8.3 Scenario Practice for Medical Disorders

Sodium Disorders and the Osmotic Demyelination Trap

Hyponatremia (Na <135 mEq/L) is the most common electrolyte abnormality in the ED, and the exam centers on matching severity to treatment. Symptoms track how fast sodium fell more than the absolute number: headache and nausea at moderate levels; seizures, coma, and herniation when Na drops below 120 mEq/L acutely.

• Severe symptomatic hyponatremia (Na <120 mEq/L with seizures or coma) is treated with 3% hypertonic saline, typically in 100–150 mL boluses, to raise sodium just enough to stop seizures.
• The cardinal safety rule: correct sodium no faster than ~8 mEq/L in 24 hours (some sources cite 6–10). Overly rapid correction causes osmotic demyelination syndrome (ODS, formerly central pontine myelinolysis)—a delayed, often irreversible quadriparesis and locked-in syndrome.
• Asymptomatic or chronic hyponatremia is corrected slowly; the danger is over-correction, not the low number itself.

Hypernatremia (Na >145 mEq/L) reflects a water deficit and presents with thirst, lethargy, and irritability; it is corrected slowly with hypotonic fluids to avoid cerebral edema. A stem with a sodium of 116 mEq/L and active seizing is the prototypical "severe symptomatic" hyponatremia and calls for hypertonic saline, not slow free-water restriction.

The cause guides the fluid choice. Hypovolemic hyponatremia (vomiting, diarrhea, diuretics) is treated with isotonic saline. Euvolemic hyponatremia most often reflects SIADH (syndrome of inappropriate antidiuretic hormone)—from CNS disease, pulmonary disease, malignancy, or drugs—and is managed with fluid restriction. Hypervolemic hyponatremia (heart failure, cirrhosis, renal failure) is managed with fluid and sodium restriction. In hyperglycemia, serum sodium falls about 1.6 mEq/L for every 100 mg/dL of glucose above normal (pseudohyponatremia), so correct the glucose rather than treating the number as a true deficit.

Recognizing pseudohyponatremia keeps you from over-treating a lab that will normalize once the glucose falls.

Potassium Disorders and ECG Recognition

Hyperkalemia is the electrolyte emergency most likely to kill quickly, and the ECG drives urgency. Changes progress predictably as potassium climbs:

The treatment order is fixed and frequently tested:

1. IV calcium gluconate (or chloride) first—it stabilizes the cardiac membrane within minutes but does not lower potassium.
2. Shift potassium into cells: regular insulin (10 units) with dextrose (25 g), and nebulized albuterol; sodium bicarbonate if acidotic.
3. Eliminate potassium: a potassium binder (e.g., patiromer/SPS), loop diuretics, or dialysis for refractory cases or renal failure.

Giving insulin requires concurrent dextrose to prevent hypoglycemia. Hypokalemia (K <3.5) causes U waves, flattened T waves, and ventricular ectopy; replace potassium and check magnesium, because hypokalemia is refractory until low magnesium is corrected.

Acid-Base Disorders: Reading the Gas

The CEN expects you to classify a blood gas and find the anion gap. Compute anion gap = Na − (Cl + HCO3), normal 8–12 mEq/L. A gap above 12 signals an unmeasured acid.

High anion gap metabolic acidosis causes are recalled by MUDPILES:

• Methanol
• Uremia
• DKA (and other ketoacidoses)
• Propylene glycol / Paraldehyde
• Isoniazid / Iron
• Lactic acidosis (sepsis, shock)
• Ethylene glycol
• Salicylates

Classify the primary disorder by pH and the two drivers: PaCO2 (respiratory) and HCO3 (metabolic).

Deep, rapid Kussmaul respirations are the lungs blowing off CO2 to compensate for the metabolic acidosis of DKA—a respiratory response to a metabolic problem, not a primary lung disorder.

Calcium, Magnesium, and a Worked Gas

Beyond sodium and potassium, the CEN tests calcium and magnesium disturbances because they drive cardiac and neuromuscular emergencies. Hypocalcemia (ionized calcium low) causes neuromuscular irritability—Chvostek and Trousseau signs, tetany, laryngospasm, and a prolonged QT that can deteriorate to torsades. It appears after thyroidectomy, in pancreatitis, in tumor lysis syndrome, and after massive transfusion (citrate binds calcium). Treat symptomatic cases with IV calcium gluconate.

Hypercalcemia (often from malignancy or hyperparathyroidism) causes the classic "stones, bones, groans, and psychiatric overtones," with a shortened QT; treat with aggressive IV normal saline and, for severe cases, calcitonin and bisphosphonates.

Magnesium is the quiet partner. Hypomagnesemia makes hypokalemia and hypocalcemia refractory and predisposes to torsades, so magnesium is replaced alongside potassium; IV magnesium sulfate is the treatment for torsades regardless of the measured level. Hypermagnesemia, usually iatrogenic in renal failure or obstetric magnesium therapy, causes hyporeflexia, hypotension, and respiratory depression—treated with IV calcium and dialysis.

A worked gas

Given pH 7.30, PaCO2 30 mmHg, HCO3 14 mEq/L: the pH is acidemic, the bicarbonate is low (the metabolic driver), and the low CO2 is the lungs compensating. This is a partially compensated metabolic acidosis—precisely the pattern of DKA, sepsis-related lactic acidosis, or a toxic ingestion. Always read pH first, then identify which value (CO2 or HCO3) explains it, then check whether the other value has compensated.