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  • 1. Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) vii–viii Preface An Atlas of Head and Neck Images, Part I Richard H. Haug, DDS Charles Lee, MD Guest Editors It has now been more than a century since the discovery of roentgen rays, and five decades since their routine incorporation into clinical practice. The past three decades have observed vast improvements in plain radiographic quality, the incorporation of computers into the imag- ing system, and the development of completely new imaging technology such as magnetic res- onance, ultrasonography, and digitalization. The use of imaging in surgical practice has become almost as much a part of the preoperative assessment as the history and physical exami- nation itself. With that in mind, it is important for the surgeon to be familiar with all imaging modalities that may improve patient assessment, and also to have a working knowledge of which images and what image hallmarks are associated with common maladies, conditions, and pathologic entities. As imaging is visual in nature, the atlas format is particularly effective in conveying such information to the clinician. An Atlas of Head and Neck Images, Parts I and II are provided as an overview of technology, and as simple guides for interpreting images of common head and neck maladies, conditions, and pathologic entities. While this atlas series is primarily directed toward oral and maxillofacial surgeons, plastic and reconstructive surgeons, and otorhinolaryngologist–head and neck sur- geons, it also will be a useful tool for radiologists, neurosurgeons, general surgeons, and the medical and dental communities at large. The first two articles in the series deal with head and neck trauma, their assessment and management. The third focuses on chest radiography in the perioperative period. The fourth article approaches the cutting edge of imaging technol- ogy with a presentation of ultrasonography of the maxillofacial region. Part II in this series be- gins with an exhaustive compendium of panoramic images. The sixth article focuses on computed tomography of the head and neck. The final articles include nuclear imaging and magnetic resonance imaging as they are applied to the head, neck and face. While this atlas series does provide an overview of signs, symptoms, etiology and pathophysi- ology of a vast array of head and neck problems, it is not meant to be a definitive treatise on 1061-3315/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 6 1 - 3 3 1 5 ( 0 2 ) 0 0 0 0 4 - 5
  • 2. viii R.H. Haug, C. Lee / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) vii–viii injury and pathology. It is intended merely to act as a guide to quickly point the practicing surgeon in the right direction when he or she encounters specific conditions and problems in head and neck surgery. It is highly visual in design, so as to act as a quick and ready reference. Richard H. Haug, DDS Division of Oral & Maxillofacial Surgery College of Dentistry Chandler Medical Center University of Kentucky 800 Rose Street, Lexington KY 40536-0297, USA E-mail address: rhhaug2@pop.uky.edu Charles Lee, MD Division of Diagnostic Radiology College of Medicine Chandler Medical Center University of Kentucky 800 Rose Street, Lexington KY 40536-0297, USA E-mail address: clee0@pop.uky.edu
  • 3. Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 Computed tomography of head injury Richard H. Haug, DDSa,*, Thomas Pittman, MDb a Division of Oral and Maxillofacial Surgery, College of Dentistry, University of Kentucky, 800 Rose Street, Room D-508, Lexington, KY 40536-0297, USA b Department of Neurosurgery, College of Medicine, University of Kentucky, 800 Rose Street, Lexington, KY 40536-0298, USA Closed head injury (CHI) is defined by Davidoff et al [1] as a ‘‘documented loss of conscious- ness and/or post-traumatic amnesia’’ in patients with nonpenetrating injury [2–4]. Lee et al [2], while correlating CHI and various facial fractures, identified 10 separate diagnoses using com- puted tomography (CT), including the following: • Transtentorial herniation • Epidural hematoma • Subdural hematoma • Intracerebral hematoma • Hemorrhagic contusion • Intraventricular hemorrhage • Subarachnoid hemorrhage • Pneumocephalus • Edema • Midline shift Recent investigations identified a high frequency of neurologic injury concomitant to facial trauma (2.0%–17.5%) [3–9]. The authors found that CHI occurred with facial fractures in 17.5% of cases, with 10% of patients suffering severe cranial injury. In addition, there was a direct relationship between some forms of facial trauma and death caused by neurologic injury [10]. It is therefore important that craniomaxillofacial surgeons (oral and maxillofacial sur- geons, otolaryngologists, head and neck surgeons, neurologic surgeons, and plastic and recon- structive surgeons) be familiar with the diagnosis and management of patients with CHI. This includes having a working knowledge of the signs and symptoms that are manifested by these patients, and familiarity with the classic imaging appearance of associated lesions. Moreover, craniomaxillofacial surgeons must have a close working relationship with their neurosurgical and radiologic colleagues to best care for this group of patients. This article provides craniomaxillofacial surgeons and radiologists with a simple guide to the various intracranial lesions found in patients with facial fractures. It is meant to be highly visual, with representative images of the common lesions seen with head injury. Although the article provides a brief review of the signs, symptoms, and management of patients with CHI, it is not meant to be a definitive treatise on head injury but a guide to point surgeons quickly in the right direction when they encounter these problems. Since 1972, CT has been the preferred means for the imaging of patients with head injury. As technology has improved, scanning times for each slice have diminished from a few minutes to, in some cases, as little as a second. Although the inability to demonstrate blood-brain barrier disruption was at one time a limitation of CT, the introduction of injectable contrast media * Corresponding author. E-mail address: rhhaug2@pop.uky.edu (R.H. Haug). 1061-3315/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 6 1 - 3 3 1 5 ( 0 2 ) 0 0 0 0 5 - 7
  • 4. 150 R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 has, in part, overcome this problem. The following images and associated descriptions represent common traumatic intracranial lesions that may be diagnosed with CT. Transtentorial herniation Frequency/incidence The incidence of CHI among patients with facial trauma has been reported to be 17.5% [8]. In a review of CHI and facial fractures by Lee et al [2], transtentorial herniation was found in 4.3% of patients with a CHI associated with facial injuries. Signs and symptoms Patients with transtentorial herniation often present with a decreased level of consciousness in combination with ipsilateral pupillary dilatation with loss of light response. Hemiparesis or decerebrate rigidity may follow. Ultimately, hypertension, bradypnea, and bradycardia can occur. Etiology/pathophysiology In transtentorial herniation, the mesial part of the temporal lobe is pushed over the edge of the tentorium, where it obliterates the ambient cistern and compresses the midbrain. The third nerve and the posterior cerebral artery run through the ambient cistern and are often affected. Herniation is usually the result of a supratentorial mass. Subdural hematomas, epidural hematomas, and contusions are the most common causes of herniation in patients with head trauma. Image of choice for diagnosis CT without contrast is the preferred imaging method. CT is performed with 3.0-mm slice thicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and end- ing at the vertex of the skull. Soft tissue windows are centered at 40 to 80 Hounsfield Units (H). Bone windows are centered at 500 to 2500 H. Image hallmark Transtentorial herniation may be difficult to detect with CT imaging. Almost invariably, pa- tients who have herniated will have other radiographic evidence of trauma to the cranium and its contents. Unilateral narrowing of the subarachnoid space around the brain stem with evi- dence of brain stem distortion in the presence of a supratentorial mass suggests the diagnosis. Obliteration of the suprasellar cistern is a reliable sign, although suprasellar mass lesions may have a similar appearance (Fig. 1). Management Transtentorial herniation is ideally managed before it occurs. Operative decompression is most likely to be successful before significant neurologic deterioration has developed. Epidural hematoma Frequency/incidence A CHI occurs in 17.5% of patients with facial fractures [6]. An epidural hematoma can be found in 6.7% of this group [2].
  • 5. R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 151 Fig. 1. Transtentorial herniation with cisternal obliteration. Signs and symptoms Epidural hematomas most frequently occur in the temporal area and are often associated with external evidence of trauma and/or a skull fracture. They are relatively less common in chil- dren and in elderly individuals presumably because, in those age groups, the dura is more adherent to the skull. Reports describe a lucid interval, a period of minimal neurologic abnor- mality immediately after the injury, followed by a progressive decline as characteristic of these lesions. Unfortunately, a lucid interval does not occur in the majority of patients with epidural hematomas and can be seen in patients with other types of intracranial pathology. Etiology/pathophysiology Epidural hematomas are generally the result of damage to the anterior or posterior branches of the middle meningeal arteries. They are commonly caused by cranial fractures that tear the artery or vein, and when displaced, strip the dura. As the collection of blood enlarges, more dura is stripped. Bleeding from middle meningeal veins, or venous sinus, or from the bone edges along a depressed fracture are less common causes of an epidural hematoma and are related to venous rather than arterial hemorrhage. Image of choice for diagnosis CT without contrast is the preferred imaging method. CT is performed with 3.0-mm slice thicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and
  • 6. 152 R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 ending at the vertex of the skull. Soft tissue windows are obtained at 40 to 80 H. Bone windows are obtained at 500 to 2500 H. Image hallmarks An epidural hematoma is a biconvex (football shaped) collection of blood between the skull and dura (Fig. 2). It is hyperdense when acute and, unlike a subdural hematoma which may be composed of blood mixed with cerebrospinal fluid (CSF), is uniformly dense. Management Small lesions that occur in the frontal or parietal areas can be observed. Most temporal hema- tomas, and essentially all large epidural hematomas, are removed. Depending on their size and Fig. 2. Epidural hematoma with classic lens or football-shaped high-density extra-axial collection. There is cortical buckling of both gray and white matter which is characteristic of epidural hematoma.
  • 7. R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 153 location, this can be accomplished through a burr hole, a craniectomy, or a craniotomy. A bleeding vessel can often, but not always, be identified. A postsurgical CT scan should be ob- tained to verify decompression. Mortality is dependent on the neurologic condition of the pa- tient at the time of decompression; the mortality rate is less than 5% in patients who are awake at the time of operation but can be markedly higher in patients who are lethargic or comatose. Subdural hematoma Frequency/incidence Subdural hematomas occur in 19% of patients who have a CHI associated with facial fractures [3]. Signs and symptoms Subdural hematomas are seen most frequently in patients who have been in a motor vehicle accident or sustained a similar high-energy impact. Most patients with acute subdural hemato- mas have a decreased level of consciousness and impaired motor function. Asymmetry of a pa- tient’s neurologic exam and a worsening neurologic status should raise suspicion of a subdural hematoma or some other compressive lesion. Etiology/pathophysiology An acute subdural hematoma is most often caused by bleeding from a lacerated area of brain or from torn emissary vessels. The blood spreads widely in the subdural space because there are no significant obstructions to flow. This accounts for the characteristic crescent-shaped appear- ance of these lesions. Image of choice for diagnosis CT without contrast is the preferred imaging method. CT is performed with 3.0-mm slice thicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and end- ing at the vertex of the skull. Soft tissue windows are obtained at 40 to 80 H. Bone windows are obtained at 500 to 2500 H. Image hallmarks Using CT, a subdural hematoma is seen as a hyperdense crescent-shaped collection that lies beneath the dura and outside the brain (Fig. 3). Compression of the brain with midline displace- ment is a common finding. Because of clot degradation and fluid absorption, density changes with time. Acute lesions tend to be hyperdense, subacute isodense, and chronic subdural hema- tomas hypodense. Management Most large subdural hematomas should be removed. This is generally done through a large cra- niotomy, which offers the most flexibility in a setting in which large areas of the brain may be in- jured. The clot is removed by gentle irrigation, suction, and traction. The source of the bleeding, if it can be identified, should be controlled. Because subdural hematomas are often seen in patients with severe brain injury, the prognosis is poor for both survival and neurologic recovery.
  • 8. 154 R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 Fig. 3. A thin left-sided subdural hematoma extending from the frontal to the parietal side. The inward displacement of the cortex is seen well. There is also transfalcine herniation with the left side of the brain under the falx and shifting into the right half of the cranium. The left lateral ventricle is completely compressed by the subdural hematoma. Intracerebral hematoma Frequency/incidence Intracerebral hematomas occur in 15.2% of patients with a CHI associated with facial fractures [2]. Signs and symptoms Symptoms caused by an intracerebral hematoma reflect its size and location. Focal deficits can occur as can nonspecific signs and symptoms of increased intracranial pressure (headache, nausea, vomiting, and confusion). Large hematomas can cause herniation. Etiology/pathophysiology Intracerebral hematomas may occur as the result of isolated trauma to the head or in association with other intracranial injuries. Isolated hematomas are generally the result of a
  • 9. R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 155 low-energy impact over a small surface area. The most common locations are the inferior frontal and temporal lobes. In these locations, the brain abuts bony ridges and the irregular surface frontal fossa. Image of choice for diagnosis CT without contrast is the preferred imaging method. CT is performed with 3.0-mm slice thicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and end- ing at the vertex of the skull. Soft tissue windows are obtained at 40 to 80 H. Bone windows are obtained at 500 to 2500 H. Image hallmarks Intracerebral hematomas appear on a CT scan as dense collections of clot that are well cir- cumscribed, homogeneous, and ovoid (Fig. 4). They are often surrounded by areas of low den- sity caused by edema. The majority of the hematomas occur in the frontal or temporal lobes. After several weeks, a hematoma may appear isodense, or of similar density to the surrounding brain tissue. At that point, they may demonstrate peripheral, or ring, enhancement. Without knowledge of prior bleeding, the CT scan at this point may be misinterpreted as tumor. Management Small hematomas (<2.0 cm) may be managed nonoperatively. Large lesions can be removed if they cause mass effect and are in a surgically accessible location. If the hematoma has been present for several days, needle aspiration may be attempted, but craniotomy is generally re- quired for evacuation of an acute clot. Hemorrhagic contusion Frequency/incidence Hemorrhagic contusions are found in 36.7% of patients with a CHI associated with facial fractures [2]. Signs and symptoms The symptoms caused by an intracerebral contusion depend on its size and location. Small contusions may be asymptomatic whereas large lesions may give rise to focal deficits or symp- toms associated with increased intracranial pressure or herniation. Etiology/pathophysiology Hemorrhagic contusion is usually caused by a sudden deceleration but may also occur as the result of an isolated trauma to the head or in association with other intracranial injuries. Iso- lated contusions are generally the result of a low-energy impact over a small surface area. The most common locations are the inferior frontal and temporal lobes. Image of choice for diagnosis CT without contrast is the preferred imaging method. CT is performed with 3.0-mm slice thicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and
  • 10. 156 R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 Fig. 4. Intracerebral hematoma in the left frontal region (high density) with associated surrounding edema. There is mass effect with shift of the midline structures to the right side. The hematoma appears to be fragmented and thus may also be referred to as adiffuse axonal injury. ending at the vertex of the skull. Soft tissue windows are obtained at 40 to 80 H. Bone windows are obtained at 500 to 2500 H. Image hallmarks Cerebral contusions are seen as inhomogeneous regions of mixed high and low density that result from edema and/or tissue necrosis admixed with blood (Fig. 5). Contusions may be single or multiple. They often have poorly defined margins. They are frequently found at the site of injury (coup) or opposite it (contracoup). Frontal, temporal tip, and occipital lesions are most common. Management Small contusions (<2.0 cm) may be managed nonoperatively and usually resolve over a pe- riod of weeks. Large lesions that are causing mass effect may be removed. Generally, this requires a craniotomy.
