Bites and Stings Pressure immobilisation bandages in first-aid treatment of jellyfish envenomation: current recommendations reconsidered Peter L Pereira, Teresa Carrette, Paul Cullen, Richard F Mulcahy, Mark Little and Jamie Seymour

MJA 2000; 173: 650-652

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Abstract

The effect of PIB is to retard the dissipation of snake venom into the circulation by impeding lymphatic flow. This protects target tissues by confining the toxin to the affected limb until the patient is treated with antivenom.

In snakebite, the venom is released into the tissues and the delivery apparatus (the snake's fangs) does not remain at the bite site. By contrast, in jellyfish stings, the venom is delivered by specialised cells (nematocysts) which have barbed shafts that adhere to the skin. Unless the nematocysts have entirely discharged their venom, applying pressure (as with PIB) has the potential to worsen the envenomation. Our anecdotal experience is that patients with jellyfish stings whose first aid includes PIB have more severe and prolonged symptoms. Furthermore, no scientific evidence supports the use of PIB in the treatment of box jellyfish stings.¹⁰

We designed an experiment to test the hypothesis that applying direct pressure to discharged nematocysts releases further venom.

To cause the nematocysts to discharge, we applied a 6 volt, 3 ampere direct current charge across the tentacles for two seconds. Such electrical augmentation is currently used to collect venom from jellyfish for antivenom production.¹¹ After removal of the tentacles, the membrane was inverted, leaving the nematocyst bodies lying within the cylinder and their penetrating shafts directed externally through the membrane. An aneroid sphygmomanometer (bladder removed) was then attached to the other end of the cylinder (Box 1) to apply pressure to the discharged nematocysts. We used a pressure of 40 mmHg, as pressures of between 40 and 70 mmHg from PIB have been found to obstruct lymphatic flow in simulated snake envenomation.¹²

Through a dissecting microscope (x 100 magnification) small beads of clear fluid were noted on the tips of the shafts (Box 2). With constant visualisation of these beads, 40 mmHg pressure was applied, and a subjective estimate was made as to whether the pressure altered the size of the beads.

To confirm the nature of these beads, the shafts from the discharged nematocysts were washed repeatedly with 2 mL of isotonic saline. The first washing was after activation of the nematocysts (A); the second (B) further cleaned the nematocysts; and the final washing (C) occurred after pressure was applied (and released). Live adult prawns (Penaeus mergenensus) were then injected with one of the three washes (0.2 mL intramuscular injection into the second abdominal segment) and their heart rate was observed every 30 seconds for a period of 10 minutes. The time to ventricular standstill was recorded as a measurement of toxicity. Each solution was administered to three prawns.

Statistical analysis

The heart rates of the nine prawns at time zero (before injection of the washings from the nematocyst shafts) were not statistically different (F_2,6 = 1.895; P = 0.230), but there were significant differences between time from injection of the washings to ventricular standstill for the three different washings (F_20,65 = 8.53; P < 0.001) (Box 3).

• Solution A: In the three prawns administered the first washing, ventricular standstill occurred within 60 seconds of injection.

• Solution B: All three prawns administered the second washing were unaffected by this inoculum during 540 seconds of observation, apart from a minor reduction in heart rate at 60 seconds for one prawn.

• Solution C: The third washing (after applying pressure), although not as potent as the first washing, caused ventricular standstill within 180 seconds in all three prawns.

We showed that Solution A (with venom from initially activated nematocysts) produced the anticipated ventricular standstill when injected into prawns. The relatively innocuous nature of Solution B, which did not produce any ventricular standstill, shows that Solution A had effectively cleaned the nematocyst of any substantial amount of venom. Solution C showed a return of toxicity after 40 mmHg pressure was applied. Thus, pressure applied to discharged nematocysts of Chiropsalmus sp. results in further venom being released.

Vinegar, presumably through a chemical process, is a potent inactivator of nematocysts' firing mechanism. Not discounting this important function, its role in first aid is limited to inactivating undischarged nematocysts. Any inference that it has a continuing protective effect with discharged nematocysts is probably incorrect, as further expression of venom from discharged nematocysts appears to be mechanical rather than triggered.

Given that the physical processes behind nematocyst discharge in all jellyfish are similar, and that nematocyst discharge operates similarly, there is sufficient reason to believe that the use of PIB on any jellyfish sting site may exacerbate the envenomation, irrespective of whether vinegar has been applied. Until evidence to the contrary is available, we recommend that applying PIB is not part of the management of this life-threatening condition. An amended first-aid protocol for jellyfish stings is given in Box 4.

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Reprints will not be available from the authors.
Correspondence: Dr P L Pereira, Department of Emergency Medicine, Cairns Base Hospital, PO Box 902, Cairns, QLD 4870.
peter_pereiraAThealth.qld.gov.au

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