Clinical Image 22: The Stuck Sub



HPI: A 27 year-old male with no significant past medical history presents to the ED with chest pain. The patient states about 30 minutes prior to arrival he was eating a meatball sub and got the feeling “like something was stuck in my chest”. He drank water in an attempt to push the food into his stomach but it did not help.  He then tried to self induce vomiting multiple times when he developed acute chest pain. Over the course of several minutes his chest pain worsened and was now associated with shortness of breath, nausea and dry heaving, dysphagia, and odynophagia. He also feels as though his voice sounds hoarse.  He denies dizziness, syncope, palpitations, or abdominal pain. He’s been otherwise well leading up to this.   

Vitals: T: 99.4 BP: 138/68 P: 86 R: 16 SpO2: 100% on room air

Physical examination: Patient found sitting up in the stretcher and appears extremely uncomfortable. He is cool and clammy. He has diminished breath sounds bilaterally. He is noted to have right facial and neck swelling as well as underlying crepitus. Heart sounds are regular rate and rhythm without murmur, rub, or gallop. He has no abdominal tenderness, guarding, rebound, or distention. No other pertinent exam findings.

Chest X-ray imaging was obtained:

Figure 1: Chest x-ray imaging on patient arrival

Figure 1: Chest x-ray imaging on patient arrival

What does the chest x-ray show and what is the presumptive diagnosis?

Pneumomediastinum concerning for esophageal rupture (Boerhaave’s Syndrome)

In the chest x-ray above we can see air tracking along the mediastinum (red arrows), as well as extensive subcutaneous emphysema tracking into the neck (green arrows).

Figure 2: Pneumomediastinum. Air can be seen tracking along the mediastinum (red arrows), and into the subcutaneous tissues of the neck (green arrows).

Figure 2: Pneumomediastinum. Air can be seen tracking along the mediastinum (red arrows), and into the subcutaneous tissues of the neck (green arrows).

The patient’s respiratory distress worsened and he became hypoxic requiring oxygen by NRB. Repeat chest x-ray demonstrated a left sided pneumothorax, as identified by a pleural line (arrows).

Figure 3: Left sided pneumothorax as identified by a pleural line (arrows)

Figure 3: Left sided pneumothorax as identified by a pleural line (arrows)

Some quick facts about Boerhaave’s Syndrome:

  • Full thickness perforation of the esophagus after a sudden increase in intraesophageal pressure, typically in the setting of forceful emesis.
  • Foreign body ingestion and food impaction may also result in perforation either directly or indirectly (forceful vomiting).
  • Blunt or penetrating neck trauma can also cause perforation, as well as instrumentation (endoscopy).
  • Most perforations are left sided and distal, although proximal perforations are more commonly seen with instrumentation.
  • Classic presentation is sudden onset, severe chest pain following forceful emesis. It often radiates into the back, abdomen, neck, and shoulders.
  • Patients are typically ill appearing, diaphoretic, dyspneic, and/or tachycardic.
  • On examination patients may have subcutaneous crepitus appreciated in the chest and neck. Hamman’s crunch, an audible crepitus appreciated on heart auscultation, is sometimes heard in the setting of pneumomediastinum.
  • Chest x-ray imaging may reveal pneumomediastinum, pneumoperitoneum, pneumothorax, subcutaneous air, or pleural effusions (typically left sided), although a normal x-ray does not rule out the diagnosis as mediastinal emphysema takes time to develop.
  • Patients can develop mediastinitis, pneumonitis, or peritonitis from the leakage of esophageal contents, which can rapidly develop into septic shock.
  • ED management includes resuscitation in the setting of septic shock, administration of broad spectrum antibiotics (consider anti-fungals as well), and surgical consultation.
  • Delay in diagnosis and treatment > 24 hours is associated with an increased rate in mortality.
  • Definitive management ranges from conservative for smaller tears with a more indolent clinical course, to surgical management for more severe perforations.

Pneumomediastinum versus Pneumopericardium: Does the distinction matter?  

Of course! The main importance is that pneumopericardium can develop tension physiology, whereas as pneumomediastinum typically does not. With pneumomediastinum, in addition to air tracking along the mediastinum, you can also see a pleural edge along the upper heart border. In this case, the pleural reflection is very thin, versus pneumopericardium in which there is a much thicker edge given the thickness of the pericardium. In pneumopericardium the air is confined to the pericardial space, where in pneumomediastinum it often decompresses into the subcutaneous tissue.

Case Conclusion:

Our patient underwent a left sided chest tube insertion for management of his pneumothorax followed by barium swallow to assess the severity of his perforation. He was found to have a small, focal, contained perforation in the distal esophagus.

