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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3733_Библиотеки_им_академика_М_И_Перельмана.pdf
Bronchial to pulmonary artery or pulmonary vein shunting should be
considered. Pleural lesions after radiotherapy or inflammation can frequently
cause shunting from systemic arteries to pulmonary artery or pulmonary vein.
If direct communication is evident, then embolization should be avoided to
prevent a systemic embolic showering.
Although rare complications including bronchial necrosis and
bronchoesophageal fistula16 have been reported, we have never had serious
complications caused by bronchial wall damage.
TIPS AND TRICKS
• Superselective catheterization with a microcatheter should be always
the ultimate goal from the technical standpoint.
• 3-D chest CT and or catheter angiography with rotational CT
capabilities should be carefully analyzed to understand the tumor
vascularization.
• Review if there are esophageal and anterior spinal branches before
starting to embolize any chest blood vessels.
• Antineoplastic agents should slowly be infused to the target artery,
avoiding backflow.
• A mixture with contrast material (1:1) is preferable to recognize the
flow.
• Immediately after completion of infusion, embolization should be
commenced.
• Embolic material should be mixed with contrast material to get good
opacity to check the free flow state.
• The end point of embolization is not arterial occlusion but
disappearance of tumor vasculature.
• Flow reduction observed on fluoroscopy during the injection of
embolic material is a good sign that the embolization procedure is
complete.
SUMMARY
Recent advancement of technology including imaging, microcatheter, and
embolic material makes it possible to approach transarterially to the lung and
mediastinal malignant lesions. Chemoembolization offers considerable
improvement of symptoms to patients with less complication compared to the
systemic chemotherapy. In the management of advanced chest malignancies,
including primary lung cancer, metastatic lung tumors, and chest wall
recurrence of breast cancer, transarterial treatment will play an important role
to control life-threatening symptoms and increase survival with quality of
life.
REFERENCES
1. Neyazaki T, Iked M, Seki Y, et al. Bronchial infusion therapy for lung
cancer. Cancer. 1969;24:912–922.
2. Osaki T, Oyama T, Takenoyama M, et al. Feasibility of induction
chemotherapy using bronchial infusion for locally advanced non-small
cell lung cancer: a pilot study. Surg Today. 2002;22(9):772–778.
3. Murakami M, Kuroda Y, Sano A, et al. Therapeutic results of non-small
cell lung cancer in stage III: combined synchronous irradiation with
bronchial artery infusion of CDDP [in Japanese]. Nihon Igaku Hoshasen
Gakkai Zasshi. 1995;55(1):44–49.
4. Nakanishi M, Umeda Y, Demura Y, et al. Effective use of multi-arterial
infusion chemotherapy for advanced non-small cell lung cancer patients:
four clinical specified cases. Lung Cancer. 2007;55(2):241–247.
5. Park HS, Kim YI, Kim HY, et al. Bronchial artery and systemic artery
embolization in the management of primary lung cancer patients with
hemoptysis. Cardiovasc Intervent Radiol. 2007;30:638–643.
6. Wang GR, Ensor JE, Gupta S, et al. Bronchial artery embolization for
the management of hemoptysis in oncology patients: utility and
prognostic factors. J Vasc Intervent Radiol. 2009;20(6):722–729.
7. De Gregorio MA, Medrano J, Laborda A, et al. Hemoptysis workup
before embolization: single-center experience with a 15-year period
follow-up. Tech Vasc Interv Radiol. 2007;10:270–273.
8. Morimoto K, Takatsuka Y, Sugitachi A, et al. Combined transcatheter
arterial embolization and regional chemotherapy for locally advanced
carcinoma of the breast. Acta Radiol Oncol. 1985;24(3):241–245.
9. Takizawa K, Shimamoto H, Ogawa Y, et al. Development of a new
subclavian arterial infusion chemotherapy method for locally or
recurrent advanced breast cancer using an implanted catheter-port
system after redistribution of arterial tumor supply. Cardiovasc Intervent
Radiol. 2009;32(5):1059–1066.
