I started the EM Res Podcast and Blog about one year ago, and things have taken off in that time.  To accommodate the growth of the podcast and the blog, I am excited to announce that I have a new website: www.emrespodcast.org.  ​

The new site offers a number of exciting advantages.  First, it offers a better aesthetic and navigation across all platforms, including smartphones and tablets.  It is overall much cleaner and easier to use.  It is also everything EM Res in one location.  You get the blog, the podcast, and the show notes all in one place.  The podcast is still on iTunes, but is also hosted here for streaming from any device.  The new format allows for easier commenting and interactivity between myself and readers/listeners.  The search functionality is much easier, allowing you to search blog posts and podcast episodes all at the same time.  I can also make more dynamic, involved posts with more capabilities than I had before.  Finally, you get one click connectivity to all my social media outlets, including Facebook, Twitter, Google, Vimeo, and Tumblr.   

For those of you who are die hard Tumblr fans and following that, the Tumblr site is not going away.  You can still follow along there, as all future blog posts and podcasts will be pushed to Tumblr as well.  ​

Thank you all for reading, listening, and making this such a fun and rewarding experience for me.  Hopefully you get as much out of it as I do.  I’m looking forward to what the next year has to bring, and please bookmark/head on over to emrespodcast.org!​

Peritonsillar Abscess

About a month ago, I posted a video with the following history and questions.  Let’s take a look at the answers: 

A 23 year old male presents to the ED with 4 days of sore throat, getting much worse over the last 24 hours.  You note that he has a muffled sounding voice.  On exam, he has trismus, uvular deviation, L sided tonsillar asymmetry, and could seriously use a breath mint.  Your attending decides to perform an intraoral ultrasound to evaluate the patient, and you see the above image.  

1. What do you see?

As correctly pointed out by a few, what you were looking at was a peritonsillar abscess, noted as the anechoic circular area adjacent to the tonsillar tissue.  This is the most common deep space infection of the head and neck.  

2.  What is the next step in management?

First, you want to make your patient comfortable.  Start with some pain medicine.  Steroids have been shown in some studies to potentially decrease hospitalization time,  and perhaps help with symptom relief, but there is question as to the risk-benefit profile.  Use your clinical discretion.  Perform intramural US to confirm the presence of a PTA and distinguish from cellulitis.  Once comfortable, you may proceed with needle aspiration (no significant evidence that aspiration or ID are different in terms of outcomes).  I prefer ultrasound guidance.  More on that in the podcast.  

3.  Should you start antibiotics or not?

Antibiotics are indicated, with Penicillin and Flagyl being 98-99% effective in the below referenced review.  Nontoxic patient can be treated as an outpatient, while those who fail aspiration or I/D or are toxic may require surgical consultation.  

Want more in depth info?  Check out the podcast!

The latest episode of the EM Res Podcast talks about where new residents should start if they are looking to get into the FOAMed world.  It can be daunting to start out, but once you get into it you’ll find it a great way to learn anytime, anywhere.  

This is by no means an exhaustive list, and if your blog or website was left off it is by no means a slight.  There are many great resources out there.  Go to www.lifeinthefastlane.com to see their full listing of EM/CC Podcasts and blogs.  Remember, start with basic core content, and branch out from there.  If you are a more seasoned EM resident or attending, go big from the start.  

Also, check out the actual responses to my Twitter poll on the top 3 FOAMed resources for the new EM Resident here. 

A Case of a Sore Throat

A 23 year old male presents to the ED with 4 days of sore throat, getting much worse over the last 24 hours.  You note that he has a muffled sounding voice.  On exam, he has trismus, uvular deviation, L sided tonsillar asymmetry, and could seriously use a breath mint.  Your attending decides to perform an intraoral ultrasound to evaluate the patient, and you see the above image.  

1. What do you see above?

2.  What is the next step in management?

3.  Should you start antibiotics or not?

From the last post: 

A 57 y/o male presents to the ED with a chief complaint of sudden loss of memory. His wife reports that when he awoke this morning he was his normal self, had coffee and ate breakfast but while his wife was showering he suddenly told her that he felt “weird”. His wife realized that he had forgotten everything that had happened not only this morning but also the night prior and was very tearful and frightened which is unlike his normal personality.  Last night he drank four beers which he usually does every weekend. His wife denies any trauma, or LOC, slurred speech or weakness. His only medical problem is hypertension. He has no significant family history, does not smoke and denies any illicit drug use. On physical examination, initially on arrival to the department he was only oriented to self but after an hour on he began to remember events from the night prior and became oriented to time and place. He was noted to persistently have trouble making new memories as he scored 0/3 when asked to recall three objects and was also noted to occasionally ask the same questions multiple times.  He can easily remember past events such as his first car and his birthday. Cranial nerves are intact, he has normal sensory and muscle strength in all four extremities bilaterally, normal finger to nose testing and also has a normal gait. The rest of the physical exam is unremarkable

1) At this time, what testing should be performed?

Answer: No further testing is needed. 

2) What is your diagnosis?

Answer: Transient Global Amnesia

3) What is the prognosis for this diagnosis?

Excellent prognosis.  The attack typically resolves in 24 hours

Transient global amnesia(TGA) is a rare condition where there is a sudden, temporary episode of memory loss that cannot be attributed to a neurologic condition such as epilepsy or stroke. Patients do not have any focal neurologic findings before or after the attack and there is no history of recent head injury; however, 1/3 of patients have an identifiable precipitating event.   Females are more likely to have an emotional precipitating event while in men the precipitating event is likely to involve physical exertion. The deficit is in short-term memory and ability to make new memories resulting in speech perseverance. Long-term memory remains intact as demonstrated in our clinical case where our patient was able to recall things such as his birthday and his first car. During the event the patient is aware of their amnesia because their consciousness is not effect often leading to anxiety. In one study, 11% of patients exhibited “emotionalism” (as our case patient experienced) and 14% “fear dying”. The average duration lasts between 2-8 hours and per diagnostic criteria resolves within 24 hours making this a rather benign disorder. The cause of TGA remains unknown at this time and about 6% of patients experience a relapse of TGA per year. These patient’s are not at an increased risk for stroke and management of these patients is simply reassurance and time. 

Resources:

1) Miller, J. W.; Petersen, R; Metter, E; Millikan, C; Yanagihara, T (1987).”Transient global amnesia: Clinical characteristics and prognosis”. Neurology 37 (5): 733–7. 

2) Quinette, P.; Guillery-Girard, B; Dayan, J; De La Sayette, V; Marquis, S; Viader, F; Desgranges, B; Eustache, F (2006). “What does transient global amnesia really mean? Review of the literature and thorough study of 142 cases”. Brain 129 (Pt 7): 1640–58. 

