Crush Injury and Crush Syndrome Dr S Pezeshki

Crush Injury and Crush Syndrome Dr. S. Pezeshki Orthopedist Azad university of Tehran Medical Branch

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

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

Definition • compression of extremities or other parts of the body that causes muscle swelling and/or neurological disturbances in the affected areas of the body • Typically affected areas of the body include lower extremities (74%), upper extremities (10%), and trunk (9%).

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

Crush Epidemiology Earthquake Victims 3 -20% of all victims Number of limbs affects risk 1 Limb 50% 2 Limbs 75% >3 Limbs 100%

Crush syndrome is localized crush injury with systemic manifestations. traumatic rhabdomyolysis (muscle breakdown) release of potentially toxic muscle cell components and electrolytes into the circulatory system. • approximately 50% of those with crush syndrome developing acute renal failure • 50% need dialysis

Clinical Presentation Sudden release of a crushed extremity may result in reperfusion syndrome == acute hypovolemia and metabolic abnormalities == lethal cardiac arrhythmias myoglobinuria == renal failure

Hypovolemia Blood and fluid sequestration(up to 12 L) Acidosis Shock and ARF release of nuclear acids and amino acids and lactic acid Metabolite imbalance Hyperkalemia , hypocalcemia , hyperphosphatemia Arrhythmia

Kobe, 1995 372 crush syndrome 202 developed ARF 78 required Hemodialysis Aggressive Fluid Management

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

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

Acute Renal Failure • Myoglobin • Brown urine • p. H • Volume Status • Acids • Renal Effects? • Myoglobin Gel • Distal tubules • Oliguric Renal Failure • Electrolyte Abnormalities • Within 3 -7 days postextrication

ARF Treatment • Aggressive Hydration • In situ IVF • GOAL: • UOP: 200 -300 cc (2 cc/kg/hr) • Alkalinization of Urine • 1 st: Bicarbonate • 2 nd: Acetazolamide • GOAL: • Urine p. H b/w 6 -7 • Forced Diuresis • Lasix • Mannitol

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

Shock • Hypovolemic Shock • >12 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 • 250 cc aliquots • Titrate to radial pulses and/or UOP

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

Dysrhythmia • Hyperkalemia • Hypocalcemia • Acidosis

Hyperkalemia • Mild (5. 5 -6. 5 m. Eq/L) • Severe (7. 5 -8. 5 m. Eq/L) • peaked T waves • Widening of the QRS • Moderate (6. 5 -7. 5 m. Eq/L) • prolonged PR interval • decreased P wave amplitude • depression or elevation of ST segment • slight widening of QRS • bundle branch • intraventricular blocks • Flat and Wide P waves • AV Blocks • ventricular ectopy • Life-threatening (>8. 5 m. Eq/L) • • loss of P waves High-grade AV blocks Ventricular dysrhythmias Widening of the QRS complex • eventually forming a sinusoid pattern.

Now, what do you see? Peaked T wave

What K is this? Widening of the QRS bundle branch intraventricular blocks Flat and Wide P waves AV Blocks ventricular ectopy

Describe the ECG. loss of P waves High-grade AV blocks Ventricular dysrhythmias Widening of the QRS complex eventually forming a sinusoid pattern.

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 • Surgery: compartment release

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

In Situ Management Prehospital setting: • Patient Access • IV Access • Administer intravenous fluids before releasing the crushed body part. (This step is especially important in cases of prolonged crush [>4 hours]; however, crush syndrome can occur in crush scenarios of <1 hour) • If this procedure is not possible, consider shortterm use of a tourniquet on the affected limb until intravenous (IV) hydration can be initiated • IV Hydration • Bicarbonate • Mannitol • Extrication

Post-Extrication Hospital setting: • Hypotension • Initiate (or continue) IV hydration—up to 1. 5 L/hour • Renal Failure • Prevent renal failure with appropriate hydration, using IV fluids and mannitol to maintain diuresis of at least 300 cc/hr Triage to hemodialysis as needed

Metabolic Abnormalities • Acidosis: Alkalinization of urine is critical; administer IV sodium bicarbonate until urine p. H reaches 6. 5 to prevent myoglobin and uric acid deposition in kidneys • Hyperkalemia /Hypocalcemia: • calcium gluconate 10% 10 cc or calcium chloride 10% 5 cc IV over 2 minutes • sodium bicarbonate 1 meq/kg IV slow push • regular insulin 5 -10 U and D 5 O 1 -2 ampules IV bolus • kayexalate 25 -50 g with sorbitol 20% 100 m. L PO or PR

Secondary Complications • Monitor casualties for compartment syndrome; monitor compartmental pressure if equipment is available; consider emergency fasciotomy for compartment syndrome • Treat open wounds with antibiotics and tetanus toxoid, and debridement of necrotic tissue • Apply ice to injured areas and monitor for the 5 P’s: pain, pallor, parasthesias, pain with passive movement, and pulselessness • Observe all crush casualties, even those who look well

Disposition • Patients with acute renal failure may require up to 60 days of dialysis treatment; unless sepsis is present, patients are likely to regain normal kidney function

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

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

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