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PubMedDate not supplied

Metabolic disturbances after head injury: abnormalities of sodium and water balance with special reference to the effects of alcohol intoxication.

Eighty-eight patients with craniocerebral trauma were studied prospectively to assess the effects of the injury on sodium and water balance. Abnormalities of serum sodium and osmolality occurred in 11 of the 76 patients who were on the study more than 24 hours, and the incidence of these abnormalities was directly related to the severity of the craniocerebral injury. Hyponatremic hypo-osmolar states were as frequent as were hypernatremia and serum hyperosmolality. The major cause of the hyponatremia was inappropriate antidiuretic hormone secretion; hypernatremia was due to dehydration and occurred predominantly in comatose patients with increased insensible fluid losses associated with pyrexia. We recommend that the initial fluid intake after craniocerebral trauma be kept between 1500 and 1800 ml/24 hours and that further fluid management be dictated by repeated serum electrolyte determinations. The electrolyte balance should be monitored continuously after a significant head injury for up to 2 weeks, because hyponatremic states sometimes develop more than 1 week after injury. The serum alcohol was measured on admission, and the level of serum alcohol correlated well with the serum osmolality on admission; thus, the degree of elevation of serum osmolality was a very good guide to the serum alcohol level. However, there was no statistically significant correlation between alcohol intoxication or chronic alcoholism and the late development of serum sodium and osmolality disturbances.

Adolescent↗
PubMed1983

[Pulmonary intoxication by accidental inhalation of a household aerosol water repellent].

Two young people, a 23 year man and his wife aged 21, are admitted in hospital because they complain of headache; nausea, dyspnea. These symptoms are related with the use of a water-reppellent spray in bad conditions; troubles appear because the product is used in an insufficiently ventilated room. At the admission time, the man suffers from coughing, polypnea, giddiness, the fever is 38 degrees, 3 C. The blood gas values are normal. The thoracic Xray is also normal. The woman is more affected the fever is 38,8 degrees C. The signs are worse and the blood value of Co is 5%. The blood gas values are: PO2 64,8 mm HG, SaO2 92,4%, PCO2 28,8 mm Hg. The chest Xray shows signs of acute pulmonary oedema. Corticoïds and furosemide give a progressive improvement. 48 h later a favorable evolution is noted in the two cases. The german manufacturer of the product gave its composition which is as follows: - petrol 17,3% - essence 15,3% - methylen chloride 13,7% - freon (trichlorofluoro-methane - dichlorofluoromethane) 42,2% - impregnant (melamine resin; organic methylic soap) 2,6% - propan butan 9,2%. The compound responsible for the symptomatology is petrol vapour which, if inhalated, is well known to produce pulmonary toxicity. The woman's condition was worse because she used the spray herself and therefore inhaled a lot a vapours. With this type of product the direction for use have to be strictly followed ie the operation must take place in a well ventilated room.

Accidents, Home↗
PubMed1994

The postmortem blood alcohol concentration and the water content.

Determination of blood alcohol concentration and water content were performed on blood specimens from 71 bodies. Two blood specimens were sampled from each body. First-specimens (short-time-specimens) were sampled from 0 to 9.6 hours postmortem, in mean 2.1 hours. Second-specimens (long-time-specimens) were sampled from 8.0 to 229.9 hours postmortem. The relation between the blood alcohol concentration and the blood water content in the two blood specimens (first and second) is described by a multiple regression equation. The equation gave as result: if the body had no signs of putrefaction, the difference in water content between the short-time-specimens and the long-time-specimens has a significant influence on the blood alcohol concentration. This was not the case if the body had visible signs of putrefaction. Then other factors influence the blood alcohol concentration more than the water content. Our study also indicates that if a blood alcohol determination is performed on whole blood, and the blood specimen was sampled shortly after death from a case of bleeding shock, a correction of the blood alcohol concentration should be done if the blood water content is higher than 82%.