3) Pantoni; Bertini, E; Lamassa, M; Pracucci, G; Inzitari, D (2005). “Clinical features, risk factors, and prognosis in transient global amnesia: a follow-up study”. European Journal of Neurology 12 (5): 350–6

Welcome back Dr. Krystle Shafer, who has the following conundrum for us:

A 57 y/o male presents to the ED with a chief complaint of sudden loss of memory. His wife reports that when he awoke this morning he was his normal self, had coffee and ate breakfast but while his wife was showering he suddenly told her that he felt “weird”. His wife realized that he had forgotten everything that had happened not only this morning but also the night prior and was very tearful and frightened which is unlike his normal personality.  Last night he drank four beers which he usually does every weekend. His wife denies any trauma, or LOC, slurred speech or weakness. His only medical problem is hypertension. He has no significant family history, does not smoke and denies any illicit drug use. On physical examination, initially on arrival to the department he was only oriented to self but after an hour on he began to remember events from the night prior and became oriented to time and place. He was noted to persistently have trouble making new memories as he scored 0/3 when asked to recall three objects and was also noted to occasionally ask the same questions multiple times.  He can easily remember past events such as his first car and his birthday. Cranial nerves are intact, he has normal sensory and muscle strength in all four extremities bilaterally, normal finger to nose testing and also has a normal gait. The rest of the physical exam is unremarkable

1) At this time, what testing should be performed?

2) What is your diagnosis?

3) What is the prognosis for this diagnosis?

From our last post: “EMS brings in a 22 year old male who has presented multiple times previously with suicidal gestures. Tonight, they state he took an unknown quantity of acetaminophen about 4 hours prior to arrival. You draw a 4 hour acetaminophen level, and it is 105 micrograms/mL. Feeling good that he is below the treatment threshold of 150 micrograms/mL, you are just about to call the psychiatrist when the patient tells you he actually ingested “Tylenol PM.” Does this matter? Is the patient medically clear?”

Pimpsmanship 101: if an attending asks you a question like that, the answer is not going to be “yes, the situation you presented me is the right answer with no change.  Medically clear.”  Unless your attending is doing some 5th level Jedi-type pimping.  

Tylenol PM is a combination of acetaminophen and dihenhydramine.  Diphenhydramine overdose is concerning in and of itself as it can cause the anticholinergic toxidrome.  In this case, however, the diphenhydramine is cause for a different concern.  

Diphenhydramine can cause delayed GI motility, potentially causing delayed acetaminophen toxicity.  In fact, any agent that causes delay in GI motility (think opioids) can cause this problem.  Because of this, your 4 hour level is not going to be reliable.  If you are concerned that a patient may have delayed motility or gives you a history of co-ingestion of any drug that causes slowed GI motility, you should check an 8 hour level, and treat if toxic based on the Rumack Nomogram.  The same goes for extended-release acetaminophen preparations (see references below)

This case and topic highlights the importance of the history in patients presenting to the emergency department with potential toxic ingestions.  In particular, remember these 3 tremendously important points:

1. When did they ingest, what did they ingest, and how much?  This obviously gives you the basics.  It also is helpful in calculating toxic doses (do you know the toxic dose of acetaminophen in mg/kg?)

2. Were there any co-ingestants?  Obviously this makes a huge difference in this case.  In all cases, you want to know the full spectrum of what you may be facing, and what toxidromes you need to look for.  

3. To what medications did they have access?  This is a crucial historical point, and this is one of those cases where not showing up with your cynical hat can prove foolish.  Remember, patients who have ingested medications often have done so with the intent to harm themselves.  Now they are talking to a doctor who is trying to save them.  They may not be straightforward with you.  Knowing what medications were available to them may give you a hint about what they really took.   

Talk to family, those who live with them, and definitely talk to your prehospital providers.  This is also a big pearl for your oral boards: If anyone is available to provide extra history, they are there for a reason.  Ask the question: is there anyone else who can provide me with additional history?  This extra history can prove to be vital.  In this case, it is the difference between treating your patient appropriately or sending them to psych to crump.  

Do you want to learn about Point of Care Ultrasound (POCUS)?  Have you ever wanted to learn about point of care echocardiography from Haney Mallemat (@CriticalCareNow)?  Have you ever wondered what I am like in non-blog, podcast or Twitter form?

You can accomplish all of these things by attending the Wellspan York Hospital Point of Care Ultrasound Conference, June 13-14, 2013.  This is a two day course that covers both basic and advanced POCUS.  Didactic sessions will be mixed with hands on scanning with live models and phantoms.  Two day attendees will earn 16 hours of Category 1 CME.  

The course itself is located in York, Pennsylvania.  We are about 45 minutes north of Baltimore, and 2 hours west of Philadelphia.  For more information, including the schedule and fees, check out: http://www.yorkhospital.edu/default.aspx?program=2&type=text&content=165

If you have any further questions, please contact me here, on Twitter (@BobStuntz), or email me (bobstuntzmd@gmail.com).  We hope to see you there!

EMS brings in a 22 year old male who has presented multiple times previously with suicidal gestures. Tonight, they state he took an unknown quantity of acetaminophen about 4 hours prior to arrival. You draw a 4 hour acetaminophen level, and it is 105. Feeling good that he is below the treatment threshold, you are just about to call the psychiatrist when the patient tells you he actually ingested “Tylenol PM.” Does this matter? Is the patient medically clear?

The answer later this week, unless you come up with it first!

Altered mental status is an all too familiar complaint to emergency physicians.  The differential is broad, and includes multiple life threatening diagnoses.  We of course think the worst: does the patient have a head bleed or a stroke?  Are they septic?  Have they ingested some life threatening drug or toxin?

All too often, we get caught up in the rush to get the patient to CT without thinking about a few common, easily diagnosed, and relatively easily fixed problems that require no radiation.  It is something we all do from time to time.  I have noted four diagnoses that I and my residents occasionally forget to look for, and wind up kicking ourselves over later.  Think about these early, and look for them routinely.  

1. Glucose: In my experience this is far and away the most commonly forgotten cause of AMS.  Glucose is the syphillis of AMS.  It can cause seizures, mimic strokes, and make a patient look like they are having an MI.  I have seen patients sent to CT for stroke and even intubated, only to later discover they have a low serum glucose.  Ask EMS for a fingerstick reading on all AMS patients.  If they did not check, you should.  Consider D for Dextrose along with disability in your ABC’s (and remember to ask for a chem stick on your oral boards!).  Treatment options range from oral glucose in the awake, to IV dextrose in those with contraindications to oral repletion (1-2 mg glucagon IM is an option if IV access is not immediately available).  What you give depends on age:

Adults: 1 mL/kg D50

Kids: 2 mL/kg of D 25

Infant/newborn: 5 mL/kg D10 

2. Hypoxia: You would think this is a simple one, but it does get missed.  A patient is not themselves at home, and a family member brings them in.  In the heat of the moment, no one tells the triage nurse they are oxygen dependent and ran out of their home O2 the day before.   This one is as simple as sticking a pulse ox on and administering supplemental O2.  

3. Hypercarbia: Seen frequently in COPD, and thus usually in an older, sicker population, we often forget to look for hypercarbia as we look for other causes of AMS.  This is as simple as getting a screening VBG or iSTAT (an iSTAT gets you your glucose as well).  As I described in a previous post, a venous pCO2 < 45 mmHg is nearly 100% sensitive in the evaluation of hypercarbia.  Remember, however, that it does not correlate well to an absolute number.  The interpretation: Normal pH and pCO2 < 45 mmHg on your VBG, and you are clear.  If the patient is acidotic or has an elevated pCO2, get an ABG to get a true evaluation and ventilate them (invasively or non invasively as indicated).  

4. Hepatic encephalopathy: You would think this would be easy: Your patient is yellow, or has a history of liver disease.  But again, patients prone to hepatic encephalopathy tend to be overall sickly, and I see extensive workups to rule out ICH, sepsis, or other causes of AMS, but lack a simple ammonia.  Do not forget to check that ammonia if the patient has any risk factors for  hepatic encephalopathy.  Treatment involves initiation of lactulose and further investigation as to the root cause.  

