All posts by TheTraumaPro

Flash Pulmonary Edema After Chest Tube Insertion

You are seeing a young man in the emergency department who gives a history of falling two days ago. He experienced chest pain at the time which has persisted, but he did not immediately seek medical care. He has noticed that he now gets winded when walking quickly or climbing stairs, and describes pleuritic chest pain.

He presents to your emergency room and on exam has a bruise over his left lateral chest wall. Subcutaneous emphysema is present, and breath sounds are absent. Chest x-ray shows a complete pneumothorax on the left.

You carefully prepare and insert a chest tube in the usual position. A significant rush of air occurs, which tapers off over 15 seconds. Here is the followup image:

About 10 minutes later you are called to his room because he is complaining of dyspnea and his oxygen saturation has decreased to 86%. Breath sounds are somewhat decreased and the tube appears to be functioning properly. You immediately obtain another chest x-ray:

What just happened? This is a classic case of unilateral “flash” pulmonary edema after draining the chest cavity. This phenomenon was first described in 1853 in a patient who had just undergone thoracentesis. It is very uncommon, but seems to occur after rapid drainage of air or fluid from the chest cavity.

Here are some interesting factoids from case reports:

  • It occurs more often in young men
  • It is most common when draining large hemo- or pneumothoraces
  • Rapid drainage seems to increase the incidence
  • It is likely due to increased pulmonary capillary permeability from inflammatory mediators or changes in surfactant
  • Symptoms typically develop within an hour after drainage

What should you do? First, if you are draining a large collection of air or blood, do it slowly. Clamp the back end of the chest tube prior to insertion (you should always do this if you value your shoes) and use it to meter the amount of fluid or air released. I typically let out about 300cc of fluid, then wait a minute and repeat until all the blood has been drained. For air, vent it for 10 seconds, then wait a minute and repeat.

In patients at high risk for this condition, apply pulse oximetry and follow for about an hour. If they still look and feel great, nothing more need be done.


  • Fulminant Unilateral Pulmonary Edema After Insertion of a Chest Tube. Dtsch Arztebl Int 105(50):878-881, 2008.
  • Reexpansion pulmonary edema after chest drainage for pneumothorax: A case report and literature overview. Respir Med Case Rep 14:10-12, 2015.
  • Re-expansion pulmonary edema following thoracentesis, Can Med Assn J 182(18):2000-2002, 2010.

Blame The Trauma Surgeon?

I just finished reading a recent paper published in the Journal of Trauma that purports to examine individual surgeon outcomes after trauma laparotomy. The paper was presented at AAST last year, and is authored by the esteemed trauma group at the University of Alabama at Birmingham. It was also recently discussed in the trauma literature review series that is emailed to members of EAST regularly.

Everyone seems to be giving this paper a pass. I won’t be so easy on it. Let me provide some detail.

The authors observe that the mortality in patients presenting in shock that require emergent laparotomy averages more than 40%, and hasn’t changed significantly in at least 20 years. They also note that this mortality varies widely from 11-46%, and therefore “significant differences must exist at the level of the individual surgeon.” They go on to point out that damage control usage varies between individuals and trauma centers which could lead to the same conclusion.

So the authors designed a retrospective cohort study of results from their hospital to try to look at the impact of individual surgeon performance on survival.

Here are the factoids:

  • Over the 15 month study period, there were over 7,000 trauma activations and 252 emergent laparotomy for hemorrhage control
  • There were 13 different trauma surgeons and the number of laparotomies for each ranged from 7 to 31, with a median of 15
  • There were no differences in [crude, in my opinion] patient demographics, hemodynamics, or lab values preop
  • “Significant” differences in management and outcomes between surgeons were noted:
    • Median total OR time was significantly different, ranging from 120-197 minutes
    • Median operation time was also different, from 75-151 minutes across the cohort of surgeons
    • Some of the surgeons had a higher proportion of patients with ED LOS < 60 minutes and OR time < 120 minutes
    • Resuscitation with red cells and plasma varied “significantly” across the surgeons
  • Mortality rates “varied significantly” across surgeons at all time points (24-hour, and hospital stay)
  • There were no mortality differences based on surgeons’ volume of cases, age, or experience level

The authors acknowledged several limitations, included the study’s retrospective and single-center nature, the limited number of patients, and its limited scope. Yet despite this, they concluded that the study “suggests that differences between individual surgeons appear to affect patient care.” They urge surgeons to openly and honestly evaluated ourselves. And of course, they recommend a large, prospective, multicenter study to further develop this idea.

