Mechanism of Aqueous Misdirection Syndrome
Aqueous misdirection (malignant glaucoma) results from posterior misdirection of aqueous humor into or behind the vitreous cavity, creating a ciliovitreal block that prevents normal anterior flow of aqueous through the pupil. 1, 2
Pathophysiologic Mechanism
The fundamental problem is abnormal aqueous flow posteriorly rather than anteriorly, which occurs through the following mechanism:
- Ciliolenticular or ciliovitreal block develops when aqueous humor becomes trapped posterior to the lens-iris diaphragm or within/behind the vitreous gel 1, 2
- This posterior misdirection causes the entire lens-iris diaphragm to shift forward, resulting in axial (central and peripheral) shallowing of the anterior chamber 1, 3
- The forward displacement occurs despite a patent peripheral iridotomy, distinguishing this from pupillary block glaucoma 1, 3
- Intraocular pressure typically elevates due to impaired aqueous outflow, though it may occasionally be normal 1
Anatomic Predisposition in Hyperopic Eyes
Middle-aged hyperopic adults are particularly susceptible due to specific anatomic features:
- Shorter axial length creates crowded anterior segment anatomy 4
- Thicker crystalline lens with age further reduces available space 4
- Anteriorly positioned ciliary body and reduced ciliary sulcus space facilitate abnormal aqueous flow patterns 4
- These eyes may have nanophthalmic features (axial length <20mm, high hyperopia, small corneal diameter <11mm), which significantly increases risk 4
Mechanism After Incisional Glaucoma Surgery
Following glaucoma surgery, several factors contribute to aqueous misdirection:
- Surgical disruption of normal anatomic relationships between lens, vitreous, and ciliary body 3
- Inflammation and ciliary body edema alter aqueous production and flow dynamics 4
- Vitreous expansion or anterior hyaloid face integrity creates a barrier preventing anterior aqueous movement 2, 5
- In eyes with intact anterior hyaloid, aqueous becomes trapped in the vitreous cavity rather than flowing forward 5
- Zonular fiber pathways may allow inappropriate fluid movement posteriorly, particularly in hyperopic eyes with already compromised anterior segment space 2
Clinical Recognition
The diagnosis requires recognizing this constellation:
- Axial anterior chamber flattening (both central and peripheral) 1, 3
- Patent peripheral iridotomy confirmed on examination 1, 3
- Absence of choroidal effusion or hemorrhage on B-scan ultrasonography 3
- Elevated or normal IOP with forward lens-iris diaphragm displacement 1
Critical Distinction from Other Mechanisms
This "pushing mechanism" differs fundamentally from:
- Pupillary block (relieved by iridotomy) 4
- Plateau iris (anteriorly rotated ciliary processes without vitreous involvement) 4
- Choroidal effusion (visible fluid collections posteriorly) 4
The key pathophysiologic insight is that aqueous humor bypasses its normal anterior route and becomes sequestered posteriorly, creating a vicious cycle of anterior chamber collapse and continued posterior misdirection that is refractory to conventional glaucoma treatments 1, 2.