ACCORDING TO AYURVEDA THE DISEASES OF SCLERA ARE CALLED AS SHUKLAGATA ROGAS. THE PROBABLE MODERN CORRELATION OF SHUKLAGATA ROGAS LIKE ARMA(PTERYGIUM) ETC. ARE EXPLAINED IN THIS PPT.

1. MODERN CORRELATION OF ALL
SHUKLAGATA ROGA
DR. PREMA. K. JIGALI
ASST. PROFESSOR, P G DEPT. OF SHALAKYA TANTRA
SVM AMC, ILKAL, KARNATAKA-587125

2. PTERYGIUM
• DEFINITION
• Derived from Greek word pterygion means wing(Buttrefly)
• A wing shaped fold of conjunctiva encroaching on cornea from either side within
the interpalpebral fissure.
• The base of the pterygium lies within the interpalpebral conjunctiva and the
apex of the triangle encroaches upon cornea.

3. • Pterygium is more commonly seen in people living in hot climates and
in those who work outdoors and it is widely accepted that pterygium is
response to prolonged effect of environmental factors such as
exposure to sunlight( uv rays),dry heat, wind and abundance of dust.
Etiology

4. Pathology
• Pathologically pterygium is a degenerative and hyperplastic condition of
conjunctiva.
• The subconjunctival tissue undergoes elastotic degeneration and proliferates
as vascularised granulation tissue under the epithelium, which ultimately
encroaches the cornea.
• The epithelium , bowman's layer and superficial stroma are destroyed.

5. Clinical features
Demography
• Age: Usually seen in old age.
• Sex: More common in males doing outdoor work than females.
• Laterality: It may be unilateral or bilateral.

8. • The normal flow of tears from temporal to nasal side towards the
punctum carries with it any dust particles entering the Conjunctival
sac thus the further irritating the nasal conjunctiva.

9. Symptoms
• Cosmetic intolerance may be the only issue in otherwise
asymptomatic condition in early stages.
• Foreign body sensation and irritation may be experienced.
• Defective vision occurs when it encroaches the pupillary area or due
to corneal astigmatism induced by fibrosis in the regressive stage.
• Diplopia may occur occasionally due to limitation of ocular
movements.

10. Signs
• Triangular fold of conjunctiva encroaching on
the cornea in the area of palpebral aperture
usually on the nasal side is typical
presentation of pterygium.
• However, it may also occur on the temporal
sides.
• Very rarely, both nasal and temporal sides are
involved (primary double pterygium)..

11. Stocker line:
• Reddish brown line of iron deposition seen
in corneal epithelium anterior to the
advancing head of pterygium.
• Stockers line is a punctate, brownish, sub
epithelial line passing vertically in front of
the invasive apex of the pterygium.
• The mechanism of iron deposition in the
development of pterygium is still unknown,
but iron level was reported significantly
higher in the pterygium tissue than in
normal conjunctiva.

12. Parts of pterygium
Parts of a fully developed pterygium are as follow:
• Head: Apical part present on the cornea,
• Neck: constricted part present in the limbal area,
• Body: scleral part, extending between limbus and canthus,
• Cap: semilunar whitish infiltrate present just in front of the head.

14. Types
• Based on the extent and progression, pterygium has been described
of three types
• Type 1: pterygium extends less than 2mm onto the cornea.
• Type 2: pterygium involves up to 4mm of the cornea.
• Type 3: pterygium encroaches on to more than 4mm of the cornea
and involves the visual axis.

19. Differential diagnosis
Pterygium must be differentiated from pseudo pterygium.
• Pseudopterygium is a fold of bulbar conjunctiva attached to the cornea.
• It is formed due to adhesions of chemosed bulbar conjunctiva to marginal
corneal ulcer.
• It usually occurs following chemical burns of the eye.
• Difference between pterygium and pseudopterygium

21. Treatment :
• Medical management is not much use
• Tear substitutes may be used in patients with small regressive
pterygium for dry eye symptoms.
• Topical steroid may be required for associated inflammation.
• Protection from u v rays with sunglasses decreases the growth
stimulus.

22. Surgical excision is the only satisfactory treatment, which may be
indicated for:
• Cosmetic disfigurement.
• Visual impairment due to regular or irregular astigmatism.
• Continued progression threatening to encroach onto the pupillary
area.
• Diplopia due to interference in ocular movements.

23. Surgical technique of pterygium excision;
• After topical anesthesia, eye is cleaned, draped and exposed using
universal eye speculum.
• Head of the pterygium is lifted and dissected off the cornea very
meticulously.
• Main mass of pterygium is then separated from the sclera underneath
and the conjunctiva superficially.
• Pterygium tissue is then excised taking care not to damage the
underlying medial rectus muscle.
• Hemostasis is achieved and the epi scleral tissue exposed is cauterized
thoroughly.
• Conjunctival limbal auto graft(CLAU)transplantation to cover the defect
after pterygium excision. It is the latest and most effective technique in
the management of pterygium. Use of fibrin glue to stick the auto graft in
place reduces the operating time as well as discomfort associated with
sutures.

