Alcohol/Poisoning

Dr Busisiwe Mashiya
Department of Forensic Medicine
SMU
Introduction
Introduction
• Forensic toxicology is a study and practce of the applicaton of toxicology for the purposes of law.
• It involves; identfiatin and quantfiatin of a drug, poison or substance in human tssue and
interpretatin of the fndings and the results.
• The results of toxicological analysis are correlated with the medical history of the deceased, the
autopsy fndings and the circumstances surrounding the death to determine whether the
substance/drug:
• Caused the death
• Was a iintributiry faitir
• Played ni rile in the death
Defnition

• Poison:
• Any substance /material which when absorbed in sufcient amounts causes ill
health or death.
• “All drugs are poison, there is not one which is not a poison. The right dose
diferentates a poison from remedy.”
• In law: diference between a medicinal drug or poison is the intenton with which
is given.
Classifcation:

• Aiiirding ti ihief symptims (mide if aitin)

• Corrosives (acids and alkalis)
• Irritants (metallic, non‐metallic, vegetable, animal, and mechanical)
• Neurotcs(cerebral, spinal)
• Cardiac poisons ( digitalis, ergot)
• Irrespirable gases or vapors ( carbon monoxide, carbon dioxide)
• Abortfacients: Potassium permanganate tablets
• Miscellaneous ( insectcides, weed killer, aspirin, paracetamol, solvent abuse, food
poisoning)
Classifcation:

• Aiiirding ti their appearanie ir use

• Agricultural
• Insectcides: Organophosphates
• Pestcides: Riat poison, parathion
• Industrial
• Acids, alkalis, heavy metals
• Domestc poisons
• Drugs, Herbal enemas
• Fungi
• Mushrooms
• Flora (plants)
• Oleander
Classifcation:

• Aiiirding ti their funitinal use:

• Accidental – e.g. cocaine, heroin
• Suicidal – e.g. tricyclic antdepressants
• Homicidal – e.g. arsenic
• Iatrogenic – e.g. insulin
Degree of toxicity:

• Depends on:
• Lethal dose:
• Indicaton of lethality of a given substance. Variaton occurs with what consttutes a
fatal level of toxin. Depends on age, race, weight, medical or surgical conditons,
route of administraton.
• LD50: An experimental reference value where at that value 50% of the experimental
populaton will die.
• expressed in the units of micrograms (or milligrams) of the substance per
kilogram of the test‐subject’s body weight in kg i.e. µg or mg/kg body weight.
• The liwer the LD50 amiunt is, the mire tixii the substanie.
Factors that afect action of poison:

• Dose
• Rioute of administraton and absorpton
• Accumulaton or storage
• Distributon, metabolism and eliminaton
• Host vs substrate factors: idiosyncrasy, age, habit, health
• Poison factors: concentraton of poison, chemical form and physical state of poison
Drugs and toxicology screens:

• Involve analytcal techniques used to identfy specifc drugs or their metabolites in a

biological matrix.
• Types:
• General – for wide range of substances.
• Seleitve – for certain groups of substances.
• Qualitatve – reportng the presence in specimen.
• Quanttatve – reportng concentraton of drug or metabolite in tssue.
• To be reported as being present in forensic cases, the drug must be absolutely
identfed and, if signifcant quantfed.
Challenges in management of
poisoning cases:

• Problem of diagnosing poisoning.

• Problem of poison identfcaton.
• Problem of result interpretaton.

• WHY?
• Diference in laboratory analytcal methods
• Quality of specimens
• Quality control at the laboratory
• If drug identfed is a prescribed drug: is it a therapeutc dose or tail end of toxic dose?
Challenges in management of
poisoning cases:

• IF NO POISONS / DRUGS WERE DETECTED IN LABORATORY ANALYSES, THIS MAY BE

DUE TO:
• Eliminaton of poison / drug by vomitng or diarrhea
• Disappearance of poison / drug from lungs by evaporaton or oxidaton
• Detoxifcaton or conjugaton or eliminaton of poison /drug afer absorpton
• Body/specimens/tssues were decomposed
• Faulty preservatves were used
• Wrong or insufcient material was sent for analysis
Examples of the drugs/toxins
encountered:

• Agricultural: Organophosphate, carbamates

• Illicit drugs : heroin, cocaine, amphetamines
• Corrosive and metallic poisoning
• Medicinal poisoning
• Organic solvents
• ALCOHOL
Organophosphates:

• Used in domestc and industrial setngs.

