Asassfeh Ayham, Zughul Ramy
General Practice, Ibn Al Haytham Hospital, Amman, JOR.
Critical Care Medicine, University of Michigan, Lansing, USA.
Cureus. 2025 Mar 11;17(3):e80427. doi: 10.7759/cureus.80427. eCollection 2025 Mar.
Ischemic colitis constitutes about half of mesenteric vasculopathies, and it shares a similar pathophysiologic process with acute and chronic mesenteric ischemia. These, in turn, can be divided into occlusive and nonocclusive mesenteric ischemia (NOMI). We present this case of a patient presenting with abdominal pain secondary to right-sided colitis, initially presumed to be infectious, but later attributed to localized NOMI. The correlation between localized NOMI, specifically right-sided colitis, and right ventricular (RV) failure has not been well described in the literature. NOMI, in general, is suspected to be secondary to splanchnic vasoconstriction, which results from sympathetic stimulation and renin-angiotensin-aldosterone system (RAAS) activation. Additionally, patients with RV failure have been shown to develop intestinal congestion due to elevated right atrial pressure (RAP), leading to bowel wall thickening and impaired mesenteric venous drainage, which may further contribute to ischemia. This mechanism suggests that both arterial hypoperfusion and venous congestion may play a role in the pathogenesis of right-sided ischemic colitis in RV failure. The predominance of ischemia in the right colon, rather than in classical watershed areas, may be attributed to preferential vasoconstriction of the superior mesenteric artery (SMA), which supplies the right colon, as well as localized venous congestion impairing mesenteric drainage in this region. Individual variability in vascular anatomy and autoregulatory responses could also contribute to this atypical presentation. This case highlights a potentially underrecognized association between RV dysfunction and right-sided ischemic colitis, emphasizing the interplay of low cardiac output, mesenteric hypoperfusion, and venous congestion. Given the absence of direct studies on this relationship, further research is needed to better understand its clinical significance.
缺血性结肠炎约占肠系膜血管病变的一半,其病理生理过程与急性和慢性肠系膜缺血相似。而急性和慢性肠系膜缺血又可分为闭塞性和非闭塞性肠系膜缺血(NOMI)。我们在此报告一例因右侧结肠炎继发腹痛的患者,最初推测为感染性病因,但后来归因于局限性NOMI。局限性NOMI,特别是右侧结肠炎与右心室(RV)衰竭之间的相关性在文献中尚未得到充分描述。一般认为,NOMI继发于内脏血管收缩,这是由交感神经刺激和肾素-血管紧张素-醛固酮系统(RAAS)激活所致。此外,已有研究表明,RV衰竭患者由于右心房压力(RAP)升高会出现肠道充血,导致肠壁增厚和肠系膜静脉引流受损,这可能进一步加重缺血。这种机制表明,动脉灌注不足和静脉充血可能在RV衰竭导致的右侧缺血性结肠炎发病机制中均起作用。右半结肠缺血而非典型分水岭区域缺血占优势,可能归因于供应右半结肠的肠系膜上动脉(SMA)的优先血管收缩,以及该区域局部静脉充血导致肠系膜引流受损。血管解剖结构和自身调节反应的个体差异也可能导致这种非典型表现。该病例突出了RV功能障碍与右侧缺血性结肠炎之间可能未被充分认识的关联,强调了低心输出量、肠系膜灌注不足和静脉充血之间的相互作用。鉴于缺乏关于这种关系的直接研究,需要进一步研究以更好地理解其临床意义。