postoperative aortic fistulas into the airways: etiology, pathogenesis, presentation, diagnosis, and...
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2003;75:1998-2006 Ann Thorac SurgMarco Picichè, Ruggero De Paulis, Alessandro Fabbri and Luigi Chiariello
diagnosis, and managementPostoperative aortic fistulas into the airways: etiology, pathogenesis, presentation,
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Postoperative Aortic Fistulas Into the Airways:Etiology, Pathogenesis, Presentation, Diagnosis, andManagementMarco Piciche, MD, Ruggero De Paulis, Alessandro Fabbri, MD, andLuigi Chiariello, MDCardiac Surgery Department, San Bortolo Hospital, Vicenza, Italy, and Chair of Cardiac Surgery, “Tor Vergata” University ofRome, Rome, Italy
Postoperative aortobronchial and aortopulmonary fistu-las are rare and late complications of cardiac surgery.They mostly complicate descending thoracic aortic pro-cedures. Hemoptysis is the main symptom, and may bemassive or intermittent. The reported interval betweenthe time of operation and the onset of hemoptysis rangesfrom 3 weeks to 25 years. Diagnostic examinations areoften unable to directly visualize a fistula. Indication forsurgical or endovascular repair mostly relies on clinicalsuspicion and nonspecific diagnostic features. Urgenttreatment is based on the association of the followingelements: (1) hemoptysis, (2) history of previous cardiac
or aortic operation, (3) presence of lung infiltrates on thechest roentgenogram, (4) lung hemorrage on the com-puted tomographic scan, and (5) and visualization of apseudoaneurysm. Aortobronchopulmonary fistulas areuniformly fatal if untreated. The overall surgical mortal-ity rate is 15.3%. There is no procedure-related mortalityafter endovascular stent grafting. A review of the En-glish-language literature from 1947 to October 2002 ispresented.
(Ann Thorac Surg 2003;75:1998–2006)© 2003 by The Society of Thoracic Surgeons
Aortic fistulas into the bronchial tree and lung paren-chyma may develop after unpredictable periods
after surgery and are often the consequence of pseudo-aneurysms. Hemoptysis, whether massive or intermit-tent, represents the most common symptom [1, 2]. Follow-ing our case report describing an aortic pseudoaneurysm(PSA) fistulizating into the right bronchial tree [3], wecompleted the study on postoperative aortobronchopul-monary fistulas (ABPFs) through a collective review ofthe literature.
Patients and Methods
We performed a MEDLINE search with the terms “aor-tobronchial fistula,” “aortopulmonary,” “aortobroncho-pulmonary,” “aortotracheal,” “pseudoaneurysm,” “post-operative,” and “hemoptysis.” References in each articlewere screened to look for any article not reported onMEDLINE. All case reports and reviews from 1947 toOctober 2002 have been included. A total of 76 patientsand 79 fistulas (3 patients were affected by two fistulas)were found. The etiology, pathogenesis, and anatomical,clinical, diagnostic, and surgical features, as well as theoutcomes, were examined.
Historical MarksThe first ABPF was described by Girardet [4] in 1914 in apatient affected by pulmonary tuberculosis. In 1934Keefer and Mallory [5] reported the first series of chronicaortic aneurysms with six autopsy cases of ABPFs. Thefirst case of postsurgical fistula was observed by Jones [6]in 1947 in an 11-year-old girl who had undergone patentductus arteriosus ligation 2 years previously.
In the 1960s Davey [7] identified the cause of fistulas inthe material used for aortic replacement, namely, Ivalongrafts. The first of three existing cases of double ABPF inthe same patient was reported by Grillo and colleagues[8] in 1968. In 1993, Ramakantan and Shah [9] firstdescribed a communication into the right bronchial tree.In 1996 Campagna and colleagues [10] and Chuter andassociates [11] separately reported successful treatmentwith endovascular stenting.
