Category Archives: Grand Rounds

Active Shooter

sources from Dr. Marc Kanter’s All NYC EM Conference lecture, enjoy:

** EM:RAP 12/2013 segment with Ilene Claudius interviewing Active Shooter expert Mike Clumpner **

 
1) Active Shooter Planning and Response in a Healthcare Setting

2) NYPD Active Shooter Recommendations and Analysis for Risk Mitigation

3) Hospital-Based Shootings in the US: 2000-2011 Kelen GD, Catlett CL, Kubit JG, Hsieh YH. Ann Emerg Med. 2012 Dec;60(6):790-798.e1. doi

4) Violence in the Health Care Setting – JAMA Commentary December 8, 2019 Vol 304

5) Dept of Homeland Security First Responder Guide for Improving Survivability in Improvised Explosive Device and/or Active Shooter incidents

6) Hartford Consensus Compendium – American College of Surgeons

7) Dept of Homeland Security Letter – Active Shooter and Complex Attack Resources

8) Tactical Emergency Combat Care Guidelines

9) FBI/Dept of Justice – A study of active shooter incidents in the US between 2000-2013

10) The San Bernardino, California, Terror Attack: Two Emergency Departments’ Respons Lee C., Walters E, et al. Western Journal of Emergency Medicine January 2016

11) Handbook Tactical Combat Casualty Care Lessons Learned No. 13-21

 

 

Under Pressure

It’s important to keep a high index of suspicion when worrying about Compartment Syndrome; keep the 6 P’s in mind. It’s also important to know how to assemble and use a compartment measurement kit if you’re searching for hard, objective data.

Stryker Setup

1.) contents of the pressure measurement kit
2.) remove contents from wrapping
3.) attach chamber to the pre-filled saline syringe
4.) place the aforementioned into the monitor/unit
5.) place needle onto chamber
6.) eject excess air, if present, from syringe
7.) zero the assembled unit at the angle you will be entering compartment
8.) insert, inject 2-3 drops of saline, and await measurement

When interpreting a compartment’s pressure, there’s the old way, and the new way:

OLD:
Normal Compartment Pressure <10 mmHg
Up to 20 mmHG = No Problem
30-50 mmHG = PROBLEM

NEW:
Delta Pressure = [Diastolic Pressure] – [Compartment Pressure]
Delta Pressure < 30 mmHg : BAD

the CBC – perhaps a bastion for the intellectually astute?

If a patient’s CD4 count is unknown, the Absolute Lymphocyte Count (ALC) can act as a temporary surrogate.

ALC= WBC x % of Lymphocytes.

Here’s a quick review of the literature:

 

One of the more highly quoted studies states a CD4 count of <200 × 10(6) cells/μL is very likely if the ED ALC is <950 × 10(6) cells/μL and less likely if the ALC is >1,700 × 10(6) cells/μL, Napoli et al (2011).

Two studies performed in non-ED setting showed a good correlation between the CD4 count and ALC. There is some question as to whether these results are applicable or generalizable to the ED population, since all of the participants were tested during routine examinations, not while they were acutely ill, Blatt et al (1993) and Fournier AM et al (1993).

Another study, from Temple University, looked at 800+ samples of CBC + CD4 on HIV+ pt’s (ED & non-ED), Shapiro NI et al (1998).

While a single ALC threshold was neither sensitive nor specific for a low CD4 count, the investigators determined two valuable cut-offs of 1000 and 2000 cells/mm3.

– An ALC less than 1000 cells/mm3 was 91% predictive in identifying patients with CD4 counts less than 200 cells/mm3 (sensitivity only 67%, but specificity 96%).
– An ALC greater than 2000 cells/mm3 was 95% predictive in identifying CD4 counts greater than 200 cells/mm3.
The authors concluded that patients with ALCs greater than 2000 cells/mm3 might be less susceptible to opportunistic infections, while those with ALCs less than 1000 cells/mm3 are at higher risk. These researchers had no access to clinical data and couldn’t account for factors such as antiretroviral therapy or the presence of acute infection such as sepsis, pneumonia, or TB.

