Transcript Crush Syndrome - UNM Emergency Department

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:
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•
•
•
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
Prolonged
Compression
2.
–
3.
Usually 4-6 hours
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
Hemodialysis
Aggressive Fluid
Management
Advances in Management
• Disaster Relief
Task Force
– Marmara,
Turkey
– Task Force:
• Trained
Personnel
• Portable HD
– 462 ARF (18%
mortality)
Limb
Compression
Myoglobinemia
• Local Pressure
• Local Tamponade
• Muscle necrosis
• Capillary necrosis
• Edema
ARF
SHOCK
Muscle Ischemia
Muscle Infarction
Acidosis &
Hyperkalemia
Extracellular
Fluid Shifts
Cardiac
Arrhythmia
Pathophysiology
•
•
•
•
•
Local Pressure
Local Tamponade
Muscle necrosis
Capillary necrosis
Edema
• Severity of
syndrome is
relative to muscle
mass involved
Pathophysiology
• 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
• 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
Limb
Compression
Myoglobinemia
• Local Pressure
• Local Tamponade
• Muscle necrosis
• Capillary necrosis
• Edema
ARF
SHOCK
Muscle Ischemia
Muscle Infarction
Acidosis &
Hyperkalemia
Extracellular
Fluid Shifts
Cardiac
Arrhythmia
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
Limb
Compression
Myoglobinemia
• Local Pressure
• Local Tamponade
• Muscle necrosis
• Capillary necrosis
• Edema
ARF
SHOCK
Muscle Ischemia
Muscle Infarction
Acidosis &
Hyperkalemia
Extracellular
Fluid Shifts
Cardiac
Arrhythmia
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
Limb
Compression
Myoglobinemia
• Local Pressure
• Local Tamponade
• Muscle necrosis
• Capillary necrosis
• Edema
ARF
SHOCK
Muscle Ischemia
Muscle Infarction
Acidosis &
Hyperkalemia
Extracellular
Fluid Shifts
Cardiac
Arrhythmia
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
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–
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–
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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?