reconstruction. to increase the risk for infection the literature ad- vocates active exploration and evacuation of all large postoperative fluid collections. A selective 12.6 Local Complications approach is more common, however. This man- agement strategy suggests surgical treatment only 12.6.1 Lymphocele and Seroma for wounds with heavy secretion and those sus- pected to be related to synthetic grafts. The opera- Background and Causes tion includes evacuating the fluid and covering Subcutaneous fluid collections in wounds are the graft with tissue, frequently by applying sev- common postoperatively, especially in the groin. eral rows of absorbable sutures. Old long-lasting When a collection is discovered within 24 h after lymphoceles have a capsule that should be excised the procedure it is usually a hematoma, but when a after ligation of afferent lymph vessels. well-demarcated fluid collection appears later during the first postoperative weeks, it is a seroma or lymphocele. Such swellings are created when degraded blood products and tissue secretions accumulate in the wound – a seroma – or when
  • 157. 12.6 Local Complications 157 12.6.2 Postoperative Leg Swelling 12.6.3 Wound Edge Necrosis Background and Causes Background and CausesAfter successful vascular reconstruction for lower Wound edge necrosis is a complication that affectsextremity ischemia over half of all patients will calf incisions used for distal reconstructions. It issuffer from more or less pronounced swelling of caused by ischemia in the wound edges. Somethe operated leg. Indeed, many vascular surgeons studies indicates that up to 15% of all proceduresargue that this is a reliable sign of a successful op- will be troubled by wound edge necrosis. Risk fac-eration. Patients with severe ischemia are the ones tors are a long operating time, severe ischemia,who will swell the most. The explanation for this and the application of self-retaining retractors thatcomplication is not clear, but a disturbed micro- are too strong. Surgical undermining of the skincirculation, a diffuse venous thrombosis, impaired and subcutaneous tissue during the operation alsolymph drainage, and reperfusion have all been increases the risk.suggested as possible causes. The swelling usuallyincreases successively and reaches its maximum Clinical Presentation2–3 weeks after reconstruction and can be expect- A few days postoperatively a red or bluish discol-ed to last several months. oration of the skin along the wound edges is noted. The discoloration can be partial, but the extent Clinical Presentation usually increases during the following day andBecause the leg is heavy, numb, stiff, and aching, might occasionally engage the entire incision. Thethe patient is usually worried about it. The edema discolored area is slowly transformed into blackis localized to the calf and foot and is apparent at necrosis without displaying signs of infection.physical examination on the 2nd or 3rd postopera- Within a week the necrosis is clearly demarcatedtive day. This usually coincides in time with the against normally perfused and vital skin. Thispatient’s resumption of ambulation. The swelling condition is often combined with a successful re-is most pronounced at the ankle level, but the construction and a swollen leg. It is important toentire leg can be involved. The diagnosis is easy to differentiate this dry necrosis from the more seri-establish, but in some cases a duplex scan is re- ous ischemic necrosis with wound breakdown,quired to differentiate this condition from deep dehiscence, and overt infection that was discussedvenous thrombosis. Duplex scanning is recom- previously in this chapter.mended for the patient who, in addition to theswelling, develops cyanosis or tenderness over the Management and Treatmentcalf muscles or has a severe and inexplicable pain Wound necrosis usually heals by itself throughin the leg. ingrowth of new skin from the wound edges. With time it will cover the entire wound surface. A pre- Management and Treatment requisite for healing is that the necrosis be loos-The leg swelling needs no specific treatment other ened and surgically removed. The healing processthan elevation and patience. This treatment is also might occasionally require several months and,sufficient when the swelling persists longer than in rare cases, a split skin graft when the necrosis2 months after the operation. Other contributing is large. Accordingly, active treatment consists ofcauses, such as cardiac failure, should, of course, superficial wound revision and dressing corrected if possible. Compression stockingswith mild compression could also be tried to re-lieve the symptoms. Mannitol, furosemide, and 12.6.4 Local Nerve Injuriesallopurinol have all been tried with no document-ed effect. An important aspect is to inform the pa- Background and Causestient about the benign nature of this condition. Sensory and motor nerve injuries are common after carotid surgery and occur distal to groin and calf incisions after vascular reconstruction in the leg. The lumbosacral plexus and the main stem of
  • 158. 158 Chapter 12 Complications in Vascular Surgery the femoral nerve can also be injured during aortic eral nerves have a considerable capacity for regen- and iliac vascular surgery. Stripping of the greater eration and the symptoms can be expected to suc- saphenous vein below the knee is also associated cessively decrease up to at least 1 year after the with a high risk for injuries to the saphenous nerve, operation. The same is valid for mainstem inju- which is why distal stripping is avoided nowadays. ries. Patients in whom the pain is considerable The mechanism of injury during all of these pro- should be offered analgesics and possibly also a cedures is usually division or ischemic damage nerve block. secondary to pressure from retractors during the procedure. Occasionally a hematoma can com- press and affect the nerve. Further Reading Adam DJ, Haggart PC, Ludlam CA, et al. Coagulopathy Clinical Presentation and hyperfibrinolysis in ruptured abdominal aortic The patient usually describes a numb and painful aneurysm repair. Ann Vasc Surg 2004; 18(5):572– skin area within the dermatome of the injured 577 nerve. The pain in nerve injuries is burning and Cherry KJ Jr, Roland CF, Pairolero PC, et al. Infected often combined with hyperesthesia. Some exam- femorodistal bypass: is graft removal mandatory? ples of injured nerves and the corresponding skin J Vasc Surg 1992; 15(2):295–303 area affected are listed in Table 12.6. Drews RE. Critical issues in hematology: anemia, thrombocytopenia, coagulopathy, and blood prod- uct transfusions in critically ill patients. Clin Chest Table 12.6. Injured nerves and corresponding symp- Med 2003; 24(4):607–622 tomatic skin areas de Figueiredo LF, Coselli JS. Individual strategies of hemostasis for thoracic aortic surgery. J Card Surg Damaged nerve Symptomatic area 1997; 12(2 Suppl):222–228 Major auricular nerve Skin around the ear lobe Fujitani RM. Revision of the failing vein graft: outcome of secondary operations. Semin Vasc Surg 1993; Branches to the Medial skin of the thigh 6(2):118–129 femoral nerve Kuestner LM, Reilly LM, Jicha DL, et al. Secondary aor- Saphenous nerve Skin medially below the toenteric fistula: contemporary outcome with use of knee and of the foot extraanatomic bypass and infected graft excision. Lumbosacral plexus Unilateral or bilateral J Vasc Surg 1995; 21(2):184–195 motor and sensory deficits Schwartz ML, Veith FJ, Panetta TF, et al. Reoperative in large areas of the legs approaches for failed infrainguinal polytetrafluo- roethylene (PTFE) grafts. Semin Vasc Surg 1994; 7(3):165–172 Taylor SM, Weatherford DA, Langan EM, et al. Out- comes in the management of vascular prosthetic Management and Treatment graft infections confined to the groin: a reappraisal. There is no effective treatment for these types of Ann Vasc Surg 1996; 10(2):117–122 nerve injuries. The patient should be informed Young RM, Cherry KJ Jr, Davis PM, et al. The results that the injury is benign despite its nuisance, and of in situ prosthetic replacement for infected aortic that it might heal and disappear with time. Periph- grafts. Am J Surg 1999; 178(2):136–140
  • 159. Acute Venous Problems 13CONTENTS 13.1 Summary13.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . 159 Thrombolysis is a viable treatment option13.2 Background and Pathogenesis . . . 159 for patients with deep vein thrombosis.13.2.1 Background . . . . . . . . . . . . . . . . . . . . . . . . . 159 Phlegmasia cerulea dolens may require13.2.2 Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . 160 surgical thrombectomy or thrombolysis as13.3 Clinical Presentation . . . . . . . . . . . . . . 160 well as fasciotomy Use of a cava filter when indicated may13.4 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . 161 save patients from pulmonary embolism13.5 Management and Treatment . . . . . 161 Patients with thrombophlebitis extending13.5.1 In the Emergency Department . . . . . 161 into the deep venous system may require sur-13.5.2 Endovascular Treatment . . . . . . . . . . . 162 gical ligation of the greater saphenous vein.13.5.3 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . 16313.5.4 Phlegmasia Cerulea Dolens . . . . . . . . 16313.5.5 Vena Cava Filter Placement . . . . . . . . 16413.5.6 Postoperative Treatment . . . . . . . . . . . 164 13.2 Background and Pathogenesis13.6 Results and Outcome . . . . . . . . . . . . . . 164 13.2.1 Background13.7 Miscellaneous . . . . . . . . . . . . . . . . . . . . . 16513.7.1 Thrombophlebitis . . . . . . . . . . . . . . . . . . 165 The main scope of this chapter is to discuss mis- Further Reading . . . . . . . . . . . . . . . . . . . 165 cellaneous venous problems, mainly thromboem- bolic disease, but not venous injuries. The latter is covered in Part I of this book which focuses on specific regions of the body. As listed in the incidence table below (Table 13.1), venous thrombosis is quite common. TheTable 13.1. Incidence of venous thromboembolism (PE pulmonary embolism, DVT deep vein thrombosis) Country Year assessed Type of disease Population Incidence per age (years) 100,000 persons per year USA 1996 30% PE Adults 90 (California) 70% DVT 15–80 Sweden 1991–2000 59% PE Women 36 41% DVT 15–44 USA 1966–1990 59% PE Adults 117 (Minnesota) 41% DVT (hospital based) Italy Before 2000 19% PE Adults 77 80% DVT (lower limb) 18–65 1% DVT (upper limb)