Three of these can be checked and treatment initiated within 5 minutes of arrival (apply a pulse ox and get an iSTAT to check a sugar and screen for hypercarbia).  While you always want to fully work up your patients with AMS, do not miss these oft forgotten, easily identified and fixed causes of AMS.   

To any American EM residents who follow the blog and/or podcast, good luck on the inservice exam tomorrow.  Remember to take the exam seriously.  While your results do not directly help or hurt your cause to become board certified EP’s, the results will give you great insight into your knowledge base, and will help you identify areas where you need to improve.  

Do whatever you normally do before big tests today.  Some people don’t touch anything study related.  I always feel the need to review last minute stuff the day before any big test.  Just do what you normally do before a big test (you’ve taken a few at this point).  

Also, if you have not yet, check out www.emergencyboardreview.com (@EMBoardReview on Twitter).  There is a nice comprehensive review on the site from Dr. David Pierce from University of Buffalo.  It is about 1hr 45 min, and a nice wrap up.  

There has been a fair amount of discussion recently about the national epidemic of prescription drug abuse in the United States.  I recently read an interesting article in EM News on the topic.  I have some personal opinions on the subject, and I feel that this is an important topic for Emergency Medicine Residents and Registrars to consider.  

First, I notice frequently that we refer to the medications for which we write as “narcotics.” This sends a shiver up my spine.  I have been told that at one point, pharmacologically “narcotics” referred to any drug with sleep inducing properties.  In the United States’ common vernacular, it has become a legal term.  Narcotics by US legal definitions include cocaine and heroin.  While I understand that amongst physicians we know what we mean by this, remember that our patients knows narcotics from TV (do you think when they say Narcotic on “Law and Order,”  they are referring to legally obtained prescriptions?).  I think when we refer to these medicines as narcotics, to the lay person we are associating ourselves with illegal drugs, making us look even more like the drug dealers inflicting this scourge on society.  I am not a drug dealer.  I would submit that we should avoid referring to what we prescribe as narcotics, and I try my best to do so myself.  (We all slip of course!)  

The question is always who is to blame for the skyrocketing abuse of these medications?  I was taught that pain was the 5th vital sign, and spent residency seeing articles in how bad we are at addressing pain in the ED.  Now I am told I am responsible for killing and addicting my patients.  What are we to do?  As a resident, you hear both sides.  Every attending with whom you work will have a different opinion.  It is going to be your job to synthesize those opinions and develop your own practice.  

I personally rarely will write for more than 1-2 day’s worth of opioid and opioid like analgesics (obviously there are exceptions to this).  I believe in this especially in the “abdominal pain NOS” and other NOS (not otherwise specified) groups, where your prescription may mask pain that should prompt their return to the ED.  I know there are other EP’s who will write for more or less.  I also hear blame placed on primary care providers.  I think we as physicians should stop trying to blame each other as there is not one group at fault for the problem.  It is clearly multifactorial.  I think there are a few things we can do to address the problem from our standpoint and make our treatment of pain better and safer for us and our patients.    

1. Talk with your patients.  Acknowledge their pain, treat them in the ED, and discuss prescription options.  We should be telling our patients of the side effects of prescriptions opioids/opioid like analgesics (constipation, overdose, addiction, impaired function, masking concerning pain).  Explain your recommendations.    

2.  Review patient records and drug databases if available.  If they are doctor shopping or shuttling prescriptions, recognize this and don’t compound the problem.  

3. Try to avoid treating Press-Gainey.  Remember, we are doctors and not concierge at the Bellagio.  If it takes a few minutes to sit down and discuss pain management with your patient, it is worth it to avoid blindly throwing Vicodin at someone who may abuse it (or let it get in the hands of their kids) just because you feel like it will make them score you higher.  This gets into the issue of people rating their doctors like a customer service industry in general, which is a debate all its own.  I know this issue is not so simple, but I think it is something that is important and that we should all talk about.  

4.  Do not punish patients who truly need it because you think everyone asking for pain meds is a “drug seeker.”  Just because the terminal cancer patient is asking for dilaudid does not mean he/she is a “drug seeker”  in the classic sense.  Perhaps they are seeking drugs because they are truly in pain.  This leads to my last point:

5.  Treat each patient as an individual with a fresh set of eyes.  One day, that “drug seeker” may going to come in with something catastrophic, and you do not want to miss that.  Just because your last 3 patients were scamming you does not mean the fourth one is doing the same.  Take each complaint seriously.  If you evaluate them and determine they do not have an emergency medical condition, by all means hit the brakes.  If you do not want to be treated like an illegal drug dealer, then do not treat your patients like an illegal drug buyer.  

ACEP recently released a clinical policy on the topic that I think presents reasonable recommendations.  This is obviously a controversial topic, and there are no absolute right answers.  As a trainee, you need to evaluate your own beliefs and learn from your supervisors.  But above all, remember, your job is to do what is right for your patients.  Do that, and you will never go wrong.  

One of the most common knee jerk reactions in medicine is to give oxygen.  Short of breath?  Oxygen.  Chest pain? O2.  Abdominal pain….you get the idea.  And why not, oxygen is harmless, right?  While we do require oxygen to live, and it is 21% of our atmospheric pressure at sea level, oxygen in the medical setting should be considered a drug.  It is a substance that you are administering to treat a medical condition, and it has been shown to have deleterious effects in the right setting.  

Situation 1

A 70 year old COPD patient is brought in by EMS with a complaint of worsening shortness of breath.  He was noted to have a pulse ox reading of 85% on EMS arrival, so a non-rebreather mask was placed.  You order a few nebulizer treatments and some steroids before you saw him, and now his oxygen is up to 98%.  You’re feeling much better about yourself, and you consult the hospitalist for admission.  An hour later, the hospitalist shows up raving about admitting an unconscious patient to the floor.  ”Why isn’t this guy going to the unit?”  You go back to check on your patient, and he is full-on gorked.  What happened?  In this case, oxygen has led to hypercapnic respiratory failure.  

The traditional teaching is that COPD patients depend on low oxygen to keep their reparatory rate up and blow off CO2.  Thus,  if you cause hyperoxia, you knock out their hypoxic reparatory drive, they retain CO2, and then they tank.  Truthfully, the hypoxic reparatory drive only accounts for about 10-15% of your respiratory drive, while CO2 levels contribute most of the rest.  So what does happen in these people when you give them high levels of O2?

A. The Haldane effect:  When we increase blood oxygen levels, hemoglobin binds to mostly oxygen (instead of CO2), leaving CO2 by itself in the blood.  As it builds up in the blood, the acute COPD patient cannot blow it off.  

B. Reversal of hypoxic pulmonary vasoconstriction: In COPD, hypoxic portions of lung are vasoconstricted to match ventilation and perfusion.  When you cause hyperoxia, this vasoconstriction eases, and you get vasodilation in these areas.  This leads to a V/Q mismatch, and increased dead space in the lung.  This again leads to poor ventilation and an increase in plasma CO2.    

