Hypernatremic, Hyperkalemic Dehydration in an 8-Month-Old with Acute Gastroenteritis Managed With Controlled Hypotonic Rehydration

Abstract

Background: Hypernatremic dehydration is a dangerous manifestation during infancy since hyperosmolality can trigger neurologic impairment and since excessive rapidity of correction may trigger cerebral edema. Even though acute gastroenteritis is typically associated with the emergence of iso- or hyponatremic dehydration, hypernatremia can also occur when the volume of free-water loss and reduced intake surpasses that of sodium loss, especially in young infants. Prerenal physiology (1) and gastrointestinal bicarbonate depletion (2), respectively, may be represented by concomitant hyperkalemia and hyperchloremia.

Case presentation: A male patient aged 8 months complained about several periods of vomiting and loose stools and a report of being drowsy with clinical signs including moderate dehydration. No previous administration of oral rehydration solution or intravenous fluids history. The first complete blood count revealed hemoconcentration (hematocrit 38.3%) and reactive thrombocytosis (platelets 470 ×10 3 /mm 3 ). Serum electrolytes demonstrated hypernatremia (Na 153.15 mmol/L), hyperchloremia (Cl 134.11 mmol/L), slight hyperkalemia (K 5.07mmol/L), and an increase in the ionized calcium (iCa 1.51 mmol/L). With close clinical and biochemical observation, controlled intravenous rehydration with 0.45% saline was initiated. After repeating the test about 6.7 hours later, the electrolytes focused on enhancement (Na 151.24 mmol/L; Cl 123.63 mmol/L; K 4.41 mmol/L; iCa 1.45 mmol/L), which matches approximately 0.29 mmol/L/h sodium correction rate, which is well within the safety extremes.

Conclusion: Physiologically consistent patterns of hypernatremia (net water loss and insufficient intake), hyperchloremia (diarrheal loss of bicarbonate and chloride retention under hypovolemia), hyperkalemia (temporarydownward changesin renal potassium excretion due to prerenal hypoperfusion +acidosis and mild hypercalcemia (hemoconcentration and impaired renal calcium clearance) are demonstrated in this case. Slow correction using hypotonic saline was linked to biochemical improvement without any known complications.