Alcoholic Intoxication↗
PubMed1980

[The role of zinc compounds in forensic chemistry].

Literary data on the intoxications with tin containing chemicals are reviewed. Attention is called to the fact, that the value of the DL of the chlorides in some works are mistaken for the sulphates and vice versa. Several cases of acute intoxication with soldering-water are reported. In these cases both the medical history and the autopsy findings referred only to intoxication with hydrochloric acid and the effect of other toxic agents was not suspected.

Diagnosis, Differential↗
PubMedDate not supplied

[Forensic medical diagnostics of nitrate and nitrite intoxication].

Nitrates and nitrites, accumulating in toxic concentrations in soil, plants, water and foodstuffs, can cause lethal intoxication. The method of isolation, identification and quantitation has been elaborated for their diagnosis. It is based on the isolation of water and subsequent chromogenic test plus photoelectrocolorimetry.

Forensic Medicine↗
PubMed1985

Serum strontium estimation as a diagnostic criterion of the type of drowning water.

The estimation of serum strontium in rabbits before and after death by drowning, in soft or hard water, or by barbiturate intoxication is highly promising as a method in medicolegal practice. It not only diagnoses drowning but also indicates the type of drowning water. Atomic absorption spectrophotometry is a good method for the estimation.

Animals↗
PubMedDate not supplied

An experimental model of self-intoxication in C57 mice.

Male C57BL/6J mice offered unrestricted access to food, water and 10% ethanol, exhibited obvious intoxication when treated with the alcohol dehydrogenase inhibitor, 4-methylpyrazole (4MP) by chronic infusion. Plasma concentrations of ethanol ranged from 156 +/- 43 mg/dl at midday to 254 +/- 31 mg/dl at midnight producing a twenty-fold increase in the total exposure to blood alcohol. Illness sufficiently severe to require intervention occurred in five of the ten mice in the experimental group, while controls treated with 4MP and offered only water to drink displayed no adverse effects. The continuation of drinking despite life-threatening toxicity suggests these mice failed to make an association between the consumption of ethanol and its consequences.

Alcoholic Intoxication↗
PubMed2001

Dementia in patients undergoing long-term dialysis: aetiology, differential diagnoses, epidemiology and management.

Dementia in patients undergoing long-term dialysis has not been clearly defined; however, four different entities have been described. Uraemic encephalopathy is a complication of uraemia and responds well to dialysis. Dialysis encephalopathy syndrome, the result of acute intoxication of aluminium caused by the use of an aluminium-containing dialysate, was a common occurrence prior to 1980. However, using modern techniques of water purification, such acute intoxication can now be avoided. Dialysis-associated encephalopathy/dementia (DAE) is always associated with elevated serum aluminium levels. Pathognomonic morphological changes in the brain have been described, but the mechanism for the entry of aluminium into the CNS is incompletely understood. The mechanisms involved in the pathogenesis of the neurotoxicity associated with aluminium are numerous. Although only a very small fraction of ingested aluminium is absorbed, the continuous oral aluminium intake from aluminium-based phosphate binders, and also of dietary or environmental origin, is responsible for aluminium overload in dialysis patients. Age-related dementia, especially vascular dementia, occurs in patients undergoing long-term dialysis as frequently as it does in the general population. The differential diagnoses of dialysis-associated dementias should include investigation for metabolic encephalopathies, heavy metal or trace element intoxications, and distinct structural neurological lesions such as subdural haematoma, normal pressure hydrocephalus, stroke and, particularly, hypertensive encephalopathy and multi-infarct dementia. To prevent DAE, dietary training programmes should aim to achieve the lowest phosphate intake and pharmacological tools should be used to keep serum phosphate levels below 2 mmol/L. To prevent vascular dementia, lifestyle modification should be undertaken, including optimal physical activity and fat intake, nicotine abstinence, and targeting optimal blood glucose, cholesterol and triglyceride levels, and blood pressure, to those outlined in current recommendations.

