Which of the following are true/false about clinical features of Fat embolism syndrome? 1. Tachypnea 2. Systemic hypoxia may occur 3. Fat globules in urine are diagnostic 4. Manifests after several days of trauma 5. Petechiae in anterior chest wall
Fat embolism syndrome: Pathophysiology: It is a common phenomenon. It is most commonly seen in patients with multiple fractures and in fractures involving lower limb especially femur. Fat originates from the site of trauma, paicularly from the injured marrow of the fractures bone and the suggestion that the fat arises from the plasma as a result of agglutination of chylomicrons is not suppoed by the vivo experiments. Circulating fat globules >10 mm in diameters occurs in most adults after close fracture of long bones and histological traces of fat can be found in the lungs and other internal organs. Few of these patients develop clinical features similar to ARDS and are known as fat embolic syndrome. Clinical presentation: The patient is usually a young adult with a lower limb fracture (especially of femur), more commonly after closed fracture of long bone (especially of femur) and more so when fractures are multiple. It usually manifests itself within 24-48 hrs, but occasionally the onset may be delayed for several days. Early warning signs (within 72 hrs of injury) are a slight rise in temperature (pyrexia) and pulse rate (tachycardia). In more pronounced cases there is breathlessness, mild restlessness, petechiae on the chest,axillae, retina and conjunctival folds, progressing to marked respiratory distress and coma in severe cases. Management: Prevention: Rough handling, inadequate immobilization and long journey to reach trauma centre are predisposing factors that must be avoided in long bone fractures. Fracture stabilization by IM nail. Stopping the emboli from reaching main circulation by tieing profunda vein (this is of doubtful value) Removing fat emboli from circulation by lipolytic agents as heparin 9 serum lipase activity) Hypeonic glucose (decrease FFA production) Offset its effect by: Vasodilation e.g. phenoxybenzamine Prompt correction of hypovolemia Prophylactic use of O2 Dextran (expand plasma volume, reduce RBC aggregation and platelet adherence) Aprotinin (protease inhibitor) decrease platelet aggregation and serotonin release. Alcohol has vasodilator and lipolytic effect Treatment of established case: Aim of treatment is maintaining adequate O2 level in the ventilation. Oxygen is the only therapeutic tool of proven use. It should be administered in sufficient amount to maintain aerial PO2 > 80 mmhg. O2 toxicity (pneumonia) is avoided by using O2 conc. below 40% Steroids are given to avoid chemical pneumonia resulting from breakdown of pneumonia fat emboli in to FFA. Surface cooling will diminish O2 demand. Ref: Apley's 8/e, page 535; Maheshwari 3/e, page 34; Miller's Anesthesia 6/e, page 2425.
1,2,3,5 true & 5 false
2,4 false & 1,3,5 true
All are true
1,3,4,5 true & 2 false