https://nova.newcastle.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:45238 Wed 26 Oct 2022 19:41:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:35037 Wed 19 Jun 2019 11:33:00 AEST ]]> 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:28884 Wed 11 Apr 2018 15:45:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:14376 12 and partial VICC, with only incomplete fibrinogen consumption, occurred in three patients. Systemic symptoms occurred in eight patients. Myotoxicity and neurotoxicity did not occur. H. stephensi venom was detected in all three H. stephensi envenomings (1.1, 44 and 81 ng/mL) for whom pre-antivenom blood samples were available, and not detected in one without envenoming. In two cases with post-antivenom blood samples, venom was not detected after tiger snake antivenom (TSAV) was given. In vitro binding studies demonstrated that TSAV concentrations of 50mU/mL are sufficient to bind the majority of free H. stephensi venom components at concentrations above those detected in envenomed patients (100 ng/mL). Eleven patients received antivenom, median dose 2 vials (Range: 1 to 5 vials), which was TSAV in all but one case, where polyvalent antivenom was used. Immediate hypersensitivity reactions occurred in six cases including one case of anaphylaxis. Envenoming by Hoplocephalus spp. causes VICC and systemic symptoms, making it clinically similar to brown snake (Pseudonaja spp.) envenoming. Based on in vitro studies reported here, patients may be treated with one vial of TSAV, although one vial of brown snake antivenom may also be sufficient.]]> Wed 11 Apr 2018 15:19:00 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:14537 Wed 11 Apr 2018 14:02:42 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:14472 Wed 11 Apr 2018 13:49:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:14410 Wed 11 Apr 2018 12:23:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:14507 1.5) in Russell’s viper envenoming, the specificity of negative WBCT20 in non-envenomed patients and directly compared paired WBCT20 and INR. Results: Admission WBCT20 was done in 140 Russell’s viper bites with coagulopathy and was positive in 56/140 [sensitivity 40% (95% confidence interval (CI): 32–49%)]. A negative WBCT20 led to delayed antivenom administration [WBCT20−ve tests: median delay, 1.78 h (interquartile range (IQR): 0.83–3.7 h) vs. WBCT20 + ve tests: median delay, 0.82 h (IQR: 0.58–1.48 h); P = 0.0007]. Delays to antivenom were largely a consequence of further WBCT20 being performed and more common if the first test was negative (41/84 vs. 12/56). Initial WBCT20 was negative in 9 non-envenomed patients and 48 non-venomous snakebites [specificity: 100% (95% CI: 94–100%)]. In 221 paired tests with INR > 1.5, the WBCT20 was positive in 91(41%). The proportion of positive WBCT20 only increased slightly with higher INR. Conclusions: In clinical practice, the WBCT20 has low sensitivity for detecting coagulopathy in snake envenoming and should not over-ride clinical assessment-based decisions about antivenom administration. There is an urgent need to develop a simple bedside test for coagulopathy in snake envenoming.]]> Wed 11 Apr 2018 11:31:16 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:14540 Wed 11 Apr 2018 10:55:00 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:44618 Tue 18 Oct 2022 08:58:32 AEDT ]]> 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:39247 Bungarus multicinctus, the Chinese krait, is a highly venomous elapid snake which causes considerable morbidity and mortality in southern China. B. multicinctus venom contains pre-synaptic PLA2 neurotoxins (i.e., β-bungarotoxins) and post-synaptic neurotoxins (i.e., α-bungarotoxins). We examined the in vitro neurotoxicity of B. multicinctus venom, and the efficacy of specific monovalent Chinese B. multicinctus antivenom, and Australian polyvalent elapid snake antivenom, against venom-induced neurotoxicity. B. multicinctus venom (1–10 μg/mL) abolished indirect twitches in the chick biventer cervicis nerve-muscle preparation as well as attenuating contractile responses to exogenous ACh and CCh, but not KCl. This indicates a post-synaptic neurotoxic action but myotoxicity was not evident. Given that post-synaptic α-neurotoxins have a more rapid onset than pre-synaptic neurotoxins, the activity of the latter in the whole venom will be masked. The prior addition of Chinese B. multicinctus antivenom (12 U/mL) or Australian polyvalent snake antivenom (15 U/mL), markedly attenuated the neurotoxic actions of B. multicinctus venom (3 μg/mL) and prevented the inhibition of contractile responses to ACh and CCh. The addition of B. multicinctus antivenom (60 U/mL), or Australian polyvalent snake antivenom (50 U/mL), at the t₉₀ time point after the addition of B. multicinctus venom (3 μg/mL), did not restore the twitch height over 180 min. The earlier addition of B. multicinctus antivenom (60 U/mL), at the t₂₀ or t₅₀ time points, also failed to prevent the neurotoxic effects of the venom but did delay the time to abolish twitches based on a comparison of t₉₀ values. Repeated washing of the preparation with physiological salt solution, commencing at the t₂₀ time point, failed to reverse the neurotoxic effects of venom or delay the time to abolish twitches. This study showed that B. multicinctus venom displays marked in vitro neurotoxicity in a skeletal muscle preparation which is not reversed by antivenom. This does not appear to be related to antivenom efficacy, but due to the irreversible/pseudo-irreversible nature of the neurotoxins.]]> Thu 28 Jul 2022 14:45:09 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:44458 Naja) cause severe local dermonecrosis and myonecrosis, resulting in permanent disabilities. We studied the time scale in which two Indian polyvalent antivenoms, VINS and Bharat, remain capable of preventing or reversing in vitro myotoxicity induced by common cobra (Naja naja) venom from Sri Lanka using the chick biventer cervicis nerve-muscle preparation. VINS fully prevented while Bharat partially prevented (both in manufacturer recommended concentrations) the myotoxicity induced by Naja naja venom (10 μg/mL) when added to the organ baths before the venom. However, both antivenoms were unable to reverse the myotoxicity when added to organ baths 5 and 20 min post-venom. In contrast, physical removal of the venom from the organ baths by washing the preparation 5 and 20 min after the venom resulted in full and partial prevention of the myotoxicity, respectively, indicating the lag period for irreversible cellular injury. This suggests that, although the antivenoms contain antibodies against cytotoxins of the Sri Lankan Naja naja venom, they are either unable to reach the target sites as efficiently as the cytotoxins, unable to bind efficiently with the toxins at the target sites, or the binding with the toxins simply fails to prevent the toxin-target interactions.]]> Thu 13 Oct 2022 15:06:33 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:14407 Sat 24 Mar 2018 08:24:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:14406 Sat 24 Mar 2018 08:24:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:14441 Sat 24 Mar 2018 08:21:00 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:14440 Sat 24 Mar 2018 08:20:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:14458 Sat 24 Mar 2018 08:19:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:14463 25 kDa. All venoms (10 μg/ml) demonstrated in vitro neurotoxicity in the chick biventer cervicis nerve-muscle preparation, with a relative rank order of: H. signata ≥ D. devisi ≥ V. annulata = E. curta > C. boschmai. CSL polyvalent antivenom neutralized the inhibitory effects of C. boschmai venom but only delayed the inhibitory effect of the other venoms. All venoms displayed PLA2 activity but over a wide range (i.e. 1–621 μmol/min./mg). The venoms of C. boschmai (60 μg/kg, i.v.), D. devisi (60 μg/kg, i.v.) and H. signata (60 μg/kg, i.v.) produced hypotensive effects in vivo in an anaesthetized rat preparation. H. signata displayed moderate pro-coagulant activity while the other venoms were weakly pro-coagulant. This study demonstrated that these understudied Australian elapids have varying pharmacological activity, with notable in vitro neurotoxicity for four of the venoms, and may produce mild to moderate effects following systemic envenoming.]]> Sat 24 Mar 2018 08:19:17 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:10648 Sat 24 Mar 2018 08:13:40 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:10030 Sat 24 Mar 2018 08:12:18 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:37203 Mon 31 Aug 2020 15:02:09 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:46615 Mon 28 Nov 2022 10:44:33 AEDT ]]> 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: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 ]]> 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: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:53857 Fri 19 Jan 2024 12:31:10 AEDT ]]> 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:15310 Fri 09 Sep 2016 16:08:51 AEST ]]>