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What is Feature of fat embolism includes all except: (PGI Dec 2010) and explain in detail?
Ans: D Commonly Manifests after several days of trauma Commonly Manifests after several days of trauma- this is rarely seen . Hence, this statement is wrong. Correct statement is- Usually manifests itself within 24-48 hours of trauma "Sputum & urine mav reveal the presence of fat a lobulesQ"- Maheswari 3rd/34 Fat Embolism Syndrome | | | | Pathophysiology * Fat embolism is a common phenomenon It is more commonly seen in patients with multiple fractures and in fractures (involving lower limb especially femurQ * 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 the vivo experiments,. * Circulating fat globules > 10 mm in diameter occur in most adults after close fracture of long bonesQ and histological traces of fat can be found in the lungs and other internal oigans. * Few of these patients develop clinical features similar to ARDS and are k/a fat embolism syndrome Clinical Presentation - The patient is usually a young adult with a lower limb (esp. femur) fracture, most commonly after closed fractures of long bone (esp) shaft femurQ and more so when fractures are multipleQ - It usually manifests itself within 24-48 hoursQ, but occasionally 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 , PectechiacQ on chest, axillae, retina & conjuctival folds; progressing to marked respiratory distress & coma in severe cases. Management * Prevention: - Rough handling, inadequate immobilization and long journey to reach trauma center predisposing factors that must be avoided in long bone fractures - Fracture stabilization by IM nail * Stopping the emboli from reaching main circulation bytieing profunda vein (? of doubtful value) * Removing fat emboli from circulation by - Lipolytic agents as heparinQ ( serum lipase activity) - Hypertonic glucose (decrease F FA production) * Offset its effect by - Vasodilation e.g. phenxv benzamine - Prompt correction of hypovlemia - Prophylactic use of O2 - DextranQ (expand plasma volume, reduce RBC aggregation and platelet adherence) - Aprotinin (this protease inhibitor) decrease platelet aggregation and serotonin release) - Alcohol has vasodilator & lipolytic effect. * Treatment of Established Case - The aim of treatment is maintaining adequate oxygen level in the ventilation. - Oxygen is the only therapeutic tool of proven useQ. It should be administered in sufficient amount to maintain arterial PO 2 > 80 mm Hg - O2 toxicity (pneumonitis) is avoided by using O2 cone, below 40%. - Steroids are given to avoid chemical pneumonitis resulting from break down of pulmonary fat emboli into FFA - Surface cooling w ill diminish O2 demand.