Chaser before tPA shots?

by Andrew Summersgill, M.D.

Before taking shots of tPA, don’t forget your CHASER: a mnemonic for when NOT to give tPA in Stroke/MI patients:

  • C: Cancer
  • H: Hemorrhagic stroke in past. Hypertension>180/>110*
  • A: Aortic dissection, AV malformations
  • S: Stroke (ischemic within the last 3 months). Sugar (glucose 400mg/dL )*
  • E: Exsanguination/active bleeding
  • R: Relative contraindications

This is a quick outline to consider before pushing lytics. There is overlap between these two subsets, and obviously the list is more comprehensive, so be sure to look up the latest guidlines.

*stroke specific (ischemic, hemorrhagic, etc)

RPM

Disasters occur when events overwhelm a response’s capabilities.

The Simple Triage and Rapid Treatment (START) is used in such extreme situations to maximize salvageable victims with available resources. This algorithm can be remembered with the acronym RPM:

  • Respirations
  • Perfusion/Pulses
  • Mental Status

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Black-tagged patients have a low likelihood of survival with available resources.
Red-tagged patients require immediate attention.
Yellow-tagged patients are in serious condition, but can be delayed.
Green-tagged patients have relatively minor injuries.

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References
Rosen’s Chapter 139, Disaster Preparedness
FEMA Hospital Emergency Response Training Manual
http://www.remm.nlm.gov/StartAdultTriageAlgorithm.pdf

Crash Course in Advanced EKG

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

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

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

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

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

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

6.) BER

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

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

An Interview with Paul Thistle

by Jonathan Lee, MD

I hate pigeon-holing Africa into a giant monolithic entity but I couldn’t help looking out into the foliage and thinking to myself, “if this isn’t Africa, I don’t know what is”? In the northeastern corner of Zimbabwe less than a hundred kilometers from Mozambique and a three hour bumpy ride from its capital, Harare, which I was pre-warned about with a “this is the part where your teeth fall out!” is Karanda Mission Hospital. It sits on top of a hill nestled in lush vegetation serving the very community it looks over. I spoke with Dr. Paul Thistle, an OB/GYN physician from Canada about his lifelong work in the country. Since graduating residency he has worked in Afghan refugee camps in Pakistan in the 1980’s and has also worked in Indonesia as well. But for most of his career he has worked in Zimbabwe, serving 19 years in rural communities not only performing surgeries but also treating patients with HIV and tuberculosis, arguably the number one killer of adults in Zimbabwe and Subsaharan Africa. I discuss what emergency medical care in rural Zimbabwe is like and how he has learned to adapt to an inadequate healthcare system.

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So you’ve worked for the last nineteen years in Zimbabwe. What made you want to work here versus Canada or the United States?

“Well, I had always known that I wanted to work in a resource poor area of the world. It’s a different environment here. People need help here. And to be honest the work is more satisfying as well.”

Tell me about Zimbabwe’s healthcare system.

“In the rural areas, 60 percent of hospitals are being run by churches and 40 percent by the government. In Harare, it’s more like 10 percent mission and 90 percent government. Currently about 15 percent of the population gets medical aid but that still leaves the majority without any access to healthcare. The government hospitals are expensive and so a lot of people even from Harare end up coming all the way up to Karanda hospital for their medical care because it is much more affordable.

Zimbabwe has had a bumpy past. There is a lot of discontent, there are no jobs, there’s certainly no health care system to speak of. There is a lot of disillusionment in the country and in the end, the people suffer.”

So, Zimbabwe has had a lot of violence in the past, most recently in 2008 during the elections. What was it like working as a physician during that time? Did you see a lot of injuries?

“We saw a lot but we didn’t see as much as you think. At Howard Hospital where I used to work we saw about 30 traumas related to the violence in our catchment of 300,000 and of those, 2 people died. Is that a lot? Well more people die in Toronto of car accidents in one day so by volume it’s not. A lot of what was on the news was sensationalized but at the same time those weren’t accidents. It was politically charged violence which is always bad but at the same time you have to stay neutral.”

I would have expected there to be a lot more. What is the prehospital medical infrastructure in Zimbabwe? Is there an EMS system here?

