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Is Tonsillectomy a Possible Treatment for IgA Nephropathy from Randomized Controlled Trial (RCT)? The most common causes of indigestion are gastroesophageal reflux and functional dyspepsia.
Other Factors Helicobacter pylori has a clear etiologic role in peptic ulcer disease, but ulcers cause a minority of dyspepsia cases. Dyspeptic patients typically report symptoms referable to the upper abdomen that may be meal-related, as with postprandial distress syndrome, or independent of food ingestion, as in epigastric pain syndrome. Discriminating functional and organic causes of indigestion mandates excluding certain historic and exam features. Because indigestion is prevalent and most cases result from GERD or functional dyspepsia, a general principle is to perform only limited and directed diagnostic testing of selected individuals. Once alarm factors are excluded (Table 54-3), patients with typical GERD do not need further evaluation and are treated empirically.
Upper endoscopy is recommended as the initial test in patients with unexplained dyspepsia who are >55 years old or who have alarm factors because of the purported elevated risks of malignancy and ulcer in these groups. For mild indigestion, reassurance that a careful evaluation revealed no serious organic disease may be the only intervention needed. Antacids are useful for short-term control of mild GERD but have less benefit in severe cases unless given at high doses that cause side effects (diarrhea and constipation with magnesium- and aluminum-containing agents, respectively).
Prokinetics like metoclopramide, erythromycin, and domperidone have limited utility in GERD.
Antireflux surgery (fundoplication) to increase LES pressure may be offered to GERD patients who are young and require lifelong therapy, have typical heartburn and regurgitation, are responsive to PPIs, and show evidence of acid reflux on pH monitoring. Some patients with functional heartburn and functional dyspepsia refractory to standard therapies may respond to antidepressants in tricyclic and selective serotonin reuptake inhibitor classes, although studies are limited. Diarrhea and constipation are exceedingly common and, together, exact an enormous toll in terms of mortality, morbidity, social inconvenience, loss of work productivity, and consumption of medical resources. Constipation, by contrast, is rarely associated with mortality and is exceedingly common in developed countries, leading to frequent self-medication and, in a third of those, to medical consultation. Although diarrhea and constipation may present as mere nuisance symptoms at one extreme, they can be severe or life-threatening at the other. While the primary function of the small intestine is the digestion and assimilation of nutrients from food, the small intestine and colon together perform important functions that regulate the secretion and absorption of water and electrolytes, the storage and subsequent transport of intraluminal contents aborally, and the salvage of some nutrients that are not absorbed in the small intestine after bacterial metabolism of carbohydrate allows salvage of short-chain fatty acids. The extrinsic innervations of the small intestine and colon are part of the autonomic nervous system and also modulate motor and secretory functions.
During the fasting period, the motility of the small intestine is characterized by a cyclical event called the migrating motor complex (MMC), which serves to clear nondigestible residue from the small intestine (the intestinal “housekeeper”). Colonic tone refers to the background contractility upon which phasic contractile activity (typically contractions lasting <15 s) is superimposed. After meal ingestion, colonic phasic and tonic contractility increase for a period of ~2 h.
Tonic contraction of the puborectalis muscle, which forms a sling around the rectoanal junction, is important to maintain continence; during defecation, sacral parasympathetic nerves relax this muscle, facilitating the straightening of the rectoanal angle (Fig.
Diarrhea is loosely defined as passage of abnormally liquid or unformed stools at an increased frequency. More than 90% of cases of acute diarrhea are caused by infectious agents; these cases are often accompanied by vomiting, fever, and abdominal pain.
The pathophysiology underlying acute diarrhea by infectious agents produces specific clinical features that may also be helpful in diagnosis (Table 55-2).
The decision to evaluate acute diarrhea depends on its severity and duration and on various host factors (Fig. The cornerstone of diagnosis in those suspected of severe acute infectious diarrhea is microbiologic analysis of the stool. Structural examination by sigmoidoscopy, colonoscopy, or abdominal computed tomography (CT) scanning (or other imaging approaches) may be appropriate in patients with uncharacterized persistent diarrhea to exclude IBD or as an initial approach in patients with suspected noninfectious acute diarrhea such as might be caused by ischemic colitis, diverticulitis, or partial bowel obstruction.
