Dural arteriovenous and spontaneous choroidal · arteriovenous fistula. Alow-flow dural fistula was thought to be more likely than a conventional high-flow carotid-cavernous fistula

British Journal of Ophthalmology, 1978, 62, 483490

Dural arteriovenous fistula and spontaneouschoroidal detachment: new cause of an old diseaseJOHN W. HARBISON, DUPONT GUERRY, AND HERBERT WIESINGERFrom the Departments of Neurology and Ophthalmology, Medical College of Virginia, USA

SUMMARY A case is presented in which bilateral spontaneous choroidal detachments appear to bethe direct result of bilateral dural arteriovenous fistula of the cavernous sinus region. Rapidresolution of the clinical signs followed bilateral orbital decompression via the transfrontal approach.Similarities in clinical presentation of both entities are reviewed and a premise for their cause-and-effect relationship elaborated. A literature search for similar unrecognised cases is discussed.The paper suggests that this association may be more frequent than published reports would imply.

Spontaneous choroidal detachment and duralarteriovenous fistulae of the cavernous sinus areuncommon clinical entities. Each produces arelatively characteristic syndrome with a constella-tion of ocular signs and symptoms. Their occurrencetogether has been previously reported on only asingle occasion (Woillez et al., 1967).A patient with this rare clinical combination

recently provided the opportunity to study exten-sively their association. The results of thisinvestigation suggest the association may not be asunusual as the current literature would suggest. Aplausible basis for the relationship of spontaneouschoroidal detachment with dural arteriovenousfistulae in the region of the cavernous sinus is nowproposed.

Case history

A 70-year-old White male professor emeritus ofinternal medicine noted irritation and a foreignbody sensation of both eyes associated with lacrima-tion, conjunctival injection, and mild lid oedema inOctober 1973. Before the onset of symptoms headmitted to much stress in his work as well as aminor fall in which he struck the right side of hishead without apparent injury. Initial therapy withtopical steroids by his private ophthalmologistprovided no improvement.A thorough medical investigation with neurological

consultation was undertaken in June 1974. No

Address for reprints: Dr John W. Harbison, Departmentof Neurology, Box 698, Medical College of Virginia,Richmond, Virginia 23298, USA

history of additional neurological, ophthalmological,endocrine, or medical symptoms was elicited. Hespecifically denied headache, ocular pain, diplopia,visual loss, or cranial bruits. A review of his pastmedical history revealed hypertensive cardiovasculardisease, coronary artery disease with angina pectoris,diverticulosis and diverticulitis, Dupuytren's con-tractures, and transient ischaemic cerebral vasculardisease characterised by transient global amnesiaand left hand inco-ordination of infrequentoccurrence.

Physical examination showed the visual acuity tobe 20/20 OU. Both pupils were noted to be dilated,the right responding poorly to direct light. Ocularmotility was normal and there was no ptosis,although mild lid oedema persisted. Hertel exoph-thalmometry registered 20 mm OU. Marked dilata-tion of conjunctival vessels was now present. Nocranial or ocular bruits were detected and therewas no increase in resistance to retropulsion of theglobe. Slit-lamp examination was normal, andapplanation tensions were 21 mmHg OU. Retinalchanges were characterised funduscopically by mildvenous engorgement, small dot haemorrhages, andarteriovenous nicking. No significant findings wererecorded on general physical or neurologicalexamination.

Laboratory studies giving normal results at thattime included: total and differential blood counts,ESR, urine analysis, BUN, glucose, serum electro-lytes, calcium, phosphorus, alkaline phosphatase,LDH, SGOT, cholesterol, bilirubin, total proteinand A/G ratio, creatinine, uric acid, serum proteinelectrophoresis and immunoglobulins, cryoglobu-lins, tuberculin and histoplasmin skin tests, and

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John W. Harbison, DuPont Guerry, and Herbert Wiesinger

Fig. 1 Top view shows conjuncti-val vascularity at the time ofadmission. Bottom view showsresolution of conjunctivalvascularity

toxoplasmin serum titres. Chest and skull x-rayswere normal. The electrocardiogram revealed aright bundle branch block, left anterior hemiblock,occasional ventricular ectopic beats, and leftventricular hypertrophy.No diagnosis was then established, though a

hyperviscosity syndrome was considered.At 2 subsequent ophthalmic examinations no

new diagnositic suggestions were provided. On 2August 1974 visual acuity OD had dropped to 20/40,and an intraocular mass was noted temporally from7 to 10 o'clock. A choroidal melanoma was sus-pected. A second opinion was requested of theauthors before proposed enucleation.

