If my patient is on antibiotics and has a history of C. difficile, should I put them on prophylactic oral vancomycin?

Example: you have a lovely 68-year old male with a history of two episodes of C. difficile infections after getting antibiotics in the setting of a hip surgery three months ago. He is admitted to your service with pneumonia and you decide he should get a 5-day course of levofloxacin. He has no abdominal pain or diarrhea (yet). Would PO vancomycin would help prevent recurrence of C. diff? 

In this case, the answer is a weak “yes.” There is no randomized controlled trial data showing that PO vanc prevents recurrence. However, there is a retrospective study of 172 patients in Quebec with a diagnosis of C. diff who were exposed to antibiotics for whatever reason within 90 days of their diagnosis. Those patients who had at least one recurrence of C. diff who got PO vanc had half the risk of getting C. diff again. Because the study looked at patients within 90 days of diagnosis, it’s unclear whether patients who had C. diff from a longer time ago would get the same benefits. A second study from 2016 of over 200 patients showed that patients who got PO vanc had a 4% risk of recurrence, whereas patients who didn’t had a 27% risk. Notably, this study only surveilled patients for 4 weeks after their antibiotic course, and the patients weren’t randomized–I got the sense that the patients who were offered PO vanc were “sicker.”

The regimen that I have seen most often is 125 mg PO vancomycin QID, but the second study, for example, reported 125 mg PO vancomycin BID or daily, so regimens are all over the place.

How long should patients continue PO vanc prophylaxis for? Again, no strong right answer. I have seen patients told to take PO vanc for only as long as they are on other antibiotics, for a week after finishing, or to do a slow taper/pulse down. However, there is a clinical trial  that has set the time course of PO vanc as 5 days after stopping other antibiotics, which sounds pretty good. What if it’s longer than a week, or a month? I did have a patient who required lifelong oral suppressive antibiotics…and we made the decision to keep her on PO vanc lifelong as well.

Do probiotics prevent recurrence of C. diff? The 2018 IDSA guidelines cite unclear evidence on whether probiotics prevent recurrence. While probiotics are fine for the general population (might as well try it if it won’t hurt), there are rare cases of fungemia/invasive infection that have been reported, in patients who are immunocompromised, have PICC lines, or are otherwise severely ill.


How is fecal microbiota transplant (FMT) performed?

Fecal microbiota transplant (FMT) is an effective and durable method of treating recurrent or refractory C. difficile infections. There are several routes of administration:

  • Nasogastric tube: patient takes PPI beforehand, NG tube is inserted, 50-60 cc of fecal slurry is pushed into the tube
  • Endoscopy: 200-250 cc of fecal slurry is delivered by flex sigmoidoscopy or colonsocopy (to the cecum)
  • Capsules: frozen capsules of slurry taken over several weeks (experimental)

Is there any difference between these different routes of delivery? Capsules were first devised at Massachusetts General Hospital; clinical trials are ongoing and they are not widely available. NG tube vs. endoscopy have been compared, and although some have not found a difference, some conclude that endoscopy is superior. For example, this study of 50 patients from the University of Alabama at Birmingham showed that patients who had endoscopy delivery of FMT had a greater rate of “cure” (improvement of symptoms in 2 weeks) and fewer repeat FMT treatments. However, you do have to evaluate each patient individually: some patients may find the idea of an NG tube too repulsive, some may be too sick to undergo endoscopy, etc. Importantly, FMT is felt to be safe for immunocompromised patients, too.

Tangent: according to the 2018 IDSA guidelines for treatment of C. diff, PO vancomycin or fidaxomicin are now considered agents of choice for a first episode of C. diff, no matter the severity. Keep your metronidazole on the shelves! It’s no longer recommended. 

Is it safe to give Tylenol to this patient with liver injury or elevated LFTs?

It is a widely held belief that Tylenol (acetaminophen, or paracetamol, depending on where you are) should not be used in patients with chronic liver disease or transaminitis because the drug will worsen liver injury or cause acetaminophen toxicity, the most common kind of drug-induced liver injury. However, underuse of Tylenol may lead to overuse of other pain medications, like NSAIDs or opiates, which come with their own problems. 

