Although food containing preformed toxins can cause illness within 1 to 6 hours, most acute gastroenteritis has at least a 12- to 48-hour incubation period (Table 183.1). Typically, the onset is gradual and is often noticed as mild dyspepsia after eating a meal. This is the meal often suspected by the patient to be the cause of the illness. However, the pathogen has usually been incubating for the last 1 to 2 days and is just starting to cause symptoms.

Table 183.1 Symptom Onset Time

ORGANISM OR PATHOGEN	Symptom Onset
Scombroid fish (poisoning)	5-60 min; average, 20-30 min
Staphylococcus	1-6 hr
Bacillus cereus	2-14 hr; average, 2-4 hr
Ciguatera fish (poisoning)	2-6 hr, ≥24 hr
Clostridium perfringens enterotoxin	6-24 hr
Vibrio parahaemolyticus	4-48 hr; average, 8-12 hr
Salmonella	8-48 hr
Shigella	24-48 hr
Plesiomonas shigelloides	24-48 hr
Cholera and noncholera Vibrio species	24-48 hr
Enterotoxigenic Escherichia coli	24-72 hr
Norovirus or rotavirus	24-72 hr
Campylobacter	2-5 days
Yersinia	1-14 days; average, 2-4 days
Aeromonas hydrophila	1-5 days
Hemorrhagic Escherichia coli O157:H7	3-8 days
Cryptosporidium and Isospora	5-10 days
Clostridium difficile	Days to month;, average, 5-14 days
Giardia	1-3 wk
Entamoeba histolytica	1 wk-1 yr

Within 1 to 2 hours after the initial dyspepsia, nonbloody vomiting often begins. If bleeding does occur, the most common cause is a Mallory-Weiss tear. This results when forceful ejection of gastric contents creates a tear in the mucosa at the junction of the esophagus and the stomach. It rarely occurs during the first episode of vomiting, and treatment is almost always supportive. An initial presence of blood, or a persistent predominance of gross blood, should prompt a search for noninfectious causes of vomiting such as a bleeding peptic ulcer or esophageal varices.

Diarrhea can occur simultaneously with vomiting, or it may be delayed for up to 48 hours after vomiting begins. In some cases, diarrhea may be the only component of clinical illness. Gross diarrheal blood is more common than hematemesis and varies by pathogen (Box 183.1). Dysentery, defined as a diarrheal stool containing gross blood, can be accompanied by fever, abdominal pain, and tenesmus.

Documentation

History

• Onset and duration

• Amount of vomiting

• Amount of diarrhea

• Presence of blood in either

• Associated symptoms

• Fever

• Headache

• Neurologic symptoms

• Pain

• Ingestion of suspicious foods in last 7 days

• Raw or undercooked (sushi)

• Well or wilderness water

• Picnics

• Exposure to people with similar symptoms

• Recent travel

• Camping or hiking (consider Giardia)

• International travel (consider simple traveler’s diarrhea or a more serious cause such as cholera, depending on location)

• Recent antibiotics or hospitalizations (consider Clostridium difficile)

• Pregnancy (increased risk of Listeria monocytogenes)

• Past medical history

• Abdominal surgical procedures (consider partial obstruction)

• Irritable bowel syndrome/inflammatory bowel disease

• Immunocompromised state

• Diabetes (look for ketoacidosis)

• Medications

• Antibiotics (consider Clostridium difficile)

• Warfarin (case reports of extreme international normalized ratio elevation in severe diarrhea have been published)

• Social history

• Alcohol or illicit drugs (consider symptoms of withdrawal)

• Sexual activity (consider pregnancy, gynecologic cause, and multiple causes in men who have sex with men)

• Animal exposure

• New pets in house (10% of dogs and cats excrete Salmonella)

• Slaughterhouse workers, farm workers, veterinarians (e.g., Bacillus anthracis, Coxiella burnetii)

• Family history

• Irritable bowel syndrome or inflammatory bowel disease

Differential Diagnosis

Vomiting and diarrhea can result from other pathologic states, or they may be iatrogenic, such as from a medication side effect. Vomiting and diarrhea can herald an endocrine emergency such as in adrenal crisis, or they may represent a completely benign event, such as diarrhea after long-distance running. Maintaining a level of suspicion for other causes is essential, to minimize the chance of missing a more dangerous disorder or to reassure a patient when the cause is benign. The following subsections describe additional diagnoses to consider.