There are of course other studies which show the ALC isn’t great
Pirzada et al (2006), and others where it is decent.

These analyses of the ALC could proof useful in many resource poor areas of the world with rising rates of HIV/AIDS as shown by these studies in India and Africa, for example.

ill & expectant

Some brief highlights from Dr. Haney Mallemat’s lecture titled “Pregnant & Sick: Management of the Critically Ill & Expectant” at the All NYC EM conference this past week.

Optimize Perfusion & Diffusion when treating the critically-ill pregnant patient.

If you treat mom, you’ll treat baby; just remember what you were TOLD:
Tilt (alleviates IVC compression, subsequently increasing venous return by 30%)
Oxygen (use Nasal Cannula, Non-Rebreathers, High Flow Humidified O2. BiPAP is bad – pregnant women have lower esophageal sphincter tone amongst other changes, which increases their aspiration risk.)
Lines (Obtain IV access above diaphragm. Avoid femoral veins, as the placenta is compressing them.)
Dates (24 weeks is the trigger for whether or not to perform a Perimortem C-Section)

Some more on Perfusion Physiology:
-25% goes of the circulating volumes goes to the placenta.
-During cardiac arrest, displacement of the uterus alleviate IVC compression (see Tilt). However, in this circumstance tilting the patient may impede effective CPR. Instead have an assistant manually displace the uterus while leaving the patient in the supine position.
-Perimortem C-sxn can increase the mother’s cardiac output by up to 80%.

And speaking of perimortem C-sxn…
EMCrit’s 2013 Conference’s Blast competition winner, Dr. Salil Bhandari, succinctly described 3 critical point to remember: 24, 4, Scissors.

24 weeks (increased chances of survival for mom and baby)
4 minutes (4 minutes of CPR… or 2 rounds)
Scissors (to make the midline cut)

EMCrit on PeriMortem C-Section – http://vimeo.com/59516684
ACLS on the pregnant patient – http://circ.ahajournals.org/content/122/18_suppl_3/S829.full#sec-35

And on Diffusion Physiology:
The growing placenta pushes upward into the diaphragm, decreasing the FRC (hurts apnea time while intubating)

Crash Course in Advanced EKG

image

Dr. Amal Mattu gave a fantastic lecture on advanced EKG interpretation at the AAEM Conference in NYC today. For those who were unable to attend, here are some highlights:

1.) Sgarbossa Criteria helps diagnose an acute MI in the setting of an LBBB. Concordance bad. Discordance good (but TOO much discordance is bad too).
Elegantly shown from EMS12lead.com – http://tinyurl.com/ndw285

2.) Wellens Syndrome describes T wave changes indicating a proximal LAD lesions.
Type 1 are deep, symmetric TWI which hit you square in the face and Type 2 are subtle, biphasic changes.
Nicely displayed here: http://pages.mrotte.com/wellens/five.png

3.) Posterior MIs present as ST depressions in V1-V3 with tall R waves (N.B., the R waves are actually evolving Q Waves)
Get a posterior lead EKG to look for ST Elevations (Leads V7-V9: http://lifeinthefastlane.com/wp-content/uploads/2011/09/posterior-leads.gif)

4.) aVR: unloved, forgotten. Elevations here can be indicative of LMCA, proximal LAD occlusions. Bad, bad, bad.

5.) STEMI vs Pericarditis? Keep this in mind:
a.) ST Elevations with reciprocal ST Depressions anywhere (except aVr or V1) = STEMI
b.) ST Elevation greater in III than II = STEMI
c.) Morphology of ST Segment is either convex or flat = STEMI

6.) BER

7.) aVL changes can present as early reciprocal changes of impending doom. A TWI in this lead alone might evolve into an inferior wall STEMI.

