Category Archives: Complications

How Much Fetal Radiation Exposure In Imaging Studies?

I periodically publish a chart that shows how much radiation exposure our patients get from various trauma imaging studies. For reference, here it is:

Test Dose (mSv) Equivalent background
radiation
Chest x-ray 0.1 10 days
Pelvis x-ray 0.1 10 days
CT head 2 8 months
CT cervical spine 3 1 year
Plain c-spine 0.2 3 weeks
CT chest 7 2 years
CT abdomen/pelvis 10 3 years
CT T&L spine 7 2 years
Plain T&L spine 3 1 year
Millimeter wave
scanner (that hands
in the air TSA thing at
the airport)
0.0001 15 minutes
Scatter from a chest
x-ray in trauma bay
when standing one 
meter from the
patient
0.0002 45 minutes
Scatter from a chest
x-ray in trauma bay
when standing three 
meters from the
patient
0.000022 6 minutes

One of the issues that trauma professionals gnash our teeth about is how much radiation the baby gets when we perform these studies on pregnant women. Well, here is just what you need. Another chart! In order to avoid confusion, I will list effective doses to the fetus in milligrays (mGy), which is how much radiation is deposited in a substance. This is a little confusing, since doses are frequently listed in millisieverts which takes the specific organ and type of radiation into effect. In general, these two units are very similar for x-rays.

A useful rule of thumb is that if the fetal dose is less than 50 mGy during any trimester, the risk of an abortion or fetal malformation is about the same as from other risks to the pregnancy. The American College of Radiology notes that exposures less than 100 mGy are “probably too subtle to be clinically detectable.”

To help in your clinical decision making, I’ve added some extra information to the table regarding fetal exposure:

Test Adult Dose (mSv) Fetal Dose (mGy)
Chest x-ray 0.1 negligible
Pelvis x-ray 0.1 negligible
CT head 2 <1
CT head and C-spine 4 10
CT chest 7 <1
CT abdomen/pelvis 10 25
Pan Scan (CTA chest, abdomen, and pelvis) up to 68 up to 56
CT pulmonary angiogram up to 40 <1

Bottom line: We still have to think hard about how we image pregnant patients! There are some alternatives available to us, including the good old physical exam, conventional x-rays, and ultrasound. MRI is possible, but is a pain in the ass for many reasons. 

CT of the head and cervical spine are fine for both mother and baby, and non-contrast imaging of the torso is within accepted limits of fetal exposure. However, the whole point of the torso scan in CT is to identify critical injuries that may lead to exsanguination like solid organ and aortic injuries. In general, those scans should always be ordered with contrast. 

If clinical suspicion is high, it may be necessary to order these higher-dose studies anyway. If the mother has an unrecognized and potentially fatal injury, the baby will not survive either. There are many, many permutations of injuries and diagnostics. These cases will put your clinical judgment to the test, for sure!

References:

  • Imaging Pregnant and Lactating patients. RadioGraphics 35:6, 1751-1765, 2015.
  • Imaging of the pregnant trauma patient. RadioGraphics 34:3, 748-763,2014.
  • Fetal doses from radio logical examinations. Br J Radiol;72(860): 773–780, 1999.
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Best Of AAST #6: Chronic Disease In Young Trauma Patients

Worldwide, the proportion of older people is growing. With that is an increase in the number of older folks with medical comorbidities like diabetes, hypertension, and obesity. Trauma professionals recognize these conditions’ negative impact on recovery after injury.

But is being young becoming the new old? The trauma group at WakeMed performed a retrospective multi-center study to tease out an estimate of the prevalence of these conditions (plus one more: alcohol/substance use) in injured young(er) people. They studied trauma patients aged 18-40 over three years, examining their charts for evidence of the conditions listed that had been previously undiagnosed.

Here are the factoids:

  • Of the 6,307 patients included, a startling 4,843 (77%) had at least one underlying disease, usually hypertension or obesity
  • Using their multivariate models, they found that age was (barely) a predictor, as were male sex ( 1.43x) and uninsured status (1.6x)
  • Only a quarter of patients had a primary care physician (PCP), but this did not increase the presence of underlying disease
  • Patients found to have these conditions were twice as likely to be referred to a PCP, although this referral rate was still very low (14% vs. 8%)
  • There was no difference in inpatient complications or hospital length of stay

The authors concluded that the undiagnosed disease burden in young adult trauma patients is high. They recommend rigorous screening measures and appropriate referrals.

Bottom line: This is an interesting abstract revealing what we all probably subconsciously recognize. Younger people are not as healthy as they once were. The numbers with obesity, diabetes, hypertension, and substance use are now staggering, with over three-quarters of patients in this convenience study impacted.

Abnormalities are often found on the lab panels drawn during a trauma activation or upon admission. Unfortunately, we do not always act on them since they don’t appear to have anything to do with the trauma.

