Topic 4.

Drug-Related and Toxin-Related Deaths

Deaths involving drugs or toxins account for a significant number of cases handled by
forensic facilities. While some of these cases may be relatively straightforward, in others, there
is often no indication of drug or toxin exposure at autopsy, either on external or internal
examination. A further difficulty arises at the scene as there may be no indicators of drug usage,
sometimes because family members or friends have ‘‘cleaned-up’’ the area. Thus, most
drug-related deaths are included in the larger population of deaths that have ‘‘no anatomic
cause of death.’’ Occasionally, there are findings that give clues to a possible drug related death.
These include recent or old needle puncture marks, needle track marks, tablets in the stomach,
or scarring of the wrists from a previous suicide attempt. Marked pulmonary edema (fluid) may
accumulate in many kinds of drug deaths resulting in a characteristic cone of foam from the
mouth or nose. Drug deaths may involve illegal (“street”) drugs, over-the-counter (OTC)
preparations, or prescription medications. In order to appropriately identify deaths related to
drugs or toxins, it is essential to perform forensic toxicology tests on postmortem blood (and/or
other tissue) samples. For this reason, forensic pathologists and death investigators should be
very familiar with the types of drugs that are routinely screened for by their forensic toxicology
laboratory. Routine “drug screens” usually identify many drugs and toxins; however, for many
others, the toxicology laboratory must be asked to specifically attempt to identify that particular
drug or toxin. In order to know which ones might be present, a thorough death and scene
investigation must be performed.
Investigation of Drug-Related Deaths
Death investigators must be able to recognize drugs and drug paraphernalia while at death
scenes. Packaging materials, containers, syringes, homemade smoking devices, scales,
prescription medications, and other items should arouse suspicion of a drug-related death.
Over-the-counter (OTC) and prescription medications should not be ignored. Collecting and
documenting all OTC and prescription medicines, and counting all pills present in each
container, is an essential part of a death investigator’s job. Interviewing survivors (family,
friends) can often reveal a history of drug use by the decedent.
Another scenario involves the “dumping” of a drug death body at a site distant from the
place of death. If a drug abuser dies at a location that is being used by other drug users, it is not
uncommon for some of the living members of the group to transport the body to a separate,
isolated location. This is presumably done so as to not disrupt the drug-use environment.
Sometimes, the helpful body transporters leave obvious signs for those who discover the body,
such as a syringe and needle, or other drug paraphernalia.
If a victim is transported to the emergency department prior to being pronounced dead, and
if there is survival in the hospital prior to death, it is important for death investigators to obtain
from the hospital laboratory any or all blood (and other tissue) samples collected from the
decedent. This collection must occur immediately upon notification of death, since many
laboratories discard samples after only a few days.
Autopsy Findings in Drug-Related Deaths
Despite the fact that there are usually no overt external (or internal) autopsy findings in
drug/toxin deaths, there are some findings that may represent clues that a drug death has
occurred. Occasionally, there are obvious findings.
Findings on external examination that suggest the possibility of a drug or toxin related death
include drug paraphernalia on the body or within the clothing, fresh needle puncture marks,
needle tracks (scars from intravenous drug administration), skin-popping scars (from injecting
drugs subcutaneously), a perforated nasal septum (from snorting drugs, such as cocaine),
stained fingers (from smoke or paint), evidence of previous suicide attempts (recent shallow
cuts or scars on arms/wrists), evidence of pill residue or dyes in vomit within or around the
mouth or on clothing, peculiar discoloration of livor mortis (bright red: carbon monoxide or
fluoroacetate; green: hydrogen sulfide), and extensive white or pink foamy, frothy pulmonary
edema fluid protruding from the mouth and/or nose. This latter finding, which is sometimes
called a “foam cone,” is not specific for drug deaths, as it can occur in a variety of non-drug
cases, but it can be seen in deaths related to opiates or inhalants.
Internal findings that suggest the possibility of a drug or toxin death include extensive liver
damage, unusual gastrointestinal contents numerous pills or pill “sludge” or “residue” within
the stomach, a dusky discoloration of the brain or widespread brain swelling, and abundant
foamy pulmonary edema fluid. The term “body stuffing syndrome” refers to a situation whereby
an individual, usually in imminent threat of being apprehended or searched by police, quickly
intentionally ingests (or hides in other body orifices) illegal or illegally-obtained drugs, in hopes
of avoiding arrest. Subsequent massive drug overdose can ensue. The term “body packing
syndrome” refers to a situation whereby an individual purposefully ingests (or hides in other
body orifices) illegal or illegally-obtained drugs, usually packaged in some type of carrying
container (balloons, condoms, plastic bag or wrap), in order to transport the drugs across
international borders, through airports, or after stealing them, with the intention of recovering
the drugs at a later time and place. As with the body stuffing syndrome, subsequent massive
overdose can occur.
