Carbon monoxide poisoning occurs after the inhalation of carbon monoxide gas. Carbon monoxide (CO) is a product of combustion of organic matter under conditions of restricted oxygen supply, which prevents complete oxidation to carbon dioxide (CO2). Carbon monoxide is colorless, odorless, tasteless, and non-irritating, making it difficult for people to detect.
Carbon monoxide is a significantly toxic gas with poisoning being the most common type of fatal poisoning in many countries.[1] Symptoms of mild poisoning include headaches, vertigo, and flu-like effects; larger exposures can lead to significant toxicity of the central nervous system and heart. Following poisoning, long-term sequelae often occur. Carbon monoxide can also have severe effects on the fetus of a pregnant woman.
The mechanisms by which carbon monoxide produces toxic effects are not yet fully understood, but hemoglobin, myoglobin, and mitochondrial cytochrome oxidase are thought to be compromised. Treatment largely consists of administering 100% oxygen or hyperbaric oxygen therapy, although the optimum treatment remains controversial.[2] Domestic carbon monoxide poisoning can be prevented by the use of household carbon monoxide detectors.
Sources
0.1 ppm - natural background atmosphere level (MOPITT)
0.5 to 5 ppm - average background level in homes[5]
5 to 15 ppm - levels near properly adjusted gas stoves in homes[6]
100-200 ppm - Mexico City central area from autos etc.[7]
5,000 ppm - chimney of a home wood fire[8]
7,000 ppm - undiluted warm car exhaust[9]
30,000 ppm - undiluted cigarette smoke[10]
Common sources of CO that may lead to poisoning include house fires, furnaces or heaters, wood-burning stoves, motor vehicle exhaust, and propane-fueled equipment such as portable camping stoves, ice resurfacers,[3] forklifts,[4] engine-driven generators,[5] and gasoline-powered tools such as high-pressure washers, concrete cutting saws, power trowels, floor buffers, and welders used in buildings or semienclosed spaces.[6] CO poisoning can also occur in scuba diving due to faulty or badly sited diving air compressors. (See Effects of relying on breathing equipment while underwater for more information.) Generators and propulsion engines on boats --especially houseboats --have resulted in fatal carbon monoxide exposures. [7] Another source is exposure to the organic solvent methylene chloride, which is metabolized to CO by the body.[8]
Polluted air often contains unhealthy levels of carbon monoxide. Many areas of the US have struggled to achieve legislated limits. Significant advances have been made since the implementation by 1990 of a vehicle emissions limit of 3.4 gpm (grams per mile), a large reduction from the previous limit of 87 gpm. [11] [12] [13] [14]
[edit] Epidemiology
Carbon monoxide poisoning is the most common type of fatal poisoning in France and the United States. It has been estimated that more than 40,000 people per year seek medical attention for carbon monoxide poisoning in the United States.[9] In many industrialized countries, carbon monoxide may be the cause of greater than 50% of fatal poisonings.[1] In the U.S., about 200 people die each year from carbon monoxide poisoning associated with home fuel-burning heating equipment.[10] The CDC reports, "Each year, more than 500 Americans die from unintentional CO poisoning, and more than 2,000 commit suicide by intentionally poisoning themselves."[11]
[edit] Suicide
As other poisons such as cyanide and arsenic were placed under increasingly stringent legal restrictions, the carbon monoxide in town gas became the principal method of suicide by poisoning.[citation needed] Suicide was also often committed by inhaling exhaust fumes of running car engines. In the past, motor car exhaust may have contained up to 25% carbon monoxide. Newer cars have catalytic converters, which can eliminate over 99% of carbon monoxide produced.[12] However, even cars with catalytic converters can produce substantial carbon monoxide if an idling car is left in an enclosed space. Furthermore, cars with faulty heaters can produce a sufficient amount of carbon monoxide to cause deaths in some instances. This is due to reduced oxygen availability, and therefore, less efficient combustion.
As carbon monoxide poisoning via car exhaust has become less of a suicide option, there has been an increase in new methods of carbon monoxide poisoning such as burning charcoal or other fossil fuels within a confined space, such as a small room, tent, or car.[13] Such incidents have occurred mostly in connection with group suicide pacts in both Japan and Hong Kong, but are starting to occur in western countries as well, such as the 2007 suicide of Boston lead singer Brad Delp.[14]
[edit] Symptoms
[edit] Acute
The earliest symptoms, especially from low level exposures, are often non-specific and readily confused with other illnesses, typically flu-like viral syndromes, depression, chronic fatigue syndrome, and migraine or other headaches.[15] This often makes the diagnosis of carbon monoxide poisoning difficult. If suspected, the diagnosis can be confirmed by measurement of blood carboxyhemoglobin.
The main manifestations of poisoning develop in the organ systems most dependent on oxygen use: the central nervous system and the heart. The clinical manifestations include tachycardia and hypertension, and central nervous system symptoms such as headache, dizziness, confusion, convulsions, and unconsciousness. CO poisoning may also produce myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, hyperglycemia, muscle necrosis, acute renal failure, skin lesions, visual and auditory problems, and respiratory arrest.[16]
One of the major concerns following CO poisoning is the severe neurological manifestations that may occur days or even weeks after an acute poisoning. Common problems encountered are difficulty with higher intellectual functions and short-term memory, dementia, irritability, gait disturbance, speech disturbances, parkinson-like syndromes, cortical blindness, and depression[17] (depression can occur in those accidentally exposed). These delayed sequelae occur in approximately 15 percent of severely poisoned patients after an interval of 2 to 28 days. It is difficult to predict who may develop delayed sequelae; however, advancing age, loss of consciousness while poisoned, and initial neurological abnormalities may indicate a greater chance of developing delayed symptoms. According to the Philadelphia poison control hotline, sequelae are generally not anticipated when exposure is not severe enough to result in loss of consciousness.
[edit] Chronic
Long term, repeat exposures present a greater risk to persons with coronary heart disease and in pregnant patients.[18] Chronic exposure may increase the incidence of cardiovascular symptoms in some workers, such as motor vehicle examiners, firefighters, and welders. Patients often complain of persistent headaches, lightheadedness, depression, confusion, and nausea. Upon removal from exposure, the symptoms usually resolve themselves.[19]
[edit] Toxicity
Carbon monoxide is a significantly toxic gas, although patients may demonstrate varied clinical manifestations with different outcomes, even under similar exposure conditions.[20] Toxicity is also increased by several factors, including: increased activity and rate of ventilation, pre-existing cerebral or cardiovascular disease, reduced cardiac output, anemia or other hematological disorders, decreased barometric pressure, and high metabolic rate.
