Substances & Homeopatic Remedies

Lachesis mutus

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Venom is proteolytic, coagulant, vasculotoxic, neurotoxic.

Initial symptoms are similar to those of bothropic envenomation: intense pain, nausea, vomiting, sweating, and excitability, but differing in the magnitude of a tremendous edema and in the absence of intensive bleeding and phlyctenae. There are also important alterations in arterial blood pressure and in the activity and concentration of coagulation factors' (Bolanos et al. 1982)

General information about snakes and bites:

The chemistry of snake venoms is complicated. Venoms are at least 90% protein (by dry weight) , and most of the proteins in venoms are enzymes . About twenty-five different enzymes have been isolated from snake venoms , ten of which occur in the venoms of most snakes . Proteolytic enzymes , phospholipases , and hyaluronidases are the most common types . Proteolytic enzymes catalyze the breakdown of tissue proteins . Phospholipases , which occur in almost all snakes , vary from mildly toxic to highly destructive of musculature and nerves . The hyaluronidases dissolve intercellular materials and speed the spread of venom through the prey’s tissue . Other enzymes include collagenases , which occur in the venom of vipers and pitvipers and promote the breakdown of a key structural componenet of connective tissues (the protein collagen) ; ribonucleases , deoxyribonucleases , nucleotidases , amino acid oxidases , lactate dehydrogenases , and acidic and basic phosphatases all disrupt normal cellular function , causing the collapse of cell metabolism , shock , and death .

Not all toxic chemical compounds in snake venoms are enzymes . Polypeptide toxins , glycoproteins , and low-molecular-weight compounds are also present in mambas and colubrids . The roles of the other components of venom are largely unknown .
Every snake’s venom contains more than one toxin , and in combination the toxins have a more potent effect than the sum of their individual effects . In general , venoms are described as either neurotoxic (affecting the nervous system) or hemotoxic (affecting the circulatory system) , although the venoms of many snakes contain both neurotoxic and hemotoxic components .

Venom componenets are broadly categorized by how they work to disrupt normal function .

Enxymes - found in all snake venoms-spur on physiologically disruptive or destructive process .
Proteolysins - found mostly in viper and pitviper venom-dissolve cells and tissue at the bite site , causing local pain and swelling .
Cardiotoxins - associated mostly with elapids ad vipers-have variable effects ; some depolarize cardiac muscles and alter heart contraction , causing heart failure .
Hemorrhagins - occurring in the venom of vipers , pitvipers , and the king cobra-destroy capillary walls , causing hemorrhages near and distant from the bite .
Coagulation - retarding compounds-found in some elapids-prevent blood clotting .
Thromboses - which some vipers have-coagulate blood and foster clot formation throughout the circulatory system .
Hemolysis - which are in the venom of elapids , vipers and pitvipers-destroy red blood cells .
Cytolysins - components of viper and pitviper venom-destroy white blood cells .
Neurotoxins - found in elapids , vipers , tropical rattlesnakes , and some North American Mojave rattlesnakes-block the transmission of nerve impulses to muscles , especially those associated with the diaphragm and breathing .
Venom composition can vary among individuals of the same species , and even in the same litter , but variation is greater among geographically different populations . For example , Mojave rattlesnakes (Crotalus scutulatus) from eastern Arizona and adjacent New Mexico have a special neurotoxin known as Mojave toxin , but their venom lacks hemorrhagic and some proteolytic properties . Venom from Mojave rattlesnakes of central Arizona lacks the Mojave but has strong hemorrhagic and proteolytic properties . Where the two populations overlap , individual rattlesnakes have a venom with intermediate properties .

Venom toxicity may also vary over time in the same individual . Generally speaking , the venom of newborn and small juvenile snakes appears to be more potent than that adults of the same species . Also , a bite from a snake that has not fed recently , such as one that has just emerged from hibernation , is more dangerous than that of one that has recently fed , because it has more venom to inject . Venom glands must replace venom lost with each strike-bite , and full replacement takes time .

Chemical Components Of Snake Venoms

Peptide bradykinin potentiators .
 Peptide bradykinin potentiators .
Proteolytic enzymes .
Hyluronidases .
Proteases .
Thrombinlike enzymes
Nerve growth factor (an enzyme) .
Other enzymes : ribonucleases , deoxyribonucleases , nucleotidases , amino acid oxidases , lactate dehydrogenases , acidic and basic phosphatases .
Glycoproteins .
Nucleotides (amino acids) .
Biogenic amines .
Acectylcholine .

