Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE JANUARY 1998 ISSUE THE POISON SLEUTHS DEATH BY PHOSGENE -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young man today. His eyes look suffused. What happened to him? Please tell me." "Good morning Tarun. The name of this 36 year old man is Manhar. He is a welder by profession and was working for the last five years as a welder in Messers Arihant Welders Ltd. Welders as you know work with hot torches, and seal metallic objects. He used to weld metallic pipes in a small confined space in basement. Yesterday he was suffering from common cold, but he reached his workplace at 9 am as usual and started welding pipes in the basement. After sometime, a cup of tea and some snacks were sent to him by the management as he was having common cold. This was not a usual practice, but as he was ill and the management wanted quick work on that day, this sympathetic gesture was made. He took tea and snacks and got back to work. Soon he started feeling as if his throat was dry and burning. His eyes began itching, and there was a copious outflow of tears. He took it merely to be an aggravation of his common cold symptoms, and kept on working. Soon however he started coughing violently. Still he did not take things seriously. He took some water to soothe his throat and continued working. When the cough became unbearable, he came up and told about this experience to the manager on duty. He asked him to relax on a side chair. Soon thereafter he died." "Oh, sure enough this is a mysterious death. What do you think happened in this case?" "A few facts about Manhar would be in order before I proceed with this story. Manhar was a Union leader, and for the last three months was fighting with the management for better working conditions and salary. I have talked to the Union and its other leaders. They all hold Manhar in great respect. They have come out with a most outrageous suggestion, and in fact that is part of the reason, why his body is with me today." "What have they suggested doctor? Please let me know." "Well, the Union leaders think that the management has secretly poisoned Manhar. There is no secret of the fact that the management did want to sack Manhar, the moment he took up the cause of workers. But they couldn't do so, because the Union threatened to go on strike. Since then the Management was thinking of various ways and means of doing away with him. The Union leaders- as well as the family members -think that the management sent poisonous tea and snacks to Manhar on that fateful day. Manhar was naive enough to think that the Management was being friendly to him, and took the tea. The fact that Manhar started having symptoms of throat irritation, redness of eyes and coughing immediately thereafter has lent strength to their suspicion." "Well come to think of doctor, even I think that he might have been poisoned." "Tarun, I have made a habit of examining the scene of crime always before starting the autopsy. So before starting the autopsy on this case, I asked police to take me to the place where he was working. I was surprised to find that he was working in a really cramped place in the basement. The place had a rather musty odour. "Perhaps you are suggesting that he died of suffocation. But he was working there daily for the last five years, and nothing happened to him!" "Yes that's right. But I looked around and found some strange looking cans there. I enquired about these cans and was told by the Management staff, that they contained dry-cleaning fluid. They were soon going to expand into dry-cleaning business and for this purpose had bought dry-cleaning fluid and had stored the cans there. Some of the cans were lying open...." "Sorry to interrupt you doctor, but is this observation of any help in this murder investigation?" "Oh yes, surely it is. When you look at all the facts, you can pinpoint the probable cause of his death." "Sorry doctor. I can't make any head or tail of the facts you have just mentioned." "Tarun dry-cleaning fluid usually contain chlorinated solvents, such as carbon tetrachloride or tricholoroethylene. I investigated about the contents of that dry cleaning fluid and found out that it contained tricholoroethylene. It is a well known fact that welding in a poorly ventilated, confined space in the presence of chlorinated solvents can cause phosgene to form rapidly in lethal concentrations. After I found the dry cleaning cans there, and saw how cramped the place was, I immediately came to the conclusion that Manhar must have died of phosgene poisoning. There were some additional pointers to my hunch. In the first place the place had a musty odour much like the actual smell of phosgene...." "But Manhar never noticed the smell. If phosgene was forming, he must have noticed it." "Phosgene is not a particularly offensive smelling gas. Its odour has been described as musty, resembling that of fresh mown hay or green corn. Of course, in high concentrations phosgene is rather pungent and mildly irritating, but Manhar was having severe cold on that day and it is quite possible that he couldn't notice the smell because of his cold. In addition to the smell, the other things, that go in favor of phosgene poisoning are the peculiar symptoms that he displayed...." "Oh, well, I am getting the idea. You certainly are a clever doctor. But let us begin from the beginning. Tell me something about phosgene first, so I could follow you better" "Tarun, Phosgene is a colorless gas, about 3.43 times heavier than air. It liquefies at 80 C. Phosgene is an acidic chloride and its chemical formula is COCl2 . It is known by several other names. Some of these are Carbonic dichloride, carbonyl chloride, carbon oxychloride, and chloroformyl chloride. It has a musty odor resembling fresh mown hay or green corn as I have already told you. Because of these peculiar properties, and especially the fact that it is heavier than air, it was used extensively in gas warfare in World War I, and caused 80 per cent of the deaths by gas in that conflict. Fortunately, gas warfare was sparingly used in World War II, otherwise the casualties could have been much more. A curious fact is that smokers report a flat, metallic taste when smoking in the presence of phosgene. Phosgene does not occur naturally and was first synthesized by Sir Humphry Davy in 1812 by means of passing carbon monoxide and chlorine through charcoal. It was quite natural for a curious mind to do such an experiment, because these two were the most poisonous gases known at that time, and one would have thought, he could perhaps create a deadlier gas by mixing the two chemically. In a way, he succeeded too, because phosgene is in fact deadlier than both the other gases. According to most estimates, Carbon monoxide can prove fatal if inhaled in a concentration of 1000 ppm for sometime....." "Sorry to interrupt you doctor, but would you tell me the meaning of ppm?" "Sure, ppm is an abbreviation of parts per million. When we talk of the toxicity of gases, we usually talk in terms of ppm. If I mix 1 cc of a poisonous gas with ordinary air in such a way that the final volume of the mixture turns out to be 1 million cc, the concentration of the poisonous gas in that mixture would be referred to as 1 ppm. Of course you can understand that to make the final mixture to be 1 million cc, I would have to use 999,999 cc of ordinary air. Similarly if I mix 1000 cc of a poisonous gas with 999,000 cc of air, the resulting mixture would measure 1 million cc and the concentration of poisonous gas in that mixture would be 1000 ppm." "Oh, that is quite clear doctor. So you were telling me about the lethality of certain gases." "Yes, I told you about the lethality of Carbon monoxide. For chlorine the fatal concentration has been estimated to be somewhat lesser; about 400 ppm, but phosgene kills rapidly in as low concentration as 50 ppm. Its lethality is compounded by the fact, that it is not a particularly irritating gas, being only mildly irritating and that too in high concentrations. Because of this curious fact, the victim does not make any attempt to run away from the gas, as he would do if he were exposed to, say, chlorine. This is what happened in Manhar's case. In fact phosgene is such a dangerous gas that cylinders of phosgene are not normally supplied by the manufacturers unless they have satisfied themselves that the purchaser and his premises are satisfactory." "But why would anyone want to buy such a deadly gas doctor?" "Tarun, Phosgene is an important industrial chemical being used in the synthesis or manufacture of isocyanates, polyurethane, polycarbonate resins, aniline dyes, pharmaceuticals, plastics, and insecticides. It is also used in the "Uranium enrichment" process. Because of its wide use in industry, there is always a danger of workers getting dangerously exposed to it. Currently it is generally agreed that a Maximum Allowable Concentration (MAC) of phosgene should be 1.0 ppm of gas, which means that during a 10 hour continuous working period, there should be no more than 0.1 ppm of the gas in the environment (0.1 ppm x 10 hours = 1 ppm). Phosgene can form by burning of several compounds, most important of which is polyurethane. This is the chemical with which furniture upholsteries are made. In December, 1987, in Tampa, Florida, an individual was filling an air mattress with a hair dryer when the mattress exploded, burned and released phosgene into the apartment. This occurred because the mattress was made of polyurethane. This gas represents one of the many hazards to fire-fighting personnel and fire victims for similar reasons. Welding in a poorly ventilated, confined space in the presence of chlorinated solvents or other halides can cause phosgene to form rapidly in lethal concentrations as I have already told you. You would be surprised to know that phosgene was also implicated in the Bhopal tragedy that occurred in our country in December 1984..." "Yes, that certainly surprises me doctor. Because I was under the impression that the gas responsible for the tragedy was Methyl Isocyanate (MIC)." "Oh, sure it was. But that was just one of the main gases involved. MIC in turn is made from phosgene and methylamine and is used as an intermediate product in the manufacture of carbamate insecticide Carbaryl, or Sevin, the chemical which Union Carbide used to make. On that fateful day nearly 50,000 pounds of stored MIC was released in vapor and liquid forms over a period of 2 hours. Because of the hypothesized reactions that took place within the storage tank and in the surrounding atmosphere, it is thought that MIC, phosgene, and hydrogen cyanide all played a significant role in this disaster." "That's certainly a good addition to my knowledge doctor. Tell me doctor, how does phosgene kill?" "Tarun, phosgene damages the body in several ways. It slowly hydrolyzes in mucus membrane water to produce carbon dioxide and hydrochloric acid. Because this hydrolysis tends to occur slowly, phosgene is less irritating to the mucous membrane of the upper airway and eyes and therefore penetrates more deeply into the lungs. Formation of hydrochloric acid within the lungs causes damage to lung cells. This causes water to ooze out of the blood into the lungs. This in turn causes lungs to become water logged, a condition medically known as pulmonary edema. This is a very important and conspicuous finding in deaths due to phosgene. I have examined Manhar's lungs, and they are severely water logged. Hydrochloric acid can also cause red blood cells to break down, a process medically known as hemolysis. This usually occurs at high concentrations. There are other complex reactions too, which cause severe kidney and liver damage." "Doctor, earlier you said that Manhar's symptoms also led you to conclude phosgene poisoning. Can you tell me what are the symptoms experienced in phosgene poisoning." "Oh sure. In concentrations of 3 ppm, phosgene causes dryness and burning of the throat. At 4 ppm, it causes eye irritation, redness of eyes, and watering of eyes. At 5-10 ppm, it causes coughing. Exposure to 25 ppm for 30 minutes is very dangerous, and even brief exposures to 50 ppm or greater is rapidly fatal. You will remember that Manhar displayed roughly the same symptoms. 80% of mortalities occur within 48 hours of the initial exposure, which may be considered as its fatal period. There are no specific diagnostic tests for phosgene exposure. A detailed and meticulous history and crime scene examination is the only likey thing to help. And that certainly has helped me. Come let us tell the police that the management is innocent. They have not given any poison to Manhar. But certainly they were careless to keep those cans in the basement. The management may be charged for being careless, but certainly the charge of murder can not be proved." "Oh, how very clever of you doctor. This was a most interesting discussion. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very deadly poison- Sodium Monofluoroacetate, commonly known as SMFA."

