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Background: Green pit vipers (GPVs), namely Trimeresurus albolabris and Trimeresurus stejnegeri accounts for most snakebites in Southern China. Green pit viper venom contains thrombin-like enzymes, resulting in defibrination syndrome. Using of clotting factor replacement after antivenom administration is controversial.

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Article Synopsis
  • - In South America, contact with certain caterpillars, especially those from the Lonomia genus, can cause serious health issues, including hemorrhagic syndromes and even death due to venom that disrupts blood clotting mechanisms.
  • - The only effective treatment for these envenomations is the Lonomia Antivenom (LAV) manufactured in Brazil; however, its efficacy against other Lonomia species, apart from L. obliqua, had not been experimentally tested before this study.
  • - This research demonstrated that LAV effectively restores normal blood clotting in rats injected with venom from Lonomia casanarensis and Lonomia orientoandensis, confirming its potential as a treatment for envenomation by these cater
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DIC is a severe complication, often resulting in multi-organ failure and fatal outcome. As any syndrome, it is polyethiologic, while a big number of its causes logically leads to various mechanisms of its forming. Main manifestations of the disseminated intravascular blood coagulation syndrome are clottage and haemorrhage.

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Neurotoxicity with persistent unilateral ophthalmoplegia from envenoming by a wild inland taipan (Oxyuranus microlepidotus, Elapidae) in remote outback South Australia.

Toxicon

October 2017

Toxinology Department, Women's and Children's Hospital, 72 King William Street, North Adelaide, South Australia, 5006, Australia; Department of Paediatrics and Reproductive Medicine, University of Adelaide School of Medicine, 30 Frome Street, Adelaide, South Australia, 5005, Australia.

Introduction: A case of life threatening envenoming by a wild specimen of the inland taipan, Oxyuranus microlepidotus, is described. There have been 11 previously well-documented envenomings by O. microlepidotus, but only 2 were inflicted by wild snakes.

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Mechanisms of early trauma-induced coagulopathy: The clot thickens or not?

J Trauma Acute Care Surg

August 2015

From the Heart, Trauma and Sepsis Research Laboratory (G.P.D., H.L.L., R.S.), Australian Institute of Tropical Health and Medicine, College of Medicine and Dentistry, James Cook University, Queensland, Australia; and Naval Medical Research Unit-San Antonio (F.R.S.); and US Army Institute of Surgical Research (A.P.C.), Uniformed Services University, JBSA-Fort Sam Houston, San Antonio, Texas.

Traumatic-induced coagulopathy (TIC) is a hemostatic disorder that is associated with significant bleeding, transfusion requirements, morbidity and mortality. A disorder similar or analogous to TIC was reported around 70 years ago in patients with shock, hemorrhage, burns, cardiac arrest or undergoing major surgery, and the condition was referred to as a "severe bleeding tendency," "defibrination syndrome," "consumptive disorder," and later by surgeons treating US Vietnam combat casualties as a "diffuse oozing coagulopathy." In 1982, Moore's group termed it the "bloody vicious cycle," others "the lethal triad," and in 2003 Brohi and colleagues introduced "acute traumatic coagulopathy" (ATC).

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