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Consultation section
Q:
I have been seeing an intraocular pressure (lOP) greater than 33 mm Hg in 25% of my one-day postoperative extracapsular cataract-posterior chamber intraocular lens patients. I do not use viscoelastic agents; I do not perform an iridectomy in uncomplicated cases. An incidence of 25% to 35% was confirmed in casual discussion with several other ophthalmic surgeons. 1. When do you routinely first measure the lOP postoperatively? 2. What do you postulate as the causes of the pressure increase? 3. Do you feel the elevated pressure is significant? 4. How do you treat elevated lOP? 5. What are your suggestions for preventing this postoperative pressure rise? Dennis D. Shepard, M.D.
Santa Maria, California
A:
consultation section Edited by Dennis D. Shepard, M.D.
568
J CATARACT REFRACT
You indicate that 25% to 35% of patients undergoing uncomplicated cataract surgery may have an elevated lOP on the first postoperative day, even when viscoelastic agents were not employed. It is interesting that this is almost the same percentage of early pressure elevations found by Ralph Kirsch following intracapsular cataract surgery some 25 years ago. The current techniques of surgery are much different than they were at that time, but the findings are essentially the same. You indicate that you do not perform an iridectomy in uncomplicated cases. I do not think that this accounts for the pressure elevations, as these cases do not represent pupillary block except in extremely rare instances. On the other hand, pupillary block glaucoma does occur after extracapsular extraction and, frankly, I am unable to find a valid reason not to do an iridectomy. I think this early pressure rise following surgery is related to distortion of the limbus by tight closure of the cataract wound. Several years ago, David Epstein, in conjunction with David Campbell, demonstrated that outflow facility, as determined by perfusion in eyebank eyes, was markedly diminished by closing a cataract incision. Tight closure of the limbal wound reduced the outflow facility by about 50%. The facility was immediately reestablished when the sutures were loosened and the decrease could be reproduced when the sutures were tightly tied. This would suggest that wound distortion by tight closure decreased outflow and could account for the early postoperative pressure
SURG- VOL 13, SEPTEMBER 1987
elevation. Such pressure elevation would be more likely to occur in eyes with glaucoma in which outflow facility is already diminished. Use of viscoelastic agents also obstructs the outflow and could further increase pressure when these agents are used. Epstein also found that irrigation of the viscoelastic material from the anterior chamber had relatively little effect in reducing this change. Fortunately, the pressure elevation from either of these causes is short-lived and of relatively little importance in eyes with healthy optic nerves. On the other hand, eyes with severe optic nerve damage from glaucoma may be irreparably damaged by this early pressure elevation. It is for this reason that in patients with badly damaged optic nerves the lOP should be measured several hours following surgery and appropriate measures to reduce pressure elevation should be used if it occurs. Immediate use of beta blockers, carbonic anhydrase inhibitors and/or hyperosmotic agents might prevent permanent loss of central vision in such instances. It is also for this reason that I, as well as several other people treating glaucoma patients, will consider a combined cataract and glaucoma operation in patients with severe optic nerve damage who require cataract surgery. This holds true ieven when the preoperative lOP can be adequately controlled on medical therapy. While the filtering procedure may not work on a permanent basis, it may well avoid the early postoperative pressure rise that can be severely damaging in these patients. Allan E. Kolker, M. D. St. Louis, Missouri
A:
Intraocular pressure elevation following extracapsular cataract extraction (ECCE) with posterior chamber intraocular lenses is commonly seen with or without viscoelastic substances. This is also noted in intracapsular cataract extractions after microsurgical techniques involving multiple small sutures used with tight wound closure. A 25% to 30% incidence of pressure rise greater than 10 mm Hg above baseline is about average. In patients with preexisting glaucoma, the pressure rise occurs more frequently and can be quite severe, rising to the 50 mm Hg to 60 mm Hg level in occasional patients. In response to the questions: l. We routinely first measure the lOP on the first day postoperatively. 2. The cause of this pressure increase is probably related to inflammatory debris and secondary aqueous and possibly humoral obstruction of the trabecular meshwork. Dr. David Campbell felt that
tight suturing distorted the trabecular meshwork and caused its occlusion. 3. The elevated pressure is probably insignificant unless it gets above 40 mm Hg, at which point vascular occlusions may occur rarely. However, in glaucomatous patients with preexisting visual field loss or optic nerve damage, it can be quite significant, causing further damage to the visual field and even obliteration in the rare patient. 4. The management of elevated lOP depends on the severity of the elevation and the condition of the optic nerve. A pressure in the mid 30s and a healthy optic nerve is probably of little significance; however, a similar pressure in an eye with a 0.8 or 0.9 cup-disc ratio and visual field loss can be damaging. The most effective means to bring pressure down are miotics, such as pilocarpine 2%. Recently, Ruiz has recognized that Pilogel applied at night will also bring the pressure down. Carbonic anhydrase inhibitors and topical beta blockers are also effective. In the glaucoma patient, in whom pressure elevation could be dangerous, we accompany filtration surgery with a modified trabeculectomy flap. A small portion of the internal lip of the trabeculectomy area is excised. In the postoperative period, the posterior edge of this trabeculectomy and scleral flap incision site can be depressed, allowing a little aqueous to escape and immediately lower the pressure. If the pressure is very high, this may have to be done twice daily. The goal is to lower the pressure to approximately 10 mm Hg to 15 mm Hg rather than lower, because one hopes to avoid secondary aqueous production. 5. Preventive measures include the use of acetylcholine chloride (Miochol®) postoperatively, topical pilocarpine, possibly Pilogel, and acetazolamide (Diamox®). Topical beta blockers can be used following surgery although I have heard of one death that was associated with the use of topical beta blocker drops applied to the eye at the end of the cataract procedure. Another preventive method is to remove all viscoelastic material from the eye at the end of the operative procedure. Even when the combined filtering procedure is done with a cataract extraction, sodium hyaluronate (Healon®) can prevent the outflow of aqueous through the filtering site and cause high pressures postoperatively. H. Dunbar Hoskins, Jr., M.D.
