Case report

Can facial arteriovenous malformation predispose to bilateral intraoperative suprachoroidal hemorrhage?

Senthil, Sirisha FRCS*; Sethi, Vani MS; Mohan, Sashwanthi MB BS; Reddy, Jagadesh C. MS; Chhablani, Jay Kumar MS

Author Information
Journal of Cataract and Refractive Surgery Online Case Reports: April 2018 - Volume 6 - Issue 2 - p 33-35
doi: 10.1016/j.jcro.2018.01.005
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Abstract

Suprachoroidal hemorrhage is one of the most serious vision-threatening complications of any intraocular surgery. It occurs because of blood collection in the potential suprachoroidal space during the intraoperative or postoperative period. The cumulative incidence of suprachoroidal hemorrhage in intraocular surgeries is reported to be 0.2% to 0.75% with older techniques of cataract surgery, which has drastically reduced to 0.03% to 0.06% with closed chamber techniques such as phacoemulsification.1

A known predisposing factor for suprachoroidal hemorrhage is sudden hypotony. Hypotony causes serous choroidal effusion that obstructs the venous outflow, leading to congestion and stretching of the long and short posterior ciliary vessels resulting in rupture with massive extravasation of blood into the suprachoroidal space.2,3

Many systemic risk factors such as advanced age, arteriosclerosis, uncontrolled or long-standing hypertension, blood dyscrasia, use of anticoagulants, diabetes mellitus, liver disease, and ocular risk factors such as Sturge-Weber syndrome, glaucoma, myopia, aphakia, pseudophakia, choroidal arteriolar sclerosis, inflamed eyes, vitrectomized eyes, and suprachoroidal hemorrhage in the fellow eye have been implicated in the development of suprachoroidal hemorrhage.1 Rare cases such as spontaneous bilateral suprachoroidal hemorrhage without ocular surgery,4 bilateral suprachoroidal hemorrhage in the postoperative period after intraocular surgery,5 and unilateral cases of intraoperative suprachoroidal hemorrhage during phacoemulsification6 have been reported in the past.

We present a rare case of bilateral limited-extent recurrent suprachoroidal hemorrhage during phacoemulsification in a patient with no known ocular or systemic risk factors; however, the patient had possible subclinical choroidal hemangioma and an operated facial arteriovenous malformation (AVM). Prompt intraoperative measures and appropriate management during the postoperative period helped in complete resolution of this dreaded complication and helped achieve a postoperative corrected distance visual acuity (CDVA) of 20/20 in both the eyes.

CASE REPORT

A 65-year-old woman had significant nuclear cataract (NS3) in both eyes with visual complaints with 20/40 vision. The rest of the anterior and posterior segment was within normal limits. Intraocular pressure (IOP) by applanation tonometry was 15 mm Hg and 16 mm Hg in the right eye and left eye, respectively. The axial length in both eyes was 22.4 mm. The patient was a mild hypertensive, well controlled on one antihypertensive medication (amlodipine [calcium channel blocker] 2.5 mg once daily) with blood pressure of 120/90 mm Hg over 2 years. She had a facial scar from a surgical procedure 25 years ago.

Phacoemulsification with intraocular lens (IOL) implantation was planned in the left eye followed by the same surgery in the right eye. During the left eye phacoemulsification after nucleus removal, there was sudden shallowing of the anterior chamber, tightening of the globe, and iris prolapse from all the ports. The iris was reposited and the wound was quickly sutured. Suspecting a suprachoroidal hemorrhage, intravenous (IV) mannitol 300 mL was given. Despite this, the globe remained hard and hence the surgery was deferred with retained cortical matter.

Ultrasound (US) B-scan revealed a localized hemorrhagic choroidal detachment with choroidal thickening, suggestive of suprachoroidal hemorrhage in the superonasal quadrant (Figure 1, A). The patient was started on topical and oral steroids. The suprachoroidal hemorrhage resolved by 3 weeks and cortical wash with secondary IOL implantation was planned. There was recurrence of the suprachoroidal hemorrhage during the secondary IOL implantation despite preoperative intravenous mannitol; however, the surgery was completed and the wound was sutured. Conservative management was started with topical steroids, antibiotics, cycloplegics, and oral steroids. One month later, the CDVA in the left eye improved to 20/25, with IOP of 13 mm Hg.

Figure 1.
Figure 1.:
Ultrasonography shows localized retinochoroidal elevation caused by suprachoroidal hemorrhage (A and B). Fundus photographs of both eyes show choroidal folds (C and D, arrow), and SS-OCT scans show thickened choroid with choroidal folds (arrow) on horizontal (E and F) and vertical scans (G and H) (SS-OCT = swept-source optical coherence tomography).

In view of recurrent episodes of suprachoroidal hemorrhage in the same eye, the patient was evaluated for possible predisposing factors and none were found. The only possible risk factor, mild systemic hypertension, was very well controlled.

