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Community-Acquired Clostridioides difficile
Community-Acquired Clostridioides difficile Cases in Children on the Rise
Increase in pediatric cases of C difficile is linked to use of broad-spectrum antibiotics, recurrent infections, and a growth in highly virulent strains.
© JENNIFER OOSTHUIZEN / CDC
Clostridioides difficile is a normal constituent of the gut microbiota.
Clostridioides difficile is a spore-forming, anaerobic, gram-positive, toxin-producing bacillus found in the gastrointestinal (GI) tract of humans and animals.1-3 Although C difficile is a normal constituent of the gut microbiota, the overcolonization of this pathogen can cause a range of colonic conditions.1
A case-controlled retrospective study conducted from January 2012 through December 2016 found the overall incidence of communityacquired Clostridioides difficile infection (CDI) cases to be 13.7 per 100,000 children per year, with a substantial increase in cases from 2012 (9.6/100,000).4 In 2018, the Centers for Disease Control and Prevention Emerging Infections Program reported 15,591 cases of C difficile in 10 states. Among children aged 1 to 17 years, the incidence of illness was 26.7 per 100,000 persons and 9.03 per 100,000 persons for community-acquired and health care-associated CDIs, respectively.5
Many factors have increased the rate of CDI in children, such as the increasing use of broadspectrum antibiotics, greater number of recurrent infections, and an increase in highly virulent strains.6,7 It is essential that health care professionals recognize the growing incidence of pediatric CDI in both the community and in health care facilities. Proper hand hygiene and minimizing overprescribing of antibiotics are essential to prevent this deadly infection in children.8 The establishment of an antibiotic stewardship
program in hospitals and private practice can greatly reduce the use of inappropriate antibiotics.8,9
Etiology and Pathogenesis
C difficile spores are acquired person to person through the fecal-oral route or via fomites on environmental surfaces or contaminated hands.2,10 As noted, certain antibiotic usage can disrupt normal GI flora and allow C difficile spores to germinate, overcolonize the colon, and alter the normal GI microbiome.2 After colonization of the colon, C difficile releases 2 pathogenic toxins (A and B); toxin B is 10 times more potent and virulent than toxin A.2,6,11 These toxins bind to receptors on the plasma membrane of the colonocyte, enter the cytoplasm, and trigger apoptosis.3 This cell death results in a progressive compensatory inflammatory reaction at the colonic mucosa that leads to diarrhea or colitis.3,12 A virulent strain of C difficile, referred to as the North American pulse type 1 (NAP1) strain, is more prevalent among hospitalacquired CDI and is associated with more severe illness.11
Signs and Symptoms
The pathogenic potential of C difficile ranges from asymptomatic colonization to toxic megacolon, septic shock, pseudomembranous colitis, and even death.3 The classic presentation of mild to moderate CDI is an acute diarrheal illness described as profuse watery diarrhea accompanied by fever and lower abdominal cramping.2
The World Health Organization defines diarrhea as the presence of 3 or more loose stools within 24 hours.3 Vomiting and bloody stools may also be present but are not common GI manifestations of CDI.2 Children with severe or fulminant disease frequently present with the classic presentation of CDI accompanied with hemodynamic instability, leukocytosis, or lactic acidosis.2
Infants younger than age 12 months frequently have asymptomatic colonization of C difficile. 2,7 The exact mechanism of this colonization is unclear, but many theories have been proposed, such as young age, protective factors in mother’s breast milk in the development of the neonatal microbiota, preferential colonization of less pathogenic strains, and lack of intestinal toxin receptors that are required for CDI.2,3,13 Colonization rates of C difficile vary widely from newborns to children younger than age 2 years.1 Genomic analysis of newborn GI tracts have demonstrated varying degrees of C difficile colonization because of maternal and placental microbiome colonization.11
