M2E Too! Mellick's Multimedia EduBlog

The M2E Too! Blog by Larry Mellick, MD, presents important clinical pearls using multimedia.

By its name, M2E Too! acknowledges that it is one of many emergency medicine blogs, but we hope this will serve as a creative commons for emergency physicians.

Thursday, October 5, 2017

I’ve heard for years in emergency medicine circles that it was impossible to preoxygenate with a bag-valve mask (BVM) unless one is actually compressing the bag and forcing oxygen flow to the patient. I recently did an informal survey of my colleagues at work, and the responses varied from confident affirmation that the BVM was an inadequate tool for preoxygenation to quasi-warnings not to tread on this dogma without first consulting anesthesia or respiratory therapy. What started as a simple quest to clarify whether the dogma about BVMs and preoxygenation was true turned into a fascinating review and new personal insights into preoxygenation.

The statement that the bag-valve mask is a poor tool for preoxygenation of the spontaneously ventilating patient is simply false. If the mask seal is excellent and the oxygen flow rate is sufficient, one can preoxygenate better with it than with the overly touted non-rebreather mask. This may not be true for all BVM brands, but holds true for the vast majority of them. Adding a PEEP valve to the BVM may not improve oxygenation for patients with healthy lungs, but there is an excellent chance that it will help patients with wet lungs by recruiting back drowning alveoli.

The non-rebreather mask and the bag-valve mask will more effectively oxygenate the patient at flush rates of oxygen. In other words, turn up the wall oxygen to its maximum levels of 50 to 60 L/min and the hyperventilating, air-hungry patient will not be able to overcome the capacity of either tool. (See the video.) An article earlier this year demonstrated that the non-rebreather mask attached to flush rates of oxygen is non-inferior to the BVM at 15 L/min. (Ann Emerg Med 2017;69[1]:1.) It naturally follows that flush rates of oxygen for the BVM would also have an additive effect.

Non-invasive ventilation (NIV) and high-flow oxygen therapy (HFOT) with humidified air are also excellent tools for preoxygenation, but NIV has to address the same problem seen with BVM preoxygenation. Both devices must be removed from the face of the apneic patient to intubate the airway. This is not a problem when using high-flow nasal cannulas or HFOT. Nevertheless, this dilemma with NIV and BVM can be resolved during that interlude of apnea just prior to rapid sequence intubation by quickly placing a standard nasal cannula with oxygen flowing at high rates.

It is absolutely fascinating to me that groupthink and myths are so common in the practice of medicine. Invariably, patients suffer to some degree as a result. Thankfully, medical researchers continue to shine their high-lumen lights through the fog and smoke screens of these medical myths and falsehoods.



Watch Dr. Mellick’s video where he shows how the non-rebreather mask and the BVM can be effectively used to oxygenate patients.

Friday, September 1, 2017

Children have this strange predilection for placing small objects in body cavities and orifices. Besides putting foreign bodies in their mouths, an act that often leads to ingestion or aspiration, the ear canals and nares are their favorite locations for depositing plastic beads, toy parts, paper materials, small vegetables, jewelry, screws, and nails, and that frequently brings them to the emergency department. Unsuccessful attempts to remove the foreign bodies in the ED lead to a consultation or referral to an ENT specialist. The timing, technique, and tools used to remove a foreign body will depend on the anatomic location, the shape of the object, the material it is made of, its consistency and texture, whether it is occlusive, and the potential risks to patient.

Magnetism is a potentially valuable tool in the emergency department that really hasn't received the respect it deserves. The cardiac pacer magnet is probably what everyone thinks of when they consider magnetism in the ED, but magnetism also can be helpful in removing metallic foreign bodies from the mouth, ears, and nasal cavities and in locating and removing ferromagnetic fragments buried under the skin and subcutaneous tissues.

Not all metals are strongly attracted by a magnetic force, but this technique will work with iron, nickel, cobalt, gadolinium, dysprosium, and alloys such as steel that contain ferromagnetic metals. Unfortunately, the majority of pediatric foreign bodies placed in the nose and ears are made of plastic, paper, vegetable matter, or other materials not affected by magnetic force, but it pays to be prepared when the foreign body is susceptible to the forces of magnetism.​

The magnets used to remove foreign bodies should ideally be powerful but small enough to access pediatric-sized nares and auditory canals. That is where rare earth magnets play an important role. These are made from the alloys of these 17 elements in the periodic table. The magnets were first developed in the 1970s, and have especially powerful magnetic fields. The neodymium magnets and samarium-cobalt magnets are two most common types of rare earth magnets used by industries and manufacturing.​