8.) Hyperacute T Wave – not just tall, pointy, and would hurt to sit on… but also can present subtlety… of normal height… with a straight initial up-sloping of a T wave.

Mini-Conference: Anorectal Abcesses

presented by Dr. Ken Adams

For the ED physician, one of our primary concerns if whether this is something that we can handle or does it require surgical management. We should feel comfortable managing perirectal abscesses but the collections in other anorectal areas such as the intersphincteric, ischiorectal and supralevator spaces require surgical management.

The most feared complication is fistula formation which can form in anywhere between 30 – 60% of anorectal abscesses. If you are going to perform an I&D of an anorectal abscess in the ED, taking a culture is of utmost importance. If the culture is growing common GI flora (Bacteroides, E. coli, Enterobacterstaph) you should be suspicious for an underlying fistula while you can feel more comfortable if your culture comes back with staph or strep as this is likely your run of the mill abscess. Incision and drainage is the definitive treatment but you should consider antibiotics if they patient displays systemic symptoms, is a diabetic or is immunosuppressed.

Acute Pulmonary Edema (Summary)

Presented by Dr. Anand Swaminathan, NYU/Bellevue.

A 65 yo M pt with PMH of ESRD, HTN, CAD comes in c/o SOB x3 days after missing hemodialysis twice in the past week. A portable CXR is ordered, and it looks similar to this:
http://radiopaedia.org/cases/apo-arrowsjpg

Acute Pulmonary Edema.
Causes: MI, PE, dysrhythmia, infection, tox, therapy non-compliance

Managment:
– firstly, supportive – ABCs, IV, o2, monitor
– Airway? less and less patients need to be intubated

The pathophysiology helps us better understand/affects our management:
– LV can’t pump blood out as fast, resulting in blood backing up.
– fluids fills the alveoli, washes out surfactant
– results in sympathetic surge.
– RAAS is activated, leading to vasconstriction and water reabsorption
– ADH released, increasing the circulating volume

Treatment Options:
1.) Nitro
Effect of sublingual nitroglycerin in emergency treatment of severe pulmonary edema, Bussmann et al.
(http://www.ncbi.nlm.nih.gov/pubmed/417614)
– decreased in LV filling pressure, decrease in cardiac output
– nitrates are good for preload (and afterload) reduction

2.) Morphine
Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis, Peacock et al.
(http://www.ncbi.nlm.nih.gov/pubmed/18356349)
– increased risk of ICU admissions, mechanical ventilation, and mortality
– (study not randomized, and more correlational than causal)

3.) Loop Diuretics
Comparison of nitroglycerin, morphine and furosemide in treatment of presumed pre-hospital pulmonary edema, Hoffman et al.
(http://www.ncbi.nlm.nih.gov/pubmed/3115687)
– pts who got morphine and furosemide did worse
– a lot of pts DON’T have fluid overload
– lots DON’T have functioning kidneys
– splanchinic circulation is clamped, so lasix won’t reach the kidney

4.) ACE Inhibitors
Rapid improvement of acute pulmonary edema with sublingual captopril, Hamilton et al.
(http://www.ncbi.nlm.nih.gov/pubmed/8673775)
– sublingual administration of captopril vs NG
– decreases afterload

5.) BiPAP
Randomized Trial of Bilevel versus Continuous Positive Airway Pressure for Acute Pulmonary Edema, Liesching et al.
(http://www.ncbi.nlm.nih.gov/pubmed/24071031)
although mechanism has not been proven:
-surfactant thought to be washed out of alveoli
– PEEP keeps alveoli open
– reduces afterload (especially versus CPAP)

**Takeaway point**
Initial APE Tx = Nitro + BiPAP

Shattering Urban Legends in Emergency Medicine.

Presented by Dr. Anand Swaminathan, NYU/Bellevue.

