Some studies reported up to 80% of patients with  irritable bowel syndrome  (IBS) have SIBO (using the  hydrogen breath test ). IBS-D is associated with elevated hydrogen numbers on breath tests while IBS-C is associated with elevated methane numbers on breath tests. [ 11 ]  Subsequent studies demonstrated statistically significant reduction in IBS symptoms following therapy for SIBO. [ 12 ] [ 11 ] [ 6 ]


Various mechanisms are involved in the development of diarrhea and IBS-D in bacterial overgrowth. First, the excessive bacterial concentrations can cause direct inflammation of the small bowel cells, leading to an  inflammatory diarrhea . The malabsorption of  lipids ,  proteins  and  carbohydrates  may cause poorly digestible products to enter into the  colon . This can cause an  osmotic diarrhea  or stimulate the colonic cells to cause a  secretory diarrhea . [ 5 ]


There is a lack of consensus however, regarding the suggested link between IBS and SIBO. Other authors concluded that the abnormal breath results so common in IBS patients do not suggest SIBO, and state that "abnormal fermentation timing and dynamics of the breath test findings support a role for abnormal intestinal bacterial distribution in IBS." [ 13 ]  There is general consensus that breath tests are abnormal in IBS; however, the disagreement lies in whether this is representative of SIBO. [ 14 ]


Certain people are more predisposed to the development of bacterial overgrowth because of certain risk factors.  These factors can be grouped into four categories: (1)  motility  disorders, impaired movement of the small bowel, or anatomical changes that lead to stasis (a state in which the normal flow of a body liquid stops); (2) disorders of the  immune system ; (3) interference with the production of proteolytic enzymes, gastric acid, or bile; and (4) conditions that cause more bacteria from the  colon  to enter the  small bowel . [ 4 ]
In some people, methanogens may reside in the oral cavity, as evidenced by reductions in breath methane levels following mouthwash with chlorhexidine. [ 15 ]  This may affect results from hydrogen-methane breath testing.


Absence or impairment of the  migrating motor complex  (MMC), a cyclical motility pattern in the small intestine, and phase III of the MMC in particular, is associated with the development of SIBO. [ 16 ]  Problems with motility may either be diffuse, or localized to particular areas.


MMC impairment may be a result of post-infectious  irritable bowel syndrome , drug use, or  intestinal pseudo-obstruction  among other causes. [ 17 ]  There is an overlap in findings between  tropical sprue , post-infectious  irritable bowel syndrome  and small intestinal bacterial overgrowth in the pathophysiology of the three conditions and also SIBO can similarly sometimes be triggered by an acute gastrointestinal infection. [ 18 ] [ 19 ] [ 20 ]  As of 2020, there is still controversy about the role of SIBO in the pathogenesis of common functional symptoms such as those considered to be components of  irritable bowel syndrome . [ 4 ]  Diseases like  scleroderma [ 21 ]  cause diffuse slowing of the bowel, leading to increased bacterial concentrations. More commonly, the small bowel may have anatomical problems, such as out-pouchings known as  diverticula  that can cause bacteria to accumulate. [ 22 ]  After surgery involving the  stomach  and  duodenum  (most commonly with  Billroth II  antrectomy), a  blind loop  may be formed, leading to stasis of flow of intestinal contents. This can cause overgrowth, and is termed  blind loop syndrome . [ 23 ]


Systemic or metabolic disorders may lead to conditions allowing bacterial overgrowth as well. For example, diabetes can cause intestinal neuropathy,  pancreatitis  leading to  pancreatic insufficiency  can impair digestive enzyme production, and bile may be affected as part of  cirrhosis of the liver . [ 24 ]  The use of  proton pump inhibitors , a class of medication used to reduce stomach acid, is associated with an increased risk of developing SIBO. [ 25 ]


Finally, abnormal connections between the  bacteria -rich colon and the small bowel can increase the bacterial load in the small bowel. Patients with  Crohn's disease  or other diseases of the  ileum  may require surgery that removes the  ileocecal valve  connecting the small and large bowel; this leads to an increased reflux of bacteria into the small bowel. [ citation needed ]  After  bariatric surgery  for obesity, connections between the stomach and the  ileum  can be formed, which may increase bacterial load in the small bowel. [ 26 ]


The diagnosis of bacterial overgrowth can be made by physicians in various ways.  Malabsorption  can be detected by a test called the  D-xylose absorption test .  Xylose  is a sugar that does not require enzymes to be digested. The  D-xylose test  involves having a patient drink a certain quantity of D-xylose, and measuring levels in the  urine  and  blood ; if there is no evidence of D-xylose in the  urine  and  blood , it suggests that the small bowel is not absorbing properly (as opposed to problems with enzymes required for digestion). [ 27 ]


The gold standard for detection of bacterial overgrowth is the aspiration of more than 10 5  bacteria per millilitre from the small bowel. The normal small bowel has less than 10 4  bacteria per millilitre. [ citation needed ]  Some experts however, consider aspiration of more than 10 3  positive if the flora is predominately colonic type bacteria as these types of bacteria are considered pathological in excessive numbers in the small intestine. The reliability of aspiration in the diagnosis of SIBO has been questioned as SIBO can be patchy and the reproducibility can be as low as 38 percent. Breath tests have their own reliability problems with a high rate of false positive. Some doctors factor in a patients' response to treatment as part of the diagnosis. [ 4 ]


Breath tests have been developed to test for bacterial overgrowth. These tests are either based on bacterial metabolism of  carbohydrates  to  hydrogen ,  methane , or  hydrogen sulfide , or based on the detection of by-products of digestion of carbohydrates that are not usually metabolized. The  hydrogen breath test  involves having the patient fast for a minimum of 12 hours then having them drink a substrate usually glucose or  lactulose , then measuring expired hydrogen and methane concentrations typically over a period of several hours. It compares well to jejunal aspirates in making the diagnosis of bacterial overgrowth. [ citation needed ]   Carbon-13  ( 13 C) and  carbon-14  ( 14 C) based tests have also been developed based on the bacterial metabolism of D-xylose. Increased bacterial concentrations are also involved in the deconjugation of bile acids. The  glycocholic acid  breath test involves the administration of the bile acid  14 C glycocholic acid, and the detection of  14 CO 2 , which would be elevated in bacterial overgrowth. [ citation needed ]


However, some physicians suggest that if the suspicion of bacterial overgrowth is high enough, the best diagnostic test is a trial of treatment.  If the symptoms improve, an empiric diagnosis of bacterial overgrowth can be made. [ 28 ]


There is insufficient evidence to support the use of inflammatory markers, such as  fecal calprotectin , to detect SIBO. [ 4 ]


SIBO may be defined as an increased number of bacteria measured via exhaled hydrogen and/or methane gas following the ingestion of  glucose , or via analysis of small bowel aspirate fluid. [ 3 ]  Nevertheless, as of 2020, the definition of SIBO as a clinical entity lacks precision and consistency; it is a term generally applied to a clinical disorder where symptoms, clinical signs, and/or laboratory abnormalities are attributed to changes in the numbers of bacteria or in the composition of the bacterial population in the small intestine. [ 4 ]  The main obstacle to accurately define SIBO is limited understanding of the normal intestinal microbial population. Future advances in sampling technology and techniques for counting bacterial populations and their metabolites should provide much-needed clarity. [ 4 ]


The  archaeon   Methanobrevibacter smithii , has been associated with symptoms of SIBO which result in a positive methane breath test. [ 29 ]  In addition to the  archaeon , a few bacteria can also produce methane, such as members of the  Clostridium  and  Bacteroides  genus. Production of methane therefore, may not be bacterial, nor limited to the small intestine, and it has been proposed that the condition should be classified as a separate 'intestinal  methanogen  overgrowth' (IMO). [ 29 ]


Treatment strategies should focus on identifying and correcting the root causes, where possible, resolving nutritional deficiencies, and administering antibiotics. This is especially important for patients with indigestion and malabsorption. [ 4 ]  Although whether antibiotics should be a first line treatment is a matter of debate. Some experts recommend  probiotics  as first line therapy with antibiotics being reserved as a second line treatment for more severe cases of SIBO.  Prokinetic drugs  are other options but research in humans is limited. [ 30 ] [ 31 ] [ unreliable source? ]  A variety of antibiotics, including  tetracycline ,  amoxicillin-clavulanate ,  metronidazole ,  neomycin ,  cephalexin  and  trimethoprim-sulfamethoxazole  have been used; however, the best evidence is for the use of  rifaximin , a poorly-absorbed antibiotic. [ 2 ]  Although  irritable bowel syndrome  has been shown to respond to the treatment of poorly-absorbed antibiotics, there is limited evidence on the effectiveness of such treatment in cases of SIBO, and as of 2020, randomized controlled trials are still needed to further confirm the eradicating effect of such treatment in SIBO. [ 4 ]
A course of one week of antibiotics is usually sufficient to treat the condition. However, if the condition recurs, antibiotics can be given in a cyclical fashion in order to prevent tolerance. For example, antibiotics may be given for a week, followed by three weeks off antibiotics, followed by another week of treatment. Alternatively, the choice of antibiotic used can be cycled. [ 28 ]  There is still limited data to guide the clinician in developing antibiotic strategies for SIBO. Therapy remains, for the most part, empiric. However, concerns exist about the potential risks of long-term broad-spectrum antibiotic therapy. [ 4 ]


Probiotics  are bacterial preparations that alter the bacterial flora in the bowel to cause a beneficial effect. Animal research has demonstrated that probiotics have barrier enhancing, antibacterial, immune modulating and anti-inflammatory effects which may have a positive effect in the management of SIBO in humans. [ 4 ]   Lactobacillus casei  has been found to be effective in improving breath hydrogen scores after six weeks of treatment presumably by suppressing levels of a small intestinal bacterial overgrowth of fermenting bacteria. [ citation needed ]   Lactobacillus plantarum ,  Lactobacillus acidophilus , and  Lactobacillus casei  have all demonstrated effectiveness in the treatment and management of SIBO. Conversely,  Lactobacillus fermentum  and  Saccharomyces boulardii  have been found to be ineffective. [ 4 ] [ failed verification ]  A combination of  Lactobacillus plantarum  and  Lactobacillus rhamnosus  has been found to be effective in suppressing bacterial overgrowth of abnormal gas producing organisms in the small intestine. [ 32 ] [ non-primary source needed ]


A combination of probiotic strains has been found to produce better results than therapy with the antibiotic drug  metronidazole . [ 33 ] [ non-primary source needed ]


An  elemental diet  has been shown to be highly effective for eliminating SIBO with a two-week diet demonstrating 80% efficacy and a three-week diet demonstrating 85% efficacy. [ 34 ] [ 35 ] [ non-primary source needed ]  An elemental diet works via providing nutrition for the individual while depriving the bacteria of a food source. [ 36 ]  Additional treatment options include the use of  prokinetic  drugs such as  5-HT 4  receptor  agonists or  motilin  agonists to extend the SIBO free period after treatment with an elemental diet or antibiotics. [ 37 ] [ non-primary source needed ]  A diet void of certain foods that feed the bacteria can help alleviate the symptoms. [ 38 ]  For example, if the symptoms are caused by bacterial overgrowth feeding on indigestible carbohydrate rich foods, following a  FODMAP  restriction diet may help. [ 38 ] [ non-primary source needed ]


