Abdominal pain is pain that you feel anywhere between your chest and groin. This is often referred to as the stomach region or belly. The evaluation of abdominal pain requires an understanding of the possible mechanisms responsible for pain, a broad differential of common causes, and recognition of typical patterns and clinical presentations. Abdominal pain can be generalized or localized to one area. Pain can also be referred – the type of pain that is perceived at a location other than the site of the painful stimulus/ origin.

Location of Pain and Potential Causes

Upper abdominal pain syndromes typically have characteristic locations: right upper quadrant pain, epigastric of midabdominal pain, or left upper quadrant pain.

Right upper quadrant abdominal pain can be caused by among other things, gallstones, inflammation of the gallbladder or bile ducts, , hepatitis, liver abscess,.

Epigastric (mid upper abdomen) pain can be caused by a heart attack, inflammation of the pancreas (pancreatitis), peptic ulcers or gastroesophageal reflux disease (GERD), inflammation in your stomach or esophagus, and indigestion.

Left upper quadrant abdominal pain can be caused by enlarged spleen, splenic abscess, or splenic rupture, among other causes.

Lower abdominal pain syndromes that are generally localized to one side include appendicitis, and diverticulitis.

Abdominal pain from some genitourinary etiologies may be localized to either side and can be due to kidney stones, urinary tract infection (UTI), kidney infection, urinary retention, and infectious colitis as well as endometriosis, ectopic pregnancy, fallopian tube inflammation among other causes.

Abdominal pain syndromes may have diffuse, nonspecific, or variable patterns of pain and could be due to obstruction, perforation of the GI tract, inflammatory bowel disease (Crohn’s disease of ulcerative colitis), gastroenteritis, bacterial peritonitis, malignancy, celiac disease, constipation, and even lactose intolerance. Abdominal pain can also be due as described above to a gynecological issue.

Abdominal pain can vary in intensity, and can be sharp, dull, mild to moderate, or severe, present with or without other symptoms, and can be acute (lasting hours to days but less than 2 weeks) or chronic (lasting for weeks to months).

When Should I Call My Doctor?

Contact your doctor immediately if you have a new onset severe pain, with or without other symptoms that may include diarrhea, nausea, vomiting, blood in vomit or stool, fever, abdominal guarding, change in bowel habits, severe constipation, or weight loss. You should also reach out to your doctor if your pain simply does not feel normal to you or, whether it is chronic or acute. Your doctor may order blood tests, stool tests, imaging and if indicated – endoscopic procedures, to rule out the cause of your pain.

Acute viral gastroenteritis is a common reason for emergency department and outpatient clinic visits in the United States. Acute viral gastroenteritis also causes outbreaks in certain closed communities, such as nursing homes, schools, and cruise ships. Restaurants and catered meals are another common source of outbreaks.

Most cases of acute infectious gastroenteritis are viral, with norovirus being the most common cause and the second most common cause of hospitalization for acute gastroenteritis. The other common pathogens causing viral gastroenteritis are rotavirus, enteric adenovirus, and astrovirus. Other nonviral causes include bacteria (e.g., Staphylococcus aureus, Campylobacter jejuni, Shigella spp., Salmonella spp., Yersinia, and Escherichia coli) and parasites (e.g., Giardia and Cryptosporidium).

In addition to large outbreaks from consumption of contaminated food and water, noroviruses are efficiently spread person-to-person. Viral gastroenteritis has pronounced peaks in the winter and spring.

Symptoms of Acute Gastroenteritis

Acute gastroenteritis is defined as the cute onset of diarrhea often accompanied by nausea and vomiting, lasting 12 to 24 hours. Fever and abdominal pain may occur as well. Classically, vomiting and diarrhea occur together; however, less commonly, either can occur alone.

Diagnosis of Acute Gastroenteritis

Clinical diagnosis — The diagnosis of acute viral gastroenteritis is made by a characteristic history of diarrhea (at least three or more times per day) of rapid onset often accompanied by nausea, vomiting, fever, or abdominal pain and characteristic physical examination of mild, diffuse, abdominal tenderness.

Laboratory testing — Routine laboratory and stool studies not required for the diagnosis of acute viral gastroenteritis; it is not necessary to determine a specific viral diagnosis. Stool studies are not routinely necessary in patients with viral gastroenteritis and are typically negative for fecal leukocytes and occult blood. Stool culture is also negative for bacterial pathogens. The presence of fecal leukocytes, occult blood, lactoferrin, or positive stool culture all indicate an inflammatory, nonviral gastroenteritis.

However, stool studies should be obtained in the following situations: adults presenting with persistent fever, dehydration, blood or pus in the stool, or other alarm symptoms and signs, and when there is clinical suspicion of a nonviral, inflammatory etiology of acute gastroenteritis. Diarrhea that lasts for more than a week should also prompt consideration of infectious and noninfectious causes.

Treatment

Acute viral gastroenteritis is usually self-limited and is treated with supportive measures (fluid repletion and unrestricted nutrition). No specific antiviral agents are available. Most important, antibiotics are not necessary, do not improve the symptoms and should not be used.

For adults presenting with acute viral gastroenteritis without signs of volume depletion, adequate volume can be maintained with sport drinks and broths. For adults presenting with mild to moderate dehydration, oral rehydration solutions may be superior to sports drinks in maintaining electrolyte balance along with hydration. Patients with severe dehydration require intravenous fluids.

Antiemetics and antimotility agents are used sometimes for excessive vomiting or excessive fluid loss from diarrhea, respectively. In known viral gastroenteritis epidemics, antibiotics are not indicated. Empiric antibiotics may have a limited role in the management of acute gastroenteritis, when it is unclear if the etiology is viral or bacterial. The role of antibiotics in bacterial gastroenteritis is discussed separately.

When to See Your Doctor

Contact your doctor If you experience:

• Severe volume depletion/dehydration

• Abnormal electrolytes or renal function

• Bloody stool/rectal bleeding

• Abnormal and/or unintended weight loss

• Severe abdominal pain

• Prolonged symptoms (more than one week)

And/or if you belong to one of the following categories:

• Hospitalization or antibiotic use in the past three to six months

• Age 65 or older

• Individuals with comorbidities (e.g., diabetes mellitus, immunocompromised)

• Pregnant

Barrett’s esophagus is the condition in which a metaplastic columnar epithelium that has both gastric and intestinal features replaces the stratified squamous epithelium that normally lines the distal esophagus. The condition develops as a consequence of chronic gastroesophageal reflux disease (GERD) and predisposes to the development of adenocarcinoma of the esophagus.

Barrett’s esophagus is usually discovered during endoscopic examinations of middle-aged and older adults; the large majority of cases go unrecognized. The mean age at diagnosis of Barrett’s esophagus is approximately 55 years. Barrett’s esophagus is two- to threefold more common in men than in women.

Risk Factors

• Gastroesophageal reflux disease (GERD) – In patients with symptomatic GERD, erosive esophagitis is an independent risk factor for Barrett’s esophagus, conferring a fivefold increased risk of Barrett’s at five-year follow-up.

