Bloating: Difference between revisions

Jump to navigation Jump to search
Line 67: Line 67:


==Pathophysiology==
==Pathophysiology==
=== Abnormal Gut Microbiota ===
===Abnormal Gut Microbiota===
There is a relationship between the types of gas produced by colonic microflora and bloating. The low producers of methane reported significantly increased bloating and cramping after the ingestion of sorbitol and fiber, and the high producers of methane revealed a lower prevalence of severe lactulose intolerance than low producers. Hence, the role of methanogenic flora may be important in the pathogenesis of bloating. <ref name="pmid8995944">{{cite journal |vauthors=Kajs TM, Fitzgerald JA, Buckner RY, Coyle GA, Stinson BS, Morel JG, Levitt MD |title=Influence of a methanogenic flora on the breath H2 and symptom response to ingestion of sorbitol or oat fiber |journal=Am. J. Gastroenterol. |volume=92 |issue=1 |pages=89–94 |date=January 1997 |pmid=8995944 |doi= |url=}}</ref>
There is a relationship between the types of gas produced by colonic [[microflora]] and bloating. The low producers of [[methane]] reported significantly increased bloating and [[cramping]] after the ingestion of [[sorbitol]] and fiber, and the high producers of methane revealed a lower prevalence of severe [[lactose intolerance]] than low producers. Hence, the role of methanogenic [[flora]] may be important in the pathogenesis of bloating. <ref name="pmid8995944">{{cite journal |vauthors=Kajs TM, Fitzgerald JA, Buckner RY, Coyle GA, Stinson BS, Morel JG, Levitt MD |title=Influence of a methanogenic flora on the breath H2 and symptom response to ingestion of sorbitol or oat fiber |journal=Am. J. Gastroenterol. |volume=92 |issue=1 |pages=89–94 |date=January 1997 |pmid=8995944 |doi= |url=}}</ref>


=== Small Intestinal Bacterial Overgrowth ===
===Small Intestinal Bacterial Overgrowth===
Patients with IBS who explicitly complain of bloating have been reported to have elevated gas production from bacterial fermentation due to small intestinal bacterial overgrowth (SIBO).<ref name="pmid17043337">{{cite journal |vauthors=Pimentel M, Park S, Mirocha J, Kane SV, Kong Y |title=The effect of a nonabsorbed oral antibiotic (rifaximin) on the symptoms of the irritable bowel syndrome: a randomized trial |journal=Ann. Intern. Med. |volume=145 |issue=8 |pages=557–63 |date=October 2006 |pmid=17043337 |doi=10.7326/0003-4819-145-8-200610170-00004 |url=}}</ref>
Patients with [[IBS]] who explicitly complain of bloating have been reported to have elevated gas production from bacterial [[fermentation]] due to [[small intestinal bacterial overgrowth]] (SIBO).<ref name="pmid17043337">{{cite journal |vauthors=Pimentel M, Park S, Mirocha J, Kane SV, Kong Y |title=The effect of a nonabsorbed oral antibiotic (rifaximin) on the symptoms of the irritable bowel syndrome: a randomized trial |journal=Ann. Intern. Med. |volume=145 |issue=8 |pages=557–63 |date=October 2006 |pmid=17043337 |doi=10.7326/0003-4819-145-8-200610170-00004 |url=}}</ref>


