International Journal of Psychiatry in Clinical Practice, 2005; 9(2): 142 /144
CASE REPORT
Acute psychological stress-induced water intoxication
SAGARIKA MUKHERJEE1, EMMANUEL S. ANTONARAKIS2, S. ASADUZZAMAN1 & JOHN R. PETERS1 1
Department of General Medicine, University Hospital of Wales, Cardiff, UK, and 2Johns Hopkins Bayview Medical Center, Baltimore, MD, USA
Abstract Excessive water drinking is a recognised feature of schizophrenia. We present here a case of excessive water drinking precipitated by acute psychological stress. A 52-year-old woman, with no previous mental health problems, was found in a state of altered consciousness and was profoundly hyponatraemic. She had consumed excess amount of water due to severe mental stress. She was treated with hypertonic saline followed by fluid restrictions. The water intoxication had caused brain damage which led to behavioural changes and impaired cognition. We describe the pathophysiology of water intoxication.
Key Words: Stress, water intoxication, hyponatraemia, psychosis
Introduction Drinking excessive amounts of water is a recognised feature of patients with chronic schizophrenia. Twenty percent of chronic schizophrenics drink excessive water and about one-fifth of them experience chronic hyponatraemia and episodes of water intoxication [1]. Water intoxication has also been reported to occur in long-distance marathon runners and army personnel. Other reported cases of water intoxication are in association with anorexia nervosa, following transurethral resection of prostate (TURP) and to escape urinary drug tests. We report a case of water intoxication in a woman without any known psychological disturbances. Case report A 52-year-old woman was found unconscious in her own home. She was usually fit and worked as a property dealer and was not on any regular medications. Her partner confirmed that she did not have any physical or mental health problems previously. Following a disagreement with her partner, she became emotionally upset and, a day prior to admission, she was extremely mentally stressed and was observed to self-induce vomiting and drink large quantities of water. The Glasgow Coma Scale (GCS) was 5/15 on admission with stable vital parameters (pulse 100/min and BP 130/70). Chest
and abdomen were clear and there were normal heart sounds. Deep tendon reflexes were present and Babinski’s reflex was positive on both sides. Baseline bloods showed: sodium 108 mmol/l, potassium 2.2 mmol/l, urea 2.2 mmol/l, and creatinine 45 mmol/l. White cell was count high. Chest X-ray and ECG were normal. Serum and urine screening for drug toxicity was negative. CSF screening for glucose, protein and white cell count was normal. Urine and blood culture showed no growth. CT scan of the brain did not show any abnormality, and there were no features of cerebral infarct. She was treated with benzyl penicillin and cefuroxime along with potassium replacement and hypertonic saline, and later restricted to 1000 ml of normal saline. Biochemistry normalised within 36 h and gradual and slow improvement of neurological status occurred. She gained consciousness but remained confused, changing from somnolence to psychomotor agitation. No focal neurological abnormalities were noted. For the next few days she was alert and awake but completely aphasic and answered all questions with an affirmative nodding of head. She was started on venlafaxine due to suspected depression and later converted to quetiapine. MRI scan of her head showed a few tiny non-specific high signal intensity foci in the cerebral white matter and these were thought to be ischaemic. There was no signal abnormality within the pons to suggest an osmotic
Correspondence: Dr Sagarika Mukherjee, 11 King George V Drive, Heath Park, Cardiff CF14 4ED, UK. Tel: /44 2920742344. Fax: /44 2920744581. E-mail: [email protected]
(Received 26 September 2004; accepted 15 February 2005) ISSN 1365-1501 print/ISSN 1471-1788 online # 2005 Taylor & Francis DOI: 10.1080/13651500510028986