Fluid and electrolyte replacement are of central importance to all forms of acute diarrhea. In moderately severe nonfebrile and nonbloody diarrhea, antimotility and antisecretory agents such as loperamide can be useful adjuncts to control symptoms. Judicious use of antibiotics is appropriate in selected instances of acute diarrhea and may reduce its severity and duration (Fig.
5-HT3 antagonists such as ondansetron and granisetron can prevent postoperative vomiting, radiation therapy–induced symptoms, and cancer chemotherapy–induced emesis, but also are used for other causes of emesis with limited evidence for efficacy.
Metoclopramide, a combined 5-HT4 agonist and D2 antagonist, is effective in gastroparesis, but antidopaminergic side effects, such as dystonias and mood and sleep disturbances, limit use in ~25% of cases. Intestinal pseudoobstruction may respond to the somatostatin analogue octreotide, which induces propagative small-intestinal motor complexes.
Centrally acting antidopaminergics, especially metoclopramide, can cause irreversible movement disorders such as tardive dyskinesia, particularly in older patients. Prophylaxis with tricyclic antidepressants, cyproheptadine, or ?-adrenoceptor antagonists can reduce the severity and frequency of attacks.
Reduced lower esophageal sphincter (LES) tone contributes to reflux in scleroderma and pregnancy and may be a factor in some patients without systemic illness.
Visceral hypersensitivity was first reported in IBS with demonstration of heightened perception of rectal balloon inflation without changes in compliance.
Functional dyspepsia, the cause of symptoms in >60% of dyspeptic patients, is defined as ?3 months of bothersome postprandial fullness, early satiety, or epigastric pain or burning with symptom onset at least 6 months before diagnosis in the absence of organic cause. Esophageal squamous cell carcinoma occurs most often with long-standing tobacco or ethanol intake. Other causes of esophageal inflammation include eosinophilic esophagitis and pill esophagitis.
Functional dyspepsia overlaps with other disorders including GERD, IBS, and idiopathic gastroparesis. Upper endoscopy is indicated to exclude mucosal injury in cases with atypical symptoms, symptoms unresponsive to acid suppression, or alarm factors. However, endoscopic findings in unexplained dyspepsia include erosive esophagitis in 13%, peptic ulcer in 8%, and gastric or esophageal malignancy in only 0.3%. Surgery is appropriate for biliary colic, whereas diet changes are indicated for lactase deficiency or celiac disease. Histamine H2 antagonists like cimetidine, ranitidine, famotidine, and nizatidine are useful in mild to moderate GERD. Alginic acid combined with antacids forms a floating barrier to reflux in patients with upright symptoms. The ?-aminobutyric acid B (GABA-B) agonist baclofen reduces esophageal exposure to acid and nonacidic fluids by reducing TLESRs by 40%; this drug is proposed for refractory acid and nonacid reflux. Worldwide, >1 billion individuals suffer one or more episodes of acute diarrhea each year. Population statistics on chronic diarrhea and constipation are more uncertain, perhaps due to variable definitions and reporting, but the frequency of these conditions is also high.
Even mild symptoms may signal a serious underlying gastrointestinal lesion, such as colorectal cancer, or systemic disorder, such as thyroid disease. The intrinsic innervation, also called the enteric nervous system, comprises myenteric, submucosal, and mucosal neuronal layers. The parasympathetic nerves convey visceral sensory pathways from and excitatory pathways to the small intestine and colon. This organized, propagated series of contractions lasts, on average, 4 min, occurs every 60–90 min, and usually involves the entire small intestine. However, short duration or phasic contractions mix colonic contents, and high-amplitude (>75 mmHg) propagated contractions (HAPCs) are sometimes associated with mass movements through the colon and normally occur approximately five times per day, usually on awakening in the morning and postprandially. It is an important cofactor in the colon’s capacitance (volume accommodation) and sensation.
The initial phase (~10 min) is mediated by the vagus nerve in response to mechanical distention of the stomach.
