The management of massive ultrafiltration distending the aneurysm sac after abdominal aortic aneurysm repair with a polytetrafluoroethylene aortobiiliac graft

AbstractCollections of serous fluid surrounding prosthetic grafts can be caused by infection or transudation of serum, and making the distinction is often troublesome. Bergamini and his colleagues1 developed a dog model of low-grade prosthetic graft contamination with Staphylococcus epidermatis. All animals developed evidence of graft infection, and 13 of 18 dogs developed a fluid-filled perigraft cyst. Signs of systemic infection, however, were present in only 1 animal, and the Staphylococcus epidermatis study strain was isolated from the tissue surrounding the graft in only 1 dog. The authors had to disrupt the biofilm to achieve positive cultures in 14 of 18 animals. This animal model seemed to conform to clinical experience and placed great emphasis on the role of indolent infections in the pathogenesis of perigraft fluid collection. It is equally clear that perigraft fluid collections may result from transudation of fluid through the prosthetic surfaces, which act similar to a dialysis membrane under certain circumstances.2-6 Noninfectious seromas are characterized generally by the accumulation of clear serous fluid with a protein and glucose content of serum and the lack of acute inflammatory cells when the sediment is examined. The need to distinguish between these 2 forms of fluid accumulation became important in the treatment of a 62-year-old man who was seen 2 ½ years after the repair of an abdominal aortic aneurysm with an aortobiiliac stretch polytetrafluoroethylene (PTFE) prosthesis. There was no evidence of infection, and there was a 12 cm cystic mass surrounding a patent PTFE prosthesis. (J Vasc Surg 1998;28:551-5.

Aneurysmal expansion of the visceral patch after thoracoabdominal aortic replacement: An argument for limiting patch size?

AbstractIntroduction: Thoracoabdominal aortic replacement requires visceral vessel revascularization and is usually performed with Crawford's inclusion technique or a large Carrel patch. This segment of retained native aorta may be prone to recurrent aneurysmal disease. We reviewed our experience with patients in whom aneurysmal expansion of the visceral patch was detected. Methods: The records of 107 patients undergoing thoracoabdominal aortic replacement operations performed or followed up at the Johns Hopkins Hospital between 1992 and 2000 were reviewed. All patients had visceral patches created for type II, III, or IV aneurysms. Visceral patches were considered aneurysmal if the maximal diameter of the aortic prosthesis and patch was 4.0 cm or more. Results: Patch aneurysmal expansion (mean, 5.4 cm) was detected in eight patients (7.5%). All three women had connective tissue disorders (mean age, 36 years), and all five men had atherosclerotic disease (mean age, 73 years). Five patients were symptom free with their aneurysms detected by surveillance computed tomography scans; two patients had back pain prompting computed tomography scans; and one patient presented with an emergency patch rupture. Aneurysmal patches were successfully revised in three patients. Two patients died in the operating room, and three patch aneurysms (< 5 cm) are still being observed. The mean time to the detection of aneurysmal expansion was 6.5 years after the original operation. Therapy consisted of replacement of a segment of the thoracoabdominal aortic graft and refashioning a smaller patch, including only the visceral artery orifices with separate attachment of the left and possibly right renal artery. Conclusions: Although Crawford's inclusion method of visceral patch construction is generally durable, patients undergoing thoracoabdominal aortic replacement require yearly surveillance for the detection of aneurysmal expansion of the visceral patch. We recommend limiting visceral patch size at the original operation by routinely excluding the orifice of the left renal artery. Patients at high risk for recurrent aneurysmal expansion, such as those with connective tissue disorders, will benefit from creating small visceral patches and possibly implanting both renal arteries separately during the original operation. (J Vasc Surg 2001;34:405-10.

