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84 B. M. Hoppenfeld and J. Cynamon
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A–C
D–G
FIGURE 7-14. A 65-year-old man, a smoker, presented with a 2-week history of progressive ischemia and rest pain in the left
calf and foot. (A) Angiogram performed from the right common femoral artery demonstrates severe stenosis of the popliteal artery at the adductor canal. (B) Occlusions are identified in all three tibial vessels. (C) ABalkin Contralateral 5.5 Fr sheath (Cook Group Company), was advanced into the external iliac artery, and the popliteal stenosis is angioplastied with a 4 mm ⫻ 4 cm balloon. (D) A SP catheter (Medi-tech, Boston Scientific Corp.) is advanced into the posterior tibial artery and the artery is laced with a total of 120,000 U of urokinase. (E) The SP catheter (Medi-tech, Boston Scientific Corp.) then is advanced into the anterior tibial artery and tibial–peroneal trunk, lacing each of these in turn (a total of 250,000 U of urokinase was used). An overnight thrombolytic drip of 120,000 U/h of urokinase is begun through a Berenstein catheter (Angiodynamics) positioned in the popliteal artery. (F). Postthrombolysis arteriogram clearly demonstrates improvement in the tibial runoff. (G) Both the posterior tibial and anterior tibial arteries again provide flow into the foot.
the Cragg catheter (MTI,) or a multi-side hole catheter that is occluded with a tip occluding wire (Angiody­namics, Cook), or a routine guidewire, causing most of the infusion to exit the side holes in a relatively even distribution. The catheter should be positioned so that the proximal side hole is at or close to the top of the clot and the distal side hole is just proximal to the end of the clot. A coaxial system (a multi-side hole catheter with an infusion wire coaxially in the catheter) may be required to achieve these levels of infusion. A typical infusion rate of urokinase would be a total of 240,000 U/hour for the first 4 hours and then reduced to be­tween 80,000 and 120,000 U/hour for the duration of
therapy. Alternatively, r-tPA 0.5 mg to 1 mg/hour can be used. Occasionally, a higher dose of 1 to 2 mg/hour will be used over a short period and then reduced to the lower 0.5 to 1 mg/hour range for overnight infu­sions. Concomitant heparin should be used sparingly to reduce the incidence of pericatheter thrombosis. We typically give a bolus of 2000 U of heparin to the patient, followed by a heparin infusion of 500 U/hour. The par­tial prothrombin time (PTT) is monitored closely and should be less than twice the normal value (this corre­sponds to a 40 to 70 range at our institution). Care should be taken not to over-anticoagulate the patient because the incidence of bleeding, including groin he-
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Vascular Recanalization Techniques
85
E–H
FIGURE 7-15. A 43-year-old woman with a patent aortobifemoral bypass graft and occluded femoral to popliteal bypass graft
presented with an acute history of right limb ischemia involving both sensory and motor loss from the midcalf to the foot. (A) Diagnostic arteriogram is performed from the left common femoral artery, demonstrating the patent aortobifemoral bypass graft. (B) The femoral-to-popliteal graft hood is opacified, but the graft is occluded. (C) A Berenstein catheter was passed into the graft. (D) An SP catheter (Medi-tech, Boston Scientific Corp.) then was advanced through the graft, into the distal graft, and the graft was laced with 250,000 U of urokinase. (E) An overnight drip of urokinase was begun at 120,000 Units/hour. (F) Postthrombolysis arteriogram demonstrates patent graft with residual thrombus in the peroneal artery. An SP catheter (Medi-tech, Boston Scientific Corp.) then was directed into the peroneal artery and was laced with 250,000 U of urokinase. Then a urokinase drip was begun from the level of the popliteal artery at 80,000 U/hour. (G) The patient was brought back to the angiosuite that afternoon. Postthrombolysis angiogram demonstrates dissolution of the peroneal thrombus. (H) Straight-line flow into the foot is restored.
matoma, retroperitoneal hematoma, and intracerebral hemorrhage, may increase with excessive anticoagula­tion combined with a lytic agent (Fig. 7-16).
Follow-up arteriography should be performed as neces­sary and when practical. When a case is started in the morning, we typically restudy the patient late in the after­noon. If the case was started in the afternoon, we restudy the patient the next morning. During the follow-up evalu­ation, the catheter position can be adjusted to optimize the lytic effect.
