Rhabdomyolysis
DEFINITION
Damage to muscle cells, with release of a large amount of cell contents
which may in turn block up the kidneys, causing acute renal failure,
amongst
other complications.
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INCIDENCE
Seen most commonly in crush injury.
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AETIOLOGY
Pathogenesis
Muscle injury.
- mostly seen in acute trauma.
- consider hereditary if recurrent.
- consider medications
- consider combo of causes eg alcohol and low K+.
Sieve
Congenital
McArdle's Tarui's
Infection
Viral and bacterial infections have been known to cause muscle
damage.
Non-infectious
Myositis
Trauma
Crushing injury.
Over-exercising
Electric shock
Burns
Seizures
Prolonged immobility
Hypo/hyperthermia
DPT
Alcohol, cocaine, amphetamines, caffeine
Opiates, antihistamines, barbiturates
PCP, CO.
Statins, succinhycholine.
Snake/bee/hornet venom.
EM
Neuroleptic malignant syndrome
Hypokalaemia
Low phosphate
Hyperthyroid
DKA
Hyperosmolar states
Hypokia
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BIOLOGICAL BEHAVIOUR
Pathophysiology
First described by Bywaters and Beall in crushed victims of the German
blitz
in WWII.
- they noted acute renal failure was hardly seen in hypovolaemia alone,
but
often seen when associated with crushing injuries.
Muscle injury.
Combination of direct injury, ischaemia and cell death.
--> muscle cell contents released: myoglobin, CPK, aldolase, LDH,
transaminases.
Also K+ release
--> cardiac complications.
Kidney Pathophysiology
Prerenal failure occurs with significant hypovolaemia.
- generally has to be <90mmHg systolic
Myoglobin pigment precipitates in renal tubules.
- obstructs tubules and is nephrotoxic through ferrihemate, a breakdown
product.
Combo of myoglobinuria, hypovolaemia and acidosis --> renal failure.
Complications
Systemic
ARF
- 5-8% of all ARF due to r.
~ 33% of r. pts will develop ARF.
Hypovolaemia
DIC
- if severe
- resolves spontaneously in days.
Metabolic derangement
- K+ high in 10-40%.
- ARF main cause of this.
- Ca++ commonly deranged, rarely symptomatic.
Localised
Compartment syndrome
- involved muscles will swell markedly.
- not until after rehydration.
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MANIFESTATIONS
Are not sensitive.
Symptoms
Local
Hx of crushing injury
- often thigh or calf
50% have muscle pain
Also stiffness.
Dark urine (reddish-brown / amber).
Systemic
Weakness, malaise.
Low grade fever.
Nausea, vomiting, abdo pain if severe.
If very severe, urea may change mental state.
Signs
Observe
Muscle swelling.
Hypovolaemia.
Decreased urine output.
Dark urine.
Palpate
Muscle tenderness.
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INVESTIGATIONS
Biochemistry
History/exam insensitive
Elevated CPK most sensitive indicator.
- level correlates with degree of muscle damage but not with likelihood
to
develop ARF.
- rises 2-12hrs post injury
- peaks 24-72hrs post injury
- then declines at 39% per day.
- so if not following this pattern suspect ongoing damage.
Us+Es.
Urine
Dipstick +ve for heme but absent for RBCs.
- myoglobin is rapidly excreted
- 26% have -ve dipstick.
Need to request specifically myoglobin assay if want a sensitive urine
test.
Haematology
ABG
Coags as baseline.
Other
If there was no physical injury, and r. is suspected, seek cause as per
clinical suspicion.
- eg glucose, LDH, albumin, toxicology screen.
- phosphate, Ca, uric acid levels.
MRI highly effective at localising rhabdomyolysis.
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MANAGEMENT
Acute
ABCs
Immobilise crush injuries
Prevent ARF
Early aggressive IV fluids.
--> the window of opportunity is short and action must be prompt to
preclude needing renal replacement therapy.
- catheterise
- rapidly correct fluid deficit, then 2.5ml/kg/hr
- mannitol / frusemide have been used in addition: maintains a high
tubular volume.
- keep urine output going well.
- some say 2ml/kg/hr, some say 200ml/hr.
- ATLS says 100ml/hr until myoglobinuria cleared.
- continue for first 24-72hrs.
Bicarbonate
- CCrISP suggests alkalinising urine to help prevent toxic effec of
acid products of myoglobin breakdown on renal tubular cells.
Treat hyperkalaemia
Treat cause
- be alert for compartment syndrome.
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References
ATLS