Book MEET 2013 by divine [id]

ENDOVASCULAR EMERGENCIES Update of endovascular approach Editors

Max Amor Patrice Bergeron Piergiorgio Cao Nicholas Cheshire Nicola Mangialardi Klaus Mathias

Preface On behalf of the MEET Directors Patrice Bergeron

The 2013 MEET edition Combo is devoted to endovascular emergencies.

Peter Schneider has selected a series of very interesting emergencies in arterial and venous lower limb vessels, Richard Mc Willams was interested in developing visceral emergencies and myself on thoracic aortic syndroms. Finaly we have also a special contribution from Gunnar Tepe on DES and DE balloons for the SFA. In the 3 chapters ,the role of endovascular technology has been highlighted and we thank warmly all the authors who have contributed to this successful e-combo.

Editorial On behalf of the MEET Directors Patrice Bergeron

This year, the MEET combo will focus on endovascular emergencies, subject pushed by all the MEET Directors. In fact, endovascular management is so widely applied in routine and emergency situations that it appeared justified to devote a special program on this topic. The MEET congress will comport sessions on aortic emergencies, aortic malperfusions and stroke management among many other situations where emergencies are resolved with endovascular technics; it was logic to complete the content with such an e-combo on endovascular emergencies.

Table of contents

1E ndovascular management of vascular emergencies of the thoracic aorta

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

a. Requirements

of Stent grafts for acute thoracic

syndroms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Patrice Bergeron, Timur Abdulamit, Jean-Christophe Trastour

b. Acute

type A dissection: is there a role for endovascular repair? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 Nicola Mangialardi, Sonia Ronchey, Eugenia Serrao, Holta Kasemi, Vittorio Alberti, Stefano Fazzini

c. I ndication of Stentgrafts Christoph Nienaber

in acute thoracic syndroms . . . 23

d. Experience

with endovasc repair of traumatic isthmic ruptures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 Eric Verhoeven, Athanasios Katsargyris

e. G lobal experience Thomas Larzon f. Endovascular

malperfusion

with TEVAR in ruptured TAA . . . . . . . . . 43

Management of acute abdominal organ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Piergiorgio Cao, Ciro Ferrer, Nunzio Montelione, Carlo Coscarella, Antonio Lorido, Gabriele Pogany

g. Endovascular

Management of acute compromised supra aortic vessels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Mario Lachat, Felice Pecoraro, Lyubov Chaykovska, Dieter Mayer, Zoran Rancic

h. Emergencies in infected thoracic Peter R. Taylor, Rachel Clough, Oli Lyons

aortic stent grafts . . . 59

2E mergency vascular procedures in the lower extremity

. . . . . . . . . . . . . . . . . . . . .

a. Arterial

access site complications: How to manage, when to operate, and when catheter-based techniques can handle it . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 Jörg Teßarek

b. Complications

of closure devices and their management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77 Nicola Pellizzari, Luca Favero, Carlo Cernetti

c. A cute

ischemia of lower extremity due to embolization of thrombosis: diagnosis and management . . . . . . . . . . . . . . . . 81 Carlo Setacci

d. Management

of acute occlusion of a bypass graft or an endovascular reconstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89 Michael Wholey

e. When

to consider fasciotomy for the endangered leg and how to do it . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97 Isabelle Van Herzeele

f. Venous

emergency: Management of phlegmasia using mechanical, chemical, or surgical thrombectomy . . . . . 103 Olivier Hartung

3 Visceral artery emergencies a. Embolic occlusion Jörg Teßarek b. Spontaneous

113

of the SMA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115

haemorrhage from liver and renal tumours . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119 Michael Wholey

. . . . . . .

c. Haemorrhage

from pancreaticoduodenal and splenic artery pseudoaneurysms in pancreatitis . . . . . . . . . . . . . . . . . . 127 Maria Antonella Ruffino, Claudio Rabbia

d. Hepatic artery Richard McWilliams

bleeding after biliary drainage . . . . . . . . . 135

e. Acute

renal failure due to suprarenal aortic occlusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137 Richard McWilliams

4 Special contribution

. . . . . . . . . . . . . . . . . . . . . . . .

141

Current

Status of Drug Eluting Stents and Drug-coated Balloons in the SFA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143 Gunnar Tepe

Authorâ&#x20AC;&#x2122;s index

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

153

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

1. E ndovascular management of vascular emergencies of the thoracic aorta a. R equirements of stent grafts for acute thoracic syndroms

Patrice Bergeron, Timur Abdulamit, Jean-Christophe Trastour RĂŠsidence du Parc private hospital, Marseille, France

Acute Thoracic Syndroms (ATS) reflect a large variety of diseases afecting the thoracic aorta in emergency. Most commonly are described: Acute Thoracic Dissection (ATD) figure 1, intra Mural Hematoma (IMH) figure 2, Aortic Ulcers (AU) figure 3 or Impending Aneurysm Rupture (IAR) figure 4.

All these diseases present an acute risk of bleeding requiring a specific treatment. Apart the medical treatment which must be optimized including blood pressure control, Stent Grafts (SG) implantation is often required to solve the problem avoiding a sudden death. SG need to respect different requirements in order to be selected for this application. 1. Anatomical requirements Besides the size of the device, conformity to the aorta and safe application are a priority. The thoracic aorta is not uniform from its origin to the diaphragm; the vessel changes direction, diameter, configuration, division and fixation. Disease, Aging and Hypertension increase these differencies, creating dilatation, elongation, tortuosities and wall degradation. All these parameters are now easily studied thanks to reconstructions from CT scan, MRI, Transoesophagal echography. Preoperative Angiography or IVUS are unnecessary and must be avoided in emergency.

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

Research of a False Chanel (FC) signing a ATD must be completed by identification of the entry tear(s), the flow direction and its reentry, arterial branches and their potential malperfusion or a spinal cord ischemia. (figures 5, 6)

A strategy must be discussed as to determine an access plan (iliac stenosis, calcifications tortuosities…) and to decide whether to cover, transpose or stent arterial branches rising from the True or FC; Finally conformability and stability of the device can be anticipated.

2. Technical requirements The introducer size must fit to the iliac access. Dilatation or stenting of the iliac arteries may be useful in case of severe narrowing or calcifications, covered stents can help for the “paving and cracking” technic. Most of the devices fit to the diameter of the iliac arteries but device progression can be limited by tortuosities and calcifications, stretching the access by using Stiff Guide Wires (GW) is essential, rarely an extra access from the arm is necessary. In some extreme aortic tortuosities it can be useful for SG progression. The most important aspect is about conformability to the aortic curvatures (figure 7) and its fragility; Rigid SG, bare stented extremity must be avoided. Ideally, the oversizing is limited to 10% except if chimps are associated to perfuse visceral arteries. When the sizing was not determined preoperatively, intra operative angiography with a calibrated pigtail allow to fix the diameter and the length of the SG. Imaging must be of high quality, Hybrid rooms allow combined endovascular and conventional procedures with a good imaging, nevertheless C arms in the OR have proved to be effective in most situations except for obese patients. The left anterior oblique view (LAO) 30° is helpful to expose the thoracic aorta and the arch. Landmarks must be relia7 ble, placement of a GW in the compromised branches allow also abail out stenting. Fusion has been reported to be useful but there are very few equipped centers. In critical situations, to treat thoraco-abdominal emergencies, sacrificing a renal or a celiac artery is acceptable with the risk of renal and hepatic disorder. In the arch, the left subclavian artery can also be covered except if providing an internal mammary artery to the coronaries or a solitary or dominant vertebral artery. Conformability of the SG is of prime importance at the arch level (figure 8). New devices from Gore, Medtronic and Cook have been designed to fit the curvature and avoid the reported SG collaps. 8 8bis When chimneys are associated, the proximal landing zone has to be increased from the classical 2cm to one more cm each chimp added; for example: 3 chimps at the arch need 5 cm (2+3) of landing zone. This allows to rub out the gutters. Each chimney implies to increase the SG oversizing. A covered stent for supplying the celiac artery or the SMA can be placed in a “Snorkel mode”, and The “Sandwich technique can also be useful in rare situations.The decision to one or the other choice must be done on a drawning to reproduce the situation. Chimneys are easier to adapt the emergent situation than branched and fenestrated SG even on off the shell basis. (figures 9,10) 14

a. Requirements of stent grafts for acute thoracic syndroms, P. Bergeron, T. Abdulamit, JC. Trastour

The length of the SG must cover the entire disease but total coverage of the Thoracic aorta for ATD is not mandatory in emergency in order to avoid any low inter costal artery supplying the spinal cord. All these advices help for device selection.

3. Biomechanical requirements SG are submitted to unexpected forces after their placement in the thoracic aorta and this can lead to migration, plication or deterioration if their biomechanical properties have been underestimated; This is why experimental and clinical studies are mandatory; Simulators under varied conditions of flow and pressure test the fabricresistance, the anchorage and the resistance to stent fractures. Finally SG require clinical trials before large diffusion; Based on these requirements of SG and on the clinical case, we have a large choice for device selection offering the best option for the treatment of acute thoracic syndroms.

1. E ndovascular management of vascular emergencies of the thoracic aorta b. Acute type a dissection: is there a role for endovascular repair? Sonia Ronchey, Eugenia Serrao, Holta Kasemi, Vittorio Alberti, Stefano Fazzini, Nicola Mangialardi

San Filippo Neri Hospital, Rome, Italy

Introduction Type A aortic dissection (TAAD) is a cardiovascular catastrophe associated with high mortality. Medical treatment is associated to poor outcome with a mortality rate around 60%. [1] Open surgical repair is the standard treatment for TAAD despite a high mortality/morbidity rate especially in high risk patients, reported up to 60%. [2] Because mortality is strongly related to both pre-operative conditions of these patients and the invasiveness of the interventions, a less invasive approach would be highly beneficial. Over the last decades endovascular therapies have emerged as the therapy of choice in patients with descending thoracic and abdominal aortic diseases. [3] The introduction of new techniques and extensive experiences have broadened the indications for these interventions, and even diseases affecting the ascending aorta can be treated. Primary reports focused on retrograde type A dissections affecting the aortic arch in which the primary entry tear was located in the descending segment. These patients were treated by stent graft placement in the descending aorta. [4] Currently, stent graft placement in the ascending aorta for the treatment of aneurysms, pseudo-aneurysms, penetrating ulcers, intramural hematoma and even type A dissections have been described in anecdotical reports. [5, 6] Computed Tomographic (CT) scan imaging studies show that endovascular repair is anatomically feasible in about 30% of patients with type A dissection with a proximal entry tear in the ascending aorta. This percentage of patients may increase up to 39% with the use of extra-anatomic bypass, like a left to right carotid-carotid bypass, in order to obtain an adequate distal landing-zone. [7, 8] We report our initial experience with endovascular repair for TAAD patients by placement of a stent graft in the ascending aorta. Our experience Between April 2009 and June 2012, 37 patients with TAAD were submitted to our hospital, at the Cardiac Surgery Department. 9 of them were considered at high risk for open surgery because of co-morbidities and/or previous sternotomy. The anatomic characteristics of these patients were studied for an endovascular approach and 4 of them respected our inclusion criteria and were addressed to a stent graft position in the ascending aorta. Inclusion criteria were: 1. entry tear in the ascending aorta; 17

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

2. distance between sinotubular junction and entry tear of at least 2 cm; 3. distance between entry tear and brachio-cephalic trunk at least 0.5 cm; 4. no signs of cardiac tamponade or severe aortic regurgitation; 5. no signs of ischemia of aortic branches; 6. adequate femoral and iliac arteries. Patients with cardiac revascularization from ascending aorta were excluded. All patients were smokers and had hypertension, 1 patient had atrial fibrillation (2 males: mean age 70 years) (table 1). Sex

Age

Co-morbidities

ASA/ Euro-score

Patient 1

III/9.42%

Patient 2

III / 34.93 %

< 8 hours

Patient 3

III-IV/37.05 %

< 8 hours

Patient 4

Hypertension, Tabaco use Hypertension, Tabaco use, previous ascending aorta replacement for type A dissection (2007) Hypertension, diabetes, dislipydemia, previous aortic valve replacement (2011) Hypertension, COPD, previous aortic valve replacement (2008), ascending aorta replacement for type A dissection (2012)

Time between symptoms and OR < 8 hours

III-IV/34.38%

2 days

Table 1: Baseline Characteristics 1 patient had prior aortic valve repair and 2 patients had previous ascending aortic repair for TAAD (in one of them was associated the aortic valve replacement) with a residual entry tear in the ascending aorta. The patients with previous ascending aortic repair were first treated with analgesic and antihypertensive therapy without results. CTA images were acquired on multislice CT-scan with 0,625 mm detector configuration (manufacturer GE VCT 64 MD light speed). Non-contrast images were first obtained, and followed by acquisition of 1,25 mm axial images and retro-reconstruction at 0,625 mm from the origin of carotid arteries to the femoral arteries after intravenous injection of 80-90 ml of non-ionic contrast (400 mg/ml). Subsequently, the acquired CTA datasets were transferred to a workstation (OsiriX 3.9.4 -64 bit) for analysis. A central lumen line was generated and the distance between the entry tear and the sinotubular junction and innominate artery were measured (figure 1).

Figure 1: A Limited Type A Dissection: center line Figure 1: B Limited Type A Dissection: 3D VR reconstruction Figure 1: C Limited Type A Dissection:3 years Follow-up CT-scan: 3D VR reconstruction Stent graft selection was based on the aortic diameter measured at the level of the entry tear, with at least 10% of oversizing in respect to the true lumen, but not exceeding the original aortic diameter. 20% of oversizing was performed in case of previous ascending aortic graft replacement (20% of over18

b. Acute type A dissection: is there a role for endovascular repair?, S. Ronchey, E. Serrao, H. Kasemi, V. Alberti, S. Fazzini, N. Mangialardi

sizing respect to the graft diameter). The presence of pericardial effusion and of aortic regurgitation was investigated with the use of transesophageal echocardiography (TEE). Three patients were operated in acute setting (< 8 h after acute onset of symptoms), one of these because of brachio-cephalic trunk symptomatic dissecting dilatation (32 mm, no neurologic signs, neck pain not responding to medical therapy) occurring 48 months after ascending aorta replacement. In one case the procedure was delayed (48 h). Written informed consent was obtained before the procedure. All the procedures were performed under general anesthesia, with surgical femoral access. A giudewire was introduced in three cases throw a percutaneous right brachial access into the aortic arch and descending aorta as a rescue for supra-aortic vessels. In one case a reversed Left Common Carotid (LCC) to Right Common Carotid (RCC) and Right Subclavian Artery (RSA) bypass was performed to obtain an adequate distal landing zone, an Amplatzer vascular plug II - 22 mm (St Jude Medical) was used to occlude the origin of the brachio-cephalic trunk. Through the femoral artery a Landerquist stiff guidewire (COOK, Inc., Bloomington, IN) was positioned into the left ventricle. Under fluoroscopic guidance the graft was advanced into the ascending aorta. Standard Cook Zenith TX2 was used in 1 case and an off the shelf device for the ascending aorta (Cook, Inc., Bloomington, IN) in 3 patients. Cardiac pacing (180 beats/min) was used to reach systolic blood pressure up to 40-60 mmHg to prevent dislodgement of the stent graft during deployment. Via a right common femoral vein a temporary ventricular pacing wire was placed in the apex of the right ventricle. Trans Esophageal Ecocardiography (TEE) and completion angiography was used to verify the competence of the aortic valve, check the patency of the coronary arteries and supra-aortic branches and to evaluate the exclusion of the dissection. Mean operating time was 128 min (range 90-215). Technical success was achieved in 100% of the patients, with complete exclusion of the entry-tear. Stent graft length ranged between 55 and 81 mm and diameter between 35 and 40 mm. No death was registered during follow up (mean 15 range 4-39 months). One patient experienced a pulmonary edema 2 months after the procedure not operative related. Control CT scans demonstrated no migration of the graft. A complete false lumen thrombosis of the ascending aorta was obtained in three patients, while in one case the false lumen in the ascending aorta was still patent, without aortic enlargement. This patient remains asymptomatic at 9 months follow up. In two patients we obtained the complete false lumen thrombosis of the descending thoracic aorta, while in the other 2 patients only a partial false lumen thrombosis (Tables 2 and 3). Diameter Number Distance Distance Ascending of entry entry entry Aorta tears tear LSCA tear STJ

Patient 1 Patient 2 Patient 3 Patient 4

AdType of Measure- Length of InTechnical ditional In-hopital stent ments procedure hospital success proce- mortality graft Stentgraft (min) morbidity dure

Cook TX2

40-31

Yes

OS Cook

38-73

215

Yes

Yes*

OS Cook

38-55

170

Yes

OS Cook

42-72

140

Yes

* LCCA-RCCA-RSA bypass + AT embolization

Table 2: Characteristics Dissection and Procedure LSCA: Left Subclavian Artery, STJ: Sinotubular Junction, AT: anonymous trunk, OS: off the shelf

Patient Patient Patient Patient

1 2 3 4

Thrombosis Length of FU Thrombosis FL FL descending (months) ascending AO AO

39 15 9 4

Yes Yes No Yes

Yes Yes Partial Partial

Ascending aortic diameter

34 30 36 34

Complications

Additional procedures

Mortality

No No No no

No No No No

Table 3: Follow-up 19

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

Discussion With increasing age population the incidence of TAAD is rising, especially in the elderly group. [9] In these patients open surgical repair is indicated, with graft replacement of the ascending aorta and, in the presence of aortic regurgitation, with valve resuspension or replacement. It has been reported that both preoperative clinical condition of the patient and invasive character of such procedures, are associated with high mortality rates, ranging up to 60% in octogenerians. [1, 2] Medical therapy alone has a comparable or even worse outcome, and therefore less invasive treatment options, like endovascular therapies, might be beneficial. [1] Our study confirmed that, in a small selected subset of patients, stent graft placement in the ascending aorta for TAAD is a feasible and may represent an effective and safe procedure.In 2000 Dorros et al. reported the first case of TAAD treated with an endovascular technique through a trans-septal approach. [10] Since then several authors have published their experiences, but the current literature remains sparse (Table 4). First author

Dorros et al. Kato et al. Wang et al. Ihnken et al. Zhang et al. Rayan et al Verhoye et al. Zimpfer et al. Senay et al. Mussa et al. Palma et al. Kische et al. Nienaber et al. Ye et al. Metcalfe et al.

Year

STENTGRAFT

Number of patients

2000

Lacteba

2001 2003 2004 2004

Homemade COV ZSTENT GENERIC BARE, GORE GIANTURCO Z

30-day Endoleak Acute (%) Mortality (%) (%)

1(100)

0(0)

CVA (%)

Late Mortality (%)

0(0)

Prev.

interv

FU (mts)

3-42

1(100)

0(0)

1(100)

0(0)

2004

GORE

2006

COOK-Z

1(100)

0(0)

2006

JOTEC

1(100)

0(0)

1(100)

0(0)

1(100)

0(0)

2007 2007 2008

GORE TAG GORE TAG BRAILE BIOMED

1 (MPA)

1 1

1 0(0)

0(0)

2008

COOK

2011

VARIOUS

9-39

2011

VARIOUS

6(60%)

1(10)

2(20)

35,5

2012

Cook

1(100)

0(0)

Table 4: Review of literature. Ye et al. reported the largest series consisting of ten patients with only midterm follow-up. [11] These results seem promising if we consider the high risk patients and their poor prognosis. As the landing-zones are located very close to the coronary and innominate arteries stent graft placement in the ascending aorta may be performed only in selected cases. Two studies have been conducted to investigate the feasibility of stentgraft placement in type A dissections. [7,8] Moon et al. showed that in a 162 patients with TAAD 32% were anatomically suitable for endovascular repair as there was absence of valvular involvement and appropriate length and diameter of proximal sealing zones. [7] Hybrid procedures could be used to extent the applicability by combining a supraaortic debranching procedure with endovascular stent graft placement. We performed this in two patients (figure 2). 20

b. Acute type A dissection: is there a role for endovascular repair?, S. Ronchey, E. Serrao, H. Kasemi, V. Alberti, S. Fazzini, N. Mangialardi

Figure 2 A: T ype A dissection after limited open repair estended to Brachio-cephalic trunk and right common carotid artery: 3D VR reconstruction Figure 2 B: TEVAR in the ascending aorta + reversed LCC -RCC - RSA bypass. Plug into the brachiocephalic trunk: 3D VR reconstruction The use of a left-to-right carotid bypass can increase the feasibility of endovascular treatment of the ascending aorta up to 40% of all TAAD patients. [8] Thorough understanding the anatomical limits of the aortic dissection and the adjacent anatomy is a necessary prerequisite before such procedure. Identification of the primary entry tear is essential for the success of stent grafting, although this may be a difficult process. The development of multi-detector-slice CT scanners and post-processing software have resulted in superior imaging with less artifacts, improving the sensitivity and specificity of this imaging modality. Three-dimensional reconstructions and virtual endoluminal imaging can be useful to assess the size and location of the intimal tear and to determine the precise length and diameter of the stent graft for successful exclusion of the dissection. [12] Other radiologic findings, like pericardial effusion, aortic diameter, the diameters of true and false lumen and the status of thrombosis of the false lumen may be helpful in planning the procedure. [13] Endovascular procedures in TAAD patients harbor considerable risks. The aortic arch manipulation with guide wires and stent grafts can lead to dissection extension or dislodgement of thrombus. To avoid such complications, in selected cases, a right carotid artery access for the stent graft can be used. This is also associated with an increased risk of stroke, so we preferred to perform all procedures from a femoral route. Aortic valve insufficiency is another important complication, which is associated with aortic dilatation due to the stent graft. This complication might be related to excessive oversizing. Based on this observation we adopted a maximum oversizing of 10%. Completion TEE should be performed in all cases to assess cardiac and aortic valve function,in combination with an angiography to confirm the patency of the supraaortic branches and coronary arteries. Development of novel devices and techniques and increasing experience in these type of procedures are fundamental, before these techniques can be widely adopted. In our experience we used in three cases a device specifically designed from Cook for the ascending aorta, with a longer shaft (100 cm) and a short tip (2 cm) (figure 3). Recently Metcalfe et al. published their experience with the implementation of a stent in a TAAD patient, designed specifically for ascending aorta, consisting of a 65 mm covered component and proximal and distal bare stents. [14] Although the use of bare stents in aortic dissections remains highly debated, as it may induce a new dissection or a re-entry tear, the results of these developments, in combination with other studies, are eagerly awaited. [15] Our experience is limited to a small, atypical, number of patients with TAAD. Three of them had previous cardiac surgery. In these patients the natural risk of retrograde dissection, cardiac tamponade or aortic rupture was lower. A reintervention was necessary because of the medical therapy failure, but open surgery was considered at high risk by a multidisciplinary team at our institute. Figure 3: Cook Off- Again, previous ascending aortic replacement is another bias of this group of the-shelf Device for patients because certainly eliminates the risk of retrograde dissection during ascending TEVAR but the presence of a mechanical aortic valve made the procedure more 21

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

technically demanding. We propose endovascular treatment of the ascending aorta in a very selected number of cases and still consider open repair the gold standard. Conclusion Endovascular treatment of TAAD by placement of a stent graft in the ascending aorta is a challenging procedure due to the proximity of the aortic arch branches and coronary arteries. Our experience shows that this technique is feasible in selected patient categories, and it seems associated with favorable results. Before this therapy can be implemented in the daily practice, further research is mandatory.

References

1. Mehta RH, Oâ&#x20AC;&#x2122;Gara PT, Bossone E et al. Acute type A aortic dissection in the elderly: clinical characteristics, management, and outcomes in the current era. J Am Coll Cardiol 2002; 40:685-692. 2. Trimarchi S, Eagle KA, Nienaber CA et al. Role of age in acute type A aortic dissection outcome: report from the International Registry of Acute Aortic Dissection (IRAD). J Thorac Cardiovasc Surg 2010; 140:784-789. 3. Dake MD, Miller DC, Semba CP et al. Transluminal placement of endovascular stent-grafts for the treatment of descending thoracic aortic aneurysms. N Engl J Med 1994; 331:1729-1734 4. Kato N, Shimono T, Hirano T et al. Transluminal placement of endovascular stent-grafts for the treatment of type A aortic dissection with an entry tear in the descending thoracic aorta. J Vasc Surg 2001; 34:1023-1028. 5. Nienaber C.A., Kishe S., Akin I., Liebold A., Weidtmann B., Incb H., Rehders T.C.. Indications, timing and results of endovascular treatment of type A aortic dissection. J Vasc Endovasc Surg 2011;18:187-91. 6. Kolvenbach RR, Karmeli R, Pinter LS et al. Endovascular management of ascending aortic pathology. J Vasc Surg 2011; 53:1431-1437. 7. Moon MC, Greenberg RK, Morales JP et al. Computed tomography-based anatomic characterization of proximal aortic dissection with consideration for endovascular candidacy. J Vasc Surg 2011; 53:942-949. 8. Sobocinski J, Oâ&#x20AC;&#x2122;Brien N, Maurel B et al. Endovascular approaches to acute aortic type A dissection: a CT-based feasibility study. Eur J Vasc Endovasc Surg 2011; 42:442-447. 9. Olsson C, Thelin S, Stahle E et al. Thoracic aortic aneurysm and dissection: increasing prevalence and improved outcomes reported in a nationwide population-based study of more than 14,000 cases from 1987 to 2002. Circulation 2006; 114:26112618. 10. Dorros G, Dorros AM, Planton S et al. Transseptal guidewire stabilization facilitates stent-graft deployment for persistent proximal ascending aortic dissection. J Endovasc Ther 2000; 7:506-512. 11. Ye C, Chang G, Li S et al. Endovascular stent-graft treatment for Stanford type A aortic dissection. Eur J Vasc Endovasc Surg 2011; 42:787-794. 12. Hornero F, Cervera V, Estornell J et al. Virtual vascular endoscopy for acute aortic dissection. Ann Thorac Surg 2005; 80:708-710. 13. Takami Y, Tajima K, Kato W et al. Can We Predict the Site of Entry Tear by Computed Tomography in Patients With Acute Type A Aortic Dissection? Clin Cardiol 2012. 14. Metcalfe MJ, Karthikesalingam A, Black SA et al. The first endovascular repair of an acute type A dissection using an endograft designed for the ascending aorta. J Vasc Surg 2012; 55:220-222. 15. Williams JB, Andersen ND, Bhattacharya SD et al. Retrograde ascending aortic dissection as an early complication of thoracic endovascular aortic repair. J Vasc Surg 2012; 55:1255-1262.

1. E ndovascular management of vascular emergencies of the thoracic aorta c. I ndications for Stentgrafts in acute aortic syndromes

Christoph A. Nienaber

Heart Center Rostock, Department of Internal Medicine I, Division of Cardiology, University of Rostock, Germany

Abstract Acute aortic syndrome and all chronic aortic conditions are subject to critical review, classification and new evaluation for medical, surgical and endovascular management. The current literature was evaluated and extracted for evidence for diagnostic and therapeutic recommendations based on natural history or interventional trials / registries. The reader will understand the variety of aortic diseases, comprehend the spectrum from acute to chronic conditions, and valueâ&#x20AC;Ż/ judge the details of therapeutic management and prognosis. On aggregate, the interest in all aortic condition is rising as a result of better understanding of disease, faster and easier diagnostics and emerging therapies with focus on modern pharmaceutical and non-surgical endovascular therapeutic options. Conclusion The spectrum of acute aortic conditions encompasses classic aortic dissection and other forms of acute aortic syndrome. On the basis of non-invasive imaging modalities the therapeutic options in the initial phase of dissection comprise blood-pressure lowering, anti-impulse medication, while definitive management favours non-traumatic non-surgical endovascular interventions in the attempt to reconstruct the dissected aorta. Acute aortic dissection should be considered a constituent of acute aortic syndrome (AAS) together with intramural hematoma (IMH), penetrating atherosclerotic ulcer (PAU) and aortic rupture. The common denominator of AAS is disruption of the media layer of the aorta with bleeding within the media layers (IMH) or separation of the layers of the aorta (dissection). In the majority of cases (90 percent), an intimal disruption is present that results in tracking of the blood in a dissection plane within the media potentially rupturing through the adventitia or back through the intima into the aortic lumen (Figure 1). The most common aortic syndrome is aortic dissection, featuring a tear in the aortic intima commonly preceded by medial wall degeneration or cystic media necrosis.[1] Blood passes through the tear separating the intima from media or adventitia creating a false lumen. Propagation of dissection can proceed in anterograde or retrograde fashion involving side branches and causing complications 23

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

such as tamponade, aortic valve insufficiency or proximal or distal malperfusion syndromes. [2-5]

Figure 1: S chematic of aortic dissection (left), penetrating ulcer (middle), and IMH (right) all causing acute aortic syndrome. Epidemiology Historically, acute aortic syndrome was attributed to syphilis; today, contributing factors are diverse (Table 1). The most common risk condition for aortic dissection or IMH is hypertension (75% history of hypertension). Other risk factors include smoking, direct blunt trauma and use of illicit drugs (such as cocaine or amphetamines). Population-based studies suggest that the incidence of acute dissection ranges from 2 to 3.5 cases per 100 000 person/years, which correlates with 6000 to 10 000 cases annually in the U.S. [6-10] There is weak evidence that aortic dissection is more common in the winter compared to warmer summer months. A review of 464 patients from IRAD reported a mean age at presentation of 63 years, with significant male predominance (65%). [7,8] The incidence of dissection appears to be increasing, independent of the aging population, to 16 per 100 000 men per annum; interestingly women may be affected less frequently, but have worse outcome as a result of atypical symptoms and delayed diagnosis. [11] It may in fact be that 2 to 3 times as many patients die from aortic dissection than from ruptured abdominal aortic aneurysm, particularly women are usually autosomal dominant and are strongest in younger patients (Marfan syndrome, Loeys-Dietz-Syndrome, Turner syndrome or Ehlers Danlos syndromes, especially type IV). [12,13] The most common mutations appear to lie in either the fibrillin gene (FBN-1) or the TGF- receptor 2 gene (TGFBR2) in Marfan and Loeys-Dietz syndromes respectively; there appears to be little difference in the clinical presentations of these two syndromes, over half of each group present with aortic symptoms. [14,15] The commonest non-syndromic mutation associated with thoracic aneurysms and dissections is in the smooth muscle cell actin gene, ACTA2, found in about one sixth of these patients. The association of mutations in genes encoding the contractile apparatus of vascular smooth muscle cells (SMC) with both aortic dissection and thoracic aneurysm indicates that SMC tonus and function may be an important phenotype influencing the response of the aorta to wall stress. Two other proximal conditions which predispose to acute aortic syndromes are annuloaortic ectasia and bicuspid aortic valve and both of these may have a genetic basis. [6] Table 1: Contributing conditions for Aortic Dissection Long-standing arterial hypertension • Smoking, dyslipidemia, cocaine/crack, amphetamine use Connective tissue disorders • Hereditary disorders • Marfan Syndrome • Loeys-Dietz Syndrome • Ehlers-Danlos Syndrome

c. Indications for Stentgrafts in acute aortic syndromes, C. A. Nienaber

• Turner Syndrome • Hereditary vascular disease • Bicuspid aortic valve • Coarctation Vascular inflammation • Auto immune disorders • Giant cell arteritis • Takayasu arteritis • Behcet’s disease • Ormond’s disease • Infection • Syphilis • Tuberculosis Deceleration trauma • Car accident • Fall from height Iatrogenic factors • Catheter/instrument intervention • Valvular/aortic surgery • Side- or cross-clamping/aortotomy • Graft anastomosis • Patch aortoplasty

Clinical Signs and Symptoms Patients with acute aortic syndromes often present in similar fashion, regardless of underlying condition such as dissection, IMH, PAU, or contained aortic rupture. Pain is the most commonly presenting symptom of acute AoD independent of age, sex, or other associated clinical complaint.7 Pooled data from >1000 patients showed that acute dissection is perceived as abrupt pain in 84% (95%; CI 80% to 89%) with initially severe intensity in 90% (95%; CI 88% to 92%). [7,18-20] Although classically described as tearing or ripping patients are more likely to describe the pain of acute dissection as sharp or stabbing, and fluctuating. Pain of aortic origin may often be confused with acute coronary syndromes. Cardiac enzymes, troponin and ECG changes may be instrumental in the diagnostic work-up, but only the absence of both D-dimer elevation and ECG-changes is considered specific to rule out acute aortic syndromes. D-dimers when elevated above 500 µg/L appear to correlate with extent and severity of acute aortic dissection, but fail to distinguish AAS from pulmonary embolism; critically elevated D-dimer should, however, prompt undelayed CT or TEE for confirmation of either life-threatening entity. [21,22] Acute aortic dissection can be classified according to either the origin of the intimal tear or whether the dissection involves the ascending aorta (regardless of the site of origin). Accurate classification is important as it drives decisions regarding surgical versus nonsurgical management. The two most commonly used classification schemes are the DeBakey and the Stanford systems. For purposes of classification, the ascending aorta refers to the aorta proximal to the brachiocephalic artery, and the descending aorta refers to the aorta distal to the left subclavian artery. The DeBakey classification system categorizes dissections based on the origin of the intimal tear and the extent of the dissection: ● Type A: All dissections involving the ascending aorta regardless of the site of origin (surgery usually recommended). ● Type B: All dissections that do not involve the ascending aorta (nonsurgical treatment usually recommended). Note that involvement of the aortic arch without involvement of the ascending aorta in the Stanford classification is labeled as Type B. ● Type I: Dissection originates in the ascending aorta and propagates distally to include at least the aortic arch and typically the descending aorta (surgery usually recommended). ● Type II: Dissection originates in and is confined to the ascending aorta (surgery usually recommended). ● Type III: Dissection originates in the descending aorta and propagates most often distally (nonsurgical treatment usually recommended). – Type IIIa: Limited to the descending thoracic aorta. – Type IIIb: Extending below the diaphragm. 25

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

The Stanford classification system divides dissections into 2 categories, those that involve the ascending aorta and those that do not. The risk of death is increased in patients who present with or develop complications of pericardial tamponade, involvement of coronary arteries causing acute myocardial ischemia/infarction, or malperfusion of the brain. [2,16,23,24] Other predictors of increased in-hospital death include age ≥70 years, hypotension or cardiac tamponade, kidney failure and pulse deficits. [25] Less appreciated predisposing factors for type A dissection include prior cardiac and valvular surgery (15%) and iatrogenic dissection with surgery or catheterization (5%). [23] In the absence of immediate surgical repair, medical management of proximal dissection is associated with a mortality of nearly 20% by 24 hours after presentation, 30% by 48 hours, 40% by day 7, and 50% by 1-month. Even with surgical repair, mortality rates are 10% by 24 hours, 13% by 7 days, and nearly 20% by 30-days (Figure 2). The most common causes of death are aortic rupture, stroke, visceral ischemia, cardiac tamponade and circulatory failure. [23,26,27] Patients with uncomplicated type B dissection have a 30-day mortality of 10% and may be candidates for long-term medical management based on anti-impulsing medication.6 However, with the evolution of ischemic complications such as renal failure, visceral ischemia, or contained rupture mortality increases to 20% by day 2, and 25% by day 30. Similar to type A dissection, advanced age, rupture, shock, and malperfusion are important independent predictors of early mortality. Nonetheless, all types of acute dissection require initial medical management until definitive treatment. Initial medical therapy Acute aortic syndrome (dissection or IMH) involving the ascending aorta are surgical emergencies; in selected cases hybrid approaches of an endovascular and open combination may be considered. [28] Conversely, acute aortic pathology confined to the descending aorta are subject to medical treatment unless complicated by organ or limb malperfusion, progressive dissection, extraaortic blood collection (impending rupture), intractable pain or uncontrolled hypertension. [15] Initial management of AAS in general, particularly in dissection of both the proximal (A) and distal (B) aorta, is directed at limiting propagation of dissected wall components by control of blood pressure and reduction of dP/dt as an anti impulse strategy. Reduction of pulse pressure to just maintain sufficient endorgan perfusion is a priority with the use of intravenous β-blockade as first-line therapy before swift surgical repair in type A lesions (Table 2). Medical Initial step in type A dissection prior to surgery Uncomplicated acute type B dissection Stable isolated aortic arch dissection Uncomplicated chronic type B dissection Surgery Type A aortic dissection Acute type B dissection complicated by Retrograde extension into the ascending aorta Dissection in fibrillinopathies (e.g. Marfan-syndrom, Loeys-Dietz-Syndrome, Ehlers-Danlos-Syndrom) Interventional Unstable acute / chronic type B dissection Malperfusion Rapid expansion (>1cm/year)

c. Indications for Stentgrafts in acute aortic syndromes, C. A. Nienaber

Critical diameter (≥5,5cm) Refractory pain Type B dissection with retrograde extension into the ascending aorta Hybrid procedure for extended type A aortic dissection

Table 2: Distribution of differential therapeutic strategies in aortic dissection. Labetalol, with both α- and β-blocking characteristics, is useful for lowering both blood pressure and dP/dt, with target systolic pressure of 100-120 mmHg and heart rate of 60-80 beats/min. Often multiple agents are required, with patients, ideally managed in an intensive care setting. Opiate analgesia should be prescribed to attenuate the sympathetic release of catecholamines triggered by pain with resultant tachycardia and hypertension (Table 3). Esmolol

Mechanism Cardioselective beta-1 blocker

Dose Load: 500 µg/kg IV Drip: 50 µg kg-1 min-1 IV. Increase by increments of 50 µg/min

Labetalol

Nonselective beta 1,2 blocker Selective alpha-1 blocker

Load: 20 mg IV Drip: 2 mg/min IV

Enalaprilat

ACE inhibitor

0.625-1.25 mg IV q 6 hours. Max dose: 5 mg q 6 hours.

Nitroprusside Direct arterial vasodilator

Begin at 0.3 µg kg-1 min-1 IV. Max dose 10 µg kg-1 min-1

Nitroglycerin Vascular smooth muscle Relaxation

5-200 µg/min IV

Cautions / contraindications - Asthma or bronchospasm - Bradycardia - 2nd- or 3rd-degree AV block -C ocaine or methamphetamine abuse - Asthma or bronchospasm - Bradycardia - 2nd or 3rd degree AV block - Cocaine or methamphetamine abuse - Angioedema - Pregnancy - Renal artery stenosis - Severe renal insufficiency - May cause reflex tachycardia - Cyanide/thiocyanate toxicity - especially in renal or hepatic insufficiency - Decreases preload - contraindicated in tamponade or other preload-dependent states - Concomitant use of sildenafil or similar agents

Table 3: Initial medical treatment in aortic dissection. Further management is dictated by the site of the lesion and evidence of complications (persisting pain, organ malperfusion), as well as by the evidence of disease progression on serial imaging. In normotensive or hypotensive patients, careful evaluation for loss of blood, pericardial effusion or heart failure (by cardiac echo) is mandatory before administering volume. Patients with profound haemodynamic instability often require intubation, mechanical ventilation and urgent bedside transoesophageal echocardiography or rapid CT for confirmatory imaging. In rare cases, the external ultrasound diagnosis of cardiac tamponade may justify immediate sternotomy and surgical access to the ascending aorta to prevent circulatory arrest, shock and ischaemic brain damage. Percutaneous pericardiocentesis as a temporary step often fails, and can accelerate bleeding and shock, and is consequently contra-indicated [29]. For many years there was consensus that patients with type B dissection should be treated medically unless life-threatening complications occur. Nevertheless, long-term medical management is associated with solving outcomes and survival estimates ranging from 60-80 percent. Even today, there is no clear indication for endovascular repair of uncomplicated type B dissection with respect to 2 years outcomes; the INSTEAD trial showed no survival advantage of stenting as opposed to best medical therapy at 2 years (best medical therapy 95.6% vs. stenting 88.9%; P=0.15) [30]. It did, however, show beneficial impact of stent-graft on aortic remodeling that may indeed beneficially impact on long-term outcomes after 5 years with a lower rate of late rupture in stented patients. 27

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

Surgical Management The aim of surgical therapy in proximal type A (type I, II) aortic dissection is prevention of rupture or development of pericardial effusion, which may lead to cardiac tamponade and death. Similarly, sudden onset of aortic regurgitation and coronary flow obstruction require urgent surgical intervention, with the aim of resecting the region of intimal tear in dissection limited to the ascending aorta and replacement by a composite or interposition graft (if the aortic valves are intact or resuspendable). When the dissection extends to the aortic arch or the descending aorta, resection of the entire intimal flap may not be possible or the patient may require partial or total arch replacement [31]. A recent report highlights the problem of either resecting or leaving unrecognised intimal tears in the arch or descending thoracic aorta, which is seen in 20-30 % and predisposes to later distal aortic reoperation [32]. Even in centres of excellence, using adjunctive measures such as profound hypothermic circulatory arrest and selective retrograde perfusion of head vessels for surgical management of arch repair, operative mortality ranges between 15 and 35 % [33]. Although gaining growing acceptance for improved outcome (5-year survival of 73 ± 6 %), profound hypothermic circulatory arrest has failed to improve early complications, survival and distal reoperation rates in patients with acute type A dissection; 30-day, 1-year and 5-year survival estimates are 81 ± 2 %, 74 ± 3 % and 63 ± 3 %, and not different from other techniques based on propensity-matched retrospective analysis [31]. The key to success is rapid surgery prior to any haemodynamic instability or deterioration (Table 4). Table 4: Distribution of differential therapeutic strategies in aortic dissection Surgery Type A aortic dissection Acute type B dissection complicated by Retrograde extension into the ascending aorta Dissection in fibrilinopathies (e.g. Marfan-syndrom, Ehlers-Danlos-Syndrom) Medical Uncomplicated acute type B dissection Stable isolated aortic arch dissection Uncomplicated chronic type B dissection Interventional Unstable acute / chronic type B dissection Malperfusion Rapid expansion (>1cm/year) Critical diameter (≥5,5cm) Refractory pain Type B dissection with retrograde extension into the ascending aorta Hybrid procedure for extended type A aortic dissection

Aortic arch in acute type A (type I and II) dissection Treatment of the acutely dissected aortic arch remains an unresolved issue. At present there is growing consensus that any dissected arch should be explored during hypothermic circulatory arrest [34, 35]. In the absence of an arch tear, an open distal anastomosis of the graft and the conjoined aortic wall layers at the junction of the ascending and arch portions is justified. Arch tears occur in up to 30 % of patients with acute dissection [35, 36]. Whenever extensive tears are found that continue beyond the junction of the transverse and descending aortic segments, or with acute dissection of a previously aneurysmal arch, subtotal or total arch replacement may be required, with reconnection of some or all supra-aortic vessels to the graft during hypothermic circulatory arrest and antegrade head perfusion [37]. In dissecting and non-dissecting aneurysms extending to the downstream aorta, an elephant trunk extension of the arch graft is an option described by Borst et al. [38]. This technique greatly facilitates later procedures on the downstream aorta. Instead of performing a conventional anastomosis between the end of the graft and the descending aorta, the graft is allowed to float freely in the aortic lumen. In a later procedure the elephant trunk section of the graft may be either connected surgically 28

c. Indications for Stentgrafts in acute aortic syndromes, C. A. Nienaber

to the distal descending aorta directly or extended with another tubular prosthesis or interventionally by a customized endovascular stent graft that may then be anastomosed at any desired downstream level of the aorta. Surgery in type B (type III) aortic dissection In the current era, the indications for active management in patients with acute type B (type III) are limited to the prevention or relief of life-threatening complications such as malperfusion syndrome, intractable pain, rapidly expanding aortic diameter or signs of imminent aortic rupture that can all be managed by interventional stent graft placement. In particular signs of malperfusion or vital aortic side-branch occlusion warrant interventional therapy via stent grafting to improve distal true lumen flow or, in rare instances, via catheter-guided side-branch stenting. Conversely, uncomplicated type B (type III) aortic dissections are at present usually treated medically, since surgical repair has no proven superiority over medical or interventional treatment in stable patients. In complicated cases, the concept of interventional stent graft placement seems to be associated with higher survival rates than the open surgical approach [39,40].

Interventional Endovascular Strategy Conventional treatment of Stanford type A (DeBakey type II, II) dissection consists of surgical reconstruction of the ascending aorta with complete or partial resection of the dissected aortic segment. Endovascular strategies have no clinical application except for relief of critical malperfusion prior to surgery of the ascending aorta by distal fenestration in cases of thoraco-abdominal extension (DeBakey type I) and peripheral ischaemic complications (Figure 4).

