Carotid-Cavernous Fistula from the Perspective of an Ophthalmologist. A Review

Abstract

Carotid-cavernous fistula (CCF) is an abnormal communication - vascular connection between arteries and veins in the cavernous sinus. Classification according to etiology is traumatic vs spontaneous. According to blood flow rate per high flow vs low flow fistula. According to anatomy of direct vs indirect: Direct (direct) CCF arises through direct communication between the internal carotid artery (ICA) and the cavernous sinus. Indirect CCF originates through indirect communication through the meningeal branches of ICA, external carotid artery and cavernous sinus (not directly with ICA) and Barrow type A, B, C, D division. Patients subjective complaints depend on the type of CCF. Most often it is pulsating tinnitus, synchronous with blood pulse. Typical findings include protrusion and pulsation of the eyeball, corkscrew vessels - arterialization of conjunctival and episleral vessels, increased intraocular pressure, not responding to local antiglaucomatous therapy, keratopathy a lagophthalmo, corneal ulcers. In the later untreated stages of CCF, secondary, venous stasis or central retinal vein occlusion can occur. Diagnostic procedures include B-scan and color Doppler ultrasonography, digital ophthamodynamometry, computer tomography, nuclear magnetic resonance and digital subtraction angiography. CCF can simulate orbitopathy, conjunctivitis symptoms, carotid occlusion, scleritis or cavernous sinus thrombosis. The ophthalmologist should recognize and indicate the necessary examinations in a timely manner. The therapy is ophthalmological, neuroradiological, sterotactic, surgical and conservative.

Full text

ČESKÁ A SLOVENSKÁ OFTALMOLOGIE 2020 1
REVIEW
CAROTIDCAVERNOUS FISTULA FROM THE
PERSPECTIVE OF AN OPHTHALMOLOGIST 
A REVIEW
SUMMARY
Carotid-cavernous fistula (CCF) is an abnormal communication - vascular connection between arteries and veins in the cavernous sinus.
Classification according to etiology is traumatic vs spontaneous. According to blood flow rate per high flow vs low flow fistula. According
to anatomy of direct vs indirect: Direct (direct) CCF arises through direct communication between the internal carotid artery (ICA) and the
cavernous sinus. Indirect CCF originates through indirect communication through the meningeal branches of ICA, external carotid artery
and cavernous sinus (not directly with ICA) and Barrow type A, B, C, D division. Patient‘ssubjective complaints depend on the type of CCF.
Most often it is pulsating tinnitus, synchronous with blood pulse. Typical findings include protrusion and pulsation of the eyeball, corkscrew
vessels - arterialization of conjunc tival and episleral vessels, increased intraocular pressure, not responding to lo cal antiglaucomatous therapy,
keratopathy alagophthalmo, corneal ulcers. In the later untreated stages of CCF, secondary, venous stasis or central retinal vein occlusion can
occur. Diagnostic procedures include B-scan and color Doppler ultrasonography, digital ophthamodynamometry, computer tomography,
nuclear magnetic resonance and digital subtraction angiography. CCF can simulate orbitopathy, conjunctivitis symptoms, carotid occlusion,
scleritis or cavernous sinus thrombosis. The ophthalmologist should recognize and indicate the necessary examinations in atimely manner.
The therapy is ophthalmological, neuroradiological, sterotactic, surgical and conservative.
Key words: carotid- cavernous stula; cavernous sinus; caput medusae; cork screw vessels; proptosis; venous stasis; exophthalmos; ocular pathology;
ultrasonography
Čmelo J.
Centre for Neuro-ophthalmology, Bratislava
Sworn declaration
The author of the study hereby declares that no conict of interest
exists in the compilation, theme and subsequent publication of this
professional communication, and that it is not supported by any
pharmaceuticals company. The author further declares that the study
has not been submitted to any other journal or printed elsewhere, with
the exception of congress abstracts and recommended procedures.
Received: 12. 2. 2020
Accepted: 3. 5. 2020
Available on-line: 30. 8. 2020
doc. MUDr. Jozef Čmelo
Centrum neurooftalmológie,
Palas-Eye s.r.o.
Škultétyho 1
831 03 Bratislava, Slovensko
palas.eye@gmail.com
INTRODUCTION
Carotid-cavernous fistula (CCF) is an abnormal com-
munication – vascular connection between the arteries
and veins in the region of the cavernous sinus (sinus
cavernosus – SC). From a topographical perspective,
the SC is a venous network of a spongiform character.
