Psychogenic polydipsia: a review of past and current interventions for treating psychiatric inpatients diagnosed with psychogenic polydipsia (PPD).
|Article Type:||Disease/Disorder overview|
(Care and treatment)
Water intoxication (Prevention)
|Publication:||Name: Annals of the American Psychotherapy Association Publisher: American Psychotherapy Association Audience: Academic; Professional Format: Magazine/Journal Subject: Psychology and mental health Copyright: COPYRIGHT 2010 American Psychotherapy Association ISSN: 1535-4075|
|Issue:||Date: Spring, 2010 Source Volume: 13 Source Issue: 1|
The purpose of the article is to provide a review of past and current treatment strategies for psychogenic polydipsia, which includes fluid restriction and behavioral and pharmacologic modalities.
Relevance of the Topic to Rehabilitation Practitioners
Approximately 80% of psychiatric patients who manifest psychogenic polydipsia suffer from schizophrenia (De Leon, Verghese, Tracy, Josiassen, and Simpson 1994).
Historically, psychiatric inpatients afflicted with psychogenic polydipsia have required day-to-day treatment from a multi-disciplinary team. The major aim is to intervene via the treatment conditions highlighted below, before the patient has consumed dangerous quantities of fluids. Achieving this goal requires assessment and treatment of abnormal drinking behavior with staff-intensive care requirements. Although a closed ward has not provided the definitive solution for the polydipsia-hyponatremia syndrome, it was identified in the past as a necessary link to successful patient discharge. More specifically, reduced levels of care (i.e., less restrictive) increased patient safety and improved quality of life in many instances (Shah & Greenberg, 1992).
A Retrospective Review
Psychogenic polydipsia refers to fluid drinking that greatly surpasses physiological requirements (Webb & Gehi, 1981). Self Induced Water Intoxication (SIWI) is a debilitating disorder that occurs mainly with patients diagnosed with schizophrenia and is an extreme manifestation of psychogenic polydipsia. The association between disturbances in water balance and schizophrenia has been recognized for almost 90 years (Rowntree, 1923).
More specifically, if fluid intake exceeds the individual's capacity for excretion, then the resultant hyponatremia (i.e., sodium depletion) may produce signs of water intoxication including: vomiting, agitation, ataxia, seizures and coma (Rosenbaum, Rothman, and Murray 1979). Disordered water homeostasis is a well recognized complication of schizophrenia, with an estimated prevalence in at least 20% of chronic psychiatric inpatients and hyponatremia in more than 10% of this population (De Leon, 2003).
Polydipsia-hyponatremia syndrome refers to a state of self-induced hyponatremia associated with the excessive drinking of fluids (i.e., any fluid available).Water intoxication, which is caused by exceeding 5% of body weight in water consumption in a 24-hour period, denotes the changes in mental and neurological status that result from reductions in serum sodium (i.e., less than 135 mmol/L) and osmolality. In the broader sense of the term, disordered fluid homeostasis may be thought to be compromised of disturbances in the intake and excretion of fluids. The term psychogenic polydipsia is a syndrome that is psychologically motivated or is a habitual voluntary need for oral fluid that exceeds the physiological requirements for fluid balance (Cosgray, Giger, Davidhizar, and Kreisl 1993). As indicated by Karp and Laureno (1993), the most serious insult to the brain's structural integrity occurs when a sudden drop in plasma osmolality is so great that the compensatory mechanism is overwhelmed. The result is cerebral edema (i.e., swelling of the brain) and the ensuing clinical manifestations of water intoxication which include (Arieff, 1984):
Physical signs of hyponatremia
* Edema of the extremities
* Abdominal distention
* Periorbital puffiness
* Nausea and vomiting
* Elevated blood pressure and pulse may indicate volume overload
Mental status changes
Observed in water intoxication and easily confused with the individual's primary psychiatric illness.
* Restlessness and pacing
Affective changes may include
* Elevated mood or euphoria
* Labile behavior
* Anger outbursts
Diligent day-to-day management of patients with psychogenic polydipsia is critical in preventing fluid intoxication. The major aim of treatment is to intervene before the patient has consumed dangerous quantities of fluids.
Course of Illness-Psychological Dependency/Addiction
Patients with schizophrenia destined to develop polydipsia hyponatremia syndrome are indistinguishable from other patients with schizophrenia at the outset of their illness (Vieweg, Rowe, and David 1984). Besides some drugs that decrease the clearance of free water, North American studies suggest that male gender, white race (versus black race), and chronicity may be associated with the development of water intoxication in polydipsic patients (Baumgart, Schmid, and Spieg 2005; Melli, Chaudhry, and Cornblath 2005). Typically, they develop psychosis in late adolescence or their early twenties, and at this stage parameters of water regulation are normal. A clinically "silent period" of 5-15 years commences during which time health care professionals consider patients to be metabolically stable. Primary polydipsia, or polydipsia not explained by medical causes, has been described as a three-stage process: simple polydipsia with accompanying polyuria, polydipsia with water intoxication, and physical complications secondary to ingestion of fluids in large quantities (Baumgart et al. 2005).
