Aneurysms of the Popliteal Artery [1st ed.] 9783030496869, 9783030496876

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Aneurysms of the popliteal artery Antonino Cavallaro Editor

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Aneurysms of the Popliteal Artery

Antonino Cavallaro Editor

Aneurysms of the Popliteal Artery

Editor Antonino Cavallaro Past Professor of General Surgery “Sapienza” University Rome Italy

ISBN 978-3-030-49686-9    ISBN 978-3-030-49687-6 (eBook) https://doi.org/10.1007/978-3-030-49687-6 © Springer Nature Switzerland AG 2021 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Foreword

“The glory of medicine is that it is constantly moving forward, that there is always more to learn.” William James Mayo, 1928

Progress in medicine has been relentless and, during the last two decades, endovascular treatment revolutionized the management of vascular diseases. Treatment of aortic and arterial aneurysms has been no exception. The publication of this comprehensive textbook on popliteal aneurysms has been timely and greatly needed by trainees, practicing vascular surgeons, and other vascular specialists. Aneurysms of the Popliteal Artery edited and in great part written by Antonino Cavallaro, past Professor of Surgery of the “Sapienza” University of Rome, Italy, is an outstanding multidisciplinary contribution to the field of aneurysm treatment, scripted in collaboration with interventional radiologists and surgical pathologists, all from leading Italian medical schools and hospitals. Stimulated by his first acquaintance with popliteal aneurysms as a young surgical pathologist, Professor Cavallaro presents us his rich and expert lifetime experience that he collected at his renowned many years of surgical practice at “Sapienza” and during the time he spent in a small bush hospital in remote Southern Cameroon. This all-inclusive, beautiful book is thoroughly searched, scholarly written, clearly presented, eminently illustrated and contains over 2100 essential references on the topic. The author takes us on a fascinating journey to discover all aspects of popliteal artery aneurysms, from little-known and long-­ forgotten historical facts to the Hunterian ligation and to detailed embryology, anatomy, and pathology of the popliteal artery and the clinical presentation of patients with popliteal artery aneurysms. The anatomy illustrations are clean and masterful. The preparations are exceptional. The pathology specimens and histology pictures are excellent and demonstrative. Evaluation with imaging studies is described in detail, and data-packed chapters with color illustrations and superb intraoperative photographs on open surgical and endovascular treatment are presented. The volume finishes with a special treat of a comprehensive review of non-­ atherosclerotic popliteal artery aneurysms, a gem you will not find in similar textbooks on this subject. The book is comprehensive in every aspect as it presents technical details and tabulates results of a whole spectrum of open and endovascular techniques. The most important message is that ultimately we need to focus on the individual patient, who presents with an a­ symptomatic v

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or symptomatic popliteal aneurysm or with severe limb ischemia caused by thromboembolism due to the aneurysm. Based on extensive review of the literature, including the most recent meta-analyses, the authors state that open surgery remains the preferred technique of repair. It should be offered to those who have a good saphenous conduit, who are young, symptomatic, or have a poor runoff. Endovascular treatment found its place in popliteal aneurysm repair, but, until further progress in technology, it should be used selectively, in those with acute and difficult presentation, in the frail, and in the elderly. This book of Professor Cavallaro hopefully will get on the bookshelf of many vascular trainees and specialists. The magnificent illustrations, the colorful tables, the beautiful printing, and the well-written text are both educational and stimulating. There is much to do in the field of aneurysm treatment to save lives, salvage limbs, and improve the quality of life of these patients. I have no doubt that those who read and consult this book will be in the forefront to fight this devastating disease. Peter Gloviczki Rochester, MN, USA

Foreword

Preface

I was a 21-year old student of medicine (3 years would still lapse to achieve the degree of MD) and, fascinated by surgery, I spent many day and night hours in the Institute of Surgical Pathology of the University of Catania. The running year was 1960, and reconstructive arterial surgery was taking the first steps; amputation for limb gangrene was rather frequent. Students were often committed to dissect the amputated limb and make a report on the conditions of the arterial tree and encouraged to use drawings and pictures. I had never encountered a popliteal aneurysm and was really astonished when I found that, in a mid-thigh amputated lower limb, the cause of gangrene was a thrombosed popliteal aneurysm: the thrombus was rather recent and extended diffusely into the tibial vessels. The aneurysm had a diameter of 32 mm and a length of 35 mm. But for the localized arterial dilatation, the arteries looked normal (the patient was 48 years old). This was the beginning of my continuing interest and attention for popliteal aneurysms. After retiring from academic and hospital activities, I decided to put hands on the clinical and literary material I had collected, in the hope of giving a realistic image of the current state of the art on this still challenging and controversial aspect of arterial pathology. My thanks go to the colleagues who accepted to contribute to this book: to Mrs. Enrica Salone, responsible for the Library of Surgery and Anesthesiology Departments of the University “Sapienza,” Rome, for the invaluable help in the bibliographic research and as a trait d’union with NILDE (National InterLibrary Document Exchange). Particular and friendly thanks to Bernardo Luraschi of the Department of Surgery “P. Valdoni” and to the Department itself, which allowed him to work with me, even after I went out from the university to become a private citizen: without the support of B. Luraschi and of his great capabilities as an artist, an expert on computer graphics and on “book building,” it would have been impossible for me to accomplish my task. Lovely thanks to my wife Rose, who agreed that I continue to dedicate many hours to “surgical problems” even after I was no more an active surgeon. Special thanks to Dr. Peter Gloviczki, who kindly and friendly accepted to read and comment on the manuscript. Rome, Italy January 2019

Antonino Cavallaro

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Contents

Part I History 1 A Surgeon’s Journey Through History Up to the End of the Nineteenth Century ��������������������������������������������������������������   3 Antonino Cavallaro 2 Modern Historical Background������������������������������������������������������  35 Antonino Cavallaro Part II The Popliteal Artery: Embryology and Anatomy 3 The Popliteal Artery: Embryology ������������������������������������������������  47 Antonino Cavallaro 4 The Popliteal Artery: Reminding Normal and Variant Anatomy����������������������������������������������������������������������  53 Antonino Cavallaro 5 Persistence of the Ischiadic Artery ������������������������������������������������  61 Antonino Cavallaro 6 Popliteal Artery Entrapment����������������������������������������������������������  73 Antonino Cavallaro Part III Popliteal Aneurysms: Pathology 7 Surgical Pathology ��������������������������������������������������������������������������  91 Pietro Gallo and Bruna Cerbelli Part IV Atherosclerotic Popliteal Aneurysms: Clinical Aspects 8 Definition, Prevalence, and Etiopathogenesis�������������������������������� 101 Antonino Cavallaro 9 The “Problem” of Arteriomegaly �������������������������������������������������� 115 Antonino Cavallaro 10 Outline of Patients with Atherosclerotic Popliteal Aneurysm������ 121 Antonino Cavallaro

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11 Clinical Presentation������������������������������������������������������������������������ 133 Antonino Cavallaro Part V Popliteal Aneurysms: Diagnosis 12 Diagnostic Procedures �������������������������������������������������������������������� 161 Alessandro Cannavale, Mariangela Santoni, Marianna Gazzetti, Fabrizio Fanelli, and Antonino Cavallaro Part VI Atherosclerotic Popliteal Aneurysms: Surgical Treatment 13 Operative Indication, Surgical Approach, and Tactics���������������� 179 Antonino Cavallaro 14 Primary Amputation, Endoaneurysmorrhaphy, Lumbar Sympathectomy, and the Use of Tourniquet���������������������������������� 193 Antonino Cavallaro 15 Treatment with Reestablishment of Circulation �������������������������� 203 Antonino Cavallaro 16 Late Sequelae of Surgical Treatment �������������������������������������������� 243 Antonino Cavallaro Part VII Atherosclerotic Popliteal Aneurysms: Endovascular Treatment 17 An Up-to-Date of Popliteal Artery Anatomy, Static and Dynamic�������������������������������������������������������������������������� 259 Antonino Cavallaro 18 Homemade and Early Stent-Grafts������������������������������������������������ 265 Fabrizio Fanelli, Pierleone Lucatelli, Carlo Cirelli, Renato Argirò, Filippo Maria Salvatori, and Antonino Cavallaro 19 The Hemobahn-Viabahn Stent-Grafts������������������������������������������ 271 Fabrizio Fanelli, Pierleone Lucatelli, Carlo Cirelli, Renato Argirò, Filippo Maria Salvatori, and Antonino Cavallaro 20 Other Stent Grafts and Hybrid Procedures���������������������������������� 287 Fabrizio Fanelli, Pierleone Lucatelli, Carlo Cirelli, Renato Argirò, Filippo Maria Salvatori, and Antonino Cavallaro 21 The Current Role of Endografting ������������������������������������������������ 295 Fabrizio Fanelli, Pierleone Lucatelli, Carlo Cirelli, Renato Argirò, Filippo Maria Salvatori, and Antonino Cavallaro

Contents

Contents

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Part VIII Non-atherosclerotic Popliteal Aneurysms 22 Behçet’s Disease�������������������������������������������������������������������������������� 313 Antonino Cavallaro 23 Kawasaki’s Disease�������������������������������������������������������������������������� 325 Antonino Cavallaro 24 Neurofibromatosis���������������������������������������������������������������������������� 331 Antonino Cavallaro 25 Fibromuscular Dysplasia���������������������������������������������������������������� 337 Antonino Cavallaro 26 Disorders of the Connective Tissue������������������������������������������������ 343 Antonino Cavallaro 27 Klippel–Trénaunay Syndrome, Parkes Weber Syndrome����������� 355 Antonino Cavallaro 28 HIV/AIDS ���������������������������������������������������������������������������������������� 361 Antonino Cavallaro 29 Mycotic Aneurysms�������������������������������������������������������������������������� 369 Antonino Cavallaro 30 Miscellaneous������������������������������������������������������������������������������������ 379 Antonino Cavallaro

Contributors

Renato Argirò, MD, PhD  Department of Diagnostic Imaging, Interventional Radiology, University “Tor Vergata”, Rome, Italy Alessandro Cannavale, MD, EBIR  Vascular and Interventional Radiology Unit, “Sapienza” University, Rome, Italy Antonino  Cavallaro, MD, FACS Past Professor of General Surgery, “Sapienza” University, Rome, Italy Bruna  Cerbelli, MD Department of Radiological, Oncological and Pathological Sciences, “Sapienza” University, Rome, Italy Carlo  Cirelli, MD Interventional Radiology Unit, “Belcolle” Hospital, Viterbo, Italy Fabrizio  Fanelli, MD, EBIR Vascular and Interventional Radiology Department, “Careggi” University Hospital, Florence, Italy Pietro Gallo, MD  “Sapienza” University, Rome, Italy Marianna Gazzetti, MD, PhD  “Villa Stuart” Hospital, Rome, Italy Pierleone  Lucatelli, MD, PhD, EBIR Interventional Radiology Unit, “Sapienza” University, Rome, Italy Filippo  Maria  Salvatori, MD  Interventional Radiology Unit, “Sapienza” University, Rome, Italy Mariangela  Santoni, MD Vascular and Interventional Radiology Unit, “Sapienza” University, Rome, Italy

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Part I History

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A Surgeon’s Journey Through History Up to the End of the Nineteenth Century Antonino Cavallaro

Aneurysms, at least external aneurysms, i.e., pulsating swellings in the neck or limbs, were certainly observed by our ancestors well before the birth of civilizations and the historical witness of these. The Papyrus Ebers (dated more than 1500  years BC) contains probably the first recorded medical description of aneurysmal disease, and the treatment appears to be committed to a surgeon using a cautery [1]. Hippocrates (ca. 460–377 bC) [2] and Celsus [3] (contemporary to the emperor Tiberius) do not write about aneurysm, while in the Indian encyclopedic treatise Sushruta Samhita [4], some diseases are mentioned that may be interpreted as related to aneurysm. Being the legendary life of Sushruta referred to the eighth to seventh century BC, a dispute arose about the priority of the Indian medicine and culture. Historians, probably moved also by some kind of national or racial pride, would debate for decades on this topic; but one must consider that the Indian and Greek cultures had continuing contacts, through the Persian empire, also before the stormy campaigns of Alexander the Great (356–323 BC), and that the Samhita was written through several centuries up to the first period of the Christian era. It is probable that both cultures, the Indian and the Greek,

A. Cavallaro (*) Past Professor of General Surgery, “Sapienza” University, Rome, Italy © Springer Nature Switzerland AG 2021 A. Cavallaro (ed.), Aneurysms of the popliteal artery, https://doi.org/10.1007/978-3-030-49687-6_1

arose and flourished in the same historical periods [5]. Rufus of Ephesus, who lived in the second half of the first century, is famous for his detailed statements on medical history-taking [6] and is commonly quoted, starting with Aetius of Amida (ca. 502–575) [7], as being the first to use the term aneurysm. Galenus (129–201), who refers to Rufus on many occasions, always demonstrating great consideration and respect, writes about the aneurysm, clearly describing how false aneurysms arise and as well that gentle compression may reduce their volume without leaving the sign of fovea, which is typical of tumors due to edema [8]. Galenus, after stating that it is difficult to treat injuries to the arteries, expresses the opinion that aneurysms are not amenable to cure. This giving-up attitude was firmly objected by Antyllus (third century) with the statement that it is not reasonable to leave to themselves all patients affected with aneurysm; Antyllus, demonstrating to have acquired a consistent experience in this field of surgery, outlines precisely the technique to be followed for successful treatment of both true (Fig.  1.1) and false aneurysms. Antyllus’ procedure is described by Oribasius (ca. 320–400) [9] together with his recommendations for a correct operative indication: • Do not attempt to treat too large aneurysms. • Do not attempt to treat aneurysms located in the neck or near the root of limbs (at or near 3

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a

b

Fig. 1.1  The Antyllu’s procedure for true or circumscribed aneurysms: (a) the aneurysm is underpassed with a needle bearing a double thread; this is cut so as to have two single threads; (b) the proximal thread is gently slipped cranially for ligature of the inflow arterial segment; (c) the distal thread is brought distally for ligature

c

d

of the outflow arterial segment; (d) the sac has been opened longitudinally, emptied, and packed with gauzes and different drugs to favor benign suppuration (evacuation of the sac content was deemed necessary, relying on the idea that the disease is due to the bad quality of the blood contained within the sac itself)

the axilla or the groin), because control of the arterial inflow is difficult or impossible. • Do not extirpate the aneurysm, as ligatures, albeit correctly placed, may slip under the impulse of blood, with ensuing lethal hemorrhage from the stump. The last procedure, i.e., resection of the aneurysm, was evidently practiced in the times of Antyllus; it is attributed to Philagrius, a physician from Epirus, who lived also during the third century [10]. For false aneurysm, Antyllus describes a method based upon mass ligature above and beyond the tumor, followed by incision of this. It is not clear if Antyllus applied his procedure both to upper and lower limb aneurysms, but probably almost exclusively arm aneurysms were treated, being easier the control of inflow. As well, being often these aneurysms a consequence of bloodletting, both true aneurysms and circumscribed false aneurysms (anévrysmes enkistés after Broca [11]) were operated with the same technique. Aetius of Amida described a variation of Antyllus’ procedure for aneurysms at elbow crease, based upon the preliminary section of the brachial artery, between ligatures, well above the aneurysm itself [12] (Fig. 1.2). Paul of Aegina (ca. 625–690) [13] textually reported the Antyllus’ procedure, without mentioning the source, however clearly stating that it is indicated to treat aneurysms consequent to

Fig. 1.2  Aetius’ method to treat brachial aneurysm at elbow crease: (a) double ligature and section of the brachial artery; (b) ligature of the artery above and beyond the sac and opening of this

arterial perforation, thus indirectly stressing the rarity of true brachial aneurysms, while mass ligature was reserved to pseudoaneurysms consequent to arterial laceration or rupture.

1  A Surgeon’s Journey Through History Up to the End of the Nineteenth Century

No other surgical procedures to treat aneurysms were described for centuries: the famous Albucasis from Cordoba (936–1013) still reports the operation described by Antyllus [14] and the same is done by Guy de Chauliac (1300–1368) [15]. The latter, however, stresses the indication, as the first therapeutic option, to external compression of aneurysm with leather apparatuses similar to those used to contain hernias. The Middle Age approaching to its end, a substantial advancement for the science and practice of surgery took place: dissection of human body, after more than a millennium of prohibition, was permitted, starting at the Salerno Medical School (at the beginning of the thirteenth century) and rapidly extended in other Medical Schools in Italy [16] and thereafter throughout many European countries. This milestone event prompted a tremendous increase in the knowledge of human anatomy and as well a progressively deeper insight into pathological conditions, which allowed the definition and the interpretation of these, culminating with the celebrated work of Morgagni [17], which was preceded by the highly remarkable treatises of Benivieni [18] and Bonet [19] (Fig. 1.3). Jean Fernel remarked how aneurysms may affect arteries throughout the entire human body

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and pointed out that they may be found in the thoracic and abdominal cavities [20]. The great surgeon Ambroise Paré (to whom a crowd of injured soldiers are indebted for having reintroduced the ligature of arteries instead of cauterization with boiling oil or hot iron) repeated almost textually Antyllus’ suggestions about the treatment of aneurysms; obviously, he considered internal aneurysms not amenable to cure and thickening and calcification of the sac walls as a natural resource apt to prolong life [21]. The enthusiastic effort to increase the knowledge about nature and man and the flourishing of a number of open-minded students gave a substantial impulse to medicine and surgery, and the ancient or Antyllus’ method was brought again on the stage. Surgeons continued to believe that direct aggression to the sac was essential to cure the aneurysm, even if the etiology of true aneurysm was not attributed to failure of the arterial wall, but related either to some kind of blood corruption or to the exaggerated impulse of blood. Extirpation (Philagrius’ method) encountered a very limited favor, one exception being the case reported by Purmann [22]: looking at the original drawing, it is evident that limb amputation would have been the alternative (Fig. 1.4).

Fig. 1.3  Front cover of the three treatises that gave rise to morbid anatomy as a science

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Fig. 1.4  The aneurysm that Purmann extirpated from the left upper limb of a lady (ref. 22)

The attention of surgeons was focused almost exclusively on aneurysms located in the upper limb; as for popliteal aneurysm, the only reasonable therapy was deemed to be amputation. Surgery for brachial aneurysm was part of the official textbooks for apprentice surgeons in the army [23], and the use of the aneurysm needle (aiguille à anévrysme) of Petit (Fig. 1.5) was recommended to underpass the brachial artery. In 1774, a Lorrainer surgeon, Keyslère, applied the method of Antyllus to popliteal aneurysm; he treated on a whole four patients, with success in three, while the fourth patient died. This surgical exploit is described in details in a letter by the Italian physician A.G.  Testa addressed to D.  Cotugno, professor at the University of Naples.The content of the letter is almost textually reported by Pelletan [25] in his Clinique Chirurgicale. Keyslère reproduced the technique attributed to Antyllus, however omitting the distal ligature. This variation of the original method had already been proposed, in the upper limb, by Guillemeau [26]. Later on, Heister [27] was apparently successful in omitting also the proximal ligature: the artery was plugged with caustic and astringent substances and ligature was reserved to cases in which plugging was not effective. Heister himself considered very dangerous to do a distal ligature on account of the possible impairment of the collateral net. The operation on brachial aneurysm by opening the sac, plugging the artery, and packing and com-

Fig. 1.5  The silver needle designed by Jean Louis Petit to pass threads under the aneurysmatic brachial artery (ref. 24)

pressing the sac, without any ligature, had been already described by Hamberger [28]. Surgery in the popliteal domain was undoubtedly facilitated by the introduction of the tourniquet, invented in 1674 by the military surgeon Morel during the siege of Besançon in the course of the war between France and Spain [29]. Some system to constrict the root of the limb to obtain an almost bloodless surgical field was already in use, but the tourniquet or garrot had the advantage of being easily tightened or loosened according to the surgeon’s requirement (Fig. 1.6). It had the disadvantage of bearing trauma to all tissues, including veins and nerves (but compression of the nerves implied a temporary loss of sensibility with reduction of pain).

1  A Surgeon’s Journey Through History Up to the End of the Nineteenth Century

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Fig. 1.6  Artist’s conception of Morel’s garrot

a

b

c

Fig. 1.7  Antyllu’s method as modified after the introduction of the tourniquet: (a) the sac is opened and the content evacuated; (b) temporary and partial release of the tourniquet to identify the proximal arterial orifice; a probe (initially a metallic female urethra catheter was used) is

introduced into the artery enabling to elevate this and an easier separation from the nerve and vein; (c) proximal ligature (same maneuvers employed for ligature of the artery distal to the aneurysm, when performed)

The tourniquet, in its initial configuration, was substituted with a series of devices, the first of which being probably the one proposed by Petit [30]: these permitted to exert compression only (or almost only) on the main artery and were ruled mechanically, thus avoiding the need for a tourniquet-dedicated assistant (Fig. 1.7). The possibility that femoral or popliteal artery could be submitted to ligature without involving by necessity the gangrene of the limb represented

an impulse toward the attempts to cure popliteal aneurysm in a less destructive way than amputation. It relied on a series of observations, starting in 1742 with Guénault and Vandenesse [31]: “… non ergo in vulnere arteriae cruralis continuo ab amputatione auspicandum” (limb amputation is not unavoidable when the femoral artery is injured). Precise statements were made by Winslow [32] and mainly by Haller [33]: “…arteriam popliteam…cum spe inter duos condylos

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ligari posse, aut exscindi, si aneurysma id requisiverit, & aeque bonam spem post eam resectione de tibia pedeque superesse…& in anastomosibus illis fiducia chirurgi ponitur…” (the popliteal artery, hopefully, may be tied between the condyles, or resected if there is an aneurysm, with good possibility of survival of leg and foot….the surgeon being confident in anastomotic connections…) (Fig. 1.8). Notwithstanding this favorable background, operative treatment of popliteal aneurysm remained, in the judgment of many physicians Fig. 1.8  The popliteal artery and its branches (from Haller, ref. 33, table V)

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and surgeons, a procedure long and painful for the patient and difficult and painstaking for the surgeon and, moreover, endangered by relevant mortality and morbidity. Gangrene was always impending, mainly when a distal ligature was applied to the lower part of the popliteal artery, as in the case reported by Monro [34]. Another dreaded complication was delayed hemorrhage either after the separation of ligatures (between the 14th and the 20th day) as pointed out by Sennert [35] or from arterial wall disruption from infection or pre-existing disease aggravated by

1  A Surgeon’s Journey Through History Up to the End of the Nineteenth Century

the trauma of ligature; surgeons attempted to prevent the consequences of delayed hemorrhage, particularly dangerous because it could manifest suddenly in the absence of medical personnel, by adding some accessory ligatures, loose but ready to be tied [25, 34] or, better, by leaving in situ, for several days after the operation, the tourniquet, the screw of which could be managed easily [36]. Sepsis, local or systemic, was however the commonest cause of failure [25] and represented the main bugbear nourishing diffidence for direct surgery. Success reported by distinguished surgeons [36–38] had the flavor of rarity, so as to deserve mention also in literary environments [39] and, on a whole, a mortality of about 50% results from a careful review of the published experiences. This could not be excessive, being very relevant, in those times, also mortality from amputation, but the impression was negative. Already Paul Barbette [40] had argued that extirpation of popliteal aneurysm could, if successful, save limb and life, but that it was better to lose a limb and save life. And the famous Percival Pott [41] stated that amputation was the best, and practically the unique, treatment for popliteal aneurysm: “Nor have I ever seen other operation than that of amputation, which has preserved the life of the patient.” Without being so radical, Syme [42] says that the old method, when applied to popliteal aneurysm, “proved most difficult and appalling.” Asepsis would change up-down the situation, but this revolutionary event was still far, and other routes to treat external aneurysms, and particularly popliteal aneurysms, were searched for and practiced. The following review is a witness of both the ingenuity and the audacity of our fathers in surgery who faced a disease dramatically evident and almost always lethal if not cured. Wandering across the large literary production on external aneurysms, from the fifteenth through the nineteenth century, a lot of therapeutic designs and essays are encountered, some of them only or almost only experimental, others tested in extensive and poorly homogeneous clinical series: none entirely satisfactory. Also, but for some scientifically built-up reviews and detailed case reports, it is not easy to argue how

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many patients met with an unwanted result of treatment. As well, the scanty mention of cases of misdiagnosis and consequent foolhardy incision of an aneurysmal growth gives only an idea about the tip of a dramatic iceberg. How many charlatans, poorly knowledgeable about aneurysms, were responsible of the incision of an aneurysm believing it was an abscess? Sometimes, this unlucky maneuver was performed also by surgeons established in their practice and acquainted with aneurysms, justified (?) by a poor knowledge of the patient’s history and by the fact that the aneurysm was heavily inflamed or scarcely pulsating [43–45].

1.1

The Valsalva’s Method (Medical or Constitutional Treatment of Aneurysms)

The method of Valsalva was conceived in Bologna University at the beginning of the eighteenth century; it is described in details by Albertini [46]. It aimed to render stable, at the lowest possible level, the status of the heart and of the circulatory system (the belief was that the main cause of aneurysms was the trauma exerted by blood impulse against the arterial walls). The patient was brought near inanition through repeated bloodletting, reduced intake of food and beverages, absolute bed rest, and avoidance of any stimulus (also psychic or emotional), sometimes refrigerants, sometimes evacuative remedies. When the patient was barely able to rise his hand, then a little addition in nourishment was allowed. This regimen could last several weeks or several months. Morgagni, who dedicated to Valsalva the first part of his work [47], also describes the method and as well its effectiveness [17], however pointing to the fact that patients were at risk of syncope or death. The beneficial effects of this regimen consisted, as pointed out by Hodgson [48] more than a century later, of the deposition of layered thrombus within the aneurysmal sac, which evolved toward consolidation, reduction of size, and loss or reduction of pulsatility, at the expense of a true debilitation. Internal aneurysms (heart, aorta), not amenable to any

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form of therapy, were the initial target of Valsalva. However, the method proved useful also in the treatment of external aneurysms. Morgagni [17] reports the cure of a popliteal aneurysm; worth of mention, the patient subsequently died for the complications of a contralateral popliteal aneurysm, and, at autopsy, also an aortic aneurysm was found.1 Sabatier [49] reports the cure of a subclavian aneurysm. Lancisi [50], Flajani [51], and Pelletan [25] consider the Valsalva’s method as not really curative but highly useful to retard the increase of the aneurysm size and to prolong life, but suggest that external aneurysms should be treated surgically whenever possible. The Valsalva’s method was progressively softened as for bloodletting and starvation, modified in several details and added with drugs such as sedatives, digitalis, and potassium iodide; the last was considered useful to reduce the activity of the cardiovascular system and also as an antiluetic agent. It remained on the stage up to the end of the nineteenth century [36, 52–55], either as an accessory to other methods of prolonged therapy or as the sole possibility of treatment for internal aneurysms [56]. In 1860, the Medical Times and Gazette [57] published a casuistic of 35 external aneurysms, most being popliteal, and of these 27 were initially treated by prolonged arterial compression with a tourniquet: in the 18 cases in which the treatment was curative, the Valsalva’s method was almost routinely associated, lasting up to 6 months. Today, the method of Valsalva may look, as really it is, not adequate and relying on a speculative process devoid of practical significance; but, framed within the medical knowledge and, mainly, the surgical possibilities of past times, it bears such amount of ingenuity and deepness of thinking as to deserve the continuing celebrity for its author; moreover, for the first time, and for a long time, it allowed patients, otherwise left to themselves, to hope that health could be gained again and sometimes to live more and better.

The anatomic specimen of this case could be observed in the Valsalva Museum, Institute of the Academy of Sciences, Bologna, Italy.

1 

1.2

Hot and Cold

Marco Aurelio Severino, surgeon in Naples, considers the aneurysm as a bloody abscess (abscessus sanguiflui) [58]; he makes mention [59] of the use of hot iron (ignis) in treating a false aneurysm in the thigh of a young patient; this, however, was cured only successively through a brilliant operative procedure after Antyllus’ method. The topic use of cold, in external aneurysms, to control the symptoms of inflammation, is probably very old. Through the centuries sixteen to nineteen, ice and refrigerants encountered a moderate but continuing favor as really curative agents, for both internal and external aneurysms, particularly as an accessory but effective remedy associated with other kinds of therapy. The relevance of ice therapy is stressed by several authors who dedicated great attention to the problem of aneurysm treatment, from Matani [60] in Italy to Sabatier [49] and Larrey [61] in France. Mention of circumscribed false aneurysms cured with ice is found in the works of Bartholin [62] and Monro [34]: both, however, report histories and events of which they became knowledgeable through other colleagues. Bartholin, in particular, was very enthusiastic about the multifaceted therapeutic properties of ice, according to the instruction received during his practice with M.A. Severino. The possibility that ice may really cure aneurysm was in general considered with reserve; however, in the Dupuytren Museum, in Paris, the specimen n. 239 [63] consists of the anatomic preparation of a popliteal aneurysm cured with ice: the popliteal artery has the appearance of a fibrous chord and the collaterals are particularly well developed and enlarged. Guerin, surgeon in Bordeaux, claimed to have cured more than one popliteal aneurysm with topical application of cold [64].

1.3

Coagulants

The injection of coagulants into the aneurysm was proposed by Monteggia, at the beginning of the nineteenth century [65]: he suggested to try this method of aneurysm consolidation before resorting for the operative treatment. After an initial

1  A Surgeon’s Journey Through History Up to the End of the Nineteenth Century

enthusiasm, several complications were reported. The method implied the temporary compression of the feeding artery to allow the concentration of the injected substance within the aneurysmal sac and avoid its diffusion into the distal arterial tree. Iron perchloride was the coagulant used more extensively, and precision syringes were constructed for the administration of the exact quantity of coagulant as programmed (Fig.  1.9). Wardrop [67] proposed the use of acetic acid.

Attempts to treat popliteal aneurysms were rare, sometimes successful [68], sometimes followed by catastrophe [69]. In 1909, Monod and Vanverts [70] concluded that there was not any evidence of the effectiveness of this method. However, the technique of inducing intra-­aneurysm coagulation revived after the introduction of the modern endovascular technologies [71]. A certain favor, however not substantiated by the results, encountered the method based on the subcutaneous injection of gelatin, proposed by Lancereaux in 1897 [72], to enhance the clotting properties of blood.

1.4

Fig. 1.9 Artist’s conception of the precision syringe designed by Pravaz and manufactured by Charrière, in Paris (modified, from Broca [11]). The cylinder was 3 cm long, with an inner diameter of 5 mm; the piston was put forward by a screw system; the metallic parts were in silver; trocars and cannulae in gold or platinum (for Charrière as a famous manufacturer of surgical tools, see ref. 66)

11

Foreign Bodies (Acupuncture, Wiring, Etc.)

The priority of acupuncture as a method of inducing blood clotting within the aneurysmal sac is contended by Velpeau [73] and Phillips [74]: the principle, tested in different experiments on the dog and the horse, is that foreign bodies introduced into the arterial lumen are able to produce clots and that these, growing and conjoining together, may bring to the obliteration of the vessel. A number of assays, using from two to many needles introduced percutaneously into the aneurysm or fully trespassing it, were attempted; but the fair results obtained with normal arteries in animals, looked hardly transferrable to aneurysms in man. Clinical application did not afford any significant results. In 1864, Moore [75] proposed the wiring of aneurysm. Apparently, he was unaware of the works of Velpeau and of Phillips; he conceived the idea after performing the autopsy of a sailor who had died of a gunshot in the chest, having found in the ascending aorta a metallic bullet embedded in fibrin; under his suggestion, Murchison introduced into an aneurysm of the ascending aorta more than 23 m of iron wire. The Moore’s method had a number of revivals, mainly for the treatment of inoperable aneurysms, and metallic wire was substituted with several kinds of foreign bodies: Bryant [76]

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12

introduced horse hair into a popliteal aneurysm, but this eventually ruptured after few days.2 Ransohoff [77] considered this method as a last resort procedure cautioning against its use for peripheral aneurysms, given the availability of many other useful methods. In 1921, D’Arcy Power [78] described the use of fine steel wire arranged into wisps that, once introduced into the aneurysm, expanded to form miniature umbrellas. Many decades later, the introduction of endovascular technology brought the method again on the stage in the treatment of several types of aneurysm, including abdominal aortic aneurysms [79], in which wiring was coupled with axillo-­femoral grafting [80], and intracranial aneurysms [81].

1.5

Thermic and Electric Energy

According to Ransohoff [77], at the end of the nineteenth century, Herne obtained the coagulation of an iliac aneurysm by the introduction of heated needles. In 1826, Home [82] introduced into an iliac aneurysm a large-bore needle (which he called acupunctorium) that was heated to the white in its external part: he demonstrated that heat could induce blood coagulation within the aneurysm; however gangrene and death ensued. Pravaz [83] is credited for the idea of using electricity to induce blood coagulation, in 1831. Phillips [74], in his experimental work on acupuncture, demonstrated the possibility of coupling this with electricity: two needles introduced into a bare artery were connected respectively with the copper and the zinc poles of a Volta’s apparatus. The first clinical applications are probably those of Petrequin [84], who, in 1845, reported to have cured with galvano-puncture two small aneurysms; he was not able to cure a brachial pseudoaneurysm because the patient refused to be submitted to further sessions of therapy, after the first one. Galvano-therapy of aneurysms was extensively studied in Italy. Ciniselli [85] reported the The anatomic specimen may be found in the Museum of Guy’s Hospital, London.

2 

cure of a popliteal aneurysm and proposed the method for the treatment of different types of aneurysm [86]. Burci [87] made a review of the problem outlining the correct (and limited) indications to the use of electricity in the treatment of aneurysms. In 1853, Boinet [88] reported the results of galvano-puncture in a collected series of 32 cases: the method was uneffective in 22 cases, and in ten cases the claimed success was questionable. In this series, the popliteal aneurysms were five, and only in two a questionable good result was obtained. Complications were frequent. In 1879, Corradi [89] proposed to couple electricity to the wiring technique of Moore [75]: the fili-galvano-puncture became known as the Moore-Corradi method. This relied on a better technology than that available in the early experiences of galvano-puncture; the foreign body (the wire) was abandoned inside the aneurysm after the passage of the electric current. Internal aneurysms, not amenable to surgical therapy, were the main target of the method, and some remarkable success was registered [90] together with a continuing endeavor to improve technology, which involved for decades some distinguished clinical researchers [91, 92]. Still in our days, the effect of electricity coupled with the introduction of foreign bodies into the aneurysm is the object of experimental and clinical research [93], however without any definitive demonstration about its effectiveness.

1.6

Needling

Needling was proposed in 1890 by Macewen [94]: fine and high tempered needles were introduced into the aneurysm, to touch and scarify the opposite inner surface, with the aim of giving rise to white thrombi adherent to the wall. These would increase in volume and produce a progressive occlusion or at least reduce the size of the sac. The results, in the four cases treated by Macewen, were not clear, and the method looked poorly attractive both at early [95] and late evaluation [96].

1  A Surgeon’s Journey Through History Up to the End of the Nineteenth Century

1.7

Manipulation

This method was proposed by Fergusson [97] in 1857: he observed the spontaneous consolidation of a large subclavian aneurysm in a patient who practiced swimming strenuously and argued that, during the athletic performance, thrombi were mobilized and occluded the outlet. On the basis of further cases, he suggested manipulation as a mean to cure aneurysm, with the aim (hope?) that massage could displace parietal thrombi and plug the distal part of the sac.

1.8

Ligature

Dominique Anel is quoted as the first to cure an aneurysm by simply tying the feeding artery. On January 30, 1710, in Rome, being present G.M.  Lancisi and other Roman surgeons, he operated on a religious who complained of a brachial pseudoaneurysm (consequent to bloodletting) which was growing in size and near to rupturing: the operation consisted of the ligature of the artery, cranial to the aneurysm and as close as possible to it; a second ligature was needed, cranial to the former, to control hemorrhage from a small muscular branch. The cure was complete and radial pulse was easily appreciable; ligatures went out after 18 and 28 days. The report of Anel [98] is largely of the epistolary type and the comment of Lancisi is enthusiastic. Anel, who was better known for his method to cure lachrymal fistula, was probably influenced by Guillemeau [26], but his operation really opened new perspectives in the treatment of aneurysms: only a unique, simple ligature was needed, omitting both the aggression to the sac and the distal ligature. Anel’s method did not meet significant favor, at least initially. Years later, J.L. Petit [99], albeit wandering for less invasive procedures, still treated brachial pseudoaneurysm by the direct aggression to the sac followed by proximal and distal ligature of the injured artery. Heister [27] continued to treat brachial aneurysms by opening the sac, under the protection of a tourniquet, omitting the distal ligature (considered dangerous for collateral circulation), and sometimes

13

he was able to omit also the proximal ligature when plugging of the artery was effective. Dupuytren [100] described four cases of brachial pseudoaneurysms in which he applied the techniques up to then available according to the requirement of each individual case, considering that Anel’s method exposes to the risk of backflow into the aneurysm, so that a distal ligature may be necessary; as well, leaving untouched the sac, healing is possible but also suppuration with ensuing drainage of pus and blood. According to Velpeau [101], Desault was the first to use Anel’s method to treat a popliteal aneurysm; this operation is only hardly mentioned in the posthumous edition of Desault’s surgical works [102], where large attention is dedicated to the method of ligating the artery soon distal to the aneurysm. It is a matter of fact that the technique of proximal ligature as the treatment of popliteal aneurysm is almost universally attributed to John Hunter, and the method is known as the Hunter’s method. In effects, as Roux [103] points out in the Prolegomeni of his not completed book Nouveaux éléments de médecine opératoire, the principle underlying the operations devised successively by Anel, Hunter, and Scarpa [104] is the same, varying only the procedure: i.e., to suppress direct bloodstream through the aneurysm. Probably, Anel was moved by a happy and lucky intuition; Hunter relied on deeply thinking about anatomy, surgery, and experimental data (being stimulated also by the results of direct aggression to the sac, which were far from satisfactory, due to the high incidence of heavy complications and mortality); Scarpa, also relying on his extensive knowledge of anatomy and surgery, proposed the way to couple the best result with the minimum risk of complication. It is not known if Hunter was aware of Anel’s method. But a probable answer is: yes. Circulation of ideas and experiences through the leading medical environments in Western Europe was really a lively one, favored by the frequent interlacing of civilian and military events in the life of physicians and especially of surgeons. One example is that of P.  Assalini, who was a

14

professor of surgery in Italy but as well a surgeon in Napoleon’s army and a tireless visiting fellow at the school of famous European surgeons. The celebrated operation of Hunter was performed to treat the popliteal aneurysm of a coach driver on December 2, 1785, and the patient left the hospital after 6 weeks completely cured and able to return to his work. Details of the operative procedure were described by surgeons who were present; while the descriptions agree on the access to the femoral artery (at the level later named Hunter’s canal) and the number of the ligatures applied to the artery (four), differences exist about the succession of ligatures. Assalini [105] reports that the first ligature was the lowest one and that this was tightened, while the three cranial were applied to lessen the impressive impulse of blood against the first ligature and that they were not completely tightened (with decreasing force from distal to cranial, thus transforming the arterial lumen into a reverse conical conduit). Home [106], the brother-in-law to Hunter, reports that the four ligatures (two couples) were successfully applied from up to down and as well that tightening was progressive but never complete. More than a century later, Heath [107], delivering the Hunterian oration, argued that, in the first three operative procedures, Hunter ligated also the femoral vein; this is hardly believable, being aware of the surgical dexterity of Hunter and as well of the reports of both Home and Assalini. Hunter’s method gained rapidly the favor of surgeons, in England as obvious but also throughout Europe. Scarpa put an end to any quarrel about the superiority of either the old or the new method, clearly stating which were, in those times, the disadvantages of the direct access to the popliteal space: • The need for a very long incision • The depth of the operative field, which made difficult the management of instruments • The proximity to the aneurysm and to the surrounding reaction often involving nerves, veins, and other structures

A. Cavallaro

• The alterations of the arterial wall, with the risk that this was easily injured or that it was not able to hold the ligature • The unavoidable damage to the ischiadic nerve, which needed to be retracted during a long part of the procedure • The short length of artery which could be dealt with, implying the risk of damage to important secondary arterial branches • The risk of injury to tibial vessels if a distal ligature had to be applied • The subsequent, almost constant and prolonged, suppuration of the popliteal space, often followed by impairment of knee motility Scarpa concluded that all the above difficulties were avoided by tying the femoral artery in the thigh and leaving the sac untouched. After the operation, he observed the reduction of aneurysm size, the vanishing of its pulsations, and the appearance of an easily appreciable pulsation of genicular arteries; as well he stated that the access to the femoral artery in the triangle was easier than at mid-thigh. However, very large popliteal aneurysms, rapidly increasing in size and near to rupture, remained, in Scarpa’s opinion, not amenable to cure, being thigh amputation, or better knee disarticulation, the only chance to save patient’s life. Ligature and arterial compression remained the preferred therapeutic options according to many authors and for many years. In 1832, Gibson [108] textually stated “The ligature, then, may be considered as the only mode of operation upon which any great reliance can be placed in the treatment of aneurism…..” In 1896, Eve [109] asserted that, in the treatment of popliteal aneurysm, ligature represented the second choice being compression the first one. And still in 1939 Miles and Wilkie [96] considered simple ligature as one of the accepted ways to cure this kind of aneurysm. The so-called Anel-Hunter’s method was largely used to treat popliteal aneurysms, and, through the years, several refinements, modifications, and details were proposed and discussed: a witness of the fact that the method could be

1  A Surgeon’s Journey Through History Up to the End of the Nineteenth Century

effective without being entirely satisfactory. The statements of the two outstanding and recognized authorities, Hunter and Scarpa, outlined the rules, but the debate about the best tactical behavior as for operative indication, timing of surgery, preparation of the patient, and surgical maneuvers remained open for decades, and, in some surgical environments, like in Ireland, the method was applied only when compressive therapy had failed [110]. Sabatier [49] stated that the ligature, above or beyond the aneurysm, was indicated in large and/or rapidly growing aneurysms; in the other cases compressive therapy was preferred, as this enabled collateral circulation to gradually and effectively develop. Ligature of the superficial femoral artery either at mid-thigh (Hunter) or at its origin (Scarpa) was progressively accepted by an increasing number of surgeons [111, 112] also in emergency conditions [113], and, experience being gained, it prevailed over the technique proposed by Anel. The latter appeared to allow a more straightforward result, being however threatened by the consistent risk of infection of the sac. Reduction of this dangerous complication was really the reason of the success encountered by Hunter’s method [45], while the other feared complication, gangrene, remained unchanged and perhaps was more frequent; in fact, the job of the collateral network was to bypass one obstruction (the coagulated aneurysm) after Anel’s method and two obstructions (also the site of the ligature) with Hunter’s technique. From this point of view, Anel’s method had also the advantage that no collateral branch emerged between the ligature and the sac [55]. Asepsis, substantially lowering the incidence of infection of the sac, would bring to reconsider favorably the Anel’s method [114]; it would also reduce the incidence of venous inflammation [115], a complication not frequent but lethal. The aim of the ligature was to produce the consolidation of the popliteal aneurysm through its filling with blood clots. True healing, according to Scarpa, was achieved when the aneurysm had been substituted by a fibrous chordiform structure. This fortunate and definitive event was

15

documented in several postmortem findings. Cooper [116] reported on the dissection of a limb operated on 7  years before: the popliteal artery was represented by a fibrous chord, being fairly developed the collateral circulation. However, from the clinical point of view, success was defined by disappearing of pulsations and progressive reduction in size; cure of the patient relied on these local changes and as well on the preservation of limb viability. In case of fusiform aneurysm of the popliteal artery, clinical cure could be achieved without obliteration of the arterial lumen, as demonstrated by autopsy finding 5 years after the treatment [117]. Disappearing of pulsations was not always immediate; Porter [52] ascribed this phenomenon to looseness of the knot, when these were no more appreciated after some hours or days. But when pulsatility of the sac persisted, remaining or returning to the preoperative levels, it was evident that collaterals continued to feed the aneurysm; in these cases, reoperation could afford cure. Savory [118] reported a case in which ligature according to Scarpa was not effective; then the femoral artery was tied again according to Hunter, without any beneficial effect; cure was finally achieved tying the artery in the popliteal space, distal to the origin of the great anastomotic branch. The same author studied 15 specimens of popliteal aneurysm preserved in the museums of London hospitals, cured by ligature of the femoral artery (from few days up to 12 years) and found that the femoral artery was fully patent in 11 (73%) and partially patent in four; he concluded that “obliteration of the artery is by no means ­necessary for the cure of the aneurism…the pressure of blood stream be reduced…by thus breaking the force of the main stream a cure will follow.” Ligature was fashioned in several ways, according to the ideas about its consequence upon the artery. Scarpa thought that adhesive inflammation was the mechanism underlying the fact that the artery remained impervious to blood also when ligatures went out and consequently suggested that ligature should flatten the artery, rather than crushing its walls, bringing into contact the opposite walls in their inner aspect, and

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used a ribbonlike string including within the knot a small cylinder of cloth, placed between the ligature and the artery. The suggestion of Scarpa was accepted by many surgeons, and apparatuses were developed apt to compress the artery, closing its lumen without the use of ligature. The presse-artère of Deschamps [101] and the arterial compressor of Assalini [105] were used successfully in several cases. They were preceded by instruments which allowed the progressive tightening of ligature as the serre-fil of Desault [102] (initially devised to treat female genital polyps accessible through the vagina) (Fig. 1.10). Scarpa’s view was not shared by others, as Jones [119] (credited for coining the term endothelium), who ascribed to blood coagulation a trigger role in producing obliteration of the arterial lumen.

a

The effects of ligature upon the artery were investigated thoroughly by several authors [114, 120–122] and fully assessed in the texts of pathology at the end of the nineteenth century [123]. Also in this field asepsis would bring a revolution, i.e., the disappearance of the process by which ligatures were eliminated by necessity through the surgical wound: this put an end to the rule of leaving one or both ends of the ligature out of the wound, in order to make easier, after some days or weeks, their extrusion or ablation; healing by the first intention became the rule in noncomplicated cases. In effects, already in the early nineteenth century, when antisepsis and asepsis were still very far from the operating theaters, it had been demonstrated [124] that a silk ligature could be cut near the knot, leaving it buried in the wound, and that if it would come out,

b

a

c

Fig. 1.10  From left to right: (a) the serre-fil of Desault (from ref. 102, Table 9). It had been devised to treat female genital polyps accessible through the vagina and also rectal

and nasal polyps; (b) the presse-artère of Deschamps (artist’s conception after the description of Velpeau, ref. 101); (c) the arterial compressor of Assalini (ref. 105)

1  A Surgeon’s Journey Through History Up to the End of the Nineteenth Century

this happened through a trifling and not painful suppurative process. Ligature of the superficial femoral artery was the principal method of treating popliteal aneurysms by proximal bloodstream interruption. In some cases, however, ligature was performed also [125] or only [126] on the external iliac artery. Ligature of the common femoral was considered contraindicated, owing to the anatomic arrangement of collaterals [127]. Pierre Brasdor, who was professor of surgery in Paris in 1798, is credited for suggesting to tie the artery beyond the aneurysm, an idea shared by Desault [102], who assessed that, when it is difficult or impossible to perform a proximal ligature, distal ligature may be effective. The method was developed and applied by Wardrop [128] and successively coupled with other kinds of treatment (galvano-puncture, injections of coagulants, etc.) to enhance the chances of aneurysm consolidation [129]. Finally, proximal and distal ligature, as suggested by Pasquier,3 was seldom applied: Boyer [38] reported a personal case in which a popliteal aneurysm was cured in this way. The chronology of the different sites on which ligature was applied, in the management of popliteal aneurysms, may be found in the work of Assalini [105], largely based on the personal witness of surgical events, and reveals some serendipitous achievements which were not followed by substantial consequences in the surgical practice. In 1781, Spezzani, dealing with a popliteal aneurysm with impending gangrene, put a ligature on the femoral artery at its lower third as a preliminary step to knee disarticulation: surprisingly, the aneurysm was cured and limb viability preserved. In 1782, Picchienati planned the amputation in a case of popliteal aneurysm and, trying to maintain the knee joint for a better prosthetic fitting, performed amputation of the leg: closure of the artery beyond the aneurysm was followed by consolidation of this. Lastly, Assalini reports that the operation of Desault (ligature of the artery above the aneurysm according to Anel)

It was not possible to find the original reference; Pasquier is quoted by Broca (ref. 11, p.  217). But many authors refer to Pasquin. 3 

17

took place in June 1785, preceding by 6 months the first case of Hunterian procedure. Besides the local and systemic complications of any surgical procedure in the pre-aseptic era, ligature of the artery was threatened by several specific complications: • New aneurysm at the site of ligature: Matas [56] collected eight cases. • Septic phlebitis [115]. • Secondary hemorrhage, often but not always complicating infection. • Suppuration of the sac, often obliging the surgeon to proceed to emergency amputation. But gangrene was the most feared specific complication, inherent to the method, the success of which depended largely on the effectiveness of collateral circulation. That collaterals could safely assure blood supply to the leg and foot was demonstrated by several experiments [122] in which the role of periarterial sympathectomy was also enlightened [130] and substantiated by a lot of clinical results. But the incidence of gangrene remained stable through the years, often requiring a major amputation, sometimes involving only the toes or the forefoot: the latter event ­rendered imperfect the cure [131] causing chronic impairment of limb function. Other forms of arterial closure, aimed at the development of collateral circulation, were proposed and tested. A mediate compression sufficient to stop hemorrhage from injured arteries was obtained by acupressure [132, 133] and wire pressure [134]: the artery was encircled, together with a quantity of surrounding soft tissues, with a long needle or a metallic wire, introduced percutaneously and twisted. None of these methods encountered significant favor, and the same happened for the methods of reduction of arterial lumen [135], the better known being the metallic bandaging devised by Halsted [136]: this consisted of a metallic band digitally applied around the artery, which was successful in curing a popliteal aneurysm and was also tested to treat aortic aneurysms [137]. The possibility of obtaining the progressive occlusion or the significant reduction of the arterial lumen, allowing the contemporary development of collaterals, continued to deserve

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the attention of surgeons involved in the treatment of aneurysms. Matas [138] tested the use of U-shaped aluminum bands molded around the artery; in case of troubles of limb viability, the wound could be reopened and the band widened; otherwise, being all ok, the band could be completely tightened at a second operation. In 1931, Chéffelar Klots [139] suggested the use of fascia lata (a strip 1 cm wide) secured around the artery; progressive shrinking would end, within few months, into the occlusion of the artery while collateral circulation developed; a brachial aneurysm was successfully treated, but the principal target of this method was carotid aneurysm. According to the exhaustive review performed by Delbet and Mocquod [131], the method of treating popliteal aneurysm by proximal ligature allowed a good rate of success: from 1877 through 1894, cure was achieved in more than 87% of the cases; however, limb function resulted chronically impaired in several cases, lowering to 71% the true clinical success. The incidence of recurrence (when very early it was rather a persistence) was low, about 5%; but recurrence was observed also several years after the operative procedure. Mortality was about 10%, being higher when considering also the results related to the pre-aseptic era [140]. In the series published in 1860 on the Medical Times and Gazette [57], mortality was absent after primary ligature and higher than 25% after secondary ligature (performed in case of failure of the compression therapy): numbers are small, but the experience is suggestive of the importance of applying ligature as a first option procedure.