Under ordinary conditions, it is less dense than air, but during fires, it accumulates on the ground, so that if poisoning causes loss of consciousness, the amount of carbon monoxide inhaled increases and the possibility of fatality is radically increased.
Carbon monoxide is life-threatening to humans and other forms of air-breathing life, as inhaling even relatively small amounts of it can lead to hypoxic injury, neurological damage, and possibly death. A concentration of as little as 0.04% (400 parts per million) carbon monoxide in the air can be fatal. The gas is especially dangerous because it is not easily detected by human senses. Early symptoms of carbon monoxide poisoning include drowsiness and headache, followed by unconsciousness, respiratory failure, and death. First aid for a victim of carbon monoxide poisoning requires access to fresh air; administration of artificial respiration and, if available, oxygen; and, as soon as possible, medical attention.
When carbon monoxide is inhaled, it takes the place of oxygen in hemoglobin, the red blood pigment that normally carries oxygen to all parts of the body. Because carbon monoxide binds to hemoglobin several hundred times more strongly than oxygen, its effects are cumulative and long-lasting, causing oxygen starvation throughout the body. Prolonged exposure to fresh air (or pure oxygen) is required for the CO-tainted hemoglobin (carboxyhemoglobin) to clear.
The effects of carbon monoxide in parts per million are listed below:
35 ppm (0.0035%) Headache and dizziness within six to eight hours of constant exposure
100 ppm (0.01%) Slight headache in two to three hours
200 ppm (0.02%) Slight headache within two to three hours
400 ppm (0.04%) Frontal headache within one to two hours
800 ppm (0.08%) Dizziness, nausea, and convulsions within 45 minutes. Insensible within two hours.
1,600 ppm (0.16%) Headache, dizziness, and nausea within 20 minutes. Death in less than two hours.
3,200 ppm (0.32%) Headache, dizziness and nausea in five to ten minutes. Death within 30 minutes.
6,400 ppm (0.64%) Headache and dizziness in one to two minutes. Death in less than 20 minutes.
12,800 ppm (1.28%)Unconsciousness after 2-3 breaths. Death in less than three minutes.
In addition, a recent report concludes that carbon monoxide exposure can lead to significant loss of lifespan after exposure due to damage to the heart muscle. [21]
[edit] Carboxyhemoglobin
Levels of carbon monoxide bound in the blood can be determined by measuring carboxyhemoglobin, which is a stable complex of carbon monoxide and hemoglobin that forms in red blood cells. Carbon monoxide is produced normally in the body, establishing a low background carboxyhemoglobin saturation. Carbon monoxide also functions as a neurotransmitter. Normal carboxyhemoglobin levels in an average person are less than 5%, whereas cigarette smokers (two packs/day) may have levels up to 9%.[22]
Serious toxicity is often associated with carboxyhemoglobin levels above 25%, and the risk of fatality is high with levels over 70%. Still, no consistent dose response relationship has been found between carboxyhemoglobin levels and clinical effects.[23] Therefore, carboxyhemoglobin levels are more guides to exposure levels than effects as they do not reliably predict clinical course or short- or long-term outcome.[24]
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Toxicology
Toxicology (from the Greek words toxicos and logos) is the study of the adverse effects of chemicals on living organisms.[1] It is the study of symptoms, mechanisms, treatments and detection of poisoning, especially the poisoning of people.
History
Mathieu Orfila is considered to be the modern father of toxicology, having given the subject its first formal treatment in 1813 in his Traité des poisons, also called Toxicologie générale.
Theophrastus Phillipus Auroleus Bombastus von Hohenheim (1493 - 1541) (also referred to as Paracelsus, from his belief that his studies were above or beyond the work of Celsus - the Roman physician from the first century) is widely regarded as "the father" of toxicology. He is credited with the classic toxicology soundbite "All things are poison and nothing is without poison; only the dose makes a thing a poison." The original German reads: "Alle Dinge sind Gift und nichts ist ohne Gift; allein die Dosis macht, dass ein Ding kein Gift ist." This is often condensed to "The dose makes the poison".
Relationship between dose and toxicity
Toxicology studies the relationship between dose and its effects on the living organism. The chief criterion regarding the toxicity of a chemical is the dose, i.e. the amount of exposure to the substance. Almost all substances are toxic under the right conditions as Paracelsus, the father of modern toxicology said, “Sola dosis facit venenum” (only dose makes the poison). Paracelsus, who lived in the 16th century, was the first person to explain the dose-response relationship of toxic substances.
Even a benign substance like water can cause harm in excessive amounts. "Dr. Adrian Cohen was saddened, but not surprised, to hear about the 28-year-old woman who died earlier this month after drinking nearly two gallons of water to try to win a radio station contest." [2]
The term LD50 refers to the dose of a toxic substance that kills 50 percent of a test population (typically rats or other surrogates when the test concerns human toxicity). LD50 estimations in animals are no longer required for regulatory submissions as a part of pre-clinical development package.[citation needed]
Toxicity of Metabolites
Many substances regarded as poisons are toxic only indirectly. An example is "wood alcohol," or methanol, which is chemically converted to formaldehyde and formic acid in the liver. It is the formaldehyde and formic acid that cause the toxic effects of methanol exposure. Many drug molecules are made toxic in the liver, a good example being acetaminophen (paracetamol), especially in the presence of alcohol. The genetic variability of certain liver enzymes makes the toxicity of many compounds differ between one individual and the next. Because demands placed on one liver enzyme can induce activity in another, many molecules become toxic only in combination with others. A family of activities that engages many toxicologists includes identifying which liver enzymes convert a molecule into a poison, what are the toxic products of the conversion and under what conditions and in which individuals this conversion takes place.
History
Mathieu Orfila is considered to be the modern father of toxicology, having given the subject its first formal treatment in 1813 in his Traité des poisons, also called Toxicologie générale.
Theophrastus Phillipus Auroleus Bombastus von Hohenheim (1493 - 1541) (also referred to as Paracelsus, from his belief that his studies were above or beyond the work of Celsus - the Roman physician from the first century) is widely regarded as "the father" of toxicology. He is credited with the classic toxicology soundbite "All things are poison and nothing is without poison; only the dose makes a thing a poison." The original German reads: "Alle Dinge sind Gift und nichts ist ohne Gift; allein die Dosis macht, dass ein Ding kein Gift ist." This is often condensed to "The dose makes the poison".
