Thoracic Trauma: What You Need to Know
It is estimated that thoracic trauma accounts for about 20%–25% of all deaths resulting from trauma. Common intrathoracic injuries resulting in death include tension pneumothorax, uncontrolled hemorrhage, airway obstruction and cardiac tamponade.2
The early presentation of severe, life-threatening intrathoracic injury can sometimes be subtle. This article reviews the pathophysiology, clinical exam findings and prehospital management of these injuries, allowing prehospital providers to better anticipate, identify and treat them in the field. For purposes of this article, thoracic trauma will be divided into three classes: chest wall injuries, pulmonary injuries and cardiovascular injuries.
Chest Wall Injuries
An intact thoracic cage is required for adequate ventilation (see Figure 1). Any blunt chest wall injury that results in inadequate ventilation can lead to hypoxia, hypercarbia and eventually acidosis and respiratory failure. Blunt chest wall injuries include rib fractures from a single rib to a flail chest, as well as sternal fractures. Alternatively, penetrating chest trauma can cause hypoxia with hypocarbia as inspiratory pressure is lost.
Rib and Sternal Fractures
Rib fractures are the most common form of significant chest injury, resulting from more than half of cases of blunt trauma to the chest. The issue with a rib fracture is not in the fracture itself; an isolated rib fracture is painful but not life-threatening. The danger with rib fractures lies with the potential for underlying injury such as pneumothorax, hemothorax, cardiac injury, and liver and spleen lacerations.
Fractures to the first three ribs are uncommon, as they are short and stiff and protected by the clavicle, scapula and muscles of the upper chest wall. A fracture to these ribs suggests significant force was transmitted into the thorax, and the risk of intrathoracic injury is high. The presence of two or more rib fractures at any level on the thoracic cage is associated with a higher incidence of internal injuries.
Ribs 4–9 are the most commonly injured because of their exposed position and relative immobility, as they are attached to the sternum anteriorly and the spine posteriorly. Fractures to ribs 9–11 are associated with increased risk of intra-abdominal injury, specifically to the liver and spleen.
Sternal fracture and costochondral separation (separation of the sternum from the ribs) are most often caused by anterior blunt force trauma, the most frequent mechanism being collision of the chest with a steering wheel. In one study, motor vehicle collisions accounted for 68% of all sternal fractures.3 Contrary to intuition, a restrained passenger is more likely than an unrestrained passenger to suffer sternal fracture. The occurrence of sternal fractures has increased threefold since the widespread use of over-the-shoulder seat belts.4 During frontal collisions (which often result in rapid deceleration), the compressive force generated when the anterior chest strikes the seat belt is often significant enough to result in sternal fracture or separation from the ribs.
An isolated sternal fracture has extremely low mortality risk, but this rises rapidly with the presence of associated injuries.2 Associated injuries that contribute to this high mortality include flail chest, aortic injury, pulmonary and myocardial contusions, intra-abdominal injuries and head injury. Because of the heart’s location directly posterior to the sternum, cardiac complications such as myocardial contusion can occur with a fractured or displaced sternum.
History and clinical exam findings
Ask all patients with thoracic trauma about their mechanism of injury. If the patient can’t provide this information, interview bystanders or determine mechanism to the extent possible from clues on scene. Determine any preexisting medical conditions that could possibly complicate the patient’s ability to compensate for developing shock. Examples are the use of anticoagulant or beta-blocking medications along with any past medical history that can be complicated by traumatic insult, such as coronary artery or respiratory disease.
Patients with rib or sternal fractures will typically present with complaints of pain worsening with movement, coughing, inspiration and palpation, dyspnea, and tachycardia. The clinical exam will often reveal crepitus, pain with palpation, and guarding and splinting of the affected area. In addition, compressing the thoracic cage at a location away from the injury site may result in pain at the injury site, as intrathoracic pressure increases and irritates the injury.
Tachycardia will most likely be present because of associated pain; the patient may be tachypneic with a shallow tidal volume, as it often hurts to take deep breaths.
Tachycardia and tachypnea may also signal respiratory compromise from associated pneumo- or hemothorax. Soft tissue injury, such as a contusion, abrasion, erythema, ecchymosis or swelling, may also be present over the fracture site.
If a patient with fractures to the lower rib cage (ribs 9–11) presents with signs and symptoms of shock and does not have signs and symptoms suggesting tension pneumothorax or hemothorax, suspect an intra-abdominal injury (such as to the liver or spleen).
Transport patients with even simple, isolated rib fractures to an emergency department for evaluation. Specific management for rib fractures depends on the degree of respiratory impairment and centers around maintaining normal respiratory function and pain relief. Most often the patient with an isolated rib fracture will require only pain control during their injury management. Giving an IV analgesic such as fentanyl can alleviate the pain; consider it early in patient management. If the patient’s respirations are inadequate or signs of hypoxia exist, administer supplemental oxygen to maintain a pulse oximetry of at least 94%. Utilize positive-pressure ventilation (PPV) as necessary to maintain respiratory function.
Patients with even seemingly benign fractured sternums should receive full spinal immobilization and supplemental oxygen, be placed on cardiac monitors and have large-bore IVs established. Assess their cardiac rhythm frequently for signs of cardiac irritability in the form of PVCs, PACs and dysrhythmias, all signs of cardiac contusion. As with rib fractures, give IV analgesics for pain control if pain interferes with the patient’s ability to breathe adequately.
A flail chest is created when three or more ribs are fractured at two or more places each, creating a freely moving segment of chest wall that moves paradoxically to the rest of the chest. Flail segments can be located anteriorly, laterally or posteriorly, and a flail sternum can result from anterior blunt force trauma that disarticulates the sternum from all the ribs (costochondral separation).
Breathing is affected by flail chest in three ways: The work of breathing is increased, tidal volume is decreased, and pulmonary contusions interfere with respiration. The work of breathing is increased by the loss of integrity of the chest wall and the resulting paradoxical movement of the flail segment. Tidal volume is decreased both by the paradoxical movement of the flail segment compressing the lung on the affected side during inspiration, and also by the patient’s reluctance to take deep breaths because of the pain produced when the flail segment moves. In addition, a flail segment is almost always associated with underlying pulmonary contusion, resulting in atelectasis and poor gas exchange across the alveolar-capillary membrane. All of these factors contribute to developing inadequate respirations and hypoxia.
Clinical exam findings
Patients with a flail chest will have considerable pain with movement and respiration, and will often have obvious soft tissue injury (abrasions, contusions, etc.) over the injured site. Paradoxical chest wall motion is the classic sign of flail chest, but may not initially be present if muscular splinting of the chest wall stabilizes the segment in place. If the patient is intubated and receiving PPV during your clinical examination, paradoxical chest wall movement may not be observable, as PPV “splints” the segment internally. Palpation of the injured area will most likely elicit tenderness or pain. In addition, crepitus and obvious loss of chest wall integrity may be palpated.
Patients with mild to moderate flail chest injury and no signs of respiratory failure can be managed with the administration of high-flow supplemental oxygen, cardiac monitoring and IV initiation with analgesia for pain control. Reducing the pain that accompanies respiration can encourage deeper breaths and increase tidal volume, decreasing the work of breathing and correcting hypoxia. Accordingly, the reduction of pain is of paramount importance in the treatment of flail chest in the conscious patient.
Patients with a flail chest and respiratory distress will likely require PPV with a bag-valve mask, and those with respiratory failure may require endotracheal intubation. PPV will serve to splint the flail segment internally and increase tidal volume, reversing developing hypoxia.
In addition to an intact chest wall, an intact and functioning pulmonary system and intrathoracic environment are required to ensure adequate ventilation. Hypoxia can develop secondary to injuries to the tracheobronchial tree, the visceral or parietal pleura, or the lung itself. Common pulmonary injuries include pulmonary contusion, simple and open pneumothorax, tension pneumothorax, hemothorax and traumatic asphyxia.
A pulmonary contusion is a bruise on the lung parenchyma. Pulmonary contusion is reported to be present in 23% of patients with significant blunt chest trauma, and occurs most often from automobile collisions with rapid deceleration.3 Pulmonary contusions can also occur from the cavitational forces generated when a high-velocity projectile such as a bullet travels through the lung, or secondary to shock waves traveling through water or air, as with an explosion.
Regardless of the mechanism, injury to the lung results in injury to capillaries and the leaking of blood into the lung tissue and alveoli. This collection of fluid in the alveoli interferes with normal alveolar-capillary gas exchange. As the patient attempts to compensate, tachypnea and respiratory alkalosis can occur. Lung sounds may be coarse with rhonchi or even diminished or absent. Tachycardia and eventually shock will ensue if things are not corrected, along with respiratory failure.
A pneumothorax occurs when air collects in the pleural space between the lung and the inside of the chest wall. It is a common complication of blunt and penetrating chest trauma and is present by default in every patient with penetrating injuries that pass through the parietal and visceral pleura. Pneumothoraces are classified as simple, open or tension.
