The Cricothyrotomy Menu

There are a variety of strategies for accessing the trachea via the neck and the terminology is confusing. Open cricothyrotomy, often referred to as surgical cricothyrotomy, is using a knife to cut a hole in the cricothyroid membrane and placing a tracheostomy tube or endotracheal through that hole. Several techniques have been described, including the no-drop technique, the rapid four-step technique, and the scalpel-bougie technique.

Percutaneous cricothyrotomy is a term usually used in distinction to surgical or open cricothyrotomy, implying a less invasive approach. Percutaneous cricothyrotomy facilitates the placement of a tracheostomy or endotracheal tube in the trachea by using either a Seldinger tube-over-dilator-over-wire technique, or a tube-over-trocar device [1, 2]. Most emergency physicians are referring to the Seldinger technique when they use the term percutaneous cricothyrotomy.

Though a needle is used in the Seldinger technique, the term needle cricothyrotomy usually refers to a less definitive procedure where a comparatively small cannula, such as a 14g angiocath, is placed into the trachea and oxygen is insufflated under pressure through the cannula; this is called transtracheal jet ventilation when a special high-flow device is used, though a bag-valve-mask is more likely to be available, if less effective, and several hard to remember maneuvers are commonly proposed that allow a BVM to be adapted for this purpose.

Wire In Trachea Readiness Technique

For patients who suddenly and unexpectedly cannot be intubated or oxygenated, the weight of evidence and opinion seems to favor an open technique [1, 2, 3, 4, 5], which appears to be faster than a percutaneous approach, more likely to be successful for those who don’t perform the procedure often (i.e. everyone), and would be used to rescue a failed percutaneous attempt. Smart people disagree on this point, however. Certainly, the goal in these scenarios is to establish oxygenation as quickly as possible by whatever means necessary, and that will differ based on provider, patient, and setting. Have a plan that works for you in your environment.

Many patients who cannot be intubated orally do not suddenly and unexpectedly crash, however. The need for a surgical airway can present itself as a land mine that explodes in front of you as you walk to your mailbox in your bathrobe, but also as a land mine that explodes as you carefully traverse a known minefield in a tank. Of course every emergency intubation is a minefield, and being cognitively and materially prepared for failure of intubation and failure of ventilation at the outset of every case is one of the characteristics of the airway expert. But while we have many options for plan A and plan B, there is still only one plan C – when intubation fails, and oxygenation fails, plan C is cricothyrotomy. Since it is clear that the most important surgical airway error is that it is delayed, several airway management paradigms [1, 2, 3] have recently emerged that explicitly encourage providers to prepare for and properly initiate cricothyrotomy.

In Scott Weingart’s CricCon taxonomy, the highest alert posture is to cut the skin and find the membrane, so that if the need arises, incising the membrane and placing the tube is simple. Most emergency practitioners, however, are uninterested in cutting the neck. On the other hand we are perfectly happy to put wires and tubes in the neck, and do it all the time in the internal jugular vein. Here lies the role of percutaneous cricothyrotomy: not as a crash technique, but as an alert posture, a readiness maneuver: when the likelihood of requiring a surgical airway is sufficiently high, place a wire in the trachea.

Placing a wire in the trachea feels more like inserting a central line than cutting the neck. Feel free to use ultrasound. [1, 2, 3] The strength of the wire-in-trachea approach is that it lures the practitioner into preparation and makes timely performance of cricothyrotomy more likely by breaking the procedure into agreeable steps. Inclination via incrementalism.

There are at least two scenarios in which wire-in-trachea readiness technique would be used:

a. An almost crash expected very difficult laryngoscopy, such as an angioedema patient who requires an airway not this very second but urgently.  If the patient is cooperative, wire is placed after rapid local anesthetic infiltration as preparations are being made for awake laryngoscopy vs. RSI. If uncooperative, wire is placed immediately after induction (concurrent with preoxygenation if using a delayed sequence strategy), just before laryngoscopy, or as laryngoscopy is beginning. This is basically an enhanced double setup.

b. In the midst of a can’t intubate, can ventilate situation. This occurs relatively commonly: laryngoscopy has failed, but LMA or bag-mask ventilation is effective, then the second laryngoscopy attempt fails, but ventilation remains effective, and then the third attempt fails, and you feel like you’re running out of tricks/tools. And you know that with every airway attempt, the glottis becomes a little more swollen, the airway gods–who have until now granted you the gift of ventilation–their patience is a little more tested, and the prospect of can’t intubate, can’t ventilate looms. So after a few failed oral attempts, while the patient is being ventilated, place the wire, then go on with as many further attempts as you want, knowing that if and when ventilation becomes ineffective (or if you have other patients to see and want to move on), cricothyrotomy is straightforward.

Logistics

Percutaneous cricothyrotomy kits are expensive and often stocked in small numbers. To utilize the wire-in-trachea readiness technique, use the needle/syringe/wire from a central line kit. Fill the syringe halfway with water/saline so that tracheal location of the needle can be confirmed by the bubbling of aspirated air.

Have your unopened percutaneous cric kit at the bedside, and when needed, 1) open the kit 2) stab the skin with the scalpel 3) slide the tracheostomy tube-over-dilator into the trachea 4) pull the wire and dilator 5) inflate the cuff 6) ventilate. Don’t forget to load the tracheostomy tube onto the dilator if not pre-loaded in your kit.

Step 2 is important: an aggressive stab must be made on the skin, along the path of the wire, similar to central line technique but larger, to accommodate a larger device.

Step 3, inserting the tube-over-dilator, is facilitated, like everything else, by the application of sterile lubricant. Use a firm twisting motion.

If oral or nasal access is successful and cricothyrotomy isn’t needed, simply pull the wire. Put a band-aid on the site; this will serve as evidence of a disarmed land mine.

Thanks to Rob and Scott for helping me develop this idea.

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References:

• 1 Fitch MT, Manthey DE, McGinnis HD, Nicks BA, Pariyadath M. Videos in Clinical Medicine: Abscess Incision and drainage (video). N Engl J Med 2077; 357:e20.

• 2 Danby FW, Margesson LJ. Hidradenitis suppurativa. Dermatol Clin. 2010Oct;28(4):779-93.

• 3 Orman, Rob. Perianal Abscess. ERCAST, Jan 2011.  http://ercast.org/perianal-abscess

• 4 Schwarz RJ, Shrestha R. Needle Aspiration of Breast Abscess. Am J Surg. 2001;l 182(2):117.

• 5 Kronfol R, Downey K. Technique of Incision and Drainage for Skin Abscess. UpToDate Online. May 2011.

• 6 Wilson W et al.  Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association and others. Circulation. 2007 Oct 9;116(15):1736-54.

• 7 Roberts, James R. Clinical Procedures in Emergency Medicine, 5th ed. 2009.

• 8 Liu C, Bayer A, Infectious Diseases Society of America, et al. Clinical practice guidelines by the Infectious Diseases Society of America for the treatment of methicillin-resistant Staphylo- coccus aureus infections in adults and children. Clin Infect Dis. 2011;52(3):e18-e55.

• 9 O’Malley GF, Dominici P, Giraldo P, Aguilera E, Verma M, Lares C, Burger P, Williams E. Routine packing of simple cutaneous abscesses is painful and probably unnecessary. Acad Emerg Med. 2009 May;16(5):470-3.

• 10 Schmitz GR. How do you treat an abscess in the era of increased community-associated methicillin-resistant Staphylococcus aureus (MRSA)? J Emerg Med. 2011 Sep;41(3):276-81.

• 11 Walraven CJ, Lingenfelter E, Rollo J, Madsen T, Alexander DP. Diagnostic and therapeutic evaluation of community-acquired methicillin-resistant Staphylococcus Aureus (MRSA) skin and soft tissue infections in the emergency department. J Emerg Med. 2012 Apr;42(4):392-9.

For abscess I&D, most of us haven’t been thinking about antibiotic prophylaxis in patients at risk for infective endocarditis. According to my interpretation of table six of this guideline, we should be. “Antibiotic prophylaxis is reasonable for procedures on respiratory tract or infected skin, skin structures, or musculoskeletal tissue only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from IE (Table 3).”

The double setup is an airway management strategy conventionally carried out in the operating room, in a stable or relatively stable patient who requires a definitive airway but is anticipated to be very difficult to intubate orally. An otolaryngologist or other surgeon fully prepares to perform a cricothyrotomy or tracheotomy–patient prepped, all equipment laid out, sterile gown and gloved, scalpel in hand–and then gives the anesthesiologist the nod, at which point the patient is induced and orotracheal intubation is attempted. If unsuccessful, anesthesia nods to surgery, who proceeds with a neck incision.

Emergency physicians are trained to manage difficult oral airways and perform cricothyrotomy–how does the double setup apply to our environment? Once the decision to intubate has been made and preoxygenation has been initiated (don’t forget the nasal cannula), ask two questions: How urgently must this patient be intubated? How difficult do I predict this airway to be?

Scenario 1: Must intubate immediately, very scary airway.

Some patients need to be intubated right now, and some patients who need to be intubated right now also are predicted to have difficult airways. The paradigmatic examples of this stressful situation are the dynamic airway insults: patients with bullets, bites or burns (neck trauma, anaphylaxis, airway burn or caustic exposure) who are already showing signs of airway embarrassment. The proper mentality in these cases is this patient is going to require cricothyrotomy, but I’m going to attempt orotracheal intubation, just to make sure. There is no time for a fancy airway assessment or fancy preparations, these patients are a test of your department’s, and your own, usual state of readiness. Patients with dynamic airways should be induced and paralyzed, because intubation will get harder with each passing minute–RSI gives you optimal conditions, as quickly as possible. Once the tools you need to perform cricothyrotomy are at the bedside, use the orotracheal technique that, in your hands, will give you your best shot at first pass success, as quickly as possible. Video laryngoscopy is a good choice. As soon as your first pass fails and not one second later, attempt ventilation (I suggest you move straight to an LMA), but you have accepted that there is a good chance that this is also unlikely to succeed and that the next step is to cut the neck. You must give yourself permission to initiate a surgical airway early in this group. An unsuccessful cricothyrotomy performed at the right time is defensible; a successful cricothyrotomy performed too late is indefensible. Both lead to terrible outcomes, one is defensible, one indefensible. Scenario 1 is an anesthesiologist’s technique compressed into an emergency physician’s timeline.

Scenario 2: Must intubate immediately, no difficult airway features. 

Lots of ED patients fall into this category, perhaps the most typical is the CNS catastrophe who presents with a GCS that can be counted on one hand. Like scenario 1, the airway attempt must proceed without extensive preparation, but both orotracheal intubation and ventilation are more likely to be successful, and this procedural reserve affords you a more measured approach. Be mindful, however, that your brief airway assessment may mislead you, and that you never know what you’re going to get when you put in the laryngoscope. You therefore have decided, before you push drugs and put in the laryngoscope, what you will do when laryngoscopy fails, and what you will do when ventilation fails, and you have the materials at the bedside to do it. Experienced emergency providers recognize procedural reserve as a luxury that the patient can revoke immediately and unpredictably, and are thus ready to transition to a scenario 1 type approach every time they push a paralytic.

Scenario 3: No urgency to intubate, very scary airway. 

When you have time to intubate, you are swimming in the anesthesiologist’s ocean and you need to use a different stroke; in fact swimming like an anesthesiologist is mostly about wearing several life jackets and surrounding yourself with lifeguards. This scenario might involve a patient with a fixed flexion deformity of the cervical spine who is slowly decompensating from a pneumonia, or a patient with an airway tumor who just took 20 long-acting diltiazem tablets and needs gastric lavage. Calling an anesthesiologist is reasonable in these cases and certainly is the right answer on an oral board exam, but an anesthesiologist may not be available (and certainly will not be available on the boards).

The approach for these patients centers on being cognitively and materially ready for plan A, B, C, and D and on awake technique. It’s also nice to have a few friends at the bedside. Exactly what is plan A-D is up to you, as long as these plans are carefully prepared, and one of them is cricothyrotomy, if the patient cannot be intubated or ventilated. This picture demonstrates an example plan A, B, C, and D and a variety of best practice points.

The patient has a variety of congenital cognitive and anatomic anomalies, was very uncooperative and required intubation for emergent MRI. He is known to be a very difficult laryngoscopy. Our plan was to use an awake technique using IM ketamine sedation to augment local anesthesia.

1. Plan A is video laryngoscopy. The intubator (in the middle) made his best attempt but could not visualize the vocal cords, so without removing the device, handed off the video laryngoscope to the assistant on the patient’s left, who was already performing suction.

2. Plan B is flexible endoscopy, which is ongoing. Note that the operators are at this point using both video screens (video laryngoscope and flexible endoscope) simultaneously.

3. The second assistant on the patient’s right has access to the equipment tray and is also the designated surgical airway operator.

4. The neck is marked, and the site has been infiltrated with lidocaine and epinephrine. The more likely is cricothyrotomy, and the more time you have to prepare, the more advanced your surgical airway preparation should be.

5. The second assistant is using his finger to pull on the right corner of the mouth. This under-utilized technique really opens things up.

6. The usual suction (in this case, the second suction) under the patient’s right shoulder is available to either the intubator or second assistant. The flexible endoscope used in this case does not have suction capability, which made the need for suction on either side more likely.

7. The head of the bed is at 30 degrees.

8. The bag-mask is on the patient’s abdomen. A common mistake is to leave the bag-mask behind the operators, hanging off the oxygen tubing, so that as the saturation is dropping, someone who is already freaking out and tangled in wires and tubes has to perform a complex dance move to get at the device.

9. The intubating LMA is ready to be inserted if emergency ventilation is required. This is our Plan C. Plan D is cricothyrotomy (either carefully if Plans A/B/C have failed but oxygenation is adequate, or quickly at any moment if intubation and oxygenation fail).

10. A variety of tubes and blades, as well as oral and nasal airways.

11. The medications and tools we used to anesthetize the airway.

12. Post-intubation equipment.

13. The ventilator is on standby, connected to end-tidal CO2 (not visible) and programmed with patient-appropriate settings.

14. This container holds our supply of bougies and is sadly empty. There is a bougie on a stand behind the video laryngoscope, not visible but easily accessible to the assistant on the patient’s left.

15. Don’t forget to use a checklist.

Scenario 4: No urgency to intubate, no difficult airway features. 

Here we’re talking about the slowly worsening guillain-barré patient, or the patient with the small subdural that the receiving hospital has asked you to intubate for transport. Seems like low risk, and it is low risk, for the patient. But these cases are actually higher risk for you, because when a patient arrives in extremis, your hand is forced and if it doesn’t go well, it’s harder to hold you responsible. In a well patient with normal anatomy who needs to be intubated, you are again in anesthesiologist territory, and you are potentially held to the higher standard of an anesthesiologist, who gets called into the chief’s office when the patient wakes up with a chipped tooth. These are great cases to practice your awake technique; you might find that you don’t mind swimming with a life jacket every once in a while.

Emergency providers are routinely called upon to react to complex scenarios that demand specific life-saving maneuvers, immediately and without warning.  The most important impediment to performing well in these situations is your own catecholamines, and the most important catecholamine reduction strategy is preparation. The extent to which you are prepared to immediately react is your usual state of readiness, and it has two parts: cognitive and material.

Cognitive readiness requires that you consider emergency scenarios and decide on a plan. This starts with a textbook (by textbook I of course mean the internet) and reading what others think you should do in a given emergency scenario. The hard part of cognitive readiness is keeping up with the endlessly changing, endlessly disagreeing opinions, and deciding how to shape them into a plan that you like and that works for you in your environment. Logistics are key.

As medical knowledge expands forever faster, perhaps the most important knowledge of all is knowing what you need to know, and knowing what you can look up. This is not an either/or so much as a spectrum of how close information needs to be to your brain. There are plans that have to live in your brain (management of a completely obstructing airway foreign body), facts that you can take 30 seconds to look up (weight-based dose of atropine), and lists that you can review at your desk (the differential diagnosis of anisocoria). Memory fails when catecholamines are high; planning for emergency scenarios involves the development and deployment of emergency references. Your emergency references must be instantly available, instantly familiar and navigable, and damn reliable. Your plan for emergency scenarios takes into account how close aspects of that plan need to be to your brain and incorporates your emergency references.

As you develop cognitive readiness, the plans you develop for emergency scenarios start with a textbook but proceed in your imagination. I call this invisible simulation, and I find that I do a lot of it in the shower. The more you invisibly simulate emergency scenarios, the more likely the demand to immediately act will be met with calm. It is the combination of recognizing when to act immediately, and doing so calmly, that is the defining characteristic of an emergency professional.

Material readiness is simpler than cognitive readiness but often neglected. Material readiness is having the equipment you need, when you need it, where you need it. Nurses and technicians are often charged with this responsibility, however, when you need suction and it’s not there, the technician being reprimanded later does not get the blood out of your patient’s airway. You will do well to make a habit, at the start of every shift, of verifying that the most important equipment is ready and in a location known to you.

It might seem like a daunting task to cognitively and materially prepare for all the scenarios that might call for immediate action, after all, anything could roll through the doors at any time, right? Well, yes, but not really.

Asphyxiation. We focus on airway preparation for good reason. The best time to go through your airway checklist is before the patient arrives. Of particular interest is the scalpel. It has been said (by me) that there are two kinds of emergency physicians: those who always carry a scalpel in their pocket, and those who will, later on in their career, always carry a scalpel in their pocket.

Suffocation. Your adrenals will appreciate it if you have a well-rehearsed plan for managing the severe asthmatic. Also, having the capability to immediately initiate noninvasive ventilation–without calling for a machine, mask, or respiratory therapist–is worth fighting for. When you are forced to intubate a patient who could have been managed with NIV, you have done your patient a disservice.

Exsanguination and serious trauma. Do you know how to get your hands on uncrossmatched blood immediately? Do you have a good sense of the key interventions to consider in the first few minutes of a trauma resuscitation?

Cardiac arrest. Do you know exactly how to use your defibrillator? What about if the paddles or pads are disconnected? Can you initiate emergency pacing? Do you have a command of ACLS pulseless arrest, or your own algorithm? Do you know how to lyse a diagnosed or strongly suspected pulmonary embolism in cardiac arrest? Do you have a plan for treating cardiac tamponade? For tension pneumothorax, all you need is your scalpel and your finger.

Difficult access. Do you know where your IO device is and how to use it?

The uncontrollably violent patient. Do you know how to activate the highest alert to hospital security? Do you know what drug to use if you only have one shot?

Anaphylaxis. Do you know exactly which preparation of epinephrine to use and how much? Also see asphyxiation, above.

Status epilepticus. Do you have a clear set of priorities when managing the seizing patient? Which drug are you going to reach for first, and what dose? What if you don’t have an IV/IO?

Contamination. Do you know where all your personal protective equipment is, including those fancy masks? How you will make a patient covered in something dangerous safe to bring into your department?

Poisoning. How do you access your antidotes (digoxin immune Fab, lipid emulsion, hydroxocobalamin, etc)?

There are other scenarios that require immediate action, but start with these ten. Be warned that spending too long in the shower will upset your roommate.

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Changes in v13:

• nasal cannula and preoxygenation sections beefed up
• added airway management strategy section
• removed incremental FiO2/PEEP chart
• roc dose changed from TBW to IBW
• added section on cricothyrotomy technique
• ultrasound added to post-intubation complications assessment
• added proviso, “pretreatment agents are always optional.”
• added S to DOPES mnemonic (breath stacking)
• added “function” to “verify cuff” for ETT
• changed phenylephrine from post to peri intubation hypotension
• fancy style enhancements

Bonus: personnel arrangement diagram

There are two kinds of hypertension encountered by emergency physicians: hypertensive emergencies, and hypertension. The term hypertensive urgency has minimal meaning, less than minimal utility, and should be abandoned.

Patients with a hypertensive emergency are critically ill. They need to be in a resuscitation area on intravenous antihypertensive drips. The hypertensive emergencies are acute pulmonary edema, aortic dissection, preeclampsia, subarachnoid hemorrhage, and hypertensive encephalopathy. Intravenous blood pressure reduction may also be indicated in acute coronary syndrome, acute ischemic stroke, and intracerebral hemorrhage. A patient with severe hypertension and arterial bleeding unable to be staunched using conventional means perhaps qualifies as a hypertensive emergency and it may be reasonable to use IV medications to lower blood pressure in these patients as well; however, if allowed to take its natural course, hypertension in these cases will surely be self-limited.

Acute renal failure is always included in the list of hypertensive emergencies, but no one knows what to do with this because while it is clear that longstanding hypertension can box your kidneys, the relationship of the elevated creatinine in the patient in front of you to the hypertension in the patient in front of you is usually impossible to determine. If an acutely ill patient has very high blood pressure and an elevated creatinine that is not known to be old, it is reasonable to treat that patient as a hypertensive emergency. A well patient with hypertension and an elevated creatinine needs to be in an internist’s clinic, not in the emergency department.

There are a variety of hyperadrenergic states such as cocaine intoxication, thyroid storm, autonomic hyperreflexia and pheochromocytoma that may resemble hypertensive emergency, but it is the hyperadrenergic state that is the therapeutic target in these instances, not the hypertension. Do not forget to actively cool patients hotter than 41°C (105°F).

Headache is not a hypertensive emergency, no matter how high the blood pressure. It is likely the headache that is causing the hypertension, not the other way around. Treat the headache and the pressure will come down. The same is true of epistaxis.

Lowering blood pressure quickly, for example with the infamous IV labetalol push, in a patient who does not have a hypertensive emergency, subjects the patient to risk of harm without chance of benefit. [ref] Many of these patients have been living with high blood pressure for a long time and quick reductions can cause quick problems, like stroke. You can bring the blood pressure down with IV meds, and this may make you feel powerful and may pacify the consultant/nurse/patient/family, but as soon as you turn around the pressure will go right back up. Fixing the number is a great pacifier but is bad for patients. The consultant/nurse/patient/family may not know better, but you are paid well to know better. It’s easier to write for 20 of IV labetalol than to explain to the consultant/nurse/patient/family, but you are paid well to explain.

All patients with hypertension, unless clearly secondary to pain or emotion (i.e. hypertension resolves with symptom resolution) should be told that they might have the disease of hypertension and their blood pressure should be rechecked in a primary care physician’s office. How strictly you arrange or recommend followup depends on how high the blood pressure is and how many other diseases the patient has. Shayne & Pitts suggest that patients who have diseases known to be caused by or worsened by hypertension (CAD, CHF, stroke, renal insufficiency, etc) are at higher risk and want to call these patients hypertensive urgency, but this is confusing and unnecessary. Just follow these patients up closely, as is consistent with basic emergency medicine principles. Even if the blood pressure were normal, you would still want these patients to follow up closely because having a lot of bad diseases is a risk factor for a bad outcome.

There is no evidence that initiating oral antihypertensive therapy in the ED makes any difference, but it’s not unreasonable and is an excellent patient satisfaction gambit. EMCREG recommends: “Consider oral antihypertensive therapy for patients with blood pressure > 180/110 mm Hg and initiate therapy in patients with blood pressure > 200/130 mm Hg.” I use amlodipine, because it has few contraindications and toxicities. Emergency physicians should not perform ancillary testing on patients with hypertension either to make sure this isn’t a hypertensive urgency, which is a disease that does not exist, or to attempt to tailor a daily antihypertensive prescription to the creatinine, or ECG, or urinalysis, or anything else. You do gunshot wounds and heart attacks and IV dilaudid seekers, let the primary care physician do hypertension.

The most common scenario where lowering blood pressure quickly makes a big difference is in acute hypertensive pulmonary edema; in this scenario it’s the blood pressure that’s the problem. The treatment is high dose nitroglycerine and noninvasive ventilation. For very distressed patients with very high blood pressure, start with a 1 mg IV push of nitroglycerine and start your drip at 200 mcg/min and stand at the bedside, watching closely, titrating the drip and giving additional boluses as needed. [ref 1, ref 2, ref 3] Patients with active myocardial ischemia and hypertension should also be on a nitro drip, titrated to relief of pain or untoward drop in blood pressure. Not patients with a positive troponin who are legs crossed reading a newspaper, not patients with undifferentiated chest pain waiting on their second enzyme, this applies to patients who are clutching their chest because their heart wants more oxygen than their coronary arteries can deliver.

The blood pressure isn’t the problem in aortic dissection, but we have good reason to believe that elevated blood pressure (and heart rate) makes things worse. If strongly suspected or confirmed, call a surgeon and aggressively dose opiates to abolish pain and anxiety as you bring heart rate down to 60 using IV esmolol (or diltiazem/verapamil if beta blockers are contraindicated); this will also reduce blood pressure. If at that point blood pressure isn’t as low as it could be, add a titratable vasodilator like nicardipine and bring pressure as low as possible while maintaining organ perfusion. [ref]

Preeclampsia is an important hypertensive emergency that is easy to overlook, especially postpartum–almost always within two weeks but possibly up to six weeks after delivery. Hypertensive pregnant or postpartum patients with signs of preeclampsia should be treated with high-dose magnesium (start with 6 g over 20 minutes). EMCREG recommends keeping blood pressure under 160/110 in the antepartum and intrapartum period and less than 150/100 if postpartum or if platelet count is < 100,000. Magnesium will have a salutary effect on blood pressure but if not at target, labetalol is the recommended agent. Other beta blockers and ACE inhibitors should be avoided in pregnancy. Delivery is the therapy of interest in most of these patients, they are therefore usually best managed on L&D.

Blood pressure management is key in subarachnoid hemorrhage, analogous to aortic dissection. Use nicardipine to keep SBP less than 160. [ref] Nimodipine, given orally, is to prevent vasospasm later on, not to lower blood pressure. There’s a lot to think about in SAH, so get some help, even if it comes from a dubious source.

Hypertensive encephalopathy is not headache, patients with hypertensive encephalopathy are encephalopathic and acutely ill. You are not going to diagnose hypertensive encephalopathy until after you’ve ruled out intracranial hemorrhage, because when a patient presents altered and looking bad with a very high blood pressure, it’s much more likely to be ICH, so that patient needs management of ABC’s and then a quick CT scan. If the CT scan is negative, and the patient continues to be altered and very hypertensive, start your nicardipine drip. If the patient’s mentation improves with lowering of blood pressure, you then say, aha, that was hypertensive encephalopathy.

Acute ischemic stroke and spontaneous intracranial hemorrhage patients often have very high blood pressure and medical science has not yet determined if patients with these conditions benefit from blood pressure reduction. For ischemic stroke, If you’re using thrombolytics, keep blood pressure under 180/105 using nicardipine or labetalol. Otherwise, the latest recommendations are to lower blood pressure above 220/120 by 15% within 24 hours. The AHA says it’s probably safe to lower systolic blood pressure to 140 in ICH patients. Otherwise they suggest blood pressure management according to this table, which isn’t confusing at all. In traumatic brain injury, leave hypertension alone; focus on preventing hypotension and teaching your consultants that ketamine does not raise ICP and is an appropriate RSI agent in this context.

Lastly, tell your patients who check their blood pressure at home and then come in for hypertension that checking blood pressure at home causes cancer.

These days, with all the fancy airway tools and techniques, placing an endotracheal tube in the trachea often feels as dramatic as placing a foley in the urethra. Your hard-fought airway skills and intestinal fortitude seem wasted. You might find yourself obscuring your intern’s view by “applying cricoid pressure” just to watch him get that same panic-induced nausea you had to suffer day in day out, all those years, glidescope be damned. Intubation these days is too friggen easy. Well it’s about to get even easier.

