Dose of Epinephrine for Patients with Anaphylaxis

Many of us are familiar with 0.3-0.5 mg IM of 1:1,000. Important to give IM and not SC.

In severe cases, consider IV Epinephrine:

• Take 1 mg of crash cart Epinephrine (1:10,000) and inject into 1 liter of normal saline
• Start drip at 1 cc/min which is 1 microgram/min
• "Titrate to life" (i.e. titrate up or down according to severity)

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Chest pain is a very high risk chief complaint in emergency medicine. And although we are told by the experts what we should write on the chart, we often struggle with finding time to do so.

Given that we can't pick up every MI, dissection, and PE, what things can we document in the chart that prove we are thorough and that we have thought about a diagnosis? And how can we document a "protective thought process" without taking too much time to do so?

Consider documenting these on your chest pain charts:

• Risk factors present/absent for ACS/MI, dissection, and PE
• Good family history
• Don't be sloppy with the history and physical exam. Doesn't matter if they help or not. Attorneys will have a field day discussing how sloppy the history and exam was. If the history and physical examination are bad get out the checkbook. 
• Pulses in upper and lower extremity
• Any leg swelling?
• Any diastolic murmur?

Documenting key pertinent negative comments in the chart shows that you are thinking (and considering MI, Aortic Dissection, and PE), and whenever this can be shown in a chart, there is more ammunition for the defense attorney. 

Pulmonary Embolism and IVC Filters

Inferior vena cava filters are placed in patients with massive DVT and /or in patients who cannot receive systemic anticoagulation.

The question is, can patients develop pulmonary embolism if a filter is already in place? The answer: yes

How does this happen?:

• Clot burden at the site of cava-filter insertion (below the filter). Clots can dislodge at this site and slip through the filter.
• Embolization around the IVC filter via retroperitoneal collaterals.

Hypertensive Encephalopathy (HE) is a clinical diagnosis and can look like many other disease entities.

HE refers to a relatively rapidly evolving syndrome of severe hypertension in association with severe headache, nausea, and vomiting, visual disturbances, convulsions, altered mental status and, in advanced cases, stupor and coma.

The key is the presence of severe hypertension. Remember, though, that 160/105 mm Hg may be high for an individual patient. Most patients with the syndrome will have diastolic pressures well in excess of 120-130 mm Hg. The only way you will know if the diagnosis is correct is to treat the BP (carefully control), work up other etiologies, and see of symptoms improve with BP control.

Beware the patient with severe HTN and seizure. Seizure may be the first, and only, symptom of hypertensive encephalopathy. 

Beta Blockade in Treating Acute Aortic Dissection

Medical therapy for acute aortic dissection is aimed at decreasing shear stress within the aorta. Although there are many agents to choose from when treating hypertension in patients with acute aortic disease, all regimens should include a beta blocker (like esmolol) unless contraindicated. Initiation of a beta blocker before another antihypertensive agent is added is crucial as this will prevent reflex tachycardia associated with vasodilators and other afterload reducers. Reflex tachycardia may worsen the dissection. 

Treatment of Cerebral Venous and Sinus Thrombosis

Thrombosis of the cerebral venous system, also known as cerebral venous and sinus thrombosis and dural sinus thrombosis, is an uncommon condition encountered in the emergency department. The diagnosis may be stumbled upon by various CT findings or by MRI and/or a high opening pressure on lumbar puncture.

The treatment of choice is full dose anticoagulation with heparin. Available studies looked at unfractionated heparin, but many experts now consider LMWH (like Lovenox) an acceptable alternative. Despite the risk of hemorrhagic transformation of a venous infarct, heparin therapy is considered the standard treatment for this condition. 

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Some Tips for Designing an Insanely Great Talk

Here are just a few things you can do to create a fantastic presentation:

• Remember: great talks mix education, entertainment, and inspiration
• Limit the number of bullet points. Text can be your enemy. Better yet, try to develop your talk without bullet points!
• Use more pictures and video. The more the better. 
• Tell stories and use emotion (people love stories and learn well from stories)
• In order to improve your speaking skills listen to recordings of yourself and watch videos of your presentations
• Spend extra time of developing an excellent opening and closing. Bombing these will seal your fate. 

Great website for making great, memorable slides:

http://www.brainslides.com/

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Pulmonary Embolism and Blood Pressure

Patients with massive PE will often develop worsening hypotension after a fluid bolus due to increased right ventricular distension and deviation of the interventricular septum towards the left side of the heart. This septal deviation decreases left heart cardiac output.

