All posts by The Trauma Pro

Technique, Video

By Request: Submental Intubation – The Video!

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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!

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Technique

By Request Again!: Submental Intubation

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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.

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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.

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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

Complications

The Impact Of NSAIDs On Fracture Healing

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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.

References:

  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.
Complications

NSAIDs And Bone Healing: How Do They Impact It?

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The arguments about whether NSAID administration has any effect on bone healing continues to be argued by our orthopedic and spine surgery colleagues. In the early days of research in this area (about 20 years ago) there were concerns in animal models that there might be a problem. Apparently lots of rats and bunnies were suffering from fractures in those days.

But physiologically, how could NSAIDS do this? Here’s a simplified diagram of how the bone healing process works.

First, an acute injury occurs and macrophages and other cells move into the area to start the inflammatory process. COX-2 receptors are highly expressed on these cells, resulting in an increase in prostaglandin E2 (PGE2) production.

PGE2 then promotes proliferation of stem cells that differentiate into osteoblasts, which in turn begin forming bone to repair the injury.  In theory, if PGE2 is reduced in the healing area there is the possibility that bone formation may be impaired, leading to non- or malunion or refracturing.

Administration of NSAIDs can block COX-1 and COX-2 receptors throughout the body. This serves to decrease prostaglandin production and hence reduces inflammation and pain. Doesn’t it follow that giving these drugs should be bad for bone formation in patients with fractures?

Not so fast! There are a number problems with this argument. First, not all NSAIDs are created alike. Here is a chart that shows where the primary focus of COX inhibition is with some common NSAIDs.

Note how the common over-the-counter drugs affect both COX-1 and COX-2, yet there are some that are more selective. So the choice of drug may be relevant.

And we can’t assume that an in vitro effect in a Petri dish of cells actually carries over into the in vivo world. Many researchers rely initially on animal models to study drug effects in vivo. Predictions based on studies of rats and bunnies frequently do not pan out in humans.

We are left with only a theory based on an understanding of the basic mechanism of bone healing. Tune in to my next post where I discuss the research that’s been done in this field and whether it actually translates into human bone healing or not.

Guidelines

Massive Transfusion: What Ratios Are People Using?

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Back in the old days (which I remember fondly), we didn’t pay too much attention to the ratio of blood to plasma. We gave a bunch of bags of red cells, then at some point we remembered that we should give some plasma. And platelets? We were lucky to give any! And to top it all off, we gave LOTS of crystalloid. Turns out this was not exactly the best practice.

But things have changed. Some good research has shown us that a nice mix of blood component products is good and too much crystalloid is bad. But what exactly is the ideal mix of blood products? And what is everybody else doing?

What are all the other trauma centers doing? An interesting medley of anesthesia and pathology groups from the University of Chicago, a Dallas-based anesthesia group, and a blood center in my home base of St. Paul, conducted a survey of academic medical centers back in 2016. They wanted to find out how many actually had a MTP and to scrutinize the details.

They constructed a SurveyMonkey survey and sent it to hospitals with accredited pathology residencies across the US. There were 32 questions in the survey, which asked for a lot of detail. As you can probably personally attest, the longer and more complicated the survey, the less likely you are to respond. That certainly happened here. Of 107 surveys sent out, it took a lot of nagging (initial email plus two nags) to get a total of 56 back.

Here are the factoids:

  • Most were larger hospitals, with 74% having 500 or more beds
  • All had massive transfusion protocols
  • Trauma center level: Level I (77%), Level II (4%), Level III (4%), Level IV (2%), no level (14%)
  • Nearly all (98%) used a fixed ratio MTP; very few used any lab-directed (e.g. TEG/ROTEM) resuscitation
  • Target RBC:plasma ratio: 1:1 (70%), 1.5:1 (9%), 2:1 (9%), other (9%)
  • Only 58% had the same RBC:plasma ratio in each MTP cooler
  • More than 86% had thawed plasma available (remember, these were generally large academic centers)
  • Half stored uncrossmatched type O PRBCs outside the blood bank, usually in the ED; only 1 stored thawed plasma in the ED
  • A total of 41% had more than one MTP (trauma, OB, GI, etc.)
  • 84% had some type of formal review process once the MTP was complete
  • About 68% had modified their MTP since the original implementation. Some increased or decreased ratios, expanded MTP to non-trauma services, decreased the number of units in each pack, changed to group A plasma from AB, or switched from ratio to TEG/ROTEM or back.

Bottom line: This is an intriguing snapshot of MTP practices around the country that is about six years old. Also remember, this is a somewhat skewed dataset. The survey was directed toward hospitals with academic pathology programs, not trauma centers. However, there is enough overlap that the results are probably generalizable. 

Most centers are (were) using MTP packs containing six units of PRBCs, and were attempting to achieve a fixed 1:1 ratio. Half of hospitals had the same number of units in each cooler, half varied them by cooler number. Nearly half had multiple flavors of MTP for different specialties. Very few used TEG/ROTEM during the initial phased of MTP. Most modified their MTP over time.

Unfortunately, I’ve not seen a similar survey repeated recently. I’m certain that practices have changed over time as our understanding of balanced resuscitation continues to advance. 

Finally, I’ve written quite a lot on most of these issues. See the links to my “MTP Week” series below.

Reference: Massive Transfusion Protocols: A Survey of Academic
Medical Centers in the United States. Anesth & Analg 124(1):277-281, 2017.

MTP week series: