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.