Category Archives: CNS

GCS At 40: The Current GCS Scale (Adult)

My last post provided some history about the original Glasgow Coma Scale (GCS). Today, I’ll provide some of the finer details of measuring the components of the current iteration of GCS (not GCS-40). I will list out the individual scale values, and explain some of the most misunderstood.

As you know, there are three components to the GCS. Let’s examine each:

Eye Opening

  • 4 – This is an easy one. The eyes are open, and they are opened spontaneously.
  • 3 – Eyes open to your voice. If your patient is asleep and they awaken, the E score is actually 4. If they only open their eyes to repeated voice prompts, then it is a 3.
  • 2 – Eyes open only to pain or stimulation. This is typically tested by squeezing a fingernail, but the exam should progress as described in the Nuances section below.
  • 1 – This one is easy, too. The eyes don’t open, no matter what.

What if the eyes are swollen shut? Then record it as E1c (c = closed).

Verbal Response

  • 5 – Your patient is oriented and converses with you spontaneously.
  • 4 – Confused. This means that you can talk with your patient and they respond in sentences, but you can detect some confusion or disorientation based on their speech.
  • 3 – Inappropriate words. Remember it this way: your patient speaks like a 3-year-old. They can say a few words but can’t construct a meaningful sentence.
  • 2 – Incomprehensible sounds. This means that your patient may moan or make noises, but does not form any words.
  • 1 – No verbal response at all.

If the airway is controlled with an endotracheal tube, then the score is recorded as V1t.

Motor response

  • 6 – Your patient obeys commands.
  • 5 – Localizes to pain. Your patient will move toward a painful stimulus in an attempt to remove it. They can move their arms/hands above their chin in response to facial stimulation.
  • 4 – Withdrawal from pain. Patients cannot move their arms above the chin.
  • 3 – Flexor response (decorticate posturing). This score, and the next one (2), are the ones that I always confuse. Just remember that the patients reach for the “core.” They flex their forearm and wrist, clench their fist, extend their legs, and point their toes (plantar flex).

  • 2 – Extensor response (decerebrate posturing). These patients bring their arms to their sides (adduct), extend the elbow but flex the wrist and fingers, and pronate the forearms. Legs and feet are the same as above.

  • 1 – No response to stimuli.

Nuances

  • Record the entire score. This means all components and modifiers. An example would be E3 V4 M4 = 11, or E1c V1t M3 = 5, or E1 V1 M2rt M3lt = 4/5
  • Alcohol or drug intoxication will interfere with accurate measurement of the GCS, especially with the verbal and eye-opening components.
  • If the motor score is asymmetric (higher on one side than the other), record the higher score. Or better yet, break out the motor scores for both sides so your friendly, neighborhood neurosurgeon has a better idea of what is going on.
  • Stimulation should proceed from fingernail squeeze, to pinching the trapezius muscle, to pressure in the supra-orbital notch, in that order. The sternal rub is to be discouraged, as it can lead to bruising.

In my next post, I’ll describe the differences in the Pediatric Glasgow Coma Scale.

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GCS At 40: The Original GCS

The Glasgow Coma Score (GCS) has been in use for more than 40 years. Since that 40th anniversary a few years back, there has been talk of updating this tried and true system. But where did this scale come from? How was it devised? And why are we looking to update it now? I’ll dig into this topic over my next several posts.

The original paper describing the GCS was published in 1974 by Graham Teasdale and Bryan Jennett. They were neurosurgeons at the Institute of Neurologic Sciences in Glasgow, Scotland (of course) and were based in the Southern General Hospital. Until this paper was published, each report in the literature described its own assessment of level of consciousness. Most divided the spectrum into various steps noted between fully alert and comatose. Unfortunately, these systems were confusing, and they varied from 3-17 steps! There was just no consensus. Some relied on a comprehensive neurologic exam, including brainstem function tests. However, none of these were really designed for repeated bedside assessment.

Teasdale and Jennett settled on three simple areas to examine: eye-opening, motor response, and verbal response. They selected easily observable responses for each of these components. Here is a copy of the original scale:

Notice that this differs from the current-day score. The motor response did not have a “withdrawal” option, so the maximum score was only 14! But that didn’t matter much at the time; the individual components were graphed out over time for inspection. A total score was not generally calculated.

Teasdale and Jennett found that inter-rater reliability for this system was excellent, compared to a 25% discrepancy for other less objective systems in use at the time. This led to its rapid adoption over the coming years.

In my next post, I’ll describe how GCS came to be used over the ensuing years.

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Using MRI To Predict Outcome From Diffuse Axonal Injury (DAI)

Has this happened to you? A patient with a serious head injury is not waking up as expected. There were a few punctate hemorrhages seen on the initial CT scan. Your neurosurgery colleague orders an MRI to “provide a prognosis on the patient’s injury.”

Is this a legitimate request? Sure, MRI is very sensitive at detecting very small hemorrhages that may signal the presence of diffuse axonal injury (DAI). But do more abnormalities on MRI equal a poorer prognosis or longer recovery time?

A group from Vanderbilt presented their data from a retrospective cohort study at EAST earlier this year.  They reviewed 7 years of data from 2006 to 2012, including all patients with a head CT positive for intracranial injury and an MRI within 2 weeks. They excluded penetrating injuries and patients with psychiatric or neurologic disorders. They analyzed information on three year mortality, functional outcome, and quality of life.

