ALCOHOLS

ETHANOL, METHANOL
Outline

Sources
Conditions of poisoning
Mechanism of toxicity
Clinical picture
Diagnosis
Treatment
 ETHANOL

ETHYL ALCOHOL
 Sources

Ethyl alcohol produced by sugar fermentation

It is colorless,
characteristic odour,
firey taste,
volatile and
highly inflammable
Conditions of poisoning

Mainly Accidental
 Metabolism

Mainly oxidized in the liver (90%)

Alcohol Aldehyde
dehydrogenase dehydrogenase TCA cycle

Ethanol Acetaldehyde Acetyl CoA

Water + Carbon dioxide
The remaining 10% excreted unchanged in breath
and urin
Mechanism of toxicity
The effects of alcohols are due to:
 Ethanol itself

 Acetaldehyde

 Metabolic changes

 Nutritional deficiencies
Mechanism of toxicity
I) Central effect:
* Descending depressant effect on CNS
(cortex is the most sensitive).
* Inhibition of VMC (False sensation of heat)
* Inhibition of antidiuretic hormone (Diuresis)
Mechanism of toxicity
II) Peripheral Effects

 CVS:
 Blood pressure ↓
 Heart rate ↑
 Cardiomyopathy
 Dysrythmia
 Coronary atherosclerosis
 Mechanism of toxicity
II) Peripheral Effects
 Gastrointestinal effect:

Gastrointestinal irritation,
Achlorhydria
Malabsorption
 Liver:

Fatty degeneration of the liver

Alcoholic cirrhosis
Impaired liver function
 Hypoglycemia
II) Peripheral Effects
 Polyneuropathy:

Due to vitamin deficiency : B1

 Polyneuropathy: axonal degeneration
gradual, bilateral and symmetric
distal more than proximal
legs more than arms
Weakness, decrease pain and temperature sense
 Mental disorders
Mental disorders are due to cortical atrophy
which is attributed to nutritional deficiency
especially thiamine and manifested by:

 Wernick’s encephalopathy

 Korsakoff’s psychosis

 Encephalitis haemorrhagica
 Wernicke’s encephalopathy is characterized
by sudden onset of the triad:

* ophthalmoplegia

* ataxia

* confusion.
 Korsakoff syndrome is characterized by:
memory impairment specifically short-term
memory loss
Clinical manifestations

Mild (effect on frontal lobe):

 Exaggerated mood
 Defective in judgment of time and place.
 Unsteady gait.
 Depression of the mental-brake leading to
abnormal behavior and sexual crimes.
 If driving, it may lead to many accidents at the
Clinical manifestations

Moderate (basal ganglia, cerebellum):

 Muscular incoordination which leads to
staggering gait, slurred speech, ataxia and
tremors of hands and lips.
 Blurred vision, diplopia and nystagmus.
 Hiccough due to: Myoclonic contraction of the
diaphragm.
 Vomiting
 Flushing: false sensation of heat while the
body temperature is low.
Clinical manifestations
Vomiting due to:
1) central emetic effect of acetaldehyde
2) Gastric irritation by concentrated beverage
Clinical manifestations
Severe (inhibition of reticular formation):
 Marked inhibition of consciousness.

 Muscular incoordination and complete

inability to move (false paralytic stage).
Clinical manifestations
 Characters of ethanol coma:
 Pallor with profuse sweating.
 Smell of alcohol.
 Subnormal temperature.
 Rapid weak pulse.
 Low blood pressure
 Reflexes are absent.
 Slow and shallow respiration
 Macewen's sign: the pupils are constricted but
dilate after pinching the skin
Diagnosis
History
Examination
Investigations
Differential diagnosis
Diagnosis … Investigations
 Screening: breath (breath test) and saliva
 Quantitative: blood alcohol level
Diagnosis … Investigations
 ABG
 Blood Glucose
 Level of legal evidence of a drunk is 0.15% in
blood (below this level, there is no impairment
of will power) in some countries it is 0.08%.
Differential Diagnosis

 Atropine poisoning in excitatory stage

 Other causes of coma (toxic, traumatic,

pathological).
Treatment
I. Emergency and supportive care
II. Decontamination
III. Antidote
IV. Enhance elimination
Treatment
I. Emergency and supportive care
 ABCs

 Treat hypothermia

 Treat acidosis

 Treat hypoglycemia
Treatment
II. Decontamination
** Gastric lavage
 within 1h
 If patient is drowsy ?? Cuffed endotracheal tube

** Emesis: contraindicated because of CNS

depression
Treatment
III. Antidote:

 No specific antidote
Treatment
IV. Enhance elimination

 Hemodialysis in
severe cases
 Symptomatic treatments:
 Vitamin Bl (thiamine) 100mg IV to avoid
Wernicke’s encephalopathy.
 Vitamin B6 to enhance alcohol metabolism.