Stress, excessive drinking of water and hyponatraemia myelinosis and cerebral infarct was also not noted. Blood results, given in Table I, show trends over time. In the next few days she appeared to be disoriented and excitable. Speech returned incompletely and was rapid, high tone, and slurred, and there was a degree of expressive and receptive dysphasia. She was seen by psychiatrist and they were unable to assess her thoughts and perceptions as she was unable to give coherent answers. She appeared distressed at her inability to express herself or relate to others and at times frightened by her environment. Cognition was impaired and mini mental test score was 7 out of 30. She had no insight into her illness. She gradually became more settled with increasing familiarity. She was transferred to the psychiatry unit and quetiapin was continued. Mental status improved, but a degree of cognitive impairment remains to date. We diagnosed her as having organic behavioural and cognitive impairment secondary to brain damage precipitated by water intoxication. Discussion Polydipsia can be defined as an impulsive behaviour leading to absorption of large amounts of water (4/ 20 l/day) without any organic disease. Its prevalence in chronic psychiatric patients can be as high as 6/ 17%. Schizophrenics represent 80% of cases reported. Some patients with polydipsia may develop hyponatraemia [2]. Hyponatraemia in water intoxication appears when three conditions are present: an abnormal thirst regulation, inappropriate antidiuretic hormone (ADH) secretion and/or excessive renal sensitivity to ADH, with an increased sensitivity of the central nervous system to hyponatraemia [3]. Polydipsia is significantly associated with male gender, smoking, celibacy and chronicity [4]. There is also a high prevalence of schizophrenia, mental
143
retardation, pervasive developmental disorders, and high frequency of somatic disorders. Our patient had no physical or mental health problems prior to this presentation. The mental stress was thought to have been precipitated by the emotional turmoil with her partner. During this time she had an episode of acute psychosis and this led to excessive water drinking and severe symptomatic hyponatraemia. There was no clinical or radiological evidence of cerebral infarction. There are reports in the literature of strong association between selfinduced water intoxication and severe psychiatric symptoms, including acute psychosis and a broad range of psychiatric symptoms. For unknown reasons life-threatening water intoxication often coincides with acute psychosis in polydipsic schizophrenic patients with chronic hyponatraemia. Psychotic exacerbations are associated with enhanced anti-diuretic hormone secretion for unknown reasons [5]. Psychogenic polydipsia alone cannot explain hyponatraemia in these patients because water intake rarely exceeds the very high excretory capacity of a normal renal diluting system. Other defects leading to abnormal water excretion must be present in these patients if hyponatraemia is to develop. These patients may have abnormalities in thirst regulation, an inappropriate ADH secretion, and an excessive response of the renal tubules to ADH [3]. When acute hyponatraemia occurs, the predominant clinical problem is overt neurological disease resulting in confusion, dysphasia, flaccidity, convulsions, coma, and ultimately death. Pathophysiology of biochemical abnormalities in water intoxication In acute water intoxication, the symptoms of hyponatraemia appear to be related to central nervous
Table I. Selected laboratory values showing trends over time. Day 1 (12:35) Day 1 (17:29) Day 2 (10:57) Plasma Sodium, mmol/l Potassium, mmol/l Calcium, mmol/l Magnesium, mmol/l Glucose, mmol/l Osmolality, mOsm/kg Albumin, g/l Protein, g/l Urea, mmol/l Creatinine, mmol/l Haemoglobin, g/dl White cells/mm3 Platelets/mm3 Urine Sodium, mmol/l Potassium, mmol/l Osmolality, mOsm/l
108 2.2 2.17 0.96 3.6 235 38 64 2.2 45 11.9 20.3 367
112 2.5
260
2.6 50
65 23 325
125 3.0 2.13 0.92 4.9 270 35 60 1.8 55 13.3 12.4 392
Day 2 (22:24)
