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Summary Table

Category	Details
Risk Factors	Elderly, hospitalized patients, heart failure, cirrhosis, nephrotic syndrome, thiazide diuretics, SSRI use, marathon runners, post-surgical patients (especially post-TURP), psychogenic polydipsia, adrenal insufficiency, hypothyroidism
Etiology	Serum sodium < 135 mEq/L caused by excess water relative to sodium. The underlying mechanism varies by volume status: hypovolemic (sodium loss exceeding water loss), euvolemic (water retention with near-normal sodium), or hypervolemic (water retention exceeding sodium retention)
Patient Presentation	Mild: nausea, malaise, headache. Moderate: confusion, lethargy, muscle cramps. Severe: seizures, obtundation, coma, respiratory arrest
Classic Physical Exam	Varies by volume status. Hypovolemic: dry mucous membranes, orthostatic hypotension, poor skin turgor. Hypervolemic: peripheral edema, ascites, JVD, pulmonary crackles. Euvolemic: clinically normal volume exam
Key Diagnostic Results	Serum sodium < 135 mEq/L, serum osmolality < 280 mOsm/kg (true hypotonic hyponatremia). Urine osmolality and urine sodium are the pivotal next steps to classify etiology
Management	Hypovolemic: normal saline. Euvolemic (SIADH): fluid restriction, salt tablets, vaptans. Hypervolemic: fluid restriction + loop diuretics. Severe symptomatic: hypertonic saline (3% NaCl). Correction rate must not exceed 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome
Keywords	"Confusion after surgery," "marathon runner with seizure," "patient on thiazides with lethargy," "low serum osmolality," "euvolemic hyponatremia," "beer potomania," "tea and toast diet," "reset osmostat"

1. Pathophysiology

Sodium is the primary determinant of serum osmolality and therefore the principal regulator of water distribution between the intracellular and extracellular compartments. The serum osmolality can be estimated using:

$$Serum\ Osmolality \approx 2[Na^+] + \frac{Glucose}{18} + \frac{BUN}{2.8}$$

When serum sodium falls, the extracellular fluid becomes hypotonic relative to the intracellular compartment. Water moves down its osmotic gradient into cells, causing cellular swelling. In the brain, this swelling is particularly dangerous because the rigid skull limits expansion. Cerebral edema is the direct cause of the neurological symptoms seen in hyponatremia, ranging from headache and confusion to seizures, herniation, and death.

The body defends against hyponatremia primarily through ADH (antidiuretic hormone / vasopressin). Under normal physiology, falling osmolality suppresses ADH release, allowing free water excretion. Hyponatremia develops when this defense fails, either because ADH is inappropriately elevated (SIADH), the kidneys cannot excrete free water (renal failure, very low solute intake), or the stimulus for ADH is non-osmotic (hypovolemia, pain, nausea, medications).

A critical concept the test-writer expects you to understand: the rate of onset determines the severity of symptoms, not just the absolute sodium level. Acute hyponatremia (developing in < 48 hours) is more dangerous because brain cells have not had time to adapt by extruding intracellular osmoles. Chronic hyponatremia (> 48 hours) may be surprisingly well-tolerated even at very low sodium levels because the brain has adapted. This adaptation, however, creates a new danger during correction: if you raise sodium too quickly in a chronically adapted brain, you cause osmotic demyelination syndrome (ODS), formerly called central pontine myelinolysis.

Before classifying the cause, you must first rule out pseudohyponatremia and hypertonic hyponatremia. Pseudohyponatremia occurs with extreme hyperlipidemia or hyperproteinemia, where the lab artifact falsely lowers the measured sodium (serum osmolality will be normal). Hypertonic hyponatremia occurs when an osmotically active solute like glucose draws water into the extracellular space, diluting sodium. For every 100 mg/dL increase in glucose above normal, sodium falls by approximately 1.6 to 2.4 mEq/L. In both cases, the serum osmolality is NOT low, so they are not true hypotonic hyponatremia.

2. Classification and Clinical Manifestation

The classification of hyponatremia is built around two axes: volume status and urine studies. This is the framework the test-writer uses to build answer choices.

