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SCIENCE IN CRIME DETECTION-21 WHAT DO THE ABRASIONS TELL US ? I had a tremendous response for my article " The use of infra-red photography in Forensic Science", published in the October,1994 issue of Crime & Detective. Many readers however could not understand properly, what I meant by infra-red rays. Mr. Suryaprabh writes from Pune," Your article on detecting blood stains was superb. But I could not understand much about infra-red rays. Could you tell me more about them in your feedback column?" Well Suryaprabh, I had decided not to put too much science in my article, but since you have asked me this question, let me tell you about infra-red rays in as simple words as I can. Ordinary light is composed of rays, which move in jumping fashion. If you had the means to see these rays, you would find that these rays move forward by jumping, much as frogs move forward by jumping. The distance through which these rays jump is different for different rays. For instance, rays of blue coloured light make very short jumps, while rays of red coloured light make very long jumps. Rays of all other colours make jumps of intermediate distance. There are some invisible rays which make shorter jumps than that made by blue coloured light. These are known as ultra-violet rays. You must have read them in connection with solar eclipse. Then there are certain other invisible rays, which make longer jumps than even the red light. These are known by the scientists as infra-red rays. Both ultra-violet and infra-red rays are very helpful to forensic scientists. Although they are themselves invisible, they make several other things visible. In the October issue we have seen, how these rays made the various blood stains visible, which were invisible otherwise. Just for the sake of additional information, I would like to add up something more. You must have heard about microwave ovens. Many of you might even be having one at home. These microwave ovens use another kind of invisible ray, knows as microwaves. These rays make jumps even longer than the infra-red rays. Similarly X-rays (which are used for diagnostic purposes in hospitals), are yet another kind of rays which make shorter jumps than even the ultra-violet rays. There are a number of other rays familiar to scientists and they make full use of them in several ways. This time I am going to you about a remarkable case which I solved about 3 years back. In 1992, I was asked to do the post-mortem examination on the dead body of a 45 year old man Pyare, who had died in a drunken brawl. He had gone to his friend Mohan's house for a drink. They started playing some kind of card game there. It involved money also, so in fact they were gambling. During the course of play, an altercation developed between the two, and Mohan, in a fit of rage threw a glass ash-tray towards Pyare. It hit Pyare on the forehead and he dropped dead immediately. Mohan had a set of two similar looking ash-trays. Many friends who used to visit his house testified that he indeed had two similar looking ash-trays. When the police searched Mohan's house after the incident, they found only one ash-tray in his house. When questioned regarding this, Mohan said that one ash-tray had broken accidentally some days back and he had thrown away the remains of that tray. Actually something else had happened. After the ash-tray hit Pyare's forehead, it fell on the floor and broke down and Mohan threw away the remains. His story was that Pyare had consumed a lot of alcohol and when he was returning home, he had fallen down the stairs and had died as a result. The police picked up the remaining ash-tray and gave it to me in the hope that it might help my work. I found that if somehow I could prove that Pyare had indeed been hit by the ash-tray, the police could nab Mohan. I did it in quite an ingenious way. Actually I found an abrasion on Pyare's forehead which gave Mohan away. But to understand properly the details of how I nabbed Mohan, we must know a little bit about abrasions. Abrasions are very superficial injuries, which are produced when the skin rubs against some rough surface (reproduce fig. 4.4 on page 126 here). If we could look at the skin under a microscope, we would find that it is constructed rather like an onion, having several layers. Just as you can peel several layers of thin coverings from an onion, the same can be done with the skin. The skin is composed of two layers, the upper being called epidermis and the lower dermis ( The upper layer is further composed of five sublayers, giving the skin a true resemblance to an onion as talked earlier, but this aspect is not necessary for the purposes of this story, so I will not elaborate it further). Epidermis does not have any blood vessels, so if something injures only the epidermis, there will be almost no bleeding. Abrasions are injuries which cause damage only to the epidermis and that's why there is usually very little bleeding from abrasions. Abrasions can be quite useful in knowing the events before death. If a person was dragged on a rough ground there will be abrasions on his back. These abrasions will tell a forensic pathologist that the person was dragged on rough ground. Not only this, these abrasions can also tell the direction in which the body was dragged. The abrasions are quite deep in the direction in which the body was being dragged. In the other direction ( i.e. the direction away from that of dragging), these abrasions can be quite superficial. This gives us the direction of dragging which can confirm or refute the statement of so-called eye witnesses. Thus if the victim was dragged by catching hold of his feet, the drag marks (abrasions) will be deeper near the feet end, and if he was dragged by catching hold of his arms, the abrasions will be deeper near the head end (reproduce fig. 4.7 on page 127 here) . In this particular case, the killer raped a young woman, and then killed her with a knife. While he was raping her, another young woman heard her cries and rushed to the spot. The scene that she saw through the bushes was too horrifying. She was too scared to come out of the bushes and help her friend. But she kept watching the killer and his actions. After satisfying his lust, the killer stabbed the woman, to remove the possibility of her going to police later. Then he dragged her by her feet, and ditched her in a nearby nallah (nallah is an Indian term which means a small stream of water - generally it refers to open sewage water stream). The killer was caught in due course of time, and the young woman, who had watched her through the bushes, gave the details of what she had seen. Her statement was challenged by the defence counsel on several grounds. It was said that she had been tutored by the police to depose against the killer. She was grilled by the defence counsel on several grounds. One of the grounds was that she had not seen the dragging of the body by the killer and was saying this merely to make the story more ghastly and also because of being tutored by the police. According to the defence story, the unfortunate woman might have fallen in the nallah just by accident. The post mortem examination showed that there were abrasions on the back, which supported the story of her being dragged by someone. Not only this, the abrasions were deeper near the feet end, and this supported the woman's story that the victim had indeed been dragged by the feet. If the abrasions are situated in more than two directions, the probability is that the deceased was dragged repeatedly in more than two directions ( reproduce fig. 4.5 on page 126 here). In this figure we see abrasions in more than two directions. This was the case of a woman who was first murdered and then thrown down a deep pit. During the fall, the body of the woman struck the wall of the pit twice, in different postures. This gave rise to two sets of abrasions, both in different directions. If this body had been given to me even without any accompanying story, I would still have been able to say, just by looking at the abrasions, that something weird had happened to the lady. It could not have been a case of simple dragging, simply because the abrasions were running in completely different directions. A case of simple dragging would have caused abrasions in one direction only. However most interesting are the abrasions which are caused by peculiar shaped objects. These are interesting because they reproduce the shape of the object causing them, and this helps us identify the object. These abrasions are known as patterned abrasions because they are exactly similar to the pattern of the object causing them. It is important to understand how they are caused. A rough object upon hitting the skin crushes the upper layers of the skin, causing abrasions. If the object has some pattern (such as the radiator or the tyre of a car), the abrasions will assume the same pattern. This happens because the pattern on the rough object crushes only those layers of the skin which come in contact with the pattern. It is rather like making the mark of a rubber stamp. A rubber stamp has certain raised areas and only those areas come in contact with the ink and subsequently with the paper. Thus we get a peculiar mark (such as the name of a company or a person). If the same stamp were made of a hard substance such as a stone, and it were strongly imprinted on the skin, a patterned abrasion will form exactly in the same shape. The patterned abrasions are thus very helpful in identifying the weapon causing them. Let us see this by a few illustrations. In one of the cases, the deceased was attacked by a `Rambo knife'. The back edge of the serrated knife produced tell-tale patterned abrasions. These abrasions clearly give the shape of the weapon. During the investigation of the case, three suspects were caught, and several knives were recovered from all of them. But only one suspect had the peculiar knife, which could have caused such peculiar looking abrasions. It could be easily proved by the forensic pathologist that only that knife could have produced the peculiar abrasions seen on the body. The suspect was prosecuted on this vital piece of evidence. Thus the patterned abrasions helped nab the killer (reproduce Fig. 4.10 on page 129 here) . In another case a man fell against a ridged tiled surface. The pattern produced on his head helped to reconstruct the events before death (reproduce fig. 4.11 on page 130 here). Normally one would have thought that he was killed, but the peculiar looking abrasions supported the story that he might have fallen against the ridged tile. Coming back to our case. I saw a pattern similar to the one shown in the figure here (reproduce fig. 4.9 on page 129 here). The head is showing a very definite and clear patterned abrasion. It consists of concentric circles. When I examined the ash-tray which was given to me, I found a similar pattern on the base. The story at once flashed in my mind. Mohan had hit Pyare with the ash-tray which had caused the peculiar looking abrasion. Like the mark of a rubber stamp, the ash-tray had left its impressions (patterned abrasions) on the forehead. Had Pyare fallen down the stairs as alleged by Mohan, he couldn't have sustained that peculiar looking abrasion. The reasoning is simple. If you see the mark of a rubber stamp anywhere on a paper, you are sure that there must be a similar stamp somewhere, and it must have been used on the paper. Similarly when I saw the patterned abrasion on the forehead (which in many ways is just like the mark of a rubber stamp, as explained earlier), I was sure that some object with a similar pattern must have been used to hit Pyare. Without that object, the mark simply could not have appeared on the forehead! Under the weight of the forensic evidence, Mohan cracked and admitted his guilt. Thus a very small and insignificant looking abrasion revealed the whole crime to me.

Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE JANUARY 1999 ISSUE THE POISON SLEUTHS DEATH BY SODIUM NITRITE -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young woman today. Her whole body seems to have a chocolate brown color. I remember last time too, I had seen a dead body with chocolate brown color. Did this woman also die of the same poison? Please tell me." "Good morning Tarun. The name of this young woman is Radhika, and she is about 25 years old. She died in her flat at about 9 am today morning. She was a junior executive in a private firm here in Delhi, and was living alone in this flat. Her family members are living in Jaipur. She was living here solely for the purpose of this job. Her parents were looking out for a match for her marriage." "Oh, I see." "Yesterday night she was fine. In fact, she met one of her neighbors Shyamala -also a 25 year old girl- at about 9pm, and she tells us that she was perfectly in good spirits. That rules out suicide...." "Wait a minute doctor. If a person is in good spirits and cheerful a day before his or her death, does it rule out suicide? Is it not possible that she was trying to mislead the neighbors by being cheerful so that nobody gets to know her intentions?" "There are other indications too. There is no suicide note. Generally a person who commits a suicide, leaves a suicide note." "Oh, I see" "Well, the police interrogated Shyamala more about her as she was the only one, who knew Radhika very well. She told the police that she (Radhika) was in love with Chaman, a 26 year old colleague in her office. Recently she had become pregnant by him, and she was pressing him for marriage. However Chaman had lost interest in her, and was trying to avoid her. Only 2 days back she had threatened him to go to his parents if he did not agree for the marriage. Chaman's parents are very religious and God-fearing, and he knew if she approached them, they would force him to marry her. To settle matters he came yesterday to Radhika's flat at about 7 pm. Shyamala knows because when he came, Radhika called her as a mediator. Shyamala tells the police that Chaman was looking very tense and jittery. She thought it was because he had such a difficult matter to resolve. Anyway she just sat there for about an hour. When she saw that the matter is going to take more time, she left the house making an excuse. When she left, Radhika was just preparing to go inside the kitchen to make tea for everyone. She offered Shyamala to go after having tea, but she just left. She however saw Chaman leaving Radhika's house only about 15-20 minutes later. She was sitting idly at her window when she saw him. He looked to be in great hurry." "Oh, I see. So did you find anything in the post-mortem that corroborates what Shyamala is saying?" "Yes, I found a 4 month old male baby inside Radhika's uterus, which definitely tells us that she was pregnant. I have kept the tissues of this fetus for his DNA profiling, which will tell us definitely if Chaman was his father or not. More about that later. What interested me was the color of her body. I told you last time (See SR December 1998 issue) that there are certain poisons which can cause methemoglobin to form inside the body. It is this compound which imparts such color to the body. Well one of such poisons is sodium nitrite. I got a hint that she might have died of sodium nitrite poisoning when I went to her flat and saw that she had unfinished breakfast on her table. She was in the habit of having a full meal in the morning itself. She had prepared Dal and Roti and must be eating it. And it was lying there unfinished. Nearby I could see some dried vomitus on the floor. Obviously when she was eating the food, she must have got sick and must have vomited. I saw a salt cellar on her table which was open. I got quite curious, when I glanced underneath the dining table and found lot of white salt like powder spilled over there. As a poison sleuth, I don't want to take chances and intuition told me there was something either in the salt cellar or in the powder spilled over the floor that we were looking for. So I quietly kept the salt cellar in my pocket and also some of the powder spilled over the floor underneath the dining table. I examined both these substances in my lab. And do you know what I found?" "What? Please tell me doctor. I am getting curious." "Tarun, I had the most extraordinary finding in the salt cellar. It had a substance looking like salt but it was not sodium chloride. It was sodium nitrite. And the salt like powder which was spilled underneath the table was nothing but sodium chloride. Do you get the picture now?" "Well, not really. I don't understand how such a curious thing happened." "To me it is clear like glass. Obviously someone replaced the salt in the cellar with sodium nitrite. And before doing this he spilled the salt underneath the table to empty the cellar so he could fill it with the poison he had brought with him. The only commonly available poison which looks and tastes like salt is sodium nitrite" "Really? Doctor I am getting curious. Please tell me more about sodium nitrite." "Tarun, as I told you earlier, sodium nitrite causes methaemoglobinaemia; even small doses of sodium nitrite can kill within a few minutes. Even the nitrates can be dangerous. Organic nitrates in fact are reduced to nitrites in the intestine. Inorganic nitrates, bismuth subnitrate excepted, are not normally reduced to nitrites in the body, but this may occur when the upper digestive tract (stomach and upper part of small intestines) is infected with nitrate-reducing bacteria, e.g. Escherichia coli. Inorganic nitrates are irritants of the stomach and, in large doses, potassium nitrate is a diuretic. A diuretic is a chemical which increases the production of urine. Poisoning by nitrites is actually not very common. It can result from mistaking this salt for common salt or Epsom salts." "Doctor, under what circumstances can sodium nitrite poisoning occur?" "Tarun, poisoning can be homicidal, accidental or suicidal. With sodium nitrite, accidental poisoning is probably most common, although homicidal poisoning is also possible as we have seen in the case of Radhika. One of the earliest reports of sodium nitrite poisoning came from Middlesborough, UK in 1936. Two adults and their daughter aged five were suddenly taken ill after the midday meal. The adults died before a doctor could reach them and their daughter died shortly after her admission to hospital. It appears they had complained to neighbors of acute abdominal pain and vomiting. Their faces went blue. Investigation showed very similar results to what I found in Radhika's case. A basin of cooking salt and a salt cellar contained sodium nitrite; the upper layer in the latter was of 98% sodium nitrite and the lower layer 98.2% common salt. Unconsumed food contained sodium nitrite, e.g. cabbage 6.5% and Yorkshire pudding 4.5%. The gastric contents of the man contained 4.275 g and those of the woman contained 1.284g of sodium nitrite. Over a gram of the poison was present in the child's vomit. The vomit of the adults was not available for analysis, but presumably they had ingested considerably more than remained in their stomachs. The source of the poison was not determined, but the man had had access to sodium nitrite in the course of his employment. Nobody knows how the mix up happened. Probably someone filled up a half empty salt cellar either intentionally or mistakenly with sodium nitrite." "Oh, that is most extraordinary and bears an eerie resemblance to the case we have on our hands." "Yeah sure. Accidental deaths due to the ingestion of sodium nitrite used in error for common salt in the preparation of soup have also occurred. Several such accidental deaths have been reported. Death in these cases occurred within a few minutes following symptoms which included nausea, headache, vertigo, urgent vomiting, profuse diarrhoea and cyanosis (bluing of the skin). Stomach contents in most of these cases contained sodium nitrite ranging from 1.74 to 84.0 mg/kg of the gastric contents. There was a more consistent concentration in the organs, e.g. in the liver, where the concentration was between 3.0 and 4.35 mg/kg. A quarter of a litre of the soup in most of these cases contained l.5 g of sodium nitrite. I must tell you that the fatal dose of sodium nitrite is from 1 to 2 g. I have already explained you the concept of fatal dose (see "Poisoning by Thallium" SR, October 1997)." "Yes doctor, I do remember you having mentioned it." "In another case, eleven men were poisoned after eating oatmeal seasoned with sodium nitrite in mistake for common salt. The men added more salt from salt shakers later shown to contain sodium nitrite. Immediately after the meal they felt sick and vomited. There was dizziness and abdominal cramps. They went blue and five lost consciousness. Methaemoglobin was later demonstrated in their blood. One of these men, aged 82, died the next morning; his organs had a diffuse brown colour. The source of the poison was nitrite used to cure meat. Only eleven of 125 persons who ate of the oatmeal were affected and these eleven had used contaminated salt shakers of which one contained 0.137% of nitrite. It was estimated they had taken at least 163 mg. In yet another case, a boy aged two months suddenly went blue, 'almost black', after his 7.0 am feed. Sodium citrate had been prescribed for the relief of indigestion and two tablets had been added to the feed. When seen in hospital, about five hours later, the appearance of the child simulated those of congenital heart disease; he