Vomiting and Diarrhea

Vomiting Without Diarrhea

Vomiting is a symptom and not a diagnosis. Gastroenteritis can be diagnosed only if signs of gastritis enteritis are clearly present, based on clinical evaluation. Vomiting can also be caused by many toxic and metabolic disorders and organ dysfunction. Ingestions, carbon monoxide, and other poisonings often incite vomiting without other signs. Early hepatitis, biliary disease, and early appendicitis may cause vomiting, with few other signs. Other important causes of isolated vomiting include those discussed in the following paragraphs.

Obstruction

A history of abdominal surgery should raise suspicions of a possible intestinal obstruction. On physical examination, abdominal distention is common, and hypoactive, high-pitched bowel sounds are in contrast to the hyperactive bowel sounds usually found in gastroenteritis.

Cyclic Vomiting

The challenge in patients with cyclic vomiting is in determining the rare episode when the symptoms may be caused by gastroenteritis, instead of being an exacerbation of the underlying disorder. Diarrhea is rare, fever should not be present, and a history of stressful triggers is often identifiable when the episode results from an exacerbation of cyclic vomiting.

Intracranial Disease

Headache is a common complaint that often accompanies acute gastroenteritis. However, vomiting also frequently occurs simultaneously with headaches caused by migraines, intracranial hemorrhage, or tumor. When the history of a headache is elicited, the physician must consider the following factors so that more dangerous disease is not overlooked. Headache that started before the onset of vomiting, or headache as the primary focus of the patient, is concerning. Similarly, a sudden, severe headache occurring while vomiting may indicate an aneurysmal rupture resulting from increased intracranial pressure during the Valsalva maneuver.

Myocardial Infarction

Atypical presentations of myocardial infarction are important to recognize. Vomiting without diarrhea in a patient with significant risk factors should prompt consideration of a cardiac cause. The concomitant presence of shortness of breath and diaphoresis, with or without chest pain, further increases the probability of myocardial infarction.

Early Pregnancy

“Morning sickness” is most common within the first 13 weeks of gestation. However, pregnancy-associated nausea and vomiting may be more severe at other times of day and may continue well past the first trimester. Not unusually, vomiting is the first symptom a woman experiences before she is aware of the pregnancy. Vomiting without diarrhea, symptoms spanning several days, and hunger between episodes should arouse suspicion of pregnancy as the cause. Inquiring about breast tenderness and missed or irregular menstrual periods can help to elicit the diagnosis. A pregnancy test should be standard in the evaluation of any woman of childbearing age who presents with symptoms of acute gastroenteritis.

Focal Pain

Patients with acute gastroenteritis often complain of abdominal pain, but the quality of this pain tends to be crampy and migratory secondary to increased intestinal motility and spasm. Mild, constant midepigastric pain is also common after vomiting because of gastritis and abdominal wall muscle exertion. In rare cases, Campylobacter and Yersinia may cause isolated cecitis, characterized by focal right lower quadrant pain in the absence of vomiting or diarrhea that mimics acute appendicitis. Severe, focal, unrelenting pain should prompt a search for other causes, however.

Focal Inflammation

Causes of focal inflammation including gastritis, pancreatitis, cholecystitis, diverticulitis, and appendicitis are suspected when pain is isolated to these respective areas.

Gynecologic Emergencies

These conditions include tubo-ovarian abscess, ovarian torsion, ruptured ectopic pregnancy, and pelvic inflammatory disease. A pelvic examination and pregnancy test are essential in the evaluation of women who complain of concomitant pelvic or lower abdominal pain.

Diffuse Pain

Perforated Viscus

A history of peptic ulcer disease, recent gynecologic or gastrointestinal instrumentation, or fever with peritoneal signs should raise the suspicion of perforated viscus.

