Hyponatremia Flashcards

1
Q

Hyponatremia

A

Definition

mild: <135mEq/L(mmol/L) in blood

moderate 120-130mEq/L

severe <120mEq/L

acute (<48hrs) or chronic

Osmolarity vs osmolality

  • Osmolality is no. solute particles per 1 kg solvent; osmolarity is no. solute particles per 1 L solvent
  • For dilute solutions, the difference between osmolarity and osmolality is insignificant. Measurements of osmolarity are temperature dependent because the volume of solvent varies with temperature (i.e., the volume is larger at higher temperatures). In contrast, osmolality, which is based on the mass of the solvent, is temperature independent. For this reason, osmolality is the preferred term for biologic systems.
  • Serum osmolality = 2 x (Na) + (Glucose) + (urea)
  • urine osmolality = 2 x (urine Na) + Urine K + (urinary urea nitrogen/2.8) + (urine glucose/18)

Presentation

usu asymptomatic unless <120mEq/L. In which case presents with:

  • headache, n/v, lethargy, confusion, irritability, muscle weakness/spasm/cramp, seizure, coma

Ask further qns to investigate possible cause:

  • Hx CCF, liver or renal disease, malignancy, hypothyroid, Addison’s disease, GI losses, psych illness, recent drug ingestion, surgery, recent IV fluids.

Causes

Meds, diarrhoea, HF, liver cirrhosis, renal disease, adrenal insufficiency, SIADH, psychogenic polydipsia/water intoxication

Diagnostic algorithm

Hypovolemic

High urinary sodium = renal losses:

  1. Addisons (adrenal insuff). Low serum osmolality.
  2. Renal failure (leading to polyuria. Na+ losing nephropathy). Low serum osmolality.
  3. Diuretics (esp thiazides), and various other meds inc carbamazepine, chlorpromazine, ADH analogs, indapamide, SSRI, amiodarone, ecstasy
  4. Osmotic diuresis (mannitol, glucosuria, urea). High serum osmolality.

Normal urinary sodium (<20mmol/L) = Extra-renal losses:

  1. skin: sweat, trauma, burns, heat
  2. GIT: D+V, fistula, SBO, villous adenoma

Hypervolemic

  1. CCF
  2. Cirrhosis
  3. Renal failure
  4. Nephrotic syndrome

Euvolemic

High urine osmolality (>500) = SIADH

  • high urinary Na >20
  • low serum osm <260

Normal urine osmolality = H2O (free water) overload

  1. Copious IVFT (esp 5% dextrose)
  2. hypothyroidism
  3. glucocorticoid insufficiency
  4. psychogenic polydypsia (low serum osm; low urine Na)

Management

Urgent

  • Presence of symptoms, severe hyponatremia (<125mmol), hypotension
  • avoid rapid correction to reduce risk of central pontine myelinolysis (demyelination of pons –> irreversible). Avoid normo or hypernatremia in first 24hrs
  • When shock present –> IV isotonic saline. Correct 1-2mmol/L per hr.
  • Chronic hyponatremia (>48hrs) patients should be fluid restricted and can be corrected at a rate of 0.5mmol/L per hr, max 8-10mmol/L per day.

Less urgent

  • asymptomatic
  • remove the cause
  • 1-1.5L FR
  • high Na diet and oral NaCl tablets

Fluid overload

  • loop diuretics

Persistent hypoNa

  • Demeclocycline (reduces ADH, leads to nephrogenic diabetes insipidus (diuresis, inability to concentrate urine). 600-1200mg/day. Caution in liver or renal disease)
  • tolvaptan
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2
Q

Medications that cause hyponatremia

A

Thiazide diuretics

  • hyponatremia usu begins within 2/52 after onset of therapy, or develops during concurrent illness. Virtually all cases of severe diuretic-induced hyponatremia have been due to a thiazide-type diuretic. Patients present similar to SIADH (euvolemic, normal renal function). Discontinuing the drug leads to improved serum Na.
  • Thiazides act in the cortex of the DCT by inhibiting Na/Cl cotransporter. This leads to decreased Na+ reabsorption, thereby decreasing the action of Na/K pump. Thiazides also impair free water excretion, by increasing water permeability and water reabsorption in the inner medullary collecting duct, an effect that is independent of ADH. In addition, pts develop polydypsia. The combined effects of natriuresis (can be of higher ion concentration than in the plasma) and water retention, precipitates hyponatremia.

A loop diuretic is much less likely to induce this problem unless the diuretic has induced volume depletion. Loop diuretics inhibit NaCl reabsorption in the thick ascending limb of the loop of Henle, which impairs the accumulation of NaCl in the medulla, which means water isn’t reabsorbed in the medullary collecting tubule, resulting in the excretion of a dilute urine.

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3
Q

SIADH

A

Causes

Meds: diuretics (thiazides), amiodarone, carbamazepine, chlorpromazine, SSRI, theophylline, indapamide. Ecstasy

cerebral disorders/any insult (tumor, meningitis)

chest (pneumonia esp legionnaires’, empyema, bronchogenic carcinoma esp SCC)

ectopic ADH (esp SCC), rare (MS, Guillain Barre, intermittent porphyria)

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