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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Necrotizing enterocolitis (NEC) sometimes occurs in term infants with congenital heart disease. This article reports a rare case of a term infant with coarctation of the aorta complex who developed NEC on the 8th day after birth. Spontaneous closure of the ductus arteriosus in the 1st week of life may cause intestinal ischemia and hypoxia with resultant NEC.
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PMID:Necrotizing enterocolitis in a term infant with coarctation of the aorta complex. 903 12

Ischemia/reperfusion (I/R) injury to the intestinal mucosa occurs in several commonly encountered clinical situations, such as necrotizing enterocolitis and nonocclusive mesenteric insufficiency. No clinically feasible technique is available for mucosal preservation during ischemia. The goal of this work was to determine whether the continuous intraluminal flow of oxygenated perfluorocarbon (PFC) could protect mucosal integrity and function in a rat model of intestinal I/R injury. Rats were subjected to ischemia by clipping the superior mesenteric artery (SMA) for 60 minutes. Reperfusion was achieved by release of the clip for 120 minutes. Animals were divided into 4 groups: Sham (laparotomy alone), I/R (I/R alone), I + PFC/R (PFC was administered during the ischemic interval only), I/R + PFC (PFC was delivered only during reperfusion). Tissue sections were examined blindly to assess mucosal integrity, and mucosal dissacharidase activities were measured to assess function. Oxygenated PFC, when administered during ischemia alone, ameliorated I/R-induced mucosal injury; however, when it was delivered during reperfusion alone, the mucosal injury worsened. When oxygenated PFC was administered throughout I/R, the degree of mucosal injury was similar to the I + PFC/R group, and dissacharidase activities were preserved when compared with the I/R group. Intraluminal perfusion of oxygenated PFC during ischemia preserves mucosal function and integrity, and may offer a new treatment modality for a variety of mesenteric ischemic disorders.
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PMID:Oxygenated intraluminal perfluorocarbon protects intestinal muscosa from ischemia/reperfusion injury. 904 54

The successful use of a combination of "patch, drain, and wait" (PDW) and home total parenteral nutrition (TPN) in the management of a case of acute, catastrophic midgut volvulus in a 2-year-11-month-old boy with near-total ischemia/necrosis of his small intestine is reported. The PDW approach to the highly effective management of acute midgut ischemia/necrosis in infancy and childhood (necrotizing enterocolitis and midgut volvulus) involves maximum gut salvage by avoidance of resection, stoma formation, or both through the use of extensive peritoneal cavity drainage by Penrose drains, TPN, and broad-spectrum antibiotics. The extensive peritoneal drainage fosters capture of enteric fistulas with the formation of enterostomies at drain exit sites, while adhesions and ischemia/inflammation-induced hypervascular obliteration of the peritoneal cavity diminish the potential for peritonitis (no peritoneal cavity, no peritonitis) and facilitate impressive salvage of seemingly hopelessly lost ischemic/necrotic gut (a simulation of the in utero ischemic gut process leading to atresias and some varying, but generally mild, gut loss) while simultaneously contributing to the resorption of absolutely non-salvageable gut and the creation of a remarkably clean and adhesion-free peritoneal cavity resembling that of a newborn infant with midgut intestinal atresia.
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PMID:Combination of "patch, drain, and wait" and home total parenteral nutrition for midgut volvulus with massive ischemia/necrosis 906 40

