TBI management

Clare

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This is a patient I recently had to manage that greatly conflicted me.

High speed road crash about 30 minutes from hospital; 20 year old unrestrained male driver with a huge spider web on the windscreen; initially trapped and extricated by the Fire Service.

Primary survey – his head was munted, huge forehead laceration, otherwise unremarkable

BP 80/50, PR 140, RR 6, snoring with intermittent apnoea, GCS 8, ECG ST

I presumed he had (1) a traumatic brain injury and (2) hypovolaemic shock from uncontrolled internal bleeding. It is also possible that this bloke was hypotensive as a result of his brain injury i.e. loss of neural control of vascular tone or something and did not have significant internal haemorrhage however I would consider it more likely he was bleeding internally given his mechanism of injury.

The treatment of TBI and presumed hypovolaemic shock in regards IV fluid therapy is conflicting because (1) the goal of TBI is achieve a relatively normal blood pressure to ensure sufficient MAP to avoid derangement of ICP/CCP while (2) fluid resuscitation in a patient with hypovolaemic shock should only be given if they have (a) no radial pulse, (b) a falling level of consciousness or (c) no recordable blood pressure however his radial pulse and blood pressure were recordable while his decreased level of consciousness was primarily due to brain injury rather cerebral hypoperfusion.

Now this is one of those “grey” areas where a patient into a sort of treatment black hole and requires significant clinical judgement. I presumed that the most critical problem was his traumatic brain injury given that the brain is significantly more sensitive to hypotension and a poorly managed TBI has much greater morbidity and mortality. I figured that if he did have internal bleeding from an artery or ruptured spleen or whatever that while this was important it was less important than a poorly managed TBI as the destination hospital had 24 hour CT and surgical facilities so any operative control of bleeding would happen fairly rapidly as an early RT call was placed to the hospital so they activated the trauma team and were prepared for him.

To that end my management was giving him enough fluid to achieve a BP of at least 110 mmHg – lower than our normal target for TBI is 120 mmHg and over what I have read as a target for uncontrolled Hypovolaemia (90 mmHg) but based upon what I felt was the most important aspect of care – i.e. preventing secondary brain injury. Our CPG does not have a BP target for uncontrolled hypovolaemia but stresses that the patient must be given the minimum amount of fluid compatible with life (which I think has previously been stated to be presence of a radial pulse).

I figured a BP of 110 mmHg would mean a MAP and CPP of at least 70 which are at the lower end of normal.

This is my first major trauma with significantly complex management and I feel very uneasy about it. The others I have had have been fairly straightforward in terms of management i.e. bloke trapped under something or whatever; I am keenly aware of the significant disability that traumatic brain injury and more-over, poorly managed TBI, has and hate to think that this young guy ends up a vegetable and loses the next 60 years of normal life because of me.

So what do you think? Do you agree with my reasoning or would you have done something differently?

PS An Intensive Care Paramedic with rapid sequence induction would have taken longer to locate and intubate than it was to take him directly to the hospital; he wouldn't take an LMA but did accept a naso-airway so with that and good old fashioned head positioning his oxygenation was relatively normal so calling for RSI wasn't really necessary, it would have been great to have but not absolutely necessary in this case.
 
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VFlutter

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To that end my management was giving him enough fluid to achieve a BP of at least 110 mmHg – lower than our normal target for TBI is 120 mmHg and over what I have read as a target for uncontrolled Hypovolaemia (90 mmHg) but based upon what I felt was the most important aspect of care – i.e. preventing secondary brain injury. Our CPG does not have a BP target for uncontrolled hypovolaemia but stresses that the patient must be given the minimum amount of fluid compatible with life (which I think has previously been stated to be presence of a radial pulse).

I figured a BP of 110 mmHg would mean a MAP and CPP of at least 70 which are at the lower end of normal.

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Tough situation. I think the ability to sedate, RSI, and titrate ETCO2 would have been beneficial.

Hypotension during TBI is associated with a really poor prognosis. Chances are you were screwed from the get go.

