Cases in the lower animals are usually the result of direct infection through some traumatic lesion of the eye.
The special feature of the disease is the rapid and abundant production in all parts of the eye of pus cells until the whole organ has become a bag of pus.
The chief diagnostic symptoms are the presence of a foul wound, the rapid advance of the phlegmonous inflammation of the conjunctiva and lids, the yellowish opacity of the cornea, and, if visible, of the aqueous humor, the prominence of the entire eyeball, the high attendant fever and the early destruction of the eye. In the domestic animals the sympathetic irritation of the second eye has not been observed so commonly as in man. If the patient survives, the pus makes its way slowly to the surface, and escapes, and the cavity granulates and heals with contraction of the eye into a small nodular mass.
The treatment of the condition is essentially antiseptic and should be made preventive if possible, as there is little hope of saving the eye if the suppurative inflammation has been already established. The wound should be treated at the earliest moment with antiseptic lotions, sublimate solution (1 ∶ 5000) or potassium permanganate solution (1 ∶ 100) or pyoktannin (1 ∶ 1000), or creolin (1 ∶ 100). When inflammation has actually set in, these should be used still more assiduously by frequent injection under the lids, or by inserting antiseptic cotton between these and the bulb.
Enucleation. When the eye has become a virtual abscess the quickest and most perfect relief is secured by the complete extirpation of the eyeball. The patient is narcotized by ether or chloroform, and a thread or hook being passed through the cornea, the globe is quickly dissected out by curved scissors. Bleeding may be checked by pressure with cotton wool steeped in tincture of the muriate of iron, and later the wound may be dressed with stupes wet with a mixture in equal parts of standard solution of sulphurous acid, glycerine and water.
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.