What is the next step in managing a 40-year-old patient with Diabetes Mellitus (DM) and Hypertension (HTN) on Indapamide (indapamide), who presents with diarrhea for 3 weeks, abdominal tenderness, and severe hypokalemia?

Management of Severe Hypokalemia in a Patient with Diabetes, Hypertension, and Diarrhea

Initial Assessment and Management

The next step in managing this patient should be to check the serum magnesium level (option C). 1

This 40-year-old patient with diabetes mellitus and hypertension on indapamide presents with a critical potassium level of 2.1 mmol/L, which requires urgent evaluation and correction. The severe hypokalemia (K+ <2.5 mmol/L) is likely multifactorial, resulting from:

1. Indapamide therapy (thiazide-like diuretic) 2, 3
2. Prolonged diarrhea (3 weeks) causing gastrointestinal potassium losses
3. Possible diabetic ketoacidosis or uncontrolled diabetes

Rationale for Checking Magnesium First

Checking magnesium is the priority for several critical reasons:

• Hypomagnesemia frequently coexists with hypokalemia in patients taking thiazide-like diuretics like indapamide 2, 4
• Potassium repletion will be ineffective if concurrent hypomagnesemia is not corrected first 1
• Indapamide increases urinary excretion of magnesium, which can result in hypomagnesemia 3
• Diarrhea causes significant magnesium losses along with potassium losses

In a study of patients with indapamide-induced electrolyte disturbances, 8 out of 11 patients had concurrent hypomagnesemia with hypokalemia 4. This makes checking magnesium levels essential before attempting potassium correction.

Why Other Options Are Less Appropriate

• Urinary potassium (Option A): While this would help determine the source of potassium loss (renal vs. extrarenal), it would not change immediate management. The patient already has a critical potassium level requiring urgent correction, and we know indapamide is contributing to renal potassium wasting 3.

• Glucose level (Option B): Although important in a diabetic patient, severe hyperglycemia would cause transcellular potassium shifts but is unlikely to be the primary cause of such profound hypokalemia (2.1 mmol/L). Additionally, correcting potassium is more urgent than checking glucose in this scenario.

• Bicarbonate (Option D): While metabolic alkalosis can occur with diuretic use and contribute to hypokalemia, checking magnesium is more critical as hypomagnesemia must be corrected first for successful potassium repletion.

Management Algorithm

1. Check serum magnesium level immediately

2. Begin potassium replacement therapy:

   • For severe hypokalemia (K+ <2.5 mmol/L): Intravenous potassium chloride at 10-20 mEq/hour via peripheral IV with continuous cardiac monitoring 1
   • If magnesium is low, administer magnesium replacement concurrently

3. Additional immediate steps:

   • Obtain ECG to assess for hypokalemia-related changes (U waves, flattened T waves, ST depression)
   • Temporarily hold indapamide 3
   • Begin workup for cause of diarrhea

4. Once stabilized:

   • Consider alternative antihypertensive medication
   • Evaluate for other electrolyte abnormalities (sodium, calcium)
   • Monitor renal function

Important Considerations

• Indapamide is associated with severe electrolyte disturbances, particularly in elderly or low-weight patients 5, 4
• Rhabdomyolysis is a potential complication of severe hypokalemia, requiring monitoring of creatine kinase 6
• Cardiac arrhythmias are a serious risk with potassium levels <2.5 mmol/L 7
• Neurological symptoms including delirium may occur with severe hypokalemia and other electrolyte disturbances 4

The combination of prolonged diarrhea and indapamide therapy creates a particularly high-risk situation for profound electrolyte disturbances that requires prompt identification and correction of magnesium deficiency before effective potassium repletion can occur.