Comment: combination risperidone and SSRI-induced serotonin syndrome.
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Biomedical subjects
Publications and source records attributed to Geoffrey K Isbister.
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OBJECTIVES: To determine whether the occurrence of paracetamol and non-paracetamol analgesic deliberate self-poisoning (DSP) and accidental paediatric poisoning was affected by two periods of recall of paracetamol products. DESIGN: Retrospective, observational audit of proportions of poisonings with tablet and capsule formulations of paracetamol, ibuprofen and aspirin products during two recall periods compared with the number of poisonings during the same periods of the previous three years. SETTING: A national poisons information centre and a regional toxicology service. MAIN OUTCOME MEASURES: Rates of DSP and accidental paediatric poisoning with paracetamol, ibuprofen and aspirin. RESULTS: During the two recall periods, there was a significant increase in ibuprofen DSP calls to the poisons information centre (RR, 1.86; 95% Cl, 1.41-2.44; P = 0.001). There was no significant change in paracetamol or aspirin DSP calls over the two recall periods. However, there was a non-significant reduction in DSP calls with paracetamol in the first recall period alone (P = 0.057). There was a significant increase in the proportion of aspirin DSP presentations for the toxicology service (RR, 3.33; 95% CI, 0.97-11.4; P = 0.043), but no significant changes in paracetamol and ibuprofen DSP presentations. For accidental paediatric ingestions there was a significant increase in the proportion of ibuprofen calls (RR, 2.35; 95% CI, 1.85-2.98; P = 0.001), but no significant change in paracetamol or aspirin calls. CONCLUSIONS: Reduced paracetamol availability increased poisoning with alternative analgesics, but had little effect on the incidence of paracetamol poisoning. Restriction of paracetamol-containing products may inadvertently increase poisoning with potentially more toxic agents.
We report two cases of envenomation by the black bellied swamp snake, Hemiaspis signata, with expert identification of the snakes. In the first case a 12 year old boy, who after the removal of the pressure immobilisation bandage, developed decreased fibrinogen levels and positive cross-linked fibrinogen degradation products (XDPs), but normal prothrombin time and activated partial prothrombin time. These changes resolved over 8h with no treatment. In the second case a 7 year old boy had local pain, swelling and axillary lymphadenopathy following the bite. These cases indicate the potential for coagulopathy and local symptoms following bites by large specimens of H. signata in young children.
Allergic reactions following contact or injury from arachnids are uncommon. There have previously only been reports of urticarial reactions following contact with large spiders from the family Theraphosidae. A 55-year-old male presented to hospital with a generalised urticarial rash following contact with a spider, identified by the person as a huntsman spider (Family: Sparassidae). The spider had crawled over both his arms for a period of minutes. About 30 min later, he developed a rash on the arms which spread to the trunk. He then developed bradycardia and hypotension that required treatment with atropine, adrenaline and histamine antagonists. He recovered within 6 h and had no further problems. The early allergic reaction in this case was most likely the result of contact with the spider.
Four cases of Red-back spider envenoming are reported in which there was minimal response to intramuscular antivenom. Intravenous antivenom was then administered in each case with almost complete resolution of symptoms. All cases were followed up to confirm the effect of treatment. This failure of intramuscular Red-back antivenom raises the question of its efficacy. There has been no controlled trial to prove that intramuscular Red-back antivenom is effective and animal work with other antivenoms has demonstrated the intramuscular formulation to have delayed and incomplete effects. Controlled studies should be undertaken to establish the effectiveness of intravenous and intramuscular Red-back antivenom.
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Clinical toxinology suffers from a long history of poor data collection. A 20-year review of MEDLINE illustrates the lack of randomized controlled trials and prospective studies in clinical toxinology. Mythology surrounds bites and stings, resulting from the general fear of many creatures such as spiders, which has not been disproved by appropriate well-designed studies. The current focus on necrotic arachnidism in many parts of the world is a good example. Previously, most studies have been retrospective, bites and stings have not been confirmed, and creatures have not been kept or have been incorrectly identified. Prospective observational studies of confirmed bites with correct identification of the creature are required in clinical toxinology. This requires a collaboration between those who can correctly identify the animals (biologists/taxonomists) and those involved in the clinical management (poison information services, emergency departments, and toxicology services). Prospective collection of data pertaining to the circumstances and effects of the bites is essential. Routine follow-up is required to identify delayed effects and the duration of immediate effects. Analysis of databases created from prospective studies will not only answer questions about the effects of different species, but will ultimately allow the development of evidence-based methods to identify animals based on the circumstances and effects of bites, rather than requiring formal identification of the culprit.
