CASE PRESENTATION
A junior resident calls you into the operating theater for advice on how to manage a problem that has arisen in the early stages of what appeared to be a routine phaco case. The patient is a healthy 70-year-old female who is a low myope. She is not taking any medication.
Until now, the operation was going well. The surgeon was just finishing the hydrodissection when the chamber shallowed fairly aggressively, resulting in iris prolapse through the main incision and a hard eye. The chamber was flat and had been impossible to deepen with viscoelastic (Figure 1).
Two months ago, the patient underwent uncomplicated cataract surgery in her other eye. What are the possible causes and how would you manage this situation?
DAVID ALLEN, FRCOphth
When faced with a problem during surgery, it is always advisable to stop and analyze what is happening in basic terms. Here, we have a situation where the iris is being pushed out of the eye. We must conclude that there is a pressure difference between the posterior surface of the iris and the outside. The pressure difference is forcing the iris out of the incision. We also know that the eye is hard; the pressure in the eye is considerably greater than atmospheric pressure.
The surgeon has either put more fluid into the eye (and into the posterior chamber) than has come out or more fluid has been added from within the eye (ie, intraocular hemorrhage). We are told that this event occurred at the end of hydrodissection, so the former is the more likely situation.
There is a particular danger with hydrodissection when the capsulorhexis is intact but small and/or the nucleus is hard. If, under these circumstances the fluid wave passes behind the nucleus, it can accumulate in the space between the nucleus and posterior capsule. This may push the nucleus forward, put pressure on the rhexis edge and produce a capsular block. Injecting more fluid simply increases the blockage.
The surgeon now needs to reinsert a cannula or spatula through the incision, gently pass it in front of the prolapsing iris, and, without injecting anything, push the nucleus backward or rock it side-to-side to break the capsular block. It may take several attempts to break the block, but when it occurs you will see an immediate redeepening of the anterior chamber. Fluid should exit the eye through the incision.
In the unlikely event that this maneuver does not correct the problem, either the capsule has been blown out and the hydrodissection fluid has been injected into the vitreous, or an intraocular (ie, suprachoroidal) bleed must be suspected. The capsule blowout is unlikely if the anterior rhexis is clearly intact, however, it could have occurred if the capsulorhexis edge is incomplete. If this is suspected, redeepen the anterior chamber with a simple pars plana needle aspiration of liquid from the anterior vitreous cavity. The appropriate surgical strategy for removal of the nucleus can then be adopted.
Alternatively, if suprachoroidal hemorrhage is the likely diagnosis, it would be best to stop surgery. Use ultrasound — if available — to confirm the diagnosis. Alternatively, gently patch the eye and return the patient to the operating room in approximately 60 minutes. Often the situation will stabilize, allowing the iris to be reposited, and the incision to be sutured. If not, a limited pars plana anterior vitrectomy may be considered to lower the pressure in the posterior segment. Reducing the IOP in this way may provoke further bleeding. It may be possible to complete the lens removal, but it is worth considering a two-stage surgery with IOL insertion as a secondary procedure.
LARRY BENJAMIN FRCS, FRCOphth, DO
Sudden onset of a hard eye has six discernable causes — two extraocular and four intraocular. The extraocular causes, orbital in origin, arise from an orbital hemorrhage or a speculum causing high orbital pressure. The latter is unlikely in this case, as the eye was soft until the complication occurred, and high orbital pressure from a speculum would usually be present from the outset of the procedure.
An orbital hemorrhage could arise late (eg, complication of sharp needle, local anesthesia), therefore ascertaining the type of local anaesthetic is important. Balloting the eye backward in the orbit will demonstrate whether or not the orbit is tense. If so, signs of increasing hemorrhage may be present with blood visible in the periorbital tissues or the subconjunctival space. If the orbit is tense and the cause appears to be an orbital hemorrhage, the procedure should be postponed — at least until signs of progressive hemorrhage have abated. This may be relatively soon (ie, minutes) or may require that the procedure is abandoned and rescheduled for another time. Consideration for general anesthesia or subtenons local anesthetic should be given at the next operation date.
An increase in orbital tension from a speculum often just requires removal of the speculum and replacement with one of a different design.
The three main intraocular causes of sudden onset of a hard eye are choroidal hemorrhage, capsular block syndrome and vitreous hydration. The first is excluded by examination with the indirect ophthalmoscope. If present, however, the eye should be protected by performing a paracentesis with a sharp blade (diamond blades are good for this) at a site distant from the wound and the procedure abandoned. A cyclodialysis spatula or similarly flat-bladed instrument is then used to reposit the iris from the new paracentesis by sweeping the iris from the inner aspect of the wound. Once completed, no further surgical procedure should be carried out. Further manipulation of the globe may cause extension of the hemorrhage, which is usually more severe.
