Chapter 24. Chest Trauma

Up to half of all trauma patients sustain some degree of thoracic injury. Twenty to twenty-five percent of all trauma deaths are directly attributable to chest trauma. Thoracic trauma is a contributing factor in another 25% of trauma deaths.

1This chapter is a revision of Chapter 22 in the 6th edition by Seth Stearley, MD, and L. Richard Boggs, MD.

Establish ABCs

The ABCs should be addressed as previously outlined in Chapters 9 and 10. There are specific considerations in evaluating the ABCs in the patient with blunt or penetrating chest trauma. The airway can be obstructed at any level from the pharynx to the trachea. Abnormalities in breathing can be caused by one or more of the following mechanisms: (1) impairments in the chest wall or musculature, eg, secondary to pain or because the chest wall motion is not coordinated; (2) impairments in gas exchange, secondary to atelectasis, contusion, or disruption of the respiratory tract; and (3) CNS impairments secondary to drugs or head trauma. Hypoxia is the most important feature of chest injury. Early interventions should attempt to insure that an adequate amount of oxygen is delivered to the portions of the lung capable of normal ventilation and perfusion. Abnormalities in circulation can be caused by blood loss, increased intrapleural pressure, blood in the pericardial sac, vascular disruption, or myocardial dysfunction. Since shock will most often be caused by blood loss, the first step should be to ensure adequate fluid resuscitation.

Pain Control

Pain may impair chest wall expansion and impede oxygenation. Pain should be relieved with small frequent doses of narcotic medications, eg, 2–8 mg of morphine or 50–100 μg of fentanyl every 30 minutes as needed. The pain level should be constantly reassessed to ensure adequate analgesia.

Several entities need to be considered in the patient with chest trauma. They can cause severe hypoxia and/or shock. The diagnoses are made clinically and need to be addressed without waiting for any diagnostic testing. Any patient presenting with any one of these entities should be treated as outlined and admitted to the hospital for further care.

Tension Pneumothorax

Tension pneumothorax develops when a one-way valve air leak occurs from either the lung or chest wall. Air enters the pleural space but cannot escape, leading to increased intrapleural pressure, collapse of the lung, and shift of the mediastinal contents to the opposite side. Tension pneumothorax can result from blunt chest injury with resultant parenchymal lung injury, but can also be secondary to positive-pressure ventilation. Occasionally a small penetrating wound can cause a valve-like effect that allows air to enter the pleural space on inspiration but not exit on expiration. The collapse of the lung leads to right to left pulmonary shunting and resultant hypoxia. In addition, increased intrathoracic pressure and pressure on the vena cava can reduce venous return to the heart and lead to decreased cardiac output and shock.

Diagnosis

Pneumothorax is characterized by respiratory distress, tachypnea, and hypoxia. There will be hyperresonance to percussion and decreased or absent breath sounds on the affected side. With tension pneumothorax, the trachea will be deviated away from the affected side. Neck veins may be distended, but this may be absent if the patient is hypovolemic. The diagnosis of tension pneumothorax is made clinically. Patients with a tension pneumothorax need immediate treatment and should not wait for X-ray. Figure 24–1 shows the chest X-ray (CXR) of a patient whose physical examination findings should have lead the physician to perform a needle decompression instead of an X-ray (not the mistake of the authors). For stable patients, in whom a pneumothorax is suspected, diagnosis is confirmed with CXR (Figure 24–2). Besides ultrasonography is quickly becoming an alternative to X-ray for rapid identification of pneumothorax. Reported sensitivity for detection of pneumothorax of 86–98% for ultrasound versus 28–75% for supine CXR makes it a potentially attractive alternative.

Treatment

The treatment for a tension pneumothorax is immediate tube thoracostomy (Chapter 6). If a chest tube is not immediately available, needle thoracostomy with a large-bore (16-gauge or less) needle in the second intercostal space in the midclavicular line will convert the tension pneumothorax into a simple pneumothorax until a tube can be placed. In this instance, the needle should be left in until a definitive chest tube can be placed. Opening the wound further with a gloved finger or a clamp can relieve a tension pneumothorax associated with a penetrating injury. For patients with a simple pneumothoraces secondary to trauma, traditional teaching has been to drain through a tube thoracostomy and admit the patient for observation. However, it has been shown that those with small pneumothoraces detected on CT scan appear at low risk for complications and may not require drainage. In addition, serial observations or simple aspiration have been shown to be safe in patients presenting later or with small simple pneumothoraces.

