Chapter 36. Gastrointestinal Emergencies

Diarrhea and vomiting are common reasons for Emergency Department visits. Although the majority of cases are of an infectious, self-limiting nature, the differential diagnosis is broad with the potential for significant morbidity and mortality. Many pathologic processes involve gastrointestinal (GI) symptoms. Included are intracranial pathology (trauma, masses, infections), cardiac disease (myocardial infarction, angina), toxic exposures (digoxin, carbon monoxide, heavy metals), acute abdominal pathology (intestinal obstruction, mesenteric ischemia), and endocrine abnormalities (diabetic ketoacidosis, adrenal insufficiency), among others. In addition, infectious causes of diarrhea and vomiting can cause significant harm, especially in the elderly, in infants, and in immunocompromised individuals (Figure 36–1).

Hypotension and Shock

Essentials of Diagnosis

• Signs of decreased perfusion
• Hypotension, tachycardia, oliguria, and orthostasis
• Cool, pale skin; dry mucous membranes; and altered mentation

Clinical Findings

Obtain complete vital signs. Look for signs of decreased perfusion (ie, cool, pale skin; altered mentation; decreased urinary output; dry mucous membranes). Hypotension (systolic pressure <90 mm Hg), tachycardia, oliguria, and orthostasis may indicate impending hemodynamic instability. Look for evidence of sepsis, GI bleed, cardiac pump dysfunction, surgical abdominal pathology, toxic exposures, endocrine abnormalities, or anaphylaxis.

Treatment and Disposition

Insert a large-bore intravenous catheter and draw blood for a complete blood count (CBC), electrolytes, renal and liver function, serum lipase, and a pregnancy test, if indicated. Type and crossmatch if significant blood loss is reported or suspected. Start supplemental oxygen, cardiac monitoring, and pulse oximetry together with normal saline volume resuscitation while the underlying cause is sought. If appropriate, initiate empiric antibiotic therapy. Hospitalize the patient for continuous monitoring, supportive treatment, and further investigation if the cause is uncertain. Initiate specific treatment once the cause is determined.

Acute Abdominal Emergencies

Essentials of Diagnosis

• Focal abdominal pain or signs of peritoneal inflammation (rebound)
• Pain that precedes the vomiting or diarrhea
• Pain out of proportion to the physical examination

Clinical Findings

Patients with acute surgical abdominal pathology may present with diarrhea and vomiting and are at risk of being mislabeled as having gastroenteritis. Inquire about the nature and location of pain and the existence of upper GI symptoms (vomiting) and lower GI symptoms (diarrhea). Determine which symptom began first. Signs and symptoms suggestive of an acute abdominal emergency include focal abdominal pain, an examination consistent with peritoneal inflammation, pain that precedes the vomiting and diarrhea, protracted vomiting with nonspecific abdominal pain, and pain out of proportion to the physical examination. Consider entities such as acute appendicitis, intestinal obstruction, mesenteric ischemia, ectopic pregnancy, GI bleed, intussusception, and gonadal torsion (Table 36–4). Serial abdominal examinations in the ED may help differentiate early acute abdominal emergencies with vomiting or diarrhea from gastroenteritis. In patients with arteriovascular disease who present with pain out of proportion to the examination, mesenteric ischemia must be ruled out.

Treatment and Disposition

Treatment ultimately depends on the cause of the symptoms. Obtain complete vital signs; gain intravenous access; and draw blood for a CBC, electrolytes, renal and liver function tests, serum lipase, pregnancy test if appropriate, and blood type and crossmatch. An acute abdominal series may demonstrate a small or large bowel obstruction. A computed tomography (CT) scan or ultrasound may help identify the cause of the acute abdomen. If intussusception is suspected, an air contrast or barium enema can be both diagnostic and therapeutic. If the patient's condition is unstable, seek appropriate surgical consultation early.

Toxic Exposures

Essentials of Diagnosis

• Cholinergic or sympathomimetic syndromes
• Ingestion of mushrooms, herbal or plant preparations, or seafood
• Occupational exposures—exposure to heavy metals, pesticides, or carbon monoxide
• Medications—digoxin, salicylates, or others

Clinical Findings

Diarrhea and vomiting are often the presenting symptoms of toxic exposures. The list of toxins is extensive (Figure 36–1). Obtain key historical information including medications, occupational exposures, use of herbal preparations, consumption of mushrooms or plant products, ingestion of seafood, exposures to heavy metals, and a history of allergic reactions. Search for specific toxin-induced syndromes such as cholinergic or sympathomimetic reactions. Consider common toxins such as digoxin, salicylates, and carbon monoxide. If neurologic symptoms exist, consider botulism or shellfish poisoning.

Treatment and Disposition

Begin treatment with the proper decontamination method. Give patients with toxic ingestions activated charcoal and a cathartic. Patients with cutaneous and inhalation exposures should be removed from the source and the contaminant diluted. Initiate supportive care and continuous monitoring. Administer specific antidotes if appropriate.

Other Emergencies

Essentials of Diagnosis

• Chest pain, shortness of breath, diaphoresis, acute pump failure
• History of cardiac, central nervous system, endocrine disease, or trauma
• Abnormal neurological examination, alteredmentation, fevers, headache
• Laboratory and physical abnormalities

Clinical Findings

Cardiac, central nervous system, or endocrine disorders may include vomiting or diarrhea as presenting symptoms (Figure 36–1). Evidence of a cardiac-related disorder includes chest pain, shortness of breath, diaphoresis, a history of cardiac disease, or evidence of acute pump failure. Indications of central nervous system pathology include a history of trauma, an abnormal neurological examination, fever, headache, and evidence of other toxic or metabolic pathology affecting the central nervous system.