 Naloxone can shorten alcoholic coma.

 Antibiotics to prevent respiratory

complications.
Cause of death
• Respiratory center depression
• Acute haemorrhagic pancreatitis
• Head injury, asphyxia, drowning, accidents
Questions?
 Metabolism

Mainly oxidized in the liver (90%)

Alcohol Aldehyde
dehydrogenase dehydrogenase Folic
acid
Methanol Formaldehyde Formic acid

Water + Carbon dioxide

The metabolite formaldehyde is 33 times more
toxic than methanol.
Mechanism of action:

 Severe depression of CNS (more than

ethanol).
 Acidosis (due to formic acid and lactic
acidosis).
 Blindness: retinal and optic nerve
degeneration due to formate accumulation
and enhanced by metabolic acidosis.
Clinical manifestations
 I- first few hours: the patient usually presents
with gastritis (nausea, vomiting, colic), back
pain (due to pancreatitis)
 II-After a latent period of 12-36 hours: the
patient presents with
 a) CNS Depression: coma (due to acidosis
and accumulation of formic acid in the CSF)
convulsion
 b) Visual: pain in eyes, photophobia, blurring
of vision and dilated fixed pupils, felling as
standing in snow field and blindness.
 c) Severe metabolic acidosis may produce life
threatening hyperkalemia.: air hunger
 D)Shock

Death is always preceded by blindness

 Laboratory investigations:
 Serum methanol
 Serum formate: a better measure of toxicity,
but are not widely available.

 Ophthalmic examination: Fundus

examination
Treatment
I. Emergency and supportive care
 ABCs

 Early ttt of Acidosis

 Coma

 convulsion
Treatment
II. Decontamination
 Gastric lavage

 within 1h
Antidote:

Ethanol
Saturate the alcohol dehydrogenase enzyme
and prevent the formation of toxic
metabolites.
Ethanol 10% in glucose solution is administered
through central venous line and titrated to
maintain a serum level of 100mg/dl and the
patient requires an intensive care unit.
Antidote

4 methyl pyrazol

Inhibits alcohol dehydrogenase enzyme

Antidote

Folic acid
 For the conversion of formic acid to carbon
dioxide and water.
 Symptomatic treatment:
Steroids are indicated if there is any evidence of
optic neuritis. It is also useful in cerebral edema.
 IV. Enhance elimination

Immediate Hemodialysis to remove methanol and

toxic metabolites ‫مهمة جدا جدا‬

General indications
Visual disturbance
Methanol level above 25-30 mg/dl
Refractory acidosis
Precipitation of renal failure
KEROSENE
 Absorption

 GIT→ slow absorption

 Respiratory tract: distribute all over the lungs

if few ml enter respiratory passage (high
vapor pressure and low surface tension)

 SKIN

NB: Kerosene is highly volatile with very low

viscosity
 VERY LOW VISCOSITY + HIGHLY VOLATILE

1
ASPIRATION PNEUMONIA
CNs
Irritation of GIT
depression

COUGH
BRONCHOSPASM
PNEUMONIA Seneitize heart to
catecholamine
C.P of kerosine toxicity
Gastrointestinal tract
 Smell of kerosene

 Burning pain from mouth to stomach

 Nausea, vomiting (risk of aspiration)

 Abdominal pain and diarrhea

C.P of kerosine toxicity
Respiratory system
 Aspiration: immediate cough and chocking

 Chemical pneumonitis: respiratory distress

 Pulmonary edema

 Respiratory arrest and death

C.P of kerosine toxicity
Cardiovascular
 Dysrythmia (atrial fibrillation, ventricular
fibirillation): Kerosene seneitizes heart to
catecholamine

Headache, blurring of vision,

convulsion, dilated pupil,
death
Diagnosis of kerosene
poisoning:

 From history , clinical picture & smell of

kerosene.
 Investigations:
 1-X-ray on the abdomen: kerosene appears as
a layer unmixed with stomach contents.
 2- X-ray on the chest for signs of pneumonia (
multiple, patchy dense areas with ill defined edges.)
 3-Arterial blood gases.
 4-ECG monitoring.
 ttt of kerosene toxicity
Hospitalisation

 Demulcents e.g water not milk

 No Emesis (for fear of aspiration pneumonia)

 Lavage OR not ? no
If >1ml/kg →wash with warm H2O After
cuffed Intubation & suction 1st
 ↓
If inhaled
 Remove to fresh air.
 Care for respiration by intermittent positive p
100% humidified O for pt pulmonary edema.(to
open collapsed alveoli)
 Corticosteroids to ↓ chem pneumonitis??
 Antibiotics for bronchopneumonia
 N.B:
 Never give Epinephrine . why?
THANK YOU