Extension from conjunctivitis, wounds, foreign bodies, bites, stings,
blows, infections, filaria. Symptoms: eye tender, closed, epiphora,
red, pannus, photophobia, congested sclera, opaque or ramified red
cornea, or diffuse red, exudation, suppuration, corneal abscess,
ulcer, perforation, prolapsus iris, panophthalmia. Focal illumination.
Recovery. Permanent cicatrix or opacity. Lesions: exudates of lymph
and leucocytes into corneal layers: embryonic tissue: vascularization:
abscess: ulcer: cicatrix: opacity: staphyloma: hypopion: prolapsus
iridis: panophthalmia. Treatment: antiseptic astringents, atropine,
leeching, derivatives, blister, seton, opacities; in severe cases
antiseptic puncture, sublimate lotion, silver nitrate, potassium
permanganate, boric acid, pyoktannin: in perforations antiseptic
bandage and eserine, iridectomy: in chronic cases mercury oxide.
Keratitis occurs in all domestic animals as a primary disease, or as an
extension from conjunctivitis.
_Causes._ Extension from acute, enzootic, infectious conjunctivitis in
sheep and cattle has been noticed by a great number of observers. Bayer
and Lohoff have studied maculated keratitis of the superficial layers in
horses. Again it has followed wounds by foreign bodies, spikes of
vegetables, particles of iron and glass, blows of whips, or insects,
stings, etc. It also occurs in connection with the local action of
particular poisons, such as variola (foot and mouth disease), canine
distemper, etc., and from the local irritations caused by trichiasis or
entropion or by the filariæ lachrymalis (ox) and palpebralis (horse).
_Symptoms._ The eye is extremely sensitive, and habitually closed, with
a profuse flow of tears, and a disposition to resist opening of the
lids. When exposed the cornea is seen to be more or less clouded and
perhaps reddened by the formation of vessels proceeding from its
sclerotic margin. This is known as _pannus_. If the anterior chamber is
still visible the pupil is found to be contracted showing photophobia.
The congestion is first visible in the sclerotic and in the absence of
pigment is most intense near the margin of the cornea. Upon the cornea
itself it is preceded by a deep white opacity, into which the
vascularity gradually extends. The whole cornea may finally become of a
bright pink hue.
The congestion of the cornea may advance to fibrinous exudation, or the
formation of pus between its layers, to molecular degeneration and the
formation of ulcer, or even to perforation and escape of the aqueous
humor. In this case prolapsus iris, panophthalmia and destruction of the
eye are likely to ensue.
Ulcer if not readily seen with unaided vision can be easily recognized
by the aid of focal illumination, and abscess can be detected by the
presence of a sharply circumscribed centre of intense opacity, white or
yellow, and some bulging of the membrane.
The pus may be absorbed, or it may escape by rupture and discharge
externally, or into the anterior chamber when the resistance is least in
that direction, and when this takes place, a dangerous internal
infective inflammation is the result.
In the slighter forms of keratitis the inflammation may come early to a
standstill, and recede, tenderness and photophobia pass off, the eyelids
may be opened, and the corneal opacities gradually disappear. If any
portion of the cornea has become vascular, that portion is liable to
remain opaque or even pink.
_Lesions._ Under the influence of an irritant on the cornea, the vessels
in the margin of the sclerotic become actively congested and pour out
lymph freely, leucocytes also escape and with the lymph pass through the
lymph channels into the substance of the corneal tissue. Here they
undergo active fission and increase, and the normal cells of the corneal
tissue multiply in like manner, so that in a short time there is an
extraordinary production of embryonic cells. Into the embryonic tissue
so formed, blood escapes from forming loops of new vessels, and this
goes on extending until the whole cornea may have become vascular.
Degenerations in the newly formed structure may result in suppuration,
(_hypopyonkeratitis_) or molecular decay and ulceration, (_ulcus
corneæ_) or organization may take place into the fibrous tissue with
contraction and permanent opacity, (_macula_) or a hyperplasia may form
in the shape of a staphyloma.
Among the other complications may be named pus in the anterior chamber
(hypopion), prolapsus of the iris, iritis and panophthalmia.
_Treatment._ In the milder form of keratitis, antiseptic astringents
with atropia sulphate are often effectual: zinc sulphate, boric acid or
alum (1 ∶ 100). Any direct mechanical cause of the irritation must be
removed, and the eye rendered as far as possible antiseptic or aseptic.
Derivatives also may be of service, and Trasbot especially advises
bleeding from the angular vein of the eye but only in the very earliest
stages. Cupping, leeching or setons may be employed. Excessive tension
may be relieved by puncture of the cornea near its margin. The remaining
opacity after the inflammation has subsided may usually be removed by
touching it daily with a camel’s hair brush dipped in a solution of
silver nitrate (1 ∶ 200).
In the more severe cases antiseptic lotions are even more essential,
mercuric chloride (1 ∶ 5000), potassium permanganate (1 ∶ 100), boric
acid (1 ∶ 100), silver nitrate (1 ∶ 200). Careful massage is of value.
Ulcers may be touched daily with a solution of silver nitrate (1 ∶ 400),
or of pyoktannin (1 ∶ 100).
Perforations must be treated by antiseptic bandage, eserin, and in case
of necessity, iridectomy as advised under perforating wounds.
Abscesses of the cornea should be opened with a flamed needle and
treated with antiseptic lotions.
Obstinate cases are often benefited by ointment of yellow oxide of
mercury 1, vaseline 10, or by the red oxide of mercury or calomel.