https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51237 Wed 28 Feb 2024 16:07:34 AEDT ]]> 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:50468 Wed 26 Jul 2023 14:52:32 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:14403 2 years) recruited to the Australian snakebite project with VICC (International Normalized Ratio [INR] > 3) were eligible. Patients were randomized 2 : 1 to receive FFP or no FFP. The primary outcome was the proportion with an INR of < 2 at 6 h after antivenom administration. Secondary outcomes included time from antivenom administration to discharge, adverse effects, major hemorrhage, and death. Results: Of 70 eligible patients, 65 consented to be randomized: 41 to FFP, and 24 to no FFP. Six hours after antivenom administration, more patients randomized to FFP had an INR of < 2 (30/41 [73%] vs. 6/24 [25%]; absolute difference, 48%; 95% confidence interval 23–73%; P = 0.0002). The median time from antivenom administration to discharge was similar (34 h, range 14–230 h vs. 39 h, range 14–321 h; P = 0.44). Seven patients developed systemic hypersensitivity reactions after antivenom administration – two mild and one severe (FFP arm), and three mild and one severe (no FFP). One serious adverse event (intracranial hemorrhage and death) occurred in an FFP patient with preexisting hypertension, who was hypertensive on admission, and developed a headache 6 h after FFP administration. Post hoc analysis showed that the median time from bite to FFP administration was significantly shorter for nonresponders to FFP than for responders (4.7 h, interquartile range [IQR] 4.2–6.7 h vs. 7.3 h, IQR 6.1–8 h; P = 0.002). Conclusions: FFP administration after antivenom administration results in more rapid restoration of clotting function in most patients, but no decrease in discharge time. Early FFP administration (< 6–8 h) post-bite is less likely to be effective.]]> Wed 11 Apr 2018 15:48:26 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:14506 Wed 11 Apr 2018 15:30:33 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:14410 Wed 11 Apr 2018 12:23:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14481 Wed 11 Apr 2018 12:14:17 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:31242 Wed 11 Apr 2018 11:11:28 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22780 Wed 11 Apr 2018 11:03:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14373 Wed 11 Apr 2018 10:50:48 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26405 Wed 11 Apr 2018 10:46:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49080 Wed 03 May 2023 16:15:11 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55885 Wed 03 Jul 2024 14:59:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44896 98% amino acid sequence similarity with short-chain postsynaptic neurotoxins from other Naja species. When compared to short-chain neurotoxins isolated from cobras in China, α-EPTX-Na1a contained novel residues K47Q (i.e. lysine to glutamine), N48T (i.e. asparagine to threonine) and G49A (i.e. glycine to alanine). In conclusion, α-EPTX-Na1a is a potent, pseudo-irreversible, short-chain neurotoxin. The high prevalence of α-EPTX-Na1a in Chinese N. atra venom is likely to explain the mild neurotoxicity experienced by envenomed patients.]]> Tue 28 Nov 2023 12:09:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14408 Tue 20 Aug 2024 11:44:00 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14537 Tue 20 Aug 2024 09:12:10 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41985 Tue 16 Aug 2022 15:55:22 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:37720 Thu 25 Mar 2021 11:51:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51188 Thu 24 Aug 2023 14:39:11 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51189 Thu 24 Aug 2023 14:38:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51185 Thu 24 Aug 2023 14:37:48 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:50904 Thu 10 Aug 2023 13:31:43 AEST ]]> 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:7323 Sat 24 Mar 2018 08:35:39 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: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: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:14474 Sat 24 Mar 2018 08:18:51 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14549 Sat 24 Mar 2018 08:18:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12441 50 values were determined. Results: Acanthophis spp. and Naja spp. venoms produced concentration-dependent inhibition of cell proliferation in both cell lines. Naja spp. venoms were significantly more cytotoxic than the most potent Acanthophis venom (i.e. A. antarcticus) in both cell lines. Naja spp. venoms also displayed higher sensitivity in L6 cells. SAIMR antivenom significantly inhibited the cytotoxic actions of all Naja spp. venoms in both A7r5 and L6 cells. However, death adder antivenom (CSL Ltd) was unable to negate