Diabetes insipidus

Central diabetes insipidus

Neurogenic or central diabetes insipidus is characterized by a lack of antidiuretic hormone (ADH) that may result from any injury to the anterior hypothalamus, pituitary stalk, or posterior pituitary gland. In acute critically ill patients, the most common causes of diabetes insipidus are surgery for pituitary tumors, cerebral trauma, intracranial hypertension, and brain death ( Table 138.1 ). Diabetes insipidus also may occur as a complication of bacterial meningitis or encephalitis, vascular aneurysm or thrombosis, drug administration, or alcohol intoxication. Injuries to the hypothalamus most often yield permanent diabetes insipidus because ADH is synthesized in the hypothalamus itself. Injuries to the pituitary stalk and neurohypophysis more commonly cause transient diabetes insipidus because hypothalamic ADH secretion can be effective even in the absence of anatomic pathways to the normal site of release. Chronic diabetes insipidus in critically ill patients generally results from tumors of the pituitary region and from the sequelae of cerebral trauma.

Clinical picture

In complete hypothalamic or pituitary injuries, diabetes insipidus generally develops 6–24 hours after the injury because previously released ADH remains circulating this long. Patients with untreated diabetes insipidus usually develop urine outputs of 10–15 L/day. When the thirst mechanism is preserved, it is activated as soon as osmolality or volemia decreases. If the patient remains conscious and is given free access to water, he or she may be able to drink large amounts and compensate for the urine losses. In other cases, the large amounts of dilute urine rapidly result in dehydration, with hypovolemia and hypotension, and in hypernatremia, with neurologic deterioration. It is important that diabetes insipidus be recognized and treated rapidly, especially in comatose or noncommunicative patients. In patients with partial diabetes insipidus, the onset of polyuria may be delayed and the volume of urine may be lower. Nevertheless, if urine is hypo-osmolar and the diabetes insipidus is not treated, dehydration and hypernatremia finally occur and cause symptoms.

Clinical signs of hypernatremia usually appear only when the plasma sodium concentration increases to greater than 155–160 mEq/L or plasma osmolality increases to greater than 330 mOsm/kg. Signs may appear sooner if hypernatremia is associated with other metabolic disorders, particularly with disorders that also increase plasma osmolality. Symptoms mainly include confusion and lethargy. Severe hypernatremia results in coma and sometimes seizures. Acute and severe dehydration and hypernatremia may lead to cerebral shrinkage, sometimes associated with subdural or intraparenchymal hemorrhages.

Clinical signs of dehydration include blood volume depletion and hypotension in the most severe cases. Biologic markers of dehydration are usually absent in ICU patients with central diabetes insipidus because the urine loss begins abruptly and commonly reaches more than 1 L/hr. The free water deficit can be estimated by the following formula:

The formula assumes that only free water has been lost and that sodium stores are normal. Most often, some sodium has been lost together with additional water, and the total water deficit is even higher than that estimated from the formula. A moderate level of hypernatremia (e.g., 155 mEq) already is associated with a free water deficit of more than 4 L and a total water deficit that may be much higher if sodium has been lost.