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Polydipsia in the chronically mentally ill: A review
Polydipsiain the ChronicallyMentallyIlk A Review Mary Ann Boyd
Poiydipsia, or excessive intake of water, is reviewed in the chronicalty mentally P 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. 0 1990 by W.B. Saunders Company.
OLYDIPSIA, or the excessive intake of water, is thought to have relatively benign physiological effects on chronically mentally ill patients, but it can lead to water intoxication and a medical emergency. In hospitalized chronically mentally ill patients, once the volume of fluid increases in the body, and the physiological effects of polydipsia approach abnormal levels, clinical manifestations become obvious. In these patients, symptoms of excessive water ingestion seem to exacerbate the symptoms of their mental illness. By the time the symptoms of polydipsia become obvious, patients require close observation and are disruptive and difficult to manage. Vomiting, urine incontinence, and profuse perspiration may also occur, requiring increased nursing care. In all cases, patients must be restricted from further intake of water. The nursing care of these mentally ill patients presents special management problems related to the frequent intake of fluid and the accompanying psychological changes and physical responses to the increase in water volume. Water intoxication was first reported as a medical problem by Rowntree in 1923. He concluded that water intoxication occurred when water was
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From the School of Nursing, Southern Illinois University at Edwardsville. Address reprint requests to May Ann Boyd, R.N., Ph.D., D.N.S., Southern Illinois University, School of Nursing, Box 1066, Edwardsville, IL 62026-1066. 0 1990 by W.B. Saunders Company. 0883-9417/9oKI403-cOO2$3.0000/0
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ingested in excess of the ability of the organism to excrete it. He identified the symptoms of water intoxication, recognized that it could lead to death if not treated, and suggested that water intoxication was due, in part, to increased intracerebral pressure because of the disturbance of the salt water equilibrium. Intravenous hypertonic sodium chloride solution was recommended for treatment. He did not describe water intoxication in psychiatric patients. Barahal (1938) is credited with first reporting water intoxication in a psychiatric patient. He presented a case study of a female diagnosed with dementia praecox, paranoid type, who was admitted in a state of water intoxication, and described her acute state, including seizures and coma. Arieti (1944) linked the “placing into mouth” activity of schizophrenics to a ‘ ‘preterminal” stage and explained oral behavior in psychoanalytic terms. These ideas were further expanded by Leiken and Caplan (1967) who suggested that psychogenic polydipsia symbolically reestablished a symbiotic relationship with mother. The drinking phenomena that leads psychiatric patients to a state of water intoxication has been called by many names. Psychogenic polydipsia was initially used to describe excessive water ingestion leading to water intoxication in psychiatric patients (Carter & Robbin, 1947; Leiken & CapIan, 1967). The terms, primary polydipsia, compulsive water drinking, hyperdipsia, and hysterical polydipsia have also been used (Sahadevan & Bay-
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liss, 1965; Wyngaarden & Smith, 1985). Other terms commonly used to describe the phenomena of excessive water ingestion leading to a state of intoxication are self-induced water intoxication in schizophrenia (SIWIS) and self-induced water intoxication in psychosis (SIWIP). According to some authors, the term primary polydipsia should be used to describe abnormal drinking behavior caused by psychiatric or neurophysiological mechanisms in the absence of need for fluids and the term secondary polydipsia should be used to describe unusually large intake of water in response to increased need from abnormal loss (diabetes insipidus or mellitus) or other external causes of thirst such as dry mouth from medication (Johnson, Breshahan, & Chan, 1985). Vieweg et al. (1988) use the acronymn PIP (psychosis, intermittent hyponatremia, and polydipsia) to describe the syndrome of patients who characteristically reside in state mental hospitals and suffer complications including generalized seizures, coma, and death secondary to hyponatremia. The purpose of this article is to review the research related to excessive water ingestion or polydipsia in psychiatric patients, the magnitude and types of problems that these patients experience, and the treatment interventions reported, as well as to propose recommendations for practice and research. Most of the reported research was found in medical journals, with the exception of three nursing articles (Ashby, 1987; Prim, 1988; Watson, 1985). The review was undertaken in order to provide a background for further research into psychiatric patients’ behavioral and physical responses to excessive water ingestion. POLYDIPSIA IN PSYCHIATRIC PATIENTS
In 1979, Jose and Perez-Cruet suggested that the incidence of water intoxication may be higher than the literature has indicated. In a survey of 239 patients, they found that 16 (6.6%) had a consistent history of compulsive water drinking; of these, eight (3.3%) had symptoms of water intoxication. In a similar study in Japan (Okura & Morii, 1986), seven cases (3.1%) of compulsive water drinking including six cases of water intoxication among 225 inpatients of a public hospital were identified. Another study reported the prevalence of polydipsia to be 17.5% for 241 male patients hospitalized
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in a Veterans Administration facility (Blumm, Tempey, & Lynch, 1983). The prevalence of polydipsia in a state psychiatric system was reported as 6.2% by Evenson, Jos, and Mallya (1987). In this study, a total of 2,201 patients were evaluated for polydipsia, and 137 patients were identified. Of these patients, 32 met the criteria for the diagnosis of water intoxication in at least one instance. The variation in prevalence rates may be explained by the different methodologies used. For example, in the studies by Jose and Perez-Cruet ( 1979), Evenson et al. (1987), and Okura and Morii (1986) the subjects, who were known for their excessive water drinking, were identified by staff. Once identified, the patients’ medical records were reviewed for confirmation. In the study by Blum et al. (1983) all patients were screened and the inclusion criteria included urine-specific gravities. The higher rate (17.5%) in the latter study suggests that patients may be chronically polydipsic, but are not identified by staff. Therefore, the reported rate of polydipsia, according to several studies, varies from 3.1% to 17.5 % of hospitalized mentally ill patients in public facilities. If these prevalence rates are supported through additional studies, there could be anywhere from 16,000 to 92,OOtJstate and federal hospitalized patients who are excessive water drinkers (NIMH , 1987). Since the early 1940s several investigations have been concerned with categorizing polydipsia in psychiatric patients as a distinct illness. It was believed that the etiology of polydipsia in psychiatric patients was due to excessive water ingestion and that it was distinct from other illnesses with similar symptoms, specifically, diabetes insipidus (DI) and inappropriate secretion of antidiurectic hormone (SIADH). Both in patients with DI and in psychiatric patients with polydipsia, excessive volumes of oral fluid intake and of urine output and low urine osmolalities were observed. However, the serum sodium levels, osmolalities and blood urea nitrogen (BUN) levels were observed to be high in patients with DI and low in psychiatric patients with polydipsia. It was thought that the high levels in the patients with DI were due to excessive renal fluid loss and subsequent dehydration and the low levels in psychiatric patients due to extracellular fluid expansion. These effects in the psychiatric patients were thought to be due
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only to excessive ingestion of water (Bartter & Schwartz, 1967; Saruta et al., 1982). When psychiatric patients with polydipsia were compared with those diagnosed with SIADH, the serum sodium levels, osmolalities, and BUNS were low in both, but in SIADH the extracellular fluid expansion was thought to be due to excessive renal water retention and not to excessive oral water intake. Consequently, it was reasoned that the SIADH patient’s concentrated urine was due to inapproriately secreted antidiuretic hormone and the psychiatric patient’s dilute urine was due to high volume throughout (Mendelson & Deza, 1976). Early research supported this distinction. In 1947, Carter and Robbins found that urine responses to hypertonic saline infusions were normal in patients in whom an antidiuretic phenomenon was operating. They thought that hypertonic saline infusions followed by urine measurement would provide an objective means that would differentiate diabetes insipidus from psychogenic polydipsia. However, in this study, there were only three subjects with psychogenic polydipsia. Clinical differentiation of those with compulsive water drinking, diabetes insipidus, and renal disease was reported by Barlow and de Wardener (1958). They found that some psychiatric patients had abnormal antidiuretic hormone secretion, but were unable to clearly identify diagnostic differences in physiological functioning. They concluded that compulsive water drinking was “probable” if there was an absence of renal disease, if intermittent polydipsia and polyuria were occurring, if there were associated gross psychological disturbances, or if there was evidence of ADH secretion. Other investigations addressing pathophysiological differences among DI, SIADH, and polydipsia leading to water intoxication in psychiatric patients include Langgard and Smith (1962) and Sahadevan and Baylis (196% who presented evidence based on two psychiatric cases each that the etiology of the water intoxication seemed to be simply excessive water ingestion without any evidence of inappropriate release of ADH. However, later research findings have not supported clearcut distinctions between polydipsia in psychiatric patients and those with DI and SIADH. Diabetes insipidus and psychogenic polydipsia