Etiology and PathogenesisAortic fistulas into the airways are more common afterdescending thoracic aorta (DTA) procedures. Duringinfancy they can be seen after patent ductus arteriosus oraortic coartaction repair [6, 7, 10–35]. In adults theyprevail after resection of DTA chronic aneurysms [36–48]. Aortic fistulas have also been reported after surgicalrepair of aortic arch [49, 50, 51] and thoracoabdominalaneurysms [52], DTA traumatic rupture [51, 53], types A[3, 22, 54, 55] and B [35, 56, 57] dissection, Takayasuarteritis [58], and aortic sarcoma (Table 1) [59]. The ABPFsencountered after surgery for tetralogy of Fallot [23],
Address reprint requests to Dr Chiariello, Cattedra di Cardiochirurgia,Universita di Roma “Tor Vergata,” European Hospital, Via Portuense 700,00149, Rome, Italy.
© 2003 by The Society of Thoracic Surgeons 0003-4975/03/$30.00Published by Elsevier Inc PII S0003-4975(02)04837-3
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aortic and mitral valves [9, 60, 61], and tumor of thoracicvertebrae represent unique cases [62]. Finally, endobron-chial expandable metal stents caused fistulas in a patientwith pediatric bronchomalacia [63], after lung transplan-tation [64], aortic dissection [55], or tracheal resection [65](Table 2).
Postoperative aortic PSAs may arise from disruption ofone or more arterial wall layers with extravasation ofblood into the surrounding spaces. The hematoma isthen held by the remaining vascular layers, fibroustissue, and sometimes the parietal pericardium. A neo-intima may develop [3]. Disruption may be related todifferent sites depending on the type of operation. Thecannulation site for cardiopulmonary bypass is the mostcommon in a review by Sullivan and associates [66].Graft-to-graft anastomosis [3], saphenous vein anasto-mosis [67], aortic and needle vent sites [68], patch suturelines, and distal or proximal suture lines in aortic replace-ment [69] have also been reported.
Inappropriately tight sutures, fragility of the host tis-sue, or inappropriate material each play a role in pseudo-anaurysm development [6]. Merrill and coworkers [70]have reported PSAs caused by silk suture fragmentationand dissolution in patients with Teflon grafts. A sutureline may also be disrupted by adjacent arteriosclerosis[53]. Bacterial or fungal infection of a prosthetic graft mayplay a role [16, 24, 25, 38, 54, 62]. As with true aneurysms,but at a faster rate, the PSA progressively enlarges andcauses compression of the airways. This results in a localinflammatory response and the phenomenon of pressurenecrosis, which increases the inflammatory process. Sta-ble adhesions may occur [66]. The lung undergoeschronic pulsate erosion exerted by the vascular mass.When the wall tension of the PSA becomes critical, itruptures into the airways [3].
A PSA is not the only possible cause of bronchopul-monary damage, which may also be due to neoaneu-rysms involving the native aortic wall next to suture lines[23, 36–38, 43, 48, 56, 58]. In other cases slow but contin-uous damage to lung parenchyma is caused by strictlyadjacent foreign material such as graft substance [7, 57],remnant of temporary bypass [50, 51], silk knots andsuture material [6, 17, 37, 46], endobronchial expandablemetal stents [55, 63–65], or kinking of an aortic stent-graft[52] (Table 3).
The left lung is much more involved than the right one.This may be explained by the short distance from theDTA. Conversely, communications between the ascend-ing aorta and the right lung are rare, and only 7 caseshave been reported so far [3, 9, 22, 51, 54, 60, 61]. Reportedsites of aortic and bronchopulmonary ends of fistulas arelisted in Table 4.
PresentationHemoptysis is the first (and often the only) symptom ofABPFs. It may be massive or intermittent, depending onthe size of the opening. The fistula is usually small and itis easily occluded by clots. It then stays closed for weeksor months; when clots lese or dislodge, the communica-tion opens again and a new bleeding ensues [6, 7, 10, 11,
14, 15, 17–23, 36, 37, 40, 41, 43–46, 50–54, 56–59, 62, 71].This process recurs several times, increasing at eachepisode until the fistula becomes large enough to causemassive passage of blood. The reported interval betweenthe time of operation and the onset of hemoptysis isvariable, ranging from 10 weeks [13] to 25 years [11, 23,72] after cardiac or aortic procedures. The interval evendecreases to 3 weeks after endobronchial expandablemetal stents implant [63]. Less frequently, massive bleed-ing appears abruptly at the first episode, representing animminent threat to life (Tables 1 and 2) [3, 49, 10, 18, 13,16, 23, 26, 38, 39, 43, 55, 58, 60, 63–65].