Classification by Volume Status

Volume Status	Mechanism	Classic Causes	Urine Na	Urine Osmolality
Hypovolemic (total body water low, sodium even lower)	Sodium loss > water loss triggers non-osmotic ADH release	Renal loss (thiazides, adrenal insufficiency, cerebral salt wasting): Urine Na > 20. Extrarenal loss (vomiting, diarrhea, burns, third-spacing): Urine Na < 20	Variable (see causes)	> 100 mOsm/kg (concentrated, kidneys holding water)
Euvolemic (total body water mildly increased, sodium normal, no edema)	Water retention without significant sodium retention	SIADH (most tested), hypothyroidism, adrenal insufficiency, psychogenic polydipsia, beer potomania, reset osmostat	> 40 (in SIADH) or < 20 (polydipsia, beer potomania)	> 100 in SIADH; < 100 in polydipsia/beer potomania
Hypervolemic (total body water high, sodium also high but water even higher)	Effective circulating volume is low, triggering ADH and sodium/water retention, but water retention predominates	Heart failure, cirrhosis, nephrotic syndrome, advanced renal failure	< 20 (HF, cirrhosis, nephrotic). > 20 (renal failure)	> 100 mOsm/kg

Classification by Severity and Symptoms

Severity	Serum Sodium	Symptoms
Mild	130 to 134 mEq/L	Often asymptomatic, subtle cognitive slowing, increased fall risk
Moderate	125 to 129 mEq/L	Nausea, headache, confusion, gait instability
Severe	< 125 mEq/L	Vomiting, seizures, obtundation, respiratory arrest, coma

Classification by Chronicity

Timeline	Definition	Clinical Significance
Acute	Develops in < 48 hours	Brain has not adapted. Higher risk of cerebral edema and herniation. More aggressive correction is safer.
Chronic	Develops over > 48 hours (or unknown duration)	Brain has adapted by losing intracellular osmoles. Lower risk of acute herniation, but higher risk of ODS with rapid correction.

3. Diagnostic Workup

Test	Purpose	Expected Finding
Serum sodium	Confirm hyponatremia	< 135 mEq/L
Serum osmolality	First branch point: rule out pseudohyponatremia and hypertonic causes	< 280 mOsm/kg confirms true hypotonic hyponatremia
Urine osmolality	Assess whether ADH is active	> 100 mOsm/kg = ADH-mediated (kidneys concentrating). < 100 mOsm/kg = non-ADH-mediated (primary polydipsia, beer potomania, low solute)
Urine sodium	Differentiate renal vs. extrarenal sodium loss (hypovolemic) or confirm SIADH (euvolemic)	> 20 to 40 mEq/L = renal losses or SIADH. < 20 mEq/L = extrarenal losses or hypervolemic states (HF, cirrhosis)
Volume status assessment	Physical exam is the second branch point	Determines hypovolemic vs. euvolemic vs. hypervolemic
TSH, morning cortisol	Rule out hypothyroidism and adrenal insufficiency before diagnosing SIADH	Must be normal to diagnose SIADH (it is a diagnosis of exclusion)
Serum uric acid	Supportive clue for SIADH	Low uric acid (< 4 mg/dL) supports SIADH due to increased renal clearance
Fractional excretion of uric acid	Helps distinguish SIADH from cerebral salt wasting	Elevated in both, but normalizes after correction in CSW while remaining elevated in SIADH

The diagnostic algorithm is the most tested aspect of hyponatremia. The test-writer will give you a sodium value and expect you to follow a stepwise approach:

Step 1: Confirm it is real. Check serum osmolality. If osmolality is normal (280 to 295), consider pseudohyponatremia. If osmolality is elevated (> 295), think about hyperglycemia or mannitol infusion. Only proceed if osmolality is low (< 280), confirming true hypotonic hyponatremia.

Step 2: Assess volume status clinically. This is where the vignette gives you physical exam clues. Edema, ascites, and JVD point to hypervolemic. Dry mucosa, tachycardia, and orthostatic hypotension point to hypovolemic. A clinically normal exam points to euvolemic.

