Corrine R Balit

Publications of Corrine R Balit

• Amisulpride overdose is frequently associated with QT prolongation and torsades de pointes.

  Authors: Geoffrey K Isbister, Corrine R Balit, Dawson Macleod, Stephen B Duffull

  Journal of clinical psychopharmacology. 08/2010; 30(4):391-5.

  This study aimed to describe the effects of the antipsychotic amisulpride in overdose, including the frequency of QT prolongation and torsades de pointes. Cases of amisulpride overdose (>1 g) wereThis study aimed to describe the effects of the antipsychotic amisulpride in overdose, including the frequency of QT prolongation and torsades de pointes. Cases of amisulpride overdose (>1 g) were recruited from 2 state poison centers and a tertiary toxicology unit over 5 years. A 1-page clinical research form was used to collect clinical information. Copies of all electrocardiograms were obtained. Electrocardiogram parameters (QRS and QT intervals) were manually measured as previously described, and plots of QT-heart rate (HR) pairs were compared with the QT nomogram. There were 83 patients with amisulpride overdoses with a median age of 29 years (interquartile range [IQR], 23-40 years), and 42 (51%) were female. The median dose ingested was 6 g (IQR, 3-13 g, range, 1.2-120 g). The median HR was 66 beats/min (IQR, 60-81 beats/min). Bradycardia occurred in 20 cases (24%), and hypotension in 19 (23%). From 440 electrocardiograms (average of 5 per case; range, 1-15), an abnormal QT-HR pair occurred in 61 cases (73%). Torsades de pointes developed in 6 cases (7%), with doses of 4, 4.6, 18, 24, 32, and 80 g. The patient taking 32 g died after a cardiac arrest. Widened QRS did not occur except transient rate-dependent bundle-branch block in 3 cases. There were significant associations of bradycardia, hypokalemia, and hypocalcaemia, with QT prolongation and torsades de pointes. Central nervous system effects were uncommon with coma in 7 cases, seizures in 2, and dystonic reactions in 2. Amisulpride overdose commonly causes QT prolongation, bradycardia, and hypotension. Torsades de pointes occurred commonly enough to suggest that amisulpride is highly cardiotoxic in overdose.

• Unintentional paediatric ingestions of angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists.

  Authors: Corrine R Balit, Simon P Gilmore, Geoffrey K Isbister

  Journal of paediatrics and child health. 11/2007; 43(10):686-8.

  AIMS: There is limited information on safety of angiotensin converting enzyme (ACE) inhibitors and angiotensin II (AII) receptor antagonists in unintentional paediatric ingestions. This study wasAIMS: There is limited information on safety of angiotensin converting enzyme (ACE) inhibitors and angiotensin II (AII) receptor antagonists in unintentional paediatric ingestions. This study was conducted with the aim of developing referral guidelines for poison information centres. METHODS: Calls to the NSW poison information centre from January 2002 to July 2004 regarding paediatric ingestion of ACE inhibitors and AII receptor antagonists were recruited and prospectively followed up. Information collected included: demographics (age, gender, weight), type of exposure (unintentional, therapeutic error), ingested dose and clinical effects. Dose was reported in defined daily doses (DDD) to compare across and within the two drug classes with respect to the normal adult dose. RESULTS: Nineteen cases of paediatric ingestion of ACE inhibitors and AII receptor antagonists were included. The median age was 2 years (Interquartile range (IQR): 20-33 months) and the median dose ingested was 1 DDD (IQR: 1-2). There were nine ACE inhibitor ingestions and 10 AII receptor antagonist ingestions. One of nine children (11%) observed in hospital developed transient hypotension but required no treatment and recovered without complication. This child ingested an ACE inhibitor and ingested >3 DDD. CONCLUSION: Unintentional paediatric ingestions of ACE inhibitors and AII receptor antagonists resulted in the majority of children remaining asymptomatic. ACE inhibitor ingestions under 2 DDD can be observed at home provided the child is asymptomatic and there is a responsible adult to observe the child. The dose required for observation in AII receptor antagonist ingestions is less clear.

