August 2017 | Volume 17 Issue 8
Editor-in-Chief: Mel Herbert, MD
Executive Editor: Stuart Swadron, MD
Associate Editor: Marlowe Majoewsky, MD
Introduction:
A Red Hot Arm
Rob Orman MD and Anand Swaminathan MD
Take Home Points
Vancomycin, piperacillin-tazobactam and clindamycin are
a reasonable combination of antibiotics in suspected nec-
rotizing fasciitis.
A small incision with a scalpel into suspected necrotizing
fasciitis can assist in diagnosis.
Patients with septic superficial thrombophlebitis have
cellulitis spreading from the vein.
The literature supporting anticoagulation in septic super-
ficial thrombophlebitis is inconclusive.
CASE
A patient had used intravenous drugs and presented with fevers
and tachycardia. The arm was swollen, red and hot. It appeared
consistent with a deep space infection. The patient was started
on a combination of vancomycin, piperacillin-tazobactam and
clindamycin due to the possibility of necrotizing fasciitis.
Antibiotic selection. The patient needs vancomycin to cover for
MRSA, strep and skin flora. Piperacillin-tazobactam will provide
broad spectrum coverage. These patients are at risk of pseudo-
monas. This also covers anaerobes. Although clindamycin cov-
ers anaerobes as well, it may play an additional role in binding
toxins in necrotizing fasciitis.
Although it was an apparent soft tissue infection, it wasn’t ob-
viously necrotizing fasciitis. Orman ordered a CT. This showed
clot in the superficial veins with surrounding cellulitis. The diag-
nosis? Septic superficial thrombophlebitis.
Surgery was consulted and took the patient to the OR.
The bedside evaluation for necrotizing fasciitis. If the patient
looks really sick and you are concerned for necrotizing fasciitis,
you can make a small incision in the skin. If you cut cellulitis (and
we have all done it thinking we were getting abscess), you get
EM:RAP Written Summary August 2017: Volume 17, Issue 8
www.emrap.org
some bleeding but not much else. If you put a scalpel into nec-
rotizing fasciitis, you get dirty, watery discharge and can bluntly
probe along with a finger or probe.
It may be difficult to distinguish between superficial throm-
bophlebitis and septic superficial thrombophlebitis. Uncom-
plicated superficial thrombophlebitis looks red over the vein.
They are less likely to be febrile or have systemic signs of illness.
Septic superficial thrombophlebitis has cellulitis spreading from
the vein and the patient may be sick and febrile.
The most likely bacteria are staph, strep and Enterobacter. If
the patient has an indwelling line, remove it. Start antibiotics.
Should the veins be removed? Practice patterns by surgeons
vary widely. DeLoughery usually tries to get the clot out. This
may not be feasible in some locations like the portal vein.
Should these patients receive anticoagulation? The litera-
ture is inconclusive. DeLoughery does not routinely start an-
ticoagulation unless there is evidence of progression of the
clot. However, he tends to anticoagulate septic thrombophle-
bitis of the viscera.
It was a busy night with a lot of sick patients. A subsequent pa-
tient had phlegmasia cerulea dolens (a severe form of deep vein
thrombosis) with tremendous venous engorgement. The patient
was transferred to IR for tPA and clot removal. Another patient
had cauda equina and went to the OR.
Gnarly Wounds
Brian Lin MD, Zach Shinar MD, Jonathan Kantor MD
Take Home Points
Wound flaps of questionable viability may be tacked
down to see if it takes.
Opinions differ on suturing lacerations of muscle.
Some zones of the extensor tendons in the hand may be
amenable to repair in the emergency department.
Central slip injuries may be identified with a modified
Elson’s test.
1
 The wound has a flap but the tissue may not survive. Some
advocate using the flap as a biologic dressing and tack it down.
Is this a good practice? Give your best try to tack down the flap.
It will either take or not. If it takes, great. Warn the patient that Neurocritical Intubation
it might not take. You don’t need to get too aggressive cutting Josh Bucher MD
tissue for fear it may not survive.
Take Home Points
Do you need to suture lacerations involving the muscle? Ac-
cording to Kantor, muscle does not hold sutures well. Fascia Intranasal medications are often underutilized.
does hold sutures well. If it is a relatively superficial muscle lac-
Set-up is minimal and administration is faster than IV
eration, you can reapproximate it by closing the fascia. Other-
medication.
wise, do your best to close up the laceration of the skin. Splint in
a position of safety and refer to the specialist. Most medications may not be given intranasally and vol-
ume is limited to 1 mL per naris.
Opinions differ on whether or not to close the muscle. Kenji
Inaba closes the muscle to eliminate dead space and achieve The intranasal route avoids first pass metabolism.
appropriate opposition of the ends of the muscle. He uses
Intranasal administration may be a good option in hospice
absorbable suture in a 2-0 or 3-0 with a tapered needle. He
patients.
uses a tension relieving suture such as a horizontal mattress.
Unlike Kantor, he does not close the fascia unless it is a large
Most patients don’t arrive in the emergency department with
defect. Patients who have had fasciotomies to relieve the
an IV in their arm. However, they do have nostrils. This provides
compartment syndrome do not have repair of their fascia and
an opportunity for the use of intranasal medications which are
do fine.
often underutilized.
The extensor tendon injury. Lin will repair extensor tendon inju-
Rech, MA et al. When to pick the nose: out-of-hospital and emer-
ries of the hand and forearm in specific zones of the hand (1-4).
gency department intranasal administration of medications. Ann
Zones 1-4 go from the fingertips to the base of the finger. It
Emerg Med. 2017 May 25. PMID: 28366351.
does not include the MCP joint (zone 5).
There are many benefits to the intranasal route when you need
It is easy to miss these injuries because there is so much
fast access. Set up is minimal and much faster than intravenous
redundancy in the extensor tendon network of the hand
medication. This may be a safer option for the patient and staff,
such as the juncturae tendinum and more than one extensor
especially with a combative patient. The pharmacokinetics are
tendon in the thumb, index finger and small finger. You can
faster than intramuscular.
completely lacerate a tendon and maintain full extension of
the digit. If you are in doubt, it is fine to extend the wound What are the drawbacks of intranasal administration? Most
margin to evaluate. If you are suspicious of injury but unable medications can’t be given intranasally. Medications such as
to identify a wound, you can close the laceration, splint and midazolam may burn with administration. The volume limitation
refer to a hand surgeon. Tendons may retract out of the field is 1 mL on each side (2 mL total).
of view.
Ideally, you are not using more than 0.5 mL per side. Admin-
Beware of the central slip injury. This can be examined with ister half of your dose in each nostril.
a modified Elson’s test. The patient presses the back of their
Many medications have multiple concentrations. For exam-
middle phalanges together. Asymmetry can indicate a central
ple, midazolam is normally stocked in one concentration for
slip injury.
IV therapy but you will want a more concentrated product for
Sometimes, the laceration may extend into the joint. This is intranasal administration. This can be a setup for medication
not always treated operatively in smaller joints. These patients errors.
may just receive a washout under digital block in the ED, splint
The atomizers are more expensive than IV and intramuscu-
and be discharged home on antibiotics. You may use a soft tip
lar routes. The commercially available atomizers cost about
catheter such as an IV catheter to irrigate the joint.
$6. However, this is a small amount of the cost of an ED visit.
Review. Chlorhexidine is better than Betadine. Normal saline There has been limited availability previously.
has not been shown better than water. Evert edges and reduce
Check out our video on EMRAP HD to learn how to make
tension. Patients may shower but remember that the wound is
your own atomizer device.
not completely repaired when sutures are removed. Muscle re-
pair can be deferred to the specialists. The pharmacokinetics are variable. Although intranasal is

2 EM:RAP Written Summary | www.emrap.org

 better than intramuscular administration, it is less reliable
than intravenous or intraosseous administration.
The most common medications administered intranasally are
benzodiazepines, pain and procedural sedation medications
and naloxone. There are some other medications that are possi-
ble. Lidocaine may be administered intranasally. Dexmedetomi-
dine also may be administered intranasally.
Patients receiving intranasal midazolam can be pretreated
with atomized lidocaine to improve comfort.
Why is the intranasal route so effective? The nasal cavity has
a rich vascular plexus which has a direct route into the blood-
stream. Any drug that can easily cross a mucous membrane will
have good absorption in the nasal cavity. Also, unlike oral ad-
ministration, first pass metabolism is avoided with the intranasal
route. The nasal mucosa is close to the brain and some studies
have found the concentration of the drug to be higher in the
CSF than in the plasma.
Although intranasal medications are more commonly given
to pediatric patients, you can give them to adult patients, es-
pecially hospice patients. Use of intranasal fentanyl can avoid
needlesticks. It is great for palliation.
The Challenging Foley
Jessica Mason MD and Eamonn Bahnson MD
Take Home Points
Most difficult Foley catheter placements may be avoided
with proper technique. What if this doesn’t work? You may require a flexible guidewire
Patients may be coached to relax the external sphincter to
allow passage.
Smaller catheters are more likely to coil and enter a false
lumen.
At 3 am, the nurse informs you that they are unable to place a
Foley catheter.
The majority of difficult Foley placements can be avoided with
proper technique. The problem is often due to the external
sphincter rather than the prostate. Unless, the patient performs
self-catheterization and is familiar with that sensation, their re-
flex will be to contract all their muscles. The catheter will come
up against the sphincter. If you can get them to relax, the cathe-
ter will slide through the external sphincter.
The anatomy. The urethra starts in the penis and then transi-
tions to the prostatic urethra before the bladder. The urethra
makes a 90 degree turn between the penile and prostatic ure-
thra. The urethra heads cranially. The external sphincter is locat-
ed here and is under somatic control.
August 2017: Volume 17, Issue 8 | www.emrap.org
What can you do? Distend
the urethra with gel or lube
and coach the patient that
they need to relax when
they feel resistance.
The Foley kits typically con-
tain a slip tip syringe rather
than a Luer lock syringe.
You can insert the slip tip
into the meatus and inject it.
How far in did the catheter
go? This can help you trou-
bleshoot. Did they meet resis-
tance at the prostatic and penile urethra junction because the
patient was uncomfortable? Is the catheter meeting resistance
due to a urethral stricture? Strictures are less common.
Try to get the patient to relax the sphincter. There is a con-
cern for causing a false tract by pushing the catheter posteri-
orly into the tissue. Although it seems counterintuitive, try a
larger catheter such as a 20 French with a coude tip. A smaller
catheter is more likely to coil and go into the false lumen.
Coude catheters have a slight angle at the tip. Make sure the
catheter is held with the coude tip pointing up at 12 o’clock to
facilitate passage cranially after passing the external sphinc-
ter. Don’t twist the catheter as you advance it. Hold the penis
with some tension to allow a direct path. The penile urethra
tends to be tortuous in the absence of erection and pulling
the penis with tension can straighten the urethra.
and confirmation of catheter placement on cystoscope.
What if prior attempts have resulted in bleeding? The safest
option is cystoscopy to allow direct visualization.
What are the most common reasons for urology consultation
regarding Foley placement?
The Foley was placed but no urine is draining. You can inject
saline and aspirate it to see if urine comes out in the syringe.
The Foley may not be all the way in. To avoid this scenario,
hub the catheter. You don’t want to inflate the balloon in the
prostatic urethra as this can result in significant bleeding, es-
pecially in a patient on blood thinners.
Placement of a Foley catheter when the penis is not visualized,
such as in edema or morbid obesity. Most commonly, people
try to blindly place the catheter in the hole in the soft tissue
where the penis is. Without tension, it will likely coil in the soft
tissue. Get an extra set of hands to help you retract the tissue.
You also can try placing the patient in Trendelenburg if they will
tolerate it. Place your hands on either side of the suprapubic
area and push down. This should allow visualization of the glans.
3
 The catheter only goes in a few centimeters before it can’t
pass. If you are concerned for a stricture, use a smaller and
more rigid catheter. Start with a 16 French and sequentially
go down to a 14 or 12 French. Use a silicone Foley which is
more rigid.
The traumatic removal of the Foley catheter. There can be a
lot of bleeding, especially if these patients are on blood thin-
ners. The inflated balloon pulled across the prostate leads to
bleeding from the friable prostate tissue. If the patient needs
a catheter or there is significant bleeding, the best strategy
is to replace the catheter. There shouldn’t be any structural
damage that would prevent you from passing the catheter.
The catheter can place pressure on the walls of the prostate
to tamponade bleeding. Inflate the balloon more than previ-
ously. Although the Foley catheter instructions state that the
balloon holds 5 mL or 30 mL, they can actually hold more than
this. A 5 mL balloon can hold almost 100 mL before it pops. A
30 mL balloon can hold a few hundred mL before it pops.
There are three reasons why Foley catheter placement may be
difficult in female patients; a morbidly obese patient, a hip or
pelvic fracture that prevents positioning to visualize urethra or
an elderly female with limited flexibility and stenosis of the va-
gina and introitus.
The main difficulty is visualization. Get an extra set of hands.
Once you can visualize the urethra, the catheter almost al-
ways goes in.
If you can’t visualize the urethra due to prolapse or stenosis,
use your finger as a guide. You can place your finger in the
vagina and move it anteriorly. Place the catheter directly over
your finger. The only place it can go is in the urethra. Elevate
the pelvis over an overturned bedpan.
Replacing a suprapubic catheter. This is the same catheter used
for a urethral Foley but it passes through a tract in the lower
abdomen directly into the bladder. Just pull the old one out and
place a new one. Just like a G-tube, 4-6 weeks should be al-
lowed to allow the tract to mature. Prior to this, there is a risk
that the bladder will fall away from the abdominal wall and urine
will leak out of the bladder. These have the potential to close
rapidly. Get something into the bladder to maintain the tract.
You can place a smaller catheter to maintain patency of the tract
and dilate later.
4 EM:RAP Written Summary | www.emrap.org
Intra-articular Lidocaine
Patrick Bafuma PA
Take Home Points
Intra-articular lidocaine can result in shorter hospital stays
and fewer complications compared to procedural sedation.
Spinal needles may make it easier to access the joint.
Chronic dislocators may not have much blood obtained
upon aspiration.
Intra-articular lidocaine versus procedural sedation for the
reduction of shoulder dislocation. An informal poll on Twitter
found procedural sedation was used 50% or more of the time
for shoulder dislocation. This takes resources and time. There
is some small risk for the patient. There is a lot of paperwork
involved.
Jiang, N et al. Intra-articular lidocaine versus intravenous anal-
gesia and sedation for manual closed reduction of acute anterior
shoulder dislocation: an updated meta-analysis. J Clin Anesth.
2014 Aug;26(5):350-9.
This meta-analysis included 9 randomized controlled trials and
over 400 patients. They found no difference in pain control.
There was a slightly longer time spent on the actual procedure
in the intra-articular lidocaine group. The time until disposition
was decreased by about 30 minutes for the intra-articular lido-
caine group and there were fewer complications.
There were no differences in patient satisfaction or success
rate of reduction.
Bafuma’s tips for intra-articular injection.
Use a spinal needle. The space you need to reach is deeper
than you think. You must aspirate blood. If you don’t see flash
you probably won’t have great analgesia. If you are getting
a lot of blood back, make sure you aren’t in a vessel before
injecting. Chronic dislocators may not have much blood in the
joint with dislocation.
You can use the ultrasound to visualize where you are going.
This may be helpful in obese patients.
Draw up about 10-20 mL of 1% lidocaine. This is about 100-
200 mg of lidocaine which is well below the toxic dose in the av-
erage 70 kg adult. Attach a 20 gauge spinal needle. Go in at an
80-90 degree angle about 1-2 cm below the lateral edge of the
acromion into the glenohumeral joint. Slowly inject over about
20-30 seconds and wait about 15 minutes before reduction.
While you are waiting, you can place the patient in the prone
position with their arm dangling off the bed. This prepares
them for scapular manipulation.
 Or if you prefer external rotation, you can have the patient
sit upright with their knees up. Have them cross their fingers
with their hand in front of their knee. This is the Davos tech-
nique. Have them gently lean backwards.
The patients may sometimes spontaneously reduce with
these techniques.
Epi In Cardiac Arrest, Again!
Rob Orman MD and Amal Mattu MD
Take Home Points
The data on epinephrine in cardiac arrest is mixed.
A recent study found patients who received epinephrine
within 19 minutes were more likely to have favorable neu-
rologic outcomes.
Cardiac arrest can be divided into three phases; electrical
phase, circulatory phase and metabolic phase.
The optimal dose of epinephrine is unclear.
There are mixed messages about the use of epinephrine in car-
diac arrest.
Tanaka, H et al. Favorable neurological outcomes by early epi-
nephrine administration within 19 minutes after EMS call for
out-of-hospital cardiac arrest patients. Am J Emerg Med. 2016
Dec;34(12):2284-2290. OPEN ACCESS LINK.
This data was primarily from Japan and Singapore. It was a
retrospective evaluation of over 119,000 patients between
2008 and 2012.
They looked at patients who were given epinephrine at vari-
ous time durations. Japan does not allow pronouncement of
death in the field unlike the United States. There is likely more
bias in the US studies.
o Later in the metabolic phase, the alpha effect may be harmful.
They compared patients who were not given epinephrine to
patients who were given epinephrine. Within the group re-
ceiving epinephrine, they compared patients who were given
epinephrine between 5-18 minutes, 19-23 minutes, 24-29
minutes and 30-62 minutes after the EMS call.
They looked at neurologic outcome at 1 month as a primary
outcome and return of spontaneous circulation as a second-
ary outcome.
What did they find? Patients who received epinephrine had
a higher rate of return of spontaneous circulation than the
patient who did not receive epinephrine. There were some
problems with this study; the epinephrine group had more
frequent public access defibrillation. However, they found
August 2017: Volume 17, Issue 8 | www.emrap.org
that patients in the earliest epinephrine had slightly better
neurologic outcomes at 1 month than the group with later
administration.
The early epinephrine group was more likely to have by-
stander CPR, shockable rhythms and slightly fast ambulance
arrival. It is unclear if the early administration of epinephrine
was the factor or the other factors that allowed for early ad-
ministration of epinephrine.
A three phase model of cardiac arrest.
The first phase is the electrical phase. This is in the first 5 min-
utes. These patients are most amenable to early defibrillation.
The second phase is probably 5-10 minutes after that. This is
the circulatory phase. The priority is to reestablish circulation.
This is probably the time period when epinephrine is most
likely to work. The studies seem to confirm this.
The third phase is the metabolic phase. This involves hyper-
kalemia, metabolic acidosis and dying myocardium. Increas-
ing evidence shows the more epinephrine that is given in this
phase, the worse the outcome. If they do survive, they have
worse neurologic function.
The optimal dose of epinephrine is unclear. There is little ev-
idence to say that the 1 mg bolus of epinephrine given every
3-5 minutes is the right dose. We often see downstream effects
of this epinephrine dose if return of spontaneous circulation is
achieved.
Epinephrine has alpha and beta effects.
Although you might think that that beta effects might be the
most useful, the beta effects can lead to cardiac ischemia, ar-
rhythmia and increased myocardial demand.
The early alpha effects seem to be the most useful in cardiac
arrest. This causes peripheral vasoconstriction. You want to
constrict the peripheral circulation to bring blood back to the
heart to increase coronary perfusion.
Peripheral vasoconstriction may decrease perfusion to the
brain with escalating doses of epinephrine.
How is Mattu teaching the use of epinephrine? From the prac-
tical standpoint, people want to follow ACLS. They are con-
cerned about medicolegal issues or criticism by teammates. It
is a complicated issue. Mattu recommends epinephrine for the
first 15 minutes, but believes escalating doses after about 15
minutes may be harmful.
5

