Pear B L
Department of Radiology, University of Colorado Health Sciences Center, Denver, USA.
Radiology. 1998 Apr;207(1):13-9. doi: 10.1148/radiology.207.1.9530294.
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.
本综述阐述了在理解肠壁积气发病机制方面不断变化的模式。尽管已提出许多理论,但实际上有四个主要的临床和诊断影像学方面的考量因素。壁内肠气最常见且最危及生命的原因是肠缺血、梗死、坏死性小肠结肠炎、中性粒细胞减少性结肠炎、肠扭转和脓毒症导致的肠坏死。在胃中,壁内气体可由气肿性胃炎或腐蚀性物质摄入引起。这些情况均为外科急症。肠壁积气继发于黏膜破坏,推测是由于消化性溃疡、幽门狭窄、环状胰腺甚至更远端梗阻导致的过度扩张所致。破坏也可由溃疡、糜烂或创伤引起,包括虐待儿童导致的创伤。破坏还可能是医源性的,如经导管空肠喂养管、支架穿孔、硬化治疗或手术或内镜创伤。在这些情况下,气体可能呈局灶性或线性。治疗取决于破坏的程度和潜在病因。黏膜破坏的一种更隐匿形式可能是由于黏膜糜烂以及急性和亚临床肠炎继发的肠隐窝缺陷所致,这使得腔内细菌气体在压力作用下渗入肠壁各层,尤其是黏膜下层(29)。肠壁积气通常表现为线性或囊性,在因使用类固醇、化疗、放疗或艾滋病而免疫功能低下的患者中更为常见。在这些情况下,肠壁积气可能是由于肠壁淋巴组织缺陷导致黏膜通透性增加,腔内细菌气体进入肠壁所致。临床和影像学表现对于区分该类患者中这种短暂性肠壁积气与暴发性危及生命的病因很重要。对于慢性阻塞性肺疾病、哮喘和囊性纤维化患者,仍必须考虑肺部病因。它可发生于气压伤和放置胸管后。它可能与干呕和呕吐相关的胸内压升高有关。肠壁积气的起源偶尔仍可能原因不明——虽有病因但无法解释。