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PubMed1996

["Polydipsia, intermittent hyponatremia and psychoses" syndrome: a diagnosis and therapeutic management of a case].

Polydipsia can be defined as an impulsive behavior leading to absorption of large amounts of water (4 to 20 litres a day), without any underlying organic disease. Its prevalence in a population of chronic psychiatric patients can be as high as 6 to 17%. Schizophrenia represents 80% of cases reported. Some patients with polydipsia may develop hyponatremia, leading to a PIP syndrome (Polydipsia intermittent hyponatremia and psychosis). Hyponatremia or water intoxication appears when three conditions are present: an abnormal regulation of thirst, an inappropriate ADH secretion and/or an excessive renal sensitivity to ADH, with an increased sensitivity of the central nervous system to hyponatremia. The clinician must first identify patients at risk to develop water intoxication and start treatment before any severe physical complication occurs. Pharmacological treatments aiming at an increase of renal free-water excretion--do not show a constant efficacy in the correction of hyponatremia, they have no action on polydipsia. The new atypical neuroleptics such as clozapine and risperidone seem to open new perspectives in the treatment of polydipsia. Controlled studies should be performed in this field.

Adult↗
PubMed1997

Psychotic exacerbations and enhanced vasopressin secretion in schizophrenic patients with hyponatremia and polydipsia.

BACKGROUND: For unclear reasons, life-threatening water intoxication often coincides with acute psychosis in polydipsic schizophrenic patients with chronic hyponatremia. In contrast, most polydipsic schizophrenic patients are normonatremic and never manifest hyponatremia. To explore whether the effect of acute psychosis on water balance differs in these 2 schizophrenic subgroups, we compared their responses to drug-induced psychotic exacerbations. METHODS: Matched polydipsic schizophrenic patients with (n = 6) and without (n = 8) hyponatremia were identified based on past and current indexes of fluid intake and hydration. A transient psychotic exacerbation was induced with an infusion of the psychotomimetic methylphenidate hydrochloride (0.5 mg/kg of body weight over a 60-second period). Antidiuretic hormone levels, subjective desire for water, and factors known to influence water balance were measured at 15-minute intervals for 2 hours. RESULTS: Except for the expected differences in plasma osmolality and sodium, basal measures were similar in the 2 groups. Following methylphenidate administration, antidiuretic hormone levels increased more in the hyponatremic patients (P < .02), despite their consistently lower plasma osmolality (P < .007). No known or putative antidiuretic hormone stimulus could account for this finding. Only basal positive psychotic symptoms (P < .09) and plasma sodium (P < .18) were even marginally associated with the peak antidiuretic hormone responses, but neither factor could explain the difference in the response by the 2 groups. CONCLUSION: Psychotic exacerbations are associated with enhanced antidiuretic hormone secretion, for unknown reasons, in schizophrenic patients with hyponatremia and polydipsia, thereby placing them at increased risk of life-threatening water intoxication.

Acute Disease↗
PubMed2004

Colonic irrigation-induced hyponatremia.

A 42-year-old Chinese woman presented with transient confusional state and memory loss due to acute water intoxicational hyponatremia complicating colonic irrigation (enemas) used as an alternative medicine to promote health. Although there is no evidence that such "antiautointoxication" technique conveys true benefit in any condition, this form of "quackery" may actually cause harm, such as water intoxication as in this case.

Acute Disease↗
PubMed1989

Effect of furosemide, bumetanide and mannitol on intracranial pressure in experimental brain edema of the rat.

Loop diuretics interfere with NaCl-KCl cotransport, which operates not only in the kidney but as well in a variety of nonepithelial cells including neuronal and glial cells. In these cells loop diuretics are able to reduce cellular volume. The present study has been performed to establish, whether furosemide or bumetanide directly modify intracranial pressure in cytotoxic brain edema. To this end, water intoxication was induced in animals acutely nephrectomized, to exclude any consequences of renal effects. Neither furosemide nor bumetanide proved effective in reducing intracranial pressure. In contrast, infusion of hypertonic mannitol solution leads to a marked, rapid reduction of intracranial pressure. The observations rule out a direct action of loop diuretics on intracranial cells to reduce intracranial pressure in water intoxicated animals.

Animals↗
PubMedDate not supplied

Primary and drug-induced disorders of water homeostasis in psychiatric patients: principles of diagnosis and management.

