Anterior & Posterior uveitis & Endophthal mitis detailed

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anterior uveitis hypopyon keratic precipitates slit lamp

This clinical photograph shows a slit-lamp examination of the anterior segment of a human eye, focusing on the cornea. The image demonstrates a characteristic clinical finding of anterior uveitis: keratic precipitates (KP). These appear as diffuse, medium-sized, brownish-gray inflammatory cellular deposits adhered to the posterior surface of the cornea (the corneal endothelium). The precipitates are distributed across the illuminated area, contributing to visible endothelial haziness. The light reflex from the slit lamp is scattered and irregular, indicating a disruption of corneal clarity and the presence of inflammatory material. This finding is highly relevant for diagnosing intraocular inflammation and monitoring the response to therapy in conditions like viral or idiopathic uveitis.

This clinical photograph shows a slit-lamp examination of the anterior segment of a human eye, focusing on the cornea. The image demonstrates a characteristic clinical finding of anterior uveitis: keratic precipitates (KP). These appear as diffuse, medium-sized, brownish-gray inflammatory cellular deposits adhered to the posterior surface of the cornea (the corneal endothelium). The precipitates are distributed across the illuminated area, contributing to visible endothelial haziness. The light reflex from the slit lamp is scattered and irregular, indicating a disruption of corneal clarity and the presence of inflammatory material. This finding is highly relevant for diagnosing intraocular inflammation and monitoring the response to therapy in conditions like viral or idiopathic uveitis.

This clinical photograph, taken via slit lamp microscopy, displays the anterior segment of a human eye with a focus on corneal pathology. The image reveals diffuse keratic precipitates (KPs) distributed primarily across the central area of the corneal endothelium. These precipitates are characterized by a 'mutton-fat' appearance, manifesting as whitish, waxy, and irregularly shaped inflammatory deposits. Such findings are indicative of granulomatous uveitis, often associated with conditions like Cytomegalovirus (CMV) hypertensive anterior uveitis or sarcoidosis. The slit lamp beam highlights the depth of these deposits on the posterior corneal surface. Additionally, a mild inflammatory reaction is noted within the anterior chamber, though cell and flare are not individually resolvable at this magnification. This visual evidence serves as a critical diagnostic marker for differentiating types of intraocular inflammation and monitoring treatment response in patients with secondary glaucoma or viral uveitis.

This clinical photograph, taken via slit lamp microscopy, displays the anterior segment of a human eye with a focus on corneal pathology. The image reveals diffuse keratic precipitates (KPs) distributed primarily across the central area of the corneal endothelium. These precipitates are characterized by a 'mutton-fat' appearance, manifesting as whitish, waxy, and irregularly shaped inflammatory deposits. Such findings are indicative of granulomatous uveitis, often associated with conditions like Cytomegalovirus (CMV) hypertensive anterior uveitis or sarcoidosis. The slit lamp beam highlights the depth of these deposits on the posterior corneal surface. Additionally, a mild inflammatory reaction is noted within the anterior chamber, though cell and flare are not individually resolvable at this magnification. This visual evidence serves as a critical diagnostic marker for differentiating types of intraocular inflammation and monitoring treatment response in patients with secondary glaucoma or viral uveitis.

A close-up clinical photograph of the anterior segment of a human eye using slit-lamp biomicroscopy. The image demonstrates active acute granulomatous anterior uveitis. Key findings include multiple keratic precipitates (KPs) on the posterior corneal surface (retrodescemetic area), indicated by white arrows. These precipitates vary in morphology from small granular spots to larger, more opaque deposits. The distribution is localized across the lower portion of the corneal endothelium, which is characteristic of inflammatory cellular accumulation in the anterior chamber. The visual evidence of these 'mutton-fat' style precipitates serves as a hallmark for granulomatous inflammation, often associated with systemic conditions such as sarcoidosis or tuberculosis. The image also displays typical slit-lamp lighting effects, including corneal reflections and a visible beam showing the depth of the anterior chamber.

A close-up clinical photograph of the anterior segment of a human eye using slit-lamp biomicroscopy. The image demonstrates active acute granulomatous anterior uveitis. Key findings include multiple keratic precipitates (KPs) on the posterior corneal surface (retrodescemetic area), indicated by white arrows. These precipitates vary in morphology from small granular spots to larger, more opaque deposits. The distribution is localized across the lower portion of the corneal endothelium, which is characteristic of inflammatory cellular accumulation in the anterior chamber. The visual evidence of these 'mutton-fat' style precipitates serves as a hallmark for granulomatous inflammation, often associated with systemic conditions such as sarcoidosis or tuberculosis. The image also displays typical slit-lamp lighting effects, including corneal reflections and a visible beam showing the depth of the anterior chamber.

