Chapter XVIII: Part 18

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.

_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.

EXOPHTHALMOS.

This consists in an increase of the media of the eye so as to cause an excessive increase in size, and an unsightly bulging outward from the orbit and between the lids. It may be said to be a more exaggerated enlargement of the eye ball, than has been already noticed under glaucoma.

It has been seen in nearly all classes of domestic animals. Everhardt and Möller reports it in horses, Hausmann, Pradal, etc., in cattle, LaNotte, in lambs, Cöster, Trasbot, etc., in dogs, and Trasbot, in birds (chickens and parrots). It has been found congenitally in lambs and at a few days old in foals, especially when weak and puny; in older animals it appears to be most frequent in the anæmic or starved animal, in the lymphatic, or, as in man, in the goitrous.

The manifest projection outward of the eye may occur as a nervous phenomenon, without intraocular pressure, and without abscess, neoplasm, or inflammation in the depth of the orbit. In a case of tuberculosis in a three year old cow, I have found this condition, with normal tension of the eyeball, but with acute tubercular meningitis of the pia, surrounding the pons and crura cerebri, a grayish exudate with lighter miliary centres, and a considerable clot of extravasated blood.

_Symptoms._ Mostly without any febrile reaction, there is a manifest enlargement and bulging of the globe of the eye, so that it stands out between the lids which can no longer cover it. The cornea, aqueous, lens, and vitreous are not usually opaque, but show only a pale, blue, opalescent tint. The pupil is often widely dilated so as to show clearly the interior of the eye. Vertiginous symptoms have been observed in the cow (Pradal), the supposed result of intraocular pressure.

_Treatment_ has had little effect when it stops short of puncture of the cornea or iridectomy.

HYDROPHTHALMOS OR BUPHTHALMUS CONGENITUS.

This has been applied to a congenital enlargement of the eyes from internal distension in children. The cases in lambs and foals quoted in the last article were evidently of this nature. They are charged on intraocular pressure acting on the delicate tissues of the embryo or unborn animal. There is not necessarily cupping of the optic disc so that persistent tension after birth cannot be insisted on.

Cases occurring in older animals, may be forms of secondary glaucoma though classed under hydrophthalmos by Mayer and others.

_Treatment_ when demanded is along the same lines as in glaucoma.

CATARACT. OPACITY OF THE LENS OR ITS CAPSULE.

Definition. Forms: lenticular, capsular, cortical, nuclear, polar,
black, diabetic, traumatic, immature, mature, senile. Causes: impaired
nutrition of lens, inflammation of iris, choroid, ciliary body,
retina; recurrent ophthalmia. Proliferation of cells. Increased
density, chemical changes, degenerations. Sugar, sodium chloride,
naphthalin. Rachitis. Senile. Blood pigment. Symptoms: shrunken bulb,
opalescent zone around cornea, angle on upper lid, shying, extra ear
activity, high stepping, better sight in twilight, homatropia,
examination facing the light, Purkinje’s images, ophthalmoscopic
examination. Prognosis hopeless. Treatment: phosphureted oil, massage,
operation in horses, discission, under antiseptic precautions,
extraction under careful antisepsis, suction.

_Definition._ Any pathological change in the lens or its capsule diminishing its transparency.

_Varieties._ The opacity may be situated either in the lens (=lenticular=) or in its capsule (=capsular=). Again, it may be in the outer part (=cortical=) or in the central part (=nuclear=) of the lens. If the opacity is on the capsule in front of the lens it is =anterior capsular=; if on the portion behind the lens it is =posterior capsular=. If the opacity is caused by black iris pigment adherent to the capsule it has been called =black cataract=. If the lenticular cataract is small and round, it is =polar=, and it may be =anterior= or =posterior polar= according as it is situated near the front or back of the lens. =Diabetic cataract= is one associated with mellituria. A =traumatic cataract= is one resulting from a wound of the lens which admits the aqueous humor and causes softening, swelling and finally solution of the substance of the lens. The =immature= or =unripe cataract= is one in which the lens is not yet wholly involved and indurated; the =mature= or =ripe=, when such consolidation has extended throughout. =Senile Cataract= is seen in old horses, dogs, cats, birds and very exceptionally in cows. This usually attacks both eyes at once. A degeneration takes place in the fibres of the lens, which are invaded by sclerosis beginning at the centre of the organ.

_Causes._ In domestic animals cataracts are commonly the result of impairment of the nutrition of the lens in connection with inflammation of the iris, choroid, ciliary body, retina, or hyaloid membrane, and above all, in solipeds, in recurrent ophthalmia. It may be assumed that a transparent tissue composed of cells can only maintain its translucency so long as the most perfect equilibrium is maintained as regards the mutual relation of the cells, the pressure of its interstitial plasma, and the chemical composition of both plasma and cell structures. The slightest deviation in any direction will impair or abolish the transparency of the tissue. In inflammation this occurs in various ways, through the increased cell multiplication and the change in the nature of the cells, through the increased exudation and the alteration of the solid parts as regards compression and relative position, and through chemical changes in the exudate which contains more salts, fibrinogenous material, etc., than the normal plasma. The same is true of all the post inflammatory degenerative processes that take place in the lens.