Characteristically, patients developing psychogenic polydipsia are first noted to be polydipsic (i.e., habitually seeking out and consuming any/all fluids) in their early thirties. By their mid-thirties, they may present with generalized seizures secondary to fluid intoxication. A generalized seizure is the first recognized problem in patients with psychogenic polydipsia in more than 80% of cases (Jos, 1984; Vieweg et al. 1984).
Besides patients with schizophrenia and schizoaffective disorder, patients with; mental retardation (Vieweg, Godleski, and Shannon 1989a); and middle-aged women with anxiety disorders (Harisprasad, Eisinger, and Nadler 1980); dementia (Vieweg, Godleski, and Shannon 1989b); and bipolar disorder (Vieweg, Godleski, Graham, Barber, Goldman, Kellogg, Bayliss, Glick, Hundley, and Yank 1990) are susceptible to developing this problem.
PAST AND CURRENT TREATMENT APPROACHES: IMPLICATIONS FOR PRACTICE
A clinical history, physical examination, and routine laboratory tests remain important sources of information to understand and treat patients with polydipsia--hyponaetremia syndrome. Clues of the developing polydipsia include reports of preoccupation with drinking, observed increased fluid consumption, nocturnal bed wetting, urinary incontinence, and worsening of the psychosis in the afternoon and early evening (Dundas, Harris, and Narasimban 2007). Whereas history, serum sodium, and osmolality produce some diagnostic certainty, a water restriction test is the "gold standard" for diagnosis (Dundas et al, 2007).
Fluid restriction and other behavioral interventions (Vieweg & Leadbetter, 1997) remains a cornerstone of treating psychiatric patients with this affliction. This intervention, either voluntary or imposed is not always successful, particularly among chronically psychotic patients. In part, this is because some schizophrenic patients with polydipsia syndrome stated they over-drink fluids to feel better (Millson, Smith, and Koczapski 1993). More recently, a study by Shekhar (2004) reported a case of a patient whose excessive fluid intake was ameliorated by treatment with the angiotensin-receptor blocker (ARB) losartian. Following a one-week baseline period characterized by marked diurnal weight gain and high fluid intake per nursing observations, this patient was initiated on losartan 25 mg/day. This treatment ameliorated her polydipsia within two days. The following week, the losartan dose was increased to 50 mg/ day, resulting in further improvement per weight measurement and nursing observations. Discontinuation of losartan was attempted the next week and the polydipsia worsened. However the patient's blood pressure and heart rate remained stable. The patient's psychiatric symptoms were not exacerbated by adding losartan, which was continued at 50mg/day. The author suggested the results in improving the course of treatment were due in part to central angiotensin pathways critical in regulation of fluid intake. Dopamine may have modulated the thirst-inducing effect of angiotensin 11 at the brain's AT1 and AT2 receptors (Verghese, de Leon, and Simpson 1993). This study suggests that polydipsia is not solely a behavioral consequence of psychosis, but may be a unique manifestation of the dopaminergic dysfunction implicated in schizophrenic psychopathology. The patient eventually required readmission because of polydipsia without causal psychiatric morbidity.
Diurnal body weight change is the most important single parameter to follow regarding a patient identified with excessive fluid drinking because it incorporates most of the variables involved in this drinking disorder. Vieweg (1993) stated behavioral approaches to thirst disturbance offer promise but are labor intensive. The research states that institutionalized, psychotic patients respond to thirst stimuli similarly qualitatively but not quantitatively. More specifically, polydipsia patients drink more fluids at comparable times during the day than do their non-polydipsia counterparts. A shift in thirst threshold--not factors such as hallucinations and delusions--explains polydipsic patterns in the polydipsia/hyponatremia syndrome (Goldman, Luchins, and Robertson (1988). In conjunction and in regard to alcoholism, it was found that alcohol abuse prevalence is higher among schizophrenics with recurrent water intoxication (SIWI) than among matched controls with normal water balance (Ripley, Millson, and Koczapski 1989). Other authors suggested that antecedent alcohol abuse in schizophrenia increases the risk of subsequently developing fluid intoxication (Blum, Tempey, and Lynch 1983); (Singh, Padi, and Bullard 1985).
Mental status changes (i.e., a change from baseline behavior) can be a prime indicator of hyponatremia. Examples include a patient with blunted affect who suddenly becomes more animated and experiences a worsening of psychosis, particularly in the afternoon, which may indicate hyponatremia. Cognitive changes include deficits in complex information processing, reduced mental flexibility and verbal fluency, impaired attention span, judgement deterioration, and increased confusion.
Medical concerns include the importance of remembering that a patient's response to hyponatremia is idiosyncratic; some patients may become more disorganized and confused whereas others become withdrawn and somnolent. Increased urine volume can result in hypotonic bladder, hydronephrosis, and renal dysfunction. Urinary incontinence, urinary tract infections, and chronic parineal irritation frequently occur. Distention of the gastrointestinal tract caused by fluid loading can cause nausea, vomiting, and abdominal pain. Behaviors associated with polydipsia include frequent trips to the bathroom and an increase in consumption of non-portable water resources. Changes in appearance (i.e., compared to baseline) are evident as patients neglect their personal hygiene.
