Tag Archives: head injury

General

Antiplatelet Therapy And Blunt Head Trauma

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All trauma professionals are aware of the evils of anticoagulation in patients who sustain traumatic brain injury. Warfarin is one of the most common anticoagulants encountered, but there is also a growing number of poor outcomes in patients with the newer, non-reversible agents.

But what about antiplatelet agents like aspirin and clopidogrel (Plavix)? Many physicians worry about these drugs, but is it warranted? Two Level I trauma centers in the Chicago area reviewed their experience. They retrospectively reviewed the records of patients over 40 years old who sustained blunt head trauma. A total of 1547 patients were identified over a 4 year period. They analyzed these records for in-hospital mortality, need for neurosurgical intervention, and length of stay.

Here are the factoids:

  • 27% of patients were taking antiplatelet agents. Patients also taking warfarin were excluded.
  • 21% were taking aspirin alone, 2% clopidogrel alone, and 4% both drugs
  • Patients taking the drugs averaged about 10 years older than those who were not
  • Overall, injury severity was relatively low (average ISS 10). A disproportionate number of more severely injured patients were not taking antiplatelet agents.
  • There was no difference of incidence of intracranial hemorrhage (45%), neurosurgical intervention (3%), or mortality (6%) between the two groups
  • Hospital length of stay averaged about 6.5 days, but long LOS was a bit more common in the antiplatelet agent group.

Bottom line: This is one more in a series of papers scrutinizing trauma and antiplatelet agents. A few previous studies have shown an adverse effect, but they have been much smaller series. I don’t believe the jury is in yet, so watch these patients carefully. A 6 or 12 hours repeat scan is probably in order, along with frequent neuro monitoring.  It’s probably not worthwhile to actively try to reverse them by giving platelets unless there is obvious life-threatening hemorrhage or sudden neurologic change (see below).

Related posts:

Reference: Outcomes in traumatic brain injury for patients presenting on antiplatelet therapy. Am Surg 81(2):128-132, 2015.

General

Trauma 20 Years Ago: Seatbelt Injuries

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Seatbelt use has increased from 58% in 1994 to a high of 85% last year. We know that seatbelt use saves lives, but trauma professionals are also aware that they can create their own injuries as well. This is a positive trade-off, because belt use prevents injuries that are difficult to treat (e.g. severe brain injury) and produces a higher number of intra-abdominal injuries that are easy to treat.

The spectrum of injuries attributed to seat belt use was finally appreciated in a journal article published 20 years ago this month. The authors wanted to catalog the various injuries seen in belted and unbelted motor vehicle occupants. They reviewed data from the North Carolina Trauma Registry, one of the most sophisticated state registries at the time. Although there were over 21,000 records in the database, only 3,901 involved motor vehicle crashes and had complete data on seatbelt use.

This study found the following:

  • Mortality was higher in those not wearing their seat belts (7% vs 3.2%)
  • Unbelted had a much higher incidence of severe head injury (50% vs 33%)
  • Overall incidence of any abdominal injury was the same for both (14%)
  • GI tract injuries were more common in the belted group (3.4% vs 1.8%)
  • Solid organ injury was the same

Bottom line: This study sparked the recognition that seatbelts reduce severe head injury but increase the incidence of some hollow viscus injuries. About 514 severe head injuries were prevented in exchange for 21 additional abdominal injuries that were generally easily repaired. Good tradeoff!

Related posts: 

Reference: The spectrum of abdominal injuries associates with the use of seat belts. J Trauma 31(6):821-826, 1991.

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Controlling Fever In Head Injury

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Fever is a well recognized side effect of head injury. Management of fever is inconsistent among physicians taking care of these patients. There is a lot of debate on the best course of action, but not so much data. Current enthusiasm for applications of hypothermia has created some reluctance to tolerate much in the way of hyperthermia. Here is my take on the currently available literature.

First, understand that there is a fundamental difference between studies that study induced hyperthermia vs those that look at spontaneous fever. This lies in the fact that the set point for temperature regulation is changed in fever, but not in hyperthermia. Therefore, it is not clear whether hyperthermia studies can truly be used to answer these questions.

Animal studies originally focused on stroke models, which showed deleterious effects from hyperthermia. TBI is very different than stroke, but some hyperthermia models did tend to show cellular damage and blood brain barrier breakdown at temperatures of 39C. However, a fever model in rats showed no outcome difference (in rats) in febrile vs normothermic animals with TBI.

A Medline search (ref 4) yielded no randomized controlled trials that could be used to guide us with regard to fever management. The lesser quality papers involved a very heterogeneous group of subjects that made it difficult to draw good conclusions. As a generalization, they found that extremes of temperature, both high and low, were probably associated with worse outcomes. One randomized prospective study showed that aggressive fever control for temperatures > 38.5C had higher mortality and more infections.

