Common Organ Injuries

Head Injury

Traumatic brain injuries are a significant cause of morbidity and mortality among patients sustaining trauma, particularly from motor vehicle crashes and falls. According to the Brain Injury Association of America, 1.5 million Americans sustain a traumatic brain injury (TBI) each year, ranging from mild concussions to fatal brain injuries.10 From 1995 to 2001 there were over 1.1 million emergency department visits, 235,000 hospitalizations, and 50,000 deaths attributed to TBI.11,12 Falls are the leading cause of TBI in children from 0 to 4 years and in adults 75 years or older, but motor vehicle— traffic causes still result in the greatest number of TBI-related hospitalizations and deaths. Assaults account for about 11 percent of annual TBI-related emergency department visits, hospitalizations, and deaths. It is estimated that 80,000-90,000 people annually experience the onset of long-term disability as the result of TBI. The cost of TBI is estimated to be $48.3 billion each year in the United States.13

The primary mechanisms of head injury include concussion, compression, deceleration, and rotational acceleration. These mechanisms can account for a number of different pathologic conditions associated with head injury, including skull fracture, concussion, brain contusion, extradural hematoma, subarach-noid hemorrhage, and diffuse axonal injury (DAI). Skull fractures may be linear or stellate, depressed or nondepressed, and may involve the cranial vault or the skull base. Basilar skull fractures may be associated with cerebrospinal fluid (CSF) leak and a higher risk for subsequent meningeal infection.

Concussion is a transient loss of consciousness that may not be associated with apparent tissue injury or neurologic deficit, although retrograde and/or antegrade amnesia is not an uncommon finding.

Cerebral contusion, or intracerebral hematoma, typically occurs in the frontal or temporal lobe and is characterized by localized tissue injury and hemorrhage. It may lead to further bleeding, elevated intracranial pressure (ICP), or posttraumatic seizure disorder.

In addition to intracerebral hematoma, intracranial hematomas may be subdural (beneath the dura) or epidural (between the skull and dura) (Fig. 2-4). Acute subdural hematomas generally are due to rupture of bridging veins between the brain and dura, whereas epidural hematomas are typically due to arterial laceration, most notably the middle meningeal artery where it crosses underneath the temporal bone. Subdural hematomas are more common, are frequently associated with underlying cerebral contusion, and the prognosis

Figure 2-4 (A) CT scan images of an acute subdural hematoma and (B) a lens-shaped epidural hematoma (asterisks). The subdural hematoma is also associated with an intraparenchymal brain contusion in the right parietal area.

is worse than for epidural hematomas because of the associated brain injury. Epidural hematomas have been classically described as producing a lucid interval in which the patient initially loses consciousness (concussion), then recovers, and finally develops progressive neurologic deterioration as the lesion expands.

DAI is a generalized shear-type injury involving axons in the brain white matter. Damaged axons are typically interspersed among normal axons and may show up on CT scan as petechial hemorrhage. MRI scanning, however, is more sensitive than CT for detecting DAI. A wide spectrum of clinical presentations—and neurologic outcomes—may result from DAI.

It is important to conduct a thorough neurologic evaluation when assessing a patient for TBI. The GCS score, as previously described, provides an objective clinical measure of the extent of the brain injury based on the patient's best eye opening, verbal, and motor responses (Table 2-4). Frequent reevaluation of a patient's neurologic status is imperative to ascertain neurologic deterioration that may require neurosurgical intervention.

Diagnosis of TBI is best accomplished by noncontrasted CT scan. This will identify any areas of hemorrhage, as well as skull fractures, retained missile fragments, and evidence of generalized brain edema or midline shift.

Prevention of secondary brain injury due to decreased perfusion and hypoxemia of the brain is of paramount importance during the initial management of TBI. Cerebral perfusion pressure (CPP), defined as the difference in mean arterial pressure (MAP) and ICP, should be kept at least at 70 mmHg. Thus, the management strategy necessarily involves controlling systemic blood pressure as well as ICP. Systolic hypotension to less than 90 mmHg has been shown to be associated with a worse neurologic outcome in patients with TBI. Such patients should be resuscitated, as any trauma patient, with crystalloid solutions and perhaps even hypertonic saline solution to maintain MAP and decrease cerebral edema. Once hypovolemia is corrected, the judicious use of vasopressors may be required to maintain the MAP in the desired range. ICP monitoring, as well as mechanical ventilation, is generally indicated for severe TBI, and may be accomplished with an intraparenchymal ICP monitor or with a ventriculostomy catheter. The latter method also allows for drainage of CSF. ICP should be kept below 20 mmHg. First-line treatments to lower the ICP include elevation of head to 30°, hyperventilation to PCO2 of 30-35 mmHg to decrease intracerebral vascular volume, and administration of mannitol, an osmotic diuretic, to reduce brain edema.14 Additionally, patients with moderate to severe TBI should receive prophylactic anticonvulsant medication. There is no role for corticosteroids in the management of TBI.15

Indications for operative intervention include increasing neurologic impairment or a mass effect causing more than 5 mm midline shift. Additionally, depressed skull fractures may need to be elevated or debrided.

