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Rhabdomyolysis

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

What causes rhabdomyolysis?

Direct Muscle Injury


Crush injuries, deep burns, electrical injuries, acute necrotizing
myopothy of certain cancers, assaults with prolonged and vicious
beating/repetitive blows

Excessive Physical Exertion


Results in state in which ATP production cant keep up with
demand exhaustion of cellular energy supplies & disruption of
muscle cell membrane
Protracted tonic-clonic seizures, psychotic hyperactivity (mania or
drug-induced psychosis)

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)

Electrolyte & Serum Osmolality Abnormalities


Chronic hypokalemia significant total body loss of K+ disrupts
Na+ K+ pump cell membrane failure, leak of toxic intracellular
contents from muscle cells
Overuse of diuretics , hyperemesis gravidarum, some drugs
(amphotericin B), hyperglycemic hyperosmolar nonketotic coma

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

Drugs, Toxins, Venoms


Ethanol depresses CNS and leads to periods of immobility;
alcohol also has toxic effects on myocytes with binge drinking
-statins
Drugs that mimic or stimulate SNS (cocaine, methamphetamines,
ecstasy, pseudoephedrine, excessive caffeine)
Chemicals & toxic plants
Snake venoms, multiple stings by wasps, bees, hornets
Pharmaceutical agents benzodiazepines, corticosteroids,
narcotics, immunosuppressants, antibiotics, antidepressants,
antipsychotics

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

Genetic & Autoimmune Disorders


Carbohydrate & lipid metabolism; muscular dystrophies,
autoimmune disorders such as polymyositis & dermatomyositis

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

Acute RF (myoglobinuric RF)

Compartment syndrome (with crush injuries) decompression


fasciotomy

DIC give FFP

Disturbances in serum & urine electrolyte levels/balance


cardiac arrhythmias

Hypovolemia

Metabolic Acidosis

Respiratory failure

Acute muscle wasting

Diagnostics

serum total CK & CK-MM (CK isoenzyme in skeletal


muscle)
Begins 2-12h post-injury, peak 1-3 days, declines 3-5 days

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

serum BUN & Cr


d/t escape of massive amounts Cr from damaged muscle

Early hypocalcemia
Deposit of Ca in necrotic muscle, soft tissues calcify in necrosis

Diagnostics cont.

Later hypercalcemia & hyperphosphatemia


Phosphate and calcium leakage from damaged muscle cells
give PO calcium carbonate/hydroxide & calcium will follow being
fixed when phosphate distribution fixed (inverse relationship)

uric acid (hyperuricemia)

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

The treatment of rhabdomyolysis includes initial


stabilization and resusitation of the pt.

Saline has been used as the fluid of choice for resusitation.

A recent prospective randomized single-blind study


compared saline or RL solution for initial resusitation.In
addition, all pts were treated with bicarbonate &
diuretics.The study found less bicarbonate & diuretics were
needed for pts receiving RL.

Over view of studies for fluid


management of Rhabdomyolysis
Study

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.

Free radical scavengers and


antioxidants
The magnitude of muscle necrosis caused by ischemiareperfusion injury has been reduced in experimental
models by the administration of free-radical scavengers .
Many of these agents have been used in the early
treatment of crush syndrome to minimize the amount of
nephrotoxic material released from the muscle
Pentoxyphylline is a xanthine derivative used to improve
microvascular blood flow. In addition, pentoxyphylline
acts to decrease neutrophil adhesion and cytokine
release
Vitamin E , vitamin C , lazaroids (21-aminosteroids) and
minerals such as zinc, manganese and selenium all have
antioxidant activity and may have a role in the treatment
of the patient with rhabdomyolysis

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

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