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Anterior uveitis
Dr. Komala
Senior resident
Ophthalmology
DEFINITION:-
The inflammation of uveal tract.
Classification-
■ I. ANATOMICAL CLASSIFICATION
■ II. CLINICAL CLASSIFICATION
■ III. ETIOLOGICAL CLASSIFICATION
■ IV. PATHOLOGICAL CLASSIFICATION
A. Anatomical Classification –
(IUSG) International Uveitis Study
Group
■ 1) Anterior Uveitis – Inflammation of iris
and anterior part of ciliary body.
■ 2) Intermediate Uveitis – Involvement of
posterior part of ciliary body and extreme
periphery of retina. (Pars planitis)
■ 3) Posterior uveitis – Retinochoroiditis,
choroiditis, retinitis, chorioretinitis
■ 4) Diffuse or pan uveitis – Involvement of
entire uveal tract
B. Clinical Classification -
■ 1) Acute – sudden symptomatic onset.
Persists for 3 weeks or less.
■ 2) Chronic – Frequently insidious and
asymptomatic. Persists for months or
years.
■ 3) Recurrent
C. Etiological Classification
One of the most difficult problems in ophthalmology.
In most of the cases, probably, allergy is the cause.
■ 1) Exogenous-
Introduction of organism into the eye through a
perforating wound or ulcer.
■ 2) Secondary infection-
Due to direct spread from adjoining structures-
■ Cornea
■ Sclera
■ Retina
3) Endogenous
4) Allergic inflammation: Result of an antigen-antibody
reaction occurring in the eye due to previous
sensitization of uveal tissue to some allergen. The
allergen is a foreign protein.
■ Most of the cases of iridocyclitis do not have any
specific cause and are probably allergic in nature.
5) Auto-immune -
Immune disorders
e.g. rheumatoid arthritis, SLE, ankylosing spondylitis,
Reiter’s syndrome, Behcet’s Syndrome.
Granulomatous Non-
granulomatous
1. Aetiology Organismal
invasion
Antigen-antibody
reaction
2. Course
a) Onset Insidious Acute
b) Duration Chronic Short
c) Inflammation Moderate Severe
D. Pathological Classification
Granulomatous Non-
granulomatous
3. Pathology
a) Lesion Circumscribed Diffuse
b) Iris Focal reaction Diffuse reaction
c) Keratic
precipitates
Mutton fat Fine plenty
d) Iris adhesions Coarse, few,
thick
Fine, plenty, thin
4.
Investigations
May be positive Negative
PATHOLOGY AND
CLINICAL SIGNS-
Inflammation of iris and ciliary body
Dilatation of blood vessels
Iris stromal edema.
SIGNS - Iris pattern altered.Iris colour
altered. Iris thickened.Also
accompanied by, ciliary congestion,
conjunctival hyperaemia and chemosis
of conjunctiva.
SIGNS –
■ Iris pattern and colour altered.
■ Iris thickened accompanied by, ciliary
congestion, conjunctival hyperaemia
and chemosis of conjunctiva.
Exudation of fibrin-rich fluid and
inflammatory cells in the tissues
Exudates escape into anterior chamber
■ Plasmoid aqueous
■ SIGNS - Aqueous flare (like the beam
of projector in smokey theatre)
Nutrition of corneal endothelium is
affected due to toxins
Corneal endothelium becomes sticky
and edematous
Cells desquamated at places
SIGN – Keratic precipitates
Inflammatory cells stick to endothelial
layer as cellular deposits .
In very intense cases, polymorphs pour
out to sink to bottom of anterior
chamber
SIGN – Hypopyon
Exudates cover the iris as a thin film and
spread over pupillary area
SIGN – Irritation of iris musculature
constrictor being more powerful than
dilator, spasm results in miosis.
If exudate is profuse
SIGN – Plastic iritis
Blockage of pupil
SIGN – impairment of sight.
