https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38528 Wed 27 Oct 2021 16:09:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45245 Daboia russelii) venom causes a range of clinical effects in humans. Hypotension is an uncommon but severe complication of Russell’s viper envenoming. The mechanism(s) responsible for this effect are unclear. In this study, we examined the cardiovascular effects of Sri Lankan D. russelii venom in anaesthetised rats and in isolated mesenteric arteries. D. russelii venom (100 µg/kg, i.v.) caused a 45 ± 8% decrease in blood pressure within 10 min of administration in anaesthetised (100 µg/kg ketamine/xylazine 10:1 ratio, i.p.) rats. Venom (1 ng/mL–1 µg/mL) caused concentration-dependent relaxation (EC₅₀ = 145.4 ± 63.6 ng/mL, R_max = 92 ± 2%) in U46619 pre-contracted rat small mesenteric arteries mounted in a myograph. Vasorelaxant potency of venom was unchanged in the presence of the nitric oxide synthase inhibitor, L-NAME (100 µM), or removal of the endothelium. In the presence of high K⁺ (30 mM), the vasorelaxant response to venom was abolished. Similarly, blocking voltage-dependent (K_v: 4-aminopryidine; 1000 µM) and Ca²⁺-activated (K_Ca: tetraethylammonium (TEA; 1000 µM); SK_Ca: apamin (0.1 µM); IK_Ca: TRAM-34 (1 µM); BK_Ca; iberiotoxin (0.1 µM)) K⁺ channels markedly attenuated venom-induced relaxation. Responses were unchanged in the presence of the ATP-sensitive K⁺ channel blocker glibenclamide (10 µM), or H1 receptor antagonist, mepyramine (0.1 µM). Venom-induced vasorelaxtion was also markedly decreased in the presence of the transient receptor potential cation channel subfamily V member 4 (TRPV4) antagonist, RN-1734 (10 µM). In conclusion, D. russelii-venom-induced hypotension in rodents may be due to activation of K_v and K_Ca channels, leading to vasorelaxation predominantly via an endothelium-independent mechanism. Further investigation is required to identify the toxin(s) responsible for this effect.]]> Wed 26 Oct 2022 19:42:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45084 Wed 26 Oct 2022 14:04:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50481  1,000 U/L). The Australian Toxicology Monitoring (ATOM) study is a prospective observational study, recruiting via two poison information centers and four toxicology units. Patients following an acute APAP ingestion presenting < 24 hours post-ingestion were recruited. Initial samples were analyzed for APAP metabolites, those measured were the nontoxic glucuronide (APAP-Glu) and sulfate (APAP-Sul) conjugates and NAPQI (toxic metabolite) conjugates APAP-cysteine (APAP-Cys) and APAP-mercapturate (APAP-Mer). The primary outcome was hepatotoxicity. In this study, 200 patients were included, with a median ingested dose of 20 g, 191 received acetylcysteine at median time of 5.8 hours post-ingestion. Twenty-six patients developed hepatotoxicity, one had hepatotoxicity on arrival (excluded from analysis). Those who developed hepatotoxicity had significantly higher total CYP metabolite concentrations: (36.8 μmol/L interquartile range (IQR): 27.8-51.7 vs. 10.8 μmol/L IQR: 6.9-19.5) and these were a greater proportion of total metabolites (5.4%, IQR: 3.8-7.7) vs. 1.7%, IQR: 1.3-2.6, P < 0.001)]. Furthermore, those who developed hepatotoxicity had lower APAP-Sul concentrations (49.1 μmol/L, IQR: 24.7-72.2 vs. 78.7 μmol/L, IQR: 53.6-116.4) and lower percentage of APAP-Sul (6.3%, IQR: 4.6-10.9 vs. 13.1%, IQR, 9.1-20.8, P < 0.001)]. This study found that those who developed hepatotoxicity had higher APAP metabolites derived from CYP pathway and lower sulfation metabolite on presentation. APAP metabolites may be utilized in the future to identify patients who could benefit from increased acetylcysteine or newer adjunct or research therapies.]]> Wed 26 Jul 2023 18:22:28 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50468 Wed 26 Jul 2023 14:52:32 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43163 Wed 24 May 2023 08:55:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23169 150 mg/kg is ingested. However, 75 mg/kg is used in many UK sources, including a flow chart on the Royal College of Emergency Medicine website, NHS trust guidelines and a 2015 BMJ Best Practice monograph.]]