The ophthalmic vein (vena ophthalmica) flows into the
SC, and the internal carotid artery (arteria carotis inter-
na – ACI) and the abducens nerve (nervus abducens)
pass through the SC. The ophthalmic and maxillary
branches of the trigeminal nerves (nervi trigemini),
trochlear nerve (nervus trochlearis) and oculomotor
nerve (nervus oculomotorius) are located on the peri-
phery of the SC (Fig. 1).
EPIDEMIOLOGY
From an epidemiological perspective, CCF is a rare
pathology. It occurs in 0.2 % of patients with cranio-
cerebral trauma [1] and as many as 3.8 % patients with
basilar skull fracture [2]. Non-traumatic CCF occurs
more frequently in women and in middle to advanced
age [3]. In the overwhelming majority fistulas are uni-
lateral, but bilateral CCFs have also been described in
the literature [4,5].
ETIOPATHOGENESIS
The most common cause (70–90 %) of CCF is trauma
[6] in the intracranial or periorbital region. Direct caro-
tid-cavernous fistulas are distinguished by a direct co-
nnection between the intracavernous segment of the

CZECH AND SLOVAK OPHTHALMOLOGY 2020
2
internal carotid artery and the cavernous sinus. These
fistulas usually have a high through-flow of arterial
blood, and are most frequently caused by a traumatic
defect in the arterial wall.
Approximately 24 % of CCFs occur non-traumatically
– spontaneously. In the case of indirect CCF, a commu-
nication is established between the SC and one or more
of the meningeal branches of the ACI, the external caro-
tid artery (arteria carotis externa – ACE) or both the ACI
and ACE. These stulas usually have a low – slow throu-
gh-ow. We encounter these stulas most frequently in
the case of disorders of the conjunctival tissues (Ehler-
s-Danlos syndrome, collagenosis), upon damage to the
vascular wall of the carotid artery (aneurysm, dissecti-
on), upon hypertension and cerebral arteriosclerosis [7],
upon atherosclerosis or in the case of rupture of an ane-
urysm. Opinions dier on the pathogenesis of indirect
CCFs. Defects in the vascular walls occur upon a bac-
kground of congenital arteriovenous malformations,
which develop spontaneously or in connection with
atherosclerosis, systemic hypertension, collagen vascu-
lar disease, pregnancy, and during or after childbirth. In
an extensive study by Debrun [9], in which 132 patients
with classication according to Barrow were examined,
75.8 % were classied as type A stulas, 3 % as type C
stulas and 21.6 % as type D stulas.
A minimal percentage of CCFs originate iatrogeni-
cally – during surgical procedures. For example, fo-
llowing a surgical procedure in the region of the pitui-
tary gland, after therapy for neuralgia of the trigeminal
nerve, thrombectomy of the carotid artery, during
operations on the ethmoid sinuses etc. [8].
Classication:
• According to etiology as traumatic vs. spontaneous.
• According to speed of blood flow as high-flow vs.
low-flow fistulas.
• According to anatomy as direct vs. indirect: Di-
rect CCF originates through direct communication
between the internal carotid artery and the caver-
nous sinus. Indirect CCF originates through indirect
communication through the meningeal branch of
the ACI, ACE and cavernous sinus (thus not directly
with the ACI).
• More precise classification is according to Barrow
[10] into four types: Barrow type A – direct CCF:
communication between the cavernous sinus and
ACI. Barrow type B – indirect CCF: dural connections
between the cavernous sinus and meningeal co-
nnections of the ACI. Barrow type C – indirect CCF:
dural connections between the cavernous sinus and
meningeal branches of the ACE. Barrrow type D – in-
direct CCF: communication between the cavernous
sinus and meningeal branches of the ACI and ACE.
The classification is presented synoptically in table 1.
Subjective complaints
Subjective complaints, similar to objective findings,
are highly influenced by whether this concerns direct
CCF (Barrow type A) or indirect CCF (Barrow types
B,C,D). Subjective complaints of direct CCF are above
all pulsating (subjectively disruptive) tinnitus, synchro-
nous with blood pulse. Headache is generally non-spe-
Fig. 1. View of cavernous sinus
ACI – internal carotid artery. N. III – oculomotur nerve. N. IV –
trochlear nerve. N. VI – abducens nerve. N. V1 – ophthalmic
branch of trigeminal nerves. N. V2 – maxillary branch of trige-
minal nerves.
