Pathophysiology
Summary
Pneumothorax is characterized by the loss of negative intrapleural pressure, manifesting as sudden dyspnea and pleuritic chest pain on the affected side, specifically sharp pain provoked by deep inspiration. Two primary types exist: primary spontaneous pneumothorax, frequently observed in tall, thin males in their early 20s, associated with the formation of apical subpleural blebs and often without any precipitating event or underlying lung disease, and secondary spontaneous pneumothorax, commonly caused by underlying conditions like COPD, high airway pressures from mechanical ventilation, blunt chest trauma, parenchymal destruction from malignancy, or pulmonary infections like M. tuberculosis. Diagnostic hallmarks include a white visceral pleural line and an absence of peripheral vessel markings on chest X-ray (CXR), as well as hyperresonant percussion and diminished breath sounds upon auscultation of the affected side due to the air filling the pleural space.
Tension pneumothorax is a critical condition where air enters the pleural space through a valve-like tear in the visceral pleura, permitting air entry but not exit. This leads to the compression of mediastinal structures and progressive enlargement of the pneumothorax, evident by tracheal deviation away from the affected lung on imaging. This can result in decreased venous return, leading to hypotension and reflex tachycardia, as well as obstruction of the superior vena cava (SVC) causing subsequent jugular vein distension (JVD). Immediate needle decompression followed by chest tube placement is imperative for management.
Other pleural conditions include hemothorax, the presence of whole blood in the pleural space that often results from ruptured intrathoracic aneurysms or trauma, and chylothorax, an accumulation of chylomicron-rich fluid with triglyceride levels >110 mg/dL. The chylous fluid usually results from trauma to the thoracic duct during surgery or thoracic duct obstruction from intrathoracic malignancies like lymphoma. In contrast to pneumothorax, which presents with hyperresonance upon percussion, hemothorax and chylothorax are characterized by dullness upon percussion of the affected side.
Lesson Outline
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FAQs
Loss of ‘negative’ intrapleural pressure in pneumothorax allows air to enter the pleural space, disrupting the pressure differential that normally keeps the lung inflated. This leads to partial or complete lung collapse, resulting in a sudden onset of dyspnea and compromised respiratory function.
Pneumothorax classically presents a sudden onset of dyspnea and pleuritic chest pain on the affected side, often exacerbated by deep inspiration. Physical examination reveals hyperresonant percussion and diminished breath sounds over the affected area, due to the presence of air in the pleural space.
Primary spontaneous pneumothorax is most frequently seen in tall, thin males in their early 20s who have no underlying lung disease and no identifiable precipitating event. Risk factors include smoking and the presence of apical subpleural blebs or subpleural bullae located at the apex of the lung.
Secondary spontaneous pneumothorax is often a consequence of pre-existing lung diseases or damage, such as COPD, malignancies, M. tuberculosis infection, and pulmonary infections like pneumonia and lung abscess. Mechanical ventilation with high airway pressures can also lead to secondary spontaneous pneumothorax. Diagnostic clues on chest x-ray include a white visceral pleural line, representing the edge of the collapsed lung, and an absence of peripheral vessel markings.
Tension pneumothorax is a critical condition requiring immediate intervention. It can cause compression of mediastinal structures, evident by tracheal deviation away from the affected lung on imaging. Additionally, it can lead to decreased venous return, resulting in hypotension and reflex tachycardia, as well as obstruction of the superior vena cava, manifesting jugular vein distension (JVD). Immediate needle decompression followed by chest tube placement is essential to prevent cardiovascular collapse.