> Wed 24 Aug 2016 16:12:42 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33902 Wed 23 Jan 2019 10:40:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34141 Wed 17 Nov 2021 16:30:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50267 Wed 12 Jul 2023 12:12:15 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14461 Wed 11 Apr 2018 16:21:58 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14464 14 y) with snake envenoming in Sri Lanka. Snake identification was by patient or hospital examination of dead snakes when available and confirmed by enzyme-immunoassay for Russell’s viper envenoming. Patients were blindly allocated in a 11 randomisation schedule to receive antivenom either as a 20 minute infusion (rapid) or a two hour infusion (slow). The primary outcome was the proportion with severe systemic hypersensitivity reactions (grade 3 by Brown grading system) within 4 hours of commencement of antivenom. Secondary outcomes included the proportion with mild/moderate hypersensitivity reactions and repeat antivenom doses. Of 1004 patients with suspected snakebites, 247 patients received antivenom. 49 patients were excluded or not recruited leaving 104 patients allocated to the rapid antivenom infusion and 94 to the slow antivenom infusion. The median actual duration of antivenom infusion in the rapid group was 20 min (Interquartile range[IQR]:20–25 min) versus 120 min (IQR:75–120 min) in the slow group. There was no difference in severe systemic hypersensitivity reactions between those given rapid and slow infusions (32% vs. 35%; difference 3%; 95%CI:−10% to +17%;p = 0.65). The frequency of mild/moderate reactions was also similar. Similar numbers of patients in each arm received further doses of antivenom (30/104 vs. 23/94). Conclusions: A slower infusion rate would not reduce the rate of severe systemic hypersensitivity reactions from current high rates. More effort should be put into developing better quality antivenoms.]]> Wed 11 Apr 2018 16:21:45 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14867 Wed 11 Apr 2018 15:51:53 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29575 Wed 11 Apr 2018 15:46:56 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14469 Wed 11 Apr 2018 15:06:10 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21003 Wed 11 Apr 2018 14:29:48 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14408 Wed 11 Apr 2018 14:19:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14862 Wed 11 Apr 2018 13:51:59 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14541 Wed 11 Apr 2018 13:36:43 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14544 Wed 11 Apr 2018 10:15:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14404 Wed 11 Apr 2018 10:15:15 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14492 c of 440 ms or 500 ms. Plotting the QT-HR pair for patients on drugs suspected or known to cause QT prolongation allows assessment of the QT interval based on normal population QT variability. This risk assessment then allows the safer commencement of drugs therapeutically or management of drug induced effects in overdose.]]> Wed 11 Apr 2018 10:07:08 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14381 Wed 11 Apr 2018 10:04:10 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19519 Wed 11 Apr 2018 09:27:43 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46919 Wed 07 Dec 2022 10:33:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50169 15 years) patients treated by an Australian state ambulance service with 1.6 mg IM administration of naloxone for respiratory depression (respiratory rate <11 breaths/min and/or oxygen saturation <93% in room air) caused by presumed opioid poisoning. The primary outcome was the proportion of presentations with severe agitation (Sedation Assessment Tool score >1) within 1 hour of naloxone administration. Secondary outcomes were the proportion of presentations with acute opioid withdrawal (tachycardia [pulse rate >100 beats/min], hypertension [systolic >140 mm Hg], vomiting, agitation, seizure, myocardial infarction, arrhythmia, or pulmonary edema), and reversal of respiratory depression (respiratory rate >10 breaths/min and saturation >92% or Glasgow Coma Scale score 15). Results: From October 2019 to July 2021, there were 197 presentations in 171 patients, with a median age of 41 years (range, 18 to 80 years); of the total patients, 119 were men (70%). The most common opioids were heroin (131 [66%]), oxycodone (14 [7%]), and morphine (11 [6%]). Severe agitation occurred in 14 (7% [95% confidence interval {CI} 4% to 12%]) presentations. Opioid withdrawal occurred in 76 presentations (39% [95% CI 32% to 46%]), most commonly in the form of tachycardia (18%), mild agitation/anxiety (18%) and hypertension (14%). Three presentations (1.5%) received chemical sedation for severe agitation within 1 hour of naloxone administration. A single 1.6 mg dose of naloxone reversed respiratory depression in 192 (97% [95% CI: 94% to 99%]) presentations. Conclusion: Severe agitation was uncommon following the administration of 1.6 mg IM naloxone and rarely required chemical sedation.]]