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Objective: Hemodialysis is currently the recommended treatment for patients with severe salicylate poisoning. Hemofiltration, unlike hemodialysis, is available in a larger number of hospitals and is better tolerated in hemodynamically unstable patients. The aim of this study was to determine whether hemofiltration is a possible alternative to hemodialysis in severe salicylate poisoning. Methods: An in vitro hemofiltration model was used, with a Hospal AN69 filter and 500mL of 4% bovine serum albumin (BSA) as the carrier solution. Three different salicylate concentrations were studied (300, 600 & 900mg/L), with six runs for each starting concentration. Hemofiltration was performed for 180mins at a BSA flow rate of 150mL/min; ultrafiltrate was replaced with deionized water. Pre-filter, post-filter and ultrafiltrate samples were taken every 5mins for the first 60mins and then every 15mins. Results: The mean total amount of salicylate removed by hemofiltration (% amount initially present ([+ or -] 95% CI)) was 53% ([+ or -] 8%) for the 300mg/L runs, 69% ([+ or -] 12%) for the 600mg/L runs and 70% ([+ or -] 2%) for the 900mg/L runs. The sieving coefficient was constant over the 180mins studied; 0.4 ([+ or -] 0.05) for the 300mg/L runs, 0.65 ([+ or -] 0.08) for the 600mg/L runs and 0.75 ([+ or -] 0.04) for the 900mg/L runs. Conclusions: This in vitro model shows for the first time that hemofiltration can provide effective clearance of salicylate at toxicologically significant concentrations. The removal of 53-70% salicylate would be expected to be clinically significant in a severely poisoned patient. Although other factors will influence overall elimination and require further evaluation, this study shows that hemofiltration has important potential in treating severe salicylate poisoning., Dargan PI, Jones AL, Salimi Gilani P, Wallace C, Widdop B. National Poisons Information Service (London), Guy's and St Thomas' NHS Trust, London, United [...]

Background: Toxicological analyses are an essential component in evaluating toxic hazards in humans. However, there is potential for misuse and, in some cases, abuse of these investigations. Overuse of analytical toxicology services occurs when physicians request analyses even though the clinical signs are unequivocal and the results will have no relevance to patient management. There has been an abysmal failure of UK laboratories to reach agreement on standard systems of units for reporting quantitative toxicological data. Most striking is the split between those laboratories who advocate SI molar units for toxicological analyses and those who are not convinced that there are any grounds for abandoning mass units. Laboratory reports that are devoid of any comments or guidance on normal and toxic ranges are of little use unless a readily accessible consultant service for interpretation is available. This is a major cause of confusion and misinterpretation that can have disastrous clinical implications. While these deficiencies are regrettable, they fall into the category of misuse rather than abuse. The latter term should apply in circumstances where the analytical tests themselves have no valid scientific merit, either because no evidence for their relevance in diagnosing toxic exposure exists or they are completely inappropriate to a particular patient. Even when the tests may have some perceived value, some laboratory practitioners are unable (or unwilling) to support the accuracy of their results by quality control data. Bone fide external quality assessment schemes are not available for many of these tests so that another measure of performance quality is missing. Where schemes do exist, the laboratories are under no mandatory obligation to take part. Reports are frequently accessible to the patient and those sections dealing with interpretation can be presented in ways that cause alarm and distress. Moreover, this practice can lead to incorrect diagnoses, use of treatments of dubious benefit and delays in establishing the true medical condition such that long term and potentially serious health effects develop. There is a pressing need to introduce some measure of control in this area. Conclusion: Laboratories should be prevented from offering tests that are not recognized as valid by a group of recognized authorities. Where the tests may be classified as useful, the laboratories should be required to satisfy the performance criteria laid down by one or more accreditation schemes. Finally, clinicians who use these should ensure that there is genuine scientific evidence for their relevance to the investigation of a particular patient, that the data is sound in terms of analytical accuracy and that they understand fully the ground on which an interpretation is made., Volans GN, Widdop B. Medical Toxicology Unit, Guy's & St Thomas' NHS Trust, London, United [...]

Since September 1974 the London Centre of the National Poisons Information Service has advocated the use of methionine for acute paracetamol poisoning and this paper presents a preliminary report of its outcome.Seventeen patients, all of whom had high plasma paracetamol levels, received oral methionine within ten hours of the ingestion of the overdose. Eleven of these patients suffered no hepatic damage, while the remaining six showed varying degrees of liver failure with a mean maximum aspartate aminotransferase (AST) of 1,098 iu/l. There were no deaths in this group. Among fourteen patients who had taken similar paracetamol overdoses and received no antidotal treatment, all developed liver damage and seven of these died. These two groups were not, however, accurately matched for dose of paracetamol, plasma paracetamol levels or interval before reaching hospital.Comparison was therefore made with two other recently published series of untreated patients. A significant reduction was noted in the incidence of liver damage and in the mean maximum AST.Although this survey was not controlled, it is suggested that oral methionine, which has a low incidence of side-effects, may be effective in reducing the incidence and severity of paracetamol-induced liver damage, provided the overdose is not massive.

Of a series of sixty patients admitted after paracetamol overdose, forty-nine developed liver damage. Seventeen patients progressed to hepatic encephalopathy, and twelve of these died from fulminant hepatic failure. All but two of the patients with bilirubin levels above 4 mg. per 100 ml. by the 3rd-5th day developed encephalopathy. It is suggested that the degree and prognosis of the liver damage in the first few days can be assessed from the serum-bilirubin and prothrombin-time. Histology of liver-biopsy specimens of those who recovered showed severe centrilobular necrosis and collapse, but no patient has progressed to cirrhosis. Although most patients appear well in the first 3 days after ingestion, it is likely that the liver damage can be prevented only in the first 24 hours.