Journal of Neuro-Ophthalmology, June 1982, Volume 2, Issue 2

Venous stasis retinopathy associated with embolic obstruction of the central retinal artery.

A case of venous stasis retinopathy in a 58-year-old male is reported. Despite carotid endarterectomy for ipsilateral internal carotid atheromatous disease, the retinopathy persisted until the embolic obstruction of the central retinal artery resolved spontaneously. Then the venous stasis retinopathy was relieved. In patients with venous stasis retinopathy and reduced arterial pressure that cannot be attributed to carotid disease, an occult but hemodynamically significant arterial obstruction posterior to or at the lamina cribrosa may be suggested.

J. Clin. Neuw-vphth.,/moJ. 2: 113-lltl, 1082. Venous Stasis Retinopathy Associated with Embolic Obstruction of the Central Retinal Artery* LARRY E. MAGARGAL, M.D. GEORGE E. SANBORN, M.D. ALBERT ZIMMERMAN, M.D. Abstract A case of venous stasis retinopathy in a 58-year.old male is reported. Despite carotid endarterectomy for ipsilateral internal carotid atheromatous disease, the retinopathy persisted until the embolic obstruction of the central retinal artery resolved spontaneously. Then the venous stasis retinopathy was relieved. In patients with venous stasis retinopathy and reduced arterial pressure that cannot be attributed to carotid disease. an occult but hemodynamically significant arterial obstruction posterior to or at the lamina cribrosa may be suggested, Introduction Venous stasis retinopathy can be a manifestation of central retinal arterial insufficiency due to ca­rotid obstruction, central retinal venous obstruc­tion. or intravascular hyperviscosity conditions. The history of a 58-year-old male presenting with an embolus that produced partial obstruction of the central retinal artery and concomitant venous stasis retinopathy is presented. The p.atient, who was found to have ipsililteral intern.al cMotid .ath­eromatous disease, subsequently underwent Cil­rotid endilrterectomy. However, the venous stasis retinopathy persisted until the embolic obstruction of the centril! retinal .artery WilS spontilneously relieved. This case suggests th.lt venous stasis ret­inopathy can develop second.ary to .In Mteri.al ob­struction anywhere in the ilfferent system from the heart to the optic disc. The relationship of venous stilsis retinopilthy 10 underlying carotid occlusive dise.:lse w.1S initiJlly described by Hedges in 19b2' and n.JOled by Kearns and Hollenhorst iI year l.:lter.~ Although the From the Retina VasculM Unit, R,"in., <",·rv,,'(·. Wdl, (y,. H,,,· pital, Thomas Jefferson Unlv('''''Y, I'hd.IJ,·lp)ll.,. I'enn>vlv~",.,. • Presented at the Tt"nth Ret,nJI CU"/"fI·'''''·. Fu"du' M.lllt!',·,· tations of Neurologic Di't"~"·' Will, [y.. Hu,pit"I, Th,'m." Jefferson UnIversity. September 15. IQ7Q. June 1982 carotid bifurcation is probably the most common site of obstruction, hemodynamically equivalent lesions located anywhere from the he.:lrt to the optic disc probably can produce chronic central retinal artery insufficiency. This arterial insuffi­ciency may manifest clinically as venous stasis retinopathy. We present a case with atheromatous internal carotid artery disease, embolization result­ing in incomplete obstruction of the central retinal artery, and hypoperfusion venous stasis. The ob­servation that the venous stasis retinopathy per­sisted following carotid endarterectomy but re­solved following dislodgement of the embolus