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< Back To Main Page. LinkedIn X (Twitter) Facebook Copy link Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Volume 26 Number 1 ( January - June ) Contents Editorials Puneet Setia Apology Laws – Are they the right answer for Medical Practitioners? By Puneet Setia India DOI: 10.5281/zenodo.14599219 Read > Papers P Shruti Knowledge and Attitude Towards End-of-Life care and Advance Directives amongst Medical Students and Postgraduates in a Tertiary care Hospital of South India By P Shruthi ¹ , J Damodharan ² 1. Professor, Department of Forensic Medicine and Toxicology 2. Former Dean and Professor, Department of General Medicine, Saveetha Medical College, Chennai, Tamil Nadu, India India DOI: 10.5281/zenodo.12666258 Read >

Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE NOVEMBER 1999 ISSUE THE POISON SLEUTHS DEATH BY CICUTOXIN -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a middle aged man today. What happened to him? Please tell me.” “Good morning Tarun. The name of this man is Radhey and he is about 54 years old. He was a carpenter by profession and had been in good health till yesterday. Yesterday morning he went to catch some fish in a nearby lake, along with his friend Shyam. Both of them were very friendly. While they were fishing, a person by the name of Lal came there and offered some sweet potatoes to them. Sweet potatoes as you perhaps know are known as ShakkarKandi in Hindustani. Both of them ate some of it. Shyam however spat out after one bite, because he thought it was not tasting how it should be. Radhey took some lusty bites from it, because he was hungry, and he liked its taste too. Half an hour after eating the plant, Radhey felt nauseated and dizzy and had stomach pains. Following this, he suddenly stiffened, fell on the ground unconscious, and made gross, irregular movements of his arms and legs. Shyam was alright by this time.” “Oh, from the story it appears to me, that Lal had given Radhey some poison mixed in sweet potatoes.” “Yeah, it sure does. The police has investigated into the background of Lal, and they have found that Lal held some grudge against Radhey. He wanted to settle an old score with him. So it does appear that Lal had a motive to give him some poison. The question is whether we can prove he gave him some poison or not. According to the only eye witness available - Shyam - the only thing Lal gave to Radhey was sweet potatoes. And sweet potatoes are not poisonous. So the police is going to have a tough time in the court proving anything against Lal. Sure enough they are banking heavily on my investigation.” “So what have you found doctor?” “Let me complete my story first. About one and a half hour after eating the sweet potatoes, Radhey was admitted to a hospital emergency room. On the way to the hospital, he was reported to have had four convulsions. I have asked the doctors who treated Radhey, about his condition when they first saw him. They tell me that when he was brought to them - at about 10 am yesterday - he was comatosed, and was bluish all over. This bluishness is known as cyanosis in medical terminology.” “Oh, that is terrible!” “Yes. He was not responding to any painful stimuli, which means he was really in a deep coma. His blood pressure was normal, but his pulse was more than twice the normal- about 150 per minute. The normal rate as you know is about 72 per minute. His breathing was stertorous. He was perspiring extensively, drooling saliva from his mouth, and his parotid glands were markedly swollen. He alternately clenched and ground his teeth and made chewing movements. His tongue was bleeding from a left sided laceration. His arms and legs showed intermittent, coarse, uncoordinated, and restless movements. He had extreme but intermittent muscle spasms, in particular of the muscles of shoulder and neck, causing throwing back of the neck. The pupils of his eyes were markedly constricted. In fact so constricted were they, that the doctors told me they were like pin points. You know that normally the pupils have a diameter of about 4mm. In this case, they were smaller than half a mm. His eyes were red. The eyeballs protruded somewhat.” “Oh, Radhey must surely have died dreadfully. What did the doctors diagnose?” “They couldn’t know what had befallen Radhey. They gave some conservative treatment, but Radhey’s condition worsened and he expired yesterday night at about 10 pm, about 14 hours after having ingested those mysterious ‘sweet potatoes’.” “Doctor, how do you think Radhey must have died? I think Lal injected some poison in those sweet potatoes.” “He probably could have done that. But by listening to the history of this case, and after talking to the doctors, I can only think of one poison.” “What is that poison doctor. Please tell me. I am getting curious.” “Tarun, the symptoms are so peculiar that there could only have been one poison- Water hemlock.” “What? Water hemlock? Never heard of it as a poison. Could you tell me more about it please?” “Tarun, Water Hemlock is a member of the genus Cicuta, of the Umbelliferae family of plants. There are nine subspecies of Cicuta, and all are very poisonous. Cicuta virosa is the common European water hemlock, and Cicuta maculata and Cicuta douglasii are the varieties found in North America. These varieties are found in India also. Common eponyms for Cicuta are cowbane, five-finger root, snake weed, wild carrot, dead man’s fingers, poison parsnip, wild parsnip, beaver poison, muskrat weed, spotted hemlock, spotted cowbane, musquash root, false parsley, fever root, mockeel root, wild dill, spotted parsley and carotte à moreau. They are found in marshy sloughs and meadows and on the banks of streams. Cicuta plants are difficult plants to identify, which may explain why Radhey mistook them for sweet potatoes. In fact, they have been mistaken for many diverse edible plants such as artichokes, celery, sweet potatoes, sweet anise, and wild parsnip. Cicuta plants are difficult to identify in the early spring, when only the fleshy swollen roots, particularly toxic at this time, are present. Later in the year, the roots are less poisonous, but the leaves and stem then contain sufficient poison to prove fatal if ingested.” “Oh, I see. What is the poisonous substance present in these plants doctor?” “Cicutoxin. Chemically, it is a highly unsaturated higher alcohol. Its formula -if you care- is: HOCH₂ (CH₂)₂ (C≡C)₂ (CH=CH)₃ CH(OH)CH₂CH₂CH₃ There is another poison in these plants, and that is Oenanthotoxin. This is found in Cicuta virosa, and is actually an isomer of cicutoxin. It was first isolated by a scientist Boehm in 1876 and was crystallized by Clarke in 1949.” “Doctor, how do these poisons actually kill the person?” “Tarun, Cicutoxin belongs to a category of poisons known as cholinergic poisons. This name comes from a natural substance found in the nerve endings, acetylcholine. You may be surprised to know that although acetylcholine is normally found in nerve endings - in fact it is essential for muscle contraction - an excess of this substance can prove dangerous to human body. Many insecticides such as organophosphorus compounds also show cholinergic effects and prove poisonous because of that.” “Oh, I see. Please tell me more about these poisons doctor.” “Cholinergic poisons exhibit two main groups of symptoms. One are called muscarinic effects, because they resemble the symptoms caused by eating a poisonous mushroom Amanita muscaria. These symptoms include salivation, perspiration and constriction of pupils. In fact, the moment I heard these symptoms from the doctor, coupled with the information that Radhey had been given “sweet potatoes” by a potential foe, I came to the conclusion that he had been given the root of some plant of the Cicuta species. The second group of symptoms is called the nicotinic effects, because they include symptoms caused by nicotine, a very poisonous alkaloid found in tobacco. Main among these symptoms are muscle twitchings and convulsions.” “Doctor, we have all the circumstantial evidence that Lal gave some poisonous roots to Radhey, but how are you conclusively going to prove in the court that Lal indeed gave him this substance?” “Tarun, I have taken the stomach contents of Radhey and have done a chemical test on that. They have proved positive for Cicutoxin and Oenanthotoxin. This surely means he has been given Cicuta roots by Lal. I did not stop at that. I specifically asked the police to raid Lal’s house. They raided and found many more such roots. Here they are, and any botanist can tell to the court that they are roots of Cicuta plants. Do we need any more proof than that?” "Surely not doctor. That was very clever of you doctor. Without your clever deduction - especially your noticing the peculiar symptoms of Radhey at the time of his death, and your sound knowledge of botany- everybody would have thought he died of some mysterious natural disease. This was a most interesting discussion doctor. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison- Brodifacoum."

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SCIENCE IN CRIME DETECTION-1 WHEN DID THE MURDER TAKE PLACE ? Many a time I have been called by the police to places where dead bodies are lying and I am asked to tell them when a particular person was done to death. This is a very important question for the police to know. Imagine a person found dead in a hotel room at 10.00 pm by a waiter. Visitors' register and statements of various hotel employees reveal that four people met that man on that day at 10 am, 1 pm, 3 pm, and 7 pm respectively. Obviously, the murder was committed by one of them. Many might imagine the last visitor to be the murderer, because, had an earlier visitor murdered the man, the next visitor would have informed the police. But this is not necessarily so. A man might knock at the door, get no answer and return. Also, a visitor with a criminal record may have been too afraid to inform about the murder, even if he had discovered the dead body. Thus, it becomes very important to tell exactly when the person died. We use a very ingenious technique to do that. A law of physics says that a hot body always comes back to the temperature of its surroundings. Thus if you keep a glass of hot milk on the table, after sometime, the milk cools down. Our bodies also work similarly. While living, however, the various life processes keep the human body warm and do not let the body cool. At the time of death, all life processes stop and the body starts cooling down. All human beings have a temperature of 98.4 0 Fahrenheit. The surrounding temperature in shade varies from 60 0 to 80 0 Fahrenheit depending upon the weather. So, after death, the body tends to cool down and come to the temperature of the environment. We do not take the temperature of the dead body by keeping the thermometer in the mouth, as is done in living beings. This is due to various reasons. For one thing, we are interested in taking the core temperature of the dead body and not the surface temperature. Core temperature is the temperature of the internal organs of the body, while surface temperature is the temperature of the skin. Surface temperature is generally lower than the core temperature. Thermometer in the mouth or axilla gives the surface temperature, which is not of much interest to us. Another reason why we do not take the mouth temperature is that the jaws become stiff after death. So, it becomes very difficult to open the mouth of a dead person and if someone forcibly inserted the thermometer in the mouth, there is every likelihood of the thermometer getting cracked. After death, the body starts cooling in a well-defined way. In summers, a dead body cools by about 0.75 0 Fahrenheit ever hour and in winters, it cools faster- by about 1.5 0 Fahrenheit every hour. The first thing that we do after arriving at the scene of crime is to insert a thermometer deed in the rectum of the dead body ( see figure 1). We insert it almost 4-5 inches deep. This gives us the core temperature of the body, in which we are interested. In fact, there are several ways to take the core temperature of the body, but this is the simplest. Many doctors prefer to make a small incision (about 0.5 cm), just below the rib margin on the right side of the body and insert the thermometer deep in this nick ( see figure 2 ) . Since the liver lies just below this nick, the thermometer gets inserted in the liver. This procedure also reveals the core temperature but many doctor do not prefer this method, because it injures the liver. Later, when the body is opened for post mortem, some difficulties may be encountered in assessing the injuries to the liver, if there are any. This is because the insertion of the thermometer may have interfered with the injuries already present in the liver. Some other doctors prefer to take the brain temperature. For this, they drill a hole in the skull and then insert the thermometer deep inside the brain. In the case of females, some doctors prefer to insert the thermometer in the vagina and take the vaginal temperature. However the most common site remains the rectum, as shown in the figure. We already know the rate of cooling of the body after death. Suppose I am called by the police at 10.00 pm to a hotel room, where a dead body is lying. I will first of all take the rectal temperature. Suppose the temperature is found to be 87 0 Fahrenheit. It is the month of February and I know that dead body cools at the rate of 1.5 0 Fahrenheit every hour in winter months. The loss in temperature is (97.4-87) 0 or about 10.4 0 Fahrenheit. Dividing it by 1.5, I get the number of hours the person has been dead to be seven. I deduct 7 hours from 10 pm (the time when I am making the examination) and arrive at the correct time of murder- 3 pm. The police summons the visitor who called the murdered man at 3 pm, and detailed questioning begins. Simple, isn't it? But as Sherlock Holmes used to say, all deductions seem simple when they are explained. They are difficult only till they remain unexplained. (Next issue: From what distance did the person fire?)

