220 J. Anaesth.

2005; 49 (3) : 220 - 222

Indian

INDIAN JOURNAL OF ANAESTHESIA, JUNE 2005

220

CAROTICOCAVERNOUS FISTULA - A Case Report

Dr. (Lt. Col.) Murthy TVSP 1 Dr. (Col.) Chandra Mohan 2
Dr. Pratyush Gupta 3 Dr. (Maj.) Bedi P. S. 4 Dr. (Brig.) Prabhakar T. 5
SUMMARY:
Direct carotid-cavernous fistulas are high-flow shunts with a direct connection between the internal carotid artery and the cavernous
sinus. The goals of treatment are to eliminate the fistula and preserve carotid artery patency1. Some patients do not show the classical
triad of symptoms viz. pulsating exophthalmos, bruit, and conjunctival chemosis. In such patients, early diagnosis and treatment are
particularly important because cortical venous drainage and a consequent risk of hemorrhage are frequently present2. A patient is
described with a traumatic caroticocavernous fistula which resulted in unilateral proptosis and diminished vision in left eye alongwith
the characteristic triad of symptoms. Successful obliteration of the fistulous connection with restoration of normal arterial and venous
flows was achieved by insertion of Guglielmi detachable coils (GDC).

Keywords : Caroticocavernous fistula, Traumatic brain injury, Dural AV fistulas, monitoring

Introduction
The caroticocavernous fistula is a specific type of
dural arteriovenousfistula characterized by abnormal
arteriovenous shunting within the cavernous sinus. A
caroticocavernous fistula results in high-pressure arterial
blood entering the low-pressure venous cavernous sinus.
This interferes with normal venous drainage patterns and
compromises blood flow within the cavernous sinus and the
orbit. Caroticocavernous fistulas represent approximately
12% of all dural arteriovenous fistulas. Type A is more
common in young males.Types B, C, and D are more
common in women older than 50 years, with a 7:1
female-to-male ratio.1,2
Case report
A 23 years old soldier was admitted as a case of
closed head injury following a road traffic accident. He
presented with left eye proptosis, diminished vision along
with features of AV fistula (bruit, thrill, proptosis). He
was managed conservatively and was later diagnosed to
have a caroticocavernous fistula. The endovascular closure
of fistula by electrodetachable coils was planned, to be
conducted under general anaesthesia. The patient did not
show any external stigmata for a connective tissue disorder.
The patient was preoperatively assessed and accepted
in ASA-II.
1.
2.
3.
4.
5.

M.D.,PDCC., Asso. Prof.,

M.D., Prof., Interventional Radiologist
M.B.B.S., FICMR., Post Graduate Resident (Anaesthesiology)
M.B.B.S., Post Graduate Resident (Anaesthesiology)
M.D. Prof. and Head, Anaesthesiology
Army Hospital (Research and Referral), New Delhi, India
Correspond to :
Lt. Col. T.V.S.P.Murthy
E-mail : tvspmurthy@ yahoo.com
(Accepted for publication on 24 - 3 - 2005 )

He was kept nil per oral after 2200 hrs the night
previous to the surgery and premedicated with diazepam
5mg at night and on morning of procedure. In the operation
theatre, he was monitored with ECG, NIBP and SpO2
(pulse oximetry). Under local anaesthesia, the left radial
artery was cannulated using a 20G cannula for recording
continuous invasive intra arterial BP monitoring and the
right basilic vein was cannulated with a 16G catheter to
monitor the CVP. Pethidine 40 mg and glycopyrrolate
0.2 mg were given intravenously as premedication on
the table. He was preoxygenated with 100% oxygen for
3 minutes, induced with thiopentone 300 mg and intubated
with pancuronium 8 mg. A 8.5 mm cuffed, reinforced
endotracheal tube was passed and anaesthesia maintained
with air, oxygen and isoflurane. A base line arterial blood
gas was done which was within the normal limits. The
urinary bladder was catheterized to monitor urine output.
Intraoperatively, moderate hypotension was
maintained and systolic blood pressure kept between 90 to
100 mm of Hg with beta blockade using metoprolol and
isoflurane (1-1.5%). A nitroglycerine infusion was prepared
and kept ready for use in case of requirement. The
intervention was started by cannulating the femoral vein
under image guidance and heparinisation with 5000 units
bolus intravenously, followed by 1000 unitshr-1 via a
continuous infusor pump to maintain anticoagulation.
The fistula was delineated on the image intensifier
(fluoroscopy) and identified. For curiosity sake and to know
the degree of arterialisation of the cavernous sinus, one of
the ports of the catheter was connected via a pressure
tubing to a transducer and zeroed at the level of the mastoids
in an attempt to measure the pressure, which to our surprise
recorded in the range between 60-80 mm Hg and depicted
an arterial/pulsatile trace on the monitor, which otherwise
would have normally been around 10-15 mmHg. The AV
fistula was successfully closed by coiling. A total of 8 GDC