24. Surgical steps

26. Recurrence of the pterygium after surgical excision is the main problem(30 to
40%). However it can be reduced by any of the following measures:
• Surgical excision with free conjunctival limbal autograft (CLAU)taken from
the same eye other eye is presently the preffered technique.
• Surgical excision with amniotic graft and mytomycin –C(0.02%) application
may required in recurrent pterygium or when dealing with a large
pterygium.
• Surgical excision with lamellar keratectomy and lamellar keratoplasty may
be required in deeply infiltrating recurrent recalcitrant pterygium.

28. Pinguecula
• . Pinguis means fat.
• It is common degenerative condition of the conjunctiva.
• It is characterized by formation of a triangular yellowish white patch on
the bulbar conjunctiva near the limbus. This condition is termed
pinguecula

29. Etiology
• Etiology of pinguecula is not known exactly.
• It has been considered as an age change, occurring more commonly
in persons exposed to strong sunlight, dust and wind.

30. Pathology
• There is an elastotic degeneration of collagen fibers of the substantia
propria of conjunctiva
• coupled with deposition of amorphous hyaline material in the
substance of conjunctiva.

31. Clinical features:
• It is a bilateral, usually stationary
condition, presenting as a
yellowish white triangular patch
near the limbus.
• Apex of the triangle is always away
from the cornea. It affects first
nasal side and then the temporal
side.
• When conjunctiva is congested, it
stands out as an avascular
prominence.

32. Complications:
• Inflammation
• Intraepithelial abscess
• Rarely calcification
• Doubtful conversion into pterygium.

33. Treatment
• No treatment required for pinguecula.
• However, when cosmetically unaccepted and if so desired, it may be
excised.
• When inflamed it is treated with topical steroid.

34. ECHYMOSIS OF CONJUNCTIVA OR
SUBCONJUNCTIVAL HAEMORRHAG:
• It is of very common occurrence.
• It may vary in extent from small petechial hemorrhage to an extensive
one spreading under the whole of the bulbar conjunctiva and thus
making the white sclera of the eye invisible.

35. ETIOLOGY:
• Subconjunctival hemorrhage may be associated with following conditions:
1.Trauma: it is the most common cause of subconjunctival hemorrhage. It may
be in the form of
a)Local trauma to conjunctiva including that due to surgery and sub
conjunctival injections
b)Retrobulbar hemorrhage which almost immediately spreads below the
conjunctiva. Mostly, it results from a retrobulbar injection and from trauma
involving various walls of the orbit.
2.Inflammation of the conjunctiva: petechial subconjunctival hemorrhages are
usually associated with acute hemorrhagic conjunctiva caused by picorna virus,
pneumococcal conjunctivitis and leptospirosis.
3.Sudden venous congestion of head: The subconjunctival hemorrhages may
owing to rupture of conjunctival capillaries due to sudden rise in pressure.
4.Bleeding disorders like purpura, hemophilia and scurvy.

36. 5. Spontaneous rupture of fragile capillaries may occur in vascular
diseases such as arteriosclerosis, hypertension and diabetes mellitus.
6. Acute febrile systemic infections such as typhoid, malaria, diphtheria,
meningococcal septicemia, measles.

37. Clinical features
• Subconjunctival hemorrhage is symptomless. However, there may be
symptoms of associated causative disease.
• On examination:
• Subconjunctival hemorrhage looks as a flat sheet of homogeneous
bright red color with well defined limits.

38. Treatment
• It is self limiting condition that requires no treatment in the absence
of infection or significant trauma.
• Most of the time it is absorbed completely within 7 to 14 days.
• During absorption color changes are noted from bright red to orange
and then yellow. In sever cases, some pigmentation may be left
behind after absorption.
• Psychotherapy and assurance to the patient is most important part of
the treatment.
• Cold compresses to check the bleeding and hot compresses may help
in absorption of blood.

39. Anatomy of sclera

40. Anatomy of sclera

41. EPISCLERITIS
• It is benign recurrent inflammation of the epi sclera, involving the
overlying Tenon's capsule but not underlying the sclera.
• It is typically affects young adults, being twice as common in women
than men.

42. Etiology;
• Idiopathic: exact etiology is unknown.
• Systemic diseases associated with episcleritis include gout, rosacea,
psoriasis and connective tissue diseases.
• Hypersensitive reaction to endogenous tubercular or streptococcal
toxins is also reported.
• Infection of episcleritis caused by herpes zoster virus, syphilis, lyme
disease.