Treatment and Disposition

Patients with a suspected cardiac, central nervous system, or endocrine causes of vomiting or diarrhea should receive aggressive evaluation and management. This may include an ECG, continuous cardiac monitoring, intravenous access, supplemental oxygen, pulse oximetry, and a complete set of labs including clotting studies and cardiac enzymes as indicated. Obtain X-rays, CT scans, and consultations as needed.

Once life-threatening conditions have been sought and treatment begun, an attempt should be made to further identify the cause of vomiting and diarrhea. Consider the following historical, physical, and laboratory investigations (Table 36–1).

History

Features of the Present Illness

Important features of the present illness include time of onset, the nature of symptoms, and duration of illness. Differentiate acute (less than 2 weeks) from chronic symptoms. Clarify the patient's use of the term diarrhea. Identify associated symptoms. Inquire about fever, abdominal pain, anorexia, diarrhea, constipation, tenesmus, myalgias, vomiting, cephalgia, and neurologic symptoms such as paresthesias, weakness, or cranial nerve palsies. Inquire about the presence of blood or mucus in the stool and about the character of the vomitus (bloody or bilious). Determine the onset and severity of diarrhea and vomiting in relation to other symptoms. Abdominal cramps after copious, watery diarrhea is consistent with gastroenteritis. However, abdominal pain followed by nausea and loose stool could represent appendicitis. The symptom complex of profuse diarrhea, fever, myalgias, and cephalgia is consistent with dysentery, whereas a symptom complex of sudden severe headache, nausea, vomiting, and loose stool could represent a process such as subarachnoid hemorrhage.

Medical and Surgical History

Inquire about the patient's medical and surgical history. Give special attention to immunocompetency. Inquire about a history of HIV, diabetes mellitus, GI bleed, abdominal surgeries, malignancies, and endocrine disease. Ask about recent chemotherapy or radiation therapy.

Medications and Antibiotic Use

Inquire about medications including prescription, over-the-counter, herbal preparations, and drugs of abuse. Give particular attention to recent antibiotic or laxative use.

Exposure Risk; Similar Illness in Others

Ask about common source exposures such as daycare or community outbreaks. Inquire about a history of hospitalization or institutionalization.

Dietary History

Inquire about unusual foods, dairy products, eggs, seafood, or unpasteurized or undercooked food. Ask about the ingestion of mushrooms or other plant products.

Travel History

Inquire about recent international travel, especially to developing countries. Forty percent of travelers to endemic regions of Latin America, Asia and Africa acquire traveler's diarrhea. Ask about recent domestic travel or outdoor activities, especially backpacking or exposure to new water sources.

Toxin Exposures

Assess the risk of exposure to toxins, including heavy metals, carbon monoxide, salicylates, and digoxin (see Figure 36–1). Ask about occupational history as it relates to toxin exposures. In farm workers, consider pesticides (organophosphate poisoning) and nicotine (green tobacco syndrome). Inquire about a history of allergic reactions.

Sexual Exposures

Inquire about sexual contacts. Amebiasis, giardiasis, campylobacteriosis, salmonellosis, and shigellosis can be transmitted by sexual contact. Chlamydia trachomatis, herpes simplex, and Neisseria gonorrhoeae are also possible causes of lower GI symptoms. HIV-positive and immunocompromised individuals are subject to infections with Cryptosporidium, cytomegalovirus, and Mycobacterium avium intracellulare.

Physical Examination

Use the physical examination to assess the patient's hydration status, evaluate for sepsis, rule out the acute abdomen, and determine the presence of blood in the stool.

General Appearance

Assess the patient's overall health. Look for evidence of volume depletion, a toxic appearance, or jaundice.

Fever

Fever is consistent with invasive bacterial or parasitic causes of gastroenteritis (ie, dysentery). Fever could also indicate a process requiring acute surgical intervention. Less commonly, fever may be associated with a viral or noninvasive bacterial gastroenteritis. Food poisoning should not be associated with fever.

Blood Pressure and Pulse Rate

Hypotension and tachycardia are typical responses to volume depletion. If the volume status is not apparent, evaluate for orthostasis with the patient supine, sitting, and standing to detect more subtle degrees of volume depletion (systolic pressure drop ≥10 mm Hg and pulse rise ≥15 beats/min). Young, healthy adults may maintain normal vital signs even with significant dehydration. Look for a blunted response in patients who are taking atrioventricular nodal blockers.

Abdominal Examination

Significant abdominal pain should prompt the search for causes other than infectious gastroenteritis. If abdominal examination elicits focal tenderness, or if signs of peritoneal inflammation are present, consider acute surgical pathology. However, subjective, diffuse, and crampy abdominal pain or tenderness may occur after extensive vomiting or diarrhea. In addition, several infectious agents, most notably Yersinia enterocolitica and Campylobacter sp., may mimic appendicitis and cause right lower quadrant pain, anorexia, low-grade fever, and vomiting preceding the onset of diarrhea. Appendicitis must be ruled out in patients with this presentation.

Rectal Examination

Perform rectal examination to detect fecal impaction, melena, or hematochezia.

Laboratory and Diagnostic Studies

Laboratory and diagnostic tests are of limited value in the routine evaluation of diarrhea and vomiting. Testing should be carried out, as indicated, in patients with a suspected noninfectious cause of vomiting or diarrhea, in those who are hemodynamically unstable, the very young, the elderly, and immunosuppressed individuals. In addition, testing may be necessary in patients with a prolonged course or in those not responding to conservative management.

