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Biomedical subjects

J A Vale

Publications and source records attributed to J A Vale.

At least 55 records · Page 3Linked to original sources
PubMed1995

Multiple-dose activated charcoal: a review of relevant clinical studies.

Although many studies in animals and volunteers have demonstrated that multiple-dose activated charcoal increases drug elimination significantly, this therapy has not been shown in a controlled study in poisoned patients to reduce morbidity and mortality. Further clinical studies are required to establish its role and the optimum dosage regimen of charcoal to be administered. Based on current evidence, multiple-dose activated charcoal should only be considered if a patient has ingested a life-threatening amount of phenobarbital (phenobarbitone), carbamazepine, theophylline, quinine, dapsone or salicylate. In all of these cases there are data to confirm enhanced elimination, though no controlled studies have demonstrated clinical benefit.

Charcoal↗
PubMed1995

Disturbances of potassium homeostasis in poisoning.

Unless renal function is impaired or rhabdomyolysis is severe, hyperkalemia is a relatively uncommon metabolic complication of poisoning. In contrast, marked hypokalemia is a more common problem and may have serious sequelae. Most potassium disturbances in acute poisoning are due to disruption of extra-renal control mechanisms, notably the activity of Na+/K+ ATPase and K+ channels. Hypokalemia occurs because of increased Na+/K+ ATPase activity (e.g. beta 2 agonist, theophylline or insulin poisoning), competitive blockade of K+ channels (e.g. barium or chloroquine poisoning), gastrointestinal losses and/or alkalosis. Hyperkalemia follows inhibition of Na+/K+ ATPase activity (e.g. by digoxin), increased uptake of potassium salts, disruption of intermediary metabolism (e.g. cyanide poisoning), activation of K+ channels (e.g. fluoride poisoning), and the presence of acidosis and rhabdomyolysis, particularly if the latter is complicated by renal failure. Hypokalemia results in generalized muscle weakness, paralytic ileus, ECG changes (flat or inverted T waves, prominent U waves, ST segment depression) and cardiac arrhythmias (atrial tachycardia +/- block, AV dissociation, VT, VF). Hyperkalemia is associated with abdominal pain, diarrhea, muscle pain and weakness, ECG changes (tall peaked T waves, ST segment depression, prolonged PR interval, QRS prolongation) and cardiac arrhythmias (VT, VF). Significant disturbances of potassium homeostasis are often unrecognized and may cause considerable morbidity and mortality. Prompt recognition and appropriate treatment of these disturbances could be life-saving.

Homeostasis↗
PubMed1994

Post-irradiation bladder dysfunction: muscle strip findings.

Strips of rat detrusor muscle were studied in an organ bath 6 months after X-irradiation at doses of 15 and 25 Gy; cystometric studies in these animals had shown a persistent and significant reduction in compliance. The organ bath study demonstrated an increase in the purinergic sensitivity of irradiated detrusor muscle as compared with control. This was significant: p < 0.0145 for the 25 Gy dose group (n = 8) and p < 0.0456 for the 15 Gy group (n = 8) at an alpha,beta-methylene-ATP concentration of 10(-4) M (Mann-Whitney U-Test). There was no difference in sensitivity to cholinergic or noradrenergic stimulation, or to electrical stimulation of the transmural nerves. The finding of purinergic hypersensitivity in irradiated muscle, coupled with ultrastructural evidence of a neural injury, raises the interesting possibility that a denervation supersensitivity phenomenon may contribute to the pathophysiology of post-irradiation bladder dysfunction.

Animals↗
PubMed1994

Choosing the correct pain relief for extracorporeal lithotripsy.