Psychotropic drugs, as well as some psychiatric disorders, can produce neurotoxic and life-threatening abnormalities of water and electrolyte balance that require prompt and appropriate medical intervention. Compulsive fluid intake by psychotic patients (primary polydipsia) can produce delirium due to water intoxication with hyponatremia. Several psychotropic drugs cause water retention by decreasing renal clearance, as in the syndrome of inappropriate antidiuretic hormone secretion. Lithium and other agents interfere with renal resorption of water to cause nephrogenic diabetes insipidus. Clinical signs in these disorders range from lethargy and confusion to stupor, seizures, coma, and death. This overview provides a conceptual framework for differentiating among and safely managing these relatively common disorders.

Antipsychotic Agents↗
PubMed1997

Intranasal desmopressin-associated hyponatremia: a case report and literature review.

We present a case of a 29-year-old woman with a long history of nocturnal enuresis who developed symptomatic hyponatremia from water intoxication shortly after beginning desmopressin. A MEDLINE search in the English language revealed 13 prior case reports. All patients presented with seizure, mental status changes, or both. Two distinct presentations occurred: one group of patients maintained a stable course with desmopressin and developed symptoms related to an outside factor. The other group of patients were new to desmopressin and had a profound water intoxication response from its use. While the underlying cause was from simple overhydration, the quickness of this unanticipated adverse effect is noteworthy. The importance of counseling to ensure a family's and a patient's understanding of the effects of desmopressin as well as monitoring electrolytes periodically may help identify and prevent this serious iatrogenic complication.

Administration, Intranasal↗
PubMed1990

Urinary arginine vasopressin in asthma: consideration of fluid therapy.

To elucidate the role of antidiuretic hormone (ADH) on water and electrolyte balance in patients with asthmatic attacks, urinary arginine vasopressin (AVP) was assayed in 28 asthmatic patients. In a 3-year-old girl with status asthmaticus who developed a grand mal seizure in association with hyponatremia, urinary AVP levels remained high and fluctuated before convulsion; the cause of the convulsion was considered to be water intoxication due to inappropriate ADH secretion. In 19 of 28 patients with moderately severe asthmatic attacks, increases in urinary AVP levels occurred before treatment (300 +/- 80 pg/ml vs. 40 +/- 24 pg/ml (normal controls), p less than 0.01); elevated AVP levels tended to fall in response to intravenous fluid therapy (appropriate ADH secretion) in 2 of 6 patients, but did not fall (inappropriate ADH secretion) in the remaining patients. It is concluded that inappropriate ADH secretion may occur in asthmatic attacks, and that in such a condition there seems to be a potential risk of water intoxication during fluid therapy, as demonstrated in the present patient.

Adolescent↗
PubMed1993

Neuroendocrine factors influencing polydipsia in psychiatric patients: an hypothesis.

Polydipsia and water intoxication cause considerable morbidity and mortality in chronic psychiatric patients. The pathophysiology of the disorder is unknown, and there is no effective treatment. Angiotensin II is an important dipsogen in animals; in humans, some conditions with abnormal thirst are associated with increased angiotensin function. Chronic D2 dopamine receptor blockade increases angiotensin II-induced thirst in animals; in humans, increased peripheral response to angiotensin II is documented. Chronic D2 blockade with typical neuroleptics may increase sensitivity to angiotensin II and induce thirst. Clozapine, which has negligible D2 blocking action may improve polydipsia. Recent case reports demonstrate improvement of polydipsia during clozapine therapy. Angiotensin II releases vasopressin; this could explain water intoxication, which occurs later in the syndrome. This paper suggests an etiological model and a treatment modality for this disorder.

Antipsychotic Agents↗
PubMed1990

Diuretics after transurethral prostatectomy: a double-blind controlled trial comparing frusemide and mannitol.

Mannitol and frusemide were compared in a randomized, controlled, double-blind trial for their effects in promoting diuresis after prostatectomy and on indices of water intoxication. The drugs had comparable diuretic effects. Sodium loss was greater with frusemide, contributing to sodium depletion after operation. Administration of frusemide was associated with more frequent need for i.v. volume expansion after operation. Plasma osmolality was greater with mannitol (289 (SD 4.2 mosmol kg-1 at 1 h after operation and 285 (5.3) mosmol kg-1 at 4 h after operation) than with frusemide (282 (7.1) mosmol kg-1 and 279 (6.7) mosmol kg-1, respectively) (P less than 0.05). Plasma concentration of sodium was significantly greater with mannitol (136.9 (3.1) mmol litre-1) than with frusemide (134.4 (2.8) mmol litre-1) only on the morning after surgery (P less than 0.05). Mannitol is an effective alternative to frusemide in inducing diuresis after prostatectomy, and may protect against water intoxication.