The  specific carbohydrate diet  ( SCD ) is a restrictive diet originally created to manage  celiac disease ; it limits the use of complex carbohydrates ( disaccharides  and  polysaccharides ).  Monosaccharides  are allowed, and various foods including fish, aged cheese and  honey  are included. Prohibited foods include cereal grains, potatoes and lactose-containing dairy products. [ 1 ]  It is a  gluten-free diet  since no grains are permitted. [ 2 ]


In 1924,  Sidney V. Haas  (1870–1964) described the first SCD for the treatment of children with celiac disease; this was known as the  banana  diet. [ 2 ] [ 3 ]  Haas described a trial with 10 children; all 8 children treated with bananas went into remission, and the two control children died. [ 4 ]  The banana SCD was the cornerstone of celiac therapy for decades until bread shortages in the Netherlands caused by World War II caused children with celiac disease to improve, which led to the isolation of wheat proteins, not starches, as the cause of celiac disease. [ 4 ]  Before the banana SCD, one out of four children with celiac died. [ 3 ]  After more research, he described the SCD as a treatment for celiac disease and  inflammatory bowel disease  (IBD) in his 1951 medical textbook  The Management of Celiac Disease ; Haas never accepted the finding that wheat gluten was the damaging part of wheat; he insisted it was starch and called the discovery about a gluten a "disservice." [ 5 ]


The diet was later re-popularized by biochemist Elaine Gottschall, the mother of one of Haas's patients, in her 1996 book  Breaking the Vicious Cycle. [ 2 ] [ 6 ]  Gottschall's daughter was reported to been cured of ulcerative colitis in two years by SCD. [ 1 ]  Gottschall described the theory of how restricting diet might reduce gut inflammation associated with various medical conditions. [ 2 ]   Gottschall asserted that the diet could "cure" a number of medical conditions without providing data. [ 6 ]    Gottschall advocated using SCD to treat  Crohn's disease ,  ulcerative colitis ,  diverticulitis ,  cystic fibrosis ,  chronic diarrhea , and  autism . [ 1 ]


The claims that the SCD is beneficial for children with autism are based on the supposition they have too much harmful bacteria in their gut.   [ 7 ]  While limited evidence suggests the SCD can be beneficial, there is a concern the restrictive nature of the diet may cause  nutritional deficiencies . [ 8 ]  Parents adopting the SCD for their children are at risk of experiencing guilt when their expectations of improvement are dashed. [ 7 ] [ 9 ]  The SCD is one of many unevidenced treatments offered for children with  special needs  that have the characteristic signs of being  pseudoscientific . [ 7 ]


A 2013 review on SCD and other exclusion diets concluded: "However, we lack large prospective controlled trials to provide the dietary recommendations patients’ desire. Taken together, studies of exclusive enteral nutrition, exclusion diets, and semi-vegetarian diets suggest that minimizing exposure of the intestinal lumen to selected food items may prolong the remission state of patients with inflammatory bowel disease. Even less evidence exists for the efficacy of the SCD,  FODMAP , or  Paleo diet . " [ 2 ]   It also said that the diet risks imposition of an undue financial burden and potentially causes malnutrition. [ 2 ]


As of 2017 [update]  there was preliminary evidence that the SCD may help relieve the symptoms of adults with inflammatory bowel disease. [ 10 ]


The Gut and Psychology Syndrome Diet (GAPS Diet) is an even more restrictive variant of the SCD, devised by a Russian neurologist. [ 11 ] [ 12 ]  The diet is promoted with claims it can treat a wide variety of conditions including autism, schizophrenia and epilepsy. [ 11 ] [ 12 ]  Like the SCD, claims of the diet's usefulness for children with autism are not supported by scientific studies. [ 11 ]   Harriet Hall  has described the GAPS diet as "a mishmash of half-truths, pseudoscience, imagination, and untested claims", [ 12 ]  and  Quackwatch  includes the GAPS Diet in its  Index of questionable treatments . [ 13 ]


Steatorrhea  (or  steatorrhoea ) is the presence of excess  fat  in  feces . Stools may be bulky and difficult to flush, have a pale and oily appearance, and can be especially foul-smelling. [ 1 ]  An oily anal leakage or some level of  fecal incontinence  may occur. There is increased fat excretion, which can be measured by determining the fecal fat level. [ 2 ]


Impaired digestion or absorption can result in fatty stools.
Possible causes include  exocrine pancreatic insufficiency , with poor digestion from lack of  lipases , loss of  bile salts , which reduces  micelle  formation, and small intestinal disease-producing  malabsorption . Various other causes include certain medicines that block fat absorption or indigestible or excess oil/fat in diet. [ 2 ]


The absence of  bile  secretion can cause the feces to turn gray or pale. Bile is responsible for the brownish color of feces. In addition to this, bile also plays a role in fat absorption, where dietary lipids are combined so that pancreatic lipases can hydrolyze them before going towards the small intestine. Without bile acids, this pathway would have a hard time occurring, which would lead to fat malabsorption and make steatorrhea more probable to occur. [ 2 ]  Other features of fat malabsorption may also occur such as reduced bone density, difficulty with vision under low light levels, bleeding, bruising, and slow blood clotting times. [ 1 ]


Orlistat  (also known by trade names Xenical and Alli) is a diet pill that works by blocking  the enzymes that digest fat . As a result, some fat cannot be absorbed from the gut and is excreted in the feces instead of being metabolically digested and absorbed, sometimes causing oily anal leakage. [ 6 ] [ 7 ] [ 8 ]  Vytorin (ezetimibe/simvastatin) tablets can cause steatorrhea in some people. [ 6 ] [ 8 ]


Some studies have shown that stool lipids are increased when whole nuts are eaten, compared to nut butters, oils or flour [ 9 ]  and that lipids from whole nuts are significantly less well absorbed. [ 10 ]


Consuming  jojoba oil  has been documented to cause steatorrhea and anal leakage because it is indigestible. [ 11 ]


Consuming  escolar  and  oilfish  (sometimes mislabelled as  butterfish ) will often cause steatorrhea, also referred to as gempylotoxism or gempylid fish poisoning or  keriorrhea . [ 12 ]


The fat substitute  Olestra , used to reduce digestible fat in some foods, was reported to cause leakage in some consumers during the test-marketing phase. As a result, the product was reformulated before general release to a hydrogenated form that is not liquid at physiologic temperature. The U.S.  Food and Drug Administration  warning indicated excessive consumption of Olestra could result in "loose stools"; however, this warning has not been required since 2003. [ 7 ] [ 13 ]


Steatorrhea should be suspected when the stools are bulky, floating and foul-smelling. [ 1 ]    Specific tests are needed to confirm that these properties are in fact due to excessive levels of fat.  Fats in feces can be measured over a defined time (often five days). [ 14 ]  Other tests include the (13)C-mixed triglycerides test and fecal  elastase , to detect possible fat maldigestion due to  exocrine pancreatic insufficiency , [ 14 ]  or various specific tests to detect other causes of  malabsorption  such as  celiac disease . [ 15 ]


Treatments are mainly correction of the underlying cause, as well as digestive enzyme supplements. [ 2 ]


Stercoral perforation [ 1 ]  is the perforation or rupture of the  intestine 's walls by its internal contents, such as hardened  feces  or foreign objects. Hardened stools may form in prolonged  constipation  or other diseases which cause obstruction of transit, such as  Chagas disease ,  Hirschprung's disease , toxic  colitis ,  hypercalcemia , and  megacolon . [ 2 ]


Symptoms can include  abdominal distension , pain, and nausea. [ 2 ]


Stercoral perforation is a rare and very dangerous, life-threatening situation, as well as a  surgical emergency , because the spillage of contaminated intestinal contents into the  abdominal cavity  leads to  peritonitis , a rapid  bacteremia  ( bacterial infection  of the  blood ), with many  complications . [ 3 ]


This article related to  pathology  is a  stub . You can help Wikipedia by  expanding it .


Stercoral ulcer  is an  ulcer  of the  colon  due to pressure and irritation resulting from severe, prolonged  constipation  due to a large bowel obstruction, damage to the  autonomic nervous system , or stercoral colitis. It is most commonly located in the  sigmoid colon  and  rectum . Prolonged constipation leads to production of fecaliths, leading to possible progression into a  fecaloma . These hard lumps irritate the rectum and lead to the formation of these ulcers. It results in fresh bleeding per rectum (i.e.  hematochezia ). These ulcers may be seen on imaging, such as a  CT scan  but are more commonly identified using  endoscopy , usually a  colonoscopy . [ 1 ]  Treatment modalities can include both surgical and non-surgical techniques.


Typical patients will present with a history of constipation, likely chronic constipation. Patient populations vulnerable to chronic constipation include, but are not limited to, the elderly, persons with  dementia , those with damage to the autonomic nervous system, infectious diseases, or intestinal vascular compromise. Some patients, due to their condition, may have limitations in reporting their symptoms. Typical symptoms can include  abdominal pain ,  abdominal distention ,  abdominal cramping ,  nausea ,  vomiting ,  fever ,  rectal bleeding , and possible  bowel perforation . [ 2 ]  Patients that develop bowel perforation may present in an acute state with severe abdominal pain and signs of perforation, such as abdominal distention,  guarding  and  rigidity , and air in the abdominal cavity. [ citation needed ]


Stercoral ulcers can lead to a complication known as stercoral colitis. Stercoral colitis is a relatively rare form of inflammatory  colitis  that can develop as a result of chronic  constipation  leading to the formation of hardened stool, known as fecaloma. Fecalomas can then lead to distention, possibly causing focal  necrosis  and possibly ulceration. Additional distention in the area can lead to compromise of the vascular supply, leading to intestinal  ischemia [ 2 ]
This form of colitis can be due to a wide range of etiologies, coinciding with most causes of constipation. Other etiologies range from a  stroke , intestinal vascular compromise, or any other damage to the  autonomic nervous system  to more rare diseases such as  Chagas disease  and  Hirschsprung's disease . [ citation needed ]


Ensuring a proper diagnosis involves a variety of tools by the clinician. An efficient  abdominal exam , along with a  rectal exam  aids in diagnosis. Typically patients will have tenderness to palpation on exam. Rebound tenderness or guarding may present with perforation of the ulcer with air leaking into the abdomen. In these patients, their exam may be far more acute with abdominal rigidity and need for immediate surgical intervention. Additionally, a rectal exam may reveal stool present in the  rectal vault , pointing to the fact that constipation has been or is still present. These patients may even have blood on their rectal exam, due to passing small amounts of stool around the ulcer and adjacent  fecaloma . [ 2 ]


Patients may have unstable vital signs if they have been having rectal bleeding, have developed stercoral colitis, and/or have had a perforation of the ulcer. These vital sign changes may be an acute fever,  elevated heart rate , and/or  decreased blood pressure . Laboratory evaluation may not be as specific in pointing to a diagnosis. Patients may have non-specific  leukocytosis  with elevated  acute phase reactants . However, these are neither specific nor sensitive so the clinician must take into account all aspects of the patient's illness to reach the diagnosis. If a patient presents with severe symptoms it may be useful to order blood cultures and preoperative labs such as  type and screen  and  coagulation testing . [ 2 ]