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endophthalmitis fundus vitreous inflammation

A color fundus photograph of a human eye demonstrating acute clinical features of endophthalmitis. The image shows significant vitreous haze (vitritis), which markedly reduces the clarity of the retinal details. The optic disc is visible as a yellowish-white structure, but its margins appear blurred. The retinal background exhibits a diffuse, deep reddish hue, indicative of severe inflammation and congestion. Key pathological findings include multifocal white retinal infiltrates scattered throughout the posterior pole and visible retinal hemorrhages, particularly in the superior peripheral quadrant. The retinal vasculature is partially obscured by inflammatory exudates and the hazy vitreous media. This image serves as an educational example of the funduscopic presentation of severe intraocular infection, often following penetrating trauma or surgery, where inflammatory debris prevents a sharp view of the underlying retina.

A color fundus photograph of a human eye demonstrating acute clinical features of endophthalmitis. The image shows significant vitreous haze (vitritis), which markedly reduces the clarity of the retinal details. The optic disc is visible as a yellowish-white structure, but its margins appear blurred. The retinal background exhibits a diffuse, deep reddish hue, indicative of severe inflammation and congestion. Key pathological findings include multifocal white retinal infiltrates scattered throughout the posterior pole and visible retinal hemorrhages, particularly in the superior peripheral quadrant. The retinal vasculature is partially obscured by inflammatory exudates and the hazy vitreous media. This image serves as an educational example of the funduscopic presentation of severe intraocular infection, often following penetrating trauma or surgery, where inflammatory debris prevents a sharp view of the underlying retina.

This diagnostic clinical photograph displays a fundus view of the human eye, characterized by extreme vitreous haze (Grade 4+) and reduced media clarity. The image demonstrates the classic presentation of endophthalmitis, where internal ocular inflammation severely obscures retinal landmarks. The optic disc, macula, and retinal vasculature are clinically invisible due to the dense, diffuse opacification of the vitreous humor. Scattered throughout the hazy medium are subtle, non-discrete vitreous exudates, appearing as irregular opacities that further degrade the image quality. This visual finding is a critical sign of intraocular infection or severe inflammation, often associated with a precipitous drop in visual acuity. The diagnostic image serves to illustrate the physical limitations of fundus examination in the presence of advanced vitritis, necessitating alternative diagnostic modalities like B-scan ultrasonography for assessing retinal attachment.

This diagnostic clinical photograph displays a fundus view of the human eye, characterized by extreme vitreous haze (Grade 4+) and reduced media clarity. The image demonstrates the classic presentation of endophthalmitis, where internal ocular inflammation severely obscures retinal landmarks. The optic disc, macula, and retinal vasculature are clinically invisible due to the dense, diffuse opacification of the vitreous humor. Scattered throughout the hazy medium are subtle, non-discrete vitreous exudates, appearing as irregular opacities that further degrade the image quality. This visual finding is a critical sign of intraocular infection or severe inflammation, often associated with a precipitous drop in visual acuity. The diagnostic image serves to illustrate the physical limitations of fundus examination in the presence of advanced vitritis, necessitating alternative diagnostic modalities like B-scan ultrasonography for assessing retinal attachment.

This clinical photograph is an ultra-widefield fundus image of a human left eye, illustrating features of endogenous endophthalmitis. The fundus exhibits a generalized orange-yellow hue with a hazy appearance, consistent with significant vitreous inflammation (vitritis). Multiple, small, yellowish-white, circumscribed chorioretinal lesions are scattered across the retina, primarily concentrated in the macular and peripapillary regions. Several of these lesions are specifically highlighted by black arrows, demonstrating their distinct, slightly elevated morphology. These clinical findings represent multifocal abscesses or 'puff ball' lesions, characteristic of fungal infections such as Candida albicans that have infiltrated from the choroid into the retinal layers. The image serves as an educational example for diagnosing ocular manifestations of systemic infections, particularly in patients with recent surgical or urological interventions. The visibility of the optic disc and retinal vasculature is slightly obscured by the overlying vitreous haze, emphasizing the severity of the intraocular inflammatory response.

