Teaching case. A six-year-old, "left amblyopia 20/200", glasses +0.75 OU, fundus "quiet" on a quick examination with a direct ophthalmoscope. The patch was worn for a year without change. On review — a relative afferent pupillary defect (RAPD) on the left and segmental disc pallor. A year was lost to a label.
PPP: the diagnosis requires an acuity deficit and a probable cause. Amblyopia without strabismus, unequal refractive error, media opacity or a structural abnormality is rare. If there is no obvious cause — a thorough search for an alternative.
RAPD is no longer a new term here (Lesson 1.5), but in the clinic it is easy to "not do" it. The swinging flashlight compares the afferent limb of the two eyes: light on the intact eye constricts both pupils; moving it to the affected eye makes both dilate, even though the light was not removed, only moved to the other eye. This is not "the pupil moves poorly" as an oculomotor sign, nor a consequence of low acuity as such. Amblyopia with a quiet disc and an intact retina does not, as a rule, produce an RAPD of a degree that would explain 20/200. If there is an RAPD — look for the optic nerve, severe retinal disease, compression, rather than doubling the patching.
What should alarm you more than "it just isn't responding to treatment".
- RAPD. Look for the optic nerve, severe retinal disease; do not escalate occlusion as the only response.
- Sudden loss of vision in a schoolchild. Amblyopia is a developmental disorder, not a vascular catastrophe. "Suddenly can't see" is not a reason to intensify patching.
- Nystagmus not explained by early bilateral deprivation.
- Visual fields that do not fit "just low acuity".
- Absence of an amblyogenic factor on repeat cycloplegia.
- A paradox: very poor acuity with tiny anisometropia and no tropia.
- Systemic red flags: neurological symptoms, prematurity with severe ROP, a family history of hereditary dystrophies.
Subtle organic disease that the PPP itself writes into the amblyopia discussion: disc hypoplasia, myelinated nerve fibres, macular traction after ROP, uveitis. Here both layers are possible: structure plus amblyopia. You treat what is plastic, without promising to lift the structural ceiling. The reverse also occurs: subtle, unrecognised retinal or optic nerve anomalies contribute to the reduction on top of strabismic or anisometropic amblyopia.
A practical rule for revising the diagnosis. If after optics and adequate occlusion/atropine with confirmed adherence there is no shift — not "another 6 hours", but fundus again, pupils again, cycloplegia again, readiness for imaging. The PPP table for adjusting treatment states separately: if treatment is unsuccessful because of underlying pathology (the example in the table is optic nerve hypoplasia), therapy is reduced or stopped.
Another mask is incorrectly measured acuity. Crowding, peeking, latent nystagmus under opaque occlusion, refusal of the patch, the "wrong" set of pictures. Before declaring resistant amblyopia, re-measure acuity with a protocol that holds up against adjacent symbols.
The boundary of the diagnostic module. The course does not make you a neurologist and does not set out an MRI protocol. It makes an ophthalmologist who does not start occlusion until the factor and the acuity have been named, and who is able to say "this may not be amblyopia".
A summary of the examination plan — in a form you can take into the clinic:
- History and risk factors.
- Brückner before mydriasis.
- Stereopsis / Worth before dissociation.
- Alignment and motility before cycloplegia.
- Acuity with crowding, monocular, with correction.
- Pupils, anterior segment, external examination (ptosis, axis).
- Cycloplegic retinoscopy.
- Fundus.
- Diagnosis only with factor plus deficit; otherwise — search for an alternative.
- Only then — the conversation about treatment.