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Sabiston Textbook of Surgery, 19th Edition. Sample Chapter 13
 

Sabiston Textbook of Surgery, 19th Edition. Sample Chapter 13

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This latest edition is every surgeon's must have to make confident surgery decisions. Featuring new chapters on Liver Transplantation, the aorta, The Difficult Abdominal Wall etc. ...

This latest edition is every surgeon's must have to make confident surgery decisions. Featuring new chapters on Liver Transplantation, the aorta, The Difficult Abdominal Wall etc.

Check out the sample chapter 13. For purchase, please visit www.asia.elsevierhealth.com

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    Sabiston Textbook of Surgery, 19th Edition. Sample Chapter 13 Sabiston Textbook of Surgery, 19th Edition. Sample Chapter 13 Document Transcript

    • Chapter 13 SurgiCal CompliCationS Mahmoud N. Kulaylat and Merril T. Dayton operations can be performed in a purely elective fashion, whereas surgical wound complications others must be done in an urgent fashion. Occasionally, the complications of thermal regulation surgeon will require that the patient lose weight before the respiratory complications operation to enhance the likelihood of a successful outcome. cardiac complications At times, a wise surgeon will request preoperative consultation renal and urinary tract complications from a cardiologist or pulmonary specialist to make certain that endocrine gland dysfunction the patient will be able to tolerate the stress of a particular gastrointestinal complications procedure. hepatobiliary complications Once the operation has begun, the surgeon can do much neurologic complications to influence the postoperative outcome. Surgeons must handle ear, nose, and throat complications tissues gently, dissect meticulously, and honor tissue planes. Performing the technical portions of the operation carefully will lower the risk for a significant complication. At all costs, sur­ geons must avoid the temptation to rush, cut corners, or accept Surgical complications remain a frustrating and difficult aspect marginal technical results. Similarly, the judicious use of anti­ of the operative treatment of patients. Regardless of how techni­ biotics and other preoperative medications can influence the cally gifted and capable surgeons are, all will have to deal with outcome. For a seriously ill patient, adequate resuscitation may complications that occur after operative procedures. The cost of be necessary to optimize the patient before giving a general surgical complications in the United States runs into millions of anesthetic. dollars; in addition, such complications are associated with lost Once the operation is completed, compulsive postoperative work productivity, disruption of family life, and stress to employ­ surveillance is mandatory. Thorough and careful rounding on ers and society in general. Frequently, the functional results of patients on a regular basis postoperatively gives the operating the operation are compromised by complications; in some surgeon an opportunity to be vigilant and seek postoperative cases the patient never recovers to the preoperative level of func­ complications at an early stage, when they can be most effec­ tion. The most significant and difficult part of complications is tively addressed. During this process, the surgeon will carefully the suffering borne by a patient who enters the hospital antici­ check all wounds, evaluate intake and output, check temperature pating an uneventful operation but is left suffering and compro­ profiles, ascertain what the patient’s activity levels have been, mised by the complication. evaluate nutritional status, and check pain levels. Over years of Complications can occur for a variety of reasons. A surgeon experience, the clinician can begin to assess these parameters and can perform a technically sound operation in a patient who is detect deviations from the normal postoperative course. Expedi­ severely compromised by the disease process and still have a tious response to a complication makes the difference between complication. Similarly, a surgeon who is sloppy or careless or a brief, inconvenient complication and a devastating, disabling hurries through an operation can make technical errors that one. In summary, a wise surgeon will deal with complications account for the operative complications. Finally, the patient can quickly, thoroughly, and appropriately. be healthy nutritionally, have an operation performed meticu­ lously, and yet suffer a complication because of the nature of the disease. The possibility of postoperative complications Surgical Wound complicationS remains part of every surgeon’s mental preparation for a difficult operation. Seroma Surgeons can do much to avoid complications by careful preoperative screening. When the surgeon sees the surgical can­ Causes didate for the first time, a host of questions come to mind, such A seroma is a collection of liquefied fat, serum, and lymphatic as the nutritional status of the patient and the health of the heart fluid under the incision. The fluid is usually clear, yellow, and and lungs. The surgeon will make a decision regarding perform­ somewhat viscous and is found in the subcutaneous layer of the ing the appropriate operation for the known disease. Similarly, skin. Seromas represent the most benign complication after an the timing of the operation is often an important issue. Some operative procedure and are particularly likely to occur when K2 13-1Townsend_Chapter 13_main.indd 1 6/10/2011 12:36:18 PM
    • 13-2  section ii  PerioPerative ManageMent large skin flaps are developed in the course of the operation, as or associated with drainage of dark red fluid out of the fresh is often seen with mastectomy, axillary dissection, groin dissec­ wound. tion, and large ventral hernias or when a prosthetic mesh Hematoma formation is prevented preoperatively by cor­ (polytetrafluoroethylene) is used in the repair of a ventral hernia. recting any clotting abnormalities and discontinuing medi­ cations that alter coagulation. Antiplatelet medications and presentation and management anticoagulants may be given to patients undergoing procedures A seroma usually manifests as a localized and well­circumscribed for a variety of reasons. Clopidogrel is given after implantation swelling, pressure or discomfort, and occasional drainage of clear of a coronary stent, ASA is given for the treatment of coronary liquid from the immature surgical wound. Prevention of seroma artery disease (CAD) and stroke, and VKA is given after implan­ formation may be achieved with placement of suction drains tation of a mechanical mitral valve for atrial fibrillation, venous under the flaps. Their premature removal often results in large thromboembolism, and hypercoagulable states. These medica­ seromas that will require aspiration under sterile conditions, tions must be temporarily discontinued before surgery. There are followed by placement of a pressure dressing. A seroma that no specific studies that have addressed the issue of timing of reaccumulates after at least two aspirations is evacuated by discontinuation of such medications. opening the incision and packing the wound with saline­ One must balance the risk of significant bleeding caused moistened gauze to allow healing by secondary intention. In the by uncorrected medication­induced coagulopathy and the risk presence of synthetic mesh, open drainage is best performed in of thromboembolic events after discontinuation of therapy. The the operating room, the incision is best closed to avoid exposure risk of bleeding varies with the type of surgery or procedure and infection of the mesh, and suction drains are placed. An and adequacy of hemostasis; the risk of thromboembolism infected seroma is also treated with open drainage. The presence depends on the indication for antithrombotic therapy and pres­ of synthetic mesh in these cases will prevent the wound from ence of comorbid conditions.1 In patients at high risk for healing. Management of the mesh depends on the severity and thromboembolism (e.g., those with a mechanical mitral valve extent of infection. In the absence of severe sepsis and spreading or older generation aortic valve prosthesis, venous thromboem­ cellulitis and the presence of localized infection, the mesh can bolism within 3 months, severe thrombophilia, recent atrial be left in situ and removed at a later date when the acute infec­ fibrillation [within 6 months], stroke or transient ischemic tious process has resolved. Otherwise, the mesh must be removed attack who are scheduled to undergo an elective major surgical and the wound managed with open wound care. procedure involving a body cavity), the VKA must be discon­ tinued 4 to 5 days before surgery to allow the international Hematoma normalized ratio (INR) to be lower than 1.5. In patients whose INR is still elevated (>1.5), low­dose vitamin K (1 to 2 mg) is 1 Causes given orally. Patients are then given bridging anticoagulation— A hematoma is an abnormal collection of blood, usually in the that is, a therapeutic dose of rapidly acting anticoagulant, intra­ subcutaneous layer of a recent incision or in a potential space in venous (IV) UFH or to LMWH. Those receiving IV UFH the abdominal cavity after extirpation of an organ (e.g., splenic (half­life, 45 minutes) can have the medication discontinued 4 fossa hematoma after splenectomy or pelvic hematoma after hours before surgery and those receiving therapeutic dose proctectomy). Hematomas are more worrisome than seromas LMWH SC (variable half­life) 16 to 24 hours before surgery. because of the potential for secondary infection. Hematoma VKA is then resumed 12 to 24 hours after surgery (takes 2 to 3 formation is related to inadequate hemostasis, depletion of clot­ days for anticoagulant effect to begin after start of VKA) and ting factors, or the presence of coagulopathy. A host of disease when there is adequate hemostasis. In patients at high risk of processes can contribute to coagulopathy, including myelopro­ bleeding (major surgery or high bleeding risk surgery) for liferative disorders, liver disease, renal failure, sepsis, clotting whom postoperative therapeutic LMWH or UFH is planned, factor deficiencies, and medications. Medications most com­ initiation of therapy is delayed for 48 to 72 hours, low­dose monly associated with coagulopathy are antiplatelet drugs, such LMWH or UFH is administered, or the therapy is completely as acetylsalicylic acid (ASA, aspirin), clopidogrel, ticlopidine, avoided. Patients at low risk for thromboembolism do not eptifibatide, and abciximab, and anticoagulants, such as ultra­ require heparin therapy after discontinuation of the VKA. fractionated heparin (UFH), low­molecular­weight heparin Patients on ASA or clopidogrel must have the medication with­ (LMWH [e.g., enoxaparin, dalteparin sodium, tinzaparin]), and held 6 to 7 days before surgery; otherwise, the surgery must be vitamin K antagonist (VKA [e.g., warfarin sodium]). delayed until the patient has completed the course of treat­ ment. Antiplatelet therapy is resumed approximately 24 hours presentation and management after surgery. In patients with a bare metal coronary stent who The clinical manifestations of a hematoma may vary with its size, require surgery within 6 weeks of stent placement, ASA and location, and presence of infection. A hematoma may manifest clopidogrel are continued in the perioperative period. In as an expanding, unsightly swelling and/or pain in the area of a patients who are receiving VKAs and require urgent surgery, surgical incision. In the neck, a large hematoma may cause immediate reversal of anticoagulant effect requires transfusion compromise of the airway; in the retroperitoneum, it may cause with fresh­frozen plasma or other prothrombin concentrate and a paralytic ileus, anemia, and ongoing bleeding caused by local low­dose IV or oral vitamin K. During surgery, adequate hemo­ consumptive coagulopathy; and, in the extremity and abdomi­ stasis must be achieved with ligature, electrocautery, fibrin glue, nal cavity, it may result in compartment syndrome. On physical or topical bovine thrombin before closure. Closed suction examination, the hematoma appears as a localized soft swelling drainage systems are placed in large potential spaces and with purplish blue discoloration of the overlying skin. The swell­ removed postoperatively when the output is not bloody andK2 ing varies from small to large and may be tender to palpation scant. Townsend_Chapter 13_main.indd 2 6/10/2011 12:36:18 PM
    • Surgical coMPlicationS  chapter 13  13-3 Evaluation of a patient with a hematoma, especially one presentation and management SeCtion ii PerioPerative ManageMent that is large and expanding, includes assessment of preexisting Acute wound failure may occur without warning and eviscera­ risk factors and coagulation parameters (e.g., prothrombin time tion makes the diagnosis obvious. A sudden, dramatic drainage [PT], activated partial prothrombin time [aPTT], INR, platelet of a relatively large volume of a clear, salmon­colored fluid count, bleeding time) and appropriate treatment. A small hema­ precedes dehiscence in 25% of patients. More often, patients toma does not require any intervention and will eventually report a ripping sensation. Probing the wound with a sterile, resorb. Most retroperitoneal hematomas can be managed by cotton­tipped applicator or gloved finger may detect a partial expectant waiting after correction of associated coagulopathy dehiscence. (platelet transfusion if bleeding time is prolonged, desmopressin Prevention of acute wound failure is largely a function of in patients who have renal failure, and fresh­frozen plasma in careful attention to technical detail during fascial closure, such patients who have an increased INR). A large or expanding as proper spacing of the suture, adequate depth of bite of the hematoma in the neck is managed in a similar fashion and best fascia, relaxation of the patient during closure, and achieving a evacuated in the operating room urgently after securing the tension­free closure. For very high­risk patients, interrupted airway if there is any respiratory compromise. Similarly, hema­ closure is often the wisest choice. Alternative methods of closure tomas detected soon after surgery, especially those developing must be selected when primary closure is not possible without under skin flaps, are best evacuated in the operating room. undue tension. Although retention sutures were used exten­ sively in the past, their use is less common today, with many acute Wound Failure (dehiscence) surgeons opting to use a synthetic mesh or bioabsorbable tissue scaffold. Causes Treatment of dehiscence depends on the extent of Acute wound failure (wound dehiscence or a burst abdomen) fascial separation and the presence of evisceration and/or refers to postoperative separation of the abdominal musculoapo­ significant intra­abdominal pathology (e.g., intestinal leak, neurotic layers. It is among the most dreaded complications peritonitis). A small dehiscence, especially in the proximal faced by surgeons and is of great concern because of the risk of aspect of an upper midline incision 10 to 12 days postoper­ evisceration, the need for some form of intervention, and the atively, can be managed conservatively with saline­moistened possibility of repeat dehiscence, surgical wound infection, and gauze packing of the wound and use of an abdominal incisional hernia formation. binder. In the event of evisceration, the eviscerated intestines Acute wound failure occurs in approximately 1% to 3% of must be covered with a sterile, saline­moistened towel and patients who undergo an abdominal operation. Dehiscence most preparations made to return to the operating room after a often develops 7 to 10 days postoperatively but may occur very short period of fluid resuscitation. Similarly, if probing anytime after surgery, from 1 to more than 20 days. A multitude of the wound reveals a large segment of the wound that is of factors may contribute to wound dehiscence (Box 13­1). open to the omentum and intestines, or if there is peritoni­ Acute wound failure is often related to technical errors in placing tis or suspicion of intestinal leak, plans to take the patient sutures too close to the edge, too far apart, or under too much back to the operating room are made. tension. Local wound complications such as hematoma and Once in the operating room, thorough exploration of the infection can also predispose to localized dehiscence. In fact, a abdominal cavity is performed to rule out the presence of a deep wound infection is one of the most common causes of septic focus or an anastomotic leak that may have predisposed localized wound separation. Increased intra­abdominal pressure to the dehiscence. Management of that infection is of critical (IAP) is often blamed for wound disruption and factors that importance before attempting to close. Management of the adversely affect wound healing are cited as contributing to the incision is a function of the condition of the fascia. When complication. In healthy patients, the rate of wound failure is technical mistakes are made and the fascia is strong and intact, similar whether closure is accomplished with a continuous or primary closure is warranted. If the fascia is infected or interrupted technique. In high­risk patients, however, continu­ necrotic, débridement is performed. The incision can then be ous closure is worrisome because suture breakage in one place closed with retention sutures; however, to avoid tension, use weakens the entire closure. of a prosthetic material may be preferred. Closure with an absorbable mesh (polyglactin or polyglycolic acid) may be preferable because the mesh is well tolerated in septic wounds Box 13-1  Factors associated With Wound Dehiscence and allows bridging the gap between the edges of the fascia without tension, prevents evisceration, and allows the underly­ technical error in fascial closure ing cause of the patient’s dehiscence to resolve. Once the emergency surgery wound has granulated, a skin graft is applied and wound intra-abdominal infection closure is achieved by advancing local tissue. This approach advanced age uniformly results in the development of a hernia, the repair of Wound infection, hematoma, and seroma which requires the subsequent removal of the skin graft and elevated intra-abdominal pressure use of a permanent prosthesis. An alternative method of obesity closure is dermabrasion of the skin graft followed by fascial chronic corticosteroid use closure using the component separation technique. Attempts Previous wound dehiscence to close the fascia under tension guarantee a repeat dehiscence Malnutrition and, in some cases, result in intra­abdominal hypertension radiation therapy and chemotherapy (IAH). The incision is left open (laparotomy), closed with a Systemic disease (uremia, diabetes mellitus) temporary closure device (open abdomen technique), closed K2Townsend_Chapter 13_main.indd 3 6/10/2011 12:36:18 PM
    • 13-4  section ii  PerioPerative ManageMent with synthetic mesh or biologic graft (acellular dermal matrix), wound (macrodeformation) and removal of extracellular fluid or closed by using negative­pressure wound therapy. (via decrease in bowel edema, evacuation of excess abdominal The open abdomen technique avoids IAH, preserves the fluid, decrease in wound size), stabilization of the wound envi­ fascia, and facilitates reaccess of the abdominal cavity. With ronment, and microdeformation of the foam­wound interface, laparotomy, the wound is allowed to heal with secondary inten­ which induces cellular proliferation and angiogenesis. The sec­ tion and/or subsequently closed with a skin graft or local or ondary effects of the vacuum­assisted closure device include regional tissue. This approach is associated with prolonged acceleration of wound healing, reduction and changes in bac­ healing time, fluid loss, and risk of complex enterocutaneous terial burden, changes in biochemistry and systemic responses, fistula formation as a result of bowel exposure, desiccation, and and improvement in wound bed preparation—increase in traumatic injury. Furthermore, definitive surgical repair to local blood perfusion and induction healing response through restore the integrity of the abdominal wall will eventually be microchemical forces.3 This approach results in successful required. A temporary closure device (vacuum pack closure) closure of the fascia in 85% of cases. However, the device is protects abdominal contents, keeps patients dry, can be quickly expensive and cumbersome to wear and may cause significant removed with increased IAP, and avoids secondary complica­ pain, cause bleeding (especially in patients on anticoagulant tions seen with laparotomy. A fenestrated, nonadherent, poly­ therapy), be associated with increased levels of certain bacteria, ethylene sheet is applied on the bowel omentum, moist surgical and be associated with evisceration and hernia formation. towels or gauze with drains are placed on top, and an iodophore­ There is also an increased incidence of intestinal fistulization impregnated adhesive dressing is placed. Continuous suction is at enterotomy sites and enteric anastomoses, and in the then applied. If the fascia cannot be closed in 7 to 10 days, the absence of anastomoses. wound is allowed to granulate and then covered with a skin graft. Surgical Site infection (Wound infection) Absorbable synthetic mesh provides wound stability and is resistant to infection. It is associated with fistula and hernia Causes formation repair, which is difficult and may require recon­ Surgical site infections (SSIs) still continue to be a significant struction of the abdominal wall. Repair with nonabsorbable problem for surgeons. Despite major improvements in antibiot­ synthetic mesh such as polypropylene, polyester, or polytetra­ ics, better anesthesia, superior instruments, earlier diagnosis of fluoroethylene (PTFE) is associated with complications that surgical problems, and improved techniques for postoperative will require removal of the mesh (e.g., abscess formation, vigilance, wound infections continue to occur. Although some dehiscence, wound sepsis, mesh extrusion, bowel fistulization). may view the problem as merely cosmetic, that view represents Although PTFE is more desirable because it is nonadherent a shallow understanding of this problem, which causes signifi­ to underlying bowel, it is expensive, does not allow skin graft­ cant patient suffering, morbidity, and even mortality, and is a ing, and is associated with chronic infections. An acellular financial burden to the health care system. Furthermore, SSIs dermal matrix (bioprosthesis) has the mechanical properties of represent a risk factor for the development of incisional hernia, a mesh for abdominal wall reconstruction and physiologic which requires surgical repair. Currently, in the United States, properties that make it resistant to contamination and/or SSIs account for almost 40% of hospital­acquired infections 3 infection. The bioprosthesis provides immediate coverage of among surgical patients. the wound and serves as mechanical support in a single­stage The surgical wound encompasses the area of the body, reconstruction of compromised surgical wounds. It is bioactive internally and externally, that involves the entire operative site. because it functions as tissue replacement or scaffold for new Wounds are thus categorized into three general categories: tissue growth; it stimulates cellular attachment, migration, 1. Superficial, which includes the skin and subcutane­ neovascularization, and repopulation of the implanted graft. ous tissue A bioprosthesis also reduce long­term complications (e.g., 2. Deep, which includes the fascia and muscle erosion, infection, chronic pain). Available acellular materials 3. Organ space, which includes the internal organs of are animal­derived (e.g., porcine intestinal submucosa, porcine the body if the operation includes that area dermis, cross­linked porcine dermal collagen) or human­ The Centers for Disease Control and Prevention has pro­ derived (e.g., cadaveric human dermis). However, the rate of posed specific criteria for the diagnosis of surgical site infections wound complications (e.g., superficial wound or graft infec­ (Box 13­2).4 tion, graft dehiscence, fistula formation, bleeding) and Surgical site infections develops as a result of contamina­ 2 hernia formation or literaxity of the abdominal wall is 25% tion of the surgical site with microorganisms. The source of these to 50%.2 microorganisms is mostly patients’ flora (endogenous source) Negative­pressure wound therapy is based on the concept when integrity of the skin and/or wall of a hollow viscus is of wound suction. A vacuum­assisted closure device is most violated. Occasionally, the source is exogenous when a break in commonly used. The device consists of a vacuum pump, can­ the surgical sterile technique occurs, thus allowing contamina­ ister with connecting tubing, open­pore foam (e.g., poly­ tion from the surgical team, equipment, implant or gloves, or urethane ether, polyvinyl alcohol foam) or gauze, and surrounding environment. The pathogens associated with a sur­ semiocclusive dressing. The device provides immediate cover­ gical site infections reflect the area that provided the inoculum age of the abdominal wound, acts as a temporary dressing, for the infection to develop. The microbiology, however, varies, does not require suturing to the fascia, minimizes IAH, and depending on the types of procedures performed in individual prevents loss of domain. Applying suction of 125 mm Hg, the practices. Gram­positive cocci account for half of the infections open­pore foam decreases in size and transmits the negative (Table 13­1)—Staphylococcus aureus (most common), coagulase­K2 pressure to surrounding tissue, leading to contraction of the negative Staphylococcus, and Enterococcus spp. S. aureus infections Townsend_Chapter 13_main.indd 4 6/10/2011 12:36:19 PM
    • Surgical coMPlicationS  chapter 13  13-5 Box 13-2  centers for Disease control and prevention  SeCtion ii PerioPerative ManageMent table  13-1  pathogens  isolated  from  postoperative  surgical  criteria for Defining a surgical site infection site infections at a University hospital Superficial incisional pathoGen percentaGe oF isoLates infection less than 30 days after surgery Staphylococcus (coagulase-negative) 25.6 involves skin and subcutaneous tissue only, plus one of the  Enterococcus (group D) 11.5 following: Staphylococcus aureus 8.7 • Purulent drainage • Diagnosis  of  superficial  surgical  site  infection  by  a  Candida albicans 6.5 surgeon Escherichia coli 6.3 • Symptoms of erythema, pain, local edema Pseudomonas aeruginosa 6.0 Deep incisional Corynebacterium 4.0 less than 30 days after surgery with no implant and soft tissue  involvement Candida (non-albicans) 3.4 infection  less  than  1  year  after  surgery  with  an  implant;  alpha-hemolytic Streptococcus 3.0 involves deep soft tissues (fascia and muscle), plus one of the  Klebsiella pneumoniae 2.8 following: vancomycin-resistant Enterococcus 2.4 • Purulent drainage from the deep space but no exten- sion into the organ space Enterobacter cloacae 2.2 • abscess  found  in  the  deep  space  on  direct  or  radio- Citrobacter spp. 2.0 logic examination or on reoperation From Weiss Ca, Statz CI, Dahms ra, et al: Six years of surgical wound surveillance • Diagnosis  of  a  deep  space  surgical  site  infection  by  at a tertiary care center. arch Surg 134:1041-1048, 1999. the surgeon • Symptoms  of  fever,  pain,  and  tenderness  leading  to  wound dehiscence or opening by a surgeon organ Space evidence to indicate that hospital­acquired MRSA is developing infection less than 30 days after surgery with no implant resistance to vancomycin (vancomycin intermediate­resistant S. infection less than 1 year after surgery with an implant and  aureus [VISA] and vancomycin­resistant S. aureus [VRSA]).5 infection;  involves  any  part  of  the  operation  opened  or  mani- Enterococcus spp. are commensals in the adult gastrointestinal pulated, plus one of the following: (GI) tract, have intrinsic resistance to a variety of antibiotics • Purulent  drainage  from  a  drain  placed  in  the  organ  (e.g., cephalosporins, clindamycin, aminoglycoside), and are the space first to exhibit resistance to vancomycin. • cultured organisms from material aspirated from the  In approximately one third of SSI cases, gram­negative organ space bacilli (Escherichia coli, Pseudomonas aeruginosa, and Enterobacter • abscess found on direct or radiologic examination or  spp.) are isolated. However, at locations at which high volumes during reoperation of GI operations are performed, the predominant bacterial • Diagnosis of organ space infection by a surgeon species are the gram­negative bacilli. Infrequent pathogens are adapted from Mangram aJ, horan tC, pearson ML, et al: Guideline for prevention group A beta­hemolytic streptococci and Clostridium perfringens. of surgical site infection. Infect Control hosp epidemiol 20:252, 1999. In recent years, the involvement of resistant organisms in the genesis of SSIs has increased, most notable in MRSA. A host of patient­ and operative procedure–related factors may contribute to the development of SSIs (Table 13­2).6 The normally occur in the nasal passages, mucous membranes, and risk of infection is related to the specific surgical procedure skin of carriers. The organism that has acquired resistance to performed and, hence, surgical wounds are classified according methicillin (methicillin­resistant S. aureus [MRSA]) consists to the relative risk of surgical site infections occurring—clean, of two subtypes, hospital­ and community­acquired MRSA. clean­contaminated, contaminated, and dirty (Table 13­3). In Hospital­acquired MRSA is associated with nosocomial infec­ the National Nosocomial Infections Surveillance System, the tions and affects immunocompromised individuals. It also risk of patients is stratified according to three important factors: occurs in patients with chronic wounds, those subjected to inva­ (1) wound classification (contaminated or dirty); (2) longer sive procedures, and those with prior antibiotic treatment. duration operation, defined as one that exceeds the 75th percen­ Community­acquired MRSA is associated with a variety of skin tile for a given procedure; and (3) medical characteristics of the and soft tissue infections in patients with and without risk patients as determined by the American Society of Anesthesiol­ factors for MRSA. Community­acquired MRSA (e.g., the ogy score of III, IV, or V (presence of severe systemic disease USA300 clone) has also been noted to affect SSIs. Hospital­ that results in functional limitations, is life­threatening, or is acquired MRSA isolates have a different antibiotic susceptibility expected to preclude survival from the operation) at the time of profile—they are usually resistant to at least three β­lactam operation.7 antibiotics and are usually susceptible to vancomycin, teico­ planin, and sulfamethoxazole. Community­acquired MRSA is presentation usually susceptible to clindamycin, with variable susceptibility SSIs most commonly occur 5 to 6 days postoperatively but may to erythromycin, vancomycin, and tetracycline. There is develop sooner or later than that. Approximately 80% to 90% K2Townsend_Chapter 13_main.indd 5 6/10/2011 12:36:19 PM
    • 13-6  section ii  PerioPerative ManageMent of all postoperative infections occur within 30 days after the patients are hospitalized for 6 days or less, 70% of postdischarge operative procedure. With the increased use of outpatient infections occur in that group. surgery and decreased length of stay in hospitals, 30% to 40% Superficial and deep SSIs are accompanied by erythema, of all wound infections have been shown to occur after hospital tenderness, edema, and occasionally drainage. The wound is discharge. Nevertheless, although less than 10% of surgical often soft or fluctuant at the site of infection, which is a depar­ ture from the firmness of the healing ridge present elsewhere in the wound. The patient may have leukocytosis and a low­grade fever. According to the Joint Commission (TJC), a surgical 4 table 13-2  risk Factors for postoperative Wound infection wound is considered infected if (1) there is drainage of grossly enVironMentaL  treatMent  purulent material drains from the wound, (2) the wound spon­ patient Factors Factors Factors taneously opens and drains purulent fluid, (3) the wound drains ascites contaminated  Drains fluid that is culture­positive or Gram stain–positive for bacteria, medications and (4) the surgeon notes erythema or drainage and opens the chronic  inadequate  emergency  wound after determining it to be infected. inflammation disinfection/sterilization procedure undernutrition inadequate skin  inadequate antibiotic  treatment obesity antisepsis coverage Prevention of surgical site infections relies on changing or Diabetes inadequate ventilation Preoperative  dealing with modifiable risk factors that predispose to surgical hospitalization site infections. However, many of these factors cannot be extremes of age Presence of a foreign  Prolonged operation changed, such as age, complexity of the surgical procedure, body and morbid obesity. Patients who are heavy smokers are Hypercholesterolemia encouraged to stop smoking at least 30 days before surgery, Hypoxemia glucose levels in diabetics must be treated appropriately, and Peripheral vascular disease severely malnourished patients should be given nutritional supplements for 7 to 14 days before surgery.8 Obese patients Postoperative anemia must be encouraged to lose weight if the procedure is elective Previous site of irradiation and there is time to achieve significant weight loss. Similarly, recent operation patients who are taking high doses of corticosteroids will have lower infection rates if they are weaned off corticosteroids or remote infection are at least taking a lower dose. Patients undergoing major Skin carriage of staphylococci intra­abdominal surgery are administered a bowel preparation Skin disease in the area of infection in the form of a lavage solution or strong cathartic, followed immunosuppression by oral nonabsorbable antibiotic(s), particularly for surgery of the colon and small bowel. Bowel preparation lowers the Data from National Nosocomial Infections Surveillance Systems (NNIS) System patient’s risk for infection from that of a contaminated case report: Data summary from January 1992–June 2001, issued august 2001. am J Infect Control 29:404-421, 2001. (25%) to a clean­contaminated case (5%). Hair is removed by clipping immediately before surgery and the skin is prepped at the time of operation with an antiseptic agent (e.g., alcohol, chlorhexidine, iodine). The role of preoperative decolonization in carriers of S. table 13-3  classification of surgical Wounds aureus undergoing general surgery is questionable, and the inFection   routine use of prophylactic vancomycin or teicoplanin (effective cateGorY criteria rate (%) against MRSA) is not recommended. Although perioperative clean no hollow viscus entered 1-3 antibiotics are widely used, prophylaxis is generally recom­ Primary wound closure mended for clean­contaminated or contaminated procedures in no inflammation which the risk of SSIs is high or in procedures in which vascular no breaks in aseptic technique elective procedure or orthopedics prostheses are used because the development of SSIs will have grave consequences (Table 13­4). For dirty or clean-  Hollow viscus entered but controlled 5-8 contaminated no inflammation contaminated wounds, the use of antibiotics is for therapeutic Primary wound closure purposes rather than for prophylaxis. For clean cases, prophy­ Minor break in aseptic technique laxis is controversial. For some surgical procedures, a first­ or Mechanical drain used Bowel preparation preoperatively second­generation cephalosporin is the accepted agent of choice. contaminated uncontrolled spillage from viscus 20-25 A small but significant benefit may be achieved with the pro­ inflammation apparent phylactic administration of a first­generation cephalosporin for open, traumatic wound certain types of clean surgery (e.g., mastectomy, herniorrhaphy). Major break in aseptic technique For clean­contaminated procedures, administration of preopera­ Dirty untreated, uncontrolled spillage from  30-40 tive antibiotics is indicated. The appropriate preoperative anti­ viscus Pus in operative wound biotic is a function of the most likely inoculum based on the open suppurative wound area being operated. For example, when a prosthesis may be Severe inflammation placed in a clean wound, preoperative antibiotics would includeK2 something to protect against S. aureus and streptococcal species. Townsend_Chapter 13_main.indd 6 6/10/2011 12:36:19 PM
