forensic Toxicology,

1. ETHYLENE GLYCOL,
Iso propyl alcohol,
BARBITURATES
DR M B SINGH
COURTESY; DR G BISWAS, SLIDE SHARE, MR MOMPATI LETSWELETSE

2. TOXICITY of
ETHYLENE GLYCOL,
BARBITURATES

3. ETHYLENE GLYCOL,
clear, colorless , odorless , non volatile liquid with bitter sweet
taste

4. ETHYLENE GLYCOL
FATAL DOSE ; 100 -200 ML.
FATAL PERIOD ; 3 DAYS.

5. Action: Ethylene glycol itself is not toxic, but the toxicity
is due to metabolites glycolic and oxalic acids which
inhibits oxidative phosphorylation.
„Oxalic acid combines with calcium to form calcium oxalate
crystals which accumulates in the proximal convoluted
tubules causing hypocalcaemia and renal failure.
„Metabolic acidosis occurs from glycolic acid.

6. ETHYLENE GLYCOL: MECHANISM OF POISONING.
• Ethylene glycol is metabolized by alcohol dehydrogenase to
glycoaldehyde, which is then metabolized to glycolic, glyoxylic,
and oxalic acids.
These acids, along with excess lactic acid, are responsible for the anion
gap metabolic acidosis.
Tissue injury is caused by widespread deposition of oxalate crystals
and the toxic effects of glycolic and glyoxylic acids.

8. SIGNS AND SYMPTOMS OF POISONING
seizures
coma
cerebral edema (in some cases)
tachycardia
tachypnea, and
hypertension or hypotension
flank pain,
costovertebral angle tenderness, and
oliguric renal failure

9. DIAGNOSIS
Laboratory tests which include
• complete blood count
• serum electrolytes
• alcohol toxicology panel with ethanol,
• blood urea nitrogen
• urinalysis
• serum ethylene glycol level
• calcium and magnesium levels

10. ANTIDOTE: ETHANOL AND FOMEPIZOLE
Fomepizole
It is thought to act as an inhibitor of alcohol dehydrogenase
and therefore prevent the formation of acidic ethylene
glycol metabolites.
It is administered in divided doses
- Loading dose, 15 mg / kg
- Maintainance dose 10 mg / kg every 4h

11. Administer fomepizole or ethanol to saturate the enzyme
alcohol dehydrogenase and prevent metabolism of
ethylene glycol to its toxic metabolites.
Ethanol (ethyl alcohol) acts as a competitive substrate for the enzyme alcohol dehydrogenase,
preventing the metabolic formation of toxic metabolites from methanol or ethylene glycol

12. SAFETY PROFILE OF FOMEPIZOLE
Generally safe but may stimulate hypersensetivty that may exhibit it self as
• mild skin rash
• heart burn
• nausea
• vomiting
• diarhoea
• loss of apettite
• dizzzines
• hangover feeling

13. Non-specific findings.
i. Organs are congested.
ii. Mucous membrane of the GIT is congested and inflamed.
iii. Cerebral oedema, chemical meningoencephalitis, liver and kidney
damage may be seen.
iv. Oxalate crystals are seen in the brain, spinal cord and kidneys.
Medico-legal aspects:
Poisoning is accidental or suicidal in nature.
Homicide may possible but very rare.
POST MORTEM APPEARANCE – ETHYLENE GLYCOL

14. Isopropanol-
Colorless volatile liquid with acetone smell
It is found in rubbing alcohol (70% isopropanol), antifreeze,
skin lotions, mouthwashes and home cleaning products.
Physical properties: It is a colorless, volatile liquid with a
faint odor of acetone, and is slightly bitter in taste.

15. Metabolism: It is well absorbed through the mucous membrane of the
respiratory tract and GIT, and reaches a peak concentration
approximately 30–120 min after ingestion.
It is metabolized in the liver and converted to acetone which is excreted in
the urine and breath.
Action: It is 2–3 times more potent than ethanol and more toxic than
methyl alcohol. Both the CNS depressant effects and the fruity odor on
the patient’s breath are due to acetone.

16. Signs and Symptoms
„The primary toxicity with isopropanol is CNS depression.
„Unlike methanol and ethylene glycol, isopropanol does not cause a
metabolic acidosis.
„It causes hypotension, cerebral depression and drunkenness. There
is loss or sluggishness of reflexes. Pupils are constricted in coma.
There are signs of renal damage.
„Death from ingestion of isopropanol is uncommon.

17. Propanol
Fatal dose: 250 ml (> 100 mg/dl in blood)
Fatal period: Few hours.
Treatment: Similar to methanol.

18. Postmortem Findings
„Externally, non-specific findings.
„Internally, the organs are congested. Lungs and kidneys
are congested and edematous. There may be renal
degeneration.
Medico-legal aspects: Poisoning is accidental, mostly by
way of external medicinal use.

