We thank Acosta et al. [1] for their critical comment on our retrospective study [2] and important clarifications regarding the nomenclature of acute mesenteric ischemia (AMI). Most importantly, the authors point out the difference between intensive care unit (ICU) patients and non-ICU inpatients or outpatients with AMI. In our cohort, over 80% of the patients have been treated in the ICU when AMI was suspected, and more than 50% were supported with vasopressors [2, 3]. Clinical signs and symptoms for AMI such as abdominal pain are unspecific and occur late in many patients [4]. Critically ill patients in the ICU frequently receive analgesics, or they are even comatose, seriously complicating clinical assessment. Due to hemodynamic instability or even cardiocirculatory arrest resulting in intestinal hypoperfusion, these patients are particularly susceptible to non-occlusive mesenteric ischemia (NOMI). Diagnostic difficulties mean that NOMI is often overlooked and only diagnosed post-mortem by autopsy [5].

The small intestine is mainly affected in patients with acute occlusion of the superior mesenteric artery (SMA). In these cases, AMI can be reliably diagnosed by clinical assessment and computed tomography angiography (CTA) in many cases. In contrast, NOMI often affects the right hemicolon [5]. Therefore, we recommend developing screening protocols for colonoscopy in critically ill patients in the ICU with a high risk of NOMI for timely detection of colon ischemia. We argue that patients after cardiac arrest, and patients with severe shock with and without mechanical circulatory support, should be critically selected for early routine colonoscopy. Colonoscopy is widely available and can be performed at the bedside in the ICU, minimizing the additional risks of patient transport, as for CTA assessment. The risk profile of colonoscopy in these patients seems to be favorable [2, 3]. Considering perfusion deficits in the SMA as the most frequent cause for AMI in critically ill patients, it is important, that the right hemicolon is assessed. If uncertainty prevails after endoscopy, or additional signs of tissue ischemia persist, CTA should be considered. Future studies should particularly assess the association of ischemia in the right hemicolon with small bowel ischemia not visible during colonoscopy.

Currently, the optimal treatment for patients with NOMI is still a matter of debate. Limited ischemic mucosal changes may recover spontaneously. However, extensive transmural ischemia requires surgery to avoid bacterial translocation and severe peritonitis. It is exactly the mismatch between serosal and mucosal signs of ischemia that warrants colonoscopy in these cases. Colonoscopy is not primarily indicated to avoid laparotomy, but rather to tailor the surgical approach, namely the extent of resection. Peritonitis and pneumatosis are therefore only relative contraindications for colonoscopy. Secondary surgery for complete colectomy after, e.g., right hemicolectomy because of overlooked mucosal ischemia in the left colon must be avoided under all circumstances.

In summary, screening colonoscopy can be a valuable tool for early detection of NOMI in critically ill patients in the ICU. Nevertheless, further studies should be designed for the definition of optimal indication and timing for colonoscopy and risk-stratified management.