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Three infants with symptoms of diabetes insipidus are described. Psychogenic polydipsia, which rarely occurs in infancy, was diagnosed. It was caused by mistakes made by the parents in bringing up these children.
Desmopressin is a commonly used, well-tolerated agent for the treatment of primary nocturnal enuresis and central diabetes insipidus. Intranasal desmopressin provides symptomatic relief with few serious complications. A 29-year-old woman with a long history of primary nocturnal enuresis began treatment with intranasal desmopressin. Although the enuresis ceased, she developed throbbing headaches, nausea, vomiting, paresthesia, lethargy, fatigue, and altered mental status over the next 7 days. When she came to the emergency room her sodium concentration was 127 mmol/L. The history of desmopressin use was not obtained at that time. She was treated with intravenous fluids and discharged. The symptoms returned and worsened over the next 4 days, and she returned to the emergency room stuporous. A repeat sodium was 124 mmol/L, and she was admitted. The history of desmopressin use was still not available. Medical evaluations included computerized tomography, lumbar puncture, complete blood counts, serum chemistries, and serologies. The next morning the woman was improved and informed clinicians of her desmopressin use. Without other causes for the hyponatremia, she was diagnosed with the syndrome of inappropriate antidiuretic hormone, presumably caused by desmopressin. Within 24 hours of fluid restriction and cessation of desmopressin, her symptoms and hyponatremia resolved. A review of the literature found 11 children and 2 adults in whom intranasal desmopressin was associated with hyponatremia, all of whom experienced seizures or altered mental status. Our patient illustrates the importance of early recognition and treatment of hyponatremia before the onset of seizures. When vague symptoms develop during desmopressin therapy, hyponatremia must be considered as part of the differential diagnosis. It may also be prudent to screen for electrolyte abnormalities in patients taking this agent to prevent serious iatrogenic complications.
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The objective of this investigation was to determine electrolyte concentration in skeletal muscles and plasma of rats during 90 days of hypokinesia (decreased motor activity) and 15 days of posthypokinesia. The animals were divided into three groups: 1) supplemented hypokinetic rats (SHR), i.e., rats subjected to hypokinesia and taking daily an additional 9 ml water per 100 g body weight plus 6 ml isotonic sodium chloride per 100 g body weight; 2) unsupplemented hypokinetic rats (UHR), i.e., rats subjected to hypokinesia; 3) vivarium control rats (VCR), i.e., rats placed under ordinary vivarium conditions. Hypokinesia was effected by keeping SHR and UHR animals in small individual cages that restricted their movements in all directions without hindering food and water intake. Determinations were made of water and electrolyte (sodium potassium, calcium, magnesium) concentrations in muscle tissue; concentration of electrolytes (sodium, potassium, calcium, magnesium, phosphorus, chloride) in plasma; body weight; fluid consumed and eliminated in urine; whole blood, red blood cell and plasma volumes; hematocrit content and plasma protein concentration. During the hypokinetic period, electrolytes and water concentration in muscle tissue and plasma electrolyte concentration changes significantly in the UHR when compared with SHR and VCR while in comparing the SHR with the VCR these same variables had no significant changes. Body weight, water balance, volume of blood, red blood cell and plasma, hematocrit and plasma protein concentration in the UHR were also significantly different when compared with the VCR. No significant difference was seen in these parameters when the SHR and VCR were compared. During the initial seven days of the posthypokinetic period the changes in these same parameters remained significantly different in the UHR when compared with the SHR and VCR while changes were insignificant when the SHR and the VCR were compared. It was concluded that daily hyperhydration may be used to attenuate or normalize water and electrolyte concentrations in muscles and plasma of rats subjected to prolonged restriction of motor activity.
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Several troops evacuated from field training sites as heat casualties were determined to be fluid overload casualties. Common features of this paradoxical syndrome were dilute primary electrolytes with physical exhaustion and muscle weakness after rapid free water intake. A pattern of skipping meals, working in a hot and humid environment, and consuming large volumes of water as "protection against becoming a heat casualty" predisposed these troops to the physical impairment that they intended to avoid. The mechanisms leading to both appropriate and inappropriate physiological responses to free water replacement are discussed as a basis for avoiding this specific heat casualty situation.
Three cases of children with suspected copper intoxication from the drinking water are described. The children presented with protracted diarrhoea, which promptly disappeared, when they were given drinking water of low copper concentration but reappeared when given their domestic water. It is concluded that the use of copper tubing in the water pipes may under certain circumstances result in the presence of copper in the drinking water and the risk of intoxication, especially in small children.
Disordered water balance affects as many as 60% of severely psychiatrically disabled persons. Most patients do not progress to the point of a medical emergency, but are in a state of mild chronic intoxication, making them unavailable for treatment and requiring nursing care to treat the effects of the chronic intoxicated state. Interventions depend on the severity of the disordered water balance and vary from teaching fluid intake control to controlling all patient access to fluids. Nursing management of water intoxication is a trial and error approach. Through a thorough assessment and close observation of the patient, the nurse can determine which interventions would be most appropriate for the patient.
Eleven water soluble chelating agents were tested as antidotes for acute beryllium sulfate intoxication in mice. The most effective of these was sodium 4,5-dihydroxy-1,3-benzenedisulfonate (Tiron). At the level of administration of beryllium used, aurin tricarboxylic acid is not an antidote.