• Lignocaine and chlorhexidine toxicity in children resulting from mouth paint ingestion: a bottling problem.

  Authors: Corrine R Balit, Anne-Maree Lynch, Simon P Gilmore, Lindsay Murray, Geoffrey K Isbister

  Journal of paediatrics and child health. 07/2006; 42(6):350-3.

  BACKGROUND: A pharmaceutical product was marketed in Australia for 'teething' in an almost identical container to a popular paediatric paracetamol preparation. The product contained lignocaine andBACKGROUND: A pharmaceutical product was marketed in Australia for 'teething' in an almost identical container to a popular paediatric paracetamol preparation. The product contained lignocaine and chlorhexidine. The similarity of the packaging resulted in large number of therapeutic errors in which the 'teething' preparation was given in error for paracetamol. As the exact dose of the erroneously administered mouth paint was known this provided an opportunity for outcome assessment of lignocaine ingestion. METHODS: Calls to two state poison information centres regarding this product were prospectively followed up. Information collected included: demographics, type of exposure, details of the exposure and adverse effects. A systematic review of the literature was used to identify all previous reported cases of lignocaine and chlorhexidine ingestion. RESULTS: There were 28 cases with complete follow up where the product was given in therapeutic errors (10 girls and 18 boys; median age 11 months; range 2 months-4 years). The mean ingested dose of lignocaine was 2.7 mg/kg (standard deviation 1.3 mg) and chlorhexidine was 0.06 mg/kg (standard deviation 0.03 mg). The largest ingested lignocaine dose was 5.9 mg/kg. Two children developed minor symptoms: one vomited twice and the other was reported to have increased salivation and difficulty with solid food for 20 min. No other adverse effects were reported. The literature review suggested that severe effects occurred with doses more than 15 mg/kg. CONCLUSION: No major adverse effects occurred with lignocaine ingestions of less than 6 mg/kg and it would be appropriate to observe these patients at home. Chlorhexidine did not appear to cause clinical effects in this low concentration.

• Which medicines do young children access from blister packs?

  Authors: Elizabeth A Hender, Corrine R Balit

  The Medical journal of Australia. 07/2005; 182(11):594.

• Funnel-web spider bite: a systematic review of recorded clinical cases.

  Authors: Geoffrey K Isbister, Michael R Gray, Corrine R Balit, Robert J Raven, Barrie J Stokes, Kate Porges, Alan S Tankel, Elizabeth Turner, Julian White, Malcolm McD Fisher

  The Medical journal of Australia. 05/2005; 182(8):407-11.

  OBJECTIVE: To investigate species-specific envenoming rates and spectrum of severity of funnel-web spider bites, and the efficacy and adverse effects of funnel-web spider antivenom. DATA SOURCES:OBJECTIVE: To investigate species-specific envenoming rates and spectrum of severity of funnel-web spider bites, and the efficacy and adverse effects of funnel-web spider antivenom. DATA SOURCES: Cases were identified from a prospective study of spider bite presenting to four major hospitals and three state poisons information centres (1999-2003); museum records of spider specimens since 1926; NSW Poisons Information Centre database; MEDLINE and EMBASE search; clinical toxinology textbooks; the media; and the manufacturer's reports of antivenom use. DATA EXTRACTION: Patient age and sex, geographical location, month, expert identification of the spider, clinical effects and management; envenoming was classified as severe, mild-moderate or minor/local effects. DATA SYNTHESIS: 198 potential funnel-web spider bites were identified: 138 were definite (spider expertly identified to species or genus), and 77 produced severe envenoming. All species-identified severe cases were attributed to one of six species restricted to NSW and southern Queensland. Rates of severe envenoming were: Hadronyche cerberea (75%), H. formidabilis (63%), Atrax robustus (17%), Hadronyche sp. 14 (17%), H. infensa (14%) and H. versuta (11%). Antivenom was used in 75 patients, including 22 children (median dose, 3 ampoules; range, 1-17), with a complete response in 97% of expertly identified cases. Three adverse reactions were reported, all in adults: two early allergic reactions (one mild and one with severe systemic effects requiring adrenaline), and one case of serum sickness. CONCLUSIONS: Severe funnel-web spider envenoming is confined to NSW and southern Queensland; tree-dwelling funnel webs (H. cerberea and H. formidabilis) have the highest envenoming rates. Funnel-web spider antivenom appears effective and safe; severe allergic reactions are uncommon.

