https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45242 Wed 26 Oct 2022 15:43:04 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:35876 Wed 26 Aug 2020 10:25:45 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33902 Wed 23 Jan 2019 10:40:16 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36093 Wed 15 Dec 2021 16:10:24 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51651 Wed 13 Sep 2023 10:02:53 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14561 c) was linearly dependent on predicted escitalopram concentration [slope = 87 ms/(mg l–1)], using a hypothetical effectcompartment (half-life of effect-delay, 1.0h). Administration of SDAC significantly reduced QT prolongation and was shown to reduce the risk of having an abnormal QT by approximately 35% for escitalopram doses above 200 mg. Conclusions: There was a dose-related lengthening of the QT interval that lagged the increase in drug concentration. SDAC resulted in a moderate reduction in fraction of escitalopram absorbed and reduced the risk of the QT interval being abnormal.]]> Wed 11 Apr 2018 13:43:06 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:3581 Wed 11 Apr 2018 12:14:02 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16538 Wed 11 Apr 2018 11:41:35 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:31378 1, the dose and timing of which is often guided by experience with the management of over-anticoagulation with warfarin therapy, rather than acute overdose. Case Report: We report a case of a 50-year-old man who ingested an unknown amount of his warfarin, venlafaxine, and paracetamol. He presented with an international normalized ratio (INR) of 2.5, which steadily increased over 24 h to 7, despite receiving an initial 1 mg of vitamin K₁. He was then treated with 5 mg vitamin K₁, and once the INR returned to 4.5, 40 h post ingestion, he was discharged home. He was also treated with a full course of acetylcysteine for the paracetamol overdose. The following day his INR rebounded to 8.5 and he suffered a spontaneous epistaxis requiring readmission; he was treated with low titrated doses of vitamin K₁. The warfarin concentration was 74.6 μg/mL 26 h post ingestion and decreased to 3.7 μg/mL over 72 h. Why Should an Emergency Physician Be Aware of This? Our case highlights the risk of a rebound elevated INR even 3 days after acute warfarin overdose despite treatment with vitamin K₁. Understanding the pharmacokinetics of vitamin K₁ in comparison with warfarin, repeat INR testing, and continued treatment with oral vitamin K₁ may help avoid complications of rebound coagulopathy in warfarin overdose.]]> Wed 06 Apr 2022 13:58:43 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45670 Wed 02 Nov 2022 16:06:29 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:44310 40 years; 35% female, 80% receiving OAT, 62% injected drugs in the preceding month). Recent opioid overdose (preceding 12 months) was reported by 7% of participants, lifetime naloxone access by 17%, and lifetime naloxone training by 14%. Compared to people receiving OAT with no additional opioid use, recent opioid, benzodiazepine (preceding six months), and hazardous alcohol use was associated with recent opioid overdose (aOR 3.91; 95%CI: 1.68-9.10) and lifetime naloxone access (aOR 2.12; 95%CI 1.29-3.48). Among 91 people who reported recent overdose, 65% had never received take-home naloxone or naloxone training. Conclusions: Among people recently using opioids or receiving OAT, benzodiazepine and hazardous alcohol use is associated with non-fatal opioid overdose. Not all factors associated with non-fatal overdose correspond to factors associated with naloxone access. Naloxone access and training is low across all groups. Additional interventions are needed to scale up naloxone provision.]]