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At least 1,135 records · Page 63Linked to original sources
PubMed1994

Patients with disordered water balance. Innovative psychiatric nursing intervention strategies.

1. Patients with disordered water balance (DWB) have difficulty with fluid intake/output and osmoregulation. These difficulties are characterized by polydipsia, polyuria, significant variation in pattern of excretion, abnormal diurnal weight gain, and behavioral changes. 2. Therapeutic milieu-management strategies for patients experiencing acute and chronic phases of DWB are the cornerstone of long-term management of these patients. 3. Implementation of the intervention and milieu-management strategies described in this article resulted in a reduction of patients requiring acute medical treatment subsequent to an acute phase of DWB.

Adult↗
PubMed1995

Rhabdomyolysis after correction of hyponatremia due to psychogenic polydipsia.

Severe neurologic complications resulting from correction of hyponatremia are common, but reports of nonneurologic sequelae are scarce. This article describes a patient in whom rhabdomyolysis developed during correction of severe hyponatremia attributable to psychogenic polydipsia. Relevant material about volume regulation in the cell is presented, and a potential mechanism of cell damage is proposed. This case report emphasizes the importance of monitoring for nonneurologic complications during correction of hyponatremia.

Adult↗
PubMed1998

Absence of changes in antidiuretic hormone, angiotensin II, and atrial natriuretic peptide with clozapine treatment of polydipsia-hyponatremia: 2 case reports.

BACKGROUND: Polydipsia-hyponatremia is a poorly understood disorder that causes considerable mortality and morbidity. Hyponatremia in polydipsia-hyponatremia has been attributed to disturbances in antidiuretic hormone (ADH) function. Improvements in polydipsia-hyponatremia during clozapine treatment offered the chance to see if levels of ADH and other hormones associated with osmoregulation changed with improvement in biochemical and clinical measures of polydipsia-hyponatremia. METHOD: In this preliminary, longitudinal study, we studied 2 male schizophrenic patients (DSM-III-R) who had polydipsia-hyponatremia. Measures were (1) biochemical and clinical: serum sodium and osmolality, urine osmolality and specific gravity, normalized diurnal weight gain, and estimated urine volume and (2) endocrine: ADH, angiotensin II, atrial natriuretic peptide, and prolactin. Measures were collected during 2 months of baseline (typical neuroleptic) and 6 months of clozapine treatment. RESULTS: Single-case statistical procedures showed significant changes in sodium levels (a.m. and p.m.), estimated urine volume, and a.m. urine specific gravity in both patients and significantly decreased diurnal weight gain in 1 patient. Both serum and urine osmolality showed improvement, but values did not reach statistical significance. Low baseline ADH levels persisted through 6 months of clozapine treatment and showed no changes in the context of improvements in serum sodium and osmolality. No significant changes were seen in levels of angiotensin II and atrial natriuretic peptide. CONCLUSION: Given the limitations of this study, there is some evidence to suggest that the improvements in serum sodium and osmolality during clozapine treatment of polydipsia-hyponatremia may not be related to serum levels of ADH, although altered ADH receptor function cannot be ruled out. These data need to be extended in larger samples.

Adult↗
PubMed2005

Treatment of the polydipsia-hyponatremia syndrome with urea.

OBJECTIVE: The polydipsiahyponatremia syndrome is difficult to control in patients with severe mental illness, and there is no established effective therapeutic approach. We investigate the effect of oral daily intake of large amounts of urea to prevent hyponatremic episodes. METHOD: Seven patients were treated during 4 to 18 months with urea (0.3-0.9 g/kg/day). Five of these patients had schizophrenia. Body weight variation between morning and evening was determined before and during the course of therapy in 5 patients. The dose of urea was increased if morning serum sodium level (SNa) was lower than 132 mmol/L. RESULTS: Urea therapy increased mean +/- SD morning SNa (from 127.5 +/- 3.4 mmol/L before initiation of urea treatment to 136.5 +/- 2.4 mmol/L during the second month of urea treatment; p < .01) and mean +/- SD urine osmolality (from 86 +/- 39 mOsm/kg H(2)O to 159 +/- 58 mOsm/kg H(2)O; p < .05), probably without changes in water intake or urine volume excretion as attested by the level of urinary creatinine concentration. Mean +/- SD body weight variation decreased from 4.5% +/- 1.0% before initiation of urea treatment to 2.8% +/- 1.0% during the second month of urea treatment (p < .05). Two patients stopped urea treatment after 1 year and subsequently developed symptomatic hyponatremia. CONCLUSION: These preliminary data show that urea appears to be an effective therapeutic approach for the polydipsiahyponatremia syndrome.