Relationship between dose and toxicity
Toxicology studies the relationship between dose and its effects on the living organism. The chief criterion regarding the toxicity of a chemical is the dose, i.e. the amount of exposure to the substance. Almost all substances are toxic under the right conditions as Paracelsus, the father of modern toxicology said, “Sola dosis facit venenum” (only dose makes the poison). Paracelsus, who lived in the 16th century, was the first person to explain the dose-response relationship of toxic substances.
Even a benign substance like water can cause harm in excessive amounts. "Dr. Adrian Cohen was saddened, but not surprised, to hear about the 28-year-old woman who died earlier this month after drinking nearly two gallons of water to try to win a radio station contest." [2]
The term LD50 refers to the dose of a toxic substance that kills 50 percent of a test population (typically rats or other surrogates when the test concerns human toxicity). LD50 estimations in animals are no longer required for regulatory submissions as a part of pre-clinical development package.[citation needed]
Toxicity of Metabolites
Many substances regarded as poisons are toxic only indirectly. An example is "wood alcohol," or methanol, which is chemically converted to formaldehyde and formic acid in the liver. It is the formaldehyde and formic acid that cause the toxic effects of methanol exposure. Many drug molecules are made toxic in the liver, a good example being acetaminophen (paracetamol), especially in the presence of alcohol. The genetic variability of certain liver enzymes makes the toxicity of many compounds differ between one individual and the next. Because demands placed on one liver enzyme can induce activity in another, many molecules become toxic only in combination with others. A family of activities that engages many toxicologists includes identifying which liver enzymes convert a molecule into a poison, what are the toxic products of the conversion and under what conditions and in which individuals this conversion takes place.
History : 20th century
The same trend continued through the Victorian era, and was still labelled as an epidemic of sorts, and with poison still being considered one of the easiest and simplest ways to commit murder.[29] However, several changes occurred in the Victorian era, such as the rise of the life insurance industry, made poisoning the 'fashionable' crime considering the guaranteed and lucrative profit in the killing of a life-ensured relative with a large price on their head.[29] But as the move into the 1900s occurred, the technology of preventing poisoning became better and more efficient, and criminal poisoning become much harder than in previous centuries.[30] Criminal poisoning had to be made cleaner and better planned to match the ever-advancing technologies employed against would-be poisoners.[30] However, because of a wider range of educated people, more people were able to understand how to use poison and were intelligent or skilled enough to plan out a logical poison-induced murder, whereas in past times, usually only a select few knowledgeable people knew enough to conduct a successful homicide.[30]
Old poisons
Poison used in the past were also present in 20th-century murders. In the early 20th century, arsenic was often used, but during the mid-century, cyanide became quite popular. It was used during World War II by captured agents of the Resistance as a means of suicide to escape the heinous torture of their enemies.[30] Nazi war leader Herman Goering even used it to kill himself the night before he was supposed to be hanged during the Nuremberg Trials.[31] Adolf Hitler had also taken a pill of cyanide shortly before the fall of Berlin along with his wife, Eva Braun.[32]
However, new poisons later became more used, so as to outmatch the knowledge of the current toxicology field of science. In this way, wielding a new and unknown poison, a poisoner could kill someone, and the death might be mistaken as an unfortunate case of a rare illness.[30] This put a new strain on toxicology and other branches dealing with poison, and they were forced to work hard to keep up with the criminals who were using poisons that they had never previously encountered.
Old poisons
Poison used in the past were also present in 20th-century murders. In the early 20th century, arsenic was often used, but during the mid-century, cyanide became quite popular. It was used during World War II by captured agents of the Resistance as a means of suicide to escape the heinous torture of their enemies.[30] Nazi war leader Herman Goering even used it to kill himself the night before he was supposed to be hanged during the Nuremberg Trials.[31] Adolf Hitler had also taken a pill of cyanide shortly before the fall of Berlin along with his wife, Eva Braun.[32]
However, new poisons later became more used, so as to outmatch the knowledge of the current toxicology field of science. In this way, wielding a new and unknown poison, a poisoner could kill someone, and the death might be mistaken as an unfortunate case of a rare illness.[30] This put a new strain on toxicology and other branches dealing with poison, and they were forced to work hard to keep up with the criminals who were using poisons that they had never previously encountered.
History : 16th–18th centuries
By the end of the 16th century, the art and popularity of poison had moved from Italy to France, where criminal poisoning was becoming more and more frequent. It is estimated that in the 1570s that there would have been about thirty thousand people in Paris alone using poison or having some connection to poison in an illegal or immoral way.[28] It was becoming something of which was described as a 'plague' or 'epidemic'.[28] And this epidemic, while obviously contributing greatly to the death toll, was also greatly affecting citizens who had no connection to poison. Many people, nobles especially, were becoming extremely afraid of poisoning. They would attend dinner parties of only the most trusted, and hired only hand-picked servants. Several instances very famous or high-born people who were very afraid of poisoning are both Henrietta Anne of England and Henry IV.[28] The princess Henrietta Anne of England was so fearful and aware of poisoning that she instantly made the assumption that she had been poisoned when she was afflicted with a peritonitis due to a duodenal ulcer, while Henry IV, while making a visit to the Louvre, was recorded to have eaten only eggs that he had cooked himself, and drank only water that he had poured for himself.[28] Later, in 1662, Louis XIV limited the sale of poisons within apothecaries, and certain poisons were not to be sold, except to people whom the shopkeeper knew well to be trustworthy.[28]
Trustworthy alchemists did, however, become hard to find during this period; many of them were con men, fooling both their patrons and the public at large into believing that Mercury, thought then to be something of a 'core' element - one of which all others were invariably composed - was convertible into gold and other fine metals. While many took advantage of this belief, others genuinely, in the name of science, attempted to make gold out of less valuable and duller elements. Such of these alchemists were driven towards the same goal of attaining three objects of high desire within alchemical circles: the Philiosopher's Stone, able to change base metals into pure gold; the Elixir of Life, which lengthened one's life expansively, and finally, the Alkahest, a substance which was capable of dissolving anything. The pursuit of these goals, as fantastical, but scientifically supported as it was, retarded greatly the progress of alchemical science, as these goals were ultimately impossible to realise. [22]
Chambre Ardente
At a similar time to the ban of poisons, priests in Notre Dame became so astounded with the number of poison-related confessions that they had listened to that they decided to inform the king about how bad the 'epidemic' of poison actually was. In response to this, the king organized an order dedicated to the investigation of poisonings called the Chambre Ardente, and the investigation itself became known as the affaire des poisons.
