EM@3AM: Hypokalemia

Background:

• Definition: serum K <3.5 mmol/L; severe when potassium falls below 2.5 mmol/L or if the hypokalemia is associated with symptoms or EKG changes (see below) (2,3).
• Why it matters in the ED: Hypokalemia can lead to lethal arrythmias, particularly in the setting of concurrent hypomagnesemia (2,4). It can also lead to respiratory failure due to severe muscle weakness/paralysis (2) and can contribute to ileus and rhabdomyolysis (5).

Causes:

• Renal losses – Loop and thiazide diuretics, hyperaldosteronism, renal tubular acidosis, aminoglycosides, cisplatin, amphotericin B (2,3,5).
• GI losses – vomiting, diarrhea, NG suctioning
• Endocrine – Cushing’s disease, steroids, diabetic ketoacidosis
• Intracellular shifting – insulin therapy, beta-agonist therapy (i.e. albuterol), alkalosis
• Malnutrition/Decreased intake – Alcoholism, eating disorders

Diagnostics:

• Serum Electrolytes/pH: K, Mg, CO2 +/- arterial blood gas (to evaluate for possible K shifting via the K⁺/H⁺exchanger to compensate for metabolic derangements).
• EKG: Flattened T waves, U waves, QT prolongation, PVCs which can lead to ventricular arrythmias including torsades de pointes (1,2,5).
• Urine potassium (if unclear etiology): Likely renal if urine K is >20 mEq/L vs Extrarenal (GI) if urine K <20 mEq/L (2,6).

ED Management and Disposition:

• Each 0.3 mEq/L drop in serum K ~100 mEq of total body K deficit (3). Levels <3.0 mEq/L requires significantly larger amounts of potassium for repletion to improve serum levels.
• PO replacement preferred when possible as it is less expensive, less likely to cause hyperkalemia, and avoids the risk of phlebitis associated with IV potassium administration (2,5).
  • IV repletion is necessary in patients with severe hypokalemia, patients who are unable to tolerate oral intake, or who are in a shock state resulting in decreased enteral absorption (6).
• Don’t forget magnesium: Hypomagnesemia (Mg <1.5 mg/dL) should be corrected to allow for potassium repletion. Hypomagnesemia causes renal potassium wasting (6).
  • For mild hypomagnesemia (1.6-2 mg/dL): Trialing oral magnesium repletion with 400 mg BID PO magnesium oxide is reasonable; 400 mg magnesium oxide = 20 mEq magnesium (7).
  • For moderate to severe hypomagnesemia (>1.6 mg/dL) or symptomatic hypomagnesemia: 2g IV magnesium over 5-15 min followed by 2 additional grams IV over 30-60 min (7).
• Rate of infusion: For routine repletion, a rate of 10 mEq/hr is standard (6). For severe hypokalemia or DKA, target a rate of 20 mEq/hr (either via a central line or split via 2 peripheral IVs to avoid phlebitis) (6). Faster infusions have higher risk of phlebitis. If >40 mEq/hr is needed, a central line is preferred as only 10 mEq/hr should run through each peripheral line. Rates should not exceed 60 mEq/hr unless there are extenuating circumstances such as cardiac arrest due to hypokalemia or recurrent malignant arrythmias with a pulse due to hypokalemia (where rates of 20 mEq IV potassium over 2-3 minutes are useful) (6).
• Monitoring: Potassium check q2-4h during IV repletion with continuous cardiac monitoring if infusing > 10mEq/hr (2,6). Continuous cardiac monitoring is necessary in IV potassium supplementation to monitor for arrythmias associated with the development of hyperkalemia.
• Identify precipitating factors and addressing the underlying cause: If hypokalemia is mild (3.0-3.5 mg/dL), the cause is presumed to resolve in the upcoming days (i.e. gastroenteritis), and patient is able to follow up outside of the hospital, discharge is safe. If hypokalemia is moderate to severe (<3.0 mg/dL), the cause is unable to be identified in the ED or not presumed to resolve in the upcoming days, admission may be warranted for further workup (i.e. nephrology, endocrinology consult) and management (2,6).
• A special note about diabetic ketoacidosis (DKA) and potassium: Insulin is the mainstay of treatment of DKA. Insulin also shifts potassium intracellularly. In DKA, potassium must be checked, and may need to be replenished, prior to the initiation of insulin therapy. The target for potassium in DKA should be K>5 (8).
  • If K is < 3.5, hold insulin to replace potassium until K>3.5. Infusion rates of 40-60 mEq/hr can be reasonable if the patient is in extremis (6).
  • If K is 3.5-5.5, replace potassium while initiating insulin therapy; use 20-40 mmol KCl per liter of IV fluid
  • If K is >5.5, start insulin therapy without replacing potassium; monitor potassium every 2-4 hours with potassium goal >5 mg/dL (6).

