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



Pelvic Fractures… a real page turner

by Jonathan Lee, MD


Pelvic structures are held together by the strong ligamentous connections surrounding it; this is disrupted in pelvic fractures. Keep in mind that the internal iliac vessels and the lumbosacral plexus are intimately associated with posterior pelvic ligaments.

MORTALITY RATE 15-25% for closed fractures, as much as 50% for open fractures… most commonly caused by hemorrhage. The pelvis can hold up to 3-4 liters of blood (nearly HALF your body’s blood volume!)



Inspection for ECCHYMOSIS; it can point you towards a bleeding pelvic fracture:

  • Periumbilical (Cullens Sign)
  • Flanks (Grey Turner Sign)
  • Iguinum / Perineum / Scrotum / Upper Thigh (Destot Sign)

Check for GROSS HEMATURIA – 21% of males and 8% of females.

Check the vagina and rectum to rule out OCCULT OPEN FRACTURES … if so: abx are imperative.

Apply gentle rotational force on each iliac crest


low sensitivity for detecting instability Get a bedside pelvic x-ray



RESUSCITATION – CABDE (worry about those catastrophic bleeds).

Consider massive transfusion!

PRBC:FFP:Platelets ideally should be transfused 1:1:1



The purpose of a pelvic binder is to CONTROL BLEEDING. It should be centered over the GREATER TROCHANTERS. Do not place over iliac crest/abdomen. Augment with internal rotation of lower extremities and taping at ankles/knees.



The most commonly used system is the young-burgess system that organizes fractures by direction of the impact force:

  • Anterior-Posterior compression
  • Lateral compression
  • Vertical Sheering


So when you check your pelvis x-ray, quickly MEASURE to see if there is >2.5cm displacement of the symphysis pubis and >1cm displacement between he sacroiliac joints! This may not only point you towards disposition (surgery vs. conservative management) but also indicates to what degree of bleeding to expect. More displacement = More sheering of vessels.

Keep in mind that 80-90% of pelvic fracture bleeds are venous. Yes, they may be brisk bleeds that present to your trauma room hypotensive, but they can also be slow bleeds. So if your patient stays in your ER longer than intended, make sure you get serial H/H’s.


by Jonathan Lee, MD


Total five species (Zaire to have the highest mortality – named after the country in which it was first discovered)

Category A Bioterrorism Agent – Agents with High transmission/dissemination and high mortality – along with Small Pox and the Bubonic Plague.

Discovered in Zaire (or current day Democratic Republic of Congo) in 1976. Named after a tributary that branches off of the Congo River that was near the site of initial outbreak.

Since 1976, there have been 14 outbreaks of Ebola Virus (including current). All have been in either in Zaire/DRC, Gabon, or Sudan.


Unclear however likely secondary to animal vector. Original host thought to be bats as they have frequently been isolated to carry the virus without actually being affected. Likely bat drops a piece of partially eaten fruit, drops it on the ground, which then other animals consume humans hunt for bushmeat…


Body fluid contact with either open skin or contact with any mucosa. Can be carried in serum, tears, urine, saliva, semen, vaginal fluids. Thought to last in sperm even post infection. Infections go up once patients get admitted to hospitals secondary to close contact. Proper personal protective equipment and hygiene is paramount to preventing spread.


Virus can invade any cell in the body however preferentially attacks three:

  • Neutrophil CD16B – Suppresses your immune system initially.
  • Endothelium – Leading to hemorrhage. Inflammation can also trigger DIC.
  • Hepatocytes – Suppresses release of cytokines. Hepatic failure furthering coagulopathy.

Keep in mind there is an incubation period ranging from 2-21 days.


Symptoms/Patient Presentation

High fever >101.5, malaise, asthenia (weakness), myalgias, nausea/vomiting, diarrhea, loss of appetite, joint pains, melena, rectal bleeding, vaginal bleeding, bleeding from gums, conjunctival hemorrhage.

Further down the road Internal/external hemorrhage, rashes including hemorrhagic vesicles/bullae, petechiae, maculopapular rash


  • CBC – WBC may not be elevated at all
  • Pt/Ptt normal
  • LFTs – with worsening hepatic failure
  • Diagnostic testing: ELISA & PCR


Serum/Plasma/ or Whole blood minimum of 4ml shipped refrigerated or frozen on ice pack/dry ice (no glass tubes) as a Category B diagnostic specimen to the CDC.



(1) Percutaneous OR mucous membrane exposure or direct skin contact with body fluids or a person with a confirmed or suspected case of EVD without appropriate personal protective equipment.

(2) Laboratory processing of body fluids of suspected or confirmed EVD cases without appropriate PPE or standard biosafety precautions. Thromobcytopenia can develop over time.