Making the Diagnosis
A thorough clinical evaluation must rule out other causes of diarrhea, such as viral enteritis, parasitic infection, bacterial infection, and inflammatory bowel disease; testing every child with diarrhea for CDI may lead to misdiagnosis and inappropriate treatment.8 Testing for CDI is indicated according to the patient’s history of new-onset diarrhea with no clearly attributable cause, such as an inflammatory bowel disease (IBD) exacerbation, laxative use, or enteral tube feedings.2 Medical providers must keep in mind that diarrheal illnesses in pediatric patients frequently have viral etiologies. Symptoms such as nausea, vomiting, or fever are more commonly associated with viral diarrhea than CDI.2 Abdominal discomfort, cramps, and diarrhea can also be present in other conditions, such as ischemic colitis, adverse effects (AEs) of medications, and postradiation colitis.2,14
Patient Risk Factors Several risk factors are associated with pediatric CDI. Prior antibiotic exposure is the most significant risk factor for both community-acquired and hospital-acquired pediatric CDI.1,2,11 The use of multiple concomitant antibiotic and prolonged antibiotic therapy also increases the risk for pediatric CDI.8 Although any antibiotic may be responsible for CDI, certain antibiotic classes have been more frequently associated with this infection. In a case-control study performed in pediatric patients, the usage of macrolides, fluoroquinolones, clindamycin, tetracyclines, and third-generation cephalosporins were found to be strong risk factors of community-acquired pediatric CDI.15 Although antibiotic exposure is frequently associated with CDI, more than 40% of children with CDI in this study did not report previous antibiotic exposure.15
Other risk factors associated with pediatric CDI include recent exposure to individuals with C difficile infection; increased length of hospitalization; diet; food additives; use of proton pump inhibitors; GI devices, such as gastrostomy (G tube) or jejunostomy tubes (J tubes); and being an organ transplant recipient.8 Pediatric patients at risk for CDI often have underlying comorbidities, such as malignancy, IBD, and being a solid organ transplant recipient (Table 1).16-18
Testing The diagnosis of pediatric CDI is made by stool tests. Major associations recommend enzyme immunoassay (EIA) for glutamate dehydrogenase (GDH) as a screening tool because
of its near 100% sensitivity.8 Glutamate dehydrogenase is an antigen that is present in CDI.1 Positive GDH screenings only indicate presence of C difficile, regardless of toxigenic or nontoxigenic strain.1,8
An initial GDH screening is typically performed in conjunction with a nucleic acid amplification test (NAAT), often through polymerase chain reaction (PCR), to detect the genes responsible for the production of toxins A and B.1,2,7 Although NAAT has been recognized as the most sensitive method for detection of C difficile, a first-line standard testing method has not been established.3
The American Academy of Pediatrics (AAP) states that the testing of children younger than age 1 year is not routinely recommended in children with diarrhea unless the patient has known risk factors, such as gut motility disorders or Hirschsprung disease, or if the patient is in the setting of a C difficile outbreak.3 Children between the ages of 1 and 2 years should not be tested unless other viral etiologies have been investigated and ruled out. Pediatric patients older than age 2 years should be tested in patients with prolonged or worsening diarrhea.3,16
Testing for alternative or concomitant enteropathogens should also be considered, including stool culture of other organisms and ova and parasite testing.1 A multistep approach for screening and confirmatory testing seems to be the best strategy for diagnosis.1,2,4 Biomarkers such as fecal calprotectin can also be ordered: an increase of this neutrophil product can be used as a marker for intestinal inflammation and may be useful in deciphering colonization vs true infection. Fecal leukocytes may also be present in stools.8
