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by Murder

  Any of these could also be toxic for the fetus, and, of course, if the victim died, the fetus would, too, unless an emergency cesarean section was performed.

  Although any of these would work, I think mercury or carbon tet would be best. I particularly like the idea of a vapor, but that doesn't fit your original plot idea.

  How Deadly Are Death Cap Mushrooms, and What Do They Do to the Victim?

  Q: In my story a murder is committed by feeding the victim a death cap mushroom. I need to know how quickly it acts and what reactions the victim would have before death.

  A: The death cap mushroom (Amanita phalloides) is the most dangerous of the mushrooms. In fact, the entire Amanita family is to be avoided. Other toxic species are the fool's mushroom (A. verna), the death angel (A. virosa), and the smaller death angel (A. bis-poriger).

  The death cap grows in the southeast United States and prefers damp forested areas. The others prefer dry pine forests or mixed wooded areas and lawns. Their cap colors vary from pale green to yellow-olive in the coastal United States and Europe and to white or light brown in the remainder of the United States. All have white gills with white spores on the underside of their caps.

  The death cap is so toxic that a single mushroom can kill. The two main toxins found in these mushrooms are amanitin, which causes a drop in blood sugar (hypoglycemia), and phalloidin, which damages the kidneys, liver, and heart. Symptoms are slow in onset, typically beginning six to fifteen hours after ingestion, and they may be delayed as much as forty-eight hours. In general, the later the onset of symptoms, the worse the chances for survival. This is because the toxins go to work on the liver and other organs almost immediately, but the late onset of symptoms delays the seeking of medical help.

  Symptoms usually begin with stomach pain, nausea, vomiting, and bloody diarrhea. When the liver is involved, jaundice will impart a yellow hue to the skin. The victim may then lapse into a coma. As the kidneys fail and as dehydration progresses due to vomiting and diarrhea, the potassium level in the blood can rise abruptly and lead to cardiac arrest and death.

  Treatment is often not helpful because, as stated above, by the time help is sought, the toxins are already working their mischief in the body. Regardless, the first order of business is to pump the stomach to remove any residual mushrooms. This would help only in the first four to six hours. After that, the mushrooms have been digested and are no longer in the stomach. The victim is moni-

  tored with blood tests for hypoglycemia, elevated potassium, and abnormal liver and kidney function. These problems are treated as they arise. Otherwise, hope and prayer are suggested.

  A quicker-acting toxin is the panther mushroom (A. pantherina) or the fly agaric mushroom (A. muscaria), both members of the Amanita family. They come in a variety of colors, from yellow to red to orange to grayish brown, and often have white patches on their caps. These contain several different poisons. Choline and muscarine cause a drop in blood pressure and pulse, nausea, dizziness, profuse sweating and salivation, tearing of the eyes, and diarrhea. Ibotenic acid and muscimol cause dizziness, headache, seizures, blurred vision, muscle cramping, loss of balance, coma, respiratory failure, and death.

  The symptoms typically begin from half an hour to three hours after ingestion. Treatment is similar to the above measures plus the use of atropine to block the effects of the muscarine and choline. Atropine must be given intravenously. Typically, 0.5 to 1 milligram is given every hour as needed to keep the heart rate and blood pressure within normal ranges.

  What Drug Available in the Nineteenth Century Could Be Used to Make a Victim Pliant but Awake?

  Q: In my story, my protagonist needs to transport a captive by rail in 1889 Europe. What drug would keep the victim semi-mobile but helpless over a weeklong railway trip?

  A: I think your best bet would be one of the opium derivatives. Laudanum (tincture of opium) and morphine were widely available. In fact, during the last half of the nineteenth century, laudanum, opium, and morphine were the drugs used most often for suicide in England. These drugs were commonly used for pain, sedation, and to calm crying babies. They weren't controlled substances as they are today. It wasn't until 1909 that an international commission took the first steps toward regulating opium.

  Laudanum was probably first created by the great physician Paracelsus. It was the addiction of Samuel Taylor Coleridge (1772— 1834) and Sir Walter Scott (1771-1832), who used it to relieve his long-standing abdominal pain from what was likely chronic gallbladder disease.

