Red eye by manojit

THE LARGEST RED EYE PRESENTATION EVER...

1. Kousik
Karmakar
MANOJIT
SARKAR
Special Thanks to ophthalmology Dept. of
MALDA MEDICAL COLLEGE & HOSPITAL

SPEAKER

2. INTRODUCTION
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FREQUENT PRESENTATION TO EYE OPD & ONE OF
THE MOST COMMON OCULAR COMPLAINT.
ETIOLOGIES ARE DIFFERENT
MUST BE ABLE TO DIFFERENTIATE BETWEEN
SERIOUS VISION THREATENING CONDITIONS AND
SIMPLE BENIGN CONDITIONS.
MANAGEMENT IS DEPEND UPON ETIOLOGIES

3. COURSE ABSTRACT
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AN OVERVIEW OF ANTERIOR SEGMENT DISORDERS
REVIEW OF CLINICAL SIGNS
CONSIDERATION ON DIFFERENTIAL DIAGNOSIS
CURRENT TREATMENT AND MANAGEMENT
MODALITIES

4. WHAT IS RED EYE
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RED EYE IS A LAYMAN ‘S
TERM.IT IS APPLIED TO
ANY CONDITION WITH
DILATATION OF
CONJUNTIVAL AND
CILLIARY VESSELS.
#REFERS TO HYPEREMIA OF
THE SUPERFICIALLY VISIBLE
VESSELS OF THE CONJUNCTIVA,
EPISCLERA,OR THE SCLERA
CAUSED BY DISORDERS OF
THESE STRUCTURES
THEMSELVES, OR OF ADJACENT
STRUCTURES LIKE THE EYELIDS,
CORNEA, IRIS, AND CILIARY
BODY

5. COMMON RED EYE ETIOLOGIES
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INFECTION
INFLAMMATION
IRRITATION
ALLERGY
TRAUMA
CHEMICALS
TUMOR
SYSTEMIC CONDITIONS

6. SIGNS OF THE RED EYES
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12.
VESICLES
FOLLICLES
CILIARY FLUSH
IRREGULAR PUPIL
PAPILLAE
FOREIGN BODY
DILATED CONJUNCTIVAL VESSELS
DISCHARGE
CORNEAL ULCER
HYPOPYON
DENDRITIC ULCER
DILATED EPISCLERAL VESSELS
1 2
3
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10
1112

7. SYSTEMATIC EVALUATION OF THE
RED EYE
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ORBIT
LIDS
LACRIMAL SYSTEM
CONJUNCTIVA AND SCLERA
CORNEA
ANTERIOR CHAMBER
IRIS AND PUPIL
RETINA AND OPTIC NERVE

8. DIFFERENTIAL DIAGNOSIS OF
RED EYE
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1.LID DISEASE
BLEPHARITIS
STYLE/CHALAZION
TRICHIASIS

2.CONJUNCTIVAL
DISEASES
CONJUNCTIVITIS
CHEMICAL REACTION
DRY EYE
PINGUECULA/
PTERYGIUM
SUBCONJUNCTIVAL
HEMORRHAGE
CONJUNCTIVAL TUMOR

3.CORNEAL DISEASE
KERATITIS
ULCER
ABRASION

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5.SCLERA
SCLERITIS
EPISCLERITIS

6.UVEAL TRACT
ANTERIOR
INTERMEDIATE
POSTERIOR

7.GLAUCOMA
ACG

8.DISEASE OF INTERNAL
COMPARTMENT
ENDOPHTHALMITIS
CELLULITIS
DACRYOADENITIS

9.FOREIGN BODY
10.OCULAR TRAUMA
Red Eye
Conjunctiv
a
Cornea Sclera
Iris and
Ciliary
Body
Anterior
Chamber
Eyelid Orbit

9. ACCORDING TO TYPE OF
REDNESS

10. ANOTHER WAY TO CLASSIFY THE
RED EYE
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RED EYE
(NON-VISION-THREATENING
DISORDERS)
SUBCONJUNCTIVAL HEMORRHAGE
CONJUNCTIVITIS
STYE
CHALAZION/INTERNAL
HORDEOLUM
BLEPHARITIS
KERATITIS
DRY EYE
PTERYGIUM/PINGUECULUM

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RED EYE
(VISION-THREATENING
DISORDERS)
IRITIS/UVEITIS
CORNEAL ULCERS
ANGLE-CLOSURE GLAUCOMA
PRESEPTAL/ORBITAL
CELLULITIS
ENDOPHTHALMITIS
HYPHEMA
TRAUMA

11. Lid DiseaseLid Disease

12. BLEPHARITIS
SUBACUTE/
CHRONIC
INFLAMMATION
OF EYELID.
TYPES:3 TYPES
A)ANT.
BLEPHARITIS
-SQ/SEBORRHEIC
-ULCERATIVE/
BACTERIAL
-MIXED
B)POST.
GENERAL SYMPTOMS:
-ITCHING
-REDNESS
-BLURRING AND DISCOMFORT OF VISION
-EPIPHORA
SIGNS:
SQ..BLEPHARITIS:
1.WHITE DANDRUFF SCALES ON THE LID
MARGIN
2.MADAROSIS
3.TYLOSIS
ULCERATIVE BLEPHARITIS:
YELLOW CRUSTS AT THE ROOTS OF EYE
LASHES

Treatment:
-removal of scale/scrub by
3%NaHCO3
-epilation in case of
ulcerative blepharitis
-antibiotic
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Meibomiantis:
Meibomian orifice
shows erythema and
edema with secretions
thick and tenacious
Often diffusely
inflamed lid margins
Oral teracycline
helpful (doxy 100 BID)

13. STYE
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Acute
suppurative
inflammation of
lash follicle.
Causative agent:
staph aureus
infection of lid.
External-glands
of Zeiss, moll.
SYMPTOMS:
-ACUTE PAIN
-SWELLING OF THE
LID
-MILD WATERING
-PHOTOPHOBIA
SIGNS:
- STAGE OF
CELLULITIS
- STAGE OF ABSCESS :
PUS POINT ON THE
LID MARGIN
TREATMENT:
-SYSTEMIC ANTIBIOTIC
-HOT COMPRESS
-EVACUATION OF PUS
-LARGE->SURGICAL APPROACH

14. CHALAZION TREATMENT

#SMALL-
-HOT COMPRESS
-STEROID
ANTIBIOTIC
-INTRA CHALAZION
INJ.DEPOT-
TRIAMCINOLONE
#MODERATE/LARGE-
EXCISION
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NON SUPPURATIVE CHRONIC
GRANULOMATOUS
INFLAMMATION OF
MEIBOMIAN GLAND
BREAKDOWN OF LIPIDS INTO
OLEIC ACID
GRANULOMA FORMATION
P/F:
-STYE
-BLEPHARITIS



