https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 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:7395 Wed 11 Apr 2018 15:21:44 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:33461 33.4µs) within the first 24 hours was associated with greatly increased risk of IMS (odds ratio = 8.9, 95% confidence intervals = 2.4-29.6, p = 0.0003; sensitivity 86%, specificity 58%). The differences in jitter between IMS+ and IMS- patients remained significant for 72 hours and increased jitter was observed in some patients for up to 216 hours. For intubated patients, the median time for jitter to normalize and median time to extubate were similar, and the two variables had a moderate positive correlation (r = 0.49, P = 0.001). Conclusions: Prolonged jitter recorded with SfEMG <24 hours of ingestion of an OP strongly correlates with subsequent occurrence of IMS. The time course of electrophysiological recovery of the NMJ was similar to the time course of respiratory recovery in IMS patients.]]> Tue 03 Sep 2019 18:17:15 AEST ]]> 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:24919 Sat 24 Mar 2018 07:14:50 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:28885 50 was 0.15 µg/ml and 0.26 µg/ml for plasma and red cell cholinesterase, respectively. Discussion. Aldicarb poisoning causes rapid onset severe toxicity with muscarinic and nicotinic excess, seizures, and decreased consciousness. Cholinesterases rapidly recover once aldicarb concentrations decrease and precede clinical recovery.]]> Fri 28 Jul 2017 15:35:00 AEST ]]>