Disorders caused by venomous snakebites and marine animal exposures gkPresentation Transcript
Disorders Caused by
Venomous Snakebites and
Marine Animal Exposures
Venomous snakes belong to the families Viperidae
(subfamily Viperinae: Old World vipers; subfamily
Crotalinae: New World and Asian pit vipers), Elapidae
(including cobras, kraits, coral snakes, and all Australian
venomous snakes), Hydrophiidae (sea snakes),
Atractaspididae (burrowing asps), and Colubridae (a large
family in which most species are nonvenomous and only a
few are dangerously toxic to humans). Bite rates are
highest in temperate and tropical regions where
populations subsist by manual agriculture. Recent
estimates indicate somewhere between 1.2 million and 5.5
million snakebites worldwide each year, with 421,000–
1,841,000 envenomations and 20,000–94,000 deaths.
The typical snake-venom apparatus consists of bilateral
venom glands situated below and behind the eye and
connected by ducts to hollow anterior maxillary teeth. In
viperids (vipers and pit vipers), those teeth are long mobile
fangs that retract against the roof of the mouth when the
animal is at rest. In elapids and sea snakes, the fangs are
smaller and are relatively fixed in an erect position. In 20%
of pit viper bites and higher percentages of other
snakebites (up to 75% for sea snakes), no venom is
released ("dry" bites). Significant envenomation probably
occurs in 50% of all venomous snakebites.
Venoms and Clinical
Envenomations by most viperids and some elapids with
necrotizing venoms cause progressive local swelling, pain,
ecchymosis, and (over a period of hours or days)
hemorrhagic bullae and serum-filled vesicles. In serious
bites, tissue loss can be significant. Systemic findings can
include changes in taste, mouth numbness, muscle
fasciculations, tachycardia or bradycardia, hypotension,
pulmonary edema, hemorrhage (from essentially any
anatomic site), and renal dysfunction. Envenomations by
neurotoxic elapids such as kraits (Bungarus spp.), many
Australian elapids [e.g., death adders (Atractaspis spp.)
and tiger snakes (Notechis spp.)], some cobras (Naja spp.),
cause neurologic dysfunction.
Venoms and Clinical
Early findings may consist of cranial nerve weakness (e.g.,
manifested by ptosis) and altered mental status. Severe
envenomation may result in paralysis, including the
muscles of respiration, and lead to death from respiratory
failure and aspiration. After elapid bites, the time of onset of
venom intoxication varies from minutes to hours,
depending on the species involved, the anatomic location
of the bite, and the amount of venom injected. Sea snake
envenomation usually causes local pain (variable),
myalgias, rhabdomyolysis, and neurotoxicity; these
manifestations occasionally are delayed for hours.
Early stages of severe, full-thickness necrosis 5 days after a Russell's
viper (Daboia russelii) bite in southwestern India
Incising wounds and/or applying suction to the bite
should be avoided, as these measures are
ineffective and exacerbate local tissue damage.
Similarly ineffective and potentially damaging are
the application of poultices, ice, and electric shock.
Techniques or devices used in an effort to limit
venom spread (e.g., lymphoocclusive bandages or
tourniquets) are ineffective and may result in
greater local-tissue damage, particularly that due
to necrotic venoms. Tourniquet use can result in
amputation and loss of function even in the
absence of envenomation.
Elapid venoms that are primarily neurotoxic and have no
significant effects on local tissue may be localized by
pressure-immobilization, a technique in which the entire
limb is wrapped immediately with a bandage (e.g., crepe or
elastic) and then immobilized. For this technique to be
effective, the wrap pressure must be precise (40–70 mmHg
in upper extremity application and 55–70 mmHg in lower
extremity application), and the victim must be carried from
the scene of the bite to avoid muscle-pump action that—
regardless of the anatomic site of the bite—will disperse
venom if the victim walks.
In the hospital, the victim should be closely monitored (vital
signs, cardiac rhythm, oxygen saturation, urine output)
while a history is obtained quickly and a rapid, thorough
physical examination is performed. For objective evaluation
of the progression of local envenomation, the level of
swelling in the bitten extremity should be marked and limb
circumferences measured every 15 min until swelling has
stabilized. During this period of observation/monitoring, the
extremity should be positioned at approximately heart level.
