Abdominal angina  is  abdominal pain  after eating caused by a reduction of blood flow to the  celiac trunk ,  superior mesenteric arteries  (SMA),  inferior mesenteric artery  (IMA), or the surrounding organs. [ 1 ]  Symptoms include  abdominal pain ,  weight loss ,  diarrhea ,  nausea ,  vomiting , and an aversion or fear of eating caused by the pain associated with eating.


Abdominal angina is caused by obstruction or  stenosis  of the  inferior mesenteric artery ,  celiac trunk , or  superior mesenteric artery . Gender, age, smoking,  hypertension ,  diabetes , and  hyperlipidemia  are risk factors for abdominal angina. The  digestive tract  relies on the celiac, superior mesenteric, and inferior mesenteric arteries for blood flow. Abdominal pain occurs when these arteries fail to provide adequate blood flow.


Abdominal angina is diagnosed using imaging to identify  stenosis . Differential diagnoses include  GERD ,  dietary sensitivities ,  constipation ,  pancreatitis , abdominal abscess,  appendicitis ,  irritable bowel syndrome ,  gastroenteritis ,  hepatitis , and gastrointestinal system inflammation.  Chronic mesenteric ischemia  requires surgical  revascularization  and treatment like  stents , transaortic  endarterectomy , or bypassing the arteries.


Abdominal angina often has a one-year delay between symptoms and treatment, leading to complications like  malnutrition  or bowel infarction. Abdominal angina is more prevalent in females with a 3:1 ratio, and the average age of onset is 60 years. Abdominal angina was first described by Dr. Baccelli in 1918 as lower abdominal pain after eating.


Symptoms of abdominal angina include postprandial  abdominal pain ,  weight loss ,  diarrhea ,  nausea ,  vomiting , and an aversion or fear of eating caused by the pain associated with eating. [ 2 ]


Abdominal angina usually starts 30 minutes after eating and persists for one to three hours. Individuals typically express the pain as a dull ache by clenching their fists over the  epigastrium  ( Levine sign ). [ 3 ]


Sometimes people may reduce their caloric intake in an attempt to decrease pain which can lead to weight loss. There may also be changes in bowel habits, most commonly diarrhea from  malabsorption  or rarely  constipation . [ 3 ]


Abdominal angina is caused by obstruction or  stenosis  of the  inferior mesenteric artery  (IMA),  celiac trunk , or  superior mesenteric artery  (SMA). [ 4 ]  More than 95% of abdominal angina is caused by stenosis of the splanchnic arteries due to local  atherosclerosis . [ 5 ] [ 6 ]  The occlusion mainly affects the ostia or the last few centimetres of the  mesenteric arteries . [ 7 ]


In rare cases, compression of the celiac trunk by the diaphragm's arcuate ligament can result in isolated occlusive disease (also known as " median arcuate ligament syndrome "). [ 5 ]  Other less common causes of vascular obstruction include  vasculitis , chronic mesenteric  venous thrombosis ,  fibromuscular dysplasia ,  radiation enteritis , and, in rare cases, extrinsic obstruction or vessel encasement by a tumour. [ 8 ]


Approximately 82% of those with abdominal angina have  diabetes .  Hyperlipidemia , which frequently causes  peripheral vascular disease , raises the risk of abdominal angina by 70% and correlates with the  atherosclerotic  aspect of the disease process. Smoking plays a part in the development of abdominal angina. Smokers account for 75% to 80% of all abdominal angina cases. Age also plays a role. The average age of onset is more than 60. This data corresponds with the vascular damage that occurs with age. Gender appears to play a role in the development of abdominal angina. Women are threefold more likely to develop abdominal angina than men.  Hypertension  is another known risk factor. Six out of ten of those with abdominal angina will be hypertensive. [ 9 ]


The  celiac ,  superior mesenteric , and  inferior mesenteric  arteries are the three primary blood vessels that support the  digestive tract .  Abdominal pain  happens because the digestive processes require increased blood flow to the stomach. The stenotic or occluded artery cannot give adequate blood flow. The pain is caused by  ischemia  of the affected tissues, which do not receive the essential perfusion to preform digestion. [ 7 ]


The gastrointestinal system has significant  collateral circulation , which may worsen in cases of vascular  stenosis . Along with the protection provided by collateral blood flow, the colon possesses various other mechanisms to prevent  ischemia , such as opening of all mesenteric capillaries, redistribution of intramural blood supply, and improved oxygen extraction. But if those are exceeded, these defensive mechanisms become overwhelmed and no longer provide protection. [ 8 ]


Some people with a single-vessel lesion experience symptoms, while others with up to three lesions are asymptomatic; hence, the number of arteries required to cause symptoms of ischemia is debatable. The occurrence of angina is determined by factors besides the number of arteries affected, such as the location of the lesion, the time of advancement of the lesions, and concurrent disorders that impact  angiogenesis . [ 8 ]


Abdominal angina is diagnosed by identifying  stenosis  with imaging. [ 10 ]  Since the symptoms of abdominal angina overlap with various other disorders, other causes of symptoms are ruled out as a part of the diagnostic process.  Gastric ulcers ,  abdominal aortic aneurysms , and  gastrointestinal cancers  can have similar symptoms and can be ruled out by  esophagogastroduodenoscopy ,  CT scans , or  MR angiogram . Other differential diagnoses include  GERD , dietary or  food sensitivities ,  constipation ,  pancreatitis , abdominal abscess,  appendicitis ,  irritable bowel syndrome ,  gastroenteritis ,  hepatitis , and inflammation of the gastrointestinal system. [ 11 ]   Duplex ultrasound ,  MR angiography ,  angiography , and  computed tomography angiography  can be used to help confirm the diagnosis of abdominal angina. [ 3 ]  Duplex ultrasound may be used to screen for abdominal angina but is not ideal for visualizing stenosis. Angiography, MR angiography, or CT angiography can be used to further visualize the celiac and mesenteric arteries. [ 12 ]


Abdominal angina is treated differently based on the severity and cause.  Antibiotics  are often used in the case of  colonic ischemia  as there is often cooccuring infections. When possible the underlying cause of abdominal angina may be treated. This includes medications to treat  heart failure ,  hypertension ,  dysrhythmia , or  hyperlipidemia . [ 13 ]


The most effective treatment for  chronic mesenteric ischemia  is surgical  revascularization  and percutaneous treatment such as  stents . [ 12 ]  Surgical treatment may include transaortic  endarterectomy  of the effected arteries or creating a retrograde or anterograde bypass in the arteries. [ 14 ]


Similarly to other  vascular disorders , abdominal angina can be slowly progressive. There is often a one-year delay between the onset of symptoms and treatment. Complications of abdominal angina such as  malnutrition  or  bowel infarction  can cause increased morbidity and mortality in this population. [ 4 ] [ 15 ]


The prevalence of abdominal angina is unknown. It is more prevalent in females than males with a ratio of 3:1. The mean age of those affected is 60 years old. [ 4 ]


The term "abdominal angina" was first used by Dr. Baccelli in 1918. He used the term to describe a group of patients who had developed lower abdominal pain after eating. In 1936 Dunphy made the connection between abdominal angina and gastrointestinal necrosis. 21 years later Mikkelson introduced a surgery which could help restore blood flow to the gastrointestinal system. Although there was early interest in research, there has been very little subsequent research in the years following. [ 16 ]


Abdominal epilepsy  is a  rare condition  consisting of  gastrointestinal  disturbances caused by  epileptiform seizure activity . [ 1 ] [ 2 ] [ 3 ] [ 4 ] [ 5 ]  It is most frequently found in children, though a few cases of it have been reported in adults. [ 6 ]  It has been described as a type of  temporal lobe epilepsy . [ 7 ]  Responsiveness to  anticonvulsants  can aid in the diagnosis. [ 8 ]  Distinguishing features of abdominal epilepsy include (1) Abnormal laboratory, radiographic, and endoscopic findings revealing  paroxysmal  GI manifestations of unknown origin (2) CNS symptoms (3) Abnormal  EEG . [ 9 ]  Most published medical literature dealing with abdominal epilepsy is in the form of individual  case reports . A 2005 review article found a total of 36 cases described in the medical literature. [ 3 ]


Abdominal epilepsy is marked by GI symptoms such as  abdominal pain  followed by uncontrollable  vomiting , usually preceded by  lethargy . Lethargy and confusion is the most common neurological symptoms associated with abdominal epilepsy. Other symptoms include generalized  tonic-clonic seizures  followed by sleep, and unresponsiveness. [ 10 ] [ 11 ]   Abdominal aura characterized by abdominal sensations precedes the abdominal seizure. This is associated with pain, nausea, hunger, gassiness especially in temporal lobe epilepsy. [ 12 ]


It is unknown as to what causes abdominal epilepsy. While a causal relationship between seizure activity and the GI symptoms has not been proven, the GI symptoms cannot be explained by other pathophysiological mechanisms, and are seen to improve upon  anticonvulsant  treatment. Because the condition is so rare, no high-quality studies exist. There have been too few reported cases to identify risk factors, genetic factors, or other potential causes. [ 10 ]


Criteria for diagnosis of abdominal epilepsy includes frequent periodic abdominal symptoms, an abnormal  electroencephalogram  (EEG) and significant improvement of gastrointestinal symptoms after taking anti-seizure medication. Medical testing for diagnosis can be completed using  MRI scans  of the brain,  CT scans  and  ultrasounds  of the abdomen,  endoscopy  of the gastrointestinal tract, and  blood tests . [ 10 ]


Typically, the diagnostic process begins with gathering information regarding the presence of common symptoms like paroxysmal abdominal pain and other gastrointestinal issues. Symptoms that persist continuously or for prolonged periods are less likely to indicate abdominal epilepsy. It's important to consider convulsions, alterations in consciousness, and other neurological symptoms alongside gastrointestinal symptoms when diagnosing abdominal epilepsy. Though every episode of it may not be accompanied by a neurological symptom. This often makes these neurological symptoms unnoticeable for the patient. [ 11 ]


This is followed by the necessary evaluation that comprises neurological and physical examination, laboratory test, abdominal imaging using CT and ultrasound, endoscopy. Next if the above are normal but the history still suggests for this syndrome an EEG must be performed. EEG findings alone too cannot distinguish between the kinds of epilepsy. Moreover, often an EEG report could be normal if an event is not accompanied by neurological symptoms. If it is doubtable a neurologist should be consulted. [ 11 ]


Like other forms of epilepsy, abdominal epilepsy is treated with anticonvulsant drugs, such as  phenytoin . Based on the clinical response additional medication may be used for complementing it or it could be used instead of phenytoin. Since no controlled studies exist, however, other drugs may be equally effective. [ 10 ]  Anticonvulsants target non-epileptic causes of abdominal pain via  sedative  mechanisms. It may also act just as a  placebo . The prognosis is generally good and most patients are benefitted from medicines alone. [ 13 ]