10. McDonald DM. Angiogenesis and remodeling of airway vasculature in
chronic inflammation. Am J Respir Crit Care Med. 2001;164:S39–S45.
11. Fan QS, Huo XK, Wang MQ, et al. Efficacy and safety of transcatheter
chemoembolization of the internal thoracic artery in patients with
hepatocellular carcinoma. Chin Med J (Engl). 2011;124:1374–1380.
12. Cauldwell EW, Siekert RG, Lininger RE, et al. The bronchial arteries:
an anatomic study of 150 human cadavers. Surg Gynecol Obstet.
1948;86:395–412.
13. Ghaye B, Dondelinger RF. Imaging guided thoracic interventions. Eur J
Respir J. 2001;17(8):507–528.
14. Chun JY, Morgan R, Belli AM. Radiological management of
hemoptysis: a comprehensive review of diagnostic imaging and
bronchial arterial embolization. Cardiovasc Intervent Radiol.
2010;33:240–250.
15. Brown AC, Ray CE. Anterior spinal cord infarction following bronchial
artery embolization Semin Intervent Radiol. 2012;29:241–244.
16. Munk PL, Morris C, Nelems B. Left main bronchial-esophageal fistula:
a complication of bronchial artery embolization. Cardiovasc Intervent
Radiol. 1990;13:95–97.
I
Section D Trauma Embolization
21
Head and Neck Trauma
Goetz Benndor
njuries to the vasculature of the head and neck can be caused by blunt
trauma during motor vehicle accidents, falls, assaults, hanging, or
sporting injuries1 and may be associated with significant morbidity and
mortality.
2–9
Whereas carotid injuries are associated with 8% to 18 %
mortality, injuries to the vertebral arteries can be associated with 17% to 38%
mortality.10 Penetrating vascular trauma is usually caused by sharp objects or
instruments, such as knives,
11–17
nail guns,18 broken glass, arrows,19 or by
bullets from gunshot injuries (GSIs).
20–24
Whereas in Western Europe and
Canada, low-velocity stab injuries are the most frequently seen, high-velocity
gunshot injuries are by far the dominant cause of penetrating vascular trauma
in the United States.
21
Iatrogenic injuries to the carotid, vertebral, and facial arteries by medical
tools or instruments are generally rare but may occur during both diagnostic
and therapeutic percutaneous procedures or during open surgical procedures.
These include injuries of the carotid during central vein catheter
placement,
25,26
inadvertent puncture of the vertebral arteries during cervical
epidural steroid injection,
27,28
or injuries to the facial and maxillary arteries
during orthognathic surgery.
29–33
Clustered location of several major arteries, some of which difficult to
reach and to control by surgical exposure, is characteristic for the head and
neck area. Vascular injuries can result in various lesions with different
clinical sequelae ranging from cerebrovascular insults (CVIs) to active
extravasation with critical blood loss. Exsanguination and ischemic stroke are
the main causal factors of morbidity and mortality for penetrating arterial
injury in the head and neck area. Mortality rate is highest in the first 24 hours
after presentation, with primary and secondary cerebral ischemic injury
accounting for the leading causes of death, followed by exsanguination.
34,35
Because blunt trauma may result in CVI, and if left untreated can lead to
stroke in 30% to 50% of all patients, with severe permanent neurologic
deficits in 48% to 58%,36 early screening and intervention is important to
improve clinical outcome.
6
Nonfatal GSI to the head and neck can be devastating, with mortality in
civilian patients ranging from 2% to 29%.
22,37,38
Vascular injury to the
carotid or vertebral arteries occurs in 15% to 25% of patients with penetrating
injuries to the neck,
39,40
and the stroke rate in patients with arterial injury
ranges is reported to be as high as 15%.
9
Immediate therapeutic measures include hemodynamic control and
preventing or decreasing morbidity associated with cerebrovascular
insufficiency or embolic phenomena.
20,41
Iatrogenic vascular trauma can present with local symptoms, stroke, or
as acute massive bleeding requiring early therapeutic management.