• Sources: aseptcide over fruit and vegetables, dewormers in animals, fy sprays, fea collars, ant‐lice
shampoo.
• Chemical names: Parathion, malathion, or chlorpyrifos.
• Manner: suicidal or accidental.
• Mechanism of acton:
• Inactvates the enzyme acetyl cholinesterase (AChE) at nerve endings leading to increase in
acetylcholine (Ach).
• ACH is found in the central and peripheral nervous system and neuromuscular junctons.
• AChE degrades Ach into choline and acetc acid.
• Increase of Ach leads to stmulaton of nicotnic and muscarinic receptors.
Organophosph
ates:
Organophosphates:

• Modes of administraton:
• Inhalaton of airborne partcles
• Ingeston through contaminated containers, not washing hands afer working with OP or poorly washed
vegetables or fruits.
• Toxicity depends on dose, duraton of exposure and mode of transmission. Inhalaton >ingeston.
• Presentaton:
• Early symptoms non‐specifc.
• Can muscarinic, nicotnic or CNS efects.
• SLUDGEM
• DUMBELS
• Nicotnic efects: muscle fasciculatons, cramping and weakness.
• Autonomic nicotnic efects: hypertension, tachycardia, mydriasis.
Organophosph
ates:
Carbamate
poisoning:
• Aldicarb (temik) is a common poison used.
• Is an insectcide and is controlled by Act 36 of
1947.
• Highly toxic.
• Rioute of administraton: inhalaton, dermal
absorpton and ingeston.
• Mechanism of acton:
• Irreversible inhibiton of acetylcholine
esterase (AChE), similar to organophosphate.
• At autopsy: small black granular substance in
the stomach.
Illicit drug poisoning: Heroin

• Heroin is produced in clandestne laboratories either from the synthetc acetylaton of morphine,
or from crude extracts of the exudates from the opium poppy (Papaver somniferum).
• Pharmacokinetcs :
• Heroin is almost totally hydrolysed to morphine before it reaches the systemic circulaton.
• Diacetylmorphine> monoacetylmorphine >6‐acetylmorphine>morphine
• Plasma concentratons of morphine correlate poorly with dose.
• Pharmacokinetc studies of intravenous heroin, show peak heroin plasma concentratons are
obtained within 2min of dosing and are not detected afer 30min.
• Smoking of heroin is not as efcient as intravenous use. When inhaled the drug is likely to
reach the brain in 20s.
Illicit drug
poisoning: Heroin
Illicit drug poisoning: Heroin

• Mechanisms of acton:
• Riespiratory depression: decrease in sensitvity of the respiratory centres to
carbon dioxide.
• Cardiovascular collapse: inhibits baroreceptor refexes, which can lead to sudden
orthostatc hypotension.
• Bronchoconstricton: leading to asthma‐like symptoms.
Illicit drug poisoning: Heroin

• Deaths associated with heroin use:

• The high mortality is in part due to viral infectons (HIV, Hep C), early onset of natural
disease and violence; however the leading cause of death is toxicity.
• Heroin deaths are largely classifed by their circumstances, i.e. knowledge of the
deceased being a user etc.
• Anatomical signs include: Pulmonary oedema and congeston of the lungs, needle
puncture marks with subcutaneous and perivenular haemorrhage and the presence of
antbodies to hepatts c and others.
Illicit drug poisoning: Cocaine

• Cocaine has been used by the Peruvian Indians for centuries for well‐being and
increased endurance, afer sucking the leaves of the plant ethroxylon coca.
• Cocaine belongs to the tropane alkaloid family, which includes hyoscine, scopolamine
and atropine.
• Pharmacokinetcs:
• Cocaine is metabolised to benzoylecgonine (BE), ecgonine methyl ester (EME) and
other metabolites.
• Peak concentratons of cocaine, following doses of 25‐40mg following oral or IV use
administratons range up to 0.35mg/L, and rise proportonally with the dose
• The duraton of acton usually parallels their blood plasma concentratons
Illicit drug
poisoning:
Cocaine
Illicit drug poisoning: Cocaine