In addition, patients with massive PE will sometimes develop higher blood pressures after intubation as positive pressure ventilation reduces preload, decreases deviation of the septum, and increases left sided cardiac output.

Pneumoperitoneum on CXR and CT

Pneumoperitoneum may be seen on an upright CXR up to 7 days after laparoscopic abdominal surgery/laparotomy and may be seen on abdominal CT for as long as three weeks after surgery. 

Risk Stratification in Pulmonary Embolism

The following are the principal markers useful for risk stratification:

• Clinical markers (shock, hypotension)
• Markers of RV dysfunction (RV dilatation, hypokinesis or pressure overload on echo, RV dilatation on CT, BNP elevation)
• Markers of myocardial injury (elevated troponin)

Patients with one or more of these markers have a higher mortality rate.

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Silent Pulmonary Embolism?

As many as 50% of patients with isolated DVT will be found to have silent pulmonary embolism (i.e. no chest pain or shortness of breath) on VQ scanning. Studies performed in the last year or so with CT scanning show that this percentage is much higher.

The clinical take-home point is NOT to get a pulmonary CTA on suspected DVT patients but to remember that many patients can and do have PE in the absence of cardiopulmonary symptoms. Pretty frightening....

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Submitted on behalf of Dr. Michael Abraham

Thyrotropin (TSH) 

• Different types of test available:
  • The first tests available were radioimmunoassay. 
  • The next type of test available is the immunometric test.

• As each test is developed there has been a trend to use the term ‘generation’ for a 10 fold increase in sensitivity. ¹

• Indications for ordering in the ED:   Hypothyroidism, Graves Disease, Hashimoto’s Thyroiditis, Thyroid storm.

• Diagnostic Accuracy
  • The original TSH benchmark was the ability to measure euthyroid (0.4 – 4mIU/L) from very low (<0.01 mIU/L) which is suggestive of Graves disease. 
  • Most new tests have a functional sensitivity of <0.02mIU/L. 
  • The clinical sensitivity and specificity have to be determined by each laboratory’s staff. This requires testing of samples over a 6-8 week period as should include a sample of the population that is being tested.²
• Average turnaround time to complete test: 
  • The tests are mainly run on large lab analyzers. There are many commercially available tests the turnaround time is dependent on the manufacturer of the machine.

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Thrombolytic Therapy for Pulmonary Embolism

Current, FDA-approved thrombolytic therapy for PE:

• tPA 100 mg over two hours-infusion
• Heparin drip should be turned off during tPA infusion and turned back on ONLY after PTT has fallen to 2 X normal
• Other drugs are being used-like Tenecteplase (TNKase), but strictly speaking, not FDA approved for thrombolysis of PE
• Most studies to date do not show that catheter-based delivery of lytics is safer than systemically administered lytics
   

Massive Pulmonary Embolism and Response to Fluids and Mechanical Ventilation

Massive pulmonary embolism leads to acute pulmonary hypertension and right ventricular overload. This leads to release of troponin and a "bowing" of the interventricular septum on echocardiography. Deviation of the septum then leads to a decrease in left-sided cardiac output. 

A few interesting clinical pearls:

• Administration of IV fluids to patients with massive PE often leads to a decrease in BP. This happens as a result of increasing preload causing further bowing of the septum and a subsequent further drop in left ventricular cardiac output, leading to hypotension. 
• Patients with massive PE who require intubation often demonstrate an increase in BP due to positive pressure ventilation causing a drop in preload and a reduction of septal bowing into the left ventricle.

Teaching When Time is Limited

We all know how difficult it can be to teach in the ED when it is busy. So how do the experts do it when there is so little time?

Just a few considerations that might make your teaching more effective and easier to do when it is busy:

• Identify the learner's needs. The time-saving rule of thumb: target, then teach. After all, how do you know what to teach if you don't know what the learners knows or needs.
• Teach rapidly. And I mean rapidly. Many of us have really come to realize over the years that less is better. As Amal says, be a sniper and don't use a shotgun. Teach one thing quickly and move on. Pick a pearl (or pitfall, etc.), lock and load, then deliver it...then STOP teaching. Much more effective than spending 20 minutes talking about stuff nobody will ever remember!
• Provide some type of feedback. Feedback is one of the most underused yet powerful teaching tools available. 