• Central (abdominal) obesity – Central obesity is a risk factor for GERD and for Barrett’s esophagus.

• Family history – Familial aggregation of Barrett’s esophagus and esophageal adenocarcinoma has been described, and Barrett’s esophagus has been found in up to 28 percent of first-degree relatives of patients with esophageal adenocarcinoma. It is unclear if this is due to common environmental exposures and/or an inherited predisposition.

• Smoking – Smoking appears to have a synergistic effect with GERD in increasing the risk of Barrett’s esophagus. In a pooled analysis of five population-based case-control studies from the International BEACON (Barrett’s Esophagus and Esophageal Adenocarcinoma Consortium), the risk of Barrett’s esophagus was 1.7 times greater in smokers than in nonsmokers without GERD, and was 1.6 times greater than in nonsmokers with GERD.

Screening Patients for Barrett’s Esophagus

Screening should be done for Barrett’s esophagus in patients with multiple risk factors for adenocarcinoma. These include a hiatal hernia, age ≥50, male sex, chronic gastroesophageal reflux disease (GERD), White individuals, central obesity, cigarette smoking, and a confirmed history of Barrett’s esophagus or esophageal adenocarcinoma in a first-degree relative. In patients with erosive esophagitis found on the initial examination, a repeat endoscopy should be performed after a three-month course of acid suppression to exclude the presence of Barrett’s esophagus. In patients with a negative screening upper endoscopy for Barrett’s esophagus, a routine follow-up upper endoscopy for screening for Barrett’s esophagus is not indicated.

Passage of minimal bright red blood most commonly occurs in a chronic intermittent pattern. Very often, small amounts of red blood on toilet paper after wiping or a few drops of blood in the toilet bowl are noticed by a person after using the bathroom. Small amounts of blood on the surface of the stool are also considered minimal, but red blood intermixed with stool is not.

A history of minimal bright red blood in stool suggests a lesion near the anal canal but must be differentiated from dark red blood in a person with a history of gastrointestinal bleeding, or maroon stool with intermixed bright red blood (which could mean that blood is coming from a small or a large intestine). However, patients’ and clinicians’ perceptions of stool color vary widely, even when assisted by a standardized color chart.

Benign findings of bright red blood in stool are common and appear to account for 90 percent or more of all episodes of minimal bright red blood in stool. The true proportion of benign etiologies may be even higher, since many young people with minimal bright red blood in stool never present for care. However, scant rectal bleeding is also a common presenting symptom of serious diagnoses, such as colorectal cancer.

Common causes of bright red blood in stool include:

• Hemorrhoids

• Anal fissures

• Polyps

• Proctitis

• Rectal ulcers

• Cancer

On examination, your doctor will obtain a comprehensive medical and social history including your medications and over-the-counter supplements, lifestyle, diet, and will conduct a thorough physical examination. The physical examination will be directed at identifying possible or definite sources of bleeding and at finding worrisome lesions that may be detectable on examination. A detailed physical examination will include inspection of the anal area and a digital rectal examination.

Laboratory and Other Testing

Laboratory testing contributes little information to the evaluation of very low risk patients but may prompt more extensive investigation in patients at intermediate risk for colonic malignancies. Your doctor may order a complete blood count (CBC) and ferritin tests, which are reasonable preliminary tests in patients over age 40, or those with other risk factors for colonic malignancy, such as family history.

Diagnostic tests

Colonoscopy or sigmoidoscopy are generally recommended when additional evaluation beyond the history and physical examination is warranted.

When to Contact Your Doctor

You should contact your doctor if you notice large amounts of red blood in your stool, in the toilet, or on toilet paper, with or without blood clots; if, in addition to seeing blood in stool, you have upper or lower abdominal pain, fatigue, diarrhea, severe constipation, fever, or weight loss. You should also contact your doctor if you see dark red blood in your stool.

Celiac disease is a small bowel disorder characterized by mucosal inflammation, villous atrophy, and crypt hyperplasia, which occur upon exposure to dietary gluten and demonstrate improvement after withdrawal of gluten from the diet. Celiac disease should be differentiated from nonceliac gluten sensitivity in order to identify the risk for nutritional deficiency and complications of celiac disease and to determine the necessary degree and duration of adherence to a gluten-free diet. The diagnosis of celiac disease also has important implications for family members who may be at risk for celiac disease and associated disorders.

Who Should Be Tested

Serologic (blood) testing for celiac disease is recommended in adults with any of the following:

• Suggestive gastrointestinal symptoms — gastrointestinal symptoms include chronic or recurrent diarrhea or constipation, malabsorption, unexpected weight loss, abdominal pain, distension, or bloating or unexplained iron deficiency anemia. Testing should therefore be performed in patients with symptoms suggestive of irritable bowel syndrome or refractory lactose intolerance.

• Extraintestinal signs/symptoms suggestive of celiac disease — patients with extraintestinal symptoms, signs, or laboratory evidence for which celiac disease is a treatable cause. This includes patients without other explanations for iron deficiency anemia, folate or vitamin B12 deficiency, persistent elevation in serum aminotransferases, dermatitis herpetiformis, fatigue, recurrent headaches, low birthweight offspring, reduced fertility, dental enamel hypoplasia, metabolic bone disease and premature osteoporosis, idiopathic peripheral neuropathy, or nonhereditary cerebellar ataxia.

Diagnostic Approach

The diagnostic approach is based on the risk for celiac disease and whether the patient is on a gluten-containing diet. All testing for celiac disease should ideally be performed while patients are on a gluten-containing diet. Individuals at low risk for celiac disease should undergo serologic testing. Patients with positive serologic testing, should undergo an upper endoscopy with small bowel biopsy to diagnose celiac disease.

Differential Diagnosis

The most common disorders in the differential diagnosis of celiac disease include irritable bowel syndrome, small intestinal bacterial overgrowth, lactose intolerance, chronic pancreatitis, microscopic colitis, and inflammatory bowel disease. Celiac disease can be differentiated from these by serologic evaluation and small bowel biopsy.

Constipation is a common complaint that may be due to a variety of causes. Appropriate management requires an evaluation for secondary etiologies, such as systemic disorders and drugs. Once secondary causes have been eliminated, idiopathic constipation may be associated with normal or slow colonic transit, defecatory dysfunction (pelvic floor dysfunction), or both.

The approach to a patient with chronic constipation will depend on whether studies indicate normal or slowed colonic transit and whether there is a defecatory dysfunction. The specific choice of agents and order of their introduction varies with the etiology of the condition.

How to Manage Chronic Constipation

Management of chronic constipation includes patient education, behavior modification, dietary changes, and laxative therapy. Severe, intractable, slow transit constipation is rare and may be treated with surgery, but with extreme caution; patients should be referred to specialized centers for a full evaluation prior to surgery.

The initial management of idiopathic chronic constipation includes patient education, dietary changes, bulk-forming laxatives, and/or the use of non-bulk-forming laxatives or enemas. Efficacy, safety, convenience, costs, and clinical response all weigh into the choice of the initial treatment selected. Patients with severe constipation have generally failed these measures and require a different approach to therapy.

