My nightmare ICL experience: fulminant endophthalmitis
Hi everyone,
I'd like to share my experience and hear the opinion of anyone with expertise in this area. I'll try to summarize everything as clearly as possible, but I realize this will still be a very long post. Thanks to anyone who takes the time to read it all.
I'm a 33-year-old male. On July 23, I underwent simultaneous bilateral ICL implantation to correct high myopia (-6.0 D in my left eye and -6.5 D in my right). I chose ICLs because laser vision correction had been discouraged due to my relatively thin corneas (around 485 µm) and large scotopic pupil diameter.
The lenses implanted were non-toric STAAR EVO+ ICLs.
The procedure itself was quick (about 5 minutes per eye) and relatively painless. The surgeon who operated on me has more than 10 years of experience and is considered one of the best in this field, at least here in Italy.
The surgery was performed at 10:00 a.m., and by 11:00 I was already back at my hotel. I was told everything had gone perfectly and that I should return the following morning for my postoperative check-up. I was prescribed antibiotic and steroid eye drops but instructed to start them the next morning because medications had already been administered during surgery.
On the way back to the hotel my vision was already fairly good. My eyes burned a little, and it was difficult to keep them open, but nothing seemed particularly concerning.
I lay down with the protective eye shields for about three hours. Around 1:00 p.m. I had something to eat. My vision was still acceptable, but I noticed mild pain in my left eye, which was watering much more than the right, and I still had difficulty keeping it open. I went back to bed and tried to sleep through the afternoon.
During those hours the burning sensation in the left eye never went away.
At around 6:00 p.m. I got up and opened the curtains. I immediately noticed that the vision in my left eye had become dramatically worse compared to just a few hours earlier, and the eye was much redder than the right one.
I contacted my surgeon, who asked me to come in immediately.
He found severe inflammation in the anterior chamber and prescribed steroid drops every 20 minutes. He thought it might be TASS (Toxic Anterior Segment Syndrome), a rare sterile inflammatory reaction usually caused by substances introduced during surgery, often the ophthalmic viscoelastic device.
I was scheduled for another examination later that evening.
During that visit I told him I had started seeing a dark, thread-like floater that looked like a piece of seaweed moving around inside my eye. He reassured me that the vitreous was completely clear and that the inflammation involved only the anterior chamber.
I returned to the hotel and started the intensive steroid treatment, but it made absolutely no difference. My vision remained the same and the eye stayed very red.
It's worth mentioning that throughout all of this I had very little actual pain. My main symptoms were burning, redness, and marked photophobia.
That evening I returned for another examination. I was told the inflammation was "stable," that I could go back to the hotel, use the drops another two or three times before bed, and come back the following morning.
I left feeling somewhat reassured, although I wasn't entirely convinced by the explanation.
The following morning my vision in the left eye had deteriorated even further. At that point I could only perceive light, and my visual field was filled with what looked like a forest of black seaweed floating around whenever I moved my eye.
At the clinic I wasn't seen by my surgeon but by one of his assistants. Among other tests he performed an ocular ultrasound. The only explanation I received was that my eye was inflamed because "the treatment hadn't been administered during the night" (which obviously wasn't something I had been instructed—or even able—to do). I was told to return a couple of hours later.
I went back to the hotel frightened and deeply discouraged. I had the growing feeling that I had entrusted myself to people who were not able to manage the situation appropriately. At that stage I still believed the inflammation was limited to the anterior chamber.
Around lunchtime my surgeon called me and instructed me to go immediately to the emergency department of the local hospital. He told me I needed my eye "cleaned out" so that I could "see a little better" and so they could collect samples for analysis.
At the hospital I was examined by the retinal team.
They immediately diagnosed acute endophthalmitis and told me I needed emergency pars plana vitrectomy to protect the retina and prevent permanent vision loss.
At that moment my world collapsed.
