more “posterior pressure,” but keep in mind the two different spaces affected—the periorbital and the suprachoroidal. Patients appreciate that the pain is diminished and surgeons can complete the case less stressfully under regional anesthesia.

We have been able to complete all procedures within 60 minutes of the onset of the AISH using this technique. The procedure remains difficult, but manageable. I will apply Q-tip pressure at intervals during the surgery to keep the effusion or hemorrhage in check and to keep the eye as soft as possible during surgery. The incision must be watertight and the infusion bottle as high as possible (if the posterior capsule is intact).

It is desirable to complete the surgery during the time frame provided by the regional block. There is psychological stress inflicted on the patient and the family by delay. However, if the surgeon is uncomfortable proceeding, or if the eye remains firm for an inordinate amount of time, there is no significant ocular morbidity involved in delaying the completion of the cataract extraction. Even after capsulotomy and/or partial phaco, treating aggressively for elevated IOP and inflammation and waiting a few days for the eye to stabilize is acceptable.

If surgery is continued, every prudent attempt must be made to remove the cataract, which is possible by following the management technique outlined here. Once the cataract has been removed, it is usually not too difficult to insert an IOL. The only exception to this guideline might be the secondary insertion of an IOL if the capsule has been severely compromised during the initial operation.17

These patients should be treated aggressively postoperatively with topical steroids and ocular pressure lowering medications. We routinely use oral systemic carbonic anhydrase inhibitors until the IOP is con-

FIGURE 8–7 A choroidal elevation may be evident on indirect examination.

trolled. The choroidal elevation is usually evident postoperatively by indirect ophthalmoscopy (Fig. 8–7) or B-scan ultrasonography (Fig. 8–8). Effusions usually resolve within 2 weeks, whereas suprachoroidal hemorrhages may require 1 to 2 months.

EXPULSIVE HEMORRHAGE

In the unfortunate event that a true expulsive hemorrhage occurs, the same basic principle applies— close the incision. Toilet the incision as well as possible; there should be no vitreous or uvea in or beyond the incision. A retina/vitreous specialist should be

consulted within 24 hours. Repair of a true expulsive hemorrhage, or a severe AISH with “kissing choroidals,” requires the help of an experienced posterior segment specialist.

TREATMENT OF MASSIVE

SUPRACHOROIDAL HEMORRHAGE

Just because a patient has a massive suprachoroidal hemorrhage does not mean that they will require secondary surgery. Each case must be judged individually. If the eye has vitreous or uvea in the incision, secondary surgery is probably indicated. Drainage of the suprachoroidal space in the immediate surgical and postoperative period is probably not helpful. Most of the time, the hemorrhage will simply recur.16,18 Massive kissing choroidals, in which there is apposition of the retinal surfaces, presents more of a dilemma. Experimental and clinical work indicate that a suprachoroidal hemorrhage begins to liquefy between 7 and 14 days; therefore, such a hemorrhage is optimally drained during this time.16 Chu et al18 used echography to follow these patients and noted that many cases resolved spontaneously without immediate retinal sequelae in spite of a mean period of retinal apposition of 15 days.

Reynolds et al19 also concluded that secondary surgery was not indicated if a kissing choroidal was the only problem. If retinal detachment or vitreous incarceration was present, vitrectomy with air-fluid exchange, combined with drainage of the suprachoroidal blood, was indicated. Scott et al20 evaluated visual acuity in eyes having appositional suprachoroidal hemorrhage and found significantly worse vision if the appositional choroidal was present for more than 14 days.

All patients having a massive suprachoroidal hemorrhage have a very guarded prognosis. Even in the best-case scenario, eyes requiring secondary surgery don’t often see well. An acuity of 20/200 or better should be judged a success in these cases. Concurrent or delayed retinal detachment is always a risk, just one more reason an experienced retina/ vitreous surgeon should be managing patients with complicated, massive suprachoroidal hemorrhage, and more reason than ever to understand the nature of positive pressure development during phacoemulsification and the management of AISH!

CONCLUSION

Treatment of an AISH has as its primary goal the prevention of expulsive hemorrhage. This is achieved by intervening at the earliest possible recognition of a suprachoroidal effusion. Treatment consists of immediate closure of the incision, external Q-tip pres-

CHAPTER 8 POSITIVE PRESSURE • 73

sure on the globe to tamponade the effusion or hemorrhage, and pharmacologic agents to decrease the postoperative IOP. If 5 to 10 minutes of significant anterior pressure does not sufficiently soften the eye, place a Honan balloon over the eye at a pressure of 50 mm Hg. Wait and watch for 10 to 60 minutes until the eye is softer, then proceed to complete the procedure. In my experience, all such cases have been completed with 90% of patients having 20/40 or better visual acuity. Most importantly, no eyes have developed an expulsive hemorrhage.7

REFERENCES

1.Arnold PN. A prospective study of a single injection peribulbar technique. J Cataract Refract Surg 1991;18: 157–161.

