Tag Archives: TBI

Medication Alert! Dabigatran and Head Trauma

First, there was warfarin, a cheap and effective way of treating deep venous thrombosis (DVT) and pulmonary embolism (PE) in trauma patients. Unfortunately, there is plenty of literature that shows the added risk that this drug poses in injured patients, particularly in head injury. Because of this, many trauma centers have developed “rapid reversal protocols” to quickly restore vitamin K dependent clotting factors in an attempt to improve outcomes. To see our protocol, click here.

Next came clopidogrel (Plavix), which is used to prevent clotting in vascular disease. It irreversibly inhibits platelet aggregation. Counteracting this drug is more complicated due to its long half-life. Platelet infusions are required, but the infused platelets are inhibited by any remaining drug in the plasma. This requires the use of lots of platelets to get some meaningful clot to form again.

Now, we have direct thrombin inhibitors (DTI). Hirudins were the first used, and were never an issue in trauma patients. And their short half-lives obviate the need for reversal. The newest DTIs (argatroban and dabigatran) are a real problem in trauma. Argatroban is not a problem, because it is given by IV only. But dabigatran (Pradaxa) has just been approved for oral use within the last year.

According to the package insert, “there is no antidote to dabigatran etexilate or dabigatran.” And also “dabigatran can be dialyzed (protein binding is low), with the removal of about 60% of drug over 2 to 3 hours; however, data supporting this approach are limited.”

We will be seeing patients taking this drug in the near future. What do we do if they are trauma victims with bleeding in critical places, like the brain? At Regions, we have developed a proposed guideline that combines oral charcoal, dialysis, transfusions and optionally, activated Factor VII. Click here to download the protocol.

If anyone has any experience with these patients, please comment below. And everyone else, keep your fingers crossed!

Related posts:


Thanks to Colleen Morton MD for developing the dabigatran reversal protocol

IOM Report: Nutrition and Traumatic Brain Injury (TBI)

The Institute of Medicine (IOM) released a report last week summarizing a project that examined the impact of nutrition on head injury. The Department of Defense requested this review because of the significant morbidity and mortality incurred by our armed forces caused by TBI.

The IOM convened a panel of experts that reviewed the available data. As with most such panels, there is a recommendation to engage in additional research. They went a step further, though, and recommended several specific avenues of research, including:

  • Determine optimum levels of blood glucose
  • Study the benefits of insulin therapy
  • Determine the optimal goals for nutrition
  • Look at the effects of supplements and various diets, CDP-choline, creatine, n-3 fatty acids, fish oil and zinc supplements

The most pressing recommendation they made was a call to standardize the feeding regimen for severe TBI patients very early after injury. Specifically, they recommend that nutritional support be started within 24 hours of injury, consisting of 50-100% of the total energy expenditure with 1 to 1.5 g protein per kg body weight. This should be continued for the first 2 weeks after injury. It appears that this intervention limits the intensity of the inflammatory response after TBI and improves outcomes. 

Reference: Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel. Click to access the document on the IOM site.

Controlling Fever In Head Injury

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.


  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.

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

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 

Nail Discoloration After Severe Traumatic Brain Injury (TBI)

Occasionally, patients who have had a severe brain injury but recovered relatively quickly may present with complaints of odd nail discoloration. This may involve fingernails and/or toenails. What gives?

This is actually a byproduct of repeated exams to determine the Glasgow Coma Scale score. A common way to determine the motor component is to squeeze the fingertip or toetip. I’ve seen some neurosurgeons use a pen to apply a great deal of force to the nail.

The discoloration is a resolving subungual hematoma. You may see different colors under different nails, depending on the age of the hematoma. Amaze your colleagues with your knowledge on this one!