Europe PMC Funders Group Author Manuscript Ophthalmol Int. Author manuscript; available in PMC 2015 February 25. Published in final edited form as: Ophthalmol Int. 2013 ; 8(3): 85–86.

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Delayed Optochiasmal Arachnoiditis following Intervention for a Subarachnoid Haemorrhage Patrick Yu-Wai-Man, PhD, FRCOphth1,2 and Christopher Neoh, FRCS, FRCOphth1 1Newcastle

Eye Centre, Royal Victoria Infirmary, Newcastle upon Tyne, NE1 4LP, United

Kingdom. 2Wellcome

Trust Centre for Mitochondrial Research, Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.

Abstract Visual morbidity following a subarachnoid haemorrhage is common among survivors and it is usually the result of vascular ischaemia at the time of the initial insult. In this report, we present an unusual case of delayed, progressive visual loss following intervention for a ruptured anterior communicating artery aneurysm. We discuss the possible etiological factors and highlight potential diagnostic pitfalls.

Introduction Europe PMC Funders Author Manuscripts

The annual incidence of subarachnoid haemorrhage (SAH) is about 1 in 10,000, with a mean age at presentation of 60 years and a male to female ratio of 2:1. It is a medical emergency with a case fatality rate approaching 50% and about a third of survivors remaining severely neurologically impaired. Visual deficits following SAH are common and relate to vascular ischaemia at the time of the acute insult or less frequently to intraocular haemorrhage (Terson’s syndrome).1 We present a rare case of delayed, progressive visual loss following intervention for a ruptured anterior communicating artery aneurysm (ACOM).

Case Report A 59-year-old woman suffered a SAH (Fisher grade 2) in April 2005 and following incomplete coiling of a left-sided ACOM, she underwent an open craniotomy with successful clipping of the residual neck. A titanium clip (Yasargil™, Braun Aesculap) was used without complications and no additional wrapping or coating materials were used to secure the aneurysm wall. A post-operative angiogram confirmed complete occlusion of the aneurysm with preservation of all the distal vessels. She had previously been fit and well with no other co-morbidities except for well controlled hypertension. She made a full recovery and on discharge had no neurological deficits.

Corresponding author: Dr Patrick Yu-Wai-Man Newcastle Eye Centre Royal Victoria Infirmary Newcastle Upon Tyne, NE1 4LP Tel: 0191-282-5447; Fax: 0191-282-6269 [email protected].

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In April 2006, she had several episodes of grand mal seizures and was seen as an emergency by the neurologists at her local hospital. She was apyrexial and her inflammatory markers and white cell count were not raised. A lumbar puncture was normal and a head computer tomography (CT) scan without contrast showed no acute haemorrhage or suspicious lesions in the vicinity of the aneurysm clip. She also reported visual blurring in her left eye that had been present for at least 3 months and on discharge, she was referred to our unit for an ophthalmological opinion. Her visual acuities were 20/30 right eye (RE) and 20/200 left eye (LE), and Ishihara test plates were 12/13 RE and 0/13 LE. The right Goldmann visual field was normal, but the left was constricted with a central scotoma. The ophthalmology resident documented left optic disc pallor with an associated relative afferent pupillary defect. Since the CT scan did not reveal any intracranial lesions compromising the anterior visual pathways, it was felt that her left visual deficits were longstanding, the result of optic nerve injury when the aneurysm was clipped. The patient was subsequently referred to the neuroophthalmology service for a second opinion.

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When the patient was reviewed two months later in the neuro-ophthalmology clinic, she had become aware of visual loss in her RE about two weeks prior to her follow-up appointment. Her visual acuities had deteriorated to 20/120 RE and hand movement LE, and Ishihara test plates were 1/13 RE and 0/13 LE. Goldmann perimetry showed a right temporal hemianopia in addition to bilateral central scotomas. An urgent MRI scan with contrast showed a cavitating, ring enhancing lesion in the vicinity of the aneurysm clip with surrounding inflammation involving the anterior visual pathways (Figure 1). The presumed abscess was drained under image guidance and she was started on high dose intravenous antibitiotics for four months via a Hickman line. No microorganisms were identified from the aspirate and serial blood cultures on admission were all negative. At her last follow-up in May 2007, her visual acuities had stabilized to 20/40 RE and count fingers LE, but there had been no visual field improvement.

Discussion The main therapeutic options for securing intracranial aneurysms are endovascular coiling and clipping. In the relatively uncommon situation where it is not possible to clip the aneurysm completely, the wall can be reinforced by wrapping it with various materials, the most popular choice being muslin gauze.1, 2 Clipping of ruptured aneurysms carries a procedure-related surgical morbidity of around 20%, but optochiasmal arachnoiditis (OCA) is a rare complication.3, 4 OCA can be triggered by a foreign body reaction to muslin and there are 30 reported cases of delayed optic neuropathy in this group, mostly within two years of the procedure.2, 5 No muslin was used in our patient, excluding this as a possible aetiological factor. What are the other possible explanations? Although no wrapping materials were used, in the absence of an open surgical exploration, it is not possible to fully exclude an inflammatory reaction to foreign material inadvertently introduced at the time of the craniotomy. Infection, however, is unlikely given the relatively long interval between the clipping procedure and the onset of symptoms. Our patient was never unwell and a full septic screen, including culture of the aspirates from the cavitating brain lesion, failed to identify any pathogenic microorganisms.