Other symptoms and signs are inconstant. Dyspneaand cough [15, 16, 18, 36, 45, 48, 60, 65], chest or back pain[23, 36, 48, 65], pulmonary rales [15, 18], hypoxemia [11,45, 47], dysphonia [28], hoarseness [48], tachypnea [45],fever [15], sepsis [11], or respiratory alcalosis [45], failure[78], or arrest [39, 58] have been reported. The patientmay be unstable hemodynamically, with hypotension[56], shock [13, 36], and cardiac arrest (Tables 1 and 2)[36].
DiagnosisHemoptysis may be present in many pathologic condi-tions. For this reason, anamnesis is extremely importantfor differential diagnosis. A history of previous cardiac oraortic operations is highly suggestive of ABPF, especiallyif DTA was involved [3].
Chest roentgenography is the first means of examina-tion (Fig 1). It may disclose a mediastinal mass or intra-parenchymal hemorrage, although imaging of lung infil-trate is nonspecific and a radiogram may even be normal[46]. Thus, additional investigations are required (Tables1 and 2).
Aortography has been widely used in the past. Thecontrast fluid may be seen directly in the fistula [31]. Ifthe contrast medium is seen only in the bronchus itrepresents an indirect sign; however, more often thefistula is occluded by clots and aortography is nondiag-nostic [37]. Dislodgment of clots with fatal hemoptysisduring injection of contrast material has been reported[9].
Conventional computed tomography (CT) was firstused for diagnosis of ABPF in 1986 [41]. It is easilyperformed in emergency conditions. With a low dose ofcontrast material it reveals lung consolidation due toparenchymal hemorrage, the diameter and contours of amass, and eventual compression of surrounding struc-tures (Fig 2). However, it is quite unlikely to yield a scanthat directly visualizes the passage of contrast from theaorta into the airways. To our knowledge, this has onlybeen reported by Riancho and colleagues [18] and byNinan and associates [61].
Bronchoscopy is able to detect the source of hemopty-sis, as it may visualize the bronchial tear [43]. However,dislodgment of occluding clots and traumatic rupture ofan adherent vascular mass are potential serious compli-cations [49, 43, 50]. As with aortography [49], someauthors recommend that a surgical team be ready foremergency operation during the procedure [49, 45].
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Table 1. Aortic Diseases and Correlate Procedures Developing Aortobronchopulmonary Fistulas: Population, Type of Procedure, Presentation, and Diagnostic Modalities
Variable AoC PDAAoC �
PDA
DTAChronic
Aneurysms
DAAChronic
Aneurysms
TAChronic
Aneurysm
DTA AcuteTraumaticRupture
Type ADissection
Type BDissection
TakayasuArteritis
AorticSarcoma
No. of patients (tot � 68) 25 5 2 19 3 2 2 4 3 2 1Age range (y) 16–62 11–45 17–20 22–75 61–71 72–74 56–82 56–58 49–62 49–54 65Gender m/f (nr) 17m/8f 2m/2f (1 nr) 1m/1f 16m/3f 3m 2m 2m 3m/1f 3m 2f 1 moNo. of fistulas (tot � 71) 26a 6a 2 19 4a 2 2 4 3 2 1Procedures developing ABPF
Graft replacement 8 . . . . . . 12 2 1 1 3 3 . . . . . .
Patch repair 9 . . . 1 3 1 . . . 1 . . . . . . 2 . . .
Primary repair 2 6 . . . . . . 1 . . . . . . . . . . . . . . . 1Aorto-aortic bypass graft 2 . . . 1 . . . . . . . . . . . . . . . . . . . . . . . .
Homograft . . . . . . . . . 1 . . . . . . . . . . . . . . . . . . . . .