    • Surgical coMPlicationS  chapter 13  13-7 SeCtion ii PerioPerative ManageMent table 13-4  prophylactic antimicrobial agent for selected surgical procedures proceDUre recoMMenDeD aGent potentiaL aLternatiVe cardiothoracic cefazolin or cefuroxime vancomycin, clindamycin vascular cefazolin or cefuroxime vancomycin, clindamycin gastroduodenal cefazolin cefoxitin, cefotetan, aminoglycoside, or fluoroquinolone +  antianaerobe open biliary cefazolin cefoxitin, cefotetan, or fluoroquinolone + antianaerobe laparoscopic cholecystectomy none — nonperforated appendicitis cefoxitin, cefotetan, cefazolin + metronidazole ertapenem, aminoglycoside, or fluoroquinolone + antianaerobe colorectal cefoxitin, cefotetan, ampicillin-sulbactam,  aminoglycoside, or fluoroquinolone + antianaerobe, aztreonam  ertapenem, cefazolin + metronidazole + clindamycin Hysterectomy cefazolin, cefuroxime, cefoxitin, cefotetan,  aminoglycoside, or fluoroquinolone + antianaerobe, aztreonam  ampicillin-sulbactam + clindamycin orthopedic implantation cefazolin, cefuroxime vancomycin, clindamycin Head and neck cefazolin, clindamycin — From Kirby Jp, Mazuski Je: prevention of surgical site infection. Surg Clin North am 89:365-389, 2009. A first­generation cephalosporin, such as cefazolin, would be contaminated instruments, avoidance of environ­ appropriate in this setting. For patients undergoing upper GI mental contamination, such as debris falling from tract surgery, complex biliary tract operations, or elective colonic overhead) resection, administration of a second­generation cephalosporin 7. Thorough drainage and irrigation of any pockets of such as cefoxitin or a penicillin derivative with a β­lactamase purulence in the wound with warm saline inhibitor is more suitable. Alternatively, ertapenem can y be used 8. Ensuring that the patient is kept in a euthermic state, for operations involving the lower GI tract. The surgeon will well­monitored, and fluid­resuscitated give a preoperative dose, intraoperative doses approximately 4 9. Expressing a decision about closing the skin or hours apart, and two postoperative doses appropriately spaced. packing the wound at the end of the procedure The timing of administration of prophylactic antibiotics is crit­ The use of drains remains somewhat controversial in pre­ ical. To be most effective, the antibiotic is administered IV venting postoperative wound infections. In general, there is within 30 minutes before the incision so that therapeutic tissue almost no indication for drains in this setting. However, placing levels have developed when the wound is created and exposed closed suction drains in very deep, large wounds and wounds to bacterial contamination. Usually, a period of anesthesia with large wound flaps to prevent the development of a seroma induction, preparation, and draping takes place that is adequate or hematoma is a worthwhile practice. to allow tissue levels to build up to therapeutic levels before the Treatment of SSIs depends on the depth of the infection. incision is made. Of equal importance is making certain that For both superficial and deep SSIs, skin staples are removed the prophylactic antibiotic is not administered for extended over the area of the infection and a cotton­tipped applicator periods postoperatively. To do so in the prophylactic setting is may be easily passed into the wound, with efflux of purulent to invite the development of drug­resistant organisms, as well as material and pus. The wound is gently explored with the serious complications, such as Clostridium difficile–associated cotton­tipped applicator or a finger to determine whether the colitis. fascia or muscle tissue is involved. If the fascia is intact, At the time of surgery, the operating surgeon plays a major débridement of any nonviable tissue is performed; the wound role in reducing or minimizing the presence of postoperative is irrigated with normal saline solution and packed to its base wound infections. The surgeon must be attentive to personal with saline­moistened gauze to allow healing of the wound hygiene (hand scrubbing) and that of the entire team. In addi­ from the base anteriorly, thus preventing premature skin tion, the surgeon must make certain that the patient undergoes closure. If widespread cellulitis or significant signs of infection a thorough skin preparation with appropriate antiseptic solu­ (e.g., fever, tachycardia), are noted, administration of IV anti­ tions and is draped in a sterile, careful fashion. During the biotics must be considered. Empirical therapy is started and operation, steps that have a positive impact on outcome are tailored according to culture and sensitivity data. The choice followed: of empirical antibiotics is based on the most likely culprit, 1. Careful handling of tissues including the possibility of MRSA. MRSA is treated with van­ 2. Meticulous dissection, hemostasis, and débridement comycin, linezolid, or clindamycin. Cultures are not routinely of devitalized tissue performed, except for patients who will be treated with antibi­ 3. Compulsive control of all intraluminal contents otics so that resistant organisms can be treated adequately. 4. Preservation of blood supply of the operated organs However, if the fascia has separated or purulent material 5. Elimination of any foreign body from the wound appears to be coming from deep to the fascia, there is obvious 6. Maintenance of strict asepsis by the operating team concern about dehiscence or an intra­abdominal abscess that (e.g., no holes in gloves, avoidance of the use of may require drainage or possibly a reoperation. K2Townsend_Chapter 13_main.indd 7 6/10/2011 12:36:19 PM
    • 13-8  section ii  PerioPerative ManageMent Wound cultures are controversial. If the wound is small, shock or with a severe illness often have associated vasoconstric­ superficial, and not associated with cellulitis or tissue necrosis, tion that results in poor perfusion of peripheral organs and cultures may not be necessary. However, if fascial dehiscence tissues, an effect accentuated by hypothermia. In a high­risk and a more complex infection are present, a culture is sent. A patient, a core temperature lower than 35° C is associated with deep SSI associated with grayish, dishwater­colored fluid, as a twofold to threefold increase in the incidence of early postop­ well as frank necrosis of the fascial layer, raises suspicion for the erative ischemia and a similar increase in the incidence of ven­ presence of a necrotizing type of infection. The presence of tricular tachyarrhythmia. Hypothermia also impairs platelet crepitus in any surgical wound or gram­positive rods (or both) function and reduces the activity of coagulation factors, thereby suggests the possibility of infection with C. perfringens. Rapid resulting in an increased risk for bleeding. Hypothermia results and expeditious surgical débridement is indicated in these in impaired macrophage function, reduced tissue oxygen tension, settings. and impaired collagen deposition, which predisposes wounds to Most postoperative infections are treated with healing by poor healing and infection. Other complications of hypothermia secondary intention, allowing the wound to heal from the include a relative diuresis, compromised hepatic function, and base anteriorly, with epithelialization being the final event. In some neurologic manifestations. Similarly, the patient’s ability some cases, when there is a question about the amount of to manage acid­base abnormalities is impaired. In severe cases, contamination, delayed primary closure may be considered. In the patient can have significant cardiac slowing and may be this setting, close observation of the wound for 5 days may be comatose, with low blood pressure, bradycardia, and a very low followed by closure of the skin or negative­pressure wound respiratory rate. therapy if the wound looks clean and the patient is otherwise doing well. treatment Prevention of hypothermia entails monitoring core tempera­ ture, especially in patients undergoing body cavity surgery or complicationS oF tHermal regulation surgery lasting longer than 1 hour, children and older adults, and patients in whom general epidural anesthesia is being con­ Hypothermia ducted.9 Sites of monitoring include pulmonary artery blood, tympanic membrane, esophagus and pharynx, rectum, and Causes urinary bladder. While the patient is being anesthetized, and Optimal function of physiologic systems in the body occurs during skin preparation, significant evaporative cooling can within a narrow range of core temperatures. A 2° C drop in body take place; the patient is kept warm by increasing the ambient temperature or a 3° C increase signifies a health emergency that temperature and using heated humidifiers and warmed IV is life­threatening and requires immediate intervention. Hypo­ fluid. After the patient is draped, the room temperature can be thermia can result from a number of mechanisms preoperatively, lowered to a more comfortable setting. A forced­air warming intraoperatively, or postoperatively. A trauma patient with inju­ device that provides active cutaneous warming is placed on the ries in a cold environment can suffer significant hypothermia, patient. Passive surface warming is not effective in conserving and paralysis can lead to hypothermia because of loss of the heat. There is some evidence that a considerable amount of shiver mechanism. heat is lost through the head of the patient, so simply covering Hypothermia develops in patients undergoing rapid resus­ the patient’s head during surgery may prevent significant heat citation with cool IV fluids, transfusions, or intracavitary irriga­ loss. tion with cold irrigant, and in patients undergoing a prolonged In the perioperative period, mild hypothermia is common­ surgical procedure with low ambient room temperature and a place and patients usually shiver because the anesthesia impairs large, exposed operative area subjected to significant evaporative thermoregulation. Many patients who shiver after anesthesia, cooling. Almost all anesthetics impair thermoregulation and however, are hypothermic. Treatment of the hypothermia with render the patient susceptible to hypothermia in the typically forced­air warming systems and radiant heaters will also reduce cool operating room environment.9 Advanced age and opioid the shivering.9 In a severely hypothermic patient who does not analgesia also reduce perioperative shivering. Propofol causes require immediate operative intervention; attention must be vasodilation and significant redistribution hypothermia. Postop­ directed toward rewarming by the following methods: eratively, hypothermia can result from cool ambient room tem­ 1. Immediate placement of warm blankets, as well as perature, rapid administration of IV fluids or blood, and failure currently available forced­air warming devices to keep patients covered when they are only partially responsive. 2. Infusion of blood and IV fluids through a warming More than 80% of elective operative procedures are associated device with a drop in body temperature, and 50% of trauma patients 3. Heating and humidifying inhalational gases are hypothermic on arrival in the operating suite. 4. Peritoneal lavage with warmed fluids 5. Rewarming infusion devices with an arteriovenous presentation system Hypothermia is uncomfortable because of the intense cold sen­ 6. In rare cases, cardiopulmonary bypass sation and shivering. It may also be associated with profound Special attention must be paid to cardiac monitoring effects on the cardiovascular system, coagulation, wound healing, during the rewarming process because cardiac irritability may be and infection. A core temperature lower than 35° C after surgery a significant problem. Similarly, acid­base disturbances must be triggers a significant peripheral sympathetic nervous system aggressively corrected while the patient is being rewarmed. Once response, consisting of an increased norepinephrine level, vaso­ in the operating room, measures noted earlier to keep the patientK2 constriction, and elevated arterial blood pressure. Patients in warm are applied. Townsend_Chapter 13_main.indd 8 6/10/2011 12:36:19 PM
    • Surgical coMPlicationS  chapter 13  13-9 malignant Hyperthermia Box 13-3  Management of Malignant hyperthermia SeCtion ii PerioPerative ManageMent Causes Discontinue the triggering anesthetic. Malignant hyperthermia (MH) is a life­threatening hypermeta­ Hyperventilate the patient with 100% oxygen. bolic crisis manifested during or after exposure to a triggering administer alternative anesthesia. general anesthetic in susceptible individuals. It is estimated that terminate surgery. 5 MH occurs in 1 in 30,000 to 50,000 adults. Mortality from give dantrolene, 2.5 mg/kg, as a bolus and repeat every 5 min,  38 MH has decreased to less than 10% in the last 15 years as a then 1 to 2 mg/kg/hr until normalization or disappearance  result of improved monitoring standards that allow early detec­ of symptoms. tion of MH, availability of dantrolene, and increased use of check  and  monitor  arterial  blood  gas  and  creatine  kinase,   susceptibility testing. electrolyte, lactate, and myoglobin levels. Susceptibility to MH is inherited as an autosomal domi­ Monitor the electrocardiogram, vital signs, and urine output. nant disease with variable penetrance. To date, two MH suscep­ adjunctive and supportive measures are carried out: tibility genes have been identified in humans and four mapped • volatile  vaporizers  are  removed  from  the  anesthesia  to specific chromosomes but not definitely identified. The muta­ machine. tion results in altered calcium regulation in skeletal muscle in • carbon dioxide canisters, bellows, and gas hoses are  the form of enhanced efflux of calcium from the sarcoplasmic changed. reticulum into the myoplasm. Halogenated inhalational anes­ • Surface  cooling  is  achieved  with  ice  packs  and  core  thetic agents (e.g., halothane, enflurane, isoflurane, desflurane, cooling with cool parenteral fluids. and sevoflurane) and depolarizing muscle relaxants (e.g., succi­ • acidosis  is  monitored  and  treated  with  sodium  nylcholine, suxamethonium) cause a rise in the myoplasmic Ca2+ bicarbonate. concentration. When an MH­susceptible individual is exposed • arrhythmias  are  controlled  with  beta  blockers  or  to a triggering anesthetic, there is abnormal release of Ca2+, lidocaine. which leads to prolonged activation of muscle filaments, culmi­ • urine  output  more  than2 ml/kg/hr  is  promoted;  nating in rigidity and hypermetabolism. Uncontrolled glycolysis furosemide (lasix) or mannitol and a glucose-insulin  and aerobic metabolism give rise to cellular hypoxia, progressive infusion  (0.2 u/kg  in  a  50%  glucose  solution)  are  lactic acidosis, and hypercapnia. The continuous muscle activa­ given  for  hyperkalemia,  hypercalcemia,  and  tion with adenosine triphosphate breakdown results in excessive myoglobulinuria. generation of heat. If untreated, myocyte death and rhabdomy­ the patient is transferred to the intensive care unit to monitor  olysis result in hyperkalemia and myoglobulinuria. Eventually, for recurrence. disseminated coagulopathy, congestive heart failure (CHF), bowel ischemia, and compartment syndrome develop. Once MH is suspected or diagnosed, the steps outlined in presentation and management Box 13­3 are followed. Dantrolene is a muscle relaxant. In the MH can be prevented by identifying at­risk individuals before solution form, it is highly irritating to the vein and must be surgery. MH susceptibility is suspected preoperatively in a administered in a large vein. When given intravenously, it blocks patient with a family history of MH or a personal history of up to 75% of skeletal muscle contraction and never causes myalgia after exercise, a tendency for the development of fever, paralysis. The plasma elimination half­life is 12 hours. Dan­ muscular disease, and intolerance to caffeine. In these cases, the trolene is metabolized in the liver to 5­hydroxydantrolene, creatine kinase level is checked, and a caffeine and halothane which also acts as a muscle relaxant. Side effects reported with contraction test (or an in vitro contracture test developed in dantrolene therapy include muscle weakness, phlebitis, respira­ Europe) may be performed on a muscle biopsy specimen from tory failure, GI discomfort, hepatotoxicity, dizziness, confusion, the thigh.10 MH­susceptible individuals confirmed by abnormal and drowsiness. Another agent, azumolene, is 30 times more skeletal muscle biopsy findings or those with suspected MH water­soluble than and equipotent to dantrolene in the treat­ susceptibility who decline a contracture test are given a trigger­ ment of MH; like dantrolene, it does not affect the heart. Its free anesthetic (e.g., barbiturate, benzodiazepine, opioid, pro­ main side effect is marked pulmonary hypertension. However, pofol, etomidate, ketamine, nitrous oxide, nondepolarizing azumolene is not in clinical use at this time. neuromuscular blocker). Unsuspected MH­susceptible individuals may manifest postoperative Fever MH for the first time during or immediately after the adminis­ tration of a triggering general anesthetic. The clinical manifesta­ Causes tions of MH are not uniform and vary in onset and severity. One of the most concerning clinical findings in a patient post­ Some patients manifest the abortive form of MH (e.g., tachy­ operatively is the development of fever. Fever describes a rise in cardia, arrhythmia, raised temperature, acidosis). Others, after core temperature, modulation of which is managed by the ante­ intubation with succinylcholine, demonstrate loss of twitches on rior hypothalamus. Fever may result from bacterial invasion or neuromuscular stimulation and develop muscle rigidity. An their toxins, which stimulate the production of cytokines. inability to open the mouth as a result of masseter muscle spasm Trauma (including surgery) and critical illness also invoke a is a pathognomonic early sign and indicates susceptibility to cytokine response. Cytokines are low­molecular­weight proteins MH. Other manifestations include tachypnea, hypercapnia, that act in an autocrine, paracrine, and/or endocrine fashion to skin flushing, hypoxemia, hypotension, electrolyte abnormali­ influence a broad range of cellular function and exhibit proin­ ties, rhabdomyolysis, and hyperthermia. flammatory and anti­inflammatory effects. The inflammatory K2Townsend_Chapter 13_main.indd 9 6/10/2011 12:36:19 PM
    • 13-10  section ii  PerioPerative ManageMent infections are preventable and are considered a “never” compli­ table 13-5  causes of postoperative Fever cation by the Centers of Medicare and Medicaid Services.13 inFectioUs noninFectioUs CR­BSI results from microorganisms that colonize the hubs or abscess acute hepatic necrosis from contamination of the injection site of the central venous acalculous cholecystitis adrenal insufficiency catheter (intraluminal source) or skin surrounding the insertion site (extraluminal source). Coagulase­negative staphylococci, Bacteremia allergic reaction hospital­acquired bacteria (e.g., MRSA, multidrug­resistant Decubitus ulcers atelectasis gram­negative bacilli, fungal species [Candida albicans]) are the Device-related infections Dehydration most common organisms responsible for CR­BSI. S. aureus bac­ empyema Drug reaction teremia is associated with higher mortality and venous throm­ bosis. Metastatic infections (endocarditis) are uncommon but endocarditis Head injury represent a serious complication of CR­BSI. The duration of 6 Fungal sepsis Hepatoma central venous catheter placement, patient location (outpatient Hepatitis Hyperthyroidism versus inpatient), type of catheter, number of lumens and Meningitis lymphoma manipulations daily, emergent placement, need for total paren­ teral nutrition (TPN), presence of unnecessary connectors, and osteomyelitis Myocardial infarction whether best care practices are followed are risk factors for BSI.14 Pseudomembranous colitis Pancreatitis Parotitis Pheochromocytoma presentation and management In evaluating a patient with fever, one has to take into consid­ Perineal infections Pulmonary embolus eration the type of surgery performed, patient’s immune status, Peritonitis retroperitoneal hematoma underlying primary disease process, duration of hospital stay, Pharyngitis Solid organ hematoma and epidemiology of hospital infections. Pneumonia Subarachnoid hemorrhage High fever that fluctuates or is sustained and that occurs 5 to 8 days after surgery is more worrisome than fever that occurs retained foreign body Systemic inflammatory early postoperatively. In the first 48 to 72 hours after abdominal Sinusitis response syndrome surgery, atelectasis is often believed to be the cause of the fever. Soft tissue infection thrombophlebitis Occasionally, clostridial or streptococcal SSIs can manifest as tracheobronchitis transfusion reaction fever within the first 72 hours of surgery. Temperatures that are elevated 5 to 8 days postoperatively demand immediate atten­ urinary tract infection Withdrawal syndromes tion and, at times, intervention. Evaluation involves studying Wound infection the six Ws: wind (lungs), wound, water (urinary tract), waste (lower GI tract), wonder drug (e.g., antibiotics), and walker (e.g., thrombosis). The patient’s symptoms usually indicate the response results in the production of a variety of mediators that organ system involved with infection; cough and productive induce a febrile inflammatory response, also known as systemic sputum suggest pneumonia, dysuria and frequency indicate a inflammatory response syndrome.11 Hence, fever in the post­ UTI, watery foul­smelling diarrhea develops as a result of infec­ operative period may be the result of an infection or caused tion with C. difficile, pain in the calf may be caused by deep by systemic inflammatory response syndrome. Fever after venous thrombosis (DVT), and flank pain may be caused by surgery is reported to occur in up to two thirds of patients, and pyelonephritis. Physical examination may show an SSI, phlebi­ infection is the cause of fever in approximately one third of cases. tis, tenderness on palpation of the abdomen, flank, or calf, or Numerous disease states can cause fever in the postoperative cellulitis at the site of a central venous catheter. period (Table 13­5). A complete blood count, urinalysis and culture, radiograph The most common infections, however, are health care– of the chest, and blood culture are essential initial tests. A associated infections—SSI, urinary tract infection (UTI), intra­ chest radiograph may show a progressive infiltrate suggestive of vascular catheter–related bloodstream infection (CR­BSI), and the presence of pneumonia. Urinalysis showing more than 105 pneumonia. Urinary tract infection is a common postoperative colony­forming units/milliliter (CFU/mL) in a noncatheterized event and a significant source of morbidity in postsurgical patient and more than 103 CFU/mL in a catheterized patient patients. A major predisposing factor is the presence of a urinary indicates a urinary tract infection. The diagnosis of CR­BSI rests catheter; the risk increases with increased duration of catheter­ on culture data because physical examination is usually unreveal­ ization (>2 days). Endogenous bacteria (colonic flora, most ing. There is no gold standard for how to use blood cultures. common E. coli) are the most common source of catheter­related Two simultaneous blood cultures or paired blood cultures (i.e., urinary tract infection in patients with short­term catheteriza­ simultaneous peripheral and central blood cultures) are com­ tion. With prolonged catheterization, additional bacteria are monly used. Peripheral blood cultures showing bacteremia and found. In the critically ill surgical patient, candiduria accounts isolation of 15 CFUs or 102 CFUs from an IV catheter indicate for approximately 10% of nosocomial urinary tract infection. the presence of a CR­BSI. In tunneled catheters, a quantitative The presence of an indwelling catheter, diabetes mellitus, use of colony count that is 5­ to 10­fold higher in cultures drawn antibiotics, advanced age, and underlying anatomic urologic through the central venous catheter is predictive of CRC­BSI. abnormalities are risk factors for candiduria.12 If paired cultures are obtained, positive culture more than2 The use of central venous catheters carries a risk of CR­BSI hours before peripheral culture indicates the presence of CR­BSI.K2 that increases hospital stay and morbidity and mortality. The After removal of the catheter, the tip may be sent for quantitative Townsend_Chapter 13_main.indd 10 6/10/2011 12:36:19 PM
    • Surgical coMPlicationS  chapter 13  13-11 culture. Serial blood cultures and a transesophageal echocardio­ days. For patients with septic thrombosis or endocarditis, SeCtion ii PerioPerative ManageMent gram are obtained in patients with S. aureus bacteremia and treatment is continued for 4 to 6 weeks. Catheter salvage is valvular heart disease, prosthetic valve, or new onset of murmur. indicated in patients with tunneled catheters that are risky to Patients who continue to have fever, slow clinical progress, and remove or replace, or in patients with coagulase­negative no discernible external source may require computed tomogra­ staphylococci who have no evidence of metastatic disease or phy (CT) of the abdomen to look for an intra­abdominal source severe sepsis, do not have tunnel infection, or do not have of infection. persistent bacteremia. Catheter salvage is achieved by antibi­ Prevention of urinary tract infection starts with minimiz­ otic lock therapy whereby the catheter is filled with antibiotic ing the duration of catheterization and maintenance of a solution for several hours. closed drainage system. When prolonged catheterization is required, changing the catheter before blockage occurs is rec­ reSpiratory complicationS ommended because the catheter serves as a site for pathogens to create a biofilm. The efficacy of strategies to prevent or general considerations delay the formation of a biofilm, such as the use of silver alloy A host of factors contribute to abnormal pulmonary physiology or impregnated catheters and the use of protamine sulfate and after an operative procedure. First, loss of functional residual chlorhexidine in reducing catheter­related UTIs has yet to be capacity is present in almost all patients. This loss may be the established.15 result of a multitude of problems, including abdominal disten­ On the other hand, most if not all CR­BSIs are preventable tion, painful upper abdominal incision, obesity, strong smoking by adopting maximal barrier precautions and infection control history with associated chronic obstructive pulmonary disease, practice during insertion. Educational programs that stress best prolonged supine positioning, and fluid overload leading to practice that targets those placing the catheter and those respon­ pulmonary edema. Almost all patients who undergo an abdom­ sible for maintenance of the catheter are important. Removal of inal or thoracic incision have a significant alteration in their catheters when they are not needed is paramount. On placing breathing pattern. Vital capacity may be reduced up to 50% of the catheter, there must be strict adherence to aseptic technique, normal for the first 2 days after surgery for reasons that are not the same as in the operating room—hand hygiene, skin antisep­ completely clear. The use of narcotics substantially inhibits the sis, full barrier precaution and stopping insertion when breaks respiratory drive, and anesthetics may take some time to wear in sterile technique occur. The subclavian vein is preferable to off. Most patients who have respiratory problems postopera­ jugular and femoral vein. Involvement of a catheter care team tively have mild to moderate problems that can be managed with for proper catheter care after insertion has proven effective in aggressive pulmonary toilet. However, in some patients, severe reducing the incidence of CR­BSIs. Antiseptic­ and antibiotic­ postoperative respiratory failure develops; this may require intu­ impregnated catheters decrease catheter colonization and bation and ultimately may be life­threatening. CR­BSIs but their routine use is not recommended. Two types of respiratory failure are commonly described. Type I, or hypoxic, failure results from abnormal gas exchange treatment at the alveolar level. This type is characterized by a low Pao2 with Management of postoperative fevers is dictated by the results a normal Paco2. Such hypoxemia is associated with ventilation­ of a careful workup. Management of the elevated temperature perfusion (V/Q ) mismatching and shunting. Clinical conditions itself is controversial. Although the fever may not be life­ associated with type I failure include pulmonary edema and threatening, the patient is usually uncomfortable. Attempts to sepsis. Type II respiratory failure is associated with hypercapnia bring the temperature down with antipyretics are recom­ and is characterized by a low Pao2 and high Paco2. These patients mended. If pneumonia is suspected, empirical broad­spectrum are unable to eliminate CO2 adequately. This condition is often antibiotic therapy is started and then altered according to associated with excessive narcotic use, increased CO2 produc­ culture results. tion, altered respiratory dynamics, and adult respiratory distress A UTI is treated with removal or replacement of the cath­ syndrome (ARDS). The overall incidence of pulmonary compli­ eter with a new one. In systemically ill patients, broad­spectrum cations exceeds 25% in surgical patients. Of all postoperative antibiotics are started, because most offending organisms exhibit deaths, 25% are caused by pulmonary complications, and pul­ resistance to several antibiotics, and then tailored according to monary complications are associated with 25% of the other culture and susceptibility results. In patients with asymptomatic lethal complications. Thus, it is of critical importance that the bacteruria, antibiotics are recommended for immunocompro­ surgeon anticipate and prevent the occurrence of serious respira­ mised patient, patients undergoing urologic surgery, implanta­ tory complications. tion of a prosthesis, or patients with infections caused by strains One of the most important elements of prophylaxis is with a high incidence of bacteremia. Patients with candiduria careful preoperative screening of patients. Most patients have no are managed in a similar fashion. The availability of fluconazole, pulmonary history and need no formal preoperative evaluation. a less toxic antifungal than amphotericin B, however, has encour­ However, all patients with a history of heavy smoking, main­ aged clinicians to use it more frequently. tained on home oxygen, unable to walk one flight of stairs The treatment of CR­BSI entails removal of the catheter, without severe respiratory compromise, previous history of with adjunctive antibiotic therapy. A nontunneled catheter can major lung resection, and older patients who are malnourished be easily removed after establishing an alternative venous must be carefully screened with pulmonary function tests. Sim­ access. Single­agent therapy is sufficient and usually involves ilarly, patients managed by chronic bronchodilator therapy for vancomycin, linezolid, or empirical coverage of gram­negative asthma or other pulmonary conditions also need to be assessed bacilli and Candida spp. in patients with severe sepsis or carefully. Although there is some controversy about the value of immunosuppression. Treatment is continued for 10 to 14 perioperative assessment, most careful clinicians will study a K2Townsend_Chapter 13_main.indd 11 6/10/2011 12:36:20 PM
    • 13-12  section ii  PerioPerative ManageMent high­risk pulmonary patient before making an operative deci­ ventilator­associated pneumonia. Tubes traversing the aerodiges­ sion. The assessment may start with posteroanterior and lateral tive tract serve as conduits for bacteria to migrate to the lower chest radiographs to evaluate the appearance of the lungs. It respiratory tract.16 The most common pathogens encountered in serves as a baseline if the patient should have problems patients with hospital­acquired pneumonia depend on prior postoperatively. antibiotic therapy. In patients with early hospital­acquired pneu­ Similarly, a patient with polycythemia or chronic respira­ monia and no prior antibiotic therapy, the most common organ­ tory acidosis warrants careful assessment. A room temperature isms are Streptococcus pneumoniae (colonizes upper airway), arterial blood gas analysis is carried out in high­risk patients. Haemophilus influenzae, Enterobacteriaceae spp. (E. coli, Klebsi- Any patient with a Pao2 lower than 60 mm Hg is at increased ella spp., and Enterobacter spp.), and S. aureus (mostly MRSA). risk. If the Paco2 is more than 45 to 50 mm Hg, perioperative Patients with early hospital­acquired pneumonia and recent morbidity might be anticipated. Spirometry is a simple test that antibiotic therapy and those with late hospital­acquired pneu­ high­risk patients undergo before surgery. Probably the most monia also have gram­negative bacilli involved. The bacteria are important parameter in spirometry is the forced expiratory occasionally resistant to first­generation cephalosporins. The volume in 1 second (FEV1). Studies have demonstrated that any organisms in patients with late­onset hospital­acquired pneumo­ patient with an FEV1 higher than 2 liters will probably not have nia and prior history of antibiotics exhibit multidrug resistance serious pulmonary problems. Conversely, patients with an FEV1 (P. aeruginosa, Acinetobacter baumannii, and MRSA). lower than 50% of the predicted value will probably have exer­ tional dyspnea. If bronchodilator therapy demonstrates an Diagnosis improvement in breathing patterns by 15% or more, broncho­ The most common cause of a postoperative fever in the first 48 dilation is considered. Consultation with the patient includes a hours after the procedure is atelectasis. Patients present with a discussion about cessation of cigarette smoking 48 hours before low­grade fever, malaise, and diminished breath sounds in the the operative procedure, as well as a careful discussion about the lower lung fields. Frequently, the patient is uncomfortable from importance of pulmonary toilet after the operative procedure. the fever but has no other overt pulmonary symptoms. Atelec­ tasis is so common postoperatively that a formal workup is not atelectasis and pneumonia usually required. With the use of incentive spirometry, deep The most common postoperative respiratory complication is breathing, and coughing, most cases of atelectasis will resolve atelectasis. As a result of the anesthetic, abdominal incision, and without any difficulty. However, if aggressive pulmonary toilet postoperative narcotics, the alveoli in the periphery collapse and is not instituted or the patient refuses to participate, frank devel­ a pulmonary shunt may occur. If appropriate attention is not opment of pneumonia is likely. The patient with pneumonia will directed to aggressive pulmonary toilet with the initial symp­ have a high fever and occasional mental confusion, and produces toms, the alveoli remain collapsed and a buildup of secretions a thick secretion with coughing, leukocytosis, and chest radio­ occurs and becomes secondarily infected with bacteria, resulting graph that reveals infiltrates. If the patient is not expeditiously in pneumonia. The risk appears to be particularly high in diagnosed and treated, this condition may rapidly progress to patients who are heavy smokers, are obese, and have copious respiratory failure and require intubation. Concurrently with the pulmonary secretions. initiation of aggressive pulmonary toilet, inducted sputum for Pneumonia is the most common nosocomial infection culture and sensitivity should be sent immediately to the labora­ occurring in hospitalized patients. Pneumonia occurring more tory. Quantitative cultures of the lower airways obtained by than 48 hours after admission and without antecedent signs of blind tracheobronchial aspiration, bronchoscopically guided infection is referred to as hospital­acquired pneumonia. Aspira­ sampling (bronchoalveolar lavage [BAL]), or protected specimen 7 tion of oropharyngeal secretion is a significant contributing brush allow more targeted antibiotic therapy and, most impor­ factor in its development. Extended intubation results in another tantly, decrease antibiotic use. Although pneumonia acquired in subset of hospital­acquired pneumonia, ventilator­associated the hospital accounts for only 5% of all patients, particularly in pneumonia—pneumonia occurring 48 hours after but within older patients, the process may rapidly progress to frank respira­ 72 hours of the initiation of ventilation. Health care–associated tory failure requiring intubation. pneumonia refers to pneumonia occurring in patients who had been hospitalized in the last 90 days, patients in nursing facilities treatment or frequenting a hemodialysis unit, and those who have received To prevent atelectasis and pneumonia, smokers are encouraged recent antibiotics, chemotherapy, or wound care. Although some to stop smoking for at least 1 week before surgery and the treat­ consider hospital­acquired pneumonia and health care– ment of patients with chronic obstructive pulmonary disease, associated pneumonia to be the same disease process, because asthma, and CHF is optimized. Adequate pain control and both have the same prevalent organisms, the prognosis is differ­ proper pulmonary hygiene are important in the postoperative ent. Hospital­acquired pneumonia arising early (<5 days) has period. A patient­controlled analgesia device seems to be associ­ better prognosis than that arising late (>5 days). Numerous ated with better pulmonary toilet, as does the use of an epidural factors are associated with increased risk for pneumonia: infusion catheter, particularly in patients with epigastric inci­ depressed immune status, concomitant disease, poor nutritional sions. Encouraging the patient to use the incentive spirometer status, increased length of hospital stay, smoking, increasing age, and cough while applying counterpressure with a pillow on the uremia, alcohol consumption, prior antibiotic therapy, presence abdominal incision site is most helpful. Rarely, other modalities of an endotracheal, nasogastric (NG), or enteric tube, and such as intermittent positive­pressure breathing and chest phys­ therapeutic proton pump inhibitor (PPI). Used to prevent iotherapy may be required. Patients on the ventilator are best stress ulceration, PPI increases colonization of the stomach kept in a semirecumbent position and subjected to proper oralK2 with pathogenic bacteria that can increase the risk of hygiene. Chlorhexidine rinse or nasal gel has been shown to Townsend_Chapter 13_main.indd 12 6/10/2011 12:36:20 PM
