Diabetes insipidus: Nursing process (ADPIE)

Harvey Nguyen is a 30-year-old male client who suffered a traumatic brain injury during a skiing accident 4 months ago.

He presents to his primary care physician, or PCP, with a report of increased thirst, increased urine output, and frequent nighttime urination.

He says he doesn’t go anywhere without a water bottle and always needs to know where the restroom is when he is away from home.

He says that he is tired all the time because he has to make frequent trips to the bathroom during the night.

His laboratory results are serum sodium 147 mEq/L; serum glucose 100 mg/dL; serum osmolality 312 mOsm/kg; urine specific gravity 1.001; and urine osmolality 248 mOsm/kg.

His PCP refers him to an endocrinologist who admits Harvey to the medical unit for a water deprivation test which confirms the diagnosis of central diabetes insipidus.

Diabetes insipidus is a condition characterized by excessive water loss through urine because the kidneys don’t reabsorb enough water.

Now, the primary hormone that regulates water reabsorption and balance in the body is ADH, also called vasopressin.

ADH is normally produced by the hypothalamus and is stored in the posterior pituitary, which are both located within the brain. To do this, the hypothalamus contains osmoreceptors, which are able to sense the osmolality of the blood.

The normal blood osmolality value is between 285 and 295 mOsm/kg. Now, when a person is dehydrated, osmolality increases, so osmoreceptors sense this and, in response, stimulate the pituitary to release the stored ADH into the blood.

ADH then travels to the kidneys to decrease water excretion in urine, and increase water reabsorption back into the blood, which ultimately helps restore normal blood osmolality.

In addition, osmoreceptors trigger the sensation of thirst. After the person drinks water, the osmolality returns to normal, and ADH secretion stops.

There are four types of diabetes insipidus. The first type is central diabetes insipidus, which is caused by a problem in the hypothalamus or pituitary gland, preventing ADH production or ADH release.