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Hypopyon corneal ulcer

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					Hypopyon corneal ulcer
Etiopathogenesis
Causative organisms. Many pyogenic organisms
(staphylococci, streptococci, gonococci, Moraxella)
may produce hypopyon, but by far the most
dangerous are pseudomonas pyocyanea and
pneumococcus.
Thus, any corneal ulcer may be associated with
hypopyon, however, it is customary to reserve the
term 'hypopyon corneal ulcer' for the characteristic
ulcer caused by pneumococcus and the term 'corneal
ulcer with hypopyon' for the ulcers associated with
hypopyon due to other causes. The characteristic
hypopyon corneal ulcer caused by pneumococcus is
called ulcus serpens.
Source of infection for pneumococcal infection is
usually the chronic dacryocystitis.
Factors predisposing to development of hypopyon.
Two main factors which predispose to development
of hypopyon in a paitent with corneal ulcer are, the
virulence of the infecting organism and the resistance
of the tissues. Hence, hypopyon ulcers are much more
common in old debilitated or alcoholic subjects.
Mechanism of development of hypopyon. Corneal
ulcer is often associated with some iritis owing to
diffusion of bacterial toxins. When the iritis is severe
the outpouring of leucocytes from the vessels is so
great that these cells gravitate to the bottom of the
anterior chamber to form a hypopyon. Thus, it is
important to note that the hypopyon is sterile since
the outpouring of polymorphonuclear cells is due to
the toxins and not due to actual invasion by bacteria.
Once the ulcerative process is controlled, the
hypopyon is absorbed.
Clinical features
Symptoms are the same as described above for
bacterial corneal ulcer. However, it is important to note
that during initial stage of ulcus serpens there is
remarkably little pain. As a result the treatment is often
undully delayed.
Signs. In general the signs are same as described
above for the bacterial ulcer. Typical features of ulcus
serpens are :
  Ulcus serpens is a greyish white or yellowish
disc shaped ulcer occuring near the centre of
cornea (Fig. 5.6).
  The ulcer has a tendency to creep over the
cornea in a serpiginous fashion. One edge of the
ulcer, along which the ulcer spreads, shows more
infiltration. The other side of the ulcer may be
undergoing simultaneous cicatrization and the
edges may be covered with fresh epithelium.
  Violent iridocyclitis is commonly associated with
a definite hypopyon.
  Hypopyon increases in size very rapidly and
often results in secondary glaucoma.
  Ulcer spreads rapidly and has a great tendency
for early perforation.
DISEASES OF THE CORNEA 97
Management
Management of hypopyon corneal ulcer is same as
for other bacterial corneal ulcer. Special points which
need to be considered are :
  Secondary glaucoma should be anticipated and
treated with 0.5% timolol maleate, B.I.D. eye drops
and oral acetazolamide.
  Source of infection, i.e., chronic dacryocystitis if
detected, should be treated by dacryocystectomy.
Complications of corneal ulcer
1. Toxic iridocyclitis. It is usually associated with
cases of purulent corneal ulcer due to absorption of
toxins in the anterior chamber.
2. Secondary glaucoma. It occurs due to fibrinous
exudates blocking the angle of anterior chamber
(inflammatory glaucoma).
3. Descemetocele. Some ulcers caused by virulent
organisms extend rapidly up to Descemet's membrane,
which gives a great resistance, but due to the effect
of intraocular pressure it herniates as a transparent
vesicle called the descemetocele or keratocele
(Fig.5.3). This is a sign of impending perforation and
is usually associated with severe pain.
4. Perforation of corneal ulcer. Sudden strain due
to cough, sneeze or spasm of orbicularis muscle may
convert impending perforation into actual perforation
(Fig. 5.4). Following perforation, immediately pain is
decreased and the patient feels some hot fluid
(aqueous) coming out of eyes.