“In theory yes. In Zimbabwe, we have private healthcare and then there’s public healthcare. In private, they may have an ambulance service depending on your insurance. Maybe you can pick up the phone and they’ll pick you up. But in the public medical system, which almost all Zimbabweans utilize, there is no emergency medical system, even in Harare. You would have to put the person in the back of the taxi and rush them in somehow.”

What about rural areas?

“Nothing, no.”

So if someone doesn’t have a car and there aren’t any taxis around which is typical in rural Zimbabwe and lets say you have some acute illness that needs to be managed, what happens?

“Well, as long as we’re talking acute, they’ll die on the way to the hospital. Or they may not even make it that far, they’ll just die at home. Or they will come in with complications, like a ruptured appendix for example. So most people can hire a car if there are vehicles around. But there isn’t a guaranteed emergency medical system. We do happen to have an ambulance truck in the hospital, but then again we can’t staff it. We don’t have a driver to go out. If somebody calls us, then we might look around for a driver and a nurse, then send it out.”

How often do you receive calls?

“Not very often, most people just walk in.”

And this isn’t a special 3 digit phone number, it’s the number to the hospital?

“That’s correct. Because nobody pays for the service, right? You’d have to have a driver on stand-by for emergency services. A nursing team would have to be available. And then there is the mileage of the vehicle. Who pays for all of this? The hospital can’t afford it. So we do have an ambulance but its the logistics of getting it out in the fields. And plus the roads are rough. Even if you have an MI or a stroke, you’re not gonna get to them within thirty minutes. And also we don’t have an intensive care unit. We’re trying to intensify our emergency response but in reality, the hospital doesn’t have a cardiac care unit or neurosurgical care. So if there is an acute cardiac or neurological emergency, what are we going to do about it? So it’s more than just one link that’s broken in the system. So if they survive an MI and make it to the hospital, we’re looking at morphine and heparin. We can’t do coagulation studies studies either so you have to make the best judgement. Normally you give morphine and an aspirin and try to reduce long term complications. So you will see it all first hand.”

So then you diagnose the MI wIth just an EKG? Can you test cardiac enzymes?

“Last time I checked, we needed to fix our EKG machine. It wasn’t working the last time I heard. And no we can’t do cardiac enzymes. So if someone comes in with crushing chest pain, you have to rely on your clinical judgement and experience.”

“Most young doctor, if you can’t make a diagnosis, you order more lab tests or imaging tests but you have to learn to make decisions based on what you have. We don’t have the luxury for extra tests.”

Doesn’t that become frustrating as a physician when you can’t diagnose?

“Yes but being a doctor isn’t just about that. You do the best you can with what you have. But kindness and compassion goes a long way. The medicine part you won’t have trouble figuring it out.”

Do you envision yourself staying in Zimbabwe in the future?

“Well we’re working it out one day at a time. You can never predict the future. Some things about home I miss and something’s about Zimbabwe I would miss. The work is better here. The job is more satisfying. The income is much lower, but that’s not the reason I would decide.”

Dr. Thistle is married to his Zimbabwean wife Pedrinah who is a nurse-midwife and has two sons, James and Alex. He lives within the compounds of Karanda Mission Hospital and frequents the “bumpy ride” to and from Harare to visit his sons and pick up groceries of which his guilty pleasure is potato chips.

ENT by Dr. V – Emergency Nosebleed and Therapy

by Ramona Vanel, MD

I remember in my third grade current events our weekly assignment was to tackle the who, what, when, where and why’s of the events. Today we will discuss the WHO, WHAT, WHEN, WHERE, WHY of nose bleeds!

  • WHO

The epidemiology of nosebleeds seems to be in a bimodal distribution:
school aged children and middle aged men.

  • WHAT

What are nosebleeds … seriously?! Ok, this seems intuitive but there is more to this question than meets the eye. We will discuss that more a bit later in this post.

  • WHEN

Most often this occurs during the winter season.

  • WHERE

This is a GREAT QUESTION. There is a difference between ANTERIOR nosebleeds and POSTERIOR nosebleed; with the majority being anterior nose bleeds.