Pharmacology Rounds:
Gonorrhea Gets Some Muscle
Rob Orman MD and Bryan Hayes PharmD
Take Home Points
Gonorrhea infections are increasingly resistant to antibiotics.
Current guidelines recommend a dose of 250 mg IM ceftriax-
one and 1 g oral azithromycin for uncomplicated infections.
PID should be treated with a 250 mg IM dose of ceftri-
axone followed by a prolonged course of doxycycline.
Although patients may be given serial doses of azithromy-
cin, they are unlikely to tolerate it.
Gonorrhea is increasingly resistant to antibiotics. The new
guidelines recommend a dose of 250 mg IM ceftriaxone in a
single dose plus 1 gram of oral azithromycin for uncomplicated
gonorrhea infections of the cervix, urethra and rectum.
The recent gonococcal isolate surveillance project found in-
creases in MIC for azithromycin and cephalosporins. This is con-
cerning for increasing resistance. The MIC is the minimum inhibi-
tory concentration, which means the lowest concentration of the
antibiotic that should be sufficient to eradicate the pathogen.
There are increasing isolates with decreased sensitivity to azi-
thromycin. In 2013, 0.6% of isolates were resistant to azithro-
mycin and just one year later, it increased to 2.5%. The rate of
resistance increased 300% in a year. The current guidelines also
cover chlamydia.
Can PID be treated with a single dose of ceftriaxone and azith-
romycin? These patients should really be treated with a single
dose of 250 mg IM ceftriaxone followed by a prolonged course
of doxycycline. Although recommendations advise patients may
take serial doses of 2g of azithromycin, this is unlikely to be tol-
erated by patients. You do not have to give the dose of azithro-
mycin if patients are given the prolonged course of doxycycline.
Pharmacology Rounds:
What Works for Acute Migraine?
Rob Orman MD and Bryan Hayes PharmD
Take Home Points
Recent guidelines on acute migraine headache manage-
ment recommend metoclopramide, prochlorperazine and
sumatriptan be offered to patients.
Dexamethasone should be offered to prevent recurrence.
Opiates may be avoided.
6 EM:RAP Written Summary | www.emrap.org
The American Headache Society just came out with guidelines
on acute migraine headache management. They separated vari-
ous medications given for migraines in the ED into recommenda-
tions of should be offered, may be offered, should be avoided or
no recommendation. Most of these medications are now generic.
Orr, SL et al. Management of adults with acute migraine in the
emergency department: the American Headache Society evi-
dence assessment of parenteral pharmacotherapies. Headache.
2016 Jun;56(6):911-40. PMID: 27300483.
There were three medications in the category of should be
offered; metoclopramide (10-20 mg IV), prochlorperazine (10
mg IV) and sumatriptan (6 mg subcutaneously).
In the category of may be offered; droperidol if available, halo-
peridol, NSAIDs, valproic acid and IV acetaminophen.
In the category of may avoid; hydromorphone, lidocaine, mor-
phine, octreotide and diphenhydramine. Many like to use di-
phenhydramine along with metoclopramide or prochlorperazine
as it may have an adjunctive effect on the headache and ad-
dresses some of the side effects (like akathisia).
Other ways to avoid akathisia with metoclopramide or
prochlorperazine include slower administration over about 15-
20 minutes. Intravenous diphenhydramine can cause euphoria.
Consider oral administration if you want to include it in your
cocktail.
In the category of no recommendation, they included ketamine
(not enough evidence), propofol and intravenous magnesium.
Magnesium is unlikely to cause problems, however.
They included dexamethasone in the category should be
offered to prevent recurrence of headaches.
Friedman, BW. Managing migraine. Ann Emerg Med. 2017
Feb;69(2):202-207. PDF LINK.
This article went through all of the medication options and
gave a progression through treatment modalities that you
can use.
The first line continues to be metoclopramide or prochlor-
perazine with adjunct dexamethasone to prevent recurrence.
Also consider droperidol if available or haloperidol. Avoid opi-
ates in these patients.
 You may not be able to identify these patients in the acute
Blood Pressure Control stroke setting as history may be limited.
in Acute Stroke Identifying modifiable delays in acute stroke evaluation
Rob Orman MD and Jon Schrock MD
and treatment. What are some things we can do to improve
door-to-infusion time?
Take Home Points
Avoid performing less meaningful tests before the CT, such
Studies in patients treated with thrombolytics for STEMI
as the EKG and chest x-ray. Getting the head CT quickly is
found a higher risk of intracranial hemorrhage if the pa-
important to determine what is going on and it should not be
tient was hypertensive.
delayed for other tests.
Labetalol or nicardipine may be used to lower blood pres-
What is the blood pressure target in a patient who will not re-
sure before thrombolytics.
ceive thrombolytics?
Hypotension may also lead to complications in stroke pa- At Shrock’s institution, they will hold all blood pressure med-
tients. They may require fluids boluses or pressor support
ications in patients with acute stroke who do not receive
to maintain adequate perfusion.
thrombolytics unless the blood pressure reaches greater than
210 mmHg.
Hypertension in stroke. Early studies found patients treated Low blood pressure and dehydration are concerning. There
with thrombolytics for STEMI were higher risk for intracranial
are some studies showing that patients with evidence of de-
hemorrhage if hypertensive. This data was extrapolated to de-
hydration such as clinical signs or an elevated BUN/creatinine
termine a maximum blood pressure of 185/110 mmHg to per-
ratio will do worse. Shrock will give these patients fluids to
mit thrombolytics.
augment circulation to the brain.
When should the blood pressure target be achieved? You want In some situations, patients with staccato symptoms who
the blood pressure below this level before initiating throm-
improve initially with fluids or have intracranial stenosis and
bolytics. You don’t want the blood pressure to increase after
are symptomatic at a lower blood pressure may be started on
thrombolytics due to increased risk of intracranial hemorrhage.
pressors. Is there a set target? No. The blood pressure sup-
Schrock uses labetalol because it is readily available, easy to ad-
port is targeted toward improvement of neurologic symptoms.
minister with rapid onset of action. If the patient has an increase
However, Shrock does not routinely start patients on pressors.
in blood pressure after administration of thrombolytics, they are
started on a continuous infusion such as nicardipine.

There is no current head-to-head comparison to suggest

labetalol or nicardipine as superior. Most centers will use Against Medical Advice
labetalol as it is easier to administer and does not require setting Rob Orman MD, Mike Weinstock MD and Kevin
up a drip. However, infusion of medication allows for tighter Rogers MD
blood pressure control and decreases swings of blood pressure.
Take Home Points
The patient arrives with stroke symptoms and a blood pressure
of 220/180 mmHg. They will go to CT. You don’t know if they Although patients may refuse procedures or medications,
have a hemorrhage or an ischemic stroke that may be treated you do not need to terminate care.
with thrombolytics. Should you give an antihypertensive prior
Leaving against medical advice requires capacity, ade-
to the scanner?
quate explanation of risks and proper documentation.
Schrock typically gives 10 mg of labetalol as the patient is
Document your discussion with the patient, including any
heading to the scanner. You don’t want to overshoot. You can
questions they asked, as this can demonstrate capacity.
give another dose as needed or set up a nicardipine drip.
There are four key aspects to capacity; ability to commu-
How long does it take labetalol to work? Usually it starts
nicate, ability to understand information, ability to under-
working in a few minutes.
stand the situation and ability to manipulate the informa-
Your goal is around 150-165 mmHg based on the limited ev- tion presented to make a logical decision.
idence available.
You do not need to document the patient’s reason for
Patients with significant hypertension on multiple medica- leaving as it may be used against you.
tions or end stage renal disease can be difficult to manage.