A Bp of 110 systolic? Assuming 110/70 that would be a MAP of ~83.

CPP = MAP (83) - ICP (let's say a high normal of 15) = 68. The optimal level during a TBI is above 70-80 mmHg. And that was calculating with an ICP of 15...what do you think it really was? Lets say it was 25 (which is way conservative) then the CPP would be 58. Mortality increases 20% for each 10mmHg below 70. What if his ICP was 40......

I personally would have been more aggressive with the MAP. Remember Cushing's triad? Hypertension is the body's natural response to maintain cerebral perfusion with increased ICP. They actually give TBI patients pressors in the Neuro ICU to maintain CPP if necessary.

Also, Nasal airway in a patient with head trauma? (See picture under my username) Did he have battle signs, raccoon eyes, etc? Posturing? Any other findings with would indicate internal hemorrhage? Rigid abdomen?
 
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Aprz

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Is 83 really a good estimate of the MAP at that HR?

Significant head trauma is a relative contraindication for nasal airways now-a-days. Fixing a bad airway is going to take precedents over the slim possibility of inserting it into the cranium.

In addition to what Chase said about other signs e.g. trismus, abnormal pupils, posturing, how did the vitals trend, and how did the patient respond to your treatments?
 
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VFlutter

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Is 83 really a good estimate of the MAP at that HR?
Thanks, I totally forgot to account for the tachycardia. But even taking the arithmetic mean it would be 90.

All that was assuming he did in fact have a TBI.
 
OP
Clare

Clare

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Tough situation. I think the ability to sedate, RSI, and titrate ETCO2 would have been beneficial.
He was 30 minutes by road to hospital; calling for RSI and then still have 30 minutes to hospital would have taken probably an hour.

A Bp of 110 systolic? Assuming 110/70 that would be a MAP of ~83.

CPP = MAP (83) - ICP (let's say a high normal of 15) = 68. The optimal level during a TBI is above 70-80 mmHg. And that was calculating with an ICP of 15...what do you think it really was? Lets say it was 25 (which is way conservative) then the CPP would be 58. Mortality increases 20% for each 10mmHg below 70. What if his ICP was 40......
I don't know what his ICP was, in this case there was no sign it was elevated (e.g. seizure, pupil dysfunction, posturing).

I personally would have been more aggressive with the MAP. Remember Cushing's triad? Hypertension is the body's natural response to maintain cerebral perfusion with increased ICP. They actually give TBI patients pressors in the Neuro ICU to maintain CPP if necessary.
There was no hypertension, BP was 80 so he was hypotensive

I figured the more aggressive we are with his blood pressure to reach the CPG target of 120 mmHg then potentially the worse it is going to be for any internal haemmorhage. No good having a guy with an intact noggin if he dies from bleeding into his chest, pelvis or abdomen but conversely the opposite is also true; no good having good control of his haemmorhage only to have him end up a vegetable.


Also, Nasal airway in a patient with head trauma? (See picture under my username) Did he have battle signs, raccoon eyes, etc? Posturing? Any other findings with would indicate internal hemorrhage? Rigid abdomen?
[/quote]

Nasal airways are not contraindicated in head trauma and it is simply taught that we should exercise care and stop if significant resistance is encountered.

There was no obvious signs of internal haemmorhage such as a rapidly distending, rigid abdomen but history of mechanism and physiological signs were highly indicative of somebody who could very well have been suffering from internal bleeding. His hypotension could have been due to a neurogenic cause i.e. loss of neural control of vascular tone regulation or something but I am not sure how likely that is. If he didn't have TBI but still had the hypotension and tachycardia then he is assumed to have uncontrolled internal haemmorhage.

Is 83 really a good estimate of the MAP at that HR?

Significant head trauma is a relative contraindication for nasal airways now-a-days. A bad airway is going to take precedents over the slim possibility of inserting it into the cranium.

Were there any other signs of TBI e.g. abnormal pupils, trismus, posturing? How did the vital trends, and how did the patient respond to treatment?
There was no signs of significant head injury other than the stated big forehead laceration where his head hit the windscreen.