In early stages, there is adhesion of iris to lens capsule
(Atropine may free the iris)
SIGN – Spots of exudate or pigment derived from posterior
layer of iris left permanently upon anterior capsule of
lens (valuable evidence of previous iritis)
Later on, the organization of the adhesion leads to formation of
fibrous bands between pupillary margin of iris and lens capsule
(atropine cannot rupture them)
SIGN – Posterior synechiae (more in lower part of pupil
due to effect of gravity)
When adhesions are localized and a
mydriatic is instilled, it causes
intervening portions of circle of pupil to
dilate.
SIGN– Festooned pupil
(due to irregular dilatation
and is a sign of present or
past iritis.)
Pigment epithelium on
posterior surface is pulled
around pupillary margin so
that patches of pigment on
anterior surface of iris are
seen.
SIGN – Ectropion of
uveal pigment (due to
contraction of
organizing exudates
upon iris)
With recurrent attacks or severe cases, the
whole circle of pupillary margin gets tied
to lens capsule.
SIGNS – Annular or ring synechiae or
Seclusio pupillae
Collection of aqueous behind iris since
aqueous drainage is hampered.
Iris is hence bowed forwards like sail.
SIGN – Iris Bombe (anterior chamber is
funnel shaped i.e. deepest in centre,
shallowest at periphery)
As iris bulges forward and comes into contact with
cornea
Adhesions of iris to cornea at periphery develop
SIGNS – Peripheral anterior synechiae
Obliteration of filtration angle (Hypertensive
iridocyclitis)
SIGNS – Rise in IOP (secondary glaucoma)
When exudate is more extensive
Organization of exudate across entire pupillary
area
Film of opaque fibrous tissue in pupillary area
SIGNS – Occlusio pupillae or Blocked
pupil
Exudates fill up posterior chamber if there is
much of cyclitis
When these adhesions organize, the iris
adheres to lens capsule.
SIGNS – Total posterior synechiae
When these adhesions organize, the iris
adheres to lens capsule.
SIGNS – Total posterior synechiae
Retraction of peripheral part of iris
Anterior chamber is abnormally deep at
periphery
In worst cases of plastic iridocyclitis
Cyclitic membrane formed
behind lens
Finally, degenerative
changes in ciliary body
Vitreous becomes fluid
Nutrition of lens impaired
SIGNS – Complicated
cataract
Phthisis bulbi will be the
eventuality.
In final stages, there is
interference with
secretion of aqueous
Fall in IOP
Eye shrinks (development
of soft eye is an
ominous sign)
SIGNS – Phthisis bulbi
Clinical Features
SYMPTOMS
■ Pain
■ Diminished vision
■ Redness of eye
■ lacrimation
■ photophobia
SIGNS
■ Signs of vascular
congestion
■ Signs of exudation
■ Signs of pupillary
changes
Clinical Features
SIGNS
■ Lid oedema
■ Circumcorneal congestion
■ Corneal signs
■ Anterior chamber signs
■ Iris signs
■ Pupillary signs
■ Lenticular changes
■ Changes in the vitreous
Clinical Features
SIGNS
■ Corneal signs
Corneal oedema
Keratic precipitates (KPs)
Mutton fat, granular, red & old KPs
Posterior corneal opacity
Clinical Features
SIGNS
■ Anterior chamber signs
■ 1. Aqueous cells. It is an early feature of
iridocyclitis.
■ – = 0 cells,
■ ± = 1–5 cells,
■ +1 = 6–10 cells,
■ +2 = 11-20 cells,
■ +3 = 21–50 cells, and
■ +4 = over 50 cells
Clinical Features
■ 2. Aqueous flare. It is due to leakage of protein
particles into the aqueous humour from damaged
blood vessels. It is demonstrated on the slit lamp
examination by a point beam of light passed obliquely to
the plane of iris.
■ Grade :
■ 0 = no aqueous flare,
■ +1 = just detectable;
■ +2 = moderate flare with clear iris details;
■ +3 = marked flare (iris details not clear);
■ +4 = intense flare (fixed coagulated aqueous
with considerable fibrin).