  • 11. R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 157 Fig. 5. Multiple foci of hemorrhage in the bilateral frontal regions and some subarachnoid blood. This can be referred to as diffuse axonal injury or hemorrhagic contusion. Intraventricular hemorrhage Frequency/incidence Intraventricular hemorrhage occurs in 7.6% of patients with a CHI associated with facial fractures [3]. Signs and symptoms The most frequent complication of intraventricular hemorrhage is obstructive hydrocepha- lus. Patients develop increased intracranial pressure with a declining level of consciousness and, ultimately, pupillary and motor abnormalities. If recognized early, the hydrocephalus usu- ally responds well to ventricular drainage. Etiology/pathophysiology Traumatic intraventricular hemorrhage can result from periventricular parenchymal or vas- cular injury and/or be a manifestation of subarachnoid hemorrhage. The subarachnoid hemor- rhage may enter the ventricular system either through the choroidal fissures in the temporal lobes, or via the intravenous tube through the lateral foramen of Luschka.
  • 12. 158 R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 Image of choice for diagnosis CT without contrast is the preferred imaging method. CT is performed with 3.0-mm slice thicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and end- ing at the vertex of the skull. Soft tissue windows are obtained at 40 to 80 H. Bone windows are obtained at 500 to 2500 H. Image hallmarks Blood within the ventricles appears hyperdense in relation to the CSF (Fig. 6). The blood can be found within or fill any part of the ventricular system. Management Ventricular drainage is required for patients who develop hydrocephalus from intraventric- ular hemorrhage. Unfortunately, the clot can clog the drain and make reliable CSF drainage difficult. There is rarely a need for operative intervention. Localized thrombolytics have been used to treat intraventricular hemorrhage but the indications are not well defined. Fig. 6. A moderate amount of intraventricular hemorrhage in the bilateral lateral ventricles.
  • 13. R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 159 Subarachnoid hemorrhage Frequency/incidence Subarachnoid hemorrhage occurs in 7.6% of patients with a CHI associated with facial fractures [2]. Signs and symptoms Subarachnoid hemorrhage likely occurs in most patients with significant head injuries. It can be difficult to recognize because small amounts of blood are poorly seen with currently available imaging techniques. The symptoms are difficult to isolate, but subarachnoid hemorrhage likely contributes to the development of chemical meningitis (neck stiffness, photophobia, elevated temperature) and post-traumatic vasospasm. Etiology/pathophysiology Either parenchymal contusions or vascular injuries can cause subarachnoid hemorrhage. Image of choice for diagnosis CT without contrast is the preferred imaging method. CT is performed with 3.0-mm slice thicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and end- ing at the vertex of the skull. Soft tissue windows are obtained at 40 to 80 H. Bone windows are obtained at 500 to 2500 H. Image hallmarks CT scan will identify bleeding into the subarachnoid space (Fig. 7). Subarachnoid hemor- rhage may appear as linear regions of high density in the basal cisterns, sylvan fissures, vertex sulci, and interhemispheric fissure. It is frequently associated with other forms of intracranial injury. Most traumatic subarachnoid hemorrhages tend to be focal and overlie the convexities. Subarachnoid hemorrhage in the basilar cisterns, especially the suprasellar cistern, is more con- sistent with ruptured aneurysm. If this pattern is seen in association with a motor vehicle acci- dent, the rupturing of the aneurysm may be the direct cause of the accident. Management The treatment of patients with traumatic subarachnoid hemorrhage is directed at the associ- ated injuries. No specific therapy is required. Pneumocephalus Frequency/incidence Pneumocephalus occurs in 14.8% of patients with a CHI associated with facial fractures [2]. Signs and symptoms The presence of air within the cranium does not produce unique signs or symptoms. Pneumo- cephalus is most often found with open cranial, temporal bone, or maxillofacial fractures. Etiology/pathophysiology Pneumocephalus usually occurs from some form of penetrating or open injury. Examples in- clude open cranial fractures, posterior table frontal sinus fractures, or maxillofacial fractures
  • 14. 160 R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 Fig. 7. Traumatic subarachnoid hemorrhage with contrast media noted in the subarachnoid space. This is the CT of a patient with a ruptured aneurysm. that interrupt the cribiform plate of the ethmoid bone. In unusual circumstances, nonpenetrat- ing closed injuries may displace the cribiform plate or posterior table of the frontal sinus and result in intracranial air. Image of choice for diagnosis CT without contrast is the preferred imaging method. CT is performed with 3.0-mm slice thicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and end- ing at the vertex of the skull. Soft tissue windows are obtained at 40 to 80 H. Bone windows are obtained at 500 to 2500 H. Image hallmarks The CT will identify air (ÿ1000 H) within the intracranial space as black areas usually mixed in with the CSF or pooling within the ventricle (Fig. 8). No matter what the window settings are, air will always appear black. Management Pneumocephalus usually resolves without surgical intervention. If pneumocephalus is associ- ated with a craniofacial fracture, reduction of the fracture will generally seal the air leak. Anti- biotic therapy directed toward cutaneous and sinus contaminants should be considered.
  • 15. R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 161 Fig. 8. Multiple areas of very dark signal centered in the suprasellar cistern and also into the bilateral sylvian fissures and ambient cistern. These are collections of air within the subarachnoid spaces related to facial fractures. Note the fracture of the left lamina papyrcea with sinus air escaping into the left orbital fat. Edema Frequency/incidence Cerebral edema occurs in 17.1% of patients with a CHI associated with facial fractures [2]. Signs and symptoms Cerebral edema can cause a variety of symptoms depending on the location and extent of the lesion. Localized edema is often associated with a contusion or hematoma. Diffuse edema can occur with widespread injury, hypoxia/hypotension, or occasionally and more commonly in children, from hyperemia. If the edema occurs in an arterial vascular territory involving both gray and white matter, then the possibility of carotid dissection with ensuing infarct should be considered in a traumatic setting. Etiology/pathophysiology Cerebral edema is defined as an increase in water content within the brain parenchyma. Edema is a common manifestation of head trauma, and can be likened to bruising of the brain. Multiple mechanisms contribute to edema formation, including increased capillary permeability, accumu- lation of toxins, failure of cellular metabolism, hypoxia, and decreased cerebral blood flow.
  • 16. 162 R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 Image of choice for diagnosis CT without contrast is the preferred imaging method. CT is performed with 3.0-mm slice thicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and end- ing at the vertex of the skull. Soft tissue windows are obtained at 40 to 80 H. Bone windows are obtained at 500 to 2500 H. Image hallmarks Cerebral edema appears by CT as a zone of low density (Fig. 9). Mass effect may be noted with associated compression, distortion, and displacement of the ventricles or parenchymal structures. With diffuse edema, there may be no normal brain for density comparison but the edema can be recognized by ventricular compression and/or loss of cisternal definition, or mid- line shift. Management The management of cerebral edema depends on the clinical setting. Intracranial pressure monitoring and treatment of increased intracranial pressure may be required. Surgery is rarely helpful. Fig. 9. A zone of low density and distortion of the ventricles.
  • 17. R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 163 Transfalcine herniation/midline shift Frequency/incidence Midline shift occurs in 19.5% of patients with a CHI associated with facial fractures [3]. Signs and symptoms The signs of midline shift reflect the area that has been injured. As the problem progresses, non- specific signs of intracranial hypertension may develop and, ultimately, herniation may occur. Etiology/pathophysiology Midline shift can be caused by an intracranial mass or a localized area of injury. If untreated, it may progress to transfalcine herniation with displacement of structures related to one hemi- sphere into the contralateral hemisphere under the midline rigid falx, hence the term transfalcine herniation. Image of choice for diagnosis CT without contrast is the preferred imaging method. CT is performed with 3.0-mm slice thicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and end- ing at the vertex of the skull. Soft tissue windows are obtained at 40 to 80 H. Bone windows are obtained at 500 to 2500 H. Image hallmarks CT scan demonstrates displacement of the midline structures, such as the wall between the two lateral ventricles, the III ventricle, or pineal gland (Fig. 10). Management Management of patients with a midline shift varies depending on the type of lesion (extra- axial, intra-axial, or mixed), the location of the lesion (bilateral or unilateral), and the clinical setting. Large clots and contusions causing a midline shift are often removed. In situations in which no operable lesions are present, management might include intracranial pressure monitor- ing, pharmacologic treatment of increased intracranial pressure, and serial CT scans. Cranial fracture Frequency/incidence The incidence of cranial fractures coincident with facial trauma has been reported to be 4.4% [7]. Signs and symptoms A patient with a cranial fracture will have sustained some form of trauma sufficient to over- come the impact-absorbing capacity of the soft tissues of the scalp or facial bones. These patients will nearly always have a facial fracture or laceration, hematoma, contusion, or abrasion of the scalp, although such evidence of external trauma occasionally can be subtle.
  • 18. 164 R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 Fig. 10. A large right-sided subdural hematoma with mass effect and shift of the midline structures to the left side. Because portions of the right hemisphere have shifted under the falx to the left side, this is consistent with transfalcine herniation. Etiology/pathophysiology An impact of a magnitude sufficient to deform the cranium beyond its elastic limits causes a cranial fracture. These fractures may be classified as linear, stellate, or depressed. A depressed fracture is one in which the outer table of one or more segments is depressed below the inner table of the surrounding skull. Image of choice for diagnosis CT without contrast is the preferred imaging method. CT is performed with 3.0-mm slice thicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and end- ing at the vertex of the skull. Soft tissue windows are obtained at 40 to 80 H. Bone windows are obtained at 500 to 2500 H. Image hallmarks Cranial fractures will appear as linear or stellate areas of diminished relative radiodensity or attenuation adjacent to normal bone on routine skull radiographs (Fig. 11). Depressed and in- driven fragments of bone can easily be seen on skull X rays and CT.
  • 19. R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 165 Fig. 11. Cranial fractures are denoted by displacement of the outer table within the inner table. Management The management of skull fractures varies depending on the following: (1) the presence or ab- sence of concomitant intracranial injury, (2) the amount that the bone fragments are displaced and whether any fragments have torn the dura. If the skull fracture is open, cutaneous wounds should be repaired, depressed fractures reduced, and consideration given to antibiotic therapy. Nondisplaced fractures may be managed with observation, as long as associated intracranial in- jury is absent. Depressed skull fractures in cosmetically important areas and those associated with significant compression of the underlying brain are often elevated. References [1] Davidoff G, Jakubowski M, Thomas D, et al. The spectrum of closed-head injuries in facial trauma victims: incidence and impact. Ann Emerg Med 1988;17:6–9. [2] Lee KF, Wagner LK, Lee YE, et al. The impact absorbing effects of facial fractures in closed-head injuries: an analysis of 210 patients. J Neurosurg 1987;66:542–7. [3] Becker DP, Gade GR, Young HF, et al. Diagnosis and treatment of head injury in adults. In: Youmans JR, editor. Neurological surgery: a comprehensive reference guide to the diagnosis and management of neurosurgical problems. Philadelphia: WB Saunders; 1990. p. 2017–48. [4] Becker DP, Gudeman SK. Textbook of head injury. Philadelphia: WB Saunders; 1989. [5] Conforti PJ, Haug RH, Likavec M. Management of closed head injury in the maxillofacial trauma patient. J Oral Maxillofac Surg 1993;51:298–303. [6] Haug RH, Savage J, Likavec M, et al. A review of 100 closed head injuries associated with facial fractures. J Oral Maxillofac Surg 1992;50:218–22.
  • 20. 166 R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166 [7] Haug RH, Adams JM, Conforti PJ, et al. Cranial fractures associated with facial fractures: a review of mechanism, type and severity of injury. J Oral Maxillofac Surg 1994;52:729–33. [8] Haug RH, Prather J, Indresano AT. An epidemiologic survey of facial fractures and concomitant injuries. J Oral Maxillofac Surg 1990;48:926–32. [9] Haug RH, Wible RT, Likavec MJ, et al. Cervical spine fractures and maxillofacial trauma. J Oral Maxillofac Surg 1991;49:725–9. [10] Plaisier BR, Punjabi AP, Super DM, et al. The relationship between facial fractures and death from neurologic injury. J Oral Maxillofac Surg 2000;58:708–12.
  • 21. Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 Radiography of the cervical spine in trauma Thad Jackson, MD, Deborah Blades, MD* Department of Neurosurgery, College of Medicine, University of Kentucky, 800 Rose Street, Lexington, KY 40536-0298, USA This article illustrates the typical clinical and radiographic findings of patients with injuries to the cervical spine and discusses basic treatment guidelines. Cervical spine injuries are frequently seen in multitrauma patients and can be devastating injuries, particularly if not identified in a timely manner. The initial evaluation is both clinical (questioning about neck pain, palpating the neck, and neurologic examination) and radiographic, if indicated. All trauma patients should be effectively immobilized until a cervical spine injury is ruled out. The initial radiographic work-up consists of anteroposterior, lateral, and open-mouth odon- toid views. If the C7-T1 junction is not seen on plain radiographs, a swimmer’s view of the cer- vical spine should be obtained. If this view remains inadequate, a computed tomography (CT) scan through the nonvisualized vertebral bodies should be obtained. Depending on the type of injury, additional radiographic studies may be indicated. Early recognition of cervical spine in- jury and consultation of a spine specialist is imperative for a good neurologic outcome. Atlanto-occipital dislocation Frequency/incidence Atlanto-occipital dislocation (AOD) is present in up to 1% of patients with cervical spine injuries. AOD has been found in 19% to 35% of autopsies of fatal cervical spine injuries. There is a higher incidence of AOD among children [1]. Signs and symptoms AOD is typically fatal [1,2]. Mortality is most frequently from anoxia caused by respiratory arrest. Among survivors, more than 70% have an associated head injury [3]. Cranial nerve pal- sies (especially types VI, IX and XII) are seen in 50% of cases. Complete quadriplegia or brain- stem injury typically results in death. Brown-Sequard or central cord syndrome may also be observed. Patients will frequently deteriorate when placed in cervical traction. The patient may be completely neurologically intact and have a good outcome [1]. Etiology/pathophysiology AOD is caused by violent trauma (typically, motor vehicle collision or pedestrian struck by car) and may be related to hyperextension with distraction [1,3]. In fatal cases, there is transection of the spinal cord; however, in cases in which the patient survived, there was angio- graphic evidence of vertebral artery injury at the C1 level where the artery penetrates the dura to become intracranial. From a mechanical view, the distal vertebral artery as well as the head is * Corresponding author. E-mail address: dblades@pop.uky.edu (D. Blades). 1061-3315/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 6 1 - 3 3 1 5 ( 0 2 ) 0 0 0 1 0 - 0
  • 22. 168 T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 freely moveable in AOD, causing the artery to be injured at the C1 level as the vertebral artery then becomes anchored to the spine within the transverse foramen. At autopsy, none of these patients had evidence for mechanical injury or transection of the cord [4]. Image of choice for diagnosis Radiographic diagnosis is difficult, which frequently delays diagnosis. Plain lateral radio- graphs are typically the first test ordered. Plain radiographic techniques for diagnosing this en- tity include the Power’s ratio, and the X-line method [5]. The opisthion and basion are often difficult to identify on plain films, making thin-slice CT (3-mm cuts) with sagittal reconstruction a more accurate way of identifying AOD (see Power’s ratio in the Image hallmarks section). If suspicion is high, reformatted CT is the test of choice. Image hallmarks There is typically massive retropharyngeal soft tissue swelling (Fig. 1). On plain lateral radio- graphs, the Power’s ratio is frequently employed. The distance from the basion to the posterior arch of the atlas divided by the distance from the opisthion to anterior arch of atlas is greater than 1.0 in all cases of AOD. A Power’s ratio of less than 0.9 is normal, whereas ratios of 0.9 to 1.0 are borderline, representing 7% of the normal population and no cases of AOD [2]. Management Initial treatment involves strict immobilization of the cervical spine. Patients are typically reduced and placed in a halo vest. It is typically recommended that the patient subsequently undergo posterior occipital to cervical fusion [1,3]. Fig. 1. Lateral radiograph with massive soft tissue swelling.
