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Journal of Nursing

Diabetes Insipidus

Karen Resseguie-Vickstrom, BSN, BBA, MBA (current DNP student) [email protected]


Diabetes Insipidus

Water is reabsorbed by the kidney that is controlled by the antidiuretic hormone (ADH) also known as vasopressin (Grossman, 2013). ADH is synthesized by cells in the hypothalamus known as the supraoptic and paraventricular nuclei that are conveyed along the hypothalamohypophysial pathway to the posterior pituitary gland for storage (Grossman, 2013). When the hypothalamus is stimulated by increased serum osmolality, it sends nerve impulses down the hypothalamohypophysial tract to the posterior pituitary gland to release the stored ADH into circulation (Lin, Liu & Lim, 2005). There are two types of vasopressin (V) receptors that the ADH exerts its efforts through and they are known as V1 and V2 (Grossman, 2013). The V1 receptors are located in the vascular smooth muscles causing vasoconstriction whereas V2 receptors are located on the tubular cells of the cortical collecting duct to control the reabsorption of water by the kidneys (Grossman, 2013). The renal mechanisms of the water reabsorption is particularly important for maintaining the body fluids osmolality (Hall 2011).

There are several stressor situations that can alter the release and increase the level of ADH to include (1) significant pain (2) trauma (3) nausea (4) surgery and (5) medication such as narcotics or certain anesthetic (Grossman, 2013). In addition to stressors a condition that also has an effect on the ADH is known as Diabetes Insipidus (DI) in which there is a deficiency or decreased response to the antidiuretic hormone (Grossman, 2013; Makaryus & McFarlane, 2006; Sand & Bichet, 2006).

Causes

Explanation to the parents should be explained that Diabetes Insipidus also known as water diabetes is marked by the inability to concentrate urine during periods of water restriction and therefore expel huge quantities of tasteless urine, usually as much as 3 to 20 liters per day, depending on the level of deficiency of ADH or renal insensitivity to ADH (Chan, & Kemp, 2013; Grossman, 2013). The polyuria output is accompanied by symptomatology of excessive thirst or polydipsia (Grossman, 2013). Individuals with a normal sense of thirst mechanism and that have fluid readily available are able to maintain proper fluid levels (Grossman, 2013). Complications arise in persons such as children whom may not be able to communicate their need for hydration and therefore inadequate fluid hydration can quickly lead to hypertonic dehydration and increased serum osmolality (Grossman, 2013). DI is classified in two forms (1) central or neurogenic DI that occurs due to a defect in the release of ADH and (2) nephrogenic DI that occurs due to the kidneys not responding to ADH (Decauyo, 2009; Makaryus & McFarlane, 2006).

Persons with central DI have lost up to 80-90 percent of ADH secreting neuron before polyuria becomes evident and in most cases the disorder has some ability to concentrate urine (Grossman, 2013). Central DI can also be considered temporary in circumstances of individuals following a head injury or surgical intervention near the hypothalamohypophysial tract (Grossman, 2013). Other causes can be the presence of a tumor or from an inherited autosomal dominant or recessive trait (Chan & Kemp 2013). Whereas the nephrogenic DI is associated with impairment of the urine concentrating ability and water storing up and may be caused by a genic factor that affects the V2 receptor that joins the ADH or aquaporin-2 protein that formulates water canals in the collecting tubules (Decauyo, 2009). Nephrogenic DI can be contributed to disorders that may include chronic medical conditions such as failure in the kidneys, sickle cell anemia, polycystic kidney disease, lithium and electrolyte disorders to include potassium depletion or chronic hypercalcemia in that these conditions interfere with the postreceptor actions of ADH in the permeability of the accumulating ducts (Grossman, 2013).

Chan and Kemp (2013) indicates that the most common forms of central DI is due to tumors, neurosurgical procedures, malformations and infiltrative lesions. It is estimated that the overall incidences occurs in 3 persons per a 100,000 population or 0.003% with a male dominate ratio of 60:40 (Chan & Kemp, 2013). The x-linked nephrogenic DI is not as common but yet exceeds the recessive variety of frequency in a ratio of 9:1 with the male mutation rate at 4 cases per million population (Chan & Kemp, 2013).

Treatment

It should be explained that treatment for DI will depend on the cause and the severity of the medical disorder and therefore a complete medical history and assessment will need to be obtained that includes the child’s daily nutritional intake, fluid intake, bowel and bladder elimination and pattern (Bass, 2014). Diagnostic work up will include laboratory values from urine samples, blood tests, a water derivation test while in the hospital to determine if dehydration occurs and a magnetic resonance imaging (MRI) of the brain, kidneys, liver and abdominal organs to check for pituitary abnormalities (Bass, 2014).

Explanation to the parents should include that persons with incomplete neurogenic DI can maintain near to normal water balance levels when cleared to ingest water in response to thirst (Grossman, 2014). Treatment of choice for central DI is a pharmacologic synthetic ADH analogue desmopressin acetate (DDAVP) or medications to include chlorpropamide and thiazide diuretics (Chan & Kemp, 2013; Grossman, 2013). Unfortunately desmopressin cannot be used to treat nephrogenic DI due to the receptor sites being defective and the kidneys responses being blocked (Chan & Kemp, 2013). Therefore treatment involves thiazide diuretics, amiloride and indomethacin or aspirin in combination with a low-solute diet (Chan & Kemp, 2013).

Long term survival is good in most cases depending on the underlying cause and as long as water remains readily available at all times to replace the enormous losses (Chan & Kemp, 2013). Due to the young child and their inability to express thirst or have access to hydration at all times, parents should be educated regarding the extreme necessity regarding water replacement (Chan & Kemp, 2013). It is extremely important to stress that should a gastrointestinal illness occur that causes a decrease intake of fluids or increased loose stools or both, medical attention is needed immediately to prevent life threatening electrolyte and fluid imbalances (Chan & Kemp, 2013).

Conclusion

Diabetes Insipidus also known as water diabetes is marked by the incapability to concentrate urine during periods of water restriction and therefore excrete huge volumes of tasteless urine due to the low sodium content (Chan, & Kemp, 2013; Grossman, 2013). DI is classified in two forms (1) central or neurogenic DI that occurs due to a defect in the release of ADH and (2) nephrogenic DI that occurs due to the kidneys not responding to ADH (Decauyo, 2009; Makaryus & McFarlane, 2006). DI is more common in males and one of the contributing factors is from an X-linked pattern of inheritance in that the males are the ones clinically affected but the females are the carriers (Elsevier, 2014). Medication management is available in conjunction with readily accessible water at all times to replace the enormous losses that occur through urination (Chan & Kemp, 2013). Enforcement to parents that this disease can easily turn to life threatening if a low-solute diet and hydration is not readily followed.

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