DNA damage and repair system in spinal cord ischemia

AbstractBackground and Purpose: Spinal cord ischemia-reperfusion injury may be initiated by a number of mediators, including reactive oxygen species. Recent studies have shown that human MutY homologue (hMYH), human 8-oxo-7,8-dihydrodeoxyguanine (8-oxoG) glycosylase (hOGG1), and human MutS homologue 2 (hMSH2) are important DNA mismatch repair genes. We hypothesized that ischemia-reperfusion injury in spinal cord causes DNA damage manifested by 8-oxoG production and activates the DNA repair system involving hMYH, hOGG1, and hMSH2. Methods: Spinal cords of rabbits were removed at 1, 3, 6, 24, and 48 hours after 30 minutes of infrarenal aortic occlusion. DNA damage was determined with 8-oxoG staining. The expression and localization of DNA repair enzymes, such as hMYH, hOGG1, and hMSH2, were studied with Western blot analysis and immunohistochemical staining. The level of apoptosis was determined with TUNEL study. Activation of caspase-3, an enzyme induced by cellular injury that leads to apoptosis by degrading cellular structural proteins, was also studied. Results: DNA damage monitored with 8-oxoG level was significantly present from 1 hour to 6 hours after reperfusion in gray matter neurons of ischemic spinal cord. The levels of hMYH, hOGG1, and hMSH2 were markedly increased in gray matter neurons at 6 hours after reperfusion. Caspase-3 was also induced at 6 hours to 24 hours after reperfusion in ischemic spinal cord. However, the peak level of TUNEL reactivity was found at 48 hours after reperfusion in spinal cord neurons. Conclusion: This study has shown, for the first time, the rapid expression of DNA damage-repair processes associated with spinal cord ischemia and subsequent reperfusion. (J Vasc Surg 2003;37:847-58.

Durability of thoracoabdominal aortic aneurysm repair in patients with connective tissue disorders

AbstractObjective: Thoracoabdominal aortic aneurysm (TAAA) repair is a durable procedure performed with reasonable perioperative mortality and morbidity in patients with atherosclerotic aortic disease. However, the long-term outcome and durability of TAAA repair performed in patients with a connective tissue disorder (CTD) is not well known. Methods: The records of 257 patients who underwent TAAA repair at the Johns Hopkins Hospital between January 1992 and December 2001 were reviewed. Survival analysis was performed with Kaplan-Meier analysis, and subgroups were compared with the log-rank test. Multivariable analysis was performed with the Cox proportional hazards model and logistic regression. Results: Patients with CTD (n = 31) were seen earlier (mean age, 48.6 ± 2.9 years) than patients without CTD (mean age, 69.1 ± 0.6 years; P < .0001, Mann-Whitney U test) and had a greater incidence rate of aortic dissection (52% versus 19%; P < .0001, χ2 test) and extent I or II aneurysm (77% versus 64%; P = .04). The perioperative (30-day) mortality rate was 6.5% in patients with CTD, which was similar to the rest of the cohort (P = .39, Fisher exact test). The incidence rate of paraparesis/paraplegia was 12.9%/6.5% in patients with CTD, and CTD was the only factor predictive of paraparesis (P = .03; odds ratio, 9.3; logistic regression). The cumulative survival rate among the entire cohort was 53.4% ± 4.4% at 5 years (Kaplan-Meier), and no difference was seen among patients with or without CTD (P = .16, log-rank test) or among different Crawford extents (P = .29). Of the two late (>6 months) deaths in patients with CTD, none were from aortic rupture or dissection, compared with two of 31 late deaths in patients without CTD. Multivariable analysis confirmed that postoperative renal failure (P = .03) predicted mortality but neither CTD (P = .93), nor Crawford extent (P = .21, Cox regression) predicted mortality. Among survivors, no mean difference was found in largest aortic diameter on follow-up imaging in patients with or without CTD (4.7 ± 0.3 cm versus 4.4 ± 0.3 cm; P = .47, Mann-Whitney U test). The cumulative graft patency rate, representing long-term graft stability and with death, rupture, dissection, or recurrent aneurysm as endpoints, was 47.5% ± 4.6% at 5 years (Kaplan-Meier) and was similar in patients with or without CTD (P = .10, log-rank test). Conclusion: TAAA repair appears to be a durable operation, with a reasonable 5-year patient survival rate and a low risk of postoperative paraplegia or additional aortic events. Patients with CTD can expect their outcome, including long-term survival and aortic stability, to be similar to patients without CTD. (J Vasc Surg 2002;36:696-703.