Residency · Residency · Internal Medicine
Electrolyte Emergencies: Hyponatremia and Hyperkalemia
Overview
Hyponatremia and hyperkalemia are the two most common and potentially life-threatening electrolyte disorders encountered on the wards. Both require systematic diagnostic algorithms and careful management to avoid iatrogenic harm. Overly rapid correction of hyponatremia causes osmotic demyelination syndrome (ODS), while hyperkalemia requires emergent treatment when ECG changes or severe elevation are present.
Hyponatremia
Definition and Classification
Hyponatremia is defined as serum sodium below 135 mEq/L. It is classified as mild (130-134), moderate (125-129), or severe (below 125). Temporal classification distinguishes acute (developing in less than 48 hours, with higher risk of cerebral edema) from chronic (developing over more than 48 hours, with higher risk of ODS with rapid correction).
Diagnostic Algorithm
The first step is to confirm true hyponatremia by checking serum osmolality. Hypotonic values (below 280 mOsm/kg) indicate true hyponatremia requiring further workup. Isotonic values (280-295) suggest pseudohyponatremia from severe hyperlipidemia or hyperproteinemia. Hypertonic values (above 295) indicate translocational hyponatremia from hyperglycemia, requiring sodium correction by 1.6-2.4 mEq/L for every 100 mg/dL of glucose above 100.
The second step is assessing volume status through clinical examination and urine studies. Hypovolemic hyponatremia with urine sodium below 20 suggests GI losses, third-spacing, or burns; with urine sodium above 20, it suggests diuretics, adrenal insufficiency, or cerebral salt wasting. Euvolemic hyponatremia with urine sodium above 20 and urine osmolality above 100 points to SIADH (the most common cause of euvolemic hyponatremia), hypothyroidism, or cortisol deficiency. Hypervolemic hyponatremia with urine sodium below 20 occurs in heart failure, cirrhosis, and nephrotic syndrome; with urine sodium above 20, it occurs in advanced CKD.
The third step is checking urine osmolality. A value below 100 mOsm/kg indicates primary polydipsia or low solute intake ("tea and toast" diet). A value above 100 indicates impaired free water excretion that is ADH-mediated.
<image>Diagnostic algorithm for hyponatremia based on serum osmolality, volume status assessment, urine sodium, and urine osmolality</image>
SIADH -- Diagnosis and Common Causes
SIADH requires euvolemia, serum osmolality below 275, urine osmolality above 100, urine sodium above 30, and normal thyroid and adrenal function. Causes include CNS disease (stroke, subarachnoid hemorrhage, meningitis), pulmonary disease (pneumonia, tuberculosis), medications (SSRIs, carbamazepine, cyclophosphamide, desmopressin), malignancy (small cell lung cancer), and physiologic stimuli such as pain, nausea, and postoperative states.
Treatment of Hyponatremia
For acute symptomatic hyponatremia with seizures or obtundation, 3% hypertonic saline is administered as a 100 mL IV bolus over 10 minutes, which may be repeated up to two additional times if symptoms persist. The target is to raise sodium by 4-6 mEq/L in the first 1-2 hours to alleviate symptoms.
For chronic hyponatremia, the maximum correction rate is 8 mEq/L in any 24-hour period, with some experts recommending 6 mEq/L or less in high-risk patients. High-risk factors for ODS include chronic hyponatremia with sodium below 120, hypokalemia, alcoholism, malnutrition, and liver disease.
Volume-dependent treatment involves isotonic saline for hypovolemic causes and fluid restriction for SIADH and hypervolemic causes. SIADH-specific treatments include fluid restriction (below 1 L/day), salt tablets plus a loop diuretic, urea (gaining adoption), and vaptans (tolvaptan, which has a limited role due to hepatotoxicity risk and cost).
If overcorrection occurs and sodium rises too fast, DDAVP 1-2 mcg IV every 6-8 hours plus D5W should be administered to lower sodium back to safe correction limits.
Osmotic Demyelination Syndrome (ODS)
Previously called central pontine myelinolysis, ODS can also affect extrapontine areas. It occurs 2-6 days after overly rapid correction and presents with dysarthria, dysphagia, quadriparesis, locked-in syndrome, and altered consciousness. MRI findings lag clinical symptoms by 1-2 weeks. The condition is largely irreversible, making prevention critical.
<image>MRI brain showing characteristic central pontine myelinolysis lesion in osmotic demyelination syndrome with corresponding clinical features</image>
Hyperkalemia
Definition and Classification
Hyperkalemia is defined as serum potassium above 5.0 mEq/L. It is classified as mild (5.0-5.5), moderate (5.5-6.5), or severe (above 6.5 or any level with ECG changes).
Pseudohyperkalemia
A hemolyzed specimen is the most common cause of pseudohyperkalemia. Other causes include prolonged tourniquet time, fist clenching, and extreme leukocytosis or thrombocytosis. The value should always be repeated before treating if clinically unexpected.
Etiologies
Decreased excretion causes include AKI, CKD, hypoaldosteronism (Type 4 RTA), and medications (ACE inhibitors/ARBs, spironolactone, amiloride, trimethoprim, NSAIDs, calcineurin inhibitors, heparin). Transcellular shift causes include acidosis, insulin deficiency, beta-blockers, digoxin toxicity, succinylcholine, and cell lysis (rhabdomyolysis, tumor lysis, massive hemolysis). Increased intake is rarely the sole cause unless impaired excretion coexists; sources include oral or IV KCl supplements and salt substitutes.
