Pathology of corneal ulcer Once the damaged corneal epithelium is invaded by the offending agents the sequence of pathological changes which occur during development of corneal ulcer can be described under four stages, viz., infiltration, active ulceration, regression and cicatrization. The terminal course of corneal ulcer depends upon the virulence of infecting
agent, host defence mechanism and the treatment received.
Depending upon the prevalent circumstances the course of corneal ulcer may take one of the three forms:
(A) Ulcer may become localised and heal;
(B) Penetrate deep leading to corneal perforation;
or
(C) Spread fast in the whole cornea as sloughing corneal ulcer.
The salient pathological features of these are as under:
[A] Pathology of localised corneal ulcer
1. Stage of progressive infiltration (Fig. 1A). It is characterised by the infiltration of polymorphonuclear and/or lymphocytes into the epithelium
from the peripheral circulation supplemented by similar cells from the underlying stroma if this tissue is also affected. Subsequently necrosis of the
involved tissue may occur, depending upon the virulence of offending agent and the strength of host defense mechanism.
2. Stage of active ulceration (Fig. 1B). Active ulceration results from necrosis and sloughing of the epithelium, Bowman's membrane and the involved stroma. The walls of the active ulcer project owing to swelling of the lamellae by the imbibition of fluid and the packing of masses of leucocytes between them. This zone of infiltration may extend to a considerable distance both around and beneath the ulcer. At this
stage, sides and floor of the ulcer may show grey infiltration and sloughing.
During this stage of active ulceration, there occurs hyperaemia of circumcorneal network of vessels which results into accumulation of purulent exudates on the cornea. There also occurs vascular congestion of the iris and ciliary body and some degree of iritis due to absorption of toxins from the ulcer. Exudation into the anterior chamber from the vessels of iris and ciliary body may lead to formation of hypopyon. Ulceration may further progress by lateral extension resulting in diffuse superficial ulceration or it may progress by deeper penetration of the infection leading to Descemetocele formation and possible corneal perforation. When the offending organism is highly virulent and/or host defence mechanism is
jeopardised there occurs deeper penetration during stage of active ulceration.
Depending upon the prevalent circumstances the course of corneal ulcer may take one of the three forms:
(A) Ulcer may become localised and heal;
(B) Penetrate deep leading to corneal perforation;
or
(C) Spread fast in the whole cornea as sloughing corneal ulcer.
The salient pathological features of these are as under:
[A] Pathology of localised corneal ulcer
1. Stage of progressive infiltration (Fig. 1A). It is characterised by the infiltration of polymorphonuclear and/or lymphocytes into the epithelium
from the peripheral circulation supplemented by similar cells from the underlying stroma if this tissue is also affected. Subsequently necrosis of the
involved tissue may occur, depending upon the virulence of offending agent and the strength of host defense mechanism.
2. Stage of active ulceration (Fig. 1B). Active ulceration results from necrosis and sloughing of the epithelium, Bowman's membrane and the involved stroma. The walls of the active ulcer project owing to swelling of the lamellae by the imbibition of fluid and the packing of masses of leucocytes between them. This zone of infiltration may extend to a considerable distance both around and beneath the ulcer. At this
stage, sides and floor of the ulcer may show grey infiltration and sloughing.
During this stage of active ulceration, there occurs hyperaemia of circumcorneal network of vessels which results into accumulation of purulent exudates on the cornea. There also occurs vascular congestion of the iris and ciliary body and some degree of iritis due to absorption of toxins from the ulcer. Exudation into the anterior chamber from the vessels of iris and ciliary body may lead to formation of hypopyon. Ulceration may further progress by lateral extension resulting in diffuse superficial ulceration or it may progress by deeper penetration of the infection leading to Descemetocele formation and possible corneal perforation. When the offending organism is highly virulent and/or host defence mechanism is
jeopardised there occurs deeper penetration during stage of active ulceration.
defences) and the treatment which augments the normal host response. A line of demarcation develops around the ulcer, which consists of leucocytes that
neutralize and eventually phagocytose the offending organisms and necrotic cellular debris. The digestion of necrotic material may result in initial enlargement of the ulcer. This process may be accompanied by superficial vascularization that increases the humoral and cellular immune response. The ulcer now begins to heal and epithelium starts growing over the edges.
4. Stage of cicatrization (Fig.1D). In this stage healing continues by progressive epithelization which forms a permanent covering. Beneath the epithelium, fibrous tissue is laid down partly by the corneal fibroblasts and partly by the endothelial cells of the new vessels. The stroma thus thickens and fills in under the epithelium, pushing the epithelial surface anteriorly.
The degree of scarring from healing varies. If the ulcer is very superficial and involves the epithelium only, it heals without leaving any opacity behind.
When ulcer involves Bowman's membrane and few superficial stromal lamellae, the resultant scar is calleda 'nebula'. Macula and leucoma result after healing of ulcers involving up to one-third and more than that
of corneal stroma, respectively.
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| Fig. 1. Pathology of corneal ulcer : A, stage of progressive infiltration; B, stage of active ulceration; C, stage of regression; D, stage of cicatrization. |
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