History of mesenteric ischemia. The evolution of a diagnosis and management.

This article has traced the evolution of our knowledge of mesenteric ischemia from the initial stage of recognition of the condition and its manifestations, through the phase of treatment after the fact-resection of gangrenous intestine, to our present-day attempts to diagnose and treat the ischemic episode before death of the bowel and patient occurs. It is history from the authors' perspective, and because of limitations of space it is, perforce, highly selective. Hundreds of valuable contributions could not be included, and their omission in no way detracts from their importance. A number of surgeons, including Williams and Bergen in this country, Marston in England, Saegesser in Switzerland, and Kieny in France, have made mesenteric ischemia a major focus of their careers and have published extensively on it. The first book devoted to all aspects of mesenteric ischemia, Vascular Disorders of the Intestines edited by Boley, Schwartz, and Williams, was published in 1971. Since that time a number of books and monographs have chronicled progress in the field. Together these references make a good foundation for newly interested investigators in the subject. The results of diagnosis and management of mesenteric ischemia have improved significantly over the past 100 years but remain poor. The best part of the history of mesenteric ischemia remains to be written.

Bloodless splenic surgery: the safe warm-ischemic time.

To assess the feasibility of a technique of bloodless splenic surgery, experiments were performed to determine the safe warm-ischemic time of the spleen. Ten mongrel dogs were divided into two groups. Group I (n = 5) underwent division of all collateral splenic vessels, followed by total splenic artery and vein occlusion for 3 hours. Group II (n = 5) underwent similar collateral devascularization, but with total occlusion of the splenic pedicle for 2 hours. All animals underwent sulfur colloid scintiscanning preoperatively and 2 weeks postoperatively. Blood specimens were analyzed for the presence of Howell-Jolly bodies and immunoglobulin (Ig) G IgG and IgM levels. Pathological examination of the spleens was performed 2 weeks postoperatively. Postoperative scintiscanning showed very poor splenic visualization in two of the five group I dogs. Pathologically these spleens had extensive necrosis. The remaining eight spleens had normal scans, and only mild congestion was noted. Howell-Jolly bodies were found in all group I dogs (mean, 14.6) but in only 2 group II dogs (mean, 0.6). In four group I dogs, a marked decrease in peripheral IgG was noted. Splenic immunoglobulin levels and peripheral IgM were similar in both groups. This study demonstrates that 3 hours of warm splenic ischemia resulted in splenic necrosis and loss of function in 40% of the dogs tested. Two hours of ischemia appears to be safe for dogs; certainly 1 hour should be safe for humans and should allow sufficient time for most splenic surgical procedures.

Aggressive approach to acute mesenteric ischemia.

An aggressive diagnostic and therapeutic approach to acute mesenteric ischemia can dramatically lower the mortality of this lethal disease. The cornerstones of this approach are the earlier and more liberal use of angiography and the use of intra-arterial infusions of vasodilators in the treatment of both nonocclusive and occlusive mesenteric ischemia.

Pathophysiology of mesenteric ischemia.

Intestinal ischemia can result from a host of pathophysiologic disturbances and, in turn, may produce a variety of adverse local and systemic consequences. Mechanisms of ischemic injury and the central role of vasoconstriction are discussed.

Hemodynamic basis of the pain of chronic mesenteric ischemia.

Tonometry, a new technique to indirectly assess intestinal blood flow, was used to determine the hemodynamic changes produced by a simulated meal in animals with a fixed, decreased splanchnic blood flow. In experiments on 14 dogs, celiac artery and superior mesenteric artery blood flow was maintained at 50 percent of normal flow by occluders and flow probes, and tonometers were placed in the stomach and small bowel to measure intramural pH, a metabolic marker of intestinal perfusion. Intramural pH was determined at 100 percent and 50 percent splanchnic blood flow, at 50 percent flow after instillation of cream into the stomach, and again when cream was placed into the small bowel. Intestinal intramural pH decreased significantly when blood flow was decreased to 50 percent, as expected, but decreased significantly again when cream was placed in the stomach. The hemodynamic explanation of the decrease when cream was placed in the stomach is a steal from the intestinal to the gastric circulation stimulated by food in the stomach. Such a steal could explain the temporal nature of the pain experienced by patients with chronic mesenteric ischemia.

The effect of metronidazole on wound healing in rats.