Fecal Cell Count

Fecal erythrocytes and, to a greater degree, leukocytes have been used as a guide to determine who should receive empiric antibiotics. Both findings are associated with inflammatory diarrhea, of which bacterial dysentery is a common cause. However, there are many noninfectious causes of inflammatory diarrhea, which may also produce fecal red and white cells. These include inflammatory bowel disease (IBD), chemotherapy and radiation therapy, hypersensitivity, and autoimmune disorders. Just as the presence of erythrocytes and leukocytes is not specific for a bacterial process, their absence by stool smear does not rule it out. Furthermore, the cell count has not been shown to be a good indicator of which patients will benefit from empiric antibiotic treatment.

Bacterial Culture of Stool

Consider bacterial culture of stool in patients experiencing a prolonged course, in infants, in the elderly, in immunocompromised patients, and in patients who appear toxic. Stool for culture can be collected in the emergency department, and, in the event that the diarrhea persists, results can be used to guide future treatment.

Stool for Ova and Parasites

Consider testing for ova and parasites in patients with chronic diarrhea, those with a history of travel to developing countries, patients with HIV infection, and those with exposure to infants in daycare.

Clostridium Difficile Toxin

Consider testing for C. difficile toxin if the patient reports recent antibiotic use or recent hospitalization. Diarrhea may be delayed as long as 12 weeks after antibiotic therapy. Clindamycin, penicillins, and cephalosporins are commonly implicated. The incidence of community-acquired infection without recent antibiotic use is well established. Consider testing in patients with severe diarrhea, abdominal pain, and foul-smelling stool, even in those without recent antibiotic use.

Escherichia Coli 0157:H7 Toxin

Test patients with suspected hemolytic-uremic syndrome for E. coli 0157:H7 toxin through a stool culture looking specifically for 0157:H7 or if available by identifying the toxin through rapid immunoassay.

Giardia Antigen

Consider testing for Giardia antigen in HIV-infected patients, in those with a history of travel to developing countries or a history of backpacking, and in those with daycare exposure.

CBC, Blood Urea Nitrogen/Creatinine, Glucose, Lipase, and Liver Function Tests

Order other blood tests as indicated, especially if significant dehydration is suspected. Liver function testing is helpful if biliary colic or cholecystitis is suspected as the cause of vomiting. Lipase should be ordered in the patient with a history of pancreatitis, significant alcohol use or epigastric pain.

Urinalysis

A urinalysis and a urine pregnancy test should be obtained if indicated.

Radiographic Evaluation

Radiographic evaluation is indicated for patients thought to have a surgical abdomen. If abnormal bowel sounds, bilious vomiting, or abdominal distention are present, consider an acute abdominal series. An abdominal CT scan or an ultrasound may be appropriate as indicated.

Referral

Referral to a gastroenterologist may be indicated in the evaluation of chronic diarrhea.

The specific agent responsible for an episode of infectious gastroenteritis is difficult to identify in the acute setting. However, viral agents account for the majority of episodes, up to 70% by some estimates. Of the remaining infectious causes, bacterial agents account for approximately 24% and parasitic agents account for 6%.

Viral Gastroenteritis

Essentials of Diagnosis

• Mild systemic symptoms; generally no fever or abdominal pain
• Fecal erythrocytes and leukocytes are uncommon
• Dehydration may be mild to severe

Clinical Findings

Most viral agents produce a secretory diarrhea. Viral cytotoxins lead to an increased cellular permeability and result in the secretion of water and electrolytes into the intestinal lumen. Unlike invasive dysentery, viral gastroenteritis usually lacks significant systemic symptoms and is not generally associated with fever and abdominal pain. Fecal erythrocytes and leukocytes are uncommon. The most frequently identified agents are Norwalk virus and rotavirus.

Treatment and Disposition

Like other causes of nondysenteric gastroenteritis (Table 36–2), viral gastroenteritis tends to be self-limiting and to require only supportive care. However, significant dehydration can occur and lead to severe illness, especially in those at the extremes of age or those with other compromising medical conditions. Patients without underlying disease, who are nontoxic, can tolerate oral intake, have normal vital signs, and have a supportive/appropriate social situation at home can usually be discharged. Patients should be given discharge instructions to return if they are unable to tolerate oral intake or have worsening symptoms.

Bacterial Gastroenteritis

Essentials of Diagnosis

• Cytotoxin-mediated bacterial gastroenteritis is clinically similar to viral gastroenteritis
• Invasive bacterial enteritis produces dysentery with fever, diarrhea, abdominal cramps, and other systemic symptoms
• Fecal erythrocytes and leukocytes are common in invasive disease

Clinical Findings

Bacterial agents may produce either an inflammatory or a secretory diarrhea. Secretory diarrhea is cytotoxin mediated and may be caused by toxins that are preformed and therefore rapid acting, as with Staphylococcus aureus food poisoning, or by toxins formed after bacterial colonization, as with Vibrio cholerae (see Table 36–2). Secretory diarrhea that affects the upper small bowel generally produces watery diarrhea. Inflammatory diarrhea is caused by direct bacterial invasion of the intestinal mucosa and often affects the distal small bowel and colon. The result is release into the intestinal lumen of water, electrolytes, blood, proteins, and mucus. The clinical presentation is dysentery and may include fever, abdominal pain, bloody diarrhea, anorexia, myalgia, cephalgia, dehydration, and weight loss. With invasive enteritis, stool smears generally contain both erythrocytes and leukocytes.

