Review Article
Detection of poisoning by substances other than drugs:
a neglected art
Neil R Badcock
From the Department of Chemical Pathology, The Women's and Children's Hospital, 72 King William
Road, North Adelaide 5006, South Australia, Australia
Emergency toxicology deals with the problems
involved in the rapid presumptive diagnosis and
treatment of suspected poisoning.1±5 In my
experience, the most frequent request by
clinicians in poisoning cases is for identi®cation
of the toxin. However, in the current era of ®scal
restraint, rationalization in the contemporary
toxicology laboratory dictates that more selec-
tive testing occur. This invariably involves
employing simple analytical techniques to detect
drugs, and testing for poisons other than drugs
is largely ignored.6±13 A comprehensive drug
screen in the hands of experienced toxicologists
will allow identi®cation of most drug classes,
actual drugs and their characteristic metabolite
patterns; recognized exceptions are a number of
quaternary ammonium compounds (water-
soluble, solvent-insoluble), such as the muscle
relaxant pancuronium chloride, the a2-agonist
clonidine, various b-adrenergic blockers (e.g.
sotalol) and b2-adrenergic agonists [e.g. salbuta-
mol (albuterol) and terbutaline]. However, there
are serious limitations when a comprehensive
drug screen is used as the sole means of
diagnosing poisoning,14±17 since these screens
rarely include poisons that are not drugs.6,9 If
evaluation of the poisoned patient is restricted to
a comprehensive drug screen, carbon monoxide
(the principal single cause of death by poisoning
in England and Wales in 199418) could go
undetected in the absence of informed discussion
between toxicologist and requesting clinician.
In reality, of course, the toxicologist may be
screening for several poisons without recognizing
this fact. The drug screen exclusivity occurs in a
climate in which there is a decrease in the number
of drug-related poisonings and an increase in those
caused by household products.19,20 This occurs, for
example, in children because of tamper-proof
containers. In this group, many poison exposure
cases involve non-pharmaceuticals, such as
petroleum distillates, bleaches, detergents,
Correspondence: Dr Neil R Badcock.
E-mail: badcockn@wch.sa.gov.au
146
Ann Clin Biochem 2000; 37: 146±157
camphor, camphor oil, mothballs, caustic soda,
paints and painting chemicals (turpentine, paint
stripper), rodent killer, ¯uoride/iron tablets,
alcohols (e.g. ethylene glycol and propanol),
insecticides (e.g. from pet care chemicals), swim-
ming pool chemicals, vitamins, heavy metals and
many other non-drugs.21±23 Most of these will not
be detected by a comprehensive drug screen, but
the patient has ingested or has been in contact with
a substance that has produced an injurious or
deadly effect. There is an urgent need for simpler,
reliable, low-cost methods for poison detection.
Rapid access to information that will assist
clinician and toxicologist should be available for
non-pharmaceutical poisonings as well as for
medications.19 A quick differential diagnosis is
desirable to help minimize damage and to ensure
that adequate treatment is initiated quickly. It is
axiomatic that the analyses must be completed
in time to be useful and that the results can be
interpreted. A poison test, even after a lengthy
analysis, can avoid months of fruitless clinical,
biochemical and haematological investigations,
especially in children. It can be an important
consideration in deciding outcome following
organ removal from poisoned donors, with
attention recently being drawn to possible graft
damage caused by some poisons.24 Knowledge
of toxins that have a tendency to cause seizures
may also prove invaluable.25 A broad-based
screen can aid in diagnosis and management,13
exclude other potential diagnoses and more
expensive tests, or eliminate the need for further
treatment. Moreover, the ®ndings may assist in
de®ning the risk of mutagenicity and genotoxi-
city for the patient.26±29
Analytical diagnosis is not always simple in
questions of poisoning. Every assistance must be
solicited. A history is useful, including:
. What labelled poisons were in the house to
which the patient had access? What is the
case history? Is there a suicide note? What
poisons are common in the area? Does

