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Background Whether intestinal dysmotility and the use of a proton pump inhibitor (PPI) either independently or together contributes to small intestinal bacterial over-growth (SIBO), and/or small intestinal fungal overgrowth (SIFO) is not known.
Human intestinal microbiota create a complex polymicrobial ecology. This is characterised by its high population density, wide diversity and complexity of interaction. Any dysbalance of this complex intestinal microbiome, both qualitative and quantitative, might have serious health consequence for a macro-organism, including small intestinal bacterial overgrowth syndrome (SIBO). SIBO is defined as an increase in the number and/or alteration in the type of bacteria in the upper gastrointestinal tract. There are several endogenous defence mechanisms for preventing bacterial overgrowth: gastric acid secretion, intestinal motility, intact ileo-caecal valve, immunoglobulins within intestinal secretion and bacteriostatic properties of pancreatic and biliary secretion. Aetiology of SIBO is usually complex, associated with disorders of protective antibacterial mechanisms (e.g. achlorhydria, pancreatic exocrine insufficiency, immunodeficiency syndromes), anatomical abnormalities (e.g. small intestinal obstruction, diverticula, fistulae, surgical blind loop, previous ileo-caecal resections) and/or motility disorders (e.g. scleroderma, autonomic neuropathy in diabetes mellitus, post-radiation enteropathy, small intestinal pseudo-obstruction). In some patients more than one factor may be involved. Symptoms related to SIBO are bloating, diarrhoea, malabsorption, weight loss and malnutrition. The gold standard for diagnosing SIBO is still microbial investigation of jejunal aspirates. Non-invasive hydrogen and methane breath tests are most commonly used for the diagnosis of SIBO using glucose or lactulose. Therapy for SIBO must be complex, addressing all causes, symptoms and complications, and fully individualised. It should include treatment of the underlying disease, nutritional support and cyclical gastro-intestinal selective antibiotics. Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.
Proton pump inhibitors (PPIs) can cause diarrhea, enteric infections, and alter the gastrointestinal bacterial population by suppressing the gastric acid barrier. Among patients that received long term PPI treatment, we evaluated the incidence of small intestinal bacterial overgrowth (SIBO; assessed by glucose hydrogen breath test [GHBT]), the risk factors for development of PPI-related SIBO and its clinical manifestations, and the eradication rate of SIBO after treatment with rifaximin.
GHBTs were given to 450 consecutive patients (200 with gastroesophageal reflux disease who received PPIs for a median of 36 months; 200 with irritable bowel syndrome [IBS], in absence of PPI treatment for at least 3 years; and 50 healthy control subjects that had not received PPI for at least 10 years). Each subject was given a symptoms questionnaire.
SIBO was detected in 50% of patients using PPIs, 24.5% of patients with IBS, and 6% of healthy control subjects; there was a statistically significant difference between patients using PPIs and those with IBS or healthy control subjects (P < .001). The prevalence of SIBO increased after 1 year of treatment with PPI. The eradication rate of SIBO was 87% in the PPI group and 91% in the IBS group.
SIBO, assessed by GHBT, occurs significantly more frequently among long term PPI users than patients with IBS or control subjects. High dose therapy with rifaximin eradicated 87%-91% of cases of SIBO in patients who continued PPI therapy.
Hydrogen breath tests are widely used to explore the pathophysiology of functional gastrointestinal disorders. Small intestinal bacterial overgrowth and carbohydrate malabsorption are disorders detected by these tests that have been proposed to be of great importance for symptoms in, for instance, irritable bowel syndrome. However, conclusions drawn from these studies are highly controversial and divergent results exist. There is also an extensive use of these tests in clinical practice with difficulties regarding interpretation of the tests and sometimes erroneous conclusions. The limitations and pitfalls of these tests will be reviewed in this article, and hopefully the occasional abuse of these tests can be turned into proper clinical and scientific use instead in the future.
To investigate non-invasively the incidence of absorption of carbohydrates in diabetic patients during an oral glucose tolerance test (OGTT) and to determine whether malabsorption may be associated with insulin secretion and insulin resistance.
A standard 75-g OGTT was performed in 82 diabetic patients. The patients received 75 g of anhydrous glucose in 225 mL of water after an overnight fasting and breath samples were collected at baseline and up to 120 min after ingestion. Breath hydrogen and methane concentrations were measured. Blood glucose and serum insulin concentrations were measured before ingestion and at 30, 60, 90, 120 min post-ingestion.
