New me: This is a possibility, but only 10-20% of antibiotic associated diarrhoea is caused by C diff. Most of the time the problem is an alteration in the bowel flora. The third potential mechanism is a direct prokinetic effect of the antibiotic, typically erythromycin.<\/p>\n
Old me: Still, it\u2019s C. diff till proven otherwise. The antibiotic must be stopped and a stool sample for C diff toxin sent.<\/strong><\/p>\n New me: The antibiotic should ideally be stopped. Whether or not stool samples need to be sent routinely is a matter of risk. The two questions I need to ask myself are:<\/p>\n <\/p>\n a) \u00a0 How likely is it that in this patient there is C. diff?<\/p>\n b)\u00a0\u00a0 If it were C. diff and I missed it, how bad would that be?<\/p>\n <\/p>\n a) What makes it likely to be C. diff?<\/span><\/p>\n This can be split into factors in the history of the presenting complaint and patient factors.<\/p>\n HPC: Fever, blood in stools, crampy pain and a tender abdomen go more with C diff; non C.diff antibiotic induced diarrhoea tends to be more of a \u2018nuisance diarrhoea\u2019 (not too severe).<\/p>\n Patient factors (according to NICE CKS):<\/p>\n 1. Advanced age <\/strong>\u2014 the rate of positive C. difficile assay results in people older than 65 years of age is 20\u2013100 times greater than the rate in people 10\u201320 years of age.<\/p>\n 2. Antibiotic treatment<\/strong> \u2014 although none can be excluded, the most commonly implicated antibiotics are:<\/p>\n Clindamycin<\/p>\n Cephalosporins \u2014 in particular second- and third-generation cephalosporins (such as cefuroxime axetil, cefixime, ceftriaxone, and cefotaxime)<\/p>\n Fluoroquinolones (such as ciprofloxacin, norfloxacin)<\/p>\n Co-amoxiclav<\/p>\n Ampicillin and amoxicillin (which may relate mainly to the volume of their use rather than being high risk)<\/p>\n 3. Underlying morbidity<\/strong> such as abdominal surgery, cancer, chronic renal disease, and tube feeding.<\/p>\n 4. Current use of a proton pump inhibitor <\/strong>(such as omeprazole and lansoprazole) or other acid-suppressive drugs (such as H2-receptor antagonists).<\/p>\n Two further important risk factor are hospitalisation<\/a> (C diff colonisation rates of about 20-30 percent, compared to 3 percent in the general population) and previous C. diff infection. In fact, the recurrence rate is around 20% for the first infection and 45-60% after the second episode in hospitalised patients.<\/p>\n <\/p>\n b) If it were C. diff, how bad would it be to miss it?<\/span><\/p>\n C. diff infection can cause anything from a self resolving bout of diarrhoea to pseudomembranous colitis, toxic megacolon, perforation of the colon, sepsis and death. As with any diarrhoea, there is always a risk of dehydration.<\/p>\n <\/p>\n Old me: OK, so what is the mechanism of C. diff infection then?<\/strong><\/p>\n New me: It\u2019s not as simple as \u2018take a culprit antibiotic –> kill off the good bacteria –> let C. diff proliferate\u2019. This mechanism does not explain why C diff occurs in outbreaks on wards, as antibiotic exposure is pretty constant from week to week.<\/p>\n It\u2019s like Quasar<\/a>.<\/p>\n When I was a kid, we used to go to Quasar. If you got shot, a voice came from your gun saying \u2018Defence shield active, active. Warning, warning\u2019. The idea was that for two seconds, the defence shield was active (you could not shoot, but could not be shot) and then you were in trouble for two more seconds (you could be shot, but could not shoot). This was terrible game design. The defence shield bit was OK, but the warning bit encouraged picking on one victim over and over.<\/p>\n Clearly I got over this and was definitely not one of the people who got picked on over and over on at his own Quasar birthday party by his own friends.<\/p>\n Antibiotics put you in the \u2018warning, warning\u2019 phase. The disruption to the bowel flora is the first hit. If you then meet C. diff whilst you are in the warning, warning phase, that is the second hit. You then go one of two ways. Most people get colonised asymptomatically. A minority get C. diff infection. It\u2019s not clear what determines your fate after the second hit, but it is probably a mixture of virulence factors and host factors.<\/p>\n http:\/\/cid.oxfordjournals.org\/content\/26\/5\/1027.full.pdf<\/a><\/p>\n <\/p>\n Old me: Oh, I see. Most of the time you can tell it\u2019s unlikely to be a C. diff infection then. <\/strong><\/p>\n New me: Yeah. NICE CKS say that if C. diff is suspected, then get a stool sample sent. If not, don\u2019t.<\/p>\n The usual rules for deciding who to admit with gastroenteritis<\/a> apply. If you suspect C. diff, assess<\/a> severity.<\/p>\n If you are going to send a stool sample for C.diff toxins, bear in mind there is a 10-20% false negative rate<\/a>. Because of this, you may have to repeat the C. diff toxin test 24 hours after a negative result if clinical suspicion remains. This is because quite a bit of toxin needs to be detected to give a positive test.<\/p>\n![\"From](\"https:\/\/i0.wp.com\/drcrunch.co.uk\/blog\/wp-content\/uploads\/2014\/04\/screen-shot-2014-04-15-at-21-30-37.png?resize=474%2C278\")
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