Alcohol intoxication

Methanol Poisoning

Dr N.A.Ruchira Nishshanka
MD (1st year)
Department of Agad Tantra
R.G.G.P.G. Ayurvedic College and Hospital,Paprola
 Methyl alcohol

(Carbinol, Wood Alcohol, Wood Naphtha Or Wood Spirits)

 Colorless
 Volatile liquid
 Odour similar to ethyl alcohol
 Has a burning taste
Found In

 Cleaning Materials,
 Solvents
 Paints
Varnishes
 Formaldehyde Solutions
 Antifreeze
Windshield Washer Fluid (30–40% Methanol)
 Duplicating Fluids
 Absorption and Excretion
 Inhalation, ingestion, dermal exposure or eye contact.

 Methanol poisoning is most often due to accidental or intentional

ingestions, and accidental epidemic poisonings due to distilling and
fermenting errors and beverage contamination

 Rapidly absorbed from the stomach, intestines, lungs and skin, and
achieves a maximal concentration 30–90 min after ingestion
• Once methanol enters the body, it is quickly absorbed from the gastrointestinal
tract and metabolized in the liver.

• Alcohol dehydrogenase breaks methanol down into formaldehyde which is then

further oxidized by aldehyde dehydrogenase to form formic which is metabolized
to folic acid, folinic acid, carbon dioxide and water.
 Fatal Dose : 60 to 200 ml
 Fatal Period : 24 to 36 hours ( may be delayed for 2 to 4 days)

 Signs and Symptoms of Toxicity

 Symptoms occur 12–24 h after ingestion
 But as the methanol continues to be metabolized, the levels of toxicity will
increase.
 The most common permanent health effect following severe poisoning is
blindness ( 10 to 20 ml. of methanol can cause blindness.), brain damage that
could result in difficulty walking/moving, damage to the peripheral nervous
system, and encephalopathy.
• CNS: Headache, dizziness, vertigo, restlessness, muscular weakness,
hypothermia, delirium, amnesia, convulsion (terminal event),
coma

• Ocular: Blurred or misty vision (snowfield vision), Fixed and dilated pupils,
Visual disturbances, like photophobia, blurred or misty vision
(snowfield vision), temporary or complete blindness due to optic
neuritis and atrophy from accumulation of formic acid within the
optic nerve.(10 to 20 ml. of methanol can cause blindness.)

• GIT : Nausea, vomiting, cramps in abdomen, spirit- like odor in the

nostrils and mouth, dehydration
• Renal : Acidosis, strongly acidic urine, scant urine
• RS : Dyspnea, cyanosis, respiratory depression.
 Treatments
 Keep the patient in a dark room or Eyes should be kept covered to prevent
further retinal damage Manage ABC
 Gastric lavage using 5%bicarbonate solution should be done, and 500 ml. of
this may be left in the stomach
 Oral administration of sodium bicarbonate, 2 g in 250 ml of water, 4 hourly.
 Activated charcoal - reduces the mortality significantly. It acts by reducing the
absorption of alcohol from the digestive tract, and by creating a concentration
gradient in favour of movement of alcohol and its metabolites back into the gut
 Folate therapy: Calcium folinate/leucovorin (calcium salt of folinic acid)
 Hemodialysis as soon as possible in case of severe poisoning.
 Symptomatic treatment.
Ethanol treatment
 Presence of ethanol will inhibit formation of toxic metabolites from
methanol and ethylene glycol because it has a much higher affinity for alcohol
dehydrogenase
Antidote
 4-methylpyrazole (fomepizole) is a competitive inhibitor of alcohol
dehydrogenase.28 It blocks the formation of formaldehyde and formic acid
and can be used instead of ethanol.
Dose: Loading dose of 15 mg/kg over 30 min, followed by 10 mg/kg every 12 h
for 4 doses, then 15 mg/kg every 12 h
 Postmortem Findings
External
 Signs of asphyxia with cyanosis and prominent postmortem staining are observed.
 Froth from the mouth may be seen.
 Pyridine may give the skin a purple color

Internal
 GIT: Mucous membrane of stomach and duodenum are congested and inflamed with small
hemorrhages. Small or large intestine or both are contracted resembling a thick pipe of a very narrow
lumen.
 Lungs: Congested and edematous.
 Liver: Necrobiosis and fatty change.
 Kidneys: Tubular degeneration.
 Brain: Edematous and focal hemorrhages.
 Urinary bladder: Mucosa congested.
ANALYSIS
 Methyl alcohol and formic acid are found in all organs, blood and urine.

 Formaldehyde cannot be demonstrated probably because ofthe rapidity with

which it combines with protein and its speedy oxidation to formic acid.

