In this article we will look at inflammation of the eye through external causes such as surgery, trauma to the eye or through spread of external infection of the eye. Such inflammatory disease of external origin is termed exogenous endophthalmitis and represents the most common type of infection. Around one in 1,000 cases are directly linked to intraocular surgery such as cataract surgery, corneal transplant ation, glaucoma trabeculectomy surgery and vitrectomy. Very rarely, it can be related to strabismus surgery (one in 30,000).
In this article, I will offer you an insight into a rare form of direct infection suffered by a contact lens wearer that eventually led to endophthalmitis and hope in some way to convey the experience of the trauma the patient had to endure before finally a positive outcome was reached. Practitioners, and our patients, tend to take contact lens wear for granted but, when an infection occurs, it is the urgency of the action we take that will determine the outcome as to whether one’s eyesight is preserved.
Case study
Sixty-three-year-old female RA had been a long standing patient at the practice, having originally worn monthly replacement contact lenses and, from 2008, daily disposable lenses. In April 2010, she developed shingles which affected her right forehead and eyelids. She was kept under observation until 2011, having to use amitriptyline for post-herpetic neuralgia. She was able to continue wearing contact lenses during this period.
In November 2011, while in Malta, she was sunbathing under a tree and unwittingly touched the tree and rubbed her eyes. Following advice given to most of our patients, she rang immediately on her return to the UK complaining of pain and discomfort to the right eye. She had not worn her contact lenses for three days and could not understand the pain in the right eye which she claimed to be worse than the pain endured following shingles.
I was in the fortunate position to experience the patient’s infection first hand and initiate the following sequence of events:
- 9/11/11 – I saw a right superior temporal corneal ulcer or abscess. There were feathered edges to the ulcer and it appeared more likely to be a deep epithelial rather than a stromal infiltrate. I referred the patient urgently to Moorfields Eye Hospitals with a likely diagnosis of microbial, fungal or Acanthamoeba keratitis on the basis of the pain. She was immediately treated with anti-Pseudomonas antibiotic (levofloxacin 5mg) and anti-fungal (econazole 1%) eye drops to be used every hour to the right eye. Also prescribed was the dilator atropine (1%) eye drops twice a day.
- 16/11/11 – the correct diagnosis of fungal Fusarium keratitis was confirmed. An increase in the abscess to double the size of that initially observed had occurred, the lesion still having the dull, feathery appearance. There were also signs of posterior pupillary synechiae (figure 1).
- 19/11/11 – the abscess in the right eye was now encroaching centrally and there were definite pupillary synechiae indicating a rampant inflammatory process. The patient was still continuing drops as earlier.
- 28/11/11 – the abscess was now central and hypopyon was visible inferiorly in the anterior chamber. Straw-yellow stromal discolouration, due to release of free haemosiderin, was observed (figure 2).
Figure 1
At this stage, step in Professor John Dart whose expertise is called upon by the eye specialists at Moorfields for many severe or complex cases.
Figure 2
- 5/12/11 – Professor Dart and his team decided to drain the hypopyon using a intracameral plasminogen activator and an amphotericin anterior chamber washout procedure.
- 13/12/11 – The inferior chamber hypopyon had now gone. Nasally, there were two iris holes and central nasally there seemed to be possible further hypopyon. A central corneal scar was still evident.
- 26/01/12 – the Fusarium keratitis was responding at last and, by February, a decision was taken to undertake cataract extraction along with a corneal transplant.
- 29/03/12 – the disease returned and two successive corneal transplants were affected by the fungus. The cataract was removed from the right eye which was left aphakic. A third right eye corneal transplant was performed using a 9mm corneal button (a procedure described as a therapeutic penetrating keratoplasty).
- April 2012 to August 2013 – the intraocular pressure was increasing in the right eye to 30mmHg so a decision was taken to prescribe anti-hypotensive eye drops (povidone-iodine tds, tafluprost at night and Azopt tds). The patient continued using amphotericin qds and levofloxacin tds daily.
