Dr.

Hisham Zein Elabdin

ALCOHOLS
Ethyl alcohol (Ethanol)
Ethyl alcohol is a colourless liquid, having a characteristic odour.
Circumstances of poisoning:
1-Ingestion of alcoholic beverages:
The presentation of a person who has drunk excessive amounts of
alcohol may be in form of acute alcohol intoxication.
If a person is used to drink alcohol for long duration with increasing
amounts, he may become addict i.e. chronic alcoholic. When he tries to
stop drinking , he will suffer from the withdrawal symptoms.
Other forms of presentations may occur when alcohol is contaminated
with other poisonous substances as methyl alcohol or metals.
2-Industrial exposure.
3-Accidental by children.
Absorption of alcohol:
Ethanol is rapidly absorbed from the gastrointestinal tract with
approximately 20%absorbed from the stomach and remainder from the
small intestine.
The absorption rate is affected by several factors including :
1- The degree of dilution, volume and type of alcoholic drink.
2- The presence of food in the stomach delays absorption.
3- Gastric motility.
4- Sex: as there is alcohol dehydrogenase enzyme in the wall of the
stomach which is more active in male than female.
Peak absorption is 30 to 90 minutes following intake.
METABOLISM OF ALCOHOL:
Alcohol dehydrogenase (ADH), the principal enzyme responsible for
ethanol oxidation, is an intracellular enzyme that is also present in the
stomach and the liver.
ADH expressed in human gastric mucosa oxidizes a small proportion of
the ingested ethanol , thus reducing the amount available for
absorption. This effect is more pronounced in men than in women and in
nonalcoholic's than in alcoholics.
About 90% of the circulating ethanol is metabolized in the liver. Ethanol
is oxidized to acetaldehyde by the action of alcohol dehydrogenase
 Dr. Hisham Zein Elabdin

(ADH). During this process NAD (Nicotinamide adenine dinucleotide) is

reduced to NADH. Acetaldehyde is oxidized again to form acetic acid by
the action of aldehyde dehydrogenase (AD). Here also NAD is reduced to
NADH.
ADH AD
Ethanol Acetaldehyde acetic acid
+ +
NAD NADH+H NAD ANDH+H
Acetic acid in presence of CoA, changes to acetyl CoA. Which enters
tricarboxylic acid cycle. Leading to oxidation in peripheral tissues.
Pathophysiology:
The effects of the alcohol may be due to ethanol itself, due to
acetaldehyde, due to the metabolic changes or due to nutritional
deficiency.
The major actions of ethanol involve enhancing the inhibitory effects of
aminobutyric acid (GABA) at GABAA receptors and blockade of the N-
methyl-D-aspartate (NMDA) subtype of glutamate, an excitatory amino
acid (EAA) receptor. Oxidation of ethanol generates an excess of
reducing potential in the cytosol in the form of NADH, with the ratio of
NADH to NAD+ being dramatically increased. This ratio, also known as
the redox potential, determines the ability of the cell to carry on various
oxidative processes. The unfavorable change in redox potential as a
consequence of ethanol metabolism contributes to the development of
metabolic disorders.
The net result will be
Accumulation of free NADH with a resultant increase in NADH: NAD
ratio, this is called redox ratio and NAD depletion.
Effects:
Certain oxidation reactions that depend on the presence of NAD will be
inhibited as:
A- Oxidation of lactate to pyruvate
Lactate pyruvate
+ +
NAD NADH+H
The increase in the amount of lactate will result in metabolic acidosis
In metabolic acidosis due to alcohol poisoning, there is high anion gap.
This is the difference in quantities between cations and anions. The
 Dr. Hisham Zein Elabdin

cations are Na+, K+, and the anions are HCO3 -, CL -. The normal anion gap
is 8 to 12 mEq/l. In alcoholic metabolic acidosis it is above 18mEq/l.
B) Acetic acid in presence of NAD enters tricarboxylic acid cycle, leading
to oxidation in peripheral tissues. If not available, acetic acid will be
shifted to fatty acid synthatase. It is utilized in the formation of free fatty
acids, which increases serum triglycerides, plasma phospholipids and
cholesterol. Accumulation of fat in liver lead to fatty liver.
 There will be inhibition of hepatic glucogenesis which results in
hypoglycemia.
 The increased lactic acid competes with uric acid for renal
excretion. The result will be secondary hyperuricaemia, this
produces attacks of gout in susceptible individuals.
 Inhibition of the release of antiduretic hormone polyuria
which results in hypotension and loss of important electrolytes .
Excretion of alcohol:
After absorption, the remaining alcohol (10%) is excreted unchanged in
urine, sweat and breath.
ACUTE ALCOHOL POISONING:
CLINICAL PICTURE:
The signs and symptoms of acute alcohol toxicity are related to the
amount of alcohol taken and also differ with the level of alcohol in blood
alcohol concentration (BAC).
1g ethanol in a drink raises the BAC 25 to 30mg/dl.
 ≤ 0.05% (50mg/100ml)
No effect, mild euphoria.
 0.05-0.10%
 Exaggerated mood.
 Increased self - confidence.
 Altered judgment.
 Impaired vision.
 Red conjunctiva.
 0.10-0.14%
 Legal intoxication level (for driving a vehicle)
 Eyes : nystagmus
 Emotional instability
 Dr. Hisham Zein Elabdin

