Medical Tidbits‎ > ‎

2015/10/23 - Medical Tidbits: Traumatic Brain Injuries

Good afternoon as I sit here in Boston in a Starbucks Coffee Shop listening to “It’s nothing like the real thing baby”

One of the reasons for sitting in the Starbucks is the aspect that like so many of you, I am currently studying for my EMS Board certification (this is a subspecialty board certification).  Several of the questions on the review test along with some of the material deals with traumatic brain injuries.   Though we are outside the “summer months” and fall has gripped the Midwest … we really do have to take into account the potential of traumatic brain injuries once the snow and ice starts to fall.


With traumatic brain injuries there are several factors that come into play with the first issue at hand being the primary injury to the brain itself.  Falling, being involved in a car accident, being smacked across the head with a baseball bat, etc and the brain gets jostled around and therefore direct injury.  There is very little that we can do for this (unless we beat someone to an accident and prevent the accident in the first place … and if you can do that … you should not be working for us !!!!).  What we can prevent is the secondary injury.  This of course is the destruction of the brain parenchyma secondary to lack of oxygen (hypoxic state).  This can either be from destruction of the blood vessels and therefore loss of blood to an area, swelling within the skull that increases pressure and therefore pushes the blood out of the skull (again causing a hypoxic state).  This phenomena is known as the Monroe-Kelly Hypothesis.   A drop in blood pressure which in turn causes a drop in perfusion to the brain parenchyma (again goes back to lack of oxygen). 


If you had not realized … there was a theme there … and that seemed to be lack of oxygen to the brain … this is a “BAD THING”.  


In the board review and also through current research from EPIC-TBI (Excellence in Prehospital Injury Care – Traumatic Brain Injury), OPALS (Ottawa Prehospital ALS study) and several other groups the treatment for TBI had changed.


First and foremost we must prevent hypoxia.  This is one of the primary “killers” for TBI.  It is reported that a single pulse ox sat < 90% will double the mortality for a patient.   This then comes into play … do we actually need to intubate a patient in the prehospital arena, or is the use of a BVM appropriate for care until the patient can get to a more definitive destination center.   Yes we have the luxury on the flight / mobile side of things of having some fancy drugs and equipment that helps us ensure a (1st) pass success rate.  Again with multiple attempts at intubation you increase the risk of hypoxia and therefore mortality for these patients.  The other thing that all of us can do if we have to intubate the patient is use “apneic oxygenation”.  Scott Weingart and Richard Levitan gives an excellent review / perspective on this at http://emcrit.org/preoxygenation/.


After hypoxia the big killer is hypotension.  A single drop in SBP below 90 mmHg in adults and children > 10 will again double the mortality of patients with TBI.  Drop the blood pressure and we drop the perfusion thereby increasing hypoxia … get your IV’s established early.  If you cannot get IV’s then place an IO.  For patients with bleeding in the prehospital arena consider early use of TXA (reminder 1 gram over 10 minutes should be administered within 3 hours of the accident / incident).   If the tank is full and the patient is creeping towards a hypotensive state then get vasopressors on these patients (again … make sure that the tank is full – if unsure then dump several liters of fluid into the patient).


The last issue comes with hyperventilation.  In the past we are taught that patients with TBI should have an EtCO2 around 30 – 35.  Well the truth is starting to show that therapeutic hyperventilation may not be that great.   In (1) research article it showed that patients with low PCO2 levels below 35 at time of admission had an increased mortality (it was listed at 77% compared to a 15% mortality rate for patients with normal PCO2 levels and 61% for elevated PCO2 levels above 45).  Is there still a role for a transient use of hyperventilation for a patient that is herniating … the truth is that we really do not know. 


So in the end … prevent hypoxia (give them some oxygen … 2 liters is appropriate … if you need then BVM the patient (intubate if you can properly secure the tube with 1 attempt).  Prevent hypotension … use fluids and if necessary TXA.  Current literature is starting to support a maintenance of an EtCO2 level between 35 – 45.

 

As always … Share the Care; Work as a Team