A simple pneumothorax occurs when a hole in the visceral pleura allows air to escape the lung and collect in the pleural space. A simple pneumothorax is most often caused when a fractured rib lacerates the pleura. It may also occur without a fracture when blunt trauma is delivered at full inspiration with the glottis closed (holding your breath), resulting in a dramatic spike in intra-alveolar pressure and alveolar rupture. This mechanism is known as the paper bag syndrome.
An open pneumothorax occurs when a hole in the chest wall and pleura allows air to collect in the pleural space. The violation of the pleural space eliminates the normally negative intrapleural pressure that exists between the lung and chest wall, causing the affected lung to collapse. Air may move in and out of the hole in the chest wall with inspiration, resulting in a sucking chest wound.
A tension pneumothorax occurs when the initial defect in the chest wall or lung acts as a one-way valve, allowing air to enter the thorax with inspiration but not escape with exhalation. With each breath, pressure within the hemithorax increases, further deflating the lung. As pressure continues to increase, the mediastinum is pushed toward the unaffected side. This shift causes the vena cava to kink, resulting in decreased venous return. This creates a chain reaction of decreased preload, decreased stroke volume, decreased cardiac output and, ultimately, decreased blood pressure. Further shifting of the mediastinum will start to interfere with expansion of the lung on the opposite side to the injury, decreasing tidal volume in the healthy lung. Obstructive shock and hypoxia are the results of tension pneumothorax.
Clinical exam findings
A closed pneumothorax may present with obvious soft tissue trauma to the chest wall if blunt force trauma was the cause. An open pneumothorax will present with a penetration in the chest wall; an impaled object may still be in place. Auscultation of lung fields may reveal normal lung sounds in the event of a small pneumothorax, or diminished or absent lung sounds with a larger one. In severe cases tachycardia and tachypnea may present. Pulse oximetry may be normal or decreased, depending on the size of the pneumothorax; often, slight tachycardia and a slightly low SpO2 (92%–94%) are all that accompany a small pneumothorax.
Though the clinical exam findings associated with simple pneumothorax may be fairly unimpressive, the signs associated with a developing tension pneumothorax can be dramatic. Initial anxiety, difficulty breathing, tachycardia and tachypnea will worsen as the affected lung collapses. SpO2 will start to fall, and skin will become increasingly pale, cool and diaphoretic as obstructive shock physiology begins.
If the tension pneumothorax progresses and a mediastinal shift occurs, tachycardia and hypotension will become profound, soon followed by decreased mental status. Lung sounds will diminish on the unaffected side, and JVD will occur as a result of decreased venous return to the heart in the absence of concomitant hypovolemia. Tracheal deviation, if observable at all, is a very late sign and occurs low in the neck. Worsening cyanosis, unconsciousness and eventually death will occur.
Treatment of simple and closed pneumothorax consists of ensuring adequate ventilation and oxygenation. In cases of isolated simple pneumothorax, patients will often be able to maintain their own airway and ventilate adequately. In such cases, administer oxygen by a device that will ensure an SpO2 of at least 94%, place the patient on the cardiac monitor and establish IV access. Monitor EtCO2 if possible and immobilize the spine if warranted. Patients will rarely require ventilatory assistance or endotracheal intubation.
In the absence of a commercial occlusive dressing, cover the penetration accompanying an open pneumothorax with an occlusive dressing taped on three sides. This effectively creates a one-way valve that will prevent air from entering the chest through the penetration during inspiration, yet allow air to escape during exhalation, preventing development of a tension pneumothorax. There are times when the occlusive dressing will not function properly, and air will accumulate in the thorax. If an occlusive dressing is applied and signs and symptoms of tension pneumothorax develop, lift the corner of the dressing to allow the chest to decompress.
The definitive treatment for a tension pneumothorax is needle decompression, a skill typically available only to ALS providers. BLS providers should provide PPV to these patients while quickly transporting to an emergency department or rendezvousing with a paramedic. Perform needle decompression (also termed needle thoracostomy) immediately after tension pneumothorax is diagnosed, prior to any other treatment. In this procedure, a large-bore needle is inserted into the second or third intercostal space at the midclavicular line just over the top of the rib. It is important to use a needle of adequate length, as needles less than 4.5 cm have been shown to have failure rates up to 65%.5 Inserting the needle into the pleural space results in a rush of air through the needle, immediate decompression of the thorax, and fairly rapid correction of the cardiorespiratory insult characteristic of tension pneumothorax. The needle is left in place, typically with a flutter valve to allow air to escape the thorax but not enter. Commercial needle thoracostomy kits are available from several manufacturers, or a kit can be made with equipment normally found on an ambulance, such as a latex glove finger.