Imaging studies have been shown to be a key aspect in diagnosing patients with stercoral ulcers and stercoral colitis. Patient status on presentation is important to take into consideration when deciding what imaging study to order. Patients who are acutely ill and showing signs of perforation will need an upright  Chest x-ray  to determine if there is free air in the peritoneum. The imaging study of choice is an  CT scan  of the abdomen with  IV contrast , considering the patient's  renal function  is adequate. Findings that can be seen are fecal impaction with dilation of the  rectosigmoid junction  commonly, but any part of the colon can be dilated. Additionally, fecalomas may be seen as masses in the colon. In the case of ulceration, the part of the colon adjacent to the fecaloma will be thickened. This thickening of the bowel will help differentiate from stercoral colitis and stercoral ulcer from fecal impaction as the colon is typically not thickened in cases of fecal impaction. [ 2 ]


Treatment of these patients is typically dependent on a case-to-case basis as the overall patient presentation has to be considered. If the patient presents in an acutely ill state with possible  sepsis  or shock, they will need adequate IV fluid hydration with possible broad-spectrum  antibiotics . Additionally, these patients may need surgery if perforation has occurred. Patients without these symptoms should be managed conservatively with either manual or endoscopically guided fecal disimpaction. A bowel regimen should also be started to ensure that bowel movements become normal.  Opioid  pain medication should be avoided as these medications can slow  colonic motility  and possibly worsen constipation. The key to management and prognosis is identifying the cause or causes of the underlying constipation. Patients should be encouraged to increase  fiber ,  fluids , and  fruits  in their habits. Osmotic and stimulant  laxatives  can also be considered to aid patients if they have trouble making the necessary changes to their diet. [ 2 ]


A  stress ulcer  is a single or multiple  mucosal  defect usually caused by physiological (not psychological)  stress  which can become complicated by  upper gastrointestinal bleeding . These ulcers can be caused by  shock ,  sepsis , trauma or other conditions and are found in patients with chronic illnesses. These ulcers are a significant issue in patients in critical and intensive care.


It was previously thought that  peptic ulcers  (a different type of ulcer) could be caused by psychological stress but this was proven false with the discovery of  Helicobacter pylori  and its role in the formation of this ulcer. Stress ulcers are a different condition and are formed by different mechanisms. The term  stress ulcer  is a proper medical term and should not be misinterpreted as indicating that these ulcers are caused by emotional stress. Here the term  stress  refers to extreme physiological changes in the body.


Another distinction between peptic and stress ulcers is their location in the upper  gastrointestinal tract . Whereas ordinary  peptic ulcers  are found commonly in the  gastric antrum  and the  duodenum , stress ulcers are usually found in the  fundic mucosa  and can be located anywhere within the  stomach  and proximal  duodenum . Stress ulcers tend to present with multiple lesions whereas in peptic ulcers this is much more uncommon.


Stress ulcers, as defined by overt bleeding and hemodynamic instability, decreased  hemoglobin , and/or need for transfusion, were seen in 1.5% of patients in the 2252 patients in the Canadian Critical Care Trials group study. [ 1 ]  People with stress ulcers have a longer ICU length of stay (up to eight days) and a higher mortality (up to four-fold) than patients who do not have stress ulceration and bleeding. [ 2 ]  While the bleeding and transfusions associated with the stress ulcerations contribute to the increased mortality, the contribution of factors like  low blood pressure ,  sepsis , and  respiratory failure  to the mortality independently of the stress ulceration cannot be ignored. [ citation needed ]


Risk factors for stress ulcer formation that have been identified are numerous and varied.  However, two landmark studies and one position paper exist that addresses the topic of risk factors for stress ulcer formation:


The ulcerations may be superficial and confined to the mucosa, in which case they are more appropriately called erosions, or they may penetrate deeper into the submucosa. The former may cause diffuse mucosal oozing of blood, whereas the latter may erode into a submucosal vessel and produce frank hemorrhage. [ 3 ]


The characteristic lesions may be multiple, superficial mucosal erosions similar to erosive  gastroduodenitis . Occasionally, there may be a large acute ulcer in the duodenum (Curling's ulcer). [ 4 ]


Generally, there are multiple lesions located mainly in the stomach and occasionally in the duodenum. They range in depth from mere shedding of the superficial epithelium (erosion) to deeper lesions that involve the entire mucosal thickness (ulceration). [ 5 ]


The pathogenic mechanisms are similar to those of erosive gastritis. [ 5 ]


The pathogenesis of stress ulcer is unclear but probably is related to a reduction in mucosal blood flow or a breakdown in other normal mucosal defense mechanisms in conjunction with the injurious effects of acid and pepsin on the gastroduodenal mucosa. [ 6 ]


Stress ulcer is suspected when there is upper gastrointestinal bleeding in the appropriate clinical setting, for example, when there is upper gastrointestinal bleeding in elderly patients in a surgical intensive care unit (ICU) with heart and lung disease, or when there is upper gastrointestinal bleeding in patients in a medical ICU who require respirators. [ citation needed ]


Stress ulcer can be diagnosed after the initial management of gastrointestinal bleeding, the diagnosis can be confirmed by upper GI endoscopy. [ citation needed ]


The need for medications to prevent stress ulcer among those in the intensive care unit is unclear. As of 2014, the quality of the evidence is poor. [ 7 ]  It is unclear which agent is best or if prevention is needed at all. [ 8 ]  Benefit may only occur in those who are not being fed. [ 9 ]  Possible agents include  antacids ,  H2-receptor blockers ,  sucralfate , and  proton pump inhibitors  (PPIs). Tentative evidence supports that PPIs may be better than H2 blockers. [ 10 ]


Concerns with the use of stress ulcer prophylaxis agents include increased rates of  pneumonia  and   Clostridioides difficile  colitis . [ 9 ]


The principles of management are the same as for the chronic ulcer. [ 11 ]  The steps of management are similar as in erosive gastritis. [ 4 ]


Endoscopic means of treating stress ulceration may be ineffective and operation required. [ 11 ]  It is believed that shunting blood away from the mucosa makes the mucous membrane ischaemic and more susceptible to injury. [ 4 ]


Treatment of stress ulceration usually begins with prevention. Careful attention to respiratory status, acid-base balance, and treatment of other illnesses help prevent the conditions under which stress ulcers occur. Patients who develop stress ulcers typically do not secrete large quantities of gastric acid; however, acid does appear to be involved in the pathogenesis of the lesions. Thus it is reasonable either to neutralize acid or to inhibit its secretion in patients at high risk. [ 12 ]


In case of severe hemorrhagic or erosive gastritis and stress ulcers, a combination of antacids and H2-blockers may stop active bleeding and prevent bleeding from happening again. In selected patients, either endoscopic therapy or selective infusion of vasopressin into the left gastric artery may help control the hemorrhage. [ 13 ]


Among those in the intensive care unit, ulceration resulting in bleeding is very rare. [ 9 ]


Superior mesenteric artery  ( SMA )  syndrome  is a  gastro - vascular  disorder in which the third and final portion of the  duodenum  is compressed between the  abdominal aorta  (AA) and the overlying  superior mesenteric artery .  This  rare , potentially life-threatening syndrome is typically caused by an angle of 6–25° between the AA and the SMA, in comparison to the normal range of 38–56°, due to a lack of retroperitoneal and  visceral fat  ( mesenteric  fat). In addition, the aortomesenteric distance is 2–8 millimeters, as opposed to the typical 10–20. [ 1 ]  However, a narrow SMA angle alone is not enough to make a diagnosis, because patients with a low BMI, most notably children, have been known to have a narrow SMA angle with no symptoms of SMA syndrome. [ 2 ]


SMA syndrome is also known as Wilkie's syndrome, cast syndrome, mesenteric root syndrome, chronic duodenal ileus and intermittent arterio-mesenteric occlusion. [ 3 ]  It is distinct from  nutcracker syndrome , which is the entrapment of the left  renal vein  between the AA and the SMA, although it is possible to be diagnosed with both conditions. [ 4 ]


Signs and symptoms include early satiety,  nausea ,  vomiting , extreme "stabbing" postprandial  abdominal pain  (due to both the duodenal compression and the compensatory reversed  peristalsis ), abdominal distention/distortion,  burping , external hypersensitivity or tenderness of the abdominal area,  reflux , and  heartburn . [ 5 ]  In infants, feeding difficulties and poor weight gain are also frequent symptoms. [ 6 ]


In some cases of SMA syndrome, severe  malnutrition  accompanying spontaneous  wasting  may occur. [ 7 ]  This, in turn, increases the duodenal compression, which worsens the underlying cause, creating a cycle of worsening symptoms. [ 8 ]


Fear of eating is commonly seen among those with the chronic form of SMA syndrome. For many, symptoms are partially relieved when in the left lateral decubitus or knee-to-chest position, or in the prone (face down) position. A Hayes maneuver, which corresponds to applying pressure below the umbilicus in cephalad and dorsal direction, elevates the root of the SMA, also slightly easing the constriction. Symptoms can be aggravated when leaning to the right or taking a  face up  position. [ 7 ]


Retroperitoneal  fat and  lymphatic tissue  normally serve as a cushion for the duodenum, protecting it from compression by the SMA. SMA syndrome is thus triggered by any condition involving an insubstantial cushion and narrow  mesenteric  angle. SMA syndrome can present in two forms: chronic/congenital or acute/induced. [ citation needed ]


Patients with the chronic, congenital form of SMA syndrome predominantly have a lengthy or even lifelong history of abdominal complaints with intermittent exacerbations depending on the degree of duodenal compression. Risk factors include anatomic characteristics such as: asthenic (very thin or "lanky") body build, an unusually high insertion of the duodenum at the  ligament of Treitz , a particularly low origin of the SMA, or  intestinal malrotation  around an axis formed by the SMA. [ 9 ]   Predisposition is easily aggravated by any of the following: poor motility of the digestive tract, [ 3 ]  retroperitional  tumors ,  loss of appetite ,  malabsorption ,  cachexia , exaggerated lumbar  lordosis ,  visceroptosis , abdominal wall laxity, peritoneal adhesions, abdominal trauma, [ 10 ]  rapid linear adolescent growth spurt,  weight loss ,  starvation ,  catabolic  states (as with  cancer  and  burns ), and history of neurological injury. [ 11 ]


The acute form of SMA syndrome develops rapidly after traumatic incidents that forcibly hyper-extend the SMA across the duodenum, inducing the obstruction, or sudden weight loss for any reason. Causes include prolonged supine bed rest, scoliosis surgery, left nephrectomy, ileo-anal pouch surgery. [ citation needed ]


SMA syndrome is usually difficult to differentiate with  anorexia nervosa . [ 12 ]  Patients with SMA syndrome can be hindered restoring weight in those with anorexia nervosa. [ 13 ]