    • Surgical coMPlicationS  chapter 13  13-13 lower the rate of ventilator­associated pneumonia. Treatment gastroesophageal reflux, even with the absence of an NG tube, SeCtion ii PerioPerative ManageMent with sucralfate as compared with a PPI for stress ulcer prophy­ and have altered GI motility. Prophylactic histamine 2 (H2) laxis may be considered for patients not at high risk for GI receptor antagonists or PPIs that increase gastric pH and allow bleeding. Proper endotracheal tube care, elimination of secre­ the gastric contents to become colonized by pathogenic organ­ tions pooling around the endotracheal cuff, frequent suctioning isms, tracheostomy, reintubation, and previous antibiotic expo­ with a closed suction technique, and use of protocols designed sure are other factors associated with an increased risk for health to minimize mechanical ventilation can lead to decreased care–related pneumonia. The risk of aspiration is high after ventilator­associated pneumonia. Once the diagnosis is made, extubation because of the residual effect of sedation, the NG and while awaiting culture results, treatment with empirical tube, and oropharyngeal dysfunction. antibiotic therapy is associated with decreased mortality. The The pathophysiology of aspiration pneumonitis is related choice of antimicrobial agent depends on the patient’s risk to the pulmonary intake of gastric contents at a low pH associ­ factors, length of hospital stay, duration of mechanical ventila­ ated with particulate matter. The severity of lung injury increases tion, prior antibiotic therapy and culture results, and immuno­ as the volume of aspirate increases and its pH decreases. The suppression. process often progresses rapidly, may require intubation soon after the injury occurs, and later sets the stage for bacterial infec­ aspiration pneumonitis and tion. The infection is refractory to management because of the aspiration pneumonia combination of infection occurring in an injured field. The pathophysiology of aspiration pneumonia is related to bacteria Causes gaining access to the lungs. Aspiration of oropharyngeal or gastric contents into the respira­ tory tract is a serious complication of surgery. Aspiration pneu­ presentation and Diagnosis monitis (Mendelson’s syndrome) describes acute lung injury that A patient with aspiration pneumonitis often has associated vom­ results from the inhalation of regurgitated gastric contents, iting and may have received general anesthesia or had an NG whereas aspiration pneumonia results from the inhalation of tube placed. The patient may be obtunded or have altered levels oropharyngeal secretions that are colonized by pathogenic bac­ of consciousness. Initially, the patient may have associated teria. Although there is some overlap between the two disease wheezing and labored respiration. Many patients who aspirate entities with regard to predisposing factors, their clinicopatho­ gastric contents have a cough or a wheeze. Some patients, logic features are distinct. however, have silent aspiration suggested by an infiltrate on a Factors that predispose patients to regurgitation and aspira­ chest radiograph (CXR) or decreased Pao2. Others have cough, tion include impairment of the esophageal sphincters (upper and shortness of breath, and wheezing that progress to pulmonary lower) and laryngeal reflexes, altered GI motility, and absence of edema and ARDS. In the great majority of patients with aspira­ preoperative fasting. A number of iatrogenic maneuvers place tion pneumonia, on the other hand, in a susceptible patient, the the patient at increased risk for aspiration in a hospital setting. condition is diagnosed after a chest radiograph shows an infil­ In the perioperative period, aspiration is more likely with urgent trate in the posterior segments of the upper lobes and the apical surgery, in patients with altered levels of consciousness, and in segments of the lower lobes. patients with GI and airway problems. Trauma patients and patients with peritonitis and bowel obstruction may have a treatment depressed level of consciousness and airway reflexes, a full Prevention of aspiration in patients undergoing surgery is stomach as a result of a recent meal or gastric stasis, or GI pathol­ achieved by instituting measures that reduce gastric contents, ogy that predisposes to retrograde emptying of intestinal con­ minimize regurgitation, and protect the airway. For adults, a tents into the stomach. Patients with depressed levels of period of no oral intake, usually 6 hours after a night meal, 4 consciousness as a result of high doses of narcotics and patients hours after clear liquids, and a longer period for diabetics, is who have suffered cerebrovascular accidents are obtunded and necessary to reduce gastric contents before elective surgery.17 have neurologic dysphagia and dysfunction of the gastroesopha­ Routine use of H2 antagonists or PPIs to reduce gastric acidity geal junction. Anesthetic drugs lower esophageal sphincter tone and volume has not been shown to be effective in reducing the and depress the patient’s level of consciousness. Diabetics have mortality and morbidity associated with aspiration and hence is gastroparesis and gastric stasis. Patients with an increased bacte­ not recommended. When a difficult airway is encountered, rial load in the oropharynx and depressed defense mechanisms awake fiberoptic intubation is performed. In emergency situa­ as a result of an altered level of consciousness are at risk for tions in patients with a potentially full stomach, preoxygenation aspiration pneumonia. is accomplished without lung inflation, and intubation is per­ Older adults are particularly susceptible to oropharyngeal formed after applying cricoid pressure during rapid­sequence aspiration because of an increased incidence of dysphagia and induction. In the postoperative period, identification of an older poor oral hygiene. Patients with a NG tube or who are debili­ or overly sedated patient, or a patient whose condition is dete­ tated are also at risk for aspiration because they have difficulty riorating, mandates instituting maneuvers to protect the patient’s swallowing and clearing their airway. The risk for aspiration airway. Postoperatively, it is important to avoid the overuse of pneumonia is similar in patients receiving feeding via an NG, narcotics, encourage the patient to ambulate, and cautiously nasoenteric, or gastrostomy tube; patients receiving nutrition via feed a patient who is obtunded, older, or debilitated. a gastrostomy tube frequently have scintigraphic evidence of A patient who sustains aspiration of gastric contents needs aspiration of gastric contents. The critically ill are at an increased to be placed on oxygen immediately and have a chest radiograph risk for aspiration and aspiration pneumonia because they are to confirm the clinical suspicions. A diffuse interstitial pattern in a supine position, have an NG tube in place, exhibit is usually seen bilaterally and is often described as bilateral, fluffy K2Townsend_Chapter 13_main.indd 13 6/10/2011 12:36:20 PM
    • 13-14  section ii  PerioPerative ManageMent infiltrates. Close surveillance of the patient is absolutely essen­ common manifestations of such injury are pulmonary edema, tial. If the patient is maintaining oxygen saturation via a face acute lung injury, and ARDS. The clinician’s ability to recognize mask without excessively high work of breathing, intubation and distinguish among these conditions is of critical importance may not be required. However, if the patient’s oxygenation dete­ because clinical management of these three entities varies con­ riorates or the patient is obtunded, the work of breathing siderably. increases, as manifested by an increased respiratory rate, and Pulmonary edema is a condition associated with accumula­ prompt intubation must be accomplished. After intubation for tion of fluid in the alveoli. As a result of the fluid in the lumen suspected aspiration, suctioning the bronchopulmonary tree will of the alveoli, oxygenation cannot take place and hypoxemia confirm the diagnosis and remove any particulate matter. occurs. As a consequence, the patient must increase the work of Administration of antibiotics shortly after aspiration is con­ breathing, including an increased respiratory rate and exagger­ troversial, except in patients with bowel obstruction or other ated use of the muscles of breathing. Pulmonary edema is usually conditions associated with colonization of gastric contents. caused by increased vascular hydrostatic pressure associated with Administration of empirical antibiotics is also indicated for a CHF and acute myocardial infarction (MI). It is also commonly patient with aspiration pneumonitis that does not resolve or associated with fluid overload as a result of overly aggressive improve within 48 hours of aspiration. Corticosteroid adminis­ resuscitation (Box 13­4). tration does not provide any beneficial effects to patients with A consensus conference has identified acute lung injury 8 aspiration pneumonitis. Antibiotic therapy with activity against and ARDS as two separate grades of respiratory failure second­ gram­negative organisms is indicated for patients with aspiration ary to injury. In contrast to pulmonary edema, which is associ­ pneumonia. ated with increased wedge and right­sided heart pressure, acute lung injury and ARDS are associated with hypo­oxygenation pulmonary edema, acute lung injury, and because of a pathophysiologic inflammatory response that leads adult respiratory distress Syndrome to the accumulation of fluid in the alveoli, as well as thickening in the space between the capillaries and the alveoli. Acute lung Causes injury is associated with a Pao2/Fio2 (fraction of inspired oxygen) A wide variety of injuries to the lungs or cardiovascular system, ratio of less than 300, bilateral infiltrates on chest radiography, or both, may result in acute respiratory failure. Three of the most and a wedge pressure less than 18 mm Hg. It tends to be shorter in duration and not as severe. On the other hand, ARDS is associated with a Pao2/Fio2 ratio of less than 200 and also has Box 13-4  conditions Leading to pulmonary edema, acute  bilateral infiltrates and a wedge pressure less than 18 mm Hg. Lung injury, and adult respiratory Distress syndrome presentation and management increased Hydrostatic pressure Patients with pulmonary edema often have a corresponding acute left ventricular failure cardiac history, recent history of massive fluid administration, chronic congestive heart failure or both. In the presence of a frankly abnormal chest radiograph, obstruction of the left ventricular outflow tract invasive monitoring in the form of a Swan­Ganz catheter for thoracic lymphatic insufficiency evaluation of pulmonary capillary wedge pressure may be indi­ volume overload cated. Patients with an elevated wedge pressure are managed altered permeability State by fluid restriction and aggressive diuresis. Administration of acute radiation pneumonitis oxygen via face mask in mild cases and intubation in more severe aspiration of gastric contents cases is also clinically indicated. In most cases, the pulmonary Drug overdose edema resolves quickly after diuresis and fluid restriction. near-drowning Patients with acute lung injury and ARDS generally have Pancreatitis tachypnea, dyspnea, and increased work of breathing, as mani­ Pneumonia fested by exaggerated use of the muscles of breathing. Cyanosis Pulmonary embolus is associated with advanced hypoxia and is an emergency. Aus­ Shock states cultation of the lung fields reveals poor breath sounds associated Systemic inflammatory response syndrome and multiple organ  with crackles and, occasionally, with rales. Arterial blood gas failure analysis will reveal the presence of a low Pao2 and high Paco2. Sepsis Administration of oxygen alone does not usually result in transfusion improvement in the hypoxia. trauma and burns In patients with impending respiratory failure, including tachypnea, dyspnea, and air hunger, management of acute lung mixed or incompletely understood pathogenesis injury and ARDS is initiated by immediate intubation plus Hanging injuries careful administration of fluids; invasive monitoring with a High-altitude pulmonary edema Swan­Ganz catheter to assess wedge pressure and right­sided narcotic overdose heart pressure is occasionally helpful. The strategy involves neurogenic pulmonary edema maintaining the patient on the ventilator with assisted breathing Postextubation obstructive pulmonary edema while the injured lung heals. A patient with severe acute lung reexpansion pulmonary edema injury or ARDS is initially placed on an Fio2 of 100% and then tocolytic therapy weaned to 60% as healing takes place. Positive end­expiratoryK2 uremia pressure is a valuable addition to ventilator management of Townsend_Chapter 13_main.indd 14 6/10/2011 12:36:20 PM
    • Surgical coMPlicationS  chapter 13  13-15 table 13-6  criteria for Weaning from the Ventilator table 13-7  risk Factors for Venous thromboembolism SeCtion ii PerioPerative ManageMent paraMeter WeaninG criteria cateGorY Factors respiratory rate <25 breaths/min general factors advancing age Hospitalization or nursing home (with or  Pao2 >70 mm Hg (Fio2 of 40%) without surgery) indwelling venous catheters Paco2 <45 mm Hg neurologic disease (plegia and paresis) Minute ventilation 8-9 liters/min cardiomyopathy, myocardial infarction, or  heart failure secondary to valve disease tidal volume 5-6 ml/kg acute pulmonary disease (adult respiratory  distress syndrome and pneumonia) negative inspiratory force −25 cm H2o chronic obstructive lung disease varicose veins inherited thrombophilia Protein c deficiency Protein S deficiency patients with this injury. Similarly, tidal volume needs to be 6 antithrombin iii deficiency to 8 mL/kg, with peak pressure kept at 35 cm H2O. Tidal Dysfibrinogenemia Factor v leiden mutation volume is set at 10 to 12 mL/kg of body weight and the respira­ Prothrombin gene mutation tory rate is chosen to produce a Paco2 near 40 mm Hg. In Hyperhomocysteinemia anticardiolipin antibody addition, the inspiratory­to­expiratory ratio is set at 1 : 2. Most Paroxysmal nocturnal hemoglobinemia patients will require heavy sedation and pharmacologic paralysis acquired thrombophilia Malignancy during the early phases of recuperation. inflammatory bowel disease Careful monitoring of oxygenation, improvement of the Heparin-induced thrombocytopenia respiratory rate with intermittent mandatory ventilation, and trauma Major surgery general alertness will suggest when the patient is ready to be Pregnancy/postpartum extubated. Criteria for extubation are listed in Table 13­6. nephrotic syndrome Behçet’s syndrome Systemic lupus erythematosus pulmonary embolism and History of venous thromboembolism Venous thromboembolism Causes Venous thromboembolism describes DVT and pulmonary Box 13-5  symptoms and signs of pulmonary embolism embolism (PE). PE is a serious postoperative complication that Pleuritic chest pain* represents a source of preventable morbidity and mortality in Sudden dyspnea* the United States and is responsible for 5% to 10% of all tachypnea in­hospital deaths. Undiagnosed PE has a hospital mortality rate Hemoptysis* as high as 30%, which falls to 8% if diagnosed and treated tachycardia* appropriately. leg swelling* Venous thromboembolism (VTE) is caused by a perturba­ Pain on palpation of the leg* tion of the homeostatic coagulation system induced by intimal acute right ventricular dysfunction injury, stasis of blood flow, and a hypercoagulable state. Risk Hypoxia factors for the development of VTE are listed in Table 13­7.18 Fourth heart sound* Thrombophilia describes hereditary and acquired biochem­ loud second pulmonary sound* ical states that predispose to VTE. One in four fatal PE cases inspiratory crackles* occurs in surgical patients. Survivors of VTE are at increased risk for recurrence. The highest risk of VTE occurs in patients *More common with pulmonary embolism. hospitalized for surgery. The prevalence of PE in patients with malignancy is 11%. The incidence of relative risk of DVT and PE in patients with inflammatory bowel disease is approximately long bones and air embolism, often related to operative proce­ 5% and 3%, respectively. In major trauma victims, the incidence dures and the presence of central lines. of DVT exceeds 50%, with fatal emboli occurring in 0.4% to 2% of cases. Critically ill and intensive care unit patients have presentation and Diagnosis multiple risk factors and are also at higher risk for VTE. Central The physiologic response to PE depends on the size of the venous catheter–related thromboses are more common with thrombus, coexisting cardiopulmonary disease, and various neu­ femoral placement. Thrombosis ranges from 4% to 28% after rohormonal effects. More than 50% of DVTs are silent and PE subclavian vein cannulation and 4% to 33% after internal may be the first manifestation of the disease. Most symptoms jugular catheterization. In patients with subclavian or axillary and signs associated with symptomatic PE are nonspecific and vein thrombosis, PE is reported in 9.4%. may be encountered with other disease states, such as MI, pneu­ Most PEs originate from an existing DVT in the legs, and mothorax, and pneumonia (Box 13­5). CXR has limited value the iliofemoral venous system represents the site from which in the diagnosis of PE and is mainly used to rule out other causes most clinically significant pulmonary emboli arise. Approxi­ of a patient’s symptoms. Approximately 5% to 10% of patients mately 50% of patients with proximal DVT develop a PE. Rare develop a massive PE that results in hemodynamic instability causes of PE include a fat embolus associated with fractures of (hypotension, with or without shock) and death. The K2Townsend_Chapter 13_main.indd 15 6/10/2011 12:36:20 PM
    • 13-16  section ii  PerioPerative ManageMent probability of an individual having PE (pretest probability) is In critically ill patients with high suspicion for PE and assessed by the sum of points given to VTE risk factors: the patients with suspected massive PE, the workup depends on patient’s symptoms, signs, and laboratory results (e.g., electrocar­ their hemodynamic stability. In stable patients, anticoagulation diogram [ECG], CXR, and arterial blood gas) most likely to be is started if there are no contraindications, VUS is performed, associated with PE. Using various scoring systems, patients are and a spiral CT scan is obtained urgently. In unstable patients, stratified into low­, moderate­, and high­probability categories. anticoagulation is started and VUS and echocardiography are Establishing the diagnosis of PE requires confirmatory tests performed. If the echocardiographic results are positive, throm­ (helical CT scan and/or a pulmonary angiogram) and ancillary bolytic therapy is started and, if negative, a pulmonary angio­ tests (venous duplex ultrasound [VUS] and a D­dimer assay). gram is obtained. Helical CT, also known as spiral CT or CT pulmonary angiog­ raphy, has high specificity (92%) and sensitivity (86%), espe­ treatment cially for central PE (main pulmonary artery or subsegmental Medications used in the treatment of venous thromboembo­ branches) and has replaced the V/Q scan as the initial test of lism are the heparins, fondaparinux, VKAs, and thrombolytic choice. In addition to the findings listed in Box 13­5, spiral CT agents. Heparin prevents the thrombin­mediated conversion of also allows diagnosis of other pulmonary causes of a patient’s fibrinogen to fibrin and stops propagation of the thrombus. symptoms. The test, however, requires IV contrast, may not be UFH is inexpensive and highly effective, enhances antithrom­ available after normal working hours, requires a cooperative botic activity of antithrombin III and factor Xa, and has a short patient to avoid artifacts, may miss emboli in subsegmental plasma half­life. LMWH primarily inactivates factor Xa and arteries, which account for 20% of all pulmonary emboli, and has a longer half­life and more predictable anticoagulant prop­ may be inconclusive in approximately 10% of cases. Pulmonary erty. VKAs (e.g., warfarin) have a delayed onset of action and angiogram is the gold standard test because it visualizes the arte­ the potential to interact with other medications. Fondaparinux rial tree directly and detects intravascular filling defects. It is used is a synthetic pentasaccharide that selectively inhibits factor Xa. less commonly, however, because it is invasive, requires expertise, Thrombolytic agents (e.g., streptokinase, urokinase, recombi­ and after­hours availability is limited. nant tissue plasminogen activator) are used in the treatment of Echocardiography is a rapid, noninvasive, available massive PE. bedside test that provides quick results in a critically ill or Treatment of PE starts with prevention. Because the great hemodynamically unstable patient. Transthoracic echocardiog­ majority of PEs originates from existing clots in the deep venous raphy (TTE) shows the hemodynamic consequences of acute system of the legs in at­risk patients, identifying patients at risk ventricular pressure overload—namely, right ventricle dysfunc­ for DVT plus applying preventive measures is the only way to tion (hypokinesia and dilation), interventricular septal flatten­ decrease VTE­related morbidity and mortality. The intensity of ing and paradoxical motion, elevated tricuspid gradient, prophylaxis must match the risk for VTE and potential compli­ pulmonary hypertension, and a patent foramen ovale.19 Dys­ cations of the medication (e.g., bleeding, heparin­induced function of the right ventricle (RV) occurs in 30% to 50% of thrombocytopenia [HITT]). According to the American College patients with PE who undergo echocardiography. The trans­ of Clinical Pharmacy (ACCP), assessment of patients into low­, esophageal echocardiogram also shows secondary changes in moderate­ and high­risk categories for VTE is based on the type cardiac chamber size and functions caused by hemodynamic of surgery performed, patient mobility, risk of bleeding, and effects of the PE and may reveal a proximal intrapulmonary or VTE risk based on the presence of additional risk factors.20 Age free­floating intracardiac clot. Echocardiography also rules out is a significant risk factor, with the risk doubling with each other causes of shock such as a pericardial tamponade. Trans­ decade beyond the age of 40 years. Most hospitalized patients esophageal echocardiography is not always available and have at least one risk factor for VTE and approximately 50% of requires specialty training. them have more than three risk factors. Pharmacologic prophy­ VUS of the extremities is used as an indirect test for laxis is an accepted and effective strategy.21 In the critically ill, diagnosing PE. Approximately one third of patients with PE heparin is first­line prophylaxis. Prophylaxis is achieved with the will demonstrate lower extremity findings consistent with administration of low­dose UFH given SC every 8 hours or DVT, and 80% of PE patients have a DVT on the venogram. LMWH given as a daily dose. Recent studies have suggested that 10 D­dimer is a degradation product of a cross­linked fibrin LMWH is more effective prophylaxis than low­dose UFH in the blood clot. Levels are typically elevated in patients with acute critically ill and is associated a with reduced risk of major hem­ thromboembolism. Of the many D­dimer tests, enzyme­ orrhage. Overt bleeding and thrombocytopenia are contraindi­ linked immunosorbent assay (ELISA) is the most sensitive, cations to chemical prophylaxis. In patients undergoing surgery, with quick results. A negative test excludes the diagnosis, but LDUF is administered (5000 U, 3 to 4 hours preoperatively and 11 a positive test does not rule in the diagnosis. then every 8 hours). Fondaparinux has emerged as an alternative 12 Based on the pretest clinical probability, a patient suspected prophylactic after major orthopedic surgery. Nonpharmacologic 9 of having PE requires a CXR, ECG, arterial blood gas (ABG) prophylaxis can be achieved with elastic stockings, graduated analysis, and D­dimer assay. If leg symptoms are present, VUS compression stockings, intermittent pneumatic compression is performed and, if positive, the patient is considered to have devices, or venous foot pumps. Compression devices are not PE and receives anticoagulant medication because treatment is associated with bleeding. They produce a satisfactory reduction similar to that for PE. If leg symptoms are absent, the spiral CT in risk for DVT in high­risk surgical patients. However, little is approach may be used. If the findings on spiral CT are subop­ known about their efficacy as sole prophylaxis in the critically timal or negative and there is a high clinical probability of PE, ill and they may be most beneficial in combination with phar­ an angiogram is obtained. This approach is not appropriate for macologic prophylaxis in the subset of high­risk patients orK2 patients with iodinated dye allergy. solely in patients for whom the risk of bleeding is high. The Townsend_Chapter 13_main.indd 16 6/10/2011 12:36:20 PM
    • Surgical coMPlicationS  chapter 13  13-17 presence of leg ulcers and peripheral vascular disease precludes and intra­abdominal procedures are most commonly associated SeCtion ii PerioPerative ManageMent the use of mechanical devices. with hypertensive events. Preoperatively, most hypertension is Anticoagulation is the standard of care treatment for VTE. essential hypertension; much less common are cases associated It prevents clot propagation and allows endogenous fibrinolytic with renovascular causes and, even rarer, vasoactive tumors. activity to dissolve existing thrombi, a process that occurs over Intraoperatively, fluid overload and pharmacologic agents may weeks and months. Incomplete resolution is not uncommon and cause hypertension. Postoperatively, a host of causative factors predisposes to recurrent VTE. The initial treatment is with are associated with hypertension, including pain, hypothermia, LMWH, UFH, or fondaparinux, followed by VKA, which is hypoxia, fluid overload in the postanesthesia period caused by administered on the same day as LMWH or UFH, with overlap fluid mobilization from the extravascular compartment, and for 5 days or longer until the target INR is achieved. In patients discontinuation of chronic antihypertensive therapy before with VTE and active cancer, anticoagulation is continued indef­ surgery. Other causes of postoperative hypertension include initely. Surgical patients within 24 hours of surgery may be intra­abdominal bleeding, head trauma, clonidine withdrawal considered for a retrievable inferior vena cava filter until antico­ syndrome, and pheochromocytoma crisis. agulation is initiated. In patients with a contraindication to anticoagulation, placement of an inferior vena cava filter pro­ presentation and management tects against PE. Most cases of hypertension are detected during the routine pre­ 13 UFH is given intravenously (a weight­adjusted bolus of operative workup. The observant surgeon will consider hyper­ 70 U/kg is followed by 1000 U/hr) to achieve a partial throm­ tension in the preoperative screening of patients, recognizing boplastin time 1.5 to 2 times the control value. aPTT is deter­ that failure to detect significant problems with hypertension can mined 6 hours after the loading dose and then on a daily basis, lead to needless hypertension­related complications. By defini­ and the dose of heparin is adjusted accordingly. UFH is easily tion, any patient who has a diastolic blood pressure higher than reversible and hence the agent of choice. LMWH is given SC 110 mm Hg must be assessed and treated preoperatively if elec­ once or twice daily (enoxaparin, 1.5 mg/kg/day, or dalteparin, tive surgery is being contemplated. Patients taking chronic anti­ 10,000 to 18,000 U/day, depending on weight). Monitoring of hypertensive medications who are undergoing elective surgery LMWH is not necessary. Both UFH and LMWH may be asso­ are instructed to continue taking the medication up to the day of ciated with HITT, and therefore the platelet count is monitored surgery. Patients receiving oral clonidine can be switched to a between days 3 and 5. Warfarin is given orally and this therapy clonidine patch for at least 3 days before surgery. In emergency is allowed to overlap with heparin therapy until the INR is cases, the medications administered during induction and main­ therapeutic for 2 consecutive days before heparin is discontin­ tenance of anesthesia will assist in bringing the blood pressure ued. Therapy is continued for more than 3 months, with the down. Intraoperatively, the anesthesiologist must carefully goal to reach an INR of 2.5. monitor blood pressure, make certain that it stays within accept­ In massive PE, the goal of therapy is to maintain hemody­ able limits, and avoid fluid overload, hypoxia, and hypothermia. namic stability, enhance coronary flow, and minimize right ven­ In the postoperative period, the patient is given adequate analge­ tricular ischemia. Once suspected, resuscitation is initiated, sia for pain control and long­term antihypertensive medications oxygen administered, and IV UFH therapy started. In the are resumed. In patients who are not able to take oral medica­ hemodynamically unstable, IV vasoactive medications are tions, beta blockers, angiotensin­converting enzyme (ACE) required. Thrombolytic therapy, if not contraindicated, has the inhibitors, calcium channel antagonists, or diuretics are given advantage of dissolving the clot rapidly, with rapid improvement parenterally or clonidine is administered as a transdermal patch. in pulmonary perfusion, hemodynamic alterations, gas exchange, Although hypertension in the postoperative period is and right ventricular function. The role of surgical embolectomy common, a hypertensive crisis is uncommon, especially after is controversial. The transcatheter technique (with or without noncardiac surgery. A hypertensive crisis is characterized by low­dose thrombolytic therapy) is another therapeutic approach. severe elevation of blood pressure associated with organ Placement of an inferior vena cava filter reduces the risk for dysfunction—cerebral and subarachnoid hemorrhage and recurrence of PE. stroke, acute cardiac events, renal dysfunction, and bleeding Novel anticoagulants under investigation include factor Xa from the operative wound. This particularly appears to be the inhibitors (direct inhibitor [hypermethylated derivative of case in carotid endarterectomy, aortic aneurysm surgery, and fondaparinux with a long half­life given IV or SC] or indirect many head and neck procedures. Diastolic hypertension inhibitor mediated by antithrombin [given orally or parenter­ (>110 mm Hg) is significantly associated with cardiac complica­ ally]) and direct thrombin inhibitors. tions and systolic hypertension (>160 mm Hg) is associated with an increased risk for stroke and death. In patients with cardiac complicationS new­onset or severe perioperative hypertension and patients with a hypertensive emergency, treatment with agents that have postoperative Hypertension a rapid onset of action, short half­life, and few autonomic side effects to lower blood pressure is essential. Medications most Causes commonly used in this setting include nitroprusside and nitro­ Hypertension is a serious problem that can cause devastating glycerin (vasodilators), labetalol and esmolol (beta blockers), complications in the preoperative, intraoperative, and postop­ enalaprilat (useful for patients receiving long­term ACE inhibi­ erative periods. Perioperative hypertension (or hypotension) tors), and nicardipine (calcium channel blocker). It is crucial in occurs in 25% of patients undergoing surgery. The risk of hyper­ the acute setting not to decrease blood pressure more than 25% tension is related to the type of surgery performed and the to avoid ischemic strokes and hypoperfusion injury to other presence of perioperative hypertension. Cardiovascular, thoracic, organs. K2Townsend_Chapter 13_main.indd 17 6/10/2011 12:36:20 PM
    • 13-18  section ii  PerioPerative ManageMent perioperative ischemia and infarction respiratory failure), increased heart rate (arrhythmias), change in mental status, or excessive hyperglycemia in diabetics. Many Cause perioperative MIs are non–Q wave NSTEMI. Periprocedural Approximately 30% of all patients taken to the operating room MI is associated with the release of biomarkers of necrosis, such have some degree of CAD. Older patients, patients with periph­ as MB isoenzymes of creatinine kinase (CK­MB) and troponins, eral artery disease, and those undergoing vascular, thoracic, into the circulation. The troponin complex consists of three major orthopedic, or upper abdominal procedures are at high subunits, T (TnT), I (TnI), and C (TnC). TnT and TnI are risk for an acute coronary syndrome in the postoperative period. derived from heart­specific genes and are referred to as cardiac 14 Major risk factors for developing CHD are smoking, family troponins (cTns). cTns are not present in healthy individuals; history, adverse lipid profiles, diabetes mellitus, and elevated their early release is attributable to the cytosolic pool and late blood pressure.22 Although management of nonoperative MI has release to the structural pool. improved, the mortality associated with perioperative MI Patients considered to have acute coronary syndrome remains approximately 30%. Perioperative myocardial compli­ should have a 12­lead ECG and placed in an environment with cations result in at least 10% of all perioperative deaths. In the continuous electrocardiographic monitoring and defibrillator 1970s, the risk for recurrence of MI within 3 months of an MI capability. Biomarkers of myocardial necrosis are measured. was reported to be 30% and, if a patient underwent surgery CK­MB has a short half­life and is less sensitive and less specific within 3 to 6 months of infarction, the reinfarction rate was than cTns. Troponins can be detected in blood as early as 2 to 15%; 6 months postoperatively the reinfarction rate was only 4 hours but elevation may be delayed for up to 8 to 12 hours. 5%. However, improved preoperative assessment, advances in The timing of elevation of cTns is similar to CK­MB but cTns anesthesia and intraoperative monitoring, and the availability of persist longer, for up to 5 to 14 days. Elevated cTn levels above more sophisticated intensive care unit monitoring have resulted the 99th percentile of normal in two or more blood samples in improvement in the outcome of patients at risk for an acute collected at least 6 hours apart indicates the presence of myo­ cardiac event. Individuals undergoing an operation within 3 cardial necrosis. Equivalent information is obtained with cTnI months of an infarction have an 8% to 15% reinfarction rate; and cTnT, except in patients with renal dysfunction, in whom between 3 and 6 months postoperatively, the reinfarction rate is cTnI has a specific role. Each patient should have a provisional only 3.5%. The general mortality associated with MI in patients diagnosis of acute coronary syndrome with UA (electrocardio­ without a surgical procedure is 12%. graphic changes of ischemia and no biomarkers in the circula­ Myocardial ischemia and MI result from the imbalance tion), STEMI, or NSTEMI. The distinction has therapeutic between myocardial oxygen supply and demand. Primary causes implications because patients with STEMI may be considered that reduce myocardial perfusion and therefore oxygen supply for immediate reperfusion therapy (fibrinolysis or percutaneous include coronary artery narrowing caused by a thrombus that intervention).22 develops on a disrupted atherosclerotic plaque, dynamic obstruction caused by spasm of an epicardial coronary artery or treatment diseased blood vessel, and severe narrowing caused by progres­ Preventing coronary ischemia is a function of identifying patients sive atherosclerosis. Secondary causes that increase myocardial prospectively at risk for a perioperative cardiac complication. oxygen requirements, usually in the presence of a fixed restricted This will allow improvement of the condition of the patient, oxygen supply (limited myocardial perfusion), are extrinsic possibly lowering the risk, selection of patients for invasive or cardiac factors that include fever and tachycardia (increased noninvasive cardiac testing, and identifying patients who will myocardial oxygen demand), hypotension (reduced coronary benefit from more intensive perioperative monitoring. Preop­ blood flow), and anemia and hypoxemia (reduced myocardial erative cardiac risk assessment includes adequate history taking, oxygen delivery). The increased circulating catecholamines asso­ physical examination, and basic diagnostic tests. The history is ciated with surgical stress further increase myocardial oxygen important to identify patients with cardiac disease or those at demand. risk for cardiac disease, including previous cardiac revasculariza­ tion, history of MI or stroke, and presence of valvular heart presentation and Diagnosis disease, heart failure, arrhythmia, hypertension, diabetes, lung Acute coronary syndrome refers to a constellation of clinical disease, and renal disease. Unstable chest pain, especially cre­ symptoms that are compatible with myocardial ischemia and scendo angina, warrants careful evaluation and probable post­ encompasses MI: ST­segment elevation myocardial infarction poning of an elective operation. Physical examination may reveal (STEMI) and depression (Q wave and non–Q wave), and unsta­ uncontrolled hypertension, evidence of peripheral artery disease, ble angina (UA)/non–ST­segment elevation myocardial infarc­ arrhythmia, or clinical stigmata of heart failure (HF). The CXR tion (NSTEMI). UA/NSTEMI is defined as ST­segment may show pulmonary edema, ECG may show an arrhythmia, depression or prominent T wave inversion and/or positive bio­ blood gas analysis may reveal hypercapnia or a low Pao2, and markers of myonecrosis in the absence of ST­segment elevation blood tests may show abnormal kidney function. The patient and in an appropriate clinical setting. The risk for myocardial who is found to have HF on physical examination or by history ischemia and MI is greatest in the first 48 hours after surgery, must have the problem treated before consideration for an elec­ and it may be difficult to make the diagnosis. The classic mani­ tive operative procedure. Guidelines for Perioperative Cardiovas- festation, chest pain radiating into the jaw and left arm region, cular Evaluation for Noncardiac Surgery, published by the is often not present. Patients may have shortness of breath, American College of Cardiology (ACA) and American Heart increased heart rate, hypotension, or respiratory failure. Periop­ Association (AHA), have stratified clinical predictors of increased erative myocardial ischemia and MI are often silent and, when perioperative cardiovascular risk leading to MI, CHF, or deathK2 they occur, are marked by shortness of breath (heart failure, into major, intermediate, and minor risks (Table 13­8) and Townsend_Chapter 13_main.indd 18 6/10/2011 12:36:20 PM