The progression from the onset of psychosis to polydipsia and hyponatremia follows a predictable course in schizophrenia (Vieweg et al. 1989a). As a rule, a relentless increase in fluid consumption is noted early in the illness. After five or more years of polydipsia, episodic hyponatremia may begin to occur, perhaps dependent on environmental variables (Bugel & Heath, 1992). Factors that can predate development of frank hyponatremia include: nicotine and caffeine abuse and treatment with certain psychotrophic medications in substance abuse. Patients who have concurrent diagnosis of schizophrenia and alcohol abuse are particularly prone to polydipsia and hyponatremia (Ripley et al. 1989).
Traditional Intervention Strategies
Once a patient is suspected of having polydipsia and episodic hyponatremia, the degree of severity of fluid dysregulation should be established. Ideally, direct measurement of oral fluid intake would determine whether a patient is polydipsic. However, this method has been found to be impractical due to the many demands on a restricted ward with this unique clinical population. Changes in the patient's body weight is the easiest method of appraisal if done regularly in a standardized fashion (i.e., patient weighed four times daily in the early a.m., mid-a.m., late p.m., and mid-evening). A 4-kilogram difference in males and 3.5-kilogram difference in females over a 24-hour period has been used as a criterion for determining excessive drinking (Hutcheon & Bevilacqua, 2005).
A behavior sampling method (e.g., Virginia Polydipsia Scale) has been developed to assess drinking behaviors. The scale has shown excellent inter-rater reliability and sensitivity to changes in psychiatric functioning caused by polydipsia (Shutty, Hundley, and Leadbetter 1992). The Virginia Polydipsia Scale involves observation of patient activities before and after any bout of drinking fluids, counting the number of cigarettes consumed, urine volume, drinking source, rate of drinking, time drinking occurred, and the amount drunk.
It also measures 20 psychiatric symptoms (e.g. anger outbursts, social withdrawal, and pacing) frequently associated with water intoxication.
Generally speaking, early polydipsic patients do not drink more frequently than matched control subjects but they do drink greater volumes with each drinking bout. They do not void as much or as often as controlled subjects. These findings are helpful clinically because they suggest that time spent at the fluid source drinking is more crucial than mere number of times drinking occurs. Behavioral sampling can help specify drinking risk periods, idiosyncratic patterns of drinking and idiosyncratic responses to "fluid loading."
Consequentially, whenever a specific behavioral management plan is indicated, behavioral observations can be used to help design, implement, and evaluate subsequent behavioral interventions. More specifically, the patient's base weight is taken when the patient is weighed after arising in the morning and before beginning to consume fluid. Following several daily measurements it becomes clear that morning weights tend to oscillate around a base weight that is identified on a weight chart. All subsequent monitoring depends on an accurate base weight. Minor fluctuations (i.e., a pound or two) in morning weight are expected and require no action. Lastly, successful long-term care depends on the patient's own ability to limit polydipsia.
One way to assess a patient's ability to limit polydipsia is to examine their objective reasons why polydipsia is so important in their lives. This can be initiated during psychosocial rehabilitation group meetings held semi-weekly (e.g., two 15-minute sessions per week). In these meetings, many patients have described a euphoric quality associated with polydipsia, although others have admitted to increased irritability. Most patients have noted a desire for stimulation, similar to other substances of abuse such as alcohol or street drugs. Developing an understanding of what influences a patient to develop an addiction for polydipsia can improve management of this dysregulation of fluid intake.
Group topics typically include repeated progress checks on a patient's ability to self-monitor and control their drinking during the past week and the development of strategies to reduce drinking. Group counseling also provides corrective feedback and encouragement for those patients who are involved in intensive behavioral protocols such as what is occurring on the locked care unit. The frequency and severity of fluid intoxication determines the level of independence a patient earns. These positive consequences include time off the unit, time off hospital grounds, or the ability to participate in rewarding activities. Management of patients who have become habitual fluid seekers (i.e., all fluids) usually occurs in a locked unit that is in itself an artificial structure of control.
Currently, there is little generalized ability regarding carryover of activities for daily living (i.e., ADL) to other settings, such as community residential treatment programs for acute and subacute SIWI patients. This is due to the nature of the polydipsia disorder and severity of both subtypes (i.e., 'sippers' versus binge drinkers) manifesting this disorder.
During the past 20 years, the use of antipsychotic medication, the "atypicals" such as clozipene treatment, has reduced the impulsive, psychotic, and anxiety-driven nature of excessive fluid consumption (Smith, Puckett, Crawford, and Elliot 2004). Unfortunately, disturbed fluid regulation is a chronic condition that often limits the effectiveness of pharmacological approaches of atypical neuroleptics. In the past, clozapine appeared to be a promising treatment. However, its side effect profile limited its use. More specifically, the patients themselves often refuse to be medication-compliant due to excessive weight gain, drooling, and weekly blood work requirements. On a positive note, clozapine's effectiveness in treating disturbed fluid regulation may be related to its greater efficacy in treating psychosis overall. It has also been effective in reversing the diurnal variation in urine output noted in patients with disturbed fluid regulation.