Abdominal radiographs or noncontrast abdominal computed tomography (CT) scans may be ordered for severe or fulminant disease to rule out colonic dilation,19 wall thickening, or perforation.2,7 Although colonoscopy with biopsy is extremely sensitive, this invasive imaging modality is only considered in atypical presentations.20
Treatment
The initial step in management of pediatric CDI is prompt cessation of the inciting antibiotic therapy.2,7,16 In very mild disease, discontinuation of antibiotics may be sufficient to reverse the disease process without use of medications.2 The continuation of antibiotic therapy puts the patient at increased risk for recurrent infection.7 If antibiotic therapy cannot be terminated because of concomitant infection, switch to an antibiotic with the narrowest spectrum.2
Empiric antibiotic therapy against C difficile should be commenced if the results of testing are delayed for greater than 48 hours or if the patient is showing signs of severe or fulminant infection.2,7 If not, it is recommended that positive laboratory results be obtained before treatment is initiated.2 Symptomatic support with aggressive intravenous (IV) fluid resuscitation is crucial in children with diarrhea.1 Antimotility drugs, such as loperamide, are discouraged because of associated poor outcomes, such as toxic megacolon or ileus, but are considered safe to use once antibiotic treatment against CDI has been initiated.2,11
Antibiotic treatment for pediatric CDI depends on the severity of illness and whether it is the first episode or a recurrence of infection (Table 2, page 24).8,21 In the 2017 updated Infectious Diseases Society of America guidelines, the severity of illness is defined as nonsevere (previously mild/ moderate), severe, and fulminant (previously complicated).8 For children with nonsevere CDI, the recommended antibiotics are metronidazole and vancomycin for 10 days.8,21 In nonsevere cases of CDI, clinical improvement with antibiotic therapy should occur within 1 to 2 days of initiation, but about 31% of pediatric cases need a second course of antibiotics.1,11
For children with severe CDI, the guidelines recommend oral vancomycin over metronidazole whereas for fulminant CDI, the guidelines recommend vancomycin for 10 days (oral or rectal) with or without metronidazole IV for 10 days.8,21
TABLE 1. CDI in Special Pediatric Populations16-18
Children with IBD • 7%-24% incidence rate • 10× the risk of developing CDI than patients without IBD • 34% recurrence rate
Children with cancer • 27% incidence rate • >15× the risk of developing CDI than patients without cancer • 26% recurrence rate
Recipients with solid organ transplant • 1.3%-31% incidence rate • 7× to 13× the risk of developing CDI than nontransplant hospitalized patients • 19.7% recurrence rate
CDI, Clostridioides difficile infection; IBD, inflammatory bowel disease.
TABLE 2. Disease Severity and Current Recommended Pediatric Dosing for CDII8,21
Disease Severity Clinical Manifestations Treatment Comments
Discontinue antimicrobial agents and begin rehydration via IV fluid
First episode, nonsevere • Nonbloody diarrhea • Mild abdominal discomfort/tenderness • WBC <15,000/mm3 • Afebrile Metronidazole: • 7.5 mg/kg/dose 3 or 4×/d × 10 days (maximum 500 mg) OR Vancomycin: • 10 mg/kg/dose 4×/d × 10 days (maximum 125 mg 4×/d) • Metronidazole is considered first-line therapy for mild to moderate diseaseI • Vancomycin and fidaxomicin are markedly more expensive than metronidazole • May consider switching metronidazole to vancomycin if no response in 5-7 days • Fidaxomicin should only be used in patients aged ≥6 years
First episode, severe disease Must have at least 1: • Severe abdominal pain • Hypoalbuminemia • Lactic acidosis • WBC >15,000/mm3 • Serum albumin ≤3 g/dL • Creatinine level 1.5× greater than baseline Vancomycin – Oral: • 10 mg/kg/dose 4×/d × 10 days (maximum 500 mg) Vancomycin – Rectal: • Age 1-3 years: 250 mg/50 mL every 6 hours • Age 4-9 years: 375 mg/75 mL every 6 hours • Age ≥10 years: 500 mg/100 mL every 6 hours • The efficacy of fidaxomicin in severe or complicated/fulminant disease for pediatric CDI needs further investigation
