Small Bowel Obstruction - Clinical Tree

Descriptions of patients with small bowel obstruction (SBO) date back to the earliest medical literature. It was not until the 19th century and the advent of anesthesia and antisepsis, however, that surgery became a recognized and effective treatment. At the same time, physiologic studies of fluid shifts, electrolyte imbalances, intravenous resuscitation, and antibiotics allowed even safer surgical approaches to patients with obstruction. Despite advances in treatment, SBO remains a common clinical problem, accounting for as many as 400,000 admissions annually in the United States, with between 30% and 40% requiring operative exploration. Moreover, these admissions are costly both in terms of time and money: the average length of stay for patients requiring operative exploration is 6 days following a laparoscopic lysis of adhesions and 11 days following a laparoscopic bowel resection, with mean hospital charges of $38,669 and $71,218 respectively, with a national burden of $2.1 billion.

At the time of initial evaluation for SBO, it is critical to determine whether a true mechanical obstruction or pseudoobstruction (dysmotility/ileus) is the cause of symptoms; this distinction will guide all subsequent treatment. Clinical judgment must also be employed to determine illness severity, resuscitation requirements, and the urgency of operative intervention. Patients may present acutely, or with a chronic and relapsing problem with symptoms ranging from modest discomfort to critical illness and shock ( Fig. 72.1 ).

Pathophysiology

The earliest response of the proximal gut to obstruction is to increase bowel wall contractility to overcome the blockage. This increase in contractility, which may occur proximal or distal to the obstruction, may result in early symptoms of diarrhea or enhanced output; however, if the obstruction persists, ultimately the contractions become less efficient and may cease altogether. At this point, proximal bowel dilatation may occur. Dilatation and the lack of contractility may allow water and electrolytes to accumulate proximal to the obstruction. Significant third-space losses in addition to vomiting may result in marked dehydration and hypovolemia. Metabolic derangement may be significant, and depends on the level of the obstruction. Proximal obstruction may result in hypochloremia, hypokalemia, and metabolic alkalosis. Concurrent, persistent vomiting can exacerbate these alterations. Obstruction of the distal small bowel results in a larger capacitance effect with enhanced volume loss. Electrolyte disturbances may be somewhat less severe; however, significant hypovolemia and even renal damage can occur. If obstruction is not relieved and these processes continue, volume loss and abdominal distention will result in decreased venous return, diaphragmatic elevation, and perhaps compromised ventilation, all of which will exacerbate the symptoms of an acute abdomen.

Under normal circumstances, the luminal content of the small bowel contains very few bacteria; up to one-third of jejunal aspirates in healthy volunteers will be sterile. Interestingly, obstruction provokes a profound change in the flora of the small intestine, with stasis permitting overgrowth of the few native species as well as being populated by reverse peristalsis from the colonic microbiota. These are most commonly Escherichia coli , Streptococcus faecalis , and Klebsiella species. Overgrowth can occur rapidly. Even prior to frank perforation with gross contamination, there is evidence that bacteria can translocate through the intestinal wall and may well contribute to a deteriorating sepsis picture if the treatment of initial obstruction is delayed.

Classification and Etiology

SBO can be classified by mechanism. The patient's symptoms and presenting signs may be caused by a functional obstruction from dysmotility, or a true mechanical obstruction. Mechanical SBO may be further classified as partial or complete obstruction, with the etiology of mechanical SBO divided into three main categories: extrinsic, intrinsic/intramural, and intraluminal.

Dysmotility

Dysmotility or ileus can be caused by a wide range of insults (see Fig. 72.1 ), and the recognition and diagnosis of pseudoobstruction is critical to avoiding an unnecessary, unhelpful operation that is likely to worsen rather than improve the clinical picture. A comprehensive, thorough history including all medications, comorbid conditions, and social history often points to a diagnosis favoring dysmotility over mechanical obstruction. The case of postoperative ileus following recent abdominal or pelvic surgery is reasonably straightforward. However, other causes including blunt trauma, pancreatitis, kidney stones, mesenteric ischemia, and retroperitoneal hematoma can also lead to ileus. Additionally, many classes of medications including opioids, some psychotropic medications, chemotherapeutic agents, and anticholinergic drugs are known to slow motility and may cause or contribute to a diagnosis of dysmotility. In select cases, pharmacologic agents such as alvimopan or methylnaltrexone may play a role in preventing or mitigating ileus. Although commonly used, there is little data to support the use of prokinetic agents such as erythromycin or metoclopramide in the setting of postoperative ileus.

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