M2E Too! Mellick's Multimedia EduBlog
E 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 30, 2014
The three videos presented this month demonstrate the technique for mixing and administering pulse dose epinephrine with actual patients. Particularly helpful is the one that demonstrates the administration of pulse dose epinephrine to a pediatric patient. What I really like about the demonstrated pediatric technique (first discussed in my Emergency Medicine News blog on anaphylaxis: http://bit.ly/1CHsX6h) is that it uses the same 1:100,000 concentration used for adults. And, the 0.1 mL/kg is easily remembered because it is the same mL/kg recommendation for the ACLS concentration of epinephrine. There is essentially nothing new to learn.
I first learned about the concept of pulse dose pressors, or as I call them, “push dose pressors,” from the EMCRIT blog by Scott Weingart, MD. (http://bit.ly/10mvXHc.) The value of push dose pressors for treating anaphylaxis presenting with hypotension was immediately apparent to me. It is stressful to treat hypotensive patients with anaphylaxis who are unresponsive to intramuscular epinephrine. Most of us cringe just a little at the thought of giving intravenous epinephrine outside cardiopulmonary arrest. Having a technique for giving well calibrated and exact doses of epinephrine makes the administration of intravenous epinephrine much more palatable. But if giving intravenous epinephrine to an adult is stressful, the angst associated with the pediatric patient is compounded. Viewing these videos should give peace of mind for treating adults and children with intravenous pulse doses of epinephrine.
Wednesday, September 03, 2014
A sucking chest wound or open pneumothorax is a fairly uncommon event off the battlefield, and civilian guidelines as a result are highly dependent on the experience of the military expert opinion concerning their management. Past recommendations were to place a three-sided occlusive dressing to allow air to egress to prevent a tension pneumothorax, but battlefield guidelines calling for an occlusive dressing closed on three of four sides have not proven to be effective or realistic. Covering the wound improves respiratory mechanics, but the three-sided occlusive dressing on bleeding chest wounds is no longer recommended. Current tactical prehospital guidelines recommend a vented chest seal or closing the wound and observing the patient for development of a tension pneumothorax if one is not available. A needle is placed in the chest to release the air if a tension pneumothorax develops.
The Tactical Combat Casualty Care Guidelines recommend a non-vented chest seal if a vented chest seal is not available, and that physicians treat by burping or removing the dressing or by needle decompression if the patient develops increasing hypoxia, respiratory distress, or hypotension, and a tension pneumothorax is suspected. (National Association of Emergency Medical Technicians, Tactical Combat Casualty Care Guidelines, Oct. 28, 2013; http://bit.ly/1pdHwIw.)
The recommendations for a vented chest seal is a change from the 2011 guidelines that recommended immediate application and securing of an occlusive material to cover the defect and subsequent monitoring of the casualty for the potential tension pneumothorax. (ItsTactical.com, Tactical Combat Casualty Care Guidelines, Aug. 8, 2011; http://bit.ly/1oe4Cjc.)
Five or six brands of chest seals are available. At least one, the SAM chest seal, comes in vented and non-vented forms. Not much research is available on this topic, but two 2013 articles looked at vented chest seals. The first article found that HyFin, SAM, and Sentinel vented chest seals were equally effective in evacuating blood and air in a communicating pneumothorax model. All three also prevented tension pneumothorax formation after penetrating thoracic trauma. (J Trauma Acute Care Surg 2013;75:150.)
The second article studying injured pigs found that vented and unvented chest seals provided immediate improvements in breathing and blood oxygenation in their model of penetrating thoracic trauma. The unvented chest seal led to tension pneumothorax, hypoxemia, and possible respiratory arrest in the presence of ongoing intrapleural air accumulation, while the vented chest seal prevented these outcomes. The outcome for the unvented chest seals was not expected because a tension pneumothorax was simulated by injecting approximately 1.4 liters of air into the thoracic cavity of the animal models. (J Emerg Med 2013;45(5):686.) A 2008 study found that the Bolin and Asherman chest seals equally prevented the development of a tension pneumothorax in this open pneumothorax model. (Injury 2008;39:1082.)