  • 160. 160 Chapter 13 Acute Venous Problems incidence varies with the population studied and Primary iliac vein thrombosis occurs most increases with age. Hospital-based studies present commonly on the left side where a stenosis fre- a larger proportion of pulmonary embolism (PE), quently is a predisposing factor. whereas community cohorts have more thrombo- sis patients. Manifestations range from a superfi- cial thrombophlebitis or a minor deep venous 13.3 Clinical Presentation thrombosis (DVT) that produces only minute symptoms to a DVT with massive embolism to the Patients with DVT experience pain and leg swell- lungs, threatening the patient’s life. While open ing that often is worse when standing or walking. surgical treatment of venous thromboembolic dis- Some patients also feel warmth and notice that the ease is rarely indicated, it is helpful to have basic leg is red. Patients with caval obstruction have knowledge about diagnosis, pathogenesis, and bilateral symptoms. These examples constitute the anticoagulation treatment. This is important for classic symptoms of DVT, but many patients do differential diagnosis and for the few instances not have any symptoms at all and present with PE when emergency endovascular or open surgical only. Signs of this condition include shortness of treatment is indicated. This chapter will also de- breath and chest pain that may be worsened by scribe the technique for surgical and endovascular deep breaths. Occasionally, patients also report treatment of acute DVT. that they have been coughing up phlegm that may be tinged with blood. Patients with phlegmasia cerulea dolens have 13.2.2 Pathogenesis similar but more severe symptoms. Discoloration is often pronounced. Pedal pulses are usually ab- When DVT occurs, clots have usually formed in sent, and the leg is very tender. Foot gangrene is the small deep veins in the calf. Patients afflicted also noted occasionally. It may therefore be mis- have hypercoagulative disorders, are taking medi- taken for arterial embolism, but misdiagnosis can cations that affect clotting that make them sus- be avoided by remembering that acute arterial ceptible to venous thrombosis, has malignancy or occlusion does not cause edema. has been immobilized for a larger period. The clot Physical examination is only 30% accurate for causes a local inflammation in the venous wall DVT and a poor way to establish the diagnosis. and adjacent tissue that may make the calf tender. The most common finding, however, is localized Because the small veins in the calf are paired, the calf tenderness. Homan’s sign – pain when dorsi- clot does not cause significant venous obstruction flexing the foot with the knee extended – is nei- or distal edema. Flow in the obstructed vein will ther sensitive nor specific and should probably not decrease, however, which increases the risk for be used. Other examination findings are visible continuing clot formation. The clot will then grow superficial collateral veins, pitting edema, and in a proximal direction and continue to obstruct swelling of the entire leg. To be significant, the lat- more veins. Also at this stage distal edema is quite ter should expand the calf circumference by more uncommon because collateral flow is extensive in than 3 cm compared with the other leg. the legs, and significant swelling does not occur Patients with primary iliac vein thrombosis until the common femoral vein is obstructed. At may present with abdominal pain in the lower this level the outflow from the deep femoral, su- quadrant, tenderness over the vascular bundle in perficial, and great saphenous vein is affected. the groin and general swelling of the leg. Continued obstruction, causing near occlusion of Patients with upper limb thrombosis have sim- all the main veins in the leg and pelvis, can lead to ilar symptoms; the most common are arm swell- a dreaded condition called phlegmasia cerulea do- ing and discoloration or pain. lens (discussed later). Any time during this pro- Scoring systems combining clinical findings cess there is also a substantial risk that clots will and medical history have been proposed to in- dislodge from the leg veins, follow the blood flow crease accuracy of the examination. If the exami- to the lungs, and cause PE. nation is positive for more than three of the signs and symptoms described above, up to 75% of the
  • 161. 13.5 Management and Treatment 161patients have evidence of DVT as diagnosed by tals this means starting with duplex scanning toduplex examination. establish the diagnosis. If signs of DVT are pres- ent, it is important to elucidate the extent of thrombosis during the examination. This infor- 13.4 Diagnostics mation is useful in the management process be- cause some patients with femoral vein, iliac vein,All patients, including those considered to have or cava thrombosis may need thrombolysis or evenonly small risk to be suffering from DVT and those a cava filter. When the DVT diagnosis is con-having arm symptoms, should undergo duplex firmed, baseline blood coagulation parameters arescanning or perhaps phlebography. The duplex ex- obtained, and low molecular weight heparin treat-amination includes visualization of the veins, ment is initiated. It is also important to excludeclots, blood flow, and vein compressibility. The other diagnoses that could contribute to thelatter is considered a direct test of DVT because a thrombosis formation. For example, clinical indi-vein with clot cannot be compressed, whereas the cations of an intraabdominal malignancy could bewalls of a healthy vein are very easy to squeeze confirmed or eliminated by computed tomogra-together by pressure with the probe. Lack of blood phy (CT). Both inpatient and outpatient protocolsflow variation with breathing is another sign can then be used for the continued treatment ofsuggesting DVT on duplex examination. Phlebog- the patients. (No further recommendations will beraphy includes cannulating a superficial foot vein given on the medical management of DVT hereand injecting contrast during fluoroscopy to because this book is intended to focus on vascularenable visualization of thrombosed veins. This surgical treatment.)method was the standard diagnostic procedure Few diagnosed patients are candidates forbefore duplex appeared as the primary choice for urgent surgical or endovascular treatment, butestablishing the DVT diagnosis. Today it is used the most common situations when it can be con-mostly when duplex is unavailable in the hospital sidered are listed in Table 13.2. Patients with upperor when it is unable to identify the deep leg veins. limb thrombosis may also benefit from urgent Another test useful for DVT diagnosis is deter- thrombolysis. The same clinical findings listedmining the concentration of the fibrin degrada- in the table are also applicable in patients withtion product D-dimer in the blood. This test has a duplex-verified axillary or subclavian vein throm-sensitivity for DVT of 90% or greater as well as a bosis.negative predictive value of 90% or greater by most If D-dimer is positive and pulmonary symp-studies. Accordingly, a negative D-dimer level (the toms are prominent in the medical history (or thecut-off level depends on the type of assay used) ina symptomatic patient with a clinically suspected Table 13.2. Clinical findings indicating that open sur-diagnosis nearly provides exclusion of DVT. There- gical or endovascular treatment should be consideredfore, it is suitable as a screening test before further in patients with duplex-verified thrombosis into femo-work-up when the diagnosis is not obvious. ral and/or iliac veins Clinical findings Treatment type(s) 13.5 Management and Treatment Young age Thrombolysis Duration of symptoms Thrombolysis 13.5.1 In the Emergency Department <10 days Pronounced symptoms ThrombolysisPatients who complain of unilateral limb swelling Contraindications Cava filter, thrombectomyand pain should be suspected to have DVT and to heparin treatmenthave a blood sample drawn for measuring D-di- Phlegmasia cerulea Thrombolysis,mer. A negative test excludes DVT or PE as the dolens thrombectomy, fasciotomyprimary diagnosis. Patients with a positive D-di- Free-floating thrombus Cava filtermer may suffer from a venous thromboembolic in vena cavadisease and need further work-up. In most hospi-
  • 162. 162 Chapter 13 Acute Venous Problems patient has chest pain or hemoptysis), a CT scan is added to the duplex and laboratory work-up to re- veal signs of PE. Furthermore, if PE is confirmed, evaluation of the heart function by echocardiogra- phy is also valuable. Such patients should also re- ceive oxygen. It must be kept in mind that patients with PE may have a negative D-dimer. If suspicion is strong, the work-up should proceed regardless of the outcome of this test. Urgent thrombolysis may be indicated in patients with massive PE ob- structing more than 50% of the vasculature. Pul- monary edema and hypotension due to right ven- tricular failure are consequences of this, and the only way to save such patients may be to remove as much of the obstruction as possible. a 13.5.2 Endovascular Treatment The purpose of thrombolytic therapy is to reduce the long-term consequences of extensive, particu- larly caval and iliac DVT. Supposedly it restores patency and preserves valve function but long- term randomized studies comparing this therapy with standard anticoagulation have not been car- ried out. It may also reveal obstructions contribut- ing to clot formation. Such stenotic segments may be treated by stenting. Thrombolytic therapy achieves more rapid clot resolution but does not significantly reduce mortality or the risk of recur- rent PE in hemodynamically stable patients. It is also associated with an increased incidence of ma- jor hemorrhage compared with heparin therapy alone. The main contraindications to thromboly- sis are listed in Chapter 10 (p. 128). b Therapy should be administered locally by catheter-directed infusion of the lytic agent into Fig. 13.1. Thrombolysis of iliac vein thrombosis before the clot. Ipsilateral or contralateral groin access is (a) and after therapy (b) commonly used. The latter reduces bleeding com- plications and decreases the risk associated with transversing the thrombus. Thrombus passage in- When the venous system is catheterized, venogra- creases the risk for clot dislodgement and PE. The phy is performed to localize and determine the ipsilateral approach avoids transversing intact distribution of the thrombosis. Treatment proto- valves, but it may be more difficult to puncture cols vary extensively. The first dose of tPA is often and catheterize the groin vein if it is occluded. Du- infused for 30 min, then the venography is repeat- plex-guided puncture could then be tried. Placing ed. If more lysis is needed the infusion is contin- a catheter in the superficial femoral or popliteal ued for 24 h or more. During this time period the veins may be impossible if the valves are intact. A result is checked repeatedly, depending on treat- jugular venous catheterization can be used if the ment progress. The bolus injection mentioned is clot involves the vena cava. It is common to use a not used in some protocols. An example of a veno- side-hole catheter with its tip placed in the clot. gram is shown in Fig. 13.1.
