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Biomedical subjects

J A Vale

Publications and source records attributed to J A Vale.

At least 91 records · Page 5Linked to original sources
PubMed1989

Hypophosphataemia and phosphaturia in paracetamol poisoning.

To find out whether the hypophosphataemia in paracetamol poisoning is due to renal loss of phosphate, serum phosphate concentrations were correlated with indices of hepatotoxicity in 273 patients who had taken an overdose of paracetamol, and the renal handling of phosphate was examined in another 40 patients. Hypophosphataemia was a feature of paracetamol poisoning, whether hepatotoxicity was present or not. It correlated with the degree of hepatic damage and was not influenced by glucose infusions. Serum phosphate correlated with renal threshold phosphate concentration, so renal loss rather than intracellular redistribution of phosphate seems to be the reason for the hypophosphataemia in paracetamol overdose, and it correlates well with other indices of severity of poisoning.

Acetaminophen↗
PubMed1989

Biofilms, bacteria and bladder catheters. A clinical study.

Biofilms were present on 16 of 33 urethral catheters examined. In 11 cases the catheter carried a different microbial flora from that of the bladder urine. The length of time the catheter was in situ did not influence biofilm formation, and all types of materials tested supported biofilm growth. Biofilms were seen on 2 of the 7 catheters where prophylactic antibiotics had been used.

Bacteria↗
PubMed1987

Who needs molar units for drugs?

The standardisation of units for drug concentration measurement in clinical medicine is an urgent necessity. The obvious choice is mass units based on the litre. A change to molar units for drug concentrations would make no sense unless drugs were also prescribed in moles, which would cause disruption and inconvenience. There would be considerable danger to patients and the change would be expensive. Most importantly, molar units for drugs will not benefit doctors or their patients. Mass units should be retained and proposals for the adoption of molar units should be abandoned.

Humans↗
PubMed1987

Paraquat poisoning: clinical features and immediate general management.

In contrast to 10-15 years ago most cases of paraquat poisoning are now due to deliberate self-poisoning with parasuicidal or suicidal intent rather than to accidental ingestion. Less commonly, poisoning may follow careless handling of paraquat during occupational use. Although paraquat can be absorbed through the skin if improperly handled, poisoning usually follows ingestion and has rarely been reported after subcutaneous, intravenous or intraperitoneal injection. Clinically, three degrees of intoxication may be distinguished. Mild poisoning occurs after the ingestion or injection of less than 20 mg of paraquat ion/kg body weight. In these cases patients are either asymptomatic or symptoms are confined to the gastrointestinal system. All patients recover fully. Moderate to severe poisoning usually follows the ingestion (rarely injection) of 20-40 mg of paraquat ion/kg body weight. Non-specific symptoms of ill health together with local gastrointestinal symptoms precede the development of renal failure (which may recover spontaneously) and pulmonary fibrosis which may not be manifest for days or weeks. Death occurs in the majority of cases but is usually delayed for 2-3 weeks. Acute fulminant poisoning follows the ingestion of substantial quantities of paraquat (greater than 40 mg of paraquat ion/kg body weight). In addition to local symptoms, multiple organ (cardiac, respiratory, hepatic, renal, adrenal, pancreatic, neurological) failure occurs. Death may supervene within hours and is never delayed for more than a few days. Initial general management has four priorities.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1987

Treatment of paraquat poisoning in man: methods to prevent absorption.

Theoretically, absorption of an ingested dose of paraquat may be reduced by gastric lavage, induced emesis, whole-gut lavage or by the oral administration of absorbent substances. Animal experiments suggest that paraquat is absorbed poorly from the stomach and absorbed incompletely (less than 5%) from the small intestine over a 1-6 h period. Although gastric lavage would therefore seem a logical way to ameliorate the toxicity of an ingested dose of paraquat, peak plasma concentrations are attained rapidly and evidence for the efficacy of gastric lavage in man is poor. In 1977, a potent emetic (PP796) was added to liquid and solid formulations of paraquat because experiments in primates had demonstrated a fivefold reduction in toxicity. In man, ingestion of formulations containing an emetic is more likely to cause spontaneous vomiting within 30 min than non-emetic preparations. However, definite evidence of benefit, as judged by improved patient prognosis, has yet to be established. Gut lavage has been shown to remove only a small proportion of an ingested dose of paraquat. At the flow rates employed in man (75 ml/min), approximately 0.5-1.0 litres of lavage fluid/h may be absorbed across the intestinal wall. Since there is a theoretical risk of increasing paraquat absorption, the use of whole-gut lavage cannot be recommended. Bipyridilium herbicides are absorbed by soil and clay minerals, and montmorillonite in particular has been shown to be a strong binding agent in vitro. Accordingly, the use of Fuller's Earth (calcium montmorillonite) and Bentonite (sodium montmorillonite) for the treatment of poisoning has been investigated in animal models.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum Compounds↗
PubMed1987

Hyperlactataemia and metabolic acidosis following paracetamol overdose.

