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Topic: SNAKE VENOM POISONING

0.0 OVERVIEW
0.2 CLINICAL EFFECTS
0.2.1 SUMMARY
A. EDEMA:
(1) In most cases, almost immediate SWELLING and EDEMA
appear. Swelling is usually seen around the injured
area within five minutes after the bite and often
progresses rapidly, involving the entire injured
extremity within an hour. Generally, however, edema
spreads more slowly over a period of 8 to 36 hours.
(2) Swelling is most marked after bites by the eastern
diamondback rattlesnake. It is less marked after
western diamondback bites, and after bites by the
prairie, timber, red, Pacific, and black-tailed
rattlesnakes, sidewinders and cottonmouths. It is
least marked after bites by copperheads.
B. PAIN: Immediately following the bite is a complaint of
most patients with poisoning by rattlesnakes. It is
most severe after eastern and western diamondback bites,
less severe after bites by the prairie and other viridis
rattlesnakes, and least severe after copperhead and
massasauga bites. WEAKNESS, SWEATING, FAINTNESS and
NAUSEA are common.
C. RATTLESNAKES, COTTONMOUTH, AND COPPERHEAD SNAKES
1. LOCAL:
a. May include punctures, pain, edema,
erythema, bleeding, ecchymosis, and
lymphangitis.
2. SYSTEMIC:
a. May include hypotension, weakness,
sweating or chills, perioral and/or
peripheral paresthesia, taste
changes, nausea and vomiting, and
fasciculations. Coagulopathies and
shock may occur in some
envenomations.
D. CORAL SNAKES
1. LOCAL:
a. Minimal reaction, punctures may be
obscure.
2. SYSTEMIC:
a. May include drowsiness, weakness,
dysphagia, dysphonia, diplopia,

headache, weakness, and respiratory
distress.
0.3 LABORATORY
A. The following immediate procedures should be carried out:
typing and cross-matching, bleeding, clotting and clot
retraction times, complete blood count, hematocrit,
platelet count and urinalysis.
B. RBC indices, sedimentation rate, prothrombin time,
arterial blood gases, sodium, potassium and chloride
determinations may be needed.
0.4 TREATMENT OVERVIEW
0.4.1 SUMMARY
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Topic: SNAKE VENOM POISONING

A. This overview contains first aid treatment only. See
main section of management for assessment and therapy
guidelines.
B. FIELD OR FIRST AID TREATMENT
1. Put victim at rest and keep warm.
2. Remove rings and constrictive items.
3. Lightly immobilize injured part in functional
positional and keep just below heart level.
4. Give plenty of reassurance.
5. Transport to medical facility as quickly as possible.
6. Do not pack in ice.
7. Use Sawyer Extractor over bite area if transport to
medical facility is to be in excess of 45 minutes.
Must be applied immediately.
8. Electroshock treatment for snakebite has been
recommended as initial therapy, but this unusual
recommendation has been demonstrated to be ineffective
in an animal model and is potentially quite dangerous.
1.0 SUBSTANCES INCLUDED
1.3 DESCRIPTION
A. There are approximately 120 species of snakes in the
United States of which 26 are venomous. Bites by
nonvenomous snakes are much more common than bites by
venomous snakes. These should be treated as simple
puncture wounds, employing an appropriate antitetanus
agent. About 25% of all bites by venomous snakes in the
United States do not result in envenomation, that is, the
snake may bite but not inject venom, or may eject it onto
the skin, as in a very superficial bite.
B. Most rattlesnakes, copperheads, water moccasins and coral
snakes tend to bite superficially but a few bites
penetrate muscle. The gravity of the poisoning will
depend upon:
1) The nature, location, depth and number of bites
2) The amount of venom injected
3) The species and size of the snake
4) The age and size of the victim
5) The victim's sensitivity to the venom
6) The microbes present in the snake's mouth
7) The kind of first aid treatment and subsequent
medical care.
C. Bites by venomous snakes may therefore vary in severity
from trivial to extremely grave. In every case, snake
venom poisoning is an emergency requiring immediate
attention and the exercise of considerable judgement.
Delayed or inadequate treatment may result in tragic
consequences. However, failure to differentiate between
the bite of a venomous and a nonvenomous snake may lead
to the use of measures that can not only cause discomfort
but may produce deleterious results.
D. It is essential that a diagnosis, based on identification
of the snake and the presence or absence of symptoms and
signs, be made before treatment is instituted. The
admitting diagnosis should indicate whether the patient
has been bitten and envenomated by a venomous snake
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Topic: SNAKE VENOM POISONING