Figure 4: Contrast-enhanced MRA of chronic type B dissection originating from the aortic arch region in MIP (A) and as volume-rendered 3D reconstruction (B). Follow-up MRA at 7 days after stent-graft placement shows a completely sealed proximal entry to the thrombosed false lumen. The diameter of the true lumen is normalized and the descending aorta is reconstructed (C). In distal dissection, however, endovascular stent graft placement has the potential to repair the aorta by sealing one (or multiple) proximal entry tears with a prosthetic-covered scaffold, thus reconstructing the previously collapsed true lumen with re-establishment of side-branch flow, and finally initiation of thrombosis of the false lumen (Table 5, Figure 5) [39-41].

Esmolol

Mechanism Cardioselective beta-1 blocker

Dose Load: 500 µg/kg IV Drip: 50 µg kg-1 min-1 IV. Increase by increments of 50 µg/min

Labetalol

Nonselective beta 1,2 blocker Selective alpha-1 blocker

Load: 20 mg IV Drip: 2 mg/min IV

Enalaprilat

ACE inhibitor

0.625-1.25 mg IV q 6 hours. Max dose: 5 mg q 6 hours.

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

Mechanism

Dose

Nitroprusside Direct arterial vasodilator

Begin at 0.3 µg kg-1 min-1 IV. Max dose 10 µg kg-1 min-1

Nitroglycerin Vascular smooth muscle relaxation

5-200 µg/min IV

Cautions / contraindications - Severe renal insufficiency - May cause reflex tachycardia - Cyanide/thiocyanate toxicity - especially in renal or hepatic insufficiency - Decreases preload - contraindicated in tamponade or other preload-dependent states - Concomitant use of sildenafil or similar agents

Table 5: Initial medical treatment in aortic dissection.

Figure 5: Chronic type B aortic dissection with partial false lumen thrombosis prior to stent-graft placement (left); Reconstructed and remodelled thoracic aorta after scaffolding of dissected segments (right). Most scenarios of malperfusion syndrome are amenable to endovascular management, considering that surgical mortality rates in patients with acute peripheral vascular ischaemic complications are similar to those in patients with mesenteric ischaemia [42,43]. In the near future, combined surgical and interventional procedures, even for proximal dissection, are likely to emerge [44,45] considering that endovascular procedures have already been applied successfully to the ascending aorta (Figure 6). Figure 6: Reconstructed type A aortic dissection with short stent-graft placed in the ascending aorta to seal the entry and induce complete reconstruction. 30

c. Indications for Stentgrafts in acute aortic syndromes, C. A. Nienaber

Indications for stent graft placement The most effective method for excluding an enlarging and dilated false lumen is the sealing of proximal entry tears with a customized stent graft. The absence of a distal re-entry tear is desirable for optimal results but not a prerequisite. Depressurisation and shrinking of the false lumen is the most beneficial result to be gained, ideally followed by complete thrombosis of the false lumen and remodeling of the entire dissected aorta: on rare occasions, this even occurs in retrograde type A dissection [46]. Similar to previously accepted indications for surgical intervention in type B dissection, scenarios such as intractable pain with descending dissection, rapidly expanding false lumen diameter, extra-aortic blood collection as a sign of imminent rupture or distal malperfusion syndrome are accepted indications for emergency stent graft placement [40,46,47]. Moreover, late onset of complications such as malperfusion of vital aortic side branches may justify endovascular stent grafting as a first option. Interventional therapy in an elective setting Medical therapy, as the first-line approach to uncomplicated type B aortic dissections, is justified because of a relatively good short-term prognosis with 85 % of patients surviving their initial hospital stay. The reported 30-day mortality of uncomplicated type B dissections ranges at 11 % versus 30 % in complicated cases with limbs or visceral ischaemia, renal failure, or contained rupture [48]. Unfortunately, the long-term outcome of medical therapy is suboptimal with a reported 50 % 5-year survival rate and delayed expansion of the false lumen in 25 % patients at 4 years. This expansion of the false lumen predisposes patients to aortic rupture or retrograde migration of the dissection plane with involvement of the ascending aorta and a consequent increased mortality rate [49-51]. Initial experience of the endovascular management of chronic aortic dissection versus open surgery was reported by Nienaber et al. [50]. Whether prophylactic use of thoracic endovascular aortic repair (TEVAR) in patients with chronic type B aortic dissections is superior to medical treatment alone was evaluated in the prospective, randomized, and controlled Investigation of STEnt grafts in Aortic Dissection (INSTEAD) trial [51]. One hundred and forty patients in a stable clinical condition at least 2 weeks after index dissection were randomly subjected to elective stent graft placement in addition to optimal medical therapy (n=72) or to optimal medical therapy alone (n=68). There was no difference inn allcause deaths, with a 2-year cumulative survival rate of 95.5±2.5 % with optimal medical therapy vs. 88.9±3.7 % with TEVAR (p=0.15). Moreover, the aorta-related death rate was not different (2,9 % vs. 5,6 %; p=0,68), and the risk for the combined endpoint of aorta-related death and progression was similar (p=0,65). Aortic remodeling occurred in 91,3 % of patients with TEVAR, but only in 19,4 % of patients under medical treatment (p<0,001). Thus, data from INSTEAD trial suggest no prognostic advantage of TEVAR within 2 years compared with monitored medical therapy for uncomplicated chronic type B dissection, suggesting that TEVAR should be reserved for complicated cases of acute or chronic descending thoracic aortic dissection, or when medical management fails. Paraplegia may occur after use of multiple stent grafts but still appears to be a rare phenomenon, especially with a stented segment of less than 20 cm. Results of short-term follow-up are excellent, with a 1-year survival rate of > 90 %; tears can be re-adapted and aortic diameters generally decrease with complete thrombosis of the false lumen.This suggests that stent placement may facilitate healing of the dissection, sometimes of the entire aorta, including abdominal segments. However, late reperfusion of the false lumen has been observed occasionally, underlining the need for stringent follow-up imaging. Interventional therapy in an emergency setting The concept of emergency stent graft placement for urgent endovascular aortic repair of dissection is attractive, and a growing number of acute type B aortic dissections undergo endovascular repair (with little evidence of periprocedural morbidity, aborted malperfusion or leakage) and reconstruction of the dissected aorta (Table 6) [50-66]. Recent reports suggest that percutaneous stent graft placement in the dissected aorta is safer and produces better results than surgery for type B dissection. Data from IRAD registry on 571 patients with acute type B aortic dissection provided better survival rates after endovascular treatment versus open surgical repair in patients with complicated type B dissection (Figure 3) [66] 31

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

Figure 3: C omparison of various treatments in patients with complicated acute type B aortic dissections. (Ref. 66) Author

Year

Technical Paraplegia (%) Success (%) Acute complicated type B dissection 43 100 0 28 97 n.a. 609 98 0.8 63 95 0 16 100 0 66 100 3.4 35 97.1 2.8 28 90 n.a. 106 99 1.8

Bortone et al. Dialetto et al. Eggebrecht et al. Xu et al. Verhoye et al. Fattori et al. Szeto et al. Khoynezhad et al. Alves et al.

2004 2005 2006 2006 2008 2008 2008 2009 2009

Parsa et al.

2010

Nienaber et al. Kato et al. Eggebrecht et al. Jing et al. Guangqi et al. Kim et al. Nienaber et al.

1999 2001 2005 2008 2009 2009 2009

12 15 28 35 49 72 72

100 Chronic type B dissection 100 100 100 100 77.6 87 95.7

2 0 0 0 0 0 0 2.8

Mortality (%)

Follow-up (month)

7 10.7 11.2 10.6 27 10.6 2.8 18 (1y) 22(5y) 18 (acute AD) 7 (chronic AD) 37 (overall) 6 (aorta-related)

21 18.1 24 48 36 1 18 36 35.9

0 0 13.6 7.6 4.8 8.2 11.1 (overall) 5.6 (aorta-related)

12 24 12 48 14.4 43 24

14.4

Table 6: R esults of endovascular stent-graft implantation in different clinical conditions (AD: aortic dissection). Long-term therapy and follow-up The long-term approach to patients with successful initial treatment of acute aortic dissection begins with the appreciation of a systemic illness. Systemic hypertension, advanced age, aortic size and presence of patent false lumen are all factors which identify higher risk, as does the entire spectrum of Marfanâ&#x20AC;&#x2122;s syndrome [51,66-70]. All patients merit aggressive medical therapy, follow-up visits and serial imaging. It has been estimated that one third of survivors of dissection will experience extension of dissection or rupture, or require surgery for aortic aneurysm formation within 5 years. Adjunctive Ă&#x;blockade is important by lowering both blood pressure and sheer wall stress (dp/dt). Blood pressure should be titrated to less than 130/80 mmHg regardless underlying disease [71-73]. Additionally, heart rate should be controlled since a heart rate < 60 bpm significantly decreases secondary adverse events 32

c. Indications for Stentgrafts in acute aortic syndromes, C. A. Nienaber

(aortic expansion, recurrent aortic dissection, aortic rupture and/or need for aortic surgery) in type B aortic dissection [74]. Choice of serial follow-up imaging is dependent on institutional availability and expertise. Previous recommendations suggest follow-up imaging at 1, 3, 6, 9 and 12 months following discharge, and annually thereafter [71]. This aggressive strategy underlines the observation that both hypertension and aortic expansion / dissection are common and not easily predicted in the first months following hospital discharge. Imaging should not be confined to the region of initial involvement since both dissection and aneurysm formation may occur anywhere along the entire length of the aorta.

References

1. Larson EW, Edwards WD. Risk factors for aortic dissection: a necropsy study of 161 cases. Am J Cardiol 1984; 53:849-55. 2. Meszaros I, Morocz J, Szlavi J, Schmidt J, Tornoci L, Nagy L, Szep L. Epidemiology and clinicopathology of aortic dissection. Chest 2000; 117:1271-8. 3. Roberts CS, Roberts WC. Aortic dissection with the entrance tear in the descending thoracic aorta. Analysis of 40 necropsy patients. Ann Surg 1991; 213:356-68. 4. Masuda Y, Takanashi K, Takasu J, Watanabe S. [Natural history and prognosis of medical treatment for the patients with aortic dissections]. Nippon Geka Gakkai Zasshi 1996;97:890-3. 5. Bogaert J, Meyns B, Rademakers FE, Bosmans H, Verschakelen J, Flameng W, Marchal G, Baert AL. Follow-up of aortic dissection: contribution of MR angiography for evaluation of the abdominal aorta and its branches. Eur Radiol 1997; 7:695702. 6. Hiratzka LF, Bakris GL, Beckman JA, Bersin RM, Carr VF, Casey DE, Eagle KA, Hermann LK, Isselbacher EM, Kazerooni EA, Kouchoukos NT, Lytle BW, Milewicz DM, Reich DL, Sen S, Shinn JA, Svensson LG, Williams DM. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM – Guidelines for the Diagnosis and Management of Patients with thoracic Aortic Disease: Executive Summary. A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. J Am Coll Cardiol 2010; 55:27-129. 7. Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, Evangelista A, Fattori R, Suzuki T, Oh JK, Moore AG, Malouf JF, Pape LA, Gaca C, Sechtem U, Lenferink S, Deutsch HJ, Diedrichs H, Marcos y Robles J, Llovet A, Gilon D, Das SK, Armstrong WF, Deeb GM, Eagle KA. The International Registry of Acute Aortic Dissection (IRAD): New insights into an old disease. JAMA 2000; 283:897-903. 8. Suzuki T, Mehta RH, Ince H, Nagai R, Sakomura Y, Weber F, Sumiyoshi T, Bossone E, Trimarchi S, Cooper JV, Smith DE, Isselbacher EM, Eagle KA, Nienaber CA; International Registry of Aortic Dissection. Clinical profiles and outcomes of acute type B aortic dissection in the current era: lessons from the International Registry of Aortic Dissection (IRAD). Circulation 2003; 108:II312-II317. 9. Olsson C, Thelin S, Stahle E, Ekbom A, Granath F. Thoracic aortic aneurysm and dissection: increasing prevalence and improved outcomes reported in a nationwide population-based study of more than 14000 cases from 1987 to 2002. Circulation 2006; 114:2611-2618. 10. Svensson LG, Kouchoukos NT, Miller DC, Bavaria JE, Coselli JS, Curi MA, Eggebrecht H, Elefteriades JA, Erbel R, Gleason TG, Lytle BW, Mitchell RS, Nienaber CA, Roselli EE, Safi HJ, Shemin RJ, Sicard GA, Sundt TM 3rd, Szeto WY, Wheatley GH 3rd;. Society of Thoracic Surgeons Endovascular Surgery Task Force. Expert consensus document on the treatment of descending thoracic aortic disease using endovascular stent-grafts. Ann Thorac Surg 2008; 85:S1-41. 11. Nienaber CA, Zannetti S, Barbieri B, Kische S, Schareck W, Rehders TC: INSTEAD Investigators. Investigation of STEnt grafts in patients with type B aortic dissection: design of the INSTEAD trial: a prospective, multicenter, European randomized trial. Am Heart J 2005; 149:592-599. 12. Nienaber CA, Fattori R, Mehta RH, Richartz BM, Evangelista A, Petzsch M, Cooper JV, Januzzi JL, Ince H, Sechtem U, Bossone E, Fang J, Smith DE, Isselbacher EM, Pape LA, Eagle KA; International Registry of Acute Aortic Dissection. Gender-related differences in acute aortic dissection. Circulation. 2004; 109:3014 –21. 13. Trimarchi S, Nienaber CA, Rampoldi V, Myrmel T, Suzuki T, Bossone E, Tolva V, Deeb MG, Upchurch GR Jr, Cooper JV, Fang J, Isselbacher EM, Sundt TM 3rd, Eagle KA; IRAD Investigators. Role and results of surgery in acute type B aortic dissection: insights from the International Registry of Acute Aortic Dissection (IRAD). Circulation 2006; 114:I357-I364. 14. Tsai TT, Evangelista A, Nienaber CA, Trimarchi S, Sechtem U, Fattori R, Myrmel T, Pape L, Cooper JV, Smith DE, Fang J, Isselbacher E, Eagle KA; International Registry of Acute Aortic Dissection (IRAD). Long-term survival in patients presenting with acute type A aortic dissection: insights from the International Registry of Acute Aortic Dissection (IRAD). Circulation 2006; 114:I350-I356. 15. Lundevall J. Traumatic rupture of the aorta, with special reference to road accidents. Acta Pathol Microbiol Scand. 1964; 62:29 –33. 16. Richens D, Kotidis K, Neale M, Oakley C, Fails A. Rupture of the aorta following road traffic accidents in the United Kingdom 1992–1999. The results of the co-operative crash injury study. Eur J Cardiothorac Surg. 2003; 23: 143–8.

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17. Fabian TC, Davis KA, Gavant ML, Croce MA, Melton SM, Patton JH Jr, Haan CK, Weiman DS, Pate JW. Prospective study of blunt aortic injury: helical CT is diagnostic and antihypertensive therapy reduces rupture. Ann Surg. 1998; 227:666 –76. 18. Attias D, Stheneur C, Roy C, Collod-Béroud G, Detaint D, Faivre L, Delrue MA, Cohen L, Francannet C, Béroud C, Claustres M, Iserin F, Khau Van Kien P, Lacombe D, Le Merrer M, Lyonnet S, Odent S, Plauchu H, Rio M, Rossi A, Sidi D, Steg PG, Ravaud P, Boileau C, Jondeau G. Comparison of clinical presentations and outcomes between patients with TGFBR2 and FBN1 mutations in Marfan syndrome and related disorders. Circulation. 2009 Dec 22; 120(25):2541-9. 19. Nienaber CA, Von Kodolitsch Y. Therapeutic management of patients with Marfan syndrome: focus on cardiovascular involvement. Cardiol Rev 1999; 7:332-41. 20. Tsai TT, Nienaber CA, Eagle KA. Acute aortic syndromes. Circulation.2005; 112:3802–13. 21. Clouse WD, Hallett JW, Jr., Schaff HV, Spittell PC, Rowland CM, Ilstrup DM, Melton LJ 3rd. Acute aortic dissection: population-based incidence compared with degenerative aortic aneurysm rupture. Mayo Clin Proc. 2004; 79:176–80. 22. Suzuki T, Mehta RH, Ince H, Nagai R, Sakomura Y, Weber F, Sumiyoshi T, Bossone E, Trimarchi S, Cooper JV, Smith DE, Isselbacher EM, Eagle KA, Nienaber CA. Clinical profiles and outcomes of acute type B aortic dissection in the current era: lessons from the International Registry of Aortic Dissection (IRAD). Circulation 2003; 108 Suppl 1:II312-7. 23. von Kodolitsch Y, Schwartz AG, Nienaber CA. Clinical prediction of acute aortic dissection. Arch Intern Med. 2000 Oct 23;160(19):2977-82. 24. Klompas M. Does this patient have an acute thoracic aortic dissection? JAMA. 2002; 287:2262–72. 25. von Kodolitsch Y, Nienaber CA, Dieckmann C, Schwartz AG, Hofmann T, Brekenfeld C, Nicolas V, Berger J, Meinertz T. Chest radiography for the diagnosis of acute aortic syndrome. Am J Med 2004; 116:73-7. 26. Eggebrecht H, Naber CK, Bruch C, Kroger K, von Birgelen C, Schmermund A, Wichert M, Bartel T, Mann K, Erbel R. Value of plasma fibrin D-dimers for detection of acute aortic dissection. J Am Coll Cardiol 2004; 44:804-9. 27. Shinohara T, Suzuki K, Okada M, Shiigai M, Shimizu M, Maehara T, Ohsuzu F. Soluble elastin fragments in serum are elevated in acute aortic dissection. Arterioscler Thromb Vasc Biol 2003; 23:1839-44. 28. Suzuki T, Distante A, Zizza A, Trimarchi S, Villani M, Salerno Uriarte JA, De Luca Tupputi Schinosa L, Renzulli A, Sabino F, Nowak R, Birkhahn R, Hollander JE, Counselman F, Vijayendran R, Bossone E, Eagle K; IRAD-Bio Investigators. Diagnosis of acute aortic dissection by D-dimer: the International Registry of Acute Aortic Dissection Substudy on Biomarkers (IRAD-Bio) experience.Circulation. 2009; 119:2702-7. 29. Isselbacher EM, Cigarroa JE, Eagle KA. Cardiac tamponade complication proximal aortic dissection: is pericardiocentesis harmful? Circulation 1994;90:2375-9. 30. Nienaber CA, Rousseau H, Eggebrecht H, Kische S, Fattori R, Rehders TC, Kundt G, Scheinert D, Czerny M, Kleinfeldt T, Zipfel B, Labrousse L, Ince H. Randomized comparison of strategies for type B aortic dissection: the Investigation of STEnt Grafts in Aortic Dissection (INSTEAD) trial. Circulation 2009;120(25):2519-28. 31. Lai DT, Robbins RC, Michell RS, Moore KA, Oyer PE; Shumway NE, Reitz BA, Miller DC. Does profound hypothermic circulatory arrest improve survival in patients with acute type A aortic dissection? Circulation 2002;106:218-28. 32. Schoor JS, Yerlioglu ME, Galla JD, Lansman SL, Ergin MA, Griepp RB. Selective management of acute type B aortic dissection : long-term follow-up. Ann Thorac Surg. 1996 ;61 :1339-41. 33. Xenos ES, Abedi NN, Davenport DL, Minion DJ, Hamdallah O, Sorial EE, Endean ED. Meta-analysis of endovascular vs open repair for traumatic descending thoracic aortic rupture. J Vasc Surg. 2008; 48:1343-51. 34. Gott VL, Greene PS, Alejo DE, Cameron DE, Naftel DC, Miller DC, Gillinov AM, Laschinger JC, Pyeritz RE. Replacement of the aortic root in patients with Marfan’s syndrome. N Engl J Med. 1999; 340:1307-13. 35. Ergin MA, O’Connor J, Guinto R, Griepp RB. Experience with profound hypothermia and circulatory arrest in the treatment of aneurysms of the aortic arch. Aortic arch replacement for acute aortic arch dissections. J Thorac Cardiovasc Surg. 1982; 84:649-55. 36. Nguyen B, Muller M, Kipfer B, Berdat P, Walpoth B, Althaus U, Carrel T. Different techniques of distal aortic repair in acute type A dissection: impact on late aortic morphology and reoperation. Eur J Cardiothorac Surg. 1999; 15:496-500. 37. Griepp RB, Ergin MA, Lansman SL, Galla JD, Pogo G. The physiology of hypothermic circulatory arrest. Semin Thorac Cardiovasc Surg. 1991;3:188-93. 38. Borst HG, Walterbusch G, Schaps D. Extensive aortic replacement using “elephant trunk” prosthesis. Thorac Cardiovasc Surg. 1983;31:37-40. 39. Ince H, Nienaber CA. The concept of interventional therapy in acute aortic syndrome. J Cardiovasc Surg (Torino) 2002;17:135-42. 40. Koschyk D, Nienaber CA, Knap M, Hofmann T, Kodolitsch YV, Skriabina V, Ismail M, Franzen O, Rehders TC, Dieckmann C, Lund G, Reichenspurner H, Meinertz T. How to guide stent-graft implantation in type B aortic dissection? Comparison of angiography, transesophageal echocardiography, and intravascular ultrasound. Circulation 2005;112:260-4. 41. Nienaber CA, Fattori R, Lund G, Dieckmann C, Wolf W, von Kodolitsch Y, Nicolas V, Pierangeli A. Nonsurgical reconstruction of thoracic aortic dissection by stentgraft placement. N Engl J Med. 1999340:1539-45. 42. Walkers PJ, Dake MD, Mitchell RS, Miller DC. The use of endovascular techniques for the treatment of complications of aortic dissection. J Vasc Surg. 1993;18:1042-51. 43. Fann JI, Sarris GE, Mitchell RS, Shumway NE, Stinson EB, Oyer PE, Miller DC. Treatment of patients with aortic dissection presenting with peripheral vascular complications. Ann Surg. 1990;212:705-13. 44. Yano H, Ishimaru S, Kawaguchi S, Obitsu Y. Endovascular stent-grafting of the descending thoracic aorta after arch repair in acute type A dissection. Ann Thorac Surg. 2002;73:288-91.

c. Indications for Stentgrafts in acute aortic syndromes, C. A. Nienaber

45. Iannelli G, Piscione F, Tommaso L, Monaco M, Chiariello M, Spampinato N. Thoracic aortic emergencies: impact of endovascular surgery. Ann Thorac Surg. 2004;77:591-6. 46. Kato N, Shimono T, Hirano T, Ishida M, Yada I, Takeda K. Transluminal placement of endovascular stent-grafts for the treatment of type A aortic dissection with an entry tear in the descending thoracic aorta. J Vasc Surg. 2001;34:1023-8. 47. Nienaber CA, Ince H, Weber F, Rehders T, Petzsch M, Meinertz T, Koschyk DH. Emergency stent-graft placement in thoracic aortic dissection and evolving rupture. J Cardiovasc Surg (Torino). 2003;18:464-70. 48. Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, Evangelista A, Fattori R, Suzuki T, Oh JK, Moore AG, Malouf JF, Pape LA, Gaca C, Sechtem U, Lenferink S, Deutsch HJ, Diedrichs H, Marcos y Robles J, Llovet A, Gilon D, Das SK, Armstrong WF, Deeb GM, Eagle KA. The international registry of acute aortic dissection (IRAD): new insights into an old disease. JAMA 2000;283:897-903. 49. Nienaber CA, Zannetti S, Barbieri B, Kische S, Schareck W, Rehders TC. INSTEAD study collaborators. Investigation of Stent grafts in patients with type B Aortic Dissection Design of the INSTEAD trial – a prospective, multicenter, European randomized trial. Am Heart J. 200;149:592-9. 50. Nienaber CA, Fattori R, Lund G, Dieckmann C, Wolf W, von Kodolitsch Y, Nicolas V, Pierangeli A. Nonsurgical reconstruction of thoracic aortic dissection by stent-graft placement. N Engl J Med. 1999;340:1539-45. 51. Nienaber CA, Rousseau H, Eggebrecht H, Kische S, Fattori R, Rehders TC, Kundt G, Scheinert D, Czerny M, Kleinfeldt T, Zipfel B, Labrousse L, Ince H; INSTEAD trial. Randomized comparison of strategies for type B aortic dissection: the Investigation of STEnt grafts in Aortic Dissection (INSTEAD) trial. Circulation 2009;120:2519-28. 52. Bortone AS, De Cillis E, D’Agostino D, de Luca Tupputi Schinosa L. Endovascular treatment of thoracic aortic disease: four years of experience. Circulation 2004;110:262-7. 53. Dialetto G, Cocino FE, Scognamiglio G, Manduca S, Della Corte A, Giannolo B, Scardone M, Cotrufo M. Treatment of type B aortic dissection: endoluminal repair or conventional medical therapy? Eur J Cardiothorac Surg. 2005;27:826-30. 54. Egggebrecht H, Nienaber CA, Neuhäuser M, Baumgart D, Kische S, Schmermund A, Herold U, Rehders TC, Jakob HG, Erbel R. Endovascular stent-graft placement in aortic dissection: a meta-analysis. Eur Heart J. 2006;27:489-98. 55. Xu S, Huang F, Yang J, Li ZZ, Wang XY, Zhang ZG, Du JH. Endovascular repair of acute type B aortic dissection: early and mid-term results. J Vasc Surg. 2006;43:1090-5. 56. Verhoye JP, Miller DC, Sze D, Dake MD, Mitchell RS. Complicated acute type B aortic dissection: mid-term results of emergency stent-grafting. J Thorac Cardiovasc Surg. 2008;136:424-30. 57. Szeto WY, McGarvey M, Pochettino A, Moser GW, Hoboken A, Cornelius K, Woo EY, Carpenter JP, Fairman RM, Bavaria JE. Results of a new surgical paradigm: endovascular repsir for acute complicated type B aortic dissection. Ann Thorac Surg. 2008;86:87-94. 58. Khoynezhad A, Donayre CE, Omari BO, Kopchok GE, Walot I, White RA. Midterm results of endovascular treatment of complicated acute type B aortic dissection. J Thorac Cardiovasc Surg. 2009;138:625-31. 59. Alves CM, da Fonseca JH, de Souza JA, Kim HC, Esher G, Buffolo E. Endovascular treatment of type B aortic dissection: the challenge of late success. Ann Thorac Surg. 2009;87:1360-5. 60. Persa CJ, Schroder JN, Daneshmand MA, McCann RL, Hughes GC. Midterm results for endovascular repair of complicated acute and chronic type B aortic dissection. Ann Thorac Surg. 2010;89:97-104. 61. Kato N, Hirano T, Ishida M, Shimono T, Cheng SH, Yada I, Takeda K. Acute and contained rupture of the descending thoracic aorta: treatment with endovascular stent-grafts. J Vasc Surg. 2003;37:100-5. 62. Eggebrecht H, Herold U, Kuhnt O, Schmermund A, Bartel T, Martini S, Lind A, Naber CK, Kienbaum P, Kühl H, Peters J, Jakob H, Erbel R, Baumgart D. Endovascular stent-graft treatment of aortic dissection: determinants of postinterventional outcome. Eur Heart J. 2005;26:489-97. 63. Jing QM, Han YL, Wang XZ, Deng J, Luan B, Jin HX, Liu XJ, Li F. Endovascular stent-graft for acute and chronic type B aortic dissection: comparison of clinical outcomes. Chin Med J. 2008;121:2213-7. 64. Guangqi C, Xiaoxi L, Wei C, Songqi L, Chen Y, Zilun L, Shenming W. Endovascular repair of Stanford type B aortic dissection: early and midterm outcome of 121 cases. Eur J Vasc Endovasc Surg. 2009;38:422-6. 65. Kim U, Hong SJ, Kim J, Kim JS, Ko YG, Choi D, Lee do Y, Chang BC, Shim WH. 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1. E ndovascular management of vascular emergencies of the thoracic aorta d. E xperience with endovasc repair of traumatic isthmic ruptures

Athanasios Katsargyris1, Eric Verhoeven1,2

1. Department of Vascular and Endovascular Surgery, Klinikum N端rnberg, Nuremberg, Germany 2. Department of Vascular Surgery, Leuven University, Leuven, Belgium

Introduction Blunt traumatic thoracic aortic injury involves most commonly the aortic isthmus region and is considered the second most common cause of death in trauma patients.[1, 2] Conventional surgical repair typically requires a high posterolateral thoracotomy commonly with cardiopulmonary bypass. This is a high-morbid procedure associated with high mortality and paraplegia rates.[3-5] Thoracic endovascular aortic repair (TEVAR) has been well established in the treatment of aneurysmal disease, but also plays a role in other thoracic aortic pathologies, including traumatic aortic isthmic rupture (TAIR).[6-8] TEVAR avoids the morbidity associated with thoracotomy, aortic cross clamping, and cardiopulmonary bypass. Although there is currently no commercially available device approved for repair of traumatic thoracic aortic injuries, off-label use of TEVAR emerges as a valuable tool to treat these severely injured acute patients. The present chapter aims to review the role and outcome of TEVAR in the management of TAIR. Traumatic aortic isthmic rupture (TAIR) More than 80% of blunt thoracic aortic injuries occur at the aortic isthmus, while other regions, such as the ascending aorta, the aortic arch branches, or the distal descending aorta are rarely involved.[9] TAIR occurs as a result of multiple different forces, including posterior movement of the sternum and compression of the aorta onto the spine, sudden increase in hydrostatic forces within the aorta, and deceleration forces that result in shearing and torsion of the fixed descending aorta.[10] Less than 25% of patients suffering TAIR survive to be evaluated in a hospital, and of those who do, up to 50% will die within 24 hours.[3, 11] The ideal timing of therapy of patients who finally survive and reach the hospital has changed over the course of the years. Although three to four decades ago TAIR was considered highly unstable and requiring emergency therapy, there has been a shift towards a more delayed intervention in combination with radiological surveillance and anti-hypertensive therapy.[12-14]

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

Endovascular vs Open surgical repair Although Level I evidence is lacking, TEVAR is increasingly used for the treatment of TAIR, due to its inherent advantages in terms of operative complexity compared to open surgery. The latter requires at a minimum a left thoracotomy, single lung ventilation, and aortic cross-clamping with complex cardiorespiratory support. Poly-trauma patients are usually not able to tolerate single lung ventilation, while cervical instability and long bone fractures can render positioning for left thoracotomy problematic.[10] The use of heparin may be also contraindicated due to the presence of concomitant injuries with increased risk for hemorrhage. Moreover, the typical trauma patient frequently is admitted in centers with limited or no open thoracic aortic experience.[3, 15] TEVAR, on the other hand, is more widespread and has been applied with success to TAIR. Emergent TEVAR for TAIR requires a considerable degree of endovascular expertise, but this is far more achievable compared to the complex anesthetic and surgical set-up required for open thoracic aortic surgery. This becomes more important at night or during weekends, when less experienced team face such surgical emergencies. One could conclude that TEVAR has a clear advantage in terms of ease of applicability compared to open surgery in most acute thoracic aortic syndrome, including TAIR. Indeed, open surgery notes higher perioperative morbidity and mortality rates in most series when compared to TEVAR.[5, 13, 16] Approximately 30% of patients die in the perioperative period, with 80% of those deaths as a result of concomitant injuries. In addition, perioperative morbidity is high including post thoracotomy pneumonia up to 60%, paralysis or paresis ranging within 6% and 30% and injury to the intrathoracic nerves up to 20%.[4,11,17-20] As mentioned above, multiple single institution studies have demonstrated encouraging results of TEVAR for TAIR. Feezor et al. reported a 0% 30-day mortality, with only one serious endograft related complication in a total of 22 patients.[21] Urgnani et al. demonstrated a 100% technical success rate and one (5%) unrelated perioperative mortality in a total 20 patients. In this study, no neurological complications were noticed.[22] Despite the above data, direct comparison of the two methods in terms of perioperative mortality and morbidity has not been studied. Prospective randomized trials are unavailable and not likely to be conducted in a timely and accurate fashion. The best available evidence comparing the two techniques originates from systematic reviews and meta-analyses of the existing literature with the largest recently published by Murad et al.[23-25] This systematic review was commissioned by the Society for Vascular Surgery (SVS) and included 7768 patients (77% males). The mortality rate was significantly lower after TEVAR, compared to open repair (9% vs. 19% respectively, p< 0.01). The risk of spinal cord ischemia (SCI) and end stage renal disease (ESRD) was higher in open repair compared with TEVAR (SCI: 9% open vs. 3% TEVAR, p<0.01; ESRD: 8% open vs. 5% TEVAR, p< 0.01). Open repair was also associated with increased risk of graft infection (11% open vs. 3% TEVAR, p<0.01) and systemic infections (13% open vs. 5% TEVAR, p<0.01). TEVAR, however, showed a trend towards increased risk for secondary interventions during follow-up, although the difference with open surgery did not reach statistical significance (p=0.07). Based on the above data, the SVS committee issued clinical practice guidelines suggesting that TEVAR for TAIR is associated with better survival and decreased morbidity compared with open repair and therefore can be preferentially performed.[26] As discussed above, it is noteworthy that this recommendation was based on low quality evidence (Grade 2, Level C). Specific considerations of TEVAR for TAIR Although TEVAR seems to be advantageous in the treatment of TAIR, some specific issues do merit further discussion. 1. Timing of TEVAR in a “stable” patient Given the 46% mortality rate noted in TAIR-patients managed conservatively, the SVS committee suggested urgent (<24 hours) repair simultaneously or immediately after other injuries had been treated, but at the latest prior to hospital discharge.[25-27] However, minority opinion was expressed that conservative management with frequent imaging surveillance might be appropriate for selected cases of “minimal aortic injury” (i.e., periadventitial defect or hematoma). 38

d. Experience with endovasc repair of traumatic isthmic ruptures, A. Katsargyris, E. Verhoeven

2. Choice of repair in young patients - TEVAR vs. Open This issue was also addressed by the relevant SVS Committee, highlighting that age should not be a factor influencing the type of repair in the acute situation. Although younger patients may have a higher risk for late complications, the lower risk of death and SCI after TEVAR compared to open surgery, override these potential concerns for the long term.[24, 28] In surgically fit patients with poor anatomy for TEVAR, however, open repair might be considered.[26] 3. Suitability of current available thoracic stent-grafts The average age of TAIR patients is < 40 years.[25] With ageing, the aorta tends to expand in diameter and the aortic arch becomes less angulated. Current commercially available thoracic stentgrafts have been developed to treat aneurysmal disease, and therefore, were designed for patients with larger normal aortas and less arch angulation. As a consequence the “off-label” use of current stent-grafts in TAIR may have limitations. Arch angulation represents one such shortcoming. Inability to adapt to increased arch angulation can result in bad apposition of the stent-graft, leading to endoleak and/or stent-graft collapse.[29] The latter is a serious complication and can lead to complete occlusion of the descending aorta, malperfusion, and death.[21] Stent-graft collapse has also been shown in cases where excessive oversizing was present.[10] When the stentgraft is oversized too much, the extra circumference cannot fully expand against the opposed aortic wall and collapses inward. TEVAR for TAIR is prone to collapse because of the relatively large size stent-grafts that were available and the small diameter aorta in young patients. On the other hand, hypovolemic shock in trauma patients can lead to significant underestimation of the “real” thoracic aorta diameter due to the resulting vasospasm.[30] This poses additional difficulties to optimal stent-graft sizing in TAIR. Two companies, W.L. Gore and associates, and Cook Inc., have improved their thoracic grafts with the aim to accommodate the angulated aortic arch better. Cook uses a pro-form system to force the first stent into the curvature. (Fig. 1) Gore has reengineered the thoracic graft (c-TAG) to improve flexibility inside an angulated arch. (Fig. 2)

Figure 1: Zenith TX2 Pro-Form (Cook Inc, Bloomington, USA) designed to improve proximal stentgraft apposition and provide accurate proximal conformity to the inner curvature of the aortic arch. Figure 2: Conformable GORE TAG (c-TAG) Device (W.L. Gore and associates, Flagstaff AZ, USA) engineered to provide increased flexibility in angulated aortic arch anatomies.

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

4. Coverage and revascularization of the left subclavian artery (LSA) Coverage and routine or selective revascularization of the LSA during TEVAR remains controversial. Although the landing zone requirements for TEVAR in TAIR may differ from aneurysmal degenerative disease, the proximity of the traumatic injury to the LSA makes coverage essential in 30-50% of the cases.[25, 31] Apart from distal arm ischemia and possible vertebrobasilar insufficiency, LSA coverage may also increase the risk of SCI due to occlusion of thyrocervical collateral arteries to anterior spinal arteries. Currently, there is no clear consensus regarding pre- or intra-operative LSA revascularization. Suggested indications to revascularize the LSA include patent left internal mammary artery used as a bypass graft to left anterior descending coronary artery, hypoplastic right vertebral artery or dominant left vertebral artery, and an incomplete vertebrobasilar system. Individualized decision additionally taking into account the availability of surgical expertise, general condition of the patient and concomitant injuries seems to be the most reasonable option.[26, 32] 5. Systemic heparinization The ability to repair TAIR without the required large doses of systemic heparin for cardiopulmonary bypass represents one important advantage of TEVAR. Multiple authors have reported TEVAR in TAIR without using heparin in view of coexistent severe injuries resulting in higher risk for hemorrhage.[13, 33] On the other hand, one has to consider that the introduction systems are large (2224F in diameter) and do temporarily occlude the blood flow at the access artery. This can result in lower limb ischemia, especially when TEVAR lasts longer in inexperienced hands. Available evidence does not allow for safe guidelines regarding routine heparinization or not. Individualized decision making while balancing the thrombophylic and hemorrhagic potential is currently suggested.[26] 6. Spinal drainage Spinal cord ischemia (SCI) occurs rarely (3%) after TEVAR for TAIR.[25] This, along with the limited coverage of the thoracic aorta, and the increased risk of epidural hematoma in a coagulopathic multi-trauma patient, does not justify routine spinal drainage. The latter should be considered postoperatively if symptoms of SCI are noticed.[26] 7. Anesthesia type Although it is possible to perform elective TEVAR under local anesthesia, the special situation in a multi-trauma patient (agitation, difficult cooperation, concomitant injuries that may require simultaneous surgery), makes local anesthesia cumbersome. Most experts agree that emergency TEVAR for TAIR should be performed under general anesthesia.[26] 8. Follow-up strategy The optimal strategy for long-term follow-up of these patients remains controversial. Although annual and life-long CTA is routinely advocated after TEVAR, this may not be the case after TEVAR for TAIR. TAIR does not represent an evolving disease process, as in the case of degenerative thoracic aortic aneurysms, but a stable post-traumatic injury. Thus, after technically successful intervention with good short- and mid-term documented outcome, further annual CTA may not be mandatory. This is important given the younger age of TAIR patients, with clear concerns of cumulative radiation and iodinated contrast exposure.[34, 35] Alternative follow-up methods, including the combination of plain X-ray and MRA should be considered whenever suitable. To our opinion, follow-up schemes (imaging method and timing) for TEVAR after TAIR should be adapted and relaxed whenever possible in view of the young patient cohort. Conclusions TEVAR for TAIR carries clear advantages over open surgery with regard to operative mortality and morbidity, and the risk of spinal cord ischemia. Newer more flexible stent-grafts such as the c-TAG and the Zenith TX2 pro-form adapt better to the angulated arch anatomy. Further developments in endovascular technology along with accumulating evidence regarding long-term durability, will underline the primordial role of TEVAR in TAIR. 40

d. Experience with endovasc repair of traumatic isthmic ruptures, A. Katsargyris, E. Verhoeven

References

1. Clancy, T.V., et al., A statewide analysis of level I and II trauma centers for patients with major injuries. J Trauma, 2001;51:346-51. 2. Richens, D., et al., The mechanism of injury in blunt traumatic rupture of the aorta. Eur J Cardiothorac Surg, 2002;21:28893. 3. Jamieson, W.R., et al., Traumatic rupture of the thoracic aorta: third decade of experience. Am J Surg, 2002;183:571-5. 4. Cowley, R.A., et al., Rupture of thoracic aorta caused by blunt trauma. A fifteen-year experience. J Thorac Cardiovasc Surg, 1990;100:652-60. 5. Ott, M.C., et al., Management of blunt thoracic aortic injuries: endovascular stents versus open repair. J Trauma, 2004;56:565-70. 6. Canaud, L., et al., Lessons learned from midterm follow-up of endovascular repair for traumatic rupture of the aortic isthmus. J Vasc Surg, 2008;47:733-8. 7. Estrera, A.L., et al., Progress in the treatment of blunt aortic injury: 12-year single-institution experience. Ann Thorac Surg, 2010;90:64-71. 8. Hoornweg, L.L., et al., Endovascular management of traumatic ruptures of the thoracic aorta: a retrospective multicenter analysis of 28 cases in The Netherlands. J Vasc Surg, 2006;43:1096-102. 9. Borsa, J.J., et al., Angiographic description of blunt traumatic injuries to the thoracic aorta with specific relevance to endograft repair. J Endovasc Ther, 2002;9:84-91. 10. Brinster, D.R., Endovascular repair of blunt thoracic aortic injuries. Semin Thorac Cardiovasc Surg, 2009;21:393-8. 11. Fabian, T.C., et al., Prospective study of blunt aortic injury: Multicenter Trial of the American Association for the Surgery of Trauma. J Trauma, 1997; 42): 374-80. 12. Pierangeli, A., et al., Delayed treatment of isthmic aortic rupture. Cardiovasc Surg, 2000;8:280-3. 13. Pacini, D., et al., Traumatic rupture of the thoracic aorta: ten years of delayed management. J Thorac Cardiovasc Surg, 2005;129:880-4. 14. Langanay, T., et al., Surgical treatment of acute traumatic rupture of the thoracic aorta a timing reappraisal? Eur J Cardiothorac Surg, 2002;21:282-7. 15. Azizzadeh, A., et al., Blunt traumatic aortic injury: initial experience with endovascular repair. J Vasc Surg, 2009;49:1403-8. 16. Broux, C., et al., Emergency endovascular stent graft repair for acute blunt thoracic aortic injury: a retrospective case control study. Intensive Care Med, 2006;32:770-4. 17. Sturm, J.T., et al., Risk factors for survival following surgical treatment of traumatic aortic rupture. Ann Thorac Surg, 1985;39:418-21. 18. Kwon, C.C., et al., Delayed operative intervention in the management of traumatic descending thoracic aortic rupture. Ann Thorac Surg, 2002;74:1888-91. 19. Razzouk, A.J., et al., Repair of traumatic aortic rupture: a 25-year experience. Arch Surg, 2000;135:913-8. 20. Chung, J., et al., Endovascular repair in traumatic thoracic aortic injuries: comparison with open surgical repair. J Vasc Interv Radiol, 2008;19:479-86. 21. Feezor, R.J., et al., Endovascular treatment of traumatic thoracic aortic injuries. J Am Coll Surg, 2009;208:510-6. 22. Urgnani, F., et al., Endovascular treatment of acute traumatic thoracic aortic injuries: a retrospective analysis of 20 cases. J Thorac Cardiovasc Surg, 2009; 138:1129-38. 23. Hoffer, E.K., et al., Endovascular stent-graft or open surgical repair for blunt thoracic aortic trauma: systematic review. J Vasc Interv Radiol, 2008;19: 1153-64. 24. Xenos, E.S., et al., Meta-analysis of endovascular vs open repair for traumatic descending thoracic aortic rupture. J Vasc Surg, 2008;48:1343-51. 25. Murad, M.H., et al., Comparative effectiveness of the treatments for thoracic aortic transection [corrected]. J Vasc Surg, 2011;53:193-199. 26. Lee, W.A., et al., Endovascular repair of traumatic thoracic aortic injury: clinical practice guidelines of the Society for Vascular Surgery. J Vasc Surg, 2011;53:187-92. 27. Demetriades, D., et al., Blunt traumatic thoracic aortic injuries: early or delayed repair--results of an American Association for the Surgery of Trauma prospective study. J Trauma, 2009;66:967-73. 28. Tang, G.L., et al., Reduced mortality, paraplegia, and stroke with stent graft repair of blunt aortic transections: a modern meta-analysis. J Vasc Surg, 2008; 47: 671-5. 29. Raupach, J., et al., Endovascular treatment of acute and chronic thoracic aortic injury. Cardiovasc Intervent Radiol, 2007;30:1117-23. 30. Van Prehn, J., et al., Difficulties with endograft sizing in a patient with traumatic rupture of the thoracic aorta: the possible influence of hypovolemic shock. J Vasc Surg, 2008;47:1333-6. 31. Peterson, B.G., et al., Utility of left subclavian artery revascularization in association with endoluminal repair of acute and chronic thoracic aortic pathology. J Vasc Surg, 2006;43:433-9. 32. Matsumura, J.S., et al., The Society for Vascular Surgery Practice Guidelines: management of the left subclavian artery with thoracic endovascular aortic repair. J Vasc Surg, 2009;50:1155-8. 33. Midgley, P.I., et al., Blunt thoracic aortic injury: a single institution comparison of open and endovascular management. J Vasc Surg, 2007;46: 662-8.

