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Ординатура / Офтальмология / Английские материалы / Veterinary Ocular Pathology A Comparative Review_Dubielzig, Ketring, McLellan_2010

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Non-surgical trauma

Chapter

 

 

5

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figure 5.7  Traumatic cataract. (A,B) Gross photographs show trauma-induced cataracts in a cat (A) and a dog (B). There is lens capsule rupture, displacement of lens fiber protein, and synechiae in both globes. (C,D) Low magnification and higher magnification of a canine post-traumatic cataract show lens capsular rupture and remodeling.

A B

C D

Traumatic lens subluxation or luxation

This is rarely seen in isolation, as the forces required to disrupt the zonular attachments of domestic animals are generally associated with other signs of severe ocular trauma.

Retinal effects (Figs 5.11, 5.12)

Because of the precise anatomic and functional organization of normal retinal tissue, it is at great risk of damage associated with contusive injury.

The neuroretinal tissue is ‘stretched’ across the posterior segment, and it has a semi-liquid consistency that makes it vulnerable to disruption by the shearing forces of a pressure wave propagating within it

This type of injury can be associated with ‘whiplash’ forces, which may result from shaking, as seen in the

shaken-baby syndrome in human infants, or from a blow to the head

If the damage is mild, the retina may not degenerate, and a return to function is possible

If the damage to the retina is locally severe, the retinal tissue undergoes rapid degeneration. The damage occurs acutely, is non-progressive over the long-term, and it is often segmental

Within the first 24 h, retinal contusion is associated with apoptosis and physical disruption

Separation of the photoreceptor processes from the outer nuclear layer is seen in acute trauma

Hemorrhage in the retina or vitreous

Within 5 days, the severely affected retinal tissue becomes liquefied and phagocytes (gitter cells) predominate

The end-stage is regional, severe retinal atrophy

Retinal detachment and retinal tears are frequently seen

A useful clue that trauma was involved as the cause of severe retinal damage is the finding of well-preserved blood vessels, seemingly ‘free in space’, separated from the atrophic retinal tissue adjacent to them.

Scleral effects, scleral rupture (Figs 5.13, 5.14)

There are over 240 cases of scleral rupture in the COPLOW collection in dogs and cats. Scleral rupture results from a deforming blow to the globe. The blow may or may not directly penetrate the globe but deformation of the globe results in rupture of the sclera at points of weakness. These weak points include the equatorial region adjacent to rectus muscle attachments and, less commonly, the posterior pole.

Most commonly, scleral rupture is the result of blunt trauma without a penetrating component (Fig. 5.13)

In these cases you will find the following features:

Segmental uveal fibrosis in the region of the scleral rupture or defect

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Veterinary Ocular Pathology

 

 

Figure 5.8  Lens capsule rupture.

 

 

(A) Gross photograph of a canine globe

 

 

showing a small lens remnant and

 

 

adhesion of iris, ciliary body, and

 

 

detached retinal tissue.

 

 

(B) Photomicrograph of a feline globe

 

 

after traumatic lens capsule rupture

 

 

showing coiling of the capsule and

 

 

cellular proliferation on both sides of the

 

 

capsular defect. (C,D) Photomicrographs

 

 

showing macrophage and multinucleate

 

 

giant cell reaction to exposed lens

 

 

proteins, which is a reliable indication of

A

B

lens capsular rupture.

C D

A scleral defect, which typically extends from the equator radially towards the posterior pole

Episcleral and orbital fibrosis with displaced fragments of pigmented uveal tissue or disorganized neural tissue of retinal origin

Episcleral damage involving peripheral nerve tissue, with neuroma formation

An example of trauma to the globe with both direct penetration and scleral rupture would be a ballistic injury (Fig. 5.14)

In these cases, you will find the following features:

An entry wound

Uveal fibrosis in association with the scleral defect

If segmental uveal fibrosis but no scleral defect is found, it can be rewarding to cut deeper into the block in search of a scleral defect

A scleral rupture starting at the equator that extends radially toward the posterior pole, but does not involve the optic disc

Possibly an exit wound

Metallic fragments

Polarized light can be very useful to identify tiny, metallic fragments, which otherwise may masquerade as melanin

Extensive episcleral and orbital hemorrhage or scarring, depending on chronicity

Displaced pigmented uveal tissue and disorganized neural tissue of retinal origin.

Comparative Comments

The retinal effects and scleral effects of blunt trauma are very similar in the human eye to those described for domestic animals.

