++
North American coral snakes include the eastern coral snake (Micrurus fulvius
fulvius), the Texas coral snake (M. fulvius tenere),
and the Arizona (Sonoran) coral snake (Micruroides euryxanthus).
The eastern coral snake is found primarily in the southeastern U.S.
The Texas and Arizona coral snakes are found primarily in the states
that bear their names. Coral snakes account for 20 to 25 bites a
year.
++
All coral snakes are brightly colored with black, red, and yellow
rings. The red and yellow rings touch in coral snakes, but they
are separated by black rings in nonpoisonous snakes, which led to
the well-known rhyme, “Red on yellow, kill a fellow;
red on black, venom lack.” This rule is not always true
outside of the U.S.
++
Coral snake venom is primarily composed of neurotoxic components that
do not cause marked local injury (Table 206-2).
A potential victim of coral snake bite should be admitted to the
hospital for observation. Coral snake venom effects may develop
hours after a bite, and effects are not easily reversed. Three to
five vials of Antivenin (Micrurus fulvius) should
be administered to patients who have definitely been bitten, because
it may not be possible to prevent further effects or reverse effects once
they develop.13 Additional doses of coral snake
antivenom are reserved for cases in which symptoms or signs of coral
snake envenomation appear. Because respiratory failure may result
from clinical effects of the neurotoxin, baseline and serial measurement
of pulmonary function parameters (such as inspiratory pressure and
vital capacity), in addition to intensive care observation, may
be useful. Prolonged ventilatory support may be required in severe
cases. The patient must be observed closely for signs of respiratory
muscle weakness and hypoventilation. Bites by the Sonoran coral
snake are mild, and antivenom is not usually needed.
++
Australian Elapid
Bites
++
Elapids are found throughout the world in tropical and warm climates. Medically
significant groups include most venomous snakes of Australia [tiger
snakes (Notechis), brown snakes (Pseudonaja), costal
taipan (Oxyuranus), death adder (Acanthophis), red-bellied
black snake (Pseudechis)] and cobras (Naja), mambas (Dendroaspis),
and kraits (Bungarus) found in Africa and southern
Asia.
++
Elapid bites produce primarily neurologic effects: tremors, salivation, dysarthria,
diplopia, bulbar paralysis with ptosis, fixed and constricted pupils,
dysphagia, dyspnea, and seizures. The immediate cause of death is
paralysis of respiratory muscles. Signs and symptoms may be delayed up
to 12 hours (Table 206-2).
++
The Elapidae possess nonretractile small- to medium-sized paired
fangs that have grooved venom channels rather than hollow venom
ducts. It is thought that the Elapidae exert voluntary control over the
injection of venom, hence the occurrence of a dry bite without envenomation.
++
The venom of the Australian elapids contains several important
components.14 Neurotoxins (tiger snake, taipan,
and death adder) act at the neuromuscular junction and cause descending
symmetric flaccid paralysis. Signs usually become apparent within
2 to 12 hours after the bite and may include ptosis, partial ophthalmoplegia
(diplopia), dysarthria, loss of facial expression, and loss of airway
control, as well as respiratory paralysis in severe cases. The procoagulant
toxins (brown snake, tiger snake, taipan) act as prothrombin converters,
leading to a venom-induced consumptive coagulopathy with fibrinogen
depletion and variable thrombocytopenia. Intracranial hemorrhage
is a recognized complication.
++
The brown snake can cause rapid collapse and death.15 Renal
impairment or failure may also result from snakebite. The mechanisms
are poorly understood and may include hypotension, myoglobinuria,
coagulopathy, and direct renal toxicity. Myolysins (tiger snake,
taipan, mulga snake) are structurally related to the neurotoxins
but instead produce rhabdomyolysis, which may result in muscle pain,
weakness, myoglobinuria, renal failure, and hyperkalemia. Rarely,
a venom-induced thrombotic microangiopathy may complicate brown
and tiger envenomation.16 Local tissue destruction
is uncommon with the bite of any Australian species, although mild
to moderate ecchymosis and swelling may occur.
++
The severity of elapid envenomation cannot be estimated by the
clinical appearance of the bite site or initial symptoms.17 Even
with severe envenomation patients may initially feel well and manifest
few untoward clinical features. Initial symptoms include nausea, vomiting,
headache, abdominal pain, diplopia, dysphonia, progressive muscle
weakness, discolored urine, and seizures. Young children may not
provide a history of snakebite, so a high index of suspicion for
elapid snakebite is needed if a child develops toxicity in a geographic
area populated with elapids.