Often patients experience increased pain during the lysis, which may be due to lysis and embolization of small clots. With continued infusion, these episodes are usually
self-limited and often resolve completely. If the pain and ischemia persist, a repeat angiogram is warranted. If em­boli are identified, the catheter or an injectable guidewire can be advanced to the emboli to continue thrombolysis, “chasing” the emboli down the leg, lacing the vessels with thrombolytics, and continuing the infu­sion until the emboli dissolve (see Fig. 7-17). When the clot is lysed, a search should be done for an underlying lesion that may have caused the graft to clot or the native artery to occlude. If a lesion is found, it should be cor­rected by angioplasty, stent placement, or surgery, which­ever is considered appropriate based on the lesion iden­tified (Fig. 7-18).
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A
B
FIGURE 7-16. Hematomas are not uncommon when treating with lysis; occasionally, they can be quite large. (A) Computed
tomography scan of the pelvis demonstrates blood in the anterior abdominal wall. (B) The hematoma extended up the retroperitoneal space, continuing into the psoas muscle and around the perirenal fat planes.
A–E
F–I
FIGURE 7-17. A 44-year-old woman presented to the emergency room with acute right foot ischemia, blue toes, and rest pain.
She is several years status post lower back surgery, having had pedicle screws placed from an anterior approach. (A) Diagnostic arteriogram is performed via the right common femoral artery. A complex, irregular lesion is identified in the left common iliac artery. It is postulated that this may have been an iatrogenic injury from the patient’s previous back surgery. (B) Occlusions of the distal anterior tibial artery. (C) Occlusions of the posterior tibial artery are noted. Most likely, these occlusions were responsible for the patient’s acute limb ischemia and postulated to be emboli off the common iliac lesion. (D)An8⫻ 40-mm Smart Stent (Cordis, Johnson & Johnson Corp.) was placed across the common iliac lesion. (E) The posterior tibial and anterior tibial arteries were laced with 2.5 mg of rt-PA through an SP catheter (Medi-tech, Boston Scientific Corp., Watertown, MA). (F) A Berenstein catheter (Angiodynamics) was left in the popliteal artery, and an overnight drip of 1 mg/hour rt-PA was begun. (G) Follow-up angiogram demonstrates resolution of the common iliac lesion. (H) After 15 hours of thrombolysis, there is normal three-vessel runoff from the popliteal artery. (I) There is reconstitution of the posterior tibial, dorsalis pedis, and plantar arteries, with minimal residual thrombus in the most distal aspect of the posterior tibial artery. The patient was pain free with a warm foot.
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A–C
87
FIGURE 7-18. A 57-year-old man presented with acute rest pain and mild sensory loss in the left foot. (A) Diagnostic arteriogram
is performed from the right common femoral artery, and a popliteal occlusion is identified. An Up and Over Balkin Contralateral
5.5 Fr sheath (Cook Group Company) was advanced into the left external iliac artery, and a Berenstein catheter was advanced to the level of the popliteal occlusion. The occlusion was crossed with a Bentson guidewire. An infusion catheter was placed within the popliteal occlusion, and an overnight urokinase drip was begun at 120,000 U/hour. (B) Postthrombolysis arteriogram demonstrates dissolution of the popliteal and tibial thrombus and identifies the underlying lesion of the popliteal artery. A 5 mm ⫻ 2 cm balloon angioplasty was performed of the popliteal stenosis. (C) Post angioplasty arteriogram demonstrates resolution of the lesion and return of straight-line flow into the tibial vessels and to the foot.
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11. Tetterroo E, Van Engelen AD, Spithoven JH, et al. Stent placement after iliac angioplasty: comparison of hemodynamic and angiog­raphic criteria. Radiology 1996;201:155.
12. Dyet JF, Gaines PA, Nicholson AA, et al. Treatment of chronic iliac
artery occlusions by means of percutaneous endovascular stent placement. J Vasc Interv Radiol 1997;8:349–353.
13. Reyes R, Maynar M, Lopera J, et al. Treatment of chronic iliacartery occlusions with guide wire recanalization and primary stent place­ment. J Vasc Interv Radiol 1997;8:1049.
