Alcohol-forensic and toxicology module.ppt

🧪 Alcohol in Toxicology: A Brief Overview
Alcohols are a diverse group of organic compounds, and in toxicology, they are classified based on their potential to cause harm. The most commonly encountered alcohols in clinical toxicology include ethanol, methanol, isopropanol, and ethylene glycol. Each has distinct pharmacokinetics, toxic effects, and treatment protocols.

🍷 Ethanol (CH₃CH₂OH)
Source: Found in alcoholic beverages, mouthwashes, and medications.

Absorption & Metabolism: Rapidly absorbed via the gastrointestinal tract; metabolized in the liver by alcohol dehydrogenase (ADH) to acetaldehyde, then to acetate.

Toxic Effects: CNS depression, hypoglycemia, hypothermia, respiratory depression, and in chronic use—liver cirrhosis and Wernicke’s encephalopathy.

Withdrawal: Can lead to tremors, seizures, delirium tremens, and death if untreated.

Treatment: Supportive care, thiamine supplementation, and benzodiazepines for withdrawal.

🧴 Methanol (CH₃OH)
Source: Found in windshield washer fluid, paint thinners, and industrial solvents.

Metabolism: Converted by ADH to formaldehyde, then to formic acid—responsible for toxicity.

Toxic Effects: Visual disturbances ("snowfield vision"), metabolic acidosis, CNS depression, and potential blindness.

Treatment: Fomepizole or ethanol (ADH inhibitors), bicarbonate for acidosis, and hemodialysis in severe cases.

🧼 Isopropanol (CH₃CHOHCH₃)
Source: Rubbing alcohol, hand sanitizers, and disinfectants.

Metabolism: Metabolized to acetone via ADH.

Toxic Effects: More potent CNS depressant than ethanol; causes hypotension, hemorrhagic gastritis, and ketosis without acidosis.

Treatment: Supportive care; dialysis rarely needed unless severe.

🚗 Ethylene Glycol (HOCH₂CH₂OH)
Source: Antifreeze, brake fluids, and industrial solvents.

Metabolism: Metabolized to glycolic acid and oxalic acid—both nephrotoxic.

Toxic Effects: CNS depression, metabolic acidosis, renal failure due to calcium oxalate crystal deposition.

Treatment: Fomepizole or ethanol, bicarbonate, calcium supplementation, and hemodialysis.

🧠 Diagnostic Considerations
Lab Tests: Blood alcohol levels, anion gap, osmolar gap, arterial blood gases, and renal function tests.

Clinical Clues: History of exposure, altered mental status, visual symptoms, and metabolic derangements.

🩺 Management Principles
Airway, Breathing, Circulation: Always prioritized.

Antidotes: Fomepizole or ethanol for methanol and ethylene glycol.

Supportive Care: IV fluids, correction of electrolyte imbalances, and monitoring for complications.

Dialysis: Indicated in severe poisoning or renal failure.

Alcohol toxicity remains a critical concern in emergency medicine and forensic toxicology. Prompt recognition and targeted intervention can significantly reduce morbidity and mortality. Understanding the metabolic pathways and clinical presentations of each alcohol type is essential for effective management.

1. Alcohols poisoning

2. •Introduction:
•Alcohols are a large chemical group which
include:
- Ethyl alcohol (ethanol).
• - Methyl alcohol (methanol).
• - Isopropyl alcohol .
• - Ethylene glycols.

3. •I. Ethyl alcohol (Ethanol)
•Introduction:
• -Medico-legal importance:
•(

1
)
Criminal acts (Sexual assault, ...).
•(

2
)
Accidents (Road accidents, fall from height, …).
• -The concentration of alcohol in the different
commonly used beverages varies from 2 % to 85%.
• -Ethanol toxicity may be acute or more commonly
chronic.

4. •[A ]Acute Ethanol Toxicity
•[I ]Pharmacokinetics:
-Absorption:
•Small intestine (80 %), stomach (20 %).
•-Metabolism & Excretion:
• -Mainly hepatic by oxidation (90%) and dehydrogenase enzyme
is responsible for this process.
• -The remaining (10%) is eliminated unchanged 5% in urine and
5% in breath.

5. •[II ]Pharmacodynamics:
• -The mechanism of ethanol intoxication is not specifically
known.
• CNS depression: by effects on specific chemical
neurotransmitters:
• -Potentiates GABA activity (Inhibitory
neurotransmitter).
• -Inhibits glutamate activity (Excitatory
neurotransmitter).

6. •Condition of Poisoning:
•It is almost always accidental among the chronic
alcoholics.
•Fatal Dose:
•Classically: 150 ml of pure alcohol.
•Fatal Period:
•It is expected in the first 1-10 hrs.

7. Effects in relation to blood level:
0.15% : Slight drunkenness.
0.25% : Heavy drunkenness.
0.35% : Coma.
0.5% : Fatal due to central respiratory depression.

8. Clinical picture of acute toxicity:
-Cortex: inhibition of cortical centers lead to free
release of emotions with euphoria,
cheerfulness, talkativeness, sexual assaults
and violence.
-Cerebellum: Staggering unsteady gait.
-Vasodilatation:
- Flushing of the face and skin with sweating and
Dehydration
-Sense of warmth but there is hypothermia.
-Hypotension and tachycardia .