There is probably some effect of decreased hypoxic respiratory drive, especially when you drive the paO2 incredibly high, but it’s true effect on hypercapnea is oven overstated (1).  This has been a contentious topic, especially in the prehospital setting.  However, there was a nice article in BMJ in 2010 that really answered the question in my opinion (2).  While it has its flaws, it showed that patients with true COPD exacerbation who received oxygen titrated to a sat of 88-92% had a significantly lower mortality rate than those who received high flow oxygen (2% versus 9%), and less incidence of hypercapnia.  

So what should you do?  First ask the patient if they know where they live normally in terms of a pulse ox. If they are always at 96% at their doctor’s office, 96% is fine.  If they live at 88%, that’s ok.  Get the non-rebreather off and titrate your oxygen to their level.  I have seen some resistance to this from nursing and prehospital providers, however, this is a great opportunity to educate and engage others in the patient’s care.  Get the mask off, put them on nasal cannula, and titrate their oxygen.  It is easy to overlook these patients, as they may initially look better, and if you do not think about this you will have someone crash on you.  

(Like COPD?  Look out for an upcoming EM Res Podcast episode…)

Situation 2 

You resuscitate a cardiac arrest patient.  You intubated them, but you never talked with the respiratory therapist about vent settings, and you never checked an ABG to titrate your oxygen.  You’re a busy man, “ain’t nobody got time for that.”  Your ICU is booked, and your patient stays in the ED for a few hours.  The intensivist has some choice words for you when he comes down and finds the vent to still be set to a FiO2 of 100%.  What’s his problem?

This is another case where oxygen has been shown to be bad for patients.  Hyperoxia following cardiac arrest has been shown to lead to increased free radical production and oxidative stress, alveolar injury and apoptosis, and increased in hospital mortality (3).  With patients across the country spending more time boarding in the ED waiting for an ICU bed, we have to realize that this is not something we can ignore.  Check ABG’s after intubation and titrate your vent settings.  

As you can see, oxygen is not always completely benign.  Titrate your oxygen in COPD patients.  Check for hyperoxia and alter your vent settings to correct it in your resuscitated cardiac arrest patients.  (This is where you need an ABG).  

On a side note, thanks for your patience with the lack of posts and podcasts in the last month.  I have been working on the Emergency Board Review Podcast series (On Twitter @EMBoardReview, and on iTunes as well!).  Hopefully you have been liking that.  If you don’t know about it, go check it out, 100% free Emergency Medicine US Board review.  Not taking the American EM Boards?  It’s still great review material for Emergency medicine no matter where you are.  Look out in the upcoming weeks and months for the EM Res Podcast and Blog to be back up at normal speed.  As always, I’d love to hear your feedback and suggestions!

1. New, A.  Oxygen: kill or cure? Prehospital hyperoxia in the COPD patient.  Emerg Med J. 2006 February; 23(2): 144–146.

2. Austin MA et al. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: Randomised controlled trial. BMJ 2010 Oct 18; 341:c5462. 

3. Kilgannon JH, et al. Association Between Arterial Hyperoxia Following Resuscitation From Cardiac Arrest and In-Hospital Mortality. JAMA Vol 303, No 21, June 2, 2010;2165-2171. 

We had some good responses, and everybody was right on.  

This is an image of Herpetic Whitlow.  Herpetic whitlow is an infection of the digits caused by herpes simplex virus (HSV).  It can be caused by HSV 1 or two.  The common pathophysiology is inoculation of the affected area through a break in the skin and subsequent exposure to bodily fluids.  

Patients present with a complaint of intensely painful lesions on the digits, usually at the distal phalanx.  A prodrome of severe pain is followed by eruption of vesicular lesions.  The prodrome may include pain felt in the upper arm or axilla as well.  The lesions appear as classic HSV, grouped vesicles on an erythematous base, and may coalesce, as in this case.  This is a self resolving illness, and usually will improved within two weeks. Treatment is symptomatic care with analgesia, although in the immunocompromised, oral antivirals should be considered.  

In children and healthcare workers, infection is usually secondary to oral HSV infection (the classic buzzword is a dental hygienist or dentist), while in adults exposure to genital HSV is more common.  

The big take home: do not attempt to incise and drain these lesions.  Doing so may lead to bacterial superinfection, delayed healing, or, the more feared complication, systemic spread.  You wouldn’t want to be the one who caused herpes encephalitis, would you?

For a more detailed overview, check out this well done Medscape article. 

What is that?

A young female presents with complaints of left thumb pain and swelling preceded by a few days of upper arm and axillary pain. She states she has not had any trauma, fevers, chills, or engaged in any high risk sexual behavior recently. She was told by a friend to come to the ED so that we could “cut it open and drain it.” You see the above cutaneous finding with no other notable abnormalities of the left upper extremity. Wat is this and are you going to cut it open?

Hey faithful readers, and belated Happy Holidays!  Sorry for the lag in posts, but I’ve been spending time with the family, and working on this…

You may remember back a few months I started doing some board review stuff, but noted it was going to be a huge project to tackle on my own.  Fortunately, Jon Schonert from EM Chatter (@EMChatter, www.emchatter.com), came to the rescue with similar interests and a keen ability to make websites.  We have gotten some help from around the EM blog and podcast world (@EMBasic, Steve Carroll to name one), and are rolling out www.emergencyboardreview.com.  

This is a work in progress, but our goal is to provide you with high quality, high yield, just-the-facts FREE board review material to help you pass the EM Inservice, Qualifying, and ConCert exams.  My introduction video can be found here, I give an audio intro on my podcast here.  

Down the road, we will be getting these on iTunes as well, and the website will be expanded.  For now, find us here:

Twitter: @EMBoardReview

Facebook and Google+: Emergency Board Review

Website: www.emergencyboardreview.com 

There’s already a lot of great content there.  The GI videos are up along with the first cardiology and ortho videos.  Keep checking back.  

As promised, here are the ABEM links to the exam info and the Model of the Clinical Practice of Emergency Medicine.  Looking forward to helping you prep for the boards!

Inservice exam

Qualifying Exam

ConCert Exam

Model of the Clinical Practice of Emergency Medicine

I got a bunch of critical care questions for the Weingart-Mallemat interview for the last podcast.  Of course, I did not have time to get them all answered, and I felt some of them were already well answered elsewhere.  So I’m going to answer a few of them with my references for good resources already out there, starting with this question:

“I have a situation that’s come up a few times recently and I haven’t been able to find a good answer to it in my lit search. Patient with a fib and in CHF. Slightly hypotensive (SBP 100-110), but not unstable or warranting cardioversion. 2 different attendings have recommended giving calcium gluconate prior to the Ca-channel blocker to “blunt the hypotensive effect”. The best explanation I’ve gotten was that it allows AV nodal blockade to occur, but the calcium influx to the peripheral vascular system prevents vasodilation.  

So: What is the pharmacokinetics for giving calcium prior to CCB in the a fib patient and is there an alternative (besides electricity) in the hypotensive patient?

In terms of the alternative to electricity and treating the crashing a fibber, I will refer  you to the EMCrit Podcast, Episode 20.  As usual, Weingart has a great approach to these patients.  The problem is (and I hate to break this to all the electricity-heads out there): cardioversion does not work in these really sick a fib patients.  These are not the younger paroxysmal a fibbers who come in for their monthly cardioversion.  They are usually chronic a fib patients, and have irritable hearts and you get a few minutes of sinus rhythm, at best, before you have them flip right back into  a fib with RVR.  So this will take some medical finesse.  Listen to his podcast, he has a fantastic approach. Make sure if there is an obvious reason they are in a fib (like being floridly sceptic), treat that source.  Make sure they have a good preload (US their IVC).  When the heart is beating that fast, it does not fill so you want your preload optimized.  Don’t be afraid to give them fluid.  