Other Components (Organic and Ignorganic)

Nontoxic organic components and organic components with unclear roles :
Carbohydrates : Neutral sugars , Amino sugars , Sialic acid .
Lipids : Cholesterol , Monoglycerides , Diglycerides , Triglycerides , Phospholipids .

Inorganic ions (which activate and deactivate enzymes) :
Macrocomponents : Calcium , Chlorine , Copper, Iron , Magnesium , Manganese , Nickel , Phosphate , Potassium , Sodium , Sulfate , Zinc .
Microcomponents : Bismuth , Gold , Molybdnum , Palladium , Platinum , Selenium , Silver . Water .
How Many Snakes Are Venomous ?
Four families of snakes (Atractaspididae , Colubridae , Elapidae , and Viperidae) include species dangerous to humans , a total of roughly 450 species or about 19% of all snake species . In none of these families are all species lethal to humans , although all atractaspidine , elapid , and viperid snakes are venomous . Generally speaking , the venoms most dangerous to humans are those of snakes that specialize on warm-blooded prey . Because human physiology is similar to that of prey , the venoms react similarly in humans .But humans are also sensitive to snake venoms adapted to kill prey other than birds or mammals .

Danger may vary with the volume of venom injected . Even a mildly toxic venom is lethal if the snake injects enough of it . Conversely , a snake with a highly toxic venom is not dangerous if it is small and incapable of breaking the skin , or if it does not bite in defense . The Sonoran coralsnakes (Micruroides euryxantus) have small mouths and usually do not break the skin when they bite . Some species have venom-delivery systems that do not permit them to deliver venom efficiently to large animals . Other species rarely come in contact with humans .
In the large family Colubridae , about one-quarter of the species (over 600 species) have fangs , or at least enlarged and grooved maxillary teeth . But only four have caused human fatalities : the African boomslang (Dispholidus typus) , Oriental tigersnake (Rhabdophis tigrina) , African birdsnake (Thelotornis kirtlandii) , and Peruvian gray falseviper (Tachymenis peruviana) . In the other three families , all species have fangs and should be considered potentially dangerous , though some are small or have venoms with weak effects on humans .

The salivas of some non-venomous colubrids have , in rare instances , caused mild to moderate poisoning in humans . In the United States , people have had reactions to bites of the black-striped snake (Coniophanes imperialis) , ringneck snake (Diadophis punctatus) , western hognose snake (Heterodon nasicus) , cat-eyed snake (Leptodeira septentrionalis) , Mexican vinesnake (Oxybelis aeneus) , western terrestrial gartersnake ( Thamnophis elegans) , common gartersnake (T . sirtalis) , and lyre snake (Trimorphodon biscutatus) . None of these snakes’ venom-delivery systems operates efficiently on humans ; most must chew for the venom to enter the wound . Symptoms of envenomation appear in fewer than 1% of gartersnake bites , though such bites are common among people who handle these snakes . It is possible that the salivas of all colubrids have a toxic component , and that some susceptible than others .

Proportions of venomous and nonvenomous snakes worldwide . Venomous snakes are here defined as those dangerous animals :

Nonvenomous snakes:
Nonvenomous colubrids : 64%
Blindsnakes : 12%
Boas and related species : 5%

Venomous snakes:
Vipers : 8%
Cobras and related species : 10%
Venomous colubrids : 1%