If a choroidal hemorrhage has not occurred, gentle balloting of the nucleus backward into the capsular bag can cure the second of the intraocular causes (ie, capsular block syndrome). Forcible hydrodissection, sending a fluid wave behind a hard nucleus, causes this syndrome. In the presence of a small capsulorhexis opening, the nucleus is forced upward by the fluid, blocking fluid from exiting the capsular bag. Further injection of fluid distends the capsular bag and forces the nucleus forward, increasing pressure in the eye. Balloting the nucleus backward can undo the capsular block and encourage fluid back into the anterior chamber; however, if the situation is not recognized in time, further injection of fluid will eventually pop the posterior capsule and may cause the nucleus to drop into the vitreous cavity.
If balloting of the nucleus does not resolve the situation, it is probable that vitreous hydration has occurred. Fluid can be injected through the zonules and into the anterior vitreous, causing forward movement of the iris/lens diaphragm and shallowing (Figure 1). If all other causes have been excluded, simply waiting 10 or 15 minutes will often allow resolution of the problem; IOP normalizes, and the anterior chamber will slowly deepen again.
The final cause of a hard eye is sudden filling of the choroidal circulation, such as when a patient coughs or strains. This is usually self-evident, but the patient may become hypercapnoeic (a potent cause of vasodilatation) if he or she is tense and not breathing normally. With increased intraabdominal pressure, the choroid may fill rapidly. This is sometimes seen when the subconjunctival injection is given. If it causes pain, the patient often tenses up, and the anterior chamber is seen to shallow at the end of the procedure.
Following this diagnostic algorithm will allow a firm diagnosis and the correct management plan to be instigated.
MARK PACKER, MD, FACS
A thorough understanding of the principles of hydrodissection may reveal the sequence of events leading to increased IOP, chamber shallowing and iris prolapse. Hydrodissection means irrigation of balanced salt solution beneath the anterior capsule edge, following completion of the capsulorhexis and preceding rotation of the lens within the capsular bag. As described in 1992 by I. Howard Fine, MD, of Eugene, Ore, cortical cleaving hydrodissection represents an adaptation of this technique to lyse corticocapsular connections, permits free rotation of the lens within the bag and facilitates eventual aspiration of cortical material during phacoemulsification of the epinucleus.1
Cortical cleaving hydrodissection includes three key steps:
1. Tenting up of the anterior capsule with the cannula tip and irrigation of balanced salt solution into the intracapsular space;
2. Observation of the fluid wave passing between the posterior capsule and the posterior lens cortex with anterior movement of the lens, capsulorhexis widening and prolapse of viscoelastic through the corneal incision; followed by
3. Discontinuation of irrigation and decompression of the capsular bag. Balanced salt solution must be released from the posterior capsule and posterior lens cortex; use the cannula to apply posterior pressure to the center of the lens within the capsulorhexis.
The anterior movement of the lens and widening of the capsulorhexis (ie, step 2) has sometimes been described as an intraoperative example of capsular block. Balanced salt solution is trapped in the capsule behind the lens, much as aqueous is trapped in the capsule behind a pseudophakic IOL, due to retained viscoelastic and osmotic pressure.2 If irrigation is continued beyond this point and the lens is soft enough or the capsulorhexis is large enough, the lens may prolapse through the capsulorhexis. If viscoelastic does not exit the anterior chamber, there is risk of a posterior capsule rupture due to increased intracapsular pressure.
In this case, the surgeon has irrigated balanced salt solution into the capsule during the first step of hydrodissection, increasing the volume of fluid in the eye. This increased volume is trapped behind the lens, which is then forced anteriorly and causes the chamber to shallow. Viscoelastic is pushed out of the eye — as it should be — but in this case, a short posterior limbal incision in conjunction with overly aggressive hydrodissection (probably in terms of both volume and flow rate) causes the iris to prolapse along with the viscoelastic. The IOP is high because the hydrodissection fluid remains trapped behind the lens, increasing the total volume of fluid in the eye.
This nasty sequence of events may be avoided. Construct a longer clear corneal incision (ie, at least
2 mm) and discontinue hydrodissection as soon as the fluid wave and anterior movement of the lens is noted. At this moment, use the side of the cannula to push the lens posteriorly and decompress the lens capsule. The action of decompressing the bag forces the hydrodissection fluid out of the bag (via the capsular fornices) lysing the capsulocortical connections.
Once they occur, management of the shallow chamber and iris prolapse involves decompression of the capsular bag by posterior force on the surface of the lens. A cannula on a syringe of cohesive viscoelastic is introduced through the paracentesis. No attempt should be made to directly reposit the iris. The cannula is advanced across the pupil and maintained in a horizontal position; the lens is pushed back. The hydrodissection fluid will burp out of the bag and the chamber will deepen. Viscoelastic can then be injected to maintain the chamber, and the iris will generally slip back inside the eye. If it does not slip back in, however, the phaco needle can be introduced, bevel up over the iris, and the lens extraction begun.