Then comes rate control and the calcium question.  Many times, in the patient with borderline pressures, reducing their heart rate will actually increase their pressure (more cardiac filling time).  But does calcium prevent hypotension with dilt?  

The pharmacology of CCB’s is nicely reviewed here.  Where people are getting this idea is actually from studies on verapamil (see this and this).  There has been one RCT looking at Ca pretreatment with Diltiazem and it could not detect any statistically significant blunting of the BP drop with Ca administration.  This is partially because almost no one got hypotensive in the study.  It is also interesting because pharmacologically, diltiazem should actually have more peripheral effect than Verapamil (Verapamil is supposed to be more cardioselective.  Dilt can be used for BP but has more cardiac effects than dihydropyridine groups).  Yet the study did not really pan this possibility out.  

My take: Ca is a safe drug to administer, and it has some good inopressor activity in its own right, so why not try it?  Optimizing electrolytes in irritable hearts is a goal anyway.  Try lower doses of dilt, and repeat.  Weingart has a link to a slow infusion he sets up.  I haven’t tried this, but same principle: lower and slower to slowly control HR and not tank BP.  I have also used digoxin loading in a few patients (0.25 mg initial dose).  Digoxin decreases chronotropy, and this does take up to 6 hours, but it also causes vasoconstriction and increased isotropy.  Reliable pharmacists have told me this can be within the first hour, and anecdotally I can say I’ve seen the patients who failed low slow dilt and needed digoxin did get better within the first hour.  Not fully better, but any better is good in this population.  

In a related post, check out my previous post of diltiazem versus metoprolol in rate control for rapid a fib.  Hope this helps, and we’ll be answering more of the left out questions as time goes on.   

Episode 8: Critical Care with Scott Weingart and Haney Mallemat

I somehow tricked Scott Weingart and Haney Mallemat into sitting down and talking EM-Critical Care with me.  We go over Critical Care fellowships and answer your questions about EM/CC.  Should all residencies be four years?  Where do the experts see our specialty in 10 years?  Should we abandon the landmark technique for central line placement?  What about video versus direct laryngoscopy?  A ton of great stuff in just an hour of your time.  Either follow the link above, or find us/subscribe on iTunes.

I have had a few cases recently where, while supervising a procedure with a resident, the procedure does not go perfectly smoothly, and I have had to step in and lend a hand.  This usually results in the resident beating themselves up.  I’m here to talk you down off the ledge. 

Remember, you are learning how to do procedures the attendings you are working with have done hundreds, or even thousands, of times.  We are naturally going to be more skilled procedurally because, as has been said, practice makes perfect.  If you compared my intubating skills to an EM attending who has been working for 15 years, they would probably have me beat.  It is the natural progression of things.  

Look at it as a learning experience.  As a resident, when I missed a procedure, it usually wound up teaching me some very good lessons about what I was doing wrong and what I could do better.  

So how can you turn these instances into positive learning experiences?

1. No matter how many times you have done a procedure, check your ego at the door.  I vividly remember the first intubation I missed as as resident.  I had had the good fortune of being successful for about 90 intubations in a row, with near half of those being on very carefully selected OR patients.  I was going in a bit cocky.  It was an obese status epileptics.  I jokingly told someone that I had done a tough intubation on a skinny guy earlier that week I thought would be easy, so this lady would probably wind up being the opposite of what I expected and be the easiest tube of my life. It was not.  I had not mentally prepared myself for the procedure, and when I got in and saw it was difficult, I panicked.  

2.  Ask the attending what they did differently, and make them give you a good answer.  On that same tube, my attending went in calmly, visualized structures, passed a bougie, and smoothly threaded the tube over that.  I asked the attending what they had done and why.  The attending jokingly responded, “I took my time, visualized my structures, and it was easy.”  I now use this as a joking phrase, but if you are an attending, explain to the resident what you did.  What did you see?  What kind of view did you get?  Why did you choose the bougie, and how do you use it?  What would you have done if that did not work?  Debrief the resident, and residents demand an adequate debriefing.  

3.  Do your own mental debriefing, and review the procedure step by step.  Did you position the patient appropriately?  Was your equipment positioned appropriately?  Did you have everything in the room that you needed?  What did you attending do differently that helped them get it?

4.  Identify where you went wrong, and make a mental note for the next time.  Maybe you had the US machine over your shoulder instead of line of sight during that central line.  Maybe the LP patient was not sitting correctly.  Perhaps you forgot a crucial piece of equipment.  Figure it out, note it, and don’t do it next time.  

5.  Take a deep breath, and relax.  This is how you learn, and you will miss procedures.  Murphy’s law dictates that your attending will come in and have a super easy time, leaving you to think they never miss procedures, and you are somehow incompetent because you do.  Everyone, at every stage in the game misses procedures.  I did an LP with a resident recently that went very smoothly for me.  A few weeks before that I had done an LP on my own when I was covering our ED during resident conference that was one of the more difficult ones I have ever done, and I had to throw in the towel.  We all miss sometimes.  

Do not freak out about these missed procedures.  Use them as a learning tool.  Approach it like a mechanic: break down every step, figure out where you went wrong, and fix it for next time.  Attendings, make sure that you talk your resident through your process and debrief them appropriately.  Making it seem easy and not explaining yourself only makes the resident feel worse, and winds up teaching them nothing.  This is a true learning opportunity.  Don’t miss it!

Well, Episode 7 is here, and I finally caved.  That’s right, I’m doing an airway talk.  

Obviously, airway is king.  As it turns out, the A in ABC’s stands for airway and not Ativan. (I know, I was surprised when I first learned that too).  There is a ton of stuff out there on airway, and I wanted to try to do the topic some justice.  Part of my job is to synthesize what is out there for you, the EM Resident.  

So I sat down with Tom Kehrl and we talked tips and tricks of the airway.  These are pearls we have learned in going to courses, listening to lectures and podcasts, and intubating a bunch of people, and supervising a bunch more.  

You can find the show notes here.  I put a ton of links to podcasts, articles, and websites that go over many of the topics we discuss.  Might be the most robust set of show notes yet, and you definitely want to be online when you check it out.  Get it on your usual podcast apparatus or click the link below:

http://emrespodcast.libsyn.com/episode-7-airway-tips-and-tricks-i

Today we have our first post from Bryan Wexler, MD.  Bryan is currently a fellow in Disaster Medicine and Emergency Management.  Check out his bio on our guest author page.  He also incidentally holds the title as the real most interesting man in the world.  Being a disaster medicine specialist, Dr. Wexler is going to tell us all about the world of disasters, how to prepare for them, and what we all need to know in future posts.  But first, an intro…

In wake of Hurricane Sandy and the immense devastation caused, states of emergency were issued and many were left homeless or without power.

For those involved in disaster planning and response the responsibilities are understood to a large extent.   However the question remains, “What does this mean for the average Emergency Medicine physician?”

One cannot prepare for every potential event and permutation, which is why an “All-Hazards” approach, with emphasis on general concepts over specific individual nuances and annexes on more likely events, is favored.  

