Australian and New Zealand Guideline for Mild to Moderate Head Injuries in Children.

OBJECTIVE: Children frequently present with head injuries to acute care settings. Although international paediatric clinical practice guidelines for head injuries exist, they do not address all considerations related to triage, imaging, observation versus admission, transfer, discharge and follow-up of mild to moderate head injuries relevant to the Australian and New Zealand context. The Paediatric Research in Emergency Departments International Collaborative (PREDICT) set out to develop an evidence-based, locally applicable, practical clinical guideline for the care of children with mild to moderate head injuries presenting to acute care settings. METHODS: A multidisciplinary Guideline Working Group (GWG) developed 33 questions in three key areas - triage, imaging and discharge of children with mild to moderate head injuries presenting to acute care settings. We identified existing high-quality guidelines and from these guidelines recommendations were mapped to clinical questions. Updated literature searches were undertaken, and key new evidence identified. Recommendations were created through either adoption, adaptation or development of de novo recommendations. The guideline was revised after a period of public consultation. RESULTS: The GWG developed 71 recommendations (evidence-informed = 35, consensus-based = 17, practice points = 19), relevant to the Australian and New Zealand setting. The guideline is presented as three documents: (i) a detailed Full Guideline summarising the evidence underlying each recommendation; (ii) a Guideline Summary; and (iii) a clinical Algorithm: Imaging and Observation Decision-making for Children with Head Injuries. CONCLUSIONS: The PREDICT Australian and New Zealand Guideline for Mild to Moderate Head Injuries in Children provides high-level evidence and practical guidance for front line clinicians.

Death adder envenoming causes neurotoxicity not reversed by antivenom--Australian Snakebite Project (ASP-16).

BACKGROUND: Death adders (Acanthophis spp) are found in Australia, Papua New Guinea and parts of eastern Indonesia. This study aimed to investigate the clinical syndrome of death adder envenoming and response to antivenom treatment. METHODOLOGY/PRINCIPAL FINDINGS: Definite death adder bites were recruited from the Australian Snakebite Project (ASP) as defined by expert identification or detection of death adder venom in blood. Clinical effects and laboratory results were collected prospectively, including the time course of neurotoxicity and response to treatment. Enzyme immunoassay was used to measure venom concentrations. Twenty nine patients had definite death adder bites; median age 45 yr (5-74 yr); 25 were male. Envenoming occurred in 14 patients. Two further patients had allergic reactions without envenoming, both snake handlers with previous death adder bites. Of 14 envenomed patients, 12 developed neurotoxicity characterised by ptosis (12), diplopia (9), bulbar weakness (7), intercostal muscle weakness (2) and limb weakness (2). Intubation and mechanical ventilation were required for two patients for 17 and 83 hours. The median time to onset of neurotoxicity was 4 hours (0.5-15.5 hr). One patient bitten by a northern death adder developed myotoxicity and one patient only developed systemic symptoms without neurotoxicity. No patient developed venom induced consumption coagulopathy. Antivenom was administered to 13 patients, all receiving one vial initially. The median time for resolution of neurotoxicity post-antivenom was 21 hours (5-168). The median peak venom concentration in 13 envenomed patients with blood samples was 22 ng/mL (4.4-245 ng/mL). In eight patients where post-antivenom bloods were available, no venom was detected after one vial of antivenom. CONCLUSIONS/SIGNIFICANCE: Death adder envenoming is characterised by neurotoxicity, which is mild in most cases. One vial of death adder antivenom was sufficient to bind all circulating venom. The persistent neurological effects despite antivenom, suggests that neurotoxicity is not reversed by antivenom.

Human anti-snake venom IgG antibodies in a previously bitten snake-handler, but no protection against local envenoming.

We report a 60 year old male bitten by snakes from the Acanthophis genus (Death adder) on two occasions who developed high titres of human IgG antibodies to Acanthophis venom detected at the time of the second bite. The patient was bitten by Acanthophis antarcticus (common death adder) on the first occasion, developed non-specific systemic effects and did not receive antivenom. Three months later he was bitten by Acanthophis praelongus (northern death adder) and he developed significant local myotoxicity associated with a moderate rise in the creatine kinase (maximum 4770 U/L). He was given antivenom 55 h after the bite and recovered over several days. Death adder venom was detected in serum at the time of the first bite, but not the second bite. Human IgG antibodies to death adder were detected on the second admission but not the first. However, despite the presence of antibodies to death adder venom and free venom not being detected, the patient still developed significant local myotoxicity.