DISCUSSION
First described in 1962 by Borsany(14), CBS still is an important
complication in head and neck cancer, with a mortality of 40% and
neurologic morbidity of 60%(1)(15). Prior radiotherapy, prior radical
neck dissection, mucocutaneous fistula, flap necrosis, wound infection,
poor nutrition and tumor recurrence can be counted as risk factors for
CBS(5)(7)(8). Tumor encasement and infiltration of carotid artery
causing inflammation and weakening of carotid artery wall, also plays an
important role(5)(9). Overall incidence of CBS in head and neck cancer
ranges from 2.5% to 4.5%(2)(5)(10). After examination of medical
records of 348 patients treated for head and neck cancer in our clinic,
8 patients with CBS treated by open approach carotid artery ligation,
were determined, having a slightly lower rate compared to the
literature(2.3%).
CBS was classified as type I(threatened) CBS occurring when carotid
artery was exposed through soft tissue breakdown, type II(impending)
with limited, sentinel bleeding and type III(rupture) with active
bleeding(1)(12). Type III is the most common type of CBS(over 60%)
followed by type II and I, respectively(12)(16). Chaloupka et al.,
reported their findings on endovascular treatment of CBS. Among 4
patients with type I, 10 patients with type II and 5 patients with type
III CBS; most common pathologic finding was pseudoaneurysms, followed by
tumor encasement(1). However, in another study, extravasation was the
most common pathologic finding(in 8 out of 10 patients), while
pseudoaneurysm was seen in only 2 patients, which could be explained as
all these 8 patients were type III CBS(17). All of our patients
presented with acute rupture(type III CBS), thus most common finding was
extravasation, followed by pseudoaneurysm.
CCA emerged as the most common site of origin of rupture in our study,
which was consistent with the literature reporting a rate of over 60%
(5)(12)(17)(18). Bleeding was found to be from CCA near bifurcation in
5(62.5%), ICA in 2(25%) and from main trunk of external carotid artery
just above bifurcation in one(12.5%) patient. However, in a study
consisting of 6 patients with CBS, ICA was found to be the most common
site(in 4 out of 6 patients), followed by CCA(2). In addition, in a
larger scale study, again ICA was reported to be the most common site
with a rate of greater than 50%, while CCA was being the least
common(1).
Previous radiotherapy is considered to be the most important risk
factor, by increasing the risk up to seven fold(6)(19), even to 14-fold
in case of a radiation dose of >70 Gy(8). After exclusion
of patients who were previously irradiated, CBS rate was found to be
only 0%–2.4%; however, when patients received radiotherapy analyzed
separately, CBS rate increases to 4.5%–21.1% (5). Free radical
production triggered by radiotherapy is considered to be causative agent
by inducing thrombosis of vaso vasorum, fibrosis of adventitia, and
premature atherosclerosis; eventually resulting in weakening of arterial
wall(19). In Estomba et al.’s study, except for one out of six patients
with CBS had a previous history of radiotherapy and cause of CBS was
proved to be radiation induced necrosis in 3 patients, pharyngocutaneous
fistula in 2 patients, and tumor recurrence in 1 patient(2). Durmaz et
al., stated that history of radiotherapy was the common future in all of
their 10 patients with CBS, 7 with recurred cancer and 5 with
pharyngocutaneous fistula(17). In a large review by Powitzky, among 140
patients and 161 CBS cases, previous history of radiotherapy was found
to be the most common shared feature(89%), followed by nodal
metastasis(69%), neck dissection(63%), necrosis(55%), mucocutaneous
fistula (40%)(12). Being another risk factor, neck dissection -
especially radical neck dissection, with stripping of the carotid – was
reported to increase the risk of CBS to eight fold(8). Among 8 patients
included in this study, all had a previous history of radiotherapy, with
3 as primary curative treatment and 5 as adjuvant treatment. 3 of the
latter also had a history of radical neck dissection. Pharyngocutaneos
fistula in 3, wound infection in 5 and necrosis at bleeding site in 6 of
the patients were seen, apart from tumor infiltration which was present
in all.
Most common tumor primary sites were larynx(23%), hypopharynx(22%) and
nasopharynx (21%)(12). In a study consisting of 10 patients with CBS,
in a six-year period, 3 had had primary tumor in larynx, 2 each in oral
cavity, hypopharynx, nasopharynx, and 1 in salivary gland(17). In our
study, primary site was oral cavity in 3(37.5%), oropharynx-hypopharynx
in 3(37.5%) and larynx in 2(25%) of the patients.
Surgical ligation has been traditionally the treatment of choice for
CBS(18)(20). However, after the introduction of the detachable balloons
specifically for treatment of impending CBS in 1984 by Osguthorpe and
Hungerford(21), there has been an increasing tendency towards
endovascular approach. Over 90% of patients reported in the past
fifteen years were treated by endovascular approach, either by stenting
or embolization; while surgical ligation was the preferred method in
less than 10%(12). Drawbacks of surgical ligation; such as hemodynamic
instability complicating perioperative management, hypotension deepened
with general anesthesia resulting in cerebral ischemia, consumption
coagulopathy due to blood loss resulting in uncontrollable
re-hemorrhage, challenging surgical dissection caused by previous
operations and radiotherapy; played role in this change of treatment
preferences(1). In a paper reporting 6 cases with CBS, among 3 patients
managed by endovascular approach, 1 had neurologic sequel; while 1
patient managed by surgical ligation also suffered neurologic
complication(2).
Regardless of the treatment choice; angiography is accepted as gold
standard for diagnosis(22), by also having the advantage of evaluating
the patency of contralateral carotid system with balloon occlusion test,
thus leading the treatment option(23)(24). Hence, every treatment should
be preceded by angiographic evaluation; yet it may not be possible in
every case due to need of emergent intervention.
Average time to CBS from initial time of diagnosis was 2.7 years, mostly
originating from proximal part of the carotid bifurcation(12). Among
patients who had a second regime of radiotherapy, median time for CBS to
occur, from beginning of re-irradiation, was 7.5 months, ranging up to
four to five years, in certain cases(10). In our patient population,
time to recurrence following primary treatment was between 6-19 months
with a mean of 8.25±5.11 months. Time from detection of recurrence or
soft tissue exposure to CBS, was from 2 to 12 months with a mean of
5.37±3.11 months, with being earlier in patients having fistula and
necrosis (6 patients; 2-4 months with a mean of 4±1.2 months). In this
regard, following massive neck or local recurrence with soft tissue
exposure, necrosis and fistula, carotid blow-out is to be expected
within 4 months and preventive measures must be undertaken during this
period.