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There are at least two ways to attain magnetism that will latch on to errant ferromagnetic foreign bodies in the emergency department. The donut-shaped cardiac pacer magnet found in almost every emergency department is a very strong rare earth magnet. When it's overlaid a screwdriver or a pair of hemostats, the cardiac pacer magnet can create a magnetized, narrow-tipped tool that will fit into smaller body cavities. Commercial pen magnets can be purchased at auto parts stores, and are small, powerful rare earth magnets that can effectively fit into most anatomical orifices. The cardiac pacer and these pen magnets can also be applied directly over metallic foreign bodies buried in the skin to help locate and pull them toward the surface to facilitate removal.​

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A potential criticism of magnet use is tool sterility. Thankfully, most of the orifices holding foreign bodies are far from sterile, and tools cleaned with the appropriate antiseptics or covered with a sterile glove should be antiseptically appropriate. Some degree of preplanning is needed to purchase the pen magnets for the emergency department and store them so that they can be easily located when needed. The strength of the magnets is critical to accomplishing the stated goals and secondarily magnetizing hemostats, forceps, and screw drivers when that technique is used. The speed and ease of removal of metallic foreign bodies will please and surprise everyone involved.

Many characteristics of these magnets make them especially useful in removing foreign bodies. First, often all that is necessary is to get close to the foreign body. Even if the pen magnet doesn't fit entirely into the ear canal, just getting close to the metallic foreign body is generally all that is needed. Similarly, there is no need to get behind the foreign body to bring it forward as is the case with balloon catheter and right angle hook removal techniques. The maneuvering required by other tools in the tight quarters of smaller body cavities can be uncomfortable. There is no need to get a grip on the object to remove it as is the case with alligator forceps or similar tools.

The actual procedure used will depend somewhat on the patient and the specific orifice holding the foreign body. Topical anesthesia will usually not be needed for the ear, but for the nose, a 1:1 mixture oxymetazoline and 4% lidocaine can be used to prevent bleeding and provide topical anesthesia. Procedural sedation may be necessary depending on the patient and the foreign body's location and characteristics. Directional traction on the helix will make the external auditory canal more accessible, and using an ENT dilator or pushing on the tip of the nose with the non-dominant hand will improve accessibility and visibility to the nares. Proximate location of the foreign body to the airway may also determine the technique used.

It is always important to confirm that a second foreign body is not lurking in the shadows. And, be sure to watch our three videos demonstrating the tools and techniques discussed above.​


Watch Dr. Mellick demonstrate how to use a pacer magnet to remove a foreign object from the ear.​


Watch a video of Dr. Mellick as a guinea pig for testing different magnets for removing a foreign body from the ear.


Watch a video of Jedidiah Ballard, DO, using a pacer magnet to remove a foreign object from the ear.​


Tuesday, August 1, 2017

Double sequential defibrillation appears to work in the electrophysiology lab, and anecdotal evidence shows that lives can be saved in the prehospital setting and in the emergency department. With all the unanswered questions swirling around it, should we use this technique? Let’s consider the evidence.

Using two sets of defibrillators fired simultaneously or in a sequential pattern to treat refractory ventricular fibrillation is a relatively new concept. A number of different names for the procedure exist, but double sequential external defibrillation (DSED) or double simultaneous defibrillation (DSD) are commonly used. This technique was first described in 1994 by Hoch, et al., in five patients who were successfully converted from ventricular fibrillation in an electrophysiology laboratory. (J Am Coll Cardiol 1994;23[5]:1141.) The patients in this report failed to convert to normal sinus rhythm with monophasic energies ranging from 200-360 joules. All of them, however, responded to double shock with a total of 720 joules. The current experience with DSD in treating atrial fibrillation is probably more robust, but the evidence for refractory ventricular fibrillation is mostly case reports and case series. Nonetheless, DSD appears to convert fibrillating hearts and save lives.

Multiple questions still surround this off-label use of defibrillators for ventricular fibrillation. There is evidence of safety based on the use of DSD in atrial fibrillation patients, but the potential risk of myocardial injury from doubling the joules administered to the patient is not completely known. Two defibrillators fired simultaneously at maximal output will deliver 400 or 720 joules depending on whether one is using a biphasic or monophasic defibrillator.

It is also unclear whether quick sequential defibrillation or simultaneous defibrillation is more beneficial. It may be a moot point, though. Simultaneously firing two defibrillators probably doesn’t ever happen when done manually, and it is possible that a short millisecond separation may allow the second set of joules to occur at the moment of greatest drop in electrical resistance following the first attempt.