Measures applied in the field (such as constriction bands or
tourniquets) should be removed once IV access has been
obtained, with cognizance that the release of such ligatures
may result in hypotension or dysrhythmias when stagnant
acidotic blood is released to the central circulation.
Large-bore IV access in one or two unaffected extremities
should be established. Early hypotension is due to pooling
of blood in the pulmonary and splanchnic vascular beds.
Later, systemic bleeding, hemolysis, and loss of
intravascular volume into soft tissues may play important
roles. Fluid resuscitation with isotonic saline (20–40 mL/kg
IV) should be initiated if there is any evidence of
hemodynamic instability, and a trial of 5% albumin (10–20
mL/kg) may be given when patients fail to respond to saline
infusion. Only after aggressive volume resuscitation and
antivenom administration (see below) should vasopressors
(e.g., dopamine) be added.
Blood should be drawn for typing and cross-matching and
for laboratory evaluation as soon as possible. Important
studies include a complete blood count to evaluate the
degree of hemorrhage or hemolysis and to identify
thrombocytopenia, studies of renal and hepatic function,
coagulation studies to diagnose consumptive
coagulopathy, and testing of urine for blood or myoglobin.
In developing regions, the 20-min whole-blood clotting test
can be used for reliable diagnosis of coagulopathy. A few
milliliters of fresh blood are placed in a new, clean, plain
glass receptacle (e.g., a test tube) and left undisturbed for
Use of Acetylcholinesterase Inhibitors
in Neurotoxic Snake Envenomation
1. Patients with clear, objective evidence of neurotoxicity after
snakebite (e.g., ptosis or inability to maintain upward gaze) should
receive a trial of edrophonium (if available) or neostigmine.
a. Pretreat with atropine: 0.6 mg IV (children, 0.02 mg/kg; minimum of
b. b. Follow with: Edrophonium: 10 mg IV (children, 0.25 mg/kg) or
Neostigmine: 1.5–2.0 mg IM (children, 0.025–0.08 mg/kg)
2. If objective improvement is evident at 5 min, continue neostigmine at
a dose of 0.5 mg (children, 0.01 mg/kg) IV or SC every 30 min as
needed, with continued administration of atropine by continuous
infusion of 0.6 mg over 8 h (children, 0.02 mg/kg over 8 h).
3. Maintain vigilance regarding aspiration risk and secure the airway
with endotracheal intubation as needed.
In the event of serum sickness (fever, chills,
urticaria, myalgias, arthralgias, and possibly
renal or neurologic dysfunction developing
1–2 weeks after antivenom administration),
the victim should be treated with systemic
glucocorticoids (e.g., oral prednisone, 1–2
mg/kg daily) until all findings resolve; the
dose is then tapered over 1–2 weeks. Oral
antihistamines and analgesics provide
additional relief of symptoms.
Morbidity and Mortality
The overall mortality rates for venomous snakebite are low
in areas with rapid access to medical care and appropriate
antivenoms. In the United States, for example, the mortality
rate is <1% for victims who receive antivenom. Eastern and
western diamondback rattlesnakes (Crotalus adamanteus
and C. atrox, respectively) are responsible for the majority
of snakebite deaths in the United States. Snakes
responsible for large numbers of deaths in other countries
include cobras (Naja spp.), carpet and saw-scaled vipers
(Echis spp.), Russell's vipers (D. russelii), large African
vipers (Bitis spp.), lancehead pit vipers (Bothrops spp.),
and tropical rattlesnakes (C. durissus).
The Golgi apparatus of the cnidoblast cells within
cnidarians such as hydroids, fire coral, jellyfish,
Portuguese men-of-war, and sea anemones
secretes specialized living stinging organelles
called cnidae (also referred to as cnidocysts, a
term that encompasses nematocysts, ptychocysts,
and spirocysts). Within each organelle resides a
stinging mechanism ("thread tube") and venom. In
the stinging process, cnidocysts are released and
discharged upon mechanosensory stimulation.
The venoms from these organisms are mixtures of
proteins, carbohydrates, and other components.