The successful use of a combination of "patch, drain, and wait" (PDW) and home total parenteral nutrition (TPN) in the management of a case of acute, catastrophic midgut volvulus in a 2-year-11-month-old boy with near-total ischemia/necrosis of his small intestine is reported. The PDW approach to the highly effective management of acute midgut ischemia/necrosis in infancy and childhood (necrotizing enterocolitis and midgut volvulus) involves maximum gut salvage by avoidance of resection, stoma formation, or both through the use of extensive peritoneal cavity drainage by Penrose drains, TPN, and broad-spectrum antibiotics. The extensive peritoneal drainage fosters capture of enteric fistulas with the formation of enterostomies at drain exit sites, while adhesions and ischemia/inflammation-induced hypervascular obliteration of the peritoneal cavity diminish the potential for peritonitis (no peritoneal cavity, no peritonitis) and facilitate impressive salvage of seemingly hopelessly lost ischemic/necrotic gut (a simulation of the in utero ischemic gut process leading to atresias and some varying, but generally mild, gut loss) while simultaneously contributing to the resorption of absolutely non-salvageable gut and the creation of a remarkably clean and adhesion-free peritoneal cavity resembling that of a newborn infant with midgut intestinal atresia.
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PMID:Combination of "patch, drain, and wait" and home total parenteral nutrition for midgut volvulus with massive ischemia/necrosis. 915 65

Although the pathogenesis of necrotizing enterocolitis remains uncertain, ischemia appears to be an important contributing factor to the development of this disorder. Reperfusion plays a major role in ischemia-related injury, and oxygen free radicals produced during reperfusion most likely contribute to the injury. These oxidants can be generated during prostanoid metabolism, which increases during reperfusion of ischemic gut in adult subjects. The present study was designed to: 1) examine the effects of superior mesenteric artery occlusion, e.g. ischemia and reperfusion in vivo on the development of histopathologic intestinal injury; 2) determine whether products of arachidonic acid metabolism, e.g. prostanoids are increased during reperfusion of ischemic gut; and 3) determine whether oxygen free radical scavengers attenuate the injury in newborn pigs. Chronically catheterized placebo-pretreated newborn pigs exposed to ischemia-reperfusion, placebo-pretreated nonischemic control pigs, and polyethylene glycol-superoxide dismutase (SOD) plus polyethylene glycol-catalase (CAT)-pretreated, ischemic pigs were studied by examining changes in intestinal circulation, oxygenation, prostanoids, and tissue injury. In the placebo-pretreated pigs, intestinal blood flow decreased to very low levels during superior mesenteric artery occlusion. During reperfusion, blood flow increased, but remained below baseline. After ischemia, oxygen uptake returned to values that were similar to baseline. Intestinal efflux of the vasodilator 6-keto-prostaglandin F1alpha was evident (p < 0.05 versus no or zero efflux) during early reperfusion. Histopathologic scoring of terminal ileal samples showed significant mucosal necrosis, surface epithelial disruption, lamina propria congestion and hemorrhage, submucosal hemorrhage, edema, and increases in cells compared with the placebo-pretreated nonischemic pigs. In the SOD plus CAT-pretreated ischemic pigs, changes in intestinal blood flow, oxygen uptake, 6-keto-prostaglandin F1alpha efflux, and the pattern of the ileal tissue injury did not differ significantly from the placebo-pretreated ischemic pigs. In summary, superior mesenteric artery occlusion for 1 h and reperfusion for 2 h resulted in severe intestinal ischemia, early postocclusive limited increases in intestinal perfusion and oxygen uptake, efflux of vasodilating prostanoids during early reperfusion, and signs of ischemic tissue injury in the placebo- and SOD plus CAT-pretreated pigs. This study demonstrates that, after superior mesenteric artery occlusion and reperfusion, severe intestinal tissue injury is detected in vivo, prostanoid efflux increases, and SOD plus CAT given just before occlusion does not attenuate the extent of injury in newborn pigs.
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PMID:Ischemia-reperfusion injury in the intestines of newborn pigs. 926 20