=== Intestinal Gas Accumulation ===
===Intestinal Gas Accumulation===
In fasting conditions, the healthy GI tract produces just about 100 mL of gas spread almost equally between 6 compartments the liver, small intestine, ascending colon, transverse colon, descending colon, and distal (pelvic) colon. The postprandial gas volume rises by around 65 percent, mainly in the pelvic colon. Excessive levels of intestinal gas have been suggested as the possible source of bloating and distension.<ref name="urlSleisenger and Fordtrans Gastrointestinal and Liver Disease- 2 Volume Set - 9th Edition">{{cite web |url=https://www.elsevier.com/books/sleisenger-and-fordtrans-gastrointestinal-and-liver-disease-2-volume-set/feldman/978-1-4160-6189-2 |title=Sleisenger and Fordtran's Gastrointestinal and Liver Disease- 2 Volume Set - 9th Edition |format= |work= |accessdate=}}</ref>
In fasting conditions, the healthy GI tract produces just about 100 mL of gas spread almost equally between 6 compartments the [[liver]], [[small intestine]], [[ascending colon]], [[transverse colon]], [[descending colon]], and distal (pelvic) colon. The [[postprandial]] gas volume rises by around 65 percent, mainly in the pelvic colon. Excessive levels of intestinal gas have been suggested as the possible source of bloating and distension.<ref name="urlSleisenger and Fordtrans Gastrointestinal and Liver Disease- 2 Volume Set - 9th Edition">{{cite web |url=https://www.elsevier.com/books/sleisenger-and-fordtrans-gastrointestinal-and-liver-disease-2-volume-set/feldman/978-1-4160-6189-2 |title=Sleisenger and Fordtran's Gastrointestinal and Liver Disease- 2 Volume Set - 9th Edition |format= |work= |accessdate=}}</ref>


=== Altered Gut Motility and Impaired Gas Handling ===
===Altered Gut Motility and Impaired Gas Handling===
Ineffective anorectal evacuation and impaired gas processing could also be the potential causes of abdominal distension and bloating.
Ineffective [[anorectal]] evacuation and impaired gas processing could also be the potential causes of abdominal distension and bloating.


=== Abnormal Abdominal-diaphragmatic Reflexes ===
===Abnormal Abdominal-diaphragmatic Reflexes===
In healthy adults, colonic gas infusion increases anterior wall tone and relaxes the diaphragm at the same time. On the contrary, patients with bloating have shown diaphragmatic contraction (descent) and relaxation of the internal oblique muscle with the same gas load. <ref name="pmid19208364">{{cite journal |vauthors=Accarino A, Perez F, Azpiroz F, Quiroga S, Malagelada JR |title=Abdominal distention results from caudo-ventral redistribution of contents |journal=Gastroenterology |volume=136 |issue=5 |pages=1544–51 |date=May 2009 |pmid=19208364 |doi=10.1053/j.gastro.2009.01.067 |url=}}</ref>
In healthy adults, colonic gas infusion increases anterior wall tone and relaxes the [[diaphragm]] at the same time. On the contrary, patients with bloating have shown diaphragmatic contraction (descent) and relaxation of the [[internal oblique muscle]] with the same gas load. <ref name="pmid19208364">{{cite journal |vauthors=Accarino A, Perez F, Azpiroz F, Quiroga S, Malagelada JR |title=Abdominal distention results from caudo-ventral redistribution of contents |journal=Gastroenterology |volume=136 |issue=5 |pages=1544–51 |date=May 2009 |pmid=19208364 |doi=10.1053/j.gastro.2009.01.067 |url=}}</ref>


=== Visceral Hypersensitivity ===
===Visceral Hypersensitivity===
The sensation of bloating may originate from abdominal viscera in patients with a functional gastrointestinal disorder, in whom normal stimuli or small variations of gas content within the gut may be perceived as bloating. The autonomic nervous system may also contribute to the modulation of visceral sensitivity and sympathetic activation is known to increase the perception of intestinal distention in these patients.
The sensation of bloating may originate from abdominal [[viscera]] in patients with a [[functional gastrointestinal disorder]], in whom normal stimuli or small variations of gas content within the gut may be perceived as bloating. The [[autonomic nervous system]] may also contribute to the modulation of [[visceral]] sensitivity and sympathetic activation is known to increase the perception of intestinal distention in these patients.


