Bloating
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Ibtisam Ashraf, M.B.B.S.[2]
Synonyms and keywords: Post-prandial abdominal fullness
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. Bloating also results from irritable bowel syndrome, gastroparesis, small intestinal bacterial overgrowth 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]
- Nongaseous form of bloating was first described by Sir James Y. Simpson. [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 bloating.
Pathophysiology
Abnormal Gut Microbiota
There is a relationship between the types of gas produced by colonic microflora and bloating. The role of methanogenic flora has always been in question when the pathogenesis of bloating is discussed. During the experiments involving the ingestion of sorbitol and fiber, it was determined that there was a significant increase in bloating in individuals with low producers of methane vs high producers. [5]
Small Intestinal Bacterial Overgrowth
Bacterial fermentation and the subsequent gas production is the potential cause of bloating in patients with irritable bowel syndrome.[6]
Intestinal Gas Accumulation
Increase levels of intestinal gas has been linked with bloating. After consuming a large meal there is 65% increase in postprandial gas volume in pelvic colon, where as during fasting, GI tract produces about 100ml of gas which spreads between liver, small intestine, ascending colon, transverse colon, descending colon, and distal (pelvic) colon.[7]
Altered Gut Motility
Gut motility is affected in many disorders mainly labeled as Intestinal dysmotility. It affects the evacuation of excessive gas produced in the GI tract during fasting as well as post-prandial.
Abnormal Abdominal-diaphragmatic Reflexes
Mechanism which leads to bloating are not well understood but studies have shown a role of abdominal-diaphragmatic reflexes, which are involves the combination of increase in the anterior wall tone and diaphragm relaxation. These reflexes are abnormal in individuals with bloating.[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 induces alteration of gut motility and increases bacterial fermentation.
Causes
The most common cause of bloating is Constipation, Pregnancy, IBS, Celiac disease, Lactose, fructose, and other carbohydrates intolerance, Pancreatic insufficiency, Gastroparesis, Diabetes mellitus, Hypothyroidism, Scleroderma, Chronic idiopathic pseudo-obstruction, Small bowel bacterial overgrowth, Acute gastroenteritis, Gastric malignancy, Ovarian malignancy, and Ascites.[10]
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.[11]
Epidemiology and Demographics
- In the USA, 15-30% of the general population has been reported to experience bloating.[12]
- A telephone survey reported a prevalence of 16% in US adults who were asked about bloating or distention during the last month.[13]
- Women were more likely than men to report bloating.[12]
- There is no racial predilection to bloating.[14]
Risk Factors
Risk factors include chewing gum, hard candy, and carbonated beverages such as soda or beer. 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
The sensation of abdominal bloating is often attributed to excessive gas in patients. However, the relationship between the volume of intestinal gas and the effects is not clear. Patients with chronic complaints of bloating and distension have heightened sensitivity to gaseous distension or exaggerated motor response to normal amounts of gas. Pains that are due to bloating will feel sharp and cause the stomach to cramp. These pains may occur anywhere in the body and can change locations quickly.
Bloating is typically benign, although it can be due to severe conditions such as intestinal obstruction and malignancy.
Patients with mild functional bloating may need merely reassurance that the condition is benign. [10]
Diagnosis
Diagnostic Study of Choice
Rome IV criteria for establishing the diagnosis of functional bloating include both of the following (for at least three months with symptom onset at least six months prior to diagnosis).[15]
●Recurrent bloating or distension, on average, at least one day per week; abdominal bloating and/or distension predominates over other symptoms
●Insufficient criteria for a diagnosis of IBS, functional constipation, functional diarrhea, or postprandial distress syndrome
History and Symptoms
History includes the onset of symptoms, the relationship to diet (eg, wheat, dairy, fructose, fiber, nonabsorbable sugars) diurnal variation, and the presence of symptoms suggestive of other functional gastrointestinal disorders, including constipation, diarrhea, and abdominal pain or postprandial fullness. Functional bloating usually have a diurnal pattern which may accompany the consumption of such foods, frequently accompanied by excessive burping or flattening. Patients may complain about deteriorating symptoms as the day progresses, particularly after meals, but they may be relieved overnight.[16]
Physical Examination
Common physical examination findings of bloating include abdominal distention with or without altered bowel sounds. However, if occult fecal blood, cutaneous findings (sclerodactyly with scleroderma, dermatitis herpetiformis in celiac disease), peripheral or autonomic neuropathy, cachexia, jaundice, or palpable masses is present then it suggests underlying organic disease. [11]
Laboratory Findings
Complete blood count
To evaluate for anemia
Serologies for Celiac Sprue[17]
- anti-tissue transglutaminase (tTG) antibodies
- endomysial antibodies (EMA)
- deamidated gliadin peptide (DGP) antibodies
Hydrogen Breath Test
For the evaluation of small intestinal bacterial overgrowth and lactose intolerance.
