Diabetes Insipidus Clinical Presentation
- Author: Michael Cooperman, MD; Chief Editor: George T Griffing, MD more...
History
The clinical presentation of diabetes insipidus (DI) depends on the cause, the severity, and the associated medical condition(s) of the patient.
The most common form of DI is that which follows trauma or surgery to the region of the pituitary and hypothalamus. It may exhibit 1 of 3 patterns: transient, permanent, or triphasic. The triphasic pattern is observed more often clinically. The 3 phases of this pattern are as follows:
- The first phase is a polyuric one that lasts 4-5 days, caused by inhibition of antidiuretic hormone (ADH). An immediate increase in urine volume and a concomitant fall in urine osmolality occur.
- The second phase is an antidiuretic one that lasts 5-6 days, resulting from the release of stored hormone. Urine osmolality rises.
- The third phase can be permanent DI, when stores of ADH are exhausted and the cells that produce more ADH are absent or unable to produce.
Polyuria, polydipsia, and nocturia (from 3-18 L) are the predominant symptoms. In infants, crying, irritability, growth retardation, hyperthermia, and weight loss may be the most apparent signs. In children, enuresis, anorexia, linear growth defects, and fatigability typically predominate. Pregnancy is associated with an increased risk of DI. When it has a nontraumatic cause, DI typically has a much more indolent course.
Many patients have a predilection for drinking cold liquids, often water. Neurologic symptoms vary with the patient’s access to water; patients with free access may have no symptoms at all.
Symptoms and signs of simultaneous anterior pituitary dysfunction may be present but are rare.
Physical Examination
The physical examination varies with the severity and chronicity of DI. The examination findings may be entirely normal. Hydronephrosis, bladder enlargement, and signs of dehydration are common. The daily urine volume is highly variable (3-20 L/d), and patient tolerance of dehydration also varies among individuals. Aside from signs of dehydration and an enlarged bladder, no specific signs of DI exist.
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].

