Ординатура / Офтальмология / Английские материалы / Applied Pathology for Ophthalmic Microsurgeons_Naumann, Holbach, Kruse_2008

hemorrhage. Drastic pressure release in eyes with acute glaucomas increases the risk of expulsive choroidal hemorrhage (see below). To prevent infection and indirect distant complications, e.g., traumatic tears, perforations of necrotizing keratitis or insufficiently closed surgical wounds, water-tight closure is required as soon as possible (see Chapters 2.2, 4).

Defects in the sensory retina, such as horseshoe tears or foramina, are one reason for retinal detachments. The other is anteriorly displaced vitreous tissue, causing traction on the sensory retina separating it from the retinal pigment epithelium (RPE). “Locations of minor resistance” are the potential “ora slit” and “foveola slit” (see below and Chapter 5.6). Various methods of extrascleral indentations by implants and intravitreal cutting and aspiration release the traction to the margins of the retinal defects (see Chapter 5.6). Other methods, like cryocoagulation (diathermy) or laser therapy, induce necroses of RPE, sensory retina and choroid followed by scar formation between the reattached sensory retina and the viable margin of underlying RPE and choroid.

2.1.2

Excess of Tissue

Congenital anomalies – hamartomas and choristomas

– inflammatory or oncologic processes, abnormal wound healing and neovascularization may lead to an excess of tissue. Malignant neoplasias may impair the function of the eye or even pose a risk for life. Depending on the dimension, removal of such processes requires “excisional biopsy,” which means complete removal of larger lesions, or limited biopsy to establish the histologic diagnosis. If a wide defect results, wound closure with mobilization of the adjacent tissue or transplantation may be necessary (for details see Chapters 3 and 5 for the individual tissue).

2.1.3

Altered Tissue In Situ

Opacities of the lens may present at birth or are acquired following trauma, other ocular or generalized diseases, or – most commonly – are associated with aging. Cataract extraction is the most frequently performed surgical procedure of all medical disciplines. Today the cloudy lens tissue is removed and a lens implant of plastic is inserted into the empty lens capsular bag. With current methods the lens epithelium cannot be removed completely. Reactive proliferation of the remaining lens epithelium always occurs. The resulting secondary cataract can be considered the product of a wound healing process of the lens epithelium and often requires a non-mechanical YAG-laser capsulotomy to reestablish a clear axis of the optic media (see Chap-

ter 5.5). All attempts to avoid secondary cataract would require removal of all lens epithelial cells. This, however, may interfere with a reliable fixation of the lens implant and/or its haptic.

Other examples of altered tissue are those in the trabecular meshwork for chronic open angle glaucomas (see Chapter 5.2), opacities of the cornea from hereditary dystrophies or acquired as a consequence of infectious or non-infectious inflammation causing scar formation (see Chapter 5.1). In 1905 Zirm demonstrated that the corneal obstacle to vision can be removed and replaced by a clear corneal graft – achieving the first successful and today by far the most often performed human tissue transplantation.

2.1.4

Displaced Tissue

Most commonly the retina or the lens is involved.

Detachment of the sensory retina used to be a cause of irreversible blindness until 1916, when Gonin showed that closure of the retinal defect can achieve a cure.

Anatomical variations explain the locations of “minor resistance” for detachment of the sensory retina:

“Ora slit”: In the pre-equatorial area the photoreceptors are only rudimentary and cannot achieve the usual interdigitation between the processes of the pigment epithelium and the outer segments of rods. As a result the adhesion is relatively weak predisposing to separation. This explains why rhegmatogenous retinal detachments usually start in the equatorial region following traction from the anteriorly displaced vitreous body, creating a retinal defect at its base.

“Foveola slit”: The outer segments of foveolar cones

– unlike rods, do not develop the relatively tight interdigitation with the processes of the foveolar pigment epithelium. This predisposes the macular region to the common “disciform” separation of the sensory retina from the RPE.

The sensory retina can also be displaced by traction from preretinal granulation tissue – retinopathy proliferans – particularly with diabetes mellitus or after traumatic vitreal hemorrhage (see Chapters 5.6, 6.1).

Dislocation of the clear lens may occur after blunt trauma, or with metabolic defects like homocystinuria or Marfan syndrome. As this may seriously disturb the optical axis, it may require removal of a clear lens (see Chapter 5.5).