1.9

pressure upon the aneurysm, leaving free from pressure enough space to allow the blood flow to continue through collateral arterioles and veins (he called the apparatus ponton, as it worked like a kind of wharf). But the method of direct compression had been already reported: Tulpius [144] cured a pseudoaneurysm of the hand, between the thumb and the forefinger, by prolonged pressure with a thin lead plate. The same method was successfully used by famous surgeons, as Sennert [35] and Hildanus [145] and later by Juncker [146]; Barbette [40] cured a small popliteal aneurysm. In general, this method was deemed useful for true aneurysms but contraindicated for false or ruptured aneurysms [147]. Heister [27], Ravaton [148], and others designed special apparatuses for mechanically adjusted compression of aneurysms, after the suggestion of Guy de Chauliac [15], who thought to manage aneurysms like hernias. Arnaud [149] devised an apparatus for the calf, stressing the importance of exerting pressure upon the arterial opening into the aneurysm. Direct compression was used, without a proper indication and without success, also in cases in

Compression

Direct compression probably represents the most instinctive way to treat external aneurysms. Occasional successes are repeatedly quoted in the medical literature. A celebrated case is the one reported in 1681 by the abbé Bourdelot [141], who served as the personal physician to the prince of Condé and to the Swedish queen Christina; he cured on himself a brachial (post-­ bloodletting) aneurysm, using, for 1 year, a self-­ made apparatus (Fig.  1.11) which exerted

Fig. 1.11  Artist’s conception of the compressing apparatus made up by Bourdelot to cure his own brachial pseudoaneurysm (from the drawing of Dionis [142] and the description of Thillaye [143])

1  A Surgeon’s Journey Through History Up to the End of the Nineteenth Century

which compression could not involve the aneurysm in its entirety [150]. Platner [151] described the steps to achieve effective compression upon arm aneurysm, after this had been emptied of its blood content: application of a compress of blotting paper chewed and soaked in wine; apposition of a cloth pack containing some hard material (coins); and the whole followed by tight bandaging. But the close and fruitful interrelationship between compression and aneurysm would really develop through the method of indirect or mediate pressure, i.e., compression upon the feeding arterial trunk: this appeared as something midway between the constitutional method of Valsalva and the abrupt interruption of bloodstream obtained with ligature, without exposing the patient to the poor results of the former and as well to the high risk of complication and death of the latter. Mediate compression was used initially in the cure of arterial traumatic lesions with the aim of lowering the quantity and the force of blood arriving to the injured site. In 1716, De Gouey [152] reported about a case in which success was achieved with a tourniquet: the pressure was initially complete, but the tourniquet was partially released after some hours. In 1742, Jussy [153] described the complete healing of an injury to the lower third of the femoral artery, using a Petit’s tourniquet which was progressively released from the 10th day on, maintaining continuously “les muscles extenseurs de la jambe dans leur plus fort raccourcissement & les fléchisseurs dans la plus grande extension.” The need of adjusting pressure according to the individual requirements and mainly to the involved part of the upper/lower limb prompted a prolonged and multifaceted series of modifications of the Petit’s tourniquet already after a short time from its introduction into the clinical practice [154]. Mediate compression was coupled with direct compression by means of complex systems of bandaging, being largely known the one proposed by Theden [155]. However, the first specific suggestion dates back to Genga [156], who, in 1673, devised a system of bandaging the upper limb to treat an arterial injury: the bandage began at finger level (each finger being bandaged carefully), con-

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tinued cranially with addition of compresses upon the lesion and arrived to the root of the limb, including a small piece of wood (of the diameter of a finger and long about 13–15  cm) applied against the course of the main artery and kept in place by the bandage (Fig.  1.12). The method, which revealed to be curative, aimed to prevent peripheral edema, to facilitate directly the healing of the arterial lesion, and to reduce the force of the main bloodstream toward the injured site. Some years later, De La Charrière [157] used a small cylindrical cushion instead of the wood. Dealing with aneurysms, compression of the feeding artery had been occasionally used in particular circumstances: by Verduc [158] to lower the impulse of blood against the ligature, after an operation according to Antyllus’ method, and by Monro [34] in a case of impending rupture of a popliteal aneurysm (he applied a tourniquet and instructed the patient how to manage the screw as soon as the aneurysm would burst). Guattani [36] (who had experienced the value of direct compression in a case of popliteal aneurysm misdiagnosed as an abscess and therefore incised) was the first to plan rationally, on a pathophysiologic ground, the compression upon the artery, cranial to the aneurysm, associating this remedy with direct compression and with Valsalva’s method “…simul cohibendo sanguinis cursum in arteria ad affectum locum tendente…” (…at the same time, reducing the bloodstream through the artery which arrives to the aneurysm…). To achieve reduction of blood flow, he used a cylindrical cushion applied along the entire course of the femoral artery and kept in place by a bandage running along the entire limb and continued with a couple of rounds at pelvic level. In this way he cured five popliteal aneurysms; in a sixth case, the aneurysm eventually burst and the patient died. Some years later, always in Rome, Flajani [51] continued successfully the experience of Guattani, stressing the importance of pressure upon the femoral artery, near its inlet into the aneurysm, to help the development of the collateral circulation (he was also successful in the operative treatment of popliteal aneurysms). The use of indirect or mediate compression as the unique or principal method to treat external

A. Cavallaro

20 Fig. 1.12  The bandage begins at finger level and continues cranially (a) with addition of compresses upon the lesion (b), including a small piece of wood (c) against the cours of the main artery, arriving to the root of the limb (d)

a

b

c

d

aneurysms dates back to 1761: Kretschmer, quoted by Bilguer [159], cured a pseudoaneurysm of the brachial artery with a tourniquet applied at the limb root continuously for 3  months. In 1795, Bruckner [160], albeit the Hunterian method was already, and increasingly, appreciated, treated a huge popliteal aneurysm with a self-made ring tourniquet which compressed the femoral artery so as to reduce, but not abolish, the pulsations of the tumor; after several months, the aneurysm was fully consolidated, and the fair pulsation of some genicular arteries was easily appreciated. In the same year, Lassus

[161] reported the curious and subsequently famous case of a 30-year-old man, complaining of popliteal aneurysm, who, having observed that pressure upon the artery in the thigh reduced the pulsations of the aneurysm, made a small cloth bag full of ashes and applied it tightly against the artery; after 8 months, the aneurysm was cured. Lassus believed that this was one of the rare cases of spontaneous cure of aneurysm; however, he argued that mediate pressure was worth of being tried before resorting for surgical treatment. The method encountered a certain favor in France and in Italy. Deschamps [162], in 1803,

1  A Surgeon’s Journey Through History Up to the End of the Nineteenth Century

reported a case of popliteal aneurysm cured by Eschards; and in 1810 Dubois [163] enlightened the advantages of progressive pressure, having cured a popliteal aneurysm in about 1 month. In Italy, Cumano [164] reported the cure of a popliteal aneurysm in 8  days, with a follow-up of 3 years. The idea was that pressure upon the femoral artery should not produce the massive coagulation of blood within the aneurysm but a progressive thrombus layering consequent to the condition of low flow. Massive coagulation would give rise to soft and poorly homogeneous clots, subjected to fragmentation and peripheral migration once the normal flow was reestablished, even if pressure was released gradually. It was evident that this treatment could be effective, but it was in general very long; moreover, continuing pressure could be painful for the patient and dangerous for the superficial tissues upon which it was applied. Dupuytren [165] acknowledged the curative potential of mediate compression, stating however that this kind of treatment was exceedingly long and often unbearable by the patient “…il est de personnes qui ne peuvent supporter son action; aussi est-on obligé, dans le plus grand nombre des cas, de récourir à la ligature, que est, en resumé, le plus efficace de tous les moyens de guérison que l’on a proposé….” Length of treatment, pain, and sloughing of the skin were really the troublesome aspects of pressure over the artery. Perhaps, the longest treatment was reported by Boyer [38]: progressive compression upon the femoral artery with a tourniquet (which at times had to be released) lasted 21 months, to achieve the cure of a popliteal aneurysm. But the cure was total and definitive, as ascertained through a clinical control after 38 years [117] and postmortem finding after a further interval of 9 years [11]. But the cure of popliteal aneurysm by indirect or mediate compression was going toward a period of true glory in Ireland, through the experience of the Dubliner surgeons. The history begins about 1820, when Todd [166] realized that a period of compression upon the femoral artery could be useful for the development of collateral circulation before proceeding to the Hunterian operation “...in many cases of aneurism, in which operations have failed,

21

from mortification of limb succeeding, the patient might have been saved by a delay sufficient to allow some progress to be able in establishing the collateral circulation….” The idea was not new, having been stressed already by Piet [167] at the beginning of the century. Todd applied this principle in two patients, who were unable to tolerate compression and were submitted to ligature; however, relying on the observations made on these two patients, he argued that compression, if prolonged and well done, could bring to the cure of aneurysm. Wilde [168] reports that Todd, before his death in 1826, succeeded in curing a popliteal aneurysm by pressure upon the femoral artery. The first official case in the Irish series was reported by Hutton [169], who cured in 20 days a popliteal aneurysm, using a tourniquet upon the femoral artery at groin, maintained in activity for 3–6  h/day; the compression therapy was performed because the patient had refused surgery. In 1846, in a first summary of the Irish experience, Wilde [168] collected 18 cases of popliteal aneurysms treated by mediate compression: 14 (77%) were cured and in four it was necessary to perform ligature. This report is inclusive of cases treated by Cusack (who, initially, was contrary to mediate compression and in favor of direct compression) and Harrison; this latter case was largely known, regarding a patient who, by himself, manufactured two tourniquets and applied them upon his femoral artery, accomplishing a double and alternate compression and curing his popliteal aneurysm. In 1851, Bellingham [110], reporting the 36th case of external aneurysm treated in Dublin by mediate compression, summarized the results in 25 popliteal aneurysms, of which 20 (80%) were cured and only one patient died (from erysipelas). On the ground of this experience, he stated that compression compared favorably with respect to ligature, as the latter, albeit assuring a high percentage of success, exposed the patient to significant risk of heavy complications and death. In effects, some years before, Crisp [170] had reported that out of 110 patients treated by Hunter’s method for popliteal aneurysm, seven (6.3%) were amputated and 12 (10.9%) died; this incidence of major complications obscured the

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great rate of success (91 patients—82.8%—were cured). In any case, according to Bellingham, amputation was still the only possible treatment for popliteal aneurysms which were of enormous dimensions or had burst becoming diffuse or had burst into the knee joint. The enthusiasm for mediate compression grew up, becoming also evident that the tourniquet could be ruled so as to only decrease the pulsation of aneurysm [171], reducing the risk of unbearable pain and of injury to superficial tissues. It gained favor also in Great Britain, where the Hunter’s operation was obviously considered as the best option. Miller [172], reporting on 29 lower limb aneurysms (six femoral, 23 popliteal) treated by mediate compression during the year 1846, observed that 25 (86%) were cured, ligature being necessary only in four. In France, mediate compression was strongly supported by Broca [11], mostly on account of the high risk of mortality following ligature; reviewing the results of the treatment of popliteal or femoro-popliteal aneurysms, as reported in the literature from 1842 through 1854, he found that

compression had been correctly applied in 139 cases, of which 127 (91%) were cured. The modalities of mediate compression were, through the years, the object of a lively debate. An apparently ideal way of using tourniquets for mediate compression was described by De La Touche [173] in 1825: he suggested the use of a number of apparatuses placed upon different points of the artery and screwed or released in order to maintain pressure on the artery without damaging the skin and stressing the patient: this looked really ideal for popliteal aneurysms. But, at last, it resulted evident [57] that a precise rule was not possible or necessary, being really important the tolerance of the patient and the judgment of the physician; as well, that cure could be achieved after an extremely variable length of treatment (only in 60% of the cases in less than 1 month). Pressure upon the artery was obtained in different ways, the simplest being represented by weights suspended with a cable [174] (Fig. 1.13). In general, mechanical apparatuses, progressively more and more sophisticated, were used,

Fig. 1.13  Types of weights used for compression upon the femoral artery. The tip of the pelote was flat or slightly convex, with a diameter of 2–3  cm. The patient had to maintain stable the position of the pelote, but it is evident that this would probably shift at each movement in bed.

The pelote was sometimes replaced with a bag containing mercury or lead shots. This type of compression was conceived by Bellingham on a Sunday, being the tourniquet damaged and lacking who was able to repair it (from ref. 174 and ref. 11 p. 812, modified)

1  A Surgeon’s Journey Through History Up to the End of the Nineteenth Century

allowing pressure to be continued or not, ruled as for its degree, and shiftable along the artery course. The tourniquets applied with straps, as the one introduced by Petit [147] (Fig.  1.14), were abandoned because of impairing the whole circulation, including collateral arterial branches and veins (Fig. 1.15). The different types of tourniquets or, better, compressing apparatuses, successively proposed and used in the clinical practice (Fig.  1.16a–g), had three fundamental components: • The one exerting pressure, or pelote: this was shaped to exert pressure only upon the artery, hopefully sparing veins and nerves; such a selective action was present already in the tourniquet of Moore [178] designed to compress only the nerve and reduce sensibility and pain during amputation.

Fig. 1.14  The tourniquet of Petit (ref. 147). A = a kind of counter-pelote, which could be shifted along the leather strap for optimal adjustment on the limb surface opposite to the site where pressure was exerted

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• The one assuring counterpressure: this was shaped as a counter-pelote or as a gutter, to receive more or less comfortably the opposite surface of the limb. • The framework connecting the two above, manufactured according to different criteria (ring, spring, arch, hinged bar). None of these instruments, however, were fully satisfactory even if the modality of mechanical compression was in some way established in its broad significance, expressed by the principle of one-artery compression [179]: i.e., pressure had to be exerted only over one arterial channel, leaving the others free for the development of collateral circulation. But the diffuse feeling was that mediate compression for the treatment of popliteal aneurysm was the method more effective and as well less dangerous for the patient. Times were sound for a simpler and more easily manageable way of exerting pressure upon the femoral artery. The importance of mediate digital compression had been enlightened by Saviard [180] at the end of the seventeenth century: this method was successfully used for 24 h to prevent hemorrhage in a case of brachial aneurysm in which the operative procedure had to be interrupted on account of patient’s intolerance (distal ligature was not performed and the backflow was relevant). In 1845, Greatrex and Robinson [181] observed that digital pressure was an effective remedy, in the treatment of a popliteal aneurysm, when the tourniquet had to be released (in their patient, surgery was deemed contraindicated owing to a great number of cases of erysipelas in the hospital). Digital pressure as a method of choice in the treatment of popliteal aneurysm was introduced in 1848 by the American surgeon Knight [182]: a popliteal aneurysm, in a patient incapable to bear any form of instrumental compression, was cured in 40 h. Always in the USA, some years later, two popliteal aneurysms were cured with double and mixed alternate compression, instrumental at mid-thigh, digital at groin [183]. In Europe, a case reported by Colles [11] gained some celebrity for its curious characteristics: a patient, hospitalized for a period of treatment in sight of

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Fig. 1.15  Evidence that straps assuring pressure upon the artery would as well compress the entirety of soft tissues over the bone, thus impairing all the circulatory net

Fig. 1.16 (a) The ring tourniquet (from ref. 11, p. 820). The counterpressure and the stability of the apparatus are assured with a small gutter. The larger part of the limb contour is not involved by pressure. (b) The tourniquet of Bigg, with a very large gutter and an archlike framework (from ref. 11, p. 816). (c) The spring tourniquet of Duval, with a very large counter-pelote (from ref. 175 and ref. 11, p.  819). (d) The tourniquet of Signoroni, relying on a hinged-­bar armor (from ref. 176 and ref. 11, p. 821). (e)

The tourniquet of Carte was largely used. Two straps in vulcanite (A) assured some degree of elasticity to the compressing mechanism (from ref. 177). (f) Broca modified the tourniquet of Carte, replacing the vulcanite straps with a vulcanite cylinder (A) through which the screw moved freely, while the framework relied on a hinged bar according to Signoroni (from ref. 11, pp. 823 and 827). (g) Apparatus for alternate compression with double tourniquet (from ref. 11, p. 831)

1  A Surgeon’s Journey Through History Up to the End of the Nineteenth Century

a

25

b c

d e

f

g

26

tourniquet treatment of popliteal aneurysm, observed that pressure upon the femoral artery diminished his symptoms; he practiced prolonged periods of digital pressure and cured by himself the aneurysm in 7 days, with great surprise of the physicians, who were not aware of the matter. Digital compression was standardized in Italy, at the University of Padua, by Vanzetti [184]: it was demonstrated that patients could be instructed to exert pressure by themselves, for periods of 5–8 min, each period followed by a short interval, on different arterial sites (carotid, brachial, radial, femoral). The patient was free overnight also when pressure was exerted by the physician or his assistants; in this case, the hand could work for about 10 min before fatigue obliged to a stop; however, this period could be prolonged up to 1 h with the support of the contralateral elbow (Fig. 1.17). The method gained favor slowly but steadily. In 1862, Southam [185] gave a vivid description of the cure, in 50  h, of a popliteal aneurysm: a crowd of students, two by two (one appreciated aneurysm pulsation), were involved. Moore [186] was obliged to stop compression with tourniquet

Fig. 1.17  Artist’s conception of digital pressure at groin with the support of the contralateral elbow

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after 17  days, owing to skin injury, and turn to digital compression with a positive result. In 1884, Holmes [55] stated that, after the results obtained by Vanzetti, digital compression should be considered the best method of treating popliteal aneurysms with mediate compression and that ligature should be reserved to cases in which compression, in any form, was not effective. As a mean, cure was obtained in 3 days with digital pressure, in 14  days when a tourniquet was used. According to him, digital compression was exquisitely selective, sparing nerves and veins, not dangerous for the skin, and easily shiftable along the artery; furthermore, it allowed to exert the minimal pressure required to abolish aneurysm pulsation; however, it involved many assistants. On the other side, instrumental compression did not require many assistants, but the surveillance of an experienced surgeon, as, if committed to students or nurses, the resulting pressure could be exaggerated. Other methods of compression were tested in the treatment of popliteal aneurysm, but they did not meet with relevant success and favor. Knee flexion was introduced by Hart [187] in 1859, after having observed that forced knee flexion reduced aneurysm pulsation. The foot and the leg were bandaged, and then the leg was forcefully bent on the thigh and bandaged to the same and to the pelvis (Fig. 1.18). The popliteal space was not bandaged, and the aneurysm, with the knee flexed, projected below the line of flexure. The aneurysm was cured, and Hart argued that this kind of treatment could be offered to patients with a small aneurysm, of relatively young age, and of tiny constitution (so that knee flexion could be tolerable for the patient and without any adverse effects on the knee joint). Shortly after, a second successful case was reported by Shaw [189], who, arguing on the physiopathologic changes produced by forced knee flexion, outlined three mechanisms favoring aneurysm consolidation: direct compression upon the aneurysm; pressure of the aneurysm upon the artery, within the popliteal space; and flow reduction from artery angulation. In 1864, Hart [190] reported a case cured in 6  days by Johnson and was able to collect on a whole 13

1  A Surgeon’s Journey Through History Up to the End of the Nineteenth Century Fig. 1.18 Artist’s conception of the Hart’s method to treat popliteal aneurysm (a). An alternative method (b) avoided foot and leg bandaging and relied on a sort of slipper fixed to the pelvis with straps (from ref. 188)

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a

b

cases cured with this method. However, 3 years later, Lawson Tait [191] delivered a substantially final, and negative, judgment on this technique, considered extremely painful and practically intolerable for the larger part of patients. Elastic compression was proposed by Reid in 1857 [192]: being the patient administered with narcotics, the entire lower limb, but for the projection of aneurysm, was submitted to total ischemia with Esmarch band [193] and a tourniquet was applied at groin before reestablishing the circulation. Rapid consolidation of the aneurysm could be obtained. Three years later, Petit [194] collected 20 cases of aneurysm treated in this way, with a success rate slightly higher than 50%. The same, rather low, success rate was confirmed by Stimson [195], analyzing the results in 62 limb aneurysms, of which 59  in the lower limb and in larger part popliteal. Delbet and Mocquod [131] delivered a substantially negative judgment on mediate compression as a way to treat popliteal aneurysm, collecting the available data up to 1888 (i.e., in the pre-aseptic era): –– –– –– ––

Digital compression: 59 cases, cure in 50% Elastic compression: 73 cases, cure in 49% Knee flexion: 19 cases, cure in 36% Instrumental compression: 223 cases, cure in 49%

These data were similar to those reported by Barwell [196]. The conclusion was that mediate compression could be still acceptable in elderly or cachectical patients provided that neurologic symptoms (either sensory or motor) were absent, the aneurysm was small and not inflamed, and the artery to be compressed was healthy; the technique, however, could be advantageous in stimulating the development of collateral circulation, in preparation to a radical operation. A glance at the status of the art in the last decades of the nineteenth century, Stromeyer [197] made a statement about the superiority of compression over the different surgical options (mostly ligature). Holmes [198], summarizing the experience of the British hospitals consisting of 212 popliteal aneurysms (almost all treated by compression or ligature) from 1861 through 1872, found cure in 78%, amputation in 6%, and death in 13%. But two true revolutions took place at the end of the century: one regarded the entire surgical world with the introduction of asepsis [199, 200] (the autoclave became a fundamental component of the surgical scenario in 1896, with von Bergmann); the other was represented by a tremendous progress in the surgical management of arterial injuries and diseases.

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131. Delbet P, Mocquod T.  Affections chirurgicales des artères. In: Le Dentu P, Delbet P, editors. Nouveau traité de medicine clinique et opératoire, vol. XI. Paris: J. B. Baillière et Fils; 1911. p. 167–84. 132. Simpson JY.  Acupressure. Edinburgh: A. & C. Black; 1864. 133. Pirrie W.  Practical considerations on acupressure. Illustrated by cases. Med Times Gaz. 1865;2:5–7, 31–4. 134. Dix J.  Wire-compression: a substitute for ligature. Med Times Gaz. 1863;1:94–6. 135. Scalone A. Un processo per la produzione di stenosi vasale. Policlinico sez Chir. 1913;20:412–8. 136. Halsted WS.  Partial, progressive and complete occlusion of the aorta and other large arteries in the dog by means of the metallic band. J Exp Med. 1909;11:373–91. 137. Stratton RT. Treatment of aneurism by direct gradual arterial closure. Report of a second case of aneurism of the abdominal aorta treated by this method. Calif St J Med. 1908;10:339–41. 138. Matas R, Allen CW. Occlusion of large arteries with removable metallic band to test the efficiency of the collateral circulation. JAMA. 1911;56:233–8. 139. Chéffelar Klots T.  The use of fascia lata for the occlusion of arteries, in case of aneurism. Ann Surg. 1931;93:635–6. 140. Norris GW. Statistics of the mortality following the operation of tying the femoral artery. Am J Med Sci. 1849;18:313–35. 141. Bourdelot PM. Lettre à Blegny. In: Planque F, editor. Bibliothèque choisie de médecine, vol. II. Paris: D’Houry; 1749. p. 481–5. 142. Dionis P.  Cours d’opérations de chirurgie, demontrées au Jardin Royal. Paris: D’Houry; 1790, fig. 44. 143. Thillaye JBJ. Traité des bandages et appareils. Paris: Crochard; 1815. p. 349–62. 144. Tulpius NP.  Observationes medicae. Amstelredami (Amsterdam): L. Elzevirum; 1652. p. 320–1. 145. Hildanus WF.  Opera observationum et curationum medico-chirurgicarum quae existant omnia. Francofurti (Frankfurt): J. Dufour; 1682. p. 225–6. 146. Juncker J.  Conspectus chirurgiae tam medicae, method stahliano conscriptae quam instrumentalis. Halae (Halle an der Saale): Orphanotrophei; 1721. p. 113–21. 147. Petit JL. Observations anatomiques et pathologiques au sujet de la tumeur qu’on nomme anévrysme. Turin: Mém. Acad. Roy. Sci.; 1736. p. 244–55. 148. Ravaton H, Sue P. Pratique moderne de la chirurgie, vol. III. Paris: Vincent; 1776. p. 510–38. 149. Arnaud G.  Mémoires de chirurgie, avec quelques remarques historiques sur l’état de la médecine et de la chirurgie en France et en Angletere, vol. I. London: J. Nourse; 1768. p. 181–219. 150. Le Dran HF. Observations de chirurgie, vol. I. Paris: G. Osmont; 1731. p. 296. 151. Platner JZ.  Institutiones chirurgiae rationalis tum medicae tum manualis in usu discentium. Venetiis: B. Albritius; 1747. p. 148–58.

32 152. De Gouey LL.  La véritable chirurgie établie sur l’expérience et la raison. Rouen: P. Ph. Cabut; 1716. p. 228–9. 153. Jussy JP.  Sur l’ouverture d’une artère guérie sans ligature. J Méd Chir Pharm. 1774;42:442–8. 154. Lassauzée. Description d’un tourniquet nouveau. J Méd Chir Pharm. 1774;41:57–65. 155. Theden JCA. Neue Bemerkungen und Erfahrungen zur Bereicherung der Wundarzneykunst und Arzneygelahrheit, vol. II.  Berlin: F.  Nicolai; 1776. p. 41–8. 156. Genga B.  Anatomia chirurgica, cioè istoria anatomica dell’ossa, e muscoli del corpo umano: con la descrizione dei vasi che scorrono per le parti esterne…. Rome: Dell’Onofri; 1687. p. 292–301. 157. De La Charrière J. Traité des opérations de la chirurgie. Paris: D. Hortemels; 1690. p. 283. 158. Verduc JB. Traité des opérations de chirurgie. Paris: D’Houry; 1688. p. 67–8. 159. Bilguer JU.  Dissertation sur l’inutilité de l’amputation des membres. Lausanne: F. Grasset & Co.; 1784. p. 107–11. 160. Brückner. Geschichte einen wahren Pulsadergeschwülst in der Knjekehle welchs ohne Operation geheilt ward. Loder J.  Chirurgie, Gebursthülfe u. gerichtliche Arzneykunde. 1797;1:248–52. 161. Lassus P.  De la médecine opératoire ou traité élémentaire des opérations de la chirurgie. Paris: F. Buisson; 1795. p. 444–93. 162. Deschamps JFL.  Anévrisme poplité. Compression de la fémorale avec un tourniquet. Guérison en onze mois. J de Sedillot. 1803;16:375. 163. Dubois P. Observations sur un anévrisme de l’artère poplitée gauche, guéri par la compression. Bull Fac Méd Paris. 1810;2(3):45–6. 164. Cumano GP.  Storia ragionata di un aneurisma popliteo guarito col mezzo della compressione, esercitata sull’arteria femorale superficiale presso il suo passaggio attraverso il terzo adduttore, mediante macchinetta conforme a quella inventata dal Prof. Dupuytren. Ann Univ Med. 1829;51:74–87. 165. Bruet JA, Brienne de Bosmont A. Leçons orales de clinique chirurgicale faites à l’Hôtel Dieu de Paris par M. le Baron Dupuytren, recuillies et publiées par une Société de Médecins, vol. IV. Paris: G. Baillière; 1834. p. 516. 166. Todd CH.  A report of cases of aneurism in which operation was performed in the Richmond Hospital, Dublin. Dublin Hosp Rep Comm Med Surg. 1822;3:91–138. 167. Piet CML.  Essay sur l’emploi de la compression, considerée comme moyen préparatoire à l’opération de l’anévrisme. Paris: N. Rénaudière; 1803. 168. Wilde W, (editor). Observations on the history of the cure of a popliteal aneurysm by compression, with cases of C.H.  Todd, Ph. Crampton, J.W.  Cusack, R. Adams and prof. Harrison. Dublin Quart J Med Sci. 1846;2:104–32.

A. Cavallaro 169. Hutton E. Case of popliteal aneurysm cured by compression over the femoral artery. Dublin J Med Sci. 1843, 23:364–8. 170. Crisp E. A treatise on the structure, diseases and injuries of the blood vessels. London: J.  A. Churchill; 1847. p. 224–34. 171. Cusack JW.  Case of popliteal aneurism, cured by compression in four days. Dublin Q J Med Sci. 1847, 4:239–40. 172. Miller J.  Principles of surgery. Philadelphia: Blanchard & Lea; 1852. p. 54. 173. De La Touche G.  Nouvelle manière d’exercer la compression médiate prolongée sur les principales artères des membres. Strasbourg: Thèse Inaugurale; 1825. 174. Bellingham O’B.  Observations upon the employment of compression in aneurism, with some statistical details. Dublin J Med Sci. 1845;27:163–76. 175. Duval MCJ.  Compresseur à pression élastique et graduée. Bull Acad Méd. 1855;21:244. 176. Signoroni B. Sopra un nuovo compressore delle arterie. Ann Univ Med. 1838;87:260–1, fasc. 177. Sarazin C.  Compresseur. In: Jaccoud SF, editor. Nouveau dictionnaire de médecine et de chirurgie pratique, vol. VIII.  Paris: J.  B. Baillière; 1868. p. 793–804. 178. Moore J.  A method of preventing or diminishing pain in several operations of surgery. London: T. Cadell; 1784. p. 26–7. 179. Walker GE.  Note on a case of popliteal aneurism treated by compression. Liverpool Med Surg Rep. 1871;5:60–78. 180. Saviard B. Nouveau recueil d’observations chirurgicales. Paris: J. Collombat; 1702. p. 151–8. 181. Greatrex E, Robinson WTC. A case of aneurism of the popliteal artery, cured by compression of the femoral artery. Med Chir Trans. 1845;28:39–43. 182. Knight J. Report of the committee on surgery. Trans AMA. 1848;1:169–70. 183. Wood IR. Report of the standing committee in surgery. Trans AMA. 1851;4:236. 184. Rosmini G.  Rapporto sulla cura degli aneurismi con compressione digitale. Ann Univ Med. 1858;165:145–55. 185. Southam G.  A case of popliteal aneurism cured by digital compression. Med Chir Trans. 1863;46:211–6. 186. Moore CH. An account of some unusual occurrences during the cure of a popliteal aneurism. Med Chir Trans. 1864;47:17–24. 187. Hart E.  A case of popliteal aneurism successfully treated by flexion of the knee joint. Med Chir Trans. 1859;42:205–8. 188. Durham AE.  Case of popliteal aneurism, successfully treated by flexion of the knee. Med Chir Trans. 1864;47:25–7. 189. Shaw A. A case of popliteal aneurysm, successfully cured by continuous flexion of the knee joint. Med Chir Trans. 1859;42:209–10.

1  A Surgeon’s Journey Through History Up to the End of the Nineteenth Century 190. Johnson HC (Hart E.) Some particulars of a case of popliteal aneurysm cured by flexion of the knee. Med Chir Trans. 1864;47:29–30. 191. Lawson Tait R.  On the treatment of femoral aneurism. Med Times Gaz. 1867;2:534–5. 192. Reid W. Report of a successful case of the application of Esmarch bloodless system to the treatment of aneurism. Lancet. 1875;2:448–9. 193. Esmarch JFA.  Ueber künstliche Blutleere bei Operationen. Sammstung klin Vorträge. 1873;2:373–84. 194. Petit HL.  De l’emploi de la compression élastique dans le traitement des anévrysmes des membres. Bull Gén Thér Méd Chir. 1878;84:458–63; 504–13; 543–56.

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195. Stimson L. On the treatment of aneurysm by elastic compression. Am J Med Sci. 1881;81:312–9. 196. Barwell R.  Aneurism. In: Ashurts J, editor. International encyclopedia of surgery, vol. III. New York: W. Wood & Co.; 1889. p. 591. 197. Stromeyer L.  Handbuch für Chirurgie. Freiburg: Herder’sche Verlagshandlung; 1867. p. 941–9. 198. Holmes T. On the surgical treatment of aneurism in its various forms. Lancet. 1875;195:637–40. 199. von Bergmann E.  Die Gruppierung der Wundkrankheiten. Beitr klin Wchschr. 1882;19:677– 9; 701–3. 200. Macnaughton-Jones H.  Asepsis and antisepsis in abdominal surgery and gynaecology. London: Baillière, Tyndall & Co.; 1898.

2

Modern Historical Background Antonino Cavallaro

2.1

 he Dawn of Reconstructive T Arterial Surgery

The first apparently successful attempt to repair injury to an artery and preserve the patency of this is credited to Lambert [1], in the early second half of the eighteenth century. According to his report to William Hunter, he suggested to a colleague in Newcastle-on-Tyne, Mr. Hallowell, to close the defect in a brachial artery, injured during bloodletting, instead of applying the usual ligatures, above and beyond the lesion. The operation, performed under the protection of a tourniquet at the upper part of the arm, implied the passage of two threads (ready to be tied at any moment during the procedure or in the p.o. course) and consisted on the application of a steel pin, about 70  mm long, through the lips of the arterial wound; the pin was secured by twisting a thread around it, as in hare-lip (Fig. 2.1). The procedure looked successful; the pin went out from the wound on the 14th day and the patient left the hospital after 1 month with a good radial pulse. Lambert, albeit gratified by this good result, was very cautious about the possibility that his idea could give rise to an established method of treating arterial lesions. And, in fact, no further A. Cavallaro (*) Past Professor of General Surgery, “Sapienza” University, Rome, Italy

© Springer Nature Switzerland AG 2021 A. Cavallaro (ed.), Aneurysms of the popliteal artery, https://doi.org/10.1007/978-3-030-49687-6_2

Fig. 2.1  The technique used to correct hare-lip (top) transferred to the treatment of an arterial lesion (bottom) according to Lambert

reports on this kind of procedure are found but for the experimental attempts of Asman [2]: he reproduced on few dogs the Lambert’s procedure and concluded that it was impossible to stop hemorrhage from an injured artery and maintain its patency. He argued that the radial pulse in the Hallowell’s patient was due to collateral circulation. In the period covering the end of the nineteenth century and the beginning of the twentieth century, there was a tremendous revival of interest 35

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36

for arterial suture, witnessed by a lot of experimental researches and as well by an increasing number of clinical reports. One of the first to confront again with arterial suture was Gluck [3], who however met with great difficulties with needles and threads, which cut the arterial edges, and reported some success with small ivory clamps. Von Horoch [4] succeeded in performing blood-tight sutures on arteries, but thrombosis ensued constantly. In 1889, Jassinovsky [5] demonstrated conclusively the possibility of suturing arterial lesions and maintaining patency of the lumen: his method of suture took only the outer coats of the artery, sparing the intima. About 10 years later, Silberberg [6] obtained the same fair results, demonstrating that it was not relevant if the suture penetrated the intima or not. But the matter of arterial suture had already reached the clinical field. The first successful arteriorraphy in man is credited to Postempski [7] who, at the third congress of the newborn Italian Society of Surgery, reported the repair of a femoral artery, which he had injured during the drainage of an abscess. A number of surgeons were able to repair wound of arteries without abolishing by necessity their patency. Jensen [8] collected the reports of eight different surgeons (the carotid artery, too, was repaired with success), and in 1909 Smith [9] found the reports of 12 additional surgeons. The clinical attempts to repair injured arteries regarded also the treatment of fully divided vessels; in effects, the experimental and clinical researches about the possibility of repairing a completely divided artery through an end-to-end technique or a graft were more attractive and as well more demanding. Achievement of this goal was pursued in different ways, including the use of mechanical devices. The technique of Payr [10] relied on the use of magnesium cylinders (which were absorbed within 3–4  weeks) (Figs. 2.2 and 2.3) and gained some favor, in lack, however, of consisting results. Hopfner [11] used the method of Payr in transplanting segments of artery from one animal to another, with good results at 1–3  months; however, when he attempted to transplant veins into the arterial system, he met constantly with thrombosis.

a

b

c

Fig. 2.2  Payr’s technique A for end-to-end arterial reconstruction, using a magnesium cylinder with a groove near one extremity. (a) One arterial stump is brought through the cylinder. (b) The margins are everted to cover and trespass the groove. (c) The other arterial stump, eventually dilated in some way, is brought to cover the former and tied upon the groove so as to procure intima-to-intima apposition

The direct end-to-end suture looked at first unsuccessful, and complex techniques of union of the two arterial stumps were devised, of which the more largely known were the cuff method of Gluck [12] and the invagination method of Murphy [13]. The former (Fig. 2.4) looks to have been confined to the domain of experimental surgery. The invagination method (Fig. 2.5) is recorded as being used in the first case of successful end-­ to-­end arterial repair in man (performed during an operation for arteriovenous fistula, it relied on a previous series of animal experiments, in which a 25% chances of success was obtained, however with permanent and not irrelevant stenosis). In 1896, in Lyon, Jaboulay [14] proposed end-­ to-­end suture with a series of U sutures (Fig. 2.6). This was probably the basis for the triumph of Carrel [15, 16] who had worked in the Jaboulay’s research laboratory (Fig. 2.7). The technique of Carrel represents the completion and the crowning of a lot of experimental researches and of clinical attempts and really means that times were sound for a novel era in

2  Modern Historical Background

37

Fig. 2.3  Payr’s technique B, with two hemicylinders of magnesium. Also in this case, intima-to-intima apposition is gained

which injured or diseased arteries could be reconstructed, besides putting the basis for organ transplantation. Based on an impressive series of successful procedures, it obscured other promising techniques, as the continuous mattress suture of Dorrance [17] (Fig.  2.8) derived from the research work of Dorfler [18]. As well, proposals for amelioration of it (theoretically), like the quadrangular technique of Frouin [19], did not encounter significant favor.

2.2

The Changing Trends in the Treatment of Popliteal Aneurysms

The advent of asepsis changed radically the prognosis of all surgical procedures; the always impending risk of infection, with its dramatic

sequels of morbidity and mortality, decreased drastically. Interest for nonsurgical treatment, like compression therapy, vanished and a manifest trend toward radical cure was evident; direct aggression to the sac and extirpation of the same became the goal of surgical procedures: the revival of Antyllus’ and Philagrius’ methods. Decrease of cases treated with ligature and increase of extirpation procedures were registered by Delbet and Mocquod [20], who also put into evidence that, after 1888, mortality rate consequent to extirpation was very low (1.4%). According to Ransohoff [21], extirpation was the ideal method to treat external aneurysms, even when rapid growth and impending rupture were suggestive for amputation as a lifesaving procedure.

A. Cavallaro

38

a

a

b

b

c

c

d d e

Fig. 2.4 The successive steps of end-to-end arterial reconstruction with the cuff method of Gluck. The cuff was initially taken from the same artery, later on from homologous arteries or was made with decalcified bone

Fig. 2.5 The successive steps of end-to-end arterial reconstruction with the method of Murphy

Monod and Vanverts [22] collected 151 cases, of which 100 treated by extirpation, with a success rate of 93% and suggested that simple incision of the sac (Antyllus’ method) was justified only when extirpation looked too difficult and dangerous pointing out to its negative consequences, as secondary hemorrhage from backflow and neurologic problems related with involvement of nerves by the prolonged and extensive process of healing. The same authors [23] outlined the main steps of the surgical procedure: • Preliminary control of hemorrhage with Esmarch band (or by arterial clamping) • Ligature of the artery beyond the sac to prevent distal embolization • Individuation of nerves outside the perianeurysmal reaction • Careful sparing of veins, unless completely occluded [24]

Fig. 2.6  The technique of Jaboulay. Each U suture takes about 1 mm of arterial tissue; stitches are applied with an interval of 1 mm from each other

This aggressive approach was not universally shared. Ligature continued to have supporters. The great Italian surgeon Durante [25], in 1905,

2  Modern Historical Background

Fig. 2.7 The universally known end-to-end arterial reconstruction by the triangulation method of Carrel

Fig. 2.8  End-to-end arterial reconstruction with the continuous mattress suture proposed by Dorrance

asserted “se togli l’agopuntura e l’introduzione di corpi estranei…ancora da tentare negli aneurismi inoperabili….di tutti i metodi curativi, oggi che

39

la legatura ci da tanti splendidi successi, non resta più nulla” (a part acupuncture and foreign bodies introduction…which should still be tried in case of inoperable aneurysm…of all the curative methods, given the splendid results offered by ligature, no other looks acceptable today). In general, however, ligature was reserved to cases in which extirpation looked very difficult: and it was a simple Hunterian ligature [26] or a fully excluding ligature above and beyond the aneurysm and as well of collaterals [27]. And compression, too, in some form, was still scantily used with reported success [28]. In 1919, Filadoro [29] reported the cure of a small popliteal aneurysm, probably luetic, with specific mercurial therapy and knee flexion of 3-month duration. Obviously, aneurysm extirpation did not abolish the risk of gangrene; the true innovation consisted of the maintenance of direct blood flow to the leg and foot after the extirpation or obliteration of the aneurysm. The first recorded attempt was performed in 1906 by the Spanish surgeon Goyanes [30, 31]. His operation (Fig. 2.9) is now universally known but remained initially obscure owing to the poor diffusion of the journal on which it was reported. Goyanes tied and cut the popliteal artery above and beyond the aneurysm and maintained bloodstream continuity using the in situ popliteal vein; both the anastomoses (artery-to-vein and, distally, vein-to artery) were fashioned end to end according to the Carrel’s technique. The operation was successful; however no news are available after the early p.o. period. The technique of bridging an arterial defect with autologous vein looked attractive, once Carrel had demonstrated the extraordinary ­potential of reconstructive vascular surgery. In 1907, Lexer [32] reported the use of autologous vein to maintain blood flow after the extirpation of a post-traumatic aneurysm of the axillary artery. The patient died in delirium tremens on the fifth p.o. day, and autopsy showed a patent venous graft (even if the artery was thrombosed at the site of proximal clamping). A vein grafting procedure in the treatment of popliteal aneurysm was reported in 1913 by Pringle [33] in Glasgow and in 1916 by Bernheim [34] in the USA.

40

Fig. 2.9  Schematic representation of the operation performed by Goyanes (from the original drawing, modified)

In his extraordinary book on cardiovascular surgery, Jeger [35] formally attests that operation for external aneurysms or arteriovenous fistulas should consist of the resection (or exclusion) of the diseased arterial segment and on venous grafting used as an interposition graft or as a bypass. An apparently simpler way to maintain direct arterial flow after aneurysm resection was investigated through the technique of end-to-end arterial suture: however, this type of reconstruction was possible only when the distance between the two arterial stumps was rather short [36, 37]. The ingenuity of Matas [38, 39] enlightened this period of innovative efforts and ideas, in

A. Cavallaro

which, however, many of the today current facilities (anticoagulants, antibiotics, fine surgical tools, etc.) were still lacking. The technique of endoaneurysmorrhaphy (the term will be introduced by Matas in 1902) was born on March 31, 1888 (Matas was aged 28): an aneurysm of the brachial artery was still pulsating after proximal and distal ligatures had been properly placed; Matas reopened the wound and, as extirpation looked very dangerous for the ulnar and median nerves, decided to open the sac and to obliterate it from inside with a series of sutures. This was later known as obliterative endoaneurysmorrhaphy. Further developments, based on the idea that intima-to-intima apposition had the same meaning than serosato-serosa apposition in Lembert’s suture, aimed to obliterate the aneurysm and as well to maintain the native artery continuity: the restorative and the reconstructive endoaneurysmorrhaphy (Fig. 2.10). According to its author, endoaneurysmorrhaphy reduced the risks of extirpation, being less traumatic and bloody and as well sparing important neighboring structure; due to the absence of trauma to collaterals, the risk of gangrene was also reduced. Matas’ procedure encountered large favor on account of its effectiveness in curing the aneurysm and of the possibility of maintaining an intact blood stream without any need of grafting procedure. In 1915, Horsley [40] collected 62 cases of endoaneurysmorrhaphy with one death (from tetanus), two gangrenes (the satellite veins had been injured and tied), and two recurrences after secondary hemorrhage (these were cases of reconstructive endoaneurysmorrhaphy). Secondary hemorrhage was not a rare c­omplication, while gangrene, when the operation was correctly performed, was practically absent [41]. The first half of the twentieth century did not register any further substantial improvement, in spite of so promising beginning, may be, also, on account of the decreasing incidence of external aneurysms. In 1939 [42] it was stated “within recent decades surgical forms of aneurysms have become much less frequent than they were once, particularly in the arteries of the extremities.”

2  Modern Historical Background

41

Fig. 2.10  Schematic representation of the different types of endoaneurysmorrhaphy. Top: obliterative. Bottom, left: restorative (in case of sacciform aneurysm). Bottom, right: reconstructive (possible in case of fusiform aneurysm, when, having introduced a probe into the arterial lumen, the two orifices were separated by a short distance

and the arterial tissues were in good conditions). Whatever the technique used, after obliteration or preservation of the arterial lumen, the sac was partially resected, if possible, and obliterated with one or more series of interrupted sutures, involving also the superficial tissues

Some decades later, Illingworth [43] would write “aneurysm of the popliteal artery was formerly a common condition, but is now rare: syphilitic arteritis was the underlying cause”. As a matter of fact, according to the report of the surgeon general on vascular surgery in World War II [44], a venous grafting procedure was performed only in one of the 13 cases of aneurysm in which maintenance of arterial continuity was attempted. Lumbar sympathectomy became a procedure frequently associated with the surgical treatment of peripheral aneurysms; initially advocated by Gage [45] in 1934, to improve collateral circulation, its specific role to prevent gangrene when dealing with popliteal aneurysm was

supported by Richards and Learmonth [46] in 1942. However, Shumacker [47], in an extensive review of the problem, concluded that “sympathectomy offers no guarantee against ischemic disaster.” But, in those years, some practical and conceptual advancements toward the current approach to popliteal aneurysm took place. Arteriography became fundamental in evaluating the collateral circulation both pre- and postoperatively, to verify its efficiency and to eventually decide for amputation [48–50]. And the spontaneous cure of aneurysm, i.e., thrombosis of the same, was no more regarded only as a lucky event but also as a danger for limb survival [51].