19. BARBITURATES: MECHANISM OF ACTION
• All barbiturates cause generalized depression of neuronal
activity in the brain.
• Interaction with a barbiturate receptor leads to enhanced gama
aminobutyric acid (GABA)-mediated chloride currents and results
in synaptic inhibition.
• Hypotension that occurs with large doses is caused by
depression of central sympathetic tone as well as by direct
depression of cardiac contractility.

20. SIGNS AND SYMPTOMS
• Lethargy
• slurred speech
• nystagmus, and ataxia are common with mild to moderate
intoxication. With higher doses, hypotension, coma, and
respiratory arrest commonly occur.
With deep coma, the pupils are usually small or mid-position; the
patient may lose all reflex activity and appear to be dead.

21. DIAGONOSIS inclused estimation of
• electrolytes level
• Glucose levels
• BUN
• creatinine,
arterial blood gases
or pulse oximetry, and chest x-ray.
Antidote - There is no specific antidote.

22. Supportive therapy -barbiturates
• gastric lavage with activated charcoal.
• Enhanced elimination
1. Alkalinization of the urine , increases the urinary elimination of
Phenobarbital but not other barbiturates. Its value in acute overdose is unproved,
and it may potentially contribute to fluid overload and pulmonary edema.
2. Repeat-dose activated charcoal has been shown to decrease the half-life
of Phenobarbital, but it has not been shown to actually shorten the duration of coma.
3. Hemoperfusion or hemodialysis may be necessary for severely intoxicated
patients not responding to supportive care (i.e., with intractable hypotension)

23. Postmortem Findings – barbiturates.
exlternal i. Mainly those of asphyxia.
ii. Cyanosis is present.
iii. Froth is seen from the mouth and nostrils.
iv. Congested face, and prominent postmortem
staining.
v. Barbiturate blisters may be seen.
Internal i. Stomach: White particles may be seen. Gastric mucosa may be eroded. Fundus
may be thickened, granular and hemorrhagic.
ii. Lungs: Congested and edematous. Bronchopneumonia, and/or petechial
may be present.
iii. Heart: Subendocardial hemorrhages may be seen.
iv. Kidneys: Degeneration of convoluted tubules.
v. Other organs: Congested

24. barbiturate automatism (self-poisoning)
definition: it is taking of barbiturate tablets repeatedly in a short interval,
because of mental confusion and memory disturbances.
cause: the patient develops a state of toxic delirium after ingestion of one or
several doses of drug,
and in the delirium or automatism state, patient himself takes
doses of drug due to loss of memory of previous drug intake, or in order to
to sleep without any intention to commit suicide and without realizing it.
Hence elderly people on therapy, need some one’s assistance in taking drug.
medico-legal aspects: barbiturate automatism may be
more pronounced with alcohol consumption.

25. MEDICO-LEGAL ASPECTS - BARBITURATES
mostly suicidal, rarely homicidal.
Barbiturates are used as ‘date rape’ drugs, since they can be easily placed
into drinks and produce a state of relaxation and disinhibition.
Accidental poisoning occurs due to an overdose (automatism).
Addiction may occur due to excessive use of barbiturates.
Occupational hazards: barbiturates may impair the mental and/or physical
abilities required for the performance of tasks, such as driving a vehicle or
operating machinery. Patients should be warned accordingly.

26. . 1.Safe limit of alcohol consumption in males and females are: AFMC 11
A. 15 and 10 units/week B. 18 and 15 units/week
C. 21 and 14 units/week D. 25 and 18 units/week
2. Blackout is due to: Maharashtra 11
A. Alcohol intoxication B. Cocaine toxicity
C. LSD toxicity D. Cyanide poisoning
3. Fatal level of ethanol in blood: NIMHAS 13
A. 100–200 mg/dl B. 200–300 mg/dl
C. 300–400 mg/dl D. > 500 mg/dl
4. In holiday heart syndrome, most common feature seen is: Odisha 09; DNB 10
A. Atrial fibrillation B. Atrial flutter
C. Ventricular fibrillation D. Ventricular flutter

27. 5. Disulfiram is useful in: TN 11
A. Alcohol dependence B. Heroin dependence
C. Cocaine dependence D. Cannabis dependence
6. Disulfiram: JIPMER 10
A. Inhibits alcohol dehydrogenase B. Inhibits aldehyde dehydrogenase
C. Both A and B D. Inhibits phosphodiesterase
7. Disulfiram-like reaction is caused by: Kerala 11
A. Acamprostate B. Metronidazole
C. Tetracycline D. Digitalis
8. Most common symptom of alcohol withdrawal is:
AI 07; FMGE 08
A. Bodyache B. Tremor
C. Diarrhea D. Rhinorrhea

28. 9. CAGE questionnaire is used in: AP 07; MP 09; NEET 13
A. Alcohol dependence B. Opiate poisoning
C. Dhatura poisoning D. Barbiturate poisoning
10. Delirium tremens seen in: DNB 10; NEET 13
A. Alcohol withdrawal B. Alcohol intoxication
C. Opioid intoxication D. Opioid withdrawal
11. All are true about delirium tremens, except: NIMHANS 10; AI 11; FMGE 11
A. Normal sleep wake cycle B. Visual hallucinations
C. Coarse tremors D. Clouding of consciousness
12. A male did not have alcohol for 2 days presented with seizures treatment given: AIIMS 13
A. Diazepam B. Phenobarbital
C. Disulfiram D. Thiamine

