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Psychogenic polydipsia — An unusual cause of hyponatremic coma and seizure
CASE CONFERENCE coma; hyponatremia; polydipsia, psychogenic; seizure
P s y c h o g e n i c Polydipsia m An Unusual C a u s e of H y p o n a t r e m i c C o m a and Seizure [Roberge R, Gemsheimer J, Sparano R, Tartakoff R, Morgenstern MJ, Rubin K, Senekjian D, Andrade R, Matthew V: Psychogenic polydipsia - - An unusual cause of hyponatremic coma and seizure. Ann Emerg Med April 1984;13:274-276.] INTRODUCTION
Joel Gemsheimer, MD: Today's case is that of a psychiatric patient who presented comatose and with a witnessed first time grand-mal-type seizure. The discussant will be Raymond Roberge, MD, Department of Emergency Medicine, Lincoln Medical and Mental Health Center, and New York Medical College.
CASE PRESENTATION Robert Sparano, MD: A 38-year-old man presented to the emergency department after having been found unconscious at home. Paramedics responding at the scene reported witnessing a grand-real-type seizure lasting approximately one minute. The patient was reported to respond to noxious stimuli by withdrawal of all extremities. The paramedics placed an oral airway, administered oxygen by nasal cannula, and transported the patient. Prior medical history, as provided by family members, revealed that the patient was a psychiatric outpatient with a longstanding diagnosis of schizophrenia. There was also a long history of intravenous drug abuse and alcohol abuse. Medications included Cogentin (benztropine) on a daily basis, and Prolixin (fluphenazine) 25 mg intramuscularly on a biweekly basis. Admission vital signs were as follows: pulse, 88 beats per minute; blood pressure, 180/120 m m Hg; respirations, 28/min; and temperature, 37.3 C. Shortly after admission, the patient sustained a second grand-mal-type seizure. He was intubated and was administered 5 mg diazepam intravenously, with resultant termination of the seizure. The patient received one ampule (50 cc) of 50% dextrose solution, four ampules (1.6 mg) naloxone, and 100 mg thiamine, without apparent response. Physostigmine, 2 rag, was administered to counteract the possibility of phenothiazine toxicity, again without apparent response. An Ewald tube was passed nasally and the stomach was aspirated of approximately 200 cc of a brownish sludge that was sent for toxicology screening and subsequently was found to be negative. A charcoal slurry was instilled into the stomach and a cathartic was administered. Physical examination revealed some nuchal rigidity. Pupils were equal and reactive. Deep tendon reflexes were equal and symmetrical. Plantar reflexes were downgoing. The chest was clear to auscultation, and the heart examination was normal. The abdomen was soft and non-distended, and hypoactive bowel sounds were present. Rectal examination revealed good sphincter tone, no masses, and guaiac-negative stool. The chest film was negative, and the electrocardiogram revealed no acute changes. Lumbar puncture was negative. Toxicology screen was negative for alcohol, phenothiazines, benzodiazepines, and barbiturates; salicylates were 3.4 mg%. The urinalysis revealed a specific gravity of 1.005, 1 to 3 WBCs, 3 to 6 RBCs, and a pH of 6.0. The CBC revealed a WBC of 18,100; hemoglobin, 13.1; and hematocrit, 37. The serum electrolytes were as follows: sodium, 105; potassium, 2.9; chloride, 73; CO2, 23; BUN, 5; glucose, 101; creatinine, 0.8~ 13:4 April 1984
Annals of Emergency Medicine
Raymond Roberge, MD Joel Gernsheimer, MD Robert Sparano, MD Randy Tartakoff, MD Mary Jo Morgenstern, MD Kenneth Rubin, MD Doris Senekjian, MD Ruben Andrade, MD Varghese Matthew, MD Bronx, New York From the Emergency Medicine Residency Program, Lincoln Medical and Mental Health Center, Bronx; and New York Medical College, New York, New York, Received for publication April 25, 1983, Accepted for publication June 29, 1983. Address for reprints: Raymond Roberge, MD, Department of Emergency Medicine, Lincoln Medical and Mental Health Center, 234 East 149th Street, Bronx, New York 10451.
