Clostridium difficile infection

Clostridium difficile infection

• 1.
  Clostridium difficile Infection
• 2.
  colon infection isacquired in association with antibiotic use and the consequent disruption of the normal colonic flora most common diarrheal illness acquired in the hospital Due to ingestion of spores of C. difficile that vegetate, multiply, and secrete toxins, causing diarrhea and pseudomembranous colitis (PMC).
• 3.
  Etiology C. difficileis an obligately anaerobic, gram-positive, spore-forming bacillus whose spores are found widely in nature (hospitals and chronic-care facilities)
• 4.
  Clindamycin, ampicillin, andcephalosporins were the first abx associated with CDI. 2nd & 3rd cephalosporins: cefotaxime, ceftriaxone, cefuroxime, and ceftazidime, are frequent agents fluoroquinolones (ciprofloxacin, levofloxacin, gatifloxacin, and moxifloxacin) are the most recent drug implicated in hospital outbreaks. Penicillin/-lactamase-inhibitor combinations: ticarcillin/clavulanate and piperacillin/tazobactam ->less risk vancomycin and metronidazole, found to cause CDI Rare cases: without prior antibiotic exposure.
• 5.
  Clinical Manifestations Diarrheais the most common manifestation Stools never grossly bloody; soft and unformed to watery or mucoid may have as many as 20 bowel movements per day fever in 28% of cases abdominal pain in 22% leukocytosis in 50%. unexplained leukocytosis (15,000 (WBCs)/L) are at high risk for complications of C. difficile infection -> toxic megacolon and sepsis. C. diff diarrhea recurs after treatment in 15–30% of cases Recurrences: due to the same strain or reinfections with a new strain.
• 6.
  Diagnosis diarrhea (3unformed stools per 24 h for 2 days) with no other recognized cause plus toxin A or B in the stool, toxin-producing C. difficile detected in the stool by (PCR) or culture, or pseudomembranes seen in the colon. PMC is a more advanced form of CDI and is seen at endoscopy in 50% of patients with diarrhea with (+) stool c/s and toxin assay for C. difficile
• 7.
  Treatment Primary CDI discontinuation of any ongoing abx is recommended as 1st step in treatment 15–23% respond to this simple measure.  current epidemic strain and rapid deterioration of patients, prompt initiation of specific CDI treatment has become the standard. hydration avoidance of antiperistaltic agents and opiates -> mask symptoms and possibly worsen disease.
• 8.
  All drugs, (vancomycin),should be given orally if possible. When IV metronidazole is administered, fecal bactericidal drug concentrations are achieved during acute diarrhea, and CDI treatment has been successful Pt with adynamic ileus, IV metronidazole tx of PMC has failed. mean time to resolution of diarrhea is 2–4 days Treatment should not be deemed a failure until a drug has been given for at least 6 days. Recommendation: metronidazole and vancomycin be given for at least 10 days patients with mild to moderate illness respond to Metronidazole 500 mg PO 3x/day for 10 days; extension of the treatment period may be needed for slow responders.
• 9.
  The severity assessmentscore age elevated temperature low albumin level elevated WBC count documentation of PMC by endoscopy treatment of CDI in the intensive care unit initiate treatment with oral vancomycin in: seriously ill patient high WBC count (>15,000/L) creatinine level 1.5 times more than the baseline
• 10.
  Recurrent CDI 15–30%of patients experience recurrences of CDI, either as relapses caused by the original organism or as reinfections following treatment. Recurrence rates are higher: 1.patients 65 years old 2.those who continue to take abx while being treated for CDI 3.those who remain in the hospital after the initial episode of CDI.
• 11.
  Patients who havea first recurrence of CDI have a high rate of second recurrence (33–65%) In the first recurrence, re-treatment with metronidazole is comparable to treatment with vancomycin  Recurrent disease, once thought to be relatively mild, has now been documented to pose a significant (11%) risk of serious complications (shock, megacolon, perforation, colectomy, or death within 30 days)
• 12.
  Approaches include theadministration of vancomycin followed by the yeast Saccharomyces boulardii administration of vancomycin followed by a synthetic fecal bacterial enema the intentional colonization of the patient with a nontoxigenic strain of C. difficile.
• 13.
  Other strategies: 1.vancomycinin tapering doses or with pulse dosing every other day for 2–8 weeks 2.sequential treatment with vancomycin (125 mg four times daily for 10–14 days) followed by rifaximin (400 mg twice daily for 14 days)
• 14.
  Severe Complicated orFulminant CdI Fulminant (rapidly progressive and severe) CDI presents the most difficult treatment challenge Patients with fulminant disease often do not have diarrhea, and their illness mimics an acute surgical abdomen Sepsis (hypotension, fever, tachycardia, leukocytosis) may result from severe CDI
• 15.
  An acute abdomen(+/- toxic megacolon):  signs of obstruction, ileus, colon-wall thickening, and ascites on abdominal CT, often with peripheral-blood leukocytosis (20,000 WBCs/L) With or without diarrhea, DDX of acute abdomen, sepsis, or toxic megacolon and patient has received antibiotics in the past 2 months sigmoidoscopy / colonoscopy to visualize PMC abdominal CT are the best diagnostic tests in patients without diarrhea.
• 17.
  Source: Harrisons OxfordHandbook of Medicine Medscape
• 18.
  http://crisbertcualteros.page.tl