Introduction

In 1956, Birch et al. reported the first case of anastomotic aneurysm in a patient after prosthetic aortic graft placement. Since then, anastomotic aneurysms have been recognized as an infrequent, although important, late complication of prosthetic arterial reconstruction. Although true native aneurysmal degeneration may occur at an anastomotic site, the majority of anastomotic aneurysms are false because they are composed of a fibrous pseudocapsule rather than the normal component layers of the arterial wall. Notably, anastomotic aneurysms have the potential for significant morbidity and mortality, and they present clinical challenges in their detection, evaluation, and management.

Incidence and Anatomic Location

Overall, anastomotic aneurysms complicate 1% to 4% of arterial anastomoses. The incidence of anastomotic aneurysms, however, is influenced substantially by anatomic location, surgical technique, time from anastomotic construction, integrity of the host artery at the original operation, and other local and systemic factors. When reporting incidence, anastomotic aneurysm formation may be described by the number of patients, or more accurately, by the number of anastomoses, as a patient with an aortobifemoral bypass, for instance, has one aortic anastomosis and two femoral anastomoses at risk.

The interval to presentation of anastomotic aneurysm has increased. , Previously seen as an early phenomenon, anastomotic aneurysms in most modern series present at a mean of 6 years following graft implantation, although associated infection can shorten this interval dramatically. Anastomotic aneurysms after reconstruction for aortoiliac occlusive disease are more likely to have late presentations (16 years vs. 9 years for aneurysmal aortic disease) and are more likely to represent degeneration of the anastomosis rather than true aneurysmal change.

The most common anatomic site of anastomotic aneurysm formation is the femoral artery, complicating from 0.5% to 24% of reconstructions. In a large retrospective analysis of anastomotic aneurysms after prosthetic reconstructions for aortoiliac occlusive disease, van den Akker et al. reported an overall incidence per patient of 13% and an incidence per anastomotic site of 4.8%, 6.3%, and 14% for aortic, iliac, and femoral anastomoses respectively. In addition, the cumulative freedom from anastomotic aneurysm formation at 15 years was 92%, 84%, and 76% for aortic, iliac, and femoral sites. This propensity of anastomotic aneurysms to form at the femoral location has been documented by others. ,

Large retrospective studies of graft-related complications for abdominal aortic aneurysm repair report a cumulative incidence of anastomotic aneurysm of 1.3% to 3.0%. , Based on three decades of experience with open repair of extent I to IV thoracoabdominal aortic aneurysms, Latz et al. reported a cumulative incidence of anastomotic aneurysms of 2.6% to 3.0%. , The incidence of aortic and iliac anastomotic aneurysms, however, is probably underestimated because of inadequate surveillance, prolonged time to recognition, and their initially quiescent behavior. Studies with routine radiologic surveillance estimate the incidence of anastomotic aneurysms of the aorta and iliac arteries to be approximately 10%, and may reach 36% by Kaplan–Meier analysis at 15 years. , ,

The documented incidence of anastomotic aneurysms following carotid endarterectomy (with or without patch angioplasty) is much lower, approximately 0.3%. However, following repair of extracranial carotid aneurysms, anastomotic aneurysms can complicate 13% to 57% of cases. The interval to presentation may occur as early as weeks following carotid intervention, although the majority of reported cases present from 5 to 12 years after reconstruction. With improved operative technique and the introduction of superior prosthetic materials, carotid anastomotic aneurysms are most commonly associated with surgical site infection and, more specifically, prosthetic infection (see Ch. 97 , Carotid Artery Aneurysms).

Pathogenesis

An anastomosis between two vascular structures is potentially subject to failure and hence aneurysm formation. Anastomotic aneurysms occur almost exclusively between prosthetic grafts and native arteries, with only rare occurrences in completely autogenous anastomoses. When a suture line between two vascular structures is disrupted, an anastomotic aneurysm may form. The egress of blood from the defect forms a pulsatile hematoma that, while in continuity with the bloodstream, becomes lined peripherally with laminated thrombus that eventually becomes encapsulated by surrounding host tissue. A fibroblastic process that initiates the formation of a tissue capsule ensues. The capsule, essentially a false aneurysm cavity, is subjected to systemic arterial pressure and may gradually enlarge, occasionally resulting in local complications of expansion, distal embolization, or rupture.

Several etiologic factors have been implicated in the pathogenesis of anastomotic aneurysms yet the relative importance ascribed to each factor varies substantially by author or institutional experience. Nonetheless, because anastomotic disruption is pivotal in anastomotic aneurysm formation, the pathogenesis may be conceptualized simplistically by considering local and systemic etiologic factors. Each factor may induce or contribute to anastomotic failure, and each has assumed prominence during various time periods. Because no robust data exist to corroborate the contribution of some of these factors to the development of anastomotic aneurysms, several factors are accepted on a theoretical basis alone ( Box 50.1 ).