  • 23. T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 169 Atlantoaxial rotatory subluxation/dislocation Frequency/incidence Rotatory subluxation at the C1-2 joint is relatively uncommon. Signs and symptoms Patients will frequently have torticollis, inability to rotate their head, facial flattening (if chronic), and upper cervical pain. The head position is sometimes described as ‘‘cock robin’’ (20° lateral tilt to one side, 20° rotation to the other side, and a slight flexion) [6]. Etiology/pathophysiology Rotatory subluxation typically occurs in children because the facet joints are smaller and more steeply inclined, and children have a larger head-to-body ratio, making the joint prone to rotational damage [7]. It can be seen spontaneously, with minor or major trauma, and can occur in association with upper respiratory infections [6]. Image of choice for diagnosis Diagnosis may be made with an open-mouth odontoid view; however, thin-cut CT from the occiput through C2 is the preferred imaging test. Image hallmarks On open-mouth odontoid view, there is typically asymmetry of the atlantoaxial joint (the C1 lateral mass that is rotated forward appears larger and closer to the midline; Fig. 2). The spinous process of the axis is tilted in one direction and rotated in the opposite direction. CT scan typ- ically shows the rotation of the atlas on the axis [6,7]. Fig. 2. (A) Anteroposterior radiograph demonstrating ‘‘cock robin’’ head position described in atlantoaxial rotatory subluxation. (B) Lateral radiograph demonstrating rotation of C1 on C2. (C) CT scan demonstrating rotation of C1 on C2.
  • 24. 170 T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 Fig. 2 (continued )
  • 25. T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 171 Management If diagnosed early (<1 week), patients can frequently be treated with closed reduction using cervical traction or a soft collar and an exercise program. Longstanding or recurrent subluxa- tion will often be treated with open reduction and fusion (C1-2) [7]. Dens fracture Frequency/incidence Dens fractures represent 10% to 15% of cervical spine fractures [2]. Signs and symptoms Common symptoms associated with dens fracture involve upper cervical pain. Patients will frequently hold their head between their hands when changing from a supine to upright posi- tion. It is estimated that 25% to 40% of patients with this fracture die at the time of the accident. Patients who survive the injury are most frequently neurologically intact [2]. Approximately 20% of patients with dens fractures present with myelopathy. In a study by Apuzzo et al [8], 44 of 45 patients were neurologically normal within 4 weeks of the event. Etiology/pathophysiology Most dens fractures are probably the result of flexion injuries secondary to violent trauma. Extension injuries may cause dens fractures, particularly those associated with posterior dis- placement. In elderly and young patients, dens fractures have been reported following falls [9]. Image of choice for diagnosis Dens fractures are typically seen on the open-mouth odontoid view. If the dens is not well visualized, anteroposterior (A-P) and lateral tomograms may be helpful. Axial CT images will frequently miss the fracture. If a CT scan is ordered, 2- to 3-mm cuts with sagittal reconstruc- tions should be performed (when a dens fracture is suspected). Image hallmarks There are three types of dens fractures; type I fractures occur through the tip of the dens (very rare), type II fractures occur through the base of the neck of the dens (most common type of dens fracture; Fig. 3), and type III fractures occur through the body of C2. Management Type I and type III fractures are typically considered stable and treated using a hard collar for a period of 8 to 14 weeks. Type II fractures have a high rate of nonunion, particularly if there is displacement (>4–6 mm) or the patient is elderly [8]. In younger patients, if there is minimal displacement, these fractures will typically be treated using halo vest immobilization. If there is significant displacement or the patient is elderly, these fractures will typically require surgical fusion (odontoid screw or posterior C1-2 fusion) [8]. Type II fractures in children will nearly always heal with immobilization alone [9].
  • 26. 172 T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 Fig. 3. (A) Lateral radiograph demonstrating a type II dens fracture. (B) Anteroposterior film demonstrating fracture through the base of the dens. (C) Tomogram demonstrating fracture through the base of the dens. (D) CT scan of type II dens fracture.
  • 27. Fig. 3 (continued )
  • 28. 174 T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 Jefferson fracture Frequency/incidence Jefferson fracture represents 10% of spine fractures [10] and is frequently associated with C2 fracture (>40% of cases) [2]. Signs and symptoms Patients very rarely have neurologic symptoms; frequently, patients complain of neck pain. Twenty-one percent of patients also have a head injury [2]. Etiology/pathophysiology Typically, an axial loading force to the skull causes this type of fracture [10]. Because the lat- eral masses of C1 and the occipital condyle have a wedge-shaped appearance, the axial loading widens the ring, resulting in four breaks in the C1 ring at their weakest locations—the bilateral lamina/vertebral artery groove junction and the bilateral anterior arch/lateral mass junction. Most fractures are also associated with tear of the transverse ligament, which allows ring wid- ening to occur and also makes this a highly unstable injury at the C1-C2 level: tear of the trans- verse ligament may further injure the cord but at a lower level than the AOD. Image of choice for diagnosis These fractures are frequently missed on lateral radiographs of the spine but are usually identified on open-mouth odontoid view of the atlantoaxial region by the overhang of C1 lat- eral masses on C2. Most of these AOD exhibit very marked prevertebral soft tissue swelling not seen to this degree with other cervical spine injuries. A thin-section (2 mm with overlapping slices) CT scan from C1-C3 with sagittal and coronal reconstructions is the imaging method of choice [2]. The Power’s ratio is only good for anterior AOD, and is negative for dislocation if it is in a posterior or longitudinal direction. The X-lines are able to diagnose all three types of AOD. The difficulty with the plain radiographic methods is identifying reliably the basion and opisthion. Image hallmarks Open-mouth odontoid view shows outward displacement of the lateral most edges of the C1 lateral mass relative to those of C2. Fracture through the anterior and posterior neural arches of C1 is seen on CT scan (Fig. 4). There is typically significant retropharyngeal soft tissue swelling. Transverse ligament tear can be directly seen when there is avulsion of the transverse ligament tubercle with a chip of bone seen within the C1 ring on CT. The unaffected tubercle can be seen on the contralateral side. If the bone is not torn, transverse ligament tear can be inferred by marked widening of the predental space in relation to the anterior arch of C1 because of forward subluxation of C1 with respect to CT. Most of the time with AOD, there is also instability at the C1-C2 level as well. Management Nondisplaced fractures (no overhang of C1 on C2) are typically treated with a hard collar. Fractures with less than 7 mm of displacement are treated with a hard collar or halo vest im- mobilization. Fractures with greater than 7 mm of displacement (implies disruption of the trans- verse atlantal ligament) are treated with halo vest immobilization [2].
  • 29. T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 175 Fig. 4. CT scan demonstrating a Jefferson fracture through the anterior and posterior neural arches of C1. Hangman’s fracture (traumatic spondylolisthesis of the axis) Frequency/incidence Traumatic spondylolisthesis of the axis, or hangman’s fracture, represents about 7% of cer- vical spine fractures [11]. Signs and symptoms Neck pain and pain with motion are frequently experienced. Patients rarely have neurologic deficits (<5%) related to the hangman’s fracture as long as they survive the initial traumatic forces. There is a high incidence of associated head injury (70%–80%) [2]. Etiology/pathophysiology Hangman’s fractures historically have been caused by distraction and hyperextension as with an execution by hanging [12]; however, most modern hangman’s fractures are caused by hyper- extension with axial loading as is frequently seen in automobile accidents. The classic scenario is an unrestrained passenger in a motor vehicle collision in which the chin of the passenger is forced into marked hyperextension on the dashboard or on the steering wheel. Image of choice for diagnosis Plain lateral radiographs identify 95% of cases based on the anterior subluxation of C2 with respect to C3 [2].
  • 30. 176 T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 Fig. 5. (A) Lateral radiograph demonstrating fracture through pedicles of C2. (B) CT demonstrating bilateral C2 pedicle fractures.
  • 31. T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 177 Image hallmarks Plain films do not demonstrate the bilateral arch fracture through the C2 pedicles well, whereas CT clearly shows the fracture (Fig. 5). Anterior subluxation of C2 on C3 is frequently seen on the plain radiographs. Less often, there may be an avulsion fracture from the anterior inferior corner of the body of C2; however, this avulsion fracture may occur by itself without a hangman’s fracture. Nevertheless, if this chip is seen, one must presume there is an associated hangman’s fracture, until the CT scan proves otherwise. Management Nonsurgical treatment is adequate in 95% of patients. For type I fractures (<3 mm of dis- placement), the patient may be treated with a hard collar or halo vest (for unreliable patients) for 12 weeks. Type II (angulation and translation of C2 on C3 of >3 mm) and type IIA (angu- lation without significant displacement) are treated with halo vest immobilization for 8 to 12 weeks followed by hard collar for a total of 3 to 4 months of immobilization. Type III fractures (pars fracture with bilateral facet dislocation at C2-3) typically require operative intervention (anterior cervical fusion of C2-3) [2]. Burst fracture Frequency/incidence Burst fractures are common in the thoracolumbar spine but are rare in the cervical spine [13]. The teardrop fracture, which is the most common in the cervical spine, may be considered to be a variation of the burst fracture. Signs and Symptoms Symptoms can vary from neck pain, radiculopathy, to complete spinal cord injury depending on the degree of spinal canal compromise [13]. Etiology/pathophysiology Burst fractures are secondary to an axial loading injury [13]. Image of choice for diagnosis Burst fractures are typically seen on lateral radiographs of the spine. Anteroposterior views are often helpful in differentiating from compression fractures (increased interpedicular distance is often seen in burst fractures). CT scan is the diagnostic test of choice as it allows accurate assessment of spinal canal compromise. Magnetic resonance imaging (MRI) is helpful in iden- tifying associated ligamentous injuries but is not necessary in most cases of burst fracture. Image hallmarks Typically, there is loss of body height and increased interpedicular distance seen on plain ra- diographs (Fig. 6A). Retropulsion of bony fragments is typically seen on plain radiographs. CT scans will often show a comminuted fracture of the vertebral body and demonstrate the associ- ated posterior element fracture (pedicle, lamina, spinous process; Fig. 6B). Management Burst fractures are typically treated with anterior body corpectomy and fusion. At times, rigid bracing or posterior fusion may be recommended [13].
  • 32. 178 T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 Fig. 6. (A) Lateral radiograph of C6 burst fracture. (B) Comminuted burst fracture including bilateral laminar fractures.
  • 33. T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 179 Compression/wedge fracture Frequency/incidence Simple compression fractures with wedge deformity of the body are uncommon in the cervi- cal spine but more commonly seen in the thoracic and lumbar regions. Signs and symptoms Patients frequently complain of neck pain at the site of the fracture. Neurologic deficits are rare with compression fractures (neurologic injury would imply instability and a more signifi- cant injury than a simple compression fracture). Etiology/pathophysiology Compression fractures are thought to be caused by flexion/axial loading forces. Image of choice for diagnosis Compression fractures are seen on plain lateral radiographs. CT scanning is helpful to ensure that there is no spinal canal compromise as would be seen in a burst fracture. Image hallmarks On plain radiographs, there is loss of vertebral body height anteriorly with preservation of the posterior vertebral body height (wedge-shaped vertebral body; Fig. 7A). On CT scan, there is cortical disruption of the anterior cortical margin of the vertebral body (Fig. 7B). Management Patients with compression fractures are typically treated using rigid immobilization (hard collar) for 6 to 12 weeks. Prior to removal of the hard collar, flexion-extension cervical spine radiographs should be obtained because there are several reports of instability associated with cervical compression fractures [14]. This instability implies ligamentous injury as well, because the simple wedge fractures are not unstable injuries unless there has been an acute loss in height of more than 50%. Subluxation facet fracture/lock Frequency/incidence Facet fractures with subluxation represent approximately 7% of cervical spine injuries ac- cording to a study by Sonntag and Hadley [15]. Bilateral and unilateral fractures are most com- monly found at the C6-7 level. Signs and symptoms Patients with unilateral facet fracture-dislocation can have a variable presentation. Sonntag and Hadley [15] found that of 31 patients, 6 were neurologically intact with pain only, 7 had root deficits only, 10 had incomplete spinal cord injuries, and 7 had complete neurologic inju- ries. Bilateral facet fracture-dislocations tend to have more significant neurologic injuries. In a study of 37 patients, 31 patients had complete spinal cord injuries and 6 had incomplete spinal cord injuries [15].
  • 34. 180 T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 Fig. 7. (A) Lateral radiograph demonstrating wedging of the C7 vertebral body as typically seen in a compression fracture. (B) CT scan of fracture through anterior portion of vertebral body. Etiology/pathophysiology Unilateral facet fracture-dislocations are thought to be caused by a flexion-rotation injury, whereas bilateral facet fracture-dislocations are thought to be caused by hyperflexion injury.
  • 35. T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 181 Image of choice for diagnosis Plain lateral radiographs are adequate in the diagnosis of unilateral and bilateral facet fracture-dislocations. A CT scan through the area will be helpful in determining the degree of disruption of the superior and inferior articular processes of the facet. Image hallmarks With unilateral facet fracture-dislocation, there is subluxation of approximately 25% of the superior vertebral body relative to the inferior vertebral body (Fig. 8). Typically there is also evidence of rotation. With bilateral facet fracture-dislocation, there is approximately 50% or greater subluxation without evidence of rotation. On CT, the affected facet joint appears to be two semicircles with the curved surfaces abutting each other, thus uncovering the facet joint itself. Normally, the flat surfaces abut each other such that the facet joint is not seen, and the two facets have an ovoid shape. Management For unilateral facet fractures, closed reduction using cervical traction is attempted. If closed reduction is successful (18 of 29 of acute fractures in the Sonntag and Hadley study), the patient is typically immobilized in a halo. If unable to achieve closed reduction, open reduction and Fig. 8. (A) Lateral radiograph of unilateral facet and associated subluxation of C4 on C5 of approximately 25% of the width of the vertebral body. (B) CT demonstrating unilateral fact fracture on the left. (C) Lateral radiograph of bilateral locked facets with subluxation of approximately 50% of the width of the vertebral body. (D) CT scan of bilateral locked facet.
  • 36. 182 T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 Fig. 8 (continued)
  • 37. T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 183 Fig. 8 (continued) internal fixation using interspinous cables or lateral mass plates are typically undertaken. A similar treatment is attempted with bilateral facet fracture-dislocations; however, the likelihood of achieving adequate closed reduction is lower (20 of 37 acute fractures) [15]. Teardrop fracture Frequency/incidence Teardrop fractures represent approximately 5% of cervical spine fractures [2]. Signs and symptoms Patients are frequently quadriplegic. They are rarely neurologically intact [2]. Etiology/pathophysiology Teardrop fractures are typically seen in the setting of an acute flexion injury with severe axial loading [16]—most commonly sustained from diving into a shallow body of water. An unrestrained automobile passenger with the head flexed and then driven into the dashboard may also sustain this injury. Even though the teardrop bony fragment itself involves the ante- rior body, it is the associated retropulsion of the posterior body into the canal that injures the spinal cord. This persistent retropulsion of the body is seen on plain radiographs in most patients [17].
