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A case is reported of water intoxication and cardiac conduction disturbances occurring as a late complication of carbamazepine therapy for trigeminal neuralgia. These uncommon but potentially hazardous complications of therapy are reported because of the wide use of carbamazepine as the agent of choice for trigeminal neuralgia and as an anticonvulsant.
The authors report a case of water intoxication in a woman who received 140 I.U. of oxytocin in 3 litres of glucose serum in 15 hours to induce a therapeutic abortion. This water intoxication led to loss of consciousness with increase in weight and hyponatraemia. The treatment consisted in restricting fluid intake, giving sodium and 20% Mannitol. A short review of the literature with an explanation of the physiopathology is given. This is the antidiuretic action of oxytocin when it is given with too much fluid without electrolytes.
Moderate-dose (15 to 20 mg/kg) bolus intravenous (IV) cyclophosphamide is increasingly being employed for the treatment of autoimmune diseases. High-dose (30 to 50 mg/kg) IV cyclophosphamide, which is used in transplantation and oncology, may cause water intolerance and water intoxication. Described herein is the first patient, to our knowledge, to develop water intoxication following administration of moderate-dose IV cyclophosphamide. A water challenge test demonstrated the absence of an underlying syndrome of inappropriate antidiuretic hormone secretion. Water intolerance was demonstrated in five additional patients receiving moderate-dose IV cyclophosphamide and hydration with hypotonic fluids. Thus, contrary to previous reports, water intoxication can occur following administration of moderate-dose IV cyclophosphamide. Patients with renal insufficiency who are receiving hypotonic fluids following moderate-dose IV cyclophosphamide administration may be at greatest risk for development of symptomatic water intoxication.
Presented is the case of a normal two-month-old girl who developed seizures secondary to water intoxication. The infant had been fed 20 to 30 oz of water daily for three days, while her usual formula was withheld because of vomiting and diarrhea. On the day of admission, the infant exhibited signs of water intoxication in the form of lethargy, vomiting, and seizures. Hyponatremia, hypothermia, and hyperglycemia were noted on admission, and are common features of the syndrome. The patient responded well to fluid restriction and salt replacement. Previous reports have attributed water intoxication to feeding mismanagement, vigorous hydration, dilute formulas, and swimming lessons.
Psychogenic polydipsia and its frequent complication, water intoxication, are well-known to psychologists. There are biochemical and psychiatric theories of psychogenic polydipsia which often correlate with each other. A 48-year-old man with chronic paranoid schizophrenia developed symptoms of psychogenic polydipsia. This provoked disturbances in electrolyte balance, resulting in a rapid decrease in serum sodium concentration and eventual death. There is a paucity of information and little awareness of this problem in the professional literature.
A 63 year old female, who was admitted to a psychiatric hospital for schizophrenia, was referred to our emergency room because of sudden loss of consciousness and convulsions. On arrival, she was drowsy and hypoxemic. Her chest X-ray showed cardiomegaly with pulmonary edema. ECG showed marked ST depression in precordial leads and serum chemistry revealed marked elevation of CPK, GOT and LDH along with hyponatremia and hypochloremia. She was immediately admitted to CCU on suspicion of acute non-transmural myocardial infarction complicated with congestive heart failure. After fluid restriction and intravenous infusion of dopamine she passed large amount of urine, and her consciousness level, electrolyte imbalance and ECG change, improved gradually. Although serum CPK level increased as high as 32,307 IU/ml, there were no signs of left ventricular asynergy on UCG and CPK isozyme analysis performed later revealed more than 99% of serum cCPK was MM-type. We concluded that water intoxication was the cause of the ECG change and the elevated serum CPK, GOT and LDH levels. There are few reports on elevated CPK level in association with water intoxication, in which rhabdomyolysis is speculated as the cause of CPK elevation. But there is no report on ECG change complicated with water intoxication. In our case, electrolyte imbalance caused by water intoxication seemed to play a major role in ST depression and QT prolongation. Although water intoxication is a rare disorder in the general population, it is not infrequent among patients with psychiatric diseases. Care must be taken when such patients present ECG change and serum enzyme elevation mimicking ischemic heart disease.