SYMPTOMS:
-NODULAR SWELLING
OF THE LID
-DROOPING OF THE
LID
SIGNS:
-PEA SHAPED
NODULE AWAY FROM
LID
-NO INFLAMMATION

15. INTERNAL HORDEOLUM
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SUPPURATIVE
INFLAMMATION OF
MEIBOMIAN GLAND
ASSOCIATED WITH
BLOCKAGE OF THE
DUCT
CAUSATIVE AGENT:
STAPH AUREUS
SYMPTOMS:
-ACUTE PAIN
-SWELLING OF THE LID
-PHOTOPHOBIA
SIGNS:
-LOCALIZED SWELLING WITH MARKED EDEMA
-PUS POINT AWAY FROM THE MARGIN
Treatment
-hot compress
-Evacuation of
pus
-eye ointment
-systemic eye
antibiotic
-incision:should be

16. TRICHIASIS
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INWARD MISDIRECTION OF CILIA
WITH NORMAL POSITION OF EYE
LID MARGIN.
SYMPTOMS:
-FB SENSATION
-PHOTOPHOBIA
-LACRIMATION
SIGNS:
-MISDIRECTED CILIA
-REFLEX BLEPHAROSPASM
-CONGESTED CONJUNCTIVA
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TREATMENT:
1.EPILATION
2.ELECTROLYSIS
3.CRYO-EPILATION
-20*C FOR 20-25 SECS BY DOUBLE
FREEZE TECHNIQUE
4.ELECTRODIATHARMY:30 MAMP
FOR 10 SECS.
5.IRRADIATION
6.ARGON LASER CILIA ABALATION

17. CONJUNCTIVALCONJUNCTIVAL

DISEASES DISEASES

18. BRIEF DESCRIPTION OF THE
FOLLOWINGS…
CONGESTION
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THREE TYPES:-
1)CONGESTION OF
CONJUNCTIVAL VESSELS
2)CONGESTION OF
CILIARY
VESSELS(CIRCUMCILIARY
OR CIRCUMCORNEAL
CONGESTION)
3)CONGESTION OF
EPISCLERAL VESSELS

19. BACTERIAL CONJUNCTIVITIS
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INFLAMMATION OF CONJUNCTIVA DUE TO
BACTERIAL INVASION.
BOTH ADULTS AND CHILDREN
SYMPTOMS:
TEARING,
FOREIGN BODY SENSATION
BURNING, STINGING
PHOTOPHOBIA
PAIN IN CASE PURULENT CONJUNCTIVITIS
SIGNS:
MUCOPURULENT OR PURULENT OR CATARRHAL
DISCHARGE
LID AND CONJUNCTIVA MAYBE EDEMATOUS
CONJUNCTIVAL CONGESTION
PAPILLARY REACTION MAY BE SEEN
CONJUNCTIVAL SWAB FOR CULTURE

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ACUTE:staph.,strepto.,pneumococcus,[MUCOPURULENT ]
HYPERACUTE: Neisseia gonorrhea [PURULENT]
CHRONIC CATARRHAL: Staph(mainly), Moraxella, e.coli,
klebsiella,proteus
ANGULAR:Moraxella axenfield[MUCOPURULENT]

20. TREATMENT
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SPRCIFIC TREATMENT:
IN CASE OF ACUTE/CHRONIC BACTERIAL CONJUNCTIVITIS:
TOPICAL ANTIBIOTICS:BROAD SPECTRUM(IDEALLY ANTIBIOTIC SHOULD BE SELLECTED AFTER CULTURE AND
SENSITIVITY TEST)
CHLORAMPHENICOL(1%),GENTAMICIN(0.3%),TOBRAMYCIN(0.3%),FRAMYCETIN(0.3%)…IF PATIENT DOES NOT
RESPOND THESE ANTIBIOTIC THEN:CIPRO/OFLO/GATI(0.3%)FLOXACIN
ANTI INFLAMMATORY AND ANALGESIC(PCM,IBUPROFEN)
IN CASE OF PURULENT CONJUNCTIVITIS:
3
R
D GEN CEPHALOSPORIN(CEFOXITIM,
CEFOTAXIM,CEFTRIAXONE),NORFLOXACIN,SPECTINOMYCIN
ANALGESIC
IN CASE OF ANGULAR CONJUNCTIVITIS:
OXYTETREACYCLIN(1%)-2-3 TIMES FOR 9-14 DAYS
ZINC LOTION/ZINC OXIDE TO INHIBIT PROTEOLYTIC FUNCTION
GENERAL MEASURES:
DARK GOGGLES
FREQUENT HAND WASHING
AVODENCE OF SHARING OF TOWEL,HANDKERCHIEF
HYGENIC

21. VIRAL
CONJUNCTIVITIS
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SYMPTOMS:
-ACUTE, WATERY RED EYE
WITH SORENESS, FOREIGN
BODY SENSATION AND
PHOTOPHOBIA
SIGNS:
-CONJUNCTIVA IS OFTEN
INTENSELY HYPERAEMIC AND
THERE MAYBE FOLLICLES,
HAEMORRHAGES,
INFLAMMATORY MEMBRANES
AND A PRE-AURICULAR NODE
-THE MOST COMMON CAUSE IS
AN ADENOVIRAL INFECTION
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TYPES OF VIRAL CONJUNCTIVITIS:
ADENOVIRAL(1-11,19)
ENTEROVIRUS
MOLLUSCUM CONTAGIOSUM
HERPES SIMPLEX

22. VIRAL CONJUNCTIVITIS CONTD…
ADENOVIRAL CONJUNCTIVITIS
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COMMONEST CAUSE OF VIRAL
CONJUNCTIVITIS
TYPES:
1)EPIDEMIC CONJUNCTIVITIS-
ADENOVIRUS 8&19
2)NON-SPECIFIC FOLLICULAR
CONJUNCTIVITIS-
ADENOVIRUS 1-11 & 19
3)PHARINGOCONJUNCTIVAL
FEVER-ADENOVIRUS 3&7
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SYMPTOMS:
REDNESS,WATERING,MILD MUCOID DISCHARGE.
PHOTOPHOBIAOCULAR DISCOMFORT,FB
SENSATION
SIGNS:
CONJUNCTIVA:HYPEREMIA,CHEMOSIS,
FOLLICLES AT PALPEBRAL CONJUNCTIVA,
PAPILLARY REACTION.PETICHIAL HE.
PSEUDOMEMBRANE FORMATION
CORNEA:SUPERFICIAL PUNCTATE KERATITIS
TREATMENT:
GEN MEASURES:
SPECIFIC:TOPICAL ANTIBIOTIC,TO[PICAL
ANTIVIRAL:CIDOFOVIR,STEROIDS
PREVENTIVE MEASURE

23. ALLERGIC CONJUNCTIVITIS
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ENCOMPASSES A SPECTRUM OF
CLINICAL CONDITION
SYMPTOMS:
ALL ASSOCIATED WITH THE
HALLMARK SYMPTOM OF
ITCHING
THERE IS OFTEN A HISTORY OF
RHINITIS, ASTHMA AND FAMILY
HISTORY OF ATOPY
SIGNS:
IT MAY INCLUDE MILDLY RED
EYES, WATERY DISCHARGE,
CHEMOSIS, PAPILLARY
HYPERTROPHY AND GIANT
PAPILLAE
TREATMENT :
CONSIST OF COLD COMPRESSES,
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Types of allergic conjunctivitis:
ACUTE
Seasonal allergic conjunctivitis (SAC)
Perennial allergic conjunctivitis (PAC)
CHRONIC
Vernal keratoconjunctivitis (VKC)
Atopic keratoconjunctivitis (AKC)
Giant papillary conjunctivitis (GPC)