First episode, fulminant disease Clinical manifestations of severe CDI accompanied by at least 1 of the following: • Hypotension • Shock • Mental status changes • Fever >38.5°C • End organ failure • Respiratory distress • Hemodynamic instability • Ileus • Gastrointestinal perforation • Toxic megacolon Vancomycin – Oral: • 10 mg/kg/dose 4×/d × 10 days (maximum 500 mg 4×/d) Vancomycin – Rectal: • Age 1-3 years: 250 mg/50 mL every 6 hours • Age 4-9 years: 375 mg/75 mL every 6 hours; • Age ≥10 years: 500 mg/100 mL every 6 hours AND/OR IV metronidazole: • 10 mg/kg/dose 3×/d × 10 days (maximum 500 mg) • Consider early surgical consultation in all patients with complicated or fulminant disease
First recurrence
Second or greater recurrence Metronidazole: • 7.5 mg/kg/dose 3 or 4×/d x 10 days (maximum 500 mg) OR Vancomycin: • 10 mg/kg/dose 3×/d × 10 days or • 10 mg/kg/dose 4×/d for 10 days (maximum 125 mg) • Repeat same antibiotic regimen as initial episode if possible
Vancomycin pulsed taper regimen: • 10 mg/kg/dose by mouth or by rectum 4×/d OR Vancomycin • for 10 days followed by Rifaximin • 10 mg/kg 3×/d for 20 days OR Fecal microbiota transplantation • Fecal microbiota transplantation should be considered after the third recurrence
Discontinuation of antimicrobial agents and rehydration via IV fluid are essential to treatment. CDI, Clostridioides difficile infection; IV, intravenous; WBC, white blood cell count.
Metronidazole is the preferred initial treatment for nonsevere pediatric CDI because of its affordability and efficacy against vancomycin-resistant enterococcus (VRE).8 Metronidazole is typically administered orally 3 times a day for 10 days. It is secreted across the intestinal mucosa, causing it to achieve high fecal concentrations. This medication is associated with more frequent AEs than vancomycin, such as nausea, vomiting, metallic taste, and abdominal cramps. Serious complications, such as encephalopathy or peripheral neuropathy, are uncommon but are still possible with metronidazole.2,7 Metronidazole is typically avoided for recurrent episodes as repeat exposure may lead to neurotoxicity.2,12 Vancomycin is not absorbed in the GI tract, causing it to achieve high fecal concentrations and, in turn, producing higher rates of recovery.16 Notable AEs of vancomycin include abdominal pain, nausea, and hypokalemia.7
Fidaxomicin is a new macrolide that was approved for use in pediatric CDI patients aged 6 months and older in February 2020.22 Fidaxomicin has minimal systemic absorption, leading to high concentrations in the colon, and may have other benefits compared with vancomycin. The SUNSHINE study was a multicenter, randomized, blinded clinical trial that enrolled pediatric patients from 39 sites to evaluate the efficacy of vancomycin and fidaxomicin in pediatric CDI. Although both treatments are effective for pediatric CDI, study results showed evidence of higher clinical response and cure and lower recurrence with the use of fidaxomicin compared with vancomycin.23 Fidaxomicin has been shown to cause less new-onset colonization of Candida and vancomycin-resistant enterococcus (VRE) species.24 Despite promising results thus far, more studies are necessary to evaluate fidaxomicin and its efficacy in recurrent pediatric CDI.
Rifaximin is an oral rifamycin derivative antibiotic that is being evaluated as an alternative initial treatment for CDI because of its favorable side effect profile.25 Rifaximin has been shown to stimulate the growth of Lactobacillus in the gut and does not significantly alter the gut flora.26 In a small, randomized, controlled trial comparing the efficacy of metronidazole with rifaximin in patients aged 12 to 18 years with IBD and nonsevere CDI, there was no statistically significant difference in the results.25 This could indicate that rifaximin could be a viable alternative for pediatric patients with CDI and coexisting IBD. Further studies are needed to provide evidence of rifaximin’s efficacy and ability to decrease recurrence rates and to gain FDA approval for use of this medication for pediatric CDI.