Here are the factoids:

  • A total of 311 patients met all inclusion/exclusion criteria, with a median age of 40 and serious injury (average ISS 29, average ICU length of stay 6 days)
  • Functional status at discharge could be assessed in 240 patients, and only 118 could be contacted for long-term followup questions
  • Only 56% of patients with severe TBI had an MRI positive for DAI
  • Functional status was lower on discharge for patients positive for DAI on MRI
  • There was no difference in Glasgow Outcome Score, quality of life, or 3 year survival in patients with MRI evidence of DAI compared to those without

Bottom line: This is a relatively large study, but there are still several weaknesses that could skew the numbers a bit. However, it appears that MRI for prognostication of outcomes in patients with clinical DAI is not very helpful. First, only about half with a clinical picture of DAI showed it on MRI. And sure, MRI may tell us a little bit about their status when they are discharged from the hospital to rehab or transitional care. But is that information very useful? It certainly does not help predict their outcome in the longer term. So why order an expensive and difficult study (think restraints, sedation, lots of pumps and monitors) to tell us what we already know based on our experience with severe TBI?

Reference: Prognosis of diffuse axonal injury with traumatic brain injury. J Trauma 85(1):155-159, 2018

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Sports Drinks And Electrolyte Replacement In TBI

Yesterday, I wrote about the (lack of) effectiveness of forcing hypernatremia in the management of TBI. However, we do know that some of our head injured patients have trouble maintaining a normal sodium level, and if it drops quickly or too far, hyponatremia can certainly cause problems. Trauma professionals have a number of tools to help fix this, including salt supplements or tablets, saline infusions, or even hypertonic saline in more difficult cases.

But what about using a sports drink to replace electrolytes? Isn’t that what athletes do? There are quite a few of these sports drinks on the market, and new ones seem to appear every week. Common examples are Gatorade, Powerade, Muscle Milk, Vitamin Water, 10-K Thirst Quencher, and many more. What if your brain injured patients eschews the salt tabs and insists on pounding down sports drinks all day?

Here is a table from an old sports medicine paper that describes the composition of a number of sports drinks from back in the day. Some, like Gatorade, are still around. (Click image to see a bigger, readable version)

Note that the electrolyte results are in mg/250cc, so I will translate to meq/liter for you. Gatorade had the highest sodium concentration at the time, 20meq/L, and one of the lowest potassiums at 3meq/L. The majority of the current day sports drinks have about the same electrolyte composition. Note that they are all a bit hyperosmolar (300+ mOsm), and this is made possible by added carbohydrate from some type of sugar. The carb is usually in the form of sucrose, dextrose, and/or high fructose corn syrup (yum!).

Bottom line: Your typical sports drink is equivalent to D30 in 0.1 normal saline. Not good for your TBI patient when consumed for sodium supplementation. It will actually drive the serum sodium down when consumed in quantity. Make sure your patients steer clear of this stuff until their brain injury is healed and they are running their next marathon.

Reference: The Effectiveness of Commercially Available Sports Drinks. Sports Med 29(3):181-209, 2000.

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Targeted Hypernatremia In Trauma Brain Injury: Does This Work?

Traumatic brain injury (TBI) frightens and confuses most trauma professionals. The brain and its workings are a mystery, and there is very little real science behind a lot of what we do for TBI. One thing that we do know is that intracranial hypertension is bad. And another is that we do have some potent drugs (mannitol, hypertonic saline) to treat it emergently.

So if we can “dry out” the brain tissue on a moment’s notice and drop the ICP a bit with a hit of sodium, doesn’t it stand to reason that elevating the sodium level constantly might keep the brain from becoming edematous in the first place? Many neurosurgeons buy into this, and have developed protocols to maintain serum sodium levels in the mid-140s and higher. But what about the science?

A nice review was published in Neurocritical care which identified the 3 (!) papers that have promoted this practice in humans with TBI. In general, there was a decrease in ICP in the patients in the cited papers. Unfortunately, there were also a number of serious and sometimes fatal complications, including pulmonary edema and renal failure requiring hemodialysis. These complications generally correlated with the degree of hypernatremia induced. Papers were also reviewed that involved patients with other brain injury, not caused by trauma. Results were similar.

Bottom line: There is no good literature support, standard of care, or even consensus opinion for prophylactically inducing hypernatremia in patients with TBI. The little literature there is involves patients with severe TBI and ICP monitors in place. There is nothing written yet that justifies the expense (ICU level care) and patient discomfort (frequent blood draws) of using this therapy in patients with milder brain injury and a reliable physical exam. If you want to try out this relatively untried therapy, do us all a favor and design a nice study to show that the benefits truly outweigh the risks. 

And if you can point me to some supportive literature that I’ve missed, please do so!

Related posts:

References:

  • Induced and sustained hypernatremia for the prevention and treatment of cerebral edema following brain injury. Neurocrit Care 19:222-231, 2013.
  • Continuous hyperosmolar therapy for traumatic brain injury-induced cerebral edema: as good as it gets, or an iatrogenic secondary insult? J Clin Neurosci 20:30-31, 2013.
  • Continuous hypertonic saline therapy and the occurrence of complications in neurocritically ill patients. Crit Care Med 37(4):1433-1441, 2009. -> Letter to the editor Crit Care Med 37(8):2490-2491, 2009.
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