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There is increasing awareness that clips used in laparoscopic surgery can rarely cause foreign body granulomas directly, requiring surgical excision.6 Interestingly, one patient has been described who developed severe pruritus following intervention for a ruptured intracranial aneurysm. Both the craniotomy wires and the clip used had been made from stainless steel (cobalt and nickel).7 Skin patch testing revealed that the patient was severely atopic to these two metals and histological analysis of the tissues adjacent to the clip and wires was consistent with a T-cell mediated type IV hypersensitivity reaction. Surgical removal of the aneurysm clip and wires resulted in complete symptoms resolution. In a recent report of eight patients with isolated, progressive visual loss after coil embolisation of paraclinoid aneurysms, the most likely explanation in this subgroup of these patients was perianeurysmal, coil-related inflammation.8 Evidence from experimental animal models also suggests that aneurysm coils can induce a chronic inflammatory response with the fibrotic thickening of the aneurysm wall being a possible protective mechanism reducing the risk of rupture.9, 10 We can only speculate as to whether our patient became sensitized to the clip or coil material used to treat her ACOM aneurysm, with the subsequent immunological reaction leading to a sterile inflammatory mass that eventually involved her anterior visual pathways.

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Our case also highlights a number of learning points for the clinician faced with a patient reporting visual loss several months after neurosurgical intervention for an aneurysm. The differential diagnosis must include muslin-induced OCA and since most patients will not know or remember the full details of their procedure, it is imperative to either request the surgical records or contact the neurosurgical team to clarify what was actually involved. Unless there is previous documentation, it can be difficult to ascertain the exact onset of the visual loss and whether it is progressive. With the benefit of hindsight, the head CT scan was a routine series performed to rule out an intracranial bleed and the sections did not allow for a detailed analysis of the area around the aneurysm clip or the anterior visual pathways. This reminds us of the potential pitfalls of only relying on “normal” reports, either from lack of access to the films or the failure to review them personally. CT is also not the best imaging modality for excluding early or subtle lesions in the parasellar region. Clinicians must therefore be extremely wary of ascribing optic atrophy and visual deficits to trauma from previous neurosurgical intervention without the benefit of an appropriate MRI scan to rule out a compressive, infiltrative or inflammatory cause.

References 1. Suarez JI, Tarr RW, Selman WR. Current concepts: Aneurysmal subarachnoid hemorrhage. N. Engl. J. Med. 2006; 354(4):387–96. [PubMed: 16436770] 2. Taravati P, Lee AG, Bhatti MT, et al. That’s a wrap. Surv. Ophthalmol. 2006; 51(4):434–44. [PubMed: 16818086] 3. Saveland H, Hillman J, Brandt L, et al. Causes of Morbidity and Mortality, with Special Reference to Surgical Complications, after Early Aneurysm Operation - a Prospective, One-Year Study from Neurosurgical Units in Sweden. Acta Neurol. Scand. 1993; 88(4):254–8. [PubMed: 8256568] 4. McLaughlin N, Bojanowski MW. Early surgery-related complications after aneurysm clip placement: an analysis of causes and patient outcomes. J. Neurosurg. 2004; 101(4):600–6. [PubMed: 15481713]

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5. Prabhu SS, Keogh AJ, Parekh HC, et al. Optochiasmal Arachnoiditis Induced by Muslin Wrapping of Intracranial Aneurysms - a Report of 2 Cases and a Review of the Literature. Br. J. Neurosurg. 1994; 8(4):471–6. [PubMed: 7811414] 6. Grubb K, Gagandeep S, Chatzoulis G, et al. Surgical clips - A nidus for foreign body reaction after hepatic resection. Surg. Laparosc. Endosc. Pct. Tech. 2005; 15(6):363–5. 7. Ross IB, Warrington RJ, Halliday WC. Cell-mediated allergy to a cerebral aneurysm clip: Case report. Neurosurgery. 1998; 43(5):1209–11. [PubMed: 9802865] 8. Schmidt GW, Oster SF, Goinik KC, et al. Isolated progressive visual loss after coiling of paraclinoid aneurysms. Am. J. Neuroradiol. 2007; 28(10):1882–9. [PubMed: 17998416] 9. Fujiwara NH, Kallmes DF. Healing response in elastase-induced rabbit aneurysms after embolization with a new platinum coil system. Am. J. Neuroradiol. 2002; 23(7):1137–44. [PubMed: 12169470] 10. Ding YH, Dai DY, Lewis DA, et al. Angiographic and histologic analysis of experimental aneurysms embolized with platinum coils, matrix, and HydroCoil. Am. J. Neuroradiol. 2005; 26(7):1757–63. [PubMed: 16091526]

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Figure 1.

T1-weighted images showing: (A) marked inflammatory changes in the suprasellar region around the aneurysm clip with swelling of the optic chiasm; and (B) a well-defined, ring enhancing lesion extending into the left gyrus rectus.

Europe PMC Funders Author Manuscripts Ophthalmol Int. Author manuscript; available in PMC 2015 February 25.

Delayed Optochiasmal Arachnoiditis following Intervention for a Subarachnoid Haemorrhage.

Visual morbidity following a subarachnoid haemorrhage is common among survivors and it is usually the result of vascular ischaemia at the time of the ...
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