(snake venom poisoning), bitten but not envonomated, or
bitten by a nonvenomous snake.
E. "Snakebite" is not a valid medical-legal diagnosis. The
identity of the offending reptile, when obtainable,
should be noted on the admitting record. It should be
borne in mind that some persons bitten by nonvenomous
snakes become excited and even hysterical, and that these
findings may give rise to disorientation, faintness,
dizziness, hyperventilation, a rapid pulse, and even
primary shock.
F. IDENTIFICATION
1. Identification of a venomous species is not always easy.
The rattlesnakes are distinguished from the nonvenomous
snakes by their two elongated, canaliculated, upper
maxillary teeth, which can be rotated from their resting
position, in which they are folded against the roof of
the mouth, to their biting position, where they are
almost perpendicular to the upper jaw. Each fang is
shed periodically and is replaced by the first reserve
fang. The pupils are vertically elliptical, but a few
nonvenomous snakes also have such pupils. The crotalids
have a deep easily identifiable pit between the eye and
the nostril. The somewhat triangular shape of the head,
the base being wider than the neck, also helps to
distinguish them from nonvenomous snakes.
2. Color and pattern are the most deceptive criteria for
identification. Identification of the offending snake
on the sole basis of fang or tooth marks is not
recommended. Some nonvenomous snakes may leave teeth
marks very similar to those produced by rattlesnakes and
rattlesnakes may leave teeth marks in addition to those
of the two upper maxillary fangs. Very often, crotalids
may strike and leave a single fang puncture wound and
this is too similar to that which might be produced by a
nonvenomous snake to be relied upon in confirming a
diagnosis.
3. CORAL SNAKE: The coral snake's upper maxillary teeth
are also elongated but they are much shorter than those
of the rattlesnakes, and they are fixed. Coral snakes
have round pupils, and can be distinguished from king
snakes, scarlet snakes and some shovel-nosed and milk
snakes, with which they are sometimes confused, by their
complete rings of black, yellow and red, the red and
yellow ring touching. "Red on yellow kill a fellow".
1.4 GEOGRAPHICAL LOCATION
A. The distribution of some of the medically more important
snakes of the United States is as follows:
SNAKES LOCATION
1. Pit vipers (Crotalidae)
a. Cottonmouths &
Copperheads
(Agkistrodon)
1) Cottonmouths TX NE IA KS OK AR MO
(A. piscivorus) TN KY IL NC SC GA AL
MS LA FL VA
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Topic: SNAKE VENOM POISONING

2) Copperheads TX NE IA KS OK AR MO
(A. contortrix) TN KY IL IN OH NC SC
GA AL MS LA FL PA NJ
MD DE VA W.VA NY
N.ENG
b. Rattlesnakes
(Crotalus)
1) Eastern Diamondback
(C. adamanteus)
2) Western diamondback CA NV AZ NM TX OK AR
(C. atrox)
3) Sidewinder CA NV AZ UT
(C. cerastes)
4) Timber TX MN WI NE IA KS OK
(C. horridus) AR MO TN KY IL IN OH
NC SC GA AL MS LA FL
PA NJ MD DE VA W.VA
NY N.ENG
5) Rock AZ NM TX
(C. lepidus)
6) Speckled CA NV AZ
(C. mitchelli)
7) Black-tailed AZ NM TX
(C. molossus)
8) Twin-spotted AZ
(C. pricei)
9) Red diamond CA
(C. ruber)
10) Mojave CA NV TX AZ NM TX
(C. scutulatus)
11) Tiger AZ
(C. tigris)
12) Western MO
(C. viridis)
Prairie ID AZ NM TX MO SD ND
(C.v. viridis) NE IA WY UT CO
Grand Canyon AZ
(C. v. abyssus)
Southern Pacific CA
(C. v. helleri)
Great Basin OR ID CA NV AZ UT
(C. v. lutosus)
Northern Pacific WA OR ID CA NV
(C. v. oreganus)
13) Ridge-nosed AZ
(C. willardi)
14) Massasauga and pigmy
(Sistrurus)
Massasauga AZ NM TX MI WI MN
(S. catenatus) NE IA CO KS OK MO
IL IN OH NY PA
Pigmy TX OK AR MO TN NC
(S. miliarius) SC GA AL MS LA FL
2. Coral snakes
(Elapidae)
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Topic: SNAKE VENOM POISONING