August 2017: Volume 17, Issue 8 | www.emrap.org 7

 When we are working through the AMA process, should we
be focused on our protection or the patient? The focus is the
patient. If you do this correctly, you will reduce your risk.
For example, you have a patient with a small bowel obstruction
that is refusing a NG tube. Some will tell the patient to leave.
Don’t do this. Patients can refuse procedures or medications.
That doesn’t mean that you need to terminate care. Sometimes
this is about negotiation. Document the care they refused.
There are three pillars of leaving against medical advice; capaci-
ty, adequate explanation of the risks and proper documentation.
Capacity is different than competence. Competence is a le-
gal decision that occurs in court. We are looking for capacity.
This is the ability of the patient to express two choices. They
have to understand the relevant information. You need to ask
questions to make sure they understand what you are telling
them. The patient has to understand the consequences of
treatment and non-treatment. You also have to explain alter-
natives to the patient.
If the patient refuses a recommended treatment but there are
alternatives, you have to provide the alternatives if reason-
able. The patient needs to show they have reasoning ability.
You need to document your discussion with the patient,
including any questions that they asked. When they start
asking questions, it supports their capacity.
There are four key aspects to capacity; ability to commu-
nicate, ability to understand information, ability to under-
stand the situation and ability to manipulate the informa-
tion presented to make a logical decision. This means they
can take the facts presented and make a logical decision
even though you disagree with it.
Communication of risks. Potential risks, potential outcomes,
alternative approaches need to be documented. Doing all of
this in a patient centered manner decreases your risk of be-
ing sued. Patients may be concerned about the cost of pro-
cedures or deductibles. You need to be prepared for this. If
you have a logical discussion with a patient who has capacity
about situations that aren’t absolute, sometimes it is more
shared decision making than AMA. It also depends on the de-
gree of risk. If the patient is high risk, it should be AMA. If the
patient is low risk and wants to follow-up with their doctor
because it will be cheaper, it may be shared decision making.
Both need to be documented.
The documentation. The AMA form documents that the dis-
cussion took place because the patient has to sign the form.
However, your documentation of capacity, risks, benefits and
alternatives in the medical record is just as important.
The patient still needs instructions of what to do and how
to follow-up. Emphasize “If you change your mind in five
8 EM:RAP Written Summary | www.emrap.org
minutes, just come right back in that door. Return any time
you want and we will treat you.”
You get some legal protection from doing this correctly.
Once the patient says that they no longer want to partic-
ipate in your care plan, they have terminated your duty. If
injury occurs after termination of duty, you will not be held
responsible. Assumption of risk defense can decrease your
liability. Evidentiary support such as your medical record is
very powerful in court.
Make sure you document that they have capacity. “I think
you have appendicitis because people with appendicitis
have pain in the right lower quadrant where you have pain. I
would like to give you antibiotics and do a CT scan. If it finds
appendicitis, I would like you to go to surgery.” “Is there an
alternative to surgery?” “There is some evidence supporting
antibiotics.” “What is the risk?” “It could burst and let pus into
your belly and give you a life-threatening infection and result
in scars that can result in bowel obstruction.”
Your duty is to try to provide as much patient centered
communication and care as they will let you.
Be as specific as possible about the risks. Several cases
have shown that general documentation is not sufficient.
We have heard mixed messages about the AMA form. It has
been described alternatively as protective and adversarial. It is
not important compared to your conversation with the patient
and documentation of the medical decision making. Have the
patient sign the form, but have a good discussion with the pa-
tient and family.
You have a patient with right lower quadrant pain and an
elevated white blood cell count. You are very worried that
the patient has appendicitis. The patient wants to go home.
Bickell, NA et al. How time affects the risk of rupture in appendi-
citis. J Am Coll Surg. 2006 Mar;202(3):401-6. PMID: 16500243.
They looked at patients with rupture and when it happened.
They found that less than 2% of patients had rupture at 36
hours. For example, the parents of a 10 year old with 12 hours
of pain refuse imaging or additional work-up. This may be a
reasonable decision that they are making based on their sit-
uation. It is unlikely to rupture so we might engage in shared
decision making.
However, shared decision making can only take place if it is a
decision between two reasonable alternative pathways. This
is not a patient with sepsis and a blood pressure of 60 who
wants to go home with oral antibiotics.
However, if you have patient who is febrile with severe pain
for more than 48 hours, this patient is going to have to sign
the AMA form if they leave.
Documentation in the chart is usually accepted at face value.
 However, signing the AMA form demonstrates that not only did Marik had some patients who were dying from sepsis and tried
the patient understand they were leaving against medical ad- giving vitamin C, thiamine and steroids. He noted dramatic re-
vice but they even signed a form. We want to prevent a lawsuit. sults and then did a before and after trial that showed an incred-
The best way is to make sure that the patient and family under- ible decrease in the comparable mortality between the groups
stand that we are concerned about them. using this regimen. However, this was a before and after trial.
This is not high level evidence. There is controversy between
Should you document the patient’s reason for leaving? Wein-
the evidence based medicine group saying that there is insuffi-
stock does not discuss the reasons behind leaving. It is easy for
cient evidence, and clinicians, who are desperate for something
us to document that the patient’s reason for leaving was trivial,
to treat their patients and view it as unlikely to harm with poten-
but it can be turned against us.
tial benefit. This is difficult to reconcile.
You have a patient who comes to the emergency department
Weingart is on the fence. He knows this is too early; he should
frequently. They have diabetes, renal insufficiency and have
not be trying this and should wait for a randomized controlled
chest pain. They are very verbally abusive to the staff. You
trial. However, he wants to try it. The problem with trying it is
work them up and they have an elevated troponin. The patient
that you won’t immediately see the results. Our biases will cause
is saying they will sue you and threatens that they will leave.
us to view a positive outcome as evidence the cocktail works
Would you have them sign an AMA form? Absolutely. There and negative outcome as a patient that was likely to do poorly
is no reason for them not to do it. If they stand up and walk regardless of intervention.
out, document what happened in an objective way. “I went
This controversy is unlikely to die soon. There is a prospective,
in to explain to the patient why I was concerned about them
randomized controlled trial in the works. The study showed an
medically and they should stay. They stood up. I told them I
incredible improvement in mortality; 32% absolute difference
would like them to sign the AMA form and they walked out.”
with an NNT of 3 for lives saved. However, the methodology is so
Documenting the expletives used by the patient in quotes flawed that the study can’t be used to change practice at this point.
will be described by the attorney as the patient advocat-
ing for care that they weren’t receiving.
How should you document the verbally abusive patient?
“The patient has chest pain which I think is very likely to be
Strayerisms:
from ACS and I’m extremely concerned about them. I have
Why Do We Intubate?
Reuben Strayer MD
gone back in the room twice to explain the seriousness of
the situation but the patient refuses to stay. I offered him
Take Home Points
to come back any time if he changes his mind. He stood up,
looked me in the eye and walked out.” Although we often say we are intubating for airway pro-
tection, we are usually intubating for another reason. It is
Both the AMA form and medical decision making are import-
important to use the correct terminology and indication.
ant and should be components of caring for a patient who
leaves AMA. It is always better to avoid a lawsuit than to win There are six reasons to intubate; airway, breathing, circu-
one. Take your emotion out of it. lation, disability, expected course and agitated delirium.
Signs of impending airway obstruction include stridor,
voice change, mishandling secretions and posturing.
Critical Care Mailbag:
Vitamin C for Sepsis? A significant proportion of people have an absent gag re-
Rob Orman MD and Scott Weingart MD flex at their baseline and the presence of a gag reflex does
not demonstrate adequate airway reflexes
Take Home Points
Intubation for airway protection. Why do we always say we are
A recent trial by Marik showing decreased mortality with
intubating for airway protection? Most of the time we don’t mean
administration of hydrocortisone, vitamin C and thiamine
that we are intubating for airway protection. Airway protection is
was not high level evidence.
a mysterious concept. Try asking five emergency providers how
More evidence is needed before changing practice. you can tell if a patient is or isn’t protecting their airway.

There are six reasons to intubate.

Marik, PE et al. Hydrocortisone, vitamin C and thiamine for the treat-
ment of severe sepsis and septic shock: a retrospective before-after Airway. However, this is not about protection but about
study. Chest. 2017 Jun;151(6):1229-1238. PMID: 27940189. obstruction. You need to get ready for a tough intubation

