LAPORAN KASUS

Case Report: Methanol Intoxication Complicated with

Acute Pancreatitis, Alcoholic Ketoacidosis,
and Intracranial Hemorrhage
Eric Rahardi*; Putu Moda Arsana**
*Resident, **Supervisor, Endocrine and Metabolic Disease Consultant,
Department of Internal Medicine, Faculty of Medicine, Brawijaya University - Saiful Anwar General Hospital,
Malang, East Java, Indonesia

ABSTRACT
Background: Methanol intoxication occur after accidental or suicidal ingestion and the toxicity is due to the formation of formaldehyde and
formic acid. Methanol ingestion can also lead to acute pancreatitis and metabolic acidosis. Brain injury can also occur as ischemia or hemorrhage.
The report is a 23-year-old male with methanol intoxication with complications of acute pancreatitis, alcoholic ketoacidosis, and intracronial
hemorrhage.
Key words: methanol intoxication, acute pancreatitis, alcoholic ketoacidosis, intracranial hemorrhage

ABSTRAK
Intoksikasi metanol dapat disebabkan karena ketidak sengajaan atau percobaan bunuh diri; toksisitas akibat terbentuknya formaldehid dan
asam format. Metanol dalam tubuh dapat menyebabkan pankreatitis akut, asidosis metabolik dan gangguan peredaran darah otak.Laporan
kasus ini mengenai laki-laki 23 tahun dengan intoksikasi metanol disertai komplikasi pankreatitis akut, ketoasidosis alkoholik dan perdarahan
intrakranial. Eric Rahardi, Putu Moda Arsana. Laporan Kasus: Intoksikasi Metanol Disertai Komplikasi Pankreatitis Akut, Ketoasidosis
Alkoholik dan Perdarahan Intrakranial.
Kata kunci: intoksisasi metanol, pankreatitis akut, ketoasidosis alkoholik, perdarahan alkoholik

INTRODUCTION
Methanolalso referred to as methyl alcohol
is used widely in commerce and industry.
Methanol toxicity is due to the formation of
two toxic metabolites, formaldehyde and
formic acid that were well absorbed from
the gastrointestinal tract, with peak levels attained 30 to 90 min after ingestion. Most incidents of toxicity occur after oral ingestion,
but significant absorption may also occur
through lungs or skin. The serum half-life after
mild toxicity is 14 to 20 hours, increases to 24
to 30 hours in severe toxicity. Following ingestion, highest concentrations are found in the
kidney, liver, and gastrointestinal tract, also
found in the vitreous humor and optic nerve.
Most methanol (90 to 95%) is eliminated by
liver, while renal excretion accounts for 2 to 5
percent; pulmonary excretion is minimal. 1,2

Alamat korespondensi

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Methanol ingestion cause high anion gap

metabolic acidosis from the production of
formic and lactic acid and CNS disturbance
ranging from inebriation and drowsiness to
obtundation, seizure, and coma. Selective toxicity of the optic nerve and basal ganglia are
well known features. Methanol ingestion can
also lead to acute pancreatitis3.4. Acute pancreatitis is a sudden inflammation of the pancreas characterized by a discrete episode of
abdominal pain and elevated serum amylase
and lipase levels. It can have severe complications and high mortality despite treatment,
while mild cases are often successfully treated
with conservative measures.
We report a patient with methanol intoxication presented with severe high-anion-gap
acidosis metabolic and intracerebral bleeding. 5

CASE PRESENTATION
A 23 year-old male was admitted to the Emergency because of severe vomiting since 8
hours before admission accompanied with
abdominal pain that spread to the back. He
also suffered from shortness of breath since 2
hours before admission. He had suffered from
headache 1 day before admission and start
to feel nausea 12 hours before admission, followed with frequent vomiting contained residual food and fluid. (His mother said that he
vomit more than 10 times). According to his
neighbor, he had a party and drank alcohol 2
days before admission. Two of his friends have
same symptoms and died in hospital. The patient had a habit to consume alcohol since 6
years ago.
On physical examination he looked severely
ill with GCS 234, pupils were isocore with

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positive light reflex, blood pressure was 90/60,
pulse rate 120 bpm, respiratory rate 40 x / min
and axillar temperature 37.9 `C
Laboratory results showed leukocyte 35,100
u/L, Potassium 8.24 mmol/L, Blood sugar 337
mg/dl, Amylase 187 U/l, Ureum 77 mg/dl, Creatinin 2.31 mg/dl, and severe metabolic acidosis with pH 6.991, BE -24.9, anion gap 30.
The patient was transferred to ICU and rehydrated with NS 2l/hour and after the hypotension was successfully treated, insulin bolus
10u IV was given and continued with Actrapid 5U/hour. Emergency hemodialysis was
planned but refused by his family. Natrium
Bicarbonate 100 mg and Calcium gluconas
1000 mg was also slowly given intravenously
to manage the metabolic acidosis and the
hyperkalemia. Folic acid 1200 mcg, pantoprazole 30 mg and thiamine 3x200 mg was also
administered.