MURTHY, MOHAN, GUPTA, BEDI, PRABHAKAR : CAROTICOCAVERNOUS FISTULA

coils were used for the closure. Post coiling the cavernous
sinus pressures fell to 8-10 mm of Hg and the bruit
disappeared dramatically. Patient was reversed on
conventional lines. The procedure lasted for 6 hours and
during the procedure cerebral antioedema (0.5 gmkg-1 of
20% mannitol) and antiepileptic (5 mgkg-1 sodium dilantin)
measures were instituted, given as slow intravenous infusions.
Post operatively the progress of patient was satisfactory
both clinically and radiologically. The patient was nursed
for 24 hrs in ICU, with continuous monitoring of ECG,
NIBP, pulse oximetry and fluid balance under optimal
sedation using midazolam. He made an uneventful recovery
and was discharged with instructions for regular followup.
Discussion
Several classifications of CCF exist depending on
anatomy, etiology and pathophysiology.3 One categorization
divides between traumatic and spontaneous fistulas. Another
classification is established according to fistulous supply to
the cavernous sinus as follows: type A: internal carotid
artery (ICA); type B: dural branches of the ICA; type C:
dural branches of the external carotid artery (ECA); type
D: combined forms.4 This leads to a further classification
into direct high flow, and indirect low flow fistulas because
therapeutic management of CCF is strongly dependent on
their haemodynamics.5,6 Finally, considering aetiology, there
are several entities responsible for the development of a
CCF: closed or penetrating head trauma, surgical damage,
rupture of an intracavernous aneurysm, connective tissue
disorders, vascular disease, and dural fistulas.7,8 Blunt
head injury can lead to shearing of intracavernous arteries,
causing the development of a fistula. Penetrating head injury
can lead to fistula formation by direct laceration of
intracavernous vessels.
Caroticocavernous and vertebral venous fistulas are
direct arteriovenous fistulas.9 Their symptoms range from
benign to extremely severe ophthalmologic or neurologic
complications. Mechanism of symptoms is mostly related
to venous drainage. Therapy is revolutionized nowadays
with endovascular techniques using mostly detachable
balloons and coils which have a high success rate and very
few complications. The efficacy and safety of detachable
balloon occlusion of direct carotid cavernous fistulas are
well established.10 However, detachable balloon techniques
have to be required for occlusion of the internal carotid
artery (ICA) in a substantial percentage of patients. New
approaches to and occlusion methods of carotid cavernous
fistulas have been described,10 with increased focus on
preserving ICA flow. These methods include the use of
two-balloon techniques, use of GDC,11,12 permanent
solidifying agents and even stents. Transvenous access
to the cavernous sinus is most often achieved via the

