Compulsive polydipsia presenting as diabetes insipidus: A behavioral approach

J. Behov. The-r. & Exp. Psychrot. Printed in Great Brsain.

Vol. 15, No. 4, pp. 353-358,

19R4

ooO5-7916184 $3.00 + 0.00 S 1984 Pergamon Presc Ltd

COMPULSIVE POLYDIPSIA PRESENTING AS DIABETES INSIPIDUS: A BEHAVIORAL APPROACH* ELIZABETH

A. KLONOFF

and DOUGLAS

J. MOORE

Case Western Reserve University Cleveland. Ohlo Summary-Although compulsive polydipsia or self-induced water intoxication is known to occur with a relatively high frequency in psychiatric patients, much of the literature has focused on medication treatment and interactions; little has been written describing alternative methods of intervention. This paper describes an inpatient treatment using both EMG biofeedback and response prevention. The relationship between compulsive appetitive behaviors and more classic presentations is discussed. Because the patient was treated on the endocrine service. the importance of adequately training non-psychiatric staff is emphasized. It is suggested that this may be a model for the behavioral management of psychiatric problems on medical/surgical wards.

ingestion, and electrolyte values consistent with SIADH represent a syndrome reflecting underlying dysfunction of the hypothalamus and limbic system. However, the emphasis has primarily been on the presence of self-induced water intoxication in psychotic individuals, despite evidence suggesting the symptom can be present in a wide variety of psychiatric disorders (Barlow and dewardener, 1959). Some investigators (e.g. Jose and PerezCruet, 1979) have suggested the condition remits spontaneously; however, others (Barlow and dewardener, 1959) have reported histories of compulsive polydipsia ranging from 4 months to 20 years. Three fatal cases have been described (Raskind, 1974; Rendell, McGrane and Cuesta, 1978). Despite this, little attention has been paid to the specific treatment of this disorder. Nixon, Rothman and Chin (1982) used demeclocycline to reduce the severity and frequency of hyponatremic episodes in a 24-yrold psychotic woman. Other investigators (e.g. Rosenbaum et al., 1979) have reported resolu-

Although first reported by Barahal in 1938, the problem of water intoxication has received little attention in the psychiatric literature. Recent investigation (Jose and Perez-Cruet, 1979) suggests that 6.6% of patients in one state mental hospital had a consistent history of compulsive water drinking lasting from a few hours to a few days. Despite the relative frequency of this problem in psychiatric settings, little has been written regarding the optimal way of managing these patients. Much of the recent literature has focused on the potential role of inappropriate antidiuretic hormone (ADH) secretion. Rosenbaum, Rothman and Murray (1979) discussed the potential causal relationship between psychosis, the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and water intoxication. Kosten and Camp (1980) have cautioned about the potential danger of SIADH in patients on piperazine phenothiazines. Raskind, Orenstein and Christopher (1975) have suggested that agitated psychotic depression, increased water

*Portions of this paper were presented at the Annual Meeting of the Association for Advancement of Behavior Therapy. Los Angeles, November 1982. Requests for reprints should be sent to: Elizabeth A. Klonoff, Behavior Therapy Clinic. Department of Psychiatry, Case Western Reserve University, Cleveland. OH 44106. U.S.A. 353

354

ELIZABETH

A. KLONOFF

tion of the polydipsia coincidentally with resolution of the psychosis, often with the use of antipsychotic medications. The purpose of the current paper is to describe the behavioral treatment of a case of compulsive polydipsia that had been refractory to other, traditional psychiatric and pharmacologic treatments.