 Loss of inhibition
 Incoordination of movements
 Impaired memory
 Difficult articulation
 0.15-0.29%

 Loss of muscle coordination.
 Marked confusion
 Staggering gait
 Slurred speech
 Disorientation
 No behavior control
 Diplopia
 Hiccough
 Vomiting
 Drowsiness
 Altered sensation and perception
 0.30 - 0.40%
 Apathy
 Sleepy
 Delirium
 Stupor
 More than 0.40%
 Anesthesia
 Coma
 Death
Management of acute poisoning :
Investigation
1- Alcohol level in breath
2- Blood alcohol level
Arterial blood gases and blood pH.
Treatment:
 A-B-C.
 Gastric lavage
 Dr. Hisham Zein Elabdin

 Activated charcoal for any coingestion

 Thiamin 100%mg/IM or IV
 Sodium bicarbonate IV, 1 mEq/kg.
 haemodialysis

CHRONIC ALCOHOL POISONING

(Alcoholism, alcohol dependence)
The definition of alcoholism as given by the WHO "Alcoholics" is :
Those excessive drinkers whose dependence on alcohol has attained
such a degree that it shows a noticeable mental disturbance or
interference with the bodily or mental health , their interpersonal and
their social and economic functions, or who show the prodromal signs of
such development. They therefore require treatment.
Alcohol dependence is characterized by tolerance, physical dependence
and withdrawal symptoms.
Clinical picture of alcohol dependence:
A- General : loss of appetite, facial rubor, bulbous red nose, breakdown
in moral status, conjunctivitis and bronchial catarrh. Nutritional
disturbances; vitamin deficiency.
B- Cardiovascular :
 Cardiomyopathy
 Cardiac hypertrophy
 Cardiac arrhythmias
 Briberi heart disease: systemic hypertension, collapsing pulse,
peripheral oedema.
 Hypertension
C- Gastrointestinal manifestations:
 Gastritis.
 Malabsorption.
 Carcinoma of the oesophagus.
D- Liver:
 Fatty liver.
 Hepatitis.
 Liver cirrhosis.
 Hepatoma.
 Dr. Hisham Zein Elabdin

E- Acute haemorrhagic pancreatitis.

F- Musculoskeletal :
Alcohol myopathy may be subclinical, acute or chronic. There is
alteration of CK, severe myoglobinuria, muscle cramps in the
extremities, weakness and atrophy in a group of muscles in the leg.
G- Peripheral neuritis (sensory) and tremors in hands.
H- Mental disorders:
 Personality change.
 Korsakoff,s psychosis.
o Amnesia and memory disturbance.
o Intellectual defect; inability to learn.
 Wernike,s encephalopathy Characterized by the triad:
o Paralysis of eye movement and nystagmus.
o Ataxia.
o Mental disturbance.
In these tow syndromes there is cortical atrophy which is believed to
be due to nutritional deficiencies especially thiamine.
 Encephalitis haemorrhagica with small areas of haemorrhagic
necrosis in the hypothalamus and along the walls of ventricles.
There is also atrophy of the cerebral cortex.
 Delirium tremens (Toxic confusion state) disorientation,
illusions, fear, visual hallucination, paranoid ideas, delusions,
restlessness, hyperactivity, tremors.
 Psychiatric syndromes as:
o Alcoholic hallucination.
o Morbid jealousy (Othello syndrome).
o Suicidal tendency.
o Alcohol delusions.
o Alcohol dementia.
MANAGEMENT OF CHRONIC ALCOHOLISM:
Investigations:
 Alcohol breath.
 Blood alcohol concentration (BAC).
 Alcohol in urine.
 Dr. Hisham Zein Elabdin

 Arterial blood gases.

 Serum electrolytes.
 Liver function tests
TREATMENT:
1- Gradual withdrawal.
2- Diet; high in vitamins and carbohydrates.
3- Psychotherapy (in groups)
4- Antabuse: Disulfiram(tetra ethyl thiuram)
Ingestion of antabuse will lead to a syndrome that starts 15 to 30
minutes after ingestion of alcohol. The syndrome is characterized by
flushing, vertigo, headache, nausea, vomiting, abdominal pain, chest
pain and hypotension. These symptoms make the person dislike
alcohol (aversion therapy).
Dose: initial 500mg once daily for seven to ten days then 125-250
mg/day orally.
Mechanism of action
Disulfiram and its metabolites block the oxidation of acetaldehyde.
Side effects of Disulfiram:
Garlic taste, rotten egg odor, headache, fatigue, drowsiness,
dermatitis, psychosis.
Treatment of Disulfiram reaction:
 Oxygen.
 Ephedrine.
 Ascorbic acid 500mg IV.
 Antihistaminic.
 Phenothiazines and fluids.
Withdrawal symptoms
1- Minor withdrawal:
6-8 hours after reaching O alcohol level:
o Nausea
o Vomiting
o Sweating
o Tachycardia
o Hypertension
o Weakness
 Dr. Hisham Zein Elabdin