Despite the fact that the inquisitors had been sponsored by the sovereign himself, they failed to catch many of the worst and most murderous poisoners, in whom probably had many connections in which were employed to evade punishment. However, in the life of the order, approximately 442 persons were caught and received punishment.[28] The work of this order did cause a backfiring, or side effect that was a magnifying in the interest of poison and how to use them, and, inexplicably, many people actually became actively involved in poison after the birth of an order made to reduce poisonings.
In Spain
While criminals based in Italy and England were the first to introduce poison as a means of murder or harm, during this period the use of poison truly was spreading all over Europe. Spain was notable for the fact that it had, by some means or another, committed several failed attempts at the disposal of Queen Elizabeth of England.[28] One person named Dr. Rodrigo Lopez, a Jewish physician, was called on by Spain to kill the queen, but he was caught and then later hanged, drawn and quartered for the act, though Elizabeth herself and Robert Cecil doubted his guilt. It is thought that some aspects, specifically a character, of Shakespeare's The Merchant of Venice may refer to or have been inspired by this Dr. Lopez. After this particular incident, the queen's food had to be tasted for poisoning, and greater security was put into effect. She was even known to have taken antidotes on a weekly basis for protection.
Conversely, royal assassination attempts by poison were also domestic in Spain, with several people and groups wanting to kill the monarchs. One successful attempt at this (probable one of few in Europe) was the poisoning of Marie Louise, the wife of Carlos II, who died suddenly in September 1689.
Trustworthy alchemists did, however, become hard to find during this period; many of them were con men, fooling both their patrons and the public at large into believing that Mercury, thought then to be something of a 'core' element - one of which all others were invariably composed - was convertible into gold and other fine metals. While many took advantage of this belief, others genuinely, in the name of science, attempted to make gold out of less valuable and duller elements. Such of these alchemists were driven towards the same goal of attaining three objects of high desire within alchemical circles: the Philiosopher's Stone, able to change base metals into pure gold; the Elixir of Life, which lengthened one's life expansively, and finally, the Alkahest, a substance which was capable of dissolving anything. The pursuit of these goals, as fantastical, but scientifically supported as it was, retarded greatly the progress of alchemical science, as these goals were ultimately impossible to realise. [22]
Chambre Ardente
At a similar time to the ban of poisons, priests in Notre Dame became so astounded with the number of poison-related confessions that they had listened to that they decided to inform the king about how bad the 'epidemic' of poison actually was. In response to this, the king organized an order dedicated to the investigation of poisonings called the Chambre Ardente, and the investigation itself became known as the affaire des poisons.
Despite the fact that the inquisitors had been sponsored by the sovereign himself, they failed to catch many of the worst and most murderous poisoners, in whom probably had many connections in which were employed to evade punishment. However, in the life of the order, approximately 442 persons were caught and received punishment.[28] The work of this order did cause a backfiring, or side effect that was a magnifying in the interest of poison and how to use them, and, inexplicably, many people actually became actively involved in poison after the birth of an order made to reduce poisonings.
In Spain
While criminals based in Italy and England were the first to introduce poison as a means of murder or harm, during this period the use of poison truly was spreading all over Europe. Spain was notable for the fact that it had, by some means or another, committed several failed attempts at the disposal of Queen Elizabeth of England.[28] One person named Dr. Rodrigo Lopez, a Jewish physician, was called on by Spain to kill the queen, but he was caught and then later hanged, drawn and quartered for the act, though Elizabeth herself and Robert Cecil doubted his guilt. It is thought that some aspects, specifically a character, of Shakespeare's The Merchant of Venice may refer to or have been inspired by this Dr. Lopez. After this particular incident, the queen's food had to be tasted for poisoning, and greater security was put into effect. She was even known to have taken antidotes on a weekly basis for protection.
Conversely, royal assassination attempts by poison were also domestic in Spain, with several people and groups wanting to kill the monarchs. One successful attempt at this (probable one of few in Europe) was the poisoning of Marie Louise, the wife of Carlos II, who died suddenly in September 1689.
History : Renaissance
By the Renaissance, the use of poisons for unlawful and reprehensible intentions had peaked; it was arguably becoming any assassin or murderer's essential tool.[26] This peaking of poison's popularity within crime syndicates and circles would probably have been due at least in part to the new discoveries that were then being made about poison.[26] Italian alchemists for one were, in the 14th and 15th century, realizing the potential of the combining of poisonous substances to create even more potent brews than the ones that had been put together,[26] and other new properties of poison were becoming clearer. A science of the study was forming, something today known as toxicology. So prominently used for homicide in society was poison that one would be fearful even to attend a dinner party for fear of having the food or drink poisoned by either the host or perhaps one of the guests.[26]
Borgia family
The very controversial Pope Alexander VI, also known at birth as Roderic BorjaCesare Borgia was the son of Pope Alexander VI, perhaps one of the most disputed popes in regards to legitimacy, having used his power to promote his five sons to high titles.[26] He was thought to be a hostile and ruthless man, and was avoided and feared. Borgia was notorious not only for being the son of a very controversial man, but also because he was thought to be a poison-wielding murderer.[26] In the following quote, Apollinaire describes what he believes is a kind of 'Borgia Recipe' used for the disposing of victims:
“ La Cantarella. That which the Borgias utilised in conjunction with arsenic without knowing it, was phosphorus, a secret which had been divulged to the Borgias by a Spanish monk, who also knew the antidote for it, as well as an antidote for arsenic; one sees, therefore that they were well armed. ”
After the death of Cesare Borgia's father, many rumors circulated proposing several theories about the cause, although most ended with the Pope having died in some horrible way involving murder, usually by poisoning.