> Tue 11 Oct 2022 16:12:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46899 p = .06), systolic blood pressure of 110 mmHg (range: 65–180) vs 125 mmHg (range: 90–184) (p = .009), respectively. Digoxin concentrations 4.4 nmol/L (range: 3.3–9) vs 4.2 (range: 2–11.2) (p = .42) and potassium concentrations 5.4 mmol/L (range: 3–11) vs 5.1 mmol/L (range: 3.5–8.2) (p = .33) were similar. Median dose of digoxin-Fab used was 1.5 vials (IQR: 1–2). There were 9 (12%) deaths in the Fab group compared to 7 (14%) in those treated with supportive care (risk difference −2.5%; 95% CI: −14 to 9%; p = .68). The median LOS was six days in both groups. Mean changes in potassium concentration [−0.5 ± 0.1 vs. −0.4 ± 0.1 mmol/L; difference −0.1 (95% CI: −.02, 0.4), p = .70] and HR within 4 h [8 ± 1 vs. 7 ± 3 bpm; difference −1.0 (95% CI: −6.7, 4.8), p = 0.74] were similar in the two groups. Conclusions: This study did not appear to show any benefit from the routine use of digoxin-Fab in patients thought to have chronic digoxin poisoning. These patients have multiple co-morbidities that may be contributing to their clinical features, other treatments are often equally effective.are often equally effective.]]> Tue 06 Dec 2022 15:39:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:40438 14 years who took an overdose of dihydropyridines (amlodipine, felodipine, lercanidipine, nifedipine) were included. Concurrent overdoses with non-dihydropyridine CCBs, alpha-blockers and beta-blockers were excluded. Patient demographics, drugs exposure details, serial vital signs, treatments and outcome were collected. Results: There were 100 patients. 68 took mixed overdoses of dihydropyridines with ARBs/ACEIs and 32 took single overdoses of dihydropyridines without ARBs/ACEIs. The mixed group had lower median nadir mean arterial pressures (62 vs 75 mmHg, p < 0.001), more frequently had hypotension (OR 4.5, 95%CI: 1.7–11.9) or bradycardia (OR 8.8, 95%CI: 1.1–70). Multivariable analysis indicated the mixed overdoses had an 11.5 mmHg (95%CI: 4.9–18.1) lower minimum systolic blood pressure (SBP) compared with the single group; other factors associated with a lower minimum SBP were higher doses [2.3 mmHg (95%CI: 1.1–3.5) lower per 10 defined daily doses] and younger age [2.2 mmHg (95%CI: 0.3–4.2) higher per decade]. A larger proportion of the mixed ingestion group received intravenous fluids (OR 5.7, 95%CI: 1.8–18.6) and antidotes and/or vasopressors (OR 2.9, 95%CI: 1.004–8.6). Conclusion: Combined overdoses of dihydropyridines with ARBs/ACEIs caused more significant hypotension and required more haemodynamic support than overdoses of dihydropyridines alone.]]> Tue 02 Aug 2022 11:11:57 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50513 Thu 27 Jul 2023 14:20:52 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34308 2 g) and paracetamol-codeine combinations presenting to a tertiary toxicology unit (1987-2013). Demographic information, clinical effects, treatment (naloxone, length of stay [LOS], mechanical ventilation) were extracted from a prospective database. Primary outcome was naloxone requirement or ventilation for respiratory depression. Results: From 4488 presentations, 1376 admissions were included with paracetamol alone (929), paracetamol-codeine combinations (346) or paracetamol-codeine-doxylamine combinations (101) without co-ingestants. Median age was 23 years (12-89 years); 1002 (73%) were female. Median dose was 12 g (interquartile range [IQR] : 7.5-20 g). Median LOS was 16 h (IQR: 6.5-27 h) and 564 (41%) were given acetylcysteine. Significantly larger paracetamol doses were ingested and more acetylcysteine given in paracetamol alone versus paracetamol combination overdoses. Seven out of 1376 patients were intubated or received naloxone (0.5%; 95% CI: 0.2-1.1%), three intubated, three given naloxone and one both. Three out of 929 patients ingesting paracetamol alone (0.3%; 95% CI: 0.1-1%) required intubation or naloxone, compared to two out of 346 ingesting paracetamol-codeine combinations (0.6%; 95% CI: 0.1-2.3%; absolute difference, 0.26%; 95% CI: -0.7-1.2%; P = 0.62). Two out of 101 patients ingesting paracetamol-codeine-doxylamine combinations (2%; 95% CI: 0.3-8%) required intubation or naloxone. Four patients were intubated for reasons other than respiratory depression: hepatotoxicity (2), retrieval (1), no data (1). Two out of 929 (0.2%) paracetamol alone overdoses had a Glasgow coma score < 9 compared to three out of 346 (0.9%) in the paracetamol-codeine group. Conclusions: Paracetamol-codeine combination overdoses are rarely associated with severe respiratory depression, with only two given naloxone and none intubated for respiratory depression.]]