A hemothorax occurs when blood collects in the pleural cavity. It can occur with both blunt and penetrating chest trauma. Hemorrhage from injury to the lung parenchyma is the most common cause of hemothorax, but the bleeding from such injuries tends to be self-limiting because of the compressive nature of the accumulating blood, the high amount of thromboplastin (a blood protein that aids in coagulation) present in the lung, and the low pulmonary arterial pressure, all of which serve to facilitate clot formation and stop bleeding. Large injuries to the lung parenchyma and to arteries and/or veins can bleed considerably (more than 1 liter) and lead to hypovolemic shock.
Injuries to the relatively small intercostal and internal mammary arteries are the source of hemorrhage more often than the hilar arteries of the lungs or other great vessels. Hemorrhage from an injured intercostal artery can be brisk, as it branches directly off the aorta and is under high pressure.6 Accumulating blood displaces and collapses the lung, reducing tidal volume and compromising ventilation, leading to hypoxia. If allowed to progress, an uncommon complication termed a tension hemothorax can develop that will present similarly to a tension pneumothorax.
Clinical exam findings
The patient with a hemothorax will present with difficulty breathing, decreased or absent lung sounds on the affected side, and a chest that is dull to percussion. In addition, signs of shock will be present, including tachycardia; tachypnea; cool, pale, diaphoretic skin; and hypotension.
Similarly to the previous conditions, management of hemothorax begins with oxygenation and IV access along with control of external bleeding. Allow for permissive hypotension, as aggressive fluid volume replacement can dilute remaining blood and its clotting factors, both of which can interfere with the body’s attempts at clot formation, bleeding control and hemostasis.
Traumatic asphyxia occurs when sudden and severe crushing forces on the chest result in the retrograde flow of blood from the right side of the heart through the superior vena cava and into the large veins of the neck and head.
Clinical exam findings
The clinical exam of the patient with traumatic asphyxia will reveal upper-extremity cyanosis, bilateral subconjunctival hemorrhage, edema and a swollen tongue. Impaired cerebral blood flow may result in neurologic deficits, altered mental status, altered level of consciousness or seizures.7
The prehospital treatment of traumatic asphyxia is supportive. Despite the dramatic appearance, the condition itself is often benign in the absence of concomitant intrathoracic or intra-abdominal injuries.8 Provide spinal immobilization if the mechanism of injury suggests the possibility of spinal column or cord injury, and give oxygen if intrathoracic injury is suspected or hypoxia is present. Initiate ALS interventions such as cardiac monitoring and fluid volume resuscitation if signs of shock are present.
Injuries to the intrathoracic components of the cardiovascular system often have devastating and immediately life-threatening effects. Common injuries include pericardial tamponade, blunt cardiac trauma and blunt aortic injury.
An acute pericardial tamponade is the accumulation of blood within the pericardium, resulting in compression of the heart, impaired cardiac filling and reduced cardiac output. Acute pericardial tamponade is most common in patients with penetrating trauma to the chest and upper abdomen, and is rarely associated with blunt force trauma. It occurs more often with stab wounds than with gunshot wounds; 60%–80% of patients with stab wounds involving the heart develop tamponade. Because of the larger, more irregular defects in the pericardium produced by gunshot wounds, tamponade develops in only about 20% of GSWs to the heart and pericardium.9
After the initial penetrating trauma, the pericardium seals, and continued hemorrhage from the injured myocardium fills the pericardial space. The pericardium is relatively inelastic, and the introduction of even small volumes (60–100 mL) of blood over a short amount of time can result in significant increases in pressure leading to tamponade physiology.6 The increased pressure in the pericardium is transmitted to the heart, compressing it and preventing adequate ventricular filling during diastole. This in turn reduces preload, stroke volume and cardiac output; hypotension ensues.
One result of the cardiac compression is an increased diastolic pressure. A narrowing pulse pressure will develop as systolic pressure falls with reduced cardiac output but diastolic pressure remains high because of cardiac compression. JVD may develop secondary to decreased venous return to the right side of the heart, though it may be absent when there is significant bleeding from other injuries. In addition to the reduced cardiac output, cardiac tamponade reduces myocardial perfusion via compression of the coronary arteries, decreasing myocardial oxygen supply during a period of increased myocardial oxygen demand, further stressing the heart.
Clinical exam findings
The classic clinical exam findings associated with cardiac tamponade include hypotension, JVD and muffled heart tones, a trio of signs known collectively as Beck’s triad. This triad is difficult to identify in the prehospital environment, as auscultation of heart sounds, and the identification of muffled ones, can prove difficult in noisy environments. As the tamponade evolves, hypotension and tachycardia will be present, as will a narrowing pulse pressure and possibly pulsus paradoxus (a drop in systolic blood pressure of more than 10 mmHg during inspiration).