Not all sucking chest wounds are created equally, however. Some current chest seals with their relatively small footprint would be unable to seal and vent large sucking chest wounds. Several years ago we treated a 4-year-old girl who was attacked by the family’s pit bulls. One of the dogs was not chained up, and grabbed her torso and tore open the chest wall, creating a large sucking chest wound. (Figure 1/video.) Multiple bite injuries were also sustained to her hand and leg. (Figure 2.)
Click here to watch a video of a 4-year-old with a sucking chest wound.
The ED who transferred her to us applied sterile petrolatum gauze and a large abdominal dressing over the wound. Her initial hypoxemia (SaO2 79% on room air) was treated with supplemental oxygen by face mask. The first chest x-ray showed no evidence of a pneumothorax and the petrolatum gauze appeared to be letting air escape, so we did not change the initial management. The patient was subsequently taken to the operating room for further management of the open pneumothorax and washout of her bite wounds. A chest tube was inserted in the operating room, and the large thoracic wound was closed.
Current recommendations for managing a sucking chest wound have changed. The old recommendation to place a piece of plastic wrap or aluminum foil on top of the wound and tape it on three sides should be considered no longer appropriate, even in the austere environment of the wilderness. (Wilderness Medicine. Philadelphia: Elsevier: 2011, p. 456.) You may still use whichever appropriate material you have in the wilderness — plastic wrap, a piece of a plastic bag — but seal the wound on four sides after maximally venting the air from the chest by timing application with full expiration. Then be sure to monitor the patient for increasing hypoxia, respiratory distress, or hypotension, and tension pneumothorax. If signs of decompensation develop, treat by burping or temporarily removing the dressing or, if necessary, by needle decompression.
Wednesday, August 06, 2014
Relative or paradoxical bradycardia in the face of severe blood loss and hypotension fits squarely in the “it-just-ain’t-right” category. It isn’t right because it happens far more frequently than we recognize, and it contradicts what we have been taught about the body’s response to hemorrhage. A definite and significant subset of hypotensive patients will not mount a tachycardia response to hypotension, and a third or more of hypotensive trauma patients will present with bradycardia. (J Trauma 1998;45:534 and 2009;67:1051; J Am Coll Surg 2003;196:679.)
But it just isn’t relative bradycardia in the face of hypotension and hemorrhage where the heart rate’s reliability as a marker for severe blood loss fails. The truth is that even though there is an association between hemorrhage and tachycardia, it is actually unreliable and nothing like the four classes of hypovolemic shock described in that well-known table published by the Advanced Trauma Life Support course. The evidence shows that the ATLS table is more wishful thinking than reality. (Resuscitation 2011;82:556; 2010;81:1142; 2013;84:309.) We still need to respect tachycardia in the face of hypotension, but heart rate is not a reliable indicator in the trauma patient. (J Am Coll Surg 2003;196:679; J Trauma 2007;62:812.)
The sensitivity and specificity of tachycardia is poor. Patients with rapid heart rates frequently do not have serious blood loss, and others who are not tachycardic will be found to be seriously hypovolemic.
Nevertheless, paradoxical bradycardia in the face of massive hemorrhage and hypotension is a fascinating physiologic response. It is very real, and has the potential to trip up the unsuspecting clinician. Several years ago, a 20-year-old woman presented to our emergency department with severe vaginal bleeding. Obstetrics and gynecology was consulted shortly after her arrival in the emergency department, but it was early in the academic year, and delay after delay occurred. Multiple calls to the on-call resident were made. Eventually, the patient demonstrated hypotension that rapidly worsened.
The paradoxical or relative bradycardia associated with her hypotension was truly impressive. Her heart rate was recorded at 58 beats per minute even when her blood pressure was 66/34 mm Hg. Emergent blood transfusion bought us time until the obstetrics gynecology consultants finally arrived to take the patient for an emergency dilation and curettage. Nevertheless, a 4 g drop in hemoglobin was documented over a relatively short period of time. And, of course, the consultants were heard blaming the emergency department for not calling them sooner. Click here to watch a video of this patient.
A number of potential explanations exist for this phenomenon. A vagal or parasympathetic response is often proposed because it is a relative common occurrence in penetrating or blunt abdominal trauma. (J Emerg Med 1989;7:335.) Some experts also say this is one stage of the body’s response to significant blood loss. Heart rate slowing allows the ventricles to fill and prevents the empty heart syndrome. In fact, tachycardia reportedly occurs after fluids and blood are replenished.