How Is Venom Injected ?
A snake’s fang correspond s to a syringe’s needle . In fact , the free end of the fang is identical to the tip of a needle . Both have sharp tips to penetrate skin and muscle , and discharge orifices near the tip . Finally , the jaw musculature surrounding the venom gland corresponds to the syringe’s plunger . The contraction of these muscles squeezes the gland , forcing venom from the lumen into the venom duct and outward through the fang .
Among the various venomous snakes , biologists have identified three distinct venom-delivery systems . There is evidence that each system evolved more than once . For instance , the folding fang of vipers and pitvipers is also found in the Australian deathadders and African stilettovipers , three groups that are not closely related . All three systems evolved from the basic snake tooth , which is slightly curved ond cone-shaped . This basic aglyphous (grooveless) tooth (a , without ; glyphe , carving or groove) occurs in all snakes , even those with fangs , and most snakes have only these grooved teeth . Evolution of grooved and , eventually , canaled teeth (fangs) occurred only on the maxillary bone of the upper jaw . The three types of venom-delivery systems differ with regard to the position of the fang on the maxillary , the nature of the venom groove or canal , and the mobility of the fang-maxillary unit .
Ancestral snakes were venomless and had only grooveless teeth . All blindsnakes , boas , pythons , and other henophidian snakes still have exclusively aglyphous teeth . The majority of the colubrid snakes-the largest and most diverse snake family-are also aglyhous , although some species have one or two enlarged rear teeth on each maxillary bone . These enlarged teeth may be separated from the front maxillary teeth by gap known as a diastema . A diastema commonly separates the enlarged rear teeth , whether grooved or not , from the smaller front maxillary teeth .
Snakes with enlarged rear maxillary teeth are termed opisthoglyphous (opiistho , behind) . In some opisthoglyphous colubrids the enlarged teeth are ungrooved , but most others have a groove on the face or the side of the enlarged tooth . Originally these elongated teeth probably served only to hold prey , and this use persists in gartersnakes (Thamnophis) . However , such teeth puncture the prey’s skin , and some saliva inevitably enters the puncture wounds . An adaptive advantage would have resulted from increasing the toxicity , digestive ability , or tranquilizing effects of saliva , and assuring its delivery deep into the wound . Any of these advantages would have driven the evolution of fangs and venom glands , producing a range of venoms and venom-delivery systems .
Evolution of venom-delivery systems proceeded in two main directions : toward fixed proteroglyhous (Protero , earlier) and toward hinged solenoglyphous fangs (soleno , pipe) . In both instances , the grooved tooth became a fang by virtue of closure of the groove and a shifting forward of the enlarged tooth to the front of the mouth .
In proteroglyphous snakes , the fangs are short because large fixed fangs would require a deepening of the mouth cavity to prevent the fangs from perforating the floor of the mouth . The proteroglyphous condition is typical of the elapid snakes (cobras , taipan , coralsnakes , seasnakes , and their relatives) . In many species , particularly the seasnakes , the fang is barely longer than the teeth behind it . Proteroglyphous snakes typically bite and hold their prey , and then chew to inject venom deep in the wound . This behaviour is virtually universal among seasnakes , whose fish prey would otherwise swim or drift away before being incapacitated an envenomating strike-bite and withdraw . The largest elapid , the king cobra (Ophiophagus hannah) , has fangs only 8 to 10 millimeters long ; fangs are less than 8 millimeters long in mambas (Dendroaspis) , less than 7 millimeters in Indian cobras (Naja naja) , and less 3 millimeters long in adult harlequin coralsnakes (Micrurus fulvius) and yellow-bellied seasnakes (Pelamis platurus) .
The hinged fangs of the vipers and pitvipers (Viperidae) represent a more intricate system that allows a snake to strike , envenomate , and withdraw from the struggling prey , thereby avoiding injury . The hinged fang sits at the front of the mouth on a short maxillary bone that can rotate forward and backward . When not in use , the fang folds backward and upward against the roof of the mouth , where it lies enclosed in a membranous sheath . During a strike , the maxilla rotates forward , erecting the fang , and the mouth opens nearly 180 degrees . AS the mouth strikes the prey , the jaws close , propelling the fangs into the prey ; the venom is injected at the time of penetration . The right and left fangs can be rotated independently , although they erect jointly . A viper often works its fangs back into their resting sheaths one at a time after swallowing its prey .
The advantage of folding fangs is that long fangs can be housed in the mouth without perforating the floor of the mouth . Viperids have significantly longer fangs than the proteroglyphous elapids , and some viperids seem to have taken the evolutionary opportunity of lengthening their fangs to the extreme . Bitis , a group of African vipers , have the longest fangs known : up to 28 millimeters in the puffadder (B . arietans) , and over 30 millimeters in large Gaboon vipers (B . gabonica) . Even in the smaller copperhead (Agkistrodon contortrix) and common European viper (Vipera berus) , fangs are 7 millimeters or longer .
Folding fangs occur in two other groups of snakes . The Australian deathadders (Acantophis) , though they are elapids , are solenoglyphous . Their folding-fang mechanism is very similar in appearance and operation to that of the vipers and pitvipers . The deathadders also have the body shape and ambush-hunting habits of many viperids , an excellent example of convergent evolution .
The African molevipers (Atractaspidinae) are also solenoglyphous . Their short maxillary bones rotate and bear long fangs , but their strike-bite differs from that of the viperids and deathadders . They are burrowers , and the confines of narrow burrows make a typical rearing strike impossible . Instead they crawl along side their prey , open their mouths slightly , and shift the lower jaw away from the prey , freeing the fang nearest the prey . With a backward and sideward stab , they embed the fang , and inject venom into their prey (typically newborn rodents and burrowing lizards) . Because they stab backward , rather than biting forward , a snake handler who grabs one behind the head often ends up with a fang embedded in a finger or thumb ; this accounts for the snake’s common name , stilettoviper .
Newborn venomous snakes are fully operational . They have fangs and inject venom when bite . Throughout the lives of all snakes , however , teeth and fangs are shed and replaced regularly . An ordinary tooth is replaced by one that form beneath it , eventually loosening and then pushing it out of its socket . Proteroglyphous and solenoglyphous fangs are replaced an a somewhat different fashion . A series of five to seven replacement fangs lies in the gums of behind and above the functional fang . these replacement fangs are arranged in a graduated series , the largest adjacent to the functional fang . AS the functional fang wears down , it is replaced by the next fang . The reserve-fang series than shifts forward , so that a replacement fang is always available to replace a damaged functional fang .
The replacement fangs do not develop fully formed but in miniature ; instead , the growth process forms the tip first and then builds up the base , thus enlarging the fang and pushing the tip outward . The hollow-needle shape is apparent early in development . Functional fangs are shed in cycles as short as ten days and as long as six to ten weeks , depending on the species and the health of the individual snake . During the replacement phase , a snake may briefly have two fangs on each side of its head .

