Tasty Morsels of Critical Care 029 | Clostridium Difficile

25 Feb

Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care fellowship exam preparation.

We see C. Diff in the ICU in a couple of contexts. Firstly the poor unfortunate soul who starts with a benign illness and gets some antibiotics and develops a fulminant colitis and shock needing colectomy and an ICU admission. Secondly we have the frequent dilemma of the prolonged ICU patient who is collecting complications like they’re merit badges. They’ve developed new shock and there’s some diarrhoea and you’re worried about c. diff.

First off some risk factors. Firstly is antibiotic exposure and topping the list would be beta-lactams and clindamycin, closely followed by the quinolones, aztreonam, and the carbapenems.

A truncated list of patient specific risk factors might go as follows:

  • age >65y
  • previous GI surgery or IBD
  • renal impairment
  • prolonged hospitalisation esp with a C. diff contact
  • gastric acid suppression (though PEPTIC trial would suggest against this is unlikely, or at least not more likely than H2RA. However I still think it’s a fair answer in an exam)
  • immunocompromised and chemotherapy patients

There are a few useful principles of prevention:

  • Hand washing – remember that spores survive alcohol and on surfaces, need soap and water
  • Isolation
  • Testing of symptomatic individuals
  • avoidance/minimising antibiotics
  • Limit PPI use and get NG tubes out ASAP

In terms of diagnosis we’re typically thinking of this in patients with diarrhoea. We send a stool sample and wait patiently by the computer for a result. But what are we actually testing? This will of course depend somewhat on your local lab but there are a few important principles. Most of the time we’re testing for a toxin produced by the bacterium. This can be toxin A or B or both. If both are +ve then cool cool cool you’ve probably got your diagnosis. If you’ve got one +ve and one -ve then IDSA recommends using nucleic acid amplification (or PCR if you like) as a tie breaker. The PCR is very very sensitive. And the issue is that the presence of c diff DNA in your poo doesn’t necessarily imply disease whereas the combination of symptoms a +ve toxin immunoassay and a PCR is much more compelling.

An important component of the diagnosis involves some form of mucosal assessment – especially in more severe cases. This can be some form of flexible boweloscopy device or a CT scan looking for colitis or mega colon.

Once you’ve made your diagnosis you’re ready to start some treatment. This can be very confusing as treatment is not only determined by severity grade but the recommendations have changed relatively recently (in 2018) so the stuff you learnt for your membership examinations may no longer be relevant.

The split here is into non severe, severe and fulminant so keep that in mind.

The split between non severe and severe, is defined by a WCC<15 and a normalish creatinine. This distinction would seem an important thing to memorise, however as far as I can work out, IDSA suggests identical treatment for both non severe and severe. Namely

  • Vance 125mg PO QDS OR fidoxamicin
  • note that metronidazole PO is no longer recommended the way it was in the mid noughties when I started.

Fulminant disease is primarily determined by shock and the presence of megacolon. This probably is something worth remembering as treatment here is significantly different. Here you give vanc 500mg PO QDS plus metro IV (which after being given IV is secreted unchanged into the GI tract via the biliary tract). For those with nasty distal disease vanc enemas can also be used which will certainly make you super popular with the nursing staff.

While rarely done, it’s really important in both clinical practice and certainly in an exam to consider taking out the whole colon. The surgeons will of course make the final decision on this but some may need a little nudge in the right direction. Potential nudges might include

  • Hypotension requiring vasopressor therapy
  • Clinical signs of sepsis and organ dysfunction
  • WCC in excess of 50
  • Lactate in excess of 5mmol/L
  • Failure to improve on medical therapy after 5 days

If you’ve managed to get all this across in your SAQ then you’re flying but if you want to go for gold then you could throw in a few comments like

  • faecal transplant – niche and not really considered until 3rd recurrence
  • IVIG as a toxin binding agent in fulminant (no substantial support)
  • there is a monoclonal antibody to bind toxin but this is really sketchy at this point

References and rationalisations

Deranged Physiology

LITFL

IDSA 2018

 

 

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