> Wed 05 Jul 2023 16:31:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49047 1%. With results dichotomised as <1.0% or ≥1.0%, our proposed new method versus the ICSH method showed almost perfect agreement [observed agreement 95%, Cohen's kappa (κ)=0.84, SE 0.04, 95% CI 0.76–0.92, p<0.005]. Inter-observer strength of agreement for our method was moderate (Fleiss' κ for comparisons between three non-unique microscopists κ=0.50, SE 0.05, 95% CI 0.41–0.59, p<0.005). Intra-observer reproducibility assessed in two microscopists ranged from substantial (Cohen's κ=0.71, SE 0.08, 95% CI 0.55–0.86, p<0.005) to borderline almost perfect agreement (Cohen's κ=0.81, SE 0.07, 95% CI 0.68–0.93, p<0.005). Schistocyte quantitation using our new method is simpler than the 2012 ICSH method and had almost perfect agreement. Our finding of moderate inter-observer agreement in quantitating helmet, triangle and crescent schistocytes is applicable to both the ICSH and our newly proposed method. This finding underscores the importance of clinicopathological correlation and repeated examinations in the context of a clinically suspected TMA.]]> Wed 03 May 2023 15:40:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21860 Tue 26 Sep 2017 14:05:54 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36181 in silico and in vitro studies have identified factor Xa as an appropriate activating agent, and the phospholipid Actin FS as a cofactor for a Xa clotting time (TenaCT) test. A proof-of-concept study was designed to (1) explore the reproducibility of the TenaCT test and (2) explore factors that could affect the performance of the test. In vitro clotting time tests were carried out using plasma from 20 healthy volunteers. The effect of enoxaparin was determined at concentrations of 0.25, 0.50, and 1.0 IU/mL. Clotting times for the volunteers were significantly prolonged with increasing enoxaparin concentrations. Clotting times were significantly shortened for frozen plasma samples. No significant differences in prolongation of clotting times were observed between male and female volunteers or between the 2 evaluated age groups. The clotting times were consistent between 2 separate occasions. The TenaCT test was able to distinguish between the subtherapeutic and therapeutic concentrations of enoxaparin. Plasma should not be frozen prior to performing the test, without defining a frozen plasma reference range. This stu dy provided proof-of-concept for a Xa-based test that can detect enoxaparin dose effects, but additional studies are needed to further develop the test.]]> Tue 25 Feb 2020 10:13:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20168 Tue 24 Aug 2021 14:23:24 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36665 max = 91 ± 1%) in pre-contracted mesenteric arteries. In contrast, E. ocellatus venom (1 μg/ml) only produced a maximum relaxant effect of 27 ± 14%, suggesting that rapid cardiovascular collapse is unlikely to be due to peripheral vasodilation. The prevention of rapid cardiovascular collapse, by 'priming' doses of venom, supports a role for depletable endogenous mediators in this phenomenon.]]> Tue 23 Jun 2020 12:29:07 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43153 Tue 13 Sep 2022 15:28:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51646 Tue 12 Sep 2023 20:13:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53624 2 years. Information about demographics, bite circumstances, species involved, clinical and laboratory features of envenoming, and treatment is collected and entered into a purpose-built database. Results: Between January 2002 and August 2020, 13 patients with suspected sea snake bite were recruited to ASP, 11 were male; median age was 30 years. Bites occurred in Queensland and Western Australia. All patients were in or around, coastal waters at the time of bite. The species involved was identified in two cases (both Hydrophis zweifeli). Local effects occurred in 9 patients: pain (5), swelling (5), bleeding (2), bruising (1). Envenoming occurred in eight patients and was characterised by non-specific systemic features (6) and myotoxicity (2). Myotoxicity was severe (peak CK 28200 and 48100 U/L) and rapid in onset (time to peak CK 13.5 and 15.1 h) in these two patients. Non-specific systemic features included nausea (6), headache (6), abdominal pain (3), and diaphoresis (2). Leukocytosis, neutrophilia, and lymphopenia occurred in both patients with myotoxicity and was evident on the first blood test. No patients developed neurotoxicity or coagulopathy. Early Seqirus antivenom therapy was associated with a lower peak creatine kinase. Conclusion: While relatively rare, sea snake envenoming is associated with significant morbidity and risk of mortality. Early antivenom appears to have a role in preventing severe myotoxicity and should be a goal of therapy.]]