24. VERNAL CONJUNCTIVITIS(SPRING
CATARRH)
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TREATMENT:
SPECIFIC TREATMENT:
1)TOPICAL STEROIDS-BETA/DEXAMETHASONE
2)MAST CELL STABILIZERS:NA CHROMOGLYCOLATE(5 %)
3)DUAL ACTION ANTIHISTAMINS:OLOPATIDINE
4)NSAIDS EYE DROPS
5)IMMUNE MODULATORS-TOPCAL CYCLOSPORINE,
TACROLIMUS
6)LUBRICATING SUBSTANCE:CARBOXYMETHYL
CELLULOSE
7)LARGE PAPILLAE:CRYO APPLICATION,BETA IRRADIATION
8)SYSTEMIC:ORAL ANTI HISTAMINS,ORAL STEROIDS
GENERAL MEASURES:
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Type 1 hypersensitivity reaction
Charecterised by “RIBS”-
R-recuuent,I-interstitial,B-usually bilateral,S-self
limiting
Usually in 4- 20 yrs of age
Symptoms:
Intense Itching
Lacrimation
Ropy discharge
redness both eye
Photophobia
Signs:

25. Summary of conjuctivitis

26. OPHTHALMIA NEONATORUM
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Neonatal conjunctivitis.
Any conjunctivitis occurs in the 1
st

28 days of life. Notifiable disease
Important: immature eye defences →
severe conjunctivitis, with membrane
formation and bleeding → serious
corneal disease and blindness.
important causative agents:
Neisseria gonorrhoea (corneal
perforation)
Chlamydia trachomatis
(chronic corneal scarring)
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Management:
refer to ophthalmologist
Swab and send for culture
test (mandatory)
N.gonorrhoeae penicillin
topically (local disease) and
systemically (systemic disease)
Chlamydia  topical
tetracycline ointment (local
disease) and systemic
erythromycin (systemic disease)
HSV  topical antivirals

27. PTERYGIU
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DEGENERATIVE CONDITION OF
SUBCONJUNCTIVAL TISSUE
SEEN USUALLY IN >40 YRS.
MALES ARE MORE SUSCEPTABLE TO
IT
NASAL SIDE IS COMMON FOR
PTERYGIUM
SYMPTOMS:
-FB SENSATION,
DIMNESS OF VISION
DIPLOPIA
SIGNS:
TRIANGULAR FOLD OF
CPONJUNCTIVAL MASS
ENCROACHING UPON THE CORNEA

28. PTERYGIUM CONTD…

29. SUBCONJUNCTIVAL HEMORRHAGE
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USUALLY ASYMPTOMATIC
BLOOD UNDERNEATH THE
CONJUNCTIVA, OFTEN IN A
SECTOR OF THE EYE
ETIOLOGY:-
-TRAUMA
-INFLAMMATIONS
-WHOOPING COUGH
-STRANGULATION
-ATHEROSCLEROSIS
-BLOOD DYSCRASIAS
-BLEEDING DISORDER
-ACUTE FEBRILE CONDITIONS
-VICARIOUS BLEEDING
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IN TRAUMATIC SUB CONJ.HEMOORHAGE,
POST.LIMIT IS VISIBLE IN LOCAL TRAUMA
TO EYEBALL TRAUMA
BUT IN HEAD INJURY ITS NOT VISIBLE
TREATMENT:
-PLACEBO THERAPY
-PSYCHOTHERAPY
-COLD COMPRESS IN INITIAL STAGE
& HOT COMPRESS IN LATE STAGE

30. DRY EYE(KERATOCONJUNCTIVITIS SICA)
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ITS CAUSE;-DECREASED TEAR
PRODUCTION
ASSOCIATED WITH:-
INCREASED AGE
FEMALE SEX
MEDICATION(E.G
ANTICHOLINERGIC)
INVESTIGATION:
SCHIRMER’S TEST
TREATMENT
APPLICATION OF ARTIFICIAL TEAR
USE OF WELL FITTING EYE
GLASSES WITH SIDE SHIELDS
CYCLOSPORINE OPHTHALMIC
DROPS

FIGURE :DRY EYE
DISEASE WITH LOSS
OF LUSTER OF THE
CONJUNCTIVAL AND
CORNEAL SURFACE

31. CONJUNCTIVAL TUMORS

32. ANTERIOR CHAMBER

33. HYPHEMA
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It is the collection of blood in
anterior chamber

It may appear as a reddish
tinge/small pool of blood at the
bottom of the iris or in the
cornea.

A sign of significant blunt or
penetrating trauma to the
globe

34. HYPOPYON
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IT IS A LEUKOCYTIC EXUDATE, SEEN
IN THE ANTERIOR CHAMBER, USUALLY
ACCOMPANIED BY
REDNESS OF THE CONJUNCTIVA
AND THE UNDERLYING EPISCLERA.
FORMATION OF THE EXUDATE W/
C SETTLES AT THE BOTTOM DUE
TO GRAVITY.
IT IS SIGHT-THREATENING
INFECTIOUS KERATITIS OR
ENDOPHTHALMITIS UNTIL PROVEN
OTHERWISE.

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Ethiologies
Fungal:-
Aspergillus and Fusarium s
p.,Behcet'sdisease,  
Endophthalmitis, and
panuveitis/
panophthalmitis

35. corneacornea

36. CORNEA: ANATOMY &
PHYSIOLOGY
12/07/2016RED EYE 36
1.
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5.
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5 layers
Epithelium
Bowman’s membrane
Stromal layer
Desscemet’s membrane
Endothelium
*N.B.: an extra layer Dua’s Layer
discovered in 2013..

Function:
Transmission of light
Refraction of light
Barrier against infection, foreign

37. CAUSES


2/14/2018RED EYE 37
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Corneal Abrasion
Corneal
Laceration
Corneal Foreign
Body
Corneal Ulcer
keratitis

38. CORNEAL ABRASION
.

2/14/2018RED EYE 38
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CORNEAL ABRASIONS ARE
DEFECT IN THE EPITHELIUM
DUE TO
TRAUMA, CONTACT LENS
WEARING;
USE FLUORESCEIN STAIN AND
BLUE LIGHT;
*DEFECT SHINE IN GREEN.

