Acute Mesenteric Ischemia: The Challenge of Gastroenterology

Yasuhara, Hiroshi

doi:10.1007/s00595-004-2924-0

Cited by 250 publications

(214 citation statements)

References 80 publications

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“…Acute mesenteric ischemia (AMI) is an abdominal-vascular emergency which is rare and has high mortality rates (60-80 %) due to late diagnosis (1)(2)(3). AMI is seen in one out of thousand but the incidence is increasing (4).…”

Section: Introductionmentioning

confidence: 99%

“…The etiology of AMI can be evaluated in 4 sub-categories: superior mesenteric artery (SMA) embolism (45-50 %), thrombosis of SMA (25 %), superior mesenteric vein (SMV) thrombosis (5-10 %), and non-occlusive mesenteric ischemia (NOMI) (20 %) (4)(5)(6)(7). Despite the differences in its etiology, intestinal gangrene and necrosis is the fatal end of AMI (3,7).…”

Section: Introductionmentioning

confidence: 99%

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The place of D-dimer and L-lactate levels in the early diagnosis of acute mesenteric ischemia

Aydın¹,

Ozban²,

Serinken³

et al. 2015

BLL

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INTRODUCTION: Acute mesenteric ischemia (AMI) is an abdominal-vascular emergency which is rare and has high mortality rates (60-80 %) due to late diagnosis (1-3). Although it is known that extravascular reasons like intestinal intussusception, volvulus, strangulated hernias and obstructions can cause intestinal gangrene, these are rarely the cause of AMI (1). MATERIALS AND METHODS: In this study, we used male Wistar-Albino rats weighing 250-300 grams obtained from Pamukkale University Experimental Research Laboratory. Animals were exposed to light-dark cycles for 12 hours and had free access to food and water. They were kept in cages for 7 days to stabilise their intestinal fl ora. In animals of group I, nothing was made other than taking 0.5 ml blood intracardially. In other animals, abdomen was reached with midline laparotomy and superior mesenteric artery (SMA) was located. In group II (operative control group), SMA was isolated and manipulated but was not ligated. In Group III (intestinal ischemia group), SMAwas isolated and ligated with 3/0 silk tie distally to the aorta. After this process, intestinal ischemia was achieved which was confi rmed by paleness and pulselessness of intestines, caecum and right colon. Later on, abdomen was closed with double 3/0 polyglactin sutures. At postoperative 1st, 4th and 6th hours 0.5 ml blood was taken intracardially from the animals in groups II and III in order to quantify D-dimer and L-lactate levels. LABORATORY TESTS: D-dimer: Blood samples which were put into tubes containing sodium citrate, were seperated from plasma with centrifugation at 4000 rpm for 7 minutes. L-lactate: Blood L-lactate levels were determined from blood taken into capillary tubes with the help of immobilised enzyme electrode technology using YSI 1500 Sport portative lactate analyzer (Yellow Springs Instruments Inc., Ohio-USA). HISTOPATHOLOGIC VERIFICATION: Two cm long intestinal samples were taken from animals in which SMA was ligated in order to achieve mesenteric ischemia and these samples were fi xed in 10 % formol. DISCUSSION: As a result, in rats with SMA occlusion serum D-dimer levels were not increased signifi cantly when compared either in the group or with the basal values of the control group and values in operative control group. Therefore, it is concluded that D-dimer is not a useful marker for early diagnosis of AMI. On the other hand, it is revealed that blood L-lactate levels began to increase signifi cantly following 4th hour of mesenteric ischemia and it is shown that this increase continued at the 6th hour. In addition, considering the utmost importance of the early diagnosis in patients with the clinical suspicion of AMI, L-lactate seems to be a suitable marker to use in emergency departments because it is achieved with a portable device that gives fast and accurate results. Nevertheless, our results are need to be supported by clinical studies with larger patient series (Tab. 2, Fig. 11, Ref. 39). Text in PDF www.elis.sk.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The place of D-dimer and L-lactate levels in the early diagnosis of acute mesenteric ischemia

