Painless thoracic aortic dissection (TAD) and syncope

Patients with TAD do not always present with chest pain. In the International Registry of Aortic Dissection (IRAD) study, 2.2% of TAD cases were painless and approximately 13% of TAD cases presented with isolated syncope (i.e. NO PAIN). Other studies have shown that as many as 15% of TAD cases are painless.

Patients with TAD may present after a syncopal episode. The underlying pathophysiology of syncope is related to proximal rupture into the pericardium with resultant tamponade.

Add TAD to your differential diagnosis of unexplained syncope, especially in older folks and especially if a patient "looks bad" and you don't have a reason.

Unusual Presentations of AAA

Many unusual presentations of AAA have been reported in the literature and include:

• Musculoskeletal complaints (thigh or groin pain)
• Bilateral testicular pain
• Unexplained inguinal pain-VERY well described
• Femoral neuropathy
• Abdominal pain and urge to deficate (and, NO, I am not making that one up)

One more note on the whole urge to deficate thing: any thing that leads to hemoperitoneum may cause this strange complaint (ruptured AAA, ruptured ectopic pregnancy).

Beware of older patients with groin pain!

Lower abdominal pain (mimicking diverticulitis) and isolated groin/hip pain are relatively common presentations of AAA and iliac artery aneurysm and rupture. As many as 15-20% of symptomatic AAAs wil present with hip and/or groin pain.

Bottom line: AAA and iliac artery aneurysm should at the very least be considered in older patients (and in patients with vascular disease) who present with unexplained groin/hip pain.

New Antihypertensive agent coming our way...

Well, we have nitroprusside, labetalol, nicardipine, fenoldopam, etc. Say hello to a new drug that is "reported" to be a great drug for ED patients with severe hypertension (emergencies)....Clevipidine (Cleviprex).

Clevidipine is an ultrashort acting calcium channel blocker that has been found to be a powerful antihypertensive medication.

Unique properties of the drug:

• Very short half life-quick on, quick off
• Not affected by renal/liver disease-drug is broken down into inactive metabolites by plasma esterases
• Reportedly as effective as nitroprusside and the other big guns we have for severe hypertension
• Starting dose is 1-2 mg/hour and can titrate up every 1-2 minutes.
• Contraindicated in patients with allergies to soy products and egg products

Remains to be seen if this drug will play in a role in the treatment of our severely hypertensive patients....stay tuned...

Aortoenteric Fistula (AEF)-Beware the Upper GI Bleed!

Important points about AEF:

• Most of the time this is a complication of AAA repair (secondary fistula)
• Fistula site normally in the duodenum (the graft erodes into the duodenum)
• "Herald bleed" seen in 20-80% of patients (bleeding stops spontaneously then stops prior to massive hemorrhage)
• Diagnostic studies frequently waste too much time. As a rule of thumb, any unstable patient with a history of AAA repair who presents with a massive GI bleed should probably be taken to the OR for emergent laparotomy. Stable patients may need to get a CT scan and/or EGD (although EGD misses many of these)
• Failure to consider the diagnosis (and act) may lead to bad patient outcomes
• Have a low threshold to call a gastroenterologist AND a surgeon when this diagnosis is being entertained. If you are wrong and it isn't an AEF, no big deal. But if you are correct, you may have saved a life!

Pearl: Suspect a aortoenteric fistula in any patient with a prior AAA repair who presents with an upper GI bleed (may also be lower GI bleed)

Great case of bradycardia today in the ED-requiring transvenous pacemaker....cause?? K 7.6

Some bradycardia pearls:

• The dose of atropine is 0.5 mg IV. Can be repeated.
• Heart transplant patients will not respond to atropine as the transplant is denervated. Go right to pacing.
• Consider glucagon if suspected beta blocker toxicity....and be prepared...most patients vomit!
• DON"T FORGET THE K! A frequent cause of weird and insuspected bradycardia. I have had at least 3 cases of bradycardia (two requiring TV pacemaker insertion in the ED) due to hyperK in the last 3-4 weeks.
• Capture of the ventricle occurs when the complexes on the monitor become wide (assuming they weren't already wide)
• Search for the cause (MI, tox, metabolic, etc.)

Hypertensive Encephalopathy

Hypertensive encephalopathy (HE) is one of the true hypertensive emergencies. Although usually seen with diastolic BPs greater than 120 mm Hg, it can occur in patients with lower numbers. And the diagnosis can be really tricky to make. Sometimes the diagnosis isn't clear until symptoms resolve from BP reduction .

