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Stopping the cascade of diabetes insipidus

HOLCOMB, SUSAN SIMMONS RN-CS, CCRN, FNP, MN

Critical care
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FIND OUT HOW TO RECOGNIZE THIS POTENTIALLY DEADLY CONDITION—AND KEEP IT UNDER CONTROL.

Diabetes insipidus

Susan Simmons Holcomb is a nurse practitioner at Walk-In Health Care of Olathe in Olathe, Kan., and a nurse practitioner in nutritional consulting at the Sastun Center of Integrative Health Care in Mission, Kan.

Figure

Figure

A few hours ago, John Ace, 57, was admitted from the operating room to your intensive care unit after surgery to repair a ruptured aortic aneurysm. He's on a ventilator, has a pulmonary artery (PA) catheter for hemodynamic monitoring, and is receiving lactated Ringer's solution at 150 ml/hour. He received 10 units of blood during surgery.

Checking his indwelling urinary catheter, you notice that for the past hour, Mr. Ace has produced 500 ml of very pale yellow urine. A specific gravity of 1.001, determined by point-of-care testing, leads you to suspect diabetes insipidus (DI).

In this article, I'll tell you how you can manage and treat this potentially deadly condition. First, let's discuss the problems that cause this condition.

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ADH secretion and action

Diabetes insipidus occurs when either the secretion or action of antidiuretic hormone (ADH) goes awry. Produced in the hypothalamus and stored in the posterior pituitary, ADH causes fluid retention or lack of diuresis. In large amounts, ADH—also known as vasopressin—constricts arterioles.

In general, the body releases ADH in response to a decrease in circulating volume, which may occur with dehydration, an increase in plasma osmolality, or hypotension. Hypoxia can occur with hypovolemia and should raise ADH release.

By conserving water, ADH helps increase blood volume and blood pressure (BP) and return serum osmolality to normal. Diabetes insipidus ensues when the hypothalamus doesn't produce enough ADH, the posterior pituitary doesn't release ADH, or the nephron can't act in response to ADH.

Diabetes insipidus occurs in two forms. If the problem involves a lack of ADH secretion because of a problem with the hypothalamus or pituitary, the patient has central DI, also called neurogenic DI. If ADH is released but fails to stimulate the nephron's collecting tubules to conserve water, the patient has nephrogenic DI.

Each type of DI springs from various sources (see Understanding the Causes), but the main symptoms are the same: polydipsia (excessive thirst) and polyuria (excessive urination). If untreated, DI can lead to symptoms associated with hypovolemic shock, including changes in level of consciousness, tachycardia, tachypnea, and hypotension. However, unlike hypovolemic shock, DI causes an increase in urine output rather than a decrease.

Also watch for signs and symptoms of hypernatremia. These include restlessness, agitation, decreased deep tendon reflexes, and seizures.

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Two tests

Diagnostic findings associated with DI include polyuria, elevated serum osmolality, decreased urine osmolality, hypernatremia, and low urine specific gravity (see Keeping an Eye on Diagnostic Findings). Two tests can determine if DI's source is central or nephrogenic: the water deprivation test and the ADH test. Because of risks associated with these tests, the physician wouldn't normally order either for a critically ill patient.

In the water deprivation test, clinicians place the patient in mild dehydration to determine if the kidneys can concentrate urine with adequate ADH stimulation. If the kidneys can't concentrate urine, then the kidneys are the source of DI and the patient has nephrogenic DI. This test is also used to differentiate between psychogenic polydipsia (excessive thirst with no physiologic basis) and DI.

In the ADH test, the patient is challenged with ADH—usually desmopressin acetate (DDAVP) at an initial dose of 0.05 to 1 ml intranasally. Urine volume is measured before and after the challenge. If the kidneys respond by concentrating urine, then the cause of DI is central. If the kidneys can't concentrate urine, then the cause is nephrogenic.

Because Mr. Ace is critically ill, neither the water deprivation test nor the ADH test was administered. But chemistries revealed a serum osmolality of 350 mOsm/kg and hypernatremia, 152 mEq/liter, indicating dehydration.