Table 1. Classication of carotid-cavernous stula
Classication of
CCF according to:
Etiology Speed of blood
ow
Anatomy Barrow
Traumatic High ow Direct Barrow type A: direct CCF: communication
between SC and ACI
Non-traumatic, or
spontaneous
Low ow Indirect Barrow type B: indirect CCF: dural connections
between SC and meningeal connections of ACI
Barrow type C: indirect CCF: dural connections
between SC and meningeal branches of ACE
Barrow type D: indirect CCF: communication
between SC and meningeal branches of ACI and
ACE

CZECH AND SLOVAK OPHTHALMOLOGY 2020 3
cific, mostly frontal and ipsilateral with the fistula, so-
metimes linked with paresthesia to pains in the face.
In the case of direct CCF, patients state retrobulbar
pulsating pressure. In the case of indirect CCF (Barrow
types B, C, D) pulsating tinnitus is minimal, occasional
or absent, and is not subjectively disruptive. Patients
not infrequently complain of deterioration of central
visual acuity and diplopia. However, patients rarely no-
tify a doctor of these complaints, and as a result it is
necessary to ask actively about any pulsation and tin-
nitus within the framework of differential diagnostics.
DIAGNOSIS
Ophthalmological diagnosis:
When damage occurs to the intracavernous segment
of the ACI, ACE and their branches, the arterial blood
from these arteries ows directly into the venous SC. In-
creased venous pressure in the SC causes dilation of the
superior ophthalmic vein (vena orbitalis superior – VOS)
and a deterioration of venous outow from the eye and
eye socket. At the same time, perfusion pressure in the
ophthalmic artery decreases, which may lead to reti-
nal ischemia and malfunction of vision. In addition to
this, increased venous pressure in the SC may lead to a
compression of the surrounding tissues such as the n.VI,
n.IV, n.III and n.V1 – ophthalmic branch of the trigeminal
nerves and the n.V2 – maxillary branch of the trigeminal
nerves. This compression may be manifested for exam-
ple as ophthalmoplegia [11]. On a background of the
above-stated pathological changes, ophthalmologists
may encounter a broad range of pathological chan-
ges in the eye and eye socket. These may sometimes
resemble other ocular diseases – stated in dierential
diagnostics below. Direct CCF always has more fruste
ocular manifestations than indirect CCF.
Typical symptoms encountered by ophthalmologis-
ts are:
• Pulsating murmur ipsilaterally with CCF in the peri-
orbital region. Protrusion of eyeball, almost always
unilateral (Fig. 2).
• Pulsation of eyeball (visible or detectable palpably).
This always appears in direct CCF, sometimes in in-
direct CCF.
• Caput medusae: corkscrew vessels – arterialisation of
conjunctival and episcleral blood vessels (Fig. 3, 4).
• Chemosis of conjunctiva + tumescence of eyelids
(Fig. 5).
• Increased intraocular pressure (IOP), not responding
to local anti-glaucomatous therapy.
• We encounter edema of the optic nerve disc only in
the case of direct CCF [12].
• Diplopia: n.VI is most often afflicted due to anatomi-
cal flow in centre of SC.
• Depending on damage to n.III ptosis of upper eyelid,
pupillomotor dysfunction.
• Keratopathy and lagophthalmos, corneal ulcers.
• Haemorrhage into vitreous body, retina.
In late untreated stages of CCF neovascular glauco-
ma, secondary angle-closure glaucoma (after a longer
time increased orbital pressure leads to congestion of
the iris) may occur [13,14]. Venous stasis causes de-
terioration of the retinal blood flow, which may lead
to central retinal vein occlusion [15]. In one clinical
trial, a “3 point signal” was demonstrated to aid timely
diagnosis of CCF: hyperaemia of the disc of the optic
nerve (DON) + dilation of retinal vein and haemorrh-
age into retina [16].