  • 163. 13.5 Management and Treatment 163 13.5.3 Operation 13.5.4 Phlegmasia Cerulea DolensHistorically, surgical thrombectomy has been lib- This serious form of DVT is, as already mentioned,erally used in patients with iliofemoral thrombo- characterized by massive thigh and calf edemasis to reduce the risk of postphlebitic syndrome and a cold, mottled foot. The risk of massive PE isdevelopment. Although several patient series have high, even for patients receiving anticoagulationpresented good results after thrombectomy, ran- therapy. Phlegmasia cerulea dolens often indicatesdomized controlled trials data is less favorable. occult malignancy which must be excluded inOne study reported a similar long-term frequency every patient.of postphlebitic syndrome when comparing the Treatment follows the principles given for DVTprocedure with low molecular weight heparin as outlined above, with the addition of fasciotomytherapy, while others found better preservation of when the arterial component is prominent. Throm-valves and fewer problems after surgery. Consid- bolysis is the primary choice when the arterialering the general surgical risk and postoperative perfusion is rendered adequate – palpable pulsescomplications such as groin infection and bleed- in the ankle arteries or good skin perfusion in theing, it is rarely indicated to perform surgical foot. If the patient lacks foot pulses, surgicalvenous thrombectomy today. It is used mostly in thrombectomy is a better strategy because it is apatients with extensive venous thrombosis who quicker way to reduce clot burden and obstruc-have contraindications for anticoagulation and tion. Long-term venous function is of minor im-lytic therapy. Another indication that remains is portance at this stage. When the arterial functionthrombus extraction in phlegmasia cerulea do- is compromised, fasciotomy should follow the sur-lens. The technique of venous thrombectomy is gical thrombectomy For some patients, amputa-described in the Technical Tips box but can be tion is the only option.quite difficult to perform if the experience ofvascular surgery is limited. TECHNICAL TIPS Venous Thrombectomy Preferably, general anesthesia is used and the pa- tralateral groin could also be used, especially if tient is given an antibiotic that covers common the thrombus is free floating but located only in wound infection bacteria. A groin incision is per- the iliac vein. Next, a rubber bandage is tightly ap- formed right over the common femoral vein, plied around the entire leg from the foot to the which is extended distally over the superficial wound to empty all distal veins from thrombus. femoral vein. These two veins and their branches Distal thrombectomy can also be done but is of- are exposed and banded. The patient is given in- ten difficult because the valves make distal pas- travenous heparin, and a transverse venotomy is sage of the Fogarty catheter impossible. Finally, a performed in the common femoral vein. The an- continuous 5-0 suture closes the venotomy, and esthesiologist is then asked to adjust the ventila- an arteriovenous fistula is created. This is achieved tion to a high positive end pressure to minimize by using a branch from the greater saphenous the risk of PE, while a #7 or #8 Fogarty catheter is vein and performing an anastomosis between its passed proximally into the vena cava and as much end and the common femoral artery. The reason of the clot as possible is extracted. This preventive for this is that the patency of the iliac vein is con- measure is insufficient if the risk for PE is high. If sidered to be better if a higher flow is achieved. It the thrombus protrudes into or involves the vena does require exposure of the artery and its branch- cava, cava filter insertion should precede surgery. es. After control of any remaining bleeding, the A balloon occluding the vena cava from the con- wound is closed.
  • 164. 164 Chapter 13 Acute Venous Problems 13.5.5 Vena Cava Filter Placement Several types of filters are available on the market, and temporary filters can be used when perma- Indications for vena cava filter placement include nent placement is not necessary; one such situa- the following: tion is the last one in the list above. The complica- Recurrent PE despite full anticoagulation tion rate after filter placement is low. Occasionally Proximal DVT and contraindications to full the filter may be dislodged into the right atrium, anticoagulation but insertion site bleeding is more common. The Proximal DVT and major bleeding while on filter can be inserted by either a jugular or femoral full anticoagulation approach. The former is preferred if the CT has Progression of iliofemoral clot despite antico- revealed extensive thrombus in the inferior vena agulation cava. The method for filter placement via the Large free-floating thrombus in the iliac vein femoral vein is briefly described in the Technical or inferior vena cava Tips box. Massive PE in which recurrent emboli may prove fatal Venous thrombectomy (during or after surgery) TECHNICAL TIPS Vena Cava Filter Placement Before the procedure it is sometimes necessary to achieved by introducing a pigtail catheter placed make sure that the iliac veins on the access side higher up. For filter placement, a larger sheath, at and the inferior vena cava are free of thrombus. least 12-French, is placed over a stiff guide wire This is done by cannulating the femoral vein using approximately to the level where the filter is to be the Seldinger technique and inserting a guide placed. The preloaded filter catheter is advanced wire and an introducer sheath. A venogram is to the implant site and released during fluoro- obtained by manual injection of contrast. Diame- scopic monitoring. After the catheter is withdrawn ter estimations and better visualization of the a venogram completes the procedure. vena cava and the renal vein location can be 13.5.6 Postoperative Treatment 13.6 Results and Outcome After thrombolysis or thrombectomy, patients There are several studies in the literature compar- should keep their leg or arm elevated and com- ing thrombolysis and anticoagulation for acute pression stockings are applied. They should be DVT, and meta-analyses suggest that the former is used day and night for at least 2 weeks postopera- more effective for clot lysis and venous patency. tively. Intermittent compression devices increase Furthermore, significantly fewer patients appear venous blood flow and probably improve patency to end up with postthrombotic syndrome when after thrombolysis and thrombectomy. For the treated with thrombolysis as compared with anti- latter, the benefit is supported by clinical stud- coagulation. Accordingly, many patients with ies. Patients should also receive long-term antico- acute iliofemoral DVT should be considered for agulation, initially with low molecular weight thrombolysis. As suspected, however, more bleed- heparin that is substituted for coumadin for at ing complications occur with this treatment strat- least 6 months. If not investigated previously, un- egy, so careful selection of patients is important. derlying coagulation disorders should be consid- Also, surgical thrombectomy appears to be more ered because this would influence the length and effective, than anticoagulation alone. In one study type of treatment this strategy was able to preserve at least half of the
  • 165. 13.7 Miscellaneous 165valves and 80% of occluded iliofemoral segments The treatment consists of analgesics, mobiliza-could be reopened. tion, and sometimes low molecular weight hepa- Few good prospective studies exist on the effi- rin subcutaneously. The latter is indicated if thecacy of vena cava filters for preventing PE, but at patient is unable to walk because of the pain.least one randomized controlled trial clearly veri- Thrombophlebitis localized to the thigh, especial-fied that filters are effective at least in the short ly close to its inflow into the common femoral veinterm. Accordingly, this study suggests that tempo- may be treated by surgical ligation to prevent con-rary filters may be advantageous. tinued thrombosis in the deep veins and PE. It is common, however, to use a duplex scan to find out the distance from the clot to the common femoral 13.7 Miscellaneous vein. Surgical ligation is recommended if this dis- tance is <1 cm. 13.7.1 ThrombophlebitisThrombophlebitis, thrombosis of a superficial Further Readingvein with secondary inflammation insurroundingtissue, is a very common condition. The exact Augustinos P, Ouriel K. Invasive approaches to treat-explanation for its occurrence is unknown, but ment of venous thromboembolism. Circulationcoagulation disturbances or local inflammation 2004; 110(9 Suppl 1):I27–I34 Haage P, Krings T, Schmitz-Rode T. Nontraumaticprobably contribute. Because varicose veins are vascular emergencies: imaging and interven-prone to be damaged by minor trauma and also tion in acute venous occlusion. Eur Radiol 2002;often have a low blood flow, they are at risk for 12(11):2627–6243thrombophlebitis. Patients with malignancy have Juhan CM, Alimi YS, Barthelemy PJ, et al. Late resultsan increased risk for this condition and if there of iliofemoral venous thrombectomy. J Vasc Surgare no apparent causes – a known coagulation dis- 1997; 25(3):417–422order or trauma – patients should be worked up to Plate G, Eklof B, Norgren L, et al. Venous thrombecto- my for iliofemoral vein thrombosis – 10 year resultsrule out other diseases or coagulation problems. of a prospective randomised study. Eur J Vasc Endo- The patient experiences pain in the extremity, vasc Surg 1997; 14(5):367–374which is quite severe and is localized along a su- Sharafuddin MJ, Sun S, Hoballah JJ, et al. Endovascularperficial vein. The skin feels tender and hot. The management of venous thrombotic and occlusivephysical examination is usually sufficient to reveal diseases of the lower extremities. J Vasc Interv Ra-the location of the thrombophlebitis as well as diol 2003; 14(4):405–423its distribution. Because thrombophlebitis in leg Watson LI, Armon MP. Thrombolysis for acute deepveins may spread to the deep system and cause vein thrombosis. Cochrane Database Syst Rev 2004; 4:CD002783DVT and even PE, it is important to find outwhether it extends into deeper veins. In the litera-ture this happens in around 10% of the cases. Ifone is in doubt, duplex scanning is recommended.