42

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A. Cavallaro

20. Delbet P, Mocquod T.  Affections chirurgicales des artères. In: Le Dentu P, Delbet P, editors. Nouveau traité de medicine clinique et opératoire, vol. XI. Paris: J. B. Baillière et Fils; 1911. p. 167–84. 1. Lambert R. “A new method of treating aneurysm” Extract of a letter from Mr. Lambert, surgeon at 21. Ransohoff J. The extirpation of aneurisms. Ann Surg. 1894;19:79–84. Newcastle-on-Tyne, to Dr. Hunter, giving an account of a new method of treating an aneurysm. Read June 22. Monod C, Vanverts JLJ.  Chirurgie des artères. In: Rapport au XXII Congrès de Chirurgie, Paris, 1909. 15, 1761. Med Observ Inquiries Soc Phys London. Paris: Alcan; 1909. 1762;2:360–4. 2. Asman C. “De Aneurismate” Dissertatio Medica 23. Monod C, Vanverts JLJ.  Traité de technique opératoire, vol. I. Paris: Masson; 1907. Inauguralis, Gröningen, March 24, 1773  in Lauth 24. Vanverts JLJ.  Volumineux anévrisme poplité. Th.  – “Scriptorum latinorum de aneurismatibus Extirpation. Presse Méd. 1902;10:1089. collectio: Lancisius, Guattani, Matani, Verbrugge, 25. Durante F.  Trattato di patologia e terapia chirurWeltinus, Murray, Trew, Asman” A.  König, gica. Rome: Società Editrice Dante Alighieri; 1905. Argentorati (Strasburg); 1785. p. 532–47. 3. Gluck T.  Ueber zwei Fälle von Aortenaneurysmen 26. Seguin. Anévrisme poplité. Ligature de la fémonebst Bemerkungen über die Nath de Blutgefässe. rale dans le canal de Hunter. Arch Méd Navale. Langenbecks Arch Klin Chir. 1883;28:548–60. 1910;94:344–9. 4. Von Horoch K.  Die Gefässnath. Allg Wien Med 27. Filippello GB.  Su un caso di aneurisma bilater Wchschr. 1888;33:263–4; 279–280 ale dell’arteria poplitea. Boll Soc Piemontese Chir. 5. Jassinovsky A. Die Arteriennath. Eine experimentelle-­ 1935;5:581–2. chirurgische Studie. Dissertatio Inauguralis, Univ. of 28. Pheidengold (Taft B.). Sur un cas d’anévrysme proTartu (Dorpat), Estonia; C. Mattiesen, Dorpat; 1889. fessionnel de l’artère poplitée guéri par la compres 6. Silberberg O. Ueber die Nath der Blutgefässe: experision. Arch Gén Méd. 1896;6:622–3. mentelle und klinische Untersuchungen. Dissertatio Inauguralis, Univ. of Breslau, T.  Schatzky, Breslau; 29. Filadoro P.  Due casi di aneurisma della poplitea di natura sifilitica. Policlinico sez Chir. 1919;26:32–7. 1899. 7. Postempski P. La sutura dei vasi sanguigni. Arch Atti 30. Goyanes Capdevila J. Nuevo trabajo de cirugia vascular plastica de las arterias por las venas o arterioplastica Soc It Chir. 1886;3:391–5. venosa aplicada como nuevo metodo del tratamiento 8. Jensen C. Uber circuläre Gefässsuture. Langenbecks de los aneurismas. Siglo Méd. 1906;53:544–8. Arch Klin Chir. 1903;69:938–98. 31. Goyanes Capdevila J.  Substitucion plastica de las 9. Smith EA.  Suture of arteries. An experimental arterias por las venas o arterioplastica venosa aplicada research. London: Oxford Univ. Press; 1909. como nuevo metodo del tratamiento de los aneuris10. Payr E.  Beitrâge zur technik der Blutgefäss- und mas. Siglo Méd. 1906;53:561–4. Nervennath nebst Mitteilungen über die Virwerdung 32. Lexer E.  Die ideale Operation des arteriellen und eines resorbierbaren Metalles in der Chirurgie. Arch des arteriellen-venosen aneurysma. Arch Klin Chir. Klin Chir. 1900;62:67–93. 1907;83:459–77. 11. Hopfner E.  Uber Gefässnath, Gefässtransplantation und Replantation von amputirten Extremitäten. Arch 33. Pringle H.  Two cases of vein grafting for the maintenance of direct arterial circulation. Lancet. Klin Chir. 1903;70:417–71. 1913;1:1795–6. 12. Gluck T.  Die moderne Chirurgie des Circulation-­ 34. Bernheim BM.  Ideal operation for aneurism of the apparatus. Beitr Klin Wchschr. 1898;129:1–29. extremity: report of a case. Bull Johns Hopkins Hosp. 13. Murphy JB. Resection of arteries and veins injured in 1916;27:93–5. continuity: end-to-end suture; experimental and clini35. Jeger E.  Die Chirurgie der Blutgefässe und des cal research. Med Record. 1897;51:73–88. Herzens. A.  Hirschwald, Berlin; 1913; reprint by 14. Jaboulay M, Briau E.  Recherches expérimentales Springer, Berlin; 1973. p. 254–62. sur la suture et la greffe artérielles. Lyon Méd. 36. Stich R, Makkas M, Dowman CE.  Beiträge 1896;81:97–9. zur Gefässchirurgie, circuläre Arteriennath 15. Carrel A.  La technique opératoire des anastomoses und Gefässtransplantationen. Beitr Klin Chir. vasculaires et de la transplantation des viscères. Lyon 1907;53:113–60. Méd. 1902;98:859–64. 37. Enderlen E.  Ein Beitrag zur idealen Operation 16. Carrel A.  The surgery of blood vessels. Bull Johns des arteriellen Aneurysma. Dtsch Med Wchschr. Hopkins Hosp. 1907;18:18–28. 1908;34:1581–2. 17. Dorrance GM.  An experimental study of suture of arteries with a description of a new suture. Ann Surg. 38. Matas R. Traumatic aneurysm of the brachial artery; incision and partial excision of the sac; recovery. Med 1906;44:409–24. News Philadelphia. 1888;53:462–6. 18. Dorfler J.  Ueber Arteriennath. Beitr Klin Chir. 39. Matas R.  An operation for the radical cure of 1899;25:781–825. aneurysm based upon arteriorrhaphy. Ann Surg. 19. Frouin A.  Sur la suture des vaisseaux. Presse Méd. 1903;37:161–96. 1908;16:233–6.

2  Modern Historical Background 40. Horsley JS.  Surgery of blood vessels. London: H. Kimpton; 1915. 41. Gibbon JH. The Matas operation in the treatment of iliac, femoral and popliteal aneurysms. Ann Surg. 1936;103:147–8. 42. Miles A, Wilkie D.  Thomson & Miles’ manual of surgery, vol. I.  London: Oxford Univ. Press; 1939. p. 243–51. 43. Illingworth E, Dick BM.  A textbook of surgical pathology. London: Churchill; 1963. p. 213–4. 44. Freeman NO, Shumacker HB Jr. Arterial aneurysms and arteriovenous fistulas. Maintenance of arterial continuity. In: Elkin DC, DeBakey ME, editors. Vascular surgery in World War II.  Washington DC: Office of the Surgeon General, Dept. of the Army; 1955. p. 266–301. 45. Gage IM.  Mycotic aneurysm of the common iliac artery; sympathetic ganglion block as an aid in development of collateral circulation in arterial aneurysms of peripheral arteries; report of a case. Am J Surg. 1934;24:667–710.

43 46. Richards PL, Learmonth JR.  Lumbar sympathec tomy in the treatment of popliteal aneurysm. Lancet. 1942;1:383–4. 47. Shumacker HB Jr. Arterial aneurysms and arteriovenous fistulas. Sympathectomy as an adjunct measure in operative treatment. In: Elkin DC, DeBakey ME, editors. Vascular surgery in World War II. Washington, DC: Office of the Surgeon General, Dept. of the Army; 1955. p. 318–60. 48. Jonckheere F, Leclerck R. Sur un anévrysme arteriel du creux poplité. Ann Soc Belg Chir. 1934;33:158–67. 49. Delgado R. Aneurisma de la arteria poplitea; arteriografia. Bol Soc Cir Rosario. 1936;3:183–91. 50. Pearse HF Jr, Warren SL. The roentgenographic visualization of the arteries of the extremities in peripheral vascular disease. Ann Surg. 1931;94:1094–104. 51. Leriche R, Froelich F.  De la gangrène dans les anévrysmes oblitérés des membres. Nature de la gangrène humide. Presse Méd. 1939;47:1626–8.

Part II The Popliteal Artery: Embryology and Anatomy

3

The Popliteal Artery: Embryology Antonino Cavallaro

The first systematic approach to the study of the development of lower limb arteries in the human embryo is probably represented by the work published in 1902 by De Vriese [1]. However, it is generally recognized, without any significant variation through years and decades, that a reliable outline of what does happen in the human embryo as a premise to the adult arterial system in the lower limb was described by Senior [2] in 1919, being the result of a detailed and certainly

painstaking research performed at New  York University. The following description, including figures, refers to the original work of Senior, largely simplified with the aim of enlightening schematically the development of the popliteal artery and of its major branches. At the 6 mm stage (Fig. 3.1), each umbilical artery derives from the union of a ventral and a dorsal root. The dorsal root, called the secondary

Fig. 3.1 6 mm embryo-right side: medial (left) and frontal view. (1) Umbilical artery. (2) Ventral root of the umbilical artery. (3) Dorsal root of the umbilical artery. (L1) First segmental lumbar artery. (L5) Fifth segmental lumbar artery. (4) Proximal component of the dorsal root of the umbilical artery. W Wolffian duct. In red: the axial artery

A. Cavallaro (*) Past Professor of General Surgery, “Sapienza” University, Rome, Italy © Springer Nature Switzerland AG 2021 A. Cavallaro (ed.), Aneurysms of the popliteal artery, https://doi.org/10.1007/978-3-030-49687-6_3

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one being its caliber smaller than that of the ventral root, is formed by the union of two arteries arising one from the fifth segmental lumbar artery just near its origin from the aorta and the other, cranial, arising directly from the aorta distal to the origin of the fourth segmental lumbar artery. The dorsal root of the umbilical artery passes upon the dorsal and then the lateral aspect of the Wolffian duct to join the ventral root; while curving around the lateral aspect of the duct, the dorsal root gives off the axial artery. At the 8.5 mm stage (Fig. 3.2), the umbilical artery arises directly from the aorta and the ventral root is no more present. The dorsal root is now independent from the fifth segmental lumbar artery. The axial artery crosses posteriorly the tibial nerve to reach its lateral aspect and traverses the entire posterior part of the lower limb down to the sole. The umbilical artery gives off the external iliac artery, the origin of which marks the limit between the common iliac artery and the internal iliac artery.

In the 12 mm embryo (Fig. 3.3), the external iliac artery has given off the inferior epigastric artery and the femoral artery. The latter grows rapidly and divides, at about mid-distance of the femur, into two branches, one of which represents the ramus communicans superior which is going to join the axial artery. The axial artery forms a marked bending indicating the site where the two arterial systems will join together. The 14  mm embryo (Fig.  3.4) presents the ramus perforans cruris, which consists of a branch arising from the axial artery in the proximal part of the leg and passing, through the space between the tibia and the fibula, onto the extensor surface. This branch follows a recurrent course toward the knee, and its proximal segment will become a part of the adult anterior tibial artery. At this stage, in which blood supply to the leg is

Fig. 3.2  8.5 mm embryo. The nervous tissue is in yellow. Medial (top) and frontal view. (1) Common iliac artery. (2) Internal iliac artery. TN tibial nerve. In red: the axial artery. In green: the external iliac artery

Fig. 3.3  12  mm embryo. (1) External iliac artery. (2) Inferior epigastric artery. (3) Femoral artery. (4) Ramus communicans superior (the dashed line with arrow outlines its course to join the axial artery)

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Fig. 3.4  14  mm embryo. (1) Ischiadic artery. (2) Deep popliteal artery. (3) Interosseous artery. (4) Ramus perforans cruris. (5) Superficial posterior tibial artery. (6) Superficial posterior peroneal artery. (7) Superior gluteal artery. TN tibial nerve, PN peroneal nerve. In the frontal view: the ramus perforans cruris, in its first part (A) will become a component of the anterior tibial artery; the ascending part (B) will persist in the adult as the anterior recurrent tibial artery

provided by the two systems, axial and femoral, the axial artery is conventionally divided into three parts: • The ischiadic artery, from the origin to the union with the femoral system through the ramus communicans superior (at, or near, the site of the adductor hiatus). From the root of the ischiadic artery the superior gluteal artery is given off. • The deep popliteal artery, from the union with the ramus communicans superior to the emergence of the ramus perforans cruris. • The interosseous artery, from the origin of the ramus perforans cruris to the termination. The deep popliteal artery gives off two relevant branches coursing through the leg: the superficial posterior tibial artery and the superficial posterior peroneal artery.

Fig. 3.5  18 mm embryo. (1) Superior gluteal artery. (2) Ischiadic artery. (3) Deep popliteal artery. (4) Recurrent anterior tibial artery. (5) Anterior tibial artery. (6) Interosseous artery. (7) Superficial posterior tibial artery. (8) Superficial posterior peroneal artery. (9) Inferior medial genicular artery. (10) Ramus communicans inferius, between the superficial posterior peroneal and the interosseous arteries. PM popliteus muscle. A, B, and C represent, respectively, the cranial, middle, and distal components of the definitive peroneal artery (frontal view). In blue: superficial popliteal artery

In the 18 mm embryo (Fig. 3.5), the skeleton mesenchyme is well defined also at foot level; a striking difference is noticed between the increasing caliber of the femoral artery and the involutive aspect of the axial artery; the superior gluteal artery has now an independent origin. The deep popliteal artery courses between the tibia and the popliteus muscle: at the proximal border of this, it gives off the inferior medial genicular artery and a short trunk deriving from the progressive union of the superficial posterior tibial and the

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superficial posterior peroneal arteries. This trunk, in the majority of the cases, will extend down to the lower border of the popliteus muscle, ­becoming the distal part of the definitive popliteal artery: now, it is called the superficial popliteal artery. Another new aspect of leg arterial apparatus is the presence of the anterior tibial artery: its proximal part being formed by the first part of the ramus perforans cruris. The interosseous artery is still present, and consequently four arterial branches traverse the leg length. A communicating branch (the ramus communicans inferius) unites the interosseous artery to the superficial posterior peroneal artery. In the adult, the peroneal artery will be represented by an upper segment (the remnant of the superficial posterior peroneal artery), a middle segment (the ramus communicans inferius), and a lower segment (the distal part of the interosseous artery). Fig. 3.6 22 mm embryo. (1) Remnant of the proximal part of the ischiadic artery. (2) Inferior medial genicular artery. (3) Deep popliteal artery. (4) Superficial popliteal artery. (5) Recurrent anterior tibial artery. (6) Ramus communicans medius. (7) Superficial posterior peroneal artery. (8) Posterior tibial artery. (9) Anterior tibial artery. PM popliteus muscle

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In the 22 mm embryo (Fig. 3.6), the ischiadic artery has lost continuity with leg arteries. Its proximal part will persist as the inferior gluteal artery, and other remnants will be represented in the adult as components of the intramuscular net depending on the branches of the deep femoral artery. The superficial posterior peroneal artery gives off a branch (the ramus communicans medius) which courses below the inferior border of the popliteus muscle and joins the deep popliteal artery opposite to the origin of the ramus perforans cruris. This branch represents the normal definitive first part of the anterior tibial artery in the adult; when the union between the proximal parts of the superficial posterior tibial and superficial posterior peroneal arteries will be complete, it will arise as a terminal branch of the definitive popliteal artery. The popliteus muscle is enclosed between the two popliteal arteries; however, the deep popliteal artery is going toward atrophy.

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The arrangements and rearrangements regarding the origin of the anterior tibial artery during embryo’s development deserve particular attention because they represent a clue to the understanding of several important variants in the termination of the adult popliteal artery. Senior described carefully the changing situations from the 20  mm through the 24.8  mm stages (Fig.  3.7). At the 20  mm stage, the first part of the anterior tibial artery is represented by the ramus perforans cruris arising from the deep popliteal artery (the middle part of the primitive axial artery); before bending toward the course of the anterior tibial artery, the ramus perforans gives off the recurrent anterior tibial artery. As well, the origin of the ramus peforans marks the end of the deep popliteal artery and the beginning of the interosseous artery (the distal part of the primitive axial artery). At the 22 mm stage, the interosseous membrane is quite evident, separating the interosseous artery from the anterior tibial artery, which now appears as the continuation of the deep popliteal artery. The latter, just above the origin of the interosseous artery, is joined by the ramus communicans medius, coming from the initial part of the superficial posterior peroneal artery. At the 24.8 mm stage, the ramus communicans medius, now arising from

the superficial popliteal artery (due to the fusion of the superficial posterior peroneal artery with the superficial posterior tibial artery), appears to be the first part of the anterior tibial artery, now coursing beyond and not above the popliteus muscle. The deep popliteal artery has disappeared, remnants being represented by some branches (inferior medial genicular artery, recurrent anterior tibial artery, and the first part of the ramus perforans cruris, participating to the formations of the anterior tibial artery); as well, a part of the deep popliteal artery, i.e., the segment between the arrival of the ramus communicans medius and the origin of the interosseous artery, is incorporated in the anterior tibial artery. The development of the muscles involved in the adult popliteal region has been the object of several studies [3–6], the more exhaustive, for our purposes, being the work of Bardeen [7, 8] to which we will refer in the following. In the 14 mm embryo, the posterior aspect of the leg is characterized by two groups of muscles: one, more superficial and lateral, comprehensive of gastrocnemius, soleus, and plantaris muscles, and the other, deeper and more medial, represented by the popliteus, the posterior tibial and the long flexor muscles.

Fig. 3.7  The origin of the anterior tibial artery (left, 20 m stage; middle, 22  mm stage; right, 24.8  mm stage); left leg, lateral view. Changes regarding the interosseous and the superficial posterior peroneal arteries are not represented in the figure, and the terms peroneal artery and posterior tibial artery are used for any of the stages. The deep popliteal artery and its branches are in red; the superficial

popliteal artery is in blue; the ramus communicans medius is in green; the anterior tibial artery is in yellow; the interosseous artery is in black (it is represented only in the left drawing). PM popliteus muscle, IO interosseous membrane. (1) Inferior medial genicular artery. (2) Peroneal artery. (3) Posterior tibial artery. (4) Ramus perforans cruris. (5) Recurrent anterior tibial artery

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above the lateral condyle of the femur, but the medial one has not yet reached the femur. The soleus begins to attach to the tibia. The definitive configuration of the medial head of the gastrocnemius muscle takes place during the latter half of the second month of embryo’s life: during its final migration there are chances of interference with the newly developed (or still developing) popliteal artery, which may be catched and displaced medially or produce some modification upon the migration itself with ensuing variations in the cranial (femoral) attachment of the muscle. These are the recognized premises to the more frequent types of popliteal artery entrapment.

Fig. 3.8  20 mm embryo. Top: the lateral head of the gastrocnemius is already inserted onto the femur, while the medial head is still migrating toward the femur. Bottom: in a deeper plane, the soleus presents only a limited, initial attachment to the tibia

The gastrocnemius group is connected with the blastema of the calcanear bone. The stage of 20 mm marks the almost definitive configuration of several muscles. The popliteus is well defined and its skeletal connections are those typical of the adult. The lower extremity of the semimembranosus appears fused with the tibial blastema near the back of the knee joint. Also the tendon of the semitendinosus muscle is well developed, however inserted a little more distally than in the adult. The cranial migration of the muscles of the gastrocnemius group is fairly evident, but not complete (Fig.  3.8): while the plantaris muscle is not yet identifiable, the gastrocnemius shows distinctly the two heads: the lateral one has reached its definitive termination

References 1. De Vriese B. Récherches sur l’évolution de vaisseaux sanguins chez l’homme. Arch Biol. 1902;18:665–730. 2. Senior HD.  The development of the arteries of the human lower extremity. Am J Anat. 1919;25:54–95. 3. Bolk J. Bezlehungen zwischen Skelet, Muskulatur und Nerven der Extremitaten, dargelegt am Beckengürtel, an dessen Muskulatur sowie am Plexus lumbo-­sacralis. Geg Morphologisches Jahrbuch. 1894;21:241–77. 4. Le Double A.  Traité des variations du système musculaire de l’homme et de leur signification au point de vue de l’anthropologie zoologique. Paris: Schleicher Fr.; 1897. 5. Schomburg H.  Entwickelung der Muskeln und Knochen des menschlichen Fusses an Serienschritten und Rekonstruktionen und unter zuhulfenhame makroskopischer Präparation. Gottingen: Dieterich; 1900. 6. Valenti G.  Sopra le prime fasi di sviluppo della muscolatura degli arti. Arch It Anat Embriol. 1902;2:272–80. 7. Bardeen CR, Lewis WH.  Development of the limbs, body wall, and back in man. Am J Anat. 1901;1:1–35. 8. Bardeen CR. Development and variation of the nerves and the musculature of the inferior extremity and of the neighboring regions of the trunk in man. Am J Anat. 1906;6:259–390.

4

The Popliteal Artery: Reminding Normal and Variant Anatomy Antonino Cavallaro

The popliteal artery courses from the adductor hiatus, where the superficial femoral artery ends, to the soleus arcade, immediately beyond which it divides into the anterior tibial artery and the tibioperoneal trunk. In general, anatomists consider the latter as the first part of the posterior tibial artery, so that the peroneal artery becomes a branch of this. To shortly describe the normal anatomy of the popliteal artery and of the neighboring structures (Figs. 4.1, 4.2, 4.3, and 4.4), we refer to the Italian treatise of anatomy by Chiarugi [1]. The adductor hiatus represents the outlet of the adductor canal (which surgeons prefer to call as the Hunter’s canal). Initially, the artery is covered by the semimembranosus muscle, having a course slightly oblique with external direction, but its larger course is almost vertical, corresponding to the major axis of the popliteal fossa and, of course, of the popliteal lozenge. Besides some muscular branches in its upper part, the popliteal artery gives off several important collaterals. The genicular arteries arise above the knee joint line (superior medial and lateral genicular arteries), at the level of this (middle genicular artery), and beyond this (inferior lateral genicular artery). The inferior medial genicular artery arises at the level of the knee

A. Cavallaro (*) Past Professor of General Surgery, “Sapienza” University, Rome, Italy © Springer Nature Switzerland AG 2021 A. Cavallaro (ed.), Aneurysms of the popliteal artery, https://doi.org/10.1007/978-3-030-49687-6_4

Fig. 4.1  Posterior view of the lower third of the femur and of the upper thirds of the tibia and fibula (right limb). Numbers indicate muscular attachment. (1) Medial head of gastrocnemius. (2) Lateral head of gastrocnemius. (3) Plantaris. (4) Popliteus. (5) Semimembranosus. (6) Soleus, medial attachment which continues distally along the middle third of the medial border of the tibia. (7) Soleus, lateral attachment

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Fig. 4.2  Posteromedial view, right limb. (1) Superficial wall of the adductor canal. (2) Superficial femoral artery and vein, saphenous nerve. (3) Saphenous nerve and great anastomotic artery. (4) Popliteal vessels. (5) Semimembranosus muscle. (6) Tendon of the sartorius muscle. (7) Tendon of the gracilis muscle. (8) Tendon of the semitendinosus muscle. (9) Popliteus muscle. (10) Lateral head of gastrocnemius. (11) Medial head of gastrocnemius. (12) Soleus muscle

joint line or immediately above it; about at the same level, there is the origin of the two sural arteries supplying directly the two bodies of the gastrocnemius muscle. The genicular arteries are important components of the knee anastomotic network, to which contribute also the great anastomotic artery, arising from the terminal part of the superficial femoral artery, and the recurrent tibial arteries. This anastomotic network plays a crucial role in assuring distal perfusion in case of ligature of the popliteal or of the superficial femoral artery. From cranial to distal, the popliteal artery lies upon the popliteal plane of the femur (through a consistent fatty pad), the knee joint capsule, and

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the popliteus muscle. The popliteal vein courses posterior and lateral to the artery, and the tibial nerve posterior and lateral to the vein; these interrelationships change at the apex of the popliteal lozenge, where fat separates the nerve from the vessels, and at the bottom of the popliteal fossa, corresponding to the interstice between the two gastrocnemius bodies, where the vein is almost medial to the artery and the nerve posterior to the artery (Fig. 4.3). The popliteus muscle is a triangular flat muscle going from the femur (beyond the lateral epicondyle) to the medial border of the tibia; passing over the tibiofibular joint, it has close interrelationship with the lateral meniscus and the knee synovial capsule. With the name of triceps muscle of the sura, anatomists indicate a complex muscular apparatus formed by the gastrocnemius and the soleus muscles which unite distally into the Achilles’ tendon. The gastrocnemius is a biceps muscle; the medial body inserts proximally onto the femur, above the medial condyle, just posterior to the adductor tubercle (also in the normal situation some muscular bundles insert directly onto the neighboring surface of the popliteal plane); the lateral body inserts proximally onto the femur, above the lateral condyle, some bundles directly onto the popliteal plane and the fibrous extension of joint capsule. The insertion of the medial head reaches a little more cranial level than the contralateral one. The cranial origin of the soleus muscle is located on the tibia (popliteal line and middle third of the medial border), on the fibula (the head, the proximal part of the lateral border, and the posterior surface), and on the fibrous arch which connects the head of the fibula with the upper part of the popliteal line of the tibia (it is commonly denominated as the soleus arcade or soleus ring). The tendon of the plantaris muscle courses between the soleus and the gastrocnemius muscles: it sometimes unites with the Achilles’ tendon, sometimes descends medially to this, and inserts separately onto the calcaneus. Proximally,

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Fig. 4.3  Posterior view of the muscles of the popliteal region, right leg. The muscles ending into the goose paw have been resected. Left: (1, 2) The two heads of gastrocnemius. (3) Plantaris. (4) Semimembranosus. (5) Biceps femoris. (6) Sartorius. (7) Gracilis. (8) Semitendinosus. Right, gastrocnemius muscle and peroneal nerve resected; semimembranosus muscle retracted. (1) Tendon of semi-

membranosus. (2, 3) Cranial part of the two heads of gastrocnemius. (4) Popliteus. (5) Plantaris. (6) Soleus. Colored circles point to the interrelationships of artery (red), vein (blue), and nerve (yellow) at different levels of the popliteal fossa. In case of duplicity of the popliteal vein, the two veins run lateral and medial to the artery in a posterior plane

this muscle begins above the lateral femoral condyle, above and medially to the insertion of the lateral head of the gastrocnemius muscle (being sometimes fused with this).

this happens in 95% of individuals. Variations in the site and modalities of branching have been the object of many investigations, not only for the sake of anatomical knowledge per se but also to enable vascular and orthopedic surgeons and interventional angioradiologists to perform their job at the best, avoiding unexpected complications and difficulties due to derangement from normal anatomy. Sometimes the research was stimulated by technical difficulties encountered during reconstructive vascular procedures requiring a popliteal or infrapopliteal distal anastomosis [3, 4], and a precise knowledge about eventual

4.1

Variants of the Terminal Branching of the Popliteal Artery (Fig. 4.5)

Usually, the popliteal artery divides into its terminal branches below the lower margin of the popliteus muscle; according to Lippert and Pabst [2],

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Fig. 4.4  Course and branches of the popliteal artery, posterior view, right limb. Nerves and veins not represented. (1) Proximal end of the lateral head of gastrocnemius. (2) Proximal end of the plantaris muscle. (3) Proximal end of the medial head of gastrocnemius. (4) Upper part of the soleus muscle. (5) Popliteus muscle. (6) Biceps femoris muscle. (7) Semimembranosus muscle. (8) Sartorius muscle. (9) Gracilis muscle. (10) Semitendinosus muscle. (11) Superior genicular arteries. (12) Middle genicular artery. (13) Inferior genicular arteries. (14) Tibioperoneal trunk. (15) Anterior tibial artery. Muscular and sural arteries not represented; the latter arise at about the same level of the inferior medial genicular artery. The dashed line represents the true level of the soleus arcade

anatomic variants of the popliteal artery is of great relevance in orthopedic procedures requiring knee arthroplasty or high tibial osteotomy [5, 6]. These investigations rely on anatomic dissection studies or angiographic findings (Table 4.1), less frequently on other methods of imaging, like duplex ultrasound [5] or MRI [6].

A. Cavallaro

When the popliteal artery ends at the normal level, i.e., at or immediately below the lower border of the popliteus muscle, some variations in its branching modality may be observed, the more frequent being trifurcation and the presence of a common anteriot tibial + peroneal trunk (Table 4.2). True trifurcation is rare, being observed in less than 1% of individuals [2], but it is usual to define trifurcation as the arising of the three terminal branches of the popliteal artery in close proximity [23], within a 0.5 cm distance [4]. Albeit trifurcation is commonly associated with a normal site of division, a case of true trifurcation of the popliteal artery at the level of knee joint has been reported [3]. The presence of a common trunk for anterior tibial and peroneal arteries is commonly associated with high division of the popliteal artery, but it has been observed also in the condition of normal site of branching. A very rare variant of the popliteal artery was described by Adachi [9]: the distal popliteal artery is double and the two branches unite distally before dividing in a normal fashion: it is the so-called island, as the two arterial segments look as circumscribing an island. Probably, this variant had been already observed [24] and two cases were recently reported by Singla [15]. But the more intriguing variant of popliteal artery branching is high division (Figs.  4.5 and 4.6), which represents also a potentially dangerous situation, if not recognized, in operative or endovascular procedures involving the knee level. It is commonly accepted that any division of the popliteal artery above the lower margin of the popliteus muscle should be defined as a high division. One of the first illustrations of this conditions is due to Haller [25] (see Fig. 1.8). In the nineteenth century, several authors observed and described the high branching of the popliteal artery in man [7, 26–29]. In 1929, Senior [30] tried to explain some of the more frequent variants of popliteal artery branching, on the basis of his previous study on embryology [31]. The clinical relevance of high division of the popliteal artery is documented by the recently continuing reports of cases and studies [32–35]. In Table 4.3 are summarized the results of a number

4  The Popliteal Artery: Reminding Normal and Variant Anatomy Table 4.1  Site of popliteal artery branching Author, year A—Anatomic studies Quain [7], 1844 Parson [8], 1898 Adachi [9], 1928 Trotter [10], 1940 Keen [11], 1961 Colborn [12], 1994 Somayaji [13], 1996 Ozgur [14], 2009 Singla [15], 2012 Thitlertdecha [16], 2013 B—angiographic studies Morris [17], 1961 Barsdley [18], 1970 Mauro [19], 1988 Kim [4], 1990 Day [20], 2006 Kil [21], 2009 Mavili [22], 2011

a

b

f

g

Limbs Branching at investigated normal site (%) 227 106 770 1168 280 84 250 40 60 230

94.4 92.4 98.2 94.7 94.9 92.9 90.0 90.0 96.8 96.9

246 235 343 605 1037 1242 535

92.7 95.8 96.8 95.6 92.9 98.7 94.0

57

Table 4.2  Variants in branching of popliteal artery (normal site of division)

Author, year Quain [7], 1844 Keen [11], 1961 Mauro [19], 1988 Kim [4], 1990 Day [20], 2006 Kil [21], 2009 Thitlertdecha [16], 2013 Sawant [23], 2013

c

Fig. 4.5  Schematic drawings of some variants in branching of the popliteal artery (right limb, posterior view). (a) Normal (90–98.7%). (b) Trifurcation (0.4–6.1%). (c) Common trunk anterior tibial and peroneal (0.4–3.3%). (d) High origin of the anterior tibial artery (0.4–13.3%).

d

Limbs 227

Common trunk ant.tib. Trifurcation and peroneal (%) (%) 0.4

280

4.3

343

4.1

1.2

605 662 1242 230

2.0 5.0 1.5 6.1

1.1

120

5.0

3.3

0.4

e

(e) Idem, coursing anterior to the popliteus muscle (0.4– 8.3%). (f) High origin of common trunk anterior tibial and peroneal. (g) Idem, passing anterior to the popliteus muscle (f + g 0.8–7.9%)

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58

Table 4.3  High division of the popliteal artery and related branching variants

Fig. 4.6  High division of the popliteal artery

of researches, mainly anatomic or radiologic; radiologists commonly refer to the line of tibial plateau as a marker of high division of popliteal artery. Abnormal branching of popliteal artery is sometimes bilateral [35]; according to Kil and Jung [21], if the branching pattern is variant in one limb, there is a 28% probability that the opposite side will also contain a variation. Significant racial or ethnic differences are not evident, even when purposedly investigated [10]; however, the very high incidence of variants reported by Sawant [23] in Mumbai deserves to be mentioned. Relevant variants of the main branches of division of the popliteal artery are related to aplasia or hypoplasia of one or two branches, with predominance of the remaining arteries or artery in supplying blood to the foot. Single case reports have been recently published by Asian researchers [36, 37]; Table 4.4 summarizes the results of some series. But for the case mentioned by Schafer and Thane [24], absence of the peroneal artery has never been reported [38] probably because this artery, at least in its distal part, is a direct deriva-

Author, year Limbs A Quain [7], 1844 227 0.4% Parson [8], 1898 106 5.7% Adachi [9], 1828 770 0.9% Trotter [10], 1168 1.5% 1940 Keen [11], 1961 280 3.6% Barsdley [18], 235 1970 Mauro [19], 343 2.3% 1988 Kim [4], 1990 605 2.9% Colborn [12], 84 1994 Somayaji [13], 250 6.4% 1996 a Tindall [5], 100 2006 Day [20], 2006 662 3.8% Szpinda [40], 76 2006 Kil [21], 2009 1242 1.2% Singla [15], 60 1.6% 2012 Sawant [23], 120 13.3% 2013 Thitlertdecha 230 0.9% [16], 2013

B 2.6% 1.9% 1,0% 2.4%

C 2.6%

D

0.8% 1.4%

0.4% 1.1% 4.2% 0.9% 0.7% 0.8% 7.1% 3.6% 6.0% 3.3% 7.9% 0.1% 1.6% 8.3% 3.3%

5.0%

1.3% 0.9%

A High origin of anterior tibial, coursing posterior to the popliteus muscle B Idem, coursing anterior to the popliteus muscle C High origin of common trunk anterior tibial and peroneal, coursing posterior to the popliteus muscle D idem, coursing anterior to the popliteus muscle N.B. other reported variant: high origin of common trunk anterior tibial and posterior tibial and high origin of peroneal (one case, Kim [4]; two cases, Day [20]) a Study with duplex scan ultrasound Table 4.4 Frequence of hypoplasia/aplasia of tibial vessels Author, year Mauro [19], 1988 Kim [4], 1990 Day [20], 2006 Kil [21], 2009 Sawant [23], 2013 Thitlertdecha [16], 2013

Limbs 343

A 2.3%

B

A + B

495 655

1.6% 0.2%

3.8% 1.1%

0.2% 0.2%

1242 120

1.7% 11,7%

5.1% 5.0%

0.8%

0.9%

2.2%

230

A Hypoplasia/aplasia of anterior tibial B Idem, posterior tibial C Idem, anterior and posterior tibial

4  The Popliteal Artery: Reminding Normal and Variant Anatomy

tive of the early arterial conduit to the lower limb, i.e., the axial artery. In case of hypoplasia or aplasia of the anterior and/or posterior tibial arteries, the peroneal artery becomes a major contributor to the blood supply of the foot: this happens in about 12% of the cases [2], and when the peroneal is the unique significant artery traversing the posterior aspect of the leg down to the foot, it gains the appellative of arteria peronea magna [39]. All the considered variations do not configure a pathological condition, but only a higher probability of misdiagnosis and improper treatment, if required.

References 1. Chiarugi G.  Istituzioni di anatomia dell’uomo, vol. II. Milan: Soc. Editrice Libraria; 1959. p. 497–515. 2. Lippert H, Pabst R.  Arterial variations in man. Classification and frequency. Munich: J.F.Bergmann; 1985. p. 60–4. 3. Sanders RJ, Alston GK.  Variations and anomalies of the popliteal and tibial arteries. Am J Surg. 1988;152:531–4. 4. Kim D, Orron DE, Skillman JJ. Surgical significance of popliteal artery variants. A unified angiographic classification. Ann Surg. 1990;210:776–81. 5. Tindall AJ, Shetty AA, James KD, Middleton A, Fernando KWK. Prevalence and surgical significance of a high-origin anterior tibial artery. J Orthop Surg. 2006;14:13–6. 6. Keser S, Sauraniar A, Barar A, Ulukent SC, Ozer T, Tuncay I.  Anatomic localization of the popliteal artery at the level of knee joint: a magnetic resonance imaging study. Arthroscopy. 2006;22:656–9. 7. Quain R.  The anatomy of the arteries of the human body with its application to pathology and surgery. London: Taylor & Walton; 1844. p. 530–43. 8. Parson FG, Robinson A.  Eighth report of the Committee of collective investigation of the Anatomical Society of Great Britain and Ireland for the year 1897-1898. J Anat Physiol. 1898;33:29–36. 9. Adachi B.  Das Arteriensystem der Japaner, vol. II. Kyoto: Maruzen; 1928. p. 196–242. 10. Trotter M.  The level of termination of the popliteal artery in the White and the Negro. Am J Physiol Anthropol. 1940;27:109–18. 11. Keen JA.  A study of arterial variations in the limbs with special reference to symmetry of vascular patterns. Am J Anat. 1961;108:245–61. 12. Colborn GI, Lumsden AB, Taylor BS, Skandalakis JE. The surgical anatomy of the popliteal artery. Am Surg. 1994;60:238–46. 13. Somayaji SN, Nayak S, Bairy KL.  Variations in the branching pattern of the popliteal artery. J Anat Soc India. 1996;45:23–6.

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14. Ozgur Z, Hulya U, Ikiz ZAA.  Branching pattern of the popliteal artery and its clinical importance. Surg Radiol Anat. 2009;131:357–64. 15. Singla R, Kaushal S, Chabbra U.  Popliteal artery branching pattern: a cadaveric study. Eur J Anat. 2012;16:157–62. 16. Thitlertdecha S, Praneatpolgrang S, Rungruang T. New patterns of the popliteal artery and its branches in Thais. Sirirai Med J. 2013;65:47–50. 17. Morris GC Jr, Beall AC Jr, Berry WB, Fesre J, DeBakey ME. Anatomical studies of the distal popliteal artery and its branches. Surg Forum. 1961;10:498–502. 18. Barsdley JL, Ataple TW.  Variations in branching of the popliteal artery. Radiology. 1970;94:581–7. 19. Mauro MA, Jacques PF, Moore M.  The popliteal artery and its branches: embryologic basis of normal and variant anatomy. Am J Radiol. 1988;150:435–7. 20. Day C, Orme R. Popliteal artery branching patterns— an angiographic study. Clin Radiol. 2006;61:696–9. 21. Kil SW, Jung GS.  Anatomical variations of the popliteal artery and its tibial branches: analysis in 1242 extremities. Cardiovasc Intervent Radiol. 2009;32:233–40. 22. Mavili E, Donmez H, Kahriman G, Ozaslamaci A, Ozcan N, Tasdemir K.  Popliteal artery branching patterns detected by digital subtraction angiography. Diagn Intervent Radiol. 2011;17:80–3. 23. Sawant SP.  A morphological study of termination of popliteal artery with its clinical significance. Int J Curr Sci. 2013;6:E94–100. 24. Schafer EA, Thane GD.  Quain’s elements of anatomy. London: Longman, Green & Co.; 1892. Part II, p. 495 25. Haller A. Iconum anatomicarum quibus aliquae partes corporis humani delineatae continentur. Fasc. V: arteriae pedis. Göttingen: Wid. A.  Vandenhoeck, Acad. Bibliopol.; 1756. p. 21–43, tab. 5. 26. Caldani LM, Caldani F.  Icones anatomicae quot quot sunt celebriores ex optimis neotericorum operibus summa diligentia descriptae et collectae, vol. I. Venice: G. Picotti; 1808, tab. 194. 27. Tiedman F.  Erklärungen der Ergänzungen wu den Abbildungen der Pulsadern der menschlichen Körpers. Heidelberg: C. Winter; 1846, tab. 51. 28. Hyrtl J.  Uber normale und abnorme Verhaltnisse des Schlagadern des Unterschenkels. Denkschr. kaiserlich. Akad. Wissenschaften Wien. 1864;23:245–88. 29. Barkow HCL.  Comparative Morphologie des Menschen und der menschenähnlichen Tiere. Vol.VI: Erläuterungen zur Schlag- und Blutader-Lehre des Menschen. Breslau: F. Hirt; 1868, tab. 8. 30. Senior HD. Abnormal branching of the human popliteal artery. Am J Anat. 1929;44:111–20. 31. Senior HD.  The development of the arteries of the human lower extremity. Am J Anat. 1919;25:54–95. 32. Klecker RJ, Winalski CS, Aliabadi P, Mina P.  The aberrant anterior tibial artery: magnetic resonance appearance, prevalence, and surgical implications. Am J Sports Med. 2008;36:720–7.

60 33. Yildiz S. A high origin anterior tibial artery and its current clinical importance. Int J Anat Var. 2010;3:180–2. 34. Singla R, Chabbra U, Kaushal S.  High division of the popliteal artery—a case report. Int J Anat Var. 2012;5:104–6. 35. Sharma K, Haque MH, Mansur DI. Bilateral high origin of anterior tibial artery and its clinical importance. Kathmandu Univ Med J. 2012;37:88–90. 36. Iiji P, D’Costa S, Nayak SR, Prabhu LV, Pai MM, Vasgaonkar R, Rai R, Sugavasi R. Hypoplastic posterior tibial artery and the enlarged peroneal artery supplying the posterior tibial region: a rare variation. J Vasc Bras. 2008;7:272–4.

A. Cavallaro 37. Kara A, Uzmansel D, Kurtoglu Z.  Bilateral hypoplastic posterior tibial arteries with histological features. Case report. Turk Klinik J Med Sci. 2009;29:1330–4. 38. Hollinshead WH. Anatomy for surgeons. New York: Harper & Row; 1969. p. 807. 39. Senior HD.  An interpretation of the recorded arterial anomalies of the human leg and foot. J Anat. 1919;53:130–71. 40. Szpinda M.  Digital-image analysis of the angiographic patterns of the popliteal artery in patients with aorto-­ iliac occlusive disease. Ann Anat. 2006;188:377–82.

5

Persistence of the Ischiadic Artery Antonino Cavallaro

Normally [1], in the adult, the internal iliac artery divides into two main trunks, the posterior continuing as the superior gluteal artery and the anterior. The latter gives off several important branches supplying the pelvic organs and divides into the internal pudendal artery and the ischiadic artery; this appears as its terminal branch or continuation. The ischiadic artery (or inferior gluteal artery) leaves the pelvis through the lower part of the greater sciatic foramen, passing under the pyriformis muscle, and then courses medial to the sciatic nerve, covered by the gluteus maximus muscle, dividing after 3–6 cm into two branches: the inferomedial branch descends between the cutaneous posterior nerve of femur and the sciatic nerve, supplying this through a small branch (the satellite artery or arteria comitans of the sciatic nerve). In 1832, Green [2] described an anomaly of the femoral artery that he believed to be unique “….the external iliac artery passed under Poupart’s ligament and immediately divided into three or four branches, which seemed to supply the place of the profunda; no superficial femoral artery could be found in the thigh;….dissecting the lower back of the thigh and leg, it was discovered that the artery, which became the popliteal…..was a branch of the internal iliac; a large artery, of the same calibre as the femoral itself usually is, passed out through the sciatic notch with the sciatic nerve….” A. Cavallaro (*) Past Professor of General Surgery, “Sapienza” University, Rome, Italy © Springer Nature Switzerland AG 2021 A. Cavallaro (ed.), Aneurysms of the popliteal artery, https://doi.org/10.1007/978-3-030-49687-6_5

This is commonly quoted as the first report of a persisting primitive ischiadic artery, later called simply as persisting sciatic artery (PSA). Green made a warning about the pitfalls offered to surgeons by such anatomical variant especially when undertaking the treatment of a popliteal aneurysm by ligature of the superficial femoral artery. Almost two centuries elapsed and a case of popliteal aneurysm in a limb with a PSA was reported [3]. In 1847, Dubrueil [4] published a beautiful drawing of a PSA continuing with the popliteal artery (Fig. 5.1). Other scanty reports appeared in the literature [5, 6], and in 1928 Adachi [7] was able to collect 15 cases (including two personal cases resulting from 1200 dissections). Reports on the finding of a PSA during dissections continued to be published, also in recent years [8–11]. The PSA has been the object of several case reports and reviews, owing to the intriguing problems posed by its presence and mainly by its pathology. The largest collected series was published by Ikezawa [12] (Table  5.1); taking into account the reports appeared successively, it is probable that more than 200 cases are currently present in the world literature. PSA is a rare anomaly: Adachi [7] found two cases out of 1200 dissections (0.16%). From the retrospective inquiry into large angiographic series [23, 24], an incidence of 0.04–0.05% results. A recent study [25] on 360 women 61

A. Cavallaro

62

Fig. 5.1  Persistent sciatic artery, from the drawing of Dubrueil [4] Table 5.1  Reviews of cases of persistent ischiadic artery Author Taylor [13] Bower [14] Vimla [15] Williams [16] Donovan [17] Becquemin [18] Shutze [19] Ikezawa [12] Maldini [20] Van Hooft [21] Abdallah [22]

Year 1966 1977 1981 1983 1984 1985 1993 1994 2002 2009 2010

No. of cases 14 31a 34 52 35 59 94 168b 88 122c 136d

22 from cadavers 43 from cadavers c From 1964 through 2007 d From 1964 a

b

s­ubmitted to angiography in sight of uterine artery embolization for the treatment of leiomyoma discovered three cases of PSA (0.8%). In

general the prevalence is considered as ranging from 0.02% to 0.05–0.06% [14, 17, 26], but it is also suggested that this rarity may be due to the fact that the anomaly remains often undiagnosed [27]. In a consecutive series of 307 patients investigated through CT angiography for suspected arterial insufficiency of the lower limbs [28], a PSA incidence of 1.6% was found. A detailed classification of PSA has been proposed by Pillet et  al. [29] and by Gauffre et  al. [30], taking into account the origin and the morphology of the anomalous artery with respect to that of the femoral system, resulting in a number of types (one relative to the origin of the ischiadic artery from the middle sacral artery) and some subtypes. However, from the clinical point of view, it looks better to follow the simple classification proposed by Bower et al. [14] considering two types: complete and incomplete. Complete is when the sciatic artery descends along the thigh to continue with the popliteal artery and incomplete when its continuity is broken or if it is connected either with the hypogastric artery or with the popliteal by way of small collateral branches. The complete form is considered expression of a total failure of the sciatic and femoral system coalescence in the embryo [31], and it is generally assumed that it represents the major blood supply to the leg and foot, but occasionally the two systems appear complete and separate [14] resulting in a dual blood supply to the popliteal artery [16, 32]. Golan et al. [33] reported the first case of bilateral complete PSA and bilateral complete femoral artery. Cases with complete PSA are the majority: in the review performed by Ikezawa et al. [12], they represent 68.5% (artery incomplete in 9.9%; 21.6% unknown). In smaller series, the artery results complete in a larger percentage, 79–90% [16, 18, 33]. According to Van Hooft et al. [21], the artery was complete in 75% of cases when unilateral and in 78% when bilateral (in three additional cases of bilateral persistence, the artery was complete on one side and incomplete on the other). The PSA was found to be bilateral in a variable percentage of cases, ranging from 22 to 54% [12, 14, 15, 18, 21, 33, 34]. The behavior of the femoral artery in the presence of PSA is variable; complete absence is rare

5  Persistence of the Ischiadic Artery

[21, 35], and incompleteness of the sciatic artery does not mean by necessity normality of the superficial femoral artery which may be aplastic or hypoplastic [32]. In general, the femoral system is present and may consist of a common-­ profunda trunk, but most often the superficial femoral artery is evident, being slender and ending at the adductor hiatus or continuing into the popliteal fossa as the descending genicular artery. Rarely, the superficial femoral is intact and the profunda totally lacking [9, 32]. The femoral artery was normal [36, 37] as found by Ikezawa et  al. [12] in 13% of the cases reviewed in the world literature: it was hypo- and aplastic in more than 54%, but its morphology was not specified in 33%. In most cases, according to Blair and Nandy [38], the function of the defective superficial femoral is assumed by an overdeveloped profunda which enters the ischiadic channel with its perforating branches. From the anatomical point of view, the PSA looks as the continuation of an enlarged hypogastric artery; it leaves the pelvis through the lower part of the sciatic foramen and courses under the gluteus maximus, thereafter descending dorsal to the adductor magnus and, passing lateral to the insertion of the latter, enters the popliteal fossa. The popliteal artery may be in a more lateral position than usual [28]. The PSA may accompany the proximal part of the posterior cutaneous nerve of the thigh or proceed within the posterior sheath of the sciatic nerve [39–43], which tends to flatten over the artery. In this case, Adachi [7] warned against misinterpretation of PSA as a hypertrophic arteria comitans. PSA may be accompanied by variants in the infragenicular arterial patterns [38] and by several malformative situations including: • Arteriovenous malformations [24, 32, 44] • Neurofibromatosis [32] • Hypoplasia of the limb [35] or hemihypertrophy [16, 36, 45] • Anomalous aortic arch [46] Concomitant persistence of the sciatic vein was reported by Golan et al. [33] and by Savov and Wassilev [47]; further imaging studies [28] put into evidence that PSA is commonly associ-

63

ated with the lack of direct drainage of the popliteal vein through the superficial femoral vein, supplied by a persistent sciatic vein or by a large anastomotic channel between the popliteal vein and the deep femoral vein. Anomalous drainage of the popliteal vein is a common finding in the contralateral unaffected limb in case of unilateral PSA [28]. Persisting sciatic vein is a frequent finding in Klippel-Trenaunay syndrome, as demonstrated with MRI [48]. Arteriomegaly of the PSA is common [49], reaching sometimes an extreme degree [50] and implying very slow flow and as well propensity to aneurysmal degeneration. The presence of unknown PSA may be the source of relevant hemorrhagic or ischemic complications in trauma patients [51, 52] and during hip surgery [53]. Balachandra et al. [54] reported a case of acute limb ischemia following kidney transplant. Rodriguez-Rivera et al. [55] put into evidence the risk of limb ischemia following endovascular treatment of abdominal aortic aneurysm with concomitant coiling of the internal iliac artery [56]. The diagnosis of persistence of the primitive sciatic artery is generally made in adult individuals, at the mean age of 45–57 years [21, 57] with extremes ranging from 6 months to 85–89 years [12, 19]. Van Hooft et al. [21] report the diagnosis of PSA in a 32-week-old fetus, and Shah et  al. [58] report a symptomatic PSA in a newborn. In one of the first reviews of clinical cases studied with angiography [34] 14/18 patients (78%) were older than 30 years. According to large reviews of clinical cases of PSA, most patients were in some way symptomatic, but as many as 11–18% were fully asymptomatic [12, 19, 21], and the presence of PSA was a rather surprising incidental finding. Patient’s complaints were related to ischemia or sciatic pain or buttock mass (painful or not): these three major symptoms were often variably coexisting. Ischemia was generally attributed to embolism from a sciatic aneurysm or thrombosis of the same, but impairment of distal blood supply resulted also from thrombosis of non-aneurysmal PSA [56, 59] and was occasionally observed in lack of any thromboembolic phenomenon [60].