As we have seen with the closing of New York University Langone Medical Center, among others following the hurricane, preparation is crucial not only for the facility itself, but also the nearby hospitals receiving an additional influx of patients.  While evacuation of a facility might be the cause of inadequate preparation or failure of plans, or might seem like an admission of defeat, ultimately it is a testament to an understanding of the safety of patients and staff.  Having good evacuation plans as well as mutual aid agreements with nearby facilities is important for continuation of care despite an adverse situation. 

The Emergency Department is essentially the front line of the hospital, and the physician its de facto leader.  With constant, well-documented problems of overcrowding, the Emergency Department has become adept at compensating and composing quick solutions to keep things running as smoothly as possible.  However, in a true disaster where resources are overwhelmed, these attempts may be inadequate.  As such, it is imperative to be familiar with ones hospital disaster plan, resources available in times of crisis, and the incident command system. 

Having a plan in place is just the beginning. Understanding the potentially far-reaching implications of events or loss of certain utilities is crucial in development of a good disaster response plan.  True preparedness also requires frequent testing of systems in order to discover and improve on inherent weaknesses as well as provide familiarity with the plan for when it is needed.

In future posts, we will go into detail about the specific components of a disaster plan and disaster management.  

Italie, Leanne; Marchione, Marilynn.  “NYU Hospital Evacuation: Hurricane Sandy Power Failure Moves More Than 200 Patients.”  The Huffington Post.  10 Oct 2012.  15 Nov 2012 http://www.huffingtonpost.com/2012/10/30/nyu-hospital-evacuation-hurricane-sandy_n_2044026.html.  

Koenig KL, Schultz CH. Koenig and Schultz’s Disaster Medicine: Comprehensive Principles and Practices. New York, NY: Cambridge University Press, American College of Emergency Physicians; 2010. eds.

A great conversation broke out the other day on Twitter, when it was asked by a US emergency physician if anyone sends home their low risk PE patients on LMWH.  An international discussion ensued, with EP’s from Sweeden, the UK, and the US to name a few discussing how they manage PE.  

Check out the initial conversation.

This discussion generated the links to a number of great references that support outpatient management of select patients with PE.  Check them out at your own leisure from the above link.  

This discussion has now been going on over the course of the weekend.  Michelle Lin also posted a great Paucis Verbis card about the PESI, or Pulmonary Embolism Severity Index score.  It is a great summary.  This link also contains a discussion amongst other great minds in emergency medicine on Twitter about this very topic.  

The resounding theme from US physicians: it seems most would like to/are willing to send low risk patients with PE home, but there is an overall fear of a bad outcome or litigation.  As was pointed out in all these discussions, our medical culture is more lawyer heavy, and the constant fear of a lawsuit makes us hesitant to take such risks.  

I agree wholeheartedly, however, with our international cohort.  This is something that is being done safely in other countries.  We regularly send home DVT patients on LMWH, something that was unheard of just years ago.  How many of these DVT patients have small PE’s that we are not picking up and do just fine?  Does it make financial sense to admit all of these people, some of whom go home in the first 48 hours anyway?  Do these patients benefit from being exposed to iatrogenic complications when we could do the same thing with them at home?

Furthermore, and perhaps more importantly, I feel we are picking up far too many PE’s.  How many people that we diagnose with small PE’s who have normal vital signs, minimal symptoms, and no residual DVT really benefit from our treatment, and how many do we harm with bleeding complications or medication reactions?  We have become so gripped with fear of the bad outcome and the ensuing lawsuit that we have lost sight of the most important question: is what I am doing helping the patient, or hurting them?

My take on all of this is that there is a fair amount of evidence that in a subset of patients with PE who have normal vitals, normal labs, and no residual DVT, and who are overall low risk with few medical comorbidities, outpatient treatment with LMWH is safe and can be done effectively as others are doing it around the world.  The PESI score is promising, but needs further external validation before you can apply it to our population as a whole.  Everyone is going to have their N=1 of the low risk patient who went home with a DVT and came back with a PE on LMWH, but you have to ask yourself, would being in the hospital have prevented that?  The answer is no.  

In order to do this in the US, as our culture stands currently, a few things need to happen. First, discussions like the ones that have been going on are a great start.  Great minds in EM need to come together and deem that this is a reasonable approach, and that it could be part of our standard of care. Second, further studies in the US need to push these boundaries and establish that this can be safely and effectively done.  Third, institutional initiatives, both from hospitals and their health systems and representative bodies such as ACEP and AAEM, are needed to come up with criteria for outpatient treatment and standardization of care.  I at this point would not send home one of these patients without that institutional support and agreement.  

The American College of Chest Physicians has suggested that patients can be discharged “early” after the diagnosis of PE is made is they are stable, low risk, have good follow up, and can inject LMWH.  Does this mean from the ED?  I’d like to think so, and the webpage I referenced would suggest that.  From my research, I cannot find any ACEP or AAEM guidelines that recommend discharge home from the ED in patients with PE.  

My hope is that soon we will be sending these patients home regularly.  For now, however, I will have to agree with Haney Mallemat and Simon Carley:

Another interesting case from Krystle Shafer, MD:

A 62 y/o Chinese American male presents to the ED with a chief complaint of nausea, generalized weakness, and vertigo. His physical exam is unremarkable with the exception of slight hand grasp weakness noted in the patient’s right hand compared to his left.  He has no noted gait abnormalities or nystagymus. His potassium is noted to be critically low at 2.4 and is repleted, and a noncontrast head CT scan is negative. The patient is diagnosed with hypokalemia secondary to viral gastroenteritis, acute vertigo, and is admitted.

Within hours of being admitted the nursing staff notes that the patient is experiencing progressive weakness. He is unable to transfer himself from stretcher to bed secondary to weakness. His entire upper right extremity is now weak and his lower extremities are becoming weak as well. He is able to lift left arm in the air for five seconds but cannot lift his right arm. Twelve hours later the patient is unable to move his arms or legs bilaterally secondary to profound weakness and is having difficulty speaking and with swallowing water. Light touch sensation remains intact on exam in his bilateral upper and lower extremities.  He continues to complain of nausea and vertigo.  He soon develops respiratory distress, and is emergently intubated.  It is thought that the patient has Guillain-Barre given the progressive nature of the condition.  

The patient had an emergent MRI, which demonstrated bilateral ventral-medial medullary infarct. This is a rare diagnosis this is often misdiagnosed as Guillan-Barre syndrome.  In 2007 there were only 40 reported cases in the medical literature and it only accounts for less than 1% of brain infarctions.  The most common presentation of this disorder is a progressive loss of motor function to the point of quadriplegia with associated dysarthria and dysphagia. Anatomically, the corticospinal tracts within the medullary pyramids as well as the hypoglossal nerve fibers are effected causing the above symptoms. Of note, light tough sensation is spared over entire body as well as sensory and motor functions for the face. Propriception and vibration sensation is however often effected as the medial lemniscal tracts are also found in the medial medulla.