was neither distressed nor febrile. A diagnosis of toxic methaemoglobinaemia was made and the remaining tablets, fortunately available, were subjected to analysis. They proved to contain 65 mg of sodium nitrite each. The infant, therefore, had ingested 130mg, the maximum dose for an adult. There are a host of other such cases of which I am aware." "Doctor please tell me a few interesting ones out of these." "In one case, two children aged two and three months respectively took feeds to which from 35 to 40g of sodium nitrite had been added in error for sodium citrate. The elder infant died. Cyanosis and blackening of the mouth were outstanding features. In another case, a boy aged two years vomited while playing with his elder brother aged nine. After a second vomit he was given a glass of water to drink. Vomiting continued and he was taken to hospital. He was deeply cyanosed, collapsed and crying with spasms of pain. Poison was taken out from the stomach with the help of a tube and oxygen was administered, but the child died at about three hours after being poisoned. Sodium nitrite was detected by analysis of his stomach contents. There was methaemoglobin in the blood. It is probable that the boy had ingested and absorbed appreciably more of the poison. The source of the poison in this case was a bottle of sodium nitrite, now nearly empty, which the elder boy had brought for the purposes of a chemical experiment. The dead child had licked the bottle. I must tell you that sodium nitrite is highly soluble in water and its taste resembles that of common salt and that is what makes it such an attractive homicidal poison. Interestingly sodium nitrite is used in machine oil also as a corrosion inhibitor, and deaths have occurred when someone accidentally drank machine oil. There is a case of a girl on record who died in this way. She was eleven years old, and drank a mouthful of machine oil accidentally, some of which she immediately spat out...." "Just a minute doctor. I think sodium nitrite is an oxidizing agent, and if I remember my chemistry alright, corrosion is an oxidative process. Then how can nitrite be used as a corrosion inhibitor?" "Tarun, sometimes oxidizers are also reducing agents. Such is the case of nitrite, which can be further oxidized to nitrate. I must tell you that the tendency of nitrite to act as an oxidizer is increased in an acid environment such as that found in the stomach. At higher pH levels its oxidizing potential is greatly decreased. Corrosion can be inhibited by using a sacrificial reducing agent such as nitrite. Sodium nitrite is also commonly put into packaged foods like meat to keep oxidation from happening. So I was telling you about that little girl. Within an hour she was unconscious and deeply cyanosed. Fortunately she recovered after proper treatment. Analysis showed that the oil contained 36.5% sodium nitrite, 7.5% of an emulsifying agent and 56.0% water. Her stomach washings contained 7-8mg/ 100 ml of sodium nitrite." "Oh, that is certainly most extraordinary!" "Tarun, sodium nitrite poisoning has happened in other ways too. Poisoning by well water drawn from badly constructed wells near farmyards may contain an appreciable amount of nitrate which makes it unfit for drinking and a source of poisoning newborn infants. This illness is however rarely fatal. About 30 cases are on record and only one, it appears, was fatal. It is apparent that the risk is only to infants of under 90 days old, who live in rural communities..." "Doctor, can boiling the water make such water safe? I have heard that boiling the water makes it cleaner." "Yes boiling the water does make it free of infective micro-organisms, because they get killed by boiling, but when the water is contaminated with a chemical substance, it gives no protection whatsoever. On the contrary, it concentrates the nitrates, which can get concentrated upto 3 times on boiling the water! Older children are unaffected, probably because they can tolerate the amount of nitrate likely to be present in their normal fluid intake. It does appear that poisoning in these circumstances is not dependent only upon the amount of nitrate ingested· It has been suggested that poisoning by nitrate will only occur in those whose gastric juice exceeds pH 4.0 and when nitrate-reducing bacteria are present in the upper digestive tract." "Doctor, this is a most extraordinary fact that you have told me. Can you tell me what is the concentration of nitrites in such contaminated water coming from wells?" "The contaminated water, usually drawn from shallow wells, of not over 75 feet deep, usually contains over 20 ppm (parts per million) of NaN03. Methaemoglobinaemia (the existence of too much methemoglobin in the blood) does not normally occur unless the water contains 30 ppm. The upper limit of nitrate should not exceed 10 ppm because as I told you earlier, if boiled the water could be concentrated threefold and thus to a dangerous concentration. Even cows which feed on beet tops rich in nitrates develop methaemoglobinaemia. This is known as the condition of 'purple' cows and is well recognized. Purple is the color the cows get when there is lot of methemoglobin in their blood." "Oh, this is most extraordinary." "There are more interesting facts Tarun. Nitrite poisoning from spinach has also occurred. During 1959-65 in Germany there were 15 cases of nitrite poisoning in infants, aged two to ten months, who had eaten spinach. Nitrite and the remains of spinach were found in the stomach contents of one of the infants. Two factors were responsible. First, the excessive use of nitrate fertilizer, which should not, but often did, exceed 80 kg/hectare. Second, bacterial activity converted the nitrate in spinach into nitrite. Samples of spinach, fresh, frozen and tinned, showed a nitrate contamination of from 40 to 2100 mg/kg. The risk arose when the feed was prepared in advance and stored overlong at room temperature. Even after cooking, a sufficient number of bacteria remained to produce nitrite. The maximum nitrate content of spinach should not exceed 200mg/kg. It has even been recommended that during the first three months infants should not be given spinach." "Doctor, such an interesting poison must have caught the fancy of suicides also. Have there been cases of suicidal poisoning too with sodium nitrite?" "Yes, sure. Suicidal poisoning with sodium nitrite has also occurred. A medical practitioner, aged 51, committed suicide in 1942 by ingesting sodium nitrite. He had been mentally ill for some time. On the night of his death he awoke his son, a medical student, and told him that his mother had suddenly been taken ill during the night. A doctor was summoned and while he was attending to the woman a bump was heard in the passage. The deceased was then found lying on the floor; he died within five minutes of his fall. Poisoning was suspected, but a search revealed only a glass of brandy and another which appeared to contain water. Toxicological analysis demonstrated 2g of sodium nitrite in the gastric contents. The blood was 'dark'. Unfortunately no analysis was made of the brandy or water, otherwise I am sure they would have found nitrite in the brandy. The deceased had given his wife some of the brandy during the night and this may have been the vehicle of poison responsible both for her illness and his death. I feel he first gave brandy laced with nitrite to his wife and then consumed the poison himself, but of course it is only a guess. But sure enough, it is possible to kill someone by lacing his or her drink with as little as 2 grams of sodium nitrite. It was believed that the poison was taken within an hour prior to his death. It was suggested by the relatives that he had died of a heart attack, but the doctor said that he had died of nitrite poisoning." "Oh, doctor. We could go on and on with such interesting stories. Tell me how you can prove Radhika died of nitrite poisoning?" "Tarun, I told you I examined both the contents of the salt cellar as well as the powder spilled over the floor. Now I will tell you what happened. Chaman came to Radhika's house not for reconciliation, but for killing her. He was sure, killing her was his only way out. He got sodium nitrite from a chemistry lab. We have still to find out, how he got hold of it, and who gave it to him. He came fully armed with this poison in a packet. When Shyamala left and Radhika went inside the kitchen to make a cup of tea, he quickly picked up the salt cellar, spilled the salt in it on the floor underneath the table and refilled it with the powder that he had brought. He knew that sometime she would consume the contents of the salt cellar thinking it was salt and she would die. It was no doubt a very clever plan, but thankfully we could catch it. The color of Radhika's body at once told me we were looking for a poison which produces methemoglobinemia, and that was Chaman's undoing. I have found an appreciable quantity of Sodium nitrite from Radhika's stomach contents, and to top it all, the police has found some left over sodium nitrite from Chaman's house too. Initially he denied having any hand in Radhika's death, but when he was told of all the medical and circumstantial evidence against him, he broke down and admitted his guilt." "Very clever doctor. This was a most interesting discussion doctor. Without your masterly deduction, Chaman could never have been caught. People might have thought, it was an accidental death. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison. You may not have even thought that it was a poison. I will tell you about death by Potassium Permanganate."

