|Year : 1999 | Volume
| Issue : 2 | Page : 126-129
Vitrectomy in takayasu's disease
Tarun Sharma, Bhushan Khare, Randeep Sharma, Mahesh P Shanmugam, Lingam Gopal
Vitreoretinal Service, Sankara Nethralaya, Vision Research Foundation, Chennai, India
Sankara Nethralaya, Vision Research Foundation, 18 College Road, Chennai - 600 006
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Sharma T, Khare B, Sharma R, Shanmugam MP, Gopal L. Vitrectomy in takayasu's disease. Indian J Ophthalmol 1999;47:126-9
Pars plana vitrectomy could provide a successful method of treating vitreous haemorrhage in Takayasu's disease.
Takayasu's disease is an idiopathic granulomatous inflammation of the wall of the aorta and its tributaries. The involved vessels may become progressively narrowed or obliterated resulting in ischaemia of the supplied area. The most characteristic ocular findings are dilatation of small vessels, microaneurysm formation and arteriovenous anastomoses. More severe ischaemia may result in peripheral retinal nonperfusion, neovascularization and vitreous haemorrhage. We performed pars plana vitrectomy for non-clearing vitreous haemorrhage in two patients with Takayasu's disease. To our knowledge, the role of vitrectomy in Takayasu's disease has not been reported.
| Case 1|| |
A 37-year-old Sri Lankan female was first examined on 10 June, 1995. She reported diminished vision in both eyes for the past 8 years. She had previously undergone treatment for bilateral chronic panuveitis, followed by bilateral intraocular lens (IOL) implantation 2 years ago. During the follow up, she developed rubeosis iridis and underwent laser photocoagulation in both eyes.
On initial examination, visual acuity was counting fingers close to face in both eyes. Slitlamp biomicroscopy of the right eye showed a small patch of iris atrophy at 9 o'clock close to pupillary border, anterior chamber flare 2+, peripheral anterior synechiae (PAS) up to anterior trabecular meshwork in the temporal half and posterior chamber IOL. The left eye showed rubeosis iridis, PAS up to anterior trabecular meshwork in the temporal half, posterior synechiae at 2 o'clock and posterior chamber IOL. There were no keratic precipitates. Conjunctival and episcleral vessels were of normal calibre. The intraocular pressures (IOP) were 11 and 12 mmHg in the right and the left eye respectively.
The right fundus showed minimal vitreous haemorrhage, fibrovascular proliferation at the optic disc, venous looping at 12 o'clock posterior to equator, scattered laser photocoagulation marks in the periphery and a pigmented macular scar. The left fundus showed an elevated fibrovascular proliferation at the optic nerve head and vitreous haemorrhage. B-scan ultrasonography showed incomplete posterior hyaloid detachment attached to a highly reflective membrane over the disc. During ocular examination, the patient felt giddy, but she was conscious and responded to verbal commands. On systemic examination, the radial pulse was not felt; however, dorsalis pedis pulse (89 per minute) was palpable. The blood pressure in the upper extremities was unrecordable. In the lower extremities, it measured 110/70 mmHg. Subsequently, she underwent a complete haematological and systemic evaluation. Haematological investigations were within the normal range except for the erythrocyte sedimentation rate (ESR) value of 61 mm at 1 hour (Westergren's method). A carotid duplex scan showed bilateral marked intimal thickening of the common carotids. She was diagnosed to have Takayasu's disease. A negative Mantoux test ruled out the underlying tubercular aetiology.
She underwent pars plana vitrectomy in the left eye. Vitreous haemorrhage was of grayish-white colour. Posterior vitreous detachment was absent and had to be induced with active suction. Intraoperative bleed was controlled immediately by raising the infusion bottle. Beyond the mid-periphery, retinal vessels were extremely attenuated. At the end of the procedure, a fill-in scatter photocoagulation was performed. The post-operative period was uneventful. She was treated with systemic corticosteroids for Takayasu's disease. Six weeks later, her best corrected visual acuity in the left eye improved to 6/60. Fundus examination of the left eye showed clear vitreous cavity and well photocoagulated attached retina.
| Case 2|| |
A 31-year-old Indian female was examined on 3 June, 1996. She reported diminished vision in the right eye for one year and was referred as a case of neovascular glaucoma. The left eye was asymptomatic. She was known to have idiopathic aortic arteritis and left hemiparesis. MRI scan showed multiple infarcts in both cerebral hemispheres [Figure - 1].