Diagnosis is very difficult, and usually one of exclusion. SMA syndrome is thus considered only after patients have undergone an extensive evaluation of their  gastrointestinal tract  including  upper endoscopy , and evaluation for various malabsorptive, ulcerative and inflammatory intestinal conditions with a higher diagnostic frequency. Diagnosis may follow  X-ray  examination revealing duodenal dilation followed by abrupt constriction proximal to the overlying SMA, as well as a delay in transit of four to six hours through the gastroduodenal region.  Standard diagnostic exams include abdominal and pelvic  computed tomography  (CT) scan with oral and IV contrast,  upper gastrointestinal series  (UGI), and, for equivocal cases, hypotonic duodenography.  In addition, vascular imaging studies such as  ultrasound  and contrast  angiography  may be used to indicate increased bloodflow velocity through the SMA or a narrowed SMA angle. [ 14 ] [ 15 ]


Despite multiple case reports, there has been controversy surrounding the diagnosis and even the existence of SMA syndrome since symptoms do not always correlate well with radiologic findings, and may not always improve following surgical correction. [ 16 ]  However, the reason for the persistence of gastrointestinal symptoms even after surgical correction in some cases has been traced to the remaining prominence of reversed  peristalsis  in contrast to direct peristalsis. [ 17 ]


Since females between the ages of 10 and 30 are most frequently affected, it is not uncommon for physicians to initially and incorrectly assume that  emaciation  is a choice of the patient instead of a consequence of SMA syndrome.  Patients in the earlier stages of SMA syndrome often remain unaware that they are ill until substantial damage to their health is done, since they may attempt to adapt to the condition by gradually decreasing their food intake or naturally gravitating toward a lighter and more digestible diet. [ citation needed ]


SMA syndrome can present in  acute , acquired form (e.g. abruptly emerging within an inpatient stay following scoliosis surgery) as well as  chronic  form (i.e. developing throughout the course of a lifetime and advancing due to environmental triggers, life changes, or other illnesses). According to a number of recent sources, at least 70% of cases can typically be treated with medical treatment, while the rest require surgical treatment. [ 5 ] [ 11 ] [ 19 ]


Medical treatment is attempted first in many cases. In some cases, emergency surgery is necessary upon presentation. [ 11 ]  A six-week trial of medical treatment is recommended in pediatric cases. [ 5 ]  The goal of medical treatment for SMA syndrome is resolution of underlying conditions and weight gain. Medical treatment may involve nasogastric tube placement for duodenal and gastric decompression, mobilization into the prone or left lateral decubitus position, [ 20 ]  the reversal or removal of the precipitating factor with proper  nutrition  and replacement of fluid and  electrolytes , either by surgically inserted jejunal  feeding tube ,  nasogastric intubation , or  peripherally inserted central catheter  (PICC line) administering  total parenteral nutrition  (TPN). Pro-motility agents such as  metoclopramide  may also be beneficial. [ 21 ]   Symptoms may improve after restoration of weight, except when reversed peristalsis persists, or if regained fat refuses to accumulate within the mesenteric angle. [ 17 ]  Most patients seem to benefit from nutritional support with  hyperalimentation  irrespective of disease history. [ 22 ]


If medical treatment fails, or is not feasible due to severe illness, surgical intervention is required. The most common operation for SMA syndrome,  duodenojejunostomy , was first proposed in 1907 by Bloodgood. [ 7 ]  Performed as either an   open surgery  or  laparoscopically , duodenojejunostomy involves the creation of an  anastomosis  between the  duodenum  and the  jejunum , [ 23 ]  bypassing the compression caused by the AA and the SMA. [ 1 ]   Less common surgical treatments for SMA syndrome include Roux-en-Y duodenojejunostomy, gastrojejunostomy, anterior transposition of the third portion of the duodenum, intestinal derotation, division of the  ligament of Treitz  (Strong's operation), and transposition of the SMA. [ 24 ]  Both transposition of the SMA and lysis of the duodenal suspensory muscle have the advantage that they do not involve the creation of an intestinal anastomosis. [ 9 ]


The possible persistence of symptoms after surgical bypass can be traced to the remaining prominence of reversed  peristalsis  in contrast to direct peristalsis, although the precipitating factor (the duodenal compression) has been bypassed or relieved. Reversed peristalsis has been shown to respond to duodenal circular drainage—a complex and invasive open surgical procedure originally implemented and performed in China. [ 17 ]


In some cases, SMA syndrome may occur alongside a serious, life-threatening condition such as cancer or AIDS. Even in these cases, though, treatment of the SMA syndrome can lead to a reduction in symptoms and an increased quality of life. [ 25 ] [ 26 ]


Delay in the diagnosis of SMA syndrome can result in fatal  catabolysis  (advanced  malnutrition ),  dehydration ,  electrolyte  abnormalities,  hypokalemia , acute gastric rupture or  intestinal perforation  (from prolonged  mesenteric ischemia ), gastric distention, spontaneous  upper gastrointestinal bleeding ,  hypovolemic shock , and  aspiration pneumonia .
 [ 1 ] [ 14 ] [ 27 ]


A 1-in-3 mortality rate for Superior Mesenteric Artery syndrome has been quoted by a small number of sources. [ 28 ]  However, after extensive research, original data establishing this mortality rate has not been found, indicating that the number is likely to be unreliable. While research establishing an official mortality rate may not exist, two recent studies of SMA syndrome patients, one published in 2006 looking at 22 cases [ 11 ]  and one in 2012 looking at 80 cases, [ 19 ]  show mortality rates of 0% [ 11 ]  and 6.3%, [ 19 ]  respectively. According to the doctors in one of these studies, the expected outcome for SMA syndrome treatment is generally considered to be excellent. [ 11 ]


According to a 1956 study, only 0.3% of patients referred for an upper-gastrointestinal-tract barium studies fit this diagnosis, and is thus a  rare disease . [ 29 ]  Recognition of SMA syndrome as a distinct clinical entity is controversial, due in part to its possible confusion with a number of other conditions, [ 30 ]  though it is now widely acknowledged. [ 1 ]  However, unfamiliarity with this condition in the medical community coupled with its intermittent and nonspecific symptomatology probably results in its underdiagnosis. [ 26 ]


As the syndrome involves a lack of essential fat, more than half of those diagnosed are  underweight , sometimes to the point of sickliness and  emaciation .  Females are impacted more often than males, and while the syndrome can occur at any age, it is most frequently diagnosed in early adulthood.  The most common co-morbid conditions include mental and behavioral disorders including eating disorders and depression, infectious diseases including tuberculosis and acute gastroenteritis, and nervous system diseases including muscular dystrophy, Parkinson's disease, and cerebral palsy. [ 19 ]


SMA syndrome was first described in 1861 by  Carl Freiherr von Rokitansky  in victims at autopsy, but remained pathologically undefined until 1927 when Wilkie published the first comprehensive series of 75 patients. [ 31 ]


American actor, director, producer, and writer  Christopher Reeve  had the acute form of SMA syndrome as a result of  spinal cord injury . [ citation needed ]  Former model Lisa Brown died in 2017 due to her SMAS after her insurance denied the potentially life saving surgery she needed. Her initial surgery failed causing her to require an intestinal transplant that was expected to cost up to $1 million leading her insurance to deny it. She planned her own funeral.  [ 32 ]   [ 33 ]


In 2017 the only US non-profit began distributing grants to those with SMAS. They are registered to the IRS under the name Superior Mesenteric Artery Syndrome Research, Awareness and Support, but also work under the DBA of SMAS Patient Assistance. They offer several resources on their website smasyndrome.com and their Facebook business page. SMAS Patient assistance works to disprove inaccurate information, educate on better diagnostic testing, and more successful surgeries such as Duodenal Deroation with LADDS.  [ citation needed ]


Tropical sprue  is a  malabsorption  disease commonly found in tropical regions, marked with abnormal flattening of the  villi  and  inflammation  of the lining of the  small intestine . [ 1 ] [ 2 ]  It differs significantly from  coeliac sprue . It appears to be a more severe form of  environmental enteropathy . [ 3 ] [ 4 ]


The illness usually starts with an attack of acute  diarrhoea ,  fever  and  malaise  following which, after a variable period, the patient settles into the chronic phase of diarrhoea,  steatorrhoea ,  weight loss ,  anorexia , malaise, and nutritional deficiencies. [ 1 ] [ 2 ] [ 3 ]
The symptoms of tropical sprue are:


Left untreated, nutrient and  vitamin deficiencies  may develop in patients with tropical sprue. [ 1 ] [ 2 ]   These deficiencies may have these symptoms:


The cause of tropical sprue is not known. [ 2 ]   It may be caused by persistent bacterial, viral, amoebal, or  parasitic infections . [ 5 ]   Folic acid deficiency , effects of malabsorbed fat on  intestinal motility , and persistent  small intestinal bacterial overgrowth  may combine to cause the disorder. [ 6 ]  A link between  small intestinal bacterial overgrowth  and tropical sprue has been proposed to be involved in the etiology of post-infectious  irritable bowel syndrome  (IBS). [ 7 ]  Intestinal immunologic dysfunction, including deficiencies in secretory immunoglobulin A (IgA), may predispose people to malabsorption and bacterial colonization, so tropical sprue may be triggered in susceptible individuals following an acute enteric infection. [ 1 ]


Diagnosis of tropical sprue can be complicated because many diseases have similar symptoms.  The following investigation results are suggestive: [ 1 ]


Tropical sprue is largely limited to within about 30 degrees north and south of the  equator .  Recent travel to this region is a key factor in diagnosing this disease in residents of countries outside of that geographical region. [ 2 ]


Other conditions which can resemble tropical sprue need to be differentiated. [ 4 ]   Coeliac disease  (also known as  coeliac sprue  or gluten sensitive enteropathy ), has similar symptoms to tropical sprue, with the flattening of the  villi  and  small intestine inflammation  and is caused by an  autoimmune disorder  in genetically susceptible individuals triggered by ingested  gluten .  Malabsorption can also be caused by  protozoan infections ,  tuberculosis ,  HIV/AIDS ,  immunodeficiency ,  chronic pancreatitis  and  inflammatory bowel disease . [ 2 ]   Environmental enteropathy  is a less severe, subclinical condition similar to tropical sprue. [ 2 ]


Preventive measures for visitors to tropical areas where the condition exists include steps to reduce the likelihood of  gastroenteritis .  These may comprise using only  bottled water  for drinking, brushing teeth, and washing food, and avoiding fruits washed with tap water (or consuming only peeled fruits, such as  bananas  and  oranges ).  Basic sanitation is necessary to reduce fecal-oral contamination and the impact of environmental enteropathy in the developing world. [ 2 ]


Once diagnosed, tropical sprue can be treated by a course of the antibiotic  tetracycline  or  sulphamethoxazole/trimethoprim (co-trimoxazole)  for 3 to 6 months. [ 2 ] [ 8 ]
Supplementation of vitamins B 12  and folic acid improves appetite and leads to a gain in weight. [ 4 ] [ 9 ]


The prognosis for tropical sprue may be excellent after treatment.  It usually does not recur in people who get it during travel to affected regions.  The recurrence rate for natives is about 20%, [ 2 ]  but another study showed changes can persist for several years. [ 10 ]


Tropical sprue is common in the  Caribbean , Central and  South America , and  India  and southeast  Asia .  In the Caribbean, it appeared to be more common in Puerto Rico and Haiti.  Epidemics in southern India have occurred. [ 2 ]


The disease was first described by  William Hillary [ 11 ]  in 1759 in  Barbados . [ 12 ]  Tropical sprue was responsible for one-sixth of all casualties sustained by the Allied forces in India and Southeast Asia during World War II. [ 2 ]  The use of folic acid and vitamin B 12  in the treatment of tropical sprue was promoted in the late 1940s by Dr.  Tom Spies  of the  University of Alabama , while conducting his research in Cuba and Puerto Rico. [ 13 ] [ 14 ] [ 15 ]


Upper gastrointestinal bleeding  ( UGIB ) is  gastrointestinal bleeding  in the  upper gastrointestinal tract , commonly defined as bleeding arising from the  esophagus ,  stomach , or  duodenum . Blood may be observed in  vomit  or in altered form as  black stool . Depending on the amount of the blood loss, symptoms may include  shock .