This clinical photograph is an ultra-widefield fundus image of a human left eye, illustrating features of endogenous endophthalmitis. The fundus exhibits a generalized orange-yellow hue with a hazy appearance, consistent with significant vitreous inflammation (vitritis). Multiple, small, yellowish-white, circumscribed chorioretinal lesions are scattered across the retina, primarily concentrated in the macular and peripapillary regions. Several of these lesions are specifically highlighted by black arrows, demonstrating their distinct, slightly elevated morphology. These clinical findings represent multifocal abscesses or 'puff ball' lesions, characteristic of fungal infections such as Candida albicans that have infiltrated from the choroid into the retinal layers. The image serves as an educational example for diagnosing ocular manifestations of systemic infections, particularly in patients with recent surgical or urological interventions. The visibility of the optic disc and retinal vasculature is slightly obscured by the overlying vitreous haze, emphasizing the severity of the intraocular inflammatory response.

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posterior uveitis retinitis choroiditis fundus photograph

This clinical photograph displays a fundus examination of the peripheral retina, illustrating diagnostic signs of posterior uveitis, specifically associated with ocular toxoplasmosis. The image captures two primary pathological features: retinal vasculitis and punctate choroiditis. Retinal vasculitis is highlighted by green arrows, showing evidence of perivascular inflammation and vascular sheathing where the retinal vessels appear thickened and slightly obscured by inflammatory exudate. Multiple punctate choroiditis lesions are indicated by red arrows; these appear as small, discrete, yellowish-white, round-to-oval spots scattered predominantly across the inferior retinal periphery. The lesions are localized deep within the retina at the level of the choroid, representing focal inflammatory foci. This visual evidence supports the educational objective of identifying peripheral manifestations of panuveitis, including the secondary vascular and choroidal responses that occur alongside primary retinitis. These findings are critical for differentiating infectious etiologies like toxoplasmosis from systemic autoimmune conditions.

This clinical photograph displays a fundus examination of the peripheral retina, illustrating diagnostic signs of posterior uveitis, specifically associated with ocular toxoplasmosis. The image captures two primary pathological features: retinal vasculitis and punctate choroiditis. Retinal vasculitis is highlighted by green arrows, showing evidence of perivascular inflammation and vascular sheathing where the retinal vessels appear thickened and slightly obscured by inflammatory exudate. Multiple punctate choroiditis lesions are indicated by red arrows; these appear as small, discrete, yellowish-white, round-to-oval spots scattered predominantly across the inferior retinal periphery. The lesions are localized deep within the retina at the level of the choroid, representing focal inflammatory foci. This visual evidence supports the educational objective of identifying peripheral manifestations of panuveitis, including the secondary vascular and choroidal responses that occur alongside primary retinitis. These findings are critical for differentiating infectious etiologies like toxoplasmosis from systemic autoimmune conditions.

This fundus color photograph illustrates clinical manifestations of posterior syphilitic uveitis. The image shows widespread, small, circular, whitish-yellowish pre-retinal lesions (indicated by black arrows) scattered across the retina. These punctate lesions, sometimes referred to as pre-retinal precipitates, are seen overlying areas of active retinitis and often represent aggregates of inflammatory cells. A generalized haziness is visible across the fundus, characteristic of vitritis (inflammation of the vitreous humor), which obscures the clarity of the underlying retinal vessels and landmarks. The optic disc is visible in the nasal periphery with relatively preserved margins. This presentation is a classic hallmark of ocular syphilis, often termed 'the great mimicker,' where inflammatory cells migrate across the retina into the vitreous. This visual material serves as an educational resource for identifying inflammatory ocular phenotypes and distinguishing pre-retinal precipitates from intra-retinal foci in the context of infectious uveitis.

This fundus color photograph illustrates clinical manifestations of posterior syphilitic uveitis. The image shows widespread, small, circular, whitish-yellowish pre-retinal lesions (indicated by black arrows) scattered across the retina. These punctate lesions, sometimes referred to as pre-retinal precipitates, are seen overlying areas of active retinitis and often represent aggregates of inflammatory cells. A generalized haziness is visible across the fundus, characteristic of vitritis (inflammation of the vitreous humor), which obscures the clarity of the underlying retinal vessels and landmarks. The optic disc is visible in the nasal periphery with relatively preserved margins. This presentation is a classic hallmark of ocular syphilis, often termed 'the great mimicker,' where inflammatory cells migrate across the retina into the vitreous. This visual material serves as an educational resource for identifying inflammatory ocular phenotypes and distinguishing pre-retinal precipitates from intra-retinal foci in the context of infectious uveitis.

