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Etiology of abdominal aortic “inflammatory” aneurysms: Hypothesis
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Etiology o f abdominal aortic "inflammatory" aneurysms: Hypothesis To the Editors:
Anent the article "Inflammatory Aneurysms of the Aorta" by Crawford et al. (J VASC SUV,G 1985; 2:113-24), your readers may be interested in a concept that I have evolved regarding the etiology of so-called inflammatory ~ibdominal aortic aneurysms. About 10% of abdominal aortic aneurysms are found at laparotomy to have thick white walls involving the duodenum, vena cava, renal veins, and the ureter and have the macroscopic appearance of retroperitoneal fibrosis. Although Walker et al? introduced the term "inflammatory aneurysm" to designate these aneurysms, bacteria or fungi have not been shown to be responsible. The diagnosis is suspected clinically by the presence of tenderness and an elevated erythrocyte sedimentation rate and is confirmed by CT scan. Apart from the technical difficulties encountered during excision and grafting of these difficult aneurysms, interest lies in the fact that the etiology is at present unknown. "Inflammatory aneurysms" do not appear to occur elsewhere in the body except, of course, those caused by obvious bacterial or fimgal infection; furthermore, the characteristic macroscopic features do not seem to be associated with small abdominal aortic aneurysms. This suggests that ~.he condition does not begin with the formation of the aneurysm but develops only after the aneurysm has reached a certain size. It is hypothesized that periaortic lymphedema followed by fibrosis is the cause of inflammatory aneurysms. The abdominal aorta has a profuse network of periaortic lymphatic vessels, most of which course longitudinally but some lie transversely and obliquely. These lymphatic vessels receive lymph from the lower extremities, the abdominal wall, the pelvic organs, and the gastrointestinal tract, some of which contain chyle lymph. It is postulated that, as an abdominal aortic aneurysm expands, those lymphatic vessels that are arranged transversely or obliquely around the abdominal aorta may become stretched or disrupted, which causes local lymphatic obstruction or the escape of lymph. In much the same way as lymphatic obstruction in the lower extremities eventually causes subcutaneous fibrosis, the same inflammatory response could occur in the periaortic tissues. The absence of profuse periarterial lymphatic channels elsewhere could
account for the absence of this intriguing pathologic entity in other situations. H. Gaylis, M~D.
Department of Surgery University of the Witwatersrand Johannesburg, South Africa REFERENCE
1. Walker DL, Bloor K, Williams G, et al. Inflammatory aneurysms of the abdominal aorta. Br J Surg 1972; 59:609-14.
The efficacy o f dextran 40 in preventing early postoperative thrombosis following difficult lower extremity bypass To the Editors:
In their recent publication "The Efficacy of Dextran 40 in Preventing Early Postoperative Thrombosis Following Difficult Lower Extremity Bypass" (J VASC SURG 1984; 1:765-73) Rutherford et al. made a useful contribution to the prevention of early thrombosis of technically difficult peripheral arterial bypasses. Although the benefits of intravenous dextran 40 in the prevention of venous thrombosis are well known, 1-3surprisingly its advantages in arterial surgery have been rarely tested. We have used dextran 40 in all peripheral arterial reconstructive surgical procedures for the past 8 years in a dose of 20 ml/hr by continuous intravenous administration for 24 hours starting immediately after induction of anesthesia and infuse it in the same dose until the fifth postoperative day. The two main beneficial characteristics of dextran 40 as a macromolecular solution are the hemodilution by its own volume causing increased flow through the graft and a dilution of all clotting factors and its effect on the structure and fimction of factor VIII with a reduction of platelet fimction.4 Questions that remain unsolved concern (1) the dose: we think it might not be advisable to administer a dose less than 20 ml/hr, since one could lose the benefit of hemodilution and increased flow; (2) the mode of administration: the elimination of low molecular weight dextran is rapid, so that it seems justified to administer the solution continuously over 24 hours; and (3) the period of admin643
