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PubMedDate not supplied

Disturbed vasopressin release in 4 dogs with so-called primary polydipsia.

Primary polydipsia is characterized by a marked increase in water intake and secondary polyuria, and in dogs often is described as a behavioral problem or a psychological disorder. We describe 4 dogs with primary polydipsia, diagnosed on the basis of a modified water deprivation test, in which further examination included serial measurements of urine osmolality (UOsm) and plasma vasopressin (VP) measurements during water deprivation and hypertonic saline infusion. The dogs, ranging in age from 4 months to 4 years, all were presented for evaluation of polyuria and polydipsia. Physical examination, routine blood chemistry, and urinalysis disclosed no specific cause for the polyuria and polydipsia. During serial measurements UOsm spontaneously reached high concentrations in 2 dogs, whereas in the other 2 dogs UOsm also fluctuated but on no occasion exceeded 1,000 mosm/kg. Primary polydipsia was diagnosed when UOsm exceeded 1,000 mosm/kg at the end of the modified water deprivation test and plasma osmolality did not exceed the upper limit of the reference range during testing. During water deprivation, plasma VP concentrations remained relatively low. The VP response to hypertonic saline infusion was abnormal, with an increased threshold value in 3 dogs, an increased sensitivity in 2 dogs, and an exaggerated response in 1 dog. It is concluded that some dogs fulfilling current criteria for primary polydipsia produce concentrated urine spontaneously throughout the day in a pattern similar to what has been observed in healthy pet dogs. This finding can be regarded as diagnostic and precludes the need for a water deprivation test. During water deprivation testing, all 4 dogs produced highly concentrated urine in the face of low basal plasma VP concentrations. The observed abnormal VP release in response to hypertonic stimulation may be interpreted as a primary disturbance in the regulation of VP secretion, although it might also be the result of overhydration caused by a primary abnormality in drinking behavior.

Animals↗

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↗

PubMedDate not supplied

[Prevalence of polydipsia and water intoxication in psychiatric inpatients].

INTRODUCTION: The prevalence of polydipsia and water intoxication among psychiatric inpatients has been described in different countries, however few studies have been conducted in Europe. The present study was aimed at evaluating the prevalence of polydipsia and water intoxication in an European Psychiatric Hospital. METHODS: SPGU (Specific Gravity of Urine) and Normalised Diurnal Weight Gain (NDWG) were evaluated among 201 inpatients. RESULTS: Risk of polydipsia and water intoxication were found among 51% of all patients. Risk of primary polydipsia was present in 25% of patients, and primary polydipsia and risk of water intoxication among 25% of all patients. CONCLUSIONS: This is one of the unique studies of polydipsia and water intoxication in psychiatric inpatients in Europe, and the first one conducted in Spain. The development of specific preventative and clinical programmes in psychiatric patients is suggested due to the clinical relevance and high prevalence of this pathology.

Adult↗

PubMedDate not supplied

[Rhabdomyolysis due to polydipsia in a patient with psychotic disorder].

Polydipsia is a frequent clinical entity in psychiatric patients, especially in those with a psychotic disorder. Acute episodes of polydipsia can produce important metabolic alterations and even coma and death. Psychogenic polydipsia is a underestimated diagnosis, due to multiple causal factors and an etiology that has not been clearly established. We present the case of a patient with psychiatric background who was seen due to a clinical situation of severe acute renal failure by high rhabdomyolysis that needed hemodialysis, due to acute polydipsia. We also review some of the epidemiological and clinical factors and etiopathogeny of the polydipsia. It is considered necessary to keep in mind the in mind the diagnosis of polydipsia in any psychiatric patient showing acute symptoms of confusion.

Drinking Behavior↗

PubMed1976

Hysterical polydipsia (compulsive water drinking) in children.

Two patients had entirely different clinical presentations of hysterical polydipsia: convulsions and coma in a 5-year-old boy with intrinsic renal disease and a single kidney, and abnormal behavior in a 3-year-old girl with normal kidneys. In neither case was the correct diagnosis made on initial evaluation. Physiological studies demonstrated primary polydipsia to be responsible for both clinical presentations. The differential diagnosis of polydipsia and polyuria is reviewed, and the nonuniform presentation of hysterical polydipsia is emphasized. In children with intrinsic renal disease, hysterical polydipsia may be life-threatening.

