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A patient with chronic fluorine intoxication from mineral water demonstrated an abnormal intense uptake of Tc-99m MDP in the whole spine, the bone metaphyseal regions, and the sternum ("tie sternum"). Results of a bone biopsy revealed an intense osteomalacia and a high fluorine concentration. Bone imaging performed one year after the patient stopped drinking mineral water was normal.
Different degrees of severity in global brain oedema were induced by varying amounts of water intoxication (50, 100, 150, and 200 ml Aqua dest./kg b.wt. intravenously) in groups of six cats, which were functionally nephrectomized. Animals loaded with physiological saline and sham-operated served as controls. Two hours following the water load, the tissue concentrations of CrP, ATP, ADP, AMP, pyruvate, glucose, and lactate were determined by optical enzymatic analysis. The results show disturbances in brain energy metabolism dependent on the severity of the brain oedema. The high energy compounds and in consequence the ATP/ADP-ratio, and respectively the energy charge potential, fall in direct relationship to the severity of the brain oedema. Lactate and lactate-pyruvate ratio increase. The energy source of the cell, glucose as well as pyruvate, significantly falls in the group with severe brain oedema. The results of the brain energy metabolism were compared with our previous study concerning the brain water content, rCBF and CPP in global brain oedema (Meinig et al. 1973). The results show that the disturbances of energy metabolism are directly related to the rCBF and are not dependent on CPP over a wide range.
BACKGROUND: To determine if ready access to a sodium-containing beverage ameliorates life-threatening water imbalance, we compared Gatorade to water in an ABA design. METHOD: Four male chronic schizophrenic inpatients with symptomatic hyponatremia drank water for 1 week, Gatorade plus water for 3 weeks, and then water again for 1 week. Afternoon plasma osmolality and morning serum sodium levels were used to estimate hydration status, and morning and afternoon urine creatinine concentrations were used to estimate fluid intake. RESULTS: During the baseline phase, subjects were mildly polydipsic and mildly overhydrated in the morning and severely overhydrated in the afternoon. All subjects stated they preferred Gatorade and appeared to consume large quantities of it. Indices of fluid intake and hydration status did not differ between the two control phases, nor between the treatment phase and the other two phases. Frequency of severe hypo-osmolemia was also unaffected. CONCLUSION: Substitution of electrolyte-containing beverages is not likely to prevent water intoxication.
We describe a case report with moderately low plasma sodium level and predominant metabolic alkalosis. Others have reported acid-base balance disorders, although no clear pathophysiological explanation has been put forward. We hypothesize that, combine with poor protein intake, mild hyperosmolar beer leads to a water intoxication syndrome, whereas strong hyperosmolar beer intake more likely induces hypochloremic metabolic alkalosis.
We have presented a case of paraplegia following spinal anaesthesia administered for a transurethral prostatic resection. Further investigation revealed a metastatic peridural compressive lesion at the level of T4. We have discussed some of the contributory factors involved, chiefly the lumbar puncture (perimedullary vascular engorgement, alterations in C.S.F. dynamics) and the possible role of intra-operative water intoxication (swelling of spinal cord cells).
Hyponatremia, an electrolyte disturbance usually without clinical significance, may sometimes lead to serious complications when overlooked or not treated appropriately. One cause of hyponatremia, the syndrome of inappropriate antidiuretic hormone (SIADH) secretion, has been associated with some drugs, including carbamazepine (CBZ). Because of its antidiuretic effects, CBZ has been used successfully to treat diabetes insipidus centralis. Possible mechanisms for the antidiuretic effects of CBZ have been proposed. Altered sensitivity to serum osmolality by the hypothalamic osmoreceptors appears likely, but an increased sensitivity of the renal tubules to circulating ADH cannot be excluded. CBZ has led to hyponatremia in patients with epilepsy, neuralgia, mental retardation, and psychiatric disorders with a frequency varying from 4.8 to 40%. Oxcarbazepine (OCBZ), which is structurally related to CBZ, has shown similar hyponatremic effects, but whether hyponatremia occurs more often than with CBZ is not yet clear. Experience with OCBZ is still limited, and there is no definite explanation for a possible difference in antidiuretic potency. Most patients with CBZ/OCBZ-induced hyponatremia are asymptomatic. In rare cases, water intoxication has been reported, necessitating treatment discontinuation.
