History and exam
Key diagnostic factors
common
recent crush injury
History of trauma with limb deformity and swelling.
Peripheral pulses are diminished compared with the opposite extremity.
Capillary refill is prolonged and distal colouration is poor.
prolonged immobilisation
This is more likely in cases with alcohol or drug abuse, as patients may lie unmoving in one position for a significant length of time.
presence of other risk factors
Key risk factors include trauma, alcohol, cocaine, amfetamine, phencyclidine, narcotics, diuretics, statins, salicylate toxicity, toxins, envenomation, inflammatory disorders, muscle hypoxia, and genetic disorders.
muscular pain or weakness
May occur after obvious trauma or recent intense exercise, but can also occur insidiously. Commonly implicated muscle groups are the extremities and the lower back.[2]
Other diagnostic factors
uncommon
general malaise
A feeling of general aches, lethargy, and being unwell.
dark urine
Dark, red urine caused by urinary myoglobin. Other causes of red urine include ingestion of beetroot, blackberries, and rhubarb and use of medications such as senna, doxorubicin, and phenothiazines.[30]
muscular swelling
Muscle swelling at an area of injury or in the setting of muscle overuse may be present.
muscular tenderness
Generalised muscle tenderness may be elicited.
diminished peripheral pulse
Compared with opposite extremity.
prolonged capillary refill
Compared with opposite extremity.
Risk factors
strong
trauma
Traumatic injuries are a common cause of rhabdomyolysis; one study has shown some degree of biochemical evidence of rhabdomyolysis (abnormal creatine kinase [CK]) among 85% of critically injured patients admitted to a trauma intensive care unit.[2][4] Trauma patients with vascular injuries or muscle ischaemia with subsequent reperfusion are at higher risk for rhabdomyolysis.[2]
Burns and electric shock may cause extensive muscle injury.
Over-exertional states may be considered muscular trauma. Rhabdomyolysis has been documented in unconditioned athletes and military recruits. A diagnosis of exertional rhabdomyolysis is made when there are severe muscle symptoms (pain, stiffness, and/or weakness) and laboratory evidence of muscle lysis (CK level >5 times the upper limit of normal or >1000 IU/L) in the setting of recent exercise.[19][20]
alcohol
Ethanol abuse is the most common aetiological factor in the development of rhabdomyolysis.[1][3][5]
It is thought to be directly toxic to myocyte membranes, inhibits calcium uptake into the cells, and disrupts sodium-potassium adenosine triphosphatase.
In addition, concurrent delirium tremens, withdrawal seizures, prolonged immobilisation and limb compression, volume depletion, and electrolyte abnormalities are alcohol-related medical problems that can cause rhabdomyolysis.
cocaine
May cause hyperdynamic muscular state.
amfetamine
May cause hyperdynamic muscular state.
phencyclidine
May cause hyperdynamic muscular state.
narcotics
May cause tissue hypoperfusion and prolonged immobilisation and limb compression.
diuretics
May lead to potassium depletion severe enough to result in rhabdomyolysis.
statins
Have a significant unwanted effect of rhabdomyolysis.[8][9] Statins currently licensed worldwide include, but are not limited to, rosuvastatin, atorvastatin, simvastatin, pravastatin, fluvastatin, and lovastatin. The mechanism is not clearly defined. Statins and other medications (e.g., daptomycin) may have a synergistic effect on muscle breakdown.[16]
salicylate toxicity
Salicylate toxicity uncouples oxidative phosphorylation, which inhibits adenosine triphosphate formation.
toxins
Such as cyanide, mercury, copper, carbon monoxide, and toluene.
envenomation
Such as snakebite, centipede bite, or bee sting.
inflammatory disorders
Dermatomyositis and polymyositis are inflammatory diseases that result in nearly universal chronic rhabdomyolysis, but complications are rare.[21]
muscle hypoxia
Any condition that disrupts blood flow to tissue may result in cellular injury to muscles. Ischaemic injury can occur through vascular occlusion or through prolonged immobilisation and limb compression. Arterial thrombosis or emboli, vasculitides such as sickle cell disease, non-ambulatory geriatric patients, or other debilitated patients, may present with evidence of myonecrosis.
genetic disorders
Hereditary rhabdomyolysis occurs rarely as genetic defects of carbohydrate and lipid metabolism.[1][5][22] The 2 most common are carnitine palmitoyltransferase deficiency and myophosphorylase deficiency (McArdle syndrome).
The diagnosis is suspected in patients with a positive family history and recurrent episodes of exercise-induced rhabdomyolysis.
weak
metabolic disorders
Metabolic and endocrine disorders may lead to hypokalaemia or hypophosphataemia.[1][5]
Adequate potassium levels are necessary to increase blood flow to anaerobic muscles and aid in the synthesis and storage of glycogen as a source of muscle energy; depleted levels can cause malaise, generalised weakness, and myalgias.
Phosphate is the predominant intracellular anion and is a necessary precursor for adenosine triphosphate formation.
Any disorder that leads to depletion of these ions may result in rhabdomyolysis. Examples include hypernatraemia, hyperosmolar state, myxoedema, thyroid storm, diabetic ketoacidosis, phaeochromocytoma, anorexia nervosa, hyperalimentation, and other malnutrition states.
infection
Infectious aetiologies occur either by direct myocyte invasion or through toxin production.
Influenza A and B are the most common viral causes, but HIV and the coxsackievirus have also been implicated.
Bacterial infection with Legionella, Francisella tularensis, Streptococcus pneumonia, Salmonella, and Staphylococcus aureus have been documented as causative in decreasing order.[5][23]
increased body temperature
Use of this content is subject to our disclaimer