sug­gests thilt the venous stasis in this case was related to embolic arterial obstruction ilt the optic disc. We believe this is the first description of such an association. Case Report A 58-year-old white male was initl.:llly seen in consultation on March II. 1976, with d historv of blu rred vision in the left eye of several mo~ths duration. His medical history revealed systemic hypertension of 25-years dur.ltion. He denied Jnv signs or symptoms consistent with pril)f episodes of am.lurosis fug.lx or transient cerebr.11 i chemi.1. His ViSU.11 .lCuity W.1S :!.O/:!.O in the right eye .1nd 20/30 in the left eye. The intr.lOcul.Jr pre~~ure \VJS 20 mm of mercury in Nch eye. Systl:'mic bllllld pressure W.:lS 150/80 mOl llf mercury. Examin.ltion of thl:' left f>ye reve.lled .In .lthf>rom.ltous plaque at the bifurc,ltion of the centr.ll retin.ll .lrtery lln the optic disc (Fig. I) .lnd tn.lrl-ed (llll.ltcr.ll vessels. TIl(' retin.ll veins were dil.lted .lIld t0rtllllUS with ('o.lfsening of llw perip.lpill.Hy c.lpill.uies. _(.It­tered dot-.lIld-bllll retin.ll henwrrh.lg<>s I,vere presenl in the midpl'riphery of the fundus (Fig. :!). The c.Hlllid pulses were 11l1rm.ll and no bruits were detl>cted by .IUScult.ltion, The ophth.:llmodyn.l­mometry re.ldings were nllrm.ll in the right eye (47/100) but were signific.lntly depressed in the left eye (10/15), These re<ldings were performed with J Bailli.ut-type instrument and are not cor- 113 Figure J. Left eye with .therom.tous pl.que Involv,ng the cent,,1 relln.ta"erv .nd e,tendlng ,nlo the supern....1b"nch retln.I."ery. Anero.1 collate,,1 ves els He present The ,nferona..1 branch retinal ve,n IS sl,ghtly megular ,n caliber rrcted for intraocul.H pressure, Intr.lv('nous fluor('scein .lngi~lgr"phy (Figs. 3d .lnd 3/'» r('vl'.lled J l-Iightly d('l.lyrd .lrm·t~l-r('tinJ circul.ltion liml' ~,f HI sl'Clmds, rdpid filling of Ih(' .!flni••1coll.ltt'r.lls, dl'IJy('d Mtl'riJI v('nous trdn­.., I limt', fu .. if,'rm ~l'••dlng "f lhe r!'linJI vrnul!'s, cOdrsening of the retinal capillaries, scattered mi­croaneurysms, and blocked fluorescence in areas corresponding to retinal hemorrhage (Fig. 4) . Thorough neurologic evaluation, including ca­rotid angiography, revealed an ulcerative plaque involving the proximal portion of the left internal Journal of Clinka] euro-ophthalmology la' (b) Figurt' 3. Artt'ridl fillin~ phdSf' f.:l} Jnd (".lrly l.lnlC'll.u v('m)u'" ph.l~l' tl,) ""f tlw t'1Ulll"l'..,t l'lIl cln~ioJ!r:r",m demon tratin~ c'XtcnMVC ~rt('riJI t ~~II.u("r..lll" byp"~""n~ ('mb",llu...\I di..~. carotid artery (Fig. 5). On M.Hch 19, 1976, the patient underwent an uncomplic<lted left c<lrotid endarterectomy. The carotid <lrtery lumen W.lS found to be <lpproxim<ltely 40%-50% obstructed .It the time of surgery. Eight days after cdrotid end­arterectomy, the p<ltient's visual acuity rem.lined 20/30 in the left eye. Repe<lt fluorescein .lngiogra- June 1982 phy showed .1 ~lightly impnwed .1rI11-tll-rC'tinJ cir­(" ulJtion tillle of 15 sC'("ond~: howC'ver, the fe.llures of Venl)lIS t.1sis pl'rsisted. Repeat ophth.llmodyn­. lmometry me.1surements were .1150 unchanged. On follow-up ex.lmin.ltion 7 months I,lter (October 12, 1976), thC' visu,11 .lcuity in the left eye remained 20/30; th<> <>mbolus .1I1d venous st.lsis retinop<lthy 115 Figure 4. RecorculJt,on ph.5r "f fluoresceon Jnl\lO~r.m ,n m,drr"phrrv 5hl.w,n!\ m,ld c,lrilLJry llonprrfuSlon. b(>Jdin~ uf veilsC:'1 WJIII(,. Jnd mIUOJn(>urv..m<. fi~un.