Thyroid Function tests[18]
Fasting Cortisol Levels[19]
Antinuclear antibodies and Scleroderma antibodies[20]
To evaluate for collagen vascular disease
Antinuclear neuronal antibodies[21]
To screen for paraneoplastic visceral neuropathy
Stool analysis
Antigen testing for Giardia
Electrocardiogram
There are no ECG findings associated with bloating.
X-ray
An abdominal x-ray may be helpful to rule out intestinal obstruction.
Echocardiography or Ultrasound
Abdominal/Pelvic Ultrasound to look for ascites and rule out ovarian cancer.
CT scan
There are no CT scan findings associated with bloating. However, it can be used to rule out intestinal obstruction.
MRI
There are no MRI findings associated with bloating.
Other Imaging Findings
Upper GI Endoscopy
The presence of alarm features including weight loss, abdominal pain, dysphagia, heartburn, and regurgitation are an indication for a diagnostic evaluation with upper endoscopy.
Other Diagnostic Studies
There are no other diagnostic studies associated with bloating.
Treatment
Medical Therapy
Education, treatment of associated disorders, and behavioral therapy
Management requires instruction to minimize air swallowing and reassurance that belching is a benign condition. Relevant behavioural interventions include the avoidance of gum chewing, smoking, consuming carbonated drinks, and gulping of food and liquids. Treatment should be started in people with persistent depression or anxiety.[22] Patients with co-existing acid reflux may need an acid reduction treatment for the control of GERD.
Effective management with excessive belching by a therapist (e.g. cognitive behavioral therapy or speech therapist)[23] with specific experience of diaphragmatic relaxation exercises has been linked with a decrease of symptoms. Diaphragmatic breathing decreases postprandial intragastric pressure and raises the pressure of the esophagogastric junction region, restoring the gradient of the gastroesophageal pressure.
Reflux inhibitors for refractory symptoms
Baclofen 10 mg three times daily can be prescribed to reduce transient lower esophageal sphincter relaxations and centrally suppress the swallowing rate, and may decrease both supragastric and gastric belching.[24]
| Abdominal Bloating and Distension [10] | |||||||||||||||||||||||||||||||||
| Evaluate for: ●Alarm Signs ●Overlapping FGID (FG,FD,IBS) ●Bacterial Overgrowth ●Dietary Intolerance Celiac Disease ●Recent Weight Gain Constipation ●Psychological disorder | |||||||||||||||||||||||||||||||||
| No | Yes | ||||||||||||||||||||||||||||||||
| ●Reassurance ●Recommend Diaphragmatic Breathing ●Diet Intervention: Low FODMAP diet ●Symptomatic medical therapy: Peppermint oil, Simethicone etc | Treat Accordingly | ||||||||||||||||||||||||||||||||
| No Response | |||||||||||||||||||||||||||||||||
| ●Trial of Rifixamin/Probiotics | |||||||||||||||||||||||||||||||||
| No Response | |||||||||||||||||||||||||||||||||
| ●Antidepressants ●Psychological therapy ●Hypnotherapy, CBT | |||||||||||||||||||||||||||||||||
| No Response | |||||||||||||||||||||||||||||||||
| ●Refer to Neurogastroenterology center ●Refer to CT or MRI Electromyography ●Refer to Abdominal Biofeedback therapy | |||||||||||||||||||||||||||||||||
Surgery
Surgical intervention is not recommended for the management of bloating.
Primary Prevention
There are no established measures for the primary prevention of bloating.
Secondary Prevention
There are no established measures for the secondary prevention of bloating.
References
- ↑ 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.
- ↑ 2.0 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.
- ↑ 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.
- ↑ "February 1887 - Volume 14 - Issue 2 : The Journal of Nervous and Mental Disease".
