HYPONATRAEMIA

Hyponatraemia < 120mmol/L

Metabolic encephalopathy
(water into brain cells + cerebral edema)

- confusion
- seizure
- coma

Rapid correction-- central pontine myelinosis
Do not increase sodium concentration by > 0.5mmol/L
cautious admin of isotonic 0.9% sodium chloride + use of loop diuretics (frusemide)

Hypertonic saline is dangerous.

Sodium deficit

140-measured Na+ x 0.2 x height(kg)

why 0.2? 20% ECF- sodium is the main cation

If ECF normal or increased-- IV water admin and sodium decreased

Will correct spontaneously if water intake is decreased
ALthough less common in surgical patient  SIADH promotes tubular reabsorption of water
Independently of sodium concentration---- inappropriately concentrated urine

(>100mOsm/L) in face of hypotonic plasma (>290mOsm/L)

Therefore urine osmolality helps to distinguish SIADH from excess IV admin. Spot measurement of urine sodium will be high

In patients with decreased ECF volume.
Hyponatraemia combined water and sodium deficiency

Diarrhoea
Diuresis
Adrenal insufficiency

Tx: 0.9% NaCl

HYEPRNATRAEMIA

Sodium level> 145mmol/L

Causes: water loss or sodium gain

Hypovolaemia
Decreased intake
Vomiting
Diarrhoea
Diuresis
Burns
Sweating
Irreversible loss from RT
Diabetes insipidus (head injury)

Hypertonic IV fluids leading hypervolaemia.

Goals: recognition of symptoms when present, identify underlying cause, correct volume disturbances, correction of hypertonicity.

Acute symptomatic hypernatraemia: defined as hypernatraemia occurring in a documented period of less than 24hours should be corrected rapidly.

Chronic hypernatraemia (>48hours) however, should be corrected more slowly due to the risks of brain edema during treatment. The brain adjusts to and mitigates chronic hypernatraemia but increasing the intracellular content of organic osmolytes.

If extracellular tonicity is rapidly decreased, water will move into the brain cells, producing cerebral edema, which may lead to herniation, permanent neurologic deficits and myelinosis.




Isotonic crystalloid to restore IV fluid rapidly
and administer water gradually to correct relative water deficit
(orally/ via nasogastric tube) or IV as 5% dextrose
or
1/4 to 1/2 NS gradually correct hypernatraemia

Brain cells adapt to high Na in ECF
Once this has occurred, rapid correction, rapid correction of severe hypernatraemia can lead to rapid rise in intracellular volume cerebral edema, seizure and permanent neurological injury.
TO decrease risk of cerebral edema, free water deficits should be replaced slowly with sodium correction of rate of less than 0;5mmol/hr or

1/4- 1/2 normal saline----- gradual correction of hypernatraemia