Nonocclusive mesenteric ischemia (NOMI) is a condition that can encompass ischemia, inflammation, and infarction of the intestinal wall. In contrast to most patients with acute mesenteric ischemia, NOMI is distinguished by patent arteries and veins. The clinical presentation of NOMI is often insidious and nonspecific, resulting in a delayed diagnosis. Patients most at risk are those with severe acute and critical disease, including major surgery and trauma. Nonocclusive mesenteric ischemia is part of a spectrum, from mild, asymptomatic, and an unexpected finding on CT scanning, through to those exhibiting abdominal distension and peritonitis. Severe NOMI is associated with a significant mortality rate. This review of NOMI pathophysiology was conducted to document current concepts and evidence, to examine the implications for diagnosis and treatment, and to identify gaps in knowledge that might direct future research. The key pathologic mechanisms involved in the genesis of NOMI represent an exaggerated normal physiological response to maintain perfusion of vital organs at the expense of mesenteric perfusion. A supply-demand mismatch develops in the intestine due to the development of persistent mesenteric vasoconstriction resulting in reduced blood flow and oxygen delivery to the intestine, particularly to the vulnerable superficial mucosa. This mismatch can be exacerbated by raised intra-abdominal pressure, enteral nutrition, and the use of certain vasoactive drugs, ultimately resulting in the development of intestinal ischemia. Strategies for prevention, early detection, and treatment are urgently needed.

The use of polymeric, compared with (semi)elemental, formulation does not lead to a significantly higher risk of feeding intolerance, infectious complications or death in patients with acute pancreatitis. Neither the supplementation of enteral nutrition with probiotics nor the use of immunonutrition significantly improves the clinical outcomes.

Guidelines lacked consensus in their recommendations for minimally invasive management of pancreatic abscess, infected pseudocyst, and infected necrosis, and few recommendations were graded according to the strength of the evidence. More prospective trials are needed to provide evidence where it is lacking, which should be incorporated into clinical practice guidelines.

The mononuclear phagocytic system (MPS), comprised of monocytes, macrophages, and dendritic cells, is essential in tissue homeostasis and in determining the balance of the immune response through its role in antigen presentation. It has been identified as a therapeutic target in infectious disease, cancer, autoimmune disease and transplant rejection. Here, we review the current understanding of the immunophenotype and function of the MPS in normal human liver. Using well-defined selection criteria, a search of MEDLINE and EMBASE databases identified 76 appropriate studies. The majority (n=67) described Kupffer cells (KCs), although the definition of KC differs between sources, and little data were available regarding their function. Only 10 papers looked at liver dendritic cells (DCs), and largely confirmed the presence of the major dendritic cell subsets identified in human blood. Monocytes were thoroughly characterized in four studies that utilized flow cytometry and fluorescent microscopy and highlighted their prominent role in liver homeostasis and displayed subtle differences from circulating monocytes. There was some limited evidence that liver DCs are tolerogenic but neither liver dendritic cell subsets nor macrophages have been thoroughly characterized, using either multi-colour flow cytometry or multi-parameter fluorescence microscopy. The lobular distribution of different subsets of liver MPS cells was also poorly described, and the ability to distinguish between passenger leukocytes and tissue resident cells remains limited. It was apparent that further research, using modern immunological techniques, is now required to accurately characterize the cells of the MPS in human liver.