a. Western coral snake
(Micruroides AZ NM TX
euryxanthus)
b. Eastern coral snake
(Micrurus fulvius) TX AR NC SC GA AL MS
LA FL
1.6 OTHER
A. CHEMISTRY
1. Snake venoms are complex mixtures, chiefly proteins,
many of which have enzymatic activities. However, the
lethal and perhaps more deleterious fractions are
certain peptides and proteins of relatively low
molecular weight. Some of these peptides may be 25
times more lethal than the crude venom. These peptides
appear to have very specific receptor sites, both
chemically and pharmacologically.
2. Snake venoms are also rich in enzymes, including:
proteinases; phospholipase A, B., C, and D; ATPase;
L-arginine-ester hydrolases; ribonuclease; alkaline
phosphatase; transaminase; deoxyribonuclease; acid
phosphatase; hyaluronidase; phosphomonoesterase; DPNase;
L-amino acid oxidase; phosphodiesterase; endonuclease;
cholinesterase; and 5'-nucleotidase endonuclease. The
venoms of the crotalids are rich in some of these
enzymes, while poor in others.
3. Although the peptides of the North American rattlesnakes
have not yet been studied in detail, preliminary
investigations indicate they are 3 to 10 times more
lethal than the crude venom, and have molecular weights
around 10,000. Several larger lethal proteins have also
been isolated but their exact composition has not yet
been determined.
2.0 CLINICAL EFFECTS
2.1 SUMMARY
A. EDEMA:
1. In most cases, almost immediate SWELLING and EDEMA
appear. Swelling is usually seen around the injured
area within five minutes after the bite and often
progresses rapidly, involving the entire injured
extremity within an hour. Generally, however, edema
spreads more slowly over a period of 8 to 36 hours.
2. Swelling is most marked after bites by the eastern
diamondback rattlesnake. It is less marked after
western diamondback bites, and after bites by the
prairie, timber, red, Pacific, and black-tailed
rattlesnakes, sidewinders and cottonmouths. It is least
marked after bites by copperheads.
B. PAIN: Immediately following the bite is a complaint of
most patients with poisoning by rattlesnakes. It is most
severe after eastern and western diamondback bites, less
severe after bites by the prairie and other viridis
rattlesnakes, and least severe after copperhead and
massasauga bites. WEAKNESS, SWEATING, FAINTNESS and
NAUSEA are common.
C. REGIONAL LYMPH NODES may be ENLARGED, PAINFUL, and
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Topic: SNAKE VENOM POISONING

TENDER.
D. HEMATEMESIS, MELENA, INCREASED or DECREASED SALIVATION,
and MUSCLE FASCICULATIONS may be seen (Russell, 1983).
E. RATTLESNAKES, COTTONMOUTH, AND COPPERHEAD SNAKES
1. LOCAL:
a. May include punctures, pain, edema,
erythema, bleeding, ecchymosis, and
lymphangitis.
2. SYSTEMIC:
a. May include hypotension, weakness,
sweating or chills, perioral and/or
peripheral paresthesia, taste
changes, nausea and vomiting, and
fasciculations. Coagulopathies and
shock may occur in some
envenomations.
F. CORAL SNAKES
1. LOCAL:
a. Minimal reaction, punctures may be
obscure.
2. SYSTEMIC:
a. May include drowsiness, weakness,
dysphagia, dysphonia, diplopia,
headache, weakness, and respiratory
distress.
G. TIMES SYMPTOM OR SIGN WAS OBSERVED/TOTAL
NUMBER OF CASES
Fang marks 100/100
Swelling and edema 80/100
Pain 72/100
Ecchymosis 60/100
Vesiculations 51/100
Changes in pulse rate 60/100
Weakness 60/80
Sweating and/or chill 37/60
Numbness or tingling of tongue 63/100
and mouth or scalp or feet
Faintness or dizziness 52/100
Nausea, vomiting or both 48/100
Blood pressure changes 46/100
Increased body temperature 15/41
Swelling regional lymph nodes 40/100
Fasciculations 33/100
Increased blood clotting time 31/60
Sphering of red blood cells 18/46
Tingling or numbness of 20/49
affected part
Necrosis 38/100
Respiratory rate changes 20/57
Decreased hemoglobin 37/100
Abnormal electrocardiogram 26/100
Cyanosis 20/100
Hematemesis, hematuria, 22/100
or melena
Glycosuria 32/97
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Topic: SNAKE VENOM POISONING