++
Diagnosis of envenomation by Australian Elapidae requires the
correlation of history of potential snakebite, clinical features
of envenomation, and laboratory investigations. Commonwealth Serum
Laboratories (CSL Ltd., Melbourne, Australia) developed a Snake
Venom Detection Kit (SVDK) to classify snake venom identified at
the bite site or in the urine. Positive SVDK identification of venom
at the bite site or in the urine assists in selecting a monovalent
antivenom, but does not represent an indication for antivenom therapy
without other evidence of systemic venom effects. SVDK testing of
blood is not recommended, because false positive and false negative
results have been described.15
++
The aim of first aid is to delay absorption of venom from the
bite site until the patient is in a facility that can administer antivenom
if required. In Australia, pressure immobilization of the involved
limb is used. The principle is to contain the venom within lymphatic
vessels and prevent systemic absorption. This is done by wrapping a
snug elastic bandage over the bite site and then extending it to
cover the entire limb. The limb is then splinted to prevent motion.
Examination of lymphatic flow rates with simulated venom has demonstrated
that, even if the upper or lower limb is appropriately bandaged
and immobilized, walking will hasten systemic envenoming.18 Use
of tourniquets is contraindicated. In the rare circumstance
that a bite is inflicted on the trunk, apply firm pressure to the
affected area without restricting breathing.
++
Any history suggestive of an elapid bite should prompt the initiation
of first aid and transport to a medical facility with appropriate
medical expertise, laboratory facilities, and antivenom supplies.
The constriction band should be maintained until envenomation is excluded
and an IV line is established, or until the patient can receive
antivenom. Once the patient is in the hospital, if there are no signs of envenomation and results
of laboratory studies are normal, the constriction band should be
removed. If the patient’s condition deteriorates immediately
after constriction band removal, reapply the band and give antivenom.
Once antivenom is infusing, the constriction band should be removed
so that venom is available for interaction with circulating antivenom.
There is no evidence that venom is inactivated by being trapped
at the bite site.15
++
Antivenom should be given only in cases in which there
is clear clinical or laboratory evidence of systemic venom effect
(Table 206-2). Clinical indications
for immediate antivenom therapy include repeated vomiting and severe
headache; neurotoxic effects such as ptosis, cranial nerve involvement,
progressive muscle weakness, or diaphragmatic involvement; or evidence
of coagulopathy. Pertinent investigations include complete blood
count, coagulation studies (including levels of fibrinogen and fibrin degradation
products), serum electrolyte levels, renal function tests, creatine
kinase level, and urine testing for hematuria or myoglobinuria.14 Abnormal
coagulation study results frequently provide laboratory evidence
of systemic venom effects before neurotoxic effects are apparent.
In the absence of clinical or laboratory evidence of venom effect,
the constriction band should be removed and the patient observed
for at least 12 hours. Coagulation studies should be repeated 2
hours after band removal and at intervals thereafter, depending
on the patient’s condition.
++
Six antivenom products, derived from equine immunoglobulin G,
are available to treat envenomation by the five groups of venomous
terrestrial Australian snakes plus the sea snakes. These six products
are monovalent antivenoms.14 A polyvalent antivenom,
also equine immunoglobulin G, neutralizes the venom of all five
major groups of dangerous Australian terrestrial snakes (Table 206-5).
++
++
If indicated, monovalent or polyvalent antivenom
should be given immediately in sufficient doses to improve coagulation
values. A child should receive the same dose of antivenom as an
adult.14 Pregnancy is not a contraindication to
antivenom therapy. Skin testing before antivenom administration
is not recommended,14 and epinephrine and supplies
for intubation should be at the bedside to treat anaphylaxis. If
the type of snake involved cannot be identified, usually two appropriate monovalent
antivenoms may be selected by correlating the clinical presentation
with knowledge of snakes found in the geographic area. Until recently,
recommended doses of monovalent antivenom and laboratory end points
for treatment had been based on clinical evidence and expert consensus.
More rigorous research now suggests that lower doses of antivenom
may be appropriate.19 Again, expert advice is recommended. The
role of polyvalent antivenom therapy is currently ill-defined. Hypersensitivity
is usually an uncommon complication of antivenom therapy in Australia,
but caution is required.20–22 A 5-day
course of prednisolone may be prescribed in an attempt to reduce
the incidence of serum sickness in those patients who receive large
doses of antivenom, but clear clinical trial data supporting this
practice are lacking.15