More subtle displacements of the lens develop with the frequently overlooked pseudoexfoliation syndrome, which is a generalized disorder of the extracellular matrix. The zonular instability caused by this process leads to phacodonesis and an increased incidence of vitreous loss during extracapsular cataract surgery and its consequences (see Chapters 5.5, 5.6, 6.3).

2.1.5

Neovascularization and Scars

Intraocular neovascularization most often originates

(1) either from the retinal vessels – always toward the vitreous, never to the outer layer of the sensory retina, or (2) from the choriocapillaris beyond Bruch’s membrane under the RPE, never to the outer choroidal layer (Fig. 2.1).

The process of preretinal vascularization into the vitreous, originating from the retinal vessels, is the cause of retinopathia proliferans particularly in diabetes mellitus, Eales and sickle-cell disease. Angiogenic factors originating from the hypoxic retina initiate also neovascularization of the ciliary body – cyclitic membranes – or on the surface of the iris – rubeosis iridis. As long as the basic metabolic and angiogenic pathology in diabetes mellitus is not sufficiently understood, pre-

vention of proliferative retinopathy remains unsatisfactory. The disturbing excessive scar tissue can be removed by pars plana vitrectomy (see Chapter 5.6).

Subretinal neovascularization originating from the choriocapillaries is the irreversible feature of so-called age related disciform macular degeneration.

Scars do not only follow mechanical or non-me- chanical trauma, but also inflammatory processes in the cornea, iris, anterior chamber, vitreous and in the border zone between the sensory retina and vitreous or RPE and choroid.

After trauma and intraocular surgery, restoration of the anterior chamber must achieve access to the surface of the trabecular meshwork in an open angle. This is essential to prevent scar formation between Fuchs’ roll of the iris and the trabecular meshwork, causing irreversible anterior synechiae and angle closure glaucoma. With current microsurgical methods adhesions

2.2

Intraocular Compared with Extraocular Surgery: Distinguishing Features and Potential Complications

Extraocular surgery of lid, orbit and the epibulbar procedures not opening the intraocular space take into consideration the special surgical anatomy and pathology, but otherwise follow the same pattern as in general

surgery in the various organs of the body (see Chapter 3).

Intraocular microsurgery with an opening in the eye wall alters the peculiar equilibrium of the tissues and spaces within the eye (Fig. 2.2, 2.3, 2.4). The normal function of the eye depends on some special features (Table 2.1): (1) blood-ocular barriers in analogy to the blood-brain barrier; (2) avascularity of the cornea, anterior chamber, lens and vitreous in order to maintain

Fig. 2.2. c Beginnings of choroidal hemorrhage, cystoid changes and hemorrhage into the outer retinal layers.

d Papilledema, retinal folds, and cystoid alteration in the outer and inner plexiform layers of the sensory retina 10 weeks after perforating injury with wound leakage. Notice thin sclera behind Elschnig’s spur (arrow). Retina arteficially detached (ARD) (PAS)

c

d

Table 2.2. Special risks of “open eye” microsurgery

1.Forward motion of iris-lens diaphragm: “vis a tergo” (Fig. 2.5)

2.Paracentesis effect: blood-aqueous barrier breakdown (Fig. 2.6)

3.Expulsive choroidal hemorrhage (Fig. 2.7)

4.Pupillary and ciliary block angle closure (Fig. 2.8)

5.Infectious endophthalmitis, acute with bacteria, subacute with fungi (Fig. 2.9)

6.Sympathetic uveitis

7.Diffuse and cystic epithelial ingrowth (Fig. 2.11 – 2.13)

8.Hemorrhage from vasoproliferative processes (Fig. 2.1)

9.“Toxic anterior segment syndrome” (TASS)

10.“Intraoperative floppy iris syndrome” (IFIS)

Induction

coil

2.2.1

Anterior Movement of the Iris-Lens Diaphragm (“Vis a Tergo”)

Any opening of the anterior chamber with loss of aqueous moves the iris-lens diaphragm forward. It is also mobile during intravitreal manipulation. Opening of the anterior chamber with leakage of aqueous always induces an acute ocular hypotony. Increased filling of the blood vessels of the posterior uvea, combined with uveal effusion, acts as an engine to push the retina, vitreous and the iris-lens diaphragm forward (Fig. 2.5).

