Anterior segment ischemia (ASI) after extraocular muscle surgery is reported to occur once more than two extraocular muscles are operated. It results from inadequate perfusion of the iris and ciliary body owing to disruption of blood supply to iris and ciliary body which mainly comes through anterior ciliary blood vessels, which are seven in number with each rectus muscle contributing two anterior ciliary vessels except lateral rectus muscle which contributes only one ciliary vessel. Primate studies have shown that 70–80% of the blood supply to the anterior segment of the eye is contributed by the anterior ciliary system in addition to collateral blood supply from the anterior episcleral arterial circle.
Incidence of severe ASI following strabismus surgery has been reported to be 30/400,000 surgeries. It mostly occurs in adults and after transposition of the vertical recti. Symptoms usually occur after 1–2 days of surgery, which include conjunctival chemosis, corneal edema, anterior chamber reaction, lens opacities, hypotony and sector iris perfusion defects. Late sequelae include correctopia, iris atrophy, cataract and on rare occasions phthisis bulbi.
There are number of risk factors which contribute towards ASI such as; micro-vascular disease, sickle cell disease, leukemia, thyroid eye disease, high myopia, previous scleral buckling, previous strabismus surgery and radiation therapy.
We report a case of traumatic left sixth nerve palsy in a 46-year-old man, who developed ASI following medial rectus recession and split thickness vertical muscle transposition (Hummelsheim) on the left eye.
A, 46-year-old Indian male presented to our hospital with complaints of inward deviation of his left eye for the last 9 months, which he developed after sustaining a head injury. The deviation was associated with horizontal diplopia, which was more in the left lateral gaze. The patient was a known hypertensive and was on medication for the past 7 years.
Examination showed best-corrected visual acuity (BCVA) of 20/20 in both eyes. The alternate cover test showed left esotropia of 25 PD in primary gaze [Fig. 1]. Ocular motility examination showed absent abduction in the left eye. Examination of the anterior segment was normal. Pupils were normal in size and were reacting to light. Fundus examination was normal in both eyes. Intraocular pressures (IOP) were 14 mmHg in each eye. Forced duction and force generation tests were negative.
Patient underwent left medial rectus recession of 5 mm from the insertion and a split-tendon transposition of the left superior and inferior rectus muscles to the lateral rectus insertion (Hummelsheim procedure) through limbal conjunctival peritomy.
On the first postoperative day, the visual axis was parallel. BCVA of the left eye was 20/60. There was moderate corneal edema with anterior chamber reaction of flare 2+ and cells 2+ on slit lamp biomicroscopy. Left eye pupil was semi-dilated and was sluggishly reacting to light. The IOP was 18 mmHg in the left eye. The posterior segment was normal. Diagnosis of ASI was made. Patient was started on topical and systemic steroids. After 1-week of steroids, visual acuity was 20/40. Corneal edema and anterior chamber reaction had reduced. The pupil was still mid dilated and was nonreacting to light [Fig. 2]. IOP was 4 mmHg in the left eye.
Patient was followed up regularly. Oral and topical steroids were tapered and stopped after 1 month. One year after the surgery, visual acuity had improved to 20/30. On anterior segment examination, the cornea was clear, the anterior chamber was quiet, the pupil was mid-dilated and nonreacting to light [Fig. 3a]. Visual axis was parallel and abduction of the left eye was in near normal [Fig. 3b]. IOP and posterior segment were within normal limits.
Our patient developed ASI following one muscle recession, and two muscle split muscle transposition, which is equivalent to two muscle surgery as the second halves of these vertical recti muscles still continue to contribute one ciliary vessel each. However, our patient was a known hypertensive, which could have been a risk factor for the development of ASI. Al Enezi and Al Wayel reported ASI in a 35 years old myopic patient following a similar procedure. They proposed that high myopia could also be a risk factor for ASI with vertical muscle surgery. A two-staged procedure with an interval of 4–6 months could have prevented ASI in our patient with hypertension as a risk factor as this would have allowed time for remodeling of the collateral circulation.
Both fornix and limbal incisions are associated with ASI. However, limbal incisions are said to predispose to more severe ischemia compared to fornix incisions as these compromise the anterior episcleral arterial circle. Fornix incision also could have been a better option for this patient.
Microscopic surgery on recti muscle for carefully dissecting anterior ciliary vessels before disinsersion can also be considered for high-risk patients as this helps to keep the anterior ciliary vessels intact and prevent ASI.
Anterior segment ischemia should be kept in mind during vertical muscle transposition in high risk patients during strabismus surgery.
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Conflicts of Interest: None declared.