Forensic Toxicology
Learning Objectives
By the end of this topic, you should be able to:
- Define forensic toxicology and distinguish it from clinical and analytical toxicology.
- Explain the clinical features and mechanism of organophosphate poisoning, cyanide poisoning, and arsenic poisoning.
- List the correct postmortem samples to collect for a suspected poisoning death and the preservative used for each.
- Describe the sequence of screening and confirmatory tests used in postmortem toxicology.
- Explain why drug-facilitated sexual assault (DFSA) samples require urgent, specific collection protocols.
- Identify common mistakes in poisoning case management and viva answers.
Quick Answer
Forensic toxicology is the branch of forensic medicine that detects and interprets poisons and drugs in the body to help determine the cause and manner of death, establish criminal liability, or prove intoxication. It matters because most poisoning deaths have no diagnostic autopsy findings — organophosphates, cyanide, and arsenic can all kill without leaving a signature lesion on the table. The diagnosis is made in the laboratory, not the mortuary, which is why correct sample collection, preservation (usually sodium fluoride, never formalin), and chain of custody are as important as the chemistry itself.
Overview
When a pathologist opens a body and finds nothing to explain death — no wound, no occlusion, no obvious disease — poison becomes the leading suspect. Unlike trauma, poisoning is a silent cause of death: the changes it produces are biochemical, not structural, so autopsy alone often cannot confirm or exclude it. Forensic toxicology exists to close that gap by chemically demonstrating what killed the person.
The specialty sits at the intersection of three demands that clinical toxicology does not face. First, the sample is usually decomposed or postmortem, so the toxicologist must correct for redistribution of drugs after death (postmortem redistribution) and interference from putrefaction. Second, the result must survive legal scrutiny, so chain of custody and confirmatory testing are non-negotiable — a screening positive is never enough to convict or acquit. Third, the toxicologist must work backward from a often-vague clinical history to decide which of thousands of possible poisons to test for, guided by circumstantial evidence, autopsy findings, and cost.
In Indian and most South Asian medico-legal practice, three poisons dominate the exam syllabus and real casework: organophosphate compounds (agricultural insecticide poisoning, the single most common poisoning death in rural India), cyanide (rapid, dramatic, used in both suicide and homicide), and arsenic (the classic "inheritance powder," still relevant because of chronic environmental exposure from contaminated groundwater and because it is detectable in hair and nails years after death).
Common Poisons
Organophosphate Poisoning
Definition. Organophosphate (OP) compounds are insecticides (malathion, parathion, chlorpyrifos, monocrotophos) that irreversibly inhibit acetylcholinesterase (AChE), causing accumulation of acetylcholine at synapses.
Explanation — how it works. Normally, AChE breaks down acetylcholine in the synaptic cleft after it transmits a nerve impulse. OP compounds phosphorylate the active site of AChE, and if untreated for too long the enzyme-inhibitor bond "ages" and becomes permanent. Acetylcholine then keeps accumulating at three receptor sites: muscarinic receptors (smooth muscle, glands), nicotinic receptors (skeletal muscle, autonomic ganglia), and central receptors (brain). The clinical picture is therefore a mixed muscarinic-nicotinic-CNS toxidrome, remembered by the mnemonic DUMBELS — Diarrhea, Urination, Miosis, Bradycardia/Bronchorrhea, Emesis, Lacrimation, Salivation — plus nicotinic effects of fasciculation, weakness, and eventually respiratory paralysis.
Example. A farm laborer found unconscious in a field next to an empty pesticide bottle, with pinpoint pupils, profuse salivation, and a strong garlic-like or kerosene-like odor on the breath — this presentation should trigger immediate suspicion of OP poisoning even before any history is available.
Real-world example. OP self-poisoning is the leading method of suicide in agricultural regions of India, Sri Lanka, and parts of Southeast Asia, because the compounds are cheap, legally available for farming, and highly lethal in small volumes. This "public health" dimension is why WHO and Indian toxicovigilance programs track OP mortality separately from other poisons.
Why it matters. Recognizing OP toxicity early changes management (atropine for muscarinic block, pralidoxime/PAM to reactivate AChE before "aging" occurs, usually within 24–48 hours) and changes the forensic sample plan (stomach wash fluid, blood cholinesterase levels, and viscera for GC analysis).