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have been described as existing in a chronic schizophrenic patient (Fricchione, Kelleher, & Ayyala, 1987). There have been several reports of psychiatric patients who were diagnosed with SIADH that was associated with massive water ingestion, confusing the physiological distinction (Clinch, 1982; Dubovsky, Grabon, Berl, & Schrier, 1973; Emsley & Taljaard, 1987; Fowler, Kronfol, & Perry, 1977; Hobson & English, 1963; Husband, Mai, & Cam&hers, 1981; Kramer & Drake, 1983; Matuk & Kalyanaraman, 1977; Peck & Schenkman, 1979; Raskin, 1974; Raskind, Orenstein, & Christopher, 1975; Raskind, Weitzman, Orenstein, Fisher, & Courtney, 1977; Singh, Padi, Bullard, & Freeman, 1985; Vieweg, Rowe, David, Yank, & Spradlin, 1984; Vincent, 1977; Zubenko, Altesman, Cassidy, & Barreira, 1984). As a result of these studies, it has been suggested that impaired excretory mechanisms influenced by the antidiuretic hormone may also play a role in the psychogenesis of water intoxication of psychiatric patients. The investigations of Raskind et al. (1977) and of Emsley et al. (1989) lend support to this view. The antidiuretic hormone was positively correlated to the degree of psychosis in six psychotic subjects when compared with a control groups by Raskind et al. The Emsley group compared levels of plasma arginine vasopressin (the antidiuretic hormone), urine output, and osmolalities of 28 healthy volunteers with 23 unmedicated patients with schizophrenia or schizoaffective disorders. The results indicated that the psychotic patients excreted a significantly lower cumulative volume and had significantly higher minimum urine osmolalities than the healthy volunteers. On separating the patients according to duration of the current illness, those with a duration of less that 24 weeks showed the most pronounced antidiuretic state. Seven of the patients were above the 0.75 percentile of 1.40 pg/mL for baseline arginine vasopressin levels. They concluded that the possibility existed that there was enhanced renal sensitivity to the antidiuretic hormone, which may explain the antidiuretic state in these patients. Attempts at identifying demographic or treatment factors that may be associated with either excessive water ingestion or water intoxication have been largely unsuccessful. It was originally thought that water intoxication may occur more
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frequently in females (Roberge et al., 1984; Resnick & Patterson, 1969), however, recent studies show the prevalence to be only slightly higher in women (60%) than in men (Evenson et al., 1988). This may reflect the population distribution of the study rather than an increased prevalence in females. The highest reported prevalence of polydipsia in a psychiatric population (17.5%) was by Blum et al. (1983), whose study occurred in an allmale institution. Iatrogenic factors such as administration of psychotropic medication (Ajlouni, Kern, Tures, Theil, & Hagen, 1974; Beckstrom, Reding, & Cerletty, 1979; DeRivera, 1975; DeSoto, Griffith, & Katz, 1985; Dhar, Ramos, & Minot, 1978; Gipson & Price, 1978; Hamburger, Langley, & Bowers, 1980; Husband, Mai, & Carruthers, 1981; Langgard & Smith, 1962; Luzecky, Burman, & Schultz, 1974; Madhusoodanan & Osnos, 1981; Miller & Moses, 1975; Matuk & Kalyanaraman, 1977; Kosten & Camp, 1980; Palladino, 1986; Peck KzSchenkman, 1979; Peterson, Pollack, Mahoney, & Fuller, 1978; Rao, Martin, Watts, & Smith, 1975; Sandifer, 1983; Shah, Wig, & Chausbury, 1973; Solammadevi, 1981; Weitzel, Shraberg, & Work, 1980; White, 1975), withdrawal of psychotropic drugs (Shen & Sata, 1983; 1984), and electroconvulsive shock therapy (ECT) (Narang, Chaudhury, & Wig, 1973; Jos, Evenson, & Mallya, 1986; Shah, Wig, & Chausbury, 1973) have been implicated in excessive water ingestion. The drug and ECT studies, for the most part, examined the effect of a specific drug such as chlorpromazine and thiothixene on the antidiuretic hormone, arginine vasopressin (AVP). In most cases there was some effect. The problem is that the relationship between the antidiuretic hormone to excessive water ingestion and water intoxication in the psychiatric patients is not understood, therefore, any conclusions drawn regarding the relationship between psychotropic administration and excessive water ingestion have to be limited. When medications including thiothixene, lithium carbonante, chorpromazine, amitriptyline, fluphenazine, and haloperidol were withdrawn in the Shen and Sata study, the patients’ water drinking behavior became worse. Six patients received dosage reduction and five patients had episodes of compulsive water drinking occurring within a week following reduction of neuroleptic dosages. Six
episodes of compulsive drinking were stopped within 24 hours by doubling the dosage of the neuroleptic agent. This suggests that the illness itself may influence excessive water drinking and water intoxication. Cigarette consumption has not been shown to be related to water intoxication (Vieweg et al., 1986). Recently, alcohol abuse has been associated with water intoxication. According to Ripley, Millson, & Kocazpski, (1989) alcohol abuse was more common among 17 schizophrenic male inpatients with self-induced water intoxication than among 17 matched schizophrenic control inpatients. The alcohol abuse had begun 8 to 22 years before the diagnosis of water intoxication. In summary, the prevalence of polydipsia in psychiatric patients has been shown to be significant. Research has not differentiated polydipsia leading to water intoxication in psychiatric patients from the DI or SIADH. Investigations into the relationship of polydipsia in psychiatric patients to these other illness states will probably continue. Iatrogenic factors such as administration of psychotropic medication and reduction of medication have both been implicated in excessive water drinking. PATIENT RESPONSES TO EXCESSIVE WATER INGESTION
Nursing is concerned with the diagnosis and treatment of human responses to health or illness. For this discussion, the human responses of patients experiencing polydipsia and water intoxication problems are organized around excessive ingestion of water or fluids, excessive urinary excretion, cognitive functioning during episodes of polydipsia and water intoxication, and potential emergencies. EXCESSIVE WATER INTAKE
Water ingestion has been targeted as a behavior that is a problem for certain chronically mentally ill patients. Excessive consumption of water can lead to a medical emergency because it involves the rapid development of severe hypotonicity, which leads to the rapid expansion of the brain and increased intracranial pressure (Goldberg, 198 1). It was consistent in all reports that patients were drinking excessive water, and it is not unusual for patients to drink several gallons in 1 day. There seems to be a compulsive nature to the
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drinking of water, and at times, even an addictive quality to it. Prim (1988) describes a compulsive, repetitive nature to the water drinking behavior in a patient who made four to eight trips to the water fountain within 1 hour. Personal experience confirms her observation. It is not unusual for patients to return to a water fountain several times, even after reminders by the staff. This author has observed patients to be very creative in obtaining fluids, including drinking from showers, bathtubs, toilet bowls, and their own urine containers. Patients have not stopped drinking even when threatened with loss of privileges. However, there has been little in the literature investigating this drinking behavior. There have been no studies that examine the relationship of the polydipsic behavior to the severity of psychiatric illness. Descriptions of behavior associated with events leading up to a state of water intoxication in psychiatric patients have been limited. Most of the case studies were of patients who were admitted in a state of water intoxication. All reported excessive water ingestion as preceding the water intoxication state. In those articles in which patients offer an explanation for their drinking behavior, it has been described as a cleansing activity with religious significance (Rendell, Magrane, & Cuesta, 1978; Dubovsky, Grabon, Berl, & Shrier, 1973). For example, one woman reported that the water would purify her sinful thoughts and another patient said that it would make him a better Christian (Fowler, Kronfol, & Perry, 1977). One patient explained the drinking behavior as a way of cleansing the body, which suggests that the behavior has been incorporated into her delusional system. However, upon observation, many patients seem very much in contact with reality and do not exhibit this type of delusional thinking. EXCESSIVE URINATION
Excessive urination and abnormal volumes of urine have been noted in patients with chronic schizophrenia. In early literature, an abnormally high volume of urinary excretion and a largerthan-normal variation in the pattern of excretion in schizophrenic patients was reported by Hoskins (1933), Hoskins and Sleeper (1933) and Sleeper and Jellinek (1936), who also noted that the polyuric patients did not experience the emotional deterioration that was characteristic of the nonpolyuric patients. Emsley et al. (1989) found that
psychotic patients excreted lower cumulative volume than the healthy volunteers. Vieweg, Rowe, David, Cumow, and Spradlin (1984) reported that male patients with a specific gravity of greater than 1.003 predictibly excreted 2,800 to 28,000 mL of urine per day. They suggested that severe hyposthenuria (specific gravity of urine, 1.003 or less) may be a biological marker for a population at risk of developing water intoxication. These patients are often incontinent during the night, have frequent urination, and often urinate in socially unacceptable places, such as hallways and comers. When one patient was asked what the nursing staff could do to help him with his chronic drinking of water, he answered that a “rubber sheet” would help. Assessment of urinary output is difficult, if not impossible, because of the inability of many of the patients to comply with the collection procedures. Vieweg et al. (1984) suggested use of urinespecific gravities as a screening tool for potential water intoxication. COGNITIVE FUNCTIONING
