Case studies on poisoning

Case study 1 Outline of case Habibul was a healthy 10 years-old boy who suffered from time-to-time with mild eczema which usually resolved itself without the need for treatment. On one occasion, however, Habibul’s eczema was much worse than normal and he complained to his mother about the itchy, painful red skin behind his knees. His mother who believed in traditional remedies consulted a local herbalist who supplied her with a paste containing ground up Nicotiana leaves, coffee beans and lime. On returning home she applied the paste to Habibul’s legs. About 30 minutes later, Habibul began to feel dizzy and nauseous and he was unsteady on his feet. Soon afterwards he vomited and started to drool and perspire. He complained of pains in his stomach and became very agitated. On admission to hospital it was noted that Habibul was sweaty and drooling but his body temperature was normal, his pupils were dilated and his pulse rate and blood pressure were both elevated. His level of consciousness varied and during one period of agitation he had a generalized seizure. With supportive care and appropriate treatment, Habibul recovered but some symptoms such as increased perspiration lasted for three days. Questions • What toxidrome best fits Habibul’s symptoms? • What is the likely toxicant and its source? • How does it produce its effects? • Why in some patients do the tachycardia, hypertension and mydriasis progress to badycardia, hypotension and miosis? • Why does muscle weakness occur in some patients? • Is the presence of lime in the herbal preparation significant? • What are Green Tobacco Sickness and Cow’s Urine Concoction? • How might poisoning of young children with this toxicant occur in the domestic environment? Case study 2 Outline of case Mike and Dean worked as car mechanics. They were good friends but Dean liked to gamble and frequently borrowed small sums of money from Mike which he normally paid back as soon as he could. However, the relationship between the two men deteriorated when, after a losing streak, Dean confessed that he could not pay back what he owed. Mike decided to teach Dean a lesson so he put about 60 mL of antifreeze fluid into Dean’s mug of sweet tea. About 20 minutes after the tea break Dean began to feel merry and started to behave as though he was thoroughly drunk. The workshop manager thought Dean had been drinking during work so he sent him home with a warning that he would be dismissed if it happened again. On the way home, Dean felt sick and started to vomit. He lost consciousness and was admitted to a local hospital. Clinical tests revealed severe acidosis with raised ketones, hypocalcaemia and the presence of microscopic crystals in urine. Dean eventually recovered but he was left blind and his hearing was impaired. Questions • What was the likely toxicant? • How is it metabolised? • Explain the outcomes of the clinical tests • Why might Dean have felt weak and why might some of his muscles have gone into tetany? • What treatments do you think Dean received and why were these treatments used? • Why are dogs and cats at risk from poisoning with this agent? • Is there any connection between this case study and cases of poisoning following ingestion of rhubarb leaves? Case study 3 Outline of case Todd had been meaning to tidy up the wood pile for some time but the weather had not been good. However, one warm sunny day he decided to get the job done. He had moved several small logs when he felt a slight pin prick sensation on the top of his right index finger. He carried on working because it was not too painful and he thought it was just a splinter of wood that had broken the skin but within 30 minutes Todd began to experience pain and muscle cramps and tremors in his right arm. Concerned that he might be having a heart attack, Todd called an ambulance and was admitted to hospital. On admission, he was alert and well orientated but the muscle cramps, tremors and pain had progressed to his back and abdomen. The felt nauseous, his nose was runny and he was sweating and salivating a lot. Clinical examination revealed a blood pressure of 185/120 mm Hg; pulse, 120 min-1; respiration, 22 min-1 but blood chemistry was normal including cardiac enzymes. During the physical examination it was noticed that there were two red spots surrounded by an area of erythema on the top of Todd’s right index finger. It was concluded that Todd was suffering from latrodectism. Questions • Todd has been bitten by something but by what? • What is the toxicant and how does it work at a cellular level? • How does the toxicant produce the symptoms described above (latrodectism)? • What treatment do you think Todd received? Session 2 - 27/4 at 15.00h in LT21 Case study 4 Outline of case Mr. Jackson was born in Bradford in 1886 and had lived and worked in the town for the last twenty-five years. He was employed at a local woollen mill as a wool sorter; a job that required him to separate wool fleeces into various qualities and then to remove the knots and foreign bodies that are often found adhered to the fleece. In a typical week, Mr. Jackson would handle hundreds of fleeces from animals such as sheep, Alpaca and Angora goats. Mr. Jackson first noticed an itchy papule (bump) on his forearm which he thought was a flea bite. However, after three days the papule developed into a small painless ulcer about 1cm in diameter. The centre of the ulcer then turned black and the surrounding tissue became swollen and very inflamed. Mr. Jackson began to feel unwell. He complained of a persistent headache, a lack of energy, loss of appetite and that he felt feverish. Mr. Jackson’s condition soon deteriorated. He developed sepsis accompanied by severe oedema and multi-organ failure. Questions • What is the disease Mr. Jackson died from and what is the likely causative agent? • Is there a connection between Mr. Jackson’s occupation and the disease? • By what routes can the