More recent studies (Sterns, Sagar, Nigwekar, and Hix 2009) have reviewed the treatment of chronic hyponatremia and stated that many hospitalized patients present with multiple conditions that are potential causes for hyponatremia (Perinanyagam, Sterns, Silver, Grieff, Mayo, and Hix 2008). Sterns et al. (2009) state they often initiate therapy with hypertonic saline because it will increase the serum sodium concentration reliably regardless of etiology. An infusion of 3% saline at 15 to 30 ml/h can be used for chronically hyponatremic patients who are neither seizing nor comatose (Mohmand, Issa, Ahmad, Cappuccio, Kouides, and Sterns 2008; Liamis, Kalogirou, Saugos, and Elisaf 2008). The authors' further state chemistries should be obtained at 4- to 6-hour intervals during the infusion and the urine output should be monitored carefully. Hypertonic saline should be discontinued after the serum sodium level has increased by 4-6 mmol/L or if a water diuresis emerges. They discourage he use of formulas to predict the increase in serum sodium concentration and stated that overcorrection of hyponatremia may complicate any form of therapy for hyponatremia; of note--patients given large volumes of isotonic saline may be more likely to overcorrect than patients given low volumes of hypertonic saline (Oh, Uribarri, Barrido, Landman, Choi, and Carroll 1989).
Currrent use of vasopressin antagonists to treat sustained hypotonic hyponatremia almost always has a mediation effect (Sterns et al. 2009). Treatment of the electrolyte disturbance with vasopressin antagonists may have advantages over currently available therapy (Greenberg & Verbalis, 2006). Vasopressin antagonists have been shown to be more effective than placebo in increasing the serum sodium concentration in patients with modest, asymptomatic hypnatremia (Schrier, Gross, Gheorghiade, Berl, Verbalis, Czerwiec, and Tolvaptan 2006; Soupart, Gross, Legros, Alfodi, Djillali, and Heshmati, 2006; Zeltser, Rosansky, van Rensburg, Verbalis, and Smith 2007). Unfortunately, there is almost no published experience with the use of these inpatients with symptomatic hyponatremia. The authors conclude that vasopressin antagonists cannot yet be recommended as single agents for the treatment of hyponatremic emergencies.
Lastly, a number of authors in the past 30 years (Illowsky & Kirch, 1988) have postulated that elevated dopamine activity may drive thirst, and provide the common link between psychotic illness and polydipsia. This relation may be related directly to the pathophysiology of schizophrenia or arise secondarily as a neuroleptic-induced dopamine supersensitivity (Leadbetter & Shutty, 1994) and supersensitivity psychosis (Chouinard, Jones, and Annable, 1978). Supersensitivity of the D2 receptors in the hypothalamic-pituary axis may explain polydipsic behavior. This would predict that polydipsic behavior occurs following chronic rather than acute treatment with antipsychotics and that it does not occur at the outset of the illness.
During the treatment period in a structured inpatient setting, many patients diagnosed with psychogenic polydipsia, whether falling in the range of mild, moderate, or severe addiction, are unable to sustain a comfortable discharge to an open ward. This is due to a high frequency potential for relapse which necessitates returning to the locked, specialized SIWI Unit.
Education of the patient, family members, and community care providers, however the discharge outcome, is fundamental to successful discharge. Typically during the treatment period each patient has been prescribed an individualized weight protocol to track diurnal weights and estimated sodium levels. The purpose and importance of these plans are emphasized to the patient's community care providers. This procedure eliminates unnecessary changes in antipsychotic medications after discharge and improves the competence of community care providers in dealing with this particular clinical population.
Before discharge from a locked unit to an open setting, a patient diagnosed with psychogenic polydipsia should be assessed regarding their ability to monitor and self-regulate fluid intake. More specifically, care providers should examine the patient's level of insight, acceptance, motivation, and cognitive skill. It is imperative that any planning for transition to community living entail a series of carefully monitored passes allowing the patient to visit these facilities before discharge. During the pass period, the patient records their body weight and is supervised initially by a staff member and is instructed how to handle elevated weights. The frequency and severity of weight gain while "on pass" is one way of measuring the patient's readiness for discharge and indicates the level of structure needed.
Discharge Risks and Hurtles
Severely mentally ill patients diagnosed with psychogenic polydipsia drink fluids excessively sometimes exceeding 10 litres per day. Keeping in mind that both polydipsia and hyponatremia can lead to significant morbidity and mortality, it is important to be cognizant that this illness accounts for as many as 18% of non-geriatric deaths in schizophrenic patients (Vieweg, David, and Rowe 1985). Various techniques of water restriction, behavioral interventions and psycho-education can be effective (Millson, Smith, and Koczapski 1993). However, it is not clear whether these techniques would be as effective in less restrictive environments (Thomas, Howe, Gaudet, and Brantley 2001). This is a crucial issue for a treatment team to operationalize in an era of de-institutionalization. In the past 10 years (Thomas et al., 2001), a study involving an out-patient behavioral approach to the treatment of psychogenic polydipsia with a nonpsychiatric, primary care, adult male patient was completed with promising results. This was done in a setting where restriction of fluid intake was not practical.