(3) Participation in funeral or other direct exposure to human remains in the geographic area where the outbreak is occurring without appropriate PPE.


(1) Spent time in facility where EVD patients are being treated (people not directly involved in patient care, or if involved in patient care used PPE).

(2) Household members of an EVD patient without high risk exposure.

(3) Persons who had direct unprotected contact with bats or primates from EVD affected countries.

Consultation with local and state health departments is recommended. Stay safe, and have a high index of suspicion.

A.I. – Aye Yai Yai

by Elizabeth Perry, MD


35 yo F presents to your Resus Room. She’s hypotensive, and not really responding to fluids, and have tried almost all of your pressors. You find out from her accompanying family members that she’s an asthmatic, steroid dependent, and hasn’t been able to make her insurance payments on time as of recent.

What’s going on? (hint: adrenal insufficiency)

A brief reminder of the adrenal gland:
Synthesizes steroid hormones (glucocorticoids – cortisol, mineralocorticoid – aldosterone, gonadocorticoids – testosterone, estrogen) in the cortex and catecholamines (epinephrine, norepinephrine, dopamine) in the cortex.

Primary Adrenal Gland Insufficiency = Addison’s
-destruction of > 90% of adrenal glands
-Results in decreased cortisol and aldosterone production
-causes: autoimmune destruction, hemorrhage (from use of warfarin,sepsis, trauma), tumor (breast and melanoma), infection (HIV, Tb, meningococcemia) or inflammatory process.
-In US 70% of primary AI is due to autoimmune disorders. Can be isolated or associated with polyglanduar autoimmune syndrome (PGA) type I or II.
About 20% of HIV patients eventually develop adrenal insufficiency, most common infectious cause in US. Worldwide most common infectious cause is TB.

Secondary Adrenal Gland Insufficiency
-insufficient production of ACTH. Occurs following disorders in the hypothalamic–pituitary axis, when CRF and/or ACTH fails to be secreted.
most common cause is suppression of HPA axis over time due to long term therapy with pharmacologic doses of glucocorticoids.
-other causes: destruction or dysfunction of the pituitary (pituitary disease, head trauma, postpartum pituitary necrosis- Sheehan Syndrome)
-mineralocorticoid (aldosterone) function intact, loss of glucocorticoid (cortisol) activity

Tertiary Adrenal Gland Insufficiency
-hypothalamic disease and suppression of CRH

The life–threatening exacerbation of adrenal insufficiency due to increased physiologic demand (infection) or decreased supply (discontinuation of steroid therapy) of cortisol. Usually occurs in response to major stress: MI, sepsis, surgery, major injury, trauma.

GI: abdominal pain, vomiting and diarrhea
CVS: dehydration, hypotension, refractory shock, poor response to inotropes/pressors

fluid resuscitation (recommendation is D5NS for both hyponatremia and hypoglycemia)
-reversal of electrolyte abnormalities
high dose hydrocortisone (100mg IV Q6 hrly): provides both glucocorticoid and mineralocorticoid effects
-IV Dexamethasone 4mg may be given if the rapid ACTH stimulation test will be part of diagnostic workup
vasopressors in patients unresponsive to fluid resuscitation (norepinephrine, dopamine, phenylephrine preferred)

Danger Zone: Signout

by Stephen Strasberg, MD

Handoff = Signout = Dangerous

It is well known that patient handoffs are a dangerous time for patients.  Information is exchanged and whenever this happens, inevitably something gets lost in the mix.

What can you do to help your patients?  Have a system.  Any system really, but just having a system in place to signout or handoff patients in a systematic way will reduce medical errors and keep your patients safer.  There are numerous systems out there.  JCAHO and WHO use SBAR.  Our friends and UNM (University New Mexico) use PLAN ED.  Here is their policy.

  • “Run the List” (go over next steps for all patients so that a clear plan is presented at handoff) within the hour leading up to the shift change with the attending.
  • Reevaluate high-risk patients (patients who have already been handed off once and/or who do not have a clear diagnosis or disposition plan) within the hour leading up to handoff.
  • Write down key lab values for acutely ill and complicated patients within thirty minutes of handoff. Time permitting, radiology findings and current vital signs should also be included.


Handoff Presentation

All providers should use the same structured format for handoff presentations in order to facilitate the consistency and completeness of communication among providers and nursing staff.