The formation of cataract from chemical alteration in the fluids is familiar in diabetic subjects,—man or beast (Altenhof). It can be produced experimentally in frogs by injecting sugar, common salt or any other readily diffusible saline solution under the skin (Kunde). Rabbits that are fed naphthalin develop cataract which radiates in lines and streaks from the pole towards the periphery and in the cortical portion of the lens. Perhaps the lamellar cataract of rachitic patients is also to be attributed to the lack of earthy salts in the plasma of the lens.

_Senile cataract_ may be hypothetically attributed to impaired nutrition, degeneration in the lens or its capsule, or less commonly to disease of the blood vessels of the eye, or gradual changes in the plasma. It occurs in horse, ox or dog at ten years old and upward.

=Anterior Capsular Cataract= sometimes results from the deposition of =blood pigment on the capsule= in cases of extravasation into the anterior chamber. This is closely allied to the black or spurious cataract which consists in the adhesion of the uveal pigment to the capsule, and its detachment from the iris.

Kunde who caused cataract in frogs by injection, subcutem or ingestion of concentrated solutions of sugar or salt, attributes the result to the sudden abstraction of water from the crystalline lens. Even the cell multiplication in inflammatory cases, he holds to favor this, since the new cells having little vitality are especially subject to granular and other deposits and degenerations, with loss of water or of transparency.

_Symptoms and diagnosis._ The examiner should apprehend cataract after internal ophthalmia. Much more so, if there is apparent diminution of the bulb, an opalescent zone around the outer border of the cornea, or a marked angle in the curvature of the upper eyelid, as usually occurs in recurrent ophthalmia. When a horse suddenly acquires a habit of shying, of starting back or to one side when approached, when confronted with strange or unexpected objects, or with deep shadows like those from electric lights, he is to be suspected. When he carries his ears in an unusually alert manner, turning one forward and the other back, when he steps higher than before to avoid unseen objects, suspicion should attach to him. If he sees better in twilight than in the full sunlight, central cataract may be feared, while the periphery which is exposed by the dilatation of the pupil in semi-darkness is still clear. In all examinations for soundness, the greatest care should be taken to exclude the possibility of overlooking an existing cataract.

In the very early stages, while internal inflammation and photophobia are still present, the pupil may be contracted so that lesion can easily escape notice. Any contraction of the pupil therefore disproportionately to the light, should demand a careful examination with the pupil dilated in darkness or by the action of atropia or homatropin. In the more advanced cases with no persistent inflammation and an advanced opacity of the lens, sensitiveness to light is greatly lessened, the pupil is dilated and the cataract is easily detected.

In cases approximating to the condition last named it is usually only necessary to place the animal in a sombre or dark building, with his head facing the light at an open door, or window and best with full sunlight. Let this fall full upon the eye, and let the observer view the pupil diagonally from each side when any opacity may be detected.

When the pupil is too narrow, several drops of a one per cent. solution of atropia sulphate may be dropped within the lower lid and left for ten minutes until the pupil is widely dilated. Then the examination may be made as above, or still better the animal may be taken into a dark chamber and examined by one of the following methods:

A light, preferably a candle, is placed in front of the eye and moved from side to side, upward and downward, so as to bring its images over all parts of the cornea and lens. In the normal eye there are reflected three images of the light, one large, clear, and upright from the anterior surface of the cornea, one, much smaller but still upright, from the anterior capsule of the lens, and one, small and inverted, from the posterior surface of the lens and capsule. Any opacity in the lens or on its posterior capsule, will cause the posterior (inverted) image to become indistinct, and as it were a diffuse white blur, as it passes over that spot. The other small (erect) image may be even clearer than normal in passing over the opaque area because of the mirror-like reflecting action of the white cloud behind it. The movement of the light so as to pass its image over all parts of its surface in succession will certainly reveal the existence and seat of the cataract, by the blurring of the inverted image of the flame.

Another method is by oblique illumination, the patient’s head being turned away from the light and the interior of the eye being lighted up by reflection from a mirror. If the pupil has been sufficiently dilated all parts of the lens can be scrutinized in this way and the slightest opacity detected by the grayish or whitish haze.

If there is still doubt as to the nature of such appearances, it may be set at rest by illuminating the depth of the eye with the ophthalmoscope when the opacities will appear as dark areas in the general red ground. (See Systematic Examination of the Eye.)