During stabilization, the skin should be decontaminated
immediately with a generous application of vinegar (5%
acetic acid), which is the all-purpose agent useful for
inactivating the nematocysts in the greatest number of
species. Rubbing alcohol (40–70% isopropyl alcohol),
baking soda (sodium bicarbonate), papain (unseasoned
meat tenderizer), fresh lemon or lime juice, household
ammonia, olive oil, or sugar may be effective, depending
on the species of stinging creature. For the sting of the
venomous box-jellyfish (Chironex fleckeri), vinegar should
be used. Local application of heat (up to 45°C/113°F),
commonly by immersion in hot water, may be as effective.
Marine Vertebrate Stings
The affected part should be immersed immediately in
nonscalding hot water (45°C/113°F) for 30–90 min or until
there is significant relief of pain. Recurrent pain may
respond to repeated hot-water treatment. Cryotherapy is
contraindicated. Opiates will help alleviate the pain, as will
local wound infiltration or regional nerve block with 1%
lidocaine, 0.5% bupivacaine, and sodium bicarbonate
mixed in a 5:5:1 ratio. After soaking and anesthetic
administration, the wound must be explored and debrided.
Radiography (in particular, MRI) may be helpful in
identification of foreign bodies.
Ciguatera poisoning is the most common nonbacterial food
poisoning associated with fish in the United States; most
U.S. cases occur in Florida and Hawaii. The poisoning
almost exclusively involves tropical and semitropical marine
coral reef fish common in the Indian Ocean, the South
Pacific, and the Caribbean Sea. Among reported cases,
75% (except in Hawaii) involve the barracuda, snapper,
jack, or grouper. The ciguatera syndrome is associated
with at least five polyether sodium channel activator toxins
that originate in photosynthetic dinoflagellates (such as
Gambierdiscus toxicus) and accumulate in the food chain.
The >150 symptoms reported include abdominal pain,
nausea, vomiting, diarrhea, chills, paresthesias, pruritus,
tongue and throat numbness or burning, sensation of
"carbonation" during swallowing, odontalgia or dental
dysesthesias, dysphagia, dysuria, dyspnea, weakness,
fatigue, tremor, fasciculations, athetosis, meningismus,
aphonia, ataxia, vertigo, pain and weakness in the lower
extremities, visual blurring, transient blindness,
hyporeflexia, seizures, nasal congestion and dryness,
conjunctivitis, maculopapular rash, skin vesiculations,
dermatographism, sialorrhea, diaphoresis, headache,
arthralgias, myalgias, insomnia, bradycardia, hypotension,
central respiratory failure, and coma.
The differential diagnosis of ciguatera includes paralytic
shellfish poisoning, eosinophilic meningitis, type E
botulism, organophosphate insecticide poisoning,
tetrodotoxin poisoning, and psychogenic hyperventilation.
At present, the diagnosis of ciguatera poisoning is made on
clinical grounds because no routinely used laboratory test
detects ciguatoxin in human blood. High-performance liquid
chromatography (HPLC) is available for ciguatoxins and
okadaic acid but is of limited clinical value because most
health care institutions do not have the equipment needed
to perform the test.
Therapy is supportive and is based on symptoms. Nausea
and vomiting may be controlled with an antiemetic such as
ondansetron (4–8 mg IV). Hypotension may require the
administration of IV crystalloid and, in rare cases, a pressor
drug. Bradyarrhythmias that lead to cardiac insufficiency
and hypotension generally respond well to atropine (0.5 mg
IV, up to 2 mg). Cool showers or the administration of
hydroxyzine (25 mg PO every 6–8 h) may relieve pruritus.
Amitriptyline (25 mg PO twice a day) reportedly alleviates
pruritus and dysesthesias. In three cases unresponsive to
amitriptyline, tocainide appeared to be efficacious.
Nifedipine has been used to treat headache. IV
infusion of mannitol may be beneficial in moderate
or severe cases, particularly for the relief of
distressing neurologic or cardiovascular
symptoms, although the efficacy of this therapy
has been challenged and has not been definitively
proved. The infusion is rendered initially as 1 g/kg
per day over 45–60 min during the acute phase
(days 1–5). If symptoms improve, a second dose
may be given within 3–4 h and repeated on the
next day. Care must be taken to avoid dehydration
in a treated patient.