The pathophysiology behind abdominal epilepsy remains speculative. Several studies indicate that  insula  and  sylvian  fissures also known as  lateral sulcus  could be related to inducing abdominal epilepsy. Their location is found to coincide with the locations of the abdomen on the  Sensory homunculus . [ 14 ]  Any pathophysiological changes in the M2 portion of  cerebral artery  which flows through  lateral sulcus  are associated with the epilepsies of the  temporal  and  parietal  regions. [ 15 ]  The abdominal symptoms are believed to be associated with the transmission of impulses from the temporal lobe to the  dorsal motor nucleus  of the  vagus  nerve via the dense direct projections. The  hypothalamus  is also believed to induce  sympathetic  pathways from the  amygdala  in the medial temporal lobe to the  GI  tract to trigger such symptoms. [ 16 ]


Cerebral tumors have been assessed to be a plausible cause of abdominal epilepsy. [ 17 ]  Right  parietal  and  occipital   encephalomalacia , biparietal  atrophy , and bilateral perisylvian  polymicrogyria  has been possibly associated with  ictal  abdominal pain associated with abdominal epilepsy. [ 18 ]


French physician and scientist  Armand Trousseau  is commonly credited as being the first to describe the condition in 1868 in a boy with  paroxysmal  GI symptoms culminating in  grand mal  epileptic seizure. [ 19 ]  The first account of abdominal epilepsy supported by EEG tracings came in 1944 in an article by M.T. Moore, followed by subsequent case reports from the same group. [ 20 ] [ 21 ]


Abdominal migraine   (AM)  is a  functional disorder  that usually manifests in childhood and adolescence, without a clear pathologic mechanism or  biochemical  irregularity. Children frequently experience sporadic episodes of excruciating central  abdominal pain  accompanied by  migrainous  symptoms like  nausea ,  vomiting , severe  headaches , and general  pallor . [ 1 ]  Abdominal migraine can be diagnosed based on clinical criteria and the exclusion of other disorders. [ 2 ]


The  US Food and Drug Administration  has not approved any drugs for the treatment of abdominal migraine. The goal of treatment is usually to prevent attacks, and this is often achieved through nonpharmacologic intervention. [ 3 ]


Research has indicated that the incidence of abdominal migraine in children falls within the range of 0.4% [ 4 ]  to 4%. [ 2 ]  The condition primarily affects children aged 3 to 10 years, with a higher prevalence in females. [ 5 ]


Midline  abdominal pain  with  paroxysmal , recurrent, acute onset attacks that last an average of 17 hours are the hallmarks of abdominal migraine. [ 6 ]  There have been reports that these attacks can last anywhere from two to seventy-two hours. [ 5 ]  Although it has also been reported to be diffuse and colicky, the pain is usually described as dull and periumbilical. 91% of patients have  anorexia , 73% to 91% have  nausea , 35% to 50%  vomit , and 93% to 100% of patients have associated  pallor . [ 7 ]  The attack usually comes to an abrupt end. [ 5 ]  The average annual frequency of abdominal migraine attacks in patients is 14. [ 6 ]


Although nonspecific prodromes can occur before attacks, abdominal migraine attacks are usually sporadic. This can include behavioral and  mood swings ,  anorexia ,  flushing ,  diarrhea , and  auras  that include  numbness ,  slurred speech ,  tingling  in the distal extremities, and flashing lights. [ 5 ]  Weeks to months may pass between episodes, and during this time patients usually experience no symptoms. [ 8 ]


Abdominal migraine has been linked to specific alterations in the  gut-brain axis , vascular dysregulation, modifications in the  central nervous system , and genetic factors. [ 9 ]


Abdominal migraine pathophysiology may involve psychological factors.  Abuse  and stressful events are two risk factors for recurrent abdominal pain, for instance. Furthermore, it has been demonstrated that kids with  functional gastrointestinal disorders  experience  mental health conditions  like  anxiety  and  depression  more frequently than kids without these conditions. [ 10 ]


There are several typical causes of attacks of abdominal migraines.  Stressors  related to work and family life, irregular sleep patterns, extended fasts and food deprivation,  dehydration , exercise, travel, high- amine  foods, foods containing flavoring, coloring, and  monosodium glutamate  (MSG), and flashing lights are a few common triggers. [ 5 ] [ 8 ]


A significant hereditary component may be involved in abdominal and other migraines due to their strong familial incidence, [ 11 ]  especially in the case of mutations affecting  cell membrane transport  ( channelopathies ). [ 12 ] [ 13 ]


While the  pathophysiology  of  functional gastrointestinal disorders  (FGIDs) has many potential contributors, the etiology of abdominal migraine is still unknown. [ 14 ]


It is thought that abnormal electrical discharge from the  hypothalamus  that travels to the cortex and  autonomic nervous system [ 15 ]  or variations in the  cerebral artery's  blood flow velocity cause attacks. [ 16 ]  In patients with FGIDs, there appears to be a disruption in the complex  brain-gut axis . [ 17 ]  Many episodic  functional gastrointestinal disorders  in childhood have been linked to  mitochondrial disease , [ 18 ]   hypothalamic-pituitary-axis  dysfunction, and  gene mutations ; these associations have not, however, been studied in patients diagnosed with abdominal migraine. [ 19 ]


It's critical to rule out organic diseases as the source of a child's symptoms while also taking the patient's functional state into account. When diagnosing abdominal migraine, a patient's complete medical history and physical examination are crucial. Additionally, any potential alarm signs and symptoms should be carefully examined. The presence of visible or occult  blood in the stool ,  dysphagia ,  hematemesis ,  bilious  vomiting,  fever , changes in growth pattern, and  weight loss   are a few examples of alarm symptoms. [ 20 ]  Further imaging and testing should be carried out if these alarm signs or symptoms are apparent. [ 21 ]


The  Rome IV criteria  state that paroxysmal bouts of intense, acute periumbilical, midline, or diffuse  abdominal pain  lasting at least an hour, exhibiting a recurrent pattern, being incapacitating, and interfering with regular activities can be used to diagnose abdominal migraine if at least two of these episodes take place over a six-month period. There should be weeks or months without any symptoms in between attacks. The following symptoms must be present in at least two instances:  pallor ,  photophobia ,  headache ,  nausea ,  vomiting , and  anorexia . Lastly, there is no other medical diagnosis that can account for the symptoms. [ 22 ]


Abdominal migraine is defined by the  International Classification of Headache Disorders  III criteria as five or more episodes of abdominal pain lasting two to seventy-two hours. A minimum of two out of three of the following criteria must also be met by the pain: dull or "just sore" quality; midline location, periumbilical, or poorly localized; and moderate to severe intensity.  Pallor ,  nausea ,  vomiting , and  anorexia  are associated symptoms that the patient should have at least two of. [ 7 ]


Abdominal migraine must be distinguished from other causes of chronic or recurrent abdominal pain. These include  irritable bowel syndrome ,  peptic ulcer disease , and  gastroesophageal reflux disease . [ 3 ]  It must also be distinguished from causes of acute abdominal pain, such as  appendicitis , as wrong diagnosis may lead to unnecessary  appendectomy . [ 23 ]


Because there are so few studies in the literature, there are no firm recommendations for the treatment of abdominal migraines. [ 24 ]  The majority of treatment options are predicated on anecdotal evidence, a small number of studies conducted on a relatively small number of children, and a close correlation between abdominal migraines and both  migraine headaches  and FGIDs. [ 25 ]


When treating patients with abdominal migraines, doctors may find the STRESS mnemonic useful. It stands for stress management, travel advice, rest, emergency symptoms, sparkling lights, and snacks to avoid. [ 26 ]


Certain triggers, like bright light, restless nights, travel, and extended fasting, should probably be minimized or avoided once they have been identified. [ 19 ]  Emotional stressors from family or school activities can be a trigger for certain kids, so it's best to minimize or stay away from them. [ 3 ]  Although there are no particular randomized trials evaluating the efficacy of biofeedback and counselling in treating abdominal migraines, it is believed that these interventions may be helpful if emotional stress is a trigger factor in the development of migraine in children. [ 27 ]


It's unclear what function  elimination diets  serve. Nonetheless, in patients experiencing both migraine and  IBS  symptoms, an  immunoglobulin G  (IgG)-based elimination diet shows promise in lowering migraine episodes. [ 28 ]  There isn't much more proof that a child's diet has a significant impact on when migraines begin. [ 29 ]


In one study, 14 children with abdominal migraine were administered  pizotifen  syrup, a  serotonin  and  histamine  antagonist. After four months, 70% of the patients said their symptoms had improved. Their symptoms were noticeably milder and less frequent. [ 30 ]   Propranolol  and  cyproheptadine  syrup were found to alleviate symptoms in a retrospective review. [ 25 ]   Flunarizine  use was found to reduce the frequency and duration of abdominal migraine attacks in another retrospective review. [ 31 ]


Analgesics ,  triptans , and  antiemetics  may be helpful for sudden attacks of abdominal migraines. It has been suggested that patients with  nausea ,  vomiting , or  anorexia  might benefit more from nasal sprays or suppositories. [ 5 ]  Acute attacks have been reported to be resolved by  acetaminophen  and  ibuprofen . [ 32 ]  Intranasal  sumatriptan  alleviated the symptoms of abdominal migraine in two children, according to a case report. [ 33 ]  In refractory cases, intravenous  sodium valproate  has been reported to resolve abdominal migraine episodes. [ 34 ]  According to a case series, intravenous  dihydroergotamine  treatment prevented abdominal migraine attacks in five out of six pediatric patients. [ 35 ]


Abdominal migraine can have a significant impact on day-to-day life. [ 36 ]  Children may  miss school  or other activities. [ 36 ]  It resolves in many patients. [ 23 ] [ 37 ]


Abdominal migraine primarily affects  children , for whom it is a common cause of chronic  abdominal pain . It may be as high as 9% or as low as 1% among children. [ 23 ]  It is rare in  adults . [ 3 ]  However, children diagnosed with abdominal migraines may have migraine headaches as adults. [ 38 ]  The mean age of diagnosis is 7 years. [ 39 ] [ 40 ]  It appears to be slightly more common in  women . [ 23 ]


This condition was first described in 1921 by Buchanan. [ 41 ]  It was once considered a controversial diagnosis. [ 42 ]  However, it is now accepted as a common cause of chronic abdominal pain in children. [ 43 ]


Aerophagia  (or  aerophagy ) is a condition of excessive air swallowing, which goes to the  stomach  instead of the  lungs . Aerophagia may also refer to an unusual condition where the primary symptom is excessive  flatus (farting) ,  belching (burping)  is not present, and the actual mechanism by which air enters the gut is obscure or unknown. [ 1 ]  Aerophagia in psychiatry is sometimes attributed to nervousness or  anxiety . [ 2 ]


Aerophagia is associated with excessively  chewing gum ,  smoking , drinking  carbonated drinks , eating too quickly, as well as anxiety, high  continuous positive airway pressure  and wearing loose  dentures . Aerophagia is also carried out deliberately as a voluntary action to increase the length and volume of a  belch , as any air successfully swallowed serves to increase the  partial pressure  in the stomach and expand a burp. [ 13 ] [ 14 ]  In people with cervical spinal blockages, inhaling can cause some air to enter the esophagus and stomach involuntarily. [ 15 ]


Aerophagia is diagnosed in 8.8% of cognitively delayed patients [ 16 ]  where the coordination between swallowing and respiration is impaired and not well-defined. [ 17 ]