This clinical photograph is a fundus image of the right eye, demonstrating hallmark features of severe posterior uveitis, specifically cytomegalovirus (CMV) retinitis in an immunocompromised patient. The image shows significant optic disc pallor and generalized vitreous haze, which obscures the fine detail of the retinal vasculature. Multiple large, confluent, white-to-off-yellow granular exudates (noted by blue arrows) are visible, concentrated around the macular area and extending into the peripheral retina, consistent with active necrotizing retinitis. A distinct area of pigmentation and thinning, indicated by a yellow arrow, represents an old, atrophic choroidal scar. The presence of these chorioretinal lesions alongside the optic nerve pallor illustrates the extensive retinal destruction and secondary optic neuropathy often seen in progressive viral infections of the retina. The educational focus is on identifying active infectious lesions versus chronic scarring and assessing the degree of vitritis and optic nerve involvement in inflammatory eye disease.

This clinical photograph is a fundus image of the right eye, demonstrating hallmark features of severe posterior uveitis, specifically cytomegalovirus (CMV) retinitis in an immunocompromised patient. The image shows significant optic disc pallor and generalized vitreous haze, which obscures the fine detail of the retinal vasculature. Multiple large, confluent, white-to-off-yellow granular exudates (noted by blue arrows) are visible, concentrated around the macular area and extending into the peripheral retina, consistent with active necrotizing retinitis. A distinct area of pigmentation and thinning, indicated by a yellow arrow, represents an old, atrophic choroidal scar. The presence of these chorioretinal lesions alongside the optic nerve pallor illustrates the extensive retinal destruction and secondary optic neuropathy often seen in progressive viral infections of the retina. The educational focus is on identifying active infectious lesions versus chronic scarring and assessing the degree of vitritis and optic nerve involvement in inflammatory eye disease.

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Uveitis (Anterior & Posterior) and Endophthalmitis

Anatomical Classification of Uveitis

Uveitis is classified by the primary anatomical site of inflammation (SUN Working Group):
TypeStructures Involved
AnteriorIris, anterior ciliary body (pars plicata)
IntermediateVitreous, pars plana, peripheral retina
PosteriorRetina, choroid (behind vitreous base)
PanuveitisAll segments
Anatomical classification of uveitis
Anatomical zones of uveitis (anterior = red, intermediate = blue, posterior = green) - Kanski's Clinical Ophthalmology

PART 1: ANTERIOR UVEITIS

Definition & Epidemiology

Anterior uveitis (AU) is inflammation of the iris and/or anterior ciliary body. It is the most common form of uveitis.
  • Iritis = iris alone
  • Iridocyclitis = iris + anterior ciliary body (clinically indistinguishable from iritis)

Types

Acute AU (AAU)Chronic AU (CAU)
OnsetSuddenInsidious or acute
LateralityUsually unilateralMore often bilateral
Duration< 3 monthsPersistent; relapse < 3 months after stopping treatment
Associated systemic diseaseLess commonMore common
Granulomatous signsUncommonOften present
PrognosisGenerally goodMore variable
Recurrent = repeated episodes separated by untreated inactive periods. Remission = no visible cells for ≥ 3 months.

Aetiology & Systemic Associations

CategoryConditions
Idiopathic~50% of all cases
HLA-B27 related~20% of AAU; ankylosing spondylitis (25% develop AU), reactive arthritis, psoriatic arthritis, IBD-related arthritis
InfectiousVZV (herpes zoster ophthalmicus), HSV, CMV, TB, syphilis, Lyme disease
Non-infectiousJIA, sarcoidosis, Behçet disease, SLE, MS, TINU syndrome, drug-induced
MasqueradeLymphoma, anterior segment melanoma, juvenile xanthogranuloma
Pathophysiology: Interleukin-6 (released by monocytes/macrophages) plays a key role in the aberrant immune response. In HLA-B27 associated cases, cross-reactivity with microbial antigens in genetically predisposed individuals is proposed. HLA-B27 is present in 50% of AAU patients with no systemic disease and 90% with associated spondyloarthropathy.

