Electrolyte abnormalities

Hyponatremia

SIADH (Syndrome of Inappropriate Antidiuretic Hormone): Euvolemic hyponatremia, associated with small cell lung cancer, CNS disorders, and certain medications
Heart failure: Hypervolemic hyponatremia due to fluid retention and dilution of sodium
Cirrhosis: Hypervolemic hyponatremia, often associated with ascites and peripheral edema
Diuretics: Particularly thiazides, can cause hypovolemic hyponatremia due to excessive sodium loss
Primary polydipsia: Excessive water intake leading to dilutional hyponatremia
Adrenal insufficiency: Hypovolemic hyponatremia due to aldosterone deficiency leading to sodium loss

Hypernatremia

Dehydration: Most common cause, due to inadequate water intake or excessive water loss
Diabetes insipidus: Central or nephrogenic, leads to excessive water loss and hypernatremia
Osmotic diuresis: Often due to uncontrolled diabetes mellitus, leading to loss of water and sodium
Hyperaldosteronism: Excessive aldosterone leads to sodium retention and water loss, contributing to hypernatremia
Excessive sodium intake: Rare, but can occur with excessive ingestion of salt or hypertonic saline administration

Hypokalemia

Diuretics: Particularly loop and thiazide diuretics, causing increased potassium excretion
Gastrointestinal losses: Vomiting, diarrhea, and nasogastric suctioning can lead to significant potassium loss
Hyperaldosteronism: Excess aldosterone increases renal potassium excretion
Insulin administration: Drives potassium into cells, reducing serum potassium levels
Alkalosis: Shifts potassium into cells in exchange for hydrogen ions, leading to hypokalemia
Magnesium deficiency: Impairs potassium reabsorption in the kidneys, leading to hypokalemia

Hyperkalemia

Renal failure: Decreased potassium excretion is the most common cause of hyperkalemia
Medications: ACE inhibitors, ARBs, potassium-sparing diuretics, and NSAIDs can reduce potassium excretion
Acidosis: Causes potassium to shift out of cells into the bloodstream
Adrenal insufficiency: Decreased aldosterone levels lead to reduced potassium excretion
Hemolysis: Release of intracellular potassium into the bloodstream due to red blood cell breakdown
Pseudohyperkalemia: Due to release of potassium during blood sample collection, not reflective of true serum levels

Hypocalcemia

Hypoparathyroidism: Most common cause, leading to decreased calcium reabsorption from the kidneys
Vitamin D deficiency: Reduces calcium absorption from the gut, leading to hypocalcemia
Chronic kidney disease: Reduced conversion of vitamin D to its active form, leading to decreased calcium absorption
Pancreatitis: Saponification of calcium in the fat necrosis process
Hypomagnesemia: Leads to impaired parathyroid hormone secretion, contributing to hypocalcemia
Rhabdomyolysis: Acute onset hypocalcemia due to precipitation of calcium in damaged muscle tissues
Massive blood transfusion: Citrate in transfused blood binds to calcium, leading to transient hypocalcemia

Hypercalcemia

Primary hyperparathyroidism: Most common cause, leading to increased calcium reabsorption in the kidneys
Malignancy: Often due to parathyroid hormone-related protein (PTHrP) secretion by tumors, or osteolytic metastases
Vitamin D toxicity: Increased intestinal calcium absorption leading to hypercalcemia
Thiazide diuretics: Decrease renal calcium excretion
Granulomatous diseases (e.g., sarcoidosis): Increased conversion of vitamin D to its active form by macrophages, leading to increased calcium absorption
Immobilization: Increased bone resorption due to lack of weight-bearing activity, leading to hypercalcemia

Symptoms and Presentation

Weakness and fatigue: Common in both hypo- and hyperkalemia, and hypercalcemia
Muscle cramps or spasms: Seen in hypocalcemia and hypomagnesemia, as well as severe hypokalemia
Confusion or altered mental state: Can be a sign of severe hypercalcemia or hyponatremia
Polyuria and polydipsia: Common in hypercalcemia and hypernatremia due to osmotic diuresis
Palpitations or arrhythmias: Seen in both hyperkalemia and hypokalemia, and sometimes in severe hypocalcemia
Tingling or numbness: Often reported in hypocalcemia due to neuromuscular irritability
Nausea and vomiting: Non-specific, but can be associated with hypercalcemia and hyponatremia

Background

Past medical history: Renal disease, heart disease, endocrine disorders such as hyperparathyroidism, or a history of malignancy
Medication history: Use of diuretics, ACE inhibitors, corticosteroids, or supplements (e.g., calcium, vitamin D)
Dietary history: Intake of potassium-rich or low-potassium foods, calcium, and sodium intake
Recent surgeries or procedures: Especially those involving the parathyroid glands, thyroid, or significant blood transfusions
Family history: Particularly of endocrine disorders, such as familial hyperparathyroidism or renal tubular acidosis
Social history: Consider alcohol use, dehydration risks, and accessibility to healthcare

Laboratory Tests

Serum electrolytes: Sodium, potassium, calcium, magnesium, and phosphate levels
Renal function tests: Urea, creatinine, and eGFR to assess renal contribution to electrolyte imbalance
Arterial blood gas (ABG): To assess for acidosis or alkalosis, which may be related to electrolyte disturbances
Hormone levels: PTH (for calcium abnormalities), aldosterone, and renin (for potassium abnormalities)
ECG: To assess for cardiac arrhythmias associated with electrolyte imbalances, particularly potassium and calcium disorders
Urine electrolytes: To assess renal handling of sodium, potassium, and calcium, particularly in cases of diuretic use or suspected renal tubular disorder
Vitamin D levels: Particularly in cases of hypocalcemia or hypercalcemia
Toxicology screen: If substance use or medication toxicity is suspected

Endocrine & metabolic