· 5. <. .1nltld .1rh"rhl~roHll ...h\n\·II\~ Ih)(htl·Ih.~lh:- uh.l~r~HI\·l· rl.h-lUe" ~.\f tht IH\'\II1l.l1 Inlt:rn.ll \,lr,.t1J .uh.'r\' .ll'p<·,lr("J <'~~('lIli,llly unl'h.Hl~('d. H,'w,'v,'r. "II M.m hiS, "177, I W.1f .ltl..r l·.lwlid ~lIr~ery, lhe VI'u.d .1l11l1y III thl' Idt ,'V,' l1.1d illlprlwed I" 20/20. J UlllllI~' "I'i.. ,-,\.1111';1,111<'" .It lh.ll lime ·.I1",,'..d 111.11 1111' ,,1.1<1'1<' h.ld dl~.ll'l',·.H('d .ll1d thE' Vl'n,'u~ ~tolsis retinopathy had resolved (Fig. 6). Ophlhollmodynamometry values were normal and ~ymmf'tricdl with the opposite eye. This eye has m.lint,lined tholt visual acuity without evidence of relinopdthy for 4 yeJrs. loumdl of Clinical Nl'uro-ophthalmology Fi~ure 6. Ldt ~y~ showln~ disdpp<'dfJn ~ of Jth~romJt{lUS pldqu,' I V".If .,tlN millJI pr~S~nIJlion R~~r~ssion "f th~ drt~ridl d", c"lIdt~rJI< dnd venous SldSIS 1& nOw evident. Discussion Venous stasis retinopathy, a described by Keams and Hollenhorst/ is characterized by an Insidious onset. diminution, or absence of venous pulsations, dilated and tortuous retinal veins, pe­ripheral microaneurysms, and small blossom­shaped retinal hemorrhages. It has been related to occlusion or severe (90% or greater) steno i of the ipsilateral internal carotid artery resulting in oph­thalmic artery insufficiency. In contrast, according to Hayreh and associates, I venous stasis retinopa­thy can be produced experimentally by complete obstruction of the central retinal vein as it surfaces from the optic nerve posterior to the lamin.:! cri­brosa. Features of an ischemic central retin.11 vein obstruction (hemorrhagic retinopathy) were only obserVed when both the central retinal vein .lOd Ihe central retinal artery were occluded simuJt,l­neously. In our review of central retin.:!1 v<'in ob. trllcti,'n~, we found a continuum of clini al Jnd Jn~ill~r.lphi, features, which vdried from hyp('rp('rm('.lbl(' p.lt­terns with basically intact retin,ll capillari('s 10 i~· chemic patterns exhibiting ext('n~ive zones of ".11'­illary nonperfusion:' The retinJI circIII.ltion W.I~ severely impaired in cases of ischemic c<'ntr.ll r<,t· inal vein obstruction more Ih,ln in CJS<'. with .1 hyperperrneable pattern. Histop.:!th(llo~ic studies indicate that the site of venous obstruction i usu­ally in the region of the laminJ cribrll..1 where arterial disease may produce compr<'ssi'1I1 of the companion central retinal v<'in wilhin their om- June 1982 mon adventitidl sheath." Therefore, it would eem thai arteridl disedse is probably a common precur­sor t venous thrombosis. However, sll1ce hyper­viscosity state can produce f('Jture of venous stasis in the dbsence of clinically detectable arteriJI di ease, venous stasis may be 'the result of other underlying mech.lOisms. . This C<1se illustrates that intra-arteriJI obstruc­tion <11. or just <1nterior to. the lamina crib rosa C<1n produce reduced retinJI arterial pre sure .lOd, in fa t, can result in venous stasis retin(lpathy, Ve­nous obstruction due to drteriJI n~mpressi,'n is an unlikely mechJnism in this c.:tse. bl"CdUSl" the ve­nous St.ISIS did not re.I,lve .IS .1 result "f c"lIJter­.1Iiz. ltion .Hound the site of obstrucli'lI1. Insle.ld. it impnw('d f,'lIowin~ pJ'S.I~E' "f Ih(' ('mb"lic "b­slru..- ti,'n. There 1V.IS no cllnic.ll or I.,b,'r.lt"rv ('\'1­denc(' "f .1Il lIndl'r1yinl' hyper"i"-,',it,, c,'ndili"n. The V('n(IUS SldSis IV.IS ,liSt, .lpr.Hently not the result "f th(' underlyin~ c.ln'Iid ,'bstn.....tlon. since II IV.'