His blood pressure came up to just over 100 mmHg with one litre of fluid and the tachycardia decreased.

This is a case involving somebody who is otherwise young, healthy and very much has his whole life ahead of him and upon whom mortality and morbidity will impact greatly. It is my first case involving complex management of major trauma where doing right by one thing may negatively affect the other (cerebral ischaemia vs. permissive hypotension).

Perhaps a few mmHg of blood pressure wasn't a major deciding factor, perhaps I am overthinking it, but I've not seen something like this before and it has, for the time being, greatly affected me.

I am not sure if my management is the real problem or if its more I am very unsure of myself because this is the first time I have encountered somebody of my own age who has significantly major trauma and whose quality of life, or even ability to lead any sort of a normal life, is likely to have been destroyed and that is very hard to see. I am not sure a bit of blood pressure was really my concern.
 
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VFlutter

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What makes you think he had a TBI then? Just the mechanism of injury? Neurogenic shock is associated with spinal cord injury not TBI. TBI usually presents with hypertension which is why I made the point about Cushing's triad and desired high MAP in TBI patients.
 
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OP
Clare

Clare

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What makes you think he had a TBI then? Just the mechanism of injury? Neurogenic shock is associated with spinal cord injury not TBI. TBI usually presents with hypertension which is why I made the point about Cushing's triad and desired high MAP in TBI patients.
History of mechanism, the huge spider web on the windscreen where his head hit and physiological signs, particularly the respiratory rate and GCS all leaf me to believe he had a TBI.
 

VFlutter

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History of mechanism, the huge spider web on the windscreen where his head hit and physiological signs, particularly the respiratory rate and GCS all leaf me to believe he had a TBI.
With bradypnea and ALOC then I would assume the ICP is increasing. And no other signs/symptoms? Pupils were PERRLA?

I still think I would be more aggressive with the pressure but I could be wrong, there are arguments going both ways.
 
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Handsome Robb

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NG tubes are the worry in head trauma. NPAs it's a caution. Basically don't force it, like Clare already said.

I'm not someone who jumps to calling for HEMS constantly but was it an option? 30 minutes by ground is a long time to manage this patient without the ability to titrate ETCO2 not to mention that trauma is a surgical disease (sorry vene, I stole your line ;) ) and no matter what you do, if he doesn't get a surgeon to crack him open and stop the bleeding nothing is going to matter. 100-110 mmHg SBP is what I've always been taught. I can't remember what PHTLS/ITLS say about it, I want to say it's 110 mmHg but don't quote me. You say calling for RSI takes that time then the 30 minutes to the hospital. Why can't the ICP meet you en route? Kill two birds with one stone that way. You meet up, they hop in push some drugs, drop a tube then continue on your way...

Can't really titrate his CPP unless you are bolting him with an ICP monitor in the field... CPP = MAP-ICP

If he's buggered for the rest of his life, it's not your fault. No way you can twist that up and make it your fault, so drop that thought. You gave him every shot he had at a decent quality of life. Without you, he'd more than likely died in that car or in the bed of a pickup on the way to the band-aid box rural ER.

Doesn't sound like neurogenic shock unless he had an SCI along with his TBI, as Chase already said as well. Definitely very possible though. You gave him an 8 on the GCS, can you break it down more for us? (x/x/x) Was he moving his extremities? Doesn't have to be purposeful but where they all moving? Personally that'd steer me away from a SCI and ultimately neurogenic shock if he was.

Without outwards signs of hemorrhage, be it internal or external, I'd personally lean towards TBI + SCI and neurogenic shock and would have been more aggressive with fluids but we can all sit here and monday morning quarterback your call to death, in the end we weren't there.

You said his abdomen was soft and not distended correct? How were his lung sounds? Pelvis intact? How about both femurs? Not saying these things are the end all to "ruling out" internal hemorrhage but if everything listed above is good you've covered the large cavities that are generally involved in fatal internal hemorrhage. Maybe this is the wrong way to think about it and someone smarter than me feel free to tell me I'm an idiot and correct me.

