GLAUCOMA.
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.