14. Sullivan TM, Childs MB, Bacharach JM, et al. Percutaneous translu­minal angioplasty and primary stenting of the iliac arteries in 288 patients. J Vasc Surg 1997;25:829–839.
15. Vorwek D, Guenther RW, Schuermann K, et al. Primary stent place­ment for chronic iliac artery occlusions: follow-up results in 103 patients. Radiology 1995;194:745.
16. Martin EC, Katzen BT, Benenati JF, et al. Multicenter Trial of the Wallstent in the iliac and femoral arteries. J Vasc Interv Radiol 1995;6:843–849.
17. Palmaz JC, Laborde JC, Rivera FJ, et al. Stenting of the iliac arteries with the Palmaz Stent: experience from a multicenter trial. Cardiovasc Interv Radiol 1992;15:291–297.
18. Palmaz JC, Sibbitt RR, Reuter SR, et al. Expandable intraluminal graft: preliminary study. Radiology 1985;156:73–77.
18a.Bolia A. Percutaneous intentional extraluminal (subitimal) reca-
nalization of crural arteries. Eur J Radiol 1998;28:199–204.
19. Bakal CW, Cynamon J, Sprayregen S. Infrapopliteal percutaneous transluminal angioplasty: what we know. Radiology 1996;200:36.
20. Brawn LA, Ramsey LE. Is improvement real with percutaneous transluminal angioplasty in the management of renovascularhyper­tension? Lancet 1987;2:1313–1316.
21. Derkx F, Schalekamp M. Renal artery stenosis and hypertension. Lancet 1994;344:237–239.
22. Dorros G, Prince C, Mathiak L. Stenting of a renal artery stenosis achieves better relief of the obstructive lesion than balloon angioplasty. Cathet Cardiovasc Diagn 1993;29:191–198.
23. Dorros G, Jaff M, Jain A, et al. Follow-up of primary Palmaz-Schatz
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stent placement for atherosclerotic renal artery stenosis. Am J Cardiol 1195;75:1051–1055.
24. Cicutok P, McLean G, Oleaga J. Renal arter y stenosis: anatomic classification for percutaneous angioplasty. AJR Am J Roentgenol 1981;137:599–601.
25. Gruentzig A, Kuhlman V, Vetter W. Treatment of renovascular hypertension with percutaneous transluminal dilatation of a renal artery. Lancet 1978;1:801–802.
26. Palmaz JC, Kopp DT, Hayashi H, et al. Normal and stenotic renal arteries: experimental balloon-expandable intraluminal stenting. Radiology 1987;164:705–708.
27. Sos TA, Pickering TG, Sniderman K, et al. Percutaneous translumi­nal renal angioplasty in renovascularhypertension due to atheroma or fibromuscular dysplasia. N Engl J Med 1983;309:274–279.
28. Soulen MDC. Renal angioplasty: underutilized or overvalued? Ra- diology 1994;193:19–21.
29. Tegtmeyer CJ, Brown J, Ayers CA, et al. Percutaneous transluminal angioplasty for the treatment of renovascular hypertension. JAMA 1981;246:2068–2070.
30. White CJ, Ramee SR, Collins TG, et al. Renal artery stent place­ment. J Endovasc Surg 1998;5:71–77.
31. Andaz S, Shields DA, Scurr JH, et al. Thrombolysis in acute lower limb ischemia. Eur J Vasc Surg 1993;7:595–603.
32. Bero CJ, Cardella JF, Reddy K, et al. Recombinant tissue plasmino­gen activator for the treatment of lower extremity peripheral vascu­lar occlusive disease. J Vasc Interv Radiol 1995;6:571–577.
33. Ouriel K, Shortell CK, Azodo MW, et al. Acute peripheral arterial occlusion: predictors of success in catheter directed thrombolytic therapy. Radiology 1994;93:561–566.
34. Ouriel K. Surgery vs. thrombolytic therapy in the management of peripheral arterial occlusion. J Vasc Interv Radiol 1995;6:48s–54s.
35. Ouriel K, Veith FJ,Sasahara AA. Thrombolysis or peripheral arterial surgery (TOPAS): phase I results. J Vasc Surg 1996;23:64–73.
36. Rauber K, Heidinger KS, Kemkes-Matthes B. Coagulation altera­tions due to local fibrinolytic therapy with recombinant tissue plas­minogen activator (rt-PA) in patients with peripheral arterial occlu­sive disease. Cardiovasc Interv Radiol 1997;20:169–173.
