Genetic muscular disorders are known risk factors for rhabdomyolysis, which may result in acute kidney injury. Recurrent episodes of acute kidney injury can lead to chronic kidney disease and eventually end-stage renal failure. We describe a patient with chronic kidney disease that developed in the setting of recurrent rhabdomyolysis, resulting in the requirement for renal transplantation. After transplantation, the maintenance of tacrolimus trough concentrations above what is typically prescribed for standard renal transplant recipients appeared to confer protection from further episodes of rhabdomyolysis. This is consistent with previous case series that demonstrated a therapeutic benefit of the calcineurin inhibitor cyclosporine in collagen VI myopathies in the nontransplant population. This case report suggests the potential application of higher tacrolimus targets in patients who have undergone renal transplantation in the setting of recurrent rhabdomyolysis leading to end-stage renal failure.
INTRODUCTION:Magnesium toxicity can occur due to decreased excretion or overconsumption and is rare in the general population. Early-onset symptoms of toxicity are nausea, flushing, weakness, and urinary retention. However, severe toxicity and its management is not well-described. We present a case of magnesium overdose with intractable hypotension. CASE PRESENTATION:A 34-year-old male presented to the emergency department after he was found unresponsive in a restaurant in the presence of empty bottles of magnesium supplements and ibuprofen. He was hypotensive, hypothermic, and emergently intubated for airway protection. His serum magnesium level was 11.7mg/dl. He was treated with gastric decontamination, intravenous calcium and admitted to the intensive care unit. Continuous Renal Replacement Therapy (CRRT) was initiated and led to a reduction in the measured serum magnesium concentration. Despite aggressive volume administration and multiple vasopressors, he had refractory shock and severe acidosis. An echocardiogram revealed adequate cardiac function; hence, he was not a candidate for Extracorporeal Membranous Oxygenation (ECMO). A trial of hydrocortisone and methylene blue also yielded no benefit to his distributive shock. His hospital course was further complicated by abdominal compartment syndrome requiring a bedside exploratory laparotomy, aspiration pneumonia, acute respiratory distress syndrome, and disseminated intravascular coagulation. Ultimately, his family elected to transition to comfort care, and the patient passed away on hospital day 4.DISCUSSION: Magnesium competitively blocks the entry of calcium into presynaptic terminals of smooth muscle cells, inhibiting the release of acetylcholinesterase, causing smooth muscle relaxation. In the setting of an overdose, this translates to refractory vasoplegia. Magnesium also alters the polarization of the cytoplasmic membrane in cardiac myocytes, causing lengthening of the action potential, thus predisposing to arrhythmias. While iatrogenic magnesium toxicity has been reported at levels of 3-5mg/dL, a level of >10mg/dL is uncommon. There may be a dose-dependent refractoriness that has not been identified in the literature so far. Treatment of severe magnesium toxicity requires urgent dialysis in conjunction with IV calcium which acts as an antagonist. If there is catecholamine resistance, methylene blue may be used to restore systemic vascular resistance. CONCLUSIONS:Severe magnesium toxicity can present with shock & acidosis. Despite dialysis and aggressive resuscitation, the vasoplegia can be refractory and lead to fatal complications, including respiratory collapse and cardiac arrest. Even with early recognition and treatment, the mortality can be high, and further studies are needed to improve outcomes.
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