Figure 4: Barium swallow demonstrating distal esophageal perforation (arrows).

Figure 4: Barium swallow demonstrating distal esophageal perforation (arrows).

He received broad spectrum antibiotics and was admitted to the cardiothoracic surgery service where he underwent successful conservative management.

Faculty Reviewers: Dr. Alyson McGregor and Dr. Robert Tubbs

More Reading:


1: Gorrochategui, M., et. al. Pneumothorax. Radiopaedia. 2017 <>.

2: Gorrochategui, M., et. al. Pneumomediastinum. Radiopaedia. 2017. <>.

3: Raymond, D., Jones, C. Surgical Management of Esophageal Perforation. UptoDate. 2017.

4: Tintinalli, et. al. Emergency Medicine. 8th Edition. 2016. 328; 511-512.


AEM Early Access 02: Ketamine for Acute Pain in the ED

Welcome to the second episode of AEM Early Access, a FOAMed podcast collaboration between the Academic Emergency Medicine Journal and Brown Emergency Medicine. Each month, we'll give you digital open access to an AEM Article in Press, with an author interview podcast and links to curated FOAMed supportive educational materials for EM learners.

    A FOAM Collaboration: Academic Emergency Medicine Journal and Brown EM

    A FOAM Collaboration: Academic Emergency Medicine Journal and Brown EM

This month's discussion: Ketamine as an Adjunct to Opioids for Acute Pain in the Emergency Department: A Randomized Controlled Trial. Karen J. Bowers MD, MS, Kelly B. McAllister, PharmD, MBA, Meredith Ray, PhD, MPH, and Corey Heitz MD, MS.

LISTEN NOW: Author Interview with Karen Bowers, MD


Karen J. Bowers MD, MS, MEd

Emergency Medicine Resident, PGY-2

Emory University School of Medicine

**This article will be open access digitally until June 30, 2017. Read it in full here.**

Article summary:

Objective: To measure and compare total opioid use and number of opioid doses in patients treated with opioids versus ketamine in conjunction with opioids, pain scores up to 2 hours after presentation in the ED and patient satisfaction in patients treated with opioids versus ketamine in conjunction with opioids, and to monitor and compare side effects in patients treated with opioids versus ketamine in conjunction with opioids.

Methods: Randomized, double-blinded, placebo-controlled trial at a single center academic emergency department evaluating the use of ketamine versus placebo in conjunction with opioids for moderate to severe pain. Patients who had received an initial dose of opioid analgesia were randomized to receive either 0.1 mg/kg ketamine or placebo prior to protocol-cased dosing of additional opioid analgesia, if required. Over 120 minutes, subjects were assessed for pain level (0-10), satisfaction with pain control (0-4), side effects, sedation level, and need for additional pain medication. Total opioid dose, including the initial dose, was compared between groups.

Results: 63 subjects were randomized to the placebo group and 53 to the ketamine group. No significant differences were found in demographics between the groups. Patients receiving ketamine reported lower pain scores over 120 minutes than patients receiving placebo (p = 0.015). Total opioid dose was lower in the ketamine group (mean SD = 9.95 +/- 4.83 mg) compared to placebo (mean SD = 12.81 +/- 6.81 mg; p = 0.02). Satisfaction did not differ between groups. Fewer patients in the ketamine group required additional opioid doses. More patients reported light-headedness and dizziness in the ketamine group. 

Conclusions: Ketamine, as an adjunct to opioid therapy, was more effective at reducing pain over 120 minutes and resulted in a lower total opioid dose as well as fewer repeat doses of analgesia. More side effects were reported in the ketamine group (51% vs. 19%), but the side effect profile appears tolerable. 


Related #FOAMed educational resources:

SGEM #130: Low Dose Ketamine for Acute Pain Control in the ED

Review of Dr. Beaudoin's (faculty at Brown University) research on low dose Ketamine for Acute pain, by EM Cases: Low Dose Ketamine Analgesia

EM Crit: "Opioid Free ED". Podcast with Dr. Motov, who published a comparison of 0.3 mg/kg of ketamine versus morphine and found it to be just as good. Also see Dr. Motov's website,, where you will find many related resources.

Our friends at NUEM review of Dr. Motov's study: Ketamine versus Morphine for Pain Control

Ped EM Morsels: Ketamine for Analgesia 

EM Docs: Ketamine for Analgesia in the ED

Faculty Reviewer: Dr. Gita Pensa

Like this podcast's hip hop ketamine anthem from The EMC (Dr Christopher Hahn)? Check him and more of his work out at, or on Twitter at @TheEMCMD.


