THREE GI STOOGES: GAS, BAD BREATH, NAUSEA
| INTESTINAL GAS —John H. Bond, MD, Professor of Medicine, University of Minnesota, and Chief, Gastroenterology
Section, Veterans Affairs Medical Center, Minneapolis
|
| Gases in intestinal tract: 5 main gases, ie, nitrogen, oxygen, carbon dioxide, hydrogen, and methane; all odorless; noxious
gases present in small concentrations (not enough volume to cause symptoms other than aroma)
|
 | Source: oxygen and nitrogen come from swallowed air; oxygen absorbed quickly and utilized by mucosal cells as it passes
through gastrointestinal (GI) tract; nitrogen poorly absorbed and most passed as flatus; nitrogen also can diffuse into lumen
from blood; carbon dioxide believed to be produced in huge volumes by reaction of bicarbonate and fatty acids produced
during digestion; bacteria in colon make large amounts of carbon dioxide (probably not many symptoms because
absorbed rapidly and excreted by lungs, although during periods of high bacterial production, flatus contains large amount
of carbon dioxide); hydrogen produced by bacteria in colon in response to presence of fermentable carbohydrate; one
third of population have bacteria capable of producing methane, although unknown why (appears to be lifelong trait)
|
| Eliminating gas: can be eructated, passed as flatus, or absorbed into blood stream and excreted from lungs
|
| Repetitive eructation: not much more than nervous habit; patients aspirate air into upper esophagus during inspiration,
then blow it out with belch, often with loud noise; patients believe they are producing large volumes of gas and concerned
they have organic disease; treat by reassurance and education; show patients what they do by having them palpate neck just
before they belch so they can sense aspiration of air into esophagus; demonstration of cause of symptom usually enough
|
| Abdominal bloating: common complaint; probably part of irritable bowel syndrome (IBS); patients believe they have
large amount of gas in GI tract; clothes feel tight; patients usually able to convince their physicians that they are making
huge amounts of gas; may have associated changes in bowel movement pattern; study found that patients with functional
symptoms had symptoms despite presence of normal volumes of gas in GI tract (visceral hypersensitivity; characteristic
of IBS); no treatment that reduces gas effective; reassure patients and treat for IBS
|
| Excessive flatulence: may be real or imagined; patients come up with large numbers of complaints they believe related;
Australian study showed normal flatulence 12.7/day for men, 7.1/day for women; speaker’s study showed average of
14 to 15/day for men, 7/day for women
|
| Beans: contain low molecular weight carbohydrate made of short-chain saccharides that cannot be digested by human
small intestine; in colon, bacteria break down molecules, producing large amounts of gas; “fartless” pinto bean invented
but not successful because of poor consistency
|
| Other causes of gas: lactase deficiency (12.5 g of lactose can result in 4283 mL of hydrogen); whole wheat flour, oats,
corn, potatoes
|
| Treatment: eliminate or reduce number of complex carbohydrates ingested, eg, pastas and breads; neither simethicone nor
charcoal help symptoms; speaker gives patients list of high- and low-gas–producing foods and instructs them to reduce
number of foods on high-gas list and increase foods on low-gas list (almost always works)
|
| BAD BREATH, BAD TASTE, BURNING MOUTH, AND HICCUPS —Kirsten Tillisch, MD, Center for Neurovisceral
Science and Women’s Health, Division of Digestive Diseases, David Geffen School of Medicine at the University of California,
Los Angeles
|
| Bad breath: >25 million Americans have chronic daily halitosis; >$4 billion spent annually on various treatments, few of
which improve condition; leads to self-consciousness, decreased quality of life, decreased social interaction; important
to patients and should not be dismissed; common misconception that bad breath caused by gastric contents or gastroesophageal
reflux disease (GERD); >90% of cases have oral cause; traced to volatile sulfur compounds released by bacteria
breaking down amino acids from food debris trapped in dental plaque and by poor oral hygiene; categorized as
endogenous and exogenous
|
| Exogenous: usually transient; dry mouth—often caused by alcohol, short-term use of medications, tobacco use (decreases
salivary flow, leading to proliferation of bacteria and less washing out of bacteria from oropharynx; foods with
high sulfur content—eg, onions, garlic, dairy products; high doses of multivitamins
|
| Endogenous: chronic form; most sources oral, eg, gingivitis, oral abscesses, oral ulcers, concretions in tonsils; long-term
use of medications, eg, antidepressants, anticholinergic agents, antihistamines, diuretics (can decrease salivary flow and
worsen bad breath); bad breath in morning often due to drying of mouth during sleep and transient increase in bacteria;