Ischemic Bowel

In patients with risk factors for peripheral vascular disease, diffuse abdominal pain along with nausea and diarrhea after eating may indicate compromised blood flow to the intestines. The onset may be more gradual in patients with slowly progressive atherosclerosis, or it may be abrupt from an embolic event to the intestinal vasculature. The physical examination is often unimpressive, given the severity of the stated discomfort (hence the finding of “pain out of proportion to examination”). A high index of suspicion should be maintained, especially in the older population, because missing the diagnosis can lead to significant morbidity and even death.

Diagnostic Testing

Diagnostic testing is often overused in infectious gastroenteritis. With symptoms lasting less than 24 hours in otherwise healthy individuals who are not at the extremes of age, no diagnostic testing is indicated, other than a pregnancy test in women of reproductive age. Exceptions include patients with severe symptoms, multiple grossly bloody stools, or hemodynamic instability, as well as testing for epidemiologic purposes if food poisoning or a bioterrorism event is suspected.^3,⁴

Laboratory or radiologic evaluation may be helpful in several situations. A bedside urine evaluation for ketones may be useful to document dehydration and to guide intravenous fluid management. In patients whose symptoms have persisted for more than 24 hours, electrolyte determinations and tests of kidney function may be indicated. If a chemistry panel is obtained, calculation of the anion gap should be done to prevent missing clues to diabetic or alcoholic ketoacidosis, toxic ingestions, or other serious conditions. Mild elevations in liver function tests are very nonspecific in acute gastroenteritis, but marked elevations could be an indication of hepatitis A infection.

Although the diagnostic yield is generally low, stool culture in patients who have unrelenting diarrhea may detect a treatable cause that can significantly shorten the course of illness.⁵ Typically, positive results take at least 2 to 3 days, and symptoms have often resolved by the time results return. For patients who develop diarrhea 3 days or more after being hospitalized, bacterial stool cultures have not been found to be helpful.⁶ Testing for ova and parasites has not shown to be cost effective unless the patient is at identifiable risk. This group includes patients with diarrhea persisting for several days after international travel to endemic regions, persons who ingest untreated water while camping or hiking, those with exposure to daycare centers, men who have sexual contact with other men, and persons who have sexual contact with patients with AIDS.⁷ If parasitic infection is suspected, three separate specimens from different time periods must be sent for ova and parasites before the test can be considered negative. Clostridium difficile testing should be performed for anyone with persistent diarrhea and a history of antibiotic use in the previous 3 months. In patients with severe diarrhea, C. difficile testing should be considered even in the absence of recent antibiotic exposure or recent hospitalization. The reason is the emergence of a hypervirulent strain, designated NAP1/BI/O27, that has caused illness in otherwise healthy individuals without the traditional risk factors for C. difficile colitis.⁸

The recommended diagnostic work-up in patients with AIDS and in others who are severely immunocompromised is more aggressive. Studies in these patients tend to yield more positive results, and symptoms are less apt to resolve without intervention. Stool should be sent for culture just as in immunocompetent patients. C. difficile testing should be performed because this remains the most common pathogen detected in patients with human immunodeficiency virus infection and diarrhea. Three separate specimens should be sent to be examined for ova and parasites, given the intermittent shedding of organisms. In addition, stool should be sent for acid-fast smear to detect Cryptosporidium, Isospora, and Cyclospora. Finally, in severely immunocompromised patients with a CD4 count lower than 100 cells/microliter, a trichrome stain should be ordered to test for microsporidium.⁹ Unlike in immunocompetent patients, in whom blood cultures are of extremely limited use, blood culture results in immunocompromised patients may be positive in up to 40% of cases and may yield a diagnosis even in the absence of positive stool culture results.¹⁰ Fungal blood cultures should also be considered, to detect Mycobacterium avium complex. In this population, if severe diarrhea persists despite negative evaluations, the patient will need endoscopic evaluation for mucosal biopsy and additional cultures.

For patients with severe abdominal pain or distention, an obstructive plain radiographic series or abdominal computed tomography scan with oral and intravenous contrast can help to differentiate other more serious causes of their symptoms. Abdominal computed tomography scans without contrast, or with oral contrast alone, may be sufficient, depending on the experience of the radiologist conducting the examination.

