All posts by The Trauma Pro

Philosophy

McSwain’s Laws Of Trauma

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I’m going to be (re)sharing the laws of trauma over the next few posts. I’ve identified a total of eleven over the past 12 years, and I wanted to share them with you.

But first, I’d like to share another trauma surgeon’s observations. Dr. Norman McSwain was an icon in trauma surgery during the early years of my career.

I knew Norm for decades and literally grew up reading about his advancements and accomplishments. Unfortunately, he passed nine years ago. It’s interesting that one never truly appreciates the magnitude of a colleague’s achievements until the person is gone.

Norm was a skilled surgeon and teacher, but his achievements were felt far outside his home in Louisiana. He was an early member of the ACS Committee on Trauma, and was very involved in the development of the Advanced Trauma Life Support and Prehospital Trauma Life Support courses. He is credited with developing the original EMS programs in both Kansas, where he took his first faculty position out of residency, and in New Orleans, his home for the remainder of his life. He spent his career at the Charity Hospital there, weathering multiple political storms over the years, as well as the big one, Hurricane Katrina. He was instrumental in achieving Level I Trauma Center status for its replacement, Interim LSU Hospital.

Norm’s accomplishments are, as many of his contemporaries who have left us, too numerous to count. I certainly won’t try to recount them here. But it was his charm, his love for his charges, and his willingness to teach every trauma professional that will always be remembered.

I’ll leave you with his 18 rules of patient care. They are timeless and will serve you well regardless of your degree and level of medical training.

In my next post, I’ll start explaining the eleven laws that I’ve developed.

Download McSwains Rules of Patient Care

Resuscitation

MTP And The Blood Availability Trap In Trauma Team Activations

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Early availability of blood is a key component in the successful resuscitation of severely injured trauma patients. All trauma centers have implemented massive transfusion protocols (MTP) to ensure rapid delivery of blood products to the trauma bay.

Unfortunately, locating the blood bank in some remote corner of the basement is common practice, as far from the trauma bay as possible. This guarantees a delivery delay once the MTP is activated. To offset this, many centers have implemented policies to make a limited quantity of blood products available in the trauma bay.

This supply can be located in a blood refrigerator located nearby. Or it may be a practice of calling for emergency release blood if the trauma professionals believe it might be necessary. Some trauma centers have codified this so that highest-level activations automatically have a cooler of blood products delivered, hopefully before patient arrival.

However, I have observed while visiting numerous centers that this often causes an unintended consequence. It can actually slow MTP activation!

How can that be, you say? It’s simple. Critically injured patients result in an intense and highly charged trauma activation. The surgeon is concentrating on keeping the patient alive and orders the emergency release blood to be hung. The resuscitation continues. “Hang another unit.” And so on.

Eventually, the temporary supply runs out. Then everybody looks at each other and does a facepalm. Nobody thought to activate the MTP!

How can this be avoided? The key is to do everything possible to activate it from the very start. Here are some tips:

  • Use an objective scoring system to trigger MTP. The two most common ones are the ABC score and the Shock Index. Both are easy to calculate, and can frequently be used based on the prehospital report. This means the MTP can be activated before the patient even arrives.
  • If you open the blood refrigerator or touch the emergency release blood, activate the MTP. This will give you two to four units to buy time for the first MTP cooler to arrive.
  • Empower everyone in the trauma bay to speak up. Make sure everyone knows the rules listed above, and encourage them to speak up if they see that any of them are met. “Team leader, should we activate the MTP?”
  • Don’t be shy! If you only transfuse one unit of refrigerator blood and stop, no harm, no foul. The unopened MTP cooler can be sent back to the blood bank with no risk of waste.

Bottom line: Don’t get suckered into forgetting to activate the MTP just because it looks like you have blood available. Automate the process so you never run out again.

General

The Peri-Mortem C-Section

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The perimortem C-section (PMCS) is a heroic procedure designed to salvage a viable fetus from a moribund mother. Interestingly, in some mothers, delivery of the fetus results in return of spontaneous circulation.

The traditional teaching is that PMCS should be started within 4-5 minutes of the mother’s circulatory arrest. The longer it is delayed, the (much) lower the likelihood that the fetus will survive.

The reality is that it takes several minutes to prepare for this procedure because it is done so infrequently in most trauma centers. Recent literature suggests the following management for pregnant patients in blunt traumatic arrest (BTA):

  • Cover the usual BTA bases, including securing the airway, obtaining access and rapidly infusing crystalloid, decompressing both sides of the chest, and assessing for an unstable pelvis
  • Assess for fetal viability. The fundus must measure at least 23 cm.
  • Assess for a shockable vs non-shockable rhythm. If shockable, do two cycles of CPR before beginning the PMCS. If non-shockable, move straight to this procedure.

Bottom line: Any time you receive a pregnant patient in blunt arrest, have someone open the C-section pack while you assess and try to improve the mother’s viability. As soon as you complete the three tasks above, start the procedure! You don’t need to wait 4 minutes! And by the way, this is usually a procedure for surgeons only. They have the speed and skills to get to the right organs quickly. If unavailable, do what you need to do, but recognize that the outcome may be even worse than it usually is.

Extremity

Vascular And Nerve Injury After Knee Dislocation

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There’s a lot of dogma in trauma care, as well as in the field of medicine generally. The knee dislocation dogma is that the incidence of vascular injury is high (around 50%) with posterior dislocation and somewhat lower with non-posterior dislocation.

At least, that’s what I learned way back when. After recently finding myself spouting off those numbers, I wondered if it was really true. Our diagnostic imaging and vascular care have increased considerably in the last few decades, so I decided to check it out.

This lovely image from EMDocs.net shows the various dislocation types. It also gives you an idea of why an associated vascular or nervous injury is so common.

(The nomenclature of the dislocation is based on the direction in which the tibia and fibula move with respect to the femur.)

The orthopedic surgery group at UCLA performed a meta-analysis of the literature on knee dislocation complications. They identified seven papers describing the injuries of 862 patients.

Here are the factoids:

  • The overall incidence of vascular injury with knee dislocation was 18%, and nerve injury was 25%
  • The incidence of vascular injury with the various types of dislocation was:
    • Posterior dislocation: 25%
    • Anterior dislocation: 19%
    • Lateral dislocation: 18%
    • Medial dislocation: 7%
    • Rotatory: 14%
  • Disruption of both cruciate ligaments as well as the lateral or medial collateral ligament had a very high incidence of vascular injury (32% and 26% respectively)
  • About 80% underwent surgical repair of the popliteal artery, but the amputation rate was 12%(!)

Bottom line: The old dogma regarding vascular injury after knee dislocation may be slightly exaggerated. However, it is still common after knee dislocation and can lead to devastating complications.

If your patient tells you that they felt a popping sensation in their knee or have a mechanism consistent with knee dislocation (e.g., pedestrian struck), be very suspicious for this injury. A thorough yet gentle exam, including good neurologic and vascular exams, should be performed. Calculating the Arterial Pressure Index (API) may be helpful but will not keep you from obtaining imaging studies. Multi-plane knee imaging is required, and a CT angiogram/runoff study should be performed to exclude a vascular problem.

Reference: Vascular and Nerve Injury After Knee Dislocation: A Systematic Review. Clin Orthop Relat Res 472(9):2621-9, 2014.

Head

What Is: A Hinge Fracture Of The Skull?

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Although very few things in medicine are new, I love it when I learn about something I’ve never heard of before. Recently, while reading an autopsy report, I ran across the term “hinge fracture of the skull.” What? Maybe if I were a neurosurgeon, I would have recognized the term. This was the perfect excuse to hit the books (or, more accurately, the internet).

A hinge fracture crosses the skull base transversely and involves the temporal and sphenoid bones. Here are diagrams of two common transsphenoidal fracture patterns, courtesy of radiopaedia.org. The red and green lines can be considered transverse (hinge) fractures.

Why the hinge analogy? Since the fracture extends entirely across the skull base, it splits the skull in two. In theory, the bones could hinge around this line, but the reality is that it usually doesn’t. It’s just a memorable name.

It takes a significant amount of force to fracture the skull like this. Although any major blunt force could do this, there is a higher association with motorcycle crashes. I found an interesting paper (cited below) that showed that if a rider’s face smashes into the back of the cycle driver, the force delivered to the rider’s mandible can cause this fracture pattern. It can also occur in falls from heights and direct trauma to the head (e.g., baseball bat).

Many patients with this injury do not survive very long due to severe CNS injury or other significant blunt-force injuries. Those who do may demonstrate these findings on exam:

  • Bruising typical of a skull base fracture. This includes Battle’s sign (bruising behind the ears over the mastoid process) and raccoon eyes (bruising around the eyes).
  • Evidence of severe TBI. Low GCS is expected due to significant force to the head.
  • Cranial nerve deficits. The path of the fracture can vary considerably and may involve one or more cranial nerves. Patients may manifest hearing loss, double vision (if awake), or facial paralysis.
  • CSF leak. Many basilar skull fractures result in otorrhea or rhinorrhea, and this one is no exception.

If your patient survives the trauma bay, diagnosis is made by CT scan. Given the location of this fracture, CT angiography should be added if a hinge fracture is identified. There is a higher probability of blunt carotid and vertebral arterial injury with this diagnosis.

Treatment of this fracture complex is beyond the scope of this post. Consult your friendly neighborhood neurosurgeon. Only they can appreciate the nuances and reconstructive needs of this injury.

Reference: Mechanism of transverse fracture of the skull base caused by blunt force to the mandible. Legal Medicine,
Volume 54, 101996, 2022.