Beyond the Basics: Thoracic Trauma
CEU Review Form Thoracic Trauma (PDF)Valid until August 3, 2007
Thoracic injuries can be very dramatic, and may present with obvious physical findings that lead to immediate identification and management during the initial and rapid trauma assessment. For example, a large open wound to the anterior thorax can be easily found upon inspection of the supine patient in a well-lit environment. On the other hand, some patients with thoracic injuries may exhibit subtle signs and symptoms that can be easily missed initially, due partly to the extremely uncontrolled environment in which EMS personnel function. A small gunshot or stab wound to the thorax can be missed when assessing a patient in a poorly lit and chaotic setting. Accurate assessment requiring differentiation of breath sounds can also be hampered by loud background noises produced by crowds, music, television, passing vehicles or your own ambulance engine. A high index of suspicion, accurate assessment and frequent reassessment are necessary to identify both the apparent and less obvious thoracic injuries that could lead to lethal consequences.
Mechanism of Injury
Thoracic injury may result from both penetrating and blunt trauma. Penetrating trauma has a tendency to be more obvious in the initial phases of assessment, due to the presence of an open wound to the thoracic wall. External bleeding may or may not be present. The amount of external bleeding is not an indicator of the potential severity of internal bleeding associated with an underlying trauma. High-velocity gunshot wounds and bullets that enter the thoracic cavity and ricochet can produce multiple organ, vascular and structural damage. The physical location of the gunshot entrance or exit wound does increase one's index of suspicion of underlying internal organ and structural damage; however, it does not provide a precise prediction of the complete scope of the internal injury. Low-velocity wounds to the chest, such as those produced by a knife, may better predict underlying organ and structural damage due to the kinematics associated with the injury.
Blunt trauma may produce gross physical findings, such as large contusions, tenderness, fractured ribs and flail segments, or relatively little external evidence of injury. The chest wall may be severely compressed during the application of blunt force, causing the internal organs to be stretched, torn and sheared. After the blunt force is removed, the chest may recoil, leaving significant, moderate or minor evidence of the temporary cavitation that occurred during impact. If little external injury is evident, one may suspect minor or no internal thoracic damage; but, the patient may be suffering from multiple and severe organ, vascular and structural injury. In both cases, rely on patient complaints and physical exam findings to increase your index of suspicion of internal organ and structural injury.
Blunt and penetrating trauma may produce injury to several structures within the thoracic cavity. Some injuries have a much higher incidence when associated with a specific mechanism, such as acute pericardial tamponade related to penetrating injury to the chest and upper abdomen, and esophageal injury associated with penetrating trauma to the neck and upper chest. Anatomical structures that have the potential to be injured in thoracic trauma are the chest wall, lung tissue, pulmonary tract, myocardium, great vessels (inferior and superior vena cava and aorta), esophagus and diaphragm. Thus, the injury may involve muscles, bones, organs and vessels.
A compromise in ventilation, oxygenation and circulation may occur due to the anatomical structures typically involved in thoracic trauma. Injuries like rib fractures and flail segment may interfere with the bellow action of the chest and lead to inadequate mechanical ventilation. Oxygenation may be impaired by a large pulmonary contusion that restricts gas exchange through the collection of blood within the alveoli and the alveolar-capillary interface, or from a large area of collapsed lung tissue resulting from a pneumothorax. Hypotension from blood loss from a hemothorax or a reduction in cardiac output from a mechanically compressed myocardium associated with an acute pericardial tamponade can produce significant circulation and tissue perfusion disturbances. Some injuries, such as a tension pneumothorax, may lead to ventilatory, oxygenation and circulation compromise, which can produce lethal results early if not rapidly identified and managed. Some injuries, such as simple rib fractures, may produce such excruciating pain that the patient intentionally hypoventilates to reduce chest wall movement and becomes secondarily hypoxic. As with any patient, the focus in the treatment of thoracic trauma is to establish and maintain adequate airway, ventilation, oxygenation and circulation. This may involve emergency management aimed at preventing further organ or structural involvement, reducing the existing life threat or minimizing progression of the pathophysiologic compromise.