Recurrent Clostridioides difficile Infection
Approximately 22% of children with an initial episode of CDI will have a recurrence.27 The guidelines for treatment for a nonsevere first recurrence is metronidazole for 10 days or vancomycin for 10 days. For a second or subsequent recurrence, vancomycin is given in a tapered and pulsed regimen or for 10 days followed by rifaximin for 20 days or fecal microbiota transplantation (FMT).8
Fecal Microbiota Transplantation
Fecal microbiota transplantation should be considered as a treatment option for pediatric patients with 3 or more recurrences for whom antibiotic therapy is not successful.6,8,28 Fecal microbiota transplantation is the administration of fecal content and gut organisms from a healthy donor’s GI tract into a patient with recurrent CDI via a nasogastric tube, colonoscopy, or enema.2,12 For patient with CDI, FMT through oral capsules is the preferred method of fecal administration.2,7 The goal of FMT is to restore the GI tract into a healthy balanced microbiome to discourage C difficile colonization and generate an immunologic response that promotes eradication of C difficile. 2
Limited data exist regarding FMT in pediatric patients, with much of that available information consisting of individual case studies.29 A few studies on FMT in pediatric CDI do show promising results, supporting the consideration of FMT as a treatment strategy for pediatric CDI. In a retrospective study that included 335 pediatric patients with CDI (age range, 11-23 years), 81% had a successful outcome after a single FMT and 86.6% had a successful outcome after a first or repeated FMT.30 Additional data is required to evaluate the efficacy and safety of FMT to support the use of this treatment in recurrent pediatric CDI. The 2019 safety alert for use of FMT in adults cannot be ignored and, as biotherapeutics are explored as a possible alternative to this treatment in adults, the use of FMT in children should also be further assessed for safety and efficacy.31
Complications/Prognosis
Recurrent CDI is the most common complication of pediatric CDI, occurring in approximately 22% of cases.27 Recurrent CDI is defined as an episode of symptom onset and positive assay results at least 60 days after the completion of a primary treatment regimen for CDI.1,2,8 Recurrent episodes can be caused by persistence of dormant spores within intestines, relapse of previous infecting strain, infection with a new strain, or low levels of antitoxin antibody levels.29 Pediatric patients with IBD are also more likely to have recurrent disease.6,25 Infection with the virulent NAP1 strain of C difficile has also been associated with an increased likelihood of recurrence.11
Studies report that approximately 3% to 7% of pediatric CDI patients develop fulminant disease.32,33 Fulminant disease is
characterized by hemodynamic instability, respiratory failure, a megacolon greater than 7 cm in diameter, hypotension, or shock.8 Aggressive and prompt diagnostic and therapeutic interventions are necessary in fulminant disease.8
Prevention
Children with suspected or confirmed CDI should be isolated with strict contact precautions enforced. C difficile spores can linger on surfaces for up to 5 months.2 Spores are resistant to extreme temperatures and alcohol-based cleaning agents, making prevention of transmission extremely difficult.2,11 When disinfecting surfaces in the child’s room or hospital room, sporicidal agents such as hypochlorite are preferred.2 Bleach, hydrogen peroxide vapor, and ultraviolet light are other methods of disinfecting hospital rooms of patients with CDI.2,11
Hospital environments are the most common source of C difficile acquisition among hospitalized pediatric patients.8 Colonization risk increases with the length of hospital stay.1 Health care personnel must wear gowns and gloves before contact with the patient occurs. Proper hand hygiene should be performed before and after contact with a pediatric patient with CDI, and after removal of gloves.2,11 Use of alcohol-based hand rubs are not adequate to eradicate C difficile spores from hands.8 Soap and water are the preferred agents for handwashing because they are more effective at removing spores from hands.2,11