  • 166. Acute Problems with Vascular Dialysis Access 14CONTENTS 14.1 Summary14.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . 167 Infections in dialysis-access fistulas can14.2 Background . . . . . . . . . . . . . . . . . . . . . . . . 167 cause erosion and lethal bleedings.14.3 Pathophysiology . . . . . . . . . . . . . . . . . . 168 Infections in dialysis accesses should not14.3.1 Occlusion and Thrombosis . . . . . . . . . 168 be debrided in the emergency department.14.3.2 Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . 168 The urgency of revision of an occluded ac-14.3.3 Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . 169 cess depends on the patient’s need for di-14.3.4 Aneurysms and Hematomas . . . . . . . 169 alysis and on available alternative dialysis14.3.5 Steal and Arterial Insufficiency . . . . . 169 options. Steal symptoms should be worked up ur-14.4 Clinical Presentation . . . . . . . . . . . . . . 170 gently and treated expeditiously.14.4.1 Occlusions and Thrombosis . . . . . . . . 17014.4.2 Other Complications . . . . . . . . . . . . . . . 17114.5 Diagnostics . . . . . . . . . . . . . . . . . . . . . . . . 17114.6 Management and Treatment . . . . . 172 14.2 Background14.6.1 Occlusion and Thrombosis . . . . . . . . . 17214.6.1.1 In the Emergency Department . . . . . 172 A prerequisite for providing hemodialysis to a pa- Operation . . . . . . . . . . . . . . . . . . . . . . . . . . 172 tient with chronic renal insufficiency is access to a14.6.1.3 Thrombolysis . . . . . . . . . . . . . . . . . . . . . . . 173 vessel with a good diameter for allowing easy14.6.2 Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . 173 puncture with the large-bore dialysis needles, thus14.6.2.1 In the Emergency Department . . . . . 173 achieving high-volume flow and effective dialysis. Operation . . . . . . . . . . . . . . . . . . . . . . . . . . 174 This is accomplished by performing vascular ac-14.6.3 Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . 174 cess procedures. Two main types of surgically cre- In the Emergency Department . . . . . 174 ated accesses for hemodialysis exist: autologous14.6.3.2 Operation . . . . . . . . . . . . . . . . . . . . . . . . . . 174 arteriovenous (AV) fistulas, usually done at the14.6.4 Aneurysms and Hematomas . . . . . . . 175 wrist, and “bridging fistulas” made when a syn- In the Emergency Department . . . . . 175 thetic ePTFE (expanded polytetrafluoroethylene) Operation . . . . . . . . . . . . . . . . . . . . . . . . . . 175 vascular graft is used as a bridge between an ar-14.6.4 Arterial Insufficiency and Steal . . . . . 175 tery and a vein. This latter type will be called an14.6.4.1 In the Emergency Department . . . . . 175 AV graft in this chapter. A common type of bridg- Operation . . . . . . . . . . . . . . . . . . . . . . . . . . 175 ing fistula is the so-called loop graft, which is tun-14.6.5 Management After Treatment . . . . . 175 neled as a loop down the palmar aspect of the fore-14.6.6 When Can the Patient arm, with its inflow and outflow anastomoses in be Given Dialysis? . . . . . . . . . . . . . . . . . . . 176 the cubital fossa (Fig.14.1). Straight AV grafts with the inflow at the wrist and outflow in the cubital14.7 Results and Outcome . . . . . . . . . . . . . . 176 fossa or in the upper arm are also common. AV Further Reading . . . . . . . . . . . . . . . . . . . 177 fistulas in the upper arm can be created either by keeping the cephalic vein at its location or by su- perficial transposition of the brachial vein to the
  • 167. 168 Chapter 14 Acute Problems with Vascular Dialysis Access Fig. 14.1. Example of an arterio- venous “loop graft” volar side of the upper arm. Both alternatives con- 14.3.1 Occlusion and Thrombosis stitute an end-to-side anastomosis to the brachial artery in the cubital fossa. Complications with Early occlusions, up to 4 weeks after access con- vascular accesses are a significant problem and struction, are usually caused by poor preoperative cause morbidity as well as mortality in an already conditions or technical errors at surgery. It is also severely ill group of patients. The high frequency common, that an AV fistula never develops and of complications is reflected in studies from the matures. This situation can be difficult to differ- United States that report at least one urgent reop- entiate from early thrombosis. Retrospective stud- eration for every third primary operation. ies report that 10–25% of all AV fistulas at the Large numbers of patients need hemodialysis wrist level fail to mature. today. In Sweden, for instance, more than 600 pa- Late occlusion is caused by a combination of tients yearly or at least two patients daily will seek many factors. Dehydration and episodes of hypo- medical attention because of more or less acute tension, for example, contribute but are only oc- problems with their dialysis accesses. The majori- casionally the main reason for an occlusion. The ty will go to hospitals with an established dialysis significance of stenosis as the cause for occlusion department and experience managing these com- increases over time. Irrespective of access type, plications, but some will be admitted at other in- stenoses are usually localized in the outflow vein stitutions for problems related to their dialysis 1–2 cm from the anastomosis. Initially the stenosis accesses. causes a resistance against the flow, which de- Therefore, it is important that most physicians creases it further, and when a critical level is and surgeons are able to recognize complications reached the access occludes. Occurrence of multi- that need urgent management. The aim of this ple stenoses is common for both types of accesses. chapter is to provide a basis for such judgment and In AV grafts stenoses are formed both in anasto- to give management recommendations. motic areas and at old puncture sites along the graft itself. The possibilities of a successful throm- bectomy are small in late graft occlusions because 14.3 Pathophysiology the risk for multiple stenoses increases with time of usage. Thrombotic occlusion in more proximal The most important acute complications occur- segments of the outflow vein, for example at an ring in dialysis accesses and leading to hospital axillary level, also occurs in a number of cases. admission are occlusion, infection, bleeding, local swellings, and arterial insufficiency in the hand distal to the access. All complications can occur 14.3.2 Infection early after the primary operation or after several years of dialysis. Swelling is usually caused by Between 11% and 35% of all AV grafts will end up pseudoaneurysms, hematomas, or seromas. The with an infectious complication. Postoperative diagnostic work-up of these complications is in wound infection after access construction belongs most cases simple, but their management is more to this category and is sometimes related to insuf- difficult. For this reason, the complications will be ficient skin suturing. Despite intensive antibiotic discussed below under separate headings. treatment such infections may spread and form an
  • 168. 14.3 Pathophysiology 169abscess around the anastomosis. In AV fistulas, NOTEinfections, other than postoperative ones, are rare; Bleeding in well-functioning AV fistulas isthe total infection rate is only 3%. Also, they are often severe due to the high blood flow inoften benign and can be treated with antibiotics the access.only. For both access types the infection mighterode the walls of the artery or vein with seriousbleeding or pseudoaneurysm formation as a con- 14.3.4 Aneurysms and Hematomassequence. Even if infections can be fulminant and lead to The reason why some AV fistula veins continuesepticemia and mortality, chronic infections with to develop over time to become a true aneurysma more insidious course and mild clinical symp- is unknown, but the magnitude of blood flowtoms are more common. AV grafts are sometimes through the access as well as vein quality contrib-contaminated at puncture, which causes an infec- ute. Pseudoaneurysms are common in synthetiction with few symptoms and a good prognosis. grafts, secondary to puncture. The frequency isHematoma development after puncture increases related to the number of punctures in the graft.the risk for such infections. They may then be The incidence is reported to be 10% for AV grafts,more aggressive, often involving the entire graft while only 2% of AV fistulas are at risk for thiswith several local abscesses developing along it. complication. As previously mentioned, infection The most common organism found in positive is another important cause of pseudoaneurysmcultures from access infections is Staphylococcus formation that often is located in anastomoticaureus, but streptococci and Gram-negative bacte- areas.ria are also common. The latter two cause more Hematomas are caused by puncture and areserious infections than Staphylococcus aureus usually absorbed within a couple of weeks. Occa-does. sionally a swelling will persist at the hematoma site for a long time. Such swellings consist of fibro- sis and serous fluid. Rarely, hematomas become so 14.3.3 Bleeding large that they need surgical treatment.Bleeding from an AV fistula or graft can occurafter trauma or incorrect puncture. A proper tech- 14.3.5 Steal and Arterial Insufficiencynique at puncture is consequently important toavoid unnecessary defects in the graft wall. Even Steal implies that the blood flow in the graft orsmall holes in the fistula vein bleed profusely be- fistula is so large that it reduces perfusion to thecause of the high flow in the access. It occasionally tissue distal to the fistula. All AV fistulas andexceeds 400 ml/min for wrist fistulas and even grafts cause some degree of steal (Fig. 14.2), buthigher in the upper arm. Infection may also, as rarely to an extent that symptoms of arterial insuf-already mentioned, lead to disastrous hemorrhage. ficiency in the hand develop. The frequency ofThis is the rationale for a liberal approach to admit symptomatic arterial insufficiency due to steal isthe patient for observation when infection in a 1–2% for AV fistulas and 5–6% for AV grafts con-dialysis access is suspected. Furthermore, the skin structed on the forearm. For accesses in the uppercovering a dilated vein of an AV fistula is often arm the frequency is even higher. Patients withthin and does not contain bleeding well. Patients diabetes have an increased risk for arterial insuf-with uremia also have a multifactorial disturbance ficiency caused by steal.of the coagulation cascade that increases the riskfor severe bleeding.