Common misunderstanding. Students often think atropine "treats" the poisoning. It only blocks the muscarinic (parasympathetic) effects — it does nothing for nicotinic weakness or respiratory muscle paralysis, which is why patients can still die of respiratory failure despite adequate atropinization, and why pralidoxime (which regenerates the enzyme) must be given as well, ideally before aging occurs.
Cyanide Poisoning
Definition. Cyanide (as HCN gas, potassium/sodium cyanide salts, or released from substances like bitter almonds and apricot kernels) is a rapidly acting cellular asphyxiant that binds cytochrome c oxidase in the mitochondrial electron transport chain, blocking aerobic respiration.
Explanation. With cytochrome oxidase inhibited, cells cannot use oxygen even though it is delivered normally by the blood — this is "histotoxic hypoxia." Anaerobic metabolism takes over, producing severe lactic acidosis. Death can occur within minutes of a large dose (the classic history is sudden collapse, almost instantaneous in massive exposure) or within an hour with smaller doses, preceded by headache, palpitations, dyspnea, and seizures.
Example. A viva-classic finding is the smell of bitter almonds on opening the stomach at autopsy — though this is genetically variable; roughly 40% of people cannot detect it due to an olfactory gene polymorphism, so its absence never rules out cyanide.
Real-world example. The 1982 Chicago Tylenol tampering deaths (seven fatalities from capsules laced with potassium cyanide) remain the textbook case demonstrating how forensic toxicology — hair analysis and viscera testing — both confirmed the poison and helped trace a common source across victims who had no contact with one another.
Why it matters. Because death can be so fast, cyanide poisoning is a recognized method for both suicide and homicide, and it is one of the few poisons with a specific antidote pathway (sodium nitrite to induce methemoglobinemia, which competes for cyanide, followed by sodium thiosulfate to convert cyanide to the far less toxic thiocyanate, excreted in urine).
Common misunderstanding. Cherry-red or pink postmortem lividity is often taught as "diagnostic" of cyanide, but it is neither sensitive nor specific — carbon monoxide poisoning produces the same color, and cyanide deaths can also show ordinary bluish lividity. Color alone is never used to confirm the diagnosis; blood and viscera analysis (microdiffusion or spectrophotometric methods for cyanide, or specifically GC) are required.
Arsenic Poisoning
Definition. Arsenic (as arsenic trioxide, "white arsenic") is a heavy metal poison that inhibits pyruvate dehydrogenase and other sulfhydryl-dependent enzymes, disrupting cellular energy metabolism, and has both acute and chronic (occupational, environmental) presentations.
Explanation. Acute arsenic poisoning classically causes severe gastroenteritis — profuse "rice-water" like vomiting and diarrhea — within hours, mimicking cholera, followed by cardiovascular collapse and, in survivors, a delayed peripheral neuropathy. Chronic low-dose exposure (e.g., contaminated groundwater in parts of West Bengal and Bangladesh) produces skin changes (melanosis, keratosis), Mees' lines (transverse white lines) in the nails, and increased risk of skin and other cancers over years.
Example. In a classic homicidal-poisoning scenario, arsenic is added repeatedly in small doses to food over weeks to months, producing a chronic illness that mimics a gastrointestinal disease rather than an obvious acute poisoning — this slow method is precisely why arsenic earned the historical nickname "inheritance powder."
Real-world example. Because arsenic is deposited in keratin, it remains detectable in hair and nails for years after exposure, and segmental hair analysis can even estimate the timing of exposure(s) along the hair shaft — this technique has been used to exhume and re-examine historical poisoning cases (including retrospective analysis of Napoleon Bonaparte's remains, though the cause of his death remains debated).
Why it matters. Arsenic's ability to persist in hair/nails long after death (unlike volatile poisons such as cyanide or alcohol, which dissipate) makes it uniquely suited to exhumation cases — a body buried months or years earlier can still yield a positive result.
Common misunderstanding. Students sometimes assume a single hair/nail test result proves timing of a single poisoning event. In reality, interpreting segmental hair analysis requires knowing hair growth rate (~1 cm/month) and requires quality-controlled cutting close to the scalp; contamination from external environmental arsenic (e.g., handling arsenical pesticides without ingestion) can also produce false elevation on the hair surface, so wash procedures before analysis matter.