Aluminum↗
PubMed1993

Acrylamide disrupts elemental composition and water content of rat tibial nerve. III. Recovery.

We have previously demonstrated that subacute and subchronic acrylamide (ACR) intoxication are associated with a loss of subcellular elemental regulation in myelinated axons and Schwann cells of rat tibial nerve (LoPachin et al., Toxicol. Appl. Pharmacol. 115, 21-34, 1992; LoPachin et al., Toxicol. Appl. Pharmacol. 115, 35-43, 1992). In the present study, rats were allowed to recover partially from subchronic oral ACR intoxication (2.8 mM in drinking water for approximately 30 days). Elemental composition and water content of tibial nerve myelinated axons and Schwann cells were measured by electron probe X-ray microanalysis. Results show that K and Cl concentrations in larger tibial nerve axons were shifted toward normal values or above. For the most part, small axons also exhibited elemental changes that reflected recovery from ACR intoxication. Mitochondria displayed elemental changes that were similar to corresponding axoplasm. Schwann cells in tibial nerve of recovering animals had altered Na, P, Cl, K, and Mg concentrations that were similar in magnitude and extent to those occurring during ACR intoxication. In contrast, myelin displayed few changes. These results suggest that the recovery process following ACR intoxication is associated with characteristic changes in subaxonal elemental composition that might be related to repair mechanisms. That recovery-related elemental changes differ from those associated with intoxication provides additional support for the hypothesis (LoPachin et al., Toxicol. Appl. Pharmacol. 115, 21-34, 1992) that perturbation of elemental regulation is a specific component of ACR neurotoxicity. The observation of persistent Schwann cell disruption during recovery might reflect either long-term secondary consequences or delayed recovery from direct injury. Further studies are necessary to resolve this issue.

Acrylamide↗
PubMed1980

Effect of L-thyroxine on renal excretion of water and electrolytes in both normal and mercury-intoxicated rats.

The urine output and the change in excretion of electrolytes (sodium, potassium, calcium, chloride, inorganic phosphate) in rats following mercury-induced acute tubular lesions showed marked recovery during L-thyroxine therapy. The kidney mechanisms responsible for this effect are discussed, considering especially the observation that rats treated with L-thyroxine have a reduced urinary output, unlike other species, including man, which react with polyuria. The oliguric effect of thyroid hormone in rats is attributed to the greater length of the vasa recta and loops of Henle.

Animals↗
PubMed1988

Nutritional copper intoxication in three German infants with severe liver cell damage (features of Indian childhood cirrhosis).

Three of the four children of two unrelated German families fell ill in the first year of life with severe hepatopathy leading to death in two of the children so far, after a progressive clinical course and severe hepatic failure. Laboratory and morphological investigations revealed a high concentration of copper in the liver and to a lesser degree in the kidneys and other organs. The liver architecture was severely altered by micronodular cirrhosis with toxic liver cell damage similar to that found in Indian childhood cirrhosis. Epidemiologically, copper intoxication of the drinking water was verified. The drinking water was obtained from wells via copper pipes. The copper content of the drinking water went as high as 3400 micrograms/l in the two families while water taken directly from the well showed normal content but had lowered pH (6.2). Both parents were clinically healthy, as was an older son who had not been exposed to copper intoxication during the first nine months of his life. Therefore, copper intoxication during the perinatal period appears to be a prerequisite for manifestation of the disease.

Chemical and Drug Induced Liver Injury↗
PubMed2001

In vivo protection of a water-soluble derivative of vitamin E, Trolox, against methylmercury-intoxication in the rat.