- 28/11/13 – a corneal transplant button and a rigid gas permeable contact lens were fitted.
- 3/05/16 – The corneal transplant remained intact and a stitch was removed, distorting the cornea. The existing contact lens wear was stopped awaiting the fitting of a new gas permeable contact lens (figure 3).
Figure 3
Fungal Keratitis
Fungal corneal infection is a very rare occurrence in the UK and few optometrists have witnessed its devastating effects. Fungal keratitis is difficult to diagnose, with limited treatment options, and usually the prognosis is poor. Predisposing factors include immunosuppression, as a result of diseases such as Aids or lymphoma or due to certain anti-cancer or transplant drugs. Topical corticosteroids, as used for example for eczema, dermatitis or psoriasis, can also be a predisposing factor.
Agricultural workers are most at risk, and a high percentage of hospital fungal keratitis patients are farmers or gardeners who suffer organic trauma to the eye. Hot and humid climates, as well as dry eye and contact lens wear, can increase susceptibility to fungal infection of the eye.
Fungal infective agents can be divided into moulds and yeasts. Moulds (or filamentary fungi) that commonly infect the cornea are the Fusarium and Aspergillus species. Yeast infection of the eye is predominantly from Candida species of yeast (as causes vaginal thrush).
Clinically, yeast infection of the cornea appears as an expanding stromal infiltrate, with minimal epithelial ulceration and a ‘button’ appearance. Filamentary fungal infections show a feathery, branching pattern and the cornea appears as dull grey, with a dry, rough texture. Severe anterior uveitis and hypopyon may accompany the corneal findings. Within two to three weeks, the characteristic corneal lesion disappears and the appearance instead resembles that of an advanced bacterial keratitis.
It is also common to see straw-yellow discolouration of the cornea which occurs when the red blood cells release haemoglobin into the aqueous humour. This diffuses across the endothelium and Descemet’s membrane into the posterior corneal stroma. Keratocytes phagocytise the haemoglobin to leave toxic haemosiderin. Haemosiderin kills the keratocytes, and the free haemosiderin diffuses through the stroma and passes anteriorly into the epithelium and a straw-yellow discolouration is observed (figure 2).
Treatment and management
A careful history should be taken as always for severe ocular pain, especially so for farm workers or gardeners and anyone with autoimmune disease or immunosuppression and who may have decreased corneal sensitivity (neurotrophic cornea). Microbial keratitis should be suspected, and a corneal scrape is indicated for microbiological analysis and confirmation of bacterial, fungal, herpes zoster or simplex viral and, most importantly, acanthamoebal presence. Pain is severe for any of these types of keratitis and immediate action is necessary to prevent sight loss.
Intense topical therapy with anti-fungal agents (econazole 1% preservative-free eye drops) are to be used every hour through day and night. Broad spectrum antibiotics (levofloxacin) are also prescribed, together with cycloplegic eye drops (atropine 1% or cyclopentolate 1%) to be used daily twice a day.
When hypopyon develops and the infection spreads undeterred, injection of amphotericin antibiotic and tissue plasminogen activator (TPA) into the anterior chamber is indicated. This procedure is called anterior chamber washout. The tissue plasminogen is a naturally occurring serine proteinase that hydrolysis fibrin. In cases of secondary endophthalmitis, intravitreal amphotericin is given followed by vitreous biopsy.
Steroids should be avoided at all cost for fungal infections for fear of rampant spreading of the fungus. Where intraocular pressure rises, anti-glaucoma medication is indicated to prevent nerve fibre damage and loss of vision. Where Candida yeast infection is suspected, then oral fluconazole (50mg to 400mg) is prescribed for seven to 14 days.
Most exogenous endophthalmitis are due to corneal surgery and optometrists may see such patients only once they have lost their sight. Figure 4 shows some examples of exogenous endophthalmitis including one where a prosthetic eye was eventually fitted for cosmetic purposes.
Kirit Patel is an optometrist in independent practice in Radlett, Herts. A new series of his case studies begins in Optician soon.