- Alterations in gastrointestinal motility occur commonly in critically ill patients.
- The small intestine is the site of obstruction in 90% of cases of mechanical bowel obstruction. Pelvic adhesions are the most common cause. Thirty percent of cases require surgery.
- Intestinal pseudo-obstruction (nonmechanical bowel obstruction) may present with clinical symptoms that are similar to mechanical obstruction. Treatment includes nasogastric suction, rehydration, and correction of causative factors.
- Ogilvie's syndrome (colonic pseudo-obstruction) is characterized by abdominal distension and marked dilation of the cecum and right colon on abdominal x-rays. Treatment with colonoscopic decompression of the right colon is successful in about 60% of patients. Intravenous neostigmine is also effective.
- The incidence of diarrhea in the critically ill is greater than 40% and is up to 60% in patients receiving enteral feedings.
- Clostridium difficile infections are generally acquired in the hospital in patients receiving broad-spectrum antibiotics. Measurement of C. difficile toxin A or B in the stool by rapid enzyme-linked immunosorbent assay (ELISA) is the most practical method for diagnosis. Treatment consists of metronidazole or vancomycin for 7 to 14 days.
- Hyperbilirubinemia is frequently seen in patients with sepsis; cytokines along with bacterial endotoxins impair transport of bile acids at the sinusoidal and canalicular membranes, resulting in cholestasis.
- The etiology of total parenteral nutrition (TPN)-associated liver dysfunction appears to be multifactorial. The diagnosis is often made after the exclusion of other causes such as the concurrent use of potentially hepatotoxic medications, biliary obstruction, infections, and underlying intrinsic liver disease.
- Critically ill patients have multiple risk factors that predispose to acalculous cholecystitis. Patients often present atypically; unexplained fever and evidence of occult infection may frequently be the only manifestations. Ultrasonography alone is of limited value in diagnosis.
- Strong clinical suspicion and early recognition of acalculous cholecystitis are essential. Because of delays in diagnosis, more than 40% of patients develop complicated disease with gangrene, abscess, or perforation of the gallbladder.
Gastrointestinal (GI) and hepatic dysfunction are common in the critically ill patient, particularly in the setting of multiple organ system failure (MOSF) and the systemic inflammatory response syndrome (SIRS). Many factors are responsible for the pathophysiologic derangements of the GI tract and liver in critically ill patients. Disordered function may be directly related to the precipitating illness of the patient, which can lead to additive morbidity, thus perpetuating a vicious cycle. Management of disordered GI and hepatic function often necessitates aggressive and sometimes invasive diagnostic and therapeutic maneuvers, placing critically ill patients at risk for iatrogenic complications. These conditions may create vexing problems in the ongoing care of patients in the intensive care unit. It is therefore imperative for the clinician to develop a thorough understanding of the pathophysiology of GI and hepatic dysfunction in the critical care patient. This knowledge will permit identification of these conditions and allow for management decisions that are appropriate and timely.
In this chapter, we review the physiology of intestinal motility, and the pathophysiology and clinical features of intestinal obstruction and pseudo-obstruction. We also review the various causes of diarrhea in the critically ill patient, as well as the pathophysiology of bacterial translocation. In addition, the relationship between hepatic dysfunction in the critically ill patient as related to infection and parenteral nutrition will be discussed. The diagnosis and management of acalculous cholecystitis will also be reviewed.
Alterations of intestinal motility are common in the critically ill patient. The following discussion will be restricted to small intestinal and colonic motility, since these are the GI organs most subject to dysfunction in the intensive care setting.
Normal Function of the Small Intestine and Colon
The contents of the small intestine and colon are subject to complex processing prior to their excretion from the rectum. As GI contents are moved through the stomach and small intestine, mixing and churning result in the reduction in size of individual particles. These smaller particles allow increased exposure of nutrients to the small intestinal mucosa. The contents of the small intestine subsequently undergo nutrient and electrolyte absorption with a net secretion of fluid. The normal transit time of a liquid bolus from the mouth to the ileocecal valve is less than 2 hours, whereas solid substances take up to 8 hours to reach the cecum.1 The colon functions as a storage organ, with solid contents remaining within the colon for an average of 35 hours prior to excretion.2 Intraluminal contents undergo solidification as they move from the proximal to distal colon as marked reabsorption of water, sodium, and chloride, and net secretion of potassium, takes place. These processes occur through highly coordinated events with regional differences within portions of the small and large intestine. The control of luminal fluid and electrolyte balance, as well as motility of the small intestine and colon, requires the integration of neuronal, muscular, and endocrine components of these organs.
Neuroanatomy of the Small Intestine and Colon
The complexity of intestinal neuroanatomy can be appreciated by the fact that the neuronal density of the gut is approximately equivalent to that of the spinal cord. This network of neuronal pathways has been described as the “brain of the gut.”3 The small and large intestine have both intrinsic and extrinsic neuronal components. The intrinsic neurons of the small intestine and colon consist of cell bodies which are located in either the submucosa (Meissner's plexus) or the intermuscular region between the circular and longitudinal muscles of the gut wall (Auerbach's plexus) (Fig. 81-1). Submucosal nerve cell bodies are most prominent in the duodenum and decrease in density in a caudal direction; intermuscular nerve cell bodies are more evenly distributed throughout the GI tract.
Schematic representation of a cross-section of the small intestine. Nerve cell bodies are seen within the submucosa (Meissner's plexus) and between the circular and longitudinal ...
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