=== Food Intolerance and Carbohydrate Malabsorption ===
===Food Intolerance and Carbohydrate Malabsorption===
A high FODMAP diet has demonstrated prolonged hydrogen production in the intestine, colonic distension by fermentation, increased colonic fluid delivery by osmotic load within the bowel lumen, and GI symptom generation. <ref name="pmid20102355">{{cite journal |vauthors=Barrett JS, Gearry RB, Muir JG, Irving PM, Rose R, Rosella O, Haines ML, Shepherd SJ, Gibson PR |title=Dietary poorly absorbed, short-chain carbohydrates increase delivery of water and fermentable substrates to the proximal colon |journal=Aliment. Pharmacol. Ther. |volume=31 |issue=8 |pages=874–82 |date=April 2010 |pmid=20102355 |doi=10.1111/j.1365-2036.2010.04237.x |url=}}</ref>
A high FODMAP diet has demonstrated prolonged hydrogen production in the [[intestine]], colonic distension by [[fermentation]], increased colonic fluid delivery by osmotic load within the bowel lumen, and GI symptom generation. <ref name="pmid20102355">{{cite journal |vauthors=Barrett JS, Gearry RB, Muir JG, Irving PM, Rose R, Rosella O, Haines ML, Shepherd SJ, Gibson PR |title=Dietary poorly absorbed, short-chain carbohydrates increase delivery of water and fermentable substrates to the proximal colon |journal=Aliment. Pharmacol. Ther. |volume=31 |issue=8 |pages=874–82 |date=April 2010 |pmid=20102355 |doi=10.1111/j.1365-2036.2010.04237.x |url=}}</ref>


=== Hard stool/Constipation ===
===Hard stool/Constipation===
Distension of the rectum by retained feces slows small intestinal transit as well as colonic transit, thus aggravating bloating in constipated patients. Constipation or hard/lumpy stool induces alteration of gut motility and increases bacterial fermentation.
Distension of the [[rectum]] by retained [[feces]] slows small intestinal transit as well as colonic transit, thus aggravating bloating in [[Constipation|constipated]] patients. Constipation or hard/lumpy stool induces alteration of gut motility and increases bacterial [[Fermentation (biochemistry)|fermentation]].


==Causes==
==Causes==

Revision as of 20:06, 31 August 2020

WikiDoc Resources for Bloating

Articles

Most recent articles on Bloating

Most cited articles on Bloating

Review articles on Bloating

Articles on Bloating in N Eng J Med, Lancet, BMJ

Media

Powerpoint slides on Bloating

Images of Bloating

Photos of Bloating

Podcasts & MP3s on Bloating

Videos on Bloating

Evidence Based Medicine

Cochrane Collaboration on Bloating

Bandolier on Bloating

TRIP on Bloating

Clinical Trials

Ongoing Trials on Bloating at Clinical Trials.gov

Trial results on Bloating

Clinical Trials on Bloating at Google

Guidelines / Policies / Govt

US National Guidelines Clearinghouse on Bloating

NICE Guidance on Bloating

NHS PRODIGY Guidance

FDA on Bloating

CDC on Bloating

Books

Books on Bloating

News

Bloating in the news

Be alerted to news on Bloating

News trends on Bloating

Commentary

Blogs on Bloating

Definitions

Definitions of Bloating

Patient Resources / Community

Patient resources on Bloating

Discussion groups on Bloating

Patient Handouts on Bloating

Directions to Hospitals Treating Bloating

Risk calculators and risk factors for Bloating

Healthcare Provider Resources

Symptoms of Bloating

Causes & Risk Factors for Bloating

Diagnostic studies for Bloating

Treatment of Bloating

Continuing Medical Education (CME)

CME Programs on Bloating

International

Bloating en Espanol

Bloating en Francais

Business

Bloating in the Marketplace

Patents on Bloating

Experimental / Informatics

List of terms related to Bloating



Resident
Survival
Guide
Bloating
ICD-10 R14.r
ICD-9 787.3

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Ibtisam Ashraf, M.B.B.S.[2]

Overview

Bloating is described as a sensation of elevated abdominal pressure that may or may not be accompanied by objective abdominal distension, i.e. noticeable enlargement of the waist. Bloating and abdominal distension may be symptoms of organic disease and possible causes should be considered first in the differential diagnosis. It is one of the most frequent problems in a wide proportion of patients with gastrointestinal disorders, but the most common cause is constipation. Aside from constipation, other causes of bloating include Irritable bowel syndrome, small intestinal bacterial overgrowth, gastroparesis, and gynecological conditions. The pathophysiology of bloating is not well understood and suggested underlying causes include visceral hypersensitivity, behavioral mediated irregular abdominal wall-phrenic reflexes, the influence of poorly ingested fermentable carbohydrates, and microbiome modification. Usually, patients are evaluated with a thorough history and physical examination, but organic disorders should be ruled out. The management strategy includes dietary modification, behavioral therapy, microbiome modulation, and medical therapy.