As stated earlier, polydipsia with hyponatremia has been primarily associated with patients who have severe psychopathology/cognitive impairment (Kirch, Bigelow, and Weinberger, 1985). Four processes are suggested to "re-engineer" a successful, treatment program for psychogenic polydipsia in a typical inpatient hospital environment to optimize potential for discharge to a reduced level of care. They include:
1. Create a vision and mission statement regarding assessment, treatment, discharge, and follow-up steps for the psychogenic polydipsic SIWI Unit.
2. Develop the staff's core competencies in behavioral management (i.e., behavior modification) and adherence to a philosophy/practice that is consistent with current standards of care regarding this dual diagnosed clinical population.
3. Develop the unit's guiding principles regarding treatment adherence for psycho-education, medication, and behavioral programming that can be tailored for each patient. Psychogenic polydipsia needs to be adequately addressed in clinical practice by correcting the hyponatremia first if the patient is symptomatic. A combination of behavioral treatments and medication has been shown to be effective in the long term, keeping in mind psychogenic-polydipsia, similar to schizophrenia, has a relapsing course warranting clinician vigilance and appropriate management.
4. Develop a comprehensive daily, weekly, and monthly reward and evaluation procedure to carefully track the behavior of each respective patient. In conjunction, developing a formalized, quarterly review to provide a feedback mechanism from a treatment team perspective regarding this difficult and complex clinical population.
The following breakdown of residential needs is provided, based on the fact that psychogenic polydipsia can become an addiction with no demonstrable cure if left untreated. A multidisciplinary team approach should be utilized to treat this problem (i.e., frequency of fluid over-consumption and severity of symptoms) and a biopsychosocial philosophy of care. More specifically, it should incorporate a pharmacological, psychosocial, and behavior management approach. Recalling that approximately 80% of psychiatric inpatients diagnosed with psychogenic polydipsia have been diagnosed with schizophrenia, the following protocol is suggested:
Three patient cohorts of clinical severity (i.e., mild, moderate, severe) should be appraised based on the frequency of fluid intoxication, sodium levels, and daily weight of each respective patient. In conjunction, two styles of fluid ingestion to intoxication should be identified which include: a) chronic "tippling" of any/all fluids throughout the day, and b) the more robust, out-of-control binge drinkers whose drinking patterns are exaggerated and easy to spot. Based on this information a streamlined, customized treatment program that is flexible and easy to modify should be created.
Residential needs include:
* Acute (uncontrolled drinking) inpatient, secure facility with controlled fluid access;
* Sub-acute (controlled drinking) securable residential milieu for patients who can better manage their habitual over-drinking with structure/support;
* Long-term (uncontrolled drinking) use the facility as the acute, however geared for a long-term, residential stay with controlled fluid access;
* Consultation Resources: External expert consultation should be made available for all programs designed to treat patients diagnosed with psychogenic polydipsia:
* Pre-admission: The expert consultant assists with diagnosis and stabilization of the patient in their own residential setting. This includes completing the St. Louis Water Intoxication Assessment as an adjunct to the Virginia Polydipsia Scale.
* Post-discharge: Transition and ongoing support by the multidisciplinary staff which would include: patient assessment/stabilization. This role changes to pre-admission if the stabilization time exceeds three months.
Historically, a reduction of the tendency to habitually seek out and over consume any/all fluids by this clinical population has been influenced by two treatment factors: a) utilizing ward restriction (i.e, confinement on the ward) for any breeches of daily protocol (e.g., baseline weight to final weight over 4 kg. for males and 3.5 kg. for females over a 24-hour period), and b) staff supervised "off ward" grounds privileges earned throughout the treatment duration. More recently (Thomas et al. 2001) "overlearning" was practiced by the inpatient reviewing skills taught in prior sessions; receiving verbal praise from the staff during weekly treatment sessions for satisfactory sodium concentration levels and progress reported by the family. Lastly, the authors suggested targeting treatment towards a return of normal sodium concentration, rather than a measurable reduction in fluid consumption.
Adherence to the aforementioned treatment paradigm utilizing behavior management principles, psycho-educational semi-weekly groups, and an empirically validated medication regime increases the potential for patient internalization and improved outcome regarding the amelioration of psychogenic polydipsia. This is usually measured qualitatively by staff observations/daily recording and quantitatively, as reflected by a reduction in the frequency of habitual fluid-seeking behavior, intoxication, and weight fluctuation.
Patients initially diagnosed with psychogenic polydipsia require a specialized closed ward with trained staff familiar with the course of treatment for this specialized client population (i.e., multidisciplinary team approach). Due to the nature of the addiction and potential for self-injurious behavior, treatment requires a milieu that balances maximizing the patients' dignity with their safety, which demands close scrutiny by the multidisciplinary team.
Discharging patients to an open ward without carefully researched transitioning protocols will, in the writer's opinion, result in the eventual relapse of the patient.
