DIABETES INSIPIDUS

Diabetes insipidus, or DI, is a condition that results when damage or destruction of the
neurons of the hypothalamus causes decreased levels of antidiuretic hormone (ADH) and severe diuresisa and dehydration occur. The deficiency results in the inability to conserve water, and if the patients thirst mechanism is not adequate, or if fluids are not accessible, the fluid balance will be altered. The two main etiologies of DI are tumors of the hypothalamus or pituitary and closed head injuries that may have damage to the supraoptic nuclei or hypothalamus. head injuries, neurosurgery, or hypophysectomy may lead to a loss of osmoreceptor function and/or damage to the area that produce antidiuretic hormone. Sometimes, a transient type of DI occurs after surgical procedures, histiocytosis, sarcoidosis, aneurysm, meningitis, encephalitis, or neoplastic conditions. All the above respond to vasopressin. DI that is nephrogenic is usually vasopressin-insensitive, and is seem in polycystic kidney disease, pyelonephritis, multiple myeloma, sarcoidosis, sickle cell disease, or any disorder that affects the kidneys.usage ethanol and phenytoin inhibit ADH secretion, and drugs such as lithium and demeclocycline inhibits ADH action in the kidney. The main goal for treatment is to prevent dehydration and electrolyte imbalances, while determination and treatment of the underlying cause occurs. Vasopressin administration will control diabetes insipidus; D-amino-D-arginine vasopressin (DDAVP) is a nasal spray that has prolonged antidiuretic effects with manimal side effects with minimal side effects. ADH deficiency is classified as neuphrogenic, drug related, primary or secondary, depending on whether the problem is caused by insufficient production of ADH or an inability of the kidney to respond to the presence of ADH. Nephrogenic diabetes insipidus: is an inherited disorder. The renal tubules do not respond to the action of ADH, which results in a poor water reabsorption by the kidneys. the actual amount of the hormone produced is not deficient. Primary diabetes insipidus: is caused by defect in the hypothalamus or pituitary gland, resulting in a lack of ADH production or release. Secondary diabetes insipidus can result from tumors within the adjacent to the hypothalamus or pituitary gland, head trauma, infectious process, surgical procedures (hypophysectomy), or metastatic tumors, usually from the lung or the breast. less often, it is caused by brain hemorrhage, brain disease, or cerebral aneurysm, which ADH production. Drug-related diabetes insipidus: is caused by lithium carbonate (eskalith, lithobid, carbolith) and democlocycline (declomycin). These drug can interfere with the respond of the kidneys to ADH.

MEDICAL CARE LABORATORY: Serum osmolality elevated, usually greater than 295 mOsm/kg; urine osmolality decreased, generally less than 500 mOsm/kg and can be as low as 30mOsm/kg; urine specific gravity low, generally 1.001 to 1.005; plasma ADH levels decreased in central diabetes insipidus; serum sodium elevated

Water deprivation test: Used to demonstrate that in the presence of simple dehydration, kidneys cannot concentrate urine; used to differentiate psychogenic polydipsia from diabetes insipidus Vasopressin test: Used in conjunction with water deprivation test to identify that the kidneys can concentrate urine with exogenous ADH and differentiates nephrogenic from central diabetes insipidus IV fluids: Required because of potential or present fluid deficits resulting from the bodys inability to conserve water Electrolyte replacement: Required bases upon patients lab levels; hypernatremia is frequently seen, so potassium levels maybe low

Hormonal replacement: Vasopressin (pitressin) or desmopressin acetate (DDAVP, stimate) is used toreplace endogenous hormone; drug increase the permeability of the renal tubular epithelium which increase reabsorption of water and allowed for concentration of urine Chlorpropamide: Diabenese used for its antidiuretic effect with DI patients; stimulates the release of ADH and helps the response of the renal tubules to ADH effects Thiazide diuretics: Chlorothiazide (diuril), hydrochlorothiazide (esidrex, hydrochlorthiazide, hydrodiuril, thiuretic) chlorthialidone (chlorthialidone, hygroton, hylidone, thalidone), indapamide (lozol), and metolazone (diulo, zaroxolyn) used to reduce the solute load and deplete sodium in order to increase water reabsorption