SCIENCE IN CRIME DETECTION-22 DEATH BY AIR INJECTION I had a tremendous response for my article "Deaths in Police custody", published in the November, 1994 issue of Crime & Detective. Mr. Shambhu Nath Gupta writes from Ludhiana, Punjab that he loved the article. However he wants to know why physical torture in police custody is known as the third degree method. Well Mr. Gupta, there is no clear cut answer to this. There are many theories as to the origin of the term "third degree". One that I am aware of is this. Generally when one utters the word "third" in connection with anything it is used as equivalent to "poor" or "inferior in quality". We commonly talk of a third division, or a third rate book. We even talk of third class people, when we want to talk about mean people. "Third degree" might refer to a poor and unscientific method of extracting information from a criminal. Torture certainly is an unscientific method of extracting information from a criminal. However Mr. Sudhir Bansal from Karol Bagh has come out with another ingenious explanation. He also liked the article and has himself volunteered information on this. He says that there are three degrees of extracting information from a criminal, the degrees increasing in severity and brutality as we go up by numbers. First degree method is to extract the truth by interrogation. Second degree method is to inflict mental torture. Third degree is the well-known method of inflicting physical torture. Sounds quite a reasonable and plausible explanation to me! Many people have asked if I could tell them something about the history of "third degree" method. Well, the use of physical torture to test a person's innocence was commonly practiced in Europe during medieval times in trial by ordeal. The principle-adapted from pagan rites by the Church-was that a person's innocence in respect of a criminal accusation could be tested by his ability to withstand pain and injury. Two of the most popular tests involved contact with boiling water and red-hot metal. In cases where there was a lack of clear guilt, the accused person was required to plunge his arm into a bowl of scalding water and retrieve a stone! If after 3 days there was evidence of burning on the skin the person was judged to be guilty. Similar tests involved walking on red hot ploughshares or gripping a piece of hot metal in the hands without the flesh being burned. The idea was that if a person was not guilty of the accusation, his innocence would protect him. So much for the third degree. This time I am going to tell you about a very ingenious way of committing murder. This is by injecting air in somebody's veins. If somebody is indeed murdered using this technique, it is extremely difficult to detect it. Yet there are ways to detect it, if the forensic pathologist is careful. The interesting thing about this sinister technique is that it uses none of the traditional gory weapons like firearms or daggers, nor does it use poisons. The murder device is quite simply and surprisingly air, which is so harmless and ubiquitous. It is almost unbelievable that such an innocuous looking thing as air could kill someone. Actually air or for that matter anything in this universe can kill a person, if it is wrongly placed in a human body. This case is also a similar case. In this case air gets ensconced in a place where it normally shouldn't be! Such cases are technically known as cases of "air embolism". The word embolism comes from Greek en, "in," and ballein, "to throw or cast". Since in this technique, air is "thrown in" or "cast in" the blood vessels, it is known as air embolism. Henceforth we will be using the term "air embolism", whenever we would refer to injection of air in the blood vessels to kill someone. Readers may be interested to know that the concept of air embolism for murder has been used time and again in crime novels, one of the best instances being in the famous writer Dorothy L. Sayer's novel where `a hypodermic of air was injected into an artery'. Before telling anything further about death by air embolism, let us first understand a little bit about the way our blood circulates in our body. This is very essential to understand how a person get killed by injection of air. Our heart is comprised of 4 chambers. There are two chambers on the right and two on the left side. The chambers on the right side are known as right atrium and right ventricle, while the chambers on the left side are known as left atrium and left ventricle. The location of these chambers will become clearer by referring to the adjacent figure (Ed: Please reproduce the figure on page 282 here. Please reproduce in colour, as this is very essential for proper understanding) . Here lungs, legs, head and arms are depicted only symbolically. Bad blood from legs, head, arms and in fact from every part of the body returns to the upper right chamber called the right atrium. The bad blood in the figure has been represented by blue colour, while the good blood has been represented by red colour. Keep referring to the figure to follow the route taken by the blood. A proper understanding of the normal route of the blood is very essential. With each contraction of the heart the right atrium sends this bad blood to the right ventricle. The right ventricle, in turn, sends this blood to the lungs via pulmonary arteries. Do not let the complicated names baffle you. Just remember that atrium and ventricles are fancy sounding names of some chambers of the heart. Ventricle is a larger chamber than atrium. Also keep in mind that "artery" is the name of a conduit which takes the blood away from the heart while vein is the name of a conduit which brings blood to the heart. The word pulmonary comes from Latin pulmo, "the lung". Thus "pulmonary artery" refers to a conduit which takes the blood away from the heart towards the lung. In the lung, the bad blood is purified. This is done by the help of the air which we breathe all the time (even at the time of sleeping). The pure blood (now depicted as red) is returned to the heart via pulmonary veins. The blood comes in the third chamber of the heart known as left atrium. Left atrium sends this blood to the left ventricle, which in turn, pumps this pure blood to the whole body via a very big conduit known as aorta. The body organs use this pure blood, and when this blood becomes impure, it is once again returned to the right atrium. And thus the circulation goes on. Now we are ready to understand how air embolism works. First of all we must appreciate that nature has made this whole system of circulation air-proof. This means that there is no way, air could enter this system of conduits and pipes. If somehow air could enter the system (such as by injection of plain air through a syringe), the air will form an "air lock" within the system. This "air lock" is quite familiar to plumbers and owners of diesel engines, where the normal flow of liquid through tubes is wholly or partially blocked by air. Quite in the same manner this air lock blocks the flow of blood through the arteries and veins, thus bringing the circulation to a halt. Let us make this a little more clearer. Air could be made to enter the circulation either through the arteries (red coloured conduits) or through the veins (blue coloured conduits). More commonly injections for murder are given in the veins. When such an injection is given, the air bubbles start travelling towards the right atrium. From right atrium they keep travelling onwards till they come to the lung. Here the capillaries are too narrow to allow the big bubbles to pass. The result is that these bubbles get entangled in the blood vessels of the lung. The whole blood traffic stops and the person dies very quickly. In fact his bad blood can not be purified by the lungs, because traffic of blood towards the lungs has been stopped. The body can not imagine that such a sinister thing has happened. It "thinks" that the blood is not getting purified because of lack of air. So it quickens the respiration. The person starts gasping. But nothing helps because the cause lies somewhere else and the person dies. The beauty of the technique lies not only in its simplicity but also in another thing-the difficulty of detection of this condition at post-mortem examination. When a person dies of air embolism, the only abnormal thing that is there within his body is a bubble of air somewhere in his blood vessels. If the forensic pathologist is not careful, the bubble would vanish the moment the body is opened. Thus in every suspected murder case, first of all I take an X-ray of the dead body. It might surprize the reader as to why one would like to X-ray a dead person. The reason is that the air bubbles are seen very well in an X-ray. When the body is still not open, the air bubbles lie undisturbed in the blood vessels and we can see where the bubbles lie. Look at the adjacent figure closely to know where I expect the air bubbles to lie in a case of air-embolism. In the place of lungs you see a network of conduits, which is partly blue coloured and partly red coloured. The air bubbles lie in this network of conduits, and many times in the pulmonary artery itself. When the X-ray of the dead body indicates that this might indeed be a case of air embolism, we open the body very carefully. Because if we do not open it carefully, the air bubbles might escape the moment the body is opened. In such cases we dissect the blood vessels under water. The detailed technique is very complicated and I do not want to confuse you by giving details of this technique. Just remember that we dissect the blood vessels under water. If air is present within the blood vessels, bubbles of air will be seen to emerge. It is like finding a leak in a bicycle tube by immersing the tube in water! Murder by air embolism is quite rare, despite the strong chances of a murderer escaping scot free in such cases. This is because such a technique requires great skill. Not everyone can handle a syringe, let alone puncture a vein successfully with it. I have a nagging fear that such type of murder might be very common among the drug addicts of our country. They are quite suited for committing such types of murder. They can handle syringes very deftly (almost as deftly as doctors, as they have to inject the drugs through the syringe all the time), and they need to do away with people fairly commonly. In my whole life, I have encountered just one case of murder by air embolism and that too when I was in Edinburgh. The case was of a doctor husband who had got tired of his nagging wife. The husband was carrying on an affair with one of his female patients and his wife had got hint of that. She was having fits of faintness for quite sometime. So one day the doctor filled up a large syringe with air and injected air into her veins under the pretext that he was giving her some drug. About 200 c.c. of air is required to kill a person by air embolism. I do not know how he managed to inject that much amount through a syringe. Even a commonly used large syringe takes in about 20 c.c. of air only. He might have used a bigger syringe or may be he repeatedly pushed the air inside by removing the piston from the syringe again and again. Well, the important thing is that he did use the air for committing the murder. He would have gone scot free, but when I asked one of the witnesses as to what were the symptoms of the lady when she was dying, I was told that she was gasping for air. This immediately alerted me. This is a symptom of air embolism as we have already seen. Coupled with this was the fact that her husband was a doctor. He was ideally suited for committing such a type of act. So before opening the body, I decided to take a radiograph (X-ray) of the body. Sure enough the bubbles of air could be seen in the deceased woman's pulmonary arteries. Then I looked at the dead woman's forearms. They showed marks of injection. Immediately I alerted the Lothian and Borders Police (the police force that mans the city of Edinburgh). A detailed interrogation was done and sure enough the doctor admitted his guilt. This was yet another victory of Forensic Medicine.