It is also unclear whether the overall increase in energy levels, the addition of a second vector of current flow, or the greater amount of heart muscle lying directly under the pads is responsible for the successes. It is clear that impedance in a patient relates to body mass and that human anatomy and chest sizes vary. It is also highly likely that the fibrillating ventricles may frequently not align perfectly with a single energy vector.

Another question needing clarification is which pad placement format is best: two sets placed side by side using the traditional anatomic locations for defibrillator pads or one set of pads placed at the traditional locations and the second set placed in an anterior-posterior location. At this time, no one knows for sure which option is more effective.

It is also unknown, or at least unclear, exactly when the dual simultaneous defibrillation should be initiated. Is DSD more effective when incorporated earlier in the attempted resuscitation of a VF arrest? It is known that the longer the patient is in ventricular fibrillation, the more resistant the heart is to being defibrillated. Obviously, the sooner we have a return of spontaneous circulation, the better the cognitive outcome for the patient. It would seem obvious that incorporating DSD sooner is better than later.

What do we know for sure? Additional vectors of current flow are added, and a higher total number of joules are delivered to the flailing heart. And almost definitely a greater cardiac topography is covered by the double sets of pads. We also know that the defibrillation process is probably never going to be exactly simultaneous because of the manual process required.

Equipment:
-Two defibrillators and two sets of pads.

Steps:
-Apply a second set of defibrillation pads in the same configuration as the existing pads but adjacent or in the anterior-posterior position. (Make sure the pads are not touching or applied on top of one another.)
-Charge both monitors to their maximum energy level (200 joules for biphasic, 360 joules for monophasic). Warn all providers not to be in contact with the patient at the time of discharge, and then charge and simultaneously push the defibrillation button on each monitor. Some recommend continuing cardiac compression until just before the defibrillation buttons are pushed. Immediately resume chest compressions. Administer appropriate ACLS medications and repeat as necessary.
-Have a video of double sequential defibrillation available.

So, should we use this technique? Let’s turn to The Aphorisms of Hippocrates: “For extreme diseases, extreme methods of cure, as to restriction, are most suitable.” (http://bit.ly/2sUkilA.) In other words, desperate times call for desperate measures, and double simultaneous defibrillation in the face of refractory ventricular fibrillation easily fits that bill.​

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Monday, July 3, 2017

The time for possible salvage and survival of a torsed testicle is commonly thought to be six to eight hours, a period that is expressed with confidence by the medical and legal professions. Survival of torsed testicles with and without subsequent atrophy is known to occur outside that critical window. My colleagues recently treated a 17-year-old boy approximately three days after the onset of right scrotal pain. He reported his pain constantly as 8/10 in severity. He didn't tell his mother for several days because he was scared, embarrassed, and hoping that the pain and swelling would resolve.

The patient was taken to the operating room approximately 70 hours after the onset of his testicular torsion. The cyanotic, 360-degree torsed left testicle pinked up and was deemed viable in the OR. The patient reported a week later that he was experiencing no pain and that his testicle seemed to be completely back to normal. Consider for a minute if the urologist had elected not to take the patient to the operating room that night. The outcome would have been much different, and an otherwise salvageable testicle would have died.

The potential for subsequent testicular atrophy is acknowledged, but no one knows for sure. Is there a clear-cut time when it is futile to rush to the operating room? If there is, it probably has to be based on other physical and ultrasonographic findings in addition to time.

It is true that torsed testes have been found to be necrotic after just six or fewer hours of pain, and scores of reports describe testicular survival following significantly longer periods. Many of these salvaged testicles have subsequently atrophied, but some also appear normal despite prolonged periods of torsion. Possible explanations for variations in testicular survival include fewer twists of the spermatic cord, the relative thickness of the torsed spermatic cord, or other anatomical aspects such as the attachment level of the tunica albuginea in the bell clapper deformity that allows persistence of critical blood flow.

The importance of understanding survival time in testicular torsion is critical; failure to recognize that testicular survival can occur even after many hours and potentially days of symptoms can lead to inappropriate delays in timely management. I am working on a systematic review of testicular survival rates and duration of torsion, and a preliminary but extensive search of the literature found 1,857 patients with surprising results. These numbers may change once our systematic review is finished, but time to surgery varied. Our tallied survival was 97.8 percent in patients whose treatment was zero to six hours since onset of symptoms, 83.1 percent for seven to 12 hours, 62.9 percent for 13-18 hours, 44.6 percent for 19-24 hours, 22.5 percent for 24-48 hours, and 7.7 percent for more than 48 hours. These survivals are almost identical to those reported by Visser, et al. (BJU Int 2003;92[3]:200.) Unfortunately, no references were included to support this graphically presented data. Our systematic review has more than 2,000 patients to date, and the survival data remains pretty much unchanged.