  • 169. 170 Chapter 14 Acute Problems with Vascular Dialysis Access Fig. 14.2. Principle of “steal” in an arteriovenous fistula placed in the wrist Table 14.1. Medical history in dialysis access occlusion History Cause Management High resistance during dialysis Outflow vein stenosis Revision “Arterial suction” during dialysis Inflow artery stenosis Revision Puncture difficulties Impaired access flow Revision (stenosis in the artery) Recently constructed access Misjudgment or technical error during Revision (<4 weeks) operation Dehydration Systemic causes (e.g., gastroenteritis) Thrombectomy Episodes of hypotension Systemic cause (e.g., medication) Thrombectomy or thrombolysis in association with dialysis Swollen and discolored hand Thrombosis/stenosis more proximally New access in the other arm; and arm in an outflow vein (e.g., external fistula thrombolysis and angioplasty compression during sleep) of stenosis 14.4 Clinical Presentation 14.4.1 Occlusions and Thrombosis Diagnosis of access complications is usually sim- The medical history and physical examination are ple. Patients often acquire good knowledge over helpful for verifying an occlusion. Some examples time about their accesses and are generally well from the medical history suggesting different aware of problems. Furthermore, during dialysis causes for graft occlusion are summarized in Table two or three times every week the function is 14.1. evaluated and the fistula examined by nurses. In AV grafts the function is evaluated by palpa- Therefore, the patient is usually admitted with an tion of a thrill and auscultation of bruits over the already established diagnosis. The surgeon’s task outflow vein. The thrill feels like a vibration in the is then to verify the diagnosis and prepare for fingers. If a thrill is noted and there is an audible treatment. bruit, the graft is patent. The direction of flow is sometimes hard to determine in AV grafts. Usu- ally the arterial anastomosis is located on the ulnar side, and the flow is directed in a loop down in the forearm with the venous limb on the radial side (Fig. 14.1). The direction of flow may, however, be the opposite. A simple way to check the flow direc-
  • 170. 14.5 Diagnostics 171tion is to occlude the graft at the tip of the loop symptoms should be included. It is also importantwith a finger and palpate for pulsation over the to note signs of infection during the examinationlimbs of the loop. These are then felt only in the of swellings and hematomas. A pulsating massarterial limb. indicates presence of an aneurysm. If such a pul- If the access is new and the arm is swollen pul- sating mass is located in the anastomotic area,sations can be difficult to find. AV grafts may the aneurysm probably originates from the suturetherefore be patent despite the inability to find a line.pulse. On the other hand, the graft can be occlud- Patients with steal complain about pain, numb-ed and still have a palpable pulse due to trans- ness, coldness, and weakness in the hand distalmission of the pulsation into the thrombus. If, to the access. The symptoms are often accentuatedin a previously well-functioning graft, there are during dialysis. As for atherosclerotic arm isch-neither bruit, thrill, nor pulsations it is occluded. emia, the patient may have aggravated symptoms The examination and evaluation of AV fistulas when using the hand in an elevated position. Thesuspected to be occluded is identical and consists examination may reveal necrotic tips of the fin-of palpation and auscultation of the outflow vein gers, pallor, and cyanosis, and only a weak radialin search of a thrill and bruit. Pulsations are easier pulse is palpated. Sometimes the pulse is totallyto evaluate in AV fistulas than in AV grafts. AV absent.fistulas can be pulseless and still work well whenthey are less than 2–3 weeks old. When they have NOTEbeen used for a while they are easy to examine Steal may cause severe ischemic problemsbecause of the increased vein size. The occurrence and should be worked up and treatedof new pulsations in an old fistula indicates a mi- promptly.nor outflow obstruction. Total absence of pulses ina vein with previous pulsations strongly indicatesocclusion. One alternative for evaluating the pa- 14.5 Diagnosticstency of an AV fistula is to carefully compressthe outflow vein somewhat in the cubital fossa or Only a few cases of access complications needaxilla (for upper arm fistulas) and then search for immediate treatment. These urgent cases need nopulsations. diagnostic work-up besides the medical history and a physical examination. The cornerstone of the work-up of dialysis access complications is 14.4.2 Other Complications otherwise duplex scanning. Diagnoses of aneu- rysms and hematomas as well as evaluation of stealThe clinical presentation of access infections is and arterial insufficiency generally require du-in line with infectious complications in general, plex. Duplex also provides sufficient informationand the patient describes pain, tenderness, fever, for treatment planning. There is no urgency inand drainage of pus. The severity of the infection working up these complications, and there isshould also be assessed because it leads manage- always time for a duplex investigation. For symp-ment. Serious infection is associated with septice- tomatic steal, angiography is used by some as themia and bleeding and may need urgent manage- first choice because of its capability to provide ament, whereas mild infections can be observed. view of the retrograde and collateral blood flow. InEarly after surgery for AV graft construction the AV graft and fistula thrombosis, diagnostic work-skin may be red and the surgical area swollen. up is rarely necessary. Accesses with poor func-Such findings in the examination suggest a reac- tion are best treated before they occlude. Accord-tion to the graft material, and it usually dissolves ingly, if a problematic access is still patent whenwithin 3–4 days. It is important to also evaluate examined, duplex should be performed liberally asthe function of the fistula and graft because infec- soon as possible to localize stenoses and provide ation may cause and be a consequence of occlusion. revision strategy. Angiography is an alternative ifWhen taking a medical history from a patient with duplex is not available.a bleeding complication, questions about infection
  • 171. 172 Chapter 14 Acute Problems with Vascular Dialysis Access 14.6 Management and Treatment TECHNICAL TIPS Thrombectomy in an AV Fistula 14.6.1 Occlusion and Thrombosis In the Emergency Department Local or regional anesthesia of the axillary plexus Acute occlusion of a hemodialysis access is not a is preferred, but if an increased risk of bleeding vascular emergency. The only possible exception is reported, it should be avoided. Protection to this principle is when a recently created AV masks and double gloves should be used because fistula occludes. After just 6–8 h the thrombus de- of the hepatitis risk. Scrub and drape the entire stroys the intima of the vein and the access cannot arm. For correction of AV fistulas, a longitudinal be salvaged. Accordingly, recent occlusions may incision at least 5 cm long over the outflow vein is be treated by thrombectomy and revision. For recommended. The distal end of the incision occlusions of longer duration little can be done to should be placed at the level of the anastomosis. save the fistula and the main concern is the pa- The fistula is exposed by sharp dissection and a tient’s uremia and urgency of dialysis. As soon as vessel loop is applied. At this stage the fistula is possible a strategy for continued access and dialy- checked again for patency by palpation or a pen sis should be formed in collaboration with the Doppler. The vein is then inspected for the pres- nephrologist. The following questions need to be ence of stenoses, which are seen as a narrowing considered to decide whether thrombectomy or combined with a poststenotic dilatation (Fig. thrombolysis should be attempted: 14.3). The stenotic area can also be palpated as a Has this access had previous problems and been segment with a thick and hard vessel wall. A trans- revised before? verse incision is made in the vein as close to the What is the chance that the access can be used anastomosis as possible. Thrombectomy in the for dialysis after thrombectomy and revision? outflow vein is performed first in a proximal di- Which alternative access routes are available? rection toward the upper arm using a #3 Fogarty catheter until no further thrombus material comes If the access has had problems and been revised out through the venotomy. If backflow is restored, previously and there is little chance that dialysis vein function is checked once more by rapidly can be continued it is often better to consider the infusing heparinized Ringer’s glucose solution. alternatives to thrombectomy. When few access Infusion of 20 ml should be easily done within possibilities are available it is reasonable to be 20–30 s with no resistance. If a large force is more aggressive with thrombectomy attempts. required, remaining thrombus or stenoses in AV grafts, on the other hand, can more often be the outflow or axillary vein is probable. The best saved by thrombectomy or thrombolysis. We rec- way to verify this is to perform an intraoperative ommend doing the operation as soon as possible, angiography and this is recommended when but not during nighttime. Thrombolysis is a good there is any uncertainty about the results. When alternative for AV graft occlusions. venous outflow is restored, the vein is clamped with a small soft vascular clamp such as a mini- Operation bulldog. At this stage systemic heparinization is A surgeon without experience in access surgery is considered; the recommended dose is half the almost never forced to perform an operation with- normal dose of 50–75 units heparin per kilogram out being able to wait for assistance. The only pos- of body weight. The next step is to insert the same sible exception to this is thrombectomy. Therefore, thrombectomy catheter toward the inflow anas- in this text only this procedure will be described tomosis and into the artery. One pull with the in detail and other operations will be discussed in catheter is usually enough to obtain a strong pul- more general terms. The technique is described in sating inflow. Finally, the vessel is clamped and the Technical Tips box. It must be remembered, the venotomy closed with interrupted 6-0 or however, that simple thrombectomy as the only 7-0 prolene sutures. The result is evaluated by procedure is rarely successful; it is primarily rec- palpating the vein and auscultating with a pen ommended in cases when an anatomical cause for Doppler. If the pulse and Doppler signals are the occlusion has been ruled out. It usually has to weak, it is necessary to continue the operation be combined with some kind of revision. with revision of the access.