Diuresis↗
PubMed1997

Hypouricemia in chronic schizophrenic patients with polydipsia and hyponatremia.

BACKGROUND: Polydipsia is a common disorder among chronic psychiatric patients. Impaired water excretion due to enhanced action and secretion of antidiuretic hormone has been reported in hyponatremic patients with polydipsia. Hypouricemia coexisting with hyponatremia is a hallmark of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The transitory coexistence of hyponatremia and hypouricemia in patients with polydipsia-hyponatremia syndrome is presented. METHOD: We examined the course of hypouricemia and hyponatremia in three schizophrenic patients with a long-standing history of polydipsia resulting in the presence of these conditions. In addition, we investigated the renal clearance of uric acid in five polydipsic patients without a previous history of water intoxication or hyponatremia (simple polydipsia). RESULTS: Both hyponatremia and hypouricemia were demonstrated in the presence of SIADH in one patient, during an episode of acute water intoxication in another, and in association with chronic hyponatremia in a patient who was following the target weight procedure. Elevated fractional excretion of uric acid percentage (FEUA%) was detected in two patients. These states appeared to be episodic or transitory. In the five patients with simple polydipsia, serum uric acid concentrations and FEUA% were maintained within the normal range. CONCLUSION: Altered uric acid regulation that resembles SIADH is present in patients with polydipsia-hyponatremia syndrome. Monitoring the uric acid concentration and FEUA% in polydipsic patients may be useful in identifying those patients with transiently impaired water excretion.

Adult↗
PubMed1990

The effect of skull and dura on brain volume regulation after hypo- and hyperosmolar fluid treatment.

This study was performed to determine the response of brain water and electrolytes to acute hypo-osmolality and hyperosmolality in animals with intact skulls and dura, in comparison with those subjected to extensive bilateral or unilateral craniectomy and opening of the dura. In rats, 4 to 5 weeks after extensive unilateral or bilateral craniectomy and opening of the dura, a 50-mOsm/kg decrease in plasma osmolality was produced by systemic administration of distilled water ("water intoxication"), or a 28-mOsm/kg increase in plasma osmolality was produced by systemic administration of either 1 M NaCl or 1 M mannitol in 0.34 M NaCl. Tissue water, Na. and K contents were determined after 120 minutes. Tissue water accumulation or water loss was proportional to the decrease or increase in plasma osmolality. The tissue water accumulation after "water intoxication," however, was less (40% of the predicted value) than that predicted for ideal osmotic behavior. The brain tissue was also found to shrink less than predicted on the basis of ideal osmotic behavior (40% of the predicted value after mannitol treatment, and 60% after NaCl administration). This nonideal osmotic response of the brain tissue is consistent with the finding in other studies and indicated a significant degree of volume regulation. Water and electrolyte changes did not differ between animals operated on and those not operated on, a fact which demonstrates that there are no effects of extensive skull and dura defects on tissue volume regulation under hypo- and hyperosmolar conditions encountered under clinical circumstances.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Do the skull and dura exert influence on brain volume regulation following hypo- and hyperosmolar fluid treatment?

The present studies were performed to determine the response of the brain water and electrolytes to acute hypoosmolality and hyperosmolality in animals with intact skull and dura, in comparison with those subjected to extensive bilateral or unilateral craniectomy and dural opening. Four to 5 weeks following extensive unilateral or bilateral craniectomy and dural opening in rats, a 50 mosm/kg decrease in plasma osmolality was produced by systemic administration of distilled water ("water intoxication"), or a 28 mosm/kg increase in plasma osmolality was produced by systemic administration of either 1 M NaCl or 1 M mannitol in 0.34 M NaCl. Tissue water, Na, and K contents were determined after 120 minutes. Tissue water accumulation or water loss was proportional to the decrease or increase in plasma osmolality. However, the tissue water accumulation following "water intoxication" was less (40% of the predicted value) than that predicted for ideal osmotic behaviour. The brain tissue was also found to shrink less than predicted on the basis of ideal osmotic behaviour (40% of the predicted value after mannitol treatment, and 60% after NaCl administration). This non-ideal osmotic response of the brain tissue is consistent with the finding in other studies and indicated a significant degree of volume regulation. Water and electrolyte changes were not different in operated and non-operated animals, demonstrating no effects of extensive skull and dura defects on tissue volume regulation under hypo- and hyperosmolar conditions of a degree that may be encountered under clinical circumstances.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Effect of adjunctive cortisol on serum sodium in a polydipsic hyponatremic schizophrenic patient.

