Compulsive Water Drinking Water Intoxication
and
J. P. A. Noonan and J. Ananth
C
OMPULSIVE water drinking is one of many causes of water intoxication. The phrase “water intoxication” was first applied by Rowntree’ to the symptoms of increased neuroexcitability produced by a sudden dilution of the body solutes through the excessive administration of water. The syndrome has been more recently defined by Finkel’ as developing if the water excess is profound or rapid in onset, so that the patient cannot excrete water fast enough to prevent positive water balance although renal diluting capacity is normal. The patient’s level of total body water increases, and he becomes hyponatremic. Crumpacker and Kriel,3 in a report of water intoxication in infants, have classified the syndrome into four etiologic groups. The first of these is transplacental water intoxication of newborn infants born to asymptomatic hyponatremic mothers. The second group is iatrogenic and includes: improper administration of fluids parenterally or otherwise, the use of medication affecting antidiuretic hormone (ADH), and the use of medication that decreases the ability to conserve sodium. The third group consists of the syndrome of inappropriate ADH due to disease. The fourth group is that in which the water intoxication is due to excessive intake alone. This latter group includes those cases of psychogenic etiology. Although there are many possible etiologies, the symptoms of the intoxication remain virtually uniform. They are primarily neurologic, consisting of anorexia, headache, blurred vision, muscle cramps, and ultimately stupor, convulsions, and death. Since the initial description of the syndrome of water intoxication by Rowntree in 1923, there has been a considerable reluctance among physicians in admitting the possibility of a purely psychogenic polydipsia resulting in water intoxication. In fact, there are repeated assertions in the literature that the condition cannot occur without a predisposing cause. A lead article in the Lancet4 assures us that “water cannot harm thirsty patients.” Linquette et al.” are equally emphatic in stating that “water intoxication therefore occurs only when there is impairment of water excretion as well as excessive water intake.” Hobson and English” warn that the assumption that normal capacities of water excretion have been exceeded is not supported by the experimental study of compulsive water drinkers who fail to develop intoxication following excessive water intake unless exogenous vasopression is administered. Demanet et al.’ report that excessive intake of fluids seemed the most important causative factor in 9 of 12 patients who developed hyponatremia and coma. In 7 of From the Department of Psychiatry, St. Mary’s Hospital. Montreal Canada. J. P. A. Noonan, M.D.; Resident in Psychiatrv, Sr. Mary’s Hospital; J. Ananth, M.D.: Assistant Professor, McGill University and Director of Psychiatric Education and Research, St. Mary’s HOTpital: Montreal. Canada. Reprint requests should be addressed to J. P. A. Noonan. M.D.. Department of Psychiatrv. Montreal General Hospital. 1650 Cedar Avenue. Montreal, H3G 1.44, Canada. c 1977 bv Grune & Stratton, Inc. Comprehensive
Psychiatry,
Vol. 18. No. 2 (March/April).
1977
183
184
NOONAN AND ANANTH
the 9 cases, the excessive intake was in the form of beer. On the other hand, Doig et al.,8 in a study of healthy subjects, suggest that water intoxication is not a hazard of beer drinking in healthy individuals. In favor of the view that factors other than excessive intake are required, is the report by Kennedy and Earleyg of profound hyponatremia resulting from a thiazide-induced decrease in urine-diluting capacity in a patient with primary polydipsia. Beresford’O describes two cases implicating hydrochlorothiazide in the onset of acute hyponatremic encephalopathy in known long-term compulsive water drinkers. The possibility that schizophrenic patients are vulnerable to water loading is raised by Hobson and English.6 They cite previous evidence of water retention in schizophrenia and speculate regarding a possible hypothalamic disorder, in some cases of schizophrenia, resulting in inappropriate release of ADH, and further state that it is difficult to evaluate the possible contribution of “emotional stress.” Thus, they imply that water intoxication in schizophrenic patients may not be psychogenic. On the basis of these findings, it is evident that excessive water intake may result in water intoxication in the presence of predisposing factors. However, the possibility that purely psychogenic polydipsia may also result in water intoxication remains controversial. Despite the controversy, there are a number of cases in the literature in which polydipsia alone has been implicated in water intoxication. Pickering and Hogan” report a case of a 9 le yr old boy who developed a severe toothache and began drinking large quantities of water for the relief of his pain, as a result of which he became water intoxicated and had a convulsion. Swanson and Iseri’* describe two cases of acute encephalopathy considered to be due to selfinduced water intoxication. One of these patients was an alcoholic, and the other ingested a large volume of water in an effort to induce defecation. Emery’” describes the case of a 47 yr old alcoholic who progressed to convulsions and coma as a result of drinking a large volume of water. Alexander et al.” report a case in which coma and convulsions were the consequence of acute water intoxication resulting from a schizophrenic delusion. Baharal’” reported one case of a physically healthy schizophrenic patient who drank large quantities of water and then convulsed. Bewley”j reported two cases of acute water intoxication from compulsive water drinking in psychiatric patients. Devereaux and McCormick” described the case of a 41 yr old schizophrenic woman whom they believed to be the most severe case of water intoxication in the literature. A 29 yr old schizophrenic male was admitted unconscious and convulsing following the ingestion of large amounts of water.