The Young Orthopod

Introduction Fat embolism syndrome follows long bone fractures . Its classic presentation consists of an asymptomatic interval followed by pulmonary and neurologic  manifestations combined with petechial hemorrhages . The syndrome follows a biphasic clinical course . The initial symptoms are probably caused by mechanical occlusion of multiple blood vessels with fat globules that are too large to pass through the capillaries. ✫ Unlike other embolic events, the vascular occlusion in fat embolism is often temporary or  incomplete since fat globules do not completely obstruct capillary blood flow because of their  fluidity and deformability. • The late presentation is thought to be a result of hydrolysis of the fat to more irritating free fatty  acids which then migrate to other organs via the systemic circulation .  Etiology Many aspects of the fat embolism syndrome remain poorly understood , and disagre

Hemorrhagic shock is a condition of reduced tissue perfusion, resulting in the inadequate delivery of oxygen and nutrients that are necessary for cellular function.  Whenever cellular oxygen demand outweighs supply, both the cell and the organism are in a state of shock. Classes Of Shock Class 1 – < 15 % loss blood volume (< 750 mL in a male weighing 70 kg) (No change in BP, pulse pressure, respiratory rate or capillary refill) Minimal tachycardia < 100 bpm Skin pallor possible Class 2 – 15–30 per cent loss blood volume ( 750–1500 mL) (No change in systolic blood pressure) ↓ Peripheral perfusion with cool, pale, clammy skin Capillary refill > 2 seconds Tachycardia > 100 bpm ↓ Pulse pressure as diastolic bp rises Increased respiratory rate (tachypnoea) of 20–30 /min Subtle mental status changes: anxiety, fear, aggression Class 3 – 30–40 per cent loss blood volume ( 1500– 2000 mL ) Marked tachycardia > 120 bpm Measurable fall in systo

I. Systemic Factors     1. Age 2. Activity level including     General immobilization Space flight   3. Nutritional status 4. Hormonal factors     Growth hormone Corticosteroids (microvascular osteonecrosis) Others (thyroid, estrogen, androgen, calcitonin, PTH, prostaglandins) 5. Diseases: DM, anemia, neuropathies, tabes 6. Vitamin deficiencies: A, C, D, K 7. Drugs: nonsteroidal antiinflammatory drugs (NSAIDs), anticoagulants, factor XIII, calcium channel blockers (verapamil), cytotoxins, diphosphonates, phenytoin (Dilantin), sodium fluoride, tetracycline 8. Other substances (nicotine, alcohol) 9. Hyperoxia 10. Systemic growth factors 11. Environmental temperature 12. Central nervous system trauma II. Local Factors      A. Factors independent of injury, treatment, or complications     1. Type of bone 2. Abnormal bone     Radiation necrosis Infection Tumors & other pathological condns 3. De