44 Diabetes insipidus Overview/pathophysiology Diabetes insipidus (DI) is a condition that can result from one of several problems. Central (neurogenic) DI is caused by a defect in the synthesis of antidiuretic hormone (ADH) by the hypothalamus or release from the posterior pituitary. Nephrogenic DI results from a defect in the renal tubular response to ADH, causing impaired renal conservation of water. The primary problem is excessive output of dilute urine. Neurogenic DI may be the result of primary DI (i.e., a hypothalamic or pituitary lesion or dominant familial trait), secondary DI (following injury to the hypothalamus or pituitary stalk), or vasopressinase-induced DI, which is seen in the last trimester of pregnancy (caused by a circulating enzyme that destroys vasopressin). Nephrogenic DI either occurs as a familial X-linked trait or is associated with pyelonephritis, renal amyloidosis, Sjögren’s syndrome, sickle cell anemia, myeloma, potassium depletion, or chronic hypercalcemia. A rare form of DI, termed psychogenic diabetes insipidus, is associated with compulsive water drinking. Another form of water consumption related DI is dipsogenic diabetes insipidus, caused by an abnormality in hypothalamic control of the thirst mechanism. This condition is most often idiopathic, but has been associated with chronic meningitis, granulomatous diseases, multiple sclerosis, and other widely diffuse brain diseases. Patients have severe polydipsia and polyuria. Lastly, a lack of vasopressin can develop during pregnancy, resulting is gestagenic diabetes insipidus. The condition may be treated with vasopressin if severe, but generally resolves 6-8 weeks following delivery. Except for when it follows infection or trauma, DI onset is usually insidious, with progressively increasing polydipsia and polyuria. DI following trauma or infection has three phases. In the first phase, polydipsia and polyuria immediately follow the injury and last 4-5 days. In the second phase, which lasts about 6 days, the symptoms disappear. In the third phase, the patient experiences continued polydipsia and polyuria. Depending on the degree of injury, the condition can be either temporary or permanent. DI must be differentiated from other syndromes resulting in polyuria. History, physical examination, and simple laboratory procedures assist in diagnosis. Other causes of polyuria include recent lithium or mannitol administration; renal transplantation; renal disease; hyperglycemia; hyperosmolality (early); hypercalcemia; and potassium depletion, including primary aldosteronism. Health care setting Acute care (either medical-surgical or intensive care unit); primary care for patient who is being managed after hypophysectomy Assessment Signs and symptoms: Polydipsia, polyuria (2-20 L/day) with dilute urine (specific gravity less than 1.007). Physical assessment: Usually within normal limits, but patient may show signs of dehydration if fluid intake is inadequate. Individuals with cranial injury, disease, or trauma may exhibit impairment of neurologic status, including altered level of consciousness (LOC) and sensory or motor deficits. History of: Cranial injury, especially basilar skull fracture; meningitis; primary or metastatic brain tumor; surgery in the pituitary area; cerebral hemorrhage; encephalitis; syphilis; or tuberculosis (TB). Familial incidence rarely is a factor. Diagnostic tests Urine osmolality: Decreased (less than 200 mOsm/kg) in the presence of disease. Specific gravity: Decreased (less than 1.007) in the presence of disease. Serum osmolality: Increased (300 mOsm/kg or greater) in the presence of disease. Vasopressin (DDAVP) challenge test: After administration of vasopressin subcutaneously or desmopressin by nasal spray, urine is collected q15-30 min for 2 hr. Quantity and specific gravity are then measured. Normally, individuals will show a concentration of urine but not as pronounced as that of persons with DI; a person with kidney disease will have a lesser response to vasopressin. Note: One serious side effect of this test is precipitation of heart failure in susceptible individuals.< div class='tao-gold-member'> Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Psychosocial support Care of the renal transplant recipient Pneumothorax/hemothorax Bronchiolitis Stay updated, free articles. Join our Telegram channel Join Tags: All-In-One Care Planning Resource Jul 18, 2016 | Posted by admin in NURSING | Comments Off on Diabetes insipidus Full access? Get Clinical Tree