Do Snakes Spit Their Venom ?
Some cobras can spray their venom for a distance of up to 2.5 meters . This action is called spitting , but it does not evolve puckering the lips and blowing the venom outward . Spitting is a defensive behaviour that has nothing to do with killing prey . Spitting cobras bite and envenomate their prey just as do other venomous snakes .

Venom-spitting apparently evolved at three separate times in the family Elapidae but in no other snake families . Two of the spitting-cobra groups are African ; one group is the African ringhal cobra (Hemachatus haemachatus) , and the second includes the black-necked cobra (Naja nigricollis) , the Mozambique spitting cobra (N . mossambica) , the Mozambique red spitting cobra (N . pallida) , and the wEst African spitting cobra (N . katiensis) . The third group of spitters is from eastern Asia and includes the golden spitting cobra (Naja sumatrana) of the Malay Peninsula and Sumatra , the Indonesian spitting cobra (N . sputatrix) of southern Indonesia , the common spiting cobra (N . philippinensis) and Samar spitting cobra (N . samarensis) of the Philippines , the Chinese and Indochinese populations of the Asian black cobra (N . atra) , and some populations of the widespread Asian monocled cobra (N . kaouthia) . These snakes live in areas inhabited by large herbivores that might trample them or large carnivores that might eat them , and thus use their venom defensively .

Spitting or spraying of venom involves no major evolutionary structural modification . The fangs of spitting cobras resemble those of their nonspitting relatives , except that the discharge orifice of the fang is greatly reduced in size and pointed more forward . When compression of the venom gland forces its secretion through the venom duct and hollow fang , the venom is not discharged from the fang as quickly as in a snake with a normal-sized discharge orifice . The venom thus backs up in the fang , creating greater pressure at the discharge opening than in a normal fang , and the venom sprays from the fang in tiny droplets instead of large drops . The snake aids expulsion of venom by forcibly collapsing its lung and blowing air out of its mouth . The air carries the venom in a pair of fine sprays aimed at the eyes of the intruder .

At close quarters , the spitting cobras have very accurate aim . If the neurotoxic venom reaches the eyes , it is quickly absorbed by the capillaries of the conjunctiva . The venom may cause temporary blindness by irritating the cornea ; extensive damage of the cornea can lead to permanenr blindness . The venom should be rinsed out of the eye as soon as possible .

Reports occasionally surface of venom-spitting by vipers or pitvipers (Viperidae) , some of which may sling venom around if agitated and striking violently . Some small West Indian boas of the genus Tropidophis are said to spit blood when disturbed ; these reports may be faulty observations of these snakes’ defensive behaviour of dripping blood from their eyes . The only true venom-spitting snakes are cobras .