• Mechanism of acton:
• Cocaine prolongs the actons of the nerves by preventng the re‐uptake if niradrenaline, dipamine and
seritinin, following release afer a nerve impulse; the net efect is to produce a similar response to
amphetamines.
• Anatomically the regions afected in the brain include: the caudate nucleus, nucleus accumbens, the
medial prefrontal cortex, the dorsal raphe and the locus coeruleus.
• Cocaine also aits as an anaestheti agent by blocking the current of sodium ions through the nerves. In
high doses this anaesthetc efect may iause iardiai arrhythmias and lead to sudden death.
• The sudden ‘high’ experienced with IV usage is caused by the sudden release of noradrenaline from the
nerve endings.
Illicit drug poisoning: Cocaine

• Pharmacological efects:
• CVS: Cocaine is a powerful vasiiinstriitir and ihrinitripe. Blood pressure and heart rate are
elevated. The acton of cocaine on the alpha adrenergic receptors of the heart causes
vasoconstricton of the coronary arteries, thereby decreasing blood supply but increasing demand.
• CNS: Cocaine produces euphiria, ariusal, an elevatin in miid and increased vigour. Anxiety and
restlessness are necessary side efects of these actons. Larger doses may even produce tremor,
tonic‐clonic seizures and dysphoria. Tactle hallucinatons are common. Users ofen experience an
increase in body temperature.
• Skeletal musile: The tone is increased. A more serious side efect includes rhabdomyolysis.
• Other: Commonly cocaine causes rhinits. Chronic use is associated with perforaton of the nasal
septum
Illicit drug poisoning: Cocaine

• Pathology associated with cocaine related deaths:

• Cocaine produces hyperaemia, tssue ischaemia, haemorrhage and sudden cardiac
collapse. These may culminate as myiiardial infaritin, ierebral haemirrhage, ir a
disseitng airti aneurysm.
• Cardiac damage is relatvely common in users including MI, myocardits,
cardiomyopathies and valvular heart disease.
• Rienal pathology includes: a degree of peri‐glomelular fbrosis, intersttal cellular
infltraton, arteriolar sclerosis and vascular changes.
• Riespiratory fndings in crack users include: chronic intersttal pneumonia with the
accumulaton of free silica within histocytes with associated mild pulmonary fbrosis.
Illicit drug poisoning: Amphetamines

• Amphetamines were frst synthesized in 1887. By the late 1920’s it was used medicinally as a replacement for
ephedrine as a nasal decongestant. By the Second World War its abuse potental was well known.
• The amphetamines are related in structure to the legal stmulants.
• Pharmaiikinetis:
• Three main routes of amphetamine metabolism: para‐hydroxylaton, beta‐hydroxylaton, deaminaton.
• These stmulants have good oral bioavailability and give maximum blood concentratons within 1 – 2
hours
• The main metabolite of methamphetamines is amphetamine.
• Detecton tmes in urine depend on the dose used and the pH of the urine. Detecton tmes range up to 1
– 2 days following usual doses.
Illicit drug poisoning: Amphetamines

• Mechanism of acton:
• Amphetamines interact with the nerves utlizing noradrenaline, dopamine and serotonin.
• They facilitate the release of neurotransmiters at the nerve terminals or replace the neurotransmiter
itself and produce an adrenaline‐like efect.
• Pharmacological efects:
• The main efects sought by drug users includes: euphoria, elevaton in mood, increased energy, vigour
and physical strength.
• Other efects: hypertension, tachycardia, muscle tremor, stereotyped behaviour, aggression, reducton
in appette, dilated bronchioles, reduced nasal congeston and increased body temperature.
• The main adverse reactons include cardiovascular complicatons, hyperaemia, rhabdomyolysis,
hallucinatons and paranoid psychotc states.
Illicit drug poisoning: Amphetamines

• Pathology associated with stmulant related deaths:

• Life threatening reactons are well documented.
• Initally these can be agitaton, fever, aggression and violence; these can rapidly
lead to very high body temperatures, tachycardia and hypertension.
• The consequences of these are rhabdimyilysis, disseminated intravasiular
iiagulatin, iinvulsiins, dehydratin, haemirrhages in the heart and bliid
vessels and renal failure.
• Post mortem fndings may include: myocardial lesions of varying age, consistent with
various phases of myofbrillary degeneraton, such as contracton bands, granulaton
tssue and scarring.
Corrosive and metallic poisoning

• Majority are used at home.