  • 172. 14.6 Management and Treatment 173 Fig. 14.3. Stenosis in an arteriove- nous fistula AV grafts ThrombolysisThe technique for thrombectomy of thrombosed Thrombolysis is an alternative to thrombectomy. ItAV grafts and fistulas is the same. Synthetic grafts has the advantage of avoiding surgery and generalare more prone to infection and antibiotic prophy- anesthesia, and central stenoses contributing tolaxis is recommended. The easiest way to expose access occlusion can be corrected by angioplasty.the graft is at the tip of the loop or in the midpor- Such proximal lesions are harder to treat by opention of a straight graft. It is better to make the skin surgery. It is a matter of debate whether throm-incision parallel and lateral to the graft then over bolysis should be performed instead of thromb-it. A transverse incision increases the risk of inci- ectomy and revision. Patients with contraindi-sion complications such as tissue necrosis and cations to thrombolysis are not candidates, butgraft infection. Alternatively, the incision can be for other groups the literature is contradictory.placed in the old scar from the primary operation Thrombolysis is certainly feasible, but recent dataover the venous anastomosis. This is favorable suggest a slight advantage for the open procedurewhen there is a history of malfunction that sug- in terms of outcome. In some hospitals, thrombol-gests a possible outflow stenosis. The dissection to ysis is attempted with a few days’ delay to reduceexpose AV grafts is sometimes cumbersome be- the risk of bleeding after a failed thrombectomy.cause of the extensive fibrosis that evolves after The thrombolytic procedure of AV grafts usu-implantation. Careless dissection can create holes ally involves catheterizing the graft where it is easyin the graft that will cause problems when flow is to puncture. For loop grafts the tip is one such site.restored. An example is extensive pulling of the A guide wire is introduced into the venous limbgraft to facilitate dissection. Bleeding from holes first, which is then substituted for a pulse sprayin the graft some distance from the skin incision is catheter via a 4-French dilator. The tip should ini-best controlled by a #4 Fogarty catheter inflated tially be placed well into the outflow vein to enableand closed with a three-way stopcock. The graft venography to rule out central stenoses. After theshould be controlled using a molded vascular tip is placed within the thrombus, a separate punc-clamp to avoid mechanical damage to the graft. ture is performed to catheterize the arterial limbOtherwise, the description in the Technical Tips in a similar way. After local heparinization throm-box for thrombectomy of AV fistulas is also valid bolysis is initiated through both catheters. Throm-for AV grafts. bolysis of AV fistulas is more difficult and the outcome cumbersome. Entrance to a fistulas is Revision achieved as close as possible to the anastomosisThe purpose of revision is to correct the problem and a venogram is obtained to visualize thethat has caused the occlusion of the access or branches of the open vein. An end-hole catheter isthreatens its function. Stenosed segments in an often used and the bolus injection omitted.AV fistula or graft are replaced with a vein orPTFE interposition graft. Patching of the stenosedarea enlarges an anastomosis that is stenosed. 14.6.2 InfectionsSometimes both interposition grafting and patchrepair need to be done. Alternatives at revision are In the Emergency Departmentto move the outflow anastomosis to a more proxi- Patients with suspected access-area infectionsmal location on the same vein or switch it to a should be admitted for observation unless thedifferent outflow vein. clinical presentation indicates a localized mild
  • 173. 174 Chapter 14 Acute Problems with Vascular Dialysis Access infection. Wounds should not be debrided in the interposition of a new piece of graft tunneled emergency department because it might cause through an area without infection. profuse bleeding. Instead, the wound should be An infected AV fistula is ligated on the inflow cleansed and dressed with pads containing an side at least 1 cm away from the infected area to antiseptic solution, and antibiotics covering Staph- avoid bleeding. A new access should not be con- ylococcus aureus should be prescribed. Before an- structed until the infection is completely healed. tibiotics are administered samples for microbio- logical culture should be gathered. If possible, the arm should be kept elevated to decrease swelling. 14.6.3 Bleeding When more severe infection is suspected, par- enteral antibiotics are recommended. If a local in- In the Emergency Department fection of an AV graft is complicated by septicemia As for all major bleeding, the wound should be the graft must be extirpated immediately. A pa- manually compressed immediately. If bleeding tient with septicemia on dialysis without signs of continues and is profuse the patient should be infection over the access can be treated with taken to the operating room for exploration and antibiotics for a couple of days before extirpation control. When finger compression is insufficient is considered. to control the bleeding, a tourniquet can be used. It is placed in the upper arm and inflated to a pres- Operation sure 50 mmHg over the systolic blood pressure. AV graft removal under local anesthesia should be To avoid damage to the skin the cuff should be avoided because exposure of the entire anastomot- padded. As soon as the bleeding site is surgically ic area is necessary, and sufficient analgesia is hard exposed and controlled the tourniquet is deflated. to achieve in infectious tissue. The skin incision is In cases of major bleeding an intravenous line is placed in the old scar from the primary operation. placed for blood sampling and volume replace- Occasionally, the graft is not incorporated and ment. surrounded with pus and fluid and can easily For minor bleedings, such as from a puncture be pulled out of its subcutaneous channel. Further site, the patient is admitted for continuing com- incisions along the graft are often needed to ex- pression and monitoring. Digital compression is pose and enable excision of the entire graft. Graft maintained for 20–30 min because it enables ade- extirpation necessitates control of all inflow and quate compression without obstructing the graft outflow vessels with vascular clamps. After the or fistula flow. If the bleeding has stopped after total graft is removed the arteriotomy is closed this time, digital compression can be substituted using an autologous vein patch. Direct suture of with a compression bandage. If bleeding continues the arterial defect should be avoided because of despite several hours of compression, the patient risk for arterial narrowing and tension in the should be worked up for a potential coagulation suture line, thus increasing the risk for continued disorder. Pharmacological treatment should be infection and bleeding. The vein can be ligated. started after considering the risk of graft throm- The brachial artery may also be ligated when the bosis. Surgical repair of minor hemorrhage should dissection to expose the arterial anastomosis is be avoided as much as possible. Rarely the source very difficult. Usually the collateral circulation is is surgical, and control and repair often necessi- sufficient. In such difficult situations an alterna- tate a fairly extensive procedure. tive when the graft is well incorporated in the area around the arterial anastomosis, is to leave a Operation 5-mm-long cuff and oversew it. This is, however, The basic principle for surgical repair of bleeding associated with a much higher risk for continued from holes in AV grafts and fistulas is to obtain infection and reoperation. During surgery sam- proximal and distal control through incisions in ples for microbiological cultures are obtained intact skin and excise and replace the injured seg- from pus or fluid in the graft tunnel. If the infec- ment with an interposition graft. This is favored tion appears to be very local, as when contami- over suturing the hole with or without a patch. nated by puncture, the access may be saved by The latter is more difficult and often causes a