39. Rx:
Supportive care
Cycloplegics(atropin,cyclopentolate)
Pain control(NSAIDS)
Topical antibiotics
Eye paches
2/14/2018RED EYE 39

40. CORNEAL LACERATION
2/14/2018RED EYE 40

41. CORNEAL FOREIGN BODY
2/14/2018RED EYE 41
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FOREIGN BODY IN OR ON CORNEA
SYMPTOMS: INTENSE IRRITATION & PROFUSE WATERING.
SIGNS: LEUCOCYTE INFILTRATION
COMPLICATIONS:
SECONDARY INFECTION AND CORNEAL ULCERATION.
MILD SECONDARY UVEITIS IS COMMON WITH IRRITATIVE
MIOSIS &
PHOTOPHOBIA.
FERROUS FOREIGN BODIES→RUST STAINING OF THE BED
OF THE
ABRASION

42. 2/14/2018RED EYE 42

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RX:
TOPICAL ANTIBIOTIC (DROP/OINTMENT)

TOPICAL NSAIDS, CYCLOPEGIC

TIGHT PATCH

2/14/2018RED EYE 43

44. KERATITIS
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INFLAMMATION OF THE CORNEA
* TYPE :
1.SUPERFICIAL
INFECTIVE
BACTERIAL
VIRAL
PROTOZOAL(ACANTHAMOEBAL)
NON INFECTIVE
AUTOIMMUNE (EG: RA, SLE)
NON AUTOIMMUNE (EG: MARGINAL KERATITIS)
2/14/2018RED EYE 44

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NON INFECTIVE:-
CENTRAL-
EXPOSURE
NEUROTROPHIC
ATHEROMATOUS
PERIPHERAL
MARGINIAL
PHLYCTENULAR KERATITIS
MOOREN’S KERATITIS
TERRIEN’S KERATITIS
ROSACEA KERATITIS
KERATITIS ASSOCIATED WITH COLLAGEN DS.
2.DEEP KERATITIS:
INTERSTITIAL KERATITIS
2/14/2018RED EYE 45

46. CORNEAL ULCER
2/14/2018RED EYE 46
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* LOSS OF CORNEAL EPITHELIUM WITH
UNDERLYING STROMAL INFILTRATION
& SUPPURATION ASSOCIATED WITH
SIGNS OF INFLAMMATION WITH OR
WITHOUT HYPOPYON
IN STRICT SENSE CORNEAL ULCER &
KERATITIS ARE NOT ALWAYS
SYNONYMOUS..
PATHOLOGY OF A CORNEAL ULCER:
STAGE OF INFILTRATION &
PROGRESSION
STAGE OF REGRESSION
STAGE OF CICATRIZATION

47. BACTERIAL CORNEAL ULCER
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CAUSES- STAPHYLOCOCCUS EPIDERMIDIS
- STAPHYLOCOCCUS AUREUS
- STREPTOCOCCUS PNEUMONIAE
- COLIFORMS
- PSEUDOMONAS
- HAEMOPHILIS

PREDISPOSING FACTORS
KERATOCONJUNCTIVITIS SICCA (DRY EYE)
A BREACH IN CORNEAL EPITHELIUM
(EG FOLLOWING TRAUMA,FOREIGN BODY,
CONTACT LENS WEAR)
UNDERLYING CORNEAL PATHOLOGY
(HERPETIC KERATOPATHY,CORNEAL EROSIONS,
2/14/2018RED EYE 47

48. 2/14/2018RED EYE 48
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* SYMPTOMS : - RED EYE
PAIN (MAIN FEATURE)  WORSENED BY
MOVEMENT OF EYELIDS
PERSISTS UNTIL HEALING OCCUR. (NOT IF
HERPES ZOSTER OPTHALMICUS)
PHOTOPHOBIA
WATERY OR MUCOPURULENT DISCHARGE
* SIGNS:-
CORNEAL HAZINESS
CILIARY CONGESTION OF THE
CONJUNCTIVA
HYPOPYON
IOP-NORMAL OR RAISED
OTHERS- IRITIS, BLEPHAROSPASM, LID
EDEMA ETC.

49. COMPLICATIONS
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ANTERIOR SYNECHIA
IRIS PROLAPSE
ADHERENT LEUCOMA
ANTERIOR STAPHYLOMA
PTHISIS BULBI
SUBLUXATION OR DISLOCATION PF LENS
ANTERIOR CAPSULAR CATARACT
CORNEAL FISTULA
EXPULSIVE HAEMORRHAGE,IRIDOCYCLITIS,
2/14/2018RED EYE 49

50. 2/14/2018RED EYE 50
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MANAGEMENT
* INVESTIGATION:-
CORNEAL SCRAPING: SCRAPES TAKEN FROM BASE OF
ULCER FOR GRAM-STAINING & CULTURE
CONJUNCTIVAL SWABS:
CONTACT LENS CASES:
* TREATMENT:-
1)GENERAL CONSIDERATIONS:
HOSPITAL ADMISSION
DISCONTINUATION OF CONTACT LENS WEAR
A CLEAR PLASTIC EYE SHIELD
DECISION TO TREAT

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•

2)LOCAL THERAPY: BROAD SPECTRUM
ANTIBIOTICS- INITIAL INSTILLATION AT
HOURLY INTERVALS DAY & NIGHT FOR 24-48
HRS

ANTIBIOTIC MONOTHERAPY :
ADVANTAGEOUS OVER DUOTHERAPY
FLUOROQUINOLONES (EG: CIPROFLOXACIN,
OFLOXACIN); MOXIFLOXACIN, GATIFLOXACIN,
BESIFLOXACIN EYE DROPS ETC..

ANTIBIOTIC DUOTHERAPY:-
EMPIRICAL THERAPY: 1
ST
LINE;
FORTIFIED CEFUROXIME(5%) FOR GRAM +VE
BACTERIA AND FORTIFIED
2/14/2018RED EYE 51

52. •
•
•






SUBCONJUNCTIVAL ANTIBIOTICS
MYDRIATICS
STEROIDS
3)SYSTEMIC ANTIBIOTICS:
POTENTIAL FOR SYSTEMIC INVOLVEMENT
SEVERE CORNEAL THINNING
SCLERAL INVOLVEMENT
PERFORATION
ENDOPHTHALMITIS
VISUAL REHABILITATION
2/14/2018RED EYE 52

53. FUNGAL ULCER
2/14/2018RED EYE 53
•
•
•
•
* ETIOLOGY:-
FILAMENTOUS FUNGI:-ASPERGILLOUS,FUSARIUM ETC
YEAST:CANDIDA
* PREDISPOSING FACTORS:-
* MODE OF INFECTION:-
OCULAR TRAUMA(AGRICULTURAL & VEGETABLE MATTERS)
SYMPTOMS:-
LESS PROMINENT THAN BACTERIAL ULCER

54. •
•
•


•
•
•
•
SIGNS:-
DRY LOOKING, YELLOWISH WHITE,INDISTINCT MARGIN;
FILAMENTOUS FUNGUS KERATITIS : DELICATE FEATHERY
FINGER LIKE PROJECTION INTO ADJACENT STROMA
SATELLITE LESIONS
RING SHAPED
CANDIDA KERATITIS: COLLAR BUTTON ABSCESS
IMMOBILE,NON STERILE HYPOPYON
IRIDOCYCLITIS
NO VASCULARIATION
2/14/2018RED EYE 54

55. •


•





* MANAGEMENT:
INVESTIGATIONS:
KOH MOUNT PREPARATION
CULTURE IN SDA MEDIA
TREATMENT:
SCRAPING & DEBRIDEMENT OF ULCER
ATROPINE EYE OINTMENT-3 TIMES DAILY
ANTIFUNGALS:
SPECIFIC:
TOPICAL: 6-8 WEEKS; NATAMYCIN(5%),
2/14/2018RED EYE 55

56. 
•
•


NYSTATIN EYE OINTMENT(3.5%)
SYSTEMIC: FOR SEVERE CASES OF DEEPER FUNGAL
KERATITIS
FLUCONAZOLE, VORICONAZOLE, KETOCONAZOLE
INTRACAMERAL, INTRACORNEAL/INTRASTROMAL:

NON SPECIFIC: GENERAL MEASURES

THERAPEUTIC PENETRATING KERATOPLASTY

2/14/2018RED EYE 56

57. VIRAL KERATITIS
•
•
•
•
•
•
•
•
•
•
•
HERPES SIMPLEX KERATITIS
CAUSES: TYPE 1 OR TYPE 2 HERPES SIMPLEX VIRUS
MOST ARE ASYMPTOMATIC
ACCOMPANIED BY:
FEVER
VESICULAR LID LESION
FOLLICULAR CONJUNCTIVITIS
PRE-AURICULAR LYMPHADENOPATHY

PATHOGNOMONIC: DENDRITIC ULCER ON CORNEA
DENDRITIC ULCER MAY HEAL WITHOUT SCAR,
BUT MAY PROGRESS TO STROMAL KERATITIS, A/
W INFLAMMATORY INFILTRATION, OEDEMA AND
ULTIMATELY LOSS OF CORNEAL TRANSPARENCY
AND PERMANENT SCARRING  IF SEVERE –
2/14/2018RED EYE 57

58. 2/14/2018RED EYE 58

59. 2/14/2018RED EYE 59




HERPES ZOSTER OPHTHALMICUS
(OPHTHALMIC SHINGLES)
CAUSE : VARICELLA ZOSTER VIRUS
AREA AFFECTED: OPHTHALMIC DIVISION OF CN V
ACCOMPANIED BY: PRODROMAL PERIOD WITH
SYSTEMICALLY UNWELL, VESICLES, LID SWELLING,
IRITIS, 2° GLAUCOMA.
RX: - ORAL ANTIVIRAL (EG: ACICLOVIR, FAMCICLOVIR)
TO REDUCE POST-INFECTIVE NEURALGIA
- TOPICAL ANTIVIRAL AND STEROIDS AND
ANTIBACTERIALS TO COVER SECONDARY INFECTION FOR
THE OCULAR DISEASE.

60. CONTACT LENS WEAR
2/14/2018RED EYE 60
•
•
•
PERIPHERAL CORNEAL VASCULARIZATION
STERILE CORNEAL ULCERATION
INFECTION-PSEUDOMOAS & ACANTHOMOEBA KERTITIS

61. PROTOZOAL KERATITIS
2/14/2018RED EYE 61
•
•
•
•
ACANTHAMOEBA KERATITIS
COMMONLY DUE TO USED OF CONTACT LENSES AND
EXPOSURE TO CONTAMINATED WATER OR SOIL.
CLINICAL FEATURES: PAINFUL KERATITIS, REDNESS OF
THE EYE AND PHOTOPHOBIA.
RX: TOPICAL CHLORHEXIDINE, POLYHEXAMETHYLENE
BIGUANIDE (PHMB) AND PROPAMIDINE.

62. NASOLACRIMAL OBSTRUCTION
•
•
•
•
•
•
•
CAN LEAD TO DACRYOCYSTITIS
PAIN, REDNESS, AND SWELLING OVER THE INNERMOST
ASPECT OF THE LOWER EYELID, TEARING, DISCHARGE
ORGANISMS
STAPHYLOCOCCI, STREPTOCOCCI, AND DIPHTHEOIDS
TREATMENT
SYSTEMIC ANTIBIOTICS
SURGICAL DRAINAGE

63. UVEAUVEA

64. INFLAMMATION OF THE UVEAL TRACT ( IRIS,
CILIARY BODY, CHOROID)

Uveitis
Anterior
Uveitis
Iritis
Iridocycli
tis
Cyclitis
Posterior
Uveitis
Choroidit
is
•
•
•
•
•
•
•
•
Inflammatory - due to autoimmune disease
Infectious - caused by known ocular and systemic
pathogens
Infiltrative - secondary to invasive neoplastic
processes
Injurious - due to trauma
Iatrogenic - caused by surgery, inadvertent trauma,
or medication
Inherited - secondary to metabolic or dystrophic
disease
Ischaemic - caused by impaired circulation
Idiopathic - a category used when thorough
evaluation has failed to find an underlying cause


AETIOLOGY

65. ASSOCIATED WITH SYSTEMIC DISEASE
•
•
•
•
•

1) sarcoidosis, TB - SOB, cough
2) Behcet’s, psoriasis - skin problems
3) ankylosing spondylitis, juvenile chronic arthritis, Reiter’s - back
pain, arthritis
4) IBD - alteration of bowel habit
5) In AIDS
Cytomegalovirus
Human syncytial virus
Cryptococcus
Toxoplasma
Candida

66. SYMPTOMS
•
•
•
•
Ocular pain
Photophobia
Blurring of
vision
Red eye
SIGNS
•
•
•
•
REDUCED VISUAL ACUITY
CILIARY INJECTION : DIFFUSE SUPERFICIAL CONJUNCTIVAL
HYPEREMIA THAT WOULD INDICATE CONJUNCTIVITIS, AS
OPPOSED TO THE CIRCUMLIMBAL REDNESS OF ANTERIOR
UVEITIS. BLURRED VISION AND PHOTOPHOBIA ARE USUALLY
ABSENT WITH CONJUNCTIVITIS.

KERATITIC PRECIPITATES ( ON CORNEAL ENDOTHELIUM) : IN
ACUTE CASES KPS MAY BE FINE AND WHITE; IN CHRONIC
CASES, LARGE AND YELLOWISH. COLORED OR PIGMENTED KPS
SUGGEST PRIOR EPISODES OF ANTERIOR UVEITIS.
CELLS/FLARE

•
•
•
•
•
Hypopyon
Vessels on iris dilated
Pigment and fibrin deposits on the anterior surface
of the lens are suggestive of synechiae. The presence
or absence of posterior subcapsular cataract should
be well documented because PSC is a frequent
complication of both the disease and the therapy.
Posterior synechiae - irregular pupil
Anterior synechiae - may occlude drainage angle

67. Marked circumcorneal
congestion with contracting
fibrin in the anterior chamber
and a pupil in mid-mydriasis.
Posterior synechiae
between iris and lens after
iridocyclitis give the pupil
the shape of cloverleaves
[festooned pupil]
IRITIS

68. INVESTIGATIONS
•
•
•
•
•
•
A FIRST EPISODE OF UNILATERAL
NONGRANULOMATOUS ACUTE UVEITIS
CAN BE DIAGNOSED BY HISTORY AND
CLINICAL EXAMINATION ALONE AND
DOES NOT NEED LABORATORY
INVESTIGATION.

IF HISTORY AND EXAMINATION ARE
NORMAL BUT THE UVEITIS IS
GRANULOMATOUS, RECURRENT OR
BILATERAL, THE FOLLOWING SCREENING
INVESTIGATIONS SHOULD BE CARRIED
OUT:
FULL BLOOD COUNT AND ESR
HLA-B27
ANTINUCLEAR ANTIBODY
SCREENING TESTS FOR SYPHILIS AND
TUBERCULOSIS
CHEST X-RAY
MANAGEMENT
General measures:
Drops to dilate the pupil (cyclopegics) such as cyclopentolate 1% or
atropine 1% should be prescribed, but this is best done by a specialist as
this treatment is contraindicated in narrow angle glaucoma.