> Thu 27 Jan 2022 15:58:08 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:186 500 ms and in seven of these causality was established based on a pre- or post-ECG with a QTc < 500 ms. Only 10% of the moclobemide cases had a heart rate (HR) > 100 beats per minute, making overcorrection of HR by Bazett's formula an unlikely cause of the findings. No cardiac arrythmias were observed other than one case of first-degree heart block. Conclusions Moclobemide prolongs the QT and QTc intervals in overdose and a 12-lead ECG should be done on all moclobemide deliberate self-poisonings. Continuous cardiac monitoring for what is otherwise a relatively benign overdose would appear to be an inappropriate use of resources but can be considered in patients with a QTc > 500 ms or with known risks for QT prolongation.]]> Thu 25 Jul 2013 09:09:31 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:8129 Sat 24 Mar 2018 08:40:04 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7015 Sat 24 Mar 2018 08:38:04 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1898 440 msec. Results: There were 469 SSRI poisoning admissions analyzed after exclusions. The median LOS for all SSRI overdose admissions was 15.3 h (IQR: 10.5–21.3) and 30 of 469 (6.4%; 95% CI 4.3–9.0%) cases were admitted to ICU. The incidence of seizures was 1.9% and coma was 2.4%. Serotonin syndrome occurred in 14% of overdoses. Comparison of median QTc intervals of the five SSRIs was significantly different (p = 0.0002); citalopram (450 IQR: 436–484) was individually different to fluoxetine (p = 0.045), fluvoxamine (p = 0.022), paroxetine (p = 0.0002), and sertraline (p = 0.001). The proportion of citalopram overdoses with a QTc > 440 msec was 68%, differing significantly from sertraline (adjusted OR: 5.11 95% CI 2.32–11.27). Comparison of median QT intervals of the five SSRIs was statistically different (p = 0.026); citalopram (400 IQR: 380–440) was individually different from sertraline (p = 0.023). Conclusions: This study shows SSRIs are relatively safe in overdose despite serotonin syndrome being common. The exception was citalopram, which was significantly associated with QTc prolongation. We believe that cardiac monitoring should be considered in citalopram overdose, particularly with large ingestions and patients with associated cardiac disease.]]> Sat 24 Mar 2018 08:33:08 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1489 24 hrs [odds ratio, 4.42; 95% confidence interval, 2.42-8.10]). The mortality for patients with aspiration pneumonitis was 8.5% compared with 0.4% for those without (odds ratio, 23; 95% confidence interval, 9-60; p < .0001), and they had a significantly higher intensive care unit admission rate. The median length of stay of patients with aspiration pneumonitis was 126 hrs (interquartile range, 62-210 hrs) compared with 14.7 hrs (interquartile range, 7-23 hrs) in patients without (p < .0001). Conclusions: Our study has shown a number of risk factors in overdose patients that are associated with aspiration pneumonitis that may allow the early identification of these patients for appropriate observation and management. Patients with aspiration pneumonitis have a significantly increased mortality and length of stay in the hospital.]]> Sat 24 Mar 2018 08:28:05 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14374 Sat 24 Mar 2018 08:23:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14873 Sat 24 Mar 2018 08:22:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14880 Sat 24 Mar 2018 08:22:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14863 90) of seizure, respectively. Results: A linear logistic regression model described the data. Simulation from the model showed that the probability of seizure was 0.05 (0.03–0.08), 0.19 (0.09–0.35) and 0.75 (0.30–0.96) at 1000, 5000 and 10 000 mg, respectively (median and 95% credible interval). At the mean dose of 2100 mg the odds ratios (OR) in the presence of SDAC, WBI and SDAC/WBI were 0.48 (0.25–0.89), 0.71 (0.35–1.22) and 0.25 (0.08–0.62), respectively. A modified Gompertz model described the time to seizure events. Simulations from the Gompertz model showed that the t₉₀ values for first seizure was 26 h and was not affected by dose or decontamination procedure. Conclusion: SDAC/WBI provided greater benefits than the sum of the independent effects of SDAC and WBI. Patients should be observed for at least 24 h for seizures based on the dose and risk of seizure occurring.]]