Apollinaire's idea was that the pope was poisoned by wine which was in fact intended for another at the dinner table, Cardinal de Corneto. Sanuto held a similar theory, except that it involved a box of sweetmeats, instead of wine.[26] The death of the pope elicited little mourning, which was expected after the debased standards of his tenure. Historical evidence suggests that the pope was indeed poisoned in some way; when his body was exhibited, it was in a shocking state of decomposition. To reduce suspicion, it was only on display at night by candlelight.[26]
Cesare Borgia's passing did not cause much sadness either, a result of the reputation that he had forged for himself. However, his sister Lucrezia did mourn for this man who had been accused of so many crimes. Lucrezia was also considered a wrongdoer, but may in fact have been held responsible for some of Cesare's misdeeds.[26]
The Council of Ten
By the 1600s, the use of poison had become an art of sorts, and, in several cities of Italy including Venice and Rome, there were actual schools teaching the ways of poison and the 'art' which had been born.[27] Earlier, in the fifteenth century, a guild of alchemists and poisoners known as the Council of Ten was formed. This cult of poison-wielding assassins carried out contracts for people who paid them enough money, and usually anyone contracted for death ended up slain, killed by an undetected dose of lethal substances of varying description.[27]
Neopoliani Magioe Naturalis
Neopoliani Magioe Naturalis was a publication first printed just before 1590 that detailed the art of poisoning, and effective methods of using poison to commit homicide. The most effective way of killing someone with poison, according to the work, was by drugging someone's wine, a method that was very popular at the time.[27] One 'very strong mixture' used in the book is the Veninum Lupinum, which consists of a mix of aconite, taxus baccata, caustic lime, arsenic, bitter almonds and powdered glass mixed with honey. The overall product is a pill approximately the size of a walnut.[27]
Borgia family
The very controversial Pope Alexander VI, also known at birth as Roderic BorjaCesare Borgia was the son of Pope Alexander VI, perhaps one of the most disputed popes in regards to legitimacy, having used his power to promote his five sons to high titles.[26] He was thought to be a hostile and ruthless man, and was avoided and feared. Borgia was notorious not only for being the son of a very controversial man, but also because he was thought to be a poison-wielding murderer.[26] In the following quote, Apollinaire describes what he believes is a kind of 'Borgia Recipe' used for the disposing of victims:
“ La Cantarella. That which the Borgias utilised in conjunction with arsenic without knowing it, was phosphorus, a secret which had been divulged to the Borgias by a Spanish monk, who also knew the antidote for it, as well as an antidote for arsenic; one sees, therefore that they were well armed. ”
After the death of Cesare Borgia's father, many rumors circulated proposing several theories about the cause, although most ended with the Pope having died in some horrible way involving murder, usually by poisoning.
Apollinaire's idea was that the pope was poisoned by wine which was in fact intended for another at the dinner table, Cardinal de Corneto. Sanuto held a similar theory, except that it involved a box of sweetmeats, instead of wine.[26] The death of the pope elicited little mourning, which was expected after the debased standards of his tenure. Historical evidence suggests that the pope was indeed poisoned in some way; when his body was exhibited, it was in a shocking state of decomposition. To reduce suspicion, it was only on display at night by candlelight.[26]
Cesare Borgia's passing did not cause much sadness either, a result of the reputation that he had forged for himself. However, his sister Lucrezia did mourn for this man who had been accused of so many crimes. Lucrezia was also considered a wrongdoer, but may in fact have been held responsible for some of Cesare's misdeeds.[26]
The Council of Ten
By the 1600s, the use of poison had become an art of sorts, and, in several cities of Italy including Venice and Rome, there were actual schools teaching the ways of poison and the 'art' which had been born.[27] Earlier, in the fifteenth century, a guild of alchemists and poisoners known as the Council of Ten was formed. This cult of poison-wielding assassins carried out contracts for people who paid them enough money, and usually anyone contracted for death ended up slain, killed by an undetected dose of lethal substances of varying description.[27]
Neopoliani Magioe Naturalis
Neopoliani Magioe Naturalis was a publication first printed just before 1590 that detailed the art of poisoning, and effective methods of using poison to commit homicide. The most effective way of killing someone with poison, according to the work, was by drugging someone's wine, a method that was very popular at the time.[27] One 'very strong mixture' used in the book is the Veninum Lupinum, which consists of a mix of aconite, taxus baccata, caustic lime, arsenic, bitter almonds and powdered glass mixed with honey. The overall product is a pill approximately the size of a walnut.[27]
Venom
Venom is any of a variety of toxins used by certain types of animals, for the purpose of defense and hunting. Generally, venom is injected while poisons are absorbed by ingestion or through the skin.
The animals most widely known to use venom are snakes, some species of which inject venom into their prey through hollow fangs; spiders and centipedes, which also inject venom through fangs; scorpions and stinging insects, which inject venom with a sting (which (in insects) is a modified egg-laying device - the ovipositor). There are also many caterpillars that have defensive venom glands associated with specialized bristles on the body, known as urticating hairs, some of which can be lethal to humans (e.g., the Lonomia moth). Venom is also found in other reptiles besides snakes such as the gila monster, and mexican beaded lizard. Other insects, such as true bugs [1], also produce venom. Venom can also be found in some fish, such as the cartilaginous fishes: stingrays, sharks, and chimaeras and the teleost fishes, which include: monognathus eels, catfishes, stonefishes and waspfishes, scorpionfishes and lionfishes, gurnard perches, rabbitfishes, surgeonfishes, scats, stargazers, weevers, carangids, saber-toothed blenny, and toadfish. In fact, recent studies have shown that there are more venomous ray-finned fishes than all other venomous vertebrates combined. Additionally, there are many other venomous invertebrates, including jellyfish, cone snails, bees, wasps and ants. The Box jellyfish is widely considered the most venomous creature in the world.[2] Some mammals are also venomous, including solenodons, shrews, the slow loris, and the male platypus.
Because they are tasked to defend their hives and food stores, bees synthesize and employ an acidic venom (apitoxin) to cause pain in those that they sting, whereas wasps use a chemically different venom designed to paralyze prey, so it can be stored alive in the food chambers of their young. The use of venom is much more widespread than just these examples, of course.
It is important to note the difference between organisms that are "venomous" and "poisonous", two commonly confused terms with regards to plant and animal life. Venomous, as stated above, refers to animals that inject venom into their prey as a self-defense mechanism. Poisonous, on the other hand, describes plants or animals that are harmful when consumed or touched. One species of bird, the hooded pitohui, although not venomous, is poisonous, secreting a neurotoxin on to its skin and feathers. The slow loris, a primate, blurs the boundary between poisonous and venomous; it has poison secreting patches on the inside of its elbows which it is believed to smear on its young to prevent them from being eaten. However, it will also lick these patches, giving it a venomous bite.
Snake venom is produced by glands below the eye and delivered to the victim through tubular or channeled fangs. Snake poisons contain a variety of peptide toxins. Snakes use their venom principally for hunting, though the threat of being bitten serves also as a defense. Snake bites cause a variety of symptoms including pain, swelling, tissue damage, low blood pressure, convulsions, and hemorrhaging (varying by the species of snake).
Doctors treat victims of a venomous bite with antivenin, which is created by dosing an animal such as a sheep, horse, goat, or rabbit with a small amount of the targeted venom. The immune system of the subject animal responds to the dose, producing antibodies against the venom's active molecule, which can then be harvested from the animal's blood and applied to treat envenomation in others. This treatment may be effective for a given person only a limited number of times, however, as that person will ultimately develop antibodies to neutralize the foreign animal antibodies injected into him. Even if that person doesn't suffer a serious allergic reaction to the antivenom, his own immune system can destroy the antivenom, before the antivenom can destroy the venom. Though most people never require one treatment of antivenom in their lifetime, let alone several, people who work with snakes or other venomous animals may. Fortunately, these people often develop antibodies of their own against the venom of whatever animals they handle, and thereby are immune without assistance of exogenous antibodies.
