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Other Diseases of the Small Intestine and Colon
Small Intestinal Bacterial Overgrowth
The microbiota of the small intestine is essential for proper immune regulation and nutrient absorption. Typically, the concentration of bacteria is less in the proximal small intestine compared with the distal small intestine. Bacterial concentration of the proximal to mid–small intestine is approximately 10 4 organisms per milliliter compared with the terminal ileum, in which the bacterial concentration may be as high as 10 9 organisms per milliliter. The colon has the highest concentration on average, reaching levels of 10 12 organisms per milliliter. The ileocecal valve acts as a barrier to prevent contamination of bacteria from the colon into the small intestine.
Clinical manifestations of small intestinal bacterial overgrowth (SIBO) include abdominal distention, excessive flatulence, diarrhea, and abdominal pain. In extreme cases, malnutrition and vitamin deficiencies caused by malabsorption of nutrients may occur.
SIBO is a condition in which there are excessive small intestinal microorganisms causing a negative impact on bowel function. Many conditions can predispose an individual to SIBO. Most of these conditions cause stagnant fecal transit, due to either a mechanical obstructive process or an underlying myopathic or neuropathic functional abnormality that leads to intestinal dysmotility. In addition, mucosal disease causing malabsorption is another factor that can lead to excessive bacterial overgrowth.
Short bowel syndrome is a condition with a clear association to SIBO. Intestinal resection of the bowel can lead to mechanical and functional obstruction from anastomotic strictures and nerve damage disrupting bowel motility. In addition, patients who have had their ileocecal valve resected are at particular risk for SIBO due to reflux of bacteria from the colon into the small intestine.
Hypochlorhydria secondary to chronic acid suppression has been implicated in causing SIBO. Gastric acid serves an important role in acting as a barrier against excessive bacterial overgrowth. The use of proton pump inhibitors (PPIs) has been associated with an increased risk of Clostridium difficile infection for this reason.
The association between intestinal microbiota and irritable bowel syndrome (IBS) has been recognized. A study in children diagnosed with IBS found that 66% of 50 children studied were found to have a positive lactulose breath test. The use of rifaximin, an antibiotic found to be effective in the treatment of SIBO, resulted in improvement of symptoms in those children who carried a dual diagnosis of IBS and SIBO.
Other conditions, including immunodeficiency, connective tissue disease, and pseudo-obstruction, also predispose individuals to SIBO.
Evaluation
Breath hydrogen and methane testing has been used to diagnose patients with intolerance to lactose, fructose, and sucrose. In addition, using lactulose as the substrate administered during testing has allowed breath testing to be applied as a diagnostic tool for SIBO. Breath test analysis, before and after the ingestion of lactulose, measures the hydrogen and methane concentration in the exhaled air. If the hydrogen concentration is greater than 20 parts per million (ppm) at any point during the testing, the patient is considered to be positive for SIBO. When glucose is the substrate being used in place of lactulose, a rise in the hydrogen level greater than 12 ppm is considered positive. If a patient has rapid small bowel transit, a false-positive breath hydrogen test can occur as the carbohydrate is rapidly delivered into the colon. An early peak should be sought as evidence of SIBO. In addition to hydrogen, methane levels should also be measured. Some organisms are primarily methane producers, and measuring hydrogen alone could lead to inaccurate test results.
Culture of jejunal aspirates can be used to diagnose SIBO. A concentration greater than 10 3 organisms per milliliter is considered positive. Dominant small bowel organisms associated with SIBO include Pseudomonas aeruginosa , Escherichia coli , Acinetobacter lwoffii , Staphylococcus species, Klebsiella pneumoniae , Streptococcus species, Acinetobacter baumannii , Enterococcus faecalis , and Enterococcus faecium .
There are several limitations to acquiring jejunal aspirates, including the invasiveness of testing (requiring endoscopy), bacterial contamination from the oral cavity, and poor reproducibility of results. In addition, bacterial overgrowth may be found in other parts of the small intestine.
Endoscopic evaluation with tissue biopsy is of limited value because the majority of SIBO cases lack inflammation, thus yielding normal results.
Management
Antimicrobial therapy has been found to be clinically effective in the treatment of SIBO. Rifaximin, which is a nonabsorbable antibiotic with minimal side effects, has been found to be very effective in treating SIBO with less likelihood of developing clinical resistance compared with other antibiotics. In one study, rifaximin at a dose of 800 mg/day for 4 weeks was found to be effective in reducing symptoms of SIBO and normalizing glucose breath testing in 50% of patients. Other antibiotics that may be used include metronidazole, amoxicillin-clavulanate, trimethoprim-sulfamethoxazole, neomycin, gentamicin, doxycycline, ciprofloxacin, and norfloxacin.
With increasing interest in nonpharmacologic management of disease, herbal therapy may have potential therapeutic benefits in the treatment of SIBO. A study comparing patients receiving rifaximin versus herbal therapy showed equivalent effectiveness on the basis of lactulose breath testing. Further studies are necessary to substantiate these findings.
There is conflicting data pertaining to the role of probiotic therapy. However, some evidence exists suggesting a supportive role for probiotic and prebiotic therapy in combination with antimicrobial treatment.
Microscopic Colitis
Microscopic colitis, as the name implies, is colonic inflammation identified on histopathologic evaluation without macroscopic evidence of inflammation. Patients present with symptoms of diarrhea and fecal urgency without a history of rectal bleeding. By definition, patients typically present with three stools or more per day, with at least one stool of liquid consistency. There are two primary subtypes of microscopic colitis: collagenous and lymphocytic. A third, or mixed, type of microscopic colitis is recognized as containing features of both collagenous and lymphocytic colitis. The incidence of microscopic colitis is 3.1 to 5.5 per 100,000 for collagenous colitis and lymphocytic colitis, respectively.