> Tue 12 Dec 2023 15:26:45 AEDT ]]> https://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33780 Tue 03 Sep 2019 18:01:49 AEST ]]> https://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14861 Thu 28 Aug 2014 12:16:27 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37720 Thu 25 Mar 2021 11:51:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42585 Thu 25 Aug 2022 15:17:17 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45649 1,000 U/L), an adduct concentration ≥1.0 nmol/ml is sensitive and specific for identifying cases secondary to acetaminophen. Our aim was to characterise acetaminophen-protein adduct concentrations in patients following acetaminophen overdose and determine if they predict toxicity. Methods: We performed a multicentre prospective observational study, recruiting patients 14 years of age or older with acetaminophen overdose regardless of intent or formulation. Three serum samples were obtained within the first 24 h of presentation and analysed for acetaminophen-protein adducts. Acetaminophen-protein adduct concentrations were compared to ALT and other indicators of toxicity. Results: Of the 240 patients who participated, 204 (85%) presented following acute ingestions, with a median ingested dose of 20 g (IQR 10–40), and 228 (95%) were treated with intravenous acetylcysteine at a median time of 6 h (IQR 3.5–10.5) post-ingestion. Thirty-six (15%) patients developed hepatotoxicity, of whom 22 had an ALT ≤1,000 U/L at the time of initial acetaminophen-protein adduct measurement. Those who developed hepatotoxicity had a higher initial acetaminophen-protein adduct concentration compared to those who did not, 1.63 nmol/ml (IQR 0.76–2.02, n = 22) vs. 0.26 nmol/ml (IQR 0.15–0.41; n = 204; p <0.0001), respectively. The AUROC for hepatotoxicity was 0.98 (95% CI 0.96–1.00; n = 226; p <0.0001) with acetaminophen-protein adduct concentration and 0.89 (95% CI 0.82–0.96; n = 219; p <0.0001) with ALT. An acetaminophen-protein adduct concentration of 0.58 nmol/ml was 100% sensitive and 91% specific for identifying patients with an initial ALT ≤1,000 U/L who would develop hepatotoxicity. Adding acetaminophen-protein adduct concentrations to risk prediction models improved prediction of hepatotoxicity to a level similar to that obtained by more complex models. Conclusion: Acetaminophen-protein adduct concentration on presentation predicted which patients with acetaminophen overdose subsequently developed hepatotoxicity, regardless of time of ingestion. An adduct threshold of 0.58 nmol/L was required for optimal prediction. Lay summary: Acetaminophen poisoning is one of the most common causes of liver injury. This study examined a new biomarker of acetaminophen toxicity, which measures the amount of toxic metabolite exposure called acetaminophen-protein adduct. We found that those who developed liver injury had a higher initial level of acetaminophen-protein adducts than those who did not. Clinical Trial registration: Australian Toxicology Monitoring (ATOM) Study–Australian Paracetamol Project: ACTRN12612001240831 (ANZCTR) Date of registration: 23/11/2012.]]> Thu 23 Mar 2023 13:56:06 AEDT ]]> 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 ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38573 Thu 18 Nov 2021 12:27:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31207 E_max model linked to a turnover model for coagulation proteins. In the joint model, an unexpected pharmacodynamic lag was identified and the estimated degradation half-life of VK-dependent coagulation proteins were in agreement with previously published values. The model provided an adequate fit to the observed data. Conclusion: The joint model represents the first work to quantify the influence of warfarin on all six VK-dependent coagulation proteins simultaneously. Future work will expand the model to predict the influence of exogenously administered VK on the time course of clotting factor concentrations after warfarin overdose and during perioperative warfarin reversal procedures.]]