64

Chronic ischemia manifested as claudication but also with rest pain and gangrene [39, 61] and onset of symptoms was often acute [30]; rest pain in absence of thromboembolism was attributed to the extreme slowing of blood flow within the tortuous and dilated PSA [62]. Acute ischemia was also frequently observed [31, 63, 64]. In about a quarter of the cases with ischemia, this was so severe as to jeopardize the limb [20] occasionally leading to amputation [65, 66]. In the report by Esaki et al. [67], acute severe ischemia was considered the consequence of thrombosis of superficial femoral artery, and a correct diagnosis of complicated PSA was established by a retrograde arteriography through the popliteal artery after amputation had been performed. In the careful review of McLellan and Morettin [34], claudication was the predominant complaint in 49% of the patients, gangrene in 12%, while in the remaining cases a buttock mass, with or without local pain, was the relevant clinical presentation. A painful gluteal mass was the chief complaint in several cases [62, 68], sometimes evidently pulsating [69] and eventually complicated by acute peripheral ischemia [70, 71]. Sciatic-like pain resulted frequently associated with aneurysm of PSA, sometimes together with an evidently pulsating mass [72] but often as an early and long-­ lasting symptom [22, 73–76] before a correct diagnosis was established. Mandell et  al. [62] observed that sciatic-like pain was triggered or enhanced in the sitting position. Of the complications of PSA, the more relevant and intriguing is represented by aneurysm. Aneurysmal degeneration of PSA is reported with variable frequence, from 15% [14, 77], when also cases observed during dissections are considered, to 41–48% [12, 14, 21]. According to Brantley et al. [31], PSA aneurysms represent 3% of all lower limb aneurysms. It is difficult to ascertain if some of the gluteal aneurysms reported in the literature were in effect PSA aneurysms. Gluteal aneurysms, which affect more frequently the superior gluteal artery, are often considered as consequent to trauma [78– 80]; trauma is recognized as an important etiologic factor also for PSA aneurysms, either iterative due to the anatomic location of the artery

A. Cavallaro

[14] or direct and unique [18]. Trauma as an etiologic factor looks acceptable for many PSA aneurysms, located at the gluteal fold behind the greater trochanter (true gluteal aneurysms are located more proximally according to Shutze et al. [19]); however PSA aneurysms have been found in the posterior aspect of the thigh [3, 46] and within the pelvis [15]. Cases of concomitant aneurysm of the internal iliac artery have been reported [42, 46] and as well several instances of diffuse dilation, with or without aneurysm, of the entire iliac-PSA-popliteal arterial axis [45, 50, 55]. While syphilis, reported in some cases as positivity of serological tests [13, 37, 39, 81, 82], is not considered a significantly possible etiologic factor, many authors wander about some kind of intrinsic frailty of PSA, not designed by nature to play the role of the principal arterial conduit to lower limb [49], which would lead to dilation and early atherosclerosis [31, 33, 82–86]. PSA aneurysms would be atherosclerotic aneurysms, being important cofactors both trauma and hemodynamics. The hypothesis of a congenital hypoplasia of the elastic component of the arterial wall [28] has not been substantiated by microscopy findings [73]. PSA aneurysms are often complicated with thromboembolism; rupture is rare. The first case of rupture was reported by Fagge [87] in 1864, and to our knowledge few additional cases have been reported [50, 88–91]. In asymptomatic cases of PSA, the arterial variant is discovered as an accidental finding [20] unrelated to any complication of PSA itself. During routine clinical or Doppler evaluation, investigation of the buttock and the posterior aspect of the thigh is generally omitted. Certainly, the occurrence of absent femoral pulse with normal popliteal and distal pulses should promptly arise a diagnostic suspicion; however, the so-­ called Cowie’s sign [35] has been observed only in five cases [21]. The presence of a buttock mass, especially if pulsating and eventually associated with sciatalgic-like pain, should represent the clue to a thorough clinical examination and immediate ultrasound evaluation. But in most cases a high level of suspicion is demanded, particularly when unexplained sciatalgic pain is the

5  Persistence of the Ischiadic Artery

unique patient’s complaint. Moreover, in obese patients, small aneurysms at the gluteal fold may be missed on palpation [33, 49, 76] even if non thrombosed. In case of acute limb ischemia from aneurysm thrombosis, the clinical diagnosis is almost impossible while it could be possible when ischemia is the consequence of embolization; however foot and leg severe ischemia in the presence of a normal femoral pulse is not a surprising occurrence as it is poorly probable to search for a PSA aneurysm without any patient’s advice. The case reported by McEnaney et  al. [92] is highly instructive: in a case of severe limb ischemia, the angiographic diagnosis of popliteo-­tibial thrombosis was established and a superficial femoral-to-posterior tibial bypass successfully performed; after a short time, the patient, for unrelated pathology, was submitted to CT evaluation of the abdomen and pelvis; this demonstrated a partially thrombosed PSA aneurysm, and at further clinical examination, a pulsating buttock mass was found. As a matter of fact, the number of clinical reports of PSA has steadily and progressively increased, thanks to the progress and diffusion of imaging technologies. After the first case demonstrated by angiography in 1960 [35], arteriography in its classic form and later with the digital subtraction technique was considered the best diagnostic tool, even if diagnostic errors continued to be reported occasionally. As reported before, in the case of Esaki et al. [67], the angiographic diagnosis of thrombosis of the superficial femoral artery was corrected after retrograde arteriography through the popliteal artery, demonstrating continuity with the hypogastric artery. With the accuracy of injecting the contrast medium cranial to the origin of the internal iliac artery, angiography dominated the stage for many years [12, 14–16, 27, 29–33, 35, 38, 41, 49, 53, 62, 64, 67, 73, 77, 82, 88]. It remains the preferred diagnostic option in several recent reports [20, 26, 43, 45, 56] and represented the clue to diagnosis in patients with acute hemorrhage [52, 93]. However, since 1985 [18], it was evident that association of angiography with CT would allow a more complete diagnosis, being able to put into evidence also thrombosed vessels and as well the interrelationships with adjacent structures [94–96] . According

65

to Jung et  al. [28], CT angiography allows the detection and the comprehensive evaluation of persistent sciatic artery and is currently considered a must in this field (Fig. 5.2). Also MRI and MR angiography have been successfully used in the diagnosis of PSA [75, 98–100], presenting the advantage of a high definition of the interrelationships between the sciatic artery and the sciatic nerve. Treatment of PSA depends on several factors, i.e., the anatomic features of both arterial systems, femoral and sciatic; the symptoms; and the age and general conditions of the patient. Asymptomatic PSA, in general accidentally discovered, without aneurysm, needs no treatment, but a close clinical and ultrasound surveillance is required, due to the consistent risk of atherosclerotic involvement, dilation, and aneurysm formation [24, 28, 101]. Controversies exist about the management of asymptomatic aneurysms; successful conservative behavior has been reported in case of fully thrombosed aneurysm [14] which may undergo significant reduction in size [102]. In 1985, Becquemin et al. [18], reviewing the literature, registered two aneurysms left untreated owing to their small volume and one patient with thrombosed aneurysm successfully treated with anticoagulants. Surveillance of asymptomatic aneurysms is suggested by Forshaw et al. [103], while Steele et al. [84] advocate the prophylactic repair due to the high risk of thromboembolic events. Up to 1985, the treatment of symptomatic or complicated PSA aneurysms was committed exclusively to surgeons. After the unlucky attempt of Kade [104] in 1876, Joffe [82] reported the first successful operation on a PSA aneurysm: in 1964, in Johannesburg, he performed obliterative endoaneurysmorrhaphy without any associate reconstructive procedure as the collateral circulation was satisfactory; the operation was complicated by permanent foot drop. The goals of the surgical therapy were evident: • To eliminate a potential embolic source and the risk of rupture • To relieve compression symptoms, if any • To assure adequate distal perfusion

66

A. Cavallaro

Fig. 5.2  Volume rendering reconstruction of CT-A study demonstrating bilateral PSA, complete in one limb and incomplete in the other. (From Cavallo Marincola et al. [97])

To achieve these goals, some relevant problems had to be solved: • The approach to gain easy control of the aneurysm, usually located near the greater trochanter, without damaging the sciatic nerve

• The management of the aneurysmal sac • The type of arterial reconstruction, when needed The classic approach to vessels and nerves in the buttock is described in details by Henry [105]: this

5  Persistence of the Ischiadic Artery

Fig. 5.3  Exposure of the sciatic nerve at buttock level (from Henry [105], simplified). Muscles are numbered as follows: (1) pyriformis, (2) gluteus medius, (3) gemellus superior, (4) obturator internus, (5) gemellus inferior, (6) quadratus femoris, (7) gluteus maximus

implies the detachment of the distal insertion of the gluteus maximus muscle, which may be hinged back uncovering the sciatic nerve coming out from the abdomen beyond the pyriformis muscle (which Henry called the key muscle) (Fig. 5.3). Few surgeons [39, 106] followed the technique of Henry; the larger part, approaching the buttock mass, preferred the less invasive procedure described by Moore [107] to avoid impairment of the nerve supply to some portions of the gluteus maximus: the incision, about 15 cm long, courses from beyond the posterior superior iliac spine to the posterior margin of the greater trochanter and is deepened by splitting the gluteus maximus along its fibers and not by division of the muscle from the iliotibial tract [77, 86, 89, 108]. Whatever the type of direct approach, it was evident that the risk of injuring the sciatic nerve was high and, moreover, that comfortable and safe access to the anomalous artery was not assured. To avoid the latter difficulty, some surgeons added an abdominal approach to gain control of the internal iliac artery [37, 39, 73, 89, 106, 109, 110].

67

In case of complete thrombosis of the aneurysm, only the problem of distal ischemia was taken into consideration, leaving undisturbed both the aneurysm and the sciatic nerve [14, 59], as the simple approach to the sac, without opening or manipulation of the same, could produce nerve damage [89]. The treatment of the sac, once surgically exposed, varied greatly. Resection, partial or complete, was performed seldom [34, 37, 41, 85]. Some surgeons proceeded to endoaneurysmorrhaphy [15, 82, 86]. More often the aneurysm was simply excluded [39, 55, 62, 73, 77, 109– 113] even if someone [42, 84] warned that exclusion might not be sufficient on account of feeding vessels inside. In 1985, the endovascular technology was introduced into the management of the complications of PSA, and this changed drastically and positively the approach to the main problems. Becquemin et al. [18] reported the first case of limb salvage by endovascular obliteration of the sac and concomitant revascularization procedure. Loh [114] successfully embolized a PSA aneurysm which had produced severe limb ischemia ending into amputation (a similar case was reported years later by Ooka [66]). Since then, obliteration of the aneurysmal sac with coils, Gelfoam, balloons, and, more recently, vascular plug became almost the rule [61, 68, 71, 92, 101, 115, 116]. Rezayat et al. [91] treated with vascular plugs a ruptured PSA aneurysm: the procedure was complicated by buttock abscess requiring surgical drainage and by foot drop. Direct surgical approach to PSA aneurysm continued to be scantily reported [110] especially when compression symptoms were a significant part of the clinical picture [61, 72, 90, 112]. Currently, simple embolization of the sac may be considered the treatment of choice for aneurysm of incomplete PSA and also when this is complete with concomitant good collateral circulation [115–117]. Arterial reconstruction is required to treat severe limb ischemia when this is the chief patient’s complaint or to prevent ischemia consequent to aneurysm treatment, as well in cases of PSA thrombosis in absence of aneurysm [56, 59, 118, 119]. A bypass excluding the PSA system

A. Cavallaro

68

has been the more frequent procedure [12, 15, 18, 22, 34, 42, 67, 68, 71, 73, 77, 92, 111, 118], but also reconstructions ending onto the PSA, distally to the aneurysm, have been reported: these were iliac-to-PSA bypasses, coursing under the inguinal ligament and then subcutaneously [90] or through the adductor muscle mass [39] or following the transobturator route [109, 110], and were in general successful, only one early failure with ensuing amputation [106]. In situ interposition grafts or inlay grafts [26, 41, 84] were initially the object of criticism, due to the anatomic position exposed to external trauma especially when sitting; however, in the short- and mid-­ term, the results were not inferior to those of bypasses. The longest follow-up in the treatment of PSA aneurysm is reported by Drodz et  al. [120] with an 18-year patency (at Doppler control) after excision and interposition graft (without foot drop). These positive results, coupled with the dramatic reduction of invasivity and the continuing improvement in technology and materials, brought to the endovascular treatment of PSA aneurysm with stent grafting. Stenting looks highly attractive, satisfying most of the requirements, i.e., exclusion of the aneurysm, maintenance or restoration of blood flow, and full respect of sciatic nerve integrity. Only when a rapid decompression is demanded owing to severe local pain or sciatic neuropathy, with or without ischemia, an inlay graft seems to be currently indicated [61, 72, 112]. In 2001, Gabelmann et  al. [121] reported good results with stent grafting of PSA in one case of aneurysm (follow-up 22 months) and in one case of severe stenosis (follow-up 18 months); they did not observe any shrinkage of aneurysm and stated that it was not yet possible to ascertain if a stent graft, in that particular anatomic situation, could endure continued compression during regular day life over a period of years. In 2005, Fearing et  al. [122] proposed stenting of PSA aneurysm by a retrograde approach through the popliteal artery to avoid difficulties in deploying a long stent via a tortuous antegrade approach through the femoral or axillary [76] access; the transpopliteal access was thereafter successfully

used by others [64], and a positive 4-year followup has been reported [123]. Fracture and thrombosis of the stent, 6 months after treatment, have been reported [124]. In spite of several positive results [125, 126], this technique is not yet universally accepted, and cases treated by embolization and reconstructive procedure continue to be reported [101]. On a whole, primary amputation is seldom reported in patients with PSA aneurysm, and surgical and/or endovascular treatment has allowed limb salvage in about 90% of the cases [21, 101]. Due to the rarity of this pathology, numbers are too small to attempt a comparison between the different therapeutic methods, also because extended follow-up is generally unavailable; as for the short- and mid-term results, no procedure looks clearly superior to others. Yang et al. [101] compared six cases of stenting (follow-up 1–48 months, mean 20 months) with six cases of interposition graft (follow-up 6–24 months, mean 16.5 months), and no difference was found. Finally, it has been observed that PSA may represent an effective—and providential—collateral route to acquired iliac and/or femoral occlusion [17, 127, 128].

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71 95. Michel C, Marcus C, Clement C, Wejroch P, Devey-­ Michel A, Menanteau B.  Persisting sciatic artery: findings using spiral CT. J Radiol. 2002;83:1847–9. 96. Abularrage CJ, Crawford R, Patel V, Conrad M.  Diagnostic strategies for the persisting sciatic artery. Vasc Endovasc Surg. 2009;29:485–9. 97. Cavallo Marincola B, Napoli A, Anzidei M, Marotta E, Boni F, Cartocci G, Bertaccini L, Noce V, Pacilé MA, Catalano C. Persistence of the sciatic artery: a case report of combined (complete and incomplete) type causing leg ischemia. Case Rep Vasc Med. 2012;2012, article ID 196798. 98. Yamaguchi M, Mii S, Kai T, Sasaka H, Mori A.  Intermittent claudication associated with persistent sciatic artery: report of two cases. Surg Today. 1997;27:863–7. 99. Erturk SM, Tatii S.  Persistent sciatic artery aneurysm. J Vasc Interv Radiol. 2005;16:1407–8. 100. Kircher MF, Lee EY, Alomari AI. MRI findings of persistent sciatic artery associated with pelvic infantile hemangioma. Clin Radiol. 2010;65:172–5. 101. Yang S, Ranum K, Malone M, Nazzal M. Bilateral persistent sciatic artery with aneurysm formation and review of the literature. Ann Vasc Surg. 2014;28(1):264.e1–7. 102. Sasaki T, Mitsunaga Y, Yoshioka K. Regression of a thrombosed persistent sciatic artery aneurysm. Heart Vessels. 2009;24:66–9. 103. Forshaw HJ, Abedin A, Wilson PA, Wilson JG.  Surveillance and conservative management of a persistent sciatic artery aneurysm. Vascular. 2005;13:187–90. 104. Kade E.  Aneurysma der Art. Ischiadica. Unterbindung der Art. Iliaca communis sinistra. St Petersb Med Wchschr. 1876;1:25–6. 105. Henry AK. Extensile exposure. 2nd ed. Edinburgh: Churchill-Livingstone; 1970. p. 180–97. 106. Blumberg L, Grant C.  Bilateral persistent sciatic artery with unilateral aneurysm and limb ischemia. J R Coll Surg Edinb. 1985;30:321–3. 107. Moore AJ.  The self-locking metal hip prosthesis. J Bone Joint Surg (Am). 1951;39-A:811–27. 108. Wolf YG, Gibbs BF, Guzzetta VJ, Bernstein EF. Surgical treatment of aneurysm of persistent sciatic artery. J Vasc Surg. 1993;17:218–21. 109. Urayama H, Tamura M, Ohtake H, Watanabe Y. Exclusion of a sciatic aneurysm and an obturator by-pass. J Vasc Surg. 1997;26:697–9. 110. Eglington TW, Gordon MK. Persistent sciatic artery aneurysm treated by exclusion and obturator by-pass. Eur J Vasc Endovasc Surg Extra. 2005;9:29–31. 111. Noblet D, Gasmi T, Mikati A, Watel A, Warembourg H, Soots G.  Persistent sciatic artery: case report, anatomy, and review of the literature. Ann Vasc Surg. 1988;2:390–6. 112. Handa GI, Coral FE, Zendrini Buzingnani V, Marques Mantovani L, Lopez Masera ES, Krauss DS, de Paula MG. Tratamento cirurgico de pseudo aneurisma de artéria isquiatica. Relato de caso e revisao da literatura. J Vasc Bras. 2011;10:256–60.

72 113. Wilms G, Storme L, Vandaele L, Baets M. CT demonstration of a persistent sciatic artery. J Comput Assist Tomogr. 1986;10:524–5. 114. Loh FK. Embolization of a sciatic artery aneurysm. An alternative to surgery: a case report. Angiology. 1981;31:472–6. 115. Song MJ, Chung CH, Hany M. Non operative management of persistent sciatic artery aneurysm. A case report. J Korean Med Sci. 1992;7:214–20. 116. Sultan GA, Pacainowski JP, Madhavaro P, McDermott R, Molloy M, Colgan M-P, Moore DJ, Shanik JD. Endovascular management of rare sciatic artery aneurysm. J Endovasc Ther. 2000;7:415–26. 117. Sogaro F, Amroch D, Galeazzi E, Di Paola F, Mancinelli P, Ganassin L. Non-surgical treatment of aneurysm of bilateral persistent sciatic artery. Eur J Vasc Endovasc Surg. 1996;12:503–5. 118. Morinaga K, Kuma H, Kuroki M, Kusaba A, Okadome K, Myazaki T, Ohtsuka K, Inokuchi K.  Occluded persistent sciatic artery. J Cardiovasc Surg. 1985;26:82–5. 119. Johansson G.  Intermittent claudication in adolescence due to incomplete persistent sciatic artery. Vasa. 1990;19:72–4. 120. Drodz W, Urbanik A, Budzynski P. A case of bilateral persistent sciatic artery with unilateral aneurysm: an 18-year period of graft patency after excision of aneurysm. Med Sci Monit. 2012;18:cs12–5. 121. Gabelmann A, Kramer SC, Wisianowski K, Tomczak R, Pamler R, Gorich J. Endovascular inter-

A. Cavallaro ventions on persistent sciatic arteries. J Endovasc Ther. 2001;8:622–8. 122. Fearing NM, Ammar AD, Hutchinson SA, Lucas ED.  Endovascular stent graft repair of a persistent sciatic artery aneurysm. Ann Vasc Surg. 2005;19:438–41. 123. Wijeyaratne SM, Wijewardene N.  Endovascular stenting of a persistent sciatic artery aneurysm via retrograde popliteal approach: a durable option. Eur J Vasc Endovasc Surg. 2009;38:91–2. 124. Girsowicz E, Georg Y, Lejay A, Ohana M, Delay C, Bouamaied N, Thaveau F, Chakfé N. Midterm failure after endovascular treatment of a persistent sciatic artery aneurysm. Ann Vasc Surg. 2014;28:1323. e7–e12. 125. Mascarenas De Oliveira F, De Souza Mourao G. Endovascular repair of symptomatic sciatic artery aneurysm. Vasc Endovasc Surg. 2011;45:165–9. 126. Venkokos C, Avgerinos EP, Chatziioannou A, Katsargyris A, Klonaris C.  Endovascular repair of a persistent sciatic artery aneurysm. Vascular. 2010;18:162–5. 127. Samson RH, Showalter DP. Persistent sciatic artery as collateral for an occluded ilio-femoral system. J Vasc Surg. 2004;40:183. 128. Tsilimparis N, Kiiaro A, Riesenmann PJ, Reeves JG. Persistent left sciatic artery eliminated need for revascularization in a 13-year old with pseudoaneurysm of the superficial femoral artery. Vasc Endovasc Surg. 2013;47:250–3.

6

Popliteal Artery Entrapment Antonino Cavallaro

Popliteal artery entrapment is recognized as a rare but not exceptional causative factor of aneurysm. Gaylis [1] found that 4 out 53 (7.5%) popliteal aneurysms were due to entrapment; in the series of popliteal aneurysms reported by Batt et al. [2], the incidence was 2.6% (3/116); when the aneurysm was bilateral, the incidence of entrapment cases was, respectively, 8.3% (1/12) and 2.3% (1/43). Stuart [3] is quoted as the first to describe muscular compression on the popliteal artery (Fig. 6.1): during the dissection of a limb amputated for gangrene consequent to thrombosis of a popliteal aneurysm, he observed the currently universally known anomaly in the course of the popliteal artery, looping around the inner margin of the medial gastrocnemius, and as well a variant in the site of proximal insertion of that muscle. An anomaly similar to that described by Stuart had been reported in 1875 by Gruber [5] (Fig.  6.2): in his case, the popliteal artery presented a segmental chronic thrombosis supplied by a marked enlargement of the arteries of gastrocnemius. Variants in the interrelationships between the neurovascular bundle, and, namely, the popliteal artery, and the neighboring musculotendinous

A. Cavallaro (*) Past Professor of General Surgery, “Sapienza” University, Rome, Italy © Springer Nature Switzerland AG 2021 A. Cavallaro (ed.), Aneurysms of the popliteal artery, https://doi.org/10.1007/978-3-030-49687-6_6

Fig. 6.1  The short note published in 1879 by T.  P. Anderson Stuart [3] (1856–1920) when he was a medical student in Edinburgh. He ended his career as the first professor and later the chairman of the board of the Medical School in Sidney [4]

structures were the object of several observations and reports by anatomists. Labatt [6] described in 1837 a double-headed medial gastrocnemius: vessels and nerve coursed, evidently compressed, between the two heads. In 1844, Quain [7] reported three observations about an unusual band of muscular fibers in close connection of the artery in the lower part of the popliteal space coursing down from a line above the femoral condyles to the gastrocnemius muscle: it 73

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A. Cavallaro

Fig. 6.2  The anomalous course of the popliteal artery found by Gruber [5]. (A) Popliteal artery. (B) Medial gastrocnemius muscle. (C) Arteria gastrocnemialis communis

separated the nerve from the vessels or the artery from the vein and was defined as a supplementary or third head of the gastrocnemius. After more than a century, Iwai et al. [8] stressed the role of the third head of gastrocnemius in the

mechanism of entrapment of the popliteal vessels and described the “gastrocnemius tertius” as a muscle arising from the posterior and inferior surface of the femur and joining the gastrocnemius, more frequently the medial head; in

6  Popliteal Artery Entrapment

Japanese, the frequency of gastrocnemius tertius would be higher than generally reported [9] (5.5% vs about 3%). The different types of gastrocnemius tertius had been thoroughly described in 1884 by Testut [10], who put into evidence that this unusual muscle could arise also from flexor muscles (semimembranosus or biceps femoris) or by the greater abductor. This was confirmed by Le Double [11], and, later, Frey [12] registered the variants (at least 12) of gastrocnemius tertius. In the last decades of the nineteenth century, several observations of an accessory, lateral, head of the medial gastrocnemius were reported [13–15]: the artery coursed between the principal and the accessory head [16] (Fig.  6.3), sometimes traversing the muscular substance. Parona [17], in 1903, reported the anomalous cranial insertion of the medial gastrocnemius, more lateral than usual, onto the metaphysis: the muscle separated the artery from the vein. In

Fig. 6.3  Accessory head of the medial gastrocnemius as illustrated by Bouglé [16]

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1938, Suzuki [18] described the compression of the popliteal artery by the tendon of the semimembranosus muscle. Popliteal artery entrapment entered the clinical stage in Leyden, with Hamming [19], who, in 1959, reported the treatment of a 12-year-old boy complaining of claudication. The young age of the patient and the peculiarity of the anatomical situation found at operation excited interest and attention, and by 1964 four additional cases had been reported [20–23]: of these, two were bilateral [22, 23], and a post-stenotic aneurysm was observed in two limbs [21, 22]. In 1965, the expression “popliteal artery entrapment syndrome” was proposed by Love and Whelan [24], being rapidly and almost universally accepted, even if French authors [25] continued to use preferentially the expression “syndrome de l’artère poplitée piégée.” Literature reviews registered eight cases in 1970 [26] and 14 cases in 1971 [27]: the latter resulted in complication by aneurysm (one case) and post-stenotic dilation (four cases). From 1959 through 1975, clinical cases amounted to 65 [28]. In 1979, Rich et al. [29] pointed to the increasing interest of this probably underestimated pathology, textually asserting “specific consideration for the diagnosis of popliteal vascular entrapment should be given to those patients in the younger athletic male population in whom intermittent claudication with exercise develops, to all younger male and female patients in whom thrombosis of the popliteal artery develops without trauma, and to all middle-aged patients in whom popliteal aneurysm develops.” The clinical field in which high suspicion for popliteal entrapment is demanded would be enlarged in the following years, including military recruits and an increasing number of female patients, and in 1999 Levien and Veller [30] again suggested that popliteal entrapment had been probably underestimated up to then. The wide spectrum of anatomical variants found to be responsible for popliteal artery flow impairment gave origin to several attempts to classification [31–35], but none looked entirely satisfactory, due to the continuing reports on new types of compression and the relevant number of

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variants (some of which really rare or unique) sometimes variously interlacing reciprocally. The concomitant involvement of the popliteal vein was observed since the early reports [36–38], and occasionally a “pure” venous entrapment was observed [39]. On a whole, vein entrapment is present in about 30% of the cases [8, 40]. In a comprehensive review [28] of 172 patients (210 limbs) treated surgically, 17 anatomical variants were identified: the medial gastrocnemius, alone or in combination with other structures, was involved in over 80% of the cases, including Stuart’s original variant (21% of all cases) and lateral attachment onto the femoral metaphysis (31% of all cases). In 1998, in Rome, the Popliteal Vascular Entrapment Forum was established [41], headed by Norman M.  Rich, and, accepting with minor changes what stated by the Society for Vascular Surgery, a ­classification was proposed (Fig. 6.4), based on the following: • Popliteal arterial and venous entrapment represent a common disease defined as popliteal vascular entrapment.

A. Cavallaro

• Anomalies are complex, and in several instances a single embryologic variant cannot fully explain the situation. Seven main types of popliteal vascular entrapment were identified: • Type I—the anatomical position of the medial head of gastrocnemius is normal or almost normal (insertion onto the superior and posterior surface of the medial condyle); the popliteal artery loops around the inner margin of the medial gastrocnemius and courses beneath the muscle to reach its normal place in the lower part of the popliteal space. • Type II—the medial head of the gastrocnemius is laterally attached, onto the femoral metaphysis. • Type III—accessory slip of the medial gastrocnemius. This accessory bundle may be tendinous, muscular, or both. If the muscular component is particularly developed, the artery looks as passing within the muscle [34, 36, 42–45].

Fig. 6.4  The four more frequent types of entrapment (see text). In type II, an example is given of the concomitant compression over the artery, the vein, and the nerve

6  Popliteal Artery Entrapment

• Type IV—the popliteal artery passes ventrally to the popliteus muscle. Entrapment from fibrous band has been sometimes assimilated to type IV [46–48]. Type IV is considered the only variant in which the nerve too may not be involved [49]. • Type V—vein entrapment, primary or associated with artery entrapment. The rarity of vein entrapment may be due to the fact that deep limb veins, which are accompanying veins to the arteries, are the last to develop, being unavailable for entrapment in the embryological stage in which it may occur [50]. • Type VI—variants. It includes complex anomalies and rare anatomical derangements. Ezaki et  al. [51] found compression by an aberrant tendinous band of the greater adductor muscle. This had been already recognized by Maistre [52] as a frequent and important component of popliteal entrapment. Compression by the plantaris muscle was identified occasionally [53] but with impressive frequency by Bouhoutsos and Daskalakis [35]. Other anatomical variants responsible for compression upon the popliteal vessels are accessory tendon of the semitendinosus muscle [33, 54], fused head of gastrocnemius [55], and medial accessory tendon of the lateral gastrocnemius [56]. Entrapment from branches of the tibial nerve has been described [29]. Reviewing the operative reports, one is brought to think that a certain overlapping of plantaris muscle, gastrocnemius tertius, and accessory bundle of medial gastrocnemius is possible in defining the anatomy and embryology of the compressing structure. • Type VII or F—functional entrapment. Levien and Veller [30] synthesized the embryological causes of the more frequent types. Persistence of the primitive popliteal artery explains type IV.  Under normal circumstances, the cranial migration of the medial gastrocnemius occurs before the development of the definitive popliteal artery. Delay in the migration of medial gastrocnemius or early formation of the latter may give origin to type I (the muscle

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catches the artery which is swept medially) or to type II (the artery partially arrests the final migration of the muscle) or to type III (the artery develops within the migrating muscle). Therefore types I–III would represent the result of a unique embryologic derangement, which may variously produce either the aberrant path of the popliteal vessels [57] or an abnormal attachment of medial gastrocnemius [31] over the normally positioned vessels. Popliteal artery entrapment is diagnosed predominantly in young adults, being 47% of patients aged 21–40 and 28% aged 20 or less [58]; extremes are at 7  years [59] and 65  years [60]. Males outnumber females 9:1 according to Andre et al. [61]; in a review of 375 cases reported from 1959 through 1990 [62], a 7.5:1 ratio was found. The number of female patients is steadily increasing (in our personal experience1 the M/F ratio is 3.5:1): currently, popliteal artery entrapment should be suspected in any young patient, regardless of sex, with symptoms of pain, paresthesia, cold foot after intensive physical activity, and as well if complaining of claudication mainly when walking upgrade or ascending stairs. Bilateral involvement was already reported in the early clinical experiences [22, 23, 53] and accounts for about 38% of all cases. Occurrence of the syndrome in consanguineous has been repeatedly observed [63–66] and once in monozygotic twins [67]. True incidence of popliteal entrapment is still obscure. Gibson et al. [57] found three cases in a series of 86 dissections (3.8%); the incidence was of 3.3% in the postmortem study published by Paulo [68]. O’Donnell [69] registered a similar incidence (4.3%) in 92 cadaver studies. Going to the clinical setting, Bouhoutsos and Daskalakis [35] treated 33 patients in a population of about 20,000 young subjects (0.16%) purposedly screened; di Marzo et  al. [70] observed the same percentage in a smaller series (2/1212; 0.16%). Personal experience has been gained at the Dept. of Surgery “P.  Valdoni,” University “La Sapienza,” Rome, and consists of 40 patients (62 limbs) treated from 1979 through 2009.

1 

A. Cavallaro

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It looks convenient to consider two stages of popliteal artery entrapment [71]: early and advanced. This relies on the pathology of the involved artery but mainly corresponds with the type of treatment required. In the early stage, the artery does not present any stable alteration, at least macroscopically; cure requires simple freeing from the compressing structure. In the advanced stages, significant stenosing lesions or thrombosis or dilation/aneurysm is present, and an associated reconstructive surgery is required, if possible; moreover, distal branches may be seriously damaged by acute or chronic embolism arising from the popliteal artery lesion. Lesions of the arterial wall have been studied in several specimens [72–75] and derive from the chronically repeated compression by a musculotendinous structure against an osseous plane; on the muscular side, they are stretch lesions, consisting of the appearance of a longitudinal smooth muscle bundle as observed in the bronchial artery as a consequence of hypertension [76]; on the osseous side they are crush lesions, with atrophy of the smooth muscle cells and of the internal elastic membrane, thickening of the intima, and eventually organized thrombus. Naylor et  al. [77], studying five specimens of occluded and resected artery, were able to define three stages of histopathologic lesions, starting with neovascularization of the adventitia and proceeding with fibrosis of the media and final fragmentation of the internal elastic lamina, fibrointimal proliferation, and superimposed thrombosis. It has been suggested [29, 47] that type IV entrapment (from popliteal muscle or fibrous transverse band) may be the most aggressive for artery disease; this could be true, as bilateral aneurysm was observed in a very young patient [46]; moreover Levien and Veller [30] reported that severe ischemia affected more than 60% of type IV cases (5/8), while its incidence was less than 30% in the whole series of 58 cases of entrapment and that the eight aneurysms observed were in type I and type IV; however anatomic lesions of the popliteal artery have been found in many musculotendinous variants. Midpopliteal artery thrombosis affected 3 out 12 patients reported by Rich et al. [29]; emphasis

on its significance and the required type of surgical approach was made by several authors [78, 79]. Post-stenotic popliteal aneurysm, first observed by Servello [21] in Padua, has been repeatedly reported [22, 25, 35, 44, 45, 48, 80], sometimes bilaterally [28, 46]. In our experience, aneurysm was present in 17% of patients (13% of limbs); in different series or reviews, the incidence of aneurysm ranged from 7 to 21% [27, 29, 81], while a simple post-stenotic dilation was observed in about 30% of the cases [27, 74]. Occasionally, the aneurysm was the first sign of entrapment [82]. As a consequence of the popliteal artery lesion, distal flow may be impaired by emboli; these may obviously arise from an aneurysm [29, 35, 83, 84] but also from mural thrombus of normal size artery [57, 85, 86]. It is a matter of fact that, especially in older patients, involvement of the tibial vessels may be observed in absence of signs of atherosclerosis: this can endanger or preclude the required reconstructive procedure. From the clinical point of view, early stage is diagnosed in younger patients with mild symptoms after intensive physical training or claudication >100  m, being rare heavy claudication (2  cm); these cases presented a statistically significant association with extra-popliteal aneurysms. In spite of a growing mass of information, the true prevalence of PAA remains speculative. More than 50  years ago, Hunter et  al. [10] concluded that apparently PAAs are less common than aneurysms of aortic bifurcation and more common than aneurysms within the chest and of the major arteries of limbs or neck. The latter assessment was confirmed by several experiences. Abelleyra et  al. [27] reported 31 peripheral aneurysms, of which 18 (58%) were popliteal. Hands and Collin [28] observed 25 femoral and 34 popliteal (57.6% of the total) aneurysms. Agrifoglio et al. [29] stated that, on the basis of the available literature, PAAs represent 62% of peripheral aneurysms. In contrast with this general consensus, Whitehouse et  al. [30] reported, during a 40-year period, 88 PAAs

and 172 femoral artery aneurysms, considering however that many PAAs are small and asymptomatic and that palpation of the groin is much easier and more reliable than that of the popliteal fossa. Trying to define, if not the prevalence, at least the eventual increase in diagnosis (and consequently the improvement in treatment), we tried to tabulate the data from several series, applying a dividing watershed represented by the year 1985, when duplex-scan apparatuses became widely available. This was a milestone event, as awareness of the importance of the disease, due to the ominous sequelae observed in undiagnosed/misdiagnosed cases, was already established following the reports of Gifford et al. [31], Wychulis et al. [32], and Bouhoutsos and Martin [33]. In the first review (Table  8.1), with the fair exception of the Mayo Clinic (reporting a mean of more than 25 cases/year), the single experiences relied on 1.5–9.8 cases/year, with only two series approaching ten cases/year. In the second

Table 8.1  Series of atherosclerotic popliteal aneurysms collected (or largely collected) before 1985 Author, year Linton [8], 1949 Janes [34], 1951a Gifford [31], 1953a Lord [35], 1957 Crawford [13], 1959 Friesen [36], 1962a,b Edmunds [37], 1965 Baird [38], 1966 Crichlow [39], 1966 Wychulis [32], 1970a Bouhoutsos [33], 1974 Buda [40], 1974 Gaylis [41], 1974 Hardy [42], 1975 Buxton [23], 1975 Evans [43], 1976c Towne [44], 1976 Tompkins [45], 1977 Chitwood [46], 1978 Inahara [47], 1978 Guvendik [18], 1980 Szilagyi [3], 1981

Study period 1942–1947 1940–1949 1913–1951 7 years 5 years 1950–1960 1948–1963 1938–1964 1953–1965 1961–1968 1958–1972 1951–1972 15 years 18 years 1963–1974 15 years 21 years 1968–1976 10 years 1963–1977 1969–1976 1964–1979

Patients 14 42 64 10 64 80 36 42 150 71 59 38 21 23 52 80 18 26 30 20 61

Aneurysms 15 63 95 13 30 100 96 51 60 231 102 81 49 29 34 86 119 26 35 44 27 86

Pts/year 2.8 4.2 1.6 1.4 5.8 5.0 1.3 3.2 18.8 4.7 2.7 2.5 1.2 1.9 3.5 3.8 2.0 2.6 2.0 2.5 3.8

Ans/year 3.0 6.3 2.4 1.9 6.0 9.1 6.0 1.9 4.6 28.9 6.8 3.7 3.3 1.6 2.8 5.7 5.7 2.9 3.5 2.9 3.4 5.4 (continued)

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104 Table 8.1 (continued) Author, year Vermilion [48], 1981c Laskar [49], 1982 Reilly [50], 1983 Whitehouse [30], 1983 Takolander [51], 1984 Downing [11], 1985 Salo [52], 1986 Mellière [53], 1986 Anton [54], 1986 Flamand [14], 1971 Raptis [55], 1986 Schellack [56], 1987 Englund [57], 1987 Lilly [58], 1988 Bacciu [15], 1988 Farina [20], 1989 Cole [59], 1989 Halliday [60], 1991 Shortell [19], 1991 Dawson [61], 1991 Roggo [62], 1993 Lowell [63], 1994a Vettorello [64], 1996 Sarcina [65], 1997 Davidovic [66], 1998

Study period 1960–1980 1970–1981 1958–1982 1943–1982 1971–1982 1960–1983 1960–1980 1970–1983 1952–1974 1975–1984 1972–1983 1965–1985 1968–1985 1978–1987 1976–1986 1972–1988 1976–1987 1982–1989 1964–1990 1958–1985 1965–1991 1980–1985 1970–1994 1974–1994 36 years

Patients 87 27 159 61 13 39 19 50 56 54 36 60 75 35 15 33 38 33 39 50 162 106 26 58 53

Aneurysms 147 32 244 88 18 61 21 73 73 87 61 95 103 59 24 47 59 51 51 77 247 161 37 69 64

Pts/year 4.1 2.3 6.4 1.5 1.1 1.6 0.9 3.6 2.4 5.4 3.0 2.9 4.2 3.5 1.4 1.9 3.2 4.1 1.4 1.8 6.0 17.6 1.0 2.9 1.5

Ans/year 7.0 2.7 9.8 2.2 1.5 2.5 1.1 5.2 3.2 8.7 5.1 4.5 5.7 5.9 2.2 2.8 4.9 6.4 1.9 2.7 9.1 26.8 1.5 3.4 1.8

In this table, as in the following one, we tried to give an idea about the experience of different authors in the field of atherosclerotic aneurysms of the popliteal artery, with exclusion of aneurysms of different etiology Only atherosclerotic PAAs are dealt with in papers at refs. 8, 13, 15, 23, 30, 34, 38, 39, 43–47, 49, 51, 52, 55, 57, 61, and 63 Papers at refs. 3, 11, 18–20, 31–33, 35–37, 40–42, 53, 60, 62, and 66 include also a small number of non-atherosclerotic PAAs. However, it was easy to extract data pertaining only to atherosclerotic PAAs Papers at refs. 48, 50, 54, 56, 58, 59, 64, and 65: not stated if all PAAs are atherosclerotic a From the Mayo Clinic, Rochester, Minnesota: overlapping of study period of ref. 31 vs ref. 34; partial overlapping of ref. 36 vs ref. 31 b In effects, Friesen et al. report having seen 110 patients (i.e., 10 pts/year), but details are given only for patients receiving surgical treatment c It is not clear if data of report at ref. 48 include data from report at ref. 43

review (Table 8.2), the Mayo Clinic remains the leading center, with more than 30 cases/year; however, eight centers reported an annual mean approaching or trespassing ten cases/year (one approaching 30 cases/year). Given the characteristics of the various experiences, essentially clinical, the impression is that PAAs are diagnosed with increasing frequency, but this is the consequence of an increased attention in the search of contralateral asymptomatic PAA or of

PAA in patients with AAA.  Large screenings are still lacking, and therefore, the true prevalence of PAA remains unknown. Perhaps PAA is not really a rare disease, and, in any case, it has been a companion of surgeons during the centuries, so as to justify and share the statement by Laskar et  al. [49]: “Il n’est pas étonnant que les premiers balbutiements de la chirurgie vasculaire se soient concentrés autour du diagnostic et du traitement des anévrismes poplités en raison de la fréquence de ces lésions.”

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Table 8.2  Series of atherosclerotic popliteal aneurysms collected (or largely collected) after 1985 Author, year Dawson [67], 1994a Carpenter [68], 1994 Gawenda [69], 1995 Duffy [70], 1998 Taurino [71], 1998 Dijkstra [72], 1998 Locati [73], 1999 Gouny [74], 2000 Irace [75], 2001 Stiegler [76], 2002 Kauffman [77], 2002 Dorigo [78], 2002 Ascher [79], 2003 Bowrey [80], 2003 Harder [81], 2003 Laxdal [82], 2004 Aulivola [83], 2004 Martelli [84], 2004 Galland [85], 2005 Stone [86], 2005 Pulli [87], 2006 Beseth [88], 2006 Huang [89], 2007b Davies [90], 2007 Curi [91], 2007 Lichtenfels [92], 2008 Dzieuciuchowicz [93], 2009 Zimmermann [94], 2010 Zaraca [95], 2010 Pulli [96], 2012 Kropman [97], 2014 Huang [98], 2014b Serrano-­Hernando [99], 2015 Mazzaccaro [100], 2015 Ronchey [101], 2015 Wagenhauser [102], 2015 Leake [103], 2016 Personal series

Study period 1985–1992 1979–1992 1981–1994 1987–1997 1980–1995 1984–1996 1982–1998 1992–1997 1990–1999 1995–2000 1968–2000 1990–2000 4 years 1988–2000 1997–2000 1974–2000 1992–2002 1985–2000 1988–2004 1995–2004 1984–2004 1981–2003 1985–2004 1988–2006 2000–2006 2000–2004 1995–2005 2000–2007 1991–2009 2005–2010 1993–2011 2005–2012 1993–2013 1998–2011 2000–2013 1996–2013 2006–2014 1981–2005

Patients 27 33 39 25 23 17 35 45 46 112 89 25 46 24 49 38 38 73 46 137 35 494 57 43 40 61 46 35 59 218 217 142 65 67 30 156 58

Aneurysms 41 54 58 42 28 23 63 52 75 65 175 109 34 67 36 70 63 56 116 55 159 43 651 72 56 60 82 63 49 81 368 271 211 94 101 50 247 82

Pts/year 3.4 2.4 2.9 1.9 1.5 1.3 7.0 4.5 7.7 3.4 8.1 6.2 3.5 6.0 1.8 3.5 2.4 4.3 4.6 6.5 1.5 24.7 3.0 6.1 8.0 5.5 5.6 1.8 9.8 11.5 28.9 6.8 4.6 4.8 1.7 17.3 2.3

Ans/year 5.1 3.9 4.3 3.2 1.9 1.8 3,7 10,4 7.5 10.8 5.3 9.9 8.5 5.1 9.0 2.6 5.7 3.5 6.8 5.5 7.6 1.9 32.6 3.8 8.0 12.0 7.4 7.9 2.6 13.5 19.4 36.1 10.0 6.7 7.2 2.8 27.4 3.3

Papers at refs. 67, 69, 70, 72, 74, 77, and 80 deal only with atherosclerotic PAAs. In addition, personal series includes only atherosclerotic PAAs Non-atherosclerotic PAAs are included in papers at ref. 73 (two cases of PA entrapment syndrome) and at ref. 83 (one case of Marfan syndrome); however, it was easy to extract data regarding only atherosclerotic PAAs Paper at ref. 89: not all atherosclerotic PAAs. Out of 236 pathology findings: atherosclerosis 233; two fibromuscular dysplasia; one thromboangiitis obliterans Papers at refs. 68, 71, 75, 76, 78, 79, 81, 82, 84–88, and 90–103: not stated if all PAAs are atherosclerotic Papers at refs. 71–73, 78, 86–88, 90, 91, and 95 deal only with cases submitted to repair (either surgical or endovascular) a Cases previously reported [61] are not included b From the Mayo Clinic, Rochester, Minnesota

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8.2

Etiopathogenesis

In the past, several factors were the object of speculation as responsible for PAA formation. Broca [104] took into consideration the abuse of alcohol and the prolonged use of mercurial drugs, but he thought that trauma and syphilis were the more frequent causes of the disease. Trauma could be acute, under the form of a contusion, but more often iterative and, in some way, inherent to daily activities. Home [105] observed a high incidence of PAA in coachmen, postilions, and horse-riding men (as cavalry soldiers), attributing the cause of chronic trauma not only to repeated strenuous movements but also to the superior border of rigid leather boots. Delbet [106] favored the traumatic etiology, observing that PAAs are more frequent in the laboring class, and also the predominant involvement of men was explained with the harder physical activity proper of male individuals. Syphilis was recognized as a frequent cause of aneurysms, but as for PAA, several doubts arose about its true role. Broca [104] observed that in colonized countries, syphilis was a diffuse disease but aneurysms were rare. Delbet [106] reported a similar and important incidence of syphilis in soldiers and sailors, but PAAs were more frequent in soldiers; contrarily, Erichsen [107] observed a particularly high incidence of PAA in sailors. Shortly before World War II, Wells et al. [108] stated that atherosclerosis is frequently the only demonstrable disease of the aneurysm wall and that trauma or strain may precipitate the dilatation and, in particular, give rise to symptoms. Linton [8] reported on 42 patients with PAA observed at the Massachusetts General Hospital in Boston during the period 1908–1947: in 35 of them, atherosclerosis was identified as the etiological factor (even if four patients were luetic); moreover, he stressed the fact that syphilis was never recognized as the etiological factor in the 25 aneurysms collected from 1938. The facts are that atherosclerotic lesions are observed also in post-stenotic aneurysms [20] and that atherosclerotic involvement per se cannot explain the predilection of aneurysmal disease for the popliteal artery.

The particular anatomic situation of the popliteal artery is considered relevant to the formation of aneurysm in this site. In 1957, Lord [35] textually wrote: “the popliteal artery is adaptable, in that it may change from a straight line course to one forming an angle of 45 degrees when the leg is fully flexed on the thigh. This change is no trick for the young, healthy, flexible vessel, but it is less readily tolerated by an artery that is more rigid and less elastic due to the presence of atheromatous plaques and deposits of Calcium in the wall...Unquestionably, frequent bending is a factor favoring the development of aneurysms in this particular vessel….” The importance of repeated trauma from flexion/extension of the knee had been already stressed by Boyd et al. [109] and by Lindbom [110]. An attractive etiopathogenetic theory is that PAA may represent a post-stenotic arterial dilatation. A clinical support to this hypothesis relies on the not rarely observed post-stenotic aneurysms in subjects affected with popliteal artery entrapment. The phenomenon is largely recognized both clinically and experimentally. Subclavian artery aneurysms due to anatomical variants in the thoracic outlet were known in the nineteenth century [111]; in 1916, Halsted and Reid [112] produced a circumscribed dilation of an artery downstream a partially occluding band. In 1954, Holman [113] thoroughly studied in the laboratory the phenomenon of post-stenotic dilatation (Fig. 8.2) and concluded: “a mass of fluid ejected through a narrow and limited constriction under high velocity strikes against a more slowly moving mass of fluid distal to the stenosis, resulting, first, in the conversion of high kinetic energy into high potential energy or lateral pressure and, second, in the lateral deflection of the rapid stream and even in a complete reversal in the direction of flow, thus producing eddies of alternating high and low pressure whose repeated impacts over prolonged periods against an elastic wall are capable of inducing structural fatigue and distention of the wall, resulting eventually and inevitably in the phenomenon of poststenotic dilatation.”

Parietal vibrations of post-stenotic aneurysms were later studied by Simkins and Stehbens [114]. Several zones of possible narrowing of the arterial line, able to produce a post-stenotic dila-

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Fig. 8.2  The post-­ stenotic dilation. Orthograde flow is not represented within the dilated segment, to enhance the effect of the lateral and retrograde deflection of stream lines. (From Holman [113], with permission)

tion of the popliteal artery at different levels, have been described (outside the anatomical variants giving rise to popliteal artery entrapment). The adductor hiatus is probably the more largely known. At this site, which is rather rigid, continuing microtraumas due to the systolic expansion of the vessel wall could be responsible for atherosclerotic lesions [115], giving rise to anatomical and functional narrowing of the vessel. Already in 1946, Lilly [116] had stressed the concept of arterial narrowing by atheromata at the distal end of Hunter’s canal; Friesen et al. [36] suggested that PAAs soon distal to the adductor hiatus may well be post-stenotic in origin. But the entire adductor canal, where the superficial femoral artery is pressed against the femur by the repeated action of the adductor muscles, may represent a zone of functional stenosis. In 1949, Boyd et al. [109] described a fibrous tunnel derived from the fascia of the deep surface of the gastrocnemius; the popliteal artery enters this tunnel after coursing freely mobile through the loose fatty tissue of the popliteal space. The fascial covering of the deep surface of the gastrocnemius would form a definite band, broad 0.25–0.50 in., attached to the capsule of the knee joint and crossing posteriorly the popliteal artery. In 1961, Gedge et  al. [117] highlighted the importance of the arcuate popliteal ligament (Fig. 8.3) in the genesis of aneurysms of the distal popliteal artery: the ligament arches upward from the head of the fibula and the lateral side of the popliteus muscle, crossing this and blending into the posterior ligaments of the knee joint. This fibrous structure, which crosses anteriorly the popliteal artery, becomes particularly sharp and prominent when the leg is fully extended.