88

PENETRATING INJURIES

Corneal penetrating injury (Fig. 5.15)

In the COPLOW collection, it is generally not possible to differentiate penetration of the cornea due to intrinsic, primary corneal disease with perforation (as discussed in greater detail in Ch. 8) from that due to penetrating trauma. Although traumatic penetrating injury to the cornea is undoubtedly important, the unique features and consequences of traumatic corneal penetrating injuries will not be specifically addressed in this chapter, because it is often not possible for the pathologist to establish the sequence of events.

Scleral penetrating injury (Figs 5.16, 5.17)

In the scleral penetrating injury cases recorded in the COPLOW collection, we have seldom been provided with a history of a traumatic event. There are features that suggest a penetrating injury to the sclera, which include the following:

Episcleral, orbital, and/or subconjunctival fibrosis or fistulating inflammation

If the inflammation is more severe in the superior part of the orbit/globe, this suggests injury related to an attack or a falling object

If the inflammation is more severe inferiorly, this suggests penetrating injury related to an oral foreign body or a stick from below

There are seven cases in the COPLOW collection, as well as cases published in the veterinary literature, with a recent history of dentistry and in some cases, accidental slippage of a dental instrument

Non-surgical trauma

Chapter

 

 

5

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figure 5.9  Lens-induced uveitis, phacoclastic uveitis. (A) Mixed Breed, 12 weeks old: prior trauma resulted in lens rupture, cataract formation, and uveitis. Pigment is present on the lens and ectropion uvea is indicated by the arrow.

(B) Vitreous protein exudation is adjacent to the ruptured lens capsule (arrow) in a traumatized dog globe. (C) Subgross photomicrograph of a canine globe showing a nearly empty lens capsular bag and protein exudates in the vitreous body secondary to the release of denatured lens proteins. (D) Gross photograph of a feline globe showing distinctive protein exudates (arrow) in the vitreous body near the posterior pole

of the lens, which is associated with posterior lens capsule rupture and lymphoplasmacytic uveitis. (E) Photomicrograph of the globe in (D) showing the granular hypereosinophilic protein characteristic of posterior lens capsular rupture in feline uveitis.

A

B C

D E

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Veterinary Ocular Pathology

*

A B C

*

D E

Figure 5.10  Metaplasia and proliferation of released lens epithelial cells. (A) Photomicrograph of a canine globe showing the iridocorneal angle with a spindle cell proliferation and broad anterior synechia secondary to lens epithelial cell proliferation and migration into the anterior chamber. Surrounding each spindle cell is a thick PAS-positive basement membrane, characteristic of lens epithelial cell origin (PAS stain). (B) Low magnification

photomicrograph showing lens capsule rupture (arrow), with proliferation and migration of metaplastic lens epithelial cells. The lens is entrapped in the anterior chamber and the proliferating cells are between the lens and the iris (PAS stain). (C,D) Photomicrographs of a traumatized dog globe showing metaplastic lens epithelial cells, labeled with immunohistochemical stain for smooth muscle actin, within the lens capsule (*) (C) and surrounding the wrinkled lens capsule (*) (D). (E) Photomicrograph of a traumatized feline globe showing the tapetum and a membrane on its inner surface composed of metaplastic lens epithelial cells. A distinct PAS-positive basement membrane surrounds individual cells (PAS stain).

90

 

 

Non-surgical trauma

Chapter

 

 

5

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figure 5.11  Traumatic retinal tear,

 

 

 

 

 

 

fundoscopy. (A) Doberman Pinscher,

 

 

 

3.5 years old: blunt trauma caused

 

 

 

 

 

 

papilledema and preretinal hemorrhage.

 

 

 

(B) Mixed Breed, 3 years old: extensive

 

 

 

posterior segment hemorrhage is present

 

 

 

after being hit by a car. The arrow points

 

 

 

to the edge of a giant retinal tear in the

 

 

 

detached retina. (C) Beagle, 1.5 years

 

 

 

old: acute blindness was present after

 

 

 

being hit by a car. Peripapillary and

 

 

 

 

 

 

horizontal linear areas of tapetal

 

 

 

 

 

 

hyperreflectivity are present (black

 

 

 

 

 

 

arrows). Abnormal tapetal pigmentation

 

 

 

is also present. (D) Non-tapetal fundus

 

 

 

of the globe in (C). Linear areas of

 

 

 

 

 

 

depigmentation and pigment migration

 

A

B

in the outer layer of the retina are

 

 

 

 

 

 

present.