Mental status of patients during periods of actual intoxication have been reported and relate to the reasons stated for the drinking of the fluids. Patients are confused, disoriented, sometimes delusional, and progress to apathy and lethargy as water intoxication becomes more severe. Most studies reported psychotic behavior and thinking as increasing in severity before patients were identified as being water intoxicated, but were not clear as to the relationship between the psychosis and intoxication. That is, did the psychosis precipitate the water intoxication or did the water intoxication precipitate the psychosis? Observation of two wards for the chronically mentally ill, where at least 30% of the 48 patients were seen by the staff as having a problem with excessive water intake, revealed that the disruptive behavior (including yelling, arguments with patients and staff, and inappropriate demands) usually occurred in the evening when there were fewer staff to cope with the disruptive behavior. Nursing management of these patients requires a larger number of staff than is usually allocated to a unit (Ashby, 1987). Observation of the patient for water intoxication requires frequent vital signs and often one-to-one observation. Once a patient is assessed as being water intoxicated, he or she may
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need to be transferred to a unit that is prepared for medical emergencies. There has been little research focusing on the cognitive aspect of psychiatric patients with polydipsia. Vieweg et al. (1984) attempted unsuccessfully to relate patients’ cognitive state as measured by the Folstein’s “mini-mental state’ ’ scores to serum sodium levels in hopes of being able to detect cognitive changes of patients approaching a state of intoxication. There is no indication in the literature of how patients explain their excessive drinking or whether it is possible to control their drinking behaviors through any cognitive restructuring . WATER INTOXICATION
Case reports have been useful in understanding the potential seriousness and clinical manifestations of water intoxication. Several case studies of psychiatric patients who became medical emergencies have been reported (Bewley, 1964; Chinn, 1974; Emsley & Taljaard, 1987; Fleischhacker, Barnas, & Ledochowski, 1987; Jos, 1984; Jose et al., 1980; Khamnei, 1983; Rae, 1976; Roberge et al., 1984). All of these case reports, with the exception of the Jos study, were of patients who were admitted in a state of intoxication, and the events leading up to their hospitalization had to be reconstructed from reports of family and friends. Jos documented that a patient had been observed drinking large amounts of water throughout the day and experienced a seizure at 3:40 p.m., suggesting that the excessive intake precipitated the intoxicated state. Vomiting followed and then another seizure at 6:30 p.m. The patients in these studies ranged in age from 19 to 53 years and represented both males and females. Most had been diagnosed with schizophrenia, but affective disorders and alcohol/drug abuse were also represented. All of the cases documented the physiological changes that occurred during acute water intoxication including seizures and low-serum sodium levels. Jose, Barton, and Perez-Cruet (1979) argued that general convulsions are the most common result of water intoxication. Other case studies of water intoxication have been reported in those who are developmentally disabled (Noonan & Ananth, 1977; McNally, Calamari, Hansen, & Kaliher, 1988) and who do not have any physical or psychiatric illness (Mellinger & Zafar, 1983).
Reports of death of psychiatric patients during an episode of water intoxication (Blotcky, Grossman, & Looney, 1980; Rendell et al., 1978; Raskind, 1974) further emphasize the potential threat to polydipsic patients. Vieweg, David, Rowe, Wampler, Bum, and Spradlin (1985) reported that of 60 patients who died before the age of 53 years in a state mental hospital, 27 patients had a schizophrenic disorder. Of those 27 patients, five ( 18.5%) died of complications of self-induced water intoxication. ASSESSMENT AND INTERVENTIONS
Measuring urine specific gravity as described by Vieweg et al. (1984) and weighing the patient as suggested by Goldman and Luchins (1987) are two nonintrusive, inexpensive interventions that may be used in assessing patients for polydipsia. These interventions are aimed at identifying an increase in fluid volume. However, the authors point out that even when used together, these methods do not identify all patients, because neither hyposthenuria nor significant weight change may be present at the time of the assessment. Treatment of water intoxication is a nursing and medical emergency. Watson (1985) outlined the nursing care of a patient in acute water intoxication. She presented a nursing care plan that identified 10 problems, from deteriorating conscious level as a result of cerebral edema, psychological problems of anxiety, and loss of privacy, to discharge planning. Sodium chloride, along with water restriction, was recommended for prevention of water intoxication (Vieweg, Rowe, David, & Spradlin, 1985). However, success with sodium chloride has been reported to be limited, because salt is rapidly lost in the urine, polyuria and hyposthenuria persist, and progressively higher doses of salt are required. Illowsky and Kirch (1988) do not recommend its use in preventing water intoxication. Medical treatment has focused on drug therapy in an attempt to stabilize serum sodium levels. Treating patients with lithium alone, and then in combination with phenytoin has been marginally successful (Vieweg et al., 1988). Demeclocycline has been reported to be successful in reducing the incidence of severe hyponatremic episodes in patients where there is mild impairment in urinary dilution (Forrest et al., 1978; Goldman & Luchins, 1985; Nixon, Rothman, & Chinn, 1982). Behavioral treatment has focused on preventing water
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intoxication of those with a known history of excessive water consumption by restricting access to water through behavior modification for a mentally retarded female (McNally, Calamari, Hansen, & Kaliher, 1988), operating a water intoxication ward designed for managing and monitoring water ingestion (Ashby, 1987) and developing individual care plans within the context of the Roy Adaptation Model (Prim, 1988). McNally et al. and Prim demonstrated success in single-case studies. Success was defined in both studies as reduction in water ingestion and in episodes of water intoxication. Ashby described the protocol that was used on the water intoxication ward, but did not report patient outcomes. A target weight procedure has been used for those patients with a history of water intoxication in an attempt to identify when water restriction is necessary. Goldman and Luchins (1987) and Delva and Crammer (1988) reported success in significantly decreasing the number of water intoxication episodes in patients by monitoring body weight and imposing water restriction when the body weight reaches 7% of a predetermined target weight for each patient. Koczapski et al. (1987) recommend that weight monitoring be used as a screening test to identify patients with subclinical disturbances in water metabolism who have not yet developed water intoxication. The one consistent intervention that is reported in the literature is restricting patients from drinking water. Common sense says that restricting water reduces the amount of fluid in the body, thereby reducing the likelihood of progressing to a water-intoxicated state. Through clinical experience, water restriction is easier said than done. Prim reported success with planning interventions by modifying a patient’s focal stimuli and providing structured activities in an attempt to divert a patient’s attention (1988). Many times staff resort to turning off the drinking fountains and locking bathrooms and showers in order to restrict access to water. Restricting access to water as an effective intervention should be investigated. RECOMMENDATIONS
FOR RESEARCH
AND PRACTICE
We know that water ingestion leading to water intoxication is a significant problem in chronic psychiatric patients and that it can lead to death. There is evidence that some chronically mentally ill patients excrete more urine than others and
some excrete less, that some drink excessive water, and in some of these patients there is an inappropriate secretion of the antidiuretic hormone, arginine vasopressin. It also has been observed that those patients who excrete more urine than others function at a higher level than those patients who do not. Water ingestion leading to water intoxication has been linked to psychiatric medications and their withdrawal, electroconvulsive therapy, psychosis, nicotine, and alcohol, but relationships have not been clearly established. Measuring urine-specific gravity and weighing patients have been suggested for screening. Interventions have focused on preventing patients from drinking to a state of water intoxication. Restricting water and monitoring body weight have been suggested. The drug, demeclocycline, is promising in the treatment of mild impairments of urinary dilution. There is much that is unknown about water ingestion leading to water intoxication. It is unclear how the patient experiences the apparent need to drink water. Is there truly an addictive nature to the behavior? If there is, how much control over water drinking can be expected of the patient? Can patients be expected to gain control over the need for water or does control need to be external? Why are the higher-functioning patients seemingly afflicted with excessive urination and need for water? Psychiatric nursing has not developed many interventions for care of these patients. There are several areas of research that need to be initiated regarding nursing care. Assessment factors, including physical and psychological ones, have not been identified. Nursing models that best explain the problems the patients experience and give direction for care have yet to be tested. Studies determining how the patient experiences the need to drink water and urinate should be explored. Most of the patient reports in the literature would suggest psychosis as an explanation of excessive water behavior. However, casual observation of patients drinking water indicates that most of the patients are not blatantly psychotic while drinking water. Future research and practice should focus on understanding the patients’ experience of polydipsia and how it relates to the patients’ level of functioning. Nursing needs to test various assessments in order to determine appropriate interventions. Acuity of nursing care needs to be addressed in terms of the nursing assignments. More is unknown about water ingestion leading to water in-
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toxication in psychiatric patients than is known. Research is sorely needed to increase the knowledge base for practice. REFERENCES Ajlouni, K., Kern, M., Tures, J., Theil, G., & Hagen, T. ( 1974). Thiothixene-induced hyponatremia. Archives of Internal Medicine, l34(12), 1103-l 105. Arieti. S. (1945). Primitive habits in the preterminal stage of schizophrenia. The Journal of Nervous and Mental Disease, 102, 367-375.