Administration, Oral↗
PubMed1989

Hyponatraemia in psychiatric patients.

Four cases of symptomatic hyponatraemia in psychiatric patients are described. All patients exhibited varying degrees of the compulsive intake of water. The initial urinary osmolalities in all cases suggested impaired clearance of free water. This may be related to an exacerbation of the psychotic state. All patients demonstrated a marked diuresis after treatment with a hypertonic (1.8%) saline solution. The underlying pathophysiology is discussed. This clinical syndrome may be associated with significant morbidity and occasional mortality that are related to the rapid development of hyponatraemia.

Aged↗
PubMed1976

Clinical, biological and pathogenic features of the syndrome of inappropriate secretion of antidiuretic hormone. A review of 26 cases with marked hyponatraemia.

Twenty-six patients with the syndrome of inappropriate secretion of antidiuretic hormone were reviewed. The underlying diseases were bronchogenic carcinoma (12 cases); myxoedema (five cases); diseases of the nervous system (five cases); bronchopneumonia, carcinoma of the oesophagus, acute intermittent porphria and chlorpropamide therapy (each one case). Serum sodium levels ranged between 104 and 125 mEq per litre. Eighteen patients presented neurological manifestations, which in 14 were considered to be due to hyponatraemia. Neurological signs included disorders of consciousness (stage I and II coma), extrapyramidal signs, asterixis and epileptic seizures. An hyponatraemic coma was the first manifestation of the syndrome in five cases. In all cases where the EEG was recorded it showed non-specific signs of metabolic coma. The fundi never showed signs of intracranial hypertension. Blood urea and creatinine levels were invariably low in the euthyroid patients; these values were normal or elevated in patients with myxoedema and hyponatraemia. Hypokalaemia was frequent, and hypocalcaemia constant. In eleven cases an excess of water intake revealed the clinical syndrome: six patients were excessive beer drinkers and five had received extensive intravenous infusions. In one case the deleterious effect of diuretics was evident, and in another, the syndrome became evident during radiotherapy of an oesophageal tumour. Treatment of the syndrome was successful in all cases. A review of the literature concerning the various pathogenic mechanisms corresponding to the different underlying diseases is presented. The concept of aberrant hormonal production by a tumour is illustrated by an electron microscopic study.

Adult↗
PubMed1999

[Recurrent hyponatremia, neurological symptoms and long-term administration of levomepromazine].

We present the case of an 84 year old lady with an episode of marked hyponatremia with acute neurological disturbances which in the latest case resolved completely after a 3 day period of fluid restriction. The more common causes of hyponatremia could be ruled out. There was no evidence for a neuroleptic drug associated change in serum sodium concentration. We conclude that the patient in this study belongs to a subset of geriatric patients in whom there is an intermittent SIADH which only becomes clinically evident when several factors coincide. The underlying mechanisms are not understood but could include the interaction of subclinical cerebrovascular disease and treatment with a neuroleptic drug in an elderly patient whose water and sodium homeostasis is compromised by the changes of normal aging which affect the many systems involved in maintaining water and sodium balance.

Aged↗
PubMed2001

Hyponatremia associated with overhydration in U.S. Army trainees.

This report describes a series of hyponatremia hospitalizations associated with heat-related injuries and apparent over-hydration. Data from the U.S. Army Inpatient Data System were used to identify all hospitalizations for hyposmolality/hyponatremia from 1996 and 1997. Admissions were considered as probable cases of overhydration hyponatremia if this was the only, or primary, diagnosis or if it was associated with any heat-related diagnosis. Seventeen medical records were identified, and the events leading to hospitalization were analyzed. The average serum sodium level was 122 +/- 5 mmol/L (range, 115-130 mmol/L). All 17 patients were soldiers attending training schools. Seventy-seven percent of hyponatremia cases occurred in the first 4 weeks of training. Nine patients had water intake rates equal to or exceeding 2 quarts per hour. Most patients were in good health before developing hyponatremia. The most common symptoms were mental status changes (88%), emesis (65%), nausea (53%), and seizures (31%). In 5 of 6 cases in which extensive history was known, soldiers drank excess amounts of water before developing symptoms and as part of field treatment. The authors conclude that hyponatremia resulted from too aggressive fluid replacement practices for soldiers in training status. The fluid replacement policy was revised with consideration given to both climatic heat stress and physical activity levels. Field medical policy should recognize the possibility of overhydration. Specific evacuation criteria should be established for exertional illness.

Fatal Outcome↗