  Opium is a white powder, while the tincture is a liquid. Either could be added to food or drink. The victim would be sleepy, lethargic, and manageable, and the dose could be easily adjusted to give the desired effect. When the victim begins to "lighten up," another dose could be given. The villain could pass off the victim's symptoms as illness rather than drugs, and no one would probably be the wiser. And when the drug is stopped, the victim would return to normal and would likely have only a fuzzy memory of events.

  What Were Some Common Poisons Available in Medieval Europe?

  Q: What would be some common poisons available to my medieval poisoner? What are their effects?

  A: There were many very effective poisons available during the medieval period and before. These are the common ones:

  Arsenic: Arsenic is a metal that is grayish in color in its pure form. Most often it is found as arsenic trioxide, which is a white powder. It can easily be added to food, where it is unlikely to be detected.

  This was the favorite poison of the treacherous French queen Catherine de Medicis. She also apparently used aqua toffana or aquetta di Napoli, which was a mixture of arsenic and cantharidin.

  Another interesting use of arsenic was in venin de crapaud. Arsenic was fed to toads or other small animals, and after they died, the carcasses were cooked to produce juices. These were added to the food or drink of the victim, with extremely toxic results.

  Acute poisoning causes severe gastric burning, nausea, vomiting, and bloody diarrhea. The victim's blood pressure drops, and he becomes weak, dizzy, cold, clammy, and confused, and may develop seizures. Death follows these painful and dramatic events.

  Belladonna (Atropa belladonna): This is a plant, and it is also called deadly nightshade. One of the active chemicals in belladonna is atropine. The name "atropine" comes from one of the three Greek Fates, Atropos, who wielded the shears that cut the thread of human life. Other active compounds include scopolamine, hyoscyamine, and hyoscine.

  One effect of belladonna is to dilate the pupils, and it is from this that its name arose. Women would use a drop in each eye to dilate their pupils, which was thought to enhance their beauty. "Belladonna" means beautiful woman.

  All parts of the plant are toxic when swallowed, and symptoms begin within an hour or so of ingestion. The signs and symptoms of atropine poisoning include dilated pupils, blurred vision, dry mouth and eyes, fever, flushed skin, abdominal cramping, confusion, disorientation, seizures, and cardiac arrest.

  Cantharidin (Cantharis vericatoria): Also called Spanish fly, it is a tasteless white powder that can be easily secreted in food or drink. Symptoms appear immediately after ingestion. Cantharidin is very irritative to every tissue it contacts, and when it is filtered from the bloodstream by the kidneys, it causes irritation of the urinary tract and thus was felt to be an aphrodisiac. In larger doses it can cause severe burning and blistering of the gastrointestinal and urinary tracts, and lead to abdominal pain, nausea, vomiting of blood, bloody diarrhea, painful and bloody urination, convulsions, a rapid pulse, a drop in blood pressure, shock, and death.

  Foxglove (Digitalis purpurea): A beautiful flowering plant it is also

  called the fairy cap, fairy bells, and fairy thimbles. These plants are the natural source of digitalis, a medication that has been in use for over a century in the treatment of heart failure and certain cardiac arrhythmias.

  All parts of the plant are toxic. Symptoms of poisoning begin in a half hour or so.
The victim experiences headache, nausea, vomiting, muscle cramping, shortness of breath, dizziness, palpitations, and finally death from cardiac arrest.

  Hemlock (Conium maculatum): This is the poison that reputedly killed Socrates. All parts of the plant are poisonous, particularly the fruit during flowering season. The active toxin is coniine, which is a neurotoxin that paralyzes muscles much like curare. Symptoms begin in a half hour, but death may take several hours.

  The first symptom is typically a loss of muscular strength, which progresses. Muscle pain and paralysis follow until the respiratory muscles fail and death ensues from asphyxia.

  Henbane (Hyoscamus niger): This is also called insane root, fetid nightshade, and poison tobacco. All parts of the plant contain hyoscyamine, a chemical also found in belladonna, and thus the signs and symptoms of poisoning with henbane are similar to those of atropine toxicity. The onset of symptoms occurs in approximately fifteen minutes.

