# Chapter 15: Core Electrolyte Disorders

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## Hyponatremia: Complete Student Study Guide

### Introduction to Hyponatremia

Hyponatremia (serum sodium \<135 mEq/L) is the most common electrolyte disorder. It is crucial to conceptualize it as a disorder of **water balance** (too much water relative to sodium), primarily controlled by Antidiuretic Hormone (ADH), rather than a simple sodium deficit.

### Systematic Diagnostic Approach

1.  **Confirm True Hypotonic Hyponatremia:** Measure serum osmolality (\<275 mOsm/kg). Rule out pseudohyponatremia (normal osmolality) and hypertonic hyponatremia (high osmolality, e.g., hyperglycemia).
2.  **Assess Volume Status:** This is key to determining the cause. Is the patient hypovolemic, euvolemic, or hypervolemic?
3.  **Check Urine Osmolality & Sodium:**
    - **Urine Osmolality \< 100 mOsm/kg:** ADH is appropriately suppressed. Think primary polydipsia or low solute intake (beer potomania).
    - **Urine Osmolality \> 100 mOsm/kg:** ADH is active. This is the most common scenario.
4.  **Urine Sodium:**
    - **\< 30 mEq/L:** Kidneys are conserving sodium. Suggests hypovolemia or hypervolemic states like heart failure/cirrhosis.
    - **\> 30 mEq/L:** Kidneys are wasting sodium. Suggests euvolemic states like SIADH or renal salt wasting.

**Serum Uric Acid:** A low serum uric acid (\<4 mg/dL) is a helpful clue that points towards SIADH.

### Treatment Principles and Correction Rates

#### Avoid Osmotic Demyelination Syndrome (ODS)!

Overly rapid correction of chronic hyponatremia is dangerous. The brain adapts to chronic low sodium, and rapid correction can cause irreversible neurologic injury.

- **Correction Goal:** Do not exceed **8-10 mEq/L in any 24-hour period.** A safer target is **6-8 mEq/L per 24 hours**, especially in high-risk patients (alcoholism, malnutrition, liver disease).
- **Acute/Symptomatic:** For severe symptoms (seizures, coma), a rapid initial increase of 4-6 mEq/L with boluses of 3% hypertonic saline is warranted to alleviate cerebral edema. Once symptoms resolve, the correction rate must be slowed.

### 2024-2025 Treatment Updates

#### Modern Hyponatremia Management

- **Hypertonic Saline:** Rapid intermittent boluses (100-150 mL of 3% saline) are now the standard for severe symptomatic cases, preferred over continuous infusions for better control.
- **Oral Urea:** Now a mainstream, evidence-based therapy for chronic SIADH. It acts as an osmotic agent to promote free water excretion. Dosing is typically 15-60g per day.
- **SGLT2 Inhibitors:** An emerging option, especially in heart failure. They induce osmotic diuresis via glucosuria, increasing free water clearance.
- **The dDAVP Clamp:** A technique used to prevent overcorrection in high-risk scenarios. Prophylactic desmopressin (dDAVP) is given to "clamp" the kidneys' ability to excrete free water, allowing for controlled correction with hypertonic saline.

## Hyperkalemia: Comprehensive Treatment Review

### Emergency Management of Severe Hyperkalemia

Severe hyperkalemia (K+ \> 6.5 mEq/L) or any level with ECG changes is a medical emergency. The treatment strategy is three-fold and should be initiated simultaneously.

#### Step 1: Stabilize the Cardiac Membrane (Immediate)

**Calcium Gluconate or Calcium Chloride:** This is the most critical first step. It does not lower serum potassium but protects the heart from arrhythmias.

- **Calcium Gluconate:** 1-2 amps (10-20 mL of 10% solution) IV over 2-5 minutes. Safer for peripheral IVs.
- **Calcium Chloride:** 1 amp (10 mL of 10% solution) IV. Contains 3x more elemental calcium but must be given through a central line to avoid tissue necrosis.

*Onset: 1-3 minutes. Duration: 30-60 minutes.*

#### Step 2: Shift Potassium Intracellularly (Temporary)

These measures buy time while definitive removal is arranged.

- **Insulin and Glucose:** 10 units of regular insulin with 25g of dextrose (1 amp of D50) IV. Onset is 15-30 minutes. Be cautious of hypoglycemia, especially in CKD patients.
- **Beta-Agonists:** High-dose nebulized albuterol (10-20 mg). Additive effect with insulin.
- **Sodium Bicarbonate:** Generally reserved for patients with concurrent severe metabolic acidosis.

#### Step 3: Remove Potassium from the Body (Definitive)

- **Loop Diuretics:** Effective if the patient has residual kidney function and is volume overloaded.
- **Potassium Binders:**
  - **Kayexalate (SPS):** Oldest agent, slow onset. Carries a risk of colonic necrosis, especially with sorbitol.
  - **Patiromer (Veltassa) & SZC (Lokelma):** Newer, safer binders for acute and chronic management. SZC has a faster onset (1 hour).
- **Dialysis:** The most effective and rapid method of potassium removal, especially in patients with kidney failure. However, practical delays in initiation are common.

