Fat embolism syndrome (FES) typically manifests within 24 to 72 hours post-injury or surgery. Fat droplets enter the bloodstream and become lodged in small blood vessels, leading to blockage and triggering a systemic inflammatory response. Suspect FES in any patient with recent fractures presenting with dyspnoea, rash, and altered consciousness. Diagnosis is often clinical as there are no specific confirmatory tests.
Fat Embolism: Rapid Onset After Injury |
- Key symptoms: Sudden breathlessness, upper body petechial rash, confusion or delirium
- Immediate ABC assessment, oxygen supplementation, and IV fluids
- Imaging: CXR to evaluate for ARDS; MRI if neurological symptoms are prominent
- Mechanical ventilation for severe respiratory distress
- Early surgical stabilization of fractures improves outcomes
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About Fat Embolism Syndrome
- FES is a rare but potentially life-threatening condition characterized by respiratory failure, neurological impairment, and cutaneous signs.
- Commonly arises after traumatic long bone fractures, particularly of the femur or pelvis, but can also occur after orthopedic surgeries.
- FES should be considered as a differential diagnosis for pulmonary embolism in patients with recent bone fractures.
Pathophysiology
- Fat embolism involves fat droplets entering the bloodstream, most commonly from bone marrow following long bone fractures.
- These droplets travel to the lungs and other organs, obstructing blood flow and leading to hypoxia, tissue injury, and a systemic inflammatory response.
- Hypoxia and inflammatory mediators can further exacerbate vascular permeability, resulting in ARDS-like symptoms.
Causes and Risk Factors
- Long bone fractures, particularly femoral and pelvic fractures
- Orthopedic surgeries involving bone marrow exposure
- Blunt trauma, acute pancreatitis, sickle cell crisis, and decompression sickness
- Intravenous lipid infusions, recent high-dose corticosteroids
Clinical Presentation
- Respiratory symptoms: Dyspnoea, tachypnoea, and hypoxia are often the earliest and most prominent signs.
- Neurological symptoms: Confusion, agitation, delirium, or coma can occur and may rapidly worsen without intervention.
- Cutaneous signs: Petechial rash, typically on the chest, axillae, and conjunctivae, is a distinctive but transient finding.
- Ocular findings: Retinal hemorrhages with fatty deposits, known as "Purtscher retinopathy."
Diagnosis
- Blood Tests: Non-specific findings may include thrombocytopenia, anaemia, and low fibrinogen levels.
- Urinalysis: Fat globules can sometimes be detected in the urine post-trauma.
- Imaging:
- CXR: Diffuse infiltrates resembling ARDS
- ABG: Shows hypoxia with potential respiratory acidosis
- CT Chest: May reveal ground-glass opacities, especially in ARDS cases
- MRI Brain: Consider for neurological involvement; may show diffuse white-matter petechial hemorrhages
Management
- Immediate resuscitation: ABCs with supplemental oxygen and mechanical ventilation as necessary
- Intensive monitoring: Admission to ICU/HDU for severe cases
- Supportive care: Fluid resuscitation, careful management of electrolytes, and maintaining hemodynamic stability
- Early fracture fixation: Reduces fat embolism risk and improves patient outcomes
- Corticosteroids: Potential benefit in decreasing inflammation; often used for severe or refractory cases but controversial
- Empiric antibiotics are generally unnecessary unless there is strong suspicion of concurrent infection.
Prognosis
- Mortality can reach 10-15% in severe cases, particularly with delayed diagnosis or intervention.
- Early recognition and prompt supportive care significantly improve prognosis, with most patients making a full recovery if treated early.
References