274/93
PSYCHOGENIC POLYDIPSIA Emergency Medicine Resiency Program - Lincoln Medical and Mental Health Center
Fig. Causes of hyponatremia (adapted from Berl et alZ). magnesium, 1.6; and calcium, 8.5. The patient was admitted with a diagnosis of hyponatremic coma. An intravenous infusion of 3% saline solution was begun at 120 cc per hour, and the patient regained consciousness in approximately four hours. On further questioning, the family revealed that on the day prior to admission the patient had begun acting bizarrely and ingesting large quantities of water throughout the day and night.
DISCUSSION Raymond Roberge, MD: The causes of coma and seizure presenting to the emergency department are numerous and varied, but most commonly involve neurological disorders, infectious agents, inhalation of noxious agents, trauma, environmental factors (eg, hypothermia), and metabolic disorders. Hyponatremia as a cause of seizure and coma is a relatively infrequent occurrence in the emergency department setting, and statistics regarding its actual incidence are lacking. Psychogenic polydipsia, one of the more uncommon causes of hyponatremia, is a clinical rarity. 1-s
Question: What is psychogenic polydipsia? Dr Roberge: Psychogenic polydipsia is a firmly established, although rarely reported, syndrome consisting of compulsive consumption of fluids due to a psychological disturbance. It is characterized by the ingestion of huge volumes of fluid over a short period of time by persons with various behavioral disorders. 6 The body is normally able to clear 15 L to 20 L per day, but excessive volumes in a short period of time overwhelm the body's clearing capabilities, resulting in acute dilutional hyponatremia. An additional aggravating factor may be the concomitant use of certain psychotropic medications, such as Mellaril (thioridazine) and Elavil (amitriptyline), which are known to induce dilutional hyponatremia. 6
Question: Which disorders must be considered in the differential diagnosis of hyponatremic coma and seizure?
Dr Roberge: The etiologies of hyponatremia can be grouped conveniently into three general categories: those with a deficit of total body water and larger deficit of total body sodium, those with an excess of total body water (psychogenic polydipsia is included in this category), and those with an excess total body sodium and larger excess total body water (Figure).7
Question: Which data are necessary in arriving at a diagnosis of psychogenic polydipsia?
Dr Roberge: The diagnosis of psychogenic polydipsia should be considered in any patient with a known psychiatric disorder who presents with a seizure and/or coma secondary to hyponatremia. Obviously the history is one of the most important criteria. Second, urinary electrolytes reveal a urinary sodium concentration of greater than 20 mEq/L because the plasma volume expansion that occurs from water retention activates a number of natriuretic mechanisms so that an increase in urinary sodium excretion occurs in spite of progressive hyponatremia, s Third, the urine specific gravity is characteristically 1.001, reflecting m a x i m u m dilution 94/275
I. Deficit of Total Body Water and Larger Deficit of Total Body Sodium (ECF Volume Depletion) Renal Losses Extrarenal Losses Diuretic excess Vomiting Mineralocorticoid Diarrhea deficiency Third space losses from Salt-losing burns, pancreatitis nephritis Muscle trauma Renal tubular acidosis II. Excess Total Body Water (Modest ECF Volume Excess - - no edema) Glucocorticoid deficiency Hypothyroidism Pain Emotion Drugs SlADH
III. Excess Total Body Sodium and Larger Excess of Total Body Water (ECF Volume Excess - - edema) Renal Extrarenal Nephrotic syndrome Cirrhosis Acute renal failure Cardiac failure Chronic renal failure
capability, 9 but may be as high as 1.005. lo Dies, Rangel and Rivera, n in their survey of the differential diagnosis between psychogenic polydipsia and diabetes insipidus, concluded that dehydration followed by the administration of vasopressin will result in a urine more concentrated in diabetes insipidus than that caused by dehydration alone. In p s y c h o g e n i c polydipsia, the urine concentration will not increase markedly over that seen following dehydration alone. Barlow and DeWordener 12 reported that only 20% of patients manifesting psychogergc polydipsia are men, and that the average age at onset of this disorder is generally over 35 years (Table).
