Pulmonary infarction is a severe medical event involving the death of lung tissue. This condition, often called a lung infarction, occurs when a specific area of the lung is entirely deprived of its necessary blood and oxygen supply. The resulting lack of perfusion leads to tissue necrosis, which is the irreversible damage of lung cells and structures. Pulmonary infarction requires immediate medical attention to prevent further complications and manage the underlying cause.
How Pulmonary Infarction Develops
The primary mechanism leading to lung tissue death is the mechanical blockage of a pulmonary artery. This blockage is most frequently caused by a thromboembolism, commonly known as a pulmonary embolism (PE), where a blood clot travels from elsewhere in the body and lodges in the lung’s vascular system. The clot abruptly cuts off blood flow to the lung segment supplied by the affected artery.
The lungs possess a unique dual circulatory system, receiving blood for gas exchange from the pulmonary arteries and oxygenated blood for the tissue itself from the bronchial arteries. This dual supply often protects the lung from true infarction, meaning many pulmonary emboli do not result in tissue death. Infarction typically develops only when the blockage is substantial or when underlying conditions, such as heart failure or pre-existing lung disease, compromise the bronchial circulation’s ability to compensate.
The most common source of the clot causing a PE is deep vein thrombosis (DVT), a blood clot forming in the deep veins of the legs. Risk factors for DVT and pulmonary infarction include prolonged immobilization, recent surgery, cancer, and inherited hypercoagulable states. The resulting lack of blood flow, or ischemia, starves the lung tissue of oxygen, leading to a wedge-shaped area of hemorrhagic necrosis that defines the infarction.
Identifying the Symptoms
The clinical presentation involves specific symptoms reflecting damage to the lung tissue and surrounding lining. One characteristic sign is pleuritic chest pain, a sharp, localized discomfort that intensifies significantly when the patient takes a deep breath or coughs. This pain stems from the irritation of the pleura, as the infarcted tissue is typically located near the lung periphery.
Patients often experience dyspnea, or shortness of breath, which can begin suddenly and worsen with physical activity. This difficulty breathing reflects the reduced capacity of the damaged lung segment to participate in gas exchange. Hemoptysis, the act of coughing up blood or bloody mucus, is another indicator associated with true infarction, resulting directly from the hemorrhagic nature of the necrotic lung tissue.
Other symptoms may accompany the acute event, including a rapid heart rate, low-grade fever, and weakness. The severity of these symptoms generally correlates with the size of the clot and the amount of lung tissue damaged. Recognizing this cluster of symptoms prompts immediate medical evaluation.
Diagnostic Procedures
Confirming pulmonary infarction requires laboratory results and specialized imaging to visualize the blockage and tissue damage. The initial laboratory test is often a D-dimer blood test, which measures a protein fragment released when a blood clot dissolves. An elevated D-dimer level suggests significant clotting activity, raising suspicion of a pulmonary embolism.
The gold-standard imaging technique to confirm a clot in the pulmonary arteries is the Computed Tomography Pulmonary Angiography (CTPA). This scan involves injecting a contrast dye into a vein and using a CT scanner to create detailed cross-sectional images of the lungs. The CTPA precisely locates the thrombus within the pulmonary vasculature and often reveals the characteristic wedge-shaped area of infarcted lung tissue.
A standard chest X-ray is frequently performed to rule out other causes of symptoms, such as pneumonia or a collapsed lung. While it cannot definitively diagnose the condition, it may show specific findings associated with infarction, such as a localized, triangular opacity known as Hampton’s Hump. Another possible sign is the Westermark sign, which indicates an area of decreased blood flow distal to the blockage.
Treatment and Recovery
Immediate management centers on stabilizing the patient and preventing new blood clots. Acute treatment involves starting anticoagulation therapy, typically with injectable heparin, to stop the existing clot from growing and reduce recurrence risk. This initial therapy is usually transitioned to an oral anticoagulant, which patients may take for at least three to six months or indefinitely.
Supportive care manages symptoms and ensures adequate oxygenation. This includes supplemental oxygen to improve blood levels and pain medication to control severe pleuritic chest pain. In rare, severe cases where the clot is massive and strains the heart, specialized thrombolytics, or “clot-busters,” may be administered to rapidly dissolve the obstruction.
Recovery time varies but can take several months, though symptom improvement often occurs shortly after starting treatment. Long-term management focuses on addressing underlying risk factors, such as managing chronic conditions or implementing lifestyle changes. The infarcted lung tissue may heal with scar tissue (fibrosis), potentially leading to some long-term reduction in lung function.