37. Semba CP, Murphy TP, Bakal CW, et al. Thrombolytic therapy with use of Alteplase (rt-PA) in peripheral arterial occlusive disease: review ofthe clinical literature. J Vasc Interv Radiol 2000;11: 149–161.
C.E. Ray Jr. and A. C. WaltmanEmbolization and Chemoembolization
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8
■■■
General Principles of Embolization
and Chemoembolization
CHARLES E. RAY JR. and ARTHUR C. WALTMAN
Transcatheter embolization is a frequently performed procedure that can be used for myriad clinical indica­tions. Whether used to stop active bleeding, as palliative therapy for benign or malignant lesions, as a form of organ ablation, or in combination with chemotherapy as primary oradjunctive therapy for malignancies, emboliza­tion procedures are becoming more common in both large medical centers and community practice settings.
This chapter outlines general principles of embolic and chemoembolic therapy, with particular attention to the techniques used and to which clinical entities may benefit from such catheter directed therapy.
■ Technique
Delivery systems
Depending on the size of the vessel or vessels to be embol­ized and the embolic agent to be used the two general types of delivery methods are selective catheter and coaxial catheter systems. Selective catheterization usually is per­formed with preformed curved catheters ranging from 5 to 7 Fr in diameter. Techniques usedin selective catheteri­zation are discussed in other chapters; most commercially available tapered end-hole catheters are sufficient for em­bolization procedures. The advent of coaxial systems has allowed superselective catheterization with minimal risk to the selected vessel. Many systems, such as the Tracker­325 system (Target Therapeutics, San Jose, CA), consist of a 3 Fr catheter with a large inner lumen diameter that allows delivery of sizable embolic materials such as Gel­foam pledgets (Upjohn, Kalamazoo, MI), or microcoils,
which do not appreciably risk occluding the catheter. By using a coaxial system, the operator may catheterize the vessel of choice virtually without regard to vessel size, thus significantly decreasing the risk of both nontarget emboli­zation and damage to the underlying vessel.
Balloon-occlusion catheters (BOCs) are useful for em­bolization procedures, particularly when alcohol is used as the embolic agent (see later). BOCs are compliant balloons designed to conform to the shape of the vessel in which they are inflated, in contrast to angioplasty bal­loons, which are designed to produce a significant radial force intended to fracture a plaque. Angioplasty balloons should not be used as BOCs, because of the notable potential risk of dissection of the vessel in which the balloon is inflated.
When large particles such as Gelfoam pledgets are used for embolization, care must be taken to use a selec­tive catheter or coaxial system with an inner diameter and taper large enough to prevent occlusion of the catheter by the embolic material. A catheter with an end-hle only also should be used to prevent inadvertent nontarget embolization through a catheter side hole. In addition, if an adhesive material such as cyanoacrylate is used, the glue must be mixed with tantalum powder for radiopacity and the deliver y catheter must be flushed with dextrose solution, because exposure of the glue to ionic com­pounds causes instant polymerization and catheter occlu­sion.
Embolic agents
The number of embolic agents has increased significantly recently; however, it must be kept in mind that a com-
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C. E. Ray Jr. and A. C. Waltman
bined approach using multiple agents is often most use­ful.
To choose the embolic agent needed, the anticipated end result of the embolization procedure must be under­stood. For instance, embolization for bleeding from a posttraumatic pseudoaneurysm has a different goal from embolization/ablation of a renal tumor preoperatively. Similarly, embolization for bleeding from a renal tumor has a purpose different from that of preoperative emboli­zation of the same pathology. Large embolic agents such as coils and Gelfoam pledgets may be used for emboliza­tion of large vessels in organs with abundant collateral supply, such as the stomach or liver, in which proximal vessels can be occluded safely without risk of tissue in­farction due to the extenssive collateral network. Large agents may be also used in tissues with an end-organ vascular supply in which the entire blood supply to the area of interest is to be occluded; however, large agents should not be used in vessels in which future emboliza­tion or transcatheter therapy is anticipated. By occlusion of the only vascular supply to a region, future selective catherization will be precluded by occluding the sole vascular access to the pathology. In contrast to large agents, liquid agents such as alcohol or glue will embolize to the most distal vascular supply and cause infarction by occluding the smallest arterioles supplying a lesion. Be­cause collateral supply occurs at a site proximal to the embolization, liquid embolization is effective in destroy­ing tissue even when there is significant parasitization or collaterization of blood supply from an adjacent source; however, it should not be used unless cell death and necrosis are the desired end results.
