[Diagnosis and therapy of water metabolism disorders].
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A case of psychogenic polydipsia is presented. A 40 year old female was brought to the emergency room after a sudden seizure at home. The patient had spontaneous eye opening, was making incomprehensible sounds and had abnormal and agitated flexion of the limbs. Severe cerebral edema was seen on the computed tomogram. The patient was found to have hypotonic polyuria and hyponatremia. Two months previously, the patient had stopped taking bromazepam (a benzodiazepine) and on the advice of a neighbour had taken plenty of water to avoid withdrawal symptoms. The diagnosis and therapy are discussed.
Juxtaglomerular complex (JGA) and kidney medullar interstitial cells (IC) in rats in acute water and salt loadings were studied. The animals were killed 1 and 2 hours later after water 0.9% and 2% natrium chloride per os administration in quantity of 5%-7% per total body weight. Plasma osmolality and plasma renin activity (PRA) was determined. In light microscopy the granulation of the JGA-cells was in accordance with PRA in all the experiment. IC were not altered in water loading. Marked diminishing of lipid granulation of the IC in all zones of papilla at 2% salt loading was observed. In electron microscopy changes in distribution and density of lipid granules of the IC in all zones of the renal papilla were noted. The lesions showed the dystrophic and necrobiotic changes in some IC, especially in central zone of papilla.
The neuroleptic malignant syndrome is a serious complication associated with the use of antipsychotic drugs that has received a great deal of interest in recent times. Although its aetiology has not been fully understood, it often occurs in association with underlying brain disease and physical debilitation. Two such cases are described. The various hypotheses concerning the aetiology and pathogenesis of this condition are also discussed.
In experiments with Wistar rats, a study was made of the content of antibody-forming cells and cytotoxic activity of normal killers after long-term administration of tritium oxide (3HOH) (370 kBq.g-1 of body mass daily, cumulative dose, 8.1 Gy, and dose rate, 8.5 cGy/day), and after gamma irradiation with corresponding doses. The long-term radiation effect caused a decrease in the immunity indices: the impairment of the immune reactions was more pronounced after the effect of 3HOH than after gamma irradiation. Damages to the immune system of mice and rats after irradiation with similar doses were compared.
In experiments with CBA mice it was shown that the long-term influence of tritium oxide administered with drinking water daily during 180 days (370 kBq.g-1 of body mass, cumulative dose 8.7 Gy, dose rate 4.5 cGy.day-1) causes the development of immunity deficiency 90 days after the onset of the administration that persists for up to 270 days. There is a 34% decrease in the average life of irradiated animals and an increase in the number of malignant neoplasms (postmortem examination was performed after natural death or killing on days 250, 350 and 450). There is a direct relationship between the occurrence of malignant neoplasms and the immunity deficiency.
The incidence of leukoses upon long-term administration of tritium oxide to Wistar rats increased by 15.6% as compared to 2.1% in controls. The repeated injection of bacterial lipopolysaccharide caused a 2.3-fold increase in the occurrence of hemoblastosis induced by the radionuclide mainly due to the increase in the proliferative activity of haemopoietic precursors because of the increased demand for mature cells.
Ten infants and children with respiratory failure, receiving standard maintenance water requirements, were treated on 13 occasions with intravenously given furosemide (1 to 2 mg/kg) because of continued impairment of oxygenation despite conventional therapy. Pulmonary auscultation and radiographs were normal or typical of the primary diagnosis. After a five-fold increase in urine output the mean Po2 rose from 61 mm Hg at a mean FiO2 of 0.7 to 140 mm Hg at an FiO2 of 0.65. The Pco2 decreased from 46 to 38 mm Hg. Interstitial pulmonary edema in these patients can be related to both their lung disease and impaired water tolerance during ventilatory therapy.
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A 10-y history of high rates of perinatal deaths and congenital anomalies in dogs in a Shetland Sheepdog kennel prompted investigations into the cause(s). Skeletal fluorosis (mottled teeth in pups, bony exostoses in adults) followed use of a commercial dog food later found to contain 460 ppm fluoride (F) from rock phosphate added as a mineral source. The effects of the water source and fluoride in dog food on female reproduction and teratogenicity were investigated in a 2-y, 2-way factorial study in the kennel. Twenty adult shelties of proven fertility were brought into the kennel and randomized into 4 treatment groups, each consisting of 4 females and 1 male. Treatments were: Group A, high F (460 ppm) dog food, well water; Group B, high F dog food, distilled water; Group C, low F (55ppm) dog food, well water; Group D, low F dog food, distilled water. Only Group C produced as many pups as expected. Overall the missed pregnancy rate (44%) in study bitches and perinatal death rate (50%) in 48 study pups paralleled the problems in shelties resident in the kennel. Higher rates for both variables in the high F and the distilled water groups seemed likely due to chance. The only major anomaly was in Group D; minor anomalies appeared in all groups. Although 460 ppm F in dog food did produce bony exostoses, we did not find convincing evidence that it adversely affected reproduction in shelties. The cause of the reproductive problems was apparently not the dog food, water, foliage, genetic factors, or infectious disease and currently remains undetermined.
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The clinical picture of metabolic encephalopathies has no aetiological specificity. It combines disturbances in conscious level dominated by disorientation and time and space and disturbances in motor activity, in particular tremor and asterixis. For each of the aetiologies studied, the following are considered: the circumstances of onset, the clinical and laboratory picture, the physiopathology and the treatment. From a diagnostic standpoint, particular emphasis should be placed upon the circumstances of onset which alone give any indication. The majority of these encephalopathies are caused by a lack of respect for simple rules in parenteral alimentation or by deficiencies. It is thus essentially an iatrogenic pathology. Treatment should be above all preventive.
We compared the diurnal weight gain of 46 patients with mental retardation to that of 21 patients with organic mental syndromes. They were weighed at 7 a.m. and 4 p.m. weekly for 3 weeks. We normalized the diurnal weight gain as a percentage by subtracting the 7 a.m. weight from the 4 p.m. weight, multiplying the difference by 100, and dividing the result by the 7 a.m. weight. Normalized diurnal weight gain was abnormal among one fourth of patients with mental retardation and two thirds of those with organic mental syndromes. Differences in age, sex, baseline weight, antipsychotic drugs, lithium, carbamazepine, blood pressure, and pulse did not explain our results. We believe that our findings provide additional evidence to separate patients with mental retardation from those with psychosis.
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