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The clinical outcome after thermal injury depends significantly on bystander action at the scene of the initial burn. Bystander action may save life, by rescue or by extinguishing flames; or by reducing medical complications which lead to death from respiratory injury or from secondary infection. Best-practice first aid may reduce the need for skin grafting; and can modify the rate and quality of healing. However, before first aid can begin, rescue and control of the incident site is crucial to the outcome of thermal injury. Bystanders are faced with an inescapable decision whether to attempt a rescue (or not), and the decision to choose the best method for the extinguishment of flames. This is the "rescue phase", currently a relatively neglected theme. In 1981, the St. John Ambulance Association introduced the primacy of "D" for "Danger" in the pedagogic first aid mnemonic, now in its current form of DRSABCD. Most secondary threats to the victim and risks to the rescuer come from high-energy sources [such as flames], and most involve a repetition of the primary incident. Current doctrine teaches four elements of how best to act in the rescue phase of a casually suffering from thermal injury. These imperatives are: (a) Assess for danger (b) Use protection if a rescue is undertaken; (c) Train in techniques for extinguishing the flames of the burning casualty; and (d) Train in the methods of physical retrieval to a safe place - where the standard dictates of DRSABCD can continue. [ABSTRACT FROM AUTHOR]

Abstract: Throughout history there have been many different and sometimes bizarre treatments prescribed for burns. Unfortunately many of these treatments still persist today, although they often do not have sufficient evidence to support their use. This paper reviews common first aid and pre-hospital treatments for burns (water—cold or warm, ice, oils, powders and natural plant therapies), possible mechanisms whereby they might work and the literature which supports their use. From the published work to date, the current recommendations for the first aid treatment of burn injuries should be to use cold running tap water (between 2 and 15°C) on the burn, not ice or alternative plant therapies. [Copyright &y& Elsevier]

Abstract: Dr Jack Handyside Barnes (1922–1985) was one of the small and elite group of Pacific marine toxinologists whose work was characterised by an uncompromising rugged persona, a focussed resolve to solve challenging problems of human clinical envenomation, and who conducted curiosity-driven research under conditions of scientific isolation. He was a pioneering advocate for the preservation of marine heritage, particularly that of the Great Barrier Reef. A former military commando who later became a general medical practitioner with extensive surgical and obstetric skills, in 1947 he was appointed the Medical Superintendent of Thursday Island in the Torres Strait. Later (from January 1953), he worked indefatigably as a general medical practitioner in Cairns, in tropical North Australia. For four decades (1945–1985), Jack Barnes undertook detailed laboratory, clinical and field research into invertebrate envenomation, particularly medusan toxinology. In 1960 he discovered the species responsible for the Irukandji syndrome, a small carybdeid named Carukia barnesi in his honour. He invented the research technique for the extraction of venom from the world''s most venomous creature, the Pacific box Jellyfish, Chironex fleckeri. By 1960, he had published taxonomic details of nematocyst structure and clinical envenomation details consequent upon stings by Physalia, Cyanea, Chironex, Chiropsalmus and Carukia. This paper is a précis of the chronology of his life, contributions and influence. [Copyright &y& Elsevier]

Abstract: Dr Ronald Vernon Southcott (1918–1998) was amongst the greatest of the Australian doctor-naturalists. His toxinological contributions included the description and naming of the box-jellyfish, Chironex fleckeri, the first definitive study (1950–1957) of the toxinology, taxonomy and biology of Australian scorpions; and the first observations in Australia of the introduced fiddleback spider, Loxosceles. His research into the medical effects of toxic fungi, poisonous plants and Australian insects was extensive. He was a founding member of the International Society on Toxinology and served on the Toxicon Editorial Board for more than 30 years. He also made extensive contributions to acarology, and to the taxonomy of mites, specifically the sub-families and genera of the Erythraeoidea. This prodigious output was achieved by one who, with the exception of war service (1942–1946), almost never travelled outside South Australia, was almost entirely self-funded and worked from his home laboratory. With Dr. P.D. Scott and C.J. Glover, he was also the authority on the fish of South Australia. Dr. Southcott was also a medical epidemiologist and senior medical administrator (1949–1978) with the Australian Commonwealth Department of Veterans’ Affairs. He served for 30 years as an Honorary Consultant in Toxicology to the Adelaide Children''s Hospital. As a zoologist and botanist of astounding breadth, he worked indefatigably in a voluntary capacity for the South Australian Museum, of which he was Museum Board Chairman from 1974 to 1982. In the pantheon of the great doctor-naturalists who have worked in Australia, he stands with Robert Brown and Thomas Lane Bancroft. [Copyright &y& Elsevier]