Open Pneumothorax (Sucking Chest Wound)

Large penetrating wounds of the thorax result in an immediate pneumothorax. There is equilibration between intrathoracic and atmospheric pressure and so negative intrathoracic pressure cannot be generated. Effective ventilation is thus impaired since air goes through the chest wall rather than into the lung resulting in severe hypoxia. The diagnosis is obvious and therapy should be instituted immediately.

Treatment

Management of an open pneumothorax should begin with assessment of the patients ABC's. All patients with a pneumothorax should be placed on 100% oxygen via nonrebreather. An occlusive dressing should be placed over the wound immediately followed by the placement of a chest tube. The occlusive dressing should be large enough to cover the wounds edges. The dressing should be taped on three side allowing air to escape from the pleural cavity but not reenter. Definitive treatment involves chest tube placement and wound closure.

Massive Hemothorax

Injury to the chest wall, great vessels, or lung can result in intrapleural bleeding or hemothorax. By definition, a massive hemothorax is defined by the rapid accumulation of greater than 1000–1500 ml of blood or one-third or more of the patient's blood volume in the chest cavity. Most commonly, a massive hemothorax is secondary to penetrating injury disrupting pulmonary or systemic blood vessels. In hemothorax associated with great vessel injury, 50% die immediately, 25% live 5–10 minutes, and 25% live 30 minutes or longer. Respiratory insufficiency is dependent on how much blood is lost. In massive injury, the affected lung is collapsed producing a right to left shunt. The loss of blood also leads to circulatory compromise.

Diagnosis

Respiratory distress, tachypnea, and variable degree of hypoxia will be present. There will be dullness to percussion and decreased breath sounds on the affected side. Depending on the degree of blood loss, hypotension and flat neck veins may be present. Pulse pressure will be narrow. Small hemothoraces may be difficult to detect on supine patients. Diagnosis is confirmed by CXR (Figure 24–3). Small hemothoraces (<350 mL) are usually visible only as a small effusion on an upright CXR. Moderate effusions (350–1500 mL) will be seen as diffuse increase in opacity on the affected side. Large (>1500 mL) effusions will have a ground glass appearance on the supine film.

Treatment

For the patients presenting with signs of massive hemothorax, tube thoracostomy should be performed immediately without waiting for diagnostic tests. For those with smaller hemothoraces, diagnosis can be confirmed before instituting therapy. Tube thoracostomy using one or two large-bore chest tubes allows for accurate assessment of current and ongoing blood loss. Autotransfusion should be considered for the patients with large bleeds (>1 L). Initial blood loss of more than 1.0–1.5 L or ongoing continuing loss of >200 mL/h for 2–4 hours requires surgery.

Cardiac Tamponade

Cardiac tamponade occurs when arterial, ventricular, or atrial injury causes blood to leak into the pericardium. True tamponade is rare and most often associated with penetrating injuries. The pericardium is acutely not very distensible and tamponade can occur even with a small amount (200 mL) of blood. The increased intrapericardial pressure compresses the heart and decreases cardiac output. In addition, venous return and cardiac filling are decreased. Increased pressure may also lead to a decrease in myocardial perfusion. These factors together lead to a decrease in cardiac output. Hypotension and shock then can result.

Diagnosis

Signs and symptoms of tamponade are nonspecific. Tachycardia and narrow pulse pressure are usually present. Beck's triad of hypotension, muffled heart tones, and distended neck veins is present in a minority of patients with tamponade from blunt trauma. Jugular venous distension may be absent because of coexisting hypovolemia. There are no specific findings on CXR that will confirm the diagnosis. Since tamponade can occur with a small effusion, heart size may not be significantly increased. Bedside focused assessment with sonography for trauma (FAST) examinations (Chapters 6 and 25) are performed in many emergency departments to quickly identify pericardial effusions in blunt and penetrating trauma patients. FAST examinations allow rapid detection of pericardial fluid, with high sensitivity and specificity. An emergency pericardiocentesis or thoracotomy can be lifesaving in an unstable patient with a pericardial effusion. In a stable patient, the diagnosis of pericardial effusion can be confirmed with transthoracic or transesophageal echocardiogram and define the hemodynamic impact. When ultrasound or echocardiography is not available, for the stable patient, CT scan is sensitive for detection of pericardial fluid. Cardiac dynamics are not assessable however.

