Article Text
Abstract
A 26-year-old woman presented at the emergency department with 4 days’ bilateral lower limb pain and swollen upper legs. Serum creatine kinase was elevated to 33 736 mmol. A diagnosis of rhabdomyolysis was made and she was treated using a rhabdomyolysis algorithm.
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Rhabdomyolysis is a syndrome characterised by muscle necrosis and the release of myoglobin, potassium, calcium and other intracellular constituents into the circulation. The severity of illness ranges from asymptomatic elevations in serum muscle enzymes to life-threatening electrolyte imbalances and acute renal failure.
Possible causes include heritable muscle enzyme deficiencies, electrolyte abnormalities, infections, drugs, toxins, endocrinopathies and statins.
Exercise-induced or exertional rhabdomyolysis is becoming increasingly important as more individuals are engaging in fitness training and are presenting with musculoskeletal complaints at the emergency department (ED).
CASE REPORT
A 26-year-old woman presented at the ED with a history of 4 days of bilateral lower limb pain.
She had started two training sessions of recreational fitness the previous week: she had two sessions of cardiotraining (Miha Circle) The Miha Circle is a circuit with six full automatic strength devices and two cardio devices. This training was followed by a session of fitness in a closed infrared cabin wherein the atmospheric temperature was approximately 38°C (InfraLigne). During this session she developed cramps in both lower limbs. The following day progressive pain in the lower limbs and walking difficulties started; after 3 days both lower limbs started to swell. The general physician prescribed diclofenac. The next day the swelling became progressive and she attended the ED.
She reported no history of trauma, surgery, immobilisation or infection. Her past medical history did not reveal any epileptic disorder, sickle cell trait, endocrinopathy or myopathy. She did not use any alcohol or drugs. She used an oral contraceptive. She did not report dark urine.
On clinical examination, both thighs were diffusely swollen but painless; there was a normal gait, normal neurological examination, no evidence of compartment syndrome, no signs of infection and no calf tenderness, also no fever.
Blood results showed creatine kinase (CK) of 33 736 mmol, lactate dehydrogenase 1501 mmol, alanine aminotransferase 242 mmol, aspartate aminotransferase 678 mmol, d-dimers 2175 ng/ml, urea 28 mg%, creatinine 0.74 mg%, potassium 4.08 (3.5–5.1 mEq/l), calcium 9.3 (8.8–10.2 mEq/l). Urinalysis was not carried out. Duplex of the limbs showed no signs of deep vein thrombosis. A diagnosis of rhabdomyolysis was made and she was treated using a rhabdomyolysis algorithm.1
She received mannitol (bolus 0.5 g/kg), 1000 ml normal saline with sodium bicarbonate (NaHCO3; 100 mEq), followed by a continuous infusion of mannitol 20% (0.1 g/kg per hour) and normal saline with NaHCO3 at 4 ml/kg per hour. She was admitted to the intensive care unit, urine output was monitored hourly and mannitol infusion adjusted as needed, urinary pH was monitored every 4 h and a bolus of NaHCO3 was given as needed. This treatment was continued until the CK level dropped below 20 000 mmol.
She was discharged after 4 days with complete resolution of symptoms and normal laboratory values and gradually resumed fitness training.
DISCUSSION
Severe or unaccustomed exertion, particularly in extremes of heat, is a well-known cause of rhabdomyolysis and has been reported in long-distance runners, bodybuilders and military recruits.2
Risk factors include: physically untrained persons; exertion occurring in extremely hot and humid conditions; or when normal heat loss through sweating is impaired or with hypokalaemia caused by potassium loss from sweating. The prevalence is higher in men than in women.
The mechanism underlying exercise-induced rhabdomyolysis remains unclear, but ischaemia and abnormal potassium release may be involved.3
The classic presentation of rhabdomyolysis includes myalgias, red to brown urine due to myoglobinuria and a more than fivefold increase above normal in serum muscle enzymes (CK).
In addition, potassium aldolase, lactate dehydrogenase and aminotransferases can be released by the muscle fibres into the bloodstream. Objective muscle weakness occurs only in those with severe muscle damage.
Myoglobinuria is observed in approximately half of the cases.
The immediate consequences of rhabdomyolysis include hyperkalaemia and hypocalcaemia caused by calcium binding by damaged muscle proteins and phosphate. Hypoalbuminaemia might result from proteinuria and leakage of protein.
In exertional rhabdomyolysis acute renal failure is more likely in patients with large muscle masses.
No randomised trials of treatment have been conducted, but by consensus intravascular volume expansion by using saline or mannitol to maintain urine output is recommended. Mannitol also acts as a free radical scavenger. Alkalinising the urine by using NaHCO3 can reduce the risk of tubular obstruction. In a large series of 382 patients with serum CK concentrations greater than 5000 U/l, 154 (40%) were treated with bicarbonate and mannitol. There was no statistically significant difference in the incidence of renal failure; however, there was a trend towards improved outcomes in patients with extremely high CK levels (>30 000 U/l) treated with bicarbonate and mannitol.4
When renal failure ensues despite these measures, continuous haemofiltration or haemodialysis will be required.
CONCLUSION
Even though the final diagnosis of exertional rhabdomyolysis is established by laboratory findings, awareness of the syndrome is essential for prompt diagnosis by the emergency physician.
Footnotes
Competing interests: None.
Patient consent: Obtained.