  • 38. 184 T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 Image of choice for diagnosis Teardrop fractures are usually seen on lateral radiographs; however, to differentiate them from a simple avulsion fracture of the anteroinferior corner of the vertebral body, a CT scan through the area in question is helpful. Teardrop fractures are associated with retropulsion of the fractured body, sagittal body fracture, and laminar fractures, which are not seen with simple avulsion fractures [17]. MRI may also be useful in evaluating the degree of ligamentous injury, the presence of an associated disc herniation, and spinal cord injury. Image hallmarks A triangular piece of bone is typically seen at the anterior inferior edge of the fractured ver- tebral body (the ‘‘teardrop’’; Fig. 9A). Frequently, there is an associated sagittal fracture of the vertebral body. This is difficult to see on the A-P view of the cervical spine because of confusing lines from the tracheal air column, nasogastric tubes, or endotracheal tubes. The fractured ver- tebral body is usually displaced posteriorly relative to the vertebral body below. Kyphosis is fre- quently seen at the site of the fracture, and there may be evidence of facet disruption. The subjacent disc space is often narrowed. There may be significant soft tissue swelling. CT scan- ning may better show the sagittal vertebral body fracture, which is frequently present, and more accurately assess the degree of spinal canal compromise (Fig. 9B) [2]. Management If the ligamentous structures (including the disc) are intact and there is no spinal cord compression, the teardrop fracture may be treated with halo immobilization for 8 to 12 weeks followed by flexion-extension cervical-spine X rays to ensure stability. If there is a large ante- rior fragment with spinal cord compression, an anterior corpectomy and fusion is typically Fig. 9. (A) Lateral radiograph of a teardrop fracture. Note the posterior subluxation of C5 on C6. (B) CT of teardrop fracture demonstrating a sagittal split in the vertebral body along with the anterior fragment.
  • 39. T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 185 Fig. 9 (continued) indicated. If there is associated posterior ligamentous injury, a combined anterior-posterior fu- sion may be indicated [2]. Clay shoveler’s fracture Frequency/incidence Clay shoveler’s fracture is uncommonly seen in trauma. It is usually seen in patients perform- ing excessive manual labor, such as grave diggers [18]. Signs and symptoms Patients complain of pain between their shoulders, which is made worse with pulling and/or lifting. There is no neurologic deficit. Patients have tenderness to palpation along the lower cer- vical/upper thoracic spine and increased pain with flexion of the head [18]. Etiology/pathophysiology Avulsion of the spinous process occurs by forces transmitted from the trapezius and other muscles attached to the spinous process. This fracture is also seen in hyperflexion and hyper- extension injuries [18,19]. As the shoveler attempts to throw the dirt off his shovel by tossing it behind his head, the clay sticks to the shovel causing a forced hyperextension load to the neck, which crowds the lower cervical posterior spinous process leading to fracture.
  • 40. 186 T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 Fig. 10. (A) C6 spinous process fracture. (B) CT of fracture through spinous process.
  • 41. T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187 187 Image of choice for diagnosis Clay shoveler’s fracture is typically seen on plain lateral radiograph; however, if there is a laminar fracture, CT may be necessary to determine if there is any encroachment on the canal. Image hallmarks There is fracture of spinous process of C7, C6, or T1 (in decreasing frequency; Fig. 10) [18]. Management This is a stable fracture. Evaluation should include flexion-extension cervical-spine radio- graphs and, if negative, only pain medication should be required. Hard-collar immobilization may be used as needed for pain control [2]. References [1] Traynelis VC, Marano GD, Dunker RO, et al. Traumatic atlanto-occipital dislocation. Case report. J Neurosurg 1986;65:863–70. [2] Greenberg MS. In: Handbook of neurosurgery. 3rd edition. Lakeland, FL: Greenberg Graphics; 1994. p. 322–24, 580–605. [3] Anderson PA, Montesano PX. Traumatic injuries of the occipital-cervical articulation. In: Camins MB, O’Leary PF, editors. Disorders of the cervical spine. Baltimore, MD: Williams & Wilkins; 1992. p. 273–83. [4] Lee C, Woodring JH, Walsh JW. Carotid and vertebral artery injury in survivors of atlanto-occipital dislocation: case reports and literature review. J Trauma 1991;31:401–7. [5] Lee C, Woodring JH, Goldstein SJ. Evaluation of traumatic atlanto-occipital dislocations. Am J Neuroradiol 1987;8:19–26. [6] Fielding JW, Hawkins RJ. Atlanto-axial rotatory fixation. Fixed rotatory subluxation of the atlanto-axial joint. J Bone Joint Surg 1977;59A:37–44. [7] Sponseller PD, Herzenberg JE. Cervical spine injuries in children. In: Clark CR, editor. The cervical spine. 3rd edition. Philadelphia: Lippincott-Raven; 1998. p. 357–71. [8] Apuzzo MLJ, Heiden JS, Weiss MH, et al. Acute fracture of the odontoid process. J Neurosurg 1978;48:85–91. [9] Ballard WT, Clark CR. Fractures of the dens. In: Clark CR, editor. The cervical spine. 3rd edition. Philadelphia: Lippincott-Raven; 1998. p. 415–28. [10] Kurz LT. Fractures of the first cervical vertebra. In: Clark CR, editor. The cervical spine. 3rd edition. Philadelphia: Lippincott-Raven; 1998. p. 409–13. [11] Gehweiler JA, Clark WM, Schaaf RE, et al. Cervical spine trauma: the common combined conditions. Radiology 1979;130:77–86. [12] Schneider RC, Livingston KE, Cave AJE, et al. ‘‘Hangman’s fracture’’ of the cervical spine. J Neurosurg 1965;22:141–54. [13] Abei M, Benzel EC. Cervical spine burst fractures. In: Clark CR, editor. The cervical spine. 3rd edition. Philadelphia: Lippincott-Raven; 1998. p. 465–73. [14] Mazur JM, Stauffer ES. Unrecognized spinal instability associated with seemingly ‘‘simple’’ cervical compression fractures. Spine 1983;8:687–92. [15] Sonntag VKH, Hadley MN. Management of cervical spine facet fracture-dislocations. In: Camins MB, O’Leary PF, editors. Disorders of the cervical spine. Baltimore, MD: Williams & Wilkins; 1992. p. 459–64. [16] Schneider RC, Kahe EA. Chronic neurologic sequelae of acute trauma to the spine and spinal cord. The significance of the acute-flexion or ‘‘tear-drop’’ fracture-dislocation of the cervical spine. J Bone Joint Surg 1956;38A:985–97. [17] Lee C, Kim KS, Rogers LF. Triangular cervical vertebral body fractures: diagnostic significance. Am J Radiol 1982;138:1123–32. [18] Hall RDM. Clay-Shoveler’s fracture. J Bone Joint Surg 1940;22:63–75. [19] Kitchel SH. Soft-tissue neck injuries. In: Clark CR, editor. The cervical spine. 3rd edition. Philadelphia: Lippincott-Raven; 1998. p. 351–5.
  • 42. Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 Chest radiography Betty J. Tsuei, MDa,*, Peter E. Lyu, DDSb a Department of General Surgery, College of Medicine, University of Kentucky, 800 Rose Street, Room C-221, Lexington, KY 40536, USA b Division of Oral and Maxillofacial Surgery, College of Dentistry, University of Kentucky, 800 Rose Street, Room D-508, Lexington, KY 40536, USA One of the most commonly performed imaging procedures is the plain chest radiograph, ac- counting for up to 50% of studies obtained in some radiology practices. Currently, radiographic evaluation of the chest is utilized in many routine settings. Preoperative radiographs are often used to screen for underlying pulmonary and cardiovascular diseases. Pleural effusions and car- diac enlargement suggestive of heart failure may be present. In the febrile patient, the chest ra- diograph is useful for visualizing pulmonary sources of fevers, such as atelectasis, viral and bacterial pneumonias, and lobar collapse. In addition, the chest radiograph is an important di- agnostic tool in the evaluation of the traumatically injured patient in which concomitant head, neck, and facial injuries may be present. Rib fractures, hemothorax, pneumothorax, and pulmo- nary contusions, and acute respiratory distress syndrome (ARDS) are commonly seen, and the hallmarks of these injuries should be readily identifiable. Finally, thoracic imaging can also detect injuries and infections that originate in the head and neck. With the many pulmonary, cardiac, esophageal, and mediastinal diseases, it is not surprising that countless volumes of ra- diology textbooks have been dedicated solely to thoracic imaging. This article touches on a few of the conditions noted previously and is intended to outline some basic findings in chest radiog- raphy. Although the article reviews clinical symptoms and treatment, it is not meant to be a de- finitive dissertation on thoracic diseases—collaboration with not only radiologists but also pulmonologists, cardiothoracic surgeons, and trauma and critical care specialists will succeed in providing accurate and timely diagnosis and appropriate medical care. Atelectasis Frequency/incidence The incidence of postoperative atelectasis is approximately 80%, but only about 20% of cases are clinically significant [1]. In a review of chest radiographs of 200 consecutive patients in the surgical ICU, 18 cases of lobar collapse were diagnosed in 17 patients (8.5%). Most cases in- volved the left lower lobe (66%), but collapse of the right lower lobe (22%) and the right upper lobe (11%) was also noted [2]. Signs and symptoms Patients may present with low-grade fever, mild leukocytosis, and mild tachypnea. In mild atelectasis, alterations in oxygenation and ventilation may not be seen. In atelectasis resulting from bronchial obstruction with significant loss of pulmonary parenchyma, patients may exhibit marked tachypnea and hypoxia. * Corresponding author. E-mail address: btsue@uky.edu (B.J. Tsuei). 1061-3315/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 6 1 - 3 3 1 5 ( 0 2 ) 0 0 0 0 6 - 9
  • 43. 190 B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 Etiology/pathophysiology Atelectasis is defined as a decrease in lung volume and can arise from several causes. Ob- structing lesions, caused by a foreign body, mucus plugging, or endobronchial tumors may re- sult in distal air resorption and atelectasis. Compressive atelectasis is caused by the compression of normal lung by an adjacent space-occupying lesion, such as a large peripheral lung tumor or bullous or lobar emphysema. Pneumothorax and pleural effusion may also result in atelectasis. One of the most common forms of atelectasis occurs when the intraluminal surfaces of alveoli collapse and adhere together. This is usually caused by a decreased tidal volume during sponta- neous respirations. Poor inspiratory volumes are common in postoperative patients as a result of sedation, anesthetic, pain, or immobility. Atelectasis can also be caused by scarring and fib- rosis in the interalveolar and interstitial space, decreasing lung compliance and reducing lung volumes. Image of choice The preferred imaging modality is a standard chest radiograph, although atelectasis may also be seen as an incidental finding on chest computed tomography (CT). Image hallmarks Hallmarks of atelectasis primarily consist of an increased opacity in the anatomic area of col- lapse. In postoperative atelectasis (Fig. 1A), this occurs primarily at the lung bases and is a bi- lateral process. Elevation of the diaphragm and displacement of the pulmonary hilum may also been seen. In cases of lobar collapse, more marked anatomic delineation is seen, such as the left upper lobe collapse (Fig. 1B). In addition to increased lobar opacity, there is often displacement of the adjacent fissure and compensatory overinflation of the normal lung. In severe cases, car- diac rotation and mediastinal shift can occur. Management Treatment of atelectasis includes aggressive pulmonary toilet to expand the collapsed por- tions of the lung. Deep breathing, forced coughing, and use of spironometry can be employed in the cooperative patient. Nebulizer treatments and nasotracheal suction to induce coughing, or positive pressure masks, may also be beneficial. In cases of lobar collapse, more aggressive measures, such as bronchoscopy to eliminate the cause of obstruction and positive pressure ven- tilation, may be required. Fig. 1C shows resolution of the left upper lobe collapse within 24 hours with vigorous pulmonary toilet. Pleural effusion Frequency/incidence Pleural effusion is usually a secondary effect from a primary disease state, and as such, the incidence varies depending on the underlying cause. In patients with congestive heart failure, the incidence of pleural effusion may be as high as 58% to 88% [3]. Effusions may also be present in 67% of patients with pericardial disease [4]. Cirrhosis and ascites are also associated with pleural effusion (6%), and as many as 11% of patients with bacterial pneumonia may exhibit concomitant pleural effusion [5]. Signs and symptoms Patients with pleural effusion may be asymptomatic if the effusion is mild. Generally, they exhibit symptoms of the underlying cause of the effusion—for example, congestive heart failure or ascites (see following subsection). Large effusions can cause respiratory compromise with
  • 44. B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 191 Fig. 1. Atelectasis. (A) Postoperative. Characteristic bibasilar platelike atelectasis (arrows). (B) Lobar collapse. Note the increased density which demarcates the left upper lobe. (C) Resolution of lobar collapse. Re-expansion of the left upper lobe collapse seen in figure 1b after 24 hours of vigorous pulmonary toilet. dyspnea, tachypnea, and hypoxia. Decreased basilar breath sounds may be found on physical examination. Etiology/pathophysiology Excess pleural fluid can be attributed to the increased transport of pulmonary interstitial fluid from the mesothelium into the pleural space. Congestive heart failure is the most common cause of transudative pleural effusion, although other disease states in which intravascular volume is
  • 45. 192 B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 Fig. 1 (continued) elevated, such as renal failure, nephrotic syndrome, and cirrhosis may also cause effusion. Sym- pathetic effusion, resulting from disease in an adjacent organ—cardiac (pericarditis), upper ab- domen (pancreatitis, splenic disease)—is also common. Infectious agents, such as bacterial pneumonia, tuberculosis, and fungal or viral infections, usually cause exudative pleural effu- sions. Malignancies, particularly breast and lung cancers, may also cause pleural effusion. Image of choice Although pleural effusion may be seen on supine chest radiography, the imaging modality of choice is an upright or lateral chest radiograph. Image hallmarks The most common manifestation of pleural effusion on upright radiograph is a fluid level in the hemithorax. Small amounts of pleural fluid may be manifest as a meniscus that blunts the costophrenic angle on the PA projection (Fig. 2A). Small effusions may also be visualized in the posterior sulcus on the lateral film. At least 175 mL of fluid is needed for the effusion to be vi- sualized on plain radiograph, whereas a large pleural effusion may completely opacify the hemi- thorax. If the patient is unable to tolerate an upright film, a lateral decubitus film with the affected side down may reveal dependent layering of fluid in the hemithorax, suggesting the pres- ence of pleural effusion. In a supine patient, the effusion is generally seen as a diffuse opacifica- tion of the affected hemithorax (Fig. 2B). Atelectasis of a lobe can also be present with pleural effusions. Management Treatment of the underlying cause of the pleural effusion often results in resolution of the effusion. In general, pleural effusion is not treated unless the patient is symptomatic. Methods of treatment in the symptomatic patient include thoracentesis or drainage with thoracostomy tube.
  • 46. Fig. 2. Pleural effusion. (A) Left pleural effusion on upright chest radiograph, demonstrating characteristic blunting of costophrenic angle and visible fluid level. (B) Right pleural effusion on supine chest film, demonstrating the diffuse increase in density through the right hemithorax.