Examination on 7 August confirmed the presenceof a pigmented mass extending from 7 to 10 o'clocktemporally OD. The mass transilluminated. Fluores-cein angiography showed only the previously notedvascular changes. A nasal visual field loss was noted.The remainder of the ocular examination wasunchanged. In view of this examination the mass wasthought to be a choroidal detachment, and thepatient was begun on oral prednisone 60 mg daily.By 19 August 1974 the choroidal detachment wasmore extensive OD, involving both the temporaland nasal segments. A temporal and inferiorchoroidal detachment was now present OS.

Three days later abrupt proptosis OD, withlimitation of motility and ptosis, occurred over aperiod of 15 minutes. The patient was placed at bedrest, and by 25 August the proptosis, motilitydefect, and ptosis had resolved.On 3 September 1974 the patient was admitted to

the Neuro-Ophthalmology Service at the Medical

College of Virginia. On admission conjunctivalvascular changes (Fig. 1) with mild chemosis and lidoedema were re-affirmed. Visual acuity OD hadfallen to light perception. Acuity OS was 20/50,could not be improved, and was associated with amoderate red/green colour perception loss. Thepupils were both widely dilated; OD remained un-responsive to light, OS normally responsive. Hertelreadings were 23 mm OD and 24 mm OS.

Ocular motility was restricted in all fields withoutptosis. Funduscopic examination demonstratedpreviously documented bilateral choroidal detach-ments. Visual field examination revealed bothtemporal and nasal defects OS; OD could not beeffectively plotted (Fig. 2). General physical andneurological examination was normal. No bruitwas heard about the head or neck. The differentialdiagnosis included endocrine exophthalmos andarteriovenous fistula. A low-flow dural fistula wasthought to be more likely than a conventionalhigh-flow carotid-cavernous fistula.

In the early morning of 7 September the patientexperienced the onset of severe orbital pain.Examination showed increase in proptosis, withHertel readings now of 28 mm OD and 26 mm OS.There was increased chemosis and lid oedema.Ocular motility was restricted in all fields (Fig. 3).The choroidal detachments were nearly complete,and visual acuity had fallen to bare light perceptionOU. Intraocular pressure was recorded at 46 mmHgOU with fairly shallow anterior chambers.The patient was immediately begun on acetazola-

mide and subjected to selective cerebral angiography.This showed bilateral 'low flow' dural arteriovenous

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Dural arteriovenous fistula and spontaneous choroidal detachment: new cause of ani old disease

90 9-3-74

Fig. 2 Tangent screen visualfield at time of admission

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Fig. 3 Marked proptosischemosis, conjunctival injection,and restriction of ocular motility

fistula draining into the cavernous sinus (Fig. 4).Because of the exacerbation of the orbital signs andsymptoms attributed to venous stasis and hypoxia,it was decided to decompress both orbits in anattempt to reverse the course of events and regainvision. Bilateral transfrontal orbital roof decompres-sion was therefore undertaken shortly after angio-graphy.The immediate postoperative course was

uneventful. The patient experienced progressiveimprovement, and by December 1974 both eyeswere quiet and white (Fig. 1). Visual acuity was20/30 OS and 20/40 OD, and ocular motility full(Fig. 5). The choroidal detachments were largelyresolved. At this point it was considered that bothfistulae had undergone thrombosis. He has continuedan asymptomatic course since then.