> Sat 24 Mar 2018 08:44:46 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7557 Sat 24 Mar 2018 08:42:05 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7354 Sat 24 Mar 2018 08:40:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:8129 Sat 24 Mar 2018 08:40:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7323 Sat 24 Mar 2018 08:35:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7335 Sat 24 Mar 2018 08:35:13 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:1660 Sat 24 Mar 2018 08:30:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14483 Sat 24 Mar 2018 08:25:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14482 Sat 24 Mar 2018 08:25:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14411 Sat 24 Mar 2018 08:24:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14374 Sat 24 Mar 2018 08:23:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14873 Sat 24 Mar 2018 08:22:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14872 Sat 24 Mar 2018 08:22:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14868 Sat 24 Mar 2018 08:21:10 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14476 Sat 24 Mar 2018 08:18:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14474 Sat 24 Mar 2018 08:18:51 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14479 Sat 24 Mar 2018 08:18:51 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14471 Sat 24 Mar 2018 08:18:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10950 Sat 24 Mar 2018 08:14:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10953 1.2 (abnormal) on admission, and the remaining 28 had an INR > 1.2 within 12 hours of the bite. Of 33 patients with myotoxicity, a combination of CK > 250 U/L and an abnormal aPTT identified all but two cases by 12 hours; one of these two was identified within 12 hours by leukocytosis. Nine cases of isolated neurotoxicity had a median time of onset after the bite of 4 hours (range, 35 min - 12 h). The combination of serial INR, aPTT and CK tests and repeated neurological examination identified 213 of 222 severe envenoming cases (96%) by 6 hours and 238 of 240 (99%) by 12 hours. Conclusion: Laboratory parameters (INR, aPTT and CK) and neurological reassessments identified nearly all severe envenoming cases within 12 hours of the bite, even in this conservative analysis that assumed normal test results if the test was not done.]]> Sat 24 Mar 2018 08:14:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10648 Sat 24 Mar 2018 08:13:40 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10032 Sat 24 Mar 2018 08:12:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10025 Sat 24 Mar 2018 08:12:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10701 Sat 24 Mar 2018 08:09:55 AEDT ]]> https://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5173 Sat 24 Mar 2018 07:47:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5485 Sat 24 Mar 2018 07:47:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5331 Sat 24 Mar 2018 07:45:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:358 Sat 24 Mar 2018 07:42:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28154 Denisonia maculata) using enzyme immunoassays. Case: A 9-year old boy was bitten by an identified Ornamental Snake. He developed nausea, vomiting, local pain, and swelling. He had a leucocytosis (white cell count, 20.8 x 10⁹/L), an elevated international normalised ratio (INR) of 1.6, but otherwise normal blood tests including D-Dimer and activated partial thromboplastin time. He was treated with Australian Black Snake antivenom because the commercial venom detection kit was positive for Black snake. He was admitted for 36 h with continuing local pain and swelling requiring parenteral analgesia. Materials and methods: Blood samples were collected with informed consent for measurement of venom and antivenom concentrations. Venom-specific enzyme immunoassays were developed using the closely related D. devisi venom with Rabbit anti-Notechis (Tiger Snake) and anti-Tropidechis (Rough-scaled Snake) IgG antibodies to detect venom in serum. Standard curves for measured venom versus actual venom concentrations were made to interpolate Denisonia venom concentrations. In vitro procoagulant and anticoagulant activity of venom was assayed. Results: Denisonia venom was detected in the pre-antivenom sample as 9.6 ng/mL D. devisi venom. No antigenic venom components were detected in post-antivenom samples and there were high antivenom concentrations. D. devisi venom had mild in vitro procoagulant activity with a minimum concentration required to clot after 5 min of 2.5-5 μg/mL and even weaker anticoagulant activity. Conclusions: Denisonia bites appear to cause local effects and possibly mild systemic envenoming (with only non-specific systemic symptoms and leucocytosis), confirmed by detection of antigenic venom components in blood. A significant coagulopathy does not appear to occur.]]