Any attempt of treatment carry-over to a milieu with a reduced level of care increases success by following a behavioral protocol. The behavioral treatment plan reinforces a slow, steady increase in access to fluids that is earned as a result of demonstrated control of drinking behavior, as influenced by the treatment strategies mentioned above. This facilitates the next stage, which is careful observation of the patients for a generalization effect, and immediate reinforcement provided those patients observed "curbing" their propensity to over-drink fluids off ward. Treating psychogenic polydipsia is a long-term project. Like any other rehabilitation procedure with a multi-disabled clientele, two steps forward and one step back can be expected! It requires a thorough examination of each patient's learning curve and careful evaluation of their respective strengths/needs before incorporating any change in the treatment protocol.
Any facility receiving patients diagnosed with psychogenic polydipsia requires an orientation regarding current treatment techniques to facilitate a comfortable transition. Deviation from the treatment protocol could jeopardize future gains and create much frustration for both patient and staff. Each unit organized to house this clinical population should obtain the Virginia Polydipsia Scale and/or the St. Louis Modified Water Intoxication Assessment to assess each patient prior to admission. This would help determine which portion of the three-stage process they fall and physical complications secondary to ingestion. As previously mentioned, data suggests that polydipsia is present in at least 20% of chronic psychiatric inpatients and hyponatremia in more than 10%. Keeping these statistics in mind, a baseline should be established from which to compare future treatment results. This allows an evaluation of each patient's long term response to treatment, measuring its efficacy and allowing adjustments to be made.
This article is approved by the following for continuing education credit:
The American Psychotherapy Association provides this continuing education credit for Diplomates and certified members, whom we recommend obtain 15 CEs per year to maintain their status.
After studying this article, participants should be better able to do the following:
1. Define psychogenic polydipsia.
2. Describe the optimal treatment for psychogenic polydipsia.
3. Define self-induced water intoxication.
KEYWORDS: psychogenic polydipsia; self induced water intoxication (SIWI); Virginia Polydipsia Scale; St. Louis Modified Water Intoxication Assessment; rehabilitation; nursing
TARGET AUDIENCE: Mental health professionals
PROGRAM LEVEL: Basic
DISCLOSURE: The author has nothing to disclose.
CE ARTICLE 2: Psychogenic Polydipsia (pages 28-35)
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CE ACCREDITATIONS FOR THIS ARTICLE
This article is approved by the following for continuing education credit:
The American Psychotherapy Association provides this continuing education credit for Diplomates and certified members, whom we recommend obtain 15 CEs per year to maintain their status.
After studying this article, participants will be better able to:
(1) Define psychogenic polydipsia.
(2) Describe the optimal treatment for psychogenic polydipsia.
(3) Define self-induced water intoxication.
KEY WORDS: psychogenic polydipsia; self induced water intoxication (SIWI); Virginia Polydipsia Scale; St Louis Modified Water Intoxication Assessment; rehabilitation; nursing.
TARGET AUDIENCE: Psychotherapy professionals
PROGRAM LEVEL: Basic
DISCLOSURE: The author has nothing in disclose.
The article examines psychogenic polydipsia (PPD), which entails a habitual voluntary need for oral fluid that exceeds the physiological requirements for fluid balance. This debilitating illness is present in at least 20% of chronic psychiatric in-patients depending on the criteria utilized. Hyponatremia refers to a low serum sodium level (i.e., less than 135 mmol/L) and the term polydipsiahyponatremia refers to a state of self-induced hyponatremia associated with the excessive drinking of fluids. Fluid intoxication occurs when an individual consumes in excess of 5% of body weight in a 24 hour period and denotes the changes in mental and neurological status that result from acute reductions in serum sodium and osmolity. Traditionally, treatment of this habituated need for excessive fluid drinking utilized multi-disciplinary teamwork, following a psycho-bio-social philosophy of care. Prognosis is still guarded for a successful recovery once a habituated pattern of fluid seeking and excessive drinking has been established.
POST CE TEST QUESTIONS (Answer the following questions after reading the article, pages 28-35)
1. What is psychogenic polydipsia?
a. Excessive urination by psychiatric inpatients
b. A habitual voluntary need for oral fluid that exceeds the physiological requirements
c. Excessive urination and bowel movements by psychiatric outpatients
d. An inability to determine the type and quantity of fluids being ingested
2. What type of treatment is optimal for this target population?
a. Psychiatric in-patients afflicted with psychogenic polydipsia require day-to-day treatment from a multi-disciplinary team
b. Outpatient therapy by a doctoral trained therapist knowledgeable in addictions
c. inpatient therapy commencing with a hl client centered approach and subsequently followed up with group counseling (closed groups)
d. Inpatient therapy commencing with both client-centered and group counseling from an "open group" format
3. What is self induced water intoxication (SIWI)?
a. A bulimic purging of excessive fluid drunk periodically throughout the day
b. Water retention due to an iatrogenic medication problem
c. Over-drinking 2% of the body weight
d. Water (i.e., any fluid) intoxication is caused by exceeding 5% of body weight in a 24 hour period and denotes the changes in mental and neurological status that result from reductions in serum sodium (i.e., less than 130 mmol/L) and osmology
4. Which inpatient population is most often associated with psychogenic polydipsia?
a. Obsessive compulsive inpatient
c. Bi-polar I inpatients
d. Schizo-affective inpatients
5. Once an individual is suspected to have psychogenic polydipisa and episodic hyponatremia what should be done?
a. Locate all fluid sources and restrict the patient's drinking
b. Investigate the living milieu of the individual and restrict water drinking until further psychobiosocial assessments can be completed
c. Discuss the situation with the multidisciplinary team at the next scheduled meeting to decide on future action
d. The degree of severity of fluid dysregulation should be established
EVALUATION: Circle one (1 = Poor 2 = Below Average 3 = Average 4 = Above Average 5 = Excellent)
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Arief, A.I. (1984). Central nervous system manifestations of disordered sodium Metabolism. Endocrinology Metabolism Clinic-North America 13: 269-294.