I had developed the rarest and most feared complication of intraocular surgery, and there was nothing left to do except undergo another emergency operation.
I was admitted and underwent surgery at 6:00 p.m. on July 24, almost exactly 24 hours after my first symptoms began.
The vitreoretinal surgeon was outstanding. She successfully removed most of the infected vitreous without causing any retinal damage. The vitreous cavity was filled with balanced salt solution (BSS), and intravitreal antibiotics were injected.
The ICL itself was left in place because it appeared completely clean and was not believed to be the source of the infection.
I remained hospitalized for seven days.
The first few days were psychologically devastating. I had already started imagining how I would live with only one functioning eye.
I was also terrified that the infection might develop in my right eye as well, since both eyes had been operated on during the same session.
Initially I was told that the retina appeared structurally intact but that nobody could guarantee complete visual recovery.
We waited for the culture results in case a second, targeted intravitreal antibiotic injection would be needed. To everyone's surprise the cultures never became positive.
This seemed very unusual given how aggressive the endophthalmitis had been, with symptoms starting only about 10 hours after surgery.
Fortunately my vision improved steadily.
By the time I was discharged I had recovered to 8/10 (20/25) visual acuity, something that genuinely surprised the retinal team.
After discharge I returned to my original surgeon for follow-up. He told me the danger had passed and that both ICLs looked perfect.
Indeed, my right eye has been completely problem-free from day one. My vision has always been excellent, my intraocular pressure has remained around 10 mmHg, and I haven't experienced any significant optical phenomena. Even the central port is visible only under very specific lighting conditions and doesn't bother me at all.
I asked him what he believed had actually happened.
He explained that because all cultures were negative, this had not been an infectious endophthalmitis but rather an "extremely rare inflammatory reaction" to the viscoelastic material—a severe TASS that subsequently progressed to involve the vitreous.
I have to admit that I remain skeptical.
I'm a physician myself (although not an ophthalmologist), and I'm comfortable interpreting medical literature and statistics.
In ICL procedures TASS has an estimated incidence of roughly 5,6 per 100,000 surgeries, whereas infectious endophthalmitis occurs in approximately 1 in 6,000 intraocular procedures.
Even if this had initially been TASS, progression to vitreous involvement after ICL implantation would be extraordinarily rare. As far as I know, I haven't found any published cases describing this sequence.
To me, culture-negative infectious endophthalmitis seems far more likely, possibly due to inadequate sampling or the large amount of antibiotics administered before the vitreous samples were collected.
Honestly, the explanation I received feels more like an attempt to avoid potential legal consequences than the most plausible medical diagnosis.
At the moment I'm back home recovering.
It's now 3 weeks days since the vitrectomy. I had my follow-up last week, and luckily everything seems to be going really well.
My left eye has almost completely recovered in terms of visual acuity.
I notice a transparent, curtain-like structure moving in my temporal peripheral vision, almost like a jellyfish and there are many small, cell-shaped floaters, which I assume are remnants of the retinal hemorrhages as they are being reabsorbed (I had quite a few of them).
The thing that concerns me most at the moment is the presence of glare exclusively in my left eye, both during the day and at night. It’s nothing debilitating, but it’s quite annoying, especially at night when looking at streetlights. I’m not sure whether it’s simply caused by the lens or whether there could be some corneal issue resulting from the TASS/endophthalmitis.
I’ve also noticed that the ring of the port projected by the ICL in my left eye isn’t perfectly circular like the one in my right eye, and it seems slightly distorted.
My right eye, on the other hand, is absolutely perfect.
My hope is that in a few months this entire experience will be nothing more than a terrible memory and that I'll finally be able to return to a normal life.
Has anyone ever encountered a case of presumed TASS progressing to vitreous inflammation after ICL implantation, or does this presentation sound much more consistent with culture-negative infectious endophthalmitis? I'd really appreciate hearing the opinion of retinal specialists or anterior segment surgeons.