If the ICP is controllable with the methods outlined above and the clinical status is stable, continued close observation is indicated.

Spine and Spinal Cord Injury

Spinal cord injury has an incidence of about 11,000 new cases each year in the United States. The average age at the time of injury is 38 years, and 78 percent of SCI occur in males. Motor vehicle crashes account for about half of the injuries, while falls are responsible for 24 percent, acts of violence cause 11 percent, and recreational sporting activities comprise about 9 percent of SCI.16

SCI can be categorized as complete or incomplete. An incomplete injury is one in which there is any degree of sensory or motor function below the level of the injury. Incomplete quadriplegia is the most common lesion, occurring about 35 percent of the time, followed by complete paraplegia (25 percent), complete quadriplegia (22 percent), and incomplete paraplegia (18 percent).16 A diagnosis of a complete SCI cannot be made with certainty during the first few days following injury because of possible confounding spinal shock. Spinal shock is a reversible condition that refers to muscle flaccidity and are-flexia seen not infrequently after SCI. It is differentiated from neurogenic shock, which is due to interruption of descending sympathetic pathways, producing vasodilatation, bradycardia, and hypotension.

Incomplete SCI may also be associated with several syndromes, including the central cord syndrome, Brown-Sequard syndrome, and anterior spinal cord syndrome. The central cord syndrome, the most common of these syndromes, is characterized by greater motor loss in the upper extremities than in the lower extremities; sensory loss is variable. It commonly occurs as a hyperextension injury (e.g., a fall forward) in a patient who has cervical spondylosis and spinal canal narrowing. The Brown-Sequard syndrome is uncommon following trauma, usually with penetrating injuries to the spine. This syndrome clinically manifests as motor loss on the side ipsilateral to the lesion and pain and temperature loss on the contralateral side. The anterior spinal cord syndrome is due to trauma or ischemia in the territory of the anterior spinal artery. Motor, pain, and temperature sensation are lost, but posterior column functions of vibration, position, and deep pressure sense are preserved. It has the worst prognosis for recovery of the incomplete syndromes discussed.

Patients, sustaining significant trauma, who have neck or spine tenderness, distracting injuries, or altered mental status due to injury or substance abuse, must be evaluated further for spine or SCI. They must remain immobilized in a cervical collar and logrolling precautions should be undertaken. A complete physical examination should be carried out, paying particular attention to any spine tenderness, deformities, and sensorimotor examination. Sacral sparing, or preservation of some perianal sensation, and the presence or absence of a bulbocavernosus reflex should be documented.

The presence of either of these findings indicates an incomplete SCI, hence a better prognosis.

Radiographic evaluation of spine and SCIs is evolving. In the past, multiple plain radiographs were used to identify fractures or subluxation. More recently, CT scanning of the cervical, thoracic, and lumbar spine with coronal and sagittal reformats have become popular due to greater sensitivity compared to plain films.17-19 MRI is usually reserved to detect soft tissue lesions, such as a herniated disk, a spinal epidural hematoma, or spinal cord contusion, that are less likely to be diagnosed with CT scan in patients with neurologic deficits. The stability or instability of spine fractures must be determined before removing spinal or logrolling precautions. This may entail further radiologic imaging, such as flexion and extension films of the cervical spine, to determine if ligamentous injury, in addition to skeletal injury, has occurred.

Airway management principles should be followed, as is the case with any trauma patient. Inline stabilization of the cervical spine must be done in preparation for orotracheal intubation. Patients with high- or midlevel cervical SCI may have respiratory insufficiency due to loss of diaphragm and/or accessory muscle function. These patients may become ventilator-dependent and are at high risk for infectious pulmonary complications.

The use of corticosteroids for SCI is somewhat controversial, but should be considered for patients who have sustained a blunt, nonpenetrating, mechanism of injury. Data from the National Spinal Cord Injury studies indicate that neurologic outcome is improved (though slightly) if steroids are given intravenously within the first 8 h of injury. Methylprednisolone is given as a bolus dose of 30 mg/kg, followed by an infusion of 5.4 mg/kg/h. If given within 3 h of injury, the infusion should last for 24 h. If given between 3 and 8 h after injury, the infusion should be continued for 48 h. The immunosuppressive effect of high-dose steroids must be weighed against the potential benefit, particularly if the steroids are to be continued for 48 h.20-22

Surgical management of spine and SCIs may be indicated to decompress the spinal cord and to stabilize an unstable axial skeleton. Once subluxation is reduced, the involved vertebrae may be operatively fused using a number of techniques incorporating bone graft, plates, and screws. External braces, such as the halo vest, may also be used to immobilize the spine without surgical intervention.

Neck Injury

The high concentration of vital structures in the neck makes the evaluation of neck injuries somewhat problematic. Consideration must be given to injuries of the aerodigestive tract, cervical vascular structures, nerves, and the cervical spine. Unfortunately, symptoms and signs may be absent or poorly predictive of injury, for example, to the esophagus, carotid, or vertebral arteries. Thus, a high index of suspicion must be maintained and multiple diagnostic modalities may be required to exclude occult injuries.

Blunt injuries to the neck are usually due to direct blows, deceleration and stretch-type mechanisms, or strangulation. Cervical spine injuries must be ruled out by careful examination, radiographic study, or both. The neck should be kept immobilized in a cervical collar until evaluation of the cervical spine is complete. Airway injury to the larynx or trachea may present with subcutaneous emphysema, shortness of breath, hemoptysis, hoarseness, or complete airway obstruction. Immediate or early control of the airway by cricothyroidotomy or tracheostomy may be required. Fiber-optic evaluation of the upper airway and the tracheobronchial tree is a useful adjunct to determine the presence or absence of an airway injury.

Blunt esophageal injuries are extremely rare, but the morbidity associated with missed pharyngoesophageal injuries mandates that patients with possible neck injuries should undergo thorough evaluation. Barium or Gastrografin swallow examination should be performed for suspected pharyngoesophageal injury; esophagoscopy should also be considered to further increase diagnostic accuracy.

Blunt cervical vascular injuries to the carotid and vertebral arteries may be completely asymptomatic or may present with a neurologic deficit either immediately or in a delayed fashion. There is likely an under appreciation of the mechanism of injury, usually a sudden deceleration, hyperextension/ neck rotation, or direct compression by automobile safety belts.23 Most blunt injuries to the carotid or vertebral arteries consist of intimal dissection, intramural hematoma, thrombotic occlusion, or pseudoaneurysm formation. Conventional angiography is considered the gold standard method of diagnosis, but the role of CT angiography is evolving.24 The majority of these patients are treated nonoperatively. Systemic anticoagulation is the therapy of choice to prevent thrombus formation, although prospective, randomized data are lacking.25 Endovascular stenting of carotid artery injuries and angioembolization of pseudoaneurysms have also added to the nonoperative management of these injuries.

Penetrating neck injuries from stab wounds or gunshot wounds have historically been classified based on the anatomic zone of injury (Fig. 2-5). Zone I injuries are those near the thoracic inlet, below the level of the cricoid cartilage. From a practical standpoint, such injuries cannot be accessed surgically by a cervical incision and require sternotomy or thoracotomy. Zone II injuries are those from the level of the cricoid cartilage to the angle of the mandible. Zone III injuries are those that occur above the angle of the mandible.

Zone I injuries are associated with injuries to the tracheobronchial tree, esophagus, and the great vessels. Evaluation of these structures by bron-choscopy, barium swallow/esophagoscopy, and angiography or CT angiog-raphy is indicated.

Figure 2-5 Zones of the neck used to classify penetrating neck wounds. (Source: Adapted from Wilson RF, Diebel L. Injuries to the neck. In Wilson RF, Walt AJ, eds., Management of Trauma: Pitfalls and Practice, 2nd ed. Baltimore, MD: Williams & Wilkins, 1996: 270-287.)