The etiology of microscopic colitis has not been definitively established. There appears to be a familial pattern and a tendency to affect women more than men. Microscopic colitis typically occurs in adulthood but may also occur in children.
Some studies have suggested that bacterial toxins may play a role. A drug-induced inflammatory response has also been suggested, especially nonsteroidal antiinflammatory drugs (NSAIDs) and PPIs. The mechanism is likely idiosyncratic given the disproportionate number of people using these medications compared with the number of patients diagnosed with microscopic colitis.
An association between celiac disease, type 1 diabetes mellitus, and immunodeficiency has been made in children diagnosed with lymphocytic colitis.
Evaluation
Radiologic and laboratory testing is typically performed to evaluate for other causes of chronic diarrhea. The diagnosis of microscopic colitis is based on histopathologic findings and requires a complete colonoscopy with random biopsies obtained throughout the colon. Performing a sigmoidoscopy alone is insufficient due to microscopic skip lesions and may miss up to 40% of cases. Colonoscopy reveals no visual evidence of inflammatory changes.
Patients with lymphocytic colitis demonstrate an increased number of intraepithelial lymphocytes (more than 20 intraepithelial lymphocytes per 100 epithelial cells) on biopsy. The major distinguishing feature of collagenous colitis is a thickened subepithelial fibrous band measuring greater than 10 μm in width ( Fig. 49.1 ).
Management
Pharmacologic treatment options vary and are typically used during flares. If an environmental exposure (i.e., medication) is thought to be causing microscopic colitis, then the primary intervention is to discontinue the inciting agent. For instance, patients with celiac disease usually respond to a gluten-free diet.
Budesonide therapy is an effective medical treatment for microscopic colitis. In one study, 86% of patients using 9 mg of budesonide daily were found to be in histologic remission after 6 weeks of therapy.
Other therapies implemented for treatment of microscopic colitis have been less successful. These include aminosalicylates, cholestyramine, glucocorticoids, antibiotics, and bismuth subsalicylate. In severe cases refractory to medical management, colectomy or diverting ileostomy may be required.
Celiac Crisis
Celiac disease is found in up to 1% of the general population. It is an autoimmune disease characterized by gluten sensitivity that leads to small intestinal inflammation featuring villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes. The diagnosis is made by serologic and small intestinal histopathologic evaluation. Patients respond well to gluten restriction, which leads to both symptom and histologic remission. Gastrointestinal signs and symptoms in children may include abdominal pain, distension, diarrhea, and failure to thrive. Extraintestinal manifestations are not uncommon and include arthralgia, anemia, transaminasemia, short stature, dental enamel defects, and dermatitis herpetiformis.
Albeit rare, patients with severe celiac disease may be susceptible to celiac crisis, a life-threatening syndrome associated with high mortality if not recognized and treated immediately. Fortunately, due to early recognition of celiac disease, the incidence of celiac crisis has declined.
Celiac crisis occurs far more frequently in children compared with adults. Patients typically present with extremely high serologic markers and severe small intestinal inflammation. Symptoms of celiac crisis include substantial diarrhea, vomiting, and dehydration, as well severe metabolic and electrolyte abnormalities. The cause of celiac crisis is likely a combination of significant intestinal inflammation compounded by an environmental trigger, which may include infection and/or surgery, further stimulating the immune system.
Evaluation
Given that this syndrome is associated with hypokalemia, hyponatremia, hypocalcemia, and hypomagnesemia, electrolytes should be immediately tested if there is clinical suspicion of celiac crisis. A hepatic function panel should be included given the high incidence of hypoproteinemia, likely secondary to poor nutrition.
Management
Treatment involves immediate removal of gluten from the patient’s diet. Most likely, the patient will require bowel rest and initiation of total parenteral nutrition. Due to the severity of this syndrome, many patients will require admission to an intensive care unit for close monitoring and treatment to restore electrolyte balance. Given these electrolyte disturbances, the patient should be placed on continuous cardiac monitoring due to the high risk of cardiac arrhythmia. Corticosteroids are commonly used to reduce the immune response and bowel inflammation.
Because of the severity of malnutrition, it is important to continue to monitor patients closely for refeeding syndrome after initiating a gluten-free diet.
Diverticular Disease
A colonic diverticulum is an outpouching of mucosa originating from the lumen of the bowel. Diverticulosis is a condition in which the colon has multiple diverticula. In many cases, this is a benign condition without symptoms. “Diverticulitis” is when the diverticula become inflamed, which leads to significant gastrointestinal symptoms. Diverticulitis is likely caused by impacted stool in the diverticula leading to infection.
Diverticular disease is common, especially in industrialized nations. Diverticula tend to occur in the rectosigmoid colon. Diverticulosis is seen in patients older than 40 years of age, with the majority occurring in patients older than 80 years of age.
Collagen cross-linking abnormalities of the colonic wall may predispose patients to develop diverticulosis. This is particularly true in patients with Ehlers-Danlos syndrome (EDS) or Marfan syndrome, who have similar abnormalities and are at high risk of developing diverticulosis at a young age. With increased collagen cross-linking, the bowel wall becomes less compliant and more susceptible to perforation.
Another mechanism in which diverticula form is related to poor fiber intake and abnormal colonic motility. Poor dietary fiber intake and slow colonic transit lead to constipation and subsequent increased intraluminal pressure from chronic straining, leading to formation of diverticula.
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