The _prognosis_ of cataract is almost invariably hopeless. I have seen newly formed opacities of the capsule clear up in a day or two, and such recovery in very slight traumatic injury and superficial exudation is recognized as possible, but a slowly forming cataract is usually there to stay. Those that clear are presumably only exudates on the capsule and not true cataracts.

_Treatment._ While exudates on the capsule may disappear under a course of purgatives and diuretics, practically nothing is to be expected from medical treatment in true cataract. The instillation of phosphorated oil (1–2 per cent.) daily into the conjunctival sac as formerly recommended, may be helpful in some of the superficially opaque membranes, but for formed cataract it has proved useless. Massage with, or without ointments can temporarily lessen ocular tension and reduce the liquids in the zonula of Zinn, and canal of Schlemm, but it is only in very exceptional recent cases, in which it has given permanent benefit, and even these were probably spurious cataracts.

The question then is essentially whether we should operate or not. In the =horse= the objections to operation are almost conclusive in all cases. The eye in which the lens has been depressed or extracted can never see objects clearly without the aid of biconvex glasses, and it is impossible to fit these to the animal. The horse that is blind can go to pasture or be driven in harness with safety, but the one that sees all objects distorted or blurred is liable to become a shyer endangering the life of his rider or driver. The greater number of cataracts in horses come from recurrent ophthalmia and are associated with opacity of the vitreous, detachment of the retina, exudates in the choroid, degeneration of the optic nerve, or other lesion which of itself would destroy vision. Almost the only object of removal of the lens in such cases would be to make an unsound horse pass for a sound one. Even this is usually unattainable because the thickened capsule remains as a dense white cloud or the opacity of the vitreous shines through the pupil. In dogs the cataract is usually associated with fewer complications, and the resulting imperfect vision is not a source of danger to man. Extraction of the opaque lens may in this case appeal so strongly to the sense of comfort of the owner that the operation may become permissible or desirable.

In man the operation may have to be delayed for a considerable time because of the unripeness of the cataract. The center of the lens may be firm and opaque while the outer layers are so soft that they would be likely to be retained in the capsule and would not only produce persistent opacity, but would be a continual threat of destruction of the eye by active inflammation. The ripeness is ascertained by careful scrutiny of the shadow of the iris during illumination of the interior of the eye. If ripe, the dark shadow of the iris approximates closely to the margin of the iris itself, whereas if the outer portion is unripe there is a clear zone of greater or less depth between the margin of the iris and the shadow reflected by the opaque portion of the lens.

In the lower animals the question is less important as we do not aim at securing perfect vision, and the danger of inflammation is therefore the main consideration. Escaping this, the aqueous humor may be expected to dissolve and remove the greater part of the still adherent lens substance, and the unsightliness of the dense white cataract is largely done away with.

=Discission.= Tearing of the capsule so as to admit the aqueous humor to the lens may be admissible in the =young= with =soft cataract=. The liquid causes gradual swelling up, solution and absorption of the lens so that in the course of a week or two the whole may be removed. It is not, however, unattended by danger, as the rapid swelling of the lens will sometimes determine an inflammation which will lead to complete destruction of the eye. The eye is first thoroughly washed with aseptic cotton and a sublimate solution (1 ∶ 1000), and is then rendered anæsthetic by cocaine (5 to 10 per cent. solution) or in the large animals general anæsthesia is produced by ether or chloroform. The eyelids are held apart by the lid speculum, the nictitans held if necessary by forceps, and the bulb steadied by seizing it with hooked forceps. A cataract needle is passed through the cornea close to its border, and carried through the pupil, previously dilated with atropia, so as to tear an opening in the anterior capsule about two-thirds the diameter of the lens. If the toughness of the capsule threatens to endanger the ciliary body by dragging upon it, two needles or fine hooks may be introduced through opposite borders of the cornea (inner and outer) and the capsule may be torn without throwing any strain on surrounding parts. The pupil must thereafter be kept dilated by atropia to obviate adhesion of the iris to the wound and the eye must be kept in comparative darkness and aseptic. If active inflammation sets in, cold, astringent or iced dressings may be called for, while if the swelling of the lens is threatening it should be at once extracted. If the eye becomes unduly tense, puncture of the cornea is indicated, and the relief of tension will sometimes start a tardy solution into renewed activity.

