Mythbusting

Chronic opiate use leads to worse surgical outcomes

No surprises here. This study looks at outcomes after major elective abdominal surgery ~500 patients on chronic opiates vs ~1900 opioid naive patients from a single center from 2008-2014.

9.2% higher costs, 12.4% longer LOS (5.9 vs 5.2 days), higher complication rate (20% vs 16%), more readmits (10% vs 6%), without a difference to discharge destination (home, SNF, etc).

On one hand, you play the hand youre given – you help the patient the best way you can. But, what if that means you detox them first? It will be interesting to see if some providers go to that extreme. Especially if they (or hospitals) are not reimbursed at a higher rate to take on the added risk / LOS / bounceback rates. I know of orthopaedics refusing surgery based on a patients weight – I can envision a scenario in which the (currently) heavily-stigmatized opiate addicted patient is deemed unfit for non-emergent surgery so that facilities and providers retain their “5 star” ratings for various non-emergent surgical procedures to gain the insurance dollars of the “educated consumer”.

Sigh. This is quite the ethical pickle.

Next question – does this spill into EM? Should we withhold 1-2 doses of opiates for fear of worse outcomes? A perforated viscous seems like a good indication for opiates if ever there was one.

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Cardiology, Critical Care, Improving Outcomes

Brady arrest? Go Full Bore.

Do you believe in full bore medicine?

(hat tip to SMACCdub for that line)

This paper puts those thoughts under the microscope a bit, and challenges us to think ahead and be prepared.

They looked at all OHCA from 2006 to 2012 with initial brady/asystolic arrests to determine if they may benefit from pre-hospital pacing, and to look at survival rates associated with various rhythms. Clear non-cardiac causes (trauma, drowning, respiratory, neurologic, suicide) were excluded.

7925 OHCA in the Netherlands

less non-cardiac (6681 patients)

less those without EKGs (~500 patients)

less ~3000 patients with VF/VT (now at 2643 patients)

less those with normo/tachycardia and those with pacers previously placed (~300 patients)

 

This leaves us with 2333 brady/asystolic (idioventricular, junctional, sinus brady, 3rd degree with/without escape, asystole) patients – or, about 30% of their OHCA.

Unwitnessed arrest still protends a poor outcome, with survival about 0.5%. However, for witnessed arrests, they report 4% survival for idioventricular / junctional arrests and 6.8% for sinus brady arrests. This seems consistent with prior studies. However, for a study trying to determine whether or not pacing is beneficial, their pace rates were quite low. They paced 11 of 220 sinus brady patients and 41 of 452 idioventricular / junctional patients, with a delay of 30.1 and 16.5 minutes to pacing respectively – with an electrical capture rate of 55% and 70% to boot.  Esssentially, they can’t answer the question “Does pacing help” with such a care gap.

So, why is this? For sinus brady, maybe patients are hanging in the 40’s-50’s and felt to be quasi-stable. Maybe its the angst of floating a pacer. Perhaps the lengthy delay for sinus brady is giving atropine, then giving it again… and maybe again- akin to pressor-angst for sepsis (giving a 4th, 5th, and 6th liter rather than starting pressors or a central line).  I imagine there is a mental barrier – whether it be not thinking about pacing or passing the buck (“I’ll let the ICU figure it out.”). The evolution of the ED-ICU model (and perhaps UPMC’s cardiac arrest unit) may be the best place to look at this type of “full bore” medicine and whether or not it would be beneficial.

But for now, there is a large gap in care. Bradycardic arrests represent about 10% of arrests, have a reasonable survival rate, and are (potentially) suboptimally managed – and you have the tools to potentially improve an outcome.  We can not say whether or not pacing is futile care for this condition.

Until then, go full bore. Your patients & their families deserve it until pacing is demonstrably shown to not be beneficial in bradycardic arrests.

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Improving Outcomes, Improving Throughput, Mythbusting, Pediatrics, Pediatrics, Pediatrics

SCI still rare in kids.

This paper demonstrates that once again, kids are quite durable.

The authors looked at 3701 patients under 19 years old evaluated for a cervical spine injury. Of the 44 patients with clinically significant cervical spine injury (CSI), 32 had plain films, none of which missed an injury.

32 out of 3701… or 0.86%

-There were ZERO patients under two years old with a CSI

Here is the caveat- one injury begets another. Of the 32 patients with CSI, ten (31%) had multiple lesions, with plain films not identifying all lesions in 4 patients. Given that, I think its fair to say CT (or admission for MRI) is warranted once an abnormality is found.

In summary, relevant cervical injuries in kids are rare (<1%), and plain films are a reasonable screening tool. CT is once again rarely needed, but beware since one injury seemingly begets another. I pretty much agree with the authors on this one,

Our calculated 100 % sensitivity (90% on PECARN, finding 168 of 186 CSI) does come with a large confidence interval and it should be expected that plain films sensitivity for CSI is likely lower in clinical practice. However, the small risk of missed injuries from plain films must be balanced against the increased risk of malignant trans- formation from performing CT scans on all children with suspected CSI.

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Mythbusting

No Magic for MagicPlex PCR.

PCR really is quite magical. You take a few drops of blood from a febrile patient and within a few hours, you can have an answer of the type of bacterium causing your “presumed noninfectious SIRS,” or, perhaps, the cause of febrile neutropenia. It may even be higher yield than good old fashioned blood cultures (x2, of course). Unfortunately, today’s article on PCR is, yet again, more “look what I can do” rather than “look at the improved outcomes!”