• Antipsychotic poisoning in young children: a systematic review.

  Authors: Geoffrey K Isbister, Corrine R Balit, Henry A Kilham

  Drug safety : an international journal of medical toxicology and drug experience. 02/2005; 28(11):1029-44.

  The aim of this review was to determine the spectrum and severity of effects of unintentional antipsychotic poisoning in children. A computerised literature search of MEDLINE (1966 to February 2005)The aim of this review was to determine the spectrum and severity of effects of unintentional antipsychotic poisoning in children. A computerised literature search of MEDLINE (1966 to February 2005) and EMBASE (1980 to February 2005) was undertaken. The Internet was searched using URL: www.google.com. The proceedings of the North American Congress of Clinical Toxicology (NACCT) and the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT) were hand searched. All cases of unintentional antipsychotic (all classes) poisoning in children aged 0-6 years were included. The data extracted included the age, weight, antipsychotic, dose, clinical effects, treatment and outcomes. The toxic dose was estimated as the lowest dose causing objective adverse effects.Sixty-eight reports were identified. Few contained all of the required information. Most of the case series included multiple antipsychotics with limited information on individual drugs or all ages with limited paediatric information. For most antipsychotics the ingestion of one tablet caused symptoms that were sometimes severe and usually lasted from 1 to 3 days. Extrapyramidal symptoms (EPS) were often delayed for up to 12-24 hours. Chlorpromazine caused CNS depression, hypotension and miosis; EPS and cardiac effects were rare, and the toxic dose was estimated to be 15 mg/kg. Haloperidol caused drowsiness (rarely coma) and over one-half of patients had neuromuscular effects (mainly EPS), with a toxic dose estimated at 0.15 mg/kg. Thioridazine caused CNS depression and potentially cardiac effects, with a toxic dose of 1.4 mg/kg. Atypical antipsychotics caused significant CNS depression (except risperidone); EPS were less common. Toxic doses were clozapine 2.5 mg/kg, olanzapine 0.5 mg/kg and aripiprazole 3 mg/kg. EPS responded to anticholinergic drug treatment.In summary, unintentional antipsychotic ingestion in children can cause severe effects that last 1-3 days, often with one tablet. Children potentially ingesting a toxic dose or who are symptomatic should be considered for assessment in hospital. Most cases resolve with good supportive care. Toxic doses are only estimates that are based on limited data and should be used with caution until prospective studies are undertaken.

• Clinical effects of exposure to the White-stemmed gum moth (Chelepteryx collesi).

  Authors: Corrine R Balit, Merilyn J Geary, Richard C Russell, Geoffrey K Isbister

  Emergency medicine Australasia : EMA. 03/2004; 16(1):74-81.

  BACKGROUND: The White-stemmed gum moth (Chelepteryx collesi) can be found in eastern Australia. The clinical effects of injuries caused by its many spine-like hairs are poorly defined and concernBACKGROUND: The White-stemmed gum moth (Chelepteryx collesi) can be found in eastern Australia. The clinical effects of injuries caused by its many spine-like hairs are poorly defined and concern about the numerous hairs that remain embedded following contact with the cocoon have led to heroic means of removal. OBJECTIVE: To examine the clinical effects of injuries by the caterpillar or cocoon of the White-stemmed gum moth. METHODS: Prospective observational study of caterpillar injuries from calls to the New South Wales Poisons Information Centre. Cases resulting from C. collesi exposure were included for analysis. Caterpillars and cocoons were expertly identified where available and a follow-up consultation of all patients was conducted. Information was collected on the circumstances of exposure, local and systemic effects and treatment. RESULTS: From the 26 included cases, seven had confirmed caterpillar contact (all children aged 1-11), six had confirmed cocoon contact and 13 had exposures consistent with C. collesi, but no caterpillar was caught. All cases occurred in summer. Of 13 confirmed exposures there was no difference between caterpillars and cocoons, and these were considered together. Affected areas were hands, feet, or both, following C. collesi being handled or trodden on. Pain was reported in all 13 cases, one with severe pain. In 10 cases pain duration was < 60 min. Six subjects had more than 100 hairs embedded (small black dots). In three cases, the hairs were surrounded by swelling and yellow discolouration. Despite the attempted removal of multiple hairs, they remained embedded for prolonged periods but caused no sequelae. CONCLUSION: The clinical effects of the White-stemmed gum moth were minor with local pain. Although hairs remained in all cases, they caused no problems. Complete removal of hairs is neither possible nor necessary, and painful and invasive methods should be avoided.

