an atlas of_head_and_neck_images__part_i__2002

Preface

An Atlas of Head and Neck Images, Part I

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 ofwhich 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 themedical 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

Charles Lee, MDRichard H. Haug, DDS

Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) vii–viii

1061-3315/02/$ - see front matter � 2002, Elsevier Science (USA). All rights reserved.

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injury and pathology. It is intendedmerely 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 andneck 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: [email protected]

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: [email protected]

viii R.H. Haug, C. Lee / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) vii–viii

Computed tomography of head injury

Richard H. Haug, DDSa,*, Thomas Pittman, MDb

aDivision of Oral and Maxillofacial Surgery, College of Dentistry, University of Kentucky, 800 Rose Street,

Room D-508, Lexington, KY 40536-0297, USAbDepartment 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 articleprovides 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: [email protected] (R.H. Haug).


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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].

150 R.H. Haug, T. Pittman / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 149–166

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.


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 relatedto venous rather than arterial hemorrhage.



thicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and

Fig. 1. Transtentorial herniation with cisternal obliteration.

151R.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.


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 orcomatose.

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.


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 areno significant obstructions to flow. This accounts for the characteristic crescent-shaped appear-

ance of these lesions.




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.


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.


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

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.


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.



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


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 removedif 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.


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.



thicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and


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 ofinjury (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.

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.


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.


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.

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.






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.


Subarachnoid hemorrhage

Frequency/incidence

Subarachnoid hemorrhage occurs in 7.6% of patients with a CHI associated with facialfractures [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 availableimaging 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.


Either parenchymal contusions or vascular injuries can cause subarachnoid hemorrhage.






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.


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


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.


CT without contrast is the preferred imaging method. CT is performed with 3.0-mm slicethicknesses, along a plane parallel to the orbitomeatal line, beginning at the ring of C1 and end-



Image hallmarks

The CT will identify air (�1000 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.

Fig. 7. Traumatic subarachnoid hemorrhage with contrast media noted in the subarachnoid space. This is the CT of a

patient with a ruptured aneurysm.


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.


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.

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.






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 parenchymalstructures. 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 pressuremonitoring 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.


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.


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 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 coincidentwith facial traumahas 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.



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 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.

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.


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 woundsshould 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


Fig. 11. Cranial fractures are denoted by displacement of the outer table within the inner table.


[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


[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.


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 patientsshould 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 beobserved. Patients will frequently deteriorate when placed in cervical traction. The patient

may be completely neurologically intact and have a good outcome [1].


AOD is caused by violent trauma (typically, motor vehicle collision or pedestrian struckby 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


E-mail address: [email protected] (D. Blades).


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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].


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.

168 T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187

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].


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].


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 onC2. (C) CT scan demonstrating rotation of C1 onC2.

169T. Jackson, D. Blades / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 167–187

Fig. 2 (continued )


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.


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].


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 issignificant 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].


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.


Fig. 3 (continued )

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].


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.


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 methodof 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 bymarked 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].


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].


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.


Plain lateral radiographs identify 95% of cases based on the anterior subluxation of C2 with

respect to C3 [2].

Fig. 4. CT scan demonstrating a Jefferson fracture through the anterior and posterior neural arches of C1.


Fig. 5. (A) Lateral radiograph demonstrating fracture through pedicles of C2. (B) CT demonstrating bilateral C2 pedicle

fractures.


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 anteriorinferior 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].


Burst fractures are secondary to an axial loading injury [13].


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].


Fig. 6. (A) Lateral radiograph of C6 burst fracture. (B) Comminuted burst fracture including bilateral laminar fractures.


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 arerare with compression fractures (neurologic injury would imply instability and a more signifi-

cant injury than a simple compression fracture).


Compression fractures are thought to be caused by flexion/axial loading forces.


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 withcervical 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].



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.

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.



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 jointitself. 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 radiographof unilateral facet andassociated subluxationofC4onC5of approximately 25%of thewidth

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.


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].


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].

Fig. 8 (continued)



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 scanthrough 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 thevertebral 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.


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].


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 tossingit 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.

Fig. 9 (continued)


Fig. 10. (A) C6 spinous process fracture. (B) CT of fracture through spinous process.