OBJECTIVES: To determine the best choice of analgesic for patients undergoing lithotripsy, and to attempt to identify factors which might predict which patients are most likely to find the procedure painful. PATIENTS AND METHODS: Sixty patients with stones in the pelvicalyceal system of the kidney were randomized prospectively to undergo lithotripsy with the Dornier MPL9000 lithotripter (Dormier Medical Systems, Marietta, GA, USA) after receiving either diclofenac 100 mg per rectum (n = 30) or pethidine 50 mg intravenously (n = 30) for analgesia. The patients completed a detailed questionnaire prior to treatment, and the level of pain perceived during lithotripsy was monitored using visual analogue scales (VASs). Arterial oxygen saturation (SaO2) was monitored before analgesia was given, throughout the treatment and for 30 min after cessation of treatment. RESULTS: The VASs were available for 56 patients and the results of pulse oximetry for 51 patients. Although a higher kilovoltage was recorded in the group who received pethidine this difference was not significant. Patients who received diclofenac or pethidine alone, showed a non-significant fall of SaO2 30 minutes after the end of treatment, although the largest fall in SaO2 observed with pethidine was 10%. Patients who received diclofenac and pethidine similarly showed a non-significant fall in SaO2. Four patients received intravenous benzodiazepines in addition to pethidine, and in this group there was a dramatic fall in SaO2 which persisted more than 30 min after the end of treatment (P < 0.0027). Diclofenac provided effective analgesia for most of the patients who underwent lithotripsy. Overall 11 patients (18%) required additional analgesia. Diclofenac or pethidine alone, in the doses used in this study, did not cause a significant drop in SaO2 during ESWL. The only response found to be of value in predicting a painful experience was fear of the dentist. CONCLUSIONS: This study shows that modern lithotripsy, in addition to being safe and effective, can be performed as an out-patient procedure using simple non-opiate analgesics. The need for stronger analgesia and/or sedation should be tailored to the needs of the individual patient, although it remains difficult to predict which patients will require such measures.

Adult↗
PubMed1994

Deaths from pesticide poisoning in England and Wales: 1945-1989.

1. Data on deaths from pesticide poisoning occurring in England and Wales between 1945 and 1989 (no data are available for 1954) have been collated; pesticides were responsible for only 1012 (1.1%) of the 87,385 deaths from poisoning (excluding those due to carbon monoxide) occurring over this 44 year period. At least 73% of all pesticide fatalities were due to suicide and overall there was a predominance of males (male:female ratio 2.4:1). No deaths from pesticide poisoning in children under 10 years have been reported since 1974 although almost 50% of suspected pesticide poisoning incidents involve this age group. 2. Herbicides were responsible for 787 (78%) fatal poisonings, 110 (11%) were caused by insecticides, 69 (6.8%) by rodenticides, 30 (3.0%) by wood preservatives and 16 (1.6%) by other pesticides. 3. The herbicide, paraquat, was responsible for 570 of 1012 (56%) deaths and, although there has been a progressive decline in the annual number of deaths from paraquat poisoning since 1982, paraquat remains the most common cause of fatal pesticide poisoning in England and Wales. 4. Sodium chlorate caused 113 (11.2%) deaths, most of these fatalities occurring between 1965 and 1983; only one death has been recorded since 1984. The phenoxyacetate herbicides resulted in 50 deaths; 2,4-D was implicated most commonly. Sixty-eight deaths were due to organophosphorus insecticides; demeton-S-methyl, malathion and mevinphos were involved most frequently. Only eight deaths resulted from organochlorine insecticides and two of these also involved an organophosphorus insecticide.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Suspected paediatric pesticide poisoning in the UK. I--Home Accident Surveillance System 1982-1988.

1. Between 1982 and 1988, 239,350 children under 10 years old attended 20 A & E Departments in England and Wales (22 departments throughout the UK in 1988) as a result of a home accident. 15,144 of 239,350 were suspected cases of poisoning and 514 attendances involved pesticides. 2. 501 of 514 children who attended hospital were under 6 years old and 41% were thought to have ingested a rodenticide, 37% an insecticide or other animal poison, 13% an herbicide or fungicide and 9% other pesticides. 3. Overall 189 of 514 children were admitted to hospital and of these 189 cases 35% were discharged home in less than one day; 94% left hospital within 2 days. 4. Using these data we estimate that over the period of study approximately 1,850 children annually attended an Accident and Emergency Department in the UK with suspected pesticide poisoning and that some 450 were admitted to hospital. However, the morbidity from this cause is low and no deaths from pesticide poisoning have been reported in children in England and Wales for more than two decades.

Accidents, Home↗
PubMed1994

Suspected paediatric pesticide poisoning in the UK. II--Home Accident Surveillance System 1989-1991.

1. Between 1989 and 1991, 121,708 children less than 10 years old attended 22 Accident and Emergency (A & E) Departments in the UK as a result of an accident at home; 6,478 of these were cases of suspected poisoning. 2. Two hundred and fifty (124 boys and 126 girls) of 6,478 cases involved pesticides. Forty two per cent of these children were thought to have been poisoned by rodenticides, 33% by a different animal poison, 13% by an herbicide or fungicide, 7% by creosote and 5% by mothballs; a pattern similar to that observed in previous years. 3. Fifty-seven of 250 children (23%) were admitted to hospital. The proportion of children admitted to hospital between 1989 and 1991 is smaller than that observed between 1982-1988 (37%). Forty-six per cent of children were discharged home within one day and 95% within 2 days, whereas between 1982 and 1988 only 35% of children were discharged within one day. No child died during the study confirming the low morbidity. 4. Using these data we estimate that between 1989 and 1991 approximately 1,500 children annually attended an A & E Department in the UK with a diagnosis of suspected pesticide poisoning and that some 350 children were admitted each year.