San Francisco, California
A:
Increased lOP immediately following cataract surgery is a very common finding. This is especially true in
J CATARACT REFRACT SURG- VOL
13, SEPTEMBER 1987
569
the era of tight wound closure with multiple interrupted or running nylon sutures. To understand the phenomenon, one only has to look at the response of the eye to less minor trauma such as laser iridotomy. Prophylactic laser iridotomy performed in fellow eyes of patients with acute angle-closure glaucoma is often associated with a brief, but substantial, lOP elevation. Older studies in the era of invasive surgical iridectomy refer to a frequent rise in lOP in the early postoperative period. Laser treatment to the retina and choroid is usually not associated with this phenomenon of elevated lOP. This would seem to indicate that there is something unique to disturbance of the anterior segment, most likely manipulation of the iris, that is the cause of the lOP increase. Recent studies would seem to implicate the release of prostaglandin as a potential villain. So it would seem that lOP elevation following ECCE with implantation of a posterior chamber intraocular lens is to be an expected occurrence. However, the level ofIOP rise and the duration of increased lOP may vary significantly depending on several factors. If there is any tendency to ocular hypertension or glaucoma preexisting the cataract surgery, the extent of the postoperative lOP increase will be intensified in duration and pressure. Incomplete removal of viscoelastic substances, watertight wound closure, residual cortical material, and extensive iris manipulation are factors that would tend to increase the incidence and extent of the postoperative pressure rise. If the patient to be operated on has a healthy optic nerve, no history of ischemic optic neuropathy, central retinal vein or artery occlusion in the fellow eye, and is without systemic risk factors for vascular occlusion such as sickle trait or hypercoagulable states, it is unlikely that the postoperative pressure elevation will be damaging. Therefore, any attempts at preventing or treating the increased lOP must be weighed against potential morbidities, inconvenience, and cost. I do not treat to prevent postoperative lOP rise, and usually elect not to treat pressure elevations up to 40 mm Hg on the first postoperative day unless there are additional indications such as corneal edema or signs of poor perfusion in the fundus. In the patient with a healthy outflow apparatus who has had an uncomplicated operation, without the use of viscoelastic agents, the lOP rise is usually short-lived. It is probably already past its peak on the morning after surgery and is usually greatly diminished at the next postoperative visit on the following day-regardless of whether treatment to reduce lOP has been instituted. Studies that support the premise that topical beta blockers may have the highest success rate in blunting the postoperative pressure rise have been reported. However, as we have come to learn, topical beta blockers are not without potentially serious systemic 570
J CATARACT
side effects. Thus, without good reason to suspect that the increased lOP, should it occur, would be damaging in a particular patient, I would argue against the use of routine anti-ocular-hypertensive medications. Should topical anti-prostaglandins ultimately prove efficacious and without significant side effects, this class of agents might be more rationally applied as a prophylaxis. Jonathan Herschler, M. D. Portland, Oregon
A:
To answer this question accurately, we reviewed 100 consecutive cases undergoing phacoemulsification with posterior chamber intraocular lens implantation. Our experience with an elevated postoperative lOP was clearly different from yours because only 2% of our patients had an lOP over 30 mm Hg as measured by applanation tonometry on the first postoperative day. One of these patients had an lOP in the 30s and the other, an lOP in the 40s. An additional 13% of patients had lOPs in the 20s. However, this series is biased because any patient who has either preexisting ocular hypertension, pseudoexfoliation, a positive family history of glaucoma, or an exceedingly long complicated phacoemulsification is routinely started on Diamox, 125 mg, immediately following surgery. Although this number is quite small, by treating the high risk patients we undoubtedly blunt the frequency of elevated postoperative pressures. Moreover, a single drop of a beta blocker (Betoptic®) is instilled at the end of each operation. Perhaps the most significant measure that we use to reduce lOP is meticulous removal of all viscoelastic agent. A miniature irrigation/aspiration tip, 1 mm in diameter, has been designed with Storz and this fits directly onto the United Surgical unit (or any other machine). At the end of the procedure, one 10-0 nylon suture is left untied and the miniature tip is inserted into the eye. Healon® is completely removed within a closed system under excellent control of the intraocular environment. The tip is first placed at the inferior angle so the irrigation washes Healon® out of the anterior chamber; then the tip is placed in the posterior chamber where it gently taps against the surface of the intraocular lens, facilitating the aspiration of Healon ® from the ciliary sulcus and from the capsular bag. I am thoroughly convinced that this very safe maneuver is responsible for our low incidence of elevated lOP the day following surgery. The precise mechanism of lOP elevation is unknown, although many of us attribute the rise to "trabeculitis." If this is the case, atraumatic surgical technique and meticulous removal of all cortical material would minimize the occurrence. There is little
REFRACT SURG- VOL 13, SEPTEMBER 1987