o Fainting
o Irritability
o Hyper reflexia
o Tremors
2- Moderate withdrawal: 24 hours after reaching O level:
o Hallucinations: visual, tactile &olfactory
o Convulsions
o Arrhythmia
3- Major withdrawal
1-7 days
o Hypertension
o Hyperthermia
o Altered mental status
o Delirium tremors: confusion, disorientation, hyperactivity,
hallucination.
Treatment of alcohol withdrawal:
1- Mild cases could be treated at home:
o Psychological assurance.
o Diet
2- Severe: in hospital:
o Frequent meals
o Fluids
o Thiamine
o Sedation: diazepam
MEDICOLEGAL ASPECT OF ALCOHOL POISONING
1- Road traffic accident
Lack of coordination, concentration and judgment, reduced visual
perception and alertness to external clues in addition to change of
behavior are factors that make a person with a high alcohol blood
level.
2- Crimes
There is a link between alcohol consumption and criminal
behavior.
3- Trauma.
 Dr. Hisham Zein Elabdin

METHYL ALCOHOL
Colorless volatile fluid
Sources
o Paint solvent
o Household cleaners
o Photocopying fluid
o Windshield washer fluid
o Industrial solvent
Circumstances of poisoning:
o Accidental
o Adulteration of alcoholic beverages
Pathophysiology:
Methyl alcohol itself is harmless but metabolites are toxic.
It is absorbed through GIT, and peak level is reached within 30-60
minutes.
 Methanol is metabolized in the liver to formaldehyde by the
action of a alcohol dehydrogenase ADH.
 Formaldehyde is further oxidized to formic acid by the action of a
group of enzymes.
 Formaldehyde is 33times as much toxic as methanol but its half
Live is 1-2 minutes. It is rapidly converted to formic acid.
 Formic acid is 6 times toxic as methanol.
 The toxic metabolite responsible for symptoms and signs is formic
acid.
 Formic acid is further oxidized to CO2.
 There is shift of the redox-ratio as in ethanol poisoning.
The main pathological effects are:
 CNS depression.
 Metabolic acidosis due to lactic acid and formic acid.
 Formic acid is responsible for the ocular toxicity, which are the
main target organ affected. It inhibits the cytochrome oxidase in
optic nerve, thus disturbing the flow of axoplasm resulting in
oedema of optic disc and swelling of myelin sheath.
 GIT irritation.
Clinical picture:
 Dr. Hisham Zein Elabdin

A latent period is present ranging from 40 minutes up to 72 hours during

which there is malaise and headache.
1- GIT manifestation: nausea, vomiting, abdominal pain, diarrhea,
anorexia.
2- CNS: Drowsiness, confusion, agitation, slurred speech, dizziness,
seizure, stupor, coma, cerebral oedema.
3- Ophthalmic: blurred vision, photophobia, visual hallucination and
pupils are sluggish or non-reactive, papilledema, hyperemic optic
disc, retinal oedema or hemorrhage.
4- Metabolic acidosis
5- Cardiopulmonary:
 Bradycardia
 Hypotension
 Tachypnea to compensate metabolic acidosis, then
respiratory failure.
MANAGEMENT:
Investigations:
1- Serum electrolytes
2- Serum osmolality
3- Arterial blood gases
4- Blood ethanol concentration BAC
5- Blood methanol level by GC/M
Toxic level 30 mg/dl.
Lethal level 80 mg/dl.
6- Urine methanol; by colour tests
7- Blood formate: level of 0.5 mg/l in severe poisoning.
8- Fundoscopic examination
9- CT of head may be needed
TREATMENT:
1- A-B-C
2- Decontamination for any coingestion . gastric lavage within 1 hour
of presentation.
3- Sodium bicarbonate 1-2 mEq/kg IV.
4- Fluids IV.
5- Ethanol infusion (competitive inhibitor for ADH).
 Dr. Hisham Zein Elabdin

 Loading dose 7.5 -10 ml/kg of 10% ethanol in Dextrose 5%

over 30 minutes.
 Maintenance dose :1-2 ml/kg/hour.
The end point should be a non detectable methanol level.
6- Calcium leucovorin (folinic acid ) 1mg/kg IV.
7- Folic acid 1 mg/kg /4hours for atotal of 6 doses.
8- New antidote: 4 methyl pyrazole (4MP, fomepzole).
 Its action is competitive inhibitor of ADH. So the toxic
metabolite formic acid will not be formed.
It has a longer duration of action and fewer adverse effects
than ethanol. No (CNS depression).
o Loading dose: 15 mg/kg IV over 30 minutes.
o Followed by 10 mg/kg every 12 hours for 4 doses
o Then 15 mg/kg every 12 hours until methanol in blood
reduced to safe levels.
It is expensive
9- Diazepam for seizures 10mg IV.
10- Haemodialysis : remove methanol and formate.
It is indicated for the following:
 Presence of symptoms.
 History of ingestion of 30 ml.
 Methanol level more than 20mg/dl.
 Ocular findings.
 Electrolytes abnormalities.
 Metabolic acidosis .
 Renal insufficiency.