Day 3
134 2.8
137 3.7 2.17 0.90
38 58 2.4 54 12.7 10.8 396
35 59 3.3 56 12.1 11.4 355
Day 6
133 4.1
Day 12
140 3.9
295
2.3 49 12.9 8.9 384
4.4 53 13.6 7.6 419
144
S. Mukherjee et al.
imbalance between intracellular and extracellular osmolality [6]. There are a number of clinical situations where overhydration may occur. If the reduction in plasma osmolality is acute */passive influx of water swells brain cells, shrinking the extracellular space around them. It is during this time that susceptibility to generalised tonic-clonic seizure dramatically increases [7]. However a cellular basis to explain how overhydration might promote epileptiform activities has been examined only recently. Neocortical and hippocampal brain slice preparations permitted an examination of new osmotic changes, alterations of cortical excitability independent of vascular damage, brain compression or other factors secondary to brain swelling. Rapid lowering of plasma osmolality in clinical situations can promote the hyperexcitability associated with generalised tonic-clonic seizure. The rate of correction of symptomatic hyponatraemia has been a subject of considerable controversy. The development of central pontine myelinosis (CPM) following rapid correction of hyponatraemia has been reported. However, this complication appears to occur in patients undergoing rapid correction of chronic hyponatraemia, after compensatory osmotic changes in brain have taken place [8]. CPM has been shown to have been either over-corrected into hypernatremic range or patients were alcoholic or had severe underlying disease. Rapid correction of acute symptomatic hyponatraemia in psychogenic water drinkers rarely results in CPM. Treatment
This has left her with global dysphasia and mild confusion. We hypothesise that psychic stress has provoked inappropriate ADH secretion. Due to an inappropriate ADH secretion, urinary osmolality was relative high despite an excessively low Na. The clinician must first identify patients at risks of developing water intoxication and start treatment before any severe physical complication occurs. Pharmacological treatments aimed at increasing renal free water excretion do not show a constant efficacy in the correction of hyponatraemia and have no action on polydipsia. Key points . Acute stress may induce behavioural changes which may result physical damage . Excessive drinking of water may be a presenting feature of acute stress manifestation . Hyponatraemia may lead to brain injury which may account for psychological disturbance Statement of interest The author has no conflict of interest with any commercial or other associations in connection with the submitted article.
References [1] Goldman MB, Morris B. Update on treatment and pathophysiology of water imbalance in schizophrenia. Psychiatr Ann 1996;26(2):93. [2] Assouly-Besse F, Seletti B, Lamarque J, Elghozi D, Petitjean F. Polydipsia, intermittent hyponatraemia and psychosis syndrome: A diagnosis and therapeutic management of a case. Ann Med Psychol 1996;154(4):259 /63. [3] Goldman MB, Luchins DJ, Robertson GL. Mechanism of altered water metabolism in psychotic patients with polydipsia and hyponatraemia. New Engl J Med 1988;318:397 /403. [4] Mercier Guidez E, Loas G. Polydipsia and water intoxication in 353 psychiatric patients: An epidemiological and psychopathological study. Eur Psychiatry 2000;15(5):306 /11. [5] Goldman MB, Robertson GL, Luchins DJ, Hedeker D, Pandey GN. Psychotic exacerbation and enhanced vasopressin secretion in schizophrenic patients with hyponatraemia and polydipsis. Arch Gen Psychiatry 1997;54(5):443 /9. [6] Chich J, Zikos D, Skopicki HA, Peterson DR, Fisher KA. Long term neurologic outcome in psychogenic water drinkers with severe symptomatic hyponatraemia: The effect of rapid correction. Am J Med 1990;88:561 /6. [7] Andrew RD. Seizure and acute osmotic change: Clinical and neurophysiological aspects. J Neurol Sci 1991;101(1):7 /18. [8] Sterns RH, Riggs JE, Schochet SS Jr. Osmotic demyelination syndrome following correction of hyponatraemia. New Engl J Med 1986;314:1535 /42. [9] Sterns RH. Severe symptomatic hyponatraemia: Treatment and outcome. Ann Intern Med 1987;107:656 /64. /
No effective pharmacological method exists for eliminating the excessive intake of fluid in patients with psychogenic polydipsia. A combination of saline infusion and fluid restriction or fluid restriction alone may help to correct electrolyte imbalance [9]. In those patients who are able to excrete free water rapidly, fluid restriction alone often leads to a rapid correction of serum Na. Optimal doses of antipsychotic and anxiolytic drugs should be used to address the compulsive nature of extreme water intake. Lithium can also be used as it blocks effect of ADH on renal tubules and increases free water excretion. Other drugs such as phenytoin, demeclocycline or naloxone have also been tried, but clozapine may be the most promising in that it actually prevents or lowers the polydipsia.
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Conclusion
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In our patient, acute psychological stress led to water intoxication followed by irreversible brain damage.