doubt that leaving excess viscoelastic material also obstructs trabecular flow. This may explain why an elevation is seen less often by those of us who are obsessive about removing all viscoelastic substance. However, Buol Heslin, M.D., recently presented a paper showing that balanced salt solution (BSS) alone, without any viscoelastic, will elevate the lOP in patients following surgery (Symposium on Cataract, IOL and Refractive Surgery, Orlando, April 1987). Therefore, it may be the surgery itself, the viscoelastic agent, or a combination of other factors that contribute to the lOP elevation. Management of the postoperative pressure rise depends upon the extent of the elevation, the susceptibility of the optic nerve, and the associated systemic vascular status. If the patient has no evidence of preexisting glaucoma or a compromised vascular system, I will not treat a pressure in the 20s. If the pressure has risen into the 30s, a beta blocker in addition to Diamox, 125 mg, orally three times a day for several days is initiated. If the pressure has risen into the 40s (or higher), a similar regimen will be started in addition to an osmotic agent administered in the office. If the patient has evidence of carotid disease, such as peripheral venous stasis retinopathy, I believe that even an lOP in the 20s can compromise arterial perfusion in the eye. Similarly, venous obstructive disease is further complicated by elevating the lOP which accounts for the high coexistence of vein occlusion and glaucoma. An aggressive approach to these patients is aimed at attaining a rapid reduction in the lOP. A most challenging patient is one who has advanced glaucoma with substantial visual field loss. If the lOP is highly elevated immediately following surgery, this patient is at risk to "snuff out" the remaining central vision. If an osmotic agent, carbonic anhydrase inhibitor, and beta blocker fail to reduce the lOP markedly, the patient is taken to the argon laser where a suture (or sutures) is cut. l I have found the Hoskins lens to be very helpful since it compresses swollen conjunctiva, facilitating suture visibility. Because conjunctiva covers these sutures as a result of careful coaptation at the conclusion of surgery, the laser-induced wound leak (with or without massage) produces a filtration bleb. The lOP is immediately reduced, removing the potential threat to the patient and allowing the lOP to be managed without surgical intervention. This technique has also proven to be of value in glaucoma patients with extensive visual field loss who cannot tolerate carbonic anhydrase inhibitors or when beta blockers are strongly contraindicated. With the exception of patients with preexisting glaucoma or systemic vascular disease, the lOP elevation following surgery has yet to cause any permanent visual loss in my experience. The complete removal of J CATARACT REFRACT
cortex with its inflammatory potential and the complete removal of Healon® with its potential for obstructing outflow are combined with the judicious use of Betoptic and Diamox in our high risk patients to attain a very low incidence of elevated lOP in the early postoperative period. Robert H. Osher, M.D. Cincinnati, Ohio REFERENCE 1. Osher RH, Cohen JS: Management of acute postoperative intraocular pressure elevation by laser-induced filtration. ] Cataract Refract Surg 12:77-78,1986
A:
1. The lOP is always measured on the first postoperative day. 2. I think the pressure increases are due to patients already having an embarrassed outflow facility, which is temporarily made worse by the cellular debris, surgical manipulation, and resulting edema and foreign material such as viscoelastic substances. 3. The significance varies with the amount of increased pressure, the condition of the optic nerve, and the discomfort it causes the patient. 4. The treatment consists of beta-blocker drops plus diuretics, which control most cases. If severe, decompression is sometimes done via a small paracentesis or loosening a suture. This is rarely necessary. 5. Careful surgery requires cleaning out all cortex possible. If a viscoelastic material is used, it should be irrigated out thoroughly followed by aspiration with the IIA tip. Also, after going several years without doing iridectomies, I finally had two pupillary blocks within one month. These were two sick patients. After this horrible experience, I started doing iridectomies routinely again. Despite all precautions, some postoperative pressure rises will still occur. Jack A. Thurmond, M. D. Weslaco, Texas
A:
1. I routinely measure the postoperative lOP at the slitlamp by applanation tonometry on the first postoperative day. 2. The pressure increase can be explained by traumatic insult to the trabecular meshwork due to the surgical location of the incision, tightness and depth of the sutures, and surgical debris left in the anterior chamber at the conclusion of surgery which must ultimately pass through the meshwork (i.e.,
SURG- VOL 13, SEPTEMBER 1987
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fibrin, heme, cortical remnants, pigment and inflammatory products). Eyes with a compromised trabecular meshwork preoperatively, such as glaucoma cases, can be expected to demonstrate increased lOP in the immediate postoperative period. 3. The elevated lOP can be significant, especially in glaucomatous eye with preexisting optic atrophy, in elderly eyes with impaired optic nerve circulation, and in cases in which the lOP may be high enough to result in patient nausea. 4. The elevated lOP can be treated with topical beta blockers, carbonic anhydrase inhibitors, and hyperosmotic agents, when clinically indicated. 5. Postoperative lOP rises may be mitigated by relatively anterior placement of the surgical incision, avoidance of tight suturing of the wound, and careful irrigation with BSS and lavage of the anterior chamber just prior to final closure so as to minimize the "debris" left in the chamber. Also, instillation of topical beta blockers on the operating table at the conclusion of surgery, as well as immediate initiation of systemic carbonic anhydrase inhibitor therapy, can be useful in situations which would be particularly susceptible to postoperative pressure elevation. Lawrence C. Pape, M.D., Ph.D.