=Linear extraction of the lens.= The animal and the eye having been prepared anæsthetically antiseptically, and midriatically as for discission, the lids are fixed with a speculum, the nictitans and the bulb with forceps, a Gräfe cataract knife is introduced through the inner side of the cornea, close to its margin and with its point parallel to the front of the iris. The handle is then raised and the cornea detached from the sclera by a series of gentle sawing motions until it has reached a point parallel to the outer margin of the cornea. If the pupil is insufficiently dilated, the iris should now be seized by forceps drawn out through the corneal wound and snipped off by scissors curved on the flat. Then the cystotome (hooked knife) is introduced with its back turned downward and carried to the further side of the capsule and close to the iris, its cutting point is turned backward and inserted in the capsule, and drawn across from side to side to make an orifice large enough for the escape of the lens. It is then given a quarter revolution so as to turn the point of the knife downward and is withdrawn from the wound back first. The lower part of the sclera and cornea is now gently pressed with a lens spoon so as to dislodge the lens from the capsule and deliver it through the corneal wound. Counter pressure may be made on the sclera at the upper part of the eye ball. The cornea is now gently stroked with cotton dipped in sublimate solution to pass all blood from the anterior chamber, and render the parts antiseptic. The iris is carefully replaced inside the cornea and any obstinately protruding parts must be excised. The eye is now covered with cotton steeped in a sublimate solution (1 ∶ 1000) and bandaged without undue pressure, and the animal tied to two sides of the stall so that it is impossible to rub the eye.

It is well to dress the eye on the second day, and if adhesion of the wound is complete it may be left without bandage at the end of a week or a fortnight.

Success depends mainly on the avoidance of infection. Therefore every indication of local or general infection should forbid the operation. Any existing infectious disease or any local eczema, conjunctivitis or disease of the lachrymal apparatus should be cured and the region thoroughly disinfected before proceeding. The head should have a good soapy wash, followed by a sponging with sublimate solution (1 ∶ 1000), the conjunctiva carefully washed out with the same and a bandage damp with it applied over the eye. This bandage is only removed on the operating table. Cloths dampened with the solution are laid on the face around the eye, the eye is cocainized with a 5 per cent. solution applied at intervals of one minute and when quite insensible the operation is commenced. The greatest care must be taken to render the hands of operator and assistants and all instruments thoroughly aseptic. The instruments are taken from a 4 per cent. solution of carbolic acid and placed in water (which has just been boiled) until needed, and to wipe the eye or make any application, sterilized cotton only is used and never touched to the eye more than once. A sublimate bandage is placed over the eye and worn for ten days or a fortnight. Then if the corneal incision is healed and pale it may be left off. The pupil should be kept dilated by a few drops of atropia daily for this length of time.

Any occurrence of iritis or choroiditis usually indicates infection and must be treated on general principles, but with especial reference to disinfection, and if this cannot be secured the eye will be almost inevitably lost.

In case of renewed opacity through thickening of the capsule an aperture must be torn in that membrane by the same method as in discission. This is commonly known as needling. It must be conducted under the same antiseptic precautions as in extraction.

_Suction._ This is only applicable to a lens which has become fluid as well as opaque. It consists in withdrawing the liquid lens through a hollow needle.

DISLOCATION OF THE LENS.

Congenital; acquired; traumatic, softening of suspensory ligament:
hinge motion, lens drops behind iris, protrudes through pupil,
cataract. Apparent increased depth of anterior chamber, tremulous
iris, projecting edge of lens like black ring. Treatment: extraction.

Dislocation of the lens may be congenital, or acquired. In the latter case it is explained by a traumatism or a liquefaction of the vitreous and coincident softening of the suspensory ligament. In either case, if the ligament is torn through in more than one-half its circumference, the lens will hang by the remainder and move on it as on a hinge so as to change its location in the different positions of the head. This is especially so where the vitreous has become abnormally fluid as there is then no resistance to the free backward movement of the lens. The writer has seen the eye of a cow affected in this way, so that the cataractous lens advances to the pupil and recedes from it as the eye is moved. In other cases the dislocated lens, being attached below only, drops down and virtually disappears behind the lower part of the iris. In still other cases it becomes wedged into the pupil, or protrudes into the anterior chamber and lies in front of the pupil and iris. The semi-detached lens sooner or later becomes opaque. A cataract with contraction of the newly formed tissue on the capsule and undue tension on the suspensory ligament may, however, precede the dislocation which is then precipitated by some shock, as a blow, fall, sneeze, cough or emesis.

The condition leads to an apparent increase in the depth of the anterior chamber, and tremulous movement of the iris, and if illuminated the impacted condition of the lens or its changes of position can be detected. If its edge is exposed it appears as a black ring.

_Treatment_ is useless, unless it be extraction of the lens, or iridectomy in suitable cases.

PERSISTENT ARTERIA HYALOIDEA.

In the embryo this artery occupies the central canal of the vitreous and extends from the optic papilla to the posterior pole of the lens. At times it persists after birth and even to mature life and is then detected as a gray or dark thread on ophthalmoscopic examination. Berlin records a case in an old horse and others in young cats, and Möller other cases in dogs. Treatment is manifestly hopeless.

OPACITY OF THE VITREOUS.

