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Physicians defined pneumothorax during the reign of Alexander the Great. Many of the early references to pneumothorax may actually have been tension pneumothorax, which can be significantly more dramatic in its clinical presentation. Needle decompression of the chest for presumed tension pneumothorax has been in practice for nearly 20 years, but few data exist in the medical literature showing the efficacy of the procedure or reviewing the field-use and incidence of the procedure.
Tension pneumothorax remains a life-threatening condition diagnosed under difficult conditions, with a simple emergency procedure as treatment (ie, needle decompression). Although commonly used, proving the efficacy of the emergency treatment or its incidence in actual population studies is nearly impossible.
Air trapped in the pleural cavity and causing shifts of the intrathoracic structure is a life-threatening emergency. Promptly recognizing this condition saves lives, both outside the hospital and in a modern intensive care unit (ICU). Because tension pneumothorax occurs infrequently and has potentially devastating effects, a high index of suspicion and knowledge of basic emergency thoracic decompression are important for all healthcare personnel.
Although some authors are now questioning the pathophysiology of tension pneumothorax, no animal models or randomized prospective trials have provided any evidence that our understanding of the cause, effects, and treatment of the disease should be changed.
The actual incidence of tension pneumothorax outside of a hospital setting is impossible to determine. The 1999 revision of the Department of Transportation (DOT) Emergency Medical Treatment (EMT) Paramedic curriculum recommends emergent needle decompression of the chest in patients exhibiting nonspecific signs and symptoms. Approximately 10-30% of patients transported to level-1 trauma centers in the US receive prehospital decompressive needle thoracostomies; however, not all of these patients actually have a true tension pneumothorax. Although this occurrence rate may seem high, disregarding the diagnosis probably results in unnecessary deaths.
The overall incidence of tension pneumothorax in the ICU is unknown. The medical literature provides only glimpses of the frequency. From the 2000 incidents reported to the Australian Incident Monitoring Study (AIMS), 17 involved actual or suspected pneumothoraces, and 4 of those were diagnosed as tension pneumothorax. A more recent review of military deaths from thoracic trauma suggests that up to 5% of combat casualties with thoracic trauma have tension pneumothorax at the time of death.
Tension pneumothorax occurs anytime a disruption involves the visceral pleura, parietal pleura, or the tracheobronchial tree. The disruption happen when a 1-way valve forms, allowing air inflow into the pleural space and prohibiting air outflow. The volume of this nonabsorbable intrapleural air increases with each inspiration because of the 1-way valve effect. As a result, pressure rises within the affected hemithorax. As the pressure increases, the ipsilateral lung collapses and causes hypoxia. Further pressure build-up causes the mediastinum to shift toward the contralateral side and impinge on both the contralateral lung and the vasculature entering the right atrium of the heart. This situation leads to worsening hypoxia and compromised venous return. The inferior vena cava is thought to be the first to kink and restrict blood flow back to the heart. It is most obvious in trauma patients who may be hypovolemic with reduced venous blood return to the heart.
Researchers still are debating the precise mechanism of cardiovascular collapse, but, generally, they believe the condition develops from a combination of mechanical and hypoxic effects. The mechanical effects manifest as kinking or compression of the superior and inferior vena cava because the mediastinum deviates and the intrathoracic pressure increases. Hypoxia leads to increased pulmonary vascular resistance via vasoconstriction. In either event, decreasing cardiac output and worsening metabolic acidosis secondary to decreased oxygen delivery to the periphery occur, thus inducing anaerobic metabolism. If the underlying problem remains untreated, the hypoxemia, metabolic acidosis, and decreased cardiac output lead to cardiac arrest and death.
Under emergency conditions, place decompression catheters in the second rib interspaced in the midclavicular line. This has been established by Wax and Leibowitz who reviewed 100 thoracic computed tomography (CT) scans measuring the distance from the midline to the internal mammary artery and the average thickness of the tissues.12 This process punctures through the skin and, possibly, through the pectoralis major muscle, external intercostals, internal intercostals, and parietal pleura. Placement in the middle third of the clavicle minimizes the risk of injury to the internal mammary artery during the emergency procedure. Place the catheter just above the cephalad border of the rib, because the intercostal vessels are largest on the lower edge of the rib.
If tension pneumothorax is suspected, make sure no contraindications exist for the placement of an emergency decompression catheter into the thorax.
Contraindications can include previous thoracotomy, previous pneumonectomy, and the presence of a coagulation disorder. These are relative contraindications, however, because tension pneumothorax is a life-threatening condition, and failure to treat expectantly can result in patient death.