New York, New York
A:
l. We recommend and we routinely measure lOP within 24 hours of surgery. Patients with glaucoma and severe optic disc damage or patients in whom lens extraction was difficult or prolonged may need to be watched more carefully because they can develop very high lOPs within hours of surgery. Under these circumstances, the patients often develop corneal edema and, often, pain. Tonometry three to four hours after surgery can detect these early pressure elevations. 2. A wide variety offactors can contribute to increased lOP in the immediate postoperative period. Retained viscoelastic material is a common cause, but apparently does not apply to the inquiring surgeon who does not use these agents. A considerable showering of melanin pigment granules can follow abrasion of the iris pigment epithelium with instruments. Another factor is retained cortical material, for in cases where pupillary dilation is not full, it is rare that all particulate lens material is removed during the cortical clean-up. Lens protein itself can impair aqueous humor outflow. In addition, patients with preexisting glaucoma or ocular hypertension who have compromised trabecular outflow may experience a greater than expected pressure 572
J CATARACT REFRACT
rise with minimal changes in particulate material in the aqueous humor. With the longer manual expression wound, compression of the trabecular meshwork by tight wound closure can also result in a marked pressure rise, as also observed with intracapsular extraction. These are entities that are not immediately obvious clinically but are common causes of increased lOP in the first few postoperative days. Severe inflammation, pupillary block, intraocular hemorrhage, mechanical displacement of the IOL, and malignant glaucoma are complications that can also lead to elevated lOP. 3. The significance of the lOP elevation is entirely dependent on the ocular symptoms, the state of the eye, and the lOP level. An eye with an already compromised optic disc may suffer additional disc damage even from a brief period of elevated lOP, while the average eye with a normal optic disc will tolerate lOPs in the 30s or even in the 40s or low 50s. However, eyes with marked elevated pressure will experience pain and corneal edema and require therapy. When the lOP approaches diastolic blood pressure, infarction of the optic nerve could occur. In addition, acute, marked lOP elevation could cause disruption of the corneoscleral wound but, in fact, this rarely occurs. Therefore, I would consider an elevated lOP significant and a cause for concern, but would observe that the majority of eyes will tolerate transient lOP elevation without adverse sequelae. 4. Aqueous suppressant agents, such as a topical beta blocker or an oral carbonic anhydrase inhibitor, are generally the most effective treatment. With severe emergent situations, an osmotic agent, administered orally or intravenously, may be required. Topical corticosteroids will minimize inflammation and may be helpful. 5. My suggestions for preventing postoperative lOP increase are as follows: Leave the anterior and posterior chambers as free of cortical material as is possible and as is consistent with preservation of the posterior capsule and safety of the procedure. Minimize undue intraocular manipulation. Avoid overly tight and overly deep corneoscleral sutures that distort the trabecular meshwork. A recent study reported lower postoperative lOP in patients who receive intraocular acetylcholine during their cataract surgery. 1 Many surgeons routinely administer beta blockers, such as timolol maleate, postoperatively. Preferring to manage each patient individually as the clinical situation demands, I do not follow this practice, but have no serious objections to it if there are no systemic contraindications to beta-blocker therapy. E. Michael Van Buskirk, M.D. Portland, Oregon
SURG-VOL 13, SEPTEMBER 1987
REFERENCE 1. Hollands RH, Drance SM, Schulzer M: The effect of acetylcholine on early postoperative intraocular pressure. Am] Ophthalmol103:749-753, 1987
A:
It is my routine to measure the lOP on the morning of the day after surgery when I see the patient in my office. Pressure increase is not uncommon and I postulate several causes. Foremost is the presence of sodium hyaluronate in the anterior chamber from surgery. It is my clinical impression that there is a very strong correlation between significantly elevated lOP and a significant amount of sodium hyaluronate left in the anterior chamber. We take great pains to remove all sodium hyaluronate from the anterior chamber at cataract surgery. I use a tapered double cannula, which I insert between sutures at the close of the procedure to exchange the sodium hyaluronate for BSS and to wash out the anterior and posterior chambers thoroughly. I push downward on the IOL, pressing it against the posterior capsule and forcing out sodium hyaluronate that may have been trapped between the implant and the capsule. I also move the cannula around to aspirate any pockets of sodium hyaluronate that may be left. It appears to be the property of sodium hyaluronate that it remains adherent to itself and that once a "pocket" of sodium hyaluronate has begun to enter the port of the aspiration cannula, the entire pocket of material will be aspirated. One can determine the presence of sodium hyaluronate in the anterior chamber by the changes in refractive index as one irrigates and aspirates and by the behavior of air bubbles in the anterior chamber. A second cause for pressure increase, one independent of the use of sodium hyaluronate, is the operative change in the blood aqueous barrier that allows a plasmoid aqueous to form. I feel that at some point in the postoperative period this plasmoid aqueous produces an osmotic effect that pulls fluid into the anterior chamber. Additionally, the liberation of partially polymerized natural hyaluronic acid from the vitreous into the anterior chamber may occur if the posterior capsule is torn during cataract surgery. I do feel that the elevated lOP can be significant, as I have seen pressures in the 70s occasionally on the first postoperative day when significant sodium hyaluronate was left in the anterior chamber. While I have not noted any definite damage to the optic nervehead from transiently elevated lOP, I feel that one sees elevated pressure primarily in patients who had a preexisting reduction in aqueous outflow. This would include all glaucoma patients. We treat the elevated lOP by preventive and therapeutic measures. All patients are given 500 mg of J CATARACT
Diamox intravenously at the close of cataract surgery. The patients are unpatched the next morning and placed routinely on Betoptic eyedrops; if preexisting glaucoma was present and had not been treated by combined surgery for glaucoma, systemic Diamox (125 mg four times daily) is also given. The Betoptic and Diamox are discontinued after five days. My suggestions for preventing postoperative lOP rise include prophylactic treatment as noted, anticipation of increased lOP in patients with glaucoma, and vigorous treatment with beta-blockers, dipivefrin hydrochloride (Propine®), high-dose systemic Diamox, and pilocarpine when pressure is significantly elevated. When very great lOP elevations are seen, the pressure can be brought down immediately with oral glycerine. When patients with chronic open-angle glaucoma that is under borderline control and has produced significant field defect are brought to cataract surgery, I generally favor combining the cataract surgical procedure with a glaucoma procedure. Our usual procedure is to perform cyclodialysis with peripheral iridectomy combined with our usual cataract extraction by phacoemulsification with posterior chamber inthe-bag lens implantation. Herbert
J.
Nevyas, M. D.
Bala-Cynwyd, Pennsylvania
A:
I routinely see my postoperative patients the day following surgery (early in the A.M.). I measure their lOP at that time. I believe even a verv minimal amount of trauma to intraocular tissue results in an inflammatory response. This reaction, in association with precipitating prostaglandin, may affect outflow. I believe the pressure rise is minimal- I have observed approximately 8% of my postoperative patients with an lOP higher than 30 mm Hg. I am convinced that this does not result in any permanent structural change of tissue function. Timoptic or Betoptic is prescribed for one week as part of my routine list of postoperative medications. If there is an lOP elevation, Diamox or methazolamide (Neptazane®) is prescribed and I measure the lOP again the following day. To prevent this postoperative pressure rise, I instill a drop of Timoptic 0.5% or Betoptic at the end of the surgery. I am not overly concerned about this transient lOP elevation. Leeds E. Katzen, M.D.