From inflammation of the ciliary body, choroid or retina. Pupil
copperas green with white points, lines or patches, move in opposite
direction from the eye, liquefied vitreous, crystals of cholesterine,
scintillance, opacity. Treatment.

Opacities visible with the ophthalmoscope usually come from effusion of blood into the vitreous, or inflammation of the retina, choroid, or ciliary body. Blood thrown into the vitreous will usually leave some permanent turbidity. In choroiditis or retinitis the ophthalmoscope may reveal the changes in these structures. A turbidity appearing in the anterior portion of the vitreous, without any apparent cause, is probably due to cyclitis which cannot be seen with the ophthalmoscope, but may cause special tenderness around the sclero-corneal zone. It is common in recurrent ophthalmia of the horse and in irido-choroiditis in animals generally, and may be a distinct feature of glaucoma. The general reflection of the pupil is copperas green, but gray or white points, lines, bars or patches may often be recognized. These being back of the lens and axis of the eye, move in the opposite direction from the line of vision, thus if the eye looks upward they descend, if it looks downward they ascend, if it turns to the right, they turn to the left and vice versa. Tested by a burning candle the three reflections remain clear and distinct unless lens or cornea are affected.

Not infrequently the vitreous is found abnormally fluid, and among its solid particles in affected horses have been found crystals of cholesterin (Jacobi) and tyrosin (Möller). In the illuminated vitreous such crystals may be seen to reflect the light like a shower of sparks (synchysis scintillans). Opacity of the vitreous has been seen in cases of amaurosis in horses (Hertwig) and glaucoma in lambs (Prinz).

_Treatment_ is rarely satisfactory, though in some recent cases, and in the absence of any other irremovable lesion, reabsorption of a slight exudate may take place, in connection with the use of mild saline laxatives and diuretics.

RETINITIS.

With choroiditis and cyclitis, albuminuria, nephritis, mellituria,
leukæmia, petechial fever, contagious pneumonia. Photophobia,
contracted pupil, redness around optic disc, enlarged retinal vessels,
white and gray spots and radiating lines, exudates, clots, fatty
degeneration. Treatment: correct primary disease.

Retinitis is usually an accompaniment of choroiditis and cyclitis, but it also occurs as a complication in a number of constitutional maladies, such as albuminuria, nephritis, mellituria, leukæmia, petechial fever, contagious pneumonia, etc. Fröhner records a case in a leukæmic horse, Peters in one suffering from petechial fever, Schindelka in cases of contagious pneumonia in the horse, and Eversbusch in recurrent ophthalmia of the horse, and under other conditions in dogs.

The attack is accompanied at the outset with much photophobia and contraction of the pupil. When this is dilated and the fundus of the eye examined with the ophthalmoscope, the retina is seen to be reddened for some distance around the optic disc and the blood-vessels are materially enlarged. Later, white or gray spots and lines are seen in and around the disc, tending to assume a radiating direction, and the retina at large, on careful examination may have a distinctly striped appearance. Brownish, reddish or light colored exudates and hæmorrhages may be made out in certain cases between retina and hyaloid, or between the retina and choroid. Fatty degeneration of the fibrous tissue is common.

_Treatment_ must be first that for the primary disease of which the retinitis is a complication, and the result will depend on how amenable that affection is to therapeutic measures. In advanced albuminuria or mellituria, the retinitis, which is usually double, is hopeless, while in contagious pneumonia, petechial fever, leukæmia and other less fatal affections, retinitis in its initial stages may recover. In cases of advanced disease with serious structural changes in the retina, recovery cannot be looked for.

DETACHMENT OF THE RETINA.

This may occur in any case of retinitis or choroiditis. It is especially common in recurrent ophthalmia in horses. It may also occur through the dragging by contracting inflammatory products in organization. Spontaneous recoveries have taken place through reabsorption, and attempts have been made by the injection of iodide lotion to hasten this, or more safely by rest and diaphoresis. Puncture and aspiration have also been tried with most varied results. As a rule in the lower animals the treatment of the inflammation, with rest, a pressure bandage, and pilocarpin will be indicated.

RETINAL HEMORRHAGE.

This occurs in inflammations of the retina or choroid, also in degenerations of the vascular walls and as a result of traumas, or poisons. Schindelka quotes a case in a dog from ptomaines, Eversbusch, one from scurvy in the dog, Appenroth, one in a calf from a blow with a cow’s horn, and others in cats and horses from traumas. It is present to a slight extent in all inflammations of the retina. With the ophthalmoscope the recent lesion appears as a bluish red blotch on a bright red ground, and the older lesion of a brownish red. Rest and a pressure bandage may be employed after subsidence of the inflammation.

TUMORS OF THE RETINA.

