Nonthrombotic embolism

Embolisms of fat, air, and amniotic fluid are uncommon but potentially life-threatening events caused when these substances enter the circulatory system. Fat emboli mostly originate from the bone marrow in patients with long bone fractures. Air can enter the circulatory system during surgical procedures (mostly neurosurgery), while amniotic fluid emboli occur during delivery. The emboli usually lodge within the pulmonary arteries and cause right ventricular outflow obstruction and circulatory collapse. Clinical features of nonthrombotic embolisms typically include acute onset of hypoxia, hypotension, and neurological symptoms (altered consciousness, seizures, coma). The diagnostic sign of fat embolism is a petechial rash on the upper body (if present), while that of venous air embolism is a mill wheel cardiac murmur. Diagnosis of any nonthrombotic embolism is primarily clinical, with arterial blood gas evaluation, ECG, and chest x-ray providing additional evidence. Treatment is mainly supportive and includes oxygenation, mechanical ventilation, and administration of vasopressors, if necessary. Mortality rates of all nonthrombotic embolisms are high.

• Definition: potentially life-threatening condition caused by the entry of fat cells, usually from bone marrow, into the circulatory system
• Etiology
  • Traumatic fat embolism (95% of cases)
    • Most commonly long bone fractures (e.g., femoral fracture)
    • Orthopedic surgeries
    • Bone marrow transplant
  • Non-traumatic fat embolism
    • Sickle cell crisis
    • Others: pancreatitis, osteomyelitis, parenteral lipid infusion
• Pathophysiology
  • Traumatic fat embolism: fat cells from bone marrow enter systemic circulation and occlude the pulmonary arterioles → right heart failure and pulmonary edema
  • Non-traumatic fat embolism: ↑ cytokine levels (e.g., CRP, TNF) → agglutination of chylomicrons in the circulation → fat emboli formation
  • Lipases metabolize the lodged fat cells (in pulmonary arterioles) → release of free fatty acids → pulmonary arteriolar endothelial injury → acute lung injury/respiratory distress
  • Emboli can enter systemic arterial circulation through a patent foramen ovale, if present → dermatological and neurological manifestations (see below)
• Clinical features
  • Symptoms develop within 12 hours to 2 weeks of the inciting insult
  • Classic triad of
    1. Hypoxia (most common symptom): tachypnea, dyspnea, cyanosis, diffuse crackles in the chest
    2. Neurological symptoms: confusion, lethargy, seizures, focal neurological deficits, coma
    3. Petechial rash (seen in up to 50% patients) : mainly seen in the axilla, chest wall, head, neck, conjunctiva, and buccal mucosa
       • Appears within 1–3 days; disappears within a week
• Diagnosis: mainly clinical
  • Complete blood count: anemia, thrombocytopenia
  • Chest x-ray: mostly normal; bilateral infiltrates may be seen
  • Microscopic examination of urine and sputum: fat droplets may be seen
  • Since there are no specific diagnostic tests, the following clinical criteria are used to diagnose fat embolism.

• Treatment: supportive care in an intensive care unit
• Prognosis: mortality rate ∼ 15%

References:^{[1][2][3][4][5]}

• Definition: : potentially life-threatening condition caused by the entry of air into circulation, often during a surgical procedure
• Etiology
  • Surgery; : neurosurgical procedures (highest risk) ; laparoscopic surgery
  • Trauma
  • Barotrauma: mechanical ventilation ; decompression sickness
  • Accidental injection of air (infusion-related errors); intentional injection of air (suicidal/homicidal intent)
  • Central venous catheter (insertion and removal)

• Treatment
  • General measures
    • Compression of the suspected site of entry (airtight sealing)
    • Correction of hypoxia and hypotension
    • Initiate CPR, if necessary
  • Position change (venous air embolism): Trendelenburg (head down position) and left lateral decubitus (Durant maneuver)
  • Central venous line insertion and direct aspiration of air bubbles from the cardiac chambers
  • Chest compression (closed cardiac massage)
• Prognosis: high mortality rate (≥ 30%)

References:^[6][7][8][9]

• Definition: rare, but life-threatening condition caused by the entry of fetal cells and debris (from the amniotic fluid) into maternal circulation
• Pathophysiology
  • Desquamated fetal cells or lanugo from amniotic fluid enter maternal circulation and embolize to the pulmonary arterioles → increased pulmonary arterial pressure, right heart failure, and pulmonary edema
  • Entry of procoagulants (thromboplastin) from amniotic fluid into maternal circulation → diffuse intravascular coagulation
  • Entry of leukotrienes from amniotic fluid into maternal circulation → triggering of an immune response → pulmonary vasospasm, alveolar capillary damage (pulmonary edema), and hypotension
• Risk factors
  • Maternal age > 30 years
  • Multiparity
  • Complicated labor (e.g., placenta previa/abruption, forceps delivery, eclampsia)
• Clinical features
  • AFE mostly occurs during labor.
  • Prodrome: nonspecific symptoms (anxiety, a sense of impending doom, shivering, cough)
  • Acute onset of
    • Respiratory collapse: hypoxia; , dyspnea, tachypnea, cough, cyanosis, basal crepitations, acute respiratory distress syndrome
    • Cardiovascular collapse: hypotension; , arrhythmias, cardiac arrest
    • Altered consciousness (drowsiness, seizures)
    • Features of disseminated intravascular coagulation
    • Multi-organ dysfunction
    • Fetal bradycardia (decelerations on cardiotocography)
• Diagnosis: mainly clinical
  • Arterial blood gas evaluation: features of respiratory acidosis
  • Complete blood count: anemia, thrombocytopenia
  • Coagulation studies: prolonged prothrombin time (PT)
  • ECG: to detect arrhythmias
  • Pulmonary artery blood sample: presence of squamous cells, hair or other fetal debris in maternal blood
• Differential diagnosis
  • Placental abruption or uterine rupture
  • Air embolism, pulmonary embolism (see above)
  • Septic shock or anaphylaxis
• Treatment
  • Correction of hypoxia: high flow oxygen or intubation and mechanical ventilation
  • Correction of hypotension/shock: vasopressors (noradrenaline or dopamine)
  • Correction of anemia and coagulopathy : transfusion of platelet/fresh frozen plasma (FFP) and packed red blood cells
  • Emergency cesarean delivery
• Prognosis
  • High maternal mortality rate
  • Neurological deficits in surviving infants

References:^{[10][11][12][13]}

• Definition: respiratory insufficiency because of embolization of bone cement material or indirect systemic effects after bone cement implantation
• Occurrence: after orthopedic procedures using bone cement material
• Pathophysiology: direct mechanical embolization and thermal effects or an immunological-mediated release of vasoactive substances; often associated with fat embolism
• Clinical features
  • Symptoms of a pulmonary embolism
  • Acute respiratory distress syndrome
• Diagnostics: CT pulmonary angiogram for the detection of mechanical embolization
• Treatment
  • Supportive (intensive care) measures, including mechanical ventilation and catecholamine therapy
  • If necessary, interventional or surgical removal of the embolic cement material