Pardon my grammar. It's late. I also realized I kinda contradict myself. Just looking at all the angles.
 

medichopeful

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Also, Nasal airway in a patient with head trauma? (See picture under my username) Did he have battle signs, raccoon eyes, etc? Posturing? Any other findings with would indicate internal hemorrhage? Rigid abdomen?
Do you have a link to that picture or article? I'd like to get a look at it and read the article if there is one!
 

Veneficus

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Many things to talk about...

The game of resuscitation.

As you mentioned, many trauma treatments compete, it is not just cardiovascular and brain.

Just last night my wife again commenting it is amazing I don't drink regularly.

I explain it like this:

Think of a chess game, only with many more pieces. Once the patient starts losing the game, you are asked to try and turn it into a win. The goal isto win as often as possible, but sometimes the position is so bad, nothing you can do will turn it around.

Blood pressure, and MAP, and perfusion. Oh my...

Based on what was described, I thinkn TBI is a good assumption, the mechanism, while not reliably predictable, also indicates potential SCI. The old guys who remember steel cars prior to airbags, seatbelts, etc. will fondly remember these findings.

I have read the post twice, I see no signs of herniation. That is not to be confused with increased ICP. Herniation is a late sign. We must also remember, GCS is not meant to decide ifwe intubate or not, it is meant to be a quantitative scoring of prognosis from brain injury. An 8 is a severe brain injury.

It is widely said in trauma surgery there are onl 5 locations that a person can die from hemorrhage. The cranial vault is not one of them. In the prehospital environment, it is not easy to find acute hemorrhage until it is very advanced. Based on the vital signs and presnetation, I would make great efforts to identify the potential site of bleeding, even by exclusion, but I personally would consider this patient bleeding until proven otherwise.

A trial of saline is not out of order. Especially an amount as small as a liter. Since Class I shock responds to saline bolus, Class II does so transiently, the bolus itself can be diagnostic. If the patient transiently responded, I would assume them still bleeding and not do it again.

I am a big supporter of permissive hypotension, but we must be realistic on what is possible or advisable without a lot of diagnostics. I would say if the patient didn't respond to the fluid bolus, or actually got worse, don't do that anymore.

Eitherway, I would not maintain a fluid infusion to maintain numbers. That I would say is a bigger concern for increased cerebral edema than 1 one time bolus.

Target numbers

Many different groups advocate different target numbers. These guidlines are designed for safety and are extremely conservative.

Permissive hypotension has a time factor depending on the pressures involved. but 80systolic for several hours is not unreasonable. 70sys for maybe an hour or two. While there will likely be loss of urine production during this time, I have consulted extensively with very respected nephrologists, one in particular with an international reputation, and I am assured the kidney can recover from this. As far as I am concerned, their experience and knowledge is significant enough to make decisions from it.

As for the effect on cerebral perfusion, perfusion assumes oxygen delivery, not just a number. I have said many times, I can normalize blood pressures on a corpse, it does not bring them back to life.

When you are thinking about maintaining a number with water, keep in mind that brain tissue as defense mechanism forms osmotically active protein, which means isotonic fluid will be drawn into the brain cell. Cellular swelling is bad. After all, it is the first step in cell injury.

A decrease in pH right shifts the saturation curve. This helps with tissue oxygenation. If you do not add any oxygen carrying capacity, and use water to increase pH, you manipulate oxygenbinding towards hemoglobin and away from tissue.

While you certainly can normalize numbers doing this, keep in mind it is a physiological defense response. When you exercise, you need more tissue oxygen. Why on earth would you do something that would lessen tissue oxygen to somebody whos life may depend on it?

Please assume crash position...

If I ever hear this on a plance, the flight attendant and I will be locked in mortal combat for one of those rear facing seats.

An unrestrained high speed accident victim is subject to forces in every direction. An aortic tear is certainly a possibility.

They come in 2 flavors.