The high flow nasal cannula is a device that has been used by neonatologists for some time, but is now making its way into adult medicine. By using special tubing, warming, and humidification, the device allows for the nasal adminstration of oxygen at upwards of sixty (60) liters per minute. This enables the delivery of 100% oxygen fraction and true positive pressure, up to around six centimeters water of PEEP. The apparatus itself has a relatively small footprint and is easier to set up than non-invasive ventilation. The oxygen hose connects to a seperate valve on the wall-mounted flowmeter, which liberates precious oxygen sources for the bag valve mask and face mask.

Being blasted with 60 liters per minute of oxygen through your nose isn’t a pleasure, but it’s much more comfortable than NIV, and of course allows the patient to talk, eat, vomit, whatever they want. Because so much water has to be added to the air, the HFNC should not be used in patients who cannot tolerate additional volume. We will see HFNC being used in the ED on many of the COPD and pneumonia patients who linger miserably on NIV, not sick enough to require ETI but not well enough to fly on simple supplemental oxygen.

But where HFNC really shines is during RSI. Put the big cannulae into your patient’s nose and let’r rip. Add a face mask or NIV or whatever your preoxygenation pleasure, then push your meds and laugh to yourself as the saturation rises during apnea. Whistle sweetly as the intern illuminates every inch of the soft palate with great determination. Hell, go see another patient and tell him to call you when he’s given up.* You remember, though, the days of the giants. When being regarded as a skilled laryngoscopist meant something. When the word airway made internists scatter like mice. When it wasn’t so easy to save a life.

*Note that hypercapnea is a consequence of apnea seperate from hypoxia. High CO2 levels are generally tolerated well, but now that we can seemingly oxygenate the apneic patient indefinitely, remember that patients with severe acidemia or intracranial insults require the expeditious establishment of ventilation as well as oxygenation.

Ventilation is the most important skill in airway management, and most of us learned to do it incorrectly.

Slideset.

As given at Emcrit’s critical care conference.

Management of Life-Threatening Asthma in the Emergency Department (pdf)

Management of Life-Threatening Asthma in the Emergency Department (png)

Regarding nebulized epinephrine: 1:1000 L-epi is 0.1% = 1 mg/ML, so 5 mL = 5 mg. 2.25% racemic epi = 22.5 mg racemic epi per mL = 11.25 mg L-epi (the active isomer) per mL, and we’re using 0.5 mL, which is 5.625 mg L-epi, so roughly  the same dose.

Dexmedetomidine (trade name Precedex) is an alpha-2 receptor agonist, similar to clonidine. Whereas clonidine provides a robust decrease in blood pressure with mild sedation, dexmedetomidine provides robust sedation with a mild decrease in blood pressure. It does not depress airway reflexes or respiration. It has a variety of potential uses in the emergency department, including procedural sedation, the facilitation of awake intubation or noninvasive ventilation, and the treatment of alcohol withdrawal. For these indications, however, we have agents that are at least as good, familiar, and a hell of a lot cheaper.

Sedation for painless procedures in children is the scenario that may push dexmedetomidine into the emergency physician’s toolkit. Kids who require sedation for CT or MR imaging would ideally be managed without placing an IV (nix etomidate), using an agent that does not cause significant cardiorespiratory depression (nix barbiturates), is otherwise safe (nix chloral hydrate, which is also unpredictable, untitratable, and lasts forever), and reliably causes kids to be still (nix ketamine).

This case series reports on 65 consecutive children sedated for CT or MRI with intramuscular dexmedetomidine, administered either once or twice at a dose of 1-4 mcg/kg, the exact dose left to provider discretion, to achieve a target Ramsay score of 4 (asleep but briskly responsive to a light stimulus). 4 patients out of 65 required a second IM dose to achieve a Ramsay score of 4. Once Ramsay 4 was achieved, no other agents were given for the duration of the procedure. The mean dose was about 2.5 mcg/kg.

All 65 children successfully completed the study. Though 9 out of 65 patients developed transient hypotension, there were no adverse events that required intervention. 65 patients is not enough to conclusively demonstrate safety, but 100% efficacy is hard to beat, and I suspect the safety profile will stand up in larger series.

Average time to sedation was 13 minutes. The average time from the end of the study to recovery was 22 minutes in the MRI group and 17 minutes in the CT group, with wide confidence intervals, i.e. there was no difference in recovery times. Since MRI is significantly longer than CT, and no sedatives were administered after the initial dose, how can this be?

Dexmedetomidine causes a different type of sedation than what we’re used to. It’s not a CNS depressant in the typical sense, it’s a powerful sympatholytic. Patients sedated with with dexmedetomidine will wake up with minimal stimulation, but when that stimulation is removed, they gently drift off to sleep. This is not a useful feature when trying to facilitate awake intubation, but it’s perfect for getting a 3 year old through the CT scanner.

Mason KP, Lubisch NB, Robinson F, Roskos R. Intramuscular dexmedetomidine sedation for pediatric MRI and CT. American Journal of Roentgenology 2011 Sep;197(3):720-5.

A common mistake made by junior emergency physicians (and sometimes not junior emergency physicians) is to identify a problem and address it without considering its precipitant. Recognizing that the patient’s symptoms are due to an exacerbation of CHF, asthma, or COPD, DKA, seizure (the med student thought it was syncope but you know better), atrial fibrillation, hypoglycemia, dehydration, hepatic encephalopathy, uremia, or electrolyte disturbance: that’s fabulous. Knowing how to treat these conditions: phenomenal. But if you really want to impress the opposite sex, or the same sex, or whatever you’re into, figure out why the patient is having this problem, now. Fortunately, the same things cause most of the common afflictions of ED patients. So here they are, the precipitants of everything:

medication changes and, especially, noncompliance

recreational intoxicants and other lifestyle choices

withdrawal (but why was this patient unable to get his fix today? there may be a further precipitant)

infection (lungs, urine, skin, CNS, abdomen, indwelling catheters and devices, soft tissue/bone)

ischemia (heart, brain, bowel)

arrhythmia

pulmonary embolism

thyrotoxicosis or hypothyroidism

occult trauma / abuse / neglect

bleeding (GI bleed, vaginal bleed, urologic bleed, retroperitoneal bleed, abdomen, thorax, thigh, street)

pregnancy (if there’s abdominal pain, bleeding, or syncope – don’t forget to rule out ectopic)

That doesn’t mean we ought to do ancillary testing to rule out these precipitants of everything; in most cases a directed history and physical is all you need. Just remember to ask the question, why is this patient having this problem, now?

{adapted from a lecture I give to first year med students, at the end of a two-week course where we teach them how to be an effective first responder in a variety of pre-hospital emergency scenarios.}

Emergency doctors staff emergency rooms. We see whatever comes in, as fast as it comes in. We are the front door of the hospital, and we never close our doors. The specialty is defined by several key characteristics, which are virtues or vices, depending on your perspective, and often they are both at the same time. So I’m going to present them as both at the same time, in a sort of pro-con format.

1. The undifferentiated patient

No other doctor routinely manages patients she knows nothing about. A typical emergency patient was found on the street in a coma. He could be minutes away from dying, or just really drunk and needs to sleep it off. We’ve got to figure it out without even knowing his name, much less his medical history or the events leading up to his present condition. Making the diagnosis is really fun.

However, Uncertainty is the currency of emergency medicine. We have to make important decisions with very little information. We are wrong a lot. Sometimes, when we’re wrong, people die. Learning to be comfortable with uncertainty is difficult.

2. Speed

Emergency physicians have to think fast and act fast.  It has been reported that emergency medicine has the highest decision density not just of any medical specialty but of any human endeavor. This is fantastic for people who have limited attention spans and require a lot of stimulation. It also makes shifts fly by; I routinely realize it’s time to start wrapping up and I feel like I just arrived.

However, when you work in the emergency room, you are working hard. It’s tiring.

3. Momentary care

Emergency physicians do not follow patients. When you’re off, you’re off. We do not carry pagers. Being off when you’re off is a big deal from a quality of life perspective – when your shift ends at six, and you make plans for eight, you’re going to be there, and you’re not going to get called away.

However, we don’t form relationships with patients, and the patients we do form relationships with are usually not the kind of patients you want to form relationships with. Emergency medicine can feel impersonal, and it’s harder to learn from your mistakes because the consequences of your mistakes often are not apparent until you’re no longer taking care of the patient. But mostly the problem is that we don’t get chocolates from our patients at holiday time.

4. Shiftwork

Scheduling for emergency docs is flexible – if I want a month off, I can just ask not to be put on the schedule for a month. Combine this flexibility with the momentary care aspect–that we don’t follow patients–and you can see how this makes for a kind of freedom that is pretty unique in medicine.

However, emergency clinicians work erratic hours, including nights. This is probably the biggest challenge for emerg docs. If you need a regular schedule to sleep right, this is not the speciality for you. The ED never closes, and so we work evenings, nights, weekends, and holidays. We take a lot of pride of being available whenever we are needed, but sometimes you can feel out of sync with the rest of the world.

5. The front door

We are the safety net for everyone and, health care reform aside, that’s not going to change anytime soon. The emergency department is on the ground floor, and when you work in the emergency department, you feel like you are connected to the community. You feel like you are helping people who really need help.

However, our workflow is dictated by whatever comes through the front doors, and this is entirely unpredictable. The emergency department is in a constant state of barely controlled chaos, and sometimes it’s uncontrolled chaos. Many of my patients are having the worst day of their lives. Many of my patients live on the margins of society and their average day is worse than the worst day of most people’s lives. It can be very challenging to take care of these patients.

6. Disease spectrum

You name it, we deal with it. No other specialty even comes close to the multiplicity of presentations and diagnoses that an emergency physician confronts in a single shift. You get to put your hand in a lot of cookie jars.

However, emergency physicians rely heavily on consultants. I spend a lot of time on the phone talking to people whom I’m giving work to, so they don’t really want to talk to me. Also, when I call a consultant, I’m talking to someone who knows more about what we’re talking about than I do. When I have a complex neurology problem, I call a neurologist and talk with her about neurology; when I have a complex dermatology problem, I call a dermatologist and speak with her about dermatology. And sometimes consultants can get really uppity and even condescending, especially the ones who never come down to the emergency department and see us reducing fractures, and defibrillating people in cardiac arrest, and delivering babies, and sewing up the laceration on the billionaire everyone’s heard of who’s lying one gurney over from the undocumented immigrant who also has a laceration and speaks a language no one’s heard of, and providing comfort care to the 96 year old taking her last few breaths, and intubating the nearly dead 10 day old with undiagnosed congenital heart disease. But constantly asking for help can be hard on the ego. You have to be comfortable not being the expert.

In addition to improving laryngeal view, there is now evidence that elevating the head of the bed prolongs apneic desaturation time. This makes good sense, and the tradition of intubating patients in the supine position should be added to the long list of Things We’ve Been Doing Wrong All This Time. Using semi-fowlers position also probably reduces the risk of regurgitation/aspiration, and is strongly recommended for all patients being intubated for upper GI bleed. But make it your routine and you will benefit when that extra little bit of glottic view, those extra few seconds of apnea, and that extra bit of protection against regurgitation really matter. There is no downside.

A middle aged gentleman presents with a basin filled with bright red blood. He’s choking, gagging and every ten seconds coughing up another huge mouthful. His daughter tells you that he has a base of tongue tumor that, 20 minutes ago, started bleeding. A lot.

Asphyxiation and exsanguination are both immediate concerns. He clearly needs to be intubated now. But how?

Awake technique is very unlikely to be successful; the patient is in extremis, blood pouring out of his mouth. He will need RSI. But you have at least two reasons to be concerned about RSI: 1. The huge amount of blood filling the oropharynx will obsure your view of the glottis. 2. The base of tongue tumor. Lord knows what you’ll see when you get in there.

The answer: Four Provider ED Double Setup.

Provider #1: Performs video laryngoscopy.

Provider #2: To the right of provider #1, performing suction.

Provider #3: To the left of provider #1, peforming suction.

Provider #4: At the patient’s side, prepared to perform cricothyrotomy.

For patients with massively bleeding oral lesions, bilateral suction, simultaneous with airway visualization, is necessary. Until recently, this was almost impossible, because only the operator can see the glottis during conventional laryngoscopy. Video laryngoscopy, however, has changed the rules. In addition to getting your eyes much closer to your target, with video laryngoscopy more than one person can participate in laryngoscopy at the same time. The magnitude of this advantage wasn’t apparent to me until a middle aged gentleman with basin filled with bright red blood presented himself in the process of both asyphyxiating and exsanguinating. I’ll bet there are other useful techniques made possible by projecting the airway onto the big screen for everyone to see. Laryngoscopy is now a team sport.

Thanks to Vishal Demla, Elizabeth Dei Rossi, Taylor Moran-Gates, Daniel Mindlin, and especially Eduardo Lacalle.

Rapid-onset antidepressant? Hot damn.

I would prefer an ethanol antidote, or a cure for secondary gain, but this is a start.

Abstract: We examined the preliminary feasibility, tolerability and efficacy of single-dose, intravenous (i.v.) ketamine in depressed emergency department (ED) patients with suicide ideation (SI). Fourteen depressed ED patients with SI received a single i.v. bolus of ketamine (0.2 mg/kg) over 1–2 min. Patients were monitored for 4 h, then re-contacted daily for 10 d. Treatment response and time to remission were evaluated using the Montgomery–Asberg Depression Rating Scale (MADRS) and Kaplan–Meier survival analysis, respectively. Mean MADRS scores fell significantly from 40.4 (s.e.m.=1.8) at baseline to 11.5 (s.e.m.=2.2) at 240 min. Median time to MADRS score ≤10 was 80 min (interquartile range 0.67–24 h). SI scores (MADRS item 10) decreased significantly from 3.9 (s.e.m.=0.4) at baseline to 0.6 (s.e.m. =0.2) after 40 min post-administration; SI improvements were sustained over 10 d. These data provide preliminary, open-label support for the feasibility and efficacy of ketamine as a rapid-onset antidepressant in the ED.

Int J Neuropsychopharmacol. 2011 May 5:1-5. PMID: 21565879

slideset available here.

