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Leprosy part 2 - a presentation at www.eyenirvaan.com
1. Pradnya Gogate B. Optom,
LEPROSY
PART 2
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2. LEPROSY : OPHTHALMIC
STRUCTURES INVOLVED
Cornea
Sclera
Iris
Ciliary body
Lens
Ocular
adnexa
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3. EYE COMPLICATIONS
Leprosy: Potentially Blinding Lesions
Lagophthalmos
(whole spectrum)
Corneal hypoaesthesia (whole spectrum)
Acute iritis and scleritis (MB leprosy)
Chronic iritis and iris atrophy (MB leprosy)
Cataract (whole spectrum)
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4. LAGOPHTHALMOS
Due
to
damage
to the facial
nerve
late result of
infiltration and
secondary atrophy of
the facial nerve and
orbicularis muscle
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5. HOW IS LAGOPHTHALMOS
ASSESSED?
Observe the Frequency and Extent of Blinking
Ask the Patient to Close the Eyes 'As in Sleep'
Ask the Patient to Close the Eyes Tightly
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6.
Treatment of Lagophthalmos is Dependent On:
1.
Duration of the lagophthalmos
2. Width of the eyelid gap, and exposure of the cornea
3. Presence or absence of corneal hypoaesthesia
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7.
Duration of lagophthalmos ≤ 6
months: prednisolone 40mg/day
slowly reducing over 12 weeks
Duration of lagophthalmos > 6
months with eyelid gap < 6 mm:
Conservative treatment, e.g.
sunglasses, 'think blink‘
Duration of lagophthalmos > 6
months with eyelid gap ≥ 6 mm:
eyelid surgery
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9. damage to the lower, exposed
part of the cornea, due to
dryness
superficial punctate keratitis
deeper corneal defect
secondarily infected
blindness by scarring or
perforation
Chronic exposure may lead to
progressive scarring
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10. TREATMENT
antibiotic eye ointment
an eye shield
An exposure ulcer is a definite indication for
eyelid surgery.
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12. CAUSES OF CORNEAL
HYPOAESTHESIA
As
a result of reversal reaction in the
trigeminal nerve (V cranial nerve).
As a result of exposure of the cornea in
lagophthalmos.
As
a result of severe scleritis and damage to
the ciliary nerves (often bilateral).
As
a result of bacterial infiltration and
secondary atrophy of ciliary and corneal nerves
(often bilateral).
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13. TREATMENT
no cure for corneal hypoaesthesia
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14. Patients should receive good health education
protection of the eyes with glasses or sunglasses
regular blinking exercises
regular inspection of the eyes
Corneal hypoaesthesia may be an indication for early
eyelid surgery
in lagophthalmos
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15. ACUTE IRITIS
only in MB patients
evidence of ENL reaction inside the eye
recur at any time
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16. SIGNS AND SYMPTOMS
redness,
pain,
photophobia, reduced
visual acuity
haziness
of the cornea
and secondary
glaucoma
unilateral
or bilateral
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17. TREATMENT
atropine
sulphate 1% twice daily, steroid eye
drops 6 times daily and steroid ointment at
night time
Systemic
steroids if there is ENL reaction
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18. SIGNS OF MB LEPROSY
(temporal) madarosis of eyebrows
early collapse of the nose
nodules on the ears
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19. TYPE 2 REACTION: ACUTE
EPISCLERITIS AND SCLERITIS
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20. EPISCLERITIS
is
a transient condition
often
as a precursor of a systemic ENL
reaction
resolves
Tx:
spontaneously and completely
topical steroids
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21. SCLERITIS
bilateral
in combination with a
severe ENL reaction
may be nodular or diffuse
and occurs with or without
acute iritis
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22.
painful
ciliary nerves may become damaged and pain
becomes less
ciliary staphylomas
subsequent scleral translucency
thinning of the sclera
In sclerosing keratitis the whole cornea may become
opaque
23. TREATMENT
Acute
scleritis is treated topically with
steroids
Oral
non steroidal anti-inflammatory drugs
(NSAID's), such as Ibuprofen (400 mg four
times daily)
Treatment
of the ENL reaction will require
high doses of systemic steroids and
clofazimine
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24. MASSIVE BACILLARY INFILTRATION:
PERI-ORBITAL COMPLICATIONS
Abnormalities occur around the eye due to infiltration
by bacilli and secondary atrophy
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25. LESIONS AROUND THE EYE
loss of eyebrows
eyelashes also become atrophic and
scanty (madarosis), and trichiasis
collapse of the nose and secondarily
blocked lacrimal sac
loose skinfold in the upper eyelids
(blepharochalasis)
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26. LESIONS WITHIN THE EYE
Ocular
leproma
Superficial
pearls
Iris
lepromatous keratitis and iris
atrophy and pinpoint pupil
Chronic
iritis
Atrophy
of the ciliary body
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27. OCULAR LEPROMA
Lepromatous nodule in the eye, usually in the region
of the lateral limbus
a ring of nodules
pinkish red or yellowish and fleshy
pinkish red or yellowish and fleshy
painless
pupil may be deformed
28. PUNCTATE AVASCULAR LEPROUS KERATITIS
AND IRIS PEARLS
PUNCTATE LEPROUS KERATITIS
faint discrete superficial infiltrates in the upper
outer quadrant of the cornea
consist of clumps of bacilli-laden cells
become tiny white opacities
finally coalesce in a diffuse haze
bilateral and asymptomatic.
Beading of the corneal nerves (diagnostic for leprosy)
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29. IRIS PEARLS
tiny white clumps (like grains of salt) extruding from the
surface of the iris
histology shows M. leprae
dislodge into the lower angle of the anterior chamber,
where they may be absorbed or give rise to anterior
synechiae
Iris pearls are pathognomonic for leprosy.
seen in longstanding MB leprosy
31. IRIS ATROPHY AND PIN-POINT PUPIL
The
iris crypts flatten
the stroma thins
deep pigmented layer of the iris become visible
full thickness iris holes appear
prominent in the stroma of the iris dilator
muscle
pupil becomes pin-point
bilateral
patient will become 'night blind'.
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32. TREATMENT
dilate the pupil with phenylephrine 2.5 - 5%
sector iridectomy
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33. CHRONIC IRITIS
no redness
flare and cells in the anterior chamber
small keratic precipitates
greyish exudates along the pupillary margin
the pupil constricts
posterior synechiae may form
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34. ATROPHY OF THE CILIARY
BODY
ciliary body is believed to be the port of entry of M.
leprae into the eye
loss of accommodation
intraocular pressure tends to be low i
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36. Prevention of blindness due to leprosy
Early diagnosis of leprosy and timely
MDT treatment
Early recognition of reactions and
effective treatment of reactions with
systemic steroids
Regular eye examination and treatment
of any complications
Lagophthalmos surgery in all patients
with a eyelid gap of ≥ 6 mm
Lens extraction in any leprosy patients
who develop blinding cataract
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