At a single tertiary care center for pediatrics, 150 MagicPlex PCR studies from 89 patients aged 2-12 years young were performed for various reasons (suspected sepsis, 55%, febrile neutropenia 25%, localized infection 12%, FUO 6%, undefined 3%). None of these patients were tested in the ED, and 149 of the 150 tests had antibiotics given before testing. 34% of patients were heme/onc patients, 17% had a stem cell transplant, 17% were ICU players, and 21% had no chronic disease. Concurrent blood cultures were drawn.

There were 60 blood stream infections identified, 5 of which were by blood culture only, 32 of which were by PCR only. For this, the authors claim a 143% increase in yield. All is not roses though, as this increase comes at the behest of 12 additional contaminants by PCR. They report their contaminant numbers are consistent with prior findings – about 90% sensitivity, 70% specific. Just under 10% of these tests led to a false positive.

Specific for what is a better question. Who is the ideal candidate for this testing? Ill appearing ICU players without a known reason? Sure. On immunosuppressants? Asplenics? transplant patients? I guess its reasonable if you dont have a source. Even in AIDS patients, pneumonia is typically common causes.

They tout, “As a matter of fact, in 24 cases out of 60, MP allowed a quick start of an appropriate, goal-directed antibiotic therapy, modifying the previous empiric regimen.” Really? An explanation of sorts would have been nice here, but they fail to provide a one liner about patient history that may have clued them in. Oh, and for every two saves, you’ll have one contaminant that you’ll jump on, bill for critical care, and start the patient on a path of antibiotics and aggressive care that they didnt need. Or set you up for premature closure. That, and magicplex missed the one Neisseria meningitidis case.

My fear is that **everyone** will get it – I mean, we can barely get providers to stop sending blood cultures on well appearing cellulitis. What happens to the pyelo without comorbidities that was on the border of getting sent home, but now gets MagicPlex, and someone decides that, despite having a transient bacteremia that was sensitive to the prescribed Levaquin, now this patient who likely could have been fine as an outpatient because they had a pan-sensitive bug now gets admitted, without measurable benefit. We still have not quite figured out when yield would be highest with magicplex. Ideally, it would be high yield in the patients who are quite ill – the UA without nitrite/leuks with 5-10 wbcs, or UA/CXR/cUS negative patient, or the febrile dialysis patient with a question of a line infection. Or the asplenic or transplant patient. But if their low yield in these situations, who cares?

As previously documented here, there is still no improvement in mortality, despite magical PCR testing. I fear that this will be the next widely overused test, that has potential to result in MUCH higher costs for the system from overdiagnosis, with currently NO added benefit.

 

PS – previous MagicPlex in the ED performed awful.

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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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Critical Care, Improving Outcomes, Mythbusting

1 in 10 EGLS saves a life.

Do current sepsis guidelines go far enough?

That was my first thought when I read today’s article. This single center ICU study looked at 220 patients divided into two categories- one category in which patients that were managed in adherence with the 2012 surviving sepsis guidelines – 20-49 ml / kg initial IV fluid bolus, continued fluid challenges until CVP of 8-12, with more given based on treating team. Noradrenaline until MAP of 65, and dobutamine for cvSO2 <70% in combination with either lactate >2 or urine output <0.5 ml / kg / hr). The other 110 patients had treatment guided by limited echo:

Treatment options looked like this:

1) IVC fluctuation <15% & normal LV function= give pressors only (discontinue IV fluid)

2) IVC fluctuation >15% & normal LV function = 20-40 ml /kg IV fluid given

3) IVC fluctuation >15% & mod/severe LV function = 10-20ml/kg IV fluid given AND initiate dobutamine 5ug/kg/min

4) IVC fluctuation <15% & mod/severe LV function = discontinue IV fluid and initiate dobutamine 5 ug/kg/min

 

These patients were pretty sick- all patients were mechanically ventilated and on noradrenaline. Limited echo was performed within 24 hours of presentation to ICU and within 36 hours of presentation to the ED (actual times were within 7-15 hours in the ICU, on average, 11 hours). Patient characteristics were pretty similar in terms of age, APACHE scores, and labs (similar ESRD/CHF percentage as well ~20% of both patient arms). Surprisingly, patients received a ridiculous amount of IV fluid from the ED – 68 (55-70) ml / kg in the echo group vs 65 (55-72) ml / kg in the standard of care arm. Yes, even with 20% of patients having ESRD / CHF – the least amount of IVF given was 55 ml / kg !

Results?

Despite all of this IV fluid given in the ED, 35% of patients still have >15% IVC collapse (!). 65% of patients had their fluid restricted, and 22% in the echo arm vs 12% in the standard of care were started on dobutamine. On Day 1 in the ICU, patients received less IVF in the echo arm (49 (33-74) ml / kg, vs 66 (42=100) ml / kg) – but still a significant amount if IVF.

28 day survival was 56% vs 66% in favor of the echo arm, with significantly less acute kidney injury (65% vs 88% for all AKI, and 19% vs 36% for stage 3 AKI).

So your NNT to save a life is 10, and 4 to reduce incidence of any AKI.

So, is this really an ED paper? Well, it depends on your area of practice. The local flavor of the authors is such that their local policy was to initiate dobutamine in the ICU and not in the ED. Are you boarding ICU players? Are your hospitalists ultrasono savvy? How involved are your intensivists in patient care while patients are awaiting an ICU bed? Are you okay with administering at least 40 ml /kg IV fluid and starting pressors on your septic shock patients? If the answer is no or “not really” to any of these questions, then the answer is yes.

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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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