1. Where you bleed out in damn near seconds.

2. The more commmon small tear, held together by ligament tension, can wait to be repaired for hours and hours, sometimes measured in days. The lower the intravascular pressure, the longer it takes to bleed out.

If you do not see a obvious bleed location, keeping in mind the occult locations like this with a slow bleed I think is a good idea.

Bottom line:

Sounds like you did your best. No worries.
 

TheLocalMedic

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To throw something in from left field from a logistics point of view...

I work in a rural area that gets lots of good grinders. We routinely deal with at least one major traffic collision per shift, so we've gotten pretty slick at dealing with major traumas and small-scale MCIs. What are your thoughts on immediately requesting a helicopter on initial dispatch? Case in point, last week we had a three car collision with a head-on and 7 patients (3 major, 2 moderates, 2 minors). Initially all we got was that it was an MVA, but my policy is that (since we're roughly 20 mins from a rural hospital and 90 minutes from a trauma center) I automatically request a helo. And I was glad I did, by the time we got to scene the helo was 10 out. I had to request two additional ambulances and an extra helo in all, but having that first bird nearby was great so that I could get that first-go trauma out of there so I could deal with the others.

I always advocate for early requests for resources if you're facing a potential trauma and you're a ways out from your hospital. If it turns out it's nothing major, you can always call everyone off, but early requests save a lot of time!
 

VFlutter

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Do you have a link to that picture or article? I'd like to get a look at it and read the article if there is one!
For some reason I was thinking about naso-tracheal intubation not a NPA


Link to article at the bottom of the page
http://www.impactednurse.com/?p=2235

I know you can not get ICP without a bolt but you can make an assumption based off signs/symptoms. It sound like increased but not yet herniation. Also, bradycardia is typically present with neurogenic shock but not always.
 

VFlutter

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What are your thoughts on immediately requesting a helicopter on initial dispatch? I automatically request a helo. And I was glad I did, by the time we got to scene the helo was 10 out. I had to request two additional ambulances and an extra helo in all, but having that first bird nearby was great so that I could get that first-go trauma out of there so I could deal with the others.

I always advocate for early requests for resources if you're facing a potential trauma and you're a ways out from your hospital. If it turns out it's nothing major, you can always call everyone off, but early requests save a lot of time!
Do you mean requesting actual response or standby? I totally agree with a standby request but calling them to scene just in case and then calling them off is a bad policy IMO.
 

Dwindlin

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Do you mean requesting actual response or standby? I totally agree with a standby request but calling them to scene just in case and then calling them off is a bad policy IMO.
While I generally agree with this, talk to the helo service. The service here does not like stand-by, they would rather just take-off and be canceled.
 

IrightI

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To throw something in from left field from a logistics point of view...

I work in a rural area that gets lots of good grinders. We routinely deal with at least one major traffic collision per shift, so we've gotten pretty slick at dealing with major traumas and small-scale MCIs. What are your thoughts on immediately requesting a helicopter on initial dispatch? Case in point, last week we had a three car collision with a head-on and 7 patients (3 major, 2 moderates, 2 minors). Initially all we got was that it was an MVA, but my policy is that (since we're roughly 20 mins from a rural hospital and 90 minutes from a trauma center) I automatically request a helo. And I was glad I did, by the time we got to scene the helo was 10 out. I had to request two additional ambulances and an extra helo in all, but having that first bird nearby was great so that I could get that first-go trauma out of there so I could deal with the others.

I always advocate for early requests for resources if you're facing a potential trauma and you're a ways out from your hospital. If it turns out it's nothing major, you can always call everyone off, but early requests save a lot of time!
I too work in the rural, with three trauma centers and a burn center about 30-40mins via helo, 2.5 by ground. For your particular call, I would have launched an aircraft, and rolled a second ambulance. All of this after recieving the first dispatch tone. Our service has a great working relationship with the area Helo EMS and they dont mind at all getting launced, and then cancelled enroute. As others have stated, its great to know that they are ten out after youve done your primary assesments.