Main Page > Vol-27 No.- 1 > Paper 1(you are here) [Epub ahead] Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Volume 27, Number 1, January - June 2026 Received: Accepted: Ref: Tsranchev I , Timonov P , Yancheva S , Hadzhieva K , Gudelova T , Sotirova M , Fasova A , Dzhambazova E , Uchikov P. Posttraumatic Ischemic Brain Stroke After Sharp Neck Injury: A Case Report Based on Autopsy . Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology [serial online], ---- ; Vol. 27, No. 1 (January - June 2026): [about 6 p]. Available from: https://www.anilaggrawal.com/forensic-medicine-and-toxicology/vol-027-no-001/27-01-paper001 . Published : -----, (Accessed: ---) Email- Ivan Tsranchev Pavel Timonov Stela Yancheva Kristina Hadzhieva Teodora Gudelova Mirena Sotirova Antoaneta Fasova Elizabet Dzhambazova Petar Uchikov Posttraumatic Ischemic Brain Stroke After Sharp Neck Injury: A Case Report Based on Autopsy Abstract Neck injuries usually are emergency medical conditions which require special medical attention. Several complications following neck trauma could be fatal, if they are not correctly treated and diagnosed. Present case is of a 56-year- old male patient sustained sharp neck trauma, who was immediately admitted for hospital treatment, with following surgical reconstruction of the left carotid artery. Two days after the surgical intervention, the patient showed clinical signs of coma and sudden respiratory and cardiac failure, resulting in a lethal outcome. Autopsy and microscopic findings revealed a life-threatening post-traumatic complication following such type of trauma. In each case of sharp or blunt neck trauma, the diagnosis “post-traumatic ischaemic brain stroke” must be ruled out as a possible serious complication by a detailed examination, including laboratory, ultrasonography, contrast angiography and various specific imaging methods. All these medical actions as standard medical algorithm can save the patient’s life. Keywords: neck injury, posttraumatic brain stroke, sharp force trauma, fatal outcome, medico-legal case Introduction In routine forensic practice, various types of trauma can contribute to neck injuries, potentially leading to severe consequences or even a fatal outcome for the patient. Death could be directly attributed to the source of the injury or as a result of a complication following such a neck injury [1]. One possible cause of death can be a post-traumatic ischaemic brain stroke after blunt or sharp neck trauma involving blood vessels in the neck, which supply the brain with blood, which in turn can be a reason for blood clots and/or emboli, causing critical cerebrovascular blood flow blockage and death of brain tissue. In these emergency cases, if such an injury to the arteries can be diagnosed at the time after the trauma, a patient could be treated with different types of anti-clotting medications to prevent thrombosis and potential stroke formation, thus saving the patient's life. Case Presenntation A 56-year-old male patient after excessive alcohol consumption fell to the floor in a bar and injured his neck on pieces of a broken glass. Immediately after, he was transported by emergency medics to the University Hospital "St George", Plovdiv, Bulgaria. After a detailed emergency room assessment, he was transferred to the Department of Vascular Surgery with the diagnosis of an "incised wound in the neck region with severance of the left carotid artery." An emergency reconstruction of the vessel wall was performed. Two days after the surgical intervention, the patient presented with clinical signs of coma and sudden respiratory and cardiac failure, resulting in a lethal outcome. After death, the body was transferred to the Department of Forensic Medicine for routine forensic examination. During the examination of the cadaver in the autopsy room, it was observed that on the frontal surface of the neck, in its upper third, just below the tip of the chin and slightly to the left, a slit-shaped incised wound was found, which had been surgically treated and stitched with 4 sutures. The length of the wound was 5cm. The edges of the wound were relatively clean and smooth; the edges were sharp. On the left half of the frontal surface of the neck, in the upper, middle and lower thirds, a large zigzag wound was found, stitched with 15 sutures. The length of the wound was 17 cm. The edges of the wound were also relatively smooth and clean, slightly congested, with scattered necrotic areas (Fig. 1). The wound was additionally assessed by performing several deep surgical cuts. A slit-shaped wound, 1 cm long and treated with one stitch, was found 2 cm to the left of the zigzag wound in the middle third of the neck. Fig.1 showing the neck region represented with a zigzag wound Fig.2 showing the left common carotid artery and inserted prosthesis inside with a greyish-reddish dense thrombus The skin in the neck area was carefully dissected, and the zigzag wound was examined in depth. The muscles in the left half of the neck were diffusely blood-soaked with a dark reddish colour. The middle third of the sternocleidomastoid muscle had impaired integrity and had undergone surgical suturing. The muscle was dissected, and the left carotid artery was reached. It was found that a 2.5 cm long section from the common carotid artery to the carotid sinus was replaced by an artificial Dacron-type prosthesis. The left common carotid artery was opened during the autopsy, and at the upper end of the inserted prosthesis, a greyish-reddish dense thrombus was found inside, adhered to the prosthesis-vessel transition (Fig. 2). The thrombus occluded the lumen of the carotid artery by about 90%. Along the course of the external carotid artery at its beginning, two transverse tears in its intima with lengths of 0.2 and 0.4 cm were found. There was a tear in the wall of the left jugular vein at the level of the described carotid artery prosthesis. The tear is sutured. Its length was 0.5 cm. During the internal examination of the cadaver, all soft tissues forming the scalp were intact, with a moist surface and a pale pink colour. The bones of the cranium were intact. The dura mater was pearly in colour and had a smooth surface. The cerebral gyri were smoothed, and the sulci were narrowed. In the left parieto-temporal region, there was a section of the cerebral cortex, sunken below the level of the surrounding brain tissue, with a pale greyish-yellowish colour, sized 4cm by 3.5 cm. We fixed the brain in a 10% formaldehyde solution for 48 hours before conducting a detailed examination. The cerebral vessels at the base of the brain were well developed without malformations. A detailed examination revealed a hard, greyish-reddish thrombus occulting the left middle cerebral artery. Consecutive sections of the brain were made. In the left parieto-temporal region of the brain, a large area of softening with a livid-greyish colour was found, with peripheral reddish haemorrhages (infarction) around it. The border between the grey and white brain matter was obliterated (Fig. 3). This area measured approximately 8 cm x 7 cm as dimensions on the surface of the left cerebral hemisphere with depth measured 7 cm in the left cerebral hemisphere. The left middle cerebral ventricle narrowed, and the left cingulate gyrus (gyrus cinguli) was shifted to the right. In the hypothalamus in the left cerebral hemisphere, a dark reddish round haemorrhage measuring 0.5 cm x 0.5 cm was also found. A similar haemorrhage was found in the basal nuclei of the left hemisphere, measuring 1 cm x 0.5 cm. Along the course of the brainstem (pons and medulla oblongata), numerous dark reddish haemorrhages measuring from punctate to 0.5 cm in diameter were found. In cross-section, the cerebellum was clear and normally developed. Fig.3 showing the infarction of brain matter over the left cerebral hemisphere Samples from brain matter were taken, and further microscopic examination was performed with H-E staining under Primo Star Zeiss microscopes with enlargements of 10x, 40x, and 100x. The detailed microscopic examination showed haemorrhages, oedema and multiple massive punctate haemorrhages in the left frontal cortex with multiple massive punctate haemorrhages in the left parietal cortex (Fig. 4), in combination with hyperaemia of blood vessels in the arachnoid layer. Additional microscopic findings were stated during this examination as follows: corpus callosum – mild oedema, hypothalamus – massive punctate haemorrhages and mild oedema, pons – areas with haemorrhages and severe oedema, medulla oblongata – severe oedema, cerebellum – oedema, cortex – mild oedema 2. Carotid artery vessel wall – part of a vessel with mixed thrombus (fig. 5). Other samples from internal organs showed no significant pathologic changes. Fig. 4 showing multiple haemorrhages and oedema in the left frontal and left parietal cortex. H-E staining. Fig.5 showing the carotid artery vessel wall – part of a vessel with mixed thrombus. H-E staining Discussion Ischaemic strokes resulting from carotid artery thrombosis following open and closed head and neck trauma have been recognised with increasing frequency recently, and these cases involve not only adults but even children [2-6]. They can lead to life-threatening consequences or even a fatal outcome if they are not diagnosed correctly [7-10]. Ischaemic strokes resulting from carotid artery thrombosis are observed in both blunt and sharp injuries, such as in the case report described above. Carotid artery thrombosis is a rare but potentially devastating complication that can follow even reconstructive surgery of any major traumatised blood vessel of the neck region [11, 12]. The non-traumatic genesis of carotid artery thrombosis, which can lead to ischemic stroke, should also be considered in such cases. The most common cause of non-traumatic carotid artery thrombosis is atherosclerosis [13]. In the presence of an unstable atherosclerotic plaque or an ulcerated atherosclerotic plaque, the endothelium of the arteries is compromised. In these cases, coagulation factors are activated, which predisposes to the formation of thrombi. In our case report during the autopsy, no atherosclerosis of the carotid arteries was detected. Other factors, of a non-traumatic nature, also predispose to the formation of thrombi in the body, such as obesity, pregnancy, smoking, arterial hypertension, and hyperlipidemia. Our case lacks previous patient history on whether the patient had any of the above-listed diseases based on medical documentation, and no pathological changes or malformations of the vessels in the brain were identified during the autopsy and on microscopy. Other causes of ischemic stroke are emboli. Most often, emboli form in the heart in the area of a post-infarction aneurysm, in the left auricle of the heart in patients with ventricular fibrillation, and in patients with bacterial endocarditis. No such conditions were found in our case report. Taking certain medications, such as oral contraceptives, can cause blood clots to form in women. Different mechanisms can cause traumatic internal carotid artery thrombosis, including direct traumatic force delivered to the neck, the head, or the oral cavity, resulting in trauma to the soft tissues or even to the cranial bones, other possible mechanisms are whiplash trauma, seatbelt trauma or even procedures in the neck region [14]. Studies have shown that factors significantly increasing the risk of developing carotid thrombosis due to carotid artery injuries include non-penetrating head injury, basilar fractures of the skull, facial fracture, cervical spinal fractures and thoracic injuries [15], with the non-penetrating head injury being the most common single associated injury. In the literature is suggested that combined injuries to the upper part of the body /head and neck injuries especially skull and spinal fractures and combined injuries to the head and chest/ increase the risk of damage to the carotid arteries. In our case the patient did not sustain any other trauma, except to the neck. In this case, we concluded that the cause of death is an ischaemic brain stroke caused by vascular injury resulting from sharp force trauma to the neck. He sustained a reconstructive operation on the traumatised section of the common carotid artery, which was replaced with an artificial Dacron-type prosthesis, despite additional anticoagulation therapy. During the autopsy, a thrombus was found adhered to the prosthesis-vessel transition. The macroscopical and histological examinations determined ischaemic brain stroke.These results imply that the carotid artery damage location is where the thrombus originated. It is therefore very