Child, Preschool↗

PubMed1982

Effects of chronic d-amphetamine on the maintenance and acquisition of schedule-induced polydipsia in rats.

The effects of chronic d-amphetamine on the acquisition of schedule-induced polydipsia and its maintenance by stimuli paired with food were evaluated in three interlocking experiments. In Experiment 1, polydipsia was induced in rats exposed to a response-independent fixed-time schedule in which a food pellet (US) was paired with a stimulus complex of lights and tone (CS) every 45 sec. When food was omitted and only the CS was presented rats drank very little water. Rats were then pretreated with 1 mg/kg d-amphetamine for 15 CS-US sessions and two or three subsequent CS-alone sessions. Animals remained polydipsic during CS-US sessions and drank little water during CS-alone sessions. However, d-amphetamine improved control exerted by the CS over drinking relative to no-drug sessions. In Experiment 2, acquisition of schedule-induced polydipsia during 10 sessions exposure to the periodic CS-US schedule was blocked in rats pretreated with 1 mg/kg d-amphetamine, compared with rats pretreated with buffer. During subsequent CS-alone sessions the temporal control of drinking by the CS was greater in the rats exposed to amphetamine. In Experiment 3, the rats that had not acquired polydipsia while under d-amphetamine in the previous experiment, all became polydipsic when pretreated with buffer. All rats remained polydipsic when re-exposed to amphetamine pretreatment. These results indicate that chronic d-amphetamine administration can facilitate control of licking and drinking by nonfood stimuli paired with food, and can block acquisition of schedule-induced polydipsia.

Animals↗

PubMed1982

Intraperitoneal preloads of water, but not isotonic saline, suppress schedule-induced polydipsia in rats.

In Experiment 1, 10 ml intraperitoneal preloads of water completely suppressed the acquisition of schedule-induced polydipsia in four of six rats. Preloads of 10 ml of isotonic saline retarded the acquisition of polydipsia slightly, but there were no significant differences in asymptotic levels of water intake between Saline Preload and Sham Preload groups. Experiments 2 and 3 demonstrated that established polydipsia was suppressed by about 10 ml when 10 ml water preloads were given; whereas, 10 ml saline preloads had no significant effect on established polydipsia. These results demonstrate that schedule-induced polydipsia is sensitive to internal states of water balance.

Animals↗

PubMed1995

Food-delay duration and the development of schedule-induced polydipsia in rats.

Twelve rats were exposed to a schedule that delivered a food pellet every 60 s (fixed time 60 s). The development of schedule-induced polydipsia was measured in terms of the water consumed and the licks per interpellet interval. Every lick by master rats initiated an unsignalled delay of 2 or 50 s in food delivery. Yoked-control rats received food at the same time as their masters, being unaffected by their own licking. Schedule-induced polydipsia developed in master rats exposed to 2-s delays, but more slowly and to a lesser extent than control animals. The development of polydipsia was prevented in master rats exposed to 50-s delays, however. When these delays were discontinued, polydipsia was obtained by master rats. The finding that the effect of the delays was modulated by their duration supports the view that the development of schedule-induced polydipsia is sensitive to control by its environmental consequences.

Animals↗

PubMed1990

Dapiprazole, a selective alpha-1 adrenoceptor antagonist, inhibits diuresis but not polydipsia produced by amphetamine in rats.

Chronic amphetamine administration has been found to produce diuresis and polydipsia in rats. We have found that dapiprazole acutely suppresses the diuretic, but not the ingestive, effects of amphetamine. To see whether diuresis is the physiological stimulus driving amphetamine-mediated polydipsia, we injected rats daily with d,l-amphetamine and the alpha-1 adrenergic antagonist dapiprazole. Throughout 19 days of treatment, dapiprazole completely prevented the increased urine output produced by amphetamine, but did not affect the development of polydipsia. This finding rules out a renal site of the primary action for amphetamine-mediated polydipsia and proposes water and electrolyte imbalance produced by chronic amphetamine administration as a model of the polydipsia and hyponatremia that develop in some psychotic patients.

Adrenergic alpha-Antagonists↗

PubMed1995

Treatment of polydipsia and hyponatremia in psychiatric patients. Can clozapine be a new option?

