should be less dilute if the allergic reaction is minimal (controlled by antihistamines and epinephrine). A
negative skin test does not preclude the possibility of an anaphylactic response to antivenom administration.
The rationale for administering antivenom is to provide early and adequate neutralization of the toxin
at the tissue site of entry before it gains systemic dominance. Except for stonefish antivenom, the product
should be administered intravenously, taking care to provide adequate doses for children and the elderly, who
have a decreased volume of distribution and increased sensitivity to venom effects. The antivenom intended
for IV administration should always be diluted with normal saline, Ringer's lactate, or dextrose 5% in water.
Marine antivenoms are produced and distributed in the Indo-Pacific regions. They include the
following:
1. Chironex fleckeri (box-jellyfish) antivenom, from Commonwealth Serum Laboratories (CSL), Melbourne,
Australia. A hyperimmune sheep globulin preparation, this may be used to neutralize the stings of Chironex
fleckeri and Chiropsalmus quadrigatus.
2. Enhydrina schistosa (beaked sea snake) sea snake antivenom, from CSL. A hyperimmune horse globulin
preparation, this may be used to neutralize the bites of most sea snakes. It is prepared by immunizing horses
with venom from E. schistosa and the Australian tiger snake Notechis scutatus.
3. Notechis scutatus (tiger snake) antivenom, from CSL. This is the antivenom of second choice against the
bites of most sea snakes.
4. Enhydrina schistosa (beaked sea snake) monovalent antivenom, from the Haffkine Institute in Bombay,
India. This may be used to neutralize the bites of most sea snakes; it is most effective against the bite of E.
schistosa.
5. Synanceja trachynis (stonefish) antivenom, from CSL. A hyperimmune horse globulin preparation, this
may be used to neutralize the stings of stonefish and more virulent scorpionfish species.
A person who is known to be sensitive to horse or sheep serum, has a positive skin test, or develops
signs of an allergic reaction or anaphylaxis during antivenom therapy requires aggressive medical
management. A recipient of antivenom should be pretreated with 50 to 100 mg of intravenous
diphenhydramine (1 mg/kg in children). After this, the initial dose of antivenom is administered at a rate no
faster than one vial each 5 minutes. If no allergic manifestation ensues, the antivenom can be administered at
a more rapid rate. If signs of anaphylaxis develop, usually heralded by an urticarial eruption or pruritus, 0.1 to
0.2 ml aliquots of antivenom should be alternated with 3 to 10 ml (0.03 to 0.1 mg) intravenous doses of
aqueous epinephrine 1:100,000 (infused over 5 to 10 minutes). Alternatively, an epinephrine drip may be
prepared as previously described in the discussion on anaphylaxis. The patient should be managed in an
intensive care unit, with electrocardiographic and blood pressure monitoring. The dose of epinephrine should
not exceed that which elevates the pulse rate above 150 beats/min. The administration of intravenous
epinephrine may cause transient hypokalemia as potassium is driven intracellularly; cessation of the
epinephrine infusion may create a transient hyperkalemia as the potassium regains entry into the extracellular
space. If a victim is highly allergic to antivenom, serious consideration should be given to supportive therapy
(including hemodialysis) without antivenom administration.
In one series, stonefish antivenom was administered to 24 victims in a dose of one or two ampoules by
the IM route, without any "immediate reactions" reported. In this same report, six victims received box
jellyfish antivenom by the IV route without immediate or delayed reactions.
SERUM SICKNESS
The formation of immunoglobulin G (IgG) antibodies in response to antigens present in antivenom
(heterologous serum) results in the deposition of immune complexes in many tissue sites, notably in the walls
of blood vessels. These complexes induce vascular permeability, activate the complement cascade and
chemotactic factors, degranulate mast cells, and trigger the release of proteolytic enzymes. Decreased levels
of C
3
and C
4
are accompanied by increased C
3a
/C
3a
des-arginine, a split product C
3
. Although immune
complexes can be measured by various tests (Raji-cell IgG assay and C
1q
-binding assay), levels of immune
complexes may not correlate with the clinical presentation. Dermal biopsy of lesional skin may reveal
leukocytoclastic vasculitis.
Symptoms are generally present within 8 to 24 days and include fever, arthralgias, malaise, urticaria,
lymphadenopathy, urticarial and morbilliform skin rashes, peripheral neuritis, and swollen joints. It is not
uncommon for the primary urticarial lesion to be noted at the injection site. Serum sickness is managed with