Probiotics The efficacy of probiotics in the prevention of pediatric CDI has been studied in randomized trials.34,35 In an analysis of 31 studies, which included 8672 patients, probiotics reduced the risk for CDI: 1.5% with probiotics and 4% without (relative risk [RR]=0.4 [95% CI, 0.3-0.52]). Baseline CDI rates from the included studies ranged from 0 to 40%, with only those studies with baseline CDI rates >5% (n=13) showing a significant reduction in CDI risk. The subgroup analysis of 6 pediatric studies with 1141 patients demonstrated a 65% reduction in the risk for CDI (RR=0.35 [95% CI, 0.19-0.63]).34
Antibiotic Stewardship Another important aspect of pediatric CDI prevention is eliminating antibiotic exposure. Antibiotic stewardship programs (ASPs) are coordinated programs that aid reduction of unnecessary antibiotic prescribing, thus helping to control pediatric CDI rates.2,8,9 Co-implementation of infection control measures with ASPs have been shown to be more efficacious than ASPs alone.2,7 These programs have been shown to significantly reduce the incidence of CDI infections in hospitalized patients, combatting the progression of the contemporary antibiotic resistance crisis.9
Unfortunately, many primary care providers do not recognize antibiotic resistance and inappropriate prescribing as a problem in their office. In a recent survey, more primary care providers agreed that antibiotic resistance was a problem in the United States (94%) than in their practice (55%) and that inappropriate antibiotic prescribing was a problem in outpatient settings (91%) but not in their practice (37%). Most respondents (91%) believed that antibiotic stewardship was appropriate in office-based practices, but they ranked antibiotic resistance as less important than other public health issues, such as obesity, diabetes, opioids, smoking, and vaccine hesitancy. 36
Conclusion
Pediatric CDI is becoming increasingly common. It is essential that health care professionals recognize the growing incidence of pediatric CDI in both the community and in health care facilities. Newer treatments such as rifaximin, fidaxomicin, and FMT are promising. More studies aiming to elucidate the efficacy of these medications in pediatric populations would further the cause of adequately preventing and treating CBI in children. ■
Heather Adams, MSPAS, PA-C, works at Women’s Wellness and Gynecology in Erie, Pennsylvania, and is an associate professor at Gannon University in the Physician Assistant program. Elizabeth Nguyen, PA-C recently graduated from the Gannon University Physician Assistant Program. She works in psychiatry at Piedmont Access to Health Services (PATHS) in Danville, Virginia.
References
1. Borali E, De Giacomo C. Clostridium difficile infection in children: a review. J Pediatr Gastroenterol Nutr. 2016;63(6):e130-e140. 2. Alvarez AM, Rathore MH. Clostridium difficile infection in children. Adv Pediatr. 2019;66:263-280. 3. Antonara S, Leber AL. Diagnosis of Clostridium difficile infections in children. J Clin Microbiol. 2016;54(6):1425-1433. 4. Miranda-Katz M, Parmar D, Dang R, Alabaster A, Greenhow TL. Epidemiology and risk factors for community associated Clostridioides difficile in children. J Pediatr. 2020;221:99-106. 5. Centers for Disease Control and Prevention. 2018 annual report for the emerging infections program for Clostridioides difficile infection. Accessed December 16, 2021. 6. Brumbaugh DE, De Zoeten EF, Pyo-Twist A, et al. An intragastric fecal microbiota transplantation program for treatment of recurrent Clostridium difficile in children is efficacious, safe, and inexpensive. J Pediatr. 2018;194:123-127.e1. 7. Hoffenberg EJ, Furuta GT, Kobak G, et al. Gastrointestinal tract. In: Hay WW, Levin MJ, Deterding RR, Abzug MJ. Current Medical Diagnosis and