Aerophagia is a dangerous potential side effect of  non-invasive ventilation  (NIV), commonly used in treatments of respiratory problems and cardiovascular critical care or in surgery when a general  anaesthetic  is required. In the case of aerophagia during NIV, it is normally diagnosed by experienced medical specialists who check on patients intermittently during NIV use for any emergent problems. The diagnosis is based on the sound heard by listening through a  stethoscope  placed outside the abdominal cavity. Using this approach, the problem is sometimes detected later than when it develops, possibly also later than necessary. Belated detection or response to aerophagia may lead to gastric distension, which in turn could elevate the  diaphragm  or cause aspiration of the stomach contents into the lungs [ 18 ]  or pneumatic rupture of the  esophagus  due to extreme gastric insufflation. [ 19 ]


Afferent loop syndrome  is an uncommon side effect of gastric surgery. [ 1 ]  The afferent loop is made up of a segment of  duodenum  and/or proximal  jejunum  located upstream of a double-barrel  gastrojejunostomy   anastomosis .  Abdominal pain  and distension are signs of increased intraluminal pressure resulting from the accumulation of enteric secretions in the obstructed afferent loop. [ 2 ]


Afferent loop syndrome may result from  volvulus , recurring  cancer , stomal  stenosis , adhesions, kinking at the anastomotic site, internal  herniation , and gastrointestinal stones. [ 1 ]


Laboratory investigations can help diagnose afferent loop syndrome, but imaging scans are required for a confirmation diagnosis. [ 2 ]  When diagnosing afferent loop syndrome,  abdominal CT  is regarded as the preferred radiographic investigation. [ 3 ]


The treatment of afferent loop syndrome is determined by the underlying cause. [ 1 ]  Surgical therapy, such as adhesiolysis,  bypass , or limb reconstruction, can usually eliminate the source in patients with benign etiologies. [ 4 ]  Treatment for patients with afferent loop syndrome due to recurrent tumors shifts to palliation. [ 1 ]


Nonbilious  vomiting ,  nausea , and abrupt onset  stomach pain  in the right upper quadrant are common symptoms in patients with acute afferent loop syndrome.  Abdominal distension  and postprandial epigastric discomfort lasting anywhere from a few minutes to an hour are common symptoms experienced by patients with chronic afferent loop syndrome. Bilious projectile  vomiting  is a typical symptom of chronic afferent loop syndrome that relieves symptoms quickly. In patients with persistent afferent loop syndrome,  steatorrhea  and  diarrhea  may exacerbate intestinal stasis.  Iron deficiency anemia  and/or  vitamin B12 deficiency  can arise from the deconjugation of bile salts by bacteria. In order to avoid postprandial pain, patients frequently quit eating, which can result in significant weight loss. [ 2 ]


Right upper quadrant abdominal and/or epigastric tenderness is the most common physical finding in afferent loop syndrome patients. There is a palpable abdominal bulge in the right upper quadrant in about one-third of people suffering from acute afferent loop syndrome. Patients may exhibit symptoms of  pancreatitis , such as  obstructive jaundice  or abdominal discomfort radiating to the side or back. Patients may show up with guarding, which is symptomatic of  peritonitis , and a stiff abdomen if intestinal perforation has occurred. [ 2 ]


Afferent loop syndrome can have either a benign or  malignant  etiology, depending on the type of obstructive lesion. Depending on where the lesion is located, there are three primary pathways that lead to benign etiology. [ 5 ]


Anastomotic stricture, foreign body impaction,  bezoars , and  enteroliths  are all potential causes of intraluminal blockage. [ 6 ]


Radiation enteritis  and scarring from marginal gastrojejunostomy ulceration are the causes of mechanical blockage of the intramural area. [ 7 ] [ 8 ]


Conditions that cause external compression include internal  hernia ,  volvulus , entrapment, compression, kinking of the afferent loop, postoperative adhesion, and intussusception of the afferent loop. [ 9 ] [ 10 ] [ 11 ]


An antecolic afferent loop's redundancy increases the danger of kinking,  volvulus , and adhesion-induced limb entrapment when the bowel length exceeds 30 to 40 cm. Conversely, the risk of an internal  herniation  developing in a retrocolic afferent loop is increased by incorrectly closed mesocolic abnormalities. [ 12 ]


Locoregional tumor recurrence impeding the afferent loop at the anastomotic site or gastric residual is frequently linked to malignant afferent loop syndrome. [ 13 ]  Additional factors contributing to blockage include peritoneal  carcinomatosis  and regional  lymphadenopathy . [ 5 ]


The preferred radiographic study for diagnosing afferent loop syndrome is thought to be  abdominal CT . [ 3 ]  An blocked intestinal segment can be directly visualized with  CT scanning . It is also possible to look at other organs that could be affected by the obstruction, like the  biliary tree  and  pancreas . [ 2 ]  When afferent loop syndrome first manifests, the abdominal midline is often crossed by a fluid-filled tubular formation that lies between the super mesenteric artery and the  aorta . [ 14 ]


Three parameters determine the treatment plan: the type of obstructive lesion, the blockage site (inframesocolic or supramesocolic), and the patency of the major  anastomoses  for the  hepaticojejunostomy  and  pancreaticojejunostomy . The standard of care for afferent loop syndrome patients is typically surgery. Adhesiolysis,  bypass surgery , and excision with repair of the obstructive malignant lesions are the surgical therapy options available. [ 15 ]


The prognosis is good for patients who receive an early diagnosis and have surgery, with the exception of cases of advanced or recurring  cancer . A delay in diagnosis is associated with a mortality rate that varies from 30% to 60%. [ 16 ]  Patients who experience afferent limb perforation and subsequent  peritonitis  and shock have poor prognoses. [ 17 ]


According to reports, 0.2% of patients after distal  gastrectomy  with  Roux-en-Y reconstruction , 1% after laparoscopic distal  gastrectomy  with Billroth II reconstruction, and 0.3–1.0% of patients following total  gastrectomy  with Billroth II or  Roux-en-Y reconstruction  have afferent loop syndrome. [ 15 ]


In 1950, Roux, Pedoussaut, and Marchal initially reported afferent loop syndrome in patients who had undergone gastric surgery and were experiencing bilious  vomiting . [ 15 ]


An  ameboma , also known as an  amebic granuloma , is a rare complication of  Entamoeba histolytica  infection, where in response to the infecting  amoeba  there is formation of annular colonic granulation, which results in a large local lesion of the bowel. [ 1 ]


The  ameboma  may manifest as a right lower quadrant abdominal mass, which may be mistaken for carcinoma,  tuberculosis ,  Crohn's disease ,  actinomycosis , or  lymphoma .


Biopsy is necessary for definitive diagnosis.


This  infectious disease  article is a  stub . You can help Wikipedia by  expanding it .


Anorectal abscess  (also known as an  anal/rectal abscess  or  perianal/perirectal abscess ) is an  abscess  adjacent to the  anus . [ 1 ]   Most cases of perianal abscesses are sporadic, though there are certain situations which elevate the risk for developing the disease, such as  diabetes mellitus ,  Crohn's disease , chronic  corticosteroid  treatment and others. It arises as a complication of  paraproctitis . Ischiorectal, inter- and intrasphincteric abscesses have been described. [ citation needed ]


It typically presents with pain and swelling in the perianal area. [ 2 ]  The pain may be dull, aching, or throbbing. It is worst when the person sits down and right before a bowel movement. After the individual has a bowel movement, the pain usually lessens. Other signs and symptoms of anorectal abscess include  constipation , drainage from the rectum,  fever  and chills, or a palpable mass near the anus. [ 3 ]


The condition can become extremely painful, and usually worsens over the course of just a few days. The pain may be limited and sporadic at first, but may worsen to a constant pain which can become very severe when body position is changed (e.g., when standing up, rolling over, and so forth). Depending upon the exact location of the abscess, there can also be excruciating pain during bowel movements, though this is not always the case. This condition may occur in isolation, but is frequently indicative of another underlying disorder, such as  Crohn's disease . [ 4 ] [ 5 ]


If left untreated, an  anal fistula  will almost certainly form, connecting the rectum to the skin. [ 3 ]  This requires more intensive surgery. Furthermore, any untreated abscess may (and most likely will) continue to expand, eventually becoming a serious systemic infection.


Abscesses are caused by a high-density infection of (usually) common bacteria which collect in one place or another for any variety of reasons.  Anal abscesses, without treatment, are likely to spread and affect other parts of the body, particularly the groin and rectal lumen. [ 3 ]   All abscesses can progress to serious generalized infections requiring lengthy hospitalizations if not treated.


Historically, many rectal abscesses are caused by bacteria common in the digestive system, such as  E. coli . While this still continues often to be the case, there has recently been an increase in the causative organism being  staphylococcus , as well as the difficult to treat community-acquired  methicillin-resistant S. aureus . Because of the increasing appearance of more exotic bacteria in anal abscesses, microbiological examination will always be performed on the surgical exudate to determine the proper course of any antibiotic treatment.


Diagnosis of anorectal abscess begins with a medical history and physical exam. Imaging studies which can help determine the diagnosis in cases of a deep non-palpable perirectal abscess include pelvic CT scan,  MRI  or trans-rectal ultrasound. These studies are not necessary, though, in cases which the diagnosis can be made upon physical exam. [ 3 ]


Anorectal abscesses are classified according to their anatomic location and the following are the most common types: perianal abscess, ischiorectal abscess, intersphincteric abscess and supralevator abscess. [ 6 ] [ 7 ]


This condition is often initially misdiagnosed as  hemorrhoids , since this is almost always the cause of any sudden anal discomfort. The presence of the abscess, however, is suspected when the pain quickly worsens over one or two days and usual hemorrhoid treatments are ineffective in bringing relief.  Furthermore, any serious abscess will eventually begin to cause signs and symptoms of general infection, including  fever  and nighttime chills.


A physician can rule out a hemorrhoid with a simple visual inspection, and usually appreciate an abscess by touch.


Anal abscesses are rarely treated with a simple course of antibiotics. In almost all cases surgery will need to take place to remove the abscess. Treatment is possible in an  emergency department  under  local anesthesia , but it is highly preferred to be formally admitted to a hospital and to have the surgery performed in an  operating room  under  general anesthesia .


Generally speaking, a fairly small but deep incision is performed close to the root of the abscess.  The surgeon will allow the abscess to drain its  exudate  and attempt to discover any other related lesions in the area. This is one of the most basic types of surgery, and is usually performed in less than thirty minutes by the anal surgical team. Generally, a portion of the exudate is sent for microbiological analysis to determine the type of infecting bacteria.  The incision is not closed (stitched), as the damaged tissues must heal from the inside toward the skin over a period of time.


The affected individual is often sent home within twenty-four hours of the surgery, and may be instructed to perform several ' sitz baths ' per day. These involve a small basin which is filled with warm water, and possibly with salts; usually fits over a toilet;  and soaks the affected area for a period of time. Another method of recovery involves the use of surgical packing. The initial packing is inserted by the surgical team, with redressing generally performed by hospital staff or a district nurse. During the week following the surgery, many patients will have some form of antibiotic therapy, along with some form of pain management therapy, consistent with the nature of the abscess.


