Isolated cecal necrosis (ICN) represents a rare yet clinically significant variant of ischemic colitis, characterized by ischemic injury to the cecal region due to prolonged disruption of intestinal blood flow. While ICN can arise from various causes, including atherothrombotic occlusions in cecal arteries and non-occlusive factors such as shock or chronic diseases, its pathogenesis remains multifactorial. Clinical presentation often mirrors acute appendicitis, with patients typically presenting with sudden right lower quadrant abdominal pain. Prompt diagnosis and surgical intervention are paramount to mitigate the risk of cecal perforation and improve patient outcomes. However, preoperative diagnosis can be challenging due to non-specific radiological findings, necessitating urgent surgical resection of the affected intestine. Despite documented cases in the literature, knowledge regarding ICN remains limited, underscoring the importance of detailed case reporting to enhance disease understanding and refine diagnostic and therapeutic approaches. Here, we present a retrospective analysis of 7 ICN cases diagnosed in our hospital between 2019 and 2024, aiming to contribute insights into the clinical spectrum, management strategies, and outcomes associated with ICN. Our study revealed a diverse array of clinical presentations, radiological features, surgical interventions, and pathological findings among ICN patients. Hypertension and diabetes mellitus emerged as common comorbidities, with acute abdomen and abdominal pain being predominant symptoms. Radiologically, cecal wall thickening was frequently observed. Surgical management predominantly involved right hemicolectomy, with varying techniques employed. Pathological examination unveiled histological alterations indicative of ischemic necrosis, inflammation, and perforation. Our findings underscore the importance of considering ICN in the differential diagnosis of acute abdominal pain, particularly in elderly patients with predisposing risk factors. Further research efforts are warranted to elucidate its pathophysiological mechanisms and optimize therapeutic approaches.
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