Category Archives: General

Leukocytosis After Splenic Injury

Any trauma professional who has dealt with spleen injuries knows that the white blood cell (WBC) count rises afterwards. And unfortunately, this elevation can be confusing if the patient is at risk for developing inflammatory or infectious processes that might be monitored using the WBC count.

Is there any rhyme or reason to how high WBCs will rise after injury? What about after splenectomy or IR embolization? An abstract is being presented at the Clinical Congress of the American College of Surgeons next month that examines this phenomenon.

This retrospective study looked at a convenience sample of 75 patients, distributed between patients who had splenic injury that was either not treated, removed (splenectomy), or embolized. Data points were accumulated over 45 days.

Here are the factoids:

  • 20 patients underwent splenectomy, 22 were embolized, and 33 were observed and not otherwise treated
  • Injury severity score was essentially identical in all groups (19)
  • Splenectomy caused the highest WBC counts at the 30 day mark (17.4K)
  • Embolized patients had mildly elevated WBC levels (13.1K) that were just above the normal range at 30 days
  • Observed patients had high normal WBC values (11.0K) after 30 days
  • Values in observed and embolized patients normalized to about 7K after 30 days; splenectomy patient WBC count remained mildly elevated at 14.1K.
  • The authors concluded that embolization does not result in permanent loss of splenic function (bad conclusion, rookie mistake!)

Bottom line: This study is interesting because it gives us a glimpse of the time course of leukocytosis in patients with injured spleens. If you need to follow the WBC for other reasons, if gives a little insight into what might be attributable to the spleen. Splenectomy generally results in a chronically elevated WBC count, which tends to vary in the mid-teens range. Embolization (in this study) transiently elevates the WBC count, but it then drops back to normal.

The big problem with this study (besides it being small) is that it fails to recognize that there are many different shades of embolization. Splenic artery? Superselective? Selective? I suspect that the WBC count in main splenic artery embolization may behave much like splenectomy in terms of leukocytosis. And the conclusion about splenic function being related to WBC count was pulled out of a hat. Don’t believe it.

Related posts:

Reference: 

Leukocytosis after Splenic Injury: A Comparison of Splenectomy, Embolization, and Observation. American College of Surgeons Scientific Forum Abstracts pg S164, 2015.

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Need Some Last Minute CME/CEU?

If you need some last minute trauma-related education credits, consider viewing or attending Trauma Education: The Next Generation. It’s tomorrow, beginning at 8:00 am Central Time at Metro State University in St. Paul.

You can watch for free via Livestream. If you want credit, register first and pay a nominal fee. Or join us live in the audience!

For details, check out the website at www.tetng.org

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Is Applying Or Removing That Cervical Collar Dangerous?

Cervical collars are applied to blunt trauma patients all the time. And most of the time, the neck is fine. It’s just those few patients that have fracture or ligamentous injury that really need it.

I’ve previously written about how good some of the various types of immobilization are at limiting movement (click here). But what happens when you are actually putting them on or taking them off? Could there be dangerous amounts of movement then?

Several orthopaedics departments studied this issue using an electromagnetic motion detector on “fresh, lightly embalmed cadavers” (!) to determine how much movement occurred when applying and removing 1- and 2-piece collars. Specifically, they used an Aspen 2-piece collar, and an Ambu 1-piece. They were able to measure flexion/extension, rotation and lateral bending.

Here are the factoids:

  • There were no significant differences in rotation (2 degrees) and lateral bending (3 degrees) when applying either collar type or removing them (both about 1 degree)
  • There was a significant difference (of 0.8 degrees) in flexion/extension between the two types (2-piece flexed more). Really? 0.8 degrees?
  • Movement was similarly small and not significantly different in either collar when removing them

Bottom line: Movement in any plane is less than 3-4 degrees with either a 1-piece or 2-piece collar. This is probably not clinically significant at all. Just look at my related post below, which showed that once your patient is in the rigid collar, they can still flex (8 degrees), rotate (2 degrees) and move laterally (18 degrees) quite a bit! So be careful when using any collar, but don’t worry about doing damage if you use it correctly.