A second characteristics that must be considered when choosing an embolic agent is the desired degree of per­manence of the occlusion. In particular, some materials are biodegradable, and recanalization of the embolized vessel should be anticipated. Most vessels embolized with Gelfoam pledgets and powder will recanalize within 2 to 3
1
weeks.
Starch microspheres represent another biode­gradable agent with an in vivo half-life of 20 to 30 min. Angiography 1 week after cross-linked collagen emboliza­tion of the hepatic artery reveals a normal hepatic arterial system and more complete return within 3 months. Autologous blood clots, a fourth degradable agent, that are currently used infrequently because of the ready avail­ability of other agents.
Polyvinyl alcohol (PVA) particles are a commonly used permanent agent, with sizes ranging from approximately 50 to 2800 lm. Embolization with PVA particles usually causes a permanent occlusion of vessels that corresponds to the size of the particles used. Other materials that have been used experimentally or in clinical trials include poly­lactic acid microspheres, mer particles dissolved in polyvinyl alcohol, dura mater.
6
4
ethylene vinylacetate copoly-
5
and human
Embolization with particulateagents isconsidered com­plete when slowing of flow, not complete statis, is visual­ized. Because all arteries will tend to “back thrombose” to the previous bifurcation point when a distal occlusion is encountered, excessive embolization will decrease out­flow enough that the entire feeding artery may throm­bose. Fluoroscopically noted reflux is another indicator that the embolization procedure should be stopped.
■ Use of embolization in Clinical settings
Nonneoplastic
Active bleeding
Hemorrhage is a clinical setting in which transcatheter embolotherapy may prove useful. Embolization of active bleeding almost always provides a less invasive form of patient management than surgical alternatives, and in certain clinical settings, such as postradiation or postsur­gical fields, it may prove to be the only viable alternative because of the difficulty of surgery in such an operative field. Active bleeding may be caused by a number of etiologies, including inflammation, neoplasm, trauma, and congenital or developmental abnormalities. Once again, the desired end result of the embolization and the degree of permanence required are essential factors in determining the embolic agent of choice.
Because bleeding caused by inflammation is usually a temporary situation (i.e., over time and with appropriate medical management, the artery will likely stop bleed­ing), a temporary embolic occlusion is usually sufficient. In such cases, embolotherapy is a temporizing procedure performed to allow coagulationor healing to occur within the vessel. In addition, because inflammatory etiologies may cause further bleeding within the same organ later, a temporary occlusion is desired so that future emboliza­tions may be performed if needed. Finally, because the desired end result is not organ ablation or cell death but
2
rather cessation of bleeding and tissue preservation, distal embolic agents, such as liquid or small particles, are usu­ally contraindicated in inflammatory causes of hemor-
3
rhage.
Two inflammatory etiologies in which embolotherapy has proven efficacious include gastrointestinal (GI) and pulmonary hemorrhage. Transcatheter embolization of GI bleeding is documented best in the setting of benign causes, such as peptic ulcer disease, erosive gastritis, and Mallory-Weiss tears. In the case of peptic ulcer disease, most patients undergo endoscopy with an attempt at sclerotherapy; however, in patients in whom sclero­therapy fails or with recurrent bleeding after initial medi­cal and endoscopic therapy, patients may be referred for angiography and possible embolotherapy. In addition, unstable patients who have massive upper GI bleeding
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may benefit from emergent embolotherapy preceding, or in lieu of, surgical therapies.
7
Embolic agents used in the treatment of peptic ulcer bleeding have included Gel­foam pledgets, stainless steel coils, PVA particles, glue, and autologous clots.
7–9
Occlusion of the more distal vasculature with agents such as glue prevents the forma­tion peripheral collateral blood supply, thereby predis­posing the embolized tissue to infection and increasing the risk of postembolization ischemic complications such as fibrosis and duodenal stenosis.
