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Show Journal of Clinical Neuro-ophthalmology 13(4): 242-249, 1993. Pulseless (Takayasu) Disease with Ophthalmic Manifestations James R. Lewis, M.D., Joel S. Glaser, M.D., Norman J. Schatz, M.D., and Duane G. Hutson, M.D. © 1993 Raven Press, Ltd., Hew York Pulseless disease (PD) is a rare disorder in which inflammation of the aorta and its major branches leads to stenosis or occlusion of these arteries. It mainly affects young Oriental women, who suffer chronic ischemic injury to tissues of the brain, orbits, upper limbs, myocardium, and kidneys. The ophthalmologic features of pulseless disease tend to be late manifestations, and can include ischemia of the retina, choroid, and anterior segment. The inflammatory process may be reversed in early stages with systemic corticosteroids, but, more frequently, significant arterial stenosis necessitates arterial bypass surgery. A 59-year-old Caucasian woman with stenosis of all four major cervical arteries presented with recurrent blurred vision, syncope, mental obtundation, and a remarkable funduscopic appearance due to bilateral orbital hypoperfusion. Her acute symptoms improved slightly on high-dose systemic corticosteroids, and then resolved completely following arterial bypass surgery. Key Words: Carotid stenosis-Anastomosis-Ocular ischemia-Pulseless disease. From the Departments of Ophthalmology, Bascom Palmer Eye Institute a.R.L., J.5.G., N.J.S) and Surgery (D.G.H.), University of Miami School of Medicine, Miami, Florida, U.S.A. This work was supported in part by a Fellowship from the E. A. Baker Foundation for the Prevention of Blindness, Toronto, Canada. Address correspondence and reprint requests to Dr. Joel S. Glaser, Bascom Palmer Eye Institute, P.O. Box 016880, Miami FL 33101, U.S.A. 242 Pulseless disease (PO) is an idiopathic chronic inflammation of the aorta and the proximal segments of its major branches, producing progressive stenosis of the great vessels with resultant end-organ hypoperfusion. Uncommon in North America, it is seen most frequently in young Oriental women, but may occur at any age, in any race, and in either gender (1). Ophthalmologic manifestations occur late in the course of the disease and, perhaps for this reason, PO has been discussed infrequently in the ophthalmic literature, reported chiefly by Japanese (2-5) and French (6-7) ophthalmologists. Indeed, Takayasu (8) was an ophthalmologist. In the case described here, a 59-year-old-woman presented with symptoms and signs of severe bilateral upper extremity and ophthalmic ischemia, along with life-threatening cerebral ischemia, and a remarkable funduscopic appearance. Arteriography disclosed stenosis of the major cervical arteries. CASE STUDY Following a minor head injury sustained in a fall in April 1988, a 59-year-old woman complained of posterior headaches and brief episodes of mild dizziness. Neurologic examination was normal except for a left carotid arterial bruit. Transcranial Doppler studies showed 100% occlusion of the proximal right internal carotid artery and mild stenosis of the left internal carotid artery, and she was started on acetylsalicylic acid 325 mg each day. Because of syncopal episodes associated with third-degree heart block, she had a cardiac pacemaker inserted on July 12, 1988. Syncope did not recur, but she continued to have occasional feelings of lightheadedness. In May 1989, she began experiencing about 10 episodes per week of blurred vision in the right eye, lasting 5 to 20 minutes. Her ophthalmol- PULSELESS DISEASE 243 ogist noted narrowed retinal arterioles in both eyes and visual acuities of 20/60 right, and 20/20 left. The decreased right acuity was attributed to cataract, but eye examination was otherwise normal. There was a left carotid arterial bruit, and no pulses were palpable in either upper extremity. Blood pressure was 80/68 in the left arm and inaudible in the right arm. By October 1989, she also complained of frequent occipital headaches, exercise-induced pain in both shoulders and hands, and jaw pain precipitated by chewing. Arteriography on October 17, 1989 showed complete occlusion of the proximal brachiocephalic (innominate) artery, with numerous costocervical and thyrocervical collaterals partially reconstituting the flow of the right subclavian and right common carotid arteries. The proximal right internal carotid artery showed high-grade stenosis. There was 40-50% stenosis of the origin of left common carotid artery, along with moderate stenosis at the origins of the left subclavian and left vertebral arteries. There was no flow at all in the proximal right vertebral artery, but this was partially restored by distal collaterals. Doppler studies revealed a right brachial systolic blood pressure of 68 mmHg, and oculoplethysmography showed ophthalmic artery pressures of 90 and 68 mmHg on the left and right