August 2017: Volume 17, Issue 8 | www.emrap.org 9

 because there is a good chance that the obstruction that
indicates intubation will make intubation difficult or impos-
sible. For example, mouth or neck infections like epiglottitis
or Ludwig’s angina, ENT tumors, foreign bodies and bleeding
into the airway. Bleeding is especially bad because the blood
that is choking your patient will also choke your videolaryngo-
scope and line of sight. Be ready.
Dynamic airway obstructions deserve special mention
as these have the possibility to rapidly evolve so that an
easy intubation may be impossible in five minutes. Neck
trauma, anaphylaxis, angioedema, thermal airway injuries,
bullets, bites and burns. When a patient with one of these
problems demonstrates one of the airway signs (stridor,
voice change, mishandling of secretions and posturing),
move quickly.
Breathing. This is probably the most common reason why
we intubate in the emergency department. These patients
have diseases that cause failure of oxygenation or ventila-
tion including asthma, COPD, pneumonia, pulmonary ede-
ma, pulmonary fibrosis, etc. Most of these patients will have
normal airways. They should be easier to intubate than the
previous group. However, they may have a high oxygenation
deficit and drop their saturation as soon as your push drugs.
You need to take specific measures to address this prior to
intubation. If you use a paralytic, you may need to go fast.
Fortunately the majority of patients who used to be intubated
for a breathing problem may be temporized or stabilized with
non-invasive ventilation.
Circulation. Intubation is often an insult to the circulation of
sick patients due to the sympatholysis of the induction agent
and the preload reduction of positive pressure ventilation.
There are some patients who require intubation to unload the
muscles of ventilation because they are at the end of their
metabolic rope. This is most commonly occurs in severe sep-
sis. Resuscitate these patients before you intubate. Use strat-
egies to minimize the impact of sympatholysis such as reduc-
ing the dose of the induction agent or using a non-paralyzing
breathing intubation technique with small tidal volumes.
Disability. Patients with neurologic catastrophes such as
intracranial hemorrhage or status epilepticus and patients
with CNS depression for overdose. These are the patients
who need to be intubated for airway protection as they can’t
protect their airway and are at risk for aspiration. These pa-
tients generally have normal airways, heart and lungs. The
focus should be on brain protection by reducing the impact
of the procedure on hemodynamics and intracranial pressure.
A less common subset of patients who need to be intubated
is those with neuromuscular weakness such as myasthenia
gravis, Guillain-Barre, etc. The gag reflex is not an acceptable
indicator of airway protection.
10 EM:RAP Written Summary | www.emrap.org
A significant proportion of people have an absent gag re-
flex at their baseline and the presence of a gag reflex does
not demonstrate adequate airway reflexes. It is hard to
justify performing a maneuver known to precipitate vomit-
ing in patients where you are concerned about their ability
to protect their airway. Evaluate the ability to handle secre-
tions. Obtunded patients who are vomiting do need to be
intubated for airway protection.
Expected course. These are the patients where you are con-
cerned they will develop an A, B, C or D reason to intubate at a
time when it will be less safe to do so, such as in the CT scanner
or during transfer to another institution. These patients are of-
ten the most challenging as you are trying to predict the future.
The preferred error considers how much harm you will do if you
are wrong and how likely you are to be wrong. If you intubate a
patient who didn’t need intubation, what harm have you done?
Some small harm. There is a risk you might not get the airway
(unlikely) or other complications. However, what is the risk of
not intubating a patient who later requires a crash intubation
which is more dangerous? If you look at it this way, most of the
time when you aren’t sure whether or not to intubate, intubate.
Feral. These are the patients who need to be intubated be-
cause they are so agitated that the best way to manage their
threat is induction and intubation. This indication is less rel-
evant now that we are comfortable using dissociative dose
ketamine as a tranquilizer. We intubate seriously injured trau-
ma patients whose agitation prevents their care but we fail to
consider this strategy in other very sick patients who are agi-
tated. Delayed sequence intubation may be the right approach
if the patient is unable to cooperate with proper preparation.
Dissociate with ketamine, prepare and paralyze (or not).
Let’s clean up our terminology about intubation. Most of the
patients we intubate are not intubated for airway protection.
Know your indications for intubation and the management pri-
orities unique to each indication.
Hand, Foot and Mouth
Stuart Swadron MD and Brittney DeClerck MD
Take Home Points
Hand, foot and mouth disease results in vesicular, necrotic
lesions on the mouth, hands and feet.
A new strain of Coxsackie may infect adults and has a wid-
er distribution of lesions.
Patients with eczema may have viral seeding of the ec-
zematous skin leading to eczema coxsackium.
The lesions associated with Coxsackie A-6 may appear
similar to impetigo with crusting.
 Hand, foot and mouth disease results in vesicular, necrotic le-
sions on the mouth, hands and feet. It is typically seen in children
less than 5 years of age. They complain of pain to the throat and
may have decreased oral intake. This is a fairly self-limited dis-
ease. The child usually has viral symptoms for a few days and then
develops vesicles. Treatment is supportive. Try to relieve the pain
and make sure the child is able to tolerate adequate oral intake.
In 2011, a new strain of Coxsackie virus, A-6, appeared. This
new strain has a different clinical presentation and a different age
group of involvement. You may not suspect hand, foot and mouth
in an adult with a wider distribution of vesicles or classic lesions.
This is very contagious. It is now more widespread and found
in teenagers and adult patients. Transmission is via droplets, fe-
cal-oral transmission and the virus can linger on surfaces.
How does the clinical presentation of A-6 differ from the typ-
ical hand, foot and mouth presentation? Patients are typically
older although children may get it. Patients will have more sys-
temic systems such as fever, arthralgias and flu-like symptoms.
The lesions are more widespread. Vesicles and erosions may
occur more diffusely on the face, classically in the nose, peri-
oral and cheek regions. They may occur on the arms, extensor
surfaces, elbows, thighs, buttocks and the groin.
What is the differential diagnosis? There are several things you
should consider when you have a febrile patient with eroded
vesicles.
Varicella. There are increased outbreaks due to decreased
vaccination.
Herpes simplex, especially eczema herpeticum. Patients
with eczema may develop a wider infection with the herpes
simplex virus as it seeds the eczematous areas. The Coxsack-
ie virus is able to do the same thing and patients may devel-
op eczema coxsackium.
Some viruses may be treated with supportive care. Others, such
as HSV or VSV may be treated with acyclovir or valacyclovir.
You should admit patients with eczema herpeticum. These are
usually sick children. Make sure that they are getting intrave-
nous antivirals.
Rickettsial pox may be seen on the East Coast. This may result
in little necrotic lesions.
The lesions associated with Coxsackie A-6 may appear similar
to impetigo with crusting.
If you are suspicious for this Coxsackie virus, what testing can
you get for confirmation? There are two types of test available.
You can check antibody titers, IgG or IgM for general viruses or
you can do PCR. These can be done in the hospital setting. It is
important to know what your lab is running. However, the IgG
and IgM do not cover the A-6 virus. If you are sending an IgM to
August 2017: Volume 17, Issue 8 | www.emrap.org
look for A-6, it won’t check for it. You might consider sending a
PCR. However, you won’t send these tests routinely. You might
consider sending it if the diagnosis is unclear or there is a possi-
bility of something more dangerous.
There have been some outbreaks of hand, foot and mouth that
have been associated with real morbidity and death. There
are some strains of enterovirus 71 associated with encephalitis
and myocarditis. Don’t forget to do a good neurologic exam or
cardiac exam. If you are discharging the patient, don’t forget to
educate them that they need to come back if they worsen.
Down Syndrome
Stuart Swadron MD and Sol Behar MD
Take Home Points
Consider thyroid problems in Down syndrome children,
especially with new pleural effusion.
New neurologic changes or neck pain should be concern-
ing for atlanto-axial instability in Down syndrome.
Children with Down syndrome are high risk for respira-
tory complications with unique airway features making
intubation difficult.
You have a sick child in the emergency department. They also
have Down syndrome. These children may have multiple com-
plications.
Common pathology in Down syndrome children.
The central nervous system. They have some degree of de-
velopmental delay. However, about a third of these children
also have a seizure disorder and you may see them present
with seizures.
Cardiovascular. They have a high rate of cardiac defects such
as the endocardial cushion defect which lead to AV canal and
ventricular septal defect. However, they can have any type of
cardiac defect. This affects about half of the population with
Down syndrome.
They also have a higher incidence of pulmonary hyperten-
sion compared to normal children (about 10%). You need to
consider this when they develop a respiratory infection.
The airway. They have larger tongues, obstructive sleep apnea
and occasional tracheal stenosis. They are a potential airway
nightmare when sick. Get out your backup airway equipment.
The gastrointestinal system. If you are dealing with a neo-
nate, there is the possibility of intestinal atresia. Constipation
is almost universal in Down syndrome. In addition, there is a
higher rate of Hirschsprung’s disease.
11
 The endocrine system. Think about the thyroid. These chil-
dren are screened annually to make sure they haven’t ac-
quired hypothyroidism. The rate of Hashimoto’s thyroiditis is
about 30% in these kids. They also have a higher than normal
rate of diabetes mellitus.
Sensory problems. These children have a higher rate of vision
and hearing issues. They are at risk for strabismus and cataracts.
They almost universally have tortuous small ear canals and high
rates of serous otitis media with subsequent hearing loss.
Leukemia. They have much higher rates than the general
population and are screened with a CBC.
Orthopedics. They are at risk for atlanto-axial subluxation
which may complicate airway management. They tend to
have subluxations of the patella, hip dysplasia and ligamen-
tous laxity. They are hypotonic.
CASE
An 11 year old boy with Trisomy 21 presented with a complaint
of chest pain and difficulty breathing. The child was very short
of breath. He had a 4 day history of cough, runny nose, low
grade fevers with mild abdominal pain and one episode of non-
bloody emesis and one episode of non-bloody stool. His only
past medical history aside from Down syndrome is a history of
asthma. He also had a history of obstructive sleep apnea for
which he used CPAP. He did not have a history of congenital
heart disease however.
His temperature was 98.7ºF, blood pressure 99/57, tachycar-
dic at 170 and tachypneic at 40 breaths per minute. His pulse
oximetry was 80% on room air.
The patient was placed on oxygen with some improvement in
saturation. He was in moderate respiratory distress and grunt-
ing. He was awake and alert but was not able to complete full
sentences. His HEENT exam revealed only rhinorrhea. His
tympanic membranes were clear. He looked well-hydrated.
He had a large tongue but no neck masses. He had decreased
lung sounds on the left without obvious wheezing and sub-
costal retractions.
There wasn’t much change with albuterol. Chest x-ray
showed an enlarged heart with some hazy densities in the left
lung zone. The costophrenic angle was poorly visualized with
pleural effusion. EKG showed sinus tachycardia. The patient
was given ceftriaxone.
The CBC was normal. However, the resident reviewed the
medical record and found a TSH that had not been addressed 3
months prior. The level was 952 with a normal range of 0.5-3.5.
The patient was started on thyroid hormone immediately.
An echocardiogram showed a normal ejection fraction and a
small pericardial effusion with no evidence of tamponade.
12 EM:RAP Written Summary | www.emrap.org
CASE
A 14 year old female with trisomy 21 presented after a week
of gait instability. She was obese. The mother had noticed that
she wasn’t ambulating normally and couldn’t stand upright.
There was no history of trauma. The patient was really anx-
ious when they tried to stand her up. She was unable to climb
the steps to the exam table. She had decreased central tone,
which can be difficult to detect in these children due to their
baseline hypotonia. She had a difficult time holding up her
trunk and neck.
It is important to remember that these children are at risk
for atlanto-axial instability and serious neck pathology. Her
neurologic exam showed intact GCS and cranial nerves. How-
ever, she had hyperactive deep tendon reflexes.
She had previously normal screening x-rays at the age of 3.
The guidelines advocating for routine screening have been
revised as children have had compression of their spinal cord
despite falsely reassuring negative screening exams.
If these patients have symptoms of C-spine compression,
you need imaging. The plain films showed atlanto-axial sub-
luxation. A subsequent MRI showed substantial atrophy at
the C1-C2 level.
She was admitted for surgical management and had some
improvement in function.
When should we suspect this? Neck pain, torticollis, difficulty
walking, abnormal gait, increased clumsiness, paresthesia or
sensory change. Do a careful neurologic exam and look for
spasticity, hyperreflexia, new clonus, plantar and extensor re-
flexes and bowel or bladder dysfunction.
CASE
A 4 month old with Trisomy 21 presented with a bad upper
respiratory infection. The child had retractions and was grunt-
ing. Pulse oximetry was 89%. There was a history of a normal
perinatal echocardiogram.
The child was given oxygen with improvement in satura-
tions. On exam, the patient had rhonchi, retractions and co-
pious nasal secretions consistent with bronchiolitis.
These children are at risk of pulmonary hypertension. You
need to make sure that these children do not experience
worsening hypoxia to prevent decompensation.
Their airways are smaller and floppier. They are more prone
to apnea with bronchiolitis. Their immune systems aren’t to-
tally normal. Down syndrome is an independent risk factor for
more severe bronchiolitis even in the absence of congenital
cardiac disease.
 Get a chest x-ray in this population to rule out pneumonia or
evidence of heart disease.
These patients may require a higher level of care.
Do you need to intubate the child? Are there bridging treat-
ments you can do? BiPAP is a great option in these children.
Consider high flow oxygen.
If you have to intubate the child, make sure you keep the neck
in a neutral position as they may have occult atlanto-axial in-
stability. They have large tongues and small airways. Have a
smaller tube size available in case their airway is really small.
Use all of your resources. If you have a Glidescope available, get
it. If you can get anesthesiology back-up, consider it.
EM:RAP on Location:
A Case of Usual Discharge
Viveta Lobo MD
A female patient presented with a complaint of “stuff coming
out down there”. The patient was seen by a resident. The res-
ident was setting up to do a pelvic exam and discovered the
patient was prostitute. She was working and felt like something
was wrong after her last client. The patient said, “I’ve had STDs
before and this does not feel like it.”
The resident performed a pelvic exam. It appeared consistent
with infection and the resident located a wadded up twenty dol-
lar bill in the vagina. The patient started swearing, “I told that
guy not to do that.”
The doctor stepped out of the room after telling the patient they
would treat her with antibiotics. When they returned to check
on the patient, the patient was gone and the room was empty.
Not only was the patient gone, but she took the twenty dollar bill
with her and it’s probably out in circulation somewhere…
Subarachnoid, Syncope,
and Cardiac Arrest
Zack Shinar MD and Joe Bellezzo MD
Take Home Points
Consider subarachnoid hemorrhage in your cardiac arrest
patients.
Consider ventricular tachycardia in your syncope patients
and look for geometric changes of the heart.
Think about pseudo PEA. These patients may be better
served by treatment for shock rather than cardiac arrest.
August 2017: Volume 17, Issue 8 | www.emrap.org
About 5% of cardiac arrests have a subarachnoid hemorrhage
as their initiating event. Why do they arrest? It is not due to her-
niation of the brain. They have a massive catecholamine surge
due to the hemorrhage. Patients have macrophage infiltration in
the left ventricle with profound myocardial dysfunction and con-
gestive heart failure with cardiac arrest. This is the same mecha-