‘” Murphy and Zelman,lg in a paper differentiating the diagnostic possibilities in cases of polyuria, give an account of a patient suffering from schizophrenia who became comatose from water drinking. This patient had been drinking water excessively for at least 5 yr. Langgard and Smith”O report two cases, a schizophrenic and a frontal lobe syndrome, who, by the ingestion of massive volumes of water without any contributory causes, exceeded their maximal water tolerance and manifested “pure water intoxication.” Resnick and Pattersonzl report the case of a 31 yr old male schizophrenic who developed convulsions and coma after having been a compulsive water drinker for many months. Thomsen et al.2’ report a case of a 38 yr old male schizophrenic who developed water intoxication as the result of a delusion. Raskind2” reports the case of a 56 yr old female psychiatric patient who developed water intoxication, was subsequently
WATER
185
INTOXICATION
given hydroflumethiazide, 50 mg, and died within 24 hr. The effect of the thiazide in this case remains an unanswerable question. All the above cases reported a specific neurologic syndrome resulting from water intoxication. We have encountered a patient who had been a compulsive water drinker for several years and who periodically manifested exacerbations of psychopathology as a result of water intoxication. To our knowledge, similar observations have not been reported previously. The following is the case report and clinical findings of our patient. CASE REPORT A 32.year-old woman was admitted to the Douglas Hospital in 1942 with a diagnosis of mental retardation and a history of wandering behavior. At that time, the physical examination was unremarkable; laboratory (urinalysis, hemogram, blood chemistry, cerebrospinal fluid), and radiologic (skull and chest x-ray) examinations were normal. Her physical and mental status remained unchanged until 1970. In July of 1970, she complained of dizzy spells and her serum electrolytes were: sodium (Na) 127 meq/liter. chloride (Cl) 8 I meq/liter, and potassium (K) 3. I meq/liter. The diagnosis was electrolyte imbalance of unknown etiology, and treatment by electrolyte replacement was instituted. Exacerhation of psychopathology, including visual and auditory hallucinations, occurred concomitantly with the dizzy spells. She complained of further dizzy spells in November of 1970. but no laboratory investigations were done at that time. In October of 1971, she was transferred to the Montreal General Hospital because of nausea and vomiting with left lower quadrant pain. At that time, she was also agitated, suffered from auditory and visual hallucinations, and exhibited compulsive hand washing. On examination, her pulse was 72 beats/min, respiration 20/min, and her blood pressure was normal. There was a systolic murmur in the left parasternal area, and T-wave inversion was noted on the electrocardiogram. On investigation, serum Na was I IO meq/liter, K was 2. I meq/liter, Cl was 66 meq/liter, and white blood cell count was Il.6OO/cu mm. An intravenous pyelogram and skull x-ray were negative. although she was found to have gallstones. The diagnosis was electrolyte imbalance due to compulsive water drinking and cholelithiasis. She was treated with electrolyte replacement, made a rapid recovery, and returned to the Douglas Hospital after 3 weeks. Following this diagnosis, the nursing notes make almost daily reference to the continued excessive water drinking, which up to that point had been well concealed by the patient and not suspected by the staff. More careful observation and inquiry established several incidences of water ingestion from the water faucet resulting in a semiconscious state. She was found to lie in the bathtub with her mouth to the faucet in such a way that the sound of running water could not be heard. Various modalities of treatment, including phenothiazines, butyrophenones. thioxanthenes and behavior therapy, have been tried. In spite of these therapeutic attempts, the compulsive water drinking of this patient has been resistant to change. This is revealed by recurrent episodic neurologic and psychiatric symptoms accompanied by electrolyte imbalance. For instance, on August I. 1973, serum Na was 126 meq/liter, K was 3.5 meq/liter, and Cl was 89 meq/liter; and on August 7, 1973, serum Na was I I2 meq/liter. K was 2.6 meq/liter. and Cl was 80 meq/liter. Becauseof repeated instances of this nature. careful vigilance to prevent excessive water drinking, including bathing only in the presence of staff, have been instituted. In spite of all these precautions, electrolyte imbalance and exacerbation of psychopathology recur periodically as a result of excessive water intake.
