The Atypical Presentation of Methanol Poisoning, and its subsequent treatment

1
The Atypical Presentationof Methanol
Poisoning, and its subsequent treatment

• Chris Reeves

Dept. of Clinical Biochemistry Metabolic
Medicine, Royal Liverpool University Hospital
2
Methanol Poisoning

• Common industrial solvent,
• antifreeze fluid, screenwash, varnishes
• Less potent than ethanol (EtOH),
• but does cause intoxication
• Mechanism of toxicity
• Relatively non-toxic before metabolic activation
  
• to its metabolites - Formaldehyde
• Formic Acid

3
Methanol Poisoning

• Clinical Features
• Drowsiness, nausea vomiting, abdo pain,
• ocular injury (blurred vision)
• gt blindness, convulsions, pancreatitis,
• respiratory failure, coma
• Laboratory Features
• Severe metabolic acidosis
• High anion gap
• High osmolal gap

4
Atypical Case Study

• Presentation 0830h
• 28 year old male
• Presented at AE
• Methanol ingestion
• History
• Lots of alcohol the night before, very drunk
• At 7am accidentally drank ½ pint from water
  bottle containing pure methanol
• Felt unwell, nausea, blurred vision, abdo
  discomfort
• Occasional Smoker Occasional Alcohol

5
Initial Biochemistry _at_ 1000h

• Na 137
• K 4.0
• Cl 101
• HCO3 27
• Urea 3.6
• Creat 102
• A.Gap 13
• Osmo 335
• (measured)

Alb 46 Prot 84 Glob 38 ALP 81 Bili
20 ALT 18 GGT 23
Glucose 6.0 Ethanol lt 2.2 Amylase
87
pH 7.38 H ion 42 pCO2 5.7 pO2
12.2 Std.HCO3 24.0 BE -0.8
(FiO2 21)
Osmo (calculated) 284 ? Osmolal Gap 51
6

• Initial Treatment
• 1L N. Saline
• 200ml oral EtOH (whisky) loading dose
• 20ml/h oral maintenance dose

1330h Methanol levels from Aintree 38.5
mmol/L (1230 mg/L)
7
Treatment Protocol
Methanol gt6 mmol/L (200 mg/L) Ethanol
Methanol gt16 mmol/L (500 mg/L) Haemodialysis

• Ethanol Therapy
• 30 ml/h when not on HD
• 60 ml/h when on HD
• Aim for level of 22 44 mmol/L
• Continue until MeOH lt 1.6 mmolL (lt50 mg/L)

National Poisons Information Service - Toxbase
(www.spib.axl.co.uk )
8
Metabolism of Alcohols
Ethanol
Methanol
Ethylene Glycol
Alcohol Dehydrogenase
Glycoaldehyde (CNS effects)
Acetaldehyde (hangover, flushing)
Formaldehyde (blindness, cerebral oedema)
Aldehyde Dehydrogenase
Glycolic Acid (metabolic acidosis)
Formic Acid (metabolic acidosis)
Acetic Acid
CO2 H20
Lactate dehydrogenase or glycolic acid oxidase
Glycoxylate (lactic acidosis)
Lactate dehydrogenase or aldehyde oxidase
Oxalate (cerebral renal damage,
hypocalcaemia)
9
Its an alcohol dehydrogenase inhibitor Dr Lewis !
Whats Fomepizole Dr Carter?
10
Effectiveness of Dual Therapy
11
Methanol half-life during ethanol administration

• MeOH t½ during
• EtOH monotherapy 43.1h (30.3-52.0)
• EtOH HD 3.5h
• dual therapy
• EtOH monotherapy greatly increased MeOH t½

Palatnick et al. Methanol half-life during
ethanol administration. Ann Emerg Med 1995 26
202-207
12
Formate kinetics in methanol poisoning

• Formate t½ during
• EtOH/Fomepizole 6.04 3.26h
• monotherapy
• EtOH/Fomepizole 1.80 0.78h
• HD dual therapy
• (Endogenous clearance 2.5-20h)

Hantson et al. Formate kinetics in methanol
poisoning. Hum Exp Toxicol 2005 24 55-59
13
Outcome

• After 3 days transferred off ITU
• Underwent reviewed by Ophthalmology
• Biochemistry ABGs remained unchanged and
  unremarkable from admission
• Discharged 6 days after admission

14
Summary

• Correct selection/interpretation of biochemical
  tests
• Enable rapid diagnosis and Rx
• Demonstrated graphically the mechanism and
  effectiveness of dual therapy

15
Summary

• Main Laboratory Features
• Severe metabolic acidosis
• High osmolal gap
• High anion gap
• However
• Early Raised OG Normal AG
• Late Normal OG Raised AG

16
Acknowledgements

• Mr Frank Tames _at_ UHA

17
(No Transcript)
18
Effectiveness of Dual Therapy