Cases reported "Dehydration"

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1/14. A case of hypopituitarism with diabetes insipidus and loss of thirst. Role of antidiuretic hormone and angiotensin ii in the control of urine flow and osmolality.

    A 20-yr-old male was found to have diabetes insipidus is association with panhypopituitarism but without any focal neurological lesion being identified. He was initially treated with steroid supplements, the features of diabetes insipidus being controlled with a thiazide diuretic. Eighteen months later the patient lost thirst sensation and stopped treatment, subsequently being re-admitted with severe dehydration, oliguria and focal neurological signs. Further investigation, including brain biopsy, confirmed the presence of an atypical pinealoma which was considered inoperable. Measurements of plasma antidiuretic hormone (ADH) and angiotensin ii (AII) concentrations during the severe dehydration showed very high levels of AII, but inappropriately low plasma ADH levels for the severity of dehydration. We consider that the evidence obtained from this case supports the view that the oliguria with hypertonic urine present during severe dehydration was due to a direct renal action of the very high AII levels, possibly supplemented by the residual ADH secretion.
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2/14. Myelodysplastic syndrome with central diabetes insipidus manifesting hypodipsic hypernatremia and dehydration.

    Central diabetes insipidus (DI) is a rare but recognized complication of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) that is caused by leukemic infiltration to the hypothalamo-neurohypophyseal system. In rare patients in whom a wide region of the hypothalamus is involved, central DI results in hypodipsic hypernatremia and dehydration. Typical DI symptoms such as polydipsia, polyuria, and marked thirst are concealed in these cases, because the hypothalamic "thirst center" cannot send thirst stimuli to the cerebral cortex. Herein we describe a patient with MDS developing into AML, who presented with hypodipsic hypernatremia and dehydration. A diagnosis of central DI was made on the ground of a low level of serum anti-diuretic hormone (ADH) despite high serum osmolality. A magnetic resonance imaging study revealed attenuation of a physiological "bright spot" of the neurohypophysis. An induction course chemotherapy including regular-dose cytarabine and daunorubicin produced a rapid improvement of hypernatremia. The bone marrow aspirate after two courses of chemotherapy showed complete remission. At that point, ADH release and the "bright spot" were recovered. In order to correctly diagnose central DI in association with hematological malignancies, we should not overlook this atypical type of DI.
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3/14. Hypothalamic adipic hypernatraemia syndrome with normal osmoregulation of vasopressin.

    Adipsic hypernatraemia is an uncommon disorder in childhood caused by a defect in the osmoregulation of thirst, leading to impairment of water homeostasis and chronic hyperosmolality of body fluids. Adipsia is often associated with an abnormality in osmoregulated vasopressin secretion due to the close proximity of the hypothalamic osmoreceptors that control thirst with those regulating vasopressin secretion. Hypothalamic lesions of diverse aetiology (vascular abnormalities, neoplasms, granulomatous diseases, trauma etc.) have been described in this syndrome. We report a 12-year-old boy with evident weight loss due to hypernatraemic dehydration with a selective defect in osmoregulation of thirst and normal vasopressin secretion with no demonstrable structural lesion. To date, only six paediatric patients with this condition have been described in the literature. Conclusion: Hypothalamic adipsic hypernatraemia syndrome must be suspected when a dehydrated patient denies thirst. The study of antidiuretic function is necessary because the osmoregulation of vasopressin secretion could be altered.
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4/14. A case report of hypodipsic hypernatremia syndrome associated with suprasellar tumor.

    A 20-year-old woman was diagnosed as hypodipsic hypernatremia syndrome in association with a variety of hypothalamic syndromes. Computed brain tomography disclosed a space occupying lesion over the region of the hypothalamus, lateral ventricle and paraventricles. Evaluation revealed defective osmoregulation of thirst and AVP release and hypothalamic syndrome. She showed no desire to drink at a plasma osmolality of above 320 mOsm/kg. Dissociation in the plasma vasopressin response to osmotic change and hemodynamic change was demonstrated in this patient. Treatment with a vasopressin analogue, desamino-D-arginine vasopressin and forced intake of water restored plasma osmolality and serum sodium levels to normal. In this case, selective osmoregulating dysfunction was presumably associated with pathologic conditions in or around the hypothalamus.
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5/14. dehydration in the elderly: insidious and manageable.