DISCUSSION
Water intoxication as a result of compulsive water drinking, although rare, has been reported most frequently among psychiatric patients. If we include the case reviewed in this paper, then 15 of the 21 reported cases of water intoxication due to polydipsia have been in patients with a psychiatric illness. This fact is very pertinent in relation to the problem of the diagnosis of this condition. The diagnosis of water intoxication due to excessive water ingestion is based primarily on a
186
NOONAN AND ANANTH
good history and a lowered serum Na, supported if possible, by the direct observation of excessive water intake, particularly in hospitalized patients. However, these psychiatric patients may not be able to provide a good history or, for some psychologic reason, they may conceal the fact of excessive water ingestion. If they do conceal this fact, it may be extremely difficult to detect the excessive water ingestion by direct observation. Our patient, because of the lack of a history and because of her ability to position herself so that she functioned as an extension of the bathtub faucet, deceived the staff and eluded diagnosis for a long time. In fact, even after hyponatremia had been documented, it was another 15 months before the diagnosis of water intoxication due to compulsive water drinking was suggested. Since no predisposing organic factor to explain the water intoxication has been detected in spite of extensive investigations over a period of years, our patient may be said to have had purely psychogenic water intoxications due to compulsive water drinking. However, among schizophrenic patients, a vulnerability to water retention has been hypothesized.6 Therefore, although we have concluded that there has been no predisposition to water intoxication in our patient, this conclusion takes cognizance of the possibility that future research will reveal organic causes for some or all of the cases of water intoxication that are now ascribable to excessive intake alone. On the basis of the difficulties we experienced in making the diagnosis and because the history of excessive water ingestion was not readily forthcoming, we assume that this condition is probably more prevalent among psychiatric patients than is recognized. We suggest, therefore, that every patient found to have periodically low serum Na without any detectable cause be observed closely for excessive water intake. It is generally assumed that water intoxication manifests as a neurologic syndrome with anorexia, headache, blurred vision, muscle cramps, alteration of consciousness, and convulsions. However, as revealed in our patient, it can also masquerade as a psychiatric syndrome with auditory and visual hallucinations, obsessive-compulsive symptoms, such as hand washing, and agitation with clear consciousness, at least initially. Such a presentation of this condition poses further difficulty in the diagnosis. The likelihood of a psychiatric presentation combined with low serum Na resulting from excessive water ingestion must be entertained and carefully evaluated in pertinent situations. Usually the treatment of water intoxication requires an urgent, planned approach based on the nature of the electrolyte disturbances, and the prognosis is excellent. Although the water intoxication can be easily remedied, compulsive water drinking is extremely difficult to treat. Surprisingly, most of the reports on this subject do not delve into this important aspect of the management of these patients. With this difficulty in mind, we therefore conclude that psychiatric patients manifesting excessive water intake require great vigilance by the staff to prevent recurrences. REFERENCES 1. Rowntree LG: Water intoxication. Intern Med 32:157-174, 1923
Arch
2. Finkel RM: Hyponatremia. North Am 56:645-649, 1972
Med
Clin
WATER INTOXICATION
3. Crumpacker
RW.
187
Kriel
RL:
Voluntary
water intoxication in normal infants. Neurology 23:1251~1255, 1973 4. Lead Article: Water intoxication. Lancet 2641425-426. 1953 5. Linquette M, Fossati P, Lefebvre J, et al: Acute water intoxication from compulsive drinking. Br Med J 2:365, 1973 6. Hobson JA. English JT: Self-induced water intoxication. Ann Intern Med 58:324-332, 1963 7. Demanet JC. Bonnyns M, Bleiberg N, et al: Coma due to water intoxication in beer drinkers. Lancet2:lllS 1117,1971 8. Doig A. Gray W, Munro JF, et al: Water intoxication in beer-drinkers. Lancet 2: I3 18. 197 I
13. Emery
R: Water
intoxication.
