Evaluation of sex differences in relative dilatation of thoracic aortic aneurysms.

OBJECTIVES: Treatment recommendations based on thoracic aortic aneurysm (TAA) diameter (D) ignore differences in proportional dilatation between patients of different body habitus and sex. This study's goal is to compare TAA diameters between sexes as a function of relative aortic size as determined by aortic size index (ASI). METHODS: This is a retrospective review of all TAA's treated between 2003 and 2008. ASI was calculated for each patient, which considers aneurysm diameter, patient's height and weight. Values for males and females were plotted separately (TAA diameter vs ASI) and the resulting linear regression equations permitted comparison of proportional dilatation between sexes. RESULTS: In 40 patients (25 males, 15 females) mean TAA diameter did not differ between sexes (6.56 +/- 0.99 vs 7.03 +/- 1.14, P = 0.18), while ASI was larger in females than males (4.21 +/- 0.85 vs 3.24 +/- 0.63, P = 0.0003). Values for ruptured and intact aneurysms did not differ. Linear regression analysis permitted comparison of TAA diameter with ASI between sexes resulting in the following equation: D(Female) = 0.91D(Male) - 0.49. This correlates a 6 cm TAA in a male with a 4.97 cm TAA in a female. CONCLUSIONS: TAA of equal diameter represent a larger proportional dilatation in females compared to males. This could influence repair thresholds that are historically diameter based.

The hybrid aneurysm repair: extending the landing zone in the thoracoabdominal aorta.

We present two cases of concomitant management of a type I thoracoabdominal aneurysm and an infrarenal aneurysm via laparotomy, open infrarenal aortic replacement, visceral bypasses from the infrarenal graft, and finally endovascular exclusion of the thoracoabdominal aneurysm. While there are other reports of hybrid procedures for patients with preexisting aortic grafts in place or with retrograde visceral perfusion from a native iliac artery for type II thoracoabdominal aneurysm, these are the first reported cases of concurrent management of a type I thoracoabdominal aneurysm and an infrarenal aneurysm using the infrarenal graft as a distal landing zone for the thoracoabdominal endograft.

Primary aorto/iliac-enteric fistula-report of 6 new cases.

The management of patients with vascular-enteric fistulas remains a challenging diagnostic and therapeutic problem for the vascular surgeon. Although fortunately quite a rare cause of gastrointestinal bleeding, reported mortality and amputation rates are very high. Fistulas between major vascular structures and the gastrointestinal tract are classified as either primary or secondary. Primary fistulas occur most commonly between an aortic aneurysm and the distal duodenum, while secondary fistulas occur following erosion of prosthetic material into the bowel following aortic reconstruction. The authors report 6 new cases of primary aortoenteric fistula: A malignant aortoenteric fistula in a patient with advanced metastatic squamous cell carcinoma involving the infrarenal aorta and duodenum, 4 cases of primary aortoenteric fistulas in patients with abdominal aortic aneurysms, and 1 iliac-enteric fistula secondary to a common iliac aneurysm. The diagnosis is often difficult to make, and although it was considered in 4 patients preoperatively, the diagnosis was not made until the time of laparotomy in all of these patients. Three patients were treated with an in-situ vascular graft, 2 others had the distal abdominal aorta oversewn and axillobilateral femoral bypass performed, and in the case involving the malignancy, the patient underwent primary aortic repair owing to the extent of the tumor process prohibiting aortic reconstruction. Three patients had primary closure of the intestine performed, and 3 required bowel resection and primary anastomosis. The overall 30-day mortality rate was 50% as 3 patients died in the early postoperative period and the remaining 3 patients survived to be discharged from hospital. One patient (17%) required bilateral above-knee amputations. Treatment of patients with vascular-enteric fistulas is a difficult problem, often associated with delayed diagnosis and high morbidity and mortality rates. Successful surgical management can be achieved with primary closure of the intestinal tract and an in-situ vascular graft or extraanatomic bypass.

Cytokines contribute to early hepatic parenchymal injury and microvascular dysfunction after bilateral hindlimb ischemia.

