# Electrolyte Emergencies: Hyponatremia, Hyperkalemia, and Hypercalcemia

## Introduction

Electrolyte disorders are among the most common laboratory abnormalities encountered in the emergency department. While many are incidental findings, severe derangements of sodium, potassium, and calcium can produce life-threatening neurologic, cardiac, and neuromuscular emergencies. The emergency physician must rapidly identify symptomatic electrolyte disorders, initiate targeted treatment, and avoid iatrogenic complications from overly rapid correction.

## Hyponatremia

### Definition and Classification

Hyponatremia is defined as a serum sodium below 135 mEq/L. It is classified as mild (130 to 134), moderate (125 to 129), or severe (below 125). The temporal classification is equally important: acute hyponatremia develops within 48 hours, carries a higher seizure risk, and is safer to correct rapidly, while chronic hyponatremia develops over more than 48 hours, and the brain has adapted, making rapid correction dangerous due to the risk of osmotic demyelination syndrome.

### Pathophysiology

Hyponatremia is almost always a disorder of water balance, not sodium balance. Classification by volume status and serum osmolality guides the workup. Hypovolemic hyponatremia results from GI losses, diuretics, or adrenal insufficiency, where total body sodium is depleted but water is depleted less. Euvolemic hyponatremia is most commonly caused by SIADH, along with hypothyroidism, psychogenic polydipsia, and medications (SSRIs, carbamazepine). Hypervolemic hyponatremia occurs in heart failure, cirrhosis, and nephrotic syndrome and is dilutional. Pseudohyponatremia from hyperglycemia, hyperlipidemia, or hyperproteinemia must also be considered; sodium should be corrected by adding 1.6 mEq/L for each 100 mg/dL of glucose above 100.

### Clinical Presentation

Mild to moderate hyponatremia produces headache, nausea, fatigue, and gait instability. Severe hyponatremia causes confusion, seizures, obtundation, coma, and respiratory arrest. Cerebral edema occurs when water shifts into brain cells down the osmotic gradient.

### Emergency Treatment

Symptomatic hyponatremia with seizures or obtundation requires immediate 3 percent hypertonic saline. The bolus dose is 100 mL of 3 percent NaCl over 10 minutes, which may be repeated up to 3 times for persistent symptoms. The target is to raise sodium by 4 to 6 mEq/L in the first 1 to 2 hours to arrest symptoms. For chronic hyponatremia, correction must not exceed 8 mEq/L in any 24-hour period (some guidelines suggest a 10 mEq/L limit). Osmotic demyelination syndrome (ODS) is a devastating complication of overcorrection in which central pontine myelinolysis causes quadriplegia, pseudobulbar palsy, and locked-in syndrome. If overcorrection occurs, D5W or desmopressin (DDAVP 2 mcg IV) should be administered to re-lower sodium.

<image>Diagnostic algorithm for hyponatremia showing stepwise evaluation by serum osmolality (low, normal, high), then volume status assessment (hypovolemic, euvolemic, hypervolemic) with corresponding causes and initial treatment for each category</image>

## Hyperkalemia

### Definition and Significance

Hyperkalemia is defined as serum potassium above 5.0 mEq/L and is classified as mild (5.0 to 5.9), moderate (6.0 to 6.4), or severe (6.5 or above). Pseudohyperkalemia from hemolyzed specimens, prolonged tourniquet time, or extreme leukocytosis or thrombocytosis should be considered, and the value should always be confirmed with a repeat specimen if unexpected.

### Etiology

Decreased excretion is the most common mechanism, resulting from renal failure, hypoaldosteronism, and medications (ACE inhibitors, ARBs, spironolactone, trimethoprim, NSAIDs). Transcellular shift causes include acidosis, insulin deficiency, beta-blocker toxicity, succinylcholine, rhabdomyolysis, tumor lysis syndrome, and massive transfusion. Increased intake is rarely the sole cause but can occur with potassium supplements or salt substitutes in renal patients.

### ECG Manifestations (Progressive)

The earliest change is peaked T waves, which are tall, narrow, and symmetric. This is followed by PR prolongation and P-wave flattening, then QRS widening (an ominous finding), then a sine wave pattern (a pre-arrest rhythm), and finally ventricular fibrillation or asystole. ECG changes correlate imperfectly with serum levels, and the clinician should treat the patient, not the number alone.

### Emergency Treatment Protocol

| Step | Agent | Dose | Onset | Mechanism | K+ Reduction | Duration |
|------|-------|------|-------|-----------|-------------|----------|
| 1. Stabilize | Calcium gluconate 10% | 10 mL (1 g) IV over 2–3 min | 1–3 min | Membrane stabilization | None (cardioprotective) | 30–60 min |
| 2. Shift | Insulin + D50 | 10 U regular insulin + 25 g dextrose IV | 15–30 min | Intracellular shift | 0.5–1.2 mEq/L | 4–6 hrs |
| 2. Shift | Albuterol (nebulized) | 10–20 mg | 15–30 min | Intracellular shift | 0.5–1.0 mEq/L | 2–4 hrs |
| 2. Shift | Sodium bicarbonate | 150 mEq in 1 L D5W | 30–60 min | Shift (weak alone) | Variable | Variable |
| 3. Eliminate | Furosemide | 40–80 mg IV | 30–60 min | Renal excretion | Variable | Dose-dependent |
| 3. Eliminate | Kayexalate | 15–30 g PO/PR | 1–6 hrs | GI exchange | 0.5–1.0 mEq/L | Slow |
| 3. Eliminate | Hemodialysis | — | Immediate | Direct removal | 1–2 mEq/L/hr | Definitive |

The first step is cardiac membrane stabilization with calcium gluconate 10 percent, given as 10 mL (1 gram) IV over 2 to 3 minutes (or calcium chloride 10 mL via central line). This does not lower potassium but stabilizes the cardiac myocyte membrane potential. Onset is 1 to 3 minutes with a duration of 30 to 60 minutes, and the dose may be repeated if ECG changes persist.