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SCIENCE IN CRIME DETECTION-31 WHEN SEX PERVERSIONS LEAD TO ACCIDENTAL HANGING This time I am going to tell you about an extremely interesting case, which had completely baffled all police experts. On 24.11.1994, I was called to a scene of death. It was a dense forest on the outskirts of Delhi. A 22 year old male, who was later identified as Pyarelal, was found hanging from the branch of a tree. Both his knees were on the ground. This in itself was not abnormal or baffling. What had baffled the police, was the fact that his penis was exposed. It was coming out of the fly of his pants which was open. (Please reproduce fig. 3 on page 164 here: Source-"Medico-legal annual 1977) . On the ground was lying a sex magazine, showing the photographs of some nude girls. To all intents and purposes, it appeared that it was a sexual revenge murder. The police had definitely ruled out suicide. It is understandable that no suicidal patient would ever commit suicide in such an embarrassing position. In fact, it is well-known to all police officers and forensic experts alike that ladies who commit suicide by drowning take care to tie their saris near the legs. This is done, because otherwise the water frequently lifts up the sari, exposing their genitals, and no lady, even after death, wants to be exposed in that way. Inspector Matadeen had formed a hypothetical story like this. Pyarelal must be a flirt. He must be carrying on an affair with some girl of the locality. Her brother or some other relative may be against this relationship. They must have asked him to refrain from this activity. Pyarelal must not have paid any attention to this. So they murdered him and then hanged him from the branch of the tree, exposing his genitals. This could be a symbolic revenge for them, showing everyone what led him to his final undoing! To be sure, cases like this are not uncommon. I have seen some similar cases, but in those cases the culprits had amputated the penis of the deceased and inserted it in his own mouth! This act shows the utter contempt the killers bore in mind for the deceased's sexual excesses. When Matadeen made enquiries, it was found that Pyare had indeed made sexual advances towards a local girl Sarita. She was considered one of the sexiest girls of the locality. She had not heeded to his advances, and had even complained to her brother Ramdayal, who was something of a local goon. Ramdayal had once beaten Pyarelal very badly and had sworn to kill him if he saw him making advances towards his sister again. Ramdayal was called at once and enquiries made. All evidence was against him. Many people of the locality affirmed that he was a local goon, and had once beaten Pyarelal very badly. They said that once he had even sworn to kill Pyarelal in front of every one. However Ramdayal pleaded total ignorance. The police was about to take him to their infamous torture chamber, when I arrived at the scene. When I saw the scene, I was sure at once that it was not a case of murder. There had to be great disturbance around, had it been a case of murder, but the surroundings were quite normal and undisturbed. There were several other factors which made me come to that conclusion. If the police were thinking on the lines of murder, it was because they were entirely unaware of an entity known as sexual hanging. Sexual hanging is a very baffling kind of phenomenon which has not been understood in its entirety till now. To understand it let us dwell on a few vital facts first. If someone restricts the entry of air in his lungs (either by conscious stoppage or respiration, or by enclosing the face by a plastic bag), his blood will receive a lesser supply of oxygen. This state is technically known as anoxia (no oxygen) or hypoxia (less oxygen). It is a well-known fact that during a state of anoxia or hypoxia, a person can enjoy sexual pleasure much more intensely. Why this happens is not very clearly understood however. Some people, especially males, come to know of this fact quite accidentally or may be through some friends. They can then induce hypoxia by putting a noose round their neck, and then relaxing their body in such a way that part of the body weight comes to rest on the noose. The noose constricts the neck, producing a state of hypoxia. The person then masturbates, looking at pictures of nude women. Once the masturbatory act is over, these people remove the noose from their neck and go back to their work. Their intention is never to kill themselves. It is only to enjoy heightened sensations of sex during hypoxic states. These persons usually return to that place the next day and masturbate again, making the same complicated arrangements. A sexual deviant may go on repeating this practice for years! Sometimes however quite accidentally the pressure on the neck increases, and the person may die inadvertently. Thus sexual hanging is neither a case of murder nor of suicide. It is a case of accidental hanging. Sometimes, the victim ties himself up in quite a complicated fashion, and then masturbates (Please reproduce fig. 2 on page 163 here: Source-"Medico-legal annual 1977) . In this figure, the person has used a dog leash and collar straps for suspension. Towels were found folded over the penis and scrotum and a collar strap was buckled about his wrists which were behind his back. Such person are suffering from a special sexual perversion known as sexual bondage. They derive pleasure in sex only after they have been tied up. Sometimes the legs may be tied up in a complicated fashio n (please reproduce fig. 6 here: Source-"Medico-legal annual 1977). In this figure you can also see a towel beneath the underpants. Besides tying themselves up, some people cover their faces with rubberized sheets (Please reproduce fig. 4 and fig. 5 on page 165 here: Source-"Medico-legal annual 1977). This produces additional hypoxia. The main problem in these cases is to differentiate whether these cases were of suicide, murder or sexual hanging. The scene of sexual asphyxia is always some quiet place, (as in the case of Pyarelal) where the complicated preparations for an act can be made without fear of discovery or disturbance. Careful examination of the scene will reveal evidence that it has been used for similar purposes in the past. This evidence may be in the form of `grooving' of a wooden beam from which a rope has been suspended. As we have seen, some of these victims have been carrying such activity for years. Repeated acts of hanging themselves may produce this `grooving' which we have just talked about. In a similar manner, if the hanging used to be done from pipes, there may be scraping away of paintwork from pipes. The paraphernalia (Please reproduce fig. 9 here: Source-"Medico-legal annual 1977) of these perverts is quite interesting. It includes protective pads, straps, hooks and even parachute rigging. Sometimes hooks are also found at the scene. This also indicates the practice of sexual hanging (Please reproduce fig. 7 and fig. 8 here: Source-"Medico-legal annual 1977). In these photographs you can see a victim suspended from hooks! In the case of Pyarelal, the diagnosis of sexual hanging was not difficult to make. The penis was extruding through the pants, which made me suspicious at once. But what clinched the issue was the presence of a nude magazine near his feet. When I searched the scene, I could recover a bag, in which Pyarelal's sexual paraphernalia was lying. I gave the verdict of sexual hanging, and Ramdayal was released. Ramdayal came to me and told me that I had saved his life, otherwise he was sure to go to the gallows. On that day I realized how useful science can be!

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:

SCIENCE IN CRIME DETECTION-41 SCIENCE IN CRIME DETECTION A clever way to identify the assault weapon ‑Dr. Anil Aggrawal In this month's column I am going to tell you about a very interesting case, which I solved sometime back. This case involves the identification of a murder weapon in a very clever way. On March 22, 1995, the police called me to a scene of crime where the dead body of a 59 year old woman was found. I received the call at about 10 am, and I reached at the place immediately. The place was a posh house in Vasant Kunj, and the lady was the sole owner of the house. She was identified as one Vindhya Kumari. She was a very rich woman who had inherited a lot of money from her parents. She was living with a 17 year old servant Ramu in the house for the last few years. Ramu would look after her day-to-day needs. He was from Nepal, and had been recommended to her by a friend. Apparently he was quite happy with Vindhya Kumari. In the morning of March 22, at about 7 pm, when the milkman knocked at her door, there was no response from inside. Sensing something serious, he called the neighbors. All of them tried to get the door open somehow, but when there was continually no response from inside, they broke open the door. As soon as the door was opened, everyone was horrified to see the dead body of Vindhya Kumari in a pool of blood on the floor. There were deep gashes on the back of her neck, as if she had been hit brutally several times with a heavy cutting weapon, such as an axe (figure 1). A search of the other rooms revealed that the safe had been broken open. Some papers were lying strewn around, but there was no sigh of cash or jewellery inside the safe. Obviously the murder had been done with the intent of robbery. And moreover it appeared to be the work of some insider, a person who knew the habits of Vindhya Kumari, as to when and where she slept, where her safe was, how much money was inside her, how best to break open the safe and so on. Immediately information to the police was sent and it arrived at the scene at about 8 am. Eventually they called me, and I arrived at the scene at about 10.30 am. Every one was naturally interested in finding where Ramu was, as he could shed great light on the murder mystery. But to everyone's surprise he was not to be found anywhere. The neighbors confirmed that they had seen him till the evening on the day before, so obviously he had disappeared the night before or at best on the morning of 22 March. Ramu's absence made him the prime suspect in the eyes of the police. Enquiries from the neighbors revealed that Vindhya Kumari had gone to bed as usual at about 9 pm, on 21st March. A lady living in a house just opposite to hers confirmed that the lights in her flat were on till about 9 pm the previous day, and she distinctly remembered seeing the lights go off at about 9 pm. It obviously meant that Vindhya Kumari was awake till 9 pm and she went to bed after that. This meant that she had died sometime between 9 pm on 21st March and 7 am on 22nd March, when the milkman arrived, and got no response. I made a preliminary examination, and from the state of her body I calculated the time of her death. I found out that she had been done away to death at about 2 am on the morning of 22nd March. A brief history about the life of Vindhya Kumari would be in order here, if only to understand the case better. She married a jobless young man at the tender age of 23, and at the time of marriage it was decided that Sawan Kumar - the man she married- would remain at her parent's house after marriage. Vindhya Kumari was the only child of her industrialist parents, and they naturally wanted that their son-in-law should stay with them. This suited Sawan Kumar, as he was from a poor family and did not have any place to live. His only asset was that he was a good-looking man. Apart from that there was nothing of note worth mentioning about him. In her youth, Vindhya Kumari was apparently taken away by his charms, and had taken the rash decision to marry him. Sawan Kumar was not very much educated, and after marriage he did not feel any need to look for a job either. He would just loaf around and live like a parasite on his wife's money. He was a gambler and a drunkard too. In such circumstances it was quite natural for him to have frequent tiffs with his wife and in-laws. For 20 long years, they carried on their life somehow, but gradually the tiffs came to such a pitch that he and his wife decided to separate. As their case did not fit into any of the divorce clauses, they could not get a divorce. However they decided to live separately. Sawan Kumar asked for a hefty amount as "alimony", but his in-laws agreed for only Rs 2000 per month. This amount was just enough for him to make his both ends meet, but would not be sufficient for him to buy alcohol or to carry on his gambling activities. He resented this very much and secretly nurtured a desire to get even with Vindhya Kumari and her parents some day. As time passed, both her parents passed away, and Vindhya Kumari was left on her own. There were strong rumors that a lot of cash, jewellery and other valuable items were lying somewhere in her large mansion. As she did not trust anyone she would keep all the money to herself. In all probability, this was known to Sawan Kumar too and as he was perpetually in need of money, he secretly desired to acquire that money. After his in-laws expired, he tried to meet Vindhya Kumari a couple of times, and would try to extort some money out of her by emotionally blackmailing her. Vindhya Kumari was a soft-hearted woman, and she did give her some money on both occasions, but refused to part with large sums of money as was demanded by Sawan Kumar. This served only to infuriate him further. On his second meeting with Vindhya Kumari, he had stayed longer at her house, and had even had a cup of tea with her. Returning back to our case. The police began pursuing Ramu hotly as they were of the firm view that he had murdered