EM Conference Pearls (8/2/17)

Pearl’s from Wed conference August 2nd 2017:

Agenda:
– Asthma/COPD: Baldino
– Sepsis Core Measures: Patel
– Pulmonary cases: Patel
– Medical student pearls (from Mike Taylor, one of our students)


Dr. Baldino: Asthma/COPD

-All that wheezes is not asthma (or COPD).
-Use diagnostics to rule out mimics such as pneumonia or ptx.
-Get the CXR in COPD exacerbation, not routinely in simple asthma exacerbation.
-Good evidence and NNT’s for benefit of ipratropium, systemic steroids, magnesium,  and BiPAP.
-Intubation last resort for asthma.  Remember to adjust I to E ratio on vent.
-Steroids at discharge for asthma/COPD.  Antibiotics at discharge for COPD.
-Discharge with a plan! (and a spacer)


Dr. Patel: Sepsis Core Measures

-Sepsis core measures are from CMS, not from SSC guidelines or Sepsis 3.0. They are not necessarily rooted in great evidence, but we have to follow them!
-Remember the 3 and 6 hour severe sepsis and septic shock bundles. Timing is based on presentation time (when chart displays severe sepsis, septic shock), not door time.  To make your life easy, just use door time to meet the metrics.
-The focused exam for septic shock can now just be documented with one statement, which is in Medhost.  Make sure to click that.
-Fluids from the field count (as your 30 cc/kg), as long as it is given as a bolus and documented on the chart.
-Antibiotic choice and timing both looked at for core measures. For choice, best to go with a monotherapy agent first to meet the metric.


Dr. Patel: Pulmonary Cases

-The term HCAP is not in the newest pneumonia guidelines from 2016.
-Treat HCAP like CAP unless the patient is going to the MICU.  If going to the MICU, cover for MRSA and Pseudomonas.

Hemoptysis:

-Minor hemoptysis (streaks in the sputum)–d/c unless CXR abnormal
-Moderate hemoptysis (frank hemoptysis)—admit for further work up and obs
-Massive hemoptysis (hemoptysis interfering with respirations)–intubate and consult pulmonary (for bronch) and IR (for possible bronchial artery embolization). If there is a suspicion of a bronchovesicular fistula or other arterial fistula, CT surgery may also need to be on board.


Medical Student Pearls

One of our current medical student’s Mike Taylor put together some info on questions that were raised in conference:

Intentional “L Main Bronchus Intubation:” (for hemoptysis)

Take Home Points from 1995 Anesthesiology Case Report:
 -Can use a double lumen ET tube with a endobronchial cuff
 -The inflated endobronchial cuff can tamponade the hemorrhaging R lung and occlude airflow into it. This allows only the L lung to be effectively intubated and the provider not have to be tasked with putting the tube in the L main bronchus
 Reference: http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1949905

Rate Control for MAT:

Take home points from Uptodate
 -Treat underlying cause
 -Maintain phos and mag levels
 -Can use CCBs or beta blockers for rate control in symptomatic pts
 Reference (requires access to UpToDate): https://www.uptodate.com/contents/multifocal-atrial-tachycardia

Bandemia Cut Offs:

Take home points from 2012 Retrospective Cohort Study:
 -With normal white counts, pts with bandemia of at least 11% had higher in hospital mortality
 -So 11% or higher could use as a cut off for admission, more aggressive treatment, etc.
 Reference: https://www.ncbi.nlm.nih.gov/pubmed/22939096

Special thanks to Chief Dan Poor PGY-4 for organizing this week’s Conference Pearls and for Mike Taylor MS-IV for his Medical Student Pearls

Brain pus

Having pus in your brain is a problem no matter how you cut it, but finding it in there can be a challenge.  While the classic triad is usually fever, headache and a focal neuro deficit, this isn’t always present.  Dave Traficante (@davetraf) just published a pretty cool case of bifrontal brain abscesses in the International Journal of Emergency Medicine of a gentlemen with this very problem.  Interestingly, he didn’t have any focal neuro deficits, but he did have a very flat affect and could care less of the pus accumulating in his brain which coincided with the frontal lobe location of his abscesses. Check it out here.

Time for Terlipressin?

Correct, we don’t have terlipressin in the US, yet… Hopefully, sometime in the not so far off future we’ll have the chance to play around with it. Essentially it’s a synthetic analog of vasopressin which we are more familiar with. There’s some written about its use in variceal bleeds and here is a cool little study from Egypt using it for refractory septic shock.

