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154 Pulmonary and Bronchial Arteries
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plications ranges from 1 to 5%. Complications include contrast reaction, transient renal dysfunction, access site hematoma, arrhythmia, and respiratory distress. Cardiac perforation is rare when pigtail catheters are used. The incidence of major complications has been reported to be less than 1%.
7,8
The most common indication for pulmonary arteriog­raphy is for a patient with an indeterminate V/Q study. Pulmonary arteriography is often performed in patients with a low-probability V/Q study with a strong clinical suspicion of pulmonar y embolism. A pulmonary arte­riogram may be performed in patients with a high-prob­ability V/Q study to confirm the diagnosis before starting anticoagulation, thrombolytic therapy, insertion of an in­ferior vena cava filter, or if the clinical suspicion for pul­monary embolism does not correlate with the result of the V/Q study.
Pulmonary embolization occurs to the lower lobes in more than 50% of patients and is bilateral in 25% of patients.
9
Pulmonary emboli may lyse spontaneously, or­ganize and incorporate into the arterial wall as a plaque, or recanalize. Partial lysis of pulmonary emboli can occur within 24 hours, and complete lysis can occur within 1 to 3 weeks.
10
The primary angiographic signs of pulmonary embo­lism include an intravascular filling defect (Fig. 15-1) and an abrupt vessel cutoff (Fig. 15-2). Overlying vessels must not be confused to be filling defects. Occasionally, a small branch is occluded flush with the origin of the vessel, which makes detection difficult. Secondary angiographic findings of pulmonar y embolism include parenchymal staining, decreased perfusion, crowded vessels, delayed venous return from the affected area, pruning of vessels, slow flow, and shunting away from the involved lung.
Pulmonary arter y catheterization most commonly is performed by the transfemoral route, but it can be per­formed from an upper-extremity vein or internal jugular vein approach. When using the common femoral vein approach, an iliac and inferior venacavogram is per­formed to exclude the presence of thrombus before the catheter is advanced into the right atrium.
Catheters used for pulmonary arteriography typically have a pigtail tip to resist catheter recoil and multiple side holes to allow for rapid contrast injection. End-hole catheters have been known to cause myocardial injury and pericardial extravasation through recoil and jet ef­fect. The Grollman-type pigtail catheter has good torque control and is angled at the distal shaft that facilitates catheter passage through the tricuspid valve and right ventricular outflow tract (Fig. 15-3). After the right ven­tricle is entered, the catheter is rotated to direct the tip toward the pulmonic valve. The catheter then is ad­vanced into the pulmonary artery. An alternative method uses a standard pigtail catheter and a tip-deflecting guidewire to angle the distal shaft of the catheter.
FIGURE 15-1. Pulmonary embolism. Intraluminal filling defect is present within a left lower lobe pulmonary artery branch (
arrow
).
FIGURE 15-2. Pulmonary embolism. An abrupt vessel cutoff is present at the right upper lobe pulmonary artery branch
arrow
).
(
FIGURE 15-3. Grollman pigtail catheter.
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The patient’s electrocardiogram must be monitored continuously for the occurrence of induced ventricular ectopic beats during catheter manipulations within the cardiac chambers. Catheter-induced ventricular tachy­cardia usually can be reversed by immediately withdraw­ing the catheter. Rarely, intravenous administration of lidocaine or electroversion may be required. If left bun­dle-branch conduction block is present, there is a risk of inducing total heart block during catheterization, and a temporary cardiac pacemaker should be placed before
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155
the catheter is introduced into the pulmonary artery. Pulmonary artery pressure can be measured using the diagnostic catheter. Some interventionalists recommend decreasing the contrast injection rate and volume in pa­tients with a pulmonar y artery systolic pressure greater than 40 mm Hg; however, no relationship between ad­ministered contrast dose and complications in patients with pulmonary hypertension has been demonstrated.
11
A technically adequate pulmonar y arteriogram to ex­clude the presence of pulmonary embolus requires selec­tive catheterization of the right and left pulmonary arter­ies, with imaging in at least the frontal and one oblique projection. The ipsilateral posterior oblique view tends to produce the least amount of vascular overlap, especially of the lower lobes (Fig. 15-4). If any injection demon­strates embolus, the examination usually can be stopped.
Massive pulmonary emboli or emboli that do not re­spond to anticoagulation may require aggressive therapy. Catheter-directed thrombolytic therapy, thromboaspira­tion, mechanical clot fragmentation, and stent place­ment have been used to treat massive pulmonary embo-
12–15
lism.