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CASE REPORT
Acute psychological stress-induced water intoxication
SAGARIKA MUKHERJEE1, EMMANUEL S. ANTONARAKIS2, S. ASADUZZAMAN1 & JOHN R. PETERS1 1
Department of General Medicine, University Hospital of Wales, Cardiff, UK, and 2Johns Hopkins Bayview Medical Center, Baltimore, MD, USA
Abstract Excessive water drinking is a recognised feature of schizophrenia. We present here a case of excessive water drinking precipitated by acute psychological stress. A 52-year-old woman, with no previous mental health problems, was found in a state of altered consciousness and was profoundly hyponatraemic. She had consumed excess amount of water due to severe mental stress. She was treated with hypertonic saline followed by fluid restrictions. The water intoxication had caused brain damage which led to behavioural changes and impaired cognition. We describe the pathophysiology of water intoxication.
Key Words: Stress, water intoxication, hyponatraemia, psychosis
Introduction Drinking excessive amounts of water is a recognised feature of patients with chronic schizophrenia. Twenty percent of chronic schizophrenics drink excessive water and about one-fifth of them experience chronic hyponatraemia and episodes of water intoxication [1]. Water intoxication has also been reported to occur in long-distance marathon runners and army personnel. Other reported cases of water intoxication are in association with anorexia nervosa, following transurethral resection of prostate (TURP) and to escape urinary drug tests. We report a case of water intoxication in a woman without any known psychological disturbances. Case report A 52-year-old woman was found unconscious in her own home. She was usually fit and worked as a property dealer and was not on any regular medications. Her partner confirmed that she did not have any physical or mental health problems previously. Following a disagreement with her partner, she became emotionally upset and, a day prior to admission, she was extremely mentally stressed and was observed to self-induce vomiting and drink large quantities of water. The Glasgow Coma Scale (GCS) was 5/15 on admission with stable vital parameters (pulse 100/min and BP 130/70). Chest
and abdomen were clear and there were normal heart sounds. Deep tendon reflexes were present and Babinski’s reflex was positive on both sides. Baseline bloods showed: sodium 108 mmol/l, potassium 2.2 mmol/l, urea 2.2 mmol/l, and creatinine 45 mmol/l. White cell was count high. Chest X-ray and ECG were normal. Serum and urine screening for drug toxicity was negative. CSF screening for glucose, protein and white cell count was normal. Urine and blood culture showed no growth. CT scan of the brain did not show any abnormality, and there were no features of cerebral infarct. She was treated with benzyl penicillin and cefuroxime along with potassium replacement and hypertonic saline, and later restricted to 1000 ml of normal saline. Biochemistry normalised within 36 h and gradual and slow improvement of neurological status occurred. She gained consciousness but remained confused, changing from somnolence to psychomotor agitation. No focal neurological abnormalities were noted. For the next few days she was alert and awake but completely aphasic and answered all questions with an affirmative nodding of head. She was started on venlafaxine due to suspected depression and later converted to quetiapine. MRI scan of her head showed a few tiny non-specific high signal intensity foci in the cerebral white matter and these were thought to be ischaemic. There was no signal abnormality within the pons to suggest an osmotic
Correspondence: Dr Sagarika Mukherjee, 11 King George V Drive, Heath Park, Cardiff CF14 4ED, UK. Tel: /44 2920742344. Fax: /44 2920744581. E-mail: [email protected]
(Received 26 September 2004; accepted 15 February 2005) ISSN 1365-1501 print/ISSN 1471-1788 online # 2005 Taylor & Francis DOI: 10.1080/13651500510028986