Designed to be used as one double-sided page.

Available in pdf form.

If you’d like to modify the checklist for your institution, I can send you the original layout (omnigraffle format) and tables (excel format).

I have watched droperidol disappear from my ED’s formulary and it makes me sad. So good for so many purposes, so convenient to use, so safe, so cheap. It had to go. The black box stamp of death.

Except that I just learned that there has been a black box warning on all fluoroquinolones since July 2008. Not only has cipro and levaquin use continued unabated, no one is even talking about their black box, I hadn’t even heard of it until just now. What else has a black box that I didn’t know about? Well, it’s an impressive list of drugs. Here are some highlights for the emergency doc:

Clindamycin: “Clindamycin phosphate therapy has been associated with severe colitis which may end fatally, it should be reserved for serious infections where less toxic antimicrobial agents are inappropriate, as described in the INDICATIONS and USAGE section.”

Clopidogrel: “Poor metabolizers with acute coronary syndrome or undergoing percutaneous coronary intervention treated with Plavix at recommended doses exhibit higher cardiovascular event rates than do patients with normal CYP2C19 function.”

Factor VIIa: “Clinical studies have shown increased risk of arterial thromboembolic adverse events with this product when administered outside the current approved indications. Fatal and non-fatal thrombotic events have been reported.”

Dihydroergotamine: “Serious and/or life threatening peripheral ischemia has been reported with coadministration of this drug with potent CYP 3A4 inhibitors (including protease inhibitors and macrolide antibiotics).”

Flumazenil: “Has been associated with seizures.”

Haloperidol: “Elderly patients with dementia related psychosis treated with atypical antipsychotic drugs are at an increased risk of death compared to placebo.” “Analyses of seventeen placebo controlled trials (modal duration of 10 weeks, largely in patients taking atypical antipyschotic drugs, revealed a risk of death in the drug treated patients of between 1.6 to 1.7 times that seen in placebo treated patients.” “Observational studies suggest that, similar to atypical antipsychotic drugs, treatment with conventional antipsychotic drugs may increase mortality.” “This drug is not approved for the treatment of patients with dementia-related psychosis.” How about that. Meanwhile, haldol rains from the sky in EDs the world over, especially on patients with dementia-related psychosis. And for good reason.

NSAIDs: “NSAIDs may cause an increased risk of serious cardiovascular thrombotic events, myocardial infarction, and stroke, which can be fatal.” “NSAIDs cause an increased risk of serious gastrointestinal adverse events including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal. These events can occur at any time during use and without warning symptoms.” Yes, NSAIDs. Ibuprofen. Black friggen box. And ketorolac has its own, massive black box.

Metformin: Huge black box around lactic acidosis. Am I the only EP sending new diabetics home on metformin?

Methotrexate: God help you if you work in one of those EDs where you’re supposed to give methotrexate to ectopics without OB involvement.

Metronidazole: “Carcinogenic in mice and rats.” “Avoid unnecessary use.”

Midazolam: “Reports of respiratory depression, airway obstruction, desaturation, hypoxia, and apnea, particularly when used with concomitant CNS depressants (e.g.opioids).”

Nitroprusside: “Can cause significant drops in blood pressure leading to irreversible ischemic injury or death.”

Procainamide: “Limit the use of this drug to patients with life-threatening ventricular arrhythmias.”

Succinylcholine: “Cardiac Arrest has been reported resulting from hyperkalemic rhabdomyolysis, most frequently in infants or children (but has occurred in adolescents) with undiagnosed skeletal muscle myopathy or Duchenne’s muscular dystrophy.”

Warfarin: “Can cause major or fatal bleeding.” No shit.

And, of course there’s the droperidol black box. It’s interesting that everyone has freaked out about the droperidol black box, which has been aggressively refuted, while we continue to use other black boxed drugs without thinking twice.

Emergency physicians often manage IV catheter malfunction causing extravasation, which can result in significant tissue necrosis. Hyaluronidase may significantly reduce tissue injury from extravasation by hydrolyzing mucopolysaccharides present in connective tissue. This results in a transient increased permeability of the tissue and subsequently enhances diffusion of liquids through the subcutaneous space. Although the irritating medication is distributed over a wider area, quick absorption minimizes tissue injury.

Hyaluronidase has been shown to reduce the extent of tissue damage following extravasation of parenteral nutrition solutions, radiocontrast media, phenytoin, promethazine, dextrose, mannitol, and the vinca alkaloid chemotherapeutic agents (e.g. vincristine, vinblastine). Hyaluronidase is well tolerated and has been used in neonates as well as adults.

Administration techniques differ, but most sources recommend making a ten-fold dilution of a 150 unit vial of hyaluronidase in NS to provide a concentration of 15 units/ml, then dividing the dose into 0.2 ml subcutaneous injections via a 25 gauge needle in 4-5 different sites along the leading edge of erythema.

Hyaluronidase is most effective if administered within the first 2 hours after an extravasation, however, it may still be beneficial when given up to 12 hours after the event.

References:
(1) Wiegand R, Brown J. Am J Emerg Med 2010;28(2):257.e1-2.
(2) Cochran ST, et al. Acad Radiol 2002;9 Suppl 2:S544-6.
(3) Kuensting LL. J Pediatr Health Care 2010;24(3):184-8.
(4) Sokol DK, et al. J Child Neurol 1998;13(5):246-7.

from:

emedhome.com

two-page .pdf
vector image .pdf
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To appear in the March 2011 issue of EM Practice Guidelines Update.

Thanks to sigrid hahn, scott weingart, kaushal shah, kit tainter, rob arntfield.

In this month’s Annals of Emergency Medicine, Sener et al report on their nicely blinded study where 182 adult subjects were randomized to one of four groups – IV or IM ketamine (at dissociative doses), with or without IV midazolam (.03 mg/kg). They conclude that midazolam reduces the incidence of recovery agitation based on their results:

Green and Krauss provide an accompanying editorial where they caution that the treatment effect as reported by Sener might be exaggerated and conclude:

“Given this compelling evidence from Sener et al, many clinicians will choose to ‘tame’ ketamine in adults by routinely coadministering midazolam. Others, according to the caveats above, will just as reasonably elect to individualize such prophylaxis, using a subjective assessment of a given patient’s risk. After all, should their prediction fail and an unpleasant reaction result, it can readily be quelled with midazolam. Regardless of these approaches, the ketamine ‘tiger’ may not be as ferocious as some fear.”

In my 2008 catalog of ketamine adverse events in adults, I describe three strategies for dosing midazolam–predissociation, preemergence, and PRN. I use the PRN strategy, and in hundreds of sedations of adults, I’ve needed to use it once. Here is my accumulated wisdom on how to use ketamine.

* Use ketamine. No other agent matches its safety, efficacy, and reliability. The only patients who should not receive ketamine are patients in whom an increase in heart rate or blood pressure would really concern you. All the other variously reported contraindications, including oral procedures and especially the concerns around ICP (this is more of an issue for RSI than PSA), can be ignored*. For very quick procedures like cardioversion, propofol is probably a better choice. Propofol also provides better muscle relaxation for ortho procedures, but these procedures often take a while, and propofol is hard to use for longer procedures. Ketofol is sexy but really offers no advantage over propofol alone for very brief procedures or ketamine alone for longer procedures.

* Be prepared to intubate. This goes for all PSA agents and procedures. Full intubation setup, paralytic in vial. In PSA, airway and breathing are everything; have all your tools ready. Laryngospasm is rare but it happens – if you’re ready for it, it’s no big deal, if not, it’s a big deal.

* Use it IM in pediatrics. Starting an IV for ketamine PSA in a child who is already suffering some other painful condition is unnecessary and therefore cruel. The best approach is to immediately treat the painful condition with atomized intranasal fentanyl, get your xrays or whatever, then give IM ketamine, 4 mg/kg. Once dissociated, you can start an IV easily and painlessly, or you can skip the IV completely and do your procedure.

* Make the patient comfortable before ketamine PSA. The response to ketamine is largely emotional. When the patient goes down agitated and in pain, she is more likely to have bad dreams and a scary emergence.

* Coach the patient pre-induction. Tell your patients that you are giving them a drug that will make them have vivid dreams, but that they can choose their dream and it can be very enjoyable, and that when they wake up, their wrist is going to feel a lot better. Offer some suggestions as you’re pushing the drug; I like describing a pleasant beach scene.

* Give them a dose of ondansetron before or during PSA. Ketamine causes post-procedure nausea and vomiting frequently. There is no literature evaluating this strategy, but in my opinion zofran works, and my opinion matters. To me.

* If giving ketamine IV, give it over 60 seconds. If you give IV ketamine in a quick bolus, you will often see apnea. This resolves by itself, but it’s really hard to watch a patient not breathing for 30 seconds. Slowing the infusion makes apnea much less likely. In order to give a slow infusion, you have to

* Either dilute the ketamine or draw it into a very small syringe. Most EDs stock 50 mg/ml and 100 mg/ml preparations (some EDs stock more than one concentration – be careful). You cannot slowly give 2 cc in a 10 cc syringe.

* Have the midazolam ready and don’t hesitate to use it if the patient appears to be experiencing psychological distress. You will rarely need it if you follow the steps above, but I’ve read some firsthand reports of bad ketamine emergence reactions and they sound truly terrifying. However, the fear of an emergence reaction is a silly reason to avoid using ketamine. Unlike the adverse reactions associated with most other PSA agents, emergence reactions are not dangerous, and are very easily treatable.

* You don’t always need to use a full dissociative dose. 1-2 mg/kg IV causes dissociation; once you’re dissociated you can’t be any further dissociated and larger doses just prolong duration of action (which can be a good thing, e.g. an intubated, hypotensive but still thrashing about patient). For a quick, only moderately painful procedure, 20 mg boluses work great. The ketamine continuum starts with analgesia (note the analgesic dose ketamine drip), to loopy (giggling, responding to questions and tolerating pain), to partly dissociated (sort of responsive to questions but indifferent to pain) to fully dissociated (awake but unresponsive to any external stimuli). That said, don’t hesitate to give a full dissociative dose if you’re not in the mood to get fancy. Dissociated is da bomb.

Sener S et al. Ketamine With and Without Midazolam for Emergency Department Sedation in Adults: A Randomized Controlled Trial. Ann Emerg Med. 2011;57:109.

Green S and Krauss B. The Taming of Ketamine— 40 Years Later. Ann Emerg Med. 2011;57:115.

Strayer RJ and Nelson LS. Adverse events associated with ketamine for procedural sedation in adults. American Journal of Emergency Medicine, Volume 26 Issue 9, November 2008, pages 985-1028.

* Here are the contraindications as reported in the 2011 ACEP Clinical Policy.
Absolute: Age less than 3 months; schizophrenia.
Relative: “Major” procedures stimulating the posterior pharynx; history of airway instability, tracheal surgery, or tracheal stenosis; active pulmonary infection or disease including URI or asthma; known or suspected cardiovascular disease; CNS masses, abnormalities, or hydrocephalus; glaucoma or acute globe injury; porphyria, thyroid disorder, or thyroid medication.

EDICTv12 [acrobat format]
Changes from version 11:

* Torso angle of 30 degrees recommended

* Nasal cannula for preoxygenation and apneic oxygenation recommended

* LMA moved from difficult to basic airway equipment

* Magill forceps moved from basic to difficult airway equipment

* Rocuronium dose changed from 1-1.2 to 1.2 mg/kg

* Reduced tidal volume wording clarified “if sepsis / prone to lung injury”

* DVT prophylaxis removed from post-intubation maneuvers

* “Verify that airway equipment is ready for next patient” added to post-intubation maneuvers

* “Consider effects of decreased preload as PEEP is augmented” warning added to PEEP chart

Another myth we can put to rest.

Of 161 patients with digoxin toxicity in one hospital over 17.5 years, 23 received calcium, and no one developed stone heart, whatever the hell that is. Pretty easy study to do, but probably the best data we’ll have on this subject. So give your calcium while you’re getting your hands on and preparing digibind.

Levine M, Nikkanen H, Pallin D. The effects of intravenous calcium in patients with digoxin toxicity. Journal of Emergency Medicine. 2011; 40(1):41-46.

Background: Digoxin is an inhibitor of the sodium-potassium ATPase. In overdose, hyperkalemia is common. Although hyperkalemia is often treated with intravenous calcium, it is traditionally contraindicated in digoxin toxicity.

Objectives: To analyze records from patients treated with intravenous calcium while digoxin-toxic.

Methods: We reviewed the charts of all adult patients diagnosed with digoxin toxicity in a large teaching hospital over 17.5 years. The main outcome measures were frequency of life-threatening dysrhythmia within 1 h of calcium administration, and mortality rate in patients who did vs. patients who did not receive intravenous calcium. We use multivariate logistic regression to ensure that no relationship was overlooked due to negative confounders (controlling for age, creatinine, systolic blood pressure, peak serum potassium, time of development of digoxin toxicity, and digoxin concentration).

Results: We identified 161 patients diagnosed with digoxin toxicity, and were able to retrieve 159 records. Of these, 23 patients received calcium. No life-threatening dysrhythmias occurred within 1 h of calcium administration. Mortality was similar among those who did not receive calcium (27/136, 20%) compared to those who did (5/23, 22%). In the multivariate analysis, calcium was non-significantly associated with decreased odds of death (odds ratio 0.76; 95% confidence interval [CI] 0.24–2.5). Each 1 mEq/L rise in serum potassium concentration was associated with an increased mortality odds ratio of 1.5 (95% CI 1.0–2.3).

Conclusion: Among digoxin-intoxicated humans, intravenous calcium does not seem to cause malignant dysrhythmias or increase mortality. We found no support for the historical belief that calcium administration is contraindicated in digoxin-toxic patients.

Aligning the external auditory meatus to the sternal notch goes a long way toward optimizing head position relative to the chest, however, this is only the best estimate. You cannot know the head position that will maximize glottic view until you get in there. The best approach is as follows:

Before even attempting insertion of the laryngoscope, put the patient’s entire occiput in the palm of your right hand. An assistant should be pulling the right corner of the mouth.

