Question
A male labourer aged 27 years was brought to the emergency department with signs and symptoms of rapid and shallow breathing, headache, vertigo, severe abdominal pain, dyspnea, motor incoordination, and slurred speech. He had a history of consuming illicit liquor 8 hours before he was brought to the emergency department. He was conscious and complained of blurred vision, fatigue and palpitation. On examination, he was found to have moderate retinal edema and blurring of the disc without any change in the fields of vision. (
- (a) What could the features of the patient be suggestive of. ( 2 mark(s)
- (b) Drugs to be given for this patient with rationale for use for each one. ( 5 mark(s)
- (c) Describe drug dependence and outline the management of Alcohol dependence. ( 4 mark(s)
- (d) Describe general measures in poisoning. 4 mark(s)
Answer
a) Suggested diagnosis Methanol (methyl alcohol) poisoning — history of illicit liquor ingestion (a common source of adulterant methanol), the latent interval before symptom onset (methanol itself is not directly toxic; its metabolites are), metabolic-acidosis-pattern symptoms (headache, abdominal pain, dyspnea/rapid breathing — compensatory for acidosis), CNS depression (vertigo, incoordination, slurred speech), and the classic ocular finding — retinal edema and disc blurring without visual field change — reflecting formic acid’s specific toxicity to the retina/optic nerve.
b) Drugs, with rationale
- Ethanol (or Fomepizole, where available) — methanol is metabolized by alcohol dehydrogenase to formaldehyde and then formic acid, the toxic metabolites responsible for the acidosis and retinal damage. Ethanol has much higher affinity for alcohol dehydrogenase than methanol, competitively blocking methanol’s conversion to its toxic metabolites; fomepizole directly inhibits the same enzyme without ethanol’s own intoxicating effects.
- Sodium bicarbonate — corrects the severe metabolic acidosis caused by formic acid accumulation.
- Folinic acid — enhances the enzymatic conversion of formic acid to less toxic, excretable metabolites, accelerating its clearance.
- Hemodialysis — removes both unmetabolized methanol and toxic formic acid directly, indicated in severe poisoning/significant acidosis.
c) Drug dependence and management of alcohol dependence Drug dependence is a state characterized by compulsive drug-seeking and use, tolerance (need for increasing doses for the same effect), and a withdrawal syndrome on cessation — encompassing both physical dependence (physiological adaptation, objective withdrawal signs) and psychological dependence (craving, compulsive use despite harm).
Management of alcohol dependence:
- Acute withdrawal: benzodiazepines (Diazepam/Lorazepam) to prevent/treat withdrawal seizures and delirium tremens; thiamine supplementation (prevents Wernicke’s encephalopathy).
- Relapse prevention/maintenance: Disulfiram (inhibits aldehyde dehydrogenase, causing an aversive acetaldehyde-accumulation reaction on alcohol intake), Naltrexone (opioid receptor antagonist, reduces alcohol’s rewarding effect/craving), Acamprosate (modulates glutamate/GABA, reduces craving).
- Psychosocial support/counseling alongside pharmacotherapy.
d) General measures in poisoning
- Remove the patient from ongoing exposure; maintain airway, breathing, circulation as first priority.
- Gastric decontamination if appropriate and within the window (activated charcoal, gastric lavage) — though of limited value for already-absorbed methanol at this stage.
- Supportive care — IV fluids, correction of electrolyte/acid-base disturbance, monitoring of vitals and organ function.
- Enhance elimination where applicable (hemodialysis, forced diuresis, urinary alkalinization depending on the poison).
- Specific antidote administration where one exists.
- Continuous monitoring for complications and, where relevant, psychiatric/social evaluation once medically stable.