Bottom line: This study is an example of a good idea gone astray. Although the authors tried to find a way to stratify patient injury (using ISS and individual AIS scores and presence of specific injuries) and intervention times (time in ED, time to OR, time in OR, op time), these variables just don’t cut it. They are just too crude. The ability to meaningfully compare these number across surgeons is also severely limited by low patient numbers. 

The authors found fancy statistical ways to demonstrate a significant difference. But upon closer inspection, many of these differences are not meaningful clinically. Here are some examples:

  • Intraoperative FFP ranged from 0-7 units between surgeons, with a p value of 0.03
  • Postoperative FFP ranged from 0-7 units, with a p value of 0.01
  • Intraoperative RBC usage was 0-6 units with the exception of one surgeon who used 15 in a case, resulting in a p value of 0.04

The claim that mortality rates varied significantly is difficult to understand. Overall p values were > 0.05, but they singled out one surgeon who had a significant difference from the rest in 22 of 25 mortality parameters listed. This surgeon also had the second highest patient volume, at 25.

The authors are claiming that they are able to detect significant variations in surgeon performance which impacts timing, resuscitation, and mortality. I don’t buy it! They believe that they are able to accurately standardize these patients using simple demographic and performance variables. Unfortunately, the variables selected are far too crude to accurately describe what is wrong inside the patient and what the surgeon will have to do to fix it.

Think about your last 10 trauma laparotomies where your patient was truly bleeding to death. How similar were they? Is there no difference between a patient with a mesenteric laceration with bleeding, an injury near the confluence of the superior mesenteric vessels, and a right hepatic vein injury? Of course there is. And this will definitely affect the parameters measured here and crude outcomes. Then add some unfavorable patient variables like obesity or previous laparotomy.

In my estimation, this paper completely misses the point because it’s not possible to retrospectively categorize all the possible variables impacting “surgeon performance.” This is particularly true of the patient variables that could not possibly be captured. The only way to do this right is to analyze each case as prospectively as possible, as close to the time of the procedure and as honestly as possible. And this is exactly what a good trauma M&M process does!

So forget the strained attempts at achieving statistical significance. Individual surgeon performance and variability will come to light at a proper morbidity and mortality conference, and should be evened out using the peer review and mentoring process. It’s not time to start blaming the surgeon!

Reference: It is time to look in the mirror: Individual surgeon outcomes after emergent trauma laparotomy. J Trauma 92(5):769-780, 2022.

By Request: Submental Intubation – The Video!

In my last post, I dusted off an old post that described a novel technique for providing a secure yet short-term airway tailored to patients who can’t have a tube in their mouth or nose. Patients undergoing multiple facial fracture repair are probably the best candidates for this procedure.

A picture may be worth a thousand words, but a video is even better. Please note that it is explicit and shows the blow by blow surgical procedure. Of note, it is a quick and relatively simple advanced airway technique. Note the cool music!

Related post:

By Request Again!: Submental Intubation

I keep getting requests regarding this technique, so I’m reposting  this updated article today, and a video of the technique next week.

Here’s one of the weirder procedures I’ve seen in some time. Imagine that you need a definitive airway, but you can’t use the face for some reason (mouth or nose). The usual choice would be a tracheostomy, right? But what if you only need it for a few days? Typically, once placed, trachs must be kept for a few weeks before decannulation is safe.

Enter submental intubation. This technique involves passing an endotracheal tube through the anterior floor of the mouth, and then down the airway. This leaves the facial bones, mandible, and skull base untouched.



The technique is straightforward:

  • After initially intubating the patient  orotracheally, a 1.5cm incision is created just off the midline in the submental area under the chin.
  • Using a hemostat, all layers are penetrated, entering the oropharynx just lateral to the tongue.
  • A 1.5cm incision is then made at the puncture site, parallel to the gum line of the lower teeth.
  • The ET tube is removed from the ventilator circuit, and the connector at the proximal end of the tube is removed.
  • The hemostat is placed through the chin incision again. The proximal end of the ET tube is curled into the oropharynx and grasped with the hemostat, then pulled out through the skin under the chin, leaving the distal (balloon) end in the trachea.
  • The connector is reinserted, and the tube is then hooked up to the anesthesia circuit again.
  • The tube is then secured using a stitch under the chin.