- To prevent adhesion of the iris to the anterior lens capsule(posterior
synechia), which can lead to iris bombe and elevated IOP
- To stabilize the blood-aqueous barrier and help prevent further
protein leakage (flare).
- To relieve pain by immobilizing the iris

When using cyclopegics, the patient should be warned that the pupil
will appear large and they will have a temporary problem with vision in
the eye in which the drops have been administered.
Medical therapy:
Steriod(PREDNISOLONE)
SURGICAL THERAPY:
Removal of the vitreous may be necessary when persistent floaters
severely impede visual acuity.This procedure may also be useful as a
combined therapeutic and diagnostic test as, once removed, the
vitreous can be analysed to exclude infection or malignancy.

69. SCLERA

70. EPISCLERITIS
•
•
•
•
•
•
•
•
Episcleritis: an acute
inflammation of subconjuctival
episcleral tissue.
Sign and symptom:
Tearing,
photophobia, and
tenderness.
Localized episcleral(s/c) hyperemia.
Treatment:
Self-limiting but NSAID and
Corticosteroids.

71. SCLERITIS
•
•
•
•
•
•
It is a severe
inflammation of
sclera may result in
melting and
perforation.
Associated with
systemic diseases
such as RA and other
connective diseases.
Sign and Symptoms:
Severe pain
aggravated with
ocular motility.
Hyperemia,

72. 1.ACUTE ANGLE-CLOSURE GLAUCOMA
2/14/2018RED EYE 72
The iris root occludes the trabecular meshwork, completely obstructing drainage
of aqueous fluid from the anterior chamber. The resulting rapid elevation of
intraocular pressure requires urgent intervention to prevent permanent visual

73. NORMAL AQUEOUS FLOW
2/14/2018RED EYE 73

74. CONT’D…
-
-
-
-
RESULTS IN A SUDDEN SEVERE RISE IN IOP
MAY BE ACUTE AND PAINFUL OR CHRONIC ASYMPTOMATIC
DUE TO OCCLUSION OF ANTERIOR CHAMBER ANGLE
MAY CAUSE PERMANENT VISUAL LOSS FROM OPTIC NERVE
DAMAGE

2/14/2018RED EYE 74

75. SIGN AND SYMPTOM
•
•
•
•
•
SYMPTOMS:
RAPID UNILATERAL LOSS OF
VISION
PERIOCULAR PAIN AND HEAD
ACHE
RED EYE
PHOTOPHOBIA
NAUSEA AND VOMITING

2/14/2018RED EYE 75

76. SIGN AND SYMPTOM CON’T…
•
•
•
•
•
•
•
•
•
SIGNS
MARKED CONJUNCTIVAL AND CILIARY INJECTION
SHALLOW AC AND CORNEAL EDEMA
DECREASED VA
AQUEOUS FLARE AND CELL
VERTICALLY OVAL, FIXED AND SEMIDILATED PUPIL
DILATED IRIS BLOOD VESSELS
SEVERELY ELEVATED IOP (50-100) MMHG
GONIOSCOPY OF THE OTHER EYE SHOWS OCCLUDABLE ANGLE

2/14/2018RED EYE 76

77. DRUGS USING FOR TREATING
GLAUCOMA
ACUTE CONGESTIVE
GLAUCOMA(NARROW ANGLE )
•
•
•
•
•
•
•
OSMOTIC AGENTS:
MANNITOL(20%) I.V
GLYCEROL(50%)ORAL
CARBONIC ANHYDRASE INHIBITORS:
ACETAZOLAMIDE,I.V,ORAL
BETA BLOCKERS:
TIMOLOL MALATE(0.5%),TOPICAL
MIOTICS:
PILOCARPINE(2%)TOPICAL
PROSTAGLANDINS:
LATANOPROST(0.005%),TOPICAL

78. DRUGS FOR TREATING PRIMAY
ANGLE CLOSURE GLAUCOMA(PACG)

•
•
HYPEROSMOTIC AGENTS:
PREPARATION:
MANNITOL(20%,I.V)
GLYCEROL(10%,ORAL)
MOA:
THEY DRAW FLUID FROM THE EYE
INTO THE CIRCULATION BY
OSMOTIC EFFECT AND REDUCE IOP
•

NOTE:
DRUGS ARE USED ONLY TO
TERMINATE THE ATTACK OF
PACG.DEFINITIVE
TREATMENT IS SURGICAL/
LASER IRIDOTOMY

79. 
•
•
•
•
•
•
•


PROSTAGLANDIN
ANALOGUES:
PREPARATION:
LATANOPROST(0.005% HS )
BIMATOPROST(0.03%.HS)
TRAVOPROST(0.004%)
MOA:
IT INCRASES THE UVEOSCLERAL OUTFLOW BY
INCREASING PERMEABILITY OF AQUEOUS
HUMOR IN CILLIARY MUSCLE.
A/E:
BLURRING OF VISION
INCREASED IRIS PIGMENTATION
DARKENING OF EYE LASHES
RARELY MACULAR EDEMA
NO SYSTEMIC SIDE EFFECTS
NOTE:
IN UVEITIS PGS ARE STRICTLY
CONTRAINDICATED DUE TO AGGRAVATION
OF THE INFLAMMATION.

A.
B.
C.
D.


•
•
•
•


PREPARATION:
Epinephrine Hydrochloride(0.5/1/2% ,OD/BD)
Dipivefrine(0.1%,OD,BD)
Brimonidine(0.2%,BD)
Apraclonidine(1%,BD)
MOA:
A & B by stimulating alpha 1 and alpha 2
receptors decrease the aqueous secretion and by
stimulating beta receptor the increase uveoscleral
and trabecular outflow and reduces IOP.
C & D by stimulating alpha 2 agonist reduce
formation aq.humor and decrease IOP
A/E:
Itching
Lid dermatitis
Follicular conjunctivitis
Mydriasis
NOTE
Apraclonidine & dipivefrine are restricted after
trabeculoplaty and iridotomy


ALPHA ADRENERGIC
AGONISTS

80. CARBONIC ANHYDRASE
INHIBITORS
•
•
•

•
•
•
•

•
•


PREPARATION:
BRINZOLAMIDE(1%,BD)
DORZOLAMIDE(2%,BD)
MOA:
IT REDUCES AQ.HUMOR FORMATION BY LIMITING
GENERATION OF BICARBONATE IONS.IN CILIARY
EPITHELIUM BY INHIBITING CARBONIC ANHYDRASE
ENZYME.
A/E:
SYSTEMIC:
MALAISE
FATIGUE
ANOREXIA
DIARRHOEA
OCULAR:
BURNING AND ITCHING
CORNEAL EDEMA
NOTE:
ACETAZOLAMIDE IS NOT USED USUALLY BECAUSE IT
MAY CAUSE BM DEPRESSION,SJ SYNDROME,APLASTIC
ANEMIA ETC

MIOTICS:
•
•
•
•
PREPARATION:
Pilocarpine(1/2/4%,TDS/
QD)
MOA:
By stimulating M3
receptor it increases
contraction of longitudinal
muscle fibres of ciliary
body and sphincter
pupillae and facilitates
the drainage of aqueous.
In trabecular outflow