Then use your right hand to gently elevate the head toward the ceiling (augmenting sniffing position) and extend the neck. If the patient is adequately relaxed, this maneuver will open the mouth and open the angle between the neck and sternum (see pics below), facilitating easy insertion of the laryngoscope.

Insert the laryngoscope blade and control the tongue. As you gently advance toward the epiglottis, continue to maneuver the head by  (a) moving it toward or away from the ceiling and (b) extending or flexing the neck, as dictated by whatever maneuvers maximize your view of the glottis.

Once the patient’s head is in the position that maximizes glottic view, you need to mobilize your right hand to either take the endotracheal tube/bougie or, if the glottic view is still inadequate, externally optimize the larynx with bimanual laryngoscopy. Most operators can easily use the laryngoscope to suspend the head of most patients in the optimal position while they use their right hand for other tasks. If the patient’s head is too heavy to comfortably hold up, an assistant can either hold the head or place a roll of sheets under the head in that position. Or:

A Novel Positioning Technique to Assist Laryngoscopy in Patients with a Potentially Difficult Airway

Waldron S, Dobson A. European Journal of Anaesthesiology. 2010; 27:921.

Dr. Waldron here describes the use of a 1 liter fluid infusion pressure bag placed under the patient’s shoulders as an easily adjustable implement to raise the head and extend the neck. Very cool. Especially if you’re short on assistants.

If you stuff a lot of sheets under the head of the patient before you begin, so that the head starts off significantly elevated compared to the chest, you limit what you can do with bimanual head optimization. I therefore recommend that when inserting the sheets, you position the ear somewhat posterior to the sternal notch, expecting that you will need to elevate the head during laryngoscopy.

Enough already with this nonsense.

Schabelman & Witting. The Relationship of Radiocontrast, Iodine, and Seafood Allergies: A Medical Myth Exposed. The Journal of Emergency Medicine, 2010 39:5 701-707.

The evidence suggests that asking if patients are allergic to shellfish or iodine has no relevance to radiocontrast allergies. This questioning perpetuates the myth of an association between shellfish, iodine, and contrast agents. Instead, ask if they have any allergies, have had a previous reaction to a contrast agent, or have evidence of atopy, such as asthma. Educate nurses and technicians to stop propagating this myth as well.

If your patient offers an allergy to iodine or shellfish, ask the patient if they mean to say that they have had a reaction to intravenous contrast in the past. Educate them that they do not have an “allergy” to iodine, and that an allergy to shellfish does not change the risk of reaction to intravenous contrast any more than any other allergy.

If your hospital does not routinely use a low osmolarity, non-ionic agent, request this type of medium for atopic patients, patients who had a reaction to an intravenous contrast agent in the past, and patients with systemic disease that increases their risk for contrast reaction.

Do not delay emergent studies for steroid premedication. Only lengthy 12h premedication protocols have shown any effect on reaction rates, and this small benefit was manifested primarily by decreasing minor reactions. No steroid protocol has shown a significant benefit in decreasing severe or fatal reactions.

Monitor all patients for at least 20 min after administration of radiocontrast.

Treat any severe reaction to radiocontrast the same way you would treat a severe anaphylactic reaction.

Picture credit: http://www.flickr.com/photos/bokchoi-snowpea/4325542571/

Also, while we’re on the topic of iodine, have you noticed that on the chlorhexidine packages it says don’t use for lumbar puncture? More nonsense.

From his PaACEP resident lecture. For children who are undergoing painless imaging studies and would not otherwise require an IV.

Dose: 25 mg/kg

Typically comes in powder form for IV use, one vial = 500 mg.

Directions suggest that you reconstitute with 50 cc NaCl, which would = 10 mg/cc.

Chudnofsky method is to reconstitute with 5 cc NaCl, mix well to get all powder into solution, now you have 100 mg/cc.

Attach to syringe an 18g angiocath without needle.

Insert into rectum, not very far (1-2 cm in small child), inject slowly to keep fluid in rectum.

Close the buttocks together, hold with 3 inch cloth tape.

According to his study (PMID 10790471), average time to sedation = 7 minutes, average time to awake = 60 minutes. Note that of 100 patients, “Six had brief oxygen desaturations that responded to repositioning, although 3 of these also were given brief bag-valve- mask ventilation per institutional protocol. One developed a continuous cough. All had complete recovery and none required intubation.” So these patients have to be on a pulse oximeter and someone has to be ready to adjust airway, provide O2, and BMV as needed. I would round down the dose to closer to 20 mg/kg.

Conscientious Sedation

Patients who scream usually get my attention and things go something like this. Bypassing the protocol on a technicality (narcotics alone without sedatives are not “conscious sedation”), I administer rapid boluses of fentanyl (150 to 200 mcg usually suffice in total). Within a minute or two, the patient enters the most euphoric experience of her recent memory, closing her eyes and beginning to smile. I signal the surgeon who starts the procedure while the patient lazily registers the discomfort, but when offered more pain medication claims “it’s OK.” I hang out in the room during the procedure, adding fentanyl if needed and catching up on paperwork. Meanwhile, content surgeons, who despite their hard shells do prefer a nonsuffering patient, wrap it up in style. When all is done, the patient looks at me with immeasurable gratitude, and I recall all the reasons for which I became a physician. My term for it: “conscientious sedation.”

It uses up ED attending time, but for all the right reasons. I start with half the intended final dose for the rare hyperresponder. There is naloxone in my pocket and I’ve never had to use it. I am ready to intubate should the need arise, but I doubt it will. I memorized side effects of fentanyl and consider risk-benefit beforehand. And yes, I think it is an adequate approach to procedural pain for most ED interventions on typical adult patients, especially when local anesthetics are appropriately used.

from: Veysman, Boris D. Annals of Emergency MedicineVolume 56, Issue 4, October 2010, Page 430

Photo: http://www.flickr.com/photos/fimbrethil/387068341

Topical proparacaine .05% (usual concentration is .5%) 2-4 drops to affected eye as often as needed for pain. Safe and effective in 15 patients.

God bless Dr. Ball et al, and god bless Canada, where medical decision-making is driven by concerns other than fear of litigation.

Now, we need a larger study. And how will I discharge a patient with dilute proparacaine?

CJEM 2010;12(5):389-94

Objective: Dogma discourages the provision of topical anesthetics to patients with corneal injuries discharged from the emergency department because of the toxicity of concentrated solutions. We compared the analgesic efficacy of dilute topical proparacaine with placebo in emergency department patients with acute corneal injuries.

Methods: We conducted a prospective randomized controlled trial of adults with corneal injuries presenting to one of 2 tertiary care emergency departments in London, Ont. Patients were randomly assigned to groups receiving either 0.05% proparacaine or placebo drops as outpatients and were followed up to heal- ing by a single ophthalmologist. Our primary outcome was pain reduction as measured on a 10-cm visual analog scale.

Results: Fifteen participants from the proparacaine group and 18 participants from the placebo group completed the study. The mean age of the patients was 38.7 (standard deviation 12.3) years and the majority were male (85%). Pain reduction was significantly better in the proparacaine group than in the placebo group, with a median improvement of 3.9 (interquar- tile range [IQR] 1.5-5.1) cm on the visual analog scale versus a median improvement of 0.6 (IQR 0.2-2.0) cm (p = 0.007). The proparacaine group was more satisfied (median level of satis- faction 8.0 [IQR 6.0-9.0] cm on a 10-cm visual analog scale v. 2.6 [IQR 1.0-8.0] cm, p = 0.027). There were no ocular compli- cations or signs of delayed wound healing in either group.

Conclusion: Dilute topical proparacaine is an efficacious analgesic for acute corneal injuries. Although no adverse events were observed in our study population, larger studies are required to evaluate safety.

Picture credit: Rakesh Rocky http://www.flickr.com/photos/22905496@N07/4259910413/

Special thanks to Reuben for inviting me to post this review from my teaching resident rotation.

Question:
Is a “corrected” CSF WBC count accurate for diagnosing meningitis for a traumatic LP?
Background:
Traumatic lumbar punctures may obscure accurate diagnoses. Many authors suggest correcting the WBC count by various methods — the most popular seem to be either 700 RBC = 1 WBC, or by using the actual patient’s RBC:WBC ratio in the blood. While this seems intuitive, does it work?
Answer:
Probably not.

Basically, no; the calculations are not helpful. But if the WBC count is MUCH higher than expected, it’s probably a positive tap.

Key points:

• The sources I could find simply assert that correction is a viable method; I could not find any actual evidence that these corrections are valid.
• Multiple small studies show that corrections are generally not accurate (including ref. 1), with ROC curves equivalent regardless of how — or if! — correction is applied
• However, a few small studies also show that bacterial meningitis may be obvious despite a traumatic tap (refs 2 & 3):

If the “observed:predicted” ratio of CSF WBCs is >10, then some authors conclude that it indicates bacterial meningitis. Sensitivity & specificity are both around 80-90% with this method.

I think a higher threshold is probably better (ratio >100) — see images below.

Example:

CBC:
5 RBC (Hgb 15; Hct 45)
5 WBC

This is a predicted ratio of 1000:1 (RBCs are reported as 10^6/mcL and WBCs are 10^3/mcL)

A purely traumatic tap in this patient would be expected to look like this:

CSF
2000 RBC
2 WBC

If the CSF looked like this:
2000 RBC
20 WBC

than it is “likely” to be bacterial meningitis (Observed:Predicted = 10)

Looking at the data, I think we can all agree that this CSF is infected:
2000 RBC
200 WBC
(Observed:Predicted=100)

Here are the results from the Bonadio paper:

Bonadio data

Looking at their raw data, the ratio of 100 looks like a much better diagnostic cutoff, although it is probably best to still treat (i.e. antibiose & admit) pending more accurate tests (i.e. culture) if the picture is less clear.

Here is a ROC curve for their data, which looks pretty good altogether:

References:

1. Greenberg RG, Smith PB, Cotten CM, Moody MA, Clark RH, Benjamin DK Jr. Traumatic lumbar punctures in neonates: test performance of the cerebrospinal fluid white blood cell count. Pediatr Infect Dis J. 2008 Dec;27(12):1047-51.
   There a number of similar small studies that all agree that adjustments are not useful.
2. Bonadio WA, Smith DS, Goddard S, Burroughs J and G Khaja. Distinguishing cerebrospinal fluid abnormalities in children with bacterial meningitis and traumatic lumbar puncture. The Journal of Infectious Diseases. July 1990: 162(1): 251-254.
3. Mayefsky, JH. Determination of leukocytosis in traumatic spinal tap specimens. The American Journal of Medicine. June 1987: 82(6): 1175.

NB I didn’t put references for any of the textbooks or papers (most of which refer to the same 2-3 textbooks) that simply assert that calculations are helpful.

30 minute presentation on optimal patient assessment in the emergency department.

garbled audio resolves at the one minute mark.

Slides and Handout.

More recent live version.

I recently assisted in the management of a patient who presented in DKA with critical acidosis and hypokalemia. This presents a variety of therapeutic challenges: what to do about insulin, which treats the acidemia but worsens the hypokalemia? How can I safely supplement potassium as aggressively as possible?

In contrast to the previously-posted recommendations from Micromedex, a protocol from the Bon Secours system in Richmond, VA presents the most clinically useful summary we have come across.

___

*If potassium < 3 meq/liter and the patient is symptomatic 40 meq/hour may be administered to intensive care patients. Hourly serum potassium determinations should be drawn to avoid severe hyperkalemia and/or cardiac arrest. Symptoms of hypokalemia include: fatigue, malaise, generalized muscle weakness, respiratory failure, paralysis; EKG changes include T wave flattening or inversion, U waves, or ST segment depression, and arrhythmia’s.

Recommended maximum dose should not usually exceed 10 meq/hour or 200 meq for a 24 hour period if the serum potassium level is greater than 2.5 meq/liter per product package insert

___

Additionally, there is literature† to support providing a baseline rate of 40 mEq/hr (through a central line) with hourly supplementation using “runs” of up to 40 mEq (through a central line). Patients having their potassium replaced this aggressively should be on a monitor and have hourly electrolyte checks.

Regarding the benefit/drawback of using insulin in DKA patients, the ADA strongly recommends withholding insulin when K < 3.3. If you want to disregard this recommendation, which I do (seems overly cautious), remember you can slow the insulin infusion rather than stop it. The key is to keep a very close eye on your blood gas/chemistry.

†Murthy, K et al. Profound Hypokalemia in Diabetic Ketoacidosis: A Therapeutic Challenge. Endocrine Practice. 2005; 11:5 p 331.

Here are the confusing recommendations From Micromedex:

* Recommended maximum rates of potassium infusion vary, although most studies suggest infusions should be 10 to 20 milliequivalents/hour; up to 50 milliequivalents/hour. Frequent biochemical and electrocardiographic monitoring is necessary when rates exceed 10 milliequivalents/hour, and the faster rates should be continued for only short periods of time (Lawson, 1976; Lawson & Henry, 1977; van der Linde et al, 1977; Porter, 1976; Beeson et al, 1979; Schwartz, 1976); (Dipiro et al, 1989).

* For use through a peripheral line, most sources recommend 40 milliequivalents/liter as the maximum concentration of potassium in an intravenous infusion (Lawson, 1976; Lindeman, 1976; Gilman et al, 1985a; Lawson & Henry, 1977), though it ranges from 20 to 80 milliequivalents/liter (van der Linde et al, 1977; Porter, 1976; Beeson et al, 1979). For central line, any concentration is allowed.

* For moderate hypokalemia (K>2.5): max of 10 mEq/hour in a concentration of up to 40 mEq/liter. The maximum 24-hour total dose is 200 mEq (Prod Info potassium chloride injection, 2004).