They enrolled 80 ICU patients that were in refractory septic shock; meaning that they had to meet sepsis criteria and have the following three criteria:

  1. SBP < 90mm Hg or MAP < 70
  2. Received at least 1000ml of IVF or CVP 8-12cmH2O
  3. Necessitated more than 0.5 mcg/kg/min of norepinephrine

The 80 adult patients were split into two, pretty well matched groups, of 40. One group received adrenaline (0.2ug/kg/min) as their second-line vasopressor and the other group received a continuous infusion of terlipressin (1.3ug/kg/hr). This study was interesting because it only lasted for the next 6 hours after the second vasopressor was started. Unfortunately, they really didn’t look at patient related outcomes, but instead their primary endpoints were:

  1. MAP > 65 mmHg
  2. Systemic vascular resistance index > 1300 dynes s/cm5/m2
  3. Cardiac index > 4 L/min/m2
  4. Oxygen delivery index (DO2I) > 550 ml/min/m2

From an Emergency Medicine point-of-view the MAP is probably what we are most familiar with and is an easy enough measure to monitor in the ED.  After initially starting with a statistically equivalent MAP before the start of the second vasopressor, to having a statistically significant difference (p<0.001) after the 6 hours is hard to ignore despite the lack of reported clinical outcomes. This was in addition to showing improved hemodynamic measures and decreased doses of norepinephrine needed in the terlipressin group. This by no means is the do-all and end-all for terlipressin, and doesn’t mean we start throwing it at everything with hypotension when it gets approved in the US. Might as well get familiar with it now though, so when it does show up there are no surprises.

Post by: Terrance McGovern DO, MPH (@drtmcg13)

BOGO on TOAs

Lower abdominal pain in women can be challenging diagnostic dilemma in the Emergency Department. We had a case of a 50-year-old woman that had been previously seen by her PMD 3 days prior and diagnosed with a “small kidney stone” without any imaging, but did get the ever-reliable percocet prescription. Needless to say, she came to the ED because her pain wasn’t getting any better and now she was having increasing lower abdominal pain with high fevers. In the ED she was febrile (T: 104.5) and tachycardic (HR: 120s), but her BP was normal. She ended up having a WBC: 17k/mm3, bands: 20% and a pretty nasty UTI. Her pain persisted and we ended up doing a CT abd/pelvis with contrast to see if she had anything brewing. From the images below you can see that she had bilateral tubo-ovarian abscesses causing bilateral hydronephrosis seen on CT and confirmed with ultrasound. She was started on ampicillin, clindamycin and gentamicin and her abscesses were drained with CT guidance, yielding 400cc of thick, brown, purulent fluid. Yum

Figure 1 Figure 2

Up to one half of all cases of tubo-ovarian abscesses occur in patients with a history of pelvic inflammatory disease (PID). The theoretical etiology of tubo-ovarian abscesses is thought to revolve around an ascending infection arising in the lower reproductive tract, into the uterus and subsequently the fallopian tubes and ovaries. While Neisseria gonorrhea and Chlamydia trachomatis are commonly associated with PID, TOAs are typically polymicrobial and rarely grow either chlamydia or gonorrhea when cultured. As with most pelvic pathology, ultrasound remains the initial diagnostic modality of choice for tubo-ovarian abscesses to best visualize the upper reproductive tract. Ultrasound remains very specific (86-98%), whereas the sensitivity ranges between 56-93%. There is evidence however that computed tomography of the pelvis with contrast may provide better sensitivity than ultrasound in evaluation of TOAs. In the Emergency Department, a triple coverage antibiotic regimen (i.e. ampicillin/clindamycin/gentamicin) should be initiated despite whether the patient is going to need surgical exploration, percutaneous abscess drainage or conservative management. If the patient’s clinical status has either worsened or not improved after 48-72 hours the gynecologist will likely proceed with minimally invasive drainage procedures that have become more readily available, similar to our case.

Post by: Terrance McGovern DO, MPH (@drtmcg13)

Top 10 Infectious Disease Updates

I recently gave an “ID Updates” lecture at AAEM’s Scientific Assembly in Las Vegas, February 2016. Here are the top 10 pearls from my lecture. Some may be review, some more cutting edge. Enjoy!

  1. Use ultrasound to help guide diagnosis and management of suspected skin and soft tissue abscesses

The literature is mixed on this one but it makes sense to use ultrasound. Ultrasound seems to increase your diagnostic sensitivity and may affect management, especially in those “gray zone cases”. If you are feeling ambitious, use ultrasound after I & D to assess the success of your I & D. Plus, it’s pretty easy to do!

Alsaawi, A et al. European Journal of EM. 2016.

 

  1. Although guidelines still recommend solely I & D as the treatment of choice for simple skin and soft tissue abscesses, maybe antibiotics are not so bad!

A recent trial from Talan et al. from NEJM supports the use of antibiotics in skin and soft tissue abscesses. Antibiotics increased clinical cure and decreased complications. The knock on this trial is the included patients would have received antibiotics anyway based on disease severity; nonetheless, antibiotics benefitted patients with little harm.

Talan D et al. New England Journal of Medicine. 2016.

 

  1. First line treatment for suspected sexually transmitted infections (cervicitis, urethritis) is dual therapy Ceftriaxone 250 mg IM and Azithromycin 1 gram po.

