Disaster Medicine: Crush Syndrome Brad Greenberg, MD Center for Disaster Medicine Department of...

Disaster Medicine:Crush Syndrome

Brad Greenberg, MDCenter for Disaster Medicine

Department of Emergency MedicineUniversity 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 (′krəsh ′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, 1995

372 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 IschemiaMuscle 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

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

• Leukotrienes – 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 IschemiaMuscle 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: 200-300cc (2cc/kg/hr)

• Alkalinization of Urine– 1st: Bicarbonate– 2nd: 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 IschemiaMuscle 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 1st 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 IschemiaMuscle Infarction

Myoglobinemia

Dysrhythmia

• Hyperkalemia• Hypocalcemia• Acidosis

What do you see?

Is this better or worse?

Hmm…

Hyperkalemia• Mild (5.5-6.5 mEq/L)

– peaked T waves

• Moderate (6.5-7.5 mEq/L) – prolonged PR interval– decreased P wave

amplitude– depression or elevation

of ST segment– slight widening of QRS

• Severe (7.5-8.5 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, 1988

• 600 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• 12-18 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?