circumstantial and clinical evidence point to
the ingestion of a speci®c poison?
. Do any of the patient's clinical symptoms ®t
the poison, and can appropriate tests be
tailored to these signs and symptoms? Can
the clinical symptoms be reliably linked to
poisons, even multiple ingestions?
. What is the smell, colour, pH and general
appearance of the sample? (Indeed, to look at
and smell the urine or stomach contents
should be routine for a good poisons
laboratory.)
. What were the speed and intensity of onset?
. Has the administration of an antidote had an
effect on the poisoning? In some instances,
use of an antidote may in itself be diagnostic.
. Can routine biochemistry, the incorporation
of external biomarkers, radiography, etc.,
serve as predictors of poisoning?
. Do any non-selective assays have value as a
®rst step in prompting speci®c tests?
. Do the negative ®ndings make a diagnosis of
poisoning unlikely, or do the range and
variety of indicators used permit poisoning
to be excluded de®nitively?
As well as the above, the clinician should be
aware of agents that cause signi®cant harm if
not detected and treated quickly. Iron and
carbon monoxide are two examples of lethal
agents that need a high index of clinical
suspicion for early recognition and require
speci®c tests and speci®c therapy to ensure a
good outcome.
It would be highly desirable if the attending
physician and/or toxicologist had access to
simple, sensitive, rapid and speci®c tests requir-
ing a minimum of equipment and yielding
results in minutes ± i.e. spot tests. Analogies in
drug screening would be the o-cresol test for
paracetamol, the Fujiwara test for chloral,
Trinder's test for salicylate, colour reaction
using photo-oxidation on thin-layer chromato-
graphy (TLC), or even the tetrabromophenol-
phthalein ethyl ester colour formation test for
certain basic drugs.30±38
Generally, because spot tests lack absolute
speci®city, false positives occur much more
frequently than false negatives.8 Conversely, a
false negative may result from a number of
conditions, including low sensitivity of the
method used, binding of the agent or its
metabolites to protein or other high molecular
weight substances, coupling of the agent or its
metabolites with highly adsorptive or reactive
Poisoning by substances other than drugs 147
compounds, metabolites that react differently to
the parent compound, evaporation of, or
chemical change in, the poison during proces-
sing, masking of colour by other substances
present, outdated or unstable reagents, or
insuf®cient solvent extraction of the com-
pound.39 Some of these pitfalls can be overcome
by including positive and negative controls in
the assay procedure; such controls should be
considered mandatory.
The spot tests described here do not constitute
complete and unambiguous toxicological screen-
ing methods. They are outlined for the purpose of
helping to provide a tentative diagnosis in the
emergency treatment of acute poisoning. The
results of these spot tests must be evaluated with
considerable discretion, which generally comes
after much experience and insight in toxicological
analysis.
HOUSEHOLD POISONS
Table 1 provides a list of dangerous household
chemicals.40±42 Many of these toxic substances
have come into common use as a result of the
rapid development of new agricultural and
pesticide poisons and because of their ease of
purchase from large hardware supermarkets.
Less than 5% of the poisons in this list will be
detected using a routine drug screen.
ANALYTICAL PREREQUISITES
Proper provision of biological specimens is
necessary for effective poison screening.10,43
Collection of specimens should preferably occur
before any drugs/antidotes are administered in
treatment.
In all cases, collect:
. Blood: 5 mL of lithium heparinized blood,
2 mL of blood with sodium ¯uoride pre-
servative and 5 mL of blood without anti-
coagulant. Avoid the use of swabs containing
alcohols and heparin containing phenolic
preservative. Protect from light and freeze
at ÿ208C after separation of plasma/serum.
. Urine: send all of the ®rst sample of urine
passed; then collect a 24-h urine sample.
Avoid preservatives, thymol, sodium azide,
etc., and refrigerate at 48C. Note whether
collection involved catheterization.
. Gastric contents: note whether this is vomit,
gastric aspirate or ®rst stomach wash.
Centrifuge or ®lter and carry out tests on
supernatant/®ltrates. Retain solid material
Ann Clin Biochem 2000: 37
148 Badcock