* For severe hypokalemia (K<2) with electrocardiographic changes and/or muscle paralysis: max rate of up to 40 mEq/hour, not exceeding a total dose of 400 mEq during a 24-hour period. Continuous cardiac monitoring is recommended (Prod Info potassium chloride injection, 2004).

* Infusions of potassium chloride 20 milliequivalents/100 milliliters of normal saline administered via the central venous route and the peripheral route over an hour to 1351 intensive care unit patients were relatively safe (Kruse et al, 1990). In addition, similar results were seen in 48 intensive care unit patients (Hamill et al, 1991).

* Recommended maximum rates of potassium infusion vary, although most studies suggest infusions should be 10 to 20 milliequivalents/hour; up to 50 milliequivalents/hour. Frequent biochemical and electrocardiographic monitoring is necessary when rates exceed 10 milliequivalents/hour, and the faster rates should be continued for only short periods of time (Lawson, 1976; Lawson & Henry, 1977; van der Linde et al, 1977; Porter, 1976; Beeson et al, 1979; Schwartz, 1976); (Dipiro et al, 1989).

Eight slides culled from my ACLS Therapeutics lecture.

Particularly important for emergency physicians.

Evaluation Algorithm

Treatment Algorithm

• In the diagnostic algorithm, having one or more element of any of the high risk categories gives you one point for that category. Maximum score is three.

• With regard to treatment, labetalol isn’t a bad single agent to start with, but it reduces BP more than HR, and our first therapeutic goal is to reduce HR; metoprolol and esmolol are therefore superior agents. Esmolol has the additional benefit of being rapidly titratable.

• Do not omit aggressive opiate analgesia in your treatment of suspected or confirmed dissection.

• Other risk factors for aortic dissection include conditions associated with increased aortic wall stress, such as hypertension (particularly if uncontrolled); pheochromocytoma; cocaine or other stimulant use; weight lifting or other Valsalva maneuver; deceleration or torsional injury (eg, motor vehicle crash, fall); and coarctation of the aorta. Conditions associated with aortic media abnormalities, which also predispose to aortic dissection, include Marfan syndrome; Ehlers-Danlos syndrome; Bicuspid aortic valve (including prior aortic valve replacement); Turner syndrome; Loeys-Dietz syndrome; familial thoracic aortic aneurysm and dissection syndrome; inflammatory vaculitides such as Takayasu arteritis; giant cell arteritis; and Behcet arteritis. Other conditions associated with aortic media abnormalities include pregnancy; polycystic kidney disease; chronic corticosteroid or immunosuppressive agent administration; and infections involving the aortic wall either from bacteremia or extension of adjacent infection.

• If there is a significant blood pressure difference between the two arms, use the higher number for treatment decisions.

Full guideline available here. Circulation. 2010;121:e266-e369

Outstanding emergency medicine-focused review of the disease here.

high-def vimo screencast here.

slideset here.

audio here.

Update, Sept 2010

Piazza et al. Management of Submassive Pulmonary Embolism. Circulation. 2010;122:1124-1129.

Here we have a different definition of massive vs. submassive:

“Patients with acute PE who have normal systemic arterial pressure and preserved RV function have an excellent prognosis with therapeutic anticoagulation alone. In contrast, patients with massive PE present with syncope, systemic arterial hypotension, cardiogenic shock, or cardiac arrest and have an increased risk of adverse outcomes, including death. Normotensive patients with acute PE and evidence of RV dysfunction are classified as having submassive PE, constitute a large population at increased risk for adverse events…”

So these authors suggest that PE+hypotension=massive=reperfusion therapy. For PE+normotension, they offer this algorithm:

So +biomarker is a requirement reperfusion. They also present a concise summary of how to lyse:

]]> http://emupdates.com/2010/06/08/pulseless-massive-and-submassive-pe-role-of-lytics/feed/ 4 http://emupdates.com/2010/05/17/bvm-ventilation-of-the-edentulous-patient/ http://emupdates.com/2010/05/17/bvm-ventilation-of-the-edentulous-patient/#comments Mon, 17 May 2010 08:56:48 +0000 reuben http://emupdates.com/?p=4527 BVM should be replaced with LMA ventilation. Aside from that, if this technique is half as effective as they suggest, we need to know about it because we bag a lot of edentulous patients.

Background: In edentulous patients, it may be difficult to perform face mask ventilation because of inadequate seal with air leaks. Our aim was to ascertain whether the "lower lip" face mask placement, as a new face mask ventilation method, is more effective at reducing air leaks than the standard face mask placement.

Methods: Forty-nine edentulous patients with inadequate seal and air leak during two-hand positive-pressure ventilation using the ventilator circle system were prospectively evaluated. In the presence of air leaks, defined as a difference of at least 33% between inspired and expired tidal volumes, the mask was placed in a lower lip position by repositioning the caudal end of the mask above the lower lip while maintaining the head in extension. The results are expressed as mean ± SD or median (25th-75th percentiles).

Results: Patient characteristics included age (71 ± 11 yr) and body mass index (24 ± 4 kg/m2). By using the standard method, the median inspired and expired tidal volumes were 450 ml (400 -500 ml) and 0 ml (0 -50 ml), respectively, and the median air leak was 400 ml (365-485 ml). After placing the mask in the lower lip position, the median expired tidal volume increased to 400 ml (380 – 490), and the median air leak decreased to 10 ml (0-20 ml) (P ± 0.001 vs. stan- dard method). The lower lip face mask placement with two hands reduced the air leak by 95% (80-100%).

Conclusions: In edentulous patients with inadequate face mask ventilation, the lower lip face mask placement with two hands markedly reduced the air leak and improved ventilation.

Racine et al. Face Mask Ventilation in Edentulous Patients. Anesthesiology 2010; 112:1190-3.

http://emupdates.com/2012/07/08/emergency-department-intubation-checklist-v13/

In this month’s Canadian Journal of Emergency Medicine, Filanovsky et al describe how studies in the 70s associate rises in ICP to ketamine, and review more recent, higher quality evidence to the contrary.

They do not mention that several of the early studies examined the influence of ketamine on ICP in non-intubated patients. Ketamine is well-known to cause brief periods of apnea, especially if pushed quickly; these short episodes are clinically inconsequential when ketamine is used for PSA and irrelevant when ketamine is used for RSI, where patients are simultaneously paralyzed. However, transient rises in pCO2 will cause cerebral vasodilation and a rise in ICP. Apnea time should therefore be minimized in patients potentially susceptible to ICP fluctuations, but this strategy applies to all induction agents used for RSI.

Filanovsky et al also review evidence suggesting that ketamine may in fact be neuro-protective in head trauma, though the jury is still out on this question. They also note the concerns around the adrenal effects of etomidate, the induction agent most often used in polytrauma. While we know that etomidate infusions increase ICU mortality, it’s so far unclear if single-dose etomidate used for RSI causes clinically consequential adrenal suppression. Irrespective of these two issues, given the tendency of ketamine to increase blood pressure, it should be the induction agent of choice in the hypotensive trauma patient, with or without head injury.

CJEM 2010;12(2):154-157

We are accustomed to relying on the monitor’s ECG tracing to determine heart rate; however, a good pulse oximeter waveform better reflects the number of perfusing beats. Note the heart rate, as measured by the pulse ox, is reported in purple in the upper-right corner of the monitor. At this point we had achieved electrical capture but not mechanical capture.

Watching the pulse oximetry graph is a slick way to guide pacemaker insertion. Cardiac sonography and placing a finger on the patient’s neck to assess the pulse are alternatives.

For RSI, all drugs are based on total (actual) body weight rather than ideal body weight, except ketamine, for which you are supposed to use ideal body weight. You can remember this by keeping in mind that ketamine is the ideal RSI agent. So ideal, that if you give it based on TBW rather than IBW as recommended, it doesn’t matter. Propofol is a little funky, they recommend IBW+TBW(.4). Morphine is dosed based on IBW, whereas you’re supposed to use TBW for fentanyl. I doubt that these recommendations are based on much science, but when you have to pick a dose, it’s something.

From Brunette, AmJEM, 2004. doi:10.1016/S0735-6757(02)42250-4

Thanks to Erin Robey for finding this for me.

“…we retrospectively reviewed 104 consecutive cases of patients with insurance leaving against medical advice in 2008 from a suburban level I trauma center that sees 57,000 ED visits per year. Our review included 19 insurance companies, including HMOs, PPOs, Medicare, Medicaid, and workman’s compensation. We found that all 104 visits where the patient left against medical advice were fully reimbursed by their respective insurance company.”

Thank you, Wigder et al.

doi:10.1016/j.annemergmed.2009.11.024

Key excerpts:

“Clinical factors suggesting a diagnosis of myocarditis in individuals with ST-segment and T-wave abnormalities include a younger patient age (younger than 40 years), complaint of recent viral illness, slowly evolving ECG changes involving more than one vascular distribution, and diffuse?rather than focal?wall motion abnormalities on echocardiogram.”

“In a study of 137 patients with endocarditis diagnosed via the Duke criteria, 50% had AV block and 61% had intraventricular block, with overlap between the 2 groups.”

Punja et al, Electrocardiographic manifestations of cardiac infectious-inflammatory disorders. American Journal of Emergency Medicine (2010) 28, 364-377.

Needle-less procedural sedation / sedation for imaging:

“After extensive discussion with the patient’s parents and NICU staff, the PPM service recommended oral administration of intravenous ketamine (10 mg?mL, Monarch Pharmaceuticals) at a starting dose of 0.5 mg (0.125 mg?kg?dose). Over 4 days, the dose was titrated to 3 mg (0.75 mg ? kg ? dose) in response to observed effect. At 15 minutes after a dose of 3 mg of ketamine, the patient was able to tolerate her dressing change without crying or resisting for 45 minutes (Figs. 1 and 2). Her ability to feed afterward was preserved. No effects on depth or rate of respiration were noted.”

Saroyan et al, Pediatric Dermatology 26:6 Nov/Dec 2009 764-766.

A meta-analysis in this week’s JAMA concludes that a negative whole-leg compression ultrasound rules out dangerous outcomes at three months in 99.3% of patients who are not anticoagulated in the interim. This is good news for emergency physicians, at least in patients whose pre-test probability for DVT is low. Unfortunately, it assumes a practice pattern that is more advanced than what is offered in most American centers. The majority of stateside radiology departments do not look at the calf in their rule-out DVT protocol. This policy is based on an outdated and dangerous belief that calf DVTs are benign.

In patients who localize to the calf, ask your radiologist to rule out DVT in the calf as well as the proximal vessels. In patients who are high risk for DVT, anticoagulate empirically; note the major bleeding risk for anticoagulation is 1.1% per year. I am concerned that JAMA readers will mistakenly assume that this paper applies to them and skip anticoagulation, repeat ultrasounds, and other strategies to reduce risk in their query DVT patients whose calves were never evaluated.

Even if you’re not interested in the shoulder, the video is a must-see for the pic of corey slovis in the background.

For 8 minute Pecha Kucha competition at Scott Weingart’s ED Critical Care Conference, January 13 2010.

http://www.theatlantic.com/doc/200912u/tamiflu

Can we stop prescribing it now? Please?

I have come to treat claims about proprietary therapies in the same way that I treat claims made in emails that start forward this to everyone you know.

“…The time to maximum plasma concentrations (Cmax) was shorter for midazolam (17.5 ± 6.5 min) than for diazepam (33.8 ±7.5 min). (P < 0.05, Table II) The IM absorption profiles for midazolam and diazepam demonstrate that there is more variability in the absorption rates of IM diazepam than those of IM midazolam (Figure 2). The mean time to peak absorption rate was shorter for midazolam (9 ±2 min) than for diazepam (13.8 ±7.5 min). The absorption of midazolam was almost complete within one hour following the im administration. However, for diazepam, considerable drug absorption continued, with larger variability, beyond one hour after the IM injection.”

Hung, Dyck, Varvel et al. Comparative absorption kinetics of intramuscular midazolam and diazepam. Can J Anaesth 1996;43:5 pp 450-5.

“Midazolam is the only benzodiazepine stable in aqueous solution and suitable for intramuscular injection. A delayed onset of action might be expected, as shown by Jawad et al., but this was not confirmed by Chamberlain et al. Intramuscular midazolam may be useful in patients when attempts to introduce an intravenous line are unsuccessful. It appeared to be well tolerated and rapidly effective for treatment of acute seizures.”

Wermeling, Archer, Manaligod et al. Bioavailability and pharmacokinetics of lorazepam after intranasal, intravenous, and intramuscular administration. J Clin Pharmacol 2001;41:1225-1231.

“We found that midazolam is superior to haloperidol and lorazepam in the sedation of violent and severely agitated patients (VSAPs) with respect to time to sedation and time to arousal. The use of midazolam in the control of VSAPs can facilitate patient care, rapidly ease the disruption to the ED, and hasten disposition.”

Nobay, Simon, Levitt et al. A Prospective, Double-blind, Randomized Trial of Midazolam versus Haloperidol versus Lorazepam in the Chemical Restraint of Violent and Severely Agitated Patients. Acad Emerg Med 2004;11:744-749.

Thanks to Sara Bingel.

also note http://zo.la/em/?p=2509

confirming what we all know to be true: epinephrine in cardiac arrest only keeps earthworms up at night. in patients with an unshockable rhythm, perform quality chest compressions and secure the airway while you search for/empirically treat for the cause of the arrest. http://zo.la/em/?p=4170

Document available here.

Recommendations relevant to emergency medicine:

1. GP IIb/IIIa receptor antagonists (abciximab/reopro or eptifibatide/integrilin) can wait for the cath lab.

2. 300 to 600 mg oral clopidogrel as soon as possible is a class I recommendation. Prasugrel is the new, more expensive clopidogrel.

3. Unfractionated heparin, LMWH, fondaparinux, and bivalirudin are all acceptable anticoagulants. If patients are waiting around and PTT is subtherapeutic, rebolus unfractionated heparin.

4. Transfer thrombolysis patients to a PCI center after giving the lytic and “considering” a “preparatory” anticoagulant and antiplatelet.