Polydipsia occurs frequently in chronic schizophrenic patients, some of whom develop intermittent hyponatremia. Most therapeutic efforts have tried to control the hyponatremia. Four schizophrenic patients, followed for more than one year, showed improvement on clozapine. Case 1 was an outpatient without history of hyponatremia who improved from polydipsia and psychosis. The last three were inpatients with polydipsia, intermittent hyponatremia, and psychosis who showed minimal improvement of psychosis but significant decrease in polydipsia and water intoxication. Case 2 relapsed to polydipsia when clozapine was discontinued on two occasions. Case 3 demonstrated polyuria during 39% of days before clozapine and in 0% of days after two weeks of clozapine. In case 4, most baseline sodium levels were abnormal, but all became normal after clozapine. A time-series analysis for intervention effects showed a significant effect of clozapine (p = .017). The limited information provided by these case reports suggest the need for controlled studies of the clozapine effect on polydipsic patients.

Adult↗

PubMed2002

Effects of clonidine in schizophrenic patients with primary polydipsia: three single case studies.

A pilot study was conducted in schizophrenic patients with primary polydipsia to determine the tolerability of adding clonidine to an existing antipsychotic drug regimen and to seek evidence of an antidipsic effect. Three patients with chronic schizophrenia and primary polydipsia underwent open controlled prospective trials of treatment with clonidine in doses of up to 800 microg/day. The trials lasted from 2 to 5 months each, and analysis of variance was used to test for changes in dependent variables on a case-by-case basis. Blood pressure and pulse declined significantly in a dose-dependent manner, but fluid intake, as assessed by measurements of weight and 24-h urine volume, was not affected. Hypotension and bradycardia limited the extent to which the dose of clonidine could be increased. The lack of evident effect of clonidine on polydipsia in this small sample and the inconsistent results of two other recent studies of clonidine in patients with schizophrenia and primary polydipsia provide little overall support for the effectiveness of clonidine treatment in primary polydipsia associated with schizophrenia.

Adrenergic alpha-Agonists↗

PubMed2004

Identifying at risk nursing home residents using a polydipsia screening tool.

Persons diagnosed with schizophrenia are considered at risk for polydipsia, a potentially life-threatening condition characterized by excessive consumption of fluids. This study examined the demographic and health-related characteristics of nursing home residents with psychiatric diagnoses (N = 70) who reside in a 92-bed facility. The prevalence of polydipsia and behavioral characteristics and symptoms as measured by a 17-item polydipsia screening tool also were described. Patients who screened positive for polydipsia (36%) exhibited behaviors that included incontinence, smoking, frequent voiding, and preference for fluid over food. A polydipsia screening program could minimize morbidity and mortality associated with this fairly prevalent condition.

Adult↗

PubMed1996

Problems and progress in the diagnosis and treatment of polydipsia and hyponatremia.

Fluid-electrolyte balance is regulated within a narrow range and disturbances in this system are unusual in animals and humans. Studies from the preneuroleptic era to date suggest that up to 25 percent of patients with schizophrenia have polydipsia, suggesting that it is related to the pathophysiology of the psychoses. Polydipsia and the related phenomenon of hyponatremia cause considerable mortality and morbidity. Prevalence studies are limited by imprecise measures available at present. The treatment was limiting water intake when patients reached critical levels of water retention, which however did not improve polydipsia. Recent case reports and open studies have shown that clozapine improves both polydipsia and water retention. The response occurs at low doses and is not related to improvement in psychosis. This may not be applicable to all patients and better understanding of the pathophysiology of polydipsia-hyponatremia would lead to more empirically derived treatments.

Behavior Therapy↗

PubMed1997

Developing a best practice model for care of patients with polydipsia.

Some psychiatric patients diagnosed with schizophrenia have a secondary diagnosis of polydipsia which is manifested by consuming excessive quantities of fluids, marked confusion, and disorientation. In most instances, these persons are less amenable to treatment and rehabilitative interventions due to the changes in cognitive and physical processes. A review of our own current practice found that we had a small group of polydipsia patients requiring a large amount of one-to-one staff time for little or no long-term benefit. Further, there was no uniform approach to identify, treat, and monitor outcomes for patients with polydipsia. A TQM team was assembled with the goal of identifying a protocol for assessing the presence of polydipsia and a care map for the treatment of confirmed cases. The outcome was the development of a care map using diagnostic procedures and interventions found in the professional literature and empirical data collected on site. A short pilot study revealed that a number of polydipsia patients on Clozaril along with other interventions were successfully discharged from the hospital.