221

inferior petrosal sinus or the superior ophthalmic vein.13

A caroticocavernous fistula is not a life-threatening disease.
The risk of visual loss and the severity of associated symptoms
must be evaluated to determine the appropriate degree and
timing of intervention. Type-A fistulas rarely resolve
spontaneously. Treatment is recommended for intolerable
bruit, progressive visual loss, and the cosmetic effects of
proptosis. Types B, C, and D fistulas have a higher incidence
of spontaneous resolution. No prior contraindications
exist for the management of these lesions. Each patient
must be evaluated individually. Generally, the lesions should
be managed as aggressively as required to abort the signs
and symptoms. Management techniques may be
contraindicated if the patient cannot tolerate the possible
complications of the treatment. In the acute setting of vision
loss and/or paralysis of cranial nerves, glucocorticosteroids
(eg, dexamethasone) may be used while waiting for definitive
diagnostic studies and treatments.
The definitive management of a caroticocavernous
fistula is obliteration of the fistulous connection with
restoration of normal arterial and venous flow. This is
achieved most often through an endovascular approach.
Important anaesthetic considerations include a proper
preoperative assessment of the patient and institution of an
appropriate anaesthetic plan for the procedure. Meticulous
monitoring in the form of central venous pressures and
invasive arterial pressures should be established to provide
hypotensive anaesthesia and at the same time be able to
prevent dangerously low cerebral perfusion and associated
hypoxic insult. Use of BIS monitoring to assess depth of
anaesthesia as well as cerebral function is also recommended.
In our case, we monitored the cavernous sinus pressures so
as to depict the strange pulsatile pattern and elevated sinus
pressures which prompted us to the conclusion of
arterialisation of the cavernous sinus. The pressures returned
to normal on successful closure of the communicating fistula.
Throughout the procedure, we maintained mild to moderate
hypotension using high concentrations of isoflurane(1-1.5%)
with low fresh gas flows (2 l/min) and beta blockade with
metoprolol to minimize blood loss. The two primary
indications for elective deliberate hypotension are: a) to
slow flow in an arteriovenous malformation feeding artery
before insertion of glue/coils, termed flow arrest and b)
to test cerebrovascular reserve in patients undergoing
carotid occlusion. Ideally, the level of sedation is decreased
so that the neurological state can be assessed during the
period of deliberate hypotension. In awake patients, nausea
and vomiting can be a problem. Droperidol or ondansetron
may be considered as part of the anaesthetic regimen.
Nitroglycerine infusion would have unnecessarily resulted
in tachycardia and cerebral steal phenomenon. Sodium
nitroprusside could also have been used but its administration

222

INDIAN JOURNAL OF ANAESTHESIA, JUNE 2005

is cumbersome and we could adequately manage the patient

without resorting to these drugs by providing adequate
anaesthetic depth. Careful management of coagulation is
required to prevent thromboembolic complications during
and after the procedure but practices differ widely.
Intracranial catheter navigation is a definite indication for
anticoagulation, which can be monitored by the activated
clotting time (ACT) as a guide for heparin therapy and was
done for this case. Mannitol was administered towards the
end to reduce the fluid load and reduce orbital edema. The
patient was also dilantinised intraoperatively to prevent any
seizures. On follow up, a check angiogram was done to
ensure that the fistula had not recurred and that no new
communications had developed.
We present the case to highlight the importance of
hypotensive anaesthesia (arterialisation of carotid sinus
leading to high pressures which could have caused
uncontrollable bleeding), precise monitoring and anaesthetic
measures to reduce edema and possible seizures. The case
is also being presented to highlight the degree of
arterialisation of the cavernous sinus, which was documented
on monitoring and which to the best of our knowledge, no
such invasive monitoring has been performed till date.
References
1. Lewis AI, Tomsick TA, Tew JM Jr. Management of 100 consecutive
direct carotid-cavernous fistulas: results of treatment with
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2. Kurata A, Takano M, Tokiwa K et al. Spontaneous carotid
cavernous fistula presenting only with cranial nerve palsies.
AJNR Am J Neuroradiol. 1993 Sep-Oct; 14(5): 1097-1101.
3. I Wanke, A Doerfler, D Stolke et al. Carotid cavernous fistula
due to a ruptured intracavernous aneurysm of the internal

carotid artery: treatment with selective endovascular occlusion

of the aneurysm. J Neurol Neurosurg Psychiatry 2001; 71: 784787 [Medline].
4. Barrow DL, Spector RH, Braun IF et al. Classification and
treatment of spontaneous carotid-cavernous fistulas. J Neurosurg
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5. Debrun GM. Endovascular management of carotid cavernous
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