NURSING DIAGNOSES Deficient fluid volume Related to: -inability to conserve water -dehydration decreased levels of ADH Defining characteristics: extreme thirst, decreased skin turgor,dry mucous membranes, hypotention, tachycardia, weight loss, dilute urine output, increase urine output, hemoconcentration, hyperosmolality, increase serum sodium Intervention: -asses and monitor vital signs. -measure intake and output every 1-2 hours and notify physician for changes. Record specific gravity measurements per protocol. -administer IV fluids as ordered. If able to take oral fluids, encourage patient PO intake -weigh patient daily -administer replacement therapy for central diabetes insipidus -administer medication therapy for nephrogenic diabetes insipidus -observe for water intoxication with pharmacologic replacement therapies -assist with diagnostic procedures such as water deprivation and vasopressin test by obtaining accurate weights, vital signs, i&o, lab specimens at proper interval, and maintaining deprivation for required amount of time -instruct patient/family member in methods to prevent dehydration when on long-term ADH therapy, as well as when hospitalize

Deficient knowledge: Related to: -potential self-care management for permanent diabetes insipidus Defining characteristics: -newly diagnose DI -request for information -questions -inaccurate follow through with instruction or medication -development of preventable complications -inability to recall information vital to disease process Intervention: -assess for patient/family member comprehension of disease and medications -instruct patient in all medications, actions, schedules to be taken, methods of administration, and importance of adherence to medical regimen -instruct patient to notify physician for excessive water retention or urinary frequency and increase amount

-discuss reasons for nonadherence to medication, if patient has previously been diagnosed with DI -discuss obtaining medical alert bracelet identifying patient as having DI

Other interventions: 1. Institute safety precautions if the patient complains of dizziness or weakness. 2. Make sure the patient has easy access to the bathroom or bed pan, and answer his calls signals promptly. 3. Give vasopressin cautiously to a patient with coronary artery disease because the drug may cause vasoconstriction. 4. Provide meticulous skin and mouth care. Use soft toothbrush and mild mouth wash to avoid trauma to the oral mucosa. 5. Keep accurate records of hourly fluid intake and urine output, vital signs, and daily weight. 6. Monitor urine specific gravity and serum electrolyte and blood urea nitrogen levels. 7. During dehydration testing, watch for signs of hypovolemic shock. 8. Check laboratory values for hyponatremia and hyupoglycemia. 9. Encourage the patient to maintain adequate fluid intake during the day to prevent severe dehydration and to limit fluid in the evening. 10. Tell the patient to record his weigh daily. 11. Inform the patient and his family about long-term hormone replacement therapy. PATHOPHYSIOLOGY: DIABETES INSIPIDUS Decrease ADH (pitressin) or low plasma ADH levels Renal tubular unresponsiveness Decrease permeability to water Excess water excreted in urine Decrease urine osmolality Decrease urine specific gravity Plasma volume loss increase plasma Osmolality increase serum sodium dehydration

hypovolemic shock

polydipsia, weakness, fever, confusion

MANAGEMENT: The management of central diabete insipidus depends on the cause and severity of the disorder. Many persons with incomplete neurogenic diabetes insipidus maintain nearnormal water balance when permitted to ingest water in response to thirst. Pharmacologic preparation of ADH are available for person who cannot be managed by conservatives measures. The preferred drug for treating chronic diabetes insipidus is desmopressin acetate (DDAVP). It usually is given orally but is also available in parenteral and nasal forms. The oral antidiuretic agent chlorpropamide may be used to stimulate ADH release in partial neurologic diabetes insipidus. It usually es reserved for special cases because of its ability to cause hypoglycemia. Both neurogenic and nephrogenic forms of the disorder respond partially to the thiazide diuretics ex. hydrochlorothiazide. These diuretics are thought to act by increasing sodium excretion by the kidneys, which lowers the glomerular filtration rate and increases reabsorption of water in the proximal tubules.