Diabetes Insipidus Treatment & Management
- Author: Michael Cooperman, MD; Chief Editor: George T Griffing, MD more...
Fluid Replacement and Pharmacotherapy
In an emergency, most patients with diabetes insipidus (DI) can drink enough fluid to replace their urine losses. Replace losses with dextrose and water or an intravenous (IV) fluid that is hypo-osmolar with respect to the patient’s serum. Avoid hyperglycemia, volume overload, and overly rapid correction of hypernatremia. A good rule of thumb is to reduce serum sodium by 0.5 mmol/L every hour. The water deficit may be calculated on the basis of the assumption that body water is approximately 60% of body weight.
In case of inadequate thirst, desmopressin is the drug of choice.[11, 12] A synthetic analogue of antidiuretic hormone (ADH), desmopressin is available in subcutaneous, intranasal, and oral preparations.[13] Generally, it can be administered 2-3 times per day. Patients may require hospitalization to establish fluid needs. Frequent electrolyte monitoring is recommended.
Alternatives to desmopressin as pharmacologic therapy for DI include synthetic vasopressin and the nonhormonal agents chlorpropamide, carbamazepine, clofibrate (no longer on the US market), thiazides, and indomethacin (limited efficacy).
In central DI, the primary problem is a hormone deficiency; therefore, physiologic replacement with desmopressin is usually effective. Use a nonhormonal drug for central DI if response is incomplete or desmopressin is too expensive. Nonhormonal drugs usually are more effective in treating nephrogenic DI.
Monitor for fluid retention and hyponatremia during initial therapy. Follow the volume of water intake and the frequency and volume of urination, and inquire about thirst. Monitor serum sodium, 24-hour urine volumes, and specific gravity. Request posthospitalization follow-up visits with the patient every 6-12 months. Patients with normal thirst mechanisms can usually self-regulate.
Postoperative setting
In patients with DI who have undergone surgery, administer the usual dose of desmopressin and give (hypotonic) IV fluids to match urine output.
After pituitary surgery, patients should undergo continuous monitoring of fluid intake, urine output, and specific gravities, along with daily measurements of serum electrolytes.[14] In patients who develop DI, administer parenteral desmopressin every 12-24 hours, along with adequate fluid to match losses. Follow the specific gravity of the urine, and administer the next dose of desmopressin when the specific gravity has fallen to less than 1.008-1.005 with an increase in urine output. When the patient can tolerate oral intake, thirst can become an adequate guide.
Dietary Measures
No specific dietary considerations exist in chronic DI, but the patient should understand the importance of adequate and balanced salt and water intake. Patients with DI also must take special precautions, such as when traveling, to be prepared to treat vomiting or diarrhea and to avoid dehydration with exertion or hot weather.
Consultations
In the setting of neurosurgery or head trauma, the diagnosis of DI may be obvious and even expected. The intensivists and the nurses who manage the patient acutely are in the best position to treat him or her acutely. In the more subtle forms of DI, and certainly in all chronic forms of DI for which therapy is expected to be indefinite, the clinical endocrinologist is an invaluable aid in establishing the diagnosis and designing therapy.
Earley LE, Orloff J. The mechanism of antidiuresis associated with the administration of hydrochlorothiazide to patients with vasopressin-resistant diabetes insipidus. J Clin Invest. Nov 1962;41(11):1988-97.
Los EL, Deen PM, Robben JH. Potential of nonpeptide (ant)agonists to rescue vasopressin V2 receptor mutants for the treatment of X-linked nephrogenic diabetes insipidus. J Neuroendocrinol. May 2010;22(5):393-9. [Medline].
Rochdi MD, Vargas GA, Carpentier E, et al. Functional Characterization of V2-Vasopressin Receptor Substitutions (R137H/C/L) Leading to Nephrogenic Diabetes Insipidus and Nephrogenic Syndrome of Inappropriate Antidiuresis; Implications for treatments. Mol Pharmacol. Feb 16 2010;[Medline]. [Full Text].
Kristof RA, Rother M, Neuloh G, et al. Incidence, clinical manifestations, and course of water and electrolyte metabolism disturbances following transsphenoidal pituitary adenoma surgery: a prospective observational study. J Neurosurg. Feb 6 2009;[Medline].
Seckl J, Dunger D. Postoperative diabetes insipidus. BMJ. Jan 7 1989;298(6665):2-3. [Medline].
Hadjizacharia P, Beale EO, Inaba K, et al. Acute diabetes insipidus in severe head injury: a prospective study. J Am Coll Surg. Oct 2008;207(4):477-84. [Medline].
Spanakis E, Milord E, Gragnoli C. AVPR2 variants and mutations in nephrogenic diabetes insipidus: review and missense mutation significance. J Cell Physiol. Dec 2008;217(3):605-17. [Medline].
Hedrich CM, Zachurzok-Buczynska A, Gawlik A, et al. Autosomal dominant neurohypophyseal diabetes insipidus in two families. Molecular analysis of the vasopressin-neurophysin II gene and functional studies of three missense mutations. Horm Res. 2009;71(2):111-9. [Medline].
Krahulik D, Zapletalova J, Frysak Z, et al. Dysfunction of hypothalamic-hypophysial axis after traumatic brain injury in adults. J Neurosurg. Nov 20 2009;[Medline].
Li G, Shao P, Sun X, et al. Magnetic resonance imaging and pituitary function in children with panhypopituitarism. Horm Res Paediatr. 2010;73(3):205-9. [Medline].
Richardson DW, Robinson AG. Desmopressin. Ann Intern Med. Aug 1985;ID - NIH5M01(2):228-39. [Medline].
Schrier RW. Systemic arterial vasodilation, vasopressin, and vasopressinase in pregnancy. J Am Soc Nephrol. Apr 2010;21(4):570-2. [Medline].
Vande Walle J, Stockner M, Raes A, et al. Desmopressin 30 years in clinical use: a safety review. Curr Drug Saf. Sep 2007;2(3):232-8. [Medline].
Ausiello JC, Bruce JN, Freda PU. Postoperative assessment of the patient after transsphenoidal pituitary surgery. Pituitary. 2008;11(4):391-401. [Medline].
Print
