David L. Dudgeon

The Role of Selective Angiography in the Diagnosis and Treatment of Hepatoportal Arteriovenous Fistula

An hepatoportal arteriovenous fistula is a unique complication of abdominal trauma. Of 5 previously reported cases, 4 resulted from penetrating injury and only 1 was attributable to blunt trauma (1, 3, 4, 7, 9). The present report documents the occurrence of hepatoportal fistula following blunt abdominal trauma in a child. The case is significant not only for its rarity, but also as a demonstration of the value of selective angiography in the diagnosis, treatment, and postoperative assessment of this lesion. An 8-year-old girl sustained a fracture of the right femur and abdominal injuries as a result of an automobile accident in January 1968. The child was admitted to a local hospital in hypovolemic shock and underwent exploratory laparotomy. At operation, bleeding from liver and right kidney lacerations was controlled with chromic catgut sutures. Renal shut-down developed postoperatively and the patient was transferred to the W. A. Shands Teaching Hospital. Six weeks later, following a prolonged convales...

Intestinal production of IL-6 initiates systemic inflammation in a murine model of intestinal ischemia reperfusion1

Abstract Purpose: Intestinal ischemia/reperfusion (I/R) injury disrupts the gut barrier and activates systemic inflammation and multisystem organ failure (MOF). Our reported murine model of intestinal I/R demonstrated dose-dependent local injury and mortality [Gastroenterology (1998) 114:A-1587]. We hypothesized that the release of proinflammatory cytokines from the gut modulates systemic inflammation. Methods: Balb/c mice underwent 50 minutes of superior mesenteric artery occlusion with reperfusion. All survived long-term (>16 hours). Controls were sham operated. Serum levels of IL-6 and TNF-α were measured at 0, 1, 4, and 16 hours by ELISA. Small bowel and liver mRNA were evaluated for production of IL-6 and TNF-α by semiquantitative RT-PCR, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) standard and a Student t-test for data analysis (p Results: Serum levels of IL-6 were significantly elevated at 4 and 16 hours versus controls ( Fig. 1 , left). The serum level of TNFα was not elevated. There was a significant elevation of IL-6 mRNA at 1 and 4 hours in the jejunum ( Fig. 1 , center) Download : Download high-res image (129KB) Download : Download full-size image FIGURE 1 . and TNFα mRNA at 4 hours. No significant increase in liver IL-6 ( Fig. 1 , right) or TNF-α mRNA was seen. Conclusions: In this model of ischemia reperfusion injury, the intestine is a major source of the proinflammatory cytokine IL-6 but not of TNF-α. The rapid appearance of IL-6 mRNA in the jejunum suggests that the intestine, not the liver, initiates systemic inflammation and MOF by a distinct cytokine pattern.

Endogenous interleukin 10 does not protect against local or systemic injury in a murine model of intestinal ischemia and reperfusion1

Abstract Purpose: Ischemia/reperfusion of the small intestine disrupts gut barrier function and activates systemic inflammation. The anti-inflammatory cytokine interleukin-10 (IL-10) is protective in murine models of acute sepsis, yet its role during gut injury is unknown. We therefore undertook to investigate this question. Methods: Mice genetically deficient in IL-10 (IL-10 −/− ) on a C57BL/10 background, their wild-type littermates, and Balb/c mice underwent 30 to 80 minutes of occlusion of the superior mesenteric artery. Sixteen hours after reperfusion, survival was documented and the small bowel scored for histologic damage. Results: The LD 50 of IL-10 −/− mice was 35 minutes of occlusion, identical to that of the wild-type mice. The small bowel of all animals that died was distended, with localized jejunal hemorrhage. LD 50 Occlusion (min) Histologic Injury Score (n = 3) C57BL/10 (IL-10 +/+ ) 35 30 3.0 ± 1.0 C57BL/10 (IL-10 −/− ) 35 30 2.0 ± 0.0 Balb/c 60 50 4.3 ± 4.0 Balb/c 60 20 0.3 ± 0.6 No significant difference in intestinal damage was observed between surviving IL-10 −/− and IL-10 +/+ mice after 30 minutes of occlusion. Balb/c mice were more resistant to intestinal ischemia, demonstrated by an LD 50 at 60 minutes of occlusion. Furthermore, equivalent mucosal damage in Balb/c mice required 50 minutes of occlusion as compared with that seen in 30 minutes with occluded C57BL/10 mice. Conclusions: Interleukin-10 does not play a significant protective role either locally or systemically in this model of ischemia/reperfusion. The resistance of the Balb/c strain suggests that an alternate mechanism modulates the response to intestinal ischemic/reperfusion injury.