> Sat 24 Mar 2018 08:21:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:10828 6 mg) were identified from a prospective database of poisoning admissions to a regional toxicology service. Data extracted included patient demographics, details of ingestion, clinical features including neurological findings and evidence of dystonias, electrocardiographic parameters (heart rate [HR], QRS, and QT intervals), complications, and medical outcomes including intensive care unit admission. In addition to descriptive statistics, visual inspection of plots of QT-HR pairs compared with the QT nomogram was performed. Results: There were 107 patients with 157 presentations, including 38 patients with 45 risperidone-alone overdoses. Of the 38 patients who ingested risperidone alone, the median age was 25 years (interquartile range [IQR],16-31 years), and 19 (50%) were female. The median dose ingested was 33 mg (IQR, 15-75 mg; range, 8-248 mg). Median length of stay was 16 hours (IQR, 8-18 hours), and none was ventilated or admitted to the intensive care unit. There were 5 cases (11%) with dystonic reactions, 26 (58%) with tachycardia (HR ≥100 beats/min), and no cases with hypotension (blood pressure <90 mm Hg). Only 1 patient (2%) recorded a decreased Glasgow Coma Scale score of 14, and there were no seizures or deaths. On review of electrocardiograms in 41 of the 45 cases where risperidone was ingested alone, there were no acute dysrhythmias. In 4 electrocardiograms (10%), there was an abnormal QT-HR pair, but all bar one were associated with an HR of greater than 110 beats/min. The median maximum QRS width was 80 milliseconds (IQR, 80-80 milliseconds; range, 40-120 milliseconds). Conclusions: Risperidone taken alone in overdose causes minimal effects. Tachycardia and dystonic reactions were the main features of toxicity. Significant cardiac and other neurological features seem to be uncommon.]]> Sat 24 Mar 2018 08:12:50 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:10751 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.]]> Sat 24 Mar 2018 08:08:22 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17736 Sat 24 Mar 2018 07:57:39 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:6608 Sat 24 Mar 2018 07:46:22 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:28180 400 mg) admitted to a tertiary toxicology unit from November 2000 to June 2013. Demographic details, information on ingestion (dose and co-ingestants), clinical effects, complications (seizures, serotonin toxicity and cardiovascular effects) and intensive care unit (ICU) admission were extracted from a clinical database. Results: There were 71 cases of tramadol overdose (median age: 41 years, range: 17-69 years; and median ingested dose: 1000 mg, interquartile range [IQR]: 800-2000 mg). Seizures were dose related and occurred in 8 patients, one of them co-ingested a benzodiazepine compared with 16 patients without seizures. There were no cases of serotonin toxicity meeting the Hunter Serotonin Toxicity Criteria. Tachycardia occurred in 27 and mild hypertension occurred in 32. The Glasgow Coma Score was < 15 in 29 and < 9 in 5 patients; three co-ingested tricyclic antidepressants and two tramadol alone (3000 mg and 900 mg). Respiratory depression occurred in 13, median dose: 2500 (IQR: 1600-3000) mg which was significantly different (p = 0.003) to patients without respiratory depression, median dose: 1000 (IQR: 750-1475) mg. Eight patients were admitted to ICU, five due to co-ingestant toxicity and three for respiratory depression. Discussion: Tramadol overdose was associated with a significant risk of seizures and respiratory depression in more severe cases, both which appear to be related to the ingested dose. There were no cases of serotonin toxicity, while opioid-like effects and adrenergic effects were prominent. Conclusion: Tramadol overdose is associated with seizures and respiratory depression, but is unlikely to cause serotonin toxicity.]]> Sat 24 Mar 2018 07:36:34 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26190 Sat 24 Mar 2018 07:24:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24457 Sat 24 Mar 2018 07:17:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22703 Sat 24 Mar 2018 07:15:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22700 a) with the effect of CVVHDF modeled as a time-dependent covariate. This suggested that there was initially good clearance with CVVHDF (4 times endogenous clearance), which rapidly declined within hours.]]