HYPONATRAEMIA

Definition

 isan electrolyte disturbance

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

 isa metabolic condition in which there is

not enough sodium in the body fluids
outside the cells.
CAUSES OF HYPONATRAEMIA

 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
 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
 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

 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.
 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

 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

 Brainherniation
 Possible coma
 Death
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