Late arterial aneurysms associated with history of traumatic arteriovenous fistulas *
(Portuguese PDF version)

Ricardo C. Rocha Moreira,1 Marcio Miyamotto,2 Rossano Jarabiza3

1. Ph.D. Chief of the Vascular Surgery Service Prof. Dr. Elias Abrão, Curitiba, PR, Brazil.
2. Vascular and Endovascular Surgeon, Vascular Surgery Service Prof. Dr. Elias Abrão, Curitiba, PR, Brazil.
3. Vascular Surgery Resident, Hospital Nossa Senhora das Graças, Curitiba, PR, Brazil.

* This work was carried out in the Service of Vascular Surgery Professor Doutor Elias Abrão (Hospital Nossa Senhora das Graças and Hospital Universitário Cajuru of the Pontifical Catholic University of Paraná).

Correspondence:
Ricardo C. Rocha Moreira
Rua Pedro Muraro, 50 casa 24
CEP 82030-620 - Curitiba, PR, Brazil
Tel.: +55 (41) 332.3233/244.8787/335.6223
Fax: +55 (41) 342.6311
E-mail: ina@onda.com.br


ABSTRACT

The long term presence of an arteriovenous fistula causes proximal dilatation of the artery that feeds it. In general, the dilatation does not regress and tends to progress after the arteriovenous fistula is surgically treated. The authors report three cases in which arterial dilatation resulted in late aneurysm formation, decades after surgical treatment of arteriovenous fistulas. In all three cases, atypical location of these aneurysms was observed. The authors could find only a few similar cases in the literature.

Key-words: aneurysm, arteriovenous fistula, trauma.
Palavras-chave: aneurisma arteriovenoso, fístula arteriovenosa, trauma.

J Vasc Br 2004;3(3):265-8


Arteriovenous fistulas (AVFs) are abnormal communications between an artery or a vein that bypass the normal anatomic capillary beds. They can be congenital or acquired, presenting with local, regional and systemic changes, depending on size, location, and lasting period of the event.1

The AVF was first described by William Hunter in 1757. Since then, several authors have carried out clinical and pathologic studies that have contributed to the understanding of local and systemic effects of AVFs, like the ones by Lewis & Drury, Reid, Rienhoff and Holman. An important event associated with AVFs is the dilation of an artery proximal to the fistulous tract. Dilation usually occurs after longstanding fistulas and it develops proximal to the fístula, persisting even after ligation.2,3

In this paper we report on three cases of aneurysms proximal to AVFs that had been already managed many years ago. In all three cases described, aneurysms developed in atypical sites, proximal to the region of the ligated fistula.

CASE REPORTS

Case 1

Male patient, 62 year-old, former professional soccer player. In 1965, at 23 years of age, he had been submitted to a meniscectomy of the right knee and during the surgical procedure underwent an iatrogenic vascular injury which resulted in an AVF between the artery and the popliteal vein. The AVF was surgically managed twice (1968 and 1972) with uneventful recovery after the last intervention. In 1991, the patient underwent acute thrombosis of the popliteal artery and was submitted to reverse saphenous revascularization of the femoral artery superficial-distal to the right popliteal artery, which seemed normal under direct visualization, without dilation. In the following years, the patient presented a pulsatile mass in the proximal right thigh. Eco-Doppler sonography and arteriography evidenced an aneurysm in the proximal femoral artery (Figures 1a and 1b). The aneurysm reached 4.5 cm in 1998, determining the indication for an elective surgical treatment. A reverse saphenous vein bypass was performed using the left-thigh vein, from the right common femoral to the femoro-popliteal that had been previously deployed.

We carried out proximal and distal ligation of the aneurysm, which underwent subsequent thrombosis. The patient recovered uneventfully and remains with local pulses in the lower limb so far.

click hereFigure 1 - Arteriography showing an aneurysm of the right superficial femoral artery; a) proximal and b) distal.