9. -Eye :
- Dilated pupil (constricted pupils but dilate on
pinching the skin (McEwin pupil)
- Nystagmus. - Conjunctival injection .
-GIT :
- Increased appetite with hypoglycemia .
- Hiccough, nausea, vomiting .
-Respiratory tract :
- Smell of alcohol in breath .
- Acidotic air hunger (deep rapid respiration).
- Respiratory center depression.

10. Investigations:
Routine:
-CBC, ABG, electrolytes, Glucose level, Urea &
creatinine, urine analysis etc.…
Specific:
-Blood & urine: using potassium bichromate .
1.15 mg of ethanol reduce 1 cc of potassium bichromate
-Breath analyzer or drunkometer: In the breath .

11. Treatment:
A- Emergency measures: (ABCD).
B- Decontamination: Gastric lavage with sodium
bicarbonate (NaHCO3)
C- Symptomatic treatment:
- Care of coma and fluids for dehydration.
- Glucose to correct hypoglycemia.
- NaHCO3 IV for metabolic acidosis.
- Correction of hypothermia.

12. D- Antidote:
- Vitamin B1 (thiamine) to avoid Wernickes encephalopathy .
- Vitamin B6 to enhance alcohol metabolism.
E- Elimination:
Hemodialysis
• Indications:
• * Extremely high blood alcohol level (more than 500mg%).
• * Severe acid-base and/or electrolyte disturbances.

13. Alcohol Dependence
Clinical picture:
-Flushing of the face especially on the nose, conjunctivits .
-Loss of appetite, loss of weight, vitamin deficiency.
-Chronic gastritis, hepatic fatty degeneration and cirrhosis.
-Sensory peripheral neuritis and optic neuritis.
-Tremors of the hands.
-Increased sexual desire and decrease power.
-Dementia: decrease mental powers, decrease intelligence
and amnesia .

14. • -Special Syndromes: There are 2 famous syndromes:

•(a
)
Wernicke’s encephalopathy:
• - Mental disturbances: confusion, dementia, ataxia,
- Diplopia and nystagmus.
•(

b
)
Korsakoff psychosis :
- Amnesia to recent events.

• - Both syndromes are due to thiamine deficiency

15. Withdrawal Syndrome
•Delerium tremens:
• -Occur 48 – 72 hrs of alcohol withdrawal.
• -Mortality rate; 15.%
The severe form consists of:
• -Restlessness, agitation, and confusion.
• -Disorientation.
-Visual and auditory hallucinations.
• -Tachycardia and hypertension.
• -Tachypnea.
• -Fever and sweating .

16. Treatment:
-Hospitalization.
-Abrupt withdrawal with sedatives.
-Good diet and vitamins: Vitamin B1, B2 ,
Folic acid and Ascorbic acid .
-Antidote :
•Disulfiram: (Antabuse)
•Action: it blocks the alcohol oxidation at the
acetaldehyde stage → severe but harmless side
effects that force the patient to stop drinking .
• -Psychological therapy

17. II. Methyl Alcohol II. Methyl Alcohol
(Methanol)(Methanol)

18. •Introduction:
-An alcohol produced by distillation of wood .
-Similar to ethanol in its color, odor and taste .
-Less expensive than ethanol .
-Used as cleaner and solvent.

19. •[1 ]Pharmacokinetics:
•Absorption: Completely absorbed from the GIT .

•Metabolism and: mainly hepatic, as follows:
Alcohl dehydrogenase
•(1
)
Methanol → Formaldehyde.

aldehyde dehydrogenase
•(2
)
Formaldehyde → Formic acid


Folate
• (

3
)
Formic acid → CO2 + H2O
.

20. •[II ]Pharmacodynamics:
• -The exact mechanism is unclear, but it has been found
that it produces:
•(

1
)
Metabolic acidosis (Formic acid & lactic acid).
•(

2
)
CNS depression; including the respiratory centre.
•(

3
)
Ocular toxicity: formic acid inhibits the cytochrome
oxidase in the optic nerve.
•(

4
)
Direct myocardial depression: It is a terminal event.
•Mode of poisoning:
•Almost always accidental among alcoholics.
•Fatal Dose: 60 ml
•Fatal Period:
•It is expected to be delayed 3-7 days.

21. Clinical Manifestation:
A Latent period of 12- 36 hours due to slow metabolism of
methanol to the toxic metabolites .
-Visual: Blurring of vision, ocular pain, decreased visual
acuity, papilledema, optic atrophy and blindness .
-Metabolic acidosis: due to toxic metabolites of methanol. It
leads to air hunger, confusion, headache and weakness .
-Gastrointestinal: Vomiting, abdominal cramps and
dehydration .
-Neurological :
- Disorientation, stupor and coma.
- Convulsions.
- Encephalopathy.
- Delayed necrosis of basal ganglia leading to muscle spasticity
and dyskinetic movements.