  • 47. 194 B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 Viral pneumonia Frequency/incidence Viral infections are common and often cause more morbidity and mortality than do bacterial infections. Most viral pneumonias occur in children and adults who are relatively immunocom- promised. Infants are particularly susceptible during the ages of 2 months to 2 years, with boys affected twice as often as girls [6]. One study indicated that 90% of influenza-related fatalities occurred in patients older than 65 years. Individuals residing in nursing homes are also partic- ularly susceptible, with a mortality rate of 30% from viral pneumonia [7]. Infection rates of vi- ruses depend on the immune status of the individual. Patients with immune suppression (chemotherapeutic agents, transplant patients, HIV) may become infected with viruses, which are usually not pathogenic (eg, cytomegalovirus). Signs and symptoms Respiratory symptoms of viral pneumonia may include cough and nonpurulent sputum. Low-grade fever, chills, headache, conjunctivitis, myalgia, anorexia, and malaise are also common. Severely affected patients show rapid progression of tachypnea, dyspnea, cyanosis, and hypoxemia. Etiology/pathophysiology Most viruses causing pneumonia travel from the upper to the lower respiratory tract. Common viral agents include influenza virus, respiratory syncytial virus, measles, picornavirus, coxsackievirus, enterocytopathogenic human orphan virus, and rhinovirus. The pathologic changes induced in the lung are similar for all viruses. Necrosis and sloughing of epithelium lead to loss of normal mucosal surface. Mucous production increases, leading to bronchiolar plug- ging, and the alveoli are often filled with fluid and leukocytes. The diagnosis of viral pneumonia is often one of exclusion. It is based on the absence of purulent sputum production, failure to culture a pathogenic bacterium, a relatively benign clinical presentation, or a white blood cell count that is normal or only slightly elevated. Image of choice The preferred imaging modality is a chest radiograph. Image hallmarks Image hallmarks can be nonspecific and depend on the extent of the disease; findings range from mild interstitial prominence (Fig. 3A) to significant air space disease (Fig. 3B), especially if bacterial superinfection occurs. Areas of patchy consolidation, air trapping, and perihilar infil- trates may also be seen [8]. Management Supportive therapy is the main course of treatment. Cell culture, serology, and detection of viral antigens can aid with diagnosis but are usually not employed, because the disease is usually self-limited with complete clinical recovery in 2 to 3 weeks. Antiviral agents, usually reserved for immunocompromised patients, include ganciclovir, acyclovir, ribavirin, amantadine, and rimantadine. The respiratory tract may become secondarily infected and result in a super- imposed bacterial pneumonia, which should be treated with the appropriate antibiotics (see following section).
  • 48. B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 195 Fig. 3. Viral pneumonia. (A) Mild diffuse interstitial changes seen in viral pneumonia. (B) Significant air space disease (right lower lobe) may be present in advanced pneumonia, or if bacterial superinfection occurs. Bacterial pneumonia Frequency/incidence There are 2 to 3 million cases of pneumonia in the United States per year. Many patients with bacterial pneumonia can be treated on an outpatient basis. The mortality rate from community-acquired pneumonia in patients who require hospitalization is 14%, and increases up to 50% in patients who require admission to the ICU [9]. Among hospitalized patients,
  • 49. 196 B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 pneumonia is the second most common and most frequently fatal nosocomial infection [10]. With mechanical ventilation, the risk of acquiring a nosocomial infection increases five to ten fold. Among mechanically ventilated patient in an ICU, the incidence of nosocomial pneumonia is 18% to 58%, with a mortality rate of 38% [11]. Signs and symptoms Patients with pneumonia may present with fever, new or increased cough, purulent sputum production, or dyspnea. Clinical findings on physical examination can include fever, tachypnea, tachycardia, rales, dullness to percussion, or decreased breath sounds. Unfortunately, some studies have indicated that these signs are only 50% specific for the diagnosis of pneumonia [12]. Nosocomial pneumonia can be more difficult to diagnose, especially in ventilated patients in the ICU. In these cases, fever, leukocytosis, sputum gram stain and culture, infiltrate on chest radiograph, and presence of purulent sputum are used for diagnosis. At least three of these find- ings should be present for the diagnosis of pneumonia to be made. Etiology/pathophysiology Infectious agents gain entry to the lung either directly by inhalation of 0.5 to 1.0 lm aerosol- ized particles or after respiration of oropharyngeal secretions. If the inoculum is unable to be cleared by the pulmonary tree, bacterial multiplication results in development of pneumonia. Because of virulence factors, certain microorganisms are more capable of avoiding pulmonary clearance mechanisms, resulting in rapid replication and damage to host tissues. Common or- ganisms that cause community–acquired pneumonia include S. pneumoniae, H. influenza, and K. pneumoniae. These organisms can often be treated with single agent or oral antibiotics. Atyp- ical pneumonia may result from Mycoplasm or Legionella species. Aspiration pneumonia may be multibacterial, and is more likely to contain anaerobic species. Hospital-acquired pneumonia usually results from more virulent bacteria, such as Pseudomonas, Enterobacter, Acinetobacter, and Staphylococcus species. These organisms may require double antibiotic coverage, or exhibit unusual resistance patterns. Image of choice The preferred imaging modality is a PA and lateral chest radiograph. The infiltrate seen on radiograph may take several weeks to resolve. Therefore, serial radiographs are not necessary as long as the clinical picture shows improvement. A follow-up radiograph should be taken to document resolution of the infection. Image hallmarks The hallmark of bacterial pneumonia is a discreet pulmonary infiltrate. Loss of discreet pul- monary borders, such as the diaphragm or cardiac silhouette, indicates an increased density in the adjacent pulmonary region. Whereas lower lobe infiltrates are the most common, aspiration pneumonia often results in an infiltrate in the right upper lobe. Fig. 4 shows the characteristic infiltrate in the right upper lobe. Management The treatment of bacterial pneumonia consists of antibiotic therapy and supportive care. Specific pharmacologic intervention is dictated by the pathogen. Community-acquired pneumo- nias may often be treated with single or oral antibiotic agents, whereas nosocomial pulmonary
  • 50. B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 197 Fig. 4. Bacterial pneumonia resulting in right upper lobe infiltrate. infections often involve more virulent organisms. In these instances, multiple antibiotics may be required, and development of drug resistance is common. Sputum cultures, microbial susceptibility, and hospital and specific unit-based bacterial biograms may be beneficial in deter- mining the antimicrobial agent of choice. In certain cases, hospitalized patients with nosocomial pneumonia may require respiratory isolation to prevent spread of the organism. Rib fractures Frequency/incidence Rib fractures are a common injury resulting from trauma to the chest wall, and are less com- mon in children because of the elasticity of the cartilage and flexibility of the bone. Isolated rib fractures have an overall incidence of approximately10%; however, 90% of patients with multi- system injuries have rib fractures. Commonly associated pulmonary injuries include pneumotho- rax or hemothorax (32%) and pulmonary contusion 26%. Rib fractures and other pulmonary injuries can result in significant hospital morbidity: one study noted that 35% of patients with rib fractures developed a pulmonary complication, with an overall mortality rate of 12% [13]. Signs and symptoms Pain is the most common symptom of rib fractures. The complications of rib fracture, such as pulmonary contusion and pneumonia, are considered more significant than the injury itself. As- sociated underlying pulmonary contusion, especially in patients with flail segments, can cause pulmonary compromise, with resultant tachypnea, dyspnea, and respiratory failure. Etiology/pathophysiology Trauma is by far the most common cause of rib fractures. In traumatic injuries, direct blows to the rib cage will create an inward fracture, potentially damaging the pleura and parenchyma
  • 51. 198 B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 of the lung. Pneumothorax, hemothorax, and pneumohemothorax are frequent concomitant findings. The specific location of the injuries can relay some important information about the direction and force of impact. Rib fractures of the first, second, or third ribs can be associated with injuries to the aortic, spine, or airway. Trauma to the lower rib cage (tenth, eleventh, or twelfth ribs) often is associated with upper abdominal trauma, such as injury to the spleen, kid- neys, or liver. Multiple segmental rib fractures involving two or more contiguous ribs constitutes a flail chest. In patients with underlying bone disease, such as tumors and osteoporosis, even minor trauma, such as coughing, may precipitate rib fractures. Image of choice The preferred imaging method for rib fractures is an upright chest radiograph. Although there are specific rib films that may be obtained, these are not often performed because the diagnosis is largely clinical and the treatment supportive. Image hallmarks Rib fractures are classically seen as an irregularity of the bony contour, especially of the rib border (Fig. 5). These findings can be quite pronounced, with overlap of the ends of the ribs and significant chest wall deformities, or they can be very subtle and easily overlooked. Clinical corre- lation with point tenderness of the chest wall can often confirm the diagnosis. Associated findings may include subcutaneous emphysema, pneumothorax, hemothorax, and pulmonary contusion. Management The complications of rib fracture are considered more important than the injury itself. Significant underlying pulmonary contusion should be treated with respiratory support and mechanical ventilation, if necessary. Pain control is an important part of treatment, because lim- ited inspiratory efforts can result in atelectasis, collapse, and secondary pneumonia. Oral or in- travenous narcotics are often utilized but can cause respiratory compromise. Epidural catheter Fig. 5. Rib fractures (arrows) after blunt thoracic trauma.
  • 52. B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 199 placement for pain control can be quite efficacious. Aggressive pulmonary toilet often is neces- sary as well. Pneumothorax Frequency/incidence Traumatic injury is one most common cause of pneumothorax. As many as 35% to 40% of patients with blunt traumatic injuries will develop some form of pneumothorax, with the inci- dence depending largely on the severity of the trauma [14]. About 40% of these pneumothoraces are occult, meaning they are apparent on CT but not on chest radiographs [15]. Primary spon- taneous pneumothorax, which commonly occurs in patients with underlying pulmonary disease, accounts for about 9000 cases of pneumothorax each year. Signs and symptoms Symptoms of pneumothorax depend on the degree of lung collapse, and small pneumothora- ces may be asymptomatic. Chest pain and dyspnea are the two main symptoms associated with the development of pneumothorax. Hypoxia may occur if the pneumothorax is large, and devel- opment of tension pneumothorax (see section on tension pneumothorax) may be lethal. Etiology/pathophysiology Spontaneous pneumothorax usually results from rupture of a subpleural emphysematous bleb, which is usually located in the apex of the lung. Blebs are present in 75% of cases of pri- mary spontaneous pneumothorax, and are especially common in patients with emphysema or other underlying pulmonary diseases. Another group of patients that appears to be at risk are young, thin, male athletes. Pneumothorax can also be iatrogenic in origin. Central line place- ment, either via subclavian or jugular approach, can cause puncture of the lung parenchyma with resultant pneumothorax. Operations of the neck, such as tracheostomy and thyroidecto- mies, can also cause pneumothorax, although this is rare. Violation of the pleura and pneumo- thorax is a common finding in trauma patients who sustain rib fractures. Image of choice The preferred imaging method for detection of pneumothorax is a PA chest radiograph taken during exhalation. Exhalation may enhance the appearance of pneumothorax by increasing the density of the lung, which increases contrast between the trapped air. Image hallmarks The hallmark of pneumothorax on chest radiograph is a lucent space between the pleural line and the chest wall. This lucency, where there is a notable absence of lung parenchymal mark- ings, is most readily apparent in the apex of the lung, especially on an upright film (Fig. 6A). Close examination may be needed to visualize the pleural line (Fig. 6B). Increased opacity of the affected lung may also be visible. Subcutaneous air may also be visualized, especially in cases of traumatic pneumothorax. Management Management of pneumothorax depends on its size and on the presentation of the patient. Small pneumothoraces may be observed and resolve spontaneously. Supplemental oxygen and incentive spirometry may be beneficial. If expectant management is undertaken, close pa- tient monitoring and serial chest radiographs should be employed. If there is significant increase
  • 53. Fig. 6. Pneumothorax. (A) Right pneumothorax seen on chest radiograph. (B) Inset from above, with pleural line indicated (arrows). Note the absence of lung parenchymal markings lateral to the pleural line.
  • 54. B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 201 in the size of the pneumothorax between films, therapeutic intervention may be required because spontaneous resolution is less likely. A large pneumothorax may require decompression with tube thoracostomy and suction. In cases of prolonged unresolved pneumothorax, thoracostomy with a Heimlich valve or pleural sclerosis may be required. Hemothorax Frequency/incidence Trauma is by far the most common cause of hemothorax. One study found that 44% of pa- tients with multiple traumatic injuries had associated hemothorax [16]. Another review found that as many as 75% of patients who sustained severe blunt or penetrating chest trauma had significant hemothorax [17]. Hemothorax usually results from injury to the lung parenchyma or, on occasion, to the intercostal or great vessels. Iatrogenic causes are less common and in- clude venous catheter placement, thoracocentesis, lung or pleural biopsy, or thoracic surgery. Signs and symptoms The clinical significance of hemothorax depends on the degree of blood loss. Symptoms can range from the asymptomatic presentation to profound hypovolemic shock. Patients may com- plain of dyspnea or shortness of breath. Physical examination findings are decreased breath sounds and dullness to percussion on the injured side. If significant respiratory compromise is present, decreased arterial saturations and hypoxia may be seen. Hemothorax may also be present in conjunction with significant pneumothorax (see section on hemopneumothorax), and the clin- ical presentation may consist of aspects of both respiratory and circulatory compromise. Etiology/pathophysiology Hemothorax usually results from injury to the chest wall or lung parenchyma. Other less common but more serious causes are hemorrhage from one of the great vessels, intercostals, in- ternal mammary arteries, or the heart. Image of choice Plain radiograph is the preferred diagnostic imaging modality, and clinical correlation is often used to confirm the diagnosis. Image hallmarks Images of hemothorax may mimic pleural effusion, because both entities consist of fluid be- tween the lung parenchyma and the chest wall (see section on pleural effusion). Unlike the fluid present in effusion, however, the blood present in hemothorax will coagulate, preventing free flow in the chest cavity. For this reason, hemothorax may be seen as a generalized density over the entire hemithorax, especially in a supine chest radiograph (Fig. 7). Other manifestations of hemothorax include the presence of a visible pleural line, with increased density between the lung parenchyma and chest wall. Because most cases of hemothorax arise after trauma, the clin- ical presentation and index of suspicion differentiate hemothorax from effusion. Management Management of hemothorax consists of measures to clear the pleural space of blood. Large caliber tube thoracostomy is often employed to accomplish this. Despite these maneuvers, clotted hemothorax can be difficult to evacuate, and in some situations, thoracoscopy or tho- racotomy may be warranted. If associated infection is present (eg, pneumonia), the pleural blood is at risk for becoming an empyema through secondary infection.
  • 55. 202 B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 Fig. 7. Left hemothorax presenting with diffusely increased density throughout the hemithorax. Hemopneumothorax Frequency/incidence Trauma is the most common cause for hemopneumothorax, which occurs less frequently than an isolated pneumothorax or hemothorax. The incidence of hemopneumothorax is 21.6%, which was reported in one retrospective study analyzing blunt trauma [18]. The incidence increases with penetrating trauma (35%–38%) [19,20]. Signs and symptoms Patients can present relatively asymptomatic or with hypovolemic shock, depending on the volume of blood loss. Patients may initially complain of dyspnea or shortness of breath. Phys- ical examination findings are decreased breath sounds and unilateral percussive dullness with areas of hyperresonance on the injured side. If significant respiratory compromise is present, de- creased arterial saturations and hypoxia may be seen. Because a hemothorax is present in con- junction with significant pneumothorax, the clinical presentation may consist of aspects of both respiratory and circulatory compromise. Etiology/pathophysiology Bleeding into the pleural space is usually due to chest wall injury or parenchymal laceration. Other more serious causes are hemorrhage from one of the great vessels, one of the intercostals or internal mammary arteries, or the heart. This condition is further complicated by pneumo- thorax, which usually results from trauma to the lung parenchyma. Image of choice The preferred imaging modality for detection of hemopneumothorax is a PA chest radiograph. Exhalation may accentuate the appearance of the pneumothorax component of this entity.