Baumgart, U., Schmid, R., & Spierl, H. (2005). Olanzapine-induced acute rhabdomyolysis. A case report. Pharmacopsychiatry 38: 36-37.
Blum, A., Tempey R.W., & Lynch W.J. (I983). Somatic findings in patients with psychogenic polydipsia. Journal of Clinical Psychiatry 44: 55-56.
Bugel, C., & Heath, H.S. (1992). Early detection of water intoxication. Journal of Psychosocial Nursing Mental Health Service 30: 31-33.
Chouinard, G., Jones., B.D., & Annable, L. (1978). Neuroleptic-induced supersensitivity psychosis. American Journal of Psychiatry 135: 1409-1410.
Cosgray, R., Giger, N., Davidhizar, R., & Kreisl. R. (1993) A program for water intoxicated patients at a state hospital. 0887-6274/93/0702-05553. 00/ USA.
de Leon, Jose. (2003). Polydipsia: A study in a long-term psychiatric unit. European Archives Psychiatry Clinical Neurosciences 253: 37-39.
deLeon, J., Verghere, C., Tracy, J.I., Josiassen, R.C., & Simpson, G.M. (1994). Polydipsia and water intoxication in psychiatric patients: A review of the epidemiological literature. Biological Psychiatry, 35, 408-419.
Dundas, B., Harris, M., & Narasimhan, M. (2007). Psychogenic polydipsia review: Etiology, differential, and treatment. Current Psychiatric Reports 9: 236-241.
Goldman, M.B., Luchin D.J., & Robertson G.L. (1988). Mechanisms of altered water metabolism in psychotic patients with polydipsia and hyponatremia. New England Journal of Medicine 318: 397-403.
Greenberg, A., & Verbalis, J.G. (2006). Vasopressin receptor antagonists. Kidney International 69: 2124-2130.
Harisprasad, M.K., Eisinger, R.P., & Nadler, R.M. (1980). Hyponatremia in psychogenic polydipsia. Archives Internal Medicine 140: 1639-1642.
Hutcheon, D.S., & Bevilacqua, M. (2005). An evaluation of a behavioral assessment protocol of psychiatric patients in a restrictive setting diagnosed with psychogenic polydipsia. Journal of the American College of Counselors, Vol. 12, No. 1: 6-25.
Illowsky, B.P., & Kirch, D.G. (1988). Polydipsia and hyponagtraemia in psychiatric patients. American Journal of Psychiatry 145: 154-158.
Jos, C. J. (1984). Generalized seizures from self-induced water intoxication. Psychosomatics 25: 153-157.
Karp, B.I., & Laureno, R. (1993). Pontine and extrapontine myelinolysis: a neurological disorder following rapid correction of lhyponatremia. Medicine 72 (6): 359-373.
Kirch, D.G., Bigelow, L.B., & Weinberger, D.R. (1985). Polydipsia and chronic hyponatremia in schizophrenic inpatients. Journal of Clinical Psychiatry 46: 179-181.
Leadbetter, R.A., & Shutty, M.S. (1994). Differential effects of neuroleptics and clozapene on polydipsia and intermittent hyponatraemia. Journal of Clinical Psychiatry 55: 110-113.
Liamis, G., Kalogirou, M., Saugos, V., & Elisaf, M. (2008). Therapeutic approach in patients with dysnatraemias. American Journal of Kidney Disease 52: 144-153.
Melli, G., Chaudhry, V., & Cornblath, D.R. (2005). Rhabdomyolysis: an evaluation of 475 hospitalized patients. Medicince (Baltimore) 84: 377-385.
Millson, R.C., Smith, A.P., & Koczapski, A.B. (1993). Self-induced water intoxication treated with group psychotherapy. American Journal of Psychiatry 150: 825-826.
Mohmand, H. K., Issa, D., Ahmad, Z., Cappuccio, J.D., Kouides, R.W., & Sterns, R.H. (2007). Hypertonic saline for hyponatremia: the risk of inadvertent overcorrection. Clinical Journal of American Soc Nephrology 2: 1110-11117.
Oh, M.S., Uribarri, J., Barrido, D., Landman, E., choi, K.C., & Carroll, H.J. (1989). Danger of central pontine myelinolysis in hypotonic dehydration and recommendation for treatment. American Journal of Medical Science. 298: 41-43.
Perianayagam, A., Sterns, R.H., Silver, S.M., Grieff, M., Mayo R., Hix, J. (2008). DDAVP is effective in preventing and reversing inadvertent overcorrection of hyponatremia. Clinical Journal of American Soc Nephrology 3: 331-336.