Wrapping . . . . . . . . . 2 . . . . . . . . . . . . . . . . . . . . .
Endovascular repair . . . . . . . . . . . . . . . 1 . . . . . . . . . . . . . . .
Endobronchial stenting . . . . . . . . . . . . . . . . . . . . . 1b . . . . . . . . .
Other repair 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Not reported 4 . . . . . . 1 . . . . . . . . . . . . . . . . . . . . .
Healthy interval Min/max 10 wks/25 y 1.9 y/16 y 5 y/16 y 1.5 y/23 y 3 y/11 y 2.5 y/10 y 13 y/25 y 12 y/6 mo 5 mo/4 y 6 y/9 y 1 yOnset of hemoptysis:
Intermittent 16 4 2 11 2 2 2 2 2 1 1Massive 6 . . . . . . 2 1 . . . . . . 2 . . . 1 . . .
Not reported 3 1 . . . 6 . . . . . . . . . . . . 1 . . . . . .
No. of patients with othersymptoms/signs
10 . . . . . . 6 2 . . . . . . . . . 1 1 . . .
Reported symptoms/signsc
Anemia 1 1 . . . . . . . . . . . . . . . . . . . . . 1 . . .
Back pain 1 . . . . . . 1 . . . . . . . . . . . . . . . . . . . . .
Cardiac arrest . . . . . . . . . 2 . . . . . . . . . . . . . . . . . . . . .
Chest pain 1 . . . . . . 2 . . . . . . . . . . . . . . . . . . . . .
Cough 1 . . . . . . 1 . . . . . . . . . . . . . . . . . . . . .
Dysphonia 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Dyspnea . . . . . . . . . 3 . . . . . . . . . . . . . . . . . . . . .
Fever 2 1 . . . . . . . . . . . . . . . . . . . . . . . . . . .
Hypotension . . . . . . . . . . . . . . . . . . . . . . . . 1 . . . . . .
Hypoxiemia 1 . . . . . . 2 . . . . . . . . . . . . . . . . . . . . .
Hoarseness . . . . . . . . . 3 . . . . . . . . . . . . . . . . . . . . .
Rales 3 . . . . . . 1 . . . . . . . . . . . . . . . . . . . . .
Renal failure 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Respir. arrest . . . . . . . . . 2 . . . . . . . . . . . . . . . 1 . . .
Resp. alkalosis . . . . . . . . . 1 . . . . . . . . . . . . . . . . . . . . .
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Transesophageal echocardiography and magnetic res-onance imaging have been used less often. Magneticresonance imaging is not practical in emergency condi-tions, and it was able to visualize the fistula tract in onecase only [21]. Transesophageal echocardiography ishelpful, as it may reveal a compressive mass along theaortic graft [3]. Doppler imaging may reveal an abnormaljet from the aorta into the surrounding spaces. RecentlyThompson and associates [47] have visualized the fistulatract in 4 patients.
Recently the technique of computed tomographic an-giography has become increasingly popular, and it hasbeen used in some cases of ABPF starting from 1996 [72].It allows tridimensional view angles, visualizes a PSA
Fig 1. Chest roentgenogram showing opacification of the right lungfield due to massive hemorrhage.
Fig 2. Computed tomogram of the chest showing an ascending aortapseudoaneurysm compressing both the superior vena cava (thin ar-row) and the aortic graft (thick arrowhead). Hemorrhage in theright lung is also visible. (Reprinted with permission from The Soci-ety of Thoracic Surgeons [Ann Thorac Surg 1999, 68, 1406–7] [3].)
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and its surrounding structures, shows both the throm-bosed and contrast-filled portion, and is less invasivethan conventional angiography [10, 27, 59]. For thesereasons we agree with Ferretti and colleagues [72], whounderline the importance of this technique also when afistula per se is not demonstrable. We favor this means ofexamination every time an episode of hemoptysis isreported in a patient with previous aortic surgery.