When to See Your Doctor

Call your doctor if you experience constipation accompanied by fever and chills, abdominal cramping and pain, blood in stool, unintended weight loss, an unexpected new onset of constipation, or constipation that developed after travel.

What Is Diarrhea?

Diarrhea is a condition where stools are loose, watery or more frequent than usual. Many people get diarrhea a few times a year and it can last several days. Some people get it more often. It could be caused by infection, inflammatory bowel disease (colitis), irritable bowel syndrome (IBS) or other conditions.

What Causes Diarrhea?

Diarrhea can be caused by food or waterborne pathogens or microbes, ingestion of certain medications, certain activities, or some medical conditions. Other causes include alcohol abuse, allergies or sensitivities to certain foods, diseases of the intestine (such as Crohn’s disease or ulcerative colitis), abuse of laxatives, overactive thyroid (hyperthyroidism), radiation therapy, some cancers, surgery on your digestive system, or trouble absorbing certain nutrients, also called “malabsorption”. Diarrhea may also follow constipation, especially for people who have irritable bowel syndrome.

Symptoms of Diarrhea

Symptoms often include abdominal bloating, cramps, thin or loose stool, watery stools, and an urgent feeling to have a bowel movement. More serious symptoms may include blood or mucus in your stool, weight loss, and fever. If you have watery stools more than three times a day and you’re not drinking enough fluids, you could become dehydrated. That can be a serious problem if it is not treated.

When Should I Call My Doctor?

Call your doctor right away if you have:

• Blood in your stool or black, tarry stools

• A fever that is high (above 101 F) or that lasts more than 24 hours

• Diarrhea lasting longer than 2 days

• Severe pain in your abdomen (especially the right lower quadrant) or rectum

• Diarrhea after coming back from a foreign country

Also, call your doctor right away if you have diarrhea and any of these signs of dehydration:

• Dark urine

• Smaller than usual amounts of urine or, in a child, fewer wet diapers than usual

• Rapid heart rate

• Headaches

• Dry skin

• Irritability

• Confusion

Certain tests can help pinpoint the cause of your diarrhea. One of the most useful is an examination of stool by PCR looking for the bacteria, viruses or parasites which can cause diarrhea. Blood tests may be helpful in looking for certain diseases or disorders. In some cases, endoscopic procedures such as colonoscopy or gastroscopy may be recommended.

Hydration is essential. It is important to drink at least six 8-ounce glasses of fluids each day. Choose electrolyte replacement drinks or soda without caffeine.

Gastroesophageal reflux disease (GERD) is a condition that develops when the reflux of stomach acid causes troublesome symptoms and/or complications. GERD is classified based on the appearance of the esophageal mucosa on upper endoscopy into the following:

• Erosive esophagitis — Erosive esophagitis is characterized by endoscopically visible breaks in the distal esophageal mucosa with or without troublesome symptoms of GERD.

• Nonerosive reflux disease — Nonerosive reflux disease or endoscopy negative reflux disease is characterized by the presence of troublesome symptoms of GERD without visible esophageal mucosal injury.

Classic symptoms of GERD are heartburn and regurgitation. Other symptoms of GERD include difficulty swallowing, chest pain, painful swallowing, and occasionally chronic cough, hoarseness, wheezing), and infrequently, nausea. The diagnosis of GERD can often be based on clinical symptoms alone in patients with classic symptoms such as heartburn and/or regurgitation. However, patients may require additional evaluation if alarm features are present, risk factors for Barrett’s esophagus, or abnormal gastrointestinal imaging performed for evaluation of their symptoms. Additional evaluation is required in selected patients with suspected GERD to rule out alternative etiologies, confirm the diagnosis of GERD, and assess for complications (e.g., Barrett’s esophagus).

Upper Gastrointestinal Endoscopy (EGD)

Upper endoscopy is indicated in patients with suspected GERD to evaluate alarm features or abnormal imaging if not performed within the last three months. Upper endoscopy should also be performed to screen for Barrett’s esophagus in patients with risk factors. On upper endoscopy, biopsies should target any areas of suspected metaplasia, dysplasia, or, in the absence of visual abnormalities, normal mucosa to evaluate for eosinophilic esophagitis. Upper endoscopy is not required to make a diagnosis of GERD. However, upper endoscopy can detect esophageal manifestations of GERD (e.g., Barrett’s metaplasia, erosive esophagitis) and can rule out an upper gastrointestinal tract malignancy. Upper endoscopy can also rule out other etiologies in patients with GERD symptoms that are refractory to a trial of proton pump inhibitor therapy.

Esophageal Manometry

In patients with suspected GERD with chest pain and/or difficulty swallowing and a normal upper endoscopy, an esophageal manometry should be performed to exclude an esophageal motility disorder. Manometry is useful in ensuring that ambulatory pH probes are placed correctly but cannot diagnose GERD.

Ambulatory esophageal pH monitoring

Ambulatory pH monitoring is also used to confirm the diagnosis of GERD in those with persistent symptoms (whether typical or atypical, particularly if a trial of twice-daily PPI has failed) or to monitor the adequacy of treatment in those with continued symptoms.

The differential diagnosis of gastroesophageal reflux disease (GERD) includes infectious esophagitis, pill esophagitis, and eosinophilic esophagitis. Other causes of dysphagia include esophageal rings/webs, and impaired peristalsis due to an esophageal motility disorder. Frequent heartburn may also be due to reflux hypersensitivity or functional heartburn. GERD can be distinguished from these conditions by pH or pH-impedance testing.

When to See Your Doctor

Contact your doctor for more questions regarding GERD or if you experience any of the following symptoms:

• New onset of indigestion especially in patient ≥60 years

• Evidence of gastrointestinal bleeding (vomiting blood or blood in stool)

• Iron deficiency anemia

• Anorexia

• Unexplained weight loss

• Difficult or painful swallowing

• Persistent vomiting

• Gastrointestinal cancer in a first-degree relative

Microscopic colitis is a chronic inflammatory disease of the colon that is characterized by chronic, watery, non-bloody diarrhea. It typically occurs in middle-aged patients and has a female preponderance. The colon appears typically normal or almost normal on colonoscopy in patients with microscopic colitis. The diagnosis is established by biopsy of the colonic mucosa demonstrating characteristic histologic changes. Microscopic colitis, first described in 1980 has two main histologic subtypes: lymphocytic colitis, more specifically defined in 1989, and collagenous colitis.

Epidemiology

Incidence and prevalence — the estimated incidence of collagenous colitis and lymphocytic colitis are 2.0 to 10.8 and 2.3 to 16 per 100,000 per year, respectively, with higher incidence in northern Europe and northern parts of North America. The increasing incidence has reached a plateau. The median age at diagnosis of microscopic colitis is approximately 65 years. Approximately 25 percent of patients with microscopic colitis are diagnosed before the age of 45 years. Although microscopic colitis has been reported in children, it is rare. Microscopic colitis has a higher incidence in women, in the range of 52 to 86 percent. Female preponderance appears to be more pronounced in collagenous as compared with lymphocytic colitis (female-to-male incidence rate ratios, 3.0 and 1.9, respectively).