Postmortem Toxicology Testing
Postmortem toxicology is not simply "clinical toxicology on a dead body." Two factors make it distinct: (1) postmortem redistribution — after death, drugs (especially basic, lipophilic drugs like digoxin, tricyclics, and opioids) diffuse from tissue reservoirs (liver, lung) into adjacent blood, so femoral blood is preferred over cardiac blood because it is more resistant to this artifact; and (2) putrefaction can generate ethanol de novo through microbial fermentation, so a positive postmortem blood alcohol result must always be interpreted alongside vitreous humor alcohol (which resists putrefactive contamination) before it is accepted as ante-mortem ingestion.
The standard sample panel collected at every suspected poisoning autopsy:
| Sample | Preservative | Why this sample |
|---|---|---|
| Stomach contents + wash | Saturated saline (no preservative needed if analyzed promptly) | Detects unabsorbed poison; largest concentration if death was rapid after oral ingestion |
| Blood (femoral, not cardiac) | Sodium fluoride + potassium oxalate | Femoral site resists postmortem redistribution and putrefactive alcohol production |
| Vitreous humor | None required (refrigerate) | Resists putrefaction longest; gold standard to confirm true ante-mortem alcohol/glucose/electrolyte levels |
| Liver, kidney | Saturated saline (never formalin) | Largest organ reservoir for many drugs and metals; used for confirmatory GC-MS/AAS |
| Urine | Sodium fluoride | Good for drug screening — concentrates metabolites; useful window even after blood levels fall |
| Hair and nails | Dry, no chemical preservative | Only samples that retain long-term or historical exposure (arsenic, heavy metals) — useful in exhumation |
Why never formalin: Formalin is a fixative used for histopathology, but it chemically reacts with cyanide, alcohol, and many organic poisons, destroying them or creating artifacts (formalin itself can generate formaldehyde-related false positives). Any viscera sent for chemical analysis must be preserved in saturated saline (or, in India, per the standard forensic protocol, in rectified spirit for some samples per local guidelines) — never in formalin, which is reserved strictly for a separate histology sample.
The testing sequence always moves from cheap/fast/sensitive screening to slow/expensive/specific confirmation — a screening test alone is never legally sufficient:
Screening tests (e.g., color spot tests like the Reinsch test for arsenic, immunoassays for drugs of abuse, thin-layer chromatography) are fast and cheap but produce false positives and cannot be used alone in court. Confirmatory tests (GC-MS for volatiles and organics, LC-MS/MS for drugs, atomic absorption spectroscopy for heavy metals like arsenic) provide the specificity needed for legal proof, because they identify a compound by its unique mass spectrum or elemental signature rather than by a color reaction or antibody cross-reactivity.
Drug-Facilitated Crimes
Definition. Drug-facilitated crimes (most commonly drug-facilitated sexual assault, DFSA, but also drug-facilitated robbery) occur when a perpetrator administers a sedating or disinhibiting substance to a victim — without their knowledge — to incapacitate or render them unable to resist or later recall the assault.
Explanation. The forensic challenge is timing. Agents commonly used — benzodiazepines (particularly short-acting ones like flunitrazepam), gamma-hydroxybutyrate (GHB), and alcohol itself in combination with either — have short elimination half-lives and are often below the detection limit of standard hospital drug screens by the time a victim presents, which is frequently delayed because the victim was unconscious or amnestic and did not realize what had happened until hours later. GHB, for example, may be undetectable in blood after about 8 hours and in urine after about 12 hours, even though it may have caused profound sedation.
Example. A victim wakes up in an unfamiliar place with no memory of the preceding several hours, a strong suspicion of assault, but a "normal" routine urine drug screen — this apparent contradiction is exactly what DFSA protocols are designed to catch, because routine hospital toxicology panels are not sensitive enough for these specific agents at the concentrations and time points typically involved.
Real-world example. Because of the narrow detection window, forensic protocols for suspected DFSA prioritize urgent collection: first voided urine (largest available volume, sent specifically for expanded/targeted DFSA panel testing, not the routine hospital screen) and blood as early as possible, ideally within 24 hours of the incident and certainly within 72–96 hours for urine. Hair analysis, taken weeks later, can sometimes retrospectively confirm a single exposure using segmental analysis, though a single-dose exposure is technically harder to detect in hair than chronic use.
Why it matters. If evidence collection is delayed because clinicians assume "if the screen was negative in the ER, nothing was given," genuine drug-facilitated assaults go undetected and unprosecuted. Forensic and emergency protocols must specifically request expanded toxicology (targeting GHB, ketamine, benzodiazepines including designer analogs) rather than relying on the routine drugs-of-abuse panel, which typically only covers a handful of common street drugs.
