Diabetes insipidus
Diabetes insipidus: Excerpt from Professional Guide to Diseases (Eighth Edition)
Diabetes insipidus (also called pituitary diabetes insipidus) is a disorder of water metabolism resulting from a deficiency of circulating vasopressin (also called antidiuretic hormone [ADH]). It’s characterized by excessive fluid intake and hypotonic polyuria. The disorder may start in childhood or early adulthood (the median age of onset is 21) and is more common in males than in females. Incidence is slightly higher today than in the past. In uncomplicated diabetes insipidus, the prognosis is good with adequate water replacement and replacement of ADH by tablet or nasal spray, and patients usually lead normal lives.
Causes and incidence
Diabetes insipidus results centrally from intracranial neoplastic or metastatic lesions, hypophysectomy or other neurosurgery, a skull fracture, or head trauma that damages the neurohypophyseal structures. It can also result nephrogenically from infection, granulomatous disease, and vascular lesions; it may be idiopathic and, rarely, familial. (Note: Pituitary diabetes insipidus shouldn’t be confused with nephrogenic diabetes insipidus, a rare congenital disturbance of water metabolism that results from renal tubular resistance to vasopressin.)
Normally, the hypothalamus synthesizes vasopressin. The posterior pituitary gland (or neurohypophysis) stores vasopressin and releases it into general circulation, where it causes the kidneys to reabsorb water by making the distal tubules and collecting duct cells water-permeable. The absence of vasopressin in diabetes insipidus allows the filtered water to be excreted in the urine instead of being reabsorbed.
Nephrogenic diabetes insipidus involves a defect in the parts of the kidneys that reabsorb water back into the bloodstream. It occurs less commonly than central diabetes insipidus. Nephrogenic diabetes insipidus may occur as an inherited disorder in which male children receive the abnormal gene that causes the disease on the X chromosome from their mothers. Nephrogenic diabetes insipidus may also be caused by diseases of the kidney (such as polycystic kidney disease) and the effects of certain drugs (such as lithium and amphotericin B).
Diabetes insipidus is rare, affecting 1 in 25,000 people. Males and females are affected equally.
Signs and symptoms
The patient’s history typically shows an abrupt onset of extreme polyuria (usually 4 to 16 L/day of dilute urine but sometimes as much as 30 L/day). As a result, the patient is extremely thirsty and drinks great quantities of water to compensate for the body’s water loss. This disorder may also result in nocturia. In severe cases, it may lead to extreme fatigue from inadequate rest caused by frequent voiding and excessive thirst.
Other characteristic features of diabetes insipidus include signs and symptoms of dehydration (poor tissue turgor, dry mucous membranes, constipation, muscle weakness, dizziness, and hypotension). These symptoms usually begin abruptly, commonly appearing within 1 to 2 days after a basal skull fracture, a stroke, or surgery. Relieving cerebral edema or increased intracranial pressure may cause all of these symptoms to subside just as rapidly as they began.
Diagnosis
Urinalysis reveals almost colorless urine of low osmolality (50 to 200 mOsm/kg, less than that of plasma) and low specific gravity (less than 1.005).
CONFIRMING DIAGNOSIS Diagnosis requires evidence of vasopressin deficiency, resulting in the kidneys’ inability to concentrate urine during a water deprivation test.
In this test, after baseline vital signs, weight, and urine and plasma osmolalities are obtained, the patient is deprived of fluids and observed to make sure he doesn’t drink anything surreptitiously. Hourly measurements then record the total volume of urine output, body weight, urine osmolality or specific gravity, and plasma osmolality. Throughout the test, blood pressure and pulse rate must be monitored for signs of orthostatic hypotension. Fluid deprivation continues until the patient loses 3% of his body weight (indicating severe dehydration). When urine osmolality stops increasing in three consecutive hourly specimens, patients receive 5 units of aqueous vasopressin subcutaneously (S.C.).
Hourly measurements of urine volume and specific gravity continue after S.C. injection of aqueous vasopressin. Patients with pituitary diabetes insipidus respond to exogenous vasopressin with decreased urine output and increased specific gravity. Patients with nephrogenic diabetes insipidus show no response to vasopressin.
Treatment
Mild cases require no treatment other than fluid intake to replace fluid lost. Until the cause of more severe cases of diabetes insipidus can be identified and eliminated, administration of various forms of vasopressin or of a vasopressin stimulant can control fluid balance and prevent dehydration. Vasopressin injection is an aqueous preparation that’s administered S.C. or I.M. several times a day because it’s effective for only 2 to 6 hours; this form of the drug is used in acute disease and as a diagnostic agent.
Desmopressin acetate can be given by nasal spray that’s absorbed through the mucous membranes, or by injection given S.C. or I.V.; this drug is effective for 8 to 20 hours, depending on the dosage. It’s also available in tablet form, to be given at bedtime or in divided doses. Hydrochlorothiazide can be used in both central and nephrogenic diabetes insipidus. Indomethacin and amiloride are also used for nephrogenic diabetes insipidus. If nephrogenic diabetes insipidus is caused by medication (such as lithium), stopping the medicine leads to kidney recovery.
Special considerations
Patient care includes monitoring symptoms to ensure that fluid balance is restored and maintained.
❑ Record fluid intake and output carefully. Maintain fluid intake that’s adequate to prevent severe dehydration. Watch for signs of hypovolemic shock, and monitor blood pressure and heart and respiratory rates regularly, especially during the water deprivation test. Check the patient’s weight daily.
❑ If the patient is dizzy or has muscle weakness, keep the side rails up and assist him with walking.
❑ Monitor urine specific gravity between doses. Watch for a decrease in specific gravity accompanied by increasing urine output, indicating the recurrence of polyuria and necessitating administration of the next dose of medication or a dosage increase.
❑ Institute safety precautions for the patient who’s dizzy or who has muscle weakness.
❑ If constipation develops, add more high-fiber foods and fruit juices to the patient’s diet. If necessary, obtain an order for a mild laxative such as milk of magnesia.
❑ Provide meticulous skin and mouth care; apply petroleum jelly, as needed, to cracked or sore lips.
❑ Before discharge, teach the patient how to monitor intake and output.
❑ Instruct the patient to administer desmopressin by nasal spray only after the onset of polyuria — not before — to prevent excess fluid retention and water intoxication.
❑ Tell the patient to report weight gain, which may indicate that his medication dosage is too high. Recurrence of polyuria, as reflected on the intake and output sheet, indicates that the dosage is too low.
❑ Teach the parents of a child with diabetes insipidus about normal growth and development. Discuss how their child may differ from others at his developmental stage.
❑ Encourage the parents to help identify the child’s strengths and to use them in developing coping strategies.
❑ Refer the family for counseling if necessary.
❑ Advise the patient with diabetes insipidus to wear a medical identification bracelet and to carry his medication with him at all times.
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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