the cytotoxic effects of Acanthophis spp. venoms. Discussion: Concentrations of the predominantly cytotoxic Naja spp. venoms used were approximately three times less than the predominantly neurotoxic Acanthophis spp. venoms. SAIMR antivenom was partially effective in neutralising the effects of Naja spp. venoms. Death adder antivenom(CSL Ltd) was not effective in negating the cytotoxic effects of venom from Acanthophis spp. These results indicate that the cell-based assay is suited to the examination of cytotoxic snake venoms and may be used in conjunction with organ bath experiments to pharmacologically characterise snake venoms. Furthermore, the results suggest that the use of a skeletalmuscle cell line is likely to bemore clinically relevant for the examination of cytotoxic snake venoms.]]> Sat 24 Mar 2018 08:17:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10132 Sat 24 Mar 2018 08:13:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10169 Sat 24 Mar 2018 08:12:31 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:10024 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:19026 7 years) with a redback spider bite and severe pain, with or without systemic effects, were randomized to receive normal saline solution (placebo) or antivenom after receiving standardized analgesia. The primary outcome was a clinically significant reduction in pain 2 hours after trial medication compared with baseline. A second primary outcome for the subgroup with systemic features of envenomation was resolution of systemic features at 2 hours. Secondary outcomes were improved pain at 4 and 24 hours, resolution of systemic features at 4 hours, administration of opioid analgesics or unblinded antivenom after 2 hours, and adverse reactions. Results: Two hours after treatment, 26 of 112 patients (23%) from the placebo arm had a clinically significant improvement in pain versus 38 of 112 (34%) from the antivenom arm (difference in favor of antivenom 10.7%; 95% confidence interval −1.1% to 22.6%; P=.10). Systemic effects resolved after 2 hours in 9 of 41 patients (22%) in the placebo arm and 9 of 35 (26%) in the antivenom arm (difference 3.8%; 95% confidence interval −15% to 23%; P=.79). There was no significant difference in any secondary outcome between antivenom and placebo. Acute systemic hypersensitivity reactions occurred in 4 of 112 patients (3.6%) receiving antivenom. Conclusion: The addition of antivenom to standardized analgesia in patients with latrodectism did not significantly improve pain or systemic effects.]]> Sat 24 Mar 2018 08:05:28 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20541 Sat 24 Mar 2018 08:02:39 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:206 Sat 24 Mar 2018 07:43:07 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28062 Daboia russelii) cause unique neuromuscular paralysis not seen in other Russells vipers. Objective: To investigate the time course and severity of neuromuscular dysfunction in definite Russells viper bites, including antivenom response. Methodology: We prospectively enrolled all patients (>16 years) presenting with Russells viper bites over 14 months. Cases were confirmed by snake identification and/or enzyme immunoassay. All patients had serial neurological examinations and in some, single fibre electromyography (sfEMG) of the orbicularis oculi was performed. Results: 245 definite Russells viper bite patients (median age: 41 years; 171 males) presented a median 2.5 h (interquartile range: 1.75-4.0 h) post-bite. All but one had local envenoming and 199 (78%) had systemic envenoming: coagulopathy in 166 (68%), neurotoxicity in 130 (53%), and oliguria in 19 (8%). Neurotoxicity was characterised by ptosis (100%), blurred vision (93%), and ophthalmoplegia (90%) with weak extraocular movements, strabismus, and diplopia. Neurotoxicity developed within 8 h post-bite in all patients. No bulbar, respiratory or limb muscle weakness occurred. Neurotoxicity was associated with bites by larger snakes (p < 0.0001) and higher peak serum venom concentrations (p = 0.0025). Antivenom immediately decreased unbound venom in blood. Of 52 patients without neurotoxicity when they received antivenom, 31 developed neurotoxicity. sfEMG in 27 patients with neurotoxicity and 23 without had slightly elevated median jitter on day 1 compared to 29 normal subjects but normalised thereafter. Neurological features resolved in 80% of patients by day 3 with ptosis and weak eye movements resolving last. No clinical or neurophysiological abnormality was detected at 6 weeks or 6 months. Conclusion: Sri Lankan Russells viper envenoming causes mild neuromuscular dysfunction with no long-term effects. Indian polyvalent antivenom effectively binds free venom in blood but does not reverse neurotoxicity.]]