Clinical Features

Symptoms

  • Rapid-onset unilateral pain, photophobia, redness, watery discharge, visual blur
  • Often preceded by mild discomfort for a few days
  • CAU may be asymptomatic until complications develop (cataract)
  • History of prior episodes is common (recurrent AAU)

Signs

1. Ciliary injection (ciliary flush) Circumcorneal conjunctival hyperaemia with a violaceous (purplish) hue - due to deep vessel involvement. Typically absent in some forms of CAU.
2. Miosis Pupillary sphincter spasm - predisposes to posterior synechiae (PS) formation.
3. Anterior Chamber Cells (most reliable indicator of activity) Graded per SUN Working Group by cell count in a 1 mm × 1 mm slit beam:
GradeCells in 1×1 mm field
0< 1
0.5+1-5
1+6-15
2+16-25
3+26-50
4+> 50
Cells also appear in anterior vitreous. Swept-source anterior segment OCT can detect individual cells.
4. Aqueous Flare Haziness from protein leakage (blood-aqueous barrier breakdown). Now considered indicative of active inflammation in most cases even at low grades - associated with higher complication risk. Graded clinically by degree of interference with iris/lens visualization; laser flare photometry gives objective measurement.
5. Hypopyon Whitish purulent layer of inflammatory cells settling inferiorly in the AC under gravity. Common in HLA-B27-associated AAU (also seen in Behçet disease, infective endophthalmitis).
6. Keratic Precipitates (KP) Inflammatory cell deposits on the corneal endothelium:
  • Usually in Arlt's triangle (inferior, triangular distribution, apex up)
  • Non-granulomatous (AAU): small, fine KPs
  • Granulomatous (CAU): medium-to-large "mutton-fat" KPs (large, greasy, composed of epithelioid and multinucleated cells)
  • Fuchs uveitis syndrome: diffusely distributed, stellate/filamentous ("stellate KPs")
  • Old KPs: pigmented or "ground-glass" appearance
Keratic precipitates - slit lamp
Keratic precipitates on the corneal endothelium in anterior uveitis
Mutton-fat KPs in granulomatous uveitis
Large "mutton-fat" KPs indicating granulomatous uveitis (associated with sarcoidosis or CMV)
7. Fibrinous Exudate Common in severe AAU, especially HLA-B27-related.
8. Iris Nodules
  • Busacca nodules: in iris stroma - granulomatous uveitis
  • Koeppe nodules: at pupillary margin - site of PS formation
  • Roseolae (syphilis), iris crystals/Russell bodies (chronic uveitis, Fuchs syndrome)
9. Posterior Synechiae (PS) Inflammatory adhesions between pupil margin and anterior lens capsule. Prevent with cycloplegics. Can progress to seclusio pupillae (360° synechiae) → iris bombé → secondary angle-closure glaucoma.
10. Iris Atrophy
  • Diffuse stromal atrophy: Fuchs uveitis syndrome
  • Patchy/sectoral: herpetic uveitis (HSV and VZV)
11. Iris Neovascularization (Rubeosis Iridis) Can occur in chronic inflammation; common in Fuchs syndrome but without synechial angle closure.
12. Secondary Glaucoma
  • AAU: usually normal/low IOP (ciliary shutdown) but can rise via trabecular obstruction by inflammatory cells, trabeculitis
  • CAU: trabecular scarring/sclerosis, synechial angle closure - more sustained elevation

Investigations

Not routinely required for:
  • Single, mild-moderate, non-granulomatous AAU with no systemic features
  • Systemic diagnosis already confirmed
  • Typical features of a specific entity (e.g. Fuchs syndrome)
Investigations warranted for:
  • Recurrent, severe, or bilateral AAU
  • Persistent/chronic AU resistant to treatment
  • Granulomatous signs
  • Associated intermediate/posterior uveitis
  • Ocular/systemic features suggesting underlying disease
Key tests:
  • HLA-B27 tissue typing (chromosome 6, MHC; present in 6-8% of White population; strongly associated with AAU, AS, reactive arthritis, psoriatic arthritis)
  • ACE, chest X-ray/CT (sarcoidosis)
  • VDRL/TPHA (syphilis)
  • Mantoux/IGRA (TB)
  • ANA, anti-dsDNA (SLE)
  • RF, ANA (JIA in children)
  • FBC, ESR, CRP

Treatment

1. Topical Corticosteroids (mainstay of AAU treatment)

Prednisolone acetate 1% or dexamethasone. Typical tapering regimen:
  • Hourly × 3 days → every 2 hours × 3 days → QID × 1 week → TDS × 1 week → BD × 1 week → OD × 1 week (total ~5-6 weeks)
  • CAU: aim for complete suppression (zero cells AND flare); more gradual taper + maintenance
Complications of topical steroids: steroid-induced IOP elevation ("steroid responders"), cataract, secondary bacterial/fungal infection, HSV keratitis recurrence.