Associated Conditions

Microscopic colitis has also been associated with several other diseases with autoimmune background (e.g., autoimmune thyroiditis, type 1 diabetes mellitus, and nonerosive, oligoarticular arthritis).

Etiology and Risk Factors Medications

Nonsteroidal anti-inflammatory drugs (NSAIDs) have been implicated as being causative or triggering flares of microscopic colitis. Several other drugs have also been implicated as potential causes of microscopic colitis, including proton pump inhibitors (PPIs), specifically lansoprazole, statins, selective serotonin reuptake inhibitors and other drugs, (e.g., pembrolizumab). Concomitant use of PPIs and NSAIDs may increase the risk even further.

Smoking

Smoking may play a role in the development of microscopic colitis and the clinical outcome. In a case-control study that included 340 patients with microscopic colitis, cigarette smoking (past or present) was associated with a significantly increased risk of microscopic colitis (odds ratio 2.1, 95% CI 1.6-2.9). On average, smokers also develop microscopic colitis more than 10 years earlier than non-smokers.

Pathophysiology

The pathogenesis of microscopic colitis is unclear; however, it is likely to be multifactorial, involving mucosal immune responses to luminal factors in a genetically predisposed individual. Although lymphocytic and collagenous colitis have a similar inflammatory cell response, it is uncertain whether they are related.

Pathogenesis of microscopic colitis

Genetic susceptibility — It is unclear to what extent a genetic predisposition is associated with the development of microscopic colitis. However, familial cases have been described. Interestingly, different members of the same family developed either lymphocytic or collagenous colitis, supporting a similar underlying pathophysiology.

Abnormal collagen metabolism — Abnormal collagen metabolism may be responsible for the thick collagen band in collagenous colitis. The prominent subepithelial matrix deposition has been attributed to increased expression of the main fibrogenic genes, procollagen I and metalloproteinase inhibitor (TIMP-1), by myofibroblastic cells and inadequate fibrinolysis [83-86]. The modification of collagen metabolism has also been explained by the expression of endogenous histamine, prostaglandins, and/or nitric oxide (NO).

Altered epithelial barrier function — an alternative hypothesis is that a defect in epithelial barrier function and luminal factors may lead to an increased transmucosal permeability of antigens and bacteria, leading to immune dysregulation and intestinal inflammation seen in microscopic colitis.

Synchronous collagenous and pseudomembranous colitis have also been described in some patients, suggesting a possible etiologic role for C. difficile. Infection with Yersinia has also been suggested as an inciting event for collagenous colitis. Furthermore, resolution of collagenous colitis has been described following treatment for Helicobacter pylori, but the association remains unclear.

Clinical Manifestations

Clinical presentation — Microscopic colitis is characterized by chronic, non-bloody, watery diarrhea. The onset of diarrhea is often insidious, but sudden onset was reported in approximately 40 percent of patients. Patients with microscopic colitis usually have between four and nine watery stools per day, but in rare cases, bowel movements can exceed 15 or up to 2 liters per day. Patients may have associated fecal urgency (70 percent), incontinence (40 percent), and nocturnal episodes (50 percent). Abdominal pain occurs in up to 50 percent of patients with active microscopic colitis (≥3 stools or ≥1 watery stool per day) [102,103]. Patients may have associated weight loss due to fluid loss or decreased oral intake. Extraintestinal symptoms, such as arthralgia, arthritis, or uveitis can occur.

Collagenous colitis seems to be a more severe type of bowel inflammation and lymphocytic colitis tends to occur earlier in life.

Laboratory findings

Laboratory findings in microscopic colitis are generally nonspecific. Mild anemia, elevated erythrocyte sedimentation rate, and autoantibodies are found in approximately one-half of patients. These autoantibodies include rheumatoid factor, antinuclear and antimitochondrial antibodies, antineutrophilic cytoplasmic antibodies, anti-Saccharomyces cerevisiae antibodies, and antithyroid peroxidase antibodies. In rare cases, patients may have a protein-losing enteropathy and associated hypoalbuminemia.

Diagnostic Approach

Diagnosis — Microscopic colitis should be suspected in patients with chronic diarrhea, particularly in middle-aged and older adults. The diagnosis of microscopic colitis is established by colonoscopy with biopsy of the colonic mucosa demonstrating characteristic histologic changes.

Evaluation — Evaluation of a patient with suspected microscopic colitis serves to exclude other causes of diarrhea and establish the diagnosis of microscopic colitis.

Differential Diagnosis — The main considerations in the differential diagnosis of microscopic colitis includes celiac disease, inflammatory bowel disease, and irritable bowel syndrome. These can be differentiated from microscopic colitis by history, laboratory evaluation, and endoscopy with biopsy.

Nausea, the unpleasant sensation of being about to vomit, can occur alone or can accompany vomiting (the forceful expulsion of gastric contents), indigestion, or other gastrointestinal symptoms. Nausea can occur without vomiting and, less commonly, vomiting occurs without nausea. Nausea is often more bothersome and disabling than vomiting. Retching differs from vomiting in the absence of expulsion of gastric content. In addition, patients may confuse vomiting with regurgitation, which is the return of esophageal contents to the hypopharynx with little effort.

Pathophysiology

Normal function of the upper gastrointestinal tract involves an interaction between the gut and the central nervous system. The motor function of the gut is controlled at three main levels: the parasympathetic and sympathetic nervous systems; enteric brain neurons; and smooth muscle cells.

Nausea

Gastric rhythm disturbance is a peripheral mechanism underlying nausea from various causes. Nausea correlates with a shift in the normal three cycle per minute gastric myoelectrical activity to increased frequency (tachygastria) or reduced frequency (bradygastria). In motion sickness induced by vection (rotating a drum with black and white vertical stripes around seated stationary subjects), tachygastria precedes nausea, which is proportional to the degree of tachygastria. Drug-induced normalization of tachygastria improves nausea.

Vomiting

Vomiting is a reflex that allows an animal or person to rid itself of ingested toxins or poisons. It can be activated by humoral or neuronal stimuli, or both.

Approach to Management

Patients with acute vomiting, typically for hours to a few days, most often present to an emergency department, whereas patients with chronic symptoms are more often initially evaluated in outpatient office settings. Emergency department physicians should expeditiously exclude life-threatening disorders such as bowel obstruction, mesenteric ischemia, acute pancreatitis, and myocardial infarction. In both urgent care and routine outpatient settings, the following three steps should generally be undertaken in patients with nausea and vomiting:

• The etiology should be sought, taking into account whether the patient has acute nausea and vomiting or chronic symptoms (at least one month in duration).

• The consequences or complications of nausea and vomiting (e.g., fluid depletion, hypokalemia, and metabolic alkalosis) should be identified and corrected.

