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FEMA US&R RESPONSE SYSTEM TASK FORCE MEDICAL TEAM TRAINING 04/97 US&R MEDICAL PROBLEMS IV. US&R MEDICAL PROBLEMS A. CRUSH SYNDROME CRUSH SYNDROME INTRODUCTION n Predictable Course... n Crush injury and crush syndrome are common in trapped • Patients survive for days in victims of collapsed structures. their entrapment n Post-extrication medical deterioration and death occur from • Patients may die shortly after potentially treatable mechanisms and so this illness is a rescue if untreated primary reason to provide the victim with prompt care within the collapsed structure. • Patients survive if treated early and aggressively CRUSH SYNDROME: PREDICTABLE SEQUELAE "in the rubble" n Patients survive entrapment for days with this injury. n Patients may die shortly after rescue if not treated. VIEW GRAPH IV A - 1 n Patients may die days to weeks later if not properly treated on scene. n Patients survive if treated early and aggressively, starting "in the rubble." CRUSH SYNDROME: FREQUENCY FEMA US&R RESPONSE SYSTEM n Tangshan data (Yong et al) TASK FORCE MEDICAL TEAM TRAINING • 28 July, 1976. 04/97 • Magnitude 7.8. • 361,300 persons injured. US&R MEDICAL PROBLEMS • 242,769 persons killed. • 20% suffered from Crush Syndrome. CRUSH SYNDROME n Armenian data (Klain et al) • 7 December, 1988. n Tangshan data • Magnitude 6.9. • Crush injuries were third most common injury. • 28 July, 1976 • Crush Syndrome was leading cause of death in patients reaching medical care. • Magnitude 7.8 • 351,300 persons injured • 242,769 persons died FEMA US&R RESPONSE SYSTEM TASK FORCE MEDICAL TEAM TRAINING MANUAL 04/97 IV. US&R MEDICAL PROBLEMS A. CRUSH SYNDROME DEFINITIONS Direct mechanical crush n Mechanical disruption of tissue secondary to severe force. n Immediate cellular effect/injury. Crush injury n Muscle cell disruption due to compression. n Time/pressure relationship. n Cellular mechanism of injury controversial: • Stretch "membranopathy" • Cellular ischemia • Re-oxygenation injury Compartment syndrome n Crush injury caused by swelling of tissue inside confining fibrous sheath of muscle compartments. n Causes further destruction of intra-compartmental muscle and nerves. Crush syndrome n The systemic manifestations caused by crushed muscle tissue. n Occurs when crushed muscle is released from compression. 2 FEMA US&R RESPONSE SYSTEM TASK FORCE MEDICAL TEAM TRAINING MANUAL 04/97 IV. US&R MEDICAL PROBLEMS A. CRUSH SYNDROME DEFINITIONS (continued) Muscle tissue in compression n Muscle tissue exquisitely vulnerable to sustained pressure. n Compression may be caused by debris or by the patient's own body weight, especially if lying on a hard surface. n "Time-frame" until crush injury depends upon the amount of pressure and patient factors: • As short as one hour if compression is severe. • 4-6 hours is the more common period until significant FEMA US&R RESPONSE SYSTEM crush occurs. TASK FORCE MEDICAL TEAM TRAINING 04/97 n Amount of tissue injury to cause Crush Syndrome variable: usually lower extremities, buttocks or entire upper extremity/pectoralis area. n Muscle tissue in compression PATHOPHYSIOLOGY OF CRUSH INJURY • Muscle tissue is exquisitively n Normal muscle cell function: vulnerable to sustained • Arterial blood provides glucose/oxygen/ nutrients to the compression cells. • Cell membrane "sequesters" cellular contents and uses • Compression from debris or complex mechanisms to transport nutrients and to body weight maintain concentration gradients across the membrane of vital electrolytes. • "Time-frame" - one to six hours • Muscle cell uses oxygen/glucose/ nutrients to produce • Amount of muscle tissue: energy for normal cell function. - lower extremities • Myoglobin rapidly transports oxygen within muscle cells - buttocks to allow normal function. - entire upper extremity • Capillaries are the smallest blood vessels in the body and pectoralis and allow efficient transfer of oxygen/glucose/nutrients to tissue/cells. • Venous blood carries away CO2 and waste products, including lactic acid, for disposal or metabolism elsewhere in the body. 3 FEMA US&R RESPONSE SYSTEM TASK FORCE MEDICAL TEAM TRAINING MANUAL 04/97 IV. US&R MEDICAL PROBLEMS A. CRUSH SYNDROME PATHOPHYSIOLOGY OF CRUSH INJURY (continued) n Cell function in crush situation: • Local arterial blood flow interrupted. • Lack of oxygen causes cells to function "anaerobically," creating lactic acid and other toxins. • Cellular membrane function is disrupted (mechanism is controversial), causing cell death and dissolution. • Intracellular contents, including myoglobin, potassium, purines (later converted to uric acid) and other toxic substances are released into the local tissue area. TASK FORCE MEDICAL TEAM TRAINING 04/97 • Local capillaries are injured and become "leaky", allowing