sides, respectively. Despite anticoagulation with Coumadin, the episodes of visual blurring continued, and an inferior altitudinal visual field defect developed in the right eye. On December 20, 1989, she underwent internal carotid endarterectomy, and postoperatively used acetylsalicylic acid. Vision progressively diminished in both eyes, the episodes of lightheadedness became presyncopal, and she became lethargic and intermittently disoriented. On December 29, 1989, ophthalmic artery pressures were undetectable by oculoplethysmography. On January 23, 1990, the patient was first seen at the Bascom Palmer Eye Institute. Best corrected vision was hand-motions at 2 ft superiorly in the right eye, and 20/200 slowly, with full fingercounting confrontational visual fields in the left eye. The pupil light reactions were sluggish, with a 3+ right relative afferent defect. There was slight iris neovascularization around the right pupillary margin. Gonioscopically, the iridocorneal angles were fully open with no evidence of neovascularization, and applanation intraocular tensions were 4 mmHg bilaterally. Fundus examination revealed retinal pigment epithelium mottling, dot hemorrhages, and microaneurysms scattered throughout both midperipheral retinas, pale optic nerve heads bilaterally, and peripapillary nerve fiber layer in-farcts more prominent in the left eye. There was no disc or retinal neovascularization. Most notable, however, was the appearance of the retinal arterioles. These were narrow, and blood flow was visibly sluggish in both eyes. In the right eye, individual rouleaux of red blood cells could literally be counted as they made their way slowly through peripapillary retinal arterioles. In the left eye, retinal venules were dilated and red blood cell rouleaux were seen (Fig. 1). In either eye, retinal arterioles could be completely collapsed by minimal digital pressure on the globe, and in the right eye simply by having the patient sit up. Pulses were absent in the upper extremities and blood pressures were unobtainable. Pulses were present in the lower extremities, and neurologic examination was otherwise normal. Fluorescein angiography showed a prolonged arm-to-retina time of 24 seconds in the left eye with marked hypoperfusion of the inferotemporal quadrant of the left choroid. The entire right retina was poorly perfused (Fig. 2). No arteriovenous anastomoses were identified. Westergren erythrocyte sedimentation rate (ESR) was elevated at 71 mm/h. A chest radiograph showed mild cardiomegaly and calcification of the aortic arch. The patient was admitted to hospital, anticoagulated with intravenous heparin, and treated with intravenous methylprednisolone 250 mg every 6 hours. She was kept in a supine, slightly headdown position to minimize postural hypoperfusion. While on this regimen, vision improved about 1 Snellen line in the left eye, brachial pulses became faintly palpable bilaterally, and ESR fell to 56 mm/h. Whenever she attempted to sit up, however, visual acuity dropped rapidly in both eyes, and she became very lightheaded and confused. Arteriography demonstrated good patency of the right internal carotid artery, complete occlusion of the brachiocephalic artery, moderate stenosis of the left subclavian artery, and marked stenosis at the origin of the left common carotid artery (Fig. 3). On February 9, 1990, the patient underwent placement of a 14 x 7-m bifurcated knitted Dacron arterial graft, proximally anastomosed end-to-side to the aortic arch proximal to the origin of the brachiocephalic artery, and distally anastomosed endto- end to the brachiocephalic and left common carotid arteries distal to their respective stenotic segments (Fig. 4). She recovered well from the surgery, heparin was discontinued, acetylsalicylic acid 325 mg daily was begun, and steroid dosage was tapered over a 2-week period. JClin Neuro-ophthalmol, Vol. 13, No.4, 1993 244 J. R. LEWIS ET AL. FIG. 1. Preoperative fundus appearance. Left: Narrowed arteriolar tree with rouleaux formation (small arrows) and dilated veins in the right eye. Right: Similar vascular appearance and prominent nerve fiber layer infarcts (large arrows) in the left eye. Four weeks postoperatively, visual acuity was counting fingers at 1 ft in the right eye, and 20/60 in the left eye. There was still a 1+ relative afferent pupillary defect in the right eye. Blood flow was restored in both retinas, with no stasis or red blood cell rouleaux. Nerve fiber layer infarcts, dot hemorrhages, and microaneurysms had resolved (Fig. 5), but there were large patches of chorioretinal atrophy in the midperiphery of the right retina. Blood pressure was 120/80 in the right arm and 70150 in the left arm. On March 8, 1990, intravenous fluorescein angiography revealed an arm-toretina time of 18 seconds in the right eye, with greatly improved perfusion to both retinas (Fig. 6). Five months