Today we are going to discuss increased intracranial pressure (ICP) and herniation. This is the first of 13 lectures to go with the upcoming Emergency Neurological Life Support Course that I co-chair.
Screen for Increased Intracranial Pressure
Matt & Mike's Ultrasound Podcast on Ocular Ultrasound
Tier 0
Head of Bed Up
Temp Normal
PaCO2 35-38 mm Hg
Control Pain/Sedate if Intubated
Tier 1
Osmotic Therapy
Mannitol or
Hypertonic Saline or
Sodium Bicarb (make sure to control PaCO2)
Tier 2
Propofol (or Phenobarb) Drip titrated to take patient to low levels of sedation scales (5-200 mcg/kg/min)
CPP Optimization
Tier 3
Decompressive Craniectomy
Induced Hypothermia
Pentobarb
Moderate Hyperventialtion (I reserve for patients who are herniating)
Want more Tier 3 therapies?
Get Thomas Scalea's Lecture on TBI/ICP
Additional New Information
More on EMCrit
Elevated intracranial pressure (ICP)(Opens in a new browser tab)
Additional Resources
You Need an EMCrit Membership to see this content. Login here if you already have one.
Professor
Nassau University Medical Center
No conflicts of interest (coi).
- EMCrit Wee (392.5) – Naughty or Nice? Bad Behavior in Healthcare with Liz Crowe, PhD - January 15, 2025
- EMCrit 392 – All Things Defibrillation with Sheldon Cheskes - January 10, 2025
- EMCrit 391 – Pericardiocentesis and Tamponade Temporization - December 27, 2024
Dear Scott, Thanks for the great podcast. Only a few notes- I would bring CPP optimisation into tier 0. We all know hypotension and reduced CPP in TBI is bad. Normal PaO2 in tier 0. Hypoxia and more recently hyperoxia ( http://archsurg.jamanetwork.com/article.aspx?articleid=1216545) are known to worsen outcomes in TBI. While optimising PaCO2 and PaO2 limit Pawp and PEEP with NMBA to limit ICP surges. Agree on position being vital. Head up and neutral, but also loosen those ett ties and c-collars. I’m with you on avoiding hypotonic solutions in TBI, but I was not aware of any good evidence of… Read more »
Peter, Great comments, thanks for writing in. CPP in tier 0 So I think I mentioned CPP maintenance is in tier 0 (generally >55-60 mm Hg) is Tier 0. CPP optimization is actually pushing the CPP beyond these levels, which in some patients will lower ICP, but also has the potential for harm (fluid overload, decreased oxygen delivery from unnecessary increases in afterload, etc.) So to be absolutely clear, CPP<60 should be immediately treated in any patient with potential for increased ICP; push the CPP to see what it does to ICP only with a good amount of knowledge of… Read more »
Great points and thanks for the response. CPP individualisation is an interesting topic and really relates to whether cerebrovascular autoregulation is maintained or not. Higher CPP tend to suit those where autoregulation is maintained (which is not as uncommon as people think in TBI, can supply references) as well as maybe hypertensives. Patients with impaired autoregulation may have better outcomes with lower CPPs.With the increasing use of cerebrovascular pressure reactivity indices and TCD, individualised CPP will probably eventually become a standard of care. The extremes of PaO2, mainly hypoxia, will increase CBF and hence cerebral blood volume and ICP from… Read more »
Peter, first, I would love to see your article, if you have a unfettered copy, I’d love to place it on the blog for all. I agree re: PbrO2; that is exactly what I meant. Higher than acceptable ICPs, but good PbrO2, maybe hold off on the more aggressive therapies. I guess it becomes philosophical whether to include this in a primer on ICP treatment for non-neurointensivists, but it is a great point to make. I think the additional monitoring modalities will be nice for CPP optimization, but even now you can plot each sequential MAP increase and the resulting… Read more »
Peter, Had to spend a while thinking this through, but it was v. good b/c I just garnered a whole new vision on Osm. Just as IV bag description of pH is useless, IV bag description of Osm is irrelevant to actual clinical effects. LR is 275 in the bag. As soon as you put it into the patient, lactate will be metabolized, most of the K will go intracellular. Net effect of LR will be to drive down sodium, in effect a slightly hypotonic solution. This all gelled when you consider D5W; mOSM/L is 250, but we essentially consider… Read more »
Great and thought provoking stuff. Certainly there is a difference in solution osmolalities but while you have accounted for the distribution of the osmotically active solutes you must also consider the solvent distribution across ECF/ICF and renal handling of solutes. A greater proportion of solvent stays in the plasma with 0.9%NaCl and along with renal Na&Cl handling means (from what I understand) there is little difference in plasma sodium between the two. http://www.ncbi.nlm.nih.gov/pubmed/12519083/? But either way I think my point is not so much CSL is better then 0.9%NaCl but simply it is not so polarised anymore that TBI=0.9%NaCl and… Read more »
Hi Scott Just wanted to get your take on the diagnostic characteristics of ONSD in he ED setting. Recent metanalysis by Dubourg: http://www.ncbi.nlm.nih.gov/pubmed/21505900 Sensitivity 90%, Specificity – 85%. 4 small trials. This is OK, but imperfect when you consider the degree of badness you might be missing in that 10%. My take is that we can use ONSD to “rule in” and crank up the interventions / trip to CT. However, it still seems foolhardy to use it for a “rule out” in all but the lowest risk scenarios. Maybe serial ONSD exams will be a future substitute for the… Read more »
So here is a post with a dozen articles. But let’s pretend that Dubourg’s tiny sample is correct, with those test characteristics, you have a LR – of 0.12. Not going to find too many tests in medicine better than that.