Proteinuria 21/97
Unconsciousness 20/100
Thirst 24/100
Increased salivation 19/100
Swollen eyelids 7/100
Retinal hemorrhage 5/64
Blurring of vision 12/100
Convulsions 1/100
Decreased blood platelets 12/25
Increased blood platelets 4/25
2.6 NEUROLOGIC
A. PARESTHESIA: A common complaint following some pit viper
bites is TINGLING or NUMBNESS over the TONGUE and MOUTH
or SCALP, and PARESTHESIA around the wound. This may
appear within 5 minutes of the bite.
2.14 HEMATOLOGIC
A. Hematological findings may show HEMOCONCENTRATION early,
then a DECREASE in RED CELLS and PLATELETS. Urinalysis
may reveal HEMATURIA, GLYCOSURIA and PROTEINURIA. The
clotting screen is often abnormal.
2.15 DERMATOLOGIC
A. ECCHYMOSIS and DISCOLORATION of the SKIN often appear in
the area of the bite within several hours. VESICLES may
form within 3 hours; generally they are present by the
end of 30 hours. HEMORRHAGIC VESICULATIONS and PETECHIAE
are common.
B. THROMBOSIS may occur in superficial vessels, and
SLOUGHING of INJURED TISSUES is not uncommon in untreated
cases. NECROSIS develops in a large percentage of
untreated victims.
B. SKIN TEMPERATURE: Is usually ELEVATED immediately
following the bite.
3.0 LABORATORY
3.2 MONITORING PARAMETERS/LEVELS
3.2.1 SERUM/PLASMA/BLOOD
A. The following immediate procedures should be carried
out: typing and cross-matching, bleeding, clotting and
clot retraction times, complete blood count, hematocrit,
platelet count and urinalysis. RBC indices,
sedimentation rate, prothrombin time, arterial blood
gases, sodium, potassium and chloride determinations may
be needed.
B. Serum proteins, fibrinogen titer, partial thromboplastin
time, and renal function tests are useful.
C. In severe envenomations the hematocrit, blood count,
hemoglobin concentration, and platelet count should be
carried out several times for the first few days, and
all urine samples should be examined, particularly for
red blood cells.
3.2.3 OTHER
A. In severe poisonings, an electrocardiogram is indicated.
4.0 CASE REPORTS
A. Riggs et al (1987) reported the case of a 29 year old man
with no prior history of snakebite, who was bitten on the
left index finger by a rattlesnake. The patient had
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Topic: SNAKE VENOM POISONING