Aristolochia rugosa and Aristolochia trilobata are recorded in a list of plants used worldwide and in the West Indies, South and Central America against snakebites and scorpion stings. Aristolochic acid inhibits inflammation induced by immune complexes, and nonimmunological agents (carrageenan or croton oil). Aristolochic acid inhibits the activity of snake venom phospholipase (PLA2) by forming a 1:1 complex with the enzyme. Since phospholipase enzymes play a significant part in the cascade leading to the inflammatory and pain response, their inhibition could lead to relief of problems from scorpion envenomation.
The animals most widely known to use venom are snakes, some species of which inject venom into their prey through hollow fangs; spiders and centipedes, which also inject venom through fangs; scorpions and stinging insects, which inject venom with a sting (which (in insects) is a modified egg-laying device - the ovipositor). There are also many caterpillars that have defensive venom glands associated with specialized bristles on the body, known as urticating hairs, some of which can be lethal to humans (e.g., the Lonomia moth). Venom is also found in other reptiles besides snakes such as the gila monster, and mexican beaded lizard. Other insects, such as true bugs [1], also produce venom. Venom can also be found in some fish, such as the cartilaginous fishes: stingrays, sharks, and chimaeras and the teleost fishes, which include: monognathus eels, catfishes, stonefishes and waspfishes, scorpionfishes and lionfishes, gurnard perches, rabbitfishes, surgeonfishes, scats, stargazers, weevers, carangids, saber-toothed blenny, and toadfish. In fact, recent studies have shown that there are more venomous ray-finned fishes than all other venomous vertebrates combined. Additionally, there are many other venomous invertebrates, including jellyfish, cone snails, bees, wasps and ants. The Box jellyfish is widely considered the most venomous creature in the world.[2] Some mammals are also venomous, including solenodons, shrews, the slow loris, and the male platypus.
Because they are tasked to defend their hives and food stores, bees synthesize and employ an acidic venom (apitoxin) to cause pain in those that they sting, whereas wasps use a chemically different venom designed to paralyze prey, so it can be stored alive in the food chambers of their young. The use of venom is much more widespread than just these examples, of course.
It is important to note the difference between organisms that are "venomous" and "poisonous", two commonly confused terms with regards to plant and animal life. Venomous, as stated above, refers to animals that inject venom into their prey as a self-defense mechanism. Poisonous, on the other hand, describes plants or animals that are harmful when consumed or touched. One species of bird, the hooded pitohui, although not venomous, is poisonous, secreting a neurotoxin on to its skin and feathers. The slow loris, a primate, blurs the boundary between poisonous and venomous; it has poison secreting patches on the inside of its elbows which it is believed to smear on its young to prevent them from being eaten. However, it will also lick these patches, giving it a venomous bite.
Snake venom is produced by glands below the eye and delivered to the victim through tubular or channeled fangs. Snake poisons contain a variety of peptide toxins. Snakes use their venom principally for hunting, though the threat of being bitten serves also as a defense. Snake bites cause a variety of symptoms including pain, swelling, tissue damage, low blood pressure, convulsions, and hemorrhaging (varying by the species of snake).
Doctors treat victims of a venomous bite with antivenin, which is created by dosing an animal such as a sheep, horse, goat, or rabbit with a small amount of the targeted venom. The immune system of the subject animal responds to the dose, producing antibodies against the venom's active molecule, which can then be harvested from the animal's blood and applied to treat envenomation in others. This treatment may be effective for a given person only a limited number of times, however, as that person will ultimately develop antibodies to neutralize the foreign animal antibodies injected into him. Even if that person doesn't suffer a serious allergic reaction to the antivenom, his own immune system can destroy the antivenom, before the antivenom can destroy the venom. Though most people never require one treatment of antivenom in their lifetime, let alone several, people who work with snakes or other venomous animals may. Fortunately, these people often develop antibodies of their own against the venom of whatever animals they handle, and thereby are immune without assistance of exogenous antibodies.
Aristolochia rugosa and Aristolochia trilobata are recorded in a list of plants used worldwide and in the West Indies, South and Central America against snakebites and scorpion stings. Aristolochic acid inhibits inflammation induced by immune complexes, and nonimmunological agents (carrageenan or croton oil). Aristolochic acid inhibits the activity of snake venom phospholipase (PLA2) by forming a 1:1 complex with the enzyme. Since phospholipase enzymes play a significant part in the cascade leading to the inflammatory and pain response, their inhibition could lead to relief of problems from scorpion envenomation.
Snakebite2
Symptoms
The most common symptoms of all snakebites are panic, fear and emotional instability, which may cause symptoms such as nausea and vomiting, diarrhea, vertigo, fainting, tachycardia, and cold, clammy skin.[8] Television, literature, and folklore are in part responsible for the hype surrounding snakebites, and a victim may have unwarranted thoughts of imminent death.
Dry snakebites, and those inflicted by a non-venomous species, are still able to cause severe injury to the victim. There are several reasons for this; a snakebite which is not treated properly may become infected (as is often reported by the victims of viper bites whose fangs are capable of inflicting deep puncture wounds), the bite may cause anaphylaxis in certain people, and the saliva and fangs of the snake may harbor many dangerous microbial contaminants, including Clostridium tetani. If neglected, an infection may spread and potentially even kill the victim.
Most snakebites, whether by a venomous snake or not, will have some type of local effect. Usually there is minor pain and redness, but this varies depending on the site. Bites by vipers and some cobras may be extremely painful, with the local tissue sometimes becoming tender and severely swollen within 5 minutes. This area may also bleed and blister.
Interestingly, bites caused by the Mojave rattlesnake and the speckled rattlesnake reportedly cause little or no pain despite being serious injuries. Victims may also describe a “rubbery,” “minty,” or “metallic” taste if bitten by certain species of rattlesnake. Spitting cobras and Rinkhalses can spit venom in their victims’ eyes. This results in immediate pain, vision problems, and sometimes blindness.
Some Australian elapids and most viper envenomations will cause coagulopathy, sometimes so severe that a person may bleed spontaneously from the mouth, nose, and even old, seemingly-healed wounds. Internal organs may bleed, including the brain and intestines and will cause ecchymosis (bruising) of the victim's skin. If the bleeding is left unchecked the victim may die of blood loss.