Eversbusch found subretinal cysts in a 24 year old horse, Merkel and others have found similar bodies in old dogs and cattle. Sarcomata and melanosarcoma are found on the surface of the choroid in gray horses, implicating the retina. The only remedy is enucleation of the bulb.

INFLAMMATION OF THE OPTIC NERVE. PAPILLITIS.

Choked disc. Neuro-retinitis. Papillo-retinitis. Nerve swelling blocks
veins. Causes: lead, tumors in brain bilateral, in orbit unilateral,
influenza, petechial fever. Symptoms: redness of optic disc, retinal
arteries contracted, veins gorged, papilla swollen (woolly), vitreous
opacity. Treatment.

This is also known as _choked disc_ from the obstruction of the return of blood by the veins of the retina which pass out at the cribriform lamina. The swelling of the nerve ending and papilla compress the veins, causing stagnation and venous congestion in the retina. When the retina is thus involved the term neuro-retinitis or papillo-retinitis is often applied.

_Causes._ The condition has been traced to lead poisoning, brain or orbital tumors, and various infectious diseases. Except in orbital tumor the disease is usually bilateral. In horses Schindelka has seen the condition in influenza and Peters in petechial fever, heart failure and dyspnœa. In a necropsy on a horse the writer found complete cataract, atrophy of the bulb to less than two-thirds the size of its fellow, thickening and furrowing of the sclera, the presence of an extensive old blood clot in the seat of the vitreous, cupping of the disc, retro-ocular neuritis with exudate inside the sheath, and a considerable reddish brown tumor of the choroid plexus on the same side. The trouble was attributed to the blow of a rope on the eye a considerable time before. The blood in the vitreous retained its dark hue and showed no evidence of microbian invasion.

_Symptoms._ To the phenomena of retinitis there is added violent injection of the capillary plexus of the papilla. The arteries of the retina are contracted while the veins are dilated and tortuous. The papilla is swollen and is said to have a woolly appearance. The vitreous may be opaque by reason of exudation or blood extravasation into its substance. Retro-ocular neuritis is usually present, and brain tumor in certain cases. Möller calls attention to the fact that with atrophy of the bulb the elliptical outline of the papilla gradually lessens and it becomes more nearly round. In dogs, too, the form of the papilla is also changed and the same author has found it distinctly triangular. The pupil may be at first strongly contracted and later freely dilated.

_Treatment_ is usually of little avail and does not differ materially from that adopted in retinitis. In tumor of the orbit pressing on the optic nerve it may sometimes be reached through the temporal fossa, but usually in all such cases enucleation of the eyeball is demanded.

RETRO-BULBAR OPTIC NEURITIS.

Definition. Neurites descendens and ascendens. Extension to bulb,
other eye, or brain. Causes: traumas, meningitis, infectious diseases,
toxins, lead, tobacco, etc. Symptoms: partial blindness: congestion of
papilla, exudates in adjacent retina. Treatment: eliminate poisons,
lead, toxins, correct precedent disease, saline laxatives, diuretics,
potassium iodide, cupping, local bleeding, counter-irritants. Hygiene.

This is inflammation of the optic nerve commencing behind the eyeball and only involving the papilla secondarily. Extension to the papilla has been called _neuritis descendens_ in contradistinction to _neuritis ascendens_ in which the inflammation extends along the nerve toward the brain. There is always a tendency to extension, it may be to the papilla and retina, it may be to the chiasma and opposite eye, and it may be inward toward the ganglia and choroid plexus.

_Causes._ Apart from traumatic causes, retro-bulbar neuritis in the domestic animals has been mainly seen in connection with constitutional or infectious diseases; in the horse with petechial fever (Peters), contagious pneumonia (Schindelka), meningitis (Peters, Straub) and parotitis (Möller). It has also followed meningitis in cattle (Nebelen). In man it has been traced to lead, tobacco, alcohol and other poisons.

_Symptoms._ At first the patient may seem partially blind without apparent cause. Later ophthalmoscopic examination reveals congestion and swelling of the papilla, and congestion (especially venous and capillary) of the retinal vessels. The discolorations in streaks and spots, from exudates and degenerations follow as noticed under papillitis. It is difficult to distinguish between this and papillitis during life.

_Treatment_ should be first directed toward the elimination of any poisons, such as lead or tobacco, which may act as a causative factor. Saline laxatives and in chronic cases potassium iodide would be indicated. Every attention should be given to the maintenance of good general health, and in acute attacks, local bleeding and counter-irritation may be resorted to.

ATROPHY. PARALYSIS OF THE OPTIC NERVE. AMBLYOPIA. AMAUROSIS.