Br Med J
21367, 1959 14. Alexander ER, Crow TJ, Hamilton SM: Water intoxication in relation to acute psychotic disorder. Br Med J l:89, 1973 15. Barahal HS: Water intoxication in mental case. Psychiatr Q 12:767-771, 1938 16. Bewley TH: Acute water-intoxication from compulsive water-drinking. Br Med J 2:864, 1964 17. Devereaux MW, McCormick RA: Psychogenic water intoxication: A case report. Am J Psychiatry 129:6288630, 1972 18. Carter TJ: Water intoxication. 21367. 1959
Br Med .I
19. Murphy FJ, Zelman S: Water metabolism and the psychiatric patient. J Urology 92:60 63, 1964
9. Kennedy RM. Earley LE: Profound hypcnatremia resulting from a thiazide-induced decrease in urinary diluting capacity in a patient with primary polydipsia. N Engl J Med 282:1185-l 186. 1970 IO. Beresford RH: Polydipsia, hydrochlorothiazide. and water intoxication. JAMA 214:8799883. 1970 I I. Pickering LK, Hogan GR: Voluntary water intoxication in a normal child. J Pediatr 78:316-318. 1971
20. Langgard H. Smith WO: Self-induced water intoxication without predisposing illness. N Engl J Med 266:378-38 1, 1962 21. Resnick MD, Patterson C: Coma and convulsions due to compulsive water drinking. Neurology l9:l 125-l 126. 1969 22. Thomsen WK. Prince B. Kilgore T: Cumpulsive water drinking. Am J Psychiatry I30:h IO, 1973
I?. Swanson AG. Iseri OA: Acute encephalopathy due to water intoxication. N Engl J Med 258:831 834, 1958
23. Raskind M: water intoxication. 30:112 ll4,1974
Psychosis, polydipsia and Arch Gen Psychiatry
and
J. P. A. Noonan and J. Ananth
C
OMPULSIVE water drinking is one of many causes of water intoxication. The phrase “water intoxication” was first applied by Rowntree’ to the symptoms of increased neuroexcitability produced by a sudden dilution of the body solutes through the excessive administration of water. The syndrome has been more recently defined by Finkel’ as developing if the water excess is profound or rapid in onset, so that the patient cannot excrete water fast enough to prevent positive water balance although renal diluting capacity is normal. The patient’s level of total body water increases, and he becomes hyponatremic. Crumpacker and Kriel,3 in a report of water intoxication in infants, have classified the syndrome into four etiologic groups. The first of these is transplacental water intoxication of newborn infants born to asymptomatic hyponatremic mothers. The second group is iatrogenic and includes: improper administration of fluids parenterally or otherwise, the use of medication affecting antidiuretic hormone (ADH), and the use of medication that decreases the ability to conserve sodium. The third group consists of the syndrome of inappropriate ADH due to disease. The fourth group is that in which the water intoxication is due to excessive intake alone. This latter group includes those cases of psychogenic etiology. Although there are many possible etiologies, the symptoms of the intoxication remain virtually uniform. They are primarily neurologic, consisting of anorexia, headache, blurred vision, muscle cramps, and ultimately stupor, convulsions, and death. Since the initial description of the syndrome of water intoxication by Rowntree in 1923, there has been a considerable reluctance among physicians in admitting the possibility of a purely psychogenic polydipsia resulting in water intoxication. In fact, there are repeated assertions in the literature that the condition cannot occur without a predisposing cause. A lead article in the Lancet4 assures us that “water cannot harm thirsty patients.” Linquette et al.” are equally emphatic in stating that “water intoxication therefore occurs only when there is impairment of water excretion as well as excessive water intake.” Hobson and English” warn that the assumption that normal capacities of water excretion have been exceeded is not supported by the experimental study of compulsive water drinkers who fail to develop intoxication following excessive water intake unless exogenous vasopression is administered. Demanet et al.’ report that excessive intake of fluids seemed the most important causative factor in 9 of 12 patients who developed hyponatremia and coma. In 7 of From the Department of Psychiatry, St. Mary’s Hospital. Montreal Canada. J. P. A. Noonan, M.D.; Resident in Psychiatrv, Sr. Mary’s Hospital; J. Ananth, M.D.: Assistant Professor, McGill University and Director of Psychiatric Education and Research, St. Mary’s HOTpital: Montreal. Canada. Reprint requests should be addressed to J. P. A. Noonan. M.D.. Department of Psychiatrv. Montreal General Hospital. 1650 Cedar Avenue. Montreal, H3G 1.44, Canada. c 1977 bv Grune & Stratton, Inc. Comprehensive
Psychiatry,
Vol. 18. No. 2 (March/April).