Aydın¹,

Ozban²,

Serinken³

et al. 2015

BLL

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“…[1][2][3] Intestinal I/R may trigger mucosal barrier damage and enteric bacterial translocation (BT), leading to development of septic complications. 4,5 The intestine contains over 100 trillion commensal bacteria that are normally restricted to the lumen.…”

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confidence: 99%

Neutrophil priming by hypoxic preconditioning protects against epithelial barrier damage and enteric bacterial translocation in intestinal ischemia/reperfusion

Huang

et al. 2012

Laboratory Investigation

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Intestinal ischemia/reperfusion (I/R) induces mucosal barrier dysfunction and bacterial translocation (BT). Neutrophilderived oxidative free radicals have been incriminated in the pathogenesis of ischemic injury in various organs, but their role in the bacteria-containing intestinal tract is debatable. Primed neutrophils are characterized by a faster and higher respiratory burst activity associated with more robust bactericidal effects on exposure to a second stimulus. Hypoxic preconditioning (HPC) attenuates ischemic injury in brain, heart, lung and kidney; no reports were found in the gut. Our aim is to investigate whether neutrophil priming by HPC protects against intestinal I/R-induced barrier damage and bacterial influx. Rats were raised in normoxia (NM) or kept in a hypobaric hypoxic chamber (380 Torr) 17 h/day for 3 weeks for HPC, followed by sham operation or intestinal I/R. Gut permeability was determined by using an ex vivo macromolecular flux assay and an in vivo magnetic resonance imaging-based method. Liver and spleen homogenates were plated for bacterial culturing. Rats raised in HPC showed diminished levels of BT, and partially improved mucosal histopathology and epithelial barrier function compared with the NM groups after intestinal I/R. Augmented cytokineinduced neutrophil chemoattractant (CINC)-1 and -3 levels and myeloperoxidase activity correlated with enhanced infiltration of neutrophils in intestines of HPC-I/R compared with NM-I/R rats. HPC alone caused blood neutrophil priming, as shown by elevated production of superoxide and hydrogen peroxide on stimulation, increased membrane translocation of cytosolic p47 phox and p67 phox , as well as augmented bacterial-killing and phagocytotic activities. Neutrophil depletion reversed the mucosal protection by HPC, and aggravated intestinal leakiness and BT following I/R. In conclusion, neutrophil priming by HPC protects against I/R-induced BT via direct antimicrobial activity by oxidative respiratory bursts and through promotion of epithelial barrier integrity for luminal confinement of enteric bacteria.

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“…Additional blood investigation revealed an extremely high serum procalcitonin level (>75 ng/mL; normal, <0.10 ng/mL). Although blood culture did not yield a causative pathogen, septic shock3 with bacterial translocation through gangrenous membrane resulting from increased intraduodenal pressure due to SMAS was considered 4. Because vascular occlusion and transmural bowel necrosis were both excluded by radiology and/or endoscopy, AMA was improved by decompression with nasogastric drainage.…”

Section: Figurementioning

confidence: 99%

Superior mesenteric artery syndrome leading to reversible mucosal gangrene

Uemura

Suzuki

Katayama

et al. 2017

Acute Medicine & Surgery

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We describe a case in which gastrointestinal distention due to superior mesenteric artery syndrome (SMAS) developed into membranous gangrene, which in turn led to septic shock in a 60‐year‐old woman with cerebral palsy and cachexia. The association with SMAS and septic shock is considered extremely rare, it is important to consider this combination especially in cachectic patients with gastric distension accompanying refractory shock unknown etiology.

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Acute Mesenteric Ischemia: The Challenge of Gastroenterology

Cited by 250 publications

References 80 publications

The place of D-dimer and L-lactate levels in the early diagnosis of acute mesenteric ischemia

The place of D-dimer and L-lactate levels in the early diagnosis of acute mesenteric ischemia

Neutrophil priming by hypoxic preconditioning protects against epithelial barrier damage and enteric bacterial translocation in intestinal ischemia/reperfusion

Superior mesenteric artery syndrome leading to reversible mucosal gangrene

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