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TAO AND CTAO AS DISTINCTIVE ENTITIES/fl;7/«- et al. 1: 5-9, 1945 19. Davis HA, King LD: A comparative study of thromboangiitis obliterans in white and negro patients. Surg Gyn Obst 85: 597-603, 1947 20. Jones WM, Jones CDP: Buerger's disease in women. A report of a case and a review of the literature. Angiology 24: 675-689, 1973 21. Goodman RM, Elian B, Mozes M, Deutsch V: Buerger's disease in Israel. Am J Med 39: 601-615, 1965 22. Craven JL, Cotton RC: Haematological differences between thromboangiitis obliterans and atherosclerosis. Br J Surg 54, 862-867, 1967 23. Abramson DI: Diagnosis and treatment of thromboangiitis obliterans. Geriatrics 20: 28-41, 1965 24. Mozes M, Cahanski G, Doitsch V, Adar R: The association of 25. 26. 27. 28. 689 atherosclerosis and Buerger's disease. A clinical and radiological study. J Cardiovasc Surg (Torino) 11: 52-59, 1970 Scheinker IM: Cerebral thromboangiiitis obliterans: Histogcnesis of early lesions. Arch Neurol Psych 52: 27-37, 1944 Denny-Brown D, Romanul FC, VanDen Noort S, Drachman DB: The problem of cerebral thromboangiitis obliterans (Winiwarter-Buerger disease). Trans Amer Neurol Assoc 85: 203-204, 1960 McLoughlin GA, Helsby CR, Evans CC, Chapman DM: Association of HLA-A9 and HLA-B5 with Bucrger's disease. Br Med J 2: 1165-1166, 1976 Gulati SM, Singh KS, Thusoo TK, Saha K: Immunological studies in thromboangiitis obliterans (Buerger's disease) J Surg Res 27: 287-293, 1979 Iatrogenic Carotid Cavernous Sinus Syndrome Downloaded from http://stroke.ahajournals.org/ by guest on May 7, 2017 M I C H A E L G. HUMMER, M . D . , A N D THOMAS J. C A R L O W , M.D. SUMMARY A hemodlalysls shunt site, subclavian artery to internal jugular rein, resulted in a "pseudo" cavernous sinus syndrome. Recognition of this rare iatrogenic complication may assist in selecting other shunt sites and prevent potential visual loss and multiple surgical procedures. Stroke, Vol 12, No 5, 1981 THE FULLY DEVELOPED clinical picture of a carotid cavernous sinus fistula (CCF) is not a diagnostic dilemma. These vascular malformations commonly are either traumatic or spontaneous.1 This report is of a iatrogenic instance with clinical signs and symptoms of a carotid cavernous sinus syndrome following a subclavian artery to internal jugular vein shunt. History A 62-year-old right-handed man had received 6 years of hemodialysis treatment for membranous glomerulonephritis. Multiple episodes of thrombophlebitis eventually consumed all common sites for peripheral hemodialysis fistulas. Renal transplantation was unsuccessful. Since all peripheral shunt sites had failed, a left subclavian artery to left internal jugular vein shunt was selected. Within three weeks after the anastomosis, he experienced holocephalic headaches and mild generalized weakness, worse on his right side. A slow but progressive reddening of his left eye was noted. He denied diplopia, subjective bruit, pain and decreased visual acuity. Neurological examination documented a mild but distinct pronation drift of the right arm without tendon reflex asymmetry. Ophthalmologic examination revealed a marked dilation and arterialization of the left conjunctival vessels and 2 mm of left proptosis From the Veterans Administration Medical Center, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM 87108. Reprints: Dr. Carlow, VA Medical Center, Neuro-Ophthalmology Laboratory, Bldg. 13, 2100 Ridgecrest SE, Albuquerque, NM 87108. (fig. 1). An ocular bruit was not heard and both globes were neither tender nor pulsating (utilizing a Schi^tz tonometer). Visual acuity was correctable to 20/25 on the right and 20/20 on the left. Pupils were 4 mm bilaterally and equally responsive to light and accomodation. Applanation tonometry readings were 12 mm Hg on the right and 10 mm Hg on the left. Vergence, version and duction extraocular movements were normal. Fundus examination showed mild dilation of the left retinal veins. Abnormal laboratory studies included: BUN 64 mg/dl, creatinine 8.5 mg/dl, total protein 5.4 gm/dl, albumin 2.9 gm/dl, prothrombin time 25.7 seconds (control 11.8) and partial thromboplastin time 67.3 seconds (normal less than 40 seconds). Urinalysis revealed a specific gravity of 1.017, 2+ glucose, 3+ protein, 2-6 wbc/hpf, and 1-3 casts/lpf. An EEG showed slowing and decreased amplitude over the left frontal area. The CT scan suggested a left frontal chronic subdural hematoma. Within a week after the subdural was evacuated the right sided weakness and the EEG improved markedly. A left carotid arteriogram, after removal of the subdural hematoma, showed slow arterial filling of the left cerebral hemisphere with all venous drainage from that side via the right transverse sinus and right internal jugular