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A number of physiologic derangements have been observed resulting from the management of head and neck cancer with resection and simultaneous bilateral neck dissection. A protocol evolved to minimize morbidity from these complications was used on seventeen patients. Eleven are alive and free of disease and there was no mortality.
We describe a non-intensive behavioral intervention using an A-B design with extended follow-up on an open psychiatric unit to reduce water intake in a 52-year-old man with the syndrome of psychosis, intermittent hyponatremia, and polydipsia. A reinforcement schedule contingent upon weight gain secondary to water intake was employed. Mean diurnal weight gain was 7.1 pounds during a 23-week baseline which dropped to 4.1 pounds following 23 weeks of treatment and at a 1-year follow-up. Estimated fluid consumption dropped from 10 liters to 4 liters daily and incidents of hyponatremia decreased by 62%.
A novel behavioral method is described for the treatment of psychogenic polydipsia in a patient suffering from chronic schizophrenia. The patient was given feedback on serum sodium concentration, likely physical consequences, and the value of reducing fluid intake. An ABAB single-case design was used, with changes in sodium concentration (charted by the patient during the treatment phases) as the dependent variable. The patient showed substantially increased sodium concentration, which was maintained despite the withdrawal of feedback. This behavioral method appears promising in settings where restriction of fluid intake is not practical or ethical.
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Six patients [5 men and 1 woman, mean age 37.3 +/- 8.2 (SD) years] with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) underwent a sequence of treatments in an effort to normalize basal serum sodium levels and thereby protect the patients against complications, including hyponatremic seizures and coma. The morning baseline group mean basal serum sodium value was 132.5 +/- 3.8 meq/liter. Over a 20-month period, the sequence of treatments was salt-added diet, lithium and phenytoin, and lithium alone. Each treatment program yielded morning group mean basal serum sodium determinations superior to baseline values, except for the program of lithium alone, which could not be tolerated. The combination of lithium and phenytoin provided a morning group mean basal serum sodium level of 140.6 +/- 3.2 meq/liter, which was superior (p less than 0.01) to all other treatment modalities. Early morning hyposthenuria persisted throughout the 20-month period of observation.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
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To investigate the hypothesis that calcitonin gene-related peptide (CGRP), a potent vasodilator, is an important physiological defence against fluid overload, plasma CGRP concentrations were measured in various degrees of fluid overload in 26 haemodialysis patients, for whom diuresis, mediated by atrial natriuretic peptide (ANP), is not a possible defence mechanism. Plasma CGRP concentrations were positively correlated with the degree of fluid excess (r = 0.815, p = 0.0001) and were significantly higher in 5 patients with severe fluid overload than in those less severely affected (143 [SE 14] vs 52 [11] pmol/l; p less than 0.001). CGRP may be an effective defence against complications of fluid overload since it can increase capitance by vasodilatation.
Neuroleptic dosage was reduced by 10% every 2 weeks in five male hyponatremic polydipsic patients with schizophrenia. Mean dose fell from 1980 +/- 1289 to 631 +/- 135 chlorpromazine equivalents/day over a mean of 12.2 weeks until behavioral relapse occurred. During this time, serum sodium did not vary from baseline levels (132.9 +/- 4.9 mEq/1), suggesting that minimizing neuroleptic dose does not alter the severity of hyponatremia in these patients.
Serum osmolality and its relationship to diaphoresis and polydipsic behavior were examined in a series of 38 episodes of neuroleptic malignant syndrome (NMS) in 29 patients. Clinical variables were associated with significantly higher serum osmolality, and diaphoresis tended to emerge earlier than polydipsia in the course of NMS. The findings of this study are consistent with the hypothesis that, at least in some NMS patients, diaphoresis leads to dehydration followed by physiologically appropriate thirst and increased oral water intake. It appears that intravenous hydration is often necessary to correct the significant free water deficit that can occur during the course of NMS.
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Polydipsia, or excessive intake of water, is reviewed in the chronically mentally ill from a nursing perspective. The purpose of this article is to review research related to excessive water ingestion, the magnitude and types of problems that these patients experience, and the treatment interventions reported. Future research and practice should focus on understanding the patient's experience of polydipsia and how it relates to the patient's level of functioning, testing assessment tools, and determining appropriate interventions.
Pre-smoking versus post-smoking amounts of drinking and voiding were compared in ten state hospital patients with schizophrenia and polydipsia. Cigarette use was significantly correlated with total amount drunk but was not associated with increased drinking or decreased voiding immediately following smoking. These findings revealed no nicotine effects upon thirst drive or urinary output, but suggest that drinking and smoking represent associated repetitive behaviors.
Plasma renin activity (PRA), urinary excretions of PGE2, 6-keto-PGF1 alpha (6KPGF), TXB2 and renal function were determined in healthy women both in normal potassium balance (N, n = 14) and in experimental potassium depletion (KD). KD was induced by natriuretic treatment--associated to replacement of net NaCl and water losses--in the presence of either normal (congruent to 50 mmol/d) or low (less than or equal to 10 mmol/d) dietary potassium intake. By using different depletive patterns, three groups with estimated cumulative potassium deficit (mean +/- SEM) of 124 +/- 38 (KD0, n = 8), 160 +/- 43 (KD1, n = 8) and 198 +/- 22 mmol (KD2, n = 6), respectively, were obtained. Renal function by the clearance (cl.) method and urinary prostanoid concentrations by the RIA method were estimated during hypotonic polyuria (oral water load) and subsequent moderate antidiuresis induced by a low-dose infusion of lysine-8-vasopressin. 1. In KD0 group the potassium depletive treatment was inefficacious in significantly reducing either the plasma potassium concentration (PK) or the urinary potassium excretion (UKV). The reductions of PK and UKV as well as the enhancement of PRA became significant in KD1 and KD2 groups. 2. The urinary prostanoid excretions were not significantly changed in the KD0 and KD1 groups while in the KD2 group they were reduced, mainly concerning the urinary 6KPGF excretion. 3. Furthermore in the KD2 group, with larger potassium depletion, some of the typical hypokalemic renal dysfunctions appeared. The data suggest that a pathophysiologically critical degree of potassium depletion is associated with an inhibited renal prostanoid synthesis as well as an increased renin secretion.