postoperatively, blood pressure was 115/65 in the right arm, and still inaudible in the left arm but with a palpable systolic pressure of 65 mmHg. Visual acuity was 1/200 in the right eye and 20/50 - 2 in the left with a 1+ right relative afferent pupillary defect. Anterior segment exam- ~ FIG. 2. Preoperative i.ntravenous fluor~scei~ ~ngiography. Left: Retinal and choroidal hypoperfusion in the right eye (82.2 seconds). Right: Delayed laminar filling of venules and poor choroidal perfusion temporal to disc in the left eye (39.2 seconds). JClin Neuro-ophthalmol, Vol. 13, No.4, 1993 PULSELESS DISEASE 245 FIG. 3. Preoperative arteriography demonstrating complete occlusion of brachiocephalic artery (straight arrows) with partial reconstitution distally by collaterals (large arrowhead), and marked stenosis of left common carotid (curved arrow) and left subclavian (small arrowhead) arteries. ination was normal with no rubeosis iridis or cataract, and intraocular tensions by applanation were 11 and 14 mmHg, right and left eyes, respectively. Retinal examination was unremarkable in the left eye. The right disc was diffusely pale with a marked generalized attenuation of the nerve fiber layer, but good arteriolar flow even with moderately firm digital compression in contrast to the posturally induced arteriolar pulsations observed preoperatively. Goldmann visual fields revealed a cecocentral scotoma and inferonasal step in the right eye, and superonasal visual field depression in the left eye. DISCUSSION Pulseless disease is a disorder of unknown etiology, characterized by chronic inflammation of the large arteries arising from the aorta, resulting in stenosis and occasionally ectasia of their lumens. The disorder was probably first recognized in 1839 by Davy (1). Takayasu (8), speaking at the 12th Congress of the Japanese Ophthalmological Society in Fukuoka in 1908, described a 21-year-old woman with a "wreathlike anastomosis surrounding the optic disc at a distance of 2 or 3 mm, surrounded by another circular anastomosis. These were anastomotic shunts of arterioles and venules.... Both the surrounding vessels and their branches had 'lumps' here and there which were seen to move from day to day." Interestingly, he did not mention the patient's pulses. Ohnishi, in a discussion following Takayasu's paper, presented a 23-year-old woman with retinal vessels that were tortuous and irregular, with aneurysmal dilatations in some vessels, others whitened completely, lack of blood vessels in the peripheral retinas, but no arteriovenous anastomoses. His patient had absent radial pulses, cold arms, diminished carotid pulses, and an abnormal appearance of the aortic arch on radiograph (4). Shimizu and Sano (9) introduced the term "pulseless disease." The North American incidence of PD is 2.6 per million per year, with a female-to-male ratio of 9:1 (10). Though there is a predilection for Orientals, PD is documented in all races (11,12), presenting most commonly in the second to fourth decades of life. Ishikawa (13) proposed an age of onset of 40 years or younger as an obligatory criterion for the diagnosis of PD. This is curious, in that 22% of the 96 patients reported in his paper exceeded this Previous ~~gdhatrt~:~~:~dm~ End-la-end anastomosis to / L9tt Common Carotid Art. Stenotic left ,Common Carotid Art. left Subclavian Art. Bifurcated Dacron Graft FIG. 4. Surgical diagram depicting aortobrachiocephalic and aortocarotid bypass. Bifurcated 14 x 7-mm Dacron graft anastomosed end-to-side to aortic arch proximally, and end-to-end to brachiocephalic and left common carotid arteries distally. J Gin Neuro-ophthalmol, Vol. 13, No.4, 1993 246 J. R. LEWIS ET AL. FIG, 5, Four weeks postoperative fundus appearance. Left: Restoration of blood flow with absence of vascular stasis in the right eye. Right: Similar vascular improvement with resolution of nerve fiber layer infarcts in the left eye. age. PO occurs as late as the seventh decade of life (14,15), and in both women and men (1,14). The pathogenesis of PO is unknown, though an autoimmune mechanism has been suggested. Antibodies against arterial wall antigens have been found (10). Coexistent tuberculosis has been common in other studies, but without consideration of the prevalence of tuberculosis in the populations studied (12,16). Furthermore, Mycobacterium tuberculosis has never been isolated from the aorta (16). Numano and associates (17) and Ishikawa (18) re-ported familial cases of Takayasu disease in twin sisters. The female predominance has suggested hormonal influence, and in fact Numano and Shimamoto (19) observed elevated urinary excretion of estrogen in women with PO. Syphilis was once the major disorder to mimic PO (10). Now, the most frequently encountered disorder in the differential diagnosis of PO is arteriosclerosis of the aortic arch and great vessels. Particularly in older individuals