Clinical Case Scenario
A 55-year-old woman with a history of severe alcohol use disorder and poor nutritional intake is brought to the ICU after a generalized tonic–clonic seizure. She is post-ictal but protecting her airway.
On examination, she appears markedly malnourished and is confused but conscious.
POCUS findings:
- Bilateral lung A-profile
- Preserved cardiac contractility on eyeball assessment
- Collapsing IVC
Vital signs:
- BP: 105/65 mmHg
- HR: 112/min
Laboratory Finding
- Sodium: 106 mmol/L
- Potassium: 1.8 mmol/L
- Chloride: 72 mmol/L
- Bicarbonate: 26 mmol/L
- BUN: 8 mg/dL
- Creatinine: 0.4 mg/dL
- Serum osmolality: 222 mOsm/kg
- Urine osmolality: 450 mOsm/kg
- Urine sodium: 12 mmol/L
She receives a 150 mL bolus of 3% hypertonic saline, after which her seizures cease.
Given her extremely high risk for osmotic demyelination syndrome (ODS), you plan to limit the serum sodium rise to ≤6 mmol/L during the first 24 hours.
The next priority is aggressive intravenous potassium chloride replacement for profound hypokalaemia.
Question: How will intravenous potassium chloride replacement influence her serum sodium correction, and what is the underlying mechanism?