Question: What is the pathophysiology of hyponatremic coma and seizure?
Dr Roberge: Serum hypoosmolality results m a shift of extracellular fluid into cells in an effort to maintain osmotic equilibrium between the extracellular fluid (ECF) and the intracellular fluid (ICF). With enough movement of ECF into brain cells, cerebral edema ensues and, if the edema is severe enough, central nervous symptoms become manifest.S
Question: At what serum level of hyponatremia do central nervous system symptoms become apparent? Dr Roberge: In chronic hyponatremia, CNS manifestations are far less common, even with serum sodium concentrations as low as 110 mEq/L, because the loss of brain solutes, principally potassium chloride, minimizes brain swelling for a given reduction in body water osmolality, 9
Annals of Emergency Medicine
13:4 April t984
TABLE. Clinical characteristics of psychogenic polydipsia-induced hyponatremia History
Behavioral disorders of varying types, more commonly schizophrenia 15
Age
More commonly > 35 yr 12
Sex
4:1 female/male ratio lo
Serum sodium
Less than 125 mEq/L but generally much lower 13
Urine specific gravity
Characteristically 1.001, but may be as high as 1.0059 ,1o
Urine sodium concentration
Greater than 20 mEq/LS
Vasopressin administration following dehyd ration
No increase in urine osmolality over that seen with dehydration alone 11
In acute water intoxication, the clinical manifestations of brain edema are observed with s e r u m sodium levels of 120 to 125 mEq/L.9,13 Early symptoms include lethargy' weakness and somnolence, which can progress rapidly to seizures, coma, and death. Question: What is the appropriate t r e a t m e n t of hyponatremia? Dr Roberge: The goal of therapy in hyponatremia is to correct the body water osmolality by raising the ratio of sodium to water in the extracellular fluid. The increase in extracellular fluid o s m o l a l i t y draws water f r o m cells and thereby reduces their volume. In chronic hyponatremia, this is accomplished by correction of the underlying disorder when the hyponatremia occurs in volume contraction states or in salt-retaining states such as those seen in congestive heart failure or hepatic cirrhosis with ascites. Because acute hyponatremia is nearly uniformly fatal, it is a tree medical emergency and requires immediate therapy. The initial goal is to raise serum sodium to a level of 125 mEq/L over a period of six hours by the administration of 3% or 5% saline solution.9 Because the desired effect is to correct the body water osmolality to approximately 250 mosm/kg of water (ie, to approximately twice the desired serum sodium concentration), a useful formula for calculating the sodium requirement is as follows: 125 - measured serum sodium x 0.6 body weight = required mEq sodium. In volume-expanded, salt-retaining states such as congestive heart failure, hypertonic infusions m a y be hazardous. In the syndrome of inappropriate antidiuretic hormone (SIADH) associated with volume expansion and sodium wasting, the administration of hypertonic saline alone will be Ineffective in correcting hyponatremia because the administered salt is excreted promptly in a relatively concentrated
13:4 April 1984
urine. In such instances, a diuretic, usually furosemide, is also administered because it induces a diuresis resulting in a urine with a sodium appreciably lower than the serum sodium and it reduces the risk of extracellular fluid volume expansion. 9
Question: Are there any other hazards encountered in this mode of therapy? Dr Roberge: Rapid elevation of the serum sodium concentration to levels greater than 125 mEq/L is hazardous because loss of brain solute represents one of the compensatory mechanisms for preserving the brain cell volume in dilutional states.9,14 Raising serum sodium rapidly to levels greater than 125 mEq/L can result in central nervous system damage due to acute brain shrinkage. 9 Psychogenic polydipsia is a rarely reported entity that may lead ultimately to coma and seizures, or even death, as a consequence of induced hyponatremia, is With the increasing trend to outpatient management of behavioral disorders, the emergency physician is more apt in the future to encounter cases of hyponatremia secondary to psychogenic polydipsia. Most definitely, psychogenic polydipsia should be considered in the differential diagnosis of any psychiatric patient who presents with a history of seizures and coma. REFERENCES 1. Roundtree LG: Water intoxication. Arch Intern Med 1923; 32:157-174. 2. Barahal HS: Water intoxication in mental case. Psychoanal Q 1938;12:767-771. 3. Hobson JA, English JT: Self induced water intoxication. Ann Intern Med 1963;58:524-532. 4. Murphy FJ, Zelman S: Water metabolism and the psychiatric patient. I Urol 1964;92:60-63. 5. Devereaux MW, McCormick RA: Psychogenic water intoxication: A case report. Am J Psychiatry 1972;129:628-630. 6. Moses M, Miller M: Drug induced dilutional hyponatremia. N Engl l Med 1974;291:1234-1237. 7. Berl T, Anderson R], McDonald KM, et al: Clinical disorders of water metabolism. Kidney Int 1976,10:117. 8. Joenike JR, Waterhouse C: Renal response to sustained administration of vasopressin and water in man. ] Clin Endocrinol 1961;21:231-242. 9. Wyngarden ]-13,Smith LH (eds): Cecil: Textbook of Medicine. Philadelphia, WB Saunders Publishing Co, 1982. 10. Resnick ME, Patterson C: Coma and convulsions due to compulsive water drinking. Neurology 1969;19:1125-1126. 11. Dies F, Rangel S, Rivera A: Differential diagnosis between diabetes insipidus and compulsive polydipsia. Ann Intern Med 1961;54:710-725. 12. Barlow ED, DeWardener HE: Compulsive water drinking. Q f Med 1959;28:235-258. 13. Gilroy J, Meyers IS: Medical Neurology. New York, Macmillan Publishing Co, 1979. 14. Lewis AJ: Mechanisms of Neurological Disease. Boston, Little Brown and Co, 1978. 15. Raskind M: Psychosis, polydipsia and water intoxication: Report of a fatal case. Arch Gen Psychiatry 1974~30:112-114.
Annals of Emergency Medicine
276/95
P s y c h o g e n i c Polydipsia m An Unusual C a u s e of H y p o n a t r e m i c C o m a and Seizure [Roberge R, Gemsheimer J, Sparano R, Tartakoff R, Morgenstern MJ, Rubin K, Senekjian D, Andrade R, Matthew V: Psychogenic polydipsia - - An unusual cause of hyponatremic coma and seizure. Ann Emerg Med April 1984;13:274-276.] INTRODUCTION
Joel Gemsheimer, MD: Today's case is that of a psychiatric patient who presented comatose and with a witnessed first time grand-mal-type seizure. The discussant will be Raymond Roberge, MD, Department of Emergency Medicine, Lincoln Medical and Mental Health Center, and New York Medical College.
