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Show J. Cljn. Nellro-ophthalmol. 4: 147-150, 1984. Optic Neuropathy from the Use of Intracranial Muslin MICHAEL X. REPKA, M.D. NEIL R. MILLER, M.D. JERRY O. PENIX, M.D. JOHN H. TRANT, III, M.D. Abstract Following repair of an anterior communicating artery aneurysm with McFadden clips and muslin, a 32-year-old woman developed a steroid-responsive optic neuropathy. When she was explored, a sterile abscess with surrounding fibrotic tissue involving the muslin was found adjacent to the right optic nerve. The patient's vision improved following removal of the abscess. Introduction The repair of an intracranial aneurysm is typically accomplished by occlusion of its base with a metal clip; however, there are broad-based or fusiform aneurysms that cannot be treated in this manner. These lesions may be wrapped with muslin, muscle, and other substances in an attempt to reinforce the ectatic vessel wall. Muslin and synthetic analogs like Gelfoam, have also been used as cushions between the aneurysm clip and normal intracranial structures. We report a case of a successful repair of an anterior communicating artery aneurysm repaired with a dip and muslin that was complicated by a postoperative optic neuropathy. Case Report A 32-year-old woman developed a severe headache associated with nuchal rigidity in July 1980. The patient had no other neurologic signs or symptoms. Lumbar puncture showed bloody cerebrospinal nuid (CSF), and arteriography demonstrated an aneurysm of the right anterior communicating artery. Two weeks later, a crani- From the DepMtments of Ophthalmology (MXR, NRM). Neu· rology (NRM). and Neurosurgery (NRM). The Johns Hopkins School of Medicine, Baltimore, Maryland; and the Department of Neurosurgery (JOP), Eastern Virginia School of Medicine, Norfolk, Virginia. September 1984 otomy was performed via a right pleryonal approach. A broad-based dilation of the anterior wall of the right anterior communicating artery was found. A McFadden angled clip was placed across the neck of the aneurysm, and the dip was supported with Gelfoam patties and thin muslin strips. The immediate postoperative course was uneventful. In September 1980, 2 months after surgery, the patient noted mild blurring of vision in her right eye. She first saw an ophthalmologist in February 1981, at which time her acuity was found to be 20/50 in the right eye and 20/20 in the left eye. There was a right afferent defect as well as mild pallor of the right optic disc. Visual field examination of the right eye demonstrated only mild constriction. The patient was followed for 2 months, over which time the acuity in the right eye had diminished to 20/100, with development of an inferior-nasal defect in the right visual field. The left eye remained normal. Because of this progressive visual loss, the patient underwent computerized tomographic (CT) scanning and selective four-vessel arteriography. These studies were thought to be normal except for nonspecific postoperative changes. The patient was placed on methylprednisolone and noted immediate improvement in vision. She was continued on this drug for 6 weeks. By the conclusion of therapy, visual acuity in the right eye had improved to 20/30 with a full visual field. The patient noted no further change in vision until 3 months laler, when she again developed blurred vision in her right eye. She was given a second 3-week course of methylprednisolone and again noted improvement in vision. The patient's visual acuity remained stable for 4 months and then began to worsen. She was therefore referred to the Neuro-Ophthalmology Unit at the Wilmer Ophthalmological Institute for evaluation. On examination, the patient's visual acuity was 20/30- in the right eye and 20/20 in the left eye. The patient could identify eight out of 10 Hardy-Rand-Rittler (HRR) pseudoisochro- 147 Repka et al. Fil'U~ 1. CT scan WIth inttavft1(JUS coottasC. A hYJlOd- ~ with ri"3 entw~ t IS prnml in thor right supr-awn.r Me, marie color plates with the right eye and 10 out of 10 with the left. There was a right afferent pupillary defect. The right visual field demonstra· ted superior and inferior arcuate defects. The left visual field was normal. There was mild pallor of the right disc. A CT scan demonstrated a hypodense area with ring enhancement just above the right anterior clinoid (Fig. I). Righi carorid arteriography demonstrated minimal elevation of the first segment of the right anterior cerebral artery, overlying a surgical clip (Fig. 2). The patient underwent repeat craniotomy from a subfrontal approach. An abscess with a dense fibrous capsule intimately associated with rotting muslin strips was present in the region of the aneurysm repair. The abscess was adjacent to, and partiaUy surrounding, the right optic nerve. Fibrous bands originating from the capsule of the abscess were present around the right optic nerve. The surface of the nerve was pale, but lysis of the fibrous bands produced immediate filling of pial vessels on its surface. Gram stain of the purulent material from the abscess cavity showed only a few nt"Utrophils and no bacteria. Aerobic, anaerobic, and fungal cultures of both the muslin and the abscess contents were obtained and ultimately