Ординатура / Офтальмология / Английские материалы / Ocular Traumatology_Kuhn_2008

452 Ferenc Kuhn

nometer may be impossible or misleading if the cornea is severely injured. An estimate via palpation by an experienced ophthalmologist is preferred over not taking the IOP at all. The fellow eye should serve as control.

2.18.3Treatment

Primarily, the underlying cause of the IOP elevation must be resolved; this is detailed below. In addition, topical agents (beta blockers, prostaglandin analogs , carbonic anhydrase inhibitors, and, occasionally, alpha agonists) are used, occasionally supported by oral carbonic anhydrase inhibitors.

If the IOP remains elevated despite maximal medical treatment, laser (argon laser iridectomy and trabeculoplasty, YAG trabeculopuncture, diode laser cyclodestruction [2, 3, 15, 17, 18, 22, 26, 28, 41]), cyclocryopexy [24], and surgery (iridectomy, trabeculectomy with or without antimetabolites [20, 30, 36], shunt implantation [31]) are the next weapons in the ophthalmologist’s armamentarium. The most commonly used antimetabolites are mitomycin-C (0.2−0.4 mg/ml) and 5-FU 5-fluorouracil (50 mg/ml) [38]. Eyes that have undergone a filtering procedure are at a higher risk of endophthalmitis (Fig. 2.18.1): if an antimetabolite has been used, the annual incidence reaches 1.3% [9]. For eyes with intractable glaucoma, retinectomy remains a viable therapeutic option [16].

2.18.4Specific Conditions

2.18.4.1Mechanical Globe Trauma

2.18.4.1.1Contusion

A blunt object with insufficient momentum to cause rupture initially compresses the eye antero-posteriorly; this is followed by a rebound effect and

Detailed description of the management is beyond the scope of this book; the reader is referred to glaucoma textbooks.

Should not be administered in the acute, only in the chronic, phase because they may increase the inflammation.

454 Ferenc Kuhn

Regarding therapy, topical corticosteroids, without antiglaucoma medications, usually suffice.

2.18.4.1.1.1.2 Damage to the Trabecular Meshwork

The trabecular meshwork is ruptured. A trabecular flap, hinged at the scleral spur, may also be present. There may be blood in Schlemm’s canal, and cyclodialysis is a common additional finding.

Regarding therapy, anti-glaucoma medications or filtering surgery are used.

2.18.4.1.1.1.3 Hyphema

Blood in the AC may coexist with damage to the trabecular meshwork or may obstruct it in a fashion similar to that described above (inflammatory debris). Total hyphema and repeat hemorrhage represent elevated risk for glaucoma development, increasing the incidence from 0−25% [27] to 25−67% [34, 39]. The risk of glaucoma is directly proportional with the size of the hemorrhage: 14% if the hyphema is one-quarter, 27% if half, and 52% if the hyphema is total.

Regarding therapy, see Chap. 2.5.

2.18.4.1.1.1.4 Lens Swelling (Phacomorphic)

This condition is much more likely to occur in children than in adults, and occur in a very short period of time (see Chap. 2.16). Aqueous enters the lens through a capsular break, and the lens rapidly becomes a space-occu- pying lesion, causing pupillary block or pushing the iris forward to prevent aqueous access to the angle.

Regarding therapy, if a cataract is present, the best option is lens extraction (see Chap. 2.7). An iris bombans may be treated with peripheral iridectomy (laser or surgical; see above), but medical treatment often needs to be added.

2.18.4.1.1.1.5 Postinflammatory

Uveitis often leads to an IOP elevation [12], due mostly to trabecular meshwork obstruction, although other mechanisms are also possible (see below).

Regarding therapy, unless another specific cause exists (e.g., synechia, sympathetic ophthalmia), corticosteroids and cycloplegics are the primary weapons.

2.18.4.1.1.2Delayed-onset Glaucomas

2.18.4.1.1.2.1Angle Recession

The ciliary body is widened due to a split between its longitudinal and circular muscles. The iris may be displaced posteriorly and the ciliary processes may become visible. Iridoand/or cyclodialysis may also be present. The IOP elevation typically occurs if at least a 180° separation is present, and even then it may be delayed by years since scarring and thus chronic obstruction of aqueous outflow are important in the pathogenesis. The recession is more likely to be an indicator, rather than cause, of the glaucoma [40]. Genetic predisposition to diminished trabecular function, present in both eyes, may partially be responsible [32]. Fewer than 10% of eyes with angle recession develop glaucoma [4], even though in eyes with contusionrelated hyphema, angle recession occurs in 70−100% [6, 23, 35].

2.18.4.1.1.2.2Blood-related

2.18.4.1.1.2.2.1Hemolytic

Blood-breakdown products and macrophages that have phagocytized them obstruct the trabecular meshwork.

Regarding therapy, AC lavage is used if medication proved unable to cure this self-limiting IOP rise.

2.18.4.1.1.2.2.2Hemosiderotic

The endothelial cells in the trabecular meshwork are responsible for the phagocytosis of hemoglobin. Iron is released in the process, causing siderosis, which usually affects other tissues of the eye as well (see Chap. 2.13).

Regarding therapy, removal of all iron particles from the eye, but antiglaucoma medications or even filtration surgery, may become necessary.

The longitudinal muscle remains attached to the scleral spur, but the circular muscle is displaced posteriorly.

456 Ferenc Kuhn

2.18.4.1.1.2.2.3Ghost Cell

In eyes with vitreous hemorrhage, red blood cells occasionally undergo a degenerative process and their cell wall is altered so that these khaki-col- ored cells become rigid and oval. If the anterior hyaloid face is disrupted or absent, these cells can enter the AC but are unable to exit through normal outflow channels, obstructing the trabecular meshwork. The condition can occur after closed or open globe trauma [5].

