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Polyuria hypernatremia

Vasopressin and desmopressin are treatments of choice for pituitary diabetes insipidus. The dosage of desmopressin is 10-40 meg (0.1-0.4 mL) in two to three divided doses as a nasal spray or, as an oral tablet, 0.1-0.2 mg two to three times daily. The dosage by injection is 1-4 meg (0.25-1 mL) every 12-24 hours as needed for polyuria, polydipsia, or hypernatremia. Bedtime desmopressin therapy, by intranasal or oral administration, ameliorates nocturnal enuresis by decreasing nocturnal urine production. Vasopressin infusion is effective in some cases of esophageal variceal bleeding and colonic diverticular bleeding. [Pg.845]

Eight years after stopping lithium because of polydipsia and polyuria, a 55-year-old woman was hospitalized with lethargy, coma, and hypernatremia (sodium concentration 156 mmol/1) after her fluid intake had been restricted (391). [Pg.146]

A 76-year-old man developed severe intractable diabetes insipidus which was attributed to lithium (395). He was hospitalized for over 2 weeks and eventually died from intestinal hemorrhage. Vigorous efforts were made to treat his polyuria, electrolyte disturbances, hypernatremia, and dehydration. He had been taking chlorpromazine, lithium, and furosemide, along with other medications, and the diagnosis of lithium-induced nephrogenic diabetes insipidus was considered because of a lack of alternative explanations. [Pg.147]

Water and electrolyte disturbances, including inappropriate antidiuresis, can occur in patients who have taken high doses of colchicine (2,3), including hypernatremia and polyuria (4). [Pg.883]

The polyuria which often accompanies lithium treatment is normally compensated for by drinking water, but when consciousness is impaired severe hypernatremia may develop. When any acute illness (particularly if associated with gastrointestinal symptoms) occurs or when new medication is given, lithium blood levels should be closely monitored, and the lithium dose adjusted. [Pg.742]

Conn s syndrome is apparently caused by an inability of the adrenal cortex to carry out 17a-hydroxylation during the biosynthesis of the hormones from cholesterol. Consequently, the disease is characterized by a high secretory level of aldosterone, which lacks a 17a-hydroxyl functional group. In addition, hypernatremia, polyuria, alkalosis, and hypertension are observed (12). [Pg.1312]

Observational studies The use of tolvaptan in short- and long-term studies in heart failure and hyponatremia has been reviewed [82 ]. In an open extension study in 4133 patients with heart failure who were followed for a mean of 10 months, 111 patients with hyponatremia took oral tolvaptan for a mean of 701 days dry mouth, thirst, and hypernatremia were more common in those who took tolvaptan the incidences of hypotension and renal failure were comparable in the two groups [83 ]. The most common adverse events that were assessed by the investigator as being potentially related to the use of tolvaptan were pollakiuria ( = 11) thirst (n = 10) fatigue (n = 6) and dry mouth, polydipsia, polyuria, hypotension, hypernatremia, dizziness, headache, peripheral edema, and acute renal failure (four patients each) [84 ]. [Pg.714]


See other pages where Polyuria hypernatremia is mentioned: [Pg.541]    [Pg.377]    [Pg.541]    [Pg.377]    [Pg.258]    [Pg.1753]    [Pg.175]    [Pg.235]   
See also in sourсe #XX -- [ Pg.84 ]




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