METHOD The patient. John. was a 24.yr-old male who presented to the endocrine service complaining of a “desperate diuretic urge” and a “dried out feeling in the chest” causing him to drink up to 13 1. of fluid per day. The patient insisted he had diabetes insipidus and demanded a complete evaluation. By his report, the symptoms had begun approx. 1s yr prior to admission when he had become dehydrated and panicked after a long walk on a hot day. The symptoms had increased to the point where, prior to admission. he had refused to leave home for fear that, if out, he might not be able to get necessary fluid. During the 1%yr interval. John had numerous medical and psychiatric work-ups, all concluding that the problem was psychogenic polydipsia. He had been treated with a number of psychotropic medications including chlorpromazine, diazepam, thioridanzine. haloperidol and lithium. all without effect. At the time of this admission. he was convinced the problem was physiological and rejected any suggestion of psychological etiology. As such, he remained on the endocrine inpatient unit throughout treatment. Initial physical examination was within normal limits. Initial laboratory values included a hematocrit value of 44.9%. The white blood cell (WBC) count was 6800/~1. The blood urea nitrogen (BUN) value was 15 mg/dl. Initial electrolyte levels were: sodium, 140 mEg/l, potassium, 4.1 mEg/l; chloride, 105 mEg/l; and bicarbonate, 24 mM/I. Urinalysis showed clear, yellow urine with a pH of 7.0 and specific gravity of 1.004. Urine osmolality was 172. Prior to beginning behavioral treatment, the medical evaluation included head CAT scan. and tomograms of the sella turcica all within normal limits. In addition, a definitive differential diagnosis between compulsive polydipsia and diabetes insipidus was obtained by restricting fluid until the patient lost approx. 3% of body weight. Five units of aqueous vasopression was then injected S.C. and urine osmolality was compared before and after the inlection. I‘his water deprivation test effectively ruled out the diagnosis of diabetes insipidus. During the hospitalization he received time-contingent drazipam (2 mg five times a day) and, if requested, 30 mg of flurazepam hydrocloride at bedtime; both medications were discontinued prior to discharge and John remains medication free.

and DOUGLAS

J. MOORE

ASSESSMENT

INSTRUMENTS

Throughout John’s stay in the hospital, nursing staff kept strict records of all fluids ingested and time and amount of urinary output. All measured intake and output was completed using standard hospital protocol for obtaining such measurements. These values were entered in his medical record. Self-monitoring

Throughout this time, the patient was instructed to record each instance of drinking and urinating. For each entry, he recorded antecedent and consequent activities and rated the strength of his urge both before and after drinking and urinating. This urge rating was on a IO-point Likert scale. Similar data were obtained 6 months and 1 yr after discharge.

TREATMENT Baseline Phase A. No behavior

therapy was conducted during this phase. Nursing staff measured input and output. As expected. their data show a dramatic decrease during the period of the water deprivation test (Day 2, Fig. 1). - Measured --- Measured 14.000

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On the fourth day of hospitalization, John began the selfmonitoring described earlier. These data suggest a gradual increase in the frequency of drinking and urination in the days following the water deprivation test (see Fig. 2).

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tntervention A careful review of the self-monitoring data yielded no reliable antecedent for the urge to drink. The patient reported significant levels of distress concurrent with an increase in this urge. The clear drop in the intensity of the urge contingent upon ingesting fluid suggested that it was the act of drinking that was functioning as a reinforcer by decreasing the aversive urge to drink. Similar to other obsessive/compulsive behaviors, this sequence was conceptualized as a behavioral chain that was being reinforced by the terminal behavior in the chain, making it appropriate to use a response prevention procedure. However, there were reports that John had become violent in the past if access to fluid was prevented. As such, a systematic, additive intervention strategy was employed to

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allow for the gradual introduction of a response prevention procedure. The patient was seen daily for 1 hr individual therapy throughout his inpatient stay. The phases of therapy, including the length of each phase, are presented in Table 1. Phase B. Following the baseline period, John began a series of relaxation training sessions using frontalis EMG biofeedback. Because he became visibly anxious whenever it was even suggested that he abstain from drinking. relaxation was chosen to provide an incompatible response. Biofeedback was used because John insisted he had a physical and not psychological disorder. Prior experience (e.g. Klonoff, Youngner, Moore and Hershey, 1983) suggests that patients emphasizing physical problems more willingly accept a biofeedback-based relaxation method.

