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RHABDOMYOLYSI
SO. Ahmadi MD.
Professor Assistant of Esfahan medical School, Emergency
Department of Al-Zahra Hospital
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Rhabdomyolysis is a syndrome characterized by injury to skeletal muscle with subsequent release of intracellular contents.
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Disruption of Na+K
+ATPase pump and
calcium transport.
PATHOPHISIOLOGY:PATHOPHISIOLOGY:
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Direct muscle injury:
- Crush
- Electrical or lightning
injury
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Drugs of abuse:- Amphetamines (including Ecstasy)- Caffeine- Cocaine- Ethanol- Heroin- Lysergic acid diethylamide- Methamphetamines- Opiates- Phencyclidine
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Excessive muscular activity:
- Contact sports
- Delirium tremens
- Dystonia
- Psychosis
- Seizures
- Sports and basic training
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Genetic disorders:
- Glycolysis and
glycogenolysis disorders
- Fatty acid oxidation
disorders - Mitochondrial and
respiratory chain metabolism
disorders
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Immunologic diseases:
- Dermatomyositis
- Polymyositis
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Bacterial:- Clostridium- Group A B-hemolytic Streptococcus- Legionnaires' disease- Salmonella- Shigella- Staphylococcus aureus- Streptococcus pneumoniae
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Viral:- Coxsackie virus- Cytomegalovirus- Epstein-Barr virus- Entrovirus- Hepatitis- Herpes simplex virus- Human immunodeficiency virus- Influenza (A and B)- Rotavirus
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Ischemic injury:
- Compartment
syndrome
- Compression
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Medications:- Barbiturates- Benzodiazepines- Clofibrate- Colchicine- Corticosteroids- Isoniazid- Lithium- Monoamine oxidase inhibitors- Narcotics- Neuroleptic agents- Phenothiazines- Salicylates- Serotonergic agents- Statins- Theophylline- Tricyclic antidepressants
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The most common causes of
rhabdomyolysis in adults appear
to be: Alcohol and drug abuse
Toxin ingestion
Trauma
Infection
Strenuous physical activity
Heat-related illness
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In the pediatric population, rhabdomyolysis is an uncommon disorder.
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Influenza virus is the
most frequently
cited infectious
cause.
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Legionella is the most
frequently reported
bacterial cause of
rhabdomyolysis.
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CLINICAL FEATURES
Myalgias, stiffness,
weakness, malaise, low-
grade fever, and dark
(usually brown) urine.
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Nausea, vomiting, abdominal
pain, and tachycardia can
occur in Severe
rhabdomyolysis.
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An elevated serum CK
level is the most sensitive
and reliable indicator of
muscle injury.
DIAGNOSIS:
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The degree of CK elevation
correlates with the amount of
muscle injury and the
severity of illness, but not
the development of renal
failure or other morbidity.
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Most investigators consider a fivefold or greater increase above the upper threshold of normal in serum CK level, in the absence of cardiac or brain injury, as the requirement for the diagnosis of rhabdomyolysis
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Serum CK begins to rise
approximately 2 to 12 h
after the onset of muscle
injury.
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Serum CK peaks within 24 to72 h
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Myoglobin elevation
occurs before CK
elevation.
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Myoglobin enters the
urine when the plasma
concentration exceeds
>5 mg/dl.
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Myoglobin causes the typical
reddish brown discoloration
when urine myoglobin exceeds
100 mg/dL.
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Because myoglobin contains
heme, qualitative tests such
as the dipstick (which uses
the orthotoluidine reaction)
does not differentiate
between hemoglobin,
myoglobin, and red blood
cells.
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suspect myoglobinuria
when the urine dipstick is
positive for blood, but no
red blood cells are
present on microscopic
examination.
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myoglobin levels may
return to normal within 1
to 6 h after the onset of
muscle necrosis.
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In one study, 26 percent
of patients with
rhabdomyolysis did not
have myoglobinuria.
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COMPLICATIONS:
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• ARF
• Metabolic derangements
• DlC
• Mechanial Complications
(e,g.,compartment syndrome
or
peripheral neuropathy)
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Acute renal failure is the
most serious complication
of rahabdomyolysis.
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Ferrihemate:
the breakdown product of
myoglobin, is responsible for the
direct toxic effect on the
kidneys.
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Prehospital Care
Once a limb is extricated, intravenous NS should be initiated at 1 Lit/h. After extrication, continue intravenous NS at 500 mL, alternating with D5NS, at 1
Lit/h. Potassium or lactate-containing solutions should be avoided.
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Emergency Department
Once in the emergency
department, aggressive
intravenous rehydration remains
the mainstay of therapy. This
treatment should be continued
for the first 24 to 72 h.
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Infusion of 2.5 ml/kg per h,
with the goal of maintaining
a minimum urine output of 2
m/kg per hour or 200 – 300
ml/h.
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Sodium bicarbonate, one
ampule (44 mEq) added to 1
L of NS or two to three
ampules (88 to 132 mEq) in
D5W to run at a rate of 100
mL/h, has been
recommended to maintain a
urine pH of 6.5 or above to
prevent the development of
ARF.
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Alkalinization is not without
risks: It can exacerbate the
hypocalcemia.
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mannitol is commonly
recommended, although
there are no prospective
studies on its benefit. This
solution may be given as 1
g/kg IV over 30 min, or as 25
g IV initially, followed by
5 g/h IV, for a total of 120
g/day.
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The use of loop diuretics
(e.g., furosemide) in
rhabdomyolysis is
controversial.
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Dialysis may be necessary
to treat rhabdomyolysis
induced ARF
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Foley catheter cardiac
monitor, hemodynamic
monitoring may be necessary
to avoid fluid overload. Serial
measurements of urine pH,
artenal pH, electrolytes, CK,
calcium, phosphorus, blood
urea nitrogen, and creatinine
should be performed.
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Hypocalcemia observed
early in rhabdomyolysis
usually requires no
treatment.
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Calcium should be given
only to treat hyperkalemia
induced cardiotoxicity or
profound signs and
symptoms of hypocalcemia.
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hypercalcemia is
frequently symptomatic
and normally responds to
saline diuresis and
intravenous furosemide.
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Hyperphosphatemia:
should be treated with
oral phosphate binders
when serum levels
exceed 7 mg/dL.
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hypophosphatemia, which
may occur late in
rhabdomyolysis, requires
treatment only when the
serum level is below
1mg/dL.
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Avoid the use of
prostaglandin inhibitors
such as nonsteroidal anti
inflammatory agents,
because of their
vasoconstrictive effects on
the kidney.
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For at least the initial 24 to
48 h, these patients should
be admitted to a monitored
bed to identify
dysrhythmias secondary to
the metabolic
complications.
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