Pulmonary embolism

Age >40 years
History of venous thromboembolism
Prolonged immobilization, including long air or ground travel
Trauma or major surgery
Hormonal contraceptives or hormonal replacement therapy
Acute illness or inflammatory diseases (such as inflammatory bowel disease)
Genetic or acquired thrombophilia
• Factor V Leiden
• Lupus anticoagulant
• Antiphospholipid antibody syndrome
• Antithrombin III deficiency
• Protein C or protein S deficiency

Critical presentation

  • With significant clot burden, right heart strain can develop, with right ventricular dilation and hypokinesis and clinical signs of right heart failure.
  • Decreased flow of blood through the right-heart system can lead to impaired left ventricular filling, causing tachycardia and systemic hypotension.
  • Pulseless electrical activity (PEA) is the most common rhythm in cardiac arrest caused by obstructive PE.

Diagnosis and evaluation

  • The evaluation for suspected PE is tailored to the level of the clinician’s suspicion for this diagnosis based on the patient’s history, physical examination, and risk factors.
  • ECG

    • ECG changes in PE are usually the result of acute pulmonary hypertension, manifesting as tachycardia, symmetrical T wave inversion in the anterior leads (V1–V4), the nonspecific McGinn–White S1Q3T3 pattern, P-wave pulmonale, and right bundle branch block.

  • Chest radiography and ultrasonography

    • A chest radiograph is rarely diagnostic for PE, but can identify alternative diagnoses.
    • “Hampton’s hump,” a pleural-based, wedge-shaped area of infiltrate, can be seen in pulmonary infarction and is suggestive of PE.
    • “Westermark’s sign,” unilateral lung oligemia, is a rare radiographic manifestation of a large PE.
    • If DVT is identified on venous ultrasonography of the lower extremities in a hemodynamically stable patient with suspected PE, anticoagulant therapy can be initiated before further testing.

  • Laboratory tests

    • The D-dimer assay, which detects the presence of fibrin degradation products, can be used as a screening test for the presence of thromboembolic disease.
    • Positive screens are nonspecific, as this test can become positive in many inflammatory states including trauma, infection, or other acute illness.
    • If a patient is deemed to have low-to-moderate clinical probability for PE estimated by clinical prediction rules (Table 34.2), a negative D-dimer test can preclude the need for further evaluation and imaging studies.
    • Troponin and brain natriuretic peptide (BNP) levels can risk-stratify patients with confirmed diagnosis of PE, but are not diagnostic tools.
    • Elevated BNP and troponin have independently been associated with increased risk of adverse outcome and death in acute PE.

  • Pulmonary imaging

    • If the clinical probability for PE is high or the D-dimer screen is positive, perform CT angiography of the lungs (Figure 34.1) or ventilation–perfusion (VQ) scintigraphy if CT is contraindicated, such as in renal failure or allergy to intravenous contrast dye.
    • Magnetic resonance angiography has insufficient sensitivity for the diagnosis of PE.
    • Due to the accuracy of noninvasive imaging, use of conventional pulmonary angiography is rare.

Feb 17, 2017 | Posted by in CRITICAL CARE | Comments Off on Pulmonary embolism

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