How Dangerous Is A Snakebite ?
A snakebite is usually not dangerous , unless it involves one of the more than two hundred species that produce a potent venom . Every day , people are bitten by nonvenomous snakes and experience only the slight discomfort caused by the snake’s teeth puncturing or scratching the skin .Of course , such wounds may be painful if the snake has long teeth , such as those of a python or large ratsnake , but serious effects are rare . Bites by nonvenomous species can be treated by washing the wound and applying an antiseptic to the punctures or scratches . Bites by venomous snakes require medical treatment . If untreated , a venomous bite may result in serious tissue or organ damage and even death . Serious secondary bacterial infections , such as gas gangrene and tetanus , may also follow venomous snakebites , and loss of a limb , finger , or toe is not uncommon . A nonvenomous snakebite usually involves several puncture marks of equal depth ; that of a venomous snake is characterized by one or two larger and deeper punctures among more shallow marks . However , tooth marks are not a reliable method for identifying the potential danger of a snakebite .

If the snake is venomous , discomfort is usually felt within a few minutes . a burning sensation or pulsating pain is often accompanied by swelling or discoloration of the tissues surrounding the wound . Such localized discomfort is particularly particularly characteristic of hemotoxic envenomation by pitvipers and true vipers , but moderate to severe local pain may also accompany neurotoxic bites of some elapids .

Medical treatment should be obtained for all elapid bites , even when there is no pain . Serious elapid bites are not usually apparent , since immediate pain does not always occur . A characteristic early sign of a serious neurotoxic elapid bite is drooping eyelids , followed by difficulty in swallowing , slurred speech , severe thirst , vertigo , and difficulty in breathing . Later , blood pressure often drops , and cardiac arrest may occur .

The most extensive study , published nearly fifty years ago , estimated that 300,000 venomous snakebites occurred throughout the world each year , almost 40,000 of which resulted death . More recent coordinated data is unavailable . The rate of death from snakebite is highest in developing nations with extensive natural snake habitat and scarce medical facilities , and lowest in developed nations with plentiful medical facilities .

The more natural the habitat , the greater the chance of encountering a venomous snake . On the Indian subcontinent , about 7,000 to 15,000 people died annually of snakebite from 1940 to 1949 , a probable mortality rate of about four deaths per 100,000 people . The most frequent culprits were the various kraits (Bungarus) , cobras (Naja , Ophiophagus) , saw-scaled vipers (Echis) , and the Russel’s viper (Vipera russelii) . In Brazil 2,000 to 4,800 persons died annually of snakebite between1929 and 1949 , mostly due to the bites of the tropical rattlesnake (Crotalus durissus) and various large species of lanceheads (Bothrops) . In the United States , by contrast , only 10 to 20 persons died of snakebite each year from 1944 to 1950 , or fewer than 0.2 per 100,000 people . Over 90% of these fatal bites were attributed to the cottonmouth (Agkistrodon piscivrus) , western rattlesnake (Crotalus viridis) , and eastern and western diamondback rattlesnakes (C . adamanteus , C .atrox) . In 1957 and 1966 , H . M . Parrish reported 6,000 to 7,000 annual envenomations by snakes in the United States , causing 14 to 15 deaths . In Canada fewer than fifteen people died of snakebite during the period 1944-1948 , and in Europe the death rate from all venomous animal bites was less than 0.5 per 100,000 people .

Today , snakebite mortality worldwide is probably about 50% of what it was when the preceding data were compiled . Modern medical treatment has improved survivorship , and treatment is more widely available . Between 1965 and 1971 , for instance, only 18 of 5,387 venomous snakebites in Malaysia and 191 of 14,578 in Thailand were fatal .


Venoms And Clinical Manifestations : Snake venoms are complex mixtures of enzymes, low-molecular-weight polypeptides, glycoproteins, and metal ions. The enzymes and polypeptides affect the human body in a multisystem fashion. Among the deleterious components are hemorrhagins that render the vasculature leaky and thus cause both local and systemic bleeding; various proteolytic enzymes that cause local tissue necrosis, affect the coagulation pathway at various steps, or impair organ function; myocardial depressant factors that reduce cardiac output; and neurotoxins that act either pre- or postsynaptically to inhibit peripheral nerve impulses. Most snake venoms can adversely affect multiple organs.

Treatment (Field Management) : First-aid or "field" measures to be used in the management of venomous snakebite should focus on delivery of the victim to definitive medical care as quickly as possible; the victim should be as inactive as is feasible to limit systemic spread of the venom. Beyond this, any measure employed should at least do no further harm.

