Surprising Hyperkalemia of 10.2 mmol/L in a Patient with Hyperglycemia: A Case Report.

Hyperkalemia is a life-threatening condition potentially leading to cardiac arrest. Here, we report a case of surprising severe hyperkalemia of 10.2 mmol/L in a diabetic patient with previously normal kidney function presenting without discernible clinical symptoms to our emergency department. The patient was admitted because of hyperglycemia of 32.8 mmol/L, which was detected during daily testing in her nursing home. The hyperkalemia was caused by prerenal failure due to hyperglycemic polyuria which led to volume depletion, and worsened by a combination of potassium-sparing drugs and potassium supplementation. The patient was treated conservatively. Eighteen hours later, the serum potassium concentration was 4.6 mmol/L. The patient could be released 6 days later. To our knowledge, this is the highest described hyperkalemia treated conservatively and survived without cardiopulmonary resuscitation.

[An old lady with hyponatremia and recurrent falls]. / Eine alte Dame mit Hyponatriämie und rezidivierenden Stürzen.

BACKGROUND: Hyponatremia is one of the most commonly seen electrolyte abnormalities in hospitalized patients. The differential diagnoses are complex once the typical causes for hyponatremia such as congestive cardiac failure, liver failure, hyperglycemia, thiazides, antipsychotic drugs or chemotherapy are excluded. Especially the differentiation between the syndrome of inappropriate ADH secretion and salt-wasting nephropathy as seen in cerebral salt wasting (CSW) can be difficult. CASE REPORT: The case of a 79-year-old lady is discussed who presented to the Emergency Department with extreme dizziness after having fallen off a ladder. Biochemistry studies revealed severe hyponatremia (Na 114 mmol/l) as well as hypochloremia (Cl 85 mmol/l), all other laboratory studies were unremarkable. The intake of a thiazide diuretic, an adrenal insufficiency and other common causes of hyponatremia were excluded. On examination, there were clinical signs of volume depletion. The serum sodium initially improved adequately after the infusion of intravenous normal saline (0.9%) only to fall again along with clinical signs of volume depletion after ceasing the infusion. A high urinary sodium excretion persisted despite hyponatremia and volume depletion. Due to the clinical course the syndrome of inappropriate ADH secretion was considered unlikely and the diagnosis of CSW established. Under therapy with fludrocortisone her sodium stabilized within the normal range and she remained free of symptoms. CONCLUSION: CSW is an important differential diagnosis of hyponatremia in the hypovolemic patient. It is due to an inadequately high urinary sodium excretion. The response to intravenous normal saline can make the diagnosis likely and distinguish it from SIADH. The exact pathophysiological mechanism behind CSW is not yet completely understood. Therapy consists of fluid and salt supplementation or mineralocorticoid substitution.