The role of local transcatheter therapy for acute pulmonary embolism has yet to be defined. Surgical pul­monary embolectomy is performed as a last resort in
A B
FIGURE 15-4. Pulmonary embolism. Selective left pulmonary arteriogram in the right posterior oblique projection A: shows overlap of the lower lobe branches. The left posterior oblique view B: clearly demonstrates a large left lower lobe embolus.
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patients with cardiopulmonary collapse who do not re­spond to transcatheter techniques.
Chronic pulmonary embolism
Repeated episodes of pulmonary embolism with failureof the pulmonary emboli to lyse or recanalize may result in pulmonary hypertension and right ventricular dysfunc­tion. Computed tomography (CT) and magnetic reso­nance imaging are useful in differentiating this disorder from other causes of chronic pulmonary artery hyperten­sion. Angiography is the definitive diagnostic procedure performed for diagnostic confirmation and preoperative planning for open thromboendarterectomy. Chronic thromboembolic disease produces webs, luminal irregu­larities, segments of abrupt vessel narrowing, and obstruc­tion (Fig. 15-5).
16
The main pulmonary arteries are usu-
ally dilated. The disease is usually bilateral.
Pulmonary arteriovenous malformations
Pulmonary arteriovenous malformations (PAVMs) are abnormal connections that develop between pulmonar y artery and pulmonary vein branches originating from abnormal development of pulmonary capillaries. The PAVM results in a right-to-left shunt. PAVMs are divided into simple and complex malformations. Simple malforma-
tions have a single segmental artery and draining vein. Complex malformations have two or more arteries that sup-
ply the PAVM with one or two draining veins (Fig. 15-6). About 80 to 90% of all PAVMs are simple, and 10 to 20%
are complex. PAVMs are found most commonly in the lower lobes and are multiple in 33 to 50% of patients and bilateral in 8 to 20%.
17,18
PAVMs may occur sporadically, but most are seen in patients with Osler–Weber–Rendu syndrome, also known as hereditary hemorrhagic telangiectasia (HHT), an autoso­mal dominant disease characterized by telangiectasias or AVMs of the respiratory tract, gastrointestinal tract, and brain. Ninety percent of patients with HHT have epis-
17–19
taxis.
About half of patients with PAVMs have HHT. The likelihood of having HHT is greater if the patient has multiple PAVMs rather than a single lesion. Family mem­bers should be evaluated because up to one third of them also have PAVMs.
Patients with PAVMs commonly have initial symptoms related to pulmonary-to-systemic shunting, such as low arterial blood oxygen leading to dyspnea and fatigue, or they may have systemic arterial embolization resulting in stroke or brain abscess. Rupture of a PAVM may result in hemoptysis or hemothorax.
The goal of PAVM treatment is occlusion of the shunt to prevent complications resulting from paradoxical em­bolization and to enhance arterial oxygen saturation. Em­bolotherapy is recommended when the feeding artery of
18
a PAVM exceeds 3 mm in diameter.
Embolotherapy
with coils or detachable balloons has become the treat-
19
ment of choice.
The use of liquid or small-particle em­bolic agents for therapeutic embolization is ineffective and may result in inadvertent systemic embolization. Therapeutic embolization is performed at the pulmo-
FIGURE 15-5. Chronic pulmonary thromboembolism. Webs
arrow
) and mural irregularities (
(
curved arrow
) are present.
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157
A B
C
FIGURE 15-6. Pulmonary arteriovenous malformation
(PAVM). A: This patient presented with a brain abscess resulting from B: a large complex right upper lobe AVM. There are two feeding arterial branches ( and a large draining vein ( by placement of embolization coils.
arrow
). C: The AVM was occluded
curved arrows
)
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nary artery branch immediately proximal to the malfor­mation. Embolotherapy is preferred over surgical resec­tion in patients with multiple PAVMs because emboliza­tion spares normal lung and allows for future embolization of enlarging PAVMs.
■ Bronchial Arteriography
Management of hemoptysis is frequently a challenging clinical problem. Most patients with mild intermittent bleeding respond to supportive therapy and to medica­tions that treat the underlying cause; however, the mor­tality rate in patients with acute massive hemoptysis is high in those who are inadequately treated, with death resulting from asphyxiation rather than from exsanguina­tion. The definition of massive hemoptysis varies in the medical literature from less than 100 mL to greater than 600 mL in 24 hours.
