Adult-Gerontology Acute Care Practice Guidelines
Definition
A.Inflammation of the colon caused by an infectious agent (i.e., bacteria, virus, or parasites). Colitis is diagnosed when the patient has diarrhea (passage of three or more unformed stools per day and has evidence of inflammation in the colon based on at least one of the following.
1.Positive fecal markers: Elevated leukocytes, positive lactoferrin, or positive calprotectin.
2.Dysentery: Many small volume stools containing obvious blood or mucus (often associated with fever and abdominal pain).
3.Mucosal inflammation as identified by colonoscopy or sigmoidoscopy.
B.Duration of symptoms.
1.Acute: 14 days or fewer (most are infectious and self-limiting).
2.Persistent: 14 to 30 days.
3.Chronic: 30 or more days (most are noninfectious).
C.Pseudomembranous colitis caused by the bacteria Clostridioides difficile in the acute care setting: Of special concern; to be highlighted in this chapter.
Incidence
A.The vast majority of colitis is viral; only 1.5% to 5.6% of stool cultures produce positive results.
B.Severe diarrhea (four or more liquid stools/day for more than 3 days) is generally bacterial.
C.In the past 10 years, C. difficile infection (CDI) has been increasing in the United States—not only in the healthcare setting but also in community. Here are the 2011 estimated incidence rates in the United States for CDI, which can no longer be considered just a healthcare-acquired disease.
1.Community-acquired CDI: 51.9 cases per 100,000. The rate of first recurrence was 13.5%, and the death rate within 30 days was 1.3%.
2.Healthcare-acquired CDI: 95.3 cases per 100,000. The rate of first recurrence was 20.9%, and a death rate within 30 days was 9.3%.
Pathogenesis
A.Diarrhea represents altered changes in the flow of water and electrolytes within an osmotic gradient. Normally the gastrointestinal (GI) tract absorbs about 8 to 9 L of fluid a day, excreting about 200 mL of water in stool.
B.Enteric pathogens, acting primarily on transporter cells or the lateral spaces between cells (which are regulated by tight junctions), alter the balance toward significantly greater excretion and less absorption.
C.Pathogens can alter absorption by either direct or indirect modulation.
1.Direct modulation involving.
a.Epithelial ion transport processes.
i.Evidence from the literature proposes that the rapid onset of diarrhea induced via enteropathogenic Escherichia coli (EPEC) may result from direct effects on intestinal epithelial ion transport processes.
b.Barrier function.
2.Indirect modulation involving.
a.Inflammation.
i.Shigella and Salmonella species cause an inflammatory diarrhea characterized by fever and polymorphonucleocytes (PMNs) in the stool.
ii.PMNs regulate absorption through cytokine secretion but also have a more direct role through the secretion of a precursor to adenosine, activating certain transmembrane conductance regulators.
b.Neuropeptides.
i.C. difficile and rotavirus infection also work indirectly through modulation of ion transport subsequent to cytokine secretion and activation of enteric nerves via neuropeptides.
c.Loss of absorptive surface.
i.Giardia lead to the loss of brush border absorptive surface and diffuse shortening of villi.
ii.Similarly, EPEC cause effacement of microvilli, which decreases the surface area for nutrient absorption and causes increased osmolarity of the intestinal contents and malabsorption.
iii.Major causes in the United States.
1)Viruses: Norovirus, rotavirus, adenoviruses, and astrovirus.
2)Bacteria: Salmonella, Campylobacter, Shigella, enterotoxigenic E. coli, and C. difficile.
3)Protozoa: Cryptosporidium, Giardia, Cyclospora, and Entamoeba.
D.CDI (nosocomial and community acquired) account for almost all cases of pseudomembranous colitis (acute colitis characterized by the formation of an adherent inflammatory membrane that overlays injury site).
1.There is multifactorial activation with enterotoxin A and cytotoxin B. In addition, there is a new strain with increased productions of enterotoxin A and cytotoxin B, as well as binary toxin, with fluoroquinolone resistance.
2.Besides the direct effect of the toxins on tight junctions, and in contrast to other pathogens, C. difficile leads to activation of neuropeptides, resulting in inflammation via a necroinflammatory reaction, which activates mast cells, nerves, vascular endothelium, and immune cells.
Predisposing Factors
A.Hospitalization, previous CDI, greater than 65 years of age, recent abdominal surgery, use of proton pump inhibitors (PPI), and living conditions (long-term care facilities).
B.International travel: Shigella, Campylobacter, Salmonella, enteroinvasive E. coli (EIEC), enteroaggregative E. coli (EAEC), and others.
C.Foodborne: Staphylococcus aureus, Bacillus cereus, Clostridioides perfringens, or E. coli.
D.Other risk factors.
1.Antibiotic exposure, healthcare exposure.
2.Exposure to C. difficile.
3.HIV or other immune deficiency.