A complete blood count is usually of little value, with rare exceptions. The stress of vomiting often causes transient leukocytosis that does not correlate with the severity or cause of illness. Hemoglobin and hematocrit determinations may be helpful in patients with hemorrhagic diarrhea for assessment of anemia. Eosinophilia may indicate an allergic or parasitic origin. Macrocytic anemia can occur with infection involving Diphyllobothrium latum, and low platelet counts can be seen in infections such as Q fever (Coxiella burnetii).

In patients with an acute onset of vomiting and diarrhea, documentation of gross blood in the stool is helpful. Checking for occult blood has not been proven to be sensitive or specific. When gross blood is absent, hemoccult testing provides little to no insight into the causative pathogen and should not be used to guide treatment. Similarly, fecal leukocyte testing has low sensitivity and specificity and should not be used to justify empiric antibiotic treatment.^11,¹²

To reiterate, most cases occur in young, otherwise healthy individuals who have had symptoms for less than 24 hours. In this population, minimal to no testing should be the rule.

Treatment and Disposition

Emergency treatment of gastroenteritis begins with airway, breathing, and circulation. Airway and breathing are rarely an issue unless large-volume hematemesis is present. Boerhaave syndrome, disruption of esophageal varices while vomiting, and severe cases of anthrax are some of the few causes of massive hematemesis.

If the patient is hemodynamically unstable, immediate intervention is required. The patient should receive fluid resuscitation with two large-bore intravenous catheters or a central line, and the physician should consider causes of illness other than simple gastroenteritis. If the patient has a recent history of international travel, review of the previous location’s endemic pathogens is essential. Countries such as Haiti have had outbreaks of cholera (Vibrio cholerae) that can lead to circulatory collapse in as little as 24 hours.

For patients who have severe allergic symptoms after ingesting fish and scombroid is suspected, treatment should be initiated with antihistamines.

For patients experiencing neurologic symptoms such as paresthesias, dysesthesias, reversal of hot and cold sensation, or even altered mental status after eating fish, ciguatera poisoning should be suspected. Although not universally accepted, mannitol, 1 g/kg of a 20% solution over 30 minutes, has dramatic effects on improving symptoms.¹³^–¹⁵

Most patients are stable, however, and are suffering from nausea, vomiting, crampy abdominal pain, and possibly diarrhea without other significant symptoms. For this group, the mainstays of treatment consist of rehydration and alleviation of symptoms through antiemetics (Fig. 183.1). The use of empiric antibiotics is not indicated in most cases.

Fig. 183.1 Treatment algorithm for adults without significant comorbid illness.

BUN, Blood urea nitrogen; Cr, creatinine.

For those patients who are hemodynamically stable and whose vomiting can be controlled, oral rehydration is adequate and is often greatly underused. Ketonemia has been implicated in gastroenteritis. In patients with significant dehydration, nausea and vomiting may continue because of circulating ketones long after the initial infectious cause has been eradicated by the body. In this circumstance, proper administration of intravenous fluids may be all that is required to resolve the patient’s symptoms. If a patient is unable to tolerate oral intake, intravenous normal saline solution is adequate for initial hydration. For patients with significant ketosis, switching to dextrose-containing compounds after initial rehydration may help to restore normal metabolic function more quickly.

Many choices of antiemetics and routes of administration are available. When choosing a medication, one should consider pregnancy class, cost, and side effects, particularly the extrapyramidal side effects of the phenothiazines and metoclopramide. Table 183.2 gives the characteristics of common antiemetic agents. If one agent fails, a switch to a different class of agent is recommended, rather than repeat administration of an agent of the same class.

Table 183.2 Commonly Used Drugs

The hazards of using antidiarrheal agents in acute gastroenteritis appear to have been overstated. For afebrile patients without grossly bloody diarrhea or a high suspicion of C. difficile colitis from recent antibiotic use, antimotility agents such as loperamide or atropine-diphenoxylate can be safely administered. Use of these drugs is recommended for large-volume diarrhea that compromises hydration status or is otherwise hindering a patient’s ability for self-care.