CASE PRESENTATION Robert Sparano, MD: A 38-year-old man presented to the emergency department after having been found unconscious at home. Paramedics responding at the scene reported witnessing a grand-real-type seizure lasting approximately one minute. The patient was reported to respond to noxious stimuli by withdrawal of all extremities. The paramedics placed an oral airway, administered oxygen by nasal cannula, and transported the patient. Prior medical history, as provided by family members, revealed that the patient was a psychiatric outpatient with a longstanding diagnosis of schizophrenia. There was also a long history of intravenous drug abuse and alcohol abuse. Medications included Cogentin (benztropine) on a daily basis, and Prolixin (fluphenazine) 25 mg intramuscularly on a biweekly basis. Admission vital signs were as follows: pulse, 88 beats per minute; blood pressure, 180/120 m m Hg; respirations, 28/min; and temperature, 37.3 C. Shortly after admission, the patient sustained a second grand-mal-type seizure. He was intubated and was administered 5 mg diazepam intravenously, with resultant termination of the seizure. The patient received one ampule (50 cc) of 50% dextrose solution, four ampules (1.6 mg) naloxone, and 100 mg thiamine, without apparent response. Physostigmine, 2 rag, was administered to counteract the possibility of phenothiazine toxicity, again without apparent response. An Ewald tube was passed nasally and the stomach was aspirated of approximately 200 cc of a brownish sludge that was sent for toxicology screening and subsequently was found to be negative. A charcoal slurry was instilled into the stomach and a cathartic was administered. Physical examination revealed some nuchal rigidity. Pupils were equal and reactive. Deep tendon reflexes were equal and symmetrical. Plantar reflexes were downgoing. The chest was clear to auscultation, and the heart examination was normal. The abdomen was soft and non-distended, and hypoactive bowel sounds were present. Rectal examination revealed good sphincter tone, no masses, and guaiac-negative stool. The chest film was negative, and the electrocardiogram revealed no acute changes. Lumbar puncture was negative. Toxicology screen was negative for alcohol, phenothiazines, benzodiazepines, and barbiturates; salicylates were 3.4 mg%. The urinalysis revealed a specific gravity of 1.005, 1 to 3 WBCs, 3 to 6 RBCs, and a pH of 6.0. The CBC revealed a WBC of 18,100; hemoglobin, 13.1; and hematocrit, 37. The serum electrolytes were as follows: sodium, 105; potassium, 2.9; chloride, 73; CO2, 23; BUN, 5; glucose, 101; creatinine, 0.8~ 13:4 April 1984
Annals of Emergency Medicine
Raymond Roberge, MD Joel Gernsheimer, MD Robert Sparano, MD Randy Tartakoff, MD Mary Jo Morgenstern, MD Kenneth Rubin, MD Doris Senekjian, MD Ruben Andrade, MD Varghese Matthew, MD Bronx, New York From the Emergency Medicine Residency Program, Lincoln Medical and Mental Health Center, Bronx; and New York Medical College, New York, New York, Received for publication April 25, 1983, Accepted for publication June 29, 1983. Address for reprints: Raymond Roberge, MD, Department of Emergency Medicine, Lincoln Medical and Mental Health Center, 234 East 149th Street, Bronx, New York 10451.
274/93
PSYCHOGENIC POLYDIPSIA Emergency Medicine Resiency Program - Lincoln Medical and Mental Health Center
Fig. Causes of hyponatremia (adapted from Berl et alZ). magnesium, 1.6; and calcium, 8.5. The patient was admitted with a diagnosis of hyponatremic coma. An intravenous infusion of 3% saline solution was begun at 120 cc per hour, and the patient regained consciousness in approximately four hours. On further questioning, the family revealed that on the day prior to admission the patient had begun acting bizarrely and ingesting large quantities of water throughout the day and night.
DISCUSSION Raymond Roberge, MD: The causes of coma and seizure presenting to the emergency department are numerous and varied, but most commonly involve neurological disorders, infectious agents, inhalation of noxious agents, trauma, environmental factors (eg, hypothermia), and metabolic disorders. Hyponatremia as a cause of seizure and coma is a relatively infrequent occurrence in the emergency department setting, and statistics regarding its actual incidence are lacking. Psychogenic polydipsia, one of the more uncommon causes of hyponatremia, is a clinical rarity. 1-s
Question: What is psychogenic polydipsia? Dr Roberge: Psychogenic polydipsia is a firmly established, although rarely reported, syndrome consisting of compulsive consumption of fluids due to a psychological disturbance. It is characterized by the ingestion of huge volumes of fluid over a short period of time by persons with various behavioral disorders. 6 The body is normally able to clear 15 L to 20 L per day, but excessive volumes in a short period of time overwhelm the body's clearing capabilities, resulting in acute dilutional hyponatremia. An additional aggravating factor may be the concomitant use of certain psychotropic medications, such as Mellaril (thioridazine) and Elavil (amitriptyline), which are known to induce dilutional hyponatremia. 6
Question: Which disorders must be considered in the differential diagnosis of hyponatremic coma and seizure?