1977
183
184
NOONAN AND ANANTH
the 9 cases, the excessive intake was in the form of beer. On the other hand, Doig et al.,8 in a study of healthy subjects, suggest that water intoxication is not a hazard of beer drinking in healthy individuals. In favor of the view that factors other than excessive intake are required, is the report by Kennedy and Earleyg of profound hyponatremia resulting from a thiazide-induced decrease in urine-diluting capacity in a patient with primary polydipsia. Beresford’O describes two cases implicating hydrochlorothiazide in the onset of acute hyponatremic encephalopathy in known long-term compulsive water drinkers. The possibility that schizophrenic patients are vulnerable to water loading is raised by Hobson and English.6 They cite previous evidence of water retention in schizophrenia and speculate regarding a possible hypothalamic disorder, in some cases of schizophrenia, resulting in inappropriate release of ADH, and further state that it is difficult to evaluate the possible contribution of “emotional stress.” Thus, they imply that water intoxication in schizophrenic patients may not be psychogenic. On the basis of these findings, it is evident that excessive water intake may result in water intoxication in the presence of predisposing factors. However, the possibility that purely psychogenic polydipsia may also result in water intoxication remains controversial. Despite the controversy, there are a number of cases in the literature in which polydipsia alone has been implicated in water intoxication. Pickering and Hogan” report a case of a 9 le yr old boy who developed a severe toothache and began drinking large quantities of water for the relief of his pain, as a result of which he became water intoxicated and had a convulsion. Swanson and Iseri’* describe two cases of acute encephalopathy considered to be due to selfinduced water intoxication. One of these patients was an alcoholic, and the other ingested a large volume of water in an effort to induce defecation. Emery’” describes the case of a 47 yr old alcoholic who progressed to convulsions and coma as a result of drinking a large volume of water. Alexander et al.” report a case in which coma and convulsions were the consequence of acute water intoxication resulting from a schizophrenic delusion. Baharal’” reported one case of a physically healthy schizophrenic patient who drank large quantities of water and then convulsed. Bewley”j reported two cases of acute water intoxication from compulsive water drinking in psychiatric patients. Devereaux and McCormick” described the case of a 41 yr old schizophrenic woman whom they believed to be the most severe case of water intoxication in the literature. A 29 yr old schizophrenic male was admitted unconscious and convulsing following the ingestion of large amounts of water.‘” Murphy and Zelman,lg in a paper differentiating the diagnostic possibilities in cases of polyuria, give an account of a patient suffering from schizophrenia who became comatose from water drinking. This patient had been drinking water excessively for at least 5 yr. Langgard and Smith”O report two cases, a schizophrenic and a frontal lobe syndrome, who, by the ingestion of massive volumes of water without any contributory causes, exceeded their maximal water tolerance and manifested “pure water intoxication.” Resnick and Pattersonzl report the case of a 31 yr old male schizophrenic who developed convulsions and coma after having been a compulsive water drinker for many months. Thomsen et al.2’ report a case of a 38 yr old male schizophrenic who developed water intoxication as the result of a delusion. Raskind2” reports the case of a 56 yr old female psychiatric patient who developed water intoxication, was subsequently
WATER
185
INTOXICATION
given hydroflumethiazide, 50 mg, and died within 24 hr. The effect of the thiazide in this case remains an unanswerable question. All the above cases reported a specific neurologic syndrome resulting from water intoxication. We have encountered a patient who had been a compulsive water drinker for several years and who periodically manifested exacerbations of psychopathology as a result of water intoxication. To our knowledge, similar observations have not been reported previously. The following is the case report and clinical findings of our patient. CASE REPORT A 32.year-old woman was admitted to the Douglas Hospital in 1942 with a diagnosis of mental retardation and a history of wandering behavior. At that time, the