Pulmonary edema is a rare complication of distance running. All 4 previously reported cases occurred after triathalons or ultramarathons. We report the first case of pulmonary edema in a healthy but untrained runner after a conventional 42-km marathon race. This is also the first reported case of pulmonary edema complicating distance running in which hemodynamic measurements have been made. The pulmonary capillary wedge pressure was low. The cardiac index was initially depressed, and the arterial-venous oxygen tension difference was high, but the latter abnormalities disappeared after volume infusion. These hemodynamic data suggest that pulmonary edema in this distance runner was predominantly noncardiogenic. The etiology of the edema is uncertain, but concurrent hyponatremia and cerebral edema were present in this patient, as in 2 previously reported cases, suggesting that neurogenic pulmonary edema caused by water intoxication may be a contributing factor in pathogenesis.
Aquaporin-4 (AQP4) is expressed in astrocytes throughout the central nervous system, particularly at the blood-brain and brain-cerebrospinal fluid barriers. Phenotype analysis of transgenic mice lacking AQP4 has provided compelling evidence for involvement of AQP4 in cerebral water balance, astrocyte migration, and neural signal transduction. AQP4-null mice have reduced brain swelling and improved neurological outcome in models of (cellular) cytotoxic cerebral edema including water intoxication, focal cerebral ischemia, and bacterial meningitis. However, brain swelling and clinical outcome are worse in AQP4-null mice in models of vasogenic (fluid leak) edema including cortical freeze-injury, brain tumor, brain abscess and hydrocephalus, probably due to impaired AQP4-dependent brain water clearance. AQP4 deficiency or knock-down slows astrocyte migration in response to a chemotactic stimulus in vitro, and AQP4 deletion impairs glial scar progression following injury in vivo. AQP4-null mice also manifest reduced sound- and light-evoked potentials, and increased threshold and prolonged duration of induced seizures. Impaired K+ reuptake by astrocytes in AQP4 deficiency may account for the neural signal transduction phenotype. Based on these findings, we propose modulation of AQP4 expression or function as a novel therapeutic strategy for a variety of cerebral disorders including stroke, tumor, infection, hydrocephalus, epilepsy, and traumatic brain injury.
Previous work has demonstrated that there is a selective increase in extracellular taurine in the brain during acute water intoxication. One aim of the present study was to investigate whether plasma taurine contributes to this increase. To this end, the concentrations of taurine, other amino acids, and ethanolamine (EA) were measured in plasma and CSF of urethane-anesthetized rats injected with 150 ml/kg body weight of distilled water. Blood pressure, blood gases, and pH, as well as plasma and CSF osmolality, were also measured. The CSF level of albumin was quantitated to study the function of the blood-CSF barrier. In separate experiments, hippocampal microdialysis was performed to determine the effects of acute plasma hypoosmolality on extracellular amino acids. Finally, the effect of water injection on hippocampal specific gravity and tissue amino acids was assessed. Blood gases and pH were essentially unchanged after water administration. Mean arterial blood pressure increased to peak levels approximately 50 mm Hg above control. Plasma osmolality decreased rapidly, whereas the depression of CSF osmolality was slower and less pronounced. The average volume of the hippocampus increased by 8%. Water injection was accompanied by a 25-fold elevation of taurine in plasma, whereas phosphoethanolamine (PEA) and EA increased moderately. A small fraction of the increase in plasma taurine might derive from blood cells because dilution of blood in vitro led to doubled plasma levels of the amino acid. Taurine, PEA, and EA increased consistently in CSF and hippocampal microdialysates. Plasma hypoosmolality transiently opened the blood-CSF barrier is reflected by augmented CSF concentrations of albumin.(ABSTRACT TRUNCATED AT 250 WORDS)
Two cases are reported in which absorption of surgical irrigant into the vascular system during transurethral resection of the prostate gland (TUR) resulted in life-threatening complications due to hypo-osmolar volume overload (also known as water intoxication or the TUR syndrome). Manifestations common to both cases were haemolysis of red cells, cardiac arrhythmias, a drop in the serum sodium level, and an elevated central venous pressure. In addition, one patient developed acute pulmonary oedema and the other hypokalaemia, confusion and visual disturbances due to cerebral oedema. Water as an irrigant for TUR should be superseded by glycine 1,5%, which is safer.
