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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3733_Библиотеки_им_академика_М_И_Перельмана.pdf
occlusion has been reported in 15% to 20% of cases with an immediate 0.4%
occurrence of stroke.
3,14
Additionally, rates of complications associated with
BOT have been reported as high as 3.2%, with potential cause of
symptomatic vascular injury in underlying diseased vasculature.
2,3,17,23,24
Reported incidences of rebleeding involving reconstructive management are
inconsistent with reports ranging from low, equal, to frequent rates of CBS
recurrence when compared to deconstructive management.
10
,14,15,22,25
Additional complications to varying degrees have been reported involving
acute thromboembolism, delayed carotid stent occlusion, stent extrusion, and
brain abscess formation.
10
,12,21,22,24,26
TIPS AND TRICKS
Reconstructive Therapy
• Preprocedural neck CTA (extending to the aortic arch) can help in
identifying the culprit lesion, vessel tortuosity, and preexisting
ipsilateral and contralateral occlusions, in addition to planning stent
sizing.
• When placing a covered stent across the bifurcation, embolization of
the ECA before stent deployment reduces risks of repeated/continued
hemorrhage from collateral filling.
• Endoleaks are often encountered involving stent placement along the
carotid bulb due to its anatomical curvature. Planned use of NBCA
from a second access could be considered in these cases.
• Given the increased incidence of recurrent hemorrhages, consider
closer imaging follow-up, aggressive reintervention, and broader stent
graft coverage on initial placement.
• In cases with wound exposure, prophylactic and therapeutic
antibiotics are suggested to decrease the risk of infection.
• As the patient’s clinical condition allows, an antiplatelet regimen is
recommended before and after covered stent placement due to the
associated risk of thromboembolic phenomenon.
Deconstructive Therapy
• Preprocedural imaging can help define anatomy, identify the
causative source, and assist in overall procedure planning.
• When embolizing the ECA and its branches, primary placement of
coils followed by liquid embolic agents provide an effective
combination to achieve hemostasis.
• Embolization should always be performed distal and proximal to
exclude potential collateral filling.
• BOT or angiographic evaluation of adequate contralateral cerebral
collateralization is crucial before ICA or CCA embolization to assess
the risk of permanent neurologic sequelae.
• In cases of permanent ICA occlusion, embolization should begin at
the petrous or cavernous segment if possible. This reduces potential
dead space (with the potential formation of a column of clot above the
occlusion site) and allows for the ophthalmic artery to fill the
remainder of the ICA in a retrograde fashion.
General
• Many times, the patient will present with complicated airway
management given the nature of the disease. Adequate resuscitation
with appropriate inotrope usage is critical to help maintain cerebral
perfusion in the setting of deconstructive therapy of the CCA/ICA.
REFERENCES
1. Borsany SJ. Rupture of the carotids following radical neck surgery in
irradiated patients. Eye Ear Nose Throat Mon. 1962;41:531–533.
2. Citardi MJ, Chaloupka JC, Son YH, et al. Management of carotid artery
rupture by monitored endovascular therapeutic occlusion (1988–1994).
Laryngoscope. 1995;1086–1092.
3. Chaloupka JC, Putman CM, Citardi MJ, et al. Endovascular therapy of
carotid blowout syndrome in head and neck surgical patients: evolving
diagnostic and management considerations. AJNR Am J Neuroradiol.
1996;17:843–852.
4. Chaloupka JC, Roth TC, Putman CM, et al. Recurrent carotid blowout
syndrome: diagnostic and therapeutic challenges in a newly recognized
subgroup of patients. AJNR Am J Neuroradiol. 1999;20:1069–1077.
5. Morrissey DD, Andersen PE, Nesbit GM, et al. Endovascular
management of hemorrhage in patients with head and neck cancer. Arch
Otolaryngol Head Neck Surg. 1997;123:15–19.
6. Maran AGD, Amin M, Wilson JA. Radical neck dissection: a 19-year
experience. J Laryngol Otol. 1989;103:760–764.
7. Shankar JJ, Maloney WJ, Vandorpe R. Amplatzer vascular plug for
occlusion of parent artery in carotid blowout with active extravasation.
Interv Neuroradiol. 2011;17(2):224–227.
8. Patsalides A, Fraser JF, Smith MJ, et al. Endovascular treatment of
carotid blowout syndrome: who and how to treat. J Neurointerv Surg.
2010;2(1):87–93.
9. Lee CW, Yang CY, Chen YF, et al. CT angiography findings in carotid
blowout syndrome and its role as a predictor of 1-year survival. AJNR
Am J Neuroradiol. 2014;35:562–567.
10. Chang FC, Lirng JF, Luo CB, et al. Carotid blowout syndrome in
patients with head-and-neck cancers: reconstructive management by
self-expandable stent-grafts. Am J Neuroradiol. 2007;28:181–188.
