Hypernatremia:
– Produced by either administration of hypertonic fluids or much more frequently, loss of thirst mechanism or failure of ADH mechanisms
– Water moves from ICF → ECF
&Cells dehydrate Because of extremely efficient
• regulatory
mechanisms such as ADH and thirst, hypernatremia generally occurs only in people with prolonged lack of thirst mechanism
• Patients with loss of ADH (Diabetes Insipidus) usually can compensate with increased fluid intake.
Causes of Hypernatremia:
• Excessive loss of maily water in prolonged fever ,. Insufficient intake of water (hypodipsia)
• GI losses
• Diabetes Insipidus (both central and nephrogenic)
• Osmotic Diuresis – DKA
• Hypothalamic lesions which affect thirst center like tumors, granulomatous diseases or vascular disease
•
Sodium Overload – Infusion of Hypertonic sodium bicarbonate for metabolic acidosis.
Symptoms of Hypernatremia:
• Initial symptoms include lethargy, weakness and irritability
• Can progress to twitching, seizures, obtundation or coma
• Resulting decrease in brain volume can lead to rupture of cerebral veins leading to hemorrhage
• Severe symptoms usually occur with rapid increase to sodium concentration
• Sodium concentration greater than 180 mEq are associated with high mortality.
Diagnosis of Hypernatremia:
• Same labs as workup for hyponatremia: Serum osmolality, urine osmolality and urine sodium
• If urine osmolality is lower than serum osmolality then DI is suspecte
• Administration of DDAVP will differentiate types of DI
Urine osmolality will increase in central DI, no response in nephrogenic DI.
Treatment of hypernatremia:
Typical fluids given in form of Dextrose 5%
• Same as hyponatremia, sodium should not be lowered by more than 12 mEq/L in 24 hours
Overcorrection can lead to cerebral edema which can lead to encephalopathy, seizures or death.
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