Sequelae of corneal perforation include :
i. Prolapse of iris. It occurs immediately following
perforation in a bid to plug it.
ii. Subluxation or anterior dislocation of lens
may occur due to sudden stretching and rupture
of zonules.
iii. Anterior capsular cataract. It is formed when
the lens comes in contact with the ulcer following
a perforation in the pupillary area.
iv. Corneal fistula. It is formed when the perforation
in the pupillary area is not plugged by iris and
is lined by epithelium which gives way
repeatedly. There occurs continuous leak of
aqueous through the fistula.
v. Purulent uveitis, endophthalmitis or even
panophthalmitis may develop due to spread of
intraocular infection.
vi. Intraocular haemorrhage in the form of either
vitreous haemorrhage or expulsive choroidal
haemorrhage may occur in some patients due to
sudden lowering of intraocular pressure.
5. Corneal scarring. It is the usual end result of
healed corneal ulcer. Corneal scarring leads to
permanent visual impairment ranging from slight
blurring to total blindness. Depending upon the
clinical course of ulcer, corneal scar noted may be
nebula, macula, leucoma, ectatic cicatrix or kerectasia,
adherent leucoma or anterior staphyloma (for details
see pages 122).
Management of a case of corneal ulcer
[A] Clinical evaluation
Each case with corneal ulcer should be subjected to:
1. Thorough history taking to elicit mode of onset,
duration of disease and severity of symptoms.
A
B
Fig. 5.6. Hypopyon corneal ulcer : A, Diagrammatic
depiction; B, Clinical photograph.
98 Comprehensive OPHTHALMOLOGY
2. General physical examination, especially for
built, nourishment, anaemia and any immunocompromising
disease.
3. Ocular examination should include:
i. Diffuse light examination for gross lesions of
the lids, conjunctiva and cornea including
testing for sensations.
ii. Regurgitation test and syringing to rule out
lacrimal sac infection.
iii. Biomicroscopic examination after staining of
corneal ulcer with 2 per cent freshlyprepared
aqueous solution of fluorescein dye or sterilised
fluorescein impregnated filter paper strip to note
site, size, shape, depth, margin, floor and
vascularization of corneal ulcer. On
biomicroscopy also note presence of keratic
precipitates at the back of cornea, depth and
contents of anterior chamber, colour and pattern
of iris and condition of crystalline lens.
[B] Laboratory investigations
(a) Routine laboratory investigations such as
haemoglobin, TLC, DLC, ESR, blood sugar, complete
urine and stool examination should be carried out in
each case.
(b) Microbiological investigations. These studies
are essential to identify causative organism, confirm
the diagnosis and guide the treatment to be instituted.
Material for such investigations is obtained by
scraping the base and margins of the corneal ulcer
(under local anaesthesia, using 2 percent xylocaine)
with the help of a modified Kimura spatula or by
simply using the bent tip of a 20 gauge hypodermic
needle. The material obtained is used for the following
investigations:
i. Gram and Giemsa stained smears for possible
identification of infecting organisms.
ii. 10 per cent KOH wet preparation for
identification of fungal hyphae.
iii. Calcofluor white (CFW) stain preparation is
viewed under fluorescence microscope for
fungal filaments, the walls of which appear
bright apple green.
iv. Culture on blood agar medium for aerobic
organisms.
v. Culture on Sabouraud's dextrose agar medium
for fungi.
[C] Treatment
I. Treatment of uncomplicated corneal ulcer
Bacterial corneal ulcer is a vision threatening
condition and demands urgent treatment by
identification and eradication of causative bacteria.
Treatment of corneal ulcer can be discussed under
three headings:
1. Specific treatment for the cause.
2. Non-specific supportive therapy.
3. Physical and general measures.
1. The specific treatment
(a) Topical antibiotics. Initial therapy (before
results of culture and sensitivity are available)
should be with combination therapy to cover
both gram-negative and gram-positive
organisms.
It is preferable to start fortified gentamycin (14
mg/ml) or fortified tobramycin (14mg/ml)
eyedrops along with fortified cephazoline (50mg/
ml), every ½ to one hour for first few days and
then reduced to 2 hourly. Once the favourable
response is obtained, the fortified drops can be
substituted by more diluted commercially
available eye-drops, e.g. :
  Ciprofloxacin (0.3%) eye drops, or
  Ofloxacin (0.3%) eye drops, or
  Gatifloxacin (0.3%) eye drops.