likely that the thrombus formed as a result of an intimal tear in the carotid artery caused by the sharp force trauma. The patient died three days later, with clinical signs of coma and sudden respiratory and cardiac failure. In summary, for patients admitted for treatment as a result of neck trauma caused by a sharp object, it is important to monitor them, especially in the first few days, for the appearance of neurological symptoms [16]. It is known that in the early stages of development of an ischaemic stroke of the brain, changes may not be visualised with standard imaging techniques like a CT scan. Therefore, numerous tests have been developed that can provide an early evaluation of a neurological condition, such as the MMSE (mini mental state examination) or Folstein test, the Hodkin-son abbreviated mental test score. Highly sensitive imaging methods have also been developed, such as diffusion-weighted magnetic resonance imaging (DWI or DW-MRI), which is highly sensitive to the changes occurring in the lesion and revealing subclinical neurological changes. These imaging-specific methods could be used in combination with specific biochemical markers, proving the diagnosis [17]. CT angiography is also a highly sensitive and informative imaging method which could be in helpful use for the correct diagnosis. Conclusion Different diagnostic methods, clinical assessing tests and biochemical markers could be used in cases of sharp force neck trauma to diagnose this type of life-threatening post-traumatic complication in trauma patients. In each case of sharp or blunt neck trauma, the diagnosis “post-traumatic ischaemic brain stroke” must be ruled out as a possible serious complication. A detailed examination, including laboratory, ultrasonography, contrast angiography and various specific imaging methods with the rich patient’s history, periodic neurologic consultation and physical examination, must be performed as a standard algorithm for medical action in such types of clinical cases. That could prevent fatal complications and can save a patient’s life. References 1. Tawil I, Stein DM, Mirvis SE, Scalea TM. Posttraumatic cerebral infarction: incidence, outcome, and risk factors. J Trauma. 2008 Apr;64(4):849-53. doi: 10.1097/TA.0b013e318160c08a. PMID: 18404047 2. Yılmaz S, Pekdemir M, Sarısoy HT, Yaka E. Post-traumatic cerebral infarction: a rare complication in a pediatric patient after mild head injury. Ulus Travma Acil Cerrahi Derg. 2011 Mar;17(2):186-8. PMID: 21644101. 3. Chaturvedi S, Sohrab S, Tselis A. Carotid stent thrombosis: report of 2 fatal cases. Stroke. 2001 Nov;32(11):2700-2. PMID: 11692038. 4. Moulakakis KG, Kakisis J, Tsivgoulis G, Zymvragoudakis V, Spiliopoulos S, Lazaris A, Sfyroeras GS, Mylonas SN, Vasdekis SN, Geroulakos G, Brountzos EN. Acute Early Carotid Stent Thrombosis: A Case Series. Ann Vasc Surg. 2017 Nov;45:69-78. doi: 10.1016/j.avsg.2017.04.039. Epub 2017 May 5. PMID: 2848362 5. Caldwell HW, Hadden FC. Carotid artery thrombosis; report of eight cases due to trauma. Ann Intern Med. 1948 Jun;28(6):1132-42. doi: 10.7326/0003-4819-28-6-1132. PMID: 18864120 6. Hockaday TD. Traumatic thrombosis of the internal carotid artery. J Neurol Neurosurg Psychiatry. 1959 Aug;22(3):229-31. doi: 10.1136/jnnp.22.3.229. PMID: 14402209; PMCID: PMC497379 7. Schneider RC, Lemmen LJ. Traumatic internal carotid artery thrombosis secondary to nonpenetrating injuries to the neck; a problem in the differential diagnosis of craniocerebral trauma. J Neurosurg. 1952 Sep; 9(5): 495-507. doi: 10.3171/jns.1952.9.5.0495. PMID: 12981571. 8. Moulakakis KG, Mylonas SN, Lazaris A, Tsivgoulis G, Kakisis J, Sfyroeras GS, Antonopoulos CN, Brountzos EN, Vasdekis SN. Acute Carotid Stent Thrombosis: A Comprehensive Review. Vasc Endovascular Surg. 2016 Oct;50(7):511-521. doi: 10.1177/1538574416665986. Epub 2016 Sep 19. PMID: 27645027 9. Julia C. Schmidt, Dih-Dih Huang, Andrew M. Fleming, Valerie Brockman, Elizabeth A. Hennessy, Louis J. Magnotti, Thomas Schroeppel, Kim McFann, Landon D. Hamilton, Julie A. Dunn, Missed blunt cerebrovascular injuries using current screening criteria — The time for liberalised screening is now. Injury, Volume 54, Issue 5, 2023, Pages 1342-1348, ISSN 0020-1383, https://doi.org/10.1016/j.injury.2023.02.019 10. Macdonald S. Brain injury secondary to carotid intervention. J Endovasc Ther. 2007 Apr;14(2):219-31. doi: 10.1177/152660280701400215. PMID: 17488181. 11. Setacci C, de Donato G, Setacci F, Chisci E, Cappelli A, Pieraccini M, Castriota F, Cremonesi A. Surgical management of acute carotid thrombosis after carotid stenting: a report of three cases. J Vasc Surg. 2005 Nov; 42(5):993-6. doi: 10.1016/j.jvs.2005.06.031. PMID: 16275459. 12. Iancu A, Grosz C, Lazar A. Acute carotid stent thrombosis: review of the literature and long-term follow-up. Cardiovasc Revasc Med. 2010 Apr-Jun; 11(2):110-3. doi: 10.1016/j.carrev.2009.02.008. PMID: 20347802.] 13. Torvik A, Svindland A, Lindboe CF. Pathogenesis of carotid thrombosis. Stroke. 1989 Nov; 20(11): 1477-83. doi: 10.1161/01.str.20.11.1477. PMID: 2815181. 14. Karnecki K, Jankowski Z, Kaliszan M. Direct penetrating and indirect neck trauma as a cause of internal carotid artery thrombosis and secondary ischaemic stroke. J Thromb Thrombolysis. 2014 Oct; 38(3): 409-15. doi: 10.1007/s11239-014-1077-2. PMID: 24748050; PMCID: PMC4143597. 15. Hayakawa A, Sano R, Takahashi Y, Fukuda H, Okawa T, Kubo R, Takei H, Komatsu T, Tokue H, Sawada Y, Oshima K, Horioka K, Kominato Y. Post-traumatic cerebral infarction caused by thrombus in the middle cerebral artery. J Forensic Leg Med. 2023 Jan; 93:102474. doi: 10.1016/j.jflm.2022.102474. Epub 2022 Dec 24. PMID: 36577210 16. Fisher M, Paganini-Hill A, Martin A, Cosgrove M, Toole JF, Barnett HJ, Norris J. Carotid plaque pathology: thrombosis, ulceration, and stroke pathogenesis. Stroke. 2005 Feb;36(2):253-7. doi: 10.1161/01.STR.0000152336.71224.21. Epub 2005 Jan 13. Erratum in: Stroke. 2005 Oct; 36(10): 2330. 17. Capoccia L, Speziale F, Gazzetti M, Mariani P, Rizzo A, Mansour W, Sbarigia E, Fiorani P. Comparative study on carotid revascularisation (endarterectomy vs stenting) using markers of cellular brain injury, neuropsychometric tests, and diffusion-weighted magnetic resonance imaging. J Vasc Surg. 2010 Mar; 51(3):584-91, 591.e1-3; discussion 592. doi: 10.1016/j.jvs.2009.10.079. Epub 2010 Jan 4. PMID: 20045614 *Corresponding author and requests for clarifications and further details:

Explore the intersection of coding and forensic science. Dr. Anil Aggrawal’s Forensic Programming page features tools, scripts, and insights that help automate forensic workflows and empower tech-savvy investigators. Tarun and Anil Aggrawal's Forensic Programming Page Hi, I am Anil Aggrawal, Professor of Forensic Medicine at the Maulana Azad Medical College, New Delhi, India. I am a lover of information and knowledge. "Knowledge is power", said Thomas Hobbes. It appears if he hadn't said it, I would have. Forensic Medicine is just one of the several subjects I love. Of course it occupies my main attention because it is my profession. I have always felt forensic professionals are very creative people. They have always wanted to do new things. Over the years they have been asking me over and over again, how they can make their own forensic pages. I made my first page, sometime in 1996, and have mostly been self-taught, through books, other web pages, discussions with friends and the like. But never in my life have I taken regular classes from a professional programmer. Lately a brilliant teacher has come in my life - my son Tarun. My Family You may want to skip this sub-heading. I wrote it mainly to please myself! But if you are curious about what these pictures are doing in a page on forensic programming, you may want to read on. I did not find these pictures abnormal at all, till Tarun asked me this question. I felt then, that this question needed to be addressed. A bit about my family first, without whose active support, these pages would not have been possible at all. The top row shows me and my wife Marygold just after marriage - sometime around 25 March 1983 (I got married on 16 March 1983). This picture was taken during our honeymoon in Mussourie and Dehradoon. The second picture was taken almost 19 years later - on 25 December 2001, when we visited our brother-in-law Sanjay Gupta in California. Among other things, it shows the inexorable stamp of time. The bottom row shows my son Tarun. He was born on 20 December 1984. The first picture was taken sometime in 1988, during our visit to Kausani, a lovely hill station in North India (it is now known mainly because the father of our nation, Mahatma Gandhi visited it once and praised this place). The second during 1996 during my visit to USA as a WHO fellow. He is trying threading his hand through the vertebra of a whale in a Washington D.C. Aquarium. Over the years he has grown into an intelligent and loving child. He is the one who is responsible for whatever I know about programming. But why the pictures? These show the two people I love most in my life (besides my mother, my two brothers and their families of course!). And it was mainly because of these two people that I could do whatever little I have been able to. If I could explore new vistas of knowledge, it was because my wife looked after me with great loving care. While she was looking after all my personal worries, I was busy learning new things. My child taught me programming like a great teacher. Hence their pictures. I would have known no programming at all without these two people in my life. Why these pages on Programming? Over the years forensic professionals from all over the world have asked me questions about the basics of computers and internet. They have asked how they could make their own web pages; how could they write their own programs to store and manipulate data (such as post-mortem data, clinical forensic medicine data and so on), and I have been answering them through Emails. Finally I decided I shall make a website which will say something about computers, internet and above all programming. No familiarity with programming is assumed from readers. They don't even have to know much about computers. The only thing they must have is a computer and the releveant program (say C++ compiler for C++, or Netscape or Internet Explorer for HTML). And they must know how to type! Programs can often be long, and it helps if you can type fast. No need to worry though if you don't know typing. Just copy and paste the programs in your compiler. Of course if you type out the program yourself, you learn faster. In this site, I hope to include simple lessons in HTML, DHTML, C++, Javascript, Perl, CGI, and whatever little I know of other programming languages. Are these pages relevant to Non-Forensic people too? Yes! Although these pages are meant specially for forensic professionals (I will be addressing their problems mainly), even non-forensic people can enjoy these pages. This is because the basic programming principles remain the same. I shall begin with C++, and then go on to other languages. You can go through lessons in order, test the various exercises in your computer and if there are any queries, you can always write Email to ask me. Books on Computers/Internet/Programming Although this site would initiate you into the world of computers, internet and programming, you can't learn everything there is to learn through these pages only. Very soon, you will begin to feel the need of proper books on these subjects. One of our main aims is to provide readers of these pages with information on latest books on computers, programming and internet in the form of book reviews. Readers may read the reviews of latest books and decide, which ones they would like to buy. A Lucrative Career in Forensic Programming Is there a career in Forensic Programming? Certainly. This specialty has skipped the attention of most professionals till now. But now more and more forensic and computer professionals are becoming aware of this specialty. To know more about careers in forensic programming and in other forensic fields, you may want to go to the forensic careers page. You may also want to go through the various books we keep suggesting on this site from time to time. It would help you get an insight into the world of computers, internet and programming, and you might be able to apply this knowledge to forensic fields effectively. From time to time, we also suggest other teaching aids such as multimedia, CDs, DVDs, Video and audio tapes. Look out for various announcements on these pages for these products. Enter There was a technical issue on our end. Try again or refresh.

Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE SEPTEMBER 1997 ISSUE THE POISON SLEUTHS POISONING BY RATTI SEEDS -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? Oh well, today you are examining the dead body of a young man. Oh, my God, what happened to him? He has a nasty looking puncture mark on his neck" "Good morning Tarun. The name of this farmer is Mahesh Lodi, and he is 25 years old. He has died in the most intriguing circumstances. About 6 days back, his neighbor Kiran visited him at about 10 in the morning, and demanded that he (Mahesh) should stop meeting his sister Geeta, with whom he was having a regular affair. Reportedly Mahesh refused to do this, as he was in deep love with her. Seeing that Mahesh was quite adamant, Kiran changed his stance and became suddenly soft. Apparently he wanted to leave his house, but before leaving, he asked Mahesh that he wanted to go to the bathroom to relieve himself. Mahesh who was quite relieved by Kiran's changed stance, happily showed him the way." "And so the matter was resolved there and then" "Not in the least Tarun. Actually Kiran and his family members had implored Mahesh on this count several times in the past too, because they wanted to marry her in a different family of their own caste, but Mahesh had refused point blank to stop meeting her. Reportedly even Geeta was adamant about this relationship, and that's why they wanted to pressurize Mahesh. This time, Kiran had come to settle this issue once and for all. After coming back from the bathroom, Kiran changed his stance once again, and began abusing Mahesh. Mahesh was completely taken aback by this renewed hostility. A physical tussle ensued between the two. During the tussle, there was naturally a liberal exchange of slaps and blows. During one such blow on the back of his neck, Mahesh felt as if something very sharp had stung him, but as he had a tough fight on his hands, he had to take care of Kiran first. Soon after he was able to push Kiran out of his house. After Kiran left the house, Mahesh tried to feel the area on the back of his neck where he had felt the sting, but as the area was behind his back, he could not examine it minutely and soon forgot about it. As he was feeling quite exhausted after the tussle, he went to the kitchen and drank a glass of water from the jug. Soon after, Mahesh started feeling unwell. The next day he had a nauseating feeling and vomited a few times. He contacted a doctor, who found that his pulse was rapid, and he was running a mild temperature. Thinking that he was probably running viral fever, he prescribed some fever lowering drugs (antipyretics) and pain killers (analgesics). But apparently there wasn't much relief. Day before yesterday, his condition worsened. He started feeling much weaker. He had diarrhoea too, and reportedly passed blood in his stools. He contacted his doctor again, who noted a peculiar puncture mark on the back of his neck, which was inflamed, which as you know means that it was looking angry red. Taking it to be a mosquito bite, he preferred to ignore it, although Mahesh was complaining of itching and local discomfort there. The doctor also noted that he had a weak but rapid pulse, cold perspiration and trembling of hands. He advised him to contact a City Hospital. But before he could arrange to go to the City Hospital, Mahesh collapsed and died. The doctor refused to give a death certificate, as he couldn't ascertain the cause of his death. So the police seized his body, and has brought it to me for post-mortem examination, so that I could tell them the cause of his death" "Very interesting indeed! It appears that Mahesh started having his symptoms only after he had a physical tussle with Kiran. The symptoms indicate that he was probably poisoned, but Kiran did not give him anything to eat. It could be that he surreptitiously mixed some poison in his water or food, before he left his house." "I can't deny this possibility, except for the fact that it is very unlikely. Kiran indeed went to the bathroom just before the fight, and it is indeed possible that instead of going to the bathroom, he went to the kitchen and mixed some poison in the water or food. But if he had done that, it was much safer for him to leave immediately after coming back from the "bathroom". Why would he unnecessarily pick up the fight?" "That indeed makes sense? Then why did he go to the bathroom? Do you sincerely think that he wanted to relieve himself?" "Doesn't seem very likely, especially considering the fact that immediately after coming from the bathroom, he changed his stance once again. I would rather say that he did go to the bathroom, but for a different purpose." "And what was that?" "To fix a poisonous needle between his fingers. These poisonous needles were probably lying in his pocket. When he went to the bathroom, he fixed one such needle between his fingers. That's why when he struck a blow on the back of Mahesh's neck, it was felt by him as a sting. In fact, with that blow, he had inserted the needle in the flesh of his neck" "Sounds quite interesting to me. But what poison could it be? "Tarun, I have dissected the area of the back of the neck, and I indeed have extricated this needle. Look, here it is." "Oh indeed, but it is not a metallic needle. Looks rather like a thorn to me" "Yes, indeed it is not a metallic needle. It is called sui or sutari in vernacular, and is made from a poisonous plant known as ratti in local language. Botanically this plant is known as Abrus precatorius." Ratti ( Abrus precatorius ) seeds "Oh, so it is a thorn from this plant?" "No, it is not a thorn of this plant. It is made after quite a painstaking effort. But before I dwell on this subject further, let me tell you a little bit more about this plant, so you can follow me more intelligently." "Please go ahead doctor. I am all ears" "Let us begin with the name of the plant, which itself tells us a lot. The name of the genus is Abrus which means graceful. It actually refers to the plant's beautiful flowers. The term precatorius is derived from precor, which means "to pray" because the seeds are often used as ornamental beans in rosaries meant for prayers. Several ornamental souvenirs are also made from these seeds. The plant is commonly known as Ratti or Gunchi in India. You might recall that ancient Indian weights and measures included tola, masha and ratti. This ratti referred to the weight of a single ratti seed. This seed was chosen as a standard weight in ancient Indian system, because its seed is fairly constant in weight; on an average, it weighs about 105 mg." "That is most interesting indeed." "There are more interesting facts related to this plant. The seed is known by several names, some of the more common ones are Rosary pea, because it is frequently used in rosaries - garlands meant for worship. For the same reason, it is also known as Buddhist's rosary bead or prayer bead. It has some other interesting names too. Some of these are Jequirity bean, Indian bean, Crab's eyes, Black-Eyed Susan and Indian Licorice. Licorice or liquorice is actually a European leguminous plant, known botanically as Glycyrrhiza glabra. The sweet tasting dried root of this plant, or an extract made from it, is used in medicine or as flavoring in confectioneries. Since the roots of abrus plant are also sweet tasting, the Europeans have named it Indian licorice. The plant is native to tropical Asia, especially India. It however grows in most warm, humid climates all over the world such as in the Caribbean islands and Florida. All parts of the plant are toxic, but the seeds contain the highest concentration of toxins." "What does this plant look like doctor? Can we identify it easily?" "Of course you can. It is a tender, twining plant which is woody at the base. The leaves are compound, featherlike, with 10 to 15 pairs of narrow leaflets 1/2 to 1 inch long. Flowers are pealike, 3/8 inch long, purple pink, yellowish or whitish. Seed pod is much like the pod of the ordinary edible pea; it is 1-2 inches long, borne in clusters, green when immature, becoming brown and dry, splitting open, and remaining on vine with seeds displayed. Seeds are quite attractive, and it is for this reason, that they are used for ornamental purposes. They are usually vivid scarlet with black spot at base. Some may be white with a black spot, others may be all white, or all black, yellow or even blue. In one pod there are about 4-6 seeds. The seed is oval or round, with a diameter of about quarter of an inch. It is pale and soft when immature, but hard, dry and glossy when ripe. "What poison do the seeds contain doctor?" "The seeds contain the deadly poison abrin, which is mainly responsible for the toxicity of this plant. It contains some other toxic substances too, but abrin is most dangerous. The sweet taste of the root is due to glycyrrhizin." "Doctor, you told me about Kiran using a sui to kill Mahesh. And you also told me that this sui is made in a very complicated way. Can you tell me more about it? And why can't one just mix the seeds in some food? What is the necessity of this complicated step of making needles out of this plant?" "Tarun, you have asked several interesting questions in one go. Let me explain them one by one. The seeds are about 100 times less poisonous when taken by mouth than when injected directly in the system. That is why killers prefer to make needles and inject them directly. The needles are made in quite an interesting way. The seeds are first decorticated i.e. their outer covering is removed. The decorticated seeds are powdered and then usually mixed with datura, opium, onion or powdered glass...." "Sorry to interrupt you doctor, but you have used several terms. What are datura and opium?" "They are also different poisons Tarun. We shall discuss them in some detail in our later meetings. For the time being you can remember that these are just some poisons which are used in this method. To be sure, their use is not an absolute necessity, as ratti seeds by themselves are quite poisonous, but apparently the killers want to leave no stone unturned!" "Wow! The killers are methodical too." "Certainly, why not. Well, the powder is then made into a paste with spirit and water, and long needles are fashioned out of this paste. The needles are about 1.5 cm in length - about the length of your thumbnail- and weigh about 100 mg on an average. These needles are then dried in the sun. When dry, they are known as suis or sutaris and are ready for use. As you know the name sui refers to a needle in Hindi. I have already told you how the killer uses these needles for killing. He may hold one or two such suis in his palm between his closely held fingers (the way one holds a cigarette; only much more tightly). The victim is then slapped in such a way that the suis penetrate the flesh. The effect is similar to giving an injection of abrin to the victim, and is thus obviously quite effective. You might be surprised to know that even animals are killed by this method. Almost the same method is used to kill animals too. Animals are usually killed for revenge. To take the revenge from an enemy, it is usual for a villager to kill his cattle! Animals may also be killed to prepare hides. The only difference in the method of killing is that in this case, the suis are attached to a wooden handle and the handle is then struck forcefully on the animal's buttocks. The needles find their way deep in the animal's flesh, from where the active ingredients slowly ooze out into the system, and the animal dies over a period of 3-4 days. The advantage of using this method, is that the injection marks of these suis look quite like viper bite (the necrosis around the marks is quite similar to that), and the owner of the cattle believes that his cattle were unfortunately bitten by the viper. Any chance of counter-revenge is thus averted. A clever killer may so arrange the distance between the two suis on a handle, as to completely mimic the distance between the two fangs of a viper!" "Oh, how very ingenious. I only wish killers could use their ingenuity for constructive purposes." "You can say that again Tarun. I sent the needle recovered from Mahesh's neck for chemical analysis, and it is found to contain high amounts of abrin. That proves my contention that Kiran indeed used the sui to kill Mahesh. I alerted the police to catch Kiran who would probably have gone scot free, but for this post-mortem examination. The police raided his house and have recovered lot of ratti seeds and some suis from his possession. In fact several ratti plants were growing in the backyard of his house. Subsequently the police questioned him. Initially he kept denying his involvement, but when faced with autopsy findings, he broke down and admitted his guilt. According to him, going to toilet was actually an excuse for fixing the needles in his palms. When Mahesh had refused to agree to his request, he had immediately made up his mind to kill him. In fact when he started out from home, he had kept this option in his mind, and for that reason, he had kept a handful of ratti needles in his pocket." "Fantastic! That indeed is a most outrageous poison solved in a most ingenious way. You indeed are a great poison sleuth. What are you going to tell me next time?" "Tarun, next time I shall tell you about a very deadly poison- Thallium. "

Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE JULY 1998 ISSUE THE POISON SLEUTHS DEATH BY DNOC -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young girl today. What happened to her? Please tell me." "Good morning Tarun. The name of this young girl is Seema, and she died this morning in the hospital. Yesterday night she had some severe problem for which her neighbors had taken her to a hospital, but there she died soon after. Well, let me tell you everything from the beginning. She is 24 years old and used to live alone. She is originally from UP, where her parents and family is still residing. She was doing a job in Delhi as a typist, and so was living here for about 2 years. She apparently had a love-affair with one of her colleagues Ramesh. They had a good relation for quite some time, and there were rumours that they were even going to marry." "Oh, I see. But how did she die?" "About a month back, Ramesh's parents fixed his marriage somewhere else, to which Ramesh also did not object much, which in effect meant, that he had tacitly consented for the marriage. When Seema came to know about it, she became mad, and there was a verbal duel between the two. Quite coincidentally, this happened in their office, and everyone saw them fighting them in this manner. That's how we know about this incident." "What was she saying during the verbal duel?" "The colleagues who were present there told the police, that the verbal duel suddenly started and went on for about 15 minutes, till their colleagues intervened. She was saying that Ramesh had shown utter meanness and had deserted her because of her looks. As you can see, she is quite fat. I have measured her height and weight. She is 157 cm in height and her weight is 76 Kg, which as you can see is quite much for her height. Apparently there were sexual relations between the two also, and she was heard saying that Ramesh used their friendship for his advantage, and is now deserting her. He never intended to marry her in the first place." "Is this accusation correct?" "Well, nobody knows for sure. But from what I hear from the office colleagues, Seema was not a very attractive girl, and no male was much interested in her, except for official relations. If Ramesh started nurturing relations with her, it's quite possible, that he was looking for some free fun. Once he had his fun, he decided to marry elsewhere." "Are you hinting that he killed Seema?" "No. Not me. I do not say anything before I have scientifically confirmed my facts. The sequence of events was this. Ramesh had visited her flat last night. Apparently the meeting was aimed at reconciliation. Ramesh wanted to explain Seema the circumstances under which he was marrying elsewhere. The fact of his visit last night is confirmed by Seema's neighbors. Even Ramesh himself has agreed to this fact. Apparently, he stayed there for about 15 minutes and then left. Sometime after he left, Seema knocked at a neighbor's door and told her she was not feeling well. She was sweating profusely, had very high fever, complained of intense thirst, and was in great distress. The neighbors immediately realized that something was terribly wrong with her. They took her to the nearby hospital. Before the doctors could ask her anything, she fell into a coma, from which she never recovered. She died after 6 hours." "Oh, I see. So how did she die? "I will tell you about that a little later, when I tell you about my scientific deductions. But before that, it would be very necessary for you to know, why this case has been brought to me. Her parents were immediately informed by the neighbors and they have arrived this morning. After hearing everything, they have put a very damning allegation on Ramesh. They say that last night during his visit, Ramesh must have given her something to eat because of which these symptoms started. The fact that the symptoms started just after Ramesh left has given credence to this allegation. The police also believes this theory. They think that Ramesh wanted to get rid of Seema, otherwise she could have made life hard for him. She could even have kept troubling him after marriage, and could even infuse all kinds of doubts in the mind of his future wife, so the best course for Ramesh was to put an end to her life." "What does Ramesh have to say in this regard?" "The police has enquired Ramesh, and he says that he did visit Seema to explain her his position. The marriage was being held at the instance of his parents, and he could not interfere in that. But Seema was not ready to listen to him. She was very depressed. After about 15 minutes of unsuccessful attempts at reconciliation, he left." "What do the doctors at the hospital say about the cause of her death?" "The doctors did not have much time to examine her. I have talked to the doctors there. They feel it could be a case of salicylate poisoning or perhaps even thyrotoxicosis." "I don't really understand these two terms. Please explain them to me." "Tarun, acetylsalicylic acid is used in modern medicine for the relief of pain. Ordinary dispirin, which is available in the market for pain relief contains 350 mg of acetylsalicylic acid. If too many tablets are ingested, one can get salicylate poisoning. The toxic dose of acetylsalicylic acid is about 200-300 mg/kg. Thus you can plainly see that for Seema who was 76 kg, the toxic dose is about 65 tablets. People may ingest pain killers for committing suicide. This practice although very common in foreign countries, is not so common in our country, mainly because people are not aware of this fact. But Seema was an educated girl, and she might be well aware of this fact. She was depressed because of recent developments and she might have ingested these tablets after Ramesh left. Ramesh obviously could not give her so many tablets to eat, and even if he had given her, she would not have eaten them. So if this case does turn out to be that of salicylate poisoning, it is quite probable that Ramesh is indeed speaking the truth, and had nothing to do with her death." "Why did the doctors at the hospital think in the first place that she was having salicylate poisoning?" "Because of her symptoms. The symptoms of high fever, thirst and profuse sweating are seen in salicylate poisoning. It might surprise you to know, that although acetylsalicylic acid is normally used for the control of high temperature, during overdose, it produces high fever itself. The doctors also noted difficulty in respiration and very rapid heart rate. Before she went into coma, she also had convulsions. These features are quite typical of salicylate poisoning. The same features are also seen in thyrotoxicosis, a disorder of the thyroid gland, in which the thyroid starts secreting excessive amounts of thyroxine. That is why the doctors gave this as the second diagnosis." "Oh, so now we have all the views. Now tell me what your investigation reveals." "Tarun, we can straightaway rule out thyrotoxicosis. In this disorder, the person is excessively lean and as you can see, Seema is very much overweight. Acetylsalicylic acid poisoning seems a more likely choice. But when I examined her hands, I found some yellow stains on them. This, and certain other findings, which I shall explain shortly, immediately alerted me in the direction of another poison- a very rare one, but one which causes exactly the symptoms exhibited by Seema" "What is that poison doctor? Please tell me. I am getting curious." "Tarun it is known as DiNitroOrthoCresol or DNOC for short." "DNOC? Never heard of this poison. Please tell me something more about this poison." "Tarun, DNOC belongs to a family of compounds known as dinitrophenols (DNP). These compounds are highly toxic and can rapidly produce death. Toxic effects often appear at blood concentrations greater than 30 mg/l while concentrations greater than 60 mg/l are associated with severe toxicity. Dinitrophenols are mainly used as pesticides. Dinitro-ortho-cresol (DNOC) and Dinitrophenol are the two main phenolic pesticides. These substances are used in agriculture chiefly as selective weed killers for cereal crops and for the destruction of potato haulm. In dilute solution they may be used as an insecticidal winter wash for fruit trees. The principal risk of poisoning is in the agricultural use of concentrated solutions for spraying crops. Absorption occurs by inhalation and ingestion and also through the skin; excretion is extremely slow so the poison tends to accumulate in the body. The risk of absorption is much greater during hot weather. Those exposed to these chemicals (such as farmers when spraying these chemicals) are generally recommended to wear respirators to avoid inhaling them. They are also subjected to periodical examination to determine the concentration of these compounds in the blood, which should not exceed 20 micrograms per gram. Dinitrophenolic compounds, especially DNOC stimulate the human metabolism very strongly. In fact DNOC can increase the tissue metabolism by 1200%! The effects of dinitrophenol in stimulating metabolism have been known since 1885, and at one time DNOC was even used in the treatment of obesity and misused for "slimming". "I couldn't understand that last point very well doctor." "Tarun, any compound which stimulates metabolism that greatly basically burns up your energy stores in the body. The main energy store in the body is the fat. If it is burnt, the person will get slim. All exercises are aimed at this only- to burn as much fat as possible. But exercise is time consuming, boring and exerting, so people are on the lookout for easy way out such as chemicals and drugs which can either reduce appetite or enhance metabolism, i.e. help burn up excessive fat. For the former effect, drugs known as amphetamines were once very popular, but they have lost favour as their side effects are too many and too serious. DNOC stimulates metabolism by as much as 1200%, i.e. it burns fats 12 times faster than in a normal man. Obviously this will form a good candidate for weight reduction." "Then why don't doctors prescribe it for weight reduction?" "Because it is a very toxic drug. But early in the century several people did take it for the reduction of weight. When fatalities started occurring, the doctors came to know about its serious toxic nature, and they advised the people against taking this drug. But it was commonly available, as it was a herbicide, so people purchased it with impunity and many overweight girls are known to have consumed it in an attempt to become slim overnight. But in fact nothing of that sort happened. They died instead. Following the deaths of several girls in this way, the availability of this drug was restricted to certain people only. But still many people can get hold of this drug and may consume it. You may be surprised to know that today DNP and DNOC can be illegally bought over the internet too! Many gullible youngsters who fall prey to these internet advisers are paying with their lives. These internet advisers are quacks who encash upon the gullibility of such youngsters. They claim that their concoction would cause a quick weight reduction, but it doesn't. It kills them instead. DNOC is about 5 times as potent as dinitrophenol. The characteristic effect of these two drugs is the uncoupling of the oxidative phosphorylation, causing a great increase in tissue metabolism......" "Sorry to interrupt you doctor. You just talked about uncoupling of oxidative phosphorylation. I don't understand this term quite well. Can you explain me please?" "Tarun, this is a technical term the details of which I may not be able to explain in such a short discussion. But I will tell you certain basics. When glucose is burnt in the body to carbon dioxide and water, it passes through 3 stages. The last stage is technically known as oxidative phosphorylation. During each stage some energy is liberated, which is stored in the form of ATP (Adenosine TriPhosphate) molecules. DNOC and other dinitrophenolic compounds inhibit the formation of ATP molecules, without inhibiting the process of oxidative phosphorylation. This means that although body is burning glucose continually, it is not getting any energy in the form of ATP molecules. This situation when energy is being produced, but is not available for the formation of ATP molecules is technically known as uncoupling of oxidative phosphorylation. This excess energy has to be dissipated in the form of heat. That is why patients poisoned by this poison show high body temperature and sweating. Since body is not getting adequate amounts of energy, it tries to burn more and more glucose in a futile attempt to get energy. Even fat stores are mobilized, but all the energy produced is dissipated as heat. This is the basis of increase of metabolic rate by these compounds." "Oh, I see. But the symptoms are also seen in salicylate poisoning. How did you know she had taken DNOC?" "By the yellow stains on her hands. This yellow staining is very typical of dinitrophenolic compounds. When these compounds come in contact with skin, they form trinitrophenol or picric acid, which is yellow in color. By the yellow stains on her hands, I immediately realized that she must have handled dinitrophenol compounds. I believe she was quite concerned about her weight, and was taking this compound reqularly in small doses. I do not know where she procured this compound from, but probably she must have contacted one of those quick weight reducing quacks, who must have given her this compound. When she was taking small doses, nothing dangerous happened. But due to recent developments, she was quite convinced that she had lost Ramesh because of her weight problem. In a bid to overcome her weight problem overnight, she must have tried to get at it in one go, and may have consumed a great amount of drug immediately after Ramesh left. That is how the symptoms appeared." "But how are you sure, Ramesh did not administer her this drug?" "Because of this drug's peculiar color, odor and taste. No one can administer this drug to another by deceit, without the other immediately coming to know about it. I have exmained her blood and have found high amount of DNOC in her blood. The levels are about 100 mg/l, which is surley a fatal level. Subsequent to this, I asked the police to search her house and look for all medication bottles there. Normally the police would never have even peeped there. But following this discovery, they looked at her almirah and did indeed find a medicine chest. They brought her entired medicine chest. I noticed 3 suspect looking bottles and put their contents to examination, and in one of these, not very surprisingly, I did find high amounts of DNOC. The police have noted the name and address of the doctor from the label of that bottle, and a party has been despatched to UP to arrest that doctor. It appears that the quack who prescribed this medicine to her is based in UP, and during one of her visits to her parents, Seema must have picked this medicine." "Oh, how very clever of you doctor. Without your clever deduction, poor Ramesh would have unnecessarily been arrested and implicated. This was a most interesting discussion. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison- Cadmium."