Continence is maintained by normal rectal sensation and tonic contraction of the internal anal sphincter and the puborectalis muscle, which wraps around the anorectum, maintaining an anorectal angle between 80° and 110°. Pseudodiarrhea, or the frequent passage of small volumes of stool, is often associated with rectal urgency, tenesmus, or a feeling of incomplete evacuation, and accompanies IBS or proctitis. The remaining 10% or so are caused by medications, toxic ingestions, ischemia, food indiscretions, and other conditions. In the immunocompetent person, the resident fecal microflora, containing >500 taxonomically distinct species, are rarely the source of diarrhea and may actually play a role in suppressing the growth of ingested pathogens. Profuse, watery diarrhea secondary to small-bowel hypersecretion occurs with ingestion of preformed bacterial toxins, enterotoxin-producing bacteria, and enteroadherent pathogens. Reactive arthritis (formerly known as Reiter’s syndrome), arthritis, urethritis, and conjunctivitis may accompany or follow infections by Salmonella, Campylobacter, Shigella, and Yersinia. Although innumerable medications may produce diarrhea, some of the more frequently incriminated include antibiotics, cardiac antidysrhythmics, antihypertensives, nonsteroidal anti-inflammatory drugs (NSAIDs), certain antidepressants, chemotherapeutic agents, bronchodilators, antacids, and laxatives. Consider empirical treatment before evaluation with (*) metronidazole and with (†) quinolone.
Workup includes cultures for bacterial and viral pathogens, direct inspection for ova and parasites, and immunoassays for certain bacterial toxins (C.
Such agents should be avoided with febrile dysentery, which may be exacerbated or prolonged by them. Asian countries,[18] United States (including Hawaii), Canada ,[19] and Scotland)[20] due to bacterial resistance. Tricyclic antidepressant agents provide symptomatic benefit in patients with chronic idiopathic nausea and functional vomiting as well as in long-standing diabetic patients with nausea and vomiting. Erythromycin increases gastroduodenal motility by action on receptors for motilin, an endogenous stimulant of fasting motor activity. Acetylcholinesterase inhibitors such as pyridostigmine are also observed to benefit some patients with small-bowel dysmotility. Combining a 5-HT3 antagonist, an NK1 antagonist, and a glucocorticoid provides significant control of both acute and delayed vomiting after highly emetogenic chemotherapy. Intravenous 5-HT3 antagonists combined with the sedating effects of a benzodiazepine like lorazepam are a mainstay of treatment of acute flares.
Others exhibit frequent transient LES relaxations (TLESRs) that cause bathing of the esophagus by acid or nonacidic fluid. Similarly, ~35% of dyspeptic patients note discomfort with fundic distention to lower pressures than healthy controls.
Most cases of heartburn occur because of excess acid reflux, but reflux of nonacidic fluid produces similar symptoms. Functional dyspepsia is subdivided into postprandial distress syndrome, characterized by meal-induced fullness, early satiety, and discomfort, and epigastric pain syndrome, which presents with epigastric burning pain unrelated to meals. Other risks include prior caustic ingestion, achalasia, and the hereditary disorder tylosis.


Biliary colic is in the differential diagnosis of unexplained upper abdominal pain, but most patients with biliary colic report discrete acute episodes of right upper quadrant or epigastric pain rather than the chronic burning, discomfort, and fullness of dyspepsia. Management of patients <55 years old without alarm factors depends on the local prevalence of H. Thyroid chemistries or calcium levels screen for metabolic disease, whereas specific serologies may suggest celiac disease. Patients with GERD should limit ethanol, caffeine, chocolate, and tobacco use due to their effects on the LES.
For severe symptoms or for many cases of erosive or ulcerative esophagitis, PPIs such as omeprazole, lansoprazole, rabeprazole, pantoprazole, esomeprazole, or dexlansoprazole are needed. H2 antagonists also reportedly improve symptoms in functional dyspepsia; however, findings of trials of this drug class likely are influenced by inclusion of large numbers of GERD patients. Sucralfate, a salt of aluminum hydroxide and sucrose octasulfate that buffers acid and binds pepsin and bile salts, shows efficacy in GERD similar to H2 antagonists.