For more precise specification of the diagnosis it is
suitable also to indicate the following examinations:
Fig. 2. Ipsilateral protrusion of eyeball upon direct carotid-ca-
vernous stula in left eye
Fig. 3. Caput medusae: corkscrew vessels – arterialisation
of conjunctival and episcleral blood vessels in left eye upon
direct carotid-cavernous fistula
Fig. 4. Caput medusae: corkscrew vessels – arterialisation
of conjunctival and episcleral blood vessels in right eye
upon direct carotid-cavernous fistula

CZECH AND SLOVAK OPHTHALMOLOGY 2020
4
• Digital ophthalmodynamometry: CCF increases
pressure in the central retinal vein, as well as episc-
leral pressure. Following endovascular therapy these
pressure parameters are normalised. Digital ophthal-
modynamometry reliably and directly enables mea-
surement of pressure in the central retinal vein, and
approximate intracranial pressure [17].
• Ultrasonography (USG): B-scan displays dilated
VOS (Fig. 6), slightly enlarged extraocular muscles
(EOM) by approx. 1–3 mm ipsilaterally, contralatera-
lly the EOMs are generally within the norm. Colour
Doppler Ultrasonography (CDU: display of colour re-
trograde blood flow in the VOS in comparison with
the other eye (Fig. 7). Typical findings are pathologi-
cal decrease of flow speed in the central retinal arte-
ry ipsilaterally in comparison with the other eye (Fig.
8) as well as enlarging of the resistance index in the
central retinal artery ipsilaterally in comparison with
the other eye.
• Radiological diagnosis: With regard to the fact
that nuclear magnetic resonance (NMR) provides a
better display of vascular structures than compu-
ter tomography (CT), it is suitable to indicate NMR
of the brain, focusing on the region of the SC. NMR
without angiography may demonstrate only dilation
of the extraocular muscles, dilation of the VOS and
potentially also enlargement of the damaged area of
the SC [18]. For this reason, in the case of suspicion
of CCF it is suitable to indicate NMR with contrast
(NMR-AG). This is very important information for the
radiologist with regard to suspicion of possible CCF.
Despite the fact that CT, NMR and NMR-AG are useful,
they do not determine CCF [19]. In some cases NMR-AG
does not display the stula, despite the presence of CCF
[20]. Specialised ophthalmological examinations such
as digital ophthalmodynamometry, USG of the eye and
orbit, including Colour Doppler examination and CDI,
NMR, NMR-AG, serve as a “springboard” for the radiolo-
gist, neurologist and neurosurgeon. Within the frame-
work of mutual co-operation, similarly as in the case of
intracranial hypertension [21], intracerebral digital sub-
traction angiography (DSA) is subsequently indicated
[22]. Although DSA is an invasive test which today has
minimal complications, such as thrombosis, cerebral va-
sospasm, nerve damage and haemorrhage, it still repre-
sents the gold standard for the diagnosis of CCF.
Dierential diagnosis
CCF has a broad range of clinical manifestations. As a
result it is important to consider also other clinical fin-
dings, or conversely, in the case of the changes stated
below, also to consider the possibility of CCF within
the framework of differential diagnostics.
Fig. 5. Pronounced extraocular haemorrhage, fruste chemosis
with subconjunctival bleeding and edema of the eyelids upon
direct carotid-cavernous stula
Fig. 6. Dilation of echo of superior ophthalmic vein (vena
orbitalis superior – VOS) with the aid of ultrasonic B-scan
upon carotid-cavernous fistula
Fig. 7. Colour display of retrograde flow and dilation of VOS
upon direct carotid-cavernous fistula with the aid of Colour
Doppler ultrasonography. Left image: Under physiological
conditions the venous blood flow is coded blue, and the
arterial flow red. In the case of carotid-cavernous fistula,
retrograde blood flow ensues, meaning a change of the
colour coding from blue to red. Right image: recording of
spectral analysis of retrograde blood flow of VOS – reverse
blood flow in VOS

CZECH AND SLOVAK OPHTHALMOLOGY 2020 5
• Inflammation of conjunctiva, episclera: CCF has
typical monocular hyperaemia (arterialisation of
conjunctival and episcleral blood vessels), with in-
creased intraocular pressure (Fig. 9). In comparison
with typical inflammations of the conjunctiva and
episclera, patients do not state burning, itching or
lachrymation.
