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?

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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?

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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:

screen-shot-2017-02-18-at-7-47-52-pm

And the number of complications:

screen-shot-2017-02-18-at-7-48-04-pm

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.”

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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).

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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.

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"Palliative" is not a dirty word, GI, Improving Outcomes, Improving Throughput, Mythbusting, Radiology

Versed, Pavlov, & the NGT

I admire & strive for efficiency, empathy, and efficacy.  Thus, if a certain painful procedure extends lengths of stay without significant benefit to the patient, I’m hesitant to order it. However, sometimes it is frowned upon to not play nice in the sandbox with our Pavlov consultants who request NG tubes for small bowel obstructions.

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Thus, if you must place an NG tube for an obstruction, keep today’s study in mind.

Up at The U (of Vermont), patients that were ordered an NG tube and were between 18 and 60 years of age were given 1 ml of intranasal atomized co-phenylcaine (lidocaine 5% with 0.5% phenylephrine to each nostril, followed by either placebo or 2 mg of IV midazolam with NG tube placement within 5 minutes of placebo or midazolam. Using a 100 mm VAS for pain and discomfort, as the primary endpoint, the patients were interviewed 15 or 45 minutes after the procedure.

After 51 total cases (23 of which qualified for the study), the trial was stopped early as several ED clinicians felt that midazolam prior to insertion was superior to topical anesthetics alone and did not want their patients randomized in the study.

Hence, the numbers are a good bit low. Only 13 patients in the control arm, and 10 in the treatment arm. The mean difference in pain scores was 31mm and 36mm for discomfort. None of the midazolam placements were rated difficult by nursing who placed the NG tube, whereas 3/13 in the control group were rated as difficult or very difficult to place.

So yes. The numbers are small, and the authors shed some light on questions we would have. They spoke about anecdotally about 1mg of midazolam for those over 60 years old or with known pulmonary disease – which they felt did not alleviate pain or discomfort. Here, I think a 1mg bolus followed by 0.5mg boluses as needed is reasonable.

They cite a paper stating that 91% of providers would change their practice if new literature showed a convenient way to reduce patient discomfort. Well, here it is. So, if Pavlov’s dog barks and you HAVE to place an NG tube, hopefully your institutional policy allows IV midazolam without considering it procedural sedation (or, potentially using intranasal midazolam for anxiolysis).

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Critical Care, GI, Improving Outcomes, Mythbusting

PPIs, ACG, and GI bleeders.

The PPI wheel is reinvented.

There is so much evidence to contradict the PPI drip, that it drives me mad that some still request a drip. We have yet another study comparing PPI bolus vs infusion for the prevention of bleeding after endoscopic submucosal dissection. Not surprisingly, as we have seen in the actively bleeding GI patient before, there was no difference in delayed bleeding or high risk ulcer stigmata with PPI bolus or drips in this study that evaluted 273 randomized patients.

Yet we continue to get push back about PPI drips. Despite this meta-analysis showing high-dose infusion for variceal hemorrhage is not beneficial, or this JAMA Internal Medicine meta-analysis  showing similar outcomes for bolus treatment vs bolus +infusion in terms of rebleeding within 3, 7, and 30 days, the need for urgent intervention, mortality, red blood cell transfusion, and length of hospital stay.  Perhaps this recent meta-analysis of 12 articles demonstrating that cirrhotic patients who use PPIs are at a higher risk of developing spontaneous bacterial peritonitis may help (OR = 2.17). While the meta-analysis looked at taking PPIs on a daily basis and future risk of developing SBP, perhaps it is not a huge stretch to suggest that an acutely ill cirrhotic GI bleeder on 8 mg per hour of your favorite PPI may be more prone to develop SBP.

 

So, what does the American College of Gastroenterology say?

Pre-endoscopic intravenous PPI (e.g., 80 mg bolus followed by 8 mg/h infusion) may be considered to decrease the proportion of patients who have higher risk stigmata of hemorrhage at endoscopy and who receive endoscopic therapy. However, PPIs do not improve clinical outcomes such as further bleeding, surgery, or death (Conditional recommendation)… After successful endoscopic hemostasis, intravenous PPI therapy with 80 mg bolus followed by 8 mg/h continuous infusion for 72 h should be given to patients who have an ulcer with active bleeding, a non-bleeding visible vessel, or an adherent clot (Strong recommendation)…. A meta-analysis of 8 trials showed that, compared to endoscopic therapy alone (sclerotherapy or EVL), endoscopic plus pharmacological (octreotide, somatostatin, vapreotide) therapy improved the initial control of bleeding and 5-day hemostasis without differences in mortality or severe adverse events… EGD, performed within 12 hours, should be used to make the diagnosis and to treat variceal hemorrhage, either with EVL or sclerotherapy (Class I, Level A).

So, even ACG acknowledges that PPIs (and octreotide, while we’re at it) did not improve outcomes, yet they advocate for their use.  Important to note, they do advocate for urgent endoscopy – which they define as within 12 hours.  Next time you have to discuss a PPI drip, you can say that ACG acknowledges that it does not improve outcomes, and that high dose PPIs may predispose your sick patient to SBP.

http://gi.org/guideline/prevention-and-management-of-gastroesophageal-varices-and-variceal-hemorrhage-in-cirrhosis/

http://gi.org/guideline/management-of-patients-with-ulcer-bleeding/

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