Methyl alcohol is used industrially and is toxic to humans. It is metabolized to formaldehyde and then formic acid, which causes acidosis and is toxic. Symptoms range from dizziness and nausea to seizures, coma and death. Treatment involves correcting acidosis with bicarbonate, using ethanol to competitively bind to the metabolizing enzyme, and potentially haemodialysis. A case study describes a man with a history of alcoholism who was poisoned by methyl alcohol, developed seizures and metabolic acidosis, and died despite aggressive treatment including stomach washing and medications.

3. Introduction
 Methyl alcohol is a non drinking type of alcohol
containing single carbon and is used in industrial and
automotive purpose.

4. MECHANISM OF ACTION
METHANOL FORMALDEHYDE FORMIC
ACID
ALDEHYDE DEHYDROGENASEALCOHOL DEHYDROGENASE
METHANOL ITSELF NOT TOXIC. FORMALDEHYDE VERY TOXIC, BUT VERY
RAPIDLY METABOLISED TO FORMIC ACID. FORMIC ACID RESPONSIBLE
FOR THE TOXICITY RELATED TO METHANOL INGESTIONS

5. MECHANISM OF ACTION
METHANOL
FORMALDEHYDE
FORMIC
ACID
ACIDOSIS
Early stage
of poisoning
ACIDOSIS
TISSUE
HYPOXIA
LACTIC ACID
PRODUCTION
CIRCULATORY
FAILURE
GENERAL TOXICITY
INCREASED FORMIC ACID TOXICITY
OCULAR
TOXICITY
INHIBITION OF MITOCHONDRIAL RESPIRATION
CIRCULUS
HYPOXICUS

6. SIGNS AND SYMPTOMS
In small doses  Dizziness (vertigo)
 Headache
 Nausea & Vomitting
 Abdominal pain
In Moderate doses Tachy cardia
 Drowsiness
 Mydriasis (dilation of the pupil)
In High doses  Metabolic Acidosis
 Convulsions
 Retinal Oedema
 COMA
 Respiratory failure and death

7. SIGNS AND SYMPTOMS
CNS – CONVULSIONS, PROGRESSING TO COMA
RETINAL - BLURRED VISION, PHOTOPHOBIA, VISUAL
ACUITY LOSS, DILATED NON-REACTIVE PUPILS,
OPTIC NERVE BECOMES OEDEMATOUS
GIT - NAUSEA, VOMITING
CARDIAC - TACHYCARDIA, HYPERTENSION PROGRESSING
TO HYPOTENSION AND CARDIOGENIC SHOCK
RESPIRATORY - TACHYPNOEA

8. INVESTIGATION
BLOOD METHANOL LEVEL (by titration method)
ABG
Fundoscopy ( to examine retinal

9. Image reference  http://www.meajo.org/article.asp?issn=0974-
9233;year=2013;volume=20;issue=1;spage=92;epage=94;aulast=Iscan

10. TREATMENT
(i) Symptomatic treatment
(ii) CORRECTION OF METABOLIC ACIDOSIS
BICARBONATE (AGGRESSIVE TREATMENT)
(iii) Ethanol ( competitive binding to ADH)
(iv) Haemodialysis
(v) Folinic acid (elemination of formic acid)
(vi) Fomepizole

11. CASE STUDY

12. Name : Mr. X Age :
Sex : Male DOA :
CHIEF COMPLAINTS :
C/O Right Shoulder pain in the morning  following which he
faints and then goes into unconscious state
 convulsions (before going unconscious) (tongue bite mark seen)
HISTORY OF PRESENT ILLNESS :
N/K/C/O – BA / HTN / Epilepsy
Consumption of high levels of alcohol (12 hrs ago)
PAST MEDICAL HISTORY :
Known Diabetic, wound present over the right foot for over 7 months
PERSONAL HISTORY/ SOCIAL HABITS
K/C/O Alcoholism – 25 yrs
Smoking – 14 yrs

13. PHYSICAL EXAMINATION :
Pt was Unconscious/ disoriented
ON EXAMINATION :
Temp : 103° F BP : 110 / 70
Pulse : 88 RR 16
SYSTEMIC EXAMINATION :
CVS: S1 S2 +ve CNS : pupils not responding (dilated)
Initially responded to painful stimuli
followed by no response
RS : NVBS P/A : Soft

14. Metabolic
acidosis
Pt. Name is hidden

15. OTHER TESTS :
CT - subcortical white matter and basal ganglia hyperintensity and low-signal-
intensity
ECG – Bradycardia
DIAGNOSIS
Alcohol Poisoning ( Methyl Alcohol)

16. TREATMENT
Initially - Stomach wash given, Commercially available Ethanol 10 %
soln (30 ml)
DRUGS DOSE R.O.A FREQ No of Days
Inj Fosolin (Fos Phenytoin)
(anti convulsant)
150 mg IV stat 1
Inj Ceftum (cefuroxime) 250 mg IV OD 1
Inj Pantocid (pantoprazole) 40 mg IV BD 1
Inj Strocit ( citicoline)
(a Neurotonics/Neurotrophics)
250 mg IV BD 1
Inj Lasix 20 mg IV Stat 1
Inj Sodium Bicarb 500 mL IV Stat 1

17. PROGNOSIS OF CASE
The Subject goes into irreversible COMA
Respiratory Depression occours ( put on mechanical ventilation)
 Sudden Cardiac Failure
 Death   