Treatment

Pericardiocentesis has been advocated in the past as both a diagnostic and therapeutic modality. However there are serious limitations. Pericardiocentesis has been reported to have up to 80% false negatives and 35% false positives. In acute injury, a large part of the pericardial blood may be clotted and therefore not aspirated through even a large-bore needle. Pericardiocentesis may injure the heart or other organs and may cause delays in getting definitive care. With these caveats, in a stable patient, ultrasound-guided pericardiocentesis has been shown to be safe and reliable. In patients who are unstable or in severe shock with signs and symptoms consistent with cardiac tamponade, immediate thoracotomy allows relief of the tamponade and control of myocardial injury.

Flail Chest

Flail chest occurs when a segment of the chest does not have bony contiguity with the rest of the thoracic cage. When negative intrathoracic pressure is generated on inspiration, the flail segment moves inward, thus reducing tidal volume. Usually a significant blunt force is required, eg, motor vehicle collision (MVC) or a fall from a height. The major problem is respiratory failure due to the underlying pulmonary injury.

Diagnosis

The two major symptoms of flail chest are pain and respiratory distress. Tachypnea with shallow respirations secondary to pain will be seen. Paradoxical chest wall movement may not be seen in a conscious patient due to splinting of the chest wall. Crepitus is often present. Even with marked flail chest, the patient may be able to compensate initially for the reduced tidal volume by hyperventilating. When fatigue or underlying pulmonary injury develops, frank respiratory failure may supervene.

Treatment

Supplemental oxygen is the first-line treatment. Pain control with intravenous morphine or fentanyl should be instituted early. Patient controlled administration (PCA) of an opiod infusion is often effective for cooperative patients. Epidural infusion of a local anaesthetic agent provides near complete analgesia allowing the patient to resume normal inspiration and cough without the risk of respiratory depression. The addition of a nonsteroidal may provide adequate relief, but should be withheld until other injuries have been excluded. Consider early intubation and mechanical ventilation in any patient with ongoing hypoxia or significant increased work of breathing. Approximately 50% of patients will need immediate intubation. Indications for early intubation include marked hypoxia, hypercapnea, or inadequate breathing. External chest wall supports (taping, sandbags) reduce pain with movement of the flail segment, but they also reduce vital capacity and may worsen respiratory function and are therefore not indicated. Surgical fixation should only be considered in cases where thoracotomy is being performed for other injuries.

A careful and thorough secondary survey will identify multiple non-life-threatening chest injuries. Their prompt recognition and treatment may lead to an overall reduction in morbidity and mortality.

Pulmonary Contusion

Pulmonary contusions are injuries of the lung parenchyma with hemorrhage and edema without associated laceration. They are the most frequent intrathoracic injuries in nonpenetrating chest trauma. They occur in approximately 30–75% of patients with significant blunt chest trauma. Pulmonary contusions typically occur at the site of impact and are often associated with other thoracic injuries such as rib fractures and flail chest, although they may occur alone. Pneumonia is the most common complication of pulmonary contusion, but their presence is a risk factor for the development of acute respiratory distress syndrome and long-term disability as well. Associated medical conditions, such as chronic obstructive pulmonary disease, increase the likelihood of complications from pulmonary contusion and should lower the threshold for early intubation.

Diagnosis

Pulmonary contusion is often silent during the initial trauma evaluation. Significant traumatic mechanism as well as the presence of other associated thoracic and extrathoracic injuries should raise one's suspicion for the presence of pulmonary contusion. The most important sign of pulmonary contusion is hypoxia. The degree of hypoxemia directly correlates with the size of the contusion. Large contusions will lead to significant respiratory distress. Other clinical findings suggestive of pulmonary contusion include dyspnea, hemoptysis, tachycardia, and other evidence of chest injury such as palpable rib fractures, chest wall bruising, decreased breath sounds, or crackles on pulmonary auscultation.