Step 3: Check urine osmolality. If urine osmolality is < 100 mOsm/kg, ADH is appropriately suppressed, and the problem is excessive free water intake (psychogenic polydipsia) or very low solute intake (beer potomania, tea-and-toast diet). If urine osmolality is > 100, ADH is active, and you move to Step 4.

Step 4: Check urine sodium. This separates causes within each volume category. In hypovolemic patients, urine Na < 20 points to extrarenal losses (GI losses, skin losses), while urine Na > 20 points to renal losses (thiazides, adrenal insufficiency, cerebral salt wasting). In euvolemic patients, urine Na > 40 with urine osmolality > 100 strongly supports SIADH.

SIADH deserves special emphasis because it is the most commonly tested cause of euvolemic hyponatremia. The diagnosis requires: hyponatremia with low serum osmolality, urine osmolality > 100 mOsm/kg, urine sodium > 40 mEq/L, clinical euvolemia, normal thyroid and adrenal function, no diuretic use. Common causes include CNS disorders (stroke, hemorrhage, trauma), pulmonary disease (pneumonia, especially Legionella; small cell lung cancer), medications (SSRIs, carbamazepine, cyclophosphamide, vincristine, NSAIDs), and pain/nausea as non-osmotic ADH stimuli.

4. Management and Treatment

Clinical Scenario	Treatment	Key Details
Severe symptomatic (seizures, coma, acute onset)	3% hypertonic saline	Bolus 100 mL IV over 10 minutes, may repeat up to 3 times if symptoms persist. Target: raise sodium by 4 to 6 mEq/L in the first few hours to stop symptoms. Do NOT exceed 8 mEq/L in the first 24 hours in chronic cases.
Hypovolemic	0.9% normal saline	Volume resuscitation restores effective circulating volume, suppresses ADH, and allows free water excretion. Monitor sodium closely as it may rise rapidly once ADH is suppressed.
Euvolemic (SIADH), mild to moderate	Fluid restriction (< 800 to 1000 mL/day)	First-line for chronic SIADH. Add salt tablets (NaCl 1 to 3 g TID) if fluid restriction alone is insufficient.
Euvolemic (SIADH), refractory	Tolvaptan (vasopressin V2 receptor antagonist)	15 mg PO daily, titrate to 60 mg daily. Causes free water excretion (aquaresis). Must be initiated in the hospital with close sodium monitoring. Contraindicated in hypovolemia and liver disease.
Hypervolemic (HF, cirrhosis)	Fluid restriction + loop diuretics	Treat the underlying condition. Furosemide helps excrete free water. Vaptans may be used in refractory cases.
Overcorrection rescue	Desmopressin (DDAVP) + D5W	If sodium rises too fast (> 8 mEq/L in 24 hours for chronic cases), give DDAVP 2 mcg IV every 8 hours + D5W infusion to re-lower sodium back into the safe correction range.

Acute stabilization of severe hyponatremia takes priority over diagnosing the cause. If a patient presents with seizures or altered consciousness, the immediate next step is 3% hypertonic saline, regardless of the underlying etiology. You do not need a urine sodium or TSH before treating a seizing patient.

For chronic hyponatremia, the critical management principle is the rate of correction. The widely accepted safe limit is no more than 8 mEq/L in any 24-hour period (some guidelines use 10 to 12 mEq/L, but exam questions almost always test the more conservative 8 mEq/L threshold). Exceeding this rate in a chronically adapted brain causes osmotic demyelination syndrome, which presents days after correction with dysarthria, dysphagia, quadriparesis, "locked-in syndrome," and characteristic pontine lesions on MRI.

There are populations at higher risk for ODS who warrant even more cautious correction (target 4 to 6 mEq/L per 24 hours): patients with chronic alcoholism, malnutrition, hypokalemia, liver disease, and those with sodium < 105 mEq/L.

An important management pearl: when treating hypovolemic hyponatremia with normal saline, the sodium may rise dangerously fast once volume is restored. This happens because ADH was being driven by hypovolemia; once volume is repleted, ADH shuts off abruptly and the kidneys dump large volumes of dilute urine. This is called autocorrection, and it is a common clinical scenario where overcorrection occurs. Preemptive DDAVP can be administered as a safety clamp in high-risk patients.