The basic principles of assessment apply to thoracic trauma. A systematic approach is critical to ensure that all potential life-threatening injuries are rapidly identified and managed. Thoracic injury is also associated with a relatively high incidence of extra-thoracic trauma, especially when a blunt mechanism of injury is involved. A shotgun approach to assessment may lead to missed or late identification of life-threatening injuries, potentially resulting in a poor patient outcome due to lack of immediate emergency intervention or failure to identify the severity of the patient condition, producing unnecessarily long on-scene times, lack of proper notification to the receiving medical facility, or an improper destination decision. Developing tunnel vision in the assessment approach and focusing just on the thoracic injury may cause the EMS practitioner to miss injuries to other body systems and cavities.
The initial assessment is designed to identify and manage life-threats to the airway, ventilation, oxygenation and circulation. As previously noted, these may all be compromised in thoracic trauma. Airway obstruction, hypoventilation, hypoxia and severe hypotension are often the primary reasons for deterioration and death in the trauma patient.
Once the scene is secured, and as you approach the patient, conduct a general impression. Through a quick body scan, identify any obvious life-threatening injuries or conditions that may require immediate management, such as an obvious open chest wound, especially if it is producing a sucking sound; blood, vomitus or other substances in the oral cavity that may result in aspiration; major bleeding (arterial or venous); or a flail segment. Provide manual spinal stabilization if a spinal injury is suspected. Establish and maintain an open airway, inspect inside the oral cavity, and suction or remove any substance that can be aspirated or lead to an airway obstruction. Carefully assess tidal volume and respiratory rate. If the tidal volume and respiratory rate are both adequate, and the patient is suspected of having a significant thoracic injury or is exhibiting signs of hypoxia, maximize oxygenation by applying a nonrebreather mask at 15 lpm. If either the tidal volume or respiratory rate is inadequate, immediately begin positive-pressure ventilation at a rate of 10 to 12 ventilations per minute (one ventilation every 5 to 6 seconds) in the adult and 12 to 20 (one ventilation every 3 to 5 seconds) in the infant and child. Be sure to provide controlled ventilation rates and volumes. Overventilation may lead to exacerbation of a pneumothorax and conversion to a tension pneumothorax; reduction of preload, cardiac output, blood pressure and perfusion, especially in patients with significantly increased intrathoracic pressure; and other secondary barotrauma.
Assess the circulation by comparing the amplitude of peripheral and central pulses, obtaining a heart rate and skin temperature, color and condition. If the thoracic trauma patient presents with pale, cool and clammy skin, tachycardia, and weak or absent peripheral pulses, you should suspect possible bleeding in the thoracic cavity, mechanical compression of the heart and great vessels, or bleeding in another area of the body.
Following the initial assessment, conduct a rapid trauma assessment to identify all other possible life-threatening injuries. Immediate life-threatening thoracic injuries include tension pneumothorax, open pneumothorax, pericardial tamponade, severe hemothorax and a flail chest. These conditions are identified through inspection, palpation, auscultation and percussion. The vital signs, including a systolic and diastolic blood pressure, heart rate, respiratory rate and skin findings, along with a pulse oximeter and end-tidal carbon dioxide reading, will provide valuable information in the recognition and differentiation of thoracic injuries. It is necessary to understand and link thoracic injury to possible findings in other areas of the body when conducting your rapid trauma assessment. As an example, inspecting the pupils is necessary not only to assess for the possibility of a brain injury, but sluggish pupillary reaction may indicate significant hypoxia related to a chest injury. Likewise, jugular venous distension, especially if associated with the inspiratory phase of respiration (referred to as Kussmaul's sign) may be an indication of a thoracic injury that has resulted in a high intrathoracic pressure (i.e., tension pneumothorax) or interference with ventricular filling and cardiac output (i.e., pericardial tamponade). This may be a subtle finding; however, a tension pneumothorax and pericardial tamponade patient may present with signs that mimic a hypovolemic patient. One would not suspect jugular venous distension in hypovolemia due to the low venous pressure. Recognizing jugular venous distension, even though it may be subtle or late, may be one sign that gets the EMS practitioner thinking about a condition other than hypovolemia. Also, do not rule out the possibility of pericardial tamponade or tension pneumothorax when jugular venous distension is not found, since a large percentage of patients with chest injury may also be hypovolemic, resulting in a low venous pressure that will preclude the jugular veins from engorging. It is necessary to think critically and process and consider all of the assessment information during the exam.
A detailed exam is only done if time and the patient's condition allow it. The detailed exam is designed to find all other injuries. Life threats should have already been identified in the rapid trauma assessment.