42
Subacute and chronic lesions such as pseudoaneurysms (PAs) or
arteriovenous fistulas (AVFs) can be initially occult and may present with
delay from weeks to months.43 Endovascular treatment (EVT) of vascular
lesions following iatrogenic trauma is identical to those caused by penetrating
or blunt trauma. Biffl et al.4 have correlated the degree of blunt injury with
clinical outcome (Table 21.1). This grading system may be used to some
degree also for penetrating trauma of the carotid and vertebral arteries.
However, it is of limited value external carotid artery (ECA) injuries, where
luminal narrowing is of no clinical importance, and does not include
management of AVFs. The distal internal maxillary artery (IMA) is a
relatively frequent location for gunshot-related injuries with massive
extravasation that often require emergent endovascular management.
Traumatic AVFs in the ECA territory are clinically relatively benign but can
cause chronic headaches, bruits, or significant cosmetic problems when
involving facial veins.44 They can usually be electively treated.
TYPES OF INJURIES
Trauma in the head and neck can result in a range of arterial and venous
injuries. Although venous injuries can also lead to hematomas and drop in
hemoglobin, their clinical presentation is often less dramatic and
angiographic detection difficult. They are usually self-limiting and rarely
require endovascular or surgical management. Arterial trauma on the other
hand can lead to rapid critical blood loss or ischemic deficits due to
downstream compromise of the cerebral circulation. The spectrum of
vascular injuries is wide and ranges from minor wall irregularities and
vasospasm caused by blast effects to the surrounding tissue to partial or
complete disruption of arterial blood flow to the central nervous system and
rupture or transection with massive extravasation and critical blood loss.
Vessel Injuries without Blood Loss
Minor Wall Irregularities (Grade I)
This most frequently observed injury (~50%) can be seen as simple
vasospasm or subtle, minimal luminal irregularities (<25%) that represent
minor intimal damages. These small lesions, sometimes only detectable on
digital subtraction angiography (DSA), do not notably narrow the arterial
lumen or compromise blood flow. Because they can be nevertheless
thrombogenic, anticoagulation or antiplatelet therapy becomes necessary
when carotid or vertebral arteries are involved. Conservative management
with warfarin, heparin, low-molecular-weight heparin (Lovenox), or
antiplatelet drugs (acetylsalicylic acid [ASA], clopidogrel) and in some cases
follow up imaging is advisable
7
,8,45
Because grade I lesion can be associated
with strokes in up to 7%,46 routine screening ideally with four-vessel
angiography (DSA) is strongly recommended.
Major Wall Irregularities and Dissections (Grade II)
These injuries can present with angiographic findings identical to
spontaneous dissections, including luminal narrowing (>25%) and associated
intimal flaps. They may be complicated by rapid intraluminal thrombus
formation and thus require a more rigorous anticoagulation regime to prevent
thromboembolism.8 Of note, studies have failed to demonstrate superiority of
anticoagulation over antiplatelet therapy in the prevention of stroke,
46,47
which can impact management in trauma patients in whom antiplatelet
therapy is generally preferred by surgeons. In select cases, endovascular
management such as stent placement may be required.
24,48,49
Routine
angiographic follow-up has been recommended, as up to 61% of patients
with grade I to II injuries will require change in management. Both,
dissections and the formation of PAs are dynamic processes, and thus show
morphologic changes over time that influence therapeutic decision making.
46
An early 7 to 10 days FU DSA is helpful to determine the acuteness of a
lesion.
Pseudoaneurysms (Grade III)
PAs are small (1 to 3 mm) or large (up to several centimeters) outpouchings
of the arterial wall caused by focal arterial damage that can lead to an
intramural or extramural hematoma with subsequent recanalization.
Depending on the extent of the injury, the wall of the PA may be covered by
tunica media, adventitia, or just thrombus material. The latter is considered
the “classical pseudoaneurysm,” with an angiographic appearance identical to
true saccular or fusiform aneurysms. Similar to spontaneous dissections,
traumatic PAs, especially with a narrow neck, may heal spontaneously with
conservative management including anticoagulation or antiplatelet therapy
and follow-up computed tomography angiography (CTA) or DSA.