Accidents, Home↗
PubMed1994

Methemoglobinemia caused by the accidental contamination of drinking water with sodium nitrite.

Sodium nitrite is used commercially as a coloring agent, a food preservative and a corrosion inhibitor. Accidental poisoning usually results from the ingestion of contaminated food and water and causes gastrointestinal irritation, vasodilatation and methemoglobinemia with subsequent tissue hypoxia. We describe an unusual case of sodium nitrite-induced methemoglobinemia following the ingestion of drinking water contaminated with a corrosion inhibitor. To our knowledge this is the first report of such a case.

Adult↗
PubMed1994

Fatal methemoglobinemia due to inhalation of isobutyl nitrite.

Isobutyl nitrite is a popular recreational drug among both homosexuals and heterosexuals as it is alleged to enhance sexual pleasure and prolong orgasm. In contrast to the ingestion of this volatile nitrite, inhalation is associated only rarely with serious sequelae, though symptomatic methemoglobinemia may occur. The case reported is the first documented fatality from inhalation of isobutyl nitrite. The widespread use of isobutyl nitrite is a cause for concern and physicians should be aware of the potentially fatal consequence of abuse, particularly in those with ischemic heart disease, and its management.

Administration, Inhalation↗
PubMed1994

Methemoglobinemia following ingestion of a monolinuron/paraquat herbicide (Gramonol)

A 59-year-old man ingested a mouthful of Gramonol with suicidal intent and was admitted to a local hospital six and a half hours later. It was noted that he looked "ashen grey" and was centrally cyanosed. The methemoglobin and plasma paraquat concentrations performed on arrival at the Regional Poisons Treatment Unit eight hours after paraquat ingestion were 52% and 1100 micrograms/L respectively; the administration of methylene blue reversed methemoglobinemia within two hours. The patient suffered extensive paraquat-induced oral, and probably esophageal, ulceration and developed multiple organ (particularly renal, respiratory and hepatic) failure and died some 10 days later. This is the most severe case of Gramonol poisoning reported both in terms of the amount of paraquat ingested and the concentration of methemoglobin formed. We believe that the methemoglobinemia in this patient was caused by monolinuron not paraquat.

Fatal Outcome↗
PubMed1993

Oral manifestations of poisoning.

The purpose of this paper is to describe the variety of chemical agents and medicines which can produce oral manifestations following poisoning. Rapid diagnosis is essential in covert cases to ensure early treatment. Furthermore, oral care is an important part of the general management of many poisoned patients.

Burning Mouth Syndrome↗
PubMed1993

Post-irradiation bladder dysfunction: development of a rat model.

The aim of this research was to establish a small animal model for the functional and morphological study of post-irradiation bladder dysfunction. Young adult female Wistar rats were X-irradiated with single doses of 10, 15, 20 or 25 Gy. Filling cystometry was performed to assess changes in reservoir function: the volume infused to produce a rise in intravesical pressure of 5 cmH2O was calculated as an index of compliance. A biphasic reduction in this index was noted in animals receiving 15-25 Gy; the first reduction developed at about 4 weeks, and the second started at 3-4 months and persisted at 6 months. Bladder tissue was taken at this time (6 months post-irradiation) for morphological study. Histological examination demonstrated an increased mast cell density in the irradiated bladders, but was otherwise non-specific; fibrosis was discernible in only half of the 18 animals studied. Electron microscopy showed focal degeneration of smooth muscle cells, and in some areas there was selective degeneration of unmyelinated axon profiles. The biphasic reduction in the compliance index is consistent with the timing of the symptoms of the acute and late irradiation reactions reported by radiotherapy patients. Changes in axon profiles and mast cell density may be of functional significance.

Animals↗
PubMed1993

Paracetamol poisoning and the kidney.

Nephrotoxicity is less common than hepatotoxicity in paracetamol overdose but renal tubular damage and acute renal failure occur even in the absence of hepatotoxicity. It is possible that antidotal therapy with agents such as N-acetylcysteine may not prevent renal toxicity and, indeed, on the basis of animal work, may actually potentiate tubular damage. Careful clinical attention should be paid to renal function in patients poisoned with paracetamol.

Acetaminophen↗