Stress, excessive drinking of water and hyponatraemia myelinosis and cerebral infarct was also not noted. Blood results, given in Table I, show trends over time. In the next few days she appeared to be disoriented and excitable. Speech returned incompletely and was rapid, high tone, and slurred, and there was a degree of expressive and receptive dysphasia. She was seen by psychiatrist and they were unable to assess her thoughts and perceptions as she was unable to give coherent answers. She appeared distressed at her inability to express herself or relate to others and at times frightened by her environment. Cognition was impaired and mini mental test score was 7 out of 30. She had no insight into her illness. She gradually became more settled with increasing familiarity. She was transferred to the psychiatry unit and quetiapin was continued. Mental status improved, but a degree of cognitive impairment remains to date. We diagnosed her as having organic behavioural and cognitive impairment secondary to brain damage precipitated by water intoxication. Discussion Polydipsia can be defined as an impulsive behaviour leading to absorption of large amounts of water (4/ 20 l/day) without any organic disease. Its prevalence in chronic psychiatric patients can be as high as 6/ 17%. Schizophrenics represent 80% of cases reported. Some patients with polydipsia may develop hyponatraemia [2]. Hyponatraemia in water intoxication appears when three conditions are present: an abnormal thirst regulation, inappropriate antidiuretic hormone (ADH) secretion and/or excessive renal sensitivity to ADH, with an increased sensitivity of the central nervous system to hyponatraemia [3]. Polydipsia is significantly associated with male gender, smoking, celibacy and chronicity [4]. There is also a high prevalence of schizophrenia, mental
143
retardation, pervasive developmental disorders, and high frequency of somatic disorders. Our patient had no physical or mental health problems prior to this presentation. The mental stress was thought to have been precipitated by the emotional turmoil with her partner. During this time she had an episode of acute psychosis and this led to excessive water drinking and severe symptomatic hyponatraemia. There was no clinical or radiological evidence of cerebral infarction. There are reports in the literature of strong association between selfinduced water intoxication and severe psychiatric symptoms, including acute psychosis and a broad range of psychiatric symptoms. For unknown reasons life-threatening water intoxication often coincides with acute psychosis in polydipsic schizophrenic patients with chronic hyponatraemia. Psychotic exacerbations are associated with enhanced anti-diuretic hormone secretion for unknown reasons [5]. Psychogenic polydipsia alone cannot explain hyponatraemia in these patients because water intake rarely exceeds the very high excretory capacity of a normal renal diluting system. Other defects leading to abnormal water excretion must be present in these patients if hyponatraemia is to develop. These patients may have abnormalities in thirst regulation, an inappropriate ADH secretion, and an excessive response of the renal tubules to ADH [3]. When acute hyponatraemia occurs, the predominant clinical problem is overt neurological disease resulting in confusion, dysphasia, flaccidity, convulsions, coma, and ultimately death. Pathophysiology of biochemical abnormalities in water intoxication In acute water intoxication, the symptoms of hyponatraemia appear to be related to central nervous
Table I. Selected laboratory values showing trends over time. Day 1 (12:35) Day 1 (17:29) Day 2 (10:57) Plasma Sodium, mmol/l Potassium, mmol/l Calcium, mmol/l Magnesium, mmol/l Glucose, mmol/l Osmolality, mOsm/kg Albumin, g/l Protein, g/l Urea, mmol/l Creatinine, mmol/l Haemoglobin, g/dl White cells/mm3 Platelets/mm3 Urine Sodium, mmol/l Potassium, mmol/l Osmolality, mOsm/l
108 2.2 2.17 0.96 3.6 235 38 64 2.2 45 11.9 20.3 367
112 2.5
260
2.6 50
65 23 325
125 3.0 2.13 0.92 4.9 270 35 60 1.8 55 13.3 12.4 392
Day 2 (22:24)