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

34. Katsargyris, A. Verhoeven EL. Part Two: Against the motion. All TEVAR patients do not require lifelong follow-up by annual CTA/MRA. Eur J Vasc Endovasc Surg, 2012;44:538-41. 35. Wong, S., et al., The role of mandatory lifelong annual surveillance after thoracic endovascular repair. J Vasc Surg, 2012;56:1786-93.

1. E ndovascular management of vascular emergencies of the thoracic aorta e. G lobal experience with TEVAR in ruptured TAA

Thomas Larzon

Department of Cardiothoracic and Vascular Surgery, Ă&#x2013;rebro University Hospital, Ă&#x2013;rebro, Sweden

Background Patients with ruptured thoracic aortic aneurysm (RTAA) are suggested to have a mortality rate of about 50% in the first six hours following onset of symptoms and only a small fraction of patients is admitted alive to hospital [1]. The traditional treatment for RTAA has been open surgery through left thoracotomy and resection of the aneurysm followed by interposition of graft. For the minority who undergo open repair, mortality and morbidity rates still remain substantial with permanent paraplegia or disabling complications after stroke [2-3]. Surgical resection has also been combined with partial cardiopulmonary bypass with segmental clamping in order to reduce paraplegia but is associated with significantly higher frequency of spinal cord dysfunction in emergency procedures [4]. Current data from nonrandomized studies of elective procedures suggest that thoracic endovascular aortic repair (TEVAR) may reduce early death, paraplegia, renal insufficiency, transfusions, reoperation for bleeding, cardiac complications, pneumonia, length of stay compared with open surgery but sustained benefits on survival have not been proven [5]. This chapter will address global experience of TEVAR in RTAA. Methods Technical aspects RTAA is treated with standard technique, although prophylactic spinal drainage is applicable only in stable patients. Hypovolemia may lead to inadequate perfusion of the spinal cord and brain, resulting in increased risk of neurological deficits. However, deep hypovolemic shock is challenging but even if it leads to circulatory arrest it can be controlled by inflation of an occlusion balloon close to the left subclavian artery [6]. When the aneurysm is located in the middle part of the descending thoracic aorta (DTA) a conventional stentgraft is used with proximal landing just distal of the left subclavian artery (zone 3) or below the arch in the straight part of the DTA (zone 4). Aneurysms involving the distal part of the DTA might necessitate intentional covering of the coeliac trunk or the use of periscope technique [7]. Aneurysms involving the proximal part of DTA might require covering of the left subclavian artery (LSA) and proximal landing in zone 2. Routine revascularization of the left subclavian artery is dependent on the preference of the surgeon and the condition of the patient. LSA can be revascularized surgically by a left carotid-subclavian bypass or by transposition or by use of a chimney-stent or stentgraft. 43

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

If the aneurysm starts just distal of the left subclavian artery (LSA), it may be necessary to extend the landing zone by covering also the left common carotid artery (LCCA) to reach the brachio-cephalic trunk (zone 1) and deploy a chimney-stent or stentgraft in the LSA [8]. In a stable patient surgical cutdown of the LCCA and a bypass with a synthetic graft is performed to the LSA either cranial of the clavicle or caudal through a separate incision. In a circulatory instable patient direct puncture of the LCCA can be performed and the LSA is either sacrificed or kept open with a chimney-stentgraft inserted through a percutaneous brachial access (Figure 1). Anesthesia Induction of general anesthesia may lead to circulatory collapse in circulatory instable patients. Local anesthesia can be considered which also has the advantage that monitoring of neurological complications is facilitated. Permissive hypotension is advised until the aneurysm has been excluded but should be followed by an increase of the mean artery pressure to diminish the risk of neurological complications. Local anesthesia can normally be used during the entire procedure but conversion to general anesthesia might be necessary if the patient has pain or suffers from other discomfort. Aortic arch Open surgical total aortic arch replacement is a demanding procedure which carries a substantial morbidity and mortality. A less invasive endovascular option is endovascular stent grafting using in situ fenestrations. After thoracic stent graft deployment in the arch, fenestrations are made for the major arch vessels. During this procedure, antegrade cerebral perfusion is maintained using a temporary bypass from the left femoral artery to both carotids perfusing both the anterior and posterior cerebral circulation [9]. The triple-barrel graft technique uses double chimney-grafts to supply blood flow to the supra-aortic vessels and is another method that can be used in patients where the proximal landing has to be in the ascending aorta (zone 0) and no other option is available [10]. Results Early reports from single-centers have indicated results in favor for TEVAR with a mortality rate of 3.1% to 11.4% [11-12]. In another hospital-based study from Michigan data from 69 patients (35 TEVAR, 34 open repair) who were treated for ruptured descending thoracic pathology (excluding blunt traumatic aortic injury) between 1993 and 2009 data were prospectively collected and retrospectively analyzed [13]. In-hospital or 30-day mortality was 11.4% in the TEVAR group compared with 26.5% in the open repair group (p=0.13). The only univariate correlate of this outcome was the presentation with hemodynamic instability (p<0.0001). Long term survival for the entire cohort was 50.7%, similar between the two groups (TEVAR 67.4 months versus open repair 65 months). In a multicentre study of seven institutions, 161 patients with rupture in the descending aorta were included between 1995 and 2010 [14]. Risk factors for the composite end point of death, permanent paraplegia and stroke in multivariate analysis were increasing age and especially hypovolemic shock. The 30-day mortality was 17.4% of the TEVAR group compared to 24.6% after open surgery (p=0.260). The composite outcome of death, stroke, or permanent paraplegia occurred in 36.2% of the open repair group compared with 21.7% of the TEVAR group (p=0.044). The aneurysm-related survival of patients treated with open repair was 64.3% at 4 years, compared with 75.2% for patients treated with TEVAR (p=0.191). In a population-based study from the United States, representing an approximate 20% random sample of all in-patient hospitalizations from 37 states, a total of 2 549 DTA (1 976 non-ruptured, 573 ruptured) open repair were identified. Patients with ruptured aneurysms were significantly older than 44

e. Global experience with TEVAR in ruptured TAA, T. Larzon

those with non-ruptured aneurysms and there was a significantly greater proportion of patients with a diagnosis of coronary artery disease (CAD) and hypertension in the non-ruptured group. Congestive heart failure and chronic renal failure was more frequent in the ruptured group. In-hospital mortality was approximately 45% for ruptured DTA regardless of hospital experience and the morbidity was almost 50% [2]. In a 12-year single center study from Ă&#x2013;rebro, 44 patients with thoracic ruptures were included between 2000 to 2011; aneurysms (59%), chronic dissections (14%), plaque ruptures (11%) and other indications as transections (16%). Twent-three patients (52%) had proximal landing in zone 1-2, 14 patients (32%) in zone 3 and 7 patients (16%) in zone 4. Chimneys were used in 10 patients (23%). The 30-day mortality was 38.6% and 1-year mortality was 43.2%. Chronic dissections had the worst outcome with a 30-day mortality of 66.7% compared to plaque ruptures (0%). Discussion Important limitations of presented studies are the retrospective observational study design. However, it will be very difficult to ever realize a randomized trial comparing the outcomes of TEVAR versus open repair of ruptured DTA. For the management of ruptures involving the aortic arch it will be even more complicated. Baseline differences have been observed between the two treatment groups, including an older mean age in the TEVAR group. The older age might be explained by refusal of treatment to very elderly patients with ruptured DTA prior to the endovascular era. Another limitation is that most open surgical interventions are performed before 2000, while all endovascular procedures are performed from 2000. The numbers of patients that are not offered any treatment are not wellknown but it can be presumed that more patients are offered treatment today when TEVAR is an option than before 2000, which makes historical comparison of data very hard. There is also a large variance in outcome where some centers have reported low mortality rates around 10% compared to population-based studies with more than 40%. One explanation might be that single centers studies represent high-experienced centers but the major explanation is probably that different patients are included in the trials. Hemodynamic instability has been identified as a strong predictor of outcome. Another reason why studies are hard to compare is the variability of aortic anatomy. Most of the studies have included just ruptured DTA where the arch has not been involved in the repair compared to our case series where a majority had involvement of the aortic arch with proximal landing of the stentgraft in zone 1 or 2. Use of the chimney technique has been vital for the repair in the aortic arch and mid-term results have been good [15]. Use of double chimney-grafts can expand the landing to zone 010. Also in situ-fenestration technique has been described to treat ruptures in the aortic arch [9] and use of an aortic occlusion balloon can be an adjunct in hemodynamic instable patients [6]. Conclusions Comparison between TEVAR and open surgery is influenced by selection bias and lack of randomized trials. However a lower rate of composite end point of death, stroke and paraplegia has been observed for TEVAR compared to open surgery in many trials and endovascular management appears to be the preferred treatment when this method is feasible. By using adjunct techniques, as the chimney technique, TEVAR is a feasible alternative to treat ruptures that affects the aortic arch.

References

1. Johansson G, MarkstrĂśm U, Swedenborg J. Ruptured thoracic aortic aneurysms: a study of incidence and mortality rates. J Vasc Surg. 1995 Jun;21(6):985-8. 2. Schermerhorn ML, Giles KA, Hamdan AD, Dahlberg SE, Hagberg R, Pomposelli F. Population-based outcomes of open descending thoracic aortic aneurysm repair. J Vasc Surg 2008;48:821-7. 3. Achneck HE, Rizzo JA, Tranquilli M, Elefteriades JA. Safety of thoracic aortic surgery in the present era. Ann Thorac Surg. 2007 Oct;84(4):1180-5; discussion 1185. 4. Minatoya K, Ogino H, Matsuda H, Sasaki H, Yagihara T, Kitamura S. Replacement of the descending aorta: recent outcomes of open surgery performed with partial cardiopulmonary bypass. J Thorac Cardiovasc Surg. 2008 Aug;136(2):431-5.

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

5. Cheng D, Martin J, Shennib H, Dunning J, Muneretto C, Schueler S, Von Segesser L, Sergeant P, Turina M. Endovascular aortic repair versus open surgical repair for descending thoracic aortic disease a systematic review and meta-analysis of comparative studies. J Am Coll Cardiol. 2010 Mar 9;55(10):986-1001. 6. Larzon T, Jansson H, HolmstrĂśm B, Lund P, Norgren L, Arfvidsson B, Berggren L, Nydahl A, Eriksson T, Jonsson T, Stenberg B. Salvage of an acutely ruptured thoracic aortic aneurysm during CPR. J Endovasc Ther. 2002 Jun;9 Suppl 2:II67-71. 7. Pecoraro F, Pfammatter T, Mayer D, Frauenfelder T, Papadimitriou D, Hechelhammer L, Veith FJ, Lachat M, Rancic Z. Multiple periscope and chimney grafts to treat ruptured thoracoabdominal and pararenal aortic aneurysms. J Endovasc Ther. 2011 Oct;18(5):642-9. 8. Larzon T, Gruber G, Friberg O, Geijer H, Norgren L. Experiences of intentional carotid stenting in endovascular repair of aortic arch aneurysms--two case reports. Eur J Vasc Endovasc Surg. 2005 Aug;30(2):147-51. 9. Sonesson B, Resch T, Allers M, Malina M. Endovascular total aortic arch replacement by in situ stent graft fenestration technique. J Vasc Surg. 2009 Jun;49(6):1589-91. 10. Shahverdyan R, Gawenda M, Brunkwall J. Triple-barrel graft as a novel strategy to preserve supra-aortic branches in arch-TEVAR procedures: clinical study and systematic review. Eur J Vasc Endovasc Surg. 2013 Jan;45(1):28-35. 11. S cheinert D, Krankenberg H, Schmidt A, Gummert JF, Nitzsche S, Scheinert S, BrĂ¤unlich S, Sorge I, Krakor R, Biamino G, Schuler G, Mohr FW. Endoluminal stent-graft placement for acute rupture of the descending thoracic aorta. Eur Heart J. 2004 Apr;25(8):694-700. 12. Doss M, Wood JP, Balzer J, Martens S, Deschka H, Moritz A. Emergency endovascular interventions for acute thoracic aortic rupture: four-year follow-up. J Thorac Cardiovasc Surg. 2005 Mar;129(3):645-51. 13. Patel HJ, Williams DM, Upchurch GR Jr, Dasika NL, Deeb GM. A comparative analysis of open and endovascular repair for the ruptured descending thoracic aorta. J Vasc Surg. 2009 Dec;50(6):1265-70. 14. Jonker FH, Verhagen HJ, Lin PH, Heijmen RH, Trimarchi S, Lee WA, Moll FL, Atamneh H, Rampoldi V, Muhs BE. Open surgery versus endovascular repair of ruptured thoracic aortic aneurysms. J Vasc Surg. 2011 May;53(5):1210-6. 15. Larzon T, Eliasson K, Gruber G. Top-fenestrating technique in stentgrafting of aortic diseases with mid-term follow-up. J Cardiovasc Surg (Torino). 2008 Jun;49(3):317-22.

1. E ndovascular management of vascular emergencies of the thoracic aorta f. E ndovascular management of acute abdominal organ malperfusion Ciro Ferrer, Nunzio Montelione, Carlo Coscarella, Antonio Lorido, Gabriele Pogany, Piergiorgio Cao

Vascular Surgery, San Camillo Forlanini, Rome, Italy

Introduction Acute aortic dissection is a relatively uncommon but life-threatening condition. In the United States, it is estimated to affect 5 to 10 people per million per year [1]. In patients with uncomplicated acute type B dissection in-hospital outcomes are generally acceptable, and 90% of patients survives to hospital discharge after receiving effective antihypertensive therapy [2]. Unfortunately about 30% of acute type B aortic dissections (ABAD), at clinical presentation, are complicated by hemodynamic instability or peripheral vascular ischemia. Ischemia caused by ABAD is a life-threatening emergency with high risk of mortality if untreated [3-6]. In addition, failure to treat such malperfusion syndromes caused by complicated ABAD results in a >50% risk of death for affected patients [1,7]. Pathogenesis Two mechanisms have been accepted as the primary causes of ischemia following aortic dissection: static obstruction due to extension of the dissection directly into visceral or lower limb arteries thus narrowing their lumen; dynamic obstruction of the vessels by dissection flap prolapse into the vessel origin [7,8]. Clinical presentation Although peripheral pulse deficit is the most frequent indicator of ischemia, mesenteric and renal infarction are the most relevant causes of morbidity and mortality in patients affected by ABAD. Malperfusion syndrome in the setting of an acute aortic dissection is deďŹ ned as one or more of the following conditions [9]: visceral hypoperfusion resulting in abdominal pain or acute abdomen, radiographic hypoperfusion of mesenteric bed and lactic acidosis; renal hypoperfusion, including oliguria or aneuria in setting of an increased renal function tests (creatinine or blood-urea nitrogen) or radiographic evidence of impaired renal artery blood ďŹ&#x201A;ow; lower extremity hypoperfusion indicated by abnormal pulse examinations in conjunction with leg pain, pallor, paresthesias, or paralysis; spinal cord hypoperfusion as noted by altered motor function of one or both of legs.

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

Therapeutic options Therapeutic options to manage visceral malperfusion are related to different anatomic features. Specific treatment guidelines are difficult to estabilish [10]. Several endovascular approaches have been proposed to relieve visceral ischemia [11]. An accurate preoperative imaging evaluation, a perfect knowledge of materials and an extensive experience in endovascular procedures are crucial factors. Furthermore, multiplanar angiography and intravascular ultrasound (IVUS) are indispensible tools in order to identificate proximal and distal tear(s), extension of the dissection, and the assessment of branch vessel perfusion from true and false lumen. - Surgical Fenestration The surgical fenestration procedure consists of creating a re-entry tear by excision of the dissection lamella, decompressing true lumen and restoring flow. The first surgical aortic fenestration was performed by Shaw in 1955 [12] and successfully relieved limb ischemia, but the patient died for renal failure. The first survivor of aortic fenestration was reported by DeBakey in the same year [13]. However most largest series were reported in 90thies by Elefteriades and Cambria [14,15]. Panetton et al reported successful fenestration in 14 patients, with an operative mortality for emergency fenestration of 43%. Neither recurrent malperfusion symptoms nor aneurismal degeneration were detected at mean follow-up of 5.1 years [16]. - TEVAR The concept of endovascular reconstruction in ABAD was first introduced by Dake et al. in 1999 based on the clinical observation that patients with spontaneous thrombosis of the false lumen have a better long-term prognosis than those without [7]. Even though the placement of an endovascular stent-graft may be technically difficult, the fundamental strategy for endovascular technique in dissected patients, is relatively simple: to provide the coverage of the proximal entry tear, more often located close to the ostium of the left subclavian artery, by implantation of a covered stent-graft to reroute the blood flow into the true lumen and thereby depressurize the false lumen [17]. Moreover it may results in an immediate release of true lumen compression with restoring antegrade flow to visceral vessels (Figure 1). Observational evidence supports TEVAR for the treatment of complicated ABAD. Many studies have shown an improved early mortality of approximately 10% with endovascular repair for complicated ABAD [18-20]. In fact TEVAR is being considered as the front-line therapy for patients with acute thoracic dissection complicated by malperfusion and recent series suggest that it is a promising treatment in the setting of ABAD with malperfusion, rupture, chest pain, and acute aortic enlargement with acceptable 30-day and 1-year mortality rates, compared with surgical and medical treatments [9, 21, 22]. Szeto et al reported a 30-day mortality rates of 2.8% and 1-year survival of 93.4% Âą 4.6% in 35 patients with acute complicated type B aortic dissection treated with TEVAR [23]. Fattori et al compared the impact of different treatment strategies on survival in 571 patients with acute type B aortic dissection. TEVAR provided better outcome, with 9.3% mortality in patients treated with stent-graft and 33.9% mortality in patients undergone open surgery [20]. - PETTICOAT TECHNIQUE This technique was introduced by Mossop and Nixon and then described by Nienaber et al in 2006 for patients with persistent true lumen collapse after standard TEVAR [24, 25]. The PETTICOAT technique (Provisional Extension To Induce Complete Attachement) consists in the positioning of an uncovered bare stent distally to a standard stent-graft covering the proximal entry tear, in order to expand true-lumen, promote false lumen thrombosis, reduce the lenght of aortic coverage and induce positive aortic remodeling [25]. The bare stent limits the number of covered intercostal arteries also de48

f. Endovascular management of acute abdominal organ malperfusion, C. Ferrer, N. Montelione, C. Coscarella, A. Lorido, G. Pogany, P. Cao

creasing the risk of spinal cord ischemia. In addition, re-expansion of the true lumen with a bare stent can facilitate adjunctive interventions such as cannulation and stenting of visceral branches if necessary during the initial procedure or during follow-up. From the first experiences in which nondedicated devices have been used, in recent years, a new specific device has been introduced. The Zenith Dissection Endovascular System (Cook Medical, Bloomington, Ind) is a dual-construct device that provides proximal sealing of the primary entry tear with a covered stent graft and distal support of the dissected true lumen with bare metal stents. Two experiences with this new dissection device were recently reported. Melissano et al in a single-center experience, reported good short-term results in 11 patients [26], with no visceral/renal arteries occlusion, retrograde dissection, deviceinduced tears in the intimal lamella. Also in the STABLE study (The Study of Thoracic Aortic Type B Dissection Using Endoluminal Repair trial) the safety and performance of this device for treatment of patients with complicated ABAD, and suitable anatomy for endovascular repair, has been evaluated. The 12-month follow-up of this prospective, non-randomized, multicenter study demonstrated acceptable clinical and anatomic results [27]. - Fenestration of the dissection lamella Before the reported application of TEVAR and PETTICOAT for ABAD some authors described an alternative approach to relieve end-organ ischemia without the need for open aortic intervention to reduce the high mortality and morbidity rates related to these procedures. Endovascular aortic fenestration, first described in 1990 by Williams et al, consists of creating a hole in the dissection lamella, connecting the two aortic lumens, with a subsequent decompression of the false lumen and increasing flow to the true lumen and its branches [28]. - Branch-vessel stenting Stenting is usually performed when static obstruction compromises branch-vessel patency. If multiple vessels require treatment, the region most susceptible to ischemia should be addressed first with selective stent placement. For this reason, priority should be given to the superior mesenteric artery (SMA) or celiac trunk obstruction, followed by at least one renal artery; this is because the gut has the least tolerance for underperfusion. Once the bowel is adequately perfused, the next most urgent target is at least one renal artery to preserve renal function (Figure 2). Conclusion Usually, the coverage of the entry tear by a stent graft results in thrombosis of the false lumen and flow increase in the true lumen, normalizing the vessel perfusion and restoring branch vessels patency. However, limb or organ malperfusion may persist after proximal aortic graft placement for an insufficient true lumen expansion or a branch vessel static obstruction. In these cases further procedures such as Petticoat Technique, percutaneous aortic fenestration or branch vessels stenting, should be associated to the intimal tear coverage. Lifelong surveillance is mandatory for patients with aortic dissection. The aorta remains diseased and they usually required further procedures.

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

References

1. Svensson LG, Kouchoukos NT, Miller DC, et al. Expert consensus document on the treatment of descending thoracic aortic disease using endovascular stent-grafts. Ann Thorac Surg 2008;85 (1 Suppl):S1-41 2. Suzuki T, Mehta RH, Ince H, et al. Clinical profiles and outcomes of acute type B aortic dissection in the current era: lessons from the International Registry of Aortic Dissection (IRAD). Circulation 2003;108(Suppl. 1):II312e7 3. Umana JP, Lai DT, Mitchell RS, et al. Is medical therapy still the optimal treatment strategy for patients with acute type B aortic dissection? J Thorac Cardiovasc Surg 2002;124:896-910 4. Miller DC, Mitchell RS, Oyer PS, et al. Independent determinants of operative mortality for patients with aortic dissection. Circulation 1984;70 (Suppl 1):I153-64 5. Fann JL, Sarris GE, Scott Mitchell R, et al. Treatment of patients with aortic dissection presenting with peripheral vascular complication. Ann Surg 1990;212:705-13 6. Tsai TT, Fattori R, Trimarchi S, et al. Long-Term survival in patients presenting with type B aortic dissection. Insights from the International Registry of Acute Aortic Dissection. Circulation 2006;114:2226-31 7. Dake MD, Kato N, Mitchell RS, et al. Endovascular stent graft placement for the treatment of acute aortic dissection. N Engl J Med 1999;340:1546-52 8. Crawford S, Crawford J. Diseases of the aorta. Baltimore, Williams & Wilkins, 1984 9. White RA, Miller C, Criado FJ, et al. Report on the results of thoracic endovascular aortic repair for acute, complicated, type B dissection at 30 days and 1 year from multidisciplinary subcommittee of the Society for Vascular Surgery Outcomes Committee. J Vasc Surg 2011:53:1082-90 10. Fattori R, Botta L, Lovato L. Malperfusion syndrome in type B aortic dissection: role of the endovascular procedures. Acta Chir Belg 2008:108:192-297 11. Bozinovsky J, Coselli JS. Outcomes and survival in surgical treatment of descending thoracic aorta with acute dissection. Ann Thorac Surg 2008;85:965-71 12. Shaw RS. Acute dissecting aortic aneurysm. Treatment by fenestration of the internal wall of aneurysm. N Engl J Med. 1955;253:331-3 13. DeBakey ME, McCollum CH, Crawford ES, et al. Dissection and dissecting aneurysm of the aorta: twenty year follow-up of five hundred twenty-seven patients treated surgically. Surgery 1982;92:1118-34 14. Elefteriades JA, Hammond GL, Gusberg RJ, et al. Fenestration revisited. A safe and effective procedure for descending aortic dissection. Arch Surg 1990;125:786-90 15. Cambria RP, Brewster DC, Gertler J, et al. Vascular complications associated with spontaneous aortic dissection. J Vasc Surg 1988;7:199-209 16. Panetton JM, Teh SH, Cherry KJ, et al. Aortic fenestration for acute or chronic aortic dissection: an uncommon but effective procedure. J Vasc Surg 2000;32:711-721 17. Nienaber CA, Fattori R, Lund G et al. Non surgical reconstruction of thoracic aortic dissection by stent-graft placement. N Engl J Med 1999;340:1539-45 18. Eggebrecht H, Nienaber CA, Neuhauser M et al. Endovascular stent-graft placement in aortic dissection. A meta-analysis. Eur Heart J 2006;27(4):489-98 19. Fattori R, Lovato L, Buttazzi K, Russo V. Evolving experience of percutaneous management of type B aortic dissection. Eur J Vasc Endovasc Surg 2006;31:115-122 20. Fattori R, Tsai TT, Myrmel T, et al. Complicated acute type B dissection: is surgery still the best option? A report from the International Registry of Acute Aortic Dissection. JACC Cardiovasc Interv 2008;1:395-402 21. Cheng D, Martin J, Shennib H, et al. Endovascular aortic repair versus open surgical repair for descending thoracic aortic disease: a systematic review and meta-analysis of comparative studies. J Am Coll Cardiol 2010; 55:986-1001 22. Kim McDonayre CE, Reynolds TS, Kopchok GE, et al. Aortic remodeling, volumetric analysis, and clinical outcomes of endoluminal exclusion of acute complicated type B thoracic aortic dissections. J Vasc Surg 2011;316-24; discussion: 324-5. 23. Szeto WY, McGarvey M, Pochettino A, et al. Results of a New Surgical Paradigm: Endovascular Repair for Acute Complicated Type B Aortic Dissection. Ann Thorac Surg 2008;86:87â&#x20AC;&#x201C;94 24. Mossop PJ, McLachlan CS, Amukotuwa SA, Nixon IK. Staged endovascular treatment for complicated type B aortic dissection. Nat Clin Pract Cardiovasc Med 2005;2:316-21; quiz 322. 25. Nienaber CA, Kische S, Zeller T, et al. Provisional extension to induce complete attachment after stent-graft placement in type B aortic dissection: the PETTICOAT concept. J Endovasc Ther 2006;13:738-46 26. Melissano G, Bertoglio L, Kahlberg A, et al. Evaluation of a new disease-specific endovascular device for type B aortic dissection. J Thorac Cardiovasc Surg 2008;136:1012-8 27. Lombardi JV,Cambria RP, Nienaber CA,et al. Prospective multicenter clinical trial (STABLE) on the endovascular treatment of complicated type B aortic dissection using a composite device design. J Vasc Surg 2012;55:629-40 28. Williams DM, Brothers TE, Messina LM, et al. Relief of mesenteric ischemia in type III aortic dissection with percutaneous fenestration of the aortic septum. Radiology 1990;174:450-2

1. E ndovascular management of vascular emergencies of the thoracic aorta g. E ndovascular management of acute compromised supra-aortic vessels Mario Lachat, Felice Pecoraro, Lyubov Chaykovska, Dieter Mayer, Zoran Rancic Vascular Surgery, Clinic for Cardiac and Vascular Surgery, University Hospital Zurich, Switzerland

Acute flow restriction to the supra-aortic vessel can occur spontaneously as a local pathology or trauma or as a consequence of aortic arch dissection extending or compromising the patency of the supra-aortic trunks. Since surgery and more recently endovascular treatment are performed on these vessels, technical problems can also lead to acute flow restriction and its acute complications. The relatively new field of landing stent-grafts near or across the origin of the supra-aortic vessels is new potential source of troubles for the brain and spine perfusion. This paper will review spontaneous and iatrogenic flow restriction to the supra-aortic trunks and how to deal on with such situations. I Acute thrombosis of supraaortic vessels (Zoran Rancic) Acute thrombosis of brachiocephalic trunk occurs often in patients with preexisting atherosclerosis arteries, but also as the initial presentation of malignant diseases, antiphospholipid syndrome. In preexisting atherosclerotic disease, acute thrombosis (acute on chronic) are usually asymptomatic due to developed collaterals around the shoulder joint, but might be presented with signs and symptoms of cerebral, and arm ischemia. In case of acute, not atherosclerosis related thrombosis clinical presentation can be devastating, even with fatal outcome [1]. In case of atherosclerotic lesions endovascular options (PTA with stenting) or surgical revascularization (extra-anatomic or ascending-to-common carotid and subclavian artery) are the possible treatment options [2]. Acute thrombosis of common carotid artery (CCA) is rare and is seen in 2% of cases in patients evaluated for acute cerebrovascular disease [3]. The commonest cause of chronic CCA thrombosis is atherosclerosis related, but in case acute thrombosis it is atrial fibrillation with thrombi originated from the heart. The clinical severity varies from asymptomatic to severe, because each differs in the time to complete occlusion of the CCA, the development of collaterals, and brain hemodynamic [4]. Mobile and acute CCA thrombi extend into the internal carotid artery (ICA) and external carotid artery (ECA). There are two types of CCA occlusion: type I, isolated CCA occlusion with ICA patent and perfused by retrograde flow originating at the Willis circle or in the ECA, and type II, occlusion if CCA with concomitant ICA and ECA occlusions. Type I is more frequent [5]. Endovascular modalities include clot removal by mechanical thrombectomy, and combined intravenous-intra-arterial thrombolysis [6, 7]. 51

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

The potential benefits of recanalization must be balanced against the risks of reperfusion haemorrhage, dissection, and distal embolism. Acute thrombosis of subclavian artery (SA) is cause most frequently in patients with thoracic outlet syndrome (TOS) through costoclavicular compression syndrome and cervical rib syndrome [8]. Less common pathologies are radiation induced acute thrombosis, mobile thrombosis of the aortic arch, and different types of arteritis (Takayasu, giant cell arteritis, and myalgia rheumatic) [9]. In the endovascular era conventional surgical treatment (Fogarty balloon thrombectomy or a carotid-subclavian bypass) with correction of underlying pathology (i.e. resection of cervical rib) [10], is often replaced by endovascular treatment modalities. The first percutaneous technique was intra-arterial thrombolysis: effective, but also time-consuming, requires continuous monitoring (ICU or IMC beds), with risk of embolism or bleeding complications. Thrombolysis is often combined with percutaneous thromboaspiration, balloon angioplasty and stent deployment. There is more reports on use various percutaneous thrombectomy devices with fragmentation of thrombus without removing it (i.e. AngioJet, ArrowTrerotola Thrombolysis system), with removing the thrombus (i.e. Hydrolyser, Starub-Rotarex) [9]. More long-term follow-up will be necessary to determine the role of endovascular technique in the surgical management of TOS. Vertebral artery originates from subclavian artery, but sometimes as direct as aortic arch branch. Thrombosis occurs as a propagation of aortic arch floating thrombus, or acute thrombosis after vulnerable plaque rupture at the level of VA origin. The proposed treatment option is medical with systemic anticoagulation and antiplatelet option [11]. After resolving the thrombus stenotic lesion at origin is treated by balloon angioplasty with or without stenting the lesion. If there is no improvement of symptoms, or thrombus resolution there are two possible options: angioplasty and stent placement under ipsilateral VA distal embolic protection (using reversal flow), or blockage of thrombosed VA from contralateral VA [12]. In cases of acute thrombus propagation from VA to basilar artery the treatment option is angioplasty followed by stenting with coronary stent. Thereafter a microcatheter is navigated intracranially with subsequent fibrinolysis [12]. The open surgical procedures, vertebral endarterectomy or bypass operations are also one therapeutic modality, so that treatment must be tailored to every patient. II Acute supraaortic vessel dissection (Felice Pecoraro) Dissection of carotid and vertebral artery are the underlying cause of stroke in less than 2% of patients but account to approximately 25% in patients younger than 45 years [13]. Etiology of supraaortic dissection (SD) can be spontaneous (generally associated to aortic dissection), traumatic or iatrogenic. Iatrogenic carotid dissection (CD) has been reported during treatment of Aortic dissection, carotid artery stenting, cerebral aneurysm repair. Clinical manifestations are usually pain, Horner syndrome or ischemia occurring usually within one week. SD treatment represents a challenge in clinical practice. In addition no guidelines exist to guide SD treatment. The treatment options vary according to etiology. In all cases prevention of vessel embolism, thrombus progression and maintenance of flow is intended [14]. Medical therapy is usually used for spontaneous SD. Its use alone (anticoagulant or antiplateled) has been proposed for patients that remain asymptomatic and the same medication is recommended in association to surgical or endovascular treatment. Surgical treatment is often demanding due to extensive length of dissection and is associated high rate of complication. Generally, intervention/surgery consists in ligation or bypass while endarterectomy is contraindicated. This approach is generally used for traumatic and SD associated to aortic dissections. Thus endovascular approach has become the first approach in patients presenting symptomatic SD not responding to medical therapy. Due to the rarity of this pathology few data are reported in literature and most of them are case reports [15]. Endovascular approach in these patients however represents an issue due to anatomical abnormalities often associated, risk of additional dissection, extending dissection, vessel rupture and pseudoaneurysm formation. The most employed tool to treat SD is angioplasty and stenting with high satisfaction rate. It is recom52

g. Endovascular management of acute compromised supra-aortic vessels, M. Lachat, F. Pecoraro, L. Chaykovska, D. Mayer, Z. Rancic

mended to avoid the use of stiff stent in tortuous vessels and choose stent diameter according to inner lumen of the target vessel. With this approach technical success rates is about 90%. Perioperative mortality, as well as occlusion, range from 0 to 10%. Recurrent transient ischemic attack (TIA) rate was reported from 0 to 10.3%. Only few midterm data are reported after endovascular treatment of SD. Estimated stroke-free survival was reported to be 93% at 1 and 6 months. In a review of 63 extracranial carotid dissections with a mean follow-up period of 15.7 months, the technical success rate was 100%. Also primary and secondary patency rates were 100%. Seven (11%) new strokes were reported with no related mortality on follow-up [16]. Another report on 12 patients reported no new clinical events, stent stenosis or occlusion on 24 months follow-up [13]. Other types of endovascular approach have been reported alone or in association to stent placement. Intravenous thrombolysis can be performed in front of stent placement. Mechanical clot extraction or local thrombolysis has been reported to be successful [14]. III Aortic dissection (Lyubov Chaykovska) One of the complications of aortic dissection is an acute injury of the supra-aortic vessels that is potentially life threatening, because it can cause cerebral malperfusion. Acute pathology of the supraaortic vessels in patients with aortic dissection was reported in patients with acute A-dissection, non-A-non-B-dissection and in case of retrograde extension of type B dissection into the aortic arch. Open surgical treatment remains a gold standard for a treatment of acute aortic dissections involving supraaortic vessels and elephant trunk (ET) is recommended. Briefly, ET is a two steps procedure, which implies at first step an open surgical aortic arch replacement with a graft inserted into the distal true lumen, which prevents blood flow leakage into the dissecting lumen at the anastomosis site and also strengthens this area. Because the distal portion of the prosthesis remains dangling in the descending aorta, the second step operation (replacement of the descending aorta or the insertion of an endovascular stent graft) is required. Subsequent studies showed that a substantial number of patients died in the interval between the 2 procedures; as a consequence, alternative surgical techniques have been explored. More recently, â&#x20AC;&#x153;frozenâ&#x20AC;? elephant trunk (FET) procedure has been proposed. The FET, is a hybrid graft consisting of a distal graft part reinforced with stents and intended to be introduced through the aortic arch and deployed in the descending aorta and a proximal part that consist of a standard surgical graft for the attachment to the aortic root. The supraaortic trunk is reimplanted as a patch into the graft. Clearly, uncertainties remain regarding the relative effectiveness of the frozen elephant trunk technique when compared with other one-stage and two-stage procedures for the management of extensive aortic dissection. Hospital mortality and major morbidity with this procedure have not been insignificant. The duration of cardiopulmonary bypass during FET implantation exceeds 4 hours and is associated with lengthy intervals of myocardial ischemia and cerebral perfusion. The prevalence of major spinal cord ischemic injury is also a matter of concern. Longer follow-up to assess the fate of the patent false lumen and the need for subsequent procedures on the remaining thoracic and abdominal aorta is essential before this procedure can be widely recommended [17, 18]. Another option for the treatment of acutely compromised supraaortic vessels in the settings of aortic dissection type B or non-A-non-B is a supraaortic debranching completed by TEVAR. [19] Reports on complete endovascular repair of supraaortic vessels in the emergency setting of aortic dissection is a rarity [20]. Chimney technique for the treatment of pathologies involving the aortic arch was used for preservation of one or more rare two supra-aortic vessels [20, 21]. Technical success was achieved in 95-97% of cases, but during follow-up there were 10-19.7% of combined type I/II endoleaks. The patency of the chimney-grafts during a mean follow-up of 8.3 months was 100%. Most common complications were stroke, paraplegia, myocardial infarction and iliac haemorrhage with 30day mortality rate of 6.5%. 53

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Branched stent-graft implantation for thoracic aortic dissection is also rare and is limited to treatment of dissection involving the left subclavian artery [22]. Study on 17 patients with aortic arch pathology (among them 7 patients with aortic dissection) reports a 100 % successful deployment rate with 100 % patency during the mean follow-up period of 26 months (range, 7 to 65 months). 3 type I endoleak, which were treated endovascularly in 2 cases (implantation of a straight stent-graft in the distal attachment site and implantation of a double-branched stent-graft) and left untreated in one patient because of very high-risk for open surgery or secondary stent grafting were reported in this study. Nevertheless, the aneurysm sac remained stable in all cases during the follow up. Two deaths occurred in the follow-up period, the causes of death were cerebral bleeding and pneumonia, both considered unrelated to the stent grafting. Recently, two cases of successful transapical TEVAR were reported in patients with type A aortic dissection, who could not be treated otherwise, opening new perspectives of endovascular treatment of this complex pathology [23, 24]. IV Iatrogenic (Mario Lachat) Even if in most cases one of the supra-aortic vessels can probably be sacrificed, the result of such procedure is highly unpredictable, especially when concerning the carotid artery, as stroke or paraplegia might be expected consequence. Therefore, the authors do recommend maintaining perfusion to any aortic arch branch [25]. In fact and after exact case study and knowledge of device behavior in different anatomies and aortic segments, supraaortic trunk unsuspected encroachment and partial or complete branch occlusion should remain very uncommon. Case study will allow determining preoperatively safe revascularization strategy and/or potential bailouts [26]. In tortuous aorto-iliac anatomy and access way, navigation and aortic stent-graft deployment in the arch or ascending aorta is less precise as than if the route to there is straight or short and therefore antegrade transaortic or transapical access might be a better choice [27]. Finally full contact of the aortic stent-graft with the aortic wall when deploying a tubular stent-graft in a tighten curve as the aortic arch, might lead to incomplete apposition of the proximal or distal stentgraft end(s) and sustained perfusion in the aneurysm sac. Therefore, more proximal landing might be necessary. Different revascularization strategies are chosen depending on which aortic arch segment the aortic stent-graft will cover and land on [25]. Endovascular solutions Periscope endograft technique.

The periscope technique has originally been described to extend TEVAR to cases where the distal landing zone was interfering with the origin of the visceral arteries [28]. The Periscope principle (see picture 1), where blow flow is retrograde to the aortic branches is also the rationale for the new 54

g. Endovascular management of acute compromised supra-aortic vessels, M. Lachat, F. Pecoraro, L. Chaykovska, D. Mayer, Z. Rancic

modular thoraco-abdominal branched stent-graft from Jotec/Hechingen which has been originally designed and developed by Lachat and Pfammatter 2011 (picture 2). The Periscope endograft technique has then been extended to the subclavian artery (picture 3) by the authors. Overall experience in the last 36 months at university hospital Zurich shows in a series of 20 consecutive patients excellent early and mid-term results. In only one case, postoperative stenting of partial periscope collapse leaded to periscope graft occlusion within 30-day period after initial procedure. But, and so far remaining 19/20 periscope grafts (95%) remained patent. Applied to the arch, the Periscope endograft technique has several major advantages. â&#x20AC;˘ This Periscope endograft technique can be combined with the chimney endograft technique and therefore reduce the number of parallel grafts that would otherwise challenge the proximal aortic stent-graft landing zone. As reported by Hans Krankenberg [29], Periscope endografts can be placed simultaneously in the left subclavian artery, the left common carotid artery and the brachiocephalic trunk which allows landing aortic stent-graft in zone 0. â&#x20AC;˘ It allows addressing distal aortic pathologies exclusively transfemorally and even under local anesthesia Chimney graft technique The Chimney endograft technique has originally been described by Frank Criado and Thomas Larzon [30, 31]. There are now several reports highlighting the advantages of the technique, especially as bailout method. At the difference with the periscope technique, direct access on the supraaortic trunk is required for the chimney endograft introduction and deployment. Probably, one Chimney endograft might be safe but two or three Chimney endograft crossing the proximal aortic stent-graft landing zone might represent a real risk for ongoing endoleakage and aortic stent-graft migration. Therefore the authors recommend combining Chimney grafts with Periscope grafts and/or conventional debranching (picture 4). Fenestrated and branched stent-graft Fenestrated and branched stent-graft will not be discussed here as these graft target a careful prospectively planed revascularization of the supraaortic vessels. We just want to mention that the Chimney and/or Periscope endograft technique might be useful bailout tools in case the fenestrated or branched stent-graft has to be rescued [32].

Open surgery

Bypass surgery Carotid-to-carotid and/or carotid-to-subclavian artery bypass surgery or subclavian artery transposition are well known techniques to provide blood flow to the supraaortic trunk in case non-fenestrated or non-branched aortic stent graft will land in zone 2 and zone 1 [33]. The authors want to mention that they prefer retropharyngeal crossover way than the pre-tracheal one that would make a tracheostomy a very challenging procedure with high risk of graft infection. In addition, the authors prefer to perform a carotid-to-infraclavicular axillary artery bypass combined with a staged transbrachialoccluder implantation as a separate second procedure (picture 5) rather than a subclavian transposition or carotid-to-subclavian artery bypass. Latter option might be quite challenging in patients with trauma of the upper thorax. For aortic stentgrafts that should land in zone 0 and in cases where a sternotomy is not an option, extra-thoracic blood supply to the supraaortic vessels will come from the lower extremity arteries. 55

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Debranching Usually, in debranching procedure blood flow is derived from the ascending aorta, which requires a median sternotomy. Careful analyze of the preoperative CT images is of upmost importance, in order to clamp the aorta where it is disease-free [33, 34]. Hybrid open and endovascular debranching Combining open debranching or bypass surgery and Chimney and/or Periscope endograft techniques is our favorite as it allows downgrading technical difficulties or complexity of both the open surgery and the endovascular procedure (picture 6).

References

1. Berlanga, B., M. Torra, and J.L. Dolz, [Brachiocephalic trunk thrombosis and antiphospholipid syndrome]. Neurologia, 2009. 24(2): p. 131-2. 2. Rancic, Z., et al., Floating aortic arch thrombus involving the supraaortic trunks: successful treatment with supra-aortic debranching and antegrade endograft implantation. J Vasc Surg, 2009. 50(5): p. 1177-80. 3. Riles, T.S., et al., Common carotid occlusion. Assessment of the distal vessels. Ann Surg, 1984. 199(3): p. 363-6. 4. Cull, D.L., et al., Internal carotid artery patency following common carotid artery occlusion: management of the asymptomatic patient. Ann Vasc Surg, 1999. 13(1): p. 73-6. 5. Gerlock AJ, G.V., Krebs C. In: Gerlock AJ, Giyanani VI, Krebs C, Duplex scanning of extracranial carotid artery occlusion. Application of Noninvasive Vascular Techniques, 1988: p. 88-111. 6. Sugg, R.M., et al., Endovascular recanalization of internal carotid artery occlusion in acute ischemic stroke. AJNR Am J Neuroradiol, 2005. 26(10): p. 2591-4. 7. Combined intravenous and intra-arterial recanalization for acute ischemic stroke: the Interventional Management of Stroke Study. Stroke, 2004. 35(4): p. 904-11. 8. Thompson, R.W., D. Petrinec, and B. Toursarkissian, Surgical treatment of thoracic outlet compression syndromes. II. Supraclavicular exploration and vascular reconstruction. Ann Vasc Surg, 1997. 11(4): p. 442-51. 9. Zeller, T., et al., Acute thrombotic subclavian artery occlusion treated with a new rotational thrombectomy device. J Endovasc Ther, 2002. 9(6): p. 917-21. 10. Mohan, S.R., T. Cheatle, and R.P. Grimley, Arterial reconstruction for upper limb ischaemia: an alternative technique. J R Coll Surg Edinb, 1990. 35(3): p. 157-3. 11. The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke. International Stroke Trial Collaborative Group. Lancet, 1997. 349(9065): p. 1569-81. 12. Pieniazek, P., et al., Use of the Parodi Anti-Emboli System and transient subclavian steal for cerebral protection during emergent vertebral artery recanalization. J Endovasc Ther, 2004. 11(4): p. 511-6. 13. Hassan, A.E., et al., Long-term clinical and angiographic outcomes in patients with spontaneous cervico-cranial arterial dissections treated with stent placement. J Neuroimaging, 2012. 22(4): p. 384-93. 14. Zach, V., et al., Common carotid artery dissection: a case report and review of the literature. J Stroke Cerebrovasc Dis, 2012. 21(1): p. 52-60. 15. Kadkhodayan, Y., et al., Angioplasty and stenting in carotid dissection with or without associated pseudoaneurysm. AJNR Am J Neuroradiol, 2005. 26(9): p. 2328-35. 16. Donas, K.P., et al., Endovascular repair of extracranial carotid artery dissection: current status and level of evidence. J Vasc Interv Radiol, 2008. 19(12): p. 1693-8. 17. Kouchoukos, N.T., Frozen elephant trunk technique for extensive chronic thoracic aortic dissection: is it the final answer? Ann Thorac Surg, 2011. 92(5): p. 1557-8. 18. Ius, F., et al., Elephant trunk procedure 27 years after Borst: what remains and what is new? Eur J Cardiothorac Surg, 2011. 40(1): p. 1-11. 19. Cochennec, F., et al., Hybrid repair of aortic arch dissections. J Vasc Surg, 2013. 5214(12): p. 02658-4. 20. Shahverdyan, R., M. Gawenda, and J. Brunkwall, Triple-barrel graft as a novel strategy to preserve supra-aortic branches in arch-TEVAR procedures: clinical study and systematic review. Eur J Vasc Endovasc Surg, 2013. 45(1): p. 28-35. 21. Antoniou, G.A., et al., Chimney technique in the endovascular management of complex aortic disease. Vascular, 2012. 20(5): p. 251-61. 22. Saito, N., et al., Feasibility of the Inoue single-branched stent-graft implantation for thoracic aortic aneurysm or dissection involving the left subclavian artery: short- to medium-term results in 17 patients. J Vasc Surg, 2005. 41(2): p. 206-12; discussion 212.