81. THE SITES OF ACTION
OF OCULAR
HYPOTENSIVE DRUGS
1.
2.
3.
4.
5.
SITE OF ACTION OF MIOTICS IN ACG :
CONTRACTION OF SPHINCTER PUPILLAE
REMOVES PUPILLARY BLOCK & REVERSES
OBLITERATION OF IRIDOCORNEAL ANGLE
SITE OF ACTION OF MIOTICS IN OAG :
CONTRACTION OF CILIARY MUSCLE PULLS ON
SCLERAL SPUR AND IMPROVES TM PATENCY
SITE OF ACTION OF A)BETA BLOCKERS,B)ALPHA
1&2 AGONISTS,C)CA INHOBITORS:ALL REDUCE AQ.
SECRETION BY CILIARY BODY.
SITE OF ACTION OF PGS :INCREASE
UVEOSCLERAL OUTFLOW BY ALTERING
PERMEABILITY
?? SITE OF ACTION OF ADRENALINE(BETA 2
AGONIST ACTION):POSSIBLY INCREASES AQ.
CONDUCTIVITY OF TM

82. ENDOPHTHALMITIS

89. PATHOPHYSIOLOGY
OCULAR INFECTION WITH INFECTIOUS BACTERIAL LOAD /WITH
IMPAIRMENT OF IMMUNE PRIVILEGE OF THE EYE ,LEADS TO
INTENSE DESTRUCTIVE INFLAMMATORY REACTION .

( BACT. TOXINS ,PROTEASES + INTENSE HOST INFLAMMATORY
RESPONSE ---------- INJURY TO RETINA ,CB, A/S STRUCTURES .

INTENSE INFLAMMATORY RESPONSE ----- NEGATIVE
MICROBIOLOGICAL STUDIES .

90. INCIDENCE
*POST CATARACT 0.07 – 0.5 %.
*POST PKP 0.11%.
*POST PPV 0.05 %.
*BLEB RELATED 0.2 – 9.6 %.
*TRAUMATIC 2.4 – 8.0 % , UP TO 40% IN RURAL AREAS WITH
IOFB.

91. MICROBIAL SPECTRUM
POST CATARACT :CNS 33-77%
STAPH. AURUS 10-21%
STREPTOCOCCI 9-19%
G –VE, FUNGI 6-22%
DELAYED ONSET (CHRONIC) POST CATARACT:
PROP. ACNE ,CORYNEBACTERIA,FUNGI.
POST GLAUCOMA SX: CNS 67% EARLY
STREPT, H INFLU.

92. SYMPTOMS+SIGNS
•
•
•
•
•
•
•
•
•

PAIN
RED EYE
DECREASED VISION
HAZY CORNEA
HYPOPYON
LID SWELLING
CHEMOSIS
DISCHARGE
PHOTOPHOBIA
Patient presents with symptoms most
commonly on the second day after surgery

93. POE: CLINICAL ASPECTS
•
•
•
•
THREE FORMS OF CLINICAL PRESENTATION CAN BE
DISTINGUISHED
ACUTE FORM, USUALLY FULMINANT, OCCURS 2-4 DAYS POST-OP,
MOST COMMONLY DUE TO S.AUREUS OR STREPTOCOCCI.
DELAYED FORM, MODERATELY SEVERE, OCCURS 5-7 DAYS POST-OP,
DUE TO S.EPIDERMIDIS, COAGULASE NEGATIVE COCCI, RARELY
FUNGAL.
CHRONIC FORM, OCCURS AS EARLY AS 1 MONTH POST-OP, DUE TO
PROPIONIBACTERIUM ACNES, S.EPIDERMIDIS OR FUNGAL.

94. PROPHYLAXIS
•
*ANTISEPTICS: 5% POVIDONE – IODINE FOR AT LEAST 3
MINUTES IS THE MOST IMPORTANT
PROPHYLAXIS IN MANY STUDIES; DECREASING
CONJ +PERIORBIT.SKIN FLORA .

*SINGLE USE INSTRUMENTS IS ALWAYS PREFERABLE ESP.
TUBES.

95. ANTIBIOTICS
•
•
•
TOPICAL ANTIBIOTICS ESP. 4
TH
GENERATION FLUOROQUINOLONES APPEARS TO BE VERY EFFECTIVE IN
REDUCING CONJ. FLORA LOAD , ACHIEVING HIGH CONCENTRATIONS IN
THE IN THE A/C(ROLE COTROVERSIAL).
ORAL ANTIBIOTICS HAS NO PROVEN ROLE
ALSO SUBCONJUNCTIVAL ANTIBIOTIC INJ AT THE END OF OT HAS NO
PROVEN ROLE.

BUT NO CONTROLLED CLINICAL TRIAL PROVE THEIR EFFECT IN REDUCING
INCIDENCE OF ENDOPH.

96. ABX
INJECTION OF INTRACAMERAL
1MG/0.1ML OF CEFUROXIME (3000UG/
ML @ A/C ) AT THE END OF SURGERY:

IT HAS BEE SHOWN THE RISK OF ENDOPH. WITH THIS REGIMEN
REDUCED BY ALMOST 5 FOLDS (ESCRS ) STUDY

NB: CEFUROXIME RESIST. MRSA,MRSE,ENT.FAECALIS,PSEUD.AUR.

97. DIAGNOSIS
*IT IS MAINLY CLINICAL.
*DELAY IN DIAGNOSIS IS NOT UNCOMMON (STEROIDS ,
COMPLICATIONS ,EXPECTED POST OP INFLAM.).
*B-SCAN IS AN AID , BUT SOME TIMES IT IS MISLEADING .
*IF DOUBT, BE SAFE AND CONSIDER IT AS ENDOPH.,
NO BODY IS BLAMING OF OVER PROTECTION BUT MISSING
SERIOUS IRREVERSIBLY DAMAGING PATHOLOGY IS THIS
THE SITUATION.

98. MANAGEMENT OF ACUTE
POST OP ENDOPHTHALMITIS
*IT IS A REAL OPHTHALMIC EMERGENCY.
*CONTROVERSIES IN MANAGEMENT :

VITREOUS TAP + A/C SAMPLING + INTRAVITREAL
ABX&STEROIDS---- IN CASES VA >=HM (EVS)
VS
PRIMARY VITRECTOMY +INTRAVITREAL ABX&STEROIDS IN ALL
CASES (ESCRS).

99. MX
ESCRS RECOMMEND PRIMARY VITRECTOMY +INTRAVITREAL
ABX&STEROIDS AS A GOLD STANDARD OF CARE :

TO: DEC. BACT. LOAD , PUS , REMOVE MOST OF THE
INFLAMMATORY DESTRUCTING CELLS AND MEDIATORS ,
REMOVING THE SCAFFOLD (VITREOUS)

100. MX
EVS RECOMMENDS :
A) VITREOUS TAP + A/C SAMPLING + INTRAVITREAL
ABX&STEROIDS---- IN CASES VA >=HM.

B) VITRECTOMY +INTRAVITREAL ANTIBIOTICS
&STEROIDS IN CASES VA < HM.
WHY ?
-COMPARATIVE RESULTS FOUNDED ( ORGANISM
VIRULENCE).
-AVOIDING DELAY VITREOUS TAP + ABX .
-AVOIDING VITR. COMPLICATIONS IN A FRAGILE RETINA .

