(BMJ)—A 3-year-old boy with acute respiratory distress was admitted to the pediatric ward. He had hx of extreme prematurity, quadriplegic cerebral palsy, global developmental delay, and a ventriculoperitoneal (VP) shunt on the L side for obstructive hydrocephalus from grade 4 intraventricular hemorrhage. The patient also had retinopathy and chronic lung disease. He was treated with albuterol and ipratropium bromide nebulization but later required IV albuterol (up to 2 µg/kg/min), aminophylline (1 mg/kg/hour), and hydrocortisone. He was irritable on baseline motor exam and had no ptosis. R pupil: 3 mm, sluggish; L pupil: 6 mm, with no reaction to light. Head CT showed no new abnormality. What’s the dx?
Postsurgical mydriasis
Pharmacological mydriasis
Physiological anisocoria
Oculomotor nerve paralysis
VP shunt malfunction
You are correct. Once ipratropium bromide reaches the cornea, it acts like atropine and produces a parasympatholytic effect. It blocks muscarinic acetylcholine receptors, resulting in paralysis of sphincter pupillae, and inhibits the ciliary muscles. This leads to mydriasis, a fixed dilated pupil, and when one side is affected, it leads to anisocoria (unequal pupils).

Few cases of ipratropium bromide–induced pharmacological anisocoria have been reported in children. Anisocoria may be physiological (simple) or secondary to eye conditions such as postocular trauma/eye surgery or oculomotor nerve paralysis. More importantly, anisocoria may be a sign of a potentially life-threatening condition from raised ICP, secondary to intracranial space–occupying lesion, intracranial hemorrhage, traumatic brain injury, meningoencephalitis, or blocked VP shunt, as was the concern in this child prior to head CT. Physiological anisocoria with pupillary inequality of >0.4 mm is present in around 20% of normal people.

BMJ Case Reports CP 2020;13:e237257