#### Urinary Obstruction: A Reversible Cause

Always consider urinary obstruction (e.g., from an enlarged prostate) in a patient with AKI and hyperkalemia. A bedside bladder scan can be diagnostic. Placing a Foley catheter can be both diagnostic and therapeutic, often rapidly resolving the hyperkalemia.

## Hypercalcemia: Evaluation and Treatment

### Systematic Evaluation

The first step is to confirm true hypercalcemia by correcting for albumin (Corrected Ca = Measured Ca + 0.8 × \[4.0 - albumin\]). The most crucial subsequent test is a \*\*PTH level\*\*.

- **High/Inappropriately Normal PTH:** Points to primary hyperparathyroidism or Familial Hypocalciuric Hypercalcemia (FHH).
- **Low/Suppressed PTH:** Points to non-PTH-mediated causes, most commonly malignancy (via PTHrP or lytic bone lesions) or vitamin D intoxication. For these non-PTH-mediated causes, the \*\*VITAMINS TRAP\*\* mnemonic is a useful tool.

#### The VITAMINS TRAP Mnemonic for Non-PTH Mediated Hypercalcemia

##### Primary Causes (VITAMINS)

- **V - Vitamins:** Vitamin D or Vitamin A intoxication.
- **I - Immobilization:** Prolonged bed rest increases bone resorption.
- **T - Thyrotoxicosis:** Increased bone turnover.
- **A - Addison's Disease:** Volume depletion and hemoconcentration.
- **M - Milk-Alkali Syndrome:** Excessive intake of calcium carbonate.
- **I - Inflammatory/Infiltrative Disorders:** Granulomatous diseases like sarcoidosis or tuberculosis (due to extrarenal 1α-hydroxylase activity).
- **N - Neoplasms:** PTHrP-secreting tumors, osteolytic metastases (myeloma, breast), or lymphomas producing 1,25-vitamin D.
- **S - Sarcoidosis:** A key example of an inflammatory disorder.

##### Additional Causes (TRAP)

- **T - Thiazides:** Decrease urinary calcium excretion.
- **R - Renal Failure:** Can lead to tertiary hyperparathyroidism.
- **A - Adrenal Insufficiency:** Another way to remember Addison's disease.
- **P - Primary Hyperparathyroidism:** Note: This is a PTH-mediated cause, but included for completeness of the mnemonic; it would be ruled out by a low PTH level.

### Acute Management of Severe Hypercalcemia (Ca \> 14 mg/dL or symptomatic)

#### Treatment Algorithm for Hypercalcemic Crisis

1.  **IV Fluids - First and Foremost:** Aggressive volume expansion with normal saline (e.g., 200-300 mL/hr) is the cornerstone of therapy. It restores GFR and enhances renal calcium excretion.
2.  **Calcitonin:** Provides rapid but transient reduction in calcium (onset 4-6 hours). Useful as a bridge therapy while awaiting the effects of other agents. Tachyphylaxis occurs in 48-72 hours.
3.  **Bisphosphonates:** The mainstay for malignancy-associated hypercalcemia. Zoledronic acid is most potent. Onset is 24-48 hours. Ensure patient is well-hydrated to reduce risk of ATN.
4.  **Loop Diuretics:** Use with extreme caution and ONLY after volume repletion is complete. No longer routinely recommended.
5.  **Denosumab:** An option for bisphosphonate-refractory hypercalcemia.
6.  **Glucocorticoids:** Effective for hypercalcemia due to vitamin D-mediated causes (e.g., granulomatous diseases, lymphomas).
7.  **Dialysis:** Reserved for severe cases with associated renal failure.

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## 📚 Sources — Chapter 12 (Electrolytes)

1.  **Spasovski G, et al.** Hyponatraemia clinical practice guideline. *Nephrol Dial Transplant.* 2014;29 Suppl 2:i1-i39. [PMID: 24569496](https://pubmed.ncbi.nlm.nih.gov/24569496/).
2.  **Hillier TA, et al.** Glucose-correction factor 2.4 (4.0 above 400). *Am J Med.* 1999;106(4):399-403. [PMID: 10225241](https://pubmed.ncbi.nlm.nih.gov/10225241/).
3.  **Baek SH, et al; SALSA.** RIB vs SCI hypertonic saline. *JAMA Intern Med.* 2021;181(1):81-92. [PMID: 33104189](https://pubmed.ncbi.nlm.nih.gov/33104189/).
4.  **Sterns RH, Grieff M, Bernstein PL.** Treatment of hyperkalemia. *Kidney Int.* 2016;89(3):546-554. [PMID: 26880451](https://pubmed.ncbi.nlm.nih.gov/26880451/) .
5.  **Whang R, Whang DD, Ryan MP.** Mg deficiency and refractory K. *Arch Intern Med.* 1992;152(1):40-45. [PMID: 1728927](https://pubmed.ncbi.nlm.nih.gov/1728927/).


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