vein. A left subclavian arteriogram documented left cavernous sinus arterialization from retrograde flow in the left internal jugular vein, transverse sinus and petrosal sinus. Blood flow was from the shunt into the left carotid cavernous sinus (fig. 2). Since venous drainage from the left cerebral hemisphere occurred through the right internal jugular vein, the left internal jugular vein was ligated above the fistula. Two months later the patient was symptom STROKE VOL. 12, No 5, SEPTEMBER-OCTOBER 1981 FIGURE 1. Iatrogenic carotid cavernous fistula syndrome. The left conjunctival vessels are engorged and distended (arrow) compared to the right normal conjunctival vasculature. free and the injection in his left eye, proptosis and retinal signs had resolved. He was maintained on home peritoneal dialysis. Discussion Downloaded from http://stroke.ahajournals.org/ by guest on May 7, 2017 This patient's constellation of symptoms and signs are similar to those of the classical carotid cavernous sinus fistula syndrome. Since the vascular shunt was not in the cavernous sinus but at a more distal site, the term "pseudo" carotid cavernous sinus syndrome seems appropriate. Cavernous sinus arteriovenous communications in- elude direct carotid cavernous fistulas (CCF) and dural meningeal shunts.1 A CCF was first described by Benjamin Tavers in 1811.1 He diagnosed a pulsating exophthalmos as an arteriovenous fistula and treated the CCF by ligating the common carotid artery. CCF's can be divided into 3 types: spontaneous (25%), traumatic (75%)' and iatrogenic. The fully developed CCF syndrome includes: ocular bruit (75%), pulsating exophthalmos (69%), diplopia (24%), conjunctival chemosis (36%), orbital pain (16%), and, less frequently, dilated and arterialized conjunctival vessels, decreased visual acuity, headache and increased intraocular pressure.* Angiographic delineation with magnification and subtraction techniques can differentiate and delineate the involved vessels. Iatrogenic causes have been described following percutaneous retrogasserian procedures,' secondary to transsphenoidal surgery* or Fogarty catheter carotid thromboendarterectomy.7> 8 The iatrogenic CCF documented here has not been previously reported. The pathogenesis and treatment of CCF are beyond the scope of this report but several excellent articles and reviews are available.*110 A fistula may disappear spontaneously in 5 to 10 percent of patients.11- " Balloon-catheter techniques1'1" and thrombotic methods'- " that preserve the carotid circulation appear to be highly satisfactory alternatives to entrapment procedures. The primary surgical objective is to prevent hypoxic ocular sequelae with attendant visual loss.16 Recognition of the potential complication of a subclavian artery to internal jugular vein shunt may help to eliminate this locale as a possible hemodialysis shunt site. Prompt surgical correction can prevent visual loss. References FIGURE 2. Left subclavian artery to left internal jugular surgical shunt. (S = shunt. IJ = internal jugular vein, EJ = external jugular vein, I = innominate vein, closed arrow = proximal end of shunt, open arrow = distal end of shunt, asterisk = tip of transfemoral catheter). 1. Glaser JS: Neuro-Ophthalmology, Hagerstown, Harper and Row, pp 336-338, 1978 2. Tavers BA: A case of aneurysm by anastomosis in the orbit, cured by ligation of the common carotid artery. Trans Med Clin 2: 1-16, 1811 3. Parsons TC, Guller EJ, Wolff HG, Dunbar HS: Cerebral angiography in carotid cavernous communications. Neurology (Minneap) 4: 65-68, 1954 4. Sanders MD, Hoyt WF: Hypoxic ocular sequelae of carotid cavernous fistula. Study of the causes of visual failure before and after neurosurgical treatment in a series of 25 cases. Br J Ophthalmol 53: 82-97, 1969 5. Sekhar LN, Heros RC, Kerber CW: Carotid cavernous fistula following percutaneous retrogasserian procedures. Report of two cases. J Neurosurg 51: 700-706, 1979 6. Takahashi M, KillefTer F, Wilson G: Iatrogenic carotid cavern- IATROGENIC CAROTID CAVERNOUS SINUS SYNDROME/Hummer and Carlo* ou3 fistula; case report. J Neurosurg 30: 498-500, 1969 7. Barker WF, Stern WE, Krayenbuhl H, Senning A: Carotid endarterectomy complicated by carotid cavernous sinus fistula. Ann Surg 167: 568-572, 1968 8. David JC, Richardson R: Distal internal carotid thromboembolectomy using a Fogarty catheter in total occlusion: technical note. J Neurosurg 27: 171-177, 1967 9. Mullan S: Treatment of carotid cavernous fistulas by cavernous sinus occlusion. J Neurosurg 50: 131-144, 1979 10. Hosobuchi Y: Carotid cavernous fistula. In Wilson CB, Hoff JT (eds) Current Surgical Management of Neurologic Disease. New York, Churchill Livingstone, pp 169-181, 1980 11. Potter JM: Carotid cavernous fistula: Five cases with "spon- 691 taneous" recovery. Br Med J 2: 786-788, 1954 12. Dandy WE: The treatment of carotid cavernous arteriovenous aneurysms. Ann Surg 102: 916-926, 1935 13. Serbinenko FA: Balloon catheterization and occlusion of major cerebral vessels. J Neurosurg 41: 125-145, 1974 14. Debrun G, Lacour P, Caron J-P et al: Detachable balloon and calibrated-leak balloon techniques in the treatment of cerebral vascular lesions. J Neurosurg 49: 635-649, 1978 15. Hosobuchi Y: Electrothrombosis of carotid cavernous fistula. J Neurosurg 42: 76-85, 1975 16. Spencer WH, Thompson HS, Hoyt WF: Ischaemic ocular necrosis from carotid-cavernous fistula. Br J Ophthalmol 57: 145-152. 