Hyponatremia

HYPONATRAEMIA

Definition  is

an electrolyte disturbance (disturbance of the salts in the blood) in which the sodium concentration in the plasma is too low (below 135 mmol/L).

 is

a metabolic condition in which there is not enough sodium in the body fluids outside the cells.

CAUSES OF HYPONATRAEMIA 

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Hypovolaemic (sodium deficit with a relatively smaller water deficit) Renal Na losses, Diuretic therapy (especially thiazides), Adrenocortical failure &Gastrointestinal Na losses, i.e.: Vomiting, Diarrhea. Euvolaemic (water retention alone) Primary polydipsia, Excessive electrolyte-free water infusion, SIADH, Hypothyroidism. Hypervolaemic (sodium retention with relatively greater water retention): Congestive cardiac failure, Cirrhosis Nephrotic syndrome, Chronic renal failure (during free water intake).

CAUSES OF SODIUM AND WATER DEPLETION     

Inadequate intake Environmental deprivation, inadequate therapeutic replacement Gastrointestinal sodium Loss Vomiting, diarrhea, nasogastric suction, external fistula Skin sodium loss Excessive sweating, burns Renal sodium loss Diuretic therapy, mineralocorticoid deficiency, tubulointerstitial disease (sometimes) Internal sequestration*Bowel obstruction, peritonitis, pancreatitis, crush injury

Hypovolemic hyponatremia    

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Hyponatraemia in association with a sodium deficit ('depletional hyponatraemia') can arise as a result of: renal salt losses during diuretic therapy or aldosterone deficiency such as in Addison's disease. gastrointestinal losses of sodium, especially following vomiting. skin losses in burns. Patients in this category have clinical features of hypovolaemia (thirst, dizziness and weakness, tachycardia, dry mouth, low urine output, hypotension). Laboratory findings supportive of this assessment include low urinary sodium concentration and elevated plasma renin activity.

euvolaemic Hyponatraemia  Patients

in the second group ('dilutional hyponatremia') have no major disturbance of body sodium content, and are clinically euvolaemic.  Excess body water may be the result of : Abnormally high intake either orally (primary polydipsia) or medically infused fluids ,(SIADH).

hypervolaemic Hyponatraemia  The

third pattern of hyponatraemia is where excess water retention is associated with sodium retention and volume expansion, as in heart failure and other edematous disorders. in congestive heart failure, total body sodium is increased, yet effective circulating volume is sensed as inadequate by baroreceptors. Increased ADH and aldosterone results, with retention of water and sodium.

Symptoms & signs

Symptoms 

Abnormal mental status    

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Confusion Decreased consciousness Hallucinations Possible coma

Convulsions Fatigue Headache Irritability Loss of appetite Muscle spasms or cramps Muscle weakness Nausea Restlessness Vomiting Anorexia nervosa

Signs and tests  The

following laboratory tests can confirm hyponatremia:  Serum osmolality  Serum sodium  Urine osmolality  Urine sodium  A complete physical examination will also be done to find the cause of this condition.

Management

Management of sodium and water depletion has two main components: treatment of the cause where possible, to stop ongoing salt and water losses  replacement of salt and water deficits, and provision of ongoing maintenance requirements, usually through the intravenous route when depletion is severe. 

Hypovolemic Hypotonic Hyponatremia

 Treatment

consists of replacement of lost volume with isotonic or half-normal (0.45%) saline or lactated Ringer's infusion. The rate of correction must be adjusted to prevent permanent cerebral damage

Euvolemic Hypotonic Hyponatremia 

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Symptomatic hyponatremia is usually seen in patients with serum sodium levels less than 120 mEq/L. If there are central nervous system symptoms, hyponatremia should be rapidly treated at any level of serum sodium concentration. A reasonable approach is to increase the serum sodium concentration by no more than 1–2 mEq/L/h and not more than 25–30 mEq/L in the first 2 days; the rate should be reduced to 0.5–1 mEq/L/h as soon as neurologic symptoms improve. The initial goal is to achieve a serum sodium concentration of 125–130 mEq/L, guarding against overcorrection. Hypertonic (eg, 3%) saline with furosemide is indicated for symptomatic hyponatremic patients.

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Asymptomatic hyponatremia In asymptomatic hyponatremia, the correction rate of hyponatremia need be no more than 0.5 mEq/L/h. Water restriction Water intake should be restricted to 0.5–1 L/d. A gradual increase of serum sodium will occur over days. 0.9% saline In asymptomatic patients whose serum sodium is less than 120 mEq/L, 0.9% saline with furosemide may be used. Demeclocycline Demeclocycline (300–600 mg twice daily) is useful for patients who cannot adhere to water restriction or need additional therapy; it inhibits the effect of ADH on the distal tubule. Fludrocortisone Hyponatremia occurring as part of the cerebral salt-wasting syndrome can be treated with fludrocortisone. Selective renal vasopressin V2 antagonists

Hypervolemic Hypotonic Hyponatremia  

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Water restriction Diuretics and V2 Antagonists To hasten excretion of water and salt, use of diuretics may be indicated. Hypertonic (3%) Saline In patients with severe hyponatremia (serum sodium < 110 mEq/L) and central nervous system symptoms, judicious administration of small amounts (100–200 mL) of 3% saline with diuretics may be necessary. Emergency dialysis should also be considered.

Complications  Brain

herniation  Possible coma  Death

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