Bloating

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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 bloating.

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

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. 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

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, non absorbable 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 typically has a diurnal pattern and It may accompany the intake of certain foods and can often be followed by prolonged burping or flattening.   Patients may complain of worsening symptoms as the day continues, 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

  • 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

Fasting Cortisol Levels

Antinuclear antibodies and Scleroderma antibodies

To evaluate for collagen vascular disease

Antinuclear neuronal antibodies

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

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. 10.0 10.1 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. 11.0 11.1 Hasler WL (September 2006). "Gas and Bloating". Gastroenterol Hepatol (N Y). 2 (9): 654–662. PMC 5350578. PMID 28316536.
  12. 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.
  13. 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.
  14. 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.
  15. 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.
  16. 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.


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