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Diabetes Insipidus

3 min read

References:

  1. Brunner & Suddarth’s Textbook of Medical-Surgical Nursing, 15th Edition, ISBN 978-197-51-6103-3, by Janice L. Hinkle, Kerry H. Cheever, and Kristen J. Overbaugh ([ebook] pp. 3896-3897)

DI is a rare disorder that occurs due to injury to the hypothalamus or pituitary gland with a deficiency of ADH (vasopressin) that results in excretion of large volumes of dilute urine and extreme thirst. DI is characterized as central, nephrogenic, or dipsogenic, as well as gestational.

Etiology

  • The primary etiology for Central DI is head trauma but other causes include surgery, infection, inflammation, brain tumors, or cerebral vascular disease. It may also be idiopathic.
  • Nephrogenic DI etiologies include kidney injury, medications (lithium), hypokalemia, and hypercalcemia. This results in a failure of the renal tubules to respond to ADH.
  • Dipsogenic (causes thirst) DI is caused by a defect in the hypothalamus and may be the result of damage to the pituitary gland from a head injury, surgery, infection, inflammatory process, or a tumor.

The onset of diabetes insipidus in adults may either be insidious or abrupt.

Clinical Manifestations

ADH acts on the distal nephron of the kidney to reabsorb water. Without its action, an enormous daily output (>250 mL/hour) of very dilute urine with a specific gravity of 1.001 to 1.005 occurs.

  1. Polyuria: >250 mL/hour
  2. Very dilute urine. Specific gravity of the urine reaches 1.001 to 1.005
  3. No abnormal urine substances. There is no glucose or albumin in normal cases.
  4. Extreme thirst. Those with DI can consume from 2 to 20 liters of fluid daily, craving cold water. Withholding fluids will not reduce urine output, and is not a viable method of controlling the disease.

Assessment and Diagnosis

  1. Fluid Deprivation Test: withhold fluids from the patient for 8 to 12 hours, or until 3% to 5% of body weight is lost. In patients with diabetes insipidus, the urine’s specific gravity fails to increase even with depleting body fluids.
    • The test is terminated immediately if tachycardia, excessive weight loss, or hypotension develops.
  2. Plasma Studies: levels of ADH in the plasma, urine osmolality, and a trial of desmopressin therapy and intravenous infusion of hypertonic saline is done as further diagnostic measures.

If diagnosis is confirmed but the cause is unknown, the patient is assessed for tumors (imaging studies) that may be causing the disorder.

Management

  1. Medical:
    • Replace ADH and identify and correct the underlying pathology.
    • Ensure adequate fluid replacement.
  2. Pharmacologic:
    • Desmopressin (oral, intranasal) is used for central DI.
    • Chlorpropamide (sulfonylurea; oral hypoglycemic agent), and Thiazide diuretics are able to potentiate the effects of ADH/vasopressin on the kidneys. They are used in mild forms of DI to enhance fluid retention despite diuretic properties. Watch out for hypoglycemia and electrolyte imbalance.

If DI is nephrogenic, previous treatments are ineffective.

Thiazide diuretics, mild salt depletion, and prostaglandin inhibitors (e.g., endomethacin, aspirin) are used to treat the nephrogenic form of DI.

  1. Nursing:
    • Continuous physical assessment: monitor for clinical manifestations of dehydration. Vital signs and intake and output are essential to monitor.
    • Patient education: prevention of complications, emergency measures e.g. signs and symptoms of hyponatremia, and medication use and administration.

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