  • WHY

This requires taking a very good history. Ask about a history of bleeding disorders such as von Willebrand, history of ITP/ HHT, history of taking blood thinners, nose picking, a recent URI, trauma, etc.

Nosebleeds are quite common to see in the ED. It is imperative that the ED physician will know how to tackle cases of both anterior and posterior nosebleeds.

Anterior nosebleeds mainly arise from the sphenopalatine artery. There is a great network of vessels that form a rich vascular network called the Kiesselbach’s plexus.

With posterior nosebleeds there is another rich network of arteries in the posterior nasal cavity. The bleeding that occurs from posterior nosebleeds are from the posterior ethmoid arteries. Keep in mind that most bleeds are anterior.

I have my own way of tackling nosebleeds, and I am sure every ED physician will have their own style to addressing it themselves.

Keep in mind the ABC’s. Make sure their airway is intact, especially with posterior nosebleeds. Check the blood pressure!

You may want to consider testing H/H and coagulation studies based on history of HHT/ ITP, history of plavix, aspirin, or coumadin use. You may want to consider imaging with a history of trauma.

Start by having an ENT kit handy which includes suction and a RapidRhino. I look at the unaffected nare make sure I can clearly identify the nasal septum (remember that bleeds can be bilateral). Remove any clots that may be visible or ask patient to blow their nose. Then, tell the patient to HOLD PRESSURE to the nose externally in the sniffing position for about 15 min. (The above image is a nice trick to keep in your back pocket to help your patients hold pressure .)

After 15 minutes, recheck to see if the bleeding has stopped. If not, then reach for your RapidRhino. Some individuals will coat their RapidRhino with bacitracin which is not only an excellent idea, but also the recommended method. This is of course to prevent infection and possible TSS (Toxic Shock Syndrome). Normally the RapidRhino is successful, without the need for further intervention.

In the event the RhapidRhino is not successful, you may choose to cauterize the bleed. It is important to visualize the bleeding vessel for cauterization. Silver nitrate is great for cauterization. Please be mindful not to perforate through the nasal septum, especially when dealing with bilateral nasal bleeds.

Patient may follow up with ENT within 1-2 days after RapidRhino is placed. There is no general consensus if antibiotics are needed for prevention of Toxic Shock Syndrome.

Posterior nosebleeds maybe be a bit more aggressive and continue to bleed regardless of nasal packing. In the event of posterior nosebleeds, one can insert a foley to tamponade the bleeding. JUST REMEMBER THE AIRWAY. All patients who receive posterior packing with either an intranasal sponge or a foley will need an ENT consult and likely admission. After foley insertion, patient will need to be monitored in the intensive care unit.

Remember, most nosebleeds are not critical and Remember your ABCs.

Reference
Tintinalli JE, Kelen GD, Stapczynski JS, Ma, OJ, Cline DM, editors. Tintinalli’s Emergency Medicine. 7th ed. New York: McGraw-Hill; 2011.

Mini-Conference: Anorectal Abcesses

presented by Dr. Ken Adams

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

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

Ice Ice Baby

presented by Dr. Vikash Mishra

911 is called for a middle-aged male found sleeping on the street by a bystander. EMS recognizes the patient as a chronic EtOH user. On arrival to ED, the pt is obtunded and only responsive to pain.

v/s: HR 60, BP 90/60, RR 18, Spo2 95%. The rectal temperature is 83 degrees (an oral temp is unable to be obtained).

Two peripherals IVs are placed, warm IV fluids are started, and a warming blanket is applied. Pt is subsequently intubated and a central line is placed.

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Significant Labs: CO2 18, BUN/Cr 34/1.5, EtOH negative, Trop 0.059, CBC normal, Coags normal, CK 1676. ABG: 7.179/42/41/64% Lactate 3.27

Diagnosis: ACCIDENTAL HYPOTHERMIA

There are 650 deaths/year in the U.S. from primary hypothermia. 66% of pts are male and occurs more commonly in the elderly due to impaired thermoregulation.