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Most injuries from spiders are due to their bites. Skin and eye injuries have been reported following contact with hairs of some theraphosid spiders (tarantulas). Some large spiders have relatively large spines on their legs and it was hypothesized that these may cause injury in some cases of suspected spider bite, and may account for "splinters" uncommonly seen at bite sites. Fifteen cases of suspected injury from spider leg spines were recruited prospectively over 3y. In all cases "splinters" were seen at the site. In II cases therewas a definite bite in addition to the spine injury. There were 2 definite cases where spines were collected, identified and confirmed to be from the spider. In most cases the spider was from the family Sparassidae (huntsman spiders). In I definite case the patient was bitten, grabbed the spider and was stabbed by the spines in the fingers; he developed redness, swelling and itchiness at the site of the injury lasting over a week. The other definite case occurred when a frozen spider was picked up for venom gland dissection; more than 5 spines became embedded in the finger causing transient pain. This study establishes for the first time that larger spiders can cause injuries with their leg spines, and this occurs commonly in conjunction with a bite by the spider. This explains the presence of "splinters" at some bite sites. The spines mainly caused a simple mechanical injury, although in 1 case there was a delayed inflammatory reaction.
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OBJECTIVE: The study aimed to provide a recommended list of performance indicators from routinely collected data that measure most aspects of the patient journey through the emergency department (ED). METHODS: Data from a large tertiary ED were used to investigate the proposed performance indicators, which fell into 7 categories: background information, time from arrival to triage, time from triage to treatment, length of stay, readmission rate, left without being seen, and deaths in the ED. MAIN RESULTS: Category 1 patients were triaged, treated, and discharged rapidly. For category 2 patients, the times from arrival to triage increased but times from triage to treatment were relatively stable. Patients in categories 3 and 4 were not triaged rapidly and both the arrival to triage and triage to treatment processes were unstable and deteriorating. The average time to treatment for patients treated outside recommended times was unstable and increasing for categories 2, 3, and 4. The number of patients who left without being seen was stable except for 2 periods, and the readmission rate was stable except for 1 period of increase. CONCLUSION: The performance indicators use only routinely collected data and clearly identify the areas in which this ED performed poorly.
Serotonin toxicity (or serotonin syndrome) has become an increasingly common and important clinical problem in medicine over the last 15 years with the introduction of many new antidepressants that can cause increased levels of serotonin (5-HT) in the central nervous system (CNS). Severe and life-threatening cases are almost exclusively a result of combinations of antidepressants (usually monoamine oxidase inhibitors and selective serotonin reuptake inhibitors). Unfortunately, the term serotonin syndrome has a number of quite different meanings, and many people writing on this subject have failed to differentiate them. This has led to false conclusions regarding the 5-HT receptor subtypes responsible for the life-threatening effects in animal and human toxicity, and suggestions of ineffective treatment strategies. This review primarily addresses the serotonin receptor subtypes that underlie the clinical manifestations of excess CNS serotonin in humans and animals, and their implications for diagnosis and treatment. More specific diagnostic criteria for serotonin toxicity are required to identify situations when specific antidotes are likely to be useful. However, the mainstay of treatment of severe cases is good supportive care and early intubation and paralysis in life-threatening serotonin toxicity.
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OBJECTIVE: To investigate the cardiotoxicity of bupropion hydrochloride in deliberate self-poisoning. METHODS: A prospective study was conducted in a national poisons information center (PIC) of cases of adult deliberate self-poisoning with medical record follow-up of the patients. Fifty-nine cases of bupropion deliberate self-poisoning managed in the hospital, in which the New South Wales PIC was contacted for advice, were evaluated from November 2000 through July 2001. Clinical effects and electrocardiographic (ECG) parameters (QRS, QT, QTc) were the main outcome measures. RESULTS: ECGs were available for 17 of the 59 patients for analysis, 9 patients (53%) were women, and median patient age was 28 years (interquartile range 22-37). The mean +/- SD ingested bupropion dose was 3.8 +/- 3.1 g. Tachycardia occurred in 13 patients (76%; 95% CI 50 to 93) and hypertension in 8 patients (47%). There were no reports of hypotension or arrhythmias. There was a significantly increased QTc of 461 +/- 34 msec in the patients with bupropion overdose compared with previously developed controls; 13 of the 17 cases had a QTc >440 msec (76%; 95% CI 50 to 93). The uncorrected QT interval did not differ from that of controls. CONCLUSIONS: A moderately prolonged QTc (>440 msec) is common in bupropion overdose. However, this may not be a result of intrinsic cardiac toxicity, but overcorrection of the QTc due to the tachycardia that occurs. It is important that the QTc is interpreted with caution in overdoses of agents that cause significant tachycardia (>100 beats/min).