After viperid bites, local mechanical suction may be beneficial if applied to the puncture wounds within 3 to 5 min. A useful device is the Extractor (Sawyer Products, Safety Harbor, FL), which delivers one atmosphere of negative pressure to the wound. Suction should be continued for at least 30 min. Mouth suction should be avoided as it inoculates the wound with oral flora and theoretically can also result in the absorption of venom by the rescuer through lesions of the upper digestive tract. A proximal lymphatic-occlusive constriction band may limit the spread of venom if applied within 30 min. To avoid compounding of tissue necrosis, however, the band should not be allowed to interrupt arterial flow. A bitten extremity should be splinted if possible and kept at approximately heart level. Incisions into the bite site should never be made, and no form of cooling or electric shock is advantageous.

For elapid or sea snake bites, the Australian pressure-immobilization technique, in which the entire bitten extremity is wrapped with an elastic or crepe bandage and then splinted, is highly beneficial. The bandage is applied as tightly as it would be to treat a sprained ankle. This technique greatly restricts the absorption and circulation of venom from the bite site. However, an assessment of the potential utility of this method in viperid poisoning requires further research, as it may compound local tissue damage following these bites.

Treatment (Hospital Management) : Once in the hospital, the victim should be closely monitored (vital signs, cardiac rhythm, and oxygen saturation) while a history is quickly obtained and a brief but thorough physical examination is performed. The level of erythema/swelling in a bitten extremity should be marked and the circumferences measured in several locations every 15 min until swelling has stabilized. Large-bore intravenous access in unaffected extremities should be obtained in the event that hypotension develops. Early hypotension is due to pooling of blood in the pulmonary and splanchnic vascular beds; hours later, hemolysis and loss of intravascular volume into soft tissues may play important roles. Fluid resuscitation with normal saline or Ringer's lactate should be initiated for clinical shock. If the blood pressure response is inadequate after the administration of 20 to 40 mL/kg body weight, then a trial of 5% albumin (10 to 20 mL/kg) is in order. If volume resuscitation fails to improve tissue perfusion, vasopressors (e.g., dopamine) should be administered. Invasive hemodynamic monitoring (central venous and/or pulmonary arterial pressures) can be helpful in such cases. Central access must be obtained with extra caution if coagulopathy is evident.

Blood should be drawn for laboratory evaluation (including determination of blood type and cross-matching) as soon as possible, before the effects of circulating venom interfere with typing. Also important are a complete blood count to evaluate the degree of hemorrhage or hemolysis, studies of renal and hepatic function, coagulation studies to identify signs of consumptive coagulopathy, and testing of urine for blood or myoglobin. In severe cases or in the face of significant comorbidity, arterial blood gas studies, electrocardiography, and chest radiography may be necessary.

Attempts to locate a source of appropriate antivenin should begin early in all cases of known venomous snakebite, regardless of symptoms. If signs or symptoms develop, they may progress rapidly, making any delay in the administration of antivenin dangerous for the victim. Antivenins rarely offer cross-protection against snake species other than those used in their production unless the species are closely related. An example of good cross-protection is in the use of Australian tiger snake (Notechis scutatus) antivenin for sea snake bites (see below). The package insert accompanying a particular antivenin should be consulted for information regarding the spectrum of coverage. In the United States, assistance in finding antivenin can be obtained 24 hours a day from the University of Arizona Poison and Drug Information Center (520-626-6016).

Rapidly progressive and severe local findings (soft tissue swelling, ecchymosis, petechiae, etc.) or manifestations of systemic toxicity (signs and symptoms or laboratory abnormalities), are indications for the administration of intravenous antivenin. The package insert outlines techniques for reconstitution of antivenin (when necessary), skin-testing procedures (for potential allergy), and appropriate starting doses. Most antivenins are of equine origin and carry a risk of anaphylactic, anaphylactoid, and delayed-hypersensitivity reactions. Skin testing does not always reliably predict which patients will have an allergic reaction to equine antivenin; a skin test can be either false negative or false positive. Before antivenin infusion, the patient should receive appropriate loading doses of intravenous antihistamines (e.g., diphenhydramine, 1 mg/kg to a maximum of 100 mg; and cimetidine, 5 to 10 mg/kg to a maximum of 300 mg) in an effort to limit acute reactions. Expanding the patient's intravascular volume with crystalloids may also be beneficial in this regard (unless contraindicated by the patient's cardiac status). Epinephrine should be immediately available, and the antivenin dose to be administered should be diluted (e.g., in 1000 mL of normal saline, Ringer's lactate, or 5% dextrose in water for adults or in 20 mL/kg for children). This volume can be decreased if necessary for the treatment of patients with compromised cardiovascular reserve. The antivenin infusion should be started slowly, with the physician at the bedside to intervene in the event of an acute reaction. The rate of infusion can be increased gradually in the absence of allergic phenomena until the total starting dose has been administered (over a period of 1 to 4 h). Further antivenin may be necessary if clinical abnormalities worsen. Laboratory values should be rechecked hourly, particularly if abnormal, until stability is ensured.