This review illustrates the changing paradigms in the understanding of the pathogenesis of pneumatosis intestinalis. Although many theories have been evoked, pragmatically there appear to be four major clinical and diagnostic imaging considerations. The most common and most emergent life-threatening cause of intramural bowel gas is the result of bowel necrosis due to bowel ischemia, infarction, necrotizing enterocolitis, neutropenic colitis, volvulus, and sepsis. In the stomach, intramural gas can be caused by emphysematous gastritis or ingestion of caustic agents. These situations represent surgical emergencies. Pneumatosis is found secondary to mucosal disruption presumably due to over-distention from peptic ulcer, pyloric stenosis, annular pancreas, and even to more distal obstruction. Disruption can also be caused by ulceration, erosions, or trauma, including the trauma of child abuse. Disruption can also be iatrogenic from intracatheter jejunal feeding tubes, stent perforation, sclerotherapy, or surgical or endoscopic trauma. In these cases, the gas may be focal or linear. Treatment depends on the extent of the disruption and the underlying cause. A more subtle form of mucosal disruption may occur due to mucosal erosions and also to defects in intestinal crypts secondary to acute and subclinical enteritides that allow intraluminal bacterial gas under pressure to percolate into the bowel wall layers, particularly the submucosa (29). Pneumatosis, often linear or cystic in appearance, is seen with increased frequency in patients who are immunocompromised because of steroids, chemotherapy, radiation therapy, or AIDS. In these cases, the pneumatosis may result from intraluminal bacterial gas entering the bowel wall due to increased mucosal permeability caused by defects in bowel wall lymphoid tissue. Clinical and imaging findings are important in the differentiation of this transient pneumatosis from fulminant life-threatening causes in this subset of patients. A pulmonary cause must still be considered in cases of chronic obstructive pulmonary disease, asthma, and cystic fibrosis. It can occur with barotrauma and after chest tube placement. It may relate to increased intrathoracic pressure associated with retching and vomiting. The possibility remains that occasionally the origin of pneumatosis intestinalis will remain cryptogenic--caused but unexplained.
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PMID:Pneumatosis intestinalis: a review. 953 Feb 94

The marked advantages and merit of pre-term and particularly pre-labor (PTPL) cesarean section (C-section) in the avoidance, and indeed, virtual elimination of severely disabling gastroschisis (GS) complications in infants diagnosed prior to birth by ultrasound has unfortunately remained controversial in the 10 to 12 years since it was first reported and strongly recommended by numerous authors. During this period, GS has remained one of the four major causes of the short-gut syndrome (SGS) in infancy and childhood and a major cause of prolonged, costly, complicated, and hazardous neonatal intensive care unit stays with requirements for total parenteral nutrition (TPN). The most serious and frequent complications of GS in infants born without PTPL C-section are the occurrence of the "peel", which greatly enlarges and rigidifies the eviscerated gut, and of "complicated GS" (intestinal atresia/s, stenosis, necrosis, perforations) (CGS). The "peel" occurs in 100% of these cases and CGS in approximately 20%. "Peel" enlargement and rigidification of eviscerated intestine in the presence of a reduced peritoneal cavity causes great difficulty in covering the eviscerated, enlarged, and rigidified gut with abdominal wall, skin, a prosthesis, etc., and frequently produces gut ischemia from excessive pressure, which may lead to necrotizing enterocolitis (NEC) and SGS as well as prolonged hospital stays. The presence of a "peel" greatly complicates the hazards of dealing with cases of CGS, as resection and anastomosis are virtually impossible in the presence of a "peel." The authors report personal experience with 77 cases of GS dating as far back as 1951; 44 of the infants were born after the onset of labor by vaginal or C-section delivery and all had some degree of "peel" formation. Of 320 cases from the literature (including some of the cases reported here), 61 (19.1%) involved CGS. Of the 33 cases born PT, and especially PL, there were no cases of "peel" and only 1 case of CGS (3.0%). This infant had a single atresia associated with a very small (1 cm) defect in the abdominal wall and no labor-induced "peel," which was easily and successfully repaired by resection and anastomosis. The 6.4-fold reduction in the occurrence of CGS by PTPL C-section (3.0% vs 19.1%) was statistically significant by the chi-square test (P < 0.05), as was the 100% elimination of the disabling "peel." If the single case of CGS associated with a very small defect and no labor or labor-associated "peel" is eliminated, the incidence of CGS in the remaining PTPL group of 32 cases falls to 0 (0% versus 19.1%, P < 0.007). PT and especially PL C-section may be expected to virtually eliminate "peel" formation and CGS and to remove GS as one of the four major causes of SGS. The findings of this report that PT labor prior to PT C-section may result in both "peel" formation and CGS further solidifies the role of labor in the production of both the "peel" and the equally disabling CGS. Failure to appreciate the central role of labor in GS complications has doubtless contributed to the persistent controversy concerning the value and importance of PTPL C-section for gastroschisis diagnosed in utero. The pediatric surgeon has an important responsibility with the obstetrician to monitor the possible occurrence of occult labor in the waning weeks of pregnancy and be prepared to do a prompt C-section if it occurs and there is adequate lung maturity. The achievement of "peel"- and CGS-free gut would greatly facilitate the use of the new Bianchi technique of gut reduction without anesthesia. The combination of the use of epidural anesthesia for the elective PTPL C-section with the Bianchi approach would spare both mother and baby any untoward effects of general anesthesia and present the potential for massive reductions in hospital costs with minimal patient manipulation and disturbance. For infants born with labor-associated "peel," re-evaluation of the suitability and effectiv
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PMID:Pre-term and particularly pre-labor cesarean section to avoid complications of gastroschisis. 1078 91