> Sat 24 Mar 2018 07:15:25 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23068 1000 U/L or abnormal ALT. Results: 654 paracetamol poisonings were treated with the new protocol; median age 29 y (15-98 y); 453 females; 576 acute and 78 staggered/chronic ingestions. In 420 (64%) acetylcysteine was stopped for low-risk paracetamol concentrations. An adverse reaction occurred in 229/654 admissions (35%; 95% CI: 31-39%): 173 (26.5%; 95% CI: 23-30%) only gastrointestinal, 50 (8%; 95% CI: 6-10%) skin only systemic hypersensitivity reactions; and three severe anaphylaxis (0.5%; 95% CI: 0.1-1.5%; all hypotension). Adverse reactions occurred in 111/231 (48%) receiving full treatment compared to 116/420 (28%) in whom the infusion was stopped early (absolute difference 20%; 95% CI: 13-28%; p < 0.0001). In 200 overdoses < 10 g, one had toxic paracetamol concentrations, but 53 developed reactions. Sixteen patients had an ALT > 1000 U/L and 24 an abnormal ALT attributable to paracetamol; all but one had treatment commenced >12 h post-ingestion. Conclusion: A 2-phase acetylcysteine infusion protocol results in a fewer reactions in patients with toxic paracetamol concentrations, but is not justified in patients with low-risk paracetamol concentrations.]]> Sat 24 Mar 2018 07:12:28 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23182 Sat 24 Mar 2018 07:10:27 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:44786 2.6 nmol/L (2 µg/L). There were no deaths from acute digoxin toxicity. Conclusions: The new practice of using small, titrated doses of Digoxin-Fab led to a considerable reduction in total usage and major savings. The clinical response to titrated doses was safe and acceptable in acute digoxin poisoning.]]> Mon 24 Oct 2022 09:17:30 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32719 Mon 23 Sep 2019 13:35:30 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32381 140-180 mmHg) occurred in 23/71 patients (32%), and tachycardia occurred in 29/74 (39%) patients. There were no abnormal QT intervals and no QRS > 120 m s. Serotonin toxicity was diagnosed by the treating physician in 7/75 (9%) patients, but only one of these met the Hunter Serotonin Toxicity Criteria. None of the 75 patients who took desvenlafaxine only (± alcohol) had seizures, were admitted to intensive care or died. In comparison, the 107 patients taking desvenlafaxine in overdose with other medications developed more pronounced toxicity. Generalised seizures occurred in 5/107 (5%), but in three of these cases co-ingestants were possible proconvulsants. Fifteen patients had a GCS ≤9 and none had an abnormal QT or QRS. Severe effects appeared to be associated with coingestants. Conclusion: Desvenlafaxine overdose causes minor effects with mild hypertension and tachycardia. The risk of seizures or serotonin toxicity is low.]]> Mon 23 Sep 2019 12:11:51 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30918 200 μg). Demographic information, clinical effects, treatment, complications (central nervous system and cardiovascular effects) and length of stay (LOS) were extracted from a clinical database or medical records. Results: From 133 admissions for clonidine poisoning (1988–2015), no medical record was available in 14 and 11 took staggered ingestions. Of 108 acute clonidine overdoses (median age 27 years; 14–65 years; 68 females), 40 were clonidine alone ingestions and 68 were clonidine with co-ingestants. Median dose taken was 2100 μg (interquartile range [IQR]: 400–15,000 μg). Median LOS was 21h (IQR: 14–35 h) and there were no deaths. Glasgow coma score [GCS] <15 occurred in 73/108 (68%), and more patients taking co-ingestants (8/68; 12%) had coma (GCS <9) compared to clonidine alone (2/40; 5%). Miosis occurred in 31/108 (29%) cases. Median minimum HR was 48 bpm (IQR: 40–57 bpm), similar between clonidine alone and co-ingestant overdoses. There was a significant association between dose and minimum HR for clonidine alone overdoses (p = 0.02). 82/108 (76%) had bradycardia, median onset 2.5 h post-ingestion (IQR: 1.7–5.5 h) and median duration 20 h (2.5–83 h), similar for clonidine alone and co-ingestant overdoses. There were no arrhythmias. Three patients ingesting 8000–12,000 μg developed early hypertension. Median minimum systolic BP was 96 mmHg (IQR: 90–105 mmHg) and hypotension occurred in 26/108 (24%). 