performed incision and oral suction before seeking
medical attention. He also had recent dental surgery and
gingival irritation and mucosal breaks. Mild edema from
the bite site to the wrist and a mild coagulopathy
developed. The most striking feature was massive
oropharyngeal edema with dyspnea, wheezing, and inability
to speak, which occurred before any antivenin was
administered. The massive oropharyngeal swelling may
have been due to absorption of venom through the injured
gingival mucosa and brings the safety of incision and
oral suction into question.
5.0 TREATMENT
5.1 LIFE SUPPORT Support respiratory and cardiovascular
function.
5.3 ORAL/PARENTERAL EXPOSURE
5.3.1 PREVENTION OF ABSORPTION
A. FIELD OR FIRST AID TREATMENT
1. Put victim at rest and keep warm.
2. Remove rings and constrictive items.
3. Lightly immobilize injured part in functional
positional and keep just below heart level.
4. Give plenty of reassurance.
5. Transport to medical facility as quickly as possible.
6. Do not pack in ice.
7. Use Sawyer Extractor over bite area if transport to
medical facility is to be in excess of 45 minutes.
Must be applied immediately.
8. Electroshock treatment for snakebite has been
recommended as initial therapy (Guderian et al, 1987),
but this unusual recommendation has been demonstrated
to be ineffective in an animal model (Howe &
Meisenheimer, 1988) and is potentially quite dangerous
(Russell, 1987).
B. INITIAL ASSESSMENT
1. Distinguish between venomous or nonvenomous snake,
other animal bite, or plant thorn injury.
2. Determine where, when, and under what conditions injury
occurred.
3. Establish time and sequence of manifestations.
4. Grade of envenomation in pit viper bites:
a. TRIVIAL ENVENOMATION: Manifestations remain confined
to or around the bite area. No systemic symptoms or
signs. No laboratory changes.
b. MINIMAL ENVENOMATION: Manifestations confined to area
of bite, with minimal edema immediately beyond that
area. Perioral paresthesia may be present, but no
other systemic symptoms or signs. No laboratory
changes.
c. MODERATE ENVENOMATION: Manifestations extend beyond
immediate bite area. Significant systemic symptoms
and signs. Moderate laboratory changes; ie, decreased
fibrinogen and platelets, and hemoconcentration.
d. SEVERE ENVENOMATION: Manifestations involve entire
extremity or part. Serious systemic symptoms and
signs. Very significant laboratory changes.
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Topic: SNAKE VENOM POISONING

e. GRADING BY NUMBERS
(1) The method of grading rattlesnake bites by numbers on
the basis of selected symptoms and signs is
inadequate. Every finding should be considered in
determining the severity of the poisoning. Pain,
swelling, ecchymosis and local tissue changes may be
absent or minimal, even after a lethal injection of
some rattlesnake venoms, and these findings are too
commonly employed as the sole guides for grading the
envenomation.
(2) For that reason, poisoning should be noted as
trivial, minimal, moderate or severe, bearing in mind
all clinical manifestations, including changes in the
blood cells and blood chemistry, deficiencies in
neuromuscular transmission, changes in motor and
sensory function, and the like.
5. Evaluate status of preadmission treatment. If
tourniquet or tight band has inadvertently been placed,
apply less constricting band proximal to tourniquet,
start IV infusion of a crystalloid solution, remove
tourniquet slowly, and observe.
5.3.2 TREATMENT
A. INITIAL TREATMENT
1. To be effective, treatment must be instituted
immediately.
2. Start IV infusion of crystalloid solution (eg, lactated
Ringer's or sodium chloride, USP). If shock or severe
bleeding present, consider colloid solutions, plasma or
whole blood.
3. Cleanse wound with soap and water.
4. Loosely immobilize affected part at heart level and in
functional position.
5. Keep patient at rest and give reassurance.
6. Give antitetanus agent for tetanus prophylaxis.
7. When patient is stable, give appropriate analgesic, if
indicated.
8. Administer sedative to produce mild sedation, if
necessary.
9. Under no conditions should injured part be placed in
ice, the bite area excised, nor should a fasciotomy be
performed at this time.
B. ANTIVENIN
1. The importance of early antivenin administration,
preferably intravenously, cannot be overemphasized. The
amount to be used will depend upon the species and size
of snake, the site of envenomation, the size of the
patient and other factors. Poisoning by water
moccasins usually requires lesser doses, whereas in
copperhead bites, antivenin therapy is usually required
only for children and the elderly or severely
envenomated.
2. Recent studies indicate efficacy of antivenin when
given within 4 hours of a bite; it is of less value if
delayed for 8 hours, and questionable value after 26
hours. However, it seems advisable to recommend its
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Topic: SNAKE VENOM POISONING

