DISEASES OF THE

ANTERIOR CHAMBER
MIKAH CHIMANGO TCHALE
PRIMARY ANGLE CLOSURE
GLAUCOMA
Elevated IOP or signs suggestive of intermittent
trabecular meshwork obstruction with glaucomatous
optic neuropathy
Types
Acute Angle-closure Glaucoma
Subacute Angle-closure Glaucoma
Chronic Angle-closure Glaucoma
ETIOLOGY OR MECHANISM
Lens-induced iridotrabecular contact
Lens size that is relatively large → iridocorneal angle
narrowing & intermittent/chronic iridotrabecular contact →
trabecular meshwork dysfunction
Decreased aqueous outflow → ↑ IOP & glaucomatous optic
neuropathy
Pupillary block
Acute lens-iris apposition
Aqueous sequestration in the posterior chamber
Anterior bowing of the iris
360˚ occlusion of the trabecular meshwork
RISK FACTORS
Older patients > 60 years
Female gender
Asians & Eskimos
Hyperopia
Nanophthalmos
AC depth < 2.5mm
Thicker lens
Lens subluxation
PRIMARY ACUTE ANGLE-CLOSURE GLAUCOMA (PAACG)
SYMPTOMS
Pain
Red eye
Photophobia
Decreased/blurred vision
Halos around lights
Headache
Nausea & emesis
SIGNS
Decreased VA *
Increased IOP *
Ciliary injection
Corneal edema *
AC cells & flare
Shallow AC & narrow angle *
Mid-dilated non-reactive pupil *
Iris bombe
Mid-dilated irregular pupil
PAS
Anterior subcapsular lens opacities
EVALUATION
Complete ophthalmic history and eye exam → pupils,
cornea, tonometry, AC, Gonioscopy, iris, lens and
ophthalmoscopy
Check visual fields
MANAGEMENT
Systemic acetazolamide, Diamox 500mg STAT then bid
Topical therapy
Topical beta blockers e.g. Timolol 0.5% q15 mins x 2 days then Bid
Topical prostaglandin analogues e.g. Xalatan 0.005%
Topical steroids e.g. Pred. acetate 1% QID
 Topical miotics e.g. Pilocarpine 1%-2% x 1 initially, then QID if
effective
Not effective if IOP > 40mmHg
Laser peripheral iridotomy (LPI)
SECONDARY ANGLE-CLOSURE
GLAUCOMA
Acute or chronic angle-closure glaucoma caused by a
variety of ocular disorders
Types
Acute Angle-closure Glaucoma
Chronic Angle-closure Glaucoma
SECONDARY ANGLE-CLOSURE GLAUCOMA
SYMPTOMS
Same as 1˚ AACG
SIGNS
Decreased VA
Increased IOP
Ciliary injection
AC cells & flare
Shallow AC & narrow angles
Mid-dilated non-reactive pupil
Iris bombe
Signs of underlying etiology
EVALUATION
Same as AACG
MANAGEMENT
Treat underlying etiology
LPI for definitive or suspected pupillary block
Topical cycloplegic e.g. Atropine 1% BD
May require pars plana vitrectomy & lens extraction
Topical steroids
Treat the increased IOP
HYPHEMA
Blood in the AC
Hyphema forms a layer of blood
Microhyphema cant be visualised with naked eye, but
with slit lamp → RBCs floating in the AC
CAUSES
Trauma (most common) → 60% have angle recession
Neovascularisation of the iris or angle
Iris lesions
Malpositioned or loose IOL
SYMPTOMS
Decreased vision
May have pain
Photophobia
Red eye
SIGNS
Normal/decreased VA
RBCs in the AC (layer/clot)
May have subconj. Hemorrhage
Increased IOP
Rubeosis
Iris sphincter tears
Deep AC
Angle recession
EVALUATION
Complete ophthalmic hx & eye exam with attention to
cornea, tonometry, AC, Iris & Ophthalmoscopy
B-scan ultrasonography to rule out open globe if unable
to visualise fundus
Lab tests → sickle cell prep & haemoglobin
electrophoresis to rule out sickle cell disease
MANAGEMENT
Topical steroids e.g. Dexa 0.1% q1h initially, then taper over
3-4 weeks as hyphema resolves
Topical cycloplegic e.g. Atropine1% BD
May require treatment of increased IOP
May require AC washout for
Corneal blood staining
Uncontrolled elevated IOP
Persistent clot
rebleed
General instructions to patient
Avoid aspirin-containing products