TABLE 1. Examples of household poisons

Medicines Fluoride, antacids, calamine, vitamins, iron, lithium, liniments, antiseptics, haematinics
Plants Foxglove, oleander, poison ivy, mushrooms, seeds/kernels, cherry, thorn apple
Insecticides Ant, cockroach, rodent and moth poisons, animal ¯ea collars and powders
Household products Acids, alkalis, camphor, carbon monoxide, bleach, drain cleaner, rug cleaner, wallpaper
cleaner, laundry ink, disc batteries, moth balls, cosmetics, essential oils, detergents
Garage Kerosene/paraf®n, ®re lighters, ®re starting tablets, ®re extinguishers, paints, painting
supplies, weedkillers, slug pellets, petrol, arsenic, lead, swimming pool chemicals, antifreeze,
fumigants, car cleaning products, hobby chemicals

and do not add preservative. Gastric contents
can be extremely useful if collected shortly
after the poison was ingested.
. Others: hair, nails, saliva, sweat and meco-
nium. Submit and retain any materials found
with the patient or that may be implicated in
the poisoning (bottles, labels, capsules, plant
material, suicide note, etc.). Testing may
involve adding reagent to the sample, or
dissolving the material to be tested in an
appropriate solvent prior to the addition of
colour reagent.
A toxicology request form should be carefully
completed and accompany the specimens to the
laboratory. Essential information that can be
obtained through such a request form includes
clinical summary (condition of patient, signs,
symptoms), drugs/poisons suspected, current
treatment and all drugs administered prior to
sample collection.44
SIGNS AND SYMPTOMS AS PREDICTORS
A careful clinical evaluation using the history,
physical examination and the more readily
available laboratory tests may allow a tentative
diagnosis and initiation of treatment.45,46 Clin-
ical ®ndings of importance include altered blood
pressure, pulse, respiration and body tempera-
ture, the presence of coma, agitation, delirium or
psychosis, and muscular weakness. An ophthal-
mological examination is also important in the
acutely poisoned patient.47 Oral burns or
dysphagia may occur following ingestion of
any strongly reactive substance, but the absence
of oral burns does not exclude the possibility of
oesophageal injury.48 Odours and skin colour
may also contribute to the diagnosis.49
The presence of a particular clinical manifes-
tation may be enough to direct attention toward
a particular group or type of poison.3 Alter-
natively, it may help to rule out other
possibilities. For example, a coma could point
to organic solvents, naphthalene etc., rather
than strychnine or dieldrin,25 as long as the
vehicle in which it is formulated is not itself an
organic solvent (e.g. kerosene or toluene).
Poisons have characteristic effects.40,42,50,51
Consequently, clinical assessment, accompanied
by knowledge of which symptoms are associated
with which causative agent, can be used to direct
poison screening efforts.45 Toxins mediate re-
cognizable patterns of symptoms by stimulating
an agonistic or antagonistic response at one or
more receptors. There are two toxidromes
associated with cholinergic poisoning: one
caused by muscarinic agonists and the other by
nicotinic agonists. Potential toxins causing these
syndromes are outlined in Table 2, together with
toxins that have anticholinergic properties and
other symptoms.
SPOT TESTS
Routine drug screening requires many analytical
tools, such as colour tests, immunoassays, Toxi-
Lab (Ansys Diagnostics, Lake Forest CA,
USA), TLC, gas±liquid chromatography, high-
performance liquid chromatography and/or gas
chromatography±mass spectrometry.2,15,52±55 In
non-drug poisoning, however, information ob-
tained from very simple, rapid, invariably
colourimetric, and inexpensive screening tests is
often invaluable, especially when combined with
conventional biochemical screening and routine
haematological analysis.40,42,56
A variety of spot tests are summarized in
Table 3.57±89 They constitute a group of simple
chemical reactions requiring limited or no sample
preparation which, through their relative non-
speci®city, can be used to indicate potential
poisons quickly or rule out the presence of select
compounds. Prominent are those that would be
performed as part of a drug screening protocol
and can also be used for the screening of certain
poisons. Although tests such as atomic absorp-
tion spectroscopy are more de®nitive, a positive
result from a relatively non-speci®c test may
direct the analyst to more speci®c tests or suggest