20
Criteria for bronchial artery em­bolization are variable, and the amount of hemoptysis may be difficult to measure; however, a patient with any amount of hemoptysis that is life threatening may benefit from bronchial artery embolotherapy.
The most common causes of massive or repeated hemoptysis include tuberculosis, bronchiectasis, pneu­moconiosis, aspergilloma, cancer, amyloidosis, sarcoi­dosis, and cystic fibrosis. These destructive lung processes cause massive hemoptysis by erosion of blood vessels in its vicinity. Hemorrhage usually arises from the bronchial arteries. The pulmonary artery is rarely a source of hemoptysis. Conditions that may result in hemorrhage arising from the pulmonary artery include a Rasmussen aneurysm (erosion of a tuberculosis cavity into a pulmo­nary artery branch), traumatic pseudoaneur ysm (e.g., over­inflation of a Swan–Ganz catheter balloon, penetrating thoracic trauma) (Fig. 15-7), and PAVMs.
Surgery can be a definitive treatment for massive
hemoptysis but is a viable option only for patients who present with localized unilateral disease. Surgery is con­traindicated for patients with diffuse, bilateral, or ad­vanced pulmonar y disease. Other contraindications to surgery include inability to localize the site of bleeding, bleeding from both lungs, and nonresectable malig­nancy. Bronchial arter y embolization is an effective pri­mary method to control massive or recurrent hemoptysis, especially in patients who are not suitable candidates for surgical resection. Bronchial arteriography and emboliza­tion can be performed in combination with surgery or medical therapy of the underlying condition. Angiog­raphic localization and embolization of the bleeding ves­sels can be used to stabilize a patient prior to surgery.
Localization of the bleeding site is often useful before arteriography because abnormal but nonbleeding vessels may be encountered in patients with diffuse or bilateral disease. Bronchoscopy can be used to identify the side and sometimes site of bleeding; however, it may be tech­nically challenging in patients with acute massive hemop­tysis. Chest radiography and CT might indicate the source of hemorrhage, but these tests are often unreli­able. If the site of hemorrhage cannot be accurately local­ized or if diffuse disease is present, all identifiable bron­chial artery branches are embolized.
The bronchial arteries are variable in number and distribution, but most arise from the descending thoracic aorta at the level of the T5–T6 vertebral bodies and the carina. The most common bronchial arter y origin vari­ations include single arteries bilaterally (30%), two bron­chial arteries on one side and a single bronchial artery on the contralateral side (45%), and four bronchial arteries with two on each side (20%) or three left and one right
21
(4%).
The most common arteriographic findings in patients with bronchial artery bleeding include enlarge­ment of the bronchial artery (diameter ⬎3 mm), hyper­vascularity, aneurysmal dilatation, prominent parenchy-
A
FIGURE 15-7. Traumatic pulmonary artery pseudoaneurysm. A: A pseudoaneurysm of the lingular branch of the left pulmonary artery resulting from a gunshot wound. B: Treatment was with coil embolization.
B
mal stain, and bronchial-to-pulmonary artery shunting
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(Figs. 15-8 and 15-9). In patients with neoplasms, the vascular supply is usually from bronchial arteries or para­sitized intercostal arteries, and multiple feeding arteries are often present. Embolization is performed, even though no contrast extravasation is identified, because contrast extravasation into a bronchus is a rare arteriog­raphic finding. If a potential bleeding source cannot be identified, a descending thoracic aortogram with the pig­tail catheter placed near the left subclavian artery may be helpful.
Nonbronchial systemic collateral arteries are a signifi-
cant bleeding source in many cases.
22
Common nonbron­chial systemic collaterals include the internal mammary artery, thyrocervical trunk, branches of the subclavian or axillary artery, intercostal arteries, and inferior phrenic artery.
Occasionally, a spinal arter y branch may arise from a bronchial artery. Careful consideration must be given to the arterial supply to the spinal cord when performing bronchial arteriography and embolization. The anterior spinal artery supplies the anterior portion of the cord and can be identified by its characteristic cephalic course with a hairpin bend in the midline within the ventral median sulcus. Many interventional radiologists consider the presence of spinal artery branches originating from the bronchial artery a contraindication to embolization (Fig. 15-10).