The traditional and most frequently employed surgical approach to perforated necrotizing enterocolitis (NEC), laparotomy and bowel resection with enterostomy creation, has been associated with an unacceptably high mortality and major morbidity (sepsis, short-gut syndrome, strictures, long-term total parenteral nutrition (TPN), prolonged and costly hospitalizations with multiple operations, the inevitable open-and-close procedure for "hopeless" extensive gut ischemia in approximately 10% of laparotomy cases, etc.). The use of the laparotomy "patch, drain, and wait" (PD&W) approach to this serious of NEC complication has provided a simple, direct, and effective means of dealing with this problem. The basic principle is to resect no gut and do no enterostomies. The details are presented here as well as the multiple types of "patching" and the importance of use of extensive direct-vision draining with bilateral small Penrose drains from the undersurfaces of both diaphragms into the pelvis with exit sites in both lower quadrants. Proper and effective patching and draining cannot be done blindly,but requires direct vision (laparotomy or laparoscopy). The critical components and timing of the "waiting" are emphasized, including the vital importance of strict avoidance of early post-drainage laparotomy in the 7- to 14-day post-drainage period (whether the drainage is percutaneous, laparotomy PD&W, or laparoscopy PD&W) due to the early, life-threatening-ending hypervascularity that occurs at this time and if left unmolested will function beneficially as life- and gut-saving "good angiogenesis". The bilateral Penrose drains capture fecal fistulas and function quite well as de-facto enterostomies as the peritoneal cavity is rapidly obliterated by adhesions and massive, florid hypervascularity/gut hypoxia triggered "good angiogenesis" (no peritoneal cavity, no peritonitis). Broad-spectrum triple antibiotics and the routine use of TPN contribute to favorable results. The lessons/experiments of nature encountered in newborns with midgut atresia(s) and remarkable levels of gut survival, in the occasional case with only meconium peritonitis and no obstruction ("auto-anastomosis") are pertinent here as the TPN of PD&W is provided in atresia(s) by the maternal-placental circulation and the sterile peritoneal cavity of atresia(s) is simulated by the combination of antibiotics and peritoneal-cavity obliteration. Life- and gut-saving "good angiogenesis" is common to both situations. A 15-year personal experience with the PD&W laparotomy approach to perforated NEC in 23 cases is reported here with no mortality in the initial 60 postoperative days, no major morbidity, and no second operation required in 70% (spontaneous "auto-anastomosis") of cases. All infants with extensive gut ischemia/necrosis (NEC totalis) who would otherwise be classified as "hopeless" and managed by open-and-close only were managed in this experience successfully by PD&W with preservation of both life and an adequate amount of gut, although a second operation was required in these cases to re-establish intestinal continuity. A particularly striking observation was the rapid transition of these infants from profound illness to near-normalcy in a matter of hours after the initiation of PD&W--much like the rapid clinical changes accompanying the lancing of a boil or an abscess. An involvement of hypoxia-induced "good angiogenesis" with marked hypervascularity and involving molecules, genes, and receptors of the vascular endothelial growth factor family of hypoxia-induced angiogenesis molecules is speculated upon, and clinical studies to document these speculations are suggested as well as studies evaluating the potential of laparoscopic PD&W. The usefulness of Argyle chest-tube "venting" and "stenting" by trans-anal passage above colonic "patched" areas as seen in 2 cases is worthy of further study and use.
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PMID:Successful use of the "patch, drain, and wait" laparotomy approach to perforated necrotizing enterocolitis: is hypoxia-triggered "good angiogenesis" involved? 1095 62