Ashby, Y. (1987). Planned change: The development of a program for the management of self-induced water intoxication. Canadian Journal of Psychiatric Nursing, 28(l),
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Barahal, H. (1938). Water intoxication in a mental case. Psychiatric Quarterly, 12. 767-771.
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Bewley, T (1964). Acute water intoxication from compulsive water drinking. British Medical Journal, 2, 864. Blotcky, M., Grossman, I., & Looney, J. (1980). Psychogenic water intoxication: A fatality. Texas Medicine, 76(l), 58-59.
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Emsley, R., & Taljaard, J. (1987). Self-induced water intoxication: A case report. South African Medical Journal, 74(2), 80-81.
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Fleischacker, W., Barnas, C., & Ledochowski, M. (1987). Hyponatremia-induced organic mental disorder may mask paranoid schizophrenia. Biological Psychiatry. 22, 650-652.
Forrest, J., Colx, J.. Hong, C., Morrison, G., Bia, M., & Singer, I. (1978). Superiority of demeclocycline over lithium in the treatment of chronic syndrome of inappropriate secretion of antidiuretic hormone. New England Journal of Medicine, 298(4), 173-177. Fowler, R., Kronfol, Z., & Perry, P. (1977). Water intoxication, psychosis, and inappropriate secretion of antidiuretic hormone. Archives of General Psychiatry, 34. 1097-1099.
Fricchione. G., Kelleher, S., & Ayyala, M. (1987). Coexisting central diabetes insipidus and psychogenic polydipsia. Journal of Clinical Psychiatry, 48(2), 75-76.
Gipson, W., & Price, T. (1978). Inappropriate ADH in a psychiatric setting. Psychiatric Opinion, 15, 43-46. Goldberg, M. (1981). Hyponatremia. Medical Clinics of North America, 65(2), 251-269.
Goldman, M., & Luchins, D. (1985). Demeclocycline improves hyponatremia in chronic schizophrenics. Biological Psychiatry, 20, 1149-1155 Goldman, M., & Luchins, D. (1987). Prevention of episodic water intoxication with target weight procedure. America Journal of Psychiatry, 144(3), 365-366.
Hamburger, L., Langley, H., & Bowers, G. (1980). The syndrome of inappropriate secretion of antidiuretic hormone associated with amitriptyline or trifluoperazine administration. Journal of Kansas Medical Society, 81, 469-470.
Hobson, J., & English, J. (1963). Self-induced water intoxication: Case study of a chronically schizophrenic patient with physiological evidence of water retention due to inappropriate release of antidiuretic hormone. Annals of Internal Medicine, 58, 324-332.
Hoskins, R., & Sleeper, F. (1933). Organic function in schizophrenia. Archives of Neurological Psychiatry, 30. 123140.
Hoskins, R. (1933). Schizophrenia from the physiological point of view. Annals of Internal Medicine, 7, 445-456. Husband, D., Mai, F., & Carruthers, G. (1981). Syndrome of inappropriate secretion of antidiuretic hormone in a patient treated with haloperidol. Canada Journal of Psychiatry, 26, 196-197.
Illowsky, B., & Kirch, D. (1988). Polydipsia and hyponatremia in psychiatric patients. American Journal of Psychiatry, 145(6), 675-683.
Johnson, R., Breshahan. D., & Chan, C. (1985). Polydipsia in
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psychiatric patients. (letter) American Journal of Psychiatry, 1#2(7), 885.
JOS, C. (1984). Generalized seizures from self-induced water intoxication. Psychosomatics, 25(2), 153-157. Jos, C., Evenson, R., & Mallya, A. (1986). Self-induced water intoxication: A comparison of 34 cases with matched controls. Journal of Clinical Psychiany, 47(7), 368370.
Jose, C., Barton, J., & Perez-Cruet, J. (1979). Hyponatremic seizures in psychiatric patients. Biologica Psychiatry, 14(5), 839-843.
Jose, C. & Evenson, R. (1980). Antecedents of self-induced water intoxication. The Journal of Nervous and Mental Disease, 168(8), 498-500.
Jose, C., & Perez-Cruet, J. (1979). Incidence and morbidity of self-induced water intoxication in state mental hospital patients. American Journal of Psychiatry, 136(2), 221222.
Khamnei, A. (1983). Acute water intoxication from compulsive water drinking. IRSC Journal of Medical Science, 11, 520.
Koczapski, A., Ibraheem, S., Ashby, Y., Paredes, J., Jones, B., & Ancill, R. (1987). Early diagnosis of water intoxication by monitoring diurnal variations in body weight. American Journal of Psychiatry, 144(12), p. 1626. Kosten, T., & Camp, W. (1980). Inappropriate secretion of antidiuretic hormone in a patient receiving piperazine phenothiazines. Psychosomatics. 21, 35 l-355. Kramer, D., &Drake, M. (1983). Acute psychosis, polydipsia, and inappropriate secretion of antidiuretic hormone. The American Journal of Medicine, 75, 712-14. Langgard, J., & Smith, 0. (1962). Self-induced water intoxication without predisposing illness. New England Jourwl of Medicine, 266(8), 378-38 1. Leiken, S., & Caplan, H. (1967). Psychogenic polydipsia. American Journal of Psychiatry, 123(12), 1573-1576.
Luzecky, M., Burman, K., & Schultz, E. (1974). The syndrome of inappropriate secretion of antidiuretic hormone associated with amitriptyline administration. Southern Medical Journal, 67(4), 495-497.
Madhusoodanan, & Osnos, R. (1981). Amitriptyline-induced hyponatremia: A case report. Mr. Sinai Journal of Medicine, 18, 431-433. Martin, D., Watts, H., & Smith, L. (1975). Inappropriate antidiuretic hormone secretion. Western Journal of Medicine, 122, 145-149.
Matuk, F., & Kalyanaraman, D. (1977). Syndrome of inappropriate antidiuretic hormone in patients treated with psychotherapeutic drugs. Archives of Neurology, 34, 374-75.
McNally, R., Calamari, J., Hansen, P., 8~Kaliher, C. (1988). Behavioral treatment of psychogenic polydipsia. Journal of Behavior Therapy and Experimenral Psychiatry, 19(l), 57-61.
Mellmger, R., & Zafar, S. (1983). Primary polydipsia. Archives of Internal Medicine, 143, 1249- 125 1. Mendelson, W., & Deza,P. (1976). Polydipsia, hyponatremia, and seizures in psychotic patients. The Journal of Nervous and Mental Disease, 162(2), 140-143.
Miller, M., Moses, A., & Rao, S. (1975). Water intoxication
and thioridazine (Mellaril). Annals of Infernal Medicine, 82, p. 852. National Institute of Mental Health. (1987). Menral Health, United States, 1987. Washington, DC: Author, p. 76. Namng, R., Cbaudhury, R., & Wig, N. (1973). Effect of electmconvulsive therapy on the antidiuretic hormone level in the plasma of schizophrenic patients. Indian Journal of Medical Research, 61(5), 766-770.