• Examples: cyanide, ethylene glycol, arsenic. Can cause immediate death if inhaled or
ingested.
• Ethylene glyiil: known as ant‐freeze found in brake fuid. Colourless, odourless, non volatle
and with sweet taste. Major problem is severe metabolic acidosis.
• Cyanide:Hydrogen cyanide and its salts are amongst the most potent, rapidly actng poisons.
It combines with the ferric iron atom of intracellular cytochrome oxidases and inhibits the
acton of these partcipants in intracellular oxidatve metabolic processes – the result is
HISTOTOXIC ANOXIA
• Arsenii: Arsenite inhibits not only the formaton of acetyl‐CoA but also the enzyme succinic
dehydrogenase. Arsenate can replace phosphate in many reactons.
Medicinal drugs poisoning

• Common medicinal drugs used for poisoning (overdose) are:

• Analgesics (asprin and paracetamol)
• Ant‐depressants
• Benzodiazepines
• Phenothiazines
• barbituates
Parafn poisoning:

• Parafn is a hydrocarbon.
• Common poisoning seen in children, accidental as it has same appearance as water.
• Pathogenesis: causes direct toxic efect on lung parenchyma causing damage to type II
pneumocytes with alteraton in surfactant producton and functon. Then leads to
hypoxia.
• Complicatons: aspiraton, chemical pneumonits, respiratory failure and secondary
bacterial pneumonia.
• If taken in large amounts causes respiratory and CNS depression.
Alcohol

• Ethanol as an alcoholic beverage has been recognized by human from c. 4200 BC,
when early scenes on potery from Mesopotamia depicted the fermentaton process.
• The word ‘Alcohol’ is derived from the Arabic word ‘Aelkohol’ meaning happiness.
• Alcohols are a group of compounds containing a hydrixyl griup, R‐OH, where Ri can
be any alkyl or substtuted alkyl group.
• The alcohols of primary importance in forensic medicine are Ethanil (CH3CH2OH) and
Methanil (CH3OH).
• Ethanol is mainly produced by fermentatin of starch, sugar and carbohydrates in
fruits and grains and other food products, partcularly rye, barley, malt and grapes.
Ethanol : Properties

• Ethanol is a iiliurless, odorless, clear liquid

• Ethanol is a vilatle, mibile, hygrisiipii and fammable fuid.
• Ethanol is characterised by the presence of a hydrixyl griup (OH) on the molecule.
• Importantly it is easily miscible with water i.e. it is WATER SOLUBLE
• It is NOT LIPID SOLUBLE, therefore obese people cannot drink more!
• Alcohol has a signifcant depressant efeit, actng on neuronal cells producing a similar efect to hypoxia.
• It has a boiling point of 78.37 OC
• It has a density of 0,789g/im3 or 0,789g/ml (at 20 OC) [1ml = 1 cm³ cubic centmetre (cc)]
• It has a molar mass of 46.07 g mil−1
Pharmacokinetics:
absorption,distribution,metabolism and elimination.

• Alcohol absorpton, distributon and eliminaton are simultaneous processes that

commence upon consumpton.

• Absirptin is the passage of alcohol into the blood.

• Distributin is the temporary placement of alcohol into various body tssues.
• Eliminatin is the removal of alcohol from the body.
 Absorption

• Ethanol is water soluble and easily absorbed from the gastro‐intestnal tract.
• Ethanol is not afected by the gastric juices and is absorbed unchanged.
• Absorpton occurs by passive difusion of alcohol through cell membranes and is governed by concentraton
diferences on either side of the cell wall. (Fick’s Law).
• Considerable variaton occurs in the rate of absorpton between individuals.

• 80% of the absorpton occurs in the small intestne (due to larger surface area & rich blood supply) and only
20% of alcohol is absorbed from the stomach.

• Peak blood concentratons of alcohol occur at about 30 min afer ingeston, although the tme to peak
concentraton (Tmax) may not occur untl 2hours, partcularly if large doses are consumed or gastric emptying
is delayed.

• Gastric emptying is important, as it governs the rate of access of the alcohol to the main absorpton surfaces,
especially the small intestnes (intestnal mucosa).
Factors that infuence absorption:

• Alcohol absorpton rate is INCREASED in:

• Accelerated gastric emptying facilitates movement of the alcohol into the small
intestne: (empty stomach, gastrectomy, habituaton)
• Alcohol absorpton is also facilitated by increased acidity such as when alcohol is
consumed with carbonated drinks
• Large volumes of the beverage:
• Medical conditons (peptc ulcer, gastrits)
• Drugs that increase gastric emptying: (ant‐emetcs, erythromycin)
• Alcohol concentraton ‐ optmal absorpton occurs from drinks with an alcohol
concentraton of between 10% and 20%.
 Factors that infuence absorption:
• Alcohol absorpton rate is DECREASED in:
• High alcohol concentraton drinks:
• Diluted drinks (less than 10%)
• Drugs that delay gastric emptying:
• Tricyclic Antdepressants (TCAD’s)
• Atropine
• Chlorpromazine
• Morphine/ Codeine
• Ant‐diarrhoea compounds
• Nicotne
• Cafeine
• Shock – decreases gastric emptying
• The presence of food, especially faty foods in the stomach:  Dilutes the alcohol  Prevents contact between alcohol and mucus
membrane
The distribution and equilibrium of
ethanol

• Once in the blood, alcohol is carried throughout the body. The alcohol difuses into tssues and fuids according
to their water content.
• Initally, the arterial blood alcohol concentraton will be higher than the concentraton in the tssues
• During the absirptin phase, the BAC if arterial bliid is greater than the tssue iinientratin of alcohol and
the BAC if venius bliid.
• At equilibrium, where the tssue has absorbed a proportonate quantty of alcohol, the BAC if arterial bliid is
equal to the BAC if venius bliid.
• Distributon of alcohol in the tssues is not equal between all tssues, as alcohol is not lipid soluble:
• The amount of alcohol in a specifc type of tssue is therefore dependant on the water content of the tssue.
• Equilibrium between the BAC and the tssue alcohol concentratons is achieved within about ine ti twi hiurs.
 The distribution and equilibrium of
ethanol
• Distributin Faitir:
• This is the factor which expresses the rato between the alcohol concentraton of a fuid or organs and the alcohol
concentraton of the body as a whole.
• It is also known as Widmark faitir or ‘r’ faitir.
• In fat persons the ‘r’ factor is relatvely low because of a relatvely low water content of the body.
• Therefore the BAC in these persons will be higher as less alcohol is absorbed from the blood by the tssues
• Muscular persons have a relatvely higher ‘r’ factor.
• The ‘r’ factor difers between men and women
• Men: 0.7
• Wimen: 0.6
• Women tend to become intoxicated faster than men do with ingeston of the same amount of alcohol:
• Decreased producton of the enzymes that metabolise alcohol
• Smaller water compartment than men due to smaller muscle mass
• Increased fat compartment
The elimination (metabolism &
excretion) of ethanol:

• Alcohol is eliminated from the body by excreton and metabolism.

• The predominant process is via metabilism in the liver.
• Other processes include expiraton in breath, urine excreton and sweatng.
• Eliminaton assumes a zeri‐irder priiess, with a constant rate of loss of ethanol.
Metabolism of alcohol (in the liver):

• Most alcohol is metabolized in a manner similar to other foods, yielding iarbin diixide
and water.
• Of the alcohol absorbed, 90% is broken down (metabolized) by the liver.
• Metabolism is mediated through the enzymes, aliihil dehydrigenase (ADH) and
aldehyde dehydrigenase in the liver.
• Hepatc alcohol dehydrogenase (ADH) converts alcohol to acetaldehyde, which in turn is
metabolised to acetate, by the enzyme aldehyde dehydrogenase, with oxidaton of the
products resultng in the producton of water and carbon dioxide.
• Both enzymes utlize the co‐factor niiitnamide adenine dinuileitde (NAD).
• This co‐factor must be present in sufcient quanttes and is a rate limitng factor.
Metabolism of alcohol (in the
liver):
Metabolism of alcohol (in the liver):

• Other enzymes capable of oxidising alcohol include: iatalase / miirisimal enzyme

ixidizing system (MEOS).
• A small amount of alcohol is metabolized by the microsomal enzyme oxidizing system.
• This amount is increased in alcoholics with increased enzyme actvity (inducton of the
MEOS) due to chronic, regular intake of alcohol.
• In a normal healthy individual, the rate of clearance (metabolism) of alcohol from the
body by the liver is 0,015g/100ml per hiur.
• This is increased in chronic drinkers to 0,02g/100ml per hour ( adaptaton involving
the increased utlizaton of alternatve pathways of metabolism)
Excretion of alcohol (though urine,
breath & skin):