Definition. Horses, dogs, cattle, sheep. Amblyopia, Amaurosis. Causes:
retinal paresis from brilliant light, of cerebral ganglia, snow
blindness, poisons, lead, opium, atropine, lolium, tobacco, carbon
bisulphide, cryptogams, mushrooms, “loco” plants, carbon monoxide,
illuminating gas, quinine, heat apoplexy, cerebral concussion, brain
parasites, exudates, pressure, degeneration, gastric or intestinal
disorder, hæmorrhage, anæmia, diarrhœa, diuresis, excessive milk
secretion, gestation, embolism. Symptoms: constant excessive
dilatation of pupil, no response to light, brilliant reflection from
retina and choroid, blue or yellow, (glass eyes); bilateral, cerebral,
tract or chiasma; unilateral, bulbar or nervous; face without
expression, ears alert, head to one side, nose elevated, nostrils
dilated, ox and dog smell ground, slow pace, high stepping, does not
dodge a feint to strike. Lesions: inflammatory exudate and retinal
atrophy, congested, “woolly” papilla, retro-bulbar congestion or
atrophy of nerve, thickening of neurilemma, tumors of orbit or foramen
optica, cœnurus, cysts, abscesses, cholesteatomata, psammomata,
hydrocephalus, meningitis, pineal hypertrophy, cranial fractures or
tumors, embolisms or aneurisms, hypertrophy of dura, apoplexy.
Treatment: remove causes, laxatives, diuretics, for lead, sulphuric
acid and potassium iodide, darkness, extract cœnurus, elevate
depressed fractures, ice, cold snow, to head, blisters, setons,
electricity, strychnia, remove tumors.

Blindness without adequate, corresponding, visible changes in the structure of the eye, has long been recognized in the lower animals, having been observed in horses, dogs, cattle and sheep. When partial it is known as amblyopia, and when complete as amaurosis or blindness. The term amaurosis is, however, being gradually eliminated from ophthalmological nomenclature in favor of that of atrophy.

_Causes._ These may be factors which act directly on the retina, as the intense light of the sun, of an electric, lime or magnesium light, of the reflection from snow, ice, water, sand, or white dust. These exhaust the power of vision by over-stimulating it, but whether the blindness is due to fatigue of the retina or of the cerebral ganglia which preside over sight, it is difficult to decide. This form is much more likely to occur in horses which spend most of their time in darkness, as in unlighted stables or mines, when they are suddenly brought into the sunlight. Snow blindness, however, from prolonged exposure, is common in animals as in man, and the case of the staghound reported by Johan, is by no means an isolated one.

Much more common are factors which act primarily on the nerve centres. Poisoning with lead, poppy, belladonna (sheep and goats, Gerlach), lolium temulentum (Klüver), tobacco, carbon bisulphide, cryptogams (musty fodder), mushrooms, astragalus mollissimus, etc., abolishes vision more or less perfectly. Common illuminating gas and carbon monoxide have shown this effect on dogs and chickens. Quinia subcutem has induced the condition in dogs (Becker and Eversbusch). More or less complete amaurosis is noticed in connection with heat apoplexy in horses and fat cattle.

Cerebral concussion from blows on the head, knocking the head against a post or wall, or from violent falls induce blindness which is to be attributed rather to lesion of the brain. The same remark applies to cases that appear during the progress of brain disease, parasitic or otherwise, to those that occur in connection with overloading of the stomach or intestines, and from gestation (Riss).

In cases appearing after severe depletion, like profuse hæmorrhage, diarrhœa, or diuresis, or excessive secretion of milk (bitch), the anæmia of both eye and brain may be taken into account.

When amaurosis develops during some inflammatory or infectious disease, as in parturition fever in cows, the immediate cause may sometimes be found in embolism of the retinal, or cerebral arteries.

_Symptoms._ The most striking feature of amaurosis is the constant excessive dilatation of the pupil. This is the same in light and darkness, and in fully developed cases the animal may be taken from perfect darkness to the full glare of sunlight or electric light without the slightest contraction of the pupil. The pupillary reflex to light is entirely lost. In the slighter cases (amblyopia) there remains some slight response of the iris to light but always far short of the normal. The widely dilated pupil admits a flood of light, and in the absence of cataract, lights up the chamber of the vitreous to an unusual degree. The blue or yellowish reflection of the tapetum is very striking, and led to the obsolete names of gutta serena and glass eyes. Sometimes the disease is unilateral and at others bilateral. In case it is unilateral there is a strong presumption that the causative lesion is in the affected eye or in the optic nerve in front of the chiasma. In the bilateral cases it is more likely to depend on disease of the brain or some more distant organ.