Fig. 8.3  Schematic representation of two potential sites of PA stenosis. (A) The adductor hiatus (dilation of the proximal PA). (B) The arcuate popliteal ligament (dilation of the distal PA). (From Gedge et al. [117], modified, with permission)

Stenosis may play a particular role when localized at a bifurcation of the arterial tree. Guvendik et  al. [18] observed that both abdominal aortic

108

and popliteal aneurysms occur upstream a bifurcation; if atherosclerosis causes narrowing of one or both limbs, this will greatly enhance the reflection of pressure waves from the bifurcation, and considerable fluctuations will occur from the meeting between orthograde and reflected waves. One of the characteristics of PAAs is the frequent association with aneurysms in other sites, leading to the observation that “popliteal aneurysms caused by atherosclerosis are only single manifestations of a generalized progressive disease.” This formal assessment, made by Friesen et al. [36] in 1962, was stressed as a basic concept by Bouhoutsos and Martin [33] in 1974. Towne et al. [44] observed that patients with PAA have an inherent tendency for aneurysmal degeneration. Dawson et al. [61] followed up for 15 years a group of 50 patients with PAA: 16 (32%) developed 23 new aneurysms (six thoracoabdominal, 11 femoral, six popliteal contralateral). Cole et  al. [59] asserted that the presence of a popliteal aneurysm indicates high probability of another aneurysm either in the contralateral limb or elsewhere. The exceptional progress in the basic sciences during the last decades has generated a series of cooperative studies between clinicians and scientists aiming to define the origin of arterial aneurysms and particularly of those which are more frequent and more frequently associated, i.e., abdominal aortic and popliteal aneurysms. The research is still ongoing, but probably at the end (if any), the role of atherosclerosis will be redefined. Lindeman et al. [118], in 2008, could assert that abdominal aortic aneurysm (AAA) is a general inflammatory condition characterized by enhanced expression and activation of pro-­ ­ inflammatory transcription factors accompanied by IL-6 and IL-8 hyperexpression and exaggerated downstream cellular responses (differently from atherosclerosis). Pioneer papers appeared in the literature between 1980 and 1990: Busuttil et  al. [119] and Menashi et  al. [120] observed the increase of elastase and collagenase activities in the wall of AAA; other authors [121–123] stressed the importance of genetic factors, given the preponderance of involvement of the male sex, particu-

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larly striking for PAA.  The hypothesis of Ward [124] was that of a systemic abnormality. MacSweeney et al. [4] studied a series of 232 patients with AAA, 24 of them being also affected with PAA. Genotyping for apolipoprotein β and type III collagen did not yield any characterization for patients having also PAA.  Fibrillin-1 genotyping yielded a significant difference between 128 patients with AAA and 24 patients with AAA and PAA. An important research was performed by Sandgren et al. [125] aimed to ascertain if there is a dilating diathesis involving the peripheral arteries of patients with AAA, starting from the hypothesis that AAA is not only a localized vascular disease but also is associated with altered mechanical properties and dilatation of distant arteries [126] and with modifications of arteriolar resistance [127]. The study group comprised 183 consecutive patients waiting for AAA repair. The common femoral artery was measured in 175 subjects (151 male) and the PA in 109 subjects (95 male). Aneurysmal disease was found in eight common femoral and four popliteal arteries. Excluding these 12 patients, no dilating diathesis could be demonstrated in the examined arteries. Starting from PAAs, the condition of generalized dilating diathesis, as hypothesized by several authors, was confirmed by Widmer et  al. [128]: 33 patients undergoing repair of a PAA during the period 1996–2000 were submitted to ultrasound measurement of infrarenal abdominal aorta and common iliac, common femoral, and contralateral popliteal arteries, finding respectively the following: • Dilation: 45.5%; 51.5%; 81.2%; 21.2% • Aneurysm: 34.2%; 34.8%; 10.6%; 45.5% Moreover, patients with multiple aneurysms showed also significantly larger diameters of the brachial and external iliac arteries. Jacobs et al. [129–131]stressed the importance of apoptosis in the wall of PAAs, emphasizing the role of inflammation; they observed a large number of cells, predominantly T lymphocytes, expressing death-promoting molecules. Loss of vascular smooth muscle cells and disruption of

8  Definition, Prevalence, and Etiopathogenesis

elastic lamellae were the more evident signs of architectural derangement in the wall of PAAs and of other peripheral aneurysms. Abdul-Hussien et al. [132] demonstrated, both in AAA and PAA: marked activation of nuclear factor kβ and activated protein 1 proinflammatory transcription factors; hyperexpression of IL-6 and IL-8 on the cellular level; profuse infiltration of macrophages, neutrophils, and T-helper cells; and increased matrix metalloproteinases 8 and 9. According to their findings, genetic and epidemiologic association between AAA and PAA suggest a common origin. That PA may behave as AA has been suggested in 2004 by Debasso et al. [133], who studied the mechanical properties of the walls of PA in healthy subjects; they observed, with increasing age, the following modifications, particularly evident in male subjects: increase in diameter, increase in stiffness, increase of intima-media thickness, and decrease of distensibility. All these findings suggested a behavior typical of a central elastic artery and not of a true muscular artery, implying susceptibility to dilation and aneurysm formation. Recently, Hurks et  al. [134], from Utrecht, published a detailed study of 38 PAAs (in 36 patients) and 198 AAAs. They found similar wall degradation for elastin disruption and smooth muscle cell decrease; however, the focus of inflammation was the intima in PAAs and the adventitia in AAAs. Cholesterol core presence was more pronounced in AAAs, while iron deposits were more frequent in PAAs, suggesting previous intramural hemorrhages possibly attributable to trauma. Similar levels of MMP-9 were observed in the two types of aneurysm, while PAAs were characterized by higher levels of MMP-2, TNF-α, TNF-β, and interferon-γ. The conclusion was that AAAs have a pathophysiologic mechanism more closely related to atherosclerosis than PAAs. A still ongoing research at the 1st Dept. of Surgery of Rome University “Sapienza” [135] is focusing attention on the levels of metalloproteinases MMP-2 and MMP-9 and of their specific inhibitors (TIMP-1 and TIMP-2) in the wall of resected PAAs, both by reverse transcription-­

109

polymerase chain reaction (RT-PCR) method and immunohistochemistry. Up to now, specimens have been divided into three groups: • 11 isolated atherosclerotic aneurysms • Eight atherosclerotic aneurysms associated with AAA • Six post-entrapment aneurysms In group 2, levels of MMPs were significantly higher, and levels of TIMPs were significantly lower. No difference in MMP and TIMP gene expression was observed between groups 1 and 3. Immunohistochemistry confirmed the results of RT-PCR. These preliminary results would suggest that single PAAs and post-entrapment PAAs may share the same origin, different from the one triggering the formation of multiple aneurysms. The studies aiming to elucidate the origin of PAAs and of arterial aneurysm in general are currently flourishing, but we are still in the dawn of this fascinating research. Finally, it must not be forgotten that sites of arterial fusion during embryogenesis could present some kind of structural weakness, which could be prone to aneurysm formation [136], and this could be true in some cases of PAA [137].

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110 8. Linton RR. The arteriosclerotic popliteal aneurysm: a report of fourteen patients treated by a preliminary lumbar sympathetic ganglionectomy and aneurysmectomy. Surgery. 1949;25:41–58. 9. Julian OC, Dye WS, Javid H, Grove WG. The use of vessel grafts in the treatment of popliteal aneurysms. Surgery. 1955;38:970–80. 10. Hunter JA, Julian OC, Javid H, Dye WS.  Arteriosclerotic aneurysms of the popliteal artery. J Cardiovasc Surg. 1962;2:404–13. 11. Downing R, Ashton F, Grimley RP, Slaney G. Problems in diagnosis of popliteal aneurysms. J R Soc Med. 1985;78:440–4. 12. Theis FV. Popliteal aneurysms as a cause of peripheral circulatory disease: with special study of oscillomographs as an aid to diagnosis. Surgery. 1937;2:327–42. 13. Crawford ES, DeBakey ME.  Surgical considerations of peripheral arterial aneurysms. Arch Surg. 1959;78:226–38. 14. Flamand JP, Goldstein M, Belenger J, van der Stricht J. Les anévrismes artériels périphériques. Acta Chir Belg. 1971;70:463–71. 15. Bacciu PP, Chiroini S, Noya G, Marongiu G, Gherli T, Cossu ML, Guazzaroni M, Dettori G. L’aneurisma dell’arteria poplitea. Diagnosi e terapia. Minerva Chir. 1988;43:1549–54. 16. Cosford PA, Leng GC, Thomas J.  Screening for abdominal aortic aneurysm. Cochrane Database Syst Rev. 2007;2:CD002945. 17. Trickett JP, Scott RA, Tilney HS.  Screening and management of asymptomatic popliteal aneurysms. J Med Screen. 2002;9:92–3. 18. Guvendik L, Bloor K, Charlesworth D.  Popliteal aneurysm: sinister harbinger of sudden catastrophe. Br J Surg. 1980;67:294–6. 19. Shortell CK, De Weese JA, Ouriel K, Green RM. Popliteal artery aneurysms: a 25-year surgical experience. J Vasc Surg. 1991;14:771–9. 20. Farina C, Cavallaro A, Schultz RD, Feldhaus RJ, di Marzo L. Popliteal aneurysms. Surg Gynec Obstet. 1989;169:7–13. 21. Hirsch JH, Thiele BL, Carter SS, Colacurcio C. Aortic and lower extremity arterial aneurysms. J Clin Ultrasound. 1981;9:29–31. 22. Batt M, Scotti L, Gagliardi JM, Cassar JP, Porcher G, Le Bas P. Les anévrysmes poplités. Notre expérience à propos de 119 cas. J Chir. 1985;132:319–25. 23. Buxton B, Morris P, Johnson N, Royle J.  The management of popliteal aneurysms. Med J Aust. 1975;2:82–5. 24. Diwan A, Sarkar R, Stanley JC, Zelenock JB, Wakefield TW.  Incidence of femoral and popliteal artery aneurysms in patients with abdominal aortic aneurysms. J Vasc Surg. 2000;31:863–9. 25. Morris-Stiff G, Haynes M, Ogunbiyi S, Townsend E, Shetty S, Winter RK, Lewis MH.  Is assessment of popliteal artery diameter in patients undergoing screening for abdominal aortic aneurysms a

A. Cavallaro worthwhile procedure. Eur J Vasc Endovasc Surg. 2005;30:71–4. 26. Magee R, Quigley F, McCann M, Buttner P, Golledge J. Growth and risk factors for expansion of dilated popliteal arteries. Eur J Vasc Endovasc Surg. 2010;39:606–11. 27. Abelleyra J, Oglietti J, Solian J, Muzzio S. Resultados del tratamiento quirurgico de los aneurismas arteriales periféricos. Pren Méd Argent. 1976;63:286–90. 28. Hands LJ, Collin J.  Infrainguinal aneurysms: outcome for patient and limb. Br J Surg. 1991;78:996–8. 29. Agrifoglio G, Papacharalambus D.  Gli aneurismi arteriosi periferici. Minerva Cardioangiol. 1976;24:342–51. 30. Whitehouse WM, Wakefield TW, Graham LM, Kazmers A, Zelenock GB, Dent TL, Lindenauer SM, Stanley JC. Limb threatening potential of arteriosclerotic popliteal artery aneurysms. Surgery. 1983;93:694–9. 31. Gifford RW Jr, Hines EA Jr, Janes JM. An analysis and follow-up of 100 popliteal aneurysms. Surgery. 1953;33:284–93. 32. Wychulis AR, Spittell JA, Wallace RB.  Popliteal aneurysms. Surgery. 1970;68:942–52. 33. Bouhoutsos J, Martin P.  Popliteal aneurysms: a review of 116 cases. Br J Surg. 1974;61:469–75. 34. Janes JM, Ivins JC.  A method of dealing with arteriosclerotic popliteal aneurysms. Surgery. 1951;29:398–406. 35. Lord JW.  Clinical behaviour and operative management of popliteal aneurysms. JAMA. 1957;163:1102–6. 36. Friesen G, Ivins JC, Janes JM. Popliteal aneurysms. Surgery. 1962;51:90–8. 37. Edmunds LH, Darling RC, Linton RR.  Surgical management of popliteal aneurysms. Circulation. 1965;32:517–23. 38. Baird RJ, Sivasankar R, Hayward R, Wilson DR.  Popliteal aneurysms: a review and analysis of 61 cases. Surgery. 1966;59:911–7. 39. Crichlow RW, Roberts B.  Treatment of popliteal aneurysms by restoration of continuity: review of 48 cases. Ann Surg. 1966;163:417–26. 40. Buda JA, Weber CJ, Mc Allister FF, Vorhees AB Jr. The results of treatment of popliteal aneurysms. A follow-up study of 86 aneurysms. J Cardiovasc Surg. 1974;15:615–9. 41. Gaylis H. Popliteal arterial aneurysm. A review and analysis of 55 cases. S A Med J. 1974;48:75–81. 42. Hardy JD, Tompkins WC Jr, Hatten LE, Chavez CM.  Aneurysms of the popliteal artery. Surg Gynecol Obstet. 1975;140:401–4. 43. Evans WE, Turnipseed WD.  Popliteal aneurysms. Vasc Surg. 1976;10:86–91. 44. Towne JB, Thompson JE, Patman DD, Persson AV. Progression of popliteal aneurysmal disease following popliteal aneurysm resection with graft: a twenty year experience. Surgery. 1976;80:426–32. 45. Tompkins WC, Smith AD, Wren HB, Bransford RM. The atherosclerotic popliteal aneurysm. Report

8  Definition, Prevalence, and Etiopathogenesis of diagnosis and treatment in twenty six cases. Am J Surg. 1977;134:813–6. 46. Chitwood WR, Stocks LH, Wolfe WG.  Popliteal artery aneurysms: past and present. Arch Surg. 1978;113:1078–82. 47. Inahara T, Toledo AC. Complications and treatment of popliteal aneurysms. Surgery. 1978;84:775–83. 48. Vermilion BD, Kimmins SA, Pace WG, Evans WE.  A review of one hundred forty seven popliteal aneurysms with long-term follow-up. Surgery. 1981;90:1009–14. 49. Laskar M, Christides C, Kim M. Anévrismes poplités athéromateux. Angéiologie. 1982;34:113–21. 50. Reilly MK, Abbott WM, Darling RC.  Aggressive surgical management of popliteal artery aneurysms. Am J Surg. 1983;145:498–502. 51. Takolander RJ, Bergqvist D, Bergentz S-E, Ericsson BF, Sigurjonsson S, Jonsson K.  Aneurysms of the popliteal artery. Acta Chir Scand. 1984;150:135–40. 52. Salo JA, Ala-Kuliju K, Ketonen P, Perhoniemi V, Meurala H, Harjola P-T.  Reconstructive surgery of popliteal aneurysms, vol. 15. Vasa; 1986. p. 170–3. 53. Mellière D, Veit R, Becquemin J-P, Etienne G.  Should all spontaneous popliteal aneurysms be operated on? J Cardiovasc Surg. 1986;27:273–7. 54. Anton GE, Hertzer NR, Beven EG, O’Hara PJ, Krajewski LP.  Surgical management of popliteal aneurysms—trends in presentation, treatment and results from 1952 to 1984. J Vasc Surg. 1986;3:125–34. 55. Raptis S, Ferguson L, Miller JH. The significance of tibial artery disease in the management of popliteal aneurysms. J Cardiovasc Surg. 1986;27:703–8. 56. Schellack J, Smith RB III, Perdue GD. Nonoperative management of selected popliteal aneurysms. Arch Surg. 1987;122:372–5. 57. Englund R, Schache D, Magee HR. Atherosclerotic popliteal aneurysms with particular regard to the contralateral side. Aust N Z J Surg. 1987;57:387–90. 58. Lilly MP, Flinn WR, McCarthy WJIII, Courtney DF, Yao JST, Bergan JJ. The effect of distal arterial anatomy on the success of popliteal aneurysm repair. J Vasc Surg. 1988;7:653–60. 59. Cole CW, Thijssen AM, Barber GG, McPhall WV, Scobie TK. Popliteal aneurysm: an index of generalized vascular disease. Can J Surg. 1989;32:65–8. 60. Halliday AV, Taylor PR, Wolfe JH, Mansfield AO.  The management of popliteal aneurysms: the importance of early surgical repair. Ann Roy Coll Surg Engl. 1991;73:253–7. 61. Dawson I, van Bockel JH, Brand R, Terpstra JL. Popliteal artery aneurysms: long-term follow-up of aneurysmal disease and results of surgical treatment. J Vasc Surg. 1991;13:398–407. 62. Roggo A, Brunner U, Ottinger LW, Largiader F. The continuing challenge of aneurysms of the popliteal artery. Surg Gynecol Obstet. 1993;177:565–72. 63. Lowell RC, Gloviczki P, Hallett JW Jr, Naessens JM, Maus TP, Cherry KJ Jr, Bower TC, Pairolero

111 PC.  Popliteal aneurysm: the risk of nonoperative management. Ann Vasc Surg. 1994;8:14–23. 64. Vettorello G, Rocca T, Taddia MC, Occhionorelli S, Santini M, Mari F, Mascoli F, Donini I. Gli aneurismi dell’arteria poplitea. Nostra esperienza a proposito di 37 casi. Minerva Cardioangiol. 1996;44:437–42. 65. Sarcina A, Bellosta R, Luzzani G, Agrifoglio G.  Surgical treatment of popliteal artery aneurysms. A 20 year experience. J Cardiovasc Surg. 1997;38:347–54. 66. Davidovic LB, Lotina SL, Kostic DM, Cinara IS, Cveltkovic SD, Markovic DM, Vojnovic BR.  Popliteal artery aneurysms. World J Surg. 1998;22:812–7. 67. Dawson I, Sie R, van Baalen JM, van Bockel JH.  Asymptomatic popliteal aneurysm: elective operation versus conservative follow-up. Br J Surg. 1994;81:1504–7. 68. Carpenter JP, Barker CF, Roberts B, Berkowitz HD, Lusk EJ, Perloff LJ.  Popliteal artery aneurysms: current management and outcome. J Vasc Surg. 1994;19:65–73. 69. Gawenda M, Sorgatz S, Müller U, Walter M, Erasmi H.  The thrombosed popliteal aneurysm with distal arterial occlusion—successful therapy by interdisciplinary management. Thorac Cardiovasc Surg. 1995;43:112–6. 70. Duffy ST, Colgan MP, Sultan S, Moore DJ, Shanik GD. Popliteal aneurysms: a 10-year experience. Eur J Vasc Endovasc Surg. 1998;16:218–22. 71. Taurino M, Calisti A, Grossi R, Maggiore C, Speziale F, Fiorani P.  Outcome after early treatment of popliteal artery aneurysms. Intern Angiol. 1998;17:28–31. 72. Dijkstra B, Fleisch J, Knight D.  Management and outcome of popliteal artery aneurysms in a New Zealand Provincial Centre. Aust N Z J Surg. 1998;68:255–7. 73. Locati P, Socrate AM, Costantini E, Campanati B.  Popliteal aneurysms: current management and outcome. Minerva Cardioangiol. 1999;47:145–55. 74. Gouny P, Bertrand P, Duedal V, Cheynel-Hocquet C, Lancelin C, Escourolle F, Nussaume O, Vayssairat M.  Limb salvage and popliteal aneurysms: advantages of preventive surgery. Eur J Vasc Endovasc Surg. 2000;19:496–500. 75. Irace L, Gattuso R, Faccenna F, Cappello F, Siani B, Stumpo R, Boiceff S, Benedetti-Valentini F.  Trattamento chirurgico degli aneurismi poplitei in elezione e in urgenza. Minerva Cardioangiol. 2001;49:251–6. 76. Stiegler H, Medler G, Baumann G. Prospective study of 36 patients with 46 popliteal aneurysms with non-­ surgical treatment. Vasa. 2002;31:43–6. 77. Kauffman P, Puech-Leao P.  Surgical treatment of popliteal artery aneurysm: a 32-year experience. J Vasc Bras. 2002;1:5–14. 78. Dorigo W, Pulli R, Turini F, Pratesi G, Credi G, Alessi Innocenti A, Pratesi C.  Acute leg ischemia from thrombosed popliteal artery aneurysms: role

112 of preoperative thrombolysis. Eur J Vasc Endovasc Surg. 2002;23:251–4. 79. Ascher E, Markevich N, Schutzer RW, Kallakuri S, Jacob T, Hingorani AP. Small popliteal artery aneurysms: are they clinically significant? J Vasc Surg. 2003;37:55–60. 80. Bowrey DJ, Osman H, Gibbons CP, Blackett RL.  Atherosclerotic popliteal aneurysms: management and outcome in forty-six patients. Eur J Vasc Endovasc Surg. 2003;25:79–83. 81. Harder Y, Notter H, Nussbaumer P, Leiser A, Canova C, Furrer M. Popliteal aneurysm: diagnostic workup and results of surgical treatment. World J Surg. 2003;27:788–92. 82. Laxdal E, Amundsen SR, Dregelid E, Pedersen G, Aune S. Surgical treatment of popliteal artery aneurysms. Scand J Surg. 2004;93:57–60. 83. Aulivola B, Hamdan AD, Hile CN, Sheahan MG, Skillman JJ, Campbell DR, Scovell SD, LoGerfo FW, Pomposelli FB Jr. Popliteal artery aneurysms: a comparison of outcomes in elective versus emergent repair. J Vasc Surg. 2004;39:1171–7. 84. Martelli E, Ippoliti A, Ventoruzzo G, De Vivo G, Ascoli Marchetti A, Pistolese GR.  Popliteal artery aneurysms. Factors associated with thromboembolism and graft failure. Intern Angiol. 2004;23:54–65. 85. Galland RB, Magee TR.  Popliteal aneurysms: distortion and size related to symptoms. Eur J Vasc Endovasc Surg. 2005;30:534–8. 86. Stone PA, Armstrong PA, Bandyk DF, Keeling WB, Flaherty SK, Shames ML, Johnson BL, Back MR. The value of duplex surveillance after open or endovascular popliteal aneurysm repair. J Vasc Surg. 2005;41:936–41. 87. Pulli R, Dorigo W, Troisi N, Alessi Innocenti A, Pratesi G, Azas L, Pratesi C. Surgical management of popliteal artery aneurysms: which factors affect outcomes? J Vasc Surg. 2006;43:481–7. 88. Beseth BD, Moore WS. The posterior approach for repair of popliteal artery aneurysms. J Vasc Surg. 2006;43:940–5. 89. Huang Y, Gloviczki P, Noel AA, Sullivan TM, Kalra M, Gullerud RE, Hoskin TL, Bower TC. Early complications and long-term outcome after open surgical treatment of popliteal artery aneurysms: is exclusion with saphenous vein bypass still the gold standard? J Vasc Surg. 2007;45:706–15. 90. Davies RSM, Wall M, Simms MH, Vohra RK, Bradbury AW, Adam DJ. Long-term results of surgical repair of popliteal artery aneurysm. Eur J Vasc Endovasc Surg. 2007;34:714–8. 91. Curi MA, Geraghty PJ, Merino OA, Veeraswamy RK, Rubin BG, Sanchez LA, Choi ET, Sicard GA.  Mid-term outcomes of endovascular popliteal artery aneurysm repair. J Vasc Surg. 2007;45:505–10. 92. Lichtenfels E, Delduque Frankini A, Bonamigo TP, Cardozo MA, Schulte AA.  Popliteal artery aneurysm surgery: the role of emergency setting. Vasc Endovasc Surg. 2008;42:159–64. 93. Dzieuciuchowicz L, Lukaszuk M, Figiel J, Klimczak K, Krasinski Z, Majewski W. Factors influencing the

A. Cavallaro clinical course of popliteal artery aneurysm. Med Sci Monit. 2009;15:CR231–r235. 94. Zimmermann A, Schoenberger T, Saeckl J, Reeps C, Wendorff H, Kuehnl A, Eckstein H-H. Eligibility for endovascular technique and results of the surgical approach to popliteal artery aneurysms at a single center. Ann Vasc Surg. 2010;24:342–8. 95. Zaraca F, Ponzoni A, Stringari C, Ebner JA, Giovannetti R, Ebner H.  The posterior approach in the treatment of popliteal artery aneurysm: feasibility and analysis of outcome. Ann Vasc Surg. 2010;24:863–70. 96. Pulli R, Dorigo W, Fargion A, Pratesi G, Alessi Innocenti A, Angiletta D, Pratesi C. Comparison of early and midterm results of open and endovascular treatment of popliteal artery aneurysms. Ann Vasc Surg. 2012;26:809–18. 97. Kropman RHJ, van Meurs A, Fioole B, van Santvoort HC, van Sambeek M, Moll FL, de Vries J-PPM. Association of sex with long-term outcomes after popliteal artery aneurysm repair. Ann Vasc Surg. 2014;28:338–44. 98. Huang Y, Gloviczki P, Oderich GS, Duncan AA, Kalra M, Fleming MD, Harmsen WS, Bower TC.  Outcomes of endovascular and contemporary open surgical repairs of popliteal artery aneurysm. J Vasc Surg. 2014;60:631–8. 99. Serrano-Hernando FJ, Martinez López I, Hernández Mateo MM, Rydings MH, Sanchez Hervás L, Rial Horcajo R, Moñuz Ducaju G, Conejero AM. Comparison of popliteal artery aneurysm therapies. J Vasc Surg. 2015;61:655–61. 100. Mazzaccaro D, Carmo M, Dellatana R, Settembrini AM, Barbetta I, Tassinari L, Roveri S, Settembrini PG. Comparison of posterior and medial approaches for popliteal artery aneurysms. J Vasc Surg. 2015;62:1512–20. 101. Ronchey S, Pecoraro F, Alberti V, Serrao E, Orrico M, Lachat M, Mangialardi N. Popliteal artery aneurysm repair in the endovascular era. Fourteen-years single center experience. Medicine. 2015;94:e1130. 102. Wagenhauser MU, Herma KB, Saghan TA, Dueppers P, Schelzig H, Duran M. Long-term results of open repair of popliteal artery aneurysm. Ann Med Surg. 2015;4:58–63. 103. Leake AE, Avgerinos ED, Chaer RA, Singh MJ, Makaroun MS, Marone LK. Contemporary outcome of open and endovascular popliteal artery aneurysm repair. J Vasc Surg. 2016;63:70–6. 104. Broca P. Des anévrysmes et de leur traitement. Paris: Labé; 1856. p. 1–48. 105. Home E.  An account of Mr. Hunter’s method of performing the operation for the cure of popliteal aneurism. In: Palmer JE, editor. The works of John Hunter. London: Longman & Co; 1837. p. 594–612. 106. Delbet P, Mocquod T.  Affections chirurgicales des artères. In: Le Dentu P, Delbet P, editors. Nouveau traité de médecine clinique et opératoire. Paris: J.B. Ballière & Fils; 1911. p. 167–84. 107. Erichsen JH.  Science and art of surgery. London: Longman, Green & Co.; 1872. p. 14–55.

8  Definition, Prevalence, and Etiopathogenesis 108. Wells AH, Coburn CE, Walker MA. Popliteal aneurysm, with report of a case. JAMA. 1936;106:1264–6. 109. Boyd AM, Ratcliffe AH, Jepson RP, James GWH.  Intermittent claudication: a clinical study. J Bone Joint Surg. 1949;31-B:325–55. 110. Lindbom A. Arteriosclerosis and arterial thrombosis in lower limb: a roentgenological study. Acta Radiol Suppl. 1950;80:1–80. 111. Poland A. On a case of fusiform and tubular aneurysm of the subclavian artery, and its successful treatment by indirect digital compression. Med Chir Trans. 1869;52:277–307. 112. Halsted WS, Reid MR. An experimental study of circumscribed dilation of an artery immediately distal to a partially occluding band and its bearing on the dilation of the subclavian artery observed in certain cases of cervical rib. J Exp Med. 1916;24:271–86. 113. Holman E.  On circumscribed dilation of an artery immediately distal to a partially occluding band: poststenotic dilatation. Surgery. 1954;36:3–24. 114. Simkins TE, Stehbens WE.  Vibrations recorded from the adventitial surface of experimental aneurysms and arteriovenous fistulas. Vasc Surg. 1974;8:153–65. 115. Palma EC.  Stenosed arteriopathy of Hunter canal and loop of the adductor magnus. Am J Surg. 1952;83:723–33. 116. Lilly GD.  The management of aneurysms of the lower extremities. Ann Surg. 1946;123:601–6. 117. Gedge SW, Spittel JA Jr, Ivins JC. Aneurysm of the distal popliteal artery and its relationship to the arcuate popliteal ligament. Circulation. 1961;24:270–3. 118. Lindeman JH, Abdul-Hussien H, Schaapherder AF, van Bockel JH, van der Thusen JH, Roelen DL, Kleemann R.  Enhanced expression and activation of proinflammatory transcription factors distinguish aneurysmal from atherosclerotic aorta: IL-6 and IL-8-dominated inflammatory responses prevail in the human aneurysm. Clin Sci. 2008;114:687–97. 119. Busuttil RW, Abou-Zamzam AM, Machleder HI.  Collagenase activity of the human aorta: a ­comparison of patients with and without abdominal aortic aneurysms. Arch Surg. 1980;115:1373–8. 120. Menashi S, Campa JS, Greenhalgh RM, Powell JT.  Collagen in abdominal aortic aneurysm: typing, content, and degradation. J Vasc Surg. 1987;5:578–82. 121. Tilson MD, Seashore MR.  Human genetics of the abdominal aortic aneurysm. Surg Gynecol Obstet. 1984;158:129–32. 122. Joahnsen K, Koepsell T. Familial tendency for abdominal aortic aneurysms. JAMA. 1986;256:1934–6. 123. Darling RC, Brewster DC, La Muraglia MG, Moncure AC, Cambria RP, Abbott WM. Are familial abdominal aortic aneurysms different? J Vasc Surg. 1989;10:39–43. 124. Ward AS. Aortic aneurysmal disease. A generalized dilating diathesis. Arch Surg. 1992;127:990–1.

113 125. Sandgren T, Sonesson B, Ryden-Ahlgren A, Lanne T.  Arterial dimensions in the lower extremities of patients with abdominal aortic aneurysm—no indication of a generalized dilating diathesis. J Vasc Surg. 2001;34:1079–84. 126. Makita S, Ohira A, Tachieda R, Itoh S, Moriai Y, Niinuma H, Nakamura M, Hiramori K. Dilation and reduced distensibility of carotid artery in patients with abdominal aortic aneurysms. Am Heart J. 2000;140:297–302. 127. Midttun M, Sejrsen P, Paaske WP.  Is non-specific aneurysmal disease of the infrarenal aorta also a peripheral microvascular disease? Eur J Vasc Endovasc Surg. 2000;19:625–9. 128. Widmer MK, Blatter S, Schmidli J, Baumgartner I, Gagl B, Carrel T, Savolainen H, Diehm N.  Generalized dilating diathesis in patients with popliteal artery aneurysms. Vasa. 2008;37:157–63. 129. Jacob T, Ascher E, Hingorani A, Gunduz Y, Kallakuri S.  Initial steps in the unifying theory of the pathogenesis of arterial aneurysms. J Surg Res. 2001;101:37–43. 130. Jacob T, Hingorani A, Ascher E.  Examination of the apoptotic pathway and proteolysis in the pathogenesis of popliteal artery aneurysms. Eur J Vasc Endovasc Surg. 2001;22:77–85. 131. Jacob T, Schutzer R, Hingorani A, Ascher E.  Differential expression of YAMA/CPP-32 by T lymphocytes in popliteal artery aneurysms. J Surg Res. 2003;112:111–6. 132. Abdul-Hussien H, Hanemaaijer R, Kleemann R, Verhaaren BF, van Bockel JH, Lindeman JH.  The pathophysiology of abdominal aortic aneurysm growth: corresponding and discordant inflammatory and proteolytic processes in abdominal aortic and popliteal artery aneurysms. J Vasc Surg. 2010;51:1479–87. 133. Debasso R, Astrand H, Bjarnegard N, RydénAhlgren A, Sandgren T, Lanne T. The popliteal artery, an unusual muscular artery with wall properties similar to the aorta: implications for susceptibility to aneurysm formation? J Vasc Surg. 2004;39:836–42. 134. Hurks R, Kropman RHJ, Pennekamp CWA, Hoefer IE, de Vries J-PPM, Pasterkamp J, Vink A, Moll FL.  Popliteal artery aneurysms differ from abdominal aortic aneurysms in cellular topography and inflammatory markers. J Vasc Surg. 2014;60:1514–9. 135. Mosiello G, Sapienza P, Fuso A, Sterpetti A, Cucina A, Di Gioia C, Coluccia P, di Marzo L.  Popliteal artery aneurysm formation: a pathogenetic dilemma. Personal commun. 136. Norman PE, Powell JS. Site specificity of aneurysmal disease. Circulation. 2010;121:560–8. 137. Mellière D, Cron J, Lange F, Qvarfordt P, Desgranges J, Becquemin J-P, Cavillon A. Some popliteal aneurysms are congenital. Cardiovasc Surg. 1998;6:42–9.

9

The “Problem” of Arteriomegaly Antonino Cavallaro

In 1942–1943, Leriche [1, 2] reported on two patients with extraordinary elongation and dilatation of the pelvic and common femoral arteries, which, before operation, were misdiagnosed as aneurysmatic. He textually assessed: “La possibilité pour les artères de s’allonger et se dilater globalement de façon regulière, sur un point de leur trajet, sans que cette dilatation ait la moindre rassemblance avec un anévrysme fusiforme et sans que l’exploration artérielle révèle la moindre cause tangible à cet état anatomique singulier.”

He called this condition arteria mega et dolicho; in one case, also the accompanying veins were involved. No microscopy findings were reported. In 1966, Staple et al. [3] were apparently the first to report a short series of patients (nine) whose pelvic and limb arteries presented alterations similar to those described by Leriche. Relying on microscopy findings, they stated that arteriosclerosis was the underlying disease. Some years later, Lea Thomas [4], from St. Thomas’ Hospital in London, confirmed this etiopathogenetic theory but observed that similar cases had been reported in pediatric patients [5, 6]. He reported the first consistent series (30 patients, all male, aged 46–75 years) and coined the widely accepted term arteriomegaly.

A. Cavallaro (*) Past Professor of General Surgery, “Sapienza” University, Rome, Italy © Springer Nature Switzerland AG 2021 A. Cavallaro (ed.), Aneurysms of the popliteal artery, https://doi.org/10.1007/978-3-030-49687-6_9

The arteriosclerotic origin was furtherly confirmed by Callum et al. [7] and by Carlson et al. [8]. However, Randall et al. [9] observed that the basic pathological lesion was represented by a marked alteration of the media consisting of the decrease and fragmentation of the elastic fibers, completely lacking in some areas; no inflammation or mucoid deposition was observed; the intima showed reactive fibrosis, and telangiectasia of the vasa vasorum was evident in the adventitia. The authors concluded that arteriosclerotic changes were superimposed and that the fundamental lesion was not arteriosclerotic. Successively, the group from St. Thomas’ [10] recognized that the term arteriomegaly is purely descriptive and that a precise definition of the disease was difficult, asserting however that arteriomegaly is a real entity (likely occurring in 6% of the population over 50 years) which represents a pathological variant of the normal dilating process due to ageing, possibly not related to arteriosclerosis. But, later on, the same group [11] suggested that arteriomegaly could represent a variant of arteriosclerosis in which the elastic layer of the arterial wall is preferentially destroyed. More recently, D’Andrea et  al. [12], on the basis of ultrastructural studies focused on the comparison between arteriomegaly and arteriosclerosis, stressed the specificity of the alterations of the elastic component in the former, suggesting an inheritability of this vascular 115

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d­ isorder. This would agree with the hypothesis of Lawrence et al. [13], who found a 36% incidence of familiarity studying the first degree relatives aged >50  years of 14 patients with arteriomegaly; this incidence was 1.5 times greater than that observed for 86 patients with abdominal aortic aneurysm. A clear definition about the nature of arteriomegaly is difficult. However, while some authors [14] are still oriented to consider it as a variant of arteriosclerosis, the prevalent trend [15, 16] is to define it as a specific disease. The circulatory alterations caused by arteriomegaly are mainly represented by a slowing of blood flow, sometimes so marked as to render difficult, in earlier studies, the angiographic visualization of distal arteries. The slow flow could be responsible for local thrombosis and/ or embolism—even in the absence of aneurysms [8]—observed in angiograms as an abrupt arterial cut-off or emboli located also in arteries apparently spared by the dilating process. Lea Thomas [4] argued that these patients are prone to embolism and the clinical corresponding behavior would consist of the fact that symptoms, if any, have sudden onset and short duration. One of the more intriguing aspects of arteriomegaly is the association with aneurysms. Hollier et al. [17] assert: “this entity, especially when associated with diffuse aneurysms at multiple levels, represents a particular process distinct from simple arteriosclerotic aneurysms occurring at multiple sites. It does not necessarily imply specific aneurysm formation, however aneurysms do occur and often are quite extensive. This diffuse aneurysmal disease that occurs in patients with arteriomegaly should be differentiated from multiple isolated arteriosclerotic aneurysms since in general more extensive, entails a higher morbidity and may require different surgical management.”

These authors considered aneurysmal disease to be diffuse when involving at least three of the arterial segments examined; they found 91 male patients (aged 36–87  years, mean, 67.5  years) with arteriomegaly and diffuse aneurysmal disease out of 5771 consecutive patients submitted to angiography of the infrarenal abdominal aorta downward the popliteal arteries during the period 1968–1982 and proposed the following classifications:

• Type I (10/91  =  11%): aneurysms present in the aorta and iliac and common femoral arteries, with arteriomegaly of the superficial femoral and popliteal arteries • Type II (7/91 = 8%): aneurysms in the common femoral, superficial femoral, and popliteal arteries, with arteriomegaly of the aorta and iliac arteries • Type III (74/91 = 81%): aneurysms in the aortoiliac, femoral, and popliteal arteries, with arteriomegaly of intervening arteries that are not specifically aneurysmal The authors stressed that arteriomegaly was observed in 300 of the 5771 angiograms (5.2%), but only 91/300 (30.3%) had also diffuse aneurysmal disease; however, as arteriomegaly appears to be a progressive arteriopathy, a number of patients with simple arteriomegaly would probably develop aneurysms. This was confirmed by the study of Barandiaran et  al. [18], who, following up for 6–146 months (mean, 76 months) 67 patients with arteriomegaly, observed that only 13 of the 31 patients initially without aneurysms remained in this condition: the number of patients with associated aneurysms passed from 36 (54%) to 54 (81%). The classification proposed by Hollier et al. [17] appears to be clinically relevant, as sudden arterial occlusion was observed in 35% of group III patients and only in 10% and 7%, respectively, of patients in group I and in group II. A classification of arteriomegaly per se, unrelated with the presence of aneurysm, is offered by Callum et al. [10], relying on 33 postmortem findings and 106 aortograms (all related to male subjects older than 50 years): • Generalized arteriomegaly, with dilatation and tortuosity of all vessels • Localized arteriomegaly: some dilated and tortuous segments and also some normal or stenotic or occluded vessels • Tortuosity without dilatation • Local dilatation without tortuosity Tortuosity was experimentally related to failure of elastin by Dobrin et al. [19]. Partially adhering to the latter classification, Bartolo et  al. [20], reviewing 1221 peripheral

9  The “Problem” of Arteriomegaly

117

arteriographies performed during 8 years, found 235 (19.2%) cases of arteriomegaly with the following distribution: • • • •

Dilatation and elongation, 132 (56%) Elongation, 41 (17.5%) Dilatation, 26 (11.1%) Simple tortuosity, 36 (15.4%)

In the first three groups, 66 patients (33.2%) presented also aneurysms. In patients with arteriomegaly, the occurrence of popliteal artery aneurysm (PAA) (Fig. 9.1) is frequent, as documented in Table 9.1. A situation theoretically different from the arteriomegaly/aneurysm association is the one called aneurysmosis [21], i.e., extensive aneurysmal change involving all or many major arteries. A certain confusion exists about this term that should indicate a particular and extreme situation of multiple arteriosclerotic aneurysms. This was emphasized in the report by Dent et al. [22], who, in a large group of 1488

patients with aneurysm affecting the abdominal aorta or its peripheral branches, identified 57 (3.9%) patients with multiple aneurysms (45 aortoiliac and peripheral, five aortoiliac and visceral, seven multiple peripheral): on a total of 271 aneurysms, 46 (17%) were popliteal. Both in the report and in the extensive discussion on it, arteriomegaly is not mentioned but for the assertion, by Dr. Dent, about the difficulty encountered in separating diffuse ectasia (meaning arteriomegaly?) from true aneurysm formation. The term aneurysmosis, as pointed out by Lawrence [23], is not included in the suggested standards for reporting on arterial aneurysms [24]; however it is used on several occasions, being considered expressive of diffuse aneurysmal disease. Belardi and Lucertini [25] proposed the following nomenclature: • Aneurysm, localized arterial dilation • Arteriomegaly, generalized enlargement of the entire arterial system without aneurysm

Fig. 9.1  PAA in a case of arteriomegaly

Table 9.1  Occurrence of PAA in patients with arteriomegaly Author, year Staple [3], 1966 a Lea Thomas [4], 1971 Carlson [8], 1975 Hollier [17], 1983 a Chan [11], 1990 D’Andrea [15], 2010 Barandiaran [18], 2012

Pts with arteriomegaly 9 30 7 300 65 18 67

Pts with aneurysm 6 20 4 91

36 (54)b

From St. Thomas’ Hospital, London Numbers in brackets are related to the end of follow-up (see text)

a

b

Number of aneurysms 13 42 15 410

Pts with PAA 2 3 36 10 14 (20)b

Number of PAAs 2 19 6 80 59

A. Cavallaro

118 Table 9.2  Incidence of arteriomegaly or diffuse aneurysmal disease in series of atherosclerotic PAAs Author, year Crichlow [26], 1966 Bouhoutsos [27], 1974 Evans [28], 1976 Vermilion [29], 1981 Laskar [30], 1982 Mellière [31], 1986 Schellack [32], 1987 Lilly [33], 1988 Lowell [34], 1994 Taurino [35], 1998 D’Andrea [15], 2010 Personal series

Number of patients 42 102a 52 87 27 50 60 35 106 23 40 58

Patients with arteriomegaly

Patients with diffuse aneurysmal disease 4 (9%)

48a (47%) 8 (15%)b 12 (14%) 12 (44%) 1 (2%)

10 (20%) 29 (48%)

19c (54%) 45 (42%) 1 (4%) 10 (25%) 2 (3%)

Reports at refs. 29, 32, 33, and 35: not stated if all aneurysms are atherosclerotic Numbers refer to aneurysms not to patients. The 48 aneurysms were observed in the group of 54 patients with dilating arteriopathy b All eight patients are part of the group with bilateral popliteal aneurysms (34 patients) in which the incidence of diffuse aneurysmal disease is therefore 24% c 17/24 patients with bilateral PAA (70%); 2/11 patients with monolateral PAA (18%) a

• Aneurysmosis, diffuse aneurysmal disease in patients with arteriomegaly. According to these authors, aneurysmosis would include the three types of arteriomegaly/aneurysm association described by Hollier et al. [17]; however, the occurrence of diffuse aneurysmal disease outside arteriomegaly remains excluded and would be considered as a particular subgroup of the first category. Keeping into account the probable confusion derived from the variant use of terms, we attempted to tabulate the incidence of arteriomegaly and diffuse aneurysmal disease in some series of PAAs (Table 9.2).

References 1. Leriche R.  Dilatation pathologique des artères en dehors des anéurismes. Vie tissulaire des artères. Presse Méd. 1942;50:641–2. 2. Leriche R. Dolicho et mégaartère. Dolicho et mégaveine. Presse Méd. 1943;51:354–5. 3. Staple TW, Friedenberg MJ, Anderson MS, Butcher HR Jr. Arteria magna et dolicho of Leriche. Acta Radiol Diagn. 1966;4:293–305. 4. Lea Thomas M.  Arteriomegaly. Br J Surg. 1971;58:690–4.

5. Beuren A, Hort W, Kalbfleisch H, Müller H, Stoermer J.  Dysplasia of the systemic and pulmonary arterial system with tortuosity and lengthening of the arteries. A new entity diagnosed during life, and leading to coronary death in early childhood. Circulation. 1969;39:109–15. 6. Ertugrul A. Diffuse tortuosity and lengthening of the arteries. Circulation. 1967;36:400–7. 7. Callum KG, Gaunt JI, Lea Thomas M, Browse NL.  Physiological studies in arteriomegaly. Cardiovasc Res. 1974;8:373–83. 8. Carlson DH, Gryska P, Seletz J, Armstrong S. Arteriomegaly. Am J Roentgenol. 1975;125:553–8. 9. Randall PA, Omar MM, Rohner R, Hedgcock M, Brenner J.  Arteria magna revisited. Radiology. 1979;132:295–300. 10. Callum KG, Lea Thomas M, Browse NL. A definition of arteriomegaly and the size of arteries supplying the lower limbs. Br J Surg. 1983;70:524–9. 11. Chan O, Lea Thomas M.  The incidence of popliteal aneurysms in patients with arteriomegaly. Clin Radiol. 1990;41:185–9. 12. D’Andrea V, Malinovsky L, Cavallotti C, Benedetti-­ Valentini F, Malinovska V, Bartolo M, Todini AR, Biancari F, Di Matteo FM, De Antoni E. Angiomegaly. J Cardiovasc Surg. 1997;38:447–55. 13. Lawrence PF, Wallis C, Dobrin PR, Bhirangi K, Gugliuzza N, Galt S, Kraiss L. Peripheral aneurysms and arteriomegaly. Is there a familial pattern? J Vasc Surg. 1998;28:599–605. 14. Yamamoto N, Unno N, Miysuoka H, Ukiyama T, Saito T, Kaneko H, Nakamura S. Clinical relationship between femoral artery aneurysms and arteriomegaly. Surg Today. 2002;32:970–3.

9  The “Problem” of Arteriomegaly 15. D’Andrea V, Cantisani V, Catania A, Todini A, Stio F, Di Matteo FM, Di Marco C, Greco R, Di Certo M, Guaitoli E, De Antoni E.  Angiomegaly and arterial aneurysms. Giorn Chir. 2010;31:429–32. 16. Mingazzini P, Leni D, Vacirca F, Corso R. Arteriomegalia: una malattia rara da non dimenticare. Il Bassini. 2013;34:38–42. 17. Hollier LH, Stanson AW, Glowiczki P, Pairolero PC, Joyce JW, Bernatz PE, Cherry KJ. Arteriomegaly: classification and morbid implications of diffuse aneurysmal disease. Surgery. 1983;93: 700–8. 18. Barandiaran JV, Hall TC, Glaves I, El-Barghouti N, Perry ET. An observational study into the management of arteriomegaly: a call for a revised classification system. Ann R Coll Surg Engl. 2012;94:250–5. 19. Dobrin PB, Schwartz TH, Baker WH.  Mechanisms of arterial and aneurysmal tortuosity. Surgery. 1988;104:568–74. 20. Bartolo M, Todini AR, Antignani PL, Izzo A. Les artériopathies ectasiantes: un chapitre oublié. J Mal Vasc. 1990;15:109–13. 21. Smith RF. In discussion on Dent et al. 159. 22. Dent TL, Lindenauer SM, Ernst CB, Fry WJ. Multiple arteriosclerotic arterial aneurysms. Arch Surg. 1972;105:338–44. 23. Lawrence PF. Reply letter. J Vasc Surg. 1999;30:581–2. 24. Johnston KW, Rutherford RB, Tilson D, Shah DM, Hollier L, Stanley JC.  Suggested standards for reporting on arterial aneurysms. J Vasc Surg. 1991;13:444–50.

119 25. Belardi P, Lucertini G.  Regarding: peripheral aneurysms and arteriomegaly: is there a familial pattern? (letter). J Vasc Surg. 1999;30:581. 26. Crichlow RW, Roberts B.  Treatment of popliteal aneurysms by restoration of continuity: review of 48 cases. Ann Surg. 1966;163:417–26. 27. Bouhoutsos J, Martin P. Popliteal aneurysms: a review of 116 cases. Br J Surg. 1974;61:469–75. 28. Evans WE, Turnipseed WD.  Popliteal aneurysms. Vasc Surg. 1976;10:86–91. 29. Vermilion BD, Kimmins SA, Pace WG, Evans WE. A review of one hundred forty seven popliteal aneurysms with long-term follow-up. Surgery. 1981;90:1009–14. 30. Laskar M, Christides C, Kim M. Anévrismes poplités athéromateux. Angéiologie. 1982;34:113–21. 31. Mellière D, Veit R, Becquemin J-P, Etienne G. Should all spontaneous popliteal aneurysms be operated on? J Cardiovasc Surg. 1986;27:273–7. 32. Schellack J, Smith RB III, Perdue GD. Nonoperative management of selected popliteal aneurysms. Arch Surg. 1987;122:372–5. 33. Lilly MP, Flinn WR, McCarthy WJ III, Courtney DF, Yao JST, Bergan JJ.  The effect of distal arterial anatomy on the success of popliteal aneurysm repair. J Vasc Surg. 1988;7:653–60. 34. Lowell RC, Gloviczki P, Hallett JW Jr, Naessens JM, Maus TP, Cherry KJ Jr, Bower TC, Pairolero PC. Popliteal aneurysm: the risk of nonoperative management. Ann Vasc Surg. 1994;8:14–23. 35. Taurino M, Calisti A, Grossi R, Maggiore C, Speziale F, Fiorani P. Outcome after early treatment of popliteal artery aneurysms. Intern Angiol. 1998;17:28–31.

Outline of Patients with Atherosclerotic Popliteal Aneurysm

10

Antonino Cavallaro

10.1 Demographics (Table 10.1) A long time has elapsed since Broca [71] could assert that the incidence of aneurysms decreases from the age of 40–45 years onward, but for those affecting the thoracic aorta; for external aneurysms, he observed a male-female ratio of 8:1. In his thorough review of 110 aneurysms treated with compression, age of patients ranged from 14 to 64 years, with a mean of 31 years. Popliteal artery aneurysm (PAA) affects prevalently adult and older individuals, with most patients in the seventh decade of life: the percentage of patients older than 60 years ranges as high as 73% [9], 77% [50], and 81% [8]. In the report of Gaylis [11], only two patients were under 40 years old. Evans et al. [13] observed that patients with bilateral aneurysms were older than those with unilateral aneurysm: in the former group, 26/34 (76.5%) were over 60 years old, and in the latter 10/18 (55.6%). In 1954, Gifford et al. [72] reported the case of an atherosclerotic PAA in a 35-year-old man: this was considered the youngest patient with an atherosclerotic PAA. Few years later, Greenstone et  al. [4] reported, in their series, a case in a 32-year-old patient.