The utility of eradication therapy in functional dyspepsia is limited, although some cases (particularly with the epigastric pain syndrome subtype) relate to this infection. Several studies have promoted the efficacy of motor-stimulating drugs in functional dyspepsia, but publication bias and small sample sizes raise questions about reported benefits of these agents. Individuals who respond less well to fundoplication include those with atypical symptoms or who have esophageal body motor disturbances.
Gas and bloating are among the most troubling symptoms in some patients with indigestion and can be difficult to treat. Among the 100 million persons affected annually by acute diarrhea in the United States, nearly half must restrict activities, 10% consult physicians, ~250,000 require hospitalization, and ~5000 die (primarily the elderly). United States population surveys put prevalence rates for chronic diarrhea at 2–7% and for chronic constipation at 12–19%, with women being affected twice as often as men. Given the heterogeneous causes and potential severity of these common complaints, it is imperative for clinicians to appreciate the pathophysiology, etiologic classification, diagnostic strategies, and principles of management of diarrhea and constipation, so that rational and cost-effective care can be delivered. The function of these layers is modulated by interneurons through the actions of neurotransmitter amines or peptides, including acetylcholine, vasoactive intestinal peptide (VIP), opioids, norepinephrine, serotonin, adenosine triphosphate (ATP), and nitric oxide (NO). Parasympathetic fibers via the vagus nerve reach the small intestine and proximal colon along the branches of the superior mesenteric artery. Thus, the colon can partially compensate for excess fluid delivery to the colon that may result from intestinal absorptive or secretory disorders. Glucose then exits the basal membrane through a specific transport protein, GLUT-5, creating a glucose concentration gradient between the lumen and the intercellular space, drawing water and electrolytes passively from the lumen. After food ingestion, the small intestine produces irregular, mixing contractions of relatively low amplitude, except in the distal ileum where more powerful contractions occur intermittently and empty the ileum by bolus transfers. Segmentation by haustra compartmentalizes the colon and facilitates mixing, retention of residue, and formation of solid stools.
Distention of the rectum results in transient relaxation of the internal anal sphincter via intrinsic and reflex sympathetic innervation. During defecation, the pelvic floor muscles (including the puborectalis) relax, allowing the anorectal angle to straighten by at least 15°, and the perineum descends by 1–3.5 cm.
Fecal incontinence is the involuntary discharge of rectal contents and is most often caused by neuromuscular disorders or structural anorectal problems.
Disturbances of flora by antibiotics can lead to diarrhea by reducing the digestive function or by allowing the overgrowth of pathogens, such as Clostridium difficile (Chap. Nearly 40% of tourists to endemic regions of Latin America, Africa, and Asia develop so-called traveler’s diarrhea, most commonly due to enterotoxigenic or enteroaggregative Escherichia coli as well as to Campylobacter, Shigella, Aeromonas, norovirus, Coronavirus, and Salmonella. Diarrhea closely following food consumption at a picnic, banquet, or restaurant may suggest infection with Salmonella, Campylobacter, or Shigella from chicken; enterohemorrhagic E. Infections with Shigella, Giardia, Cryptosporidium, rotavirus, and other agents are very common and should be considered.
Infectious diarrhea is one of the most frequent categories of nosocomial infections in many hospitals and long-term care facilities; the causes are a variety of microorganisms but most commonly C. Diarrhea associated with marked vomiting and minimal or no fever may occur abruptly within a few hours after ingestion of the former two types; vomiting is usually less, abdominal cramping or bloating is greater, and fever is higher with the latter. Yersiniosis may also lead to an autoimmune-type thyroiditis, pericarditis, and glomerulonephritis. Most episodes of acute diarrhea are mild and self-limited and do not justify the cost and potential morbidity rate of diagnostic or pharmacologic interventions. Oral sugar-electrolyte solutions (iso-osmolar sport drinks or designed formulations) should be instituted promptly with severe diarrhea to limit dehydration, which is the major cause of death.
Bismuth subsalicylate may reduce symptoms of vomiting and diarrhea but should not be used to treat immunocompromised patients or those with renal impairment because of the risk of bismuth encephalopathy. Many physicians treat moderately to severely ill patients with febrile dysentery empirically without diagnostic evaluation using a quinolone, such as ciprofloxacin (500 mg bid for 3–5 d). The classification of chronic diarrhea by pathophysiologic mechanism facilitates a rational approach to management, although many diseases cause diarrhea by more than one mechanism (Table 55-3).
