https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 2-methyl-4-chlorophenoxyacetic acid (MCPA) and bromoxynil herbicide ingestion https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33902 Wed 23 Jan 2019 10:40:16 AEDT ]]> Neurotoxicity in Sri Lankan Russell's viper (Daboia russelii) envenoming is primarily due to U1-viperitoxin-Dr1a, a pre-synaptic neurotoxin https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33132 Tue 28 Aug 2018 12:56:55 AEST ]]> Acute esophageal injury and strictures following corrosive ingestions in a 27 year cohort https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33604 12), 8 strong acids (pH < 2), 29 domestic bleaches, 30 other domestic products, 6 non-domestic products and three unknown. Three patients died in hospital within 24 h (phenol, sodium azide, HCl). Two developed strictures (both strong alkalis): one had complete esophageal destruction; another developed a stricture after 25 d (inpatient grade 2A endoscopy). 24 patients were asymptomatic and discharged without complication. 65 patients were symptomatic (4 catastrophic injuries). 61 reported sore mouth/throat (50), abdominal pain (21), chest pain (17), dysphagia (13); 28 had an abnormal oropharyngeal examination. 25/61 symptomatic patients underwent inpatient endoscopy: normal (3), grade 1 (5), grade 2 (15) and grade 3 (2). Of 88 patients, 12 died (3 inpatients, 9 unrelated), 28 couldn't be contacted and 48 were contacted after 1.7-24 y, including two with strictures. Five couldn't be interviewed (normal endoscopy (1), no dysphagia (3) and stroke (1). 4/41 interviewed reported dysphagia but no objective evidence of stricture. Principal conclusions: All inpatient deaths and severe complications were apparent within hours of ingestion, and occurred with highly corrosive substances. One delayed stricture occurred, not predicted by inpatient endoscopy.]]> Thu 22 Nov 2018 16:43:22 AEDT ]]> The pharmacokinetics of sertraline in overdose and the effect of activated charcoal https://nova.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 (Cmax). 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 ]]> Hematologic effects and complications of snake envenoming https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27226 D-dimer may assist in early diagnosis, but fibrinogen levels often add little in the clinical setting. Bedside investigations would be ideal, but point-of-care testing international normalized ratio and whole blood clotting tests have been shown to be unreliable in VICC. The major complication of VICC is hemorrhage, including intracranial hemorrhage which is often fatal. The role of antivenom in VICC is controversial and may only be beneficial for some types of snakes including Echis spp where the duration of abnormal clotting is reduced from more than a week to 24 to 48 hours. In contrast, antivenom does not appear to speed the recovery of VICC in Australian snake envenoming. Other treatments for VICC include factor replacement, observation and prevention of trauma, and heparin. An Australian study showed that fresh-frozen plasma speeds recovery of VICC, but early use may increase consumption. There is no evidence to support heparin.]]> Mon 23 Jul 2018 13:17:15 AEST ]]> Massive paracetamol overdose: an observational study of the effect of activated charcoal and increased acetylcysteine dose (ATOM-2) https://nova.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 ]]>