■ Aqueous Flare
Clinical Features
SIGNS
■ Anterior chamber signs
3. Hypopyon. When exudates are heavy and thick,
they settle down in lower part of the anterior chamber
as hypopyon (sterile pus in the anterior chamber)
4. Hyphaema (blood in the anterior chamber): It may
be seen in haemorrhagic type of uveitis.
■ Hypopyon in anterior uveitis
Clinical Features
SIGNS
■ Iris signs
1. Loss of normal pattern.
2. Changes in iris colour.
3. Iris nodules
4. Posterior synechiae.
5. Neovascularsation of iris
Clinical Features
SIGNS
■ Pupillary signs
1. Narrow pupil.
2. Irregular pupil shape.
3. Ectropion pupillae
4. Sluggish pupillary reaction
5. Occlusio pupillae
Clinical Features
SIGNS
■ Lenticular signs
1. Pigment dispersal over anterior lens capsule
2. Exudates
3. Complicated cataract
■ Change in the vitreous
Anterior vitreous may show exudates and
inflammatory cells after an attack of acute
iridocyclitis.
■ Fuch’s heterochromic iridocylitis
■ Posner Schlossman syndrome.
Fuch’s heterochromic
iridocylitis
■ Fuchs’ heterochromic iridocyclitis is a
chronic nongranulomatous type of low
grade anterior uveitis.
■ It typically occurs unilaterally in middle-
aged persons.
Fuch’s heterochromic
iridocylitis
■ The disease is characterised by:
■ (i) heterochromia of iris,
■ (ii) diffuse stromal iris atrophy,
■ (iii) fine KPs at back of cornea,
■ (iv) faint aqueous flare,
■ (v) absence of posterior synechiae,
■ (vi) a fairly common rubeosis iridis,
sometimes associated with
neovascularisation of the angle of anterior
chamber
■ (vii)comparatively early development of
complicated cataract and secondary
glaucoma (usually open angle type).
■ Treatment. Topical corticosteroids .
Posner Schlossman syndrome.
■ Recurrent attacks of acute rise of intraocular
pressure (40-50 mm of Hg) without
shallowing of anterior chamber associated
with,
■ fine KPs at the back of cornea, without any
posterior synechiae,
■ epithelial oedema of cornea,
■ a dilated pupil, and a white eye (no
congestion).
Posner Schlossman syndrome.
■ The disease typically affects young adults, 40
percent of whom are positive for HLA-BW54.
■ Treatment. It includes medical
treatment to lower IOP along with a short
course of topical steroids.
Differential Diagnosis
Character Conjunctivitis Iridocyclitis Glaucoma
Infection Superficial Deep ----
Secretion Mucopurulent Watery Watery
Pupil Normal Small,
irregular
Large, Oval
Character Conjunctivitis Iridocyclitis Glaucoma
Media Clear Sometimes
pupil
opaque
Corneal
oedema
Tension Normal Usually
normal
High
Pain Mild Moderate
with first
division of
trigeminal
Severe and
entire
trigeminal
Character Conjunctivitis Iridocyclitis Glaucoma
Tenderness Absent Marked Marked
Vision Good Fair Poor
Onset Gradual Usually
gradual
Sudden
Systemic
complications
Absent Little Prostration
and
vomiting
Complications of Uveitis
■ Hypertensive uveitis – Secondary glaucoma
■ Endothelial opacities in cornea due to formation of keratic
precipitates
■ Hypopyon and hyphaema
■ Suppurative uveitis may progress to end-ophthalmitis or
pan-ophthalmitis
■ Toxic matter goes into lens – complicated cataract.
■ Post inflammatory atrophy of zonules – subluxation of
lens
■ Vitreous – opacification of vitreous, liquification of gel,
shrinkage of gel, retinal detachment
Contd..