Women are rarely affected; in the different reported series, the percentage of female patients ranges from 0 [4, 9, 13, 18, 30, 32, 33, 43, 44, 56, 58, 67, 73] to 10% [62], 12.3% [45], and 19.3% [39]. On the whole, women represent about 4% of all patients with an atherosclerotic PAA. The cause of this sporadic involvement is not known, even if genetic factors linked to sex are intuitively responsible. Towne et al. [14] observed that women were older than men: in their series, 32% of the 75 male patients were over 70 years old, and all the five female patients were over 75 years old. All the ten female patients reported by Reilly et  al. [23] were over 80 years old. This intriguing and unexplained fact was recently confirmed by Kropman et al. [66], observing that the mean age of 185 male patients was 66 years, significantly lower than the mean age of 17 female patients (71 years).

10.2 A  ssociated Diseases and Risk Factors Many patients affected with a PAA present several associated morbid conditions, and this is not surprising, considering that they are often older and that the genesis of the aneurysms is in general arteriosclerosis.

A. Cavallaro (*) Past Professor of General Surgery, “Sapienza” University, Rome, Italy © Springer Nature Switzerland AG 2021 A. Cavallaro (ed.), Aneurysms of the popliteal artery, https://doi.org/10.1007/978-3-030-49687-6_10

121

A. Cavallaro

122 Table 10.1  Distribution of age and sex in some series of atherosclerotic PAAs Author, year Linton [1], 1949 Janes [2], 1951 Lord [3], 1957 Greenstone [4], 1961 Friesen [5], 1962 Hunter [6], 1962 Edmunds [7], 1965 Baird [8], 1966 Crichlow [9], 1966 Wychulis [10], 1970 Gaylis [11], 1974 Buxton [12], 1975 Evans [13], 1976 Towne [14], 1976 Tompkins [15], 1977 Chitwood [16], 1978 Inahara [17], 1978 Guvendik [18], 1980 Vermilion [19], 1981 Jackaman [20], 1982 Laskar [21], 1982 Whitehouse [22], 1983 Reilly [23], 1982 Takolander [24], 1984 Mellière [25], 1986 Anton [26], 1986 Raptis [27], 1986 Englund [28], 1987 Schellack [29], 1987 Lilly [30], 1988 Cole [31], 1989 Farina [32], 1989 Shortell [33], 1991 Ramesh [34], 1993 Dawson [35], 1994 Lowell [36], 1994 Carpenter [37], 1995 Gawenda [38], 1995 Vettorello [39], 1996 Sarcina [40], 1997 Taurino [41], 1998 Duffy [42], 1998 Dijkstra [43], 1998 Borowicz [44], 1998 Gouny [45], 2000 Rosenthal [46], 2000 Irace [47], 2001 Dorigo [48], 2002 Galland [49], 2002

Patients 14 42 10 9 64 27 82 36 42 152 38 23 52 80 18 26 30 20 87 14 27 61 159 13 50 110 36 75 60 35 38 33 39 31 77 106 33 39 26 58 23 24 17 16 35 22 45 89 58

Male 13 41

Female 1 (7.1%) 1 (2.4%)

9 62 26 81 33 42 148 37 21 52 75 17 25 28 20 84 13 26 59 149 12 46 108

0 2 (3.2%) 1 (3.8%) 1 (1.3%) 3 (8.4%) 0 4 (2.7%) 1 (2.7%) 2 (8.7%) 0 5 (6.3%) 1 (5.6%) 1 (3.9%) 2 (6.7%) 0 3 (3.5%) 1 (7.2%) 1 (3.8%) 2 (3.3%) 10 (6.3%) 1 (7.7%) 4 (8%) 2 (1.9%)

75 59 35 37 33 39 30 77 103 32 37 21 55 22 23 17 16 30 22 41 85 56

0 1 (1.7%) 0 1 (2.7%) 0 0 1 (3.3%) 0 3 (2.9%) 1 (3.1%) 2 (5.2%) 5 (19.3%) 3 (5.2%) 1 (4.4%) 1 (4.2%) 0 0 5 (14.3%) 0 4 (8.9%) 4 (4.5%) 2 (3.5)

Age (mean) 49–79 (65) 48–88 (65.5) 47–73 (61.5) 32–75 (57.5) 21–83 (60) 38–77 (60) 41–93 (68) 42–86 27–93 42–85 (66) 42–86 39–93 57–101 (72) 49–81 (66) (66.7) 42–90 (60) 52–86 (71) 41–76 (67) 40–96 (70) 40–77 (65) 35–82 (62) 50–90 (66) (66.3) 21–86 (66) 34–82 (65) (65) 48–82 (63) 52–83 (67.7) 49–84 (65) 50–90 (70.5) 41–85 (64) 43–84 (66.6) (65.8) 42–85 (64) 39–81 (66) 42–82 (63.5) 64–83 (73) 46–75 (63) 43–88 (71) 46–81 (61) 28–91 (66) 46–86 (68)

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Table 10.1 (continued) Author, year Kauffman [50], 2002 Ascher [51], 2003 Bowrey [52], 2003 Mahmood [53], 2003 Harder [54], 2003 Martelli [55], 2004 Aulivola [56], 2004 Laxdal [57], 2004 Stone [58], 2005 Pulli [59], 2006 Huang [60], 2007 Davies [61], 2007 Lichtenfels [62], 2008 Dzieuciuchowicz [63], 2009 Zimmermann [64], 2010 Zaraca [65], 2010 Kropman [66], 2014 Serrano-Hernando [67], 2015 Mazzaccaro [68], 2015 Ronchey [69], 2015 Leake [70], 2016 Personal series

Patients 112 25 46 41 24 38 38 49 46 137 289 48 40 61 46 35 202 142 65 67 156 58

Male 106 24 45 38 22 35 38 46 46 130 281 45 36 57 44 34 185 142 64 55 150 58

Female 6 (5.4%) 1 (4%) 1 (2.2%) 3 (7.3%) 2 (8.4%) 3 (8.9%) 0 3 (6.2%) 0 7 (5.2%) 8 (2.8%) 3 (6.3%) 4 (10%) 4 (6.6%) 2 (4.4%) 1 (2.9%) 17 (8.5%) 0 1 (1.6%) 12 (18%) 6 (3.8%) 0

Age (mean) 39–93 41–89 (74) 43–94 (73) (68) (67) (68) 18–87 (67.1) 33–88 (69) 42–92 (72) 28–91 (68) 17–88 (70) 46–88 (69) 40–87 (71.3) 38–84 (57) 31–95 (71.5) 43–86 (67) (67) (69.3) (67.6) (69) (71.4) 52–88 (64)

Only atherosclerotic PAAs are dealt with in papers at refs. [1, 2, 4, 6, 8, 9, 12–17, 20–22, 24, 27, 28, 34, 36, 38, 42, 43, 45, 50, 52] In papers at refs. [11, 15, 18, 25], not all PAAs are atherosclerotic; however, it was easy to extract data relative to patients with atherosclerotic PAAs Papers at refs. [5, 7, 10, 22, 56] include some patients with non-atherosclerotic PAAs: 4, 2, 2, 3, 1, respectively Paper at ref. [60] includes some non-atherosclerotic PAAs Not stated if all PAAs are atherosclerotic in papers at refs. [19, 23, 26, 29–31, 33, 37, 39–41, 44, 47, 48, 51, 54, 55, 57–59, 61–70]

Heart disease (mainly coronary artery disease) affected 48% (1358/2810) of the patients, with extremes from 19 to 25% [9, 27, 41, 45, 50, 55] up to 60% [6, 8, 15, 56, 70] (personal series). Ramesh et  al. [34] observed a higher incidence of thrombosed PAAs in subjects with cardiovascular disease. Hypertension was the more frequent associated disease, affecting 53% of the patients (1583/2980), with wide variations from less than 30% [15, 16, 18, 34, 74] to more than 70% [44, 62, 64, 69] (personal series). An incidence of 50% or more is reported in 27/52 of the series in Table 10.2.

The incidence of cerebrovascular disease was 12% (246/2112), ranging from less than 5% [12, 19, 63] to more than 20% [15, 32, 41]. Diabetes was rather rare (5% or less) in some series [7, 11, 40, 41, 58]; however, its incidence was 20% or more in others [10, 30, 44, 46, 51, 56, 58, 62, 69, 70] with a global incidence of 15% (426/2901). The occurrence of chronic obstructive pulmonary disease (COPD) is registered in 12 series (952 patients) with an incidence of 16%. Gaylis [11] observed that most of his patients were smokers. Of 1831 patients (28 series), 1153 (63%) were smokers.

A. Cavallaro

124 Table 10.2  Associated diseases and risk factors in patients affected with atherosclerotic PAA Author, year Hunter [6], 1962

Pts 27

Edmunds [7], 1965

82

Baird [8], 1966

36

Crichlow [9], 1966 Wychulis [10], 1970

42 152

Bouhoutsos [75], 1974

71

Gaylis [11], 1974

38

Buxton [12], 1975

23

Towne [14], 1976

80

Tompkins [15], 1977

18

Chitwood [16], 1978

26

Inahara [17], 1978 Guvendik [18], 1980 Vermilion [19], 1981

30 21 87

Laskar [21], 1982

27

Whitehouse [22], 1983

61

Reilly [23], 1982

159

Takolander [24], 1984 Anton [26], 1986

13 110

Raptis [27], 1986 Salo [74], 1986 Schellack [29], 1987

36 21 60

Lilly [30], 1988

35

Cole [31], 1989

38

Farina [32], 1989

33

Shortell [33], 1991 Ramesh [34], 1993 Lowell [36], 1994 Carpenter [37], 1995 Sarcina [40], 1997

39 31 106 33 58

Heart 20 (74%) 35 (43%) 24 (67%) 8 (19%) 67 (44%) 26 (37%) 21 (55%) 11 (48%) 25 (31%) 11 (61%) 10 (38%) 8 (27%) 7 (33%) 43 (49%)

Hypert.

CVD

Diabet.

48 (59%)

11 (13%)

4 (5%)

11 (31%)

8 (22%)

3 (8%)

20 (48%) 102 (67%) 31 (44%)

3 (7%) 28 (18%)

4 (9%) 52 (34%)

7 (10%)

1 (1%)

14 (37%)

2 (5%)

2 (5%)

10 (44%)

1 (4%)

40 (50%)

10 (12%)

12 (15%)

5 (28%)

4 (22%)

2 (11%)

7 (27%)

2 (8%)

10 (33%) 6 (29%) 33 (38%)

2 (7%) 2 (9%) 3 (3%)

8 (30%) 20 (33%) 52 (33%) 5 (38%) 47 (43%) 9 (25%) 8 (38%) 31 (52%)

3 (5%)

8 (13%)

62 (39%)

23 (14%)

17 (11%)

4 (31%) 65 (59%)

11 (10%)

19 (17%)

6 (17%)

2 (6%) 2 (9%)

14 (37%) 14 (42%) 9 (29%) 49 (46%) 5 (15%)

None

19 (23%)

94 (62%)

11 (7%)

Most

7 (18%)

20 (28%)

4 (22%)

1 (6%)

32 (37%)

5 (19%)

26 (96%) 31 (51%)

8 (13%)

21 (60%)

Tobac.

15 (17%)

23 (38%)

23 (64%) 3 (14%) 37 (62%)

COPD

40 (67%) 15 (43%)

7 (20%) 6 (16%)

17 (52%)

8 (24%)

20 (51%) 4 (13%) 55 (52%)

6 (19%) 20 (19%)

16 (48%) 21 (36%)

5 (15%)

14 (42%)

27 (82%)

5 (13%) 17 (16%) 3 (9%) 3 (5%)

78 (74%) 22 (38%)

5 (15%)

10  Outline of Patients with Atherosclerotic Popliteal Aneurysm

125

Table 10.2 (continued) Author, year Taurino [41], 1998

Pts 23

Heart 5 (22%)

Hypert. 15 (65%)

CVD 5 (22%)

Diabet. 4 (17%)

12 (50%)

9 (37%)

2 (8%)

Duffy [42], 1998

24

Borowicz [44], 1998

16

13 (81%)

9 (56%)

Locati [76], 1999

48

27 (56%)

3 (6%)

Gouny [45], 2000

35

8 (23%)

19 (54%)

5 (14%)

Rosenthal [46], 2000

22

8 (36%)

12 (55%)

9 (41%)

Kauffman [50], 2002

112

28 (25%) 9 (36%)

57 (51%)

12 (11%)

25

Harder [54], 2003

24

Martelli [55], 2004

38

8 (21%)

25 (66%)

3 (8%)

5 (13%)

Aulivola [56], 2004

38

24 (63%)

4 (11%)

8 (21%)

Laxdal [57], 2004

49

28 (74%) 22 (45%)

17 (35%)

4 (8%)

2 (4%)

Stone [58], 2005 Pulli [59], 2006

46 137

Huang [60], 2007

289

Lichtenfels [62], 2008

40

Dzieuciuchowicz [63], 2009 Zimmermann [64], 2010

61 46

Kropman [66], 2014

202

Ronchey [69], 2015

67

Leake [70], 2016 Personal series

156 58

13 (52%)

5 (20%)

13 (54%)

2 (8%)

18 (39%) 71 (52%)

12 (26%) 9 (7%)

192 (66%) 36 (90%)

46 (16%) 4 (10%)

9 (22%)

34 (56%)

1 (2%)

7 (11%)

33 (72%) 67 (33%) 28 (42%) 98 (63%) 39 (67%)

99 (49%)

20 (30%)

75 (48%)

37 (24%) 6 (10%)

None

6 (10%)

5 (20%) 18 (75%) 19 (50%) 32 (84%) 22 (45%)

62 (45%) 41 (14%)

101 (74%) 81 (28%) 35 (87%) 51 (84%) 36 (78%) 81 (40)

12 (18%) 24 (15%) 12 (21%)

39 (58%) 61 (39%) 57 (98%)

26 (13%)

63 (94%)

42 (72%)

13 (34%) 6 (16%)

8 (17%) 29 (14%)

Tobac. 20 (87%) 22 (92%) 16 (100%) 23 (48%) 28 (80%) 14 (64%)

15 (13%)

Ascher [51], 2003

30 (22%) 128a (44%) 22 (55%) 23 (38%)

COPD 4 (17%) 5 (21%)

0

Heart: mainly coronary artery disease and also congestive heart failure CVD cerebrovascular disease, including stroke, COPD chronic obstructive pulmonary disease Papers at refs. [6, 8, 9, 12, 14–17, 21, 22, 24, 27, 34, 36, 42, 45, 46, 50, 74] deal only with atherosclerotic PAAs Papers at refs. [32, 56, 75] include also non-atherosclerotic PAAs, but it was easy to extract data pertaining to atherosclerotic PAAs Some patients with non-atherosclerotic PAAs are included in papers at refs. [7] (2/82), [10] (2/152), [11] (5/43), [18] (1/21), and [76] (2/48) and in paper at ref. [60] Not stated if all aneurysms are atherosclerotic in papers at refs. [19, 23, 26, 29–31, 33, 37, 40, 41, 44, 51, 54, 55, 57–59, 62–64, 66, 69, 70] a Cardiovascular disease in general

A. Cavallaro

126

10.3 Concurrent Contralateral and Extrapopliteal Aneurysm As outlined in Table  10.3, patients with a PAA have high chances of having contralateral PAA and aneurysms in other major arteries. This

was highlighted in 1953 by Gifford et  al. [77], who stressed the importance of both a careful initial evaluation and an extended followup: “a long and more detailed follow-up plus a more careful search for extrapopliteal aneurysms  …  would undoubtedly reveal the presence of more aneurysms.” In their series of 69

Table 10.3  Series of atherosclerotic PAAs: associated aneurysms

Author, year Janes [2], 1951 Gifford [77], 1953 Lord [3], 1957 Greenstone [4], 1961 Hunter [6], 1962 Friesen [5], 1962 Edmunds [7], 1965 Baird [8], 1966 Crichlow [9], 1966 Wychulis [10], 1970 Bouhoutsos [75], 1974 Gaylis [11], 1974 Buxton [12], 1975 Evans [13], 1976 Towne [14], 1976 Tompkins [15], 1977 Chitwood [16], 1978 Inahara [17], 1978 Guvendik [18], 1980 Vermilion [19], 1981 Szilagyi [78], 1981 Jackaman [20], 1982 Laskar [21], 1982 Whitehouse [22], 1983 Reilly [23], 1983 Takolander [24], 1984 Downing [79], 1985 Mellière [25], 1986 Anton [26], 1986 Raptis [27], 1986 Schellack [29], 1987 Englund [28], 1987 Lilly [30], 1988 Cole [31], 1989 Farina [32], 1989 Shortell [33], 1991 Dawson [35], 1991 Ramesh [34], 1993 Lowell [36], 1994 Carpenter [37], 1995 Gawenda [38], 1995

Pts 42 64 10 9 27 60 82 36 42 152 71 38 23 52 80 18 26 30 21 87 61 14 27 61 159 13 40 50 110 36 60 75 35 38 33 39 50 31 106 33 39

Patients with bilateral PAA 21 (50%) 31 (48%) 3 (30%) 3 (33%) 15 (56%) 36 (60%) 26 (32%) 15 (42%) 18 (43%) 89 (59%) 31 (44%) 11 (29%) 11 (48%) 34 (65%) 39 (49%) 8 (44%) 9 (35%) 14 (47%) 7 (33%) 60 (69%) 25 (41%) 13 (93%) 5 (18%) 27 (44%) 85 (53%) 5 (38%) 22 (55%) 23 (46%) 50 (45%) 25 (69%) 35 (58%) 28 (37%) 24 (68%) 21 (55%) 14 (42%) 12 (31%) 27 (54%) 12 (39%) 55 (52%) 21 (64%) 19 (49%)

Patients with extrapopliteal aneurysms

AAA

17 (27%)

8 (12%)

IA 1 4

FA 2 9

Oth. 1 3

7

4 4 44 29 4 6

2

14 3 2 5

1 1

30 27 3 1 23 23 2 13 21 9 10 37 12 5

2

6 (22%) 15 (25%) 12 (15%) 8 (22%) 6 (14%) 69 (45%) 9 (26%)

25 (31%) 6 (33%) 11 (42%)

47 (54%) 5 (36%) 6 (22%)

6 (46%) 16 (40%) 28 (56%) 43 (39%) 41 (68%) 36 (48%)

19 (57%)

82 (77%) 20 (61%) 17 (43%)

6 (17%) 6 (14%) 53 (35%) 23 (32%) 5 (13%) 5 (22%) 25 (48%) 15a (19%) 5 (28%) 8 (30%) 11 (37%) 6 (29%) 35 (40%) 28 (46%) 3 (21%) 1 (4%) 38 (62%) 34 (21%) 5 (38%) 8 (20%) 16 (32%) 35 (32%) 17 (47%) 32 (53%) 21 (28%) 8 (23%) 12 (32%) 12 (36%) 20 (51%) 18 (36%) 12 (39%) 54 (51%) 19 (58%) 16 (41%)

37 9

3 1 3 22 2 3 22 13 4 17 2 48 3 5 9 17 9

34 4

21 7 30 2 29

5

2

2 2

1

3

6 6 2

10  Outline of Patients with Atherosclerotic Popliteal Aneurysm

127

Table 10.3 (continued)

Author, year Sarcina [40], 1997 Taurino [41], 1998 Duffy [42], 1998 Dijkstra [43], 1998 Borowicz [44], 1998 Locati [76], 1999 Gouny [45], 2000 Galland [49], 2002 Kauffman [50], 2002 Stiegler [80], 2002 Ascher [51], 2003 Bowrey [52], 2003 Mahmood [53], 2003 Harder [54], 2003 Martelli [55], 2004 Aulivola [56], 2004 Laxdal [57], 2004 Stone [58], 2005 Pulli [59], 2006 Huang [60], 2007 Lichtenfels [62], 2008 Dzieuciuchowicz [63], 2009 Zimmermann [64], 2010 Zaraca [65], 2010 Kropman [66], 2014 Serrano Hernando [67], 2015 Mazzaccaro [68], 2015 Leake [70], 2016 Personal series

Pts 58 23 24 17 16 48 35 58 112 46 25 46 41 24 38 38 49 46 137 289 40 61 46 35 202 142 65 67 58

Patients with bilateral PAA 9 (15%) 5 (22%) 16 (67%) 6 (35%) 10 (62%) 17 (35%) 17 (49%) 34 (59%) 63 (56%) 19 (41%) 9 (36%) 21 (46%) 19 (46%) 12 (50%) 18 (47%) 25 (66%) 24 (49%) 9 (20%) 22 (16%) 156 (53%) 20 (50%) 21 (34%) 17 (37%) 14 (40%) 150 (74%) 69 (49%) 29 (45%) 34 (51%) 24 (41%)

Patients with extrapopliteal aneurysms 12 (52%)

14 (87%)

AAA 7 (12%) 12 (52%) 4 (58%) 7 (41%) 10 (62%) 16 (33%) 9 (26%) 25 (43%) 31 (28%)

IA

FA 2

9

7

6

13 7

Oth.

2

17 (37%) 30 (65%)

14 (37%)

47 (34%) 192 (66%) 24 (60%) 24 (39%)

30 (46%) 22 (38%)

9 (36%) 15a (41%) 11b (27%) 7 (29%) 12c (32%) 16 (39%) 25 (51%) 23 (50%) 42a (31%) 157 (54%) 10 (25%) 11 (18%) 11 (30%) 9 (26%) 112 (55%) 49 (34%) 18 (28%) 28 (42%) 18 (31%)

1 1 4 2 9 5 168 6 8

4 10 7 2

1

4 6 3 110 5 9

4 2 2 29 2 1

4

9

1

1

2

1

AAA abdominal aortic aneurysm, IA aneurysm of iliac arteries, FA aneurysm of femoral arteries Numbers of IAs and FAs refer in general to aneurysms, not to patients:   •  Crichlow [9]: 4 pts with bilateral FA   •  Janes [2]: 1 pt with bilateral IA, 2 pts with bilateral FA   •  Jackaman [20]: 1 pt with unilateral IA, 1 pt with bilateral IA, 3 pts with bilateral FA   •  Laskar [21]: 2 pts with unilateral IA, 1 pt with bilateral IA, 1 pt with unilateral FA   •  Whitehouse [22]: 8 pts with unilateral IA, 14 pts with bilateral IA, 7 pts with unilateral FA, 16 pts with bilateral FA   •  Englund [28]   •  Ascher [51]: 1 pt with bilateral IA, 4 pts with unilateral FA   •  Downing [79]: 5 pts with unilateral FA, 4 pts with bilateral FA   •  Personal series: 1 pt with bilateral IA, 2 pts with bilateral FA Papers at refs. [2, 4, 6, 8, 9, 12–17, 21, 22, 24, 27, 28, 34–36, 38, 42, 43, 45, 49, 50, 52] deal only with atherosclerotic PAAs Some non-atherosclerotic PAAs are included in papers at refs. [3, 5, 11, 25, 75, 77, 78], but it was easy to extract data pertaining to atherosclerotic PAAs A small number of non-atherosclerotic PAAs are included in papers at refs. [7] (2/82), [10] (2/152), [18] (1/21), [56] (1/64), [76] (2/48), and [79] (1/40); paper at ref. [60] includes some non-atherosclerotic PAAs Not stated if all aneurysms are atherosclerotic in papers at refs. [19, 23, 26, 29–31, 33, 37, 40, 41, 44, 51, 53–55, 57–59, 62–68, 70] a Aortoiliac aneurysms b Aortic or iliac aneurysm c 1/12 aortoiliac aneurysm

A. Cavallaro

128

PAAs (64 atherosclerotic), they observed that 4/8 AAAs and 3/9 femoral aneurysms were not present initially and manifested during followup. Towne et al. [14] reported that 5/39 contralateral PAAs were diagnosed during the follow-up (23  months–11  years). The occurrence of new contralateral aneurysms during follow-up was confirmed by other authors: Downing et al. [79] (3/22), Sarcina et al. [40] (2/11), Kauffman et al. [50] (6/63), and Mahmood et al. [53] (1/19). Dawson et al. [35] observed new aneurysms during a 5-year follow-up: popliteal contralateral, six (initially 21); femoral, 11 (initially 19); and thoracoabdominal aorta, six (initially 0). They calculated that the probability of new aneurysms, after the initial repair, was 6% at 1  year and 49% at 10  years; in particular, at 10 years, the probability was 100% in patients with bilateral PAA vs 30% in patients with unilateral PAA; other relevant risk factors for the development of new aneurysms were age >65 years and hypertension.

From Table 10.3, it results that the occurrence of a contralateral PAA ranges from 15 to 93% (mean, 49%), while extrapopliteal aneurysms occur in 14–87% (mean, 42%) and AAAs in 4–62% (mean, 31%). Already in 1951, Janes and Ivins [2] observed extrapopliteal aneurysms in three patients with bilateral PAA. The particular association between bilateral PAAs and extrapopliteal aneurysms was further confirmed by other authors (Table 10.4). In 2002, Galland and Magee [49] reevaluated the interrelationship between thrombosis of PAA at presentation and presence of other aneurysms, confirming what initially reported in 1993 [34]: 39 patients with thrombosed PAA presented 28 (72%) contralateral and 19 (49%) abdominal aortic aneurysms; 11 patients with patent PAA presented six (32%) contralateral and six (32%) abdominal aortic aneurysms. All the above data would support the theory that PAA is, in many cases, the sign of a diffuse and progressive arterial aneurysmal disease

Table 10.4  Occurrence of extrapopliteal aneurysms in patients with unilateral or bilateral PAA Author, year Baird [8], 1966

Extra A M 3/21 (14%)

B 5/15 (33%)

Evans [13], 1976 Vermilion [19], 1981

6/27 (22%)

41/60 (68%)

4/18 (22%)

12/22 (55%)

Whitehouse [22], 1983 Downing [79], 1985 Schellack [29], 1987 Cole [31], 1989 Carpenter [37], 1995 Duffy [42], 1998 Huang [60], 2007

58/123 (47%)

123/156 (79%)

AAA M

B

IA M

B

FA M

B

4/18 (22%) 6/27 (22%) 19/34 (56%)

21/34 (62%) 35/60 (58%) 19/27 (70%)

3/27 (11%) 8/34 (24%)

19/60 (32%) 14/27 (52%)

4/27 (15%) 12/34 (35%)

26/60 (43%) 11/27 (41%)

8/25 (32%) 5/17 (24%) 6/12 50% 4/8 (50%) 56/123 (42%)

24/35 (69%) 8/21 (38%) 13/21 62% 10/16 (62%) 101/156 (65%)

Extra A extrapopliteal aneurysm, AAA abdominal aortic aneurysm, IA iliac aneurysm, FA femoral aneurysm Papers at refs. [8, 13, 22, 40] deal only with atherosclerotic PAAs Paper at ref. [79] includes one (1/40) non-atherosclerotic PAA; paper at ref. [60] includes some non-atherosclerotic PAAs Not stated if all PAAs are atherosclerotic in papers at refs. [19, 29, 31, 37]

10  Outline of Patients with Atherosclerotic Popliteal Aneurysm

deserving life-long surveillance. In addition, an isolated and noncomplicated PAA, observed during follow-up, could represent a different and less aggressive type of arterial disease.

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Clinical Presentation

11

Antonino Cavallaro

In 1936, Wells et al. [1] described the nature of symptoms due to the presence of the aneurysmal mass: interference with knee movements, impairment of venous return, pressure on adjacent popliteal nerve causing numbness, and pains of varied severity and location. They also stressed the sequelae of events leading to rupture: “gradual stretching and absorption of ligaments and erosion of bone may proceed until the aneurysm ruptures externally into the soft tissues or into the knee joint. This complication is a constant and serious menace in any case of this disease.” Gifford et al. [2] tried to distinguish symptoms attributable to arteriosclerosis obliterans beyond a non-thrombosed aneurysm but agreed that in the 17 cases of chronic ischemia they observed in this condition, impairment of the leg/foot arterial circulation could be the consequence of repeated embolism from the endoaneurysmal thrombus. Similarly, Linton [3] had recognized that in most popliteal artery aneurysms (PAAs), there was evidence of obliterative arterial disease; however, whereas all aneurysms in his series were patent and pulsating, only in 3/14 extremities distal pulses were not appreciable; he stressed that pathologic examination, in all cases, “revealed a laminated blood clot consisting of partially organized and fresh thrombi … so loosely attached

A. Cavallaro (*) Past Professor of General Surgery, “Sapienza” University, Rome, Italy © Springer Nature Switzerland AG 2021 A. Cavallaro (ed.), Aneurysms of the popliteal artery, https://doi.org/10.1007/978-3-030-49687-6_11

that if … had been dislodged, emboli of the arteries distal to the aneurysm would have occurred….” The report by Gifford et al. [2] deserves a particular mention, as it was the first one to document, based on large numbers, the relevant incidence of serious complications both at presentation and during a careful follow-up (mean, 50 months; max, 318 months): out of 100 aneurysms (95 atherosclerotic), 49 were complicated at presentation; thrombosis, 20; embolism, 14; gangrene, ten; vein compression, 19; nerve compression, ten; and rupture, 12; during the followup, 10/49 complicated aneurysms underwent ­ further complications, and 13, initially noncomplicated, became complicated. Attempting to tabulate the clinical findings at presentation, we found it difficult to be precise, owing to the varying methods in describing symptoms and to the fact that a single aneurysm could produce more than one relevant symptom; however, an almost exhaustive picture about clinical presentation may be inferred from consultation of both Tables 11.1 and 11.2. Trying to analyze the clinical presentation of PAAs and, mainly, to define the genesis of the adverse events linked to their complications, one should always keep in mind what was stated by Wells et al. [1] more than 80 years ago: “popliteal aneurysm vary from others in that they … are subjected to frequently unheralded, sudden complications.” In the same period, Blakemore [63] asserted that the possibility of gangrene is ever 133

A. Cavallaro

134 Table 11.1  62 series of atherosclerotic PAAs: clinical presentation (symptoms, signs) Chronic ischemia Author, year (1) Linton [3], 1949 (2) Gifford [2], 1953 (3) Lord [4], 1957 (4) Greenstone [5], 1961 (5) Hunter [6], 1962 (6) Friesen [7], 1962 (7) Edmunds [8], 1965 (8) Baird [9], 1966 (9) Crichlow [10], 1966 (10) Wychulis [11], 1970 (11) Buxton [12], 1975 (12) Evans [13], 1976 (13) Towne [14], 1976 (14) Tompkins [15], 1977 (15) Chitwood [16], 1978 (16) Inahara [17], 1978 (17) Guvendik [18], 1980 (18) Szilagyi [19], 1981 (19) Vermilion [20], 1981 (20) Laskar [21], 1982 (21) Jackaman [22], 1982 (22) Whitehouse [23], 1983 (23) Reilly [24], 1983 (24) Graham [25], 1983 (25) Takolander [26], 1984 (26) Downing [27], 1985 (27) Mellière [28], 1986 (28) Anton [29], 1986 (29) Raptis [30], 1986 (30) Schellack [31], 1987 (31) Englund [32], 1987 (32) Lilly [33], 1988 (33) Cole [34], 1989 (34) Farina [35], 1989 (35) Shortell [36], 1991 (36) Dawson [37], 1991 (37) Ramesh [38], 1993 (38) Roggo [39], 1993 (39) Carpenter [40], 1994 (40) Gawenda [41], 1995 (41) Taurino [42], 1998 (42) Duffy [43], 1998 (43) Locati [44], 1999 (44) Gouny [45], 2000 (45) Irace [46], 2001 (46) Kauffman [47], 2002 (47) Dorigo [48], 2002 (48) Bowrey [49], 2003 (49) Mahmood [50], 2003 (50) Ascher [51], 2003

Pts 14 69 10 9 27 64 82 36 42 152 23 52 80 18 26 30 21 62 87 27 14 61 159 33 13 40 52 110 36 60 75 35 38 36 39 50 31 167 33 39 23 24 48 35 45 112 89 46 45 25

Ans 15 100 13 12 42 73 98 51 60 233 34 86 119 26 35 40 28 87 147 32 27 88 244 52 18 62 77 160 61 95 110 59 59 50 51 71 43 252 54 58 28 40 65 52 75 142 109 67 52 34

Asympt. IC 3 4 35 17 3 15 1 23 12 17 94 12 25 17* 7 17 7 37 49 4 13 39 112 16 4 17 41 77 7* 44 14 26** 25 13 15 29 18 61 21 27 3 17 27 20 18* 40 58 30 29 14

1 16* 36 22 14 5 42 14* 4 9 9 6 30 66 4 12 42 9 2 19 4 65 6* 13

RP/N

13* 5 4 28 11 19

33* 12 10 13 8 54 8 25 9 3 10 14 18 3* 28

7 5 79 11 7 3 16

19 11

76 5

103

8 6 5 15 6*

3 5 9 4 9*

2 19 11 19 24

24 2 5 6

5 2 23 7 1 11 11 7 2 15 5

21*

15**

15 2 26

8

11*

15

7**

16

Acute Mass ischemia related symptom 1 11 41 4 5 3 11* 36 23 22 32 14 21 23 62 1

13 3 17 10 6* 72 24 19 14 6

10 23 1** 11 4 12 1 10 6 3 3 11 7 3 6* 30 3 1 4

11  Clinical Presentation

135

Table 11.1 (continued) Chronic ischemia Author, year (51) Laxdal [52], 2004 (52) Aulivola [53], 2004 (53) Martelli [54], 2004 (54) Pulli [55], 2006 (55) Huang [56], 2007 (56) Kropman [57], 2007 (57) Lichtenfels [58], 2008 (58) Dzieuciuchowicz [59], 2009 (59) Mazzaccaro [60], 2015 (60) Wagenhauser [61], 2015 (61) Leake [62], 2016 (62) Personal series

Pts 49 39 38 137 289 66 40 61 65 30 156 58

Ans 57 51 42 159 358 110 60 82 77 42 186 82

Asympt. 17 15 12 67 144 57 28 18 16 77 48

IC 6 8 5 51 90 15 5 21 18 14 28 22

RP/N 28 8 6 50 12 9 10 3 10 43 11

Acute Mass ischemia related symptom 6 13 7 11 5 30 5 74 36 13 14 16 3 23 10 17 4 2 34 4 1 0

Pts number of patients, Ans number of aneurysms, IC intermittent claudication, RP/N rest pain/necrosis, including blue toe syndrome, Mass related symptoms difficulty in knee movements, local pain, vein/nerve compression, rupture (2) 95/100 atherosclerotic aneurysms in 64/69 patients (5, 13, 29, 45) Numbers* refer to patients, not to lesions (6) 69/73 atherosclerotic aneurysms in 60/64 patients (7) 96/98 atherosclerotic aneurysms in 80/82 patients (10) 231/233 aneurysms were atherosclerotic in 150/252 patients (17) 27/28 atherosclerotic aneurysms in 20/21 patients (18) 86/87 atherosclerotic aneurysms in 81/82 patients (27) 75/77 atherosclerotic aneurysms in 50/52 patients (32) Numbers** refer to 48 operated limbs (34) 47/50 atherosclerotic aneurysms in 33/36 patients: three aneurysms from entrapment syndrome were symptomatic (38) 247/252 atherosclerotic aneurysms in 162/167 patients (43) 63/65 atherosclerotic aneurysms in 46/48 patients (52) The series includes one aneurysm from Marfan disease and two mycotic aneurysms (not among those which ruptured) (19, 23, 28, 30, 32, 33, 39, 44, 45, 47, 49–51, 53, 54, 56–61): not stated if all atherosclerotic aneurysms (55) Microscopy diagnosis of atherosclerosis in 232/236 cases (on a whole of 358 cases) Some authors exclude a number of contralateral aneurysms, and consequently, in the table, the number of aneurysms is inferior to that effectively observed (in brackets): e.g., (16), 40 (44); (51), 57 (70); (53), 42 (56); (59), 77 (94); (61), 186 (247). The number of asymptomatic aneurysms at diagnosis is therefore higher than reported, provided that excluded aneurysms are probably small and not complicated

present because of the danger of thrombosis and rupture. These statements, fully confirmed by decades of experience, stimulated the attention of physicians and have determined the criteria on which surgical treatment (and currently also endovascular treatment) is offered to the patient.

11.1 S  ize and Morphology of the Aneurysm: Is There Any Relationship with Symptoms/Complications? Following the suggestion by Szilagyi et al. [19], patients with a PAA ≥2 cm in diameter have been considered, almost routinely, candidates for

interventional treatment. However, the same authors formally expressed that “the probability of sudden thrombosis or embolism, the two important noxious events in the natural history of this disease, is probably not importantly dependent on the aneurysmal size.” Several authors [8, 23, 64, 65] have stressed the concept that the size of the aneurysm is not correlated with embolism or thrombosis. Friesen et al. [7] did not find possible to statistically relate aneurysm size with complications, and others have experienced that small aneurysms are prone to complications just like larger ones. Bouhoutsos and Martin [66] assert that “a small aneurysm is as great a danger for the limb as is a larger one.” Barker [67] reminded how many times, when

A. Cavallaro

136 Table 11.2  61 series of atherosclerotic PAAs: clinical presentation (complications) Author, year (1) Linton [3], 1949 (2) Gifford [2], 1953 (3) Lord [4], 1957 (4) Greenstone [5], 1961 (5) Hunter [6], 1962 (6) Friesen [7], 1962 (7) Edmunds [8], 1965 (8) Baird [9], 1966 (9) Crichlow [10], 1966 (10) Wychulis [11], 1970 (11) Buxton [12], 1975 (12) Evans [13], 1976 (13) Towne [14], 1976 (14) Tompkins [15], 1977 (15) Chitwood [16], 1978 (16) Inahara [17], 1978 (17) Guvendik [18], 1980 (18) Szilagyi [19], 1981 (19) Vermilion [20], 1981 (20) Laskar [21], 1982 (21) Jackaman [22], 1982 (22) Whitehouse [23], 1983 (23) Reilly [24], 1983 (24) Graham [25], 1983 (25) Takolander [26], 1984 (26) Downing [27], 1985 (27) Mellière [28], 1986 (28) Anton [29], 1986 (29) Raptis [30], 1986 (30) Schellack [31], 1987 (31) Englund [32], 1987 (32) Lilly [33], 1988 (33) Cole [34], 1989 (34) Shortell [36], 1991 (35) Dawson [37], 1991 (36) Ramesh [38], 1993 (37) Roggo [39], 1993 (38) Carpenter [40], 1994 (39) Gawenda [41], 1995 (40) Taurino [42], 1998 (41) Duffy [43], 1998 (42) Locati [44], 1999 (43) Gouny [45], 2000 (44) Irace [46], 2001 (45) Kauffman [47], 2002 (46) Dorigo [48], 2002 (47) Bowrey [49], 2003 (48) Mahmood [50], 2003 (49) Ascher [51], 2003 (50) Laxdal [52], 2004

Pts 14 69 10 9 27 64 82 36 42 152 23 52 80 18 26 20 21 62 87 27 12 61 159 33 13 40 52 110 36 60 75 36 38 39 50 31 167 33 39 23 24 48 35 45 112 89 46 45 25 41

Ans 15 100 13 12 42 73 98 51 60 233 34 86 119 26 35 40 28 87 147 32 27 88 244 52 18 62 77 160 61 95 103 59 59 51 71 43 252 54 58 28 40 65 52 75 142 109 67 52 34 57

Thrombosis 1 20 3 6 11 20 23 22 16 65 16 30 16 17 9 7 66 11 6 21 89 15 7 9 23 70 27 36 16** 31 28 37 22 115 33 28 13

19 42 24 15 14 7

Embolism 14 3 3 28 17 19 23 5 27 5* 3 7

3 34 8 5 32 4 3

Vein compr. Nerve compr. Rupture 2 19 10 12 2 2 2 1 0 3 13 12 11 5 1 4 6 2 4 14 6 3 41 15 6 1 0 4 2* 2* 0 0 0 5 1 0 3 1 2 11

12

0

6 8

8 6** 3 4

2

1 6

3 5 30

2 0 4 3 1 2 4 1**

2 58 4 3

4 5 1 0

3 6

1 8 1 6 2 4 25

2 1 1

1 1 1 2

5

3 2

3 1 2 4

11  Clinical Presentation

137

Table 11.2 (continued) Author, year (51) Aulivola [53], 2004 (52) Martelli [54], 2004 (53) Pulli [55], 2006 (54) Huang [56], 2007 (55) Kropman [57], 2007 (56) Lichtenfels [58], 2008 (57) Dzieuciuchowicz [59], 2009 (58) Mazzaccaro [60], 2014 (59) Wagenhauser [61], 2015 (60) Leake [62], 2016 (61) Personal series

Pts 39 38 137 289 66 40 61

Ans 51 42 159 358 110 60 82

Thrombosis 11 10 34 95 12 16 47

Embolism 3 8 2 28

65 30

77 42

17 14

3 11

3

1

156 58

186 82

50 29

5

0

0

4

Vein compr. Nerve compr. Rupture 6 1 3 2 5 20 0 1 1

4 0

(2) During follow-up, ten aneurysms underwent further complications, and 13, initially not complicated, became complicated: complications during follow-up were thrombosis/embolism, 11; gangrene, 14; vein compression, 5; nerve compression, 2; and rupture, 4. On the whole, 62/100 aneurysms (of which 95 were atherosclerotic) underwent one or more significant complications (3) Of three thromboses, two were acute, one defined insidious (6) All 20 thromboses were acute (7) Of four ruptured aneurysms, three were atherosclerotic (9) Of three ruptures, one was iatrogenic, following repeated attempts at biopsy for a suspected popliteal tumor (10) Out of 233 cases, 106 were uncomplicated and 111 presented complications from aneurysm; in other 16 cases, complications were attributed to diffuse atherosclerotic disease, not properly to aneurysm. As the entire series comprises one mycotic and one dissecting aneurysm, it is not clear if all the six ruptured aneurysms were atherosclerotic (13) Numbers refer to patients, not to limbs* (20) Thrombosis: seven acute and four subacute (24) Three further thromboses were observed during the follow-up; rupture affected bilateral aneurysms in the same patient (32) Numbers refer to 48 operated limbs** (34) Of 28 thromboses, 19 were acute (35) Of 37 thromboembolisms, 11 were acute (36) Of 22 thromboses, 19 were acute

long femoropopliteal endarterectomy was frequently performed, the cause of an extensive femoral occlusion was individuated in the thrombosis of a small (2  cm; and the same was true for the presence of mural thrombus: ≤2 cm, 9/14 (64%) and >2 cm, 14/20 (70%). Some authors, however, did not share these findings. Varga et al. [68], reviewing for the UK Joint Vascular Research Group (19 surgeons) 137 patients with 200 PAAs, found that 58 aneurysms with mural thrombus averaged in diameter 29 mm while 23 aneurysm without mural thrombus had a mean diameter of 21.5 mm. In a series from Poland [59], larger aneurysms were more frequently symptomatic and had ischemic symptoms than smaller ones; however, the difference did not reach statistical significance, and there was not any difference in diameter between cases with limb-threatening ischemia and those without.

138

Most of the experiences support the concept that smaller aneurysms are risk-free; as of now, the cut-off at 2  cm in diameter for selecting patients for surgical/endovascular treatment is empirical, relying on some kind of tradition and not on a scientific/statistical basis, even if some surgeons [69] asserted to have never seen a thrombosed PAA with a diameter 39% (765/1930), and in 13 series (59%) ([41, 43, 44, 48–51, 55, 62], personal series), it was 40% or more. A number of asymptomatic aneurysms are completely thrombosed; the lack of symptoms in this condition is probably more frequent than suspected [66] especially in older patients with arteriosclerotic occlusive disease because of low requirements in physical activity, good collateral circulation, or heavy symptoms in the contralateral limb. This form of spontaneous healing is reported in several series. A thrombosed aneurysm was diagnosed in 4–38% of symptomless limbs [9, 29, 65]; Bouhoutsos and Martin [66] reported eight cases, of which three were associated with an abdominal aortic aneurysm and five with contralateral ischemic symptoms. Asymptomatic limbs with a patent aneurysm and incidental distal occlusion or silent embolic events [35, 40, 74] represent a group at particular risk for acute thrombosis and ischemia, owing to the reduction of the infrapopliteal arterial bed, and should be considered and managed as symptomatic [76]. As one of the major controversies regards how to manage asymptomatic aneurysms, it is important to know which is the natural history of these lesions (Table  11.3). Looking at the table, it is amazing to see how different are the data reported in the different experiences. Certainly, patients

A. Cavallaro

and aneurysms may be quite different from one report to another, and sometimes, the follow-up is short. In addition, the reasons of nonoperative treatment may be quite variable, ranging from medical contraindications to refusal by the patient, from the occurrence of more urgent health problems (as an abdominal aortic aneurysm or severe symptoms in contralateral limb) to (why not?) ideologic trends of the surgeon. However, these striking differences, coupled with the very low rate of complications in some series, would in part justify the slogan [79]: “a symptomless limb can only be made worse by arterial surgery.” The final sensation is that the behavior of an asymptomatic PAA is really quite unpredictable, and this should always be present in the mind when planning the best management option of these patients.

11.4 C  hronic Ischemia and Acute Ischemia Chronic ischemia on clinical presentation was present in 41% (1406/3440) of limbs with a PAA.  Intermittent claudication was observed in 22% (809/3730), ranging from 4–8% [28, 58, 80] to 41–49% [9, 13, 29, 81]. Rest pain/necrosis was the complaint in 18% (592/3362) with extremes at 4–8% [8, 9, 45, 60] and 41–49% [39, 40, 52]; in the latter group, we included arbitrarily limbs with the blue toe syndrome, as very distal embolic events may result in digital gangrene; Bouhoutsos and Martin [66] described 18 cases of digital gangrene with palpable pedal pulses. The onset of symptoms was a picture of acute ischemia in 29% (736/2530) ranging from 1–10% ([11, 27, 43], personal experience) to 37–51% [5, 42, 47, 80]. Acute ischemia may reveal otherwise unsuspected thrombosed PAA. Dardik and Dardik [82] reported two cases initially misdiagnosed as embolic occlusion of the femoral artery; a similar case was described by Jackaman et  al. [22] In particular, the advent of intra-arterial thrombolysis has enlightened this possibility. Hamelink and Elliott [83] reported that in 3/34 (9%) cases of acute limb ischemia treated with intra-arterial

11  Clinical Presentation

141

Table 11.3  Fate of untreated PAAs, asymptomatic at diagnosis Author, year (1) Wychulis [11], 1970 (2) Buxton [12], 1975 (3) Anton [29], 1976 (4) Englund [32], 1987 (5) Farina [35], 1989 (6) Hands [77], 1991 (7) Roggo [39], 1993 (8) Dawson [74], 1994 (9) Lowell [73], 1994 (10) Schellack [31], 1997 (11) Stiegler [78], 2002 (12 Mahmood [50], 2007 (13) Vrijenhoek [65], 2013

Aneurysms 87 9 15 14 14 16 45 42 64 26 19 7 42

Follow-up months (mean) 12–96 (3.7) 12 1–261 (66) 3–119 12–192 (50) 4.5–30

Complicated 27 (31%) 2 (22%) 4 (27%) 7 (50%) 5 (36%) 0 15 (33%) 25 (60%) 12 (19%) 2 (8%) 0 5 (71%) 1 (2%)

Uncomplicated 33 7 11 7 9 8 17 52 24 17 2 41

Pts. died 31

7

2

(1) Of 31 who died, four were complicated before death, and one of these died of complication after surgery. In effect, 60 cases (69%) remained uncomplicated until death or end of follow-up (3) Of four complicated, two were amputated (4) Of seven complicated, two were amputated (6) One lost to follow-up; seven died while asymptomatic. In effect, 15/16 (94%) remained asymptomatic until death or end of follow-up (7) All patients complained of ischemic symptoms during the follow-up and all were operated on (8) Complicated: mean follow-up, 18  months; maximum, 65  months. Uncomplicated followed-up for 4–96  months (mean, 39) (9) Of 12 complicated limbs, three were amputated (11) At diagnosis, all aneurysms had a diameter 2 cm would compress the vein; however, most patients have a normal venous drainage (as determined by air plethysmography). Involvement of the popliteal vein appears related not only to aneurysm size but also to the eventual perianeurysmal inflammatory reaction, as witnessed by the dense adhesion frequently observed [1, 95] between the vein and the sac; this could be the consequence not only of the prolonged and traumatic contact between the two vessels but also of blood leakage [5]. In the case reported by Goncu et al. [98], the vein was adherent to a large (80  ×  110  mm) aneurysm, and the nerve too was involved, with foot drop still present 10 months after the successful treatment of the aneurysm. Foot drop was present also in one case of vein compression reported by Mahmood et  al. [50] An extreme

case of vein involvement is described by Rossi et  al. [101]: the popliteal vein was ruptured, being stretched and avulsed by a giant (85 mm) PAA; the clinical picture mimicked aneurysm rupture.

11.9 Nerve Involvement Nerve involvement is a nonfrequent complication of PAA. It is mentioned in 18 series with an incidence of 7% (80/1109). In other six series, the incidence is reported together with that of vein involvement: 9% (41/458). When mentioned, this complication ranges from 0–1% [2, 8, 15] to 10–13% [11, 27]. Lord [4] observed symptoms of pressure on the popliteal nerve in 2/13 cases (15%). Nerve damage may manifest as pain, numbness, weak leg, or foot drop. It is debated if it derives only from compression and stretching or also from occlusion of vasa nervorum [102]. It may be correlated with aneurysm thrombosis [33] or rapid increase of aneurysm size [103]. Frequently, foot drop does not regress even after successful treatment of the aneurysm. Rarely, foot drop may derive also from compartment syndrome, which may be acute from thrombosis [104] or chronic exertional from repeated embolism [105].