Radiographic findings by CXR may range from patchy interstitial infiltrates to complete lobar opacification. CXR will initially miss a substantial number of pulmonary contusions, but as a result of ongoing hemorrhage and edema, radiographic evidence of contusion is usually apparent within 6 hours of injury. Since the size of the contusion may help predict the clinical course for the patient, thoracic CT may provide additional useful information. Animal studies suggest that CT will identify contusions in 100% of those with experimentally induced pulmonary injury; therefore, CXR should be followed by CT in the patients where suspicion for undetected injury is high and identification of the injury will alter their management.

Treatment

Early recognition and treatment of pulmonary contusion is essential to preventing long-term complications. The mainstay of treatment is supportive care and consists of the careful use of intravenous fluids so as to keep the patient euvolemic, supplemental oxygen, chest physiotherapy, and if severe, the use of mechanical ventilation with positive end-expiratory pressure.

Disposition

Most patients with radiographic evidence of pulmonary contusion or clinical findings suggestive of pulmonary contusion should be admitted for monitoring and respiratory support. Exceptions to this would include young adults with minor contustions and no underlying pulmonary disease.

Myocardial Contusion

It is estimated that 15–20% of patients sustaining significant thoracic trauma have some degree of cardiac involvement. Myocardial contusions are distinct areas of hemorrhage that are typically subendocardial but may extend transmurally. The right ventricle is most commonly involved due to its proximity to the sternum. Contusions of the myocardium typically produce wall motion abnormalities that may lead to conduction defects, dysrhythmias, or a decrease in cardiac output leading to cardiogenic shock.

Diagnosis

The clinical presentation of myocardial contusion is nonspecific. Patients are often asymptomatic but may complain of chest pain, have subtle ECG changes, or present with hypotension secondary to cardiac dysmotility. Specific standardized criteria for the diagnosis of myocardial contusion do not exist. Studies of blunt trauma patients looking for evidence of cardiac contusion have classically used one or more of the following criteria:

1. ECG—A normal ECG does not exclude the possibility of myocardial contusion, but it is the best screening tool. An ECG should be obtained in all patients with significant thoracic trauma, particularly if there are concomitant injuries such as flail chest, rib fractures, or pulmonary contusion. An ECG should also be obtained in trauma patients complaining of chest pain, with unexplained hypotension, and those with a history of coronary artery disease. The most common finding by ECG in myocardial contusion is sinus tachycardia (ST) followed by nonspecific ST and T wave changes. Right bundle branch block is also commonly seen. A range of dysrhythmias and conduction disturbances may be evident however, including ST elevation, atrial fibrillation, atrial flutter, premature ventricular contractions, ventricular tachycardia, ventricular fibrillation, first-degree heart block, and right bundle branch block. While a normal ECG cannot 100% exclude the presence of a myocardial contusion, the literature suggests that very few patients with normal ECGs develop complications.

2. Biochemical markers—There is much debate in recent literature regarding the value of obtaining cardiac enzymes in the evaluation of the patient with potential myocardial contusion. Creatine kinase MB (CK-MB) is nonspecific for cardiac injury in the setting of trauma and is often elevated in cases of skeletal muscle, diaphragm, liver, or bowel injury. Both Troponin T and Troponin I have been shown to be very specific for cardiac injury in trauma but have poor sensitivity. Cardiac enzymes have not been shown to predict the development of complications or need for hospital admission.

3. Echocardiography—Transthoracic and transesophageal echocardiography should not be used as screening tools for myocardial contusion. They are best used in the evaluation of patients with unexplained hypotension or persistent ECG abnormalities to exclude other potential cardiac injuries such as pericardial tamponade and ventricular rupture. While both studies will identify wall motion abnormalities that are consistent with myocardial contusion, they have not been shown to predict or prevent clinical complications.

Treatment

There is no particular treatment for myocardial contusion other than to treat the potential complications as they arise. Patients should be monitored at all times. Dysrhythmias should be treated as discussed in previous chapters. There is no role for the administration of prophylactic antidysrhythmics. Patients who subsequently develop myocardial infarction should be treated as such, but thrombolytics should not be used in the trauma patient.