MEGACASE: 75 yo F with history of ESRD on HD presents to your E.D. after a looooong bus ride with unilateral leg swelling, shortness of breath, hemoptysis, and a recent history of hip surgery. Your thorough history further reveals that the patient has asthma, a severe shellfish allergy, and has had contrast reactions in the past. To make matters worse, the patient is writhing in pain on the stretcher complaining of right flank pain radiating to the groin and a history of renal calculus last year. And for some reason, this patient is still finding the time to tell you she has a “sore throat,” with fever, cough, tonsillar exudate and cervical lymphadenopathy. Oh yeah, and her throat snaps shut like a bear-trap if she has penicillin.

You just finished prepping the exam room, when…

image

1.) Do patients with ESRD need emergent dialysis after receiving IV contrast?

NO

There may be a slightly increased risk of pulmonary edema with iodinated contrast secondary to higher molecular weights, but most hospitals use non-iodinated contrast now. Patients may continue their current dialysis schedule so long as they are dialysed within 24-72 hrs post-contrast administration, regardless of anuric/oliguric status. Check out wha t the American College of Radiology says:
“… Unless an unusually large volume of contrast medium is administered or there is substantial underlying cardiac dysfunction, there is no need for urgent dialysis after intravascular iodinated contrast medium administration.” ACR, version 9, pg 26. (http://www.acr.org/quality-safety/resources/contrast-manual)

2.) Is pretreatment necessary/effective in preventing adverse reactions to IV contrast?

NAH

“The efficacy of corticosteroid and/or antihistamine prophylaxis is unknown, though some have suggested this practice. However, given the likely differing mechanisms between acute and delayed reactions, as well as the extreme rarity or nonexistence of severe delayed reactions, premedication prior to future contrast-enhanced studies is not specifically advocated in patients with solely a prior history of mild delayed cutaneous reaction.” ACR, version 9, page 40. (http://www.acr.org/quality-safety/resources/contrast-manual)

3.) Ok, ok, how about flomax for renal stones? Everybody’s doing it.

Take it or leave it.

Most studies are equivocal showing no benefit. However, one recommendation that pervades the literature is that if you are going to use it, save it for distal stones. (http://www.ncbi.nlm.nih.gov/pubmed/21149761)

4.) I’ve heard pen allergic patient’s should never, ever get cephalosporins because the rate of cross-reactivity is 10%. This has to be true.

Listen, pal…

Well, when penicillins and cephalosporins were first produced, the were often made in the same factories – this 10% figure is more likely related to cross-contamination during the production process, not cross-reactivity. The actual rate is closer to 1-3%. There may be higher rates with 1st or 2nd generation cephalosporins, but 3rd generation or higher seem to be fine. Furthermore, the proportion of patients claiming to have a PCN allergy, that actually have a true PCN allergy, is 3%. Overall, the rate of anaphylaxis to cephalosporin in patient’s with a history of anaphylaxis to PCN in 0.001%.

Remember the rule of 3’s: 3% actually have it, 3% will have a reaction and 3rd gen cephalosporin or higher is best. (http://www.ncbi.nlm.nih.gov/pubmed/21742459)

Brian Hayes of UM puts it best on ALiEM:
http://academiclifeinem.com/busting-the-myth-the-10-cephalosporin-penicillin-cross-reactivity-risk/

5.) I know antibiotics can’t prevent PSGN. I get it, I know. But what about for Acute Rheumatic Fever (ARF)?

This one’s gotta be right.
As it turns out: not really. The rate of ARF is so low in industrialized nations, that the CDC does not track incidence of the disease any more. (In aboriginal populations, older thinking still holds strong; ARF remains problematic and necessitates antibiotic therapy). The risk of sequela from the disease is significantly and statistically low, and it is a self-limiting process. A Cochrane review demonstrated “resolution and improvement of pain in participants with sore throat” when comparing the efficacies of steroids and antibiotics. (http://www.ncbi.nlm.nih.gov/m/pubmed/23076943/)