Day 3
134 2.8
137 3.7 2.17 0.90
38 58 2.4 54 12.7 10.8 396
35 59 3.3 56 12.1 11.4 355
Day 6
133 4.1
Day 12
140 3.9
295
2.3 49 12.9 8.9 384
4.4 53 13.6 7.6 419
144
S. Mukherjee et al.
imbalance between intracellular and extracellular osmolality [6]. There are a number of clinical situations where overhydration may occur. If the reduction in plasma osmolality is acute */passive influx of water swells brain cells, shrinking the extracellular space around them. It is during this time that susceptibility to generalised tonic-clonic seizure dramatically increases [7]. However a cellular basis to explain how overhydration might promote epileptiform activities has been examined only recently. Neocortical and hippocampal brain slice preparations permitted an examination of new osmotic changes, alterations of cortical excitability independent of vascular damage, brain compression or other factors secondary to brain swelling. Rapid lowering of plasma osmolality in clinical situations can promote the hyperexcitability associated with generalised tonic-clonic seizure. The rate of correction of symptomatic hyponatraemia has been a subject of considerable controversy. The development of central pontine myelinosis (CPM) following rapid correction of hyponatraemia has been reported. However, this complication appears to occur in patients undergoing rapid correction of chronic hyponatraemia, after compensatory osmotic changes in brain have taken place [8]. CPM has been shown to have been either over-corrected into hypernatremic range or patients were alcoholic or had severe underlying disease. Rapid correction of acute symptomatic hyponatraemia in psychogenic water drinkers rarely results in CPM. Treatment
This has left her with global dysphasia and mild confusion. We hypothesise that psychic stress has provoked inappropriate ADH secretion. Due to an inappropriate ADH secretion, urinary osmolality was relative high despite an excessively low Na. The clinician must first identify patients at risks of developing water intoxication and start treatment before any severe physical complication occurs. Pharmacological treatments aimed at increasing renal free water excretion do not show a constant efficacy in the correction of hyponatraemia and have no action on polydipsia. Key points . Acute stress may induce behavioural changes which may result physical damage . Excessive drinking of water may be a presenting feature of acute stress manifestation . Hyponatraemia may lead to brain injury which may account for psychological disturbance Statement of interest The author has no conflict of interest with any commercial or other associations in connection with the submitted article.
References [1] Goldman MB, Morris B. Update on treatment and pathophysiology of water imbalance in schizophrenia. Psychiatr Ann 1996;26(2):93. [2] Assouly-Besse F, Seletti B, Lamarque J, Elghozi D, Petitjean F. Polydipsia, intermittent hyponatraemia and psychosis syndrome: A diagnosis and therapeutic management of a case. Ann Med Psychol 1996;154(4):259 /63. [3] Goldman MB, Luchins DJ, Robertson GL. Mechanism of altered water metabolism in psychotic patients with polydipsia and hyponatraemia. New Engl J Med 1988;318:397 /403. [4] Mercier Guidez E, Loas G. Polydipsia and water intoxication in 353 psychiatric patients: An epidemiological and psychopathological study. Eur Psychiatry 2000;15(5):306 /11. [5] Goldman MB, Robertson GL, Luchins DJ, Hedeker D, Pandey GN. Psychotic exacerbation and enhanced vasopressin secretion in schizophrenic patients with hyponatraemia and polydipsis. Arch Gen Psychiatry 1997;54(5):443 /9. [6] Chich J, Zikos D, Skopicki HA, Peterson DR, Fisher KA. Long term neurologic outcome in psychogenic water drinkers with severe symptomatic hyponatraemia: The effect of rapid correction. Am J Med 1990;88:561 /6. [7] Andrew RD. Seizure and acute osmotic change: Clinical and neurophysiological aspects. J Neurol Sci 1991;101(1):7 /18. [8] Sterns RH, Riggs JE, Schochet SS Jr. Osmotic demyelination syndrome following correction of hyponatraemia. New Engl J Med 1986;314:1535 /42. [9] Sterns RH. Severe symptomatic hyponatraemia: Treatment and outcome. Ann Intern Med 1987;107:656 /64. /
No effective pharmacological method exists for eliminating the excessive intake of fluid in patients with psychogenic polydipsia. A combination of saline infusion and fluid restriction or fluid restriction alone may help to correct electrolyte imbalance [9]. In those patients who are able to excrete free water rapidly, fluid restriction alone often leads to a rapid correction of serum Na. Optimal doses of antipsychotic and anxiolytic drugs should be used to address the compulsive nature of extreme water intake. Lithium can also be used as it blocks effect of ADH on renal tubules and increases free water excretion. Other drugs such as phenytoin, demeclocycline or naloxone have also been tried, but clozapine may be the most promising in that it actually prevents or lowers the polydipsia.
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Conclusion
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In our patient, acute psychological stress led to water intoxication followed by irreversible brain damage.
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