Disposition

Asymptomatic stable patients with normal ECGs and no evidence of other thoracic injury may be safely discharged from the emergency department. Elderly patients and those with a history of coronary artery disease, significant blunt thoracic trauma, ECG changes, or hypotension should be admitted for monitoring.

Diaphragmatic Hernia

Diaphragmatic hernias have been reported in 1–5% of patients sustaining blunt chest or abdominal trauma. They result either by direct violation of the diaphragm or significant intra-abdominal or intrathoracic pressure applied to the diaphragm resulting in its rupture. The right side is affected up to three times less than the left because it is relatively well protected by the liver. Up to 50% of these injuries are missed on the initial trauma evaluation, and their delayed presentation may not be clinically significant until herniation of abdominal contents through the diaphragm results in obstruction, incarceration, strangulation, perforation, or even death. Once a tear in the diaphragm occurs, it will not heal spontaneously, allowing for the herniation of abdominal contents into the chest cavity. Delayed presentations of blunt diaphragmatic rupture have been reported up to 50 years after the primary traumatic event.

Diagnosis

Patients with diaphragmatic hernias may be asymptomatic, particularly in the acute phase, or may present with symptoms of bowel obstruction. Delayed presentation is common with nonspecific respiratory or bowel complaints since early diagnosis is difficult to establish and often missed.

1. CXR—The CXR is a valuable screening tool in detecting blunt diaphragmatic rupture. The initial X-ray is interpreted as normal in up to 50% of acute cases but will be abnormal in almost 100% of those with delayed presentations. Findings on an upright CXR suggestive of diaphragmatic rupture include elevation or irregularity of the diaphragmatic border, unilateral pleural thickening, obvious herniation of abdominal contents into the chest cavity, and the presence of a nasogastric tube in the chest cavity (Figure 24–4).

2. CT—CT scans are often used preoperatively in the hemodynamically stable patients but have had less than satisfactory results in reporting isolated diaphragmatic injuries. Right-sided lesions are often missed because the contour of the right diaphragm is difficult to discern from the contour of the liver.

Treatment

Surgical reduction of the hernia and repair of the diaphragm is mandatory in all patients with diaphragmatic rupture. Care should be taken to avoid abdominal injury when placing a chest tube in patients with concomitant hemothorax or pneumothorax.

Esophageal Disruption

Esophageal disruption or perforation is an infrequent injury sustained secondary to blunt trauma. The mechanism of injury is unclear, but most occur during high-speed motor vehicle collisions and are typically associated with other serious thoracic injuries. While their occurrence is rare, the reported mortality is more than 20% because of its resultant complications of mediastinitis, which include pericarditis, pneumonitis, empyema, and even aortic erosion.

Diagnosis

Esophageal injuries are difficult to diagnose. The symptoms and signs are often nonspecific and masked by other serious injuries. It should always be suspected in the patient with evidence of serious neck, thoracic, back, or abdominal injury. Patients may complain of throat pain, dysphagia, odynophagia, hoarseness, choking, chest pain, hematemesis, dyspnea, or continued neck pain despite appropriate treatment and immobilization. Neck redness, swelling, unexplained tachycardia, subcutaneous emphysema of the neck or chest, and bloody nasogastric tube contents may be found on physical examination.

Radiologic signs on CXR suggestive of esophageal injury include pneumomediastinum, widened mediastinum, and left pleural effusion. Gastrograffin followed by barium swallow and esophagoscopy are probably the best diagnostic tools available for the detection of esophageal perforation; however, detailed exploratory surgery may be necessary for definitive diagnosis.

Treatment

Treatment of esophageal perforations depends on the location and the extent of the injury. Nonoperative management with drainage, antibiotics, and nutritional support may be appropriate for select injuries, but most require aggressive surgical management to prevent extensive spread of infection to the mediastinal and pleural cavities.

Aortic Disruption

Traumatic aortic rupture is a common cause of death in blunt trauma. Injury is typically caused by rapid deceleration and shearing forces sustained in motor vehicle accidents, falls, and crush injuries and most commonly involves the descending segment of the aorta just past the origin of the left subclavian artery. More than 80% of patients die at the scene. Another 10–20% of patients with aortic disruption will die within the first hour. Rapid diagnosis and treatment is essential for limiting the mortality associated with these injuries.

