Clinical Picture: Diabetic Ketoacidosis with Evolving Hypokalemia

This 15-year-old girl presents with classic features of Diabetic Ketoacidosis (DKA): severe abdominal pain, vomiting, cold extremities (poor perfusion), tachycardia, and hypotension. Her labs confirm this:

• Blood glucose 400 mg/dL — hyperglycemia
• Blood pH 6.9 — severe metabolic acidosis
• Urine ketones +++ — ketosis
• Serum creatinine 1.4 mg/dL — mild pre-renal azotemia from dehydration

She is correctly started on IV fluids and insulin. Four hours later she develops an inability to lift her limbs — acute, ascending flaccid weakness. In the setting of DKA treatment, this is the hallmark presentation of insulin-induced hypokalemia.

Why This Happens

Patients in DKA are almost always total-body potassium depleted (from osmotic diuresis, vomiting, and acidosis-driven cellular shifts), even though the initial serum potassium may appear normal or high because acidosis pushes potassium out of cells. Once insulin therapy begins:

• Insulin activates the Na⁺/K⁺-ATPase pump, driving potassium into cells.
• Correction of acidosis with fluids further shifts potassium intracellularly.
• The result is a rapid fall in serum potassium, unmasking the pre-existing total-body deficit.

Severe hypokalemia causes profound muscle weakness (including inability to lift limbs), areflexia, and — critically — life-threatening cardiac arrhythmias and respiratory muscle paralysis if uncorrected. This is why potassium must be monitored closely and repleted proactively during DKA management (insulin is typically withheld or paused if K⁺ falls below ~3.3 mEq/L).

Option-wise Analysis

• Intravenous normal saline — Already part of ongoing initial DKA management for volume resuscitation; it does not address the new neuromuscular symptom of limb weakness, which is specifically due to potassium shift.
• Potassium repletion (Correct Answer) — The new-onset inability to lift limbs after starting insulin is the classic clinical clue for insulin-induced hypokalemia. Prompt potassium replacement is essential to prevent cardiac arrhythmia and respiratory failure, and is the immediate next step.
• Urine sample for ketones — Ketonuria has already been documented (+++) at presentation; repeating this test does not explain or address the new limb weakness.
• Intravenous sodium bicarbonate — Bicarbonate is reserved for extreme, refractory acidosis (generally pH < 6.9 with hemodynamic instability) and is not routinely used in DKA due to risks including paradoxical worsening of hypokalemia by further driving potassium intracellularly — the opposite of what this patient needs.

Therefore, the correct next step is potassium repletion to correct the insulin-induced hypokalemia responsible for her limb weakness and to prevent potentially fatal complications.