Toxicology Issues
With any substance (drug, poison) that is present in a person’s body, there are a variety of
terms that are used to describe processes involving that substance. The “route” of exposure or
administration describes how the substance gets into a person’s blood stream. Common routes
are ingestion (through the GI tract), injection (via a needle intravenously, intramuscularly, or
subcutaneously), inhalation (breathing it in, either directly or via burning or smoking it), and
insufflation (snorting). The term “metabolism” describes how the human body breaks down the
substance. Two common locations for drug/toxin metabolism are the liver and the bloodstream
itself, where various enzymes can break down certain substances. A substance that is formed by
the breakdown of a “parent” substance is referred to as a “metabolite,” or a “breakdown
product.” With certain drugs, a metabolite might be “active,” meaning it has pharmacological
properties, often similar to the parent drug/toxin. Many other metabolites are “inactive,”
meaning that they do not have pharmacological properties. How the body actually gets rid of a
drug, usually via metabolism and excretion (often via the kidneys), is referred to as
“elimination.” The “half-life” (designated as t1/2) of a drug/toxin is the length of time it takes for
the body to eliminate half of the substance that was originally present. There are certain drugs
that have very short half-lives. With some of these, postmortem metabolism can continue to
occur, using blood enzymes that remain partially active after death. As such, pathologists often
rely on toxicology tests identifying a metabolite in order to establish that a death was related to
a particular drug’s toxicity.
One of the most important factors in identifying drug- or toxin-related deaths is the forensic
toxicology laboratory. Knowing the correct samples to obtain, the proper packaging and storage
protocols, and maintaining the proper chain of custody are all necessary to obtain the most
optimum toxicology results. Forensic pathologists and death investigators should be aware of
the drugs and toxins that are normally screened for in a particular toxicology laboratory’s
screening tests. A “qualitative” test signifies whether a substance is present (positive) or not
(negative). For a test to have forensic significance, a second methodology must be used with
positive results. In most laboratories, the second, confirmatory test is also “quantitative,” in that
a specific level of the drug/toxin is determined. A common confirmatory method is gas
chromatography−mass spectroscopy (GCMS). For certain substances, samples must be referred
to a larger, reference laboratory. Several tubes of blood and urine should be collected (if
possible) in every forensic case.
Urine is frequently used for screening tests. Although such tests can be useful in directing a
toxicology laboratory toward a particular drug/toxin, it is important to remember that, in order
to determine whether or not a given drug or toxin has contributed to death, the blood levels are
what is most important. The best source of blood is peripheral blood, which is most easily
obtained from the femoral (groin) blood vessels. Samples of blood should be collected in tubes
with sodium fluoride preservative (gray-top tubes), tubes with no preservative (red-top tubes),
and tubes with appropriate preservatives for carboxyhemoglobin (carbon monoxide) testing,
which vary from laboratory to laboratory. Urine samples should be collected in containers with
no preservative. Other body fluids and tissues can also be collected, including vitreous fluid,
cerebrospinal fluid (CSF), bile (from the gallbladder), gastric (stomach) contents, and various
solid organs (liver, kidney, brain, muscle). Pathologists should work with their toxicology
laboratory to determine which samples are best to retain.
All samples should be labeled with the decedent’s name, as well as the sample site (for
example: “femoral blood”). Occasionally, testing of hair is required. This can be performed at
special reference laboratories, and sometimes can provide a timeline for drug/toxin exposure. A
relatively significant amount of hair (a group of hair strands at least 1/4 to 3/8 inch in diameter)
should be collected if such testing is to be performed. In cases where heavy metal poisoning is
of concern, a fingernail or toenail can be retained for potential testing.
