Harvey's Garden

Nonthrombotic embolism

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Air Embolism

  • Epidemiology & Risk Factors

    • Iatrogenic (Most common): Central venous catheter (CVC) insertion/removal (esp. if pt is sitting up or taking a deep inspiration). c
    • Surgical: Neurosurgical procedures in the sitting position (e.g., posterior fossa tumor resection), cardiothoracic surgery.
    • Barotrauma: Scuba diving (rapid ascent), positive pressure ventilation (alveolar rupture).
    • Trauma: Penetrating chest trauma.

  • Clinical Features

    • Venous Air Embolism (VAE): Sudden onset dyspnea, tachypnea, hypoxemia, cough.
    • Hemodynamics: Obstructive shock (hypotension, tachycardia, ↑ JVP, sudden ↓ in ETCO2).
    • Auscultation: “Mill-wheel” murmur (loud, churning, continuous machine-like murmur over the precordium).
    • Arterial Air Embolism (AAE): Occurs via paradoxical embolism (e.g., patent foramen ovale[PFO], ASD) or direct pulmonary vein entry. Presents with acute neurologic deficits (stroke-like sx, altered mental status, seizures) or myocardial ischemia.

  • Diagnosis

    • Initial/Screening: Primarily a clinical diagnosis. Intraoperative monitoring shows sudden drop in end-tidal CO2 (ETCO2) due to ↑ alveolar dead space.
    • Confirmatory/Gold Standard: Transesophageal echocardiogram (TEE). Most sensitive modality; visualizes air bubbles in the right atrium/ventricle or crossing a PFO.
    • Key Labs/Imaging: ABG shows hypoxemia and hypercapnia. CT head/chest may reveal air pockets but is rarely done acutely due to HD instability.

  • Differential Diagnostics

    • Thrombotic Pulmonary Embolism: Diff by timeline and triggers (e.g., prolonged immobility, active cancer vs. sudden onset during CVC removal); lacks the classic mill-wheel murmur.
    • Tension Pneumothorax: Diff by unilateral absent breath sounds, hyperresonance to percussion, and tracheal deviation.
    • Acute Myocardial Infarction: Diff by classic ECG findings (ST elevations), though AAE can cause coronary ischemia; onset is typically less abrupt than an iatrogenic air embolism.

  • Management

    1. Immediate/First-line:
      • Stop further air entry: Immediately occlude the CVC site/leak (or flood surgical field with saline).
      • Positioning: Place pt in Left lateral decubitus AND Trendelenburg (Durant’s maneuver). Mechanism: Traps air in the right ventricular apex, preventing it from entering and obstructing the right ventricular outflow tract (RVOT) and pulmonary artery.
      • Oxygenation: Administer 100% O2 (creates a diffusion gradient that accelerates resorption of nitrogen from the air bubble).
    2. Second-line: Aspiration of air via a CVC (if the catheter tip is already situated in the right atrium). Provide hemodynamic support (IVF, vasopressors).
    3. Refractory/Special Circumstances: Hyperbaric Oxygen Therapy (HBOT). Treatment of choice for Arterial Air Embolism (especially with severe neurologic deficits or HD instability) to rapidly decrease bubble size.

  • Complications

    • Cardiovascular collapse and cardiac arrest (due to RVOT obstruction), Cardiac arrhythmia
    • Cerebral infarction (stroke).
    • Myocardial infarction.
    • Death.

Fat Embolism Syndrome

  • Epidemiology & Risk Factors
    • Long bone fractures (femur, tibia, pelvis).
    • Orthopedic surgery (e.g., intramedullary nailing).
    • Severe burns, liposuction, acute pancreatitis, bone marrow transplant.
    • Fat droplets are microscopic and lodge in the pulmonary capillary beds and microvasculature (subsegmental/terminal arterioles). c So no filling defects on CTA.
      • Unlike thromboembolic PE, which has large, organized blood clots lodge in macrovasculature (main, lobar, or segmental pulmonary arteries).
  • Clinical Features
    • Latency: Usually 24–72 hours post-injury.
    • Classic Triad:
      • Respiratory: Dyspnea, tachypnea, hypoxemia (can progress to ARDS).
      • Neurologic: Altered mental status (AMS), confusion, lethargy, focal deficits (usually transient).
      • Petechial Rash: Non-palpable, petechiae in a vest-like distribution (neck, axillae, chest, subconjunctival). Occurs in only 20-50% but is highly specific.
    • Fever, tachycardia, thrombocytopenia.
  • Diagnosis
    • Clinical Diagnosis: Based on Gurd’s criteria (classic triad + minor criteria). No single gold-standard diagnostic test.
    • Initial/Screening:
      • Pulse oximetry/ABG (shows hypoxemia, ↑ A-a gradient).
      • CXR (normal initially; progresses to bilateral diffuse patchy infiltrates / “snowstorm” pattern). c
        • Pulmonary endothelial lipase breaks down the embolized neutral fat into Free Fatty Acids (FFAs). FFA toxicity triggers a massive local inflammatory response (neutrophil activation, cytokine release), leading to ARDS.
    • Key Labs:
      • CBC (thrombocytopenia, anemia).
      • Urine/sputum analysis (may show lipid droplets, but low sensitivity/specificity).
    • Imaging/Other:
      • Brain MRI: Indicated for unexplained AMS. Shows “starfield pattern” (diffuse, punctate hyperintensities on DWI).
      • CTPA: Often obtained to rule out thromboembolic PE; may show ground-glass opacities but cannot directly visualize fat emboli in subsegmental vessels.
  • Differential Diagnostics
    • Thromboembolic Pulmonary Embolism (PE): Diff by lack of petechial rash, lack of early AMS, later onset (usually >3-5 days post-op/injury vs 24-72h for FES). CTPA shows filling defects in main/lobar arteries.
    • Acute Respiratory Distress Syndrome (ARDS): Diff by absence of petechial rash and focal neurologic deficits; triggered by sepsis, trauma, or severe pancreatitis.
    • Transfusion-Related Acute Lung Injury (TRALI): Diff by acute onset during or within 6 hours of blood product transfusion; no petechiae.
    • Alcohol Withdrawal Delirium (DTs): Diff by history of heavy alcohol use, autonomic hyperactivity (severe tremors, diaphoresis, hallucinations), lack of respiratory distress/petechiae.
  • Management
    • First-line (Supportive):
      • Supplemental O2; mechanical ventilation (intubation + PEEP) if ARDS develops.
      • Hemodynamic support (IVF, vasopressors if shock).
    • Prevention (Key Step): Early stabilization and operative fixation of long bone fractures (within 24 hours of injury).
    • Refractory/Adjunct: Systemic corticosteroids (methylprednisolone) may be considered in high-risk patients, but evidence is controversial; not routinely recommended over supportive care.
  • Complications
    • ARDS (primary cause of mortality).
    • Permanent neurologic deficits (stroke, cognitive impairment).
    • Multi-organ dysfunction syndrome (MODS).

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