systemic diseases, eg, postnasal drip, sinusitis, lung abscess, autoimmune disease, diverticulum in esophagus, achalasia,
bowel obstruction (rare); pseudohalitosis from psychologic causes (ie, patients who do not have bad breath but
concerned and convinced they do)
|
| Diagnosis: carefully assess for systemic disease; evaluate patient’s medications; consider GERD as cause; look in
oropharynx for abnormalities
|
| Treatment: oral hygiene; dietary advice; chlorhexidine mouthwash most effective; zinc mouthwashes suggested; referral
to dentist
|
| Bad taste: differential diagnosis similar to that of bad breath; medications most prominent cause (can cause bad taste, altered
taste, or lack of taste); GERD possible cause; psychogenic or hallucinatory bad taste
|
| Mechanisms by which medications alter taste: some decrease access to taste receptors (by drying oral mucosa or causing
swelling of taste pores); altering chemical environment or salivary content; acting as direct agonists or antagonists to
taste receptors; changes in membrane potential or neurotransmitter function; altered taste can occur immediately after
starting medications or weeks later; stopping medication may help but can take months before normal taste returns;
more common in older patients and those with lower body mass index
|
| Medications that can alter taste: antimicrobials (eg, metronidazole) most common; terbinafine (Lamisil; ≈3% of patients);
lipid-lowering agents; angiotensin-converting enzyme (ACE) inhibitors (eg, captopril has dose-related bitterness or sour
or salty taste in ≤7% of patients); antidepressant agents common offenders
|
| Diagnosis and management: similar to that of bad breath; perform oral examination; take careful drug history; discontinue
nonessential medications (warn patient that it may be some time before symptoms resolve); suspect GERD if bad
taste first thing in morning, after meals, or associated with regurgitation (trial of proton pump inhibitor [PPI] recommended);
treat dry mouth with artificial saliva preparations; mouthwash may or may not help; wait (studies show most
idiopathic dysgeusias resolve in ≈2 yr); reassurance
|
| Burning mouth syndrome: defined as unremitting oral burning in absence of detectable oral mucosal changes; may be
primary or secondary; associated with—vitamin B12 deficiency (rare disorder; usually associated with other symptoms
and laboratory abnormalities, particularly anemia); type 2 diabetes (controversial); infectious diseases (eg, early Candida
infection); epidemiology—more common in women (7:1) in middle age range; prevalence 1% to 15%; constant; often associated
with bad taste and/or subjective sense of dry mouth; lasts 3 to 6 mo; etiology—unknown; suspected etiologies include
local nerve trauma or neuritis, possibly caused by parafunctional habits, eg, bruxism, repeated cheek biting or tongue
thrusting or other abnormal mouth movements, eg, nervous tics; ill-fitting dentures; food allergies; psychogenic causes, eg,
comorbid depression or anxiety (some patients respond to antidepressants); not modulated by particular stresses
|
| Management: diagnose correctly; rule out secondary cause; examine mouth for visible lesions; evaluate dentures; reassure
patient; no good evidence for any treatments, although tricyclic antidepressants used most commonly; paroxetine
(selective serotonin receptor inhibitor [SSRI]) used; topical capsaicin (Capzasin) thought to be helpful
|
| Hiccups: thought to be mediated by vagal afferents, phrenic nerve efferents, and probably some sympathetic input as well;
can cause repeated spasm that can vary; usually transient but can become prolonged (rare; more common in older population);
can occur at any age; more common in men than women (5:1); most common in postsurgical and hospitalized patients,
and those with medical illness, particularly stroke
|
| Transient hiccups: associated with emotional stress; predisposing factors include alcohol, gastric distention, sudden excitement
or shock, change in temperature, esophageal distention (rare); self-limited; avoiding triggers relatively easy in
patients prone to recurrent hiccups
|
| Prolonged hiccups: risk factors include significant medical illness, metabolic problems, intrathoracic or intra-abdominal disease
(eg, pneumonias, abscesses, tumors in area of diaphragm); herpes zoster shown to cause hiccups in rare cases (improve
with antiviral therapy; tend to occur before skin lesions develop); associated with central nervous system (CNS)
disease (particularly stroke), intra-abdominal disease, and some drugs (eg, benzodiazepines, general anesthetics)
|
| Evaluation: obtain electrolytes, chest x-ray, abdominal film to look for excessive gastric distention
|
| Therapies: nonpharmacologic therapies that people try at home not studied or particularly helpful; placing nasogastric
tube helpful in some patients with or without gastric distention; chlorpromazine (Thorazine) or baclofen most commonly