In conclusion, different diagnostic modalities are po-tentially able to directly visualize a fistula tract; however,our review discloses that only in exceedingly rare cases
Table 2. Nonaortic Diseases and Correlate Procedures Developing Aortobronchopulmonary Fistulas: Population, Type ofProcedure, Presentation, and Diagnostic Modalities
Variable
MitralValve
Disease
AorticValve
Disease
Mitral andAortic Valve
DiseaseTetralogyof Fallot
PulmonaryFibrosis
VertebraTumor
Bronchomalacia/Tracheomalacia
No. of patients (tot � 8) 1 1 1 1 1 1 2Age (y) 25 54 25 40 48 25 14/40Sex f m f m m f 2mNo. of fistulas (tot � 8) 1 1 1 1 1 1 2Procedures developing ABPFs
MVC 1 – – – – – –AVR – 1 – – – – –MVR � AVR – – 1 – – – –VSD closure – – – 1 – – –Vertebra metallic device – – – – – 1 –Endo-bronchial stenting – – – – 1 (after lung
transplantation)– 2 (1 after tracheal
resection; 1pediatricbronchomalacia)
Healthy interval 6 months 2 months 2.5 years 17 years 13 months 1 year 3 weeks/7 yearsOnset of hemoptysis
Intermittent – – – 1 – 1 –Massive – 1 1 – 1 – 2Moderate, single episode 1 – – – – – –
Other symptoms or signs:Chest pain 1 – – – – – 1 (adult patient)Dyspnea – – – – 1 – 1 (adult patient)Respiratory distress – – – – 1 – –Swelling 1 1 – – – – –
DiagnosticsCT – 1 1 1 – – 1 (pediatric
patient)AOR 1 1 1 1 – 1 1 (adult patient)BR – – – 1 1 – –
AOR � aortography; AVR � aortic valve replacement; BR � bronchoscopy; CT � computed tomography; MVC � mitral valvecommissurotomy; MVR � mitral valve replacement; VSD � ventricular septal defect.
Table 3. Mechanical Causes of Bronchopulmonary Damage
Cause N (%)
Pseudoaneurysms 47 (59.4%)Neoaneurysms 8 (10.1%)Knots and suture material 4 (5%)Graft substance 2 (2.5%)Remnant of temporary bypass 2 (2.5%)Endovascular stent-graft 1 (1.2%)Endobronchial stent 4 (5%)Unknown or not reported 11 (13.9%)
Table 4. Anatomy of the Fistulous Pathway
Sites of Aortic and Bronchopulmonary Ends N (%)
DTA—Left upper lobe parenchyma 19 (24%)DTA—Left lower lobe parenchyma 9 (11.3%)DTA—Left main stem bronchus 8 (10.1%)DTA—Left lower lobe segmental bronchus 2 (2.5%)DTA—Left upper lobe segmental bronchus 6 (7.5%)DTA—Left lung or bronchial tree, exact site not
reported26 (32.9%)
DAA—Left upper lobe parenchyma 2 (2.5%)AA—Right upper lobe parenchyma 2 (2.5%)AA—Right main stem bronchus 3 (3.8%)AA—Right upper lobe segmental bronchus 1 (2.5%)AA—Right middle lobe segmental bronchus 1 (2.5%)
AA � ascending aorta; DAA � distal aortic arch; DTA � descend-ing thoracic aorta.
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was this visualization practically achieved. Thus, indica-tion for surgical or endovascular repair mostly relies onclinical suspicion and nonspecific diagnostic features.
We advise urgent treatment based on the association ofthe following elements: (1) hemoptysis, (2) history ofprevious cardiac or aortic operation, (3) presence of lunginfiltrates on a chest roentgenogram, (4) lung hemorrageon a computed tomographic scan, and (5) visualization ofa PSA.
ManagementIf left untreated, ABPFs are uniformly fatal [1]. In ourreview, all 8 untreated patients died due to massivehemoptysis (Table 5). Thus, management of the airwaysmust be immediate and must first include bleedingcontrol by selective endotracheal intubation. The inflatedcuff of a Carlens tube [73] or a Fogarty embolectomycatheter [17] may be positioned into the bleeding side ofbronchial tree to protect the contralateral side fromhemorrage. Otherwise a single-lumen endotracheal tubemay be positioned in the healthy main stem bronchus[58]. Some authors recommend using a rigid broncho-
scope as an airway and suction conduit while waiting forsurgery [2].