2. Cycloplegic Agents

Prevent PS, break fresh synechiae, relieve ciliary/pupillary spasm:
  • Cyclopentolate (12-24 h duration)
  • Homatropine (3 days)
  • Atropine (7-10 days)
  • Phenylephrine 2.5% or 10% (supplementary, to break PS)
  • Mydricaine No. 2 (subconjunctival injection of adrenaline + atropine + procaine): for fresh PS resistant to drops

3. Periocular / Intravitreal Steroids

For severe or refractory cases. Injections into sub-Tenon space or intravitreal depot.

4. Systemic Therapy

Oral corticosteroids: 10-35 mg prednisone/day for moderate-severe or bilateral cases
Steroid-sparing immunosuppressives (supervised by uveitis specialist, after excluding active TB, checking haematological/renal/hepatic function):
ClassDrugs
AntimetabolitesMethotrexate, mycophenolate mofetil, azathioprine
Calcineurin inhibitorsCyclosporin A, tacrolimus (T-cell critical uveitis: VKH, birdshot)
Alkylating agentsCyclophosphamide, chlorambucil
Anti-TNF biologicsInfliximab, adalimumab, etanercept, golimumab, certolizumab (effective in neutrophil/macrophage-critical: Behçet, sarcoidosis)
IL-6 inhibitorsTocilizumab
Anti-CD20Rituximab (B-cell critical, e.g. ANCA+ scleritis)
Goal of therapy: steroid-free remission. Biologics (adalimumab/infliximab) have improved outcomes in vision-threatening chronic uveitis. Anti-TNF monotherapy or combination with azathioprine carries small but significant lymphoma risk.

PART 2: POSTERIOR UVEITIS

Definition

Posterior uveitis encompasses retinitis, choroiditis, and retinal vasculitis. Often there is combined involvement:
  • Retinochoroiditis (originates in retina, extends to choroid)
  • Chorioretinitis (originates in choroid, extends to retina)

Clinical Presentation

Symptoms depend on lesion location:
  • Peripheral lesion → floaters
  • Macular lesion → impaired central vision
  • Vitritis can accompany any form and causes diffuse visual haziness

Patterns of Inflammation

Retinitis

  • Focal, multifocal, geographic, or diffuse
  • Active: whitish retinal opacities with indistinct borders (surrounding oedema)
  • Resolving: borders become better defined, lesion scars

Choroiditis

  • Focal, multifocal, geographic, or diffuse
  • Does not usually cause vitritis without concurrent retinal involvement
  • Active: round, yellow nodule in the choroid

Retinal Vasculitis

  • Primary or secondary (adjacent to retinitis focus)
  • Venous involvement (periphlebitis) more common than arterial (periarteritis)
  • Active: yellowish/grey-white patchy perivascular cuffing, sometimes with haemorrhage
  • Quiescent: perivascular scarring (do not mistake for active disease)
Posterior uveitis - retinitis, choroiditis, vasculitis
(A) Retinitis with indistinct whitish opacities; (B) active choroiditis yellow nodule; (C) retinal vasculitis with perivascular cuffing - Kanski's Clinical Ophthalmology
Toxoplasmosis retinitis with vasculitis
Peripheral retina: retinal vasculitis (green arrows) and punctate choroiditis lesions (red arrows) in toxoplasmosis

Important Causes of Posterior Uveitis

InfectiousNon-infectious
Toxoplasmosis (most common infectious cause worldwide)Sarcoidosis
CMV retinitis (immunocompromised, HIV)Birdshot retinochoroidopathy (HLA-A29)
HSV/VZV acute retinal necrosis (ARN)Serpiginous choroidopathy
TuberculosisVogt-Koyanagi-Harada (VKH) syndrome
Ocular histoplasmosis (OHS)Sympathetic ophthalmia
ToxocariasisMultifocal choroiditis and panuveitis (MCP)
SyphilisPunctate inner choroidopathy (PIC)
Candida (endogenous)MEWDS, APMPPE, AZOOR

Investigations (Multimodal Imaging)