Historical Perspective

  • Bernheim in 1891 described a woman who said, "I go up and down like an accordion."[1] and Later on in 1900 Kaplan, wrote on ventre en accordéon.[2]
  • Sir James Y. Simpson described it and demonstrated nongaseous bloating. [3]
  • According to Kaplan, in the 19th century in Europe, the intestines of the patient were punctured with a trocar in cases of suspected intestinal obstruction. In this way, it was discovered that there was no gas involved in cases of hysteric bloating.
  • It was also considered a "tumor" that vanished when the patient was anesthetized and returned when they were conscious.[4]
  • Lordosis association with bloating was described by Krukenberg in 1884. [2]
  • Bloating was first described by Alvarez of the Mayo Clinic in 1949 in a woman with a psychiatric problem.[2]

Classification

There is no established system for the classification of [disease name].

OR

[Disease name] may be classified according to [classification method] into [number] subtypes/groups: [group1], [group2], [group3], and [group4].

OR

[Disease name] may be classified into [large number > 6] subtypes based on [classification method 1], [classification method 2], and [classification method 3]. [Disease name] may be classified into several subtypes based on [classification method 1], [classification method 2], and [classification method 3].

OR

Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.

OR

If the staging system involves specific and characteristic findings and features: According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].

OR

The staging of [malignancy name] is based on the [staging system].

OR

There is no established system for the staging of [malignancy name].

Pathophysiology

Abnormal Gut Microbiota

There is a relationship between the types of gas produced by colonic microflora and bloating. The low producers of methane reported significantly increased bloating and cramping after the ingestion of sorbitol and fiber, and the high producers of methane revealed a lower prevalence of severe lactose intolerance than low producers. Hence, the role of methanogenic flora may be important in the pathogenesis of bloating. [5]

Small Intestinal Bacterial Overgrowth

Patients with IBS who explicitly complain of bloating have been reported to have elevated gas production from bacterial fermentation due to small intestinal bacterial overgrowth (SIBO).[6]

Intestinal Gas Accumulation

In fasting conditions, the healthy GI tract produces just about 100 mL of gas spread almost equally between 6 compartments the liver, small intestine, ascending colon, transverse colon, descending colon, and distal (pelvic) colon. The postprandial gas volume rises by around 65 percent, mainly in the pelvic colon. Excessive levels of intestinal gas have been suggested as the possible source of bloating and distension.[7]

Altered Gut Motility and Impaired Gas Handling

Ineffective anorectal evacuation and impaired gas processing could also be the potential causes of abdominal distension and bloating.

Abnormal Abdominal-diaphragmatic Reflexes

In healthy adults, colonic gas infusion increases anterior wall tone and relaxes the diaphragm at the same time. On the contrary, patients with bloating have shown diaphragmatic contraction (descent) and relaxation of the internal oblique muscle with the same gas load. [8]

Visceral Hypersensitivity

The sensation of bloating may originate from abdominal viscera in patients with a functional gastrointestinal disorder, in whom normal stimuli or small variations of gas content within the gut may be perceived as bloating. The autonomic nervous system may also contribute to the modulation of visceral sensitivity and sympathetic activation is known to increase the perception of intestinal distention in these patients.

Food Intolerance and Carbohydrate Malabsorption

A high FODMAP diet has demonstrated prolonged hydrogen production in the intestine, colonic distension by fermentation, increased colonic fluid delivery by osmotic load within the bowel lumen, and GI symptom generation. [9]

Hard stool/Constipation

Distension of the rectum by retained feces slows small intestinal transit as well as colonic transit, thus aggravating bloating in constipated patients. Constipation or hard/lumpy stool induces alteration of gut motility and increases bacterial fermentation.

Causes

Disease name] may be caused by [cause1], [cause2], or [cause3].

OR

Common causes of [disease] include [cause1], [cause2], and [cause3].

