Case Presentation: A 48-year-old female with a past medical history of opioid dependency and right hip arthroplasty presented with complaints of fevers and purulent drainage at her surgical site. Pertinent exam findings included fever, tenderness, and erythema on her right hip. Initial creatinine, bicarbonate, and magnesium were within normal limits. She underwent irrigation and debridement with initiation of IV antibiotics. Hospitalization was complicated by post-operative blood loss anemia, acute kidney injury, hypoglycemia, hypotension, and hyperkalemia, peak potassium 6.5 mmol/L. Treatment included IV fluid and blood transfusions with improvement in anemia and kidney function. Hyperkalemia persisted despite treatment with IV insulin, sodium polystyrene sulfonate, furosemide and sodium bicarb infusion. Initial work-up included urine osmolal gap and trans-tubular potassium gradient which reflected hyporeninemic hypoaldosteronism. Additional lab work revealed serum ACTH 1.5 pg/ml, random cortisol 7.5 mcg/dL, TSH 0.24 mcIU/ml, and free T4 0.5ng/dL. Nephrology and Endocrinology were consulted for assistance with refractory hyperkalemia and hypoaldosteronism. Cosyntropin stimulation test revealed an intact adrenal response despite low baseline ACTH and cortisol levels. Continued hypoglycemia and hypotension prompted concern for secondary adrenal insufficiency and functional evaluation of the pituitary with serum prolactin and IGF-1. Empiric stress-dose steroids lead to resolution of hypotension, hyperkalemia, and hypoglycemia.
Discussion: The etiology of the patient’s refractory hyperkalemia remained unclear despite extensive workup and resolution of kidney injury. As hyperkalemia can precipitate fatal arrhythmias, identifying the etiology and initiating management is crucial. Serology revealed functional adrenal glands. Thyroid studies with low ACTH level raised suspicion for secondary insufficiency; prolactin and IGF-1 levels, ordered to evaluate pituitary function, were normal. Literature suggests that cortisol acts on potassium via a mineralocorticoid-like effect. The patient was empirically treated with a course of high dose IV steroids with excellent response and subsequent normalization of hyperkalemia. Her clinical status continued to improve with normal ACTH and cortisol on recheck 4 weeks after discharge.
Conclusions: The evaluation of adrenal function is essential in the workup of refractory hyperkalemia. The use of stress dose steroids reflects a potentially effective therapeutic strategy. Diagnosis can be challenging and may ultimately reflect a multifactorial etiology. If a clinician is unable to identify the source for hyperkalemia, treatment with a trial of steroids should be considered. Further diagnostic investigation is needed to delineate management when multiple etiologies are suspected.