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Treating central DI

Treatment for DI depends on whether it's central or nephrogenic. To treat central DI, the physician uses ADH replacement (see Choices for Replacing Antidiuretic Hormone), most commonly intranasal DDAVP.

Unlike other preparations, intranasal DDAVP has no effect on smooth muscle and won't increase BP or be as likely to cause arrhythmias. When replacing ADH, be sure to monitor for volume overload and hyponatremia.

More recently, clinicians have used pituitrin, a bovine extract from the posterior pituitary that contains oxytocin and vasopressin. Given in minute amounts, this preparation seems to control fluid status better, with minimal adverse reactions. Use a syringe pump to deliver the precise dosage ordered.

Table. C

Table. C

Among the other treatments for central DI:

  • chlorpropamide (Diabinese), which seems to decrease thirst
  • carbamazepine (Tegretol), which may have a similar action to chlorpropamide
  • thiazide diuretics, which I'll discuss in detail as a treatment for nephrogenic DI
  • indapamide (Lozol), which may work similarly to thiazide diuretics.

The physician starts Mr. Ace on intranasal DDAVP, 0.05 ml twice a day. Using the PA catheter to monitor hemodynamic status, you follow his hemodynamics closely for signs of volume overload such as increasing PA and pulmonary capillary occlusion pressures.

You also monitor his lungs for signs of volume overload, such as crackles, and watch his urine output. Adjust fluid replacement each hour. You also closely monitor serum and urine chemistries and serum and urine osmolality.

Treatment for central DI also includes fluid replacement. In acute cases, you can replace fluids fairly rapidly. But in chronic cases of DI, replace fluid slowly to avoid cerebral edema.

In either case, derive the amount of fluid replacement from the calculated water deficit (water deficit in liters = [plasma sodium − 140]/140 × estimated total body water in liters). You'd perform slow replacement by correcting the first 50% of the water deficit in the first 12 to 24 hours and the remaining 50% over 1 to 2 days. Fluid choice is based upon the patient's urine electrolytes, serum electrolytes, or both.

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Treating nephrogenic DI

Therapy for nephrogenic DI includes a low-salt diet and diuretics. The physician orders diuretics to force sodium loss, which enhances water reabsorption. Diuretics may decrease the glomerular filtration rate, allowing water reabsorption at the proximal tubule rather than at the collecting duct. This bypasses the need for water reabsorption at the collecting duct under the influence of ADH.

In the past, physicians ordered hydrochlorothiazide alone or in combination with indomethacin (Indocin). More recently, they've used hydro-chlorothiazide plus amiloride. This combination works better than hydrochlorothiazide alone, has fewer adverse effects, and is better tolerated than hydrochlorothiazide plus indomethacin. The usual dose of hydrochlorothiazide is 50 to 100 mg daily with 50 mg of indomethacin every 8 hours or hydrochlorothiazide plus amiloride (50 mg/5 mg), one tablet daily.

In some cases, the physician will use the oral antidiabetic chlorpropamide (Diabinese) to stimulate ADH release from the posterior pituitary. The intention is to augment collecting tubule response to ADH.

Because chlorpropamide is a sulfonylurea, monitor the patient's blood glucose levels very carefully. The hypoglycemic effects of sulfonylureas are difficult to predict and reverse, so this isn't considered first-line therapy.

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Targeting the cause

Besides initiating these treatments, the physician will try to eliminate the cause of DI, whether central or nephrogenic.

For instance, nephrogenic DI is a potential complication of lithium therapy, most commonly used for bipolar disease. The physician will need to try another therapy to prevent DI from continuing or recurring. If central DI results from head injury, infection, or hypoxia, the DI should resolve as those conditions improve.

Mr. Ace begins to respond to DDAVP therapy. On day five, he's successfully weaned from the ventilator; on day six, his PA catheter is removed. By day seven, he's transferred to the step-down unit. He's monitored closely for weight, urine output, osmolality, and electrolytes. As he stabilizes further, he'll be weaned from DDAVP.

Because Mr. Ace experienced hypoxia from the aortic aneurysm, he's temporarily impaired and can't perform activities of daily living on his own. You arrange for transfer to a rehabilitation facility until he can again care for himself. His health care providers will need to keep his mucous membranes moist and prevent skin breakdown from lack of self-care and changes in volume status. A patient with chronic DI, whether central or nephrogenic, will need lifelong medication. He'll have to carefully monitor his weight and keep follow-up visits with his primary health care provider. However, chronic DI doesn't shorten the life span.