Treatment: Pediatrics. 24th ed. New York, New York: McGraw Hill Education; 2018:647-648. 8. McDonald LC, Gerding DN, Johnson S, et al. Clinical practice guidelines for Clostridium difficile infection in adults and children: 2017 update by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA). Clin Infect Dis. 2018;66(7):e1-e48. 9. Baur D, Gladstone BP, Burkert F, et al. Effect of antibiotic stewardship on the incidence of infection and colonisation with antibiotic-resistant bacteria and Clostridium difficile infection: a systematic review and meta-analysis. Lancet Infect Dis. 2017;17(9):990-1001. 10. Bauer MP, Kuijper EJ. Potential sources of Clostridium difficile in human infection. Infect Dis Clin North Am. 2015;29(1):29-35. 11. Noor A, Krilov LR. Clostridium difficile infection in children. Pediatr Ann. 2018;47(9):e359-e365. 12. Clayton JA, Toltzis P. Recent issues in pediatric Clostridium difficile infection. Curr Infect Dis Rep. 2017;19(12):49. 13. Borali E, Ortisi G, Moretti C, et al. Community-acquired Clostridium difficile infection in children: a retrospective study. Dig Liver Dis. 2015;47(10):842-846. 14. Manthey CF, Eckmann L, Fuhrmann V. Therapy for Clostridium difficile infection - any news beyond metronidazole and vancomycin? Expert Rev Clin Pharmacol. 2017;10(11):1239-1250. 15. Adams DJ, Eberly MD, Rajnik M, Nylund CM. Risk factors for communityassociated Clostridium difficile infection in children. J Pediatr. 2017;186:105-109. 16. Hourigan SK, Sears CL, Oliva-Hemker M. Clostridium difficile infection in pediatric inflammatory bowel disease. Inflamm Bowel Dis. 2016;22(4):1020-1025. 17. Kim J. Editorial commentary: Clostridium difficile in pediatric oncology patients: more questions than answers. Clin Infect Dis. 2014;59(3):404-405. 18. Luo R, Weinberg JM, Barlam TF. The impact of Clostridium difficile infection on future outcomes of solid organ transplant recipients. Infect Control Hosp Epidemiol. 2018;39(5):563-570. 19. De Giacomo C, Borali E. Clostridium difficile in children: a multifaceted infection. J Pediatric Infect Dis. 2016;1:12. 20. McConnie R, Kastl A. Clostridium difficile, colitis, and colonoscopy: pediatric perspective. Curr Gastroenterol Rep. 2017;19(8):34. 21. Campbell CT, Poisson MO, Hand EO. An updated review of Clostridium difficile treatment in pediatrics. J Pediatr Pharmacol Ther. 2019;24(2):90-98. 22. Skinner AM, Scardina T, Kociolek LK. Fidaxomicin for the treatment of Clostridioides difficile in children. Future Microbiol. 2020;15(11):967-979. 23. Wolf J, Kalocsai K, Fortuny C, et al. Safety and efficacy of Fidaxomicin and vancomycin in children and adolescents with Clostridioides (Clostridium) difficile infection: a phase 3, multicenter, randomized, single-blind clinical trial (SUNSHINE). Clin Infect Dis. 2020;71(10):2581-2588. 24. Okumura H, Fukushima A, Taieb V, Shoji S, English M. Fidaxomicin compared with vancomycin and metronidazole for the treatment of Clostridioides (Clostridium) difficile infection: a network meta-analysis. J Infect Chemother. 2020;26(1):43-50. 25. Gawronska A, Banasiuk M, Lachowicz D, Pituch H, Albrecht P, Banaszkiewicz A. Metronidazole or rifaximin for treatment of Clostridium difficile in pediatric patients with inflammatory bowel disease: a randomized clinical trial. Inflamm Bowel Dis. 2017;23(12):2209-2214. 26. Ng QX, Loke W, Foo NX, Mo Y, Yeo WS, Soh AYS. A systematic review of the use of rifaximin for Clostridium difficile infections. Anaerobe. 2019;55:35-39. 27. Nicholson MR, Thomsen IP, Slaughter JC, Creech CB, Edwards KM. Novel risk factors for recurrent Clostridium difficile infection in children. J Pediatr Gastroenterol Nutr. 2015;60(1):18-22. 28. Gurram B, Sue PK. Fecal microbiota transplantation in children: current concepts. Curr Opin Pediatr. 2019;31(5):623-629. 