11. Sovik E, Klow NE, Brekke M, et al. Elective placement of covered
stents in native coronary arteries. Acta Radiol. 2003;44:294–301.
12. Chang FC, Luo CB, Lirng JF, et al. Complications of carotid blowout
syndrome in patients with head and neck cancers treated by covered
stents. Interv Neuroradiol. 2008;14(suppl 2):29–33.
13. Chang FC, Lirng JF, Luo CB, et al. Patients with head and neck cancers
and associated postirradiated carotid blowout syndrome: endovascular
therapeutic methods and outcomes. J Vasc Surg. 2008;47(5):936–945.
14. Lesley WS, Chaloupka JC, Weigele JB, et al. Preliminary experience
with endovascular reconstruction for the management of carotid blowout
syndrome. AJNR Am J Neuroradiol. 2003;24(5):975–981.
15. Pyun HW, Lee DH, Yoo HM, et al. Placement of covered stents for
carotid blowout in patients with head and neck cancer: follow-up results
after rescue treatments. AJNR Am J Neuroradiol. 2007;28(8):1594–
1598.
16. Zhao LB, Shi HB, Park S, et al. Acute bleeding in the head and neck:
angiographic findings and endovascular management. AJNR Am J
Neuroradiol. 2014;35:360–366.
17. Miller T, Burns J, Farinhas J, et al. Covered stents safely utilized to
prevent catastrophic hemorrhage in patients with advanced head and
neck malignancy. J Neurointerv Surg. 2012;4(6):426–434.
18. Koutsimpelas D, Pitton M, Külkens C, et al. Endovascular carotid
reconstruction in palliative head and neck cancer patients with
threatened carotid blowout presents a beneficial supportive care
measure. J Palliat Med. 2008;11(5):784–789.
19. Maldonado TS, Rosen RJ, Rockman CB, et al. Initial successful
management of type I endoleak after endovascular aortic aneurysm
repair with n-butyl cyanoacrylate adhesive. J Vasc Surg. 2003;38:664–
670.
20. Chen YL, Wong HF, Ku YK, et al. Endovascular covered stent
reconstruction improved the outcomes of acute carotid blowout
syndrome. Experiences at a single institute. Interv Neuroradiol.
2008;14(suppl 2):23–27.
21. Sorial E, Valentino J, Given CA, et al. The emergency use of endografts
in the carotid circulation to control hemorrhage in potentially
contaminated fields. J Vasc Surg. 2007;46(4):792–798.
22. Zussman B, Gonzalez LF, Dumont A, et al. Endovascular management
of carotid blowout. World Neurosurg. 2012;78(1–2):109–114.
23. Mathis JM, Barr JD, Jungreis CA, et al. Temporary balloon test
occlusion of the internal carotid artery: experience in 500 cases. AJNR
Am J Neuroradiol. 1995;16:749–754.
24. Warren FM, Cohen JI, Nesbit GM, et al. Management of carotid
“blowout” with endovascular stent grafts (case reports). Laryngoscope.
2002;112:428–433.
25. Hoppe H, Barnwell SL, Nesbit GM, et al. Stent-grafts in the treatment of
emergent or urgent carotid artery disease: review of 25 cases. J Vasc
Interv Radiol. 2008;19:31–41.
26. Wan WS, Lai V, Lau HY, et al. Endovascular treatment paradigm of
carotid blowout syndrome: review of 8-years experience. Eur J Radiol.
2013;82(1):95–99.
M
Section C Thoracic Embolization
18
Hemoptysis
Miguel A. De Gregorio • Alicia Laborda
assive hemoptysis, also known as life-threatening hemoptysis, is a
serious, critical condition that necessitates urgent assessment and
treatment of the patient. Despite advances in the treatment of
massive hemoptysis, it still imposes a high-risk condition. According to
published data, in any given year, 28% of pulmonologists witness a case of
death due to massive hemoptysis.
1
The lungs receive blood from the pulmonary artery and bronchial
systems under normal conditions. In pathologic situations, systemic arteries
can penetrate into the lung and irrigate contained injuries. The low-pressure
pulmonary system tends to produce small-volume hemoptysis, whereas
bleeding from the bronchial system, which shares systemic pressure, tends to
be profuse.
2
Conservative medical treatment of patients with expectoration of 300 to
600 mL of blood per day is associated with mortality in 50% to 100% of the
patients affected,3 with asphyxia rather than hemorrhage commonly being the
cause of death.4 Although surgical treatment of massive hemoptysis is
associated with mortality rates between 7.1% and 18.2%, it can reach up to
40% when surgery is performed urgently.
5
Since embolization of the bronchial artery was first described by Remy
et al.6 in 1973, it has become the main option for the treatment of massive
hemoptysis, either at first presentation or in case of recurrence. Various
studies have demonstrated its effectiveness, safety, and usefulness.
7–15
However, surgery plays an important role in the treatment of massive
hemoptysis caused by certain diseases, such as pulmonary hydatidosis,
bronchial adenoma, and aspergilloma that is refractory to other treatments.
