RHABDOMYOLYSI

SO. 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.

Disruption of Na+K

+ATPase pump and

calcium transport.

PATHOPHISIOLOGY:PATHOPHISIOLOGY:

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

cited infectious

cause.

Legionella is the most

frequently reported

bacterial cause of

rhabdomyolysis.

CLINICAL FEATURES

Myalgias, stiffness,

weakness, malaise, low-

grade fever, and dark

(usually brown) urine.

Nausea, vomiting, abdominal

pain, and tachycardia can

occur in Severe

rhabdomyolysis.

An elevated serum CK

level is the most sensitive

and reliable indicator of

muscle injury.

DIAGNOSIS:

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 myoglobin exceeds

100 mg/dL.

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 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.

The use of loop diuretics

(e.g., furosemide) in

rhabdomyolysis is

controversial.

Dialysis may be necessary

to treat rhabdomyolysis

induced ARF

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 binders

when serum levels

exceed 7 mg/dL.

hypophosphatemia, which

may occur late in

rhabdomyolysis, requires

treatment only 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

dysrhythmias secondary to

the metabolic

complications.