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Wilderness Medical Society - snowmass 2005 (Page 327)

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Wilderness Medical Society - snowmass 2005
MARINE ENVENOMATIONS
Paul S. Auerbach, M.D.
Abridged from Wilderness Medicine, 4
th
edition, St. Louis, Mosby, 2001
The science of poisons, biotoxicology, is divided into plant poisons, or phytotoxicology, and animal poisons,
or zootoxicology. "Toxinology" connotes the science of toxic substances produced by or accumulated in
living organisms, their properties and their biological significance for the organisms involved. Animals in
which a definite venom apparatus is present are sometimes called phanerotoxic, while animals whose body
tissues are toxic are termed cryptotoxic. Naturally occurring aquatic zootoxins may be designated as oral
toxins (which are poisonous to eat and include bacterial poisons and products of decomposition), parenteral
toxins (venom produced in specialized glands and injected mechanically (by spine, needle, fang, fin, or dart),
and crinotoxins (venom produced in specialized glands and administered as slime, mucous, and gastric
secretion). Within these three subdivisions, further classifications are by phylogeny, chemical structure, and
clinical syndrome.
Although all venoms are poisons, not all poisons are venoms. According to the theory that offensive
venoms are generally oral (mouth and fang) and defensive venoms are aboral (tail and sting) or dermal (barb
and secretion), the majority of marine venoms are defensive. In the evolutionary scheme it appears that
venomous fish seek specific self-defense, whereas poisonous fish are noxious in a nonspecific manner. A brief
comparison of the features of venoms and poisons shows that poisons produced in skin, muscle, blood, or
organs are generally heat stable (115
o
to 120
o
F), gastric acid stable, and carry seasonal toxicity. They are not
"released" and may lack a well-defined biologic function. Venoms are more commonly heat labile, gastric
acid labile, and nonseasonal in toxicity. They can be released in varying amounts and have evolved for
conquest and defense.
In snakes the latency, toxicity, and duration of a venom effect are related to the route of envenomation.
Intravascular injection is significantly more lethal than intraperitoneal or transcutaneous injection, as
determined by the measured lethal dose of 50% survival of the group (LD
50
). This principle is not commonly
applied to marine venoms because few encounters involve direct intravascular invasion.
Most venoms are high molecular weight amalgams of vasoactive amines, proteolytic enzymes, and
other biogenic compounds. These substances denature membranes, catabolize cyclic 3',5'-adenosine
monophosphate, degranulate mast cells, provoke histamine release, initiate arachidonate metabolism,
accelerate coagulopathy, interfere with cellular transport mechanisms, disrupt metabolic pathways, impede
neuronal transmission, and evoke anaphylaxis and shock. Frustratingly, although many marine venoms are
composed of protein and polypeptide subunits, they lack sufficient immunogenicity to allow development of
antitoxins or antivenoms. Poisons represent metabolic by-products and are usually of smaller molecular
weight.
Taxonomy of marine animals can sometimes be confusing. The hierarchical distinctions are made in
descending order: kingdom, phylum, class, order, family, genus, and species.
Antivenom Administration
A number of marine envenomations, such as those by the box-jellyfish and certain sea snakes, may
require the administration of specific antivenom. Marine antivenoms are raised in sheep and horses and
therefore are antigenic in humans, inducing both immediate and delayed hypersensitivity. Most authorities
recommend that a skin test should be performed for sensitivity to horse serum, if the clinical situation permits,
after a sea snake envenomation. (There is rarely time for a skin test with a Chironex envenomation, which
requires immediate intervention.) This should be done only after deciding to administer antivenom and not to
determine whether antivenom is necessary. The purpose of sensitivity testing is to allow adequate prophylaxis
against anaphylaxis. The skin test is performed with an intradermal injection into the upper extremity of 0.02
ml of a 1:10 dilution of horse serum test material in saline, with 0.02 ml saline in the opposite extremity as a
control. Erythema and pseudopodia are present in 15 to 30 minutes in a positive response. Because antivenom
contains many times the protein content of horse serum used for skin testing, the use of antivenom for skin
testing may increase the risk of anaphylactic reaction. If the skin test is positive, the antivenom intended for
IV infusion should be diluted in sterile water to a 1:100 concentration for administration. Successive vials

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