use up to 30 hours in all severe cases of crotalid
poisoning.
3. When the offending snake is an imported species, the
physician should consult the nearest Poison Control
Center for guidance on the availability and choice of
antivenin. The larger zoos of the country usually
stock supplies of antivenins and have emergency
programs for dispensing them, and addresses of
consulting physicians.
4. Skin test (See antivenin brochure). If positive,
patient should be treated in an intensive care setting,
if antivenin is necessary to save life or limb.
5. Administer Antivenin (Crotalidae) Polyvalent IV in
dilution, initially at a slow rate and then at a faster
rate (15 to 20 minutes per vial) if no reaction occurs.
a. Minimal envenomation 5 to 8 vials; moderate 8 to 12;
severe 13 to 30+. No antivenin is indicated in
trivial bites.
b. To administer, dilute each vial to 50 to 200 ml (eg, 5
vials in 250 to 1000 ml diluent), and give
intravenously by continuous infusion. Reduce volume
of diluent as required in pediatric patients.
c. Attempt to give total dose during first four to six
hours.
d. Use after 24 hours to reverse coagulopathy.
6. Administer North American Coral Snake Antivenin
(Micrurus fulvius) IV in continuous drip.
a. If there is a definite bite, 3 to 5 vials in diluent
(eg, 250 to 500 ml of sodium chloride injection, USP)
should be given as early as possible.
b. If symptoms and signs develop, 3 to 5 additional vials
should be administered, and more as indicated.
7. If necessary to administer IM, give in buttocks. DO
NOT give IM unless IV administration is absolutely
impossible.
8. Never inject antivenin into a toe or finger.
9. If patient has a reaction to the antivenin, discontinue
its use for 5 minutes, give diphenhydramine IV, and
then start antivenin more slowly under close
observation, and with shock cart at hand. If a further
reaction occurs, discontinue antivenin and seek
consultation.
10. Measure circumference of involved part just above bite
and 10 and 20 cm above this point. Record every 15
minutes during antivenin administration and every 1 to
2 hours thereafter to document edema.
11. Have tourniquet, oxygen, epinephrine, shock drugs,
tracheostomy equipment and positive-pressure breathing
apparatus available.
C. SUPPORTIVE MEASURES
1. Observe patient for minimum of 4 hours in all cases of
snakebite.
2. DO NOT leave patient unattended.
3. Vasopressors should only be used short-term to treat
hypotension. Parenteral fluid challenge is usually
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Topic: SNAKE VENOM POISONING

adequate.
4. Heparin is not recommended for coagulopathies.
5. Broad spectrum antibotic if severe tissue involvement.
6. Plasma, albumin, whole blood or platelets, as
indicated.
7. Limit IV fluids during period of acute edema.
8. Liquid or soft diet, as tolerated.
9. Maintain airway.
10. Oxygen or positive-pressure breathing as necessary.
11. Antihistamines or steroids to treat allergic reactions
to antivenin or venom. DO NOT USE STEROIDS DURING
ACUTE PHASE OF POISONING, except in conditions of shock
or severe allergic reactions.
D. FOLLOW-UP CARE
1. Cleanse and cover wound with sterile dressing.
2. Debridement, if necessary, third to tenth day. Elevate
extremity slightly if swelling is severe and there are
no systemic manifestations or abnormal laboratory
findings.
3. Soak part for 15 minutes 3 times daily in 1:20 Burow's
solution.
4. Paint wound twice weekly following debridement with an
aqueous dye of brilliant green 1:400, gentian violet
1:400, and N-acriflavin 1:1000. Apply antimicrobial
cream (Neomycin or similar) at bedtime.
5. Physical therapy evaluation on 3rd or 4th day; start
active exercise immediately.
5.3.4 PATIENT DISPOSITION
5.3.4.5 OBSERVATION CRITERIA
A. Observe patient for minimum of 4 hours in all cases of
snakebite.
6.0 RANGE OF TOXICITY
6.6 LD50/LC50
A. Data on the toxicity of crotalid venoms is shown in the
table:
Avg length Approx yield
of adult dry venom IP LD50 IV LD50
(inches) (mg.) (mg/kg) (mg/kg)
Rattlesnakes
Eastern 32-65 370-700 1.89 1.68
diamondback
Western 30-65 175-320 3.71 1.29
diamondback

Red diamond 32-52 120-350 6.69 3.70
Timber 32-54 75-100 2.91 2.63
Prairie 32-46 35-100 1.60 1.61
Southern 32-48 75-150 3.71 1.29
Pacific
Great Basin 32-46 75-150 2.20 1.70
Mojave 22-40 50-90 0.23 0.21
Sidewinder 18-30 18-40 4.00 1.82
Moccasins
Cottonmouth 30-50 90-145 5.11 4.00
Copperhead 24-36 40-70 10.50 10.92
Coral snakes
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Topic: SNAKE VENOM POISONING