The second step promotes intracellular potassium shift. Regular insulin 10 units IV plus D50 25 grams (50 mL) IV has an onset of 15 to 30 minutes and lowers potassium by 0.5 to 1.2 mEq/L; glucose must be monitored hourly for 4 to 6 hours, as hypoglycemia occurs in up to 75 percent of patients. Nebulized albuterol 10 to 20 mg has an additive effect with insulin and an onset of 15 to 30 minutes. Sodium bicarbonate 150 mEq in 1 liter of D5W has a weak effect as monotherapy but is useful when concurrent metabolic acidosis is present.

The third step is potassium elimination. Loop diuretics (furosemide 40 to 80 mg IV) are useful if renal function is adequate and the patient is euvolemic. Sodium polystyrene sulfonate (Kayexalate) has slow onset, limited evidence, and a risk of intestinal necrosis, and its use has declined. Newer potassium binders such as patiromer and sodium zirconium cyclosilicate (Lokelma) have faster onset and better safety profiles. Hemodialysis is the definitive treatment for severe, refractory hyperkalemia, especially with renal failure.

<image>ECG progression of hyperkalemia showing four rhythm strips: normal baseline, peaked T waves at K+ 6.0, widened QRS at K+ 7.5, and sine wave pattern at K+ 8.5 with annotations at each stage</image>

## Hypercalcemia

### Definition and Etiology

Hypercalcemia is defined as total serum calcium above 10.5 mg/dL (always corrected for albumin: corrected calcium equals measured calcium plus 0.8 times the difference between 4.0 and the albumin level). Ionized calcium above 5.2 mg/dL is more accurate and not affected by albumin. Severity is classified as mild (10.5 to 12.0), moderate (12.0 to 14.0), or severe/crisis (above 14.0). Primary hyperparathyroidism (in outpatients) and malignancy (in inpatients) account for over 90 percent of cases. Malignancy-related causes include PTHrP-secreting tumors (squamous cell, renal cell), osteolytic metastases (breast, myeloma), and lymphoma (1,25-vitamin D production). Other causes include granulomatous disease (sarcoidosis), thiazide diuretics, vitamin D toxicity, milk-alkali syndrome, immobilization, and thyrotoxicosis.

### Clinical Presentation -- "Stones, Bones, Groans, and Psychiatric Moans"

The classic mnemonic captures the spectrum: stones (nephrolithiasis, nephrocalcinosis), bones (bone pain, pathologic fractures, osteoporosis), groans (abdominal pain, nausea, vomiting, constipation, pancreatitis), and psychiatric moans (confusion, lethargy, depression, coma). Cardiac effects include a shortened QT interval, Osborn waves, bradycardia, and heart block, and hypercalcemia potentiates digoxin toxicity.

### Emergency Treatment

Volume resuscitation with normal saline at 200 to 500 mL per hour is the cornerstone, as most patients are significantly volume depleted from hypercalcemia-induced nephrogenic diabetes insipidus. Loop diuretics (furosemide) should be given only after adequate volume resuscitation to promote calciuresis and must not be given before rehydration. Calcitonin 4 IU/kg subcutaneously or IM every 12 hours has rapid onset (4 to 6 hours) with a modest effect (lowering calcium by 1 to 2 mg/dL) but develops tachyphylaxis within 48 hours. Bisphosphonates (zoledronic acid 4 mg IV over 15 minutes or pamidronate 60 to 90 mg IV over 2 to 4 hours) have an onset of 2 to 4 days and are definitive for malignancy-related hypercalcemia. Denosumab is used for bisphosphonate-refractory cases. Hemodialysis is reserved for severe, life-threatening hypercalcemia with renal failure or cardiac instability. Glucocorticoids are effective for granulomatous disease and lymphoma-related hypercalcemia (hydrocortisone 200 mg IV then 50 mg every 8 hours).

<image>Treatment algorithm for hypercalcemia of malignancy showing initial aggressive IV saline hydration, followed by parallel administration of calcitonin for rapid effect and zoledronic acid for sustained effect, with decision points for refractory cases including denosumab and hemodialysis</image>

## Clinical Pearls

Symptomatic hyponatremia with seizures requires emergent 3 percent hypertonic saline -- a 100 mL bolus over 10 minutes is safe and effective and should not be delayed for confirmatory labs. In chronic hyponatremia, overcorrection is more dangerous than undercorrection, and correction should be limited to 8 mEq/L per 24 hours, using DDAVP proactively if correction outpaces targets. Calcium is the first drug in severe hyperkalemia -- it does not lower potassium but prevents cardiac arrest while other therapies take effect. Dextrose should always be given with insulin for hyperkalemia, and glucose should be monitored for at least 4 to 6 hours, as iatrogenic hypoglycemia is the most common complication. In hypercalcemia, aggressive saline hydration is the cornerstone of initial therapy, and furosemide should only be added after the patient is volume replete.

## References

1. Sterns RH. "Disorders of Plasma Sodium -- Causes, Consequences, and Correction." *New England Journal of Medicine*. 2015;372(1):55-65.
2. Long B, et al. "Controversies in Management of Hyperkalemia." *Journal of Emergency Medicine*. 2018;55(2):192-205.
3. Minisola S, et al. "The Diagnosis and Management of Hypercalcaemia." *BMJ*. 2015;350:h2723.
4. Palmer BF, Clegg DJ. "Diagnosis and Treatment of Hyperkalemia." *Cleveland Clinic Journal of Medicine*. 2017;84(12):934-942.