  • 174. 14.6 Management and Treatment 175narrowing and increases the risk of postoperative 14.6.4 Arterial Insufficiency and Stealthrombosis. For large amounts of bleeding, theprocedure can be performed in a bloodless field In the Emergency Departmentobtained by tourniquet occlusion. Arterial insufficiency secondary to steal is not managed urgently. Diagnostic work-up with du- plex or angiography is usually necessary to plan an 14.6.4 Aneurysms and Hematomas adequate treatment strategy. Administration of analgesics should be initiated as soon as possible, In the Emergency Department and opioids are often required. Even in patientsPatients with a thin skin layer covering a clinically with severe ischemic symptoms, ligature of graftssuspected aneurysm are at risk for fistula rupture. or fistulas can be performed during office hours.These aneurysms should therefore be subject to Occasional patients with therapy-resistant painsurgical excision. Urgent management is particu- might need urgent surgery.larly important when there are signs of infectionbecause such aneurysms may cause septic emboli- Operationzation in addition to severe bleeding. The patient In patients with severe symptoms of hand ischemianeeds urgent work-up with duplex scanning to the AV fistula or graft must be closed. This isdifferentiate such infected aneurysms from other achieved by exposing the vein in the anastomoticfluid collections that do not need urgent manage- area and clamping the artery. The vein is thenment. divided and closed by sutures 1 or 2 cm from the Hematomas that not are infected are best left to anastomosis. Upper arm AV fistulas are treated thereabsorb. Exceptions are hematomas that com- same way. Attempts to reduce blood flow at thispress the access and might impair its flow. Duplex level by wrapping a vein or synthetic patch aroundis helpful for evaluating whether this is the case. the fistula have anecdotally been successful. Occa-If the hematoma is expanding rapidly, within a sionally, work-up of arterial insufficiency causedcouple of hours, blood flow in the access is almost by AV fistulas in the wrist reveals retrograde flowalways threatened. Such expansion is usually in the hand. These patients can sometimes be im-caused by graft laceration and should be immedi- proved by simply transforming the anastomosisately repaired. Old and stable hematomas can, as from side-by-side to end-by-side. Usually, however,an alternative, be treated by puncture and aspira- ligation of the entire fistula is required.tion if the function of the access is at risk. To avoid AV grafts causing steal are excised as describedinfection the puncture should be performed as far in the section on infection, but the access may beaway from the graft as possible. saved by using a different technique. It constitutes a bypass from the brachial artery above the inflow Operation anastomosis to a level below it. The bypass is thenTrue aneurysms with an overlying skin defect in followed by ligature of the brachial artery just dis-AV fistulas are excised after proximal and distal tal to the proximal bypass anastomosis. With thiscontrol. Venous interposition grafting repairs the method relief of ischemic symptoms with main-defect. Surgical treatment of pseudoaneurysms in tained access function has been reported.AV grafts also requires control proximal and dis-tal to the aneurysm. The aneurysm is then openedand the connection between the sac and graft 14.6.5 Management After Treatmentlumen is oversewn. Resection and interpositionof a new piece of graft is often required, however. The principles for management after treatment areIn the anastomotic area, pseudoaneurysms are similar for all complication types. Surgical woundsbest excised and the defect repaired with a patch. should be inspected frequently during the firstA hematoma threatening the graft’s function is 24 h. Bleeding problems are common after throm-treated the same way as aneurysms. bectomy and revision as well as after procedures for infection and steal. Function is also monitored closely. Patency is checked by auscultating for
  • 175. 176 Chapter 14 Acute Problems with Vascular Dialysis Access bruits and palpating for thrills over the outflow Table 14.2. Location of stenosis in 357 arteriovenous vein. After AV graft procedures, the vein is in- graftsa (based on four studies) sonated at the vein and graft anastomosis site. Localization Frequency It is important to ensure that the patient is hy- drated and has an acceptable blood pressure. This Venous anastomosis 63% is often a difficult task in uremic patients. If a ste- In vein away from the anastomosis 18% nosis is suspected in the access but is not mended In inflow artery 10% for some reason, a duplex scan is ordered as soon In graft 12% as possible to verify and localize it before the access In a central vein 1% reoccludes. Postoperative heparinization beyond a 36% had more than one localization the dialysis treatment is rarely needed. Patients treated for infection should continue on antibiot- ics until the results of bacterial cultures arrive or the infection is healed. tulas are preferred over AV grafts. The reason is that if an AV fistula develops – which about 75% does – it will probably work well for many years 14.6.6 When Can the Patient with few complications. Compared with AV grafts be Given Dialysis? stenoses in the outflow vein develop later in AV fistulas;the mean difference is in the range of For all problems with dialysis accesses an impor- 4–5 months. AV grafts, however, have the advan- tant issue is the patient’s need for dialysis. Insert- tage of early dialysis, and at least 70% of all grafts ing a temporary catheter in the neck or groin are patent one year after implantation. Later AV should be weighed against the possibility of a suc- grafts are prone to develop stenoses and infection cessful operation. A basic rule is that a revised di- complicates this type of access in much higher alysis access should be allowed at least a couple of frequencies. The locations of stenoses in AV grafts days to heal after the procedure to avoid bleeding are listed in Table 14.2. complications. Dialysis requires heparinization, The result of thrombectomy for treatment ac- which in combination with uremic patients’ ten- cess occlusion is poor. For example, one study dency for coagulopathy increases the risk for evaluating AV grafts reported a 75% immediate bleeding. During dialysis clots in the suture line success, but the 30-day patency was 45%. At are dissolved and bleeding is likely. Such bleeding 6 months only 18% of the grafts could be used for is often difficult to treat. Moreover, interposed dialysis and at 1 year only 3% could. A contribut- vein grafts have thin walls and are easy to damage ing factor to these results is probably that some during puncture. Vein grafts needs at least 10–14 stenoses are missed at thrombectomy and are not days to be arterialized, and PTFE grafts should be corrected. This is supported in the literature, incorporated in surrounding tissue to minimize which reports that half of all occluded AV grafts the risk for bleeding. Accordingly, if the need for have no identifiable cause of occlusion. When dialysis is urgent and the risk of surgical bleeding angiography was performed in the same patient after revision is considered small, dialysis can be group, 92% had at least one stenosis. When throm- performed the first postoperative day providing bectomy was combined with revision the results that the puncture can be made in an old part of the were somewhat better: 60% of the grafts were access and that the heparin dose during dialysis is patent after 30 days and 25% at 6 months. In adjusted. most studies, multiple revisions are often needed to achieve acceptable results. Only a few AV fistu- las can be saved by thrombectomy according to 14.7 Results and Outcome the literature, which is why this operation should not be performed often. It is generally better to In Sweden AV fistulas constitute about 80% of create a new access if the occlusion lasts longer all dialysis accesses constructed. This percentage than 8 h and when the fistula occludes early after varies internationally, but the trend is that AV fis- construction.