Ann Clin Biochem 2000: 37

 Poisoning by substances other than drugs 149

TABLE 2. Physiological responses to various poisons

Signs/symptoms Likely poison(s)

General
Diarrhoea, urination, miosis, bradycardia, Organophosphates, betel nut, pilocarpine, carbachol,
bronchorrhoea, emesis, lacrimation, salivation acetylcholine, poisonous mushrooms
(DUMB-BELS)
Tachycardia, hypertension, weakness or paralysis, Insecticides, nicotine, spider venom
muscle fasciculations
Delusions, hallucinations, convulsions, coma Volatile substance abuse
Salivation, lacrimation, urinary incontinence, Carbamates
diarrhoea, gastrointestinal cramping, emesis
Breath odour
Bitter almonds Cyanide
Garlic Malathion, parathion, arsenic, phosphorus, tellurium
Alcohol Phenols, alcohols
Ethereal (sweet) Ether
Stale tobacco Nicotine
Acetone/penetrating Lacquer
Coal gas Carbon monoxide
Acrid Paraldehyde
Phenolic (disinfectants) Creosotes, phenols
Shoe polish Nitrobenzene
Pears Chloral
Colour of skin and mucous membranes
Hyperaemia Cyanide, alcohol
Jaundice/yellow skin Mushrooms, nitro compounds, phosphorus, picric acid,
carbon tetrachloride, atrabine
Cyanosis Aniline, nitrobenzene, nitrites, nitrates, parathion,
chlorates, marking ink
Cherry red or pink skin Carbon monoxide, cyanides
Pallor Benzene, lead, naphthalene, chlorates, solanine, ¯uoride,
plant poisons, carbon monoxide
Blue-grey skin Silver salts
Blue-black gum line Bismuth, lead, mercury
Skin rash Antimony, arsenic, turpentine, coal-tar derivatives
Etching of the skin Corrosives
Discolouration of mouth or pharynx, distension Any poison
and spasticity of the abdomen
Vomiting, neck stiffness Strychnine
Red (boiled lobster) skin/desquamation Boric acid
Respiration
Increased Dinitrophenol, cyanide, carbon monoxide
Wheezing Cholinesterase inhibitors
Eyes
Miosis Carbamate pesticides, organophosphates
Mydriasis Barium, benzene, thallium, camphor
Temperature
Increased Arsenicals, boric acid, camphor, dinitrophenols
Decreased Aconite (herbal preparations), ether, chloroform, nitrites
Sweating Organophosphate insecticides
Genitourinary system
Anuria Mercurials, bismuth, chloride, carbon tetrachloride,
turpentine

the need for further evaluation. In an environ- completed in minutes. The analytical time
ment in which ef®ciency is paramount, the use of required to carry out all the procedures listed is
established protocols and screening assays is approximately 3 h, but, by modifying the proce-
preferable. Most individual spot tests can be dure to incorporate only those poisons suspected