showed no growth. One week postoperatively, the patient's visual acuily was 20/40 with a full field in the right eye. Six months later, acuity was 20/30 in the right 148 eye. Twenty-two months postoperatively. the acuity had improved to 20/20. with a full periph· eral field. H-R-R color vision was six of six plates in each eye. Discussion The use of reinforcing and hemostatic materials for aneurysm surgery began in the early years of neurosurgery. In 1911, Cushingl commented on the use of muslin for hemostasis dUring aneurysm repair, while 00U2 first described the use of muslin (cotlon gauze) for reinforcing the surgical repair of an aneurysm. Sachs) studied the pathologiC effects of cotton wrapping material. and found that a dense fibrotic response developed when this material was placed intracranially. He also noted that a similar response occurred when just a few wisps of cotton were left in the neurosurgical field inadvertently. There is one previous report4 documenting three cases of optic neuropathy following wrapping of an ant"Urysm with muslin. None of these patients was explored. The first patient had a progressive deterioration of vision OVeT 24 days with recovery in just a few days. The second patient had a fluctuating course with eventual return to nonnal acuity and field. She had a second distinct attack in both eyes with fever and cerebrosinal fluid leukocytosis with eventual im- Journal of Clinical Neura-ophthalmology Optic Neuropathy Figure 2. Righi carotid arteriogram. An aneurysm clip is present just inftrior to the first SE'gment or the right anttrior ctrcbral arttry and pro;e<:ts into tht rtgion normally occupiE'd by the right optic ntrvt. Tht clip and the segment of artery are eltvatro by an avascular mass. provement of her vision. The third patient had a progressive left optic neuropathy over 5 months with moderate return of function over the subsequent 6 months. None of these patients was treated surgically or medically. In each of these cases, the suggested mechanism of ischemia seems improbable. A more likely cause of the optic neuropathy was a waxing-waning inflammatory response to the implanted muslin. Our patient had surgery during which the right anterior communicating artery was clipped and wrapped with muslin. Postoperatively, she developed a recurrent right optic neuropathy that was sensitive to steroids. The optic neuropathy could have been caused by several mechanisms in this patient: ischemia, compression, and inflammation. Simple ischemia seems unlikely, since ischemic optic neuropathy is of sudden onset, and there usually is no significant recovery of vision. Compressive optic neuropathies are usually slowly progressive like that in our patient and may show some improvement during steroid therapy.s Inflammatory optic neuropathies often respond dramatically to steroid therapy. We suspect that out patient's optic neuropathy was probably caused by all three mechanisms. lnflammation is likely because of the steroid responsiveness of the process, the enhancing mass on CT scan, as well as the abscess found at September 1984 surgery. Compression of the optic nerve can be implicated because of the dense fibrotic reaction that resulted in the formation of a mass near the right optic nerve.6 Ischemia might have been involved since the pial vessels on the surface of the optic nerve appeared to fill after the fibrous bands were cut. This case emphasizes that the intracranial use of foreign bodies, such as muslin, can incite an inflammatory response along with fibrosis and abscess formation. If this response is sufficiently close to the optic nerve, a progressive or recurrent, yet potentially correctable optic neuropathy probably caused by a combination of inflammation, compression, and ischemia might ensue. Based on our case, we suggest that muslin wrapping be avoided whenever possible, especially near the optic nerve. If a patient develops an optic neuropathy after use of muslin, craniotomy may eventually be necessary to restore visual function. References 1. Cushing. H.: The control of bleeding in operations for brain tumors. With the desCription of silver clips for the occlusion of vessels inacessible to the ligation. AmI. Surg. 54: 1-19, 1911. 2. Dolt, N.M.: Intracranial aneurysms: Cerebral arteriography: Surgical treatment. TrailS. Merl. Chir. 149 Repka et at Soc. Edilrburgh 112: 219-234, 1933. 3. Sachs, E., Jr,: The fate of muscle and cotton wrapped about intracranial arteries and aneurysms. A laboratory and clinico-pathological study. Acta Neurochir. 26: 121-137, 1972. 4. Carney, P.G., and Oatey, P.E.: Muslin wrapping of aneurysms and delayed visual failure. A report of three cases. j. (lin. Neuro-ophthalmol, 3: 91-96, 1983. S. Hirst, L.W" Miller, N.R., Kumar, A.J., and Udvarhelyi, G.B.: Medulloblastoma causing a corticosteroid- responsive optic neuropathy. Am. J. Ophthal- 150 mol. 89: 437-442,1980. 6. Cogan, D.G.: Neurology of the Visual System. Charles C Thomas. Springfield, Illinois, 1980, p. 217. Acknowledgment This work was supported in part by a National Eye Institute Fellowship 2T32EY0747 (Dr. Repka). Write for reprints to: Neil R. Miller, M.D., B-107, Maumenee Bldg., Johns Hopkins Hospital, Baltimore, Maryland 21309. Journal of Clinical Neuro-ophthalmology |