physical examination was unremarkable; laboratory (urinalysis, hemogram, blood chemistry, cerebrospinal fluid), and radiologic (skull and chest x-ray) examinations were normal. Her physical and mental status remained unchanged until 1970. In July of 1970, she complained of dizzy spells and her serum electrolytes were: sodium (Na) 127 meq/liter. chloride (Cl) 8 I meq/liter, and potassium (K) 3. I meq/liter. The diagnosis was electrolyte imbalance of unknown etiology, and treatment by electrolyte replacement was instituted. Exacerhation of psychopathology, including visual and auditory hallucinations, occurred concomitantly with the dizzy spells. She complained of further dizzy spells in November of 1970. but no laboratory investigations were done at that time. In October of 1971, she was transferred to the Montreal General Hospital because of nausea and vomiting with left lower quadrant pain. At that time, she was also agitated, suffered from auditory and visual hallucinations, and exhibited compulsive hand washing. On examination, her pulse was 72 beats/min, respiration 20/min, and her blood pressure was normal. There was a systolic murmur in the left parasternal area, and T-wave inversion was noted on the electrocardiogram. On investigation, serum Na was I IO meq/liter, K was 2. I meq/liter, Cl was 66 meq/liter, and white blood cell count was Il.6OO/cu mm. An intravenous pyelogram and skull x-ray were negative. although she was found to have gallstones. The diagnosis was electrolyte imbalance due to compulsive water drinking and cholelithiasis. She was treated with electrolyte replacement, made a rapid recovery, and returned to the Douglas Hospital after 3 weeks. Following this diagnosis, the nursing notes make almost daily reference to the continued excessive water drinking, which up to that point had been well concealed by the patient and not suspected by the staff. More careful observation and inquiry established several incidences of water ingestion from the water faucet resulting in a semiconscious state. She was found to lie in the bathtub with her mouth to the faucet in such a way that the sound of running water could not be heard. Various modalities of treatment, including phenothiazines, butyrophenones. thioxanthenes and behavior therapy, have been tried. In spite of these therapeutic attempts, the compulsive water drinking of this patient has been resistant to change. This is revealed by recurrent episodic neurologic and psychiatric symptoms accompanied by electrolyte imbalance. For instance, on August I. 1973, serum Na was 126 meq/liter, K was 3.5 meq/liter, and Cl was 89 meq/liter; and on August 7, 1973, serum Na was I I2 meq/liter. K was 2.6 meq/liter. and Cl was 80 meq/liter. Becauseof repeated instances of this nature. careful vigilance to prevent excessive water drinking, including bathing only in the presence of staff, have been instituted. In spite of all these precautions, electrolyte imbalance and exacerbation of psychopathology recur periodically as a result of excessive water intake.
DISCUSSION
Water intoxication as a result of compulsive water drinking, although rare, has been reported most frequently among psychiatric patients. If we include the case reviewed in this paper, then 15 of the 21 reported cases of water intoxication due to polydipsia have been in patients with a psychiatric illness. This fact is very pertinent in relation to the problem of the diagnosis of this condition. The diagnosis of water intoxication due to excessive water ingestion is based primarily on a
186
NOONAN AND ANANTH
good history and a lowered serum Na, supported if possible, by the direct observation of excessive water intake, particularly in hospitalized patients. However, these psychiatric patients may not be able to provide a good history or, for some psychologic reason, they may conceal the fact of excessive water ingestion. If they do conceal this fact, it may be extremely difficult to detect the excessive water ingestion by direct observation. Our patient, because of the lack of a history and because of her ability to position herself so that she functioned as an extension of the bathtub faucet, deceived the staff and eluded diagnosis for a long time. In fact, even after hyponatremia had been documented, it was another 15 months before the diagnosis of water intoxication due to compulsive water drinking was suggested. Since no predisposing organic factor to explain the water intoxication has been detected in spite of extensive investigations