The presentation is variable and includes:

• Seizures
• Altered mental status
• Coma
• Vomiting

The goal of treatment is to reduce the BP NO MORE THAN 25% (of the MAP) within the first few hours. In addition, drugs like Hydralazine (which may lead to a precipitous decline in BP) and Clonidine (which can alter mental status) should be avoided.

Medications to consider for treating HE include intravenous drips-Fenoldopam, Nicardipine, Labetalol. Drugs like Nipride are probably best avoided since cyanide toxicity may alter a patient's mental status further.

Todays pearl pertains to a great new blog put together by Dr. Michelle Lin, entitled "Academic Life in Emergency Medicine." The blog is superb and is a great resource for anyone interested in academic EM.

Today's posting is about teaching when time is limited and Michelle discusses a really good article written by Irby, et al. This article addresses a topic that is very pertinent to us in the ED, how to teach when it is busy. Isn't it always busy?

Tips from the article:

1. Identify the learner needs (can't be successful without this important step)
2. Teach rapidly (great tips for how to do this in the ED)
3. Provide feedback (students are starving for this)

Want more??? Gotta check out the article....

Here is the link to the site:

http://AcademicLifeinEM.blogspot.com/ 

Enjoy!

The Alcoholic Patient in the ED

Well, we have all been there....EMS rolls in with "another drunk guy" found down in the street. The nurses tell you, "he is here all the time...he is just drunk." You should be scared any time you hear this phrase uttered. Always be a little nervous about this group of patients and you won't fall victim to many of the pitfalls that some of us have experienced.

Pearls and Pitfalls in Caring for the Intoxicated Patient in the ED:

• Get a glucose early. Many of these patients are hypoglycemic when they arrive.
• Assume the worst and NEVER tell yourself or others,"He's just drunk." That statement is the kiss of death. Always assume there is occult trauma present. Did they fall and sustain a head bleed, splenic injury, hip fracture?
• Reevaluate during your shift. There is nothing worse than placing an intoxicated patient in a room and ignoring them, only to find out that hours (or shifts) later that they won't wake up.
• Consider a head CT. Although you can't scan them all, have a low threshold to image them. They fall all the time, and you will be surprised at how many subdural hematomas you pick up when you scan this group of patients. If you don't image, perform reassessments frequently during your shift.

Some Pearls on ED Teaching:

• Don't teach so much. Limiting the number of points taught will lead to increased retention. Quality, not quantity.
• Make sure your learners are "with you." If the learner isn't attentive, forget it. Move and and return to teaching when the learner is ready. You are wasting your time if they are paying attention.
• Be creative in adapting your teaching style when it is busy. You don't have to be at a dry erase board drawing metabolic pathways (sorry Fermin) to be teaching. Simply discussing your thought process outloud is a great way of teaching "on the fly."
• Be flexible and remember: the focus should be on the learner (what they get out of it) and not the teacher. Many forget that when they teach in the ED.

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Transvenous pacing

We had a very interesting case the other day in the ED. A 60 yo male presented after a syncopal episode. After arriving in the ED he was awake (with a pulse of 50) but then became asystolic, without warning. He then woke up and 10 minutes later became asystolic again. He then woke up again. So, we decided to put in a transvenous pacer.

Some considerations when putting in a transvenous pacer:

• You need to use a small cordis (e.g. 6 French)
• Right IJ is the preferred approach so that when the balloon is inflated you will have easy entry into the right heart
• You will need transvenous pacing wires, obviously.
• Once you open the wire kit, you will find 2 adaptors that fit over the two ports of the pacemaker wire. Snap them on, then these connect to the ventricular leads of the pacer box-ignore the atrial side. Here is the key: the POSITIVE lead connects to the PROXIMAL port on the pacemaker (PROXIMAL=POSITIVE) and the distal lead connects to the distal port.
• Turn the pacer on then set rate to 80 or so. And start the mAmp at 20.
• Advance the wire through the Cordis and after the wire has cleared the Cordis, blow up the balloon with a syringe and lock it.
• The key is in determining capture: While the patient is on the monitor, and as the wire is being slowly advanced, look for pacer spikes and the development of wide complexes. This indicates electrical capture. Be sure to check for mechanical capture by checking the patient's pulse.
• After capture, the mAmps can be turned down to the capture point.
• DON'T forget that transcutaneous pacing is clearly the first option as this is easy to initiate.