nism that occurs with patients with Takotsubo and voodoo.
Think about this in your cardiac arrest patients, especially if
they had a headache. Patients with cardiac arrest from intra-
cranial hemorrhage have a terrible prognosis.
Is it ok to give anticoagulant to these patients? If the patient
has some prodrome or history concerning for subarachnoid
hemorrhage, Shinar obtains a CT scan prior to anticoagulation.
A 2007 study in Stroke found 4% of patients with missed sub-
arachnoid hemorrhage had a recent ED visit for syncope.
Vermeulen, MJ et al. Missed diagnosis of subarachnoid
hemorrhage in the emergency department. Stroke. 2007
Apr;38(4):1216-21. PMID: 17322078.
Syncope and cardiac arrest are not the same but may be relat-
ed. We have a concept of sudden cardiac death. There is also
abortive sudden cardiac death; the patient that died and came
back. These patients complain of syncope. How do we assess
for the possibility of ventricular tachydysrhythmia?
Probably only about 20% of patients with cardiac arrest due
to ventricular tachycardia had an MI. Another 15% likely had
electrolyte abnormalities, prolonged QTc, etc. However, the
majority doesn’t have acute disease but rather old coronary
disease. They have some cardiac insult and ischemic area that
causes them to have a plaque of the ventricle that acts as a
mechanism for inducing ventricular tachycardia.
You can think about this similarly to SVT when you have an
electrical problem with re-entry causing a high ventricular
rate. The same thing occurs in the ventricle but instead of
going around the AV node, you are going around this ischemic
area. What does this mean? In patients with old coronary dis-
ease, you need to consider if their syncope was due to a ven-
tricular tachydysrhythmia.
The San Francisco Syncope rules describe congestive heart
failure as a risk factor for bad outcome. This was prospec-
tively validated with 98% sensitivity and 56% specificity to
predict serious adverse outcomes in a month. However, a
subsequent validation study by another group found sensi-
tivity of 74%. The rule is positive if any of the following are
present; history of congestive heart failure, hematocrit less
than 30, abnormal EKG, shortness of breath and blood pres-
sure less than 90 mmHg at triage.
ACEP describes risk factors of heart failure, coronary dis-
ease, structural heart disease, abnormal EKG and hematocrit
less than 30, older age and comorbidities.
13
 How can you identify these patients? Do they have a geo-
metric change of their heart? Do they have signs of an old
heart attack, CHF or cardiomegaly? Patients with dilated car-
diomyopathy can have electricity repolarize around the heart
and increase risk of ventricular tachycardia.
Pseudo PEA. This describes the scenario where the heart is still
beating but it is not beating strongly enough to appreciate a
pulse. This could be PEA where patients do not have forward
flow from the heart and have electromechanical dissociation or
it could be a patient in profound shock. The last thing we want
to do to a patient in profound shock is to start chest compres-
sions and give superhuman doses of epinephrine. If you do chest
compressions on a beating heart, you may compress when the
heart is trying to relax and decrease the cardiac output, decreas-
ing the coronary artery perfusion pressure and increasing the
chance of them entering true cardiac arrest.
A study by Norm Paradis showed decreased CPP.
Paradis, NA et al. Coronary perfusion pressure during exter-
nal chest compression in pseudo-EMD, comparison of sys-
tolic versus diastolic synchronization. Resuscitation. 2012
Oct;83(10):1287-91. LINK.
We want to identify patients in pseudo PEA. We can do
this easily with an ultrasound. If the patient has good cardi-
ac function, maybe we should avoid chest compressions and
treat shock. If the patient has a blood pressure of 50 or 60
mmHg and is in shock, would you give them a milligram of
epinephrine or micro doses to raise their blood pressure? It is
unclear where this transition occurs. Arterial lines can really
help you in this situation.
A study in Slovenia performed ultrasound on prehospital
patients with PEA. If they saw cardiac activity, they treated
for shock. They had tremendous improvement in survival to
discharge.
Prosen, G et al. Impact of modified treatment in echocardio-
graphically confirmed pseudo-pulseless electrical activity in
out-of-hospital cardiac arrest patients with constant end-tidal
carbon dioxide pressure during compression pauses. J Int Med
Res. 2010 Jul-Aug;38(4):1458-67. PMID: 20926019.
Paper Chase 1:
Pacemakers and MRI
Sanjay Arora MD and Michael Menchine MD
Take Home Points
Patients with pacemakers and AICDs may undergo
non-thoracic MRI with pre- and post-MRI programming.
This study was performed in patients with newer genera-
tion devices.
14 EM:RAP Written Summary | www.emrap.org
In the one patient who accidentally underwent MRI while
their ICD was on, the ICD had device failure.
Russo, RJ et al. Assessing the risks associated with MRI in pa-
tients with a pacemaker or defibrillator. N Engl J Med. 2017 Feb
23;376(8):755-764. PMID: 28225684.
The bottom line: with pre- and post-MRI programming, pa-
tients with pacemakers and AICDs may undergo non-thoracic
MRI.
There are now MRI conditional pacemakers. However, the
majority of pacemakers in circulation are not MRI conditional.
In general, all of the guidelines recommend avoidance of MRI
when the patient does not have an MRI conditional pacemaker
for fear the magnet will dislodge the internal lead, alter the inter-
nal circuitry or heat the leads resulting in tissue damage. Since
2000, more recent devices have fewer ferromagnetic parts and
may be safer for MRI. MRI conditional pacers and defibrillators
are safe for MRI but only under certain circumstances. They still
require preprogramming.
In this study, they conducted a prospective multi-center eval-
uation of adults with non-MRI conditional pacemaker/ICD
undergoing a non-thoracic MRI across the United States. The
study protocol involved pre-scanning and turning the pacers
and ICDs off. If the subject was completely pacer dependent
then the pacer was set to asynchronous pacing mode. After the
scan, the devices were reprogrammed and interrogated.
Subjects had to have a thoracic ICD or pacer implanted after
2000 and undergo an extrathoracic MRI. They were moni-
tored by a team of people capable of intervening if there were
complications.
The primary composite endpoint was pacer or ICD failure
(death, generator or lead failure, loss of capture, new ar-
rhythmia, etc). Secondary endpoints were electrical issues
like P wave or R wave amplitude decrease suggesting the
pacer or ICD was experiencing more resistance or problems.
What did they find? They conducted the protocol on 1000 pac-
er cases and 500 ICD cases. 35% of the MRIs were of the brain,
about 40% involved the spine and about 10% were of the lower
extremity or pelvis.
4 patients reported feeling something weird in their chest like
heating but they did not experience complications. No pa-
tient who underwent the study protocol had a major problem.
However, the one patient who accidentally underwent MRI
while their ICD was left on had device failure.
There were some minor secondary endpoints reached in
about 1-4% of the pacer group and 20% of the ICD group but
these were not considered major issues (for example, the P
wave decreased in amplitude).
 Some patients had multiple MRIs over time and there was no
relationship between the number of MRIs and these outcomes.
What does it mean? It shows that under precise clinical set-
tings, MRI probably can be done in patients with newer pacers
and ICDs with minimal risk to the device. However, the clinical
settings are stringent and require device reprogramming before
and after the MRI. If it isn’t done, the one case demonstrated
failure of the device. Some aggressive stroke centers may try to
implement MRI procedures to work through this but overall this
may affirm our current ED practice of avoiding MRI in patients
with pacers/ICDs as a bad idea.
Paper Chase 2:
Epi, Anaphylaxis, and the Elderly
Sanjay Arora MD and Michael Menchine MD
Take Home Points
We are much less likely to give epinephrine to older pa-
tients with anaphylaxis.
Intramuscular administration of epinephrine has fewer
side effects than intravenous administration.
The most common serious cardiovascular complications
included ventricular tachycardia and troponin elevation
but no patients died.
Kawano, T et al. Epinephrine use in older patients with anaphylaxis:
Paper Chase 3:
clinical outcomes and cardiovascular complications. Resuscitation.
Lysis of Intermediate Risk PE
Sanjay Arora MD and Michael Menchine MD
2017 Mar;112:53-58. PMID: 28069483.
The bottom line: we are much less likely to give epinephrine
to older patients with anaphylaxis than younger patients. This
study also found that IM epinephrine in the older group led to
fewer adverse cardiac effects compared to IV.
Anaphylaxis is defined as a serious allergic reaction that is
rapid in onset and may cause death. This is bad. The sickest
patients do receive epinephrine but we often hesitate in older
patients for fear of cardiac complications. Is this myth or reality?
Is it better to administer epinephrine IV or IM?
The authors of this study conducted a retrospective study at 2
urban hospitals. They evaluated the EMR to identify all patients
with a diagnosis of allergic reaction. They reviewed the charts of
these patients to look for evidence of anaphylaxis with a history of
allergen exposure with hypotension, shortness of breath, etc. They
separated the patients into two cohorts; young patients between
17 and 50 years of age and older patients greater than 50 years.
The primary outcome of interest was the proportion of pa-
tients who received epinephrine. The secondary outcome was
cardiovascular complications such as ventricular fibrillation,
stroke, elevated troponin, STEMI, etc.
August 2017: Volume 17, Issue 8 | www.emrap.org
They identified almost 3000 patients with allergic reactions.
492 met the criteria for anaphylaxis. About 25% of these pa-
tients (122 patients) were older.
What did our practice look like? 61% of patients with ana-
phylaxis in the younger cohort received epinephrine com-
pared to 36% in the older cohort.
Cardiovascular complications occurred in 5 patients who re-
ceived epinephrine. 4 of these patients were in the older co-
hort, 1 in the younger cohort. These complications included
ventricular tachycardia and elevated troponin but no patients
died. In the older cohort, 3 out of the 4 patients received IV
epinephrine compared to only one who received intramuscu-
lar. The patient who received IM epinephrine had a transient
ST depression that resolved spontaneously. They also reported
more frequent dosing errors when epinephrine was given IV.
What does this mean? Conclusions are limited due to the small
number of patients in the study but this is likely the largest trial to
date looking at this issue. Due to the retrospective design, it is un-
clear why some patients received epinephrine and others didn’t.
It may be that the providers did not give epinephrine to patients
with a history of cardiac disease and the complication rate may be
higher if given to all comers. Epinephrine clearly is safe in young-
er patients. It is pretty safe in older patients. If you are going to
give it, give it intramuscularly rather an IV in older patients.
Take Home Point
A 3 year follow-up study of patients with submassive PE
found that about 30% will have mild dyspnea and func-
tional limitation regardless of whether or not they received
thrombolytics.
Konstantinides, SV et al. Impact of thrombolytic therapy on the
long-term outcome of intermediate-risk pulmonary embolism. J Am
Coll Cardiol. 2017 Mar 28;69(12):1536-1544. PMID: 28335835.
The bottom line: this 3 year follow-up study of patients with
submassive PE found that about 30% will have mild dyspnea
and functional limitation regardless of whether or not they
were given thrombolytics.
There is still a lot of debate about the management of pulmo-
nary embolism. The only thing we seem pretty sure about is us-
ing thrombolytics for pulmonary embolism with cardiovascular
collapse. The data on thrombolytics in submassive PE has been
difficult to interpret. Submassive PE or intermediate risk PE is
usually defined as having right ventricular strain and positive
cardiac biomarkers.
15
 After years of small trials, the Pulmonary Embolism Throm-
bolysis Trial (PEITHO) trial showed that thrombolytics were
associated with a lower rate of hemodynamic deterioration
but had a higher risk of major bleeding and no difference in
mortality. The net effect of this is that most people aren’t
keen to give thrombolytics. However, a subsequent small trial
suggested that tPA prevented long-term chronic pulmonary
hypertension. The debate continued about whether IV tPA
was a good idea.
What did they do? This was a continuation of the PEITHO tri-
al. They followed up the subjects from the original study which
consisted of 1005 patients from sites around the world for two
years. Patients were randomly assigned to receive tPA and hep-
arin versus heparin alone for submassive PE. 28 sites participat-
ed in long term follow-up accounting for 709 of the original pa-
tients. They conducted a chart review at each site for outcomes
and did a clinical and echocardiographic study for any patient
they could find.
What did they find? Of the 709 people followed for 2 years,
the overall mortality was similar among those who received tPA
versus the control group (20% versus 18%). This was not statis-
tically significant.
They were only able to conduct actual clinical follow-up on
175 patients in the tPA group and 183 patients in the placebo
group. They found that 36% in the tPA group and 30% in the
control group had persistent dyspnea or functional limitation.
On echocardiography, mild right ventricular dysfunction was
seen in 44% of the tPA group and 37% of the placebo group.
Chronic pulmonary hypertension was pulmonary hyperten-
sion was diagnosed in only of the tPA group and 3% of the
placebo group. This was not statistically significant.
What does this mean? Overall, these findings support recom-
mendations that submassive PE be treated with anticoagulants
and supportive care with tPA to be reserved for cases where he-
modynamic compromise occurs. We still don’t know if interven-
tional cardiology techniques to remove clot portend any short
or long-term benefit for submassive PE.
Paper Chase 4:
Keeping Opioids Safe at Home
Sanjay Arora MD and Michael Menchine MD
Take Home Points
A survey study found high rates of unsafe storage of pre-
scription opiates among adults with children in the home.
The majority of adults do not have a strong opinion re-
garding the effort to lock up opiates giving us the oppor-
tunity to influence them.
16 EM:RAP Written Summary | www.emrap.org
McDonald, EM. Safe storage of opioid pain relievers among adults
living in households with children. Pediatrics. 2017 Mar;139(3).
PMID: 28219969.
The bottom line: this survey study found high rates of unsafe
storage of prescription opiates among adults with children in
the home.
The opioid epidemic could be called America’s largest public
health problem. In 2014, more than 10 million people report-
ed using opiates non-medically. Children and adolescents are at
particularly high risk of first time abuse as the chance of parents
or grandparents having opiates lying around is high.
Does this really happen? Yes. Among children less than 6 years
old hospitalized for ingestion of pills, opiates are the most com-
monly implicated medication. To minimize the risk of children
getting into prescription opiates, most national organizations
suggest providers promote safe use (use only what you need),
storage (in a locked cabinet) and disposal (give back unused
medications).
This is an area where we can make a difference. How much
difference can we make?
The study randomly selected almost 5000 adults with children
less than the age of 18 from a national web based panel. The
response rate was close to 98%. The sample was divided into
parents with children between 1-6 years of age and 7-17 years
of age.
Overall, about a third of participants with young children
said they stored opiates safely. This dropped to 12% in the
group with older children.
A larger study looking at all households with and without
kids found only 1 in 10 people stored their opiates safely.
They asked questions about attitudes via the health beliefs
model and about three-quarters of those surveyed thought
that children who accessed opiates could suffer serious
health consequences. About 70% agreed that storing opiates
in a locked cabinet would be a good way to prevent access.
Only about 15% felt that it was not worth it.
When answering detailed questions about the effort behind
locking up opiates, almost 50% were neutral. This is a good
thing as there is a large percentage that isn’t locking up their
opiates and may be influenced.
There is a lot of pressure on us to help fix the opioid epidemic
including prescribe less, look up databases, etc but this seems
like something we can actually do that has the potential for
impact. Lock up those pills!
 interest. The outcome of interest was development of an ar-
Paper Chase 5: rhythmia that developed within 8 hours of ED presentation and
Do All Chest Pain Patients required some form of management. Development of ischemic
Need Monitoring changes was not an outcome. During the validation phase, all
Sanjay Arora MD and Michael Menchine MD patients remained hooked up to the monitor for at least 8 hours.