Table 1. Phases of treatment Label on Figs. 14

Length of each phase (days)

A

4

B

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Phase Baseline (staff monitored intake and output affected by administration of vasopressin) Patient begins EMG biofeedback Patient not allowed to discuss symptoms Patient to relax for 5 minutes prior to drinking and urinating Began involvement of parents Patient to decrease discomfort rating before drinking by 2 ratingpoints Patient to decrease discomfort rating before drinking by 3 rating points Patient to attempt to drink no more frequently than every 1% hours All fluids and urinal obtained from nurses’ station No more than 20 cc fluid every 2 hours at pre-selected times Discharged from hospital

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ELIZABETH

A. KLONOFF

The patient was seen daily for this training. and was required to practice the relaxation exercises twice a day for 20 min. He recorded his level of relaxation before and after each practice session on a IO-point Likert scale. In addition, all social reinforcement for his symptoms was removed. Nursing staff no longer inquired about them, and all input and output records, as well as urine tests (e.g. specific gravity, osmolality). were completed with John having no knowledge of the results. Nursing was instructed to attempt to direct the conversation toward his likes and dislikes and. if he was unable to converse without describing symptoms. the conversation was terminated. All conversation was carefully documented in the Nursing Notes, which were reviewed daily. Progress notes were used explicitly to reinforce staff for compliance with our instructions. Phusr C. Once John was able to demonstrate increased ability to relax. he was then instructed to attempt to relax for 5 min prior to any instance of drinking or urinating. Thus. the negative reinforcer (that is, removal of the subjective feeling of distress by ingesting water) was delayed by a constant time interval. This also introduced a graduated response prevention paradigm. Phase D. At this point the parents, who had not visited the patient since admission. were seen. The importance of not providing social attention for John’s discussion of symptoms was emphasized. From this point on, both the parents and the patient were seen together at regular intervals in addition to the individual sessions. Phase E. By this phase, John was able to relax sufficiently well to use criterion levels of relaxation as part of the treatment. Using the l-10 Likert scale. he was required to decrease his level of discomfort by two rating points before each instance of drinking regardless of how long it took him to do so. Phase F. The patient was now required to decrease his discomfort rating by three rating points prior to the ingestion of any fluid. In addition. he was instructed to attempt to drink no more frequently than once every 1% hr. Although he was able to do this. when instructed to delay drinking for 2 hr. he had a more difficult time. Phase G. Because John demonstrated limited ability to control his own urge to drink over a 2-hr period. a more complete response prevention program was instituted. All fluids and the urinal were kept at the nurses’ station. The patient was allowed no more than 200 cc fluid every 2 hr at pre-selected times. Relax&ion for 5 min was a prerequisite to obtaining fluid. The 200 cc was to be divided into at least four swallows. with a period of relaxation among them. If John felt anxious during the time he was not allowed water, he was to practice relaxation. To discourage “cheating” his bathroom door was locked and he was restricted to the ward during the first few days of treatment; these restrictions were dropped prior to discharge.

The patient continued in weekly therapy following discharge, Approximately half of the sessions included John’s parents. Focus of the therapy included: familial relations. social skills. sexual identity. vocational choices and increasing activity. At no time did the therapy focus on the polydipsia. At periods of 6 months and I yr after discharge, John was asked again to monitor his drinking for I-2 weeks.

and DOUGLAS

J. MOORE

RESULTS Figure 2 demonstrates self-monitored frequency of drinking and urinating both while in the hospital and at 6 months and I yr follow-up. Figures 3 and 4 reflect the patient’s urge ratings before and after each instance of drinking and urinating respectively. As these graphs clearly 9-

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demonstrate, this comprehensive response prevention intervention was able dramatically to decrease both drinking and urinating even after John was discharged and at the follow-up periods. Reports from the parents confirmed the success of the intervention. The patient also provided information regarding the amount of fluid ingested each time he drank. By his report, at 6 months follow-up he was drinking an average of 6.53 cups (approx. 1567 cc) per day; at 1 yr follow-up, he was drinking an average of 8.7 cups (approx. 2091 cc) per day. Both values are well within the normal expected ingestion levels and, in fact, are below the levels measured by nursing at the time of discharge. This suggests that not only did the frequency of drinking remain at acceptable levels during the follow-up period, but also that the total amount ingested per day remained acceptable. In addition, John reports increased social activities; the successful completion of three semesters of community college; increased pleasant events; and decreased feelings of anxiety and depression.