This abstract makes it clear that the disease burden in this group is high. It is very likely that those affected will probably develop complications at an earlier age and will suffer a decrease in their overall healthspan as they age. The only and most important thing we can do is pay attention and set our patients up with a primary care physician on discharge to begin working on their potential health problems.

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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.

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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How Fast Do Trauma Patients Die?

For years, I’ve taught my residents participating in trauma activations, “Your patient is bleeding to death until proven otherwise.” This concept served as the basis of the [poorly documented] “Golden Hour” and for decades has directed our efforts at getting patients to a center with an immediately available OR as quickly as possible.

Donald Trunkey published the first paper illustrating the trimodal distribution of death in 1983 in Scientific American. A crude graph showed the large spike in early deaths that occurred within this first hour. But the paper was mainly observational and was not based on quantitative data.

Wouldn’t it be nice to know how quickly these injured patients were dying, and of what? The trauma group at the University of Pennsylvania massaged data in the state trauma database, focusing on patients who died of their injuries during the first four hours. They created two variables to more objectively compare times, the TD5 and the TD50. These are the time at which 5% and the time at which 50% (median) had died, respectively.

The Pennsylvania Trauma Outcomes Study database contains a huge amount of data. During the 11 years of the study, a total of 6,547 met the mortality criteria for analysis.

Here are the factoids:

  • The mechanism of injury was about 60% blunt / 40% penetrating, with an average ISS of 33
  • The majority of these patients (85%) were hypotensive before their death, meaning that they were likely bleeding to death on arrival
  • The  overall TD5 was 23 minutes, and the TD50 was 59 minutes
  • These numbers were shorter for penetrating injuries, TD5=19 minutes and TD50=43 minutes
  • Patients who were not hypotensive lived a little longer: TD5=44 minutes and TD50 = 2 hours 18 minutes
  • 77% of patients died in the ED and 19% in the OR. The remainder died in the ICU.

This chart shows the TD5 by mechanism and type of surgery. This represents when after arrival, patients start dying due to their injuries. Penetrating injury plus hypotension kills the fastest at 19 minutes and head injuries the slowest at 1:20.

Bottom line: The authors clearly show how soon seriously injured patients start to die. It’s less than 20 minutes in victims of penetrating injury with early hypotension. And the time between the “just start do die” point (TD5) and the “half are dead” point (TD50) is frighteningly short, just an additional twenty minutes!

There appears to be a bit of a grace period in patients who arrive with a normal blood pressure. Their TD50 is extended out to about two hours. All this means is that they are bleeding more slowly, but it is still killing them.

A good rule of thumb is that ANY hypotensive patient should make you justify why you are NOT ALREADY IN THE OPERATING ROOM! Dawdling in the trauma bay or performing unnecessary scans will push your patient much closer to the point of no return. Look at the huger percentage of patients in this study who died in the ED.

Remember, your patient is bleeding to death in front of your eyes, and the only place you can stop it is the OR!

Reference: Defining the optimal time to the operating room may
salvage early trauma deaths, J Trauma 76(5):1251-1258, 2014.

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Predicting VTE Risk In Children

There’s a lot of debate about if and at what age injured children develop significant risk for venous thromboembolism (VTE). In the adult world, it’s a little more clear cut, and nearly every patient gets some type of prophylactic device or drug. Kids, we’re not so certain about at all.

The Children’s Hospital of Wisconsin tried to tease out these factors to develop and implement a practice guideline for pediatric VTE prophylaxis. They prospectively reviewed over 4000 pediatric patients admitted over a 6 year period.

It looks like the guideline was developed using some or all of this data, then tested using regression models to determine which factors were significant. The guideline was then tweaked and a final model was implemented.

Here are the factoids:

  • 588 of the patients (14%) were admitted to the ICU, and 199 of these were identified as high-risk by the guidelines
  • Median age was 10 (this is always important in these studies)
  • VTE occurred in 4% of the ICU patients, and 10% of the high-risk ones
  • Significant risk factors included presence of central venous catheter, use of inotropes, immobilization, and GCS < 9

Bottom line: This abstract confuses me. How were the guidelines developed? What were they, exactly? And the results seem to pertain to the ICU patients only. What about the non-ICU kids? The abstract just can’t convey enough information to do the study justice. Hopefully, the oral presentation will explain all.

I prefer a very nice analysis done at the Oregon Health Science University in Portland. I wrote about this study earlier this year. The authors developed a very useful calculator that includes most of the risk factors in this model, and a few more. Input the specific risks, and out comes a nice score. The only issue is, what is the score threshold to begin prophylaxis and monitoring? Much more practical (and understandable) than this abstract. Check it out at the link below.

References:

  1. Evaluation of guidelines for injured children at high risk for venous thromboembolism: A prospective observational study. J Trauma Acute Care Surg. 2017 May;82(5):836-844.
  2. A Clinical Tool for the Prediction of Venous Thromboembolism in Pediatric Trauma Patients. JAMA Surg 151(1):50-57, 2016.
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