Nixon, R., Rothman, J., & Chin, W. (1982). Demeclocycline in the prophylaxis of self-induced water intoxication. American Journal of Psychiatry, 139(6), 828-830.
Noonan, J., & Ananth, J. (1977). Compulsive water drinking and water intoxication. Comprehensive Psychiatry, 18(2), 183-187.
Okura, M., & Morii, S. (1986). Polydipsia, polyuria, and water intoxication observed in psychiatric inpatients. Tokushima Journal of Experimental Medicine, 33. l-5. Palladino, A. (1986). Hyponatremia associated with carbamazepine therapy. American Journal of Psychiatry, 143(9), 1190. Peck, P., & Schenkman, L. (1979). Haloperidol-induced syndrome of inappropriate secretion of antidiuretic hormone. Clinical Pharmacological Therapy, 26, 442-444. Peterson, J., Pollack, R., Mahoney, J., & Fuller, T. (1978). Inappropriate antidiuretic hormone in patients treated with psychotropic drugs. Archives of Neurology, 34(14), 374-375.
Prim, R. (1988). Water intoxication and psychosis syndrome. Journal of Psychosocial Nursing, 26( 11). 16-18. Rae, J. (1976). Self-induced water intoxication in a schizophrenic patient. Canadian Medical Association Journal, 114, p. 438. Rao, K., Miller, M., & Moses, A. (1975). Water intoxication and tbioridazine. Annals of Inrernal Medicine, 82, p. 61. Raskind, M. (1974). Psychosis, polydipsia, and water intoxication. Archives of General Psychiarry, 30, 112-l 14. Raskind, M., Orenstein, H., & Christopher, T. (1975). Acute psychosis, increased water ingestion, and inappropriate antidiuretic hormone secretion. American Journal of Psychiatry, 132, 907-910.
Raskind, M., Weitzman, R., Orenstein, H., Fisher, D., & Courtney, N. (1977). Is antidiuretic hormone elevated in psychosis? A pilot study. Biological Psychiatry, 13(3), 385-390.
Rendell, M., McGrane, D., & Cuesta, M. (1978). Fatal compulsive water drinking. Journal of rhe American Medical Association, 240, 2557.
Resnick, M., & Patterson, C. (1969). Coma and convulsion due to compulsive water drinking. Neurology, 19, 1125-1126.
Ripley, T., Millson, R., & Koczapski, A. (1989). Self-induced water intoxication and alcohol abuse. American Journal of Psychiatry, 146(l),
102-103.
Roberge, R., Gemsheimer, J., Sparano, R., Tartakoff, R., Morgerstem, M., Rubin, K., Senekjian, D., Andrade, R., & Mattber, V. (1984). Psychogenic polydipsia: An unusual cause of hyponatremic coma and seizure. Annals of Emergency Medicine, 13(4), 274-276.
Rowntree, L. (1923). Water intoxication. Archives of Internal Medicine, 32, 157-174.
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POLYDIPSIA Sahadevan, M., & Bayliss, V. (1965). Compulsive water drinking. A report of two cases. Journal of Association of Physician India, 13, 755-757.
Saruta, T.. Fujimaki, M., Ogihara, T., Saito, 11,Konishi, K., & Kondo, K. (1982). Evaluation of the reninangiotension system in diabetes insipidus and psychogenic polydipsia. Nephron, 132, 14-17. Sandifer, M. (1983). Hyponatremia due to psychotropic drugs. Journal of Clinical Psychiatry, 44, 301-303.
Shah, D., Wig, N., & Chausbury, R. (1973). Antidiuretic hormone levels in patients with weight gain after chlorpromazine therapy. Indian Journal of Medical Research, 61(S), 711-176.
Shen, W., & Sata, L. (1984). Self-induced water intoxication and hyper-dopaminergic state. (letter) American Journal of Psychiatry, 141(10), 1305-1306. Shen, W., & Sata, L. (1983). Hypothalamic dopamine receptor supersensitivity? A pilot study of self-induced water intoxication The Psychiatric Journal of the University of Ottawa, 8(3), 154-158.
Sheritz, S., Jameison, R., Petrie, W., and Crook, J. (1980). Compulsive water drinking treated with high dose propranolol. The Journal of Nervous and Mental Health, 168(4), 246-248.
Singh, S., Padi, M., Bullard, H., & Freeman, H. (1985). Water intoxication in psychiatric patients. British Journal of Psychiatry. 146, 127-131. Sleeper, F., & Jellinek, E. (1936). A comparative physiologic, psychologic, and psychiatric study of polyuric and nonpolyuric schizophrenic patients. The Journal of Nervous and Mental Disease, 83, 557-563.
Solammadevi, S. (1981). Inappropriate antidiureses during amitriptyline therapy. Southern Medical Journal, 74, 775776.
Vieweg, W., David, J., Rowe, W., Peach, M., Veldhuis, F., & Spradlin, W. (1986). Correlation of cigarette-induced increase in serum nicotine levels with arginine vasopressin concentrations in the Syndrome of Self-Induced Water Intoxication and Psychosis (SIWIP). Canadian Journal of Psychiatry, 31(2), 108-l 11. Vieweg, W., David, J., Rowe, W., Wampler, G., Bums, W., & Spradlin, W. (1985). Death from self-induced water
intoxication among patients with schizophrenic disorders. The Journal of Nervous and Mental Disease, 173(3), 161-165.
Vieweg, W., Rowe, W., David, J., Cumow, R., & Spradlin, W. (1984). Patterns of urinary excretion among patients with self-induced water intoxication and psychosis. Psychiatry Research. 15, 71-79.
Vieweg, W., Rowe, W., David, J., & Spradlin, W. (1985). Oral sodium chloride in the management of schizophrenic patients with self-induced water intoxication. Journal of Clinical Psychiatry, 46(l), 16- 19. Vieweg, W., Rowe, W., David, J., Yank, G., & Spradlin, W. (1984). The “mini-mental state” examination in the syndrome of self-induced water intoxication and schizophrenic disorders (SIWIS): A pilot study. International Journal of Psychiatry in Medicine, 14(4), 347-359.
Vieweg, W., Weiss, N., David, J., Rowe, W., Godleski, L., & Spradlin, W. (1988). Treatment of psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) using lithium and phenytoin. Biological Psychiatry, 23, 25-30.
Vincent, F. (1977). Inappropriate ADH secretion (letter). Archives of Neurology, 34, 725.
Watson. M.S. (1985). Water intoxication. Nursiq Times, ( I), 40-42.
Weitzel, W., Shraberg, D., & Work, J. (1980). Inappropriate ADH secretion: The role of drug rechallenge. Psychosomatics, 21(9), 711-179. White, M., & Fetner, C. (1975). Treatment of syndrome of inappropriate secretion of antidiuretic hormone with lithium carbonate. New England Journal of Medicine, 293, 390-392.
Wyngaarden, J., & Smith, L. (Eds.). (1985). Cecil textbook of medicine. Philadelphia, PA: W.B. Saunders. Zerbe, R., Stropes, L., & Robertson, G. (1980). Vasoptessin function in the syndrome of inappropriate antidiuresis. Annual Review of Medicine, 31 I 315-327.
Zubenko. G.. Altesman, R., Cassidy, J., & Barreira, P. ( 1984). Disturbances of thirst and water homeostasis in patients with affective illness. American Journal of Psychiatry. 141(3), 436-437.
Poiydipsia, or excessive intake of water, is reviewed in the chronicalty mentally P 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. 0 1990 by W.B. Saunders Company.