Diagnosis

Aortic injury should be considered in all patients involved in rapid deceleration accidents such as motor vehicle collisions at speeds greater than 30 miles/h or falls from greater than 10 feet. Clinical signs and symptoms suggestive of aortic injury include chest pain, back pain, dyspnea, hoarseness, intrascapular murmur, and extremity pain caused by ischemia. Patients may be hypertensive, hypotensive, or may present with pseudocoarctation where the upper extremities are hypertensive and the lower extremities have minimal blood pressure and pulse deficits. Thirty percent of patients with traumatic aortic injury have no external signs of trauma to the chest. Other patient factors that can raise a clinician's index of suspicion for TAI include age >50, unrestrained driver, ejected passenger or pedestrians struck by a motor vehicle.

1. CXR—CXR is a screening tool for blunt aortic injury and is commonly used to determine the need for further studies. Mediastinal widening more than 8 cm is the most commonly cited abnormality on CXR that leads to further workup. Other findings suggestive of aortic injury include indistinct aortic knob, left mainstem bronchus depression, tracheal deviation to the right, nasogastric tube deviation, widening of the right paratracheal stripe (>5 mm), apical capping, and obliteration of the space between the pulmonary artery and the aorta (Figure 24–5). Despite its use as a screening tool, CXRs are normal in 2–5% of patients with aortic injury.

2. Angiography—Angiography has historically been the gold standard for diagnosis of aortic injury but is rarely employed in clinical practice today. Angiography is expensive, time consuming, invasive, and requires a large dye load. Because the clinical indicators for blunt aortic injury are often nonspecific, a large number of negative aortograms have been performed in the past. Over the last decade, CT of the chest has been used in the evaluation of aortic injury with angiography saved for those patients with indeterminant findings by CT.

3. Chest CT—CT is less expensive than angiography and can be performed much more quickly. With the newer-generation scanners and the use of intravenous contrast and consistent protocols, the sensitivity and specificity for aortic injury approaches 100%, particularly when criteria for positive scans include periaortic hematoma along with direct signs of aortic injury.

Treatment

Treatment of blunt aortic injury includes pharmacologic management of blood pressure in combination with prompt surgical or endovascular repair.

Tracheobronchial Injury

Injury to the trachea or bronchus as a result of blunt trauma is relatively uncommon but can be quite severe. Approximately 80% of patients with tracheobronchial injuries die before reaching a hospital. Tracheobronchial injuries are usually the result of motor vehicle accidents and crush injuries. Right-sided bronchial injuries occur more commonly and are typically more severe, while almost 80% occur within 2 cm of the carina. The diagnosis of tracheobronchial injury is missed in at least 25% of patients during the initial trauma evaluation.

Diagnosis

Failure to recognize tracheobronchial injury during the initial trauma evaluation is common. Patients may be comfortable on room air or may present in acute respiratory distress. The most common clinical symptoms and signs suggestive of injury to the trachea or bronchus are dyspnea and subcutaneous emphysema of the neck or upper thoracic region, but may also include hoarseness, hemoptysis, hypoxia, and persistent pneumothorax despite appropriate tube thoracostomy. CXR findings indicative of tracheobronchial injury include subcutaneous emphysema, pneumomediastinum, pneumothorax, and peribronchial air.

Treatment

All patients in respiratory distress with suspected tracheobronchial injury should be endotracheally intubated, preferably over a bronchoscope if time allows. Blind intubation is discouraged as it may result in the complete disruption of small tracheal lacerations. Stable patients with suspected trauma to the trachea or bronchi should undergo immediate bronchoscopy for definitive evaluation and localization of the injury followed by operative repair.

Rib Fractures

Rib fractures are the most common injury sustained in blunt thoracic trauma. They are usually sustained in motor vehicle accidents. Fractures of the first rib usually indicate severe trauma because of the necessary force to produce such an injury. Fractures may cause localized pain, crepitance, pain with inspiration, and dyspnea and may even cause pneumothorax or hemothorax. Mortality increases with the number of ribs involved. The pain associated with rib fractures may lead to hypoventilation, atelectasis, retained secretions, and finally pneumonia.

