Handling complications after Ahmed tube placement
The Ahmed valve can effectively reduce intraocular pressure. In this case, presenting at Cleveland Clinic’s Cole Eye Institute, heightened suspicion of valve failure led to the resolution of persistent postoperative hypotony after Ahmed tube placement in a 62-year-old intellectually challenged man being treated for advanced primary open-angle glaucoma.
Cleveland Clinic is a non-profit academic medical center. Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services. Policy
Intraocular pressure (IOP) was well-controlled in the low- to mid-teens with maximal tolerated topical therapy and oral carbonic anhydrase inhibitors — until acetazolamide was discontinued due to intractable metabolic acidosis that had become increasingly difficult to control with sodium bicarbonate. IOP rose to the mid-40s with microcystic edema and decreased visual acuity.
Ophthalmologist Stella Paparizos, MD, used Ahmed tube placement rather than a trabeculectomy due to uncertainty over the patient’s ability to tolerate in-office postoperative manipulation and take long-term care of a bleb.
On the first postoperative day, there was suspicion of aqueous leak around the tube tract site and early peripheral choroidals because of anterior chamber shallowing. The patient was started on atropine ophthalmic solution, along with a topical antibiotic and steroid.
On the third postoperative day, the IOP was 18, with subsequent narrowing of the anterior chamber. The patient returned to the operating room for drainage of choroidal effusions and reformation of the anterior chamber. Trypan blue confirmed the absence of a leak around the tract site. After the conjunctiva was closed using a running Prolene suture, Healon-5 was injected into the anterior chamber.
“We thought this problem would resolve on its own,” says Dr. Paparizos, “but on follow-up, we found even less space in the front of the eye where the structures were actually touching.” Dr. Paparizos ultimately used a 7-0 Vicryl suture to ligate the tube near its insertion into the plate. “We had to treat the valved tube as if it never had a valve at all,” she noted.
Persistent post-operative hypotony after Ahmed tube placement, in the absence of conjunctival or tube tract leaks, suggested a faulty valve. The tube was ligated, essentially treated like a non-valved device. This resolved the anterior chamber instability.
“Postoperative hypotony can occur for many reasons,” says Dr. Paparizos, “and it can be a challenge to identify the correct etiology.” A postoperative decrease in aqueous production can lead to transient hypotony and shallowing of the anterior chamber. Aqueous leak around the tube at the site of scleral insertion leads to over-filtration. Valve failure, as suggested in this case, may be due to natural variation in resistance among each device, or be secondary to over-aggressive priming of the sensitive silicone valve mechanism or manipulation of the valve box with forceps.
“This case reminds surgeons who place Ahmed tube shunts that valve function is not guaranteed,” says Dr. Paparizos. Postoperative hypotony and a shallow anterior chamber should raise suspicion of a faulty valve. Ligation of the tube should be considered during chamber reformation if a reoperation is warranted.
“A partial ligation of the Ahmed tube using Prolene and Vicryl sutures can decrease the incidence of postoperative hypotony without affecting the final success rate of the procedure,” she says.
Studies continue to indicate effectiveness and safety
Study highlights the value of quantitative ultra-widefield angiography
Switching medications may decrease treatment burden and macular fluid
Interventions abound for active and stable phases of TED
Corneal imaging and interpretation play a major role
Effect of low-dose atropine and dual-focus contact lenses is unknown in patients with comorbid eye conditions
How to screen for and manage treatment-triggered uveitis
Minimally invasive surgery is effective for uveitic and steroid-induced glaucoma too