Psychogenic polydipsia in a patient with anorexia nervosa

JOURNAL

OF ADOLESCENT

HEALTH

CARE

1985;6;404-406

Psychogenic Polydipsia in a Patient with Anorexia Nervosa KATHLEEN

M.

MYERS,

M.D.,

M.P.H.,

M.S.

This report describes the first reported case of compulsive water drinking (CWD) in an adolescent with anorexia nervosa (AN). The CWD appears to be a bulimic behavior with potentially serious medical complications. The concurrence of AN and CWD suggests possible hypothalamic dysfunction of food and water regulation.

AND

MARK

SCOTT

SMITH,

M.D.

Abnormalities of ADH secretion have been reported in anorexia nervosa (7), although there are no documented cases of concurrent CWD. Our patient with CWD and anorexia nervosa further suggests possible impairment of water metabolism in anorexia and the need to carefully pursue a history of polydipsia in AN patients.

KEY WORDS:

Adolescent psychogenic polydipsia Compulsive water drinking and anorexia nervosa Compulsive water drinking as a form of bulimia Psychogenic polydipsia without psychosis

Psychogenic polydipsia (CWD) is a well-recognized syndrome in psychotic disorders (1) which is much less frequently associated with milder psychopathologies (2,3). Intriguing are the few reported CWD patients with central nervous system impairment (4,5), pregnancy (4), and no psychopathology (2,3). To our knowledge, this is the first reported case of anorexia nervosa (AN) associated with compulsive water drinking (CWD). Morbidity and mortality in CWD are due to the hyposmolar state and hyponatremia that may lead to dementia, seizures, coma, and death (6). Generally, neurologic symptoms clear with correction of the hyponatremia, although patients may establish a new equilibrium with a lowered serum osmolality due to the secretion of antidiuretic hormone (ADH) (1,3).

From the Children’s Orthopedic Hospifal and Medical Center, Departments of Child Psychiatry bnd Pediakics, Seattle, Washington. Address rearint reauests to: Dr. Kathleen M. Myers, Departmenf of Child Psych&y and behavioral Medicine, Children< Orthopedic Hospital and Medical Center, 4800 Sandpoint Way, N.E., P.O. Box C5371, Seattle,

WA

98105.

Manuscript 404 0197-0070/85/$3.30

accepted

September

Case Report A 15-year-old girl was admitted to the adolescent ward of the Children’s Orthopedic Hospital and Medical Center for treatment of anorexia nervosa complicated by psychogenic polydipsia and a hyponatremic seizure. She had begun dieting two years prior to admission (PTA) at a weight of 73 kg and within nine months lost 16 kg. During that time she started drinking several liters of water daily allegedly in an effort to control her appetite. Eight months PTA she began binge eating and vomiting while maintaining her weight at 57 kg. She denied abuse of diuretics or laxatives. By five months PTA her weight had decreased to 48 kg and she had ceased her bulimia but continued to drink several liters of water each day. Two months PTA she acutely drank 11 liters of water over 2 hr; this was apparently triggered by an argument with her mother, A tonic-clonic seizure occurred. Admission serum sodium at another hospital was 107 mEq/L, and potassium was 3.0 mEq/L. Urine specific gravity was 1.004. Computed axial tomography of the head was unremarkable. With fluid restriction and hypertonic saline infusion, her sodium stabilized at 130 mEq/L and she was discharged. Over the next five weeks her weight dropped to 40 kg, CWD continued at 9 liters a day, and she became confused and combative. She was then admitted to our

hospital. Physical examination revealed a cachectic female who was 170 cm tall with a weight of 40 kg. Blood pressure was llOl90 without orthostasis, and the pulse rate was 40 per

minute. Except for acrocyanosis, signs of malnutrition, and

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poorly developed secondary sex characteristics, physical examination was within normal limits. Initial laboratory revealed a serum sodium of 126 mEq/L, potassium 3.8 mEq/L, chloride 94 mEq/L, and bicarbonate 22 mM/L. Serum osmolality was 225 mOsm/L and urine specific gravity was 1.001 with a spot urine sodium excretion of 10 mEq/L. Thyroid studies were normal with T3 (RU) 25.5%, T 4 9.9~g/dl, TSH 2.32 ~IU/ml. Total protein albumin, glucose, blood urea nitrogen, creatinine, hemoglobin, and white blood count were all within normal limits. • Psychiatric evaluation revealed the patient to be completely oriented with an immature manner and speech. Her affect was labile with expressions of worthlessness, suicide ideation, and fear of being alone. There was no formal thought disorder and no ideation of cleansing her "sinfulness" with water. Cognitive processes were concrete and she attributed her drinking to thirst, health, and appetite control. Within her family there was obvious overinvolvement of the patient and her mother, with the father assuming a passive role. Her mother endorsed recurrent depression in herself. The patient met DSM-III criteria for anorexia nervosa with fear of obesity, a disturbed body image, weight loss greater than 25% of original body weight, refusal to maintain appropriate body weight, and no known underlying physical illness. A Minnesota Multiphasic Personality Inventory (MMPI) using adolescent norms showed all scales below 50 except for a 2-scale elevation to 72, suggesting depression without psychosis. Unrestricted on the adolescent ward the first evening, she surreptitiously drank several liters of water. At 0800 the next morning her serum sodium was 125 mEq/L; but by 1800 it was down to 115 mEq/L. She remained asymptomatic. She was transferred to the Inpatient Psychiatric Unit at the University of Washington Hospital (UWH). At UWH her weight gain was irregular, averaging 0.6 kg/week for the first four weeks. With water restriction to approximately two liters a day, her serum sodium quickly stabilized in the normal range, but her urine specific gravity remained in the 1.002 range. She did not comply with an accurate measurement of her fluid balance and when monitoring of intake was relaxed, serum sodium would fall below 130 mEq/L. An empirical trial of thiothixene 6 mg/day was begun after the second week in an attempt to modulate her labile affect and irrational cognitive state which impaired her treatment compliance. By the fourth week she was less labile and more compliant with the behavioral contingency of maintaining serum sodium. However, she began consuming salt packets in order to continue CWD without hyponatremia. Depressive symptoms increased and some lability persisted. Therefore, trazadone was begun and increased to 200 mg/day by the seventh week at which time she weighed 45.9 kg but still had periodic hyponatremia (< 126 rnEq/L). By the tenth week she weighed 48.2 kg. Her mood and thinking were moderately improved, but continued CWD precluded discharge for another four weeks.