This is clinically different from Guillain-Barre syndrome (which only affects the peripheral nerves) because it is typically not an ascending paralysis, facial muscles are spared, and autonomic dysfunction is absent. Diffusion-weighted MRI reveals a characteristic “heart-appearance” in the medulla as it did with our patient.  Like all strokes, these infarcts are closely linked to hypertension and arteriosclerosis: but what happens such that both sides of the medulla are infarcted at the same time? In patients who have bilateral infarct it is suspected that they have an anomalous branch of the vertebral artery which supplies both sides of the medial medullary instead of the normal expected circulation of bilateral branches of the anterior spinal artery. Overall prognosis is poor for these patients and they often suffer from quadriplegia for the rest of their lives.

Need a refresher on Guillain-Barre?

1. Look for a history of URI or GI infection preceeding symptoms.  
2. This is an acute demyelinating polyneuropathy that affects peripheral nerves
3. Early on, people experience extremity paresthesias, and then progress to a rapidly ascending symmetric muscle weakness
4. Hyporeflexia may be present (lower motor neuron sign), and patients may have autonomic dysfunction
5. Respiratory muscles and cranial nerves are involved later
6. Onset is hours to days
7. Treatment: Supportive care, IVIG, possibly plasma exchange

Ma,L et al. Bilateral medullary infarct presenting as Guillan-Barre-like syndrome”. Clinical neurology and neurosurgery. 2011; 113: 589-591. 

Tokuoka, K et al. “A case of bilateral medullar infarction presenting with “heart appearance sign”. Tokai J Exp Clin Med. 2007; 32 (3): 99-102.

AAEM.  A Focused Review of the Core Curriculum. 

A 32 y/o female presents with complaints of shortness of breath.  She has a leg immobilizer on, and had noticed some swelling in that leg earlier this week.  She is tachycardic, and had a pulse ox of 70% when EMS picked her up.  She is 98% on 6 L nasal cannula, but when she tries to exert herself in any way, she desats to the upper 80’s.  She is tachycardic, but her blood pressure is normal.  You take a look at her heart and you see the above image.  What is going on?  The answer, case, and outcome to come later this week in a new EM Res Podcast Case Conference.  

Hey everyone.  First, just wanted to say sorry for the 2 week or so absence.  My wife and I just recently had our second child, and between going back to work after paternity leave and not sleeping, I’ve been a bit preoccupied.  I’m back on a better schedule now, so thanks for your patience and understanding.  The next podcast, part 2 of the RUSH exam, should be out in the next few days.  

I recently was told of a case that got me thinking.  The situation and names have been changed to protect the innocent, or guilty as it were.  A young man presented to an ED with a foreign body that was, lets say, stuck on a very sensitive part of the body.  When he showed up, it had been on for a few hours.  He was in extreme pain.  A medical student picked up the case, and with the nurse, took it upon themselves to remove the foreign body, under the guise that it was “limb threatening” (At least I’m calling it a limb).  This was done without any attending or resident supervision.  Furthermore, the patient had no idea this was a student.  Fortunately the offending agent was removed, and the patient did well.  

As a medical student, or a junior resident, it can be tempting to take something like this on by yourself.  In a competitive world of residency and job applications, you want to stand out and look like a star.  The thought of doing a procedure on your own that saves a life or limb is tempting, and I can see how someone would want to impress their residents, upper levels or attendings.  You don’t want to be seen as passive.  You want to be aggressive, see patients, do procedures, and impress those around you while learning at the same time.  

I also remember the feeling as a med student of being the “third wheel.”  You do not want to bother people who are already busy, and you do not want the people you are trying to impress thinking you are needy.   But remember, being a cowboy and doing it on your own can backfire in a major way.  

First, most medical students are doing rotations at academic institutions, or institutions where at the very least the attendings want to work with medical students.  Obviously, if you are a resident, your attendings want to teach.  Teaching is what we are here for, and we will always take an interruption to help perform a  life or limb saving procedure.  We expect you to come to us.  

Second, even if you perform the procedure successfully, some people will see you as reckless, someone who is willing to take big risks and feels like they do not need help.  This makes it less likely down the road that you will be sought out for procedures.  

Third, we have a tough job in the ED.  We have a few minutes to inspire confidence and trust in our patients.  If a paint has something done under the presumption that a doctor is performing a procedure, or you do not fully inform them of your title and role, this can cause a serious amount of distrust if the patient discovers a student was doing an unsupervised procedure.  This puts the student at a disadvantage, as we already know patients are reluctant to have students perform procedures to being with.  

Finally, and most importantly, there is the risk to the patient.  Your job as a physician and student physician is to always take the best care of the patient possible.  You may think you know what you are doing and be completely wrong, or you may know what you are doing and have a bad outcome.  Regardless, you need to be directly supervised when performing any procedure unless told otherwise.  

So what is a student, or junior resident, to do?  Observe the following rules:

1. Err on the side of caution.  If you have any doubt as to what you are doing, or any question about the care you are providing, get help.  

2.  Don’t worry about appearing weak.  We want you to come get help in a critical situation.  We want to be involved, and we want to teach you.  

3.  Do not sit on critical patients.  Get a senior or attending involved early.  If you feel you cannot leave their side (i.e. performing CPR), send someone to get help.  

4.  Be aggressive, but know your limits.  If you have a question, run it by a senior.  ”This patient is tachycardic and borderline hypotensive, is it ok if I go see them, or do you want to see them with me?”

5.  Do not do any procedure without at least discussing it with someone senior to you.  

And finally, but informally, if a hacksaw is involved, you definitely should not be doing it on your own!

Alright Dr. Shafer, what is the answer to your 2 year old with a fever?

As was well pointed out in one of the comments, the differential diagnosis includes scarlet fever, rubella, and Kawasaki’s disease, as well as toxic shock syndrome.  The patient clinically does not likely have rubella, as she is up to date on her immunizations, and kids should get their first MMR between 12 and 15 months of age, plus the clinical picture does not really fit.  Labs were drawn, and a throat culture was taken.  Rapid strep was negative, with a subsequent negative culture, and labs (CBC, CMP, LDH, and CRP) revealed the following abnormalities: LDH 360, CRP 8.4, AST 107, ALT 67.  Given the concern for possible Kawasaki’s disease and abnormal labs, she was admitted to pediatrics.  On day five, she continued to develop high fevers which became unresponsive to acetaminophen  and additionally developed edema of her hands and feet. On day six she was given IVIG and high-dose aspirin. Within hours after her infusion of IVIG, her fevers resolved and by day seven she began tolerating PO, rash had almost completely disappeared, and her hands and feet were less edematous than the day prior. By day 8 the child was fever free for 24 hours and she was discharged home. Her cardiac echo was negative for coronary artery aneurysm.  So, the answers are as follows:

A) What is the diagnosis: Kawasaki Disease

B) What additional tests outside of the above need to be done: Echocardiogram

C) What is the pathology, treatment, and disposition: Pathology includes a progression of arterial lesions with accompanying vasculitis, endothelial activation and injury. The cause of Kawasaki’s remains unknown. Disposition includes hospital admission with IVIG and ASA therapy (see below)

D) Are mom and her unborn baby going to be ok: There are no reported incidences of this disease affecting pregnancy

Kawasaki’s disease was first noted  by Tomisaku Kawasaki in 1961.  He published the first Japanese case report of the disease in 1967 and by 1974 he published the first English language case report of 50 Japanese patients presenting with a complex of symptoms including fever and rash that was linked to coronary artery vasculitis. It is possible that this was a new disease that emerged in first in Japan and then emanated to the western world through Hawaii versus an established disease that  was previously misdiagnosed; regardless, it is now a well-known entity that is not defined by nation boundaries. Kawaski’s disease is defined by the American Heart Association Guidelines as fever for at least five days and four or more of five clinical criteria:

1.  Conjunctival injection

2.  Cervical lymphadenopathy

3.  Oral mucosal changes

4.  Polymorphous rash

5.  Swelling or redness of extremities.

A diagnosis could also be made if only 3 criteria with fever are present in the setting of coronary artery disease in kids.  