Upper gastrointestinal bleeding can be caused by  peptic ulcers ,  gastric erosions ,  esophageal varices , and rarer causes such as  gastric cancer . The initial assessment includes measurement of the  blood pressure  and  heart rate , as well as  blood tests  to determine the  hemoglobin .


Significant upper gastrointestinal bleeding is considered a  medical emergency .  Fluid replacement , as well as  blood transfusion , may be required.  Endoscopy  is recommended within 24 hours and bleeding can be stopped by various techniques. [ 1 ]   Proton pump inhibitors  are often used. [ 2 ]   Tranexamic acid  may also be useful. [ 2 ]  Procedures (such as  TIPS  for variceal bleeding) may be used. Recurrent or refractory bleeding may lead to need for  surgery , although this has become uncommon as a result of improved endoscopic and medical treatment.


Upper gastrointestinal bleeding affects around 50 to 150 people per 100,000 a year. It represents over 50% of cases of gastrointestinal bleeding. [ 2 ]  A 1995 UK study found an estimated mortality risk of 11% in those admitted to hospital for gastrointestinal bleeding. [ 3 ]


Persons with upper gastrointestinal bleeding often present with  hematemesis ,  coffee ground vomiting ,  melena , or  hematochezia  (maroon-coloured stool) if the hemorrhage is severe.  The presentation of bleeding depends on the amount and location of hemorrhage. A person with upper gastrointestinal bleeding may also present with complications of  anemia , including  chest pain ,  syncope ,  fatigue  and  shortness of breath . [ citation needed ]


The  physical examination  performed by the  physician  concentrates on the following things: [ citation needed ]


Laboratory findings include  anemia ,  coagulopathy , and an elevated  BUN-to-creatinine ratio .


A number of medications increase the risk of bleeding including  NSAIDs  and  SSRIs .  SSRIs  double the rate of upper gastrointestinal bleeding. [ 4 ]


There are many causes for upper gastrointestinal hemorrhage.  Causes are usually anatomically divided into their location in the upper gastrointestinal tract. [ citation needed ]


People are usually stratified into having either  variceal  or non-variceal sources of upper gastrointestinal hemorrhage, as the two have different treatment algorithms and prognosis. [ citation needed ]


The causes for upper gastrointestinal hemorrhage include the following:


The strongest predictors of an upper gastrointestinal bleed are black stool, age <50 years, and blood urea nitrogen/creatinine ratio 30 or more. [ 8 ] [ 9 ]  The diagnosis of upper gastrointestinal bleeding is assumed when  hematemesis  (vomiting of blood) is observed. [ citation needed ]


A  nasogastric aspirate  can help determine the location (source) of bleeding and help understand the best initial diagnostic and treatment plan. Nasogastric aspirate has a sensitivity of 42%, specificity 91%,  negative predictive value  64%, positive predictive value 92% and overall accuracy of 66% in differentiating upper gastrointestinal bleeding from bleeding distal to the  ligament of Treitz . [ 8 ]  A positive aspirate is more helpful than a negative aspirate (If the aspirate is positive, an upper gastrointestinal bleed is likely; if the aspirate is negative, the source of a gastrointestinal bleed is probably, but not certainly, lower). A smaller study found a sensitivity of 79% and specificity of 55%, somewhat opposite results from Witting. [ 10 ]  The accuracy of the aspirate is improved by using the Gastroccult test. [ citation needed ]


Determining whether blood is in gastric contents, either vomited or aspirated specimens, may be a challenge when determining the source of the hemorrhage. Slide tests are based on  orthotolidine  (Hematest reagent tablets and Bili-Labstix) or guaiac (Hemoccult and Gastroccult). There is some evidence that orthotolidine-based tests more sensitive than specific, the Hemoccult test's sensitivity reduced by the acidic environment; and the Gastroccult test be the most accurate. [ 11 ]  The sensitivity, specificity, positive predictive value, and negative predictive value have been reported as follows: [ 10 ]


Holman used simulated gastric specimens and found the Hemoccult test to have significant problems with non-specificity and false-positive results, whereas the Gastroccult test was very accurate. [ 12 ]
Holman found that by 120 seconds after the developer was applied, the Hemoccult test was positive on  all  control samples.


A scoring system called the  Glasgow-Blatchford  bleeding score found 16% of people presenting with upper gastrointestinal bleed had Glasgow-Blatchford score of "0", considered low. Among these people there were no deaths or interventions needed and they were able to be effectively treated in an outpatient setting. [ 13 ]
 [ 14 ]


Score is equal to "0" if the following are all present:


The predictive values cited are based on the prevalences of upper gastrointestinal bleeding in the corresponding studies. A  clinical calculator can be used to generate predictive values for other prevalences. [ citation needed ]


The initial focus is on  resuscitation  beginning with airway management and fluid resuscitation using either intravenous fluids and or blood. [ 15 ]  A number of medications may improve outcomes depending on the source of the bleeding. [ 15 ]   Proton pump inhibitor  medications are often given in the emergent setting before an endoscopy and may reduce the need for an endoscopic haemotstatic treatment. [ 16 ]  Proton pump inhibitors decrease gastric acid production. [ 16 ]  There is insufficient evidence to determine if proton pump inhibitors decrease death rates, re-bleeding events, or the need for surgical interventions. [ 16 ]  After the initial resuscitation has been completed, treatment is instigated to limit the likelihood of re-bleeds and correct any anemia that the bleeding may have caused. Those with a  Glasgow Blatchford score  less than 2 may not require admission to hospital. [ 17 ]


Based on evidence from people with other health problems  crystalloid  and  colloids  are believed to be equivalent for peptic ulcer bleeding. [ 15 ]  In people with a confirmed peptic ulcer, proton pump inhibitors do not reduce death rates, later bleeding events, or need for surgery. [ 18 ]  They may decrease signs of bleeding at endoscopy however. [ 18 ]  In those with less severe disease and where endoscopy is rapidly available, they are of less immediate clinical importance. [ 16 ]   Tranexamic acid  might be effective to reduce mortality, but the evidence for this is weak. [ 15 ] [ 19 ]  But the evidence is promising. [ 20 ]   Somatostatin  and  octreotide  while recommended for variceal bleeding have not been found to be of general use for non-variceal bleeds. [ 15 ]


For initial fluid replacement colloids or  albumin  is preferred in people with cirrhosis. [ 15 ]  Medications typically includes  octreotide  or if not available  vasopressin  and  nitroglycerin  to reduce portal pressures. [ 21 ]  This is typically in addition to  endoscopic banding  or  sclerotherapy  for the varices. [ 21 ]  If this is sufficient then  beta blockers  and  nitrates  may be used for the prevention of re-bleeding. [ 21 ]  If bleeding continues then balloon tamponade with a  Sengstaken-Blakemore tube  or  Minnesota tube  may be used in an attempt to mechanically compress the varices. [ 21 ]  This may then be followed by a  transjugular intrahepatic portosystemic shunt . [ 21 ]


If large amounts of pack red blood cells are used additional  platelets  and  fresh frozen plasma  should be administered to prevent  coagulopathies . [ 15 ]  Some evidence supports holding off on blood transfusions in those who have a  hemoglobin  greater than 7 to 8 g/dL and only moderate bleeding. [ 15 ] [ 22 ]  If the INR is greater than 1.5 to 1.8 correction with fresh frozen plasma,  prothrombin complex  may decrease mortality. [ 15 ]


Upper endoscopy within 24 hours is the recommended treatment. [ 15 ] [ 23 ]  The benefits versus risks of placing a  nasogastric tube  in those with upper gastrointestinal bleeding are not well known. [ 15 ]   Prokinetic agents  to empty the stomach such as  erythromycin  before endoscopy can decrease the amount of blood in the stomach and thus improve the operators view. [ 15 ]  This erythromycin treatment may lead to a small decrease in the need for a blood transfusion, but the overall balance of how effective erythromycin is compared to potential risks is not clear. [ 15 ] [ 23 ]  Proton pump inhibitors, if they have not been started earlier, are recommended in those in whom high risk signs for bleeding are found. [ 15 ]  It is also recommended that people with high risk signs are kept in hospital for at least 72 hours. [ 15 ]
Blood transfusions are not generally recommended to correct anemia, but blood transfusions are recommended if the person is not stable (cardiovascular system instability). [ 22 ]  Oral iron can be used, but this can lead to problems with compliance, tolerance, darkening stools which may mask evidence of rebleeding and tends to be slow, especially if used in conjunction with proton pump inhibitors.  Parenteral  Iron is increasingly used in these cases to improve patient outcomes and void blood usage. [ citation needed ]


Depending on its severity, upper gastrointestinal bleeding may carry an estimated mortality risk of 11%. [ 3 ]  However, survival has improved to about 2 percent, likely as a result of improvements in medical therapy and endoscopic control of bleeding. [ 24 ]


About 75% of people presenting to the  emergency department  with gastrointestinal bleeding have an upper source. [ 9 ]  The diagnosis is easier when the people have  hematemesis . In the absence of hematemesis, 40% to 50% of people in the emergency department with gastrointestinal bleeding have an upper source. [ 8 ] [ 10 ] [ 25 ]


Very early onset inflammatory bowel disease  ( VEOIBD ) is a type of  IBD  which starts in people younger than 6 years of age. According to age we can distinguish more specifically two categories within the VEOIBD diagnosis - neonatal  IBD  (patients younger than 1 month) and infantile  IBD  (patients younger than 2 years old). [ 1 ]


VEIOBD patients present with severe form of the disease that responds poorly to conventional therapies. The symptoms often include not only gastrointestinal tract, but also other tissues, such as  pituitary gland ,  spleen ,  liver ,  skin ,  respiratory tract  or  blood . [ 1 ]


On the other hand, other types of  primary immunodeficiency  can often manifest with IBD-like symptoms, too. These include the  IPEX syndrome ,  Wiskott-Aldrich syndrome ,  XIAP syndrome  or  chronic granulomatous disease . [ 2 ]


Inflammatory bowel diseases  (IBDs), such as  Crohn's disease  (CD) or  Ulcerative Colitis  (UC), are chronic inflammatory conditions of the  gastrointestinal tract . Up-to-date findings show that the pathogenesis is influenced by both environmental and genetic factors. A considerable number of  monogenic  disorders can be found especially among patients with VEOIBD. Causal mutations can be found in genes involved in epithelial barrier formation ( COL7A1 ,  FERMT1 ),  innate  ( CYBB ,  G6PC3 ), as well as the  specific immune response  and immune regulation ( IL10 ,  IL10RA ,  FOXP3 ). [ 3 ]