Common misunderstanding. A negative standard urine drug screen is often misread as proof that the victim was not drugged. In fact, standard immunoassay panels used in most emergency departments test only for a limited set of common drugs (opioids, cannabinoids, cocaine, amphetamines) at cutoffs designed for drugs-of-abuse screening, not for GHB or many benzodiazepines at the low concentrations relevant to a single-dose covert administration — a negative result on that panel says almost nothing about DFSA agents.
Key Terms
| Term | Definition |
|---|---|
| Forensic toxicology | Application of toxicological analysis to legal questions — cause of death, criminal liability, or intoxication. |
| Toxicokinetics | How a poison is absorbed, distributed, metabolized, and eliminated by the body. |
| Postmortem redistribution | Diffusion of drugs from tissue reservoirs into adjacent blood after death, artificially raising levels in samples like cardiac blood. |
| Chain of custody | Documented, unbroken record of who collected, handled, and transported a sample, required for evidence to be admissible in court. |
| Screening test | A rapid, sensitive but non-specific test (immunoassay, color spot test, TLC) used to narrow the list of possible poisons. |
| Confirmatory test | A highly specific test (GC-MS, LC-MS/MS, AAS) required to legally prove the identity of a poison. |
| Vitreous humor | Fluid in the eye, resistant to putrefaction, used as the most reliable postmortem sample for alcohol and electrolyte levels. |
| Cytochrome c oxidase | Mitochondrial enzyme blocked by cyanide, halting aerobic respiration and causing histotoxic hypoxia. |
| Acetylcholinesterase (AChE) | Enzyme that breaks down acetylcholine; irreversibly inhibited by organophosphates, causing cholinergic crisis. |
| Aging (in OP poisoning) | Chemical process by which the OP-AChE bond becomes permanent, after which the enzyme can no longer be reactivated by oxime drugs like pralidoxime. |
| Mees' lines | Transverse white lines on the nails seen in chronic arsenic poisoning. |
| Drug-facilitated sexual assault (DFSA) | Sexual assault in which the victim is incapacitated by covertly administered sedating or disinhibiting drugs. |
Common Mistakes
Misconception 1: "If the autopsy shows no obvious cause of death, poisoning can be ruled out." Why it's wrong: Most systemic poisons (organophosphates in low dose, cyanide, many drug overdoses) leave no macroscopic or even microscopic lesion — the diagnosis is entirely chemical, not morphological. Correct explanation: A "negative" autopsy in the absence of trauma or natural disease should raise, not lower, the suspicion of poisoning, and mandates a full viscera and fluid sample panel be sent for toxicological analysis before the cause of death is finalized.
Misconception 2: "Cherry-red lividity always means cyanide poisoning." Why it's wrong: Cherry-red or pink discoloration of lividity and blood is also produced by carbon monoxide poisoning (carboxyhemoglobin) and can occasionally be seen with hypothermia; it is neither sensitive (many cyanide deaths show ordinary lividity) nor specific for cyanide. Correct explanation: Color findings at autopsy are only a clue to guide which confirmatory test to order (e.g., specific cyanide assay vs. carboxyhemoglobin spectrophotometry) — they are never used alone to establish the cause of death.
Misconception 3: "A negative routine toxicology screen rules out drugging in a suspected DFSA case." Why it's wrong: Standard hospital drug-of-abuse immunoassays only detect a narrow set of common drugs and are not validated for GHB or many benzodiazepines at the low, single-dose concentrations typical of covert administration, and these agents clear from blood/urine within hours. Correct explanation: Suspected DFSA cases require urgent, targeted toxicology (expanded panel including GHB, ketamine, and benzodiazepine analogs) collected as early as possible — a negative routine screen provides essentially no reassurance and should never be used to dismiss the victim's account.
