A severe hypernatremia with multiple organ failure- what is the prognosis?

[Sujit]

Hello, my 63 year old friend admitted to the emergency Hospital for a gradual onset of coma. His medical history is marked with type II diabetes, diagnosed ten years ago and treated with 5 mg of glibenclamide. It is not complicated of macro and microangiopathy. She also has an old Hypertension discovered in the same year, and was treated with 10 mg Amlodipine. Clinically, neurological examination notes a Glasgow of 8/15 (Y2, V2, M4) and an isolated left hemiplegia. There was neither meningeal syndrome nor attacks of cranial nerves. She was febrile at 39°c without development of specific infectious appeal. Lumbar pits are free and painless. Diuresis was almost zero in 100ml during the first 24 hours. Blood pressure are rather low for a known and treated hypertensive patient. She was 90/60 mmHg with no signs of shock, but tachycardia at 133/min. Cardiac auscultation is normal without perceived cardiovascular breath. Vascular axes were weakly perceptible. It was stable on the respiratory plan with Oxygen saturation of 95% within room air without auscultatory and radiological home. The skin examination notes a dry skin and mucous membranes, a flattening of the superficial veins, sunken eyes and a persistent skin fold. There is no hepatomegaly or splenomegaly, or jaundice. A severe hypernatremia with multiple organ failure- what is the prognosis?

[Shubhendu]

@sujit Hypernatremia, defined as a rise in the serum sodium concentration to a value exceeding 145 mmol per liter, is a common electrolyte disorder. Because sodium is a functionally impermeable solute, it contributes to tonicity and induces the movement of water across cell membranes. Therefore, hypernatremia invariably denotes hypertonic hyperosmolality and always causes cellular dehydration, at least transiently. Although correction of transient increases in plasma osmolality is usually well tolerated, correction of chronic plasma hypertonicity with rehydration therapy may be accompanied by brain swelling, herniation, and death. The clinical differences between acute and chronic osmolar disorders can be understood through a consideration of the different mechanisms by which cells in the brain regulate their volume in response to brief and sustained osmotic challenges.