Antipsychotic Agents↗

PubMed1996

Clozapine reduces water-drinking behavior in schizophrenic patients with polydipsia.

Disordered water balance, or polydipsia, is an underassessed and underreported phenomenon present in the severely psychiatrically disabled population. Prevalence rates for polydipsia range from 6.2 to 20%. We followed up five male patients (mean age 43) with chronic schizophrenia who met the Kane criteria for being treatment nonresponders and who, in addition, had marked polydipsia. Three patients had previously received medical care for hyponatremia and had to be placed on fluid restriction when admitted to the hospital. All patients exhibited polydipsia despite high doses of typical antipsychotic drugs. Each patient was treated openly with clozapine (range 450-800 mg/day) for at least 6 months. In each case, there was a decline in the Brief Psychiatric Rating Scale score (preclozapine mean, 63; postclozapine mean, 46), and a marked reduction in fluid-seeking behavior. All fluid restrictions could be lifted, and the patients were discharged from the hospital. During a mean follow-up period of 17 months, during which patients were evaluated weekly, polydipsic behavior that required intervention had not been noted. We conclude that clozapine may be a highly effective treatment for polydipsia in patients with treatment-refractory schizophrenia. Future studies may aim to delineate neurobiologic mechanisms.

Adult↗

PubMed1994

Polydipsia amongst adults with a learning disability in an institution.

A hospital-based adult learning disabled population (n = 371) was screened for polydipsia with the help of a purpose-designed questionnaire. Polydipsia was defined as excessive drinking of more than 3 l of non-alcoholic fluid over a 24-h period. Altogether, 23 (6.2%) subjects were found to have polydipsia. The polydipsic group was compared with the whole hospital population on variables such as age and IQ distribution. A matched group of 23 individuals without a history of polydipsia was drawn from the same hospital population. The polydipsic and the matched group were compared using various biochemical and psychological measures. Thirty-five per cent of polydipsic patients, compared to 13% of the matched group, showed evidence of compensated hyponatraemia. This difference was not significant. There was no significant difference between the polydipsic and the matched group in the frequency of psychiatric illness, behavioural problems or autism. There also was no significant difference in the IQ levels of the polydipsic patients and the total hospital population. Polydipsia in this population is largely seen as part of an abnormal behavioural repertoire without any evidence of possible organic cause, except unidentified diabetes mellitus. Klein Levin syndrome and pica were represented in the polydipsic group, but not amongst the matched group.

Adult↗

PubMed1988

Polydipsia and hyponatremia in psychiatric patients.

Many psychiatric patients have polydipsia and polyuria without identifiable underlying medical causes. Hyponatremia develops in some polydipsic patients and can progress to water intoxication with such symptoms as confusion, lethargy, psychosis, and seizures or death. This syndrome is sometimes called "compulsive water drinking," "psychogenic polydipsia," and "self-induced water intoxication." Although the underlying pathophysiology of the syndrome is unclear, several factors have been implicated in producing polydipsia and symptomatic hyponatremia. These include a possible hypothalamic defect, the syndrome of inappropriate secretion of ADH (SIADH), and neuroleptic medication. Evaluation of psychiatric patients with polydipsia includes a search for other medical causes of polydipsia, polyuria, hyponatremia, and SIADH. Treatment modalities currently available include fluid restriction and medications.

Adult↗

PubMed1996

Screening patients with mental retardation for polydipsia.

OBJECTIVES: To determine whether caregiver responses to a screening question are a reliable method of identifying polydipsia (excessive water drinking) in institutionalized residents with mental retardation. To review the etiology, acute and chronic clinical manifestations, and care of polydipsia and water intoxication. METHOD: This paper presents an assessment of interrater reliability for a screening question for polydipsia using responses of primary caregivers of preidentified polydipsia cases (n = 32) and matched controls (n = 33) in a large Canadian institution for developmentally handicapped adults. A chart review of all cases of identified water intoxication is also provided. The behavioural outcomes of preventive measures for water intoxication are described. RESULTS: The screening instrument was reliable, having a kappa (interrater reliability) of 0.73. Several case descriptions illustrate typical presentations of water intoxication in this population. CONCLUSIONS: Polydipsia is reliably identified by caregiver responses to a screening question. It should be screened for regularly to ensure appropriate care to prevent important acute and chronic complications.

Adult↗