5. Keep serum glucose below 180.

6. NSTEMI/UA patients going to the cath lab should get aspirin and clopidogrel (or prasugrel).

This is from my presentation Evidence-based management of corneal abrasion, which I gave at McGill grand rounds in 2005.

Here is a nice, concise review.

Will unfortunately increase the number of pediatric head CT scans, I believe. Here is a cheat sheet, courtesy of Michelle Lin.

Journal of Emergency Medicine 37:4 p419

20 mg over 10 minutes then 20 mg/hour, titrated to effect.

ketamine 50 mg/mL

add 5 cc ketamine to 250 cc NS = 1 mg/mL

Bolus: 20 cc @ 120 cc/hour (10 minutes) then
Drip: 20 cc / hour

[weight-based dosing is .3 mg/kg over 10 minutes and .3 mg/kg/hr]

MSSM PCA and Opioid Recs

mucosa: .09% (9 in 10,000)

receptive anal intercourse: 1 to 30%
insertive anal intercourse: .1 to 10%
receptive vaginal intercourse: .1 to 10%
insertive vaginal intercourse: .1 to 1%

NEJM 361;18 p1769

RASP Tool

http://www.cjem-online.ca/v5/n1/p46

UK HIV PEP Sexual Exposure Guideline 2011

Emerg Med J. 2009 Nov;26(11):807-10.

Rob Orman ERCAST Reversal Guide

EBM EMCC Coagulopathy Reversal

Excerpted from MSSM M&M teaching points:

* Head-injured patients who are anticoagulated are at risk for delayed intracranial bleeding after a negative head CT. Options for managing this risk include a period of ED observation, admission to the hospital, and discharge with strict precautions/supervision (with or without a scheduled return visit). These strategies may or may not be combined with a repeat head CT. The duration of increased risk is not known but is thought to be somewhere between 24-72 hours, though delayed bleeds have presented even later than this.

* Intracranial bleeding with coagulopathy is a medical and surgical emergency that is both immediately life-threatening and responsive to ED therapies. These therapies should not wait for consultant collaboration and, where suspicion of ICH is sufficient, initiation of these therapies should not wait until confirmation of ICH.

* For patients with life-threatening bleeding on warfarin: administer vitamin K 10mg IV over 10 minutes and prothrombin complex concentrate. Dosing of PCC is not firmly established and can be based on both weight and INR, but 50 units/kg is a reasonable starting point in an emergency. An alternative is FFP, which should be administered at a dose of 15 ml/kg. At Sinai, a unit of FFP contains anywhere between 150 and 350 cc FFP; assume 200 cc for estimation purposes. FFP is blood type-specific; the blood bank needs to know the patient’s blood type but does not need a blood sample to cross-match.

* PCC reverses INR much more quickly than FFP, is easier to handle, and does not have the volume concerns of FFP. However, it is much more expensive than FFP and is associated with more thrombotic complications than FFP. In patients who are at particular risk of thrombosis, or when bleeding is not life-threatening, consider the benefit:harm between the two options.

* For patients with life-threatening bleeding on unfractionated heparin, stop the heparin infusion. Then administer protamine at a dose of 1 mg/100 u heparin given within the past 30 minutes, .75 mg/100 u heparin given 30-60 minutes ago, .5 mg/100 u heparin given 60-120 minutes ago, and .3 mg/100 u heparin given more than 2 hours ago.

* For patients with life-threatening bleeding on low molecular weight heparin, protamine is only partially effective (consider this before administering LMWH in a patient more likely to bleed – unfractionated heparin may be a better choice). The dose of protamine is 1 mg IV per 1 mg LMWH given in the last 10 hours. If LMWH is causing life-threatening bleeding unresponsive to protamine, consider activated Factor VII.

* For patients with life-threatening bleeding on plavix or aspirin, administer DDAVP at a dose of .3 mcg/kg with 6 units of platelets.

* For patients with life-threatening bleeding and liver failure with INR > 1.2, administer vitamin K 10 mg IV along with either PCC or FFP.

* For patients with life-threatening bleeding and renal disease associated with platelet dysfunction, administer DDAVP at a dose of 20 mcg. FFP or cryoprecipitate may also be used for additional procoagulant effect if necessary.

* For patients with life-threatening bleeding and thrombocytopenia, transfuse platelets to a level of at least 50,000.

Anyone over 15kg gets 17g. Rx: Miralax 17g daily. Mix one capful or packet in 4-8oz fluid (For an adult or bigger kid, mix in 8oz. For a small kid, mix in 4oz.)
10-15kg: 8.5g po daily. Dissolve one-half capful in 2-4oz fluid (again you pick based on the size/age of the kid)
5-10kg: 4.2g po daily. Dissolve one-half capful in 4oz fluid. Give half the dissolved solution (2oz) and discard remainder.

Thanks to Erin Robey

* Accidental arterial cannulation is usually benign but should be detected before dilation to avoid significant vessel injury. When performing an ultrasound-guided central line, the point where the needle tip enters the vein must be in the visualized ultrasound field. This may be accomplished by entering the skin with the needle a short distance away from the probe, rather than immediately adjacent to the probe, which will lead to the tip entering the vein out of the vertical plane visualized on the screen. Alternatively, the tip of the needle can be tracked into the vein by sliding the probe along the skin as the needle tip approaches the vein, keeping the tip in the visualized ultrasound field.

* If venous placement is not certain, verification may be performed using a number of techniques.
**A quick blood gas may be helpful if the PaO2/SaO2 values are conclusive; unfortunately blood gas results may lie in between definitively arterial and venous values.
** Transducing the pressure waveform is effective but takes time to set up.
** A brief and definitive technique uses a quick pressure column setup as follows:

1. Insert the guidewire, remove the needle.
2. Slide the conventional angiocath that comes in all central line kits over the wire, remove the wire.
3. Attach an extension set to the angiocath. An extension set comes in the introducer kit for this purpose. For triple lumen kits, ask the nurse to give you an extension set, or use the circular plastic sheath that stores the guidewire as extension tubing.
4. Keeping the tubing parallel to the floor, allow 20-30 cm of blood to fill the tube.
5. Hold the tube straight up to the ceiling. If the angiocath is in a vein, the column of blood will fall back down to the level of the CVP. If the angiocath is in an artery, the column of blood will continue to rise.
6. If the angiocath is in the vein, thread the guidewire, pull out the angiocath and continue Seldinger technique as usual. If the angiocath is in the artery, either remove the angiocath and hold pressure or call vascular surgery for advice.

** To estimate how low a bag of saline needs to be so that it does not overcome arterial blood pressure, use the formula SBP/2 = height in inches. For example, if the patient has an SBP of 70 mmHg, this corresponds to a height of 35 inches. If the fluid bag is hanging more than 35 inches above a patient with an SBP of 70, it will flow into an artery, fooling the unsuspecting observer into thinking the catheter is in a vein. Therefore, to verify venous placement by attaching a bag of saline, the bag of saline must be lower in inches than half of the patient’s systolic blood pressure.

Demonstrations and discussions of full sterile technique, quick pressure column technique, and a number of other central line-related topics can be found on Haru Okuda and Scott Weingart’s central line project page:

http://ehced.org/howtos/centrallineproject/central-lines.htm

Variable dosages and several preparations have been found to be effective. Guidance can be found at the National Center for Complementary and Alternative Medicine’s web site. One good option is Lactobacillus GG (Culturelle, 10 billion colony forming units/capsule) one capsule orally daily for children, two for adults.

20 drops/cc

therefore

2 drops per second = 6 mcg/min

Nynke van Dijk, MD, et al Journal of the American College of Cardiology
Effectiveness of Physical Counterpressure Maneuvers in Preventing Vasovagal Syncope
Vol. 48, No. 8, 2006
In this study, we assessed the effectiveness of physical counterpressure maneuvers (PCM) in daily life. There is presently no evidence-based therapy for vasovagal syncope. Current treatment consists of explanation and life-style advice. Physical counterpressure maneuvers have been shown to raise blood pressure and to control or abort vasovagal episodes in laboratory conditions.
We performed a multicenter, prospective, randomized clinical trial, which included 223 patients age 38.6 (????15.4) years with recurrent vasovagal syncope and recognizable prodromal symptoms. One hundred and seventeen patients were randomized to standardized conven- tional therapy alone, and 106 patients received conventional therapy plus training in PCM. The median yearly syncope burden during follow-up was significantly lower in the group trained in PCM than in the control group (p ???? 0.004). During a mean follow-up period of 14 months, overall 50.9% of the patients with conventional treatment and 31.6% of the patients trained in PCM experienced a syncopal recurrence (p ???? 0.005). Actuarial recurrence- free survival was better in the treatment group (log-rank p ???? 0.018), resulting in a relative risk reduction of 39% (95% confidence interval, 11% to 53%). No adverse events were reported. Physical counterpressure maneuvers are a risk-free, effective, and low-cost treatment method in patients with vasovagal syncope and recognizable prodromal symptoms, and should be advised as first-line treatment in patients presenting with vasovagal syncope with prodromal symptoms. (The PC-Trial; http://www.controlled-trials.com/isrctn/trial/45146526/0/ 45146526.html; ISRCTN45146526) (J Am Coll Cardiol 2006;48:1652-7) ? 2006 by the American College of Cardiology Foundation

I would add, as far as pain is concerned, that I have used this device
in quite a few awake infants and young children. We see a tertiary
population, often with underlying disease making PIV access difficult;
I have personally watched the pain response in these patients to PIV
attempts, and have found it much LESS painful to insert an EZ IO in
awake patients. We have done this without local infiltration with
lidocaine. One key is NOT to start and stop the drill as it goes
through the skin – I have seen residents do this and it twists the
skin which hurts. As long as the trigger is held until the needle is
in the bone, patients cry much less than they do with PIV placement.

The caveat, however, is that infusion through the IO definitely
appears painful. We now routinely instill 1cc of 1% lidocaine through
the IO, then wait 2 minutes before pushing fluids (this isn’t
necessary, of course, in an emergent resuscitation of an unconscious
patient). Another technique is to put 2-3 cc of 1% lidocaine in the
bag of IVF that you are infusing which seems to decrease infusion pain
well.

Garth Meckler, MD, MSHS
Fellowship Director and Assistant Section Chief
Pediatric Emergency Medicine
Oregon Health & Science University

Annals of Emergency Medicine, May 2009

This post has been superseded by this one.

All BP values are linked with or as in SBP of 220 or a DBP of 120.

No end organ damage

Administering antihypertensive therapy in the ED for the purpose of acutely lowering blood pressure in patients without end-organ damage is discouraged.

Commence oral antihypertensive therapy if BP > 200/120. Consider commencing oral therapy if BP > 180/110.

A basic metabolic panel is recommended before starting a patient on antihypertensives. Avoid ACE inhibitors in woman of childbearing potential. All hypertensive patients require follow-up.

Acute Ischemic Stroke not being treated with thrombolysis

Unless concomitant condition requiring BP control, do not treat until over 220/120. Keep above 140/90. Use labetalol or nicardipine.

Spontaneous Intracerebral Hemorrhage not SAH

If signs of high ICP, keep MAP below 130 or SBP below 180. If no signs of high ICP, keep MAP below 110 or SBP below 160. Use labetalol, nicardipine, or esmolol.

Subarachnoid Hemorrhage

Keep SBP below 160 until clipped or vasospasm occurs. Use labetalol, nicardipine, or esmolol. Oral nimodipine is used for vasospasm prophylaxis, not treatment of hypertension, though it may lower blood pressure.

Traumatic Brain Injury

Do not treat hypertension. Keep CPP between 50 and 70, but do not use vasopressors.

Acute Coronary Syndrome

Reduce by 20-30% if > 160/100 with IV/SL nitro or beta blocker.

Avoid thrombolytics if > 185/110

Heart Failure / Pulmonary Edema

Treat hypertensive and normotensive pulmonary edema patients with IV/SL nitro or ACE inhibitor.

Hypertensive encephalopathy

Reduce MAP by 25% over eight hours with labetalol, nicardipine, or esmolol.

Aortic Dissection

Keep SBP below 110, unless symptomatic hypotension, using morphine, beta blocker (metoprolol, esmolol, labetolol), followed by vasodilator (nicardipine, nitroprusside). Calcium channel blocker (verapamil, diltiazem) may be used instead of beta blocker. Avoid beta blocker if aortic regurgitation or cardiac tamponade. Remember to measure BP in both arms. [My note: target heart rate is 60-80]

Preeclampsia or Eclampsia

Keep SBP < 160 and DBP < 110 if prepartum or intrapartum. Use 150/110 if postpartum or platelets < 100,000. Use IV labetalol or hydralazine or oral nifedipine. ACE inhibitors and esmolol are contraindicated. Treatment for eclampsia should also include magnesium, 6 g over 20 minutes, then 2 g per hour.

Cocaine

Asymptomatic hypertension does not require treatment. If treatment is required, benzodiazepines are first-line therapy. If cocaine-related ACS, add nitroglycerine or IV phentolamine. Avoid beta blockers, including labetalol.

http://www.annemergmed.com/issues/contents?issue_key=S0196-0644(08)X0002-2

- High-flow oxygen is commonly used for cluster headache. Might it work for all-comers with headache?

- This was a tiny randomized trial with three groups: 17 to high-flow oxygen for 15 minutes, 14 to high-flow air for 15 minutes, and 17 to nothing for 15 minutes prior to standard medical therapy. The oxygen group did far better with regard to time to relief, 40 vs. 110 or 120 minutes; length of stay was 57 vs. 210 or 180 minutes; CT was less; less pharmacotherapy was needed, 29% (oxygen group) vs. mid-80s% in the other groups; and headache intensity was much less using visual analog scale.

- Assuming no contraindications to high-flow oxygen, this small trial, if confirmed, could change the way we treat all headaches.

- Put high-flow oxygen on your next headache patient, and see if it works.

