Tag Archives: TBI

Abstracts

EAST 2018 #1: Plasma Over-Resuscitation And Mortality In Pediatric TBI

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The first EAST abstract I will discuss is the very first to be presented at the annual meeting. This is a prospective, observational studied that was carried out at the University of Pittsburgh. It looked at the association between repeated rapid thromboelastography (rTEG) results in pediatric patients and their death and disability after plasma administration. They specifically looked at the degree of fibrinolysis 30 minutes after maximum clot amplitude and tried to correlate this to mortality.

For those of you who need a refresher on TEG, the funny sunfish shape above shows the clot amplitude as it increases from nothing at the end of R, hits its maximum at TMA, then begins to lyse. The percent that has lysed at 30 mins (LY30%) gives an indication if the clot is dissolving too quickly (LY30% > 3%) or too slowly (LY30% < 0.8%).

The authors selected pediatric patients with TBI and performed an initial rTEG, then one every day afterward. They looked at correlations with transfusion of blood, plasma, and platelets.

Here are the factoids:

  • A total of 101 patients under age 18 were studied, with a median age of 8, median ISS of 25, and 47% with severe TBI (head AIS > 3)
  • Overall mortality was 16%, with 45% having discharge disability
  • On initial analysis, it appeared that transfusion of any product impeded fibrinolysis, but when controlling for the head injury, only plasma infusion correlated with this
  • Increasing plasma infusion was associated with increasing shutdown of fibrinolysis
  • The combination of severe TBI and plasma transfusion showed sustained fibrinolysis shutdown, and was associated with 75% mortality and 100% disability in the remaining survivors
  • The authors conclude that transfusing plasma in pediatric patients with severe TBI may lead to poor outcomes, and that TEG should be used for guidance rather than INR values.

Bottom line: There is a lot that is not explained well in this abstract. It looks like an attempt at justification for using TEG in place of chasing INR in pediatric TBI patients. This may be a legitimate thing, but I can’t really come to any conclusions based on what has been printed in this abstract so far.

Here are some questions for the authors to consider before their presentation:

  • There seem to be a lot of typos, especially with < and > signs in the methods.
  • Disability is a vague term. What was it exactly? Was it related to TBI or the other injuries as well?
  • These children also appear to have had other injuries, otherwise why would they need what looks like massive transfusion activation? Why did they need so much blood? Could that be the reason for their fibrinolysis changes and poor outcomes?
  • I can see the value of the initial rTEG, and maybe one the next day. But why daily? What did you learn from the extra days of measurements? Would a pre- and post-resuscitation pair have been sufficient?
  • Plasma is the focus of this abstract, but it does not describe how much plasma was given, or whether there was any departure from the usual acceptable ratios of PRBC to plasma administration.
  • Big picture questions: Most importantly, why would you think that poor outcomes, which are the focus of this paper, are related to plasma administration? Why haven’t we noticed this correlation before? And how does daily TEG testing help you identify and/or avoid this? What questions raised here are you going to pursue?

Reference: EAST 2018 Podium paper #1.

Head

Is Decompressive Craniectomy Any Better Than Craniotomy?

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Severe TBI consists of a primary injury to the brain, followed by swelling, vascular, and ischemic problems which may cause a secondary injury. Much of the critical care management of this injury involves avoiding or ameliorating secondary injury. This is typically accomplished via medical means first, and through surgical procedures when medical management is insufficient.

Two types of surgical decompression are currently practiced: craniotomy and evacuation of blood/clot, and decompressive craniectomy with removal of a bone flap. The latter can be performed prophylactically before severe swelling occurs, or therapeutically as a damage control procedure when ICP is refractory to all other measures.

There has been a decades-old debate as to whether craniectomy, which is a major undertaking with months of skull/bone flap management, is actually worthwhile. Most studies have examined the utility of damage control craniectomy for refractory ICP. The results have not really been convincing one way or the other.