Metronidazole is gaining increasing acceptance as a perioperative antimicrobial agent. We studied the effect of metronidazole on wound healing in Sprague-Dawley rats, which received seven daily intraperitoneal injections of either metronidazole, 20 mg/kg/day, (simulating a therapeutic course) or equivalent volumes of physiologic saline solution. On the second day of treatment 25 treated rats and 20 control rats had full-thickness circular skin defects created on the back and standardized midline celiotomy incisions. The fascial incisions were closed with staples, and the abdominal skin was closed with silk sutures. On the seventh postoperative day all rats were put to death. The breaking strength of 1 cm wide segments of skin and fascial celiotomy wounds was measured, and the contraction of the open back wounds was computed. There was no significant difference in wound contraction or skin wound breaking strength, but fascial wound breaking strength was lower in treated rats than in control rats (283 versus 548 gm mean; 2 p less than 0.001). To determine whether metronidazole permanently altered or only temporarily delayed fascial wound healing, 39 additional rats treated with metronidazole and 40 control rats underwent celiotomies as described above on the second day of a 7-day course of treatment. Fascial wound breaking strength was measured 2, 3, and 5 weeks after operation. The wound breaking strength in rats treated with metronidazole remained significantly lower than that of control rats at 2 and 3 weeks (860 versus 1005 gm at 2 weeks and 1071 versus 1369 gm at 3 weeks; both 2 p less than 0.05), but at 5 weeks there was no significant difference between treated and control groups (1358 versus 1399 gm). Metronidazole apparently interferes with early fascial wound healing, but the wounds of treated rats ultimately attain the same strength as untreated controls.

Qualitative and quantitative fluorescein fluorescence in determining intestinal viability.

Clinical evaluation and qualitative (visual) and quantitative (fluorometric) fluorescence for predicting intestinal viability were compared in an animal model of temporary arterial occlusion with early revascularization. Quantitative fluorescence was determined with a perfusion fluorometer after an intravenous bolus of fluorescein. Qualitative fluorescence was determined by examination under a Wood's lamp in a darkened room. The effectiveness of each diagnostic technique in determining nonviability was expressed in terms of sensitivity, specificity, and accuracy. All three methods had 100 percent specificity; only bowel deemed nonviable proved to be so. Quantitative fluorescence also had a 100 percent sensitivity, but clinical evaluation and qualitative fluorescence had only a 33 and 11 percent sensitivity, respectively (some segments of bowel that were ultimately nonviable were not correctly predicted to be so). The inaccuracy of qualitative fluorescence was due to the fact that ischemic intestine with a hyperfluorescent pattern often progressed to necrosis. Fluorometric quantitation identified those hyperfluorescent segments that were viable. This study suggests that visual fluorescence is not reliable in assessing intestinal viability after early revascularization after arterial occlusion, but quantitative fluorometric fluorescence is reliable in almost all instances.

Vascular ectasias of the right colon in the elderly: a distinct pathologic entity.

Vascular ectasias (angiodysplasias, arteriovenous malformations) of the cecum and ascending colon are a frequent cause of lower intestinal bleeding in the elderly that has been overlooked by clinicians and pathologists. Their nature and etiology have been poorly understood until recently. This article reviews the previous literature and presents a complete and detailed description of these lesions based on the examination of 87 areas showing vascular ectasia from 26 colons. Their morphology spans a spectrum from small focal early lesions to multiple large late lesions. The early lesions are characterized by markedly dilated, large, tortuous submucosal veins with minimal dilatation of their tributaries in the mucosa. The late lesions showed further dilatation of submucosal veins and venules and extensive replacement of the overlying mucosa by racemose collections of dilated and thin walled venules and capillaries, three of which demonstrated rupture into the colonic lumen. The pathology of these lesions is considered to be specific enough to establish vascular ectasias of the colon as a distinct entity.

The pathophysiologic basis for the angiographic signs of vascular ectasias of the colon.

Three reliable diagnostic signs were identified on angiograms from 25 patients with ectasias of the right colon: (a) a slowly emptying dilated, tortuous, intramural vein; (b) a vascular tuft; and (c) an early filling vein. The frequency of these signs and the order of their occurrence reflect the different stages in the evolution of ectasias. The earliest and most frequent sign, the slowly emptying vein, reflects ectatic changes in a submocosal vein resulting from chronic intermittent partial obstruction. The vascular tuft represents more advanced lesions and corresponds to extension of the degenerative process to the venules in the mucosa. An early filling vein reflects an arteriovenous communication through a dilated arteriolar-capillary-venular unit-a mucosal ectasia.