Cefixime used to be a first line alternative (instead of Ceftriaxone), however, it is no longer with increasing resistance patterns. Bottom line—give dual therapy! Consider challenging patients who have a PCN allergy with Ceftriaxone. If you’re not going to give dual therapy with Ceftriaxone/Azithromycin, the reason better be good!

www.cdc.gov

 

  1. Newest GI recommendations state that antibiotics probably do not reduce symptom duration for uncomplicated CT proven diverticulitis.

Yes, I said it—no antibiotics for acute uncomplicated diverticulitis! Certainly, we would like to see more literature in this area, but the literature we do have show antibiotics do not improve symptoms. Antibiotics may however decrease complications, as per the guidelines. I’d like to see more here, but check out the references and see for yourself.

Strate L et al. Gastroenterology. 2015.

 

  1. Non-operative management of appendicitis is an option.

We’re not here yet in the U.S. but they are in Europe. In the newest Lancet study, 73% of patients who received non-operative management did not require an appendectomy out to one year. Those that failed non-operative management did not have complications of sepsis, abscess, or rupture compared to the operative group. The theory for non-operative management is not all appendicitis is an obstructive process that requires removal; some may respond to medical therapy.

Salminen P et al. JAMA. 2015.

 

  1. Timing of antibiotics does not reduce mortality from severe sepsis/septic shock.

CMS dictates we administer antibiotics within 3 hours of diagnosing severe sepsis/septic shock in the ED. It’s a core measure we need to meet. But it does not reduce mortality per a recent systematic review from Critical Care. Timing of antibiotics may be important, but antibiotic selection is probably more important.

Sterling S et al. Critical Care Medicine. 2015.

 

  1. Irrigation pressures do not matter in the management of open fractures.

In the OR, whether patients with open fractures get very low pressure, low pressure, or high pressure irrigation, re-op rates are the same!

The Flow Investigators. New England Journal of Medicine. 2015.

 

  1. Consider use of corticosteroids in inpatients with pneumonia.

Adjunctive prednisone in pneumonia reduced inpatient stay.

Angela Blum C et al. Lancet. 2015.

 

  1. It is thought that Strep sp. are the predominant organisms in cellulitis. But maybe not!

If Bactrim works as well as Clinda, Strep may not be the king organism in undifferentiated skin and soft tissue infections. Check out the reference.

Miller L et al. New England Journal of Medicine. 2015.

 

  1. Respect lactate!

We know lactate is not specific. But in the setting of infection or suspected sepsis, respect it if it is positive, even if in the intermediate range. Intermediate level lactates had a 30 day mortality of 15%.

Singh M et al. Annals of EM. In Press.

Post by: Nilesh Patel, DO (@nnpatel1291

Stressed vs unstressed volume

Dr. Rory Spiegel, from EMNerd, wrote a recent piece in Clinical and Experimental Emergency Medicine about how our undying love for left ventricular function in shock patients is perhaps overdoing it and the focus should rather be on the venous return. In the 1950’s Guyton et al described the three factors that affect venous return: 1. Right atrial pressure 2. Mean systemic pressure (Pms) 3. Vascular resistance.

The Pms is something that we don’t refer to often in critical care, but as Spiegel argues, should receive more respect than it does. In simple terms, Pms provides the pressure needed to produce a gradient from the venous return into the right atrium for forward flow. Spiegel provides a great analogy using a bathtub and bucket model to explain the physiology, but I’m going to attempt another analogy using a water balloon.

The Pms is composed of the blood within the venous system and the pressure exerted by the vascular bed. In the water balloon analogy, the water within the balloon is the venous blood volume and the physical balloon is the vascular bed. You can imagine, there is a certain amount of water that a water balloon can hold before the balloon starts to expand and enlarge, this is the unstressed volume. As you fill the balloon it grows and the pressure exerted by the walls of the balloon increases, this is called the stressed volume. The stressed volume produces increased Pms and subsequently increases venous return to the right atrium. Now, think of a septic shock patient as an old, ratty balloon that has been inflated too many times and has lost of lot of its elasticity. The amount of water needed in these septic balloons to get to a stressed volume is much more than a normal, healthy, brand-new balloon. Hence why we start with multiple liters of fluid resuscitation in septic shock patients, to try to get them to a stressed volume and improve the venous return. When this doesn’t work, we move onto vasopressors to clamp down on the vascular bed (squeeze the balloon) as another means of increasing Pms and venous return.

With summer around the corner, it’s going to be hard to ignore the similarities between helping your kid prepare for their next water balloon battle and dumping 30cc/kg of fluid into that old ratty, septic water balloon. Check out Spiegel’s piece in Clinical and Experimental Emergency Medicine for great review of mean systemic pressure and its relation to stressed and unstressed volume here.

Post by: Terrance McGovern DO, MPH (@drtmcg13)