Veysman BD et al. Annals of Emergency Medicine, Volume 54, Issue 3, Pages S71-S71

Antimigraine efficacy has been well demonstrated in multiple high-quality clinical trials for chlorpromazine, metoclopramide, and prochlorperazine, and droperidol. In general, these medications are inexpensive, well tolerated, and at least as efficacious, if not more so, than any agent to which they have been compared. These medications should therefore be considered first-line therapy for acute migraine in the ED setting.

Of the four agents mentioned above, chlorpromazine has fallen out of favor because of profound orthostasis that may accompany administration of this medication. Of the remaining three agents, droperidol is probably the most effective, with 2-hour headache relief rates approaching 100%. The ideal dose, as determined by a high-quality dose-finding study, is 2.5 mg. This medication is commonly used and exceedingly safe, but a recent FDA warning about QT prolongation has caused some clinicians to perform an EKG before medication administration.

Prochlorperazine administered in doses of 10 mg is also highly effective, although not quite as effective as droperidol. Metoclopramide is typically administered as a 10-mg intravenous dose but has been well tolerated and efficacious when administered as repeated successive doses of 20 mg.

Metoclopramide, prochlorperazine, and droperidol can all be accompanied by extrapyramidal symptoms, particularly akathisia, which often goes unrecognized. Prophylactic administration of diphenhydramine is a reasonable course of action, as are slower intravenous drip rates.

Metoclopramide has a favorable pregnancy rating and a long history of use for treatment of hyperemesis gravidarum. It is the most appropriate parenteral agent for treatment of acute migraine in pregnancy.

Emergency Medicine Clinics of North America Volume 27, Issue 1, February 2009, Pages 71-87

SaO2 = oxygen saturation as measured by blood analysis (e.g. a blood gas)

PaO2 = partial pressure of oxygen in the blood, as measured by blood analysis

(Risks described are approximations for a 45-year-old person; risks are halved for 70- year-olds, doubled for 20-year-olds, and quadrupled for young children)
??Mr. Smith. The best way I can diagnose your pain is a CT scan. This means having radiation exposure. I will explain how much radiation. You are always exposed to ?background’ radiation from the ground, stars, air, and food. To use money as an example, it is 2 cents per hour (20 lrad ? hr). For comparison, a chest x-ray is $2 and the abdominal CT scan is $1,000 of radiation. Risk of cancer during your lifetime increases by about 1 ? 1,000 for every $1,000 of radiation exposure. Of 1,000 people, about 420 will have cancer in their lifetimes. Therefore, every $1,000 of radiation increases the cancer risk from 420 to 421 of 1,000. About half the cancers are fatal.

You can see that the risk of cancer from the CT scan is low. For every 1,000 patients getting your scan, only 1 will probably get cancer because of it. I recommend the scan for you because I believe the benefit of diagnosis outweighs the risk. If you dis- agree, we can discuss other options that avoid radiation exposure, but these may be less helpful in diagnosing your pain. A delay in diagnosis also carries a risk of complications or death.”

Veysman, Acad Emerg Med 2009 16:1 p95

also

SmartEM.org CT Consent 2011

also, from Michelle Lin:

standard green IV:
18 gauge (1 mm) x 30 mm angiocath
max flow rate = 105 ml / minute

standard grey IV:
16 gauge (1.3 mm) x 30 mm angiocath
max flow rate = 220 ml/min

procedural IV:
18 gauge x 64 mm angiocath
max flow rate = 85 ml/min

medial (blue) & proximal (white) lumen of triple lumen catheter:
18 gauge x 190 / 180 mm
max flow rate = 26 ml/min

distal (brown) lumen of triple lumen catheter:
16 gauge x 200 mm
max flow rate = 52 ml/min

cordis / introducer:
8.5 french (2.8 mm) x 100 mm
max flow rate = 126 ml / minute
max flow rate with pressure bag @ 300 mmHg: 333 ml / minute

Myasthenia gravis decreases the sensitivity to depolarizing agents (Sux) and therefore a larger dose should be used.

Andrus summary, based on the CDC recommendations

age <7 years: DTaP

age <7 years with pertussis contraindicated DT

7-18: Tdap

7-18: with pertussis contraindicated: DT

age > 18 if > 10 years give Tdap

CDC Recommendations for Tetanus in pregnancy

Commercial Names

DTap (lower concentrations of antigens, acellular pertussis): daptacel

Tdap (higher concentrations of antigens, acellular pertussis): adacel

DTP (lower concentrations of antigens, killed whole cell pertussis – for age <6): trivax

Td (higher concentrations of antigens, no pertussis): no commercial name

Tetanus toxoid (higher concentration, only tetanus): no commercial name

2. Wolff-Parkinson-White syndrome (WPW): the most common form
of preexcitation, WPW is associated with the classic triad of
short PR interval, QRS complex widening greater than 100 milli-
seconds, and the delta wave (slurred upstroke of the QRS com-
plex). It is important to remember that delta waves, although the
most well known of the triad, are often absent in many leads.
The short PR interval is actually the most consistent finding in
all of the leads.

3. Brugada syndrome: Brugada syndrome is a purely electrical
phenomenon (meaning that patients have structurally normal hearts)
that is associated with unpredictable episodes of ventricular
tachycardia. Patients may have sudden death, but if the arrhythmia
terminates spontaneously, the patient presents instead with syncope.
The resting ECG demonstrates a right bundle branch block
morphology with STE in leads V1 to V2.

4. Hypertrophic cardiomyopathy (HCM): hypertrophic cardiomyopa-
thy may be associated with episodes of ventricular tachyarrhyth-
mias, usually associated with exertion, in relatively young patients.
The ECG manifestations of HCM are often nonspecific (high
voltage in the precordial leads, left atrial enlargement, tall R waves
in right precordial leads, and abnormal Q waves in the inferior and/
or lateral leads) [32]. However, the combination of high voltage
with deep, narrow Q waves in the inferior and/or lateral leads is
highly specific for this entity.

5. Prolongation of the QT interval: patients with a prolonged QTc
interval are at risk for torsades de pointes. Patients are at highest risk
when the QTc interval is greater than 500 milliseconds. Major causes
of prolonged QTc interval include hypokalemia, hypocalcemia,
hypomagnesemia, hypothermia, elevated intracranial pressure, acute
cardiac ischemia, sodium channel blocking drugs, and hereditary long
QT syndrome.

Dovgalyuk Am J Emerg Med. 2007 Jul;25(6):688-701

Michelle Lin Brugada Syndrome Card:

A frequently encountered problem in clinical practice is a patient who presents with acidosis and hyperglycemia. It has been my experience that the correct calculation of the anion gap in the face of hyperglycemia is often confusing. An example would best serve to illustrate the point. Assume a patient who is admitted with new-onset diabetes mellitus and has the following blood test results: glucose level, 700 mg/dL; sodium level, 128 mEq/L; chloride level, 97 mEq/L; and bicarbonate level, 21 mEq/L. The anion gap in this patient is [Na] ?([Bicarbonate] + [Cl]) = 128 ?(97 + 21) = 10, a value within normal limits; the patient has a mild non-anion gap acidosis. However, physicians often correct the sodium level in the face of hyperglycemia by adding 1.6 mEq/L to the sodium concentration for each 100-mg/dL increment in glucose levels above 100 mg/dL. This correction does not apply to the calculation of the anion gap in patients with acidosis and hyperglycemia because the water moving from the intracellular compartment to the extracellular compartment as a result of the hyperglycemia equally dilutes all electrolytes, including the chloride and bicarbonate. If in this case the sodium level is "corrected" for the hyperglycemia, it will be calculated as 138 mEq/L and lead to a falsely elevated calculated anion gap of 20. Thus, the patient’s condition would be erroneously diagnosed as severe anion gap acidosis, most probably diabetic ketoacidosis.

Tomer, Y. Annals of Internal Medicine 129:9 p753

* The mainstay of treatment for severe asthma is nebulized albuterol; the initial dose is 5 mg (note this is two bullet packs) x 3 for moderate to severe asthma and continuous nebulized albuterol for life-threatening asthma. Dosing for pediatrics varies, but an easy and reasonable approach is to give half dose for small children (2.5 mg) and full dose for larger children. The important thing is to make lots of smoke.

* For severe asthma, anticholinergic therapy should be added to ?2 agonists, the conventional dose is 500 mcg ipratropium bromide (Atrovent), given with the first three albuterol treatments in both adults and children.

* Corticosteroids should also be administered to all patients suffering a significant asthma exacerbation. Accepted dosing is 100-200 mg IV methylprednisolone per day or 40-60 oral prednisone per day. Pediatric dosing varies, but a dose of 1 mg/kg for both preparations is often used.

* In cases of severe asthma, it is not necessary to push oxygen saturation above 90-92%.

* In cases of severe asthma, data supports the use of intravenous magnesium. The dose is 2 g in adults and 50 mg/kg in children, infused over 20 minutes. Magnesium does not benefit patients with mild or moderate asthma.

* In cases of life-threatening asthma, consider subcutaneous or intramuscular epinephrine, especially in younger patients with good hearts. The dose is .3-.5 mg of the 1:1000 preparation (1 mg/mL). Pediatrics dose is .01 mg/kg.

* Non-invasive ventilation is of proven benefit in severe asthma, in a patient who can cooperate. Initial settings should an EPAP/CPAP/PEEP of 5 cm water; if BiPAP is used, initial IPAP should be 8 cm water. Improved results are noted if the patient is allowed to hold the unstrapped mask to her face at first, before strapping down the mask. Note that nebulized albuterol therapy must continue.

* In cases of life-threatening asthma, consider delivering a helium-oxygen mixture, which may improve air and medication delivery in very severe asthma exacerbations. Heliox is available at both MSSM and EHC through respiratory therapy. The preferred mixture is 80% helium, 20% oxygen.

* Data is conflicting, but case reports suggest that high dose ketamine may prevent intubation in severe asthma. The dose used in one pair of successful cases was 2 mg/kg bolus followed by an infusion of 2 mg/kg/hour, titrated as needed.

* Intubation of the asthmatic is a last resort. If necessary, maximize expiratory time by using small tidal volumes (6 ml/kg), rate of 8-10 per minute, with a high flow rate of 80-100L/min in a square waveform, which corresponds to a I:E time of 1:4 to 1:6. Ketamine (2 mg/kg) should be used for induction of the asthmatic for intubation.

* If an intubated asthmatic suddenly deteriorates, disconnect the ventilator and consider manually decompressing the chest (pushing down to assist with expiration). Consider tube displacement and obstruction (e.g. with mucus), and consider tube or needle thoracostomy for pneumothorax.

* Aminophylline does not appear to confer additional benefit over appropriately-dosed albuterol therapy in the emergency department.

reproduced from Emerg Med J 2008;25:435-436

In vitro investigation of the antibacterial effect of ketamine.

Gocmen S, Buyukkocak U, Caglayan O.

Department of Microbiology, Faculty of Medicine, Kirikkale University, Kirikkale, Turkey. jsedef@yahoo.com

PMID: 18521797 [PubMed - indexed for MEDLINE]

oh, and it’s an anticonvulsant as well.

- Hypoxia (Place LMA or ETT, provide 100% oxygen)
- Hypovolemia (Bedside ultrasound for free abdominal fluid/AAA, consider a NS bolus – if suspicion for hemorrhage is high, administer uncross-matched blood)
- Hypo/hyperkalemia (Consider calcium chloride, especially in the patient with suspected renal insufficiency)
- Hypoglycemia (Consider D50)
- Hypothermia (Warm the cold patient)
- Hydrogen ion/acidosis (Consider bicarb, especially if toxicology is suspected)
- Toxins (In addition to bicarb, consider empiric antidotes – cyanide kit, digibind, naloxone, intralipid)
- Tamponade (Perform bedside ultrasound)
- Tension pneumothorax (Perform bedside ultrasound / consider needle or tube thoracostomy)
- Thrombosis (Consider thrombolysis for AMI or, especially PE)
- Trauma (The entire cranium and posterior thorax should be inspected if occult trauma is entertained)

Although the administration epinephrine (and, formerly, atropine) is emphasized in codes, these agents do not benefit arrested patients. Your only chance to reanimate a patient in PEA or asystole is to reverse the underlying cause. Take your own pulse, take a step back, and think Hs and Ts.

World J Surg (2006) 30: 1265

Critical Care 2007 11_R1

Emergency Medicine Journal 25:166

From Ann EM 2008;51:2 p208

1. age < 50

2. HR < 100

3. SpO2 ? 95%

4. No unilateral leg swelling

5. No hemoptysis

6. No recent trauma or surgery

7. No prior DVT or PE

8. No hormone use

Wells:

1. Clinical signs and symptoms of DVT? (+3)

2. Pulmonary embolism is most likely diagnosis (+3)

3. HR > 100 (+1.5)

4. Immobilization of ?3 days or surgery in previous 4 weeks (+1.5)

5. Previous PE or DVT (+1.5)

6. Hemoptysis (+1)

7. Malignancy with treatment in past 6 months, or palliative (+1)

Score ?4 qualifies to rule out with D dimer [JAMA 295 (2): 172-9]

http://www.mdcalc.com/wells-criteria-for-pulmonary-embolism-pe

Dryden Outpatient Opiate Withdrawal Rx 2011

Annals of EM 2007;49:4 p457

2. Pulmonary embolism

3. ESRD

4. Myopericarditis

5. Stanford A dissection

6. Acute heart failure

7. Strenuous exercise

8. Cardiac toxins

9. Ablation therapy / cardioversion / defibrillation

10. Cardiac infiltrative disorders (sarcoid, amyloid)

11. Heart transplant (+trop can last 3 months)

12. Cardiac contusion after blunt chest trauma

13. Sepsis / critical illness

14. Rhabdomyolysis

Korff S, Katus HA, Giannitsis E. Differential diagnosis of elevated
troponins. Heart 2006;92:987-993.

JAMA 289:16 2123

From Wiebe CJEM July 2007

/ croup asthma

Link to website with guide in other languages.