Substance Abuse
Some drugs, depending on their physical and chemical properties and their concentrations
in the body, will exert their most toxic or lethal effects in an acute manner, while others will take
a longer period of time to act. In general, deaths associated with substance abuse may be
related to acute or chronic complications. Acute substance abuse indicates that the death was
related to direct toxic effects of the drug shortly after administration. In a delayed overdose, the
drug produces damage to the body over hours or days following acute intoxication, with
complications that may include coma, sepsis, brain swelling, and herniation. This process may
evolve over days with the drug(s) metabolized from the body. The underlying process that set
off this sequence of events is the acute intoxication.
Acute and Chronic Alcoholism
Death occurring from acute alcoholism is usually classified as natural, although this may not
always be the case. A young adult at a party trying to impress friends may attempt to guzzle a
liter of whisky. This is more than enough alcohol at one time to kill most adults. In this case, the
manner of death would be accident. Sometimes depressed people with an acute triggering
event, tell their family that they are going to “drink themselves to death.” After several days of
drinking large quantities of alcohol, they die. If you can establish the intent to do harm, the
manner of death would be suicide. If someone at a party drinks alcohol from a funnel and a
hose, by pouring the alcohol themselves, and then dies, the manner of death would be
accident. If someone holds the hose and pours the alcohol for them, the manner of death
should be homicide.
The deaths of individuals with a history of chronic alcoholism, including varying degrees of
liver disease, intoxications, and withdrawal, are mostly certified as natural. Chronic alcoholics
who stop drinking abruptly may get the “shakes” and eventually experience seizures leading to
death. Withdrawal of many other drugs without other underlying natural disease will not
typically cause death.
Ethanol (ethyl alcohol or EtOH) is what is commonly known as drinking alcohol. There are
numerous alcoholic beverages, ranging from “near-beers,” which have such low levels (<0.5%)
that they are not legally considered alcoholic beverages, to beer (3–8% alcohol by weight), to
wine (10–20%), to various distilled liquors, such as vodka, rum, gin, scotch, brandy, whiskey, and
bourbon, which may contain 40–50% alcohol by weight.
The usual route of administration of EtOH is via GI absorption after oral ingestion. The EtOH
is absorbed predominantly in the small intestines. Food may slow absorption. A vast majority of
EtOH is metabolized within the liver by enzymes that convert EtOH to acetaldehyde and then
acetic acid. A small percentage of EtOH within the blood is excreted in the urine, sweat, and
breath. The average non-alcoholic person’s ability to eliminate EtOH is about two thirds to one
drink per hour.
The toxic effects of EtOH encompass a spectrum of changes within numerous organ systems.
Within the CNS, EtOH has a depressant effect. Wernicke−Korsakoff encephalopathy, cerebellar
vermis atrophy, contral pontine myelinolysis (CPM), and seizures can occur. The liver changes
include steatosis, hepatitis, and cirrhosis. GI system effects include portal hypertension,
esophageal varices, peptic ulcer disease, gastritis, Mallory−Weiss syndrome (lacerations of
esophagus from vomiting), and pancreatitis. EtOH is considered a cardiac irritant, with
intoxicated persons being at increased risk of an arrhythmia. In addition, chronic use can result
in a dilated cardiomyopathy. Chronic alcoholics tend to be malnourished, have vitamin
deficiencies (especially thiamine), and are prone to electrolyte disturbances, such as occurs in
the low-salt vitreous electrolyte pattern. Deaths related to chronic alcoholism, without
accompanying acute intoxication, should be ruled as natural deaths. This includes deaths
related to alcohol withdrawal (delirium tremens).
It is important to obtain blood samples with care in cases where there is suspected alcohol
use, and trauma played a role in the person’s death. The best specimen for postmortem EtOH
determination is peripheral blood (femoral) collected in a gray-top tube (containing sodium
fluoride as a preservative). Heart blood samples should be avoided, since EtOH can diffuse
across the gastric wall and diaphram. “Blind” attempts at cardiac puncture in cases where an
autopsy is not going to be performed should also be avoided, since the stomach can be
inadvertently punctured; EtOH contained within the stomach in such instances will create an
artifactually elevated blood ethanol level. It is important to remember that a serum EtOH level
is approximately 12–18% higher than the corresponding whole “blood alcohol concentration”
(BAC). In cases with a significant amount of survival following injury and before death (such as
several days), evaluation of blood contained in hematomas (for example, a subdural hematoma)
may show ethanol levels consistent with circulating blood levels at the time of injury, even
though circulating blood levels immediately prior to death (and in samples collected at autopsy)
are negative.
