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Action: Communicate knowledge of musculoskeletal trauma
Conditions: Given a lecture in a classroom environment
Standards: Received a minimum score of 75% on a written exam IAW course standards
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Reason
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Agenda
Identify the clinical presentation, and management of rhabdomyolysis
Identify the clinical presentation, and management of compartment syndrome
Identify the clinical presentation, and management of crush injury and crush syndrome
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Rhabdomyolysis
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Rhabdomyolysis
Rhabdomyolysis is a serious syndrome due to a direct or indirect muscle injury
It results from the death of muscle fibers and release of their contents into the bloodstream
This can lead to complications such as renal (kidney) failure
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RhabdomyolysisCauses
Must think about risk factors because classic signs may be absent in 50% of cases
Extreme muscle strain, especially in someone who is an untrained athlete. This can happen in elite athletes too. And it can be more dangerous if there is more muscle mass to break down
Crush injuries
Long‐lasting muscle compression
Electrical shock injury, burn, heat stroke
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RhabdomyolysisCauses
Strenuous exercise or unaccustomed muscular activity (i.e. siezure)
Drug or alcohol abuse
Certain disease processes (i.e. viruses)
Bacterial infections leading to toxins in tissues or the bloodstream (sepsis)
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Clinical Presentation
Muscle pain, especially in the shoulders, thighs or lower back
Muscle weakness or trouble moving arms or legs
Abdominal pain
Nausea or vomiting
Fever, rapid heart rate
Confusion, dehydration, fever, or lack of consciousness
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Clinical Presentation
Dark (tea‐colored) urine
Oliguria or anuria
Urine or serum myoglobin
Dipstick + for blood, but no intact RBCs on spun specimen
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Complications Early
Hyperkalemia
Hypocalcemia
Hepatic inflammation
Cardiac arrhythmia and/or arrest
Late
Hypercalcemia
Renal failure
DIC
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Complications
Early or late
Compartment syndrome
•May occur after fluid resuscitation. This serious compression of nerves, blood vessels, and muscles can cause tissue damage and problems with blood flow.
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Management (TMEP)Aggressive hydration is the cornerstone of
treatment
Normal saline 1 ‐ 2L bolus IV/IO followed by 500 ml ‐1L per hour
Avoid Ringer’s lactate due to the potassium content
Titrate to achieve target urine output of > 200 ml/hour
• Consider urinary alkalinization to achieve urine pH > 6.5 Mix Sodium Bicarbonate 40 mEq (1 ampule/bristojet) in 500 ml normal saline. Run at 100 ml/h
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Management (TMEP)
Reassess vital signs and mental status frequently
Foley catheter to facilitate measuring urine output
Utilize cardiac monitoring if available
Electrolyte and metabolic complications can cause dysrhythmias
Urgent evacuation
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Potential Problems/Complications Monitor for signs and symptoms of hyperkalemia (cardiac dysrhythmia)
Administer 1 gm calcium and 40 mEq sodium bicarbonate (1 ampule) IV/IO
Hypocalcemia (provoked by sodium bicarbonate)
Peri‐oral tingling, muscle tetany, increased deep tendon reflexes, QT prolongation on cardiac monitor • Stop sodium bicarbonate infusion
Avoid loop diuretics such as furosemide (Lasix), which may increase myoglobin precipitation in kidneys and provoke acute renal failure
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Additional Management
Mannitol
Only use once urinary flow is established
1 to 2 gm/kg at a rate of 5 gm/hr
Don’t exceed 200 gm/24 hrs
Alternate with NS
Forced diuresis
Decompresses edematous muscles
Continue until urine myoglobin has cleared
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Compartment Syndrome
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Compartment Syndrome
Occurs when excessive pressure builds up inside an enclosed space in the body
Increased compartment pressure compromises circulation and function of compartment tissues
Prolonged elevation of tissue pressure leads to muscle death and nerve damage
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Common Causes
Any mechanism that increases the volume of blood or tissue within the compartment can cause a compartment syndrome
External forces
Tight cast or constrictive dressing
Venous tourniquet
Vascular
Hemorrhage
Ischemic‐reperfusion injury
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Common Causes
Orthopedic
Tibial and forearm fractures
Soft tissue injury
Prolonged limb compression
Crush injury
Burns
Envenomation
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Clinical Presentation
The classic “P’s”
Pain
Parasthesia
Poikilothermia
Pallor
Pressure
Paralysis
Pulselessness
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Pain
Disproportionate to physical exam findings
Earliest and most consistent sign
Aggravated by passive stretching
Most sensitive sign
Diffuse, deep, unremitting, and poorly localized
Not relieved with immobilization
Often difficult to control with narcotics
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Paresthesia
Tingling, burning
Diminished sensation
Two‐point discrimination
Light touch
Sensory disturbance generally precedes motor dysfunction
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Poikilothermia, Pallor, and Pressure
Poikilothermia
Cold distal extremity compared to the contralateral side
Pallor
Pale color
Pressure
Compartment is swollen and firm on palpation
Measurable increase in tissue pressure
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Pressure
Compartment pressure can be measured