Management of pericardial tamponade centers on airway control, oxygenation, and support of ventilation and circulation. Signs and symptoms of pericardial tamponade can mimic those of tension pneumothorax, although the presence of bilateral lung sounds can rule out the latter. For patients who are hypotensive, rapid volume expansion with isotonic crystalloid will increase venous pressures, resulting in increased preload and increased cardiac output, elevating systolic pressures. In some systems, pericardiocentesis can be performed for patients in extremis; however, this is most safely performed in the hospital with ultrasound guidance. In this procedure a needle is inserted into the pericardial space to withdraw blood. Aspiration of as little as 5–10 mL may result in dramatic clinical improvement.6
Blunt Cardiac Trauma
Blunt cardiac trauma is a term that represents a spectrum of myocardial injury that includes myocardial concussion, myocardial contusion and myocardial rupture. The term myocardial concussion, or commotio cordis, describes an acute form of blunt cardiac trauma that does not result in direct injury to the myocardium. Myocardial contusion occurs when the myocardium is bruised, most often by blunt force trauma. Myocardial rupture is the acute traumatic rupture of the atrial or ventricular wall.
Myocardial concussion is usually produced by a sharp, direct blow to the sternal area that stuns the myocardium and results in brief dysrhythmia, hypotension and possibly loss of consciousness. If the dysrhythmia resolves spontaneously, the patient will likely survive with no discernable damage to the myocardium. Alternatively, sudden cardiac death can occur secondary to a more severe or prolonged dysrhythmia. This has been observed in athletes who are struck in the chest with baseballs or other objects. In these cases, the treatment is rapid defibrillation followed by standard ACLS care.
A myocardial contusion usually results from blunt force trauma to the sternal area that compresses the heart between the sternum and spinal column, resulting in injury to the myocardium. Myocardial injury can include hemorrhaging within the myocardium, edema, ischemia and necrosis, all resulting in cardiac dysfunction.
Myocardial rupture occurs when blunt force trauma results in an increase of intraventricular or intra-arterial pressure significant enough to rupture the myocardial wall. It is most often the result of high-speed motor vehicle crashes; it is almost always immediately fatal.10
Clinical exam findings
The clinical exam of the patient with a cardiac contusion will reveal soft tissue injury (e.g., abrasions, contusions, ecchymosis) and possibly skeletal injury (fractured ribs, flail segment, flail sternum) on the anterior chest wall near the sternum. Sinus tachycardia and cardiac dysrhythmia are possible, and hypotension can present in severe cases. The most common signs of cardiac rupture include hypotension; tachycardia; JVD; cyanosis of the head, neck, arm and upper chest; unresponsiveness; distant heart sounds; and concomitant chest trauma.6
Blunt Aortic Injury
The term blunt aortic injury describes a spectrum of injury that ranges from small tears in the aortic intima (the innermost layer of an artery) to complete transection of the aorta, which is almost always fatal. Up to 90% of patients with blunt aortic injury die at the site of the accident or within hours of hospital admission. Wherever it falls on the spectrum, blunt aortic injury is a life-threatening injury, and is usually the result of an unrestrained frontal collision or violent lateral blunt impact to the chest.
The descending aorta is fixed to the anterior surface of the spinal vertebrae. During deceleration, the aorta will decelerate at the same rate as the body, whereas the heart and unfixed aortic arch tend to continue to move after the descending aorta has come to a halt. The resulting shearing and tearing forces put stress on the aorta at the ligamentum arteriosum, and tearing can occur.
Clinical exam findings
Clinical signs for blunt arterial injury may be unimpressive despite its severe nature; up to 50% of patients will have no external signs of chest trauma. A high index of suspicion, based on an understanding of a rapid-deceleration mechanism of injury and the signs and symptoms of shock, should suggest the possibility of blunt aortic trauma.
Management of blunt aortic injury includes airway management, oxygenation and ventilation, and fluid volume replacement in patients with profound hypotension secondary to suspected aortic transection. Do not perform aggressive fluid volume administration in patients who are not hypovolemic, as increased intravascular volume could result in greater shear forces on the injured vasculature and worsening of the injury. As with all other trauma, rapid transport to a trauma center is paramount.
Thoracic trauma includes many potentially devastating injuries. Some, such as tension pneumothorax and pericardial tamponade, can be quickly reversed with lifesaving interventions. With a high index of suspicion, thorough physical exam and aggressive management, prehospital providers can improve these patients’ odds of survival.
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9. Karrel R, et al. Emergency diagnosis, resuscitation, and treatment of acute penetrating cardiac trauma. Ann Emerg Med 1982; 11: 504.
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