Vindhya Kumari, and had decamped with all the cash and jewellery. To every one's surprise he returned all by himself on April 1. The police was secretly keeping an eye on the house of Vindhya Kumari. As soon as Ramu arrived at the house, the pounced upon him and arrested him. This seemed to surprise him a lot, and he tried to protest meekly, but the police would not listen to him. A search of his baggage revealed a large dagger, and the police immediately came to the conclusion that this was the dagger used to kill Vindhya Kumari. Ramu was taken to the "torture chamber", and given a thorough beating. He kept insisting that he had gone to Nepal to meet his parents after taking due permission from his employer Vindhya Kumari. His story was that he was working with Vindhya Kumari till 21st evening. He had already asked for permission to leave for Nepal, about a week earlier. He recalled that when he was asking for permission, even Sawan Kumar had come there to ask for some money, and he had even shared a cup of tea with his mistress. He had himself prepared the tea for both of them. Ramu asserted that this story could be confirmed from Sawan Kumar. He further said that he left the house at about 7 pm on 21st, as he had to take the 9 pm train. This seemed to fit well with the neighbors' observation who had seen him till 21st evening. As far as the dagger was concerned, his story was that he had brought it from Nepal to give it as a present to one of his friends, who had earlier requested him to bring one from Nepal. The police did not believe his story one iota and sent the dagger to me for the blood stain analysis. They believed that I would find Vindhya Kumari's blood over it. But when I examined the dagger, I did not find any blood over it. The police believed that Ramu had washed the dagger thoroughly. However I thought that Ramu was innocent. If indeed he had killed Vindhya Kumari, and had decamped to his country with all the cash, there was no need for him to come back, and least of all to bring back the murder weapon. I decided to concentrate on Sawan Kumar. The police was of the opinion that Sawan Kumar would never do such a thing. After all he was getting some regular income from his ex-wife. Why would he kill her and put his own income in jeopardy? I decided to give his house a thorough search anyway. On 15th April, the police raided his house (mainly under my pressure), and searched it thoroughly. They did not find anything of note. I arrived sometime after the police had entered, and I spotted an ornamental leather scabbard hanging from the wall. The police had not cared to search it, as it was taken to be an ornamental weapon, but I unhooked the scabbard from the wall, and took out the weapon from it. It turned out to be a khukhri (figure 3). A khukhri is a heavy curved knife, not unlike a chopper, commonly used in Northern India. It apparent had been bought by Sawan Kumar as an ornamental weapon. The blade was clean and showed very early rust along the edge, suggesting that it had been washed quite recently, i.e. within the last month or so. The cutting edge was irregularly jagged from heavy use. The moment I examined the weapon, I knew I had the killer in my hand. I had preserved the skull of Vindhya Kumari, which showed deep cuts due to the weapon (figure 2 A). As one can see clearly, these cuts show a definite pattern. The cutting edge of the khukhri also showed some pattern (the pattern of raggedness), and if I could match the two patterns, I could be sure that the khukhri found at Sawan Kumar's house had indeed been used to kill Vindhya Kumari. The ragged pattern of the khukhri had produced the peculiar pattern on Vindhya Kumari's skull, and my job now was to match the two patterns. I cut a Lifebuoy soap with the khukhri. In the process, it left its distinctive marks of raggedness over the soap (figure 2 B). Now under the microscope, I painstakingly matched the two patterns, i.e. the one found on Vindhya Kumari's skull and that produced on the soap. To my utter satisfaction, the pattern matched perfectly. This meant only one thing; that the khukhri had indeed been used to kill Vindhya Kumari. The chances of two entirely different weapons, producing exactly the same cut marks, were so remote that the possibility of another weapon being used in the murder could virtually be ruled out. The police now began interrogating Sawan Kumar more assiduously. Initially he resisted, but when faced with hard scientific facts, he broke down and admitted his guilt. He had always wanted to "kill the golden goose" and get all the " golden eggs" in one go. He knew every little detail about his ex-wife's house. He knew her habits as well, as to when she slept, where she slept and so on. During one of his recent visits to her house he had listened to the talks between Ramu and Vindhya Kumari, in which Ramu was requesting for a week's holiday starting from 21st March. Vindhya Kumari had granted him the holiday while Sawan Kumar was still in the house begging for more money. Sawan Kumar now knew that on 21st evening she would be alone in her house. He decided to kill two birds with one stone. He would kill her on 21st night itself and since Ramu would not be in the house, no body would know who killed her. There would be no one to protect her either, or to raise a hue and cry. Moreover everybody would conveniently suspect Ramu, as he would be absent from the house. For this murder he decided to use his khukhri which used to hang from the wall of his house as an ornament. After the murder, he came home, washed the khukhri thoroughly, and put it back in place. His mistake was that he thought that no one would suspect him. Even if someone came to his house on a routine checking, no one would take a notice of an ornamental weapon. Lastly even if someone took notice of it, it would be impossible for someone to connect the murder with this weapon. So his reasons for keeping the khukhri in his own house were fairly sound. On the contrary, if he had disposed of the khukhri by throwing it somewhere, the chances were quite large that it would be discovered by someone sooner or later, and then the chances of this khukhri being traced back to him were enormous. There were many people in the locality who knew that this kind of khukhri belonged to him. So he decided not to do away with his khukhri and keep it back in its place. This was a perfect murder plan by Sawan Kumar, but unfortunately for him, careful forensic work took him to the gallows. (Dr. Anil Aggrawal) S-299 Greater Kailash-1 New Delhi-110048 INDIA Ph: 91-11-6465460 FAX:91-11-5759476 (NOTE TO THE EDITOR: KINDLY RETURN THESE PHOTOGRAPHS AFTER USE, AS THEY BELONG TO MY PERSONAL COLLECTION. ALSO PLEASE PROVIDE ME THE NEGATIVES OF PHOTOS USED IN MY ARTICLES FROM MARCH 1996 TILL AUGUST 1996. THANKS.)

SCIENCE IN CRIME DETECTION-18 USE OF INFRARED PHOTOGRAPHY IN FORENSIC SCIENCE Last year I came across a very interesting case. The case related to a businessman Mr. Valecha. He had about 5 Acres of land in NOIDA, on which he wanted to build a factory relating to paper business. Somehow, some financial problems arose and Mr. Valecha could not build a factory immediately after acquiring that land. The land was lying vacant as a result. As there was nobody to look after the land, and also because Mr. Valecha became very complacent, the land remained unguarded for about 2 years. In between those two years Mr. Valecha kept going to Japan to finalize the details of technology transfer relating to paper factory. So perhaps his not visiting the factory site was somewhat justified too. After about 2 years all the deals were finalized and Mr. Valecha was able to acquire a loan of about Rs. 2 crores from the Govt. Now when he reached the site of factory he found that the place had been occupied by one local goon Mahto. He was running some liquor business from there. When Mr. Valecha asked him to vacate the land, he asked him to get lost. This infuriated Mr. Valecha very much and he contacted the police to help him in this matter. Valecha had good contacts in the police and he was sure he could get the things done. Unfortunately for Valecha, Mahto had good contacts too. Not only did he know higher‑ups in the police, he had contacts with the Underworld dons too and even with some local influential politicians. It was believed that he was paying regularly something to them, and was always actively engaged in the political campaigns of those leaders. Thus having him moved through local police contacts was not likely to be of much consequence, and that was what actually happened. The local SHO did try his level best in the beginning, but very soon when he realized the enormity of the task he had inadvertently taken, he lost all interest in the case. There was no option left for Mr. Valecha than to go to court, but this would have taken several years obviously, and Mr. Valecha could not hold on to his Govt. loan till that time. The loan would lapse only after 2 months, if Mr. Valecha could not use that loan till that time. And Valecha did not want the loan to lapse at any cost. It was under these circumstances that Valecha took a very impetuous decision. Somebody suggested to him that he should strike a deal with Mahto. Perhaps he would take a few lakhs Rupees and vacate the land himself. Valecha liked this idea and approached Mahto. He had imagined that the deal would be finalized in a few lakh Rupees. He was prepared to pay up to Rs.5 lakhs for having that land vacated. However when he talked with Mahto he was dumbstruck when Mahto kept before him a demand of Rs. 50 lakhs. This was beyond the capacity of Valecha. Try hard as he would, he could not bring Mahto to reduce his demand. Repeated discussions with various representatives of Valecha also did not bring any fruitful results. Valecha was quite exasperated now. At this stage somebody suggested to him that there was a local goon MunnaLal who could help him. MunnaLal specialized in murder. He would charge a hefty sum from his client and do away with anyone indicated by his client. When MunnaLal was contacted he agreed to kill Mahto for a sum of Rs. one lakh. As Valecha had no other option, he agreed to this. On May 15, 1993 Valecha gave a phone call to Mahto and told him that he had arranged for Rs. 50 lakhs as desired by him and he could come to Valecha's house any time to collect it. Mahto jumped at the suggestion and replied that he will be there on that very night. The time was fixed for 10 pm. This suited Valecha and MunnaLal, who wanted to do away with Mahto. Valecha had a plush house in Golf Links area. The house was tastefully decorated. MunnaLal reached Valecha's house at 8 pm sharp. He was a hatchet specialist. He had brought his hatchet with him. The plan was to kill Mahto with the hatchet and then to do away with the body. At 10 pm the door bell rang. Valecha opened the door and found Mahto standing in the doorway. Till now everything was going according to plan. Mahto was asked to take a seat. He sat on a modular sofa. This is a modern kind of sofa which can be converted into a bed at night (reproduce fig. 1 on page 191 here). The upholstery on the sofa was of a dark red colour. Mahto took the left side of the sofa. While Valecha engaged Mahto in talks, MunnaLal came from behind and struck hard on Mahto's head. Mahto immediately dropped dead. After this both Valecha and MunnaLal disposed of the body of Mahto by throwing it away in the bushes of the Ridge area. When the body of Mahto was recovered by the police the next day, they started investigation. Their line of investigation led them to Valecha. When one of Valecha's servants was questioned, he told the whole story to the police. He was present in the house when the incident had taken place. When the police started building up the case against Valecha, they were quite dismayed to find that the bed on which Mahto was alleged to be sitting did not show any blood stain. This seemed to refute the story given by the servant. But in fact the stains were not visible because the upholstery of the sofa was of red colour. Here the police was in great dilemma. If they showed the normal pictures of the sofa in the court, it would have been extremely difficult for them to convince the judge that a murder had indeed been committed on that sofa, simply because the sofa did not show any blood stain. It was at this point when they approached me for help. I made use of a special kind of light ray called the infra‑red ray. This type of ray can not be seen by the eye, but it can make several invisible things visible. After taking the photograph in infra‑red ray exposure, the blood stains were clearly visible ( reproduce fig. 2 and fig. 3 on page 192 here). One can see a large patch of blood on the left side of the sofa. The close‑up photograph shows many fine areas of blood splashing. The contrast appears dramatic when you compare these two figures with fig.1 which has been taken in normal light. In fig.1, although blood stains are present, they are hardly visible. The police then got encouraged and asked me to take the photographs of MunnaLal's shirt also. MunnaLal was wearing a black shirt at the time of murder, and police had taken that shirt into custody. But that shirt was not showing any signs of blood, and because of that police had got discouraged very much (reproduce fig. 5 on page 194 here) . But when the same shirt was photographed in infra‑red rays, it showed blood stains very clearly (reproduce fig.4 on page 193 here). Thus the infra‑red photography helped the police immensely in building up evidence against Valecha and MunnaLal. The honorable court accepted the photographic evidence, and both of them were convicted. This was yet another victory for Forensic Science!