12/108 patients were intubated, but only 2 were clonidine alone cases. Treatments included activated charcoal (24), atropine (8) and naloxone (23). The median total naloxone dose was 2 mg (IQR: 1.2–2.4 mg), but only one patient given naloxone was documented to respond with partial improvement in GCS. Discussion: Clonidine causes persistent but not life-threatening clinical effects. Most patients develop mild central nervous system depression and bradycardia. Naloxone was not associated with improved outcomes.]]> Mon 23 Sep 2019 12:03:58 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26752 -1, 5340 l and 130 l h^-1, respectively. The calculated half-life of sertraline following overdose was 28 h (IQR 19.4-30.6h). When given up to 4 h post-overdose, SDAC significantly increased the clearance of sertraline by a factor of 1.9, decreased the area under the curve and decreased the maximum plasma concentration (C_max). Conclusions: Sertraline had linear kinetics in overdose with parameter values similar to those in therapeutic use. SDAC is effective in increasing clearance when given 1.5 to 4 h post-overdose.]]> Mon 23 Sep 2019 11:21:00 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23876 3 g) admitted to a toxicology unit over 20 years. Cases were identified from a prospective database and data extracted included demographics, dose, coingestants, clinical effects, investigations, treatment and outcomes. Results: There were 36 acute metformin overdose cases. Median age 41 years old (15–68 years old); 25 were female. Median ingested dose was 10 g (interquartile range (IQR): 5–16.1 g; range: 3.5–50 g), with coingestants taken in 34 presentations. Gastrointestinal symptoms were present in 12/36, tachycardia in 10, bradycardia in three, hypotension in four and hypoglycaemia in eight. Hypotension and bradycardia were consistent with coingestants taken. Blood pH and lactate levels were available in 25/36. Median lowest pH was 7.35 (IQR: 7.28–7.38) and acidosis (pH < 7.35) occurred in 11/25. Median peak lactate was 3.9 mmol/L (IQR: 2.6–5.2 mmol/L). There was a statistical association between dose and lactate (r = 0.51; P = 0.01) and dose and pH (r = −0.70; P = 0.0001). Hyperlactataemia (lactate >2 mmol/L) without acidosis occurred in 10/25, and hyperlactataemia with acidosis in 11/25; five had lactic acidosis. The median time to peak lactate in 10 presentations with peak lactate >2 was 6 h (2–19 h). There were six intensive care unit admissions, one for lactic acidosis, and five related to coingestants. There were no deaths. Conclusion: Metformin overdose is characterised by hyperlactataemia and minor gastrointestinal effects, with a few large ingestions progressing to lactic acidosis. Coingestants are common and may dominate toxicity.]]> Mon 23 Jul 2018 12:56:16 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47473 14 years who ingested ≥10 g or 200 mg/kg (whichever is less) of MR paracetamol. Data collected included demographics, ingestion history, pathology results, treatments, and outcomes including hepatotoxicity (ALT >1000 U/L). Results: In total, 116 patients were recruited, 85(73%) were female. The median dose ingested was 32 g (IQR: 20–49 g) and median time to presentation was 3 h (IQR: 2–9 h). 78(67%) had an initial paracetamol concentration above the nomogram line (150 mg/L at 4 h). A further 12(10%) crossed the nomogram after repeat paracetamol measurements, of which five crossed after two non-toxic levels 4 h apart. Six had a double paracetamol peak, in three occurring >24 h post-ingestion. 113(97%) received acetylcysteine of which 67 received prolonged treatment beyond the standard 21 h. This was because of an elevated paracetamol concentration at the completion of acetylcysteine in 39 (median paracetamol concentration 25 mg/L, IQR: 16–62 mg/L). 21 (18%) developed hepatotoxicity, including six treated within 8 h of ingestion. Activated charcoal and double doses of acetylcysteine did not significantly decrease the risk of hepatotoxicity. Conclusions: Drug regulatory authorities are considering restrictions on MR paracetamol preparations. Following an acute MR paracetamol overdose, this study found that many patients had a persistently elevated paracetamol concentrations, many required prolonged treatment and some developed liver injury despite early acetylcysteine treatment. Furthermore, activated charcoal and increased acetylcysteine did not appear to significantly alter the risk of liver injury. Hence, research into better treatment strategies is required.]]