On initial examination, visual acuity was light perception in the right eye and 6/12 in the left. Slitlamp biomicroscopy of the right eye showed dilated episcleral blood vessels, aqueous flare 2+, rubeosis iridis, mid-dilated pupil, and a near total cataract. The left eye anterior segment was normal. The intraocular pressures were 12 and 6 mmHg in the right and left eye respectively. There was no view of the fundus in the right eye and left fundus was normal. B-scan ultrasonography of the right eye showed a complete posterior hyaloid separation. She underwent complete physical examination. All haematological investigations were within normal ranges except for ESR of (65 mm at 1 hour). Peripheral pulses in the upper extremities were absent and a bruit was present over the right carotid artery. However, dorsalis pedis pulse (84 per minute) was felt. Similarly, blood pressure in the upper extremities was unrecordable. In the lower extremities, it measured 200/100 mmHg. A carotid doppler showed diffuse intimal thickening and narrowing of both carotid vessels and subclavian arteries [Figure - 2] She was treated for aortitis and systemic hypertension.
She underwent pars plana lensectomy and vitrectomy in the right eye under local anaesthesia. Vitreous haemorrhage was red in colour. Intraoperatively mid-peripheral vascular anastomoses and attenuated peripheral vessels were observed in all quadrants [Figure - 3]. A scatter photocoagulation was performed. The postoperative period was uneventful and 6 weeks later, her best corrected visual acuity was 6/60 in the right eye. At one-year follow up, she maintained her visual acuity of 6/60 in the right eye. However, rubeosis iridis persisted. Fundus fluorescein angiography showed leakage of fluorescein dye from optic disc neovascularisation [Figure - 4]. A fill-in scatter photocoagulation was performed. During this visit, the fellow eye showed rubeosis iridis and severe capillary dropout in the peripheral quadrants [Figure - 5]. Scatter photocoagulation was performed in the left eye also.
| Discussion|| |
The diagnosis of Takayasu's disease is based on characteristic clinical features: decreased or absent peripheral pulse in upper extremities; a marked reduction in blood pressure in the upper extremities; and marked proliferation of the intima of common carotids on carotid duplex scan. Increased ESR suggested increased activity of the disease.
The ocular signs in both patients occurred as a result of decreased inflow of blood, consequent to vaso-occlusive lesions in the common carotids. Retinal vascular lesions belonged to stage 4 as per the classification of Uyama and Asayamma (stage 1, dilatation of small vessels; stage 2, capillary microaneurysm formation; stage 3, arteriovenous anastomoses; and stage 4, further ocular complications). Neovascularisation of the optic disc has also been observed by Tanaka et al.
Differential diagnosis of Takayasu's disease includes chronic uveitis, ocular ischemic syndrome, and other proliferative vascular retinopathies. Absence of keratic precipitates and cells in the anterior chamber distinguishes Takayasu's disease from chronic uveitis. Ocular ischemic syndrome rarely develops in patients below 50 years, and males are more frequently affected. Further, characteristic systemic findings including signs of cerebral ischaemia establish the diagnosis of Takayasu's disease. Ophthalmologists must suspect pulseless disease if there is no increased intraocular pressure despite angle closure due to rubeosis iridis. These patients have a propensity to develop cataract at an early age because of chronic ocular ischaemia. The surgical trauma of cataract operation is well tolerated. Vitreous surgery is not complicated as complex manoeuvres of membrane peeling or delamination are not required. Intraocular bleed is controlled instantaneously by raising the infusion bottle because of low perfusion in central retinal artery. Intraocular diathermy therefore, is not needed. After the control of intraocular bleed, the infusion bottle should be lowered to prevent the risk of permanent occlusion of central retinal artery. During endophotocoagulation, caution should be exercised to avoid treatment to mid-peripheral arteriovenous shunts. It is interesting to note that despite adequate laser treatment, regression of iris neovascularization may not occur as observed in patients with proliferative diabetic retinopathy or central retinal vein occlusion. Further, treatment with systemic corticosteroids for Takayasu's disease should be monitored by a physician.
| References|| |
Takayasu S. A case with curious changes in the central retinal artery. Nippon Ganka Gakkai Zasshi
Douglas AJ. Ocular manifestations of the rheumatic diseases. In:Tasman W, Jaegar EA, editors. Duane's Clinical Ophthalmology.
Philadelphia:Lippincott-Raven Publishers; 1996. Vol 5. p 26.
Wand M. Neovascular glaucoma. In:Albert DM, Jakobiec FA, editors. Principles and Practice of Ophthalmology:Clinical Practice.
Philadelphia:WB Saunders Company; 1994. Vol 3. p 1498.
Tanaka T, Shimuzu K. Retinal arteriovenous shunts in Takayasu disease. Ophthalmology
Brown G, Coscas G, Gutman FA, Horth D, Gitter KA. Ophthalmic manifestations of carotid artery disease. In:Singerman LJ, Jampol L M, editors. Retinal and Choroidal Manifestations of Systemic Disease.
Baltimore:Williams and Wilkins; 1991. p 143.
Uyama M, Asayama K. Retinal vascular changes in Takayasu's disease (pulseless disease). Occurrence and evolution of the lesion. In:Delaey JJ, editor. International Symposium on Fluorescein Angiography.
The Ghent, Hague:W Junk Publishers; 1976. p 549-54.
[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5]