  Poisonous mushrooms were also widely available.

  What Are the Effects of Rhubarb Ingestion?

  Q: One of my characters is fed raw rhubarb leaves torn up in a salad as an attempt to poison her. How soon would she react, and what would the reaction be? If she is taken to the hospital, what treatment would she receive? Are there any long-term complications? What is the recovery period?

  A: Rhubarb (Rheum rhaponticum) contains oxalic acid, which is the toxic substance in poisonings. It is found in the leaves and also in the stalks of several subspecies of rhubarb. Oxalic acid causes problems in two ways. The first is topical injury due to its irritant effects, and the second is "internal," occurring after it is absorbed into the body

  Oxalic acid is very irritating to the GI tract and causes mouth, throat, and esophageal pain as well as weakness, shortness of breath, stomach pain with nausea, vomiting, and possibly bleeding. Because there is a delayed onset of symptoms, your victim may not know something was wrong for several hours after eating the leaves. This delay is part of what makes rhubarb so treacherous. If it caused vomiting to occur more quickly, less internal damage would result, since the vomiting would empty the stomach. The amount of the oxalic acid that gets absorbed is directly related to how long the rhubarb remains in the stomach. Less time, less absorption, less internal problems.

  These internal problems are due to the chemical properties of oxalic acid. When oxalic acid is absorbed into the bloodstream, it reacts with calcium in the blood to form calcium oxalate. This reaction consumes the blood's calcium, and the level of calcium falls to low levels. Since calcium is necessary for the proper electrical function of the heart, these low levels can cause cardiac arrest and death. Also, the calcium oxalate produced in the bloodstream by this chemical reaction is filtered through the kidneys, where it can clog up the microscopic tubules and severely damage the kidneys. This can cause burning urination and lead to permanent loss of kidney function. Dialysis and/or kidney transplantation may be required.

  The first steps in treatment consist of emptying any residual plant from the stomach and neutralizing any oxalic acid to prevent its absorption. The more quickly this is done, the better. Forced vomiting, using an emetic (a drug that causes vomiting), or stom-

  ach lavage (washing out the stomach with a tube inserted through the nose and into the stomach) will remove any residual plant product. A common emetic is ipecac syrup. A couple of teaspoons given orally will cause vomiting in five to ten minutes. Then milk or any other calcium-containing liquid can be given orally or via the lavage tube. This binds up, or reacts with, the oxalate before it gets absorbed. In this way the calcium oxalate is formed in the stomach rather than in the bloodstream, where it works its worst mischief, and can be lavaged away.

  Also, calcium in the form of calcium gluconate is given by a slow intravenous (IV) drip to raise the calcium level in the blood to normal. Large amounts of IV fluids are given to flush the kidneys and remove any oxalate before it can damage them.

  In the emergency room your victim would likely have a thick rubber lavage tube passed through her nose and into her stomach. The stomach would be lavaged with milk or calcium citrate. An IV would be placed for calcium gluconate infusion and to give several liters of D5NS (5 percent dextrose normal saline solution), and blood tests would be run to evaluate kidney function and assess blood calcium levels. An EKG would be done immediately, and she would be admitted to the ICU for monitoring of her cardiac rhythm.

  Prognosis and long-term problems would depend on the degree of exposure and the rapidity of treatment. Recovery could be as short as twenty-four hours if treatment is effective and no cardiac or kidney complications occur, and she could have no long-term problems. Or she could suffer cardiac arrest and undergo CPR. She could suffer kidney failure and require short- or long-term dialysis, or she may need a kidney transplant at a later date.

  Does Selenium Make an Effective Poison?

  Q: I read recently about a murder case involving selenium and might want to use this in my current novel. What is

  selenium, and how does it work as a poison? What are the symptoms of poisoning, and if the intended victim survived, what medical treatment would be required?