Discussion

The initial clinical description of spontaneouschoroidal detachment has been attributed to vonGraefe in 1854 (McDonald et al., 1964). Ursin (1965)found 100 reported cases. Small series (McDonaldet al., 1964; Preisler, 1965; Rosen and Lyne, 1968;Davis et al., 1973; Scheie and Morse, 1974), as wellas single cases (Horay, 1935; Karaske, 1935;Csillag, 1937; Mathews and Moodie, 1955; Lewallen,1957; McClure, 1967; Woillez et al., 1967;Brockhurst and Lamb, 1973) of spontaneous exuda-tive or serous choroidal detachment continue to bereported, emphasising the infrequency of thisclinical entity.By definition spontaneous choroidal detachment

excludes separation of the choroid related to intra-

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4a

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4b

4bFig. 4a Lateral view of the left coommon carotid arteryinjection. There is early filling of the posterior cavernoussinus (curved arrow)Fig. 4b Frontal view of left common carotid arteryinjection with manual cross-compression of right carotidartery. Early filling of cavernous sinus is seen medially(arrow)

Fig. 5 Coinplete resolution_postoperatively of proptosis,chemosis, conjunctival injection,a1(1 ociuloniiotor restriction

ocular surgery, trauma, obvious focal infection orhaemorrhage, and traction effects in a phthisical eye.It has been associated with many local ocular aswell as systemic diseases (Schepens and Brockhurst,1963; Gupta et al., 1965). Common among thesehas been ocular inflammation: iridocyclitis, tenonitis,and scleritis.

Spontaneous choroidal detachment most com-monly presents over the age of 55, with a predilectioni

for males. Presenting symptoms consist of visualimpairment often associated with pain, photo-phobia, and epiphora. Visual loss of significantdegree is commonly associated with shallowness ofthe anterior chamber, hypotony, retinal venousstasis, and contraction of the visual field. Additionalsigns included: increased intraocular pressure,proptosis, conjunctival injection, and non-rhegmatogeniouls retinal detachment. The course is

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Dural arteriovenous fistula and spontaneous choroidal detachment: new cause ofan old disease

often characterised by remission and recurrence ofsymptoms.A number of theories have been considered with

regard to the aetiology of spontaneous exudative orserous choroidal detachment. Although its causeremains elusive, it is generally accepted that avascular process producing choroidal congestion isthe source of transudation, which results in thechoroidal separation (Verhoeff and Waite, 1925;Capper and Leopold, 1956; Lewallen, 1957; Cogan,1960; Davis et al., 1973; Scheie and Morse, 1974).This concept is experimentally supported by Aaberg'swork in the owl monkey (Aaberg, 1974). Mostauthors agree that many diseases can produce this'vasculopathy'. This has led Velzebor (1960) tosuggest that choroidal detachment should beconsidered a symptom rather than a separate clinicalentity. Perhaps spontaneous choroidal detachmentshould be considered a secondary clinical entitysymptomatic of a primary disease productive ofsignificant alterations of intraocular haemodynamicswhich include changes in choroidal vascularitycapable of inciting transudation.

Carotid-cavernous sinus fistulae with their high-flow arteriovenous communication have been easilyrecognised since Traver's initial description in 1811.In recent years, with the advent of such majoradvances in the technology of cerebral angiographyas selective catheterisation, magnification, andsubtration, a second type of arteriovenous com-munication has been recognised (Hayes, 1963;Takekawa and Holman, 1965; Mingrino and Moro,1967; Clemens and Lodin, 1968a; Newton andHoyt, 1968; Rosenbaum and Schechter, 1969;Newton and Hoyt, 1970; Taniguchi et al., 1971;Houser et al., 1972; Aminoff, 1973; Schlezinger andSchatz, 1973; Katsioris et al., 1974). These duralarteriovenous fistulae are 'low flow' communicationsbetween small meningeal branches of both theexternal and internal carotid arteries and basalvenous sinuses, frequently the cavernous sinus orits tributaries. Although the exact pathophysiologyof the dural arteriovenous fistula is obscure,current theories include the spontaneous opening ofcongenital arteriovenous shunts (Clemens andLodin, 1968b; Aminoff, 1973) and the rupture ofthin-walled dural arteries within venous sinusessecondary to minimal trauma (Katsioris et al., 1974)or straining (Taniguchi et al., 1971), with pre-existent vascular disease playing an uncertain role(Newton and Hoyt, 1970).A clinical entity generally distinct from the more

florid ocular syndrome of carotid-cavernous fistulaeresults from the 'low flow' character of these smalldural arteriovenous communications. The presenta-tion is commonest over the age of 50, with an

apparent predisposition in women. The mostfrequent presenting symptoms are headache ororbital pain of unilateral occurrence and oftensevere nature. Diplopia is usual and an ipsilateralabducens paresis typically the source. Mild non-pulsating proptosis, conjunctival injection, chemosis,and increased intraocular pressure are generallypresent.