In children who do not meet all of the classic criteria (most common in children under one years of age), measurement of high ESR and/or CRP levels as well as slight elevations in serum transaminase levels indicate diagnosis of atypical forms of the disease. This is important to note as children with atypical forms of the disease have notoriously higher rates of coronary artery aneurysms if untreated.  Of all children diagnosed with the disease, 15-25% of children will develop coronary artery aneurysm as a sequela of the vasculitis if left untreated. First line treatment, which should be administered within ten days of symptom onset, is a single infusion of IVIG (evidence rating of A) given in conjunction with high-dose aspirin, divided into four doses (evidence rating of C). Low dose aspirin should then be continued for 6-8 weeks following onset of symptoms if no cardiac abnormalities are present and indefinitely if coronary sequelae develop. Of note, despite treatment, 3-5% of children will still develop coronary aneurysms. 

In our patient, she presented with four days of fever and 4/5 clinical criteria.  By day 5, even had she not developed hand lesions, she would have had all the criteria for diagnosis.  And anytime someone has a rash and fever, you know what the family is going to ask: “Is this contagious?”  You can tell mom she is going to be OK, and so will her unborn baby.  

Sources:

1) Burns, J et. al. Kawasaki Disease: A Brief History. Pediatrics. 2000; 106 (2): e27

2) Freeman et.al. Kawasaki Disease: Summary of American Heart Association Guidelines. American Family Physician. 2006; 74(7): 1141-1148. 

The following case was submitted by Krystle Shafer, MD (pictured above).  Dr. Shafer is an EM-1 at my institution.  She went to University of Maryland (just like me, fear the Turtle!) for medical school.  She has a special interest in pediatrics and critical care, and we will certainly be hearing more from her down the road.

A one and a half year old female presents to the emergency department with a chief complaint of high fever with a home rectal temperature reported as 105 F despite administration of tylenol. Her fever initially started four days ago with tmax of 102.7 F. She has seen her pediatrician twice over the past four days who provided reassurance that this was a viral illness and advised to continue tylenol at home; despite this treatment, every day her fever has gotten higher and higher. On day two of her illness her parents report that they noted the development of an itchy rash that initially started as a couple bumps on her chest and back.   However, as her fever increased her rash became blotchier and more confluent such that it now covers her entire body, sparing the palms and soles. The day prior to her emergency department visit mom reports that the child stopped drinking pedilyte secondary to complaints that it is burning her mouth. Mom also notes that yesterday her eyes looked red and that the tip of her tongue was also bright red.  Today she has noted a white film covers her tongue. Review of systems is positive for a nonproductive cough and vomiting once during the course of her illness.

Physical exam reveals rectal temp 104.3F, mild tachycardia for her age, and a mildly increased respiratory rate.  She is in mild distress, but has no significant increased work of breathing.  HEENT reveals bilateral conjunctival injection, posterior cervical lymphadenopathy, and white patches on tongue.  Her lungs are CTAB.  CV exam shows the heart to have a regular rate/rhythm with no murmur.  She has a diffuse maculo-papular rash that spares the palms and soles.

1. Based on the information provided, what is the suspected diagnosis? 

2.  What diagnostic tests, if any, would you perform?

3.  What is the pathology of this condition? What is the treatment and disposition if your suspected diagnosis is correct?

4. Mom is currently in her first trimester of pregnancy with her second child.  Is this diagnosis potentially harmful to the fetus?

The Answer: Intussusception (congrats to @DamonTedford and @AndrewACNP1 on Twitter for getting it right!)

Intussusception is a a telescoping of one part of bowel into a distal pat of bowel (the proximal, inner portion of the telescope is referred to as the intussusceptum and the receiving distal portion is called the intussuscipien).  

• Most commonly seen between ages 3 months and 5 years.  60% of cases occur in the first year of life, and it peaks between 6 and 12 months
• Most common location: Iliocecal Junction
• Classic presentation and buzzwords include: Intermittent colicky abdominal pain, RUQ (or RLQ) mass, vomiting, current jelly stools

This can be a difficult diagnosis to make as your patients, as noted above, are commonly between 6 and 12 months and unable to provide a great history.  There are multiple features that can clue you in, however.  When kids present with bilious vomiting, they have an obstructive process until proven otherwise.  Children with intussusception will often have colicky pain, with intermittent lethargic periods.  They will have periods of fussiness and irritability where they draw their knees up to the chest, followed by periods of peacefulness or even lethargy.  In fact, a few cases I have seen have had lethargy as part of the parent's concern for bringing them in.  Remember, the boards always talk about current jelly stools, however this is a late and concerning finding (occurring in less than half of cases).  

Ultrasound is a great initial diagnostic modality to use that does not involve radiation, and does not require specialty services (so you can do this at your shop even if you do not have immediate availability of pediatric surgery).  Sensitivity and specificity have been reported up to 98-100%.  However, remember that it is most useful when the patient is in pain, and this can make it difficult.  The colicky pain followed by lethargy may result from telescoping and un-telescoping of bowel, so if performed during lethargic or painless periods or by an inexperienced sonographer it may not yield useful information.  Patients with a non-diagnostic US and high clinical suspicion for intussusception need barium or air-contrast enema and pediatric surgery consultation.  The board answer is that barium or air-contrast enema is the gold standard as it is both diagnostic and therapeutic.  

The classic US finding, as seen in the previous clip and the above images, is the target sign.  In this, the hypoechoic intussuscipien surrounds the hyper echoic intussusceptum.  This previous video also shows some free fluid around the bowel.  This, of course, can be done at the bedside by EM physicians.  Common false positives include stool, IBD, and misidentified anatomy.  In saggital you can also see a "pseudo kidney" sign, with multiple layers of edematous bowel wall mimicking the appearance of a kidney.  

Up to 90% can be reduced non-operatively, and there is a 5-10% recurrence rate (usually in the first 24 hours after reduction).  Our patient was transferred to the closest pediatric surgical center.  Enema was unsuccessful, and operative intervention was needed.  He underwent an uncomplicated operation and post-operative course.  

1. Emergency Medicine: A Focused Review of the Core Curriculum.  AAEM.  p 130-131. 

2. Halm, B.  Diagnosis of intussusception using point of care ultrasound in the ED: Case report. American J of Emerg Med (2011) 29, 354.    

3. Great SAEM resource on pediatric POC US

A 10 month old comes to the ED with his mother with concern for dehydration.  Mom states he has 2 brothers at home with diarrhea and vomiting recently, and she thinks this child caught the same bug.  The child is actually quite sleepy on exam, even bordering on lethargic.  As you are talking to mom, he begins to scream and flex his hips.  Mom says he has been doing this today, screaming for awhile and then having periods of quiet.  During this episode, you obtain the above ultrasound of the abdomen.  What do you see?  What is the treatment of this condition?  What is the role of Ultrasound in diagnosis?