Asynchrony PEM: Pediatric Airway Obstruction


Team A to the trauma room! You start assessing your patient’s C-A-Bs, and you’re stuck on Airway… this kid is struggling to BREATHE!

Foreign bodies are terrifying, but there are many causes of pediatric upper airway obstruction, such as croup, epiglottitis, angioedema, abscesses -- it's a big, scary picture.

So let’s take a moment to back up a little bit. What does upper airway obstruction sound like? Well, let’s first start with some physics (feel free to completely skip over this part, but as an engineer I couldn’t help myself). We’re going to take a walk down memory lane and bring back some old friends, namely the Bernoulli Principle and Poisseuille’s Law. Remember this equation?

The important variables here are Q (flow), P (pressure), and r (radius). As radius decreases, flow decreases. Applied to our patient population, a 1mm reduction in the 4mm diameter of a neonatal airway results in a 75% decrease in airflow. When the velocity increases to compensate, this exerts negative pressure on the walls of the lumen, precipitating airway collapse. This is what happens when you fly a plane, as illustrated in this video! (only listen to 1:05 through 1:38) and in the figure below:

Well, that was fun!

Now let’s talk about how the sound you’re hearing can tell you about the nature of obstruction. There are a couple of different types of stridor: inspiratory, expiratory, and biphasic. What does the sound we hear tell us about the location of the blockage? Take a look at the figure below, and let’s go back to those principles we just spoke about.

  Ida JB, Thompson DM. Pediatric stridor. Otolaryngol Clin North Am. 2014 Oct;47(5):795-819. doi: 10.1016/j.otc.2014.06.005


Ida JB, Thompson DM. Pediatric stridor. Otolaryngol Clin North Am. 2014 Oct;47(5):795-819. doi: 10.1016/j.otc.2014.06.005


Above the glottis, the hypermobile soft tissues of the airway will collapse with the negative pressure of an inspiratory force, causing inspiratory stridor. The glottis is more limited in its ability to expand or collapse with increased air velocity, thus stridor is likely to be audible in both phases of the respiratory cycle. Below the level of the vocal cords, sounds will depend upon whether they are intra- or extra-thoracic. If intra-thoracic, dynamic collapse will occur on expiration, when there is positive intra-thoracic pressure on the airway. The opposite is true above the thorax. Alright, if you made it to this point, hopefully you have a solid understanding of all those crazy respiratory sounds you might hear in the Peds ED!

Now that we know what we’re listening for, what’s on our differential for our patient who’s struggling to breathe? What could be obstructing our patient’s airway? Here is an overview of some things to keep on your differential, and which kids are susceptible to which causes of obstruction (and includes a section on foreign body aspiration.) If you prefer the lecture format, this podcast may be a great intro to the topic for you. I guess in the UK they use nebulized adrenaline, which here we call racemic epinephrine. Here’s another nice overview of upper airway obstruction differential and management from Don’t Forget the Bubbles .

What is the most common cause of upper airway obstruction in children? I’ll give you a hint - it sounds like this:this .

You guessed it, croup! Remember that steeple sign? Read this from PEMBlog. Read some more on croup here on Don’t Forget the Bubbles. Also ALiEM has a nice pocket card on croup for your smartphone. Remember, it’s important to keep these kids calm, because agitation causes tachypnea -- which increases negative intrathoracic pressure, which further draws air past that already narrow airway, generating “lift” and increasing the obstruction (see the physics explanation above). As common as croup is, beware of recurrent croup,  which should be a red flag to start thinking of other causes, including anatomic abnormalities.

Let’s talk a little about some other important items on the differential: Epiglottitis, peritonsillar abscess, pharyngitis, and angioedemaEM Cases has a great podcast  on this. Start at 1:23. Here’s another great review of differentiating causes of stridor and drooling. Pediatric EM Morsels has a short review of bacterial tracheitis.  Lastly, be wary of this feared complication of upper airway obstruction: negative pressure pulmonary edema.

What about stridor that has been going on for a while? What kinds of things should be on our differential for the little ones? Take a look at this case from Las Vegas EM.

Here’s another diagnosis to keep in mind - Vocal Cord Dysfunction. This can present to the ED as wheezing, stridor, or upper airway obstruction, and often goes misdiagnosed for a prolonged period of time. It is not uncommon for these patients to receive unnecessary treatments including bronchodilators, intubation, and tracheostomy due to failure to properly diagnose the condition.

Let’s put ourselves to the test with this great case from PEM Academy.

Finally, what do you do if this kid with a critical upper airway obstruction fails non-invasive measures? Here’s a good overview of intubating a kid with stridor from Don’t Forget the Bubbles .

That's it -- now you're ready to be the hero in your next pediatric upper airway emergency. 

See you next time in Asynchrony EM!