> Sat 24 Mar 2018 07:36:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26936 Sat 24 Mar 2018 07:27:31 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27040 Sat 24 Mar 2018 07:25:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27073 4) serum samples were available from 255 Russell's viper (Daboia russelii) envenomed patients. Enzyme-linked immunosorbent assay was used to measure venom, antivenom and venom-antivenom (VAV) complexes. In 79/255 (31%) there was persistent/recurrent venom detected despite antivenom being present. In these post-antivenom samples, VAV was also detected at the same time as venom was detected. Anti-horse (aH) antiserum was bound to UltraLink (UL) resin and added to in vitro venom-antivenom mixtures, and 15 pre- and post-antivenom samples from patients. There was significantly less free venom detected in in vitro venom-antivenom mixtures to which ULaH had been added compared to those without ULaH added. In 9 post-antivenom patient samples the addition of ULaH reduced venom detected by a median of 80% (69%-88%) compared to only 20% in four pre-antivenom samples. This suggests that the detection of persistent/recurrent venom post-antivenom is due to bound and not free venom.]]> Sat 24 Mar 2018 07:25:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24919 Sat 24 Mar 2018 07:14:50 AEDT ]]> https://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24683 Sat 24 Mar 2018 07:10:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23182 Sat 24 Mar 2018 07:10:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50616 Mon 31 Jul 2023 14:29:01 AEST ]]> https://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50379 Mon 24 Jul 2023 13:02:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32502 4h. Median peak venom concentration in 25 patients with systemic envenoming and a sample available was 8.4ng/L (1-3212 ng/L). No venom was detected in post-antivenom samples, including 20 patients given one vial initially and five patients bitten by inland taipans. Discussion: Australian taipan envenoming is characterised by neurotoxicity, myotoxicity, coagulopathy, acute kidney injury and thrombocytopenia. One vial of antivenom binds all measurable venom and early antivenom was associated with a favourable outcome.]]> Mon 23 Sep 2019 13:46:15 AEST ]]> https://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49547 1000 U/L). Snake species was determined by expert identification or venom specific enzyme immunoassay. Analysis included patient demographics, clinical findings, pathology results, treatment and outcomes (length of hospital stay, complications). Results: 1638 patients were recruited January 2003–December 2016, 935 (57%) were envenomed, 148 developed myotoxicity (16%). Snake species most commonly associated with myotoxicity were Notechis spp. (30%), Pseudechis porphyriacus (20%) and Pseudechis australis (13%). Bite site effects occurred in 19 patients. Non-specific systemic symptoms occurred in 135 patients (91%), specific signs and symptoms in 83. In 120 patients with early serial CK results, the median peak CK was 3323 U/L (IQR;1050–785100U/L), the median time to first CK >500 U/L was 11.1 h and median time to peak CK of 34.3 h. White cell count was elevated in 136 patients (93%; median time to elevation, 4.9 h). 37 patients had elevated creatinine, six were dialysed. Two patients died from complications of severe myotoxicity. Antivenom given before the first abnormal CK (>500 U/L) was associated with less severe myotoxicity (2976 versus 7590 U/L). Non-envenomed patients with elevated CK had rapid rise to abnormal CK (median 3.5 h) and less had elevated WCC (32%). Conclusion: Myotoxicity from Australian snakes is relatively common and has systemic effects, with significant associated morbidity and mortality. CK is not a good early biomarker of mytoxicity. Early antivenom may play a role in reducing severity.]]> Mon 22 May 2023 08:45:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44536 2 (PLA₂), and L-amino acid oxidase (LAAO) – in the venom of 39 species of Australian elapids (40% of terrestrial species diversity) and used linear parsimony and BayesTraits to investigate any correlation between enzyme activity and phylogeny or diet. Results: PLA₂ activity ranged from 0 to 481 nmol/min/mg of venom, and LAAO activity ranged from 0 to 351 nmol/min/mg. Phylogenetic comparative methods, implemented in BayesTraits showed that enzyme activity was strongly correlated with phylogeny, more so for LAAO activity. For example, LAAO activity was absent in both the Vermicella and Pseudonaja/Oxyuranus clade, supporting previously proposed relationships among these disparate taxa. There was no association between broad dietary categories and either enzyme activity. There was strong evidence for faster initial rates of change over evolutionary time for LAAO (delta parameter mean 