Treatment and Disposition

Among patients with gastroenteritis, those with dysentery tend to experience the greatest morbidity and mortality. Several invasive bacterial agents, most notably Salmonella and Shigella, may result in bacteremia, sepsis, and death. This is especially of concern in the elderly, infants, and the immunocompromised. However, any bacterial agent can cause significant harm in susceptible patients. Worldwide, V. cholerae accounts for a significant number of deaths annually. Treatment depends on the causative agent; however, in the acute setting an empiric strategy is often required (see below). Consider collecting stool for laboratory analysis in the patient with prolonged dysentery to guide future treatment.

Parasitic Enteritis

Essentials of Diagnosis

• Acute amebic dysentery may be clinically similar to bacterial dysentery
• Consider parasitic causes in patients with chronic diarrhea, a travel history to developing countries, or a history of institutionalization or immunocompromise

Clinical Findings

Parasitic agents are rarely identified in the ED. Acute amebic dysentery, caused by Entamoeba histolytica, may be difficult to distinguish clinically from dysentery of a bacterial cause. Consider parasitic causes in patients with a travel history to developing countries, in institutionalized patients, or in immunocompromised patients. Also consider parasitic causes in those with a prolonged course and in those not responding to conventional treatment. Laboratory analysis of stool may be of benefit for diagnosing suspected parasitic enteritis.

Treatment and Disposition

Treatment is best determined by the results of stool analysis. In the acute setting, empiric treatment may be required (see next section).

Supportive Care

Initial treatment consists of supportive care with special attention to the patient's hydration status. For many patients, this may be the only treatment necessary. Oral rehydration may be used for mild to moderate dehydration. In pediatric patients, oral rehydration can be accomplished by giving 50–100 mL/kg of a glucose–electrolyte solution over 4 hours.

In patients with evidence of more severe dehydration, initiate intravenous fluid resuscitation with normal saline or lactated Ringer's solution. Give pediatric patients a bolus of 20 mL/kg of normal saline and repeat as needed. Because children are particularly susceptible to hypoglycemia after prolonged vomiting and poor oral intake, a rapid bedside glucose determination should be performed in ill-appearing pediatric patients.

Empiric Chemotherapy

Interruption of the fecal–oral pathway should be the initial treatment for infectious gastroenteritis and can be accomplished by adherence to strict hygiene. Viral and noninvasive bacterial gastroenteritis, as well as many cases of bacterial dysentery, tend to be self-limiting and to require only supportive therapy. Initiate empiric antibiotic treatment in patients with a suspected invasive bacterial process and severe diarrhea, systemic symptoms, fever, and abdominal pain or in those who appear toxic. Fecal cell count is of limited utility in deciding whom to treat. Admit patients with this presentation if they are immunocompromised, have complicating medical conditions, are elderly, or are infants. For these patients, base ultimate treatment on culture results. Young, healthy adults may be candidates for outpatient treatment if they meet basic discharge criteria including ability to tolerate oral intake and having normal vital signs.

Because the results of cultures are usually unavailable in the acute setting, treatment must be empiric and guided by knowledge of common causes of dysentery (Table 36–3). Ciprofloxacin, 500 mg orally twice daily for 3–5 days, is the drug of choice. Azithromycin is an option in children and pregnant women. Use empiric treatment with caution in pediatric patients and the elderly because of an association with hemolyticuremic syndrome (HUS). This association has been shown with both ciprofloxacin and TMP-SMZ and is most strongly associated with treatment of enterohemorrhagic E. coli 0157:H7. HUS follows a diarrheal illness and is characterized by hemolytic anemia, renal failure, and thrombocytopenia. Most cases are in children and the elderly, but people of any age can be affected. Salmonella and Shigella have also been implicated. If possible, treatment in these patients should be based on culture results. If C. difficile infection is suspected, stool should be tested for C. difficile toxin and treatment initiated with metronidazole.

Because no broad empiric strategy exists for the treatment of parasitic agents, drug therapy is best guided by laboratory analysis. However, if amebic dysentery is of concern, treatment with metronidazole should be considered. A second agent, such as iodoquinol, is needed after initial treatment.

Symptomatic Treatment

Antiemetics

Intravenous hydration helps reduce emesis and should be used as initial therapy. Often this is the only therapy needed. For patients with uncontrollable, protracted vomiting, the use of an antiemetic can be considered. However, these agents may cause somnolence and complicate evaluation in a potentially septic population. In addition, side effects are common, especially dystonic reactions with the phenothiazines (prochlorperazine or promethazine). If patients can tolerate some oral intake, a trial of oral antiemetics is reasonable. In children, ondansetron given as a single oral dose may prevent the need for intravenous rehydration. A single oral dose can be followed by repeated small doses of an oral rehydration solution. The following are some available antiemetic options:

• Prochlorperazine (Compazine)—Adults, 5–10 mg intravenously, or 25 mg rectally; children >10 kg, 0.1 mg/kg rectally every 6 hours (use is contraindicated in children <10 kg)
• Ondansetron (Zofran)—Adults, 4–8 mg intravenously or orally every 4–6 hours; children, 0.1 mg/kg
• Promethazine (Phenergan)—Adults, 12.5–25.0 mg intravenously or rectally; children, 0.25–1.0 mg/kg rectally every 4–6 hours; use promethazine with caution in the elderly as it can alter mental status
• Metoclopramide (Reglan)—Adults, 5–10 mg intravenously; children, 0.1–0.2 mg/kg intravenously every 6–8 hours

Antidiarrheal Agents

Antimotility and antisecretory agents should be used with caution. Of concern is the association of morphine administration with Salmonella and Shigella bacteremia. An additional association has been suggested between the use of opiates, loperamide, or diphenoxylate with atropine and the precipitation of toxic megacolon in patients with ulcerative colitis or antibiotic-associated colitis. Antimotility and antisecretory agents should generally not be used in febrile patients with dysentery. They can generally be used in patients that do not have fever and have nonbloody diarrhea that is not severe. In the acute setting, benefits often do not outweigh possible risks of using these agents. Commonly used agents and some associated risks are listed below:

• Loperamide (Imodium)—avoid in patients with antibiotic-associated colitis, IBD, or dysentery
• Bismuth subsalicylate suspension (Pepto-Bismol)—avoid in pediatric patients because of concern about Reye syndrome; it may cause salicylate toxicity
• Kaolin-pectin suspension (Kaopectate)—may cause constipation, bloating; avoid if intestinal obstruction is suspected
• Diphenoxylate with atropine (Lomotil)—avoid in pediatrics patients; may precipitate toxic megacolon in patients with IBD; may cause central nervous system depression
• Opiates—avoid in patients with antibiotic-associated colitis, IBD, or dysentery

Treatment of Dehydration

A patient with vomiting and diarrhea is at risk for dehydration. The clinician must assess hydration status using vital signs, and examination of mucous membranes and capillary refill. Associated symptoms such as lightheadedness on standing also provide insight into the patient's hydration status. The severely dehydrated patient generally needs intravenous volume replacement with isotonic fluids. For mild or impending dehydration, oral fluid replacement is often adequate. Infants with impending dehydration or even mild to moderate dehydration can usually be successfully rehydrated over 3–4 hours with the administration of frequent, small amounts of an oral rehydration solution.

Disposition

Hospitalization is rarely required for vomiting or diarrhea due to food poisoning or viral gastroenteritis. Even though symptoms may be severe, the vomiting or diarrhea rarely persists long enough to require inpatient parenteral hydration. Patients with dysentery and a toxic appearance, severe dehydration, or persistent vomiting or diarrhea; those with complicating medical conditions; and the very young or elderly may require hospitalization. Patients should meet basic discharge criteria including stable vital signs, benign abdominal exam, and ability to tolerate oral intake before leaving the emergency department. Hospitalization may be required in the following cases:

• extremes of age—newborns and the very elderly tolerate fluid depletion poorly;
• systemic toxemia, as indicated by high fever and rigors;
• possible toxic exposures requiring further evaluation or treatment;
• massive diarrhea or extreme dehydration;
• severe vomiting (preventing oral replenishment) with diarrhea;
• for further evaluation of unexplained causes of vomiting or diarrhea;
• poor home environment where required support cannot be provided.

Inflammatory Bowel Disease

Essentials of Diagnosis

• Usually longstanding diarrhea, abdominal pain, malaise, weight loss, and fever are some of the nonspecific signs and symptoms
• In general, Crohn's patients have nonbloody diarrhea and ulcerative colitis patients have bloody diarrhea
• Patients often have family history of inflammatory bowel disease

Clinical Findings

IBD is the term used to describe the two likely autoimmune disorders, Crohn's disease and ulcerative colitis that cause chronic and often debilitating GI symptoms. Patients with Crohn's disease or ulcerative colitis may have ongoing symptoms for years without a specific diagnosis of the disease. Because symptoms may worsen slowly, patients may delay presenting for evaluation. Crohn's disease can involve any segment of the GI tract from the mouth to the anus and causes a transmural inflammation of the bowel. With transmural involvement, complications such as fistulae, abscesses, small bowel obstruction, or perforation can occur. Perianal disease (fistulae and abscesses) can occur as well in Crohn's disease. Patients with ulcerative colitis have disease limited to the mucosa and submucosa of the colon beginning in the rectum and spreading proximally with no skip areas. Typical symptoms include pain, tenesmus, and rectal bleeding. The typical course for patients with Crohn's disease includes intermittent exacerbations of abdominal pain, vomiting, and severe nonbloody diarrhea and fever followed by relatively symptom-free periods of remission. Many patients with the disease have frequent exacerbations requiring treatment with immunosuppressants. Because Crohn's disease often involves the terminal ileum, patients may have right lower quadrant pain that can be confused with appendicitis if a more careful history of recurrent symptoms is not obtained. Frequent diarrhea and rectal bleeding are common with exacerbations of ulcerative colitis. Diagnosis of IBD is suggested by history but can be more firmly established with endoscopy and histology of biopsies. During exacerbations, patients may present to the ED for evaluation. Especially for Crohn's disease, contrast enhanced CT of the abdomen is the study of choice to determine if complications such as abscess, microperforation, or obstruction have developed. Consider toxic megacolon, a condition in which the bowel dilates and may become ischemic leading to the clinical picture of sepsis, if severe abdominal pain or distention is evident. This condition, which has a mortality of 50%, can occur during severe exacerbations of IBD.

Management and Disposition

When patients with IBD present to the ED during exacerbations, management depends on the degree of dehydration, ability to maintain oral intake, and abdominal examination findings. If available, consultation with a patient's gastroenterologist is usually advisable for an IBD patient in the ED. Typical medical therapy for exacerbations includes bowel rest, intravenous fluids, close monitoring of electrolytes, intravenous antibiotics and steroids, and often will require admission for control of symptoms. If surgical conditions such as obstruction, abscess, fistula, or toxic megacolon are identified, consult a surgeon on an emergency basis.

Gastroesophageal Reflux Disease

Essentials of Diagnosis

• Substernal midline burning pain after eating and when recumbent
• Postprandial reflux of gastric contents into the posterior pharynx or the mouth

Clinical Findings

Gastroesophageal reflux disease (GERD) is a common disorder causing substernal burning discomfort often radiating toward the neck. Symptoms are usually worse after eating or when reclining and are often improved, if only temporarily, by antacids. The condition develops when high-concentration acidic gastric secretions damage the protective epithelial mucosa and cause esophagitis. Other symptoms of GERD include nausea, sore throat, hoarseness, and wheezing. Occasionally gastric fluids and small amounts of undigested food will reflux into the posterior pharynx, mouth, or upper airway. Because symptoms of acute coronary syndrome may overlap with those of GERD, consider an ECG and rule out myocardial infarction protocol for patients in which it is difficult to accurately differentiate the two conditions.