43. Pathology
• Histologically, there occurs localized lymphocytic infiltration of
episcleral tissue associated with
• edema and
• congestion of overlying tenons capsule and conjunctiva.

44. Clinical features:
• Symptoms:
• It is characterized by redness, mild ocular discomfort described as
gritty, burning or foreign body sensation.
• Rarely, mild photophobia and lacrimation.

45. • Sign:
• On examination two clinical types of episcleritis, simple and nodular
may be recognized.
• 1.simple episcleritis: it is characterized by sectorial (occasionally
diffuse)inflammation of episclera. The engorged episcleral vessels are
large and run in radial direction beneath the conjunctiva.
• Nodular episcleritis: it is characterized by pink or purple flat nodule
surrounded by injection, usually 2-3 mm away from the limbus. The
nodule is firm, tender, can be move separately from the sclera and
the overlying conjunctiva also moves freely.

46. Differential diagnosis:
• Simple episcleritis may be confused rarely with conjunctivitis.
• Nodular episcleritis may be confused with inflamed pinguecula,
swelling and congestion due to foreign body lodged in bulbar
conjunctiva and very rarely with scleritis.

47. Treatment
• 1. Topical NSAIDs, e.g, ketorolac 0.3%
• 2. Topical mild corticosteroid eye drops e.g, flurometholone or loteprednol
instilled 2-3 hourly.
• Topical artificial tears e.g, 0.5% carboxy methyl cellulose have soothing effect.
• Cold compresses applied to the closed lids may offer symptomatic relief from
ocular discomfort.
• Systemic NSAIDs may be required in recurrent cases.

48. Scleritis
• Scleritis refers to a inflammation of the sclera proper.
It is a comparatively serious disease which may consensual impairment and
even loss of vision if treated inadequately. Fortunately incidence is less than
that of episcleritis.
It usually occurs in elderly patients(40 to 70 years) involving females more
than males.

49. Etiology
Overall about 50% cases of scleritis are associated with some systemic
diseases, most common being connective tissue diseases.
Common conditions are as follows:
1. Autoimmune collagen disorders, especially rheumatoid arthritis(most
common systemic association), is the most common association. About
0.5% of patients suffering from seropositive rheumatoid arthritis
develop scleritis. Other associated collagen disorders are wegners
granulomatosis(most common vasculitis), polyarteritis nodosa, systemic
lupus erythromatosus and ankylosing spondylitis.
2. Metabolic disorders like gout and thyrotoxicosis have also been reported
to be associated with scleritis.
3. Some infections, particularly herpes zoster ophthalmicus, chronic
staphylococcal and streptococcal infection have also been known cause
infectious scleritis.

50. 4. Granulomatous diseases like tuberculosis, syphilis, sarcoidosis, leprosy can
also cause for scleritis.
5. Miscellaneous conditions like irradiation, chemical burns, vogt koyanagi
harada syndrome, bechets disease and rosacea are also implicatedin the
etiology.
6. Surgically induced scleritis is a rare complication of ocular surgery. It occurs
within 6 months postoperatively.
7. Idiopathic in many cases of scleritis, cause is unknown.

51. pathology
• Histopathological changes are that of a chronic granulomatous disorder
characterised by fibrinoid necrosis, destruction of collagen together
with infiltration by polymorphonuclear cells, lymphocytes, plasma cells
and macrophages. The granuloma surrounded by multinucleated
epitheloid giant cells and old and new vessels.

52. Classification
Scleritis can be classified as follows:
A. Non-infectious scleritis
I. Anterior scleritis(98%)
a. Non necrotizing scleritis(85%)
1. Diffuse
2. Nodular
B. Necrotizing scleritis(13%)
1. With inflammation
2. Without inflammation
II. Posterior scleritis(2%)
B. Infectious scleritis

53. • Clinical features
• Symptoms
• Pain: patients complain of moderate to severe pain which is deep and
boring in character and often wakes the patient early in the morning.
Ocular pain radiates to the jaw and temple.
• Redness may localized or diffuse.
• Photophobia and lacrimation may be mild to moderate.
• Diminution of vision may occur occasionally.

54. Signs:
A. Non infectious scleritis
Salient features of different clinical types of non infectious scleritis are as
below:
I. Anterior scleritis
a. Non necrotizing anterior scleritis
1. Non necrotizing anterior diffuse scleritis. It is the commonest variety,
characterized by widespread inflammation involving a quqdrant or
more of the anterior sclera. The involved area is raised and salmon pink
to purple in color.
2. Non necrotizing anterior nodular scleritis. It is characterized by one or
two hard, purplish elevated immovable scleral nodules,

55. Complications:
These are quite common with necrotizing scleritis and include sclerosing
keratitis, keratolysis, complicated cataract and secondary glaucoma.
Investigations:
Following laboratory studies may helpful in identifying associated systemic
diseases.
1. TLC, DLC and ESR.
2. Serum level of complement, immune complexes, rheumatoid factor,
antinuclear antibodies(s.l.e) and and L.E cells survey.
3. FTA-ABS, VDRL for syphilis.
4. Serum uric acid for gout.
5. Urine analysis.
6. Mantoux test.
7. X-ray chest, paranasal sinuses, sacroiliac joint and orbit.

