Irukandji syndrome is a distressing condition characterised by pain, hypertension and tachycardia. Some develop cardiac failure and there have been two reported deaths. Magnesium sulphate has become the standard of care despite minimal evidence. The aim of this study was to investigate if magnesium would reduce analgesic requirement and length of stay for patients with Irukandji syndrome.
This was a double-blind, randomised controlled clinical trial. Patients with Irukandji syndrome who required parenteral opioid analgesia were randomised to receive either 10 mmol of magnesium as a bolus, and then a 5 mmol/h magnesium infusion for 6 h or saline. Fentanyl patient-controlled analgesia was commenced to allow patients to self-regulate their pain relief. The primary outcome measure of the study was comparison of total analgesic requirements between the two groups. The secondary outcome measure was to compare length of stay.
The study ran from November 2003 to May 2007. Thirty-nine patients were enrolled in the study; 26 were male with a median age of 28. Twenty-two received magnesium. There was no significant difference in the morphine equivalent dose used, peak CK, peak troponin, peak pulse, peak blood pressure, peak mean arterial pressure (MAP), percentage MAP rise and length of stay for those receiving magnesium compared with placebo.
Our study did not demonstrate a benefit in the use of magnesium in the treatment of Irukandji syndrome. As such the current use of magnesium needs to be reconsidered until there is good evidence to support its use.
[Show abstract][Hide abstract] ABSTRACT: Irukandji stings are a leading occupational health and safety issue for marine industries in tropical Australia and an emerging problem elsewhere in the Indo-Pacific and Caribbean. Their mild initial sting frequently results in debilitating illness, involving signs of sympathetic excess including excruciating pain, sweating, nausea and vomiting, hypertension and a feeling of impending doom; some cases also experience acute heart failure and pulmonary oedema. These jellyfish are typically small and nearly invisible, and their infestations are generally mysterious, making them scary to the general public, irresistible to the media, and disastrous for tourism. Research into these fascinating species has been largely driven by the medical profession and focused on treatment. Biological and ecological information is surprisingly sparse, and is scattered through grey literature or buried in dispersed publications, hampering understanding. Given that long-term climate forecasts tend toward conditions favourable to jellyfish ecology, that long-term legal forecasts tend toward increasing duty-of-care obligations, and that bioprospecting opportunities exist in the powerful Irukandji toxins, there is a clear need for information to help inform global research and robust management solutions. We synthesise and contextualise available information on Irukandji taxonomy, phylogeny, reproduction, vision, behaviour, feeding, distribution, seasonality, toxins, and safety. Despite Australia dominating the research in this area, there are probably well over 25 species worldwide that cause the syndrome and it is an understudied problem in the developing world. Major gaps in knowledge are identified for future research: our lack of clarity on the socio-economic impacts, and our need for time series and spatial surveys of the species, make this field particularly enticing.
[Show abstract][Hide abstract] ABSTRACT: Although Chironex fleckeri and Carukia barnesi cause significant human envenomation, research into their effects in human models or human cells has been limited. In this in vitro study we have presented data that shows that although C. fleckeri is highly cytotoxic to human cardiac and skeletal muscle cells, C. barnesi is not cytotoxic at all concentrations tested to both cardiac and skeletal muscles cells. We also demonstrate that in vitro C. fleckeri venom cardiocytotoxic activity is significantly attenuated when heated to 44°C for 20 minutes. There is a similar attenuation with skeletal cells at 46°C.
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