Case 2

Male patient, 71 years-old, retired businessman. At the age of 14 he had an accidental wound caused by knife on the right thigh. In the following years, the patient developed with intermittent claudication, edema, varices and skin changes in the left lower extremity. A diagnosis of postraumatic AVF in the right thigh had been made in another service, at the age of 28 years-old. The patient had been submitted to surgical correction of the AVF with implantation of a PTFE prosthesis, which developed with infection and had to be withdrawn after 6 months. In the second surgery, an access was made in the right iliac fossa, apparently for the ligation of the external iliac artery. Symptoms associated with AVF disappeared, except claudication pain during long-distance walking. Forty years after the AVF correction, at the age of 68, a pulsatile mass was found in the right iliac fossa. The ultrasonography and computed tomography investigations evidenced an aneurysm in the right common iliac artery, involving the terminal aorta, and occluding the external, femoral and common iliac arteries (Figure 2). Deep femoral and popliteal arteries were patent. The patient was submitted to surgical management (Figure 3) for an endoaneurysmorraphy and interposition of a bifurcated 14 x 7 mm Dacron graft from the origin of the common iliac artery up to the right internal iliac artery (one branch) and to the right deep femoral artery (the other branch). The operation had no complications and the patient has been reported asymptomatic so far.

click hereFigure 2 - Angiotomography showing an aneurysm o the common right iliac artery.

click hereFigure 3 - Aneurysm of the right common iliac artery (surgical aspect).

Case 3

Male, 43 years-old, salesman. The patient was hospitalized with intermittent claudication during medium distances walking started after an operation in the right leg, more than 20 years ago. History of AVF during childhood developed after an injury in the right popliteal fossa caused by a steel wire of a farm equipment. At the age of 21, the patient was submitted to surgical management in another service without symptoms of AVF. He continued, however, with intermittent claudication in the same extremity during medium-distance walking. Arteriography evidenced an aneurysm in the aorto-iliac-femoral axis, from the distal artery to the common femoral artery, with a maximum diameter of 5 cm in the common iliac artery.

The patient was submitted to surgical management for the interposition of a straight Dacron graft, from the non-aneurysmatic portion of the distal aorta to the right deep femoral aorta, once the superficial femoral artery was occluded. It was termino-terminal anastomosed and there were not complications during surgery. The patient has recovered uneventfully and followed for six months, after that, contact was lost.

DISCUSSION

Dilation and distension of arteries that feed a congenital or acquired AVF are well-known events. According to Broca, the artery proximal to the AVF dilates, causing alterations in the arterial wall, which becomes extremely thin, dilated in a conic-like form, semi-transparent, and easily collapsing like a vein wall. In later studies, Holman has made a minute examination on the dilation phenomena.4

In general, arteries that feed congenital or acquired AVFs bulge. In acquired AVFs this is also frequently seen. In these cases, the extent of alterations, either local or regional and systemic will be inversely proportional to the resistance of the communication passageway between the artery and the vein. Resistance is directly dependent on the passageway length and inversely related to its diameter. As the extension of the communicating portion is mostly virtual, the most important factor is the communication diameter, which can be the same caliber as the proximal artery.5,6

The physiopathology of the proximal artery dilation is not totally clear. Hemodynamic factors probably contribute to such alterations in the proximal artery. The increase of the blood flow velocity seems to play an important role in this mechanism. Some researchers suggest that the endothelium recognizes the hemodynamic stress, stimulating the realease of the endothelium-derived relaxing factor on smooth muscle cells of the arterial wall, resulting in vasodilatation.7 Besides, the flow and the chronically increased caliber of the artery proximal to the fistula may damage the elastic fibers of the artery wall. Once the artery is irremediable injured, it may dilate even after the fistula has been ligated.8 Another possibility includes the effect of arterial wall vibration. The fact that dilation is frequently noticed in regions close to the AVF gives credibility to this theory. Vibration has shown to play an important role in the poststenotic dilation: an anatomic alteration which is not different from the formation of the aneurysm in the proximal artery.9,10

Although the arterial wall can thicken in the beginning, it usually undergoes degenerative alterations, with atrophy of the media of smooth muscular cells, decrease of elastic tissue and a tendency of showing atherosclerotic alterations, becoming thin and friable. These alterations may remain irreversible if the AVF persist for several years.3,5,9