We have been taught for years that heart rate is an integral vital sign in the assessment of patients at risk of hemorrhagic shock, but it just isn’t reliable. And it will mockingly try to trick you at the extreme when the heart rate paradoxically slows in the face of hemorrhagic shock. Don’t get caught unaware!
Wednesday, July 02, 2014
Looks can be deceiving. I was not supposed to have a difficult airway, but we found out the hard way that wasn’t true. I was about to undergo an exploratory laparotomy for suspected appendicitis in 1989, and my wife was adamant that an attending anesthesiologist perform my intubation. The anesthesiology resident at a large Midwest teaching hospital made a claim that I suspect many of us did as we advanced through training and began to feel procedurally invincible. He claimed that the attending anesthesiologist rarely did intubations, and that the residents who performed them daily were more prepared. Unaware of any unique issues with my airway and wanting to be a good patient, I didn’t attempt to override the resident.
I woke up from anesthesia with a swollen, bleeding, and extremely painful pharynx, and my right central incisor was abraded and roughened. We learned that the resident made four attempts before the attending took over and successfully placed the airway. The soft tissue injury to the pharynx resolved with time, and my dentist filed the tooth smooth again. Subsequent surgeries, however, included a successful bougie intubation and a not-so-pleasant awake intubation.
This May, my shoulder pain reached a point where I knew it was time for surgery again. My left rotator cuff muscle needed to be repaired, just like the right one had years before. Intubation methods were a necessary topic of conversation with my anesthesiologist again.
My “3-3-2” airway assessment is abnormal on two counts. Instead of three fingers, my mouth will only open to allow two and maybe part of a third finger between the upper and lower incisors. The second “3” is the distance between the mentum and the hyoid bone. This gives an idea of how much space is available for the tongue to be displaced during laryngoscopy. My facial anatomy appears fine in this regard. The “2” refers to the position of the larynx in relation to the base of the tongue. Two or more fingerbreadths between the hyoid bone and the upper anterior edge of the thyroid cartilage are ideal. This signifies that the larynx is located sufficiently beyond the base of the tongue. I barely get one fingerbreadth with this measurement. These two variances add up to a markedly anterior larynx and a difficult-to-visualize airway. I have never been told what my Cormack-Lehane classification is, but my Mallampati score is a Class II.
Visualization of Glottis: Cormack-Lehane Classification
Grade 1: Full view of glottis and vocal cords
Grade 2: Vocal cords and glottis are partially visible
Grade 3: Only epiglottis seen; glottis is not visible
Grade 4: Glottis and epiglottis are not visible
Visualization of Upper Airway: Mallampati Class
Class I: Faucial pillars, soft palate, and uvula visualized
Class II: Faucial pillars and soft palate visualized; uvula not seen (masked by tongue)
Class III: Only soft palate and base of uvula visualized
Class IV: Faucial pillars, soft palate, and uvula not visualized (only hard palate visualized)
The anesthesiologist who agreed to take my case chose a fiberoptic intubation using nebulized lidocaine, a Parker Flex-Tip endotracheal tube with the unique beaked tip, and the endoscope plastic oral airway guide. In fact, we agreed to make a teaching video of my procedure, even knowing it might not be pretty. It wasn’t. Everything the anesthesiologist did was technically correct. Unfortunately, the lidocaine nebulization failed to anesthetize my airway. That, however, was my fault. Instead of consistently inhaling the 4% lidocaine, I stopped multiple times to greet acquaintances in the operating room and to direct the filming of my video. My reward was vigorous coughing and bucking as the endotracheal tube and fiberoptic scope were inserted.
The intravenous midazolam also caused a short period of apnea, and it was a little unnerving to listen to the pulse oximetry monitor alarm drop in pitch when I reviewed the video later. I couldn’t actually tell how low my oxygen saturation went, but the oxygen was turned up, and the first reported reading was of 93%. Thankfully, I have no memory of these events.
The truth is that events like this happen all the time despite our best-laid plans, and they are the substance of life in the ED that keeps us simultaneously on our guard (paranoid) and humble. I love the video because it shows a few of the realities of difficult airway management that can be instructional for learners. Click here to watch a video of the interscalene brachial plexus block used for my shoulder surgery.
Have you ever had a patient with a difficult airway like mine? How did you manage it? What tips do you have for difficult intubations?