A recent meta-analysis (ref 3) found that TBI patients with fever stayed in the hospital and ICU longer. This translated into an extra $14,000 per patient. Precise reasons for the longer stay cannot be accurately determined, but it might be expected that patients with fever would undergo time-consuming searches for possible infectious sources.

Finally, a very recent prospective study (ref 1) at a single institution that did not try to alter temperature found that the optimum survival occurred in a group of patients whose temperatures remained between 36.5 and 38C.

Bottom line: Literature support for aggressive management of fever is poor. If there were a clear correlation with temperature maintained at or slightly below normal, we’d probably have figured it by now. Fever up to 38 degrees C probably does not need to be treated in head injured patients. However, this does not eliminate the need to continue surveillance for infectious complications.

References:

  1. The effect of spontaneuous alterations in brain temperature on outcome: a prospective observational cohort study in patients with severe traumatic brain injury. J Neurotrauma 27(12):2157-2164, 2010.
  2. Induced normothermia attenuates intracranial hypertension and reduces fever burden after severe traumatic brain injury. Neurocrit Care 11(1):82-87, 2009.
  3. Brain injury and fever: hospital length of stay and cost outcomes. J Intensive Care Med 24(2):131-139, 2009.
  4. The significance of altered temperature after traumatic brain injury: an analysis of investigations in experimental and human studies: part 2. Br J Neurosurg 22(4):497-507, 2008.
General

Trauma 20 Years Ago: ED Intubation For Head Injury Is Safe

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How far we have come! It’s now commonplace to intubate trauma patients in the ED using rapid sequence induction followed by orotracheal tube placement. However, 20 years ago we were still gnashing our teeth about safety.

In 1991, the group at UMDNJ Newark looked at 100 consecutive trauma patients with suspected head injury who were paralyzed and intubated in the ED. Half of the intubations were performed by a surgeon, the other half by an anesthesiologist. Fifty seven patients were intubated orally and 40 nasally(!). Three required cricothyroidotomy after failure to intubate due to facial fractures.

The majority of these patients had head scans performed; 59% were positive and 15 required emergent neurosurgical procedures. No patients were found to have a neurologic deficit from the intubation even though seven were eventually found to have cervical spine injuries. Only one patient developed an aspiration pneumonia.

The authors concluded that paralysis and intubation in the ED was safe. It helped facilitate the diagnostic workup because they could control combative patients. Up to that time, the only alternative was heavy sedation, which carried its own risks. 

Interesting points on how far we have advanced:

  • Intubation in the ED did not used to be routine. There was a great deal of anxiety before this procedure
  • Nasal intubation was still fairly commonplace
  • The cricothyroidotomy rate was high
  • Intubation was usually performed by a surgeon or anesthesiologist 
General

What INR is Safe for Ventriculostomy Placement?

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Intracranial pressure monitoring has been shown to benefit patients with severe brain injuries. Neurosurgeons are reluctant to place these invasive monitors in patients with abnormal coagulation studies, and many times expect the coags to be completely normal. Is this reasonable? Brain injury itself can raise the INR. When is it safe to place one of these monitors?

Researchers at the University of Alabama – Birmingham performed a retrospective review of their experience with 71 patients who underwent ventriculostomy with a range of INR values. None of these patients were on warfarin. Eighty one ventriculostomies were performed after an average of 1.5 attempts. They looked at the incidence of new hemorrhage seen on CT after placement. They found:

  • Patients with an INR < 1.2 had a 9% incidence
  • Patients with an INR from 1.2 to 1.4 had a 4 % incidence
  • Patients with an INR > 1.4 had an 8% incidence

If the neurosurgeon, is unwilling to place the ventriculostomy until the INR is normalized, there may be several additional sources of morbidity:

  • Additional brain injury that is not known and treated due to the lack of an ICP monitor
  • Potential infectious and other complications (transfusion reaction, TRALI) from plasma administration
  • Cost for the transfusion products

The patients who did have hemorrhage generally had a small focal area. The one significant hemorrhage occurred in a patient on clopidogrel (Plavix). 

Bottom line: The numbers are small, and this is retrospective work. Based on their study, the authors are comfortable placing ventriculostomies in patients not on Coumadin with an INR up to 1.6 without plasma administration beforehand. Colpidogrel should be considered as a separate risk factor.

Reference: The relationship between INR and development of hemorrhage with placement of ventriculostomy. Bauer DF et al. J Trauma, in Press Aug 27, 2010.