Venom emitted from cobras, most sea snakes, mambas, and other elapids contain toxins which attack the nervous system. The victim may present with strange disturbances to their vision, including blurriness. This is commonly due to the venom paralyzing the ciliary muscle, which is responsible for focusing the lens of the eye, but can be the result of eyelid paralysis as well. Victims will also report paresthesia throughout their body, as well as difficulty speaking and breathing. Nervous system problems will cause a huge array of symptoms, and those provided here are not exhaustive. In any case, if the victim is not treated immediately they may die from respiratory failure.
Venom emitted from some Australian elapids, almost all vipers, and all sea snakes causes necrosis of muscle tissue. Muscle tissue may begin to die throughout the body, a condition known as rhabdomyolysis. Dead muscle cells may even clog the kidney which filters out proteins. This, coupled with hypotension, can lead to kidney failure, and, if left untreated, eventually death.
Treatment
It is not an easy task determining whether or not a bite by any species of snake is life-threatening. A bite by a North American copperhead on the ankle is usually a moderate injury to a healthy adult, but a bite to a child’s abdomen or face by the same snake may well be fatal. The outcome of all snakebites depends on a multitude of factors; the size, physical condition, and temperature of the snake, the age and physical condition of the victim, the area and tissue bitten (e.g., foot, torso, vein or muscle, etc.), the amount of venom injected, the time it takes for the patient to find treatment, and finally the quality of that treatment.
Snake identification
Identification of the snake is important in planning treatment in certain areas of the world, but is not always possible. Ideally the dead snake would be brought in with the patient, but in areas where snake bite is more common, local knowledge may be sufficient to recognize the snake.
In countries where polyvalent antivenins are available, such as North America, identification of snake is not of much significance.
The three types of venomous snakes that cause the majority of major clinical problems are the viper, krait and cobra. Knowledge of what species are present locally can be crucially important, as is knowledge of typical signs and symptoms of envenoming by each species of snake.
A scoring systems can be used to try and determine biting snake based on clinical features,[9] but these scoring systems are extremely specific to a particular geographical area.
First Aid
Snakebite first aid recommendations vary, in part because different snakes have different types of venom. Some have little local effect, but life-threatening systemic effects, in which case containing the venom in the region of the bite (e.g., by pressure immobilization) is highly desirable. Other venoms instigate localized tissue damage around the bitten area, and immobilization may increase the severity of the damage in this area, but also reduce the total area affected; whether this trade-off is desirable remains a point of controversy.
Because snakes vary from one country to another, first aid methods also vary; treatment methods suited for rattlesnake bite in the United States might well be fatal if applied to a tiger snake bite in Australia. As always, this article is not a legitimate substitute for professional medical advice. Readers are strongly advised to obtain guidelines from a reputable first aid organization in their own region, and to beware of homegrown or anecdotal remedies.
However, most first aid guidelines agree on the following:
Protect the patient (and others, including yourself) from further bites. While identifying the species is desirable in certain regions, do not risk further bites or delay proper medical treatment by attempting to capture or kill the snake. If the snake has not already fled, carefully remove the patient from the immediate area.
Keep the patient calm and call for help to arrange for transport to the nearest hospital emergency room, where antivenin for snakes common to the area will often be available.
Make sure to keep the bitten limb in a functional position and below the victim's heart level so as to minimize blood returning to the heart and other organs of the body.
Do not give the patient anything to eat or drink. This is especially important with consumable alcohol, a known vasodilator which will speedup the absorption of venom. Do not administer stimulants or pain medications to the victim, unless specifically directed to do so by a physician.
Remove any items or clothing which may constrict the bitten limb if it swells (rings, bracelets, watches, footwear, etc.)
Keep the patient as still as possible.
Do not incise the bitten site.
Many organizations, including the American Medical Association and American Red Cross, recommend washing the bite with soap and water. However, do not attempt to clean the area with any type of chemical.
note: Treatment for Australian snake bites (which may differ to other areas of the world) stringently recommends against cleaning the wound. Traces of venom left on the skin/bandages from the strike can be used in combination with a snake bite identification kit to identify the species of snake. This speeds determination of which antivenin to administer in the emergency room.
[edit] Pressure immobilization
Pressure immobilization is not appropriate for cytotoxic bites such as those of most vipers,[10][11][12] but is highly effective against neurotoxic venoms such as those of most elapids.[13][14][15] Developed by Struan Sutherland in 1978,[16] the object of pressure immobilization is to contain venom within a bitten limb and prevent it from moving through the lymphatic system to the vital organs in the body core. This therapy has two components: pressure to prevent lymphatic drainage, and immobilization of the bitten limb to prevent the pumping action of the skeletal muscles. Pressure is preferably applied with an elastic bandage, but any cloth will do in an emergency. Bandaging begins two to four inches above the bite (i.e. between the bite and the heart), winding around in overlapping turns and moving up towards the heart, then back down over the bite and past it towards the hand or foot. Then the limb must be held immobile: not used, and if possible held with a splint or sling. The bandage should be about as tight as when strapping a sprained ankle. It must not cut off blood flow, or even be uncomfortable; if it is uncomfortable, the patient will unconsciously flex the limb, defeating the immobilization portion of the therapy. The location of the bite should be clearly marked on the outside of the bandages. Some peripheral edema is an expected consequence of this process.
Apply pressure immobilization as quickly as possible; if you wait until symptoms become noticeable you will have missed the best time for treatment. Once a pressure bandage has been applied, it should not be removed until the patient has reached a medical professional. The combination of pressure and immobilization can contain venom so effectively that no symptoms are visible for more than twenty-four hours, giving the illusion of a dry bite. But this is only a delay; removing the bandage releases that venom into the patient's system with rapid and possibly fatal consequences.
The most common symptoms of all snakebites are panic, fear and emotional instability, which may cause symptoms such as nausea and vomiting, diarrhea, vertigo, fainting, tachycardia, and cold, clammy skin.[8] Television, literature, and folklore are in part responsible for the hype surrounding snakebites, and a victim may have unwarranted thoughts of imminent death.
Dry snakebites, and those inflicted by a non-venomous species, are still able to cause severe injury to the victim. There are several reasons for this; a snakebite which is not treated properly may become infected (as is often reported by the victims of viper bites whose fangs are capable of inflicting deep puncture wounds), the bite may cause anaphylaxis in certain people, and the saliva and fangs of the snake may harbor many dangerous microbial contaminants, including Clostridium tetani. If neglected, an infection may spread and potentially even kill the victim.