> Sat 24 Mar 2018 07:39:43 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:24767 Pseudechis porphyriacus) causes non-specific systemic symptoms, anticoagulant coagulopathy, myotoxicity and local effects. Current management for systemic envenoming includes administration of one vial of tiger snake antivenom within 6 h of the bite to prevent myotoxicity. We present a case of severe rhabdomyolysis in a 16 year old male which developed despite early administration of one vial of tiger snake antivenom. Free venom was detected after the administration of antivenom concurrent with rapidly decreasing antivenom concentrations. The case suggests that insufficient antivenom was administered and the use of larger doses of antivenom need to be explored for red-bellied black snake envenoming.]]> Sat 24 Mar 2018 07:14:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55771 Sat 22 Jun 2024 12:11:38 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50633 Mon 31 Jul 2023 15:59:57 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: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.]]> Mon 26 Aug 2024 10:53:42 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:56269 Mon 26 Aug 2024 10:48:46 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: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:19519 Mon 19 Aug 2024 15:34:38 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28884 Mon 19 Aug 2024 14:50:08 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50978 Mon 14 Aug 2023 15:25:10 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50970 Mon 14 Aug 2023 15:19:54 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40416 Oxyuranus scutellatus) envenoming causes life-threatening neuromuscular paralysis in humans. We studied the time period during which antivenom remains effective in preventing and arresting in vitro neuromuscular block caused by taipan venom and taipoxin. Venom showed predominant pre-synaptic neurotoxicity at 3 µg/mL and post-synaptic neurotoxicity at 10 µg/mL. Pre-synaptic neurotoxicity was prevented by addition of Australian polyvalent antivenom before the venom and taipoxin and, reversed when antivenom was added 5 min after venom and taipoxin. Antivenom only partially reversed the neurotoxicity when added 15 min after venom and had no significant effect when added 30 min after venom. In contrast, post-synaptic activity was fully reversed when antivenom was added 30 min after venom. The effect of antivenom on pre-synaptic neuromuscular block was reproduced by washing the bath at similar time intervals for 3 µg/mL, but not for 10 µg/mL. We found an approximate 10–15 min time window in which antivenom can prevent pre-synaptic neuromuscular block. This time window is likely to be longer in envenomed patients due to the delay in venom absorption. Similar effectiveness of antivenom and washing with 3 µg/mL venom suggests that antivenom most likely acts by neutralizing pre-synaptic toxins before they interfere with neurotransmission inside the motor nerve terminals.]]> Mon 11 Jul 2022 14:44:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37583 16 years), who presented with a confirmed snakebite from August 2013 to October 2014 were recruited from Anuradhapura Hospital. Demographic data, information on the circumstances of the bite, first aid, health-seeking behaviour, hospital admission, clinical features, outcomes and antivenom treatment were documented prospectively. There were 742 snakebite patients [median age: 40 years (IQR:27–51; males: 476 (64%)]. One hundred and five (14%) patients intentionally delayed treatment by a median of 45min (IQR:20-120min). Antivenom was administered a median of 230min (IQR:180–360min) post-bite, which didn’t differ between directly admitted and transferred patients; 21 (8%) receiving antivenom within 2h and 141 (55%) within 4h of the bite. However, transferred patients received antivenom sooner after admission to Anuradhapura hospital than those directly admitted (60min [IQR:30-120min] versus 120min [IQR:52-265min; p<0.0001]). A significantly greater proportion of transferred patients had features of systemic envenoming on admission compared to those directly admitted (166/212 [78%] versus 5/43 [12%]; p<0.0001), and had positive clotting tests on admission (123/212 [58%] versus 10/43 [23%]; p<0.0001). Sri Lankan snakebite patients present early to hospital, but there remains a delay until antivenom administration. This delay reflects a delay in the appearance of observable or measurable features of envenoming and a lack of reliable early diagnostic tests. Improved early antivenom treatment will require reliable, rapid diagnostics for systemic envenoming.]]> Fri 23 Aug 2024 12:47:45 AEST ]]> 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 16 Aug 2024 17:17:46 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15310 Fri 06 Sep 2024 14:46:16 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17286 Fri 06 Sep 2024 14:38:21 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51342 Fri 01 Sep 2023 13:34:38 AEST ]]>