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:


[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:



Chest radiography

Betty J. Tsuei, MDa,*, Peter E. Lyu, DDSb

aDepartment of General Surgery, College of Medicine, University of Kentucky,

800 Rose Street, Room C-221, Lexington, KY 40536, USAbDivision 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 upperlobe (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.


E-mail address: [email protected] (B.J. Tsuei).


PII: S 1 0 6 1 - 3 3 1 5 ( 0 2 ) 0 0 0 0 6 - 9



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 lungvolumes.

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

190 B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211

dyspnea, tachypnea, and hypoxia. Decreased basilar breath sounds may be found on physical

examination.


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

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.

191B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211

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.

Fig. 1 (continued)


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.

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, whichare 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.


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 pneumoniais 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 reservedfor 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).


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,

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.


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.


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 maybe 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


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 nosocomialpneumonia 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 pulmonaryinjuries 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.


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

Fig. 4. Bacterial pneumonia resulting in right upper lobe infiltrate.


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, ortwelfth 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. Althoughthere 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.


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.


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 ofthe 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


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.

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 hadsignificant 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. Hemothoraxmay 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.


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 ofhemothorax 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.


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 bothrespiratory and circulatory compromise.


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 intercostalsor 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.

Fig. 7. Left hemothorax presenting with diffusely increased density throughout the hemithorax.


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 bloodmay 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.


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 suspicionmust 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.

Fig. 8 (continued)



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 shiftwith 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).


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.


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 thepulmonary 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 thatcan 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


predispose patients to the development of ARDS, and in these patients, the incidence of ARDSmay 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].


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. Althoughthe 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

Fig. 10. Right upper lobe pulmonary contusion.


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 decreasein 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.


Mediastinitis

Frequency/incidence

Acute suppurative infection of the mediastinum, regardless of the cause, is associated withgreat 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 maybe 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, maybe present.


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.


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.

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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. Sonographicimages 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.


E-mail address: [email protected] (R. Schon).


PII: S 1 0 6 1 - 3 3 1 5 ( 0 2 ) 0 0 0 0 9 - 4


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).


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).


Because it is noninvasive, easy to apply, and inexpensive, sonography is the first imagingmethod 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.

214 R. Schon et al / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 213–241

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.

Fig. 1 (continued )

215R. 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 foundon 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.


Sialadenitis can be caused by radiation and viral or bacterial infection. Acute streptococcus

staphylococcus sialadenitis arises by retrograde infection in an obstructed gland. Degenerationof 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.


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 comparedwith 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.


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 changeswithin 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.

Fig. 2 (continued )


Salivary retention cyst

Frequency/incidence

After injury or abscess of the parotid gland, saliva may be retained within the gland.

Fig. 2 (continued )


Signs and symptoms

Symptoms of a salivary retention cyst is nonpainful swelling with fluctuation (Fig. 3A).


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.


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.


The pleomorphic adenoma derives primarily from myoepithelia—sometimes adipose, chon-

droid, and osseous elements may be present in these tumors. The pleomorphic adenoma shows aslow growth with a minor risk for malignant transformation [1].


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.

Fig. 3 (continued )


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].

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.



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).

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.


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 Sjogren syndrome are less common than Whartin tumor. The disease predominately

affects middle-aged women. Lymphomas may develop in the setting of Sjogren syndrome.

Fig. 5 (continued )


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.


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. Sjogren

syndrome may present as primary or secondary disease with other autoimmune disorders, such

as rheumatoid arthritis [4].


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.


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 thecervical 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).


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.


For the evaluation of cervical lymph node enlargement, sonography is the imaging method ofchoice. 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.


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.


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).


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].


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.


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.


After diagnosis of the underlying odontogenic cause using X ray, such as panoramic views,

the presence of an abscess can be investigated by sonography.


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.


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.

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.


Anomalies may develop in the development of the first, second, and fourth branchial arches.


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].

Fig. 8 (continued )


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.

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.


Signs and symptoms

Cervical swelling, which can be painful, may be present (Fig. 11A, Fig. 11D).


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).


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-

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.


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.

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].

Fig. 11 (continued )


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 ofthe 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].


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 maybe infiltrated and destroyed.


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 cranialnerves, 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].


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.


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.


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].


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.



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 ofthe 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.


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 causemalignancies 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.



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