It is unclear whether internal packing of the perianal abscess influences time taken for healing, wound pain, development of fistulae, or abscess recurrence. [ 8 ]


The patient usually experiences an almost complete relief of the severe pain associated to his/her abscess upon waking from anesthesia; the pain associated with the opening and draining incision during the post-operative period is often mild in comparison.


Additional images of anorectal abscess


Anismus  or  dyssynergic defecation  is the failure of normal relaxation of  pelvic floor  muscles during attempted  defecation . It can occur in both children and adults, and in both men and women (although it is more common in women). It can be caused by physical defects or it can occur for other reasons or unknown reasons. Anismus that has a behavioral cause could be viewed as having similarities with  parcopresis , or psychogenic fecal retention. [ citation needed ]


Symptoms include  tenesmus  (the sensation of incomplete emptying of the rectum after defecation has occurred) and  constipation . Retention of stool may result in fecal loading (retention of a mass of stool of any consistency) or  fecal impaction  (retention of a mass of hard stool). This mass may stretch the walls of the rectum and colon, causing  megarectum  and/or  megacolon , respectively. Liquid stool may leak around a fecal impaction, possibly causing degrees of liquid fecal incontinence. This is usually termed  encopresis  or soiling in children, and  fecal leakage , soiling or liquid  fecal incontinence  in adults.


Anismus is usually treated with dietary adjustments, such as  dietary fiber  supplementation. It can also be treated with a type of  biofeedback  therapy, during which a sensor probe is inserted into the person's  anal canal  in order to record the pressures exerted by the pelvic floor muscles. These pressures are visually fed back to the patient via a monitor who can regain the normal coordinated movement of the muscles after a few sessions.


Some researchers have suggested that anismus is an over-diagnosed condition, since the standard investigations or  digital rectal examination  and  anorectal manometry  were shown to cause paradoxical sphincter contraction in healthy controls, who did not have constipation or incontinence. [ 1 ]  Due to the invasive and perhaps uncomfortable nature of these investigations, the pelvic floor musculature is thought to behave differently compared to normal circumstances. These researchers went on to conclude that paradoxical pelvic floor contraction is a common finding in healthy people as well as in people with chronic constipation and fecal incontinence, and it represents a non-specific finding or laboratory artifact related to untoward conditions during examination, and that true anismus is actually rare.


Symptoms include:


To understand the cause of anismus, an understanding of normal colorectal anatomy and physiology, including the normal defecation mechanism, is helpful. The relevant anatomy includes: the  rectum , the  anal canal  and the muscles of the  pelvic floor , especially  puborectalis  and the  external anal sphincter . [ citation needed ]


The  rectum  is a section of bowel situated just above the anal canal and distal to the  sigmoid colon  of the  large intestine . It is believed to act as a reservoir to store stool until it fills past a certain volume, at which time the defecation reflexes are stimulated. [ 4 ]  In healthy individuals, defecation can be temporarily delayed until it is socially acceptable to  defecate . In continent individuals, the rectum can expand to a degree to accommodate this function. [ citation needed ]


The anal canal is the short straight section of bowel between the rectum and the  anus . It can be defined functionally as the distance between the anorectal ring and the end of the  internal anal sphincter . The internal anal sphincter forms the walls of the anal canal. The internal anal sphincter is not under voluntary control, and in normal persons it is contracted at all times except when there is a need to defecate. This means that the internal anal sphincter contributes more to the resting tone of the anal canal than the external anal sphincter. The internal sphincter is responsible for creating a watertight seal, and therefore provides continence of liquid stool elements. [ citation needed ]


The  puborectalis  muscle is one of the pelvic floor muscles. It is  skeletal muscle  and is therefore under voluntary control. The puborectalis originates on the posterior aspect of the  pubic bone , and runs backwards, looping around the bowel.


The point at which the rectum joins the anal canal is known as the anorectal ring, which is at the level that the puborectalis muscle loops around the bowel from in front. This arrangement means that when puborectalis is contracted, it pulls the junction of the rectum and the anal canal forwards, creating an angle in the bowel called the anorectal angle. This angle prevents the movement of stool stored in the rectum moving into the anal canal. It is thought to be responsible for gross continence of solid stool. Some believe the anorectal angle is one of the most important contributors to continence. [ 5 ]


Conversely, relaxation of the puborectalis reduces the pull on the junction of the rectum and the anal canal, causing the anorectal angle to straighten out. A  squatting posture  is also known to straighten the anorectal angle, meaning that less effort is required to defecate when in this position. [ 6 ]


Distension of the rectum normally causes the internal anal sphincter to relax (rectoanal inhibitory response, RAIR) and the external anal sphincter initially to contract (rectoanal excitatory reflex, RAER). The relaxation of the internal anal sphincter is an involuntary response. The external anal sphincter, by contrast, is made up of skeletal (or striated muscle) and is therefore under voluntary control. It can contract vigorously for a short time. Contraction of the external sphincter can defer defecation for a time by pushing stool from the anal canal back into the rectum. Once the voluntary signal to defecate is sent back from the brain, the abdominal muscles contract (straining) causing the intra-abdominal pressure to increase. The pelvic floor is lowered causing the anorectal angle to straighten out from ~90 o  to <15 o  and the external anal sphincter relaxes. The rectum now contracts and shortens in  peristaltic waves , thus forcing fecal material out of the rectum, through the anal canal and out of the anus. The internal and external anal sphincters along with the puborectalis muscle allow the feces to be passed by pulling the anus up over the exiting feces in shortening and contracting actions. [ citation needed ]


In patients with anismus, the puborectalis and the external anal sphincter muscles fail to relax, with resultant failure of the anorectal angle to straighten out and facilitate evacuation of feces from the rectum. These muscles may even contract when they should relax (paradoxical contraction), and this not only fails to straighten out the anorectal angle, but causes it to become more acute and offer greater obstruction to evacuation.


As these muscles are under voluntary control, the failure of muscular relaxation or paradoxical contraction that is characteristic of anismus can be thought of as either maladaptive behavior or a loss of voluntary control of these muscles. Others claim that puborectalis can become  hypertrophied  (enlarged) or  fibrosis  (replacement of muscle tissue with a more fibrous tissue), which reduces voluntary control over the muscle.


Anismus could be thought of as the patient "forgetting" how to push correctly, i.e. straining against a contracted pelvic floor, instead of increasing abdominal cavity pressures and lowering pelvic cavity pressures. It may be that this scenario develops due to stress. For example, one study reported that anismus was strongly associated with sexual abuse in women. [ 7 ]  One paper stated that events such as pregnancy, childbirth, gynaecological descent or neurogenic disturbances of the brain-bowel axis could lead to a "functional  obstructed defecation syndrome " (including anismus). [ 8 ]  Anismus may develop in persons with  extrapyramidal motor disturbance  due to  Parkinson's disease . [ 9 ]   This represents a type of  focal dystonia . [ 10 ]  Anismus may also occur with  anorectal malformation ,  rectocele , [ 11 ]   rectal prolapse [ 12 ]  and  rectal ulcer . [ 12 ]


In many cases however, the underlying pathophysiology in patients presenting with obstructed defecation cannot be determined. [ 13 ]


Some authors have commented that the "puborectalis paradox" and "spastic pelvic floor" concepts have no objective data to support their validity. They state that "new evidence showing that defecation is an integrated process of colonic and rectal emptying suggests that anismus may be much more complex than a simple disorder of the pelvic floor muscles." [ 13 ]


Persistent failure to fully evacuate stool may lead to retention of a mass of stool in the rectum (fecal loading), which can become hardened, forming a  fecal impaction  or even  fecaliths . [ citation needed ]


Liquid stool elements may leak around the retained fecal mass, which may lead to paradoxical diarrhoea and/or fecal leakage (usually known as  encopresis  in children and  fecal leakage  in adults). [ 14 ] [ 15 ] [ 16 ] [ 17 ]


When anismus occurs in the context of intractable  encopresis  (as it often does), resolution of anismus may be insufficient to resolve encopresis. [ 18 ]  For this reason, and because biofeedback training is invasive, expensive, and labor-intensive, biofeedback training is not recommended for treatment of encopresis with anismus.


The walls of the rectum may become stretched, known as  megarectum . [ 19 ]


In the  Rome IV classification , diagnostic criteria for "functional defecation disorders" are as follows: [ 20 ]


2 subcategories exist within the functional defecation disorders category:


For all of these Rome-IV diagnoses, diagnostic criteria must have been fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis. [ 20 ]  The subcategories F3a and F3b are defined by age- and gender-appropriate normal values for the technique. [ 20 ]


Previous Rome criteria recommended that anorectal testing is not usually indicated in patients with symptoms until patients have failed conservative treatment (e.g., increased dietary fiber and liquids; elimination of medications with constipating side effects
whenever possible). [ citation needed ]


Several definitions have been offered:


Physical examination can rule out anismus (by identifying another cause) but is not sufficient to diagnose anismus.


The measurement of  pressures  within the rectum and anus with a  manometer  (pressure-sensing probe).


defecating proctogram , and  MRI defecography


Anismus can be subcategorized into 4 types based on the results of anorectal manometry testing: [ 22 ]


Anismus is classified as a functional defecation disorder. It is also a type of rectal outlet obstruction (a functional outlet obstruction). Where anismus causes constipation, it is an example of  functional constipation . Many authors describe an " obstructed defecation syndrome ", of which anismus is a cause. [ 24 ]


The  Rome II classification  functional defecation disorders were divided into 3 types, [ 25 ]  however the symptoms the patient experiences are identical. [ 26 ]


It can be seen from the above classification that many of the terms that have been used interchangeably with anismus are inappropriately specific and neglect the concept of impaired propulsion. Similarly, some of the definitions that have been offered are also too restrictive.