In general, the arterial dilation occurs in regions proximal to the fistula site and it is in general synchronized with long-term AVFs. Late developed aneurysms secondary to chronic AVFs management are not very frequent and a few cases are reported in the literature.3,11-16 In the literature review by Mellière in 1997, 17 cases had been reported.17 Most cases were late aneurysms in atypical sites developed decades after the surgical management of long-term AVFs. It was postulated that alterations in the arterial wall proximal to the AVF may be irreversible, depending on time that it has remained open and on the size of the hemodynamic stress. These alterations seem not to be limited to regions close to the fistula, affecting also the entire arterial bed of the damaged side. When alterations in the arterial wall are not reversible, any increase in the local hemodynamic stress may form aneurysms. This would explain the formation of atypical aneurysms in cases 1 and 3, where increase in the peripheral resistance caused by the ligation of right external iliac and right superficial femoral arteries, has respectively lead to an aneurysmatic dilation close to a previous and chronically compromised bed. The ligated arteriovenous fistula itself can lead to significant hemodynamic alterations due to the increase in the peripheral resistance which, over the years, could influence the proximal dilation event. Such hypothesis is confirmed by the fact that the venous graft in these places does not present any sign of dilation, after fistula ligation, even after 14 years.16

We conclude that, even after the correction of an AVF that remained open for a long period of time, structural alterations in the arterial wall remain along the arterial axis of the affected side. This entire region remains subject to aneurysmatic degenaration resulting from external and even spontaneous factors.

REFERENCES

1. Brito CJ. Fístulas AV traumáticas de longa duração. Rev Col Bras de Cir 1969;7:5.

2. Linder F. Acquired arteriovenous fistulas: report of 223 operated cases. Ann Chirur Gynaecol 1985;74:1-5.

3. Sako Y, Varco RL. Arteriovenous fistula: results of management of congenital and acquired forms, blood flow measurements, and observations on proximal arterial degeneration. Surgery 1970;67:40-61.

4. Holman E. The physiology of an arteriovenous fistula. Am J Surg 1955;89:1101-8.

5.Trout HH III, Feinberg RL. Vascular anomalies and acquired arteriovenous fistulas. In: Dean RH, Yao JST, Brewster DC, editors. Diagnosis and treatment in vascular surgery. East Norwalk: Appleton & Lange; 1995. p. 309-324.

6. Worthington G, Schenk JR, Martin W, Leslie MB, Portin BA. The regional hemodynamics of chronic experimental arteriovenous fistulas. Surgery, Gynecology & Obstetrics 1960;44-50.

7. Vanhoutte PM, Rubanyi GM, Miller VM, Houston D. Modulation of vascular smooth muscle contraction by the endothelium. Ann Rev Physiol 1986;48:307-20.

8. Greenhill NS, Stehbens WE. Scanning electron microscopic study of afferent arteries on experimental femoral arteriovenous fistulae in rabbits. Pathology 1987;19:22-7.

9. Sumner DS. Arteriovenous communications and congenital vascular malformations: hemodynamics and pathophysiology of arteriovenous fistulae. In: Rutherford RB, editor. Vascular surgery. Philadelphia: WB Saunders; 1995. p. 1166-1191.

10. Holman E. Clinical and experimental observations on arteriovenous fistulae. Ann Surg 1940;112:840-78.

11. Ray JF, Smullen WA, Lolley DM, et al. On the possible need for reoperation to control proximal aneurysms in instances of longstanding traumatic arteriovenous fistula. J Cardiovasc Surg (Torino) 1979;20:197-200.

12. Graham JM, McCollum CH, Crawford ES, et al. Extensive arterial aneurysm formation proximal to ligated arteriovenous fistula. Ann Surg 1980;191:200-2.

13. Gross C, Kobinia GS, Bruecke P. Late arterial aneurysm formation proximal to a ligated peripheral arteriovenous fistula. Vasa 1986;15:184-6.

14. Mellière D, Barres G, Saada F, et al. Late arterial aneurysm proximal to corrected post-traumatic arteriovenous fistula. J Cardiovasc Surg (Torino) 1987;28:510-5.

15. Ozcan F, Baki C, Piskin B, et al. Aneurysmatic dilatation of popliteal and femoral artery due to long-standing traumatic arteriovenous fistula. Vasa 1990;19:79-81.

16. Hartung O, Garcia S, Alimi YS, et al. Extensive arterial aneurysm developing after surgical closure of long-standing post-traumatic popliteal arteriovenous fistula. J Vasc Surg 2004;39:889-92.

17.Mellière D, Hassen-Khodja R, Cormier JM, Le Bas P, Mikati A, Ronsse H. Proximal arterial dilatation developing after surgical closure of long-standing posttraumatic arteriovenous fistula. Ann Vasc Surg 1997;11:391-6.


J Vasc Br - Official Publication of the Brazilian Society of Angiology and Vascular Surgery