Baltimore, Maryland
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I have been seeing an intraocular pressure (lOP) greater than 33 mm Hg in 25% of my one-day postoperative extracapsular cataract-posterior chamber intraocular lens patients. I do not use viscoelastic agents; I do not perform an iridectomy in uncomplicated cases. An incidence of 25% to 35% was confirmed in casual discussion with several other ophthalmic surgeons. 1. When do you routinely first measure the lOP postoperatively? 2. What do you postulate as the causes of the pressure increase? 3. Do you feel the elevated pressure is significant? 4. How do you treat elevated lOP? 5. What are your suggestions for preventing this postoperative pressure rise? Dennis D. Shepard, M.D.
Santa Maria, California
A:
consultation section Edited by Dennis D. Shepard, M.D.
568
J CATARACT REFRACT
You indicate that 25% to 35% of patients undergoing uncomplicated cataract surgery may have an elevated lOP on the first postoperative day, even when viscoelastic agents were not employed. It is interesting that this is almost the same percentage of early pressure elevations found by Ralph Kirsch following intracapsular cataract surgery some 25 years ago. The current techniques of surgery are much different than they were at that time, but the findings are essentially the same. You indicate that you do not perform an iridectomy in uncomplicated cases. I do not think that this accounts for the pressure elevations, as these cases do not represent pupillary block except in extremely rare instances. On the other hand, pupillary block glaucoma does occur after extracapsular extraction and, frankly, I am unable to find a valid reason not to do an iridectomy. I think this early pressure rise following surgery is related to distortion of the limbus by tight closure of the cataract wound. Several years ago, David Epstein, in conjunction with David Campbell, demonstrated that outflow facility, as determined by perfusion in eyebank eyes, was markedly diminished by closing a cataract incision. Tight closure of the limbal wound reduced the outflow facility by about 50%. The facility was immediately reestablished when the sutures were loosened and the decrease could be reproduced when the sutures were tightly tied. This would suggest that wound distortion by tight closure decreased outflow and could account for the early postoperative pressure
SURG- VOL 13, SEPTEMBER 1987
elevation. Such pressure elevation would be more likely to occur in eyes with glaucoma in which outflow facility is already diminished. Use of viscoelastic agents also obstructs the outflow and could further increase pressure when these agents are used. Epstein also found that irrigation of the viscoelastic material from the anterior chamber had relatively little effect in reducing this change. Fortunately, the pressure elevation from either of these causes is short-lived and of relatively little importance in eyes with healthy optic nerves. On the other hand, eyes with severe optic nerve damage from glaucoma may be irreparably damaged by this early pressure elevation. It is for this reason that in patients with badly damaged optic nerves the lOP should be measured several hours following surgery and appropriate measures to reduce pressure elevation should be used if it occurs. Immediate use of beta blockers, carbonic anhydrase inhibitors and/or hyperosmotic agents might prevent permanent loss of central vision in such instances. It is also for this reason that I, as well as several other people treating glaucoma patients, will consider a combined cataract and glaucoma operation in patients with severe optic nerve damage who require cataract surgery. This holds true ieven when the preoperative lOP can be adequately controlled on medical therapy. While the filtering procedure may not work on a permanent basis, it may well avoid the early postoperative pressure rise that can be severely damaging in these patients. Allan E. Kolker, M. D. St. Louis, Missouri
A:
Intraocular pressure elevation following extracapsular cataract extraction (ECCE) with posterior chamber intraocular lenses is commonly seen with or without viscoelastic substances. This is also noted in intracapsular cataract extractions after microsurgical techniques involving multiple small sutures used with tight wound closure. A 25% to 30% incidence of pressure rise greater than 10 mm Hg above baseline is about average. In patients with preexisting glaucoma, the pressure rise occurs more frequently and can be quite severe, rising to the 50 mm Hg to 60 mm Hg level in occasional patients. In response to the questions: l. We routinely first measure the lOP on the first day postoperatively. 2. The cause of this pressure increase is probably related to inflammatory debris and secondary aqueous and possibly humoral obstruction of the trabecular meshwork. Dr. David Campbell felt that
tight suturing distorted the trabecular meshwork and caused its occlusion. 3. The elevated pressure is probably insignificant unless it gets above 40 mm Hg, at which point vascular occlusions may occur rarely. However, in glaucomatous patients with preexisting visual field loss or optic nerve damage, it can be quite significant, causing further damage to the visual field and even obliteration in the rare patient. 4. The management of elevated lOP depends on the severity of the elevation and the condition of the optic nerve. A pressure in the mid 30s and a healthy optic nerve is probably of little significance; however, a similar pressure in an eye with a 0.8 or 0.9 cup-disc ratio and visual field loss can be damaging. The most effective means to bring pressure down are miotics, such as pilocarpine 2%. Recently, Ruiz has recognized that Pilogel applied at night will also bring the pressure down. Carbonic anhydrase inhibitors and topical beta blockers are also effective. In the glaucoma patient, in whom pressure elevation could be dangerous, we accompany filtration surgery with a modified trabeculectomy flap. A small portion of the internal lip of the trabeculectomy area is excised. In the postoperative period, the posterior edge of this trabeculectomy and scleral flap incision site can be depressed, allowing a little aqueous to escape and immediately lower the pressure. If the pressure is very high, this may have to be done twice daily. The goal is to lower the pressure to approximately 10 mm Hg to 15 mm Hg rather than lower, because one hopes to avoid secondary aqueous production. 5. Preventive measures include the use of acetylcholine chloride (Miochol®) postoperatively, topical pilocarpine, possibly Pilogel, and acetazolamide (Diamox®). Topical beta blockers can be used following surgery although I have heard of one death that was associated with the use of topical beta blocker drops applied to the eye at the end of the cataract procedure. Another preventive method is to remove all viscoelastic material from the eye at the end of the operative procedure. Even when the combined filtering procedure is done with a cataract extraction, sodium hyaluronate (Healon®) can prevent the outflow of aqueous through the filtering site and cause high pressures postoperatively. H. Dunbar Hoskins, Jr., M.D.