2.Updegraff SA, Peyman GA, McDonald MB. Pupillary block during cataract surgery. Am J Ophthalmol 1994; 117:328–332.

3.Osher RM. Emergency treatment of vitreous bulge and wound gaping complicating cataract surgery. Am J Ophthalmol 1957;44:409–411.

4.Tsai JC, Barton KA, Miller MH, et al. Surgical results in malignant glaucoma refractory to medical or laser therapy. Eye 1997;11:677–681.

5.Wolter JR, Garfinkle RA. Ciliochoroidal effusion as precursor of suprachoroidal hemorrhage: a pathologic study. Ophthalmic Surg 1988;19:344–349.

6.Beyer CF, Peyman GA, Hill JM. Expulsive choroidal hemorrhage in rabbits: a histopathologic study. Arch Ophthalmol 1989;107:1648–1653.

7.Arnold PN. Study of acute intraoperative suprachoroidal hemorrhage. J Cataract Refract Surg 1992;18: 489–494.

8.Speaker MG, Guerriero PN, Met JA, et al. A case-control study of risk factors for intraoperative suprachoroidal expulsive hemorrhage. Ophthalmology 1991;98:202–210.

9.Bukelman A, Hoffman P, Oliver M. Limited choroidal hemorrhage associated with extracapsular cataract extraction. Arch Ophthalmol 1987;105:338–341.

10.Eriksson A, Koranyi G, Seregard S, et al. Risk of acute suprachoroidal hemorrhage with phacoemulsification. J Cataract Refract Surg 1998;24:793–800.

11.Davison JA. Acute intraoperative suprachoroidal hemorrhage in extracapsular cataract surgery. J Cataract Refract Surg 1986;12:606–622.

12.Davison JA. Acute intraoperative suprachoroidal hemorrhage in capsular bag phacoemulsification. J Cataract Refract Surg 1993;19:534–537.

13.Blumenthal M, Grinbaum A, Assia EI. Preventing expulsive hemorrhage using an anterior chamber maintainer to eliminate hypotony. J Cataract Refract Surg 1997;23:476–479.

14.Hayreh SS, Weingeist TA. Experimental occlusion of the central artery of the retina: IV. Retinal tolerance time to acute ischemia. Br J Ophthalmol 1980;64:818– 825.

15.Maumenee AE, Schwartz MF. Acute intraoperative choroidal effusion. Am J Ophthalmol 1985;100:147– 154.

16.Lakhanpal V. Experimental and clinical observations on massive suprachoroidal hemorrhage. Trans Am Ophthalmol Soc 1993;91:545–652.

17.Bryant WR. Secondary intraocular lens implantation in eyes that experience suprachoroidal hemorrhage during primary cataract surgery. J Cataract Refract Surg 1989;15:629–634.

18.Chu TG, Cano MR, Green RL, et al. Massive suprachoroidal hemorrhage with central retinal apposition:

a clinical and echographic study. Arch Ophthalmol 1991;109:1575–1581.

19.Reynolds MG, Haimovici R, Flynn HW Jr, et al. Suprachoroidal hemorrhage: clinical features and results of secondary surgical management. Ophthalmology 1993;100:460–465.

20.Scott IU, Flynn HW Jr, Schiffman J, et al. Visual acuity outcomes among patients with appositional suprachoroidal hemorrhage. Ophthalmology 1997;104: 2039–2046.

Each type of phaco procedure has subtle distinctions that may lead to inconsistent surgical outcomes. Each procedure has potential hurdles that may lead to complicated outcomes. This chapter and Chapters 10 to 14 define each procedure and examine the steps leading to successful outcomes and the pitfalls leading to complications.

CATARACTOGENESIS

The classification of cataracts is artificial but useful to categorize particular cataract qualities. This allows the surgeon to plan effective surgery based on the expected cataract qualities.

