Rhabdomyolysis is a syndrome that caused injury to the framework and exit otat muscle cell contents (myoglobin, potassium, phosphate, etc..) Into the plasma.
These diseases include life-threatening diseases. Acute renal failure which is a serious complication resulting from rhabdomyolysis and its main patofisilogi mechanism caused by renal vasoconstriction, intraluminal stone formation and direct myoglobin toxicity.
CAUSE toxic
Rhabdomyolysis can be caused by various toxins and drugs, a direct effect of these toxins on muscle (metabolic poisons) or just an indirect factor or as a predisposing factor of rhabdomiolisis case.
Direct toxic effect:
Amatoxins
Carbon monoxide
Colchicine
Ethylene glycol
Snakebite
Indirect effects:
Excessive hyperactivity or muscle stiffness (dystonia)
Long seizure
Hyperthermia
Compression due to muscle immobilisasi old (as in a coma)
CAUSE non-toxic
Immobilisasi long for various reasons (such as in patients with commas)
Direct trauma to the muscle
Excessive muscle activity
Sports
Seizures
Immunological
Dermatomyosits
Polymyositis
Ischemic muscle injury
Accident
Vein occlusion
Metabolic disorders
Hipokalemi
Hypophosphataemia
Coxsackie virus infection, influenza
CLINICAL FEATURES
Clinical features vary widely. In conscious patients, the main complaint is the soft, stiffness and cramps in muscles, with weakness and loss of muscle function. Maybe not obtained myalgia (muscle pain) or pain at least at first.
In coma patients, the induration at suspected ektremitas must rhabdomiolisis. Skin discoloration due to ischemic tissue injury (discoloration, blisters) can be seen in the affected area.
On physical examination found the presence of a palpable swelling of muscles such as wood (woody) that get worse after parenteral rehydration. Great muscle swelling can cause a compartment syndrome, which marked the loss of arterial pulsation.
Dark urine color (reddish brown) is a classic sign of rhabdomyolysis. Signs of dehydration (due to fluid in terperangkapnya tissue injury) may be accompanied by oliguria. In rhabdomyolysis caused by severe poisoning, signs of muscle damage could be overlooked if signs of disease / disorder the main cause (such as, agitation very, seizures, hipertermi) dominate the clinical picture. Signs of a complication of rhabdomyolysis (eg., hiperkalaemia, acute renal failure, metabolic acidosis, disseminata intravascular coagulation (DIC) and, rarely, a failed breath) can be a major clinical findings.
Investigations
An increase in serum creatine phosphokinase levels more than five times the normal value (without the heart and brain disease) is a sensitive indicator of rhabdomyolysis.
Discharge due Myoglobinaemia content myocyte (miosit) into the plasma. In acute conditions, excessive mioglobinuria can occur and cause changes in urine color (reddish brown). Findings positive reaction orthotoluidine (Hematest), without in any red blood cells in urine, a sure sign of myoglobinuria. The existence of the following laboratory results: hyperkalaemia, hypocalcaemia, hyperphosphataemia, hyperuricaemia, elevated levels of serum urea and creatinine, increased AST (SGOT) and LDH can be found. Creatinine may increase disproportionately in relation to renal failure due to the release of preformed creatine from muscle tissue damage.
Management
The first goal of treatment is to save the vital functions, determining the cause and save healthy tissue.
Diazepam
Given in case of excessive muscle activity (eg patients who rebelled or spasm), Dosos initials (5 to 10 mg IV slowly, may be increased up to maximum 30 mg).
Liquids
Intravenous crystalloid should be given to maintain a good urine output (> 3 to 4 mls / hour).
Furosemide / Mannitol
Diuretics: furosemide or Mannitol given if the fluid itself is less satisfactory results (inadequate).
Sodium bicarbonate
Alkalinisasi urine neprotoksisitas intended to prevent myoglobin (myoglobin nephrotoxicity), but their effectiveness can not yet conclusively proven.
Calcium
Hipokalsemi, commonly found in rhabdomyolysis, rarely cause symptoms, if unaccompanied by other electrolyte disturbances, and because it rarely requires treatment.
Hemodialysis
Hemodialysis done if there is acute renal gagagl (GGA) and or a life-threatening complications (such as hiperkalemi.
Fasciotomy
Fasciotomi done if there are any serious complications such as compartment syndrome.
[Image: fasciotomi1.jpg]
CLINICAL MONITORING
Monitoring (monitoring) needs to be done such as clinical
vital signs
Urine output
Cardiac rhythm
Serum sodium, potassium, and calcium
Haematocrit / hemoglobin
Arterial blood gases
Creatine phosphokinase activity
Serum creatinine and blood urea
AST (SGOT) and LDH
Hematest (orthotoluidine reaction): if Hematest positive results, must be removed through haematuria possibility mikroscopis urine examination.
Calculate platelets (platelet count), levels of fibrinogen, partial thromboplastin and prothrombin times to detect the existence of thrombositopeni or disseminatedintravascular coagulation.
POTENTIAL COMPLICATIONS / SYMPTOMS REST
Old muscle weakness is the main complaint after the occurrence of rhabdomyolysis. Peripheral neuropathy with neurological deficit is the result of ischemic nerve because compartement syndrome. Acute renal failure secondary to rhabdomyolysis has a good prognosis if performed early therapy.