    • Surgical coMPlicationS  chapter 13  13-19 table  13-8  clinical  predictors  of  increased  perioperative   table 13-9  cardiac risk stratification for noncardiac surgical  SeCtion ii PerioPerative ManageMent cardiovascular  risk  Leading  to  Myocardial  infarction,  heart  procedures Failure, or Death LeVeL oF risK risK Factor LeVeL oF risK risK Factor High (cardiac risk often  emergency major operations, particularly in  >5%) the elderly Major unstable coronary syndromes aortic and other major vascular surgery   acute or recent Mi with evidence of  Peripheral vascular surgery considerable ischemic risk as noted by clinical  anticipated prolonged surgical procedures  symptoms or noninvasive studies associated with large fluid shifts and    unstable or severe angina (canadian class iii   blood loss or iv) Decompensated heart failure intermediate (cardiac  carotid endarterectomy Significant arrhythmias risk generally <5%) intraperitoneal and intrathoracic surgery   High-grade atrioventricular block orthopedic surgery   Symptomatic ventricular arrhythmias in the  Prostate surgery presence of underlying heart disease   Supraventricular arrhythmias with an  low (cardiac risk  endoscopic procedures uncontrolled ventricular rate generally <1%) Superficial procedures Severe valve disease cataract surgery Breast surgery intermediate Mild angina pectoris (canadian class i or ii) Previous Mi identified by history or pathologic  From eagle Ka, Berger pB, Calkins h, et al: aCC/aha Guideline Update for peri- evidence operative Cardiovascular evaluation for Noncardiac Surgery—executive Summary. Q waves a report of the american College of Cardiology/american heart association task compensated or previous heart failure Diabetes mellitus (particularly insulin dependent) Force on practice Guidelines (Committee to Update the 1996 Guidelines on peri- renal insufficiency operative Cardiovascular evaluation for Noncardiac Surgery). anesth analg 94:1052-1064, 2002. Minor advanced age abnormal electrocardiogram (e.g., left ventricular  hypertrophy, left bundle branch block, St-t  abnormalities) rhythm other than sinus (e.g., atrial fibrillation) Shortness of breath and chest pain remain the two postop­ low functional capacity (e.g., inability to climb one  erative symptoms that must always be carefully evaluated and flight of stairs with a bag of groceries) History of stroke never written off as postoperative discomfort. Subtle changes in uncontrolled systemic hypertension the ST segment and T wave hint of possible ischemia or MI. Evaluation of a patient suspected of having an intraoperative or postoperative MI includes immediate assessment by electrocar­ diography and measurement of biomarkers of myocardial necro­ stratified cardiac risk into high, intermediate, and low (Table sis. Constant electrocardiographic monitoring is required so that 13­9).21 the development of any potentially lethal arrhythmia can imme­ The ACC/AHA guidelines permit more appropriate use of diately be treated. If the level of cardiac function is a concern, preoperative testing (echocardiography, dipyridamole myocar­ echocardiography is considered. Cardiac troponin levels identify dial stress perfusion imaging, traditional exercise stress test, or patients with myocardial necrosis but do not identify the cause angiography) and beta blocker therapy, with probable cancella­ of necrosis. Cardiac­specific troponin levels begin to rise by 3 tion of the elective operative procedure.23 An algorithm for hours after myocardial injury. A troponin I level more than 1 ng/ perioperative cardiovascular evaluation is presented in Figure mL is specific, and elevations persist for 7 to 10 days. Troponin 13­1. The role of preoperative coronary artery revascularization T elevations persist for 10 to 14 days after MI. Medical manage­ has yet to be determined. Percutaneous transluminal coronary ment of myocardial ischemia and MI includes immediate angioplasty may be beneficial in reducing perioperative cardiac administration of high­flow oxygen, transfer to the intensive care morbidity in a select group of patients. unit, and early involvement of a cardiologist. Patients identified as being at high risk for myocardial The goal of management of myocardial ischemia is to pre­ events in the perioperative period are managed with beta serve the maximal amount of myocardial muscle possible, as well blockers, careful intraoperative monitoring, maintenance of as improve coronary blood flow and decrease myocardial work. perioperative normothermia and vital signs, and continued post­ Immediate administration of beta blockers (oral or IV, dose­ operative pharmacologic management, including the adminis­ titrated to decrease heart rate to less than 70 beats/min) and tration of adequate pain medication. Given several days before aspirin (160 to 325 mg) is essential. Beta blockers are not indi­ 15 surgery and continued for several days afterward, beta blockers cated for patients with bradycardia, hypotension, severe left (e.g., atenolol) have been shown to reduce perioperative myo­ ventricular dysfunction, heart block, or severe bronchospastic cardial ischemia by 50% in patients with CAD or CAD risk disease. Nitroglycerin (given as a continuous IV infusion after a factors.24 Patients with chronic stable angina continue with their loading dose) alleviates pain and is beneficial for patients with antianginal medications, and beta blockers are continued to the MI complicated by HF or pulmonary edema. Systemic heparin­ time of surgery and thereafter. An ECG is obtained before, ization (or SC LMWH), if not contraindicated, is administered. immediately after, and for 2 days after surgery. Patients are In most cases, thrombolytic therapy is contraindicated in the monitored for 48 hours, and in high­risk patients for 5 days, postoperative period and can be used only in the situation in after surgery and cardiac enzyme levels are also checked. Invasive which minor surgery is performed. Studies have shown that hemodynamic monitoring is appropriate for patients with left emergency stricture dilation and coronary artery stenting may ventricular dysfunction, fixed cardiac output, and unstable be more effective than thrombolytic therapy. ACE inhibitors angina or recent MI. may be given early after MI, especially anterior MI or with a K2Townsend_Chapter 13_main.indd 19 6/10/2011 12:36:21 PM
    • 13-20  section ii  PerioPerative ManageMent Proposed surgery Emergent Detailed risk assessment deferred to post-op period Elective or urgent Cardiac Risk factors and Cardiac evaluation vascularization no recent cardiac in last 2 years, asymptomatic in last 5 years work-up and stable No further Clinical No further testing predictors testing Major predictors of risk Minor Intermediate predictors of risk (unstable chest pain, CHF, predictors with good to excellent function symptomatic arrhythmias, of risk (prior MI, stable angina, severe valvular disease) compensated CHF) Evaluation and Surgery Risk level treatment before of surgery elective surgery High risk Intermediate risk Surgery Further Surgery testing Surgery Figure 13-1  algorithm for perioperative cardiovascular evaluation for noncardiac surgery. Patients with major predictors of risk and patients  with  intermediate  predictors  of  risk  and  a  planned  high-risk  procedure  undergo  additional  testing  and  resultant  indicated  treatment  before  elective surgery. CHF, congestive heart failure; MI, myocardial infarction. (adapted from eagle Ka, Brundage BH, chaitman Br, et al: guidelines  for perioperative cardiovascular evaluation for noncardiac surgery. report of the american college of cardiology/american Heart association  task Force on Practice guidelines. J am coll cardiol 27: 910-945, 1996.) low left ventricular ejection fraction, and probably continued as Other serious sequelae from acute MI include CHF, arrhyth­ a long­term therapy. Angiography must be strongly considered mias, and thromboembolic complications. if the patient has ongoing myocardial ischemia that does not respond to pharmacologic therapy. presentation and management Observant physicians will watch a patient with an acute MI closely for evidence of the aforementioned complications. Car­ cardiogenic Shock diogenic shock usually develops rapidly over a short period and is marked by hypotension and respiratory failure. Aggressive Causes management is required to save the life of a patient with this Cardiogenic shock is one of the most serious sequelae of acute devastating condition. Immediate institution of mechanical ven­ MI. Presumably, 50% or more of left ventricular muscle mass is tilation with a high Fio2, and occasional monitoring with a irreversibly damaged, leading to a substantial reduction in Swan­Ganz catheter, is important. For patients who do not cardiac output and resulting hypoperfusion. Other possible, less respond to pharmacologic and conservative management, intra­ frequent causes of cardiogenic shock include ruptured papillary aortic balloon pumps and ventricular assist devices may be life­ muscle or ventricular wall, aortic valvular insufficiency, mitral saving. For patients who have adequate myocardial reserve, regurgitation, and ventricular septal defect. Cardiogenic shock coronary artery bypass may occasionally be indicated. Cardiac is a highly lethal condition that results in the death of up to transplantation remains the gold standard treatment of end­K2 75% of patients unless immediate management is instituted. stage HF. Townsend_Chapter 13_main.indd 20 6/10/2011 12:36:21 PM
    • Surgical coMPlicationS  chapter 13  13-21 postoperative cardiac arrhythmias Box 13-6  Management of postoperative cardiac  SeCtion ii PerioPerative ManageMent arrhythmias Causes Cardiac arrhythmias are common in the postoperative period cardiology consultation and are more likely to occur in patients with structural heart Monitoring of the patient on a telemetry floor or in the intensive  disease. Cardiac arrhythmias are classified into tachyarrhyth­ care unit mia, bradyarrhythmia, and heart block. Tachyarrhythmia is 12-lead ecg and long strip to differentiate between atrial and  further subdivided into supraventricular (sinus, atrial, nodal) ventricular arrhythmia and ventricular (premature ventricular contraction [PVC], clinical assessment ventricular tachycardia, ventricular fibrillation). Sustained • vital signs supraventricular arrhythmia in patients undergoing major • Peripheral perfusion noncardiac surgery may be associated with an increased risk • cardiac ischemia and congestive heart failure for a cardiac event (e.g., heart failure, MI, unstable angina) • level of consciousness and cerebrovascular event.24 Factors associated with increased treatment of arrhythmia risk for supraventricular arrhythmias are increasing age, history • tachyarrhythmia of heart failure, and type of surgery performed. Sinus tachy­ • unstable: cardioversion cardia and atrial flutter or fibrillation are the most common • Stable types of tachyarrhythmia. Sinus tachycardia is caused by pain, Supraventricular  tachyarrhythmia:  Beta  blockers  fever, hypovolemia, anemia, anxiety and, less commonly, heart (esmolol),  ibutilide,  or  alternatives  (e.g.,  digoxin,  failure, MI, thyrotoxicosis, and pheochromocytoma. Atrial calcium channel blockers, amiodarone) flutter or fibrillation occurs commonly in patients with elec­ Paroxysmal  supraventricular  tachyarrhythmia:  vagal  trolyte imbalance, history of atrial fibrillation, and chronic stimulation or adenosine. Digoxin, amiodarone, or  obstructive lung disease. calcium channel blocker if adenosine fails Ventricular ectopy occurs in one third of patients after Multifocal  atrial  tachycardia:  Beta  blocker,  calcium  major noncardiac surgery and risk factors associated with an channel blocker, or amiodarone increased risk for PVCs include the presence of preoperative ventricular  tachycardia:  lidocaine,  procainamide,  or  PVCs, history of CHF, and cigarette smoking. Postoperative risk amiodarone factors include hypoxia, acute hypokalemia, and hypercapnia. • Bradyarrhythmia Ventricular arrhythmias consist of largely benign and sustained • Sustained: atropine or β-adrenergic agonist ventricular tachycardia and fibrillation. Nonsustained ventricu­ • transient: no therapy lar tachycardia commonly occurs during or after major vascular • Heart  block:  Persistent  high-grade  second-  or  third-degree  procedures. block; insertion of a permanent pacemaker presentation rate are indicated in the treatment of arrhythmias that traverse The physiologic impact of an arrhythmia depends on its type the node and dangerous in those that do not. Beta blockers and duration and the patient’s underlying cardiac status and are avoided in patients with a low ejection fraction and bron­ ventricular response. Most arrhythmias are transient and chospastic lung disease. The ultimate goal of therapy is to benign and are not associated with symptoms or physiologic achieve sinus rhythm and, if not possible, prevention of com­ changes. Occasionally, sinus tachycardia may precipitate isch­ plications associated with arrhythmias must be addressed (e.g., emia and PVCs, and unsustained ventricular tachycardia may anticoagulants given to patients with atrial fibrillation for precipitate ventricular tachycardia. Arrhythmias may also rep­ more than 48 hours). The management of postoperative resent a prelude to hemodynamic compromise, especially in arrhythmias is outlined in Box 13­6. patients with severe heart disease or a history of MI or cardiomyopathy. Both bradyarrhythmia and tachyarrhythmia postoperative Heart Failure may decrease cardiac output. Symptoms associated with arrhythmias include palpitations, chest pain, shortness of Causes breath, dizziness, loss of consciousness, cardiac ischemia, and Heart failure is a clinical syndrome characterized by any struc­ hypotension. tural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.25 Several risk factors treatment predispose to the development of heart failure, the most sig­ The patient’s underlying cardiac status is the key to manage­ nificant of which are CAD, hypertension, and increasing age. ment of arrhythmias. Arrhythmias may signal the presence of Poorly controlled heart failure represents one of the most serious reversible causes or precipitating factors that must be sought cardiac risk factors for a preoperative patient, whereas patients and dealt with, and treatment is based on the presence of with well­managed heart failure generally do well during an adverse hemodynamic effects of the arrhythmia, not its mere operation. Many factors can lead to new­onset heart failure or presence. In tachyarrhythmia, control of the ventricular decompensation of preexisting heart failure in the perioperative response is essential, and distinction between arrhythmias that period, including perioperative myocardial ischemia or MI, traverse the atrioventricular node (atrial fibrillation, ectopic volume overload, hypertension, sepsis, occult cardiac valvular atrial tachycardia) from those that do not (ventricular tachy­ disease, PE, and new­onset atrial fibrillation. The risk for heart cardia, fibrillation) is paramount. Antiarrhythmics that alter failure is greatest immediately after surgery and in the first 24 atrioventricular node conduction and control the ventricular to 48 hours after surgery. K2Townsend_Chapter 13_main.indd 21 6/10/2011 12:36:21 PM
    • 13-22  section ii  PerioPerative ManageMent presentation management of pain, including operative injection of local anes­ Patients with poorly controlled heart failure or new­onset heart thetics, may also diminish the incidence of urinary retention. failure suffer from shortness of breath and wheezing. Physical Judicious administration of IV fluids during the procedure and examination often reveals tachycardia, a narrow pulse pressure, in the immediate postoperative period, especially in patients low pressure or orthostatic hypotension, jugular venous disten­ who have undergone anorectal surgery for benign disease, may tion, peripheral edema, rales, and general evidence of poor similarly diminish the likelihood of postoperative urinary reten­ peripheral perfusion. The ECG may reveal an MI, ventricular tion. Furthermore, awareness how much time has passed since hypertrophy, atrial enlargement, or arrhythmias. A CXR may the last voiding to the present time is crucial in preventing acute indicate cardiomegaly, pulmonary edema, and pleural effusion. retention. Most patients should not go more than 6 to 7 hours Echocardiography assesses ventricular function and provides without passing some urine, and an observant clinician will information about regional wall motion and valve function. make certain that no patient goes longer than that before under­ going straight catheterization. treatment General management principles for acute urinary retention Management of patients with heart failure is directed at optimiz­ include initial straight catheterization or placement of a Foley ing preload, afterload, and myocardial contractility. Afterload catheter, especially in older patients and patients who have reduction is accomplished by lowering the vascular resistance undergone anterior resection because they may be unable to against which the heart must contract, and ACE inhibitors are sense the fullness associated with retention. In high­risk patients, a cornerstone of therapy for heart failure. Nitrates (venodilator) cystoscopy and cystometry may be required. and hydralazine (vasodilator) reduce excessive preload and are used as an alternative in patients who cannot tolerate ACE acute renal Failure inhibitors. β­Adrenergic blockade (selective or nonselective) for heart failure has proved effective in reducing mortality in patients Causes with ischemic and nonischemic heart failure.26 Digoxin (a sym­ Acute renal failure (ARF) is characterized by a sudden reduc­ patholytic agent) has traditionally been used for patients with tion in renal output that results in the systemic accumulation heart failure in sinus rhythm. Its use has decreased given the of nitrogenous wastes. This hospital­acquired renal insuffi­ superior and definitive beneficial effects of ACE inhibitors and ciency is more prevalent after major vascular procedures (rup­ beta blockers. Diuretics are necessary in all patients with heart tured aneurysm), renal transplantation, cardiopulmonary failure for the management of volume overload and relief of bypass procedures, major abdominal cases associated with symptoms of congestion. Calcium channel blockers are used septic shock, and major urologic operations. It may also occur only for the treatment of hypertension or angina not adequately in procedures in which there is major blood loss, with transfu­ controlled with other agents, such as ACE inhibitors or beta sion reactions, in serious diabetics undergoing operations, in blockers. Inotropes increase cardiac contractility and are used in life­threatening trauma, with major burn injuries, and in mul­ the critically ill and patients with end­stage heart failure. tiple organ system failure. Hospital­acquired renal insuffi­ ciency adversely affects surgical outcomes and is associated renal and urinary tract complicationS with significant mortality, especially when dialysis is required. Two types of ARF have been identified, oliguric and nonoligu­ urinary retention ric. Oliguric renal failure refers to urine in which volumes less than 480 mL are seen in a day. Nonoliguric renal failure Causes involves output exceeding 2 liters/day and is associated with The inability to evacuate a urine­filled bladder is referred to as large amounts of isosthenuric urine that clears no toxins from urinary retention. This is a common postoperative complication the bloodstream. Factors leading to ARF can be inflow, paren­ seen with particularly high frequency in patients undergoing chymal, or outflow, historically referred to as prerenal, renal, perianal operations and hernia repair. Urinary retention may also or postrenal, respectively (Table 13­10). occur after surgery for low rectal cancer when an injury to the In normal kidneys, effective perfusion of the glomeruli is nervous system affects bladder function. Most commonly, maintained by an autoregulatory mechanism involving the affer­ however, the complication is a reversible abnormality resulting ent and efferent arterioles. Any factor that interferes with or from discoordination of the trigone and detrusor muscles as a disrupts this mechanism results in ARF. Afferent constriction or result of increased pain and postoperative discomfort. Urinary efferent dilation decreases the glomerular filtration rate. Inflow, retention is also occasionally seen after spinal procedures and or prerenal, failure is secondary to hypotension, which causes may occur after overly vigorous IV administration of fluid. afferent arteriolar constriction and efferent dilation, nonsteroidal Benign prostatic hypertrophy and, rarely, a urethral stricture anti­inflammatory drugs (NSAIDs), which inhibit afferent vaso­ may also be the cause of urinary retention. dilation, and gram­negative sepsis, which causes decreased peripheral vascular resistance while increasing renal vasocon­ presentation and management striction. Renal vascular stenosis and thrombosis can also be Patients with postoperative urinary retention will complain of a causes, although these are much less common. Outflow, or dull constant discomfort in the hypogastrium. Urgency and postrenal, ARF is caused by tubular obstruction from debris, actual pain in this area occur as the retention worsens. Percus­ crystals, or pigments, ureteric obstruction, or urinary bladder sion just above the pubis reveals fullness and tenderness. outflow obstruction. Ischemia, toxins, or nephritis cause paren­ To prevent urinary retention, the population at greatest chymal ARF. concern, older adults and patients who have undergone low The incidence of contrast­induced nephropathy has beenK2 anterior resection, must be watched carefully. Adequate increasing. Tubular damage can occur within 48 hours of dye Townsend_Chapter 13_main.indd 22 6/10/2011 12:36:21 PM
    • Surgical coMPlicationS  chapter 13  13-23 table 13-10  causes of postoperative acute renal Failure SeCtion ii PerioPerative ManageMent inFLoW or prerenaL parenchYMaL or renaL oUtFLoW or postrenaL Sepsis renal ischemia cellular debris (acute tubular necrosis) Medications Drugs (aminoglycosides, amphotericin) crystals   nonsteroidal anti-inflammatory drugs iodinated contrast media   uric acid   angiotensin-converting enzyme inhibitors interstitial nephritis   oxylate intravascular volume contraction Pigment   Hypovolemia   Myoglobin   Hemorrhage   Hemoglobin   Dehydration   atherosclerotic emboli   third spacing   cardiac failure administration. Diabetic patients with vascular disease are at risk complicated. Careful history taking may identify patients with for major renal injury when contrast agents are administered. preexisting renal dysfunction. Patients with large fluid losses Administration of contrast to hypovolemic patients and those from the GI tract (e.g., diarrhea, vomiting, fistula, high ileos­ with preexisting renal dysfunction guarantees some degree of tomy output) often have associated profound dehydration. In renal injury. The tubular injury is generally self­limited and such cases, the rise in the blood urea nitrogen (BUN) level is reversible. Diabetic patients with creatinine clearance lower than usually more than the rise in the creatinine level and the ratio 50 mL/min who receive 100 mL of contrast dye, however, can of BUN to creatinine is more than 20. On the other hand, sustain severe tubular damage and may require dialysis. Blunt examination of the patient may reveal distended neck veins, rales trauma with associated crush injuries place the patient at risk in the lungs, and a cardiac gallop—all signs that a failing heart for ARF because of high serum levels of hematin and myoglobin, may be underperfusing the kidneys as the cause of the oliguria. both of which are injurious to the renal tubules. ARF is a Brown urine in the Foley bag in a trauma patient raises suspicion prominent feature in patients with acute compartment syn­ of myoglobinuria and requires rapid hydration, diuresis, and drome.27 Growing awareness of this problem has led surgeons alkalinization of the urine. Evaluation of spun urine is helpful. to intervene surgically, often resulting in dramatic improvement The presence of hyaline casts indicates hypoperfusion and the in renal function and preservation of renal filtering capacity. presence of coarse granular casts indicates acute tubular necrosis. Lipoid casts are found with NSAID­ and contrast­induced presentation and management nephropathy and white and red cell casts are found with pyelo­ Prevention of hospital­acquired renal insufficiency requires the nephritis. In patients with prerenal azotemia, the concentrating following: identification of patients with preexisting renal dys­ ability of the nephrons is normal, thereby resulting in normal function; avoidance of hypovolemia, hypotension, and medica­ urine osmolality and fractional excretion of sodium (>50 mOsm/ tions that depress renal function; and judicious use of nephrotoxic liter and FENa <1%, respectively). Conversely, with acute tubular drugs. In the presence of renal impairment, the dose of antibiot­ necrosis, the concentrating ability of the kidney is lost and the ics given for serious infections must be adjusted. The risk for patient produces urine with an osmolality equal to that of serum contrast­induced nephropathy is reduced by adequate hydration and high urine sodium levels (350 mOsm and >50 mOsm/liter, 16 and premedication with a free radical scavenger (e.g., respectively; Table 13­11). The best laboratory test for discrimi­ N­acetylcysteine) or the use of alternative contrast (e.g., gado­ nating prerenal from renal azotemia is probably FENa. In prer­ linium). Renal hypoperfusion is avoided by optimizing cardiac enal patients, FENa is 1% or less, whereas in renal azotemia output and volume expansion. Administration of fluid must be patients it often exceeds 3%. particularly judicious in patients with a history of heart failure. Once ARF is diagnosed, one has to ascertain whether the Monitoring renal function in all surgical patients, at times hypoperfusion of the kidney is caused by hypovolemia or cardiac including creatinine clearance, is a sound clinical practice. Early failure. Distinguishing the two is critical because giving heart intervention in cases of postrenal obstruction and abdominal failure patients more fluid exacerbates an already failing system. compartment syndrome can obviate the development of renal Similarly, giving diuretics to a hypovolemic patient can worsen injury. the renal failure. If the prerenal patient has no history of cardiac Anuria that suddenly develops postoperatively in an other­ disease, administration of isosmotic fluid (normal saline or lac­ wise healthy individual with no preexisting renal disease is tated Ringer’s solution, or blood in patients who have hemor­ postrenal in nature until proven otherwise. A kink in the Foley rhaged) is indicated. The IV fluid can be given rapidly (1 liter catheter or obstruction must be cleared. In patients who have over a 20­ to 30­minute period) in young patients with healthy undergone major pelvic surgery, ligation of the ureters is suspect. hearts and a Foley catheter in place to measure hourly urine If renal ultrasound or a CT scan shows hydronephrosis, imme­ output, and must be administered until the patient is producing diate surgical treatment is indicated. Postrenal causes of ARF are a minimum of 30 to 40 mL/hr of urine. If fluid administration the most dramatic and straightforward to diagnose and treat, does not result in improvement of the oliguria, placement of a with significant immediate improvement after treatment. central venous pressure or Swan­Ganz catheter is indicated to ARF is otherwise diagnosed when there is a rise in the measure left­ or right­sided heart filling pressure. In the presence serum creatinine level, decrease in creatinine clearance, and of CHF, diuretics, fluid restriction, and appropriate cardiac urine output less than 400 mL/day (<20 mL/hr). Distinguish­ medications are indicated. Ultrasound may show renal atrophy, ing between prerenal and renal azotemia, however, is reflecting the presence of chronic metabolic disease. K2Townsend_Chapter 13_main.indd 23 6/10/2011 12:36:21 PM
    • 13-24  section ii  PerioPerative ManageMent table 13-11  Diagnostic evaluation of acute renal Failure paraMeter prerenaL renaL postrenaL urine osmolality >500 mosm/liter = Plasma variable urinary sodium <20 mosm/liter >50 mosm/liter >50 mosm/liter Fractional excretion of sodium <1% >3% variable urine, plasma creatinine leve >40 <20 <20 urine, plasma urea level >8 <3 variable urine, plasma osmolality <1.5 >1.5 variable Treatment of ARF includes the management of fluid and Box 13-7  indications for hemodialysis electrolyte imbalance, careful monitoring of fluid administra­ tion, avoidance of nephrotoxic agents, provision of adequate Serum potassium > 5.5 meq/liter nutrition, and adjustment of doses of renally excreted medica­ Blood urea nitrogen > 80-90 mg/dl tions until recovery of renal function. Most urgent in manage­ Persistent metabolic acidosis ment of ARF is treating hyperkalemia and fluid overload. acute fluid overload Hyperkalemia can be managed with a sodium­potassium uremic symptoms (pericarditis, encephalopathy, anorexia) exchange resin, insulin plus glucose, an aerosolized β2­adrenergic removal of toxins agonist, and calcium gluconate. Insulin and β2­adrenergic ago­ Platelet dysfunction causing bleeding nists shift potassium intracellularly. Hyperkalemia­associated Hyperphosphatemia with hypercalcemia cardiac irritability (prolonged PR interval or peaked T waves) is urgently treated with the administration of a 10% calcium glu­ conate solution over a 15­minute period, as well as simultaneous 17 IV administration of glucose and insulin (10­U IV bolus with corticosteroid secreted from the adrenal cortex, is under the 50 mL of a 50% dextrose solution, followed by continuation of influence of adrenocorticotropic hormone (ACTH) released glucose to prevent hypoglycemia). A β2­adrenergic agonist is from the pituitary gland, which in turn is under the influence given as a nebulizer containing 10 to 20 mg in 4 mL of saline of hypothalamic corticotropin­releasing hormone; both hor­ over a period of 10 minutes or as an IV infusion containing mones are subject to negative feedback by cortisol itself. Cortisol 0.5 mg. Calcium gluconate is given as 10 mL of a 10% solution is a stress hormone. over a 5­minute period to reduce arrhythmias. Refractory hyper­ Chronic adrenal insufficiency may result from primary kalemia associated with metabolic acidosis and rhabdomyolysis destruction of the adrenal gland or be secondary to a disease requires hemodialysis. In less severe hyperkalemia, an ion state or disorder involving the hypothalamus or anterior pitu­ exchange resin (sodium polystyrene [Kayexalate]) in enema form itary gland. Primary adrenal insufficiency is most frequently will help lower potassium levels. Phosphate levels also require caused by autoimmune adrenalitis (Addison’s disease), in which careful monitoring. Hypophosphatemia can induce rhabdomy­ the adrenal cortex is destroyed by cytotoxic lymphocytes. Sec­ olysis and respiratory failure and is treated with the oral admin­ ondary adrenal insufficiency is most commonly caused by long­ 18 istration of Fleet Phospho­Soda. Hyperphosphatemia with term administration of pharmacologic doses of glucocorticoids. hypercalcemia increases the risk for calciphylaxis and is treated Chronic use of glucocorticoids causes suppression of the with the administration of phosphorus binders (calcium carbon­ hypothalamic­pituitary­adrenal axis, induces adrenal atrophy, ate) or dialysis. IV fluids are monitored with an emphasis on and results in isolated adrenal insufficiency. fluid restriction and occasional use of catheters to measure right­ Acute adrenal insufficiency may occur as a result of and left­sided heart filling pressure to avoid fluid overload. abrupt cessation of pharmacologic doses of chronic glucocor­ When supportive measures fail, consideration must be ticoid therapy, surgical excision or destruction of the adrenal given to hemodialysis.28 Indications for hemodialysis are listed gland (adrenal hemorrhage, necrosis, or thrombosis in in Box 13­7. Although some hemodynamic instability may patients with sepsis or antiphospholipid syndrome), or surgi­ occur during dialysis, it is usually transient and may be treated cal excision or destruction (postpartum necrosis) of the pitu­ with fluids. Dialysis may be continued on an intermittent basis itary gland. In addition, so­called functional or relative acute until renal function has returned, which occurs in most cases. adrenal insufficiency may develop in critically ill and septic patients. endocrine gland dySFunction presentation and Diagnosis adrenal insufficiency The clinical manifestations of adrenal insufficiency depend on the cause of the disease and associated endocrinopathies.29 Causes Symptoms and signs of chronic primary and secondary adrenal Adrenal insufficiency is an uncommon but potentially lethal insufficiency are similar and nonspecific—fatigue, weakness, condition associated with failure of the adrenal glands to anorexia, weight loss, orthostatic dizziness, abdominal pain,K2 produce adequate glucocorticoids. Cortisol, the predominant diarrhea, depression, hyponatremia, hypoglycemia, eosinophilia, Townsend_Chapter 13_main.indd 24 6/10/2011 12:36:21 PM