OR

The most common cause of [disease name] is [cause 1]. Less common causes of [disease name] include [cause 2], [cause 3], and [cause 4].

OR

The cause of [disease name] has not been identified. To review risk factors for the development of [disease name], click here.

Differentiating bloating from other Diseases

Bloating must be differentiated from Lactose intolerance, Fructose intolerance, Celiac disease, Pancreatic insufficiency, Irritable bowel syndrome, Functional dyspepsia, Functional bloating, Constipation, Diabetes, Scleroderma, Pseudo-obstruction: acute or chronic, Gastroparesis, Acute adynamic ileus, Gastric outlet obstruction, Small bowel obstruction, SMA syndrome, Colonic obstruction, Volvulus, Gastrointestinal/Ovarian Malignancy, Ascites, Pregnancy, and Obesity/adiposity.[10]

Epidemiology and Demographics

  • In the USA, 15-30% of the general population has been reported to experience bloating.[11]
  • A telephone survey reported a prevalence of 16% in US adults who were asked about bloating or distention during the last month.[12]
  • Women were more likely than men to report bloating.[11]
  • There is no racial predilection to bloating.[13]

Risk Factors

Risk factors include chewing gum, hard candy, and carbonated beverages such as soda or beer. Additionally, people may swallow excess air if they are anxious or have an upper respiratory infection. Foods that can produce excess bowel gas include leafy greens, beans, and bran foods. Dairy products can lead to bloating and flatulence in people who are lactose intolerant.

Screening

There is insufficient evidence to recommend routine screening for bloating.

Natural History, Complications, and Prognosis

If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].

OR

Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].

OR

Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.

Diagnosis

Diagnostic Study of Choice

The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met: [criterion 1], [criterion 2], [criterion 3], and [criterion 4].

OR

The diagnosis of [disease name] is based on the [criteria name] criteria, which include [criterion 1], [criterion 2], and [criterion 3].

OR

The diagnosis of [disease name] is based on the [definition name] definition, which includes [criterion 1], [criterion 2], and [criterion 3].

OR

There are no established criteria for the diagnosis of [disease name].

History and Symptoms

The majority of patients with [disease name] are asymptomatic.

OR

The hallmark of [disease name] is [finding]. A positive history of [finding 1] and [finding 2] is suggestive of [disease name]. The most common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3]. Common symptoms of [disease] include [symptom 1], [symptom 2], and [symptom 3]. Less common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3].

Physical Examination

Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].

OR

Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

The presence of [finding(s)] on physical examination is diagnostic of [disease name].

OR

The presence of [finding(s)] on physical examination is highly suggestive of [disease name].

Laboratory Findings

An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].

OR

Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].

OR

[Test] is usually normal among patients with [disease name].

OR

Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].

OR

There are no diagnostic laboratory findings associated with [disease name].

Electrocardiogram

There are no ECG findings associated with [disease name].

OR

An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

X-ray

There are no x-ray findings associated with [disease name].

OR

An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

Echocardiography or Ultrasound

There are no echocardiography/ultrasound findings associated with [disease name].

OR

Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

CT scan

There are no CT scan findings associated with [disease name].

OR

[Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

MRI

There are no MRI findings associated with [disease name].

OR

[Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

Other Imaging Findings

There are no other imaging findings associated with [disease name].

OR

[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

Other Diagnostic Studies

There are no other diagnostic studies associated with [disease name].

OR

[Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].

Treatment

Medical Therapy

There is no treatment for [disease name]; the mainstay of therapy is supportive care.

OR

Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].

OR

The majority of cases of [disease name] are self-limited and require only supportive care.

OR

[Disease name] is a medical emergency and requires prompt treatment.

OR

The mainstay of treatment for [disease name] is [therapy].

OR   The optimal therapy for [malignancy name] depends on the stage at diagnosis.

OR

[Therapy] is recommended among all patients who develop [disease name].

OR

Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].

OR

Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].

OR

Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].

OR

Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].

Surgery

Surgical intervention is not recommended for the management of [disease name].

OR

Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]

OR

The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].

OR

The feasibility of surgery depends on the stage of [malignancy] at diagnosis.

OR

Surgery is the mainstay of treatment for [disease or malignancy].