~ (wi r('lieved f,'II,'win~ ".H"tid end­. lrt<·r('ct<lIny·' In f., ..t. .111 inl('rtl.11 c.H,'tid "bstruc­ti,' n "f 40% t" SO% w""ld l'l' IInlikd\' t" prl,duc(' ..ignific.1I11 ,'phlh.llmi.. .lflt'ry p"rf"si"n insuffi­eil ·ncy. nin,,-t Mtni.11 Prt'~~lIrt' n·,-,'rdll1~s durin~ sur~ic.11 pn'n'd"n'~ th.lt ,'cclude thl' inlernJI (oJ­wtid h.lV(, ~Iwwn th.lt little. if Jny, pressure reduc­IiI'" l'ccurs dislJI t" .1 stl'lwsis l,f 010% t" 50%. and th.lt no hem"t.!yn.lmi..-.llly signifi..-.lI1t pressure re­ducti,' n occurs until .111 "bstru ti,m of approxi­m.' tdy 80% is re.lLhed.~ This supports clinical ob­s(' rv.ltiol1s Ih.:tl venous sl.lsis rl'tinl'pathy in carotid 117 .Htl?ry disl'.ISl' is seen only with Sl?Vl're (90% or nwre) stellllsis llf the internal CJrotid artery.H In •lddition, .llthllu~h the preoperativl' ophth<llmo­dyn. lIlH)ll1l'tric ll1eJsurl'ml'nts WNl' consistl'nt with .1 signific.mt reduction in retinJI Mtl'ry pressure, they did nllt improve following l'ncl.uterectomy sur~ery, but Wl'rl' normJI Jfter thl' l'mbolic ob­struction r('solved. On rl'Ct'nt ev,lluJtion, 5 ye.us Jfter his end­JrlCrel'tllmy, the p.ltient hdd not experil'nced any symphlms of olm.lurosis fugdx, other trdnsient is­chemic l'pisodl's, or recurrence of the venous stdsis rctinop.lthy. The dngiogrdphic studies, ophthal­modyn. lmometric measurements, (lnd clinical course in this case suggest thdt venous stasis reti­nopJthy coln be due to reduction of arterial pressure anterior to the Idmind cribrosd. In patients with venous stdsis retinopdthy, drteridl disc collaterals, dnd reduced arterial pressure that cannot be attrib­uted to cdrotid disease, dn occult but hemodyndm­iCdlly significant drterial obstruction at, or iust posterior to, the Idmina cribrosa may be present. References I. Hedgf?s, T.R., Ophthalmoscopic findings in internal carotid occlusion. Bull. Hopkins Hasp. 3: 89-97, 19b2. 2. Kearns, T.P., and Hollenhorst, R.W., Venous st<lsis retinop<lthy of occlusive dise<lse of the c.lrotid .lrtery. Proc. M<lYo Clin. 38: 304-312, 1963 3. H<lyreh, 5.5., Van Heuven, W.A.J., and Hayreh, M.5.: Experimental rf?tinal vascular oc~luslOn. l. P<lthogenesis of central retinal vein occlUSion. Arch. Ophthdlmol. 96: 31'1-323, 1978. 4. Mdgdrgal, L.E., Brown, C.C, Augsburger, !.].. and P<lrrish, R.K.: Neovdscular glaucomd followmg cen, tral retinal vein obstruction. Ophth,Jlmology 88: 1095-1101, 198!. 5. reen, W.R., Chan, CC, Hutchins. C.M., <lnd Terry. I.M., Central retindl vein occlusion: A prospective histup..thologic..l study of 25 f?yes in 28 Cdses. Retin.. I: 27-55, 198!. b. Neupert, ].R., Brubdker. R.F., Kearns, T.P., and Sundt, T.M., R.. pid resolution of venous stasis reti­nopdthy <lfter carotid endarterectomy. Am. f. Oph­thJ/ mol. 81: 600-602, 1978. 7. R.. nd, R. W.: Retinal <lrterial pressure studies asso­Ciated with cervic<ll carotid artery occlusion in the treatment of cerebral <lneurysms. Bull. Los Angeles Neural. Soc. 21: 175-187, 1956. 8. Kearns, T.P., Siekert, R.C., <lnd Sundt, T.M.: The ocular aspects of carotid artery bypass surgery. Tr,lns. Am. Ophth,llmol. Soc. 247-265. 1978. Acknowledgments This study W,lS supported in p.. rt by the Retina Re­sf? arch and Development Foundation, <lnd the Pennsyl­vanid Lions Sight Conservation Eye Research Founda­tion, Inc., Philadelphia. PennsylvAnia. Write for rf?prints to: LHry E. M<lg<lrg<lI, M.D., Retina Vascular Unit, Wills Eye Hospital. • 'jnth and Walnut Streets, Philadelphia, Pennsylvania 19107. Journal of Clinic<ll Neuro-ophthalmology