Diagnosis

CXR is the screening tool of choice for the detection of rib fractures, although up to 50% of rib fractures cannot be detected on CXR. CT scan will often diagnose occult rib fractures. Dedicated rib views of the chest are unnecessary because they are not generally helpful in the management of patients with rib fractures.

Treatment

Rapid mobilization, respiratory support, and pain management are the mainstays of treatment for the patient with multiple rib fractures. Continuous body positioning and oscillation therapy prevent hypoventilation and atelectasis by promoting redistribution of ventilation and perfusion to various lung segments. Mechanical ventilation allows for healing of the ribs and prevention of complications in the patient with respiratory failure. Incentive spirometry is excellent supportive therapy in stable patients. Pain control is paramount in facilitating adequate ventilation. Epidural anesthesia with bupivicaine controls pain without causing sedation and impairing the cough reflex.

Disposition

Young, healthy patients with isolated rib fractures without evidence of other serious underlying injury may be treated with pain medications and deep breathing exercises with incentive spirometry. They do not require routine admittance or serial radiographic studies. Admission should be considered for elderly or other patients with serious underlying lung disease and isolated rib fractures. These patients have a higher complication rate due to a higher prevalence of hypoventilation, atelectasis, and pneumonia.

Sternal Fracture

Most sternal fractures are associated with a direct blow. They are most common in postmenopausal females presumably secondary to osteopenia.

Diagnosis

Pleuritic midline chest pain with focal tenderness over the sternum may be present. There may be some pain with respiration, but there should be no pulmonary compromise. Pulmonary contusions or blunt cardiac injury may accompany sternal fracture and should be considered. A rare complication of sternal fractures is a posterior sternoclavicular dislocation which can result in mediastinal displacement of the clavicular heads with accompanying superior vena caval obstruction.

Treatment

In the absence of complications, therapy for sternal fractures is mainly symptomatic. Give adequate analgesia with narcotics as necessary and encourage deep breathing.

Disposition

Patients with isolated sternal fractures, with no evidence of other injuries, can be safely sent home. Patients with cardiovascular complications should be admitted. Admission should also be considered for patients in whom analgesia cannot be obtained with standard doses of narcotics or those who have limited social support.

Systemic Air Embolism

Lung trauma in which there is laceration of air passages, lung parenchyma, or blood vessels may result in a direct communication between these structures. Air can enter the pulmonary venous system as a result of a gradient caused by low pulmonary venous pressure (hypovolemia) or increased airway pressure (positive-pressure ventilation, tension pneumothorax). Pulmonary venous air embolizes systemically including coronary and cerebral circulation. Air embolization occurs most commonly after penetrating trauma.

Diagnosis

There are several findings that are suggestive of air embolism. Hemoptysis, circulatory, and CNS dysfunction immediately after initiation of positive-pressure ventilation are suggestive. Focal neurologic abnormalities in the absence of head injury are common. Circulatory arrest after the initiation of mechanical ventilation suggests air embolism. Fundoscopic examination may reveal air in the retinal vessels. Air in arterial blood gases (not due to froth) is diagnostic. Transesophageal echocardiography has been suggested as a diagnostic tool.

Treatment

Oxygenation is the first-line treatment. Selective lung ventilation has been advocated as a means of isolating the affected lung and stopping or minimizing the flow of gas into the circulation. Alternatively, high-frequency ventilation has been shown to be effective by allowing decreased ventilatory volumes and pressures. For moribund patients, thoracotomy and clamping of the hilum of the affected lung has been advocated. Cerebral air embolism has been treated with hyperbaric oxygen therapy, but other priorities may preclude or delay its use.

Traumatic Asphyxia

Severe crush injury of the thorax or abdomen can cause retrograde flow of blood from the right heart into the great veins of the head and neck.

Diagnosis

There is purplish-bluish color of the face and neck. Subconjuntival and retinal hemorrhages are common. Intracerebral bleeds are uncommon, but loss of consciousness or neurologic abnormalities can be caused by cerebral hypoxia. The clinical significance of traumatic asphyxia is the possibility of intrathoracic injuries associated with the severe crushing force.