Forensic Science Fiction The mystery of the assassinated prince When I got a telephone call from the Indian High Commission in Timbuktoo, I was relaxing in my bed with a cup of coffee and the morning newspaper. My wife was sitting besides me, and we were gossiping. Nothing irritates me more at such times than a telephone call. With some measure of irritation, I picked up the receiver. “Is it Dr. Aggrawal, Professor of Forensic Medicine at the Maulana Azad Medical College?”, a faint voice asked from the other side. “That’s right”, I replied. “Dr. Aggrawal, I am Abhinav Sinha, High Commissioner of the Indian High Commission in Timbuktoo. We are in a great problem. We have a doctor here, who is being falsely framed in a medical negligence case. I am convinced he is innocent. Could you please come and help us?” and without waiting for my reply, added, “Your tickets are being sent to your house, along with some money to take care of your travel expenses. All the hospitality here will be taken care of by us.” “Look.. .”, I protested, “I don’t know what your problem is, and I am really not sure I can help you in this case. Moreover I can’t possibly leave my college for any great length of time.” “Everything has been taken care of sir. Your trip is official. You will be treated as on duty. All expenses paid. Please come as soon as possible”, and he hung up. I was quite nonplussed, and I was almost sure, it was some practical joker trying to play a fast one on me. But within five minutes, I received a phone call from the Ministry repeating the same thing almost verbatim. Within half an hour, a government official came to my house with some travelers cheques and a club class return air ticket to Timbuktoo. There was an accompanying letter from someone higher up in the Ministry asking me to proceed to Timbuktoo immediately. It also said that I would be treated as on duty. There was no option now. The flight was at 9 pm. I looked at my watch. It was still 8 am. I had about 13 hours for preparations. I requested my wife to start packing. For those, who are not aware of Timbuktoo, it is a very tiny principality somewhere in the Middle of Africa - quite near Lake Victoria. It is a hereditary monarchy. Elections have never taken place here. Kings have been ruling this principality since time immemorial from the same family clan. Mostly the eldest son gets the chance to rule, but sometimes court intrigues result in murders, and the younger brother gets the throne. There have been cases, when a still younger brother has in turn killed his second brother and got the throne! In short, the history of this principality is rife with murders, court intrigues, treachery, debauchery and so on. Our country had no diplomatic relations with this country till sometime back, but recently in the wake on the so-called Non Aligned Movement, we had developed diplomatic relations with them. A small mission had been opened there, which was staffed by just six people. One of them was a young Indian doctor, whose main job was to look after the Indian officials and their families, as the medical fraternity in that principality was really in a very nascent stage. After a relatively comfortable nine hour flight, I landed at the King Hassan Airport in Timbuktoo. The High Commissioner of the mission was there personally to take me to my hotel. Along with him was the young doctor posted in the Mission. His name was Dr. Harish. While I was being driven to my hotel, I looked out of my window, and was amazed at the clean air and greenery all around in that tiny nation. Coming from New Delhi, it was certainly a very welcome change. The hotel was comfortable and clean. After I took bath and changed, the duo narrated their story to me, and it was something like this: Ndubuisi Eke was the king of this nation since about three years. He had a younger brother called Mombutu Eke, who wanted to usurp his throne. On 18 February 2001 - a Sunday - when Ndubuisi was taking his morning stroll, one unidentified man came from somewhere and stabbed him in the neck. The attack was so sudden that Ndubuisi’s two bodyguards couldn’t do anything. However there were rumors that they had been “bought” and did not try to stop the attacker on purpose. There was an immediate commotion all around, and in the mêlée that ensued, the attacker managed to slip away. Again people who had an ear to the ground said that this was also stage managed. The killer was someone hired by Ndubuisi’s younger brother Mombutu, who wanted to usurp his throne. As luck would have it, Ndubuisi did not die immediately thereafter. He did however receive a nasty gash in the neck. As the whole of Timbuktoo did not have a reasonably smart surgeon, he was brought to Dr. Harish in the Indian Embassy. To be sure, he too was young and rather inexperienced, but better than the best Timbuktooan doctor. Dr. Harish tried his best to save Ndubuisi, but he died immediately after arriving at the hospital. No autopsy was ever conducted on the body, and the body was cremated in haste. Mombutu Eke ascended the throne immediately thereafter. However the public - who loved Ndubuisi no end - was restless. In Mombutu, they saw a killer and usurper. There were hushed voices all around. And perhaps to silence his critics - and perhaps to clear him as well - Mombutu ordered an enquiry against Dr. Harish. It certainly was against diplomatic norms. But as far as Mombutu was concerned, it didn’t matter as his throne was in jeopardy. He wanted to show that the wound received by Ndubuisi was not fatal, and the death occurred instead because of Dr. Harish’s negligence. It was where I came into picture. I was to prove that Dr. Harish had tried his best. There was no negligence on his part and the death occurred prima facie because of the wound. But how could I do that? Had Ndubuisi’s body been with us, it would have been a relatively simple matter for me. All that I needed to do in that case was to conduct a thorough autopsy on his body to find out the correct cause of death. But the body had already been cremated in haste. Now all I had in my possession were some reports prepared by Dr. Harish, when Ndubuisi first arrived at the hospital. I interviewed Dr. Harish in great detail. He was young and inexperienced, but certainly a very bright doctor. Obviously he was terrified. He was being prosecuted in an alien land, and if found guilty, they could send him behind bars for a lengthy period of time. Something had to be done very fast. Fortunately Dr. Harish had prepared a very detailed injury report. I read the injury report over and over again, and found that the most significant part was that his left sternocleidomastoid had received a gash 6x2x4.5 cm in size. It was that wound which appeared fatal to me. But the volume of blood that Ndubuisi lost was not very much. Dr. Harish had immediately sutured the wound. At a rough guess, he had lost about 500 cc of blood. Now that is not sufficient to cause death by shock. One would require at least 2000 cc for that. Obviously Ndubuisi had died because of some other reason. But what? That was the million dollar question. I could not sleep that night. I kept thinking the whole night. And I do not know when I fell asleep. But soon I started dreaming. I saw Ndubuisi going down and down in deep water. He was struggling to stay at the surface. But something was taking him down and down. Bubbles of air were streaming through his nostrils. Bubbles of air.. .. I woke up with a start. It came to my mind in a flash. It had to be air embolism! Perhaps I was thinking about air embolism subconsciously. That is why I dreamed of those air bubbles, perhaps. For recapitulation, let me state what air embolism is. It was Rudolf Virchow, the famous 19th Century German pathologist who introduced the term embolus and embolism into modern medicine. In 1856 he applied the term embolus to a loose clot in the blood stream. These words are of Greek origin and come from the Greek word “emballe” meaning to throw in, or to lay in or to put in as a stopper, peg or bolt. A loose blood clot in the circulation indeed acts as a stopper or a peg. As long as it travels in vessels bigger than its size, it is alright, but as soon as it encounters a vessel smaller than its own size, it gets stuck there, acting as a stopper or a peg. Many of you would be surprised to know that embolism is used in a general sense too, meaning the adding or “throwing in” of an extra day to the year. In relation to medicine, we usually speak of embolism in relation to blood clots which travel from leg veins upwards and get lodged in pulmonary arteries. This is a serious condition causing almost instantaneous death. Under certain conditions - as when veins are cut - air can get sucked inside the veins. It forms a bubble inside and this bubble travels towards the heart along with the blood stream, and gets lodged in the pulmonary arteries just as a blood clot does. A bubble of air is incompressible, and there is no way the blood stream can negotiate this bubble. Inside the vein this bubble acts just like a blood clot. That is, it blocks the circulation just as effectively as does ordinary blood clots, causing immediate death. It is almost as if someone had