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Crush syndrome - Dr Bipul Borthakur
- 1. CRUSH SYNDROME Moderator: Dr.Bipul Borthakur Professor, Dept Of Orthopaedics SMCH
- 2. DEFINITION Crush syndromeis the systemic manifestation of RHABDOMYOLYSIS caused by prolonged continuous pressure on muscle tissue. Crush syndrome includes crush injury and compartment syndrome.
- 3. CAUSES OF CRUSHSYNDROME Immobility against firm surface for > 1 hour Drug or alcohol intoxication. Carbon monoxide poisoning. Cerebrovascular accident. Head trauma with coma. Elderly with hip fracture. Improper positioning of surgical patient. Assault with beating. Pneumatic antishock garment(PASG OR MAST)
- 4. PATHOPHYSIOLOGY Stretch of musclesarcolemma Sarcolemma permeability increases Influx of sodium, water and extracellular calcium into the sarcoplasm
- 5. Results in cellularswelling , ↑sed intracellular calcium , disrupted cellular function & respiration ↓sed ATP production Subsequent myocytic death
- 7. CLINICAL FEATURES Petechiae, blisters and muscle bruising. Myalgia, muscle paralysis and sensory deficit are common. Fever, cardiac arrhythmia, pneumonia, (tea or cola) coloured urine, oliguria and renal failure. Nausea, vomiting, agitation and delirium are seen in delayed rescue patients
- 9. CONTENTS RELEASED DURING RHABDOMYOLYSIS& THEIR EFFECTS • Hyperkalemia & cardiotoxicity • Provoked by hypocalcemia & hypovolemia. Potassium • Hyperphosphatemia. • Metastatic calcification. Phosphate • Myoglobinuria. • Nephrotoxicity. Myoglobin
- 10. • Elevation ofserum ck level Creatine kinase • Disseminated intravascular coagulationThromboplastin • Metabolic acidosis & aciduria Organic acids
- 11. INVESTIGATIONS Complete haemogram. ECG Arterial blood gas analysis, myoglobin. Serum creatinine kinase (CKMM) > 1000IU/I with clinical feature is taken as an indicator of crush syndrome. Peaks in 1 to 3 days. Normal range 25-175U/I. Serum aldolase, myoglobin degradation.
- 12. Serum lacticacid, AST, ALT and LDH show steady rise. Serum urea and creatinine – steep rise after prolonged crush. Serum potassium show early rise and is predictor for dialysis. Intracompartmental pressure monitoring if > 30mm Hg fasciotomy may be required.
- 13. TREATMENT Medical management 1.Fluid replacement 2.Ventilatory support 3.Correction of metabolic acidosis 4. Dialysis if required Surgical management 1. Emergency fasciotomy 2. Debridement of nacrotic tissue 3. Delayed VAC and skin grafting
- 14. FLUID RESUSCITATION Itis the mainstay of treatment 0.9% normal saline is preferred. Early most preferably within first 6 hours is essential. To counter metabolic acidosis bicarbonate and lactate or even oral citrate is essential. 50 mmol of bicarbonate for every lit of isotonic saline is used.
- 16. Diuresis- This isto maintain effective kidney function. Mannitol diuresis is indicated in setting of compartment syndrome. Dialysis- Important predictive factors:- 1. Anuria 2. Fluid overload 3. ↑sed creatinine level 4. ↑sed BUN and bicarbonate level
- 17. Potassium >7meq/l is independent and important predictive factor for dialysis. It may be required for 15 days. Hyperbaric oxygen- It ↓ses outflow from vascular compartment Reduces tissue edema promotes wound healing by fibroblast proliferation Reduces anaerobic bacterial growth
- 18. Multiple broadspectrum non nephrotoxic antibiotic may be needed. Surgery- Laparotomy and thoracotomy with debridement of necrosed muscles. Fasciotomy if compartmental pressure rises can be done as early as possible. Fractures need fixation and conservative amputations may have to be performed.
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