The question remains, however, why some torsed testicles appear to be necrotic even though the pain was less than six hours. Based on evidence that suggests this is more commonly seen in younger patients and because some patients have pain honeymoons, it is my opinion that the dead testicles had actually been torsed for much longer.​

I am confident the data are going to prove that we should not give up when suspected testicular torsion patients present many hours past the commonly taught six to eight hours. We will have done our patients and their torsed testicles a huge favor if we will aggressively and expediently manage their initial care in the emergency department.

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Watch a video of Dr. Mellick discussing torsion in a 14-year-old.​


Watch a video of Dr. Mellick discussing an unusual presentation of torsion in a 15-year-old.​​


Thursday, June 1, 2017

Are you one of those clinicians who frequently finds himself frustrated with asthma patients who improve to a point but not enough to discharge home? Even though this has to be a common problem, no one seems to talk or write much about it. I was feeling deeply frustrated about these patients, and it led me to serious clinical introspection. Why does everyone write about the crashing asthma patient, but hardly anyone addresses the problematic patient with improving but recalcitrant bronchospasm?

Most articles typically cover every available therapeutic option, including the proverbial “kitchen sink” for managing severe asthma emergencies. Kitchen-sink recommendations generally include continuous albuterol nebulization, intravenous magnesium sulfate, intramuscular epinephrine or terbutaline, noninvasive (NIV) positive pressure ventilation, helium-oxygen administration, and ultimately intubation and ventilation using ketamine. It is time, however, to give “out-the-door” asthma management a little respect and attention.

Typically, emergency department asthma protocols will include repeated albuterol treatments with at least two of those treatments combined with nebulized ipratropium bromide. Corticosteroids are also administered orally or intravenously. When these initial interventions fail, most practitioners continue to treat the bronchospasm with additional doses of albuterol and ultimately continuous nebulization of the β2 agonist.

This is where logic seems to fade. Continuing to hammer the patient with the same medication and the same receptors seems a little illogical. Wouldn’t it make more sense to switch to other medications that target different pulmonary smooth muscle receptors and the inflammatory factors associated with the bronchoconstriction? Nevertheless, most clinicians maintain a relatively limited number of therapeutic tools in their toolbox when it comes to routinely managing asthma. Consequently, many patients are ultimately admitted to the hospital for ongoing management when some of them could have been discharged home.

What other options do we have? Truthfully, a lot of new magic bullets don’t really exist for acutely managing asthma. What about looking again at some of the older, proven interventions that have been benched for the newer, shinier treatments? Maybe we should be treating the known common inflammatory factors associated with asthma more aggressively. The following treatment options seem to be working anecdotally, especially for my pediatric asthma patients. Beginning with the strongest evidence first, these tools for your asthma tool box may help you get a few more patients home.

Inhaled Corticosteroids
One of the best supported asthma management options is inhaled corticosteroids. The literature is consistently positive, and appears to support nebulized steroids in addition to other systemic corticosteroids. In our pediatric emergency department, we typically give one dose of oral dexamethasone (0.6 mg/kg) up to a maximum of 16 mg for asthma exacerbations that have been ongoing for one to two days and are resistant to home management. Other options are effective, but my choice for an inhaled or nebulized corticosteroid is 0.5 mg of budesonide. A review article and a Cochrane review of the benefits of inhaled corticosteroids provide supporting evidence for routinely adding this intervention for patients with recalcitrant bronchospasm. (Respir Med 2007;101[4]:685; Cochrane Database Syst Rev 2012;12:CD002308.)

Intramuscular or Nebulized Epinephrine
Epinephrine, of course, has always worked for bronchospasm. Older clinicians will remember when subcutaneous epinephrine administered every 20 minutes was one of the few treatment options available. Despite the tears caused by the painful injections, it worked. In fact, many older papers described injected and nebulized epinephrine as being therapeutically similar to agents such as terbutaline or albuterol. (Ann Allergy 1983;50[6]:398; Clin Pharm 1983;2[1]:45.) Besides having a few more side effects, epinephrine, a nonselective β2 agonist, also fell to the wayside because it was far easier and less objectionable to nebulize medications than give painful injections to children and adults. If they use it at all, most clinicians reserve epinephrine for the patient presenting with severe and status asthma.