The diagnosis and management of Zone II injuries are controversial.26 In the past, mandatory exploration of Zone II penetrating injuries was advocated for all wounds that disrupted the platysma. However, the negative exploration rate was as high as 67 percent, and the morbidity of a negative neck exploration was not insignificant.27,28 The advantage of mandatory neck exploration is close to 0 percent missed injury rate and possibly a reduction in hospital costs associated with obtaining multiple diagnostic studies. Presently, a selective surgical approach is generally indicated, reserving operative neck exploration for injuries found on examination or by diagnostic study and, perhaps, for high caliber or bilateral Zone II gunshot wounds to the neck. If a policy of selective surgical management is followed, it is imperative that diagnostic studies are promptly available to rule out aerodi-gestive tract and vascular injuries. The expanded use of CT scanning, including CT angiography, as a screening modality to evaluate the carotid and vertebral arteries, as well as the aerodigestive tract, may limit the need for other, conventional, diagnostic studies.

Finally, Zone III injuries are high in the neck, usually precluding operative intervention. Injuries to consider in Zone III are to the carotid and vertebral arteries, thus, either CT angiography or conventional arteriography is indicated.

Thoracic Injury

Thoracic injuries, whether from penetrating or blunt mechanisms, account for significant morbidity and mortality following trauma. It is likely that thoracic injuries, such as traumatic aortic injury, tension pneumothorax, and cardiac tamponade, are a major cause of mortality in patients who die at the scene of injury or prior to arrival at the hospital.29

Evaluation of a patient following chest injury must be expeditious. Cardiogenic or hemorrhagic shock and respiratory failure may ensue quickly after sustaining traumatic chest injuries. Injuries that must be immediately considered in an unstable patient after arrival to the emergency department include tension pneumothorax, cardiac tamponade, massive hemothorax, traumatic aortic injury, and diaphragmatic rupture.

Tension pneumothorax should be a clinical, not a radiographic, diagnosis in the majority of cases. Tension pneumothorax occurs when lung or open chest wall injury results in an accumulation of air in the pleural space under pressure as the result of a one-way valve phenomenon. The lung on that side totally collapses, and the pressure in the hemithorax causes the mediastinum to shift to the opposite side. Cardiac diastolic filling is impaired, resulting in cardiogenic shock. Diagnosis of tension pneumothorax is made by the observation of respiratory distress, tachycardia, hypotension, distended neck veins, and unilateral absence of breath sounds. Immediate treatment is needle decompression of the affected hemithorax by a large bore needle in the second intercostal space in the midclavicular line. This maneuver decompresses the tension component of the pneumothorax and allows for the placement of a thoracostomy tube as the definitive treatment of the pneumothorax.

Cardiac tamponade is another entity to consider in an unstable patient following chest trauma. Beck's triad, consisting of hypotension, distended neck veins, and muffled heart sounds, is the classic description of cardiac tamponade, but it is not uncommon for the complete triad to be absent.30 Hypovolemia due to blood loss, for example, may result in flat neck veins, even in the presence of tamponade. The finding of pulsus paradoxus, whereby the systolic pressure falls by more than 10 mmHg with inspiration, is another sign of cardiac tamponade, but may be difficult to ascertain in the emergency setting. Ultrasound may be a very useful diagnostic adjunct to evaluate for fluid in the pericardial sac, but it should not delay resuscitation or intervention. Pericardiocentesis using a subxiphoid approach may be life-saving in instances of cardiac tamponade. Thoracotomy or median ster-notomy are best performed in the operating room for definitive diagnosis and treatment.

Massive hemothorax may occur following penetrating or blunt trauma. Signs and symptoms of unilateral chest injury, such as multiple rib fractures, dullness to percussion, and decreased ipsilateral breath sounds are suggestive of hemothorax, which can be confirmed by a portable chest radiograph.

It is important to keep in mind that several hundred milliliters or more of fluid in the chest cavity are needed to appreciate a significant hemothorax on a supine radiograph. The initial treatment of a hemothorax is a large bore (at least no. 32 or 36 French catheter) chest tube. Most hemothoraces, approximately 90 percent, are treated only with a chest tube and do not require operative intervention. Indications for surgery are (1) greater than 1500 mL out of the chest tube on insertion, or (2) continued chest tube output of greater than 200-300 mL/h for several hours.