Certain important indications are to be drawn from the expression of the face, the position of the head and ears and the mode of locomotion. In all blind animals the face is without expression. The dilated pupils give no suggestion of mind looking through them, they have on the contrary an uniform stony stare. There is no sense of fire or life, but the face is like a dull sculptured mass. The immobile face finds a sharp contrast in the alertness of the ears, which may be carried one forward and another back, but fixed and yet ready to turn to catch every sound. In the horse the head is usually carried a little to one side for the same reason, and with the nose elevated (_star-gazer_) and nostrils dilated. The ox inclines to carry the head low, while the dog keeps his nose near the ground to guide himself by the sense of smell. All blind animals are disposed to move slowly and carefully, and the horse acquires a habit of _high stepping_ to avoid stumbling.

A common and important test where both eyes are equally affected and cannot be contrasted with each other, is to strike the lower part of the face with the hand and immediately threaten to repeat the blow. If the animal can see, it will seek to jerk the head out of the way as soon as the hand is raised for the second blow, while if blind there will be no such movement provided the motion of the hand has not been such as to induce a current of air on the face.

_Lesions._ Blindness, or the general symptoms of amblyopia or amaurosis, may attend on the atrophy of the retinal fibres in connection with inflammatory exudation or blood extravasation on, in, or beneath, the retina. In other cases the lesion is in the papilla which is inflamed and swollen with the woolly aspect characteristic of choked disc. In others there is congestion of the optic nerve behind the bulb, with exudation into its substance or beneath its sheath, or the nerve has already undergone extensive atrophy with thickening of its neurilemma. In other cases there is atrophy of the arteria centralis retinæ, or tumors of the orbit or optic foramen pressing upon the nerve. Cases of this kind are reported in the larger animals by Leblanc and Tscheulin, and in dogs and ducks by Hilbert.

Much more frequently the determining lesions are situated in the brain or its meninges. In sheep it is very common from the development of cœnurus cerebralis over the optic lobes. Kühnert found a cyst with delicate walls in the brain of a horse affected in this way. Amaurosis is occasionally seen in connection with the cerebral abscesses which form in complicated cases of strangles or in pyæmia, also in cases of cholesteatoma of the choroid plexus. Other conditions of its occurrence are hydrocephalus, meningitis, hypertrophy of the pineal gland, fracture of the cranium, tumors of the cranium or dura mater, embolism or aneurism of the cerebral arteries, hypertrophy and induration of the dura mater (ox, Leblanc), or sanguineous apoplexy. In a certain number of cases there may be no lesion of brain or eye, or only a congestion of the former in connection with lead poisoning, rye grass poisoning or other gastric disorder, or of gestation.

_Treatment._ Success will depend on the sympathetic nature of the condition or on the transient and removable character of its causative factor. When the condition is but a symptom of overloaded stomach or a transient poisoning by vegetable or mineral agents a direct recovery may be expected to follow their disuse and elimination from the system. This may be hastened by the exhibition of laxatives and diuretics, and in the case of lead by sulphuric acid followed by iodide of potassium. In cases of snow blindness it is only necessary as a rule to place the animal in the shade until the over-stimulation shall have subsided. In all these cases the attack has come on abruptly and without any local symptom of ocular hyperæmia and this with the preservation of the general senses can always be looked on as a favorable indication.

In cases that come on slowly and which are accompanied by symptoms of vascular disturbance or structural changes in the eye, or brain, treatment is likely to be less successful. Nevertheless cœnurus may be removed by surgical means, depressed fractures may be elevated, and acute cerebral and meningeal congestions may be met by appropriate measures. If the cerebral congestion is acute, free bleeding from the jugular with a strong purgative and the application of ice or cold water to the head may prove useful. Apparent benefit has also followed the use of blisters on the face or back of the ear, of setons, and later of a weak electric current and strychnia. Tumors also may be advantageously removed.

But in cases marked by destruction of the retina or papilla, by congestion or atrophy of the optic nerve, by destructive disease of the optic foramen, or of the brain or its meninges, treatment is futile.

ANOPHTHALMOS. ATROPHY OF THE EYEBALL. PHTHISIS BULBI. MICROPHTHALMOS.

In some cases the eye is congenitally absent (_Anophthalmos_). In others it is abnormally small. One such case came under the notice of the author in which the eyeball was represented by a small black sphere about half an inch in diameter moved by the ocular muscles. The dam of the filly, born with this defect, had, during the pregnancy, a burdock entangled in the forelock and causing a violent ophthalmia which was supposed to have lasted for months. In other cases there is a fistula opening from the vitreous behind.

Cases of wasting and atrophy of the eye follow on exudates into the vitreous and their subsequent contraction, or on suppuration and granulation as noted under _internal ophthalmia_, _recurrent ophthalmia_, and _panophthalmia_. The condition may also result from atrophy or degeneration of the optic nerve or of its cerebral ganglia (thalamus, corpora quadrigemini, geniculata, etc.). These conditions are irremediable.

LUXATIO BULBI. DISLOCATION OF THE GLOBE OF THE EYE.