HYPERNATRAEMIA

This infant is suffering from nephrogenic diabetes insipidus caused due to a defect in the interaction of ADH with its receptor.

Lab findings in this condition includes hypernatremia, low urine sodium, low urine osmolality, and elevated plasma osmolality.

Treatment of this condition consists of increased fluid intake and sodium restriction.

Due to defect in the interaction of ADH with its receptor patients does not respond to DDAVP.

Ref: Essential Paediatrics by OP Ghai, 6th Edition, Page 466

Ans. is ‘b’ i.e., Fludrocortisone

Fludrocortisone has maximum mineralocorticoid activity, so it will cause maximum hypernatremia. Hypernatremia is proportional to the mineralocorticoid efficacy of steroids.

Ans. is `c’ i.e., Nil by mouth

T/T of Hypernatremia :‑

• As hypernatremia develops, water moves out from I.C.F. to E.C.F. to maintain equal osmolality inside and outside the cell. So the intracellular fluid decreases.
• To compensate for this the brain cells generates idiogenic osmoles to increase the intracellular osmolality and prevent the loss of brain water. This mechanism is not instantaneous and is most prominent when hypernatremia has developed gradually.
• If the hypernatremia is corrected rapidly by administration of fluids, the E.C.F. osmolality lowers rapidly, and
• now the I. C.F becomes hyperosmotic in comparison to the E.C.F. So, now there is movement of water from serum
• into the brain cells to equalize the osmolality in the two compartment. This results in brain swelling and most
• commonly it manifests as seizures in infants. (This is clinically similar to hyponatremia)
• Because of the dangers of overtly rapid correction, hypernatremia should not be corrected rapidly.
• The goal is to decrease the serum sodium by less than 12-10 mEq/L even, 24 hr, at a rate of 0.5-10 mEq/h.
• In patients with chronic hypernatremia (hypernatremia that has been present for longer than 48 hours).
• The treatment regimen is
• 5 percent dextrose in water, intravenously
• At a rate of (1.35 mL/hour x patient’s weight in kg), or
• About 70 mL per hour in a 50 kg patient and 100 mL per hour in a 70 kg patient.
• The goal of this regimen is to lower the serum sodium by a maximum of 10 meq/L in a 24-hour period (0.4 meq/ L/hour).
• In patients with known acute hypernatremia (hypernatremia that has been present for 48 hours or less).
• The treatment regimen is (see ‘Initial fluid repletion regimen’ above) :-
• 5 percent dextrose in water, intravenously, at a rate of 3 to 6 mL/kg per hour
• The serum sodium and blood glucose should be monitored every one to two hours until the serum sodium is lowered below 145 meq/L.
• Once the serum sodium concentration has reached 145 meq/L, the rate of infusion is reduced to 1 mL/kg/hour and continued until normonatremia (140 meq/L) is restored.
• The goal of this regimen is to lower the serum sodium by 1 to 2 meq/L per hour and to restore normonatremia in less than 24 hours.
• Patients with diabetes insipidus will also require desmopressin therapy, which is discussed elsewhere.
• Hyperglycemia may develop with rapid infusions of 5 percent dextrose; to avoid increased water losses from glycosuria, a slower rate of infusion or a change to 2.5 percent dextrose in water may be required after several hours.
• Risk of correctionof hypernatremia.
• The treatment goal for chronic hypernatremia is designed to lower the serum sodium by 10 meq/L in 24 hours (12 meq/L in 24 hours is considered the maximum safe limit, 10 meq/L in 24 hours is chosen to increase to safety

Ans. is `c’ i.e., Renal losses

Major causes of hypernatremia

Unreplaced water loss (which requires an impairment in either thirst or access to water)

• Insensible and sweat losses
• Gastrointestinal losses
• Central or nephrogenic diabetes insipidus o Osmotic diuresis
• Glucose in uncontrolled diabetes mellitus
• Urea in high-protein tube feedings
• Mannitol
• Hypothalamic lesions impairing thirst or osmoreceptor function
• Primary hypodipsia
• Reset osmostat in mineralocorticoid excess

Water loss into cells

• Severe exercise or seizures

Sodioutn overload

• Intake or administration of hypertonic sodium solutions

Ans. is ‘c’ i.e., Periodic paralysis

• Periodic paralysis, is seen in hyponatermia

Clinical features of Hypernatremia :‑

• Most patients with hypernatremia are dehydrated and have the typical signs and symptoms of dehydration.
• Hypernatremia even without dehydration causes central nervous system symptoms that tend to parallel the degree of sodium elevation and the acuity of the increase.
• Patients are irritable, restless weak and lethargic
• Some have high pitched cry and hyperpnea.
• Alert patient are very thirsty.
• Hypernatremia causes fever although many patients have underlying process that contributes to the fever
• Except for dehydration, there is no clear direct effect of hypernatremia on other organs or tissues except the brain.

Complication of hypernatremia :‑

• Brain hemorrhage is the most devastating consequence of hypernatremia. As the extracellular osmolarity increases water moves out of brain cells, resulting in decrease in brain volume. This can result in tearing of intra cerebral veins and bridging vessels as the brain moves away from the skull and the meninges. Patient may have subarachnoid, subdural and parenchymal hemorrhage.
• Seizure and coma are possible sequale of the hemorrhage even though seizures are more common during t/t.
• Thrombotic complications are common in severe hypernatremic dehydration and include stroke, dural sinus thrombosis, peripheral thrombosis and renal vein thrombosis.
• The intracranial tension can be increased due to hemorrhage

Ans. is ‘b’ i.e., Decreased insensible losses

Major causes of hypernatremia

• Unreplaced water loss (which requires an impairment in either thirst or access to water)
• Insensible and sweat losses
• Gastrointestinal losses
• Central or nephrogenic diabetes insipidus
• Osmotic diuresis
• Glucose in uncontrolled diabetes mellitus
• Urea in high-protein tube feedings
• Mannitol
• Hypothalamic lesions impairing thirst or osmoreceptor function
• Primary hypodipsia
• Reset osmostat in mineralocorticoid excess

Water loss into cells

• Severe exercise or seizures

Sodioum overload

• Intake or administration of hypertonic sodium solutions