• Targeted therapy should be provided, when possible (e.g., surgery for bowel obstruction or malignancy). In other cases, the symptoms should be treated.

Most patients with chronic nausea and vomiting that is unexplained after routine evaluation should undergo upper GI endoscopy to identify gastric obstruction or other disorders that should have specific therapy.

However, endoscopy and other routine tests are often normal, suggesting an idiopathic (functional) etiology.

Differential Diagnosis

Specific Disorders

Acute

Infectious causes — Acute gastroenteritis is second only to the common cold as a cause of lost productivity. Bacterial, viral, and parasitic pathogens cause this illness which is characterized by diarrhea and/or vomiting. Vomiting is especially common with infections caused by rotaviruses, enteric adenovirus, norovirus, and Staphylococcus aureus.

Infection with the acute respiratory syndrome SARS-Cov-2 virus (COVID-19) often causes gastrointestinal symptoms, especially diarrhea, abdominal pain, anorexia, nausea, and vomiting, and these symptoms can precede respiratory manifestations.

Postoperative nausea and vomiting —About one-third of surgical patients have nausea, vomiting, or both after receiving general anesthesia.

Vestibular neuritis — this acute labyrinthine disorder is characterized by rapid onset of severe vertigo with nausea, vomiting and gait instability.

Chemotherapy-induced nausea and vomiting — Nausea and vomiting are common side effects of cancer chemotherapy. Anticipatory antiemetic therapy is indicated when highly emetogenic chemotherapy regimens are given.

Chronic

Nausea and vomiting of pregnancy — up to 74 percent of pregnant women suffer nausea and/or vomiting, and 50 percent have vomiting alone.

Gastroparesis — the term gastroparesis applies to delayed gastric emptying as found from scintigraphic gastric emptying testing or other procedure in the absence of mechanical obstruction. Idiopathic and diabetic gastroparesis are the two most common groups.

Gastroesophageal reflux — Nausea can occasionally be the presenting symptom of gastroesophageal reflux disease and usually responds to management of GERD.

Gastric outlet obstruction — Pyloric stenosis can occur from malignancy or peptic ulcer disease. Inflammatory edema associated with ulcers may respond to acid suppression therapy and nasogastric suction. However, fibrotic strictures may persist after ulcer healing. Endoscopic balloon dilation, surgery, and self-expanding metal stenting are treatment options.

Eosinophilic gastroenteritis — Benign eosinophilic infiltration of the gut is uncommon, but its diagnosis is especially important as steroid therapy is usually effective.

Chronic idiopathic intestinal pseudo-obstruction — Chronic intestinal pseudo-obstruction is usually secondary to an underlying disorder affecting neuromuscular function that suggests mechanical bowel obstruction of the small or large bowel in the absence of an anatomic lesion that obstructs the flow of intestinal contents.

Treatment

The management of acute and chronic nausea and vomiting may differ, and vomiting can be more responsive than nausea. Drug treatment is standard practice.

When to See Your Doctor

You should call your doctor if you vomit blood, have severe abdominal pain, fever, experienced unexplained weight loss, if your symptoms have lasted for more than a month or are debilitating and do not improve. Call your doctor if you have fever, chills, or other symptoms in addition to nausea and vomiting that last more than 24 hour and do not seem to be improving. You should contact your doctor right away if you experienced nausea and vomiting following a head injury.

In some patients, irritable bowel syndrome (IBS) symptoms arise following an episode of diarrhea or acute gastroenteritis which is often caused by microbial contamination of food or water. This phenomenon, known as post-infectious IBS (PI-IBS), denotes the persistence of abdominal discomfort, bloating and diarrhea and/or constipation that continue despite clearance of the inciting pathogen.

PI-IBS can be caused by viruses, such as norovirus, bacteria such as Campylobacter, or parasites like Giardia, Entamoeba histolytica, Cyclospora or Cryptosporidium, and can last for weeks, months, or even years. PI-IBS can be managed with dietary modifications, probiotics, medications, as well as other therapies.

Small intestinal bacterial overgrowth (SIBO) is a condition in which the small bowel is colonized by excessive aerobic and anaerobic microbes. Several disorders predispose to SIBO by altering mucosal defenses. Patients may have more than one predisposing cause. As an example, the high prevalence of SIBO in older adults may be due to small intestinal dysmotility or the chronic use of acid inhibitors such as PPIs.

SIBO is usually associated with abnormally high counts of multiple organisms in the small intestine. Data suggests that in traditional SIBO, the most common organisms are Escherichia coli and Klebsiella. Facultative anaerobes can injure the intestinal surface by direct adherence and production of enterotoxins. Aerobic bacteria produce enzymes and metabolic products that can induce epithelial cell injury.

Symptoms of SIBO

The majority of patients with SIBO present with bloating. Other common symptoms include flatulence, abdominal discomfort, chronic watery diarrhea, constipation, or mixed diarrhea/constipation. Physical examination is usually normal in patients with SIBO. However, in some cases, the abdomen may be distended.

Laboratory and Endoscopic Findings

Laboratory abnormalities are usually associated with severe bacterial overgrowth or when SIBO occurs in association with an underlying anatomic abnormality. Laboratory findings including macrocytic anemia, B12 deficiency, and the presence of fecal fat. Patients may also have low levels of thiamine and niacin and elevated serum folate and vitamin K levels.

The endoscopic appearance and histopathology of the small intestine and colon is normal in most patients with SIBO.

Diagnosis of SIBO

The diagnosis of SIBO should be suspected if bloating, flatulence, abdominal discomfort, or chronic diarrhea is present. The diagnosis is established with a positive carbohydrate breath test. We perform a carbohydrate breath test to diagnose SIBO and measure hydrogen and methane as it is simple and non-invasive.

No additional evaluation is needed to diagnose SIBO. However, we obtain additional tests to diagnose laboratory abnormalities associated with SIBO and to rule out other causes of similar symptoms (e.g., celiac disease), which may co-exist with SIBO on a case-by-case basis. In patients with severe diarrhea or iron deficiency anemia, we perform endoscopic evaluation with colonoscopy and, if indicated, an upper endoscopy with small bowel biopsy.

Carbohydrate breath test

Breath tests are based on the principle that metabolism of a test dose of carbohydrate substrate (e.g., lactulose, glucose) by the bacterial flora leads to the production of an analyte (hydrogen, methane, and hydrogen sulfide), which is absorbed and ultimately excreted in the breath. Lactulose is a nonabsorbable substance that is normally metabolized by gut bacteria in the colon with the production of hydrogen, hydrogen sulfide, and/or methane. In individuals without SIBO, the administration of lactulose results in a single peak in breath hydrogen within two to three hours due to the metabolism of lactulose by colonic flora. In patients with SIBO, administration of lactulose results in an early peak in breath hydrogen levels due to metabolism by small bowel bacteria.

Treatment of SIBO

SIBO can be treated with non-absorbable antibiotics, and dietary and lifestyle changes. Antibiotic therapy is typically begun after confirming SIBO by breath test. The selection of antimicrobial regimens is based on the pattern of bacterial overgrowth, the prevalence of risk factors for drug-resistance (recent or repeated prior exposure), relevant antibiotic allergies, and cost.