After a final position check, the surgical procedure can commence. Cool!


There are a number of variations on this technique, so you may encounter slightly different descriptions. The tube can be pulled at the end of the procedure, or left for a few days to ensure safe extubation, if needed.


A small series of 10 patients undergoing this technique was reviewed, and there were no short or long term problems. Scarring under the chin was acceptable, and was probably less noticeable than a trach scar.

Bottom line: This is a unique and creative method for intubating patients with very short-term airway needs while their facial fractures are being fixed. Brilliant idea!

Tomorrow: Submental intubation – the video!

Reference: Submental intubation in patients with panfacial fractures: a prospective study. Indian J Anaesth 55(3):299-304, 2011.

Photo source: internet

The Impact Of NSAIDs On Fracture Healing

In my last post I discussed some of the basic effects of NSAIDs on bone healing. Now let’s see if theory applies to practice.

In 2003, several papers brought to light possible interactions between these drugs and fracture healing. Specifically, there were questions about these drugs interfering with the healing process and of increasing the number of delayed unions or nonunions. But once again, how convincing were these papers, really?

It would seem to make sense that NSAIDs could interfere with bone healing. The healing process relies heavily on the regulation of osteoblast and osteoclast function, which itself is regulated by prostaglandins. Since prostaglandins are synthesized by the COX enzymes, COX inhibitors like the NSAIDs should have the potential to impair this process. Indeed, animal studies in rats and rabbits seem to bear this out.

But as we have seen before, good animal studies don’t always translate well into human experience. Although a study from 2005 suggested that NSAID administration in older patients within 90 days of injury had a higher incidence of fracture nonunion, the study design was not a very good one. It was equally likely that patients who required these drugs in this age group may have been at higher risk for nonunion in the first place.

A meta-analysis of human studies was performed in 2011. Out of 558 potential studies, only 5 met criteria review. (This is yet another reminder of the sheer amount of sub-par research out there.) The authors found that short-term use (< 14 days) of normal dose NSAIDS was not associated with non-union. High doses of ketorolac (> 120mg/day) and diclofenac sodium (> 300mg total) did have an association. But remember, this does not show causation. There are many other factors that can impede healing (smoking, diabetes, etc).

A study from 2016 examined the effect of ketorolac administration on fracture healing in patients undergoing repairs of femoral and tibial fractures. It did not find an association between non-union and ketorolac, but did find one with smoking. Unfortunately, the study was small (85 patients given ketorolac, 243 controls without it). It probably does not have the statistical power to detect any difference with the NSAID. A power analysis was not provided in the methods section.

Bottom line: Once again, the animal data is clear and the human data less so. Although there are theoretical concerns about NSAID use and fracture healing, there is still not enough solid risk:benefit information to abandon short-term NSAID use in patients who really need them. NSAIDs can and should be prescribed in patients with short-term needs and simple fractures, and consider COX-1 specific drugs like ketorolac while your patient is in the hospital. And we do have some evidence that high-dose NSAIDs may have some impact, so stick to the usual doses for just as long as they are needed for pain management.


  1. Effects of nonsteroidal anti-inflammatory drugs on bone formation and soft-tissue healing. J AM Acad Orthop Surg 12:139-43, 2004.
  2. Effect of COX-2 on fracture-healing in the rat femur. J Bone Joint Surg Am 86:116-123, 2004.
  3. Effects of perioperative anti-inflammatory and immunomodulating therapy on surgical wound healing. Pharmacotherapy 25:1566-1591, 2005.
  4. Pharmacological agents and impairment of fracture healing: what is the evidence? Injury 39:384-394, 2008.
  5. High dose nonsteroidal anti-inflammatory drugs compromise spinal fusion. Can J Anaesth 52:506-512, 2005.
  6. Nonsteroidal Anti-Inflammatory Drugs and Bone-Healing: A Systematic Review of Research Quality. JBJS Rev 4(3), 2016.
  7. High-dose ketorolac affects adult spinal fusion. Spine 36(7):E461-E468, 2011.
  8. Ketorolac administered in the recovery room for acute pain management does not affect healing rates of femoral and tibial fractures. J Orthop Trauma 30(9):479-482, 2016.