    • Surgical coMPlicationS  chapter 13  13-25 Box 13-8  rapid adrenocorticotropic hormone stimulation  table 13-12  relative corticosteroid potency compared With  SeCtion ii PerioPerative ManageMent test in patients With adrenal insufficiency hydrocortisone • Determine baseline serum cortisol level. GLUcocorticoiD  MineraLocorticoiD  • give 250 µg cosyntropin iv (or iM). actiVitY actiVitY • Measure  serum  cortisol  levels  30  to  60 min  after  Short-Acting cosyntropin is given. Hydrocortisone 1 1 • results cortisone 0.8 0.8 • normal  adrenal  function:  Basal  or  postcorticotropin  plasma  cortisol  concentration  is  at  least  18 µg/dl  Intermediate-Acting (500 nmol/liter)  or  preferably  20 µg/dl  (550 nmol/ Prednisone 4 0.25 liter). Prednisolone 4 0.25 • Primary adrenal insufficiency: cortisol secretion is not  increased. Methylprednisolone 5 trace • Severe secondary adrenal insufficiency: cortisol levels  triamcinolone 5 trace increase a little or not at all because of adrenocortical  Long-Acting atrophy. Dexamethasone 20 trace adapted from Druck p, andersen DK: Diabetes mellitus and other endocrine problems. In Stillman rM (ed): Surgery: Diagnosis and therapy, New York, 1989, Lange, p 205. decreased libido and potency. Patients with primary hypoadre­ nalism also show manifestations of elevated plasma levels of corticotropin and hyperpigmentation of the skin and mucous membranes. Patients with secondary disease, in contrast, ini­ without an obvious source of infection. Hyponatremia is usually tially have neurologic or ophthalmologic symptoms (headaches, present and does not respond to saline infusion. A sodium level visual disturbances) before showing signs of hypothalamic­ less than 120 mmol/liter is dangerous and may lead to delirium, pituitary­adrenal axis disease (hypopituitarism). Manifestations coma, and seizures. Hypoglycemia and azotemia may also be of hypothalamic­pituitary­adrenal axis suppression include present. An ECG will occasionally reveal low voltage and peaked hypoadrenalism, decreased levels of corticotropin, and manifes­ T waves. To diagnose the condition, cortisol and corticotropin tations of other hormone deficiencies (e.g., pallor, loss of hair in concentrations are checked and the short corticotropin stimula­ androgen­dependent areas, oligomenorrhea, diabetes insipidus, tion test performed. hypothyroidism). Laboratory test abnormalities, including hyponatremia, treatment hyperkalemia, acidosis, hypoglycemia or hyperglycemia, normo­ Prevention and avoidance of adrenal insufficiency are achieved cytic anemia, eosinophilia, and lymphocytosis, are present to a by a thorough preoperative history, detailed instruction of variable extent. The diagnosis, however, is established by measur­ patients receiving chronic corticosteroid therapy regarding the ing the morning plasma cortisol concentration. A level higher dangers of abrupt termination of the medication, and adequate than 19 µg/dL (525 nmol/liter) rules out adrenal insufficiency perioperative corticosteroid administration. Specific patients and less than 3 µg/dL (83 nmol/liter) indicates its presence. A with rheumatoid arthritis, inflammatory bowel disease, or auto­ basal plasma corticotropin level exceeding 100 pg/mL (22 nmol/ immune disease and recipients of organ transplants are targeted. liter), low or low­normal basal aldosterone level, and increased In the critically ill, a high index of suspicion can prevent a fatal renin concentration are indicative of primary hypoadrenalism. outcome. A stress dose of hydrocortisone (100 mg) may be given 19 The rapid corticotropin stimulation test to determine adrenal with induction of anesthesia. For minor surgical procedures, the responsiveness is the diagnostic procedure of choice when testing usual maintenance dose is continued postoperatively. For major for primary adrenal insufficiency (Box 13­8). surgical procedures, a stress dose (100 mg) is continued every 8 To confirm the diagnosis of secondary adrenal insuffi­ hours until the patient is stable or free of complications and then ciency, the metyrapone test is performed. An insufficient tapered to the usual maintenance dose. increase in plasma 11­deoxycortisol and a low plasma cortisol Symptomatic patients are treated with hydrocortisone or concentration (<8 µg/dL) after the oral administration of cortisone. Fludrocortisone (substitute for aldosterone) is also metyrapone indicate the presence of secondary adrenal insuffi­ administered to patients with primary disease. Patients who have ciency. Magnetic resonance imaging (MRI) allows evaluation received more than 20 mg of prednisone daily (or equivalent 20 of the pituitary­hypothalamic region in patients with neuro­ dose of another corticosteroid; Table 13­12) for more than 3 logic and ophthalmologic symptoms and CT is used to weeks within the previous year and patients with Cushing’s evaluate the adrenal glands in patients with primary hypoadre­ syndrome who are undergoing surgery are presumed to have nalism. hypothalamic­pituitary­adrenal axis suppression and must be The diagnosis of acute adrenal insufficiency can be espe­ treated in a similar fashion. cially difficult to make in the critically ill. The condition is Treatment of functional acute adrenal insufficiency involves suspected in patients exhibiting manifestations of preexisting or immediate, rapid administration of high­dose hydrocortisone or undiagnosed chronic adrenal insufficiency in whom unexplained methylprednisolone, with appropriate monitoring until clinical hypotension or hemodynamic instability develops despite fluid improvement is seen. Hypovolemia and hyponatremia are cor­ resuscitation, as well as ongoing evidence of inflammation rected with saline infusion. K2Townsend_Chapter 13_main.indd 25 6/10/2011 12:36:21 PM
    • 13-26  section ii  PerioPerative ManageMent Hyperthyroid crisis Box 13-9  Management of thyroid crisis Causes identification and treatment of the precipitating factor Supportive care Hyperthyroidism refers to a sustained increase in the synthesis • oxygen of thyroid hormones, and thyrotoxicosis is a clinical syndrome • iv fluid therapy that results from an abnormal elevation of circulating levels of • Sedation (chlorpromazine) thyroid hormone, regardless of cause. Thyroid hormones are • venous thromboembolism prophylaxis with heparin under the influence of pituitary gland thyroid­releasing hormone, • Dexamethasone which in turn is under the influence of hypothalamic thyrotropin­ Fever: antipyretics and cooling releasing hormone; both are subject to negative feedback by the Heart failure: Digoxin and diuretics thyroid hormones. Thyroid hormones have physiologic effects atrial fibrillation: iv heparin on many organ systems, but the greatest effect is on the cardio­ Beta blockers: oral propranolol, 60-80 mg/4 hr (or diltiazem),  39 vascular system. to reduce the heart rate below 100 beats/min. in very sick  Thyroid crisis is a medical emergency that occurs in thy­ patients,  esmolol  is  given  iv  and  reserpine  is  given  to  rotoxic patients with toxic adenoma or toxic multinodular patients refractory to large doses of propranolol. goiter, but most often in patients with Graves’ disease. The Propylthiouracil or methimazole crisis is frequently precipitated by a stressful event and charac­ lugol’s solution given 4 hr after propylthiouracil terized by exacerbation of hyperthyroidism and decompensa­ Plasmapheresis  and  charcoal  plasma  perfusion  or  exchange  tion of one or more organ systems. Mortality is high, ranging transfusion reserved for recalcitrant cases if no response in  from 20% to 50% if the crisis is unrecognized and left 24-48 hr untreated. once euthyroidism achieved, definitive therapy must be consid- ered to prevent a second crisis presentation and Diagnosis Clinical manifestations of hyperthyroidism include nervousness, fatigue, palpitations, heat intolerance, weight loss, atrial fibrilla­ Definitive therapy for Graves’ disease is accomplished with tion (in older patients), and ophthalmopathy characterized by radioactive iodine or surgery. Radioactive iodine has obvious eyelid retraction or lag, periorbital edema, and proptosis. The advantages in older, high­risk patients but needs to be avoided onset of thyroid crisis is sudden and manifested by accentuation in children, pregnant women, and patients with large toxic of the symptoms and signs of thyrotoxicosis and organ system adenomas. By using doses of 123I in the range of 10 mCi (5 to 21 dysfunction, including hyperpyrexia, tachycardia out of propor­ 15 mCi) and subsequent levothyroxine, thyrotoxicosis can be tion to fever, dehydration and collapse, central nervous system successfully managed in 85% to 90% of patients. The main side dysfunction (delirium, psychosis, seizure, coma), cardiac mani­ effect of radioactive iodine is hypothyroidism. Surgery usually festations, GI symptoms, and liver dysfunction. includes one of two operations, total thyroidectomy or a lobec­ The diagnosis of thyrotoxicosis requires demonstration of tomy on one side with a subtotal lobectomy on the other side. elevated levels of circulating thyroid hormone and suppressed Total thyroidectomy is associated with a lower recurrence rate thyroid­stimulating hormone (TSH) levels and identification than subtotal thyroidectomy is (4% to 15%) but requires life­ of the cause of the thyrotoxicosis. Free thyroxine (T4) and triio­ long T4 replacement postoperatively. Excision of the lesion is dothyronine (T3) represent the small unbound fraction of indicated for toxic adenoma, whereas total thyroidectomy is total thyroxine that is biologically active and correlate directly indicated for toxic multinodular goiter. Before surgery, patients with the presence and severity of thyroid dysfunction. Thyroid must be made euthyroid with antithyroid drugs, and iodine is scintigraphy with technetium pertechnetate (99mTcO4−) or given for 7 days before surgery. iodine 123 (123I) provides information about the functional anatomy of the gland. In Graves’ disease, there is diffuse uptake; Hypothyroidism in Plummer’s disease (toxic multinodular goiter), there is an inhomogeneous pattern with hot, cold, and warm areas, Causes and with Goetsch’s disease (toxic solitary nodule), there is Hypothyroidism is characterized by low systemic levels of intense activity in the area of the nodule, with suppression of thyroid hormone and may be exacerbated in the postoperative paranodular tissue. period in patients with preexisting chronic hypothyroidism or as a result of severe stress. Severe illness, physiologic stress, and treatment drugs may inhibit the peripheral conversion of T4 to T3 and In addition to the identification and treatment of the precipitat­ induce a hypothyroid­like state. Hypothyroidism may be ing factor(s) and supportive care, specific medications (e.g., primary (e.g., surgical removal, ablation, disease of the thyroid iodine, propylthiouracil, β­adrenergic blockers, dexamethasone) gland), secondary (e.g., hypopituitarism), or tertiary (e.g., hypo­ that target hormonal synthesis and release and block peripheral thalamic disease). effects of the hormone are administered (Box 13­9).30 Steroids are required to block the peripheral conversion of T4 to T3 and presentation and Diagnosis as a supplement because there is increased steroid demand and Patients with chronic hypothyroidism may be asymptomatic or, turnover and decreased physiologic effectiveness. Cardioversion rarely, have the severe form (myxedema coma) characterized by for supraventricular tachyarrhythmia is ineffective during the coma, loss of deep tendon reflexes, cardiopulmonary collapse,K2 thyrotoxic storm. and high mortality(≈40% to 50%). Most, however, demonstrate Townsend_Chapter 13_main.indd 26 6/10/2011 12:36:21 PM
    • Surgical coMPlicationS  chapter 13  13-27 cold intolerance, constipation, brittle hair, dry skin, sluggish­ criteria of SIADH include hyponatremia with hypotonicity of SeCtion ii PerioPerative ManageMent ness, weight gain, and fatigue. The impact of hypothyroidism is plasma, urine osmolality in excess of plasma osmolality, increased greatest on the cardiovascular system, with effects such as bra­ renal sodium excretion, absence of edema or volume depletion, dycardia, hypotension, impaired cardiac function, conduction and normal renal function. abnormalities, pericardial effusion, and increased risk for CAD. In the critically ill (e.g., those with trauma or sepsis), hypothy­ treatment roidism is associated with worsening of pulmonary function, Management of SIADH includes treatment of the underlying a predisposition to pleural effusion, and susceptibility to disease process and removal of excess water (i.e., treatment of hypothermia. the hyponatremia). Fluid restriction is the mainstay of manage­ The ECG usually shows bradycardia, low voltage, and pro­ ment of chronic SIADH. IV administration of normal saline is longed PR, QRS, and QT intervals. In patients with primary used only in significantly symptomatic patients with chronic hypothyroidism, serum total T4, free T4, and free T3 levels are SIADH or those with symptomatic acute SIADH, with a dura­ low, whereas the TSH level is elevated. In secondary disease, the tion of less than 3 days. Correction must occur at a rate of TSH level, free T4 index, and free T3 are low. Distinguishing the 0.5 mmol/liter/hr until the serum sodium concentration is two is important because adrenal insufficiency is present in 125 mg/dL or higher. Rapid correction leads to serious perma­ secondary disease and administration of levothyroxine must be nent neurologic damage. Diuretics such as furosemide occasion­ accompanied by cortisol or the disease could be exacerbated. ally help correct the imbalance. In some cases, IV administration of 3% saline solution may be required, but correction must be treatment done in a constant, sustained fashion because overly rapid cor­ Patients with known hypothyroidism who are receiving replace­ rection can result in seizure activity. ment hormonal therapy and are in the euthyroid state do not require any special treatment before surgery but are instructed gaStrointeStinal complicationS to continue taking their medications. In patients with symptom­ atic chronic hypothyroidism, surgery is postponed until a euthy­ ileus and early postoperative Bowel obstruction roid state has been achieved. Patients with myxedema coma or those showing clinical Causes signs of significant hypothyroidism (e.g., severe postoperative Early postoperative bowel obstruction denotes obstruction hypothermia, hypotension, hypoventilation, psychosis, obtun­ occurring within 30 days after surgery. The obstruction may be dation) are immediately treated with thyroid hormone, con­ functional (i.e., ileus), caused by inhibition of propulsive bowel comitant with the IV administration of hydrocortisone, to avoid activity, or mechanical as a result of a barrier. Ileus that occurs an addisonian crisis. IV levothyroxine or T3 may be given until immediately after surgery in the absence of precipitating factors oral ingestion is possible. and resolves within 2 to 4 days is termed primary or postoperative ileus. On the other hand, ileus that occurs as a result of a pre­ cipitating factor and is associated with a delay in return of bowel Syndrome of inappropriate antidiuretic function is termed secondary, adynamic, or paralytic ileus.31 Hormone Secretion Mechanical bowel obstruction may be caused by a luminal, mural, or extraintestinal barrier. Causes The precise mechanism and cause of postoperative ileus are The syndrome of inappropriate antidiuretic hormone secretion not completely understood. Several events that occur during an (SIADH) is the most common cause of chronic normovolemic abdominal surgical procedure and in the perioperative period hyponatremia. Hyponatremia is defined as a serum sodium con­ may interfere with or alter the contractile activity of the small centration lower than 135 mmol/liter. SIADH is diagnosed in bowel, which is governed by a complex interaction among the any patient who remains hyponatremic despite all attempts to enteric nervous system, central nervous system, hormones, and correct the imbalance in the presence of persistent antidiuretic local molecular and cellular inflammatory factors. Surgical stress activity from elevated arginine vasopressin levels. Vasopressin is and manipulation of the bowel result in sustained inhibitory a naturally occurring antidiuretic hormone that regulates free sympathetic activity and release of hormones and neurotrans­ water excretion. It is synthesized in the hypothalamus, trans­ mitters, as well as activation of a local molecular inflammatory ported to the posterior pituitary, and stored until specific stimuli response that results in suppression of the neuromuscular appa­ cause it to be secreted into the bloodstream. Thirst, hypovole­ ratus.32 In the immediate postoperative period, restricted oral mia, nausea, hypoglycemia, and drugs are among the many intake and postoperative narcotic analgesia also contribute to stimuli for vasopressin. Disorders and conditions that predispose altered small bowel motility. Opiates and opioid peptides in the to this relatively rare condition include trauma, stroke, anti­ enteric nervous system suppress neuronal excitability. After tran­ diuretic hormone–producing tumors, drugs (ACE inhibitors, section and reanastomosis of the small bowel, the distal part of dopamine, NSAIDs), and pulmonary conditions. the bowel does not react to the pacemaker (found in the duo­ denum), and the frequency of contractions decreases. Other presentation conditions listed in Box 13­10 are associated with or result in The clinical features of SIADH include anorexia, nausea, vomit­ adynamic ileus. ing, obtundation, and lethargy. With more rapid onset, seizures, Mechanical early postoperative small bowel obstruction coma, and death can result. Clinical expression of the syndrome is commonly caused by adhesions (92%), a phlegmon or is caused by hyponatremia and is a function of the degree of abscess, internal hernia, intestinal ischemia, or intussusception. hyponatremia, as well as the rapidity of its onset. The cardinal Intussusception occurring in the postoperative period is K2Townsend_Chapter 13_main.indd 27 6/10/2011 12:36:21 PM
    • 13-28  section ii  PerioPerative ManageMent Box 13-10  causes of intestinal paralytic ileus The diagnosis of bowel obstruction is usually based on clinical findings and plain radiographs of the abdomen.33 Pancreatitis However, in the postoperative period, differentiation between intra-abdominal infection (peritonitis or abscess) adynamic ileus and mechanical obstruction is imperative retroperitoneal hemorrhage and inflammation because the treatment is completely different. A CT scan, electrolyte abnormalities abdominal radiographs, and small bowel follow­through are lengthy surgical procedure and prolonged exposure of abdom- variably used to establish the diagnosis and assist in treatment inal contents decision making. In adynamic ileus, abdominal radiographs Medications (e.g., narcotics, psychotropic agents) reveal diffusely dilated bowel throughout the intestinal tract, Pneumonia with air in the colon and rectum. Air­fluid levels may be inflamed viscera present, and the amount of dilated bowel varies greatly. With mechanical bowel obstruction, there is small bowel dilation with air­fluid levels and thickened valvulae conniventes in the relatively uncommon and is a rare occurrence after colorectal bowel proximal to the point of obstruction and little or no gas surgery. A phlegmon or abscess may be caused by leakage of in the bowel distal to the obstruction. A CT scan is more intestinal contents from a disrupted anastomosis or by iatrogenic accurate for differentiating functional from mechanical injury to the bowel during enterolysis or closure of laparotomy obstruction by identifying the so­called transition point or incision. With mechanical obstruction, there is an increased cutoff at the obstruction site in cases of mechanical obstruc­ incidence of discrete, clustered contractions proximal to the tion. It also determines the level (high or low) and degree of obstruction that propel the intestinal contents past the point of obstruction (partial versus high­grade or complete), differenti­ obstruction (in cases of partial obstruction) and result in cramps. ates between uncomplicated and complicated (compromised In high­grade or complete obstruction, the contents do not bowel, perforation) obstruction, and identifies specific types of move distally, but accumulate in the proximal part of the bowel obstruction (closed­loop obstruction, intussusception). In and initiate retrograde contractions that empty the small bowel addition, CT may identify other associated disease states (e.g., contents into the stomach in preparation for expulsion during bowel ischemia, phlegmon, abscess, pancreatitis). Small bowel vomiting. follow­through is indicated if the clinical picture of postopera­ tive small bowel obstruction is confusing, radiographs of the presentation abdomen are not diagnostic, or the response to expectant Postoperative ileus affects the stomach and colon primarily. After management is inadequate. A standard battery of laboratory laparotomy, small bowel motility returns within several hours, tests is also obtained, including a complete blood cell count gastric motility within 24 to 48 hours, and colonic motility in with differential, determination of amylase, lipase, electrolyte, 48 to 72 hours. Secretions and swallowed air are not emptied magnesium, and calcium levels, and urinalysis. from the stomach, and gastric dilation and vomiting may occur. The return of bowel activity is heralded by the presence of bowel treatment sounds, flatus, and bowel movements. Preventive measures must be started intraoperatively and con­ Patients with early postoperative small bowel obstruction tinued in the immediate postoperative period. A concerted effort do not show manifestations of bowel activity or have temporary must be made during any abdominal operation to minimize return of bowel function. In adynamic ileus, the stomach, small injury to the bowel and other peritoneal surfaces, the recognized bowel, and colon are affected. In mechanical obstruction, the source of adhesion formation. During the operation, the surgeon obstruction may be partial or complete, may occur in the prox­ must handle the tissues gently and limit peritoneal dissection to imal part of the small bowel (high obstruction) or in the distal only what is essential. The bowel must not be allowed to desic­ part of the small bowel (low obstruction), and may be a closed­ cate by prolonged exposure to air without protection. Moist loop or open­ended obstruction.33 There is stasis and progressive laparotomy pads must be used to cover the bowel and must be accumulation of gastric and intestinal secretions and gas; the moistened frequently if contact with the bowel is prolonged. bowel may lose its tone and dilate, thereby resulting in abdom­ Instrument injury to the bowel must be avoided. Given the inal distention, pain, nausea and vomiting, and obstipation. The importance of adhesion formation and the large magnitude of extent of the clinical manifestations varies with the cause, degree, serious problems related to adhesions, adjunctive measures, such and level of obstruction. Patients with high mechanical small as antiadhesion barriers, may be considered. A number of anti­ bowel obstruction vomit early in the course and usually have no adhesion barriers are available, including an oxidized cellulose or minimal distention. The vomitus is generally bilious. Patients product and a product that is a combination of sodium hyal­ with distal obstruction, on the other hand, vomit later in the uronate and carboxymethyl cellulose. These agents may inhibit course and have more pronounced abdominal distention. The adhesions wherever they are placed. However, a decrease in the vomitus may initially be bilious and then becomes more fecu­ number of adhesions at the site of application does not lent. Differentiation between adynamic ileus and mechanical necessarily translate into a decrease in the rate of small bowel obstruction can be difficult. With adynamic ileus, patients have obstruction. diffuse discomfort but no sharp colicky pain and a distended In the postoperative period, electrolyte levels are monitored abdomen. They often have a quiet abdomen, with few bowel and any imbalance corrected. Alternative analgesia to narcotics, sounds detected on auscultation with a stethoscope. With such as NSAIDs and placement of a thoracic epidural with local mechanical obstruction, high­pitched, tinkling sounds may be anesthetic, may be used when possible. Intubation of the detected. Fever, tachycardia, manifestations of hypovolemia, and stomach with an NG tube needs to be applied selectively.K2 sepsis may also develop. Routine intubation does not confer any appreciable effect and Townsend_Chapter 13_main.indd 28 6/10/2011 12:36:21 PM
    • Surgical coMPlicationS  chapter 13  13-29 is associated with discomfort, inhibits ambulation, and predis­ microvascular permeability, exudation of fluid with resultant SeCtion ii PerioPerative ManageMent poses to aspiration, sinusitis, otitis, esophageal injury, and elec­ interstitial edema, bowel wall edema and ascites occurs. trolyte imbalance. The use of prokinetic agents does not alter In healthy individuals, IAP ranges from subatmospheric to the outcome after colorectal surgery and other pharmacologic 5 mm Hg and fluctuates with respiration, body mass index, and manipulations, such as parasympathetic agents, adrenergic activity. Following uncomplicated abdominal surgery, IAP blocking agents, and metoclopramide, also have no impact on ranges from 3 to 15 mm Hg. IAP reflects intra­abdominal resolving postoperative ileus.32 The role of early postoperative volume and abdominal wall compliance. With increased volume, feeding remains unclear. there is a decrease in compliance and any further change in Once early postoperative obstruction is suspected or diag­ volume results in an increase in pressure, leading to IAH. In the nosed, a three­step approach is essential to guarantee a favorable early stages of IAH, changes in organ function are not detectable outcome—resuscitation, investigation, and surgical interven­ and of questionable clinical significance. With further increase tion.33 Emergency relaparotomy is performed if there is a closed­ in IAP, deleterious effects are observed in the intra­ and extra­ loop, high­grade, or complicated small bowel obstruction, abdominal organs and abdominal wall.27 Upward displacement intussusception, or peritonitis. Adynamic ileus is treated by of the diaphragm results in decreased thoracic volume and com­ resolving some of the abnormalities listed in Box 13­10 and pliance and increased intrapleural pressure. This results in an waiting expectantly for resolution, with surgery not usually increase in peak airway pressure (PAP), ventilation­perfusion being required. Partial mechanical small bowel obstruction is (V­P) mismatch, hypoxia, hypercapnia, and acidosis. When IAP also initially managed expectantly and for a longer period, 7 to reaches 25 mm Hg, there is an increase in end­respiratory pres­ 14 days, if the patient is stable and clinical and radiologic sure to achieve a fixed tidal volume. However, modest IAH can improvement continues. During this time, nutritional support exacerbate acute lung injury, inhalation injury, or respiratory is initiated and surgical intervention is performed if there are distress syndrome. Compression of the inferior vena cava and signs of deterioration or no improvement. portal vein occurs and results in decreased venous return, and therefore a decrease in preload and pooling of blood in the splanchnic and lower extremity vascular beds, and increased acute abdominal compartment Syndrome peripheral vascular resistance. Venus return decreases with IAP higher than 20 mm Hg. As a result, cardiac output (CO), Cause cardiac index, and right atrial and pulmonary artery occlusion Abdominal compartment syndrome (ACS) describes increasing pressures decrease. Increased intrathoracic pressure also decreases organ dysfunction or failure as a result of IAH. IAH is present left ventricular compliance, thus reducing contractility and when there is a consistent increased IAP value higher than further decreasing the CO. Ventricular compliance is reduced 12 mm Hg, determined by a minimum of three measurements when IAP is higher than 30 mm Hg. Cardiac output decreases, conducted 4 to 6 hours apart, measured at the end of expiration despite normovolemia or apparent high filling pressures and a in a relaxed patient. ACS may be primary or secondary and normal ejection when the IAP is 20 to 25 mmHg. Systemic develops when IAP is 20 mm Hg or higher, with or without delivery of oxygen (O2) decreases and whole body oxygen con­ abdominal perfusion pressure (APP) less than 50 mm Hg (at sumption is significantly reduced at an IAP higher than least three measurements performed 1 to 3 hours apart); it is 25 mmHg. associated with failure of one or more organ systems that was Direct compression of the kidneys and obstruction of not present previously. venous outflow, with resultant increase in prerenal vascular Primary ACS develops as a result of pathologic IAH caused resistance and shunting of blood from the cortex to the medulla, by intra­abdominal pathology and secondary ACS develops in results in a decrease in the glomerular filtration rate, renal the absence of intra­abdominal primary pathology, injury, or plasma flow, glucose reabsorption, and urine output. In the intervention. Primary ACS is most commonly encountered in postoperative patient admitted to the intensive care unit with victims of multiple trauma, especially after damage control an IAP higher than 18 mm Hg, renal function is impaired by surgery, and develops as a result of ileus caused by bowel edema 30%, independent of prerenal circulation. With an IAP higher and contamination, continued bleeding, coagulopathy, packing than 25 mm Hg, renal output decreases in 65% of patients and used to control bleeding, capillary leak, and massive fluid resus­ in 100% of patients with an IAP higher than 35 mm Hg. citation and transfusion. Closure of a noncompliant abdominal Compression of the mesenteric vasculature leads to a decrease wall under tension in these situations is associated with IAH in in splanchnic perfusion, mesenteric venous hypertension, and 100% of cases. In nontrauma patients, IAH and possibly primary decreased hepatic arterial flow. This results in severe intramuco­ ACS have been reported to occur in patients with ascites, retro­ sal acidosis, intestinal edema, and visceral swelling, increased peritoneal hemorrhage, pancreatitis, or pneumoperitoneum and intestinal permeability, and possible bacterial translocation. after reduction of chronic hernias that have lost their domain, Gastric intramucosal acidosis develops with IAP higher than 20 repair of ruptured abdominal aortic aneurysm, complex abdom­ to 25 cm H2O or 15 mm Hg. Elevated central venous pressure inal procedures, and liver transplantation. Secondary ACS is in interferes with venous cerebral outflow, with consequent cere­ part iatrogenic and commonly encountered in patients with bral pooling and increase in intracerebral pressure. Also, with shock requiring aggressive fluid resuscitation with crystalloids, diminished CO and increasing intracerebral pressure, cerebral thermally injured and shock trauma victims, critically ill hypo­ perfusion pressure decreases. Interleukin 6 (IL­6) and IL­1B thermic and septic patients, and those who have sustained levels increase in response to increased IAP. Blood flow to the cardiac arrest. Shock and ischemia increase capillary permeabil­ abdominal wall decreases with a progressive increase in IAP. ity; combined with excessive crystalloid resuscitation (leading to This may result in an increased rate of abdominal wound com­ dilution of plasma) and gut reperfusion, which further increase plications. K2Townsend_Chapter 13_main.indd 29 6/10/2011 12:36:22 PM
    • 13-30  section ii  PerioPerative ManageMent Diagnosis Box 13-11  prevention of abdominal  The clinical manifestations of primary and secondary ACS are compartment syndrome similar. However, the effects of secondary ACS are more subtle, so the diagnosis may be missed and the clinical deterioration of Patients at risk for iaH and abdominal compartment synd  ome  r the patient is usually attributed to severity of the primary illness are  identified  (e.g.,  major  trauma,  complex  abdominal  or occurrence of irreversible shock. Secondary ACS often occurs procedure). during aggressive fluid resuscitation in patients with burns, organ function is monitored and assessed: extra­abdominal injury, or sepsis. Patients with ACS have diffi­ • lungs: Hypercapnia, hypoxia, difficult ventilation, ele- culty breathing or are difficult to ventilate and exhibit rising PAP, vated  pulmonary  artery  pressure,  drop  in  Pao2/Fio2  decreased volumes, hypoxia, worsening hypercapnia, and dete­ ratio,  decreased  compliance,  intrapulmonary  shunt,  riorating compliance. Oliguria rarely occurs in the absence of increased dead space respiratory dysfunction or failure. The CO is reduced, despite • Heart:  Decreased  cardiac  output  and  cardiac  index  apparent high filling pressures, and vasopressor therapy is and need for vasopressors required. The abdomen becomes distended and tense and neu­ • Kidneys: oliguria unresponsive to fluid therapy rologic deterioration may occur. The central venous pressure, • central  nervous  system:  glasgow  coma  scale  score  22 pulmonary capillary wedge pressure (PCWP), and PAP become <10  or  neurologic  deterioration  in  the  absence  of  elevated and acidosis develops. Anuria, exacerbation of pulmo­ neurotrauma nary failure, cardiac decompensation, and death ultimately • abdomen: Distention; ct scan to check for fluid col- occur. lections, narrowing of inferior vena cava, compression  Use of the urinary bladder catheter has been the gold stan­ of the kidneys, and rounding of abdomen dard and is the indirect method used to measure IAP.28 IAP is intra-abdominal  pressure  is  measured  and  monitored  with  a  measured in the following ways: (1) using a regular Foley cath­ urinary bladder or gastric catheter. 23 eter, disconnect from drainage tubing, directly inject 50 mL, other tests to check organ dysfunction: clamp, insert needle, and measure; (2) a three­way Foley cath­ • gastric mucosal pH eter with saline is injected into one port and IAP is measured • near-infrared  spectroscopy  to  measure  muscle  and  through the other; or (3) a regular Foley catheter is serially con­ gastric tissue oxygenation nected to a three­way stopcock and a transducer. Other measure­ • abdominal  perfusion  pressure  =  mean  arterial  pres- ment kits have now become commercially available. Once sure − intra-abdominal pressure measured, the pressure is graded: GI (IAP < 10 to 15 cm H2O), • renal filtration gradient = mean arterial pressure − 2×  GII (IAP < 16 to 25 cm H2O), GIII (IAP < 26 to 35 cm H2O), intra-abdominal pressure and GIV (IAP > 36 cm H2O). • ct scan Measures to lower iaH: treatment • Drainage of intra-abdominal fluid collections The prevention of primary ACS entails leaving the peritoneal • Muscle relaxation cavity open in patients at risk for IAH and after high­risk surgical avoid  primary  closure  of  the  incision—laparotomy  or  mesh,  procedures. Patients at risk for secondary ACS receiving crystal­ Bogota bag, biomesh, or vacuum-assisted closure. loid resuscitation must be monitored closely and, when given 24 more than 6 liters in a 6­hour period, IAP must be measured. In addition to blood pressure and urine output, monitoring APP decompression may be considered when the abdomen is tense (APP = mean arterial pressure − IAP) by continuously measuring and signs of extreme ventilatory dysfunction and oliguria IAP throughout resuscitation is a helpful indicator of the resus­ develop. In grade IV IAH, with signs of ventilator and renal citation end point. Routine measurement of IAP must also be failure, decompression is indicated. In patients with severe head considered in critically ill patients because IAH is the leading injury and IAP higher than 20 mm Hg, even without overt cause of chest wall impairment in ARDS. Monitoring gastric pH ACS, or intractable intracranial hypertension without obvious can detect cases of secondary ACS early after admission to the head injury, abdominal decompression must be considered. intensive care unit. A high incidence of suspicion is paramount, Unlike primary ACS, in which reopening of the preexisting especially in cases of secondary ACS in which the onset is insidi­ laparotomy incision for decompression can be easily done, ous and manifestations are subtle. Patients exhibiting the prodro­ there is usually reluctance to perform a formal laparotomy for mal phase of ACS benefit from timely intervention to relieve the decompression in cases of secondary ACS, especially in the IAH and prevent progression to ACS (Box 13­11). Conservative absence of primary intra­abdominal pathology. If nonoperative fluid resuscitation, administration of analgesia, sedatives and measures (see earlier) prove ineffective, fascial release without pharmacologic paralysis, patient positioning, drainage of intra­ exposing the peritoneal cavity using minimally invasive tech­ abdominal fluid, escharotomy, renal placement therapy, and niques has proven effective in lowering IAP in experimental diuretics are measures that may prevent progression to ACS. animals.34 Decompression (formal laparotomy) is an emergency Optimizing treatment and identifying patients with and is performed in the operating room. Decompression leads IAH­ACS likely to benefit from decompression is a challenging to reduction of IAH, severe hypotension as a result of sudden task. The decision to intervene surgically is not based on IAH decrease in systemic vascular resistance, and abrupt increase in alone but rather on the presence of organ dysfunction in asso­ the true tidal volume delivered to the patient, with washout of ciation with IAH. Few patients with a pressure of 12 mm Hg the byproducts of anaerobic metabolism from below the dia­ have any organ dysfunction, whereas IAP higher than 15 to phragm. This results in respiratory alkalosis, decrease in effec­K2 20 mmHg is significant in every patient. With grade III IAH, tive preload, and a bolus of acid, potassium, and other Townsend_Chapter 13_main.indd 30 6/10/2011 12:36:22 PM