FIGURE 15-8. Bronchial arteriogram. Left bronchial arte­riogram in a patient with massive hemoptysis from sarcoidosis. Findings include bronchial artery enlargement and hypervas­cularity.
23
Some researchers, however, have described
J. E. Silberzweig 159
FIGURE 15-9. Bronchial artery to pulmonary artery shunting.
Right bronchial arteriogram in a patient with massive hemop­tysis from tuberculosis. Findings include bronchial artery (
) to pulmonary artery (
row
vascularity.
curved arrow
) shunting and hyper-
ar-
successful bronchial artery embolization with no resul­tant neurologic complications in the presence of spinal artery branches. These procedures were performed with nonionic contrast and large embolization particles to pre-
24,25
vent unintentional embolization of spinal feeders.
Be­cause of the remote possibility of spinal cord injury from bronchial artery embolization, a neurologic examination should be performed before bronchial arteriography is done.
The most commonly used agents are polyvinyl alcohol (PVA) particles and Gelfoam pledgets. PVA particle sizes between 250 and 700 l are used. Smaller particles could pass through small spinal artery branches or bron­chial–pulmonary artery shunts. It is essential that the catheter be well seated and that there is no obvious risk of spinal artery embolization. If the spinal arteries are seen and the catheter can be advanced distal to their origin, embolic material can be placed from that location.
Visceral selective catheters, such as the Cobra, Sim­mons, or Mikaelsson, typically are used for bronchial artery catheterization. A coaxial microcatheter is often used for catheterization of bronchial artery branches. Use of a conventional 5Fr catheter placed within the origin of the bronchial artery may not allow passage of embolic materials into peripheral branches because the catheter may be occlusive and prevent flow beyond the catheter tip. Use of a microcatheter permits superselec­tive bronchial artery catheterization and embolization
26
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FIGURE 15-10. Spinal artery branch. The right bronchial ar­tery and superior intercostal artery arise from a common bron­chial intercostal trunk. An anterior spinal artery branch ( arises from the superior intercostal artery (
curved arrow
arrow
). Em­bolization of the right bronchial artery was performed after placing a microcatheter distal to the origin of the intercostal artery and spinal artery branch.
without occluding flow into the bronchial artery and occluding branches such as the spinal artery.
Bronchial artery embolization can be expected to pro­vide initial control of hemorrhage in 75 to 90% of pa­tients. Technical failure results from an inability to iden­tify and catheterize the bronchial arteries. Failure to catheterize a bronchial artery occurs in up to 10% of
23,27
patients.
The most common causes of recurrent bleeding include incomplete initial embolization or fail­ure to identify all bleeding vessels, recruitment of collat­eral vessels, recanalization of embolized vessels, and pro-
23,27
gression of disease.
Late rebleeding (i.e., after 6 months) may occur in up to 20% of patients initially controlled by bronchial artery embolization. This prob­lem is not unexpected, however, because embolization is a palliative procedure and does not directly treat the underlying disease.
Complications from embolotherapy occur in about 2 to 5% of cases and include nontarget embolization, bron­chial or esophageal necrosis, and subintimal aortic injec-
26,27
tions.
The most severe complication of bronchial ar-
tery embolization is ischemic injury to the spinal cord from contrast- or embolization-related injury, because radicular spinal arteries may arise from bronchial arteries or from intercostobronchial trunks. The reported fre­quency of this complication is less than 1%.
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2. Garg K, Welsh CH, Feyerbend AJ, et al. Pulmonary embolism: diagnosis with spiral CT and ventilation-perfusion scanning-corre­lation with pulmonary angiographic results or clinical outcome. Radiology 1998;208:201–208.
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13. Greenfield LJ, Proctor MC, Williams DM, Wakefield TW. Long-term experience with transvenous catheter pulmonary embolectomy. J Vasc Surg 1993;18:450–457.
14. Uflacker R, Strange C, Vujic I. Massive pulmonary embolism: pre­liminary results of treatment with the Amplatz thrombectomy de­vice. J Vasc Interv Radiol 1996;7:519–528.
15. Lang EV, Barnhart WH, Walton DL, Raab SS. Percutaneous pulmo­nary thrombectomy. J Vasc Interv Radiol 1997;8:261–266.
16. Auger WR, Fedullo PF, Moser KM, et al. Chronic major-vessel thromboembolic pulmonary artery obstruction: appearance at angiography. Radiology 1992;182:393–398.