When carbohydrate malabsorption was defined as subjects with an increase of at least 10 ppm (parts per million) in hydrogen or methane excretion within a 2-h period, 28 (34%) had carbohydrate malabsorption. According to the result of increased breath test, 21 (75%) patients were classified as small bowel bacterial overgrowth and 7 (25%) as glucose malabsorption. Patients with carbohydrate malabsorption were older and had poor glycemic control as compared with those without carbohydrate malabsorption. The HOMA value, the sum of serum insulin during the test and the Delta insulin/Delta glucose ratio were greater in patients with carbohydrate malabsorption.
Insulin resistance may be overestimated by using these markers if the patient has carbohydrate malabsorption, or that carbohydrate malabsorption may be present prior to the development of insulin resistance. Hence carbohydrate malabsorption should be taken into account for estimating insulin resistance and beta-cell function.
Small intestinal bacterial overgrowth (SIBO) has been proposed to be common in irritable bowel syndrome (IBS), with altered small-bowel motility as a possible predisposing factor.
To assess the prevalence of SIBO, by culture of small-bowel aspirate, and its correlation to symptoms and motility in IBS.
162 patients with IBS who underwent small-bowel manometry and culture of jejunal aspirate were included. Cultures from 26 healthy subjects served as controls. Two definitions of altered flora were used: the standard definition of SIBO (>/=10(5) colonic bacteria/ml), and mildly increased counts of small-bowel bacteria (>/=95th centile in controls).
SIBO (as per standard definition) was found in 4% of both patients and controls. Signs of enteric dysmotility were seen in 86% of patients with SIBO and in 39% of patients without SIBO (p = 0.02). Patients with SIBO had fewer phase III activities (activity fronts) than patients without SIBO (p = 0.08), but otherwise no differences in motility parameters were seen. Mildly increased bacterial counts (>/=5x10(3)/ml) were more common in patients with IBS than in controls (43% vs 12%; p = 0.002), but this was unrelated to small intestinal motility. No correlation between bacterial alterations and symptom pattern was observed.
The data do not support an important role for SIBO according to commonly used clinical definitions, in IBS. However, mildly increased counts of small-bowel bacteria seem to be more common in IBS, and needs further investigation. Motility alterations could not reliably predict altered small-bowel bacterial flora.
Capsule endoscopy (CE) is a unique tool to visualize the mucosa of the small intestine. Chronic intestinal dysmotility (CID) is a group of rare disorders of gastrointestinal motility that often are complicated by bacterial overgrowth. The aim of this study was to determine the prevalence of small bowel mucosal abnormalities in patients with CID. We also studied the usefulness of CE in the diagnosis of intestinal dysmotility.
We conducted a prospective study using CE in 18 patients; six with myopathic, 11 with neuropathic and one with indeterminate CID. A control group was used for comparison of small bowel transit.
Mucosal breaks (erosions and ulcerations) were found in 16/18 (89%) patients. The capsule reached the caecum in 11/18 (61%) patients with a median transit time of 346 minutes. In the control group the capsule reached the caecum in 29/36 (81%) cases with a median transit time of 241 minutes. The difference in transit time was not significant (p = 0.061) in this material. The capsule was retained in the stomach in 3/18 patients. None of the patients developed symptoms or signs of mechanical obstruction.
A high frequency of mucosal breaks and signs of motility disturbances were seen in CID patients. CE is feasible for the examination of small bowel mucosa in patients with CID. The relevance of observed mucosal abnormalities in CID remains uncertain.
There has been increasing interest in small intestinal bacterial overgrowth (SIBO) after reports of a link with irritable bowel syndrome (IBS), yet our understanding of this entity is limited.
Our aim was to estimate the yield of patients undergoing duodenal aspirate culture, and to identify symptoms and features that predict SIBO.
A medical chart review of patients who had undergone duodenal aspirate culture at an academic medical centre in 2003 was performed to record clinical characteristics and culture results. The associations between aspirate results and symptoms, medical diagnoses and medication use were assessed using logistic regression.
A total of 675 patients had available aspirate results. Mean age of the sample was 53 (s.d. 17) and 443 (66%) were female patients. Overall, 8% of aspirates were positive for SIBO; 2% of IBS patients had SIBO. Older age, steatorrhoea and narcotic use were associated with SIBO (P < 0.05). PPI use was not associated with SIBO, but was associated with bacterial growth not meeting criteria for SIBO (P < 0.05). Inflammatory bowel disease (IBD), small bowel diverticula and pancreatitis were positively associated with an abnormal duodenal aspirate (P < 0.05), but other conditions including IBS were not associated with SIBO.