8
Central occlusion with larger agents, such as coil occlusion of the gastroduode­nal artery, allows collateral vessels to supply the distal tissue and precludes tissue infarction without compromis­ing success of the embolization procedure.
8
Gelfoam pledgets are the most commonly used agent; however, because temporary occlusion may or may not be suffi­cient, permanent central occlusion with coils is another possible therapeutic alternative.
7–9
In the setting of mas­sive upper GI bleeding without angiographic evidence of a bleeding site, embolization of the left gastric artery with Gelfoam pledgets or coils decrease the risk of recurrent GI bleeding (0% versus 50%).
10
Embolization of the left gastric artery without angiographic documentation of bleeding can be justified because approximately 85% of gastric hemorrhage is caused by a lesion supplied by the left gastric artery.
11
Embolotherapy for GI bleeding from benign causes other than peptic ulcer disease also has been successful. One study demonstrated technical success in all patients treated with emergent Gelfoam pledget and coil embo­lotherapy for active small intestinal hemorrhage; five of six (83%) patients survived hospitalization.
9
Similar suc­cess rates have been noted in other studies for pathology as varied as jejunal ulcers, pseudoaneurysms, and Meckel’s diverticulum.
12
Transcatheter embolotherapy in the treatment of he-
moptysis also has proved efficacious.
13,14
Because of the dual vascular supply to the lungs, the likelihood of postembolization tissue infarction is low, even with use of distal embolic agents such as PVA particles or liquid agents. Most pulmonary hemorrhages resulting from be­nign causes arise from the bronchial circulation; embo­lotherapy, therefore, typically is performed through the systemic circulation rather than the pulmonary arteries. There is great variability in the number and origins of the bronchial arteries; 43% of patients demonstrate a com­mon trunk supplying the left and right bronchial arteries, and most patients demonstrate two or three bronchial arteries in total.
15
Although they are small in the normal setting, the bronchial arteries become significantly en­larged in the setting of chronic inflammatory disease. Concurrent with bronchial arter y enlargement, systemic­to-pulmonary artery communications develop, exposing the pulmonary arterial bed to greatly elevated pressures and causing rupture of the pulmonar y arteries into con-
tiguous airways.
16
It is therefore from these pulmonary arteries that bleeding arises; however, pressure in the pul­monary arteries normalizes after the bronchial arteries are embolized, causing cessation of bleeding. Although rare, bleeding arising directly from the pulmonary circu­lation can be seen with Rasmussen aneurysms or pulmo­nary arteriovenous malformations (AVMs).
17
If embolotherapy of the bronchial artery is being con­sidered, caution should be exercised because of the po­tential origin of anterior spinal artery branches from the bronchial circulation. Contributions to the anterior spi­nal artery from the right bronchial artery are seen in approximately 5% of patients, whereas contributions from the left bronchial artery are decidedly rare. Branches supplying the anterior spinal artery are angiog­raphically visualized by a characteristic “hairpin” course that is anterior to the vertebral column; the artery then descends or ascends in the midline. Although emboliza­tion procedures can be performed with coaxial catheteri­zation of the bronchial artery beyond the origin of the spinal branches, the possibility of severe cord compro­mise must be considered before such a procedure is un­dertaken. Experimental evidence suggests that particles larger than 250 lm are too large to enter small spinal feeders
18
and therefore may be used safely in bronchial artery embolization. Some authors advocate that spinal cord infarction is a potential rather than real possibility, with reported cases of transverse myelitis occurring be­fore the advent of nonionic contrast media.
19
Benign disease processes that cause bronchial arterial bleeding include infectious causes such as tuberculosis and aspergillosis and noninfectious inflammatory causes such as bronchiectasis, pulmonary sarcoid, and cystic fibrosis.
14,17
Chronic inflammatory processes can cause significant recruitment of collateral vessels from the sub­clavian, axillary, internal mammary, intercostal, and phrenic arteries.
20
In the setting of persistent or recurrent hemoptysis following successful bronchial artery emboli­zation, repeat diagnostic angiography as well as em­bolotherapy of other potential collateral vessels should be undertaken. Some authors advocate bronchial artery em­bolization as a preemptive therapy in patients with cystic fibrosis before they develop potentially massive hemop-
21
tysis.