PSYCHOGENICPOLYDIPSIA

405

Discussion We cannot find a documented report of polydipsia or water intoxication in anorexia nervosa. Our patient met DSM-III criteria for anorexia nervosa with no evidence of psychosis or primary depression. Improyed nutrition, fluid and electrolyte balance, as well as the probable organizing effects of psychotropic medications appear to have been the major factors in her partial clinical improvement. Her polydipsia may comprise a form of bulimia with water "binging" and diuresis "purging." We have seen one other anorectic patient who also drank excessively and precipitated a hyponatremic seizure. Polydipsia may not be u n c o m m o n in anorexia nervosa, but it rarely progresses to clinical complications. A brief review of other reported cases of polydipsia or irregularities of water metabolism suggests that hypothalamic dysfunction may account for this patient's symptoms (8,9). Polydipsia that occurs with psychosis generally resolves with remission of the psychosis. However, a stable chronic hyponatremic state not uncommonly persists due to an apparent downgrading of the "osmostat" and erratic ADH secretion (1,3). Unlike these patients, our anorexic adolescent could produce normonatremia with fluid restriction, suggesting grossly intact neurohypophyseal function. However, the persistent CWD, despite some stabilization of the anorexia, suggests that there may be unexplained underlying dysfunction. Her surreptitious salt intake indicated that she was more interested in actually drinking than in maintaining a hyponatremic state due to "inappropriate thirst" as was describe d•by Mellinger (10). His patient experienced excessive thirst whenever plasma osmolality exceeded 270 mOsm/1, but had an appropriate response to fluid deprivation and vasopressin administration, suggesting a normal neurohypophyseal axis. Our patient drank without relation to serum sodium and maintained normal baseline serum sodium, thus differentiating her from the patients with "inappropriate thirst" and psychosis, respectively. Gold studied water metabolism in a series of anorectic patients with polyuria and normonatremia (7). These patients demonstrated abnormally low or erratic secretion of ADH unrelated to serum sodium. The polyuria persisted into the recovery phase and could not be explained by the ADH abnormalities. Although Gold commented that polydipsia could explain these findings, a history of water intake was not reported. Since hypoglycemia simultaneously stimulates thirst, hunger, and ADH secretion, Gold postulates an afferent link between neurogenic con-

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MYERSAND SMITH

trol of food and water balance in this population. There are no metabolic studies on our patient to compare to Gold's series. Clinically ~ however, the coexistence of AN and CWD and his observation that polydipsia could explain his findings suggest that a history of water intake should be carefully evaluated in anorexic patients. Further work on the neurogenic control of food and water balance in these patients seems warranted.

References 1. Hariprasad MK, Eisinger RP, Nadler IM. Hyponatremia in psychogenic polydipsia. Arch Intern Med 1980;140:1639-42. 2. Chinn T. Compulsive water drinking. J Nerv Ment Dis 1974;158:78-80.

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3. Barlow ED, DeWardner HE. Compulsive water drinking. Q J Med 1959;28:235-58. 4. Shalev E, Goldstein D, Zuckerman H. Compulsive water drinking in pregnancy. Int J Gynecol Obstet 1980;18:465-7. 5. Stuart CA, Neelson FA, Lebovitz HE. Disordered control of thirst in hypothalamic-pituitary sarcoidosis. N Eng J Med 1980;303:1078-82. 6. Rendell M, McGrane D, Cuesta M. Fatal compulsive water drinking. JAMA 1978;240:2557-9. 7. Gold PW, Kaye W, Robertson GL, et al. Abnormalities in plasma and cerebrospinal fluid arginine vasopressin in patients with anorexia nervosa. N Engl J Med 1983;308:1117-23. 8. Fitzsimmons MA. The hypothalamus and drinking. Br Med Bull 1966;22:232-7. 9. Hernandez L, Hoebel BG. Basic mechanisms of feeding and weight regulation. In: Stunkard A, ed. Obesity. Philadelphia: W. B. Saunders, 1980. 10. Mellinger RC, Zafar MS. Primary polydipsia: syndrome of inappropriate thirsL Arch Intern Med 1983;143:1249-51.