  A: Selenium is a nonmetallic element in the same chemical family as sulfur, oxygen, polonium, and tellurium. It is an essential element for life, and its deficiency can lead to various medical problems, the most important being cardiomyopathy (a weakening of the heart muscle). Interestingly, Marco Polo may have discovered the first cases of selenium poisoning when he described a disease called "hoof rot," which occurred in horses in the Nan Shan and Tien Shan Mountains of Turkestan. The soil in that area is rich in selenium.

  Selenium poisoning is rare, although it does occur in industrial situations. Its principal applications are in the manufacture of glass, ceramics, photoelectric cells, semiconductors, steel, and vulcanized rubber. The most toxic forms are selenium dioxide (Se02) and selenious acid (H2Se04).

  Acute poisoning is most often lethal. The ingestion or inhalation of selenium dioxide or selenious acid (found in gun bluing solutions) can cause a dramatic drop in blood pressure, due to its toxic effects on the heart muscle, and a dilation (opening up) of the blood vessels throughout the body, which can lead to cardiac arrest and death. It can cause severe burns to the skin and the lining of the mouth as well as the lungs, where bleeding and pulmonary edema (lungs filling with water) may result. A reddish pigmentation of the teeth, hair, and nails coupled with a garlic-like odor on the breath are typical of acute poisoning.

  Chronic poisoning occurs with long-term, low-level exposure. The victim's skin may develop a reddish hue, and a pruritic (itchy) scalp rash may appear. The hair becomes brittle and breaks easily or falls out. The nails become brittle and display red or yellowish white transverse or longitudinal lines. The breath smells of garlic, and the victim may complain of a metallic taste in the mouth. Nausea, vomiting, fatigue, irritability, emotional lability, depression, tremors, and muscle tenderness may also occur.

  The diagnosis of selenium poisoning, either in the living or at autopsy, is made by testing the victim's blood and urine for increased selenium levels. At autopsy, findings would likely include congestion in the lungs and kidneys, patchy scarring and enlargement of the heart, edema and swelling of the brain, and a orange-brown discoloration of the skin and internal organs.

  For those who survive, treatment consists of stopping any chronic exposure and using intramuscular doses of dimercaprol (also called BAL, or British Anti-Lewisite). BAL acts as a chelating agent by binding the selenium and removing it from the body via the kidneys. The usual schedule is the injection of 3 to 5 milligrams per kilogram of body weight every four hours for two days, every six hours on the third day, and then every twelve hours thereafter for ten days.

  For your purposes, either an acute or a chronic poisoning could work, depending on whether you want the character to die right away or slowly over a month or so. Gun bluing solutions contain lethal amounts of selenious acid, and a couple of table
spoons added to food or drink could kill the person in a couple of hours. Adding a little here and there day by day would accomplish a chronic poisoning. The victim would gradually become sicker. His appetite would disappear, his weight would drop, and nausea and vomiting would occur. His hair would fall out, and he would become weak, short of breath, and irritable. His hands would develop a tremor, and he might develop heart failure and pulmonary edema. His doctor might diagnose heart disease or gastroenteritis or even the flu. Selenium poisoning would never enter his mind. He would treat him with digitalis and diuretics or suggest fluids, aspirin, and rest. As the condition progressed, the victim might be hospitalized and then die of progressive heart failure. Since death from heart failure is a common occurrence, the death would likely be written

  off to plain old heart failure—that is, until your protagonist became suspicious and tracked down the true cause of the victim's demise.

  How Quickly Would Someone Die After Drinking Alcohol Laced with Xanax?

  Q: One of my characters crushes Xanax tabs and then adds the powder to another's Scotch. Both men have been drinking. Would the Xanax interact quickly with the alcohol to depress the central nervous system? How much should be used to achieve the desired effect? Would there be any immediate reaction to the mix (that is, vomiting)? What would the specific symptoms be as the character slips into unconsciousness, and how soon would death occur?

  A: Xanax (alprazolam) is a short-acting sedative in the benzodiazepine family (along with Valium, Halcion, Restoril, Ativan, and others). It is a relatively safe sedative, but when mixed with alcohol, it can be deadly. Of course, it depends on the dosage of both the Xanax and the alcohol as well as the underlying health, size, and age of the victim. People with chronic lung or heart disease are more susceptible, as are the young and the old.