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23. Roselli, E.E., et al., Transapical endovascular ascending repair for inoperable acute type a dissection. JACC Cardiovasc Interv, 2013. 6(4): p. 425-6. 24. Kolbel, T., et al., Customized transapical thoracic endovascular repair for acute type A dissection. Ann Thorac Surg, 2013. 95(2): p. 694-6. 25. Feezor, R.J., et al., Risk factors for perioperative stroke during thoracic endovascular aortic repairs (TEVAR). J Endovasc Ther, 2007. 14(4): p. 568-73. 26. Patterson, B.O., et al., Importance of aortic morphology in planning aortic interventions. J Endovasc Ther, 2010. 17(1): p. 73-7. 27. Kolbel, T., et al., Transapical access for thoracic endograft delivery. Vascular, 2011. 19(6): p. 308-12. 28. Lachat, M., et al., Complete endovascular renal and visceral artery revascularization and exclusion of a ruptured type IV thoracoabdominal aortic aneurysm. J Endovasc Ther, 2010. 17(2): p. 216-20. 29. Krankenberg, H., et al., Endovascular repair of ascending aortic aneurysm by transapical approach and periscope technique. J Endovasc Ther, 2013. 20(1): p. 13-7. 30. Criado, F.J., A percutaneous technique for preservation of arch branch patency during thoracic endovascular aortic repair (TEVAR): retrograde catheterization and stenting. J Endovasc Ther, 2007. 14(1): p. 54-8. 31. Larzon, T., et al., Experiences of intentional carotid stenting in endovascular repair of aortic arch aneurysms--two case reports. Eur J Vasc Endovasc Surg, 2005. 30(2): p. 147-51. 32. Yoshida, R.A., et al., Total endovascular debranching of the aortic arch. Eur J Vasc Endovasc Surg, 2011. 42(5): p. 627-30. 33. Antoniou, G.A., et al., Hybrid treatment of complex aortic arch disease with supra-aortic debranching and endovascular stent graft repair. Eur J Vasc Endovasc Surg, 2010. 39(6): p. 683-90. 34. Brozzi, N.A. and E.E. Roselli, Endovascular therapy for thoracic aortic aneurysms: state of the art in 2012. Curr Treat Options Cardiovasc Med, 2012. 14(2): p. 149-63.

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1. E ndovascular management of vascular emergencies of the thoracic aorta h. E mergencies in infected thoracic aortic stent grafts

Peter Taylor, Rachel Clough, Oli Lyons

Guy’s & St Thomas’ NHS Foundation Trust, King’s College London, King’s Health Partners, London, United Kingdom

The management of infected thoracic stent grafts is one of the most challenging in the vascular repertoire. Approximately 1-4% of thoracic endografts will become infected over time. [1-5] Emergencies relate to either exsanguination, overwhelming sepsis or the spread of the sepsis either directly to adjacent structures or by emboli to distant sites. This abstract is based upon the personal experience of the author. There is no level one evidence to help with management in this field. Exsanguination Infected thoracic aortic stent grafts may suddenly present with haemorrhage resulting in massive haematemesis from an aorto-oesophageal fistula, haemoptysis from an aorto-bronchial fistula or rarely from the skin via an aorto-cutaneous fistula. Endoscopy may be required to exclude common causes of gastrointestinal or respiratory tract haemorrhage if the cross sectional imaging does not show obvious infection of the stent graft. The presence of a fistula is associated with a worse outcome in terms of survival compared to those patients who have no fistula. [6] The bleed is caused by the infection affecting and weakening the aortic wall adjacent to the stent graft, until it can no longer withstand systemic blood pressure. Occasionally there is a herald bleed which warns of the imminent catastrophe, but the first haemorrhage can be fatal. Management is based upon the anatomical position of the infected device, the fitness of the patient for open surgery, any previous surgery and the haemodynamic status of the patient. If the patient is salvageable, resuscitation should be limited to maintaining consciousness while allowing “permissive hypotension” to tamponade the blood loss. Bloods should be sent for urgent cross match and uncross-matched blood should be available with clotting factors and platelets. Patients who are haemodynamically unstable should be treated immediately with either open or endovascular repair to stop the bleeding. The advantage of endovascular repair is that haemorrhage can be controlled rapidly with minimal physiological insult to the patient. However it is only a matter of time before the infection spreads to the newly placed endograft. This procedure is a “bridge to definitive repair” because of the high incidence of continued or new aortic infection and fistulae formation.[7,8] The most difficult management decision is the timing of the definitive procedure. The patient is often clinically well after the initial haemorrhage has been controlled and the infection has responded to antibiotic therapy. However, these secondary endografts will inevitably become infected at some 59

1. ENDOVASCULAR MANAGEMENT OF VASCULAR EMERGENCIES OF THE THORACIC AORTA

stage in the future although this can take many months. The risks of the definitive procedure have to be weighed carefully against the benefits. Open surgical repair of haemodynamically unstable patients for infected thoracic aortic stent grafts carries very high risks. Definitive open surgical repair includes removal of the prosthesis with either in situ or extra-anatomic repair. Removal of the prosthesis can be performed after extra-anatomic repair has been performed if the patient is haemodynamically stable. Alternatives include in situ replacement with a homograft/allograft or antibiotic/silver impregnated prosthetic graft. [9] In-situ replacement requires partial left heart bypass with routine use of a cerebrospinal fluid drain to reduce the incidence of paraplegia. Wrapping the in-situ replacement with omentum or intercostal muscle seems to be advantageous in preventing re-infection. [10,11] Approximately 20% of in-situ grafts become infected and require replacement. Extra-anatomic bypass of the thoracic aorta can be performed from the ascending aorta to the infrarenal aorta using a median sternotomy and midline abdominal incision. This can be aided by mobilizing the right colon and the duodenum. If the origins of the arch or visceral vessels are involved then extra-anatomic bypass can be used to revascularise them. This is easier to perform for the aortic arch than for visceral arteries. Sometimes if the patient has had previous surgery such as pleurodesis or previous aortic or cardiac surgery, the dissection can be hazardous and the risk of the procedure increases. A patient with an infected graft had bilateral axillofemoral grafts to revascularise both legs with retrograde perfusion of the mesenteric and renal arteries. These sufficed while the infected graft was removed from the descending thoracic aorta which was oversewn proximally and distally and the infection abolished. An extra-anatomic graft from the ascending aorta to the infrarenal aorta completed a successful third stage some months later. Infection Deep seated aortic infection will eventually result in rigors with high swinging fevers. Overwhelming sepsis can result in multi-organ failure. Antibiotics may control the infection for a time, but unless the prosthesis is removed the sepsis will continue resulting eventually in the death of the patient. The infection may spread directly to adjacent structures such as the spine causing osteomyelitis and in extreme circumstances resulting in spinal cord compression. The sudden onset of neurological signs in the lower limbs and/or problems with control of bladder or bowel function is an indication that urgent decompression is required. Usually in patients fit for surgery this requires a joint procedure with cardiovascular and spinal surgeons. Infected endoprostheses may also shower septic emboli into the distal vascular beds. This may cause multiple small aneurysms akin to those originally described with subacute bacterial endocarditis. One patient who suffered multiple septic emboli to the muscles of the calves responded briefly to antibiotics before a fatal aortic haemorrhage supervened. In patients unfit for heroic open surgery drainage and irrigation of the infected aortic sac can be performed under radiological control and can prove useful in the short term to gain control of infection and to identify the causative organism. In our experience antibiotics should be continued for life to prevent a recrudescence of the infection. An alternative approach is to stop the antibiotics when the blood cultures are negative and the ESR and C-reactive protein have returned to normal. However, the endograft infection usually flares again within a relatively short time. [6] Some patients require long term parenteral antibiotics which can be administered with the aid of a portacath or a long central catheter inserted via a peripheral vein. The results of conservative techniques to control infection tend to have an early survival advantage over excisional procedures with reconstruction. However long term survival is clearly favoured by removing the infected prosthesis. Another advantage of prosthetic removal is the opportunity to perform extensive debridement of the surrounding infected tissues. Management of infected endoprosthesis: Patient haemodynamically stable: Antibiotics parentally. Establish drainage and irrigation. If unfit for surgery: life-long antibiotics If the patient is fit for surgery: consider open repair with removal of the endoprosthesis and in situ or 60

h. Emergencies in infected thoracic aortic stent grafts, Peter Taylor, Rachel Clough, Oli Lyons

extra-anatomic reconstruction with omental or intercostal muscle wrap. Life-long antibiotics. Patient haemodynamically unstable: Antibiotics parentally. Seal the leak with: a. endovascular repair followed by open repair when/if the patient is fit enough. Life-long antibiotics b. Open surgery if the patient is fit enough with removal of the endoprosthesis and in situ or extraanatomic reconstruction with omental wrap. Life-long antibiotics.

References

1. Heyer KS, Modi P, Morasch MD et al. Secondary infections of thoracic and abdominal endografts. J Vasc Interven Radiol 2009;20:173-9 2. O’Connor S, Andrew P, Batt M et al. A systematic review and meta-analysis for aortic graft infection. J Vasc Surg 2006;44:38-45 3. Setacci C, De Donato G, Setacci F et al. Management of abdominal endograft infection. J Cardiovasc Surg 2010;51:33-41 4. Brinster CJ, Fairman RM, Woo EY et al. Late open conversion and explantation of abdominal aortic stent grafts. J Vasc Surg 2011;54:42-7 5. Hannon RJ,Wolfe JH, MansfieldAO.Aortic prosthetic infection: 50 cases treated by radical or local surgery. Br J Surg 1996;83:654-8 6. Clough RE, Black SA, Lyons OT et al. Is endovascular treatment for mycotic aortic aneurysms ever justified? Eur J Vasc Endovasc Surg 2009;37:407-12 7. Marone EM, Mascia D, Kahlberg A, Tshomba Y, Chiesa R. Emergent endovascular treatment of a bleeding recurrent aortoenteric fistula as a “bridge” to definitive surgical repair. J Vasc Surg 2012;55:1160-3 8. Daneels ML, Verhagen HJ, Teijink JA et al. Endovascular repair for aorto-enteric fistula: a bridge too far or a bridge to surgery. Eur J Vasc Endovasc Surg 2006;32:27-33 9. Vogt PR, Brunner-La Rocca, Carrel T et al. Cryopreserved arterial allografts in the treatment of major vascular infection: a comparison with conventional surgical techniques. J Thorac Cardiovasc Surg 1998;116:965-72 10. Uchida N, Katayama A, Tamura K et al. In situ replacement for mycotic aneurysms on the thoracic and abdominal aorta using rifampicin-bonded grafting and omental pedicle grafting. Ann Thorac Surg 2012;93:438-42 11. C ivilini E, Bertoglio L, Melissano G, Chiesa R. Aortic and esophageal endografting for secondary aortoenteric fistula. Eur J Vasc Endovasc Surg 2008;36:297-9

2. EMERGENCY VASCULAR PROCEDURES IN THE LOWER EXTREMITY

2 Emergency vascular procedures in the lower extremity a. Arterial access site complications: how to manage, when to operate and when catheter based interventions can handle it

Jörg Teßarek

St. Bonifatius Hospital, Lingen, Germany

Introduction Endovascular treatment has become the first choice option for the majority of vascular diseases with lower morbidity and mortality compared to surgical procedures. The development of devices and the reduction of their passing profile has helped to further reduce the complication rate associated with arterial or venous access [1]. But despite the ongoing process of device optimisation and continuing improvements of pre-procedural imaging for accurate planning of a procedure the risk of access site complications remains an issue, which includes individual technical mistakes as well as device related access complications. Ultrasound guided puncture or vessel closure devices have developed as precious tools for more safety of the overall performance. On the other hand the growing complexity of the procedures in combination with aggressive antiplatelet therapy or anticoagulation increases both, the risk of acute thrombosis and the risk of bleeding due to incomplete puncture site sealing [2]. Additionally, remaining implants like the intraluminal anchor of a closure device or the fibrin sponge outside the vessel can result in thrombus formation and embolisation originating from the access site or deep tissue infection. In case of an adverse event related to arterial access there is no “golden rule” for actions to be taken. Decision making surely depends on the severity and acuteness of the complication, the extent of vessel damage as well as the expertise available at that very moment. Furthermore, the majority of endovascular procedures are performed following a dedicated anticoagulation or platelet inhibiting regime. Coronary interventions for acute coronary syndrome or valve replacement require medication regimes different from those for peripheral interventions. Many patients receive antiplatelet therapy or anticoagulation prior to and during the index procedure, which has to be taken into account when planning the re-intervention or surgical bail out. Decision making in case of access site complications The documentation of the initial procedure in written or electronic form must be available the same way as the staff expertise for the execution of the bail out. A maximum information must be obtained in a minimum of time to decide for open surgical or endovascular trouble shooting. 65

2. EMERGENCY VASCULAR PROCEDURES IN THE LOWER EXTREMITY

Other potential reasons for a deterioration of a patients health status must be considered such as gastrointestinal bleeding ( instead of retroperitoneal bleeding), acute neurologic symptoms or heart failure with low output (instead of acute peripheral artery thrombosis). The clinical relevance of the patients comorbidities -already indicated by the underlying PAD- might be intensified by severe blood loss, acute changes in the coagulation status, the acid-base balance and physiologic response to malperfusion or reperfusion. Diagnostic steps include blood samples to determine the current coagulation status (anticoagulation medication, anti-platelet therapy, serum fibrinogen level etc.) and the amount of blood loss. For imaging ultrasound or CT scans have to be available. Table 1 and 2 display an exemplary â&#x20AC;&#x153;how we do itâ&#x20AC;? pathway for decision making in case of bleeding complications or acute limb ischemia. Any pathway has to be adapted to the individual situation of the local setting. Not every vascular department offers 24h/7d service with the complete endovascular and surgical bail out portfolio.

Table 1: s hows a potential pathway in case of bleeding complication: The severity of the bleeding complication and the availability of expertise determine the choice of treatment such as prolonged compression therapy, injection of thrombin or surgical suture. Delayed onset of bleeding at a puncture site always bears the risk of a local infection. Then the primary aim of treatment is to achieve hemostasis independent from the reason for bleeding. Further diagnostic imaging is conducted for detection of the bleeding site and for planning of a definite bail out procedure.

a. Arterial access site complicationsâ&#x20AC;Ś, J. TeĂ&#x;arek

Table 2: P otential treatment pathway in case of access related ischemia: the standardized diagnostic steps differ concerning the time frame, which is determined by the severity of the ischemia and the clinical symptoms. Occlusions at the access site can result from local complications as well as from embolisation or anticoagulation disorders. Bleeding complications The medication with effective anticoagulants or platelet inhibitors and the use of device diameters up to 27F (endografts, percutaneous access for valve replacement) result in a higher risk of bleeding complications at the puncture site, which can occur at any time during or after the procedure or as a delayed event, even when closure devices have been used. The clinical symptoms can vary between local pain related to a clinically irrelevant small hematoma and bleeding with slow progress but sudden onset of symptoms such as flank pain, circulatory collapse or progressive shock symptoms due to haemorrhage. Contained bleeding with formation of a pseudoaneurysm can result in acute or delayed symptoms with pain (Figure 1) related to the elevated tissue pressure or compression of the surrounding structures. Continuing bleeding can result in myocardial or cerebral symptoms related to hypotension and local organ malperfusion. The critical stage of anaemia is patient dependent. Healthy young patients will tolerate a higher bloodloss than the vascular patient with pre-existing impaired perfusion of the brain or the heart.

Figure 1: T he left picture shows an extensive hematoma after arterial access for PTA via the axillary artery with perforation of the skin 8 days after the initial procedure. The patient was 67

2. EMERGENCY VASCULAR PROCEDURES IN THE LOWER EXTREMITY

suffering from swelling and pain in the arm and was treated for a potential thrombosis without diagnostic ultrasound for three days. A 6x100 mm Viabahnâ&#x201E;˘ device (Gore Inc., Flagstaff, Arizona, USA) was used for sealing. The hematoma was drained with complete healing and no neurologic deficits under antibiotic therapy. The patient was put on dual antiplatelet therapy for 6 month (according to the recommendation for antiplatelet therapy from Gore Inc.) directly after the procedure.

Treatment options Manual compression followed by compression bandage has been and still is the most simple and effective technique to avoid local bleeding complications for devices up to 6F. Meanwhile a diversity of closure devices facilitates bleeding control without time and man power consuming compression with pre-suturing technique for devices up to 27F. Nonetheless, bleeding complications can occur. 1. hematoma In case of local pain and diffuse or local hematoma at the access site colour coded (or contrast enhanced) ultrasound is the first choice diagnostic tool to detect extravasation with or without active bleeding. If no bleeding or clinical relevant compression of the surrounding structures is present conservative treatment should be chosen. The need for transfusion is indicated by the haemoglobin level and the comorbidities. A several fold evaluation of the skin under the compression bandage is necessary to avoid compression related ulceration and infection. Re-do ultrasound is mandatory prior to discharge. 2. local bleeding (pseudoaneurysm) A pseudoaneurysm, which represents a form of contained extravasation, can develop immediately or as a late event after ambulation. The natural course is further growth with the increasing risk of sudden rupture. When a patient presents with local swelling and pain at the puncture site an immediate ultrasound examination is mandatory. If active bleeding (pseudoaneurysm) can be diagnosed ultrasound guided compression with additional 24hours of compression bandage and bed rest can result in successful sealing of the puncture site. The patient should be kept under close surveillance with circulation monitoring and repeated ultrasound examination of the puncture site and evaluation of the skin. Depending on the morphology and size of the hematoma ultrasound guided thrombin injection with prolonged compression bandage to stabilize the fresh clot represent an effective treatment. Thrombin initiates an immediate thrombus formation in the hematoma cave which can result in sufficient sealing of the puncture site. If the false aneurysm has a wide neck injection of thrombin bears the risk of displacement of the agent into the vessel lumen with subsequent thrombusformation in other vessel territories. Local prominent thrombus might protrude into the lumen with partial occlusion of the vessel. Additionally, the prominent part of the thrombus is exposed to the blood flow which might result in distal embolisation. In pseudoaneurysms with narrow neck injection of thrombin and compression can be used very successfully without requiring additional procedures. The success of the ultrasound guided therapy can be estimated during the examination. Surgical repair as a primary option is necessary only for those pseudoaneurysms where no other technique is suitable (wide aneurysm neck, extensive retroperitoneal hematoma, acute symptoms of compression or compartment syndrome, incompressible hematoma (figure 2) or the acuteness of the symptoms require evacuation of a hematoma or abscess for depressurising the tissue.

a. Arterial access site complications…, J. Teßarek

Figure 2: P icture 1 shows a false aneurysm after percutaneous EVAR. The vessel showed almost no perivascular fibrosis. After resection of the capsule the sutures of the Perclose™ system are visible (arrow) and the right picture shows the high flow of the after unintentional declamping. When local skin infection or necrosis with ulceration is present a local surgical approach should be avoided to prevent deep tissue layers infection (Szilagy III°). Alternatively, extensive surgical repair with extraanatomical bypass can present the most suitable option but with a higher risk for adverse events. An endovascular approach should be preferred even if it apparently represents a bridging method. Coil embolisation or bridging with a covered stent can be used to solve the bleeding complication until the patient is in an appropriately stable situation for a definite surgical solution with preservation of perfusion and wound debridement. 3. acute active bleeding Whenever active bleeding occurs hemostasis is the first aim. Manual compression has to be applied immediately and depending on the circulation status the patient must be brought to the ultrasound lab for further diagnostic imaging or to the operating theatre. With no detectable groin hematoma at the puncture site but signs of bleeding/ blood loss a retroperitoneal hematoma has to be excluded. In obese patients this might require a CT scan to detect the leaking vessel segment and to decide for surgery or endovascular treatment. Figure 2 shows a case of retroperitoneal hematoma after puncture related injury of the dorsal side of the external iliac artery above the pubic bone. 69

2. EMERGENCY VASCULAR PROCEDURES IN THE LOWER EXTREMITY

Figure 3: T his figure shows a color coded duplex ultrasound image of a huge hematoma on the dorsal side of the distal external iliac artery after high puncture. The dorsal wall above the pubic bone if punctured or injured cannot be sufficiently compressed. Injuries like this are strongly dependent on the puncture technique and the kind of needle used. The drawing (middle) displays the anatomy with the femoral artery (red oval), the inguinal cord (yellow oval), pubic bone (grey circle) and mussels (brown). The black arrow indicates the not compressible segment of the artery. Hemostasis cannot be achieved by compression or closure devices if the bleeding originates from the dorsal wall. Sealing in this case was achieved using a Wallgraft™ (Boston Scientific, Mass., USA) introduced from the contralateral groin. If extensive extravasation or local pain is present after sealing of the leak surgical drainage or depressurising is recommendable to prevent infection and long lasting symptoms related to the organized masses in the retroperitoneum. Closure device relate complications With the development of closure devices such as the Angioseal™ (St. Jude Medical, St. Paul, Minnesota, USA) or Starclose™ (Abbott Inc., Abbott Park, Illinois, USA) and the continuing decrease of device passing profile bleeding complication have become less probable although more aggressive anticoagulants or platelet inhibitors are used. A variety of studies has shown that the experience of the user and the appropriate use of the devices are crucial for successful sealing [3]. Bleeding complications, dissection, thrombosis or infection at the puncture site represent potential complications when closure devices are used inappropriately or outside the IFU (Instructions For Use). The risk of embolisation or infection is 1.0% and 0.5% resp. [4]. Some of the systems available are contraindicated in calcified vessels, which reflects the need for ultrasound guided puncture to avoid plaques shift, rupture or false positioning of the anchor inside the lumen without wall contact. When bleeding occurs further actions depend on the characteristics of the device used. The Angioseal™ has an biodegradable anchor which remains inside the vessel. Bleeding complication can result from a false positioning of the anchor or/and fibrin sponge resulting in a gap between the vessel wall and the device. To achieve hemostasis the same stepwise approach as mentioned above can be used. Bleeding after using a Prostar™ for percutaneous EVAR requires a different approach. If the sutures did not dig into the vessel wall and the wire is still in place a second closure device can be used for sealing. Pledgets (little rectangular formed pieces of felt) can be fixed on the vessel wall for sealing always followed by 24 hours compression and ultrasound control. If this does not help to achieve sealing the fascia lata technique offers a surgical solution with limited exposure of the tissue. The subcutaneous tissue is dissected and a U-turn like suture is used to close the fascia lata resulting in sealing of the puncture whole. Only if this technique does not show sufficient sealing a surgical exposure of the complete vessel for clamping and suture is mandatory. 70

a. Arterial access site complications…, J. Teßarek

Vessel occlusion and ischemia related to closure devices Dependent on the device used the underlying reason for acute or delayed vessel occlusion is different. Diagnostic steps Post-procedural vessel occlusion at the puncture site can result from a variety of reasons and show various degrees of severity. Local plaques rupture or complete dissection of the iliac artery might be the underlying reason. The clinical relevance depends on the length of occlusion and the degree of inflow impairment. Ultrasound and CT- or MR-angio might be used for planning of the secondary intervention. Blood samples have to be taken for determination of the anticoagulation status, potential drops of platelets (heparin induced thrombocytopenia) or thrombophilia and signs of tissue necrosis. treatment options Vessel thrombosis after Angioseal™ can result from flow limitation due to mismatch between lumen diameter and the natural thrombusformation at the level of the remaining anchor. The more complex problem consists in sponge placement inside the vessel lumen or dissection of plaques by the retracted anchor, which also might result in bleeding first but then in acute vessel thrombosis and ischemia. Then surgical revision with recovery of the sponge and anchor and reconstruction of flow is necessary. If the vessel remains patent despite anchor related stenosis and haemostasis is achieved surgical reconstruction is not mandatory. The stenosis can be corrected using the Turbohawk™ (EV3 Covidien, Dublin, Ireland) which allows early treatment shortly after the index procedure. In the authors experience 12 patients have been treated this way with reconstruction of the stenotic femoral bifurcation or the superficial and profunda femoral artery with a follow up of 9-31 months. Patients were treated 18 hours to 14 days after the initial procedure (peripheral and coronary interventions) without bleeding or embolisation. Figure 3 shows the results of one of the procedures.

Figure 4: T he left picture shows the occluded superficial femoral artery. The arrow indicates the anchor site. The profunda and the superficial femoral artery was probed with a 0.0014” wire each (middle left) and the directional arterectomy was performed using ultrasound. The second wire was kept in place in case of embolic events or injury of the vessel for endovascular bail out. The origin of the SFA showed a tight stenosis after the use of the closure device and seems to be ectatic after the procedure, during the follow up no further dilatation occurred. The specimen from the chamber were examined and showed foreign material and inflammatory response.

2. EMERGENCY VASCULAR PROCEDURES IN THE LOWER EXTREMITY

In case of access vessel thrombosis after percutaneous EVAR limb stenosis, dissection of the external iliac artery or plaques rupture might cause occlusion. The Perclose™ related reasons are mainly plaques shift with flow limiting stenosis or complete obstruction. The needles of the system might catch prominent plaques from the dorsal wall while being retracted. This results in displacement of the dorsal inner layers with a higher thrombogenicity or complete dissection and disruption of blood flow. The majority of closure device related thrombotic occlusions or stenosis offer the use of thrombolysis or mechanical thrombectomy via a contralateral or transcubital approach. Table 2 shows different treatment options dependent on the acuteness of the ischemia and the given anatomy.

Table 2: p athway in case of access related ischemia: the standardized diagnostic steps concerning the time frame, which is determined by the severity of the ischemia and the clinical symptoms. Occlusions at the access site can result from local complications as well as from embolisation or anticoagulation disorders. To regain perfusion different endovascular options are at hand. The Angiojet™ (Medrad Bayer Healthcare, Leverkusen, Germany) or the Rotarex™ (Straub Medical, Switzreland) are aspiration devices that can be used in combination with local thrombolysis to recover perfusion. Adjunctive procedures like stenting or directional arterectomy can be used providing that the wire has passed the lesion. Otherwise surgical reconstruction and thrombectomy is necessary.

a. Arterial access site complications…, J. Teßarek

Figure 5: T he pictures show a thromboembolic occlusion of the superficial femoral artery after percutaneous implantation of an endograft for infrarenal aneurysm. The SFA is treated using a Rotarex™ device with ultrasound guided antegrade access to achieve complete recovery thrombus. A transbrachiale approach was not possible due to lack of device length. Infection after arterial access The overall risk of local infection after arterial puncture for intervention is estimated below 1% while the risk of post-surgical reconstruction is much higher ranging from 22-30% [5] for femoral endarterectomy or above the knee bypass surgery. Local infections at the puncture site can result in vessel wall arrosion with acute or contained bleeding (infectious pseudoaneurysm). This development can be accompanied by fever or septic emboli with purpura like skin changes distal to the access site, which already indicates the systemic disease. Infection can be present as a local problem limited to the subcutaneous tissue and skin or as an extended disease with septic metastasis in other the spleen or the brain and tissue necrosis (Figure 6).

Figure 6: T he figure shows an infection of the puncture site (sealing with closure device) with peripheral necrosis due to embolisation. The symptoms started 12 days after the initial procedure (contralateral SFA) with elevated body temperature and small purpura like necrotic lesions at the foot, which resulted in a necrosis of digit 1-3 (right). CT-scan displayed an infection at the puncture site After removal of the necrotic skin (left) purulent secretion mingled with blood was evident (middle). After CT scan a venous obturator bypass was implanted with additional resection of the infected femoral bifurcation and amputation of D 1-3. Wound healing in the groin lastet more than 4 weeks with vacuum therapy. 73

2. EMERGENCY VASCULAR PROCEDURES IN THE LOWER EXTREMITY

A rare reason for puncture site infection can result from puncturing a femoral or inguinal hernia with bowel injury and local contamination and inflammation. The infection can involve the vessel wall as well as the abdominal cave with peritoneal signs. This complication requires surgical revision and inspection of the abdominal cave to decide whether bowel resection is necessary or not. Ultrasound guided puncture is the most efficient tool to prevent and to avoid such disasters. The more widespread use of closure devices even after thrombolysis seems to increase the risk of infection. The puncture site must be regarded as contaminated after 6 hours and therefore closure devices, leaving fibrin sponges or sutures as foreign material directly at the vessel wall are contraindicated in these situations. Prevention of access site complications The description of different treatment options as mentioned in the text above do show, that the decision for either endovascular, surgical or conservative treatment remains dependent on various factors. This includes the patient related risk factors as well as the situation in the local setting. At least it is an individual decision. The different access sites show different complication risks [6-7]. It is mandatory to examine the patient prior to the scheduled intervention for appropriate planning of the procedure and the potential bail out. Some very easy but essential tests are known to prevent complications. Radial access Allen Test: examine the radial and ulnar artery in terms of patency and calcification. Compression, device related temporary malperfusion or thrombosis can provoke acute ischemia of the hand especially when the palmar arch is incomplete. Cubital/brachial access Ultrasound examination is mandatory to evaluate the risk of malperfusion, thrombosis or severe damage if 6-7F sheath diameters are necessary for the procedure. A central origin of the ulna or radial artery can result in a reduced diameter of the target vessel. Axillary access ultrasound guide puncture is mandatory because effective compression of the vessel is difficult. A hematoma or surgical access bears the risk of neurologic deficits and wound infection Femoral access Femoral access should be performed using ultrasound guided puncture to prevent plaquesshift, puncture of the external iliac artery through the inguinal cord or puncture of the profunda femoris. This has a higher risk of bleeding complication when compression is used and bears the risk of acute occlusion when closure devices are used. Popliteal access Retrograde recanalization of long or complex SFA lesions can be performed coming from the P1-segment or using a puncture in the popliteal fossa. These punctures are made under ultrasound control or angiographic control. Ultrasound guide puncture has the benefit of avoiding radiation exposure of the operators hand and eyes (radiation protection guidelines). Retrograde access via the tibial vessel Retrograde recanalization of long or complex BTK or popliteal lesions can be performed coming from the tibial vessels or pedal vessels or using a puncture of the tibial anterior or tibial posterior (rare cases peroneal artery). These punctures are made under ultrasound control or angiographic control. Ultrasound guide puncture has the benefit of avoiding radiation exposure of the operators hand or eyes.

a. Arterial access site complications…, J. Teßarek

Références

1. Cragg A, et al., Hematoma formation after diagnostic angiography, effect of catheter size; J Vasc Interv Radiol 2, 231-233, 1991 2. Muller D. et al.; Peripheral vascular complications after conventional and complex percutaneous coronary interventional procedures; Am. J. Cardiol. 69; 63-68, 1992 3. Eisenack M, Umscheid T, Teßarek J, Torsello GF, Torsello GB. Percutaneous endovascular aortic aneurysm repair: a prospective evaluation of safety, efficiency, and risk factors; J Endovasc Ther. 2009;16(6):708-13 4. Eric K. Hoffer, MD and Robert D. Bloch, MD Percutaneous arterial closure JVIR 14:865-886 (2003) 5. AWMF Guidelines for PAD treatment of the German Society for Vascular and Endovascular Surgery and Vascular Medicine, 2008) 6. Bogart D. et al.; Femoral artery catheterization complications: a study of 503 consecutive patients; Cathet. Cariovasc. Diagn. 34; 8-13, 1995 7. Khoury M. et al. Influence of arterial sites and interventional procedures on vascukar complications after cardiac catheterization.; Am. J. Surg. 164, 205-210, 1992

2 Emergency vascular procedures in the lower extremity b. C omplications of closure devices and their management

Nicola Pellizzari, Luca Favero, Carlo Cernetti

S. Giacomo Hospital, Castelfranco Veneto, Italy

Vascular closure devices (VCD) are widely used as an alternative to traditional manual compression after percutaneous intervention. Vcd are used in 38% of patients worldwide and 55% of patients in u.S. VCD are categorized as compression devices, suture-based devices, collagen plug-based devices, or clip-based devices. In the setting of diagnostic catheterization, a large meta-analysis reported a risk of vascular complications similar to mechanical compression (no advantage reported with VCD). The rate of complications after pta is higher with vcd compared to manual compression (difference are reported with specific vcd, more infections reported with vasoseal). The most common vcd-related complications are device failure, hematoma, pseudoaneurysm, retroperitoneal bleeding, infection, vessel dissection/thrombosis, embolization and nerve lesion. Vascular complications are differently managed, no large series about specific treatments are reported in licterature. Device failure is more common with suture-based device and is usually treated with additional manual compression. But other complication can occur: 1. Hematoma usually is self-limiting, in some cases it needs prolonged manual compression. 2. Hemorrage is often related to device-failure and can be due even to multiple puncture and it can be treated with manual compression, with mechanical compression device or surgical repair. 3. Pseudoaneurysm is the most common complication with collagen plug device, treatment includes ultrasound guided compression, echo-guided thrombin injection or surgical repair. 4. Retroperitoneal bleeding is a life-threatening complication usually managed with percutaneous approach using ballon tamponade, stent-graft placement or coils, alternatively surgery can be considered. In all these complications carefull monitoring of blood pressure cardiac rhythm and haemoglobin is mandatory. Infection is often related to a pseudoaneurysm and it requires antibiotic therapy, surgical exploration and repair. Vessel occlusion is due to wall dissection, thrombosis and plug embolization. Percutaneous treatment of vessel occlusion needs a controlateral femoral, brachial or radial access. Crossing site of occlusion, balloon dilation and stent placement is the most common method used to address this problem. Embolization can be treated with embolectomy or surgical removal through artery cutdown. Complications occur more often in the presence of anticoagulant therapy , severe atherosclerosis, heavy calcification, small-sized femoral artery (<5 mm) and high or low common femoral stick. To prevent complications, it is recommended to carefully identify common femoral 77

2. EMERGENCY VASCULAR PROCEDURES IN THE LOWER EXTREMITY

artery puncture sites (by eco guidance or fluoroscopic localization of fermoral head centerline). Itâ&#x20AC;&#x2122; s very important to understand that there is a learning curve with each specific vcd. When necessary, choose a different access (radial for carotid, iliac and renal intervention).

Vessel occlusion after VCD SFA occlusion after angioseal placement

Vessel occlusion after VCD Vessel occlusion after VCD crossing the occlusion with wire balloon angioplasty of SFA

Vessel occlusion after VCD vessel Vessel occlusion after VCD CFArecanalization after PTA SFA stenting

Vessel occlusion after VCD final result after stenting

Pseudoaneurysm treatment SFA pseudoaneurysm before and after eco-guided thrombin injection Complications management 78

b. Complications of closure devices and their management, N. Pellizzari, L. Favero, C. Cernetti

Comparison of manual closure and VCD

Delayed Hemostatis Delayed time to ambulation Intravascular component Extravascular component Risk of infections Risk of embolism Primary healing Secondary healing Technical failure Operator failure

Manual +++ +++ n/a n/a + + No Yes + +

VasoSeal + + n/a Yes ++++ ++ No Yes ++ ++

AngioSeal + + Yes Yes ++ +++ No Yes ++ +

Sulture-mediated + + Yes Yes ++ ++ Yes No +++ +++

Clip/Staple + + n/a Yes + + Yes No ++ ++

Table 1: comparison of different VCD References

1. MR Pate, H Jneid, CP Derdeyn et al. Arteriotomy closure device for cardiovascular procedures: a scientific statement from the American Heart Association; Circulation. 2010; 122: 1882-1893 2. E Nikolsky, R Mehran, A Halkin et al. Vascular complication associated with arteriotomy closure device in patients undergoing percutaneous coronary procedures; a meta-analysis. JACC. 2004; vol. 44, No. 6, 2004, Sept 15, 2004:1200-9 3. VD Vidi, ME Matheny, US Govindarajulu et al. Vascular closure device failure in conteporary practice. JACC Intervention, vol. 5, No 8. 2012, Aug 2012: 837-44 4. JH Deuling, RP Vermeule, RA Anthonio. Closure of the femoral artery after cardiac catheterization: a comparison of Angioseal, Starclose and manual compression. Catheter Cardiovascular Interv. 2008 Mar 1; 71(4): 518-23 5. NR Smilowitz, AJ Kirtane, WA Gray et al. Practices and complications of vascular closure devices and manual compression in patients undergoing elective transfemoral coronary procedures. Am J Cardiol. 2012 Jul 15; 110(2): 177-82 6. M Brueck, D Bandorski K rauber et al. Percutaneous transluminal dilatation of inadvertent partial or complete occlusion of the femoral artery caused by Angioseal deployment for puncture site after cardiaca catheterization. J Invasive Cardiol. 2010 Aug; 22(8): 353-7 7. A Lupi, A Rognoni, GG Secco et al. Different spectrum of vascular complications after Angioseal deployment or manual compression. J Invasive Cardiol. 2012 Mar; 24(3): 90-6 8. S Haulon, R Hassen Khodja, CW Proudfoot. A sistematic literature review of the efficacy and safety of the prostar XL device for the closure of large femoral arterial access site in patients undergoing percutaneous endovascular aortic procedures. Eur J Vasc Endovasc Surg. 2011 Feb; 41(2): 201-13 9. MR Sohail, AH Khan, DR Holmes et al. Infectious complications of percutaneous vascular closure devices. Mayo Clin Proc. 2005 Aug; 80(8): 1011-5 10. BG Schwartz, S Burstein, C Economides et al. Reviw of vascular closure devices. J Invasive Cardiol. 2010 Dec; 22(12):599-607 11. DR Tavris, Y Wang, S Jacobs et al. Bleeding and vascular complications at the femoral access site following percutaneous coronary intervention: an evaluation of hemostasis strategies. J Invasive Cardiol. 2012 Jul; 24(7):328-34 12. ID Moussa, SR Bailey, A Colombo. Complications of interventional cardiovascular procedures: a case-based atlas. 2012 Demos Medical Publishing

2 Emergency vascular procedures in the lower extremity c. Acute ischemia of lower extremity due to embolization of thrombosis: diagnosis and management

Carlo Setacci

Vascular and Endovascular Surgery - University of Siena, Siena, Italy

History of acute limb ischemia treatment The history of acute limb ischemia (ALI) treatment consists primarily of rudimental instruments and suboptimal performance in clot removal, despite various efforts to improve procedures and techniques. In the 1960s, the amputation and death rates following attempts at removal were as high as 50%. At that time there were three operative alternatives for the resolution of acute arterial occlusions: an attempt to remove the clot, an attempt to remove as much as possible of the thrombosis and clot using instruments not specifically designed for embolus removal, or amputation. The need for a solution was therefore obvious, but the problem remained unresolved until the development of the balloon thromboembolectomy catheter, called the â&#x20AC;&#x153;Fogarty catheterâ&#x20AC;? after its inventor and developer, Dr. Thomas J. Fogarty. Encouraged by his mentor Dr. J. Cranley, he had the idea of placing a balloon on the end of a urethral catheter and, through various observations and bench-testing, he developed a system by tying the pinky finger of a number 5 surgical glove onto the end of an urethral catheter. The first clinical use was successful, but the academic community ignored this new approach and at first Fogartyâ&#x20AC;&#x2122;s journal submissions were turned down. The procedure was considered dangerous, above all because scraping the endothelium was believed to cause immediate re-thrombosis of the artery. Consequently no existing medical company would agree to manufacture the device, and Dr. Fogarty continued to produce it for his personal use [1]. The first publication [2] occurred in 1963 and consisted of two illustrations and two pages of text. Nonetheless, adoption of the device remained slow until a patient won a lawsuit against a physician and hospital for not employing the device. After this, its use rapidly became widespread and a number of companies began to manufacture the balloon catheter. Surgical embolectomy has therefore been considered the preferred mode of intervention for acute arterial embolic occlusion for many years. In the 1970s a new alterative and less invasive approach was offered by intra-arterial fibrinolysis. This technique was soon considered a safe and effective adjunct in acute arterial embolic occlusion requiring balloon catheter thromboembolectomy, [3] and specifically for revascularization when multiple distal infra-popliteal clots compromise a limb, such as in an acutely ischemic leg resulting from an occluded popliteal aneurysm with no visible run-off on the angiogram. Catheter-directed thrombolysis is based on the principle that activation of fibrin-bound 81

2. EMERGENCY VASCULAR PROCEDURES IN THE LOWER EXTREMITY

plasminogen to the active enzyme plasmin is the most effective means of lysing pathologic thrombi. Direct delivery of a thrombolytic agent produces increased plasmin activity at the desired location, protects intrathrombus plasmin from circulating antiplasmins, and permits effective thrombolysis at a reduced dose. The intrathrombus delivery of plasminogen activators has enjoyed greater success than systemic lytic therapy for arterial and graft occlusions. In the mid-1990s, three randomized trials of thrombolytic therapy versus surgical revascularization (i.e., Rochester, Surgery versus Thrombolysis for Ischemia of the Lower Extremity [STILE] [4], Thrombolysis or Peripheral Arterial Surgery [TOPAS] [5]) failed to prove the superiority of thrombolytic therapy over surgical revascularization. A meta-analysis published in 2000 by Palfreyman et al. [6] showed no significant differences between thrombolysis and surgery in terms of major amputation and mortality rates. However, there was an increased risk of hemorrhage with thrombolysis (RR 2.94), and sub-group analysis suggested that short-duration occlusions (numbers needed to benefit [NNB]=3) and occluded grafts (NNB=4) may benefit from thrombolysis. This meta-analysis concluded that despite the theoretical advantages of thrombolysis, there is still insufficient evidence to justify its widespread use, except in graft occlusions and short-duration ischemia. However, the major limitation of this data comparing endovascular vs. surgical therapies for ALI lies in its consideration of fibrinolysis as the only endovascular solution available, whereas many other intraluminal procedures have been developed over the last decade. In the interim, the use of endovascular techniques has increased, with catheter-directed thrombolytic therapy being bolstered by the use of percutaneous mechanical thrombectomy devices and the selective application of angioplasty, stenting, mechanical thrombolysis, thrombus fragmentation and intraluminal thromboaspiration. The concept of hybrid approaches for acute limb ischemia now includes the combination of a number of these surgical and endovascular options, which are capable of overcoming the specific limitations that characterize the traditional approach. The concept of hybrid approaches for acute limb ischemia Although improvements in surgical techniques and perioperative patient care have occurred over the years, the results available document a persistently high medical need for patients presenting with ALI, with a reported 30-day amputation rate of 5-12%, mortality risk of 10-38%, and combined incidence of amputation and death of 25% to 37.5% at 6-month follow-up [7-10]. In fact, arterial thromboembolectomy carries the highest morbidity and mortality risk of any vascular operation, with the exception of the treatment of ruptured aortic aneurysms. The most efficient treatment for an acute arterial embolism is operative embolectomy using Fogartyâ&#x20AC;&#x2122;s balloon catheter, especially if a single large artery is involved. Unfortunately, although the early surgical success of arterial thromboembolectomy often seems acceptable, the early clinical outcome still remains unsatisfactory. This may be related to the incomplete restoration of perfusion (i.e. residual thrombus in distal vessels not reached by balloon catheter thromboembolectomy) or the propagation of residual thrombi. Both experimental and clinical studies have shown that embolectomy is frequently incomplete, with persistent thrombus remaining in the majority of patients. Plecha and Pories [11] angiographically demonstrated residual thrombus in 36% of patients who had undergone balloon catheter thromboembolectomy. The thrombus was seen in the small distal arteries and arterioles inaccessible to the balloon technique and observed lining the artery that was treated by the balloon catheter. Using fiberoptic angioscopy, White et al. [12] documented residual thrombus in the arterial lumen and adherent to the vessel wall in 82% of patients. Greep et al. 3 showed that nearly all patients treated with the balloon catheter thromboembolectomy technique had to have additional thrombus removed with a modified wire basket catheter retrieval system. Residual thrombus compromises the clinical outcome, leading to poor revascularization and an increased risk of tissue loss. In such a situation a meticulous intraoperative assessment of the adequacy of clot removal is decisive. Completion angiography can identify residual thrombus, underlying steno-occlusive lesions, or vessel injuries due to balloon catheter passage, which can be corrected by endovascular techniques. The use of endovascular solutions, including balloon angioplasty, stent82

c. Acute ischemia of lower extremity due to embolization of thrombosis: diagnosis and management, C. Setacci

ing and thromboaspiration immediately after surgical clot removal, is considered the first example of hybrid intervention for acute limb ischemia (type I hybrid solution, table 1). Other possible hybrid interventions for ALI include the combination of surgical techniques with loco-regional pre- or postembolectomy thrombolysis (type II Hybrid solution, table 1), and the combination of endovascular techniques with loco-regional thrombolysis (type III Hybrid solution, table 1). I II III

Hybrid intervention for acute limb ischemia Surgery + Endovascular (embolectomy, endarterectomy, bypass) (fluoroscopically assisted thromboembolectomy, balloon angioplasty, stenting and thromboaspiration) Surgery + Fibrinolysis (embolectomy, endarterectomy, bypass) (loco-regional pre- or post-operative thrombolysis) Fibrinolysis + Endovascular (loco-regional pre- or post-operative thrombolysis) (balloon angioplasty, stenting and thromboaspiration)

Surgery + endovascular (type I hybrid solution for ALI) The increasing availability of digital fluoroscopic imaging in the operating room, as well as vascular surgeons’ familiarity with the equipment and endovascular techniques, has further increased the number of hybrid procedures performed as adjuvants to open vascular procedures for ALI. Intraoperative completion angiography permits the identification of defects after Fogarty thromboembolectomy, thus preventing early re-occlusion. In fact, intraoperative angiography has been reported as the most reliable method of ensuring that complete clearance of the whole arterial tree has been achieved [13-15]. It should also be kept in mind that there are two categorical causes of acute arterial occlusion embolism and thrombosis - which tend to present with quite different degrees of severity of acute limb ischemia. Generally, an embolus suddenly lands in an “unprepared” arterial tree, while arterial thrombosis develops in segments with gradually increasing arterial narrowings that, over time, stimulate the development of collateral circulation. Thus, an embolus tends to produce more acute and limb-threatening ischemia than arterial thrombosis. Over the last few decades the treatment of ALI has become significantly more complex, largely due to a substantial decrease in the number of young patients presenting with embolism secondary to rheumatic valvular disease and atrial fibrillation and, conversely, a marked increase in elderly people with advanced atherosclerosis presenting with thrombosis and a far more complex disease pattern. The use of hybrid solutions is highly recommended in such complex cases of arterial thrombosis. The use of intraoperative fluoroscopy and the performance of fluoroscopically assisted thromboembolectomy greatly improves the results. Lipsitz et al. [16] reported the role of fluoroscopically assisted thromboembolectomy, underlining how this solution facilitates catheter passage through tortuous, diseased arteries, identifies residual thrombus and underlying lesions (figure 1), reduces vessel damage caused by balloon over-inflation (figure 2), and decreases the risk of catheter-induced dissection (figure 3) or atherosclerotic plaque displacement.