 Anticoagulants such as EDTA, heparin , methanarnine and formalin give a

positive test for methanol.
Cause of Death:
Death is mainly due to acidosis from production of organic acids,
and CNS depression is a minor factor
Medico legal aspects
May be used accidentally.
Intentional faulty sale.
It is used as intoxicating beverage when ethanol is not available.
Suicides & homicides may occur, but not common
Accidental poisoning may be seen in children as methanol is a
constituent of commonly available liquids.
 Methanol Poisoning: An Autopsy-Based Study at
the Tertiary Care Center of Uttarakhand, India

Vikas Vaibhav , Pawan K. Shukla , Raviprakash Meshram , Ashish R. Bhute , Abhishek Varun , Prashant Durgapal 1.
Forensic Medicine and Toxicology, All India Institute of Medical Sciences, Rishikesh, IND 2. Forensic Medicine, All
India Institute of Medical Sciences, Raipur, IND 3. Forensic Medicine, All India Institute of Medical Sciences,
Rishikesh, IND 4. Forensic Medicine, All India Institute of Medical Sciences, New Delhi, IND 5. Pathology, All India
Institute of Medical Sciences, Rishikesh, IND Corresponding author: Vikas Vaibhav, [email protected]
 Aims and objective
• This study describes postmortem and histopathological findings to
understand the internal progression of methanol poisoning.
• The study also aims to examine clinical, biochemical, and histological
changes seen with methanol poisoning.
 Materials and methods
• This study describes the methanol poisoning tragedy that occurred in February
2019 in the Haridwar district of Uttarakhand.
• It involved more than 200 people, of which 31 people died and 169 people
survived following treatment.
• Ninety-one patients were admitted to the hospital, four were brought dead, four
died within a few hours of admission (designated as early deaths), and four
died between 10 and 45 days of hospitalization (designated as late deaths).
• The deaths were divided into two categories:
 Hospital deaths (i.e., brought in alive but died during treatment; n = 8)
 Brought death (n = 4).
• A medicolegal autopsy was performed on all 12 deaths.
• Gross external and internal findings were noted, and routine viscera
and blood were preserved and sent to Uttarakhand's Forensic Science
Laboratory (FSL) to estimate methyl alcohol.
• A section of the optic nerve was taken from the optic chiasma for
histopathological examination.

Data collection
• Data were collected retrospectively; hospital records were reviewed to
obtain relevant information, including incidence history, clinical
examination, biochemical profile, treatment, and outcome.
• Relatives of the deceased who were brought dead were also
interviewed to get relevant details.
 Results
• All of the deceased were men and were of low socioeconomic status.
• Their mean age was 37.7 years (range 21-70), and 67% (n = 8) of all
victims were in the age range of 30-50 years.
• All of the deceased were brought to our center within 24 hours of
methanol ingestion.
• The average methyl alcohol level reported among hospital deaths and
brought dead was 116.08 mg/dl and 224.6 mg/dl, respectively
• Among hospital deaths, all patients were brought in a coma.
• The blurred vision had been their most common complaint, identified in
75% (n = 6), followed by vomiting and abdominal pain, while 50% (n = 4)
had features of respiratory insufficiency.
• Mean pH and bicarbonate levels among hospital deaths were 6.61 mmol/l
and 6.18 mmol/l, respectively.
• Biochemical investigations revealed features of acute renal failure among
those who died in the hospital
• The mean postmortem interval was 13.5 hours
• An autopsy revealed signs of hypoxia in all cases.
• Internal organs were congested.
• Severe metabolic acidosis leading to the respiratory failure was the cause of death in early
deaths.
• Cerebral and pulmonary edema consequent upon septicemic shock was the cause of late
deaths.
• A case with the most extended survival duration showed cerebral edema with intra cerebral
hemorrhage involving bilateral basal ganglia and the intra-thalamic region, surrounded by
necrotic tissues
• Cirrhotic liver, along with features of renal failure, was an additional internal finding in late
deaths.
• Optic nerve histopathology showed no demyelination or axonal necrosis; however, mild
edematous changes were evident.
FIGURE 1: Intracerebral hemorrhage (shown by yellow arrows) involving bilateral basal
ganglia and the intra-thalamic region surrounded by necrotic tissues seen on the sagittal
section of the cerebrum
 Discussion
• This research adds to our understanding of the acute effects of
methanol poisoning by evaluating and comparing the clinical and
autopsy profiles of deceased persons.
• The primary cause of mortality in early deaths was metabolic acidosis
leading to respiratory failure.
• Sepsis leading to multi-organ failure was the primary cause of late
deaths.
• Formic acid, the oxidation by-product of methyl alcohol, is responsible
for metabolic acidosis.
• As metabolic acidosis increases, mortality also increases
• The mean age of victims in this study was 37.7 years. Males between
30 and 50 years, belonging to low socioeconomic groups, were the
most affected
• The average methanol level among hospital and brought deaths were
116.08 mg/dl and 224.6 mg/dl, respectively. However, according to
several studies, the fatal methanol level may vary.
• The same methanol level may have a variable outcome in different
people .
• This could be attributed to a number of factors such as differences in
demographic profiles, comorbid conditions, tolerance levels, and
metabolic rates
• The most common symptoms reported by victims of methanol poisoning
are gastrointestinal , visual disturbances and neurological phenomena
• In the present study, all of the hospital deaths presented with coma.
• Cerebral and pulmonary edema were observed in all cases but were more
apparent in late deaths
• Intra cerebral hemorrhage involving basal ganglia and thalamus was
present in the longest surviving individual, while fatty changes were
evident in older victims.
• Histopathology of the optic nerve from optic chiasma showed mild
edematous changes without demyelination or axonal necrosis.
Conclusions
• Methanol poisoning is one of the manmade disasters in the developing
world.
• There are various adverse effects of different organs and organ
systems inside the body.
• Timely intervention and diagnosis can save several lives.
• The organ-directed meticulous autopsy can help autopsy surgeons in
establishing the diagnosis and thus help the judiciary in delivering
justice to the sufferers.
Thank You!