  • 176. Further Reading 177 Further Reading Huber TS, Buhler AG, Seeger JM. Evidence-based data for the hemodialysis access surgeon. Semin DialBush RL, Lin PH, Lumsden AB. Management of throm- 2004; 17(3):217–223 bosed dialysis access: thrombectomy versus throm- Lew SQ, Kaveh K. Dialysis access related infections. bolysis. Semin Vasc Surg 2004; 17(1):32–39 ASAIO J 2000; 46(6):S6–S12Green LD, Lee DS, Kucey DS. A metaanalysis compar- Schanzer H, Eisenberg D. Management of steal syn- ing surgical thrombectomy, mechanical throm- drome resulting from dialysis access. Semin Vasc bectomy, and pharmacomechanical thrombolysis Surg 2004; 17(1):45–49 for thrombosed dialysis grafts. J Vasc Surg 2002; Tordoir JH, Dammers R, van der Sande FM. Upper ex- 36(5):939–945 tremity ischemia and hemodialysis vascular access. Eur J Vasc Endovasc Surg 2004; 27(1):1–5
  • 177. General Principles of Vascular Surgical Technique 15CONTENTS 15.1 Summary15.1 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . 179 Always use atraumatic technique and spe-15.2 Background . . . . . . . . . . . . . . . . . . . . . . . . 179 cial vascular instruments.15.3 Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . 180 For proximal and distal control, all inflow and outflow vessels must be controlled and15.4 Control of Bleeding clamped prior to repair or arteriotomy or and Clamping . . . . . . . . . . . . . . . . . . . . . . 180 venotomy.15.4.1 Proximal Endovascular Blind application of vascular clamps in a Aortic Control . . . . . . . . . . . . . . . . . . . . . . 182 bleeding traumatic wound as dangerous.15.5 Vascular Suture . . . . . . . . . . . . . . . . . . . . 182 A nonsecure distal intimal edge is always a15.5.1 Choice of Suture Material . . . . . . . . . . 184 risk for dissection and creation of an inti-15.6 Arteriotomy . . . . . . . . . . . . . . . . . . . . . . . . 184 mal flap causing occlusion. Veins are vulnerable and extreme care is15.7 Closure with Patch necessary during dissection and repair. (Patch Angioplasty) . . . . . . . . . . . . . . . . 184 A vascular suture should always be tied15.8 Interposition Graft . . . . . . . . . . . . . . . . 186 with the artery clamped.15.8.1 Autologous Vein . . . . . . . . . . . . . . . . . . . 18715.8.2 Synthetic Vascular Prosthesis . . . . . . . 18715.9 Veins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 188 15.2 Background15.10 Other . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19015.10.1 Drains . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190 For surgeons who do not routinely perform vascu-15.10.2 Infection Prophylaxis . . . . . . . . . . . . . . . 190 lar operations it might be helpful to recapitulate the basic vascular surgical technique to facilitate their management of common vascular emergen- cies. First, it is always necessary to obtain control of and clamp all branches to the of interest vascu- lar segment to make a vascular operation possible at all. The rationale for being extra cautious with blood vessels is that they are extremely sensitive to trauma, which can induce undesired thrombo- genic activity on the intimal surface. Furthermore, their structure of separated wall layers demands special consideration to avoid dissection and oc- clusion. A successful vascular operation requires the surgeon to pay constant attention to technical details to avoid jeopardizing the entire operation.
  • 178. 180 Chapter 15 General Principles of Vascular Surgical Technique 15.3 Exposure Good exposure is always mandatory for optimiz- ing the prerequisites for reconstruction or repair. Exposure of most specific vascular segments is described in the corresponding chapter (e.g., ex- posure of the superficial femoral artery in the groin for embolectomy is covered in the chapter on acute leg ischemia). With a few exceptions (for instance, the trans- verse incision in the cubital fossa for exposing the brachial artery), a longitudinal skin incision over the vessel is used. The incision is made approxi- mately 2 cm longer in each direction than the re- quired exposed vessel length. An incision that is too small increases the risk for wound complica- tions in the skin and other tissues with already impaired perfusion due to unnecessary trauma from retractors. Familiarity with the anatomy is essential because it is not always possible to be guided by palpation of a pulse or hard arterioscle- rotic plaques. Use small, blunt, self-retaining re- tractors to achieve tension in the tissue to facilitate dissection. When approaching the vessel special atraumatic vascular instruments should always be Fig. 15.1. a Pass a right-angle clamp gently through used. Never use a toothed forceps in the vicinity of the soft tissue on the dorsal aspect of the artery and a blood vessel. The correct plane of final exposure direct it away from larger veins to avoid iatrogenic inju- is the outer soft layer of the adventitia. A common ries. Caution! Avoid accidental penetration of the dor- error is exaggerated caution in trying to obtain ex- sal wall of the artery. b Gently lift the artery with the vessel-loop to achieve tension in the tissue, thus facili- posure in a layer that is too superficial. The adven- tating the dissection titia is characterized by a visible net of vasa vaso- rum. It is important to be aware of the differences between a healthy and a diseased artery. The for- mer is soft, easily compressible, and has a grey/red NOTE color. This is what can be expected in trauma pa- Good exposure of the segment to be tients who are mostly young and otherwise healthy. repaired, including space enough to allow When there is no pulse in the artery it may even be safe clamping, is essential for a successful difficult to distinguish it from a vein. An arterio- vascular operation. Always use special sclerotic artery in a patient with peripheral vascu- atraumatic vascular instruments when lar disease is yellow/white and has a thick and approaching the vessel. often hard or calcified wall. Expose the anterior and lateral aspects of the artery and use a right-angle clamp with its tip 15.4 Control of Bleeding turned away from the adjacent larger vein – thus and Clamping avoiding accidental perforations – to surround the posterior aspect with a vessel-loop of fabric or In all vascular procedures, including vascular rubber. By lifting the vessel-loop, tension can be trauma, proximal and distal control is mandatory achieved in the tissue, thus facilitating the dissec- before attempting repair or doing an arteriotomy. tion in an atraumatic way (Fig. 15.1). All branches It is desirable to have a completely empty vascular should be saved because they are potential impor- segment in order to perform a vascular opera- tant collaterals. tion without unnecessary technical difficulties. To
  • 179. 15.4 Control of Bleeding and Clamping 181 Fig. 15.2. Different methods for controlling bleeding are demon- strated. From left to right: doubly applied vessel-loop, “bulldog” (small metallic vascular clamp), balloon catheter, loop of ligature, vascular clampachieve this, all branches for inflow as well as out- A vascular clamp should be chosen with anflow from the segment must be controlled. Before angle and shape that minimally disturbs the surgi-clamping, systemic anticoagulation is usually nec- cal exposure during the rest of the procedure. Toessary unless contraindicated by bleeding risk. avoid disrupting the often dorsally located plaquesThe standard dose is 100 units/kg body weight in arteriosclerotic arteries, clamps should prefer-of heparin given intravenously, but in practice, ably be applied horizontally and closed just enough5,000 units is usually adequate for an adult patient. to stop the blood flow (Fig. 15.3).It is important to be aware that the activity of Temporary vascular clamps can be manufac-heparin is halved within 1–2 h, so a repeated dose tured using vessel-loops or umbilical tape and aof 2,500 units might be required, especially if the piece of rubber tubing (Fig. 15.4).surgeon notices increased clotting activity in the When there is active traumatic bleeding, aoperating field. For local heparinization, flushing blindly applied vascular clamp can be dangerouswith a solution of 5,000 units of heparin in 500 ml and should be avoided. For full control, the injuredRinger’s acetate or Ringer’s glucose (10 units/ml) is vascular segment must be exposed. The bleedingrecommended. vessel can be controlled by finger compression, a Control of the flow in the exposed vascular seg- “peanut,” or a “strawberry” until the vessel hasments is achieved with different types of vascular been mobilized and the bleeding controlled. If thisclamps or with vessel-loops of cotton fabric or technique is not possible, external compressionrubber. Doubly applied 2-0 or 3-0 ligatures can and packing of the wound with dressings underalso be used for smaller branches. Intraluminal compression can be used while dissection is per-control with balloon catheters can also be effective formed and adequate exposure obtained, but this(Fig. 15.2). usually results in significant blood loss. Fig. 15.3. Arteriosclerotic plaques are usually located dorsally in the artery. The clamp should be placed horizontally to avoid plaque frac- ture and fragmentation
  • 180. 182 Chapter 15 General Principles of Vascular Surgical Technique In larger arteries such as the aorta, a Foley catheter of appropriate size can be used for the same pur- pose. Special catheters from different manufactur- ers are also available for occluding arteries. When balloons are used for proximal control they are easily dislocated and even blown out by the arte- rial pressure. This can be avoided by having an assistant manually support the catheter or by applying a vascular tape around the artery just proximal to the arteriotomy, thus preventing the balloon from being further dislocated distally. NOTE Never open a blood vessel without having proximal and distal control. 15.4.1 Proximal Endovascular Aortic Control When available, this alternative is of great poten- Fig. 15.4. A temporary vascular clamp is made by pull- tial importance for patients with severe intraab- ing a double vessel-loop through a piece of rubber tub- dominal bleeding after rupture of aneurysms as ing to make a snare around the vessel, which is locked well as traumatic vascular injuries. It is further by an ordinary clamp described in Chapter 7 (p. 85). 15.5 Vascular Suture In certain situations, such as in scar tissue, thorough dissection of a vascular segment can be When vessels are sutured, the suture should in- technically very challenging and should thus be clude all the layers of the vessel wall. The adventi- avoided. Balloon occlusion can be a very good tia is the most important layer for the mechanical alternative for distal as well as temporary proxi- strength of the vascular wall. The adventitia mal control. Control is, however, best achieved by should not be allowed to be interposed between surgical exposure and clamping of a more proxi- the approximated edges of the arteriotomy be- mal segment, while balloon occlusion is always an cause that can disturb the healing process. This alternative for distal control. Embolectomy cathe- can be avoided by everting the edges to allow inti- ters of adequate size connected to a three-way ma-to-intima approximation. stopcock and a saline-filled syringe are used. In- When vessels are being sutured, the needle’s spection of the open segment, under continuous point should be placed at a 90° angle against evacuation of blood from the backbleeding the vascular wall, and thereafter its circular shape is branches with suction, allows identification of the used to push it through the wall to avoid un- orifice into which the catheter should be inserted. necessary tearing. It is important to place the needle After insertion the balloon is insufflated