Regarding therapy, vitrectomy is necessary to remove the reservoir of the ghost cells and AC lavage to cleanse the outflow channels [1].

ZPearl

Irrigation of the AC for eyes with glaucoma secondary to ghost cells will not permanently reduce the IOP if the resupply of such cells from the vitreous cavity has not been addressed.

2.18.4.1.1.2.3Lens-related

2.18.4.1.1.2.3.1Subluxation and Luxation

The displaced lens can cause pupillary or angle block. In the former case, iris bombans may also be seen (see below); in the latter case, closure of the angle is easy to recognize on gonioscopy or with the UBM.

Regarding therapy, a pupillary block can be managed with (laser or surgical) iridectomy; otherwise, the lens needs to be removed.

2.18.4.1.1.2.3.2Phacolytic

Lens proteins, recognized by the body’s immune system as an alien material, leak through the capsule. The phagocytized material obstructs the trabecular meshwork. The IOP can be very high.

Regarding therapy, lens removal is indicated, preceded by medical treatment to lower the IOP and reduce the vascular engorgement.

Lens swelling may also cause late-onset glaucoma, although an early (acute) IOP rise is morel likely (see above).

A prolapsed vitreous may contribute to the blockage.

458 Ferenc Kuhn

•Initial visual acuity of <20/200

•Older age

In addition to the many conditions listed above under contusion, the following consequences of an open globe injury can lead to elevated IOP.

2.18.4.1.2.1Anterior Synechiae

Abnormal adhesion forms between the iris and the cornea as a result of inflammation or aqueous leak through an open wound and consequently flat AC. The consequence is reduced aqueous access to the angle.

Therapy proceeds according to the etiology: surgical closure of the wound; corticosteroids to reduce the inflammation; or breaking of the synechiae (see Chap. 2.5).

2.18.4.1.2.2Posterior Synechiae

As a result of inflammation, adhesion develops between the iris and the anterior lens capsule. The pupil is partially or totally immobile, and its shape is irregular. Communication between the posterior chamber and the AC is reduced. If the block is complete, the iris is bulging forward between its root and the pupillary margin (iris bombans), pushed by the aqueous that cannot reach the angle (see Chap. 2.5).

Regarding therapy, iridectomy or synechiolysis (see Chap. 2.5) is used. If the inflammation is still present, topical corticosteroids must be used.

2.18.4.1.2.3Epithelial Downgrowth or Fibrous Ingrowth

The spreading epithelial blanket or scar tissue covers the outflow channels. The condition may develop due to the injury itself or from surgery; the IOP elevation can be fairly high and difficult to treat. Prevention is crucial, avoiding full-thickness sutures in limbal wound repair (see Chap. 2.2) and placing the paracentesis slightly central to the limbus (see Chap. 2.5).

Regarding therapy, surgery is the primary weapon: cyst/cell/scar tissue removal; cryopexy; and endodiathermy [25, 37]. Removal of a scar must be done very carefully to avoid tissue rupture and bleeding (see Chap. 2.5).

2.18.4.1.2.4Toxicosis

Both a ferrous (siderosis) and a copper (chalcosis) IOFB can cause IOP elevation (see Chap. 2.13).

Regarding therapy, if recognized early, the IOFB can be removed and result in IOP normalization; otherwise, antiglaucoma medications, or even filtration surgery, may be needed. With time the ciliary body may be destroyed by the disease, which can also help lower the IOP [7].

2.18.4.2Chemical Trauma

The IOP shows an initial spike after the injury (probably due to tissue shrinkage and increased uveal blood flow), followed by a period of normal or even low IOP if there is extensive ciliary body damage. Finally, chronic IOP elevation is found, due to inflammation and scarring of the angle.

Regarding therapy, in addition to the specific therapy for the chemical injury itself (see Chap. 3.1), proper antiglaucoma medications (see above) have to be used, along with anti-inflammatory treatment and cycloplegia. Surgery is needed if the IOP cannot be controlled medically.

2.18.4.3Orbital Hypertension

The typical underlying condition is hemorrhage, whether caused by trauma or a retro- (para-) bulbar injection; systemic anticoagulant therapy is a risk factor [8].11 In the worst cases, even the LP may be lost.

Regarding therapy, emergency lateral canthotomy may have to be performed if the IOP is so high that the central retinal artery is compressed.

2.18.4.4“Iatrogenic”: Following Closure of a Cyclodialysis Cleft

Once the detached ciliary body is reattached, the previously low IOP can rapidly reach extreme values (see Chap. 2.8).

11In rare cases, the cause is orbital congestion in patients undergoing hydration therapy in cases of severe thermal burn. Another very rare etiology may be emphysema from one of the sinuses after an orbital fracture.

460 Ferenc Kuhn

DO:

•follow the IOP closely after a serious injury, especially if risk factors for the development of secondary glaucoma are present

•if medical treatment is inefficient to bring the IOP down, consider surgery early

DON’T:

•be overconfident that treatment of a certain pathology (i.e., removal of a hyphema) will solve the IOP problem; other etiologies (i.e., ghost cell formation) may contribute as well and may also require treatment

•forgo consulting a glaucoma specialist if the IOP elevation persists

Summary

Glaucoma is probably a far more common complication of closed or open globe trauma than presumed. The treatment may be simple, eliminating the underlying cause, but it may also be complex and difficult:

the IOP elevation may be nonresponsive to medical treatment and require surgical intervention. In such cases, a glaucoma specialist must be consulted.