ECG Changes (Progressive)
ECG changes progress through peaked T waves (the earliest sign), prolonged PR interval, widened QRS complex, loss of P waves, and finally a sine wave pattern progressing to ventricular fibrillation or asystole. Critically, ECG changes do not reliably correlate with potassium level: some patients develop arrhythmias at potassium of 6.0 while others tolerate levels above 7.0.
Acute Management
Acute hyperkalemia management rests on three pillars.
| Treatment Pillar | Agent | Dose | Onset | Duration | Mechanism |
|---|---|---|---|---|---|
| Membrane stabilization | Calcium gluconate 10% | 10 mL IV over 2-3 min | 1-3 min | 30-60 min | Stabilizes cardiac membrane (does NOT lower K+) |
| Intracellular shift | Insulin + dextrose | 10 U regular insulin + D50 25-50 g IV | 15-30 min | 4-6 h | Drives K+ into cells |
| Intracellular shift | Albuterol (nebulized) | 10-20 mg | 15-30 min | 2-4 h | Beta-2 mediated shift |
| Intracellular shift | Sodium bicarbonate | 50-150 mEq IV | 30-60 min | Hours | Limited except in severe acidosis |
| Elimination | Loop diuretics | Furosemide 40-80 mg IV | 30-60 min | Hours | Renal K+ excretion |
| Elimination | SZC (Lokelma) | 10 g PO TID | 1-2 h | Hours | GI K+ binding (preferred binder) |
| Elimination | Patiromer (Veltassa) | 8.4 g PO | 7-48 h | Hours | GI K+ binding (chronic use) |
| Elimination | Hemodialysis | — | Immediate | — | Definitive for refractory/ESRD |
The first pillar is cardiac membrane stabilization, which acts within minutes. Calcium gluconate 10% (10 mL IV over 2-3 minutes) is preferred, or calcium chloride via central line. Onset is 1-3 minutes with a duration of 30-60 minutes. This does not lower potassium but protects the heart while other treatments take effect. The dose is repeated if ECG changes persist.
The second pillar is intracellular potassium shifting, which works over minutes to hours. Regular insulin 10 units IV with D50 25-50 g IV (to prevent hypoglycemia) has an onset of 15-30 minutes and a duration of 4-6 hours. Nebulized albuterol 10-20 mg has an onset of 15-30 minutes and should be used in combination, not alone. Sodium bicarbonate 50-150 mEq IV has limited efficacy except in severe acidosis and is not first-line.
The third pillar is potassium elimination, which takes hours. Loop diuretics (furosemide 40-80 mg IV) work if adequate renal function is present. Sodium polystyrene sulfonate (Kayexalate) 15-30 g orally has a slow onset (hours), limited evidence, and carries a risk of colonic necrosis; it is falling out of favor. Patiromer (Veltassa) 8.4 g orally is a newer potassium binder that is better tolerated with onset of 7-48 hours, useful for chronic management. Sodium zirconium cyclosilicate (Lokelma/SZC) 10 g orally three times daily has faster onset (1-2 hours), is well-tolerated, and is emerging as the preferred binder. Hemodialysis is the definitive treatment for severe or refractory hyperkalemia or hyperkalemia with AKI/ESRD.
<image>ECG progression of hyperkalemia from peaked T waves through widened QRS to sine wave pattern, alongside treatment algorithm with three pillars of management</image>
Chronic Hyperkalemia Management
Chronic management includes dietary potassium restriction, medication review and adjustment (ACE inhibitors/ARBs and MRAs may be dose-reduced rather than discontinued if cardio-renal benefit is significant), chronic potassium binders (patiromer, SZC) that enable continued use of RAAS inhibitors in CKD and heart failure, optimization of diuretic therapy, and correction of metabolic acidosis with sodium bicarbonate supplementation.
Clinical Pearls
In hyponatremia, TSH and cortisol must always be checked before diagnosing SIADH because hypothyroidism and adrenal insufficiency are treatable mimics. Proactive DDAVP administration (the "DDAVP clamp") can prevent overcorrection in high-risk patients by administering DDAVP when starting therapy and controlling sodium rise with hypertonic saline. Potassium level drops approximately 0.3-0.5 mEq/L per unit of insulin given, and dextrose must always be co-administered with glucose checked hourly for 4 hours. In DKA, initial potassium may be normal or high despite massive total body depletion because insulin therapy will rapidly lower serum potassium, requiring aggressive replacement. Sodium bicarbonate is not effective for shifting potassium in isolation and should only be considered with concurrent severe acidosis. Kayexalate has minimal evidence for acute efficacy and carries a risk of colonic necrosis; newer binders (SZC, patiromer) are preferred.
References
- Spasovski G, et al. Clinical Practice Guideline on Diagnosis and Treatment of Hyponatraemia. Eur J Endocrinol. 2014;170:G1-G47.
- Sterns RH. Disorders of Plasma Sodium. N Engl J Med. 2015;372:55-65.
- Palmer BF, Clegg DJ. Diagnosis and Treatment of Hyperkalemia. Cleve Clin J Med. 2017;84:934-942.
- Packham DK, et al. Sodium Zirconium Cyclosilicate in Hyperkalemia. N Engl J Med. 2015;372:222-231.
- Verbalis JG, et al. Diagnosis, Evaluation, and Treatment of Hyponatremia: Expert Panel Recommendations. Am J Med. 2013;126:S1-S42.
