Fat Embolism SyndromeFat embolism refers to the presence of fat globules in lung parenchyma and peripheral circulation after fracture of a long bone or other major trauma. And fat embolism syndrome reflects a serious systemic manifestation as a consequence to these emboli.
- Fat embolism is a common phenomenon it is more commonly seen in patients with multiple fractures and in fractures (involving lower limbs especially femur)
- Fat originates from the site of trauma, particularly from the injured marrow of the fractured bones and the suggestion that the fat arises from the plasma as a result of agglutination of chylomicrons is not supported by in vivo experiments.
- Circulating fat globules>10 ยตm in diameter occur in most adults after close fracture of long bones and histological traces of fat can be found in the lungs and other internal organs.
- The patient is usually young adult with a lower limb (esp. femur) fracture, most commonly after closed fractures of long bone (esp. shaft femur) and more so when fractures are multiple.
- It usually manifests itself with in 24-48 hoursQ, but occasionaly the onset may be delayed for several days.
- Early warning signs (with in 72 hours of injury) are a slight rise in temperature (pyrexia) and pulse rate (tachycardia)Q
- In more pronounced cases there is breathlessness, mild mental confusion or restlessness, pectechiae on chest, axillae, retina & conjuctival folds; progressing to marked respiratory distress & coma in severe cases.
- Pulmonary Manifestations
- Tachypnea (increased respiration rate) with cyanosis
- Dyspnea (breathlessness)
- Low oxygen content often with a normal CO2 reading indicating there is inadequate oxygenation
- PO2<60 mmHg
- Chest x-ray show snow storm appearance and mottling -a sign which rapidly disappears in a day or two.
- Cerebral Manifestation
- Mild mental confusion or restlessness
- Cerebral signs may regress & recur, suggesting repeated flooding of the circulation with fresh emboli.
- โCutaneous Manifestation
Diagnostic petechial rash seen on
- Front & back of chest
- Retinae and
- Conjunctiva of lower lid
There is no characteristic laboratory test However suggestive findings are
- Thrombocytopenia (platelets โค1.5 lacks)
- P02 <60 mm Hg (8 kpa)
- Fall in hemoglobin value
- Microscopy of blood, sputum & urine for fat globules (gurd test)
- Fundoscopy of retina to see emboli, striate haemorrhages and fluffy exudates
- NCCT Head: shows characteristic focal emboli showers intracerebral region.
- Rough handling, inadequate immobilization and long journey to reach trauma centre are predisposing factors that must be avoided in long bone fractures.
- Fracture stabilization
- Removing fat emboli from circulation by
- Lipolytic agents as heparin (โ serum lipase activity)
- Hypertonic glucose (decrease FFA production)
- Offset its effect by
- Vasodilation eg phenoxy benzamine
- Prompt correction of hypovolaemia
- Prophylactic use of O2
- Dextran (expand plasma volume, reduce RBC aggregation and platelet adherence)
- Aprotinin (this protease inhibitor decrease platelet aggregation and serotonin release)
- Treatment of Established Case
- The aim of treatment is maintaining adequate oxygen level in the blood. If necessary by using intermittent positive pressure ventilation.
- Oxygen is the only therapeutic tool of proven use. It should be administered in sufficient amount to maintain arterial P02 >80 mm Hg
- O2 toxicity (pneumonitis) is avoided by using O2 conc. below 40%
- Steroids are given to avoid chemical pneumonitis resulting from break down of - pulmonary fat emboli into FFA.