Related post:

Reference: Motion generated in the unstable cervical spine during the application and removal of cervical immobilization collars. J Trauma 72(6):1609-1613, 2012.

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Delayed Intracranial Hemorrhage In Patients On Anticoagulants

A sizable portion of our population is taking one type of anticoagulant or another. Heck, even golf star Arnold Palmer and comedian Kevin Nealon are on Xarelto! Any trauma professional, and anyone who reads the package insert, knows that there is an increased risk of bleeding if they are injured while taking these drugs, whether it be warfarin or the new, novel anticoagulants.

But does the risk stop soon after injury? That is the presumption at many hospitals that initially treat these patients. They are seen in the ED, examined, scanned, and sent home if nothing is found. Is this a safe practice?

I have personally seen a patient who had an initially clean CT present within 12 hours after ED discharge with a catastrophic bleed and die. Yes, this is anecdotal, but I have talked to other trauma professionals with similar experiences. If this were just a minor complication, no big deal. But they died. Big problem for everyone involved.

So what does the literature say? Unfortunately, it consists of a collection of relatively small studies. Here are the collected factoids that I can glean from them:

  • Most are retrospective, observational studies 
  • Most are from a single hospital, which may miss readmissions to other facilities in the area
  • The delayed bleeding rate is about 0.5% to 1%
  • Some papers recommended discharging patients with a normal head CT and giving them instructions to return if new symptoms develop (this is what happened with my patient; what if they live alone or in a care center where these may not be recognized?!)
  • A few papers did identify patients needing neurosurgical intervention or who died
  • Immediate bleeds were more common with antiplatelet agents, delayed bleeds were more common with warfarin
  • I could find nothing that looked at this problem in patients taking novel anticoagulants like Pradaxa or Xarelto

Bottom line: The literature provides little guidance at this point. A good multi-institutional trial is needed to generate the numbers to tell us what to do. While we get around to this, I recommend that a selective brief observation (12 hrs) protocol be adopted. This protocol recognizes that subclinical bleeding may be present on initial presentation, and that a little more time is needed for it to declare itself.

Here is a link to our protocol. If the initial head CT is negative and the INR is less than 2.5, we will only discharge the patient if all of these criteria are true:

  • Age < 65
  • No skull fx
  • No new focal neurologic deficits
  • No soft tissue injury visible on CT (hematoma, laceration)
  • GCS = 15
  • No persistent vomiting
  • Brief TBI screen passed (Short Blessed Test, link here)

Most do not pass all of these, usually failing the age criterion. They are admitted for observation and neurologic monitoring for 12 hours, at which time the head CT is repeated. If it is still normal, then they can go home.

And although this protocol was designed with warfarin in mind, we apply it to patients taking novel anticoagulants like Pradaxa and Xarelto as well. We’ve had no epic fails yet, but I keep my fingers crossed!

Related posts:

References:

  • Management of minor head injury in patients receiving oral anticoagulant therapy: a prospective study of a 24-hour observation protocol. Ann Emerg Med 59(6):451-455, 2012.
  • Immediate and delayed traumatic intracranial hemorrhage in patients with head trauma and preinjury warfarin or clopidogrel use. Ann Emerg Med 59(6):460-468, 2012.
  • Delayed intracranial hemorrhage after blunt trauma: are patients on preinjury anticoagulants and prescription antiplatelet agents at risk? J Trauma 71(6):1600-1604, 2011.
  • Low risk of late intracranial complications in mild traumatic brain injury patients using oral anticoagulation after an initial normal brain computed tomography scan: education instead of hospitalization. Eur J Neurol 21(7):1021-1025, 2014.
  • Can anticoagulated patients be discharged home safely from the emergency department after minor head injury? J Emerg Med 46(3):410-417, 2014.
  • Patients with blunt head trauma on anticoagulation and antiplatelet medications: can they be safely discharged after a normal initial cranial computed tomography scan? Am Surg 80(6):610-613, 2014.
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