BackgroundDeath 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 FindingsDefinite 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/SignificanceDeath 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.
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.
Objective: Acute severe behavioural disturbance (ASBD) is a condition seen with increasing frequency in EDs. It poses a significant risk to the patient and those around them. Little is known about the epidemiology or most effective management in the paediatric population. The aim of the present study is to clarify the practice of senior emergency doctors in Australia when managing paediatric ASBD. Methods: The present study was a voluntary electronic questionnaire distributed to and undertaken by senior medical staff in EDs affiliated with the Paediatric Research in Emergency Departments International Collaborative (PREDICT) network. Respondents reported on exposure to and confidence in managing paediatric ASBD and their current practices. Results: A total of 227 (33%) clinicians completed the survey between February and May 2020. Most clinicians were caring for at least two young people with ASBD each week (72%), felt confident regarding the majority of components of management and referred to local clinical practice guidelines (69%). Agitation/ sedation rating scales were seldom used (19%). There was a significant variation in self-reported management practices. The choice of whether to use medication at all, the medication chosen and route of administration all varied greatly. Respondents were more willing to provide parenteral medication to young people reported as having recreational drug intoxication (84%) than those with neurodevelopment disorders (65%) when the same degree of agitation was reported. Conclusions: Within Australia, there is considerable variation in paediatric ASBD practice, in particular regarding medication provision. Further prospective research is required to inform best clinical practice.
In the setting of severe acute asthma, electrocardiographic abnormalities are not uncommon and some patients will develop reversible systolic dysfunction. However, acute myocardial infarction and potentially fatal arrhythmias are rare. We report the case of a middle-aged indigenous male who suffered an ST-elevation myocardial infarction and then pulseless ventricular tachycardia arrest while still in the acute phase of treatment for status asthmaticus.
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