Misdiagnosis early in the course is the rule.Migraine, cluster headaches, endocrine exophthal-mos, chronic conjunctivitis, episcleritis, iritis, andorbital tumour have been the most frequentdiagnostic errors. The absence of an objective bruitis widely accepted as the major pitfall in diagnosis.A significant number of patients without an objectivebruit, however, will provide historical evidence forone at some point in the clinical course. Thepresentation of the fistula is spontaneous and thecourse frequently characterised by remission andrecurrence of typical signs and symptoms. It may bebilateral but most frequently is unilateral. Some caseshave been asymptomatic and incidentally indentified.

If spontaneous choroidal detachments and duralarteriovenous fistulae have more than a chanceassociation, common signs and symptoms should bedefinable, providing a plausible cause-and-effectrelationship. The cohesive elements must then gainsupport from clinical observations. These criteriaappear to be satisfactorily confirmed in the followingdiscussion.

It is clear from the review of cases available in theliterature of both spontaneous choroidal detachmentand dural arteriovenous fistulae of the cavernoussinus that a group of signs and symptoms arecommon to selected cases of both clinical entities.These include: mild proptosis, conjunctival injection,orbital pain, moderate increase in intraocularpressure, and evidence of retinal venous stasis.Further, both share a spontaneous mode of onsetand a course frequently characterised by remittingand recurrent symptomatology. Finally, both tendto resolve spontaneously after periods measured inweeks to months.A single case reported by Woillez et al. (1967)

provides the only previous documentation of theassociation of spontaneous choroidal detachmentand carotid-cavernous sinus fistulae. Their casediffers from ours in that it was a unilateral post-traumatic carotid-cavernous fistula with the choroi-dal detachment occurring in the ipsilateral eyefollowing a third surgical procedure directed atobliteration of the 'high flow' fistula. Our case moreclearly substantiates a significant association, if notcause-and-effect relationship, of spontaneous cho-roidal detachment and 'low flow' dural arteriovenousfistulae. Another case report of interest in the

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Table 1 Tabulation of documented andpossible cases of associated dural arteriovenousfistula and serous choroidal detachment

Conjunctival OculomotorAuthor Case Age Sex Clinical diagnosis Proptosis injection abnormality Pain

D Harbison 1 70 M Bilateral choroidal detachment and Yes Yes Yes YesO et al. bilateral dural A-V fistulaeCU Cogan 1 53 F Bilateral retinal detachment and Yes Yes Yes YesM 1960 carotid-cavernous fistula (presumptive)EN Woillez 1 38 M Carotid-cavernous fistula, choroidal Yes Yes Not recorded YesT et al., and retinal detachment ipsilaterallyE 1967D

Preisler 1 63 M Tenonitis-scleritis with ipsilateral Yes Yes Yes Yes1964 choroidal detachment

Lewallen 1 103 M Orbital cellulitis or tumour, with Yes Yes Not recorded Yes1957 bilateral exudative retinal detachments

Csillag 1 34 F Exudative retinal detachment. Yes Yes Yes Yes1937 Tentative scleritis and MS

pHoray 1 46 M Exudative retinal detachment. Yes Yes Not recorded Yes

0 1935 Tentative bilateral scleritis

S Scheie 1 28 M Spontaneous choroidal detachment No Yes No Yes1974 2 64 F Spontaneous choroidal detachment Yes Yes No No

episcleritis

McClure 1 66 M Bilateral choroidal detachment No No No Yes

B 1967

L Ursin 1 63 F Acute glaucoma with choroidal No Yes No Yes1965 detachment

E McDonald 1 61 M Choroidal detachment and dysthyroid Yes Yes No No1964 exophthalmous