Abstract: The medical management of those envenomed by snakes, spiders and poisonous fish in Australia featured extensively in the writings 19th century doctors, expeditioners and anthropologists. Against the background of this introduced medical doctrine there already existed an extensive tradition of Aboriginal medical lore; techniques of heat treatment, suction, incision and the application of plant-derived pharmacological substances featured extensively in the management of envenomed victims. The application of a hair-string or grass-string ligature, suctioning of the bite-site and incision were practised in a variety of combinations. Such evolved independently of and pre-dated such practices, which were promoted extensively by immigrant European doctors in the late 19th century. Pacific scientific toxinology began in the 17th century with Don Diego de Prado y Tovar''s 1606 account of ciguatera. By the end of the 19th century more than 30 papers and books had defined the natural history of Australian elapid poisoning. The medical management of snakebite in Australia was the focus of great controversy from 1860 to 1900. Dogmatic claims of the supposed antidote efficacy of intravenous ammonia by Professor G.B. Halford, and that of strychnine by Dr. Augustus Mueller, claimed mainstream medical attention. This era of potential iatrogenic disaster and dogma was brought to a conclusion by the objective experiments of Joseph Lauterer and Thomas Lane Bancroft in 1890 in Brisbane; and by those of C.J. Martin (from 1893) and Frank Tidswell (from 1898), both of Sydney. The modern era of Australian toxinology developed as a direct consequence of Calmette''s discovery, in Paris in 1894, of immune serum, which was protective against snakebite. We review the key contributors and discoveries of toxinology in colonial Australia. [Copyright &y& Elsevier]

The four-link chain of the motor unit represents the contemporary end-point of some two millennia of evolving knowledge in neuroscience. The paradigm shift in neuromuscular epistemology occurred in the mid-17th century. In 1666, the newly graduated Dutch doctor, Jan Swammerdam (1637–1680) published his former investigations of dissected nerve–muscle preparations. These experiments comprised the quantum leap from observation and speculation, to that of experimentation in the field of neuroanatomy and neurophysiology. In what he termed ‘A Curious Experiment’ he also described the phenomenon of intrinsic muscle excitability – “I cannot observe that the muscle in the living animal ever absolutely ceases from all motion”. Eighty years later (1752), von Haller demonstrated experimentally that irritability (contractility) was an intrinsic property of all muscular tissue; and distinguished between the sensibility of nerve impulses and the irritability of muscular contraction. This experimental progression from Swammerdam to von Haller culminated in 1850, when Claude Bernard''s studies in experimental pharmacology confirmed that muscle was a functional unit, independent of any electrical innervation via its supplying nerve. This account comprises an audit of Swammerdam''s work in the perspective of neuromuscular knowledge. [Copyright &y& Elsevier]

Abstract: Objective: To determine the numbers of paediatric scald injuries associated with the practice of inhaling warmed vapour or warm-humidification of rooms for treatment of upper respiratory tract infection (URTI). Methods: Cases comprised a 6-year consecutive series of scalds in children 0–14 years attending the Royal Children''s Hospital (RCH) in Brisbane, Australia. All scalds were sustained either directly from a container of hot water, or by room humidification. Results: During 2001–2006, 27 children were treated for scald injury associated with breathing humidified air. Aged from 7 months to 14 years, 44% were under 3 years old and the modal age was 1 year. Injuries included steam burns to the hands from commercial vapour-producing devices in children younger than three, and spills from containers of hot water which resulted in larger scalds to multiple body sites in children aged 5–14. No child received an airway scald from hot vapour. Two children required grafts and four had a prolonged hospital stay. Total body surface area (TBSA) scalded, ranged from 1% to 15% and the majority of burns were deep dermal partial thickness. Conclusions: The common practice of warm-humidification of inspired air as home treatment of URTI''s carries an under-recognised risk of serious scalding. An alternative means of providing humidified air is to sit with your child in a closed bathroom whilst running the shower for a short time. If warm humidification is to be used, increased awareness of the risk by both parents and health professionals may reduce the incidence of this serious burn. [Copyright &y& Elsevier]