The bites of insects and other arthropods may be a minor nuisance or may lead to serious medical problems, including transmission of insect-borne illnesses and severe allergic reactions. Reactions to the bites of mosquitoes, ticks, black flies, horse and deer flies, sand flies, stable flies, biting midges, fleas, centipedes, and biting mites can be very serious and can lead to chronic health issues.

Insect bites are different from insect stings. Stings involve the injection of venom into the victim and may cause reactions ranging from local irritation to life-threatening anaphylaxis.

Arthropods that commonly bite humans include:

• Mosquitoes

• Ticks

• Kissing bugs

• Bed bugs

• Black flies

• Horse and deer flies

• Sand flies

• Stable flies

• Biting midges

• Fleas

• Centipedes

• Biting mites

• Chiggers

• Lice

• A small number of types of spiders

Common diseases that are spread to people by mosquitoes include:

• Malaria

• Dengue

• Ckikungunya virus

• West Nile virus

• Zika virus

• Japanese Encephalitis

• Yellow Fever

Other diseases spread to humans by ticks, flies, and other bugs:

• Lyme Disease

• Anaplasmosis

• Babesiosis

• Ehrlichiosis

• Powassan Virus Disease

• Borrelia

• Rocky Mountain Spotted Fever (RMSF)

• Tick-borne encephalitis (TBE)

• Trypanosomiasis

• Leishmaniasis

• Myiasis

• Loiasis

• Chagas disease

When to See Your Doctor

You should call your doctor if you develop fever, chills, headache, other flu-like symptoms, skin rash, diarrhea, vomiting, severe joint pain, or other symptoms during or after travel especially after travel to endemic regions. Some diseases like malaria and Yellow Fever can be life-threatening and you should be evaluated right away.

Enteric fever is characterized by severe systemic illness with fever and abdominal pain. The organism classically responsible for the enteric fever syndrome is Salmonella enterica serotype Typhi (formerly S. typhi). Other Salmonella serotypes, particularly S. enterica serotypes Paratyphi A, B, or C, can cause a similar syndrome; however, it is usually not clinically useful or possible to reliably predict the causative organism based on clinical findings.

Epidemiology

Worldwide, eteric fever is most prevalent in impoverished areas that are overcrowded with poor access to sanitation. Incidence estimates suggest that south-central Asia, Southeast Asia, and southern Africa are regions with high incidence of S. Typhi infection (more than 100 cases per 100,000 person-years). Other regions of Asia and Africa, some parts of Latin America, the Caribbean, and Oceania have a medium incidence of 10 to 100 cases per 100,000 person-years. These estimates, though, are limited by lack of consistent reporting from all areas of the world and are based on extrapolation of data across regions and age groups. More recent population-based studies from Latin America, in particular, are lacking, and surveillance suggests that rates have declined substantially over the past 30 years, though intermittent outbreaks continue to occur.

Because humans are the only reservoir for S. Typhi and S. Paratyphi A, a history of travel to settings in which sanitation is poor or contact with a known typhoid case or carrier is useful for identifying people at risk of infection outside of endemic areas, although a specific source or contact is identified in a minority of cases. Transmission from an index case to a contact is rarely documented in resource-rich settings.

Many travelers who subsequently develop enteric fever have not received appropriate vaccination despite guideline recommendations. Among 580 cases of vaccine-preventable diseases among returned international travelers reported to the GeoSentinel Surveillance Network between 1997 and 2007, confirmed or probable enteric fever (due mainly to S. Typhi, but also S. Paratyphi) was the most common. Only 38 percent of those with enteric fever had a pre-travel clinical encounter. However, the possibility of S. Typhi infection in returning travelers with a history of vaccine receipt should not be discounted, since the vaccine is not completely effective.

Patients who acquire infection abroad are usually older than those who acquire disease in United States outbreaks and are more likely to have drug-resistant infection. S. Typhi outbreaks in the United States are most often foodborne; they are generally limited in size but can cause substantial morbidity.

Chronic carriage

Chronic Salmonella carriage is defined as excretion of the organism in stool or urine >12 months after acute infection. Rates of chronic carriage after S. Typhi infection range from 1 to 6 percent. Chronic carriage occurs more frequently in women and in patients with cholelithiasis or other biliary tract abnormalities. Chronic carriage in the urine is rare and almost always associated with an abnormality in the urinary tract (e.g., urolithiasis, prostatic hyperplasia) or concurrent bladder infection with Schistosoma.

Chronic carriers are asymptomatic; however, they represent an infectious risk to others, particularly in the setting of food preparation. The story of “Typhoid Mary,” a cook in early 20th century New York who infected approximately 50 people (three fatally), highlights the role of asymptomatic carriers in maintaining the cycle of person-to-person spread, especially in areas of lower transmission. For this reason, eradication of carriage when identified should be attempted.

Clinical Features

Enteric fever is a febrile illness with onset of symptoms 5 to 21 days after ingestion of the causative microorganism in contaminated food or water. In general, lower inocula are associated with longer incubation times. However, both the incubation period and inoculum needed to cause disease to vary depending upon host factors such as age, gastric acidity, and immunologic status. The majority of patients with enteric fever present with abdominal pain, fever, and chills.

Classic Presentation

In the first week of illness, rising fever and bacteremia develop. While chills are typical, frank rigors are rare. Relative bradycardia or pulse-temperature dissociation may be observed. In the second week of illness, abdominal pain develops and “rose spots” (faint salmon-colored macules on the trunk and abdomen) may be seen. During the third week of illness, hepatosplenomegaly, intestinal bleeding, and perforation due to ileocecal lymphatic hyperplasia of the Peyer’s patches may occur, together with secondary bacteremia and peritonitis. Septic shock or an altered level of consciousness may develop. In the absence of acute complications or death from overwhelming sepsis, symptoms gradually resolve over weeks to months.

Effect of antimicrobial therapy

The clinical features of enteric fever have changed dramatically in the antibiotic era. When case series from the United States in the 1930s were compared with series from the 1970s and 1980s, the prevalence of splenomegaly fell from 63 to 10 percent, and the prevalence of rose spots fell from 30 to 1.5 percent. Intestinal bleeding was also less frequent.

Other clinical manifestations

The symptoms, signs, and complications of enteric fever vary widely in different series and may be related to age, geographic area, the causative organism, or the time at which patients seek medical care.

Gastrointestinal manifestations

Reports in the pre-antibiotic era suggested that constipation occurred more frequently than diarrhea. Subsequent reports suggest that these symptoms occur with approximately equal frequency or that diarrhea may be more common, particularly in young children and in adults with HIV infection. Specifically, the incidence of diarrhea in children with culture proven typhoid fever was 78 percent in a series from Australia and 50 percent in a report from Vietnam. Constipation occurs in approximately 30 percent of individuals, perhaps more frequently in adults. Intestinal perforation generally occurs more frequently among adults than children and is associated with high mortality rates.