    dehydration in the elderly results from inadequate water replacement, and associated mortality may be high when dehydration is severe. The elderly are at an elevated risk for dehydration, due to decreased thirst perception, decreased water intake, abnormal vasopressin responses to osmotic stimuli, and a predisposition to mild nephrogenic diabetes insipidus. In addition, elderly patients with chronic physical and/or mental disabilities are often unable to drink or obtain water themselves. For these high-risk patients, the physician's role is to initiate measures to prevent dehydration, including fluid orders and intake documentation.
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6/14. A question of balance--dehydration in the elderly.

    The maintenance of optimal water balance is a priority for homeostasis; unfortunately, the aging process adversely affects the mechanisms of water balance, making it more difficult for the body to adequately defend itself against water loss. Four major age-related changes predispose the elderly to dehydration and hypernatremia: a decrease in total body water, an altered sense of thirst, a decrease in the renal urine concentrating ability, and a decrease in the effectiveness of ADH. In the case of fluid balance, careful assessment cannot be overemphasized due to the fact that there are few symptoms unique to dehydration that readily allow a nurse to know that fluid imbalances are involved.
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7/14. Recurrent hypertonic dehydration due to selective defect in the osmoregulation of thirst.

    A 6-year-old girl with recurrent episodes of hypertonic dehydration was studied. She denied thirst even with a plasma osmolality as high as 421 mosmol/kg. The hypernatremia was associated with an ability to concentrate urine (854 mosmol/kg). Volume expansion with water corrected hypernatremia (162 to 148 mEq/l) and resulted in an increased urine flow and urinary dilution (137 mosmol/kg) because of suppression of endogenous vasopressin (AVP) release (5.1 pg/ml). Hypertonic saline infusion raised the plasma AVP level (25.6 pg/ml) in response to changes in plasma osmolality (305 to 330 mosmol/kg) and led to a maximal urine osmolality of 818 mosmol/kg. With chronic forced fluid intake, the patient maintained a normal serum sodium concentration (range, 135-145 mEq/l) with a urine osmolality as low as 65 mosmol/kg. These findings are consistent with an isolated defect in the osmoregulation of thirst as the cause of the chronic hypertonic dehydration without deficiency in AVP secretion.
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8/14. Impaired arginine-vasopressin secretion associated with hypoangiotensinemia in hypernatremic dehydrated elderly patients.

    Nine elderly patients, some with preceding dementia, presented with adipsia, progressive dehydration, impaired consciousness, and hypernatremia following common acute infections without gastrointestinal disturbance. Studies before rehydration revealed inappropriately low plasma arginine-vasopressin (AVP) levels for plasma osmolality, insufficiently concentrated urine, absolutely or relatively low plasma angiotensin ii (A-II) concentrations (compared with plasma renin activity and plasma angiotensin I concentrations), and low serum angiotensin I-converting enzyme activities. The plasma AVP concentrations were positively correlated with the plasma A-II concentrations (r = .677) but not with plasma osmolality. The plasma AVP level was raised by an intravenous infusion of A-II in one patient. These findings suggest the following sequence of events: impaired A-II production caused impairment of thirst perception, renal-concentrating capacity, and AVP secretion and contributed to development of hypernatremic dehydration in these elderly patients.
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9/14. Severe hypernatremia in a patient with psychiatric illness.

    A 17-year-old schizophrenic developed severe hypernatremia during a period of psychosis. The thirst-deficient abnormality that caused this hypernatremia resolved when his psychosis improved. The primary disorders causing a thirst deficiency leading to hypernatremia fall into three categories: lesions of the central nervous system, mineralocorticoid excess, and drug side effects. None of these disorders was found in our patient. We conclude that psychosis can severely impair the thirst mechanism directly.
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10/14. Hypernatremic dehydration in children with severe psychomotor retardation.

    Three cases of hypernatremic dehydration in children with severe psychomotor retardation are described. All the children were receiving processed foods that contained extremely high amounts of sodium and were unintentionally deprived of free water. Salt and water intake must be monitored closely in children who can neither communicate thirst nor regulate their diet.
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