56. Treatment
A. Non-infectious scleritis.
I. Non necrotizing scleritis. It is treated by:
Topical steroid eye drop
Systemic indomethacin 75mg twice a day until inflammation resolves.
II. Necrotizing scleritis. It is treated by:
Topical steroids
Oral steroids on heavy dosses, tapered slowly.
Immunosuppresive agents may required in non responsive cases.
Surgical treatment, in the form of scleral patch graft may required to
preserve integrity of the globe in extensive scleral melt and thinning.

57. B. Infectious scleritis:
Antimicrobial therapy, both with topical and oral agents is required in an
aggressive manner.
Surgical debridement is found useful by debulking the infected scleral
tissue and also facilitating the effect of antibiotics.

58. Comparison between Scleritis and Episcleritis
EPISCLERITIS
• Irritation
• Bright red
• Blanch
SCLERITIS(3P)
• Pain
• Purple
• Persist

59. Xerophthalmia
• The term xerophthalmia reserved to cover all the ocular
manifestations of vitamin A deficiency, including not only structural
changes affecting the conjunctiva, cornea and occasionally retina, but
also the biophysical disorders of retinal rods and cones functions.
Etiology:
• It occurs either due to dietary deficiency of vitamin A or
• its defective absorption from the gut.

60. WHO classification(1982)
The new xerophthalmia classification(modification of original 1976
classification) is as follows:
• XN Night blindness
• X1A Conjunctival xerosis
• X1B Bitots spots
• X2 Corneal xerosis
• X3A corneal ulceration/ keratomalacia affecting less than one-third
corneal surface.
• X3B Corneal ulceration affects more than one third corneal surface
• XS Corneal scar due to xerophthalmia.
• XF Xerophthalmic fundus.

62. • Clinical features:
• Conjunctival xerosis:
( xero-dry or dehydrated; osis-degenerative process)
• it consists of one or more patches of dry, lusterless, non wettable
conjunctiva. These patches almost always involve the interpalpebral
area of the temporal quadrants and often the nasal quadrants as well. In
more advanced cases, the entire bulbar conjunctiva may be affected.
• Typical xerosis may be associated with Conjunctival thickening, wrinkling
and pigmentation.

63. • Bitots spot: its an extension of the xerotic process seen in X1A.
• It’s a raised, silvery white, foamy, triangular patch of keratinized
epithelium, situated on the bulbar conjunctiva in the interpalpebral
area. It is usually bilateral and temporal and less frequently nasal.

64. X2(Corneal xerosis)
• The earliest change in the cornea is punctate keratopathy which begin
in the lower nasal quadrant followed by haziness and or dryness.
Involved cornea lacks lustre.

65. X3A AND X3B(corneal
ulceration/keratomalacia)
• Stromal defects occurs in this stage due to colloquate necrosis and
take several forms.
• Small ulcers(1-3mm)occur peripherally; they are characteristically
circular, with steep margins and are sharply demarcated.
• Large ulcers and area of necrosis may extend centrally or involve the
entire cornea

67. XS(Corneal scar)
• Healing of stromal defects results in corneal scars of different
densities and sizes which may or may not cover the pupillary area.

68. XFC(Xerophthlmic fundus)
• It is characterized by typical seed like, raised, whitish lesions scattered
uniformly over the part of the fundus at the level of optic disc.

69. Treatment
It includes local ocular therapy, vitamin A therapy and treatment of
underlying cause.
1.Local ocular therapy.
• For conjunctival xerosis artificial tears should be instilled every 3-
4nhours.
• In the stage of keratomalacia, fullfledged treatment of bacterial
corneal ulcer should be instilled.
2.Vitamin A therapy. Treatment schedules apply to all stages of active
xerophthalmia viz. XN, X1A, X1B, X2, X3A AND X3B.
3. Treatment of underlying cause such as PME and other nutritional
disorders, diarrhea, dehydration and electrolyte imbalance.

70. VITAMIN A THERAPY
• Therapeutic dose: 2 lakh IU orally on two successive days.
• Prophylactic dose:
• Children <12 months of age- 1 lakh IU once every 4-6 months
• Children above 12 months of age- 2 lakh IU every 4-6 months
• Newborn – 50,000 IU at birth

71. VITAMIN A THERAPY
Women of childbearing age 3 lakh IU within one month of giving birth
Pregnant and Lactating women – 5,000 IU everyday or 20,000 IU once a
week

72. Thank you