Neurologic manifestations

Although headache is a frequent symptom reported in 44 to 94 percent of cases, other neurological manifestations including disordered sleep patterns, acute psychosis, myelitis, and rigidity have been observed but are uncommon, as are meningitis and focal central nervous infections with S. Typhi. Patients with severe enteric fever may develop “typhoid encephalopathy,” with altered consciousness, delirium, and confusion.

Other extraintestinal manifestations

Other protean symptoms have been reported to varying degrees. Cough is not rare and has been observed in approximately 20 to 45 percent; join and muscle pain occur in about 20 percent. Focal extraintestinal manifestations, including involvement of the hepatobiliary, cardiovascular, respiratory, genitourinary, musculoskeletal, and central nervous systems, have been described as a result of bacteremic seeding, but are observed infrequently.

Laboratory Abnormalities

• Patients with enteric fever frequently have anemia and either leukopenia or leukocytosis; leukopenia with left shift is typically seen in adults, while leukocytosis is more common in children. If observed in the third week of illness, leukocytosis should prompt suspicion of intestinal perforation.

• Abnormal liver function tests are frequently observed

• Although nonspecific, serum C-reactive protein (CRP) is often elevated in patients with enteric fever.

• Cerebrospinal fluid studies are usually normal or reveal a mild pleocytosis (<35 cells/mm3), even in patients with neuropsychiatric symptoms.

Special Populations

Children — certain clinical manifestations associated with enteric fever occur with different frequency in children compared with adults. Even among infants, there is variability in the severity of the disease.

HIV-infected patients — the severity of enteric fever does not appear to be markedly increased in the setting of HIV infection, in contrast to nontyphoidal salmonellosis, in which higher complication rates are seen with HIV coinfection. However, there is some evidence that immunocompromised patients fare poorly with typhoidal infections.

Chronic carriers — in general, chronic carriers do not develop recurrent symptomatic disease. They appear to reach an immunologic equilibrium in which they are chronically colonized, usually in the biliary tract, and may excrete large numbers of organisms, but have a high level of immunity and do not develop clinical disease. Chronic carriers frequently have high serum antibody titers against the Vi antigen, although the evidence for the utility of this test for identifying carriers is mixed.

Diagnosis

Approach — the possibility of enteric fever should be considered in a febrile patient living in, traveling from, or visiting from an endemic area. Duration of fever for more than three days or accompanying gastrointestinal symptoms (abdominal pain, diarrhea, or constipation) should heighten the suspicion. The diagnosis of enteric fever is made by isolating S. Typhi or Paratyphi from a culture specimen in the setting of a compatible clinical illness. However, culture of most specimens is not highly sensitive, and other diagnostic tests (such as culture-independent methods and serology) are of limited clinical utility. Furthermore, even positive cultures usually require several days to incubate. Thus, when cultures are negative or not available, as in some resource-limited settings, the diagnosis of enteric fever is often made presumptively on the basis of a protracted febrile illness without other explanation. Empiric therapy is often appropriate in the absence of an alternative diagnosis because of the risk for severe sequelae with untreated enteric fever; nevertheless, it is important to recognize that the clinical syndrome of enteric fever is nonspecific, and the positive predictive value of a clinical diagnosis even in high-burden settings is typically less than 50 percent.

Culture — blood cultures are positive in 50 to 70 percent of patients with typhoid, depending upon the series and culture techniques used. Blood cultures may require several days of incubation. The diagnosis can also be made by culture of stool, urine, rose spots, or duodenal contents (via string capsule). Stool culture is positive in up to 30 to 40 percent of cases, but is often negative by the time that systemic symptoms bring patients to medical attention.

Limitations of serology — serologic tests such as the Widal test are of limited clinical utility in endemic areas because positive results may represent previous infection.

Culture-independent diagnostic tests — Newer rapid antibody-based diagnostic tests have only moderate diagnostic accuracy in field testing.

An enzyme-linked immunosorbent assay for antibodies to the capsular polysaccharide Vi antigen may be useful for detection of carriers in high-risk populations but has had limited success in identifying carriers in community-based screens due to high-background prevalence of Vi-antibody levels in endemic populations. Anti-Vi antibodies are not useful for the diagnosis of acute illness.

Polymerase chain reaction (PCR)-based diagnostics have had limited sensitivity in most studies given the low concentration of bacteria during bacteremia. Newer approaches are in development; antibody tests to detect serum immunoglobulin A against hemolysin E are promising.

When to See Your Doctor

Call your doctor if you return from a trip with symptoms suggestive of typhoid fever, including fever, diarrhea, constipation, abdominal pain and cramping, blood on stool, disturbed sleep pattern, psychosis, joint or muscle pain.

Ulcerative colitis is characterized by recurring episodes of inflammation limited to the mucosal layer of the colon. It commonly involves the rectum and may extend in a proximal and continuous fashion to involve other parts of the colon.

Clinical Manifestations
Patients with ulcerative colitis usually present with diarrhea, which may be associated with blood. Bowel movements are frequent and small in volume as a result of rectal inflammation. Associated symptoms include colicky abdominal pain, urgency, tenesmus, and incontinence. Patients with mainly distal disease may have constipation accompanied by frequent discharge of blood and mucus.

The onset of symptoms is usually gradual, and symptoms are progressive over several weeks. Symptoms may be preceded by a self-limited episode of rectal bleeding that occurred weeks or months earlier. The severity of symptoms may range from mild disease with four or fewer stools per day with or without blood to severe disease with more than 10 stools per day with severe cramps and continuous bleeding.

Patients may have systemic symptoms including fever, fatigue, and weight loss. Patients may also have dyspnea (shortness of breath) and palpitations due to anemia secondary to iron deficiency from blood loss, anemia of chronic disease, or autoimmune hemolytic anemia. The presence and severity of systemic symptoms depends on the clinical severity of the intestinal disease.

Physical examination is often normal, especially in patients with mild disease. Patients with moderate to severe ulcerative colitis may have abdominal tenderness to palpation, fever, hypotension, tachycardia, and pallor. Rectal examination may reveal evidence of blood. Patients with prolonged diarrhea symptoms may have evidence of muscle wasting, loss of subcutaneous fat, and peripheral edema due to weight loss and malnutrition.

Acute Complications
Severe bleeding — bleeding may be severe in up to 10 percent of patients. Massive hemorrhage occurs in up to 3 percent of patients with ulcerative colitis at some time in their disease course and may necessitate urgent colectomy.

Fulminant colitis and toxic megacolon — Patients with ulcerative colitis may develop fulminant colitis with more than 10 stools per day, continuous bleeding, abdominal pain, distension, and acute, severe toxic symptoms including fever and anorexia. Patients with fulminant colitis are at high risk of developing toxic megacolon as the inflammatory process extends beyond the mucosa to involve the muscle layers of the colon.

Perforation — perforation of the colon most commonly occurs as a consequence of toxic megacolon. However, it may also occur in the absence of toxic megacolon in patients with the first episode of ulcerative colitis due to lack of scarring from prior attacks of colitis. Perforation with peritonitis has been associated with 50 percent mortality in patients with ulcerative colitis.