Nebulized epinephrine, however, probably works just as well as intramuscular epinephrine, and possibly delivers a greater quantity of epinephrine with minimal side effects. Both regular epinephrine (5 mg maximum) and racemic epinephrine (11.25 mg maximum) can be nebulized to treat asthma and croup. It seems to be much easier to use the commercially supplied preparations of racemic epinephrine for nebulization current available. Again, there is good evidence for the effectiveness of nebulized racemic epinephrine to treat asthma. (CJEM 2007;9[4]:304; Acad Emerg Med 2000;7[10]:1097; Am J Emerg Med 2006;24[2]:217; J Crit Care 2004;19[2]:99; Allergy 1980;35[7]:605.) When the effectiveness of nebulized albuterol seems to have petered out and you sense a need for something else, consider a trial of nebulized racemic epinephrine.

Antihistamines
The triggers of an asthma exacerbation are commonly divided into allergic and nonallergic etiologies. In fact, it is possible that allergies trigger asthma attacks in 60 to 90 percent of children and 50 percent of adults. (Medscape. April 13, 2017; http://bit.ly/2oXKp4s.) Mite and cockroach antigens are known to increase asthma morbidity, and are commonly found in the environment. (J Allergy Clin Immunol 2015;136[1]:38.) Histamine is a known inflammatory mediator in the pathophysiology of asthma. IgE binds to high-affinity receptors on the surface of mast cells and basophils, leading to mast cell and basophil degranulation. Mast cell mediators, histamine, pro-inflammatory cytokines, and proteases are released, leading to an early allergic response.

Consequently, it seems intuitive that antihistamines could play a role in treating asthma. Unfortunately, evidence for the benefit of first-generation antihistamines in asthma is relatively limited. This may be secondary to the fact that antihistamines were avoided in asthma for many years. Clinicians were taught to avoid antihistamines out of concerns for possible drying and inspissation of airway secretions. Current research on second-generation antihistamines suggests benefit, however. (Am J Med 2002;113[Suppl 9A]:2S; Curr Opin Allergy Clin Immunol 2002;2[1]:53; Treat Respir Med 2006;5[3]:149; J Allergy Clin Immunol 2003;112[4 Suppl]:S96.) Clinical studies have shown mixed results, but no detrimental effects were noted. Despite weaker evidence, the addition of intravenous or oral antihistamines during an acute asthma event seems safe, reasonable, and disease mechanism-based. And it is possible that antihistamines could prove to be synergistic with other anti-inflammatory interventions.

Ibuprofen or NSAIDs
Another even more controversial option is the use of the anti-inflammatory drug, ibuprofen, in asthma. Ibuprofen is a nonselective inhibitor of the enzyme cyclooxygenase (COX), which is required for the synthesis of prostaglandins via the arachidonic acid pathway. This pathway is active in the pathogenesis of asthma. (Pharmacotherapy 1997;17[1 Pt 2]:3S.) (Figure 1.)

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Figure 1. Stylized cell depicting the mechanism of action of ibuprofen. (Pharmacogenet Genomics 2015;25[2]:96.)  Pharmacodynamics ©PharmGKB. Reprinted with permission from PharmGKB and Stanford University.

Ibuprofen is often immediately rejected as a therapeutic intervention for asthma because of concerns about exacerbating asthma in the context of aspirin sensitivity. Literature analysis seems to indicate that the use of ibuprofen in the pediatric population does not exacerbate asthma morbidity. (Paediatr Drugs 2004;6[5]:267; Clin Ther 2007;29[12]:2716.) As stated by one author: "Given the infrequent occurrence of aspirin/NSAID sensitivity in children with asthma, it seems reasonable to allow the use of ibuprofen in this population unless there is a personal or family history of aspirin-induced asthma. In addition, the inflammatory pathogenesis of asthma, anti-inflammatory effect of ibuprofen, and evidence suggesting ibuprofen may reduce morbidity in children with asthma raises the intriguing possibility that ibuprofen might actually have therapeutic benefit for at least some children with asthma." (Paediatr Drugs 2004;6[5]:267.)

A paper by Lesko, et al., stated that rather than supporting the hypothesis that ibuprofen increases asthma morbidity among children who are not known to be sensitive to aspirin, their study suggested that compared with acetaminophen, ibuprofen may reduce such risks. (Pediatrics 2002;109[2]:E20.) Finally, another study recommended that ibuprofen be withheld for at least 24 hours prior to investigations utilizing allergen bronchoprovocation because a single dose of ibuprofen was found to inhibit early and late asthmatic responses to allergen bronchoprovocation. (Allergy Asthma Clin Immunol 2016;12:24.) The evidence is limited, but ibuprofen should theoretically decrease the inflammatory factors causing bronchospasm in asthma through its actions on the arachidonic acid pathway.​

If you find yourself regularly frustrated with asthma patients who only partially improve, consider putting back into the game some or all of these older, previously benched bronchodilators and anti-inflammatory treatment modalities.