An abnormal increase in stool water content, volume, or frequency (≥3 stools above baseline in 24 hours) for <14 days duration
Most commonly secondary to infectious etiology; often...
Duration of symptoms <14 days
Historical clues for dehydration: orthostatic hypotension, dizziness, increased thirst, decreased urine output, or altered mental status
Description of ...
Oral rehydration and electrolyte management are key to successful treatment.
Oral intake, as tolerated—“if the gut works, use it”
IV fluids if patient cannot tolerate oral rehy...
Early oral refeeding is encouraged. Regular diets are as effective as restricted diets.
The traditional bananas, rice, applesauce, toast (BRAT) diet has little evidence-based support (...
da Cruz Gouveia MA, Lins MTC, da Silva GAP. Acute diarrhea with blood: diagnosis and drug treatment. J Pediatr (Rio J). 2020;96(Suppl)1:20–28.
...
R19.7 Diarrhea, unspecified
A09 Infectious gastroenteritis and colitis, unspecified
A08.4 Viral intestinal infection, unspecified
A04.9 Bacterial intestinal infection, unspecified
K52.2 Allergi...
Viruses are the most common causes of acute diarrheal illness in the United States.
Consider broad infectious etiologies if patients are immunocompromised (Cytomegalovirus, Cryptosporid...
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Figure 73.1. Electron photomicrograph of <italic>Vibrio cholerae</bold>.
Figure 73.3. Model of cholera toxin showing the five binding subunits surrounding a single active (<italic>A</bold>) subunit.
<bold><italic>Figure 15-20</bold> Mechanisms of bacterial enterocolitis.</bold> Diarrhea can be caused by (<bold>A</bold>) bacterial toxin formed in food before ingestion, (<bold>B</bold>) toxin formed in the intestinal tract after infection, or (<bold>C</bold>) direct invasion of infective organisms in the bowel wall.
<bold><italic>Figure 15-20</bold> Mechanisms of bacterial enterocolitis.</bold> Diarrhea can be caused by (<bol...
<bold>FIGURE 16-2</bold> <bold>The pathogenesis of cholera and enterotoxigenic <i>Escherichia coli</i> (ETEC) infections.</bold> The organisms colonize the mucosal surface via microbial adhesins—for example, colonization factor antigen (Cfa) of enterotoxigenic <i>E. coli.</i> The factor that binds <i>V. cholerae</i> to cells is not clearly defined, but a toxin coregulated pilus (Tcp) causes the organisms to adhere to one another and form mic...
<bold>FIGURE 16-2</bold> <bold>The pathogenesis of cholera and enterotoxigenic <i>Escherichia coli</i> (ETE...
<bold>FIGURE 16-3</bold> <bold>The pathogenesis of enteropathogenic <i>Escherichia coli</i> (EPEC).</bold> First, the organism attaches to the small bowel epithelial cell via a bundle-forming pilus (BfpA). Subsequently, a type III secretion system bridges to the cell and delivers a membrane receptor protein, Tir, and other effectors to the host cell. In a third stage, intimin on the bacterial surface mediates intimate adherence to the cell by binding to the newly d...
<bold>FIGURE 16-3</bold> <bold>The pathogenesis of enteropathogenic <i>Escherichia coli</i> (EPEC).</bol...
Clostridial diseases. Clostridia in the vegetative form inhabit the gastrointestinal tract of humans and animals. Spores pass in the feces, contaminate soil and plant materials, and are ingested or enter sites of penetrating wounds. Under anaerobic conditions they revert to vegetative forms. Plasmids in the vegetative forms elaborate toxins that cause several clostridial diseases. Food poisoning and necrotizing enteritis. Meat dishes left to cool at room temperature grow large numbers of cl...
Clostridial diseases. Clostridia in the vegetative form inhabit the gastrointestinal tract of humans and animals. Spores pass in the feces...