Extraintestinal manifestations — Although ulcerative colitis primarily involves the bowel, it is associated with manifestations in other organ systems. Although less than 10 percent of patients with inflammatory bowel disease (IBD) have an extraintestinal manifestation (EIM) at initial presentation, 25 percent of patients have an EIM in their lifetime.

Musculoskeletal — arthritis/arthropathy is the most frequent EIM of IBD. IBD is associated with both a nondestructive peripheral arthritis, which primarily involves large joints, and ankylosing spondylitis. Other musculoskeletal manifestations of IBD include osteoporosis, osteopenia, and osteonecrosis. The musculoskeletal manifestations of IBD are discussed in detail, separately.

Eye — The most frequent ocular manifestations of IBD include uveitis and. Scleritis, iritis, and conjunctivitis have also been associated with IBD. Affected patients may be asymptomatic or complain of burning, itching, or redness of the eyes.

Skin — the most frequent skin lesions associated with IBD include erythema nodosum and pyoderma gangrenosum.

Hepatobiliary — primary sclerosing cholangitis, fatty liver, and autoimmune liver disease have been associated with IBD. Patients with primary sclerosing cholangitis are usually asymptomatic and identified only due to an isolated elevation in the serum alkaline phosphatase concentration. Patients may present with fatigue, pruritus, fevers, chills, night sweats, and right upper quadrant pain.

Hematopoietic/coagulation — patients with IBD are at an increased risk for both venous and arterial thromboembolism.

Autoimmune hemolytic anemia has been associated with IBD. Patients with anemia may be asymptomatic or have nonspecific symptoms including dyspnea, fatigue, and palpitations.

Pulmonary — pulmonary complications of IBD, although rare, include airway inflammation, parenchymal lung disease, serositis, and thromboembolic disease. Symptoms range in severity from asymptomatic decreases in diffusion capacity to disabling bronchiectasis with cough and mucopurulent sputum production.

Laboratory Findings

Patients with severe ulcerative colitis may have anemia, an elevated erythrocyte sedimentation rate (≥30 mm/hour), low albumin, and electrolyte abnormalities due to diarrhea and dehydration.

Patients with ulcerative colitis and primary sclerosing cholangitis may have an elevation in serum alkaline phosphatase concentration.

Fecal calprotectin or lactoferrin may be elevated due to intestinal inflammation but are nonspecific.

Imaging
Abdominal imaging is not required for the diagnosis of ulcerative colitis but may be performed in patients who present with symptoms of colitis. Abdominal radiography is usually normal in patients with mild to moderate disease, but may identify proximal constipation, mucosal thickening or “thumbprinting” secondary to edema, and colonic dilation in patients with severe or fulminant ulcerative colitis.

Double contrast barium enema may be normal in mild ulcerative colitis. Findings on barium enema may include a diffusely reticulated pattern with superimposed punctate collections of barium in micro ulcerations. In more severe disease, there may be spiculated collar button ulcers, shortening of the colon, narrowing of the luminal caliber, pseudopolyps, and filiform polyps. Barium enema should be avoided in patients who are severely ill since it may precipitate ileus with toxic megacolon. (See “Toxic megacolon”, section on ‘Clinical manifestations’.)

Computed tomography (CT) and magnetic resonance imaging (MRI) may demonstrate marked thickening of the bowel wall, but this finding is nonspecific. CT and MRI have lower sensitivity than barium enema for the detection of subtle early mucosal disease but are equivalent in patients with established and severe disease.

Ultrasound with Doppler may demonstrate a thickened hypoechoic mucosal layer in patients with active ulcerative colitis. More severe cases may be associated with transmural bowel wall thickening. However, these sonographic findings are not specific for ulcerative colitis and may be seen in colitis due to other causes.

Laboratory studies — stool studies should include stool polymerase chain reaction (PCR) for C. difficile toxin, routine stool cultures (Salmonella, Shigella, Campylobacter, Yersinia), and specific testing for Escherichia coli O157:H7 [25]. Microscopy for ova and parasites (three samples) and a Giardia stool antigen test should also be performed, particularly if the patient has risk factors such as recent travel to endemic areas.

Testing for sexually transmitted infections, including C. trachomatis, N. gonorrhoeae, HSV, and Treponema pallidum, may be warranted, particularly in men who have sex with men or patients with severe rectal symptoms including urgency and tenesmus.

A complete blood count, electrolytes, albumin, and markers of inflammation (erythrocyte sedimentation rate or C-reactive protein [CRP]) should be obtained to assess disease severity.

Colonoscopy and biopsy — Biopsies of the colon obtained on endoscopy are necessary to establish the chronicity of inflammation and to exclude other causes of colitis. An ileocolonoscopy allows for evaluation of the terminal ileum for inflammation that would be suggestive of Crohn disease and to determine the endoscopic extent and severity of colonic disease. However, a colonoscopy should be avoided in hospitalized patients with severe colitis because of the potential to precipitate toxic megacolon. In such patients, a flexible sigmoidoscopy should be performed, and evaluation limited to the rectum and distal sigmoid colon.

Differential Diagnosis

The differential diagnosis of ulcerative colitis includes other causes of chronic diarrhea.

• Crohn disease

• Infectious cause

• Radiation colitis

• Diversion colitis

• Solitary rectal ulcer syndrome

• Graft versus host disease

• Diverticular colitis

• Medication-associated colitis

When to See Your Doctor

You should call your doctor and undergo appropriate medical evaluation if you experience symptoms associated with ulcerative colitis.

Symptoms of Upper GI Bleeding

Patients with acute upper gastrointestinal (GI) bleeding commonly present with hematemesis (vomiting of blood or coffee-ground-like material) and/or melena (black, tarry stools). Other additional symptoms may include abdominal or epigastric pain, fatigue, dizziness, fever, abdominal cramping, and shortness of breath. Sometimes upper GI bleeding occurs slowly over time and patients may present with fatigue due to iron deficiency anemia from chronic blood loss.

Common causes of upper GI bleeding include:

• Peptic ulcer (often presents with upper abdominal pain)

• Esophageal ulcer (may present with gastroesophageal reflux, or difficulty swallowing)

• Mallory-Weiss tear – present with vomiting, retching, or coughing prior to throwing up blood

• Variceal hemorrhage or portal hypertensive gastropathy (patients often have jaundice – yellow skin or sclera of the eyes)

• Abdominal distention (ascites)

• Malignancy – often presents with difficulty swallowing

• Early satiety, involuntary weight loss.

When to See Your Doctor

You should contact your doctor if you vomit blood, have black, tarry stools, and have any symptoms mentioned above. Your doctor will examine you and order laboratory tests that will include a complete blood count, serum chemistries, liver tests, and coagulation studies. The initial evaluation of patients with acute upper GI bleeding involves an assessment of hemodynamic stability. Diagnostic studies (usually endoscopy) follow, with the goals of diagnosis, and when possible, treatment of the specific disorder.