0.2), but no such pattern in PLA₂ (delta parameter mean 0.64). There were some exceptions to the phylogenetic patterns of enzyme activity: different PLA₂ activity in the ecologically similar sister-species Denisonia devisi and D. maculata; large interspecific differences in PLA₂ activity in Hoplocephalus and Austrelaps. Conclusions: We have shown that phylogeny is a stronger influence on venom enzyme activity than diet for two of the four major enzyme families present in snake venoms. PLA₂ and LAAO activities had contrasting evolutionary dynamics with the higher delta value for PLA₂ Some species/individuals lacked activity in one protein family suggesting that the loss of single protein family may not incur a significant fitness cost.]]> Mon 17 Oct 2022 09:03:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28057 Daboia russelii) envenoming is reported to cause myotoxicity and neurotoxicity, which are different to the effects of envenoming by most other populations of Russell’s vipers. This study aimed to investigate evidence of myotoxicity in Russell’s viper envenoming, response to antivenom and the toxins responsible for myotoxicity. Methodology and Findings: Clinical features of myotoxicity were assessed in authenticated Russell’s viper bite patients admitted to a Sri Lankan teaching hospital. Toxins were isolated using high-performance liquid chromatography. In-vitro myotoxicity of the venom and toxins was investigated in chick biventer nerve-muscle preparations. Of 245 enrolled patients, 177 (72.2%) had local myalgia and 173 (70.6%) had local muscle tenderness. Generalized myalgia and muscle tenderness were present in 35 (14.2%) and 29 (11.8%) patients, respectively. Thirty-seven patients had high (>300 U/l) serum creatine kinase (CK) concentrations in samples 24h post-bite (median: 666 U/l; maximum: 1066 U/l). Peak venom and 24h CK concentrations were not associated (Spearman’s correlation; p = 0.48). The 24h CK concentrations differed in patients without myotoxicity (median 58 U/l), compared to those with local (137 U/l) and generalised signs/symptoms of myotoxicity (107 U/l; p = 0.049). Venom caused concentration-dependent inhibition of direct twitches in the chick biventer cervicis nerve-muscle preparation, without completely abolishing direct twitches after 3 h even at 80 μg/ml. Indian polyvalent antivenom did not prevent in-vitro myotoxicity at recommended concentrations. Two phospholipase A2 toxins with molecular weights of 13kDa, U1-viperitoxin-Dr1a (19.2% of venom) and U1-viperitoxin-Dr1b (22.7% of venom), concentration dependently inhibited direct twitches in the chick biventer cervicis nerve-muscle preparation. At 3 μM, U1-viperitoxin-Dr1a abolished twitches, while U1-viperitoxin-Dr1b caused 70% inhibition of twitch force after 3h. Removal of both toxins from whole venom resulted in no in-vitro myotoxicity. Conclusion: The study shows that myotoxicity in Sri Lankan Russell’s viper envenoming is mild and non-life threatening, and due to two PLA2 toxins with weak myotoxic properties.]]> Mon 11 Mar 2019 12:11:05 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51419 120 mg) admitted to two tertiary toxicology units between March 2007 and May 2021. Demographic information, details of ingestion (dose, co-ingestants), clinical effects, investigations (ECG parameters including QT interval), complications (coma [GCS < 9], serotonin toxicity, seizures and cardiovascular effects), length of stay [LOS] and intensive care unit [ICU] admission were extracted from a clinical database. Results: There were 241 duloxetine overdoses (>120 mg), median age 37 years (interquartile range [IQR]: 25–48 years) and there were 156 females (65%). The median dose was 735 mg (IQR: 405–1200 mg). In 177 patients, other medications were co-ingested, most commonly alcohol, paracetamol, quetiapine, diazepam, ibuprofen, pregabalin and oxycodone. These patients were more likely to be admitted to ICU (12 [7%] vs. none; p = 0.040), develop coma (16 [9%] vs. none; p = 0.008) and hypotension [systolic BP < 90 mmHg] (15 [8%] vs. one; p = 0.076). Sixty four patients ingested duloxetine alone with a median dose of 840 mg (180–4200 mg). The median LOS, in the duloxetine only group, was 13 h (IQR:8.3–18 h), which was significantly shorter than those taking coingestants, 19 h (IQR:12–31 h; p = 0.004). None of these patients were intubated. Six patients developed moderate serotonin toxicity, without complications and one had a single seizure. Tachycardia occurred in 31 patients (48%) and mild hypertension (systolic BP > 140 mmHg) in 29 (45%). One patient had persistent sympathomimetic toxicity, and one had hypotension after droperidol. Two patients of 63 with an ECG recorded had an abnormal QT: one QT 500 ms, HR 46 bpm, which resolved over 3.5 h and a second with tachycardia (QT 360 ms, HR 119 bpm). None of the 64 patients had an arrhythmia. Conclusion: Duloxetine overdose most commonly caused sympathomimetic effects and serotonin toxicity, consistent with its pharmacology, and did not result in coma, arrhythmias or intensive care admission, when taken alone in overdose.]]