Other antidepressants such as mirtazapine and olanzapine also may exhibit antiemetic effects.
Intravenous erythromycin is useful for inpatients with refractory gastroparesis, but oral forms have some utility. Pyloric injections of botulinum toxin are reported in uncontrolled studies to reduce gastroparesis symptoms, but small controlled trials observe benefits no greater than sham treatments. Some agents with antiemetic properties including domperidone, erythromycin, tricyclics, and 5-HT3 antagonists can induce dangerous cardiac rhythm disturbances, especially in those with QTc interval prolongation on electrocardiography (ECG). Unlike other drugs in the same class, the 5-HT3 antagonist palonosetron exhibits efficacy at preventing delayed chemotherapy-induced vomiting. Antihistamines such as meclizine and doxylamine, antidopaminergics such as prochlorperazine, and antiserotonergics such as ondansetron demonstrate limited efficacy. Small studies report benefits with antimigraine agents, including the 5-HT1 agonist sumatriptan, as well as selected anticonvulsants such as zonisamide and levetiracetam.
Overeating and aerophagia override the barrier function of the LES, whereas reductions in esophageal body motility or salivary secretion prolong fluid exposure. The relation of these defects to symptom induction is uncertain; studies show poor correlation between symptom severity and degrees of motor dysfunction.
Others with dyspepsia exhibit hypersensitivity to chemical stimulation with capsaicin or with acid or lipid exposure in the duodenum. Functional dyspepsia is associated with chronic fatigue, produces reduced physical and mental well-being, and is exacerbated by stress. Alkaline reflux esophagitis produces GERD-like symptoms most often in patients who have had surgery for peptic ulcer disease. Twenty percent of patients with gastroparesis report a predominance of pain or discomfort rather than nausea and vomiting.
Associated symptoms include regurgitation of acid or nonacidic fluid and water brash, the reflex release of salty salivary secretions into the mouth. Other alarm features include unexplained weight loss, recurrent vomiting, occult or gross bleeding, jaundice, palpable mass or adenopathy, and a family history of gastrointestinal neoplasm.
The benefits and cost-effectiveness of this approach have not been validated in controlled studies. Other measures in GERD include ingesting a low-fat diet, avoiding snacks before bedtime, and elevating the head of the bed. However, because most indigestion is caused by GERD or functional dyspepsia, medications that reduce gastric acid, modulate motility, or blunt gastric sensitivity are used. A meta-analysis of 18 controlled trials calculated a relative risk reduction of 10%, with a 95% confidence interval of 6–14%, favoring H. Some clinicians suggest that patients with the postprandial distress subtype may respond preferentially to prokinetic drugs.
Dysphagia, gas-bloat syndrome, and gastroparesis are long-term complications of these procedures; ~60% develop recurrent GERD symptoms over time. Dietary exclusion of gas-producing foods such as legumes and use of simethicone or activated charcoal provide benefits in some cases. Diarrhea and constipation are among the most common patient complaints presenting to internists and primary care physicians, and they account for nearly 50% of referrals to gastroenterologists. Alterations in motor and sensory functions of the colon result in highly prevalent syndromes such as irritable bowel syndrome (IBS), chronic diarrhea, and chronic constipation. The myenteric plexus regulates smooth-muscle function through intermediary pacemaker-like cells called the interstitial cells of Cajal, and the submucosal plexus affects secretion, absorption, and mucosal blood flow. The distal colon is supplied by sacral parasympathetic nerves (S2–4) via the pelvic plexus; these fibers course through the wall of the colon as ascending intracolonic fibers as far as, and in some instances including, the proximal colon. A variety of neural and nonneural mediators regulate colonic fluid and electrolyte balance, including cholinergic, adrenergic, and serotonergic mediators. There is increased appreciation of the intimate interaction between the colonic function and the luminal ecology. The predominant phasic contractions in the colon are irregular and non-propagated and serve a “mixing” function. As sigmoid and rectal contractions, as well as straining (Valsalva maneuver), which increases intraabdominal pressure, increase the pressure within the rectum, the rectosigmoid angle opens by >15°. Common enteric pathogens often cause a more severe and protracted diarrheal illness, and, particularly in persons with AIDS, opportunistic infections, such as by Mycobacterium species, certain viruses (cytomegalovirus, adenovirus, and herpes simplex), and protozoa (Cryptosporidium, Isospora belli, Microsporida, and Blastocystis hominis) may also play a role (Chap.