Management and Disposition

Patients with GERD are usually given recommendations for lifestyle modification such as a list of foods to avoid (eg, caffeine, chocolate, fatty foods, alcohol, and peppermint) which lower the esophageal sphincter pressure. Patients with GERD should be advised to stop smoking for two reasons: (1) smoking decreases salivation that neutralizes acidic secretions in the distal esophagus and (2) smoking lowers the esophageal sphincter pressure. Other foods to avoid include those that lower the gastric pH such as orange juice, red wine, and colas. Medications that can exacerbate reflux symptoms by lowering the esophageal sphincter pressure include calcium channel blockers, β-agonists, anticholinergics, diazepam, estrogen, narcotics, progesterone, and theophylline. One simple modification includes raising the head of the bed at least 6 inches if heartburn or other symptoms such as coughing, wheezing, or laryngospasm are prominent at night. Pharmacologic treatment consists of H2-blockers twice daily for mild symptoms or proton pump inhibitors once daily for moderate to severe disease. Patients should follow up with a primary-care physician for further evaluation. Some patients may benefit from outpatient esophagogastroduodenoscopy, since longstanding GERD is associated with Barrett's esophagitis and esophageal cancer.

Esophageal Rupture

Essentials of Diagnosis

• Classic triad of vomiting, lower chest pain, and subcutaneous emphysema is occasionally present
• Hamons sign is a crunch-like sound from movement of mediastinal air
• More likely to occur today from instrumentation of the esophagus than spontaneous rupture with vomiting
• Hypotension, tachycardia, dyspnea, and fever are ominous signs, and rapid diagnosis and treatment are essential to achieve the best chance at survival

Clinical Findings

Esophageal rupture also known as Boerhaaves syndrome may occur from a variety of causes. Forceful vomiting, instrumentation of the esophagus, or blunt or penetrating trauma to the chest can all cause esophageal rupture. Once gastric and oral secretions leak out of the esophagus into the mediastinum or pleural cavity, an inflammatory and septic process begins. Patients may develop severe tachycardia, hypotension, respiratory distress, or other signs of sepsis associated with mediastinitis. Clinicians must keep a high index of suspicion for this condition because the longer the mediastinal soilage persists, the worse the patient's chances for a successful outcome. The classic triad of vomiting, lower chest pain, and subcutaneous emphysema is unfortunately not common. Hamons sign is a crunch-like sound caused by the presence of air moving within the mediastinum. Esophageal rupture should be considered in patients with vomiting, fever, and chest pain. While rarely normal in Boerhaaves syndrome, chest X-ray may demonstrate pneumomediastinum, pneumoperitoneum, either-sided pleural effusions, or pneumothoraces. For patients with fever or chest pain in setting of chest trauma, recent esophageal instrumentation, or forceful vomiting, an aggressive approach to diagnosis is recommended. Esophageal fluoroscopy using water soluble contrast may be required for diagnosis. If the initial study is negative, a barium esophagram should be performed for complete evaluation. For critically ill patients who are unable to tolerate a fluoroscopic study, a contrast-enhanced CT of the chest may demonstrate extra esophageal air and/or paraesophageal fluid and suffice for diagnosis.

Management and Disposition

Successful management of esophageal rupture depends on timely definitive treatment including decontamination of soilage in the mediastinum and in general primary repair of the esophageal injury. In the ED, management of the patient should focus on rapid stabilization of the ABCs, including intubation if respiratory compromise is developing or already present. Large-bore peripheral or central intravenous access is required for fluid resuscitation. Intra-arterial pressure monitoring is advisable. To prevent further contamination of the mediastinum, patients should be kept NPO and a nasogastric tube placed for gastric decompression. Broad-spectrum intravenous antibiotics should be initiated. Emergency consultation with a cardiothoracic surgeon is necessary as treatment is almost always surgical, however potential management options include esophagectomy, stent placement, surgical repair of the tear, and conservative treatment. Early referral should be initiated if the patient presents to a facility without the surgical or critical care expertise to manage esophageal rupture.

Esophageal Foreign Body

Pediatric Esophageal Foreign Body

See also Chapter 50.

Clinical Findings

Children commonly swallow foreign bodies, which are most often coins. Fortunately, most pass from the hypopharynx into the esophagus without causing airway obstruction. (See Chapter 50 regarding management of pediatric airway foreign body obstruction). Because of the size of coins, children may have difficulty spontaneously clearing the foreign body from the esophagus. A radiograph that visualizes the neck, chest, and abdomen is very useful to identify and track the progress of metallic foreign bodies such as a coin (see Figure 50–10). One other metallic foreign body that deserves special mention includes the button battery. Button batteries are small discs about the size of a pill or a piece of candy that can cause significant mucosal irritation and even perforation if left in place.

Management and Disposition

Once a coin or other object passes through the lower esophageal sphincter into the stomach, it is very likely to traverse the entire GI tract without difficulty. Objects that become stationary in the esophagus or those associated with pain, difficulty swallowing, drooling, or difficulty breathing should be removed on an emergency basis. To prevent significant complications, button batteries should be removed on an emergency basis by endoscopy when identified. Once a coin enters the stomach in an asymptomatic patient, outpatient follow-up with a primary-care physician is acceptable. Parents should be instructed to return to the ED if abdominal pain, vomiting, or fever develops.