put an arterial clamp over that place! Detecting ordinary blood clots in pulmonary arteries, or for that matter anywhere else in the body, is relatively easy, but detecting air embolism is a different game altogether. It remains one of the most challenging tasks faced by a forensic pathologist. The reason is that the moment you open pulmonary arteries, the bubble is going to disappear in the air. For this reason, forensic pathologists usually dissect the heart under water in suspected cases of air embolism, but believe me it is a very difficult and challenging procedure. Nobody loves it. There is a silver lining though. If you are suspecting air embolism in a case, before you start the autopsy, one of the best things you can do is to X-ray the body. If an air bubble is present in the heart or pulmonary arteries, it will show up in the X-rays. So you conduct this difficult procedure only in the cases in which you see the bubble in the X-rays, and leave out the rest. In fact, the X-ray plate itself is proof that the person died of air embolism and many forensic pathologists don’t take the trouble to dissect the heart under water after that. But we all know, no post mortem was ever conducted on Ndubuisi. Even if it had been conducted, I am doubtful, if anyone would have been able to detect the cause of death as air embolism, as there was no forensic pathologist in the whole of Timbuktoo. I was now in a very unenvious position. I did not have the dead body of Ndubuisi, and I had to prove that he had died of air embolism. That was the only way to save Dr. Harish. Only then we could prove conclusively that it was the initial stab wound which caused the death (by air embolism), and not negligence on the part of Dr. Harish. But how could I do it? That was the million dollar question. In the evening, I was sitting by the lakeside looking at the beautiful lake and the birds leisurely floating in it. I was recalling my younger days, when we had to send almost all bodies for X-rays, in which we suspected air embolism. Then for many months, our X-ray unit was out of order, and we had to start the autopsy without the benefit of the initial X-ray plates. This meant that effectively we had to open all hearts under water and nobody liked that. You have to make a sac in the pericardial cavity by making appropriate cuts in the pericardium; then you fill that pericardial sac up with water with an assistant holding up both the flaps of pericardium with forceps; and then finally you inserted the blade in the pulmonary artery and under various heart cavities, twisting and turning it expecting a bubble to rise through water. Not many forensic pathologists love this. And many complained. To solve the problem, I came up with an interesting formula. I had for long observed that more people tend to die of embolism if the cut was longer and deeper. Similarly if the muscle involved was more voluminous, chances of air embolism were higher than if the muscle were less voluminous. Thus if someone got a 5 cm cut in gluteus maximus, he would stand much greater chances of getting air embolism than if he got a cut of the same size in, say, temporalis muscle. It was because temporalis muscle is less massive than gluteus maximus. Could I turn this observation into a strict mathematical formula, I had asked myself at that time. And quite interestingly I did come up with an interesting formula. It was: E=mc² Now if you think you are already familiar with the formula, probably you are wrong. E in our formula stands for Embolism (rate of), m for muscle mass (in grams) and c was a somewhat complicated parameter, which I called the “Cut factor”. I had observed that air embolism tended to depend both on the length and the depth of the cut, but depth had a greater effect on producing air embolism than the length. Thus if the length of the cut was twice, the chances of air embolism in a person would be doubled, but if the depth was twice, the chances would be four times. To take this observation into account, I put the Cut factor equal to [(cut depth)2 x (cut length)]. The interesting thing about this formula was that this stands true across all animal species. Once this formula was in place, we applied it in some experimental animals too, namely rats, guinea pigs, hamsters and pigs. To my satisfaction the formula proved true in all cases. Now as you can see, this formula actually gives the rate of embolism. To put it in other words, it would give you the probability that the person might have suffered air embolism. What we did with this formula was to look at the muscle which was cut and the size of the cut, and put the numbers in the formula (we had to put the decimal back by four digits, i.e. we had to effectively divide the figure by 10,000 to arrive at the correct rate of probability). If we got a figure, say, 50, it effectively meant that the person had a 50% chance of getting air embolism. If we got a figure of, say, just 2, there was just a two percent chance of getting air embolism and the forensic pathologist could perhaps look the other way and forget about dissecting the heart under water. Gradually all forensic pathologists in our institution got round to opening the heart under water if the figure was greater than 50. This made sense too, because if the probability of getting an air embolism is greater than 50%, you must take enough trouble to find it out. For those, who are able to follow me only vaguely, I would illustrate with an example. Gluteus maximus’ weight on the average is 493 g. Now if it sustains a cut which is 5 cm long and 3 cm deep, what are the chances that the person would die of air embolism? We would calculate it as follows: The cut is 5 cm long and 3cm deep. Since the cut factor is equal to [(cut depth)² x (cut length)], simple mathematics would show that it would be 45. Now putting this figure in our earlier formula E=mc² We get 493 x 452 or 998325 We put four decimals behind and we get 99.8325. This means that a person getting a 5 cm long and a 3 cm deep cut would stand a 99.8325% chances of getting an air embolism. This is well near hundred percent, and I would certainly like to take all trouble to dissect the heart under water. Over the years this formula had gained International acceptance, and almost every forensic pathologist was using it in his day-to-day practice. Could I use this formula in Ndubuisi’s case? Then suddenly I remembered that Dr. Harish had been careful enough to record the dimensions of the cut quite accurately. I jumped and ran back to my hotel room. Once inside the hotel room I phoned Dr. Harish immediately and in a most excited voice asked him to give me the dimensions of the cut. He was a little surprised at my strange request but gave the figures to me. The dimensions were 6x2x4.5 cm. Now my only problem was to find out the weight of the sternocleidomastoid muscle. I am no anatomist and did not know its weight at all. But fortunately I have many good anatomists as friends. One of them is Dr. R.K.Suri, Professor of Anatomy at our own medical college. I immediately made an overseas call, forgetting the time difference completely. It was 2 am in India, and he picked up the phone with some measure of irritation. “Dr. Suri, what is the weight of Sternocleidomastoid muscle?” “Is it Dr. Aggrawal?” he asked in great irritation. “Never mind. The weight?” I insisted. “Why! it is 153 grams. But why do you ask this question in the thick of the night?” He was obviously quite nonplussed. “Thanks” I said, ignoring his question completely, banged the receiver back and got back to crunching numbers. The cut factor in this case would be 121.5 as the length of the wound was 6 cm and its depth 4.5 cm. Now putting all the figures in our good old formula E=mc², we get: 153x(121.5)2 =153 x 14762.25 or 2258624.25 Putting the decimal back by four points, we arrive at the figure 225.862425 I jumped on my feet in glee. The probability of getting air embolism was even greater than 100! To a mathematician it may look silly, but we had encountered such figures before. It meant that the person was sure to get air embolism. Everything was clear now. With such a deep cut on his Sternocleidomastoid muscle, Ndubuisi stood a 225% chance of getting air embolism. In other words, he died of air embolism. That was for sure. We immediately filed our answer in the Law Ministry of Timbuktoo. I am given to believe that the Ministry was going to dismiss that answer too, but before doing that they took the advice of some international forensic experts, and all of them advised that my reasoning was watertight and there was no scope of rebutting it. In fact if they did it, they would go down in the eyes of the International Community as an utterly unjust nation, and would stand the risk of getting completely isolated. Mombutu obviously did not want to take this risk. Dr. Harish was immediately cleared of all charges. I returned back to India, and the very next day went to Dr. Suri and thanked him for the help he rendered us. He was still very very angry with me, especially because I had banged the phone on him, but when he heard the great service he had rendered for our nation, he forgot all anger and is once again a very great friend of mine.

Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE SEPTEMBER 1999 ISSUE THE POISON SLEUTHS DEATH BY YELLOW KANER -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a very young girl today. What happened to her? Please tell me.” “Good morning Tarun. The name of this six year old girl is Radha. Her father is a Secretary to the Government of India, and fairly well-to-do person. He had only one child. Yesterday she was playing along with her friends under a tree in a park near her house. The time was around 4 pm. There were about 5-6 other boys and girls with her. They were apparently fine when they were playing. Suddenly Radha started vomiting. She had diarrhoea too. She was rushed to the hospital, where the doctors thought she was having gastro-enteritis, and she was being treated along those lines. The doctors also noted some additional symptoms. I have talked to the doctors who treated her. And they say that they noted clamminess of skin, coldness in extremities, dilation of pupils, sunken eyes and delirium. The pulse was slow and feeble in the beginning, but later it became fast and irregular. After a few hours she had convulsions, then paralysis, and finally death. She died at about 8 am in the morning today." "Oh, that is most terrible doctor? Why do you think she died? Did she die of any natural disease? Or did she die of infections such as gastro-enteritis?" "Tarun, it doesn't look like natural death to me. The symptoms are pointing towards a poison which affected her heart. So probably we are talking about some heart poison here. I have gone to the place where she was playing, and I was surprised to see that there were lot of Yellow Kaner plants in the garden where she was playing. These plants are known to botanists as Cerbera thevetia or Thevetia peruviana. In normal everyday parlance, they are known as Pila kaner or be-still tree. I am inclined to believe that either she took the seeds of that plant by mistake, or somebody gave it to her on purpose.” “That’s most preposterous. I have seen Kaner plants growing along the roads, but I never believed it was such a dangerous poison” “Oh, sure they are poisonous. The yellow oleander or be-still tree is a native of tropical America and is now widely cultivated as an ornamental shrub in tropical and subtropical regions of the world, including India. It is a small shrub with milky sap. Leaves are evergreen, alternate, ribbon like, about 6 inches long, 3/16 to 3/8 inch wide, dark and glossy above and pale beneath. Flowers are more or less fragrant, funnel form, yellow or peach-colored, rarely white, 2 to 3 inches long and to 2 inches wide, the five lobes spirally twisted and not spreading. Fruit is somewhat diamond-shaped -distinctly so in cross section. It is about one and half inches wide and 5/8 inch thick. It turns from green to yellow; then the thin layer of flesh becomes completely dehydrated, the skin becomes black and wrinkled and disintegrates, exposing the bony, light brown, attractive stone, which contains two to four flat gray seeds. The sap of the plant may cause skin inflammation in sensitive individuals. Chewing the bark or seed kernel causes a slight numbing sensation and a feeling of heat in the mouth, and purging. Ingestion of a toxic dose causes burning in the mouth, tingling of the tongue, dryness of the throat, headache, vomiting, purging, excitement followed by drowsiness.” “Sounds like a very dangerous plant to me. Are all parts of the plant poisonous? Also please tell me, which poisons are found in this plant?” “Except for the thin layer of flesh covering the stone, all parts of the plant are poisonous, especially the seeds, which contain 3.6 to 4 per cent of the cardiac glycoside thevetin. This toxin is one eighth as potent as ouabain and very similar to digitalis in activity, about which we have talked last time. Also present are thevetoxin (C30H46O10), similar to but less toxic than thevetin; neriifolin (C33H61O30) more potent than thevetin in action on cat heart; peruvoside (C30H44010); and also ruvoside (C30H46010). There has also been reported a bitter principle that acts on the central nervous system and produces tetanoid convulsions.” “Doctor, how much portion of the plant can cause death in a human being?” “Nothing is positively known about the fatal dose in human beings, although experiments have been done on animals. Fifteen to twenty grams of dry leaves are fatal to the horse; lesser amounts are fatal to cattle. Since such fatal experiments can not be conducted on human beings, our knowledge of the fatal dose of Cerbera thevetia depends upon actual cases of death which have occurred following its ingestion. A single seed has caused death in a child; 8 to 10 seeds in an adult. About 5-10 leaves of the plant are also said to be fatal. The root is very poisonous.” “Oh, I see.” “Tarun, this plant is a very popular ornamental in warm regions of both hemispheres, especially in dry coastal areas because of its resistance to drought and salinity and because it is not eaten by goats and cattle. It is often planted in numbers as a hedge. Grazing animals instinctively avoid this plant, and that is why this is a very popular plant as a hedge in India. Besides India, it is also found in other parts of the world. It is occasionally seen in the southern half of Florida and California, is very common in the West Indies, Latin America, Africa, and the Orient. In the Hawaiian Islands it has been declining in popularity with the realization that it is the most frequent local cause of human poisoning. The fruit flesh is eagerly consumed by chickens and is casually eaten by humans in Ghana and Queensland. The handsome stones, after polishing, are worn as pendants, tied together as rattles, or strung with other seeds in necklaces. Many myths and legends are associated with this plant. In the West Indies, the stone is carried in the pocket in the belief that it will ward off hemorrhoids. In East Africa, it is put in the hand of an infant at birth as a good luck token. Quantities of the seeds have been exported from Hawaii to the mainland of the United States for extraction of thevetin as a substitute for digitalis, but 40 per cent of the patients receiving this drug have suffered gastrointestinal disturbances. Indian scientists believe the more recently discovered peruvoside holds greater promise in cardiac therapy. In Africa, the seed kernels are occasionally chewed to cause purging. In the Philippines, half of one leaf is given as an emetic and purgative. The sap and bark have been utilized in small amounts to treat malarial fever as well as to induce vomiting and purging, but overdoses have caused paralysis and death. The sap has been applied to sores and ulcers, also to tooth cavities and decayed teeth to relieve toothache. It is said to cause the teeth to disintegrate. In Brazil, the seed is taken as an abortifacient. In Indonesia, immigrants from India have been seen to dry and smoke the leaves. The toxicity of the plant has been generally known since the sixteenth century. Its Sanskrit name "Ashwamarak" is translated as "horse killer. Early European explorers in tropical America reported that the Indians used the seed for homicidal purposes. In India, the seeds are commonly employed for suicide and homicide, and in Bombay they are used for killing cattle. They have poisoned pigs in Queensland.” “Looks like a very interesting plant to me. Have there been cases of poisoning with this plant before?” “Several cases of Yellow Kaner poisoning have been recorded in India. In 1900, a woman in India took two seeds in a suicide attempt. The following day, she experienced vomiting, purging, pain in the throat, headache, and fainting spells alternating with drowsiness. Her pupils were normal; heart action was weak and pulse slow. She recovered after three days of treatment. In November 1962, a four-year-old boy in Poona, India, swallowed a seed at 6 P.M., vomited 15 to 20 times, was hospitalized, was found very restless, with sunken eyes but normal pupils, dry tongue, and cold extremities. An electrocardiogram showed severe abnormalities. The following morning diarrhea occurred; on the second day the pulse became irregular, and it remained so for 36 hours. Treatment was continued for eight days; then the child was discharged with normal pulse and heart action. Some interesting cases have come from Queensland, Australia. In one case, a 3-year-old girl played "tea parties" under a yellow oleander tree in her backyard. She later developed persistent vomiting, sweating and bradycardia. Cardiac arrest occurred during her transfer to hospital and she could not be resuscitated. Another young girl was "dared" by her brother to eat the fruit of the yellow oleander. She did, and later developed severe vomiting and a variety of cardiac arrhythmias which persisted for three days before she recovered. In southwest Africa, two European children were poisoned by eating the seeds, and one died in six hours. In Southern Rhodesia, a death occurred two hours after ingestion of one seed." "Looks like this plant has really caused deaths! In this case doctor, how are you going to prove to the court of law that this child died of Cerbera thevetia poisoning?" "Tarun, I have examined her stomach, and have found remains of some leaves which look very much like Cerbera thevetia leaves. This is a very strong indication that she was given the leaves of Yellow Oleander to eat. I did not stop at that. I examined the extracts of her heart muscle and it demonstrated the presence of poisons found in Thevetia leaves or fruit. This is ample proof for any court of law to assume that Radha died of Yellow oleander poisoning. Actually when I saw Kaner plants growing in the garden nearby, I got suspicious. I thought that there might be some foul play involved in this. I found out that the father of this girl, one Mr. Sharma, had sacked one of his juniors Katkar about a year before, and since then Katkar held a grudge against Mr. Sharma. I may tell you that Katkar was a fairly intelligent man, and in his college, he had studied botany and chemistry with keen interest. Apparently he was aware of the poisonous nature of the Cerbera thevetia plant. He wanted to get even with Mr. Sharma very keenly. He had observed that there were Cerbera thevetia plants in the nearby garden, and that Mr. Sharma's only child Radha used to play there. On that fateful day, he came to the child and somehow coaxed her to chew those leaves. I really don't know what he told to the child, but her friends who were playing at a short distance away are saying that they did see Katkar talking to Radha, and Radha subsequently chewing the leaves of Kaner plant. You might think that it is very silly for a child to listen to such strangers, but you must keep in mind that a six year child does not have much judgement of her own. She apparently chewed some leaves on Katkar's insistence and that was the cause of her death. Come, let us tell the police to catch Katkar, because it is he who is responsible for her death. "That was very clever of you doctor. Without your clever deduction everybody would have thought Radha 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. You would normally think it to be a vitamin, essential for growth, but it is a very dangerous poison too. I will talk about Vitamin A next time."