Ann Clin Biochem 2000: 37

150 Badcock
TABLE 3. Spot tests (many are adaptations/extensions of some commonly used spot tests for drugs)
Test
Acid hydrolysis, o-cresol/
ammonia53,57
Aminolaevulinic acid
(ALA)78±80
Basophilic stippling (zinc
protoporphyrin)42
Blood colour53,77
Cholinesterase inhibition test
(pseudocholinesterase ± acute;
true cholinesterase ± chronic)4
Clinitest (Ames{)
Conway/dichromate53,61,75
Coproporphyrin80
Digoxin immunoassay77
Diphenylamine57,61±63
Direct ultraviolet spectrophoto-
metry59,60 (standard scan
350±220 nm; standard zero
order, ®rst and second
derivatives)
Dithionite/alkali53
Ethyl alcohol assay (EMIT§)83
Exposure biomarkers [glucaric
acid, thioethers, urinary
bacterial assay for mutagenic
activity (as an equivalent to
thiocyanate in de®ning
smoking status)]84±87
Fluorescence42
Fujiwara (pyridine/NaOH)30,58
Gas chromatography64±66
Gastric contents (odour)1,53
Ann Clin Biochem 2000: 37
Sample Common analyte(s) Additional poisons detected
Urine, gastric Paracetamol Iodine, iodide, radio-opaque material
contents (purple fumes), sulphide (yellow
fumes), bromide (reddish-brown
fumes); aniline, nitrobenzene (blue),
ethylenediamine (green)
Urine, plasma Lead Gold, vinyl chloride, hexachloroben-
zene, polychlorinated biphenyls, poly-
brominated biphenyls, dioxin, lindane,
silver, 2,4,5-T (2,4,5-trichlorophenox-
yacetic acid), lead (ALA increased)
Blood Lead Mercury, bismuth (430 stippled red
cells per 10 000 cells)
Blood Carbon monoxide Cyanide (cherry-red), nitrates, nitrites,
chlorates, aniline, dyes (chocolate),
solanine, lead, chlorates, naphthalene,
plants, snake bite (anaemia)
Serum, red Organophosphate Carbamates
cells
Urine Acetone Isopropanol, hippuric acid (purple)
Blood, urine, Ethanol Methanol, chloroform, aldehydes (e.g.
gastric contents metaldehyde), ethylene glycol (green-
blue)
Urine, hair, Lead Heavy metals ± chronic exposure (co-
nails proporphyrin increased)
Urine Digoxin Aconitine alkaloids, colchicine, cardiac
glycosides (cross-reactivity)
Gastric Ethchlorvynol Hypochlorites, chlorates, dichromates,
contents phenazopyridine nitrites, bromates, peroxides, iodates,
vanadates, glyceryl trinitrate, perman-
ganates (blue)
Diluted gastric Compounds with high Disinfectants, pesticides (paraquat),
contents, absorbances herbicides (ametryne), rodenticides
ingested (warfarin)
material
Urine, gastric Paraquat, diquat Benzalkonium, cetylpyridinium chlor-
contents ides (blue-black)
Gastric Ethanol Methanol, isopropyl alcohol (increased
contents absorbance change)
Urine Various Various
Urine, gastric Fluorescein Ethylene glycol (from antifreeze
contents colourant), also calcium oxalates
(glycolic acid tests as con®rmation)
Urine, gastric Chloral hydrate Chloroform, carbon tetrachloride,
contents 2,4,5-T, toxaphene, dichloral phena-
zone, strobane, methyl bromide, chlor-
amphenicol, trichloroethylene (red-
purple colour in pyridine)
Blood, urine, Volatile compounds Pesticides
gastric contents
Gastric Volatile Lysol, camphor, creosotes, methyl sal-
contents icylate (characteristic odours)
(Continued)
 Poisoning by substances other than drugs 151

TABLE 3. (Continued)