4.Chemotherapy.
5.Enteric tube feeding or other GI tract manipulation.
6.Inflammatory bowel disease (IBD) or other chronic GI disease.
Subjective Data
A.Common complaints/symptoms.
1.Mild: Watery diarrhea three or more times a day, abdominal cramping.
2.Severe: Watery diarrhea 10 or more times a day with abdominal cramping and pain.
May also be associated with fever, dehydration, and rapid heart rate.
B.Common/typical scenario.
1.Careful, detailed history of present illness: Important because it can suggest likely cause of the diarrhea.
a.Duration—acute, persistent, chronic, or change in periodicity.
b.Frequency and characteristics of stool.
i.Small bowel origin—watery, large volume, abdominal cramping, bloating, or gas.
ii.Large bowel origin—frequent, regular small volume stools, often tenesmus with bowel movements, and inflammatory signs (i.e., fever and bloody or mucoid stools) are common.
iii.Inflammatory signs suggest enteric viruses (e.g., cytomegalovirus [CMV], adenovirus), invasive bacteria (e.g., Salmonella, Shigella, Campylobacter), or cytotoxic pathogen such as C. difficile.
C.Family and social history.
1.Food exposure—raw or undercooked meat, seafood, unpasteurized dairy products. Timing is important.
a.Less than 6 hours with nausea and vomiting, likely S. aureus or B. cereus.
b.8–16 hours—likely C. perfringens.
c.Greater than 16 hours—viral or possibly E. coli enterotoxigenic pathogen.
2.Other exposures.
a.Animals (e.g., poultry, petting zoos): Salmonella.
b.Travel to resource limited areas (increased risk of pathogens and certain bacteria).
c.Occupation—Day-care centers likely for Giardia, Shigella, or Cryptosporidium.
d.Recent hospitalizations—increased likelihood of CDI.
e.Antibiotic use—increased likelihood of CDI.
f.Use of PPI—can increase risk of infectious diarrhea.
D.Review of systems.
1.Neurologic—lightheadedness, dizziness.
2.Dermatologic—dry skin.
3.Genitourinary—frequency of urination and color.
4.Abdominal—diarrhea, nausea, pain anywhere in the abdomen, bloody stools, loss of appetite, bloating, or distension.
Physical Examination
A.Volume status: Hypovolemia.
1.Dry mucous membranes.
2.Tenting of skin or diminished skin turgor.
3.Change in mental status.
4.Dizziness, lightheadedness, and orthostatic blood pressure.
5.Hypotension.
B.Complications: Ileus or peritonitis.
1.Abdominal distention.
2.Abdominal tenderness with percussion or gentle palpitation.
3.Rebound tenderness.
4.Abdominal rigidity.
Diagnostic Tests
A.Blood studies: Often not needed for patients with infectious diarrhea but helps determine status of the acutely ill patient.
1.Serum electrolytes if volume depletion is a concern: Screening for hypokalemia and acute kidney injury (AKI).
2.Complete blood count (CBC)—may be of limited help.
a.Platelet count—concern for hemolytic uremic syndrome.
b.Leukocytosis—consistent with CDI.
3.Blood cultures—if high fever is present, or sepsis is a concern.
4.Lactate, CPR, procalcitonin (PCT) level if patient has signs and symptoms of sepsis.
B.Stool studies: Often unnecessary if patients have no comorbidities: Infectious colitis generally resolves on its own. However, these tests should be completed for those with severe illness, high-risk comorbidities, or suggestive history.
1.Fecal leukocytes—findings of white blood cell (WBC) count on a test result does not differentiate between IBD and infectious colitis.
2.Acute bloody diarrhea: Bacterial colitis.
a.Cultures for enterohemorrhagic E. coli (EHEC) and Entamoeba.
b.Shiga toxin direct testing: For many strains of Shiga toxin-producing E. coli (STEC).
3.Stool culture.
a.Shigella, Salmonella, and Campylobacter are routinely sought.
b.If STEC, noncholera Vibrio, or Yersinia is suspected, alert the lab to look for these, because specialized techniques are required.
4.Ova and parasites (O&P): For patients with persistent diarrhea or who are immunocompromised. Unlike bacterial pathogens, which are shed continuously, O&P are shed intermittently.
5.C. difficile toxin: For patients who currently take or have recently taken antibiotics or have been hospitalized or recently been in a healthcare facility.
C.Imaging (CT): Not usually warranted unless patient is presenting with acute abdomen.
D.CDI.
1.Leukocytosis: Can be marked in severe disease (>15,000 cells/μL).
2.Volume depletion—elevated creatinine (Cr), blood urea nitrogen (BUN), reduced estimated glomerular filtration rate (GFR).
3.Elevated lactate.
4.Predictors of mortality.
a.WBC greater than 35,000 cells/μL or less than 4,000 cells/μL.
b.Significant banding (>10%).