The embolic material of choice in patients with enlarged bronchial vessels and chronic inflammatory processes isPVA particles largerthan 250 lm butnot large enough to occlude the vasculature at the proximal artery level. These agents embolize distal enough to preclude significant collateral vessel recruitment while allowing re­peat embolotherapy to be performed if needed. Larger permanent agents such as coils are contraindicated be­cause repeat embolotherapy will be difficult, if not impos­sible, because of the proximal vessel occlusion. Success rates for hemostasis following bronchial artery emboliza­tion range from 77% to 91%.
13–15,17
The success rates do
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C
FIGURE 8-1. A 68-year-old man who fell from a ladder, and sustained multiple pelvic and femoral fractures. A: Anteroposterior
digital subtraction angiogram of the pelvis demonstrating contrast extravasation ( artery and traumatic pseudoaneurysm arising from the left iliolumbar artery ( pudendal artery demonstrating contrast extravasation ( artery arising from the external pudendal ( origin for gelfoam embolization. C: Selective injection of the right external pudendal artery and embolization with Gelfoam pledgets using a coaxial catheter system demonstrating complete cessation of contrast extravasation. Flow to the inferior epigastric artery is preserved by using the coaxial system. D: Selective injection of the left iliolumbar artery demonstrating the pseudoaneurysm (
open arrow).Arrow
open arrow
denotes tip of 3 Fr coaxial catheter. (
). A 3 Fr coaxial catheter was placed distal to the inferior epigastric artery
arrow
) arising from the right external pudendal
open arrow
arrow
) arising from a branch vessel. Note the replaced inferior epigastric
Continued
)
). B: Selective injection of the right external
D
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93
E
FIGURE 8-1. (
coils and demonstrating complete occlusion of the traumatic pseudoaneurysm. F: Final postprocedure angiogram demonstrating complete cessation of contrast extravasation and occlusion of the pseudoaneurysm noted in (A).
not appear to differ significantly among the various in­flammatory causes.
Continued
)E.Selective injection of the left iliolumbar artery showing embolization with Gelfoam pledgets and
teriography and embolotherapy are not considered im­mediately necessary for patient survival. In patients in whom persistent bleeding is suspected following external
Trauma
In addition to inflammatory causes of bleeding, emboliza­tion may be used in patients presenting with hemorrhage following trauma; However, in the setting of trauma the underlying nature of the vessels as well as the desired endpoint differ greatly from those seen in the setting of chronic inflammatory disease. In mostinstances, posttrau­matic bleeding involves previously healthy vessels that un­dergo acute changes such as transection or pseudoaneu­rysm formation; temporizing measures are frequently all that are required to allow the vessel to undergo the heal­ing process or to stabilize the patient preoperatively. Be­cause of these differences, the embolic agents differ from those seen with hemorrhage from chronic inflammatory diseases.
Hemorrhage associated with pelvic fractures is one of the most frequent traumatic settings in which embolo­therapy is used. Fractures in which the constraining liga­ments of the pelvis are damaged are most likely to cause severe hemorrhage; placement of an external orthopedic fixation device stabilizes the pelvis in addition to stopping venous, osseous, and minor arterial hemorrhage.
22
Exter­nal fixation devices, therefore, are recommended in pa­tients who are hemodynamically stable and in whom ar-
fixation, diagnostic angiography is necessary to exclude an arterial source of hemorrhage. It is estimated that approximately 7% to 11% of patients with pelvic fractures will require embolization.
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The most common sources of arterial hemorrhage fol­lowing pelvic trauma are branches of the internal iliac arteries (Fig. 8-1). Cut-film angiography is the preferred method for initial diagnostic angiography done because of the presence of bowel motion artifact in the pelvis during digital subtraction angiography (DSA), although DSA may be sufficient in patients who are hemodynami­cally unstable and in whom time is crucial. It is recom­mended that distal aortogram be done before selective catheterization of the internal iliac arterie is performed because of the possibility of concomitant arterial damage
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to other vessels,
followed by selective angiography of both internal iliac arteries. In most cases, temporary oc­clusion to stop active extravasation is sufficient, because arterial spasm, thrombosis, and possibly arterial repair will occur once the patient is hemodynamically stable. Because of the rich collateral network within the pelvis, tissue infarction is an uncommon complication of em­bolization with large agents. Although coils have been used with success, permanent occlusion usually is not
F