Signs of other chest injuries that may be identified during the rapid trauma assessment or detailed physical exam may include rib fractures, simple pneumothorax, simple hemothorax, pulmonary contusion and cardiac contusion. The signs, symptoms and management of the most immediate life-threatening conditions are discussed in the following section.
Specific Thoracic Injuries
The most immediate life-threatening thoracic injuries that require rapid recognition and intervention and expeditious transport are tension pneumothorax, open pneumothorax, flail chest, massive hemothorax and acute pericardial tamponade. Unfortunately, EMS intervention for hemothorax and acute pericardial tamponade is limited to prompt recognition, supportive care and immediate transport to an appropriate medical facility capable of managing the chest injury. Thus, the following discussion will focus on tension pneumothorax, open pneumothorax and flail chest, where the EMS practitioner must intervene with specific emergency management.
A tension pneumothorax occurs from disruption of the parietal pleura, visceral pleura or tracheobronchial tree associated with blunt or penetrating trauma, or iatrogenically from certain medical procedures, such as use of positive end-expiratory pressure (PEEP) with ventilation or central venous catheter insertion. Also, too aggressive ventilation with high pressure and excessive tidal volumes may convert a simple pneumothorax to a tension pneumothorax.
The disruption allows air to escape into the pleural space. Typically, injury to the pleural lining creates a one-way valve that allows air to enter the pleural space during periods of negative intrathoracic pressure associated with inhalation; however, when air attempts to escape with the increase in intrathoracic pressure, the one-way valve is forced closed, trapping the air in the pleural space. With each inhalation, more air enters the pleural space and becomes trapped. The air begins to build rapidly, collapsing the lung. Due to the nature of the tissue that comprises the lung, it has a natural tendency to recoil and collapse, similar to a rubber band when stretched and released. When the water seal is broken between the visceral and parietal pleura, the lung will continue to exert a pulling effect inward and to recoil while continuing to create a relative negative pressure inside the pleural space that promotes air entry.
As the air collects in the pleural space on the injured side, the volume and pressure continue to build. This will eventually cause the mediastinum to shift away from the injured hemithorax and move contralaterally toward the uninjured hemithorax, resulting in compression of the uninjured lung, right atrium and vena cava. Because the injured lung is already collapsed, compression of the uninjured lung will lead to severe ventilatory and oxygenation compromise. The patient will exhibit signs of severe respiratory distress and hypoxia. Compression of the vena cava and right atrium will lead to a reduction in preload, left ventricular end-diastolic filling volume and cardiac output. Hypotension, tachycardia and other signs of poor perfusion will become evident. A tension pneumothorax causes both significant respiratory and circulation compromise, making it an immediate life-threatening condition that requires rapid identification and intervention.
Early signs and symptoms associated with a tension pneumothorax are:
- Chest pain
- Decreased breath sounds on the injured side.
Late findings in a tension pneumothorax are:
- Altered mental status
- Hyperexpanded chest wall from hyperinflation of the pleura on the injured side (asymmetrical chest wall)
- Severe respiratory distress to respiratory failure
- Severely decreased or absent breath sounds on the injured side
- Decreased breath sounds on the uninjured side
- Hypotension (may indicate impending cardiovascular collapse)
- Increased resistance to bag-valve ventilation
- Bradypnea (ominous sign of impending respiratory or cardiac arrest)
- Pulsus paradoxus (decrease in systolic blood pressure by >10 mmHg during inhalation)
- A reduction in peripheral pulse amplitude during inspiration
- Jugular venous distention (may be seen early during inspiration or not at all if the patient is hypovolemic)
- Displacement of the apical pulse
- Tracheal deviation away from the injured side (late, inconsistent and very difficult to accurately assess and find)
- Hyperresonance on the injured side
- Subcutaneous emphysema.