Test Sample Common analyte(s) Additional poisons detected

53
Gastric contents (colour) Gastric Blue ferrous Dye from rat poison, tablet, capsules,
contents phosphate etc. (various)
Gastric contents (pH; normal Gastric Acid Alkali
pH 3±4)53 contents
LaBrosse spot test76 Urine Vanillylmandelic acid Styrene (violet)
Malondialdehyde81,82 Urine, blood Lipid peroxidation Heavy metals, carbon tetrachloride,
paraquat
Merckoquant test strips (Merck Gastric Arsenic, nitrate, nitrite Manganese, chloride lead, iron, chro-
KGaA*) contents mate, bromide, iodide, zinc, copper,
cyanide (colours indicated on analytical
kits)
Paracetamol/ammonia (positive Urine, gastric Naphthalene, para- Chlorothion, creosote, benzene, resor-
paracetamol control minus contents thion, phenols cinol, EPN, dicapthion, methylpar-
o-cresol) athion (blue)
Platinum wire ± ¯ame57,63,67 Gastric Barium salts Lithium (crimson-red), thallium, cop-
contents per (green), sodium (orange-yellow)
77,88,89
Radiology Abdominal Radio-opaque Chlorinated pesticides, hydrocarbons,
radiograph or material arsenic, enteric coated material, iron
ultrasound tablets, mercury, lead, lithium (radio-
opaque)
Reinsch57 Urine, gastric Arsenic Antimony, bismuth (black), mercury
contents (silver), sulphur, tellurium (dull black)
[NB: heavy metal poisonings have
resulted following exposure to herbal
medicines, especially tonics, aphrodi-
siacs and treatment for eczema]
Rothera's68,69 Urine, gastric Ketones g-Butyrolactone (blue)
contents
Silver nitrate (nitric acid, barium Gastric Anions Bromide, iodide (yellow), cyanide
3,4
chloride) contents (grey), chloride, hypochlorite, various
acids, thiocyanate (white)
Toxi-Lab A{ (standard protocol) Urine, gastric Basic drugs Thymol, phenol, cresol, naphthol, ma-
contents lathion, strychnine, nicotine, turpentine
(Rf and colours)
Toxi-Lab A{ (Badcock: xanthine, Urine, gastric Theophylline Alkaloids, xanthines, nitrogenous bases
pre-extraction modi®cation)70,71 contents (enhanced stain)
Toxi-Lab A{ (residue, alkaline Urine Thioethers Hydrocarbons, arylamines/halides/es-
hydrolysis, Ellman's reagent, ters, nitro/cycloalka(e)nes, sulphur,
412 nm)72,73 mustards (enhanced absorbance)
Toxi-Lab{ (alcohol) Plasma Ethanol Methanol, ethylene glycol (blue spot)
Toxi-Lab B{ (aliquot in separate Urine Hippuric acid Benzene, toluene, xylene, benzoate,
well, benzenesulphonyl chloride styrene (red-orange), nitrobenzoyl
in pyridine)74 chloride (yellow)
Toxi-Lab B{ (standard protocol: Urine, gastric Acidic drugs Warfarin (yellow spot)
acidi®ed KMnO4 solution contents
following HgCl2/diphenyl-
carbazone)
Trinder's35 Urine Salicylates Methyl salicylate, benzene, phenol,
ketones, oxalates, thiocyanates, azides
(violet), acetic acid (orange-red), tur-
pentine (violet-blue)
Turmeric paper1 Gastric Borates Iodates, nitrites, bleach, chlorates,
contents bromates (bleached turmeric paper)
42
Urine colour Urine Metabolic Lead, aloe (rose colour), turpentine,
phenols (blue) cascara, phenolphtha-
lein, senna, ¯uorescein (orange) nitro-
benzene (brown)
Urine odour42 Urine Metabolic disorder Turpentine (violets), chloroform
(sweet), disinfectants (phenolic)

*E Merck, Darmstadt, Germany. {Ansys Diagnostics Inc., Lake Forest CA, USA. {Bayer Diagnostics, Mulgrave,
Australia. §Enzyme Multiplied Immunoassay Technique, Behring Diagnostics, Cupertino CA, USA. EPN=phenyl-
phosphonothioic acid O-ethyl O-(4-nitrophenyl) ester.