…
■ macular edema
■ optic neuritis – undergoes atrophy – optic nerve
atrophy
■ occlusive pupillae
■ seclusion pupillae
■ Ectropion of uveal pigment
■ Hypotony – atrophic bulbi
■ Secondary squint
■ Iris atrophy
Investigations
■ Local
■ Vision, refraction, fundus examination
■ IOP by Schiotz Tonometer
■ Slit Lamp examination
■ Focal –
■ ENT, Dental, Genito-urinatory
examination for septic focus.
■ For associated systemic disorders –
■ CBC, ESR, MT, X-ray chest – Tuberculosis
■ Urine, Blood examination-Diabetes
■ VDRL, Kahn Test – syphilis
■ Urethral smear – gonorrhoeae
■ Urine culture – for UTI
■ Blood culture – Septicemia
■ ASLO Titre, C-reactive protein – for
rheumatic disorders
■ Screening test for auto immune disorders
Treatment
1. Of iridocyclitis
2. Of complications and sequelae.
Treatment of Iridocyclitis
■ Drugs used –
■ Mydriatics
■ Steroids
■ Cytotoxic agents
■ Cyclosporin
Essentials of treatment of
anterior uveitis
Dilatation of pupil with atropine
■ Hot application
■ Control of acute phase of inflammation
with steroids
Atropine
■ Acts in 3 ways
■ by keeping the iris and ciliary body at rest
■ by diminishing hyperaemia
■ by preventing formation of posterior
synechiae and breaking down any already
formed.
Method of administration and
dose:
■ Atropine may be used in form of drops or
ointment (1%) ,every four hours is usually
sufficient.
■ When pupil is well dilated, twice a day
suffices.
■ If atropine irritation ensues, one or the other
substitutes for this drug may be used.
e.g. Homatropine, Cyclopentolate.
Mydriasis -the sub-conjunctival injection
of 0.3 ml. of mydricaine, a mixture of
atropine, procaine and adrenaline.
To avoid relapse-Atropine, or its
equivalent -continued for at least 10
days to a fortnight after the eye
appears to be quiet.
■ Hot application
■ extremely soothing to patient by
diminishing the pain.
■ of therapeutic service in increasing the
circulation.
Corticosteroids
■ Administered as drops or ointment, or more
effectively as subconjunctival injections are
of great value in controlling the
inflammation in the acute phase.
■ Occasionally, results are dramatic and eye
becomes white with great rapidity.
■ Minimize damages of antigen antibody
reaction.
Aspirin
■ Is very useful in relieving pain but if it
is intense, stronger preparation are
required.
■ Cyclosporin
-T-cell immunosuppressive drug. Used in
resistant cases.
■ Broad spectrum antibiotic
- In case of suppurative uveitis.
■ Specific Chemotherapy for Tuberculosis,
syphilis, gonorrhoea.
■ Increasing body resistance by multi-vitamins.
Treatment of complications
and sequelae-
■ Secondary glaucoma-
■ Before formation of posterior or
peripheral synechiae,- intensify
atropinisation in order to allay the
inflammatory congestion.
■ Corticosteroids - topically and
acetazolamide - systematically are
very useful in such cases..
Annular synechiae-
■ Iridectomy ‘
■ ( No operative procedure of this kind must be
undertaken during an acute attack of iritis if it can
be avoided. Reason – operation will set up a
traumatic iritis which will result in the opening
getting filled with exudates.)
■ preventive iridectomy- Since ring synechiae is
the result of recurrent attacks, iridectomy can be
performed during quiescent interval.
■ Difficulty – iris is atrophied, friable. Haemorrhage is
common. Synechiae can be broken with YAG Laser.
■ Hypopyon and Hyphaema may need
evacuation and A.C. Wash.
■ End-ophthalmitis – intravitreal injection of
Decadron and Gentamicin
■ Pan ophthalmitis – Evisceration
■ Iris Bombe
Medical – 1. Atropine 2. Diamox
Surgical – 1. 4-dot Iridotomy
■ using von Graefe’s knife
■ YAG Laser for breaking posterior synechiae
THANK YOU!

