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INTRODUCTION

In addition to being essential for adequate nutrient absorption, normal gastrointestinal motility is crucial for maintaining an appropriate balance of microorganisms and proper function within the gut.1 It also serves as a major defense mechanism against infection of the gut, and limits the propagation of bacteria to pathologic levels.1 Gastric atony, also referred to as gastroparesis, can be defined as the inability of the stomach to contract normally, causing a delay in the movement of food out of the stomach. Causal factors for gastric atony can be classified as either medical or idiopathic. The most common medical cause is diabetes mellitus, whereas less common medical conditions include neurologic disorders, connective tissue disorders, critical illness, and surgery.

In the nonsurgical patient with medical comorbidities, disruption of the normal motility can lead to atony, resulting in often devastating symptoms that severely impact nutrition and quality of life. Diabetic gastroparesis is thought to be the result of the dysregulation of the autonomic nervous system, a system that is intimately related to the neural functioning of the stomach. Similarly, the impact of neurologic disorders on gastric motility is often a consequence of the parallel functioning of neurotransmitters within the central nervous system and those found in enteric neurons. Disturbance of the former can lead to disruption of the latter and gastric atony. With connective tissue disorders, gastric atony is of critical importance, given the tendency of these patients to develop severe and complicated reflux resulting from lower esophageal sphincter hypotension and significantly impaired esophageal peristaltic amplitude. Critical illness greatly impairs the use of enteral nutrition and results in a sustained catabolic state that depletes the patient’s caloric reserves, leading to decreased immune function, impaired wound healing, and ultimately increased morbidity and mortality.2 This disruption can further result in bacterial overgrowth, translocation, pneumonia, and sepsis. While multiple therapeutic options exist for medical gastric atony, patients may often spend a majority of their life with discomfort and in search of the appropriate management.

In the postoperative setting, gastric atony, or failure of the stomach to empty, must, by definition, not be related to any other common postsurgical complication such as wound infection, intraperitoneal abscess, electrolyte disturbances, pancreatitis, thromboembolic disorders, pneumonitis, or cardiovascular complications. While a variety of factors may cause postoperative ileus, the specific categorization of atony must include “dysfunction causing a prolonged postoperative course defined as more than 14 days elapsing between the primary surgical intervention and planned discharge of the patient from the hospital.”3

In general, there are a variety of techniques employed to treat gastric atony including medical management, endoscopic techniques, and surgical intervention. Future directions will focus on greater development of these treatment strategies either alone or in combination to improve the daily functioning of these patients. The purpose of this chapter is to review the biology, physiology, diagnosis, treatment options, and persistent clinical challenges that describe this often complex and ...

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