Methylmercury (MeHg) is a well-known neurotoxicant. MeHg-intoxication causes a disturbance in mitochondrial energy metabolism in skeletal muscle and apoptosis in cerebellum. We report the first in vivo effectiveness of antioxidant Trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carhoxylic acid), a water soluble vitamin E analog, against the MeHg-induced cellular responses. Treatment with Trolox (6-hydroxy-2.5,7,8-tetramethylchroman-2-carboxylic acid) clearly protects MeHg-treated rat skeletal muscle against the decrease in mitochondrial electron transport system enzyme activities despite the retention of MeHg. Tdt-mediated dUTP nick-end-labeling method clarified that Trolox is effective for protecting cerebellum from MeHg-induced apoptosis. These data indicate that MeHg-mediated oxidative stress plays an important role in the in vivo pathological process of MeHg intoxication. Trolox may prevent some of clinical manifestations of MeHg-intoxication in humans.

Animals↗
PubMed1978

Comparative effects of dihydroergotoxine (DHET) on CBF and metabolism changes produced by experimental cerebral edema, hypoxia and hypertension.

Dihydroergotoxine (DHET) perfused in the dog (100 microgram/kg) presenting a cerebral per-hypocapno-anemic syndrome reduces cerebral hyperemia, increases cerebral venous PO2, despite the rise in CMRO2 and favors glucose oxidation by the brain. DHET (20 mg/kg p.o.) is able to drop mean, diastolic and systolic arterial blood pressures in renal-hypertensive rats having a cerebral edema induced by triethyltin intoxication without affecting cerebral water and sodium levels which are increased in the controls. DHET (50 microgram/kg i.v.) can also improve EEG changes produced by a traumatic edema but does not exert (200 microgram/kg i.v.) any effect on EEG changes produced in the rabbit by lithium chloride intoxication.

Anemia↗
PubMed1990

Swainsonine toxicosis suppresses appetite and retards growth in weanling rats.

Two groups of weanling rats were treated with swainsonine, the toxin responsible for 'pea-struck' and locoism in grazing animals, for 21 days. The initial dose rate was 46 mg kg-1 d-1 in one group, and 7.6 mg kg-1 d-1 in the other. Food and water intake, urinary volume and bodyweight gain were recorded for each rat and compared with those for pair-fed and ad libitum fed control individuals. At both dose rates, swainsonine caused marked retardation of growth consequent to profound suppression of appetite. In intoxicated rats, intake of water was also diminished.

Alkaloids↗
PubMed1988

Intoxication at home due to carbon monoxide production from gas water heaters.

Forensic medicine has a role to play in the community not only when dealing with criminal cases. When the forensic scientist observes fatalities that could have been prevented, he has an obligation to respond with the purpose of preventative measures. In a short period in Copenhagen there were a number of fatalities due to the production of carbon monoxide from gas water heaters. The gas water heaters were in most cases malfunctioning due to sooted convectors and installed without a flue, but at the time of installation maintenance checks were not mandatory, and if carried out they were often unprofessional. It is emphasized that even with well functioning equipment, the danger of intoxication exists when using a heater without a flue over an extended period, if the apartment is thoroughly insulated. The oxygen will then be used in the combustion and CO produced. The symptoms are insidious and uncharacteristic. Examples are described where physicians have failed to diagnose the condition in patients in adjoining apartments. The authorities finally responded to the medical reports with new regulations and with a favourable result. The responsibility with regard to the control of technical installations in a technically advanced society is discussed.

Accidents, Home↗
PubMed1976

Urine sodium, potassium and osmolality in two rat strains selected for their different ethanol preferences.

Urine sodium, potassium and osmolality were investigated during water and ethanol diuresis in two rat strains, AA and ANA, which drink voluntarily different amounts of ethanol. At the start of each experiment the rats were in a positive water balance. During ethanol intoxication the AA strain excreted more urine than the ANA strain. In ethanol experiments the osmolality of the urine was higher in the AA strain than in the ANA strain. With ethanol amounts of 2.4 g/kg body weight and 4.8 g/kg of body weight, urinary sodium and potassium output was greater in AA rats than ANA rats. When only water was introduced urine volumes and the excretion of sodium and potassium during 180 min were greater in ANA males than in AA males.

Animals↗