44 Diabetes insipidus Overview/pathophysiology Diabetes insipidus (DI) is a condition that can result from one of several problems. Central (neurogenic) DI is caused by a defect in the synthesis of antidiuretic hormone (ADH) by the hypothalamus or release from the posterior pituitary. Nephrogenic DI results from a defect in the renal tubular response to ADH, causing impaired renal conservation of water. The primary problem is excessive output of dilute urine. Neurogenic DI may be the result of primary DI (i.e., a hypothalamic or pituitary lesion or dominant familial trait), secondary DI (following injury to the hypothalamus or pituitary stalk), or vasopressinase-induced DI, which is seen in the last trimester of pregnancy (caused by a circulating enzyme that destroys vasopressin). Nephrogenic DI either occurs as a familial X-linked trait or is associated with pyelonephritis, renal amyloidosis, Sjögren’s syndrome, sickle cell anemia, myeloma, potassium depletion, or chronic hypercalcemia. A rare form of DI, termed psychogenic diabetes insipidus, is associated with compulsive water drinking. Another form of water consumption related DI is dipsogenic diabetes insipidus, caused by an abnormality in hypothalamic control of the thirst mechanism. This condition is most often idiopathic, but has been associated with chronic meningitis, granulomatous diseases, multiple sclerosis, and other widely diffuse brain diseases. Patients have severe polydipsia and polyuria. Lastly, a lack of vasopressin can develop during pregnancy, resulting is gestagenic diabetes insipidus. The condition may be treated with vasopressin if severe, but generally resolves 6-8 weeks following delivery. Except for when it follows infection or trauma, DI onset is usually insidious, with progressively increasing polydipsia and polyuria. DI following trauma or infection has three phases. In the first phase, polydipsia and polyuria immediately follow the injury and last 4-5 days. In the second phase, which lasts about 6 days, the symptoms disappear. In the third phase, the patient experiences continued polydipsia and polyuria. Depending on the degree of injury, the condition can be either temporary or permanent. DI must be differentiated from other syndromes resulting in polyuria. History, physical examination, and simple laboratory procedures assist in diagnosis. Other causes of polyuria include recent lithium or mannitol administration; renal transplantation; renal disease; hyperglycemia; hyperosmolality (early); hypercalcemia; and potassium depletion, including primary aldosteronism. Health care setting Acute care (either medical-surgical or intensive care unit); primary care for patient who is being managed after hypophysectomy Assessment Signs and symptoms: Polydipsia, polyuria (2-20 L/day) with dilute urine (specific gravity less than 1.007). Physical assessment: Usually within normal limits, but patient may show signs of dehydration if fluid intake is inadequate. Individuals with cranial injury, disease, or trauma may exhibit impairment of neurologic status, including altered level of consciousness (LOC) and sensory or motor deficits. History of: Cranial injury, especially basilar skull fracture; meningitis; primary or metastatic brain tumor; surgery in the pituitary area; cerebral hemorrhage; encephalitis; syphilis; or tuberculosis (TB). Familial incidence rarely is a factor. Diagnostic tests Urine osmolality: Decreased (less than 200 mOsm/kg) in the presence of disease. Specific gravity: Decreased (less than 1.007) in the presence of disease. Serum osmolality: Increased (300 mOsm/kg or greater) in the presence of disease. Vasopressin (DDAVP) challenge test: After administration of vasopressin subcutaneously or desmopressin by nasal spray, urine is collected q15-30 min for 2 hr. Quantity and specific gravity are then measured. Normally, individuals will show a concentration of urine but not as pronounced as that of persons with DI; a person with kidney disease will have a lesser response to vasopressin. Note: One serious side effect of this test is precipitation of heart failure in susceptible individuals.< div class='tao-gold-member'> Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Psychosocial support Care of the renal transplant recipient Pneumothorax/hemothorax Bronchiolitis Stay updated, free articles. Join our Telegram channel Join Tags: All-In-One Care Planning Resource Jul 18, 2016 | Posted by admin in NURSING | Comments Off on Diabetes insipidus Full access? Get Clinical Tree