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Anterior Uveitis: Causes, Signs, and Treatment

  • 1. Anterior uveitis Dr. Komala Senior resident Ophthalmology
  • 3. Classification- ■ I. ANATOMICAL CLASSIFICATION ■ II. CLINICAL CLASSIFICATION ■ III. ETIOLOGICAL CLASSIFICATION ■ IV. PATHOLOGICAL CLASSIFICATION
  • 4. A. Anatomical Classification – (IUSG) International Uveitis Study Group ■ 1) Anterior Uveitis – Inflammation of iris and anterior part of ciliary body. ■ 2) Intermediate Uveitis – Involvement of posterior part of ciliary body and extreme periphery of retina. (Pars planitis) ■ 3) Posterior uveitis – Retinochoroiditis, choroiditis, retinitis, chorioretinitis ■ 4) Diffuse or pan uveitis – Involvement of entire uveal tract
  • 5. B. Clinical Classification - ■ 1) Acute – sudden symptomatic onset. Persists for 3 weeks or less. ■ 2) Chronic – Frequently insidious and asymptomatic. Persists for months or years. ■ 3) Recurrent
  • 6. C. Etiological Classification One of the most difficult problems in ophthalmology. In most of the cases, probably, allergy is the cause. ■ 1) Exogenous- Introduction of organism into the eye through a perforating wound or ulcer. ■ 2) Secondary infection- Due to direct spread from adjoining structures- ■ Cornea ■ Sclera ■ Retina
  • 7. 3) Endogenous 4) Allergic inflammation: Result of an antigen-antibody reaction occurring in the eye due to previous sensitization of uveal tissue to some allergen. The allergen is a foreign protein. ■ Most of the cases of iridocyclitis do not have any specific cause and are probably allergic in nature.
  • 8. 5) Auto-immune - Immune disorders e.g. rheumatoid arthritis, SLE, ankylosing spondylitis, Reiter’s syndrome, Behcet’s Syndrome.
  • 9. Granulomatous Non- granulomatous 1. Aetiology Organismal invasion Antigen-antibody reaction 2. Course a) Onset Insidious Acute b) Duration Chronic Short c) Inflammation Moderate Severe D. Pathological Classification
  • 10. Granulomatous Non- granulomatous 3. Pathology a) Lesion Circumscribed Diffuse b) Iris Focal reaction Diffuse reaction c) Keratic precipitates Mutton fat Fine plenty d) Iris adhesions Coarse, few, thick Fine, plenty, thin 4. Investigations May be positive Negative
  • 11. PATHOLOGY AND CLINICAL SIGNS- Inflammation of iris and ciliary body Dilatation of blood vessels Iris stromal edema. SIGNS - Iris pattern altered.Iris colour altered. Iris thickened.Also accompanied by, ciliary congestion, conjunctival hyperaemia and chemosis of conjunctiva.
  • 12. SIGNS – ■ Iris pattern and colour altered. ■ Iris thickened accompanied by, ciliary congestion, conjunctival hyperaemia and chemosis of conjunctiva.
  • 13. Exudation of fibrin-rich fluid and inflammatory cells in the tissues Exudates escape into anterior chamber ■ Plasmoid aqueous ■ SIGNS - Aqueous flare (like the beam of projector in smokey theatre)
  • 14. Nutrition of corneal endothelium is affected due to toxins Corneal endothelium becomes sticky and edematous Cells desquamated at places
  • 15. SIGN – Keratic precipitates Inflammatory cells stick to endothelial layer as cellular deposits .
  • 16. In very intense cases, polymorphs pour out to sink to bottom of anterior chamber SIGN – Hypopyon
  • 17. Exudates cover the iris as a thin film and spread over pupillary area SIGN – Irritation of iris musculature constrictor being more powerful than dilator, spasm results in miosis. If exudate is profuse SIGN – Plastic iritis Blockage of pupil SIGN – impairment of sight.