Figure 2 Table of The Blood Sugar

The hemodynamic condition was improved

markedly following these measures. The pH
and kalium levels were back to normal. Despite this, the patient remained unresponsive
and became unconscious. Because of the initial high level of methanol (124,3 mg/dl)) and

Figure 3 Ct Scan Result

CDK-209/ vol. 40 no. 10, th. 2013

the severity of acidosis, severe neurological

damage was to be expected.
CT scan was performed and showed 48 ml
intracerebral hemorrhage in right fronto temporo parietal lobe with perifocal edema.
Vitamin K (3x10 mg), mecobalamin (3x500mcg), and mannitol infusion 250 ml in 24 hours
was given. After 8 days in ICU, the patient
was moved to the Stroke Unit for CVA management, but his family decided to took him
home because of financial problem. He died
at home after 3 days.
DISCUSSION
Criteria for therapy initiation in patients with
known or suspected methanol poisoning:
Plasma methanol >20 mg/dL or
Recent history of methanol ingestion
in toxic amounts and an osmolar gap > 10
mOsm/L or
Suspected methanol ingestion with at
least 2 of the following: Arterial pH <7.3, Serum bicarbonate <20 mmol/L and Osmolar
gap >10 mOsm/L
The clinical features of methanol intoxication
usually present after a latent period of 12-24
hours following methanol ingestion. This latent period corresponds to the time needed
to convert methanol to formic acid by alcohol
dehydrogenase in the liver, the metabolite
responsible for the acidosis and the toxic effects. This patients had clinical symptoms 24
hours after drinking.
Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. The patient came

with hyperketonemia, high anion gap metabolic acidosis but without significant hyperglycemia.
Diagnosis is by history and findings of ketoacidosis without significant hyperglycemia. Alcoholic ketoacidosis is a metabolic complication
of alcohol use and starvation characterized by
hyperketonemia and high anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis is attributed to the
combined effects of alcohol and starvation
on glucose metabolism.
Clinical features of acute pancreatitis (abdominal pain and vomiting) together with
elevation of plasma concentrations of pancreatic enzymes (amylase, lipase) are the cornerstones of diagnosis. Pancreatic enzymes are
released into the circulation during an acute
attack; blood levels peak early, and decline
over 34 days.
Alcohol use (approximately 35%) is a major
cause of acute pancreatitis. Most commonly,
the disease develops over 5-15 years; alcoholics are usually admitted with an acute exacerbation of chronic pancreatitis. Several case
reports have described sole large alcohol load
to precipitate a first attack. This features corresponds to our patient; he had drunk alcohol
since 6 years ago and came with abdominal
pain and severe vomiting and elevated amylase.
Brain injury in methanol toxicity is characterized by lesions affecting both basal ganglia
and subcortical regions. These lesion could be
ischemic/necrosis or hemorrhage, selectively
affecting bilateral putamen. It has been suggested that the putamen is at particular risk
because of its high metabolic demand and
located in end-zone of vascular perfusion. The
precise mechanism of necrosis and hemorrhage in case of methanol toxicity remains
a matter of debate. It may represent a direct
toxic effect of methanol and its metabolite formic acid - as well as secondary injury to anoxia and acidosis. More recent study suggest
that methanol induced cerebral vasospasm as
a consequence of a large rise in intracellular
calcium. These events could play a crucial role
in methanol-induced cerebral edema, brain
ischemia/necrosis and hemorrhage. It is also
demonstrated that methanol elevates calcium ions in cerebral vascular muscle cells.

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CONCLUSION
This case is a patient with methanol intoxication presented with severe high-anion-gap
acidosis metabolic, complicated with intracerebral bleeding and acute pancreatitis. The
treatment was supportive, acidosis metabolic
correction, rapid glucose regulation with insulin. Patient was discharged because of financial problem and died at home.

Figure 4 Methanol Metabolism

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