Sleep with head of bed elevated at 30 ˚ angle
Protect the eye with metal shield at all times
Remain on bed rest
ENDOPHTHALMITIS
Intraocular infection localised or involving anterior and
posterior segments
Can be acute, subacute or chronic
ETIOLOGY
Postoperative (70%)
Acute postoperative (<6 weeks after surgery)
94% gram tve bacteria & 6% gram –ve bacteria
Delayed postoperative (>6 weeks after surgery)
Propionibacterium Acnes
Staphylococci
Fungi → Aspergillus & Candida
 Conjunctival filtering bleb associated
 Streptococcus, staphylococci, H. Influenzae
Post-traumatic (20%)
Bacillus
Staphylococcus
Gram –ve organisms
 Endogenous (2-15%)
Rare
Usually fungal
Bacterial endogenous → S. aureus & Gram –ve bacteria
Occurs in debilitated, septicemic or immunocompromised pxs,
especially after surgical procedures
RISK FACTORS
After cataract surgery → <0.1%
Loss of vitreous
Poor wound closure
Disrupted posterior capsule
Prolonged surgery
 Penetrating trauma → 4%-13%
High as 30% after injuries in rural setting
SYMPTOMS
Pain
Photophobia
Red eye
Decreased vision
May be asymptomatic
Chronic uveitis appearance in delayed onset &
endogenous cases
SIGNS
Decreased VA
Lid edema
Proptosis
Conjunctival injection
Chemosis
Wound abscess
AC cells & flare
Corneal edema
Hypopyon
Poor red reflex
KPs
Vitritis
May have tve Seidel test
EVALUATION
Complete ophthalmic hx with attention to surgery and
trauma
Complete eye exam → VA, conjunctiva, sclera, cornea,
tonometry, AC, vitreous cells, red reflex &
ophthalmoscopy
Seidel test to rule out wound leak or open globe
B-scan ultrasonography if unable to visualise fundus
Lab tests: STAT evaluation of intraocular fluid cultures &
smears
Medical consultation for endogenous endophthalmitis
TREATMENT OF ACUTE POSTOPERATIVE ENDOPHTHALMITIS
If vision is better than LP, then AC & vitreous tap to
collect specimens for culture & Intravitreal antibiotics
If vision is LP only, then AC tap, pars plana vitrectomy &
Intravitreal antibiotics → vitreoretinal specialist
Intravitreal antibiotics ± steroids
Vancomycin 1mg/0.1ml or Ceftazidime 2.25mg.0.1ml
Dexamethasone 0.4mg/0.1ml → controversial
Subconjunctival antibiotics ± steroids
Vancomycin 25mg or Gentamicin 20mg
Dexamethasone 12-24mg
 Topical broad-spectrum fortified antibiotics
 Topical steroids e.g. Dexa 0.1% q1-2h initially
 Cycloplegic agent e.g. Atropine 1% tds
 Systemic IV antibiotics
Marked inflammation, severe cases, rapid onset
Controversial → EVS found no benefit with systemic antibiotics
ANTERIOR UVEITIS
Inflammation of the anterior uvea
Anterior uvea → iris & ciliary body
Exudation of WBCs & protein into the AC 2˚ breakdown
of the blood-aqueous barrier
Increased vascular permeability
TYPES
Iritis → inflammation of iris
Cyclitis → inflammation of pars plicata of ciliary body
Iridocyclitis → inflammation of iris & pars plicata of ciliary
body
ETIOLOGY
Mostly idiopathic or isolated with HLA-B27
Trauma
Infection
Malignancy
Medications
INFECTIOUS ANTERIOR UVEITIS
Cytomegalovirus (CMV)
Ebola virus disease
Herpes simplex & HZO
Lyme disease
Syphilis
Tuberculosis
NON-INFECTIOUS ANTERIOR UVEITIS
Non-granulomatous
Ankylosing spondylitis *
Reiter’s syndrome (Reactive Arthritis) *
Inflammatory Bowel Disease *
Psoriatic Arthritis
Whipple’s Disease
Juvenile Rheumatoid Arthritis *
Granulomatous
Sarcoidosis
Multiple sclerosis
Behcet’s disease
Sjogren's syndrome
SYMPTOMS
Pain
Tearing
Photophobia
Red eye
May have decreased vision
SIGNS
Normal or decreased VA
Ciliary injection
Miosis
Posterior synechiae
AC cells & flare
Aqueous cells
Early feature
Grading ????