San Francisco, California
A:
Increased lOP immediately following cataract surgery is a very common finding. This is especially true in
J CATARACT REFRACT SURG- VOL
13, SEPTEMBER 1987
569
the era of tight wound closure with multiple interrupted or running nylon sutures. To understand the phenomenon, one only has to look at the response of the eye to less minor trauma such as laser iridotomy. Prophylactic laser iridotomy performed in fellow eyes of patients with acute angle-closure glaucoma is often associated with a brief, but substantial, lOP elevation. Older studies in the era of invasive surgical iridectomy refer to a frequent rise in lOP in the early postoperative period. Laser treatment to the retina and choroid is usually not associated with this phenomenon of elevated lOP. This would seem to indicate that there is something unique to disturbance of the anterior segment, most likely manipulation of the iris, that is the cause of the lOP increase. Recent studies would seem to implicate the release of prostaglandin as a potential villain. So it would seem that lOP elevation following ECCE with implantation of a posterior chamber intraocular lens is to be an expected occurrence. However, the level ofIOP rise and the duration of increased lOP may vary significantly depending on several factors. If there is any tendency to ocular hypertension or glaucoma preexisting the cataract surgery, the extent of the postoperative lOP increase will be intensified in duration and pressure. Incomplete removal of viscoelastic substances, watertight wound closure, residual cortical material, and extensive iris manipulation are factors that would tend to increase the incidence and extent of the postoperative pressure rise. If the patient to be operated on has a healthy optic nerve, no history of ischemic optic neuropathy, central retinal vein or artery occlusion in the fellow eye, and is without systemic risk factors for vascular occlusion such as sickle trait or hypercoagulable states, it is unlikely that the postoperative pressure elevation will be damaging. Therefore, any attempts at preventing or treating the increased lOP must be weighed against potential morbidities, inconvenience, and cost. I do not treat to prevent postoperative lOP rise, and usually elect not to treat pressure elevations up to 40 mm Hg on the first postoperative day unless there are additional indications such as corneal edema or signs of poor perfusion in the fundus. In the patient with a healthy outflow apparatus who has had an uncomplicated operation, without the use of viscoelastic agents, the lOP rise is usually short-lived. It is probably already past its peak on the morning after surgery and is usually greatly diminished at the next postoperative visit on the following day-regardless of whether treatment to reduce lOP has been instituted. Studies that support the premise that topical beta blockers may have the highest success rate in blunting the postoperative pressure rise have been reported. However, as we have come to learn, topical beta blockers are not without potentially serious systemic 570
J CATARACT
side effects. Thus, without good reason to suspect that the increased lOP, should it occur, would be damaging in a particular patient, I would argue against the use of routine anti-ocular-hypertensive medications. Should topical anti-prostaglandins ultimately prove efficacious and without significant side effects, this class of agents might be more rationally applied as a prophylaxis. Jonathan Herschler, M. D. Portland, Oregon
A:
To answer this question accurately, we reviewed 100 consecutive cases undergoing phacoemulsification with posterior chamber intraocular lens implantation. Our experience with an elevated postoperative lOP was clearly different from yours because only 2% of our patients had an lOP over 30 mm Hg as measured by applanation tonometry on the first postoperative day. One of these patients had an lOP in the 30s and the other, an lOP in the 40s. An additional 13% of patients had lOPs in the 20s. However, this series is biased because any patient who has either preexisting ocular hypertension, pseudoexfoliation, a positive family history of glaucoma, or an exceedingly long complicated phacoemulsification is routinely started on Diamox, 125 mg, immediately following surgery. Although this number is quite small, by treating the high risk patients we undoubtedly blunt the frequency of elevated postoperative pressures. Moreover, a single drop of a beta blocker (Betoptic®) is instilled at the end of each operation. Perhaps the most significant measure that we use to reduce lOP is meticulous removal of all viscoelastic agent. A miniature irrigation/aspiration tip, 1 mm in diameter, has been designed with Storz and this fits directly onto the United Surgical unit (or any other machine). At the end of the procedure, one 10-0 nylon suture is left untied and the miniature tip is inserted into the eye. Healon® is completely removed within a closed system under excellent control of the intraocular environment. The tip is first placed at the inferior angle so the irrigation washes Healon® out of the anterior chamber; then the tip is placed in the posterior chamber where it gently taps against the surface of the intraocular lens, facilitating the aspiration of Healon ® from the ciliary sulcus and from the capsular bag. I am thoroughly convinced that this very safe maneuver is responsible for our low incidence of elevated lOP the day following surgery. The precise mechanism of lOP elevation is unknown, although many of us attribute the rise to "trabeculitis." If this is the case, atraumatic surgical technique and meticulous removal of all cortical material would minimize the occurrence. There is little
