Diabetes insipidus is a rare condition that occurs when the kidneys are unable to conserve water during the process of filtering blood. This form of diabetes is different than diabetes mellitus or "sugar" diabetes. Both forms of diabetes are associated with excessive urination, but have different causes and treatments. Show
Diabetes insipidus is caused by a lack of antidiuretic hormone (ADH), also called vasopressin, which prevents dehydration, or the kidney's inability to respond to ADH. ADH enables the kidneys to retain water in the body. The hormone is produced in a region of the brain called the hypothalamus. It is stored and released from the pituitary gland, a small gland at the base of the brain. When diabetes insipidus is caused by a lack of ADH, it is called central diabetes insipidus. This form of the disease can be caused by damage to the hypothalamus or pituitary gland. When the condition is caused by a failure of the kidneys to respond to ADH, the condition is called nephrogenic diabetes insipidus, which may be inherited. This form of the disease involves a kidney defect that prevents the body from reabsorbing water back into the bloodstream. It is the rarest form of this uncommon disease. Our Approach to Diabetes InsipidusUCSF is an international leader in endocrinology care. Our team provides comprehensive consultations, evaluations and treatments for a wide range of hormone disorders, such as diabetes insipidus. We treat this condition with a medication called desmopressin acetate, or DDAVP. The medication is similar to antidiuretic hormone, the hormone implicated in diabetes insipidus. We will adjust the dosage for each individual to find the right balance between controlling symptoms and avoiding complications. Our goal is to help our patients return to healthy, normal lives. 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. Which manifestation does the nurse expect to find in a patient diagnosed with diabetes insipidus DI?Signs and symptoms of diabetes insipidus include: Being extremely thirsty. Producing large amounts of pale urine. Frequently needing to get up to urinate during the night.
How is nephrogenic diabetes insipidus diagnosed?Tests used to diagnose diabetes insipidus include:. Water deprivation test. While being monitored by a doctor and health care team, you'll be asked to stop drinking fluids for several hours. ... . Magnetic resonance imaging (MRI). An MRI can look for abnormalities in or near the pituitary gland. ... . Genetic screening.. Which symptom should the nurse monitor the client for that is diagnosed with diabetes insipidus?The two main symptoms of diabetes insipidus are the frequent urge to pass high volumes of diluted urine and excessive thirst. These symptoms are also known as polyuria and polydipsia, respectively, and they are two of the three polys of diabetes.
How is true diabetes insipidus and nephrogenic diabetes insipidus diagnosed?To differentiate central and nephrogenic diabetes insipidus, perform a water deprivation test and desmopressin (DDAVP) trial. Typically a 7-hour deprivation test is adequate to diagnose diabetes insipidus. Primary polydipsia may require longer dehydration periods.
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A patient is diagnosed with nephrogenic diabetes insipidus which order would the nurse question
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