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Original Contribution

Penetrating Chest Trauma

August 2004

“Prehospital Pathophysiology” provides an opportunity for EMS providers to either refresh their knowledge related to the etiology of a certain disease or expand their knowledge base regarding common and not-so-common disease processes. This column is for both basic- and advanced-level prehospital care providers. The authors hope that through this column, EMS providers will gain a more thorough understanding of disease processes. If you would like to see a specific topic addressed in this column, send your request via e-mail to emseditor@aol.com.

Penetrating chest trauma most frequently involves mechanisms such as stabbing and gunshot wounds (GSW), although there are a variety of ways the chest can be penetrated—some of them very dramatic (industrial incidents, fence poles).

This article focuses specifically on hemothorax, pneumothorax, tension pneumothorax and pericardial tamponade. Also discussed will be assessment and treatment problems relating to the pathophysiology of these injuries.

Physiology/Pathophysiology

Penetrating chest trauma frequently creates serious or fatal injury because of the vital structures and processes that are housed within the chest cavity. Maintaining adequate intrapleural and intrapulmonic pressures within the chest cavity is essential for adequate breathing.

The lungs are surrounded by thin, durable membranes called pleura. The parietal pleura lines the chest wall. The visceral pleura is attached to the surface of the lung. Between the two pleural layers is a small amount of fluid, which serves both as a lubricant and a means to provide surface tension to keep the lungs inflated. A fluid bond between the visceral and parietal pleura creates a steady pull between the two pleural layers, which leads to a constant intrapleural negative pressure. The fluid bond is analogous to a water glass being placed upside down on a wet countertop. When the glass is pulled straight upward, the fluid bond creates a suction (negative pressure) and the glass can’t be pulled upward off the countertop unless the fluid bond seal is broken. The lung is comprised of elastin fibers that have a natural recoil tendency. This recoil property wants to pull the lung inward away from the thoracic wall; however, the fluid bond in the pleural space overcomes the elastin recoil and keeps the lungs from completely collapsing. If the fluid bond were eliminated, the lungs would collapse to approximately 5% of their normal resting size. The integrity of the pleural layers and appropriate pressure within the chest are essential for adequate breathing. A break in the continuity and integrity of the pleural layer would reduce the fluid bond and allow the elastin recoil to collapse the lung.

It is believed that the pleural space can hold between 3–4 liters of blood or air. Air will cause a dramatic reduction in surface tension when the pleura lose contact with each other, resulting in the inability to expand the affected lung. The volume of blood that can collect in the pleural space is enough to cause exsanguination. Blood or other fluids in the pleural space can also cause alveolar collapse in the areas where these substances are present.

It should be noted that during deep exhalation, the diaphragm rises as high as T4/T5. This means that an injury in the area of diaphragmatic movement may involve the chest, abdomen or both. A final issue with anatomy is that many providers fail to consider the patient’s “upper back” part of the chest cavity. The upper back is actually the posterior of the chest cavity and must be considered during assessment and care of the patient, especially in the event of penetrating trauma leading to pneumothorax or tension pneumothorax.

Hemothorax

Hemothorax is a collection of blood in the pleural space. As noted above, this space will hold between 3–4 liters of blood. Although blood in this capacity will prevent gas exchange due to alveolar collapse, it also can cause death from blood loss without one drop of blood ever leaving the body. This means that hemothorax can affect the body in two ways: hemodynamically and by impeding alveolar gas exchange.

The blood from hemothorax can come from two general areas: extrapleural and intrapleural, which includes the great vessels of the body in the mediastinum. The most common and often most profuse bleeding is caused by laceration of the extrapleural intercostal or internal mammary arteries. On the underside of each rib, and slightly toward the inside, is a vein, artery and nerve. This is important to remember in regards to placement of decompression needles.

Intrapleurally, bleeding from damage to the lung parenchyma is usually limited because of self-compression and the relative low pressures in these vessels. Of course, a rupture of the great vessels contained in the mediastinum, including the aorta and the superior and inferior venae cava, will cause a massive hemothorax.

When assessing the patient with a hemothorax, you will likely find signs of hypo-volemic shock and a mechanism of injury consistent with penetrating chest injury to include GSW, stabbing or even a closed chest injury, if it causes injuries to blood vessels. In hemothorax, you would find a dull sound on percussion over affected areas. It is important to note that many of these patients are placed supine on a backboard, which may diminish the accuracy of auscultation or percussion, especially in minor to moderate hemothorax, by causing a distribution of the blood over a greater area, masking pertinent physical findings.

Pneumothorax

A pneumothorax occurs when the integrity of the chest wall is compromised allowing air to enter, frequently caused by a penetrating wound. However, a pneumothorax may also occur spontaneously or due to a medical condition like a ruptured bleb in a chronic obstructive pulmonary disease (COPD) patient. In this case, we are limiting discussion to the penetrating chest injury.