22. -Respiratory depression: follow air hunger .
-CVS: Shock
- Cardiogenic: follow myocardial ischemia, acidosis
and hyperkalemia induced depressed myocardial
contractility.
- Vasoplegic: Depression of VMC

23. •Laboratory evaluation:
• - Arterial blood gases & electrolytes.
- Glucose, urine analysis, urea & creatinine .
- ECG .
- Chest X-ray .
- Fundus examination .
- Methanol blood level: Levels above 25mg/ dl are
indications for antidotes and hemolysis.

24. •Treatment:

1 -Emergency measures: ABCD.

2 -Decontamination: Gastric lavage:

25. • 3- Specific measures: (Antidote)
•(A
)
Ethanol:
•Ethanol is a competitive inhibitor of methanol at the
dehydrogenase enzyme i.e. it is metabolized by the same
enzyme with higher affinity.
•Aim: is to decrease the conversion of methanol into the more
toxic metabolites.
Target: is to keep the blood ethanol level at a level range of
100 mg/dl
•(B
)
4-Methyl-pyrazole: (4-MP = Fomepizole)
•Action: Alcohol dehydrogenase inhibitor.
•(C
)
Folic acid and Folinic acid:
•Action: Converts formic acid to CO2 and water i.e. it enhances
methanol elimination

27. •III. Ethylene glycols
•Introduction:
•It is one of the most serious and dramatic
poisons that encountered in clinical toxicology.
•It is used for many purposes as:
• -In many chemical processes as solvents.
• -Antifreeze in combustion engines.
• -Cosmetic preparations.
• -Medical uses: Elixir “antibiotic” of sulfonamide .

28. •Pharmacotoxicity:
• -The major toxic effects result from the
accumulation of its 4 major highly toxic
metabolites; Aldehydes, glycolate, oxalate,
and lactate.
• Toxicity is extremely high due to:
• - The high toxic effects of the metabolites.
• - The occurrence of severe acidosis.
• - The direct toxic effect of the alcohol itself on
the eye.

29. •Mode of poisoning:
• -It is almost always accidental by alcoholics .
• -Suicidal attempts are rare, while the homicidal use
is not reported.
•Fatal dose:
•It is so variable from one individual to another :
•240-970 mL.
•Fatal period:
•Death may be rapid within the first 12-24 hours
(CNS & CVS), or delayed up to 3-5 days (renal
involvement).

30. •Clinical presentation: The patient usually pass into 3 phases :
•First phase: Starts within 30 min. – 12 hr. post-ingestion.
• -Clinical picture:
• *The patient is drunk with no alcoholic smell.
• *G.I. upset: Nausea, vomiting and hematemesis.
• *CNS manifestations:
• - Diplopia and nystagmus.
• - Paralysis of the muscles of gait and eyes.
• - Hyporeflexia.
• - Convulsions and coma.
•Second phase: Starts within 12-24 hr. post-ingestion.
•There are disposition of Ca-oxalate in:
• * Vascular tree: Mild hypertension.
• * Myocardium: CHF and tachycardia .
• * Lung parenchyma: Pulmonary edema.
•Third phase: Starts within 1-3 days post-ingestion.
•There are disposition of Ca-oxalate in kidneys with:
• * Loin pain and tenderness .
• * Acute tubular necrosis or even acute renal failure.

31. •Treatment:
•The treatment of ethylene glycol intoxication is
identical to that of methanol toxicity, including
the usage of ethanol as a specific antidote.

32. •IV. Isopropyl alcohol
•Introduction:
•It is one of the most widely used alcohols in:
• -Industrial purposes: as a solvent.
• -Household products: as a vehicle or solvent in
many products as skin lotions, hair tonics,
window cleaning fluids, ….. etc.
• -Medical uses: as a vehicle of many therapeutic
products and as a sterilizing agent.

33. •Mode of poisoning:
• -Almost always accidental: particularly
occupational exposure and wrong ingestion by
children.
• -Homicidal and suicidal: Not reported.
•Fatal Dose:
•It is so variable: 20-240 mL., according to the
concentration of the commercial form.
•Fatal Period:
• -It is expected in the first week after ingestion.
• -It is more toxic than ethanol but less toxic than
methanol.

34. •Clinical Presentation:
•It is similar to that of ethanol, but more serious.
•Thus, there may be:
• - Deep coma.
• - Respiratory failure or arrest.
- Cardiomyopathy and pericarditis.
• - Cardiac arrhythmias .
• - Severe hypotension or even circulatory collapse.
• - Severe dehydration.
• - Haemorrhagic gastritis.
• - Ketonuria (acetone in urine).

35. •Treatment:
•[I ]General measures:
• - Gastric lavage or emesis.
• - Ensure patent airway.
• - Start O2-therapy immediately, and artificial ventilation, if
indicated.
• - Activated charcoal: is not effective in eliminating this agent.
•[II ]Specific measures: (antidote)
• Unfortunately, no specific antidote is available up to date.
•[III ]Symptomatic & supportive measures:
• Two main lines must be fulfilled:
•(1
)
Preservation of fluid balance and blood pressure by:
• * Fluid replacement.
• * Vasopressors: Dopamine.
•(2
)
Haemodialysis: To decrease the serum alcohol level as
possible.