The management of a life-threatening envenomation in a victim with an apparent allergy to antivenin requires significant expertise. Consultation with a poison specialist, an intensive care specialist, or an allergist is recommended. Often, antivenin can still be administered in these situations under closely controlled conditions and with intensive premedication (e.g., with epinephrine, antihistamines, and steroids).

Care of the bite wound should include application of a dry sterile dressing and splinting of the extremity with padding between the digits. Because of the risk of central spread of venom, an extremity should be elevated only when antivenin is available. Tetanus immunization should be updated as appropriate. The use of prophylactic antibiotics is controversial, as the incidence of secondary infection following venomous snakebite appears to be low. Many authorities, however, prescribe a broad-spectrum antibiotic (such as ampicillin or a cephalosporin) for the first few days.

If swelling in the bitten extremity raises concern that subfascial muscle edema may be impeding tissue perfusion (muscle-compartment syndrome), intracompartmental pressures should be checked watched for at least 6 to 8 h before discharge. An occasional viperid "dry" bite progresses to significant toxicity after a delay of several hours, and the onset of systemic symptoms is commonly delayed for a number of hours after bites by several of the elapids (especially the coral snakes) and sea snakes. Patients bitten by these reptiles should be observed in the hospital for 24 h.

Morbidity And Mortality : The overall mortality rates for venomous snakebite are low in areas of the world with rapid access to medical care and appropriate antivenin. In the United States, for example, the mortality rate is 1 percent for victims who receive antivenin. Eastern and western diamondback rattlesnakes (Crotalus adamanteus and Crotalus atrox, respectively) are responsible for most snakebite deaths in the United States. Snakes responsible for large numbers of deaths in other regions of the world include the cobras (Naja species) of Asia and Africa, the carpet and saw-scaled vipers of the Middle East and Africa (Echis species), Russell's viper (Vipera russelli) of the Middle East and Asia, the large African vipers (Bitis species), and the lancehead pit vipers of Central and South America (Bothrops species).

The incidence of morbidity in terms of permanent functional loss in a bitten extremity is difficult to estimate but is probably substantial. Such loss may be due to muscle, nerve, or vascular injury or to scar contracture. In the United States, such loss due to snakebite tends to be much more common and severe after rattlesnake bites than after bites by copperheads or water moccasins.

What Is Antivenom ?
Antivenom is a serum that is commercially produced to neutralize the effects of envenomation by venomous snakes . The fresh snake venom used to produce antivenom is obtained either by manually milking a sinkae or by electrical stimulation . Venom is extracted from captive snakes every twenty or thirty days . In manual milking , the snake is held behind its head and induced to bite a thin rubber diaphragm covering a collecting vessel while the handler applies pressure to the snake’s venom glands . The pressure is maintained until no more venom is discharged . In electrical stimulation , electrodes are touched to the opposite sides of the snake’s head , causing the muscles around the venom gland to contract , expelling venom into a collection container . The venom is freeze-dried (the preferred method) , or dried with the help of a drying agent or a vacuum .

Healthy horses , usually seven to eight years old , are injected at regular intervals with non-lethal doses of a solution prepared from the freeze-dried venom until they build up an immunity to the venom . The dosage can then be slowly increased over time to create greater immunity . The horse’s immune system neutralizes the venom by producing antibodies (specialized proteins) . These horse antibodies in turn neutralize the same venom when injected into humans .

To obtain the antibodies , a small amount of blood (6 to 8 liters) is regularly removed from the horse’s jugular vein . The blood is combined with a sodium-citrate solution , to prevent coagulation and degradation , and the globulin to which the antibodies are attached is separated out and purified . About twenty-five laboratories throughout the world produce antivenoms for the venomous snakes in their regions .