For hypokalemia coexisting with hyponatremia: potassium repletion raises serum sodium because potassium is an intracellular cation that exchanges with sodium. You must account for potassium given when calculating total correction rate.

5. Differential Diagnosis and Distractors

Diagnosis	Why It Looks Similar	Key Discriminator
Cerebral salt wasting (CSW) vs. SIADH	Both present with hyponatremia after CNS injury (SAH, neurosurgery). Both have elevated urine sodium and urine osmolality.	CSW is hypovolemic (high urine output, negative fluid balance, orthostatic changes). SIADH is euvolemic. CSW is treated with saline; SIADH with fluid restriction. Giving saline to SIADH will worsen hyponatremia.
Psychogenic polydipsia vs. SIADH	Both are euvolemic hyponatremia.	Polydipsia has urine osmolality < 100 mOsm/kg (dilute urine, ADH is suppressed). SIADH has urine osmolality > 100. Look for psychiatric history, "drinking large amounts of water."
Beer potomania vs. SIADH	Both euvolemic, both hyponatremic.	Beer potomania has low urine osmolality (< 100) due to very low solute intake, not ADH excess. History of heavy beer consumption with poor dietary intake is the giveaway.
Adrenal insufficiency vs. SIADH	Both can be euvolemic with high urine sodium. Cortisol deficiency causes non-osmotic ADH release, mimicking SIADH labs perfectly.	You must check morning cortisol or ACTH stimulation test before diagnosing SIADH. Adrenal insufficiency will also show hyperkalemia and hypotension (SIADH does not cause hyperkalemia).
Hypothyroidism vs. SIADH	Severe hypothyroidism can cause euvolemic hyponatremia through decreased free water clearance.	Check TSH. Hypothyroidism-induced hyponatremia is rare and occurs only in severe cases (myxedema). Required as a rule-out before diagnosing SIADH.
Hyperglycemia-induced hyponatremia vs. true hyponatremia	Patient appears hyponatremic on labs.	Serum osmolality is elevated or normal, not low. Correct sodium for glucose: for every 100 mg/dL glucose above 100, add 1.6 to 2.4 mEq/L to the measured sodium. If corrected sodium is normal, this is not true hyponatremia.
Pseudohyponatremia	Low sodium on basic metabolic panel.	Serum osmolality is normal. Caused by severe hypertriglyceridemia or paraproteinemia (multiple myeloma). A lab artifact, not a clinical problem.

6. Traps and High-Yield Pearls

The single most common way students lose points on hyponatremia questions is failing to follow the diagnostic algorithm in order. The test-writer builds vignettes that punish you for jumping to a diagnosis without first checking serum osmolality. A patient with hyperglycemia and low sodium does NOT have true hyponatremia, and treating it as such is a classic wrong answer. Always confirm hypotonic hyponatremia before classifying by volume status.

The second major trap is confusing SIADH with cerebral salt wasting after a neurosurgical or SAH scenario. The vignette will include subtle volume status clues (high urine output and orthostatic vital signs for CSW vs. normal volume exam for SIADH). Choosing the wrong one leads you to the opposite treatment: saline for CSW, fluid restriction for SIADH.

The third trap involves overcorrection. The test-writer loves to present a patient whose sodium corrects too quickly after normal saline infusion for hypovolemic hyponatremia. The expected answer is DDAVP plus D5W to deliberately re-lower the sodium. Students who do not know about the overcorrection rescue protocol will choose to simply "monitor," which is incorrect.

A frequently missed pearl: thiazide diuretics cause hyponatremia, but loop diuretics generally do not (or do so far less commonly). Thiazides impair the diluting segment in the distal tubule without interfering with the medullary concentrating gradient, so ADH can still concentrate urine. Loop diuretics wash out the medullary gradient, impairing both concentration and dilution, which paradoxically protects against severe hyponatremia.

Finally, remember that potassium correction counts toward sodium correction. If you give KCl to a hyponatremic, hypokalemic patient, the potassium enters cells and sodium exits, raising the serum sodium. If a patient receives both hypertonic saline and aggressive potassium repletion simultaneously, the combined effect can push correction beyond the safe threshold. The test-writer expects you to account for this.

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