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doubt that leaving excess viscoelastic material also obstructs trabecular flow. This may explain why an elevation is seen less often by those of us who are obsessive about removing all viscoelastic substance. However, Buol Heslin, M.D., recently presented a paper showing that balanced salt solution (BSS) alone, without any viscoelastic, will elevate the lOP in patients following surgery (Symposium on Cataract, IOL and Refractive Surgery, Orlando, April 1987). Therefore, it may be the surgery itself, the viscoelastic agent, or a combination of other factors that contribute to the lOP elevation. Management of the postoperative pressure rise depends upon the extent of the elevation, the susceptibility of the optic nerve, and the associated systemic vascular status. If the patient has no evidence of preexisting glaucoma or a compromised vascular system, I will not treat a pressure in the 20s. If the pressure has risen into the 30s, a beta blocker in addition to Diamox, 125 mg, orally three times a day for several days is initiated. If the pressure has risen into the 40s (or higher), a similar regimen will be started in addition to an osmotic agent administered in the office. If the patient has evidence of carotid disease, such as peripheral venous stasis retinopathy, I believe that even an lOP in the 20s can compromise arterial perfusion in the eye. Similarly, venous obstructive disease is further complicated by elevating the lOP which accounts for the high coexistence of vein occlusion and glaucoma. An aggressive approach to these patients is aimed at attaining a rapid reduction in the lOP. A most challenging patient is one who has advanced glaucoma with substantial visual field loss. If the lOP is highly elevated immediately following surgery, this patient is at risk to "snuff out" the remaining central vision. If an osmotic agent, carbonic anhydrase inhibitor, and beta blocker fail to reduce the lOP markedly, the patient is taken to the argon laser where a suture (or sutures) is cut. l I have found the Hoskins lens to be very helpful since it compresses swollen conjunctiva, facilitating suture visibility. Because conjunctiva covers these sutures as a result of careful coaptation at the conclusion of surgery, the laser-induced wound leak (with or without massage) produces a filtration bleb. The lOP is immediately reduced, removing the potential threat to the patient and allowing the lOP to be managed without surgical intervention. This technique has also proven to be of value in glaucoma patients with extensive visual field loss who cannot tolerate carbonic anhydrase inhibitors or when beta blockers are strongly contraindicated. With the exception of patients with preexisting glaucoma or systemic vascular disease, the lOP elevation following surgery has yet to cause any permanent visual loss in my experience. The complete removal of J CATARACT REFRACT
cortex with its inflammatory potential and the complete removal of Healon® with its potential for obstructing outflow are combined with the judicious use of Betoptic and Diamox in our high risk patients to attain a very low incidence of elevated lOP in the early postoperative period. Robert H. Osher, M.D. Cincinnati, Ohio REFERENCE 1. Osher RH, Cohen JS: Management of acute postoperative intraocular pressure elevation by laser-induced filtration. ] Cataract Refract Surg 12:77-78,1986
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1. The lOP is always measured on the first postoperative day. 2. I think the pressure increases are due to patients already having an embarrassed outflow facility, which is temporarily made worse by the cellular debris, surgical manipulation, and resulting edema and foreign material such as viscoelastic substances. 3. The significance varies with the amount of increased pressure, the condition of the optic nerve, and the discomfort it causes the patient. 4. The treatment consists of beta-blocker drops plus diuretics, which control most cases. If severe, decompression is sometimes done via a small paracentesis or loosening a suture. This is rarely necessary. 5. Careful surgery requires cleaning out all cortex possible. If a viscoelastic material is used, it should be irrigated out thoroughly followed by aspiration with the IIA tip. Also, after going several years without doing iridectomies, I finally had two pupillary blocks within one month. These were two sick patients. After this horrible experience, I started doing iridectomies routinely again. Despite all precautions, some postoperative pressure rises will still occur. Jack A. Thurmond, M. D. Weslaco, Texas
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1. I routinely measure the postoperative lOP at the slitlamp by applanation tonometry on the first postoperative day. 2. The pressure increase can be explained by traumatic insult to the trabecular meshwork due to the surgical location of the incision, tightness and depth of the sutures, and surgical debris left in the anterior chamber at the conclusion of surgery which must ultimately pass through the meshwork (i.e.,
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fibrin, heme, cortical remnants, pigment and inflammatory products). Eyes with a compromised trabecular meshwork preoperatively, such as glaucoma cases, can be expected to demonstrate increased lOP in the immediate postoperative period. 3. The elevated lOP can be significant, especially in glaucomatous eye with preexisting optic atrophy, in elderly eyes with impaired optic nerve circulation, and in cases in which the lOP may be high enough to result in patient nausea. 4. The elevated lOP can be treated with topical beta blockers, carbonic anhydrase inhibitors, and hyperosmotic agents, when clinically indicated. 5. Postoperative lOP rises may be mitigated by relatively anterior placement of the surgical incision, avoidance of tight suturing of the wound, and careful irrigation with BSS and lavage of the anterior chamber just prior to final closure so as to minimize the "debris" left in the chamber. Also, instillation of topical beta blockers on the operating table at the conclusion of surgery, as well as immediate initiation of systemic carbonic anhydrase inhibitor therapy, can be useful in situations which would be particularly susceptible to postoperative pressure elevation. Lawrence C. Pape, M.D., Ph.D.