Vibriosis  or  vibrio infection  is an infection caused by  bacteria  of the genus  Vibrio . About a dozen species can cause vibriosis in humans, with the most common in multiple countries across the  Northern Hemisphere  being  Vibrio parahaemolyticus ,  Vibrio vulnificus , and  Vibrio alginolyticus . [ 1 ] [ 6 ]   Vibrio cholerae , can also commonly cause vibriosis, though only those strains that do not produce cholera-specific toxins: non-O 1 or non-O 139. [ 9 ]  Bacteria that produce these toxins are classified by the World Health Organization as causing  cholera , which is a more severe disease. [ 1 ]  Vibriosis is also an animal disease, and can cause harm to wild and farmed fish among others. [ 10 ]


The genus  Vibrio  includes various species that can cause illness in humans, including  Vibrio parahaemolyticus  and  Vibrio vulnificus . These bacteria thrive in warm, brackish water and are often found in  shellfish  such as  oysters ,  clams , and  mussels . [ 1 ]


Vibriosis can be contracted through:


The symptoms of vibriosis can vary depending on the species involved:


Vibriosis incidence is influenced by  environmental  factors such as  water temperature  and  salinity . Warmer temperatures, including in relation to  global warming , have been linked to increased prevalence of vibriosis as  Vibrio  bacteria thrive in warmer conditions. [ 11 ] [ 12 ]


In some regions, vibriosis is referred to as "bath-sore fever" or "bathing fever" due to its association with warm water activities, especially during unusually warm summers. The term highlights the seasonal nature of the infections, which typically occur during the warmer months when people are more likely to engage in water-related activities. [ 5 ]


Diagnosis of vibriosis involves:


Treatment of vibriosis depends on the severity and type of infection:


Preventative measures to reduce the risk of vibriosis include:


Whipple's disease  is a  rare   systemic  infectious disease caused by the  bacterium   Tropheryma whipplei . First described by  George Hoyt Whipple  in 1907 and commonly considered as a gastrointestinal disorder, Whipple's disease primarily causes  malabsorption , but may affect any part of the human body, including the heart, brain, joints, skin, lungs and the eyes. [ 1 ]  Weight loss, diarrhea, joint pain, and arthritis are common presenting symptoms, but the presentation can be highly variable in certain individuals, and about 15% of patients do not have the standard signs and symptoms. [ 2 ]


Whipple's disease is significantly more common in men, with 87% of patients diagnosed being male. [ 3 ]  When recognized and treated, Whipple's disease can usually be cured with long-term antibiotic therapy, but if the disease is left undiagnosed or untreated, it can ultimately be fatal. [ 3 ] [ 4 ]


The most common symptoms are  diarrhea ,  abdominal pain ,  weight loss , and  joint pains . The joint pains may be due to migratory nondeforming arthritis, which may occur many years before any digestive-tract symptoms develop; they tend to involve the large joints, but can occur in any pattern and tend not to damage the joint surface to the point that the joint becomes deformed. Fever and  chills  occur in a small proportion of people. [ 5 ]


In its more advanced form,  malabsorption  (insufficient absorption of nutrients from the diet) leads to  wasting  and the enlargement of  lymph nodes  in the abdomen. Neurological symptoms (discussed below) are more common in those with the severe form of the abdominal disease. Chronic malabsorptive diarrhea leads to the poor absorption of fat, causing  steatorrhea  (fatty, offensive-smelling stool), flatulence, and abdominal distension. Protein-losing enteropathy may also occur, causing depletion of  albumin , a blood protein, which may lead to  peripheral edema  caused by the lowered  oncotic pressures . [ 5 ]


Hyperpigmentation of the skin occurs in almost half; some also have skin nodules. Various eye problems, such as  uveitis , may occur; this is typically associated with deteriorating vision and pain in the affected eye.  Endocarditis  (infection of the  heart valve ) has been reported in a small number of cases, sometimes in people with no other symptoms of Whipple's disease; this is typically noticed as breathlessness and leg swelling due to fluid accumulation as the heart is unable to pump fluid through the body. [ 5 ]


Of those affected by Whipple's disease, 10–40% have problems related to the involvement of the  brain ; the symptoms relate to the part of the brain that is affected. The most common problems are  dementia ,  memory loss ,  confusion , and decreased  level of consciousness . Eye-movement disturbances and myorhythmia (rapidly repetitive movements of the muscles) of the face, together referred to as oculomasticatory myorhythmia, are highly characteristic for Whipple's disease. Weakness and poor coordination of part of the body,  headaches ,  seizures , and a number of more uncommon neurological features are present in some cases. [ 5 ]


T. whipplei  is one of the  Actinomycetes , and is a distant relative of the  Mycobacterium avium complex , explaining in part why Whipple's disease is similar to the diseases caused by MAC bacteria. [ 6 ]  The disease is common in  farmers  and those exposed to soil and animals, suggesting that the infection is acquired from these sources. [ 5 ]


Individuals who are most susceptible to the disease are those with decreased ability to perform intracellular degradation of ingested pathogens or particles, particularly within macrophages. Several studies indicate that defective  T-lymphocyte  (particularly TH1 population) function may be an important predisposing factor for the disease. [ 7 ]  In particular, circulating cells which are  CD11b  (also known as integrin alpha) expressive are reduced in susceptible individuals. CD11b has a vital role in activation of macrophages to destroy intracellularly ingested  T. whipplei  bacteria. [ 6 ]


Common clinical signs and symptoms of Whipple's disease include diarrhea, steatorrhea, abdominal pain, weight loss, migratory arthropathy, fever, and neurological symptoms. [ 8 ]  Weight loss and diarrhea are the most common symptoms that lead to identification of the process, but may be preceded by chronic, unexplained, relapsing episodes of nondestructive seronegative arthritis, often of large joints. [ 9 ]


Endoscopy  of the  duodenum  and  jejunum  can reveal pale yellow shaggy mucosa with erythematous eroded patches in patients with classic intestinal Whipple's disease, and small bowel  X-rays  may show some thickened folds. Other pathological findings may include enlarged  mesenteric lymph nodes , hypercellularity of  lamina propria  with "foamy macrophages", and a concurrent decreased number of  lymphocytes  and  plasma cells , per high power field view of the biopsy. [ citation needed ]


Diagnosis is made by  biopsy , usually by  duodenal   endoscopy , which reveals  PAS -positive  macrophages  in the lamina propria containing non acid-fast , Gram-positive bacilli. [ 5 ] [ a ]   Immunohistochemical  staining for antibodies against  T. whipplei  has been used to detect the organism in a variety of tissues, and a  polymerase chain reaction -based assay is also available, [ 5 ]   which can be confirmatory if performed on blood,  vitreous  fluid,  synovial  fluid, heart valves, or  cerebrospinal fluid . [ 11 ]  PCR of saliva, gastric or intestinal fluid, and stool specimens is highly sensitive, but not specific enough, indicating that healthy individuals can also harbor the causative bacterium without the manifestation of Whipple's disease, but that a negative PCR is most likely indicative of a healthy individual. [ 5 ]


Treatment is with  penicillin ,  ampicillin ,  tetracycline , or  co-trimoxazole  for one to two years. [ 2 ]  Any treatment lasting less than a year has a relapse rate around 40%. [ citation needed ]  Expert opinion as of 2007 is that Whipple's disease should be treated with  doxycycline  with  hydroxychloroquine  for 12 to 18 months. [ 3 ]  Hydroxychloroquine increases antibiotic and bactericides activity against the replication of the bacteria in acidic vacuoles of macrophages by increasing the macrophage intraphagosomal pH. [ 12 ]  Sulfonamides ( sulfadiazine  or  sulfamethoxazole ) may be added for treatment of neurological symptoms. [ 3 ]


The disease is regarded as extremely rare, with an  incidence  (new number of cases per year) of one case per million people. The patients are predominantly male, with various studies and sources typically reporting a ratio between 2:1 and 3:1 of male to female patients. [ 13 ]  In the United States and some other countries, it occurs predominantly in those of  Caucasian ethnicity , suggesting a possible  genetic predisposition  in that population. [ 5 ] [ 13 ]   T. whipplei  appears to be an environmental organism that is commonly present in the gastrointestinal tract, but remains asymptomatic. [ 5 ]  Several lines of evidence suggest that some defect—inherited or acquired—in immunity is required for it to become pathogenic. [ 14 ]  The possible immunological defect may be specific for  T. whipplei , since the disease is not associated with a substantially increased risk of other infections. [ 15 ]  The disease is usually diagnosed in  middle age  (median 49 years). Studies from  Germany  have shown that age at diagnosis has been rising since the 1960s. [ 5 ]


Whipple described the disease in 1907 in a paper in the now-defunct  Bulletin of Johns Hopkins Hospital . The patient was a 36-year-old medical missionary. Whipple referred to the disease as "intestinal  lipodystrophy ". [ 1 ]  It was long presumed to be an infectious disease, but the causative organism was only fully identified in 1992. [ 16 ]  In 2003, doctors from  Johns Hopkins Hospital , together with the French microbiologist  Didier Raoult  applied novel diagnostic methods to stored tissue samples from Whipple's original patient, and demonstrated  T. whipplei  in these tissues. [ 3 ] [ 17 ]


Alcohol flush reaction  is a condition in which a person develops flushes or blotches associated with  erythema  on the face, neck, shoulders, ears, and in some cases, the entire body after consuming  alcoholic beverages . The reaction is the result of an accumulation of  acetaldehyde , a metabolic byproduct of the  catabolic  metabolism of  alcohol , and is caused by an  aldehyde dehydrogenase 2  deficiency. [ 4 ]


This syndrome has been associated with lower than average rates of alcoholism, possibly due to its association with adverse effects after drinking alcohol. [ 5 ]  However, it has also been associated with an increased risk of  esophageal cancer  in those who do drink. [ 4 ] [ 6 ] [ 7 ]


The reaction is informally termed  Asian flush  due to its frequent occurrence in  East Asians , with approximately 30 to 50% of Chinese, Japanese, and Koreans showing characteristic physiological responses to drinking alcohol that includes facial flushing,  nausea , headaches and a  fast heart rate . The condition may be also highly prevalent in some  Southeast Asian  and  Inuit  populations. [ 4 ] [ 2 ] [ 3 ] [ 8 ]


The most obvious symptom of alcohol flush reaction is flushing on a person's face and body after drinking alcohol. [ 4 ]  Other effects include "nausea, headache and general physical discomfort". [ 9 ]  People affected by this condition show greater reduction in  psychomotor functions  on alcohol consumption than those without. [ 10 ]


Many cases of  alcohol-induced respiratory reactions , which involve  rhinitis  and worsening of  asthma , develop within 1–60 minutes of drinking alcohol and are due to the same causes as flush reactions. [ 11 ]


Disulfiram , a drug sometimes given as treatment for alcoholism, induces effects similar to alcohol flush or hangover causing the  disulfiram-alcohol reaction . It inhibits  acetaldehyde dehydrogenase , causing a five-to ten-fold increase in the concentration of acetaldehyde in the body after drinking alcohol, as happens spontaneously in people subject to flush. [ 12 ] [ 13 ]