The patient is often in critical condition at the momentof diagnosis, requiring emergency surgery. Rapid insti-tution of CPB through the femoral vessels is indicatedbefore starting thoracotomy or sternotomy if resuscita-tion is executed during transport into the operatingtheater [32]. Nevertheless we deem that, even in stablepatients, surgical or endovascular treatment should beperformed without delay to prevent clot dislodgment andmassive bleeding.
Various surgical approaches have been described. TheDTA may be approached through a single [29, 32, 37] ordouble left posterolateral thoracotomy. The latter israrely used; it has been carried out at the fourth [21, 32]intercostal space proximally and at the seventh [21] orninth [32] distally. Although excessively invasive, theassociation of left thoracotomy and median sternotomyachieves optimal exposition of the supradiaphragmaticaorta [16, 22]. A simple aortic cross-clamping can be usedin case of limited extension of a PSA [17, 28, 60], but leftatrial–femoral [21, 37, 46] and femoral–femoral [24, 32, 36]bypass, instead of the traditional Gott shunt [41, 65], aremore often used to ensure distal perfusion.
When the fistula is located in the ascending aorta,femoral–femoral cannulation should be established be-fore opening the sternum, as the false aneurysm maypotentially rupture during sternotomy. In the only re-ported case of successful off-pump repair the femoralartery had been preventively cannulated [3].
The aortic end of the fistula may be treated by direct [3,6, 49, 8, 13, 14, 17, 23, 36, 65] or patch [49, 19, 20, 40, 50, 61]closure, subclavian artery flap repair [15], extraanatomicbypass grafting [16, 22, 26, 27, 31, 62], homograft implan-tation [25], and, more often, prosthetic graft insertion [19,21, 23, 28, 29, 32, 34, 37, 38, 41, 44, 46, 51, 53, 57, 60, 72](Table 6).
Surgical repair of the bronchial or pulmonary endsmay consist of primary closure [3, 6, 49, 13, 22, 46, 50, 53,56, 60, 61], partial lobe resection [49, 15, 23, 28, 29, 41, 43,44, 72], lobectomy [14, 51], or pneumonectomy [32, 40, 63]
Table 5. Overall Mortality in Patients Affected byPostoperative Aortobronchopulmonary Fistulas
Patients NMortality
N (%)
Untreated patients 8 8 (100%)Patients undergone endovascular
procedures15 1 (6.6%)
Patients undergone surgicalprocedures
52 8 (15.3%)
Patients undergone n-butyl-cyanoacrylate occlusion
1 0
Total 76 17 (22.3%)
Table 6. Management of the Aortic End of 71 Aortobronchopulmonary Fistulasa
Procedure Type N (%) Surgical Procedure Type N (%)
Surgical procedures 55 (77.4%)Primary repair 11 (15.4%)Patch repair 6 (8.4%)Subclavian flap repair 1 (1.4%)Graft replacement 23 (32.3%)Homograft implant 1 (1.4%)Extraanatomic bypass graft 8 (11.2%)Unfinished repair 4 (5.6%)
Endovascular procedures 15 (21.1%)n-Butyl-cyanoacrylate occulsion 1 (1.4%)
a Eight of 79 fistulas were untreated.
2003Ann Thorac Surg REVIEW PICICHE ET AL2003;75:1998–2006 POSTOPERATIVE AORTOBRONCHOPULMONARY FISTULAS
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(Table 7). It is not carried out when exclusion of thefistula at the aortic end (as with endovascular treatment)is considered to be adequate [37].
The pseudoaneurysm, if present, should be removedalong with all prosthetic material if infection is suspected[57]. Cryopreserved vascular homografts may help toeradicate the infection [25]. Specimens for microbiologi-cal investigation should always be taken during opera-tion. We agree with others who advise preventive anti-biotic therapy for 3 to 6 weeks postoperatively in case ofno evidence of infection [25, 30, 57].