New York, New York
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l. We recommend and we routinely measure lOP within 24 hours of surgery. Patients with glaucoma and severe optic disc damage or patients in whom lens extraction was difficult or prolonged may need to be watched more carefully because they can develop very high lOPs within hours of surgery. Under these circumstances, the patients often develop corneal edema and, often, pain. Tonometry three to four hours after surgery can detect these early pressure elevations. 2. A wide variety offactors can contribute to increased lOP in the immediate postoperative period. Retained viscoelastic material is a common cause, but apparently does not apply to the inquiring surgeon who does not use these agents. A considerable showering of melanin pigment granules can follow abrasion of the iris pigment epithelium with instruments. Another factor is retained cortical material, for in cases where pupillary dilation is not full, it is rare that all particulate lens material is removed during the cortical clean-up. Lens protein itself can impair aqueous humor outflow. In addition, patients with preexisting glaucoma or ocular hypertension who have compromised trabecular outflow may experience a greater than expected pressure 572
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rise with minimal changes in particulate material in the aqueous humor. With the longer manual expression wound, compression of the trabecular meshwork by tight wound closure can also result in a marked pressure rise, as also observed with intracapsular extraction. These are entities that are not immediately obvious clinically but are common causes of increased lOP in the first few postoperative days. Severe inflammation, pupillary block, intraocular hemorrhage, mechanical displacement of the IOL, and malignant glaucoma are complications that can also lead to elevated lOP. 3. The significance of the lOP elevation is entirely dependent on the ocular symptoms, the state of the eye, and the lOP level. An eye with an already compromised optic disc may suffer additional disc damage even from a brief period of elevated lOP, while the average eye with a normal optic disc will tolerate lOPs in the 30s or even in the 40s or low 50s. However, eyes with marked elevated pressure will experience pain and corneal edema and require therapy. When the lOP approaches diastolic blood pressure, infarction of the optic nerve could occur. In addition, acute, marked lOP elevation could cause disruption of the corneoscleral wound but, in fact, this rarely occurs. Therefore, I would consider an elevated lOP significant and a cause for concern, but would observe that the majority of eyes will tolerate transient lOP elevation without adverse sequelae. 4. Aqueous suppressant agents, such as a topical beta blocker or an oral carbonic anhydrase inhibitor, are generally the most effective treatment. With severe emergent situations, an osmotic agent, administered orally or intravenously, may be required. Topical corticosteroids will minimize inflammation and may be helpful. 5. My suggestions for preventing postoperative lOP increase are as follows: Leave the anterior and posterior chambers as free of cortical material as is possible and as is consistent with preservation of the posterior capsule and safety of the procedure. Minimize undue intraocular manipulation. Avoid overly tight and overly deep corneoscleral sutures that distort the trabecular meshwork. A recent study reported lower postoperative lOP in patients who receive intraocular acetylcholine during their cataract surgery. 1 Many surgeons routinely administer beta blockers, such as timolol maleate, postoperatively. Preferring to manage each patient individually as the clinical situation demands, I do not follow this practice, but have no serious objections to it if there are no systemic contraindications to beta-blocker therapy. E. Michael Van Buskirk, M.D. Portland, Oregon
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REFERENCE 1. Hollands RH, Drance SM, Schulzer M: The effect of acetylcholine on early postoperative intraocular pressure. Am] Ophthalmol103:749-753, 1987
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It is my routine to measure the lOP on the morning of the day after surgery when I see the patient in my office. Pressure increase is not uncommon and I postulate several causes. Foremost is the presence of sodium hyaluronate in the anterior chamber from surgery. It is my clinical impression that there is a very strong correlation between significantly elevated lOP and a significant amount of sodium hyaluronate left in the anterior chamber. We take great pains to remove all sodium hyaluronate from the anterior chamber at cataract surgery. I use a tapered double cannula, which I insert between sutures at the close of the procedure to exchange the sodium hyaluronate for BSS and to wash out the anterior and posterior chambers thoroughly. I push downward on the IOL, pressing it against the posterior capsule and forcing out sodium hyaluronate that may have been trapped between the implant and the capsule. I also move the cannula around to aspirate any pockets of sodium hyaluronate that may be left. It appears to be the property of sodium hyaluronate that it remains adherent to itself and that once a "pocket" of sodium hyaluronate has begun to enter the port of the aspiration cannula, the entire pocket of material will be aspirated. One can determine the presence of sodium hyaluronate in the anterior chamber by the changes in refractive index as one irrigates and aspirates and by the behavior of air bubbles in the anterior chamber. A second cause for pressure increase, one independent of the use of sodium hyaluronate, is the operative change in the blood aqueous barrier that allows a plasmoid aqueous to form. I feel that at some point in the postoperative period this plasmoid aqueous produces an osmotic effect that pulls fluid into the anterior chamber. Additionally, the liberation of partially polymerized natural hyaluronic acid from the vitreous into the anterior chamber may occur if the posterior capsule is torn during cataract surgery. I do feel that the elevated lOP can be significant, as I have seen pressures in the 70s occasionally on the first postoperative day when significant sodium hyaluronate was left in the anterior chamber. While I have not noted any definite damage to the optic nervehead from transiently elevated lOP, I feel that one sees elevated pressure primarily in patients who had a preexisting reduction in aqueous outflow. This would include all glaucoma patients. We treat the elevated lOP by preventive and therapeutic measures. All patients are given 500 mg of J CATARACT
Diamox intravenously at the close of cataract surgery. The patients are unpatched the next morning and placed routinely on Betoptic eyedrops; if preexisting glaucoma was present and had not been treated by combined surgery for glaucoma, systemic Diamox (125 mg four times daily) is also given. The Betoptic and Diamox are discontinued after five days. My suggestions for preventing postoperative lOP rise include prophylactic treatment as noted, anticipation of increased lOP in patients with glaucoma, and vigorous treatment with beta-blockers, dipivefrin hydrochloride (Propine®), high-dose systemic Diamox, and pilocarpine when pressure is significantly elevated. When very great lOP elevations are seen, the pressure can be brought down immediately with oral glycerine. When patients with chronic open-angle glaucoma that is under borderline control and has produced significant field defect are brought to cataract surgery, I generally favor combining the cataract surgical procedure with a glaucoma procedure. Our usual procedure is to perform cyclodialysis with peripheral iridectomy combined with our usual cataract extraction by phacoemulsification with posterior chamber inthe-bag lens implantation. Herbert
J.
Nevyas, M. D.
Bala-Cynwyd, Pennsylvania
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I routinely see my postoperative patients the day following surgery (early in the A.M.). I measure their lOP at that time. I believe even a verv minimal amount of trauma to intraocular tissue results in an inflammatory response. This reaction, in association with precipitating prostaglandin, may affect outflow. I believe the pressure rise is minimal- I have observed approximately 8% of my postoperative patients with an lOP higher than 30 mm Hg. I am convinced that this does not result in any permanent structural change of tissue function. Timoptic or Betoptic is prescribed for one week as part of my routine list of postoperative medications. If there is an lOP elevation, Diamox or methazolamide (Neptazane®) is prescribed and I measure the lOP again the following day. To prevent this postoperative pressure rise, I instill a drop of Timoptic 0.5% or Betoptic at the end of the surgery. I am not overly concerned about this transient lOP elevation. Leeds E. Katzen, M.D.
Baltimore, Maryland
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