an increased serum portion of the blood to extrude into the tissue. • The re-introduction of oxygen into the tissue later may cause additional "re-oxygenation" injury by creating other toxins such as free radicals, superoxides and n Effects of crush injury thromboxane. • Lactic acid production • Potassium/other electrolyte release • Myoglobin release n Effects of muscle cell crush injury (summarized) • Other toxins created/released (superoxides, free O2 radicals, etc.) • Lactic acid production. • Uric acid production • Potassium and other electrolytes release. • Capillary leak • Myoglobin released. • Thromboxane, prostaglandins and • Other toxins released/created (super-oxides, free other immune system substances radicals, etc.). generated • Lysosomal enzyme release. • Muscle cell enzymes released • Uric acid production. • Capillary leak. • Thromboxane, prostaglandins and other immune system substances generated. • Muscle cell enzymes (CPK, etc.) which are useful for in- hospital tests to approximate the amount of tissue destruction. 4 TASK FORCE MEDICAL TEAM TRAINING 04/97 FEMA US&R RESPONSE SYSTEM TASK FORCE MEDICAL TEAM TRAINING MANUAL 04/97 IV. US&R MEDICAL PROBLEMS n Effects of releasing compressed tissue A. CRUSH SYNDROME • Capillary leak - Error! FEMA US&R RESPONSE SYSTEM - hypovolemia TASK FORCE MEDICAL TEAM TRAINING 04/97 - hypotension CRUSH INJURY - shock • Severe metabolic acidosis - V-fib n All these effects are local only until the tissue is released and reperfused by blood. • High serum potassium - n Crush cardiac injury dysrhythmia or standstill n That is why patients may remain entrapped for days with a severe crush injury and yet appear systemically stable when • Myoglobin/uric acid/renal toxins - reached by rescuers. • Effects are LOCAL ONLY until kidney failure tissue is released and re-perfused by blood n Upon release of compression, blood flow is restored to the • Other toxins - crushed area and multiple adverse processes begin. lung/liver/renal injuries • Reason that patients survive n Effects of releasing compressed tissue: entrapment despite severe • Capillary leak Þ Hypovolemia/hypotension/shock. crush injury • Severe metabolic acidosis Þ V-fib. • High serum potassium level Þ Cardiac arrhythmia or standstill. • Adverse processes begin • Myoglobin/Uric acid/other "toxins" Þ kidney failure. immediately upon tissue release • Leukotrienes and other cell mediators: - lungs Þ adult respiratory distress syndrome - liver Þ cellular injury Error! CRUSH SYNDROME: MAJOR CAUSES OF DEATH n Hypovolemia. n Dysrhythmia. n Renal failure. OTHER CAUSES OF DEATH n Adult Respiratory Distress Syndrome (ARDS): severe lung injury. n Sepsis. n Other electrolyte disturbances. 5 FEMA US&R RESPONSE SYSTEM TASK FORCE MEDICAL TEAM TRAINING MANUAL 04/97 n Ischemic organ injury (gangrene). 6 TASK FORCE MEDICAL TEAM TRAINING 04/97 FEMA US&R RESPONSE SYSTEM TASK FORCE MEDICAL TEAM TRAINING MANUAL 04/97 IV. US&R MEDICAL PROBLEMS n Myoglobin A. CRUSH SYNDROME • "Spills" into urine at low serum levels CRUSH SYNDROME: POTENTIAL CLINICAL MANIFESTATIONS • Causes reddish-brown urine n Pre-release of entrapment: color in high concentrations • Painless crushed extremity (hypesthesia or anesthesia). • Detectable using urinalysis • Distal pulses +/- present. "dip-strip" n Post-release of entrapment: • May precipitate in kidney tubules, contributing to renal failure • Agitation. • Continued hypesthesia/anesthesia, or • Solubility in urine influenced • Severe pain in crushed extremity. by urine pH • Muscle function decreased/paralysis. • Progressively marked swelling of the area. • Systemic problems. CRUSH INJURY: DIAGNOSIS n High index of suspicion. n Identifying potential crush mechanism. n Looking for subtle signs and symptoms. n Urinary myoglobin post-release. MYOGLOBIN n "Spills" into urine at relatively low serum levels. n Causes reddish-brown urine color in high concentrations. n Lower concentrations detected by positive orthotolidene ("hemoglobin" test) on urinalysis dip-strip. n May precipitate in kidney tubules, contributing to renal failure by obstruction and heme-iron-mediated lipid peroxidation process. n Solubility in urine is markedly influenced by urine pH. 7 FEMA US&R RESPONSE SYSTEM TASK FORCE MEDICAL TEAM TRAINING MANUAL 04/97 IV. US&R MEDICAL PROBLEMS A. CRUSH SYNDROME MYOGLOBIN (continued) FEMA US&R RESPONSE SYSTEM TASK FORCE MEDICAL TEAM TRAINING 04/97 n Solubility of myoglobin in urine (Zager RA, Lab Invest 1989; 60: 619-629.) (50 mg myoglobin/ml urine) Urine pH % Precipitated n Myoglobin — 8.5-7.5 0% Solubility in Urine... 6.5 4% (50 mg myoglobin/ml urine) 5.5 23% 5.0 46% Urine pH % Precipitated <5.0 73% 8.5-7.5 0% 6.5 4% THERAPEUTIC MODALITIES 5.5 23% 5.0 46% <5.0 73% n Hypovolemia • Normal Saline (Ringer's
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