• A small porton of alcohol is excreted unchanged, i.e. leaving the body as unchanged
alcohol through the urine and breath. It is this later process that allows for breath
alcohol testng.
• Alcohol is therefore also eliminated in urine and breath and, in negligible amounts, in
sweat and faeces:
• Approximately 5% of absorbed alcohol is exireted unihanged in the breath, with
a further 5% exiretin in urine.
• The average rate of metabolism (& eliminaton) of alcohol is 0,015g/100ml ti
0,02g/100ml per hiur
• Alcoholics show an enhanced eliminaton rate compared with social drinkers.
The blood alcohol
curve:
The blood alcohol curve:

• The rising limb of the blood alcohol concentraton (BAC) curve:

• represents the increasing blood concentratons caused by a greater fow of alcohol into the blood than the eliminaton of alcohol from
the blood
• The slope of the rising limb depends on the amount of alcohol ingested and the speed of ingeston
• The amount of alcohol ingested also determines the peak of the alcohol curve.
• The peak:
• At this point the rate of absorpton and eliminaton are equal
• Riange: 15 ‐ 90 mins
• Multple peaks can occur during the declining phase when further rises occur as in persons drinking small quanttes with long intervals
• The deilining limb:
• Eliminaton exceeds absorpton
• Mellanby efeit:
• A person is more sensitve to the efects of alcohol at same concentratons in the rising limb than the declining limb
The blood
alcohol
curve:
Blood alcohol calculations:

• Widmark’s firmula :
• In the twentes, Erik MP Widmark, a Swedish scientst, developed a formula (which is stll used today). The quantty of alcohol in the
body at the tme when blood sample is taken ( not tme of incident) can be calculated.
• A = p x i x r x 10
• A = total mass of alcohol in the body expressed grams
• p = mass of the person in kilograms.
• c = concentraton of alcohol in the blood expressed in g/100ml (g%)
• 10 = conversion factor
• r = distributon factor = alcohol concentraton in the body alcohol concentraton in the blood
• The ‘r’ factor is a constant for each species. It varies in each species according to the water content of the body tssues.
• Generally, the following values are accepted.
• Women 0.5 – 0.6 (0.55)
• Average men 0.6
Blood alcohol calculations:

• Using the formula, the concentraton of alcohol found in the blood can be translated
into amount of alcohol in the body at the tme of sampling.
• Example:
• 70kg man with blood alcohol concentraton of 0.10g per 100ml of blood. Using
the formula, the total alcohol in body:
• A = p x i x r x 10
• 70x0.1x0.7x10= 49 grams of alcohol
Blood alcohol calculations:

• Calculaton of quantty of alcohol before the alleged ofence: The Windmark’s formula
consumed.
• For example: the man claims to have taken Windhoek lager (4 grams in every 100ml
of 340ml can):
• Each can: 100ml contain 4g
• 340ml= 4gx340ml/100ml=13.6g
Blood alcohol calculations:

• Back calculaton: if we want to know the concentraton of alcohol at the tme of the incident.
• Windmark based his formula for back calculaton on constant decrease in concentraton of alcohol in
blood during the declining limb of blood alcohol curve. The constant fgure is called β , which is a fall
in alcohol concentraton in g/1000ml per minute.
• “β “ is constant per hour, between 0.01 and 0.02g%
• Cv = Ct + (B60 x t) where
• Cv = alcohol concentraton at the tme of the incident/ofence
• Ct = alcohol concentraton in the specimen in g%
• B60= decreases in the alcohol concentraton between 0,01 and 0,02g% hour, average 0,015g%.
• t = the tme‐interval in hours from the tme of the incident/ofence to the taking of the specimen
Blood alcohol calculations:

•• Example:
• A man with a body mass of 70 kg is involved in MVA at 20h00 and is arrested for drunk
driving. A sample of blood is taken at 24h00 the same day, and found to be 0.2g%.
What was the blood alcohol level at tme of accident? (assuming that person had
absorbed all alcohol)
• C(v)= 0.2
Correlation of clinical degree of
intoxication with blood alcohol

• Blood alcohol levels rarely correlate directly with clinical fndings in practce:
• Experience, skill and knowledge of doctor
• Suspect’s ability to adapt
• Tolerance or resistance
• Mellanby efect
• Dose‐response efect
• Presence of other drugs such as hypnotcs, medicines and diseases.
References:

• Saukko P, Knight B. Knight’s Forensic Pathology, 3rd edn. London: Arnold, 2004
• Simpson's Forensic Medicine by Jason Payne‐James, Riichard Jones, Steven Karch, John Manlove, 13th Internatonal
Student Editon, Hodder Arnold: August 26, 2011
• Previous Forensic Pathology notes