Most snakebites, whether by a venomous snake or not, will have some type of local effect. Usually there is minor pain and redness, but this varies depending on the site. Bites by vipers and some cobras may be extremely painful, with the local tissue sometimes becoming tender and severely swollen within 5 minutes. This area may also bleed and blister.
Interestingly, bites caused by the Mojave rattlesnake and the speckled rattlesnake reportedly cause little or no pain despite being serious injuries. Victims may also describe a “rubbery,” “minty,” or “metallic” taste if bitten by certain species of rattlesnake. Spitting cobras and Rinkhalses can spit venom in their victims’ eyes. This results in immediate pain, vision problems, and sometimes blindness.
Some Australian elapids and most viper envenomations will cause coagulopathy, sometimes so severe that a person may bleed spontaneously from the mouth, nose, and even old, seemingly-healed wounds. Internal organs may bleed, including the brain and intestines and will cause ecchymosis (bruising) of the victim's skin. If the bleeding is left unchecked the victim may die of blood loss.
Venom emitted from cobras, most sea snakes, mambas, and other elapids contain toxins which attack the nervous system. The victim may present with strange disturbances to their vision, including blurriness. This is commonly due to the venom paralyzing the ciliary muscle, which is responsible for focusing the lens of the eye, but can be the result of eyelid paralysis as well. Victims will also report paresthesia throughout their body, as well as difficulty speaking and breathing. Nervous system problems will cause a huge array of symptoms, and those provided here are not exhaustive. In any case, if the victim is not treated immediately they may die from respiratory failure.
Venom emitted from some Australian elapids, almost all vipers, and all sea snakes causes necrosis of muscle tissue. Muscle tissue may begin to die throughout the body, a condition known as rhabdomyolysis. Dead muscle cells may even clog the kidney which filters out proteins. This, coupled with hypotension, can lead to kidney failure, and, if left untreated, eventually death.
Treatment
It is not an easy task determining whether or not a bite by any species of snake is life-threatening. A bite by a North American copperhead on the ankle is usually a moderate injury to a healthy adult, but a bite to a child’s abdomen or face by the same snake may well be fatal. The outcome of all snakebites depends on a multitude of factors; the size, physical condition, and temperature of the snake, the age and physical condition of the victim, the area and tissue bitten (e.g., foot, torso, vein or muscle, etc.), the amount of venom injected, the time it takes for the patient to find treatment, and finally the quality of that treatment.
Snake identification
Identification of the snake is important in planning treatment in certain areas of the world, but is not always possible. Ideally the dead snake would be brought in with the patient, but in areas where snake bite is more common, local knowledge may be sufficient to recognize the snake.
In countries where polyvalent antivenins are available, such as North America, identification of snake is not of much significance.
The three types of venomous snakes that cause the majority of major clinical problems are the viper, krait and cobra. Knowledge of what species are present locally can be crucially important, as is knowledge of typical signs and symptoms of envenoming by each species of snake.
A scoring systems can be used to try and determine biting snake based on clinical features,[9] but these scoring systems are extremely specific to a particular geographical area.
First Aid
Snakebite first aid recommendations vary, in part because different snakes have different types of venom. Some have little local effect, but life-threatening systemic effects, in which case containing the venom in the region of the bite (e.g., by pressure immobilization) is highly desirable. Other venoms instigate localized tissue damage around the bitten area, and immobilization may increase the severity of the damage in this area, but also reduce the total area affected; whether this trade-off is desirable remains a point of controversy.
Because snakes vary from one country to another, first aid methods also vary; treatment methods suited for rattlesnake bite in the United States might well be fatal if applied to a tiger snake bite in Australia. As always, this article is not a legitimate substitute for professional medical advice. Readers are strongly advised to obtain guidelines from a reputable first aid organization in their own region, and to beware of homegrown or anecdotal remedies.
However, most first aid guidelines agree on the following:
Protect the patient (and others, including yourself) from further bites. While identifying the species is desirable in certain regions, do not risk further bites or delay proper medical treatment by attempting to capture or kill the snake. If the snake has not already fled, carefully remove the patient from the immediate area.
Keep the patient calm and call for help to arrange for transport to the nearest hospital emergency room, where antivenin for snakes common to the area will often be available.
Make sure to keep the bitten limb in a functional position and below the victim's heart level so as to minimize blood returning to the heart and other organs of the body.
Do not give the patient anything to eat or drink. This is especially important with consumable alcohol, a known vasodilator which will speedup the absorption of venom. Do not administer stimulants or pain medications to the victim, unless specifically directed to do so by a physician.
Remove any items or clothing which may constrict the bitten limb if it swells (rings, bracelets, watches, footwear, etc.)
Keep the patient as still as possible.
Do not incise the bitten site.
Many organizations, including the American Medical Association and American Red Cross, recommend washing the bite with soap and water. However, do not attempt to clean the area with any type of chemical.
note: Treatment for Australian snake bites (which may differ to other areas of the world) stringently recommends against cleaning the wound. Traces of venom left on the skin/bandages from the strike can be used in combination with a snake bite identification kit to identify the species of snake. This speeds determination of which antivenin to administer in the emergency room.
[edit] Pressure immobilization
Pressure immobilization is not appropriate for cytotoxic bites such as those of most vipers,[10][11][12] but is highly effective against neurotoxic venoms such as those of most elapids.[13][14][15] Developed by Struan Sutherland in 1978,[16] the object of pressure immobilization is to contain venom within a bitten limb and prevent it from moving through the lymphatic system to the vital organs in the body core. This therapy has two components: pressure to prevent lymphatic drainage, and immobilization of the bitten limb to prevent the pumping action of the skeletal muscles. Pressure is preferably applied with an elastic bandage, but any cloth will do in an emergency. Bandaging begins two to four inches above the bite (i.e. between the bite and the heart), winding around in overlapping turns and moving up towards the heart, then back down over the bite and past it towards the hand or foot. Then the limb must be held immobile: not used, and if possible held with a splint or sling. The bandage should be about as tight as when strapping a sprained ankle. It must not cut off blood flow, or even be uncomfortable; if it is uncomfortable, the patient will unconsciously flex the limb, defeating the immobilization portion of the therapy. The location of the bite should be clearly marked on the outside of the bandages. Some peripheral edema is an expected consequence of this process.
Apply pressure immobilization as quickly as possible; if you wait until symptoms become noticeable you will have missed the best time for treatment. Once a pressure bandage has been applied, it should not be removed until the patient has reached a medical professional. The combination of pressure and immobilization can contain venom so effectively that no symptoms are visible for more than twenty-four hours, giving the illusion of a dry bite. But this is only a delay; removing the bandage releases that venom into the patient's system with rapid and possibly fatal consequences.
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