• Prospective study of centipede bites in Australia.

  Authors: Corrine R Balit, Mark S Harvey, Julianne M Waldock, Geoffrey K Isbister

  Journal of toxicology. Clinical toxicology. 02/2004; 42(1):41-8.

  BACKGROUND: There are limited reports of definite bites by centipedes with expert identification, which are required for attribution of particular clinical effects to different species. OBJECTIVE: ToBACKGROUND: There are limited reports of definite bites by centipedes with expert identification, which are required for attribution of particular clinical effects to different species. OBJECTIVE: To describe the clinical effects of centipede bites in Australia. METHODS: Prospective study of calls regarding centipede exposures to a state poison information center, from December 2000 to March 2002. Information collected included demographics, details of the exposure, local effects, systemic effects, and treatment. Collected centipedes were identified by an expert. All subjects were followed until clinical effects had resolved. RESULTS: Of 48 centipede exposures, 3 were centipede ingestions with no adverse effects and one was a contact reaction to the centipede that resulted in erythema and delayed itchiness. Of 44 definite centipede bites, the centipedes obtained and formally identified in 14 cases were from the genera Scolopendra (5), Cormocephalus (6), and Ethmostigmus (3). Of these 14 bites, 13 occurred distally (hands or feet). Pain occurred in all 14 cases and was severe in 7 patients. Redness/red mark occurred in 53%, swelling/raised area in 43%, and itchiness in 14%. No systemic effects were reported. Ethmostigmus spp. and Scolopendra spp. caused more severe effects. Of the bites, 57% occurred indoors and 50% at night. Treatment consisted of supportive measures including ice packs and simple analgesia, and 4 patients reported pain relief after immersing the bite area in hot water. Similar clinical effects were reported in the other 30 definite centipede bites. CONCLUSIONS: Australian centipede bites cause minor effects with moderate to severe pain, associated with localized swelling and erythema in bites by the genera Ethmostigmus and Scolopendra. Hot water immersion may potentially be beneficial for centipede bites. The genus Scolopendra occurs worldwide and the results may have international applicability.

• Quetiapine poisoning: a case series.

  Authors: Corrine R Balit, Geoffrey K Isbister, L Peter Hackett, Ian M Whyte

  Annals of emergency medicine. 12/2003; 42(6):751-8.