The terms congenital and developmental cataract encompass lens opacities noted at birth and during infancy, respectively. Juvenile cataract denotes onset during the period of childhood to adolescence. Presenile refers to onset between early adulthood and age 60 years, with the term senile cataract used for cataracts that develop thereafter. Cataracts developing during the juvenile period and the presenile period are often due to ocular disease, trauma, or the use of steroids. These cataracts may indicate the carrier state or early phase of genetic disease.1

Biochemical changes that consistently occur in cataracts include increased water content, loss of potassium, increased calcium, increased oxygen consumption, decreased glutathione, and decreased ascorbic acid. Many of these changes may be the result, rather than the cause, of cataracts.2

Histopathologic and ultrastructure analysis are seldom suggestive of a specific etiology, showing changes common to all subcapsular, cortical, or nuclear sclerotic cataracts.1

The following outline is an overview of the major types and causes of cataracts:

A.Major categories of congenital cataracts2

1.Remnants of the tunica vasculosa lentis

a.In the iris these are observed as pigmented pupillary membranes attached at the collarette.

b.In the anterior capsule they are a single or group of spots, which may be pigmented and are attached to the anterior capsule.

c.In the posterior capsule they are Mittendorf dots or white spots attached to the posterior capsule just inferior and nasal to the posterior pole of the lens. They rarely affect vision.

2.Polar: These cataracts may be either anterior or posterior and affect the subcapsular cortex and lens capsule. They may be either hereditary or secondary to intrauterine inflammatory processes. They may have a significant effect on vision depending on size and location.

3.Sutural: These cataracts involve the Y sutures. Often hereditary, they rarely affect sight.

4.Capsular: These cataracts are a small opacification in the anterior epithelium and lens capsule, sparing the cortex. They may protrude into the anterior chamber. They rarely affect vision.

5.Zonular: These cataracts involve opacification in the outer fetal and inner adult nucleus. They appear as fine white dots, haze, or linear spokes. They are always bilateral and are due to hereditary or other noxious stimuli during pregnancy. They are likely to affect vision.

76 • COMPLICATIONS IN PHACOEMULSIFICATION

B.Major categories of senile and presenile cataracts2

1.Nuclear: These cataracts are characterized by increasing hardness and pigmentation of the nucleus with age. There is usually slow progression with gradual loss of sight and color discrimination.

2.Cortical: Water vacuoles begin between cortical fibers and progress to transparent clefts. They then become cloudy, imbibe water, and may swell. When mature they are white and may develop a tense capsule due to an osmotic gradient pulling water into the lens. When the endonucleus becomes rock hard and floats within the liquid cortex the cataract is labeled Morgagnian.

3.Subcapsular: These cataracts begin as sheen on the anterior or posterior capsule. They then progress to white opacities with formation of vacuoles, eventually forming a plaque. Posterior subcapsular cataracts may fibrose due to metaplasia of lens epithelial cells, which may then grow into the posterior capsule. Rapid growth my lead to substantial visual loss.

C.Major categories of acquired cataracts2

1.Trauma

a.Physical injury without direct lens injury may cause a posterior subcapsular cataract (PSC).

b.Radiation after a latent period of up to 20 years may cause an anterior subcapsular cataract (ASC) or PSC. The necessary exposure is 500 to 600 rad.

c.Electrical current may cause protein coagulation of the lens with subsequent cataract formation.

2.Metabolic

a.Diabetes mellitus is the most common metabolic cause of cataract development. An increased concentration of glucose in the aqueous humor will result in increased concentration of glucose within the lens. Aldose reductase will then convert glucose to sorbitol, which remains within the lens. This will create an osmotic gradient drawing water into the lens. Initially this will induce myopia but eventually results in loss of lens clarity.

b.In Wilson’s disease the copper pigment accumulates in an anterior subcapsular location and appears like a sun flower.

3.Toxic

a.The most common toxic agent causing cataracts is steroids. In one study 30 to 40% of patients taking 10 mg of prednisone for 2 years for rheumatoid arthritis developed cataracts. Almost all will develop them if high-dose steroids are administered for 4 years. PSC is the usual type and is often rapidly a cause for visual disturbance.3

b.Chlorpromazine may cause dose-related melanin-like pigment accumulation in the anterior subcapsular lens.4

c.Amiodarone causes a nonvisually significant cataract.

d.Secondary

i.Iridocyclitis will often cause a PSC.

ii.Fuchs heterochormic iridocyclitis will cause a cortical cataract to develop.

iii.Systemic diseases such as myotonic dystrophy will cause anterior subcapsular polychromatic opacities.

iv.Congenital disease, such as galactosemia or rubella.

COMPLICATIONS IN THE COURSE OF

THE PHACO PROCEDURE

Throughout the phacoemulsification segment of any type of procedure, the most serious complication is the creation of a rent in the posterior capsule with or without vitreous loss. The posterior capsule can rupture during phaco resultant to the following causes:

1.Extention of a preexisting tear in the anterior capsulotomy: A known or occult tear in the anterior capsule may extend around the equator with the posterior pressure of the irrigating fluid. In addition, the mechanical posterior pressure of the phaco tip pressing on the nucleus during sculpting may cause extension of the tear. Finally, separation of the nuclear segments after sculpting or in preparation for chopping may stress the capsular bag, resulting in extension of a noncontinuous capsulotomy.