The first priority of management upon identification of a tension pneumothorax is to reduce the pressure of the affected pleural space. If an occlusive dressing has been applied to an open pneumothorax, remove the dressing and allow any built-up air to escape. Be sure to leave the dressing off for a few exhalations. If this is ineffective, or if the patient does not have an open pneumothorax, you must proceed with needle decompression of the affected pleural space. This is achieved by inserting a 10- to 14-gauge over-the-needle catheter into the second or third intercostal space on the anterior chest at the midclavicular line. Preferably use a 2" over-the-needle catheter that will penetrate the subcutaneous tissue, muscle and other chest wall structures and actually enter the pleural cavity. A catheter that is too short may never enter the pleural cavity. A rush of air may be heard or felt, and the patient's condition may rapidly improve when the needle is inserted. Remove the needle stylet and leave the catheter in place. With the catheter in place, the tension pneumothorax will be converted to a simple open pneumothorax that will result in no immediate life-threatening consequences. Be sure to tape and secure the catheter in place to avoid accidental misplacement, which may lead to subsequent production of another tension pneumothorax. A flutter valve can be made from the tip of an examination glove and secured to the hub of the catheter.
Ensure that you have established and are maintaining an adequate airway, ventilation and oxygenation. If ventilating the patient, use minimal rates and tidal volumes. Rapidly transport the patient to an appropriate medical facility capable of managing thoracic trauma. En route, initiate an intravenous line, if time and the patient's condition permit. Continuously reassess the patient, and be cognizant of redevelopment of a tension pneumothorax.
When air enters the pleural space through an open wound in the chest wall and parietal pleura, it is termed an open pneumothorax. As the air enters the pleural space, it collapses the lung, as in a simple pneumothorax. The difference between the two is that in an open pneumothorax, air enters the pleural space from a wound to the chest wall and not from the injured lung. This creates a conduit for air to enter the chest when the intrathoracic pressure becomes negative during inhalation. If the opening in the chest is large enough, a majority of the air will follow the pathway of least resistance and enter the pleural space directly through the open wound, bypassing the respiratory tract and lungs. A large or significant wound is thought to be two-thirds the internal diameter of the trachea. In an average-sized adult, that means the wound may only need to be the size of a nickel to be significant.
If a majority of airflow is into the pleural space and not the lungs, the patient will develop hypoxia rapidly from lack of effective ventilation and oxygenation. The patient will appear to be breathing as the chest wall moves during inspiration and expiration; however, with each chest wall expansion, the negative pressure that is created inside the thorax draws more air into the open wound, causing the lung to collapse further. If not impeded by skin, muscle, bone or other tissue, the open wound may allow air to escape during exhalation. One might think that this would then pose no real danger for the patient, since air is escaping with each breath. However, remember that the significant wound will draw the majority of air into the pleural space and not the lung, drastically reducing lung ventilation and oxygenation. Even with the escape of air during exhalation, the patient will deteriorate rapidly from the loss of effective alveolar ventilation. If the air is prevented from escaping during exhalation, it may quickly develop into a tension pneumothorax. If the patient is initially assessed in a quiet environment and the open wound is large enough, it may be possible to hear a sucking sound with inhalation and possibly with exhalation. This rare episode is referred to as a "sucking chest wound."
Signs and symptoms are:
- Open wound to the thorax
- Decreased breath sounds on the affected hemithorax
- Subcutaneous emphysema
- Deteriorating SpO2 reading
- Frothy blood at open wound
- Other signs of respiratory distress.
The priority in managing an open pneumothorax is to occlude the open wound to the thorax immediately upon identification. Initially occlude it with a gloved hand as soon as it is found, and, as rapidly as possible, apply an occlusive dressing taped on three sides. Plastic wrap, Vaseline gauze, aluminum foil or a commercial device like the Asherman chest seal can be used. Once the wound is sealed, proceed with standard trauma care, including establishing and maintaining an airway and ventilation, maximizing oxygenation, maintaining circulation, rapid transport and initiating an intravenous line en route to the medical facility. Carefully reassess the patient, since the open pneumothorax can develop into a tension pneumothorax, especially if an injured visceral pleura allows air to escape internally into the pleural space from the injured lung.
A flail chest is defined differently by various sources. Most define it as two or three adjacent ribs fractured in two or more places, which creates a free-floating segment within the chest wall. The flail could be anterior, posterior, or involve the sternum with fractured ribs on both sides. It typically takes a significant blunt force applied to the thorax to produce a flail segment. In patients with some type of pathology that causes the ribs to weaken, such as osteoporosis, less force may be required to create a flail chest. When such significant force is applied to the chest, the lung has a tendency to become contused. Thus, a common second injury, which may be more lethal than the flail chest, is an underlying pulmonary contusion.
