METHANOL POISONING

1. D R . S H A H E E R S U L A I M A N C
METHANOL POISONING

2. METHANOL
 clear,
 volatile,
 colorless,
 slightly sweet-tasting alcohol at room temperature
 Methanol is commonly found in windshield wiping
fluid, antifreeze(particularly brake line antifreeze),
embalming fluid, and fuel for camp stoves.

3. METABOLISM
 Absorbtion
GI Tract:rapidly
half life:5 minutes
peak concetration reach in 30 to 60 min
Lungs
transdermal

5.  ELIMINATION
 1st order kinetics in very low conc.
 half life-2 to 3 hour
 In poisoned patient-Zero order kinetics
 Half life 24 hour
 By ADH inhibition half life become 50 hours
 Formic acid :half life is nearly 20 hours

6.  Formic acid + Fe inhibit mitochondrial
cytochrome oxidase interfere with oxidative
metabolism lactic acidosis ,tissue hypoxia
and inhibition of intracellular respiration
 Formic acid formate + H+
 Decreasing pH promotes formic acid diffusion across
cell membranes, in particular to the central nervous
system

7.  Formic acid uniquely targets the optic disk of the
retina and retrolaminar optic nerve, potentially due
to the high amount of blood and cerebrospinal fluid
(CSF) flow through the choriocapillaris.
 These cells are more susceptible to cellular hypoxia
due to low levels of mitochondria and cytochrome
oxidase

9. CINICAL FEATURES
GI TRACT
 Abdominal discomfort
 Vomiting
 Acute pancreatitis
 Hemorrhagic gastritis
CNS
 Slurred speech
 Ataxia
 Confusion
 CNS depression

10.  VISUAL
 seeing spots with blurred
 altered visual fields,
 blindness.
 Visual disturbances occur in 30% to 70% of patients.
Early ophthalmologic findings
 reduced pupillary response to light
 hyperemia of the optic disc.
 Peripapillary retinal edema
 loss of optic disk cupping follow and often leads to
decreased visual fields and central scotomata.
 Retinal dysfunction can be reversible.
 Optic atrophy and optic neuropathy suggest a poor
prognosis for visual recovery.

11.  CVS:
 Tachycardia
 rarely have significant cardiac dysrhythmias
 As acidosis progresses, a compensatory tachypnea develops.
 shock, seizures, myoglobinuria and rhabdomyolysis have
been reported.
 Death typically results from respiratory failure and sudden
respiratory arrest, with cerebral edema and multiorgan
failure.
 Prognosis after methanol ingestion correlates with the
degree of acidosis, time to presentation, and initiation of
treatment.
 The strongest predictor of morbidity and mortality
is the degree of acidosis,

12.  Patients that survive the acute toxicity of methanol
can have permanent complications, including
blindness and neurologic deficits.
 A Parkinson-like extrapyramidal syndrome, with
bradykinesia, tremor, and dementia, can occur.
 necrosis of the putamen and subcortical white matter
 polyneuropathy, encephalopathy, ataxia, and
cognitive deficits

13. DIAGNOSIS
ABG
 High anion gap metabolic acidosis and an elevated
osmolar gap
 Due to the latency period of methanol metabolism, a
normal anion gap does not exclude methanol
ingestion.
 AG = [Na+ ]− ([HCO3− ]+[Cl− ])
 Decreased albumin can falsely elevate the AG;
 AG corrected = AG+ (2.5×[4.4 −measured serum
albumin- figge equations

14. Double gap-elevated osmolar and anion gap

15.  CT/MRI-for altered mental status patients
 Bilateral necrosis of putamen
 Non specific
Blood methanol level
 peak methanol concentrations greater than 50
mg/dL indicate significant and serious exposure
fundoscopy

16. MANAGEMENT
 correction of acidosis,
 inhibition of the production of toxic metabolites
 elimination of the parent alcohol and its toxic
metabolites
 GI decontamination has limited to no value.
 Bicarbonate
 treat a serum pH less than 7.3 with intravenous
(IV)sodium bicarbonate

17.  Bicarbonate can be administered via intermittent
boluses, combination of a bolus and infusion, or
infusion alone, based on the severity of symptoms
 Administer bolus sodium bicarbonate at 1 to 2
mEq/kg and infuse 150 mEq/L of sodium
bicarbonate in 5% dextrose at 1.5 to 2 times the
maintenance fluid rate

18.  Fomepizole and ethanole
inhibition of ADH

19. Side effect
Headache
Nausea
Dizziness
Phlebitis
Reversible liver transaminase elevation

20. Ethanol
 maintain serum ethanol concentrations between 100 and
150 mg/dL.
 The affinity of ADH for ethanol is 10 times greater than
for methanol
 worsening CNS and respiratory depression, with
hypotension, vomiting, phlebitis, and hypoglycemia
 Patients who present early after methanol ingestion
without acidosis can potentially be treated with ADH
inhibition alone

21. Hemodialysis
 acidosis (pH < 7.3),
 renal failure,
 vision abnormalities with methanol exposure,
 electrolyte imbalances unresponsive to conventional
therapy (ie, hyperkalemia),
 Hemodynamic instability,
 methanol or EG concentration more than 50 md/dL
 Traditional endpoints for discontinuing HD or ADH
inhibition are a normal acid-base status and methanol-
EG concentration less than 20 mg/dL.

22. Folinic acid
 50 mg IV Q4H

23. THANK YOU