Three months after the left eye surgery, phacoemulsification in the right eye with IOL implantation with preoperative precautions was planned. However, a similar condition of suprachoroidal hemorrhage was also noted intraoperatively in the right eye. When the suprachoroidal hemorrhage was suspected, the eye was patched, IV mannitol was administered, and 30 minutes later, limited vitrectomy was performed and the cataract surgery was completed with IOL implantation in the bag. Postoperative US B-scan confirmed limited suprachoroidal hemorrhage in all quadrants (Figure 1, B). With conservative management, the suprachoroidal hemorrhage resolved and good visual recovery was achieved by 4 weeks. The US B-scan showed a resolved suprachoroidal hemorrhage with thickened choroid. The fundus photograph showed choroidal folds (Figure 1, C and D), enhanced-depth imaging, swept-source optical coherence tomography (SS-OCT) showed retinal pigment epithelial corrugations with marked thickening of the choroid in both the eyes (right eye, 505 μm; left eye, 560 μm), comparable to an age-matched woman (Figure 1, E to H), suggestive of subclinical choroidal hemangioma.

On detailed evaluation and reviewing all the patient's previous medical reports, there was history of surgery for AVM on the lower lip and chin (in the midline) 25 years ago, with ligation of the left inferior alveolar artery that helped to regress the AVM (Figure 2). The rest of the systemic examination and evaluations were within normal limits and there were no other vascular malformations noted.

Figure 2.
Figure 2.:
Composite shows operated scar on the chin and neck region (A), X-ray with contrast shows AVM (B, arrow) and no engorged episcleral vessels on the external eye photograph (C) (AVM = arteriovenous malformation).

DISCUSSION

Intraoperative suprachoroidal hemorrhage can occur in the presence of choroidal vascular engorgement, choroidal vascular sclerosis, and vascular fragility. Fragile vessels when exposed to sudden decompression with fluctuation in IOP dynamics can result in bleeding that results in sudden elevation in IOP and a hard globe in a closed globe setting or expulsion of intraocular contents in an open globe. A rise in IOP in a closed globe helps to tamponade the hemorrhage and prevent further bleeding, and it limits the suprachoroidal hemorrhage in the absence of other risk factors such as a large aphakic eye, and so forth. As in our case, the suprachoroidal hemorrhage was limited, possibly because of closed globe surgery.

Our patient had history of being operated for AVM on the lower lip and chin (Figure 2, A). The feeding artery here was the left inferior alveolar artery, a branch of the external carotid artery (Figure 2, B). The venous drainage of this area is via the facial vein to the cavernous sinus; hence, it is unlikely that there was a direct relationship from the facial AVM and the choroidal vascular abnormality that was noted.

Increased choroidal thickness in our case was likely caused by an underlying choroidal vascular abnormality, possibly a hemangioma. We propose that a subclinical choroidal hemangioma was a predisposing factor for suprachoroidal hemorrhage in this patient. Subclinical choroidal hemangioma might not have external signs as in eyes with raised episcleral venous pressure and hence might not be obvious clinically; however, it could be detected by measuring thickness with SS-OCT.7 Hence our recommendation is that, in the presence of facial or any other systemic AVMs, a B-scan US and enhanced-depth imaging of the choroid might help rule out a coexisting choroidal vascular abnormality. In the presence of a first eye suprachoroidal hemorrhage, the other eye has a high risk for a similar complication. It is important to educate the patient and take appropriate precautions for the other eye surgery to prevent recurrence of this complication. If one cannot prevent it, at least we can detect it early and treat appropriately. What could we have done differently in our patient to prevent recurrence of suprachoroidal hemorrhage in the other eye? Using an anterior chamber maintainer at the beginning of the surgery to prevent IOP fluctuations could have helped.8 Also, prophylactic sclerotomies would have had a role to play, to drain the suprachoroidal bleed if it happened intraoperatively. Increased choroidal thickness after uneventful phacoemulsification has been reported,9 although it was much less than what was seen in our case.

There are 2 cases reported in the literature with no predisposing factor causing intraoperative suprachoroidal hemorrhage during intraocular surgery.10 These eyes required drainage of the suprachoroidal hemorrhage, during which fleshy vascular lesions suggestive of abnormal plexus of episcleral veins were noted suggesting a vascular anomaly that could have predisposed to suprachoroidal hemorrhage. In our patient, we did not find any features suggestive of abnormal dilated anterior episcleral plexus of vessels (Figure 2, C). We do not know whether there were any posterior episcleral vascular anomalies because drainage of the suprachoroidal hemorrhage was not done. Hence, the possible risk factor in our patient was a choroidal vascular abnormality in both eyes that was detected on SS-OCT.

In conclusion, we present a case of choroidal vascular abnormality in the presence of facial AVM leading to suprachoroidal hemorrhage that was successfully managed conservatively with a good visual outcome. Detailed ocular evaluation including SS-OCT is recommended preoperatively in the presence of any facial AVM to rule out a potential risk factor that could lead to serious intraoperative complications of suprachoroidal hemorrhage.

Disclosures:

None of the authors has a financial or proprietary interest in any material or method mentioned.

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