Aqueous flare
Due to leakage of protein particles into AH from damaged blood
vessels
Marked in non-granulomatous uveitis
Minimal in granulomatous uveitis
Grading
Grade 0 → no aqueous flare
Grade 1 → just detectable
Grade 2 → moderate flare with clear iris details
Grade 3 → marked flare (iris details not clear)
Grade 4 → intense flare (fixed coagulated aqueous with fibrin
Keratic precipitates (KPs)
Mutton fat KPs
Occur in granulomatous anterior uveitis
Composed of epitheliod cells & macrophages
Large, thick, fluffy KPs with grey or waxy appearance
Small & medium KPs (Granular KPs)
Occur in non-granulomatous uveitis
Composed of lymphocytes
Small, discrete, dirty white KPs
Red KPs
Seen in haemorrhagic uveitis
Formed in addition to inflammatory cells
RBCs take part in composition
Old KPs
Sign of healed uveitis
Shrink, fade, pigmented & irregular in shape
Old mutton fat KPs → ground glass appearance
Decreased corneal sensation
Usually decreased IOP in early stages
Iris nodules
Typically occur in granulomatous uveitis
Koeppe’s nodules
Situated at pupillary border; may initiate posterior synechiae
Busacca’s nodules
Situated near the collarrete
Large but less common than Koeppe’s nodules
EVALUATION
Complete case history
Past ocular hx of herpetic keratitis & trauma
Past medical hx of collagen vascular disease, autoimmune
disorders & infections
Medications
Diet → consumption of raw or poorly cooked meat
Social hx → unprotected sex, IV drug use
Other exposures → cats & dogs, individuals with infectious
disease e.g. TB, Syphilis
Complete eye exam → corneal sensation, character &
location of KPs, tonometry, pupils, AC, iris (nodules &
atrophy), vitreous cells & ophthalmoscopy
Lab testing
Purpose
Eliminate a dx
Rule out systemic infections that cause uveitis
Confirm diagnosis
General principles
Defer testing if 1st episode of mild, unilateral, nongranulomatous
uveitis not associated with systemic sxs or signs
Defer testing if the cause is known e.g. trauma
Testing should be done if uveitis become more severe, bilateral,
diffuse or new sxs or signs appear
 MANAGEMENT
Primary goals
i. Immobilise the iris & ciliary body to decrease pain &
prevent exacerbation of the condition
ii. Quell the inflammatory response
iii. Identify the underlying cause
Cycloplegia is crucial step in addressing the 1st goal
Topical cycloplegic agents e.g. Atropine 1% BD
Cyclopentolate is not potent to achieve cycloplegia in the
inflamed eye → should be avoided
Topical steroids are used to address ocular inflammatory
response
Gold standard for uveitis mgmt. → Pred. Acetate 1%
In severe cases, steroids applied q15 to 30 mins, however,
steroids should be instilled q3-4hrs initially
Unresponsive cases to conventional therapy, consider
Injectable Periocular or intraocular or oral steroids
Oral NSAIDs
Systemic immunosuppressants

 Comanagement with rheumatologist or internist

CLINICAL PEARLS
Cases of acute anterior uveitis 2˚ to blunt ocular trauma
generally resolve without incident & don’t recur
Comprehensive, dilated fundus evaluation is mandatory
in all cases of uveitis
When in doubt regarding the potency or frequency of
topical steroids, it is usually better to overtreat than to
undertreat
Cases of uveitis 2˚ to infections or autoimmune diseases,
often require months of therapy, & some individuals may
need to use topical steroids indefinitely to control the
inflammation
Clinicians who are uncomfortable with such long-term
management are advised to refer pxs to a clinician with
experience in treating uveitis.
HYPOTONY
Low IOP ≤5 mmHg

ETIOLOGY
Increased outflow → excessive drainage of aqueous &
vitreous fluid
Trauma
Surgery → wound leak, bleb over filtration
Choroidal effusion
Retinal detachment
Decreased production → ciliary body shutdown
Uveitis
Medications causing ciliary body toxicity → Mannitol,
anaesthetic agents
Ocular ischemic syndrome
Phthisis bulbi
Systemic diseases → bilateral hypotony e.g. dehydration,
ketoacidosis, uraemia
SYMPTOMS
Asymptomatic
May have pain & decreased vision
SIGNS
Normal or decreased VA
Low IOP
May have hyperopic shift
Corneal folds & edema
Positive seidel test
AC cells & flare
Shallow AC
Cataract
Structural & functional changes in the posterior segment
EVALUATION
Complete case hx → trauma, surgery, medication,
systemic conditions
Complete eye exam → cornea, tonometry, AC,
ophthalmoscopy
Seidel test to rule out open globe or wound leak in
traumatic or postsurgical cases
B-scan ultrasonography if unable to visualise the fundus
MANAGEMENT
Treat underlying etiology
Topical cycloplegic e.g. Cyclopentolate 1% or Atropine
1% BD to TID
Topical antibiotics QID for wound leak
Topical & systemic steroids, especially uveitis cases
Contact lens or patch pressure for small wound leaks
Surgical procedures
HYPOPYON
Layer of WBCs in the AC
Pseudohypopyon → layer of other cells in the AC
including pigment cells, ghost cells, tumour cells or
macrophages
Etiology
Inflammation → uveitis
Infections → corneal ulcer, endophthalmitis
SYMPTOMS
Pain
Red eye
Decreased vision
SIGNS
Normal or decreased VA
Conjunctival injection
WBCs in the AC
AC cells & flare
Any other signs of the underlying etiology
EVALUATION
Complete case hx
Complete eye exam → sclera, cornea, tonometry, AC,
iris, lens & ophthalmoscopy
Lab tests → cultures & smears for corneal ulcer or
endophthalmitis
MANAGEMENT
Treat underlying etiology
Monitor treatment response by hypopyon resorption