    • Surgical coMPlicationS  chapter 13  13-31 byproducts delivered to the heart, where they cause arrhythmia or platelet inhibitor therapy will identify patients at high risk SeCtion ii PerioPerative ManageMent or asystolic arrest. Hence, decompression is performed after for postoperative bleeding. adequate preload with volume has been established. Most In general, bright red blood is considered to come from a patients respond to decompression and survive. Once stable, colonic or distal small bowel source. Melanotic stools suggest a the patient may be returned to the operating room for defini­ gastric cause of the bleeding. However, rapid bleeding at any site tive closure. If primary closure is not possible, closure may be may result in bright red blood. Bleeding from the anastomosis effected with skin flaps only, composite mesh, bioprosthesis, may be a slow ooze or a rapid hemorrhage that can lead to bilateral medial advancement of rectus muscle and its fascia hypotension. Patients who appear to have lost a significant with lateral skin relaxation incisions, or tissue expanders and amount of blood have associated tachycardia or hypotension or myocutaneous flaps. have a significant decrease in hematocrit level. postoperative gastrointestinal Bleeding treatment To prevent stress ulceration and decrease the risk for bleeding, Causes patients at risk must receive aggressive fluid resuscitation to Postoperative GI bleeding is one of the most worrisome com­ improve oxygen delivery and prophylaxis that neutralizes or plications encountered by general surgeons. Possible sources in reduces gastric acid. Patients with respiratory failure and coagu­ the stomach include peptic ulcer disease, stress erosion, a lopathy benefit the most from prophylaxis. Maintaining the Mallory­Weiss tear, and gastric varices, in the small intestine, gastric pH above 4 is essential to minimize gastric mucosal arteriovenous malformations and bleeding from an anastomosis injury and propagation of injury by acid. This can be achieved and, in the large intestine, anastomotic hemorrhage, diverticu­ with antacids, H2 blockers, M1 cholinoreceptor antagonists, losis, arteriovenous malformations, and varices. sucralfate, or PPIs. In the critically ill, GI bleeding caused by stress ulceration The basic principles of management of postoperative GI is a serious complication. The incidence of bleeding from stress bleeding include the following: ulceration has decreased in the past 15 years, mainly because of 1. Fluid resuscitation and restoration of intravascular improved supportive care, superior acid suppression, and volume enhanced resuscitative measures. Clinically significant bleeding 2. Checking and monitoring clotting parameters and that leads to hemodynamic instability, the need for transfusion correcting abnormalities, as needed of blood products, and occasionally operative intervention 3. Identification and treatment of aggravating factors occurs in less than 5% of cases and is associated with significant 4. Transfusion of blood products mortality. Risk factors for stress ulceration are listed in Box 5. Identification and treatment of the source of the 13­12. bleeding In general, management of GI bleeding is best conducted presentation and Diagnosis in the intensive care unit setting. Fluid resuscitation with isos­ When considering the source of the hemorrhage, a previous motic crystalloids is begun after securing venous access. Blood history is important when assessing the patient. A history of samples are sent to assess the hematocrit, platelet count, pro­ peptic ulcer disease and previous upper GI bleeding lead one to thrombin time, partial thromboplastin time, and INR. If the consider a duodenal ulcer. Severe trauma, major abdominal INR is elevated, vitamin K and fresh­frozen plasma are admin­ surgery, central nervous system injury, sepsis, or MI may be istered. Platelet transfusion is administered to patients with a associated with stress ulceration. An antecedent history of violent prolonged bleeding time or to those who have been taking emesis leads to consideration of a Mallory­Weiss tear, and a antiplatelet drugs; desmopressin acetate may also be given to history of portal hypertension or variceal bleeding is a clue patients in renal failure. Hypothermia, if present, is corrected. regarding the presence of esophageal varices. A previous history Blood transfusion is recommended when tachycardia and of diverticulosis may indicate that the hemorrhage is diverticular hypotension refractory to volume expansion are present, with a in nature. With a recent surgical history of intestinal anastomo­ hemoglobin concentration in the 6­ to 10­g/dL range and the sis, oozing from the suture or staple line may be the source of extent of blood loss is unknown, a hemoglobin concentration GI bleeding. In distal colorectal anastomoses, bleeding may be less than 6 g/dL, and rapid blood loss more than 30%, as well the first sign of anastomotic breakdown. A previous history of as in patients at risk for ischemia or those with an oxygen extrac­ aortic aneurysm repair may indicate the presence of an aorto­ tion ratio more than 50%, with a decrease in Vo2.35 An NG duodenal fistula. A history of intake of NSAIDs or anticoagulant tube is placed and the effluent checked for the presence of blood. Nonbloody bilious drainage almost rules out a gastroduodenal source of the bleeding. If blood is present, lavage with saline at Box 13-12  risk Factors for Development of stress erosions room temperature is performed. Identification and treatment of the source of bleeding can Multiple trauma be achieved with endoscopy, angiography or, occasionally, lapa­ Head trauma rotomy. Endoscopic control of bleeding can be achieved with an Major burns injection of epinephrine, electrocoagulation, laser coagulation, clotting abnormalities heater probe, argon plasma coagulator, clip application, banding, Severe sepsis or any combination of these modalities, depending on the source Systemic inflammatory response syndrome of bleeding. Visceral angiography is indicated for patients who cardiac bypass are actively bleeding or when endoscopy fails to control the intracranial operations bleeding. Once an actively bleeding vessel is identified, K2Townsend_Chapter 13_main.indd 31 6/10/2011 12:36:22 PM
    • 13-32  section ii  PerioPerative ManageMent embolization (e.g., with Gelfoam, autologous blood clot, coils) dermal layer of skin, excessive bowel tension, or peristomal often controls the bleeding. Infusion of vasopressin may be used infection. in patients with severe stress ulceration, diverticulosis, and Stomal prolapse is most alarming to the patient and can ongoing bleeding. Bleeding from an intestinal anastomosis and result in incomplete diversion of stool, interfere with the stoma stress ulceration usually cease with expectant management. appliance, lead to leakage of stool, or become associated with Rarely, a patient with an anastomosis may require a reoperation obstructive symptoms and incarceration. Parastomal hernia for­ to resect the anastomosis and reconnect the bowel. Similarly, mation occurs to some degree in most patients. A peristomal surgery for stress ulceration is reserved for patients who fail fistula is often a sign of Crohn’s disease, may result from a deep medical management. Usually, a generous gastrotomy is per­ suture used to mature the stoma, or may be caused by trauma 25 formed to evacuate the blood clots and oversew sites of active from an appliance. bleeding; uncommonly, total or subtotal gastrectomy, with or Chemical dermatitis is caused by contact of the stoma without vagotomy, is performed. Recurrence with both effluent with peristomal skin as a result of a large opening in the approaches is prevented in 50% to 80% of cases. faceplate or leakage from an ill­fitted faceplate. Chemical der­ matitis is initially manifested as erythema, ulceration (ileostomy Stomal complications effluent), encrustation (urostomy effluent), or pseudoepithelio­ matous hyperplasia. Infectious dermatitis may be caused by Causes fungus, bacteria, tinea corporis, or C. albicans. Allergic derma­ Stomas are widely used in the treatment of colorectal, intestinal, titis may be related to any of the stomal equipment (e.g., face­ and urologic diseases. An intestinal stoma can be an ileostomy, plate, tape, belt), with skin manifestations appearing at the site colostomy, or urostomy, end, loop, or end­loop, temporary or of contact. Traumatic dermatitis occurs during change of the permanent, diverting or decompressing, or continent or incon­ stomal device, from stripping of adhesive, or as a result of fric­ tinent. A tube cecostomy and a blowhole are considered tempo­ tion or pressure from the stomal device or supportive belt. rary decompressing colostomies performed in emergencies. Traumatic dermatitis is manifested as erythema, erosion, and Stomal complications are the result of several causative factors. ulceration. Technical factors are most important in minimizing the compli­ Stoma patients are at risk for diarrhea and dehydration. cation rate of stoma construction and are largely preventable. The risk for dehydration depends on the type of stoma, under­ Stomal complications are numerous (Table 13­13) and range lying primary disease process, and any concomitant bowel resec­ from a bothersome problem with fit of the stomal appliance to tion; it commonly occurs in older patients, in hot weather, major skin erosion and bleeding. Early complications are con­ during strenuous exercise, and in association with short bowel sidered those that occur within 30 days after surgery. syndrome. Cutaneous manifestations of the disease may develop in the presentation and Diagnosis damaged peristomal skin in patients afflicted with certain skin Ischemic necrosis results from impaired perfusion to the termi­ conditions, such as psoriasis. Pyoderma gangrenosa may develop nal portion of the bowel as a result of a tight aperture, overzeal­ in patients with inflammatory bowel disease, and parastomal ous trimming of mesentery, or mesenteric tension. Stomal varices may develop in patients with liver disease. retraction occurs early as a result of tension on the bowel or ischemic necrosis of the stoma. Late retraction is caused by treatment increased thickness of the abdominal wall with weight gain. To prevent most stomal complications, adherence to sound sur­ Stenosis occurs as a result of a small aperture, so­called natural gical technique is imperative. Application of the technical points maturation, ischemia, recurrence of Crohn’s disease, or develop­ shown in Box 13­13 ensures the construction of a healthy and ment of carcinoma. Mucocutaneous separation develops as a well­positioned stoma in patients undergoing surgery. In emer­ result of ischemia, inadequate approximation of mucosa to the gencies and difficult cases such as the obese, distended bowel, and shortened mesentery, to ensure delivery of a viable stoma free of tension, the fascial aperture may be made larger, the table 13-13  stomal complications bowel may have to be extensively mobilized, the ileocolic artery Complication and inferior mesenteric artery may have to be divided at their cateGorY earLY Late origin, windows may need to be created in the mesentery, the stoma may be brought out at a site with less subcutaneous fat Stoma Poor location Prolapse retraction* Stenosis (above the umbilicus), or alternative stomas may be selected. ischemic necrosis Parastomal hernia After construction of a stoma, a dusky appearance indicates Detachment Fistula formation some degree of ischemia. The ischemia may be mucosal or full abscess formation* gas opening wrong end odor thickness, and the extent and depth of ischemia dictate the need Peristomal skin excoriation Parastomal varices for immediate revision of the stoma. Viability of the stoma is Dermatitis* Dermatoses checked with a test tube and a flashlight or endoscopy. Necrosis cancer extending to and beyond the fascia requires immediate reopera­ Skin manifestations of  inflammatory bowel  tion. Ischemia limited to a few millimeters is observed and may disease not result in any long­term sequelae. Repair of stomal retraction Systemic High output* Bowel obstruction often requires laparotomy. nonclosure Skin­level stenosis can be repaired locally and stenoses from *May also develop as a late complication. other causes can be repaired via laparotomy. Complete separa­K2 tion or detachment usually requires revision. Repair of end Townsend_Chapter 13_main.indd 32 6/10/2011 12:36:22 PM
    • Surgical coMPlicationS  chapter 13  13-33 Box 13-13  technical aspects of stoma construction table 13-14  Factors associated With increased risk for Clos- SeCtion ii PerioPerative ManageMent tridium difficile colitis abdominal Wall aperture excision of circular piece of skin approximately 2 cm in size cateGorY risK Factors Preservation  of  subcutaneous  fat  to  provide  support  for  the  Patient-related factors increasing age stoma Preexisting renal disease Preexisting chronic obstructive lung disease transrectus muscle placement of the stoma impaired immune defense Fascial aperture to admit two fingers underlying malignancy underlying gastrointestinal disease Stoma Selection of normal bowel for the stoma treatment-related  Preoperative bowel cleansing factors antibiotic use adequate mobilization of bowel to avoid tension on the stoma immunosuppressive therapy Preservation of blood supply to end of bowel (marginal artery  Surgery of  the  colon  and  last  vascular  arcade  of  small  bowel  mes- Prolonged hospital stay entery must be preserved) Facility-related factors intensive care units Small bowel serosa must not be denuded of >5 cm of mesen- caregivers long-term facilities tery maturation Primary maturation of end stoma or afferent limb of loop ileos- tomy avoidance of traversing skin with sutures during maturation bacterium C. difficile. Several factors are associated with increased risk for CDC (Table 13­14). There has been an increased inci­ other maneuvers* dence and diagnosis rate of C. difficile infection (CDI) in hos­ tunneling of bowel through extraperitoneal space of abdominal  pitalized patients, as well as an increase in severity, requiring wall admission to the intensive care unit, treatment failure of the Mesenteric-peritoneal closure disease, colectomies, and 30­day mortality (4.7% in 1992 to Fixation of mesentery or bowel to fascial ring 13.8% in 2003).36,37 These changes are caused by increased 26 use of supportive rod with loop stomas awareness of the disease, advanced age of inpatients, with numer­ *May be performed but have not been proved to be effective in preventing post- ous comorbidities, ubiquitous use of antibiotics, and emergence operative complications. and spread of a hypervirulent strain. Historically, cephalospo­ rins, clindamycin, and ampicillin­amoxicillin were most com­ monly associated with CDI. Fluoroquinolones, as a class of stomal prolapse can be achieved locally by making a circumfer­ antibiotics, have emerged as the most prone and at increased risk ential incision at the mucocutaneous junction, excision of to cause CDI, and the increased use of newer generation fluo­ redundant bowel, and rematuration. Repair of loop stomal pro­ roquinolones is implicated in outbreaks of a fluoroquinolone­ lapse is achieved by local revision to an end stoma. Laparotomy resistant strain. Since 2000, a hypervirulent toxinotype III strain may be required for the treatment of recurrent prolapse and of C. difficile (designated BI/NAP1/027 strain) has been identi­ prolapse associated with a parastomal hernia. Large permanent fied in Canada, the United States, and England. Virulence of or complicated parastomal hernias are treated by relocating the the wild­type C. difficile bacteria is related to enterotoxin A and stoma or reinforcing the fascia ring with mesh (synthetic or cytotoxin B encoded by the genes tcdA and tcdB. Polymorphisms biomaterial). Treatment of a peristomal fistula entails resection or partial deletions (18­base pair deletion) in tcdC may lead to of the diseased or involved segment of bowel and relocation of increased production of toxins A and B at levels 16 and 23 times the stoma. Treatment of mucosal islands ranges from ablation higher than the wild type. with electrocautery to relocation of the stoma. Antibiotic use continues to precede almost all cases of Treatment of chemical dermatitis entails cleaning the infection. Of patients contracting CDC, 90% have received damaged skin, the use of barriers, and a properly fitting stomal antibiotic therapy and 70% have been treated with multiple management system. Candida dermatitis is best treated with antibiotics. Patients receiving prolonged courses of antibiotic nystatin powder. Allergic dermatitis is treated by removal of the therapy are particularly susceptible, and those receiving prophy­ offending item and symptomatic relief is produced by oral anti­ laxis are also at risk. Prolonged hospital stay allows exposure to histamine or topical or oral steroid therapy. Traumatic dermati­ contaminated environmental surfaces by more susceptible tis is treated by patient education and application of a skin people. Intensive care and long­term facility units are not only barrier under the tape is used to secure the faceplate in place. sites of heavy environmental contamination, but also house Occasionally, in cases of severe dermatitis, the patient will have critically ill and vulnerable patients. Impaired host immune to be admitted to the hospital and placed on TPN while the defense as a result of advanced age, surgery, immunosuppressive skin around the stoma heals enough to allow subsequent place­ medications, HIV, and chemotherapy are major risk factors. The ment of an appliance. proportion of immunocompromised patients infected with C. difficile has increased from 20% to 30% in the past decade. Clostridium difficile colitis Surgical patients account for 45% to 55% of CDC, and the highest rates of infection are noted in patients undergoing Causes general and vascular surgery. C. difficile is a gram­positive anaer­ C. difficile colitis (CDC) is an inflammatory bowel disease obic spore­forming bacillus; approximately 5% to 35% of bac­ caused by toxins produced by unopposed proliferation of the teria do not produce toxins and thus do not cause colitis. The K2Townsend_Chapter 13_main.indd 33 6/10/2011 12:36:22 PM
    • 13-34  section ii  PerioPerative ManageMent organism produces a capsule that resists degradation by phago­ more prominent and are associated with systemic signs of toxic­ cytes. The spore is heat­resistant, persists in the environment for ity. Diarrhea may be absent in 5% to 12% of cases; the WBC months and years in a dormant phase, and survives on inanimate count may be depressed but is most commonly increased with objects. Approximately 3% to 5% of the general population has a rapid elevation (>20,000 cells/mm3) and bandemia (>30%). the organism in their stool. This increases to 8.6% of patients A leukemoid reaction is a prominent feature that may suggest with hematologic malignancies and 10% to 25% of adults CDC or herald the onset of fulminant disease. Frank peritoneal during hospitalization. signs and toxic megacolon may develop and rapidly progress to Antibiotic use leads to a disturbance in the microflora of shock. Toxic megacolon usually develops slowly and is charac­ the colon and allows the nosocomial organism to grow, prolifer­ terized by obstipation, a dilated colon, and systemic toxicity. In ate, and produce toxins. Toxin A, an enterotoxin, causes cell fulminant disease, the toxin assay is negative in 12.5% of cases. rounding, mucosal damage and inflammation, and release of CT scanning is diagnostic and typically shows a boggy, edema­ inflammatory mediators. Toxin B is a potent cytotoxin that tous, and thickened colon wall (>3 mm) in 88%, pancolitis in causes identical cell rounding and activates the release of cyto­ 50%, serous ascites in 35%, pericolic inflammation in 35%, a kines from human monocytes. The toxins translocate to the clover leaf or accordion sign in 20%, and megacolon (transverse portal circulation. Phagocytosis of toxins by macrophages in the colon >8 cm) in 25% of cases. Sigmoidoscopy shows pseudo­ liver results in the elaboration of several cytokines that act in the membranes in 90% of cases versus 23% in mild cases. propagation of the systemic septic response. treatment presentation and Diagnosis Treatment of CDC starts with prevention. However, this is dif­ Overgrowth of the toxigenic strain of C. difficile results in a ficult because disinfectants may eliminate C. difficile but not the variety of disease states, with varied clinical courses. Watery highly resistant spores, antibiotics are ineffective in clearing diarrhea is the hallmark symptom and usually starts during or stools of carriers and although effective, steam sterilization is shortly after antibiotic use. One dose of antibiotic can result in expensive. Judicious use of antibiotics, application of standard the disease, but the incidence with prophylactic antibiotics hygiene measures to hospital staff, use of disposable gloves and increases with extended use of antibiotics beyond the recom­ single­use disposable thermometers, and ward closure and mended period. Approximately 25% to 40% of patients become decontamination in case of outbreaks are important for decreas­ symptomatic 10 weeks after completion of antibiotic therapy. ing the mortality and morbidity associated with CDC. The stools are foul­smelling and may be positive for the presence Once a diagnosis of CDC is made, medical therapy and of occult blood. In mild to moderate cases, systemic signs of timely surgical intervention improve recovery and lower the infection are absent or present to a mild degree. In severe colitis, mortality rate. Death is related to delay in diagnosis, reliance on the diarrhea becomes associated with abdominal cramps and negative toxin assay, less than total abdominal colectomy, and anorexia, abdominal tenderness, dehydration, tachycardia, a additional patient­related factors. Infections with C. difficile raised leukocyte (white blood cell [WBC]) count, and bandemia usually follow a benign course. Although some patients respond (>10%). Pseudomembranous colitis is the more dramatic form to discontinuation of antibiotic therapy, others require treat­ of the disease and develops in 40% of patients who are signifi­ ment and respond within 3 to 4 days, and symptoms resolve in cantly symptomatic. 95% to 98% within 10 days. Vancomycin (125 mg, four times/ 27 Cell cytotoxin assay in tissue culture is a highly sensitive day) is given orally, down the NG tube or given or as an enema, and specific test for the detection of toxin B (rounding effect) or metronidazole (Flagyl) is given orally (250 mg, four times/ and is the gold standard diagnostic test for CDC. ELISA that day) or IV (500 mg, three times/day) for 2 weeks. Antimotility detects toxin A or B in stool is highly sensitive and specific. agents and narcotics are avoided. IV fluid therapy is instituted Unlike the stool cytotoxic test, which requires 24 to 48 hours, to correct dehydration. In the absence of ileus, oral intake is results with ELISA are obtained within hours, the test is less allowed. Approximately 25% to 30% of patients develop recur­ expensive, and does not require specific training. Endoscopy rent disease as a result of reinfection with a second strain or reveals nonspecific colitis in moderate disease (mucosal edema reactivation of toxigenic spores that persist in the colon. Treat­ and patchy erythema) or pseudomembranes in severe disease. ment of relapse is similar to that of the primary infection. In The presence of pseudomembranes may be limited to the prox­ patients with recurrent attacks, pulsed vancomycin therapy, imal colon in 10% of cases and the rectum may be spared in combination therapy with vancomycin and rifampicin, or the 60% of cases. Radiographs of the abdomen may be normal or administration of competitive organisms (e.g., Lactobacillus aci- show adynamic ileus, colonic dilation, thumb printing, or haus­ dophilus and Saccharomyces cerevisiae) may be tried. tral thickening. CT scans may show a thickened and edematous Most patients with CDI respond to medical treatment but, colon wall and free peritoneal fluid. occasionally, the disease progresses to a more severe form, such Approximately 2% to 5% of patients develop fulminant as fulminant colitis, despite appropriate and timely medical colitis, despite timely medical therapy, and may succumb to treatment. Fulminant colitis is characterized by severe systemic cytokine­mediated cardiovascular collapse and death. This fre­ inflammatory response (fever, hypotension, tachycardia, leuco­ quently develops in hospitalized and postoperative patients but cytosis, and/or requirement for volume resuscitation), shock, may occur in the out of hospital setting. At­risk patients are the multiple organ failure, and death caused by toxin­induced immunocompromised or those taking multiple antibiotics, inflammatory mediators (e.g., IL­8, macrophage inflammatory patients with a previous diagnosis of C. difficile infection, those protein­2, substance P, tumor necrosis factor­α [TNF­α]) with vasculopathy, older adults, those with chronic obstructive released locally in the colon. Hypotension that requires vasopres­ pulmonary disease, and those in renal failure. In fulminant sor support despite adequate volume resuscitation, lactate levelK2 colitis, abdominal cramps, distention, and tenderness become 5 mmol/liter or higher, respiratory failure and ventilator support, Townsend_Chapter 13_main.indd 34 6/10/2011 12:36:22 PM
    • Surgical coMPlicationS  chapter 13  13-35 and an increase in organ dysfunction are alarming premortem prophylaxis, modern surgical techniques, and advances in SeCtion ii PerioPerative ManageMent signs.36,38 patient care, the need for mechanical bowel preparation has been Colectomy is indicated when medical treatment fails or questioned. Studies have shown that mechanical bowel prepara­ when the patient develops hemodynamic instability, fulminant tion results in adverse physiologic changes and structural altera­ disease, toxic megacolon, or peritonitis. The timing of interven­ tions in the colonic mucosa and inflammatory changes in the tion is not well established. Although the end point of failure of bowel wall. Furthermore, some studies have suggested that its medical therapy is not known, a 24­ to 48­hour trial is consid­ use in elective cases is not only unnecessary but also associated ered minimal. Early intervention commits the patient to a major with increased anastomotic leaks, intra­abdominal and wound surgical procedure and an ileostomy, and a delayed intervention infections, and reoperation.39 Proponents of intraoperative is associated with high mortality (35% to 75%).36­38 lavage have also become content with simply decompressing the Once the patient develops fulminant CDC, multiple organ dilated colon and milking away fecal matter in the area of the failure, and hypotension, surgical intervention is less likely to be anastomosis instead of aggressive cleansing. Although there is a beneficial. Mortality is also increased with advanced age (>65 trend toward elimination of cleansing of the colon in elective years), prolonged duration of CDI, length of medical treatment, and emergent colon resection, one must be cautioned against and elevated serum lactate levels.36­38 Consequently, to lower abandoning the practice completely, especially for anterior resec­ mortality of severe CDI, patients at risk for fulminant disease tions, in which the presence of stool in the rectum poses a are identified and the clinical features of the disease must be problem with the use of staplers. recognized. Most importantly, surgical intervention must be The level of the anastomosis in the GI tract is important. considered during a critical window that precedes the onset Although small bowel, ileocolic, and ileorectal anastomoses are of multiple organ failure and hemodynamic collapse from considered safe, esophageal, pancreaticoenteric, and colorectal prolonged septic shock. Early surgical intervention noted in anastomoses are considered high risk for leakage. In the esopha­ recent years (2000­2006 versus 1995­1996) has changed the gus, lack of serosa appears to be a significant contributing factor. outcome, with a decrease in mortality from 65% to 32%.36,37 In the pancreas, the texture of the gland and size of the pancre­ The procedure of choice is total abdominal colectomy and ileos­ atic duct, presence of pancreatic duct obstructive lesions, experi­ tomy. Lesser procedures are less effective and associated with ence of the operating surgeon, and probably the type of enteric high mortality (70%) compared with 11% with abdominal anastomosis are implicated (see later). In the rectum, the highest colectomy. leak rate is found in anastomoses in the distal rectum, 6 to 8 cm from the anal verge. anastomotic leak Adequate microcirculation at the resection margins is crucial for the healing of any anastomosis. Factors interfering Causes with the perianastomotic microcirculation include smoking, Numerous factors can cause or are associated with an increased hypertension, locally enhanced coagulation activity as a result of risk for anastomotic leak (Table 13­15). Mechanical bowel prep­ surgical trauma, perianastomotic hematoma, and presence of aration has long been considered a critical factor in preventing macrovascular disease. In colorectal anastomoses, relative isch­ infectious complications after elective colorectal surgery. In emia in the rectal remnant is a factor because its blood supply emergencies, surgeons have resorted to on­table colonic lavage is derived from the internal iliac artery via the inferior hemor­ to cleanse the colon and primary anastomosis, with good results. rhoidal vessels, contribution from the middle hemorrhoidal With decreased morbidity rates as a result of effective antibiotic artery is minimal and, at best, variable because the vessels are mostly absent and, when present, are unilateral. Total mesorec­ tal excision, neoadjuvant therapy, and extended lymphadenec­ tomy with high ligation of the inferior mesenteric artery are table 13-15  risk Factors associated With anastomotic Leak additional contributing factors. DeFinitiVe Factors iMpLicateD Factors Intraluminal distention is believed to be responsible for technical aspects: Mechanical bowel preparation rupture of an anastomosis. The mechanical strength of the anas­   Blood supply Drains tomosis is important and, in the early period, is dependent on   tension on the suture line advanced malignancy sutures or staples, with endothelial cells and fibrin­fibrinonectin   airtight and watertight  Shock and coagulopathy anastomosis complex additionally contributing to the tension force. Con­ struction of a watertight and airtight anastomosis is therefore location in the gi tract: emergency surgery   Pancreaticoenteric Blood transfusion essential. Antiadhesive agents may predispose to leaks because   colorectal Malnutrition they isolate the anastomosis from the peritoneum and omentum     above the peritoneal obesity reflection and, as found in animal studies, decrease anastomotic bursting     Below the peritoneal gender reflection pressure and hydroxyproline levels.40 local factors: Smoking Intra­abdominally placed open rubber drains are not   Septic environment Steroid therapy   Fluid collection neoadjuvant therapy helpful and, if left for more than 24 to 48 hours, are associated with an increased risk of infection. In the pelvis, drains have Bowel-related factors: vitamin c, iron, zinc, and cysteine    radiotherapy deficiency been shown in some studies to be associated with a higher leak   compromised distal lumen Stapler-related factors: rate. Conversely, drains may remove blood, cellular debris, and   crohn’s disease   Forceful extraction of the stapler   tears caused by anvil or gun  serum that act as good culture media for perianastomotic sepsis insertion or abscess formation. Local sepsis affects the integrity of the   Failure of the stapler to close anastomosis negatively as it reduces collagen synthesis and increases collagenase activity, which results in increased lysis of K2Townsend_Chapter 13_main.indd 35 6/10/2011 12:36:22 PM
    • 13-36  section ii  PerioPerative ManageMent collagen at the anastomosis. Defunctioning or protective stomas leakage of intestinal contents. The leakage may be diffuse do not decrease the overall leak rate but rather minimize the throughout the peritoneal cavity (uncontrolled leak) or become severity and sequelae of perianastomotic contamination and walled off by omentum, abdominal wall, and contiguous loops decrease the reoperation rate. Defunctioning stomas, however, of bowel, pelvic wall or adhesions from prior operations. If a deprive the colon of short­chain fatty acids, resulting in exclu­ surgical drain is present, intestinal contents are discharged onto sion colitis and delay in epithelialization of the anastomosis, and the skin. Intra­abdominal fluid collections may contain intesti­ are associated with altered collagen metabolism observed in left­ nal contents, frank pus, or pus mixed with intestinal contents. sided anastomoses. If the fluid collection is drained surgically or percutaneously, Bevacizumab, an angiogenesis inhibitor, is associated with there is an initial discharge of purulent material followed by increased risk for surgical site complications. It is a humanized feculent material heralding the formation of an enterocutaneous monoclonal antibody that targets vascular endothelial growth fistula (controlled fistula). If allowed to drain through the surgi­ factor (VEGF). VEGF is a critical factor for the survival of cal incision or abdominal wall, surgical wound infection and endothelial cells and is selectively present in the neovasculature dehiscence with evisceration or an abdominal wall abscess may of growing tumors. Bevacizumab binds with high specificity and occur. If the fluid collection burrows into a contiguous structure affinity to VEGF, inhibiting the binding of VEGF to its recep­ such as the urinary bladder or vagina, spontaneous drainage tors and negatively affecting angiogenesis and/or the remodeling occurs, with the formation of an enterovesical or enterovaginal of the existing network of blood vessels. Bevacizumab is used in fistula. combination with standard chemotherapy IFL (irinotecan, Hence, after the index surgery, a patient may have an initial 5­fluorouracil [FU], and leucovorin) in the treatment of patients normal postoperative course or may not have been progressing with metastatic colorectal cancer. In animal studies, antiangio­ as expected. The early warning signs of anastomotic leak are genic cancer therapy inhibits dermal wound healing in a dose­ malaise, fever, abdominal pain, ileus, localized erythema around related fashion and compromises healing of colonic anastomoses. the surgical incision, and leukocytosis. Patients may also develop In patients with metastatic colorectal cancer, it increases the risk bowel obstruction, induration, and erythema in the abdominal of surgical site complications—spontaneous dehiscence of wall, rectal bleeding, or suprapubic pain. There may be an initial primary anastomosis and colocutaneous fistula formation from excessive drainage from the surgical wound or surgical wound an anastomosis. Such complications may occur up to 2 years dehiscence and/or evisceration. An intra­abdominal fluid collec­ after surgery.41 The mechanism is probably related to micro­ tion or abdominal wall abscess may be identified and drained thromboembolic disease leading to bowel ischemia, inhibition surgically or percutaneously. Patients may also experience pneu­ of angiogenesis in the microvascular bed of the new anastomosis, maturia, fecaluria, and pyuria. Once a fistulous communication inhibition of neoangiogenesis in postradiated tissue, and reduc­ is established, problems related to the loss of intestinal contents, tion in the number of newly formed vessels in granulation tissue perifistula skin, surgical wound, and malnutrition soon ensue. surrounding anastomotic sites. Risk factors for delayed anasto­ Sepsis is a prominent feature of anastomotic leakage and motic complications include a history of anastomotic complica­ results from diffuse peritonitis or localized abscess, abdominal tions, radiotherapy, and rectal location of anastomoses. wall infection, or contamination of a sterile site with intestinal Emergency bowel surgery is associated with high morbidity contents. Abdominal wall infection develops as a result of and mortality, in part because of sepsis and anastomotic leakage. contact of purulent material with the muscle and subcutaneous This is related to the poor nutritional status of the patient, pres­ tissue, tissue necrosis associated with fascial sutures, and/or ence of underlying malignancy, immunocompromised state, contact of corrosive intestinal juices with the abdominal wall, presence of intra­abdominal contamination or sepsis, and hemo­ resulting in chemical erosion and extension of the infectious dynamic instability. Transfusion, on the one hand, causes process. Nonclostridial necrotizing infections of the abdominal impaired cell­mediated immunity and predisposes to infection wall occur, particularly with fistulas of the lower GI tract that and, on the other hand, alleviates anemia and improves the contain high concentrations of Enterobacteriaceae, nongroup oxygen­carrying capacity of red blood cells that may have a A beta­hemolytic streptococci, and anaerobic cocci or positive impact on healing. Obesity increases the difficulty and penicillin­sensitive Bacteroides spp. Contamination of the complexity of the surgery, has been shown to be associated with urinary bladder with intestinal contents (enterovesical fistula) increased postoperative complications, and is an independent results in urosepsis. risk factor for an increasing leakage rate, especially after a low colorectal anastomosis. Steroids affect healing by decreasing col­ treatment lagen synthesis, delaying the appearance of the inflammatory Treatment of anastomotic leakage starts with prevention. In reaction, and reducing the production of transforming growth elective cases, nutritional support for 5 to 7 days is appropriate factor­β and insulin­like growth factor in wounds, which are for patients who are malnourished or have lost significant essential for wound healing. amounts of weight. Mechanical and chemical bowel prepara­ tions are still recommended by many surgeons prior to colorec­ presentation and Diagnosis tal resection. In patients receiving or who have received Anastomotic leak is a dreadful complication to encounter. It bevacizumab, the appropriate interval between the last dose results in sepsis and enteric fistula formation, leads to reopera­ administered and the surgery is not known. The terminal half­ tion and a possible permanent stoma, and is associated with life of the medication is long—20 days—so wound healing decreased survival and increased local recurrence rate after cura­ complications are documented up to 56 days after treatment. It tive resection of cancer, and possibly leads to death.42 is advisable to delay elective surgery for at least 4 to 8 weeks or, The clinical manifestations are the result of a cascade of preferably, three half­lives (60 days) after treatment. In patientsK2 events that start with loss of integrity of the anastomosis and with newly constructed anastomoses who are candidates for Townsend_Chapter 13_main.indd 36 6/10/2011 12:36:22 PM