  • 56. B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 203 Image hallmarks Signs of both pneumothorax and hemothorax will be seen on chest radiograph (Fig. 8A). The pneumothorax component can been seen as a distinct pleural line (Figs. 8A and 8b, white arrow) with absence of peripheral lung parenchymal markings. On an upright film, the pleural blood may be seen at the base of the lung, and an air-fluid level may be visualized if the blood has not coagulated (Fig. 8A, black arrow). In Fig. 8A, note the presence of rib fractures (outlined arrow), which are likely responsible for the hemopneumothorax. On a supine film, only the he- mothorax may be clearly visible. Management Management of pneumohemothorax consists of measures to clear the pleural space of blood and reexpand the collapsed portion of lung. Large-caliber tube thoracostomy is usually em- ployed to accomplish this. Despite these maneuvers, clotted hemothorax can be difficult to evac- uate, and in some situations, thoracoscopy or thoracotomy may be warranted. If associated infection is present (eg, pneumonia), the pleural blood is at risk for becoming an empyema through secondary infection. Fig. 8. Hemopneumothorax. (A) Hemothorax and pneumothorax seen on upright chest radiograph. Black arrow indicates fluid level and blunting of costophrenic angle from hemothorax. White arrow indicates pleural line and apical pneumothorax. Outlined arrows indicate the presence of multiple rib fractures which are likely the cause of the hemopneumothorax. (B) Inset of left lung apex from above, illustrating the presence of the pleural line (white arrow) and the apical pneumothorax.
  • 57. 204 B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 Fig. 8 (continued) Tension pneumothorax Frequency/incidence The major cause of tension pneumothorax is trauma. The incidence of tension pneumothorax from trauma is approximately 10% in severe blunt thoracic injuries. Approximately 5% of pa- tients who present with simple pneumothorax develop a tension pneumothorax when placed on positive pressure mechanical ventilation [21]. Signs and symptoms Tension pneumothorax is a life-threatening entity, and a high degree of clinical suspicion must be employed, especially in patients with traumatic injuries or after procedures in which pneumothorax may occur. Unilateral decreased breath sounds and contralateral tracheal devi- ation may be present but are usually late findings. Progressive dyspnea, tachycardia, and hypo- tension can occur, and the patient’s clinical condition may deteriorate rapidly to the point of cardiorespiratory arrest.
  • 58. B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 205 Etiology/pathophysiology Tension pneumothorax occurs when the pleural injury causes air to enter the pleural cavity during inspiration and a one-way valve effect prevents this air from escaping. With progressive inspiration, the pneumothorax increases in size, and this can cause significant mediastinal shift with impaired cardiac venous return and hemodynamic collapse. Image of choice The diagnosis of tension pneumothorax should ideally be made from clinical evaluation, because even a minor delay (such as obtaining a chest radiograph) may be lethal. Nonetheless, tension pneumothorax can be readily visualized on chest radiograph. Image hallmarks Significant collapse of the pulmonary parenchyma is clearly seen (Fig. 9). Shift of the trachea (arrow) and mediastinal structures to the contralateral side may be present. In severe cases, the entire mediastinum may be shifted into the contralateral hemithorax. Management Immediate needle decompression of tension pneumothorax can be life saving. Thoracostomy tube placement should then be instituted, and further management of the pneumothorax should be undertaken when the patient is stable (see section on pneumothorax). Fig. 9. Left tension pneumothorax. Note the complete collapse of the left lung parenchyma with tracheal deviation to the right (arrow).
  • 59. 206 B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 Pulmonary contusion Frequency/incidence Pulmonary contusion is a frequent sequela of blunt chest trauma, and usually is evident on radiographic examination within 6 hours of the initial trauma. It is most often associated with rib fractures, flail chest, and sternal fractures and can occur in up to 56% to 70% of patients with severe blunt chest trauma [14]. Signs and symptoms The most common symptoms of pulmonary contusion are usually related to the associated chest injuries. Thus, pain from rib fractures, sternal fractures, or soft tissue contusions may be the initial symptoms. Patients may also present with dyspnea and tachypnea. Physical exami- nation findings may include ecchymosis over the involved chest wall, point tenderness of the rib cage from associated bony injuries, and decreased breath sounds on the injured side. In cases of severe pulmonary contusion, hypoxemia and significant alveolar-arterial gradient on arterial blood gas examination may also be present. Etiology/pathophysiology The initial traumatic event leads to leakage of blood and edema fluid into the interstitial and alveolar spaces. This leads to alveolar collapse and extravasation of blood and plasma into the alveoli. Inadequate ventilation of the injured lung parenchyma can lead to significant ventila- tion-perfusion mismatch and arterial hypoxemia. Image of choice The preferred imaging modality for detection of pulmonary contusion is a chest radiograph. Image hallmarks The hallmark of pulmonary contusion is an increased density of the affected lung parenchy- ma, which results from the alveolar and interstitial edema (Fig. 10). The presence of associated chest trauma, such as rib fractures, is common and is generally located in the proximity of the pulmonary contusion. These findings are usually present within 1 hour of injury; however, in as many as 30% of patients, radiographic evidence of pulmonary contusion may not be apparent until several hours later. Management The management of pulmonary contusion largely consists of respiratory support. Supple- mental oxygen, pulmonary toilet, and adequate pain control are some initial measures that can be utilized. Significant pulmonary contusion may require intubation and mechanical venti- lation. Ventilatory maneuvers to treat hypoxia are similar to those methods used to treat ARDS (see following section). Pain management issues may be especially important in cases where rib fractures are present (see section on rib fractures). Acute respiratory distress syndrome (ARDS) Frequency/incidence ARDS is a subset of acute lung injury (ALI), a pathophysiologic syndrome with a range of severity and outcomes rather than a single disease. The exact incidence of ARDS is difficult to determine; however, there are distinct risk factors (see Etiology/pathophysiology), which
  • 60. B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 207 Fig. 10. Right upper lobe pulmonary contusion. predispose patients to the development of ARDS, and in these patients, the incidence of ARDS may be as high as 40% with associated mortalities of up to 90% in some studies [22–24]. Signs and symptoms Most patients demonstrate similar clinical and pathologic features, irrespective of the etiol- ogy of ALI. During the acute phase (first 24 hours), there are limited signs and symptoms of ARDS, with a relatively normal physical examination and chest radiograph. During the next 48 hours (latent period), there is often an observable increase in the work of breathing and mi- nor abnormalities on physical examination and chest radiograph. After a few days have passed, acute progressive respiratory failure is common, with decreases in oxygenation and lung com- pliance and the development of the characteristic diffuse infiltrates on chest radiograph. Finally, in severe cases of ARDS, marked severe hypoxemia refractory to standard ventilatory man- agement, increased intrapulmonary shunting, and associated organ dysfunction may be present [24]. Etiology/pathophysiology There are many associated risk factors for the development of ARDS, including aspira- tion, sepsis, shock, massive hemorrhage, and large-volume transfusion of blood products. Trauma-associated injuries, such as long bone fractures, fat embolism, pulmonary contusion, head injury, and multiple transfusions, are also risk factors for the development of ARDS. Other less common risks for ARDS include inhalation of smoke or toxic gases, near drowning, and drug ingestions. The pathophysiology behind the development of ARDS is increased alveolar- capillary membrane permeability, which causes acute interstitial and alveolar edema. Although the exact mechanisms of these permeability changes are not known, the marked increase in extra- vascular lung water results in a picture of ‘‘noncardiogenic’’ pulmonary edema, which is a hall- mark of ARDS. As the syndrome progresses, aggregates of plasma proteins, cellular debris, and fibrin adhere to the denuded alveolar surface, forming hyaline membranes, and the alveolar septum thickens over the next 3 to 10 days as it is infiltrated by proliferating fibroblasts, leuko- cytes, and plasma cells. Eventual fibrosis of the alveolar septa and hyaline membranes can oc- cur. Although these histologic changes are characteristic of ARDS, not all patients with the
  • 61. 208 B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 syndrome progress through this entire pathologic process. Some patients will recover within sev- eral days and never develop fibrosis, while others progress to end-stage fibrotic lung disease. Image of choice The most common imaging modality used to assess patients with respiratory distress is the plain radiograph. Image hallmarks Findings of ARDS can be difficult to distinguish from other causes of respiratory compro- mise, primarily cardiogenic pulmonary edema. In general, however, bilateral diffuse infiltrates extending to the periphery of the lung fields are ARDS hallmarks (Fig. 11). The absence of findings that are characteristic of cardiogenic edema, such as enlarged heart size or central edema, may also support the diagnosis of ARDS. Nonetheless, many of these radiographic find- ings will overlap, and clinical correlation is necessary. Management Underlying causes of ARDS, such as infection, shock, or traumatic injury, should be identi- fied and treated. The remainder of treatment largely consists of supportive ventilatory care. One cornerstone of therapy is the use of positive end-expiratory pressure, which results in a decrease in physiologic shunt fraction and recruits unventilated tissue into the well-aerated zone. Com- monly accepted ventilatory techniques used in the treatment of ARDS include minimizing tidal volumes and peak pressures in an effort to recruit dependent, collapsed alveoli while avoiding overdistension and the repeated opening and closing of airways [23]. Changes in the ventilatory mode, such as the use of pressure-controlled ventilation and prone positioning, are other tech- niques that may also be beneficial in the treatment of ARDS. Fig. 11. Acute respiratory distress syndrome (ARDS). Note the presence of bilateral diffuse infiltrates which are a hallmark of this disease.
  • 62. B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 209 Mediastinitis Frequency/incidence Acute suppurative infection of the mediastinum, regardless of the cause, is associated with great mortality. The most common cause of acute mediastinitis is esophageal perforation. Cur- rently, 77% of these esophageal perforations arise from endoscopic procedures, with only a small percentage occurring after vigorous emesis (Boerhaave syndrome). The mortality rate from esophageal disruption is 10% to 50%, and can be higher if the injury is not immediately diagnosed and treated [25]. Other forms of mediastinal infection can originate in the oropharynx and descend into the mediastinum, and mortality rates for descending necrotizing mediastinitis are greater than 50% [26]. Less common causes of mediastinal infections include penetrating trauma and postsurgical infections. Signs and symptoms Classic symptoms of esophageal injury consist of severe chest pain, often acute, occurring after esophageal instrumentation or an episode of severe emesis. This pleuritic chest pain may be exacerbated by breathing or coughing, and can be associated with dysphagia, fever, and vary- ing degrees of airway obstruction resulting from dissection of large amounts of air and acute inflammation within the mediastinal fascial planes. Patients with mediastinitis arising from in- fection in the oropharynx present with dysphagia, limitation of motion, and insidious neck pain. Other symptoms include fever, mild leukocytosis, neck stiffness, anorexia, odynophagia, regur- gitation, nasal obstruction, swelling of glands, snoring, and dyspnea. Because the mediastinal fascial planes are contained, infection spreads rapidly causing stridor and respiratory obstruc- tion. Within hours, signs of systemic toxicity, including fevers, chills, and hypotension, may be present. Etiology/pathophysiology Infectious agents can gain entry into the mediastinal space through violation of the esophagus, tracheobronchial tree, or chest wall. Because the fascial planes of the mediastinum are well de- veloped, infection can spread rapidly in these compartments, causing rapid systemic toxicity and clinical deterioration. Posterior involvement of the mediastinum can suggest tuberculous or pyogenic spinal infections. Postoperative complications after cardiac intervention are often re- lated to poor flap construction and sternal instability. Descending necrotizing mediastinitis arises from oropharyngeal infections (eg, odontogenic, peritonsillar, or retropharyngeal), which spread through the retropharyngeal space and other fascial planes to enter the mediastinal space. Image of choice There are several images that can be useful in the detection of mediastinitis. In cases where esophageal perforation is suspected, an upright chest radiograph may show signs of mediastinal air. Gastrograffin swallow may also confirm the diagnosis and delineate the extent of injury. In cases of mediastinitis where an oropharyngeal source is suspected, CT scan of the neck may be useful in determining the location of the original infection and the extent of mediastinal violation. Image hallmarks Hallmarks of mediastinitis on plain radiograph include the presence of air in the mediasti- num (Fig. 12). Mediastinal widening and air-fluid levels may be seen, and pneumothorax or hydropneumothorax may be present, especially if the infection has entered the pleural cavity. Extravasation of contrast on swallowing study is seen with esophageal perforation. A CT scan of the neck and chest may show mediastinal air, fluid, or soft tissue stranding, which suggests inflammation.
  • 63. 210 B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 Fig. 12. Mediastinal air (arrows) seen in a patient with esophageal perforation. Management Broad-spectrum aerobic and anaerobic antibiotic therapy should be started immediately, but surgical treatment of the underlying factors is usually necessary, especially in cases of severe in- fections. For infections that are located above the fourth thoracic vertebra, standard transcer- vical mediastinal drainage may be adequate. When the infection is extensive, an aggressive combination of transcervical, subxiphoid, or transthoracic drainage is indicated. In the face of airway compromise, a tracheostomy should be performed if the patient displays signs of res- piratory distress. References [1] Brooks-Brunn JA. Postoperative atelectasis and pneumonia: risk factors. Am J Crit Care 1995;4:340–9. [2] Shevland JE, Hirleman MT, Hoang KA, et al. Lobar collapse in the surgical intensive care unit. Br J Radiol 1983;56:531–4. [3] Mattison LE, Coppage L, Alderman DF, et al. Pleural effusions in the medical ICU: prevalence, causes, and clinical implications. Chest 1997;111:1018–23. [4] Gotsman I, Fridlender Z, Meirovitz A, et al. The evaluation of pleural effusions in patients with heart failure. Am J Med 2001;111:375–8.
  • 64. B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211 211 [5] Marel M, Zrustova M, Stasny B, et al. The incidence of pleural effusion in a well-defined region. Epidemiologic study in central Bohemia. Chest 1993;104:1486–9. [6] Glezen WP, Denny FW. Epidemiology of acute lower respiratory disease in children. N Engl J Med 1973;288: 498–505. [7] Bradley SF. Influenza in the elderly: prevention is the best strategy in high-risk population. Postgrad Med 1996;99:138–9, 143–9. [8] Gharib AM, Stern EJ. Radiology of pneumonia. Med Clin North Am 2001;85:1461–5. [9] Marston BJ, Plouffe JF, File TMJ, et al. Incidence of community-acquired pneumonia requiring hospitalization. Results of a population-based active surveillance study in Ohio. The Community-Based Pneumonia Incidence Study Group. Arch Intern Med 1997;157:1709–18. [10] Centers for Disease Control and Prevention . Guidelines for prevention of nosocomial pneumonia. MMWR Morb Mortal Wkly Rep 1997;46:1–79. [11] Jimenez P, Torres A, Rodriguez-Roisin R, et al. Incidence and etiology of pneumonia acquired during mechanical ventilation. Crit Care Med 1989;17:882–5. [12] Metlay JP, Kapoor WN, Fine MJ. Does this patient have community-acquired pneumonia? Diagnosing pneumonia by history and physical examination. JAMA 1997;278:1440–5. [13] Ziegler DW, Agarwal NN. The morbidity and mortality of rib fractures. J Trauma 1994;37:975–9. [14] Gaillard M, Herve C, Mandin L, et al. Mortality prognostic factors in chest injury. J Trauma 1990;30:93–6. [15] Winchell RJ. Trauma, definitive care phase: chest injuries. In: Greenfield LJ, Mulholland MW, Oldham KT, Zelenock GB, Lillemoe K (editors). Surgery, scientific principles and practice (3rd edition). Philadelphia: JB Lippincott; 2001 p. 320–33. [16] Kulshrestha P, Iyer KS, Das B, et al. Chest injuries: a clinical and autopsy profile. J Trauma 1988;28:844–7. [17] Light RW, Broaddus VC. Pneumothorax, chylothorax, hemothorax, and fibrothorax. In: Murray J, Nadel J, Mason R, Boushey H (editors). Textbook of respiratory medicine (3rd edition). Philadelphia: WB Saunders; 2000 p. 2501–66. [18] Shorr RM, Crittenden M, Indeck M, et al. Blunt thoracic trauma. Analysis of 515 patients. Ann Surg 1987;206: 200–5. [19] Madiba TE, Thomson SR, Mdlalose N. Penetrating chest injuries in the firearm era. Injury 2001;32:13–6. [20] Vasquez JC, Castaneda E, Bazan N. Management of 240 cases of penetrating thoracic injuries. Injury 1997;28:45–9. [21] Light RW. Tension pneumothorax. Intensive Care Med 1994;20:468–9. [22] Fowler AA, Hamman RF, Good JT, et al. Adult respiratory distress syndrome: risk with common predispositions. Ann Intern Med 1983;98:593–7. [23] Hudson LD, Milberg JA, Anardi D, et al. Clinical risks for development of the acute respiratory distress syndrome. Am Rev Respir Crit Care Med 1995;151:293–301. [24] Foner BJ, Norwood SH, Taylor RW. The acute respiratory distress syndrome. In: Civetta JM, Taylor RW, Kirby RR, editors. Critical care. 3rd edition. Philadelphia: Lippencott-Raven; 1997. p. 1825–39. [25] Craddock DR, Logan A, Mayell M. Traumatic rupture of the esophagus and stomach. Thorax 1968;23:657–62. [26] Lalwani AK, Kaplan MJ. Mediastinal and thoracic complications of necrotizing fasciitis of the head and neck. Head Neck 1991;13:531–9.