Fundus autofluorescence (FAF):
  • Detects lipofuscin/melanin in RPE cells
  • Hyperfluorescence in: MEWDS, serpiginous choroidopathy, AZOOR
Optical coherence tomography (OCT):
  • Macular oedema, vitreomacular disease, structural damage
  • Inner retinal infiltrates: Behçet disease, viral infections
  • Outer retinal changes: PIC, MEWDS, APMPPE, serpiginous choroiditis
  • Choroidal granulomas: sarcoidosis, TB, VKH
Fluorescein Angiography (FA):
  • Active inflammatory retinal foci: early hypofluorescence → late hyperfluorescence
  • Retinal vasculitis, optic disc swelling, subretinal fluid
  • "Window defect" (RPE loss) vs. masking (pigment clumping)
Indocyanine green angiography (ICGA):
  • Investigation of choice for predominantly choroidal inflammation
  • Choriocapillaris inflammation: patchy hypofluorescent areas (APMPPE, serpiginous)
  • Stromal choroiditis: focal hypofluorescence → late diffuse hyperfluorescence (VKH, sympathetic ophthalmia)
Investigations not generally required when:
  • A compatible systemic diagnosis is already confirmed
  • Obvious clinical pattern suggests specific entity

Treatment

Follows same principles as anterior uveitis. Choice of systemic immunosuppression guided by underlying immunology:
  • T-cell critical uveitis (VKH, birdshot retinochoroidopathy): calcineurin inhibitors (cyclosporin, tacrolimus)
  • Neutrophil/macrophage critical uveitis (Behçet, sarcoidosis): anti-TNF agents (infliximab, adalimumab)
  • B-cell critical (scleritis with ANCA+): rituximab
  • Infectious causes require specific antimicrobial therapy first (e.g. pyrimethamine + sulfadiazine + folinic acid for toxoplasmosis; ganciclovir for CMV; aciclovir for HSV/VZV ARN)

PART 3: ENDOPHTHALMITIS

Definition

Endophthalmitis is extensive inflammation of the internal ocular tissues (vitreous and/or aqueous chambers), most commonly from infection. It is one of the most serious, vision-threatening ophthalmic emergencies.

Classification by Route of Entry

TypeRouteCommon Causes
Exogenous (post-surgical)Breach in eye wall post-opStaph. epidermidis, Staph. aureus, Strep. sp., gram-negatives
Exogenous (post-traumatic)Penetrating injuryBacillus cereus, gram-negatives (often virulent, rapid)
Bleb-relatedInfected filtering blebStreptococcus sp., Haemophilus influenzae, Staph. sp.
Endogenous (metastatic)Haematogenous spreadCandida (IVDA, immunocompromised), Klebsiella (diabetics, East Asia), Aspergillus
Incidence of post-cataract endophthalmitis: ~<0.03%

Common Organisms

VirulenceOrganismsCourse
HighToxin-producing gram-positives (Strep. sp., Staph. aureus), gram-negatives (Pseudomonas, Bacillus cereus)Rapidly destructive
Low (indolent)Propionibacterium acnes, Staph. epidermidisInsidious, chronic, less destructive

Clinical Features

Symptoms:
  • Rapid decrease in vision (often the first symptom)
  • Ocular pain (follows visual loss)
  • Redness, photophobia, lid swelling
Signs (in order of severity):
  • Anterior uveitis (AC cells and flare) - often the first sign on slit lamp
  • Hypopyon (whitish inferior AC level) - substantial in endophthalmitis
  • Vitritis/vitreous exudate - impairment of red reflex
  • White/milky vitreous opacity (vitreous abscess in severe cases)
  • Chemosis and periorbital oedema
  • In bleb-related: white milky bleb + severe injection
  • Corneal oedema
Post-surgical (post-cataract) endophthalmitis typically presents 1-7 days post-op with rapid deterioration.
Bleb-related endophthalmitis is clinically distinct: white milky bleb (similar to blebitis but more severe), substantial hypopyon, vitritis, and impaired red reflex.