Primary Prevention

There are no established measures for the primary prevention of [disease name].

OR

There are no available vaccines against [disease name].

OR

Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].

OR

[Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].

Secondary Prevention

There are no established measures for the secondary prevention of [disease name].

OR

Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3].

References

  1. Schott H (1984). "[Mesmer, Braid and Bernheim: on the history of the development of hypnotism]". Gesnerus (in German). 41 (1–2): 33–48. PMID 6378725.
  2. 2.0 2.1 2.2 ALVAREZ WC (August 1949). "Hysterical type of nongaseous abdominal bloating". Arch Intern Med (Chic). 84 (2): 217–45. doi:10.1001/archinte.1949.00230020020002. PMID 18138437.
  3. Dunn PM (May 2002). "Sir James Young Simpson (1811-1870) and obstetric anaesthesia". Arch. Dis. Child. Fetal Neonatal Ed. 86 (3): F207–9. doi:10.1136/fn.86.3.f207. PMC 1721404. PMID 11978757.
  4. "February 1887 - Volume 14 - Issue 2 : The Journal of Nervous and Mental Disease".
  5. Kajs TM, Fitzgerald JA, Buckner RY, Coyle GA, Stinson BS, Morel JG, Levitt MD (January 1997). "Influence of a methanogenic flora on the breath H2 and symptom response to ingestion of sorbitol or oat fiber". Am. J. Gastroenterol. 92 (1): 89–94. PMID 8995944.
  6. Pimentel M, Park S, Mirocha J, Kane SV, Kong Y (October 2006). "The effect of a nonabsorbed oral antibiotic (rifaximin) on the symptoms of the irritable bowel syndrome: a randomized trial". Ann. Intern. Med. 145 (8): 557–63. doi:10.7326/0003-4819-145-8-200610170-00004. PMID 17043337.
  7. "Sleisenger and Fordtran's Gastrointestinal and Liver Disease- 2 Volume Set - 9th Edition".
  8. Accarino A, Perez F, Azpiroz F, Quiroga S, Malagelada JR (May 2009). "Abdominal distention results from caudo-ventral redistribution of contents". Gastroenterology. 136 (5): 1544–51. doi:10.1053/j.gastro.2009.01.067. PMID 19208364.
  9. Barrett JS, Gearry RB, Muir JG, Irving PM, Rose R, Rosella O, Haines ML, Shepherd SJ, Gibson PR (April 2010). "Dietary poorly absorbed, short-chain carbohydrates increase delivery of water and fermentable substrates to the proximal colon". Aliment. Pharmacol. Ther. 31 (8): 874–82. doi:10.1111/j.1365-2036.2010.04237.x. PMID 20102355.
  10. Hasler WL (September 2006). "Gas and Bloating". Gastroenterol Hepatol (N Y). 2 (9): 654–662. PMC 5350578. PMID 28316536.
  11. 11.0 11.1 Jiang X, Locke GR, Choung RS, Zinsmeister AR, Schleck CD, Talley NJ (June 2008). "Prevalence and risk factors for abdominal bloating and visible distention: a population-based study". Gut. 57 (6): 756–63. doi:10.1136/gut.2007.142810. PMC 2581929. PMID 18477677.
  12. Sandler RS, Stewart WF, Liberman JN, Ricci JA, Zorich NL (June 2000). "Abdominal pain, bloating, and diarrhea in the United States: prevalence and impact". Dig. Dis. Sci. 45 (6): 1166–71. doi:10.1023/a:1005554103531. PMID 10877233.
  13. Ho KY, Kang JY, Seow A (October 1998). "Prevalence of gastrointestinal symptoms in a multiracial Asian population, with particular reference to reflux-type symptoms". Am. J. Gastroenterol. 93 (10): 1816–22. doi:10.1111/j.1572-0241.1998.00526.x. PMID 9772037.


Template:Skin and subcutaneous tissue symptoms and signs Template:Nervous and musculoskeletal system symptoms and signs Template:Urinary system symptoms and signs Template:Cognition, perception, emotional state and behaviour symptoms and signs Template:Speech and voice symptoms and signs Template:General symptoms and signs


Template:WikiDoc Sources