16
In such cases, prior urgent bronchial artery embolization facilitates surgical
treatment and improves results because it allows scheduled rather than urgent
surgery to be undertaken.5 Surgery also represents the treatment of choice
when bronchial artery embolization fails repeatedly or is insufficient to
control massive life-threatening hemorrhage.
17
Currently, when embolization of the bronchial artery fails, the use of
endoscopically implanted thrombin preparations has been proposed on the
basis of its high success rate.
18
CLINICAL BACKGROUND AND PHYSICAL
EXAMINATION
Most hemoptysis are generally small, do not require urgent action, and can be
treated medically. It is crucial to differentiate hematemesis from hemoptysis.
Before assuming a lower respiratory source of the bleeding, it is important to
consider whether the blood may be coming from a nonpulmonary source,
such as the upper airway or the gastrointestinal tract. Alkaline pH, foaminess,
or the presence of pus may sometimes suggest the lungs as the primary
source of bleeding rather than the stomach.
Other data such as age, nutritional status, and comorbidities may assist
to the diagnosis and management of hemoptysis.
Epistaxis or expectoration without cough suggests that the source of
bleeding is in the upper respiratory tract, whereas expectoration accompanied
by cough indicates bleeding from the lower bronchial tree.
19
It is difficult to quantify the amount of blood expectorated. In general,
patients tend to overestimate, and besides, it is difficult to quantify the
amount of blood retained in the alveolar space and the bronchial tree.
Clinical symptoms depend on several factors such as the underlying
disease and causes of hemoptysis and the importance and amount of
bleeding. Fever, hypoxia, tachycardia, and tachypnea are going to be the most
important symptoms that may accompany a hemoptysis. The final cause of
death in hemoptysis is not hypovolemia due to blood loss but asphyxiation by
drowning.
ETIOLOGY
There are many causes of hemoptysis. Their frequency has varied with time.
In the past, lung tuberculosis was the first and main cause, but the main cause
nowadays is bronchiectasis. Salajka20 has summarized the main hemoptysis
causes in the acronym BATTLE CAMP (Table 18.1).
Hemoptysis, which can be life threatening, complicates the course of
50% to 85% of patients with an aspergilloma.21 Tuberculosis can cause
massive hemoptysis through multiple mechanisms: active cavitary or
noncavitary lung disease can cause small or large amounts of bleeding.
Active disease can cause sudden rupture of a Rasmussen aneurysm
(aneurysm of the pulmonary artery that slowly expands into an adjacent
cavity because of inflammatory erosion of the external vessel wall until it
bursts).
21
Many inflammatory or immune disorders can produce hemoptysis, such
as Goodpasture syndrome, idiopathic pulmonary hemosiderosis, lupus
pneumonitis, and Wegener granulomatosis. Other clinical situations can also
explain a hemoptysis: coagulopathy, thrombocytopenia, or use of
anticoagulants.
Iatrogenic etiology, especially due to either percutaneous or
transbronchial lung biopsy, is a cause of hemoptysis, which is usually minor
and transient and occurs in 5% to 10% of percutaneous lung biopsies, but
massive hemorrhage and death have also been reported. Hemoptysis has been
described in 6% of habitual smokers of free-base cocaine (“crack”) and has
been associated with diffuse alveolar hemorrhage.
When hemoptysis is recurrent and coincident with menstruation, it can
be caused by intrathoracic endometriosis, usually involving the pulmonary
parenchyma but occasionally affecting the airways.
21
As it has already been commented previously, blood can come from the
pulmonary artery. The main causes of pulmonary origin are as follows:
pulmonary embolism; pulmonary arteriovenous malformation, either with or
without underlying Rendu-Osler-Weber syndrome; and elevated pulmonary
capillary pressure (mitral stenosis, significant left ventricular failure,
congenital heart disease, severe pulmonary hypertension). Pulmonary artery
perforation from a Swan-Ganz catheter can also produce hemoptysis.
Depending on the study, up to 30% of patients with hemoptysis have no
cause identified even after careful evaluation. In a series of 67 patients with
cryptogenic hemoptysis, prognosis was generally good, and most patients had
resolution of bleeding within 6 months of evaluation.
22
In our series23 of 314 patients, the most frequent causes of massive
hemoptysis were bronchiectasis (31.5%), followed by acute tuberculosis or
scar tissue caused by tuberculosis (18.1%) and chronic bronchitis (14.9%).
Other causes are shown in Table 18.2.
Multislice computed tomography (CT) represents the technique of
choice for the etiologic diagnosis of nonmassive hemoptysis. Together with
fiber bronchoscopy, they can settle down a very high percentage of the most
important and severe causes of hemoptysis. Nevertheless, the use of the CT
and the fiber bronchoscopy is discussed in acute massive hemoptysis, where
arteriography can establish the diagnosis with good precision and, at the same
time, contribute to its treatment.