But what about prophylactic decompressive craniectomy (DC) to avoid future ICP problems while the patient is in the ICU? The surgical group at the University of Arizona at Tucson performed a five year retrospective review of their experience. Using propensity score matching, they identified 99 severe TBI patients who underwent DC (33) or craniotomy only (CO, 66). A power analysis showed that this sample size should be sufficient to demonstrate a significant difference.

Here are the factoids:

  • Both groups were similar with respect to age, GCS, ISS, AIS-head, and type of bleed
  • 26% died and 63% were discharged to rehab or skilled nursing facility
  • When comparing DC to CO groups, there were no differences in mortality, discharge to skilled nursing facility, discharge GCS or Glasgow Outcome Scale
  • There were more complications in the DC group, including shunt insertion for hydrocephalus (9% vs 0%), and reoperation (12% vs 2%)
  • Rates of wound infection and ventriculitis were the same for both groups (0-3%)

Bottom line: Although the study is small, it supposedly had enough patients for identification of significant differences. And basically, it didn’t show a positive difference for prophylactic decompressive craniectomy. There is certainly some opportunity for selection bias by the neurosurgeons that cannot be controlled for by this retrospective design. But it is yet another piece of the decompressive craniectomy puzzle. 

Overall, the literature support for either prophylactic or damage control craniectomy is not very strong. If it were, we would have identified some real benefits by now. What we don’t know is if there are specific subgroups of severe TBI patients who might benefit from it. So if your center is not involved in a project to study this, you should probably ask your neurosurgeons to base their practice only on what we know about this procedure to date. 

Head

What Happens To Your Average Subarachnoid Hemorrhage?

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Management of traumatic brain injury (TBI) is a common issue faced by trauma professionals. And isolated subarachnoid hemorrhage (SAH) is one of the more common presentations. In many centers, this diagnosis frequently results in admission to the hospital, neurosurgical consultation, and repeat imaging.

Is this too much care? We adopted a practice guideline nearly two years ago based on our own clinical experience that eliminated the last two. Patients were still admitted for neurologic monitoring for 16 hours. But is even this too much?

What we really need is a better understanding of the natural history of uncomplicated traumatic SAH. Well, a study from Sunnybrook and the University of Toronto does just that. They performed a 17 year meta-analysis of the literature on isolated SAH with mild TBI (GCS 13-15). They pared their initial literature search of nearly 2900 studies down to the usual few, 13 in this case. All but one were retrospective, of course, and they had the usual design flaws.

Here are the factoids:

  • How many patients eventually needed neurosurgical intervention?  0 (Well, almost zero. It was 0.0017%, to be exact.)
  • How many had progression of the SAH? About 6%
  • How many had neurologic deterioration? 0.75%, which included two  patients with increased headache and one with some confusion. Two developed intraparenchymal hemorrhage (one was on anticoagulants)
  • How many died? Only 1 died from neurologic causes, and that patient was anticoagulated at the time of injury.

Bottom line: It looks like we may be overdoing it for patients with isolated SAH and mild TBI. The natural history seems to be fairly benign, unless the patient is taking anticoagulants. The type of drug was not specified, so warfarin, aspirin, clopidogrel, and the newer anticoagulants should all be included.

Perhaps it’s time to update the our practice guidelines further. It looks like most of these simple, isolated SAH can be evaluated and released. However, if the GCS is 13 or 14, they should still be admitted for monitoring for a short period. And if on anticoagulants, admission with a repeat CT is in order.

Related posts:

Reference: The clinical significance of isolated traumatic subarachnoid hemorrhage in mild traumatic brain injury: A meta-analysis. J Trauma , published ahead of print, July 8 2017.

CNS

Could There Be A Simpler GCS?

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The Glasgow Coma Scale (GCS) has been around forever. Or really, for about 45 years. It was actually developed in the early 1970s and known as the Coma Index. It was further refined into the GCS, when 1 was selected as the minimum component score. Ever since, it has been used as a common language among clinicians to communicate gross neurologic function and trends.

But it is still somewhat complicated. Oh no it’s not, you say? Then why do so many trauma resuscitation rooms have it posted on the wall? There are three components, each with a different number of possible values. And frankly, some are harder to remember than others. Decerebrate vs decorticate, right?