Amphetamines and Similar Substances
Amphetamines are stimulant drugs. There are numerous drugs classified as amphetamines.
Several amphetamines have legitimate medicinal uses but most are used solely for recreational
abuse. Some of these are referred to as “designer drugs” − they may be ingested, injected,
smoked or snorted. The primary effects are on the CNS and cardiovascular systems, including
possible hallucinations, psychosis, and elevation of blood pressure. Deaths related to the toxic
effects of amphetamines may be related to CNS seizure activity or cardiac arrhythmias.
Tolerance may occur with amphetamines. Unlike certain other drugs, where a specific level
must be present in order to consider the death as an “overdose,” the mere presence of
amphetamines within the decedent, in the absence of another explanation for death, is
considered enough evidence to rule the cause of death as being due to the toxic effects of
amphetamines. Examples of amphetamines include: amphetamine, methamphetamine,
dextroamphetamine (Adderal), methylphenidate (Ritalin), methathinone (CAT),
methylenedioxyamphetamine (MDA), 3,4-methylenedioxymethamphetamine (MDMA or
“ecstasy”), methyl-2,5-dimethyoxyamphetamine (DOM), and paramethoxyamphetamine (PMA).
Chronic methamphetamine users frequently develop “meth mouth,” a condition of poor
oral hygiene, resulting in loss of teeth, probably related to a combination of drug-induced
teeth-grinding (bruxism), dry mouth (xerostomia), and general lack of concern.
MDMA (“ecstasy”) produces a massive serotonin rush and is very common within the rave
scene. The drug is described as a stimulant followed by a hallucinogen “chaser.”
Barbiturates
Barbiturates are a group of depressant drugs, which are divided in three basic groups,
depending on their timing of onset and duration of action (short-acting, intermediate-acting,
and long-acting). The drugs are typically ingested or injected and have a sedative-hypnotic
effect. Overdose results in coma and death. Medicinally, they are frequently used in anesthesia
or as anticonvulsants. Examples include phenobarbital, secobarbital, amobarbital, and
pentobarbital.
Although barbiturate abuse has fallen out of favor, occasional overdoses are still
encountered. Classic descriptions of some of the lesions associated with barbiturate abuse
include the presence of “barbiturate blisters” on the skin, necrosis of a particular structure in
the brain referred to as the “globus pallidus,” and the identification of polarizable crystals seen
under the microscope when looking at the stomach lining (if the drug was ingested).
Cocaine
Cocaine is a substance that leads to severe psychological or physical dependence. It is found
in the leaves of a South American shrub called Erythroxylon coca and is one of the most potent
of the naturally occurring central nervous system (CNS) stimulants. It acts in the nervous system
by inhibiting the reuptake of the neurotransmitters dopamine and norepinephrine. First isolated
in 1855, it has been used medicinally as a local anesthetic. However, because of its high
potential for abuse, the use of cocaine for clinical situations has become severely limited. When
cocaine is taken for illicit reasons it is either taken as the water-soluble hydrochloride salt by
nasal inhalation (“snorting”), intravenous injection, or as the free-base (“crack”) by smoking.
Regardless of the chemical form or route of administration, once cocaine is administered it is
rapidly absorbed and distributed throughout the body.
The half-life of cocaine is relatively short (30–60 minutes). Cocaine is metabolized to
norcocaine (active), ecgonine methyl ester, benzoylecgonine (BE), and ecgonine. Metabolism
within the bloodstream can continue after death. For this reason, blood samples should be
collected in tubes containing sodium fluoride, a substance that inhibits the enzymes that break
down cocaine. In the presence of ethanol, the substance “cocaethylene” can be produced
within persons using cocaine. Cocaethylene is unique in that it is produced in the body by a
combination of two other drugs (cocaine and ethanol), and it is pharmacologically active
(similar to cocaine), with a half-life of over an hour and a half. BE’s half-life is around 4–5 hours.
Cocaine metabolites can be detected in the urine for several days after use. In order to rule a
death as being related to the toxic effects of cocaine, there should be evidence of cocaine or
metabolites (such as BE) within postmortem blood samples. Even in the absence of measurable
cocaine within postmortem blood samples, a death can still be ruled as being caused by cocaine
toxicity, so long as metabolites are present in the blood and there is no other explanation for
death. The absence of measurable cocaine in these cases is explained by cocaine’s short
half-life, as well as the postmortem interval (between death and collection of sample), which
allows for postmortem metabolism within the blood.