Antibiotics are rarely indicated in the empiric treatment of acute gastroenteritis, for many reasons. Viruses remain the most common causes of acute gastroenteritis in the general population, and these infections resolve without intervention. Most bacterial causes are self-limited and are eradicated by the host defenses in a short time. Common adverse reactions of most antibiotics are nausea or diarrhea, occurring in up to 10% of patients. Although certain antibiotics are more prone to causing C. difficile colitis, any antibiotic can predispose patients to this complication. Administering antibiotics to patients with non-typhi Salmonella infections is ineffective and may lead to a prolonged carrier state. If the patient has contracted illness from Escherichia coli serotype O157:H7, antibiotics will have no effect on the symptoms but may lead to an increased incidence of hemolytic-uremic syndrome. Finally, empiric treatment with antibiotics contributes to the alarming development of resistant pathogens in the general patient population. Empiric antibiotics are usually ineffective, may complicate the picture, may even harm the patient, and contribute to the formation of resistant organisms.

The indications for empiric antibiotics are very narrow. If a patient appears toxic, has a fever higher than 101° F and bloody diarrhea, or is hemodynamically unstable, antibiotics may be helpful. Grossly bloody diarrhea alone is not an indication for empiric antibiotic use, and again, bloody diarrhea may be caused by E. coli O157:H7. This serotype does not usually cause a fever, and therefore empiric antibiotics prescribed for grossly bloody diarrhea in conjunction with a temperature greater than 101° F should not raise concerns of inducing hemolytic-uremic syndrome.

Another indication for empiric antibiotics involves acute gastroenteritis in the setting of travel to areas endemic for traveler’s diarrhea. The most common pathogens include enterotoxigenic E. coli, Shigella, Salmonella, and Campylobacter. In many cases, prompt use of a fluoroquinolone can lead to relief of symptoms within hours. Unfortunately, resistance to this class of drugs and to many other antibiotics is rising throughout the world, and treatment failures are becoming more common. Of the foregoing pathogens, Campylobacter has a high enough resistance to fluoroquinolones that erythromycin is now the drug of choice in these infections. For continued empiric treatment of traveler’s diarrhea in patients who do not respond to fluoroquinolones, azithromycin may be used. Sending stool cultures before the initiation of antibiotics can be helpful, given the high rates of resistance, in anticipation of potential treatment failures. Table 183.3 gives specific antibiotic regimens for symptomatic patients in whom the pathogen is identified.

Table 183.3 Antibiotic Regimens for Identified Pathogens

ORGANISM OR PATHOGEN	ANTIBIOTIC TREATMENT	COMMENT
Unknown (if empiric therapy deemed necessary)	Ciprofloxacin 500 mg bid × 3 days or TMP-SMX DS bid × 3 days

Resistance high in tropics Unknown with recent antibiotic exposure; treat empirically for Clostridium difficile colitis Metronidazole 500 mg PO tid × 10 days Also effective IV or Vancomycin 125 mg PO qid × 10 days Not effective IV Campylobacter

Erythromycin 500 mg bid × 5 days

Azithromycin 500 once daily × 3 days

Not fluoroquinolones because of resistance Salmonella Ciprofloxacin 500 mg bid × 7-10 days or Azithromycin 1 g, then 500 mg once daily × 7 days Total 7 days
For inpatient treatment or Ceftriaxone IV Coxiella burnetii Doxycycline 100 mg PO bid × 15-21 days Listeria monocytogenes

Usually self-limited, efficacy of oral antibiotics unknown; susceptible to ampicillin and TMP-SMX

For suspected or known bacteremia, parenteral antibiotics required:

Ampicillin 2 g IV q4h with or without gentamicin (first week only) × 14 days

TMP-SMX 20 mg/kg/day of trimethoprim IV divided q6h × 14 days

Shigella

Ciprofloxacin 750 mg PO once daily × 3 days

Azithromycin 500 mg once daily × 3 days

Yersinia

For severe symptoms:

Doxycycline 100 mg IV bid + tobramycin or gentamycin 5 mg/kg/day once daily × 7-10 days

Supportive care if mild symptoms Vibrio parahaemolyticus Does not shorten the course In vitro susceptibilities to ciprofloxacin Hemorrhagic Escherichia coli O157:H7 Antibiotics not effective; may be detrimental Aeromonas or Plesiomonas

Azithromycin 500 mg PO once daily × 3 days

Ciprofloxacin 750 mg once daily × 3 days

Staphylococcus Antibiotics not effective Clostridium perfringens enterotoxin Antibiotics not effective Bacillus cereus Antibiotics not effective Cholera and noncholera Vibrio species