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Diligent action

To meet the challenge of DI, you'll need to keep the patient's volume and electrolyte status under control with diligent attention to the details of intake and output and chemistries. Monitor the patient closely and intervene immediately if complications develop.

Teaching the patient and his family about the syndrome, if acute, or the disease, if chronic, will go a long way to alleviating their concerns and fears. With appropriate care, acute DI is curable and chronic DI is manageable.

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UNDERSTANDING THE CAUSES

Central diabetes insipidus (DI)

  • Congenital—familial, idiopathic, or from Wolfram syndrome, a rare autosomal recessive condition associated with DI, diabetes mellitus, optic atrophy, and deafness
  • Central nervous system (CNS) tumors—primary, metastatic, or benign
  • Cerebrovascular disease/trauma—head injury, anoxic encephalopathy, surgical, cerebral aneurysm, cavernous sinus thrombosis
  • Infections that affect the CNS—tuberculosis, syphilis, mycoses, toxoplasmosis, encephalitis, meningitis
  • Granulomatous—sarcoidosis, histiocytosis X (multi-focal Langerhans cell granulomatosis)
  • Pregnancy—vasopressinase-induced (seen in the last trimester and in the puerperium, often associated with preeclampsia or hepatic dysfunction; circulating vasopressinase destroys vasopressin). Also can be caused by Sheehan's syndrome, a rare complication, usually from excessive blood loss and shock during childbirth with resulting partial destruction of the pituitary.

Nephrogenic DI

  • Congenital—vasopressin V-2 receptor defect, aquaporin-2 water channel defect
  • Obstructive uropathy
  • Chronic tubulointerstitial disease—analgesic nephropathy, sickle-cell anemia, multiple myeloma, amyloidosis, sarcoidosis, Sjögren's syndrome, lupus, polycystic kidney disease, pyelonephritis, medullary cystic disease, acute tubular necrosis
  • Medications—lithium, amphotericin B, phenytoin, ethanol, other drugs such as steroids, anticholinergics, rifampin, aminoglycosides
  • Electrolyte problems—hypercalcemia, hypokalemia
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KEEPING AN EYE ON DIAGNOSTIC FINDINGS

These findings point to a diagnosis of diabetes insipidus, but further testing is needed to determine if the cause if central or nephrogenic.

  • Polyuria—2 to 20 liters/day (normal urine output, 1 to 1.5 liters/day)
  • Elevated serum osmolality—>300 mOsm/kg (normal, 280 to 300 mOsm/kg)
  • Decreased urine osmolality—<300 mOsm/liter (normal, 300 to 1,400 mOsm/liter)
  • Hypernatremia—>145 mEq/liter (normal sodium level, 135 to 145 mEq/liter)
  • Decreased urine specific gravity—<1.005 (normal, 1.005 to 1.03)
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SELECTED REFERENCES

Alspach, J. (ed): Core Curriculum for Critical Care Nursing. Philadelphia, Pa., W.B. Saunders Co., 1998.
    Corwin, E.: Handbook of Pathophysiology, 2nd edition. Philadelphia, Pa., Lippincott Williams & Wilkins, 1999.
      Ferry, R., et al.: “Hyponatremia and Polyuria in Children with Central Diabetes Insipidus: Challenges in Diagnosis and Management,” Journal of Pediatrics. 138(5):744–777, May 2001.
      Gawlinski, A., and Hamwi, D.: Acute Care Nurse Practitioner: Clinical Curriculum and Certification Review. Philadelphia, Pa., W.B. Saunders Co., 1999.
        Kugler, J., and Hustead, T.: “Hyponatremia and Hypernatremia in the Elderly,” American Family Physician. 61(12):3623–3630, June 15, 2000, http://www.aafp.org.
          Nickolaus, M.: “Diabetes Insipidus: A Current Perspective,” Critical Care Nurse. 19(6):18–30, December 1999.
          © 2002 Lippincott Williams & Wilkins, Inc.