OBJECTIVE: To determine whether or not risperidone is efficacious in treating self-induced water intoxication in patients with chronic schizophrenia. METHOD: We carried out a prospective 11-month open-label study using risperidone to treat 8 men with chronic schizophrenia and self-induced water intoxication. RESULTS: The 8 men were not able to reduce their fluid consumption compared with their baseline intake. Risperidone, however, significantly decreased the Brief Psychiatric Rating Scale (BPRS) scores of this very chronic group. CONCLUSIONS: Although risperidone decreased schizophrenic symptoms, it did not have significant efficacy in treating self-induced water intoxication. This study may have implications for the treatment of addictive behaviour.
A new case of oxytocin-induced water intoxication is reported in a 30 year old gravid woman. The severe symptoms of this uncommon complication are principally neurological; biological signs are a hyponatraemia with low plasma osmolality. Usually, biological and clinical signs are rapidly cleared up by treatment, but maternal death or neonatal water intoxication may occur. Such accidents must be prevented by clinical monitoring, watching out for alarm signals (oliguria is always found, resulting from the effect of oxytocin on the kidney), minimum fluid and proportional salt intakes, careful monitoring of oxytocin infusion rates, facilitated by the use of a constant flow-rate pump.
This report describes two cases of schizophrenia inpatients with polydipsia, intermittent hyponatremia, and water intoxication. Case 1, a 38 year-old male, developed polydipsia after seven years duration of schizophrenia, with a daily intake of water of more than 10 liters as a result of auditory hallucination suggestion. Nocturnal hyponatremia, agitation and exacerbation of psychosis were noted during admission. After 12 treatments of electroconvulsive therapy, the symptoms of psychosis and polydipsia declined. Case 2, a 42 year-old male, had also been a case of schizophrenia for about twenty years, and developed polydipsia with more than 5 liters of daily water intake in a chronic psychiatric hospital for a period of 5 years schizophrenia. He claimed that he enjoyed the pleasure of drinking water. The symptom of water intoxication had been noted intermittently in the past year, leading to at least two seizures. Finally the patient was transferred to our ward due to agitated mood, self-destructive behavior, consciousness loss, and motor weakness. The clinical features, differential diagnosis and treatment concept of polydipsia and water intoxication were also discussed in context.
Eight cases of convulsive coma by water intoxication without predisposing disease in the majority of instances in psychiatric patients, added to 25 cases from the literature make it possible to describe a stereotyped picture of "psychogenic" water intoxication. This includes episodes of polydipsia preceding convulsions and altered conscious level, accompanied by severe hyponatraemia. Cure occurs spontaneously after an acute hypotonic polyuric phase. Study of free water clearances and dynamic ADH suppression tests demonstrate hypovasopressinism which is difficult to inhibit, with "lower osmoreceptor reset". This abnormality is transient and sometimes relapsing.
Intravenous high-dose cyclophosphamide infusion, usually performed to treat malignant neoplasms, is known to cause water intoxication. Intravenous cyclophosphamide pulse therapy (IVCY) is increasingly being employed for the treatment of rheumatic diseases as well. Recently, water intoxication has been reported to occur even after low-to-moderate doses of IVCY. In the present paper, we describe a case of polyarteritis nodosa in a patient in whom water intoxication developed after IVCY at a moderate dose. Hydration is usually performed to maintain sufficient urine flow to avoid cystitis. Based on our case and a review of the literature, it is recommended that hydration should be carefully performed during IVCY in order to avoid water intoxication, especially when treating elderly patients.
