0.35 سم مكعب

الانسداد الرئوي ١٠١: فهم الأساسيات

المتحدث: Dr Aditya Agrawal

Consultant Pulmonologist Bombay Hospital & Medical Research Centre, Apollo Spectra and Breach Candy

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وصف

Pulmonary embolism (PE) is a critical medical condition characterized by the sudden blockage of one or more arteries in the lungs, typically caused by a blood clot that travels from another part of the body, often the legs (deep vein thrombosis). This obstruction can impede blood flow and oxygen exchange, leading to symptoms like chest pain, shortness of breath, and in severe cases, life-threatening complications. Rapid diagnosis through imaging studies, such as CT pulmonary angiography, and prompt treatment, often involving blood thinners and occasionally surgical interventions, are crucial to prevent further complications and ensure the patient's well-being.

ملخص

  • Pulmonary embolism (PE) is a blockage in the pulmonary artery or its branches, most commonly caused by a thrombus, but also potentially by tumor cells, air, fat, or amniotic fluid. Understanding pulmonary circulation is key, as the embolus often originates as a clot in the lower extremities due to injury and coagulation. PE is classified based on origin, temporal presentation, location, severity, and cause.
  • Classifying PE by chronicity includes acute (asymptomatic, symptomatic, or fatal), subacute (2-12 weeks post-symptom onset), and chronic (pulmonary hypertension group 4 for at least 6 months). Severity is categorized as massive (high-risk), submassive (intermediate-risk), or mild (low-risk). High-risk PE involves hemodynamic instability, requiring aggressive treatment, while intermediate-risk involves right ventricular dysfunction without hypotension. Classification is important for estimating 30-day mortality risk.
  • Risk factors significantly contribute to PE development. Strong risk factors include orthopedic dysfunction such as trauma, fractures, and hip or knee replacements. Moderate risks involve autoimmune conditions, cancer, immobility, and blood disorders. Weaker risk factors consist of bed rest, poorly controlled diabetes, high blood pressure, and immobility during travel or at home. Increasing age and inherited risks like Factor V Leiden mutation also elevate PE risk.
  • Clinical signs and features of PE can be varied. Classic signs like chest pain, dyspnea, and hemoptysis are present in less than 20% of cases. Common symptoms include breathlessness, chest pain, cough, palpitations, syncope, cyanosis, and diaphoresis. PE can present as pulmonary hemorrhage or infarction, isolated breathlessness, or circulatory collapse. Hemodynamic stability is defined by the absence of cardiac arrest or obstructive shock.
  • Diagnostic evaluation starts with assessing the likelihood of PE. If high, imaging modalities like CTPA or VQ scan are indicated. Chest x-rays should be performed in elderly patients to check for cardiopulmonary disease. The PERC rule identifies low-risk patients who can be ruled out for PE using a D-dimer test. D-dimer tests are sensitive but have low specificity and can be affected by age, cancer, and pregnancy.
  • Other diagnostic tools include ECGs, chest x-rays, 2D echocardiography, and pulmonary angiography. ECGs may show S1Q3T3, T-wave inversions, and sinus tachycardia. Chest x-rays may reveal vascular congestion, Westermark sign, or Hampton's hump. CT pulmonary angiography is considered the gold standard for PE diagnosis. Echocardiography can detect right ventricular dysfunction.
  • Treatment of PE depends on severity. Confirmed PE cases require assessment for bleeding risk. Those without high bleeding risk but with high PESI scores should be hospitalized. Acute PE management focuses on anticoagulation. High-risk patients may require reperfusion therapy and hemodynamic support. The treatment recommendations revolve around therapeutic anticoagulation for at least 3 months.
  • NOACs are recommended as first-line treatment for outpatients. After 6 months of therapeutic anticoagulation, a reduced dose of NOACs may be considered. If NOACs are unsuitable, aspirin or sulodexide may be considered for extended VTE prophylaxis. For patients with cancer and PE, weight-adjusted subcutaneous low molecular weight heparin should be considered for the first six months.

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