Alcohol flush reaction is a condition that is experienced more frequently by people of East Asian descent, giving rise to names such as "Asian flush" or "Asian glow". [ citation needed ]


Around 20–30% of East Asians carry the rs671 (ALDH2*2) allele on chromosome 12, which results in a less functional  acetaldehyde dehydrogenase  enzyme, responsible for the breakdown of acetaldehyde, and accounts for most incidents of alcohol flush reaction worldwide. According to the analysis by  HapMap  project, 20% to 30% of people of Chinese, Japanese, and Korean ancestry have at least one  ALDH2*2  allele, while it is rare among Europeans and sub-Saharan Africans. [ 8 ]


The rs671 allele is native to  East Asia  and most common in southeastern China. Analysis correlates the rise and spread of rice cultivation in  South China  with the spread of the allele. [ 5 ]  The reasons for this positive selection are not known, but it has been hypothesized that elevated concentrations of acetaldehyde may have conferred protection against certain parasitic infections, such as  Entamoeba histolytica . [ 14 ]


Additionally, in around 80% of  East Asians , the rapid accumulation of acetaldehyde is worsened by another gene variant; in this case the allele  ADH1B*2 ,  which results in the  alcohol dehydrogenase   enzyme  converting alcohol to toxic  acetaldehyde  more quickly than other gene variants common outside East Asia. [ 5 ] [ 15 ]


Those with facial flushing due to ALDH2 deficiency may be  homozygotes , with two alleles of low activity, or  heterozygotes , with one low-activity and one normal allele. Homozygotes for the trait find consumption of large amounts of alcohol to be so unpleasant that they are generally protected from  esophageal cancer , but heterozygotes are able to continue drinking. However, an ALDH2-deficient drinker has four to eight times the risk of developing esophageal cancer as a drinker not deficient in the enzyme. [ 4 ] [ 7 ]


Because most East Asians have a  variant  in the  ADH gene , this risk is lowered somewhat because the  ADH  variant reduces the risk of esophageal cancer four-fold. However, ALDH2-deficient people who do not carry this ADH variant are at the highest risk of cancer as these risk factors act in a multiplicative manner through increasing exposure time to salivary acetaldehyde. [ 7 ]


The idea that acetaldehyde is the cause of the flush is also shown by the clinical use of  disulfiram  (Antabuse), which blocks the removal of acetaldehyde from the body via ALDH inhibition. The high acetaldehyde concentrations described share similarity to symptoms of the flush (flushing of the skin, accelerated heart rate, shortness of breath, throbbing headache, mental confusion and blurred vision). [ 16 ]


For measuring the level of flush reaction to alcohol, the most accurate method is to determine the level of acetaldehyde in the blood stream. This can be measured through a breathalyzer test or blood test. [ 17 ]  Additionally, measuring the amount of alcohol metabolizing enzymes  alcohol dehydrogenases  and  aldehyde dehydrogenase  through  genetic testing  can predict the amount of reaction that one would have. [ citation needed ]


Anorectal varices  are  collateral  submucosal blood vessels  dilated  by backflow in the veins of the  rectum . [ 1 ]  Typically this occurs due to  portal hypertension  which shunts venous blood from the  portal system  through the  portosystemic anastomosis  present at this site into the  systemic venous system . [ 2 ] [ 3 ]  This can also occur in the  esophagus , causing  esophageal varices , and at the level of the  umbilicus , causing  caput medusae . [ 4 ]  Between 44% and 78% of patients with portal hypertension get anorectal varices. [ 3 ] [ 5 ]


Blood from the superior portion of the  rectum  normally drains into the  superior rectal vein  and via the  inferior mesenteric vein  to the  liver  as part of the  portal venous system . Blood from the middle and inferior portions of the  rectum  is drained via the  middle  and  inferior rectal veins . In  portal hypertension , venous resistance is increased within the  portal venous system ; when the pressure in the portal venous system increases above that of the  systemic , blood is shunted through the  portosystemic anastomoses . The shunting of blood and consequential increase of pressure through the collateral veins causes the  varicosities . [ citation needed ]


The terms  rectal varices  and  haemorrhoids  are often used interchangeably, but this is not correct. [ 6 ]  Haemorrhoids are due to prolapse of the  rectal venous plexus  and are no more common in patients with portal hypertension than in those without. [ 7 ]  Rectal varices, however, are found only in patients with portal hypertension and are common in conditions such as  cirrhosis . [ 8 ]


Unlike esophageal varices, rectal varices are less prone to bleeding, are less serious when a bleed does occur, and are easier to treat because of the more accessible location. [ 9 ]  However, in some cases, rectal varices can result in severe bleeding.  [ 10 ]


Typically, treatment consists of addressing the underlying portal hypertension. Some treatments include portosystemic shunting, ligation, and under-running suturing. [ 5 ]  Insertion of a  transjugular intrahepatic portosystemic shunt  (TIPS) has been shown to alleviate varices caused by portal hypertension. [ 1 ]  Successful treatment of portal hypertension that subsequently reduces anorectal varices provides a confirmation of the initial diagnosis, allowing for a distinction between varices and hemorrhoids, which would not have been alleviated by reduction of portal hypertension. [ citation needed ]


Autoimmune gastrointestinal dysmotility  ( AGID ) is an  autoimmune disease   autonomic neuropathy  affecting the  gastrointestinal  organs and  digestive system  of the body. Dysmotility is when the strength or coordination of the  esophagus ,  stomach  or  intestines   muscles  do not work as they should. [ 1 ]


Often AGID is a symptom of other problems, including  colon cancer ,  lupus , lung, breast, or  ovarian   carcinoma  or  thymoma . or other diseases.


AGID is diagnosed with a complete medical history, exam of patients motility and with special blood tests looking for autoantibodies consistent with neurologic autoimmunity. [ 2 ]  Blood tests included evaluations of immunofluorescence (neuronal nuclear and cytoplasmic antibodies), radioimmunoprecipitation assays (neuronal and muscle plasma membrane cation channel antibodies), and enzyme-linked immunosorbent assay (muscle striational antibodies). A finding, along with medical history, of ganglionic neuronal acetylcholine receptor and N-type voltage-gated calcium channel autoantibodies in the blood stream would result in a medically acceptable diagnosis of AGID. [ 3 ]


Medications to relieve nausea and vomiting or to enhance mobility may be helpful, as may  cholinesterase inhibitors .   Immunotherapy  and  plasma exchange  have also been reportedly effective. [ 4 ]   Pyridostigmine  is a pharmaceutical treatment option for patients with AGID. [ 3 ]
In severe cases patients with AGID are required to abandon eating foods, requiring them to get nourishment through a process called  parenteral nutrition , where the patient is fed via a permanent  IV  and the liquid  nourishment  is infused directly in the blood stream, as opposed to a feeding tube. [ 5 ]


Azotorrhea  is the excessive discharge of  nitrogenous  substances in the  feces  or  urine . As in when people eat a diet high in  protein  they may suffer from increased amount of  amino acid  byproduct (nitrogen) being broken and excreted through defecation or urination. [ 1 ] [ 2 ]


Creatorrhea  is the abnormal  excretion  of  muscle fibre  in  feces . [ 1 ]  The term is made from the prefix  creat-  or  creato-  which comes from Greek  kreas  meaning " flesh ". The suffix  -rrhea  (or  -rrhoea ) comes from Greek  -rrhoia  meaning "flow," hence discharge. [ citation needed ]


Digestion of food is achieved through a mixture of  mechanical  and  chemical processes . Failure to produce or secrete chemicals known as  digestive enzymes  can lead to failure digesting or breaking down specific components of ingested food. [ citation needed ]


Where there is a failure to produce, release, or convert  trypsinogen —an inactive enzyme precursor or  zymogen —muscle fibres are not properly digested and are therefore released in the feces. Trypsinogen is produced in the pancreas and released into the  alimentary canal  where it is converted to the active enzyme  trypsin . [ 2 ]
Inflammation of the  pancreas , or  pancreatitis  can therefore precipitate this condition, [ 3 ]  as can  cystic fibrosis [ 4 ]  which also affects the production of digestive enzymes.


An  enterocutaneous fistula  ( ECF ) is an abnormal communication between the  small  or  large bowel  and the skin that allows the contents of the  stomach  or intestines to leak through an opening in the skin. [ 1 ]


The  mnemonic   HIS FRIENDS  can be used to memorize characteristics which impede the closure of  ECF. [ 2 ]


H: high output
I: IBD
S:short tract


Congenital types: tracheoesophageal, vitellointestinal duct, patent urachus, rectovaginal


Acquired: trauma (postoperative), radiation, malignancy, infection


Low-output fistula: < 500 mL/day


High-output fistula: > 500 mL/day


Low-output fistula: < 200 mL/day


Moderate-output fistula: 200–500 mL/day


High-output fistula: > 500 mL/day [ 3 ]


The majority will close spontaneously within approximately 6 weeks. If it has not closed by 12 weeks, it is unlikely to do so and definitive surgery should be planned. The median time to definitive repair from  fistula  onset was 6 months (range 1 day to 28 months). The 6-month time course is commonly utilized by groups with significant experience treating fistulas, owing to the trend in encountering a less hostile abdomen than in the early phases. [ 4 ]  Some evidence also suggests that  somatostatin  can be an effective treatment with respect to reducing closure time and improving the spontaneous closure rate of enterocutaneous fistulas. [ 5 ]


Functional abdominal pain syndrome  ( FAPS ),  chronic functional abdominal pain  ( CFAP ), or  centrally mediated abdominal pain syndrome  ( CMAP ) is a  pain syndrome  of the  abdomen , that has been present for at least six months, is not well connected to gastrointestinal function, and is accompanied by some loss of everyday activities. The discomfort is persistent, near-constant, or regularly reoccurring. The absence of symptom association with food intake or  defecation  distinguishes functional abdominal pain syndrome from other  functional gastrointestinal illnesses , such as  irritable bowel syndrome  (IBS) and  functional dyspepsia . [ 1 ]


Functional abdominal pain syndrome is a  functional gastrointestinal disorder  meaning that it is not associated with any organic or structural pathology. Theories on the mechanisms behind functional abdominal pain syndrome include changes in descending modulation,  central sensitization  of the spinal  dorsal horn , peripheral enhancement of the  visceral pain  afferent signal, and, central amplification.


The diagnosis of functional abdominal pain syndrome is made based on clinical features and diagnostic criteria. A thorough clinical history must be taken to accurately diagnose functional abdominal pain syndrome. Diagnostic testing to rule out organic disorders should only be done when alarm features are present. Differential diagnosis of functional abdominal pain syndrome includes a variety of other  functional gastrointestinal disorders .


There is no well-established treatment for functional abdominal pain syndrome. General measures such as a positive  physician-patient relationship  are beneficial.  Antidepressants  are often used to treat other  functional gastrointestinal disorders  and may be helpful in treating functional abdominal pain syndrome. Psychological interventions including various forms of  therapy  can also be helpful. While the exact presence of functional abdominal pain syndrome is unknown studies show that it affects between 0.5% and 2% of  North Americans . Functional abdominal pain syndrome is more common in women than men and usually occurs in the fourth decade of life.