Older age, steatorrhoea, narcotic use, IBD, small bowel diverticula and pancreatitis were associated with small intestinal bacterial overgrowth based on abnormal duodenal aspirate culture results. However, no clear associations of true small intestinal bacterial overgrowth with IBS or PPI use were detected, in contrast to recent speculation.
Controversy still surrounds the question whether yeasts found in the gut are causally related to disease, constitute a health hazard, or require treatment.
The authors present the state of knowledge in this area on the basis of a selective review of articles retrieved by a PubMed search from 2005 onward. The therapeutic recommendations follow the current national and international guidelines.
Yeasts, mainly Candida species, are present in the gut of about 70% of healthy adults. Mucocutaneous Candida infections are due either to impaired host defenses or to altered gene expression in formerly commensal strains. The expression of virulence factors enables yeasts to form biofilms, destroy tissues, and escape the immunological attacks of the host. Yeast infections of the intestinal mucosa are of uncertain clinical significance, and their possible connection to irritable bowel syndrome, while plausible, remains unproved. Yeast colonization can trigger allergic reactions. Mucosal yeast infections are treated with topically active polyene antimycotic drugs. The adjuvant administration of probiotics is justified on the basis of positive results from controlled clinical trials.
The eradication of intestinal yeasts is advised only for certain clearly defined indications.
Tests of gastric, small intestinal and colonic motor function provide relevant physiological information and are useful for diagnosing and guiding the management of dysmotilities. Intraluminal pressure measurements may include concurrent measurements of transit or intraluminal pH. A consensus statement was developed and based on reports in the literature, experience of the authors, and discussions conducted under the auspices of the American Neurogastroenterology and Motility Society in 2008. The article reviews the indications, methods, performance characteristics, and clinical utility of intraluminal measurements of pressure activity and tone in the stomach, small bowel and colon in humans. Gastric and small bowel motor function can be measured by intraluminal manometry, which may identify patterns suggestive of myopathy, neuropathy, or obstruction. Manometry may be most helpful when it is normal. Combined wireless pressure and pH capsules provide information on the amplitude of contractions as they traverse the stomach and small intestine. In the colon, manometry assesses colonic phasic pressure activity while a barostat assesses tone, compliance, and phasic pressure activity. The utility of colonic pressure measurements by a single sensor in wireless pressure/pH capsules is not established. In children with intractable constipation, colonic phasic pressure measurements can identify patterns suggestive of neuropathy and predict success of antegrade enemas via cecostomy. In adults, these assessments may be used to document severe motor dysfunction (colonic inertia) prior to colectomy. Thus, intraluminal pressure measurements may contribute to the management of patients with disorders of gastrointestinal and colonic motility.
Candida proliferation in the gastrointestinal tract was responsible for diarrhoea in six patients. Their common presentation was multiple loose or watery bowel movements, without blood or mucus but sometimes associated with abdominal cramps, and lasting as long as 3 months. Yeast cells were most easily identified by direct microscopic examination of stool specimens. Symptoms disappeared in all patients after 3 to 4 days of oral nystatin therapy.
Intraluminal pressures were measured in the gastric antrum and at different levels of the upper small intestine in 18 normal subjects to investigate whether or not the interdigestive motor complex, identified in several animal species, occurs in man and, if so, to determine its characteristics. In all normal subjects, the activity front of the interdigestive motor complex was readily identified as an uninterrupted burst of rhythmic contraction waves that progressed down the intestine and that was followed by a period of quiescence. Quantitative analysis of various parameters of the complex and simultaneous radiological and manometrical observations revealed that it resembled closely the canine interdigestive motor complex. To test the hypothesis that disorders of this motor complex may lead to bacterial overgrowth in the small intestine, similar studies were performed in 18 patients with a positive (14)CO(2) bile acid breath test and in an additional control group of 9 patients with a normal (14)CO(2) breath test. All but five patients had normal interdigestive motor complexes. The five patients in whom the motor complex was absent or greatly disordered had bacterial overgrowth as evidenced by (14)CO(2) bile acid breath tests before and after antibiotics. These studies establish the presence and define the characteristics of the normal interdigestive motor complex in man. They also suggest that bacterial overgrowth may be due to a specific motility disorder i.e., complete or almost complete absence of the interdigestive motor complex.
Bacterial overgrowth and intestinal pseudo-obstruction may succeed abdominal radiotherapy, and absence of intestinal migrating motor complex (MMC) has been reported in bacterial overgrowth. The aims of this study were to address the relationship between intestinal patterns of motility and gastrointestinal microflora and to elucidate the pathogenesis of late radiation enteropathy.