Ripley, T.L., Millson, R.C., & Koczapski, A.B. (1989). Self-induced water intoxication and alcohol abuse. American Journal of Psychiatry 146: 102-103.
Rosenbaum, J.F., Rothman, J.S., & Murray, G.B. (1979). Psychosis and water intoxication. Journal of Clinical Psychiatry 40: 287-291.
Rowntree, L.G. (1923). Water intoxication. Archives of Internal Medicine, 32, 157-174.
Schrier, R., Gross, P., Gheorghiade, M., Berl, T., Verbalis, J.G., & Czerwiec, F.S (2006). Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. New England Journal of Medicine 355: 2099-2112.
Shaw, P.J., & Greenberg, W. M. (1992). Polydipsia with hyponatremia in a state hospital population. Hospital and Community Psychiatry, 43 (5) 509-511.
Shekhar, A (2004). Losartan for treatment of psychogenic polydipsia. The Annals of Pharmacotherapy Vol. (38): 1750-1751.
Shutry, M.S Jr., Hundley, P.L., & Leadbetter, R.A. (1992). Development and validation of a behavioral observation measure for the syndrome of psychosis, intermittent hyponatremia and polydipsia. Journal of Behavioral Therapy and Experimental Psychiatry 23: 213-219.
Singh, S., Padi, M.H., & Bullard, H. (1985). Water intoxication in psychiatric patients. British Journal of Psychiatry 146: 127-131.
Smith, R.P., Puckett, B.N., Crawford, J., & Elliott, R.L. (2004). Quetiapine overdose and severe rhabdomyolysis. Journal of Clinical Psychopharmacology 24: 343.
Soupart, A., Gross, P., Legros, J.J., Alfodi, S., Djillali, A., & Heshmati, H. (2006). Successful long-term treatment of hyponatremia in syndrome of inappropriate antidiuretic hormone secretion with satavaptan (SR-121463B), an orally active vasopressin V2 receptor antagonist. Clinical Journal of American Soc Nephrology. 1: 1154-1160.
Sterns, R.H., Sagar, U., Nigwekar, M.D., & Hix, J.K.(2009). The treatment of hyponatremia. Seminars in Nephrology, Vol 29, 3: 282-299.
Thomas, J.L., Howe, J., Gaudet, A., & Brantley, P.J (2001). Behavioral treatment of chronic psychogenic polydipsia with hyponatremia: a unique case of polydipsia in a primary care patient with intractable hiccups. Journal of Behavior Therapy and Experimental Psychiatry 32: 241-250.
Verghere, C., de Leon J., & Simpson, G.M. (1993). Neuroendocrine factors influencing polydipsia in psychiatric patients: an hypothesis. Neuropsychopharmacy 9: 157-166.
Vieweg, W.V.R., Rowe, W.T., & David, J (1984). Evaluation of patients with self-induced water intoxication and schizophrenic disorders (SIWIS). Journal of Nervous and Mental Disorders 172: 552-555.
Vieweg, W.V.R., Godleski, L.K., & Shannon, C. (1989a). Diurnal weight gain among patients with mental retardation. American Journal of Mental Retardation 93: 558-565.
Vieweg, W.V.R., Godleski, L.K., & Shannon, C. (1989b). Normalization of abnormal diurnal weight gain among chronically psychotic geriatric patients. Is abnormal diurnal weight gain a risk factor in chronic psychosis? Journal of Nervous Mental Disorders 177: 542-545.
Vieweg, W.V.R., David, J.J., & Rowe, W.T (1985). Death from self-induced water intoxication and schizophrenic disorders. American Journal of Psychiatry 141: 1258-1260.
Vieweg, W.V.R., Godleski, L.S., Graham, P, Barber, J., Goldman, F., Kellogg, E., Bayliss, E.V., Glick, J., Hunley, P.L., & Yank, G.R. (1990). Abnormal diurnal weight gain among institutionalized patients with manic depressive spectrum disorders. Psychiatric Medicine 8 (4): 129-134.
Vieweg, W.V.R., & Leadbetter, R.A. (1997). Polydipsia-hyponatraemia syndrome: epidemiology, clinical features and treatment. CNS Drugs 7: 121-138.
Vieweg, W.V.R. (1993). Behavioral approaches to polydipsia. Biological Psychiatry 34: 125-127.
Webb, W.L. & Gehi, M. (1981). Electrolyte and fluid imbalance: neuropsychiatric manifestations. Psychosomatics 22: 199-203.
Zeltser, D., Rosansky, S., van Rensburg, H., Verbalis, J.G., & Smith, N. (2007). Assessment of the efficacy and safety of intravenous conivaptan in euvolemic and hypervolemic hyponatremia. American Journal of Nephrology 27: 447-457.
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By Donald Hutcheon, EdD, RPsych; and Michael Bevilacqua, BSc
Don Hutcheon, EdD, RPsych, DAPA is a senior psychologist at Riverview Psychiatric Hospital. located in Coquitlam, a suburb of Vancouver, British Columbia. In addition to his job duties on three inpatient wards, Dr. Hutcheon has operated a part-time private practice and consulting business for the past five years.
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