11.10 Local Pain When not associated with rupture [87] or infection, local pain is a sign of rapid enlargement of the aneurysm [3, 17]. Gifford et al. [2] described a case of local severe pain from acute enlargement of a PAA requiring urgent treatment: up to then, the aneurysm was uncomplicated and not known.

11.11 Rupture Rupture of atherosclerotic PAAs (excluding cases complicated by infection) is a rare event. Reviewing 44 series, we found an incidence of

11  Clinical Presentation

3.1% (111/3542). This complication is absent in some experiences [5, 12, 15, 16, 24, 56] while it appears rather frequent in others, reaching 8–15% [2, 7, 27]. Sie et al. [106] (from Leiden, The Netherlands) thoroughly studied the problem: reviewing 29 series, published in 1953–1994, they found an incidence of 2.5%, but they reported an incidence of 4.8% (6/124) in their personal series; of the six ruptured aneurysms, the complication represented initial presentation five times, and one initially asymptomatic aneurysm ruptured 2 months after the diagnosis; in all cases, a contralateral aneurysm was present. Rupture was more frequent until the early 1960s, probably because a reduced awareness about PAA and its complications and the limited availability of imaging techniques allowed PAAs to reach large dimensions. Rarely, PAA rupture produces hypovolemic shock, and often, it remains contained within the popliteal fossa, giving origin to hematoma or pseudoaneurysm; in the latter case, patient’s history may be very long (2 years in the case reported by Tschen et al. [107]). Rupture may be ominous for limb survival, being limb-threatening ischemia a relatively frequent manifestation, as collateral circulation and venous return may be damaged by the expanding mass. In early reports, amputation has been reported as high as 50–100% [14, 64]. The different clinical presentations of rupture are schematically outlined in Fig. 11.2. Some cases of rupture may be defined as iatrogenic: Galland and Magee [70] mentioned a case of rupture during anticoagulation for acute thrombosis of a contralateral aneurysm (the case had been the object of a report by Pittathankal et  al. [108]). Of the three cases of rupture described by Crichlow and Roberts [10], one was the consequence of attempts to biopsy of the popliteal mass. We were able to find a detailed (or almost detailed) description of 60 cases of PAA rupture (Tables 11.5 and 11.6): the incidence of limb salvage appears high, but the large numbers are obscured by the poorly defined follow-up (or by its short extension) in many reports.

147

Fig. 11.2  Schematic drawing of the possible consequences of a PAA rupture. Arrowheads indicate rupture into the vein or into the synovia, giving rise to arteriovenous fistula or to hemarthros. Lesser arrow: compression and damage to the nerve (in yellow). Greater arrow: compression on the vein (venous hypertension, thrombosis). The artery, distal to the aneurysm, may be compressed or thrombosed, and this, together with compression damage of collaterals, may produce ischemia, rendered more dangerous by the obstacle to venous return. On the left: the hematoma may expand under the skin, producing hemorrhage (rare) or ecchymosis (frequent). (From Sie et  al. [106], with permission, modified)

In 2000 [120], endovascular treatment has entered the stage also in the treatment of this complication: 9/26 cases (35%), and the early results may be defined gratifying, with uniform success of the technique also in one case of arteriovenous fistula [133]; mean age of the nine patients was 78 years; two patients, 88 [132] and 83  years old [136], respectively, died p.o. from respiratory failure and sepsis of pulmonary origin; the procedure was successful in a 96-year-­ old patient [137].

Patient (sex, age) M, 81 “...” F, 39 “...” F, 73 M, 56

M, 40

M, 64 M, 79 M, 74

M, 66

M, 78 M, 78 M, 52 , 72 , 66

, 64 , 90 , 70 , 92 M, 63 M, 64 M 62 M, 62

Author, year (1) McHugh [109], 1951 (2) “...” (3) Julian [87], 1955 (4) “...” (5) “...” (6) Gage [110], 1957

(7) Seror [111], 1957

(8) Silverman [112], 1957 (9) Friesen [7], 1962 (10) “...”

(11) Enjalbert [113], 1966

(12) Downing [27], 1985 (13) “...” (14 “...” (15) “...” (16) Barroy [114], 1986 (17) Reed [115], 1991 (18) Bilotta [116], 1991 (19) Roggo [117], 1993 (20) “...”

(21) “...” (22) “...” (23) “...” (24) “...” (25) Manouguian [118], 1996 (26) Gawenda [41], 1997 (27) “...” (28) Sie [106], 1997 Massive hematoma Pain, hematoma Pain, leg swelling Acute pain

Pain and swelling distal thigh Mild leg edema, cyanosis

Pain, heavy limb

Pain+progressive impairment of limb function Pain, edema, cyanosis Pain, swelling, acute onset claud.

Clinical presentation Painful swollen leg, blebs Painful swollen leg Acute local pain Acute local pain Pain, swelling Painful popl. swelling, abscess-like

Table 11.5  Ruptured atherosclerotic popliteal artery aneurysms

Resection; ok but died after 5 weeks from cardiac failure Lumb. sympathect. + resection: gangrene, amputation Lumb. sympathect. + resection: ant. tib. compartment syndrome, amputation (rupture into the popl. vein) oblit. endoaneurysmorrhaphy + lumbar sympathectomy: ok Saphenous vein graft: ok Saphenous vein graft: ok Hunterian ligation: ischemic leg Hunterian ligation: amputation Resection + end-to-end anastomosis: ok (rupture into the popl. vein) Exclusion+aut. vein bypass: ok (thrombosed aneurysm) Exclusion and revascularization Aut. vein graft: chronic ischemia; follow-up 9 years Dacron graft; thrombosed at 5 years; new bypass with vein; ok for further 7 years Dardik graft: initially ok, later on claudication; f.-up 7 years PTFE graft: ok 30 months Aut. vein graft: ok 21 months PTFE graft: ok 3 months Partial resection + PTFE graft: ok 2 years Exclusion + prosthetic graft: ok 45 months Exclusion + aut. vein graft: ok 37 months Aut. vein bypass: ok 25 months, died from myocardial infarct.

Treatment and outcome Thigh amputation Thigh amputation Resect. + aut. vein graft: severe claudication Resection + aut. vein graft: ok 5 months Resection + aut. vein graft: ok 2 months Lumb. sympath. block+opening & exclusion of aneurysm+ forefoot amput.: ok 8 years Non-obliterative endoaneurysmorrhaphy: ok 3 months

148 A. Cavallaro

M, 72 M, 71

M, 71 M, 78 M, 75 M, 91 M, 56 M, 56 M, 74

M, 74 M, 75 M, 75 M, 75 M, 83 M, 78 F, 88 M, 86 M, 61 M, 75

M, 88

M, 66 F, 46

M, 84

M, 43 M, 66 M, 60 M, 43

(29) “...” (30) “...”

(31) “...” (32) “...” (33) “...” (34) Illig [119], 1998 (35) Ihlberg [120], 2000 (36) Juhl [121], 2001 (37) Canbaz [122], 2002

(38) Pittathankal [108], 2003 (39) Soffiatti [123], 2005 (40) Chervenkoff [124], 2005 (41) Barbato [125], 2006 (42) Parmer [126], 2006 (43) Sanjay [127], 2007 (44) Ponton [128], 2009 (45) Rits [129], 2009 (46) Meka [130], 2010 (47) Smith [131], 2010

(48) Izquierdo [132], 2010

(49) Pratesi [133], 2010 (50) Agrafiotis [134], 2012

(51) Tschen [107], 2013

(52) Coksun [135], 2014 (53) “...” (54) “...” (55) “...”

Pain, popl. swelling, cold foot Pain, popl. swelling, erythema Pain, popl, swelling Pain, popl. swelling, cold foot

Double thigh mass

Pain, limb swelling Pain, swelling

Swollen limb

Swelling, bruising Painful swollen leg Pulsatile mass Pain, swelling Pitting limb edema, distal thigh mass Swelling, pulmonary embolus Edema, recurrent cellulitis Pain, hematoma Massive edema Swollen painful leg

Acute pain Acute claud. and rest pain Painful, red, swollen leg Swollen ecchymotic distal leg Pain, limb swelling Distal thigh mass Painful mass

Leg swelling hemarthros Flapping foot, acute pain

(continued)

Aut. vein bypass: ok 77 months Dacron bypass: ok but peroneal nerve paresis; died 3 months from myocardial infarct. Dacron bypass: ok but died 1 month myocardial infarct. Dacron bypass: mild claud., died 30 months myoc. infarct. Aut. vein bypass: ok but died 40 months from pneumonia Resection + interposition vein graft + fasciotomy: ok 1 year Stent grafting: ok 5 months Exclusion, in situ fem-popl. bypass: ok 1 year Resection of aneurysm and pseudoaneurysm + PTFE graft: ok 16 months Exclusion + aut. vein bypass: ok Exclusion; PTFE graft: ok Excl. + interp. PTFE graft: ok Endoaneurysmorrhaphy + interp. vein graft: ok 3 months (thrombosed aneurysm); unroofing & decompression: ok Exclusion, opening & packing, PTFE graft: ok 6 weeks Stent graft: ok 15 months 2 Viabahn endografts: ok 1 year Stent grafting; aspiration of non-clotted blood: ok(?) 1 year (distal popliteal occluded); occlusion of aneurysm neck with Amplatz plug: ok 6 months 2 Viabahn endografts + intra-arterial thrombolysis: ok but died p.o. (respirat. failure) (arteriovenous fistula); 2 Viabahn endografts: ok 3 months Evacuation of pseudoaneurysm + resection + vein interp. graft: ok 3 months Evacuation of 2 old hematomas with pseudocapsule; giant thrombosed aneurysm untouched: ok Aut. vein interp. inlay graft + distal embolectomy: ok 52 months Aut. vein interp. inlay graft: ok 31 months Aut. vein interp. inlay graft: ok 27 months Aut. vein interp. inlay graft + distal embolectomy: ok 26 months

11  Clinical Presentation 149

M, 96

(60) Brown [137], 2016

Swelling, bruising

Clinical presentation Pain, popl. swelling, cold foot Pain, popl. swelling, erythema Pain, popl. swelling, erythema Pain, swelling

Treatment and outcome Aut. vein interp. inlay graft + distal embolectomy: ok 2 months Aut. vein. interp. inlay graft: ok 28 months Aut. vein interp. inlay graft: ok 60 months 2 Viabahn endografts: ok, but died p.o. from sepsis of pulmonary origin Endografting (Viabahn endograft): ok 15 weeks

(1) and (2) Same patient: the second, contralateral, aneurysm ruptured 2 weeks after the first operation. The patient died. At autopsy, a ruptured aneurysm of the right femoral artery was found (3) and (4) Same patient: the second aneurysm ruptured 24 h after the first one. On the side with resulting severe claudication, the distal anastomosis is defined as “very difficult.” Chronic symptoms were not relieved by lumbar sympathectomy (6) Patient with strongly positive Wassermann reaction; the remaining of ruptured aneurysm is described as full of “typical syphilitic plaques”; pathology support to this diagnosis is lacking (8) A diagnostic roentgen sign is described: interruption of the calcified vessel outline and dispersal of calcified flecks (10) Gangrene of the anterior compartment attributed to the fact that resection of the aneurysm involved the distal popliteal artery and the first part of the anterior tibial artery (28)–(33) The aneurysm was excluded or resected (30) and (31) Same patient: the left aneurysm ruptured 2 months after the right one (35) Patient with severe dyspnea from deficit of α-1-antitrypsin: retrograde application, through the infragenicular popliteal artery, of a Hemobahn stent graft (W.L.  Gore, Flagstaff, AZ, USA). This is apparently the first endografting procedure successfully performed to treat a ruptured popliteal aneurysm (44) The endograft was a covered stent Zenith (Cook, Bloomington, IN, USA). Documented, also at follow-up, a side branch endoleak (46) Four Viabahn (W.L.  Gore, Flagstaff, AZ, USA) endoprostheses were successfully used, followed by two traditional procedures of clotted blood evacuation and tissue debridement. After 1 year, due to repeated infections of the popliteal fossa, the stent grafts were explanted, and a bypass with cryopreserved vein was performed (47) The Amplatz plug (AGA Med Ltd., Birmingham, UK) is made of a nitinol wire mesh compressed to allow delivery through a catheter; after release, it returns to its original shape, occluding the target vessel

Patient (sex, age) M, 66 M, 47 M, 63 F, 83

Author, year (56) “...” (57) “...” (58) “...” (59) Ono Moraes [136], 2015

Table 11.5 (continued)

150 A. Cavallaro

11  Clinical Presentation

151

Table 11.6  Ruptured atherosclerotic popliteal artery aneurysm: details of cases from Table 11.5

Case no. 1 2 3 4 5 6 7 8 9 11 16 17 18 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 43 46 47 48 49 50 51 52 55 56 59 60

Time from onset of symptoms to diagnosis/ treatment 3 weeks Immediate 3 weeks < 1 day 10 days 1 month 3 months 1 month 3 months 1 month 5 days 2 days 3 months

Thigh or popliteal mass Pulsating Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes

Immediate 1 week Acute 1 month Acute Acute Acute Acute 10 hrs 2 months 2 months Acute

Distal pulses Non-pulsating present No Yes Yes Yes Yes Yes No No No

Yes Yes Yes Yes Yes Yes

5 days 6 weeks 1 week Some weeks Acute 2 days 2 months 2 years

Yes Yes Yes Yes Yes

15 days 1 day

Yes Yes

No Yes Yes Yes No

Initial diagnosis correct Yes Yes Yes Yes No Yes Yes No Yes Yes No No No

Yes

Yes Yes

Yes No

No Yes

Yes Yes No No No

No Yes Yes No

Yes Yes

No No Yes Yes No No No No No

Non-correct initial diagnosis: 5, 16, 17, 34, 37, 43, 60: venous problems, mainly deep vein thrombosis or thrombophlebitis 8: phlegmasia cerulea dolens 18: sarcoma 50: musculo-tendinous problems, hemorrhagic Baker’s cyst, sarcoma 52–58: the delay between the onset of symptoms and diagnosis was 2–30 days (mean, 12 days) 59: erysipelas In case 34, edema was so marked that examination of the popliteal space was impossible

Yes No

No No

A. Cavallaro

152

11.12 Infection Infection of a PAA is a rare complication, which, however, represents a significant threat for limb and life because it affects often frail and older individuals. A large variety of pathogens may be responsible for this complication, with a prevailing role of Staphylococcus aureus and Salmonella. In effect, Salmonella enteritidis is being reported with increasing frequency as the pathogen responsible for infection of aneurysms and of intimal atherosclerotic lesions [138].

We were able to collect 17 cases of infected PAA (Table  11.7): the reports indicate that the aneurysm was preexistent to the infectious event, sometimes only highly suggestive of this; occasionally, our judgement may be wrong, and the aneurysm may be infective in origin, not infected (e.g., cases 3 and 16) (see also mycotic aneurysm, Chap. 29). The clinical presentation was often (82%) that of a feverish patient, aged in most cases 70  years or more (the youngest being 58  years old, the oldest 91), with marked involvement of

Table 11.7  Cases of infection of atherosclerotic popliteal aneurysm Author, year (1) Perdue [139], 1967 (2) “...” (3) Wilson [140], 1995 (4) Baty [141], 1998 (5) Hopton [142], 1998

Patient (sex, age) Initial event M, 74 Urinary infection M, 70 Urinary infection M, 88 Abdominal pain, vomiting M, 91 Laser treatm. Villous rectal tumor F, 87 Gastroenteritis

Blood culture

Neg. Campylobacter fetus

(6) Alonso B [143]. 2001 7) Witijes [144], 2003

M, 70

Diarrhea, fever

M, 70

(8) Ysa [145], 2007

M, 73

BCG treatment for bladder cancer Diarrhea

(9) Dickinson [146], 2007 (10) Papavassiliou [147] 2008

M, 72

Pneumonia

M, 72

Pneumonia

(11) Schimmer [148], 2009 (12) Jammal [149], 2011

M, 86

Sepsis

(13) Bani-­hani [150], 2012

M, 85

Sepsis

Staphylococcus aureus

(14) Fisk [151], 2012

M, 62

Insertion of pacemaker

Staphylococcus aureus

M, 58

Salmonella enteritidis

E. coli

Streptococcus pneumoniae Neg.

Staphylococcus aureus Salmonella Bredeney

Specimen culture Treatment and outcome Proteus Thigh amputation mirabilis E. coli Endoaneurysmorrhaphy: ok 1 year Salmonella Resection + vein graft: group D died p.o. Neg. Exclusion + decompr. + fem-popl. bypass prosth. graft: ok 1 year Salmonella Exclusion + decompr. + enteritidis extra-anat. bypass fem.-ant. tibial: ok 20 months Resection + vein bypass: ok 3 months Thrombosed aneurysm, antituberc. therapy: ok 41 months Neg. Resection + extra-anat. fem-popl. vein bypass: ok 7 months Neg. Resection + fem-popl. vein graft: ok 6 months Listeria Thrombosed aneurysm; monocytogenes ligation + subtot. resect: ok 18 months Stent grafting: ok 6 months Salmonella Bredeney Staphylococcus aureus + Streptococcus group G

Resection + (finally) fem-popl. vein bypass: ok 3 years Stent grafting: ok 2 years

Not treated

11  Clinical Presentation

153

Table 11.7 (continued) Author, year (15 MoyPetersen [152], 2014 (16) Melendez [153], 2015 (17) Cervantes G [154], 2015

Patient (sex, age) Initial event M, 66 Coronary artery bypass M, 85 Sepsis M, 60

Diarrhea

Blood culture

Campylobacter fetus Salmonella sp.

Specimen culture Treatment and outcome Staph. Aureus Exclusion + decompr. + vein bypass: ok 1 year Campylobacter Resection+vein bypass: ok fetus Salmonella sp. Resection+vein bypass: died p.o. from myoc. infarct

(1) Nonviable limb at admission; died after 4 months from cerebral hemorrhage (3) Severely anemic at admission: refused transfusion being Jehovah’s witness (7) Aneurysm not appreciated clinically, but revealed by MRI; exhaustive investigations were triggered by the diagnosis of specific granulomatous hepatitis (9) Coexistence of ipsilateral infected femoral aneurysm; specimen cultures negative but pneumococcal PCR positive (11) Apparently, this is the first case of successful endovascular (Viabahn, W.L. Gore, Flagstaff, AZ, USA) treatment of an infected and ruptured PAA (12) Instructive case: dehiscence of the end-to-end reconstruction after 3 days; resection of the arterial edges and interposition of an antibiotic soaked graft; after 5 days, to prevent further complications, explantation of the graft and fempopl. bypass with autologous reversed vein (13) Need of two successive operative drainages of infected hematoma within 2 months from stent grafting (14) PET-TC: increased uptake by aneurysms of right common iliac, right common femoral, left popliteal arteries; presence of abdominal aortic aneurysm. After 4  months of antibiotic therapy, PET-TC control suggested eradication of infection; stent grafting of the aortic aneurysm. After 6 months, peri-stent inflammation, followed by sepsis and death

the general status in half of the cases, complaining of severe local pain (70%) and presenting a swollen leg (65%). A tender pulsating mass in the popliteal fossa was observed in about twothirds of the cases. Instrumental diagnosis relied, starting from case 3, on duplex ultrasound scan, often followed by computed tomography (CT) or magnetic resonance imaging (MRI). In three cases, gas bubbles were revealed by ­imaging studies. Arteriography, either traditional or digital, was performed in about half of the cases. Positron emission tomography–computed tomography (PET-TC) was performed in case 14 and imaging with labeled leukocytes in cases 7 and 9. Coexistent popliteal vein thrombosis was diagnosed in cases 3 and 5. In 1998, Smits et al. [155], from Gröningen, described a case of empyemic thrombosed aneurysm in which the diagnosis was made only at operation. Rupture, contained but more often frank, was observed in all cases, but for cases 7 and 14 (non-operated on) and case 15. Surgical treatment varied according to the individual case requirement and, obviously, the surgeon’s preference. Worth of attention is the surgical tactics recently used (cases 15 and 16): vein bypass through the medial approach fol-

lowed by direct aggression to the aneurysm through the posterior approach, having turned prone the patient. Very interesting are the results of stent-­grafting procedures (cases 11 and 13), with not only early gratifying results but also a positive 2-year follow-up in the second case. Considering the high risk ranking of most of these patients, the endovascular option could become the preferred one, even if associated minor surgical procedures (drainage of abscess/hematoma) or delayed traditional reconstructions would be required. In these patients, the role of the infectious disease specialist is of paramount importance both for treatment and surveillance, given the implant of a foreign body into a contaminated field.

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155 treatment of popliteal artery aneurysms: is exclusion with saphenous vein bypass still the gold standard? J Vasc Surg. 2007;45:706–15. 57. Kropman RHJ, De Vries J-PPM, Moll FL. Surgical and endovascular treatment of atherosclerotic popliteal artery aneurysms. J Cardiovasc Surg (Torino). 2007;48:281–8. 58. Lichtenfels E, Delduque FA, Bonamigo TP, Cardozo MA, Schulte AA. Popliteal artery aneurysm surgery: the role of emergency setting. Vasc Endovascular Surg. 2008;42:159–64. 59. Dzieuciuchowicz L, Lukaszuk M, Figiel J, Klimczak K, Krasinski Z, Majewski W. Factors influencing the clinical course of popliteal artery aneurysm. Med Sci Monit. 2009;15:CR231–5. 60. Mazzaccaro D, Carmo M, Dellatana R, Settembrini AM, Barbetta I, Tassinari L, Roveri S, Settembrini PG. Comparison of posterior and medial approaches for popliteal artery aneurysms. J Vasc Surg. 2015;62:1512–20. 61. Wagenhauser MU, Herma KB, Saghan TA, Dueppers P, Schelzig H, Duran M. Long-term results of open repair of popliteal artery aneurysm. Ann Med Surg. 2015;4:58–63. 62. Leake AE, Avgerinos ED, Chaer RA, Singh MJ, Makaroun MS, Marone LK. Contemporary outcome of open and endovascular popliteal artery aneurysm repair. J Vasc Surg. 2016;63:70–6. 63. Blakemore AH. Treatment of aneurysm by amputation. Surg Clin N Am. 1938;18:409–14. 64. Gaylis H. Popliteal arterial aneurysm. A review and analysis of 55 cases. S A Med J. 1974;48:75–81. 65. Vrijenhoek JEP, Mackaay AJC, Moll FL.  Small popliteal artery aneurysms: important clinical consequences and contralateral survey in daily vascular surgery practice. Ann Vasc Surg. 2013;27:454–8. 66. Bouhoutsos J, Martin P.  Popliteal aneurysms: a review of 116 cases. Br J Surg. 1974;61:469–75. 67. Barker WF. Discussion on Shortell et al. J Vasc Surg. 1991;14:777–8. 68. Varga ZA, Locke-Edmunds JC, Baird RN, The Joint Vascular Research Group. A multicenter study of popliteal aneurysms. J Vasc Surg. 1994;30:171–7. 69. Rivers S. Discussion on Shortell et al. J Vasc Surg. 1991;14:777. 70. Galland RB, Magee TR.  Popliteal aneurysms: distortion and size related to symptoms. Eur J Vasc Endovasc Surg. 2005;30:534–8. 71. Galland RB, Magee TR.  Management of popliteal aneurysm. Br J Surg. 2002;89:1382–5. 72. Pittathankal AA, Dattani R, Magee TR, Galland RB.  Expansion rates of asymptomatic popliteal artery aneurysms. Eur J Vasc Endovasc Surg. 2004;27:382–4. 73. Lowell RC, Gloviczki P, Hallett JW Jr, Naessens JM, Maus TP, Cherry KJ Jr, Bower TC, Pairolero PC.  Popliteal aneurysm: the risk of nonoperative management. Ann Vasc Surg. 1994;8:14–23. 74. Dawson I, Sie R, van Baalen JM, van Bockel JH.  Asymptomatic popliteal aneurysm: elective

156 operation versus conservative follow-up. Br J Surg. 1994;81:1504–7. 75. Borowicz MR, Robison JG, Elliott BM, Brothers TE, Robinson CK.  Occlusive disease associated with popliteal aneurysms: impact on long term graft patency. J Cardiovasc Surg (Torino). 1998;39:137–40. 76. Dawson I. Management of popliteal aneurysm. Br J Surg. 2003;90:249–50. 77. Hands LJ, Collin J.  Infrainguinal aneurysms: outcome for patient and limb. Br J Surg. 1991;78:996–8. 78. Stiegler H, Medler G, Baumann G. Prospective study of 36 patients with 46 popliteal aneurysms with nonsurgical treatment. Vasa. 2002;31:43–6. 79. Hands L, Collin J, Morris PJ.  A warning from 12 years of popliteal aneurysm treatment. Br J Surg. 1989;76:416. 80. Crawford ES, DeBakey ME.  Surgical considerations of peripheral arterial aneurysms. Arch Surg. 1959;78:226–38. 81. Buda JA, Weber CJ, Mc Allister FF, Vorhees AB Jr. The results of treatment of popliteal aneurysms. A follow-up study of 86 aneurysms. J Cardiovasc Surg (Torino). 1974;15:615–9. 82. Dardik H, Dardik I. Popliteal aneurysm thrombosis simulating femoral embolic occlusion. Am Surg. 1974;40:593–06. 83. Hamelink JK, Elliott BM.  Localized intraarterial streptokinase therapy. Am J Surg. 1986;152:252–6. 84. Lancashire MJR, Torrie EPH, Galland RB. Popliteal aneurysms identified by intra-arterial streptokinase: a changing pattern of presentation. Br J Surg. 1990;77:1388–90. 85. Bowyer RC, Cawthorn SJ, Walker JW, Giddings AEB.  Conservative management of asymptomatic popliteal aneurysm. Br J Surg. 1990;77:1132–5. 86. Theis FV. Popliteal aneurysms as a cause of peripheral circulatory disease: with special study of oscillomographs as an aid to diagnosis. Surgery. 1937;2:327–42. 87. Julian OC, Dye WS, Javid H, Grove WG. The use of vessel grafts in the treatment of popliteal aneurysms. Surgery. 1955;38:970–80. 88. Evans WE, Conley JE, Bernhard V. Popliteal aneurysms. Surgery. 1971;70:762–7. 89. Lilly GD.  The management of aneurysms of the lower extremities. Ann Surg. 1946;123:601–6. 90. Keynes GL, Morel MP.  Popliteal aneurysms. With report of a case. Br J Surg. 1943;31:155–7. 91. Shumacker HB Jr, Wayson EE.  Spontaneous cure of aneurysms and arteriovenous fistulas, with some notes on intrasaccular thrombosis. Am J Surg. 1950;79:532–44. 92. Walsh JJ, Williams LR, Driscoll JL, Lee JF.  Vein compression by arterial aneurysms. J Vasc Surg. 1988;8:465–9. 93. Giustra PE, Root JA, Mason SE, Killoran PJ. Popliteal vein thrombosis secondary to popliteal artery aneurysm. Am J Roentgenol. 1978;130:25–7.

A. Cavallaro 94. Brenot R, Bernard A, Sicard C, Weiller M, David M.  Anévrismes poplités révélés par des manifestation veineuses. Lyon Chir. 1983;79:128–9. 95. Mingoli A, Farina C, Feldhaus RJ, Schultz RD. Popliteal aneurysm presenting as thrombophlebitis of the lower extremity: a case report. J Vasc Surg. 1991;25:732–7. 96. Kotval PS, Shah PM, Babu SC, Charalel J, Reiter B. Popliteal vein compression due to popliteal artery aneurysm: effects of aneurysm size. J Ultrasound Med. 1995;14:805–11. 97. Bergan JJ, Trippel OH. Management of giant popliteal aneurysm. Arch Surg. 1963;86:146–53. 98. Goncu T, Tiryakioglu O, Sezen M, Yavuz S.  Giant popliteal aneurysm with deep vein thrombosis, foot drop and arteriomegaly. BMJ Case Rep. 2009;2009:bcr 11.2008.1243. 99. Bernhard VM Discussion on Towne et al. 44 100. Haaverstad R, Fougner R, Myhre HO.  Venous hemodynamics and the occurrence of leg oedema in patients with popliteal aneurysm. Eur J Vasc Endovasc Surg. 1995;9:204–10. 101. Rossi FH, Veith FJ, Lipsitz EC, Izukawa NM, Oliveira LA, Silva DG. Giant femoropopliteal artery aneurysm and vein rupture. Vascular. 2004;12:263–5. 102. Beaudry Y, Stewart JD, Errett L. Distal sciatic nerve compression by a popliteal artery aneurysm. Can J Neurol Sci. 1989;16:352–3. 103. Selvam A, Shetty K, James NV, Shah RR, Shankar K, Locker AP. Giant popliteal aneurysm presenting with foot drop. J Vasc Surg. 2006;44:882–3. 104. Dellanna M, Torsello G, Graupe F, Mackrodt H-G, Stock W.  Das akute Compartmentsyndrom des Unterschenkels—Komplikation eines Aneurysma der A. poplitea. Zentralbl Chir. 1997;122:193–6. 105. Knight JL, Au K, Whitley MA. Popliteal aneurysm presenting as chronic exertional comparment syndrome. Orthopedics. 1997;20:166–9. 106. Sie RB, Dawson I, van Baalen JM, Schultze Kool LJ, van Bockel JH.  Ruptured popliteal aneurysms. An insidious complication. J Vasc Surg. 1997;13:432–8. 107. Tschen JA, Samakar K, Patel ST, Abou-Zamzam A Jr. Asymptomatic ruptured giant popliteal aneurysm. J Vasc Surg. 2013;58:1090. 108. Pittathankal AA, Richards T, Galland RB.  Anticoagulation of a thrombosed popliteal artery aneurysm complicated by rupture of a contralateral aneurysm. Eur J Vasc Endovasc Surg. 2003;5:28–9. 109. McHugh JV. Spontaneous rupture of bilateral popliteal aneurysms. Ann Surg. 1951;133:131–4. 110. Gage M. Inflamed arterial popliteal aneurysm simulating acute abscess. Ann Surg. 1957;145:893–7. 111. Seror A. Rupture à bas bruit d’un anévrisme poplité spontané. Endoanévrismorraphie oblitérante. Afr F Chir. 1957;15:93–7. 112. Silverman JJ, Hurwitt ES. Subcutaneous rupture of a popliteal aneurysm, with a diagnostic roentgen sign. Arch Intern Med. 1957;100:314–8.

11  Clinical Presentation 113. Enjalbert A, Gedeon A, Mathe J, Gouzi J-L. Fistule artério-veineuse spontanée au cours de l’évolution d’un anévrisme artériel poplité. Mém Acad Chir. 1966;92:357–8. 114. Barroy JP, Barthel J, Locufier JL, Bosschaerts T, Goldstein M.  Atherosclerotic popliteal aneurysm. Report of one ruptured popliteal aneurysm. Survey and analysis of the literature. J Cardiovasc Surg (Torino). 1986;27:42–5. 115. Reed MK, Smith BM.  Popliteal aneurysm with spontaneous arteriovenous fistula. J Cardiovasc Surg (Torino). 1991;32:482–4. 116. Bilotta W, Walker H, McDonald DJ, Sundaram M. Case report 651. Thrombosed, leaking popliteal aneurysm. Skeletal Radiol. 1991;20:71–2. 117. Roggo A, Hoffmann R, Duff C, Brunner U, Largiader F. Wie oft rupturiert das Aneurysma der Arteria poplitea? Helv Chir Acta. 1993;60:145–6. 118. Manouguian S.  Akute Ruptur eines Aneurysmas der Arteria poplitea: Fallbericht. Zentralbl Chir. 1996;121:405–7. 119. Illig KA, Eagleton MJ, Shortell CK, Ouriel K, DeWeese JA, Green RM. Ruptured popliteal artery aneurysm. J Vasc Surg. 1998;27:783–7. 120. Ihlberg LHM, Roth WD, Alback NA, Kantonen IK, Lepantalo M. Successful percutaneous endovascular treatment of ruptured popliteal artery aneurysm. J Vasc Surg. 2000;31:794–7. 121. Juhl CM, Sandemann J.  Rumperet popliteaaneurisme. Ugeskr Laeger. 2001;163:4879–80. 122. Canbaz S, Ege T, Sunar H, Saygin C, Duran E.  Bilateral popliteal aneurysm with rupture and pseudoaneurysm formation on the left. Eur J Vasc Endovasc Surg. 2002;3:36–8. 123. Soffiatti Mesquita Oliveira R, Aliperti Ferreira D, Alvez Terra J Jr, de Mara Lenza R, de Assis Filho AC, Nunes W.  Rupture of a popliteal artery aneurysm: case report and review of the literature for the past 50 years. J Vasc Bras. 2005;4:105–10. 124. Chervenkoff V, Govedarsky V, Maximov D, Daskalov A, Stoinova V.  Rupture of a giant popliteal artery aneurysm, associated with type III aortic dissection: a case report. Eur J Vasc Endovasc Surg. 2005;9:101–3. 125. Barbato HA, Tavars CM, Volpini CA, Gomes Petisco AC, Rossi FH, Dagli MF, Vasconcelos Oliveira LA, Izukawa NM.  Aneurisma da artéria poplitea com rotura e formaçao de pseudo-aneurisma. J Vasc Bras. 2006;5:148–50. 126. Parmer SS, Skelly CL, Carpenter JP. Ruptured popliteal aneurysm. A case report. Vasc Endovascular Surg. 2006;40:71–4. 127. Sanjay P, Lewis H. Deep vein thrombosis and pulmonary embolus associated with a ruptured popliteal aneurysm—a cautionary note. World J Emerg Surg. 2007;2:34. 128. Ponton A, Garcia I, Amaiz E, Bernal JM, Bustamante M, Gonzales-Tutor A, Revuelta JM.  Endovascular repair of a ruptured giant popliteal aneurysm. Ann Vasc Surg. 2009;23:412e1–4.

157 129. Rits Y, Erben A, Ricotta JJ II. Endovascular repair of a ruptured giant popliteal artery aneurysm. Perspect Vasc Surg Endovasc Ther. 2009;21:190–4. 130. Meka M, Wixon CL, Mondy SJ, Busken C.  Endovascular exclusion of a ruptured popliteal aneurysm. Am Surg. 2010;76:338–9. 131. Smith RJP, Gajendragadkar PR, Winterbottom AP, Cooper DG, Hayes PD, Boyle JR.  Endovascular occlusion of a ruptured popliteal artery aneurysm. Vasc Endovascular Surg. 2010;44:298–301. 132. Izquierdo Lamoca LM, Blanch AM, Leiva HL.  Endovascular therapy for a ruptured popliteal aneurysm. Cath Cardiovasc Intervent. 2010;75:427–9. 133. Pratesi G, Marek J, Fargion A, Pulli R, Dorigo W, Pratesi C.  Endovascular repair of a ruptured popliteal artery aneurysm associated with popliteal arteriovenous fistula. Eur J Vasc Endovasc Surg. 2010;40:645–8. 134. Agrafiotis AC, Horn D, Segers B, Lemaitre J, Bosschaerts T.  Ruptured aneurysm of the popliteal artery. Is the diagnosis still difficult. Minerva Chir. 2012;67:355–60. 135. Coskun I, Demirturk OS, Turnel HA, Andic C, Gulcan O.  Positive clinical outcome of the saphenous vein interposition technique for ruptured popliteal artery aneurysm. Surg Today. 2014;44:1674–7. 136. Ono MA, Yoshikazu NR, Franchini RF, Viotto EF, Bogdan CR. Relato de caso: aneurisma roto de artéria poplitea. J Vasc Bras. 2015;14:189–92. 137. Brown SL, Lewis M, Morrow DR.  Endovascular repair of ruptured popliteal artery aneurysms: a case report and review of the literarure. Eur J Vasc Endovasc Surg Short Rep. 2016;32:24–8. 138. Fernandez-Guerrero ML, Aguado JM, Arribas A, Lumbreras C, de Gorgolas M. The spectrum of cardiovascular infections due to Salmonella enteric. A review of clinical features and factors determining outcome. Medicine. 2004;83:123–38. 139. Perdue GD Jr. Mycotic aneurysms associated with urinary tract infections. Am J Surg. 1967;113:710–2. 140. Wilson P, Fulford P, Smith JV, Dodd P, Walker MG.  Ruptured infected popliteal artery aneurysm. Ann Vasc Surg. 1995;9:497–9. 141. Baty V, Hein B, Selton-Suty C, Schumacher H, Peiffert B, Danchin N, Cherrier F.  Anévrysme mycotique poplité révélateur d’une endocardite à Campylobcter fetus. Presse Méd. 1998;27:357–8. 142. Hopton BP, Scott DJA. Ruptured popliteal aneurysm infected with Salmonella enteritidis: an unusual cause of leg swelling. Eur J Vasc Endovasc Surg. 1998;15:272–4. 143. Alonso-Bartolomé P, Alonso VH, Aurrecoechea E, Acha O, Blanco R, Martinez-Taboada VM, Rodriguez-Valverde V.  Mycotic (infected) aneurysm of the popliteal artery and arthritis following Salmonella bacteremia. Clin Exp Rheumatol. 2001;19:325–8. 144. Witjes JA, Vriesema JLJ, Brinkman K, Bootsma G, Barentsz JO. Mycotic aneurysm of the popliteal

158 artery as a complication of intravesical BCG therapy for superficial bladder cancer. Case report end literature review. Urol Int. 2003;71:430–2. 145. Ysa A, Bustabad MR, Arruabarrena A, Perez E, Lopez-Vidaur I, Garcia-Alonso JA.  Rupture of an infected popliteal aneurysm. Case report and review of the literature. Eur J Vasc Endovasc Surg. 2007;14:39–44. 146. Dickinson KJ, Parry DJ, Sandoe JA, Gough MJ.  Multiple peripheral pneumococcal aneurysms without aortic involvement: a unique case confirmed with the novel use of a molecular diagnostic technique. J Vasc Surg. 2007;45:1253–5. 147. Papavassiliou VG, Xanthopoulos DK, Argitis VP, Loupou CE, Dervisis CL, Vorou RM, Arvanitis DP.  Infected ruptured popliteal artery aneurysm by Listeria monocytogenes. A case report and review of the literature. J Cardiovasc Surg (Torino). 2008;49:245–8. 148. Schimmer W, Somjen GM.  Endovascular repair of a ruptured, mycotic popliteal aneurysm. Aust N Z J Surg. 2009;79:560–1. 149. Jammal MH, Guidon J, Chiche L, Tselikas L, Tiev K-P, Tolédano C, Josselin-Mahr L, Gain M, Cabane J, Kettaneh A.  Salmonella bredeney: une cause rare d’anévrysme mycotique. Rev Méd Interne. 2011;32:e12–4.

A. Cavallaro 150. Bani-Hani MG, Elnahas L, Plant GR, Ward A, Moawad M. Endovascular management of ruptured infected popliteal artery aneurysm. J Vasc Surg. 2012;55:532–4. 151. Fisk M, Peck LF, Miyagi K, Steward MJ, Lee SF, Macrae MB, Morris-Jones S, Zumia AI, Marks J.  Mycotic aneurysms: a case report, clinical review and novel imaging strategy. Q J Med. 2012;105:181–8. 152. Moy Petersen JC, Hernandez-Lahoz OI, Couto MD, Vidal Insua JJ, Garcia CR. Surgical management of an infected popliteal artery aneurysm. Vasc Spec Int. 2014;30:94–7. 153. Melendez BA, Hollis HW Jr, Rehrong TF. Mycotic popliteal aneurysm rupture secondary to Campylobacter fetus. Ann Vasc Surg. 2015;29:122. e9–e11. 154. Cervantes GV, Simào da Silva E, De Luccia N.  A rare presentation of ruptured infected popliteal artery aneurysm with massive local emphysema. Vasc Med. 2015;20:491–2. 155. Smits TM, van den Dungen JJAM, Schraffordts KH, Mooyaart EL, Hoekstra HJ.  Een zwelling distal in het bovenbeen. Ned Tijdschr Geneeskd. 1998;142:1697–701.

Part V Popliteal Aneurysms: Diagnosis

Diagnostic Procedures

12

Alessandro Cannavale, Mariangela Santoni, Marianna Gazzetti, Fabrizio Fanelli, and Antonino Cavallaro

12.1 Primary Diagnosis Until the introduction of ultrasound diagnostics into the clinical practice, primary diagnosis of popliteal artery aneurysm (PAA) was essentially clinical [1, 2]. However, since 1937, Theis [3] advised that when the aneurysmal sac is small, diagnosis may be difficult, as the symptoms of intermittent claudication or foot coldness may overshadow the unusual finding in the popliteal space. Wychulis et al. [4] defined the diagnosis as usually obvious on clinical examination, also for thrombosed aneurysms, the latter presenting as firm and nonpulsatile masses usually somewhat movable. Agrifoglio et  al. [5] confirmed the latero-lateral passive mobility, remarking also, in patent aneurysms, the presence of a systolic bruit, substantially unchanged during proximal compression and enhanced during distal compres-

A. Cannavale · M. Santoni Vascular and Interventional Radiology Unit, “Sapienza” University, Rome, Italy M. Gazzetti “Villa Stuart” Hospital, Rome, Italy F. Fanelli (*) Vascular and Interventional Radiology Department, “Careggi” University Hospital, Florence, Italy e-mail: [email protected] A. Cavallaro Past Professor of General Surgery, “Sapienza” University, Rome, Italy © Springer Nature Switzerland AG 2021 A. Cavallaro (ed.), Aneurysms of the popliteal artery, https://doi.org/10.1007/978-3-030-49687-6_12

sion. Anyway, it was evident that on physical examination only, a number of PAAs, especially if small or asymptomatic or non-pulsating, risked to be missed. When the problem of small and/or asymptomatic aneurysms, particularly those contralateral to a symptomatic one, was still underestimated, the reliability of clinical primary diagnosis appeared rather high: 81–98% [6–8]. Guvendik et  al. [9] reported that the diagnosis was always clinical in a series of 28 patients (with 32% nonpulsatile aneurysm). In the experience of Alpert et al. [10] in 38/43 cases (88%), there was a palpable popliteal mass, and 28/38 (74%) were not pulsatile. However, a number of aneurysms were discovered during amputation or in amputated specimens or at postmortem examination [6, 11–15]. In addition, frequently, the diagnosis of PAA was established during operations for limb ischemia [11, 16–18], in lack of any preoperative suspicion; this happened in 5/40 cases (12.5%) in the experience of Inahara and Toledo [14]. The intraoperative surprise was particularly striking in case of urgent treatment for acute limb ischemia [10, 15, 19, 20]. Bouhoutsos and Martin [12], in their classic paper, reported that out of 116 PAAs (of which 102 were atherosclerotic), 19 (16.4%) were discovered during a femoropopliteal reconstruction for limb ischemia, two (1.7%) during a Gritti-Stokes amputation, and 12 (10.4%) were revealed by an aorto-arteriography performed for ischemic symptoms. 161

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Palpation appeared reliable in case of relatively large aneurysms: according to Inahara and Toledo [14], most of the aneurysms diagnosed by palpation had a diameter superior to 3.0  cm; moreover, these authors observed that it may be difficult to distinguish large but normal popliteal arteries from aneurysms. Shortly after the introduction of ultrasound in daily practice, Collins et  al. [13] observed that probably about 50% of PAAs had not been detected clinically. In more recent series, it is confirmed that diagnosis based only on clinical examination may be poorly reliable [21, 22]. According to Ascher et al. [23], only 15/34 (44%) small aneurysms were suspected at palpation and if asymptomatic, only 5/14 (36%). However, if it is clear that physical examination per se is not fully reliable for primary diagnosis of PAA, it is also evident that the problem of missed diagnoses, misdiagnosis, and poor diagnostic capability in general depends mainly on cultural ground. In 1985, Downing et al. [20] reported on 62 aneurysms, of which 58 (93.5%), pulsatile or not, were appreciable at palpation; the initial diagnosis was missed on several occasions: in 26/35 (74%) cases referred by a general practitioner and in 6/17 (35%) cases referred by other hospitals; misdiagnosis conditioned a significant delay of the necessary treatment in seven patients, resulting in six amputations and one chronic ischemia. Currently, the more reliable mean for primary diagnosis is certainly US examination; however, in most cases, US should allow the confirmation of a clinical diagnosis or, at least, of a clinical suspicion: the former either the latter should represent, almost always, the initial step indicating the need or opportunity of instrumental investigations. In this sense, we agree with those authors [24–26] who assert that the diagnosis of PAAs is essentially clinical. This assessment is founded not only on the ability in physical examination of the lower limbs of the patient but principally on awareness and a high index of suspicion, the latter derived also from a meticulous and often time-consuming anamnesis [12, 20, 27, 28]. The mainstays in anamnesis and physical examination (besides the obvious finding of a mass, pul-

sating or not, at inspection or palpation) are the following: • Family history of aneurysmal disease • Aneurysms at other locations, present or repaired, including the contralateral side • Acute onset of ischemia, often with gradual improvement • Acute severe ischemia with prominent contralateral popliteal pulse or contralateral amputation • Isolated ischemic skin lesions at foot level • Prominent pulsation in the distal subsartorial or popliteal space • Chronic ischemia with strong femoral pulse and absent popliteal pulse • Absent pedal pulses, present popliteal pulse, in nondiabetic patients Particularly intriguing and difficult may be the diagnosis of PAA in a limb presenting with threatening acute ischemia. In this setting, the advent and large diffusion of intra-arterial thrombolysis opened new scenarios. In 1990, two reports aired from UK hospitals (Royal Berkshire and Royal Surrey County) dealt with the discovery of a PAA only after thrombolysis. In the former [29], of five PAAs complicated by acute ischemia, only one was palpable and correctly interpreted, pre-treatment, as the cause of the acute event. In the latter [30], of eight cases with thromboembolic complications of a PAA, two were diagnosed only after thrombolysis. A new mode of presentation of a PAA was therefore identified [26], allowing the statement that intra-­ arterial thrombolysis would add to the number of PAAs unknown before acute complications [31] (Fig. 12.1).

12.2 Imaging Techniques 12.2.1 Plain X-Ray In the past, it represented the possibility of visualizing the presence of a PAA [32]. Gifford et al. [6] reported that plain X-ray confirmed the presence of PAA in 28/100 cases; in an additional

12  Diagnostic Procedures

a

163

b

c

Fig. 12.1  Patient presenting with acute limb ischemia, no palpable mass in the popliteal space, good femoral pulse, and distal pulses absent. (a) Angio-CT demonstrating popliteal artery thrombosis with absent run-off. (b, c)

After thrombolysis, evidence of PAA and acceptable run-­ off (in this case, however, already at the first examination, suggestive calcifications were evident) (courtesy of P. Sapienza, MD)

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case, the aneurysm was unsuspected clinically. Wychulis et al. [4], studying with plain X-ray 169 cases of PAA, observed a positive finding in 138 (82%) under the form of a popliteal mass or calcifications. This time-honored investigation is obsolete for the study of PAA; however, occasionally, the calcified walls of the popliteal artery, aneurysmatic or not, may be observed in a knee X-ray, particularly in the lateral projection.

12.2.2 Xeroradiography This technique was used in the past and consisted of recording the X-ray generated images on a selenium-coated plate. Using an intravenous contrast medium, vascular images could be obtained [33]. The advent of computed tomography (CT) and magnetic resonance (MR) has relegated xeroradiography among the obsolete techniques [34].

12.2.3 Arteriography Since the beginning of the modern era in the treatment of PAAs, arteriography has been widely used; however, it was evident, already in the earlier experiences, that its diagnostic value as for the presence, the size, and the morphology of the aneurysm was relatively limited. Janes and Ivins [32] observed that at arteriography, the size of the aneurysm resulted often smaller than expected on the basis of the dimensions of the pulsatile mass. According to Edmunds et al. [2], arteriography is remarkably inaccurate in denoting a PAA; in patent aneurysm, the frequent presence of parietal concentric thrombus may lead to the evidentiation of a non-dilated lumen, rendering the interpretation of images difficult and tricky, with ensuing underestimation [35]. Szilagyi et al. [36] stressed the importance of a careful screening of the lumen, looking at irregularities and angulation. In the experience of McGowan et al. [37], in 2/11 cases, arteriography failed to evidentiate any dilatation; arteriography may miss the diagnosis in up to one-third of the cases [16, 20]. However, the intraluminal thrombus may not be concentric,

Fig. 12.2  PAA with thrombus projecting into the lumen

arteriography clearly demonstrating its protrusion into the dilated lumen (Fig. 12.2). Even more deceiving, of course, appeared the diagnostic value of arteriography in case of aneurysm thrombosis, possibly complicated by occlusion of the superficial femoral artery [4]. Albeit satisfactorily diagnostic only in some experiences [9], angiography has been routinely used as the only way to obtain reliable information on the inflow tract, the collaterals, and the outflow tract [1, 2, 11, 24, 38, 39]. Raptis et  al. [40] defined arteriography as the most important examination to plan the operative treatment, and the same is assessed by Halliday et al. [25] who performed arteriography in every case, switching to digital subtraction angiography (DSA) since 1985. Irace et  al. [21] proposed, as diagnostic workup after duplex scan, both CT (or MR) and arteriography (only arteriography in ruptured aneurysms). According to Harder et al. [41], DSA is the only necessary examination after a positive

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ultrasound study. In effect, before the diffusion of CT angiography and MR a­ ngiography, there was a general consensus on the necessity of angiography to plan the surgical treatment, often beginning with the choice of approach, and in particular to define the site of the distal anastomosis, i.e., on the lower popliteal or on infrapopliteal vessels [27, 42] (Figs. 12.3 and 12.4). In effect, a careful definition of the state of leg vessels is of crucial importance to assess surgical indication and oper-

ative planning. Still in 2008, Paraskevas et al. [43] considered equally reliable, in the study of the outflow tract, angiography and CT angiography. Arteriography, however, may be completely deceptive in achieving information on the tibial arteries in case of aneurysm thrombosis, especially if acute. Lack of visualization may be the consequence of a very slow flow, but also in case of true occlusion, vessels could be adequately cleared by thromboembolectomy or

Fig. 12.3  Patient operated on in 1978 (sudden worsening of chronic ischemia). Arteriography showing a diseased and aneurysmatic popliteal artery with involvement of the proximal part of tibial arteries. Extended medial approach allowed successful thromboembolectomy of tibial ves-

sels, resection of the diseased arterial segment, and vein interposition between the superficial femoral artery and the tibioperoneal trunk. Left: lateral projection. Right: anteroposterior projection and operative specimen

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a

b

c

Fig. 12.4  Patient operated on in 1980. Rare case of coexisting aneurysmal lesions of the popliteal artery and of the tibioperoneal trunk. (a) Arteriography. (b) Detail of the

distal aneurysm. (c) Operative specimen of the popliteal aneurysm. (d) Operative specimen of the infrapopliteal aneurysm

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d

Fig. 12.4 (continued)

thrombolysis: i.e., failed visualization of tibial arteries on arteriography should not be viewed pessimistically, as stressed by Baird et  al. [44] already in 1966, due to the fact that tibial artery occlusion beyond a popliteal artery aneurysm is likely due to embolism rather than atherosclerotic narrowing. Some authors [15] prefer to omit ­preoperative arteriography and to perform on table arteriography through the popliteal artery (this choice implies a medial access). Currently, the trend is to use DSA for endovascular treatment and to rely on CT angiography, especially in situation of acute ischemia from thrombosis/embolism.