OLYDIPSIA, or the excessive intake of water, is thought to have relatively benign physiological effects on chronically mentally ill patients, but it can lead to water intoxication and a medical emergency. In hospitalized chronically mentally ill patients, once the volume of fluid increases in the body, and the physiological effects of polydipsia approach abnormal levels, clinical manifestations become obvious. In these patients, symptoms of excessive water ingestion seem to exacerbate the symptoms of their mental illness. By the time the symptoms of polydipsia become obvious, patients require close observation and are disruptive and difficult to manage. Vomiting, urine incontinence, and profuse perspiration may also occur, requiring increased nursing care. In all cases, patients must be restricted from further intake of water. The nursing care of these mentally ill patients presents special management problems related to the frequent intake of fluid and the accompanying psychological changes and physical responses to the increase in water volume. Water intoxication was first reported as a medical problem by Rowntree in 1923. He concluded that water intoxication occurred when water was
P
From the School of Nursing, Southern Illinois University at Edwardsville. Address reprint requests to May Ann Boyd, R.N., Ph.D., D.N.S., Southern Illinois University, School of Nursing, Box 1066, Edwardsville, IL 62026-1066. 0 1990 by W.B. Saunders Company. 0883-9417/9oKI403-cOO2$3.0000/0
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ingested in excess of the ability of the organism to excrete it. He identified the symptoms of water intoxication, recognized that it could lead to death if not treated, and suggested that water intoxication was due, in part, to increased intracerebral pressure because of the disturbance of the salt water equilibrium. Intravenous hypertonic sodium chloride solution was recommended for treatment. He did not describe water intoxication in psychiatric patients. Barahal (1938) is credited with first reporting water intoxication in a psychiatric patient. He presented a case study of a female diagnosed with dementia praecox, paranoid type, who was admitted in a state of water intoxication, and described her acute state, including seizures and coma. Arieti (1944) linked the “placing into mouth” activity of schizophrenics to a ‘ ‘preterminal” stage and explained oral behavior in psychoanalytic terms. These ideas were further expanded by Leiken and Caplan (1967) who suggested that psychogenic polydipsia symbolically reestablished a symbiotic relationship with mother. The drinking phenomena that leads psychiatric patients to a state of water intoxication has been called by many names. Psychogenic polydipsia was initially used to describe excessive water ingestion leading to water intoxication in psychiatric patients (Carter & Robbin, 1947; Leiken & CapIan, 1967). The terms, primary polydipsia, compulsive water drinking, hyperdipsia, and hysterical polydipsia have also been used (Sahadevan & Bay-
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liss, 1965; Wyngaarden & Smith, 1985). Other terms commonly used to describe the phenomena of excessive water ingestion leading to a state of intoxication are self-induced water intoxication in schizophrenia (SIWIS) and self-induced water intoxication in psychosis (SIWIP). According to some authors, the term primary polydipsia should be used to describe abnormal drinking behavior caused by psychiatric or neurophysiological mechanisms in the absence of need for fluids and the term secondary polydipsia should be used to describe unusually large intake of water in response to increased need from abnormal loss (diabetes insipidus or mellitus) or other external causes of thirst such as dry mouth from medication (Johnson, Breshahan, & Chan, 1985). Vieweg et al. (1988) use the acronymn PIP (psychosis, intermittent hyponatremia, and polydipsia) to describe the syndrome of patients who characteristically reside in state mental hospitals and suffer complications including generalized seizures, coma, and death secondary to hyponatremia. The purpose of this article is to review the research related to excessive water ingestion or polydipsia in psychiatric patients, the magnitude and types of problems that these patients experience, and the treatment interventions reported, as well as to propose recommendations for practice and research. Most of the reported research was found in medical journals, with the exception of three nursing articles (Ashby, 1987; Prim, 1988; Watson, 1985). The review was undertaken in order to provide a background for further research into psychiatric patients’ behavioral and physical responses to excessive water ingestion. POLYDIPSIA IN PSYCHIATRIC PATIENTS
In 1979, Jose and Perez-Cruet suggested that the incidence of water intoxication may be higher than the literature has indicated. In a survey of 239 patients, they found that 16 (6.6%) had a consistent history of compulsive water drinking; of these, eight (3.3%) had symptoms of water intoxication. In a similar study in Japan (Okura & Morii, 1986), seven cases (3.1%) of compulsive water drinking including six cases of water intoxication among 225 inpatients of a public hospital were identified. Another study reported the prevalence of polydipsia to be 17.5% for 241 male patients hospitalized
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in a Veterans Administration facility (Blumm, Tempey, & Lynch, 1983). The prevalence of polydipsia in a state psychiatric system was reported as 6.2% by Evenson, Jos, and Mallya (1987). In this study, a total of 2,201 patients were evaluated for polydipsia, and 137 patients were identified. Of these patients, 32 met the criteria for the diagnosis of water intoxication in at least one instance. The variation in prevalence rates may be explained by the different methodologies used. For example, in the studies by Jose and Perez-Cruet ( 1979), Evenson et al. (1987), and Okura and Morii (1986) the subjects, who were known for their excessive water drinking, were identified by staff. Once identified, the patients’ medical records were reviewed for confirmation. In the study by Blum et al. (1983) all patients were screened and the inclusion criteria included urine-specific gravities. The higher rate (17.5%) in the latter study suggests that patients may be chronically polydipsic, but are not identified by staff. Therefore, the reported rate of polydipsia, according to several studies, varies from 3.1% to 17.5 % of hospitalized mentally ill patients in public facilities. If these prevalence rates are supported through additional studies, there could be anywhere from 16,000 to 92,OOtJstate and federal hospitalized patients who are excessive water drinkers (NIMH , 1987). Since the early 1940s several investigations have been concerned with categorizing polydipsia in psychiatric patients as a distinct illness. It was believed that the etiology of polydipsia in psychiatric patients was due to excessive water ingestion and that it was distinct from other illnesses with similar symptoms, specifically, diabetes insipidus (DI) and inappropriate secretion of antidiurectic hormone (SIADH). Both in patients with DI and in psychiatric patients with polydipsia, excessive volumes of oral fluid intake and of urine output and low urine osmolalities were observed. However, the serum sodium levels, osmolalities and blood urea nitrogen (BUN) levels were observed to be high in patients with DI and low in psychiatric patients with polydipsia. It was thought that the high levels in the patients with DI were due to excessive renal fluid loss and subsequent dehydration and the low levels in psychiatric patients due to extracellular fluid expansion. These effects in the psychiatric patients were thought to be due
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only to excessive ingestion of water (Bartter & Schwartz, 1967; Saruta et al., 1982). When psychiatric patients with polydipsia were compared with those diagnosed with SIADH, the serum sodium levels, osmolalities, and BUNS were low in both, but in SIADH the extracellular fluid expansion was thought to be due to excessive renal water retention and not to excessive oral water intake. Consequently, it was reasoned that the SIADH patient’s concentrated urine was due to inapproriately secreted antidiuretic hormone and the psychiatric patient’s dilute urine was due to high volume throughout (Mendelson & Deza, 1976). Early research supported this distinction. In 1947, Carter and Robbins found that urine responses to hypertonic saline infusions were normal in patients in whom an antidiuretic phenomenon was operating. They thought that hypertonic saline infusions followed by urine measurement would provide an objective means that would differentiate diabetes insipidus from psychogenic polydipsia. However, in this study, there were only three subjects with psychogenic polydipsia. Clinical differentiation of those with compulsive water drinking, diabetes insipidus, and renal disease was reported by Barlow and de Wardener (1958). They found that some psychiatric patients had abnormal antidiuretic hormone secretion, but were unable to clearly identify diagnostic differences in physiological functioning. They concluded that compulsive water drinking was “probable” if there was an absence of renal disease, if intermittent polydipsia and polyuria were occurring, if there were associated gross psychological disturbances, or if there was evidence of ADH secretion. Other investigations addressing pathophysiological differences among DI, SIADH, and polydipsia leading to water intoxication in psychiatric patients include Langgard and Smith (1962) and Sahadevan and Baylis (196% who presented evidence based on two psychiatric cases each that the etiology of the water intoxication seemed to be simply excessive water ingestion without any evidence of inappropriate release of ADH. However, later research findings have not supported clearcut distinctions between polydipsia in psychiatric patients and those with DI and SIADH. Diabetes insipidus and psychogenic polydipsia