  • 18. In early stages, there is adhesion of iris to lens capsule (Atropine may free the iris) SIGN – Spots of exudate or pigment derived from posterior layer of iris left permanently upon anterior capsule of lens (valuable evidence of previous iritis) Later on, the organization of the adhesion leads to formation of fibrous bands between pupillary margin of iris and lens capsule (atropine cannot rupture them) SIGN – Posterior synechiae (more in lower part of pupil due to effect of gravity)
  • 19. When adhesions are localized and a mydriatic is instilled, it causes intervening portions of circle of pupil to dilate. SIGN– Festooned pupil (due to irregular dilatation and is a sign of present or past iritis.)
  • 20. Pigment epithelium on posterior surface is pulled around pupillary margin so that patches of pigment on anterior surface of iris are seen. SIGN – Ectropion of uveal pigment (due to contraction of organizing exudates upon iris)
  • 21. With recurrent attacks or severe cases, the whole circle of pupillary margin gets tied to lens capsule. SIGNS – Annular or ring synechiae or Seclusio pupillae
  • 22. Collection of aqueous behind iris since aqueous drainage is hampered. Iris is hence bowed forwards like sail. SIGN – Iris Bombe (anterior chamber is funnel shaped i.e. deepest in centre, shallowest at periphery)
  • 23. As iris bulges forward and comes into contact with cornea Adhesions of iris to cornea at periphery develop SIGNS – Peripheral anterior synechiae Obliteration of filtration angle (Hypertensive iridocyclitis) SIGNS – Rise in IOP (secondary glaucoma)
  • 24. When exudate is more extensive Organization of exudate across entire pupillary area Film of opaque fibrous tissue in pupillary area SIGNS – Occlusio pupillae or Blocked pupil Exudates fill up posterior chamber if there is much of cyclitis When these adhesions organize, the iris adheres to lens capsule. SIGNS – Total posterior synechiae
  • 25. When these adhesions organize, the iris adheres to lens capsule. SIGNS – Total posterior synechiae Retraction of peripheral part of iris Anterior chamber is abnormally deep at periphery In worst cases of plastic iridocyclitis
  • 26. Cyclitic membrane formed behind lens Finally, degenerative changes in ciliary body Vitreous becomes fluid Nutrition of lens impaired SIGNS – Complicated cataract Phthisis bulbi will be the eventuality.
  • 27. In final stages, there is interference with secretion of aqueous Fall in IOP Eye shrinks (development of soft eye is an ominous sign) SIGNS – Phthisis bulbi
  • 28. Clinical Features SYMPTOMS ■ Pain ■ Diminished vision ■ Redness of eye ■ lacrimation ■ photophobia SIGNS ■ Signs of vascular congestion ■ Signs of exudation ■ Signs of pupillary changes
  • 29. Clinical Features SIGNS ■ Lid oedema ■ Circumcorneal congestion ■ Corneal signs ■ Anterior chamber signs ■ Iris signs ■ Pupillary signs ■ Lenticular changes ■ Changes in the vitreous
  • 30. Clinical Features SIGNS ■ Corneal signs Corneal oedema Keratic precipitates (KPs) Mutton fat, granular, red & old KPs Posterior corneal opacity
  • 31. Clinical Features SIGNS ■ Anterior chamber signs ■ 1. Aqueous cells. It is an early feature of iridocyclitis. ■ – = 0 cells, ■ ± = 1–5 cells, ■ +1 = 6–10 cells, ■ +2 = 11-20 cells, ■ +3 = 21–50 cells, and ■ +4 = over 50 cells
  • 32. Clinical Features ■ 2. Aqueous flare. It is due to leakage of protein particles into the aqueous humour from damaged blood vessels. It is demonstrated on the slit lamp examination by a point beam of light passed obliquely to the plane of iris. ■ Grade : ■ 0 = no aqueous flare, ■ +1 = just detectable; ■ +2 = moderate flare with clear iris details; ■ +3 = marked flare (iris details not clear); ■ +4 = intense flare (fixed coagulated aqueous with considerable fibrin).