presenting with this syndrome, arteriosclerosis may be superim- FIG. 6,. Fo~r wee~s postoperative intraveno~s fluo~e~cei~ angiography. Left: Restoration of retinal and choroidal perfUSion In the nght eye (30.1 seconds). Right: Similar Improvement in the left eye (64.1 seconds). J Clin Neuro-ophthalmol, Vol. 13, No.4, 1993 PULSELESS DISEASE 247 posed upon an underlying inflammatory process, or it may be argued that arteriosclerosis is the sole disease process, without invoking an underlying arteritis. According to Ishikawa (13), the orifices and proximal segments of branches of the aortic arch are very susceptible to arteriosclerosis. However, the return of brachial pulses and symptomatic improvement on corticosteroid treatment, as was observed in our patient, favors a diagnosis of reversible arterial inflammation (11). Giant cell arteritis is usually considered a disease of small and medium-sized arteries, but could conceivably coexist with PD. The two disorders share much in common clinically and histopathologically, but in the elderly patient, giant cell arteritis tends to manifest more fulminant systemic inflammatory symptoms, whereas Takayasu disease in elderly patients lacks the systemic inflammatory prodrome, presenting predominantly with vascular occlusive symptoms (20). Thromboangiitis obliterans (Buerger disease), though pathologically similar, occurs almost always in medium-sized arteries and veins in the legs of men (16). Preocclusive prodromal symptoms of PO may include myalgias, arthralgias, fatigue, fever, sweats, and weight loss. As stenosis of the great vessels progresses, signs and symptoms develop due to upper extremity, cerebral, ocular, myocardial, and renal ischemia. Arm claudication is a frequent manifestation. The slow progression of occlusive disease often allows collateral vessel formation. In proximal carotid artery stenosis, for example, anastomoses from thyrocervical trunk and vertebral artery enlargement often protect the patient from neurologic deficit. As was the case in our patient, syncope has also been reported in association with effort and postural change (6,11). Other systemic manifestations include headache, paresthesias, seizures, systemic hypertension, jaw claudication, anemia, angina, cardiac dysrhythmias, myocardial infarction, transient ischemic attacks, and strokes (10). Physical signs may include pulselessness in one or both arms, a difference in blood pressure between the two arms, very low or unobtainable blood pressure in one or both arms, carotid artery tenderness, carotid or subclavian artery bruits, and murmur of aortic valve regurgitation (11). Ophthalmologic manifestations are late occurrences in the course of PD. Patients may complain of transient visual obscuration or blurring upon assuming an erect posture (7) and, as demonstrated by the present case, this visual loss may persist until the patient resumes the supine position. Retinal findings in patients with PO imply high-grade vascular compromise of intracranial vessels (21). Hirose (2) reported the following funduscopic changes in Takayasu disease: dilatation, tortuosity and/or irregular diameter of central retinal blood vessels, abnormal blood flow, metamorphosis of retinal vessels into white lines, perivascular inflammatory changes, and intraretinal hemorrhages. Hirose (4) also described the dynamic fundus appearance which occurs due to the diminution of regional blood flow: "faint shadows running through the vein centripetally," and "vague shadows [in the artery] pass quickly in a centrifugal direction." As the condition progresses, blood clumps and stagnates. Didier and associates (7) studied the retinopathy of Takayasu disease using intravenous fluorescein angiography. Microaneurysms, formed by saccular or fusiform dilatation of precapillary arterioles and postcapillary venules, were found throughout the retina and were more numerous than has generally been observed in diabetic retinopathy. Arteriovenous anastomoses presented first in the retinal periphery and, with time, advanced toward the posterior pole. Retina peripheral to these shunts was nonperfused. Tanaka and Shimizu (5), using rapid-sequence intravenous fluorescein angiography, identified retinal arteriovenous shunts in the midperiphery of 24 eyes in 12 patients, all with advanced stages of PD. These were inconspicuous on funduscopy. The elaborate wreathlike peripapillary arteriovenous shunts described by Takayasu have turned out to be an unusual finding. On fluorescein angiography, arm-to-retina circulation time in Takayasu disease is prolonged to 20 seconds or more, and complete retinal arteriolar filling may take as long as 30 seconds from injection (6). Late ophthalmologic complications of PO can include vitreous hemorrhage, secondary cataract, rubeosis iridis with neovascular glaucoma, and anterior segment ischemia, which can become fulminant to the point