Forty-one consecutive female patients with symptoms of late radiation enteropathy were examined by prolonged ambulatory manometry, culture of gastric and duodenal samples with quantification of gram-negative bacilli (GNB) by the glucose gas test, the [14C]D-xylose breath test, and determination of pH and short-chain fatty acids in gastric juice.
The intensity of MMC explained 61% (P < 0.001) and 71% (P < 0.001) of the variability of GNB in the stomach and duodenum, respectively, corresponding to the severity of disease. Abnormal MMC index and presence of irregular bursts were the best predictors of GNB (86%; P < 0.001, multiple regression). Fasting gastric pH explained gastric bacterial counts (63%; P < 0.001) but did not predict GNB.
Impaired motility emerges as a causal factor for gastrointestinal colonization with GNB, whereas hypochlorhydria facilitates unspecific gastric colonization. Abnormal motility and GNB in the proximal small intestine are essential factors in the pathogenesis of severe late radiation enteropathy.
The aim of this study was to provide a detailed comparison of motor activity in the duodenum and jejunum and between men and women studied by prolonged ambulatory manometry.
Thirty healthy volunteers (17 males) underwent prolonged ambulatory recording of duodeno-jejunal motility using a catheter with five built-in strain-gauge transducers (two duodenal and three jejunal). Manometric data was obtained during an extended period of fasting, the postprandial period and during sleep.
There was a wide range of durations of the migrating motor complex (MMC), but at least one phase III was detected during 6 h of fasting, or 6 h of sleep in each subject (0.52+/-0.04 phase III/hour during fasting vs 0.59+/-0.04 during sleep, p=0.1). There was marked variation in the duration and pattern of phase III. Postprandially, frequency of contractions and motility index were maximal in the first 2 h after the meal, in both the duodenum and jejunum. There were no substantive differences between males and females or between the duodenum and jejunum.
We conclude that upper small bowel motility is little affected by gender or segment.
Current tests of gastric and small intestinal motor function provide relevant physiological information, but their clinical utility is controversial. This article reviews the current procedures, indications, significance, pitfalls, and guidelines for gastrointestinal motility measurements by scintigraphy, gastroduodenojejunal manometry, and surface electrogastrography in humans. Methods included review of literature and discussions in closed and open fora among investigators, including presentations for peer review at focused (Iowa City American Motility Society Symposium, December 1995) and national meetings (American Gastroenterological Association, May 1996, and American Motility Society, September 1996). The current tests are generally complementary; scintigraphy is typically the first test in the evaluation of gastric motor function and often confirms the clinical suspicion of dysmotility. Manometry identifies patterns suggestive of myopathy, neuropathy, or obstruction but may be most helpful when it shows entirely normal findings, because manometry helps in part to exclude dysmotility as a cause of symptoms. Electrogastrography may identify dysrhythmias or failure of signal power to increase postprandially; rhythm abnormalities may be independent of impaired emptying among dyspeptic patients. The best validated and clinically most significant results pertain to transit tests; manometry may contribute importantly to the diagnostic process; and the significance of electrogastrography remains to be fully elucidated.
The physiology and pathophysiology of small bowel motility are reviewed with particular focus on the motility patterns and periods that are detected by intraluminal manometry. Motility patterns are groups of phasic pressure waves resulting from contractions of the circular muscle layer of the small bowel that are organized by the enteric nervous system. Phase III of the migrating motor complex, the hallmark of the fasting motility period, thus reflects enteric neuromuscular function. Response to meal challenge also involves the CNS, reflexes beyond the gut and endocrine responses. Although specific disease diagnosis cannot be made by motility studies of the small bowel, the functional integrity is revealed. The normal occurrence of the essential patterns and periods of motility and the absence of distinctly abnormal patterns evidence preserved function, whereas the opposite indicates clinically significant dysmotility. Certain motility patterns are occasionally seen both in health and disease, and increased prevalence indicates a moderate dysfunction of yet unclear significance. Bacterial overgrowth with Gram-negative bacilli is the consequence of severe small bowel dysmotility, and a diagnosis that can be predicted by a motility study. Testing can be useful in the clinical management of paediatric and adult patients also by predicting the prognosis and response to enteral nutrition and medical therapy. Further studies are, however, needed to take full advantage of motility testing in clinical practise.