Profoundly dehydrated patients, especially infants and the elderly, require IV rehydration.
Empirical treatment can also be considered for suspected giardiasis with metronidazole (250 mg qid for 7 d). Domperidone, a D2 antagonist not available in the United States, exhibits prokinetic and antiemetic effects but does not cross into most brain regions; thus, anxiety and dystonic reactions are rare.
Some individuals with functional heartburn without increased acid or nonacid reflux are believed to have heightened perception of normal esophageal pH and volume.
Ten percent of patients with heartburn exhibit normal esophageal acid exposure and no increase in nonacidic reflux (functional heartburn). Eight to 20% of GERD patients exhibit esophageal intestinal metaplasia, termed Barrett’s metaplasia, a condition that predisposes to esophageal adenocarcinoma (Chap. Intestinal lactase deficiency as a cause of gas, bloating, and discomfort occurs in 15–25% of whites of northern European descent but is more common in blacks and Asians. Atypical symptoms include pharyngitis, asthma, cough, bronchitis, hoarseness, and chest pain that mimics angina.
Ambulatory esophageal pH testing using a catheter method or a wireless capsule endoscopically attached to the esophageal wall is considered for drug-refractory symptoms and atypical symptoms like unexplained chest pain. Patients with functional dyspepsia also may be advised to reduce intake of fat, spicy foods, caffeine, and alcohol. Up to one-third of GERD patients do not respond to standard PPI doses; one-third of these patients have nonacidic reflux, whereas 10% have persistent acid-related disease. The 5-HT1 agonist buspirone may improve some functional dyspepsia symptoms by enhancing meal-induced gastric accommodation.


The utility and safety of endoscopic therapies (radiofrequency ablation, transoral incisionless fundoplication) to enhance gastroesophageal barrier function have unproved durable benefits for refractory GERD. Low FODMAP (fermentable oligosaccharide, disaccharide, monosaccharide, and polyol) diets and therapies to modify gut flora (nonabsorbable antibiotics, probiotics) reduce gaseous symptoms in some IBS patients.
Acute infectious diarrhea remains one of the most common causes of mortality in developing countries, particularly among impoverished infants, accounting for 1.8 million deaths per year. The enteric nervous system receives input from the extrinsic nerves, but it is capable of independent control of these functions. The chief excitatory neurotransmitters controlling motor function are acetylcholine and the tachykinins, such as substance P. Angiotensin and aldosterone also influence colonic absorption, reflecting the common embryologic development of the distal colonic epithelium and the renal tubules. The resident microorganisms, predominantly anaerobic bacteria, in the colon are necessary for the digestion of unabsorbed carbohydrates that reach the colon even in health, thereby providing a vital source of nutrients to the mucosa.
Voluntary relaxation of the external anal sphincter (striated muscle innervated by the pudendal nerve) in response to the sensation produced by distention permits the evacuation of feces. Pseudodiarrhea and fecal incontinence occur at prevalence rates comparable to or higher than that of chronic diarrhea and should always be considered in patients complaining of “diarrhea.” Overflow diarrhea may occur in nursing home patients due to fecal impaction that is readily detectable by rectal examination.
Acute infection or injury occurs when the ingested agent overwhelms or bypasses the host’s mucosal immune and nonimmune (gastric acid, digestive enzymes, mucus secretion, peristalsis, and suppressive resident flora) defenses. Petersburg) may have increased risk of Giardia-associated diarrhea; visitors to Nepal may acquire Cyclospora. Invasive bacteria and Entamoeba histolytica often cause bloody diarrhea (referred to as dysentery). In some cases of moderately severe febrile diarrhea associated with fecal leukocytes (or increased fecal levels of the leukocyte proteins, such as calprotectin) or with gross blood, a diagnostic evaluation might be avoided in favor of an empirical antibiotic trial (see below). The aforementioned clinical and epidemiologic associations may assist in focusing the evaluation.