Eastern coral 16-28 2-6 0.97 0.23
9.0 PHARMACOLOGY/TOXICOLOGY
9.2 TOXICOLOGIC MECHANISM
A. The common practice of dividing snake venoms into such
groups as neurotoxins, hemotoxins, cardiotoxins and the
like, has led to much misunderstanding and to grave
errors in clinical judgement. Chemical, pharmacological
and clinical studies have shown these divisions to be
both superficial and misleading.
B. Snake venoms are complex mixtures and the physician
attending a patient with snake venom poisoning must
remember that he is faced with a case of multiple
poisoning, perhaps three or more toxic reactions, with
pharmacological changes that may occur simultaneously or
consecutively.
C. It should also be remembered that the effects of various
combinations of the venom components, and of metabolites
formed by their interactions, can be complicated by the
response of the victim. The release of
autopharmacological substances by the envenomated patient
may complicate the poisoning and make treatment more
difficult.
D. The venoms of pit vipers produce deleterious local tissue
effects, changes in blood cells, defects in coagulation,
injury to the intimal linings of the vessels and changes
in blood vessel resistances. The hematocrit may fall
rapidly and platelets may disappear. Pulmonary edema is
common in severe poisoning and bleeding phenomena may
occur in the lungs, peritoneum, kidneys and heart. These
changes are often accompanied by alterations in cardiac
dynamics and renal function.
E. Most of our crotalid venoms produce relatively minor
changes in transmission at the neuromuscular junction,
the notable exception being the venom of the Mojave
rattlesnake, which also produces far less tissue
destruction. The early cardiovascular collapse seen in
an occasional patient bitten by a rattlesnake is due to a
marked fall in circulating blood volume. Although
cardiac dynamics may be disturbed, in most cases the
heart changes may be secondary to the decrease in
circulating blood volume.
F. Coral snake venom causes more marked changes in
neuromuscular transmission and in conduction in nerves,
but death may occur from cardiovascular collapse quite
apart from the neurotropic changes.
12.0 REFERENCES
12.1 GENERAL REFERENCES
1. Conant R: Field Guide to Reptiles and Amphibians.
Houghton Mifflin, Boston, 1958.
2. Dowling H, Minton SA & Russell FE: Poisonous Snakes of the
World, U.S. Government Printing Office, 1968.
3. Garfin SR, Castilonia RR & Mubarak SJ: The effects of
antivenin on intramuscular pressure elevations induced by
rattlesnake venom. Toxicon 1985; 23:677-680.
4. Guderian RH, MacKenzie CD & Williams JF: High voltage
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Topic: SNAKE VENOM POISONING

shock treatment for snake bite (letter). Lancet 1986;
2:229.
5. Howe NR & Meisenheimer JL Jr: Electric shock does not save
snakebitten rats. Ann Emerg Med 1988; 17:245-256.
6. Jimenez-Porras JM: Biochemistry of snake venoms. Clin
Toxicol 1970; 3:389.
7. Klauber LM: Rattlesnakes, Univ Calif Press, Berkeley,
1956.
8. Lee CY: Snake Venoms, Springer, Berlin, 1979.
9. McCullough N & Gennaro J: Evaluation of venomous snakebite
in the southern United States from parallel clinical and
laboratory investigations. J Fla Med Assoc 1963; 49:959.
10. Minton SA: Venom Diseases. C.C. Thomas, Springfield,
Illinois, 1974.
11. Picchioni AL et al: Snake Venom Poisoning (chart),
American Association of Poison Control Centers and
American College of Emergency Physicians, 1984.
12. Picchioni AL, Hardy DL, Russell FE et al: Management of
poisonous snakebite. Vet Hum Toxicol 1984; 26:139-140.
13. Riggs BS, Smilkstein MJ, Kulig KW et al: Rattlesnake
evenomation with massive oropharyngeal edema following
incision and suction (Abstract). Presented at the
AACT/AAPCC/ABMT/CAPCC Annual Scientific Meeting,
Vancouver, Canada, September 27-October 2, 1987.
14. Russell FE: Snake venom poisoning, In: Cyclopedia of
Medicine, Surgery & the Specialities, Persol, G.M. (Ed),
F.A. Davis, Philadelphia, 1971.
15. Russell FE: Snake Venom Poisoning. JB Lippincott,
Philadelphia, 1980; Scholium International, Great Neck,
NY, 1983.
16. Russell FE: A letter on electroshock for snakebite. Vet
Hum Toxicol 1987; 29:320.
17. Russell FE & Brodie: Venoms of reptiles, In: Chemical
Zoology, Vol IX, Academic Press, New York, 1974.
18. Russell FE & Puffer H: Pharmacology of snake venoms.
Clin Toxicol 1970; 3:433.
12.2 CONSULTANTS
A. Wyeth Laboratories maintains a national 24-hour emergency
medical information number at (215) 688-4400. They will
accept collect calls in an emergency situation.
1. ATLANTA P.O. Box 4365 Atlanta, Georgia 30302 Tel: (404)
873-1681
2. BALTIMORE 101 Kane Street Baltimore, Maryland 21224 Tel:
(301) 633-4000
3. BOSTON (ANDOVER) P.O. Box 1776 Andover, Massachusetts
01810 Tel: (617) 475-9075
4. CHICAGO (WHEATON) P.O. Box 140 Wheaton, Illinois
60189-0140 Tel: (312) 462-7200
5. CLEVELAND P.O. Box 91549 Cleveland, Ohio 44101 Tel:
(216) 238-9450
6. DALLAS P.O. Box 38200 Texas 75238 Tel: (214) 341-2299
7. KANSAS CITY P.O. Box 7588 No. Kansas City, Missouri
64116 Tel: (816) 842-0680
8. LOS ANGELES P.O. Box 5000 Buena Park, California 90620
Tel: (714) 523-5500 (Buena Park); (213) 627-5374 (Los
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Topic: SNAKE VENOM POISONING