Functional abdominal pain syndrome is characterized by frequent or chronic  stomach pain  and a reduction in everyday activity. [ 2 ]  The pain is persistent, near-constant, or regularly reoccurring. The pain is not related to food intake or  defecation . [ 1 ]  Functional abdominal pain is usually periumbilical and is not accompanied by  weight loss ,  vomiting ,  diarrhea , nocturnal symptoms, or slowed growth. [ 3 ]  Typically, the level of abdominal pain in functional abdominal pain syndrome seldom varies, with maximum pain being felt the majority of the time. functional abdominal pain syndrome is frequently coupled with a proclivity to experience and report additional  somatic symptoms  of discomfort, such as  chronic pain  believed to be connected to the gynecological or  urinary systems . [ 1 ]


Functional abdominal pain syndrome is a  functional gastrointestinal disorder . [ 4 ]   Functional gastrointestinal disorders  (FGD) are common medical conditions characterized by recurrent and persistent gastrointestinal symptoms caused by improper functioning of the enteric system in the absence of any identifiable organic or structural  pathology , such as  ulcers ,  inflammation ,  tumors  or masses. [ 5 ]


The pain from functional abdominal pain syndrome is thought to be caused by changes in descending modulation,  central sensitization  of the spinal dorsal horn, peripheral enhancement of the  visceral pain  afferent signal, and, lastly, central amplification. [ 2 ]


Peripheral sensitization, also known as elevated ascending visceral afferent signalling, can happen following  GI tract   inflammation  or damage. [ 6 ]  For example, about one-third of individuals with  IBS  report that their symptoms started after an acute infection episode; this is a phenomenon known as postinfectious IBS (PI-IBS). [ 7 ]  PI-IBS has consistently been linked to the existence of a low-grade inflammatory infiltrate. [ 8 ]  According to theory, this inflammatory infiltration results in increased sensitivity and field of peripheral receptors, the latter of which causes  hyperalgesia  by recruiting and activating  nociceptors  that were previously silent. [ 2 ]  Furthermore, it was discovered that the best indicators of who would develop PI-IBS were stress, as measured by traumatic life events, and a  neurotic personality  features. [ 8 ]  These convergent lines of data support the hypothesis that  inflammation  and/or injury in a psychologically predisposed person may cause visceral afferents to become peripherally sensitized, increasing the amount of nociceptive information that ascends to the spinal dorsal horn. [ 2 ]


Peripheral  nociceptors  become more sensitive, which increases the amount of impulses that reach the spinal dorsal horn.  Central sensitization  may result from an increase in the frequency and amplitude of peripheral signals that reach the spinal dorsal horn. An increase in presynaptic  glutamate  release causes  central sensitization  by removing the  magnesium  ion block of the  N-methyl-d-aspartate  (NMDA) receptor. The end result is an overall increase in dorsal horn neuron responsiveness, which frequently lasts longer than the initial shock when combined with the activation of other important enzymes. [ 2 ]


The anterior  cingulate cortex  is home to the majority of the central descending modulatory systems. These modulatory systems allow afferent signals from the periphery to be gated, which allows for the amplification or even restriction of the signal. They interface with the spinal dorsal horn. [ 2 ]  The pro-nociceptive condition that characterizes many chronic visceral pain syndromes is thought to be mostly caused by anomalies in the descending pain modulatory system. [ 9 ]


Since pain is the primary symptom of functional abdominal pain syndrome, obtaining a complete medical history and conducting a comprehensive physical examination continue to be essential components of the diagnosing process. [ 10 ]  The functional abdominal pain syndrome patient should be asked to provide a thorough history that thoroughly examines the timeline of pain occurrences, especially in connection with surgery, infection, or traumatic life events. [ 2 ]


In a patient with functional abdominal pain syndrome, the clinical examination should be normal by definition. Nonetheless, as a starting point, it is important to look closely for the existence of abdominal scars from prior operations or investigations. Similarly,  Carnett's sign , which involves palpating a sore spot both before and after the patient tenses their  abdominal wall , could be helpful. [ 2 ]


Diagnostic testing to rule out organic disease should not be done frequently in the absence of alarm signs, similar to other functional GI problems (ie, unexplained  weight loss , bloody bowel movements,  abdominal mass ,  anorexia ). If the physical examination yields negative results, no more diagnostic testing is necessary. [ 11 ]


The  Rome IV  diagnostic criteria for functional abdominal pain syndrome is as follows: [ 12 ]


To fit the  Rome IV  diagnostic criteria for functional abdominal pain syndrome the patient must fit all of the above criteria and the criteria must be met over the past three months, with the onset of symptoms occurring at least six months before diagnosis. [ 12 ]


When diagnosing functional abdominal pain syndrome, a number of other  functional GI illnesses  should be taken into account initially.  IBS  may be taken into consideration if the pain is accompanied by changes in bowel motions (frequent, loose stools or harder, infrequent stools). Functional gall bladder disease or  sphincter of Oddi dysfunction  should be considered if the pain is significant, occurs at different intervals (not daily), and is located in the right upper quadrant or  epigastrium . Consider  functional dyspepsia  if the discomfort is in the  epigastrium  and does not meet the criteria for functional gallbladder disease. [ 11 ]


There is no definite agreement on how to best manage functional abdominal pain syndrome in adults. As a result, the majority of currently employed therapies are founded on data and firsthand knowledge from other  functional bowel diseases  and  chronic pain syndromes . It is helpful to categorize therapy modalities into three groups: psychological interventions, pharmaceutical therapies, and general measures. [ 2 ]


The  doctor-patient interaction  is essential to the management of a patient with functional abdominal pain syndrome and to a successful outcome. A crucial component of treatment is, in particular, validating a patient's symptoms in a caring, interdisciplinary setting. In the framework of routine outpatient reviews, the patient and the doctor should also decide on and establish realistic treatment goals. [ 2 ]


Antidepressants , especially low-dose  tricyclic antidepressants  (TCAs), have been shown to be beneficial in the treatment of  functional gastrointestinal disorders  and  chronic pain . [ 13 ]  They may also be helpful in the treatment of functional abdominal pain syndrome due to their dual effects of direct pain management and antidepressant properties. [ 1 ]


Trials utilizing  tricyclic antidepressants  have generally outperformed those using  selective serotonin-reuptake inhibitors  in other  chronic pain disorders . [ 14 ]   Venlafaxine  and  duloxetine  are two examples of more recent medications with combined  serotonin and norepinephrine reuptake inhibitors  (SNRIs), which have been shown to reduce pain in some somatic pain disorders and may be helpful in functional abdominal pain syndrome. [ 15 ]  Patients with co-occurring  anxiety  and  depression  may benefit from both  SNRIs  and  selective serotonin-reuptake inhibitors  (SSRIs). The majority of  analgesics , such as  aspirin  and  nonsteroidal anti-inflammatory medications , don't really help much, maybe because they mostly have peripheral effects. [ 1 ]  Because of the risk of addiction and narcotic bowel syndrome, narcotic  analgesics  should be avoided. [ 16 ]


There hasn't been a study explicitly looking at adult functional abdominal pain syndrome and psychological  therapy . Studies on non-gastrointestinal pain diseases and other painful  functional gastrointestinal illnesses , however, point to the potential benefit of psychological therapies. [ 1 ]  Stress management,  hypnosis , [ 17 ]  dynamic or  interpersonal psychotherapy , [ 18 ] [ 19 ]  and  cognitive behavioral therapy  are among the interventions that may prove advantageous. [ 20 ] [ 21 ]  The most effective way to manage impairment resulting from refractory  chronic pain  may be to refer patients to pain treatment clinics for multidisciplinary treatment programs. [ 22 ]  While the previously discussed psychological treatments have demonstrated improvements in mood, coping,  quality of life , and health care costs, their effect on specific visceral or  somatic symptoms  is less clear, indicating that their most effective application may be in conjunction with symptomatic treatment. [ 20 ] [ 23 ]


Due to a lack of data and methodological challenges in distinguishing functional abdominal pain syndrome from other more prevalent  functional gastrointestinal diseases  like  IBS  and  functional dyspepsia , the epidemiology of the disease is not fully understood. Nonetheless, compared to  functional dyspepsia  or  IBS , functional abdominal pain syndrome is generally thought to be a less frequent. [ 1 ]  The stated prevalence rates in  North America  are between 0.5% and 2%, and they are consistent with reports from other nations. [ 24 ] [ 25 ] [ 26 ]  The condition affects women more frequently than men (3:2), with a peak in prevalence occurring in the fourth decade of life. [ 27 ] [ 28 ]


Gastrointestinal diseases  (abbrev.  GI diseases  or  GI illnesses ) refer to diseases involving the  gastrointestinal tract , namely the  esophagus ,  stomach ,  small intestine ,  large intestine  and  rectum ; and the  accessory organs of digestion , the  liver ,  gallbladder , and  pancreas .


The oral cavity is part of the gastrointestinal system and as such the presence of alterations in this district can be the first sign of both systemic and gastrointestinal diseases. [ 1 ]  By far the most common oral conditions are  plaque -induced diseases (e.g.,  gingivitis ,  periodontitis ,  dental caries ). Oral symptoms can be similar to lesions occurring elsewhere in the digestive tract, with a pattern of swelling, inflammation, ulcers, and fissures. If these signs are present, then patients are more likely to also have anal and esophageal lesions and experience other extra-intestinal disease manifestations. [ 2 ]   Some diseases which involve other parts of the GI tract can manifest in the mouth, alone or in combination, including:


Oesophageal diseases include a spectrum of disorders affecting the  oesophagus . The most common condition of the oesophagus in Western countries is  gastroesophageal reflux disease , [ 4 ]  which in chronic forms is thought to result in changes to the  epithelium  of the oesophagus, known as  Barrett's oesophagus . [ 5 ] : 863–865


Acute  disease might include  infections  such as  oesophagitis , trauma caused by the ingestion of corrosive substances, or rupture of  veins  such as  oesophageal varices ,  Boerhaave syndrome  or  Mallory-Weiss tears . Chronic diseases might include  congenital  diseases such as  Zenker's diverticulum  and  esophageal webbing , and  oesophageal motility disorders  including the  nutcracker oesophagus ,  achalasia ,  diffuse oesophageal spasm , and  oesophageal stricture . [ 5 ] : 853, 863–868


Oesophageal disease may result in a  sore throat ,  throwing up blood , difficulty  swallowing  or  vomiting . Chronic or congenital diseases might be investigated using  barium swallows ,  endoscopy  and  biopsy , whereas acute diseases such as reflux may be investigated and diagnosed based on  symptoms  and a  medical history  alone. [ 5 ] : 863–867


Gastric diseases refer to diseases affecting the  stomach . Inflammation of the stomach by infection from any cause is called  gastritis , and when including other parts of the gastrointestinal tract called  gastroenteritis . When gastritis persists in a chronic state, it is associated with several diseases, including  atrophic gastritis ,  pyloric stenosis , and  gastric cancer . Another common condition is  gastric ulceration ,  peptic ulcers . Ulceration erodes the  gastric mucosa , which protects the tissue of the stomach from the stomach acids. Peptic ulcers are most commonly caused by a bacterial  Helicobacter pylori   infection . [ 5 ]   Epstein–Barr virus  infection is another factor to induce gastric cancer. [ 6 ] [ 7 ]