DISCUSSION The results of this intervention suggest that, at least in this case, the problem of compulsive polydipsia was amenable to behavioral interventions. Through a combination of response prevention, differential reinforcement and relaxation, this patient was able to decrease his abnormal fluid consumption to more normal levels. In many respects this treatment was similar to treatments of severe obsessive/compulsive disorder already described in the literature (e.g. Foa and Goldstein, 1978; Foa et al., 1983). However, one difference between the presentation of compulsive appetitive behaviors, like polydipsia, and the more classic presentation of obsessive/compulsive disorder (i.e. washers and checkers) may make treatment of compulsive appetitive disorders more problematic. In the classic presentation, objective, externally afrreed-uoon criteria for enfzaaine in the

POLYDIPSIA

357

behavior in a non-obsessive fashion can be identified (e.g. washing the hands when there is visible dirt or before meals). However, for obsessive appetitive behaviors, the criteria for engaging in the behavior is a private event, such as feeling thirsty or hungry. One cannot prevent the response of eating and drinking entirely, and in fact, in non-obsessive individuals the probability of eating or drinking is in some way related to the strength of the urge, that is to feeling thirsty or hungry. The difficulty in treating obsessive appetitive behaviors, then, comes from attempting to maintain the relationship between strength of urge and the behavior while simultaneously reducing the dysfunctional aspects of the eating or drinking behavior. In this patient this was achieved by decreasing both the frequency of the urge and the amount ingested. As response prevention paradigms are used with other disorders involving appetitive behaviors, such as bulimia (SchlesierStropp, 1984), this difficulty in formulating objective, external criteria may need to be addressed more directly. Standard exposure and response prevention may need to be modified in order to ensure that an appropriate relationship between strength of urge and eating or drinking is maintained. Clearly, this is an area where additional research is needed. This intervention was unique in another important way. It was implemented on a regular medical/surgical unit rather than a psychiatric ward. Medical/surgical nurses, burdened by routine acute care requirements, often experience caring for a “psychiatric” patient as a particular problem. This may be especially true for behavioral approaches, which often rely heavily upon staff for implementation. In this case, nursing staff was trained to know explicitly what behaviors to reinforce at what times. This training was enhanced through modelling, roleplaying, feedback and explicit reinforcement during the course of treatment. This model differs from traditional psychiatric consultation by the implementation and following through of a specifically designed treatment plan. That is, we actually provided

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A. KLONOFF

the treatment rather than making recommendations and having the untrained staff implement them independently. Concurrently, this model does not require the “psychiatric milieu” and full-time psychiatric care associated with an inpatient psychiatric ward. The instruction and reinforcement of staff necessitated by this treatment was not any greater than if the patient had been on a non-behavioral psychiatric ward. Therefore, this collaborative effort between staff on a medical/surgical ward and behavioral therapists provides an alternative model to traditional consultation/liaison and innatient nsvchiatric care. Increased attention to the process of introducing and conducting behavioral treatments in non-psychiatric environments may increase the impact of behavior therapy in a medical setting. 1

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REFERENCES Barahal H. S. (1938) Water intoxication in a mental case. Psychiatric Q 12, 767-771, Barlow E. D. and dewardener H. E. (1959) Compulsive water drinking. Q. J. Med. 28, 235-258.

Ackno&dgements-The follow-up management

authors gratefully of this patient.

acknowledge

and DOUGLAS

J. MOORE

Foa E. B. and Goldstein A. (1978) Continuous exposure and complete response prevention in the treatment of obsessive
Jeffrey

W. Janata

and Jane

Buder

for their assistance

in the