NOMI causes segmental, discontinuous intestinal vascular obstruction without organic occlusion of the mesenteric vascular trunk [1]. NOMI generally affects patients older than 50 years suffering from myocardial infarction, congestive heart failure, aortic insufficiency, and renal or postoperatively following cardiac surgery [5]. Only one report has discussed NOMI occurring during treatment for acute stroke [6].
The American Society for Parenteral and Enteral Nutrition and Society of Critical Care Medicine 2009 recommendations for early initiation of enteral nutrition [7] have promoted early enteral nutrition for critically ill patients worldwide. Accordingly, stroke patients have undeniably benefited from early enteral nutrition in many ways.
However, NOMI is a disadvantage of early enteral nutrition. Although early enteral nutrition is cautiously administered in patients with known risk factors, enteral nutrition is aggressively used in stroke patients. Given the increasing frequency of NOMI in stroke patients (including suspected cases and cases not treated surgically), we evaluated whether, due to several factors, stroke patients might be at higher risk for NOMI.
One of the pathogenetic mechanisms of NOMI is a mismatch in the oxygen demand-and-supply ratio in the intestine, particularly in the vulnerable superficial mucosa, that is induced by early enteral nutrition [8, 9]. Thus, early enteral nutrition, which is often started earlier in stroke patients because they do not have organic bowel problems, should be recognized as a risk factor for NOMI. Furthermore, for various reasons, stroke patients undergo tracheostomy, followed by early enteral nutrition.
We consider it is preferable to start enteral nutrition after tracheostomy with a small amount or the day after tracheostomy. Of course, pathological condition leading to tracheostomy has greater effect on intestinal peristalsis. Although tracheostomy does not directly affect intestinal movement, we think it does have an indirect effect on decreased intestinal movement. Under such circumstances, early enteral nutrition may be a risk factor for NOMI.
In addition, nicardipine, which is used for strict blood-pressure control, has an inhibitory effect on the gastrointestinal smooth muscle and may cause paralytic ileus (which is a well-known side effect that tends to be ignored). Moreover, administering early enteral nutrition in ileus may lead to bacterial overgrowth and progressive edema, thereby impairing intestinal mucosal blood supply and causing ischemic injury [10].
Many stroke patients have high vascular risks, and optimal intestinal blood flow may not be maintained during strict blood-pressure control. All of the above-mentioned cases occurred under strict blood-pressure control, and two patients developed NOMI early after tracheostomy following resumption of enteral nutrition.
For the above-mentioned reasons, patients with acute stroke should be considered to be at a high risk for NOMI.