Figure 1: a) underlying lesions and residual thrombus after Fogarty’s balloon catheter passage; b) final result after stenting. Figure 2: a) vessel damage (* arterial spasm) caused by Fogarty’s balloon over-inflation, and resisual thrombosis (**) at the origin of anterior tibial artery not reached by balloon catheter; b) final result after transluminal balloon angioplasty 83 Figure 3: a) popliteal dissection induced by Fogarty’s balloon catheter; b) final result after angioplasty and stenting

2. EMERGENCY VASCULAR PROCEDURES IN THE LOWER EXTREMITY

In fact the most significant advantage of fluoroscopically assisted thromboembolectomy is that it allows the operating surgeon to directly view and control the amount of balloon inflation, greatly reducing the risk of arterial damage. This visualization complements the operatorâ&#x20AC;&#x2122;s sense of friction with the balloon as it is pulled across the intima of the vessel. Without fluoroscopy the efficacy of thromboembolectomy depends on subjective evaluation of the thromboembolic specimen, inflow, and visual estimation of the adequacy of backflow. More recently, the addition of the guidewire lumen in the Fogarty Thru-Lumen embolectomy catheter allows for a far better controlled, more reproducible and accessible technique for thrombectomy and embolectomy. This catheter incorporates the same compliant, concentric balloon technology and catheter as the standard Fogarty catheter, but adds a further lumen that can be used to guide the catheter over a wire, or deliver fluids. Some advantages of image-guided, over-the-wire thrombectomy are: - Wire passage prior to catheter deployment is a strong indicator of embolic or thrombostenotic etiology. The possibility of passing a wire is a strong predictor of outcome. A variety of techniques can be employed to traverse lesions inaccessible to a catheter alone. - Distal positioning of the balloon is made possible by wire and image guidance. This prevents multiple passages with an inflated balloon and increases the likelihood of complete treatment with a single balloon passage. - The infusion of local contrast or therapeutic agents is accomplished by gently inflating the balloon and delivering the agent through the guidewire lumen. This allows for delivery of a lower volume but more concentrated contrast or therapeutic agent (e.g., thrombolytic agents, nitroglycerin, etc.). - The access site can be chosen with more freedom because the proximity to branch points is not as crucial to catheter passage when using selective over-the-wire catheterization techniques. For example, there is limited need to expose the distal popliteal artery in approaching tibial vessels. Finally, intraoperative fluoroscopy both helps determine the need for and guides adjunctive procedures such as angioplasty and stenting. These procedures can be performed at the time of thromboembolectomy, thus simplifying and speeding treatment (figure 4). Zaraca et al. [17] recently reported their experience with selective or routine intraoperative angiography in 380 thromboembolectomies over a 12-year period. They noted that the routine use of intraoperative angiography influences the clinical outcome of these patients. In particular, the routine use of intraoperative angiography results in a higher rate of extension of the procedure due to residual lesions (hybrid procedures) and in a lower reocclusion rate at 24 months. Surgery + fibrinolysis (type II hybrid solution for ALI) The rationale of intraoperative thrombolysis is that residual thrombus in the originally occluded artery, as well as thrombus in runoff and branch vessels inaccessible to the balloon catheter, can be lysed. As demonstrated in experimental conditions, intraoperative intra-arterial thrombolysis can potentially dissolve residual thrombus, leading to improved revascularization. Quinones-Baldrich et al. [18] studied an experimental model of adjunctive intraoperative intra-arterial thrombolysis following balloon catheter thromboembolectomy and showed significantly increased blood flow following infusion of streptokinase. This study consisted of 38 canine hind limbs with acute ischemia. Residual clots were found in 85% of limbs after balloon embolectomy. Intraoperative streptokinase use brought about angiographic improvement in all the limbs, with significantly increased blood flow but no bleeding complications. In a follow-up study, they were able to successfully restore extremity circulation in all patients and avoid popliteal artery exploration in 80% of patients with acute limb-threatening ischemia. Other clinical confirmations of this experi84

c. Acute ischemia of lower extremity due to embolization of thrombosis: diagnosis and management, C. Setacci

mental approach have been reported by various authors. Norem et al. [19] treated 19 patients who underwent balloon catheter thromboembolectomy with intraoperative intraarterial streptokinase infusion. Following infusion, the additional thrombus was retrieved with a subsequent balloon catheter thromboembolectomy, which was accompanied by angiographic improvement in all patients. Parent et al. [20] intraoperatively infused intraarterial plasminogen activators in 17 patients with angiographic evidence of residual thrombus in the infrapopliteal arteries following operative thromboembolectomy. With a dwell time of 30 minutes, they achieved successful lysis in 88% of patients. It has also been demonstrated in a canine animal [21] model that intraoperative infusion of urokinase after acute ischemia has a local protective effect, resulting in less skeletal muscle infarction and edema compared to the control group. The in vivo canine gracilis muscle model with acute ischemia, induced by clamping the inflow vessel for 5 hours, gained significantly more weight following reperfusion and was more indurated and swollen (signifying more tissue injury) compared to the experimental muscle, which received 30,000 U urokinase over 5 minutes with an additional 15 minutes dwell time. In the case of a combined surgical approach with fibrinolysis, there is a persistent concern that patients will face an increased risk of bleeding, although the potential benefit of intraoperative intraarterial thrombolysis may be clear. However, this concern is largely unjustified as, especially when the infusion of plasminogen activator is performed distally to the proximal clamp on the artery (above the arteriotomy) or directly in the distal vessels after selective catheterization, the concentration of lytic agent is very high in the areas of residual thrombus, thereby improving the chances of lysis of residual clots, without causing a systemic effect. Once the plasminogen activator contacts and binds to fibrinbound plasminogen, plasmin is produced locally, stimulating lysis. If the limited dose of plasminogen activator or the plasmin that is produced escapes into the systemic circulation, it will be rapidly neutralized by circulating inhibitors. A multicenter, randomized, blinded, and placebo-controlled trial [22] comparing the regional and systemic effects of intraoperative intra-arterial urokinase infusion during lower extremity revascularization not only confirmed the safety of intraoperative thrombolysis, without increasing bleeding complications, but also revealed a significantly better survival rate in patients receiving intraoperative intra-arterial urokinase compared to placebo-treated patients. The choice of lytic therapy depends on many factors, such as the location and anatomy of lesions, duration of the occlusion, patient risk factors (co-morbidities) and procedure-related risks [23-25]. As emboli newly arrived in the leg may have previously resided for some time at their site of origin, such ‘old’ emboli may be more resistant to pharmacological thrombolysis than ‘recent’ in-situ thrombus. Contraindications to pharmacologic thrombolysis must be taken into consideration. Comerota et al. [22] also reported a particular technique in the case of persistent thrombus after balloon catheter embolectomy, especially in multivessel acute occlusion in the run-off bed, when a single or even double bolus dose of intra-arterial thrombolytic agent has been inadequate. They suggest a high-dose isolated limb perfusion technique, with or without the use of a pump oxygenator. This technique selectively delivers maximal doses of a plasminogen activator into the run-off bed. Inflation of a proximal tourniquet to supra-systolic pressure at the level of the distal thigh together with catheterization and drainage of the effluent vein deny the possibility of a systemic fibrinolytic effect. Another acute event that can benefit from a hybrid approach is the thrombosis of a popliteal artery aneurysm, which is both limb- and life-threatening. Due to thrombo-embolisation of the run-off arteries, there is a significant risk of major amputation despite emergency intervention. Historically, surgical thrombectomy of the crural arteries and additional femoro-popliteal or femorocrural bypass grafting were the treatments of choice. In the 1980s, however, intra-arterial catheter-directed thrombolysis was successfully performed to improve arterial runoff before surgical re-vascularisation and increase the patency rates of peripheral bypass surgery [26]. In a recent systematic review [27] of the clinical outcome of acute leg ischemia due to thrombosed popliteal artery aneurysm (PAA), preoperative thrombolysis followed by exclusion of the popliteal aneurysm with bypass surgery was found to bring about a significant improvement in 1-year primary graft patency compared to surgery alone (crural thrombectomy and bypass surgery). Notably there were no significant differences in amputation rate between the two 85

2. EMERGENCY VASCULAR PROCEDURES IN THE LOWER EXTREMITY

treatment strategies. Although endovascular stenting has been used successfully in the management of popliteal aneurysm over the last few years, data on endovascular approaches for thrombosed PAAs, alone or in combination with surgery, are still scarce. Fibrinolysis + endovascular (type III hybrid solution for ALI) In 1974, Dotter et al. [28] reported the feasibility of using transcatheter streptokinase infusions to treat arterial and graft occlusions. Since that time, there have been a number of advances in catheter-directed thrombolytic therapy. Current methods include a variety of fibrin-specific thrombolytic agents and multiple methods for local delivery (e.g., pulse-spray, intrathrombus bolus technique), as well as the adjunctive use of mechanical thrombectomy devices. McNamara and Fischer [29] introduced the concept that a primary approach to ALI via administration of trombolytic agents could be the preferred treatment, particularly when the occluded segment can be successfully traversed with a guidewire (i.e., guidewire traversal test). They suggested that attempts should be made to pass a guidewire through the acute thrombus in order to initiate thrombolysis. Should this be impossible, a short period of thrombolysis may be initiated. If a wire can still not be passed after this short period of time, other methods of revascularization should be taken into consideration. Failure to pass a guidewire is not an absolute contraindication to thrombolytic therapy, but rather a predictor of poorer outcome [30-31]. Intravenous administration of thrombolytic agents should not be performed for ALI. A randomized parallel group study showed that intravenous administration of tissue plasminogen activator led to a higher incidence of hemorrhagic complications and less successful thrombolysis than intra-arterial delivery [32] . Even in the case of successful thrombolysis, repeat angiography should be performed to define the vascular anatomy and areas of disease that may require additional treatment. When thrombolysis reveals underlying localized arterial disease, catheter-based revascularization becomes an attractive option. Stenoses and occlusions are rarely the sole cause of ALI or even severe chronic symptoms, but they commonly lead to superimposed thrombosis and should therefore be treated to avoid recurrent thrombosis. Moreover, the speed and long-term efficacy of intra-arterial thrombolysis can be enhanced with use of adjunctive techniques. These techniques will help achieve two clinically important endpoints: they may be used in conjunction with thrombolysis to remove insoluble material or debulk the thrombus to accelerate the restoration of flow, and they may be used to correct underlying lesions at the time of thrombolysis or in the periprocedural period. The procedures that may be used in conjunction with or independently of pharmacologic thrombolysis include catheter suction thromboembolectomy and mechanical thromboembolectomy. The latter uses a variety of systems, including a saline solution jet spray with an associated Venturi effect and an additional external suction or a high-speed rotating impeller. According to this concept, dissolution of the thrombus occurs within an area of continuous mixing referred to as the ‘‘hydrodynamic vortex.’’ This selectively traps, dissolves, and evacuates the thrombus. Non-recirculation devices, which function primarily by direct mechanical thrombus fragmentation, have been used less frequently for peripheral arterial disease because of the higher risk of peripheral embolization and higher potential for vascular injury. The efficiency of mechanical thrombectomy devices mainly depends on the age of the thrombus; fresh thrombus responds better than older organized clots. Rotational (e.g., Helix; Microvena, White Bear Lake, MN) and hydraulic (e.g., Hydrolyzer; Cordis, Miami, FL, and AngioJet; Possis Medical, Minneapolis, MN) recirculation devices are available. Experience with these devices is limited and confined to small series [33-35]. Many of these catheter devices allow concurrent pulse-spray administration of a thrombolytic agent. This technology has the potential to minimize the two main drawbacks of endovascular ALI therapy, i.e. the long duration of thrombolytic infusion that is needed to establish full arterial perfusion, and hemorrhagic complications. The percutaneous aspiration thrombectomy technique uses a large-bore catheter connected to a syringe to aspirate clots from vessels. This technique, first described by Sniderman et al. [36], can be used alone or in conjunction with thrombolytic therapy, as well as with surgical thromboembolectomy or endoluminal angioplasty and stenting. In a retrospective study of 102 patients with acute arterial embolic occlusions, primary angiographic success (defined as reperfusion in a previously completely occluded vascular segment) was obtained in 87.3% of cases [37]. In another 86

c. Acute ischemia of lower extremity due to embolization of thrombosis: diagnosis and management, C. Setacci

study with patients who had acute embolic occlusions, percutaneous aspiration thrombectomy was successful in 77 out of 90 limbs (86%), although 200,000 U urokinase was required in 74 cases [38]. Percutaneous aspiration thrombectomy is typically used as an adjunct to thrombolysis in acute arterial occlusion, or it can be used as a salvage therapy to remove distal emboli after incomplete surgical thromboembolectomy. More recently Rathi et al. [39] reported their initial experience with a particular balloon catheter that allows for simultaneous low-pressure angioplasty and delivery of thrombolytics in situ in patients with arterial thrombosis. Their results suggest that this procedure is safe to use as an adjunct to other techniques in the treatment of acute limb ischemia. Conclusion Fluoroscopic guidance can facilitate and improve many aspects of standard open vascular procedures. Conversely, the ability to perform open interventions can facilitate the performance of many endovascular interventions. It is becoming increasingly important to be familiar with both open and fluoroscopically guided techniques in order to treat the full spectrum of vascular disease in an optimal fashion. Contemporary treatment of patients with acute limb ischemia includes both open and endovascular techniques, and advances in technology continue to make interventions easier and safer. These techniques constitute the armamentarium of therapeutic strategies that, when applied to specific clinical scenarios, hold the potential to reduce the morbidity and mortality previously associated with acute vascular occlusion. However, the greatest gains in improving outcomes in these patients will be more consistent and prompt recognition of the disease, followed by rapid, standardized therapy to minimize the risk of limb loss and subsequent reperfusion-related injury.

References

1. Fogarty T. Historical reflections on the management of acute limb ischemia. Semin Vasc Surg. 2009 Mar;22(1):3-4. 2. Fogarty TJ, Cranley JJ, Krause RJ, Strasser ES, Hafner CD: A method for extraction of arterial emboli and thrombi. Surg Gynecol Obstet 116:241- 244, 1963 3. Greep JM, Aleman PJ, Jarrett F, et al.: A combined technique for peripheral arterial embolectomy. Arch Surg 1972; 105:869-874 4. The STILE Investigators. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischaemia of the lower extremity. Ann Surg 1994; 220: 251-8 5. Ouriel K, Veith FJ, Sasahara AA, for the Thrombolysis Or Peripheral Arterial Surgery (TOPAS) Investigators. A comparison of recombinant urokinase with vascular surgery as initial treatment for acute arterial occlusion of the legs. N Engl J Med 1998; 338: 1105-11 6. Palfreyman SJ, Booth A, Michaels JA. A systematic review of intra-arterial thrombolytic therapy for lower-limb ischaemia. Eur J Vasc Endovasc Surg. 2000; 19: 143-57. 7. Aune S, Trippestad A. Operative mortality and long-term survival of patients operated on for acute lower extremity ischemia. Eur J Vasc Endovasc Surg 1998; 15: 143-6. 8. Braithwaite BD, Davies B, Birch PA, et al. Management of acute leg ischemia in the elderly. Br J Surg 1998; 85: 217-20. 9. Nypaver TJ, White BR, Endean ED, et al. Non traumatic lower-extremity acute arterial ischemia. Am J Surg 1998; 176: 147-52 10. Pemberton M, Varty K, Nydahl S, et al. The surgical management of acute limb ischaemia due to native vessel occlusion. Eur J Vasc Endovasc Surg 1999; 17: 72-6 11. Plecha FR, Pories WJ: Intraoperative angiography in the immediate assessment of arterial reconstruction. Arch Surg 1972; 105:902-907 12. White GH, White RA, Kopchok GE, et al.: Angioscopic thromboembolectomy: Preliminary observations with a recent technique. J Vasc Surg 1988; 7:318-325, 1988 13. Bosma HW, Jorning PJ. Intra-operative arteriography in arterial embolectomy. Eur J Vasc Surg 1990;4:469-472. 14. Mc Kenzie FN, Wall WJ, Heimbecker RO. Value of intraoperative arteriography in arterial embolectomy surgery. Can J Surg 1976;19:223-226. 15. Fogarty TJ, Amitava B. Acute arterial occlusion. In: Sabiston DL ed. Textbook of Surgery. 15th ed. Philadelphia: WB Saunders, 1997. pp 1723-1730. 16. Lipsitz EC, Veith FJ, Wain RA. Digital fluoroscopy as a valuable adjunct to open vascular operations. Semin Vasc Surg. 2003; 16: 280-90. 17. Zaraca F, Stringari C, Ebner JA, Ebner H. Routine versus selective use of intraoperative angiography during thromboembolectomy for acute lower limb ischemia: analysis of outcomes. Ann Vasc Surg. 2010; 24: 621-7.

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18. Quinones-Baldrich WJ, Ziomek S, Henderson TC, et al.: Intraoperative fibrinolytic therapy: Experimental evaluation. J Vasc Surg 1986; 4: 229-236. 19. Norem RF, Short DH, Kerstein MD: Role of intraoperative fibrinolytic therapy in acute arterial occlusion. Surg Gynecol Obstet 1988; 167: 87-91 20. Parent FN III, Bernhard VM, Pabst TS III, et al.: Fibrinolytic treatment of residual thrombus after catheter embolectomy for severe lower limb ischemia. J Vasc Surg 1989; 9: 153-160. 21. Belkin M, Valeri CR, Hobson RW: Intraarterial urokinase increases skeletal muscle viability after acute ischemia. J Vasc Surg 9:161-168, 1989 22. Comerota AJ, Rao AK, Throm RC, et al.: A prospective, randomized, blinded, and placebo-controlled trial of intraoperative intra-arterial urokinase infusion during lower extremity revascularization. Regional and systemic effects. Ann Surg 1993; 218: 534-541. 23. Korn P, Khilnani NM, Fellers JC, et al. Thrombolysis for native arterial occlusions of the lower extremities: clinical outcome and cost. J Vasc Surg 2001; 33:1148 –1157. 24. Swischuk JL, Fox PF, Young K, et al.. Transcatheter intraarterial infusion of rt-PA for acute lower limb ischemia: results and complications. J Vasc Interv Radiol 2001; 12:423– 430. 25. Nehler MR, Mueller RJ, McLafferty RB, et al.. Outcome of catheter-directed thrombolysis for lower extremity arterialbypass occlusion. J Vasc Surg 2003; 37:72–78. 26. Schwarz W, Berkowitz H, Taormina V, Gatti J. The preoperative use of intra-arterial thrombolysis for a thrombosed popliteal artery aneurysm. J Cardiovasc Surg 1984; 25: 465-468. 27. Kropman RH, Schrijver AM, Kelder JC, Moll FL, de Vries JP. Clinical outcome of acute leg ischaemia due to thrombosed popliteal artery aneurysm: systematic review of 895 cases. Eur J Vasc Endovasc Surg. 2010; 39: 452-7. 28. Dotter CT, Rosch J, Seaman AJ. Selective clot lysis with low-dose streptokinase. Radiology 1974; 111:31–37. 29. McNamara TO, Fischer JR. Thrombolysis of peripheral arterial and graft occlusions: improved results using high-dose urokinase. AJR Am J Roentgenol 1985; 144:769–775. 30. Ouriel K, Shortell CK, Azodo MV, Gutierrez, OH, Marder VJ. Acute peripheral arterial occlusion: predictors of success in catheter-directed thrombolytic therapy. Radiology 1994; 193:561–566 31. Shortell CK, Ouriel K. Thrombolysis in acute peripheral arterial occlusion: predictors of immediate success. Ann Vasc Surg 1994; 8:59–65. 32. Berridge DC, Gregson RH, Hopkinson BR, Makin GS. Randomized trial of intra-arterial recombinant tissue plasminogen activator, intravenous recombinant tissue plasminogen activator and intra-arterial streptokinase in peripheral arterial thrombolysis. Br J Surg 1991; 78:988 –995. 33. Gorich J, Rilinger N, Sokiranski R, et al. Mechanical thrombolysis of acute occlusion of both the superficial and the deep femoral arteries using a thrombectomy device. AJR Am J Roentgenol 1998; 170:1177–1180. 34. Uflacker R. Mechanical thrombectomy in acute and subacute thrombosis with use of the Amplatz device: arterial and venous applications. J Vasc Interv Radiol 1997; 8:923–932. 35. Tadavarthy SM, Murray PD, Inampudi S, Nazarian GK, Amplatz K. Mechanical thrombectomy with the Amplatz device: human experience. J Vasc Interv Radiol 1994; 5:715–724. 36. Sniderman KW, Bodner L, Saddekni S, Srur M, Sos TA. Percutaneous embolectomy by transcatheter aspiration. Work in progress. Radiology 1984; 150: 357–361. 37. Wagner HJ, Starck EE. Acute embolic occlusions of the infrainguinal arteries: percutaneous aspiration embolectomy in 102 patients. Radiology 1992; 182: 403–407. 38. Wagner HJ, Starck EE, Reuter P. Long-term results of percutaneous aspiration embolectomy. Cardiovasc Intervent Radiol 1994; 17:241–246. 39. Rathi S, Latif F, Exaire JE, Hennebry TA. Use of simultaneous angioplasty and in situ thrombolysis with a specialized balloon catheter for peripheral interventions. J Thromb Thrombolysis. 2009; 28: 77-82.

2 Emergency vascular procedures in the lower extremity d. M anagement of acute occlusion of a bypass graft or an endovascular reconstruction

Michael Wholey

Christus Santa Rosa Medical System, San Antonio, USA

Introduction There are several types of vascular bypass grafts as well endovascular reconstructions that are subject to acute arterial occlusions. These involve the surgical bypass grafts to treat diseased abdominal aorta, iliac arteries and lower extremity arteries. Acute occlusions of arterial bypass grafts and endovascular reconstructions is a real emergency for it can result in loss of limb, organ failure and death if not treated quickly. Vascular occlusion results in release of free oxygen radicals leading to cell membrane damage and can cause intra and extracelluar edema leading to compartment syndrome, prolonged ischemia and gangrene. Mortality can lead to 7-29% mortality. Types of vascular bypass grafts and endovascular reconstruction Aortic bifemoral bypass (or aortobifemoral bypass) is a surgical procedure performed in patients with atherosclerotic disease of the infrarenal aorta and iliac vessels. The aortic bifemoral bypass grafts are among the most durable treatment modalities for the abdominal aorta and pelvis. Meta-analysis of multiple studies reveals that the long-term patency of aortic bifemoral bypass grafts ranges from 91% at 5 years to 80% at 10 years. Patency rates are lower if the procedure is performed in patients with ischemic rest pain, ulcerated toes, or coexisting distal disease [1-3]. There are several extra-anatomic bypass grafts, such as the axilofemoral bypass graft and the femoral-femoral bypass graft. Femorofemoral bypass grafts are durable with patency rates at 5 years between 74-90% [4]. Early complications occurred in approximately one fifth of these patients within the first 30 days after surgery [4]. Surgical bypass grafts include grafts from the femoral artery to the popliteal artery above or below the knee as well as bypass grafts to the feet. The results of bypass surgery vary enormously depending on the type of graft (prosthetic or vein graft), the severity of the arterial disease and the site of the graft. In femoro-popliteal grafts above the knee, the 5-year patency is approximately 80% for vein grafts [5]. In femoro-popliteal venous bypass grafts below the knee, patency is approximately 65% [5]. Results for artificial grafts (PTFE) are worse. For above knee PTFE femoropopliteal bypass grafts, patency is about 60% [5]. Results for more complex procedures to the calf vessels are usually slightly worse than these figures. Endovascular reconstructions are often in reference to abdominal aortic endovascular stent 89

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grafts or EVAR. EVAR data is now approaching 10-year results. EVAR (United Kingdom Endovascular Aneurysm Repair) 1 and 2 trials were recently delivered [6]. EVAR 1 showed that at 10 years, compared with open repair, EVAR has a lower operative mortality, but at six years the advantage of abdominal aortic aneurysm-related mortality is lost [6]. Another endovascular reconstruction may be in reference to expanded polytetrafluoroethylene (ePTFE)/nitinol self-expanding stent graft (stent graft) such as the Gore Viabhan in treating SFA disease. Patency results have shown 1-year primary patency rates varying between 44% and 86%, with secondary patency rates between 58% and 93% [7]. Graft occlusions 1. Aortobifemoral Bypass Graft Graft occlusion usually occurs many years after the operation and may present as unilateral claudication or rest pain. Recurrence of symptoms is a sign that one of the distal limbs of the graft is narrowed or occluded [1-3]. (Refer to Figures 1-4)

Figure Figure

Figure 1a: 7 3 year-old male with one day history of acute right leg pain has initial angiogram showing aortobifemoral artery bypass graft occluded right leg and diminished flow seen to the left limb. Figure 1b: Catheter pulled down showed a buckling of the end to side proximal anastomosis with flow seen on left limb of the graft. Figure 1c: View of the left limb reveals anastomosis of limb to PFA with occluded SFA and high grade stenosis of the left CFA. 1d: Once left limb seen, the right limb occlusion was addressed. Diagnostic catheter was advanced up and over the bifurcation showing complete occlusion of the left leg. 1e: Angioplasty with a 3 mm balloon catheter was performed creating a channel for the thrombolytics. An infusion catheter 4 Fr with 30 cm infusion length was placed initially with sideholes in both limbs of the aortobifem graft. TPA was administered for 1 mg/hr and patient was brought back 5 hours later in the evening. 1f: Follow up angiogram reveals flow in the right limb of the graft with PFA only identified. Limited flow to the right leg note. 1g: Balloon angioplasty of the graft anastomosis was performed with distal protection for residual thrombus. Limited improvement seen. Cutting balloon with a Boston Scientific 4.0 mm (Natick, MA) was then performed. Infusion catheter was exchanged for shorter length infusion to treat right leg. Overnight infusion was then performed with 1 mg/hr. 1h: After 20 hours of infusion, final angiogram shows occluded SFA reconstituting the popliteal and trifurcation flow. 1i: Flow via posterior tibial to the foot.

d. Management of acute occlusion of a bypass graft or an endovascular reconstruction, M. Wholey

Figure 2a: 5 8 year old male with acute right lower extremity occlusion involving right limb of aortoiliac bypass graft and suspected right femoral popliteal bypass graft. Access from left CFA reveals the left limb and the native right common and a portion of the internal iliac. Figure 2b: With manipulation with a 5 Fr Simmons I catheter and a regular hydrophilic wire, able to get access into the occluded right iliac limb. Once across, a 4 Fr Glidecatheter is advanced slowly to the CFA to start infusion of tPA Figure 2c: Gentle manipulation of the Glidewire and Glidecatheter into the occluded right femoral popliteal graft is performed Figure 2d: Infusion catheter with 30 cm length has been placed and tPA administered overnight. Next morning improvement of the right limb is noted. Native right occluded iliac is seen adjacent to the graft Figure 2e: Same run as 2f with stenosis identified near the CFA anastomosis. PTA was then performed with 5mm balloon catheter and new infusion catheter was advanced into the thrombosed right femoral popliteal graft and tPA was continued Figure 2f: After overnight infusion, able to open the occluded femoral popliteal bypass graft. One vessel runoff to the foot was seen

Figure 3a: P atient with occluded right axilary-femoral bypass graft. Pulse in arm but cold, acute ischemia of right leg Figure 3b: Arterial access was achieved in both cephalad and caudal directions with two infusion catheters placed in criss-cross method Figure 3c: Start of thrombolytic administration to try to open right leg. Urokinase was given in this old case Figure 3d: After 24 hours, able to reopen the ax-fem graft Figure 3e: Fow restored to the CFA and SFA Figure 3f: Distal anastomic disease seen at level of adductor canal which was later operated and corrected later

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Figure 4a: Hx. 63 yr male sp rt ext iliac stent 6 mos and s/p neck resection for esophageal cancer was noted to have absent femoral pulse Figure 4b: 4 Fr Glide catheter used to determine extent of clot Figure 4c: 5 mm EPI Filter placed below in SFA and Angiojet Possis with power pulse spray performed above Figure 4d: Post Angiojet with minimal improvement Figure 4e: Following Possis and 5 mm PTA, filter is overrun and had to removed and new filter placed to finish treating native lesion 2. F emoral-popliteal Bypass Graft Operative therapy for femoral-popliteal artery disease includes in situ and reversed autogenous saphenous vein bypass grafts, placement of polytetrafluoroethylene (PTFE) or other synthetic grafts, and thromboendarterectomy. Operative mortality ranges from 1 to 3%. [8] The long-term patency rate depends on the type of graft used, the location of the distal anastomosis, and the patency of runoff vessels beyond the anastomosis. Patency rates of femoralpopliteal saphenous vein bypass grafts at 1 year approach 90% and at 5 years, 70 to 80%. Five-year patency rates of infrapopliteal saphenous vein bypass grafts are 60 to 70%. In contrast, 5-year patency rates of infrapopliteal PTFE grafts are less than 30%. (Refer to Figures 5-6)

Figure 5a: O ld case revealing elderly male with occluded right femoral popliteal bypass graft. Initially, guidewire could not be passed into occluded graft. According the STILES report that had just been published, 28% of STILES cases called technical failures for inability to get wire access across lesion. Here, given the inability to gain access, we parked an endhole diagnostic catheter at stump of the graft and started thrombolytic therapy (Urokinase) Figure 5b: After 4 hours of leaving end hole catheter at stump, we were able to access the fem-pop graft and begin more thrombolytic theray Figure 5c: After 24 hours, able to open the graft revealing two vessel runoff to the foot

d. Management of acute occlusion of a bypass graft or an endovascular reconstruction, M. Wholey

Figure 6a: Patient with occluded femoral popliteal bypass graft. Contralateral access obtained and occlusion found in proximal bypass graft. Occasionally it is difficult to find the origin of the bypass graft. Ultrasound is helpful in determining the graft origin. Four hours of thromboytic therapy was performed and the patient returned in the afternoon Figure 6b: Once the graft was partially opened, a microcatheter was advanced coaxially through the infusion catheter to treat the popliteal and infrapopliteal thrombus Figure 6c: After overnight infusion, little improvement in the popliteal artery and distal graft. Possis AngioJet was then employed to reduce clot build up Figure 6d: After 48 hours of infusion, finally able to open the graft and the flow infrapopliteal to the foot 3. Abdominal aortic endovascular stent grafts or EVAR. After endoleak and device migration, limb thrombosis is the most common postoperative complication. [9] Reported limb thrombosis prevalence ranges between 0.7% and 6.4% [9-12] and can occur immediately postoperative (up to 50% of limb thrombosis cases occur during the first postoperative month 5) or months to years after surgery. The overall annual incidence rate is as high as 3.2% [13]. (Refer to Figure 7) Figure 7: S tent graft for abdominal aortic aneurysm repair revealing the sharp, high bifurcation of the iliac limbs. Brachial access is preferred for treating occluded limbs. If femoral access is performed, then often a Simmons I or II catheter can be placed at the limb origin. If possible, a 4 Fr Glidecath may be advanced over the bifurction to treat the distal iliac and leg Diagnosis of occlusions Acute arterial occlusion frequently presents with the five Pâ&#x20AC;&#x2122;s, sudden pain, pallor, pulselessness (loss of the pulse), paresthesias (abnormal sensations) and paralysis. All five of these symptoms may or may not be present. Frequently, patients present in the emergency room with these symptoms. Surgical history, medications and previous imaging studies must be obtained. Blood chemistries including creatinine and coagulation status must be evaluated. Vascular surgery consult is obtained. Patients must be transferred to ICU or SICU with nursing staff familiar with acute arterial occlsions and management of multiple drips. Hydration should begin at once in non-dialysis patients. Immediate arterial Doppler evaluation is done to document level of occlusion. We will start heparin drips immediately, and when ready for angiography, we often use ultrasound to gain access in one stick. We have used MRA or CTA of the abdomen, pelvis, and lower extremities to assess the occlusion and distal disease on several occasions when angiography is not available immediately. Angiography is still the gold standard for it shows the occlusion and flow, which can be shown accurately in MRA/CTA. Treatment modalities Surgical modalities for acute arterial occlusions include amputation, endartectomy, the use of Fogarty embolectomy balloon catheter, intraoperative thrombolytic therapy and creating a new bypass graft. Amputation is used for life threatening irreversible arterial occlusion. Endovascular cut down and use of Fogarty balloon catheter is used for acute profound arterial occlusions where sensory motor deficits are present and patients cannot undergo the time required for endovascular treatment options. Lim93

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its of the Fogarty balloon catheter include residual thrombus left after treatment, inability to clear branch vessel occlusions, and risk of injury to arterial endothelium leading to more thrombogenic and spastic conditions. For acute and subacute arterial occlusions with viable limbs, endovascular treatment options would be considered. Endovascular options for treatment of acute arterial occlusions for bypass grafts and endovascular reconstructions include; Thrombolytic therapy or referred to as pharmacologic catheter-directed thrombolysis, Percutaneous aspiration thrombectomy (PAT), Mechanical thrombectomy, Rheolytic aspiration (Medrad Possis system), Adjunctive Therapy, Balloon mounted, self expandable and covered stents systems, or other adjunctive treatments, such as laser or atherectomy. Thrombolytic Therapy: Thrombolytic therapy for the treatment of acute arterial occlusions of surgical bypass grafts and EVAR has had a long tradition for managing these difficult cases. It remains an initial treatment option for patients presenting with Rutherford category l or 2 acute limb ischemia. Benefits include restoration of flow quickly, identifying the lesion if present which can be treated later, converting to elective surgery if necessary, restoration of collateral circulation, and avoiding trauma to small arteries. The administration of thromblytic therapy helps to restore flow to the foot and distal vessels which were unattainable with regular surgery. Types of infusion catheters vary on length of catheter, length of infusion sideholes, French size and wire compatibility. Manufacturers include Cragg-McNamaraâ&#x201E;˘ Valved Infusion Catheter (Covidien, Plymouth, MN), Angiodynamics Infusion Catheters (Latham, NY), and Cook infusion cathters (Bloomington, IN). Limitations to thrombolytic therapy include: duration of therapy sometimes 1-2 days of treatment, probability of complication increases with duration, expense, intensive care monitoring, serial arteriography. Risk of intracranial hemorrhage is approximately 1-2% of all cases with 5-15% systemic bleeds. One of the most frustrating aspects of thrombolytic therapy, especially with the use tissue plasminogen activator or tPA, is its inability to treat old or chronic clot past 2-3 weeks in existence. Previously, urokinase despite its problems, had been effective in chronic clot; we performed a study in which it was effective in lysing clot that was 6 months or older in approximately 70% of the cases [14]. Because of FDA issues in the US, urokinase has been pulled off the US market. We anxiously await other drugs in the pipeline to treat thrombus. What are factors for thrombolytic success? Identification Of Underlying Stenoses, Location And Severity Of Underlying Stenoses, Status Of Runoff Vessels, Viability Of Limb, Catheter Positioning Tips for treatment include the following: - Contraindications for Lysis: Recent major surgery (10 days), Recent major trauma, Active bleeding, Recent stroke and Intracerebral neoplasm - Access: make sure it is only one stick and an anterior wall only. Use ultrasound with a micropuncture set system if needed to avoid multiple arterial access. - Antiobotics should be given prior to the procedure and during treatment to avoid graft infection. - Treat inflow stenoses prior to infusion catheter placement - We will often employ distal protection below the level of clot when intervention is performed to prevent as much distal embolization as possible. - When placing the infusion catheter, be mindful of small vessel diameter with the infusion catheter, especially with the infrapopliteal circulation; often the 4 Fr infusion catheter must stay above the knee joint and if needed access coaxial system with infusion wire. - Total occlusion distally may require gently probe with a 0.014â&#x20AC;? wires in the lower leg infrapopliteal to help deliver channel of flow. Be very careful to avoid dissection distally. - Dosage: We will frequently run tPA at 1 mg with infusion rates 20-30 cc/hour in combination with Heparin 500 units IV. For very urgent cases, we will increase to 2 mg/hours for several hours and return to lab for follow up. - Length of therapy is usually overnight, occasionally we will go 48 hours but risks for bleeding and complications increase exponentially - Labs: upon catheter placement, check CBC and fibrinogen and repeat q8 hours. If platelets start to 94

d. Management of acute occlusion of a bypass graft or an endovascular reconstruction, M. Wholey

fall or if fibrinogen approaches 120, you will need to reduce TPA dose or bring to lab immediately for follow up (Refer to Figures 1-4 for further tips and recommendations) Percutaneous aspiration thrombectomy (PAT) Catheter thrombectomy with monorail catheters such as Pronto (Vascular Solutions, Minneapolis, MN) and Export AP (Medtronics, Minneapolis, MN) are simple to perform but are limited in their ability to aspirate material of large size and its ability to continually aspirate without becoming plugged up. They are useful in treating infrapopliteal and small vessel occlusions, but offer little to treat large bypass grafts. Another method includes advancing a guide of diagnostic catheter over the wire, aspirating with the wire removed, then advancing over the wire for second attempt. Because of vessel damage and crossing a lesion twice, this method is not often used. Mechanical Thrombectomy: Rheolytic thrombectomy with the AngioJet rheolytic thrombectomy system (Medrad Interventional/ Possis, Minneapolis, MN) is frequently used before or after or in place of thrombolytic therapy. The catheter, in theory, works isovolumetrically; that is, the volume of saline infused via the jets is approximately equal to the volume of thrombus debris evacuated from the catheter. The AngioJet catheter has been reported to aspirate more than 75% of the thrombus in patients presenting with ALI involving native vessels and grafts removing a bulk of the thrombosed segment and uncovering true areas of disease. Another approach with the AngioJet catheter is called the power pulse spray technique and has been reported to have 90% success rates. This technique involves thrombolytic drug infusion through the PMT catheter while occluding the outflow port and is followed by thrombus aspiration. Drawbacks include inability to treat old or chronic clot. Potential to induce distal embolization is of concern when treating a vessel near branch points. Embolization rates have been recorded as high as 56% of two series [16]. The efficacy of the device is limited by the size of the effluent lumen, a property that is dependent on the size of the device. Another limitation is that a significant amount of red blood cell hemolysis resulting in hemoglobinemia and hemoglobinuria. There is the potential for fluid overload due to intravascular irrigation. Fatalities from hyperkalemia have been noted and caution is recommended in treating children and patients with chronic renal failure. Treatment tips with the Possis catheter include recommendation of run times â&#x20AC;&#x201C; 10 min. occlusion and 5 min. patent vessel. It removes approx. 0.5cc blood and saline/sec. Improved efficacy with lower profile wires. Benefit of lacing with thrombolytic beforehand or using thrombolytics concomitantly, referred as power pulse spray. Overall results for the rheolytic device are helpful. In a good study by Papillion et al., they reported immediate technical success rate was 28% (n = 12) [16]. Twenty-one (49%) patients required adjunctive catheter-directed thrombolysis (CDT) for success [16]. Additional endovascular procedures were performed in 30 patients (70%), with a resulting overall success rate of 77% (n = 33). [16] Adjunctive Therapy: Adjunctive therapies for treatment of acute arterial occlusions include various measures after the graft or stent graft is reopened. These involve treating the anastomotic stricture if present with balloon angioplasty and possible stent placement. Close coordination with vascular surgery staff is essential for often, patients will return for surgical revision. Distal disease is frequently a complicating factor and will require endovascular intervention with balloon angioplasty, atherectomy, laser, and/ or stent placement. Conclusions Recognition of acute arterial occlusion of surgical bypass grafts and endovascular reconstructions is the first step in dealing with this difficult situation. Imaging of the problem is next with ultrasound followed by CTA or MRA of abdomen, pelvis and lower extremities or immediately to angiography depending upon the clinical situation. Level of occlusion is determined and coordination with vascular surgery is obtained to determine whether endarterectomy and embolectomy is needed versus endovascular options. For severe cases, where there is no more time available, surgery is preferred. 95

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For aortobifem bypass grafts with focal occlusion near the common femoral artery, with unobstructed flow distally to the foot, surgical embolectomy is simpler and faster than endovascular. Endovascular often results in clearing the iliac limb, but then chasing the clot down to the trifurcation and possibly foot. Endovascular treatment is preferred with extensive clot in the leg and foot that surgery will not be able to clear. If you have time, i.e. Rutherford Class 1-2 (pt can still feel and move extremities), we will perform endovascular treatment including clearing inflow obstructions and begin catheter directed thrombolytics with tPA. The use of the mechanical thrombectomy devices is another option to help debulk the extensive clot present, but be careful of its risks including distal embolization, hemolysis and in ability to treat old clot. We will use mechanical thrombectomy occasionally before starting thrombolytic therapy. After the major vessels are opened. We will assess what caused the occlusion and try to treat it if possible, or will refer the patient for surgical revision. When treating with endovascular means we frequently employ distal protection.