> Mon 23 Jan 2023 11:05:44 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34253 1000 U/L). Results: Two hundred paracetamol overdoses were analysed, reported median dose ingested was 50 g (interquartile range (IQR): 45-60 g) and median paracetamol ratio 1.9 (IQR: 1.4-2.9, n = 173). One hundred and ninety-three received acetylcysteine at median time of 6.3 h (IQR: 4-9.3 h) post-ingestion. Twenty-eight (14%) developed hepatotoxicity, including six treated within 8 h of ingestion. Activated charcoal was administered to 49(25%), at median of 2 h post-ingestion (IQR:1.5-5 h). Those receiving activated charcoal (within 4 h of ingestion), had significantly lower paracetamol ratio versus those who did not: 1.4 (n = 33, IQR: 1.1-1.6) versus 2.2 (n = 140, IQR: 1.5-3.0) (p < .0001) (paracetamol concentration measured ≥ 1 h after charcoal). Furthermore, they had lower rates of hepatotoxicity [unadjusted OR: 0.12 (95% CI: < 0.001-0.91); adjusted for time to acetylcysteine OR: 0.20 (95%CI: 0.002-1.74)]. Seventy-nine had a paracetamol ratio ≥2, 43 received an increased dose of acetylcysteine in the first 21 h; most commonly a double dose in the last bag (100 to 200 mg/kg/16 h). Those receiving increased acetylcysteine had a significant decrease risk of hepatotoxicity [OR:0.27 (95% CI: 0.08-0.94)] . The OR remained similar after adjustment for time to acetylcysteine and paracetamol ratio. Conclusion: Massive paracetamol overdose can result in hepatotoxicity despite early treatment. Paracetamol concentrations were markedly reduced in those receiving activated charcoal within 4 h. In those with high paracetamol concentrations, treatment with increased acetylcysteine dose within 21 h was associated with a significant reduction in hepatotoxicity.]]> Fri 22 Feb 2019 16:55:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45740  3000 mg were identified in each unit’s database. Excluded were cases of chronic exposure, hospital presentation > 24 hours after ingestion, and cases without a salicylate concentration. Included in our analysis was demographic data, clinical effects, investigations, complications, and treatment. Results: There were 132 presentations in 108 patients (79 females (73%)). The median age was 28 years (range: 13–93 years). The median dose ingested was 7750 mg (IQR: 6000–14,400 mg). There were 44 aspirin-only ingestions. Mild toxicity (nausea, vomiting, tinnitus or hyperventilation) occurred in 22 with a median dose of 160 mg/kg. Moderate toxicity (acid–base disturbance, confusion) occurred in 16 with a median ingested dose of 297 mg/kg. There were no cases of severe toxicity (coma or seizures) due to aspirin alone. The median peak salicylate concentration was 276 mg/L (IQR: 175–400 mg/L, range: 14–814 mg/L). There was a moderate association between dose ingested and peak concentration (Pearson r = 0.58; 95% CI 0.45–0.68). Activated charcoal was administered in 36 (27%) cases, which decreased the median peak salicylate concentration (34.2 to 24.8 mg/L/g (difference: 9.4, 95% CI: 1.0–13.1)). Bicarbonate was administered in 34 (26%) presentations, decreasing the median apparent elimination half-life from 13.4 to 9.3 h (difference: 4.2 h, 95% CI: 1.0–6.5 h). Conclusions: Acute aspirin overdose caused only mild to moderate effects in this series. Early administration of activated charcoal decreased absorption and use of bicarbonate enhanced elimination.]]> Fri 19 Apr 2024 12:58:48 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:40047 A priori standards were developed for acceptance or rejection of individual criteria. Results: Survey response was 100%. A minimum set of essential criteria for reporting cases of QT interval prolongation and drug-induced TdP in overdose setting are provided and a 35-item checklist is presented. Conclusions: We report a QT reporting checklist to ensure published case reports and series describing drug-induced QT interval prolongation in poisoning can contribute to the fund of knowledge of QT interval prolongation, TdP and other malignant dysrhythmias.]]> Fri 15 Jul 2022 10:11:12 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49393 Fri 12 May 2023 14:34:18 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41752 Fri 12 Aug 2022 11:35:18 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24829 Fri 03 Dec 2021 10:34:14 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24299 Fri 01 Apr 2022 09:26:14 AEDT ]]>