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have been described as existing in a chronic schizophrenic patient (Fricchione, Kelleher, & Ayyala, 1987). There have been several reports of psychiatric patients who were diagnosed with SIADH that was associated with massive water ingestion, confusing the physiological distinction (Clinch, 1982; Dubovsky, Grabon, Berl, & Schrier, 1973; Emsley & Taljaard, 1987; Fowler, Kronfol, & Perry, 1977; Hobson & English, 1963; Husband, Mai, & Cam&hers, 1981; Kramer & Drake, 1983; Matuk & Kalyanaraman, 1977; Peck & Schenkman, 1979; Raskin, 1974; Raskind, Orenstein, & Christopher, 1975; Raskind, Weitzman, Orenstein, Fisher, & Courtney, 1977; Singh, Padi, Bullard, & Freeman, 1985; Vieweg, Rowe, David, Yank, & Spradlin, 1984; Vincent, 1977; Zubenko, Altesman, Cassidy, & Barreira, 1984). As a result of these studies, it has been suggested that impaired excretory mechanisms influenced by the antidiuretic hormone may also play a role in the psychogenesis of water intoxication of psychiatric patients. The investigations of Raskind et al. (1977) and of Emsley et al. (1989) lend support to this view. The antidiuretic hormone was positively correlated to the degree of psychosis in six psychotic subjects when compared with a control groups by Raskind et al. The Emsley group compared levels of plasma arginine vasopressin (the antidiuretic hormone), urine output, and osmolalities of 28 healthy volunteers with 23 unmedicated patients with schizophrenia or schizoaffective disorders. The results indicated that the psychotic patients excreted a significantly lower cumulative volume and had significantly higher minimum urine osmolalities than the healthy volunteers. On separating the patients according to duration of the current illness, those with a duration of less that 24 weeks showed the most pronounced antidiuretic state. Seven of the patients were above the 0.75 percentile of 1.40 pg/mL for baseline arginine vasopressin levels. They concluded that the possibility existed that there was enhanced renal sensitivity to the antidiuretic hormone, which may explain the antidiuretic state in these patients. Attempts at identifying demographic or treatment factors that may be associated with either excessive water ingestion or water intoxication have been largely unsuccessful. It was originally thought that water intoxication may occur more
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frequently in females (Roberge et al., 1984; Resnick & Patterson, 1969), however, recent studies show the prevalence to be only slightly higher in women (60%) than in men (Evenson et al., 1988). This may reflect the population distribution of the study rather than an increased prevalence in females. The highest reported prevalence of polydipsia in a psychiatric population (17.5%) was by Blum et al. (1983), whose study occurred in an allmale institution. Iatrogenic factors such as administration of psychotropic medication (Ajlouni, Kern, Tures, Theil, & Hagen, 1974; Beckstrom, Reding, & Cerletty, 1979; DeRivera, 1975; DeSoto, Griffith, & Katz, 1985; Dhar, Ramos, & Minot, 1978; Gipson & Price, 1978; Hamburger, Langley, & Bowers, 1980; Husband, Mai, & Carruthers, 1981; Langgard & Smith, 1962; Luzecky, Burman, & Schultz, 1974; Madhusoodanan & Osnos, 1981; Miller & Moses, 1975; Matuk & Kalyanaraman, 1977; Kosten & Camp, 1980; Palladino, 1986; Peck KzSchenkman, 1979; Peterson, Pollack, Mahoney, & Fuller, 1978; Rao, Martin, Watts, & Smith, 1975; Sandifer, 1983; Shah, Wig, & Chausbury, 1973; Solammadevi, 1981; Weitzel, Shraberg, & Work, 1980; White, 1975), withdrawal of psychotropic drugs (Shen & Sata, 1983; 1984), and electroconvulsive shock therapy (ECT) (Narang, Chaudhury, & Wig, 1973; Jos, Evenson, & Mallya, 1986; Shah, Wig, & Chausbury, 1973) have been implicated in excessive water ingestion. The drug and ECT studies, for the most part, examined the effect of a specific drug such as chlorpromazine and thiothixene on the antidiuretic hormone, arginine vasopressin (AVP). In most cases there was some effect. The problem is that the relationship between the antidiuretic hormone to excessive water ingestion and water intoxication in the psychiatric patients is not understood, therefore, any conclusions drawn regarding the relationship between psychotropic administration and excessive water ingestion have to be limited. When medications including thiothixene, lithium carbonante, chorpromazine, amitriptyline, fluphenazine, and haloperidol were withdrawn in the Shen and Sata study, the patients’ water drinking behavior became worse. Six patients received dosage reduction and five patients had episodes of compulsive water drinking occurring within a week following reduction of neuroleptic dosages. Six
episodes of compulsive drinking were stopped within 24 hours by doubling the dosage of the neuroleptic agent. This suggests that the illness itself may influence excessive water drinking and water intoxication. Cigarette consumption has not been shown to be related to water intoxication (Vieweg et al., 1986). Recently, alcohol abuse has been associated with water intoxication. According to Ripley, Millson, & Kocazpski, (1989) alcohol abuse was more common among 17 schizophrenic male inpatients with self-induced water intoxication than among 17 matched schizophrenic control inpatients. The alcohol abuse had begun 8 to 22 years before the diagnosis of water intoxication. In summary, the prevalence of polydipsia in psychiatric patients has been shown to be significant. Research has not differentiated polydipsia leading to water intoxication in psychiatric patients from the DI or SIADH. Investigations into the relationship of polydipsia in psychiatric patients to these other illness states will probably continue. Iatrogenic factors such as administration of psychotropic medication and reduction of medication have both been implicated in excessive water drinking. PATIENT RESPONSES TO EXCESSIVE WATER INGESTION
Nursing is concerned with the diagnosis and treatment of human responses to health or illness. For this discussion, the human responses of patients experiencing polydipsia and water intoxication problems are organized around excessive ingestion of water or fluids, excessive urinary excretion, cognitive functioning during episodes of polydipsia and water intoxication, and potential emergencies. EXCESSIVE WATER INTAKE
Water ingestion has been targeted as a behavior that is a problem for certain chronically mentally ill patients. Excessive consumption of water can lead to a medical emergency because it involves the rapid development of severe hypotonicity, which leads to the rapid expansion of the brain and increased intracranial pressure (Goldberg, 198 1). It was consistent in all reports that patients were drinking excessive water, and it is not unusual for patients to drink several gallons in 1 day. There seems to be a compulsive nature to the
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drinking of water, and at times, even an addictive quality to it. Prim (1988) describes a compulsive, repetitive nature to the water drinking behavior in a patient who made four to eight trips to the water fountain within 1 hour. Personal experience confirms her observation. It is not unusual for patients to return to a water fountain several times, even after reminders by the staff. This author has observed patients to be very creative in obtaining fluids, including drinking from showers, bathtubs, toilet bowls, and their own urine containers. Patients have not stopped drinking even when threatened with loss of privileges. However, there has been little in the literature investigating this drinking behavior. There have been no studies that examine the relationship of the polydipsic behavior to the severity of psychiatric illness. Descriptions of behavior associated with events leading up to a state of water intoxication in psychiatric patients have been limited. Most of the case studies were of patients who were admitted in a state of water intoxication. All reported excessive water ingestion as preceding the water intoxication state. In those articles in which patients offer an explanation for their drinking behavior, it has been described as a cleansing activity with religious significance (Rendell, Magrane, & Cuesta, 1978; Dubovsky, Grabon, Berl, & Shrier, 1973). For example, one woman reported that the water would purify her sinful thoughts and another patient said that it would make him a better Christian (Fowler, Kronfol, & Perry, 1977). One patient explained the drinking behavior as a way of cleansing the body, which suggests that the behavior has been incorporated into her delusional system. However, upon observation, many patients seem very much in contact with reality and do not exhibit this type of delusional thinking. EXCESSIVE URINATION
Excessive urination and abnormal volumes of urine have been noted in patients with chronic schizophrenia. In early literature, an abnormally high volume of urinary excretion and a largerthan-normal variation in the pattern of excretion in schizophrenic patients was reported by Hoskins (1933), Hoskins and Sleeper (1933) and Sleeper and Jellinek (1936), who also noted that the polyuric patients did not experience the emotional deterioration that was characteristic of the nonpolyuric patients. Emsley et al. (1989) found that
psychotic patients excreted lower cumulative volume than the healthy volunteers. Vieweg, Rowe, David, Cumow, and Spradlin (1984) reported that male patients with a specific gravity of greater than 1.003 predictibly excreted 2,800 to 28,000 mL of urine per day. They suggested that severe hyposthenuria (specific gravity of urine, 1.003 or less) may be a biological marker for a population at risk of developing water intoxication. These patients are often incontinent during the night, have frequent urination, and often urinate in socially unacceptable places, such as hallways and comers. When one patient was asked what the nursing staff could do to help him with his chronic drinking of water, he answered that a “rubber sheet” would help. Assessment of urinary output is difficult, if not impossible, because of the inability of many of the patients to comply with the collection procedures. Vieweg et al. (1984) suggested use of urinespecific gravities as a screening tool for potential water intoxication. COGNITIVE FUNCTIONING
