Rhabdomyolysis medical therapy
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Medical Therapy
The main therapeutic measure is hyperhydration (by administering intravenous fluids), and, if necessary, the use of osmotic diuretics (to prevent fluid overload). Alkalinization of the urine with bicarbonate reduces the amount of myoglobin accumulating in the kidney.
Hydration should be aggressive and patients may require as much as 10 liters of fluid. The fluid may be third spaced into muscle. Once the patient has been hyperhydrated, then forced diuresis is utilized. The urine can be alkalinized with D5W + 2/3 amp Bicarbonate. However, be aware that this may worsen hypocalcemia. Avoid replacement of calcium since it will chelate with phosphate. When rhabdomyolysis resolves, patients will often become hypercalcemic. Patients may require dialysis for hyperkalemia, uremia or volume overload.
As the electrolytes are frequently deranged, these may require correction, especially hyperkalemia (elevated potassium levels in the blood). Calcium levels are initially low (hypocalcemia), as circulating calcium precipitates in the damaged muscle tissue, presumably with phosphate released from intracellular stores. When the acute renal failure resolves, vitamin D levels rise rapidly, causing hypercalcemia (elevated calcium). Although this resolves eventually, high calcium levels may require treatment with bisphosphonates (e.g., pamidronate).
If the exacerbating cause includes overdose of skeletal muscle relaxants and/or tricyclic antidepressants, the treatment protocols include gastric decontamination. This procedure is fairly effective because the anticholinergic effects of tricyclics and cyclobenzaprine delay gastric emptying; and, therefore, it becomes possible to obtain tablet residues even after significant time elapse. Ventricular arrhythmias, QRS widening, or intraventricular conduction abnormalities should be treated with sodium bicarbonate 1 meq/kg IV bolus and repeated if arrhythmias persist. This should be followed by IV infusion of sodium bicarbonate to produce an arterial pH of 7.5; the mechanism of sodium bicarbonate's action in this role is unknown.[1] However, sodium bicarbonate's beneficial effect on kidney function is known to be via the effects of alkalinization both increasing the urinary solubility of myoglobin leading to its increased excretion[2] and stabilizing ferryl myoglobin complex so preventing myoglobin-induced lipid peroxidation.[3][4]
References
- ↑ Chabria SB (2006). "Rhabdomyolysis: a manifestation of cyclobenzaprine toxicity". Journal of occupational medicine and toxicology (London, England). 1: 16. doi:10.1186/1745-6673-1-16. PMID 16846511.
- ↑ Zager RA (1989). "Studies of mechanisms and protective maneuvers in myoglobinuric acute renal injury". Lab. Invest. 60 (5): 619–29. PMID 2716281.
- ↑ Moore KP, Holt SG, Patel RP; et al. (1998). "A causative role for redox cycling of myoglobin and its inhibition by alkalinization in the pathogenesis and treatment of rhabdomyolysis-induced renal failure". J. Biol. Chem. 273 (48): 31731–7. PMID 9822635.
- ↑ Holt S, Moore K (2000). "Pathogenesis of renal failure in rhabdomyolysis: the role of myoglobin". Exp. Nephrol. 8 (2): 72–6. PMID 10729745.