References

1. Zelenock GB, Huber TS, Messina LM, et al. Aorta bifemoral bypass. In:Mastery of Vascular and Endovascular Surgery. Lippincott Williams & Wilkins; 44. 2. Haimovici H, Ascher E, Hollier LH, et al., Eds. Haimovici’s Vascular Surgery. 3. Cronenwett JL, Wayne Johnston. Rutherford’s Vascular surgery. 2nd. 4. Pursell R, Sideso E, Magee TR, Galland RB. Critical appraisal of femorofemoral crossover grafts. . Br J Surg. 2005 May;92(5):565-9. 5. Pereira CE, Albers M, Romiti M, Brochado-Neto F, Pereira CA. Meta-analysis of femoropopliteal bypass grafts for lower extremity arterial insufficiency Journal of Vascular Surgery Volume 44, Issue 3, September 2006, Pages 510–517. 6. Greenhalgh R Landmark EVAR Trials: EVAR 1 and 2 10-year follow-up results. Vascular News April 11, 2010 Results of Charing Cross Meeting 7. Doomernik DE, Golchehr B, Lensvelt MM, Reijnen MM..The role of superficial femoral artery endoluminal bypass in long de novo lesions and in-stent restenosis. J Cardiovasc Surg (Torino). 2012 Aug;53(4):447-57 8. Maron D and Perler B. PAD in the United States PAD: LONG-TERM MORTALITY 3/9/2010 http://www.vascularweb. org/practiceresources/Documents/BrandingPDFs/perler_pad.ppt 9. Hobo R, Buth J; EUROSTAR collaborators. Secondary interventions following endovascular abdominal aortic aneurysm repair using current endografts. A EUROSTAR report. J Vasc Surg. 2006;43:896-902. 10. EVAR trial participants. Endovascular aneurysm repair versus open repair in patients with abdominal aortic aneurysm (EVAR trial 1): randomised controlled trial. Lancet. 2005;365:2179-2186. 11. E VAR trial participants. Endovascular aneurysm repair and outcome in patients unfit for open repair of abdominal aortic aneurysm (EVAR trial 2): randomised controlled trial. Lancet. 2005;365:2187-2192. 12. Prinssen M, Verhoeven EL, Buth J, et al.; Dutch Randomized Endovascular Aneurysm Management (DREAM)Trial Group. A randomized trial comparing conventional and endovascular repair of abdominal aortic aneurysms. N Engl J Med. 2004;351:1607-1618. 13. Van Marrewijk CJ, Leurs LJ, Vallabhaneni SR, et al.; EUROSTAR collaborators. Risk-adjusted outcome analysis of endovascular abdominal aortic aneurysm repair in a large population: how do stent-grafts compare? J Endovasc Ther. 2005;12:417-429 14. Kasirajan K, Gray B, Beavers F, et al. Rheolytic thrombectomy in the management of acute and subacute limb-threatening ischemia. J Vasc Interven Radiol 2001;12:413–421. 15. Papillion P, Sprouse R, Allen K, Greer M, Lesar C, Erdos L, Myers S, Fisher d. Percutaneous Mechanical Thrombectomy of Acute Lower Extremity Ischemia. Vascular Disease ManagementVolume 5 - Issue 5 - Sept/Oct 2008 16. Wholey M, Wholey M. COMPARISON OF UROKINASE TREATMENT FOR ACUTE, SUBACUTE AND CHRONIC ARTERIAL OCCLUSIONS Cardiac Catheterization and Intervention 1998, 44:159-169

2 Emergency vascular procedures in the lower extremity e. W hen to consider fasciotomy for the endangered leg and how to do it

Isabelle Van Herzeele

University Hospital Ghent De Pintelaan, Gent, Belgium

Compartment syndrome is a condition in which elevated pressures within an osseofascial compartment cause vascular compromise, leading to ischemia of the limb and potentially life threatening complications. Acute compartment syndrome occurs when tissue pressure within a closed muscle compartment exceeds the perfusion pressure, resulting in muscle and nerve ischemia. It typically occurs subsequent to a traumatic event (blunt trauma with or without fracture), vascular injuries with ischemia reperfusion injuries, frank bleeding into the myofascial spaces or acute limb ischemia. The cycle of events leading to acute compartment syndrome starts when the tissue pressure exceeds the venous pressure and impairs blood outflow. Lack of oxygenated blood and accumulation of waste products result in pain and decreased peripheral sensation due to nerve irritation. Late manifestations of compartment syndrome include the absence of a distal pulse, hypoesthesia, extremity paresis, and occur when the elevating tissue pressure eventually compromises arterial blood flow. If left untreated or if inadequately treated, the muscles and nerves within the compartment undergo ischemic necrosis. Severe cases may lead to renal failure by rhabdomyolysis. Diagnosis is made by clinical suspicion and/or tissue pressure measurement (>30mmHg). The definitive surgical therapy for compartment syndrome is emergent fasciotomy (compartment release). The goal of decompression is restoration of muscle perfusion, and ideally this should be performed within 6 hours. Prognosis is very dependent on patientâ&#x20AC;&#x2122;s comorbidities, early recognition and treatment. History The original description of the consequences of rising intra compartmental pressures is attributed to Richard von Volkmann. His 1872 publication documented nerve injury and subsequent contracture from compartment syndrome following a supracondylar fracture. That injury remains known as the Volkmann contracture. Although long bone fractures are the most common cause of compartment syndrome, other injuries (penetrating injury, gunshot wounds, crush injury, bleeding) can lead to compartment syndrome. Approximately 50 years after von Volkmannâ&#x20AC;&#x2122;s paper, Jepson described ischemic contractures in dog hind legs caused by limb hypertension after experimentally induced venous obstruction. 97

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Wilson first described the exertion compartment syndrome in 1912. Mavor, in 1956, reported the first chronic compartment syndrome. Since then, various cases of compartment syndrome have been reported in the literature, and discussion remains on the pathophysiology and treatment options. In the 1970s, the importance of measuring intra compartmental pressures became apparent. Owen et al published a series of articles describing the use of the wick catheter for pressure measurement. He documented high compartmental pressures in various circumstances. Pathophysiology Muscle groups and associated nerves and vessels are surrounded by rigid osseofascial structures that define the different compartments in the extremities, with their own relatively fixed volume. Introduction of excess fluid or overdone volume constriction increases pressure and decreases tissue perfusion, until no oxygen is available for cellular metabolism. The mechanism can be: 1/ Reduction in volume (tight cast, constrictive dressings), 2/ Increase in content (haemorrhage on fracture, blunt trauma, coagulopathy caused by anticoagulation, IV infiltration or drug abuse), 3/ Vascular reperfusion (after arterial repair). Tissue perfusion is proportional to the difference between capillary perfusion pressure (CCP) and the interstitial fluid pressure, calculated by the formula: LBF = (PA - PV)/R (Local blood flow = (local arterial pressure - venous pressure) / local vascular resistance). Normal myocyte metabolism requires a 5-7 mm Hg oxygen tension, which can readily be obtained with a CPP of 25 mm Hg and an interstitial tissue pressure of 4-6 mm Hg. When the interstitial pressure exceeds the CPP, capillaries collapse and muscle and tissue ischemia occur. Skeletal muscle responds to ischemia by releasing histamine like substances that even increase vascular permeability. Plasma leaks out of the capillaries, and relative blood sludging in the small capillaries occurs, worsening the ischemia. The myocytes lyse, and myofibrillar proteins fall apart into osmotically active particles, attracting water from the blood compartment. A relatively small increase in osmotically active particles in a closed compartment attracts sufficient fluid to cause a further rise in intramuscular pressure. When tissue blood flow is diminished further, muscle ischemia and subsequent cell edema worsen. This vicious cycle of worsening tissue perfusion continues and escalates. Compartment pressures return to normal after a fasciotomy. The general consensus is that intra compartemental pressures (ICPs) greater than 30mm Hg require intervention. If such high compartmental pressures are left untreated, within 6-10 hours, muscle infarction, tissue necrosis, and nerve injury occur. Patients with hypotension suffer irreversible injury at lower absolute pressures. This implies that trauma patients are at increased risk. For unclear reasons, compartment syndrome associated with surgical positioning manifests later, with a mean time of 15-24 hours postoperatively. In addition to local morbidity, cellular destruction and alterations in muscle cell membranes lead to the release of myoglobin, resulting in renal injury. Advanced compartment syndrome may result in rhabdomyolysis, and conversely, rhabdomyolysis may result in compartment syndrome. Mortality is usually due to renal failure or sepsis from difficult wound management. Diagnosis Clinical assessment A high level of suspicion of compartment syndrome is a must. The earliest and most important symptom is pain, greater than expected due to the injury alone, severe pain at rest should raise the red flag. In the anterior compartment, the superficial peroneal nerve is usually affected early with loss of sensation in the web space between the first two toes. The affected compartment will begin to feel tense or hard, compared to the contralateral side. The pathognomonic five Pâ&#x20AC;&#x2122;s (Pain, Pallor, Paresthesias, Paralysis and Pulselessness) are late signs, 98

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irreversible injuries have taken place by the time they have manifested. (Figure 1) Distal pulses or open wounds do NOT exclude a compartment syndrome. Tissue pressure measurement Measurement of compartment pressures is a valuable step in the diagnosis, especially in the unconscious patient. Three primary methods are used most frequently: a handheld manometer, a simple needle manometer system, and the wick or slit catheter technique. Both manometer methods involve injecting a small quantity of saline into a closed compartment and measuring the resistance from tissue pressure e.g. Strycker STIC monitor (Figure 2). The slit catheter technique involves inserting a catheter into the compartment and monitoring the pressure via a transducer. Accuracy depends upon proper device calibrations and placement. All compartments in the affected extremity should be measured, as one compartment can be high while others are normal. The general consensus is that absolute intra compartemental pressures (ICPs) greater than 30mm Hg require intervention. Patients with hypotension may suffer from irreversible injury at lower absolute pressures, hence trauma patients are at increased risk, and should be treated earlier. Patients with peripheral arterial occlusive disease may also need a fasciotomy at a much lower compartment pressure due to an insufficient perfusion pressure of the limb. Indeed, some urge prophylactic fasciotomy in high-risk patients at normal pressures to prevent compartment syndrome.

3. 4.

Anatomy Lower leg The lower leg is divided into 4 compartments. A fifth compartment has been documented, but the clinical significance of this compartment has yet to be established. (Figure 3) The 5 compartments are as follows: 1. The anterior compartment is the space contained between the tibia, interosseous membrane, fibula, and anterior intermuscular septum. It includes the tibialis anterior muscle, the extensor digitum longus muscle, the extensor halluces longus muscle and the peroneus tertius muscle. The lateral compartment is contained by the anterior and posterior intermuscular septum, the fibula and the deep fascia. It includes the peroneus longus and brevis muscle, and the common peroneal nerve. The superficial posterior compartment is surrounded by the deep fascia of the leg, and contains the gastrocnemius, soleus, and plantaris muscle. The deep posterior compartment lies between the tibia, interosseous membrane, fibula and deep transverse fascia. Posterior tibial artery and vein and the tibial nerve, as well as the flexor digitorum and hallucis longus muscle, the popliteus muscle and the tibialis posterior muscle lie in this compartment. The tibialis posteriorcompartment is a more recently described subdivision of the deep posterior compartment. It consists of the tibialis posterior, which has been shown to have its own fascial layer. 99

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Foot The foot has 4 compartments: 1. The interosseous or intrinsic compartment: contains the 4 intrinsic muscles between the first en fifth metatarsals 2. The medial compartment: contains the abductor hallicus and the flexor hallicus brevis muscle. 3. The central or calcaneal compartment: contains the flexor digitorum brevis, quadrantus plantae, and the adductor hallicus. 4. The lateral compartment: contains flexor digiti minimi brevis and abductor digiti minimi. Upper leg The thigh contains 3 compartments: 1. The anterior compartment: rectus femoris muscle, semimembranosus, semitendinosus. 2. The posterior compartment: bisceps femoris muscle The medial compartment: adductor muscles. Surgical fasciotomy Lower leg fasciotomy The ‘two incision four compartment fasciotomy’ is the most reliable technique for treating or preventing a compartment syndrome in the lower leg. Understanding of the underlying anatomy and landmarks prior to incision are important, because distortion of the anatomy is likely to occur once the incision is made. The lateral incision (Figure 4) is made in a line one finger breath anterior to the edge of the fibula. In the swollen extremity the fibula can be difficult to palpate, so draw a line from the fibular head to the lateral malleolus to mark the course of the fibula. Scin incision should be generous and care should be taken not to injure the peroneal nerve. To find the intramuscular septum it may help to follow perforating vessels to the fascia as they enter at the intramuscular septum. The fascia’s of the anterior and lateral compartments are opened with scissors in an ‘H’ shaped fashion, extending the full length of the fascia compartments. Identification of the septum and the deep peroneal nerve ensures entry into both the lateral and anterior compartments. The medial incision (Figure 5) is made one finger breath posterior to the medial edge of the tibia, generous in length, and taking care of the great saphenous vein. Incision of the superficial fascia is opening the superficial posterior compartment. Entering into the deep posterior compartment asks blunt dissection of the soleus muscle from the tibia. Identification of the neurovascular bundle confirms entry into the deep posterior compartment. The muscles in each compartment should be assessed for viability: pink, bleeding when cut, contracting when stimulated. Fasciotomy of the foot All four compartments of the foot must be released. This can be done by 2 dorsal incisions and 1 medial incision. Upper leg fasciotomy Compartment syndrome of the thigh is uncommon because of the large volume that the thigh requires to increase the interstitial pressure. Case reports highlight the diverse mechanisms of injury: quadriceps tendon rupture, drug popping, crush injury, thigh contusion, aggressive resuscitation in trauma setting, aneurysm, following joint replacement, deep venous thrombosis, vascular injury (penetrating 100

e. When to consider fasciotomy for the endangered leg and how to do it, I. Van Herzeele

trauma and gunshot wounds) and fractures. It affects about 0.3% of trauma patients and a vascular injury has often contributed to development of this thigh compartment syndrome (57.7%). In 70% of the cases the compartments in the lower limb also need to be released. The fascial compartments of the thigh blend anatomically with the hip, allowing extravasation of blood or fluid outside the compartment. The compartments of the thigh are released through a single, long, lateral incision to access the anterior compartment directly and posterior compartment through the lateral intermuscular septum. After these compartments have been released, a repeat evaluation of the medial (adductor) compartment is performed. This is usually sufficient to relieve the pressure. If pressures remain elevated, the medial compartment is released via a separate incision. (Figure 6) Prognosis Compartment syndrome outcome depends on the time from injury to diagnosis, on time to intervention, and the technique used. Complications that may occur after fasciotomy are infection, hemorrhage, nerve damage e.g. superficial peroneal nerve and damage of the long saphenous vein. Rorabeck and Macnab reported almost complete recovery of limb function if fasciotomy was performed within 6 hours. Matsen found necrosis after 6 hours of ischemia, which currently is the accepted upper limit of viability. When fasciotomy was performed within 12 hours after the onset of acute compartment syndrome, Sheridan and Matsen reported that normal limb function was regained in 68% of patients. However, when fasciotomy was delayed 12 hours or longer, only 8% of patients had normal function. Thus, little or no return of function can be expected when the diagnosis and treatment are delayed. Some even advocate that it is better that if fasciotomy has been delayed for more than 12 hours, to explore the compartments via a small incision. If muscles are reacting on stimulation, the compartments should be released, if not – closed and allow for tissues scarring to happen in attempt to avoid infection and amputation. Long-term follow-up of patients who have undergone fasciotomies has shown good results, with a return to premorbid activity level. Pain also has been found to significantly improve. In the lower leg, the results of fasciotomies for posterior compartment syndrome are not as good as those for the anterior compartment. A possible explanation is that it is difficult to do a complete decompression of the deeper posterior compartment, because of the morbidity associated with this intervention. In general, early diagnosis with prompt appropriate treatment, results in good outcomes. Wound healing is an important issue. Berman et al. reported the “shoelace technique” in 1994 enabling approximation of the skin edges gradually; often resulting in successful wound closure without need for a skin graft. A matched series of 34 consecutive patients with and without (“shoelace technique”) VAC wound closure after fasciotomy were studied with the main parameter of interest: the time to “definitive closure” (delayed primary closure with sutures or skin graft coverage) of the wounds. Managed with VAC, the average time to definitive closure for both the lateral and the medial wounds was 6.7 days; as for the control patients, the average time to definitive closure was 16.1 days. This difference in time to wound closure between the VAC group and the non-VAC group was statistically significant. Experimental work has shown vacuum-assisted wound management to be effective in hastening the resolution of wound edema, enhancing local blood flow, promoting granulation tissue, and lowering bacterial colonization. 101

2. EMERGENCY VASCULAR PROCEDURES IN THE LOWER EXTREMITY

Conclusion Compartment syndrome is an emergency, because it may be limb threatening, cause renal impairment by rhabdomyolysis and can even be a life threatening. Acute compartment syndrome occurs when tissue pressure within a closed muscle compartment exceeds the perfusion pressure, progressing to venous congestion, and interfering with arterial blood flow, resulting in muscle and nerve ischemia. It typically occurs subsequent to a traumatic event such as fracture or acute limb ischemia. Late manifestations of compartment syndrome include extreme pain post procedure, absence of a distal pulse, hypoesthesia, extremity paresis, when the elevated tissue pressure eventually compromises arterial blood flow. If left untreated or if inadequately treated, the muscles and nerve within the compartment undergo ischemic necrosis. Severe cases may lead to renal failure by rhabdomyolysis. Diagnosis is made by clinical suspicion and/or tissue pressure measurement (>30mmHg). The definitive surgical therapy for compartment syndrome is emergent generous fasciotomy. The goal of decompression is restoration of muscle perfusion within 6 hours. Prognosis is very dependent on early recognition and treatment, and good when adequate fasciotomy is performed within 6 hours.

References

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•M asquelet, AC. Acute Compartment Syndrome of the Leg: Pressure Measurement and Fasciotomy. Orthop Traumatol Surg Res. 2010; 96(8): 913-7. •F rink M, Hildebrand F, Krettek C, Brand J, Hankemeier S. Compartment syndrome of the lower leg and foot. Clin Orthop Relat Res. 2010 Apr; 468(4): 940-50. • Yang CC, Chang DS, Webb LX. Vacuum-assisted closure for fasciotomy wounds following compartment syndrome of the leg. Journal of Surgical Orthopaedic Advances 2006, 15(1): 19-23. • American college of Surgeons. Injuries to the extremities: Compartment Syndrome and Fasciotomy. Anatomically based surgery for Trauma Course. Lab Manual Extremity Chapter 4: 1-13. •P earse MF, Harry L, Nanchahal J. Acute compartment syndrome of the leg. Fasciotomies must be performed early, but good surgical technique is important. BMJ. 2002 September 14; 325(7364): 557–558. •K anlic E, Pinski S, Verwiebe E, Saller J, Smith W Acute morbidity and complications of thigh compartment syndrome: a report of 26 cases. Patient Safety in Surgery 2010, 4:13 •H ori D, Noguchi K, Nomura Y, Lefor A, Tanaka H Small incision fasciotomy in a patient with compartment syndrome and peripheral arterial occlusive disease Ann Thorac Cardiovasc Surg 2012 •B erman SS, Schilling JD, McIntyre KE, Hunter GC, Bernhard VM Shoelace technique for delayed primary closure of fasciotomies Am J Surg 1994, 167(4): 435-6

2 Emergency vascular procedures in the lower extremity f. V enous emergency: Management of phlegmasia using mechanical, chemical, or surgical thrombectomy

Olivier Hartung

Service de Chirurgie Vasculaire, Centre Hospitalier Universitaire Nord, Marseille, France

Abstract If anticoagulation and venous compression are the gold standard treatment of deep venous thrombosis (DVT), a clot removal strategy can be proposed in order to reduce acute complications, recurrent DVT and late occurrence of postthrombotic syndrome. Different techniques are available, including surgical thrombectomy, catheter directed thrombolysis and pharmacomechanical thrombolysis. The latest recommendations recognized the interest of these treatments in selected cases of acute iliofemoral DVT. It was also pointed out that iliocaval obstructive lesions should be treated by concomitant stenting. Introduction Deep venous thrombosis (DVT) of the lower limbs is an acute condition which main complications are extension, phlegmasia cerulea, pulmonary embolism (PE) and at long term recurrence and postthrombotic syndrome (PTS). Anticoagulation and venous compression are always needed, but, in some cases, an interventional treatment can be performed in order to reduce the risk of occurrence of complications. Its goal is to remove the thrombus while avoiding fragmentation and embolization in order to maintain venous patency and preserve valve function. We will herein review the techniques, indications and results of the clot removal strategies for iliofemoral DVT. Definitions [1] Acute DVT: venous thrombosis occurred within the last 14 days. Iliofemoral DVT: complete or partial thrombosis of any part of the iliac vein and/or the common femoral vein, with or without associated femoropopliteal DVT. Femoropopliteal DVT: complete or partial thrombosis of the popliteal vein, femoral vein, and/or deep femoral vein. Proximal DVT: complete or partial thrombosis of the popliteal vein, femoral vein (formerly known as the superficial femoral vein), deep femoral vein, common femoral vein, iliac vein, and/or inferior vena cava (IVC). 103

2. EMERGENCY VASCULAR PROCEDURES IN THE LOWER EXTREMITY

Techniques All patients should be under heparin and have compression therapy since the diagnosis of DVT is made. Pretreatment workup All patients candidate for a thrombus removal strategy should have an imaging work-up in order to explore the thrombosis to determine the cephalad extension of the thrombus, the age of the thrombus and search for anatomic variation and for underlying chronic lesions (May-Thurner syndrome, post thrombotic lesions…) (figure 1). It should also explore the pulmonary arteries for PE. It should also search for contra indication to the technique, mainly malignant disease and lesions at risk of bleeding (cerebral arterio-venous malformations, cerebral aneurysms…). The best way to obtain these informations is to perform an angio CT scan. Duplex scan is also of value in that condition to have infra inguinal data on the extension and the age of the clot. In case of pregnancy MRI can replace CT scan in order to avoid irradiation. Moreover thrombophilic status should be explored. Figure 1: angio CT scan showing a thrombosed left common iliac vein with a severe stenosis of its distal part by compression of the right common iliac artery (black arrow) Catheter directed thrombolysis (CDT) (figure 2) Catheterization access approach is mostly performed on the popliteal vein. It is recommended to perform it under ultrasonographic guidance in order to reduce the risk of bleeding due to arterial puncture. Infusion is commonly performed through a multiple-side-hole catheter embedded in the thrombus and lysis is monitored at venography. Different protocols of CDT exist depending on the thrombolytic agent, the speed of infusion and its duration. The Society of Interventional Radiology suggested in 2009 [1] the use of urokinase 120,000 to 180,000 units/hour, tissue plasminogen activator 0.5 to 1.0 mg/hour, reteplase 0.25 to 0.75 units/hour, or tenecteplase 0.25 to 0.5 mg/hour. For best results, the drug should be diluted to allow infusion of higher fluid volumes (generally 25–100 mL/h), which maximizes dispersion of the drug within the thrombus. The use of a lacing dose or a “frontloaded” regimen in which a higher dose is used for the first few hours of treatment is optional. The procedure should be ended when lysis is completed or if no additional lysis is achieved within the last 12 hours. Intravenous heparin therapy must be administrated during and after the procedure (100-500 IU/hr). Laboratory parameters of surveillance are APTT, thrombin time, fibrinogen, antithrombin, fibrin, D-Dimer, hemoglobin and platelets. Depending on prior anticoagulant treatment INR or anti-Xa was measured for adjustment of heparin starting. The patients are monitored in an intensive care unit or not. Figure 2: Thrombolysis for acute left femoroiliac DVT in a patient who previously had left common iliac vein stenting for postthrombotic disease A: initial phlebography B: phlebography 10 minutes after injection of a bolus of 300000 UI of urokinase C: phlebography after 4 hour of CDT : presence of residual adherent clot which was treated by thromboaspiration and stenting. 104

f. Venous emergency: Management of phlegmasia using mechanical, chemical, or surgical thrombectomy, O. Hartung

Pharmaco-mechanical thrombectomy (PMT) In this modality, a mechanical device is added to thrombolysis. Different types of catheter can be used: - thromboaspiration using the Venturi effect or Vortex: the Angiojet (Medrad, USA), the Amplatz Thrombectomy device (Microvena, USA), the Oasis thrombectomy system (Boston Scientific, Natick, USA), the Rotarex and Aspirex (Straub Medical, Wangs, Switzerland), the Hydrolyser (Cordis, Warren, USA). - mechanical fragmentation of the clot: the Trellis peripheral infusion system (Covidien, USA) and the Arrow-Trerotola thrombectomy device (Arrow International, Reading, USA). - ultrasound accelerated thrombolysis: the EKOS EkoSonic Endovascular System (EKOS corporation, USA) using high frequency, low power sound waves which makes the thrombus more permeable and allows the thrombolytic to penetrate deeper. The goal of PMT is to use a mechanical effect in order to accelerate clot dissolution and reduce the quantity of thrombolytic agent. These procedures are commonly performed through a popliteal approach. Surgical thrombectomy (ST) [2] In case of femoroiliac DVT, surgical approach of the common femoral vein is performed and surgical loops are passed around the veins. Then an intravenous heparin bolus is given and a venotomy is performed at the inferior and lateral side of the sapheno femoral junction. At this moment, the anesthesiologists are asked to use a positive end of expiration pressure (PEEP) of 10 cm H2O during the whole thrombectomy time in order to prevent from PE. Iliac thrombectomy is performed using a large Fogarty catheter cautiously (figure 3). Limb, popliteal and femoral veins thrombectomy is then performed without using any endovenous instrumentation. All the tapes are tightened and sturdy massage of the limb and the tight is performed, starting at the foot to unstick the clot. The tapes are briefly untightened to release the clot and the maneuver is repeated until no more clot come back. The venotomy is then closed using a 6/0 polypropylene running suture. The great saphenous vein is sectioned at 10cm of the sapheno-femoral junction in order to be used for construction of an arterio-venous fistula (AVF) with a latero-terminal anastomosis between the superficial femoral artery and the saphenous vein. The AVF is closed 6 weeks later either by surgical approach or percutaneous embolization with coils or the Amplatzer device. In case of IVC involvement, the IVC is approached through a right transperitoneal subcostal route. Figure 3: surgical thrombectomy: A: iliac thrombectomy using a large Fogarty catheter B: view of the iliac clot C: the venotomy was closed and an arteriovenous fistula was constructed between the great saphenous vein and the superficial femoral artery Stenting Stenting is used to treat lesions that could compromise patency after a clot removal strategy. It is indicated in case of May-Thurner syndrome but also in case of persistence of adherent clot, underlying post thrombotic obstructive disease, extrinsic compression (retroperitoneal fibrosis, tumorsâ&#x20AC;Ś). It must be performed during the procedure using large (14-18 mm in diameter in iliac veins, 20-24 mm in IVC) and long (at least 6cm) self-expanding stents.

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Figure 4: Stenting at the end of a surgical thrombectomy of a left femoroiliac DVT: A: iliocavography showing a severe stenosis at the end of the left common iliac vein B: result after stenting using two 16 mm Wallstent. C: iliocavography through the arteriovenous fistula at 6 weeks D: arteriography after deployment of an Amplatzer in the AVF: closure of the AVF IVC filters Their goal is to avoid PE. They are used since their introduction by Greenfield in 1973. The optional filters developed during the 90’s have the advantage of removability when there are no more indications to keep them in place.

Literature review Surgical thrombectomy (ST) There was no mortality and no symptomatic PE in recent series reported by experienced groups (table 1) [2-7]. Eklöf reported a 1% mortality rate on 203 consecutive patients [8]; both deaths were not related to the thrombosis. Plate [9] reported 45% of positive perfusion scan at the admission and 20% of additional defects postoperatively, but none when an AVF was constructed. In a report with a mean follow up of more than eight years, we reported patency and valvular competence rates of respectively 84% and 80% at five years and 84% and 56% at 13 years [10]. These results are consistent with the literature review of Eklöf [8]. Plate reported before the era of stenting a prospective randomized study comparing ST with AVF and anticoagulation (N = 31) to medical treatment only (N = 32) [11]. No early death occurred but one medically treated patient had pulmonary embolism. In the surgical group the rate of early reocclusion was 13%. Ten years follow-up showed reduced leg swelling and ulcer rates, less severe sequelae and less iliac vein occlusion in the surgical group while there was more reflux at duplex scan in the medical group [12]. In our experience [2], 38% of patients were contraindicated for thrombolysis due high risk of bleeding complications. The median length of stay was 8 days. Table 1: results of the recent publications on surgical thrombectomy [2-7] Author

Acute results

Blattler 2004 (3)

Schwarzbach 2005 (4)

No major bleeding No symptomatic PE No symptomatic PE

Husmann 2007 (5)

Hartung 2008 (2)

Holper 2010 (6) Lindow 2010 (7)

106

FU M 12 21

No major bleeding No symptomatic PE 1 major bleeding (IVC) No symptomatic PE

10% femoral hematoma No symptomatic PE

Late results N recurrence No new PTS PP 80% All patients C0-3 PP 82% Reflux 11% PP 79%, SP 86% Reflux 24% Median VDS 1 VCSS 3 PP 74%, SP 84% Reflux 2% No patient C4-6 PP 75% C2-4 20%, C5-6 : 0%

f. Venous emergency: Management of phlegmasia using mechanical, chemical, or surgical thrombectomy, O. Hartung

FU: follow-up; M: month; PE: pulmonary embolism; IVC: inferior vena cava; NS: not specified; PP: primary patency; SP: secondary patency; PTS: postthrombotic syndrome; C: clinical class of CEAP. Moreover Pillny [13] reported 97 cases of venous thrombectomy during pregnancy or after delivery without maternal death and one postoperative fetal death. After a mean follow up of six years, patency rate was 89.5%, and 56.3% of the patients had no post-thrombotic syndrome, while only 3.5% had leg ulceration. Catheter directed thrombolysis (CDT) In 2004, The Cochrane PVD group [14] reviewed all the publications describing randomized controlled trials of thrombolysis versus anticoagulation for acute DVT. Complete clot lysis and improvement in venous patency occurred significantly more often with thrombolysis at early and late follow-up. Significantly less post-thrombotic syndrome and less leg ulceration occurred in those receiving thrombolysis. Venous function was improved at late follow up, but not significantly. Out of 668 patients, those receiving thrombolysis had significantly more bleeding complications but their incidence reduced over time with introduction of stricter selection criteria. There was no effect on mortality but no conclusions can be drawn on PE and DVT recurrence rates. The results of the more recent trials on CDT are summarized in table 2. Comparative and prospective randomized trials proved the superiority of CDT over medical treatment for femoro-iliac DVT. Table 2: results of recent trial on CDT. Author Year (ref) AbuRahma 2001 (15)

18 CDT 33 BMT Elsharawy 2002 (16) 18 CDT 17 BMT Laiho 2004 (17) 16 CDT 16 STL Ogawa 2005 (18) 14 CDT 10 CDT + IPC + filter Park 2008 (19) 34 CDT

Baekgaard 2010 (20)

101 CDT

Enden 2012 (21)

101 CDT 108 BMT

Acute results PE 0% / 6% Major bleeding 11%/6% PE 0 % / 6% No bleeding Bleeding 38% / 44% No symptomatic PE No bleeding Lysis < in CDT alone New PE at V/Q scan 25% Bleeding 6% Death/PE : 0 Major bleeding 0 20 bleeding (3 major)

FU M 51 6

NS 47 50 24

Late results Patency 69% / 18% CEAP 0-2 78% / 30% No obstruction 72% / 12% Reflux 11% / 41% Obstruction 31% / 50% CEAP 0-2 62% / 31% Obstruction 83% / 43% Reflux 33% / 21% VDS > in CDT alone PTS 21% Rethrombosis 32% 82% patency without reflux No C4-6, 7 C3 IF Patency 65% / 47% PTS 41% / 55%

FU: follow-up; M: month; PE: pulmonary embolism; CDT: catheter directed thrombolysis; BMT: best medical treatment; STL: systemic thrombolysis; IPC: intermittent pneumatic compression; V/Q scan: ventilation/perfusion lung scan Pharmacomechanical thrombectomy (PMT) Table 3 summarizes the results of the main trials on PMT [22-34]. Many authors showed that the procedure length, the hospital length of stay, the amount of thrombolytics and the per-patient cost of therapy were reduced with PMT when compared to CDT. Moreover PMT can be performed in patients with contraindications to CDT.

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Table 3: results of trial on PMT Author Year (ref) Kim 2006 (22) Cynamon 2006 (23) Lin 2006 (24)

Acute results

14p/19ll A 23p/26ll CDT

Complete lysis 84%/80% Major bleeding 5%/8% Lysis II/III 79% Major bleeding 8% Lysis III 75%/70% A : major bleeding/LOS reduced No symptomatic PE No major bleeding

24 A 52 A 46 CDT

Lee 2006 (25)

25 PTD

O’Sullivan 2007 (26)

19 T 30 (18T/12A) T CDT 47 (60% ll) Ekos 43 p (81% ll) T/A/T+A 14 A

No symptomatic PE No major bleeding No symptomatic PE No major bleeding Lysis II/III 93%/79% Major bleeding 0%/8.5% 70% complete lysis Major bleeding 3.8% No symptomatic PE No major bleeding No major bleeding

2024 p/ 2203 l T 25 ATD or R

No symptomatic PE No major bleeding Lysis II/III 100% No symptomatic PE No systemic bleeding PE 0%/4% (1 lethal) Bleeding 2%/1% LOS 2.7/5.8

Arko 2007 (27) Hilleman 2008 (28) Parikh 2008 (29) Rao 2009 (30) Gasparis 2009 (31) Dietzek 2010 (32) Shi 2011 (33) Sharifi 2012 (34)

91 T or A 92 BMT

FU M

Late results

PP 68%/64%

PP 85% Clinical success 92% Reflux 8% aPP 100%

1 6

Patency 90% Competence 88%

5 24

95% without rethrombosis 21% obstruction 36% reflux 93% VDS <1 VCSS <5

1 PTS

Recurrence 4.5%/16% PTS 7%/30%

FU: follow-up; p: patients; l: limbs; PE: pulmonary embolism; BMT: best medical treatment; PEVI: percutaneous endovenous intervention; T: Trellis; A: Anjiojet; T+A: Trellis + Anjiojet; PP: primary patency; aPP: assisted primary patency; ll: lower limb; ATD: Amplatz thrombectomy device; R: Rotarex; PTD: Arrow-Trerotola percutaneous thrombectomy device; LOS: length of stay IVC filter during clot removal strategy If there are no indications for IVC filters during or after surgical thrombectomy, they are often deployed while using the endovascular procedures for clot removal, most of the time through an internal jugular vein percutaneous access. Kölbel [35] reviewed the phlebography of 40 consecutive patients treated by CDT and found emboli in the filter in 45% but none had clinically symptomatic PE ; emboli were less frequent in patients with hypercoagulable disorder. Sharifi [36] published in 2012 the results of the Filter – PEVI Trial, a prospective randomized study regarding the use of IVC filter during percutaneous endovenous treatment of proximal DVT. Despite many bias, it showed that the use of IVC filter reduces the risk of PE during interventional treatment of proximal DVT and that predictors of iatrogenic PE were PE at admission; involvement of two or more adjacent venous segments with acute thrombus; inflammatory form of DVT and vein diameter of ≥7 mm with preserved architecture. Recommendations Clot removal strategies: Different societies published their recommendations regarding the use of a clot removal strategy in 2011 and 2012 [37-39] which are summarized in table 4. The American Heart Association [37], the American Venous forum and the Society of Vascular Surgery [38] recognize the interest of the interventional treatment in case of young patients at low risk of bleeding 108

f. Venous emergency: Management of phlegmasia using mechanical, chemical, or surgical thrombectomy, O. Hartung

complications with acute iliofemoral DVT to prevent PTS. Moreover they strongly suggest the use of these techniques in case of circulatory compromise due to the DVT. The American College of Chest Physicians [39] made more restrictive recommendations but were addressed to proximal DVT which include iliofemoral DVT but also popliteal and femoral DVT. Table 4: recommendations for clot removal strategies in acute iliofemoral DVT [37-39] Clot removal strategies for acute IF DVT AHA 2011 (37) IFDVT with limb-threatening circulatory compromise Transfer in center with expertise if indications are present Reasonable in case of - rapid thrombus extension despite anticoagulation - symptomatic deterioration despite anticoagulation First line treatment to prevent PTS in selected patients at low risk of bleeding Surgical thrombectomy by experienced surgeons Systemic fibrinolysis should not be given routinely No CDT/PMT for chronic symptoms (>21D) or high risk of bleeding complications AVF / SVS 2012 (38) Ambulatory patients with good functional capacity and first episode of IF DVT <14D Limb-threatening ischemia due to IF DVT PMT more than CDT if resources available ST if thrombolytic therapy is contraindicated AACP 2012 (39) Proximal DVT : anticoagulant over CDT, PMT, systemic thrombolysis and ST Patients who are most likely to benefit from interventional treatment who attach a high value to prevention of PTS, and a lower value to the initial complexity, cost, and risk of bleeding with these treatments, are likely to choose interventional therapy over anticoagulation alone. In case of thrombus removal, anticoagulant therapy at same intensity and duration

Grade I/C I/C IIa / C IIa / B IIa / B IIb / B III / A III / B

2C 1A 2C 2C 2C

IFDVT: iliofemoral deep venous thrombosis; CDT: catheter directed thrombolysis; PMT: pharmacomechanical thrombectomy; D: days; ST: surgical thrombectomy; PTS: postthrombotic syndrome. Stenting: AHA 2011 guidelines: s tent placement in the iliac vein to treat obstructive lesions after a thrombus removal strategy for acute DVT is reasonable (Class IIa; Level of Evidence C) [37]. AVF/SVS 2012 Guidelines: self-expanding stents should be used to treat ilio-caval obstructive lesions during any kind of thrombus removal strategy for acute DVT (grade 1C) [38]. IVC filters There are no specific recommendations for deployment of IVC filters during a clot removal strategy. Conclusion The interventional treatment of acute iliofemoral DVT is the best way to prevent postthrombotic syndrome. Different modalities are available and the choice must be done according to the centerâ&#x20AC;&#x2122;s experience, the respective contra-indications and the evaluation of the risk of the procedure. Stenting should be used to treat the obstructive ilio-caval lesions.

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References

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1. Vedantham S, Thorpe PE, Cardella JF, Grassi CJ, Patel NH, Ferral H, Hofmann LV, Janne d’Othée BM, Antonaci VP, Brountzos EN, Brown DB, Martin LG, Matsumoto AH, Meranze SG, Miller DL, Millward SF, Min RJ, Neithamer CD Jr, Rajan DK, Rholl KS, Schwartzberg MS, Swan TL, Towbin RB, Wiechmann BN, Sacks D; CIRSE and SIR Standards of Practice Committees. Quality improvement guidelines for the treatment of lower extremity deep vein thrombosis with use of endovascular thrombus removal. J Vasc Interv Radiol. 2009 ; 20 : S227-39. 2. Hartung O, Benmiloud F, Barthelemy P, Dubuc M, Boufi M, Alimi YS. Late results of surgical venous thrombectomy with iliocaval stenting. J Vasc Surg. 2008 ; 47 : 381-7. 3. Blattler W, Heller G, Largiader J, Savolainen H, Gloor B, Schmidli J. Combined regional thrombolysis and surgical thrombectomy for treatment of iliofemoral vein thrombosis. J Vasc Surg 2004 ; 40 : 620-5. 4. Schwarzbach MH, Schumacher H, Bockler D, Furstenberger S, Thomas F, Seelos R, et al. Surgical thrombectomy followed by intraoperative endovascular reconstruction for symptomatic iliofemoral venous thrombosis. Eur J Vasc Endovasc Surg 2005 ; 29 : 58-66. 5. Husmann MJ, Heller G, Kalka C, Savolainen H, Do DD, Schmidli J, et al. Stenting of common iliac vein obstructions combined with regional thrombolysis and thrombectomy in acute deep vein thrombosis. Eur J Vasc Endovasc Surg 2007 ; 34 : 87-91. 6. Holper P, Kotelis D, Attigah N, Hyhlik-Durr A, Bockler D. Longterm results after surgical thrombectomy and simultaneous stenting for symptomatic iliofemoral venous thrombosis. Eur J Vasc Endovasc Surg 2010 ; 39 : 349-55. 7. Lindow C, Mumme A, Asciutto G, Strohmann B, Hummel T, Geier B. Long-term results after transfemoral venous thrombectomy for iliofemoral deep venous thrombosis. Eur J Vasc Endovasc Surg 2010 ; 40 : 134-8. 8. Eklöf B, Negle´n P. Venous thrombectomy. In: Raju S, Villavicencio JL, eds. Baltimore, MD, USA: Williams & Wilkins 1997:512–527. 9. Plate G, Ohlin P, Eklöf B. Pulmonary embolism in acute iliofemoral venous thrombosis. Br J Surg 1985; 72:912–915. 10. Juhan CM, Alimi YS, Barthelemy PJ, Fabre DF, Riviere CS. Late results of iliofemoral venous thrombectomy. J Vasc Surg 1997 ; 25 : 417–422. 11. P late G, Einarsson E, Ohlin P, Jensen R, Qvafordt P, Eklöf B. Thrombectomy with temporary arteriovenous fistula: The treatment of choice in acute iliofemoral venous thrombosis. J Vasc Surg 1984 ; 1 : 867-76. 12. Plate G, Eklöf B, Norgren L, Ohlin P, Dahlström JA. Venous thrombectomy for iliofemoral vein thrombosis--10-year results of a prospective randomised study. Eur J Vasc Endovasc Surg. 1997 ; 14 : 367-74. 13. Pillny M, Sandmann W, Luther B, Gerhardt A, Zotz RB, et al. Deep venous thrombosis during pregnancy and after delivery: indications for and results of thrombectomy. J Vasc Surg 2003 ; 37:528–532. 14. Watson L, Armon M. Thrombolysis for acute deep vein thrombosis. Cochrane Database Syst Rev 2004; 4:CD002783. 15. AbuRahma AF, Perkins SE, Wulu JT, Ng HK. Iliofemoral deep vein thrombosis: conventional therapy versus lysis and percutaneous transluminal angioplasty and stenting. Ann Surg. 2001 Jun;233(6):752-60. 16. Elsharawy M, Elzayat E. Early results of thrombolysis vs anticoagulation in iliofemoral venous thrombosis. A randomised clinical trial. Eur J Vasc Endovasc Surg. 2002 ; 24 : 209-14. 17. Laiho MK, Oinonen A, Sugano N, Harjola VP, Lehtola AL, Roth WD, Keto PE, Lepäntalo M. Preservation of venous valve function after catheter-directed and systemic thrombolysis for deep venous thrombosis. Eur J Vasc Endovasc Surg. 2004 ; 28 : 391-6. 18. Ogawa T, Hoshino S, Midorikawa H, Sato K. Intermittent pneumatic compression of the foot and calf improves the outcome of catheter-directed thrombolysis using low-dose urokinase in patients with acute proximal venous thrombosis of the leg. J Vasc Surg. 2005 ; 42 : 940-4. 19. Park YJ, Choi JY, Min SK, Lee T, Jung IM, Chung JK, Chung JW, Park JH, Kim SJ, Ha J. Restoration of patency in iliofemoral deep vein thrombosis with catheter-directed thrombolysis does not always prevent post-thrombotic damage. Eur J Vasc Endovasc Surg. 2008 ; 36 : 725-30. 20. Baekgaard N, Broholm R, Just S, Jørgensen M, Jensen LP. Long-term results using catheter-directed thrombolysis in 103 lower limbs with acute iliofemoral venous thrombosis. Eur J Vasc Endovasc Surg. 2010 ; 39 : 112-7. 21. Enden T, Haig Y, Kløw NE, Slagsvold CE, Sandvik L, Ghanima W, Hafsahl G, Holme PA, Holmen LO, Njaastad AM, Sandbæk G, Sandset PM; CaVenT Study Group. Long-term outcome after additional catheter-directed thrombolysis versus standard treatment for acute iliofemoral deep vein thrombosis (the CaVenT study): a randomised controlled trial. Lancet. 2012 ; 379 : 31-8. 22. Kim HS, Patra A, Paxton BE, Khan J, Streiff MB. Adjunctive percutaneous mechanical thrombectomy for lower-extremity deep vein thrombosis: clinical and economic outcomes. J Vasc Interv Radiol. 2006 ; 17 : 1099-104. 23. Cynamon J, Stein EG, Dym RJ, Jagust MB, Binkert CA, Baum RA. A new method for aggressive management of deep vein thrombosis: retrospective study of the power pulse technique. J Vasc Interv Radiol. 2006 ; 17 : 1043-9. 24. Lin PH, Zhou W, Dardik A, Mussa F, Kougias P, Hedayati N, et al. Catheter-direct thrombolysis versus pharmacomechanical thrombectomy for treatment of symptomatic lower extremity deep venous thrombosis. Am J Surg 2006 ; 192 : 782-8. 25. Lee KH, Han H, Lee KJ, Yoon CS, Kim SH, Won JY, et al. Mechanical thrombectomy of acute iliofemoral deep vein thrombosis with use of an Arrow-Trerotola percutaneous thrombectomy device. J Vasc Interv Radiol 2006; 17 : 487-95. 26. O’Sullivan GJ, Lohan DG, Gough N, Cronin CG, Kee ST. Pharmacomechanical thrombectomy of acute deep vein thrombosis with the Trellis-8 isolated thrombolysis catheter. J Vasc Interv Radiol. 2007 ; 18 : 715-24. 27. Arko FR, Davis CM 3rd, Murphy EH, Smith ST, Timaran CH, Modrall JG, Valentine RJ, Clagett GP. Aggressive percutaneous mechanical thrombectomy of deep venous thrombosis: early clinical results. Arch Surg. 2007 ; 142 : 513-8.

f. Venous emergency: Management of phlegmasia using mechanical, chemical, or surgical thrombectomy, O. Hartung

28. Hilleman DE, Razavi MK. Clinical and economic evaluation of the Trellis-8 infusion catheter for deep vein thrombosis. J Vasc Interv Radiol. 2008 ; 19 : 377-83. 29. Parikh S, Motarjeme A, McNamara T, Raabe R, Hagspiel K, Benenati JF, et al. Ultrasound-accelerated thrombolysis for the treatment of deep vein thrombosis: initial clinical experience. J Vasc Interv Radiol 2008;19(4):521e8. 30. Rao AS, Konig G, Leers SA, Cho J, Rhee RY, Makaroun MS, Chaer RA. Pharmacomechanical thrombectomy for iliofemoral deep vein thrombosis: an alternative in patients with contraindications to thrombolysis. J Vasc Surg. 2009; 50: 1092-8. 31. Gasparis AP, Labropoulos N, Tassiopoulos AK, Phillips B, Pagan J, Cheng Lo, Ricotta J. Midterm follow-up after pharmacomechanical thrombolysis for lower extremity deep venous thrombosis. Vasc Endovascular Surg. 2009 ; 43 : 61-8 32. Dietzek AM. Isolated pharmacomechanical thrombolysis of deep venous thrombosis utilizing a peripheral infusion system: Manuf. Int Angiol. 2010 ; 29 : 308-16. 33. Shi HJ, Huang YH, Shen T, Xu Q. Percutaneous mechanical thrombectomy for acute massive lower extremity deep venous thrombosis. Surg Laparosc Endosc Percutan Tech. 2011 ; 21 : 50-3. 34. Sharifi M, Bay C, Mehdipour M, Sharifi J; TORPEDO Investigators. Thrombus Obliteration by Rapid Percutaneous Endovenous Intervention in Deep Venous Occlusion (TORPEDO) trial: midterm results. J Endovasc Ther. 2012 ; 19 : 273-80. 35. KĂślbel T, Alhadad A, Acosta S, Lindh M, Ivancev K, GottsĂ¤ter A. Thrombus embolization into IVC filters during catheterdirected thrombolysis for proximal deep venous thrombosis. J Endovasc Ther. 2008 ; 15 : 605-13. 36. Sharifi M, Bay C, Skrocki L, Lawson D, Mazdeh S. Role of IVC filters in endovenous therapy for deep venous thrombosis: the FILTER-PEVI (filter implantation to lower thromboembolic risk in percutaneous endovenous intervention) trial. Cardiovasc Intervent Radiol. 2012 ; 35 : 1408-13. 37. Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ, Jenkins JS, Kline JA, Michaels AD, Thistlethwaite P, Vedantham S, White RJ, Zierler BK; American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; American Heart Association Council on Peripheral Vascular Disease; American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011 ; 123 : 1788-830. 38. Meissner MH, Gloviczki P, Comerota AJ, Dalsing MC, Eklof BG, Gillespie DL, Lohr JM, McLafferty RB, Murad MH, Padberg F, Pappas P, Raffetto JD, Wakefield TW; Society for Vascular Surgery; American Venous Forum. Early thrombus removal strategies for acute deep venous thrombosis: clinical practice guidelines of the Society for Vascular Surgery and the American Venous Forum. J Vasc Surg. 2012 ; 55 : 1449-6. 39. Kearon C, Akl EA, Comerota AJ, Prandoni P, Bounameaux H, Goldhaber SZ, Nelson ME, Wells PS, Gould MK, Dentali F, Crowther M, Kahn SR; American College of Chest Physicians. Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 ; 141 : e419S-94S.

