Which of the following can cause mydriasis, except: Anticholinergics, Cocaine, Amphetamine, or Organophosphate (OP)?

Organophosphates Cause Miosis, Not Mydriasis

Among the listed substances, organophosphate is the only one that typically causes miosis (pupillary constriction) rather than mydriasis (pupillary dilation).

Mechanism of Action and Pupillary Effects

Substances Causing Mydriasis:

1. Anticholinergics

   • Block muscarinic acetylcholine receptors in the iris sphincter muscle
   • Prevent pupillary constriction, resulting in mydriasis 1
   • Examples include atropine, glycopyrrolate, and other antimuscarinic agents

2. Cocaine

   • Blocks reuptake of norepinephrine at sympathetic nerve terminals
   • Increases sympathetic stimulation to the iris dilator muscle
   • Produces mydriasis as a characteristic finding 2

3. Amphetamine

   • Increases release of norepinephrine and other catecholamines
   • Enhances sympathetic stimulation to the iris dilator muscle
   • Results in pupillary dilation

Organophosphate Effects on Pupils:

• Organophosphates cause miosis (pupillary constriction)
• Mechanism: Inhibit acetylcholinesterase, leading to excess acetylcholine at muscarinic receptors 3, 4
• The parasympathetic excess results in characteristic miosis, not mydriasis
• This is part of the classic "SLUDGE" syndrome (Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis) 4

Clinical Manifestations of Organophosphate Poisoning

Organophosphate toxicity presents with two distinct sets of effects:

1. Muscarinic Effects (Parasympathetic Excess):

   • Miosis (pupillary constriction) - key distinguishing feature
   • Bradycardia
   • Bronchospasm and bronchorrhea
   • Hypersalivation
   • Lacrimation
   • Urination and defecation
   • Vomiting and diarrhea 3, 4

2. Nicotinic Effects:

   • Can occasionally cause mydriasis in some cases (paradoxical effect)
   • Tachycardia
   • Fasciculations progressing to muscle weakness and paralysis
   • Hypertension 3

Important Clinical Considerations

• While organophosphates predominantly cause miosis, some mixed presentations can occur:

  • In severe poisoning, nicotinic effects may sometimes predominate
  • Mixed poisonings (e.g., organophosphate with pyrethroid) may show variable pupillary responses 5

• Atropine is the primary antidote for organophosphate poisoning:

  • Blocks muscarinic effects including miosis
  • Converts the miotic pupil to a mydriatic one during treatment 6
  • Does not reverse nicotinic effects like muscle weakness 3

• Oximes (e.g., pralidoxime) are used to reactivate acetylcholinesterase:

  • Most effective when administered early before "aging" occurs
  • Help reverse nicotinic effects 3, 4

Remember that pupillary examination is a crucial diagnostic tool in toxicology, and understanding the expected pupillary response can help differentiate between various toxidromes.