10.4 Fluid, Electrolyte & Acid-Base Disorders

Diagnostic Approach to Hyponatremia & Hypernatremia

Sodium disorders represent imbalances of water homeostasis rather than total body sodium content. On USMLE Step 2 CK, evaluating hyponatremia follows a systematic 3-step diagnostic algorithm.

                         [ Measured Serum Na <135 mEq/L ]
                                        |
                         [ Step 1: Check Serum Osmolality ]
                                        |
         +------------------------------+------------------------------+
         |                              |                              |
   [ High (>295) ]              [ Normal (280-295) ]           [ Low (<280) ]
  Hypertonic Hyponatremia      Pseudohyponatremia             Hypotonic Hyponatremia
  (Hyperglycemia, Mannitol)    (Hypertriglyceridemia)                  |
                                                        [ Step 2: Assess Volume ]
                                                                       |
         +--------------------------------+----------------------------+
         |                                |                            |
   [ Hypovolemic ]                  [ Euvolemic ]                [ Hypervolemic ]
   Urine Na <20: GI Loss / Dehydration  SIADH (Urine Osm >100)      Heart Failure
   Urine Na >20: Diuretics / Addison   Psychogenic Polydipsia       Cirrhosis / Nephrotic

Clinical Management of Hyponatremia & Correction Limits

• Osmotic Demyelination Syndrome (ODS / Central Pontine Myelinolysis): Occurs when chronic hyponatremia is corrected too rapidly (>8 mEq/L in 24 hours). Rapid extracellular hypertonicity draws water out of pontine myelin sheath cells, causing dysarthria, dysphagia, paraparesis, or locked-in syndrome.
• Severe Symptomatic Hyponatremia: Patients presenting with seizures, confusion, or coma require immediate hypertonic 3% saline bolus (100–150 mL) to raise serum sodium by 4–6 mEq/L over 1–2 hours, symptomatically reversing acute cerebral edema.
• SIADH Treatment: First-line therapy for asymptomatic euvolemic hyponatremia is fluid restriction (<800–1000 mL/day). Oral salt tablets, loop diuretics, or vasopressin receptor antagonists (vaptans) are added if fluid restriction fails.

Hypernatremia

Hypernatremia (serum Na+ >145 mEq/L) reflects a deficit of free water relative to solute. Causes include Diabetes Insipidus (DI):

• Central DI: Deficiency of ADH release from posterior pituitary (head trauma, pituitary lesions). Responds to exogenous desmopressin (dDAVP) with a >50% increase in urine osmolality.
• Nephrogenic DI: Renal resistance to ADH (lithium toxicity, hypercalcemia, hypokalemia). Does not respond to desmopressin; managed with thiazides and amiloride.
• Correction Rate Limit: Overly rapid correction of hypernatremia with hypotonic fluids risks cerebral edema (water shifts into brain cells). Correct at a maximum rate of <10 mEq/L/day.

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Potassium Disorders

Hyperkalemia Management Sequence

Hyperkalemia (serum K+ >5.2 mEq/L) causes cardiac membrane instability leading to fatal arrhythmias (sine waves, ventricular fibrillation). Treatment follows a precise 3-phase emergency protocol:

1. Membrane Stabilization (Immediate): Intravenous Calcium Gluconate (or Calcium Chloride). Restores cardiac membrane threshold potential without altering serum potassium level. Mandatory if ECG shows peaked T waves, PR prolongation, or QRS widening.
2. Intracellular Potassium Shunting (Rapid onset, temporary):
   • Insulin (10 units regular IV) plus 50% Dextrose (50 mL): Drives K+ into cells via Na+/K+ ATPase stimulation.
   • Inhaled Albuterol (10-20 mg): Beta-2 adrenergic agonist driving intracellular K+ shift.
   • Sodium Bicarbonate IV: Used primarily if severe metabolic acidosis is present.
3. Potassium Elimination from Body (Definitive):
   • Loop Diuretics (Furosemide): Increases renal K+ excretion in patients with preserved renal function.
   • Cation Exchange Resins / Potassium Binders: Patiromer or Sodium Zirconium Cyclosilicate (SZC).
   • Hemodialysis: Definitive therapy in severe AKI/ESRD.

Hypokalemia & Hypomagnesemia

Hypokalemia (serum K+ <3.5 mEq/L) causes muscle weakness, cramps, constipation, and ECG abnormalities (flattened T waves, ST depression, U waves). On Step 2 CK, if hypokalemia is refractory to oral/IV potassium replacement, check and correct serum magnesium. Hypomagnesemia disinhibits the Outer Medullary Potassium (ROMK) channels in renal collecting ducts, causing continuous urinary potassium wasting.

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Acid-Base Interpretation & Renal Tubular Acidosis

Systematic 4-Step Acid-Base Workflow

1. Assess pH: Acidemia (<7.35) vs. Alkalemia (>7.45).
2. Identify Primary Process: Compare pH change with pCO2 and serum HCO3⁻.
3. Calculate Anion Gap (if Metabolic Acidosis present): $$\text{Anion Gap} = [\text{Na}^+] - ([\text{Cl}^-] + [\text{HCO}_3^-]) \quad (\text{Normal: } 8 - 12\text{ mEq/L})$$
   • High Anion Gap Metabolic Acidosis (HAGMA) (>12 mEq/L): Mnemonic MUDPILES (Methanol, Uremia, Diabetic Ketoacidosis, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates).
   • Normal Anion Gap (Hyperchloremic) Metabolic Acidosis (8-12 mEq/L): Mnemonic HARDASS (Hyperalimentation, Acetazolamide, Renal Tubular Acidosis, Diarrhea, Addison disease, Spironolactone, Saline infusion).
4. Evaluate Compensation:
   • Winters' Formula for Metabolic Acidosis: Predicts expected pCO2: $$\text{Expected } p\text{CO}_2 = (1.5 \times [\text{HCO}_3^-]) + 8 \pm 2$$
     • If measured pCO2 > expected pCO2 -> Concurrent Respiratory Acidosis.
     • If measured pCO2 < expected pCO2 -> Concurrent Respiratory Alkalosis.

Renal Tubular Acidosis (RTA) Summary