Patient (age, sex, name, room number and chief complaint)
Label with working diagnosis or differential diagnosis
Assessment (key elements of history, physical exam, labs, diagnostic imaging)
Next steps and nursing assessment (pending labs, diagnostic imaging, consultants)
Everything else (social issues, handed off before, systems issues)


General Handoff Guidelines:

  • Plan to spend 1 to 3 minutes on each patient, depending on complexity
  • Spend approximately 5 minutes on clinical teaching
  • Be on time and prepare for handoff early so that handoffs can start when scheduled
  • Organize handoffs by doing selected “bedside waking rounds”


Proven Techniques for Effective Handoffs

  • Incorporate the use of written notes and/or electronic medical records (EMR) in handoff (has been proven to reduce physical exam and lab result memory errors, especially for patients who have been in the ED for prolonged periods of time)
  • “Repeat back”: accepting provider repeats plan of care to outgoing provider to create closed-loop verification of critical information
  • Engage in interactive questioning
  • Reduce interruptions
  • Reduce signal-to-noise ratio (background noise)


Other General Recommendations

  • Officially admitted patients (have bed request and orders) should have a very brief handoff by the outgoing resident to the accepting attending; if the patient had admitting orders at the time of the previous handoff the outgoing attending provides the handoff to the accepting attending.
  • Within 15 minutes of the end of handoff, the accepting resident should assign himself or herself as the resident provider in the FirstNet tracking system.
  • Within the first 2 hours of the shift, patients that were handed off should have had their chart, laboratory and other findings reviewed and the resident should have physically introduced himself or herself.
  • Handoff communication guidelines (based on Grice’s Maxims)
  1. Include only relevant information.
  2. Be brief.
  3. Be orderly by using the PLAN ED framework.
  4. Be honest. If someone asks a question that you are not 100% sure about (i.e. lab value or result of a scan), find out the answer after the handoff and follow up with the most accurate answer.

Tick Tock Torsion: Time is Tissue

by Michael Daignault, MD

Approximately 0.5% of all patient visits to the Emergency Departent (ED) are acute scrotal pain. The differential is long, and includes epidiymitis, orchitis, testicular torsion, torsion of the testicular appendage, testicular trauma, and herniation of abdominal contents into scrotum. In the ED, we are most concerned with testicular torsion, testicular trauma, and herniation. As they say in CVA, time is brain. In this case, TIME IS TESTICLE. This article focuses on evaluation of acute scrotal pain for torsion, as well as the application of bedside ultrasound to evaluate for testicular torsion.

Torsion occurs when the spermatic cord twists around its axis, cutting off vascular flow to the testicle and surrounding structures in the scrotum. Bedside testicular ultrasound can be a very useful adjunct to the history and physical exam in evaluating a patient for torsion. First, IV access should be obtained for laboratory analysis and most importantly to provide analgesia. A urinalysis should also be obtained if possible. Once analgesia is achieved, the patient should be in the supine position with legs spread apart. Ideally the scrotum should be supported with a sling fashioned from a towel and the penis should be covered with a towel that is taped to the abdominal wall (or the patient can be asked to support his penis in a cephalad position). A high-frequency linear ultrasound probe is then applied perpendicular to the penile shaft to obtain transverse view of the scrotum.

In this “saddle view,” both testicles can be viewed in the same window, as in the following picture:

The definitive treatment for torsion is surgery, so in the ED, we are concerned solely with identifying patients who are immediate candidates to go to the OR. As such, on bedside ultrasound, we want to identify patients with a testicle that has decreased or absent blood flow. Change the settings on your ultrasound machine to “doppler” or “color doppler” and first slide the probe while staying in transverse view to the unaffected testicle. You should see multiple pulsations in both red and blue color throughout the testicle signifying vascular flow. It doesn’t matter whether you have more red or more blue. The key is to have a baseline of “normal” vascular flow in your patient so as to compare to the affected testicle.

Next, gently slide the probe (again while staying in transverse view) to the testicle in question. You are looking for a demonstrable reduction or absence in vascular flow compared to the unaffected testicle. In the following image, there is clearly a reduced flow to the right testicle in this patient compared to the left.



Again, bedside ultrasound for testicular torsion should be used as an adjunct to the physical exam and a good history taking. Absence of cremaster reflex remains the most sensitive sign (90-100%) in diagnosing torsion. Complete ultrasound evaluation of the acute scrotum is obviously much more comprehensive than what I have outlined above, but is beyond the scope of both this article and the purview of the emergency physician. However, visualized absence of vascular flow on bedside ultrasound should prompt immediate urology consult and preparation for the OR.


For more info on scrotal ultrasound:

Images from:

Bradycardia Recap

by John Marshall, MD

– Bradycardia (HR <60) can be caused by SA & AV nodal disease

In patients with symptoms of instability (chest pain, AMS, hypotension)… remember: ABC’s, IV, O2, monitor.