12.2.4 Ultrasonography There are three modalities of visualization of echoed ultrasound signal: A-mode, TM-mode, and B-mode. A (amplitude)-mode gives a linear representation of echoes depending on their amplitude.

TM (time motion)-mode allows to depict graphically moving anatomical structures: e.g., it finds application in the study of cardiac valve dynamics. B (brightness)-mode is the most widely used in the clinic and consists of representing a digital image in which the interfaces which send echoes are more intense and will appear white, while those that do not generate signal will appear black, with an intermediate gray scale [45]. The ultrasound (US) scanning may be performed both along the length and the diameter of a vessel. The aneurysms are characterized by anechogenic lumen and hyperechogenic leaf corresponding to the wall [46]. Based on Doppler effect, US examination of blood vessels allows the study of flow characteristics, according to two modalities: continuous wave Doppler and pulsed wave Doppler [47]. Continuous wave Doppler does not allow the selective detection of a signal, depending on its depth, because the ultrasonic probe detects the signal from any vessel located within the US beam headquarters; however, it has a very wide

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diffusion in the study of superficial vessels, where no significant vascular overlapping takes place. While the probe used for continuous wave Doppler consists of two piezoelectric crystals (one for US beam emission and the other for reception), the pulsed Doppler probe contains one crystal that alternates the US delivery ­function with the receiving one, thus allowing, after a tomographic evaluation of which vessel to study, to obtain a Doppler signal not affected by the depth problem. The pulsed wave Doppler may be applied according to three different modes [48]. In echo-­ Doppler captures, sampling takes place in real time along a line represented by a slider positioned into the vessel to be studied, under US guidance, and allows to obtain a curve describing the flow trend. Color Doppler and power Doppler represent the flow using a colorimetric scale: sampling is not a selected volume but rather an area of interest. In the context of color Doppler, by convention, the red color represents the approaching blood signal, while the blue one represents the flow moving away. Power Doppler allows the measure of intensity and variations of flow over time: the result is a monochromatic representation of the flow, which does not allow to express an evaluation of velocity but is well suited to the study of slow flow and tortuous anatomic district. In the late 1970s [49], at Washington University, Strandness succeeded in combining the B-mode imaging system with a Doppler flow detector, giving origin to the prototype of duplex scan apparatuses. Duplex scan allows to determine the presence and morphology of a PAA, differentiating it from pseudoaneurysms and other popliteal masses, as well as the eventual presence of intraluminal thrombus; the type of intra-­ aneurysmal blood flow, if any; and the characteristics of the inflow tract, the run-off, and the collaterals. B-mode ultrasound began to dominate the stage in diagnosing PAAs from the middle 1970s. One of the first cases (if not properly the first) was described by Sarti et al. [50], who used also A-mode to detect pulsatility; however, only at arteriography they could ascertain the communi-

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cation of the artery with the mass. Rapidly, several reports appeared in the literature, confirming the advantages of US technology [51] in diagnosing PAAs even if not present on clinical examination [13] or not patent and not appreciated at arteriography [52]. Both the possibility of detecting intraluminal thrombus, considered as a precise indication to surgical treatment [24], and the reliability in defining aneurysm size are very important [35]. The superior diagnostic capability of US over arteriography was resolutely asserted [36, 37, 53]. Diagnostic US represents a routine procedure since the second half of the 1970s [54, 55] (Fig. 12.5). Availability of duplex scan and the possibility of performing duplex arteriography further highlighted the diagnostic role of US (Fig. 12.6). In a series of 30 PAAs (in 24 patients), Beseth et al. [56] reported that, in most cases, preoperative evaluation relied only on US.  Ascher et  al. [23] used B-mode imaging for the detection of intraluminal thrombus, followed only by duplex arteriography: also in case of acute aneurysm thrombosis, this may allow the study of outflow vessels, which may not be visualized by contrast arteriography. With this technique, 10/201 cases

Fig. 12.5  1978: our first B-mode documentation of a PAA and its intraluminal thrombus

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Fig. 12.6  Current appearance of a duplex scan study of PAA (courtesy of F. Napoli MD)

of acute threatening limb ischemia were recognized as consequent to acute thrombosis of a PAA [57]. Currently, the potential diagnostic value of US in vascular surgery will probably be enhanced by the use of second-generation ultrasound contrast agents [58].

12.2.5 Computed Tomography (CT) CT allows to analytically explore body districts and structures that are not adequately evaluable with x-ray, at the expense of the high dose of patient exposure and limited contrast resolution. The addition of water-soluble iodine contrast medium administered intravenously allows to study the arterial and venous structures, using techniques such as bolus and bolus tracking to program the spiral CT acquisitions in order to

obtain the convenient enhancement of the structures being examined. Current machines permit the large volume acquisition during the administration of iodine contrast medium and the subsequent multiplanar and three-dimensional reconstruction, obtaining angiographic-like images (e.g., applying maximum intensity projection (MIP) algorithms, after removing the signal from bone structures). CT plays an extremely important role in the diagnostic workup of PAAs, both in acute and chronic situations [59]. Earlier indications, aiming to define the morphology and the anatomical interrelationships of the PAA (Fig.  12.7), were soon modified in order to study the entire arterial system of lower limbs, from abdominal aorta downward, given the frequent association of contralateral and/or extrapopliteal aneurysms. Lower extremity CT angiography can be performed on all the currently available multidetector-­

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a

b

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suggesting a recent thrombotic apposition [61]. The superiority of CT vs. US in depicting the precise characteristics of endoluminal thrombus has been asserted by Lilly et al. [62]. The importance of multislice CT angiography in the diagnosis of PAA has been stressed in several reports [63–65]. Three-dimensional and multiplanar reconstructions are particularly useful in planning surgical or endovascular treatments, demonstrating the degree of aneurysm extension in the sagittal and coronal planes, the relationships with the adjacent structures, and the quality of inflow and outflow. The place of CT angiography as the second line and fundamental investigation, after ultrasonography, has been suggested since the early 1990s [66] and established in more recent years [67] (Fig. 12.8). Huang et  al. [68], from the Mayo Clinic, in 2007, asserted that three-dimensional CT scanning has become the most important pre-­ procedural imaging study, switching to MR angiography in case of renal insufficiency. MR angiography could be also preferred in case of incidentally discovered, asymptomatic, PAA, especially in younger patients, to save radiation dose.

12.2.6 Magnetic Resonance Fig. 12.7  Patient studied in 1996. (a) Contrast arteriography. (b) CT imaging

row CT scanners, with a dedicated imaging protocol for lower extremity run-off evaluation [60]; this imaging procedure allows the identification of the aneurysm, clearly differentiating it from ectasia, and an exhaustive description of its characteristics: location, length, transverse diameter (evaluated perpendicularly to major vascular board), presence of calcification, and, in particular, the type of the eventual ­thrombotic apposition. Detailed information on the eventual intraluminal thrombus is given: if concentric or eccentric, the maximum thickness, the look of its edges, and the possible presence of hyperdensity

Magnetic resonance is particularly useful in the study of intraluminal thrombus [69] (Fig. 12.9): in T1 sequences, lower signal is related to more rapid laminar flow, intermediate signal to organized thrombus, while media-adventitia appear as a surrounding ring of lower intensity; very peculiar is the appearance in T2 sequences: circular areas of very high signal intensity, corresponding to clot (methemoglobin) with interspersed areas of low intensity. Holden et al. [70] suggest MR angiography as the best technique for preoperative assessment, after US examination that remains the mainstay for initial diagnosis and evaluation: axial sequences before contrast allow accurate assessment of size extent; then, MR angiography

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a

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b

Fig. 12.8  Currently available CT angiography imaging. A 70-year-old man, with history of previous endovascular repair of thoracic aorta dissection and abdominal aortic aneurysm, was referred for follow-up of the stent grafts and assessment of lower limb vasculature due to intermittent rest pain in his right calf and foot. (a) CT angiography of thoracic and abdominal aorta was extended to the lower limbs, showing bilateral fusiform PAA. (b, c) Sagittal

c

d

e

MIP (maximum intensity projection) shows the inflow and the outflow of the right PA. (d) Coronal MIP reconstruction of the anterior tibial artery that has diffuse hypodense disease (arrows) likely due to distal embolization from the PAA. (e) Coronal MIP reconstruction shows a diffusely diseased peroneal artery; occlusion of the posterior tibial artery

sequences define the inflow, eventually associAdvantages of MR angiography over CT angiated stenosing lesions, and patency of tibial ography, besides the absence of ionizing radiaarteries. tions, are the accurate characterization of mural Peripheral MR angiography implies the use of thrombus (acute vs. chronic) and the capability of a gadolinium contrast agent; recently, the use of studying the run-off vessels without concern of gadofosveset trisodium has been suggested to parietal calcifications; with CT angiography, calenhance spatial resolution [71]. However, there cified plaques may cause diffuse streak artifacts are also sequences allowing to get angiographic and limit the lumen assessment [70]. However, images without the use of contrast media the evaluation of tibial vessels may be limited [72–74]. because of superimposed venous enhancement. MR angiography examination requires longer Most recent protocols use a hybrid technique acquisition time and is more operator dependent in which a portion of the gadolinium is diluted than CT angiography; however, the post-­ and utilized to acquire a four-dimensional acquiprocessing reconstructions are more automated sition of the tibial and pedal vessels. Time-­ and faster. A peripheral MR angiography image resolved MR angiography [75] offers the benefit usually subtracts the background structures, of both morphology and temporality, allowing highlighting only the enhanced vessels, thereby the blood flow to be visualized in real time as it eliminating possible issues from adjacent struc- enters the popliteal artery and the infrapopliteal tures such as bones [73]. vessels).

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a

b

c

d

Fig. 12.9  Case of large-size PAA studied in 1987. (a) Echography. (b) Arteriography. (c) MR imaging. (d) Operative specimen, opened: the huge concentric thrombus, with onion-like appearance

12.2.7 Differential Diagnosis Problems of differential diagnosis may arise in the presence of a nonpulsatile popliteal mass [5]. In effect, at clinical examination, particularly in lack of a suggestive anamnesis, a thrombosed PAA may be confused with a number of benign and malignant pathologies [76, 77]. Crichlow and Roberts [38] highlighted the problem of distinguishing a thrombosed PAA from tumors and Baker’s cysts, as well as the possibility of the abscess-like presentation of a ruptured PAA, as reported by Gage [78]. But, in case of rupture, misdiagnosis is not infrequent (see Chap. 11). Initial misdiagnosis as a Baker’s cyst has been reported in a number of cases [37]. Baker’s cysts may be associated with impairment of arterial flow from compression upon the popliteal artery [79], but vein compression is more frequent:

Langsfeld et al. [80] found a Baker’s cyst in 3.1% of 3072 cases studied for suspected deep vein thrombosis (DVT) (and in 92%, there was no any sign of DVT). In 1956, Taber and Lawrence [81] reported the case of a popliteal mass, which, after non-conclusive needle aspiration, was submitted to surgical exploration; in effect, it was a PAA and the abundant hemorrhage was controlled with a hasty suture producing severe distal ischemia; patient and limb were rescued with a bypass (arterial homograft) performed after transfer to a university hospital. Then, several cases of PAAs initially misdiagnosed as Baker’s cysts and submitted to invasive diagnostic procedures or to surgical exploration have been reported [2, 82]. Numbers are small, but the suspicion about a not rare initial misdiagnosis is strong. Still in 2009, Hashimoto et al. [83] reported a case of puncture of a supposed Baker’s cyst: the ensuing hemorrhage was controlled by prolonged compression,

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followed by the correct treatment of the PAA. Solheim and Wilhelmsen [84], on the basis of their experience, assert that the confusion between Baker’s cysts and PAAs is common enough to warrant constant attention. Since the early experience with ultrasound investigation of the popliteal space [85], the diagnosis of Baker’s cyst should be rather easy. However, about 20% of Baker’s cysts may be complex [86], with multiple lobulations, septations, and extension into the calf: in such cases, MRI may be very useful. More difficult and intriguing may be the differential diagnosis of soft tissue tumors. Ross et al. [69] described the case of a huge popliteal mass initially diagnosed as sarcoma, on the basis of plain x-ray and MRI; open biopsy revealed the vascular nature of the mass, and arteriography confirmed the diagnosis of PAA.  In the case reported by Davidovic et al. [87], the initial diagnosis of muscle tumor led to surgical exploration; as a result, the patient was transferred to a vascular service with a ruptured and infected PAA. Also in the case report by Funahashi et al. [88], the correct diagnosis of PAA was possible only during operation for a mass which had been defined as a tumor on the basis of echography, angiography, and MRI. Bigatel et al. [89] reported two cases of suspected PAA (one 6 years after exclusion and bypass) in which fine needle aspiration (FNA) revealed the sarcomatous nature of the mass. Similarly, Cristaudo et  al. [90] posed the initial diagnosis of enlarging PAA 18  months after exclusion and bypass. FNA allowed the diagnosis of primary angiosarcoma (in this case, however, the patient was already affected by metastatic spread). A case of popliteal angiosarcoma 4 years after exclusion and bypass of PAA is described by Cherchi and Camparini [91]. Conversely, Lee et al. [92] report the case of a heterogeneous mass compressing a femoropopliteal bypass suspected to be a sarcoma on the basis of spindle cells found in the FN aspirate, while the correct diagnosis was enlarging PAA: the previous (12 years) treatment of PAA by exclusion and bypass had been missed on initial anamnesis. It is clear that a meticulous anamnesis and the careful interpretation of imaging studies would, almost always, lead to the correct diagnosis;

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however, sometimes, this could be really difficult. Smits et al. [93] reported four cases of popliteal mass in which MRI did not allow a conclusive diagnosis, possible only at surgical exploration; these cases were respectively liposarcoma, pyomyositis, pseudoaneurysm, and empyemic thrombosed PAA. Coexistent PAA (previously excluded) and angiosarcoma are an exceptional occurrence [94]. Rarely, and ascertained only at microscopy [95], a PAA may harbor the so-called Masson’s pseudoangiosarcoma or intravascular papillary endothelial hyperplasia [96], which is commonly considered [97] an unusual reactive thrombotic organization.

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12  Diagnostic Procedures 50. Sarti DA, Louie JS, Lindstrom RR, Nies K, London J.  Ultrasound diagnosis of a popliteal artery aneurysm. Radiology. 1976;121:707–8. 51. Scott WW Jr, Scott PP, Sanders RC. B-scan ultrasound in the diagnosis of popliteal aneurysms. Surgery. 1977;81:436–41. 52. Davis RP, Neiman HL, Yao JST, Bergan JJ. Ultrasound scan in diagnosis of peripheral aneurysms. Arch Surg. 1977;112:55–8. 53. Takolander RJ, Bergqvist D, Bergentz S-E, Ericsson BF, Sigurjonsson S, Jonsson K.  Aneurysms of the popliteal artery. Acta Chir Scand. 1984;150:135–40. 54. Anton GE, Hertzer NR, Beven EG, O’Hara PJ, Krajewski LP. Surgical management of popliteal aneurysms: trends in presentation, treatment and results from 1952 to 1984. J Vasc Surg. 1986;3:125–34. 55. Dawson I, van Bockel JH, Brand R, Terpstra JL.  Popliteal artery aneurysms: long-term follow-up of aneurysmal disease and results of surgical treatment. J Vasc Surg. 1991;13:398–407. 56. Beseth BD.  The posterior approach for repair of popliteal artery aneurysms. J Vasc Surg. 2006;43:940–5. 57. Kallakuri S, Ascher E, Hingorani A, Markevitch N, Schutzer R, Hou A, Nahata S, Jacob T, Yorkowich W. Impact of duplex arteriography in the evaluation of acute lower limb ischemia from thrombosed popliteal aneurysms. Vasc Endovascular Surg. 2006;40:23–5. 58. Bredhal K, Mestre XM, Vila Coll R, Ghulam QM, Sillesen H, Eiberg J. Contrast-enhanced ultrasound in vascular surgery: review and update. Ann Vasc Surg. 2017;45:287–93. 59. Wright LB, Matchett WJ, Cruz CP, James CA, Culp WC, Edit JF, McCowan TC.  Popliteal artery disease: diagnosis and treatment. Radiographics. 2004;24:467–79. 60. Cook TS.  Computed tomography angiography of the lower extremities. Radiol Clin N Am. 2015;54:115–30. 61. Jarraya M, Simmons S, Farber A, Tevtelbovm O, Naggara N, Guermazi A. Uncommon diseases of the popliteal artery: a pictorial review. Insights Imaging. 2016;7:679–88. 62. Lilly MP, Flinn WR, McCarthy WJIII, Courtney DF, Yao JST, Bergan JJ. The effect of distal arterial anatomy on the success of popliteal aneurysm repair. J Vasc Surg. 1988;7:653–60. 63. Beregi JP, Djabbari M, Desmoucelle F, Willoteaux S, Wattine L, Louvegny S.  Popliteal vascular disease: evaluation with spiral CT angiography. Radiology. 1997;203:477–83. 64. Piccoli G, Gasparini D, Smania S, Sponza M, Marzio A, Vit A, Bazzocchi M. Multislice CT angiography in the assessment of peripheral aneurysms. Radiol Med. 2003;106:504–11. 65. Deglise S, Qanadli SD, Rizzo E, Ducrey N, Doenz F, Haller C, Denys A, Corpataux J-M. Long-term follow-­up of surgically excluded popliteal artery aneurysms with multi-slice CT-angiography and Doppler ultrasound. Eur Radiol. 2006;16:1323–30.

175 66. Roggo A, Brunner U, Ottinger LW, Largiader F. The continuing challenge of aneurysms of the popliteal artery. Surg Gynecol Obstet. 1993;177:565–72. 67. Mezzetto L, Scirgine L, Pacca R, Puppili G, Perandini S, Veraldi GF.  Treatment of popliteal artery aneurysms by means of cryopreserved homograft. Ann Vasc Surg. 2015;29:1090–6. 68. Huang Y, Gloviczki P, Noel AA, Sullivan TM, Kaira M, Gullerud RE, Hoskin TL, Bower TC. Early complications and long-term outcome after open surgical treatment of popliteal artery aneurysms: is exclusion with saphenous vein bypass still the gold standard? J Vasc Surg. 2007;45:706–15. 69. Ross GJ, Ross LV, Hartz WH, Fairman RM.  Case report 723. Skeletal Radiol. 1992;21:190–3. 70. Holden A, Merrilees M, Mitchell N, Hill A. Magnetic resonance imaging of popliteal artery pathologies. Eur J Radiol. 2008;67:159–68. 71. Galizia MS, Ward E, Rodriguez H, Collins J, Carr J.  Improved characterization of popliteal aneurysms using gadofosveset-enhanced equilibrium phase magnetic resonance angiography. J Vasc Surg. 2013;57:837–41. 72. Velazquez OC, Baum RA, Carpenter JP.  Magnetic resonance angiography of lower-extremity arterial disease. Surg Clin N Am. 1998;78:519–37. 73. Jens S, Koelemay MJ, Reekers JA, Bipat S. Diagnostic performance of computed tomography and contrast-­ enhanced magnetic resonance angiography in patients with critical limb ischaemia and intermittent claudication: systematic review and meta-analysis. Eur Radiol. 2013;23:3104–14. 74. Altaha MA, Jaskolka JD, Tan K, Rick M, Schmitt P, Menezes RJ, Wintersperger BJ.  Non-contrast-­ enhanced MR angiography in critical limb ischemia: performance of quiescent-interval single-shot (QISS) and TSE-based subtraction techniques. Eur Radiol. 2017;27:1218–26. 75. Hadizadeh DR, Marx C, Gieseke J, Schild HH, Willinek WA.  High temporal and high spatial resolution MR-angiography (4D-MRA). RoFo. 2014;186:847–59. 76. Beals RK, Lee TG, Knochel JQ, Henderson S.  Ultrasound as a diagnostic aid in the evaluation of popliteal swelling. Clin Orthop Relat Res. 1980;149:220–3. 77. Scully RE, Mark EJ, McNeely BU, Osteen RT, Rosenberg AE.  Case records of the Massachusetts General Hospital—Case 49–1991: a 46-year-old man with a mass in the popliteal fossa. N Engl J Med. 1991;325:1635–43. 78. Gage M.  Inflamed arterial popliteal aneurysm simulating acute abscess. Ann Surg. 1957;145:893–7. 79. Olcott CIV, Mehigan JT.  Popliteal artery stenosis caused by a Baker’s cyst. J Vasc Surg. 1986;4:403–5. 80. Langsfeld M, Matteson B, Johnson W, Wascher D, Goodnough J, Weinstein E.  Baker’s cyst mimicking the symptoms of deep vein thrombosis: diagnosis with venous duplex scanning. J Vasc Surg. 1997;25:658–62.

176 81. Taber RE, Lawrence MS.  Resection and arterial replacement in the treatment of popliteal aneurysms. Surgery. 1956;39:1003–12. 82. Galland RB, Magee TR.  Management of popliteal aneurysms. Br J Surg. 2002;89:1382–5. 83. Hashimoto W, Yamada T, Matsumaru I.  Popliteal artery aneurysms and popliteal phymas. Ann Thorac Cardiovasc Surg. 2009;15:64–7. 84. Solheim K, Wilhelmsen T.  Popliteal aneurysms. Scand J Thorac Cardiovasc Surg. 1972;11:255–8. 85. McDonald DG, Leopold GR. Ultrasound B-scanning in the differentiation of Baker’s cyst and thrombophlebitis. Br J Radiol. 1972;45:729–32. 86. Janzen DL, Peterfy CG, Forbes JR, Tirman PFJ, Genant HK. Cystic lesions around the knee joint: MR imaging findings. Am J Radiol. 1994;163:155–61. 87. Davidovic LB, Lotina SL, Kostic DM, Cinara IS, Cveltkovic SD, Markovic DM, Vojnovic BR. Popliteal artery aneurysms. World J Surg. 1998;22:812–7. 88. Funahashi S, Furuyama T, Hamatsu T, Inoue H, Tomisaki S, Iso Y.  A case of an aneurysm of the popliteal artery differentiated with difficulty from a soft tissue tumor of the lower limb. J Jap Surg Ass. 2003;54:2054–7. 89. Bigatel DA, Franklin DP, Meschter SC, Elmore JR, Youkey JR. Popliteal sarcomas masquerading as popliteal aneurysms. Case reports. Vasc Endovascular Surg. 1998;32:627–32.

A. Cannavale et al. 90. Cristaudo A, Steffen C. Not just a popliteal aneurysm: a case of metastatic epithelioid angiosarcoma. Eur J Vasc Endovasc Surg. 2012;23:e50–2. 91. Cherchi M, Camparini S.  Late presentation of popliteal angiosarcoma after previously treated popliteal artery aneurysm. Eur J Vasc Endovasc Surg. 2017;54:463. 92. Lee C, Deitch JS, Gwertzman GA, D’Ayala M, McGagh DA, Gosh B, Zenilman M.  Enlargement of previously ligated popliteal aneurysm causing venous bypass graft occlusion. Ann Vasc Surg. 2005;19:909–12. 93. Smits TM, van den Dungen JJAM, Schraffordts KH, Mooyaart EL, Hoekstra HJ.  Een zwelling distal in her bovenbeen. Ned Tijdschr Geneeskd. 1998;142:1697–701. 94. Di Saverio G, Magne JL, Farah I, Pasquier BE.  Angiosarcoma associated with aneurysm of the popliteal artery. Eur J Surg. 1995;161:53–5. 95. MacMahon GG, Mikhail HM, Molyneux J, Thomas DV, Hicks RCJ.  Masson’s pseudoangiosarcoma in a popliteal aneurysm: tumor or thrombus? Cause or effect? Ann Vasc Surg. 2010;24:257e1–3. 96. Masson M.  Hemangioendothelioma végétante intravasculaire. Bull Soc Anat. 1923;93:517–23. 97. Del Rio E, Aguilar A, Sanchez YE. Intravascular papillary endothelial hyperplasia: a reorganizing thrombus. Int J Dermatol. 1992;31:713–4.

Part VI Atherosclerotic Popliteal Aneurysms: Surgical Treatment

Operative Indication, Surgical Approach, and Tactics

13

Antonino Cavallaro

13.1 Operative Indication At the beginning of the second half of the last century, both the certainty about the need of surgical treatment for symptomatic/complicated PAAs and the quandary about what to do for asymptomatic ones entered the stage. Just to cite only some relevant reports: –– Linton [1], reviewing the experience in 1929– 1947 at Massachusetts General Hospital, observed that of 22 limbs with a PAA (in 15 patients), 11 underwent primary amputation at presentation and 6 were waiting for treatment. –– Janes and Ivins [2], from the Mayo Clinic, stressed the importance of surgical treatment before the onset of complications, highlighting the likelihood of embolic events with ensuing occlusion of distal vessels. –– Gifford et al. [3] followed up (mean 46 months) 45 PAAs initially noncomplicated: 13 (29%) became complicated and 5 limbs were lost. –– Wychulis et al. [4] published a meticulous and extended follow-up of 57 symptomatic PAAs not submitted initially to surgical treatment: significant worsening was registered in 19 (33.3%). They also followed up for years 87

A. Cavallaro (*) Past Professor of General Surgery, “Sapienza” University, Rome, Italy © Springer Nature Switzerland AG 2021 A. Cavallaro (ed.), Aneurysms of the popliteal artery, https://doi.org/10.1007/978-3-030-49687-6_13

small PAAs, asymptomatic/uncomplicated at presentation: 25 (31%) became symptomatic or complicated (5 were operated on with one postoperative death and 3 limbs were amputated). In Chap. 11, we tried to analyze some series in which a conservative treatment was chosen for asymptomatic PAAs, with conflicting results and the sensation that the eventual onset of complications is scarcely predictable. The continuing trend is to operate on PAAs with a diameter of 2  cm or more and/or with mural thrombus. This attitude, in particular regarding the size, dates back to Szilagyi et  al. [5], who suggested that a PAA 25 mm). They observed that risk factors for an accelerated growth were initial diameter and presence of thrombus, concluding, however, that the growth rate is generally unpredictable.

A. Cavallaro

Lack of complications has been reported also for large aneurysms: Ginzburg et al. [22] reported an 80-year-old patient with a PAA of 4 × 3 cm, with inside thrombus, complaining of mild claudication, who remained stable for size and symptoms during 4 years. But it is wise to keep present that a swallow does not make a summer. Focusing on the current situation, there are two criteria generally used to establish surgical indication, none of them however having an absolute value: 1. Size. The diameter of 20 mm is considered the watershed dimension. However (see Chap. 11), also smaller aneurysms may undergo significant complications. This limit is lowered to 17 mm [9] on account of the good results of preventive surgery. Stone et  al. [23] put the limit at 17.5 mm, following anyway the basic criterium of a diameter double than that of the normal adjacent artery. From Royal Berkshire Hospital, UK [24], comes the suggestion of putting the cutoff at a diameter of 30 mm as no complication was observed following up 5 PAAs 10 mm. Distal landing zone not beyond the infragenicular popliteal artery B: Mismatch >2 mm between proximal and distal landing zones; acute ischemia at presentation C: p.o. medication ASA 100 mg initially; after 2009, ASA 100 mg and clopidogrel 75 mg for 6 months and then clopidogrel 75 mg indefinitely E: Non-percutaneous H: See C I: Duplex ultrasound; median follow-up 22 months Speziale et al. 2015 [18]; two centers; Jan. 2004 to Dec. 2013; retrospective; 53 cases A: Symptomatic (12/53, 22,6%; pre-op. thrombolysis 8); asymptomatic if diam. > 20 mm or huge mural thrombus; landing zones at least 15 mm; at least one runoff vessel patent B: Age 5 mm between proximal and distal landing zones D: General or local E: Percutaneous up to 9F diameter of the introducing sheath F: Oversize 10–15% G: At least 20 mm H: Clopidogrel 75 mg, ASA 100 mg I: Duplex scan; mean follow-up 37.4 ± 29.3 months Note: distal landing zones: 50 below the knee level; three tibioperoneal trunk (ant. tib. artery occluded) Ronchey et al. 2015 [19]; single center; 2000–2013; retrospective; from Jan. 2004 included in Speziale et al. [18]; 25 cases A: Symptomatic (pre-op. thrombolysis 4); asymptomatic if diameter > 20 mm; landing zones at least 15 mm B: No runoff vessel patent C: Up to 2010, only patients at high risk for conventional surgery; later on, all patients with unavailable greater saphenous vein D: General 20%; local 80% E: Cut-down 68%, percutaneous 32% F: Oversize 1 mm K: Dual antiplatelet regimen for at least 1 month I: Duplex scan; mean follow-up 49 months (1–145) Leake et al. 2016 [20]; single center; Jan. 2006 to March 2014; retrospective; 76 cases A: Seven acute ischemia (four pre-op. thrombolysis); five claud./rest pain; three rupture; 61 asymptomatic. Landing zone below the aneurysm of adequate diameter and at least 20 mm before any tibial takeoff; runoff score 30 months follow-up. Two cases were reported, always in 1999, by De Blas et al. [9] One case presented with acute ischemia and was initially treated with thrombol20.5 Gore-Excluder (W.L. Gore & ysis and successively with stenting with two Ass., Flagstaff, AZ, USA) Wallstent: after 11  months, loss of overlapping ePTFE combined with a thin non-permeable was treated with additional stenting with patency layer of ethylene propylene attached to a nitinol maintained for 25  months after the first procedure. The second case, too, presented with acute stent frame.

20  Other Stent Grafts and Hybrid Procedures

ischemia from thrombosis of the superficial femoral artery and of a graft used to treat an aneurysm of the upper PA; after thrombolysis, an aneurysm of the middle PA was put into evidence; treatment with a Wallstent allowed patency of the reconstruction with aneurysm thrombosis up to 47  months. In both cases, control angiography immediately after stenting revealed only minimal blood leakage through the mesh. But the use of bare stents was overcome by the availability of stent grafts. From May 2009, however, the introduction of the Multilayer Flow Modulator (Cardiatis, Isnes, Belgium) has brought a new paradigm, shifting from the concept of structural barrier to that of functional barrier [10]. This tubular self-­ expanding stent consists of multilayer braided wires of cobalt alloy and acts after the Venturi effect. The main and peculiar functions of the stent were clearly outlined by E.B. Diethrich at a meeting of the Arizona Heart Foundation on June 8, 2014 (retrievable through the Internet): • It eliminates the flow vortex pressure (with the ensuing wall damage) and redirects flow in the same direction of systolic pressure. • Not allowing the vortex to be formed, a laminar flow is produced in the main channel and toward collaterals. These theoretical and experimental characteristics would allow flow maintenance in the main artery and collaterals and produce organized clots in the sac with progressive shrinkage of the same; also, the risk of rupture should be lowered [11]. On these bases, aneurysms have been reclassified following the morphology (saccular, fusiform) and the presence of collaterals (from the neck, from the sac, from both). Maintained patency of collaterals has been demonstrated in several instances as well as the sac shrinkage. Henry et al. [12] have observed that sac shrinkage may take weeks or months to be complete, depending on several factors, such as the diameter of the

289

efferent vessel, the initial aneurysm size, the weakness of the sac walls, and the presence of collaterals; moreover, the Venturi effect may be reduced in case of ostial stenosis, suggesting the opportunity of PTA before stenting [10]. The use of MFM to treat PAAs (Fig. 20.2) is still scantily reported, while relatively abundant is the literature for aortic and visceral aneurysms. Sfyoeras et  al. [13], reviewing the literature, found 1 case reported in a full article [14] and 4 cases in 12 published abstracts of international congresses. Ruffino et  al. [10], in the second report of the Italian multicenter registry on repair of peripheral and visceral aneurysms with the MFM (June 2009–June 2010: 1-year results), quote six cases, and no occlusion is mentioned; in one case, however, a type-III endoleak was observed at 3  months for loss of overlapping between the two stents (successfully treated with additional stent). This occurrence suggested that overlapping, if any, should be at least of 3 cm. Thakar and Chadhuri [15] treated six aneurysms in five patients, all cases with satisfactory landing zones and three-vessel outflow. Three stents occluded within 6  months, two (in the same patients) owing to a prothrombotic state (factor V Leiden), and one in a case of omission of the antiplatelet therapy; three stents were patent at a follow-up of 5.8  months (3–12), one showing shrinkage in spite of a persistent endoleak, while two showed narrowing at the knee joint level. Henry et al. [12] reported one case occluded at 30 days for poor compliance to antiplatelet therapy, successfully treated with fibrinolysis and PTA. Antoniou et al. [16] treated three patients with bilateral aneurysm. All six procedures were patent at a follow-up of 7.6  months, but three had required reintervention, two for thrombosis treated with thrombolysis and PTA and one for stent dislocation treated with additional stenting. Borges-Dominguez et  al. [2] reported two cases, of which one occluded at 12 days and was treated conservatively.

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a

b

c

Fig. 20.2 (a) Selective angiography of the popliteal artery, with the knee flexed (left) and extended, shows aneurysm of the popliteal artery with collaterals emerging from the distal neck. (b) Control angiography after stent-

ing with a multilayer flow modulator. (c) Color Doppler control at 6  months: patency of the stent and complete exclusion of the aneurysmal sac

20.7 Hybrid Procedures

particularly the avoidance of surgical access to the knee and leg regions. The hybrid procedure proposed by Joyce et al. [17] has been described above as a variant to the use of the Cragg EndoPro System. Puech-Leão et al. [18] (Fig. 20.3) constructed a graft with a 20-cm-long segment of saphenous vein sutured to a Palmaz stent at its upper extremity, after stripping the valves with a valvulotome. With the patient in the prone position, the distal

Hybrid procedures have been proposed to couple the advantages of endovascular technology with those of classic surgery, at the same time trying to avoid the drawbacks of stent grafting and the potentially dangerous steps of the latter. Albeit ingenuous and really feasible, they do not satisfy some of the attractive premises of endovascular procedures like the reduced operative time and

20  Other Stent Grafts and Hybrid Procedures

a

b

c

d

Fig. 20.3  The hybrid procedure proposed by Puech-Leão et al. [18]. (a) A 20-cm-long segment of saphenous vein has been harvested, the valves stripped with a valvulotome and the proximal end enlarged by two opposite vertical incisions and the application of two triangular vein patches. (b) A Palmaz stent is sutured to the enlarged part of the vein; only 1 cm of stent is left uncovered. (c) The stent is manually compressed over a balloon (not represented). (d) The stented graft has been introduced through the transected distal popliteal artery and the stent dilated and fixed in the superficial femoral artery; the distal anastomosis is fashioned end-to-end: the proximal end includes the stumps of the artery and of the vein graft (from the original, with permission, modified)

popliteal artery was prepared and transected and the graft was delivered through the proximal stump, dilating the stent when the deliver was

291

complete. Finally, the popliteal artery was reanastomosed end-to-end, including the distal stump of the vein graft. The procedure was successful, and patency was documented after 2 months. Rosenthal et al. [19, 20] treated 10 cases with an in situ saphenous vein bypass and successive coil embolization of the PAA (Fig.  20.4); comparing this series with a contemporary series of classic surgery (12 cases submitted to bypass and ligature above and beyond the aneurysm), they observed that the proposed procedure implied a longer operative time but a reduced blood loss and the absence of wound complications (in 7/10 cases, only two incisions were sufficient), as well as a shorter inhospital stay (2.1 days); in the classic group, 3 patients had wound complications and inhospital stay was 6.2 days. At a mean follow-­up of 13.6 months (4–23), one bypass occlusion was observed in each group. More recently, Hingorani et al. [21] proposed a technique to repair behind the knee PAAs, when the posterior approach was deemed inadequate and the medial one is nonoptimal. The technique avoids dissection around the aneurysm, reducing blood loss and morbidity. They performed a bypass ending onto the distal popliteal or posterior tibial artery, after the popliteal artery had been ligated distal to the aneurysm; then, coils were delivered into the sac through the superficial femoral artery, and finally, the popliteal artery was ligated cranial to the aneurysm. This would substitute the direct treatment of aneurysm sac by resection or opening and branch occlusion from inside, which the authors usually performed with aneurysms located above or beyond the knee. Out of the 88 patients observed in the period 2001–2006, 13 were treated with this hybrid technique aimed to prevent continuing growth of the aneurysm from retrograde perfusion through the branches. At a follow-up of 11.6 ± 9.6 months, the technique was successful in 12 cases, but in 1 case, continuing size increase by reperfusion was observed and ligation of collaterals was performed through a posterior approach.

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a

b

c

d

Fig. 20.4  The hybrid procedure proposed by Rosenthal et al. [19, 20]. (a) After endoscopic excision of valves and coil occlusion of the collaterals, the saphenous vein has been transected and the stump is ready for anastomosis onto the common femoral artery. (b) The distal popliteal artery has been divided and the proximal stump oversewn.

References 1. Ferreira M, Medeiros A, Monteiro M, Lanziotti L.  Alternativa técnica no tratamento endovascular dos aneurismas de artéria poplitea. J Vasc Bras. 2008;7:44–8. 2. Borges DR, Camacho Oliveira Araüjo A. Endovascular treatment of popliteal artery aneurysm. Early and midterm results. Rev Col Bras Cir. 2015;42:37–42. 3. Nishi M, Zen K, Yamaguchi S, Asada S, Kambayashi D.  Popliteal artery aneurysm treated with implantation of a covered stent graft (Fluency) reinforced with a nitinol stent S.M.A.R.T.  Cardiovasc Interv Ther. Published online 18 November 2015. 4. Henry M, Amor M, Henry J, Klonaris C, Tzvetanov K, Buniet JM, Amicabile C, Drawin T. Percutaneous endovascular treatment of peripheral aneurysms. J Cardiovasc Surg (Torino). 2000;41:871–83. 5. Cina CS, Moore R, Maggisano R, Kucey D, Dueck A, Rapanos T. Endovascular repair of popliteal artery aneurysms with Anaconda limbs: technique and early results. Catheter Cardiovasc Interv. 2008;72:716–24. 6. Mohan IV, Bray PJ, Harris JP, May J, Stephen MS, Bray AE, White GH.  Endovascular popliteal aneurysm repair: are the results comparable to open surgery? Eur J Vasc Endovasc Surg. 2006;32:149–54.

(c) After completion of the bypass, a catheter is introduced into the artery, caudal to proximal anastomosis, to deliver coils within the aneurysm. (d) Final aspect of the aneurysm and of the popliteal artery (from the original, with permission, modified)

7. Kaur P, Semder C, Denning D, Korona M Jr, Edwards JC.  Endovascular treatment of a popliteal artery aneurysm associated with arteriomegaly. J Surg Res. 2007;137:306. 8. Müller-Hülsbeck S, Link J, Schwarzenberg H, Walluscheck KP, Heller M.  Percutaneous transluminal stent and stent-graft placement for the treatment of femoropopliteal aneurysms: early experience. Cardiovasc Intervent Radiol. 1999;22:96–102. 9. De Blas M, Merino S, Ortiz F, Egana J, Lobrano MB, Lopera J, Gonzalez A, Maynar M. Treatment of popliteal artery aneurysms with uncovered Wallstents. Cardiovasc Intervent Radiol. 1999;22:336–3. 10. Ruffino MA, Rabbia C, The Italian Cardiatis Registry Investigators Group. Endovascular repair of peripheral and visceral aneurysms with the Cardiatis multilayer flow modulator: one-year results from the Italian Multicenter Registry. J Endovasc Ther. 2012;19:599–610. 11. Fossaceca R, Guzzardi G, Stanca C, Cerini P, DiGesù I, Carriero A. Effectiveness of the multilayer stent in the treatment of peripheral vascular diseases. Eur Soc Radiol Congress ECR 2012, poster C-0647. 12. Henry M, Benjelloun A, Henry I, Wheatley G.  The multilayer flow modulator stent for the treatment of arterial aneurysms. J Cardiovasc Surg (Torino). 2013;54:763–83.

20  Other Stent Grafts and Hybrid Procedures 13. Sfyoeras GS, Dalainas I, Giannakopoulos TG, Antonopoulos K, Kakisis JD, Liapis CD.  Flow-­ diverting stents for the treatment of arterial aneurysms. J Vasc Surg. 2012;56:839–46. 14. Pulli R, Dorigo W, Fargion A, Pratesi G, Alessi IA, Angiletta D, Pratesi C.  Comparison of early and midterm results of open and endovascular treatment of popliteal artery aneurysms. Ann Vasc Surg. 2012;26:809–18. 15. Takar T, Chadhuri A. Early experience with the multilayer aneurysm repair stent in the endovascular treatment of trans/infragenicular popliteal artery aneurysms: a mixed bag. J Endovasc Ther. 2013;20:381–8. 16. Antoniou GA, Schiro A, Smyth JV, Murray D, Farquharson F, Serracino-Inglott F.  Multilayer stent in the treatment of popliteal artery aneurysms. Vasa. 2012;41:383–7. 17. Joyce WP, McGrath F, Lehay AL, Bouchier-Hayes D.  A safe combined surgical/radiological approach

293 to endoluminal graft stenting of a popliteal aneurysm. Eur J Vasc Endovasc Surg. 1999;10:489–91. 18. Puech-Leão P, Kauffman P, Wolosker N, Maiera AM.  Endovascular grafting of popliteal ­ aneurysm using the saphenous vein. J Endovasc Surg. 1998;5:64–70. 19. Rosenthal D, Atkins C, Shuler FW, Jerius HS, Clark MD, Matsuura JH. Popliteal artery aneurysm treated with a minimally invasive endovascular approach: an initial report. J Endovasc Surg. 1998;5:60–3. 20. Rosenthal D, Matsuura JH, Clark MD, Kirby LB, Knoepp LF.  Popliteal artery aneurysms: is endovascular reconstruction durable? J Endovasc Ther. 2000;7:394–8. 21. Hingorani AP, Ascher E, Marks N, Shiferson A, Puggioni A, Tran V, Patel N, Jacob T. Hybrid approach for treatment of behind the knee popliteal artery aneurysms. Vascular. 2009;17:290–2.

The Current Role of Endografting

21

Fabrizio Fanelli, Pierleone Lucatelli, Carlo Cirelli, Renato Argirò, Filippo Maria Salvatori, and Antonino Cavallaro

As a matter of fact, endovascular treatment of popliteal artery aneurysms (PAAs) has dramatically increased, during a relatively short period. This is not a uniform phenomenon; in 2014, Björck et al. [1], reviewing data (from Jan. 2009 to Jan.2013) from eight countries, found a great variability, from zero (Switzerland: 0/87 PAA repairs) to 29.5% (Sweden: 146/495) and a maximum of 34.7% (Australia: 153/441). Cervin et  al. [2], consulting the Swedish Vascular Registry, observed an almost fourfold increase of endovascular procedures (E) in the period 2008–2012, compared with the early period 1994–2001. Galiñanes et al. [3], studying the phenomenon through the registries of US Medicare population for the period 2005–2007, observed the increase of E from 11.7% to 23.6%; F. Fanelli (*) Vascular and Interventional Radiology Department, “Careggi” University Hospital, Florence, Italy e-mail: [email protected] P. Lucatelli · F. M. Salvatori Interventional Radiology Unit, “Sapienza” University, Rome, Italy C. Cirelli Interventional Radiology Unit, “Belcolle” Hospital, Viterbo, Italy R. Argirò Department of Diagnostic Imaging, Interventional Radiology, University “Tor Vergata”, Rome, Italy A. Cavallaro Past Professor of General Surgery, “Sapienza” University, Rome, Italy © Springer Nature Switzerland AG 2021 A. Cavallaro (ed.), Aneurysms of the popliteal artery, https://doi.org/10.1007/978-3-030-49687-6_21

conversely, open procedures (O) decreased from 88.3% to 76.4%. Eslami et al. [4], retrieving data from 290 centers in the USA and Canada, observed the increase of E from 34.8% in 2010 to 47.6% in 2013. Trying to analyze the reasons for this really impressive success of E is not an easy matter, given the absence of randomized trials (but for the weak attempt of Antonello et al. [5]). A scientific background for the building of statements defining if E is superior to O or at least represents an equivalent alternative to O is still lacking. On the other side, many cases of PAA could be treated by endografting. Zimmermann et  al. [6], reviewing their experience in the period 2000–2007, tried to define how many of the cases they treated surgically could have been managed with endovascular procedure: considering as inclusion criteria for endografting the patency of iliofemoral tract, the existence of landing zones of at least 2 cm, and the patency of at least one outflow vessel, they observed that 22 (60%) aneurysms were considered eligible for endografting, two (5%) relatively eligible (but with complete sac thrombosis), and only 13 (35%) inappropriate. No doubt that E, owing to its truly reduced invasivity, is frankly attractive. With the refinements of the profile of devices, most cases may be treated percutaneously, relying on local anesthesia. General anesthesia is still reported in some experiences, ranging from 10–20% of the 295

F. Fanelli et al.

296 Table 21.1  Comparison of mean in-hospital stay (days) between open (O) and endovascular (E) procedures Author Pulli [15] Stone [16] Galinanes [3] Huang [17]

Study period Jan. 2000 to Dec. 2011 2001–2011

Leake [19]

2005–2007 Jan. 2005 to June 2012 2010–2013 Jan. 1994 to Nov. 2014 2006–2014

Wooster [20]

1999–2013

c

c

Eslami [4] Von Stumm [18]

c

O 10.4

E 4.4

7.3a 14.0b 4 4.2a

3.4a 5.0b 1 1.9a

3.8 7.3

1.4 3.5

5.8 4.6a 12

1.6 1.3a 2

Only elective cases Only urgent cases c Review, non-original data a

b

cases [7, 8] to about 50% [9], but local anesthesia was used in the totality of cases of several series [10–14]. Reduced in-hospital stay is another immediately apparent (and statistically significant) advantage of E (Table 21.1).

21.1 Review and Meta-analysis of the Results of Endografting Treatment of PAAs From 2007, several papers appeared in the literature attempting to compare the global results of endovascular and open surgical treatments of PAAs and to define what should be considered the gold standard. They relied on the available published data as well as on dedicated registries and Medicare database. The search for this El Dorado is still ongoing and will probably remain fruitless until the concept of gold standard does not undergo a more realistic configuration (Tables 21.2 and 21.3). Some papers offer an approximative survey and a rough evaluation of the problem, without an adequate statistical evidence; however, being based on large numbers (keeping into account the rarity of the disease), they may be orientative, putting into evidence how difficult it is to enunciate precise statements in this field.

More scientific papers attempt to perform a meta-analysis with final statistical strength, but this obliges to include into the study a low number of reports and consequently a number of cases that may be nonrepresentative of the patients effectively treated in daily practice in a certain period of time. Almost all the papers end with the auspice for a randomized trial, but we all are knowledgeable about the difficulties of such a project, given the relative rarity of PAA. Up to now, only one randomized trial is available, the one launched by Antonello et al. [5], but it was transformed into a prospective comparative study. In any case, it is highly interesting to follow the evolution of opinions about PAA endografting and the conclusions to which the various authors arrived after a certainly painstaking (and sometime ambitious) survey and analysis of a large amount of nonhomogeneous data. In 2010, the Journal of Vascular Surgery published a debate between R.D. Moore and A.B. Hill [43] regarding the definition of the gold standard in the treatment of PAA.  Each of them accomplished earnestly the respective task, Moore in favor of open surgery and Hill in favor of endovascular repair, but reading between the lines, the impression is that a firm belief was lacking. Hill stressed the concept that surgery for asymptomatic aneurysm is truly prophylactic and that, consequently, the surgical risk should be minimum; elective patients are mostly older males with comorbidities and often associated aneurysms, and open surgery requires multiple or long incisions with the risk of wound complications, leg edema, prolonged hospital stay, and slow return to normal. Endovascular repair offers comparable patency rates without the associated local and/or systemic complications. What emerged from the debate as well as from the commentary of the section editor, T.L. Forbes [44], is that the surgical gold standard is ill defined, as different procedures are part of the open treatment. But, moreover, we believe that the concept of gold standard should be modified, as we take care of patients and not simply of a disease. As a ­consequence, maybe, it would be better to speak of best option that should be tailored according to

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2007, Curi et al. [21]: E 15 and O 41 Comorbidities similar in the two groups; however, E patients were older; more symptomatic cases in O; and all urgent cases in O A: Results at 24-month follow-up E O Primary patency 83% 88% Secondary patency 100% 92% Survival 90% 90% 2007, Antonello et al. [22]: E 21 and O 27 (during the study period, 38.3% of all the observed cases were not included into the study) B: Results up to 72-month follow-up E O 12 months 36 months 72 months 12 months 36 months 72 months Primary patency (%) 80.9 71.4 71.4 100 94.4 88.1 Secondary patency (%) 90.5 85.7 85.7 100 94.4 88.1 2012, Pulli et al. [23]: E 21 and O 43 Main differences between the two groups: E, more asymptomatic cases (25% vs. 48%); E, less cases with