Topical dilation as first-line treatment for fibrin membrane pupillary-block glaucoma following uncomplicated cataract surgery

Discussion

This case report describes the successful treatment of fibrin membrane pupillary-block glaucoma by managing it as a secondary angle closure case using topical pupil dilation. The treatment effectively broke the pupillary block and thereby avoided the need for more invasive procedures suggested by other authors such as Nd:YAG membranotomy, Nd:YAG peripheral iridotomy or injection of intracameral tissue plasminogen activator.1–4 Following the normalisation of the IOP, the inflammation was successfully treated with topical dexamethasone and the patient reached a CDVA of 1.0.

A review of the literature shows that only a very small number of case reports have been published on fibrin membrane pupillary-block glaucoma. Most recently, Pallamparthy and Rajendrababu reported a less severe case of a man with diabetes in his 50s with an IOP of 25 mmHg, successfully treated with Nd:YAG peripheral iridotomy.4 Khan and Elashry likewise applied the Nd:YAG laser, but chose to perform a membranotomy. The patient suffered from diabetic retinopathy, previous central retinal vein occlusion as well as mixed connective tissue disease.2 The Nd:YAG membranotomy required 167 applications of 1.6–1.9 mW.

Khor et al reported on three patients with fibrin pupillary-block glaucoma in immediate relation to cataract surgery. In one of these cases, they initially treated with pupil dilation which broke the membrane and lowered the IOP. Nevertheless, they proceeded with both Nd:YAG membranotomy and peripheral iridotomy on the following day despite normal IOP, stating that although pupil dilation may detach the pupil edge from the membrane, the results are unpredictable.1

Yoshino et al reported a different approach where they injected intracameral tissue plasminogen activator in order to fibrinolyse the membrane and thereby broke the patient’s pupillary block successfully.3

With the low number of cases reported, no consensus on treatment exists. Topical dilation may be considered the least invasive approach and as such preferable. However, it may not be effective or sufficient in all cases. Khor et al, without further evidence, stated that the results of medical dilation were unpredictable.1 In our patient, this was not the case, though the treatment course did require close patient follow-up. Another argument to try topical pupil dilation is that in the case of a symptomatic high IOP, the other suggested treatments typically would require IOP-lowering medication in order to relieve the patient’s symptoms, in which case, topical dilation might as well be added. If the fibrin membrane is successfully loosened from the iris, more invasive procedure can be avoided and if not, one may proceed to either membranotomy, peripheral iridotomy or intracameral tissue plasminogen activator.

Nd:YAG membranotomy has been reported to break the membrane. However, as inflammation is the cause of the problem, one could argue that it is better to avoid aggravating this with a destructive laser treatment. Furthermore, the procedure may be difficult to perform if the increased IOP has caused considerable corneal oedema. In a similar manner, peripheral iridotomy may be complicated by corneal oedema as well as peripheral iridocorneal contact, which jeopardises the corneal endothelial cells. In addition, iridotomy is known to have a lower success rate in inflammatory secondary angle closure because the sticky aqueous acts as a glue between the iris and the cornea. Fibrinolysis of the membrane with intracameral tissue plasminogen activator was reported to have prompt effect. It does however require a new intracameral procedure shortly after cataract surgery. Additionally, the period with raised IOP may be prolonged if a surgeon and an operating room are not promptly available. From a logistical standpoint, it must be assumed that all eye clinics have dilating eye drops, whereas access to a YAG laser or tissue plasminogen activator is not certain.

Our patient differed on two key parameters. First, she had not been diagnosed with diabetes, as opposed to all the patients in the above-mentioned case reports. Second, she presented with the fibrin membrane pupillary-block glaucoma 2 days after uncomplicated cataract surgery. In the previous reported cases, presentation varied from day 5 to 30 postoperatively.

Given the short time span from surgery to the development of fibrin membrane pupillary-block glaucoma, the inflammatory response must have been considerably more severe than in the average patient. A possible intrinsic reason for the increased inflammatory response is hard to hypostasise as the patient had no known inflammatory diseases. The use of high-dosage ultrasonic power when performing phacoemulsification in eyes with severe cataract can provoke a more severe inflammatory response as can any lens cortex left behind after the surgery. However, according to the referring surgeon, the phacoemulsification was uneventful and we found no cortex left behind. The post-cataract surgery treatment was nepafenac 3 mg/mL once a day. Though this treatment is Food and Drug Administration approved and studies have shown it to be equivalent to nepafenac 1 mg/mL three times a day, missing a dosage, either intentionally or unintentionally, must be considered to be more severe with only one dosage a day.5 Though the patient indicated to have been compliant, the possible unintentional lack of compliance in combination with a severe inflammatory response may be part of the explanation for the development of the fibrin membrane. A considerable number of cataract surgeons adhere to the post-cataract surgery treatment regimen of combined nepafenac and dexamethasone. While for this particular patient, the addition of dexamethasone in her postoperative regimen may have been beneficial, a randomised trial of 456 patients with cataract showed no added effect of dexamethasone on early postoperative inflammation.6

Given the clinical presentation, only 2 days after cataract surgery, several differential diagnoses may be considered. The original referral diagnosis was aqueous misdirection, which would fit with the elevated IOP shortly after surgery and the shallow anterior chamber. Another possible differential diagnosis to consider is toxic anterior segment syndrome (TASS). TASS typically presents 24–48 hours post-surgery and the inflammation is located in the anterior chamber. With no consensus on the exact definition or diagnostic criteria for TASS, it is difficult to say whether this was TASS, a variant of TASS or a distinct entity from TASS. Lastly, during the entire treatment regimen, continued awareness to the possibility of post-surgical endophthalmitis is important.

Based on our case report, we suggest that topical dilation should be used as first-line treatment along with IOP-lowering medication, similar to most other secondary angle closure conditions. This strategy is minimally invasive, safe, fast and readily available. If dilation is successful in breaking the fibrin membrane pupillary block, the patient has been successfully treated and if not, the attempted dilation does not prevent the application of either Nd:YAG membranotomy, Nd:YAG peripheral iridotomy or intracameral tissue plasminogen activator.