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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.

Friday, October 10, 2014

Diseases and complications associated with intravenous drug use are many and varied. These three videos demonstrate three skin findings associated with drug addiction and IV drug use: the track marks associated with repeated intravenous injection, the piloerection that accompanies withdrawal, and the diffuse petechiae from septic emboli of life-threatening infective endocarditis.


Click here to see the track marks associated with repeated intravenous injection.



Click here to see the piloerection that accompanies withdrawal.


Click here to see the diffuse petechiae from septic emboli of life-threatening infective endocarditis.



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;


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. (, Tactical Combat Casualty Care Guidelines, Aug. 8, 2011;


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[1]: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[9]: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[3]:534 and 2009;67[5]:1051; J Am Coll Surg 2003;196[5]: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[5]:556; 2010;81[9]:1142; 2013;84[3]: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[5]:679; J Trauma 2007;62[4]: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[4]: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?

Wednesday, June 04, 2014
Limb exsanguination is no longer the most common cause of preventable death on the battlefield because of emergency tourniquets. Hemorrhage control for wounds in the junction between the trunk and the limbs and in the neck are an obvious care gap, most commonly in the pelvic area, including the buttocks and groin proximal to the inguinal ligament. (US Army Med Dep J 2011 Apr-Jun:38.) Managing hemorrhagic shock also requires support of central aortic pressure to maximize perfusion of the brain and heart and to control bleeding effectively.
Noncompressible torso hemorrhage is recognized as the leading cause of death in trauma, but definitive hemorrhage control has been challenging. A review of combat casualties from 2001 to 2011 showed that the most common sites of lethal hemorrhage were truncal (67.3%), junctional (19.2%), and peripheral-extremity (13.5%). (J Trauma Acute Care Surg 2012;73[6 Suppl 5]:S431.)
The direct application of pressure over the distal aorta with an abdominal tourniquet and the insertion of a resuscitative endovascular balloon to occlude the aorta (REBOA) has recently come to the forefront as a potential life-saving option. The problem is bleeding from noncompressible vascular injuries. Traumatic or iatrogenic injuries to the common iliac, external iliac, internal iliac, profunda femoral, and superficial femoral can cause bleeding that is extremely difficult to control. (J Cardiovasc Surg (Torino) 2012;53[4]:495.) Exsanguination from one of these vessels can occur in minutes or even seconds.
Pulsed-wave Doppler measurements have documented that blood flow to the common femoral artery can be stopped by applying direct pressure over the distal abdominal aorta or proximal iliac artery. (Prehosp Disaster Med 2006;21[6]:379.) A number of reports have now documented the ability to stop blood flow to these major vessels with the Abdominal Aortic and Junctional Tourniquet (AAJT) and the REBOA. (Mil Med 2013;178[11]:1196; J Trauma Acute Care Surg 2013;75[1]:122; J Trauma Acute Care Surg 2013;75[3]:506.) Major trauma center experience with REBOA suggests that it is feasible and effective for proactive aortic control in patients with end-stage shock from blunt and penetrating mechanisms. (J Spec Oper Med 2013;13[3]:1.) Likewise, real-life experience with the AAJT also suggests that it can save lives. (J Spec Oper Med 2013;13[2]:1; Surgery 2011;150[3]:400.)

The AAJT and REBOA are relatively new concepts in emergency medicine, and their potential benefits and roles in managing life-threatening bleeding remain untapped to a significant degree. A respectable amount of research has been done for these tools and the FDA has approved several different applications of the AAJT, so it’s time to get broader clinical and research experience with them.
The AAJT has other applications besides inguinal and groin hemorrhage. The FDA approved it for life-threatening axillary hemorrhage, and it has been used off-label for life-threatening neck hemorrhage.