 

 

 

 

C D

A full-thickness scleral defect

This finding is good evidence of a penetrating injury but, unfortunately, is seldom found in the standard plane of section

Some evidence of direct damage within the globe, that includes at least one of the following (Fig. 5.17):

Lens capsule rupture

Fistulous inflammatory tracts that extend through the uvea or retina

Bacterial sepsis

Identification of a fragment of foreign material in the section

By far the most common foreign body found in tissues in the COPLOW collection is a plant fragment (32 cases). However, hair, mineral (three cases), bone, feather, metal, and plastic have also been found. Porcupine quills are not uncommon as causes of penetrating or perforating ocular injury in certain geographic locations.

Suppurative endophthalmitis (Fig. 5.18)

Suppurative endophthalmitis is the most common consequence identified in eyes removed after a penetrating injury

Among dogs, the brachycephalic breeds (also prone to keratitis) are most likely to have suppurative endophthalmitis

The Shih Tzu is the most commonly represented canine breed, accounting for 121 of the 954 cases in the COPLOW collection with this diagnosis

Larger hunting breeds, perhaps due to their propensity for running through brush, are also prone to endophthalmitis related to perforating/penetrating injuries

Common morphologic features of suppurative endophthalmitis associated with penetrating injury include (Fig. 5.18):

A similarity in the degree of suppurative exudates throughout all of the compartments of the globe

Lens capsule rupture

Liquefactive necrosis of the retina

Focal or multifocal, very localized neovascular extensions from the choroid into the subretinal space

At COPLOW, these neovascular extensions are often referred to as ‘volcanoes’ because of their eruptive appearance

A very early change, seen in acute cases, is the appearance of suppurative infiltrate within the choriocapillaris, before other exudates are apparent.

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Veterinary Ocular Pathology

 

 

Figure 5.12  Retinal trauma, microscopic.

 

 

(A) Photomicrograph showing the effects

 

 

of recent trauma on the retina from a

 

 

canine globe penetrated by a pellet 5 h

 

 

before enucleation. There is hemorrhage

 

 

and a segmental loss of structural

 

 

integrity. (B) Photomicrograph of the

 

 

retina from a young horse necropsied

 

 

24 h after a head trauma showing

 

 

segmental apoptosis of photoreceptors

A

B

and disruption of inner and outer

segments. (C) Photomicrograph of the

 

 

 

 

retina from a dog necropsied 5 days

 

 

after head trauma showing segmental

 

 

retinal disruption, necrosis and phagocyte

 

 

accumulation. (D) Photomicrograph

 

 

showing complete retinal atrophy with

 

 

remaining macrophage cells (gitter cells)

 

 

(arrow) 10 days after blunt trauma.

C D

*

*

A B C

Figure 5.13  Ballistic foreign bodies in the globe. (A) Anterior view of a canine globe removed shortly after penetrating trauma from a shotgun injury. (B,C) A dog globe (B) and a cat globe (C) show disorganization of ocular tissues associated with bullet fragments (*) visible within the globe.

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Non-surgical trauma

Chapter

 

 

5

 

 

 

 

 

 

 

 

 

 

 

 

 

 

A B C

D E F

Figure 5.14  Scleral rupture, blunt trauma. (A–F) A montage showing six dog and cat globes with scleral rupture associated with blunt trauma. Scleral rupture in blunt trauma starts at the equator, where the sclera is thinnest, and extends towards the posterior pole.

93

Veterinary Ocular Pathology

Figure 5.15  Traumatic corneal perforation. (A,B) Gross photographs of a canine globe with traumatic corneal perforation and iris prolapse. (C,D) Low magnification photomicrographs of the same globe showing iris tissue prolapsed through the cornea and entrapped, leading to swelling, edema and vascular proliferation.

A B

C D

Septic implantation syndrome (‘cat scratch’ injuries) (Figs 5.19, 5.20) (see also Ch. 10)

This is a canine and feline syndrome of endophthalmitis, often resulting from cat scratch injury, that can be defined by a specific set of morphologic criteria:

There are 75 canine and 20 feline eyes in the COPLOW collection with endophthalmitis and features of ‘septic implantation syndrome’

All ages are affected but there is a bias towards younger animals

A definitive history of known cat scratch injury is seldom provided. However, when the inciting cause is known, it is often related to an incident involving a cat scratch

A feature of this syndrome is a period of latency, during which the globe is relatively quiet, between the inciting injury and the onset of endophthalmitis that leads to enucleation

A latency period of several months is typical, but latencies as long as 2 years have been observed among the cases in the COPLOW collection

This syndrome is characterized by the following morphological features:

Suppurative and histiocytic inflammation which intimately surrounds the lens

Broad posterior synechiae, with spindle cells and collagen that are consistent with temporal chronicity

Lens capsule rupture with suppurative inflammation extending into the lens substance

94

About 60% of cases have identifiable bacterial colonies within the lens substance but away from the inflammatory cell infiltrate

In affected canine eyes, bacteria are usually Gram-positive cocci

In feline cases there is more likely to be a mixed population of bacteria.