    • Surgical coMPlicationS  chapter 13  13-37 bevacizumab therapy, evaluation of the anastomosis prior to Drains and octreotide can be used when an anastomosis is per­ SeCtion ii PerioPerative ManageMent initiation of therapy with fine­cut CT scanning, barium enema, formed to a soft pancreas with a small duct and in lower surgi­ and colonoscopy allows identification of patients at risk for cal volume centers or centers with a high leak rate (>10%). anastomotic complications. In emergencies, especially in hemo­ Pancreatic duct stents (placed intraoperatively) continue to be dynamically unstable, immunocompromised, and nutritionally used, despite the lack of data to suggest that they decrease the depleted patients, in the presence of fecal peritonitis, significant leak rate.43 A pancreatic stent placed prior to a distal pancreatec­ bowel dilation, and edema, an anastomosis is best avoided tomy decompresses the pancreatic duct by abolishing the pres­ because a leak may prove fatal. sure gradient between the pancreatic duct and duodenum and Construction of an anastomosis that is at low risk for dis­ may decrease the risk of fistula formation, thus allowing the site ruption requires the following: of a leak to seal. 1. Adequate exposure, gentle handling of tissues, aseptic Once an anastomotic leak is suspected or diagnosed, precaution, and meticulous, careful dissection resuscitation is started immediately because patients are in the 2. Adequate mobilization so that the two attached postoperative period and have been without nutrition. Further­ organs have a tension­free anastomosis more, they have a contracted intravascular volume because of 3. Correct technical placement of sutures or staples with third spacing and lost intestinal contents, and may have an little variance electrolyte imbalance. Intravascular volume is restored with 4. Matching of the lumina of the two organs to be con­ crystalloid fluids and a blood transfusion if anemia is present nected, which can be done by various techniques and electrolyte imbalances are corrected. Oral intake is stopped 5. Preservation of the blood supply to the ends of struc­ and the bowel is put at rest to decrease luminal contents and tures to be anastomosed GI stimulation and secretion. A NG tube is placed if obstruc­ Sufficient microcirculation is essential for healing of the tive symptoms are present. Infected surgical wounds are opened, anastomosis. In intestinal anastomoses, the marginal artery of and any abdominal wall abscesses are incised and drained. the colon and last vascular arcade of small bowel mesentery must Reoperation is indicated if there is diffuse peritonitis, intra­ be preserved. The small bowel serosa must not be denuded of abdominal hemorrhage, suspected intestinal ischemia, major mesentery more than 3 to 4 cm for hand­sewn anastomoses. In wound disruption, or evisceration. Reoperation is a major the distal colon, to ensure a tension­free anastomosis, the may undertaking and is associated with significant mortality and be required: inferior mesenteric artery may be divided at its morbidity. The procedure is bloody and carries the risk of bowel origin, windows created in the mesentery of the small bowel up injury. Primary closure of the leaking point only is avoided to the third portion of the duodenum, and small branches inter­ because failure is certain. rupted between the arcades, creating mesenteric windows and The management of duodenal and proximal jejunal leaks dividing the ileocolic vessels at their origin. For intestinal and is a challenging task. In these situations, transgastric placement colorectal anastomoses, there is no difference in the rate of of a jejunal tube helps divert gastric and biliopancreatic secre­ anastomotic leakage between hand­sewn and stapled anastomo­ tions and placement of drains in close proximity to the leak ses and among various stapling techniques, provided that sound allows external drainage of the intestinal contents. Pyloric exclu­ surgical technique is followed. The decision to construct a one­ sion and gastrojejunostomy should be used judiciously in these or two­layer intestinal anastomosis is a matter of preference. A situations. Management of jejunal, ileal, and colorectal leaking colorectal anastomosis is easier to perform in one layer. However, anastomoses depends on the severity and duration of contamina­ since the advent of stapling devices, an anastomosis deep in the tion, condition of the bowel, and hemodynamic stability of the pelvis has most commonly been stapled. The technique is not patient. In a critically ill and unstable patient, especially one only faster but also improves asepsis because the anastomosis is with fecal peritonitis, a damage control type of procedure is performed in a closed fashion compared with a hand­sewn anas­ performed—the anastomosis is taken down, the ends of the tomosis, which is considered an “open anastomosis” and allows bowel are stapled, peritoneal lavage is performed, and the inci­ for more contamination. In low anterior resection, the omentum sion is left open. A second­look laparotomy with stomal forma­ may be advanced to the pelvis and placed around the colorectal tion is performed in 24 to 48 hours or once the patient is more anastomosis. This maneuver may lower the rate of anastomotic stable. Otherwise, in the small bowel, an anastomosis may be leak or disruption but mostly appears to decrease the severity of performed or the ends of the bowel are delivered as stomas; in the complication. Drainage of a colorectal anastomosis is the colon, the proximal end of the colon is brought out as a advisable in difficult cases and when technical problems are colostomy and the distal end closed or brought out as a mucous encountered, or when neoadjuvant therapy has been used. fistula; and, in the rectum, the distal end is closed and the Defunctioning stomas are used for extraperitoneal anastomoses, proximal end of the colon delivered as a stoma. A proximal when technical difficulties are encountered, or after neoadjuvant diverting stoma with drainage of the pelvis is not adequate treat­ therapy. ment of leaking colorectal anastomoses associated with diffuse When constructing a pancreaticoenteric anastomosis, a peritonitis. If the abdomen is left open, covering the bowel with pancreaticojejunostomy is equivalent to pancreaticogastrostomy. the greater omentum (if available) or a biologic implant protects An end to side–duct to mucosa pancreaticojejunostomy is asso­ the bowel and prevents desiccation and spontaneous fistula for­ ciated with a lower leak rate compared with an end­to­end mation. Negative­pressure wound therapy is best avoided when invaginating pancreaticojejunostomy; obliteration of the main bowel is exposed, especially in the presence of unprotected pancreatic duct with protamine gel or human fibrin sealant, or suture or staple line.44 suture closure of the remnant pancreas without an anastomosis, In the absence of diffuse peritonitis and evisceration, a CT is associated with the highest leak rate.43 The routine placement scan may identify single or multiple abscesses, pneumoperito­ of drains in proximity to pancreatic anastomoses is controversial. neum, ascites and, at times, extravasation of oral contrast into K2Townsend_Chapter 13_main.indd 37 6/10/2011 12:36:22 PM
    • 13-38  section ii  PerioPerative ManageMent the peritoneal cavity. Multiple abscesses require open drainage, course. They then start showing the manifestations of leakage of a single intra­abdominal abscess can be drained percutaneously, intestinal contents (see earlier). The seriousness and severity of and a pelvic abscess can be drained transrectally or transvagi­ these manifestations depend on the surgical anatomy and phys­ nally. Following drainage, an external fistula may develop. The iology of the fistula. Anatomically, the fistula may originate from management of a controlled fistula is outlined in the next the stomach, duodenum, small bowel (proximal or distal), or section. If percutaneous drainage fails to control sepsis, reopera­ large bowel. The tract of the fistula may erode into another tion is indicated. At the time of open drainage of a pelvic abscess, portion of the intestines (enteroenteric fistula) or another hollow if there is any doubt about the origin of the abscess (de novo organ (enterovesical), thus forming an internal fistula, or into abscess versus abscess secondary to a small anastomotic leak that the body surface (enterocutaneous and pancreatic fistula) or has sealed), a defunctioning stoma is constructed unless there is vagina (enterovaginal fistula), thus forming an external fistula. complete disruption of the anastomosis. In that case, the ends A mixed fistula describes an internal fistula associated with an of the bowel are exteriorized as a stoma. A pancreaticojejunos­ external fistula. A superficial fistula drains on top of an open or tomy leak, if small, can be treated by placing a drain next to the granulating wound; in a deep fistula, the tract traverses the leak. However, for an anastomosis that has almost fallen apart, abdominal cavity and drains onto the skin. Physiologically, the the patient will probably require completion pancreatectomy. A fistula is classified as high or low output on the basis of the patient who has a bile duct leak will require drainage of the volume of discharge in 24 hours. The exact definition of low infection and placement of a drain next to the leak or, in the and high output varies from 200 to 500 mL/24 hr. However, case of a large leak, may require bile duct reconstruction. three different categories are recognized—low output (<200 mL/24 hr), moderate output (200 to 500 mL/24 hr), intestinal Fistulas and high output (>500 mL/24 hr). The ileum is the site of the fistula in 50% of high­output fistulas. The discussion in this Causes section focuses mainly on external fistulas. A fistula represents an abnormal communication between two Sepsis is a prominent feature of postoperative intestinal epithelialized surfaces, one of which is a hollow organ. In the fistulas and is present in 25% to 75% of cases. As noted earlier, GI tract, a fistula may develop between any two digestive organs sepsis is the result of diffuse peritonitis or localized abscess, or between a hollow organ and the skin and may be develop­ abdominal wall or necrotizing infection, or contamination of a mental or acquired. Acquired fistulas account for most GI fistu­ sterile hollow organ with intestinal contents. las and can be traumatic, spontaneous, or postoperative in Loss of intestinal contents through the fistula results in nature. hypovolemia and dehydration, electrolyte and acid­base imbal­ GI fistulas are most commonly iatrogenic, develop after an ance, loss of protein and trace elements, and malnutrition. In a operation, and may occur anywhere in the GI tract. Esophageal, high intestinal fistula, it also results in loss of the normal inhibi­ aortoenteric, and rectal fistulas are not discussed in this section. tory effect on gastric secretion, thus resulting in a gastric hyper­ In the past, acquired GI fistulas most commonly developed as a secretory state. With high­output enterocutaneous fistulas, there result of a difficult appendectomy. At present, they commonly is also intrahepatic cholestasis related to the loss of bile salts, occur as the result of anastomotic breakdown, dehiscence of a disruption of enterohepatic circulation, and bacterial overgrowth surgically closed segment of stomach or bowel, unrecognized in the defunctionalized intestine. Malnutrition results from loss iatrogenic bowel injury following adhesiolysis, or during closure of protein­rich secretions, lack of nutrient intake, loss of absorp­ of a laparotomy incision. Occasionally, they develop after instru­ tion caused by bypass of the gut (e.g., gastrocolic, duodenocolic, mentation or drainage of a pancreatic, appendiceal, or diver­ high enterocutaneous fistulas), and sepsis that sets the stage for ticular fluid collection or abscess. The presence of intrinsic nutritional deficiency and rapid breakdown of body muscle mass. intestinal disease, such as Crohn’s disease, radiation enteritis, In gastroduodenal and proximal small bowel fistulas, the output distal obstruction, or a hostile abdominal environment, such as is high and the fluid loss, electrolyte imbalance, and malabsorp­ an abscess or peritonitis, are predisposing factors for fistula for­ tion are profound. In distal small bowel and colonic fistulas, the mation. The risk is also higher in emergencies when the patient output is low and dehydration, acid­base imbalance, and malnu­ may be malnourished or poorly prepped. trition are uncommon. Significant electrolyte imbalance occurs Gastric fistulas are uncommon and frequently occur after in 45% of patients and malnutrition occurs in 55% to 90%. resection for cancer and less frequently after resection for peptic Skin and surgical wound complications develop as a result ulcer disease, necrotizing pancreatitis, an antireflux procedure, of contact of GI effluent with skin or the wound. Effluent der­ or bariatric surgery. Pancreatic fistulas develop as a result of matitis results from the corrosive effect of intestinal contents, disruption of the main pancreatic duct or its branches secondary which cause irritation, maceration, excoriation, ulceration, and to trauma or postoperatively following pancreatic biopsy, distal infection of the skin. Fecal dermatitis is marked by erythema pancreatectomy, pancreaticoduodenectomy, pancreatic necro­ and desquamation and may encourage skin sepsis. Superficial sectomy, and surgery on the stomach, biliary tree, or spleen. and deep surgical wound and necrotizing infections also develop. Intestinal fistulas develop after resection for cancer, diverticular Pain and itching by contact of effluent with unprotected skin is disease, inflammatory bowel disease, or closure of a stoma. intolerable and affects the morale of the patient. presentation and Diagnosis treatment Enterocutaneous fistulas are usually associated with a triad of Postoperative intestinal fistulas are not a new problem but rather sepsis, fluid and electrolyte imbalance, and malnutrition. Patients continue to be a challenging clinical scenario. Their etiogenesis are usually in the postoperative period and may not be progress­ has changed and their management continues to evolve. In theK2 ing as expected or may have an initial normal postoperative past, the main focus of management involved suctioning of the Townsend_Chapter 13_main.indd 38 6/10/2011 12:36:22 PM
    • Surgical coMPlicationS  chapter 13  13-39 table 13-16  Factors affecting healing of external intestinal Fistulas SeCtion ii PerioPerative ManageMent Factors FaVoraBLe UnFaVoraBLe Surgical anatomy of the fistula long tract, >2 cm Short tract, <2 cm Single tract Multiple tracts no other fistulas associated internal fistulas lateral fistula end fistula nonepithelialized tract epithelialized tract origin (jejunum, colon, duodenal stump, and  origin (lateral duodenum, stomach, and ileum) pancreaticobiliary) no adjacent large abscess adjacent large abscess Status of the bowel no intestinal disease intrinsic intestinal disease (crohn’s disease, radiation enteritis,  recurrent or incompletely resected cancer) no distal bowel obstruction Distal bowel obstruction Small enteral defect, <1 cm large enteral defect, >1 cm condition of the abdominal  intact Disrupted (fistula opens into the base of the disrupted incision) wall not diseased infiltrated with malignancy or intestinal disease no foreign body Foreign body (mesh) Physiology of the patient no malnutrition Malnutrition no sepsis Sepsis output of the fistula no influence influence intestinal effluent and early surgical intervention. This approach also associated with a decreased rate of healing of GI fistulas. has proven ineffective and is associated with significant patient Infected surgical wounds are opened and drained, abdominal morbidity and mortality and a high reoperation rate. At present, wall abscesses are incised and drained, and intra­abdominal fluid management requires the involvement of a surgeon, nutritionist, collections are drained percutaneously or surgically. Percutane­ enterostomal therapist, interventional radiologist, and gastroen­ ous drainage is tolerated better and allows changing a complex terologist; it entails initial medical treatment to allow spontane­ fistula (fistula associated with an abscess) to a simple fistula that ous healing of the fistula, early surgical intervention in a select has a better chance of spontaneous closure. A small pigtail cath­ group of patients, and planned definitive surgery for patients eter may be changed to a larger catheter that allows irrigation of whose fistulas have failed to heal. External intestinal fistulas the abscess cavity, later injection of contrast to assess resolution result in prolonged hospital stays and enormous cost to the of the abscess, and study of the anatomy of the fistula. hospital and are associated with significant patient disability, Nutrition is one of the most important factors contributing morbidity, and mortality (6% to 30%). Although spontaneous to a successful outcome in the management of intestinal fistulas. closure occurs in 40% to 80% of cases, operative intervention TPN must be started early after the correction of electrolyte may be required in 30% to 60% of cases. imbalance and repletion of volume. TPN allows bowel rest, The first step in the management of a GI fistula is to which decreases output, eliminates negative nitrogen balance, prevent its occurrence. Reducing the likelihood of an anasto­ improves the patient’s nutritional status, allows better timing of motic leak requires adherence to sound surgical principles and the operation when needed, increases the rate of recovery, and proper techniques (see earlier). Should a fistula form, manage­ may slightly improve the closure rate once sepsis is controlled. ment involves several phases that are applied systematically and Trace elements, multivitamins, vitamin K, and medications such simultaneously (Table 13­16). as octreotide may be added to the TPN. TPN is the initial Once a leak is diagnosed or suspected, management nutritional support for any patient with a fistula and is contin­ involves resuscitation, TPN, correction of electrolyte imbal­ ued in patients with high­output fistulas or patients who cannot ances, and transfusions, as appropriate. Oral intake is stopped tolerate oral intake. Somatostatin (SMS) analogues (e.g., octreo­ and the bowel is put at rest, thus decreasing luminal contents tide, with a long half­life) help in management of the fistula by and reducing GI stimulation and secretion. An NG tube is reducing GI secretions and inhibiting GI motility, thus control­ placed if obstructive symptoms are present. Routine NG place­ ling and reducing its output. Their value in healing intestinal ment is not helpful and subjects the patient to complications, fistulas is yet to be proven and routine use is limited because such as sinusitis and aspiration. Broad­spectrum IV antibiotic they are not without side effects. Somatostatin leads to cellular therapy is started and later adjusted according to cultures. apoptosis, villous atrophy, and interruption of intestinal adapta­ The indications for early surgical intervention have been tion, and may be associated with acute cholecystitis. Enteral discussed earlier. Otherwise, resuscitation is continued. Treat­ nutrition (low­residue diet, elemental diet, liquid whole protein ment with H2 antagonists or PPI helps decrease peptic ulceration diet) is administered to patients with low­output small bowel and may decrease fistula output but does not aid in the closure and colonic external fistulas. Fistuloclysis (i.e., infusion of nutri­ of fistula. Accurate measurement of output from all orifices and tion directly through the fistula into the bowel distal to the the fistula is paramount in maintaining fluid balance. Effective fistula) is another option to deliver enteral nutrition to patients control of all sources of sepsis is important because continued whose fistula has not healed spontaneously, provided there is sepsis is a major source of mortality that results in a state of more than 75 cm of healthy bowel distal that is in continuity hypercatabolism and the failure of exogenous nutritional support with the fistula.45 Fistuloclysis is safer and less expensive than to restore and maintain body mass and immune function; it is TPN and prevents atrophy of the bowel distal to the fistula. K2Townsend_Chapter 13_main.indd 39 6/10/2011 12:36:22 PM
    • 13-40  section ii  PerioPerative ManageMent Early control of fistula output is essential to protect the intra­abdominal inflammatory reaction occurs 10 to 21 days perifistula skin from the corrosive effects of intestinal effluent, after surgery and lasts for 6 to 8 weeks before starting to resolve. promote healing of damaged skin and surgical wounds, and A 6­month period is required for a neoperitoneal cavity to facilitate nursing care of the patient. Early involvement by an develop in fistulas within a laparoscopy wound. A simple enterostomal therapist and wound care team cannot be overem­ fistula—single fistula with direct communication between the phasized. Protection of the skin is achieved with barriers, seal­ bowel and skin, a short tract and small enteral opening, and ants, adhesives, and pouches. Negative­pressure wound therapy associated with other favorable factors—can be closed 12 weeks another treatment strategy whereby the continuous suction of after the index surgery. A complex fistula—a fistula with a long fistula output minimizes contact between intestinal contents and tract and associated with other internal fistulas, large abscess surrounding tissue. Hence, it protects perifistula skin, reduces cavity, fistula that opens into the base of a disrupted wound, or the need for dressing changes, promotes wound healing, and other unfavorable factors—is closed 6 to 12 months after the even accelerates fistula closure, especially in deep fistulas. Closure index surgery. Complex fistulas associated with intrinsic intesti­ has been reported to occur in 46% to 84% of cases.46 nal disease require definitive surgical intervention once the initial Once initial sepsis is controlled, nutrition provided, and sepsis is controlled because spontaneous closure is highly unlikely wound and fistula care provided, studies are performed to define and extirpation of the diseased bowel is essential. In patients the surgical pathology of the fistula (origin, course, length of the with Crohn’s disease, infliximab (Remicade) may also be used to fistula) and condition of the bowel (presence of intrinsic intes­ aid in closure of the fistula in a select group of patients. tinal disease, presence of distal obstruction, continuity of the A controlled ECF that opens into the base of an inter­ bowel) and to evaluate resolution of the intra­abdominal abscess. rupted wound requires abdominal wall construction at the time A fistulogram is performed by injecting a water­soluble contrast of definitive repair of the fistula. The fistulizing segment must medium or barium through an existing drain or by inserting a not be excluded or bypassed to avoid the risk of blind loop 5 Fr pediatric feeding tube or a Foley catheter into the external syndrome. The fistula is excised, continuity of the GI tract rees­ opening of the fistula. A fistulogram delineates the anatomy of tablished, and freshly constructed anastomosis wrapped with the fistula and identifies associated cavities, other fistulas, and omentum, if available. Gastric, duodenal, and proximal jejunal distal obstructions. A contrast enema demonstrates the presence fistulas that cannot be resected without major surgical procedure of a colocutaneous fistula in 90%, a colovesical fistula in 34%, are best managed with a Roux­en­Y intestinal anastomosis. The and a coloenteric fistula in most cases. Enteroclysis allows eval­ laparotomy incision is closed primarily or with durable well­ uation for intrinsic intestinal disease. Cystoscopy identifies the vascularized coverage. Autogenous tissue reduces the risk of fistula opening in 40% of enterovesical fistulas but the findings infection. Pedicle or free flaps with microvascular reconstruction of localized bullous edema, with erythema and possible ulcer­ may be considered; however, component separation when the ation, are suggestive of the diagnosis in most patients. GI endos­ rectus muscle is intact, with or without augmentation with acel­ copy allows direct visualization of colonic, intestinal, and lular dermal matrix or synthetic mesh, is the preferred proce­ gastroduodenal mucosa. A CT scan allows evaluation for the dure.47 Postoperative morbidity, ventral hernia formation, and resolution of intra­abdominal abscesses and presence of intrinsic recurrent ECFs develop in approximately 20% to 25% of cases. intestinal disease. Biologic material (e.g., acellular human or porcine dermal With such an orchestrated approach, most external fistulas matrix, porcine submucosa) used for visceral overlay protection heal spontaneously. Factors associated with spontaneous healing or reconstruction is another viable option in this setting of or failure to close are listed in Table 13­16. After control of compromised operative field because the implant resists infec­ sepsis, approximately 60% to 90% of external intestinal fistulas tion and, when postoperative infection occurs, removal of the with favorable factors will close spontaneously with medical implant is not necessary. However, the product is expensive and management, 90% will close within 4 to 6 weeks, and less than the procedure is associated with a high rate of hernia formation 10% in months 2 and 3. There are limited therapeutic options and abdominal wall laxity.48 Occasionally the incision is closed 28 for ECFs that fail to close—accept the fistula as a stoma await­ in stages. The incision may be left open (laparotomy), an absorb­ ing optimal time for definitive closure or attempt direct closure. able mesh (polyglactin or polyglycolic acid) may be used to Direct repair is applicable to a superficial bud fistula bridge the fascial defect, or negative­pressure wound therapy can whereby limited dissection is performed to identify and close the be instituted. Once granulation tissue is formed, a split­thickness edges of the fistula extraperitoneally and protect the suture line skin graft is applied. with a biologic dressing, with or without tissue adhesive. New innovative approaches, such as transcatheter injection Although several attempts may be required to achieve successful of diluted thrombin, endoscopic tissue sealant or clip applica­ closure of the fistula, the surgery is a local low­risk procedure tion, and porcine small intestinal submucosa have been used in and can be repeated. Definitive repair requires careful planning recalcitrant cases or as adjunctive therapy to hasten healing of and may be a daunting task. Definitive closure requires a waiting the intestinal fistula, with some success. period of 8 to 12 weeks, and requires that sepsis be controlled, nutrition provided, and skin is protected. The waiting period is pancreatic Fistulas crucial to allow recovery of immunologic competence, improve­ Overall, the physiologic classification, diagnosis, management, ment of nutritional status, and resolution of the period of dense and outcome of postoperative external pancreatic fistulas are inflammatory reaction. There are no well­established guidelines similar to that for external intestinal fistulas. However, pancre­ to help in determining the timing of surgery. However, the expe­ atic fistulas have additional distinctive features. Following pan­ rience of the surgeon, general condition of the patient, softness creaticoduodenectomy, texture of the pancreas, size of the of the abdominal wall and abdominal cavity, and surgical pancreatic duct, blood supply to the stump, and volume ofK2 anatomy of the fistula must be taken into consideration. A dense pancreatic juice produced are the most significant risk factors Townsend_Chapter 13_main.indd 40 6/10/2011 12:36:22 PM
    • Surgical coMPlicationS  chapter 13  13-41 for fistula formation. Pulmonary problems, autodigestion, and for most postoperative biliary injuries and strictures. The rate of SeCtion ii PerioPerative ManageMent erosion into adjacent organs are additional significant morbidi­ major bile duct injury after laparoscopic cholecystectomy ranges ties associated with pancreatic fistulas. Sepsis and hemorrhage from 0.4% to 0.7%, as opposed to 0.2% after open cholecys­ are associated with significant mortality (20% to 40%) and tectomy.49 Bile leak may be caused by a bile duct injury, cystic result in prolonged hospitalization and increased hospital duct stump leak, divided accessory duct, or injury to the intes­ expense. Postoperative pancreatic fistula is diagnosed when there tine. Acute cholecystitis, a foreshortened cystic duct, anomalies is drain output of any measurable volume of fluid after postop­ of the biliary tree, hemorrhage from injury to the cystic or erative day 3 with an amylase content more than three times the hepatic artery, dissection with thermal instruments in the serum amylase activity. More often, the fluid amylase content is triangle of Calot, and failure to define the anatomy in the tri­ 29 in the tens of thousands. The fistula is demonstrated on a fistu­ angle of Calot clearly are among the most important logram or CT scan. factors associated with a higher frequency of duct injury after Efforts to decrease the morbidity and mortality of pan­ laparoscopic cholecystectomy. creatic fistulas after pancreaticoduodenectomy focus on pre­ The most common injury sustained during the laparo­ venting, decreasing, and controlling pancreatic leaks at the scopic procedure is complete transection at or below the hepatic 30 pancreatic­enteric reconstruction (see earlier, “Anastomotic duct bifurcation. Other less complex injuries include occlusion Leak”). The benefit of perioperative somatostatin or its ana­ of the duct with a clip, thermal injury, avulsion of the cystic 31 logue have been evaluated in two meta­analysis studies. One duct, and partial laceration. study noted that somatostatin and octreotide reduce the rate of biochemical fistula but not the incidence of clinical anasto­ presentation and diagnosis motic dehiscence, whereas the other noted a significant reduc­ Most bile duct injuries are not identified at the time of surgery. tion in pancreatic fistula rate but no significant difference in Early in the postoperative period, patients may have manifesta­ postoperative mortality. Intraoperatively, a modified side to tions related to a bile leak or have signs of a bile duct stricture end pancreaticojejunal anastomosis provides a tension­free later. Bile leaking from a lacerated divided duct may accumulate anastomosis to a pancreatic stump, with adequate blood in the subhepatic space and form a biloma or seep into the supply and unobstructed flow of pancreatic juice in optimal. peritoneal cavity and result in bile ascites. Patients in this situ­ Common to this modified pancreaticojejunostomy is mobili­ ation have right upper quadrant pain, fever, nausea, abdominal zation of the pancreatic stump to allow invagination of 3 to distention, and malaise. The bile, on the other hand, may drain 4 cm of pancreatic stump into the jejunum, ablation of the through an intraoperatively placed drain and be manifested as a jejuna mucosa in the area of the jejunum­pancreas interface, bile leak. In this setting patients, may have leukocytosis and a suturing the capsular edge of the pancreatic stump to mucosa slightly elevated bilirubin level. Patients with a clipped bile duct of the everted jejunum, or the use of traction sutures between do not usually have symptoms but do have elevated liver enzyme the capsular edge and jejunum proximal edge to avoid slip­ levels. Bile duct strictures are usually accompanied by cholangi­ 32 page of the stump out of the jejunum. tis, pain, fever, chills, and jaundice. Once a pancreatic fistula has formed, medical treatment Diagnosis of bile duct injury requires the use of nuclear results in spontaneous closure in almost all fistulas after a pan­ medicine imaging to demonstrate the presence of a leak or creaticoduodenectomy and in up to 80% of all other cases of obstruction, a CT scan to identify bile collections or ascites, and pancreatic fistulas. Octreotide therapy is beneficial because it ERCP to define the type and level of injury accurately. Percuta­ significantly reduces fistula output and decreases the time to neous transhepatic cholangiography is indicated in cases of com­ fistula closure. Endoscopic retrograde cholangiopancreatogra­ plete transection to define the proximal anatomy and site of phy (ERCP) is valuable because it defines the pancreatic duct injury. Magnetic resonance cholangiopancreatography is becom­ anatomy and ductal obstruction and allows the placement of a ing the test of choice to diagnose late strictures and define the stent that bypasses the high­resistance areas of the sphincter of bile duct anatomy. Oddi, ductal strictures, and calculi, thus allowing pancreatic secretions to follow the path of least resistance. The stent may treatment also block the ductal opening of the fistula. Operative treat­ Prevention of bile duct injury starts with proper surgical tech­ ment of a benign pancreaticocutaneous fistula depends on the nique and adequate identification of the anatomy. The anatomic location of the fistula (proximal versus distal portion of the variability associated with severe inflammation creates a low pancreas) and status of the pancreatic duct (dilated versus ste­ threshold for converting a laparoscopic to an open cholecystec­ notic duct). High excision of the fistula with fistuloenteros­ tomy. During laparoscopic cholecystectomy, the infundibulum tomy has been associated with the best results. Pseudocyst of the gallbladder must be retracted laterally and inferiorly to enterostomy is associated with an unacceptable recurrence and expose the triangle and widen the cystic–common bile duct failure rate. angle. Dissection of the cystic duct and artery must commence close to the infundibulum of the gallbladder. The cystic duct and artery are divided once the anatomy is clearly delineated. HepatoBiliary complicationS Excessive traction on the gallbladder must be avoided because it will result in tenting of the common duct. If there is bleeding Bile duct injuries in the area of the cystic duct, blind clipping and cautery must be avoided and adequate exposure must be achieved, even if Causes placement of another port is required. If there is an unexpected The most dreaded complication of gallbladder surgery is injury bile leak, unusual anatomy, or a second bile duct identified, to the extrahepatic bile duct system. Cholecystectomy accounts or when technical difficulties and excessive bleeding are K2Townsend_Chapter 13_main.indd 41 6/10/2011 12:36:22 PM