  • 65. Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 Ultrasonographic imaging of head and neck pathology Ralf Schon, DDS, MD*, Jurgen Duker, DDS, MD, ¨ ¨ ¨ Rainer Schmelzeisen, DDS, MD Department of Oral and Maxillofacial Surgery, Albert-Ludwigs-University, Klinik und Poliklinik fur ¨ Mund-Kiefer-Gesichts Chirurgie, Hugstetter Straße 55, D-79106 Freiburg im Breisgan, Germany This article demonstrates the properties of sonographic images for the diagnosis of soft tissue pathologies in the head and neck. Ultrasonography in medicine has been used as an imaging technology since 1950. Developments in computer technology have allowed modern ultrasound machines to produce real-time high-quality images of soft tissues; however, limitations must be considered. A total reflection of sonographic waves on bone and a complete extinction behind air-filled cavities, such as the oral cavity and the paranasal sinus, limit the sonographic investi- gation to soft tissues. Ultrasonography is recommended as the first imaging technique of choice for suspected soft tissue pathology in the head and neck. It is noninvasive, inexpensive, quick to perform, and can easily be performed in children and pregnant women. Unlike with computed tomography (CT) and magnetic resonance imaging (MRI), injectable contrast media or sedation in infants (both requiring intravenous tube placement) is not needed for sonography. Typical indications for sonographic evaluation in the head and neck include infection, cysts, salivary gland diseases, neck masses, and neoplasms. In the head and neck, a 7.5-MHz scanner is routinely used for sonography. Sonographic images in B-mode (brightness mode) show the texture and borders between tissues as a black- and-white picture. Color duplex sonography allows the visualization of moving tissues, such as blood cells. Relative movement toward the scanner is color-coded red and relative movement away from the scanner, blue. The visualization of tissue perfusion, such as in hyperemia in in- flammatory changes, vascularization of tumors, and for the evaluation of the location of blood vessels relative to pathologic findings, adds valuable diagnostic information to the B-mode picture. Dynamic sonographic evaluation techniques demonstrate in real time mobility and compressibility of the investigated tissues. Color Doppler mode allows for the quantitative eval- uation of the perfusion in larger vessels. The interpretation of sonographic images for head and neck surgeons not used to sono- graphic images may be initially difficult because the sonographic images are not produced in de- fined axial and coronal planes, such as those known for CT and MRI. A basic knowledge of the sonographic anatomy of the head and neck is required for the understanding of sonographic findings. Typical effects in sonographic imaging such as echo enhancement behind tissues, which causes lower attenuation compared with the surrounding tissues (such as in pleomorphic adeno- mas of salivary glands or cystic lesions) or total reflection of the sonographic waves with a shad- owing effect behind strong reflectors, eg, bone or stones of the salivary glands, may be evident. These effects can be used to interpretate the ultrasonographic image. This article presents sonographic images of typical pathologic findings in the head and neck and correlates these pathologies with the clinical picture. * Corresponding author. E-mail address: schoen@zmk2.ukl.uni-freiburg.de (R. Schon). ¨ 1061-3315/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 6 1 - 3 3 1 5 ( 0 2 ) 0 0 0 0 9 - 4
  • 66. 214 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ Sialolithiasis of salivary glands Frequency/incidence The most common cause of salivary obstruction is the formation of intraductal sialolith. Sialoliths are most frequently found in the submandibular gland (Fig. 1A) [1]. Signs and symptoms Patients present with recurrent swelling, which usually occurs during eating and drinking. Typical chronic changes of the gland may occur after some years (Fig. 2D). Etiology/pathophysiology Formation of viscous mucous plaques can occur in the ducts and may result in the obstruc- tive changes [1]. Mineralization of plaques causes firm stone-like sialoliths (Fig. 1A, B). Image of choice for diagnosis Because it is noninvasive, easy to apply, and inexpensive, sonography is the first imaging method of choice for diagnosis of suspected salivary gland disease. Depending on the degree of mineralization, sialoliths may show in X rays (Fig. 1A) [2]. Sialography gives indirect infor- mation on the presence of a stone in the ductal system, and obstructive changes within the gland may be obvious. Stones of the submandibular glands are often located at the posterior border of the mylohyoid muscle (Fig. 1A). Fig. 1. Intraductal sialolith of the submandibular gland is demonstrated in sialography. (A) Contrast media in the intraglandular ductal system shows the obstruction within the gland caused by the stone located posterior to the mylohoid muscle. (B) In B-mode sonography, the stone is obvious as a strong reflector with a posterior shadowing effect. (C) Inflammatory reaction in sialolithiasis with hyperemia of the submandibular gland is evident in color duplex sonography.
  • 67. R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ 215 Fig. 1 (continued ) Image hallmarks The sialolith shows a strong echo caused by the complete reflection of the ultrasonic wave. Posterior to the sialolith, the echo is extinguished, and a shadow posterior to the stone is present (Fig. 1B). Hyperemia as inflammatory reaction of the gland tissue is demonstrated by color du- plex sonography (Fig. 1C). Management The preferred therapy is the surgical removal of the stone. Removal from an intraoral root is possible when the stone is located in the anterior part of the submandibular or parotid duct. If a stone is located below the mylohyoid muscle, the submandibular gland has to be removed to- gether with the stone by a submandibular approach. Care has to be taken not to harm the lin- gual nerve, which crosses over the duct.
  • 68. 216 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ Sialadenitis Frequency/incidence Acute sialadenitis most often affects the submandibular gland rather than the parotid and mi- nor salivary glands. The frequency of acute exacerbation of a chronic infection of the salivary gland increases with the degree of obstructive changes of the gland tissue. Signs and symptoms Acute sialadenitis leads to a massive swelling of the affected gland (Fig. 2A). Pus may be found on palpation of the salivary gland at the exit of the duct. The skin overlying the affected gland is usually swollen and red. Patients complain of massive pain, and mouth opening can be limited. Etiology/pathophysiology Sialadenitis can be caused by radiation and viral or bacterial infection. Acute streptococcus staphylococcus sialadenitis arises by retrograde infection in an obstructed gland. Degeneration of acina is seen along with interstitial inflammatory cell infiltrates [1]. Multiple or single abscesses may form in acute glands (Fig. 2E). Changes in the immune system or electrolytes may also cause inflammation of the salivary glands. Image of choice for diagnosis Color duplex sonography is the imaging method of choice for the diagnosis of sialadenitis. Image hallmark In the sonographic image, the gland is massively enlarged in side comparison. Hyperemia of the acute gland is seen in color duplex sonography (Fig. 2B). A chronic recurrent infection Fig. 2. (A) Acute sialadenitis with swelling of the left parotid gland. (B) Color duplex sonography shows hyperemia of the massively enlarged gland. In chronic sialadenitis, hyperemia is less obvious compared with findings in acute sialadenitis. (C) A swelling of the right parotid gland is less obvious in a patient with chronic parotitis. (D) Pathological changes of the salivary gland tissue with multiple microabscesses caused by recurrent sialadenitis is evident in sonography and (E) sialography.
  • 69. R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ 217 Fig. 2 (continued ) with less massive enlargement of the parotid gland presents with irregular echogenic structures within the gland (Fig. 2C). Microabscesses and sclerotic changes of the gland appear as multiple hypoechoic or inhomogeneous lesions (Fig. 2D). Further information on pathologic changes within the gland may be gained by sialography (Fig. 2E). Management The management of acute infection is antibiotic therapy. After recurrent infections with per- manent changes of the salivary gland, tissue removal of the gland becomes necessary.
  • 70. 218 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ Fig. 2 (continued ) Salivary retention cyst Frequency/incidence After injury or abscess of the parotid gland, saliva may be retained within the gland.
  • 71. R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ 219 Signs and symptoms Symptoms of a salivary retention cyst is nonpainful swelling with fluctuation (Fig. 3A). Image of choice for diagnosis Sonography, using B-mode for the demonstration of cystic lesions, is the imaging method of choice. Image hallmarks The salivary retention cyst has a regular border and an hypoechoic echo. The lesion is com- pressible with the transducer (Fig. 3B). Enhancement of the sonographic echo posterior to the cyst is seen. Management The management of a salivary retention cyst is surgical, with removal or drainage. Drainage of the cyst into the duct system or the oral cavity can be performed under intraoperative sono- graphic guidance. Pleomorphic adenoma Frequency/incidence Pleomorphic adenoma is the most common benign salivary gland tumor, with the highest in- cidence in the parotid gland. Most pleomorphic adenomas arise in women in their 30s and 40s. Fig. 3. (A,B) A patient with a fluctuating swelling of the left parotid gland without signs of acute infection shows a cystic lesion in the sonographic picture. The space occupying the hypoechoic lesion shows a regular border and is compressible. (B) Enhancement of the sonographic echo posterior to the cyst is evident.
  • 72. 220 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ Fig. 3 (continued ) The second most common salivary gland tumor is the Whartin tumor (papillary cyst adenoma lymphomatosum), which occurs more frequently in men. Whartin tumor is often present in both parotid glands [1]. Signs and symptoms The tumor presents as a firm mobile swelling of the gland. The adenoma is usually painless and does not affect the facial nerve. The growth of the tumor over a period of several months is often reported by patients. Etiology/pathophysiology The pleomorphic adenoma derives primarily from myoepithelia—sometimes adipose, chon- droid, and osseous elements may be present in these tumors. The pleomorphic adenoma shows a slow growth with a minor risk for malignant transformation [1]. Image of choice for diagnosis With typical patient history, tumor location, and palpation of the tumor, B-mode sonogra- phy is the imaging method of choice. Image hallmarks The lesion presents as a hypoechoic mass with a regular border and cannot be compressed. The echo enhancement posterior to the lesion is typical (Fig. 4). In Whartin tumor, a polycystic appearance of the lesion may be seen sonographically.
  • 73. R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ 221 Fig. 4. The noncompressible hypoechoic intraparotid mass is preauricularly located and presents a regular border. Posterior echo enhancement, a typical sign in pleomorphic adenoma, is less obvious compared with fluid-filled cystic lesions. Management The management of suspected pleomorphic adenoma is surgical. Histological findings such as malignancies may define further treatment. Malignant neoplasm of the parotid gland Frequency/incidence The more common malignancies of the salivary glands are mucoepidermoid carcinoma (28%), acinus cell carcinoma (23%), adenocarcinoma (16%), and adenocystic carcinoma (9%) [3]. Epithelial malignancies of the salivary glands are less common and the most common site is the parotid gland. Signs and symptoms Patients present with an induration or swelling of the gland, which is often painful (Fig. 5A). In contrast to benign lesions, malignancies of the parotid gland may present with facial nerve palsy. Etiology/Pathophysiology Malignant tumors of the major glands are typically invasive. Some low-grade malignancies may derive from surrounding tissues. Most often, the malignancies arise de novo. The malignant transformation of benign neoplasms is rare [1].
  • 74. 222 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ Fig. 5. (A) A patient presented with a painful swelling of the left parotid gland. A beginning weakness of the orbicular branch of the facial nerve was noted. (B) MRI in axial and coronal view demonstrated the invasive growth of an adenocystic carcinoma of the parotid gland. (C) In sonography, the neoplasm of the salivary gland shows an irregular border and an inhomogeneous echo pattern with unechoic, hypoechoic, and echodense structures. Micronerve reconstruction of the facial nerve using a sural nerve graft was performed immediately after surgical removal of the tumor. Secondarily, a deepithelialized parascapular flap was used for tissue augmentation. Monitoring of the buried flap was performed by color duplex sonography. (D) The postoperative appearance of the patient 24 months after tumor resection, postoperative radiation, and 6 months after soft tissue augmentation. Image of choice for diagnosis The imaging method of choice for primary evaluation of a swelling in the area of the parotid gland is sonography (Fig. 5C). Further information on the extent of a tumor or the infiltration of the neighboring anatomic structures may be gained by CT and/or MRI (Fig. 5B). Image hallmarks Malignant tumors of the salivary glands show an irregular border and an inhomogeneous echo pattern with unechoic, hypoechoic, and echodense structures. There may be dorsal shad- owing and dorsal signal enhancement behind the lesions (Fig. 5C). The infiltration of adjacent anatomic structures with invasion of muscles or destruction of the ascending ramus of the man- dible is visible by sonography (Fig. 5C). Management Surgical management is the therapy of choice. Depending on the extent of the tumor and the pathohistologic findings after tumor resection, radiation and/or chemotherapy may be indicated (Fig. 5D).
  • 75. Fig. 5 (continued )
  • 76. 224 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ Fig. 5 (continued ) ¨ Intraparotid lymph nodes in Sjogren syndrome Frequency/incidence Intraparotid lymph nodes may be present in Sjogren syndrome. Benign lymphoid epithelial ¨ lesions of Sjo ¨gren syndrome are less common than Whartin tumor. The disease predominately affects middle-aged women. Lymphomas may develop in the setting of Sjogren syndrome. ¨
  • 77. R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ 225 Signs and symptoms Visible swelling in the parotid gland area may be present (Fig. 6A). Xerostomia is usually the main oral symptom; dry eyes is the main ocular symptom. Etiology/pathophysiology Sjogren syndrome, also known as sicca syndrome, is a chronic, progressive autoimmune dis- ¨ ease characterized by lymphocyte infiltration of the salivary and lacrimal gland with loss of the secretory epithelium. Parotitis can be caused by periductal and acinal infiltration. Sjo ¨gren syndrome may present as primary or secondary disease with other autoimmune disorders, such as rheumatoid arthritis [4]. Image of choice for diagnosis Sonography is the imaging method of choice for the diagnosis of swelling in the area of the salivary glands. The diagnosis of Sjogren syndrome is verified by Schirmer test to evaluate the ¨ lacrimal secretion and pathohistologic evaluation of the mucosal specimen. Image hallmarks Intraparotid groups of lymph node tissues with hyperemia are visualized by color duplex sonography (Fig. 6B). Fig. 6. (A) A patient with Sjogren syndrome presented with a swelling in the area of the parotid gland. (B) Color duplex ¨ sonography demonstrates multiple intraparotid lymph nodes with hyperemia.