Diagnosis

Vitreous tap (vitreous aspirate) - gold standard:
  • Gram stain + culture + sensitivity
  • Vitreous culture is more sensitive than aqueous alone
  • Anterior chamber tap (aqueous aspirate) also performed
B-scan ultrasound:
  • Performed when media opacification prevents fundal view
  • Shows vitreous echoes (inflammatory exudate) and helps assess retinal detachment

Treatment

1. Intravitreal Antibiotics (immediate, cornerstone of treatment)

Standard regimen:
  • Vancomycin 1 mg/0.1 mL (gram-positive cover) +
  • Ceftazidime 2-2.25 mg/0.1 mL (gram-negative cover)
  • Both injected simultaneously into the vitreous cavity
Repeat intravitreal antibiotics after 48 hours if no improvement.
For bleb-related endophthalmitis: ceftazidime 2 mg/0.1 mL + vancomycin 2 mg/0.1 mL intravitreal.
Note: Systemic antibiotics are generally NOT effective (poor intraocular penetration) except for fluoroquinolones.

2. Topical Antibiotics

For cases with associated corneal involvement (e.g. corneal ulcer). Started simultaneously.

3. Corticosteroids

  • Topical steroids started 48 hours after intravitreal antibiotics (not immediately)
  • Intravitreal dexamethasone 400 mcg may be given with antibiotics in some regimens
  • Oral prednisolone as adjunct

4. Oral Fluoroquinolones

Moxifloxacin or ciprofloxacin for 10-14 days (achieves reasonable intraocular levels).

5. Pars Plana Vitrectomy (PPV)

Endophthalmitis Vitrectomy Study (EVS) guidelines (post-cataract):
  • Immediate vitrectomy is superior to vitreous tap alone when presenting visual acuity = light perception (LP) or worse
  • When vision is better than LP, vitreous tap + intravitreal antibiotics gives equivalent results
Indications for PPV in clinical practice:
  • Vision LP or worse
  • No improvement after 48 hours of intravitreal antibiotics
  • Bleb-related endophthalmitis (PPV considered at 48 hours)
  • Fungal endophthalmitis
  • Dense vitreous opacity / inability to visualize retina
PPV reduces microbial + inflammatory debris burden and allows treatment of concurrent vitreoretinal pathology (e.g. retinal detachment).

6. Antifungals (for fungal endophthalmitis)

  • Systemic: voriconazole or amphotericin B (systemic and intravitreal)
  • Intravitreal: amphotericin B 5-10 mcg/0.1 mL

Special Case: Bleb-Related Endophthalmitis

Organisms are significantly more virulent than post-cataract cases → very poor outcome even with early treatment (blindness/eye loss). Aggressive regimen immediately:
  1. Vitreous + aqueous samples obtained immediately
  2. Intravitreal vancomycin 2 mg + ceftazidime 2 mg
  3. Repeat at 48 hours; consider PPV
  4. Oral fluoroquinolones 10-14 days
  5. Topical steroids after 48 hours

Prophylaxis Against Endophthalmitis

  • Preoperative povidone-iodine (5%) instillation to conjunctival sac
  • Perioperative topical antibiotics
  • Intracameral antibiotic injection (e.g. cefuroxime) at end of cataract surgery - most effective prophylactic measure
Endophthalmitis - vitreous haze and retinal infiltrates
Endophthalmitis: vitreous haze with multifocal white retinal infiltrates and haemorrhages
Fungal endogenous endophthalmitis
Endogenous Candida endophthalmitis: vitritis + multifocal yellowish-white chorioretinal "puff ball" lesions

Quick Comparison: Uveitis vs. Endophthalmitis

FeatureAnterior UveitisPosterior UveitisEndophthalmitis
Primary locationAnterior chamberRetina/choroidVitreous + AC
PainModerateVariable (often painless)Severe
Vision lossMild-moderateCentral if macula involvedRapid, severe
CellsAC cells + flareVitreous cells, retinal lesionsAC + vitritis + hypopyon
Red reflexUsually preservedUsually preservedImpaired/absent
KPsYesNoCan be present
HypopyonHLA-B27, BehçetRareProminent
AetiologyImmune/infectiousImmune/infectiousAlmost always infectious
UrgencyUrgent (same day)UrgentOphthalmic emergency
Core treatmentTopical steroids + cycloplegicsSystemic immunosuppression / antimicrobialsIntravitreal antibiotics ± PPV

Sources:
  • [Kanski's Clinical Ophthalmology, 10th ed.](Kanski's Clinical Ophthalmology, ch. 12 - Uveitis) - primary reference throughout
  • [Goldman-Cecil Medicine, International Ed.](Goldman-Cecil Medicine, Vol. 2, Ch. 391 & 457) - systemic associations and endophthalmitis management
  • Robbins & Cotran Pathologic Basis of Disease - pathological basis
  • Tintinalli's Emergency Medicine - emergency management principles
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