METHANOL POISONING

METHANOL POISONING

1. DR.SHAHEER SULAIMAN 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

4. ELIMINATION 1 st 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

5. 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

6. 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

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

8. 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 .

9. 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 ,

10. 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

11. 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

12. Double gap-elevated osmolar and anion gap

13. 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

14. 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

15. 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

16. Fomepizole and ethanole inhibition of ADH

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

18. 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

19. 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 .

20. Folinic acid 50 mg IV Q4H

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