Food Bolus Impaction

Clinical Findings

Adults more commonly become symptomatic with esophageal foreign bodies in the setting of food bolus impaction. When food bolus impaction occurs, it is usually a combination of the nature of the food that was swallowed and presence of pathology in the esophagus. Meat that is partially chewed is a common source of impaction. Esophageal abnormalities that predispose to impaction include benign stricture, Shatzki's ring, or esophageal spasm with esophagitis in the distal esophagus. Patients are usually symptomatic with dysphagia, chest pain, inability to handle oral secretions, and vomiting. A chest X-ray is unlikely to demonstrate the food bolus impaction, but it may demonstrate an air–fluid level in the esophagus. A contrast radiographic study is not recommended as it will complicate endoscopy if the food bolus impaction does not spontaneously clear.

Management and Disposition

Glucagon 1 mg intravenous has been used to relax the lower esophageal sphincter and potentiate clearance of the esophageal impaction. Studies suggest that if the food bolus is meat, glucagon is unlikely to facilitate passage of the bolus but most gastroenterologists still recommend its use. Symptomatic patients require urgent endoscopy to relieve the esophageal obstruction. Endoscopy has a high success rate of removing the obstruction. If obstructive symptoms improve, a trial of fluids is reasonable to determine if the food bolus has moved and the obstruction has resolved. If spontaneous clearance occurs, patients should have outpatient follow-up with possible endoscopy arranged to determine if underlying esophageal pathology contributed to the problem.

Acute Gastritis and Peptic Ulcer Disease

Essentials of Diagnosis

• Nausea, vomiting, epigastric abdominal pain, and mild tenderness to palpation
• May have coffee ground hematemesis or guaiac positive stool
• History of exposure to GI irritants such as NSAIDs or alcohol

Clinical Findings

Patients with acute gastritis often present complaining of epigastric abdominal burning type pain associated with nausea or vomiting. Food may relieve or exacerbate symptoms. Often there is a history of exposure to GI irritants such as NSAIDs, alcohol, and cocaine. Other etiologies include radiation exposure during cancer therapy, infectious causes such as Helicobacter pylori, or other bacteria, viruses, fungi, or parasites. The pain associated with peptic ulcer disease is nonradiating, burning, and classically occurs 2–3 hours after a meal. Gastric and duodenal ulcers are associated with H. pylori infection and NSAID use. Duodenal ulcers are also are linked to cigarette smoking. Laboratory evaluation should include hepatic function tests, lipase, hemogram (if significant blood loss is a concern), urinalysis, and urine pregnancy test if indicated. If abdominal discomfort is severe, consider an acute abdominal series or CT of the abdomen to exclude perforated viscus. Consider a gallbladder ultrasound if the patient is at risk for gallstones (hypercholesterolemia or positive family history of cholelithiasis) or has right upper quadrant abdominal tenderness or pain. Remember to include acute coronary syndrome in the differential of epigastric abdominal pain in patients with risk factors for the condition such as age over 40, hypertension, diabetes, and positive family history. In such cases consider an ECG and/or rule out myocardial infarction protocol if symptoms are suspicious for anginal equivalent.

Treatment and Disposition

Acute gastritis is a clinical diagnosis that can be definitively confirmed by endoscopy. Endoscopy for acute gastritis is in general a nonemergency diagnostic procedure. Patients diagnosed with acute gastritis who have mild abdominal discomfort, no peritoneal signs, and are tolerating oral fluids may be discharged from the ED. Discharge instructions should include avoidance of irritants that may be contributing to the condition (NSAIDs or alcohol). Pharmacologic treatment can be with over-the-counter antacids, H2-blockers (cimetidine, ranitidine or famotodine), or proton pump inhibitors (omeprazole). Patients should follow-up with a primary-care physician for reevaluation and possible referral for endoscopy. Patients with severe dehydration and/or intractable nausea and vomiting should be admitted to the hospital or to an observation unit for serial abdominal examinations and rehydration. Intravenous omeprazole may provide symptomatic relief.

Patients with suspected gastric or duodenal ulcers should be counseled to eliminate risk factors such as smoking and NSAID use. They should be referred to primary care for H. pylori testing and treatment if indicated. Proton pump inhibitors, though more expensive than H2 blockers, have been shown to produce faster healing rates of ulcers. Proton pump inhibitors may also provide more rapid pain relief.

Patients with severe pain, significant confirmed or suspected blood loss from ulcers should be admitted. Patients with confirmed or suspected perforated ulcer should receive emergent surgical consultation and admission.

Alcoholic Hepatitis

Essentials of Diagnosis

• History of heavy alcohol consumption
• Nausea, malaise, and low-grade fever
• Evidence of hepatic dysfunction such as abnormal coagulation studies, hyperbilirubinemia, or moderately elevated AST

Clinical Findings

Alcoholic hepatitis (AH) should be suspected in any patient with a history of heavy alcohol use presenting with nausea, malaise, and low-grade fever. Other presenting symptoms and signs may include jaundice, anorexia, right upper quadrant pain, hepatomegaly, or ascites. Alcoholic hepatitis develops in up to 35% of heavy drinkers and can present on a spectrum from slightly tender hepatomegaly to fulminant hepatic failure. Stigmata of chronic liver disease are often present including palmar erythema, spider angiomata, and gynecomastia. While low-grade fever (usually not higher than 101°F) is often present in AH, infectious etiologies should also be considered. Because abdominal pain is not common with AH, suspect other etiologies such as spontaneous bacterial peritonitis, pancreatitis, or hollow viscus perforation in alcoholic patients with abdominal pain complaints. Right upper quadrant tenderness and hepatomegaly are common findings related to hepatic inflammation and swelling associated with AH. Common abnormal laboratory studies include elevated PT, elevated unconjugated hyperbilirubinemia, moderately elevated AST, and only mildly elevated ALT with the ratio of AST:ALT typically in a 2:1 pattern.