1. Many polydipsic schizophrenics exhibit enhanced antidiuretic hormone (ADH) activity and thus are hyponatremic and suffer life-threatening water intoxication. Excess cortisol inhibits ADH, while cortisol insufficiency produces impairments in water balance resembling those seen in hyponatremic schizophrenics. Furthermore, hyponatremia normally upregulates cortisol receptors on the neurons which synthesize ADH, which should make them more sensitive to the effects of cortisol. 2. The author treated a hyponatremic schizophrenic, whose water imbalance was unresponsive to standard clinical interventions including clozapine, with a 4-week open trial of 60 mg cortisol daily, followed by a three week taper. 3. Mean serum sodium levels appeared to increase modestly from 114.3 to 118.5 mEq/l while the patient received adjunctive cortisol (P < .06). 4. While a modest effect was seen, the results do not suggest that adjunctive cortisol will reverse hyponatremia, and instead support other data indicating that these patients exhibit a central resistance to glucocorticoid actions.

Adult↗
PubMed1975

[Effect of generalized edema on blood flow distribution in the brain].

The correlation between increase in brain tissue pressure and cerebral blood flow distribution was studied in generalized brain edema induced by water intoxication in cats. Brain tissue pressure increased as the brain edema progressed. The intracranial vascular component was suggested to play a certain role in the volume buffering capacity at increased intracranial pressure. Transtentorial redirection of carotid blood flow observed in the early stages of water intoxication, is related to tissue pressure gradients. The meaning of tissue pressure gradients for blood flow distribution is discussed.

Animals↗
PubMed1998

Olfactory deficits in patients with schizophrenia and severe polydipsia.

BACKGROUND: The present study was designed to assess olfactory function in severely polydipsic/hyponatremic patients with schizophrenia who also had intermittent water intoxication. METHODS: The University of Pennsylvania Smell Identification Test and an olfactory acuity battery were administered to three groups of male subjects: 9 patients with schizophrenia and severe polydipsia/hyponatremia, 9 control nonpolydipsic/normonatremic patients with schizophrenia, and 9 normal controls. RESULTS: Male patients with severe polydipsia/hyponatremia and intermittent water intoxication had marked olfactory acuity and identification deficits when compared to the patient control group of similar age and age at illness onset, and to normal controls. CONCLUSIONS: The finding of deficient acuity (detection threshold) in the polydipsic/hyponatremic group but not the nonpolydipsic, normonatremic group suggests that for this subgroup, abnormalities of olfactory sensory function may occur in a pattern previously reported for other brain disorders such as Alzheimer's disease.

1-Butanol↗
PubMed1998

Rhabdomyolysis after correction of hyponatremia due to psychogenic polydipsia possibly complicated by clozapine.

OBJECTIVE: To report a case of rhabdomyolysis related to rapid correction of hyponatremia attributable to compulsive drinking of water, possible complicated by clozapine use. CASE SUMMARY: A 42-year-old white man treated with clozapine for schizophrenia was admitted for a generalized seizure. Marked hyponatremia due to psychogenic polydipsia was present. He developed a marked elevation of creatine kinase concentrations after correction of hyponatremia with hyperosmolar sodium solution, without clinical signs of rhabdomyolysis. DISCUSSION: Rhabdomyolysis associated with hyponatremia due to water intoxication has been reported in 17 patients to date. A possible explanation may lie within the framework of the calcium-sodium exchange across the skeletal muscle cell membrane. By increasing muscle cell permeability, clozapine treatment may possibly enhance the destruction of muscle cells. CONCLUSIONS: Hyponatremia due to water intoxication and concurrent use of clozapine should be considered in the differential diagnosis of rhabdomyolysis, especially in the severely psychiatrically disabled population.

Adult↗
PubMed1992

The incidence of hyponatremia in prolonged exercise activity.

Hyponatremia is a medical condition characterized by decreased concentration of sodium in the blood, which may occur in participants in endurance and ultraendurance athletic events. Slower competitors and nonacclimatized individuals appear to be at greater risk of becoming hyponatremic, especially if they experience salt depletion as a result of sweating or water intoxication. Clinical signs and symptoms of hyponatremia, which can range from muscle cramps and mental confusion to convulsions and coma, may not manifest themselves until well after the end of the event. Death may occur if hyponatremia is not properly diagnosed and treated. Medical personnel treating this condition should be cautious not to confuse water intoxication with dehydration, which produces similar symptoms. To prevent hyponatremia, participants should acclimatize themselves to race conditions prior to the event. In addition, endurance athletes should be encouraged to ingest low sodium concentrate drinks during events lasting longer than 4 hours.

Journal Article↗