Sea green pupil. Causes: intraocular pressure from serous choroiditis,
deranged fifth nerve, increased blood pressure, inflammatory
obstruction of sclero-corneal canal, irritation of the ciliary
ganglion. Symptoms: excessive tension and firmness of the globe,
anterior chamber shallow, iris contracted, sluggish, pupil grayish or
yellowish green, cupping of optic disc, pulsations of retinal
arteries. Acute inflammatory form, simple form, secondary form.
Convexity of pupil with synechia. Traumas. Luxations. Atheromas.
Lesions: inflammation of the iris, choroid, ciliary body or cornea,
round cell infiltration, cupped optic disc, atrophy of optic nerve,
hydrophthalmos. Treatment: massage, puncture of aqueous, iridectomy,
eserine, cocaine, antiseptic bandage.
This has been so named from the sea green color of the pupil. The nature
of the disease has been much debated and up to the present time
ophthalmologists are far from being agreed as to its true pathology. All
are agreed as to the essential feature of the malady, namely, increased
tension of the eye ball, but every case of increased tension of the bulb
is not recognized as glaucoma, and the true cause of the persistent and
progressive increase of pressure in cases recognized as glaucoma is not
absolutely settled.
_Causes._ The immediate cause of the condition is the increased
intraocular pressure, on this all are agreed, but as to the cause of
this pressure there is difference of opinion. Gräfe attributed it to a
serous choroiditis: Donders to deranged innervation of the 5th cranial
nerve which controls secretion; others to increased blood pressure;
others to inflammatory contraction at the sclero-corneal border where
the principal drainage canal of the aqueous humor lies. The increased
blood pressure theory appears to be contradicted by the fact that
exalted blood pressure, as in fever, does not tend to glaucoma. The
arrest-of-drainage-of-the-aqueous theory seems to be contradicted by the
reduction of the anterior chamber while the theory would demand its
increase. Priestly-Smith injected the sheep’s eye with a pressure of
water of 30 centimetres high, but while he caused an increased outflow
he failed to induce distinct glaucoma. Möller tied the ophthalmic vein
of the horse, but he also failed to produce glaucoma. “By artificial
stimulation of the ciliary ganglion in dogs, the internal tension of the
eye can be noticeably and permanently increased, and we may therefore
assume that when this ganglion is stimulated, the secretion of fluid is
increased, and that glaucoma depends upon an analogous process” (Fick).
It would seem that necessity demands at the same time an obstruction of
the normal drainage through nervous influence or otherwise. Schœn
ascribes glaucoma to overexercise of the accommodation, a cause which
would hardly be expected to operate in dogs. As bearing on the nervous
causation Fick mentions that in man glaucoma is often preceeded and
accompanied by trigeminal neuralgia. Again the symptoms of glaucoma
often appear in the course of recurrent ophthalmia in the horse.
While it seems impossible to ascribe the disease to any single definite
cause there appears to be good reason to accept as factors in different
cases, a derangement of trigeminal innervation, an irritation of the
ciliary ganglion, and an inflammation affecting the region of the
ciliary circle and the sclero-corneal line.
_Symptoms._ The tension of the eye ball is excessive as ascertained by
pressure of the finger, or by the spring tonometer. If the increase of
tension has come on suddenly, the cornea is somewhat cloudy, and less
sensitive to the touch. If one eye only is attacked the contrast between
the two is very marked and diagnostic. The anterior chamber is
diminished in size by the projection forward of the iris and lens. The
iris is usually contracted so as to show a dilated pupil reflecting a
smoky, grayish green or yellowish green hue. The iris is either
irresponsive to light or responds very slowly and imperfectly. With the
ophthalmoscope the most marked features are the “cupping” or depression
of the optic disc by pressure, and the pulsations in the retinal
arteries. These pulsations are especially easily seen at the margin of
the depression which represents the seat of the lamina cribrosa and the
point of entrance of the optic nerve. They are rendered even more
manifest by pressure on the eye. They are due to the prompt emptying of
the blood vessels by the intraocular pressure, so that these are only
momentarily filled at each cardiac systole.