Pearls:

• Correct magnesium to allow for effective potassium repletion (2,5).
• Do not use dextrose containing fluids for repletion—they can worsen hypokalemia via insulin-mediated shifts (5).
• Never administer KCl as a bolus—infuse slowly and under cardiac monitoring (5,6).
• Closely monitor EKG and repeat serum K levels during repletion (e.g. q2-4h) (5,6).
• In myocardial infarction or critically ill patients, aiming for K ≥ 3.5 mmol/L is optimal; data suggests 3.5-4.5 mmol/L may be safest (6).

A 32-year-old man presents to the ED with an acute onset of profound lower extremity weakness that began this morning after a high-carbohydrate meal the previous night. He reports no trauma, back pain, or sensory deficits. His vital signs show an HR of 110 bpm, BP of 135/80 mm Hg, RR of 16/min, and T of 37.2°C. Physical exam reveals symmetric flaccid paralysis of the lower extremities with hyporeflexia, and an ECG shows U waves and a prolonged QT interval. What is the most appropriate next step in care?

A) Administer calcium gluconate for presumed hypocalcemia

B) Administer potassium gluconate and obtain thyroid function tests

C) Initiate high-dose corticosteroids for suspected myasthenia gravis

D) Perform a lumbar puncture to evaluate for Guillain-Barré syndrome

E) Perform urgent MRI of the spine to rule out cord compression

Correct answer: B

This patient presents with classic features of thyrotoxic periodic paralysis (TPP), a rare but serious complication of hyperthyroidism characterized by acute, reversible episodes of muscle weakness due to hypokalemia. The history of a high-carbohydrate meal, which can precipitate TPP by driving potassium intracellularly via insulin release, combined with symmetric flaccid paralysis, hyporeflexia, and ECG findings (U waves, prolonged QT interval) suggestive of hypokalemia, strongly supports this diagnosis. Administration of potassium gluconate will reverse the paralysis and prevent life-threatening dysrhythmias, while thyroid function tests (e.g., TSH, free T4) are essential to confirm underlying hyperthyroidism, most commonly due to Graves disease in TPP.

TPP predominantly affects young male patients (20–40 years) and seems to be most prevalent in East Asian populations. Risk factors include male sex (20:1 male-to-female ratio), hyperthyroidism (often undiagnosed), and triggers such as high-carbohydrate intake, exercise, or stress, which shift potassium into cells. Signs and symptoms include sudden-onset muscle weakness (typically proximal and lower extremity), hyporeflexia, and sparing of sensory and cranial nerve function. Hypokalemia (serum potassium often < 3.0 mEq/L) is a hallmark, though total body potassium is normal, reflecting intracellular redistribution rather than actual depletion. Diagnosis relies on clinical presentation, hypokalemia, and evidence of hyperthyroidism (suppressed TSH, elevated free T4).

In the ED, TPP is treated by focusing on correcting hypokalemia and stabilizing the patient while addressing the underlying hyperthyroidism. Intravenous potassium chloride (e.g., 10–20 mEq/hour with cardiac monitoring) rapidly reverses paralysis, but caution is needed to avoid rebound hyperkalemia as potassium shifts back extracellularly during recovery. Instead, a recommended treatment approach is slow, incremental potassium repletion if possible (unless the potassium is severely low). Nonselective beta-blockers (e.g., propranolol) can stabilize cardiac effects and reduce thyroid hormone effects acutely, while definitive treatment of hyperthyroidism (antithyroid drugs, e.g., methimazole) can be initiated after consultation with endocrinology. Patients require close monitoring for dysrhythmias or respiratory failure, though respiratory involvement is rare. Education on avoiding triggers (e.g., high-carbohydrate meals) is also key during discharge planning.

Calcium gluconate (A) is used for hypocalcemia, which may cause tetany, seizures, or ECG changes (prolonged QT due to ST segment lengthening), but not U waves or flaccid paralysis. This patient’s presentation and ECG findings align with hypokalemia, not hypocalcemia, making calcium administration inappropriate and potentially harmful.

Myasthenia gravis (C) typically causes fatigable weakness, often involving ocular or bulbar muscles, and is not associated with hypokalemia or ECG changes like U waves. This patient’s symmetric flaccid paralysis and metabolic trigger (carbohydrate meal) are inconsistent with myasthenia. Corticosteroids are not indicated for TPP and could worsen hyperthyroid effects.

Guillain-Barré syndrome (GBS) (D) presents with ascending weakness, often postinfection, with areflexia and potential sensory deficits or albuminocytologic dissociation on cerebrospinal fluid analysis. However, this patient’s acute onset after a carbohydrate load, lack of sensory symptoms, and ECG findings consistent with hypokalemia point to TPP rather than GBS. Lumbar puncture is unnecessary and delays critical potassium repletion.

Spinal cord compression (E) typically causes sensory deficits, hyperreflexia below the lesion, and bowel and bladder dysfunction, none of which are present here. The metabolic trigger, hyporeflexia, and ECG abnormalities suggest TPP, not a structural lesion. Imaging would delay treatment and is not indicated based on this clinical picture.

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