Iatrogenic medication errors reported to the Victorian Poisons Information Centre.

BACKGROUND: Iatrogenic medication errors are a cause of medical morbidity and mortality. They result in significant cost to the Australian healthcare system each year. There is limited Australian evidence describing the iatrogenic errors occurring within the hospital system. AIMS: To examine and describe iatrogenic medication errors occurring in Victorian healthcare settings through the analysis of referrals to a state Poisons Information Centre (PIC). METHODS: A retrospective review of iatrogenic medication errors reported to the Victorian PIC (VPIC) from community and hospital healthcare settings from January 2015 to December 2019. RESULTS: Over a 5-year period, 357 iatrogenic errors were identified, 63% (n = 224) of which occurred in a hospital setting. The remaining errors occurred in a community healthcare setting. One in five patients were symptomatic from the medication error at the time of the call to the VPIC, and a change in management was required in 45% (n = 165) of all cases. Five percent (n = 17) of patients developed moderate to severe clinical toxicity as determined by the recorded poisoning severity score, and 88% (n = 18) of these required critical care management. Incorrect medication dosing accounted for 62% (n = 221) of errors. Common medication dosing errors included: double dose (51%, n = 114), incorrect medication administered (14%, n = 49), incorrect route (9%, n = 31), incorrect patient (6%, n = 22) and adult dose given to a child (4%, n = 15). CONCLUSIONS: Iatrogenic errors are occurring in the Victorian health care system. These errors can result in serious morbidity. Identification of causative factors and investment in preventative strategies will likely reduce associated morbidity and healthcare costs.

Oxycodone/naloxone preparation can cause acute withdrawal symptoms when misused parenterally or taken orally.

CONTEXT: Oral oxycodone/naloxone preparations are designed to reduce the incidence of constipation associated with oxycodone use. The low oral bioavailability (< 2%) of naloxone makes the precipitation of the acute opioid withdrawal symptoms unlikely following oral oxycodone/naloxone exposure. The incidence of acute opioid withdrawal symptoms following both oral and intravenous administration of oxycodone/naloxone preparations has not been described. OBJECTIVE: The aim of the study was to investigate the incidence and circumstances associated with oxycodone/naloxone-induced acute opioid withdrawal. METHODS: An observational case series of acute opioid withdrawal following oxycodone/naloxone administration were selected from all calls received by the Victoria Poisons Information Centre from January 2012 to December 2014. Data collected included patient demographics, reported symptoms, type of caller, intentional or accidental exposure and advice given. RESULTS: There were 107 reported exposures to oxycodone/naloxone preparations. Route of exposure was oral in 92 (86%) and intravenous injection of crushed tablets in 14 (14%) of cases, respectively. Nine callers had a history of long-standing opioid treatment and developed withdrawal symptoms with oral oxycodone/naloxone. Temporal relationship between first dose, increased dose and chewing tablets was described. There were 14 exposures to crushed oxycodone/naloxone tablets injected intravenously; all precipitated an acute withdrawal state. DISCUSSION: The development of opioid withdrawal symptoms with intravenous injection of oxycodone/naloxone is likely a result of bypassing first-pass metabolism. Withdrawal symptoms after ingesting increased dose, first dose or chewing oxycodone/naloxone suggests that there is a systemic absorption of naloxone in opioid-dependent callers. CONCLUSION: Oxycodone with naloxone tablets can lead to acute opioid withdrawal symptoms if crushed and injected parentally. First dose, increased dose and chewing of these opioid-naloxone combination tablets in opioid-dependent people can also result in acute opioid withdrawal symptoms or diminished pain relief.

The epidemiology of chemical eye exposures reported to the Victorian Poisons Information Centre.