  STUDY OBJECTIVE: We describe the effects of quetiapine in overdose. METHODS: Quetiapine poisonings were identified from a prospective database of poisoning admissions to a regional toxicologySTUDY OBJECTIVE: We describe the effects of quetiapine in overdose. METHODS: Quetiapine poisonings were identified from a prospective database of poisoning admissions to a regional toxicology service. Data extracted included details of ingestion, clinical features, investigations (including ECG), and other outcomes (length of stay and ICU admission rate). RESULTS: There were 45 cases of quetiapine overdose, of which 18 patients with quetiapine assay results were included. Median length of stay was 35 hours (interquartile range [IQR] 14 to 42 hours) for the 18 patients, and 9 were admitted to the ICU. The median ingested dose was 3.5 g (IQR 1.7 to 6.2 g), and reported ingested dose was highly correlated with estimated peak drug concentration (r(2)=0.84; P<.0001), confirming patient-provided history of ingestion. Seizures occurred in 2 patients, delirium occurred in 3 patients, and mechanical ventilation was required in 4 patients. No arrhythmias or deaths occurred. Six of the 18 patients ingested quetiapine alone, with a median length of stay of 35 hours, and 3 were admitted to the ICU. In 1 patient who ingested 24 g, hypotension and seizures occurred. For 10 patients for whom ECGs were available and who had ingested no cardiotoxic drugs, tachycardia occurred in 8 patients. For these 10 patients, the mean corrected QT (QTc) interval was increased at 487 ms, but the mean uncorrected QT interval was 349 ms. Reported dose and peak quetiapine concentrations were significantly associated with ICU admission and length of stay more than 24 hours. A reported dose less than 3 g and a Glasgow Coma Scale score not less than 15 predicted patients not requiring ICU admission or length of stay more than 24 hours. CONCLUSION: Quetiapine overdose causes central nervous system depression and sinus tachycardia. In large overdoses, patients may require intubation and ventilation for associated respiratory depression. Although a prolonged QTc occurs, its clinical significance is unclear because it is most likely caused by an overcorrection caused by the tachycardia. In our experience, a reported dose of less than 3 g for patients who are not drowsy (with a Glasgow Coma Scale score of 15) at least 4 hours after ingestion and who did not coingest another toxic agent defined a group not requiring ICU admission or inpatient admission greater than 24 hours.

• Prospective study of definite caterpillar exposures.

  Authors: Corrine R Balit, Merilyn J Geary, Richard C Russell, Geoffrey K Isbister

  Toxicon : official journal of the International Society on Toxinology. 12/2003; 42(6):657-62.

  Exposure to caterpillars results in a variety of clinical effects depending on the species involved. The aim of this study was to describe the clinical effects from caterpillar exposures withinExposure to caterpillars results in a variety of clinical effects depending on the species involved. The aim of this study was to describe the clinical effects from caterpillar exposures within Australia. Cases were recruited prospectively from calls to a poison information centre. Subjects were included if they had a definite exposure and they had collected the caterpillar or cocoon. The caterpillars were identified to genus and species level where possible. There were 36 included cases: two were contact exposures to caterpillar contents, one was an ingestion of a caterpillar and the remaining 33 patients had definite reactions from caterpillar or cocoon exposure. There were five families of caterpillars identified in the study: Arctiidae, Limacodidae, Anthelidae, Lymantriidae and Sphingidae, many of which occur worldwide. Clinical effects ranged from severe pain to an urticarial response depending on the species involved. There were no adverse effects following ingestion in this study. Treatment consisted primarily of removal of the caterpillar or cocoon. Other treatment measures consisted of symptomatic treatment such as ice packs and antihistamines. This is the first prospective study of caterpillar exposures within Australia and demonstrates that exposures can result in a variety of reactions depending on the family and species involved.

• Australian scorpion stings: a prospective study of definite stings.

  Authors: Geoffrey K Isbister, Erich S Volschenk, Corrine R Balit, Mark S Harvey

  Toxicon : official journal of the International Society on Toxinology. 06/2003; 41(7):877-83.

  There is little information on scorpion stings in Australia. The aim of this study is to describe the circumstances and clinical effects of stings by Australian scorpions. Cases of scorpion stingsThere is little information on scorpion stings in Australia. The aim of this study is to describe the circumstances and clinical effects of stings by Australian scorpions. Cases of scorpion stings were collected prospectively from calls and presentations to Australian poison information centres and emergency departments from February 2000 to April 2002. Only definite scorpion stings where the scorpion was immediately collected and expertly identified were included. There were 95 patients, 33 males and 62 females, with a mean age of 32 (SD 19.5; range 1-71) and 23 children (age<15 years). Three families of scorpions caused all stings: Buthidae (79), Bothruiridae (11, all Cercophonius spp.) and Urodacidae (five, all Urodacus spp.). The majority of stings (76%) were by one genus of scorpion Lychas spp. Seventy one percent of stings occurred between 6pm and 8am and 82 (86%) occurred indoors. Sixty percent of stings occurred on distal limbs. The median duration of effects was 6 h (interquartile range (IQR): 1-24 h). Immediate localised pain occurred in all cases and was severe in 76 cases (80%). Other local effects included red mark/redness (66%), tenderness (35%), numbness (12%) and paraesthesia (11%). Minor systemic effects (nausea, headache and malaise) occurred in 11% of cases. There were no deaths or major systemic envenoming. Less severe effects were observed for the larger Urodacus species, compared to Lychas spp. Scorpion stings in Australia do not appear to cause severe or life-threatening effects, even in children. This differs from other parts of the world, where severe envenoming is reported. The major clinical effect is severe pain, consistent with other scorpion stings. Most stings occurred indoors and at night.