of mydriasis, anterior uveitis, orbital pain, profound loss of vision, hypotony and phthisis bulbi (7). Elevation of ESR has been noted in 78% (11) to 84% (10) of patients. As in our patient (71 mmlh), this elevation tends to be modest in patients over the age of 40 (15). Leukocytosis and thrombocytosis have been reported. Elevated circulating immune complexes (22), IgG, gamma globulin, and anti-streptolysin-O titer, as well as abnormal serum complement C'3 and C'4 levels (20), have been observed. These findings support an autoimmune etiology, but have not proven clinically useful. I Clin Neuro-ophthllimol, Vol. 13, No.4, 1993 248 J. R. LEWIS ET AL. Chest radiographic findings have included mediastinum and aortic knob widening, thoracic aorta irregularity, and calcification of the aorta. Arteriography demonstrates stenosis of the great vessels, beginning near their origins from the aortic arch. Duplex Doppler ultrasound may allow progression and regression of stenosis to be followed noninvasively (20). The natural history of PO is variable and uncertain, and therefore treatment remains controversial. Many cases have demonstrated lowering of the ESR, return of pulses and symptomatic improvement on systemic corticosteroids. Anticoagulation has also been employed. One case demonstrated angiographic regression of carotid stenosis after 32 months of steroid and warfarin (23). Of the 32 patients reported by Hall and associates (11), 29 received steroids, and 13 were able to discontinue them eventually. A decrease in ESR occurred in all the steroid-treated patients, and this correlated with a decrease in inflammatory symptoms; 9%, however, also required immunosuppressives, such as azathioprine or cyclophosphamide. In a case reported by Tanaka and Shimizu (5), in whom the disease was advanced with moderate retinopathy, steroid treatment resulted in an improvement of arm-to-retina circulation time from 24 to 18 seconds. Despite this, the patient developed progressive retinopathy with disc neovascularization, large areas of retinal capillary nonperfusion, and diminishing visual acuity. Reed and associates (20) reported a 54-year-old Caucasian woman with Takayasu disease in whom fever, arm claudication, and hypertension all improved within a month on high-dose prednisone. There have been no controlled studies to prove or disprove the long-term efficacy of these treatments. Surgical procedures have included endarterectomy, saphenous vein and Dacron aortoarterial bypass grafts, extracranial-intracranial bypass grafts, aneurysm resection, aortic valve replacement, patch grafts for aneurysms, and nephrectomies for intractable renovascular hypertension. Successful transluminal balloon angioplasty of left subclavian and left common carotid arteries has also been reported (24). Robbs and associates (12) described the use of bifurcated Dacron grafts anastomosed end-to-side to the ascending aorta, and then endto- end to various combinations of neck arteries with excision of diseased arterial segments and oversewing of the proximal ends of the arteries. Because of concerns that performing surgery during the active phase of PO could result in graft occlusion, anastomotic breakdown, or aneurysm formation, most patients have received a course of JClin Neuro-ophthalmol, Vol. 13, No.4, 1993 corticosteroids to control active inflammation preoperatively, and the grafts have generally worked well. In a series of 30 surgically treated patients reported by Takagi and associates (25), 26 patients (ages 5 to 47 years) were alive, and 23 had good function of their reconstructed arteries, with postoperative follow-up of at least 10 years in all cases. They reported one patient still doing well 24 years after having a bypass graft placed from the aorta to the left internal carotid artery. In their carotid reconstruction cases, they noted improvement of visual disturbances, relief of syncopal attacks, and disappearance of retinal microaneurysms. In a 38year- old woman with stenosis of all four cervical vessel systems due to Takayasu disease, Didier and associates (7) reported improved visual acuity, decreased arm-to-retina circulation time, disappearance of microaneurysms, and focal "chorioretinal atrophy" following placement of a bifurcating graft from aorta to both common carotid arteries. Untreated, PO has been found to run a chronic, progressive course. Ishikawa (18) identified four poor prognostic factors for survival: hypotensive ischemic retinopathy, hypertension from renal artery stenosis, aortic regurgitation, and aortic or arterial aneurysms. The event-free lO-year survival rate in the absence of any of these manifestations was 97%. In the presence of one or more of these, 10-year event-free survival dropped to 59%. Reports of symptomatic improvement on steroid treatment have varied from 20 to 100% (26). 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