Comparison and Connections
| Feature | Organophosphates | Cyanide | Arsenic |
|---|---|---|---|
| Mechanism | Irreversible AChE inhibition → cholinergic excess | Cytochrome c oxidase inhibition → histotoxic hypoxia | Inhibits pyruvate dehydrogenase / sulfhydryl enzymes |
| Onset | Minutes to hours | Seconds to minutes (very rapid) | Hours (acute) or years (chronic) |
| Classic clinical clue | Miosis, salivation, garlic/kerosene odor | Sudden collapse, possible bitter-almond odor (not universal) | "Rice-water" vomiting/diarrhea (acute); melanosis, Mees' lines (chronic) |
| Antidote | Atropine + pralidoxime (PAM) | Sodium nitrite + sodium thiosulfate | Dimercaprol (BAL) / DMSA (chelation) |
| Best confirmatory sample | Blood cholinesterase level, stomach contents, viscera GC | Blood/viscera cyanide assay (microdiffusion, spectrophotometry) | Hair, nails, urine, viscera by AAS — persists longest after death |
| Typical manner of death seen | Predominantly suicide (agricultural poisoning) | Suicide or homicide | Homicide (chronic, covert) or environmental/occupational exposure |
Practice Questions
Recall
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What is the antidote combination used in organophosphate poisoning, and what does each component do? Answer guidance: Atropine blocks the muscarinic effects of excess acetylcholine (secretions, bradycardia); pralidoxime (PAM) reactivates acetylcholinesterase before the enzyme-inhibitor bond "ages" and becomes permanent — neither drug alone is sufficient.
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Which postmortem sample is preferred for alcohol estimation and why? Answer guidance: Vitreous humor, because it resists putrefactive contamination and the artifactual generation of alcohol by microbial fermentation, unlike blood.
Understanding
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Explain why cardiac blood is avoided in favor of femoral blood for postmortem drug quantitation. Answer guidance: After death, drugs sequestered in tissue reservoirs like the liver and lungs diffuse into adjacent blood (postmortem redistribution); cardiac blood is close to the liver/lungs and can show falsely elevated drug concentrations, while femoral blood, being anatomically distant, better reflects ante-mortem levels.
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Why is a screening test alone never sufficient to prove poisoning in a legal setting? Answer guidance: Screening tests (immunoassay, color spot tests, TLC) are designed for sensitivity and speed, which makes them prone to false positives from cross-reacting substances; only a confirmatory test with a distinct chemical/spectral signature (GC-MS, LC-MS/MS, AAS) provides the specificity legally required to identify a compound beyond reasonable doubt.
Application
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A farm worker is found unresponsive with pinpoint pupils, profuse salivation, and muscle fasciculations near an empty pesticide container. What poison should be suspected, what immediate treatment is indicated, and what sample should be sent urgently? Answer guidance: Organophosphate poisoning; give atropine (titrated to dry secretions) plus pralidoxime as early as possible before enzyme aging occurs; send stomach wash/contents and blood for cholinesterase level and confirmatory GC analysis.
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A suspected DFSA victim presents to the emergency department 20 hours after the alleged incident with only partial memory of events, and the routine hospital urine drug screen is negative. What should the forensic team do next? Answer guidance: Do not accept the routine screen as conclusive — collect first-available urine and blood for an expanded, targeted DFSA toxicology panel (GHB, ketamine, benzodiazepines and their analogs) as soon as possible, since these agents clear within hours to a day and routine immunoassays do not cover them.
Analysis
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Compare cyanide and arsenic poisoning in terms of speed of action and the type of postmortem sample most useful for confirming each. Why does this difference matter for exhumation cases? Answer guidance: Cyanide acts within seconds to minutes and is volatile, so it dissipates quickly after death and is best confirmed from fresh blood/viscera taken soon after death; arsenic acts more slowly (or chronically) and deposits durably in keratinized tissue (hair, nails), remaining detectable for years. This means cyanide poisoning becomes very difficult to prove in an exhumed body long after death, whereas arsenic poisoning can still be confirmed from hair or nail analysis even after prolonged burial.
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A body is found with no external injuries and a completely unremarkable autopsy. The investigating officer wants to close the case as "natural death" since nothing was found. Critically evaluate this conclusion using the concept of postmortem toxicology testing. Answer guidance: An unremarkable autopsy does not exclude poisoning, since most systemic poisons (OP compounds in modest doses, cyanide, many drugs) leave no anatomical trace; the case should not be closed until the full sample panel (stomach contents, femoral blood, vitreous, liver/kidney, urine, hair/nails) has been collected with correct preservatives and sent through both screening and confirmatory toxicology testing — only after a negative, appropriately broad toxicology workup (correlated with a normal clinical history) can natural death be reasonably concluded.