OBJECTIVE: We aimed to determine the epidemiology of chemical eye exposures reported to the Victorian Poisons Information Centre, Australia. METHODS: This was a prospective case series comprising consecutive calls to the Victorian Poisons Information Centre that related to chemical eye exposures (January 2009-2010). Data included patient demographics, place and cause of exposure, nature of the chemical, symptoms and advice given. Patients were telephoned 48 h later to determine the outcome and whether the advice had been taken. RESULTS: One thousand four hundred and eighty patients were enroled (45.7%, aged <16 years) with 937 (63.3%) followed up. Cleaning agents (32.6%), topical personal products (25.4%), industrial agents (11.8%), herbicides/pesticides (5.7%), petroleum products (4.2%) and miscellaneous agents (20.3%) comprised the exposure groups. Men were exposed to significantly more industrial agents (74.8 vs. 25.2%) and fewer topical personal agents (31.3 vs. 68.7%) than women, (P<0.001). Children were exposed to significantly more topical personal agents (65.2 vs. 34.8%) and fewer industrial agents (28.7 vs. 71.3%) than adults (P<0.001). The median time between exposure and the call for advice was significantly shorter for children (P<0.001). Eight hundred and ten (54.7%) patients were advised that medical care was not required. The remainder were advised to seek care or were already receiving care. At follow-up, only 63 (6.7%) patients were symptomatic. Eight hundred and fifty patients (90.8%) had complied with the advice given. There were no compliance differences between men/women and children/adults (P>0.05). CONCLUSION: Most exposures are of little consequence. However, there are clear epidemiological differences between sex and age groups. These findings will help inform prevention strategies.

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

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) 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.

Therapeutic errors involving adults in the community setting: nature, causes and outcomes.

OBJECTIVE: To compare the nature of therapeutic errors made by adults in community residential units (CRU) and private homes (Home). METHODS: This was an analytical case series of therapeutic errors, involving adults, reported to the Victorian Poisons Information Centre (January 2006 to March 2007). The main outcome measures were the nature, causes and outcomes of the errors and actions taken or recommendations for avoidance. RESULTS: Ninety-seven CRU and 611 Home residents (cases) were enrolled. These groups took 243 (median 2) and 785 (median 1) medications in error, respectively (p<0.001). The medication administrators were predominately staff members (94.8%) and the cases themselves (95.9%), respectively (p<0.001). The CRU cases more frequently had an incorrect medication(s) or another person's medication(s) and the Home cases a double dose or incorrect dose (p<0.001). Wide ranges of medications were taken in error with cardiac and respiratory medications being more common among the Home cases. Four (4.1%, 95% CI 1.3-10.8) CRU and 16 (2.6%, 95% CI 1.6-4.3) Home cases were referred to hospital. No case followed up had a serious outcome. Error cause differed significantly between the groups (p<0.001). Staffing issues and human factors were common within the CRU and Home groups, respectively. CONCLUSIONS: Therapeutic errors in the community are preventable and differ considerably between the CRU and Home settings. IMPLICATIONS: Prevention initiatives are indicated with particular attention to CRU staffing, training and procedural issues.

Therapeutic errors among children in the community setting: nature, causes and outcomes.

AIM: This study aimed to determine the epidemiology of therapeutic errors among children in the community setting. METHODS: This was a prospective, observational study of 491 consecutive cases reported to the Victorian Poisons Information Centre, between January 2006 and March 2007. A total of 450 (91.7%) parents/carers were followed up by telephone approximately 48 h after the initial call. The main outcome measures were the nature, causes and outcomes of the errors and actions taken or recommendations given to avoid future errors. RESULTS: The majority of children (334, 68.0%, 95% confidence interval (CI) 63.7, 72.1) were aged

The safety of edible fungi purchased at Melbourne markets.

OBJECTIVE: To determine if toxic mushroom species are sold at Melbourne fruit and vegetable markets. METHODS: We purchased a specimen of every mushroom on sale at six large Melbourne markets on four separate days evenly spread during the period April to June, 2005. These specimens were identified by a specialist mycologist at the Royal Botanic Gardens Melbourne. RESULTS: Ten edible mushroom species, but no toxic species, were identified. CONCLUSIONS: Mushrooms purchased from Melbourne markets appear to be safe. IMPLICATIONS: While this study provides no evidence that public health is at risk from mushrooms sold at Melbourne markets, it has important limitations. Ongoing periodic surveillance is warranted.