29. 13. Chronic alcoholic assaulted his neighbour. He had quit drinking 4 days
back but now has delirium tremens. He is: AIIMS 11
A. Fully responsible B. Family is responsible
C. Partially responsible D. Not responsible
14. All are associated with Wernicke’s encephalopathy, except: FMGE 10; NEET 13;
NIMHANS 13; UPSC 14
A. Cog wheel rigidity B. Alteration in mental function
C. VIth nerve palsy D. Ataxia
15. Constellation of neuropathy, muscle weakness and wasting, cardiomegaly,
edema, ophthalmoplegia, confabulation strongly suggest: KCET 13
A. Hysteria B. Thiamine deficiency
C. Lead poisoning D. Intracerebral hemorrhage

30. 16. Wernicke-Korsakoff’s syndrome is due to the deficiency of: FMGE 10; JIPMER 10;
NIMHANS 14
A. Pyridoxine B. Thiamine
C. Vitamin B12 D. Riboflavin
17. Vitamin deficiency seen in alcoholic with dementia: AP 08; Maharashtra 09; JIPMER
A. Thiamine B. Vitamin B12
C. Riboflavin D. Pyridoxine
18. A 55-year-old man presents with a 10 day history of confusion. His friend mentions
that he drinks 15 units of alcohol per day. Which of the following strongly
suggests a diagnosis of Korsakoff’s psychosis: Karnataka 07; Jharkhand 11; KCET 12; PGI
A. Delusional beliefs B. Poor long-term memory
C. Auditory hallucinations D. Confabulation

31. 19. Area of the brain is usually not involved in WernickeKorsakoff syndrome: Karnataka
11
A. Periventricular gray matter B. Mammillary bodies
C. Hippocampus D. Thalamus
20. True about alcohol paranoia: AI 10
A. Tremors B. Fixed hallucinations
C. Fixed delusions D. Wrist and foot drop
21. Criminal responsibility of an intoxicated person is under: AIIMS 14
A. Sec. 82 IPC B. Sec. 84 IPC
C. Sec. 85 IPC D. Sec. 90 IPC
22. Widmark’s formula is used for measurement of blood levels of: NIMHANS 10; AFMC
11
A. Benzodiazepines B. Barbiturates
C. Alcohol D. Cocaine

32. 23. The most reliable method of estimating blood alcohol level is: Kerala 09
A. Cavett’s test B. Breath alcohol analyzer
C. Gas liquid chromatography D. Thin layer chromatography
24. The chemical used for qualitative and quantitative assessment of alcohol in
the expired air is: KCET 12
A. Aniline B. Diphenylamine
C. Potassium ferrocyanide D. Potassium dichromate
25. In contaminated liquor poisoning, all of the following are true, except:
JIPMER
A. Metabolic alkalosis B. Blindness
C. Treatment is with ethanol D. Toxicity is due to methanol

33. 26. Not true about methyl alcohol poisoning: AIIMS 13
A. Effects are due to formic acid B. Fomepizole competitively inhibits aldehyde dehydrogenase
C. Metabolic acidosis D. Blindness
27. Ethanol is used for ethylene glycol poisoning because it is a: JIPMER 13
A. Competitive inhibitor of aldehyde dehydrogenase
B. Higher affinity for alcohol dehydrogenase
C. Chemically combines and neutralizes ethylene glycol
D. Competitive inhibitor of alcohol dehydrogenase
28. Fomepizole is used for: CMC (Vellore) 14
A. Ethanol poisoning B. Methanol poisoning
C. Opium poisoning D. Barbiturate poisoning
29. All causes metabolic acidosis, except: Kerala 07
A. Methanol B. Ethanol
C. Salicylate D. Isopropanol

34. 30. High anion gap acidosis is seen in all the following, except: DNB 10; Odisha 11
A. Diabetic ketoacidosis B. Lactic acidosis
C. Renal tubular acidosis D. Methanol poisoning
31. Antidote for ethylene glycol poisoning: DNB 09; Punjab 12; NEET 13
A. Methyl violet B. Fomepizole
C. Fluconazole D. Ethyl alcohol
32. Ethylene glycol when ingested affects kidney by forming: NEET 13
A. Formaldehyde B. Oxalates
C. Phytates D. Phosphates
Answers
1. c 2. A 3. c 4. A 5. A 6. B 7. B 8. B 9. A 10. A
11. A 12. A 13. D
14. A 15. B 16. B 17. A 18. D 19. c 20. c 21. c 22. c 23. c
24. D 25. A 26. B 27. B & D 28. B 29. D 30. c 31. B 32. B

35. Thanking you……
time to relax but be sober