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3. Visceral artery emergencies a. E mbolic occlusion of the SMA: endovascular or surgical treatment of acute mesenteric ischemia

Jörg Teßarek

St. Bonifatius Hospital, Lingen, Germany

Introduction Embolic events in the mesenteric vasculature with subsequent acute mesenteric ischemia often show fatal outcome due to misinterpretation of the clinical symptoms and delayed or not appropriately coordinated therapeutic response. The estimated probability for a correct diagnose after the initial diagnostic steps is only 30% which has been shown by autopsy results. The question that remains unanswered is: What is the optimal pathway for a patient presenting with an acute abdomen and the supposed diagnose of acute mesenteric ischemia. Is an endovascular approach feasible and until when is it worthwhile to achieve beneficial results. Or whether a laparotomy with or without vascular reconstruction or bowel resection remains the gold standard. Methods A web based literature research including peer review publications and congressional presentations was made using the key words: “acute mesenteric ischemia”, “embolic occlusion of the SMA”, “surgery” and “endovascular approach”. The treatment options and their results were compared to figure out whether a change of paradigms from surgery to endovascular or hybrid solutions for this disease entity could be recommended based on the published study or single center results. Results More than 240 publications were reviewed. Until now there is no published randomized or prospective trial that compares the results of open surgery and endovascular treatment for acute mesenteric ischemia related to embolic occlusion of the superior mesenteric artery. The vast majority of publications presents retrospective analyses, single center experiences or case reports and mandate a dedicated pathway for the supposed diagnose of acute mesenteric ischemia. The patient should undergo a strict diagnostic protocol with ultrasound, blood sample to screen for bowel ischemia and CT-angiography with high resolution imaging. Several recent publications mandate a sophisticated approach with either an endovascular treatment for those patients with no peritoneal signs but immediate surgery for patients with evidence of bowel infarction or necrosis. Spray thrombolysis with aspiration using sheaths with detachable valves, aspiration devices like the Medrad Angiojet™ system or the Rotarex™ has shown to be feasible with a survival rate of up to 90% independent from the time window between onset of symptoms, admission to the hospital and commencing of treatment. 115

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Conclusion The endovascular techniques can be feasible for revascularisation of acute visceral artery occlusions as long as no peritoneal signs are present, otherwise a surgical approach must be recommended. The implementation of a dedicated pathway and the use of high quality diagnostic imaging such as high resolution multiphase CT-angiography turned out to be crucial for decision making. The availability of the surgical and endovascular expertise in one place is an additional decisive factor. Acute embolic mesenteric occlusions and the age independent comorbidity of the patients mandate a multidisciplinary approach with treatment of the bowel ischemia and the underlying reason for embolism. Key Words: acute mesenteric ischemia, rotational thrombectomy, aspiration thrombectomy, thrombolysis References 1. Acosta S, Ogren M, Sternby NH, Bergqvist D, Björck M.; Incidence of acute thrombo-embolic occlusion of the superior mesenteric artery--a population-based study; Eur J Vasc Endovasc Surg. 2004 Feb;27(2):145-50) 2. Acosta S.; Epidemiology of mesenteric vascular disease: clinical implications; Semin Vasc Surg. 2010 Mar;23(1):4-8. 3. Vivek Srivastava, Vaibhav Pandey and Somprakas Basu; Intestinal Ischemia and Gangrene in “Gangrene - Current Concepts and Management Options”; Edited by Dr. Alexander Vitin; ISBN 978-953-307-386-6; Publisher InTech, August 2011 4. Misawa S, Sakano Y, Muraoka A, Yasuda Y, Misawa Y; Septic embolic occlusion of the superior mesenteric artery induced by mitral valve endocarditis; Ann Thorac Cardiovasc Surg. 2011;17(4):415-7 5. Wyers MC; Acute mesenteric ischemia: diagnostic approach and surgical treatment; Semin Vasc Surg. 2010 Mar;23(1):9-20 6. Türkbey B, Akpinar E, Cil B, Karçaaltincaba M, Akhan O.; Utility of multidetector CT in an emergency setting in acute mesenteric ischemia. Diagn Interv Radiol 2009;15:256-61 7. Grothues F, Bektas H, Klempnauer J.; Surgical therapy of acute mesenteric ischemia; Langenbecks Arch Chir. 1996;381(5):275-82; [Article in German] 8. S. R. Sheeran, S. J. A. Sclafani; Successful intraarterial recombinant tissue plasminogen activator therapy for acute embolic occlusion of the superior mesenteric artery; Emergency Radiology, June 2001, Volume 8, Issue 3, pp 152-155 9. Acosta S, Sonesson B, Resch T; Endovascular therapeutic approaches for acute superior mesenteric artery occlusion; Cardiovasc Intervent Radiol. 2009 Sep; 32(5):896-905 10. Björnsson S, Björck M, Block T, Resch T, Acosta S; Thrombolysis for acute occlusion of the superior mesenteric artery; J Vasc Surg. 2011 Dec;54(6):1734-42. 11. Moore M, McSweeney S, Fulton G, et al. Reperfusion hemorrhage following superior mesenteric artery stenting.Cardiovasc Intervent Radiol. 2008;31(suppl 2):S57-S61

Table 1: Risks for arterial or venous occlusion in AMI Arterial embolism or thrombosis

Venous thrombosis

Pre-existing Cardiac disease:

Portal hypertension

- atrial fibrillation

Inflammation

- recent myocardial infarction

Postop period, trauma

- congestive heart failure

Prothrombotic state

digitalis therapy

Chronic renal failure

Previous arterial emboli

Congestive heart failure

Hypercoagulable state Hypovolemia, shock

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a. Embolic occlusion of the SMA, Jörg Teßarek

Figure 1: T he figure displays a potential pathway in case of AMI. The short description of peritoneal signs include free abdominal fluid or gas and mural gas in the bowel or intrahepatic gas. With these signs of progressive ischemia surgery is mandatory.

Figure 2: T his picture shows the access to the SMA after exposure of the mesenteric root and the vessels origin (arrow). The clot or embolic debris can be removed by using an retrograde and antegrade access with a Fogarthy™ catheter and stenting of the origin of the artery can be performed, if necessary. Therefore a completion angiography is mandatory. The light blue area indicates the pancreas, the gray areas represent retractors.

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Figure 3: T he images show an occlusion of all mesenteric arteries in a patient presenting with acute onset of abdominal pain. 4 weeks prior to the acute event the patient was operated for supposed acute cholecystitis (clips in b, see arrow). After CT-angiography a transcubital approach was chosen to recanalise the SMA. Aspiration and thrombolysis was performed via a 6F sheath with a detachable valve. After aspiration a balloon expandable stent was placed and further thrombolysis was performed for residual thrombi. (f) and (g) display a residual stenosis at one of the segment branches which was accepted. The patient showed slightly elevated lactic acid serum levels during the procedure. The thrombolysis was stopped after 24 hours with no signs of peritonitis or reperfusion syndrome such as abdominal compartment.

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3. Visceral artery emergencies b. S pontaneous haemorrhage from liver and renal tumours

Michael Wholey

Christus Santa Rosa Medical System, San Antonio, USA

Introduction Spontaneous hemorrhage into the subcapsular or perinephric space is usually the result of rupture of a renal tumor, such as angiomyolipoma or renal cell carcinoma (RCC) [1]. In most cases, CT permits the radiologist to clearly differentiate a mass from the surrounding hematoma. The diagnosis of an underlying angiomyolipoma is based on the identification of low-attenuation areas of fat in a large heterogeneous mass. On contrast-enhanced CT, the presence of a solid mass with less contrast enhancement than the adjacent renal parenchyma suggests RCC (Refer to Figure 1 a, b).

Figure 1 a, b shows a renal cell carcinoma left kidney with heterogenous contrast enhancement, less than surrounding renal parenchyma. Axial and coronal reconstructions. However, small tumors may initially be obscured by the hematoma; therefore, follow-up imaging after resolution of the initial hematoma is essential [1]. Angiomyolipomas (AML) are benign slow growing tumours composed of a variable mixture of blood vessels, smooth muscles and fat [2] (Refer to Figure 2). Figure 2: Angiomylipoma showing composed of a variable mixture of blood vessels, smooth muscles and fat.

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It may be associated with tuberous sclerosis but are mostly sporadic [3]. Most angiomyolipomas are small and asymptomatic [2]. They are often an incidental finding on imaging done for other purposes. Occasionally, they may cause hematuria or flank pain from spontaneous hemorrhage which is usually retroperitoneal, and this rarely may result in acute abdomen and shock [3]. Renal AML is a relatively infrequent benign tumour observed in 0.3% of the population and accounts for 3% of all solid renal masses [2]. As many as 25% of patients with renal AML can present with spontaneous rupture and subsequent haemorrhage into the retroperitoneum [4] Massive retroperitoneal hemorrhage It is known that spontaneous perirenal haemorrhage is from AML also known as Wunderlich’s syndrome has been found in up to 10% of patients and represents the most significant and feared complication [5,6,7]. Spontaneous renal or perirenal hemorrhage may also result from coagulopathy or vasculitis, such as polyarteritis nodosa and Wegener’s granulomatosis. Rarely, the accumulation of blood in the perinephric subcapsular space can compress the renal parenchyma, leading to ischemia and subsequent high renin hypertension (Page kidney) [8]. Massive hemoperitoneum caused by spontaneous rupture of the liver is a rare event, most often associated with benign and malignant hepatic neoplasms [9]. There have been several reports in the literature of liver hemorrhage related to pregnancy, and other more rare conditions such as coagulation disturbances, connective tissue disease, and hypereosinophilic syndrome [9]. For hepatic neoplasms, rupture of an underlying hypervascular hepatic adenoma usually occurs in young women receiving long-term oral contraceptive therapy, whereas the highest incidence of bleeding hepatocellular carcinoma has been reported in Asian countries in cirrhotic patients with tumors located at the periphery of the liver [10,11]. (Refer to Figure 3 a, b) Role of interventional radiology has been crucial in reducing the morbidity and mortality of such traumatic injuries especially involving pelvic and solid organs as the spleen, liver and kidney. Using this expertise in trauma management, interventionalists use the Figures 3 a, b: CT and subsequent angiogram for large hepatocelluar same techniques and pacarcinoma that resulted in bleeding with subsequent embolization. tient management experience in treating spontaneous hemorrhage from liver and renal tumors. Technique Optimal trauma management requires a multidisciplinary team, including surgeons and interventional radiologists, coupled with modern facilities and equipment. Rapid assessment and treatment is vital in the management of patients with significant abdominal spontaneous hemorrhage [11].The haemodynamic stability of the patient is key to management yet it is not easy to define. Shocked, unstable patients can be quickly identified and need rapid transfusion while urgent assessment and then treatment of the injury takes place [12]. Haemodynamic stability may be defined as hemorrhagic shock not worse than Class 2, i.e. patients are normotensive, have elevated or normal pulse rate, respiratory rate <30/min, normal or decreased pulse pressure (arterial pulse amplitude), and have a rapid response to the initial fluid therapy of 2 L crystalloid [13]. Patients who are stable or rapidly become stable with fluid resuscitation are suitable for CT, which will allow appropriate treatment decisions to be made. The access and use of multi-detector computed tomography (MDCT) is crucial for rapid and complete CT diagnosis and improved clinical outcomes including reduction in ICU and hospital bed stays [12]. The multi-detector computer tomography (MDCT) without followed with intravenous contrast help to define the area of concern and bleeding. Sagital and coronal reconstructions and 120

b. Spontaneous haemorrhage from liver and renal tumours, Michael Wholey

multiplanar images are used to further delineate the tumor and the bleeding site as well as the arterial feeders and communication. CT findings include the contrast blush, pseudoaneurysm, contained bleed or frank extravasation. Good high resolution CTA images help define the arterial selection and subselection needed to treat the bleeding. If the patient is deemed not a patient for just observation and conservative management and the CT/CTA scan is positive for bleed, angiography is ordered. The patient is immediately brought to the angiographic suite and both femoral arteries are prepped and cleaned. We will have arterial Doppler available for patients with decreased pulses due to blood loss. We will place a 5 French arterial sheath in the common femoral artery and advance a 5 French Pigtail catheter for a quick assessment of the aorta and its major branches. For hepatic tumors, we will select the celiac trunk with a 4-5 Fr cobra catheter. Under roadmap, we will carefully advance the catheter with a 0.035â&#x20AC;? glidewire. (Refer to Figures 4 a-d)

Figures 4 a-d: Reveal the follow up embolization for case shown in Figure 3a,b. Cobra catheter selected the common hepatic artery. Oblique and magnified DSA images help to reveal the bleeding left hepatic artery. Microcatheter is used to subselect the targeted artery. Once in place, embolization is performed with microparticles (size 150-300 microns) to effectively occlude flow. Going further into the right or left hepatic artery can cause significant spasm, so we will leave the 4-5 French diagnostic catheter in the common or proper hepatic artery. Angiogram of the liver with oblique projections will show the tumor and the bleeding site. We will carefully map out which vessel or vessels lead directly to the bleeding site. Once the route is targeted, we will advance a microcatheter and subselect the artery to the bleeding site. Contrast injection is done lightly for sometimes it will illicit more bleeding. For renal tumors, pigtail injection helps to reveal whether accessory renal arteries are present. The main renal is selected with a 4-5 French cobra catheter and contrast injection will show the bleeding site. The renal artery anatomy is divided into an anterior and a posterior branch and from these arise segmental branches. From these arise interlobar, then arcuate and then interlobular branches. The type of embolization can vary depending upon several factors. First, is how stable or unstable is the patient. If it is truly life threatening and you do not have any time to spare, then access to the common femoral artery, selection of the artery and quick arterial blockage is paramount. (Refer to Figure 5 a-c).

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For very active bleeding that is life threatening, we will carefully and quickly stop the flow with microcoils (0.018” tornado or diamond shaped) blockading the vessel. This is useful for vessels that sheared off or directly leading to the bleeding side. (Refer to Figure 6 a-c).

Figure 6 a-c: Likewise, trauma in a 12 year old boy in the right lobe of the liver from motor vehicle injury requiring quick selection of the proper hepatic artery to demonstrate the large active extravastion in the right lobe of the liver. Initially it appears to be originating from the upper branch but with subselection, the lower branch is the culprit and effective microcoil embolization stops the bleeding. If the bleeding is coming off a side branch, or if you are not able to get access into the small vessel, it is important to go past the bleeding site and embolize and then pull proximally and embolize, forming an effective blockade. (Refer to Figure 7 b). The 0.018” or 0.035” coil tornado shaped coil contain synthetic fibers to promote hemostasis. (Refer to Figure 7 c) Figures 7a-c demonstrate simple principle for embolizing with coils in acute settings to stop flow immediately. If the vessel is sheared off as in Figure 7a, the angiogram will show a truncation. There may or may not be active extravasation into soft tissues or organ. Here you deploy two or more coils to seal up the vessel with end result being a complete blockade. If the vessel is torn or a sidebranch pulled off with the result being that the hemorrhage is effected by antegrade and potentially retrograde flow (from collaterals), then it is important to seal the injury from both sides. You embolize the distal end first, and then move quickly for bleeding will increase until you seal the proximal end. The last image Figure 7c shows a 0.035” coil tornado shaped coil with the synthetic fibers to promote hemostasis. For those life threatening cases, where every second really matters and where the vessel is large diameter, you could consider using an Amplatz occluder coil through the 5 Fr catheter. (Refer to Figure 8) Figure 8: Amplatz Vascular Plug (St Jude Medical, St Paul, MN, USA) is very effective in providing immediate occlusion and can be delivered in a 5 Fr catheter. 122

b. Spontaneous haemorrhage from liver and renal tumours, Michael Wholey

Combination of embolic coils and microparticles are often used in difficult tumors such renal angiomyolipoma. For most tumors, especially within the liver, embolization will be done with microparticles, or transarterial embolization (TAE). These microparticles are chosen over microcoils because the tumors will often require reintervention with further microembolization or drug delivery; coils will block the main arterial pathway making it more difficult in the future. (Refer to Figure 9) Figure 9: Microparticels are produced by several companies in vary sizes (measured in microns) and in varying types of material. Here is Embospheres, (Guerbet Biomedical, Louvres, France) Additionally, for tumors, complete or nearly complete embolization is required. Particles are able to occlude the main as well as collateral flow feeding the tumor. The embolic particles vary in terms of size and composition [14]. Sizes used are typically 100-300 microns in diameter [14]. Some centers have used smaller particles, 40 microns, as long as there is no significant shunting within the liver to the hepatic veins [14]. If there is rapid flow through the tumor to the venous system, then larger size particles are used. The type of particle has evolved over the past decade. Gelfoam sponge powder was one of the first embolic agents used, but the efficacy was reported to be low because it stayed only temporarily within the tumor vascular mesh [14]. Polyvinyl-alcoholic foam (PVA) is reported to be too heterogeneous in shape and size to be effective [15,16]. PVA performance of this material can be unpredictable, primarily because the particles clump and aggregate within the vessel lumen, thereby causing occlusion of larger peripheral vessels and allowing the development of new feeding arteries distal to the target lesion, leading to poor clinical outcomes [14]. In the past two decades, several spherical embolic agents have been developed, including trisacryl gelatin microspheres (Embospheres, Guerbet Biomedical, Louvres, France), collagen-coated microspheres, dextran microspheres, and PVA microspheres [16-20]. The development and refinement of spherical embolic particles has dramatically increased the treatment armamentarium for liver tumors, especially HCC or â&#x20AC;&#x153;hypervascularâ&#x20AC;? liver lesions [19]. Spherical embolics help to reduce or avoid particle clusters within peripheral vessels and allow for a deeper penetration in the neoplasm vasculature, with permanent and effective staining [14]. Alternative embolization techniques include the use of alcohol which is used for treating renal tumors such as renal cell carcinoma. (Refer to Figure 10 a-d).

Figure 10 a-d show a large right renal cell carcinoma presenting with significant hematuria. Work up reveals tumor extension into renal vein and IVC. Selection of the left renal artery shows the extent of tumor with characteristic neovacularity. Occlusion balloon catheter in the main renal artery allows for alcohol injection denuding the renal artery and stopping flow. 123

3. VISCERAL ARTERY EMERGENCIES

It is administered through an occlusion balloon catheter placed in the main renal artery. Prior to administration, volume of contrast is used to determine how much it requires to fill the renal artery and its branches. The balloon is deflated allowing blood flow to return. Then the pure alcohol is given slowly. Careful attention must be given to alcohol administration: it is very dangerous for any shunt to the venous circulation as well as for its difficulty in administration-it is not radiopaque. Patients when stable will normally undergo nephrectomy. Other treatment modalities for renal and hepatic tumors include the administration of transarterial chemotherapy (TACE). When a blood vessel supplying tumor has been selected, alternating aliquots of the chemotherapy dose and of embolic particles, or particles containing the chemotherapy agent, are injected through the catheter. Devices can be delivered percutaneously through the skin and directly into the tumor of radiofrequency or thermal ablation. Both ablation and TACE are administered with tumors that are stable and not hemorrhagic. Complications The embolization procedure for hepatic and renal tumors can induce tumour necrosis in more than 50% of patients. The resulting necrotic material releases cytokines and other inflammatory chemicals into the blood stream, which can lead to post-embolization syndrome [21]. This is due to hepatic artery obstruction with an acute ischemia, characterized by fever, abdominal pain and ileus [21]. A minority develop severe infectious complications such as an abscess within the necrotic tissue. This is a potentially fatal event, although percutanous drainage can be utilized in order to prevent the septicaemia and sepsis. Cholecystitis can also occur [21]. Renal artery embolization associated complications including coil migration, incomplete embolization, and groin haematoma (in 5.0%â&#x20AC;Ż[22]. (Refer to Figure 11). Figure 11: shows a coil that has migrated down to the right profunda femoral artery past the sheath. Access had to be obtained from the contralateral left femoral access with a snare to capture and remove the coil as quickly as possible to avoid the clot buildup. Symptoms of post-infarction syndrome were common, with 74.4% of patients having flank pain, nausea, or vomiting; the vast majority of these symptoms were mild and self-limited [22]. Conclusion Fortunately, spontaneous hemorrhage of hepatic and renal tumors is not common. For liver causes, the most common causes for liver tumors are hemorrhagic hepatocelluar carcinomas and metastatic disease. For renal hemorrhagic tumors, these would include angiomyolipoma and renal cell carinoma. The interventional treatment and embolization of these hemorrhagic tumors have been established in the core treatment traumatic injuries of solid organs: stabilize the patient first with adequate resuscitation, obtain an immediate CTA of the abdomen and pelvis and then transport the patient immediately to the angiographic suite. Once the angiographic studies reveal the site of bleeding, diagnostic catheter is placed near the main artery and microcatheters are used to subselect the targeted vessel. Once in position, depending upon the patientâ&#x20AC;&#x2122;s clinical status and that of the tumor, either microcoils and/or embolic particles are used. Occasionally, alcohol is administered for renal cell carcinoma prior to nephrectomy. Afterwards, though complications are generally rare, post-infarction syndrome especially with renal cases are frequent.

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b. Spontaneous haemorrhage from liver and renal tumours, Michael Wholey

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1. Belville JS, Morgentaler A, Loughlin KR, Tumeh SS. Spontaneous perinephric and subcapsular renal hemorrhage: evaluation with CT, US and angiography. Radiology 1989;172 : 733–738 2. Hajdu et al. Angiomyolipoma of kidney Report of 27 cases and review of the literature J Urol 1969 3. Anderson and Hatcher et al. Renal angiomyoliopma Prog. Urol 1990 4. Wong, McGeorge and Clark Renal angiomyolipoma: areview of literature and a report of 4 cases Br J Urol1981 5. Chesa Ponce N et al. Wunderlich’s syndrome as the first manifestation of a renal angiomyolipoma 6. Oesterling et al. The management of renal angiomyolipoma J Urol 1986 7. Pekka A. et al. Spontaneous Subcapsular or Perirenal Haemorrhage Caused by Renal Tumours: A Urological Emergency Scandinavian Journal of Urology and Nephrology 1999 8. Pintar TJ, Zimmerman S. Hyperreninemic hypertension secondary to a subcapsular perinephric hematoma in a patient with polyarteritis nodosa. Am J Kidney Dis 1998;32 : 503–507. 9. Klein K, Shapiro AM. Spontaneous Hepatic Rupture with Intraperitoneal Hemorrhage without Underlying Etiology: A Report of Two Cases. ISRN Surgery, vol. 2011, Article ID 610747, 3 pages, 2011. 10. Casillas VJ, Amendola MA, Gascue A, Pinnar N, Levi JU, Perez JM. Imaging of nontraumatic hemorrhagic hepatic lesions. RadioGraphics 2000; 20:367–378 11. 5. Kim HC, Yang DM, Jin W, Park SJ. The various manifestations of ruptured hepatocellular carcinoma: CT imaging findings. Abdom Imaging 2008; 33:633–642 12. Wallis A, Kelly M, Jones L. Angiography and embolisation for solid abdominal organ injury in adults - a current perspective. World Journal of Emergency Surgery 2010, 5:18 13. Hilty MP, Behrendt I, Benneker LM, et al.: Pelvic radiography in ATLS algorithms: A diminishing role? WJES 2008 2008, 3:11 14. Bonomo G, Monfardini L, Della Vigna P, Orgera G,Pedicini V, Orsi F. Does Microparticle Size Affect Bland Embolization Outcomes of Local Treatment for Liver Malignancies? Vasc Disease Mngt Volume 6 - Issue 5 - Sept/Oct 2009 15. Jack CR, Forbes G, Dewanjee MK, et al. Poly-vinyl alcohol sponge for embolotherapy: Particle size and morphology. Am J Neuroradil 1985;6:595–597. 16. Derdeyn C, Moran C, Cross D, et al. Polyvynil alcohol particle size and suspension characteristics. Am J Neuroradil 1995;16:1335–1343. 17. Laurent A, Beaujex R, Wassef M, et al. Trisacryl gelatin microspheres for the therapeutic embolization, I: Development and in vitro evaluation. Am J Neuroradiol 1996;17:533–540. 18. Derdeyn CP, Graves VB, Salamat MS, et al. Collagen-coated acrylic microspheres for embolotherapy: In vivo and in vitro characteristics. Am J Neuroradiol 1997;18:647–653. 19. Dion JE, Raniìkin RN, Vinuela F, et al.. Dextran microsphere embolization: Experimental and clinical experience with radiologic-pathologic correlation. Work in progress. Radiology 1986;160:717–721. 20. Siskin GP, Dowling K, Virmani R, et al. Pathologic evaluation of spherical polyvinyl alcohol embolic agent in a porcine renal model. J Vasc Interv Radiol 2003;14:89–98 21. Rammohan A, Sathyanesan J, Ramaswami S, Lakshmanan A, Senthil-Kumar P, Srinivasan U, Ramasamy R, Ravichandran P (2012). “Embolization of liver tumors: Past, present and future”. World J Radiol. 4 (9): 405–12. 22. Schwartz M, Smith E, Trost D, Vaughan ED, Renal artery embolization: clinical indications and experience from over 100 cases. BJU International Volume 99, Issue 4, pages 881–886, April 200

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3. Visceral artery emergencies c. H aemorrhage from pancreaticoduodenal and splenic artery pseudoaneurysms in pancreatitis

Maria Antonella Ruffino, Claudio Rabbia

Vascular Interventional Radiology, San Giovanni Battista Hospital, Torino, Italy

Abstract Gastrointestinal bleeding due to ruptured pseudoaneurysm is a rare but potentially fatal complication of both acute and chronic pancreatitis. Pesudoaneurysm is the result of vessel wall erosion induced by proteolytic pancreatic enzymes during the inflammatory process which may lead to either formation of pseudoaneurysm or hemorrhage into a preexisting pseudocyst. The splenic artery is the most commonly involved vessel, due to its contiguity with the pancreas, followed by the gastroduodenal artery, pancreaticoduodenal, hepatic, and left gastric artery. These lesions can bleed not only into a preexisting pseudocyst, but also into the gastrointestinal tract, pancreatic duct, retroperitoneum, or peritoneal cavity, with subsequent hemorrhage. Patients with arterial complications can be asymptomatic or present with severe abdominal pain, in different location according to the bleeding site, gastrointestinal bleeding, and shock. A prompt diagnosis of pancreatic pseudoaneurysms remains challenging, althought new developments in diagnostic imaging technique, such as ultrasound, duplex Doppler ultrasound, and computed tomography, and a prompt use of diagnostic and therapeutic angiography, had led to an earlier diagnosis of these complications, while endoscopy is indicated to rule out other causes of gastrointestinal bleeding. The management (surgical or endovascular) of this life-threating complication is still controversial and data reported in literature are limited to small series or case reports. Surgical intervention (arterial ligation with drainage of a pseudocyst or a partial pancreatectomy) and endovascular therapy (embolization with coils, glue, or other liquid embolic agents, or deployment of a covered stent, with or without concomitant coil embolization), as a single approach or a temporizing method followed by a second intervention, are both valid terapeutical approaches. Unfortunately, in some cases, surgical procedure is limited by patientâ&#x20AC;&#x2122;s clinical state and inflammatory changes that can make surgical control of bleeding extremely challenging. During the last two decades, endovascular therapy has grown as the treatment of choice for arterial bleeding management in pancreatitis, with an high technical success and low morbidity and mortality rates. Recent studies in literature show also a statistically significant advantage of embolization, with a rebleeding rate of 12% compared to 37% after operative treatment. The aim of this article is to summarize the critical aspect of diagnostic and therapeutical approach to haemorrhage from pancreaticoduodenal and splenic artery pseudoaneurysms in pancreatitis.

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Introduction The incidence of acute and chronic pancreatitis has been increasing during the last years, with severe form of acute pancreatitis occurring in about 20-30% of patients, and consequent higher incidence of local and systemic complications of the disease [1]. Major arterial haemorrhage is a rare but rapidly fatal complication of pancreatitis with an incidence in reported series ranging from 1.3% to 14% [2-4], greater in chronic pancreatitis (7-10%), than acute pancreatitis (1-6%) [5]. The most common origin of bleeding is ruptured peripancreatic pseudoaneurysm. The splenic artery is the most commonly involved vessel, due to its contiguity with the pancreas, accounting for 60-65% of all pseudoaneurysms in chronic pancreatitis [6], followed by the gastroduodenal artery (20% to 25%), pancreaticoduodenal (10%-15%), hepatic (5%-10%), and left gastric artery (2%-5%) [6-9]. The overall mortality rate due to a ruptured pseudoaneurysm in pancreatitis can be as high as 34-52% [10] as they can cause rapid blood loss. The pathogenesis of pseudoaneurysm may be the uncontrolled, severe inflammation leading to local spread of exocrine proteolytic and lipolytic enzymes causing necrosis of vessel walls and autodigestion of pancreatic or peripancreatic arteries that start dilating. This mechanism results in formation of an aneurysm (when the dilated artery is within a pseudocyst and the blood is still contained within a complete arterial wall), of a pseudoaneurysm (when there is a rupture of the aneurysm into the pseudocyst), or an active intraperitoneal haemorrhage [11]. Severe haemorrhage may also be related to development of pancreatic and peripancreatic abscess. Another cause of haemorrhage in pancreatitis is represented by iatrogenic complications of pancreatic surgery. Technical manoeuvres can damage directly the vessel wall and, combined to proteolytic digestive enzyme action, may lead to vessel rupture. Most of the patients suffering from chronic pancreatitis with pseudoaneurysms are asymptomatic, and they are usually diagnosed through imaging work-ups. When they are symptomatic, clinical finding cannot be distinguished from patients with pancreatitis, unless it is complicated. They can also present a pulsatile mass. Clinical symptom can be different depending on the location of the pseudoaneurysm rupture. It can break into the duodenum, with consequent upper gastrointestinal haemorrhage, or into a pseudocyst, with retroperitoneal haemorrhage, or in the ductus of Wirsung, causing hemosuccus pancreaticus [12]. In 3% of patients with pseudoanurysms there is haemorrhage. Surgical and percutaneous drainages for treatment of pancreatic fluid collection also raise the risk of vascular lesions. In untreated patients, the mortality rate of these arterial complications is 90%, but in treated patients it ranges from 15% to 50% [13-16]. The treatment of choice of pancreatitis arterial complications is still controversial: their low incidence precludes randomized trial evaluation of therapeutic options, thus, their management is still based on single-institutional small series data or case reports. Surgery consists of ligation or repair of the damaged artery and external drainage, Roux-en-Y cystojejunostomy, or distal pancreasectomy, but the inflammatory changes can make surgical control extremely challenging [17]. Surgical mortality ranges from 11% to 23% [18,19]. When the pseudoaneurysm is located deep within the parenchima, surgery can be unsuccessful in as many as 70% of cases [20]. In the last years, endovascular therapy has grown as the first-line option for arterial bleeding management, as a single therapy or as a temporizing measure in conjunction with surgery [21-25]. The procedures have a low morbidity and mortality rate (70% to 100%) [26,27]. Imaging Noninvasive imaging techniques, such as ultrasound (US), duplex Doppler US, and computed tomography angiography (CTA), and a prompt use of diagnostic and therapeutic angiography had led to a earlier diagnosis of vascular complications of pancreatitits, reducing morbidity and mortality rates. Endoscopy Endoscopy can be helpful in diagnosis of more common causes of gastro-intestinal (GI) bleeding, such as peptic ulcers, stress or erosive gastritis, Mallory-Weiss tears, and gastroesophageal varices. Failure to demonstrate upper GI bleeding is related to fundal gastric varices, intermittent bleeding through the papilla or a bleeding source beyond the reach of the endoscope (i.e., small intestinal varices or rupture of a pseudocyst into the intestine) [28]. 128

c. Haemorrhage from pancreaticoduodenal and splenic artery pseudoaneurysms in pancreatitis, M. A. Ruffino, C. Rabbia

Ultrasound US can perform diagnosis of pseudoaneurysm demonstrating the presence of the lesion along the target vessel: characteristic appearance of a turbolent arterial flow within an anechoic mass is indicative for a pseudoaneurysmatic lesion. Color Duplex US should be used for the evaluation of all peripancreatic fluid collections to avoid misinterpretation of aneurysm or pseudoaneurysm as a simple or complex fluid collection. Doppler can establish the diagnosis showing the typical â&#x20AC;&#x153;to-and-froâ&#x20AC;? wave-form. It may also demonstrate portal vein thrombosis with varices. This imaging modality has high sensitivity and specificity but it can be limited by deep location of visceral pseudoaneurysms, calcifications and local ileus. Contrast-enhanced US (CEUS) has been recommended as a first-choice imaging technique for the assessment of patients with acute pancreatitis, especially when iodine medium contrast in contraindicated [29]. Moreover, US is portable, readily available, relatively fast, and involves no ionizing radiation or medium contrast. Computed Tomography CT angiography, thank to its multidetector technology and faster rotation times, and its great spatial and temporal resolution, is very informative and accurate in diagnosing bleeding sites [30]. Contrast agents with higher iodine concentrations led to improved vascular enhancement. CTA is a sensitive and accurate technique for detection of major arterial hemorrhage in inflammatory pancreatic disease and should be considered as the first investigation in diagnosis and for planning intervention. It can demonstrate the extent of the pseudoaneurysmal lesion and its thrombotic component, and it can also demonstrate the relation with the surrounding viscera. Image acquisition is accomplished during the arterial phase when pancreatic parenchymal and portal venous enhancement is relatively weak. Highquality maximum intensity projection reconstructions can direct the interventionalist to an acute bleeding vessel, saving time and contrast. If a vascular abnormality is diagnosed on CT, angiography is usually requested urgently with the purpose to confirm the diagnosis and perform the treatment. Unstable patients with massive GI bleed may go directly to angiography. For most of patients the bleeding site will be readily apparent angiographically. Angiography Once considered the gold standard imaging for the detection of a visceral artery pseudoaneurysm or for the site of active bleeding in patients with pancreatitis, angiography has lost its diagnostic meaning becoming a therapeutic tool rather than a purely diagnostic one. It allows evaluation of the arterial bed, identifying the supplying vessel and assessing side branches. Detailed characteristics of pseudoaneurysms obtained during angiography, such as parent vessel size and aneurysm neck, can aid in planning treatment. It allows also localization of bleeding site in those patients for whom endoscopy or CT scan was negative. Angiography has a sensitivity of 100% for the detection of arterial bleeding in patients with pancreatic pseudoaneurysms [31]: failure to detect bleeding may be attributed to intermittent bleeding, or the fact that bleeds may have a venous rather than arterial origin [32]. Another limit of this imaging technique is the need of ionizing radiation and iodinated contrast. It remains also an invasive modality with additional risk of vascular complications such as dissection, pseudoaneurysm rupture, or vessel thrombosis, hematomas and femoral artery pseudoaneurysms. Treatment of haemorrhage Pancreatic pseudoaneurysms represent an emergent clinical condition, because the risk of their rupture is very high, while some undergo spontaneous thrombosis. Their management depends on different factors as site of source of bleeding, haemodynamic stability, and coagulation status of the patient. Treatment should be administered as soon as possible. Endoscopic Ultrasound Therapy (EUS therapy) Bleeding from peptic ulcers, stress gastritis, varices are treated with an endoscopic approach. In particular cases of visceral pseudoaneurysm, where the lesions are difficult in reaching via catheterization and they are located in close proximity of the endoscope, it is possible to perform a direct puncture of the pseudoaneurysm with injection of histoacril glue or thrombin under endoscopic ultra129

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sound control [33,34]. The procedure can be performed with the patient under conscious sedation. Other alternatives for thrombin or histoacril glue are ethylene vinyl alcohol copolymer (mixed or not with micronized tantalum powder), N-butyl-2-cyanoacrylate with or without coils, and endovascular coils alone. Complications of EUS-therapy are, as for endovascular therapy, distal embolisms and immunoreaction (for what concerns thrombin administration). Failure of endoscopic therapy can be related to intermittent bleeding or a bleeding not reachable by the endoscope. Ultrasound-guided thrombin injection Percutaneous thrombin injection under ultrasound guidance has been successfully used in treatment of iatrogenic and traumatic femoral and other peripheral arteries pseudoaneurysms, providing a safe and fast alternative to open surgical repair or ultrasound-guided compression. In those particular cases where the pseudoaneurysm is visualized by US, thrombin can be injected directly into the lesion until the cessation of flow. The effectiveness of this treatment is not well established, but many cases have been reported in Literature [35-37]. The potential complications of this procedure include distal embolization, native artery thrombosis, and anaphylaxis [38]. Surgical treatment Management of ruptured pseudoaneurysms used to be surgery, which is associated with high morbidity and mortality. Surgery is indicated in instable patients, lack of angiographic availability or its failure, but it has some limits. Because of pancreatic tissue and pseudocyst wall friability, oversewing of the bleeding site can be unsuccessful in providing hemostasis. Tight adhesion due to pancreatic inflammation distorts normal anatomy and makes surgery complex. When ligation of the bleeding artery is not possible, the only alternative is a pancreatic resection with a mortality rate of 43% for pancreatic head resection, and 16% for pancreatic body and tail [39]. For pseudoaneurysm near the pancreatic head, a Whipple procedure is usually performed, while a distal pancreatectomy with or without splenectomy is indicated for lesions around the pancreatic body or tail. Delayed bleeding post-pancreatic surgery has a reported prevalence of 5-12%: in this case, catheter angiography is very helpful in resolving the complication. Endovascular therapy With the development of imaging techniques and interventional percutaneous procedures, patients with arterial pancreatic complications are now treated with endovascular therapy. Procedures have a low morbidity and mortality, with a technical success of 70% to 100% [27] and a recurrent bleeding rate ranging from 18-37% [40], even if data about long-term hemostasis after successful embolization are limited. The overall mortality related to angiographic failure or complication is reported to be 14% in patients with chronic pancreatitis. Trans-arterial embolization provides a minimally invasive and effective alternative to surgery. Embolizing the splenic artery prior to surgical necrosectomy may significantly reduce intraoperative blood loss for patients with hemorrhagic necrosis. Coagulopathy, sepsis, and renal failure are relative contraindications to percutaneous transcatheter embolization. Initial diagnostic angiography can be performed through a short 5-Fr femoral sheath. CTA should obviate the need for abdominal aortography to delineate the arterial anatomy. In order to achieve a successful embolization, it is mandatory to get as close to the bleeding vessel as possible. The celiac axis and the superior mesenteric artery can be selectively cannulated with a variety of catheters. A 4-Fr hydrophilic Cobra catheter (e.g. Glide Catheter; Terumo/MediTech, Boston Scientific, Waltham, MA) may be sufficient for access and embolization, but sometimes, due to vessel tortuosity, a microcatheter is often required. In case of acutely angulated branches, a SOS Omni, a 5-Fr Cobra 2, or a Simmons 2 catheter â&#x20AC;&#x153;parkedâ&#x20AC;? in the proximal arterial trunk can give sufficient stability for microcatheter access. There are many microcatheter for selective and superselective access: these are 3-Fr outer diameter, with 0.021- to 0.027-in inner diameter. Most microcatheters allow higher flow rate injection making them suitable for infusion and less likely to occlude with glue. There are also many guidewires, several of which are steerable with a torque device and hydrophilic. For artery with extensive collateral circulation, aggressive coil embolization can be performed with low risk of distal ischemia, such as the celiac trunk or the proximal branches of SMA, as the inferior pancreaticoduodenal artery. In case 130

c. Haemorrhage from pancreaticoduodenal and splenic artery pseudoaneurysms in pancreatitis, M. A. Ruffino, C. Rabbia

of pseudoaneurysms, coil embolization is performed distal and proximal to the lesion (sandwich technique), in order to prevent backflow from the collateral circulation. In case of a splenic artery, placing the distal coil as close to the aneurysm as possible improves the chances of reconstitutions of arterial inflow to the spleen, reducing the risk of splenic infarction (figures 1, a-d).

