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Panhypopituitarism can be a problem in pediatric patients, usually secondary to tumor or to aggressive dissection of tumor.[252] Acute ICU problems that result include support of the adrenal axis and abnormalities of ADH.
Diabetes insipidus can have a central, renal, or psychogenic origin. The central mechanism is the most common form found in ICU patients. Absence of ADH results in polyuria and polydipsia; patients with a critical disease may not be able to meet the thirst requirement, and severe hypovolemia may then develop. Diabetes insipidus can be precipitated by brain tumor, head trauma, neurosurgery, and clinical brain death.[253] [254] Treatment in the setting of the ICU is fluid replacement or, if unwieldy, replacement of hormone with the following: aqueous vasopressin (Pitressin), 0.1 to 1.0 mL intramus-cularly (duration, 4 to 6 hours); Pitressin tannate in oil, 0.25 to 1.0 mL intramuscularly (duration, 24 to 72 hours); or desmopressin acetate intranasal, 2.5 to 10 μg twice daily (duration, 10 to 11 hours).[255] The clinical syndrome may be transient or chronic, and close supervision of fluid intake and output is essential.
The syndrome of inappropriate secretion of ADH describes hyponatremia and hypo-osmolality from inappropriate urinary losses of sodium and free water in patients with normal kidneys. Urine osmolality is greater than serum osmolality. This syndrome can be precipitated
This disease is usually self-limited, and the only real problem occurs if the diagnosis is not considered and the level of hyponatremia is low enough to cause CNS dysfunction. Seizures are rare until serum sodium is less than 120 mEq/dL. Care should be taken to raise serum sodium levels slowly. This syndrome is treated by fluid restriction and, in severe cases, by the infusion of hypertonic or isotonic saline.
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