Disaster Medicine: Crush Syndrome Brad Greenberg, MD Center for Disaster Medicine Department of Emergency Medicine University of New Mexico

Goals and Objectives Understand historical underpinnings Define Crush Syndrome Describe the epidemiology Describe the natural course Describe treatment Understand the implications for resource allocation

History World War One: –Meyer-Betz Syndrome –Noted in extricated soldiers –Triad of: muscle pain weakness brown urine

Bywaters’ Syndrome Battle of Britain, May 1941 Multiple subjects Trapped for 3-4 hours Then developed: –Shock –Swollen Extremities –Dark Urine Survived  Renal Failure  Died of Uremia

Battle of Britain Retrospective Descriptive Study –Successful extrication –Death with: Oliguria Pigmented Casts Limb Edema Associated Shock Hypothesis that muscle breakdown was the cause

All in the Name of Science Animal Model: Rabbit –Identified myoglobin as culprit molecule Postulated Therapies: –Alkalinization of Urine –Among other things…

Science and Technology Dictionary (McGraw Hill) crush syndrome (′kr ə sh ′sin′drōm) (medicine) A severe, often fatal condition that follows a severe crushing injury, particularly involving large muscle masses, characterized by fluid and blood loss, shock, hematuria, and renal failure. Also known as compression syndrome.

Functional Definition Any injury that has: 1.Involvement of Muscle Mass 2.Prolonged Compression –Usually 4-6 hours 3.Compromised local circulation

Epidemiology Earthquakes Bombings Structural Collapse Trench Collapse “Down and Out”

Epidemiology Tangshan, 1976 –242,800 dead (20%) Armenia, 1988 –50,000 dead –600 needed Hemodialysis

Crush Epidemiology Earthquake Victims –3-20% of all victims –Number of limbs affects risk 1 Limb  50% 2 Limbs  75% >3 Limbs  100% Structural Collapse –40% of survivors (Those requiring extrication)

Structural Collapse 10% survive with severe injuries 7/10 develop crush syndrome 80% dead 10% survive with minor injuries

Advances in Management In situ fluid resuscitation –Israel, 1982 –1/8 developed ARF Aggressive Fluid Resuscitation, post-extrication –Japan, 1995

Kobe, crush syndrome 202 developed ARF 78 required Hemo- dialysis Aggressive Fluid Management

Advances in Management Disaster Relief Task Force –Marmara, Turkey –Task Force: Trained Personnel Portable HD –462 ARF (18% mortality)

Extracellular Fluid Shifts ARF Cardiac Arrhythmia Limb Compression Local Pressure Local Tamponade Muscle necrosis Capillary necrosis Edema SHOCK Acidosis & Hyperkalemia Muscle Ischemia Muscle Infarction Myoglobinemia

Pathophysiology Local Pressure Local Tamponade Muscle necrosis Capillary necrosis Edema Severity of syndrome is relative to muscle mass involved

Syndrome usually requires 4-6 hours of compression Mechanisms of muscle cell injury: –Immediate cell disruption –Direct pressure on muscle cells –Vascular Compromise (4 hours) Microvascular pressure Edema and/or Compartment Syndrome Bleeding Pathophysiology

Crushed +/- ischemic muscle –Deficiency in ATP –Failure of Na/K ATPase –Sarcolemma Leakage (Influx of Ca) –Lysis if muscle cell membrane –Leaks K, Ca, CK, myoglobin Hypovolemia –Fluid Sequestration –Increased osmoles in EC space

Cell Death Platelet Aggregation Vasoconstriction Hemorrhage Increased Vascular Permeability Edema Hypoxia

Products of Muscle Breakdown Amino acids & other organic acids –Acidosis –Aciduria –Dysrhythmias Creatine phosphokinase –laboratory markers for crush injury Free radicals, superoxides, peroxides –further tissue damage

Products of Muscle Breakdown Histamines: –Vasodilation –Bronchoconstriction Lactic acid –acidosis –Dysrhythmias Le u kotrienes –lung injury –hepatic injury. Lysozymes –cell-digesting enzymes that cause further cellular injury Myoglobin –precipitates in kidney tubules, especially in the setting of acidosis with low urine pH; leads to renal failure Nitric oxide –causes vasodilation which worsens hemodynamic shock

Products of Muscle Breakdown Phosphate –hyperphosphatemia causes precipitation of serum calcium –Hypocalcemic dysrhythmias Potassium –dysrhythmias Worsened when associated with acidosis and hypocalcemia. Prostaglandins –Vasodilatation –lung injury Purines (uric acid) –Nephrotoxic Thromboplastin –disseminated intravascular coagulation (DIC)

Crush Syndrome Potassium Phosphate Purines Lactic Acid Thromboplastin Creatine Kinase Myoglobin Hypovolemic Shock Hyperkalemia Metabolic Acidosis Compartment Syndrome Acute Renal Failure