used and best studied; small studies on omeprazole (Prilosec); cisapride; treat underlying disorder
|
| EVALUATION AND TREATMENT OF CHRONIC NAUSEA AND VOMITING —Richard W. McCallum, MD, Professor
of Medicine, University of Kansas Medical Center, and Director, Center for Gastrointestinal Nerve and Muscle Function,
Kansas City
|
| Anatomy and wiring of vomiting reflex
|
| Types of nausea: serotonin (5HT)-dominant (eg, patients with migraine); opioid-dominant (eg, patients on opioids and
narcotics); dopamine-driven (generic nausea), acetylcholine-driven; histamine-driven (as in diphenhydramine
[Benadryl]-sensitive patients), progesterone- driven (as in menstrual cycle fluctuations before periods), 5HT-driven (serotonin
released from enterochromaffin cells in gastroenteritis, anything that causes necrosis, irritation, eg, radiation); drug
induced (eg, chemotherapy, ipecac, digoxin; miscellaneous)
|
| Differential diagnosis: consider pregnancy; disorders that can present with nausea and vomiting include endocrine disorders
(eg, Addison’s disease), ophthalmologic problems (eg, glaucoma), middle ear infections, chemotherapy, cancer
(cachexia, paraneoplastic syndromes, centrally mediated tumors), angina; nausea and/or vomiting before patient gets out
of bed may be renal failure, intracranial tumor, pregnancy, gastroparesis, withdrawal from drugs
|
| Gastric physiology: for first 30 min after meal, food stored in proximal stomach and stomach distending, relaxing, and accommodating
through vagal nerve input; stomach triturates solid material at 3 cycles/min average until particles small
enough to be emptied into pylorus and duodenum; most mechanisms aimed at stopping stomach from emptying to give it
time to mix and grind food, eg, release of cholecystokinin (CCK), peptide YY (PYY); motility hormone (motilin) promotes
gastric emptying
|
| Patients feeling full, bloated and uncomfortable halfway through meal: endoscopy, biopsy, computed tomography
(CT), and ultrasonography negative; lack of accommodation—body of stomach and proximal fundus not relaxing
enough to allow food to rest in stomach; may be cause of nonulcer dyspepsia; gastric emptying may be normal;
must promote accomodation by relaxing proximal body and fundus of stomach with drug therapy, eg, buspirone (BuSpar),
amitriptyline (Elavil), tegaserod (Zelnorm); impairment of gastric electrical rhythm—eg, tachygastria, bradygastria;
electromechanical coupling lost and stomach paralyzed (nervous stomach); if this lasts long enough, result is
impaired motility and delayed gastric emptying; may have concomitant small bowel problem complicating picture
|
| Delayed gastric emptying: now have standardized meal and test to measure motility; diabetic patients most common;
idiopathic cases, perhaps caused by viral syndrome; postgastric surgery decreasing, but postfundoplication increasing;
pseudo-obstruction (eg, children with neurologic interference with small bowel or diffuse motility problem of muscle or
nerve); Parkinson’s disease; collagen vascular diseases (eg, scleroderma); anorexia; CNS disorders; paraneoplastic syndromes;
autonomic neuropathies
|
| Rumination syndrome: previously called psychogenic vomiting; most commonly missed diagnosis; patient vomits
within minutes of eating meal or drinking water and has failed all therapy; caused by reflex; also called conditioned vomiting;
treat with biofeedback, breathing techniques, diaphragmatic relaxation techniques, education, hypnosis, diet (small
meals, small volume, low fat)
|
| Diabetic patient with ketoacidosis and vomiting: treat with intravenous (IV) ketorolac
|
| Treatment: treat aggressively, using scopolamine patch, domperidone, or metoclopramide (Reglan); may use dronabinol
(Marinol); use ondansetron sparingly (for chemotherapy and radiation, not for day-to-day treatment of nausea and
vomiting); tricyclic antidepressants helpful in patients with cyclic vomiting syndrome; use metoclopramide for motility;
use domperidone for 25% of patients who cannot tolerate metoclopramide; low-dose erythromycin to stimulate
motilin receptor agonist; tegaserod 6 mg 3 to 4 times daily stimulates gastric motility
|
| Gastric neurostimulation: blocks nausea by high-frequency low-energy stimulation of nausea centers; Enterra device—
uses low-energy vibration (330 µsec); shown to reduce nausea and vomiting significantly for 12 mo; improves upper GI
symptoms, quality of life, and long-term morbidity problems; associated with reduction in hemoglobin (Hb)A1C in diabetics;
does not accelerate gastric emptying; reduces hospital stay
|
Educational Objectives
| The goal of this program is to educate the listener about intestinal gas, bad breath, bad taste, burning mouth syndrome, hiccups,
and nausea and vomiting. After hearing and assimilating this program, the clinician will be better able to:
|
| 1. Name the 5 gases found in the intestinal tract and describe their natural history inside the body.