BOX 50.1
Factors Associated with the Development of Anastomotic Aneurysms

Local

  • Arterial wall degeneration

  • Suture line disruption

  • Prosthetic graft failure

  • Infection/inflammation

  • Technical errors

  • Mechanical stress

Systemic

  • Smoking

  • Hyperlipidemia

  • Hypertension

  • Anticoagulation

  • Systemic vasculitides

  • Generalized arterial weakness

Local Factors

Arterial Wall Degeneration

Degeneration of the host arterial wall is often associated with progression of atherosclerosis, which compromises vessel integrity and impairs a critical component of the vascular anastomosis. , , A consistent operative finding at exploration for anastomotic aneurysm is an intact unit of suture and prosthesis that has nonetheless separated from an attenuated arterial wall. In a cohort of 45 patients with 49 anastomotic aneurysms, Skourtis et al. demonstrated the contribution of host arterial degeneration. After operative treatment, 28 arterial specimens were examined microscopically and demonstrated a reduction or absence of elastic fibers in the media and replacement of smooth muscle cells by acellular fibrous connective tissue. Hyaline degeneration of the media and adventitia was also appreciated. In these instances, however, it can be difficult to differentiate anastomotic false aneurysm development from true aneurysmal degeneration of the native vessel.

Suture Line Disruption

Prosthetic graft anastomosis with a native artery depends indefinitely upon the integrity of the suture line, as no lasting union occurs as it would between two native vessels. Suture material, particularly silk, was recognized as a central factor contributing to anastomotic aneurysm formation in early reports. Silk suture gradually dissolves and is eventually resorbed by phagocytosis and other processes. This discovery culminated in the abandonment of silk suture for vascular anastomosis. Unfortunately, several successors of silk, including polyethylene and nylon, were also implicated in anastomotic aneurysm development, in general because of loss of tensile strength and ultimate suture disruption. Monofilament polypropylene (Prolene, Ethicon, Livingston, Scotland) suture was introduced commercially in 1969 and has enjoyed favor among vascular surgeons primarily because of its minimal tissue reactivity, low thrombogenicity, inherent resistance to infection, low coefficient of friction during suturing, and excellent maintenance of tensile strength without biodegradation. Despite these advantages, polypropylene suture readily frays and fractures, particularly with instrumentation and indiscriminate handling ( Fig. 50.1 ). Polytetrafluoroethylene (PTFE) suture is preferred by some surgeons because of its favorable suturing characteristics and relatively inert behavior in tissues, although its breaking strength is half that of polypropylene.

Figure 50.1, Electron Microscopy of Polypropylene Suture.

Nonsuture methods of vascular anastomosis that have recently been explored include rings, staples, clips, cuffs, stents, and adhesives. Purported advantages of nonsuture methods include decreased tissue reactivity, diminished vessel trauma, and technical simplicity and efficiency. Only clips are associated with an acceptable complication profile. However, these methods have been reported in only small case series, and before adoption can become widespread, long-term data are needed, especially regarding the incidence of anastomotic aneurysm formation.

Graft Failure

Both early and modern generations of prosthetic grafts have infrequently been incriminated as important factors in anastomotic aneurysm formation. Although knitted and, less commonly, woven polyester grafts dilate over time, they consistently maintain their structural integrity. Notwithstanding, several investigators have associated textile graft dilatation and compliance mismatch between the graft and host artery with development of anastomotic aneurysms. Thus, prosthetic grafts may indirectly contribute to late anastomotic disruption. , , A potential disadvantage of woven polyester grafts is their tendency to fray with handling. However, incorporation of a greater margin of graft into the anastomosis functionally eliminates this feature as a cause of late anastomotic failure (see Ch. 66 , Prosthetic Grafts).

Infection and/or Inflammation

Inflammatory states are recognized causes of anastomotic aneurysms, and are frequently the etiology when they occur in the early postoperative period. An inflammatory process may occur in response to implantation of prosthetic materials, postsurgical hematoma or lymphocele, or acquired vasculitides, such as Behçet disease. Inflammation caused by acute or indolent graft infection may also lead to anastomotic aneurysm formation ( Fig. 50.2 ). Even in the absence of clinical signs of infection, bacterial isolates, especially coagulase-negative staphylococci, have been isolated from as many as 60% to 80% of excised graft material. Although streptococci or staphylococci are the commonly implicated pathogens in graft infections, anerobic species such as Propionibacterium have also been isolated from anastomotic aneurysms.

Figure 50.2, Infected Anastomotic Aneurysm Involving the Distal Femoropopliteal Bypass Graft.

Technical Errors

Meticulous attention to suturing, including incorporation of generous portions of the arterial wall, especially in arteries subjected to concurrent endarterectomy, is paramount in preventing eventual anastomotic breakdown. Graft tension during construction of an anastomosis also contributes to late disruption and aneurysm formation. Incorrect suture handling, such as grasping the suture with forceps or clamps, may fracture sutures and predispose an anastomosis to late failure. The use of sutures of adequate strength and size also assists in minimizing technical errors.

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