But what about using the AAJT or REBOA instead of cross-clamping the aorta when an open thoracotomy is performed? One animal study specifically looked at the use of REBOA for that purpose. (Can Med Assoc J 1964;91:128.) The AAJT would obviously occlude the aorta lower than the thoracic diaphragm cross-clamping location typically used during open thoracotomy, but cross-clamping the aorta during an open thoracotomy has been fraught with difficulty and plagued by operator inexperience. Many an esophagus has been inadvertently cross-clamped, and the traumatic injury to the aorta and its branching vessels from dissection and cross-clamping can be significant. The lower-placed AAJT would not occlude blood flow to the kidneys and the superior mesenteric artery, but maybe it’s not a bad idea to preserve blood flow to the kidneys and mesentery in addition to the brain and heart.
The biggest drawbacks to the REBOA are the technical skills required for insertion and the actual time it takes to insert the balloon. I want something fast when my patient is hemorrhaging uncontrollably, and that is where the AAJT fills the bill: it can be applied in less than 60 seconds. It’s possible these two tools can be used together effectively, with the AAJT being applied immediately to allow additional time for REBOA placement.
REBOA for stopping uncontrolled bleeding in pelvic fractures has been reported as quite effective. Again, it would be great to see some experience with the application of the AAJT for that same indication. Researchers reported in 1964 that compression of the aorta with the heel of the hand just above the bifurcation of the common iliac arteries was an effective way of controlling catastrophic pelvic hemorrhage during laparotomy. (Ann Emerg Med 2013 Oct 23; doi: 10.1016/j.annemergmed.2013.09.026.) More recent reports describe external manual compression for abdominal bleeding associated with penetrating injuries and ruptured abdominal aortic aneurysms. (J Anesth 2002;16[2]:164; Obstet Gynecol 2014;123[4]:804.) Pelvic binding and the AAJT might slow blood loss significantly in pelvic fractures.
Postpartum hemorrhage is another life-threatening emergency that can occur after a Caesarean section or vaginal delivery. It is one of the most common obstetric maternal complications, and is responsible for approximately half of severe maternal morbidity. (Transfusion 2014 Mar 12; doi: 10.1111/trf.12550.) Worldwide, postpartum hemorrhage is a common etiology of maternal death, and uterine atony is the major associated cause. (WHO Guidelines; External manual compression of the aorta is a common treatment for life-threatening post-partum hemorrhage. (Anaesth Intensive Care 1994;22[5]:571.) A commonly referenced case report describing successful management of a hemorrhaging patient with this technique was published in 1994. (Circulation 1993;88[4 Pt 1]:1916.) Again, here is another condition where it seems the AAJT could play a life-saving role in slowing uterine bleeding while other interventions are being started.
Applying the abdominal tourniquet during CPR has been discussed as one way to shunt blood flow selectively to the heart and brain, meeting CPR’s goal of maintaining blood flow to the vital organs until the heart can once again function independently. Aortic compression to augment cardiopulmonary resuscitation has been written about for decades. The results were variable, though, and a number of well-done papers demonstrated improved resuscitation parameters and outcomes when the aorta was occluded during CPR. (Am J Emerg Med 2002;20[5]:453; Resuscitation 2001;50[3]:319; Resuscitation 1999;40[3]:171; Resuscitation 2011;82[8]:1087; Resuscitation 2007;75[3]:515; Crit Care Med 1997;25[6]:1003.)
Applying the AAJT during CPR is a study that simply must be done. A significant step forward will have occurred in advanced cardiac life support if a distinctly positive outcome similar to the animal studies is found.
Both these tools can save lives for a wide spectrum of different life-threatening conditions. Unfortunately, the AAJT and the REBOA are currently relatively unknown and not being used. Emergency medicine and trauma programs need to include training in how to apply the AAJT and how to insert the REBOA. And, of course, we need increased research and assessment of various clinical applications.

Additional information about the Abdominal Aortic Junctional Tourniquet can be found at

Dr. Mellick disclosed that he has no conflicts of interest related to the AAJT, but that the chairman of his department, Richard Schwartz, MD, is one of its inventors.
About the Author

Larry Mellick, MD
Dr. Mellick is a professor of emergency medicine and pediatrics at Georgia Regents University in Augusta, the former chairman of emergency medicine at Georgia Regents Health System, and a professor of emergency medicine and pediatrics at Georgia Regents Medical Center and Children’s Hospital of Georgia.

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