You are correct in seeing that the pt has a head injury, however your assessment doesnt support a TBI in its entirity. When I think of a TBI, im looking for unequal pupils, MOI, possible seizures, CSF from the ears, and battle signs. With RR of 6 with periods of apnea, im curious to see how you obtained a GCS of 8...I was thinking lower. These, you state, were all clear. Another concern for me is the V/S that you obtained. They are trending for Cushings Triad, but not neurogenic shock. With Neurogenic shock, V/S will appear to be normal due to the loss of Sympathetic tone due to the spinal injury. Human nature is to have an elevated BP and Pulse due to experienceing pain, so I would be expecting to see those refelcted in my VS upon inital hook-up. I would attribute the hypotension to internal bleeding, my guess would be a hot belly, spleen...how was his pelvis?

For your pt, RSI would have been done rather quickly. Having him knocked down, allows us to control many things that would be geared with ETCO2. For this head injury pt, the target goal of 30-35 should be obtained with an 02 sat of at least 96%. All can be titrated with proper bagging and o2 admin. We would solve the pressure problem hopefully with two large bore IVs, both runnin NS or if evidence of significant blood loss, hang one line NS and the other run Ringers through blood tubing. Our Helos carry blood, so thats all ready for them if they choose to use it. From that point forward, it would be supportive until the bird arrives....as others have said....he needs a surgeon.
 

Veneficus

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You are correct in seeing that the pt has a head injury, however your assessment doesnt support a TBI in its entirity. When I think of a TBI, im looking for unequal pupils, MOI, possible seizures, CSF from the ears, and battle signs. With RR of 6 with periods of apnea, im curious to see how you obtained a GCS of 8...I was thinking lower. These, you state, were all clear..
What you describe are either late signs or a very massive injury.

Waiting to see if a person has unequal pupils or a seizure after a blow to the head is a fail in my opinion.

We would solve the pressure problem hopefully with two large bore IVs, both runnin NS or if evidence of significant blood loss, hang one line NS and the other run Ringers through blood tubing.
How does that solve the problem?
 

IrightI

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What you describe are either late signs or a very massive injury.

Waiting to see if a person has unequal pupils or a seizure after a blow to the head is a fail in my opinion.



How does that solve the problem?
Exactly, signs of Herniation. No where did I say that I would wait and not do anything until I saw these signs. These are things that Im going to be expecting my pt to demonstrate while in my presence if im going down a TBI road with a significant head bleed. If, in fact, you do have those late signs than thats a whole different ball game. Trying to maintain a perfusing pressure without worsening the herniation is key. read: 190/110. That, of course is not solved with NS infusions, but labetalol. Im sure im preaching to the choir on this subject.

Again, didnt say that was my end all, be all solution. That would be just a start. Just as you mentioned in your earlier post, if the first liter doesnt work, then shut it down and move on. Im with ya on that.
 

VFlutter

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Exactly, signs of Herniation. No where did I say that I would wait and not do anything until I saw these signs. These are things that Im going to be expecting my pt to demonstrate while in my presence if im going down a TBI road with a significant head bleed. If, in fact, you do have those late signs than thats a whole different ball game. Trying to maintain a perfusing pressure without worsening the herniation is key. read: 190/110. That, of course is not solved with NS infusions, but labetalol. Im sure im preaching to the choir on this subject.

Again, didnt say that was my end all, be all solution. That would be just a start. Just as you mentioned in your earlier post, if the first liter doesnt work, then shut it down and move on. Im with ya on that.
TBIs like anything else are on a continuum of severity. Not every TBI will result in herniation. What she described is at least a moderate-severe TBI based on GSC and LOC.

If the hypotension was refractory to fluids then what would you do? If this was indeed neurogenic then is the problem volume or something else? Phenylephrine anyone?

Edit: You sure labetalol is the drug to use? Are there any potential complications in a TBI patient

On a side note: I spent last semester in the Neuro Step down and ICU. That was by far the most depressing and challenging experience of my healthcare career.
 
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