50,51
Follow-up imaging is important to detect trends of progression or regression
that impact therapeutic decision making.52 A decrease in size usually
indicates healing and justifies conservative management. No signs of
regression or enlarging PAs may require interventional therapy. Some
authors suggest surgical repair,53 and no clear consensus when to treat
asymptomatic dissections or PAs currently exist. However, most operators
tend to recommend EVT, and only if there is evidence for worsening on FU
imaging.
8,54–57
Treatment options are bare metal or covered stents with or
without deployment of coils or liquids into the aneurysmal sac. Covered
stents may be used in larger wide-necked lesion but can be associated with
parent vessel occlusion.57 If simple stenting shows no trend of occlusion
within 3 to 6 months, coils are usually safe to deploy through the stent
meshes,54 or double stenting is performed.55 Alternatively, coils can be
placed in jailing technique during initial stenting. Recently introduced flow
diverter can be used as well but represent a rather expensive solution.
58
Liquids such as N-butyl cyanoacrylate ([NBCA] Trufill; DePuy
Orthopaedics, Inc., Warsaw, Indiana) and Onyx (Covidien, Irvine, California)
can be very efficient to achieve rapid occlusions43 but have a clearly higher
(unnecessary) risk of distal migration into the cerebral circulation.
Depending on availability, both CTA and DSA can be used for
screening and follow-up studies. Because detection of minor vascular injuries
and visualization of small changes during follow-up can be obscured
especially in patients with GSIs and bullet fragments that cause metallic
artifacts,59 the author has a strong preference for DSA. Especially, patients
with penetrating trauma are oftentimes of relatively young age without
significant underlying vascular diseases, which minimizes the risk of
neurologic deficit posed by supra-aortic or cerebral angiography that is less
than 1% in experienced hands. In our institution, a protocol with at least one
short-term angiogram within 7 to 10 days followed by 4 weeks and 3 months
is in place.
Occlusions (Grade IV)
Similar to spontaneous dissections, severe arterial injury may lead to an
enlarging hematoma in the vessel wall or in the surrounding tissue and to
occlusion the arterial lumen. The consequences of interrupting the carotid
blood flow on the cerebral circulation depend to a large degree on the
functional status of the circle of Willis, but stroke may occur in up to 50%.
46
Vertebral artery (VA) occlusion can be fully compensated by collateral
supply of a contralateral VA or ipsilateral cervical anastomoses. If this
collateral circulation is insufficient, cerebellar infarcts or, even worse, a
devastating basilar artery occlusion may occur especially in cases with
unfavorable anatomy or advanced atherosclerosis.60 Due to the dual supply to
the posterior fossa, complete VA occlusions may be less dangerous than
nonocclusive lesions (grades I to III).46 On the other hand, even a minimal
intimal damage is potentially thrombogenic, thus early detection and
anticoagulation or antiplatelet therapy can be crucial. Further, it is important
to be aware that a completely occluded artery following trauma may
recanalize and become a new source of thromboembolic strokes. Therefore,
prophylactic anticoagulation may be indicated.
Arteriovenous Fistulas
AVFs are not included in Biffl’s grading 4 and rarely caused by blunt trauma.
They are more frequently observed following penetrating vascular injuries.
61
Simultaneous injury to arterial and venous vessels creates a channel for
arterial blood to reenter the circulation. Traumatic AVFs are usually “singlehole” high-flow lesions that can be small or occult in the beginning, and thus
not detectable during initial diagnostic screening, but develop with varying
delay.
43,62–64
EVT of traumatic AVFs is more or less identical to the one of
congenital lesions and performed using stents, coils, detachable balloons, or
embolic liquids depending on location and angioarchitecture of the
lesion.
44,65,66
As for all arteriovenous shunting lesions, treatment is effective
only when the fistula site itself is permanently occluded (either most distal
arterial or most proximal venous segment, or both) and can often be
performed as planned procedure (Fig. 21.1).