This review examines the evidence for the development of adverse effects due to prolonged gastric acid suppression with proton pump inhibitors. Potential areas of concern regarding long-term proton pump inhibitor use have included: carcinoid formation; development of gastric adenocarcinoma (especially in patients with Helicobacter pylori infection); bacterial overgrowth; enteric infections; and malabsorption of fat, minerals, and vitamins.
Prolonged proton pump inhibitor use may lead to enterochromaffin-like cell hyperplasia, but has not been demonstrated to increase the risk of carcinoid formation. Long-term proton pump inhibitor treatment has not been documented to hasten the development or the progression of atrophic gastritis to intestinal metaplasia and gastric cancer, although long-term studies are required to allow definitive conclusions. At present, we do not recommend that patients be tested routinely for H. pylori infection when using proton pump inhibitors for prolonged periods. Gastric bacterial overgrowth does increase with acid suppression, but important clinical sequelae, such a higher rate of gastric adenocarcinoma, have not been seen. The risk of enteric infection may increase with acid suppression, although this does not seem to be a common clinical problem with prolonged proton pump inhibitor use. The absorption of fats and minerals does not appear to be significantly impaired with chronic acid suppression. However, vitamin B12 concentration may be decreased when gastric acid is markedly suppressed for prolonged periods (e.g. Zolllinger–Ellison syndrome), and vitamin B12 levels should probably be assessed in patients taking high-dose proton pump inhibitors for many years.
Thus, current evidence suggests that prolonged gastric acid suppression with proton pump inhibitors rarely, if ever, produces adverse events. Nevertheless, continued follow-up of patients taking proton pump inhibitors for extended periods will provide greater experience regarding the potential gastrointestinal adverse effects of long-term acid suppression.
Intragastric growth of non-Helicobacter pylori bacteria commonly occurs during acid-suppressive therapy. The long-term clinical consequences are still unclear.
To investigate the luminal and mucosal bacterial growth during gastric acid inhibition, in relation to the type and duration of acid-inhibitory treatment, as well as to concomitant H. pylori infection.
A total of 145 patients on continuous acid inhibition with either proton pump inhibitors (n=109) or histamine2-receptor antagonists (H(2)RAs, n=36) for gastro-oesophageal reflux disease, and 75 dyspeptic patients without acid inhibition (control group) were included. At endoscopy, fasting gastric juice was obtained for pH measurement and bacteriological culture. Gastric biopsy specimens were examined for detection of H. pylori (immunohistochemistry) and of non-H. pylori bacteria (modified Giemsa stain-positive and immunohistochemistry-negative at the same location).
Non-H. pylori flora was detected in the gastric juice of 92 (41.8%) patients and in the gastric mucosa of 109 (49.6%) patients. In gastric juice, prevalence rate for non-H. pylori bacteria was higher in patients taking proton pump inhibitors than controls and those taking H(2)RAs (58.7% vs. 22.6% and vs. 30.6%, P < 0.0001 and P < 0.003, respectively), but did not differ statistically between H(2)RAs and controls. In gastric mucosa, prevalence rates for non-H. pylori bacteria were higher in patients taking proton pump inhibitors and H(2)RAs than in the controls (antrum: 46.9% and 48.6% vs. 25%, P < 0.05 for both; corpus: 52.2% and 56.8% vs. 23.7%, P < 0.001 for both), but did not differ between proton pump inhibitors and H(2)RAs. Both luminal and mucosal growth of non-H. pylori bacteria were significantly greater in H. pylori-positive than -negative patients taking proton pump inhibitors (P < 0.05 for both). Luminal growth of non-H. pylori flora increased with the intragastric pH level, whilst mucosal bacterial growth increased with the duration of acid inhibition.
Non-H. pylori flora not only contaminates the gastric juice but also colonizes the gastric mucosa of a large proportion of patients treated long-term with acid inhibition. The relationship between H. pylori and non-H. pylori bacteria in the pathogenesis of atrophic gastritis and gastric cancer needs further elucidation.
Infections of the skin and the mucous membranes due to Candida species may occur either in immuncompromised or in non-immuncompromised patients. This is in contrast to systemic candidiasis (e.g. candidemia) which is only seen in severely immunocompromised patients. Bloodstream infections caused by Candida species are increasingly recognized in critical ill adult and pediatric individuals, with significant associated morbidity and mortality. Candida albicans is the single most common fungal species causing nosocomial infections. However, non-Candida albicans spp., including fluconazole-less-susceptible Candida glabrata, have become more common pathogens. In some patient populations such as hematological (neutropenic) patients Non-C. albicans species are detected much more frequently as compared to non-neutropenic patients in the intensive care. Non-C. albicans species are more likely to occur in patients, who receive or have received antifungal therapy with azoles (e.g. fluconazole). In this review the current epidemiological trends in mucosal and invasive candidiasis are discussed with regard to the role of non-Candida albicans species as the causative agent in immunocompromised patients.