- ↑ 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.
- ↑ 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.
- ↑ "Sleisenger and Fordtran's Gastrointestinal and Liver Disease- 2 Volume Set - 9th Edition".
- ↑ 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.
- ↑ 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.
- ↑ 10.0 10.1 10.2 Mari A, Abu Backer F, Mahamid M, Amara H, Carter D, Boltin D, Dickman R (May 2019). "Bloating and Abdominal Distension: Clinical Approach and Management". Adv Ther. 36 (5): 1075–1084. doi:10.1007/s12325-019-00924-7. PMC 6824367 Check
|pmc=value (help). PMID 30879252. - ↑ 11.0 11.1 Hasler WL (September 2006). "Gas and Bloating". Gastroenterol Hepatol (N Y). 2 (9): 654–662. PMC 5350578. PMID 28316536.
- ↑ 12.0 12.1 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.
- ↑ 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.
- ↑ 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.
- ↑ Mearin F, Lacy BE, Chang L, Chey WD, Lembo AJ, Simren M, Spiller R (February 2016). "Bowel Disorders". Gastroenterology. doi:10.1053/j.gastro.2016.02.031. PMID 27144627.
- ↑ Tack J, Talley NJ, Camilleri M, Holtmann G, Hu P, Malagelada JR, Stanghellini V (April 2006). "Functional gastroduodenal disorders". Gastroenterology. 130 (5): 1466–79. doi:10.1053/j.gastro.2005.11.059. PMID 16678560.
- ↑ Mari A, Abu Backer F, Mahamid M, Amara H, Carter D, Boltin D, Dickman R (May 2019). "Bloating and Abdominal Distension: Clinical Approach and Management". Adv Ther. 36 (5): 1075–1084. doi:10.1007/s12325-019-00924-7. PMC 6824367 Check
|pmc=value (help). PMID 30879252. - ↑ Mari A, Abu Backer F, Mahamid M, Amara H, Carter D, Boltin D, Dickman R (May 2019). "Bloating and Abdominal Distension: Clinical Approach and Management". Adv Ther. 36 (5): 1075–1084. doi:10.1007/s12325-019-00924-7. PMC 6824367 Check
|pmc=value (help). PMID 30879252. - ↑ Mari A, Abu Backer F, Mahamid M, Amara H, Carter D, Boltin D, Dickman R (May 2019). "Bloating and Abdominal Distension: Clinical Approach and Management". Adv Ther. 36 (5): 1075–1084. doi:10.1007/s12325-019-00924-7. PMC 6824367 Check
|pmc=value (help). PMID 30879252. - ↑ Mari A, Abu Backer F, Mahamid M, Amara H, Carter D, Boltin D, Dickman R (May 2019). "Bloating and Abdominal Distension: Clinical Approach and Management". Adv Ther. 36 (5): 1075–1084. doi:10.1007/s12325-019-00924-7. PMC 6824367 Check
|pmc=value (help). PMID 30879252. - ↑ Mari A, Abu Backer F, Mahamid M, Amara H, Carter D, Boltin D, Dickman R (May 2019). "Bloating and Abdominal Distension: Clinical Approach and Management". Adv Ther. 36 (5): 1075–1084. doi:10.1007/s12325-019-00924-7. PMC 6824367 Check
|pmc=value (help). PMID 30879252. - ↑ Disney B, Trudgill N (April 2014). "Managing a patient with excessive belching". Frontline Gastroenterol. 5 (2): 79–83. doi:10.1136/flgastro-2013-100355. PMC 5369716. PMID 28839757.
- ↑ Hemmink GJ, Ten Cate L, Bredenoord AJ, Timmer R, Weusten BL, Smout AJ (January 2010). "Speech therapy in patients with excessive supragastric belching--a pilot study". Neurogastroenterol. Motil. 22 (1): 24–8, e2–3. doi:10.1111/j.1365-2982.2009.01371.x. PMID 19650772.
- ↑ Blondeau K, Boecxstaens V, Rommel N, Farré R, Depeyper S, Holvoet L, Boeckxstaens G, Tack JF (April 2012). "Baclofen improves symptoms and reduces postprandial flow events in patients with rumination and supragastric belching". Clin. Gastroenterol. Hepatol. 10 (4): 379–84. doi:10.1016/j.cgh.2011.10.042. PMID 22079512.
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