Fig. 1 a: c eliac trunk selective angiography shows pseudoaneurysm of the splenic artery in a patient with diagnosis of chronic pancreatitis. Both hepatic and left gastric arteries are patent Fig. 1 b: a guiding catheter was positioned at the ostium of the splenic artery in order to perform the embolization distally and proximally (sandwich technique) to the pseudoaneurysm, avoiding reperfusion. Fig. 1 c: fluoroscopy control show the correct deployment of coils 1 cm proximally and 1 cm distally to the splenic artery tear Fig. 1 d: selective angiography of celiac trunk shows complete exclusion of the splenic artery and of the pseudoaneurysm from the arterial flow. The spleen is reperfused by collateral branches arising from gastric artery Where there is lack of collateral vascularization, it is mandatory to evaluate the pseudoaneurysm neck size: if it is narrow, the lesion may be treated with catheter directed delivery of coils into the sac itself or excluded by placement of a covered stent. If the neck is wide, a covered stent graft alone may provide exclusion of the pseudoaneurysm. The risk of direct embolization of a pseudoaneurysm with coils is the risk of coils backing out into the target artery. Another technique is based on the use of a bare stent deployed across the lesion neck followed by catheter-directed coil embolization through the stent net. The stent acts like a barrier confining the coils within the sac. In case of instable patient, even a inexpendable artery must be sacrificed and occlude when the deployment of a stentgraft is not possible, i.e. in case of small and tortuous branches to difficult access even with microcatheters. Fibered coils are made up of wound steel, platinum, or tungsten wires, with attached synthetic fibers to maximize thrombogenicity. They are the embolic material of choice for pseudoaneurysm occlusion. Coils are available in different shapes (straight, helical and tapered helical) with a range of sizes from 1 to 20 mm to fit the vessel diameter. They are generally manufactured in either 0.018- or a 0.035-in. system to facilitate deployment through a microcatheter or a 5-Fr catheter. Coils are deployable by saline flush, however with the use of a pushing wire. Smaller diameter coils (0.014in.) designed for intracranial aneurysm are also available and may be detachable and retrievable. They are affixed to a delivery wire and can be detached by a threaded, pneumatic spring-loaded, or electrolytic mechanism of deployment. If a detachable coil is positioned suboptimally, it can be easily retracted and repositioned. They generally have not thrombogenic fibers. It is not mandatory to fill the aneurysmal sac, as long as the efferent and afferent arteries are occluded. Packing the sac with coils can increase the risk of rupture, is very expansive, and time-consuming. Occlusion of small vessels and multiple collateral sources may be attempted using also liquid embolic agents such glue. N-butyl cyanoacrylate (NCCA) polymerizes immediately upon contact with an ionic medium such as saline or blood. A non-ionic environment is therefore required for preparation. NBCA causes complete vessel occlusion, it is non radiopaque and it is typically mixed with ethiodized oil (Lipiodol). An accurate evaluation of flow rate across the pseudoaneurysm is required to calculate the glue:contrast ratio, as this affects viscosity and polymerization rates. Glue is more difficult to control than coils, but it facilitates occlusion distal to the microcatheter tip. There is also the potential risk of catheter 131

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occlusion or entrapment and loss of access. Visceral pseudoaneurysms have been embolized also with ethylene vinyl alchol copolymer (Onyx; EV3, Plymouth, MN, USA), material with low viscosity that in a single injection simultaneously fill numerous downstream vascular channels before polymerizing into a hard cast (41). Another option for occluding these small vessels is the use of Gelfoam, a relatively safe but temporary embolic material that provides an adequate time for the vascular injury to heal [42], even if it may be rapidly absorbed by pancreatic proteolytic enzymes. Amplatzer vascular plug (AVP, St. Jude Medical, St. Paul, MN, USA) can provide fast and complete occlusion of large artery feeding a pseudoaneurysm, such as the splenic artery, faster then with placement of multiple coils. Placement of covered stent across visceral artery pseudoaneurysms, with preservation of distal flow, has become technically feasible in recent years with smaller and more flexible delivery system. Use of stentgraft remains limited by anatomic suitability and risk of stent migration, thrombotic occlusion/intestinal ischemia, and potential infarction. After the embolization, it is mandatory to perform a complete celiac and SMA angiogram to evaluate that no other collateral vessels feed the pseudoaneurysm, or endoleak complicate stentgraft deployment. Supplementary branches must be selectively embolized and significant endoleaks treated by balloon angioplasty of the stent graft or by deployment of an additional stentgraft. Some small endoleaks tend to undergo thrombosis spontaneously due to their low rate of blood flow. Pseudoaneurysm rupture during the procedure is rare and mostly unrelated to the procedure. Non-target coil embolization and maldeployment of a stent-graft are technique-related and may occur because of inappropriate vessel-sizing or device selection [43]. Rebleeding is a potential complication of endovascular management with a rate, in recent reported series, ranging from 11% to 27% [44]. The prognosis for patients with rebleeding is very poor: 7 of 9 patients died. The management of bleeding recurrence must be individually tailored. CT follow up imaging must be considered in particular in patients where procedure fails or have further bleeding, changing viewing windows as necessary, as artefact from coils may obscure pathology; a precontrast study is mandatory, as dense old blood/thrombus within the aneurysm can be mistaken for enhancement. Solid organ ischemia can sometimes occur with consequent development of an abscess due to exogenous bacteria introduction by percutaneous means, retrograde transport of entheric pathogens via a reversed portal flow, and immunosopression [45,46]. Intraparenchimal and intraperitoneal abscesses can often be percutaneously or surgically drained. Splenic infarction is not rare but is typically clinically silent and usually managed conservatively. Conclusion Haemorrhage from pancreaticoduodenal and splenic artery pseudoaneurysms in pancreatitis is a condition that requires urgent treatment because of its potentially fatal consequences. Endovascular treatment can be considered the first-choice, effective and minimally invasive therapeutic option associated with a high success rate and few complications in patients hemodinamically stable. In case of success, no further treatment may be needed. If the embolization failed, patient can undergo another endovascular attempt or operative treatment. In order to achieve technical and clinical success it is mandatory a prompt diagnosis so the best interventional treatment (transarterial embolization, endovascular stenting or percutaneous thrombin injection) can be performed.

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c. Haemorrhage from pancreaticoduodenal and splenic artery pseudoaneurysms in pancreatitis, M. A. Ruffino, C. Rabbia

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39 Zyromski NJ, Vieira C, Stecker M, et al. Improved outcomes in postoperative and pancreatitis-related visceral pseudoaneurysms. J Gastrointest Surg 2007;11:50-55 40. Izaki K, Yamaguchi M, Kawasaki R, et al. N-butyl-cyanoacrylate embolization for pseudoaneurysms complicating pancreatitis or pancreatectomy. J Vasc Interv Radiol 2011;22:302-308 41. Lopera JE. Embolization in trauma: principles and techniques. Semin Intervent Radiol 2010;27:14-28 42. Hyare H, Desigan S, Brookes JA, et al. Endovascular management of major arterial hemorrhage as a complication of inflammatory pancreatic disease. J Vasc Interv Radiol 2007;18:591â&#x20AC;&#x201C;596 43. Kirby JM, Vora P, Midia M, et al. Vascular Complications of Pancreatitis: Imaging and Intervention. Cardiovasc Intervent Radiol (2008) 31:957â&#x20AC;&#x201C;970 44. Sanada Y, Kondo H, Goshima S, et al. Liver abscess after common hepatic artery embolization for delayed hemorrhage following pancreaticoduodenectomy: a case report. Case Report Med 2010;28-43 45. Madoff DC, Denys A, Wallace MJ, et al. Splenic arterial interventions: anatomy, indications, technical considerations, and potential complications. Radiographics 2005;25 Suppl 1:S191-S211

3. Visceral artery emergencies d. H epatic artery bleeding after biliary drainage

Richard McWilliams

Royal Liverpool University Hospital, Liverpool, United Kingdom

Haemorrhage from a hepatic artery pseudoaneurysm after biliary drainage may present as a life threatening emergency. Once suspected the diagnosis may be easily made at CT angiography if there is a large pseudoaneurysm. Therapeutic endovascular options include hepatic artery occlusion with embolization coils or covered stent insertion if a major hepatic artery is involved. The classical presentation is with upper abdominal pain, upper gastrointestinal bleeding and jaundice. Access to the hepatic artery can be difficult and a strategy must be developed with reference to the CT dataset. The techniques and equipment overlap considerably with those used to gain stable visceral artery access and stent placement during complex EVAR. The following clinical case demonstrates most of these points. A 70 year old man with cholangiocarcinoma underwent percutaneous biliary drainage and placement of an internal/external biliary drain (Figure 1). This was subsequently converted to internal biliary drainage with a meFigure 1: Transhepatic tallic self-expanding stent (Figure 2). cholangiogram showing biliary obstruction. Two months after this during a protracted hospital stay due to post-ERCP pancreatic necrosis, he became septic and dropped his haemoglobin to 6.6g/dL. He had previously undergone aortic surgery and the differential diagnosis included haemobilia and aorto-enteric fistula. Enhanced CT scanning showed no evidence of an aorto-enteric fistula nor was there evidence of hepatic artery pseudoaneurysm. There was no air in the bile ducts and haemobilia was suspected (Figure 3).

Figure 2: A self-expanding biliary stent has been inserted.

Figure 3: Axial CT section showing absence of air in the biliary tree. Air is expected with a patent biliary stent.

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A percutaneous cholangiogram showed blood clot in the bile ducts and a biliary drain was placed (Figure 4). After one week the drain was removed but after a further week he had more gastrointestinal bleeding and was found to be bleeding from the ampulla of Vater at endoscopy. CT angiography did not reveal the cause of bleeding and did not show a pseudoaneurysm. The following day he had significant further bleeding and catheter angiography was performed. This was made difficult by a stenosed coeliac axis origin (Figure 5). The initial angiograms showed no obvious bleeding (Figure 6) but selective catheterisation of the common hepatic artery showed a small Figure 4: Percutaneous pseudoaneurysm of the right hepatic artery near the upper end of the cholangiogram showing biliary stent (Figure 7). A 7Fr 55cm Cook flexor sheath was introduced extensive blood clot in the to the coeliac trunk over a stiff guidewire and a 6mm / 22mm Atrium biliary tree covered stent placed across the pseudoaneurysm (Figure 8). Establishing stable access for the stent used the standard sequence of steps used in fenestrated EVAR: initial placement of soft hydrophilic wire through a Sidewinder 1 catheter, then use of a hydrophilic catheter, then a stronger wire followed by a standard catheter and finally an Amplatz wire and Cook flexor sheath. Review of the CT scans allowed a retrospective diagnosis of a small pseudoaneurysm but this was not well shown as this area was compromised by metallic artefact from the stent and its markers. There was no further bleeding after one year of follow up.This case illustrates the challenges in the diagnosis and treatment of hepatic artery pseudoaneurysms causing arteriobiliary fistulae and massive haemobilia. Figure 5: Sagittal CT MIP image shows coeliac axis stenosis

Figure 6: Coeliac axis angiogram shows no obvious abnormality

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Figure 7: Magnified selective right hepatic angiogram shows a pseudoaneurysm at the level of the upper biliary stent.

Figure 8: The pseudoaneurysm has been treated with a 6mm/22mm Atrium covered stent.

3. Visceral artery emergencies e. Acute renal failure due to suprarenal aortic occlusion

Richard McWilliams

Royal Liverpool University Hospital, Liverpool, United Kingdom

Two cases of renal failure associated with chronic infrarenal aortic occlusion are described. Successful renal revascularisation was performed with restoration of renal function. The circumstances are similar with longstanding infrarenal aortic occlusion and late progression to suprarenal occlusion. In both cases one of the kidneys was atrophic and the other remained grossly normal but was thought to have a chronic ostial stenosis which occluded. A collateral blood supply was enough to maintain viability of the kidney but both patients required dialysis. A transbrachial approach was used to revascularise the kidneys. Case 1 A 57 year old lady with a history of pseudoxanthoma elasticum and chronic infrarenal aortic occlusion presented in renal failure (Figure 1). The right kidney was atrophic but the left kidney was of normal size and there was flow in renal branches from a collateral supply (Figures 2 and 3).

Figure 1: 3D CT reconstruction showing chronic aortic occlusion

Figure 2: Axial CT image showing aortic occlusion but there is contrast medium in the left renal artery

Figure 3: Thick MIP image from CT dataset showing reconstitution of the left renal artery beyond the aortic and ostial occlusion

She was started on dialysis but did not dialyse well and had intractable pulmonary oedema. She was considered too ill for open surgical bypass. After one month of problematic dialysis the nephrology team were considering withdrawal of dialysis and a request was made to our service for endovascular intervention. Recanalisation looked feasible but planning from the CT dataset indicated that a renal stent would partially cover an already stenosed superior mesenteric artery as the stent passed from 137

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the occluded to the patent aorta (Figure 4). An Atrium stent was placed in the SMA to protect this (Figure 5) and the left renal artery recanalised and stented with a self-expanding stent (Figures 6, 7). Following this she had a massive diuresis, her renal function normalised and her lungs improved markedly.

Figure 4: Lateral angiographic image showing SMA stenosis

Figure 5: An Atrium stent has been placed in the SMA

Figure 6: Left renal angiogram after the occlusion was crossed

Figure 7: Angiogram after deployment of left renal stent

Case 2 A 58 year old man was admitted anuric to our intensive care unit. Initial ultrasound showed atrophy of the left kidney. The right kidney measured 10.9cm in length and looked structurally normal with no hydronephrosis. A CT scan five years earlier had shown infrarenal aortic occlusion with left renal artery occlusion and a patent right renal artery. A repeat CT study showed progressive disease with additional occlusion of the right renal artery (Figures 8, 9). There was enhancement of the right renal artery due to collateral blood supply but the patient was dialysis dependent. Open surgical repair was thought to be too high a risk and endovascular treatment was planned. A left brachial approach was used with a 90cm sheath. The occlusion was crossed and a 7mm x 6cm Fluency stent placed (Figure 10). Balloon dilatation to 7mm was performed and there was a tight waist at the level of the renal artery ostium (Figure 11).

Figure 8: CT MIP image showing atrophy of the left kidney and normal sized right kidney

Figure 9: CT MIP Figure 10: Right renal showing showing arteriogram after crossing aortic occlusion with the occlusion reconstitution of the right renal artery

Figure 11: Balloon dilatation after deployment of the Fluency stent

The intention was to assess the appearance of the SMA after renal stent deployment and decide if a parallel stent was required in the SMA which could have been partially covered by the renal stent. At this point the patient became acutely unwell, very soon after balloon angioplasty. This was thought due to flash pulmonary oedema which did not respond to medical management. He was transferred to intensive care for emergency dialysis. His oedema resolved and his renal function returned and he became independent of dialysis. US and later CT scanning showed partial coverage of the SMA by the 138

e. Acute renal failure due to suprarenal aortic occlusion, Richard McWilliams

Fluency stent but there was no haemodynamic effect from this and no symptoms of mesenteric ischaemia. No intervention was performed on the SMA. He was well on discharge from hospital and remains off dialysis more than one year after the intervention. Conclusion Renal function may be salvaged in patients with infrarenal occlusion which progresses above the renal arteries. We suspect there was chronic renal artery stenosis in these two cases which encouraged a collateral supply to develop and this supply maintained the viability of the kidneys until the renal arteries were successfully revascularised. There are technical challenges in these cases as the renal stent needs to be taken significantly higher than the renal artery ostium in view of the aortic occlusion which progresses cranially to the next patent vessel: the SMA. The potential for compromise of the SMA depends on where the stent is expected to lie and also if the stent is fabric covered. A strategy for this must be part of the procedural plan.

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4. Special contribution Current Status of Drug Eluting Stents and Drug-coated Balloons in the SFA

Gunnar Tepe

Institute for Diagnostic and Interventional Radiology, Academic Hospital, RoMed Clinics Rosenheim, Germany

Introduction Percutaneous transluminal angioplasty has an expanding role as a primary minimally invasive treatment option for patients suffering from peripheral arterial occlusive disease. However, Percutaneous transluminal angioplasty entails a high incidence of restenosis of up to 50 % in the first year after the intervention.[1-3] Restenosis rather than being a recurrence of occlusive arterial disease can be seen as a local arterial response to what Andreas Gruentzig called the â&#x20AC;&#x2DC;controlled injuryâ&#x20AC;&#x2122; of angioplasty and is characterised by growth of smooth muscle cells, roughly analogous to a scar forming over an injury. Therefore, the interest of researchers and physicians turned towards methods to suppress neointimal growth and restenosis such as systemic pharmacotherapy, irradiation, and local drug delivery. Considerable research on the delivery kinetic has been done.[4, 5] It is possible to deliver a drug within the first hours or days. In contrast slow release over the period of a few months can be obtained. Each drug might have different needs of the delivery kinetic. It has been shown that especially with drugs like sirolimus and everolimus a slow and longer release has to be performed in order to prevent restenosis whereas paclitaxel seems to be effective also with a shorter elution profile.[6] Besides all these variables it is important how the drug is attached to the stent struts. The drug might be adsorbed with no coating or embedded in a special coating material. Because the coating is still there when the drug has already gone the coating must no induce inflammation which subsequently results in neointimal proliferation. In addition the coating might contribute to a higher thrombogenicity.[7, 8] The last variable which might be modified is the drug itself. Anti-inflammatory immune-modulators (e.g. sirolimus, tacrolimus, dexamethason), antiproliferative drugs (such as methothrexate and taxol), migration inhibitors (like batimastat and probucol), or drugs which promote healing and reendothelialization (e.g. vascular endothelial growth factor, advanced coatings) might be used.[9, 10] Most of the currently used drugs have more than one action which interferes with the process of restenosis. Different ways for local drug delivery In the case of short time drug delivery there are different methods in order to get the drug in the arterial wall. One is as coating on the surface of stents â&#x20AC;&#x201C; the other possibility to deliver the drug during balloon inflation as a coating on balloons.[11] In case of DES there are several variables besides the drug. One is the stent and the other one is the coating. The design of the stent should ideally deliver the drug quite homogenous. In addition the coating allows to have different delivery kinetics 143

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– fast release, slow release, or even different drug could be release at the same time or one after the other. In case of drug coated balloons the so called spacer is very important. The spacer attaches the drug to the balloon surface and allows the drug to get quickly delivered into the vessel wall. It is not only the delivery of 1-3 minutes during balloon inflation but also the fact how long the drug is retained in the wall which is influenced by the spacer and the drug formulation. Even the delivery takes place over minutes the drug is retained in the vessel wall over weeks. This and the special characteristics of the drug especially paclitaxel makes it possible that despite short delivery there is long-term effect. During inflation the drug has to come of the balloon surface and has to be delivered into the vessel wall.[12-14] Even the same drugs were taken as a coating material there is considerable difference in the delivery efficacy of each balloon. Therefore it has to be pointed out that each drug coated balloons is different even the same drug might have been chosen Drug Eluting Stents in the femoropoliteal arteries There have been only three different DES reported in clinical trials. Sircocco was the first randomized trial with a DES in the femoropopliteal arteries[15, 16]. In this prospective multicentre randomized trial a total of 93 patients either received a siolimus coated nitinol stent of the same uncoated stent which is still available as the SMART stent (Cordis). The amount of drug was equivalent to the coronary approach – nevertheless due to the properties of the self-expanding stent the coating was different. This was followed by a much quicker release and a certain inflammation driven by the coating. The study was performed in two phases because after an interim analysis a quite high stent fracture rate was seen. Therefore the lesion length was reduced to 14.5 cm. This resulted in a mean lesion length of 8.3 cm. The primary endpoint was % diameter stenosis measured by an independent core lab based on an invasive anigiography after 6 months. After 6 months the % diameter stenosis was 22.5% in the sirolimus coated stent group versus 30.9% in the uncoated SMART stents. Nevertheless this benefit was lost in long term. After 24 months the in-stent restenosis rate measured by duplex ultrasound was 22.9% versus 21.1%. The lack of benefit lead to the termination of this program. Strides was the second trial which evaluated drug eluting stents[17]. The Strides stents were coated with Everolimus. In addition to the different drug also the release kinetic was much slower compared to the Sirocco stents. The so called Dynlink-E was a slow-eluting stent releasing 80% if his total content over three months. The study was a single arm study which was performed in 11 European sites. In total 104 patients were included. The mean lesion length was 9 cm. The primary endpoint was the restenosis rate measured with DUS. In addition at 12 months an angiography was performed. The results of the Strides DES were compared with a historical group of the Vienna study which compared the uncoated version of the Dynalink-E stent with PTA. It turned out that even the results of the DES looked favourable at 6 months, after 12 months no significant benefit compared to the historical control group was observed. The restenosis rates of the coated and the uncoated stent were nearly identical which also lead to the termination of this program. The Zilver PTX stent is the third DES which has been tested in a clinical study. This DES is a stent with a polymer-free paclitaxel coating (dose 3 µg/cm2) on the abluminal side of the stent struts[18]. The Zilver PTX stent was tested in a single-arm “all-comers” registry mainly done in Europe and a prospective study comparing the Zilver PTX stent against PTA mainly done in the US. Currently only the data of the registry have been published. In this registry up to 4 stents (with a length of 8 cm each) could be implanted. In addition even patients with in-stent restenosis could be treated within the protocol. In this single arm study a total of 787 patients received a mean of 2.2 DES per patient for a mean lesion length of 100±82 mm. 22% of the lesions were longer than 15 cm. After 12 months the fracture rate was 1.5%. The freedom of target lesion revascularization was 91.1% after 12 months and 84.3% after 24 months. The 12 months primary patency rate (evaluated by DUS with a peak velocity ratio of <2.5) was 86.2%. The authors concluded an approximately 50% reduction in restenosis compared to published bare metal stents. In addition several sub-studies including the use of DES in in-stent restenosis were 144

Current Status of Drug Eluting Stents and Drug-coated Balloons in the SFA, Gunnar Tepe

done. The Zilver PTX stent showed very high patency rates even in these challenging lesions. One example is given in figure 1. Figure 1: A patient with an in-stent restenosis of the SFA (left) was recanalized and treated with two Zilver PTX stents (middle). After 9 months no restenosis was noted (right)

The randomized study compared the Zilver PTX stent with the PTA. The study had two randomization protocols. If the PTA was thought not been successful the patients either received a DES or a bare Zilver stent. In this study a total of 479 patients were treated at 55 clinical trial sites in the US, Japan, and Europe. Approximately half of the patient of the PTA group underwent a second randomization. At the end from those patients who failed to primary PTA n=61 received a Zilver PTX stent and n=59 a bare Zilver stent. The mean treated lesion length was 63 and 66 mm, respectively. The primary patency was 83.1% in the Zilver PTX group and 64.3% in the PTA group. Patients who underwent standard of care angioplasty with provisional bare metal stents had significantly poorer patency rates compared to revascularization with the Zilver PTX (83.1% with the Zilver PTX vs. 32.8% with angioplasty vs. 65.3% with optimal angioplasty. To examine the drug effect, the investigators conducted a head-to-head comparison of secondary randomization to provisional stenting with Zilver PTX or BMS with patency rates of 89.9% and 73% at 12 months. This difference was significant. Only recently the 3 year data were released. At that time point the primary patency was 79.6% in the Zilver PTX stents compared to 56.3% in the uncoated stents. This is a reduction of restenosis rate of approximately 50% by the drug coating. Both the safety and the clinical success of the Zilver PTX stents lead to both, the CE mark and the FDA approval of this stent. Currently the Zilver PTX stent is the only nitinol based self-expanding drug eluting stent. Drug eluting balloons in the femoropopliteal arteries Since that time the first results of the Paccocath drug eluting balloon became available the enthusiasm on the drug eluting balloon technology was so great that besides bigger established companies also small startup-companies invested in basic research of drug eluting balloons 19. Table 2 summarizes the different companies and their approaches to develop a drug eluting balloon. This table is not complete because a lot of groups are currently working on drug eluting technologies. Nevertheless all approaches use Paclitaxel as component on their balloon surface. In addition the drug content on the balloon ranges in the same area of 2 to 3 Âľg Paclitaxel/mm2 balloon surface. The main difference of the balloons is the adjunct on the balloon which is very important to fix the drug on the balloon surface until balloon inflation. The drug carrier has also to enhance the drug uptake in the vessel wall. Therefore it follows that drug carrier is a very important factor which might result in a clinical effective delivery or in an un-effective delivery. Therefore each balloon has to be tested for safety and effectiveness even using the same drug Paclitaxel as active component. There have never been so many trials for prevention of restenosis in the lower limb than in these days â&#x20AC;&#x201C; and this is because all different drug eluting balloons have tested. The safety and success of one drug 145

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eluting balloon cannot be extrapolated to another device. Besides this there will be no reimbursement for unproven devices. The studies can be structured in three different types: a) Proof of concept (safety and efficacy). These studies have to compare the uncoated with the coated balloon. b) Additional indications. From the current results we do not know how the drug eluting balloons perform in certain indications. Therefore these indications have to be tested like a. SFA: In- stent restenosis b. SFA: with stents c. SFA: with artherectomy c) All comer registries for evaluation of the DEBs in clinical real-world setting. The THUNDER trial[3] is a German, randomized, blinded, multicenter study comparing Paccocath® paclitaxel-coated and conventional uncoated balloon catheters with respect to efficacy and tolerance in inhibiting restenosis in the femoro-popliteal arteries. In this trial, which included a two-year follow-up, a total of 154 patients with Rutherford class 1 – 5 symptoms and stenosis or occlusion of the superficial femoral or popliteal arteries was enrolled. Patients were either treated with an uncoated balloon (= control group), with a Paccocath® balloon (~ 3µg/mm2 Paclitaxel) or with an uncoated balloon and paclitaxel dissolved in the contrast medium, i.e., Ultravist®; 17.1 mg paclitaxel in 100 mL. The primary endpoint was late lumen loss (LLL) of vessel segment at 6 months; the secondary outcomes measures included binary restenosis, target lesion revascularization (TLR), and thrombosis. Mean lesion length was 7.4 cm; 27% of lesions were total occlusions, and 36% have been treated previously. At 6-, 12 and 24-month follow-up, treatment of patients with Paccocath® balloons was found to be associated with significant reductions in late lumen loss compared to patients of the control group or patients treated with paclitaxel dissolved in the contrast medium. Importantly, the rate of target lesion revascularization (TLR) at 6, 12 and 24 months after intervention remained significantly lower in the Paccocath group compared with both other groups. Interestingly, TLR rates were less than 10% for each time interval whereas for the plain balloon group the highest restenosis rates were found until 1 year with a remarkable reduction between 12 and 24 months. Compared to the Paccocath group, TLR rates for the patients treated with paclitaxel dissolved in the contrast medium was significantly higher at 6-month follow-up but comparable low after 12 and 24 months. Only 4% of the patients in the Paccocath group received additional stents in target lesion (versus 22% in the control group). No increase in thrombotic or embolic events was observed in the Paccocath group. The THUNDER trial is still ongoing and awaits results from 5-year follow-up. In the FEMPAC (Inhibition of Restenosis in Femoropopliteal Arteries: Paclitaxel-Coated Versus Uncoated Balloon: Femoral Paclitaxel Randomized Pilot Trial) trial 20, 87 patients with Rutherford class 1 to 5 with femoro-popliteal artery occlusion or stenosis were randomly assigned to the treatment with either standard balloon angioplasty or the Paccocath® balloon. Forty-two patients were allocated to the control group (= uncoated balloon) and 45 patients to the Paccocath group. At 6-month follow-up, patients treated with the Paccocath® balloon had significantly reduced LLL compared with the control subjects. The difference between both treatment groups was maintained 18-24 months after intervention. No adverse events attributable to paclitaxel were reported. Furthermore, patients in the coated balloon group also showed improvement in Rutherford class, but no difference in the improvement in ankle brachial index was found. Nine percent of the patients in the Paccocath group vs. 14% in the control group required additional stent implantation in target lesion. Compared to the THUNDER trial, LLL the control group was lower in this study. Nevertheless, the FemPac trial confirmed the results of the THUNDER trial, demonstrating that short-term exposure of injured peripheral arteries to paclitaxel may be sufficient to inhibit restenosis. Both studies create new hope to surrender the problem of restenosis development especially in the SFA area. 146

Current Status of Drug Eluting Stents and Drug-coated Balloons in the SFA, Gunnar Tepe

The LEVANT 1 trial [Tepe ISET 2013] enrolled 101 patients with femoro-popliteal de novo lesions that had to be pre-dilated with an undersized balloon. If pre-dilatation was successful, the patients were randomized to be treated either with a paclitaxel coated MOXY™ balloon (drug dose ~ 2µg/mm2 Paclitaxel; n = 37) or a standard balloon (control group; n=38) sized according to the reference vessel diameter. Patients with insufficient result after pre-dilatation received a stent and were than randomized for post-dilatation using either a MOXY™ balloon (n=12) or a standard balloon (n=14). Primary endpoint was the angiographic LLL at 6 months follow-up. At 6-month follow-up, LLL and TLR rates were significantly reduced in the MOXY group (0.46 mm in the DCB group and 1.09 mm with uncoated balloons). Besides these angiographic results only recently the clinical results 24 months after the index procedure were released. The rate of TLRs was significantly reduced in the MOXY™ balloon group. Nevertheless the LEVANT 1 study showed some technical limitation of the DEBs and the endovascular procedure which lead to reduced efficacy of the DCBs. First if all due to the manufacturing process some of the DCBs did not open during inflation process. Some were twisted which followed that the DCB did not reach out to the vessel wall surface and therefore could not deliver the drug. In addition it was found out that in several patients DCBs were used which were too short. It follows that they ended in the atherosclerotic plaque which lead to a lack of efficacy at the end of the treatment area. Biolux PI Data of another DEB where presented but not published until now. The Passeo Lux-18 was developed by Biotronic also using PTX as active drug at a dose of 3 µg/mm2. A total 60 patients have been randomized either receiving the DCB or and uncoated balloon. The lesion length of 5.1 cm (DCB) and 6.9 cm (bare balloon) was slightly less compared to the other trials. At 6 months the binary restenosis rate could be significantly reduced by the DCB. (11.5% vs. 34.6%). In contrast at that time point the TLR rate did not differ between the groups. Nevertheless it turned out that in the 12 months interval the DCBs showed significant benefit also in respect to the TLR rate. The Passeo-Lux 18 balloon is currently the only DCB which lacks a CE mark. Nevertheless this does not seem to be related to both the safety and the efficacy profile. In the Pacifier trial Werk et al. randomized 91 patients either to receive a drug coated balloon In.Pact Pacific (Medtronic) or an uncoated balloon[21]. The primary end point was late lumen loss at 6 months assessed by blinded angiographic core lab analysis. Average lesion length was 7.0 and 6.6 cm for the DCB and the uncoated balloon respectively. 6 months angiography showed that the DCB was associated with significantly lower late lumen loss (-0.01 vs. 0.65 mm) and reduced restenosis rate (8.6% vs. 32.4%). This benefit was also reflected by the reduced rate of TLR at 12 months (7.1% vs. 27.9%). These four trials were summarized in a recently published meta-analysis of randomized trials comparing PTX-coated angioplasty versus uncoated balloon angioplasty[22]. The authors concluded that these devices were safe and effective reducing the restenosis rate. Further trials with DCBs vs. uncoated balloons in the SFA either ongoing or with no presentation of the data until now The ADVANCE 18 multi-center trial was initially designed to enroll 100 patients with symptomatic femoro-popliteal artery Rutherford category 2 to 4 comparing the treatment of de novo or restenotic lesions including instent lesions with either the Advance 18 PTX™ balloon or the conventional Advance™ balloon. In the meantime, the sample size was increased to 150 patients. Lesion length ranges from 4 to 19 cm. Primary study endpoint is the angiographic 6-month LLL with a follow-up period of 24 months. The Advance-18 DCB is the product of Cook. Even Cook obtained a CE for the DCB, this balloon is currently not available for clinical use. The FREERIDE study is a multicenter study to compare the DCB of Eurocor with uncoated balloons. The Eurocor DCB also uses PTX as active component. The drug is attached with Shellak to the balloon 147

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surface. In total 280 patients will be randomized either receiving a DCB or an uncoated balloon. In Q IV 2012 approximately 40 patients were already entered in the study. Further studies for FDA approval in the SFA Both Lutonix/BARD and Medtronic are currently aiming for an FDA approval of their DCB. Both companies finished their enrollment of US studies comparing the DEB with the uncoated balloon in several hundred of patients. The aim was to compare the pure effect of the DCB which lead to a remarkable low stenting rate. Big all-comers registries Both Medtronic and Lutonix/BARD are currently enrolling in “all-comers” registries. Medronic is currently doing a 1500 world-wide patient trial (In.Pact Global) with several subgroups especially investigation long lesions, in-stent restenosis and subintimal angioplasty. All lesions in the subgroups will be followed by DUS evaluated by a core lab. Also Lutonix/BARD is doing two somewhat smaller registries. The aim of this kind of studies is to investigate the effect of DCB in the all-day clinical reality also capturing rare side effects or limitations. Unlike the other controlled studies there are almost no exclusion criteria. The idea is to support the data of their SFA trials aiming for FDA approval.

DCB studies for further indications

In-stent Restenosis The FAIR (Femoral Artery In-Stent Restenosis) multi-center trial compares the treatment of instent restenosis in a length up to 20cm in patients randomly assigned to either IN.PACT Admiral™ drug eluting balloon angioplasty or standard balloon angioplasty with Admiral™ Extreme balloons (control group) in 118 patients. Primary study endpoint is freedom of restenosis as detected by duplex ultrasound after 6 months. The Copa Cabana Study is an investigator initiated prospective randomized study to compare Cotavance drug coated balloon (Medrad) with uncoated balloons in the SFA and popliteal arteries. The study is aimed at 100 patients. Currently approximately 60 patients have been entered into the trial. The primary endpoint is late lumen loss detected by angiography at 6 months follow-up. The difference between this and the other in-stent restenosis trials is that the investigators use angiography in addition with an independent core lab for the primary endpoint. Also the study lesions are allowed to be longer compared with the other trials. The PACUBA study is a monocenter study investigating the Eurocor Freeride DCB. 60 patients are currently randomized to either receive a DCB or an uncoated balloon. To date 36 patients have been treated within the protocol. Follow-up will be at 6 and 12 months with DUS or CTA. Further indications: The FREEWAY Stent study investigates the effect of the Eurocor DCBs on the TLR rate of stented femoral artery lesions. All lesions receive a stent. This nitinol stent is either post-dilated with a DCB or an uncoated balloon. Like the Freeride study a total of 280 patients will be randomized. The primary endpoint is the clinical driven TLR rate at 6 months. In an interim analysis in January 2013 there was a benefit for the Freeway DCB (2.5% TLR rate vs. 10.2% with the uncoated balloon) in a total of 79 patients. A possible further indication of DCBs is the use in AV-fistula. This indication in investigated in several small investigator initiated trials especially with the In.Pact DCBs. Besides this the below-the knee use for prevention of amputation in CLI patients is also investigated in several trials. Because this indication would aim for an independent book chapter (both for DES and DEBs) this topic will not be 148

Current Status of Drug Eluting Stents and Drug-coated Balloons in the SFA, Gunnar Tepe

further described. Further publications on DCBs in the SFA In addition the ongoing prospective trials there have been also some publications on data obtained with DEBs in several indications. All these publications are either registries with no control group or small cohort studies. Micari et al. published their registry evaluating the PTX coated In.Pact balloon in a total of 105 patients[23]. The mean lesion length of 7.6 cm did not differ from all the other trials. Only 12.3% of the lesions required stenting. At 12 months follow-up 92 of 105 patients were evaluable. The primary patency rate was 83.7% and the TLR 7.6%. Interestingly they could show a significant improvement of Quality of Life and absolute claudication distance followed by the DEB treatment. In the DEBELLUM trial Fanelli et al. randomized 50 consecutive patients with 122 lesions in the femoropoliteal or below the knee arteries either to receive a DEB (In.Pact) or an uncoated balloon[24]. After 6 months a significant effect of the DCB was noted. The TLR rate was reduced from 23.6% to 6.1%. The positive effect of DCBs was reflected by a higher patency rate in the SFA as well as in below the knee arteries. Only recently two publications were focused on possible further indications of drug coated balloons. Stabile et al. reported their results using the In.Pact DCB in a total of 39 patients with in-stent restenosis[25]. With this treatment they could obtain an astonishing high patency rate of 92.1% after 12 months. The mean lesion length was 8.3 cm. Cioppa et al. have pre-treated heavily calcified arteries with atherectomy in 30 patients (Turbohawk)[26]. They reported no side effects of the combined treatment. After one year the TLR rate was 10%. In summary, in various trials the efficacy and safety of the paclitaxel coated balloon could be shown. This technology together with alternative local drug delivery methods will change the endovascular therapy in the future. It is currently unknown for which indication DEBs and for which indications the Zilver PTX drug eluting stent should be used.

Tables Table 1: Ways and variables for local drug delivery To be modified Stent based

Short-time contact

a) stent design (homogenous delivery) b) delivery kinetic c) coating vs. adsorption d) drug a) mode of delivery (on a balloon, with a fluid) b) adjuncts/coating c) drug

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Table 2: Drug Coated Balloons. Companies and Products DEB Brand Manufacturer Drug Drug Carrier (Type)

References

150

IN.PACTÂ´ balloons CE MedtronicInvatec

SeQuent Please CE B.Braun

Urea (Molecule Spacer)

Iopromide (Contrast Media)

Cotavance Pantera Lux CEBayerMedrad Ultravist 370 (Contrast Media)

Biotronik

DIOR II

Elutax

Advance

Lutonix

CE Eurocor

CE AachenResonance

CE Cook

CE Lutonix

None

Unknown

PAC LITAX E L BTHC (ConShellac trast Media (Resin) Analog)

1. Bertomeu V, Morillas P, Gonzalez-Juanatey JR et al. Prevalence and prognostic influence of peripheral arterial disease in patients &gt;or=40 years old admitted into hospital following an acute coronary event. Eur J Vasc Endovasc Surg 2008;36(2):189-196. 2. Baril DT, Marone LK, Kim J, Go MR, Chaer RA, Rhee RY. Outcomes of endovascular interventions for TASC II B and C femoropopliteal lesions. J Vasc Surg 2008;48(3):627-633. 3. Tepe G, Zeller T, Albrecht T et al. Local delivery of paclitaxel to inhibit restenosis during angioplasty of the leg. N Engl J Med 2008;358(7):689-699. 4. Grube E, Silber S, Hauptmann KE et al. TAXUS I: six- and twelve-month results from a randomized, double-blind trial on a slow-release paclitaxel-eluting stent for de novo coronary lesions. Circulation 2003;107(1):38-42. 5. Stone GW, Ellis SG, Cox DA et al. One-year clinical results with the slow-release, polymer-based, paclitaxel-eluting TAXUS stent: the TAXUS-IV trial. Circulation 2004;109(16):1942-1947. 6. Wiskirchen J, Schober W, Schart N et al. The effects of paclitaxel on the three phases of restenosis: smooth muscle cell proliferation, migration, and matrix formation: an in vitro study. Invest Radiol 2004;39(9):565-571. 7. Carter AJ, Jenkins S, Sweet W et al. Dose and dose rate effects of beta-particle emitting radioactive stents in a porcine model of restenosis. Cardiovasc Radiat Med 1999;1(4):327-335. 8. Virmani R, Guagliumi G, Farb A et al. Localized hypersensitivity and late coronary thrombosis secondary to a sirolimuseluting stent: should we be cautious? Circulation 2004;109(6):701-705. 9. Schmehl J, Tepe G. Current status of bare and drug-eluting stents in infrainguinal peripheral vascular disease. Expert Rev Cardiovasc Ther 2008;6(4):531-538. 10. Tepe G. Drug-eluting stents for infrainguinal occlusive disease: progress and challenges. Semin Vasc Surg 2006;19(2):102108. 11. Speck U, Scheller B, Abramjuk C et al. Neointima inhibition: comparison of effectiveness of non-stent-based local drug delivery and a drug-eluting stent in porcine coronary arteries. Radiology 2006;240(2):411-418. 12. Scheller B, Speck U, Schmitt A, Bohm M, Nickenig G. Addition of paclitaxel to contrast media prevents restenosis after coronary stent implantation. J Am Coll Cardiol 2003;42(8):1415-1420. 13. Scheller B, Speck U, Abramjuk C, Bernhardt U, Bohm M, Nickenig G. Paclitaxel balloon coating, a novel method for prevention and therapy of restenosis. Circulation 2004;110(7):810-814. 14. Scheller B, Speck U, Romeike B et al. Contrast media as carriers for local drug delivery. Successful inhibition of neointimal proliferation in the porcine coronary stent model. Eur Heart J 2003;24(15):1462-1467. 15. Duda SH, Pusich B, Richter G et al. Sirolimus-eluting stents for the treatment of obstructive superficial femoral artery disease: six-month results. Circulation 2002;106(12):1505-1509. 16. Duda SH, Bosiers M, Lammer J et al. Sirolimus-eluting versus bare nitinol stent for obstructive superficial femoral artery disease: the SIROCCO II trial. J Vasc Interv Radiol 2005;16(3):331-338. 17. Lammer J, Bosiers M, Zeller T et al. First clinical trial of nitinol self-expanding everolimus-eluting stent implantation for peripheral arterial occlusive disease. J Vasc Surg 2011;54(2):394-401. 18. Dake MD, Scheinert D, Tepe G et al. Nitinol stents with polymer-free paclitaxel coating for lesions in the superficial femoral and popliteal arteries above the knee: twelve-month safety and effectiveness results from the Zilver PTX singlearm clinical study. J Endovasc Ther 2011;18(5):613-623. 19. Tepe G, Schmitmeier S, Zeller T. Drug-coated balloons in peripheral arterial disease. Eurointervention 2011;7 Suppl K:K70-6. doi: 10.4244/EIJV7SKA13.:K70-K76. 20. Werk M, Langner S, Reinkensmeier B et al. Inhibition of restenosis in femoropopliteal arteries: paclitaxel-coated versus uncoated balloon: femoral paclitaxel randomized pilot trial. Circulation 2008;118(13):1358-1365. 21. Werk M, Albrecht T, Meyer DR et al. Paclitaxel-Coated Balloons Reduce Restenosis After Femoro-Popliteal Angioplasty: Evidence From the Randomized PACIFIER Trial. Circ Cardiovasc Interv 2012;5(6):831-840. 22. Cassese S, Byrne RA, Ott I et al. Paclitaxel-coated versus uncoated balloon angioplasty reduces target lesion revascularization in patients with femoropopliteal arterial disease: a meta-analysis of randomized trials. Circ Cardiovasc Interv 2012;5(4):582-589. 23. Micari A, Cioppa A, Vadala G et al. Clinical evaluation of a paclitaxel-eluting balloon for treatment of femoropopliteal arterial disease: 12-month results from a multicenter Italian registry. JACC Cardiovasc Interv 2012;5(3):331-338.

Current Status of Drug Eluting Stents and Drug-coated Balloons in the SFA, Gunnar Tepe

24. Fanelli F, Cannavale A, Boatta E et al. Lower limb multilevel treatment with drug-eluting balloons: 6-month results from the DEBELLUM randomized trial. J Endovasc Ther 2012;19(5):571-580. 25. Stabile E, Virga V, Salemme L et al. Drug-eluting balloon for treatment of superficial femoral artery in-stent restenosis. J Am Coll Cardiol 2012;60(18):1739-1742. 26. Cioppa A, Stabile E, Popusoi G et al. Combined treatment of heavy calcified femoro-popliteal lesions using directional atherectomy and a paclitaxel coated balloon: One-year single centre clinical results. Cardiovasc Revasc Med 2012;13(4):219-223.

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152

Authorâ&#x20AC;&#x2122;s Index A

Timur Abdulamit . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Vittorio Alberti . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

Patrice Bergeron . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

Piergiorgio Cao . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Carlo Cernetti . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77 Lyubov Chaykovska . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Rachel Clough . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59 Carlo Coscarella . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47

Ciro Ferrer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Luca Favero . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77 Stefano Fazzini . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 Olivier Hartung . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103

Athanasios Katsargyris . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 Holta Kasemi . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

Mario Lachat . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Thomas Larzon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Antonio Lorido . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Oli Lyons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59

153

154

Nicola Mangialardi . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 Dieter Mayer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Richard McWilliams . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135, 137 Nunzio Montelione . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Christoph Nienaber . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

Gabriele Pogany . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Felice Pecoraro . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Nicola Pellizzari . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77 Claudio Rabbia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127 Zoran Rancic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Sonia Ronchey . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 Maria Antonella Ruffino . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127 Carlo Setacci . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81 Eugenia Serrao . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

Peter R. Taylor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59 Jรถrg Teร arek . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65, 115 Gunnar Tepe . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143 Jean-Christophe Trastour . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

Eric Verhoeven . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 Isabelle Van Herzeele . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97 Michael Wholey . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89, 119

155