Ann Clin Biochem 2000: 37

152 Badcock
clinically, this time can be reduced considerably.
On most occasions, the poison ingested will re¯ect
the clinical condition of the patient.
Biological specimens that are highly pigmen-
ted, visually contaminated (e.g. with food
particles) or proteinaceous may require isolation
procedures. Spot tests are then applied to the
extracted and concentrated residues.4 These tests
may involve direct colour formation of the
sample with added reagent or dissolving the
material to be tested in an appropriate solvent.
All reagents are stable for at least 3 months
when stored at room temperature and protected
from direct sunlight.
The most useful methods for initial screening
are those that combine two or more major
groups of poisons. As with all screening tests, a
positive result is presumptive and points towards
more speci®c assays. Intuition also plays a role
in a general screen.
Essential spot tests
Several toxins require rapid identi®cation.59,90,91
Those discussed here (Table 4) should be offered
on an emergency basis. Although symptoms
from ingestion of cyanide and iron may appear
very rapidly, they may also not manifest for
several hours. Further, following carbon mon-
oxide poisoning, the victim may appear normal
upon the regression of symptoms, but perma-
nent cerebral damage cannot be excluded. Delay
in the appearance of symptoms or the apparent
absence of after-effects can give rise to a false
sense of security. Treatment with the appro-
priate antidote is urgent, and can save lives.
HAIR AND NAILS
In theory, hair and nails would appear to be
ideal biological indicators since sampling is non-
invasive, the medium is inde®nitely stable on
storage, and a temporal pro®le of exposure
along the hair or nail length is possible.92±95
Further, trace element concentrations in hair
are approximately 10-fold greater than in blood
or urine.96
TABLE 4. Spot tests that are essential if there is any suspicion that the listed poisons have been ingested
Test
Lee±Jones test (NaOH/FeSO4/HCl)
K3FeCN6 (potassium ferricyanide)
K4FeCN6 (potassium ferrocyanide)
NH4OH
Ann Clin Biochem 2000: 37
In practice, however, there are severe limita-
tions on the use of hair and nails as systemic or
internal indicators of exposure. It is virtually
impossible to avoid external contamination by
ubiquitous heavy metals (e.g. lead), and there
are no accurate validation techniques for
assessing hair cleaning, although this in itself
may prove a valid external exposure indicator if
not an internal indicator. Hair analysis is useless
for thallium because thallium is not incorpo-
rated into hair.93
In addition to methodological hazards, the
biokinetics of heavy metals in hair and nails are
not understood suf®ciently well to allow their
reliable use as biological indicators.
ANTIDOTES
Antidotes, administered after presumptive iden-
ti®cation of the poison, can also be diagnos-
tic.40,42,97±102 For example, the cholinesterase
inhibitor physostigmine, when used as an
antidote, can reverse toxic anti-muscarinic
effects. Table 5 lists some antidotes and
protective agents used to treat acute poisoning.
NATURAL TOXINS
Most naturally occurring toxins are very com-
plex and cannot be easily identi®ed by normal
laboratory methods. Therefore, the identi®ca-
tion of natural toxins and the diagnosis of
toxicity may be dif®cult. However, the labora-
tory has a very important role in the manage-
ment of these patients.41,42,103
Plants containing cardiac glycosides
Patients poisoned by plants containing cardiac
glycosides (e.g. foxglove) will have elevated
glycoside levels (digoxin, digitoxin); plants
containing warfarin will cause an elevation in
the prothrombin time.
Plants containing hepatotoxins
Elevations in liver enzymes may be the ®rst
manifestation of toxicity caused by plants and
mushrooms that contain hepatotoxins.
Sample Poison
Gastric contents Cyanide
Gastric contents Fe2+
Gastric contents Fe3+
Blood Carbon monoxide
 Poisoning by substances other than drugs 153

TABLE 5. Antidotes and their application

Antidote Use

Activated charcoal Many types of overdose

Atropine Organophosphate poisoning
2,3-Dimercaptosuccinic acid Oral chelating agent for lead, mercury, arsenic poisoning
(DMSA)
Desferrioxamine Given intravenously or intramuscularly for chelating iron
Dimercaprol (British anti- Chelates mercury, arsenic, lead
Lewisite, BAL)
Calcium disodium edetate Primarily used to chelate lead
Amyl nitrite Cyanide
Ethanol Competes for alcohol dehydrogenase, thereby preventing the production of the
toxic metabolites of methanol and ethylene glycol
Folic acid, leucovorin In conjunction with ethanol in the treatment of methanol (folinic acid) poisoning
Haemodialysis Lithium
Hyperbaric oxygen Carbon monoxide, hydrogen sulphide and carbon tetrachloride toxicity
Methylene blue Methaemoglobinaemia
4-Methylpyrazole (investiga- Methanol and ethylene glycol poisoning
tional)
Physostigmine To reverse effects from poisoning with an anticholinergic agent
Pralidoxime Organophosphate poisoning
Pyridoxine Poisoning with isoniazid, monomethyl hydrazine (Gyromitra esculenta mushroom)
and, in combination with ethanol, in the treatment of ethylene glycol poisoning
Thiamine hydrochloride In conjunction with ethanol in the treatment of ethylene glycol poisoning