Multiple Myeloma + Altered Mental Status=Hyperviscosity Syndrome

Although the differential diagnosis of altered mental status is quite extensive, a patient with multiple myeloma and altered mental status should prompt consideration of one important, albeit not too common, condition.....hyperviscosity syndrome.

Some important pearls:

• This syndrome occurs when excessive amounts of protein (immunoglobulin) are secreted by myeloma (plasma) cells.
• Excessive circulating protein leads to sludging and ischemia in lung and brain tissue, lesding to hypoxia and altered mental status, respectively.
• You will only pick up this diagnosis by thinking about it, so multiple myeloma + altered mental status = hyperviscosity syndrome
• Treatment is with IVF and plasmapheresis (heme onc consult)
• And don't forget common stuff, like stroke, subdural hematomas, meningitis, etc.

Risk of PE/DVT in patients with microalbuminuria....another risk factor to consider??

Microalbuminuria (protein in the urine) is a known risk factor for arterial thromboembolic disease, and recent studies suggest that arterial thromboembolism and venous thromboembolism (VTE) have common risk factors. In a prospective community-based cohort study in the Netherlands, researchers enrolled 8574 adults (age range, 28-75) who were followed for 9 years. People with insulin-dependent diabetes or pregnancy were excluded.

Of 129 identified episodes of VTE, roughly half were deep venous
thromboses, and half were pulmonary embolisms. The annual VTE incidence
rate was 0.12% in patients with normoalbuminuria (<30 mg/24 hours)
versus 0.40% in those with microalbuminuria. After adjustment for known VTE
risk factors and other factors (including hypertension, known coronary arterydisease, and elevated C-reactive protein level), the hazard ratio for
VTE in people who had microalbuminuria, compared with those who had
normoalbuminuria, was 2.0.

Comment: The importance of this study is not in the clinical value of
usingmicroalbuminuria as a marker for VTE risk, because the absolute risk
conferred by microalbuminuria is very low, and the therapeutic
implicationsare unclear. Rather, this study suggests that microalbuminuria is a
marker for endothelial dysfunction in both arterial and venous systems, and it
suggests a mechanism for how statins interact with the endothelium to
prevent VTE (JW Cardiol Mar 29 2009).

So, does this affect us as emergency physician? Unclear. But it may very well mean that we might be dealing with a new risk factor that needs to be taken into consideration when evaluating patients with chest pain or SOB. Obviously, we might need medical records to find this risk factor...can you imagine asking a patient if they have microalbuminuria?

Show References

Giving a Lecture-Pearls and Pitfalls

Giving a lecture is filled with many potential pearls and pitfalls. Here are just a few important points that are frequently discussed:

• Stick to NO MORE than 3-4 take home points (people cannot remember more than that)
• Really spend a lot of time on the opening and closing (know them cold). This is what people will remember.
• Try to divide your talk into 5-10 minute chunks of material and DO NOT try to cover too much material....big mistake
• Perhaps one of the most important aspects of giving a really good talk is practice. You should know your material well enough that you could give it if the power went out and the computer crashes. Practice is essential...and it should "out loud." This is often neglected and it shows when unprepared speakers get up in front of an audience.
• Practice speaking without the use of verbal fillers ("ums"). This will improve as you practice more and more. Getting rid of these fillers may make the difference between a really good talk and an average talk. PRACTICE, PRACTICE, PRACTICE speaking without using them!

For an entertaining discussion of the pearls and pitfalls if giving a presentation check out the May episode of EMRAP: Educators' Edition on iTunes (also on the website www.emrap-ee.com). There is a great discussion by Greg Henry, Mel Herbert, and Amal Mattu. Check it out. It's free!

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Questioning Learners in the ED-Wait Times

When teaching medical students and residents, consider that the literature shows that we tend to wait only a few seconds (some studies say 3 seconds-which seems like a long time when you are waiting for a response) for a response. Bottom line, it has been demonstrated that many learners have the answer and will respond if simply given the time. Hard to do sometimes in a busy ED. Learners who aren't given time to respond will quickly learn that if they simply wait long enough the answers will be given to them.

So, when asking a question (NOT pimping) to a medical student or resident, simply wait a little longer. They may very well surprise you with the answer.

