Gastrointestinal motility can be markedly deranged in critical illness. This can have a number of important clinical sequelae—the most obvious of which is impaired delivery of enteral nutrition, which can result in malnutrition, if not recognized and treated. Impaired gastric emptying and lower esophageal sphincter function may allow reflux of gastric contents into the esophagus during enteral feeding, especially in the recumbent position. This situation, combined with the loss of normal airway reflexes in the sedated and sometimes paralyzed patient, results in aspiration, which can be subclinical and therefore unrecognized, impairing respiratory function and predisposing to ventilator-associated pneumonia. Another proposed consequence of gastrointestinal dysmotility in the critically ill is intestinal stasis with bacterial overgrowth, potentially leading to bacterial translocation and nosocomial sepsis. However, this has never been conclusively demonstrated in humans.
Esophageal Motility
The gastroesophageal sphincter has reduced activity in critical illness, which can have important clinical consequences. Basal lower esophageal pressures are reduced when compared to health and acid reflux occurs frequently during fasting and gastric feeding. Furthermore, reflux contents remain in the esophagus for prolonged periods as clearance is markedly impaired. Most reflux episodes occur because of very low or, in some cases, absent lower esophageal sphincter pressures. Reflux episodes are also associated with straining and coughing on the endotracheal tube.
Gastric Motility
Gastric motility can be markedly abnormal in critical illness resulting in slow gastric emptying and reduced ability to tolerate nasogastric delivery of nutrients. The stomach may be functionally divided into proximal and distal parts and, in order to achieve optimal gastric emptying, the motility of these regions needs to be coordinated. During critical illness, not only is the motility of each region disturbed, but also the motor integration between the proximal and distal stomach is disrupted.
Fundal tone is important for normal gastric emptying of liquid nutrient and, is, therefore, likely to be fundamental to the gastric emptying of liquid formulae in the critically ill patient. In health, proximal gastric relaxation occurs in response to the presence of duodenal nutrient. In critical illness, accommodation of the proximal stomach in response to small intestinal nutrient is delayed and there is increased retention in the proximal stomach. These abnormal patterns of motility are likely to result in delayed distribution of ingesta to the distal stomach, which will slow gastric emptying and, potentially, increase the risk of gastroesophageal reflux.
Reduced fasting antral motility, which is characterized by the absence, or reduction, of the antral component of phase 3 of the interdigestive migrating motor complex (MMC), occurs in critical illness and is associated with slow gastric emptying. An absence or reduction of antral phase 3 activity may predispose to colonization of the stomach with microbial pathogens. In critically ill patients this could have serious consequences, as it may be a precursor of ventilator-associated pneumonia.
In health, the rate of gastric emptying is directly related to antral activity and, hence, delayed gastric emptying may be associated with weak and/or disordered antroduodenal contractions. Reduced postprandial antral activity has been reported in critically ill patients. Furthermore, erythromycin markedly increases antral wave activity and accelerates gastric emptying in this group. Thus, a direct relationship between gastric emptying and antral activity in the critically ill has been established.
Pyloric activity (phasic and tonic) is integral to the regulation of gastric emptying. Both increased basal pyloric pressure and more frequent phasic contractions have been demonstrated in critically ill patients, and these abnormalities have been shown to correlate with slow gastric emptying ( Fig. 1 ).
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