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Nursing Care Plan | NCP Diabetes Insipidus

The disorder diabetes insipidus (DI) is characterized by excretion of large amounts of dilute urine. Diabetes insipidus can be of central (neurogenic) or renal (nephrogenic) origin. In central diabetes insipidus, excess urine is caused by insufficient amounts of antidiuretic hormone (ADH, also known as plasma vasopressin). Renal diabetes insipidus occurs when the kidney has a decreased responsiveness to ADH. The overall incidence of diabetes insipidus in the general population is approximtely 3 cases per 100,000 population.

Normally, body water balance is partially regulated by ADH, which is produced in the hypothalamus and is released from the posterior pituitary gland when body fluids become more concentrated than usual (serum osmolarity 283 mOsm/L). ADH causes water reabsorption in the distal portions of the nephron of the kidney by increasing the number of pores in the distal tubular system to allow for water reabsorption. ADH deficiency leads to little or no reabsorption; as a consequence, dilute urine formed in more proximal parts of the nephron is excreted essentially unchanged. The loss of solute-free water causes mild dehydration, a rise in plasma osmolality, and the stimulation of thirst.
Nursing care plan
Complications are most likely in patients with decreased mental alertness because their impairment makes it less likely they will drink in response to their stimulated thirst. The most serious complication of untreated diabetes insipidus is hypovolemia that may lead to hyperosmolarity, loss of consciousness, circulatory collapse, shock, and central nervous system (CNS) damage.

Neoplasms, infiltrative lesions, malformations, and neurosurgical procedures in the area of the pituitary gland are the most common causes of diabetes insipidus. Other causes of diabetes insipidus include trauma to the pituitary gland, vascular changes such as stroke and aneurysm, infection, pregnancy, and unknown reasons. The brain swelling that accompanies anoxic brain death may also lead to diabetes insipidus. In addition, certain drugs (lithium, demeclocycline, methoxyflurane, or amphotericin) or metabolic conditions can induce diabetes insipidus. Approximately 50% of the patients who develop diabetes insipidus have a familial or idiopathic (from unknown causes) form. In addition, congenital diabetes insipidus in neonates occurs as a result of malformation of the CNS.

Nursing care plan assessment and physical examination
Generally patients with suspected diabetes insipidus complain of excessive urination (polyuria), excessive thirst (polydipsia), and nocturia (excessive urination at night). The onset is often abrupt. Urinary output is usually in the 4 to 15 L per day range but can be as high as 30 L per day. Assess the patient for a past history of known causative factors: recent surgery, head trauma, or medication use. The patient may also report a history of weight loss, lightheadedness, weakness, intolerance to activity, and constipation. Parents may notice that children are more irritable than usual and may have sleep disturbances and anorexia.

Diabetes insipidus is associated with few physical signs. Except in unusual cases, dehydration is not sufficient to be evident on the physical exam. Look for signs and symptoms of dehydration: decreased tear formation, dry lips and mouth, complaints of excessive thirst, skin tenting, and dizziness. In spite of signs of dehydration, urine is clear or pale yellow and in copious amounts. You may note tachycardia, orthostatic changes in blood pressure, and decreased muscle strength.

Assess the patient’s ability to cope with a chronic illness and the financial resources to manage a chronic illness.

Nursing care plan primary nursing diagnosis: Alteration in urinary elimination related to polyuria.

Nursing care plann intervention and treatment plan
The treatment of diabetes insipidus is primarily pharmacologic. In addition to medication, fluid replacement to maintain vascular volume is essential. Rapid correction of hypernatremia is potentially dangerous because of the possibility of a rapid shift of water into brain cells, which increases the risk of seizures or cerebral edema. The water deficit is corrected gradually over 2 to 3 days with water by mouth or nasogastric tube or intravenously with half- or quarter-isotonic saline.

The most important nursing interventions focus on maintaining an adequate balance of fluid intake and output. Discuss dietary restriction of salt with the patient and family. The patient should also avoid coffee, tea, or other caffeinated substances since caffeine has exaggerated diuretic effects. The patient needs easy access to the bathroom, bedpan, or urinal. If the patient has muscle weakness or impaired mobility, make sure the pathway for ambulation to the bathroom is free from all obstructions to limit the risk of patient falls. Monitor the response to all medications and treatments by measuring the urine specific gravity daily as part of assessment data. Normal specific gravity is greater than 1.010. To identify the intake and output balance, monitor and carefully record the oral fluid intake and urine volume over a 24-hour period.

Encourage the patient to wear a medical identification bracelet and to carry any medications at all times. Note that some medications needed for a chronic disease, such as desmopressin acetate (DDAVP), are quite expensive. If the family does not have insurance coverage that includes medications, explore methods to obtain the needed medications. Refer the family to social service if necessary. Urge the patient and family to express their feelings about the patient’s condition; if they are having difficulty in coping, arrange for a counseling session.

Nursing care plan discharge and home health care guidelines
To prevent dehydration, teach the patient to use the thirst mechanism as a stimulus to drink oral fluids. To prevent polyuria, teach the patient to restrict salt and to avoid caffeine-containing products. Be sure the patient understands all medications, including the dosage, route, action, adverse effects, and the need for routine laboratory monitoring for DDAVP (plasma osmolarity). Ensure that the patient has access to the appropriate medications.
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