Plasma lactate concentrations and acid-base status were determined in 53 patients poisoned with paracetamol. Eleven patients (Group 1) had plasma paracetamol concentrations below the standard treatment decision line; 19 cases (Group 2) presenting within 15 h of overdose had plasma paracetamol concentrations above the treatment line and received N-acetylcysteine. The remaining 23 patients (Group 3) arrived at hospital too late (more than 15 h after overdose) for treatment with N-acetylcysteine to be completely effective. Compensated metabolic acidosis was present on admission in 55 per cent of Group 1 and 42 per cent of Group 2 patients, and a further 21 per cent of cases in Group 2 had an uncompensated metabolic acidosis. Half the patients in Group 3 were acidotic: 22 per cent had a compensated and 26 per cent an uncompensated metabolic acidosis. On admission, the mean plasma lactate concentration was elevated in both Group 2 and Group 3 patients though not in Group 1 cases. Plasma lactate concentration then fell to normal in patients in Group 2 but became mildly elevated again in some cases at a time which coincided closely with the peak in serum aspartate aminotransferase activity. In patients presenting within 15 h of overdose there was a significant correlation between the elevation in plasma concentrations of lactate and paracetamol at admission. In patients presenting late (Group 3), plasma lactate remained elevated for longer than in Group 2 and acidosis and hyperlactataemia were prominent features in the four patients who died. This study demonstrates first that hyperlactataemia, with or without significant acid-base disturbance, is common following paracetamol overdose particularly in those who are severely poisoned. As uncompensated metabolic acidosis is found in 20 per cent of patients who present early and require protective therapy, it should be sought and corrected if it does not remit spontaneously. Second, half the patients presenting too late for effective treatment are acidotic and those with an uncompensated metabolic acidosis resistant to correction have a poor prognosis. Paracetamol poisoning should be considered in the differential diagnosis of metabolic acidosis of unknown aetiology.

Acetaminophen↗
PubMed1986

Paraquat poisoning.

Explore the source record for details and available documents.

Combined Modality Therapy↗
PubMed1986

Factitious Cushing's syndrome.

In this report we describe a patient who produced the clinical and laboratory features of Cushing's syndrome by injecting himself for many months with hydrocortisone. Factitious Cushing's syndrome is a variant of the Münchausen syndrome and should be considered if tests used to establish the diagnosis of Cushing's syndrome appear incongruous particularly in subjects with access to medical intelligence and drugs.

Adult↗
PubMed1986

Non-narcotic analgesics. Problems of overdosage.

The first cases of fulminant hepatic failure due to paracetamol poisoning were reported in 1966, and in the United Kingdom this condition is now responsible for more cases of acute hepatic failure than any other cause. Adults account for the majority of serious and fatal cases of paracetamol poisoning and it is extremely rare for young children to ingest sufficient paracetamol to cause more than minimal liver damage. A single measurement of the plasma paracetamol concentration is an accurate predictor of liver damage provided that it is taken not earlier than 4 hours after ingestion of the overdose. Peak disturbance of liver function occurs 2 to 4 days after the overdose, often accompanied by mild jaundice, after which recovery is usually rapid and complete. In a few patients, fulminant hepatic failure, manifested by increasing jaundice and encephalopathy, may develop by the third to fifth day. Acute renal failure may complicate paracetamol poisoning, often in the context of severe liver damage. Renal failure, which is often non-oliguric, typically becomes apparent 24 to 72 hours after overdosage. The treatment of paracetamol intoxication should include gastric lavage, which has been shown to be of value for up to 6 hours after ingestion of a paracetamol overdose. Further general treatment may include parenteral fluid replacement and a prophylactic infusion of dextrose (5-10%) in patients at risk of hepatic failure. Specific protective agents in those patients at risk of paracetamol-induced liver damage include N-acetylcysteine and methionine which are most effective if given within 8 to 10 hours of ingestion of the overdose. Hepatic and renal failure should be managed conventionally. In recent years in the United Kingdom there has been a gradual decline in the number of hospital admissions and the number of deaths from aspirin poisoning. Salicylates in overdose directly stimulate the respiratory centre and so cause a respiratory alkalosis. Metabolic acidosis occurs in severe poisoning because of impairment of the oxidative metabolism of energy substrates. At very high salicylate concentrations respiratory depression may occur, possibly associated with neuroglycopenia, adding respiratory acidosis to the worsening metabolic acidosis. In addition to a mixed acid-base disturbance, hypokalaemia and hypoglycaemia may be present. Nausea and vomiting increase the fluid deficit. If dehydration is sufficiently severe, decreasing cardiac output may hasten development of lactic acidosis and acute renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)

Analgesics↗
PubMed1986

Indomethacin poisoning.

Two cases of indomethacin poisoning with supporting analytical data are described and the literature, which is limited to two reports, is reviewed. In overdose, indomethacin may produce the following non-life threatening symptoms: nausea, vomiting, abdominal pain, anorexia, drowsiness, headache, tinnitus, restlessness and agitation. The terminal elimination half-life in our two cases was respectively 6.8 hr and 2.9 hr which is similar to that found following a therapeutic dose.

Adolescent↗