A long used objective scoring system, the Maddrey Discriminant Function (MDF) score has been employed to determine the severity of an episode of AH. Taking into account the bilirubin and absolute value of the prothrombin time, this system has been criticized as being only moderately sensitive and specific and perhaps missing those patients with a low score but significant mortality.

The Glasgow Alcoholic Hepatitis Score (GAHS) is a new tool to help accurately predict mortality at 28 and 84 days when measured at days 1 and 7 (See Table 36–4). It is a simple system incorporating five variables (age, serum bilirubin, blood urea, prothrombin time, and white blood cell count) and has been shown to be a more accurate predictor of outcome than the MDF score. Additionally, it can help identify those patients who would benefit from corticosteroids.

Treatment and Disposition

While controversial, treatment of AH with corticosteroids (prednisolone 40 mg/d for 4 weeks followed by a taper) is generally recommended for patients with MDF >32 or GAHS ≥9 with spontaneous encephalopathy and no contraindications such as GI bleed, hepatorenal syndrome, sepsis, or viral hepatitis. Patients with severe AH or who are symptomatic should be hospitalized preferably in an ICU setting until the condition stabilizes. Close attention should also be paid to blood glucose levels, coagulation studies, signs and symptoms of Wernicke encephalopathy, and acute alcohol withdrawal. For patients with coagulopathy and concurrent bleeding, transfusion with fresh frozen plasma should be considered. In general, AH is an inflammatory condition that is likely to resolve slowly if alcohol is avoided. With persistent alcohol intake, patients with AH are likely to develop progressive cirrhosis and hepatic failure. Patients with mild AH who can tolerate fluids and are hemodynamically stable may be candidates for outpatient treatment. These patients should be counseled to undergo treatment for alcoholism, as abstinence from alcohol is the only treatment available to prevent the condition from deteriorating into advanced hepatic failure. Unfortunately, even with total abstinence from alcohol, some patients will continue to have progressive hepatic dysfunction from alcoholic liver disease and often will develop residual cirrhosis.

Hemorrhoids

Essentials of Diagnosis

• Perianal mass associated with itching, bleeding, and/or pain
• Bleeding is usually bright red blood
• Careful inspection of the perineum and digital rectal examination are necessary for diagnosis as other causes of rectal pain such as perianal abscess or anal fissure are common

Clinical Findings

Careful history and physical examination should be performed in patients with anorectal complaints. Bleeding is the most common presenting symptom associated with hemorrhoids. Usually the bleeding from hemorrhoids is bright red although significant blood loss or associated anemia is rare. Darker bleeding or blood mixed in with stool are not characteristic of hemorrhoidal bleeding and suggest that the source is more proximal. General guidelines recommend that patients with rectal bleeding should undergo a more complete evaluation including anoscopy and sigmoidoscopy as an outpatient. Careful inspection may reveal an anal fissure, which can cause severe anal pain that is classically worst after defecation. Patients with portal hypertension from chronic liver disease develop anal canal varices, which are clinically different from hemorrhoids. Pain from hemorrhoids is generally associated with thrombosis. An important clinical distinction is origin of the hemorrhoid relative to the dentate line. Hemorrhoids that originate above the line are “internal” and those that originate below are “external.” Internal hemorrhoids are less common and do not have overlying sensory epithelium, and therefore they are generally nonpainful. Determine the origin (internal vs external), degree of prolapse, and reducibility of hemorrhoidal tissue. Thrombosed external hemorrhoids are common and cause acute pain, a perianal lump, and bleeding when overlying skin becomes eroded from irritation. Thrombosed internal hemorrhoids produce bleeding and mucus production and when prolapsed may be tender. If gangrenous, however, internal hemorrhoids are extremely painful. Although fortunately rare, fever and urinary retention can be ominous signs of severe perineal necrotizing infection associated with infected hemorrhoids.

Treatment and Disposition

Treatment depends on the degree of thrombosis and whether the hemorrhoid is an internal or external hemorrhoid. Most nonthrombosed and nonincarcerated hemorrhoids are treated medically with instructions for sitz baths and good perianal hygiene, stool softeners, high-fiber diet, and pain control. While over-the-counter topical medications and suppositories including steroids are often recommended for symptomatic control of hemorrhoids, there is no evidence that these measures alter the time course of the disease. Acutely painful thrombosed external hemorrhoids are usually bluish to purple in color, are firm, and very tender to touch. Patients with symptomatic thrombosed external hemorrhoids may be excised in the ED using local anesthesia with epinephrine and removal of the overlying skin with an elliptical incision and completely evacuating the clot. Only hemorrhoids that are clearly thrombosed should be excised in the emergency department to avoid significant bleeding. Contraindications to excision of external hemorrhoids in the ED include bleeding disorders, immunocompromised state, or significant hemodynamic instability. After excision, the wound can be packed with gauze or gelfoam, and sitz baths initiated within 24 hours. Consult a general surgeon for incarcerated thrombosed internal hemorrhoids or those associated with excessive bleeding, which should be surgically treated in the operating room. Patients discharged from the ED should have specific instructions to return to the ED for fever, significant bleeding, or severe pain or inability to void as these may be indicative of significant complications such as infection. After excision, patients should also return to the ED or a primary-care physician in 48–72 hours for a wound check.