Abstract: It was not until the last decade of the 19th century that an experimental approach (led by Bancroft in Queensland and Martin in Sydney and Melbourne) brought a higher plane of scientific objectivity to usher in the modern era of Australian toxinology. This Australia era, 1895–1905, coincided with and in some respects was the result of the new knowledge emerging from Europe and the Americas of the therapeutic effects of antitoxins. The subsequent systematic study of Australian venoms and toxins through to the 1930s and beyond, by Tidswell, Fairley, Ross, Kellaway and Cleland, set the foundation for Australia''s leading reputation in venom research. As elsewhere, this development was to revolutionise the medical management of those victims who in the past had died in Australia from our venomous and toxic fauna. Morgan, Graydon, Weiner, Lane and Baxter at the Commonwealth Serum Laboratories emphasised the importance of cooperation between those expert at catching and milking the venomous creatures and those developing the antivenoms. Commercial antivenom manufacture began in Australia in 1930 with the tiger snake antivenom. This was followed by other antivenoms for the other important species (1955: taipan; 1956: brown snake; 1958: death adder; 1959: Papuan black snake; 1961: sea snake; 1962: polyvalent) including the first marine antivenoms in the world (1956: stonefish antivenom; 1970: box jellyfish) culminating, in 1980, with the release of the funnel web spider antivenom. More recent activity has focused on veterinary antivenoms and production of new generation human antivenoms for export (CroFab and ViperaTAB). This paper reviews some of the milestones of Australian toxinology, and antivenom development in particular, during the 20th century. [Copyright &y& Elsevier]

Background: Dopamine is a key modulator of striatal function and learning and might improve motor recovery after stroke. Previous small trials of dopamine agonists after stroke provide equivocal evidence of effectiveness on improving motor recovery. We aimed to assess the safety and efficacy of co-careldopa plus routine occupational and physical therapy during early rehabilitation after stroke.Methods: This double-blind, multicentre, randomised controlled trial of co-careldopa versus placebo in addition to routine NHS occupational and physical therapy was done at 51 UK NHS acute inpatient stroke rehabilitation services. We recruited patients with new or recurrent clinically diagnosed ischaemic or haemorrhagic (excluding subarachnoid haemorrhage) stroke 5-42 days before randomisation, who were unable to walk 10 m or more, had a score of less than 7 points on the Rivermead Mobility Index, were expected to need rehabilitation, and were able to access rehabilitation after discharge from hospital. Participants were assigned (1:1) using stratified random blocks to receive 6 weeks of oral co-careldopa or matched placebo in addition to routine NHS physiotherapy and occupational therapy. The initial two doses of co-careldopa were 62·5 mg (50 mg of levodopa and 12·5 mg of carbidopa) and the remaining doses were 125 mg (100 mg of levodopa and 25 mg of carbidopa). Participants were required to take a single oral tablet 45-60 min before physiotherapy or occupational therapy session. The primary outcome was ability to walk independently, defined as a Rivermead Mobility Index score of 7 or more, at 8 weeks. Primary and safety analyses were done in the intention-to-treat population. The trial is registered on the ISRCTN registry, number ISRCTN99643613.Findings: Between May 30, 2011, and March 28, 2014, of 1574 patients found eligible, 593 (mean age 68·5 years) were randomly assigned to either the co-careldopa group (n=308) or to the placebo group (n=285), on an average 18 days after stroke onset. Primary outcome data were available for all 593 patients. We found no evidence that the ability to walk independently improved with co-careldopa (125 [41%] of 308 patients) compared with placebo (127 [45%] of 285 patients; odds ratio 0·78 [95% CI 0·53-1·15]) at 8 weeks. Mortality at 12 months did not differ between the two groups (22 [7%] vs 17 [6%]). Serious adverse events were largely similar between groups. Vomiting during therapy sessions, after taking the study drug, was the most frequent adverse event and was more frequent in the co-careldopa group than the placebo group (19 [6·2%] vs 9 [3·2%]).Interpretation: Co-careldopa in addition to routine occupational and physical therapy does not seem to improve walking after stroke. Further research might identify subgroups of patients with stroke who could benefit from dopaminergic therapy at different doses or times after stroke with more intensive motor therapy.Funding: Medical Research Council. [ABSTRACT FROM AUTHOR]