The rectal cooling test is suggested to differentiate between rectal inertia and impaired relaxation/paradoxical contraction  [ 27 ]


Other techniques include  manometry ,  balloon expulsion test ,  evacuation proctography  (see  defecating proctogram ), and MRI defecography. [ 28 ]   Diagnostic criteria are:  fulfillment of criteria for  functional constipation , manometric and/or EMG and/or radiological evidence (2 out of 3), evidence of adequate expulsion force, and evidence of incomplete evacuation. [ 28 ]   Recent dynamic imaging studies have shown that in persons diagnosed with anismus the  anorectal angle  during attempted  defecation  is abnormal, and this is due to abnormal (paradoxical) movement of the  puborectalis muscle . [ 29 ] [ 30 ] [ 31 ]


Initial steps to alleviate anismus include dietary adjustments and simple adjustments when attempting to defecate. Supplementation with a  bulking agent  such as  psyllium  will make stool more bulky, which decreases the effort required to evacuate. [ 23 ]  Similarly, exercise and adequate hydration may help to optimise  stool form . The anorectal angle has been shown to flatten out when in a  squatting position , and is thus recommended for patients with functional outlet obstruction like anismus. [ 5 ]  If the patient is unable to assume a squatting postures due to mobility issues, a low stool can be used to raise the feet when sitting, which effectively achieves a similar position. [ citation needed ]


Treatments for anismus include biofeedback retraining, botox injections, and surgical resection. Anismus sometimes occurs together with other conditions that limit (see  contraindication ) the choice of treatments.  Thus, thorough evaluation is recommended prior to treatment. [ 32 ]


Biofeedback  training for treatment of anismus is highly effective and considered the gold standard therapy by many. [ 18 ] [ 33 ] [ 34 ]
Others however, reported that biofeedback had a limited therapeutic effect. [ 35 ]


Injections of  botulin toxin type-A  into the  puborectalis muscle  are very effective in the short term, and somewhat effective in the long term. [ 36 ]  Injections may be helpful when used together with biofeedback training. [ 37 ] [ 38 ]


Historically, the standard treatment was  surgical resection  of the puborectalis muscle, which sometimes resulted in fecal incontinence. Recently, partial resection (partial division) has been reported to be effective in some cases. [ 35 ] [ 39 ]


Paradoxical anal contraction during attempted defecation in constipated patients was first described in a paper in 1985, when the term anismus was first used. [ 40 ]  The researchers drew analogies to a condition called  vaginismus , which involves paroxysmal (sudden and short lasting) contraction of  pubococcygeus  (another muscle of the pelvic floor).  These researchers felt that this condition was a spastic dysfunction of the anus, analogous to 'vaginismus'. However, the term anismus implies a psychogenic etiology, which is not true although psychological dysfunction has been described in these patients. Hence:


Latin  ani  - "of the anus"
Latin  spasmus  - "spasm"


(Derived by extrapolation with the term vaginismus, which in turn is from the Latin  vagina  - "sheath" +  spasmus  - "spasm")


Many terms have been used synonymously to refer to this condition, some inappropriately. The term "anismus" has been criticised as it implies a  psychogenic  cause. [ 41 ]  In the most widely accepted classification systems ( ICD-11  and  Rome-IV ), the term "dyssynergic defecation" is preferred. [ 21 ] [ 20 ]  As stated in the Rome II criteria, the term "dyssynergic defecation" is preferred to "pelvic floor dyssynergia" because many patients with dyssynergic defecation do not report sexual or urinary symptoms, [ 25 ]  meaning that only the defecation mechanism is affected.


Other synonyms include:


Anorectal disorders  include conditions involving the anorectal junction [ 1 ]  as seen in the image. They are painful but common conditions like  hemorrhoids , tears,  fistulas , or  abscesses  that affect the  anal  region. [ 2 ] [ 3 ]  Most people experience some form of anorectal disorder during their lifetime. [ 4 ]   Primary care physicians  can treat most of these disorders, [ 2 ]  however, high-risk individuals include those with  HIV , roughly half of whom need surgery to remedy the disorders. [ 4 ]  Likelihood of  malignancy  should also be considered in high risk individuals. [ 5 ]  This is why it is important to perform a full history and physical exam on each patient. [ 5 ]  Because these disorders affect the  rectum , people are often embarrassed or afraid to confer with a  medical professional . [ 2 ]


Surgical Therapy. [ 5 ]


Surgical Therapy (for chronic fissures or when non-surgical therapy fails) : Anal Dilation, [ 8 ]   Lateral Internal Sphincterotomy ,  Advancement Flaps ,  Fissurectomy .


Itchiness , a  burning  sensation,  pus  discharge,  blood , and  swelling  in around the  rectum  and  anus , [ 4 ]   diarrhea . [ 12 ]  Other common symptoms include anal spasm, Bleeding with defecation [ 8 ]  and painful defecation. [ 5 ]


Doctors uses a variety of tools and techniques to evaluate the type of anorectal disorder, including  digital  and  anoscopic  investigations,  palpations , and  palpitations . The initial examination can be painful because a  gastroenterologist  will need to spread the  buttocks  and probe the painful area, which may require a  local anesthetic . [ 2 ]


Treatments range from recommendations for  over-the-counter products  to more invasive  surgical procedures .


Among the most common outpatient advice given to patients with less severe disorders include a high- fiber  diet, application of  ointment , and increased water intake. More serious procedures include the removal of affected tissue, injection of  botulinum  toxin, or surgically opening the  fistula  tract in the  sphincter  muscle. [ 2 ]


A  bezoar  ( / ˈ b i z ɔː r /   BEE -zor ) is a mass often found trapped in the  gastrointestinal system , [ 2 ]  though it can occur in other locations. [ 3 ] [ 4 ]  A  pseudobezoar  is an indigestible object introduced intentionally into the digestive system. [ 5 ]


There are several varieties of bezoar, some of which have  inorganic  constituents and others  organic . The term has both modern (medical, scientific) and traditional usage.


Esophageal bezoars discovered in nasogastrically fed patients on mechanical ventilation and sedation are reported to be due to the precipitation of certain food types rich in casein, which are precipitated with gastric acid reflux to form esophageal bezoars. Bezoars can also be caused by  gastroparesis  due to the slowing of gastric emptying, which allows food to form a bolus. [ 12 ]


The word  bezoar  is derived from the  Persian   pād-zahr  ( پادزهر ), literally  ' antidote ' . [ 13 ]  The myth of the bezoar as an antidote reached Europe from the Middle East in the 11th century and remained popular until it started to fall into disrepute by the 18th century. [ 14 ]  People believed that a bezoar had the power of a universal  antidote  and would work against any  poison  – a drinking glass that contained a bezoar could allegedly neutralize any poison poured into it.


Ox bezoars ( niu-huang  ( 牛黃 ) or   calculi bovis ) are used in  Chinese herbology [ vague ]  to treat various diseases. They are  gallstones  or gallstone substitutes formed from ox or cattle  bile . Some products allegedly remove  toxins  from the body.


The   Andalusian  physician  Ibn Zuhr  ( d.  1161), known in the West as Avenzoar, is thought [ by whom? ]  to have made the earliest description of bezoar stones as medicinal items. [ 15 ]  Extensive reference to bezoars also appears in the  Picatrix .


In 1567, French surgeon  Ambroise Paré  did not believe that it was possible for the bezoar to cure the effects of any poison and described an experiment to test the properties of the stone. A cook in the King's court was sentenced to death and chose to be poisoned rather than hanged, under the condition that he would be given a bezoar after the poison. Paré administered the bezoar stone to the cook, but it had no effect, and the cook died in agony seven hours after taking the poison, proving that – contrary to popular belief – the bezoar could not cure all poisons. [ 16 ]


Modern examinations of the properties of bezoars by Gustaf Arrhenius and Andrew A. Benson of the  Scripps Institution of Oceanography  show that when bezoars are immersed in an arsenic-laced solution, they can remove the poison. The toxic compounds in arsenic are  arsenate  and  arsenite ; each is acted upon differently by the bezoars: arsenate is removed by being exchanged for phosphate in  brushite  found in the stones, while arsenite is bound to sulfur compounds in the protein of degraded hair, which is a key component in bezoars. [ 17 ]


A famous case in the  common law  of England ( Chandelor v Lopus , 79 Eng Rep. 3, Cro. Jac. 4,  Eng. Ct. Exch.  1603) announced the rule of  caveat emptor  ("let the buyer beware") if the goods purchased are not in fact genuine and effective. The case concerned a purchaser who sued for the return of the purchase price of an allegedly fraudulent bezoar.


Bezoars were important objects in  cabinets of curiosity  and in natural-history collections, mainly for their use in early-modern pharmacy and in the study of animal health. [ 18 ] [ 19 ]


The  Merck Manual of Diagnosis and Therapy  notes that consumption of unripened  persimmons  has been identified as the main cause of epidemics of intestinal bezoars and that up to 90 percent of bezoars that occur from excessive consumption require surgery for removal. [ 20 ]


A 2013 review of three databases identified 24 publications presenting 46 patients treated with Coca-Cola for phytobezoars. Clinicians administered the cola in doses of 500 ml (18 imp fl oz; 17 US fl oz) to up to 3,000 ml (110 imp fl oz; 100 US fl oz) over 24 hours, orally or by  gastric lavage . A total of 91.3% of patients had complete resolution after treatment with Coca-Cola: 50% after a single treatment, with others requiring cola plus  endoscopic  removal. Doctors resorted to surgical removal in four cases. [ 21 ]


Bile acid malabsorption  ( BAM ), known also as  bile acid diarrhea , is a cause of several gut-related problems, the main one being chronic  diarrhea . It has also been called bile acid-induced diarrhea, cholerheic or choleretic enteropathy, bile salt diarrhea or bile salt malabsorption. It can result from  malabsorption  secondary to  gastrointestinal disease , or be a primary disorder, associated with excessive  bile acid  production.  Treatment with  bile acid sequestrants  is often effective. Depending on the severity of symptoms, it may be recognised as a disability in the United Kingdom under the Equality Act 2010.


A persistent (chronic) history of  diarrhea , with watery or mushy, unformed stools, (types 6 and 7 on the  Bristol stool scale ), sometimes with  steatorrhea , increased frequency and urgency of  defecation  are common manifestations, often with  fecal incontinence  and other gastrointestinal symptoms such as abdominal swelling,  bloating  and  abdominal pain . [ 2 ] [ 3 ] [ 1 ] [ 4 ]


People with this disorder often report impairments of  mental health  and  well-being , including  fatigue ,  dizziness ,  anxiety  about leaving home (primarily due to fear of fecal incontinence),  depression , one survey reports. [ 1 ]  It contributes in delays in diagnosis. [ 1 ]


Bile acids  (also called  bile salts ) are produced in the  liver , secreted into the  biliary system , stored in the  gallbladder  and are released after meals stimulated by  cholecystokinin . They are important for the  digestion  and  absorption  of fats (lipids) in the  small intestine . Usually over 95% of the bile acids are absorbed in the terminal  ileum  and are taken up by the liver and resecreted. This  enterohepatic circulation  of bile acids takes place four–six times in 24 hours and usually less than 0.5 g of bile acids enter the  large intestine  per 24 h. When larger amounts of bile acids enter the  large intestine , they stimulate water secretion and  intestinal motility  in the  colon , which causes symptoms of chronic  diarrhea . [ 5 ]


The  ileum  is very efficient at absorbing the glyco- and  taurine -conjugated forms of the bile salts. The  apical sodium-dependent bile salt transporter  (ASBT, IBAT, gene symbol  SLC10A2 ) is the first step in absorption at the brush-border membrane.  The cytoplasmic  ileal bile acid binding protein  (IBABP, ILBP, gene symbol  FABP6 ) and the basolateral heterodimer of  OSTα  and  OSTβ  transfer bile acids through and out of the cell where they eventually enter the  portal vein .  These bile acid transporters are all highly expressed in the ileum but not in the liver, jejunum or colon. [ 6 ]   When expression of these specialized transporters is reduced, the intestine is less efficient at bile acid reabsorption (Type 1 bile acid malabsorption). If  intestinal motility  is affected by gastro-intestinal surgery, or bile acids are deconjugated by  small intestinal bacterial overgrowth , absorption is less efficient (Type 3 bile acid malabsorption).  A very small proportion of the patients with no obvious disease (Type 2 bile acid malabsorption) may have mutations in ASBT, [ 7 ]  but this mutation is not more common in most patients and does not affect function. [ 8 ]