|
| 2. List three common symptoms related to gas and explain their management.
|
| 3. Describe the etiology of bad breath and its treatment.
|
| 4. Explain the work-up and management of burning mouth syndrome and hiccups.
|
| 5. Discuss the treatment of chronic nausea and vomiting.
|
Discussed on This Program
Amitriptyline HCl [Elavil]
Baclofen [Lioresal, Lioresal Intrathecal]
Buspirone HCl [BuSpar]
Capsaicin (several trade names)
Captopril [Capoten]
Charcoal, activated [Actidose, CharcoAid, Liqui-Char]
Chlorpromazine HCl [Thorazine]
Cisapride [Propulsid]
Diphenhydramine HCl [Benadryl, others]
Domperidone [Motilium] (investigational)
Dronabinol [Marinol]
Erythromycin (several trade names)
Ketorolac tromethamine [Acular, Toradol]
Metoclopramide [Reglan, others]
Omeprazole [Prilosec, Rapinex]
Ondansetron HCl [Zofran]
Paroxetine HCl [Paxil]
Scopolamine HBr (hyoscine HBr) [Isopto Hyoscine, Scopace]
Simethicone (several trade names)
Tegaserod maleate [Zelnorm]
Terbinafine HCl [DesenesMax, Lamisil]
Suggested Reading
Buchanan J et al: Burning mouth syndrome. Clin Evid 12:1899, 2004; Furne JK et al: Factors influencing frequency
of flatus emission by healthy subjects. Dig Dis Sci 41:1631, 1996; Olden KW et al: Chronic nausea and vomiting:
new insights and approach to treatment. Curr Treat Options Gastroenterol 8:305, 2005; Pollack MJ: Intractable
hiccups: a serious sign of underlying systemic disease. J Clin Gastroenterol 37:272, 2003; Quirynen M et al: The efficacy
of amine fluoride/stannous fluoride in the suppression of morning breath odour. J Clin Periodontol 29:944, 2002;
Sanjay S et al: Baclofen in the treatment of intractable hiccups. J Assoc Physicians India 51:324, 2003; Smith HS et
al: Management of hiccups in the palliative care population. Am J Hosp Palliat Care 20:149, 2003; Suarez F et al: Differentiation
of mouth versus gut as site of origin of odoriferous breath gases after garlic ingestion. Am J Physiol 276:G425,
1999; Suarez F et al: Insights into human colonic physiology obtained from the study of flatus composition. Am J Physiol
272:G1028, 1997; Suarez FL et al: An understanding of excessive intestinal gas. Curr Gastroenterol Rep 2:413,
2000; Suarez FL et al: Identification of gases responsible for the odour of human flatus and evaluation of a device purported
to reduce this odour. Gut 43:100, 1998; van Steenberghe D et al: Effect of different mouth rinses on morning
breath. J Periodontol 72:1183, 2001.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. For this issue, Dr. Tillisch
reports all recommended drugs for symptoms discussed are off-label uses; Dr. McCallum reports interest in Novartis Pharmaceuticals
Corp., Medtronic Inc., research support from Janssen Pharmaceutical, and some off-label use of drugs.
Drs. Bond, Tillisch, and McCallum were recorded February 19-20, 2005, in Beverly Hills, California, at Gastroenterology
and Hepatology for the Primary Care Physician, sponsored by the David Geffen School of Medicine at the University
of California, Los Angeles, Division of Digestive Diseases, and the Office of Continuing Medical Education.
The Audio-Digest Foundation thanks the speakers and the sponsor for their cooperation in the production of this program.
|
