GI, Improving Outcomes, Mythbusting

The Better Poop Route.

This is a study comparing PO vs colonoscopy inserted fecal microbiota transplant for cdiff with the primary outcome the proportion of patients without a recurrence 12 weeks after stool transplantation.


Survey says- it doesnt matter how you do it, but both have their ups and downs.


While PO meds were significantly less costly, it was significantly less pleasant (44% vs 66% rated it “not at all unpleasant”) – understandably so as patients took FORTY capsules- under direct observation no less- which were made from a singular 80-100g donation. Colonoscopy implantation was performed with placement of 360cc of “fecal slurry in the cecum” – and was significantly more expensive ($874 vs $308). Colonoscopy patients had a 12.5% rate of minor adverse events vs 5.4% of the PO group (mostly nausea/vomiting or abdominal discomfort).

Further fun facts, participants most frequently characterized fecal transplants as “innovative treatment” (63% of patients), a “natural remedy” (41%), and “unpleasant, gross, or disgusting” (30%); which is surprisingly realistic to how providers feel about this same treatment.

Its nice to see the lower cost, less invasive treatment work equally well (both clocked in at about 95% rates of non-recurrence at 12 weeks), but geez, 40 tablets of poop seems a bit more like a lost dare than a medical necessity.

Critical Care, GI, Improving Outcomes, Mythbusting

Less transfusions, the better, platelet style.

Over 4 years, the Mayo clinic reviewed over 40,000 ICU patients, and sought to determine if prophylactic platelets for critically ill thrombocytopenics matter.

Of these 40,000 ICU patients, they excluded anyone who received RBCs within 24 hours prior to the PLT count that triggered transfusion “to minimize the risk of including those with active bleeding” … The primary outcome was essentially to determine if transfusing platelets led to more RBC transfusions, and, secondarily, all-cause mortality, ICU and hospital free days (among others). Seems backwards, but whatever.

So what falls out of this data?

For all comers, in a propensity matched cohort, one transfusion begets another – (46.3 % of those with platelet transfusions also had an RBC transfusion vs 10.4% of those without platelet transfusions who had an RBC transfusion). Interestingly, those transfused platelets had less ICU free days (22.7 vs 20.8), more hospital free days (15.8 vs 13). When you look specifically at the ~5000 patients with <50k platelet counts and compare those who were/were not transfused platelets, there was no change in ICU mortality, 30 day mortality, ICU-free days, or hospital free days. While this was underpowered to determine statistical significance for those with platelet counts <50k, it is not hard to imagine a larger study to suggest similar benefits of not transfusing these patients- particularly since this study saw fewer hospital free days and fewer ICU free stays (10.2 vs 7.8 days and 19.9 vs 18.3 days respectively) – favoring a more restrictive transfusion strategy (but again, not meeting statistical significance, perhaps due to so few patients with <50k PLT).

This is not the first study I have seen suggesting empiric transfusion or outright canceling of procedures based on platelet counts between 50k and 150k is essentially bunk, and that prophylactic platelet therapy is of little benefit, if not outright harmful. There is even a flicker of a signal that prophylactic platelet transfusions >20k may not be beneficial – but this has yet to be definitively shown true -yet.

I can not agree more with the last words to the authors, “Finally, it must be acknowledged that while clinical trajectories did not improve for the cohort as a whole after platelet transfusion, it is possible that certain subpopulations may indeed benefit from the intervention, though these subgroups have yet to be identified.”

GI, Improving Outcomes, Mythbusting

NG tubes. just. wont. die.

My angst for the NGT has been explained in a previous post, and while this study adds to said angst, it sadly comes short of putting a nail in the coffin in the debate with surgical colleagues.
This is a retrospective single center study which enrolled 181 ED patients with SBO from September 2013 to Sept 2015, and essentially grouped patients according to whether or not a nasogastric tube was placed (49% of patients did not receive the dreaded NGT). Looking at a multitude of factors, they attempted to tease out items associated with nasogastric tube placement, and if there were any appreciable benefits to NGT placement.

Ultimately, if you are over age 70 (37% NGT+ vs 19% NGT-),  have a malignancy (30% NGT+ vs 17% NGT-), or had a prior SBO (56% NGT+ vs 32% NGT-) you’re more likely to have an NGT because, hey, one good NGT deserves another.  NGT+ patients were also less likely to have “likely / early SBO” (19% NGT+ vs 40% NGT-) on CT imaging as well.

All in all, while I’d love to point at the mean length of stays (7 days for NGT+ vs 4.2 days for NGT-; median 5 days vs 3 days), and non-statistically significant resection rates of 13% vs 9% as indications that the NGT is not needed…. well, we’re not exactly comparing apples to apples. The NGT+ patients were sicker- they were older, had higher malignancy rates, had a slightly higher surgical rate, and were more likely to have “definite SBO” on CT. Sadly, this is not the paper to put the NGT argument to rest.  We still need a larger study, preferably with matched controls, to fully put this dinosaur to rest.


Someone?  please? … anyone? please?

GI, Mythbusting

Haloperidol- one anti-emetic to rule them all.

When all else has failed, and the patient does not meet admission criteria, where do patients go?  Obs, of course!  I view it as a valuable tool to augment my ED armamentarium.  Specifically, for instances like, say, gastroparesis or cyclic vomiting.

This randomized, double-blind, placebo-controlled trial was performed at two urban hospitals looking at patients with a previous diagnosis of gastroparesis comparing conventional therapy + placeo to conventional therapy + 5mg of IV haloperidol.  They looked at pain severity and nausea every 15 minutes for 1 hour.  Secondary outcomes were disposition status (hospital admission or discharge), ED length of stay, and nausea resolution at 1 hour.  Sadly, they only looked at 33 patients total over a two year study period.

While the two groups were similar in terms of the conventional therapy received, in the haloperidol group, disposition was made sooner and more patients were discharged home, with a significant reduction in pain at one hour (on a scale of 0-10, a mean improvement of 5.37 vs 1.11 in favor haloperidol), as well a reduction in nausea at one hour (scale of 0-5, improvement of 2.7 vs 0.72 in favor of haloperidol).  Fewer patients were admitted (26.7% vs 72.2%) who received haloperidol, with median length of stay shorter for haloperidol (4.8 hrs vs 9 hrs).  Surprisingly, patients in the haloperidol group experienced no adverse events, including QT prolongation and dystonic reactions.  This is probably due to small sample size.

This does not address haloperidol as sole treatment,  and at only a few dozen patients in this study, certainly does not solidify haloperidol’s use as first line.  However, it does add to the pile of data showing haloperidol as safe and efficacious in these patients.  As an aside, if your hospital is anything like mine, you can not give haloperidol IV, so I’ve trialed 5-10mg IM.  Over the last 4-5 years, I’ve become fond of IM haloperidol for refractory vomiting, and (anecdotally) I’ve used it dozens of times with high rates of success.

So yes, better analgesia, decreased nausea, fewer admissions, and decreased LoS with haloperidol.  Pretty much everything you want.  I just wish a broader study in non-specific abdominal pain with vomiting would compare haloperidol as singular treatment and compare it to standard care.

Look, there are some patients who are vomiting so profusely that they seemingly require an exorcism.  For those patients, I think adding a bit of haloperidol for symptomatic relief does not have much downside, I just wouldnt go mixing multiple QT prolonging agents at once.

So, I ask, whats downside?

Improving Throughput, Mythbusting

More No-Value Care: pre-procedure INR for cirrhotics

You have a cirrhotic patient in front of you. They need a procedure. You reflexively order a cbc, comprehensive metabolic panel, and PT/INR because you’d like to know about their platelets/ liver enzymes / coagulation ability.

Or maybe it’s a consultant who refuses to do a procedure the patient needs until you order these tests.

And then the platelets come back at 40; or maybe the INR returns at 1.4. Now what?