    • 13-42  section ii  PerioPerative ManageMent encountered, intraoperative cholangiography helps identify the Box 13-14  causes of acute Delirium anatomy and any injuries. Early conversion to an open proce­ dure must also be considered. advanced age Once a leak is diagnosed intraoperatively, immediate alcohol intoxication and withdrawal repair must be performed. The procedure is converted to an Drugs (overdose or withdrawal) open one and the extent of duct injury is assessed. An acces­ • anticholinergic  drugs  (tricyclic  antidepressants,  sory duct can be ligated, partial transection of the common antihistamine) duct can be repaired over a T tube, a divided duct or almost • oral hypoglycemic agents circumferential transection of the common duct can be • antibiotics (cephalosporins) repaired with an end­to­end anastomosis over a T tube, and a • Histamine receptor blocking agents high injury can be repaired with a Roux­en­Y biliary enteric • anti-inflammatory drugs (e.g., steroidal, nonsteroidal) anastomosis. If repair of a high duct injury is difficult, drains • anticonvulsant medications are placed in the subhepatic space and the patient is referred • anxiolytics (diazepam) to a tertiary center. • narcotics A leak or injury identified early in the postoperative period • cardiac medications (beta blockers, digoxin) is treated as follows. The biloma is drained percutaneously, and Structural brain abnormalities (e.g., edema, transient ischemic  a sphincterotomy is performed, a stent is placed, or both can be attack, neoplasm) done if ERCP demonstrates a leak or partial narrowing. Surgical Metabolic and hemodynamic disturbances intervention is indicated for patients with major obstruction of • electrolyte imbalance the bile duct, major injury, or suspicion of a bowel injury. After • Hypoglycemia adequate resuscitation, administration of antibiotics, and ade­ • Hypoxemia quate drainage, patients are watched for a few days to make • Hypovolemia certain that they are not septic at the time of the operation. If endocrine dysfunction there is evidence of adequate control of the leak, the surgeon • thyrotoxicosis may wait up to 5 to 7 days for inflammation in the area to • Hypothyroidism subside before undertaking operative repair. Meticulous and • adrenocortical insufficiency careful dissection is required in this area because there is usually Sepsis and infections loss of common bile duct substance. After identifying the source respiratory  dysfunction  (e.g.,  respiratory  failure,  pulmonary  of the bile extravasation, dissection plus débridement of nonvi­ embolism, chronic obstructive pulmonary disease) able common bile duct is prudent. Once it has been ascertained liver, renal, cardiac disease (e.g., congestive heart failure, renal  that there is tissue with good integrity, a Roux­en­Y limb can be failure) anastomosed to the common bile duct. Multiple drains are left trauma (surgical or otherwise) around the site of the repair. critical illness and intensive care unit stay neurologic complicationS delirium, cognitive disorder, and psychosis Cause consciousness and changes in cognition. They may have reduced Delirium refers to a state of acute confusion and is a common ability to focus, decreased levels of awareness, and difficulty with complication of surgery. Numerous factors are implicated in attention. In addition, they may have hallucinations and altered causing delirium (Box 13­14). The presence of a structural brain psychomotor activity and sleep­wake cycle. These changes have disorder (infarct) increases the individual’s susceptibility to delir­ a tendency to fluctuate during the course of the day and are ium. Anticholinergic medications and conditions that decrease worse at night (sundowning). The severity of these manifesta­ the production of acetylcholine can precipitate delirium. In tions depends on the underlying cause. addition, a planned operation with loss of the patient’s routine The incidence of postoperative delirium and cognitive dis­ schedule, stress of the disease process, fear of the operation, loss orders in geriatric patients varies with the type of surgery per­ of personal control, placement in an unfamiliar environment, formed and preexisting dementia. Postoperative anemia addition of mind­altering pain medications, and pain can lead (secondary to acute blood loss), electrolyte imbalance, sepsis, to dramatic alterations in behavior in postoperative patients. At malnutrition, bladder catheterization, physical restraints, particularly high risk for behavioral disorders in the postopera­ extended duration of anesthesia, infection, and respiratory com­ tive period are older patients, patients with a previous history of plications are significant precipitating factors. substance abuse or psychiatric disorders, and children. The most immediately threatening disorder encountered by physicians is delirium tremens, which may occur 48 hours to 14 presentation and Diagnosis days after acute alcohol withdrawal. In addition, delirium Early in the postoperative period, a patient may become acutely tremens is associated with extreme autonomic hyperactivity. agitated, uncooperative, and confused. Patients with a previous Early signs of delirium tremens include fever, tremor, and tachy­ psychiatric disorder may, however, become more withdrawn and cardia, and late signs include confusion, psychosis, agitation, and depressed. Some patients may become noncommunicative and seizures. Because of the serious underlying nutritional and emotionally flat and may withdraw from any emotional medical deficiencies, these patients have s moderately high mor­K2 exchange. Patients may also show an altered level of tality, which approaches 20% in some series. Townsend_Chapter 13_main.indd 42 6/10/2011 12:36:22 PM
    • Surgical coMPlicationS  chapter 13  13-43 treatment presentation and management SeCtion ii PerioPerative ManageMent Management of delirium and cognitive disorders in a postop­ Seizures characterized by convulsions, rhythmic myoclonic erative patient is a frustrating and challenging clinical scenario. activity, loss of consciousness, and change in mental status are Prevention starts with the identification of high­risk individuals often associated with fecal and urinary incontinence, lack of before surgery and careful follow­up thereafter. Minimizing the neurologic responsiveness, and postevent amnesia. On recogniz­ dose or eliminating medications that interrupt mental function ing evidence of seizure activity, the patient must be carefully must be considered. Optimizing fluid status, providing nutrition restrained so that injury is not sustained during convulsions and and adequate pain control, and removing restraints early, includ­ is carefully observed. Administration of IV benzodiazepines is ing the Foley catheter, are essential. Early ambulation and trans­ essential to stop the seizure activity and is the standard for fer from the intensive care unit are encouraged. immediate care. Phenytoin (Dilantin) is the most commonly Treatment of patients with acute confusion or a sudden used anticonvulsant for new­onset generalized or focal seizures. change in behavior after surgery requires the following: It may be administered IV during acute convulsions or PO for 1. Recognition of the disorder maintenance. Phenytoin has several side effects, including rash 2. Close observation and monitoring and liver dysfunction. Occasionally, phenobarbital may be used 3. Identification and elimination of the precipitating but, because of sedation, is not an agent of choice. The two most factor commonly used agents for maintenance after seizures or for 4. Treatment of any associated laboratory abnormalities someone with status epilepticus are carbamazepine (Tegretol) 5. Selective use of imaging or other studies to rule out and valproic acid. Neither of these agents can be given IV and an organic brain lesion thus are used for maintenance only. Gabapentin can be admin­ 6. Application of measures to protect the patient and istered when the patient’s condition is refractory to other agents. staff After adequate control of the seizure, a diagnostic workup for 7. Treatment its cause is initiated. This includes a detailed history and physi­ A history of drug or alcohol abuse and of cardiac, pulmo­ cal examination, history of previous medication and drug use, nary, renal, or liver disease or psychiatric illness must be sought. WBC count to rule out occult infection, and electrolyte and A list of medications used in the perioperative period must be metabolic assessment. CT or MRI is indicated for a patient with checked. Clinical evaluation is performed to look for evidence new­onset seizure activity because tumors are often the cause. of sepsis or a recent neurologic event. A thorough neurologic Similarly, an electroencephalogram is obtained at some point to examination is performed while focusing on the level of con­ look for abnormal waveform activity. sciousness and presence of focal neurologic deficits, ataxia, paresis, or paralysis. Cognitive tests are conducted. Blood Stroke and transient ischemic attacks samples are sent to check for evidence of infection and to iden­ tify metabolic, electrolyte, nutritional, and blood gas abnor­ Causes malities. A CXR and urinalysis are performed to look for a A stroke in the perioperative period is devastating and correlates source of infection. An ECG is obtained to look for evidence of with the type of operative procedure performed, age of the MI. CT or MRI, and occasionally a spinal tap, may be helpful patient, and presence of risk factors for cardiovascular disease. in select cases. Strokes are more commonly associated with cardiovascular pro­ Measures to protect the patient and staff may include the cedures. Although older adults with cardiovascular disease are at occasional use of physical restraints, reassurance by speaking to a higher risk for a stroke, younger individuals are not exempt, the patient, and allowing family members to be involved in especially those with an underlying inherited thrombophilia. patient care. Medical therapy includes haloperidol, a neuroleptic Postoperative strokes may be ischemic or hemorrhagic in 33 (0.5 to 2 mg, given IV or IM to achieve a rapid effect and then nature. Ischemic strokes most commonly result from periopera­ PO for maintenance therapy). Benzodiazepines are the drug of tive hypotension or overzealous control of hypertension, or from choice for acute alcohol withdrawal. Other medications, includ­ cardioemboli in patients with atrial fibrillation. Other sources ing haloperidol (to control psychosis), beta blockers (to control of cardioemboli include MI and bacterial endocarditis. An autonomic manifestations), and clonidine (to control hyperten­ embolus arising from DVT and traversing a patent foramen sion) are given in addition to benzodiazepine to patients with ovale (i.e., paradoxical embolization) may be responsible for acute alcohol withdrawal. strokes of unknown cause. Hemorrhagic strokes are less common and are mostly related to therapy with anticoagulants. Factors Seizure disorders related to coagulation disorders, such as chronic abuse of alcohol, acquired immunodeficiency syndrome (AIDS), cocaine use, Causes bleeding diathesis, and preexisting cerebrovascular anomalies, Seizures are caused by paroxysmal electrical discharges from the are associated with an increased risk for hemorrhagic stroke. cerebral cortex and may be primary or secondary. Primary causes include intracranial tumor, hemorrhage, trauma, and idiopathic presentation and management seizure activity. Secondary causes include metabolic derange­ In all cases of stroke, the neurologic changes represent a dramatic ment, sepsis, systemic disease processes, and pharmacologic departure from normal patient function. A focal alteration in agents. Patients at particularly high risk for postoperative seizure motor function, alteration in mental status, aphasia, or occasion­ include those with a previous history of epilepsy and patients ally unresponsiveness may be noted. Hemorrhagic strokes are acutely withdrawing from alcohol or medications or receiving uncommon, and their effect can be more devastating than isch­ other pharmacologic agents, including antidepressants, hypogly­ emic strokes that are transient (occurring for seconds to minutes) cemic agents, and lidocaine. or reversible (occurring for minutes to hours). In truly K2Townsend_Chapter 13_main.indd 43 6/10/2011 12:36:23 PM
    • 13-44  section ii  PerioPerative ManageMent irreversible injury, the impact on the patient’s overall health is refractory case. If the bleeding fails to stop, packing for an immeasurable, and the patient’s ability to function and enjoy a extended period with petroleum jelly–covered strip gauze may good quality of life is severely compromised. be required. Removal of the packing in 1 to 3 days is usually Prevention of a perioperative stroke starts with the identi­ associated with successful treatment of refractory epistaxis, fication of at­risk patients. Patients with hypertension must along with treatment of the underlying condition or reversal receive adequate treatment, and overzealous correction must be of anticoagulation. avoided. Patients with atrial fibrillation benefit from prophylaxis A more serious scenario is posterior nasal septal bleeding, with anticoagulants. Patients with a carotid bruit must be eval­ which on occasion can be life­threatening. If all attempts to uated with noninvasive vascular studies and treated accordingly. stop anterior nasal septal bleeding are unsuccessful, one may Patients undergoing a high­risk surgical procedure (e.g., carotid infer the probability of a posterior nasal hemorrhage, which endarterectomy) may be monitored intraoperatively with tran­ may necessitate placement of a posterior pack of strip gauze scranial Doppler and electroencephalography. Adequate hydra­ covered in petroleum jelly ointment. For particularly refractory tion and monitoring in the perioperative period to avoid cases, a Foley catheter with a 30­mL balloon can be passed hypotension and fluctuations in blood pressure are essential to through the nasal passages and, after the pack is placed, pres­ avoid ischemic strokes. sure can be applied to it by pulling on the Foley catheter. This On recognizing the clinical signs and symptoms of a stroke, type of epistaxis may require concomitant anterior nasal packing the patient must have an IV line placed and be monitored for to be successful. The packs on a difficult hemorrhage such as cardiac arrhythmias. Coagulation parameters are assessed for the this may need to be left in place for 2 to 3 days. For epistaxis presence of a coagulopathy, and blood is sent for culture and that defies all attempts at conservative management, ligation of determination of the sedimentation rate to check for bacteremia the sphenopalatine artery or anterior ethmoidal artery may be and bacterial endocarditis. A diagnostic workup is started imme­ required. diately to distinguish between hemorrhagic and ischemic stroke with a CT scan or MRI of the brain. Further tests depend on acute Hearing loss the clinical scenario, such as echocardiography to assess the heart Abrupt loss of hearing in the postoperative period is an uncom­ for structural disease, carotid duplex scanning to assess patency mon event. An immediate physical examination is performed to of the carotid artery, and cerebral angiography to evaluate for ascertain the degree of hearing loss. Unilateral hearing loss is vascular anomalies. Therapy is dictated by the underling mech­ generally associated with obstruction or edema related to an NG anism of the stroke. A hypertensive hemorrhagic stroke is treated or feeding tube. Bilateral hearing loss is more often neural in by aggressive control of the hypertension, an embolic stroke nature and is usually associated with pharmacologic agents, such (cardiogenic or secondary to inherited thrombophilia) is treated as aminoglycosides and diuretics. Examination with an otoscope by anticoagulation (in the absence of a contraindication) to will often reveal the presence of cerumen impaction or edema prevent recurrence, and a hemorrhagic stroke is treated by rever­ from a middle ear infection. If the otologic examination is com­ sal of the coagulopathy with protamine, if secondary to heparin, pletely normal, neural injury related to the agents just men­ or platelet transfusion, if secondary to antiplatelet therapy. Man­ tioned should be suspected. These drugs need to be discontinued nitol and dexamethasone are given to reduce cerebral swelling. immediately and hearing monitored over the ensuing 2 to 3 days Treatment of any underlying cardiac arrhythmia is imperative to to see whether recovery occurs. For cerumen impaction, use of prevent recurrent embolization. Surgical intervention is indi­ a delicate speculum under direct vision is indicated. If the cated for patients with a localized hematoma or vascular anomaly, hearing loss is associated with edema related to an NG tube, depending on the location and size of the hematoma, status of merely removing the NG tube will result in resolution of the the patient, and accessibility of the aneurysm. Thrombolytic edema. therapy (recombinant tissue plasminogen activator) is effective in restoring cerebral blood flow and minimizing brain injury if nosocomial Sinusitis instituted early after the onset of an embolic event. Otherwise, Nosocomial sinusitis is a recognized complication in the criti­ low­dose aspirin therapy is the standard for acute ischemic cally ill. Left untreated, sinusitis may be complicated by brain infarction and, in patients who continue to have symptoms, abscess formation, postorbital cellulitis, and nosocomial pneu­ antiplatelet agents (e.g., clopidogrel bisulfate, ticlopidine hydro­ monia. Patients at high risk for sinusitis are those receiving chloride) are added. ventilatory support via a nasotracheal tube and those with nasal colonization with gram­negative bacteria. Also at risk are patients ear, noSe, and tHroat complicationS with facial trauma, those with an NG or feeding tube, and patients who have received antibiotic therapy. epistaxis Most nosocomial sinusitis occurs in the second week of Epistaxis may be associated with primary blood dyscrasias hospitalization, and the maxillary sinuses are the most com­ such as leukemia and hemophilia, excessive anticoagulation, monly affected. The classic signs encountered with community­ and hypertension. Epistaxis is divided into two general catego­ acquired sinusitis (e.g., facial pain, malaise, fever, and purulent ries, anterior and posterior. Anterior trauma is often caused by nasal discharge) may not be present because the patient is usually contusion or laceration of the nasal septum or turbinates unconscious and intubated, has other sources of infection, and during insertion of an NG or endotracheal tube. Firm pres­ is receiving analgesics and antipyretics. The diagnosis is often sure applied between the thumb and index finger to the nasal made when CT is performed to look for a source of fever and ala and held for 3 to 5 minutes is generally successful in stop­ the sinuses are included in the cuts. The CT scan generally shows ping most cases of anterior epistaxis. Occasionally, packing thickened mucosa and the presence of an air­fluid level or opaci­K2 with strip gauze for 10 to 15 minutes will aid in a particularly fication of the sinus. Townsend_Chapter 13_main.indd 44 6/10/2011 12:36:23 PM
    • Surgical coMPlicationS  chapter 13  13-45 Once diagnosed or suspected, nasal tubes are removed, Surgeons endorsed by the American Association of Cardiovascular SeCtion ii PerioPerative ManageMent decongestant is administered, and antibiotic therapy targeting and Pulmonary Rehabilitation and the Society for Academic Emer­ the two most common organisms, S. aureus and Pseudomonas gency Medicine. J Am Coll Cardiol 50:e1–e157, 2007. spp., is given. Other organisms that play a major role in noso­ comial infections, such as MRSA and vancomycin­resistant Patients with angina, particularly unstable angina, represent a high-risk Enterococcus and Acinetobacter spp., are also included in the group for surgery. The paper provides practical guidelines for the man- coverage. With such treatment, clinical response occurs in 48 agement of this challenging group of patients. 34 hours and a clinical and radiologic cure occurs in two thirds of patients. Failure of medical therapy leads to surgical drain­ Anderson DJ, Kaye KS, Classen D, et al: Strategies to prevent surgi­ age of the sinus involved. In rare cases, severe intractable cal site infections in acute care hospitals. Infect Control Hosp Epide­ sinusitis may require a drainage procedure via an operative miol 29(Suppl 1):S51–S61, 2008. technique. Surgical site infections (SSIs) remain a serious cause of significant post- parotitis operative morbidity, increased cost, and poor outcomes. This paper Parotitis most commonly occurs in an older man with poor provides a realistic strategy for lowering or preventing SSIs in the acute oral hygiene and poor oral intake, with an associated decrease care hospital setting. in saliva production. The pathophysiology involves obstruction of the salivary ducts or an infection in a diabetic or immuno­ Cooper MS, Stewart PM: Corticosteroid insufficiency in acutely ill compromised patient. The patient is noted to have significant patients. N Engl J Med 348:727–734, 2003. edema and focal tenderness surrounding the parotid gland, which eventually progresses to involve edema of the floor of This paper discusses the topic of functional adrenal insufficiency the mouth. If left undiagnosed and untreated, the parotitis in critically ill patients and outlines the workup and treatment can cause life­threatening sepsis. In the worst case scenario, strategies. the infection can dissect into the mediastinum and cause stridor from partial airway obstruction. Patients with advanced Dronge AS, Perkal MF, Kancir S, et al: Long­term glycemic control parotitis will have dysphagia and some respiratory occlusion. If and postoperative infectious complications. Arch Surg 141:375–380, the diagnosis of parotitis is being entertained, the patient 2006. receives IV, high­dose, broad­spectrum antibiotics with good coverage of Staphylococcus, the most common agent cultured This paper addresses the importance of glycemic control as it relates to from this disease. In the presence of a fluctuant area, incision postoperative infections. plus drainage is indicated, with care taken to avoid the facial nerve. Rarely, advanced disease may even require emergency Eagle KA, Berger PB, Calkins H, et al: ACC/AHA Guideline Update tracheostomy. Most patients with parotitis will have the condi­ for Perioperative Cardiovascular Evaluations for Noncardiac 35 tion arise 4 to 12 days after the initial operation. Because of Surgery—Executive Summary. A report of the American College of the rapid progression of this disease, one must be aware of the Cardiology/American Heart Association Task Force on Practice diagnosis and, when present, institute immediate therapy, Guidelines. (Committee to Update the 1996 Guidelines on Periop­ including occasional emergency surgery for patients with an erative Cardiovascular Evaluation for Noncardiac Surgery). Anesth obvious fluctuant area. Analg 94:1052–1064, 2002. This important report from the ACC and AHA carefully outlines the Selected reFerenceS management of patients with cardiac risk factors who will undergo a Almanaseer Y, Mukherjee D, Kline­Rogers EM, et al: Implementa­ noncardiac operation. tion of the ACC/AHA guidelines for preoperative risk assessment in a general medicine preoperative clinic: Improving efficiency and pre­ Geerts WH, Bergqvist D, Pineo GF, et al: Prevention of venous serving outcomes. Cardiology 103:24–29, 2005. thromboembolism: American College of Chest Physicians Evidence­ Based Clinical Practice Guidelines (8th Edition). Chest 133:381S– This paper describes the clinical predictors of increased cardiovascular 453S, 2008. risk leading to acute cardiac events in surgical patients. Implementation of these predictors may also allow better selection of patients who The ACCP offers evidence-based guidelines for preventing deep vein require more specific preoperative cardiac evaluation and beta blocker thrombosis in postoperative patients. therapy. Heller L, Levin SL, Butler CE: Management of abdominal wound Anderson JL, Adams CD, Antman EM, et al: ACC/AHA 2007 dehiscence using vacuum­assisted closure in patients with compro­ guidelines for the management of patients with unstable angina/non­ mised healing. Am J Surg 191:165–172, 2006. ST­Elevation myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice This paper deals with the concept of integration of vacuum-assisted Guidelines (Writing Committee to Revise the 2002 Guidelines for closure systems in the management of wound dehiscence. the Management of Patients With Unstable Angina/Non­ST­ Elevation Myocardial Infarction) developed in collaboration with the Lin HJ, Spoerke N, Deveney C, et al: Reconstruction of complex American College of Emergency Physicians, the Society for Cardio­ abdominal wall hernias using acellular human dermal matrix: A single vascular Angiography and Interventions, and the Society of Thoracic institution experience. Am J Surg 197:599–603, 2009. K2Townsend_Chapter 13_main.indd 45 6/10/2011 12:36:23 PM
    • 13-46  section ii  PerioPerative ManageMent repair in a compromised surgical field. Arch Surg 144:209–215, The development of a biologic prosthesis that can be placed in a con- 2009. taminated field during hernia repair has provided a relatively new treat- 3. Heller L, Levin SL, Butler CE: Management of abdominal wound ment paradigm for the management of these complex patients. This dehiscence using vacuum­ assisted closure in patients with com­ paper is a retrospective review of a single institute’s experience with one promised healing. Am J Surg 191:165–172, 2006. type of biologic prosthesis. 4. Mangram AJ, Horan TC, Pearson ML, et al: Guideline for preven­ tion of surgical site infection, 1999. Hospital Infection Control Migneco A, Ojetti V, Testa A, et al: Management of thyrotoxic crisis. Practices Advisory Committee. Infect Control Hosp Epidemiol Eur Rev Med Pharmacol Sci 9:69–74, 2005. 20:250–278, 1999. 5. Awad SS, Elhabash SI, Lee L, et al: Increasing incidence of This paper outlines the manifestations and treatment of an uncommon methicillin­resistant Staphylococcus aureus skin and soft­tissue but potentially devastating complication of thyrotoxicosis. infections: Reconsideration of empiric antimicrobial therapy. Am J Surg 194:606–610, 2007. Moore AFK, Hargest R, Martin M, et al: Intra­abdominal hyper­ 6. National Nosocomial Infections Surveillance (NNIS): System tension and the abdominal compartment syndrome. Br J Surg 91: Report, Data Summary from January 1992–June 2001, issued 1102–1110, 2004. August 2001. Am J Infect Control 29:404–421, 2001. 7. Culver DH, Horan TC, Gaynes RP, et al: Surgical wound infec­ This paper is important because it details the pathophysiology of intra- tion rates by wound class, operative procedure, and patient risk abdominal hypertension and abdominal compartment syndrome and index. National Nosocomial Infections Surveillance System. Am attempts to provide guidelines for medical and surgical management of J Med 91:152S–157S, 1991. patients in whom these complications develop. 8. Anderson DJ, Kaye KS, Classen D, et al: Strategies to prevent surgical site infections in acute care hospitals. Infect Control Hosp Perry SL, Ortel TL: Clinical and laboratory evaluation of thrombo­ Epidemiol 29(Suppl 1):S51–S61, 2008. philia. Clin Chest Med 24:153–170, 2003. 9. Buggy DJ, Crossley AW: Thermoregulation, mild perioperative hypothermia and postanaesthetic shivering. Br J Anaesth This review outlines the causes and workup of patients with a hyperco- 84:615–628, 2000. agulable state and provides recommendations for testing this high-risk 10. Rosenberg H, Antognini JF, Muldoon S: Testing for malignant group of patients. hyperthermia. Anesthesiology 96:232–237, 2002. 11. Jawa RS, Kulaylat MN, Baumann H, et al: What is new in cyto­ Sailhamer EA, Carson K, Chang Y, et al: Fulminant Clostridium kine research related to trauma/critical care? J Intensive Care Med difficile colitis: Patterns of care and predictors of mortality. Arch Surg 21:63–85, 2006. 144:433–439, 2009. 12. Bukhary ZA: Candiduria: A review of clinical significance and management. Saudi J Kidney Dis Transpl 19:350–360, This recent description of a more virulent, resistant, and aggressive form 2008. of C. dificile makes this paper highly relevant. 13. Centers for Medicare and Medicaid Services (CMS), HHS: Medi­ care program; changes to the hospital inpatient prospective Simon TL, Alverson DC, AuBuchon J, et al: Practice parameter for payment systems and fiscal year 2008 rates. Fed Regist 72: the use of red blood cell transfusions: Developed by the Red Blood 47129–48175, 2007. Cell Administration Practice Guideline Development Task Force of 14. Edwards JR, Peterson KD, Andrus ML, et al: National Healthcare the College of American Pathologists. Arch Pathol Lab Med 122: Safety Network (NHSN) Report, data summary for 2006, issued 130–138, 1998. June 2007. Am J Infect Control 35:290–301, 2007. 15. Ksycki MF, Namias N: Nosocomial urinary tract infection. Surg This paper is the result of a consensus conference held by the College Clin North Am 89:475–481, ix–x, 2009. of American Pathologists regarding blood transfusion and its usefulness 16. American Thoracic Society; Infectious Diseases Society of America: for the treatment of surgical patients. Guidelines for the management of adults with hospital­acquired, ventilator­associated, and healthcare­associated pneumonia. Am J Slim K, Vicaut E, Panis Y, et al: Meta­analysis of randomized clinical Respir Crit Care Med 171:388–416, 2005. trials of colorectal surgery with or without mechanical bowel prepara­ 17. Practice guidelines for preoperative fasting and the use of pharma­ tion. Br J Surg 91:1125–1130, 2004. cologic agents to reduce the risk of pulmonary aspiration: applica­ tion to healthy patients undergoing elective procedures: A report This paper sheds light on the usefulness of mechanical bowel prepara- by the American Society of Anesthesiologist Task Force on Preop­ tion before colorectal surgery. 36 erative Fasting. Anesthesiology 90:896–905, 1999. 18. Heit JA, Silverstein MD, Mohr DN, et al: Risk factors for deep vein thrombosis and pulmonary embolism: a population­based reFerenceS case­control study. Arch Intern Med 160:809–815, 2000. 1. Douketis JD, Berger PB, Dunn AS, et al: The perioperative man­ 19. Goldhaber SZ: Echocardiography in the management of pulmo­ agement of antithrombotic therapy: American College of Chest nary embolism. Ann Intern Med 136:691–700, 2002. Physicians Evidence­Based Clinical Practice Guidelines (8th 20. Geerts WH, Bergqvist D, Pineo GF, et al: Prevention of venous Edition). Chest 133:299S–339S, 2008. thromboembolism: American College of Chest Physicians 2. Diaz JJ, Jr, Conquest AM, Ferzoco SJ, et al: Multi­institutional Evidence­Based Clinical Practice Guidelines (8th Edition). ChestK2 experience using human acellular dermal matrix for ventral hernia 133:381S–453S, 2008. Townsend_Chapter 13_main.indd 46 6/10/2011 12:36:23 PM
    • Surgical coMPlicationS  chapter 13  13-47 21. Eagle KA, Berger PB, Calkins H, et al: ACC/AHA Guideline and problem­oriented, New York, 2001, Zuckschwerdt, pp SeCtion ii PerioPerative ManageMent Update for Perioperative Cardiovascular Evaluation for Noncar­ 102–113. diac Surgery—Executive Summary. A report of the American 34. Kirkpatrick AW, Balogh Z, Ball CG, et al: The secondary abdom­ College of Cardiology/American Heart Association Task Force on inal compartment syndrome: Iatrogenic or unavoidable? J Am Practice Guidelines (Committee to Update the 1996 Guidelines Coll Surg 202:668–679, 2006. on Perioperative Cardiovascular Evaluation for Noncardiac 35. Simon TL, Alverson DC, AuBuchon J, et al: Practice parameter Surgery). Anesth Analg 94:1052–1064, 2002. for the use of red blood cell transfusions: Developed by the Red 22. Anderson JL, Adams CD, Antman EM, et al: ACC/AHA 2007 Blood Cell Administration Practice Guideline Development Task guidelines for the management of patients with unstable angina/ Force of the College of American Pathologists. Arch Pathol Lab non­ST­Elevation myocardial infarction: A report of the American Med 122:130–138, 1998. College of Cardiology/American Heart Association Task Force 36. Seder CW, Villalba MR, Jr, Robbins J, et al: Early colectomy may on Practice Guidelines (Writing Committee to Revise the 2002 be associated with improved survival in fulminant Clostridium Guidelines for the Management of Patients With Unstable difficile colitis: An 8­year experience. Am J Surg 197:302–307, Angina/Non­ST­Elevation Myocardial Infarction) developed in 2009. collaboration with the American College of Emergency Physi­ 37. Sailhamer EA, Carson K, Chang Y, et al: Fulminant Clostridium cians, the Society for Cardiovascular Angiography and Interven­ difficile colitis: Patterns of care and predictors of mortality. Arch tions, and the Society of Thoracic Surgeons endorsed by the Surg 144:433–439; discussion 439–440, 2009. American Association of Cardiovascular and Pulmonary Reha­ 38. Pepin J, Vo TT, Boutros M, et al: Risk factors for mortality fol­ bilitation and the Society for Academic Emergency Medicine. lowing emergency colectomy for fulminant Clostridium difficile J Am Coll Cardiol 50:e1–e157, 2007. infection. Dis Colon Rectum 52:400–405, 2009. 23. Almanaseer Y, Mukherjee D, Kline­Rogers EM, et al: Implemen­ 39. Slim K, Vicaut E, Panis Y, et al: Meta­analysis of randomized tation of the ACC/AHA guidelines for preoperative cardiac risk clinical trials of colorectal surgery with or without mechanical assessment in a general medicine preoperative clinic: improving bowel preparation. Br J Surg 91:1125–1130, 2004. efficiency and preserving outcomes. Cardiology 103:24–29, 2005. 40. Uzunkoy A, Akinci OF, Coskun A, et al: Effects of antiadhesive 24. Polanczyk CA, Goldman L, Marcantonio ER, et al: Supraven­ agents on the healing of intestinal anastomosis. Dis Colon Rectum tricular arrhythmia in patients having noncardiac surgery: clinical 43:370–375, 2000. correlates and effect on length of stay. Ann Intern Med 129: 41. August DA, Serrano D, Poplin E: “Spontaneous,” delayed colon 279–285, 1998. and rectal anastomotic complications associated with bevacizumab 25. Hunt SA, Baker DW, Chin MH, et al: ACC/AHA guidelines for therapy. J Surg Oncol 97:180–185, 2008. the evaluation and management of chronic heart failure in the 42. Branagan G, Finnis D: Prognosis after anastomotic leakage in adult: Executive summary. J Heart Lung Transplant 21:189–203, colorectal surgery. Dis Colon Rectum 48:1021–1026, 2005. 2002. 43. Stojadinovic A, Brooks A, Hoos A, et al: An evidence­based 26. Bonet S, Agusti A, Arnau JM, et al: Beta­adrenergic blocking approach to the surgical management of resectable pancreatic agents in heart failure: benefits of vasodilating and non­vasodilating adenocarcinoma. J Am Coll Surg 196:954–964, 2003. agents according to patients’ characteristics: A meta­analysis of 44. Orgill DP, Manders EK, Sumpio BE, et al: The mechanisms of clinical trials. Arch Intern Med 160:621–627, 2000. action of vacuum­assisted closure: More to learn. Surgery 146: 27. Moore AF, Hargest R, Martin M, et al: Intra­abdominal hyper­ 40–51, 2009. tension and the abdominal compartment syndrome. Br J Surg 45. Teubner A, Morrison K, Ravishankar HR, et al: Fistuloclysis can 91:1102–1110, 2004. successfully replace parenteral feeding in the nutritional support 28. Karsou SA, Jaber BL, Pereira BJ: Impact of intermittent hemodi­ of patients with enterocutaneous fistula. Br J Surg 91:625–631, alysis variables on clinical outcomes in acute renal failure. Am J 2004. Kidney Dis 35:980–991, 2000. 46. Wainstein DE, Fernandez E, Gonzalez D, et al: Treatment of 29. Cooper MS, Stewart PM: Corticosteroid insufficiency in acutely high­output enterocutaneous fistulas with a vacuum­compaction ill patients. N Engl J Med 348:727–734, 2003. device. A ten­year experience. World J Surg 32:430–435, 2008. 30. Migneco A, Ojetti V, Testa A, et al: Management of thyrotoxic 47. Wind J, van Koperen PJ, Slors JF, et al: Single­stage closure of crisis. Eur Rev Med Pharmacol Sci 9:69–74, 2005. enterocutaneous fistula and stomas in the presence of large 31. Postoperative Ileus Management Council: Proceedings of Con­ abdominal wall defects using the components separation tech­ sensus Panel to Define Postoperative Ileus. Colorectal surgery nique. Am J Surg 197:24–29, 2009. consensus report, Atlanta, 2006, Thomson American Health 48. 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    • AUTHOR QUERY FORM Dear Author During the preparation of your manuscript for publication, the questions listed below have arisen. Please attend to these matters and return this form with your proof. Many thanks for your assistance. Query Query Remarks References 1 AU: Pls. check dosage & initial it 2 AU: ??? laxity? 3 AU: still current? 4 AU: this is now the name of this org. 5 AU: still true? 6 AU: OK as edited, as meant? 7 AU: OK as edited? 8 AU: add ref.? 9 AU: OK as edited? 10 AU: ref. no.? 11 AU: pls. define. 12 AU: Pls. check dosage & initial it 13 AU: Pls. check dosages & initial 14 AU: do you mean CAD? 15 AU: Pls. check dosage & initial it 16 AU: both OK as edited? Both 50 mOsm/liter? And both “>”? 17 AU: Pls. check dosages & initial 18 AU: haven’t there been concerns raised about its use? 19 AU: Pls. check dosage & initial it 20 AU: Pls. check dosage & initial it 21 AU: Pls. check dosage & initial it 22 AU: OK as edited? 23 AU: of what? 24 AU: of crystalloid? 25 AU: OK, as meant?Townsend_Chapter 13_main.indd 1 6/10/2011 12:36:23 PM
    • Query Query Remarks References 26 AU: update this 8-year-old figure? 27 AU: Pls. check dosages & initial 28 AU: please define. 29 AU: please give a figure, with unit; this is too vague. 30 AU: Pls. check cross reference; section title OK? 31 AU: ref. nos.? 32 AU: “60” was deleted here; OK? 33 AU: Pls. check dosage & initial it 34 AU: meaning unclear; plese check. 35 AU: which operation? 36 AU: this has been updated; use this ref. instead?Anesthesiology 114:495- 511, 2011. 38 AU: Pls. check dosages & initial 39 AU: Pls. check dosage & initial itTownsend_Chapter 13_main.indd 2 6/10/2011 12:36:23 PM