17. Guttmacher AE, Marchuk DA, White RI Jr.Hereditary hemorrhagic telangiectasia. N Engl J Med 1995;333:918–924.
18. Coley SC, Jackson JE. Pulmonary arteriovenousmalformations. Clin Radiol 1998;53:396–404.
19. White RI Jr, Pollak JS, Wirth JA. Pulmonar y arteriovenous malfor­mations: diagnosis and transcatheter embolotherapy. J Vasc Interv Radiol 1996;7:787–804.
20. Fernando HC, Stein M, Benfield JR, Link DP. Role of bronchial
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artery embolization in the management of hemoptysis. Arch Surg 1998;133:862–865.
21. Kadir S. Regional anatomy of the thoracic aorta. In: Atlas of Normal and Variant Angiographic Anatomy. Philadelphia: WB Saunders; 1991:49.
22. Keller FS, Rosch J, Loflin TG, et al. Nonbronchial systemic collat­eral arteries: significance in percutaneous embolotherapy for hemoptysis. Radiology 1987;164:687–692.
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24. Mauro MA, Jaques PF, Morris S. Bronchial artery embolization for control of hemoptysis. Semin Interv Radiol 1992;9:45–51.
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H.Spindola-Franc o, S. Segal, B. G. Fish, and M. A. GreenbergDiseasesof the Thorac ic Aorta
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16
■■■
Diseases of the Thoracic Aorta
HUGO SPINDOLA-FRANCO, SCOTT SEGAL, BERNARD G. FISH,
and MARK A. GREENBERG
Medical and surgical treatment as well as recently devel­oped interventional catheter procedures for the treat­ment of aortic diseases requires precise delineation of the pathological disorders. Concurrent with the development of these new techniques, the emergence of new imaging modalities such as magnetic resonance imaging (MRI), spiral computed tomography (CT), and transesophageal echocardiography (TEE) have revolutionized our ability to diagnose these complex conditions. Once considered the gold standard, angiography remains important only when other techniques are inconclusive.
Acquired diseases of the aorta such as ectasia, aneu­rysm, dissection, and its variants occur as a result of de­generative processes in older persons. These processes are accelerated in persons who have underlying connec­tive tissue disorders such as Marfan syndrome and in those with hypertension and atherosclerosis. Of these entities, acute aortic dissection or rupture may represent a surgical emergency. Aortic trauma also results in an acute emergency requiring the most expeditious diagno­sis and surgical management. Aortic arteritis syndromes are caused by inflammatory diseases such as giant cell arteritis and Takayasu arteritis, which may lead to aortic insufficiency or obstructive lesions. Aortitis also occurs during late stages of syphilis. Complications of catheter and surgical procedures also may require surgical inter­vention. Recognition of these complications has become more important as more procedures are performed. Sec­ondary involvement of the aorta by neoplasms, abscesses, and hematomas are a challenge to the clinician. Modern imaging techniques have become essential in the diagno­sis and management of these entities.
Congenital diseases of the aorta constitute a smaller
segment of the population with aortic disease. common entities are preoperative and postoperative coarctation of the aorta and patent ductus arteriosus. Other uncommon disorders occasionally are encoun­tered, including vascular rings, cervical aortic arch, inter­ruption of the aortic arch, and anomalous origin of a pulmonary artery.Pulmonary artery slingand ductusarte­riosus sling are rarely encountered. Bronchial arteries are dilated in cyanotic congenital heart disease with pulmo­nary atresia and may be hemodynamically significant as a source of pulmonary blood flow.Coil embolizationmay be necessary before surgical correction of these entities. Pul­monary sequestrations are supplied by vessels arising from the aorta and may be treated by coil embolization.
■ Aortic Dissection
Aortic dissection consists of an intimal tear in the wall of the aorta that causes separation of the intramural layers, usually between the middle and outer thirds of the media, creating a false lumen(Fig. 16-1). Blood in the false lumen may reenter the true lumen via a second intimal tear, or it may rupture through the adventitia into the periaortic tissues. Most commonly, dissections are believed to be caused by cystic medial necrosis. Proximal dissections tend to occur in younger persons who often are found to have Marfan syndrome (Figs. 16-2 and 16-3). Less commonly, inherited connective tissue disorders such as osteogenesis imperfecta, Turner syndrome, and Ehlers-Danlos syn­drome may be associated with proximal dissections. Distal dissections occur more commonly in older patients with hypertension. Other less common causes include
1,2
The most
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