Treatment and Disposition

There is no specific therapy except oxygenation. Other injuries should be treated appropriately. Patients should be hospitalized for observation.

Commotio Cordis

Commotio cordis is the condition of sudden cardiac death or near sudden cardiac death after blunt, low-impact chest wall trauma in the absence of structural cardiac abnormality. Ventricular fibrillation is the most commonly reported induced arrhythmia in commotio cordis. Young male athletes aged 5–18 years are particularly at risk for this catastrophe. It has been described after blows to the chest from baseballs, softballs, hockey pucks, and other objects. Death is usually instantaneous, and successful resuscitation is uncommon.

Penetrating trauma to the chest is usually inflicted by stabbing or gunshot but can include other foreign bodies and impalement injuries as well. Stab wounds commonly injure the ascending aorta while gunshot wounds more typically injure the descending thoracic aorta, although laceration of the pericardium and any of the thoracic great vessels may occur.

Diagnosis

Information regarding the type of weapon, length or caliber of weapon, distance from the weapon, and amount of hemorrhage at the scene can be very helpful when evaluating the patient with penetrating thoracic trauma. Most patients are hemodynamically unstable and a rapid but thorough examination is essential. The ABCs should be addressed first.

During the secondary survey, the patient should be evaluated for signs of vascular injury including unequal blood pressures of the extremities, new vascular bruits, and the classic signs of pericardial tamponade: distended neck veins, muffled heart sounds, and hypotension. A CXR should be obtained immediately to identify pneumothorax, hemothorax, or foreign body. Placing radioopaque markers at the sites of wound entry and exit can be helpful in the interpretation of the CXR. Bedside emergency FAST examinations for the evaluation of pericardial tamponade can be extremely helpful in identifying the need for thoracotomy in the penetrating trauma patient with signs of shock. The same life-threatening and potentially life-threatening injuries described in blunt trauma can occur with penetrating trauma to the chest as well and should be managed as discussed in those sections.

Treatment

Significant shock should be addressed immediately with intravenous fluid boluses and blood transfusion, although there is some data to suggest that aggressive fluid resuscitation may increase the amount of uncontrolled hemorrhage and subsequent mortality. Patients with pericardial tamponade require emergent pericardial window or thoracotomy. Tube thoracostomy should be performed in all patients with evidence of pneumothorax or hemothorax. Autotransfusion is indicated in patients with large hemothoraces. Patients with initial chest tube blood loss exceeding 1500 mL, significant ongoing hemorrhage of >200 mL/h for 2–4 hours, or persistent hypotension should be taken directly to the operating room. Impaled objects should never be removed in the emergency department as they may actually provide tamponade to surrounding vascular structures. Those patients should be stabilized with removal of the object performed in the operating room. Angiography is the gold standard for the evaluation of hemodynamically stable patients at high risk for great vessel injury based on the trajectory of the wound, although CT angiography has increasingly demonstrated reliability.

Asymptomatic patients sustaining low-risk peripheral wounds with normal physical examinations and negative initial CXRs may be safely discharged to home after a 3-hour observation and repeat negative CXR. Those who develop delayed pneumothorax during this observation period require tube thoracostomy and admission.

Role of Emergency Department Thoracotomy

The role of emergency department thoracotomy is controversial. Indications for thoracotomy are (1) penetrating thoracic wound with agonal state or recent loss of vital signs, deterioration or cardiac arrest after care has been initiated, or uncontrolled hemorrhage from the thoracic inlet or out of a chest tube; (2) need for open cardiac massage or occlusion of the descending thoracic aorta to provide increased blood flow to the heart and brain prior to a laparotomy; and (3) suspected subclavian vessel injury with intrapleural exsanguination. Contraindications to thoracotomy include penetrating trauma with no signs of life in the field or blunt trauma with no signs of life on arrival in the emergency department. Thoracotomy is not indicated unless a qualified surgical backup is present.

Emergency department thoracotomy is best used in patients sustaining penetrating thoracic injuries whom have witnessed a cardiopulmonary arrest in the emergency department or lose signs of life during a short transport to the emergency department. Survival rates for cardiac injuries and stab wounds are typically better than noncardiac injuries and gunshot wounds. Thoracotomy for penetrating injuries yields an overall survival rate of approximately 11%.