The loss of small intestinal mucosal surface area is a relatively common clinical situation seen in both the pediatric and adult population. The most frequent causes include mesenteric ischemia, trauma, inflammatory bowel disease, necrotizing enterocolitis, and volvulus. Following surgical resection, the remnant intestine compensates or adapts to the loss of native bowel by increasing its absorptive surface area and functional capacity. Unfortunately, many patients fail to adapt adequately, and are relegated to lifelong intravenous nutrition. Research into intestinal adaptation following small bowel resection (SBR) has evolved only recently from the gross and microscopic level to the biochemical and genetic level. As understanding of this process has increased, numerous therapeutic strategies to augment adaptation have been proposed. Epidermal growth factor (EGF) is an endogenous peptide that is secreted into the gastrointestinal tract and able to influence gut ontogeny, as well as mucosal healing. Early studies have demonstrated its ability to augment the adaptive process. Focusing on a murine model of massive intestinal loss, the morphological, structural, biochemical, and genetic changes that occur during the intestinal adaptive process will be reviewed. The role of EGF and its receptor as critical mediators of the adaptive process will be discussed. Additionally, the ability of EGF to augment intestinal proliferation and diminish programmed cell death (apoptosis) following SBR will be examined. Enhancing adaptation in a controlled manner may allow patients to transition off parenteral nutrition to enteral feeding and, thereby, normalize their lifestyle.
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PMID:Epidermal growth factor is critical for intestinal adaptation following small bowel resection. 1105 64

The term intestinal necrosis is nothing but a clinical and pathological concept and always includes intestinal ischemia, whether or not occlusive. In a broad sense, necrotizing enterocolitis involves intestinal ischemia associated to an infectious entity. The precipitating factor for necrosis is very often difficult to identify. Necrotizing enterocolitis occurs in 90% of cases in premature neonates and is less frequent amongst other neonates, being rare in older children and adults. The authors present two clinical cases: one 7 year-old with a history of chronic neutropenia and an eleven-year old with severe cognitive impairment, dysmorphic features and behavioural disturbances. They were both admitted to hospital due to an acute abdominal condition and shock. The necrosis implied the resection of a jejunal segment in one of the cases, and a subtotal colonic resection in the other. Despite the surgery and medical support therapy, they both died due to multiple system organ failure--3 hours and fourteen days after surgery, respectively. In the second case, death occurred subsequent to a second surgery for resection of a segment of necrotic ileum. Necropsy showed an extensive necrosis of the remaining intestine in both cases. These two cases evolved as necrotizing enterocolitis of the child. In one of the cases it was possible to establish the exclusion diagnosis of neutropenic enterocolitis. The etiopathogenic mechanisms are reviewed, including thrombotic, obstructive (both extrinsic and endoluminal), inflammatory, non-occlusive ischemic and infectious. The authors stress the general therapeutic measures, the relevance of early surgical intervention and the use of subsidiary diagnostic/therapeutic technologies, such as serum and urine title of intestinal fatty acid binding protein or selective arteriography.
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PMID:[Intestinal necrosis in children]. 1123 98


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