When an opening is created between the outside environment and the pleural space, intrathoracic and environmental pressures have a tendency to attempt to equalize. With the break in the pleural fluid bond, the ability of the injured pleura and lung to expand is severely limited. The extent of the pneumothorax can vary greatly, depending on the type of wound, location of the wound and whether the wound seals itself spontaneously. Be sure to auscultate the chest thoroughly. Percussion over the hyperinflated pleura will produce a tympanic or hollow sound known as hyperresonance. A decrease in breath sounds and hyperresonance may be heard only over the apices in small pneumothoraces; thus, be sure to assess this area thoroughly.

A significant complication of a pneumothorax is development of a tension pneumothorax. This occurs when a pneumothorax causes air to build up in the pleural space on the injured side, leading to a significant increase in intrathoracic pressure in one hemithorax. This can occur when an open pneumothorax seals itself and air continues to escape from the injured lung, or when tissue associated with an open chest wound creates a flutter valve effect, allowing air to enter but sealing the wound when air attempts to escape. The lung on the affected side will usually collapse.

As pressure builds on the injured side of the chest, it begins to cause a shift of the mediastinum toward the uninjured side of the chest. The mediastinal shift begins to compress the uninjured lung and also may kink the inferior and superior venae cava, reducing venous return to the right side of the heart. The reduction in venous return will reduce the preload of the left ventricle, leading to a decrease in cardiac output and consequential poor perfusion and hypotension. Thus, a tension pneumothorax creates not only a respiratory compromise but also a cardiovascular compromise.

Tension pneumothorax presents with respiratory distress, jugular venous distention (JVD), diminished breath sounds, tachycardia and narrow pulse pressure. Although tracheal deviation and jugular venous distention are commonly cited signs of this condition, they both occur late in the condition. It is difficult to detect tracheal deviation at a level above the suprasternal notch; however, it is usually easier to palpate a shift in the trachea than to see it.

Pericardial Tamponade

Pericardial tamponade is defined as abnormal fluid or amounts of fluid in the pericardial sac, which causes compression of the heart and diminished cardiac output.

Although tamponade is relatively rare, when it does occur, it is often due to a stab wound to the heart. The knife enters through the pericardium and into a chamber. The ventricles are most commonly involved, with a slight predominance to the right due to its anatomic position in the chest. When tamponade develops, the pericardium seals itself but bleeding from the heart continues to fill the sac, causing increased pressure on the heart and reducing the size of the ventricle, which in turn reduces the end-diastolic filling volume and leads to a drop in cardiac output. As little as 50–75ml of blood can cause diminished cardiac output.

Tamponade seen in the field is most commonly associated with an open chest wound, but, in some cases, may be caused by blunt trauma. Common signs and symptoms are JVD, narrow pulse pressure, signs of hypo-perfusion and muffled heart sounds. Kussmaul’s sign, which is an engorgement of the jugular veins during inhalation, may also be seen in pericardial tamponade. This is related to an increase in venous pressure. Beck’s triad consists of hypotension, decreased heart sounds and JVD (increasing venous pressure). While widely reported as characteristic of tamponade, in practice it is seen in less than half of patients with tamponade. This is compounded by the difficulty in obtaining heart sounds in a moving ambulance while maximizing the “golden hour.”

Table I helps distinguish between the different penetrating chest injuries. While it appears that each has a distinct presentation, distinguishing between these conditions in the presence of massive chest trauma can be challenging. Knowing the signs and symptoms, backed by the pathophysiology, will help you make important treatment decisions (e.g., needle decompression of the chest) in the face of challenging trauma calls

Bibliography

  • Hemothorax (Emergency Medicine) accessed online at www.emedicine.com on May 5, 2004.
  • Hubble MW, Hubble JP. Principles of Advanced Trauma Care. Albany, NY: Delmar Publishers, 2002.
  • Marx J, et. al. (eds). Rosen’s Emergency Medicine, 2nd Edition. St. Louis, MO: Mosby, 2002.
Table 1: Differential Diagnosis of Massive Hemothorax, Tension Pneumothorax and Cardiac Tamponade
Assessment Massive Hemothorax Tension Pneumothorax Cardiac Tamponade
Pulse Rapid Rapid Rapid
Blood Pressure Low Low Low
Pulsus paradoxus No Yes Possibly
Heart sounds Audible Audible Muffled
Neck veins Flat Distended Distended
Percussion Dull Hyperresonant Normal
Trachea Midline/deviated Deviated Midline
Chest symmetry Normal/asymmetrical Asymmetrical Normal
Breath sounds Absent/rhonchi/rales Absent Present

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