Primary bile acid diarrhea (Type 2 bile acid "malabsorption") may be caused by an overproduction of bile acids. [ 5 ] [ 9 ]  Several groups of workers have failed to show any defect in ileal bile acid absorption in these patients, and they have an enlarged bile acid pool, rather than the reduced pool expected with malabsorption. [ 10 ]  The synthesis of bile acids in the liver is negatively regulated by the ileal hormone fibroblast growth factor 19 ( FGF19 ), and lower levels of this hormone result in overproduction of bile acids, which are more than the ileum can absorb. [ 9 ]


A study found that patients suffering from bile acid diarrhea are characterized by a dysmetabolic and prediabetic-like profile, with higher postprandial concentrations of glucose, insulin and glucagon, compared with matched healthy controls. [ 11 ]  The underlying mechanisms are not fully understood. Furthermore, gut microbiome composition differs from that of people who do not suffer from bile acid diarrhea. [ 12 ] [ 13 ] [ 14 ]


Several methods have been developed to identify the disorder but there are difficulties with all of them. [ 15 ]  Diagnosis of bile acid malabsorption is easily and reliably made by the  SeHCAT  test.  This  nuclear medicine  test involves two scans a week apart and so measures multiple cycles of bile acid excretion and reabsorption.  There is limited radiation exposure (0.3 mSv).  Retention of SeHCAT at 7 days is normally above 15%; values less than 15%, 10% and 5% predict respectively mild, moderate and severe abnormal retention and an increasing likelihood of response to  bile acid sequestrants . [ 16 ]   This test is not licensed in the USA, and is underutilized even where it is available. [ 17 ] [ 18 ]   Older methods such as the  14 C-glycocholic breath test are no longer in routine clinical use. [ 19 ]


Measurement of  7α-Hydroxy-4-cholesten-3-one , (C4), a bile acid precursor, in serum, shows the increased bile acid synthesis found in bile acid malabsorption. [ 20 ]  This test is an alternative diagnostic means when available.  Fasting blood  FGF19  values may have value in the recognition of the disease and prediction of response. [ 21 ]


The various biomarkers give similar diagnostic yields of around 25% in patients with functional bowel disorders with diarrhea. [ 19 ]   In countries such as the US, where SeHCAT is not available, fecal bile acids and C4 are available to make the diagnosis. [ 19 ]


Bile acid malabsorption was first recognized in patients with  ileal disease . [ 22 ]  When other causes were recognized, and an idiopathic, primary form described, [ 23 ]  a classification into three types was proposed: [ 24 ]


Bile acid sequestrants  are the main agents used to treat bile acid malabsorption. [ 25 ]   Cholestyramine  and  colestipol , both in powder form, have been used for many years. Unfortunately, many patients find them difficult to tolerate; although the diarrhea may improve, other symptoms such as abdominal pain and bloating may worsen.


Colesevelam  is a tablet which is well tolerated and has been shown in placebo-controlled, randomized clinical trials to be effective. [ 26 ] [ 27 ] [ 28 ] [ 29 ]


The  farnesoid X receptor  agonist  obeticholic acid  has shown clinical and biochemical benefits in a proof of concept study. [ 30 ]   Tropifexor  is another farnesoid X receptor agonist that has been studied, showing improvements in biochemistry and colonic transit. [ 31 ]


Liraglutide , a  GLP-1 receptor agonist  had unexpected effects in clinical cases with co-existing bile acid diarrhoea [ 32 ]  which led to a randomised, double-blind, active-comparator, non-inferiority clinical trial. [ 33 ]  This trial demonstrated superiority in favour of liraglutide compared with colesevelam in reducing stool frequency and improved pathophysiological markers, suggesting it may be a new, safe and more effective treatment compared with current established, cheaper treatment modalities.


Bile acid malabsorption is common in Crohn's disease but not always recognized.  Most people with previous ileal resection and chronic diarrhea will have abnormal SeHCAT tests and can benefit from bile acid sequestrants. [ 4 ]


People with primary bile acid diarrhea are frequently misdiagnosed as having  irritable bowel syndrome . [ 17 ]  When SeHCAT testing  is performed, the diagnosis of primary bile acid diarrhea is commonly made. In a review of 18 studies of the use of SeHCAT testing in diarrhea-predominant irritable bowel syndrome patients, 32% of 1223 people had a SeHCAT 7-day retention of less than 10%, and 80% of these reported a response to cholestyramine, a bile acid sequestrant. [ 16 ]


A study from 2023 investigating the epidemiology of bile acid diarrhea in Denmark, found that people suffering from bile acid diarrhea seemed to have more co-morbidities, lower levels of income and education and more health care contacts compared with matches not suffering from bile acid diarrhea. [ 34 ]


Estimates of the population prevalence suggest that 1% of the adult population could have primary bile acid diarrhea (Type 2 bile acid malabsorption). [ 16 ]


A nationwide cohort study indicates an association between bile acid diarrhea and  gastrointestinal cancers . [ 35 ]


Blind loop syndrome , also known as  stagnant loop syndrome , [ 1 ]  is a state that occurs when the normal bacterial flora of the  small intestine  proliferates to numbers that cause significant derangement to the normal physiological processes of digestion and absorption. In some cases of blind loop syndrome, overgrowth of  pathogenic  non- commensal  bacteria has also been noted. It has long been understood that from birth, and throughout life, large amounts of bacteria reside symbiotically within animal gastrointestinal tracts such as the  human gastrointestinal tract . The understanding of this  gut flora  has even led to novel treatments for bowel irregularity that utilize  so called " probiotics " or good bacteria that aid in normal digestion.
The problem of blind loop syndrome arises when the bacterial colonies residing in the upper gastrointestinal tract begin to grow out of control or are altered in their makeup thereby creating a burden on the normal physiological processes occurring in the small intestine. This results in problems, among others, of:   vitamin B12 deficiency , fat malabsorption and  steatorrhea , fat-soluble vitamin deficiencies and intestinal wall injury. [ citation needed ]


Most of the symptoms of blind loop syndrome are non specific but nevertheless warrant the utmost attention. These include: [ citation needed ]


As a result of the concomitant vitamin and mineral deficiencies that occur as a result of the malabsorption associated with blind loop syndrome patients with advanced cases should be investigated for: [ citation needed ]


Blind loop syndrome is a complication of surgical operations of the abdomen, as well as  inflammatory bowel disease  or  scleroderma . Another cause is jejunoileal diverticula. [ 2 ]


The overgrowth of bacteria in the small intestine is prevented by various mechanical and chemical factors which include the constant peristaltic movement of contents along the length of the gastrointestinal tract and the antibacterial properties of gastric secretions, pancreatic secretions and  bile . [ citation needed ]


It follows that a disruption of any of these factors could lead to bacterial overgrowth and indeed blind loop syndrome has been found to occur in persons with anatomical anomalies that result in stagnation. Blind loop syndrome has also been associated with  achlorhydria , dysmotility,  fistulae , and  strictures . Chronic or high dose  opioid  therapy may contribute to blind loop syndrome by reducing gastric motility. [ citation needed ]


Due to the disruption of digestive processes by the overgrowth of intestinal bacteria; malabsorption of bile salts, fat and fat-soluble vitamins, protein and carbohydrates results in damage to the mucosal lining of the intestine by bacteria or via the production of toxic metabolites.


A physical examination may reveal a mass or distention of the abdomen. Tests which may be useful for diagnosis include: [ citation needed ]


The treatment of blind loop syndrome follows two basic principles. When a patient presents with symptoms of blind loop syndrome, the treating physician basically has two recognized options for management:


Although it would seem to be the better way to go in terms of management, there has been recent criticism on the need for such testing because of reliability issues. However, there are options such as the  glucose breath test  and jejunal  aspiration  the explanations of which are beyond the scope of this current article.  [ citation needed ]


The "treat empirically" route also has its difficulties, which have all come under wide debate and study. Recommendations are varied but seem to find some common ground around the notion that treatment should be individualized to the specific circumstances under which a patient has developed blind loop syndrome since these circumstances affect the complex microbial make up of the affected bowel.  Tetracyclines  have been the mainstay of treatment for blind loop syndrome, but recent studies have concluded  rifaximin  to be very effective in the treatment of blind loop syndrome. However, a study by Di Stefano et al. concluded  metronidazole  to be more effective than  rifaximin  in the treatment of blind loop syndrome. [ citation needed ]


Surgical management is reserved for fixing anatomical causes of bowel obstruction that interfere with normal function once they are amenable to such intervention. These conditions include: [ citation needed ]


Bowel infarction  or  gangrenous bowel  represents an irreversible injury to the intestine resulting from insufficient blood flow. It is considered a  medical emergency  because it can quickly result in  life-threatening infection  and death. [ 1 ]  Any cause of bowel  ischemia , the earlier reversible form of injury, may ultimately lead to infarction if uncorrected. The causes of bowel ischemia or infarction include primary vascular causes (for example,  mesenteric ischemia ) and other causes of bowel obstruction. [ 2 ]


Primary vascular causes of bowel infarction, also known as  mesenteric ischemia , are due to blockages in the arteries or veins that supply the bowel. Types of mesenteric ischemia are generally separated into acute and chronic processes, because this helps determine treatment and prognosis. [ 3 ]


Bowel obstruction is most often caused by intestinal  adhesions , which frequently form after abdominal surgeries, or by chronic infections such as  diverticulitis ,  hepatitis , and  inflammatory bowel disease . The condition may be difficult to diagnose, as the symptoms may resemble those of other bowel disorders. [ 4 ]   Bowel volvulus  describes a specific form of bowel obstruction, where the intestine and/or mesentery are twisted, resulting in ischemia. [ 5 ]


The only treatment for bowel infarction is immediate surgical repair and eventually  removal of the dead bowel segment . [ 1 ]


Patients who have undergone extensive resection of the small bowel may develop  malabsorption , indicating the need for dietary supplements.