Fleischer 1 42 M Choroidal detachment R/O melanoma Not recorded Not recorded Not recorded Not recorded1921 2 35 M Choroidal detachment, R/O intraocular Not recorded Yes Not recorded Not recorded

tumour

Karasek 1 32 F Posterior scleritis, retrobulbar neuritis No Yes Yes Yes1935 and choroidal detachment

present discussion is that of Cogan (1960). Hepresented an instance of bilateral exudative non-rhegmatogenous retinal detachment occurring inassociation with a presumed but unproved carotid-cavernous sinus fistula. One wonders ifa spontaneouschoroidal detachment did not precede the retinalseparation. In addition the clinical picture reportedsuggests a low-flow dural fistula as opposed to ahigh-flow carotid-cavernous fistula.

In reviewing published reports of spontaneouschoroidal detachment one can identify a number ofcases based on the previously noted signs and symp-toms in which an occult dural arteriovenous fistulaof the cavernous sinus can reasonably be suspectedas the cause (Lewallen, 1957; McDonald et al., 1964;Preisler, 1965; Ursin, 1965; McClure, 1967; Scheieand Morse, 1974). These cases have been tabulatedand recorded in Table 1 along with the apparently

proved cases as possible cases of choroidal detach-ment secondary to dural arteriovenous fistula.

It appears relatively clear that a dural arterio-venous fistula in which the venous drainage isdirected arteriorly into the superior and inferiororbital veins will result in increased orbital as well asocular venous pressure. This in conjunction withreduced mean arterial pressure resulting from arterialshunting will produce tissue hypoxia. This sequenceof events clearly provides the intraocular haemo-dynamic basis necessary for choroidal congestion,transudation, and finally detachment, as well as theadditional clinical signs and symptoms common toboth entities (Sanders and Hoyt, 1969). If thesemechanisms are accepted, it would seem establishedthat dural arteriovenous fistulae of the cavernoussinus region are one of the primary disease entitiesproductive of secondary choroidal detachments.

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Dural arteriovenous fistula and spontaneous choroidal detachment: new cause ofan old disease

Intraocular Retinalpressure venous stasis Course

Increased Yes Bilateral resolution over 4 months followingtranscranial orbital decompression

Not recorded Cloudy Spontaneous resolution in 4 monthsvitreous

Decreased Yes Spontaneous resolution in 3 days

Not recorded No Treated with local and systemic steroids,mydriatic and antibiotics. Resolved in4 weeks

Increased No Spontaneous resolution in 2 weeks.Treated with antibiotics

Normal Yes Spontaneous resolution after waxing andwaning course

Not recorded Yes Spontaneous resolution after waxing andwaning course

Decreased No Waxing and waning courseNormal No Resolved in 1 month

t OD No Treated with steroids. Spontaneousl OS resolution in 5j months

Increased No Spontaneous resolution in 2 weeks

[ncreased No Eye enucleated for suspected melanoma

Increased Yes Eye enucleated for suspected melanomancreased Yes Waxing and waning course. Patient died

of other disease

!4ormal Disk and Waxing and waning course withretinal spontaneous resolutionoedema

The case presented as well as those identified andsuspected in the literature lends clinical support tothis contention.

If this premise is accepted, it would seem reason-able to consider selective cerebral angiography inappropriate cases presenting spontaneous choroidaldetachments. These cases should exhibit a significantnumber of those features common to dural arterio-venous fistulae. We would suggest these include:proptosis, conjunctival injection, increased intra-ocular pressure, pain, and diplopia. If a realisticdiagnosis approach to the investigation of spon-taneous choroidal detachment is pursued, we mayexpect the incidence of inciting dural arteriovenousfistulae to be appropriately determined.

Presented to the American Ophthalmological Society,Hot Springs, Virginia, 29 May 1975.

References

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Aminoff, J. M. (1973). Vascular anomalies in the intracranialdura mater. Brain, 96, 601-612.

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Dural arteriovenous and spontaneous choroidal · arteriovenous fistula. Alow-flow dural fistula was thought to be more likely than a conventional high-flow carotid-cavernous fistula