• Endocrine orbitopathy: “red” eye, protrusion, subjecti-
vely pressure behind the eye, ocular hypertension may
occur not only in CCF but also in endocrine orbitopathy
(EO). However, hyperaemia upon EO (pseudoconjuncti-
vitis) is passive, in contrast with active arterialisation of
the conjunctival vessels. Hyperaemia and tumescence of
the eyelids in EO are more pronounced in early morning
(or after longer period in recumbent position). Arteriali-
sation of the conjunctival vessels is constant upon CCF.
Protrusion upon EO is never pulsating, the same applies
to subjective pressure behind the eyes. Ocular hyperten-
sion in EO is usually bilateral, and we measure dierent
values of IOP in dierent directions of gaze – orthopho-
ria, sursumduction and deorsumduction [23]. Upon CCF
the IOP value is constant in all directions of gaze, and it is
also possible to see pulsation of applanation semicircles
upon applanation tonometry. Finding on B-scan ultra-
sonography: dilation of echo of VOS and tumescence of
direct extraocular muscles [24], and above all Colour Do-
ppler enables dierentiation of CCF from EO. Likewise, if
the nding does not respond to therapy for EO, it is ne-
cessary to consider CCF [25]. Vascular malformation: pa-
tients do not state any subjective retrobulbar pressure/
sound. The method of choice is USD and UCD diagnosis
(Fig. 10, 11).
• Retrobulbar haemorrhage: similarly not stated
by the patient, no subjective retrobulbar pressure/
sound. The method of choice is USG and UCD dia-
gnosis.
• Orbitopathy of malignant origin: No pulsation, no
subjective retrobulbar pressure/sound. The method
of choice is NMR, CT, USG and UCD diagnosis [26].
• Carotid occlusion: The method of choice is UCD of
the carotid system, USG / UCD of the eye and eye
socket, NMR, CT examination.
• Posterior scleritis: Although retrobulbar pain is
present in scleritis, it is not pulsating synchronously
with pulse. This condition is unequivocally differen-
tiated from CCF by USG and UCD.
• Orbitocellulitis: CCF does not manifest pathological
inammatory markers, physiological number of leu-
kocytes. Diagnosis is similar as for scleritis USG + UCD.
• Thrombosis of SC: requires radiological examinati-
on by NMR with notification of differential diagnosis
of CCF and suspect thrombosis.
PREVENTION
As regards preventive measures, none exist. All that
is possible is to conduct a thorough examination of
all the patients who have suffered a head injury. This
applies especially to those cases where the person had
symptoms of skull fracture. These symptoms include
periorbital haematoma, subconjunctival haemorrh-
Fig. 9. Typical monocular hyperaemia (arterialisation of conjun-
ctival and episcleral vessels) with increased intraocular pressure
upon carotid-cavernous stula in comparison with passive hy-
peraemia upon conjunctivitis
Fig. 10. Vascular malformation of conjunctival and periscleral
vessels
Fig. 8. Pronounced decrease of ow speed in central retinal ar-
tery upon direct carotid-cavernous stula ipsilaterally in com-
parison with other eye

CZECH AND SLOVAK OPHTHALMOLOGY 2020
6
age, acute diplopia etc. It is necessary to diagnose CCF
as soon as possible in order to ensure timely therapy
and also to exclude the development of various com-
plications.
Prognosis:
An ophthalmologist is often the first doctor to come
into contact with a patient with CCF.
In the case of untreated CCF (especially direct CCF)
there is a danger of severe ocular changes. According
to the degree of severity of CCF, protrusion of the ey-
eball, chemosis of the conjunctiva, increased IOP to
ischemic neuropathy of the optic nerve, central reti-
nal vein occlusion and secondary glaucoma may oc-
cur within the course of a few days or up to several
months. In addition to ocular complications, there is
a large risk of intracerebral haemorrhage, pulmona-
ry embolism, and neuropathy of the cranial nerves
passing through the SC.
Approximately 20 to 30 percent of all dural fistu-
las lead to loss of sight, usually as a consequence of
uncontrolled glaucoma, ischemic neuropathy of the
optics or chorioretinal dysfunction.
Upon a diagnosis of indirect CCF, it is necessary also
to examine the haemocoagulation parameters and
conduct an oncological screening examination, since
a clinical trial from 2017 determined a link between
indirect CCFs, hypercoagulation and malignancy [27].