If stool studies are unrevealing, flexible sigmoidoscopy with biopsies and upper endoscopy with duodenal aspirates and biopsies may be indicated. Selection of antibiotics and dosage regimens are otherwise dictated by specific pathogens, geographic patterns of resistance, and conditions found (Chaps.
The main side effects of domperidone relate to induction of hyperprolactinemia via effects on pituitary regions served by a porous blood-brain barrier. Placing a feeding jejunostomy reduces hospitalizations and improves overall health in some patients with drug-refractory gastroparesis.
Miscellaneous therapies with benefit in chemotherapy-induced emesis include cannabinoids, olanzapine, and alternative therapies like ginger.
The role of hiatal hernias is controversial—most reflux patients have hiatal hernias, but most with hiatal hernias do not have excess heartburn.
Functional MRI studies show increased activation of several brain regions, emphasizing contributions from central nervous system factors. As with idiopathic gastroparesis, some cases of functional dyspepsia result from prior infection. Some patients with acid reflux on esophageal pH testing do not report heartburn, but note abdominal pain or other symptoms.
High-resolution esophageal manometry is ordered when surgical treatment of GERD is considered.
Gastric emptying testing is considered to exclude gastroparesis for dyspeptic symptoms that resemble postprandial distress when drug therapy fails and in some GERD patients, especially if surgical intervention is an option.
Furthermore, heartburn typically responds better to PPI therapy than regurgitation or atypical GERD symptoms. Acotiamide promotes gastric emptying and augments accommodation by enhancing gastric acetylcholine release via muscarinic receptor antagonism and acetylcholinesterase inhibition. The utility of low-FODMAP diets, antibiotics, and probiotics in functional dyspepsia is unproven.
Recurrent, acute diarrhea in children in tropical countries results in environmental enteropathy with long-term impacts on physical and intellectual development.
The sympathetic nerve supply modulates motor functions and reaches the small intestine and colon alongside their arterial vessels. A careful history and physical examination generally allow these conditions to be discriminated from true diarrhea. Established clinical associations with specific enteropathogens may offer diagnostic clues. Yersinia invades the terminal ileal and proximal colon mucosa and may cause especially severe abdominal pain with tenderness mimicking acute appendicitis. The syndrome of postinfectious IBS has now been recognized as a complication of infectious diarrhea. If a particular pathogen or set of possible pathogens is so implicated, then either the whole panel of routine studies may not be necessary or, in some instances, special cultures may be appropriate as for enterohemorrhagic and other types of E. Brainerd diarrhea is an increasingly recognized entity characterized by an abrupt-onset diarrhea that persists for at least 4 weeks, but may last 1–3 years, and is thought to be of infectious origin.
Postvagotomy gastroparesis may improve with near-total gastric resection; similar operations are now being tried for other gastroparesis etiologies. Analgesics cause dyspepsia, whereas nitrates, calcium channel blockers, theophylline, and progesterone promote gastroesophageal reflux. Gastric malignancies include adenocarcinoma, which is prevalent in certain Asian societies, and lymphoma.
Small-intestinal bacterial overgrowth may cause dyspepsia, often associated with bowel dysfunction, distention, and malabsorption. A low LES pressure predicts failure of drug therapy and provides a rationale to proceed to surgery. Breath testing after carbohydrate ingestion detects lactase deficiency, intolerance to other carbohydrates, or small-intestinal bacterial overgrowth. Some individuals respond to doubling of the PPI dose or adding an H2 antagonist at bedtime.
188 and 348) include 10–14 days of a PPI or bismuth subsalicylate in concert with two antibiotics.
Herbal remedies such as STW 5 (Iberogast, a mixture of nine herbal agents) are useful in some dyspeptic patients. Sympathetic input to the gut is generally excitatory to sphincters and inhibitory to non-sphincteric muscle. In health, the ascending and transverse regions of colon function as reservoirs (average transit time, 15 h), and the descending colon acts as a conduit (average transit time, 3 h). Cruise ships may be affected by outbreaks of gastroenteritis caused by agents such as norovirus.