PURPOSE: Hepatic dysfunction may contribute to death from multiple organ dysfunction after abdominal aortic surgery. Several factors are likely responsible, and the purpose of this study was to determine whether the cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin 1 (IL-1) are involved in initiating this remote hepatic injury. METHODS: In a normotensive rat model of 4-hour bilateral hindlimb ischemia/reperfusion (I/R), we measured systemic TNF-alpha and IL-1 levels throughout the I/R period. Rats were randomly assigned to either the 3-hour control group, the 3-hour I/R group, or the I/R group with administration of a polyclonal antibody (PAb) to TNF-alpha (I/R + TNF-alpha PAb). Direct evidence of lethal hepatocyte injury through the labeling of nuclei by propidium iodide (per 10(-1)mm(3)) and altered microvascular perfusion were assessed by using intravital microscopy. RESULTS: Systemic TNF-alpha peaked at 83.97 pg/mL (P <.05, n = 5) at 30 minutes of reperfusion and returned to baseline in 60 to 90 minutes. No significant change in systemic IL-1 was detected (P <.05, n = 4). Alanine aminotransferase increased 2.5-fold in the I/R group through 3 hours of reperfusion (P <.05, n = 4), and TNF-alpha PAb did not attenuate this alanine aminotransferase increase (P <.05, n = 6). Lethal hepatocyte injury increased by 8-fold in the I/R group compared with the control group (P <.05, n = 5), whereas TNF-alpha PAb significantly reduced this injury (P <.05, n = 4). No regional differences in injury were noted within the acinus. Total perfusion within the microvascular unit did not drop; however, significant flow heterogeneity was observed. The proportion of continuously perfused sinusoids declined in the I/R group after 3 hours of reperfusion in both periportal (62.0 +/- 2.2, P <.05) and, to a lesser, although significant, degree, in the pericentral regions (73. 2 +/- 1.73, P <.05). CONCLUSION: By scavenging extracellular TNF-alpha with a PAb, we provide direct evidence that TNF-alpha contributes to, but is not solely responsible for, early remote hepatocellular injury and microvascular dysfunction. The administration of TNF-alpha PAb reduced lethal hepatocyte injury in both regions of the acinus and also improved perfusion in the periportal region (76.8 +/- 5.41, P <.05), but not in the pericentral region. This suggests that TNF-alpha released during reperfusion mediates early remote hepatocellular injury and microvascular dysfunction after a remote ischemic insult.

Initiation of remote hepatic injury in the rat: interactions between Kupffer cells, tumor necrosis factor-alpha, and microvascular perfusion.

Severe trauma may initiate a systemic inflammatory response, which in turn may result in remote organ injury. After limb ischemia/reperfusion (I/R), intravital fluorescence microscopy was applied to the livers of normotensive rats to investigate the initiation of remote injury to the liver. Additionally, we determined whether Kupffer cell activation and tumor necrosis factor-alpha (TNF-alpha) were involved, via perfusion deficits, in such injury. TNF-alpha, measured by immunoassay, peaked at 30 minutes of reperfusion, but returned to baseline within 60 minutes. Limb I/R resulted in significant increases to global hepatocellular injury measured by alanine transaminase (ALT) and lethal hepatocyte injury as seen with intravital fluorescence microscopy. Although the number of perfused sinusoids went unchanged, a significantly augmented perfusion heterogeneity was measured. After 1.5 hours of reperfusion, both TNF-alpha and Kupffer cells were shown to contribute to global hepatocellular injury (e.g., ALT). After 3 hours, TNF-alpha was no longer essential for this injury, suggesting that some other mechanism(s) activated Kupffer cells and initiated hepatocellular injury. Using propidium iodide and fluorescence microscopy, we found that both TNF-alpha and Kupffer cell activation were necessary to drive hepatocytes toward lethal injury. No additional benefits were observed with a combination of TNF-alpha inhibition and Kupffer cell suppression. These results not only implicate both Kupffer cells and TNF-alpha in the initiation of remote hepatic injury, but suggest that sinusoidal perfusion deficits are not essential for the initiation of such injury. Other mechanism(s) are likely involved in the pathogenesis of remote hepatic parenchymal injury.

Small-bowel necrosis associated with jejunal tube feeding.

OBJECTIVES: To report 3 cases of small-bowel necrosis after jejunal tube feeding and to review the literature concerning this condition. DESIGN: A 5-year retrospective review. SETTING: A 560-bed university-affiliated tertiary-care teaching hospital. PATIENTS: Three patients who had bowel necrosis out of 386 who received jejunal tube feedings. RESULTS: The patients experienced small-bowel necrosis as a consequence of jejunal feeding. The ischemic necrosis was preceded by progressive abdominal pain, distension and high nasogastric output. All 3 patients required extensive small-bowel resection. Although survival was rare in previous reports, our 3 patients survived after prompt surgical intervention and small-bowel resection. CONCLUSIONS: Although the death rate for this condition approaches 70%, timely recognition and surgical intervention can save the patient's life.