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SHEEBA HAKAK
AMNCH
DEFINITION
DEFINITION
Rhabdomyolysis is the breakdown of
muscle fibers, specifically of the
sarcolemma of skeletal muscle,
resulting in the release of muscle
fiber contents (myoglobin) into the
bloodstream.
HISTORY
The association between
rhabdomyolysis and ARF was first
established during world war II.After
the bombing of London,crush victims
developed AKI with pigmented casts
in renal tubules at autopsy.
PATHOPHYSIOLOGY
pathophysiology
pathophysiology
Mechanism of ARF
causes
Muscle Ischemia
Interference with O2 delivery to cells and therefore limiting
production of ATP
Generalized ischemia from shock & hypotension, carbon monoxide
poisoning, profound systemic hypoxemia, localized compression
leading to skeletal muscle ischemia, tissue compression d/t
immobilization of muscle, intoxicated/comatose down for long
periods, immobilization from acute SCI, compartment syndrome,
Causes cont.
Temperature Extremes
Excessive Cold muscle perfusion, ischemia; freezing causes
cellular destruction
Excessive Heat destroys cells & metabolic demands (every
degree temp = metabolic demand by ~ 10%) & if body cant
keep up with requirement, cellular hypoxia anaerobic
environment
Malignant hyperthermia, neuroleptic malignant syndrome (d/t
psychotropic medications)
Causes cont.
Infections
Pneumococcal & Staphylococcus aureus sepsis, salmonella &
listeria infections, gas gangrene, NF
Can destroy large quantities of muscle tissue through generation
of toxins or direct bacterial invasion
Causes cont.
Endocrinologic Disorders
Either wasting or hypermetabolic conditions
K+ wasting diabetic ketoacidosis, hyperosmolar nonketotic
coma, hyperaldosteronism
Na+ depletion Addison disease
sympathetic stimulation & metabolic demands beyond
sustainability thyroid storm & pheochromocyoma
Clinical Presentation
Many features are nonspecific
Triad :muscle pain ,weakness and
dark urine
Varies depending on underlying
condition
Features
Local
Systemic
Clinical Presentation
Local features
Muscle pain
Tenderness
Swelling
Bruising
Weakness
Systemic features
Tea-colored urine
Fever
Malaise
Nausea
Emesis
Confusion
Agitation
Delirium
Anuria
Potential Complications
Hypovolemia
Metabolic Acidosis
Respiratory failure
Diagnostics
serum myoglobin
Until filters into urine causing characteristic coke-colored urine
serum K+
Major cause of morbidity/mortality d/t muscle breakdown &
release K+ which further by acidosis & RF
Give calcium gluconate/chloride cautiously so as to prevent
hypodynamic instability
Early hypocalcemia
Deposit of Ca in necrotic muscle, soft tissues calcify in necrosis
Diagnostics cont.
ABC
To detect hypoxia and acidosis & when giving sodium bicarb
therapy
Clotting Studies
Useful in detecting DIC
Urinalysis
Will reveal presence of protein, brown casts, uric acid crystals
Urine Dipstick
Quick initial test
Myoglobin will react to hemoglobin reagent on stick if positive,
Treatment
ABC
Fluids
Treat hyperkalaemia
Fluids
design
Brown et al
2004
No.of
patients
treatment
conclusion
Retrospectiv 1771
e
Bicarbonate,
mannitol&sa
line VS.
saline
No
improvemen
t over saline
alone
Homsi et al
1997
Retrospectiv 24
e
Bicarbonate,
mannitol &
saline
vs.saline
No
improvemen
t over saline
alone
Cho et al
2007
prospective
Lactated
ringer
vs.saline
Decreased
amount of
NAHCO3 &
diuretics
given with
LR solution
200
Mannitol
Mannitol
The diuretic effect of mannitol is
controversial as it may further
exacerbate hypovolumia,metabolic
acidosis&pre renal AKI
Alkalinisation of urine
Alkalinization of the urine with sod bicarb has been
suggested to minimize renal damage after
rhabdomyolysis.
Although mannitol and NAHCO3 are frequently
considered the standard of care in preventing AKI,little
evidence exists to support the use of these agents.
In a retrospective study of 24pts,vol expansion with
saline alone prevented progression to renal failure,&
the addition of mannitol&NAHCO3 had no additional
benefit
Brown and colleagues CK >5000U/L
154(40%) received mannitol and bicarbonate
228 (60%) didnt
No significant difference in renal failure ,dialysis,or mortality
between the groups.
Alkalization continues..
Use of carbonic anhydrase inhibitors
has been suggested when ph >7.45
after NAHCO3 therapy or if there is
continued aciduria despite alkalemia.
HBO therapy
HBO therapy also has been
advocated for treatment of crush
injuries because of its effects to
increase perepheral o2transport.
A RDBS examined the effect of HBO
on wound healing.36 pts were
divided into 2 groups ,one received
HBO therapy & other conventional
therapy.complete healing was
achieved for 17 pts in HBO grp v/s 10
Dialysis
Despite optimal treatment ,pts may
still develop AKI with severe acidosis
& hyperkalemia (daily haemodialysis
or haemofiltration may be necessary)
Remove urea and potassium