Persons with hemochromatosis are especially prone to invasive, even fatal, enteric infections with Vibrio species and Yersinia infections and should avoid raw fish. Similarly, acute gastroenteritis may precede the diagnosis of celiac disease or Crohn’s disease.
Conditions causing chronic diarrhea can also be confused with acute diarrhea early in their course. It may be associated with subtle inflammation of the distal small intestine or proximal colon. Antibiotic coverage is indicated, whether or not a causative organism is discovered, in patients who are immunocompromised, have mechanical heart valves or recent vascular grafts, or are elderly. Implanted gastric electrical stimulators may reduce symptoms, enhance nutrition, improve quality of life, and decrease health care expenditures in medication-refractory gastroparesis, but small controlled trials do not report convincing benefits. Other stimuli that induce reflux include ethanol, tobacco, and caffeine via LES relaxation. Eosinophilic infiltration of the duodenal mucosa is described in some dyspeptics, particularly with postprandial distress syndrome.
Poor esophageal body peristalsis raises concern about postoperative dysphagia and directs the choice of surgical technique. Visceral afferents convey sensation from the gut to the central nervous system (CNS); initially, they course along sympathetic fibers, but as they approach the spinal cord they separate, have cell bodies in the dorsal root ganglion, and enter the dorsal horn of the spinal cord.
The colon is efficient at conserving sodium and water, a function that is particularly important in sodium-depleted patients in whom the small intestine alone is unable to maintain sodium balance.
Acute diarrhea can also be a major symptom of several systemic infections including viral hepatitis, listeriosis, legionellosis, and toxic shock syndrome. This confusion may occur with inflammatory bowel disease (IBD) and some of the other inflammatory chronic diarrheas that may have an abrupt rather than insidious onset and exhibit features that mimic infection.
Molecular diagnosis of pathogens in stool can be made by identification of unique DNA sequences; and evolving microarray technologies have led to more rapid, sensitive, specific, and cost-effective diagnosis. Celiac disease, pancreatic disease (chronic pancreatitis, malignancy), hepatocellular carcinoma, Menetrier’s disease, infiltrative diseases (sarcoidosis, eosinophilic gastroenteritis), mesenteric ischemia, thyroid and parathyroid disease, and abdominal wall strain cause dyspepsia. Nonacidic reflux may be detected by combined esophageal impedance-pH testing in medication-unresponsive patients. Many patients started on a PPI can be stepped down to an H2 antagonist or be switched to an on-demand schedule. Afferent signals are conveyed to the brain along the lateral spinothalamic tract and the nociceptive dorsal column pathway and are then projected beyond the thalamus and brainstem to the insula and cerebral cortex to be perceived. Diarrhea or constipation may result from alteration in the reservoir function of the proximal colon or the propulsive function of the left colon.
Antibiotic prophylaxis is only indicated for certain patients traveling to high-risk countries in whom the likelihood or seriousness of acquired diarrhea would be especially high, including those with immunocompromise, IBD, hemochromatosis, or gastric achlorhydria. Gluten sensitivity in the absence of celiac disease is reported to evoke unexplained upper abdominal symptoms. Other afferent fibers synapse in the prevertebral ganglia and reflexly modulate intestinal motility, blood flow, and secretion.
Constipation may also result from disturbances of the rectal or sigmoid reservoir, typically as a result of dysfunction of the pelvic floor, the anal sphincters, the coordination of defecation, or dehydration. Use of ciprofloxacin, azithromycin, or rifaximin may reduce bacterial diarrhea in such travelers by 90%, though rifaximin is not suitable for invasive disease, but rather as treatment for uncomplicated traveler’s diarrhea. Extraperitoneal etiologies of indigestion include congestive heart failure and tuberculosis. Finally, physicians should be vigilant to identify if an outbreak of diarrheal illness is occurring and to alert the public health authorities promptly.
In each of these patient subsets, upper endoscopy is reserved for those whose symptoms fail to respond to therapy.



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