Following a successful medical procedure, ocular
pulsation and murmur disappear within a number of
hours to a few days. Dilated, congested conjunctival
blood vessels, papilloedema, ocular hypertension and
retinopathy usually return to the norm within the cour-
se of weeks to months. The speed and range of impro-
vement depends on the severity of the ocular symp-
toms during the presence of CCF. In the case of indirect
CCFs, regression is certain within 6 months at the latest.
In direct CCF there may not be a complete disappearan-
ce of protrusion, ophthalmoparesis or loss of sight. With
regard to the fact that dural carotid-cavernous stulas
are sometimes re-channelled following embolization or
they create new abnormal vessels, it is necessary to mo-
nitor the patient and regularly observe psycho-physical
functions, the ocular fundus, intraocular pressure and
potentially also retrobulbar pressure by means of di-
gital ophthalmodynamometry. However, embolisation
of a CCF is linked with a number of risks which inclu-
de thrombosis and reopening of the stula. Cases have
been described of worsening of angle-closure glauco-
ma within two months of the closure of a carotid-caver-
nous stula [28]. Embolisation also increases the risk of
thrombosis, especially in fragile veins [29].
THERAPY
Ophthalmological:
Treatment is standard as in the case of other causes. In
the case of secondary keratopathy from protrusion of the
eyeball and inability to close the eyelids, use ocular lubri-
cants or tarsorrhaphy. More suitable is local application of
medical botulotoxin to the upper eyelid. Persistent diplo-
pia can be treated with prismatic correction, or if the eye is
protruding with keratopathy, by occlusion of the eye.
In the case of pronounced ocular hypertension and se-
condary glaucoma, it is appropriate to choose the correct
anti-glaucomatous agents. Even though the majority of
cases of ocular hypertension are caused by increased
episcleral venous pressure, some of them are caused by
closure of the anterior chamber angle or neovascularisa-
tion of the iris. In the case of an increase of episcleral ve-
nous pressure, anti-glaucomatous agents with carboan-
hydrase blockers are suitable. If this does not correct the
ocular condition and CCF persists, it is possible to indi-
cate laser iridoplasty or other surgical procedures. In all
cases of ocular hypertension in CCF it is appropriate to
monitor also indirect signs of intracranial hypertension
(ICH), or as the case may be approximate values of ICH
with the aid of digital ophthalmodynamometry.
In patients with mild ocular symptoms, it is possible
to wait and observe whether indirect CCF closes spon-
taneously, which takes place in 20–50 percent of indi-
rect CCFs [30].
During this observation period, the patient’s visual
functions, IOP and ocular fundus should be monitored
regularly.
In the case of ischemia and subsequent proliferative
retinopathy and neovascular glaucoma, it is suitable
to indicate panretinal photogocoagulation or another
adequate therapy.
Conservative therapy:
As mentioned previously, the clinical course of CCF
may spontaneously fluctuate or disappear completely.
As a result, in the case of CCF it is also possible tempo-
rarily – before a surgical solution – to use conservative
therapy. This consists in the manual compression of
the ipsilateral jugular carotid artery several times per
day over the course of 4–6 weeks.
In conservative therapy it is also necessary to ensure re-
gular observation of psycho-physical functions, IOP and
the ocular fundus. Higashida, Barrow et al. [11,31] state that
conservative management may be eective in approxima-
Fig. 11. Periorbital hemangioma in right eye

CZECH AND SLOVAK OPHTHALMOLOGY 2020 7
tely 30 % of indirect CCFs and 17 % of direct cases of CCF.
Neuroradiological therapy:
The purpose of treatment is to close the stula, and at
the same time to maintain the through-ow of the caro-
tid vascular system. There are a number of therapeutic
options, which are being improved over the course of
time. One of these is endovascular embolisation with a
combination of detachable air balloons, catheters, stents
or liquid embolic substances. Application is either by
arterial or venous approach. It is possible to treat more
than 90 % of cases successfully in this manner [32].
Stereotactic radiotherapy:
This is minimally invasive, but has a long latency pe-
riod of 6–12 months: the time from performance of the
procedure until closure of the fistula [33,34]. Stereo-
tactic radiotherapy may be an option for treatment of
indirect CCFs, but is not performed for direct CCFs.
Surgical procedure:
If the patient is not capable of embolisation for heal-
th reasons, or if embolisation fails, a surgical procedu-
re comes into consideration – ligation of the internal
carotid artery.
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