over a period of years, our patient may be said to have had purely psychogenic water intoxications due to compulsive water drinking. However, among schizophrenic patients, a vulnerability to water retention has been hypothesized.6 Therefore, although we have concluded that there has been no predisposition to water intoxication in our patient, this conclusion takes cognizance of the possibility that future research will reveal organic causes for some or all of the cases of water intoxication that are now ascribable to excessive intake alone. On the basis of the difficulties we experienced in making the diagnosis and because the history of excessive water ingestion was not readily forthcoming, we assume that this condition is probably more prevalent among psychiatric patients than is recognized. We suggest, therefore, that every patient found to have periodically low serum Na without any detectable cause be observed closely for excessive water intake. It is generally assumed that water intoxication manifests as a neurologic syndrome with anorexia, headache, blurred vision, muscle cramps, alteration of consciousness, and convulsions. However, as revealed in our patient, it can also masquerade as a psychiatric syndrome with auditory and visual hallucinations, obsessive-compulsive symptoms, such as hand washing, and agitation with clear consciousness, at least initially. Such a presentation of this condition poses further difficulty in the diagnosis. The likelihood of a psychiatric presentation combined with low serum Na resulting from excessive water ingestion must be entertained and carefully evaluated in pertinent situations. Usually the treatment of water intoxication requires an urgent, planned approach based on the nature of the electrolyte disturbances, and the prognosis is excellent. Although the water intoxication can be easily remedied, compulsive water drinking is extremely difficult to treat. Surprisingly, most of the reports on this subject do not delve into this important aspect of the management of these patients. With this difficulty in mind, we therefore conclude that psychiatric patients manifesting excessive water intake require great vigilance by the staff to prevent recurrences. REFERENCES 1. Rowntree LG: Water intoxication. Intern Med 32:157-174, 1923
Arch
2. Finkel RM: Hyponatremia. North Am 56:645-649, 1972
Med
Clin
WATER INTOXICATION
3. Crumpacker
RW.
187
Kriel
RL:
Voluntary
water intoxication in normal infants. Neurology 23:1251~1255, 1973 4. Lead Article: Water intoxication. Lancet 2641425-426. 1953 5. Linquette M, Fossati P, Lefebvre J, et al: Acute water intoxication from compulsive drinking. Br Med J 2:365, 1973 6. Hobson JA. English JT: Self-induced water intoxication. Ann Intern Med 58:324-332, 1963 7. Demanet JC. Bonnyns M, Bleiberg N, et al: Coma due to water intoxication in beer drinkers. Lancet2:lllS 1117,1971 8. Doig A. Gray W, Munro JF, et al: Water intoxication in beer-drinkers. Lancet 2: I3 18. 197 I
13. Emery
R: Water
intoxication.
Br Med J
21367, 1959 14. Alexander ER, Crow TJ, Hamilton SM: Water intoxication in relation to acute psychotic disorder. Br Med J l:89, 1973 15. Barahal HS: Water intoxication in mental case. Psychiatr Q 12:767-771, 1938 16. Bewley TH: Acute water-intoxication from compulsive water-drinking. Br Med J 2:864, 1964 17. Devereaux MW, McCormick RA: Psychogenic water intoxication: A case report. Am J Psychiatry 129:6288630, 1972 18. Carter TJ: Water intoxication. 21367. 1959
Br Med .I
19. Murphy FJ, Zelman S: Water metabolism and the psychiatric patient. J Urology 92:60 63, 1964
9. Kennedy RM. Earley LE: Profound hypcnatremia resulting from a thiazide-induced decrease in urinary diluting capacity in a patient with primary polydipsia. N Engl J Med 282:1185-l 186. 1970 IO. Beresford RH: Polydipsia, hydrochlorothiazide. and water intoxication. JAMA 214:8799883. 1970 I I. Pickering LK, Hogan GR: Voluntary water intoxication in a normal child. J Pediatr 78:316-318. 1971
20. Langgard H. Smith WO: Self-induced water intoxication without predisposing illness. N Engl J Med 266:378-38 1, 1962 21. Resnick MD, Patterson C: Coma and convulsions due to compulsive water drinking. Neurology l9:l 125-l 126. 1969 22. Thomsen WK. Prince B. Kilgore T: Cumpulsive water drinking. Am J Psychiatry I30:h IO, 1973
I?. Swanson AG. Iseri OA: Acute encephalopathy due to water intoxication. N Engl J Med 258:831 834, 1958
23. Raskind M: water intoxication. 30:112 ll4,1974
Psychosis, polydipsia and Arch Gen Psychiatry