  • 34. Clinical Features SIGNS ■ Anterior chamber signs 3. Hypopyon. When exudates are heavy and thick, they settle down in lower part of the anterior chamber as hypopyon (sterile pus in the anterior chamber) 4. Hyphaema (blood in the anterior chamber): It may be seen in haemorrhagic type of uveitis.
  • 35. ■ Hypopyon in anterior uveitis
  • 36. Clinical Features SIGNS ■ Iris signs 1. Loss of normal pattern. 2. Changes in iris colour. 3. Iris nodules 4. Posterior synechiae. 5. Neovascularsation of iris
  • 37. Clinical Features SIGNS ■ Pupillary signs 1. Narrow pupil. 2. Irregular pupil shape. 3. Ectropion pupillae 4. Sluggish pupillary reaction 5. Occlusio pupillae
  • 38. Clinical Features SIGNS ■ Lenticular signs 1. Pigment dispersal over anterior lens capsule 2. Exudates 3. Complicated cataract ■ Change in the vitreous Anterior vitreous may show exudates and inflammatory cells after an attack of acute iridocyclitis.
  • 39. ■ Fuch’s heterochromic iridocylitis ■ Posner Schlossman syndrome.
  • 40. Fuch’s heterochromic iridocylitis ■ Fuchs’ heterochromic iridocyclitis is a chronic nongranulomatous type of low grade anterior uveitis. ■ It typically occurs unilaterally in middle- aged persons.
  • 41. Fuch’s heterochromic iridocylitis ■ The disease is characterised by: ■ (i) heterochromia of iris, ■ (ii) diffuse stromal iris atrophy, ■ (iii) fine KPs at back of cornea, ■ (iv) faint aqueous flare, ■ (v) absence of posterior synechiae,
  • 42. ■ (vi) a fairly common rubeosis iridis, sometimes associated with neovascularisation of the angle of anterior chamber ■ (vii)comparatively early development of complicated cataract and secondary glaucoma (usually open angle type). ■ Treatment. Topical corticosteroids .
  • 43. Posner Schlossman syndrome. ■ Recurrent attacks of acute rise of intraocular pressure (40-50 mm of Hg) without shallowing of anterior chamber associated with, ■ fine KPs at the back of cornea, without any posterior synechiae, ■ epithelial oedema of cornea, ■ a dilated pupil, and a white eye (no congestion).
  • 44. Posner Schlossman syndrome. ■ The disease typically affects young adults, 40 percent of whom are positive for HLA-BW54. ■ Treatment. It includes medical treatment to lower IOP along with a short course of topical steroids.
  • 45. Differential Diagnosis Character Conjunctivitis Iridocyclitis Glaucoma Infection Superficial Deep ---- Secretion Mucopurulent Watery Watery Pupil Normal Small, irregular Large, Oval
  • 46. Character Conjunctivitis Iridocyclitis Glaucoma Media Clear Sometimes pupil opaque Corneal oedema Tension Normal Usually normal High Pain Mild Moderate with first division of trigeminal Severe and entire trigeminal
  • 47. Character Conjunctivitis Iridocyclitis Glaucoma Tenderness Absent Marked Marked Vision Good Fair Poor Onset Gradual Usually gradual Sudden Systemic complications Absent Little Prostration and vomiting
  • 48. Complications of Uveitis ■ Hypertensive uveitis – Secondary glaucoma ■ Endothelial opacities in cornea due to formation of keratic precipitates ■ Hypopyon and hyphaema ■ Suppurative uveitis may progress to end-ophthalmitis or pan-ophthalmitis ■ Toxic matter goes into lens – complicated cataract. ■ Post inflammatory atrophy of zonules – subluxation of lens ■ Vitreous – opacification of vitreous, liquification of gel, shrinkage of gel, retinal detachment Contd..