Deaths related to cocaine use typically result from cardiovascular or central nervous system
effects. Within the cardiovascular system cocaine may induce arrhythmias, marked increase in
blood pressure, myocardial infarcts (heart attacks), and cerebrovascular hemorrhages. Within
the CNS, cocaine may induce seizures, hyperthermia, panic attacks, and intense paranoia with
delirium. Any of these may be associated with a lethal outcome. “Excited delirium” is classically
described in cocaine users, characterized by hyperthermia, superhuman strength, agitation,
paranoia, delirium, and often sudden death. Many in-custody deaths have excited delirium as a
major contributing factor.
Unlike certain drugs and toxins, there is no “safe” level of cocaine. A relatively small amount
can induce a fatal arrhythmia in a long-time user or a first-time user. In certain situations, there
may be a massive overdose. The typical settings are the “body packing syndrome” or the “body
stuffing syndrome,” wherein a person attempts to transport or hide cocaine within the GI (or
other) systems. Some longterm effects associated with chronic cocaine use include an enlarged
heart, advanced coronary artery atherosclerosis, and a perforated nasal septum (in persons who
snort cocaine). It is not unusual to encounter a case in which there is underlying heart disease
(cardiomegaly and/or atherosclerosis) that is sufficient, by itself, to explain death, but with
toxicologic evidence of recent cocaine use, i.e. significant levels of BE (but not necessarily
cocaine itself). When such a situation occurs, it is appropriate to consider both the underlying
disease and cocaine toxicity as contributing factors in death.
Opiates
Opiates are a class of narcotic drugs that are frequently abused. The term “narcotic”
describes a drug that is able to induce sleep. Opiates, therefore, are depressants. There are
many opiates and related compounds that are used for legitimate medical purposes. Morphine,
hydrocodone, oxycodone, fentanyl, propoxyphene, and methadone all have useful
pharmacologic properties, often as analgesics (pain relievers). Another common medical use for
some of the less-potent opiates, such as codeine and dextromethorphan, is cough suppression.
Opiates having no legitimate medicinal use include heroin and opium.
The physiologic effects of opiates include CNS depression and analgesia (pain relief). At
moderately high doses, opiates can cause euphoria, a sense of warmth, pinpoint pupils, nausea,
urinary retention, and constipation. Higher doses may result in drowsiness, sedation, respiratory
slowing, and a depressed cough reflex. Opiate overdose usually results in respiratory depression
and failure. Other effects can include hypotension (low blood pressure), a decreased heart rate,
and cold/clammy skin. Tolerance is a well-known phenomenon amongst opiate users, such that
higher and higher doses may be required in order for a user to experience the effects that they
desire.
At autopsy, persons dying from opiate toxicity frequently demonstrate abundant pulmonary
edema fluid, often with pink to white frothy fluid having been expelled through the mouth and
nose (a “foam cone”). Depending on the route of administration, needle tracks or “skin
popping” scars (from subcutaneous injection) may be evident. Microscopic examination may
reveal the presence of polarizable foreign material from pills that have been ground up,
dissolved, and injected into veins, and is usually seen at skin injection sites and within the lungs.
There may be gross evidence of constipation (impacted stool within the bowels) and/or urinary
retention (a markedly distended bladder).
Psychoactive Drugs of Abuse (Hallucinogens)
Hallucinogens are substances that have the ability to cause changes in a person’s perception
of reality. The term “psychedelic” is applied to some of the drugs in this category. Included in
this category of drugs is one of the most commonly used drugs of abuse, marijuana, as well as
LSD, PCP, mescaline, and mushrooms.
Marijuana
Marijuana is another name for the plant Cannabis sativa, the leaf of which may be smoked
or ingested. The drug is used for its euphoric effects; however, other possible effects are
lethargy, drowsiness, hunger (the “munchies”), thirst, memory loss, anxiety, paranoia, psychosis,
tachycardia (increased heart rate), increased blood pressure, decreased motor coordination,
and reddening of the eyes. Marijuana is not known to be lethal due to physiologic toxicity;
however, it is frequently involved in lethal accidents, where marijuana intoxication may well be
considered a causal factor in the accident. Blood THC levels of greater than 5–10 ng/mL indicate
recent use. THC and 11-hydroxyTHC levels decline rapidly after use. Blood 11-carboxy-THC can
remain elevated for several days after use and urinary carboxy-THC can be detected for several
months.

