What is diabetes insipidus?Diabetes insipidus is a condition that results from insufficient production of the antidiuretic hormone (ADH), a hormone that helps the kidneys and body conserve the correct amount of water. Normally, the antidiuretic hormone controls the kidneys' output of urine. It is secreted by the hypothalamus (a small gland located at the base of the brain) and stored in the pituitary gland and then released into the bloodstream. ADH is secreted to decrease the amount of urine output so that dehydration does not occur. Diabetes insipidus, however, causes excessive production of very diluted urine and excessive thirst. The disease is categorized into groups. Two of the groups are described below: Show
Causes of diabetes insipidus:Diabetes insipidus can be caused by several conditions, including the following:
What are the symptoms of diabetes insipidus?The following are the most common symptoms of diabetes insipidus. However, each individual may experience symptoms differently. Symptoms may include:
The symptoms of diabetes insipidus may resemble other conditions or medical problems. Always consult your physician for a diagnosis. How is diabetes insipidus diagnosed?In addition to a complete medical history and medical examination, diagnostic procedures for diabetes insipidus may include:
Treatment of diabetes insipidus:Treating diabetes insipidus depends on what is causing the disease. Specific treatment for diabetes insipidus will be determined by your physician based on:
Treatment may include modified antidiuretic hormone drugs administered either as injections, pills, or intranasal spray. For more information, contact the Pituitary Center.To arrange evaluations and request appointments, patients can call 410-955-9270 to speak with an agent who can begin the scheduling process. Learn more. Whether you're crossing the country or the globe, we make it easy to access world-class care at Johns Hopkins.  Approach ConsiderationsFluid replacementMost patients with diabetes insipidus (DI) can drink enough fluid to replace their urine losses. When oral intake is inadequate and hypernatremia is present, replace losses with dextrose and water or an intravenous (IV) fluid that is hypo-osmolar with respect to the patient’s serum. Do not administer sterile water without dextrose intravenously, as it can cause hemolysis. To avoid hyperglycemia, volume overload, and overly rapid correction of hypernatremia, fluid replacement should be provided at a rate no greater than 500-750 mL/h. A good rule of thumb is to reduce serum sodium by 0.5 mmol/L (0.5 mEq/L) every hour. The water deficit may be calculated on the basis of the assumption that body water is approximately 60% of body weight. Desmopressin and other drugsIn patients with central DI, desmopressin is the drug of choice. [37, 38] A synthetic analogue of antidiuretic hormone (ADH), desmopressin is available in subcutaneous, IV, intranasal, and oral preparations. [39] Generally, it can be administered 2-3 times per day. Patients may require hospitalization to establish fluid needs. Frequent electrolyte monitoring is recommended during the initial phase of treatment. 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 nonsteroidal anti-inflammatory drugs (NSAIDs). Because of side effects, carbamazepine is rarely used, being employed only when all other measures prove unsatisfactory. NSAIDs (eg, indomethacin) may be used in nephrogenic DI, but only when no better options exist. 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. MonitoringMonitor 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 urinary 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. Dietary measuresNo specific dietary considerations exist in chronic DI, but the patient should understand the importance of an adequate and balanced intake of salt and water. A low-protein, low-sodium diet can help to decrease urine output. PrecautionsPatients with DI 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. Patients should ensure access to water at their destination when traveling. Travels through deserts are best undertaken at night to avoid the excessive dehydration that can occur during day travel. Postoperative SettingAfter pituitary surgery, patients should undergo continuous monitoring of fluid intake, urinary output, and specific gravities, along with daily measurements of serum electrolytes. [40] 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. In patients with DI who have undergone surgery of any kind, administer the usual dose of desmopressin and give (hypotonic) IV fluids to match urinary output. ConsultationsIn the setting of neurosurgery or head trauma, the diagnosis of DI may be obvious, and even expected. The intensivists and nurses who manage the patient acutely are in the best position to provide acute care. 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. Medical genetics consultation is appropriate if there is a family history of DI and an inherited form is suspected.
Author Romesh Khardori, MD, PhD, FACP (Retired) Professor, Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, Eastern Virginia Medical School Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society Disclosure: Nothing to disclose. Coauthor(s) Jagdeesh Ullal, MD, MS, FACE, FACP, ECNU Clinical Associate Professor of Medicine (Endocrinology and Metabolism), Clinic Lead for Inpatient and Subspecialty Diabetes, UPMC Center for Diabetes and Endocrinology, University of Pittsburgh Medical Center Jagdeesh Ullal, MD, MS, FACE, FACP, ECNU is a member of the following medical societies: American Medical Association, International Society for Clinical Densitometry, Medical Society of Virginia Disclosure: Nothing to disclose. Chief Editor George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine George T Griffing, MD is a member of the following medical societies: American Association for Physician Leadership, American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society, International Society for Clinical Densitometry, Southern Society for Clinical Investigation Disclosure: Nothing to disclose. Acknowledgements Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment Frederick H Ziel, MD Associate Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Physician-In-Charge, Endocrinology/Diabetes Center, Director of Medical Education, Kaiser Permanente Woodland Hills; Chair of Endocrinology, Co-Chair of Diabetes Complete Care Program, Southern California Permanente Medical Group Frederick H Ziel, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Federation for Medical Research, American Medical Association, American Society for Bone and Mineral Research, California Medical Association, Endocrine Society, andInternational Society for Clinical Densitometry Disclosure: Nothing to disclose. What is the best treatment for diabetes insipidus?Treatments. The medication used to treat this disorder is called desmopressin acetate (DDAVP), which is similar to the antidiuretic hormone (ADH), also called vasopressin, produced by your body.
Can central diabetes insipidus go away?There's no cure for diabetes insipidus. But treatments can relieve your thirst and decrease your urine output and prevent dehydration.
Does diabetes insipidus need treatment?Mild cranial diabetes insipidus may not require any medical treatment. Cranial diabetes insipidus is considered mild if you produce approximately 3 to 4 litres of urine over 24 hours. If this is the case, you may be able to ease your symptoms by increasing the amount of water you drink to avoid dehydration.
What happens if diabetes insipidus is left untreated?Without treatment, diabetes insipidus can cause dehydration and, eventually, coma due to concentration of salts in the blood, particularly sodium.
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