> Mon 04 Sep 2023 14:57:19 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30276 Fri 24 Aug 2018 09:02:03 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53857 Fri 19 Jan 2024 12:31:10 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30363 Bungarus spp.) and taipans (Oxyuranus spp.) suggest that antivenom does not reverse established neurotoxicity, but early administration may be associated with decreased severity or prevent neurotoxicity. Small studies of snakes with mainly post-synaptic neurotoxins, including some cobra species (Naja spp.), provide preliminary evidence that neurotoxicity may be reversed with antivenom, but placebo controlled studies with objective outcome measures are required to confirm this.]]> Fri 18 Sep 2020 15:18:23 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25369 Bungarus caeruleus and Bungarus fasciatus venoms was neutralised by all antivenoms except TCAV, which did not neutralise pre-synaptic activity. Post-synaptic neurotoxicity of Ophiophagus hannah was neutralised by all antivenoms, and Naja kaouthia by all antivenoms except IPAV. Pre- and post-synaptic neurotoxicity of Notechis scutatus was neutralised by all antivenoms, except TCAV, which only partially neutralised pre-synaptic activity. Pre- and post-synaptic neurotoxicity of Oxyuranus scutellatus was neutralised by TNPAV and APAV, but TCAV and IPAV only neutralised post-synaptic neurotoxicity. Post-synaptic neurotoxicity of Acanthophis antarcticus was neutralised by all antivenoms except IPAV. Pseudonaja textillis post-synaptic neurotoxicity was only neutralised by APAV. The a-neurotoxins were neutralised by TNPAV and APAV, and taipoxin by all antivenoms except IPAV. Antivenoms raised against venoms with post-synaptic neurotoxic activity (TCAV) cross-neutralised the post-synaptic activity of multiple snake venoms. Antivenoms raised against pre- and post-synaptic neurotoxic venoms (TNPAV, IPAV, APAV) cross-neutralised both activities of Asian and Australian venoms. While acknowledging the limitations of adding antivenom prior to venom in an in vitro preparation, cross-neutralization of neurotoxicity means that antivenoms from one region may be effective in other regions which do not have effective antivenoms. TCAV only neutralized post-synaptic neurotoxicity and is potentially useful in distinguishing pre-synaptic and post-synaptic effects in the chick biventer cervicis preparation.]]> Fri 18 Sep 2020 15:17:43 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53167 Fri 17 Nov 2023 11:43:46 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50090 Fri 14 Jul 2023 11:48:12 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18589 Fri 13 Jul 2018 15:49:03 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22947 Fri 13 Jul 2018 15:45:17 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17286 Fri 09 Sep 2016 16:17:26 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45713 Fri 04 Nov 2022 10:27:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51341 1.5 (Incomplete VICC = INR>1.5 and complete VICC = ≥3.0). Results: A total of 272 confirmed snakebites (Russell’s viper[76], hump-nosed viper[89], non-venomous snakes[51] and unidentified bites[56]) were recruited (median age: 42 y [interquartile range: 30- 53 y]; 189 males [69%]). On admission, 82 (30%) had incomplete VICC (INR >1.5 and <3) and 77 (28%) had complete VICC (INR ≥3). Sixteen (6%) developed clinically apparent bleeding. The WBCT-15 had the best sensitivity of 47% for detecting VICC and 68% for complete VICC. The sensitivities of the WBCT-20, WBCT-25, CBCT-5 and CBCT-10 was 30–35%. The sensitivities of all tests were better in detecting complete VICC, VICC in Russell’s viper bites and more than 2 h post-bite. The WBCT-15 test had a sensitivity of 76% for VICC in confirmed Russell’s viper bites. For detection of VICC, CBCT-t had an an excellent sensitivity of 97%, but a poor specificity of 35% for an optimal cut-off of >6.25 min. Conclusion: WBCTs are poorly diagnostic for VICC in Russell’s viper and hump-nosed viper envenoming, missing up to two-thirds of patients for some tests. The WBCT-15 was the best test, improving for more severe VICC and greater than 2 h post-bite.]]> Fri 01 Sep 2023 13:35:05 AEST ]]>