29. Groves HE, Allen UD. Winning with poo? Fecal microbiome transplantation as an emerging strategy for the management of recurrent Clostridioides difficile infection in children. Pediatr Transplant. 2020;24(1):e13651. 30. Nicholson MR, Mitchell PD, Alexander E, et al. Efficacy of fecal microbiota transplantation for Clostridium difficile infection in children. Clin Gastroenterol Hepatol. 2020;18(3):612-619.e1. 31. Hourigan SK, Nicholson MR, Kahn SA, Kellermayer R. Updates and challenges in fecal microbiota transplantation for Clostridioides difficile infection in children. J Pediatr Gastroenterol Nutr. 2021;73(4):430-432. 32. Tschudin-Sutter S, Tamma PD, Milstone AM, Perl TM. The prediction of complicated Clostridium difficile infections in children. Infect Control Hosp Epidemiol. 2014;35(7):901-903. 33. Crews JD, Anderson LR, Waller DK, Swartz MD, DuPont HL, Starke JR. Risk factors for community-associated Clostridium difficile-associated diarrhea in children. Pediatr Infect Dis J. 2015;34(9):919-923. 34. Goldenberg JZ, Yap C, Lytvyn L, et al. Probiotics for the prevention of Clostridium difficile-associated diarrhea in adults and children. Cochrane Database Syst Rev. 2017;12(12):CD006095. 35. Goldenberg JZ, Mertz D, Johnston BC. Probiotics to prevent Clostridium difficile infection in patients receiving antibiotics. JAMA. 2018;320(5):499-500. 36. Zetts RM, Garcia AM, Doctor JN, Gerber JS, Linder JA, Hyun DY. Primary care physicians’ attitudes and perceptions towards antibiotic resistance and antibiotic stewardship: a national survey. Open Forum Infect Dis. 2020;7(7):ofaa244.
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LEGAL ADVISOR
CASE
NP Sued for Missed Hip Fracture
A litigious patient mistakenly believes that a misdiagnosis is grounds for malpractice.
ANN W. LATNER, JD
In early January, a 76-year-old patient, Mrs R, was brought by her husband to the emergency department (ED) of a local hospital after sustaining a fall outside her home. Working in the ED that night was Ms W, a family nurse practitioner, and Dr T, the ED physician.
Ms W went into the examination area to speak with Mrs R, who complained of left groin pain that radiated to her lower back. When Ms W asked if anything triggered the pain, Mrs R said that several packages were left outside her door and when she leaned over to pick them up, she fell and has experienced pain since.
Ms W took a medical history and then performed a physical examination of the patient. She noted that Mrs R’s lower back was tender toward the sacral area and that the patient was unable to perform a straight leg raise because of pain. The differential diagnosis included hip fracture, and Ms W ordered radiographs of the patient’s pelvis, including the femoral neck and knee.
After the radiograph results were back, Ms W conferred with Dr T, the ED physician. Dr T interpreted the images as showing no indication of a fracture and Ms W concurred. Meanwhile, the patient had been given pain medication and was doing better.
Mrs R was told that she would be discharged with pain medication and Ms W instructed her to follow up with her primary care provider. Ms W noted in the medical record that the patient’s condition had improved and that she advised the patient to contact her doctor for follow-up.
Two hours after she left the first hospital, the patient had her husband take her to another hospital where she complained about the same pain that she had sought treatment for at the first hospital.
At the second hospital, a computed tomography (CT) scan of Mrs R’s pelvis was conducted. The CT scan revealed a hip fracture. An orthopedist who was consulted recommended that
A medical malpractice case requires a duty owed to the patient, breach of that duty, injury caused by the breach, and damages
Cases presented are based on actual occurrences. Names of participants and details have been changed. Cases are informational only; no specific legal advice is intended. Persons pictured are not the actual individuals mentioned in the article.
