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Dr.Nafeeya Department of Forensic Medicine and Toxicology
CRUSH SYNDROME Dr.Nafeeya Department of Forensic Medicine and Toxicology
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overview Introduction etiology Pathogenesis Complications
Medicolegal importance PM FINDINGS
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INTRODUCTION Crushing injury prolonged pressure Devascularization
Crush syndrome is the systemic manifestation of muscle cell damage resulting from pressure or crushing. Crush syndrome ( by waters' syndrome) is a life threatening medical condition characterized by major shock and kidney failure following a crushing injury to skeletal muscle. It occurs in crushing accidents such as Industrial accidents, Natural disaster, Wars, Road traffic accidents etc. Crushing injury prolonged pressure Devascularization
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Some other causes Drug or alcohol intoxication
Cerebrovascular accident Head trauma with coma Elderly with hip fracture Improper positioning of surgical patient Building collapse Earthquakes Landslides Bombings Construction accidents Moulivakkam building collapse 2014
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Causes-rhabdomyolysis
traumatic Non traumatic Multiple trauma Crush injury Surgery Coma Immobilization exertional Non exertional Exertion Seizures Metabolic myopathies Malignant hyperthermia Neuroleptic malignant syndrome Ethyl alcohol Drugs Infection Electrolytes
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Pathogenesis Compressive force-cellular hypoperfusion-hypoxia
Decrease ATP-failure of ATPase pump & sarcolemma leakage Cell lysis – release inflammatory mediators Platelet aggregation Vasoconstriction Increased vascular permeability
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Mechanism of rhabdomyolysis
Ca influx Activation of phospholipase cOMPRESSION Decreased ATP production Persistent contraction ISCHEMIA Increased neutrophill Mitochondrial dysfunction REPERFUSION Increased PMN Free radicals **sternberg**
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Electrolyte abnormalities Arrhythmias Arrest Late >72 hrs
Complications Diagnosis Serum creatine kinase Serum myoglobin Serum lactic acid Aspartate aminotransferase, Alanine aminotransferase lactate dehydrogenase Serum uric acid Serum calcium Early –[12-72hrs] Shock Electrolyte abnormalities Arrhythmias Arrest Late >72 hrs Renal failure DIC Myocytosis Sepsis Early and late Acute compartment syndrome
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shock Hypovolemic shock Death Multiorgan failure
Decreased venous return Decreased preload Organ dysfunction Perfusion failure & tissue hypoxia Decreased cardiac output hypotension
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Electrolyte disturbance
Hyperkalemia Hypercalcemia Rhabdomyolysis Hyperphosphatemia Hypocalcemia
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Renal failure Acute Tubular Necrosis Myoglobulin
Binds Tamm-Horsfell protein Stimulates free radical formation Lipid peroxidation destruction of phospholipid bilayer Clinical presentation Tea-coloured or “motor oil” urine Positive urine dip for blood, few RBC on microscopy Urine or serum myoglobin
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Acute tubular necrosis -kidney
LAB-Blood culture,elevated CK,abnormal RFT Urine- myoglobulin
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Release of myogloblin in general circulation
Myoglobin is released from damaged muscle tissue (rhabdomyolysis), which has very high concentrations of myoglobin. Filtered - kidneys Toxic - renal tubular epithelium - acute kidney injury. Myoglobin is a sensitive marker for muscle injury. Clinical presentation Myglobulin-urine >1.5mg/dl-2-3 hours Increased in 2-3 hours Increased levels, which indicate cardiac muscle injury or death, occur in about 3 hours
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Compartment syndrome Elevated pressure in closed fascial compartment > 30 mmhg Compartment pressure > capillary perfusion pressure Vascular compromise, myoneural damage, tissue hypoxia Children ↑ risk: smaller spaces, less elastic 6Ps pain Pallor Paralysis Paresthesia Pulseless Poikilothermy Fasiotomy
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Compartment syndrome Crush syndrome
Prolonged continuous pressure on the skeletal muscle Cal n Na rush Potassium ,uric acid leaks out Acidosis ,hyperkalemia Result in arrythmias , shock ,and death Deep tissue injury to skeletal muscles Accumulation of blood and edema around the muscle Restrict expansion Increase fluid build up under pressure Tissue ischemia and necrosis
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disseminated intravascular coagulation
Increased clotting Consumption of platelets Increased consumption of clotting factors Thrombus formation Hemorrhagic syndrome DIC **Sternberg’s**
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Martius Scarlet Blue Stain
Pm findings: **sternberg**
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Medicolegal importance
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CRUSH TIME The time of injury and cell death varies with the crushing force involved. Skeletal muscle can tolerate ischemia for up to 2 hours without permanent injury >1h likely to result in crush syndrome Reported after 2hrs Can tolerate up to 2h warm ischemia 4-6 hours ,anatomical , functional changes >6 hours, muscle necrosis **SCHWARTZ'S**
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Medicolegal Cause of death – did the injury kill the person or not
Cause any Underlying disease Age of injury /time since injury Bleeding Clotting ,pus formation,granulation tissue,healing of fracture Manner of death –violent or unnatural
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MEDICOLEGAL IMPORTANCE
Traumatic /Crush asphyxia Crushing abrasions Crush fractures Accidental –crush injury Homicidal –assailants jump , jack knifing Suicidal –Mentally ill Burns , electrocution Poisons – mercury salts ,carbon tetracholoride
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AUTOPSY FINDINGS Face lips –swollen ,congested External Internal
Upper body- congested, cyanosed , nose ,ear , mouth bleeding present, Pallor Amputated parts Internal Congested brain Degeneration and necrosis Petechial hemorrhages Congested organs Kidneys – bilateral swelling,shock kidney,
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references Sternberg’s Diagnostic Surgical Pathology Sixth Ed.
Rosai and Ackerman's Surgical Pathology 11th Edition Schwartz's principles Of Surgery 11th edition Comprehensive clinical neprology richard J johnson 5th edition Bardale Rajesh-Principles of Forensic Medicine and Toxicology Knight's Forensic Pathology 4th edition Anil Aggrawal textbook of forensic medicine and toxicology. Narayan reddy essential of forensic medicine
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