101. •
•
INRAVITREAL ANTIBIOTICS CAN BE
REPEATED EVERY 48 HOURS
ACCORDING TO THE RESPONSE
ORAL OR IV ANTIBIOTICS HAVE
LITTLE ROLE.

102. •
•
•
•
HENCE, INTRAVITREAL INJECTIONS ARE TREATMENT OF
CHOICE.
THUS VANCOMYCIN 1 MG IN (0.1 ML) IS GIVEN
INTRAVITREALLY ALONG WITH
CEFTAZIDIME(CONCENTRATION OF 2.25 MG/0.1 ML TO BE
SAFE)
VANCO TO COVER GRAM+VE ORGANISMS AND CEFTAZIDIME
FOR GRAM NEGATIVE
AMIKACIN CAN BE USED INSTEAD OF CEFTAZIDIME BUT IS
HAVING RETINOTOXICITY MORE THAN CEFTA

103. OCULAR TRAUMA

104. EYE INJURY
BIRMINGHAM EYE TRAUMA
TERMINOLOGY(BETT)
•
OPEN GLOBE CLOSED GLOBE

LACERATING CONTUSION(BLUNT)

PENETRATING LAMELLAR
LACERATION
PERFORATING
INTRAOCUAR FB
RUPTURE

105. CONTUSION(BLUNT INJURY)
•
MECHANISM: -DIRECT
-INDIRECT
-CONTRE-COUP

106. VARIOUS EFFECTS:
EYELID-LACERATION
-ECCHYMOSIS
-EMPHYSEMA
CONJUNCTIVA-SCH
-CHEMOSIS; CONJ.LACERATION

107. LID LACERATION

108. •
CORNEA-ABRATION
-RUP. OF DESCEMETS MEM.
-STROMA EDEMA
-BLOOD STAINING OF CORNEA
-CORNEAL RUPTURE

109. CORNEAL ABRASION

110. BLOOD STAINING OF CORNEA

111. CORNEAL FOREIGN BODY

113. FOREIGN BODY TREATMENT
•
•
•
•
•
•
•
ANESTHETIZE EYE
REMOVE FB
COTTON SWAB (DON’T WORSEN ABRASION!)
KIMURA SPATULA
+/- NEEDLE TIP
ANTIBIOTIC AND +/- PATCH
1-2 DAY FOLLOW-UP WITH EYE DOC

114. SCLERA:
•
RUPTURE—ASSO.WITH-UVEAL PROLAPSE
-VITREOUS PROLAPSE
-INT. OCULAR BLEEDING

115. HYPHEMA(BLOOD IN ANT
CHAMBER)
•
•
MAJOR ARTERIAL CIRCLE
CAPILLARIES OF MINOR ARTERIAL CIRCLE

116. OTHER CAUSES
•
•
•
•
•
•
•
INTRA-OP & POST OP
HERPETIC IRIDOCYCLITIS
RUBEOSIS IRIDIS
BLOOD DYSCRASIAS
INT. OCULAR MALIGNANCY
IDIOPATHIC
JUVENILE XANTHO-GRANULOMA

117. MANAGEMENT
•
•
•
•
•
•
REST IN PROPPED UP POSITION
ANTIBIOTIC
TOPIN
TIMOLOL
STEROID
ACETAZOLAMIDE
PARACENTESIS

118. INDICATION OF PARACENTESIS
•
•
•
•
NOT ABSORBED 5-7 DAYS
HIGH IOP
BLOOD STAINING OF CORNEA
TOTAL HYPHEMA

121. IRIS
•
•
•
IRIDODIALYSIS-D SHAPED PUPIL
ANTI-FLEXION OF IRIS
TRAUMATIC ANIRIDIA

123. PUPIL
•
•
•
MYDRIASIS
D-SHAPED PUPIL
IRREGULAR PUPIL

124. LENS
•
•
VOSSIUS RING
CONCUSSION CATARACT
ROSETTE-SHAPED
SUBLUXATION

126. VITREOUS
•
•
•
LIQUIFACTION
DETACHMENT
HAEMORRHAGE
CHOROID
RUPTURE
HAEMORRHAGE

127. RETINA
•
•
•
•
•
•
COMMOTIO RETINAE(BERLIN’S EDEMA)
MACULAR CYST
MACULAR HOLE
RETINAL HAEMORRHGE
RETINAL TEAR
RETINAL DETACHMENT

128. RETINAL HEMORRHAGE

129. OPTIC DISC HEMORRHAGE

130. OPTIC NERVE
•
AVULSION—OPTIC ATROPHY
IOP
HYPOTONY
GHOST CELL GLAUCOMA
ANGLE RECESSION GLAUCOMA

131. ORBIT
•
•
PROPTOSIS
BLOW-OUT FRACTURE

133. INTRA OCULAR FOREIGN
BODY(IOFB)
•
•
SIDEROSIS BULBI—FE-IRREVERSIBLE
CHALCOSIS BULBI-CU--REVERSIBLE

134. CHEMICAL INJURIES
•ALKALI > ACID

136. HUGHES AND ROPER-HALL
CLASSIFICATION
•
GRADE 1-CORNEAL EPI. DAMAGE GOOD
NO LIMBAL ISCHAEMIA

2-CORNEA-HAZY-IRIS SEEN
1/3 LIMBAL ISCHAEMIA FAIR

3-TOT. LOSS OF CORNEAL EPITHELIUM
½ LIMBAL ISCHAEMIA GUARDED

4-TOT. CORNEA OPAQUE
>1/2 LIM. ISCHAEMIA POOR

137. TREATMENT
•
•
•
•
THOROUGH WASH
TOPICAL STEROID
TOPICAL ANTIBIOTIC
ANTI GLAUCOMA DRUGS

138. SYMPATHETIC OPHTHALMITIS
•
•
•
•
PENETRATING/SURGICAL
GRANULOMATOUS UVEITIS
TRAUMATISED EYE –EXCITING
FELLOW EYE –SYMPATHIZING
80% --3 MONTHS OF TRAUMA
90%--1 YEAR

139. PATHOGENESIS
•
•
AUTOIMMUNO REACTION TO ANTIGENS IN UVEAL TISSUE,
UVEAL PIGMENTS & RETINAL S-ANTIGEN

AGGREGATION OF LYMPHOCYTES & PLASMA CELL
SCATTERED THROUGHOUT UVEAL TISSUE

140. CLINICAL FEATURE
•
•
•
•
PHOTOPHOBIA
LOSS OF ACCOMODATION
EXCITING-CILIARY CONG.
SYMPHATHIZING-RETROLENTAL FLARE
MUTTON- FAT KP
FUNDUS-DALEN –FUCHS ‘ NODULE
COMPLICATION –CATARACT
-SEC. GLAUCOMA
-PHTHISIS BULBI

141. TREATMENT
•
STEROID-TOPICAL
SUB-TENON
SYSTEMIC
IMMUNO-SUPPRESSIVE
ENUCLEATION WITHIN 2 WEEKS—INJURED EYE