This review in the British Journal of Clinical Pharmacology goes through studies of healthy adults and adults with liver disease, including cirrhosis to look at the evidence for our fear of Tylenol. Essentially, the studies on Tylenol are small, and ALT naturally fluctuates (thus some of the previous methodology linking rise in ALT and Tylenol may have been questionable). The authors conclude that heavy alcohol use, malnutrition/fasting, underweight status, and sepsis may put patients at risk for acetaminophen toxicity, but Tylenol is still not 100% contraindicated for these groups. They state:

We have not found any case reports of hepatotoxicity secondary to therapeutic doses of paracetamol in adults with pre‐existing CLD who did not have at least one of these risk factors.

Therapeutic dose of acetaminophen is 4 g/24 hours. Therefore, it’s recommended that if you have patients with the above risk factors, aim to give them 2-3 g/24 hours. If they are developing rapidly deteriorating liver function (acute liver injury or failure), then it might be time to stop.
Continue reading

How long does this person have to be NPO for?

Being NPO for an add-on surgical case (only to be told at 5 PM that there’s no chance the case will happen today) is a low-grade form of torture, and patients are always anxious to know when and if they can even have a little bit of water for their parched mouths. The nurse wants to know what time Mr. Smith should get his aspirin with a little apple juice if the case is scheduled for 11 AM. What’s the answer?

Screen Shot 2018-07-08 at 9.43.47 AM.png
Nicely prepared table from the learning module “Anesthesia for Internists” from the Society of Hospital Medicine

What is a pericardial window?

A window is also called a transthoracic pericardiostomy, a surgical procedure done for large and/or recurrent pericardial effusion in which a 4-cm flap of pericardium is removed from the heart so that pericardial fluid can drain into the chest cavity. The pericardial flap can be used for biopsy (if there is concern for infectious or malignant pericardial effusion). When a pericardial window is performed, there may initially be a large-bore drain as well. However, the point of the window is to allow fluid to continuously drain into the chest cavity until the tissue fibroses and scars and the window “closes.” Only 5-10% of patients who get a window will have reaccumulation of the effusion, as demonstrated in this study.

Screen Shot 2018-07-07 at 12.27.44 PM.png
Source: http://onsopcontent.ons.org/Publications/SIGNewsletters/images/PDFs/acc/Table1.pdf


The least invasive technique for relieving pericardial effusion is pericardiocentesis; the most invasive is pericardiectomy. A pericardial window is somewhere in-between. (There is also something called balloon pericardiotomy which is analogous to balloon valvuloplasty.) Risks include arrhythmia, infection, clot, and very rarely, cardiac perforation.

When pericardiocentesis is performed, there may be a decision to place a pericardial drain (a small-bore catheter) to allow extra fluid to be removed. The drain is usually removed when output decreases to 25-50 cc over 24 hours. Unfortunately, up to 60% of patients who receive pericardiocentesis may have reaccumulation of the effusion.


Screen Shot 2018-07-07 at 12.34.55 PM.png



Eye-“itis:” differences between keratitis, episcleritis, scleritis, and uveitis

The eye-“itis”es can be pretty confusing for those of us who don’t regularly use an ophthalmoscope to visualize changes in blood vessels, free-floating cells, deposits, and detritus. (The last time an internal medicine resident diagnosed uveitis on slit lamp/fundoscopy was…? Sorry to my ophtho friends.) Here are some slides I made to help distinguish the “itis”es (organized from anterior to posterior):

***N.B.: One important cause of “red eye” not discussed here is ACUTE ANGLE CLOSURE GLAUCOMA. Conjunctivitis is also not discussed.

Screen Shot 2018-07-06 at 5.06.48 PM.png

Screen Shot 2018-07-06 at 4.58.18 PM.png

Screen Shot 2018-07-06 at 5.07.23 PM.png

Screen Shot 2018-07-06 at 4.58.34 PM.png