Etiology o f abdominal aortic "inflammatory" aneurysms: Hypothesis To the Editors:
Anent the article "Inflammatory Aneurysms of the Aorta" by Crawford et al. (J VASC SUV,G 1985; 2:113-24), your readers may be interested in a concept that I have evolved regarding the etiology of so-called inflammatory ~ibdominal aortic aneurysms. About 10% of abdominal aortic aneurysms are found at laparotomy to have thick white walls involving the duodenum, vena cava, renal veins, and the ureter and have the macroscopic appearance of retroperitoneal fibrosis. Although Walker et al? introduced the term "inflammatory aneurysm" to designate these aneurysms, bacteria or fungi have not been shown to be responsible. The diagnosis is suspected clinically by the presence of tenderness and an elevated erythrocyte sedimentation rate and is confirmed by CT scan. Apart from the technical difficulties encountered during excision and grafting of these difficult aneurysms, interest lies in the fact that the etiology is at present unknown. "Inflammatory aneurysms" do not appear to occur elsewhere in the body except, of course, those caused by obvious bacterial or fimgal infection; furthermore, the characteristic macroscopic features do not seem to be associated with small abdominal aortic aneurysms. This suggests that ~.he condition does not begin with the formation of the aneurysm but develops only after the aneurysm has reached a certain size. It is hypothesized that periaortic lymphedema followed by fibrosis is the cause of inflammatory aneurysms. The abdominal aorta has a profuse network of periaortic lymphatic vessels, most of which course longitudinally but some lie transversely and obliquely. These lymphatic vessels receive lymph from the lower extremities, the abdominal wall, the pelvic organs, and the gastrointestinal tract, some of which contain chyle lymph. It is postulated that, as an abdominal aortic aneurysm expands, those lymphatic vessels that are arranged transversely or obliquely around the abdominal aorta may become stretched or disrupted, which causes local lymphatic obstruction or the escape of lymph. In much the same way as lymphatic obstruction in the lower extremities eventually causes subcutaneous fibrosis, the same inflammatory response could occur in the periaortic tissues. The absence of profuse periarterial lymphatic channels elsewhere could
account for the absence of this intriguing pathologic entity in other situations. H. Gaylis, M~D.
Department of Surgery University of the Witwatersrand Johannesburg, South Africa REFERENCE
1. Walker DL, Bloor K, Williams G, et al. Inflammatory aneurysms of the abdominal aorta. Br J Surg 1972; 59:609-14.
The efficacy o f dextran 40 in preventing early postoperative thrombosis following difficult lower extremity bypass To the Editors:
In their recent publication "The Efficacy of Dextran 40 in Preventing Early Postoperative Thrombosis Following Difficult Lower Extremity Bypass" (J VASC SURG 1984; 1:765-73) Rutherford et al. made a useful contribution to the prevention of early thrombosis of technically difficult peripheral arterial bypasses. Although the benefits of intravenous dextran 40 in the prevention of venous thrombosis are well known, 1-3surprisingly its advantages in arterial surgery have been rarely tested. We have used dextran 40 in all peripheral arterial reconstructive surgical procedures for the past 8 years in a dose of 20 ml/hr by continuous intravenous administration for 24 hours starting immediately after induction of anesthesia and infuse it in the same dose until the fifth postoperative day. The two main beneficial characteristics of dextran 40 as a macromolecular solution are the hemodilution by its own volume causing increased flow through the graft and a dilution of all clotting factors and its effect on the structure and fimction of factor VIII with a reduction of platelet fimction.4 Questions that remain unsolved concern (1) the dose: we think it might not be advisable to administer a dose less than 20 ml/hr, since one could lose the benefit of hemodilution and increased flow; (2) the mode of administration: the elimination of low molecular weight dextran is rapid, so that it seems justified to administer the solution continuously over 24 hours; and (3) the period of admin643