a

Fig. 2.5. Lens-iris diaphragm moving forward by uveal hyperemia and effusion (“vis a tergo”): During open eye surgery the mean arterial blood pressure is an important factor determining the location of the iris-lens diaphragm within the eye. Microincisions of the cornea and “positive pressure” in the anterior chamber reduce the risk of protrusion. a Device for measuring the movement of the iris-lens diaphragm in the cat after wide open corneal trephination (Heuser and Gieler, 1979)

Fig. 2.5. b Movement of iris lens from forward with artificial increase of arterial blood pressure by adrenaline. c Lowering of the arterial blood pressure by sodium nitroprusside makes the irislens diaphragm move backward into the eye. The motor for anterior or posterior movement of the iris-lens diaphragm is the filling of the choroidal vessels and “uveal effusion” (Gieler and Heuser 1979)

The degree of blood filling of the choroidal vessels in the “open eye” depends on the mean arterial blood pressure. This process can be reduced by lowering the arterial and venous blood pressure and/or exerting “positive pressure” (Blumenthal) in the anterior chamber, e.g., by infusion and working in an almost “closed system.”

Self-sealing cornea wound architecture achieves quick tamponade of tiny incisions in the cornea and minimizes the effects of acute ocular hypotony and paracentesis – but in principle both always occur temporarily. However, squeezing of the anterior chamber, e.g., by lid specula, may be followed by aspiration of fluid from the ocular surface (“gulp phenomenon”), particularly if located in the lidfissure increasing the risk of postoperative endophthalmitis (see 2.2.5 and Chapter 5.5).

2.2.2

Paracentesis Effect

Breakdown of the blood-ocular barriers (Fig. 2.6): A hyperemia of all intraocular vessels and a breakdown at the blood-aqueous barrier is associated with any acute ocular hypotony: the non-fenestrated endothelial layer of the iris capillaries and the zonulae occludentes of the ciliary body open up and permit a leakage of serum proteins into the tissue and posterior and anterior chamber: This can be measured in vivo by laser tyndallometry. The plasmoid aqueous reduces the transparency and increases the risk of iris-synechia. A lowering of intraocular pressure also affects the zonulae occludentes of the blood-retinal barrier in the RPE (Verhoeff ’s membrane) and those of the retinal capillaries:

c1

c3

Bv

CE

St

c2

c4

Sensory retina

RPE

Bruch’s membrane

Choroid

breakdown of the blood-retinal barrier: “Physiologic defects” of the blood-ocular barriers are recognizable in the transition of iris root to ciliary body and at the optic disc margin (see Chapter 5.7).

After reliable closure of the wound in the eye wall, blood-ocular barrier breakdown is reversible in hours, days or weeks. Cystoid maculopathy (see 4.7, and 5.6).

2.2.4

Pupillary and Ciliary Block

Pupillary and ciliary block with acute and delayed secondary angle closure glaucoma can be the consequence of defective wound healing (see Chapter 5.2) (Fig. 2.8).

2.2.3

Expulsive Choroidal Hemorrhage and Uveal Effusion

Acute or chronic persisting ocular hypotony occurs if defective wound healing of the entrance results in an external fistula or cyclodialysis causes excessive uveal scleral outflow. Both acute and chronic ocular hypotony initiate an uveal effusion and can lead to an expulsive hemorrhage originating from a tear in the posterior ciliary artery entering into the choroidal vessels (Fig. 2.2, 2.3, 2.4, 2.7). The risk of this catastrophe is increased with high arterial blood pressure and in high myopes, where the ciliochoroidal vasculature is attenuated (Fig. 2.7). In nanophthalmus the scleral wall is thickened; this may block the outflow via the vortex veins and accelerate an uveal effusion (see above, Chapter 4.6).

CH

e1

GCL

INL

ONL

PR

RPE

Fig. 2.6. e Blood-retinal barrier: e1 Semithin section of the retina (CH choroid, GCL ganglion cell layer, INL inner nuclear layer, ONL outer nuclear layer, PR photoreceptor layer, RPE retinal pigment epithelium). e2 Electron micrograph of the retinal pigment epithelium (RPE) (BM Bruch’s membrane, CC choriocapillaris). e3 Detail of e2 showing tight junctions (arrows) between retinal pigment epithelial cells. e4 Retinal capillary (En endothelium, Nf nerve fibers, Pe pericyte). e5 Detail of e4 showing tight junctions (arrows) between endothelial cells (b–d Courtesy of U. Schlötzer-Schrehardt 2007)

RPE

BM

Nf

En

Pe

e4

e3

e5