causative agent infect the body? • How would Mr. Jackson be treated today? • What safety precautions would you put in place to reduce the risk to wool sorters of contacting the disease? • Are there any other groups of workers at risk from this condition? • In the context of this case study, what is the connection between Gruinard Island off the coast of Ross and Cromarty in Scotland and some letters sent around the USA in late 2001? • Does the causative agent have any potential military/terrorist uses? • Does the causative agent produce toxins and, if so, how do they work? Case study 5 Outline of case Mr and Mrs Briscombe lived in the South West of Britain where they owned and managed a public house, parts of which dated back to the sixteenth century. Their relationship had never been easy and in the last few years Mr Briscombe had started to drink too much and had physically abused his wife on a number of occasions. Mrs Briscombe felt trapped. There were no children, most of her family were dead or living aboard and her husband’s behaviour towards her ensured she had no self-esteem or financial independence. It is not clear when Mrs Briscombe decided to kill her husband but it seems likely she got the idea of how to do it whilst supervising a delivery of beer. One of the delivery men remarked that the cellar must be very old judging from the large wooden beams and rough stone floor. He also mentioned that there were some loose wires on the walls and ceiling and that these might be dangerous. Mrs Briscombe had rarely gone into the cellar but on this occasion, she decided to have a look around to see if any electrical repairs might be necessary. It was during this inspection that she noticed something that suggested a simple chemical might make a suitable poison for her husband. A little bit of research at a local library suggested she could buy the poison via the internet; that it is soluble in water and imparts a sweet taste. Indeed, she discovered that it had been used to sweeten wine. Later in the year, Mr Briscombe started to complain of short bouts of severe abdominal pain, especially at night. In addition, he lost his appetite, had not slept well for some time and suffered from constipation. His GP thought the anorexia, abdominal pain and insomnia were the result of constipation and suggested he try some glycerine suppositories. However, his health continued to worsen. His muscles and joints began to ache and his right arm became very weak. Subsequently, he was admitted to hospital were tests revealed anaemia, hypertension and impaired renal function. He died of renal failure. On autopsy, a thin blue-black line was noted between the gums and teeth. This and the deceased’s symptoms suggested to the pathologist that Mr Briscombe had been poisoned and chemical analysis of his blood confirmed this. When questioned by the police, Mrs Briscombe revealed that her husband drank a lot of beer and was in the habit, on a morning, of drawing off the first few pints for his own consumption. Mrs Briscombe disposed of the poison so when police asked to search the pub the only possible cause of Mr Briscombe’s death was found in the cellar. This impression was strengthened when analysis of Mrs Briscombe’s blood revealed she had also been exposed to the poison that killed her husband. Despite some doubts about whether the amount of poison in Mr Briscombe’s body could be accounted for through accidental exposure, Mrs Briscombe evaded justice. Questions • What agent do you think poisoned Mr Briscombe? • Why do you think Mrs Briscombe evaded justice? • Why was the victim anaemic? • What is the target organ(s) damaged by the likely intoxicant and is the damage reversible? • What other major incidents of human poisoning have occurred with this agent? • Are there any specific treatments for poisoning with this agent? • In the 18 & 19th Century this agent caused ‘Devonshire colic’. What alcoholic beverage is associated with this condition and how do you think it occurred? Case study 6 Outline of case Bill lost his job in 1929 and had been living in a shantytown on the edge of Oklahoma City for the past year. He survived on the free food distributed from the City’s breadlines and soup kitchens and on the pittance, he earned from casual work. Bill like a drink and, despite Prohibition, he had always managed to obtain alcohol either from local bootleggers or by buying Jamaican ginger extract from local drug stores. ‘Jake’ as it was called was a patent medicine that contained a high percentage of alcohol. Bill preferred illicit alcohol to Jake because the latter contained enough ginger to give it an unpleasant taste. However, Jake was cheap and times were hard, so most of Bill’s alcohol came in this form now. Bill’s illness started with gastrointestinal disturbances such as nausea, abdominal pain and diarrhoea. About ten days later he developed soreness in his leg muscles and several days after the occurrence of this symptom, he noticed that his toes would not move. This was soon followed by bilateral foot drop which made it difficult to walk without the aid of a cane. As Bill’s illness progressed he became unable to walk and worse: Bill gradually became unable to feed himself because of weakness in his fingers and the onset of bilateral wrist drop. He was admitted to hospital. Tests revealed that there was no impairment of tactile, pain or temperature sensation in the affected limbs. The flaccid paralysis of Bill’s limbs lasted for many months but his ability to walk properly was permanently impaired; a disability that became known as the ‘Jake walk’. Questions • What toxicant is believed to have caused Bill’s illness? • What is the target tissue of this toxicant? • How did the toxicant get into the ‘Jake’? • Is there any relationship between Bill’s illness and organophosphate-induced delayed neuropathy? • What is the likely target molecule(s)?    

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