38.1: Aspirin

Flushed face, edema of the face, skin rash, tinnitus, deafness, hyperpnea, nausea, vomiting, hematemesis, melaena, hypoprothrombinemia, acute renal failure, pulmonary edema, respiratory arrest.
Fatal dose: 5 to 10 gm.
Fatal period: A few minutes to a few hours.

38.2: Paracetamol

Paracetamol (acetaminophen) is a non-narcotic analgesic and antipyretic.
It acts by inhibiting prostaglandin synthesis.
It can produce severe liver damage due to the accumulation of a highly toxic intermediate metabolite: nacetylepbenzoquinone (NAPQ) in overdosage.
Normally in therapeutic dosage, this metabolite is detoxified by glutathione.

Within the first 24 hours, it can produce — anorexia, nausea, vomiting, and epigastric pain.
- This will be followed by the disappearance of all discomforts giving a false sense of relief in the next 24 hours.
After 48 to 96 hours it can result in progressive hepatic encephalopathy noticed by vomiting, jaundice, hepatic pain, confusion, coma, coarse flapping tremors of hands (asterixis) gastrointestinal hemorrhage, cerebral edema, renal tubular necrosis, etc.
There may be cardiac arrhythmias, hemorrhagic pancreatitis, disseminated intravascular coagulation, etc.; death often takes place in this stage.
In cases where this does not happen, the patient goes into the next stage of recovery, which begins in about 5-7 days and the patient gradually becomes completely normal in about 2–3 months' time.
Fatal dose: 10 to 25 gm.
Fatal period: Up to five days.
Toxicity Rating: 4

Gastric lavage.
Oral methionine 10 gm in 12 hours over 4 doses or IV cysteamine prevents hepatic damage if given within 10 hours.
Cysteamine 1 gm IV in 10 minutes and 400 mg in 5 percent dextrose over, 4 and 8 hours.
Vitamin K, charcoal hemoperfusion, hypertonic glucose IV for cerebral edema.
N-acetyl cysteine (NAC) is the specific antidote of choice. Orally given at 1330 mg/kg weight in 3 days, while give IV at 300 mg/kg over 20 hours.
General/ supportive measures such as IV electrolytes and rehydration, vitamin K for bleeding tendencies, mannitol for cerebral edema, etc.

It is an effective murder method as even though modern methods of postmortem assay now exist, such complex investigations are unlikely to be launched unless there is some suspicion attached to what usually looks like a natural death.
It is a potent hypoglycemic agent and if the severe lowering of blood sugar persists for many hours, then brain damage and death will occur.
In massive doses, especially intravenously, death can take place within a few hours.
If death from insulin is suspected, then a search of the body must be made for recent needle marks and the surrounding skin, subcutaneous tissue, and underlying muscle excised and sent unfixed for assay.
Blood samples should also be taken, as modern analytical methods can now distinguish between human, bovine, and porcine insulin and detect adjuvants such as zinc, which assists in tracing the origin of the extrinsic insulin.
Postmortem samples should be taken as soon as possible after death and the plasma immediately separated from the cells and kept deep-frozen until analysis.
Postmortem blood glucose levels are generally unhelpful in confirming hypoglycemia, but vitreous humor may be more useful.
Oral hypoglycemic agents, such as sulphonylureas and biguanides, may be taken in overdose, either suicidally or accidentally, producing hypoglycemia, hypokalemia, and acidosis.

Flushed face, edema of the face, skin rash, tinnitus, deafness, hyperpnea, nausea, vomiting, hematemesis, melaena, hypoprothrombinemia, acute renal failure, pulmonary edema, respiratory arrest.
Fatal dose: 5 to 10 gm.
Fatal period: A few minutes to a few hours.

Paracetamol (acetaminophen) is a non-narcotic analgesic and antipyretic.
It acts by inhibiting prostaglandin synthesis.
It can produce severe liver damage due to the accumulation of a highly toxic intermediate metabolite: nacetylepbenzoquinone (NAPQ) in overdosage.
Normally in therapeutic dosage, this metabolite is detoxified by glutathione.

Within the first 24 hours, it can produce — anorexia, nausea, vomiting, and epigastric pain.
- This will be followed by the disappearance of all discomforts giving a false sense of relief in the next 24 hours.
After 48 to 96 hours it can result in progressive hepatic encephalopathy noticed by vomiting, jaundice, hepatic pain, confusion, coma, coarse flapping tremors of hands (asterixis) gastrointestinal hemorrhage, cerebral edema, renal tubular necrosis, etc.
There may be cardiac arrhythmias, hemorrhagic pancreatitis, disseminated intravascular coagulation, etc.; death often takes place in this stage.
In cases where this does not happen, the patient goes into the next stage of recovery, which begins in about 5-7 days and the patient gradually becomes completely normal in about 2–3 months' time.
Fatal dose: 10 to 25 gm.
Fatal period: Up to five days.
Toxicity Rating: 4

Gastric lavage.
Oral methionine 10 gm in 12 hours over 4 doses or IV cysteamine prevents hepatic damage if given within 10 hours.
Cysteamine 1 gm IV in 10 minutes and 400 mg in 5 percent dextrose over, 4 and 8 hours.
Vitamin K, charcoal hemoperfusion, hypertonic glucose IV for cerebral edema.
N-acetyl cysteine (NAC) is the specific antidote of choice. Orally given at 1330 mg/kg weight in 3 days, while give IV at 300 mg/kg over 20 hours.
General/ supportive measures such as IV electrolytes and rehydration, vitamin K for bleeding tendencies, mannitol for cerebral edema, etc.

It is an effective murder method as even though modern methods of postmortem assay now exist, such complex investigations are unlikely to be launched unless there is some suspicion attached to what usually looks like a natural death.
It is a potent hypoglycemic agent and if the severe lowering of blood sugar persists for many hours, then brain damage and death will occur.
In massive doses, especially intravenously, death can take place within a few hours.
If death from insulin is suspected, then a search of the body must be made for recent needle marks and the surrounding skin, subcutaneous tissue, and underlying muscle excised and sent unfixed for assay.
Blood samples should also be taken, as modern analytical methods can now distinguish between human, bovine, and porcine insulin and detect adjuvants such as zinc, which assists in tracing the origin of the extrinsic insulin.
Postmortem samples should be taken as soon as possible after death and the plasma immediately separated from the cells and kept deep-frozen until analysis.
Postmortem blood glucose levels are generally unhelpful in confirming hypoglycemia, but vitreous humor may be more useful.
Oral hypoglycemic agents, such as sulphonylureas and biguanides, may be taken in overdose, either suicidally or accidentally, producing hypoglycemia, hypokalemia, and acidosis.