Extracellular Fluid Shifts ARF Cardiac Arrhythmia Limb Compression Local Pressure Local Tamponade Muscle necrosis Capillary necrosis Edema SHOCK Acidosis & Hyperkalemia Muscle Ischemia Muscle Infarction Myoglobinemia

Acute Renal Failure Myoglobin –Brown urine pH –Volume Status –Acids Renal Effects? Myoglobin Gel –Distal tubules –Oliguric Renal Failure –Electrolyte Abnormalities Within 3-7 days post-extrication

ARF Treatment Aggressive Hydration –In situ IVF –GOAL: UOP: cc (2cc/kg/hr) Alkalinization of Urine –1 st : Bicarbonate –2 nd : Acetazolamide –GOAL: Urine pH b/w 6-7 Forced Diuresis –Lasix –Mannitol

Extracellular Fluid Shifts ARF Cardiac Arrhythmia Limb Compression Local Pressure Local Tamponade Muscle necrosis Capillary necrosis Edema SHOCK Acidosis & Hyperkalemia Muscle Ischemia Muscle Infarction Myoglobinemia

Shock Hypovolemic Shock –>10 L can sequester in the area of crush injury –Study by Oda Annals of EM, 1997 Kobe, 1995 Most commom cause of death (66%) in the 1 st 4 days

Shock Treatment Early Aggressive Resuscitation –IVF –Blood Products –Other products? –Close Monitoring Oral Rehydration –Not so good… IV Access –Peripheral –Central –Intraosseus Bolus Therapy –250cc aliquots –Titrate to radial pulses and/or UOP

Extracellular Fluid Shifts ARF Cardiac Arrhythmia Limb Compression Local Pressure Local Tamponade Muscle necrosis Capillary necrosis Edema SHOCK Acidosis & Hyperkalemia Muscle Ischemia Muscle Infarction Myoglobinemia

Dysrhythmia Hyperkalemia Hypocalcemia Acidosis

What do you see?

Is this better or worse?

Hmm…

Hyperkalemia Mild ( mEq/L) –peaked T waves Moderate ( mEq/L) –prolonged PR interval –decreased P wave amplitude –depression or elevation of ST segment –slight widening of QRS Severe ( mEq/L) –Widening of the QRS bundle branch intraventricular blocks –Flat and Wide P waves –AV Blocks –ventricular ectopy Life-threatening (>8.5 mEq/L) –loss of P waves –High-grade AV blocks –Ventricular dysrhythmias –Widening of the QRS complex eventually forming a sinusoid patern.

Now, what do you see?

What K is this?

Describe the ECG.

Management What are your management options?

Management Alkalinization –Bicarbonate –Acetazolamide Calcium –Ca Gluconate –Ca Chloride Beta-Agonists –Albuterol, etc. Insulin/Glucose Potassium Binding Resins –Kayexalate

Hypocalcemia Signs –Chvostek’s –Trousseau’s Tetany Seizures Hypotension ECG Changes –Bradycardia –arrhythmias –Long QT segment

Treatment? Implications of Hyperphosphatemia? –Metastatic calicification –Rebound hypercalcemia Treat only if symptomatic.

Acidosis Myocardial Irritability Precipitates Arrhythmia May be refractory to treatment Treatment already discussed

Physical Examination Signs & Symptoms of Crush Injury –Skin Injury –Swelling –Paralysis –Paresthesias –Pain –Pulses –Myoglobinuria

In Situ Management Patient Access IV Access IV Hydration –Bicarbonate –Mannitol Extrication

Post-Extrication Physiologic Changes –Reestablish circulation Perfused fluids into damaged tissue Cell components enter venous circulation

Post-Extrication Complications

Delayed Causes of Death ARF ARDS Sepsis Ischemic Organ Injury DIC Electrolyte Disturbances

“Renal Disaster” Epidemiology

Sever, et al. Spitak, Amenia Earthquake, Crush Victims 225 Needed HD –Sufficient supplies –Inefficient response Resource Issues –Allocation Problems –Personnel –Support Stucture Developed a method to respond to large-scale events requiring hemodialysis –Tested in Turkey, Iran, Pakistan

Renal Disaster Logistics –Dialysis 1-3x/day days

But wait! What about chronic renal patients? How many patients per machine? Where do you get supplies? How do you organize your response? Who get to decide who receives dialysis? Who operates the machinery? How do you monitor progress? Where can you get laboratory support? With appropriate use of resources… …a substantial number of lives can be saved.

Crush Syndrome Treatment –Early IV Fluid –Close fluid management –Correct electrolyte abnormalities –Consider dialysis as a life-saving therapy

Local Relief Efforts Assess Severity of Renal Disaster Determine status of local infrastructure Estimate consumption of hospital resources and supplies Prepare work schedules for personnel Estimate need for dialysis Deliver supplies and personnel For each patient: –8-10 sets of HD equipment –4-5 units of blood products –5 liters of crystalloid per day –15g of Kayexalate

Questions?