(b) Systemic antibiotics are usually not required.
However, a cephalosporine and an aminoglycoside
or oral ciprofloxacin (750 mg twice daily)
may be given in fulminating cases with
perforation and when sclera is also involved.
2. Non-specific treatment
(a) Cycloplegic drugs. Preferably 1 percent atropine
eye ointment or drops should be used to reduce
pain from ciliary spasm and to prevent the
formation of posterior synechiae from secondary
iridocyclitis. Atropine also increases the blood
supply to anterior uvea by relieving pressure
on the anterior ciliary arteries and so brings
more antibodies in the aqueous humour. It also
reduces exudation by decreasing hyperaemia
and vascular permeability. Other cycloplegic
which can be used is 2 per cent homatropine
eye drops.
DISEASES OF THE CORNEA 99
(b) Systemic analgesics and anti-inflammatory
drugs such as paracetamol and ibuprofen relieve
the pain and decrease oedema.
(c) Vitamins (A, B-complex and C) help in early
healing of ulcer.
3. Physical and general measures
(a) Hot fomentation. Local application of heat
(preferably dry) gives comfort, reduces pain
and causes vasodilatation.
(b) Dark goggles may be used to prevent
photophobia.
(c) Rest, good diet and fresh air may have a
soothing effect.
II. Treatment of non-healing corneal ulcer
If the ulcer progresses despite the above therapy the
following additional measures should be taken:
1. Removal of any known cause of non-healing
ulcer. A thorough search for any already missed
cause not allowing healing should be made and
when found, such factors should be eliminated.
Common causes of non-healing ulcers are as
under:
i. Local causes. Associated raised intraocular
pressure, concretions, misdirected cilia,
impacted foreign body, dacryocystitis,
inadequate therapy, wrong diagnosis,
lagophthalmos and excessive vascularization
of ulcer.
ii. Systemic causes: Diabetes mellitus, severe
anaemia, malnutrition, chronic debilitating
diseases and patients on systemic steroids.
2. Mechanical debridement of ulcer to remove
necrosed material by scraping floor of the ulcer
with a spatula under local anaesthesia may hasten
the healing.
3. Cauterisation of the ulcer may also be considered
in non-responding cases. Cauterisation may be
performed with pure carbolic acid or 10-20 per
cent trichloracetic acid.
4. Bandage soft contact lens may also help in
healing.
5. Peritomy, i.e., severing of perilimbal conjunctival
vessels may be performed when excessive corneal
vascularization is hindering healing.
III. Treatment of impending perforation
When ulcer progresses and perforation seems
imminent, the following additional measures may help
to prevent perforation and its complications:
1. No strain. The patient should be advised to
avoid sneezing, coughing and straining during
stool etc. He should be advised strict bed rest.
2. Pressure bandage should be applied to give
some external support.
3. Lowering of intraocular pressure by
simultaneous use of acetazolamide 250 mg QID
orally, intravenous mannitol (20%) drip stat, oral
glycerol twice a day, 0.5% timolol eyedrops twice
a day, and even paracentesis with slow evacuation
of aqueous from the anterior chamber may be
performed if required.
4. Tissue adhesive glue such as cynoacrylate is
helpful in preventing perforation.
5. Conjunctival flap. The cornea may be covered
completely or partly by a conjunctival flap to
give support to the weak tissue.
6. Bandage soft contact lens may also be used.
7. Penetrating therapeutic keratoplasty (tectonic
graft) may be undertaken in suitable cases, when
available.
IV. Treatment of perforated corneal ulcer
Best is to prevent perforation. However, if perforation
has occurred, immediate measures should be taken
to restore the integrity of perforated cornea.
Depending upon the size of perforation and
availability, measures like use of tissue adhesive glues,
covering with conjunctival flap, use of bandage soft
contact lens or therapeutic keratoplasty should be
undertaken. Best is an urgent therapeutic
keratoplasty.

				
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posted:9/16/2012
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Description: Common Eye Disease