With great interest we read the recent article by Reintam Blaser et al. describing the current status of managing acute mesenteric ischemia (AMI) in the critically ill patient [1]. We would like to congratulate the authors for their thorough and balanced review of the present diagnostic and therapeutic options in these patients and especially agree on the importance of further research in exploring the least understood AMI entity associated with the highest mortality, namely non-occlusive mesenteric ischemia (NOMI).

Traditionally linked primarily with post-cardiac surgery patients, our group, along with others, has more recently shown that NOMI can also occur in diverse medical intensive care patients with septic shock and multi-organ failure [2, 3]. Early diagnosis of NOMI remains very challenging given the lack of biomarkers and specific clinical signs in critically ill, non-awake patients. However, we recently identified unclear rapid deterioration of organ-function and vasopressor dose as earlier clinical signs than ischemic injury-related markers such as transaminases, creatine-kinase or lactic acid dehydrogenase [2]. Treatment of NOMI beyond correcting hypovolemia and cardiac output remains equally challenging.

In our experience, patients diagnosed with potential additional NOMI, especially those presenting with septic shock and multi-organ failure, often exhibit high levels of instability, rendering abdominal exploration for surgeons exceptionally challenging. As an alternative, intra-arterial vasodilatory therapy directly in the superior mesenteric artery has been explored for a long time as a minimal-invasive approach to improve splanchnic perfusion [4]. In the absence of randomized controlled studies, comparative analyses have repeatedly demonstrated a potential survival benefit in patients undergoing additive intra-arterial vasodilatory therapy when compared to conservative therapy alone [2, 4, 5]. Our group has prospectively investigated potential predictors of response to intra-arterial vasodilatory therapy using both clinical as well as perfusion angiography data [3]. This study identified a reduction of serum lactate concentration of more than 2 mmol/l in the first 24 h after the intervention as a strong predictor of treatment success, e.g. patients with such a lactate reduction had a 26% lower mortality (59% vs. 85%) [3]. Measurement of non-routine biomarkers of intestinal ischemia at study inclusion revealed that transmural ischemia might be already present in most of these patients although computed tomography contrast imaging did not indicate any signs of transmural necrosis at this time, likely further indicating the therapeutic dilemma still seen in these patients.

Does NOMI remain an untreatable disease in the critically ill?

Robert Kennedy said once: “Some men see things as they are and ask, “Why?” I dream things that never were and ask, “Why not?”. Let us collaborate to enhance our capabilities in comprehending, diagnosing and treating NOMI in critically ill patients.