  • 1st.) Atropine 0.5mg q3-5 min, for a maximum of 3mg (can cause paradoxical bradycardia)
  • 2nd.) TransCutaneous pacing, or… Pressors (Epinephrine & Dopamine: Beta 1 activity increases AV node flow and SA conductivity)
  • 3rd.) TransVenous pacing + expert consultation

Mobitz type 2 or greater are dispo’ed to CCU (AV blocks may deteriorate into complete block).

Only people to send home are people without comorbidity and received no urgent intervention



  • – identifying a block, but missing inferior MI
  • not having pacer pads ready while giving atropine
  • – sending someone home that appears better
  • atropine may worsen ischemia in someone with ischemic disease
  • – atropine may not work in infra-nodal blocks

The Challenging AIrway

by Jason Greenman, MD

I recently returned from the Levitan (@airwaycam) Yellowstone Advanced Airway Course (#YAAC) last week. It was an awesome experience to get out to the mountains and do some didactic and hands on airway learning. To start with, the view of the Grand Tetons from the course venue was awesome. Would definitely recommend a trip to Wyoming.

photo 1

Here are a few high yield pearls from the course

Have the mind of a warrior when approaching the airway. Be positive and have a clear plan. Call it the challenging airway, not the difficulty airway. Call it the time dependent airway, not the crash airway. Call it the surgically inevitable airway, not the failed airway.

Preoxygenation is key. Get your patient into a position that will maximize preoxygenation. Try the ear to sternal notch position. Use the jaw thrust maneuver to open the airway (NOT the chin lift). Consider putting your patient into reverse trendelenburg to increase FRC.

Focus on the nose. “Blow some O’s up the nose during preoxygenation. Use the expression NODESAT (nasal oxygenation during efforts securing a tube). Studies show that high flow passive nasal oxygenation significantly increases the time before desaturation in the apneic patient.

If you don’t already know, cricoid pressure is OUT! Don’t do it! All the literature shows there are still real risks of aspiration, while causing possible airway obstruction and difficulty in passing the ET tube. Instead, use bimanual laryngoscopy to improve your view, which is external laryngeal manipulation by the laryngoscopist.

Keys to first pass success. Hold the scope low and make it an extension of your forearm. Make intubation a stepwise process. First find the uvula, then keep calm and do epiglottoscopy, followed by laryngoscopy, and then tube delivery. To maximize tube delivery, keep your stylette in a straight to cuff shape with a 35 degree curve. This allows for a narrower long axis dimension and better maneuverability. After passing the cords, consider turning the tube clockwise (to the right) to prevent catching the tracheal rings.

Consider nasal intubation if oral intubation is impossible, or laryngoscopy will be difficult secondary to oral pathology, and if the patient is breathing well and not hypoxic. Use sedation (ketamine is best!), topicalize with lidocaine 4% and afrin. Bevel towards the septum. If blind, listen for breath sounds, or the preferred method is to use fiberoptics if its available. Pass the tube through the cord on inspiration. Depth of insertion to 26-28cm.

photo 3

The hardest part about doing a surgical airway is deciding to do the surgical airway. When your heart starts racing you lose fine motor skills, so instead feel the framework of the airway, move side to side, top to bottom to find your landmark. Do the “Laryngeal Handshake” with the nondominant hand, feel the rhomboid: hyoid, then thyroid, then cricoid. Rest your dominant cutting hand on the sternum for stabilization. During the procedure use good economy of movement, don’t waste effort with extra hand movements. Make your incision vertically through the skin, than horizontally through the cricoid, don’t worry you’ll be cutting into the cartilaginous cage.

photo 2

After an unsuccessful intubation attempt, don’t get stuck on stupid, don’t fixate , try something newMove down your intubation algorithm quickly and confidently.

For more information, check out the course website at or Dr. Levitan’s website at

Managing the Bleeding Tracheostomy

by John Marshall, MD

Early Bleeding: soon after tracheostomy insertion. Think issues with hemostasis. Usually benign, i.e. from manipulation, bleeding from nearby site.

Late bleeding: months after placement.  Possibly a life threatening emergency. Sentinel bleed from innominate artery. Other causes: infection, granulation tissue.



ABC’s. Attention to clearing airway, suctioning.

Call for help: senior resident/surgery/ENT/ (institution dependent)

Examine tracheostomy site: cuffed vs uncuffed (differentiated by the presence of a pilot balloon port in cuffed, just like endotracheal tubes)


If large bleed attempt to control bleed:

Inflating cuff SLOWLY (up to 10-35 cc air)

– If bleeding continues, apply pressure at sternal notch or attempt intubation with OTT, ensuring cuff is distal to stoma opening.

– Addition of blood products if needed.

– All cases to OR for urgent surgical repair.



Shaukat, Iqbal, Akhtar, Tracheo-innominate fistula formation; a rare complication of tracheostomy, 2013.

Emergency Medicine in the South Bronx