Hypothermia = temp< 35 degrees C (95 degrees F) and classified by severity:
Mild 32-35 C (90-95 F), Moderate 28-35 C (82-90 F), Severe <28 C (82 F)

EtOH is the most common contributory factor to hypothermia.

DDX: Must consider anything causing altered mental status based on the history and physical. Also must consider any conditions that are due to Increased Heat Loss, Decreased Heat Production, or Impaired thermoregulation

Diagnostic Testing: Labwork is generally of little help. A variety of electrolyte derangements can be seen as well as renal failure in the severely hypothermic. Of note, the severely hypothermic can have a coagulopathy related to enzyme dysfunction from the cold and acidosis. ABG’s can be difficult to interpret in the hypothermic patient, but can demonstrate a variety of derangements, e.g. metabolic (lactic) acidosis, respiratory acidosis or alkalosis. Imaging studies are of little utility, but the pt’s presentation and the differential diagnosis of the altered mental status may necessitate a Brain CT.

EKG: Numerous EKG changes can be seen in hypothermia, including prolonged intervals, ectopy, AV blocks, bradycardia, and a variety of atrial & ventricular arrhythmias. Classic finding is an Osborn J-Wave seen in 80% of hypothermia cases (this pt’s EKG had them in leads V3-V6. The pt also had AFib, a QRS of 132, and QTc of 493)

Treatment:
1.) Mild Hypothermia: passive rewarming
2.) Moderate Hypothermia: passive rewarming, active external rewarming
3.) Severe Hypothermia: active external rewarming, active internal rewarming, extracorporeal blood warming

Passive external Rewarming: Remove from the environment and wet/cold clothing, blankets.
Active external Rewarming: Warm blankets, heating pads, hot water bottles
Active internal Rewarming: Warm IV Fluids, warm/humidified air
Extracorporeal Rewarming: hemodialysis/filtration, etc.

Be aware of Core Temperature Afterdrop: Continued decrease in the pt’s temp even after removed from the environment and started rewarming. One possible explanation is that peripheral extremity rewarming returns cold acidemic blood to the core, causing further temperature drop and acidosis. Another possibility is peripheral vasodilation when warming causes circulatory collapse. No consensus exists regarding how to best prevent or treat afterdrop.

References
Mulcahy, A. (2009). Accidental Hypothermia: An Evidence-Based Approach. Emergency Medicine Practice, 11(1).

Omeprazole before endoscopy in GI bleeds

PPIGIBleed

http://www.nejm.org/doi/full/10.1056/NEJMoa065703

Week 3.

• Conclusions
o In pt with bleeding peptic ulcers, improvements in clinical outcomes appreciated with those who received pretreatment with omeprazole prior to endscopy
o Optimal acid suppression with omeprazole aids in clot formation showing
• Fewer actively bleeding ulcers were seen on endoscopy
• Reduction in the need for endoscopic treatment
• Accelerates signs of bleeding resolution (ulcers with clean bases)- allowing for early discharge
o Omeprazole proves to stabilize clots, prevent recurrent bleeding, initiate healing

52 in 52: Angioplasty vs ‘Lytics in AMI

LyticsvsPCI

http://www.nejm.org/doi/full/10.1056/NEJMoa025142

Our second week installment of ALiEM’s 52 Articles in 52 Weeks.
(More info @ http://academiclifeinem.com/52-articles-in-52-weeks-landmark-em-articles-2013/)

Quick Fix:
Previous studies demonstrated the superiority of PCI over thrombolytics in treating STEMIs. Not all hospitals have cath labs, so is there benefit to transferring STEMI pts presenting in the community to facilities that can perform PCI?

This study’s composite endpoint demonstrated there was a benefit; the composite consisted of mortality, reinfarction, and stroke. There was a 75% relative risk reduction of reinfarction seen in PCI over ‘Lytics. However, “the reduction in the risks of death and stroke did not reach statistical significance.

It’s also worth mentioning that 4% of the pts screened were not stable enough to be transferred. Of 559 pts who eventually did get transferred, 35 developed arrhythmias, with no deaths en route, leading the authors to conclude “the transfer of patients was found to be safe.

Emergency Medicine in the South Bronx