Ciprofloxacin 1 g × 1

Doxycycline 300 mg × 1 dose

Azithromycin 500 mg PO once daily × 3 days

Scombroid fish (poisoning) Antihistamines; antibiotics not effective Ciguatera fish (poisoning)

Antibiotics not effective

Mannitol 1 g/kg 20% solution over 30 min for symptom relief

Enterotoxigenic Escherichia coli

Ciprofloxacin 750 mg once daily × 1-3 days

Azithromycin 1 g PO x 1

Clostridium difficile Metronidazole 500 mg PO tid × 10 days Also effective IV or Vancomycin 125 mg PO qid × 10 days Not effective IV Norovirus or rotavirus Antibiotics not effective Cryptosporidium Antibiotics poorly effective Isospora or coccidia

TMP-SMX DS bid for 10 days

Ciprofloxacin 500 mg bid × 7 days

87% effective Giardia Tinidazole 2 g PO × 1 or Nitazoxanide 500 mg PO bid × 3 days or Metronidazole 250 mg tid × 5 days or Paromomycin 25-35 mg/kg/day divided tid × 7 days In pregnancy Entamoeba histolytica

Metronidazole 500 mg tid × 10 days followed by

Paromomycin 25-35 mg/kg/day divided tid × 7 days

Enterobius vermicularis Albendazole 400 mg × 1
or
Mebendazole 100 mg chewed × 1
or
Pyrantel pamoate 11 mg/kg (maximum, 1 g) × 1 Repeat dose × 1 in 2 wk
Repeat dose × 1 in 2 wk
Repeat dose × 1 in 2 wk Taenia saginata or Taenia solium

Praziquantel 5-10 mg/kg PO × 1

Niclosamide 2 g PO × 1

Diphyllobothrium latum

Praziquantel 5-10 mg/kg PO × 1

Niclosamide 2 g PO × 1

bid, Twice daily; DS, double strength; IV, intravenously; PO, orally; qid, four times daily; tid, three times daily; TMP-SMX, trimethoprim-sulfamethoxazole.

From DuPont HL. Bacterial diarrhea. N Engl J Med 2009;361:1560-1569.

In general, patients who are hemodynamically unstable at any point in their stay, who have persistent pain, or who continue to vomit frequently should be admitted until oral intake can be tolerated and pain improves. If a noninfectious origin has not been ruled out and symptoms continue, admission should also be considered. Patients with severe comorbid illness, and those who take multiple medications that would be affected by poor oral intake or malabsorption, may also need to be admitted.

Diabetic patients may be particularly challenged by acute gastroenteritis. Infection combined with an inability to take hypoglycemic medications may increase their blood glucose concentrations and may exacerbate their dehydration. Diabetic patients may become hypoglycemic, given their decreased intake in the setting of long-acting hypoglycemic medications, and physicians should have a low threshold for admitting these individuals. If an insulin-dependent patient is discharged, a basal rate of insulin must be continued. Cutting the usual dose of insulin in half, or instructing the patient to take the long-acting insulin only and checking blood glucose levels regularly, may be sufficient. Discussion with the primary care physician before discharge facilitates outpatient management.

Patients with persistent nausea but no vomiting can usually be discharged with an antiemetic and careful instructions for maintaining hydration. Persistent diarrhea alone is not an indication for admission, unless the patient is immunocompromised and has significant dehydration on presentation.

Dietary recommendations are always of great concern to patients on discharge. Many complex regimens involve significant dietary restrictions, based on limited scientific data. Patients should be advised that the number-one priority is to stay hydrated. If solid foods do not sound appealing, then they should not be encouraged. For patients with mild diarrhea or persistent nausea, water or commercially available sports drinks should be adequate. These drinks are not properly balanced for more severe dehydration. If the patient is having large volumes of diarrhea or fluid losses, a balanced glucose and electrolyte solution with or without starches is recommended. Oral rehydration solutions are available in many pharmacies. An effective solution can be made at home by adding one-half teaspoon of salt, one-half teaspoon of baking soda, and four tablespoons of sugar to 1 L of water.¹⁸

Once a patient becomes interested in solid foods, a bland diet of bananas, rice, apples, and toast (the BRAT diet) traditionally has been recommended. No data support the BRAT diet, and patients should be encouraged to eat small amounts of whatever appeals to them, with a few exceptions. Both caffeine and alcohol have direct stimulatory effects on the bowel and therefore may worsen symptoms. In addition, a few patients encounter temporary lactose intolerance after gastroenteritis. If dairy products exacerbate symptoms, then refraining from these products for 1 to 2 weeks should allow the intestines to restore their normal function.