What did they find? They included 796 patients with chest pain
Take Home Points
from the two centers. The mean age was 64. 66% had a normal
Patients who are free from chest pain and have a normal or non-specific ECG. Only 15 patients (1.9%) developed an ar-
or non-specific ECG are unlikely to develop arrhythmia rhythmia. Most were atrial fibrillation. There were two cases of
within 8 hours of ED presentation and may be safely re- SVT and one case of ventricular tachycardia. The rule was 100%
moved from cardiac monitors. sensitive but only 36% specific.
Patients with prolonged intervals, left bundle branch What does it mean? Given that less than 2% of patients with
block and left ventricular hypertrophy were considered to chest pain developed a cardiac dysrhythmia, it seems silly to
have abnormal EKGs. keep them all on the monitor. The Ottawa Chest Pain Cardiac
Monitoring Rule represents a first step at trying to provide evi-
Only 1.9% of monitored patients developed an arrhyth-
dence for when patients can safely be brought off the monitor.
mia. The majority were atrial fibrillation with rare SVT and
This probably affirms your practice of taking patients off a mon-
ventricular tachycardia.
itor when they are well-appearing with a normal EKG. This study
affirms this as a safe practice. This doesn’t suggest that anyone
Syed, S et al. Prospective validation of a clinical decision rule to iden- who fails the rule needs monitoring.
tify patients presenting to the emergency department with chest
pain who can safely be removed from cardiac monitoring. CMAJ.
2017 Jan 30;189(4):E139-E145. PMID: 28246315. Difficult Conversations
Sam Ashoo MD
The bottom line: this is a prospective evaluation of the Ottawa
Chest Pain Cardiac Monitoring Rule that found patients who are
Take Home Points
free from chest pain and have normal or non-specific ECG do
not develop unexpected arrhythmia within 8 hours of ED pre- Difficult conversations with other physicians should ideally
sentation and may be safely removed from cardiac monitors. happen outside of the work environment and not on shift.
Evaluation and management of ED patients with chest pain is Don’t be accusatory but provide observations. Be direct.
challenging. The complaint is common but only 10% will have
Physicians also experience mental illness that may be ex-
anything resembling a serious cardiac syndrome and most these
acerbated by our environment.
are not life-threatening. However, the American Heart Associa-
tion recommends patients undergo cardiac monitoring for sev-
You are an ED director and one of your partners has been con-
eral hours during their evaluation. This is fairly resource inten-
stantly negative. How do you start a conversation?
sive, especially with increased crowding and bed demand.
The best approach is a direct approach with some finesse. Pull
However, there have not been any widely used, validated
the person in a private area or have the conversation outside of
decision support tools that use evidence to allow patients to
work. Get coffee or lunch.
come off the monitor so this decision is usually left to physi-
cians or local policy and procedures. How do you start the conversation? Don’t be accusatory but
give your observation. “I’ve noticed you’ve been more negative
What did they do? The authors conducted a prospective valida-
lately. You seem more aggressive and anxious. Is there some-
tion of the Ottawa Chest Pain Cardiac Monitoring Rule at two
thing going on?”
academic centers between 2013 and 2015.
If this doesn’t yield a result, you can consider using a personal ex-
The Ottawa Chest Pain Cardiac Monitoring Rule is very
ample. “I remember early in my career, I used to dread my shifts and
straightforward. Patients may be removed from monitoring if
I had a high anxiety level. It wasn’t until a few years that I calmed
they are free from chest pain and have normal or non-specific
down and lost my anxiety. Is this what is going on with you?”
ECGs. Abnormal ECGs included prolonged intervals, left bun-
dle branch block, left ventricular hypertrophy, etc. Ask about their family. “How are things with your children? Is
everything ok outside the department? Do you think you are
The authors collected the time the patient became free of
working too much? Do you need some time off?”
chest pain and analyzed the ECGs blind to the outcome of