SCIENCE IN CRIME DETECTION-10 WHAT DO THE FINGERPRINTS TELL US ? Sometimes seemingly trivial clues can be very helpful in detecting crime. A fascinating case came my way about 3 years back, which I solved with practically no clues‑ well, almost. I only had a very trivial clue which no person would have even imagined to be helpful in the least. But let me begin my story from the beginning. On the morning of August 19, 1990, the body of Sunita Babbar was found in her flat in Ghaziabad. Somebody had killed her hitting her head with a heavy rod. She was married two years back and had a one year old son. Her husband Rajesh Babbar a clerk in a local private office was getting Rs. 3000/‑ per month. they were living in a joint family‑the whole family occupying a common ancestral house. The night before the killing, all members of the joint family except Rajesh, Sunita and their little son were out. They had gone to the shrine of Vaishno Devi for pilgrimage. Since a few months, tension was brewing up in the house regarding the meagre dowry Sunita had brought. Sunita's mother-in-law Tejwanti wanted that Sunita's father should have giving them a colour TV, so that the whole family could enjoy with it. However, Sunita's father could not fulfil this demand despite his best efforts. This had led to some tension in the house. Sunita's mother‑in‑law Tejwanti and sister‑in‑law Lali sometimes used to misbehave with her. Sunita's husband Rajesh used to keep quite and steered himself out of this tension. Sunita was quite tensed up with the behavior of her in‑laws. She had even written a couple of letters to her parents about this. In the evening of August 18, Sunita and her husband Rajesh were watching their black and white TV in the drawing room, while their son Raju was sleeping in the other room. At about 9.30 pm. Rajesh's friend Ashok Talwar came and invited him to his house for drinks, as he had recently got the promotion. Rajesh jumped at this offer and immediately got ready to accompany him. When Rajesh went to his bedroom to get ready, Ashok sat near Sunita and began staring at her with lustful eyes. Sunita never appreciated his such habits. Once he had tried to make an obscene pass at her and she had even complained about this to her husband, but Rajesh had laughed the matter off. Sunita had a hunch that Ashok secretly wanted to have sex with her. She had once mentioned this fact in her diary too. When Rajesh came back from his bedroom after getting ready, Sunita requested him not to go away leaving her and her son alone in the house. Rajesh did not want to miss the offer of a free drink. He assured Sunita that he will be back around 11 pm. Sunita knew he has giving a false assurance to her, but there was no option for her. Reluctantly she closed the door behind her. Then she went into her room and having nothing better to do, started writing her diary. She was in the practice of writing her diary since last ten years. This diary ultimately fell into the hands of the police from where the police came to know of many facts about her. Ashok Talwar's earlier lustful behavior and his behavior and intention on the night of August 18, was also mentioned in the diary. Apparently Sunita waited for Rajesh upto 12 at midnight and then slept. Rajesh hadn't come by that time. The police apprehended Rajesh from the house of Ashok Talwar. Rajesh told the police that on the night of August 18, when he had gone to Ashok Talwar's house, Talwar had offered him drink after drink till he blanked out at Talwar's residence itself. Ashok Talwar was a shady character. He couldn't answer police queries very well as to what had prompted him to take away Rajesh to his house on that fateful night, when he knew very well that Sunita would be alone. He persisted in saying that he wanted to give Rajesh a treat on his promotion. On enquiry the police found that Talwar had indeed got a promotion about 3 months back. The question was why he gave a treat to Rajesh after such a long period? Apparently there was no sense in giving a party after such a long gap. To the police Talwar could not give any reasonable answer to this question. Another remarkable fact was that no other person had been invited for that party. In fact it could hardly be called a party. For all intents and purposes, it appeared that Talwar wanted to have Sunita alone on that night. Police inspector Chauhan developed a very weird but convincing theory from his investigations. According to him, Talwar was having a lustful eye on Sunita for a long time, but he was not getting a proper chance. When on August 18, Rajesh's family left for Vaishno Devi, Talwar noticed the opportunity. If he could somehow draw Rajesh away from his house, Sunita would be alone and he would be able to quench his lust. So he came to Rajesh's house at 9.30 pm. and took him away on a very flimsy ground. At his residence, Talwar, completely boozed Rajesh till he lost his consciousness. In the midnight around 12 pm. he came to Sunita's house and rang the bell. Sunita opened the door thinking Rajesh had returned. Thus Talwar gained entry to Sunita's house easily. There he raped her and either killed her afterwards intentionally or she died without his intention to kill her, during the course of rape itself. Frequently during the acts of rape, the rapist tries to stifle the cries of the victim by pushing a pillow against her face. Quite possibly, after Talwar was through with Sunita, he found to his horror that he had inadvertently killed Sunita and then he bolted away, came back to his house and slept. The theory seemed very plausible and all the known facts seemed to fit in perfectly well in this story. It was at this stage, that I was called by the police inspector Chauhan to inspect Sunita's body and the scene of crime. Post‑mortem examination revealed that Sunita had died because of a head injury. Somebody had hit her head with a heavy rod. There were no signs of suffocation. This was a major blow to Chauhan's hypothesis. Yet he insisted that he was right. He had an intuition that Talwar was the killer. He now said that Talwar must have raped Sunita first and then deliberately killed her. This was also a plausible alternative. All in all we couldn't find much to disprove Chauhan's hypothesis. An examination of Sunita's genitals revealed that she was used to sexual intercourse and one act of sexual intercourse had been performed on her shortly before her death. I could not say much about the timing of the act. It could be just before her death or as long as 10‑12 hours before her death. I fixed her time of death (see 'Crime & Detective' February 1993 , page 90) as 2 am on August 19. This meant that the act of sexual intercourse could have taken place anytime after 2 pm on August 18. this was not of much help as Sunita was alone with her husband on August 18, till 9.30 pm. and that act could reasonably have been done by Rajesh himself. Chauhan was desperate to prove himself right and he went to Rajesh and interrogated him. Certainly a strange question to ask from a recently bereaved husband, yet the investigation had to be completed. Rajesh admitted demurely that he and Sunita had sexual intercourse on that day at about 5 pm. Chauhan's theory was still not busted because even after this, Talwar could have indulged in sex with her. I had not said that Sunita had only one act of intercourse. The only thing I could say was that she had engaged in sex shortly before her death. Nobody could have said anything about the number of acts she had gone through. I now concentrated on the scene of crime‑ the place where Sunita's body was found and not before long I found two short clippings of nail on the floor. It appeared that Sunita had violently resisted on attack on her and during the scuffle, the assailant tried to scratch her. During this act the nail of the assailant broke and fell on the ground. When we examined Talwar's hands all his nails had been recently clipped. Chauhan insisted that Talwar had become aware of his broken nails and to hide this fact he had clipped all his nails. Anyway, I managed to take a small sliver of nail from each of Talwar's fingers. In 2 hours, I was able to tell Chauhan with cent per cent certainty that Talwar was not the culprit. How did I do this feat? Well! before I go ahead, look at your nails very carefully. You will find long striations over them, some of them are thick and some are thin. These striations are there in a fixed pattern in each individual. Every individual could be recognized positively by his unique pattern of nail striations. I tried to match the striations of the broken nails, I had found on the floor with the striations of nail silvers I had clipped from Talwar's hands. I tried hard to match them but couldn't match them at all. We can look at the nail clippings in three major ways. Fig 1 shows all these three ways. One is to look at the untreated fingernail. A better way is to first put a thin layer of metal on the fingernail and then look at it. Another way is to look at it between crossed Polaroid films. Very few crime specialists like to look at the nails in the last way but for the sake of completeness I have mentioned all the ways. Another important fact to remember is that the striations would not match even in twins sisters. Both fingernails have been taken from the left little finger. You can easily find out that the striations do not match at all. The striations also do not change over a period of time. They remain constant and are thus a very valuable tool for positive identification. Fig 3 shows 4 clippings form the same person, taken over a period of 10 years. You can see that all striations match perfectly with each other. So, these clippings really came as a boon for Talwar. He had been arguing about his innocence from the moment he was apprehended but nobody was ready to believe him. In fact all the available evidences pointed so strongly at him that nobody could think in a different way. Now, that Talwar was exonerated, the police made more searches. Rajesh reported very soon that from his almirah some jewellery and cash were missing. The theory now shifted to that of burglary. Three noted burglars of the area were apprehended after 15 days. I took nail clippings of all the three and could say positively that out of them Kartar Singh was the one, who had committed the burglary and murder. His nails striations matched perfectly with those I found on the floor. On sustained interrogations Kartar Singh admitted his guilt. In the court too, Kartar Singh confessed his crime. The court gave due importance to my medical evidence and Kartar Singh was jailed for life. It was at that moment that Talwar came to me and touched my feet. It was my evidence based on science, which had exonerated him. I sometimes think now, what would have happened, had I not found those clipping, had I not found those clippings? Sooner or later Rajesh would have discovered that his cash and jewellery were missing. But, could merely that finding, in the absence of clippings, have saved Talwar? Could Talwar's lawyer successfully plead in the court that it was the work of a burglar and not of Talwar, because cash and jewellery were missing? I think no, because the prosecution could have argued that Talwar took away cash and jewellery just to give it the look of burglary. Talwar would have been in a difficult position to counter such argument. In fact, in past, sexual murders have been committed by family friends, who have done just this to give the whole situation a look of burglary. Anyway, even if court would have given him the benefit of doubt (which I feel impossible). Talwar would have undergone the agony of a long court ordeal. The finding of nail clippings exonerated him completely in just one go. ***