Ophthalmologists recognize three varieties of glaucoma: =acute
inflammatory glaucoma=, =simple glaucoma= without apparent inflammation,
and =secondary glaucoma=, the result of another disease.
=Acute inflammatory glaucoma= is the one condition in which, in the
absence of a midriatic, inflammation is associated with dilated pupil.
It is liable to occur in a series of attacks, which increase in
severity, hence its supposed identity with recurrent ophthalmia in the
horse. The entire group of symptoms have, however, been rarely or never
seen in the horse. They are distinctly more common in dogs.
=Simple glaucoma= comes on more slowly, becomes chronic and is to be
recognized by the physical symptoms in the absence of inflammation,
notably by tension of the bulb, diminution of the anterior chamber and
cupping of the optic disc.
=Secondary glaucoma= is the direct result of some other disease of the
eye:
Complete posterior synechia acts by confining the liquid which is
secreted, to the posterior chamber whence it finds no ready outlet
through the pupil, and causes a marked bulging forward of the iris and
tension of the eyeball.
Slighter anterior synechia in the form of cicatricial adhesions between
iris and cornea in the sclero-corneal margin, acts by blocking the
principal drainage canal of the aqueous humor, which lies in this angle.
Traumatic injuries implicating the capsule of the lens and admitting the
aqueous humor freely to the lens substance determines softening,
swelling and so much irritation as to increase the secretion largely and
determine intraocular tension.
The same may result from luxation of the lens and irritation of the
ciliary circle by dragging.
Other causes are disease (atheroma) of the retinal vessels and the
growth of tumors in the interior of the eye.
_Lesions._ These are very varied. Inflammation of the iris, ciliary body
and choroid and even of the cornea is not uncommon. The iris and ciliary
body show round cell infiltration, as may also the choroid. In the
ciliary body this is likely to be especially abundant along the drainage
canal (canal of Schlemm) thereby reducing its calibre. Leber and Fuchs
found drops of liquid in the epithelium and cornea. One of the most
significant lesions in man is the cupping or depression of the lamina
cribrosa of a depth in ratio with the force of the intraocular pressure,
and inflammation or atrophy of the optic nerve, back of the eye. Möller,
however, has never been able to find actual cupping of the optic papilla
in animals, but instead thereof a general distension of the outer coats
of the eye, a hydrophthalmos. In view of the fact that these coats have
the same structure and nearly the same relative thickness as in man,
this throws considerable doubt on the supposed identity of glaucoma in
man and cases which have been considered such in the lower animals. The
comparative absence of pulsations in the retinal arteries in animals
adds to the uncertainty.
_Treatment._ Although such cases lack some of the diagnostic symptoms of
glaucoma in man, yet they agree with that in the increase of the
intraocular pressure, and demand similar measures for relief. Some
reduction of the tension can be secured by careful massage over the
eyeball so as to favor the progress of the lymph out of the bulb. A
prompt but rather transient relief can be obtained from evacuation of
the aqueous humor by puncture with a lancet close to and parallel with
the margin of the cornea. The most effective treatment is, however, by
iridectomy. On account of the great power of the muscles in the lower
animals it is usually desirable to anæsthetize the patient and then
fixing the eyeball with a pair of rat-tooth forceps, an incision is made
close in front of the upper border of the cornea, and the lancet slowly
withdrawn. A pair of iridectomy forceps are then introduced and the iris
seized and drawn out through the wound, and a portion snipped off with a
pair of fine scissors. The iris is then pushed back into the anterior
chamber, and a drop of eserin solution placed in the eye. The parts and
instruments must be rendered thoroughly aseptic before the operation,
and the eye cocainized both before and after. The eye should be kept
covered for some time with a cloth wet with a solution of mercuric
chloride (1 ∶ 5000) or other antiseptic.
Appropriate treatment may be employed in case of coexistent
inflammation, or to improve the general health.