Show References

The One Minute Preceptor Model of Teaching in the ED

This is a teaching strategy that most of us are very familiar with. Why? Because many, if not most, of us do it every day. We listen to a case, get a committment from the learner, probe for supporting evidence, and then give a teaching pearl and offer learning resources.

Perhaps one of the biggest pitfalls in teaching is NOT WAITING for the learner to answer to question. How often have you asked a question to a medical student and gave the answer? How often has a student presented a case and then they clammed up and didn't commit to a diagnosis or treatment plan?

A simple strategy for teaching success:

• Make learners "jump out there" and give you a diagnosis and treatment plan, i.e. get a commitment. Do your best to keep your mouth closed for a few seconds
• Give learners time to answer. You will be surprised. A few more seconds of waiting makes a big difference.

Diagnostic Errors in the Emergency Department

Believe it or not, there is actually a field of medicine that is devoted to examining how physicians think in clinical practice, i.e. how we make diagnostic decisions. Much of the work on this has been done by Pat Croskerry. This is extremely important for emergency physicians because we frequently have to make split second medical decisions with little to no information.

Why is this so important? If we can understand where errors are made, we can actually improve our own diagnostic skills and reduce our errors rates.

Some key pitfalls that we all fall victim to:

• Bias-this refers to the chart that says under past medical history "fibromyalgia, interstitial cystitis, bipolar, chronic constipation." This type of chart has set us up to potentially miss a diagnosis because our thought processes shut down before we have even started. Ever miss a diagnosis or almost make a mistake because of your feelings about a patient (sometimes BEFORE seeing them)? This is bias. Being aware of this dangerous pitfall in practice is the first step in preventing bias-related mistakes.
• Premature closure of the differential diagnosis-Now, we do this a lot in medicine. Some diagnosis falls in our lap (patient gives it to us, or a consultant tells us that is what it is) and we fail to r/o other things on our list. Key mistake we make is related to not considering other entities on the differential diagnosis. Take home point: Don't narrow the differential diagnosis until it is time to do so.

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The One Minute Preceptor-Microskills in Teaching

Most clinical teaching takes place in the context of busy clinical practice where time is at a premium. Microskills enable teachers to effectively assess, instruct, and give feedback more efficiently. This model is used when the teacher knows something about the case that the learner needs or wants to know.

Most of already do this on a daily basis when a learner (student or resident) presents a case to us.

• Get a commitment (Make them commit to a diagnosis and/or management strategy)
• Probe for supporting evidence (why do they think this patient with CP has an MI?)
• Teach general rules
• Reinforce what was right
• Correct mistakes

One of the biggest pitfalls in teaching, particularly to medical students, is the first skill, getting a commitment. Let (i.e. make) the student commit to a diagnosis and treatment plan and avoid spoonfeeding them.

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Nitroprusside-Friend or Foe?

Nitroprusside is a direct venous and arteriolar vasodilator and is very effective at lowering blood pressure. It has been used for the treatment of hypertensive emergencies for many years and most of are comfortable with using it.

The problems with the drug:

• May cause precipitous drops in BP and lead to overshoot of BP target goals
• The drug is inactivated by light so the infusion bag and tubing must be protected  from light
• Frequently causes nausea, vomiting, and muscle twitching
• Most importantly, cyanide (CN) is released from nitroprusside in a dose-dependent fashion and may cause clinical toxicity
• Good alternatives exist: Fenoldopam as an example. Just as effective and without any of these side effects.

Show References

Documentation of the Chest Pain Patient

Chest pain is a high risk entity in emergency medicine. And since many patients we see with chest pain are eventually discharged, we should consider what our charts should look like should we discharge a patient who has a missed life-threatening diagnosis. In other words, what would an attorney look for?

Considerations for the chart:

• Consider documenting some type of medical decision making in the chart. What were you thinking? Why didn't you think the patient needed cardiac enzymes, a CT, or admission? The chart should support your decision to send the patient home.
• Document a thorough history...enough said
• Document risk factors for the deadliy causes of chest pain (ACS, PE, dissection, etc.). This is frequently missing on charts.
• Consider documenting important, pertinent negative "chest pain physical exam findings," such as a normal leg exam (frequently missing on missed PE charts), no murmurs, equal pulses. Comments like this in the chart prove that you were thinking about a differential diagnosis. A question to ask yourself is, "Does my physical exam look like I was searching for the bad players of chest pain?"