Commercial kits available
Measure pressure within 5 cm of any fracture
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Paralysis and Pulselessness
Paralysis
Late finding from prolonged ischemia
Permanent damage may already be present
Pulselessness
Least reliable sign
CS is a disorder of microvasculature and rarely affects major vessels
Pulses are present in 90% of patients
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Clinical Presentation
Maintain a high index of suspicion with polytrauma patients
Pain greater than expected due to the injury alone is your earliest and best clue
Open wounds do not exclude CS
The presence of pulses and normal capillary refill does not exclude CS
CS can develop up to 48 hours after the event
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Complications
Rhabdomyolysis
Myoglobinuria
Renal failure
Volkmann contracture
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Management
Maintain extremity at heart level ‐
DO NOT ELEVATE
Supplemental oxygen
Fluid resuscitation
Remove constrictive casts or dressings
Evacuate to surgical facility for immediate fasciotomy
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Surgical FasciotomyNot in your scope of practice
Long incisions through the skin and fascia
Allows tissue swelling without pressure elevation
May require delayed grafting
Should be performed immediately after making the diagnosis
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Crush Injury and Crush Syndrome
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Injury vs Syndrome
Crush INJURY ‐ occurs when a body part is subjected to a high degree of force or pressure
Can produce compartment syndrome
Crush SYNDROME ‐ the systemic manifestation of muscle cell and capillary endothelial damage‐ what happens after the injury occurs
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Crush Syndrome
Major shock and renal failure after a crushing injury to skeletal muscle
Imagine “rhabdomyolysis on steroids”
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Reperfusion Syndrome
Devastating systemic effects can occur when the crushing pressure is suddenly released, without proper preparation of the patient
Initiates inflammatory response
Hypovolemia, hypotension, myocardial depression, hyperkalemia, and acidosis
Immediate release of toxins can have catastrophic systemic consequences
Be aware of development of crush syndrome starting as early as 4 hours post injury
The medications used to treat crush syndrome are not part of the standard ATP aid bag and require development of a separate crush injury kit
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Management (TMEP)
Warnings
The principles of hypotensive resuscitation according to TCCC DO NOT apply in the setting of extremity crush injury requiring extrication
In the setting of a crush injury associated with non compressible (thoracic, abdominal, pelvic) hemorrhage, aggressive fluid resuscitation may result in increased hemorrhage
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Management (TMEP)
Warnings
With extremity injuries, tourniquets should NOT be applied during Phase 1 unless there is hemorrhage which is not controllable by other means
Be aware of development of cardiac dysrhythmias due to hyperkalemia immediately following extrication
Maintain patent airway (NPA, OPA, etc.) and adequate ventilation
Monitor O2 sat with pulse ox and administer high flow oxygen if available
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Management (TMEP)
Phase 1: Immediate (cont.)
Give initial bolus of 1 to 1.5 L of NS PRIOR to attempts at extrication and continue at 1.5 L/hr
• Ringer’s lactate is not recommended due to the potassium content
Maintain urine output at greater than or equal to 200 cc/hr. If possible, insert Foley catheter.
Assess and reassess mental status
Follow Pain Management Protocol (TMEP)
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Management (TMEP)
Phase 1: Immediate (cont.)
Consider prophylactic antibiotics ‐
• Ertapenem (Invanz) 1 gm IV
Utilize cardiac monitoring if available
Mannitol (administer 1 to 2 gm/kg at a rate of 5gm/hr)
• Ensure urine output has been established prior to using Mannitol
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Management (TMEP)
Phase 2: Immediately PRIOR to extrication
Apply tourniquets to crushed extremities, if possible
Sodium Bicarbonate ‐
•1 mEq/kg IV immediately prior to extrication.
• Additional dosing of Sodium bicarbonate may be required if dysrhythmias or cardiac arrest persist after giving calcium chloride or gluconate.
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Management (TMEP)
Phase 3: Immediately FOLLOWING extrication
CPR should be initiated if cardiac arrest develops following extrication. DO NOT follow the TCCC guidelines on cardiac arrest.
If extrication is greater then 4 hours OR in the presence of dysrhythmias, administer Calcium Chloride (1 gm, 10 ml of 10% solution) or Calcium Gluconate (1 gm, 10 ml of 10% solution)
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Management (TMEP)
Phase 3: Immediately FOLLOWING extrication
(cont.)
Calcium should not be given in bicarbonate containing solutions due to precipitation of calcium carbonate
Additional dosing of Sodium bicarbonate may be required if dysrhythmias or cardiac arrest persist after giving calcium chloride or gluconate
Following extrication, once the patient is stabilized, be prepared to treat hyperkalemia as tourniquets are released
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Questions?
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Terminal Learning Objective
Action: Communicate knowledge of musculoskeletal trauma
Conditions: Given a lecture in a classroom environment
Standards: Received a minimum score of 75% on a written exam IAW course standards
2/17/2016
17
Slide 49JSOMTC, SWMG(A)
Agenda
Identify the clinical presentation, and management of rhabdomyolysis
Identify the clinical presentation, and management of compartment syndrome
Identify the clinical presentation, and management of crush injury and crush syndrome