A growing number of studies seem to suggest that small intestinal bacterial overgrowth (SIBO) is a common clinical problem. Although various techniques are available to make this diagnosis, tradition has accepted small bowel aspirate (>10(5) cfu/ml) as a gold standard. In this systematic review, the validity of culture and other diagnostic testing for SIBO is evaluated.
We performed a systematic review of the literature from 1966 to present using electronic databases (PubMed and OVID). Full paper review of those abstracts that fulfilled preset criteria was carried out to evaluate the validity of various tests in diagnosing SIBO. Finally, all papers were evaluated against published standards for studies on diagnostic testing.
Seventy-one papers met the criteria for detailed review. Studies were very heterogeneous with regards to patient populations, test definitions, sample size, and methods in general. Small bowel colony counts appeared elevated in most gastrointestinal diseases compared to controls. The traditional definition of >10(5) cfu/ml was usually indicative of stagnant loop conditions. Although, numerous diagnostic tests were studied, not even culture papers met the quality standards described by Reid et al. Breath testing and other diagnostic testing suffered therefore from the lack of a gold standard against which to validate in addition to the poor quality.
There is no validated diagnostic test or gold standard for SIBO. In this context, the most practical method to evaluate SIBO in studies at this time would be a test, treat, and outcome technique.
Whether dietary fructose intolerance causes symptoms of irritable bowel syndrome (IBS) is unclear. We examined the prevalence of fructose intolerance in IBS and long-term outcome of fructose-restricted diet.
Two hundred and nine patients with suspected IBS were retrospectively evaluated for organic illnesses. Patients with IBS (Rome II) and positive fructose breath test received instructions regarding fructose-restricted diet. One year later, their symptoms, compliance with, and effects of dietary modification on lifestyle were assessed using a structured interview.
Eighty patients (m/f=26/54) fulfilled Rome II criteria. Of 80 patients, 31 (38%) had positive breath test. Of 31 patients, 26 (84%) participated in follow-up (mean=13 mo) evaluation. Of 26 patients, 14 (53%) were compliant with diet; mean compliance=71%. In this group, pain, belching, bloating, fullness, indigestion, and diarrhea improved (P<0.02). Of 26 patients, 12 (46%) were noncompliant, and their symptoms were unchanged, except belching. The mean impact on lifestyle, compliant versus noncompliant groups was 2.93 versus 2.57 (P>0.05).
About one-third of patients with suspected IBS had fructose intolerance. When compliant, symptoms improved on fructose-restricted diet despite moderate impact on lifestyle; noncompliance was associated with persistent symptoms. Fructose intolerance is another jigsaw piece of the IBS puzzle that may respond to dietary modification.
Several previous studies have suggested that pathological colonization of the proximal gastrointestinal (GI) tract may be associated with septic morbidity. However, the prevalence of this in surgical patients is unknown and there is little information on factors that might predispose to this phenomenon. The aim of this study was to assess the preoperative variables that are associated with pathological colonization of the proximal GI tract in surgical patients.
Nasogastric aspirates were obtained from 502 surgical patients to identify abnormal colonization. Several preoperative variables were tested to identify association with pathological colonization of the proximal GI tract. Postoperative septic morbidity was recorded prospectively in all patients.
Enterobacteriaceae were identified in 78 of 502 patients (15.5%), 124 of 502 (24.7%) had multiple organisms, and 157 of 502 (31.3%) had Candida in the nasogastric aspirates. Age >70 y and emergency surgery were associated with presence of Enterobacteriaceae. Age >70 y was also associated with the presence of multiple organisms (with or without Enterobacteriaceae). Colonization with Enterobacteriaceae or presence of multiple organisms in the proximal GI tract was associated with postoperative septic morbidity. Preoperative total parenteral nutrition was associated with Candida colonization in the upper GI tract, but not with sepsis.
Pathological colonization of the proximal GI tract with Enterobacteriaceae or multiple organisms is associated with increased incidence of postoperative sepsis. Age >70 y and emergency surgery were the two preoperative variables associated with pathological colonization in surgical patients. Preoperative total parenteral nutrition is associated with fungal colonization but this is not associated with septic morbidity.