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![Page 1: Disaster Medicine: Crush Syndrome Brad Greenberg, MD Center for Disaster Medicine Department of Emergency Medicine University of New Mexico.](https://reader038.fdocuments.us/reader038/viewer/2022103004/56649cea5503460f949b52bb/html5/thumbnails/1.jpg)
Disaster Medicine:Crush Syndrome
Brad Greenberg, MDCenter for Disaster Medicine
Department of Emergency MedicineUniversity of New Mexico
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Goals and Objectives
• Understand historical underpinnings
• Define Crush Syndrome• Describe the epidemiology• Describe the natural course• Describe treatment • Understand the implications for
resource allocation
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History
• World War One: – Meyer-Betz
Syndrome– Noted in
extricated soldiers
– Triad of: • muscle pain • weakness• brown urine
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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
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Battle of Britain
• Retrospective Descriptive Study– Successful
extrication– Death with:
• Oliguria• Pigmented Casts• Limb Edema• Associated Shock
• Hypothesis that muscle breakdown was the cause
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All in the Name of Science
• Animal Model: Rabbit– Identified
myoglobin as culprit molecule
• Postulated Therapies:– Alkalinization of
Urine– Among other
things…
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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.
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Functional Definition
Any injury that has:
1. Involvement of Muscle Mass
2. Prolonged Compression
– Usually 4-6 hours
3. Compromised local circulation
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Epidemiology
• Earthquakes• Bombings• Structural
Collapse• Trench Collapse• “Down and Out”
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Epidemiology
• Tangshan, 1976– 242,800 dead
(20%)
• Armenia, 1988– 50,000 dead– 600 needed
Hemodialysis
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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)
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Structural Collapse
• 10% survive with severe injuries
• 7/10 develop crush syndrome
• 80% dead
• 10% survive with
minor injuries
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Advances in Management
• In situ fluid resuscitation– Israel, 1982– 1/8 developed
ARF
• Aggressive Fluid Resuscitation, post-extrication– Japan, 1995
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Kobe, 1995
372 crush syndrome
202 developed
ARF
78 required Hemo-dialysis
Aggressive Fluid Management
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Advances in Management
• Disaster Relief Task Force– Marmara,
Turkey– Task Force:
• Trained Personnel
• Portable HD
– 462 ARF (18% mortality)
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Extracellular Fluid Shifts
ARF
Cardiac Arrhythmia
Limb Compression
• Local Pressure• Local Tamponade• Muscle necrosis• Capillary necrosis• Edema
SHOCK
Acidosis &Hyperkalemia
Muscle IschemiaMuscle Infarction
Myoglobinemia
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Pathophysiology
• Local Pressure• Local Tamponade• Muscle necrosis• Capillary necrosis• Edema
• Severity of syndrome is relative to muscle mass involved
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• 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
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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
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Cell Death
• Platelet Aggregation
• Vasoconstriction• Hemorrhage• Increased Vascular
Permeability• Edema• Hypoxia
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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
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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
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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)
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Crush Syndrome
• Potassium• Phosphate• Purines• Lactic Acid• Thromboplastin• Creatine Kinase• Myoglobin
• Hypovolemic Shock
• Hyperkalemia• Metabolic Acidosis• Compartment
Syndrome• Acute Renal Failure
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Extracellular Fluid Shifts
ARF
Cardiac Arrhythmia
Limb Compression
• Local Pressure• Local Tamponade• Muscle necrosis• Capillary necrosis• Edema
SHOCK
Acidosis &Hyperkalemia
Muscle IschemiaMuscle Infarction
Myoglobinemia
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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
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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
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Extracellular Fluid Shifts
ARF
Cardiac Arrhythmia
Limb Compression
• Local Pressure• Local Tamponade• Muscle necrosis• Capillary necrosis• Edema
SHOCK
Acidosis &Hyperkalemia
Muscle IschemiaMuscle Infarction
Myoglobinemia
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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
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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
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Extracellular Fluid Shifts
ARF
Cardiac Arrhythmia
Limb Compression
• Local Pressure• Local Tamponade• Muscle necrosis• Capillary necrosis• Edema
SHOCK
Acidosis &Hyperkalemia
Muscle IschemiaMuscle Infarction
Myoglobinemia
![Page 33: Disaster Medicine: Crush Syndrome Brad Greenberg, MD Center for Disaster Medicine Department of Emergency Medicine University of New Mexico.](https://reader038.fdocuments.us/reader038/viewer/2022103004/56649cea5503460f949b52bb/html5/thumbnails/33.jpg)
Dysrhythmia
• Hyperkalemia• Hypocalcemia• Acidosis
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What do you see?
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Is this better or worse?
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Hmm…
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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.
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Now, what do you see?
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What K is this?
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Describe the ECG.
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Management
• What are your management options?
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Management
• Alkalinization– Bicarbonate– Acetazolamide
• Calcium– Ca Gluconate– Ca Chloride
• Beta-Agonists– Albuterol, etc.
• Insulin/Glucose• Potassium
Binding Resins– Kayexalate
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Hypocalcemia
• Signs– Chvostek’s– Trousseau’s
• Tetany• Seizures• Hypotension
• ECG Changes– Bradycardia – arrhythmias– Long QT segment
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Treatment?
• Implications of Hyperphosphatemia?– Metastatic
calicification– Rebound
hypercalcemia
• Treat only if symptomatic.
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Acidosis
• Myocardial Irritability
• Precipitates Arrhythmia
• May be refractory to treatment
• Treatment already discussed
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Physical Examination
• Signs & Symptoms of Crush Injury– Skin Injury – Swelling – Paralysis– Paresthesias– Pain – Pulses – Myoglobinuria
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In Situ Management
• Patient Access• IV Access• IV Hydration
– Bicarbonate– Mannitol
• Extrication
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Post-Extrication
• Physiologic Changes– Reestablish
circulation
• Perfused fluids into damaged tissue
• Cell components enter venous circulation
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Post-Extrication Complications
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Delayed Causes of Death
• ARF• ARDS• Sepsis• Ischemic Organ Injury• DIC• Electrolyte Disturbances
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“Renal Disaster”Epidemiology
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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
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Renal Disaster
• Logistics– Dialysis
• 1-3x/day• 12-18 days
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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.
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Crush Syndrome Treatment
– Early IV Fluid– Close fluid management – Correct electrolyte abnormalities– Consider dialysis as a life-saving
therapy
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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
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Questions?