Clinical and postmortem toxicology
Clinical toxicology begins with physiological stabilization and a structured exposure assessment. A toxidrome is a pattern that guides urgent reasoning, not absolute chemical identification. Opioid-associated respiratory depression, anticholinergic dryness, sympathomimetic diaphoresis and cholinergic secretions illustrate useful contrasts. Mixed exposures, underlying disease and treatment can alter the picture. An antidote question should not be read as permission to omit airway, circulation, monitoring or poison-specialist support.
Mechanisms help explain hazards and treatment priorities. Acetaminophen toxicity involves a reactive metabolite and depletion of protective pathways. Organophosphate and carbamate poisoning affect cholinergic transmission but differ in enzyme recovery and related treatment considerations. Toxic alcohol metabolites can produce acid-base disturbances and organ injury. Carbon monoxide impairs oxygen delivery and utilization; standard pulse oximetry may look reassuring despite a serious exposure. Exact drug regimens and decontamination procedures require the appropriate clinical protocol and individual assessment.
Postmortem toxicology adds another layer of uncertainty. Collection site, timing, preservation, decomposition and redistribution can change measured concentrations. Peripheral and cardiac blood are not interchangeable, and a tissue reservoir can produce a misleadingly high central concentration. Comparing appropriate blood, vitreous, urine and other samples may help, but no specimen completely removes all uncertainty. Interpret a result with the scene, medical history, resuscitation and other findings.
A screening immunoassay and a confirmatory analytical result answer different questions. Cross-reactivity can cause a positive screen without confirmed presence of the target drug. Detection of a metabolite establishes a particular exposure inference, not necessarily impairment at a specific time or sole causation of death. A concentration may be potentially lethal in a reference setting yet still require consideration of tolerance, interactions and specimen quality before a causal opinion is assigned.
Postmortem ethanol may arise partly from microbial production, while glucose and other analytes can change after death. A low postmortem blood glucose alone does not establish fatal hypoglycemia. Ketoacidosis interpretation can involve ketone measurements, vitreous findings and the history, rather than nonspecific fatty change alone. Maintain a distinction between analytical identification, evidence of exposure, evidence of a physiological effect and the integrated medical conclusion about contribution to death.