When the chamber initially shallows, the inexperienced junior resident will undoubtedly fear the worst (ie, expulsive suprachoroidal hemorrhage). It is worth pointing out that the bright red reflex eliminates this possibility from consideration. It is also unlikely that a myope would develop choroidal effusions, which are generally associated with nanophthalmic eyes.
At an early stage in the procedure, given the timing of the chamber shallowing, it is also unlikely that the shallowing is due to posterior pressure (such as may be seen with patient discomfort and squeezing). Another cause of posterior pressure — chronic obstructive pulmonary disease — is excluded by the patient's health history.
In short, we have a simple complication of hydrodissection. Avoidance and appropriate management techniques flow naturally from an understanding of the basic principles of intraocular fluid dynamics.
VLADIMIR PFEIFER, MD
Due to (1) the provided history and (2) since the patient did not feel pain, the likelihood of expulsive hemorrhage is minimal. The most possible cause is back flush of balanced salt solution during hydrodissection. The balanced salt solution, moving through zonules and into the posterior chamber, pushed the lens forward and flattened the anterior chamber.
The eye is firm and full. Nothing can go in before something is taken out. Pressure behind the lens allows the anterior chamber to deepen. We should not reposition the iris, deepen the anterior chamber or even touch the iris.
A 25-gauge vitrectomy handpiece is used to perform vitreous tap 4 mm behind the exposed limbus or sclera. An incision, using a 20-gauge MVR blade 4 mm behind the limbus through pars plana, is then performed. A vitrectomy cutter is introduced and vitreous tap is done, decreasing pressure in the eye and pushing the lens backward. The iris can then be pushed into the anterior chamber using vicoelastic with a high viscosity.
The shorter the iris prolapse time better it is for the patient. Phaco is then continued in a normal fashion. If the iris is floppy at the side of the incision and continuing phaco from this side would be difficult (ie, resulting in iris touch or tendency for prolapse), a new incision should be performed ≥90º away. Phaco is performed through this new incision. If the first incision is not watertight, it should be sutured before continuing with phaco.
There were no iris prolapses in the case presentation, only a flat anterior chamber. Therefore, the surgery could be interrupted and the patient sent to the recovery room. After 1 or 2 hours, the chamber would deepen by itself, and surgery could be continued safely.
BRIAN LITTLE, FRCS, FRCOphth, DO
After demonstrating that the speculum was not pressing onto the eye and that the orbit was soft, a cyclodialysis spatula was used through one of the sideports to sweep the prolapsed iris back inside, close the eye and then balotte the nucleus backward to attempt to break any capsular block. This maneuver successfully decompressed the inflated capsular bag, resulting in a forward gush of fluid, accompanied by simultaneous deepening of the chamber. This confirmed capsular block, and the phaco was then successfully and safely completed (Figure 2). Had the bag not decompressed, the incision would have been sutured and the procedure abandoned to get a diagnostic B-scan that would exclude suprachoroidal hemorrhage or a ruptured posterior capsule. If neither had been present, then vitreous hydration would have been the likely culprit, and this would settle spontaneously, allowing safe completion of the procedure the next day. This is a worrying conundrum that requires a clear head and a systematic algorithm to identify the specific cause and take effective and appropriate action.
Cosection editor Brian Little, FRCS, FRCOphth, DO, is clinical head of cataract service at the Royal Free Hospital, in London. Dr. Little is a member of the CRSToday Europe Editorial Board. He may be reached at brianlittle@blueyonder.co.uk.
Cosection editor Khiun F. Tjia, MD, is an anterior segment surgery specialist at the Isala Clinics, in Zwolle, Netherlands. Dr. Tjia is a member of the CRSToday Europe Editorial Board. He may be reached at K.Tjia@Isala.nl or +31 38 424 2980.
David Allen, FRCOphth, is from the Sunderland Eye Infirmary, in Sunderland, UK. He states that he holds no financial interest in the products or companies mentioned. Dr. Allen may be reached at David@allen50.fsnet.co.uk.
Larry Benjamin, FRCS, FRCOphth, DO, is in the department of ophthalmology at Stoke Mandeville Hospital, in Aylesbury, UK. He has a long-standing interest in microsurgical skills training. Dr. Benjamin states that he holds no financial interest in the products or companies mentioned. He may be reached at larry.benjamin@btopenworld.com.
Mark Packer, MD, is clinical assistant professor at the Casey Eye Institute, department of ophthalmology, Oregon Health and Science University, and is in private practice at Drs. Fine, Hoffman & Packer LLC. Dr. Packer may be reached at mpacker@finemd.com or +1 541 687-2110.
Vladimir Pfeifer, MD, is director of the Dr. Pfeifer Eye Surgery Center and head of the anterior segment surgery department, University Eye Clinic Ljubljana, in Slovenia. Dr. Pfeifer states that he holds no financial interest in the products or companies mentioned. He may be reached at pfeifer@pfeifer.si or +00 38 641 641 734.