Bowel obstruction , also known as  intestinal obstruction , is a mechanical or  functional obstruction  of the  intestines  which prevents the normal movement of the products of  digestion . [ 2 ] [ 5 ]  Either the  small bowel  or  large bowel  may be affected. [ 1 ]  Signs and symptoms include  abdominal pain ,  vomiting ,  bloating  and not passing  gas . [ 1 ]  Mechanical obstruction is the cause of about 5 to 15% of cases of  severe abdominal pain of sudden onset  requiring admission to hospital. [ 1 ] [ 2 ]


Causes of bowel obstruction include  adhesions ,  hernias ,  volvulus ,  endometriosis ,  inflammatory bowel disease ,  appendicitis ,  tumors ,  diverticulitis ,  ischemic bowel ,  tuberculosis  and  intussusception . [ 1 ] [ 2 ]  Small bowel obstructions are most often due to adhesions and hernias while large bowel obstructions are most often due to tumors and volvulus. [ 1 ] [ 2 ]  The diagnosis may be made on plain  X-rays ; however,  CT scan  is more accurate. [ 1 ]   Ultrasound  or  MRI  may help in the diagnosis of children or  pregnant  women. [ 1 ]


The condition may be treated conservatively or with  surgery . [ 2 ]  Typically  intravenous fluids  are given, a  nasogastric (NG) tube is placed through the nose into the stomach  to decompress the intestines, and  pain medications  are given. [ 2 ]   Antibiotics  are often given. [ 2 ]  In small bowel obstruction about 25% require surgery. [ 6 ]  Complications may include  sepsis , bowel  ischemia  and  bowel perforation . [ 1 ]


About 3.2 million cases of bowel obstruction occurred in 2015 which resulted in 264,000 deaths. [ 3 ] [ 7 ]  Both sexes are equally affected and the condition can occur at any age. [ 6 ]  Bowel obstruction has been documented throughout history, with cases detailed in the  Ebers Papyrus  of 1550 BC and by  Hippocrates . [ 8 ]


Depending on the level of obstruction, bowel obstruction can present with  abdominal pain ,  abdominal distension , and  constipation . Bowel obstruction may be complicated by  dehydration  and  electrolyte abnormalities  due to vomiting; respiratory compromise from pressure on the  diaphragm  by a distended abdomen, or  aspiration  of vomitus; bowel  ischemia  or  perforation  from prolonged distension or pressure from a foreign body and subsequently  sepsis  due to  bowel flora . [ 9 ]


In small bowel obstruction, the  pain  tends to be colicky (cramping and intermittent) in nature, with spasms lasting a few minutes. The pain tends to be central and mid-abdominal. Vomiting may occur before constipation. [ 10 ]  Common physical exam findings may include signs of  dehydration , abdominal distension with tympany, nonspecific abdominal tenderness, and high pitched tinkly bowel sounds. [ 11 ]


In large bowel obstruction, the pain is felt lower in the abdomen and the spasms last longer. Common symptoms include abdominal pain, distension, and severe constipation. [ 12 ]  Constipation occurs earlier and vomiting may be less prominent. Proximal obstruction of the large bowel may present as small bowel obstruction. [ 13 ]  Patients may notice a history of bloating and narrowing of stools before the onset of more severe symptoms. Symptoms can present quickly in the cases of  volvulus  and can present over a longer period of time in the setting of cancer. Common physical exam findings may include a palpable  hernia , abdominal distension with tympany, nonspecific lower abdominal tenderness, and a rectal mass. [ 6 ]


The main diagnostic tools are  blood tests ,  X-rays  of the abdomen, CT scanning, and  ultrasound . If a mass is identified,  biopsy  may determine the nature of the mass. [ citation needed ]


Radiological  signs of bowel obstruction include bowel distension (small bowel loops dilated >3 cm) and the presence of multiple (more than 2) air-fluid levels on supine and erect abdominal  radiographs . [ 16 ]  Ultrasounds may be as useful as CT scanning to make the diagnosis. [ 17 ]


Contrast enema  or small bowel series or CT scan can be used to define the level of obstruction, whether the obstruction is partial or complete, and to help define the cause of the obstruction. The appearance of water-soluble contrast in the cecum on an abdominal radiograph within 24 hours of it being given by mouth predicts resolution of an adhesive small bowel obstruction with  sensitivity  of 97% and  specificity  of 96%. [ 18 ]


Colonoscopy , small bowel investigation with ingested camera or push  endoscopy , and  laparoscopy  are other diagnostic options.


Differential diagnoses  of bowel obstruction include:


Causes of  small bowel  obstruction include: [ 2 ]


After abdominal surgery, the incidence of small bowel obstruction from any cause is 9%. In those where the cause of the obstruction was clear, adhesions are the single most common cause (more than half). [ 22 ]


Causes of large bowel obstruction include: [ 23 ]


Outlet obstruction is a sub-type of large bowel obstruction and refers to conditions affecting the anorectal region that obstruct  defecation , specifically conditions of the pelvic floor and anal sphincters. Outlet obstruction can be classified into four groups. [ 24 ]


Treatment of small and large bowel obstructions are initially similar and non-operative management is usually the initial management strategy as the majority of small bowel obstruction resolve spontaneously with non-operative management. [ 25 ] [ 26 ]  Patients are monitored by the surgical team for signs of improvement and resolution of the obstruction on imaging; if the obstruction does not clear then surgical management for the treatment of the causative lesion is required. [ 27 ]  In malignant large bowel obstruction, endoscopically placed self-expanding metal  stents  may be used to temporarily relieve the obstruction as a bridge to surgery, [ 28 ]  or as  palliation . [ 29 ]  Diagnosis of the type of bowel obstruction is normally conducted through initial plain  radiograph  of the abdomen, luminal contrast studies,  computed tomography scan , or  ultrasonography  prior to determining the best type of treatment. [ 30 ]


Further research is needed to find out if parenteral nutrition is of benefit to people with an inoperable blockage of the bowel caused by advanced cancer. [ 31 ]


In the management of small bowel obstructions, a commonly quoted surgical aphorism is: "never let the sun rise or set on small-bowel obstruction" [ 32 ]  because about 5.5% [ 32 ]  of small bowel obstructions are ultimately fatal if treatment is delayed. Improvements in radiological imaging of small bowel obstructions allow for confident distinction between simple obstructions, that can be treated conservatively, and obstructions that are surgical emergencies ( volvulus , closed-loop obstructions,  ischemic bowel , incarcerated  hernias , etc.). [ 2 ]  Exam findings of bowel compromise requiring immediate surgery include: severe abdominal pain, signs of  peritonitis  such as rebound tenderness,  elevated heart rate , fever, and elevated inflammatory markers on lab work, such as  lactic acid . [ 33 ] [ 34 ]


A small flexible tube ( nasogastric tube ) may be inserted through the nose into the stomach to help decompress the dilated bowel. This tube is uncomfortable but relieves the abdominal cramps, distention, and vomiting.  Intravenous therapy  is utilized and the urine output may be monitored with a  catheter  in the  bladder . [ 35 ] [ 36 ]


Most people with SBO are initially managed conservatively because in many cases, the bowel will open up. Some adhesions loosen up and the obstruction resolves. The patient is examined several times a day, and  X-ray images  are made to ensure he or she is not getting clinically worse. [ 37 ]


Conservative treatment involves insertion of a  nasogastric tube , correction of dehydration and  electrolyte  abnormalities.  Opioid  pain relievers may be used for patients with severe pain but alternate pain relievers are preferred as opioids can decrease bowel motility. [ 38 ] Antiemetics  may be administered if the patient is vomiting. Adhesive obstructions often settle without surgery. If the obstruction is complete surgery is usually required.


Most patients improve with conservative care in 2–5 days. When the obstruction is cancer, surgery is the only treatment. Those with  bowel resection  or  lysis  of adhesions usually stay in the hospital a few more days until they can eat and walk. [ 39 ]


Small bowel obstruction caused by  Crohn's disease , peritoneal  carcinomatosis , sclerosing  peritonitis ,  radiation enteritis , and postpartum bowel obstruction are typically treated conservatively, i.e. without surgery.


The prognosis for non-ischemic cases of SBO is good with mortality rates of 3–5%, while prognosis for SBO with ischemia is fair with mortality rates as high as 30%. [ 40 ]


Cases of SBO related to cancer are more complicated and require additional intervention to address the  malignancy , recurrence, and  metastasis , and thus are associated with a more poor prognosis. [ 41 ]  Surgical options in patients with malignant bowel obstruction need to be considered carefully as while it may provide relief of symptoms in the short term, there is a high risk of mortality and re-obstruction. [ 42 ]


All cases of abdominal surgical intervention are associated with increased risk of future small-bowel obstructions. Statistics from U.S. healthcare report 18.1% re-admittance rate within 30 days for patients who undergo SBO surgery. [ 43 ]  More than 90% of patients also form adhesions after major abdominal surgery. [ 44 ]
Common consequences of these adhesions include small-bowel obstruction, chronic abdominal pain, pelvic pain, and infertility. [ 44 ]


Callous ulcer  is a chronic nonhealing  ulcer  with hard indurated base and inelastic margins. [ 1 ]   It usually contains unhealthy pale  granulation tissue . It may last for months to years and does not show any tendency to heal. [ 2 ]


This cutaneous condition article is a  stub . You can help Wikipedia by  expanding it .


Campylobacteriosis  is among the most common  infections  caused by a  bacterium  in humans, often as a  foodborne illness . It is caused by the  Campylobacter   bacterium , [ 2 ]  most commonly  C. jejuni . It produces an inflammatory, sometimes bloody,  diarrhea  or  dysentery  syndrome, and usually cramps, fever and pain.


The  prodromal symptoms  are fever, headache, and  myalgia , which can be severe, lasting as long as 24 hours. After 1–5 days, typically, these are followed by  diarrhea  (as many as 10 watery, frequently bloody, bowel movements per day) or  dysentery ,  cramps ,  abdominal pain , and  fever  as high as 40 °C (104 °F). In most people, the illness lasts for 2–10 days. It is classified as invasive/inflammatory diarrhea, also described as bloody diarrhea or dysentery. [ citation needed ]


There are other diseases showing similar symptoms. For instance, abdominal pain and tenderness may be very localized, mimicking  acute appendicitis . Furthermore,  Helicobacter pylori  is closely related to  Campylobacter  and causes  peptic ulcer disease . [ citation needed ]


Complications include  toxic megacolon ,  dehydration  and  sepsis . Such complications generally occur in young children (< 1 year of age) and immunocompromised people. A chronic course of the disease is possible; this disease process is likely to develop without a distinct acute phase. Chronic campylobacteriosis features a long period of sub- febrile  temperature and  asthenia ; eye damage,  arthritis ,  endocarditis  may develop if infection is untreated. Occasional deaths occur in young, previously healthy individuals because of blood volume depletion (due to dehydration), and in people who are elderly or immunocompromised. [ citation needed ]


Some individuals (1–2 in 100,000 cases) develop  Guillain–Barré syndrome , in which the nerves that join the spinal cord and brain to the rest of the body are damaged, sometimes permanently. [ 3 ]


In patients with  HIV , infections may be more frequent, may cause prolonged bouts of dirty brown diarrhea, and may be more commonly associated with  bacteremia  and  antibiotic resistance . In participants of unprotected anal intercourse, campylobacteriosis is more localized to the distal end of the  colon  and may be termed a  proctocolitis . The severity and persistence of infection in patients with AIDS and  hypogammaglobulinemia  indicates that both cell-mediated and humoral immunity are important in preventing and terminating infection. [ citation needed ]


Campylobacteriosis is caused by  Campylobacter  bacteria (curved or spiral, motile, non–spore-forming,  Gram-negative  rods). The disease is usually caused by  C. jejuni , a spiral and comma-shaped bacterium normally found in cattle, swine, and birds, where it is nonpathogenic, but the illness can also be caused by  C. coli  (also found in cattle, swine, and birds),  C. upsaliensis  (found in cats and dogs) and  C. lari  (present in seabirds in particular). [ citation needed ]


One effect of campylobacteriosis is tissue injury in the  gut . The sites of tissue injury include the  jejunum , the  ileum , and the  colon .  C jejuni  appears to achieve this by invading and destroying epithelial cells. [ citation needed ]