Lysergic Acid Diethylamide (LSD)

 LSD represents the prototypical psychoactive drug. The usual route of administration is oral,
via consumption of thin squares of LSD-laced gelatin (“blotters” or “dots”). Alternatively, the
drug may be snorted. LSD use results in a variety of effects, including impaired judgment,
hallucinations, apid emotional changes, possible psychosis, and flashbacks (“post-hallucinogen
perception disorder”). Hyperthermia and excited delirium may also occur. A general term used
to describe the effects of LSD is “trip,” with users experiencing a “good trip” or a “bad trip.”
Anxiety and paranoia tend to accompany bad trips. Death can be related to accidental injury
sustained during acute intoxication.
Poisons
Arsenic
Arsenic is considered one of several “heavy metals” that can be toxic or lethal. The metal is
ubiquitous (existing nearly everywhere) within the environment, but can be more concentrated
in certain locations, such as bodies of water, and, hence, in the fish that reside therein. It is also
present in a variety of products, including ceramics and certain pesticides. Routes of exposure
include ingestion and inhalation. Arsenic poisons various enzymes within the body causing
acute and chronic toxicity. Symptoms include abdominal pain, nausea, vomiting, diarrhea, as
well as various cardiovascular, respiratory, and CNS effects. Arsenic poisoning may result in a
garlic odor of the breath. Chronic poisoning may cause thickened areas of skin, particularly on
the palms and soles. A long-term complication is skin cancer. In chronic toxicity, persons may
develop transverse white lines on their nails referred to as “Mee’s lines.” Since arsenic is
ubiquitous, it is normally present in very low.
Lead
Lead is relatively ubiquitous as well. It is present in pollution, older paints, certain forms of
fuel, batteries, plastics, insecticides, ceramics, and some Chinese herbal medicines. It may be
ingested or inhaled. Lead toxicity, or “plumbism,” results in a variety of physiologic effects,
including anemia because of decreased hemoglobin production, abnormal calcium metabolism,
GI hemorrhage, weakness, neurologic dysfunction (paralysis, encephalopathy), and kidney
problems. Normal blood lead levels are less than 10 μg/dL (0.1 mg/L). In cases of lead
poisoning, pathologists may see pink inclusions within certain kidney cells under the
microscope, as well as protein droplets within the CNS. Burton’s “lead lines” represent blue
discoloration of the gums, at the base of the teeth. X-ray examination in children may show
radiodense accumulation of lead within the growth plates at the ends of long bones −these are
also referred to as “lead lines.”
Mercury
Mercury is a metal that is a liquid at room temperature. It is present in a variety of
substances, ranging from certain medicines to batteries to paint to dental fillings to fish. It may
be ingested or inhaled. The CNS is the primary target of mercury poisoning, causing long-term
deficits, including dementia. Other organ systems affected include the kidneys and the GI
system.
Organophosphates
Organophosphates are commonly used as insecticides. They inhibit acetylcholinesterase,
which normally functions at nerve endings to break down acetylcholine, which is a
neurotransmitter. In the presence of organophosphates, the acetylcholine is not properly
metabolized so there is continued nerve transmission, or overstimulation of the target of the
nerve ending. This results in a wide variety of symptoms, including sustained muscular
contractions for certain muscle groups, depressed muscular function elsewhere, increased
secretions, increased sweating, increased GI tract motility, increase urination, respiratory
depression, and behavioral and neurologic effects. Organophosphate exposure can be by
ingestion, inhalation, or transcutaneously (skin absorption). Cholinesterase levels/activity can
be accurately measured in postmortem blood samples. Decreased levels suggest that
organophosphate poisoning has occurred.
Strychnine
Strychnine is a very potent poison. It is produced from the plant Strychnos nuxvomica,
which is native to southern Asia and Australia. Its primary use today is as a pesticide (rat
poison). Occasionally, the substance is reported as a contaminant in various street drugs, such
as LSD, cocaine, and heroin. Numerous routes of exposure may occur, including ingestion and
inhalation. The poison is an inhibitor of a neurotransmitter within the CNS. Acute toxicity is
characterized by agitation, being easily startled, restlessness, painful muscle spasms, jaw
tightness, and possibly difficult breathing. The urine may become dark. High doses can lead to
respiratory failure, neurologic deficits, and death.