A true flail segment has the ability to move independent of the remaining chest wall. Thus, when the chest wall is expanding, the negative intrathoracic pressure will draw the free-floating flail segment inward as the remainder of the chest moves outward. As the chest wall begins to reduce its size during exhalation, positive intrathoracic pressure causes the free-floating flail segment to move outward. This abnormal chest wall movement may interfere with effective generation of intrathoracic pressure and lung inflation.
The pulmonary contusion allows blood to seep into the alveolar-capillary interface and within the alveoli. This interferes with the ability of oxygen and carbon dioxide to cross the alveolar membrane and alveolar-capillary interface and enter into the capillary, impeding effective gas exchange.
The flail segment and pulmonary contusion will cause respiratory compromise. Both conditions may lead to severe hypoxia and hypercarbia.
Pain associated with the rib fractures is typically a predominant complaint, along with signs and symptoms of respiratory distress. Severe pain may cause the patient to intentionally hypoventilate, leading to hypoxia and hypercarbia. Respiratory distress, hypoxia and hypercarbia may also be associated with a large pulmonary contusion. A poor SpO2 reading; pale, cool and clammy skin; and cyanosis may be present.
Paradoxical movement is often thought to be the predominant sign of a flail segment. However, when ribs fracture, the intercostal muscles may spasm, causing the flail segment to be initially stabilized. Thus, paradoxical movement may be initially missed upon inspection of the chest; however, palpation will reveal the unstable segment. This is one reason why palpation of the chest is necessary during the rapid trauma assessment. As intercostal muscles fatigue, the flail segment becomes more apparent upon inspection.
Like the other chest injuries, emergency management is aimed at establishing and maintaining an airway, effective ventilation, oxygenation and circulation. Due to the significant pain associated with multiple rib fractures, pain management should be considered. Remember, the patient may be intentionally hypoventilating due to the pain and not as a result of some other respiratory pathology. If respiratory rate or tidal volume are ineffective, begin positive pressure ventilation with a bag-valve device. Maximize oxygenation by nonrebreather mask at 15 lpm in the adequately breathing patient, or attached to the bag-valve device through a reservoir if providing assisted ventilation. Stabilizing the flail segment with sandbags or other devices is no longer recommended. The patient may be able to self-splint using a pillow and his own arm. An intravenous line should be initiated. Be judicious in the administration of fluid, since it may worsen the underlying pulmonary contusion. Rapidly transport the patient to a medical facility capable of managing the chest injury.
Many other chest injuries can occur when blunt or penetrating trauma is applied to the thorax. Regardless of the injury, it is important to approach each type patient with the intent to effectively establish and maintain an airway, ventilation, oxygenation and circulation. This may include some of the specific aforementioned interventions. Along with rapid transport, these principles should provide the basis for thoracic emergency care.
Bledsoe BE, Porter RS, Cherry RA. Essentials of Paramedic Care, 2nd edition. Upper Saddle River, NJ: Prentice Hall, 2007.
Dalton AL, Limmer D, Mistovich JJ, Werman HA. Advanced Medical Life Support: A Practical Approach to Adult Medical Emergencies, 3rd edition. Upper Saddle River, NJ: Prentice Hall, 2007.
Rosen P, Barkin RM, et al. Emergency Medicine Concepts and Clinical Practice, 5th edition. Mosby, 2002.
Solomone J, Pons P, eds. Prehospital Trauma Life Support, 6th edition. St. Louis, MO: Mosby, 2007.
CEU Review Form Thoracic Trauma (PDF)Valid until August 3, 2007
Joseph J. Mistovich, Med, NREMT-P, is a professor and chair of the Department of Health Professions at Youngstown (OH) State University, author of several EMS textbooks and a nationally recognized lecturer.
Daniel D. Limmer, AS, EMT-P, is a paramedic with Kennebunk Fire-Rescue in Kennebunk, ME, and EMS Program Coordinator at York County Community College in Wells, ME. He is the author of several EMS textbooks and a nationally recognized lecturer.
William S. Krost, BSAS, NREMT-P, is an operations manager and flight paramedic with the St. Vincent/Medical University of Ohio/St. Rita's Critical Care Transport Network (Life Flight) in Toledo, OH, and a nationally recognized lecturer.
Dan Limmer, Joe Mistovich and Will Krost are all featured speakers at EMS EXPO, October 11-13, in Orlando, FL. For more information, visit www.emsexpo2007.com.