Comparative Comments

The sequelae of perforating injuries in the human eye are similar to those discussed in the COPLOW collection.

CHEMICAL INJURY (Fig. 5.21)

In contrast to the situation in human ocular pathology services, submissions to COPLOW from cases affected by known chemical injury are extremely rare.

Acid burn

Acid exposure to tissue causes an instantaneous coagulation of the most superficial tissues, with precipitation of proteins, but the effect does not extend deeply.

A B

C

Acute: coagulation necrosis of superficial epithelial and stromal tissues

Chronic: granulation tissue response.

Alkali burn

Alkali exposure causes extensive damage due to its ability to penetrate deeply into ocular tissue.

Acute: There is swelling and loss of the corneal epithelium and coagulation of conjunctival blood vessels. Tissue swelling and vascular damage extend deep into the tissue, with intraocular extension of these effects

Chronic: tissue atrophy, collagenolytic lysis, and granulation tissue. Keratomalacia is associated with the release of collagenases from corneal epithelial and stromal cells, and from neutrophils.

Non-surgical trauma

Chapter

 

 

5

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figure 5.16  Traumatic penetrating injury.

(A) Gross photograph of a canine globe with endophthalmitis due to a penetrating injury. (B) Subgross photomicrograph of a canine globe penetrated by a migrating porcupine quill. The arrow indicates the point of scleral penetration. (C) Photomicrograph showing the scleral penetration point from a slipped dental instrument.

Snake bite (Fig. 5.22)

There are three cases in the COPLOW collection of venomous snake bites directly to the globe.

The damage is dominated by tissue lysis, presumed to be related to lytic factors in the venom

Retinal and optic nerve tissue are notably destroyed, and seemingly liquified.

PROPTOSIS AND OPTIC NERVE

TRAUMA (Figs 5.23, 5.24)

There are 82 cases in the collection with a history of proptosis (anterior prolapse of the globe, which becomes entrapped by the eyelid margins behind the globe equator).

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Veterinary Ocular Pathology

A B C

D E F

Figure 5.17  Endophthalmitis with a foreign body. (A–E) A montage of gross photographs of canine and feline globes with scleral penetrating injuries. White arrows in images (B), (C) and (D) indicate the points of penetration or tracks within the globe. (E) Low magnification photomicrograph showing a plant foreign body (black arrow) imbedded in the globe near the optic nerve.

Of these 82, 80 are dogs and only two are cats. Brachycephalic breeds, young dogs, and small terrier breeds are over-represented

The time between proptosis and subsequent enucleation ranges from hours to months

The morphologic features in enucleated canine globes with a history of proptosis include:

Global optic nerve necrosis

Most globes removed following proptosis have immediate total necrosis of the optic nerve tissue

If removed within 4 days of proptosis, degeneration of the neuropil and apoptotic nuclear profiles will be observed within the optic nerve

If removed 5–10 days after proptosis, optic nerve tissue malacia, dominated by macrophage cells (gitter cells) will be observed

If removed 2 weeks or more after proptosis,

profound atrophy and fibrosis of the optic nerve will be observed

Retinal effects

The effects of retinal contusion (as described previously) may be observed

Detachment and/or retinal tear

Segmental malacia followed by atrophy

A loss of retinal ganglion cells secondary to the optic nerve trauma may be observed and, when seen, the loss of ganglion cells occurs within days of the traumatic episode

Corneal effects

In proptosed eyes, acute and profound corneal necrosis occurs, because of desiccation, loss of innervation and/or loss of blood supply to the anterior segment. There can be a full-thickness devitalization of the corneal stroma. This is purportedly more likely to occur if avulsion of more than two extraocular muscles is recognized

Loss of corneal sensation or reduced ability to blink may also contribute to chronic keratitis, following surgical replacement of a proptosed globe

In rare cases, total infarction of the globe may occur after proptosis resulting in global necrosis of ocular tissues

Orbital effects

Muscle damage, orbital hemorrhage, and other effects of soft tissue trauma can lead to inflammation or scar tissue in the episclera and orbital tissue.

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