So what if someone told you that a single GCS component works just about as well as the whole bunch? Researchers have been piecing this together for years, focusing on the motor component of GCS (mGCS). There are two flavors of simplified score: mGCS and Simplified Motor Score (SMS). The mGCS is just what it sounds like: the full motor component of GCS, ranging from 1-6. The SMS is further simplified from the mGCS: mGCS of 1-4 tranlsates to SMS 0, mGCS 5 = SMS 1, and mGCS 6 = SMS 2. In my opinion, this is actually more complicated because you have to remember not only the 6 mGCS levels, but also the cutoffs to convert it to SMS.

Finally, a group from Oregon Health Sciences University in Portland performed a nice meta-analysis of the best individual studies.

Here are the factoids:

  • Only papers that compared total GCS (tGCS) to mGCS or SMS were included, and only if they analyzed a receiving operator characteristic curve. The statistics appeared sound.
  • tGCS was very slightly better than either mGCS or SMS at predicting:
    • in-hospital mortality
    • neurosurgical intervention
    • emergency intubation
    • severe TBI

Bottom line: Overall, the total GCS is slightly (just a few percent) better at doing the things listed above, compared to the motor score alone or the “simplified” (really?) motor score. Is this clinically significant in the field? Probably not. And its mere simplicity makes it appealing. 

However, there is one major problem to adopting the mGCS for use outside the hospital. Inertia. As I mentioned, we have been using the full GCS score for almost 50 years. Pretty much every trauma professional is familiar with the GCS or knows where to look up the details. But I suspect that those clincicians who assume care of the patient once in the hospital, and especially the intensive care unit (neurosurgeons) will never allow the use of an abbreviated scale. Good idea, but sorry, it won’t catch on in the real world.

Head

Do We Really Need To Consult Neurosurgery For Mild TBI?

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We consult our neurosurgeons too often. Think back on all the head injured patients you have admitted and placed a neurosurgical consult. How many times did they recommend something new or different, or take them to surgery? Not very often, I would guess.

This is becoming a hot topic. Check out the references below to read about a few other studies that have taken a similar approach.

The trauma group at Scripps Mercy in San Diego retrospectively reviewed their admissions to determine how often patients with mild TBI (GCS > 13) and some degree  intracranial hemorrhage required neurosurgical intervention, even if they were intoxicated or taking anti-platelet or anticoagulant drugs. A total of 500 patients were studied over a 28 month period.

Here are the factoids:

  • 49 (10%) of patients required some sort of neurosurgical intervention (41 craniotomy/craniectomy, 8 ICP monitors)
  • 93% of patients had neurosurgical consultation, and made additional recommendations in only 10 (2%),none of which changed management
  • There was no clinical difference in GCS between those who received an intervention and those who did not
  • Epidural and subdural hematomas were significant predictors of neurosurgical intervention
  • Intoxication or use of anti-platelet or anticoagulant drugs was not associated with intervention. These were present in 30% of all patients!
  • Unsurprisingly, ICU and hospital length of stay were longer in patient who underwent an intervention

Bottom line: As I said, this seems to be a hot research topic. And in this study, the numbers are getting larger and the criteria more inclusive (alcohol and anticoagulants allowed).

Neurosurgeons play a very important role in patients with more moderate to injury to their brain, and with spine injuries. But their input may not be needed in many patients with milder injuries. These data suggest that, in patients with GCS > 13, only subdural and epidural hematomas require consultation because they are much more likely to require intervention. 

This parallels a practice guideline we have in place where patients with subarachnoid or small intraparenchymal hemorrhage, or a linear skull fracture are managed by the trauma service without neurosurgical consultation. We do involve them if there is any intracranial hemorrhage with a history of anticoagulant use, however.

We all need to use our neurosurgeons wisely, and this paper helps to clarify situations where they may and may not be needed. 

Related posts:

Reference: Routine neurosurgical consultation is not necessary in mild blunt traumatic brain injury. J Trauma 82(4):776-780, 2017