C. jejuni  can also cause a latent autoimmune effect on the nerves of the legs, which is usually seen several weeks after a surgical procedure of the abdomen. The effect is known as an acute idiopathic demyelinating polyneuropathy (AIDP), i.e. Guillain–Barré syndrome, in which one sees symptoms of ascending paralysis, dysaesthesias usually below the waist, and, in the later stages, respiratory failure. [ citation needed ]


Some strains of  C jejuni  produce a  cholera -like enterotoxin, which is important in watery diarrhea observed in infections. The organism produces diffuse, bloody, edematous, and exudative enteritis. In a small number of cases, the infection may be associated with  hemolytic uremic syndrome  and  thrombotic thrombocytopenic purpura  through a poorly understood mechanism. [ citation needed ]


The common  routes of transmission  for the disease-causing bacteria are fecal-oral, person-to-person sexual contact, [ citation needed ]  ingestion of contaminated food (generally unpasteurized (raw)  milk  and undercooked or poorly handled  poultry ), and waterborne (i.e., through contaminated  drinking water ). Contact with contaminated poultry, livestock, or household pets, especially puppies, can also cause disease. [ 4 ]


Animals farmed for meat are the main source of campylobacteriosis. A study published in  PLoS Genetics  (26 September 2008) by researchers from Lancashire, England, and Chicago, Illinois, found that 97 percent of campylobacteriosis cases sampled in Lancashire were caused by bacteria typically found in chicken and livestock. In 57 percent of cases, the bacteria could be traced to chicken, and in 35 percent to cattle. Wild animal and environmental sources were accountable for just three percent of disease. [ 5 ] [ 6 ]


The infectious dose is 1000–10,000 bacteria (although ten to five hundred bacteria can be enough to infect humans).  Campylobacter  species are sensitive to  hydrochloric acid  in the  stomach , and acid reduction treatment can reduce the amount of  inoculum  needed to cause disease. [ citation needed ]


Exposure to bacteria is often more common during travelling, and therefore campylobacteriosis is a common form of  travelers' diarrhea . [ citation needed ]


Campylobacter  organisms can be detected by performing a  Gram stain  of a stool sample with high  specificity  and a  sensitivity  of ~60%, but are most often diagnosed by stool culture. Fecal  leukocytes  should be present and indicate the diarrhea to be inflammatory in nature. Methods currently being developed to detect the presence of  Campylobacter  organisms include antigen testing via an  EIA  or  PCR . [ citation needed ]


The World Health Organization recommends the following: [ 7 ]


The infection is usually  self-limiting , and in most cases, symptomatic treatment by liquid and  electrolyte replacement  is enough in human infections. [ 8 ]


Antibiotic treatment only has a marginal effect on the duration of symptoms, and its use is not recommended except in high-risk patients with  clinical complications . [ 9 ]


Erythromycin  can be used in children, and  tetracycline  in adults. Some studies show, however, that  erythromycin  rapidly eliminates  Campylobacter  from the stool without affecting the duration of illness. Nevertheless, children with  dysentery  due to  C. jejuni  benefit from early treatment with erythromycin. Treatment with antibiotics, therefore, depends on the severity of symptoms.  Quinolones  are effective if the organism is sensitive, but high rates of quinolone use in livestock mean that quinolones are now largely ineffective. [ 10 ]


Antimotility agents, such as  loperamide , can lead to prolonged illness or intestinal perforation in any invasive diarrhea, and should be avoided.   Trimethoprim/sulfamethoxazole  and  ampicillin  are ineffective against  Campylobacter . [ citation needed ]


In the past, poultry infections were often treated by mass administration of  enrofloxacin  and  sarafloxacin  for single instances of infection. The FDA banned this practice, as it promoted the development of  fluoroquinolone -resistant populations. [ 11 ]
A major broad-spectrum  fluoroquinolone  used in humans is  ciprofloxacin . The increasing resistance of the  Campylobacter  to fluoroquinolones and  macrolides  is of a major concern. [ citation needed ]
A different approach, propagated within the EU is that  Campylobacter  mitigating measures should be undertaken mainly at the primary production level. An update of potential control options was released by EFSA on 30 April 2020. Vaccination, feed, and water additives, discontinued thinning,  employing few and well-trained staff, drinkers that allow standing water, addition of disinfectants to drinking water, hygienic anterooms, designated tools per broiler house were listed as most effective in mitigating the risk of Campylobacter in chicken thus reducing the risk of human campylobacteriosis. [ 12 ]


Campylobacteriosis is usually self-limited without any mortality (assuming proper hydration is maintained). However, there are several possible complications. [ citation needed ]


Campylobacter  is one of the most common causes of human bacterial  gastroenteritis . [ 13 ]  For instance, an estimated 2 million cases of  Campylobacter   enteritis  occur annually in the  U.S. , accounting for 5–7% of cases of gastroenteritis. Furthermore, in the  United Kingdom  during 2000,  Campylobacter jejuni  was involved in 77.3% in all cases of laboratory confirmed  foodborne illness . [ 14 ]  About 15 of every 100,000 people are diagnosed with campylobacteriosis every year, and with many cases going unreported, up to 0.5% of the general population may unknowingly harbor  Campylobacter  in their gut. [ citation needed ]


Unfortunately, the true incidence of campylobacteriosis is unknown in most countries, especially developing countries. The reasons are among others underreporting, difficulties with diagnosis and differences in reporting systems in different countries. [ 15 ]


A large animal reservoir is present as well, with up to 100% of poultry, including  chickens ,  turkeys , and waterfowl, having asymptomatic infections in their intestinal tracts. Infected  chicken  feces may contain up to 10 9  bacteria per 25 grams, and due to the animals' close proximity, the bacteria are rapidly spread to other  chickens . This vastly exceeds the infectious dose of 1000–10,000 bacteria for humans. [ citation needed ]


In January 2013, the  UK 's  Food Standards Agency  warned that two-thirds of all raw chicken bought from UK shops was contaminated with campylobacter, affecting an estimated half a million people annually and killing approximately 100. [ 16 ]


In August–September 2016, 5,200 people fell ill with campylobacteriosis in  Hastings , New Zealand, after the local water supply in Havelock North tested positive for the pathogen  Campylobacter jejuni . [ 17 ] [ 18 ]  Four deaths were suspected to be due to the outbreak. [ 19 ]  It is suspected that after heavy rain fell on 5–6 August, water contamination from flooding caused the outbreak, although this is the subject of a government Inquiry. [ 20 ]  It is the largest outbreak of waterborne disease ever to occur in New Zealand. All schools in Havelock North closed for two weeks, with the Hastings District Council advising an urgent notice to boil water for at least one minute before consumption. This notice was lifted on 3 September, with the outbreak officially under control. [ citation needed ]


According to  Centers for Disease Control and Prevention , a multistate outbreak of human  Campylobacter  infection has been reported since 11 September 2017. In all, 55 cases were reported from 12 states (Florida, Kansas, Maryland, Missouri, New Hampshire, New York, Ohio, Pennsylvania, Tennessee, Utah, Wisconsin and Wyoming). Epidemiological and laboratory evidence indicated that puppies sold through  Petland  stores were a likely source of this outbreak.  Out of 55 cases reported, 50 were either employees of Petland or had recently purchased a puppy at Petland, or visited there before illness began. Five people out of 55 cases reported were exposed to puppies from various sources. [ 21 ]


Campylobacter  can spread through contact with dog  feces . It usually does not spread from one person to another. However, activities such as changing an infected person's diapers or sexual contact with an infected person can lead to infection. Regardless of where they are from, any puppies and dogs may carry  Campylobacter  germs. [ 21 ]


Carbonated soda treatment of phytobezoars  is the use of  carbonated soda  to try to dissolve a  phytobezoar . Bezoars consist of a solid and formed mass trapped in the  gastrointestinal system , usually in the  stomach . [ 1 ] [ 2 ] [ 3 ]  These can also form in other locations. [ 4 ] [ 5 ]


Carbonated soda has been proposed for the treatment of gastric phytobezoars. In about 50% of cases studied, carbonated soda alone was found to be effective in gastric phytobezoar  dissolution . Unfortunately, this treatment can result in the potential of developing  small bowel obstruction  in a minority of cases, necessitating surgical intervention. [ 1 ]  It is one of many other stomach disorders that can have similar symptoms. [ medical citation needed ]


Gastric phytobezoars are a form of  intestinal  blockage and are seen in those with poor gastric motility. The preferred treatment of bezoars includes different therapies and/or fragmentation to avoid surgery. Phytobezoars are most common and consist of various undigested substances including  lignin ,  cellulose ,   tannins ,  celery ,  pumpkin  skin,  grape  skins,  prunes ,  raisins , vegetables and fruits. [ 1 ]  Phytobezoars can form after eating  persimmons  and  pineapples . These are more difficult to treat and are referred to as  diospyrobezoars . [ 6 ]


Carbonated soda may help to dissolve phytobezoars. [ 7 ]  It can be given by a  naso-gastric tube  in children. [ 8 ]  Carbonated soda can also be given by mouth and during  endoscopy . [ 9 ]  It is effective in about half of the cases. [ 7 ]


It promotes dissolution by endoscopic techniques in the majority of the patients left, leading to a final success rate up to 91.3%. [ 6 ]  In some cases, regular use of  Coca-Cola  resulted in no recurrence 3–15 months after the first episode. [ 6 ]  Treatment has varied widely. Coca-Cola has been administered either as drinking beverage or as lavage. Some are treated with various combinations of drink, injection and irrigation. The volume of Coca-Cola in treatment varies along with daily dose and time of treatment. Dosages varied from 500 mL up to 3000 mL and treatment period 24 hours to 6 weeks. When lavage is used, a double-lumen nasogastric tube or two separate tubes using 3000 mL of Coca-Cola is administered during a 12-hour period. [ 6 ]   Alternative treatments are the use of cellulase, acetylcysteine, papain, pancreatic enzymes, saline solution, 0.1 N HCl and sodium bicarbonate. The protocol for the treatment of phytobezoars with Coca-Cola, i.e., dosage and timing, has not been standardized; further investigation has been encouraged. [ 1 ]


Trichobezoars  do not respond to treatment with Coca-Cola but instead this type may have to be surgically removed. [ 9 ]  Persimmon diospyrobezoars sometimes are resistant to Coca-Cola and require a different treatment. This can include endoscopic fragmentation and/or surgical approaches especially in urgent cases where the patient exhibits gastrointestinal bleeding. [ 1 ] [ 6 ]


Adverse effects have been observed with the use of papain such as gastric ulcer, hyponatremia and oesophageal perforation. [ 6 ]  These effects have not been observed with the use of Coca-Cola. Glucose levels during the administration of Coca-Cola have not been addressed. [ citation needed ]


In addition to Coca-Cola,  meat tenderizer  has been used to dissolve bezoars of the stomach. [ 10 ] [ 11 ]  When treatment with Coca-Cola is combined with endoscopic methods, the success of treatment approaches 90%. [ 6 ]   The mechanism by which Coca-Cola dissolves the bezoar is based upon its low pH, CO 2  bubbles, and  sodium bicarbonate  content. [ 9 ]