Dr Roberge: The etiologies of hyponatremia can be grouped conveniently into three general categories: those with a deficit of total body water and larger deficit of total body sodium, those with an excess of total body water (psychogenic polydipsia is included in this category), and those with an excess total body sodium and larger excess total body water (Figure).7
Question: Which data are necessary in arriving at a diagnosis of psychogenic polydipsia?
Dr Roberge: The diagnosis of psychogenic polydipsia should be considered in any patient with a known psychiatric disorder who presents with a seizure and/or coma secondary to hyponatremia. Obviously the history is one of the most important criteria. Second, urinary electrolytes reveal a urinary sodium concentration of greater than 20 mEq/L because the plasma volume expansion that occurs from water retention activates a number of natriuretic mechanisms so that an increase in urinary sodium excretion occurs in spite of progressive hyponatremia, s Third, the urine specific gravity is characteristically 1.001, reflecting m a x i m u m dilution 94/275
I. Deficit of Total Body Water and Larger Deficit of Total Body Sodium (ECF Volume Depletion) Renal Losses Extrarenal Losses Diuretic excess Vomiting Mineralocorticoid Diarrhea deficiency Third space losses from Salt-losing burns, pancreatitis nephritis Muscle trauma Renal tubular acidosis II. Excess Total Body Water (Modest ECF Volume Excess - - no edema) Glucocorticoid deficiency Hypothyroidism Pain Emotion Drugs SlADH
III. Excess Total Body Sodium and Larger Excess of Total Body Water (ECF Volume Excess - - edema) Renal Extrarenal Nephrotic syndrome Cirrhosis Acute renal failure Cardiac failure Chronic renal failure
capability, 9 but may be as high as 1.005. lo Dies, Rangel and Rivera, n in their survey of the differential diagnosis between psychogenic polydipsia and diabetes insipidus, concluded that dehydration followed by the administration of vasopressin will result in a urine more concentrated in diabetes insipidus than that caused by dehydration alone. In p s y c h o g e n i c polydipsia, the urine concentration will not increase markedly over that seen following dehydration alone. Barlow and DeWordener 12 reported that only 20% of patients manifesting psychogergc polydipsia are men, and that the average age at onset of this disorder is generally over 35 years (Table).
Question: What is the pathophysiology of hyponatremic coma and seizure?
Dr Roberge: Serum hypoosmolality results m a shift of extracellular fluid into cells in an effort to maintain osmotic equilibrium between the extracellular fluid (ECF) and the intracellular fluid (ICF). With enough movement of ECF into brain cells, cerebral edema ensues and, if the edema is severe enough, central nervous symptoms become manifest.S
Question: At what serum level of hyponatremia do central nervous system symptoms become apparent? Dr Roberge: In chronic hyponatremia, CNS manifestations are far less common, even with serum sodium concentrations as low as 110 mEq/L, because the loss of brain solutes, principally potassium chloride, minimizes brain swelling for a given reduction in body water osmolality, 9
Annals of Emergency Medicine
13:4 April t984
TABLE. Clinical characteristics of psychogenic polydipsia-induced hyponatremia History
Behavioral disorders of varying types, more commonly schizophrenia 15
Age
More commonly > 35 yr 12
Sex
4:1 female/male ratio lo
Serum sodium
Less than 125 mEq/L but generally much lower 13
Urine specific gravity
Characteristically 1.001, but may be as high as 1.0059 ,1o
Urine sodium concentration
Greater than 20 mEq/LS
Vasopressin administration following dehyd ration
No increase in urine osmolality over that seen with dehydration alone 11