2.Phaco through the equator: During any phaco procedure, while attempting to phaco the peripheral aspect of the nucleus, the equatorial bag may be accidentally emulsified, resulting in a rent along with possible secondary extension. This can occur during sculpting near the equator with high vacuum settings. The nucleus will occlude the phaco tip. The resultant postocclusion

FIGURE 9–2 Inadvertent tear caused by phaco through the nucleus and posterior capsule.

surge may lead to aspiration of the epinucleus, cortex, and capsule. This will result in a capsular tear. Similarly, emulsification of a soft nucleus near the equator may have a comparable result (Fig. 9–1). In the presence of poor hydrodissection, the aspiration of cortex still attached to the capsular bag may actually pull the equatorial bag into the phaco tip with a resultant tear (see Chapter 15, Figure 15–3).

3.Phaco through the nucleus and posterior capsule:

This can occur at almost any time during the procedure. The phaco tip can penetrate the nucleus posteriorly. Early in the procedure during sculpting, especially with high vacuum, the tip may occlude. The subsequent surge will draw the posterior epinucleus, cortex, and posterior capsule into the tip. The mechanism is the same when, during phaco of the epinucleus, the tip can be passed through the epinucleus with aspiration of the posterior capsule and vitreous (Fig. 9–2).

Attention to detail, recognition of the predisposing factors for complications, and appropriate intervention to prevent complications are the attributes that lead to successful outcomes. Chapters 10 to 14 examine the subtleties of each type of phaco technique so that impending complicated surgical procedures can be identified and repaired prior to the emergence of the complication.

REFERENCES

1.Streeten BW. Pathology of the lens. In: Albert DM, Jakobiec FA, eds. Principles and Practice of Ophthalmology. Philadelphia: WB Saunders; 1994:2198.

2.American Academy of Ophthalmology. Basic and Clinical Science Course, 1996–1997. San Francisco: AAO; 1996:30–35.

3.Williamson J, Paterson RWW, McGavin DDM, et al. Posterior subcapsular cataracts and glaucoma associated with long-term oral corticosteroid therapy in pa-

tients with rheumatoid arthritis and other conditions. Br J Ophthalmol 1969;53:361–372.

4.Siddall JR. The ocular toxic findings with prolonged and high dosage chlorpromazine intake. Arch Ophthalmol 1965;74:460–464.

Attention to surgical detail and knowledge of alternative techniques are especially important in performing a complication-free phacoemulsification procedure. This chapter describes the major phases of the four-quadrant in situ phacoemulsification technique,1 commonly called “divide and conquer,” the flow of the procedure, typical problem-causing areas, and solutions to common problems. Specific details of each original surgical technique, variations, and applications are found in the references and in appropriate courses.

HISTORY

Nuclear splitting techniques1–3 evolved and were popularized following the advent of capsulorrhexis,4 which made subluxation of the lens nucleus into the pupillary plane difficult. These techniques enabled the surgeon to confine emulsification within the capsular bag and more easily manage smaller sections of the nucleus. The nucleus may be divided into sections or quadrants with vertical splits1,2 or delaminated internally by circumferentially separating an inner from an outer nucleus5; the two approaches may be combined by delaminating the nucleus and then splitting the internucleus vertically.3

Figure 10–1 shows the locations of lens nucleus areas created by the phacoemulsification sculpting process that will be referred to in this chapter.

PHACOEMULSIFICATION STAGES AND

PROBLEMS ENCOUNTERED

CAPSULOTOMY NONCONTIGUOUS

If there is a tear in the edge of the anterior capsulotomy, some of the maneuvers required for this nucleus management technique, such as nucleus rotation and cracking, might cause the tear to extend peripherally and then posteriorly. If the capsulotomy edge is torn after the nucleus has been hydrodissected and freely rotated, cracking may be safely accomplished, provided the crack is oriented perpendicular to, rather than directed toward, the capsular tear.

INCOMPLETE HYDRODISSECTION

If the nucleus has not been completely loosened by hydrodissection, it will be difficult or impossible to rotate. Often this is not appreciated until after the first trough has been sculpted and an attempt is made to rotate the nucleus to sculpt the second trough. In this situation the procedure should be interrupted so that repeat hydrodissection of the nucleus can be accomplished. This will allow for free rotation of the nucleus prior to continuing with the emulsification procedure. Failure to do so risks compromising zonular integrity.