Acute or chronic psychogenic polydipsia is a not uncommon finding in psychiatric patients. Water intoxication either results from the intake of large amounts of fluid within a short period of time and/or from a reduction of the renal "free water clearance". The latter can be caused iatrogenically by the administration of certain drugs or by the "Syndrome of Inadequate Secretion of ADH" (SIADH). Water intoxication results in cerebral oedema and may ultimately lead to death. A case is reported of iatrogenically-induced water intoxication in a patient with chronic psychogenic polydipsia.
This cross-sectional survey attempts to establish the prevalence of polydipsia and water intoxication at a state hospital (N = 360) using staff diagnosis, specific gravity of the urine (SPGU), weight changes, and chart review. There were 150 [42%, 95% confidence interval (CI) 37-47%] patients diagnosed as polydipsic by the staff or by SPGU. At least 93 (26%, CI 21-30%) had primary polydipsia not explained by other causes. Chart review identified 17 (5%, CI 3-7%) patients with a history of water intoxication. Using a case-control study design, schizophrenia, extended duration of hospitalization, and heavy smoking were associated with primary polydipsia in a logistic regression analysis (respective odds ratios were 1.6, 1.8, and 3.6). All patients with a history of water intoxication were Caucasian (versus 83% in those without a history) and had significantly more extended hospitalizations (94 vs. 49%). Future case-control studies should combine longitudinal identification of true cases and controls and exhaustive collections of clinical information in a standardized way.
In uncharacteristic clinical symptomatology the excess of water or the water intoxication render themselves conspicuous less by the signs of an increased fluid content than by central-nervous disturbances. Among the results of laboratory examinations the hypoosmolarity measured cryoscopically always, the hyponatraemia in most cases prove the excess of free water. Exceptions are discussed. A decreased capacity of the elimination of water pathogenetically plays a larger role than primarily excessive water supply. Apart from acute and chronic renal insufficiency the various forms of the Schwartz-Bartter-syndrome (inadequate ADH-secretion) play an increasingly more important role. The therapy demands the reduction of every supply of free water, the treatment of the evoking cause and only in cases of exception the administration of hypertonic saline solution, at the most dialysis treatment.
Three cases of psychosis, polydipsia, and water intoxication are presented as examples of a syndrome that is potentially unrecognized in psychiatric settings. Diagnostic and etiologic considerations, with particular attention to the syndrome of inappropriate antidiuretic hormone secretion (SIADH), are discussed through a review of relevant literature. A schema for a routine psychiatric evaluation is described that will minimize overlooking this association of psychosis and disturbed water balance.
Oxytocin-induced water intoxication is an uncommon iatrogenic condition with serious potential morbidity and mortality, which is preventable with a rational approach to therapy. Its pathogenesis, management and prevention are discussed.
UNLABELLED: Severe hyponatremia is associated with a mortality rate of more than 50%, primarily from cerebral edema and central nervous system dysfunction. Water intoxication is an unusual but potentially lethal cause of perioperative hyponatremia. We report a patient with severe postoperative hyponatremia resulting from excessive perioperative water consumption. Anesthesiologists should maintain an index of suspicion for hyponatremia from water intoxication in patients with neurologic symptoms during the perioperative period. Routine preoperative instructions regarding maximum perioperative water intake and inquiry into any concurrent alternative medical therapies may help to avoid this preventable complication. IMPLICATIONS: Water intoxication is an unusual but potentially lethal cause of perioperative hyponatremia. We report a patient with severe postoperative hyponatremia resulting from excess perioperative water consumption.
This case report concerns two schizophrenic patients with "psychogenic" polydipsia, without any underlying somatic disease. Although case A showed a correlation between excessive water intake and severity of psychomotor disturbance, this could not be safely diagnosed as a water intoxication because the sodium serum level was normal. The lowered sodium serum level in case B, however, allowed us to conclude that the manifestation of grand mal was a sign of a genuine water intoxication. 27 casuistic studies on 67 patients with the syndrome of self-induced water intoxication in schizophrenics are then reviewed. Finally, a variety of diagnostic and pathogenetic problems of this syndrome is discussed, with special reference to the role of inadequate ADH secretion.