Do we need to transfuse platelets or FFP? Well, this case series looked at 852 consecutive cirrhotics from Jan ’11 – March ’14 who needed an invasive procedure the decision to transfuse PLT / FFP at attending discretion. Here’s a breakdown of their patient demographics:


And the number of complications:


Now, sadly, despite discussing the World Health Organization classification for bleeding events, they did not really get into the severity of bleeding events. With that said, complications were unrelated to platelet count, INR, CHILD classes, and MELD score. Only 1 in 379 paracentesis had a bleeding event, and only 2 of 228 TIPS/ CVC/ PICC/ hemodialysis/ I&D procedures had an event.

Perhaps most importantly, while attempts to normalized PLT and INR values, PLT/FFP transfusions barely affected the corresponding abnormalities, the scheduled invasive investigations were carried out in the presence of still subnormal parameters- with no or only a few bleeding complications.

Ergo, I agree with the authors, – “we have verified clinically the futility of this recommendation.”

Critical Care, Improving Outcomes, Mythbusting, Neurology

Compazine… for infectious disease?

Today’s article’s (1, 23 ) are a break from the usual trials that are typically discussed and a bit more “benchside medicine” than bedside medicine.  In fact, let’s look at this as an early request for one of the 12 trials of Christmas.

Phenothiazines have demonstrated in vitro (as well as some in vivo) activity for gram positive cocci, mycobacteria, amoeba (4; 5), and some gram negative rods.

It should be noted that Klebsiellae, pseudomonads and acenetobacters were highly resistant to almost all of these drugs.

The MIC for phenothiazines are usually not reached with conventionally used doses, but these compounds do enhance the activity of various antibiotics to which various bacteria are susceptible (including vancomycin), and even decrease the MIC of resistant organisms.

So where am I going with all of this? For starters, lets look at some common causes of meningitis, in no specific order:

Strep pneumo (gram positive); group B strep (gram positive); staph aureus (gram positive); Listeria (gram positive); Neisseria meningitidis (gram neg diplococci); H flu (gram neg)

All things phenothiazines are thought to have activity against.

You’re likely to be giving patients with potential meningitis something for pain (I hope?), so why not go with compazine?  Likewise, patients whom you may suspect bacteremia from a cellulitis, why not give compazine to, ummm, “counteract the nausea” associated with the opiates you gave for pain control?

I think this falls into the unlikely to harm, might help category, and is seemingly a ripe area for research.  Is this practice changing?  Nope, not at all.  Food for thought, but until compazine is proven unsafe in an infectious process, I will continue my love affair with compazine for headaches, nausea, and vomiting (regardless of suspected etiology).

GI, Improving Outcomes, Mythbusting

Rethinking Diverticulitis

For those savvy FOAM early adopters that have been referring to diverticulitis as the sinusitis of the colon, this one is for you.

While diverticulitis management (or lack thereof) has been discussed periodically – specifically in regards to antibiotics being of no use in the uncomplicated form of diverticulitis – here comes a new study to suggest we have to at least rethink our referral patterns.

The Danish national registry was mined for a population-based cohort study, for a total of 445,456 included patients over 18 years, of whom 40,496 had a diagnosis of diverticulitis. They then compared other patients in a 1:10 ratio (diverticulitis: no diverticulitis) matched for sex and age within 1 year. Of note, the matched group also did not have a diagnosis of diverticulosis either.

Basically, the risk of developing colon cancer was 4.3% in the diverticulitis group and 2.3% in the matched cohort. This was statistically significant (P <0.001, incident ratio 1.86), and remained when adjusting for confounders (OR 2.20)…

Pro-inflammatory states cause more cancer? Perhaps. We know they cause more thromboembolism and early coronary disease already. Bottom line – while an NNT of 50 is nothing fantastic, we see this condition regularly, so reconsider providing strong follow up to your patient, whether that be PMD or GI, especially if they’re in the age where they are due for a colonoscopy anyway.