1973 Transient Vertical Monocular Hemianopsia with Anomalous Retinal Artery Branching Downloaded from http://stroke.ahajournals.org/ by guest on May 7, 2017 E D W A R D R. W O L P O W , M . D . AND RICHARD G. L U P T O N SUMMARY A 62-year-old man reported 6 stereotyped attacks of transient loss of vision in the lateral visual field of the right eye and was subsequently found to hare right internal carotid artery occlusion. Fundoscopy revealed an anomalous central retinal artery branching whereby a single stem vessel supplied the superior and inferior nasal quadrants of the retina. Circulatory Insufficiency in this anomalous stem could explain the occurrence of vertical monocular bemianopsia as an unusual manifestation of ipsilateral carotid artery atherosclerosis. Stroke, Vol 12, No 5, 1981 TRANSIENT monocular blindness as an indicator of ipsilateral internal carotid artery atheroma was first emphasized by Fisher.1 When the transient blindness is not total, a horizontal hemianopsia or a quadrantanopsia is most often reported by the patient.* This is consistent with the usual pattern of arterial supply to the retina whereby a single superior and inferior branch of the central retinal artery supplies a territory above and below the optic disc. This patient presents an instance of vertical monocular hemianopsia that may have been due to an appropriate retinal vascular anomaly. In such a patient, description of a vertical monocular hemianopsia might be interpreted by the physician to represent a misreporting of a homonymous hemianopsia. Report of the Patient With no previous history of retinal or cerebral vascular disease, a 61-year-old hypertensive man described 2 spells per day for 3 consecutive days of loss of vision in the temporal half visual field of the right eye lasting about one minute each time. He had been careful to cover each eye separately and was quite certain the field loss was as reported. Hospitalization was advised but he put this off for 11 months. During this time there were no transient or permanent retinal or cerebral attacks. Examination of the right ocular fundus (fig.) showed an anomalous retinal arteriolar pattern whereby a single common From the Division of Neurology, Mt. Auburn Hospital, Cambridge, MA 02138. stem bifurcated (arrow) to supply the superior and inferior nasal quadrants. The temporal quadrants were supplied in the usual fashion and the vascular pattern of the left ocular fundus was normal. No embolic material was noted. Transfemoral angiography showed total occlusion of the right internal carotid artery just distal to its origin. Blunting of the stump suggested an old occlusion. Discussion Transient monocular vertical hemianopsia has been described only rarely2-' and an adequate explanation for it has not been provided. Permanent monocular vertical hemianopsia has been reported as an uncommon result of emboli to the superior and inferior retinal artery branches on the same side of the retina.4 The basic anatomical pattern of division of the central retinal artery into a superior and an inferior retinal artery is only rarely anomalous and global, altitudinal or quadrantic field loss is to be expected. There is variation as to where, in relation to the optic disc, the division into a superior and an inferior retinal artery branch occurs.8 Single instances have been reported in asymptomatic individuals where one central retinal artery branch divides to supply the superior and the inferior nasal or temporal half of the retina.'"8 The only large-scale search for such anatomical variations was undertaken by Awan9 who found, on examining the eyes of 2100 people, that the temporal half-retina was supplied by a single branching artery in 19 eyes and the nasal half-retina Iatrogenic carotid cavernous sinus syndrome. M G Hummer and T J Carlow Stroke. 1981;12:689-691 doi: 10.1161/01.STR.12.5.689 Downloaded from http://stroke.ahajournals.org/ by guest on May 7, 2017 Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1981 American Heart Association, Inc. All rights reserved. Print ISSN: 0039-2499. 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