Angeles)
9. MEMPHIS P.O. Box 1698 Memphis, Tennessee 38101 Tel:
(901) 353-4680
10. PEARL CITY (HAWAII) 96-1185 Waihona Street Unit C1,
Pearl City, Hawaii 96782 Tel: (808) 456-4567
11. PHILADELPHIA (PAOLI) P.O. Box 61 Paoli, Pennsylvania
19301 Tel: (215) 878-9500
12. ST. PAUL P.O. Box 64034 St. Paul, Minnesota 55164 Tel:
(612) 454-6270
13. SEATTLE P.O. Box 5609 Kent, Washington 98064-5609 Tel:
(206) 872-8790
B. CONSULTANTS
1. Richard W. Carlson, M.D., Ph.D., Mount Carmel-Mercy
Hospital and Medical Center, 6071 W. Outer Drive
Detroit, Michigan 48235.
2. Roger Conant, Sc.D., Biology Department, University of
New Mexico, Albuquerque, New Mexico 87131 (for
identification of snakes).
3. David Hardy, M.D., Route 15, Box 259, Tucson, Arizona
85715.
4. L. P. Laville, Jr., M.D., The Baton Rouge Surgical
Group, Doctors Plaza, 3955 Government Street, Baton
Rouge, Louisiana 70806.
5. Lawrence Leiter, M.D., 21530 W. Golden Triangular Road,
Saugus, California 91350.
6. Sherman A. Minton, Jr., M.D., Indiana University Medical
Center, 1100 West Michigan Street, Indianapolis, Indiana
46207, (317) 264-7671 or 264-7842 (office), (317)
849-2596 (home).
7. Findlay E. Russell, M.D., Ph.D., Department of
Pharmacology and Toxicology, College of Pharmacy,
University of Arizona, Tucson, Arizona 85721.
8. L.H.S. Van Mierop, M.D., Department of Pediatrics,
University of Florida, College of Medicine, Gainsville,
Florida 32610.
9. Charles H. Watt, M.D., 900 Gordon Avenue, Thomasville,
Georgia 31792.
10. S. R. Williamson, M.D., 307 Medical Tower, Norfolk,
Virginia, (804) 625-7406 (804) 484-7151.
11. Willis A. Wingert, M.D., Univ. of So. Calif. Med.
Center, 1129 N. State Street, Los Angeles, California
90033, (213) 226-3600 (714) 626-3935.
13.0 AUTHOR INFORMATION
A. Written by: Findlay E. Russell, M.D., PhD., 06/81
B. Reviewed by: Findlay E. Russell, M.D., PhD., 06/84
C. Revised by: Findlay E. Russell, M.D., PhD., 07/86;
01/88

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