Snakes attempting suicide by self-poisoning is greatest

The snake-bite victim usually dies from a diffuse
coagulopathy or renal failure secondary to
myoglobinuria.104 There have been some recent
advances in the diagnosis of snake bite in
Australia using an enzyme-linked immunosor-
bent assay105,106 to determine the species of snake
responsible for the bite. This test has been used
in the ®eld and has been fairly reliable. There are
no tests currently available for determining pit
viper envenomation. Laboratory assessment of
coagulation is helpful.
OTHER PREDICTORS
As well as spot tests, clinical information and
biomarkers, there are other predictors of
poisonings. These include demographic vari-
ables (gender, age, race, educational level),
calendar season, location (metropolitan or
non-metropolitan), exposure to chemicals at
work, by students in science or technology
classes and so on.107±111 For example, children
aged less than 3 years and boys were most often
the victims of accidental poisoning,112 and the
incidence of poisonings was 80% higher during
the working hours of the day than during the
late afternoon, evening hours or the weekends,
the times when both parents are usually at
home.113 With adults, however, the risk of
in the early evening (20:00±21:00 h), whereas the
risk of successful suicide by self-poisoning is
greatest during the late morning (10:00±
13:00 h).114±116
LABORATORY BIOCHEMISTRY
Many routine biochemical tests can provide
markers for the presence of poisons and can be
helpful in the diagnosis of both acute and
chronic poisoning and in assessing prognosis.
Laboratory tests should include serum osmol-
ality, electrolytes, glucose and urea and estima-
tion of the anion and osmolar gaps.45,117,118 The
electrocardiogram can also provide useful in-
formation.119
As examples, hypokalaemia occurs in barium
poisoning, hyponatraemia can result from many
causes, including water intoxication, hypocal-
caemia can occur in ethylene glycol poisoning
and hyperkalaemia or hypernatraemia occurs in
iatrogenic, accidental or deliberate overdose
with potassium or sodium salts. Metabolic
acidosis with a raised anion gap may result
from severe poisoning with boric acid, carbon
monoxide, cyanide, iron, ethylene glycol, metha-
nol, ¯uoroacetates and paraldehyde.41,42 Table 6
summarizes abnormal laboratory biochemistry
in non-drug poisonings.

Ann Clin Biochem 2000: 37

154 Badcock

TABLE 6. Biochemical abnormalities associated with toxins

Abnormality Potential toxins

Hypocalcaemia Oxalates, potassium phosphate, ethylene glycol, ¯uorine, organic tin compounds
Hypercalcaemia Vitamin D
Hyponatraemia Dilution (e.g. water intoxication)
Hypernatraemia Dehydration, sodium, potassium salts
Hypokalaemia Barium salts
Hyperkalaemia Foxglove, scilliroside
Hypoglycaemia Alcohols, lithium, calcium salts, pyridoxine, akee, plant toxins
Hyperglycaemia Nicotine
Increased osmolar gap Methanol, ethanol, glycerol, isopropanol, ethylene glycol
Metabolic acidosis with Iron, lithium, carbon monoxide, cyanide, benzyl alcohol, toluene, methanol,
raised anion gap paraldehyde, ethylene glycol, strychnine
Respiratory acidosis Carbon monoxide, cyanide

When combined with other biochemistry,
these laboratory tests are likely to be even more
useful in clinical toxicology. For example,
calcium oxalate or hippurate crystals in the
urine of a patient with a high anion gap,
metabolic acidosis and increased serum osmolar
gap will provide a rapid result of great value as
an indicator of ethylene glycol poisoning;
similarly, increased osmolar gap and anion
gap, metabolic acidosis and ocular ®ndings
strongly suggest methanol poisoning.120 Blood
glucose is increased after lead or alcohol
poisoning and serum uric acid is also increased
after alcohol ingestion.
CONCLUSION
Several simple chemical reactions can be used to
indicate or rule out the presence of potential
poisons. When they form part of, or can be
readily adapted from, a routine drug screening
protocol, the range of the screen is broadened.
These colour or spot tests are direct tests that
involve limited or no sample preparation. They
can provide at least an initial indication of
poisons present or absent, and an uncon®rmed
identi®cation of the poison or family of poisons,
often within minutes of receiving specimens. A
positive result initiates more speci®c con®rma-
tory tests or suggests the need for further
evaluation.
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Accepted for publication 25 August 1999
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