• Valproate overdose: a comparative cohort study of self poisonings.

  Authors: Geoffrey K Isbister, Corrine R Balit, Ian M Whyte, Andrew Dawson

  British journal of clinical pharmacology. 04/2003; 55(4):398-404.

  AIMS: Based on individual case reports of massive overdoses, valproate is often regarded as having significant toxicity. This study aimed to describe the epidemiology of valproate poisoning and theAIMS: Based on individual case reports of massive overdoses, valproate is often regarded as having significant toxicity. This study aimed to describe the epidemiology of valproate poisoning and the spectrum of its clinical effects. METHODS: Consecutive valproate poisonings were identified and compared with other anticonvulsant overdoses and all other poisonings, from a prospective database of poisoning admissions presenting to a regional toxicology service. National prescription data for the same period were obtained. RESULTS: There were 79 patients with valproate poisoning from January 1991 to November 2001, 15 cases with valproate alone. Of the 15 cases, drowsiness occurred in two patients (both taking> 200 mg kg-1), vomiting occurred in four and tachycardia in five. In patients co-ingesting other medications, moderate to severe effects were consistent with the co-ingestants. There was one death not directly related to valproate. One patient had metabolic acidosis and thrombocytopaenia consistent with severe valproate toxicity. Comparison of valproate, carbamazepine, phenytoin and control groups showed that length of stay for both phenytoin and carbamazepine was significantly longer than for valproate (P < 0.0001), and there was a significantly increased risk of intensive care unit admission for carbamazepine vs valproate (OR 2.73; 95% CI 1.22, 6.28; P = 0.015). Although valproate prescriptions increased over the 10 years, there was relatively greater increase in the incidence of valproate poisoning. The odds of a valproate overdose in 1992 compared with carbamazepine were 0.29 (95% CI 0.07, 1.28; P = 0.141), but in 2001 were 2.73 (95% CI 1.38, 5.39; P = 0.004). CONCLUSIONS: Valproate causes mild toxicity in the majority of cases. Massive overdoses of greater than 400 mg kg-1 can cause severe toxicity, but these are uncommon. The older anticonvulsants phenytoin and carbamazepine remain a greater problem than valproate in overdose.

• Randomized controlled trial of topical aspirin in the treatment of bee and wasp stings.

  Authors: Corrine R Balit, Geoffrey K Isbister, Nicholas A Buckley

  Journal of toxicology. Clinical toxicology. 02/2003; 41(6):801-8.

  BACKGROUND: The New South Wales Poisons Information Centre (NSW PIC) has been recommending the use of topical aspirin paste for bee and wasp stings since the early 1980s. Anecdotal evidence fromBACKGROUND: The New South Wales Poisons Information Centre (NSW PIC) has been recommending the use of topical aspirin paste for bee and wasp stings since the early 1980s. Anecdotal evidence from calls suggested it was effective in reducing the swelling and duration of pain, but a literature search found no evidence to support this. OBJECTIVE: The objective of this study was to assess the effectiveness of advice given by a PIC to apply topical aspirin for the treatment of bee and wasp stings. METHODS: Patients were recruited from callers to the NSW PIC who reported a bee or wasp sting. They were randomly assigned, using a 2:1 ratio, to two different treatment advices: to apply an ice pack (control group), or to apply an ice pack and topical aspirin paste (treatment group). Initial follow-up was within 24-48 hours. Primary outcome was the presence of swelling at 12 hr. Secondary outcomes included the presence of pain at 12 hr, the presence of itchiness, and duration of redness. RESULTS: There were 37 patients who received treatment advice and 19 in the control group. Of the 37 patients advised to apply aspirin, 21 (57%) had no swelling at 12 hr compared with 14 of the 19 (74%) patients with ice alone (difference -17%; 95% CI: -47-12%; p = 0.26). Eighty-one percent (30/37) of patients advised to apply aspirin had no pain at 12 hr compared with (18/19) 95% of the others (-14%; 95% CI: -39-14%; p = 0.34). The median duration of redness was 6 hr [interquartile range (IQR): 2-48 hr] in those advised to apply aspirin paste compared with 2 hr (IQR: 0-10 hr) in those that only applied ice (p = 0.04). CONCLUSIONS: Topical aspirin paste was not effective in reducing the duration of swelling or pain in bee and wasp stings, and significantly increased the duration of redness. Symptoms rapidly subsided with ice alone as treatment.