FAQ
1. Why is formalin never used to preserve viscera samples meant for toxicology? Formalin is a fixative for histopathology; it chemically reacts with and destroys many poisons (including alcohol and cyanide) and can create false results. Viscera for chemical analysis must go in saturated saline in a separate, clearly labeled container from any histology sample.
2. Why does the smell of bitter almonds not reliably diagnose cyanide poisoning? Detecting the smell depends on a genetic trait — roughly 30–40% of people cannot smell it at all due to an olfactory receptor variant. Its presence supports the diagnosis, but its absence never excludes cyanide; a proper cyanide assay on blood or viscera is required either way.
3. Why is vitreous humor so valuable in postmortem toxicology? The eye is a relatively closed, protected compartment, so vitreous humor resists bacterial invasion and putrefaction far longer than blood. This makes it the most reliable sample for confirming true ante-mortem alcohol and electrolyte levels, avoiding the confounding effect of postmortem ethanol production by putrefactive bacteria.
4. Can hair analysis really tell you when someone was poisoned? For poisons that deposit steadily in the hair shaft as it grows (notably arsenic and other heavy metals), yes — since hair grows at a fairly predictable rate (about 1 cm per month), segmental analysis along the shaft can localize approximately when an exposure occurred. This is far less reliable for a single covert drugging in DFSA cases, where the dose is small and doesn't leave hair as a first-line detection sample.
5. Why do organophosphate poisoning patients sometimes deteriorate again after seeming to improve? This is the "intermediate syndrome" — a delayed (often 24–96 hours after apparent recovery) onset of proximal muscle weakness and respiratory difficulty, thought to relate to prolonged AChE inhibition and receptor downregulation at the neuromuscular junction. It is distinct from the initial cholinergic crisis and from delayed OP-induced neuropathy, and it is why OP poisoning patients need extended monitoring even after atropinization controls the acute symptoms.
Quick Revision
- Forensic toxicology confirms poisoning chemically when autopsy findings are absent or nonspecific — a "clean" autopsy never rules out poison.
- Organophosphates irreversibly inhibit acetylcholinesterase → cholinergic crisis (DUMBELS + nicotinic weakness); treat with atropine (muscarinic) + pralidoxime (reactivates enzyme, must be given before "aging").
- Cyanide blocks cytochrome c oxidase → histotoxic hypoxia and very rapid death; antidote is sodium nitrite then sodium thiosulfate; bitter-almond smell is present in only ~60–70% of people (genetic).
- Arsenic inhibits pyruvate dehydrogenase; acute form mimics cholera (rice-water stools); chronic form causes melanosis and Mees' lines; deposits in hair/nails for years, ideal for exhumation cases.
- Standard postmortem sample panel: stomach contents, femoral blood (NaF/oxalate), vitreous humor, liver/kidney (saturated saline), urine, hair/nails — never formalin for chemistry samples.
- Femoral blood is preferred over cardiac blood because postmortem redistribution artificially raises drug levels near the liver and lungs.
- Vitreous humor is the gold-standard sample for alcohol because it resists putrefaction and post-mortem alcohol generation.
- Testing always proceeds screening (immunoassay, color spot, TLC — fast, sensitive, non-specific) → confirmatory (GC-MS, LC-MS/MS, AAS — specific, legally required).
- Drug-facilitated sexual assault agents (GHB, benzodiazepines, ketamine) clear from blood/urine within hours, so a negative routine ED drug screen does not exclude DFSA — urgent, expanded, targeted testing is required.
- Chain of custody must be unbroken from collection to lab report, or the toxicology result can be challenged and excluded in court regardless of its scientific accuracy.
Related Topics
Prerequisites
- Basic toxicology principles (toxicokinetics, dose-response, mechanisms of cellular injury)
- Autopsy technique and postmortem changes (needed to understand what an "unremarkable" autopsy does and does not exclude)
Related Topics
- Postmortem Interval and Changes (interpreting putrefaction's effect on toxicology samples)
- Asphyxial Deaths (cyanide and CO both cause histotoxic/chemical asphyxia)
- Medico-Legal Autopsy and Chain of Custody
Next Topics
- Specific Poisons in Detail (corrosives, heavy metals beyond arsenic, plant and animal poisons)
- Sexual Offences and Medico-Legal Examination (for the clinical/forensic workup of DFSA)
- Forensic Psychiatry and Fitness to Stand Trial (where intoxication as a legal defense is examined)