Thirty-four cases of hyponatremic seizures occurring in psychiatric patients as a result of self-induced water intoxication are reviewed. Clinical and pathophysiological correlates of the condition are outlined.
A boy is described who developed clinically significant hyponatraemia during carbamazepine treatment. After eight years treatment with carbamazepine the boy began to have grand mal seizures which were clearly related to hyponatraemia. This disappeared when carbamazepine was stopped. Afterwards the boy was more alert and did not have seizures any more. The serum concentrations of sodium and potassium and serum osmolality were subsequently investigated in 94 other children under our care who received carbamazepine. No abnormal values were found. Serum osmolality was not related to serum concentration of carbamazepine in these children. It is concluded that water intoxication during carbamazepine treatment can occur also during childhood, but that it is probably not a common side effect.
The clinical course is described of an infant who accidentally received an adult dose of Syntometrine (synthetic oxytocin + ergometrine) at delivery. The infant soon became ill with convulsions and ventilatory failure, and later with water intoxication. Similar reported cases are reviewed and recommendations are given for the management of future cases.
The effect of different doses of clofibrate and carbamazepine on water metabolism was compared in a patient with psychogenic polydipsia. A definite relationship was found between the doses of both drugs and the antidiuretic effect. Daily 2--4 g clofibrate was ineffective, but 6--8 g induced the syndrome of inappropriate secretion of ADH. 600 mg carbamazepine a day induced a marked antidiuretic response which could be further augmented by administering daily 1200--1800 mg. The discrepancy between the effective "hypolipidemic" and "antidiuretic" dose of clofibrate may perhaps explain the lack of reports on water intoxication induced by this agent, despite of its entensive use in clinical practice.
The pathophysiology of polydipsia in patients with schizophrenia is inadequately understood. This study aims to investigate the genetic influence on polydipsia in schizophrenia, and is comprised of a family study and an association study. First, we screened in-patients in 14 psychiatric hospitals and found a total of 36 pairs of a proband and his/her first-degree relative, both of whom were diagnosed with schizophrenia. Among these pairs, a significant familial concordance of polydipsia was found (Fisher's exact test, two-sided, P = 0.0014; odds ratio, 88.20; 95% confidence interval, 7.31-1064.34). These results indicate that genetic factors may underlie the pathophysiology of polydipsia in patients with schizophrenia. Subsequently, we examined the genetic association between polydipsia/water intoxication and the angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism in patients with chronic schizophrenia (polydipsics: n = 65; non-polydipsics: n = 97) because several lines of evidence suggested that ACE might be involved in the development of polydipsia in schizophrenia. The D allele of ACE was found to be associated with a non-significant trend toward an increased risk of polydipsia (P = 0.086). Furthermore, a significant allelic association was found between the D allele of ACE and water intoxication (P = 0.0392). This significance remained after the data were adjusted for confounding variables by regression analysis. These results suggest that the ACE D allele may be a risk factor for polydipsia/water intoxication in patients with schizophrenia.
The potomania or primary polydipsia is associated to schizophrenia in 20% of cases. Authors reports a case of a patient 27 old years, that suffering from hebephrenia who presented potomania. It was necessary to eliminate secondary polydipsia. The main complication resulting from potomania is water intoxication. Neurobiological or psychological hypothesis were suggested related to the etiopathogeny of this association. Some biological or comportemental therapy were effective in this context.
This report describes the investigation of a spontaneous grand mal seizure in a 55-year old woman, being treated with drugs and ECT for depression. The spontaneous seizure was due to hyponatremia caused by self-induced water intoxication, although psychotrophic medication may have contributed by lowering the seizure threshold. The diagnosis of hyponatremia is discussed.
Observations of 181 foreign body introductions in 99 patients are reported. It is possible to differentiate between an oral, transanal, transcutaneous, transurethral, transvenous, transaural way and exceptional cases. Orally introduced foreign bodies up to a length of 12-15 cm usually pass spontaneously: longer foreign bodies must be removed endoscopically or surgically. A special problem is connected with foreign bodies which are swallowed together in a parallel position and form a cross in the stomach. Intravenously introduced foreign bodies like metallic mercury and copper wire were well tolerated by the patients. - Individual observations concern a patient who swallowed a screw driver (about 10 cm in length) and water intoxication in 3 patients (one of whom died) who drank 9-17 liters during 1-2 hours.