Complications

Significant complications are fortunately quite rare following gastroenteritis. The following are important to keep in mind when treating a patient with current symptoms or a recent history of acute gastroenteritis.

Lactose Intolerance

The most common minor complication is temporary lactose intolerance, which usually resolves spontaneously. As symptoms of the primary infection improve, patients may ingest milk products. However, if dairy products result in worsening bloating and cramping symptoms, then patients are advised to avoid these products for 1 to 2 weeks. Rarely does the intolerance become more chronic. Similarly, steatorrhea, or fat malabsorption, may occur transiently, particularly after a rotavirus infection, but it also resolves spontaneously.

Profound International Normalized Ratio Elevations in Patients Taking Warfarin

Case reports in patients taking warfarin have noted significant coagulopathies occurring in acute gastroenteritis. Although these disorders are usually associated with episodes lasting several days, one case occurred after a single day of diarrhea. The mechanism is presumed to be a decreased vitamin K level in the body, from both decreased oral intake and malabsorption within the intestine.^19,²⁰ Prothrombin time and international normalized ratio should be checked in patients taking warfarin, and close follow-up with repeat blood tests can prevent potential bleeding complications.

Esophageal Injury

Any patient who is forcefully retching may suffer a tear in the mucosal surface of the esophagus, called a Mallory-Weiss tear, and this can lead to blood in the vomitus. Patients usually have little to no associated pain, and bleeding almost always resolves spontaneously, but occasionally, endoscopic intervention is required to acquire hemostasis. A more serious complication results when complete transmural disruption occurs in the esophagus. Known as Boerhaave’s syndrome, it is usually accompanied by significant pain and is associated with a high mortality. A chest radiograph is almost always positive for mediastinal or intra-abdominal free air. Emergent surgical consultation and aggressive resuscitative management are essential.

Bowel Necrosis

Clostridium perfringens normally causes self-limited gastroenteritis. However, in rare cases, it can lead to enteritis necroticans, which rapidly progresses to shock and death.

Diabetic Ketoacidosis

Diabetic patients may become significantly dehydrated in combination with high blood glucose levels, especially if these patients are unable to take their usual oral hypoglycemic agents. In severe circumstances, acute gastroenteritis may lead to diabetic ketoacidosis, coma, and death. A low threshold for electrolyte testing and measurement of the anion gap can help to detect the patient in danger of this complication.

Thrombotic Thrombocytopenic Purpura and Hemolytic-Uremic Syndrome

E. coli 0157:H7 hemorrhagic colitis has been associated with the hemolytic-uremic syndrome and with thrombotic thrombocytopenic purpura. Using antibiotics to treat gastroenteritis caused by this pathogen does nothing to eradicate the disease, but it may increase the incidence of these complications.

Neurologic Complications

Campylobacter has been associated with a more severe form of Guillain-Barré syndrome that occurs even in patients with asymptomatic infections who have no signs of gastroenteritis.²¹ Most neurologic symptoms from ciguatera poisoning resolve in days to weeks, but some long-term dysesthesias have been documented up to 2 years later.¹³ Shigella can cause seizures and other neurologic symptoms, especially in children.

Other Organ System Involvement

Although rare, invasive bacterial pathogens have been associated with systemic complications such as cholecystitis, pancreatitis, meningitis, endocarditis, and osteomyelitis.²² Patients suffering from amebic colitis resulting from E. histolytica can develop a hepatic abscess. Bacillus anthracis may cause a spectrum of illness from minimal symptoms to shallow oral ulcers, massive lymphadenopathy with tissue edema, and fulminant upper and lower gastrointestinal bleeding. Severe cases of C. difficile colitis have led to protein-losing enteropathy with ascites and peripheral edema.²³

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