Transcript RHABDOMYOLYSIS - Isfahan University of Medical Sciences

RHABDOMYOLYSIS
O. Ahmadi MD.
Professor Assistant of Esfahan
medical School, Emergency
Department of Al-Zahra Hospital
Rhabdomyolysis
is
a
syndrome characterized
by injury to skeletal
muscle with subsequent
release of intracellular
contents.
PATHOPHISIOLOGY:
Disruption of Na+K +ATPase
pump and calcium transport.
Direct muscle injury:
- Crush
- Electrical or lightning injury
Drugs of abuse:
- Amphetamines (including Ecstasy)
- Caffeine
- Cocaine
- Ethanol
- Heroin
- Lysergic acid diethylamide
- Methamphetamines
- Opiates
- Phencyclidine
Excessive muscular activity:
- Contact sports
- Delirium tremens
- Dystonia
- Psychosis
- Seizures
- Sports and basic training
Genetic disorders:
- Glycolysis and glycogenolysis
disorders
- Fatty acid oxidation disorders Mitochondrial
and
respiratory
chain metabolism disorders
Immunologic diseases:
-
Dermatomyositis
-
Polymyositis
Bacterial:
- Clostridium
- Group A B-hemolytic Streptococcus
- Legionnaires' disease
- Salmonella
- Shigella
- Staphylococcus aureus
- Streptococcus pneumoniae
Viral:
- Coxsackie virus
- Cytomegalovirus
- Epstein-Barr virus
- Entrovirus
- Hepatitis
- Herpes simplex virus
- Human immunodeficiency virus
- Influenza (A and B)
- Rotavirus
Ischemic injury:
- Compartment syndrome
- Compression
Medications:
- Barbiturates
- Benzodiazepines
- Clofibrate
- Colchicine
- Corticosteroids
- Isoniazid
- Lithium
- Monoamine oxidase inhibitors
- Narcotics
- Neuroleptic agents
- Phenothiazines
- Salicylates
- Serotonergic agents
- Statins
- Theophylline
- Tricyclic antidepressants
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
In the pediatric population,
rhabdomyolysis
is
an
uncommon disorder.
Influenza virus is the
most
frequently
infectious cause.
cited
Legionella
frequently
is
the
reported
most
bacterial
cause of rhabdomyolysis.
CLINICAL FEATURES
Myalgias,
malaise,
stiffness,
low-grade
weakness,
fever,
dark (usually brown) urine.
and
Nausea,
vomiting,
abdominal
pain, and tachycardia can occur
in Severe rhabdomyolysis.
DIAGNOSIS:
An elevated serum CK level is
the most sensitive and reliable
indicator of muscle injury.
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.
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
Serum CK begins to rise
approximately 2 to 12 h
after the onset of muscle
injury.
Serum CK peaks within
24 to72 h
Myoglobin elevation occurs
before CK elevation.
Myoglobin enters the urine
when
the
plasma
concentration exceeds >5
mg/dl.
Myoglobin
causes
the
typical
reddish brown discoloration when
urine
mg/dL.
myoglobin
exceeds
100
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.
suspect myoglobinuria
when the urine dipstick is
positive for blood, but no red
blood cells are present on
microscopic examination.
myoglobin levels may return
to normal within 1 to 6 h
after the onset of muscle
necrosis.
In one study, 26 percent of
patients
with
rhabdomyolysis did not have
myoglobinuria.
COMPLICATIONS:
• ARF
• Metabolic derangements
• DlC
• Mechanial Complications
(e,g.,compartment syndrome or
peripheral neuropathy)
Acute renal failure
is
the
most serious complication of
rahabdomyolysis.
Ferrihemate:
the breakdown product of myoglobin,
is responsible for the direct toxic
effect on the kidneys.
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.
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.
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.
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.
Alkalinization
is
not
without
risks: It can exacerbate the
hypocalcemia.
mannitol
recommended,
is
commonly
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.
The use of loop diuretics (e.g.,
furosemide) in rhabdomyolysis
is controversial.
Dialysis may be necessary to
treat
induced ARF
rhabdomyolysis
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.
Hypocalcemia observed
early in rhabdomyolysis
usually requires no
treatment.
Calcium should be given only to
treat
hyperkalemia
induced
cardiotoxicity or profound signs
and symptoms of hypocalcemia.
hypercalcemia is frequently
symptomatic
and
normally
responds to saline diuresis
and intravenous furosemide.
Hyperphosphatemia:
should be treated with oral
phosphate
serum
mg/dL.
binders
levels
when
exceed
7
hypophosphatemia,
may
occur
rhabdomyolysis,
treatment
only
which
late
in
requires
when
the
serum level is below 1mg/dL.
Avoid
the
use
of
prostaglandin inhibitors such
as
nonsteroidal
anti
inflammatory agents, because
of
their
vasoconstrictive
effects on the kidney.
For at least the initial 24 to 48
h, these patients
should be
admitted to a monitored bed to
identify
secondary
dysrhythmias
to
complications.
the
metabolic