Direct contact between the vascular reconstruction andthe pulmonary tissue should be avoided to preventfurther erosive damage. The repaired aorta should becovered by the remains of the pseudoaneurysmal wall[51, 60] or by surrounding viable tissue such as thoracicwall muscles [49, 65], pleural [49, 20, 62] or pericardial [49,19, 20, 28, 65] flaps, thymic fat [23], or omental pedicle [46,50]. Otherwise bovine pericardium may be used [28].
Since 1996 endovascular procedures have been used byCampagna and colleagues [10] and by Chuter and asso-ciates [11] to treat ABPFs. So far 10 groups of investiga-tors have described endovascular stenting in 15 patients[10, 11, 30, 33, 35, 47, 48, 58, 59, 71]. There was no mortalityrate associated with these procedures. These data con-trast with the high mortality rate of open surgical repair.We found that 8 (16%) of 50 patients who had undergone
surgical treatment of DTA fistulas died intraoperativelyor early after surgery [18, 19, 24, 39, 43, 45, 52, 63] (Table8). Surgical mortality is due to complexity of procedures.A challenge is presented by coexistence of emergencyconditions and difficulties of redo operations. Hemor-rage, prolonged ventilatory compromise, kidney failure,paralysis, or graft infection may easily worsen the prog-nosis [47].
On the other hand possible complications of an aorticstent graft are migration [52], interruption of spinal chordintercostal blood supply [10], structural defects [30], ar-terial injury [33], infection (if it is located in a septicenvironment) [35], and even ABPF [52]. In our reviewonly 1 patient had complications requiring ileofemoralbypass and embolectomy [33]. With the latest generationof devices, which are considered easier to deploy, moresuitble to the aortic contour, and less likely to migrate[47], stent grafting appears very promising. With futuregenerations of devices, one may expect that complica-tions will be even less likely. Among patients who un-derwent endovascular treatment there was one deathdue to unrelated causes [71]. The overall mortality rate isreported in Table 5.
Finally, in July 2002 Hiraki and colleagues [74] reportedthe successful treatment of a postoperative ABPF byinjecting into the pathway n-butyl-cyanoacrylate mate-rial using a microcatheter tip. Rapid, strong solidificationof this substance permitted immediate occlusion. Embo-lization of fistulas has already been adopted in othercontexts; however, application to ABPFs, although wor-thy of interest, requires accurate case selection andfurther experimentation.
In conclusion, our review disclosed several aspects ofpostoperative ABPFs. Among them, operative deathswere exclusively related to fistulas of the DTA; 5 patientswith fistulas of the ascending aorta successfully under-went surgery [3, 22, 51, 60, 61] and 2 died before treatment[9, 54]. The overall surgical mortality rate was 15.3%.
Although in this setting more experience with endo-vascular repair and long-term follow-up would be desir-able, our review suggests that stent grafting represents
Table 7. Management of the Bronchopulmonary End of 71Aortobronchopulmonary Fistulas
Type of repair N (%)
Pneumonectomy 3 (4.2%)Lobectomy 2 (2.8%)Partial lobe resection 9 (12.6%)Primary repair 14 (19.7%)No repair 17 (23.9%)Not reported 26 (36.6%)
Table 8. Management of the Aortic End: Procedure-Type–Related Results
Type of ProcedureTreated
Fistulas, NSuccessful
Treatment, N (%)Procedure-Related
Mortality, N (%)
Endovascular procedures 15 15 (100%) 0Surgical procedures of DTA 50 42 (84%) 8 (16%)
6 intraoperatively2 early postoperatively
Surgical procedures of AA 5 5 (100%) 0n-Butyl-cyanoacrylate occlusion 1 1 (100%) 0
Total procedures 71 62 (87.3%) 8 (11.2%)
AA � ascending aorta; DTA � descending thoracic aorta.
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the tool of choice to treat postoperative ABPFs involvingthe DTA.
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2003;75:1998-2006 Ann Thorac SurgMarco Picichè, Ruggero De Paulis, Alessandro Fabbri and Luigi Chiariello
diagnosis, and managementPostoperative aortic fistulas into the airways: etiology, pathogenesis, presentation,
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