  • 49. … ■ macular edema ■ optic neuritis – undergoes atrophy – optic nerve atrophy ■ occlusive pupillae ■ seclusion pupillae ■ Ectropion of uveal pigment ■ Hypotony – atrophic bulbi ■ Secondary squint ■ Iris atrophy
  • 50. Investigations ■ Local ■ Vision, refraction, fundus examination ■ IOP by Schiotz Tonometer ■ Slit Lamp examination ■ Focal – ■ ENT, Dental, Genito-urinatory examination for septic focus.
  • 51. ■ For associated systemic disorders – ■ CBC, ESR, MT, X-ray chest – Tuberculosis ■ Urine, Blood examination-Diabetes ■ VDRL, Kahn Test – syphilis ■ Urethral smear – gonorrhoeae ■ Urine culture – for UTI ■ Blood culture – Septicemia ■ ASLO Titre, C-reactive protein – for rheumatic disorders ■ Screening test for auto immune disorders
  • 52. Treatment 1. Of iridocyclitis 2. Of complications and sequelae.
  • 53. Treatment of Iridocyclitis ■ Drugs used – ■ Mydriatics ■ Steroids ■ Cytotoxic agents ■ Cyclosporin
  • 54. Essentials of treatment of anterior uveitis Dilatation of pupil with atropine ■ Hot application ■ Control of acute phase of inflammation with steroids
  • 55. Atropine ■ Acts in 3 ways ■ by keeping the iris and ciliary body at rest ■ by diminishing hyperaemia ■ by preventing formation of posterior synechiae and breaking down any already formed.
  • 56. Method of administration and dose: ■ Atropine may be used in form of drops or ointment (1%) ,every four hours is usually sufficient. ■ When pupil is well dilated, twice a day suffices. ■ If atropine irritation ensues, one or the other substitutes for this drug may be used. e.g. Homatropine, Cyclopentolate.
  • 57. Mydriasis -the sub-conjunctival injection of 0.3 ml. of mydricaine, a mixture of atropine, procaine and adrenaline. To avoid relapse-Atropine, or its equivalent -continued for at least 10 days to a fortnight after the eye appears to be quiet.
  • 58. ■ Hot application ■ extremely soothing to patient by diminishing the pain. ■ of therapeutic service in increasing the circulation.
  • 59. Corticosteroids ■ Administered as drops or ointment, or more effectively as subconjunctival injections are of great value in controlling the inflammation in the acute phase. ■ Occasionally, results are dramatic and eye becomes white with great rapidity. ■ Minimize damages of antigen antibody reaction.
  • 60. Aspirin ■ Is very useful in relieving pain but if it is intense, stronger preparation are required.
  • 61. ■ Cyclosporin -T-cell immunosuppressive drug. Used in resistant cases. ■ Broad spectrum antibiotic - In case of suppurative uveitis. ■ Specific Chemotherapy for Tuberculosis, syphilis, gonorrhoea. ■ Increasing body resistance by multi-vitamins.
  • 62. Treatment of complications and sequelae- ■ Secondary glaucoma- ■ Before formation of posterior or peripheral synechiae,- intensify atropinisation in order to allay the inflammatory congestion. ■ Corticosteroids - topically and acetazolamide - systematically are very useful in such cases..
  • 63. Annular synechiae- ■ Iridectomy ‘ ■ ( No operative procedure of this kind must be undertaken during an acute attack of iritis if it can be avoided. Reason – operation will set up a traumatic iritis which will result in the opening getting filled with exudates.) ■ preventive iridectomy- Since ring synechiae is the result of recurrent attacks, iridectomy can be performed during quiescent interval. ■ Difficulty – iris is atrophied, friable. Haemorrhage is common. Synechiae can be broken with YAG Laser.
  • 64. ■ Hypopyon and Hyphaema may need evacuation and A.C. Wash. ■ End-ophthalmitis – intravitreal injection of Decadron and Gentamicin ■ Pan ophthalmitis – Evisceration ■ Iris Bombe Medical – 1. Atropine 2. Diamox Surgical – 1. 4-dot Iridotomy ■ using von Graefe’s knife ■ YAG Laser for breaking posterior synechiae