  • 78. 226 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ Management The treatment of this autoimmune disease is based on the patient’s symptoms. Replacement of saliva and tears may limit mucosal injury caused by reduced secretion. In severe cases, ste- roids and immunosuppressive agents are indicated [2]. Malignant lymphoma Frequency/incidence Neoplasms originating in lymphatic tissue can occur at any age, although the highest inci- dence occurs in patients aged 60 to 70 years. Manifestation of malignant lymphomas in the cervical and inguinal lymph nodes is common. Signs and symptoms Patients may present with reduced general condition, with fever, loss of weight, and anemia; however, patients are often asymptomatic. Swelling of lymph nodes in single or multiple loca- tions may be present (Fig. 7A). Etiology/pathophysiology Malignant lymphomas comprise histologically different diseases of the lymphatic tissues, such as Hodgkin and non-Hodgkin lymphomas. The cause of malignant lymphomas is not clearly understood, although it may be related to a viral factor. An increase of incidence in HIV-positive patients has been reported. Image of choice for diagnosis For the evaluation of cervical lymph node enlargement, sonography is the imaging method of choice. Other imaging techniques, such as CT and MRI, are indicated for staging purposes and for the evaluation of extended neoplasms, which can infiltrate bone. The diagnosis is verified by pathohistologic evaluation. Image hallmarks An enlargement of one of multiple lymph nodes may be present. Lymphatic tissue or groups of lymph nodes may show hyperemia. Margins in-between the lymph nodes and to the sur- rounding tissues may not be defined (Fig. 7B). Management The histologic finding defines the treatment of choice and the prognosis. The oncologic ther- apy with chemotherapy and/or radiotherapy, depending on the histopathologic finding, is the first line of treatment. Surgical intervention may be indicated in rare cases. Thyroglossal duct cyst Frequency/incidence Thyroglossal duct cysts (TDCs) are usually not apparent at birth. The majority of lesions are diagnosed in the first 20 years of life.
  • 79. R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ 227 Fig. 7. (A) A patient presented with an asymptomatic swelling in the left canine fossa. The swelling was treated as a suspected odontogenous infection by a dental practitioner with repeated incisions for 6 months. (B) In color duplex sonography, a well-vascularized neoplasm without clear margins was evident. A highly malignant B-cell lymphoma was diagnosed after biopsy. (C) The extend of the tumor with infiltration of the maxillary sinus is demonstrated in CT.
  • 80. 228 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ Signs and symptoms TDCs are typically located in the midline between the hyoid bone and the thyroid cartilage. A swelling of the anterior floor of the mouth may be present (Fig. 8A). Etiology/pathophysiology The thyroglossal duct connects the foramen cecum and the developing thyroid. The duct usu- ally atrophies after the thyroid descends to its final position. Parts of the duct may be persistent and become cystic in nature. Malignancies may develop in TDCs [5]. Image of choice for diagnosis The cystic formation in the midline can be investigated by noninvasive sonography. The lesion can also be demonstrated by CT with contrast media (Fig. 8B). Image hallmarks A hypoechoic cystic mass in the midline of the anterior floor of the mouth is demonstrated pre- and postoperatively (Fig. 8C,D). The lingual artery is seen next to the cystic lesion (Fig. 8E). Management Surgical removal of the cyst is recommended. Sublingual infection formation Frequency/incidence Abscess formation in the submandibular space with perimandibular abscess formation is more common than sublingual abscess formation. Signs and symptoms Firm painful swelling of the floor of the mouth and in the sublingual area is found in sublin- gual infection (Fig. 9A). The mouth opening may be limited. The clinical diagnosis of an early sublingual abscess or infiltration of the floor of the mouth may be difficult to make because fluc- tuation is not always present. Etiology/pathophysiology The most common cause for sublingual and perimandibular abscess formation is odonto- genic infection. Nonodontogenic causes include cystic lesions, sialadenitis, lymphadenitis, or soft tissue injuries. The infection may spread from the submandiblar space into the sublingual space because of the connection at the posterior aspect of the diaphragm oris. Image of choice for diagnosis After diagnosis of the underlying odontogenic cause using X ray, such as panoramic views, the presence of an abscess can be investigated by sonography.
  • 81. R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ 229 Fig. 8. (A) A patient presented with a nonpainful swelling in the midline of the anterior floor of the mouth. (B) CT performed with contrast prior to referral of the patient demonstrates the lesion located in the midline. (C) The sonographic images in two planes with the transducer placed in a vertical and horizontal position in the submental area demonstrate the cystic lesion preoperatively and (D) after surgical removal. (E) The lingual artery is seen postoperatively in power mode.
  • 82. 230 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ Fig. 8 (continued ) Image hallmarks Hyperemia of the left sublingual area without signs of abscess formation is demon- strated in an acute inflammatory reaction. The transducer is placed in a vertical and horizontal position to produce images in two planes (Fig. 9B). Management The treatment of choice may differ concerning the degree of the infection. When there is no sign of abscess formation, treatment of the underlying dental cause and antibiotic treatment are indicated. Drainage of an abscess by intraoral or extraoral incision is needed when an abscess has already formed.
  • 83. R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ 231 Fig. 8 (continued ) Second branchial cleft cyst Frequency/incidence The second branchial cleft cyst (BCC) represents approximately 95% of all BCCs. The first BCC represents approximately 1% of these cysts [6]. Signs and symptoms The swelling in the midportion of the anterior aspect of this sternocleidomastoid muscle can be palpable and visible (Fig. 10A). Recurrent swelling in this area may be present because of inflammation. Etiology/pathophysiology Anomalies may develop in the development of the first, second, and fourth branchial arches. Image of choice for diagnosis Soft tissue anomalies can be seen using sonography. Image hallmark A fluid-filled, unechoic, compressible cystic process is demonstrated next to the carotid ar- teries using color duplex sonography (Fig. 10B). Management Second branchial and brachial cleft cysts are structural abnormalities and do not resolve spontaneously. Therefore, complete surgical excision is the treatment of choice [5].
  • 84. 232 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ Fig. 9. (A) Firm, painful swelling of the floor of the mouth and in the sublingual area is found in sublingual infection. Noninvasive sonographic investigation can be easily performed in infants and children. (B) Using color duplex sonography with the transducer placed in the submental area, hyperemia as a sign of the inflammatory reaction without abscess formation was evident. Cervical lymph node metastasis Frequency/incidence Most lymph node metastasis in the head and neck region originate from squamous cell car- cinomas. Metastatic disease of other neoplasms, such as malignant melanoma, prostate and breast adenocarcinoma, or tumors of unknown primary origin, are less common.
  • 85. R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ 233 Fig. 10. (A) A patient presented with a swelling of the midportion of the sternocleidomastoid muscle. (B) A fluid-filled unechoic cystic process is demonstrated next to the carotid arteries by color duplex sonography. The compressibility of the cystic lesion was seen when compression was applied with the transducer. Signs and symptoms Cervical swelling, which can be painful, may be present (Fig. 11A, Fig. 11D). Etiology/pathophysiology Cervical lymph node metastasis is frequently found in patients with squamous cell carcinoma of the oropharyngeal cavity. Carcinomas of other origin may cause also nodal metastasis (Fig. 11D, E). Image of choice for diagnosis Sonography has a high accuracy for the demonstration of pathologic findings of cervical lymph nodes compared with CT and MRI. Image hallmarks The echo-free central aspect of a lymph node metastasis is a typical sign for central necrosis in the tumor mass (Fig. 11B). Compression or infiltration of the internal jugular vein or infiltra-
  • 86. Fig. 11. (A) A patient presented with cervical swelling on the right side. (B) Color duplex sonography demonstrates a lymph node metastasis with central necrosis and compression of the internal jugular vein. (C) Cervical metastasis in another patient with infiltration of the internal jugular vein is evident in color duplex sonography. (D) A patient presented with a swelling with a similar clinical appearance as that in (A). (E) Color duplex sonography shows a well- vascularized tissue, a metastatic disease of a thyroid carcinoma.
  • 87. R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ 235 Fig. 11 (continued ) tive growth of lymph node metastasis may be an important prognostic findings (Color Fig. 11B, C). A high degree of vascularization is not typical for metastasis of squamous cell carcinomas but can be present in other neoplasms, such as thyroid malignancies (Fig. 11D, E). Management Tumor resection is the treatment of choice. Pathohistologic findings after ablative tumor sur- gery and neck dissection may indicate radiotherapy and/or chemotherapy. Glomus vagale tumor Frequency/incidence Approximately 3% to 5% of all paragangliomas originate from the vagus nerve. The female to male ratio is approximately 3 to 1, and the mean age of patients is 48 years [7].
  • 88. 236 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ Signs and symptoms Patients with glomus tumours present with a slow-growing painless neck mass; pulsation of the mass may be palpable. When the tumor is located in the pharyngeal area, bulging of the lateral pharyngeal wall may be present. In extensive cases where the recurrent laryngeal nerve and hypoglossal nerve are involved, paralysis of the soft palate and a back-drop phenom- enon of the posterior pharyngeal wall may be evident. Vagal nerve paralysis with hoarseness and aspiration may develop [7]. Etiology/pathophysiology Paragangliomas show a unique anatomic feature. The cervical tumor forms finger-like pro- jections, which may invade fissures and foramens of the skull base. Bone as well as dura may be infiltrated and destroyed. Image of choice for diagnosis The cervical tumor can be detected using sonography (Fig. 12A); however, for the diagnosis and further evaluation of the tumor when located next to the skull base, medial to the mandible, and near the pharyngeal, MRI and MR angiography are recommended to demonstrate the ex- tend of the tumour and the degree of its vascularization (Fig. 12B, C). Image hallmarks A highly vascularized tumor next to the carotid artery is demonstrated using color duplex sonography (Fig. 12A). The extend of the tumour with bulging of the lateral pharyngeal wall and the vascularization are demonstrated in MRI, MR angiography, and conventional catheter angiography for preoperative immobilization (Fig. 12B–D). Management The surgical removal of the tumor is indicated because tumor growth causes further destruction of bone as well as dura. The tumor can be approached by submandibular incision. Temporary osteotomy of the mandible to access the superior pharyngeal space may be necessary. When an intracranial extension of the tumor is present, a craniotomy for the complete removal of the lesion and the involved dura is indicated. After complete resection, recurrence is rare [8]. Embolization prior to tumor resection is recommended be- cause bleeding of the tumor is a possible complication. There is a risk of damage to cranial nerves, the hypoglossal, and the facial nerve when the tumor is located next to the jugular foramen [8]. Hemangioma Frequency/incidence With an incidence of 3% in newborns and a development in the first 3 months of infancy, hemangioma is the most common congenital lesion. Almost 12% of 1-year-olds present with a hemangioma. The head and neck are the most common sites for the development of heman- gioma [5].
  • 89. R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ 237 Fig. 12. A patient presented with an asymptomatic right cervical swelling. (A) Using color duplex sonography, a well- vascularized tissue was obvious next to the carotid arteries. (B,C) MR angiography and conventional catheter angiography during preoperative embolization show the vascularization of the tumor.(D) MRI demonstrates the extend of the infiltrative growing tumor with bulging of the lateral pharyngeal wall.
  • 90. 238 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ Fig. 12 (continued ) Signs and symptoms Hemangioma can appear as cutaneous skin lesions, subcutaneous masses, or both, as com- pound lesions. Cutaneous lesions appear as erythematous masses. Subcutaneous lesions can present as soft, cystic, and compressible lesions with bluish discoloration of the overlying skin (Fig. 13A). The high degree of perfusion may be palpable and audible. Etiology/pathophysiology Hemangiomas may develop from arrested mesenchymal vascular primordial and are there- fore true congenital malformations rather than neoplastic processes. They usually grow rapidly until the age of 6 to 8 months. They then slowly and spontaneously resolve over the next years. Fifty percent of hemangiomas are resolved by the age of 5 years, 70% by the age of 7 years, and almost all will spontaneously resolve by the age of 12 years [9,10]. Image of choice for diagnosis Sonography is the imaging technique of choice because it is noninvasive and easy to perform in infants without sedation or the use of contrast media.
  • 91. R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ 239 Fig. 12 (continued )
  • 92. 240 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ Image hallmarks Color duplex and color Doppler sonography allow for the qualitative and quantitative anal- ysis of the vascularization within the lesion (Fig. 13B, C). The depth of soft tissue infiltration of the lesion can be measured. The results can be used for close follow-up and monitoring of the growth, especially during the first 8 months. Management Hemangiomas tend to involute spontaneously. Therefore, observation and sonographic fol- low-up of the lesion is indicated. Approximately 10% to 30% of hemangiomas require treatment Fig. 13. (A) Subcutaneous hemangioma of the left cheek presents in a 5-month-old patient as soft, cystic, compressible lesions with bluish discoloration of the overlying skin. (B) The high degree of perfusion, which may be palpable and audible, and the depth of infiltration of the lesion is demonstrated by color duplex sonography. (C) Color Doppler sonography allows for the qualitative and quantitative analysis of the vascularization pattern in the lesion.
  • 93. R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241 ¨ 241 Fig. 13 (continued ) because of threatening function, or potential disfiguration or obstruction. Extensive surgery with or without preoperative embolization may be indicated. Because of surgical removal of the infiltrative growing hemangioma, there may be disturbance of normal growth or damage of vital structures. To avoid damage, control of the lesions by systemic or intralesional steroids are the first line of therapy. Laser treatment has also been used [5,11]. Radiotherapy can cause malignancies and is therefore obsolete. References [1] Ellis GL, Auclair PL, Gnepp DR. Surgical pathology of the salivary glands. Philadelphia: WB Saunders; 1992. [2] Langlais RP, Kasle MJ. Sialadenitis: the radiolucent ones. Oral Surg Oral Med Oral Pathol 1975;40:686–90. [3] Eversole L. Salivary gland pathology. In: Fu Y-S, et al, editors. Head and neck pathology with clinical correlation. New York: Churchill Livingstone; 2001. p. 242–90. [4] Campbell SM, Montanaro A, Bardana EJ. Head and neck manifestations of autoimmune disease. Am J Otolaryngol 1983;4:187–216. [5] Kellman RM, Freije JE. Clincal considerations for non-neoplastic lesions of the neck. In: Fu Y-S, et al, editors. Head and neck pathology with clinical correlations. New York: Churchill Livingstone; 2001. p. 665–9. [6] Cote DN, Gianoli GJ. Fourth branchial cleft cysts. Otolaryngol Head Neck Surg 1996;114:95. [7] Uruquhart AC, et al. Glomus vagale: paraganglioma of the vagus nerve. Laryngocope 1994;104:440. [8] Samii M, Draf W. Surgery of the skull base. An interdisciplinary approach. Berlin: Springer; 1989. p. 414–25. [9] Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics. Plast Reconstr Surg 1982;69:412. [10] Philipps SE, Constantino PD, Houston GD. Clinical considerations for neoplasms of the oral cavity and oropharynx. In: Fu Y-S, et al, editors. Head and neck pathology with clinical correlations. New York: Churchill Livingstone; 2001. p. 472–3. [11] Waner M, Suen JY, Dinehart S. Treatment of hemangiomas of the head and neck. Laryngoscope 1992;102:1123.