• Bupropion poisoning: a case series.

  Authors: Corrine R Balit, Christa N Lynch, Geoffrey K Isbister

  The Medical journal of Australia. 02/2003; 178(2):61-3.

  OBJECTIVE: To investigate the toxicity of bupropion hydrochloride in deliberate self-poisoning in adults and accidental ingestion by children. DESIGN AND SETTING: Prospective study of casesOBJECTIVE: To investigate the toxicity of bupropion hydrochloride in deliberate self-poisoning in adults and accidental ingestion by children. DESIGN AND SETTING: Prospective study of cases identified from calls to the New South Wales Poisons Information Centre (NSW PIC), with follow-up through hospital medical records. PARTICIPANTS: Patients with bupropion poisoning managed in hospital, about whom the NSW PIC was contacted for advice, from 1 November 2000 to 31 July 2001 (59 adults and 10 children). MAIN OUTCOME MEASURES: Clinical effects, adverse outcomes (including seizures and death) and treatment. RESULTS: 45 of the 59 adults were followed up (76%), 19 of whom had taken bupropion alone. Major clinical effects of bupropion included sinus tachycardia (83%), hypertension (56%), seizures (37%), gastrointestinal symptoms (37%) and agitation (32%). Seizures were dose-dependent, with those having seizures ingesting a significantly higher median dose (P = 0.02). All seizures were brief and self-limiting. 29 patients received decontamination therapy. 10 patients required pharmacological sedation, 10 were admitted to intensive care and six were intubated. None died. Eight of 10 accidental ingestions by children were followed up (80%); one child had symptoms (vomiting and hallucinations). CONCLUSIONS: Bupropion overdose caused significant clinical effects in adults, but few in children.

• Paracetamol recall: a natural experiment influencing analgesic poisoning.

  Authors: Corrine R Balit, Geoffrey K Isbister, Jennifer Peat, Andrew H Dawson, Ian M Whyte

  The Medical journal of Australia. 03/2002; 176(4):162-5.

  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 recallOBJECTIVES: 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.

• Puffer fish poisoning: a potentially life-threatening condition.

  Authors: Geoffrey K Isbister, Julie Son, Frank Wang, Catriona J Maclean, Cindy S-Y Lin, Josef Ujma, Corrine R Balit, Brendon Smith, D G Milder, Matthew C Kiernan

  The Medical journal of Australia. 177(11-12):650-3.

  Puffer fish poisoning has been documented rarely in Australia. It results from ingesting tetrodoxtoxin found in the liver, ovaries, intestines and skin of the fish. Over a recent 16-month period, 11Puffer fish poisoning has been documented rarely in Australia. It results from ingesting tetrodoxtoxin found in the liver, ovaries, intestines and skin of the fish. Over a recent 16-month period, 11 cases of puffer fish poisoning were reported to the NSW Poisons Information Centre. Symptoms of poisoning may include paralysis, respiratory failure, numbness, paraesthesia, nausea and ataxia. Health professionals should be aware of the condition so as to institute early and appropriate management.

• Bupropion overdose: QTc prolongation and its clinical significance.

  Authors: Geoffrey K Isbister, Corrine R Balit

  The Annals of pharmacotherapy. 37(7-8):999-1002.

  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) ofOBJECTIVE: 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).