Mental status of patients during periods of actual intoxication have been reported and relate to the reasons stated for the drinking of the fluids. Patients are confused, disoriented, sometimes delusional, and progress to apathy and lethargy as water intoxication becomes more severe. Most studies reported psychotic behavior and thinking as increasing in severity before patients were identified as being water intoxicated, but were not clear as to the relationship between the psychosis and intoxication. That is, did the psychosis precipitate the water intoxication or did the water intoxication precipitate the psychosis? Observation of two wards for the chronically mentally ill, where at least 30% of the 48 patients were seen by the staff as having a problem with excessive water intake, revealed that the disruptive behavior (including yelling, arguments with patients and staff, and inappropriate demands) usually occurred in the evening when there were fewer staff to cope with the disruptive behavior. Nursing management of these patients requires a larger number of staff than is usually allocated to a unit (Ashby, 1987). Observation of the patient for water intoxication requires frequent vital signs and often one-to-one observation. Once a patient is assessed as being water intoxicated, he or she may
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need to be transferred to a unit that is prepared for medical emergencies. There has been little research focusing on the cognitive aspect of psychiatric patients with polydipsia. Vieweg et al. (1984) attempted unsuccessfully to relate patients’ cognitive state as measured by the Folstein’s “mini-mental state’ ’ scores to serum sodium levels in hopes of being able to detect cognitive changes of patients approaching a state of intoxication. There is no indication in the literature of how patients explain their excessive drinking or whether it is possible to control their drinking behaviors through any cognitive restructuring . WATER INTOXICATION
Case reports have been useful in understanding the potential seriousness and clinical manifestations of water intoxication. Several case studies of psychiatric patients who became medical emergencies have been reported (Bewley, 1964; Chinn, 1974; Emsley & Taljaard, 1987; Fleischhacker, Barnas, & Ledochowski, 1987; Jos, 1984; Jose et al., 1980; Khamnei, 1983; Rae, 1976; Roberge et al., 1984). All of these case reports, with the exception of the Jos study, were of patients who were admitted in a state of intoxication, and the events leading up to their hospitalization had to be reconstructed from reports of family and friends. Jos documented that a patient had been observed drinking large amounts of water throughout the day and experienced a seizure at 3:40 p.m., suggesting that the excessive intake precipitated the intoxicated state. Vomiting followed and then another seizure at 6:30 p.m. The patients in these studies ranged in age from 19 to 53 years and represented both males and females. Most had been diagnosed with schizophrenia, but affective disorders and alcohol/drug abuse were also represented. All of the cases documented the physiological changes that occurred during acute water intoxication including seizures and low-serum sodium levels. Jose, Barton, and Perez-Cruet (1979) argued that general convulsions are the most common result of water intoxication. Other case studies of water intoxication have been reported in those who are developmentally disabled (Noonan & Ananth, 1977; McNally, Calamari, Hansen, & Kaliher, 1988) and who do not have any physical or psychiatric illness (Mellinger & Zafar, 1983).
Reports of death of psychiatric patients during an episode of water intoxication (Blotcky, Grossman, & Looney, 1980; Rendell et al., 1978; Raskind, 1974) further emphasize the potential threat to polydipsic patients. Vieweg, David, Rowe, Wampler, Bum, and Spradlin (1985) reported that of 60 patients who died before the age of 53 years in a state mental hospital, 27 patients had a schizophrenic disorder. Of those 27 patients, five ( 18.5%) died of complications of self-induced water intoxication. ASSESSMENT AND INTERVENTIONS
Measuring urine specific gravity as described by Vieweg et al. (1984) and weighing the patient as suggested by Goldman and Luchins (1987) are two nonintrusive, inexpensive interventions that may be used in assessing patients for polydipsia. These interventions are aimed at identifying an increase in fluid volume. However, the authors point out that even when used together, these methods do not identify all patients, because neither hyposthenuria nor significant weight change may be present at the time of the assessment. Treatment of water intoxication is a nursing and medical emergency. Watson (1985) outlined the nursing care of a patient in acute water intoxication. She presented a nursing care plan that identified 10 problems, from deteriorating conscious level as a result of cerebral edema, psychological problems of anxiety, and loss of privacy, to discharge planning. Sodium chloride, along with water restriction, was recommended for prevention of water intoxication (Vieweg, Rowe, David, & Spradlin, 1985). However, success with sodium chloride has been reported to be limited, because salt is rapidly lost in the urine, polyuria and hyposthenuria persist, and progressively higher doses of salt are required. Illowsky and Kirch (1988) do not recommend its use in preventing water intoxication. Medical treatment has focused on drug therapy in an attempt to stabilize serum sodium levels. Treating patients with lithium alone, and then in combination with phenytoin has been marginally successful (Vieweg et al., 1988). Demeclocycline has been reported to be successful in reducing the incidence of severe hyponatremic episodes in patients where there is mild impairment in urinary dilution (Forrest et al., 1978; Goldman & Luchins, 1985; Nixon, Rothman, & Chinn, 1982). Behavioral treatment has focused on preventing water
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intoxication of those with a known history of excessive water consumption by restricting access to water through behavior modification for a mentally retarded female (McNally, Calamari, Hansen, & Kaliher, 1988), operating a water intoxication ward designed for managing and monitoring water ingestion (Ashby, 1987) and developing individual care plans within the context of the Roy Adaptation Model (Prim, 1988). McNally et al. and Prim demonstrated success in single-case studies. Success was defined in both studies as reduction in water ingestion and in episodes of water intoxication. Ashby described the protocol that was used on the water intoxication ward, but did not report patient outcomes. A target weight procedure has been used for those patients with a history of water intoxication in an attempt to identify when water restriction is necessary. Goldman and Luchins (1987) and Delva and Crammer (1988) reported success in significantly decreasing the number of water intoxication episodes in patients by monitoring body weight and imposing water restriction when the body weight reaches 7% of a predetermined target weight for each patient. Koczapski et al. (1987) recommend that weight monitoring be used as a screening test to identify patients with subclinical disturbances in water metabolism who have not yet developed water intoxication. The one consistent intervention that is reported in the literature is restricting patients from drinking water. Common sense says that restricting water reduces the amount of fluid in the body, thereby reducing the likelihood of progressing to a water-intoxicated state. Through clinical experience, water restriction is easier said than done. Prim reported success with planning interventions by modifying a patient’s focal stimuli and providing structured activities in an attempt to divert a patient’s attention (1988). Many times staff resort to turning off the drinking fountains and locking bathrooms and showers in order to restrict access to water. Restricting access to water as an effective intervention should be investigated. RECOMMENDATIONS
FOR RESEARCH
AND PRACTICE
We know that water ingestion leading to water intoxication is a significant problem in chronic psychiatric patients and that it can lead to death. There is evidence that some chronically mentally ill patients excrete more urine than others and
some excrete less, that some drink excessive water, and in some of these patients there is an inappropriate secretion of the antidiuretic hormone, arginine vasopressin. It also has been observed that those patients who excrete more urine than others function at a higher level than those patients who do not. Water ingestion leading to water intoxication has been linked to psychiatric medications and their withdrawal, electroconvulsive therapy, psychosis, nicotine, and alcohol, but relationships have not been clearly established. Measuring urine-specific gravity and weighing patients have been suggested for screening. Interventions have focused on preventing patients from drinking to a state of water intoxication. Restricting water and monitoring body weight have been suggested. The drug, demeclocycline, is promising in the treatment of mild impairments of urinary dilution. There is much that is unknown about water ingestion leading to water intoxication. It is unclear how the patient experiences the apparent need to drink water. Is there truly an addictive nature to the behavior? If there is, how much control over water drinking can be expected of the patient? Can patients be expected to gain control over the need for water or does control need to be external? Why are the higher-functioning patients seemingly afflicted with excessive urination and need for water? Psychiatric nursing has not developed many interventions for care of these patients. There are several areas of research that need to be initiated regarding nursing care. Assessment factors, including physical and psychological ones, have not been identified. Nursing models that best explain the problems the patients experience and give direction for care have yet to be tested. Studies determining how the patient experiences the need to drink water and urinate should be explored. Most of the patient reports in the literature would suggest psychosis as an explanation of excessive water behavior. However, casual observation of patients drinking water indicates that most of the patients are not blatantly psychotic while drinking water. Future research and practice should focus on understanding the patients’ experience of polydipsia and how it relates to the patients’ level of functioning. Nursing needs to test various assessments in order to determine appropriate interventions. Acuity of nursing care needs to be addressed in terms of the nursing assignments. More is unknown about water ingestion leading to water in-
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