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
    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
        (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
 
 

           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)
         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
        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
        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
        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.
      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
        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
         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
   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
     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
        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
14.0  SOURCE INFORMATION
      Distributed through the Cobra Information Site
      WWW at http://Cobras.net

Myths and legends have always captivated us but sometimes not for the right reasons. They alter the facts and rope us into believing that there is truth behind them. One reptile that is the subject of many legends is the snake. 

Read on to find out six common misconceptions revolving these interesting creatures.  

1. When feeding, snakes dislocate their lower jaw

Ouch, that sounds painful! Can a creature, like a snake, really be that hungry to swallow something larger than its own head?! This myth seems to suggest so, but the truth is more comfortable to swallow. 

The fact is that serpents are superbly flexible. Their lower jaw is divided into two halves called “mandibles.” These bones aren’t joined like ours are. Instead, they have a stretchy ligament that attaches the mandibles and helps them to move apart once dinner is on.  

2. Certain serpents are poisonous

Some snakes are indeed dangerous, and being near them isn’t such a good idea. However, it can get a touch confusing when you refer to these slithery reptiles as being poisonous and venomous. The two terms cannot be used interchangeably as they have different meanings.

While poison gets to work when ingested, inhaled, or absorbed through the skin, venom is any toxic substance administered through fangs, stingers, and so on. Poisonous snakes are rare, but it’s the venomous ones you want to watch out for. There are more than a whopping 600 venomous reptiles out there! Venomous North American Snakes are ones to bear in mind.

3. Rattlesnakes rattle before lashing out, without fail!

This certainly sounds quite believable! You’d think a rattlesnake would rattle away before pouncing on their prey. However, contrary to popular belief, this is a common misconception. 

Our serpentine buddies use their rattling mechanism to warn potential attackers by vibrating their tails. They don’t have to sound the warning either and can choose to skip the rattling part altogether. So next time you are crossing through a rattlesnake infested area, tread carefully! 

4. Say what? Snakes are deaf!

Our reptile friends lack eardrums, which would make you think they can’t hear airborne sounds. However, reasonably new research suggests otherwise. Regardless of lacking eardrums, snakes still have inner ears that attach to their jawbones. When resting or moving, they can pick up on vibrations in the ground, such as footsteps. Once movement is flagged up by their nifty jaw, the soundwaves are transmitted to their brain and processed.

In 2011, biologist Christian Christensen observed the brains of some ball pythons – Python regius. He found that his test subjects had no problem detecting low-frequency airborne sounds because their skulls vibrated in sync with them! So snakes aren’t deaf, after all! 

5. Slithery serpents asphyxiate their prey

We can finally put the strangulation assumption to bed now. Many believed that boas and pythons fatally choked their victims. What has been fund with recent research is that they kill by restricting their prey’s blood flow. Dr. Scott Boback and his team put to work this myth that has been circulating for many years, and now, thanks to their hard work, we can finally say that snakes don’t strangle their victims. 

6. Serpents are jam-packed with slime 

Snakes are most certainly not as grimy as they are thought to be. Covered and oozing in slime, they most certainly aren’t. Instead, they’re coated with dry scales and can feel like even sand flowing through your fingers when handled. Sounds a lot nicer than slime, that’s for sure!

So there you have it, folks! Six common misconceptions about snakes debunked right here!