A case of fatal envenomation by a captive puff adder (Bitis arietans) in Malaysia

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Abstract

<p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="first" dir="auto" id="d6427439e93">The Puff Adder (Bitis arietans) is a viper native to Africa and the Middle East. Envenomation by this species often requires the administration of appropriate antivenom in order to achieve a favorable outcome. A patient was bitten in both hands by a captive B. arietans presented to a teaching hospital in Malaysia. The patient developed painful progressive swelling on both limbs that extended to the chest, hypotension, hypokalemia with worsening anemia, thrombocytopenia, coagulopathy, and severe metabolic acidosis. The patient was managed supportively while waiting for the appropriate antivenom, Antivipmyn-Africa, from the Singapore Zoo. The patient developed cardiorespiratory arrest twice and did not recover from the second. The patient was pronounced dead 23 hours post-incident. The local unavailability of the appropriate antivenom may be the most important factor that contributed to the patient's death. There is also a need to amend the Malaysian Wildlife Act in order to prevent such cases from recurring. </p>

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Trade in live reptiles, its impact on wild populations, and the role of the European market

Mona van Schingen, Gabriele Gentile, Thomas Ziegler … (2016)

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Current Treatment for Venom-Induced Consumption Coagulopathy Resulting from Snakebite

Kalana Maduwage, Geoffrey K. Isbister (2014)

Venomous snakebite is considered the single most important cause of human injury from venomous animals worldwide. Coagulopathy is one of the commonest important systemic clinical syndromes and can be complicated by serious and life-threatening haemorrhage. Venom-induced consumption coagulopathy (VICC) is the commonest coagulopathy resulting from snakebite and occurs in envenoming by Viperid snakes, certain elapids, including Australian elapids, and a few Colubrid (rear fang) snakes. Procoagulant toxins activate the clotting pathway, causing a broad range of factor deficiencies depending on the particular procoagulant toxin in the snake venom. Diagnosis and monitoring of coagulopathy is problematic, particularly in resource-poor countries where further research is required to develop more reliable, cheap clotting tests. MEDLINE and EMBASE up to September 2013 were searched to identify clinical studies of snake envenoming with VICC. The UniPort database was searched for coagulant snake toxins. Despite preclinical studies demonstrating antivenom binding toxins (efficacy), there was less evidence to support clinical effectiveness of antivenom for VICC. There were no placebo-controlled trials of antivenom for VICC. There were 25 randomised comparative trials of antivenom for VICC, which compared two different antivenoms (ten studies), three different antivenoms (four), two or three different doses or repeat doses of antivenom (five), heparin treatment and antivenom (five), and intravenous immunoglobulin treatment and antivenom (one). There were 13 studies that compared two groups in which there was no randomisation, including studies with historical controls. There have been numerous observational studies of antivenom in VICC but with no comparison group. Most of the controlled trials were small, did not use the same method for assessing coagulopathy, varied the dose of antivenom, and did not provide complete details of the study design (primary outcomes, randomisation, and allocation concealment). Non-randomised trials including comparison groups without antivenom showed that antivenom was effective for some snakes (e.g., Echis), but not others (e.g., Australasian elapids). Antivenom is the major treatment for VICC, but there is currently little high-quality evidence to support effectiveness. Antivenom is not risk free, and adverse reactions can be quite common and potentially severe. Studies of heparin did not demonstrate it improved outcomes in VICC. Fresh frozen plasma appeared to speed the recovery of coagulopathy and should be considered in bleeding patients.

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Snakebite nephropathy.

Visith Sitprija (2006)

There is a broad clinical spectrum of renal involvement in snakebite. Besides the local and systemic symptoms, clinical renal manifestations vary from mild proteinuria, haematuria, pigmenturia to acute renal failure. Bites by haemotoxic snakes and myotoxic snakes are the common causes of renal involvement especially acute renal failure. Therefore, renal failure is often associated with haemorrhagic diathesis, intravascular haemolysis and rhabdomyolysis. Renal pathological changes include mesangiolysis, glomerulonephritis, vasculitis, tubular necrosis, interstitial nephritis and cortical necrosis. Tubular necrosis is an important pathological counterpart of acute renal failure. Haemodynamic alterations induced by cytokines and vasoactive mediators leading to renal ischaemia are important in the pathogenesis of acute renal failure. Haemolysis, intravascular coagulation and rhabdomyolysis are important contributing factors. Direct nephrotoxicity can be induced by the venom through metalloproteases and phosphilipase A2. Immunologic mechanism plays a minor role in the pathogenesis of the renal lesion.