Traumatic aortic injury may occur following a deceleration-type injury such as a motor vehicle crash or a fall from a significant height. It is estimated that 16 percent of deaths, due to immediately fatal automobile crashes, are due to rupture of the aorta; it is estimated that approximately 8000 deaths a year in the United States are attributable to great vessel injury.31,32 The most common site of aortic injury following blunt trauma is at the liga-mentum arteriosum just past the takeoff of the left subclavian artery. This location of injury, corresponding with the area of maximal fixation of the aorta, is subject to high shear stress and torsion with deceleration-type mechanisms of injury. A high index of suspicion for aortic injury must be maintained in patients sustaining a significant mechanism of injury. Due to the potential for multiple injuries in patients who present with possible aortic injury, the initial workup consists of an anteroposterior (AP) chest radiograph. Although limited, particularly in obese patients, the chest radiograph may provide important findings that are associated with traumatic aortic rupture (Table 2-7). Helical contrast-enhanced CT scanning of the chest has emerged as a highly sensitive and specific screening test for blunt aortic rupture.33,34 If the CT scan shows no periaortic hematoma or irregularity of the contour of the aorta, aortic injury can be ruled out. Aortography, however, is still considered the gold standard for diagnosis at this time. Figure 2-6 depicts some of the radiographic findings associated with traumatic aortic injury. Patients diagnosed with aortic injury should have their blood

Table 2-7 Findings Associated with Traumatic Aortic Injury on Plain Chest Radiograph

• Widened mediastinum

• Obliteration of the aortic knob and aortopulmonary window

• Deviation of trachea, esophagus, or nasogastric tube to the right

• Depression of left mainstem bronchus

• Fractures of sternum, scapula, first or second ribs

• Widened paratracheal stripe

Figure 2-6 Radiographic findings in traumatic aortic injury. (A) Plain chest radiograph showing a widened mediastinum. (B) CT scan showing intimal flap in the descending thoracic aorta, which is surrounded by hematoma. (C) Aortogram demonstrating aortic disruption distal to the left subclavian takeoff, the usual site for blunt aortic injury.

Figure 2-6 Radiographic findings in traumatic aortic injury. (A) Plain chest radiograph showing a widened mediastinum. (B) CT scan showing intimal flap in the descending thoracic aorta, which is surrounded by hematoma. (C) Aortogram demonstrating aortic disruption distal to the left subclavian takeoff, the usual site for blunt aortic injury.

Figure 2-6 (Continued)

pressure tightly controlled to below a systolic pressure of 110 or 120 mmHg to diminish the chance of in-hospital free rupture and exsanguination. Repair of the aorta is indicated with an interposition graft or, if feasible from a technical standpoint, the more recent method of endovascular stenting.35

Traumatic diaphragmatic rupture with herniation of abdominal viscera into the chest (Fig. 2-7) can also be life threatening. Hemorrhage, torsion of the herniated abdominal contents leading to ischemia, and mediastinal shift from mass effect leading to cardiac failure all must be considered in the acute setting. These injuries should be treated via an abdominal approach to fully assess the extent of abdominal visceral injury.

In addition to the immediately life-threatening thoracic injuries described above, several other specific entities related to blunt or penetrating chest trauma deserve mention. Among these are rib fractures/flail chest, pulmonary contusion, blunt cardiac injury, and transmediastinal gunshot wounds.

Flail chest is defined as an unstable chest wall resulting from fractures to three or more adjacent ribs, with each rib fractured in more than one location. Paradoxical motion of the chest wall occurs during respiration. There is frequently an underlying pulmonary contusion that contributes to respiratory insufficiency and increased work of breathing, necessitating mechanical

Figure 2-7 Plain chest radiograph depicting traumatic diaphragmatic herniation. Note the indistinct left hemidiaphragm and the nasogastric tube extending into the left chest.

ventilation. Treatment involves careful fluid management to prevent fluid overload, vigorous pulmonary toilet to prevent atelectasis and pneumonia, and adequate analgesia, including consideration of a thoracic epidural catheter.

Blunt cardiac injury can rarely result in chamber rupture, valvular disruption, or pericardial tamponade, but more commonly, myocardial contusion occurs. Definitive diagnosis of myocardial contusion can be established only by pathology, but the clinical diagnosis is inferred by ECG changes, including conduction abnormalities and arrhythmias, and echocardiogra-phy, which may be indicated to look for wall motion abnormality. Most arrhythmias will manifest in the first 24 h following injury, so patients should be placed in a monitored setting during this time period.36

With regard to penetrating trauma, transmediastinal gunshot wounds may be associated with injuries to multiple structures, including the heart and great vessels, lung parenchyma, tracheobronchial tree, esophagus, bones, and spinal cord. Helical CT scanning is a useful test to help define the missile tract and specific injuries, but it may not obviate the need for further diagnostic tests such as esophagography/esophagoscopy and bronchoscopy.37 Indications for surgery depend on the findings of the diagnostic workup.

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