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新生儿坏死性小肠结肠炎的病理学和发病机制

Author
Richard J Schanler, MD
Section Editor
Steven A Abrams, MD
Deputy Editor
Melanie S Kim, MD
Translators
曾凌空, 主任医师

引言

坏死性小肠结肠炎(necrotizing enterocolitis, NEC)是新生儿最常见的胃肠道急症,表现为肠黏膜缺血性坏死[1]。该病与炎症、肠道产气微生物侵袭以及气体进入肌层和门静脉系统有关。

NEC在活产儿中的发病率为1/1000-3/1000,主要见于早产儿,在极低出生体重儿[(very low birth weight, VLBW),即出生体重(birth weight, BW)小于1500g]中的发病率为6%-7%。尽管早期发现和积极治疗已经改善了该病的临床结局,但在新生儿重症监护病房的幸存者中,尤其是在VLBW中,NEC造成了相当多的远期并发症。

虽然早在1965年就已首次描述了NEC的病因,但至今仍不十分明确[2-4]。基于现有证据,本专题将总结NEC的病理和发病机制。该病的临床特征、治疗和预防将单独讨论。 (参见“新生儿坏死性小肠结肠炎的临床特征和诊断”“新生儿坏死性小肠结肠炎的治疗”“新生儿坏死性小肠结肠炎的预防”)

病理学

NEC的病理表现主要源于肠梗死引起的改变[5]。根据疾病进展和是否存在基础致病因素,其特异性病理表现有差异。大部分患者的末端回肠和结肠受累,而严重患者则整个胃肠(gastrointestinal, GI)道均受累。

大体病理检查上,肠道呈现肿胀和出血。偶尔,可沿肠系膜缘出现浆膜下积气。坏疽性坏死发生在对系膜缘,而且可能发生穿孔。随着肠道的恢复,会出现肠壁增厚、纤维粘连和狭窄区域。

                

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Literature review current through: 2017-06 . | This topic last updated: 2017-03-09.
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