Phacolytic uveitis is a type of lens-induced uveitis (LIU). It occurs when lens proteins (mainly cortical components) leak into the aqueous humor due to spontaneous rupture of a hypermature cataract, residual cortex after cataract surgery, or lens capsule damage from ocular trauma, leading to breakdown of immune tolerance and intraocular inflammation.
It typically presents unilaterally with ciliary injection, keratic precipitates, anterior chamber and vitreous opacities, and often elevated intraocular pressure. It is classified as non-infectious uveitis.
The AAO Adult Cataract PPP (2021) specifies that cataract surgery is indicated when the lens causes inflammation and secondary glaucoma (phacolytic, lens particle, or phacoantigenic) 2).
Lens-induced uveitis is classified into the following three types based on the pathogenic mechanism.
| Type | Mechanism | Nature of Inflammation | Main Cause |
|---|---|---|---|
| Phacolytic uveitis (this disease) | Macrophage phagocytosis of lens protein | Non-granulomatous to mild granulomatous | Hypermature cataract, residual cortex after surgery, trauma |
| Phacoanaphylactic uveitis | Type III allergy to lens protein | Strongly granulomatous | Trauma, post-surgery |
| Inflammation due to retained lens material | Direct reaction to retained lens material | Acute inflammation | After cataract surgery |
Phacolytic glaucoma is a different clinical phenotype of the same pathophysiological mechanism. Macrophages that have phagocytosed lens proteins obstruct the trabecular meshwork, impairing aqueous humor outflow. When inflammatory findings are prominent, it is called uveitis; when elevated intraocular pressure is the main feature with few inflammatory findings, it is called glaucoma. However, both may coexist 1).
There are no clear data on prevalence or incidence. It is classified as non-infectious uveitis. It occurs unilaterally with no sex predilection. When caused by spontaneous lens dissolution, it is mainly seen in elderly individuals 1). Risk factors include hypermature cataracts, ocular trauma, and retained lens cortex after cataract surgery.
They are essentially the same pathological mechanism. Macrophages that have phagocytosed lens proteins obstruct the trabecular meshwork. When inflammatory findings are prominent, it is called uveitis; when elevated intraocular pressure is the main feature with little inflammation, it is called glaucoma. The two can coexist.
After cataract surgery or trauma (with large amount of residual lens material)
Severe inflammation occurs 2–3 days after surgery.
Ciliary injection, keratic precipitates (mutton-fat KP), and anterior chamber and vitreous opacity appear.
Ocular hypertension due to fibrin exudation and posterior synechiae are observed.
When inflammation is severe, vitreous opacity occurs.
Persistent cases (late-onset postoperative)
It develops as chronic iridocyclitis occurring some time after surgery.
Ciliary injection, mutton-fat keratic precipitates, and persistent anterior chamber and vitreous opacity are present.
Sometimes accompanied by elevated intraocular pressure.
Spontaneous Capsular Rupture in Hypermature Cataract
Flashing substances (macrophages phagocytosing lens proteins) are observed in the anterior chamber.
Presents with sudden eye pain, redness, and high intraocular pressure with corneal edema.
The presence of elevated intraocular pressure despite a deep anterior chamber is important for differentiation from acute angle-closure glaucoma.
Sometimes hypopyon is observed.
In a representative case from the Japanese Society for Ocular Inflammation Uveitis Clinical Practice Guidelines (2019), an 81-year-old female presented with marked conjunctival and ciliary injection, anterior chamber opacity, hypopyon, and inability to visualize the intraocular structures. B-mode ultrasound revealed faint opacities in the anterior vitreous1).
Against a background of hypermature cataract, the anterior chamber shows shimmering opacities (macrophages phagocytosing lens proteins), accompanied by mutton-fat keratic precipitates and elevated intraocular pressure. The presence of elevated intraocular pressure despite a deep anterior chamber is important for differentiating from acute angle-closure glaucoma.
The direct cause is leakage of lens proteins into the aqueous humor due to disruption of the lens capsule. Immune tolerance breaks down, and macrophages massively phagocytose lens proteins, circulating in the anterior chamber.
There are no established diagnostic criteria1). If there is traumatic rupture of the lens capsule or a large amount of residual cortex after cataract surgery, and onset occurs within days to weeks postoperatively, this condition is highly likely. Diagnosis can be made if the presence of residual lens material is evident1).
It is important to observe exposure of lens material into the anterior chamber and vitreous cavity1).
| Differential Diagnosis | Key Points for Differentiation |
|---|---|
| Post-cataract surgery infectious endophthalmitis | When residual lens material is scarce. Differentiate by bacterial culture and PCR. |
| Delayed bacterial endophthalmitis (e.g., P. acnes) | Onset weeks to months after surgery. White plaque on the lens capsule. |
| TASS | Onset within 24 hours post-surgery. Non-infectious, diffuse corneal edema. |
| Lens-induced uveitis | Type III allergic mechanism. More severe granulomatous inflammation. Prominent mutton-fat KP. |
| Sympathetic ophthalmia | Late-onset, bilateral. Exudative retinal detachment in the fundus. |
Differentiation based solely on clinical findings is often difficult. Bacteriological tests (culture, PCR) of aqueous humor or vitreous fluid and histopathological detection of lens components are used for differentiation. However, even if bacteria are not detected, infection cannot be completely ruled out, and comprehensive judgment is necessary.
Early diagnosis and initiation of treatment are most important.
If a large amount of lens material remains, surgical removal is essential and the most effective treatment.
| Residual lens amount | Treatment strategy | Surgical method |
|---|---|---|
| Large amount | Surgical removal → postoperative steroid eye drops | PEA or ICCE ± anterior vitrectomy |
| Small amount (expect spontaneous absorption) | Steroid eye drops + intraocular pressure-lowering drugs + mydriatics → observation | Surgery if ineffective |
| Very small amount | May heal with observation alone | — |
| With elevated intraocular pressure | Beta-blocker + carbonic anhydrase inhibitor ± anterior chamber irrigation | Lens removal is definitive treatment |
Medications for drug therapy:
If the lens material is small and spontaneous absorption is expected, observation with steroid eye drops and intraocular pressure-lowering medications may be possible, but if a large amount remains, surgical removal is the definitive treatment. Long-term steroid use is not recommended; if the effect is insufficient, consider surgery promptly.
Lens proteins are normally enclosed within the lens capsule and exist as “sequestered antigens” that do not come into contact with the immune system. When the lens capsule is damaged (due to trauma, surgery, or spontaneous rupture in hypermature cataracts), lens proteins leak into the aqueous humor, triggering inflammation through the following mechanisms.
Pathogenesis:
Dual mechanism of intraocular pressure elevation:
Pathophysiological differences between phacolytic uveitis and phacoanaphylactic uveitis5):
Differentiation from sympathetic ophthalmia1): Lens-induced uveitis is unilateral and rarely causes exudative retinal detachment in the fundus.
Prognosis and course:
Macrophages that have phagocytosed lens proteins, or the high-molecular-weight soluble lens proteins themselves, obstruct the trabecular meshwork (the drainage pathway for aqueous humor), impeding aqueous outflow and causing an increase in intraocular pressure.