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Some considerations in the patient with a penetrating vascular injury (gunshot, stab):

• Obtain ankle-brachial index on all patients and document
• An ABI <0.9 indicates the need to perform an arterial study
• Traditional approach to penetrating extremity injury has been to perform angiography
• Recent (good) studies have shown that CTA of the involved extremity is just as good if not better than angiography, and a lot of centers have moved to CTA
• Obtain vascular surgery consultation if there is any concern for an arterial injury. Never hurts to err on the side of caution. 

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A review of the PERC rule...

The "PERC Rule"  is used to assess a patient's risk for probability of PE in the emergency department. It involves evaluating the presence or absence of 8 clinical criteria to arrive at a pretest probability.  And remember, this rule is supposed to be used for patients with really low pretest probability where you weren't concerned about PE to begin with. Some experts claim that "PERC negative" on the chart proves you considered PE in the differential diagnosis. But the test isn't designed to be used on EVERY patient as a means to rule out PE. Only use if you thought about the disease in a low risk patient and didn't plan on getting a d-dimer or further testing. 

The criteria are (all must be YES):

age < 50 years

heart rate less than 100 beats per minute

room air oxygen saturations 95% or greater

no prior deep venous thrombosis [DVT] or PE

no recent trauma or surgery (4 weeks)

no hemoptysis

no exogenous estrogen

no clinical signs suggestive of DVT (Unilateral leg swelling on visual inspection

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Secondary Hypertension...say what?

We obviously see tons of patients in the ED with hypertension, and we are very comfortable with both symptomatic and asymptomatic presentations. Most of these patients have essential or primary hypertension. Some patients, however, may have secondary hypertension (i.e. something is causing it). Although we will refer patients to a primary care physician for further management and workup it is worth discussing when to suspect other diagnoses as the cause of the hypertension. Is it out job necessarily to diagnose these conditions in the ED? No. 

Causes of secondary hypertension to consider:

• Obstructive sleep apnea
• Renal disease
• Renal artery stenosis (think older person with HTN and abdominal bruit)
• Coarctation (young person with HTN-ever wonder why pediatricians palpate upper and lower extremity pulses in the office?)
• Cushing's disease (excess cortisol-patient may have new diabetes, have abdominal striae, and easy bruising)
• Hyperaldosteronism (due to an adrenal tumor)...think about if a patient comes to the ED and is repeatedly hypokalemic and hypertensive
• Pheochromocytoma (episodes of flushing, hypertension, palpitations, etc.)
• Hypothyroidism (not myxedema coma or storm)...commonly causes elevated diastolic BP. 
• Hyperthyroidism 

Consider the ABCDE mnemonic:

A-Accuracy (is it really htn?), Apnea, Aldosteronism

B-Bruits, Bad Kidneys

C-Catecholamines, Coarctation, Cushing's 

D-Drugs, Diet

E-Endocrine

Aren't you glad you didn't do a Medicine residency???

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Some not too uncommon complications of Type B (distal) aortic dissection:

• Malperfusion syndrome-occurs when the dissection flap occludes a major vessel (e.g. SMA occlusion leading to bowel infarction)
• Occlusion of the spinal arteries and lower extremity arteries can lead to fleeting signs and symptoms-one minute they have left leg pain and ischemia, the next minute they don't. This is pretty classic for acute, distal aortic dissection. 
• Frank rupture (dissected aortic wall is weak and prone to aneurysm formation and subsequent rupture)
• Assume that rupture has occurred (may be intrathoracic or intrabdominal) in a Type B patient who crashes unexpectedly
• Retrograde extension into the proximal aorta is not common but does occur. Have a low threshold to whip out the sono if the patient deteriorates. 

Acute Mesenteric Ischemia

Although we all know the classic presentation of acute mesenteric ischemia (AMI), it can be tough to diagnose.

Some pearls about AMI:

• Embolization to the superior mesenteric artery (SMA) is the most frequent cause of AMI.
• Most patients present with acute, severe abdominal pain. 
• Classic presentation: acute severe abdominal pain with a paucity of physical examination findings
• Presence of tenderness in most cases indicates bowel infarction has already occurred
• The disease may be more insidious in patients with diseased mesenteric vessels (presence of collaterals). These patients may very well NOT present with acute, severe pain.
• Must have a high index of suspicion (i.e.-suspect this disease in patients at risk who present with abdominal pain)
• If you are standing at the bedside and you say, "Self, this looks like AMI," then rally the troops BEFORE labs and before CT. Get a surgeon to see the patient as soon as possible. Tell them you think the patient has AMI. Get them to move. "TIme is bowel."