In acute water intoxication, the clinical manifestations of brain edema are observed with s e r u m sodium levels of 120 to 125 mEq/L.9,13 Early symptoms include lethargy' weakness and somnolence, which can progress rapidly to seizures, coma, and death. Question: What is the appropriate t r e a t m e n t of hyponatremia? Dr Roberge: The goal of therapy in hyponatremia is to correct the body water osmolality by raising the ratio of sodium to water in the extracellular fluid. The increase in extracellular fluid o s m o l a l i t y draws water f r o m cells and thereby reduces their volume. In chronic hyponatremia, this is accomplished by correction of the underlying disorder when the hyponatremia occurs in volume contraction states or in salt-retaining states such as those seen in congestive heart failure or hepatic cirrhosis with ascites. Because acute hyponatremia is nearly uniformly fatal, it is a tree medical emergency and requires immediate therapy. The initial goal is to raise serum sodium to a level of 125 mEq/L over a period of six hours by the administration of 3% or 5% saline solution.9 Because the desired effect is to correct the body water osmolality to approximately 250 mosm/kg of water (ie, to approximately twice the desired serum sodium concentration), a useful formula for calculating the sodium requirement is as follows: 125 - measured serum sodium x 0.6 body weight = required mEq sodium. In volume-expanded, salt-retaining states such as congestive heart failure, hypertonic infusions m a y be hazardous. In the syndrome of inappropriate antidiuretic hormone (SIADH) associated with volume expansion and sodium wasting, the administration of hypertonic saline alone will be Ineffective in correcting hyponatremia because the administered salt is excreted promptly in a relatively concentrated
13:4 April 1984
urine. In such instances, a diuretic, usually furosemide, is also administered because it induces a diuresis resulting in a urine with a sodium appreciably lower than the serum sodium and it reduces the risk of extracellular fluid volume expansion. 9
Question: Are there any other hazards encountered in this mode of therapy? Dr Roberge: Rapid elevation of the serum sodium concentration to levels greater than 125 mEq/L is hazardous because loss of brain solute represents one of the compensatory mechanisms for preserving the brain cell volume in dilutional states.9,14 Raising serum sodium rapidly to levels greater than 125 mEq/L can result in central nervous system damage due to acute brain shrinkage. 9 Psychogenic polydipsia is a rarely reported entity that may lead ultimately to coma and seizures, or even death, as a consequence of induced hyponatremia, is With the increasing trend to outpatient management of behavioral disorders, the emergency physician is more apt in the future to encounter cases of hyponatremia secondary to psychogenic polydipsia. Most definitely, psychogenic polydipsia should be considered in the differential diagnosis of any psychiatric patient who presents with a history of seizures and coma. REFERENCES 1. Roundtree LG: Water intoxication. Arch Intern Med 1923; 32:157-174. 2. Barahal HS: Water intoxication in mental case. Psychoanal Q 1938;12:767-771. 3. Hobson JA, English JT: Self induced water intoxication. Ann Intern Med 1963;58:524-532. 4. Murphy FJ, Zelman S: Water metabolism and the psychiatric patient. I Urol 1964;92:60-63. 5. Devereaux MW, McCormick RA: Psychogenic water intoxication: A case report. Am J Psychiatry 1972;129:628-630. 6. Moses M, Miller M: Drug induced dilutional hyponatremia. N Engl l Med 1974;291:1234-1237. 7. Berl T, Anderson R], McDonald KM, et al: Clinical disorders of water metabolism. Kidney Int 1976,10:117. 8. Joenike JR, Waterhouse C: Renal response to sustained administration of vasopressin and water in man. ] Clin Endocrinol 1961;21:231-242. 9. Wyngarden ]-13,Smith LH (eds): Cecil: Textbook of Medicine. Philadelphia, WB Saunders Publishing Co, 1982. 10. Resnick ME, Patterson C: Coma and convulsions due to compulsive water drinking. Neurology 1969;19:1125-1126. 11. Dies F, Rangel S, Rivera A: Differential diagnosis between diabetes insipidus and compulsive polydipsia. Ann Intern Med 1961;54:710-725. 12. Barlow ED, DeWardener HE: Compulsive water drinking. Q f Med 1959;28:235-258. 13. Gilroy J, Meyers IS: Medical Neurology. New York, Macmillan Publishing Co, 1979. 14. Lewis AJ: Mechanisms of Neurological Disease. Boston, Little Brown and Co, 1978. 15. Raskind M: Psychosis, polydipsia and water intoxication: Report of a fatal case. Arch Gen Psychiatry 1974~30:112-114.
Annals of Emergency Medicine
276/95