August 2017: Volume 17, Issue 8 | www.emrap.org 17

 Be direct. “I’m your partner. It is my job to make sure you have
a long and good career at our hospital. As part of that, I need
to make sure you are functioning well and your mental state is
good so that you can have longevity in your career. At the rate
you are going, that won’t happen. Complaints are increasing and
medical care is starting to suffer. Nurses don’t want to talk to
you. This causes problems with patient care. They won’t come
to you with information you need to know to treat your patient.
You will miss things like vital sign or exam abnormalities. These
things are important and you won’t get that information. I’m
here to help you. Tell me what is going on.”
It could be something innocent or something that will require
treatment. Ashoo received a series of complaints about a physi-
cian that culminated in an encounter with a suicidal patient. The
patient was suicidal after the death of the dog. The physician told
her not to feel sad because they eat dogs in China. When Ashoo
discussed the complaint with him, he thought he was being fun-
ny. The common thread of the complaints was his sarcasm.
Ashoo said, “There are appropriate and inappropriate times
to be sarcastic. It should be avoided in the patient-physician
interaction. It is not the best approach.”
Mental illness does not spare physicians. We work in a pressure
cooker environment. Mild mental illness can be exacerbated by
our environment. This is often not discovered until the physician
is in practice and exposed to the stressors all at once. You need
to be able to have this conversation.
The approach is always the same. “Hey, I care about your ca-
reer. I want you to have a great longevity. Here are some things
we’ve noticed. The nurses don’t want to talk to you. The con-
sultants complain you are aggressive with them when they give
you no for an answer. If you lose your cool with the consultant,
you are losing the battle on behalf of your patient. Run through
your rationale with the consultant. If it doesn’t yield a result, try
a different approach. Go up the chain of command. You have
resources you can use.”
“We’ve had people with anxiety disorders that have taken
medications. Physicians need help like anyone else. Is that what
is going on with you?”
1) Don’t delay. Have the conversation early because time will
damage this physician’s career.
2) Be direct. Couch it as trying to help the physician’s career and
longevity.
3) Use personal examples.
4) Do your research. Review the chart involved in the complaint.
5) Ask about underlying mental illness. There are so many avenues
for treatment. It is important to address it and talk about it.
18 EM:RAP Written Summary | www.emrap.org
None of these conversations or scenarios is easy. Your partners
will learn to appreciate you and your practice more if you devel-
op a method for addressing this early.
A family complained about a physician being uncaring and
committing malpractice. The nursing staff was trying to find the
physician to treat ventricular fibrillation. The physician walked
in, looked at the monitor, said “Shock him” and walked back out
when the patient went back into a normal sinus rhythm.
Ashoo talked to the physician. The physician was deaf in one
ear and unable to hear the room from where he was sitting.
He couldn’t hear them yelling for him until someone came to
find him.
The physician got a hearing aid with significant improve-
ment. His relationship with the nursing staff has improved
now that he can hear them.
Don’t have these conversations during a shift.
From the Mailbag
Rob Orman MD and Anand Swaminathan MD
We received several emails on the recent segment on anxiety
and chest pain.
From Jedd Roe MD. “I was listening to May EM:RAP on the
way into shift and really enjoying the chest pain and anxi-
ety discussion. I was delighted to hear about Paul and Jeff’s
study that addressed an issue we so frequently see. Ironically
enough, the first patient I saw was exactly what they were
discussing. I typically ask about stressors in the patient’s life
and was getting positive answers about her job when her hus-
band leapt out of his chair like a student in class, dying to be
called on, and said how wife had been up until 4 am the previ-
ous day and worked late through the night. One thing I do in
these cases besides the HEART score is to give a small dose of
benzodiazepine like [I use a] GI cocktail. I know it has no diag-
nostic significance but it often makes them feel better. I don’t
give them anything to go home with but I discuss stress man-
agement techniques and put those in the discharge plans.”
“I honestly don’t feel the malpractice risk concerns many
of our colleagues described. I’ve always felt it was ok to
introduce that stress and anxiety may be a contributor and
as long as you told the patient about concerning symptoms
of ischemia to prompt return, your treatment plan is immi-
nently defensible.”
From Graham Inglesby. “This to me is an essential component
of every low risk chest pain patient that I’m planning on dis-
charging. It is one thing to fly by and say ‘Things look great!
See your doctor ASAP.’ Taking one to two extra minutes at
 bedside can change the entire encounter. For the patient I
have a gestalt that anxiety or stress may be a likely etiology of
their presentation, I often follow a script after their work-up
is complete.”
“How are you feeling? Better? Good. We’ve done a lot of tests
because we take chest pain really seriously. So far things look
great. We’ve taken a look at your heart with an EKG, some blood
tests that show no damage right now. An x-ray shows your
lungs, your heart and your bones all look good. Why else does
our chest hurt? Sometimes it might be life just getting to us. So
how are things going? Any troubles at home or work, family or
finances. I can run a lot of tests here but I don’t have a stress
meter. However, just looking at you, it seems like there is some-
thing troubling you.”
“About a third of patients will have waterworks. They will open
up for a moment and say what is troubling them. Most will feel
such catharsis and relief that someone took the time to make
sure they are safe and actually listen to them. Of course I give
my usual chest pain precautions, offer outpatient resources,
hold their hand and get them going. This makes for a reward-
ing encounter for me and the patient. I still diagnose them with
nonspecific chest pain and give them stress reduction tips in
their discharge paperwork.”
Ross B had this to say regarding the segment on cardioversion
of atrial fibrillation based on the study showing the risk of
August 2017: Volume 17, Issue 8 | www.emrap.org
thromboembolism following ED cardioversion is very low. “I’m
wondering about the description of patients sent home after
rhythm control who were not anticoagulated. My understand-
ing of the CHADs2 and CHADs2Vasc score is that they calcu-
late the risk of clot in patients with chronic atrial fibrillation, not
those patients with paroxysmal atrial fibrillation or those who
had atrial fibrillation but are cardioverted into normal sinus
rhythm. Can you comment on how to rationally approach those
patients and if these scores are applicable?”
The heterogeneity of atrial fibrillation makes prognostica-
tion challenging. A simple rule is that the stroke risk is similar
in those with paroxysmal and chronic atrial fibrillation. Most
use CHADs or CHA2DS2-VASc because it helps us gauge
risk. If they score high, they may be higher risk for stroke and
might need to start anticoagulation from the emergency de-
partment. If they have a low score or it is the first episode,
you might start aspirin and defer the decision for additional
anticoagulation to the primary care physician.
More recent guidelines are not recommending aspirin or
other anticoagulation for otherwise healthy patients with
a low CHADs score. The Canadian Cardiovascular Society
Guidelines does not recommend aspirin or anticoagulation in
a patient with a low CHADs score and without coronary or ar-
teriovascular disease. http://www.onlinecjc.ca/article/S0828-
282X(16)30829-7/fulltext
19
 NOTES

20 EM:RAP Written Summary | www.emrap.org