Further, I would never use OcUS to rule out an intracranial bleed, you use it r/o the need for immediate ICP treatment. When positive, it is an indication to HAUL ASS to imaging. If it turns out to be a false positive, all you have wasted is some intern stretcher pushing time.
Hi Scott, I am a PGY-4 and when I rotated through our institutions neuroICU, One of the neurointensivists told me that he was unhappy when patients with obviously elevated ICP were intubated in the ED. He felt that we were likely not giving enough sedation/analgesia at the time in our hurry to get the tube in and were likely hurting patients by futzing around with the airway as well as possibly inadequate sedation post-intubation, all causing massive increases in ICP. He demonstrated this by going up to one of our intubated patients with an EVD and shaking the ETT just… Read more »
Doing a clean neuro-stable intubation in a patient with high ICP requires a bunch of knowledge, experience and planning. There is nothing special about it being performed by any individual specialty. Whoever does it needs to be excellent both before, during, and after. His complaint should be that these intubations are not uniformly being performed well. It should not be a complaint that they are being performed in the ED. Until medicine understands that specialty guarantees very little in terms of competence, we will continue to deal with these issues in a way that is not helpful to patient care.
Hey Scott
Writing from the UK where we don’t have a huge tradition of ED crit care and the drug availability is a bit different – what are your thoughts on thiopentone as opposed to propofol for the sedation? I remember it being hypothesised that it provided better suppression of brain metabolic demands but not sure whether there’s anything to support that?
Kirsty
absolutely, this was a mainstay prior to the ascendance of propofol.
Hey Scott, Not sure if you are going to address this in later podcasts, but how do you go about managing blood pressure in your patients with severely hypertensive bleeds? We know hematoma expansion is associated with poor outcomes in patients with ICH, and from the INTERACT trial it appears that BP control can reduce hematoma expansion (without evidence of a patient orientated benefit). The feasibility study from the ATACH trial was done and showed we could reduce the BP, but there appeared (granted in a very small pilot study) to be some non-statistically significant safety concerns. Anyways, before the… Read more »
What are your thoughts on the hypotensive patient and using propofol as the sedative of choice. I was wondering if it’s still worth using over other sedatives that may not cause as much hypotension when you’re beginning to need pressors to maintain a sufficient MAP to keep the CPP at goal. Basically, does propofol + a pressor have more benefits than other sedatives that may not require a pressor?
Propofol is nice b/c if you go too far, you can turn it off. In a hypotensive patient all of the pressors will drop BP from loss of endogenous catechol. So it becomes a style issue. No reason you couldn’t use midazolam for these patients, which is just a bit more hemodynamically stable.
In regard to your recommendation to do optic nerve u/s to screen for increased ICP, why not just look at the fundus for the presence of venous pulsations? It is quick and easy once learned, and requires no special equipment. If venous pulsations are present, ICP is less than 190 cm H2O and thus is not elevated. Absence of venous pulsations suggests that ICP is higher than that, although 10% of normals may have it. Also helps distinguish papilledema from pseudopapilledema. J Neurol Neurosurg Psychiatry 2003;74:7–9
If indeed you find it quick and easy, go for it. Most do not. When I have my panoptic and the patient gaze is midline, I agree not so bad. Trying it with the wall opthalmascopes is a no go. The ultrasound exam is truly quick and easy and has far more literature to validate it.
ok, i am clearly way behind but…….
Where’s ketamine? As I have to often sedate the head pt with borderline BP, might not ketamine be the answer?
Mike
Hi everyone- as a new listener, I would like to ask the community about another non-surgical intervention in this context: Reversal of anticoagulation in anticoagulation-associated intracranial hemorrhage (aaICH), which is a condition I see quite often. We routinely get these patients´ INR back to normal within the first hour with Prothrombin Complex or FFP. In my opinion, the evidence for doing this is rather small, and there seems to be a trend towards the idea that it doesn´t help at all. (Dowlatshahi et al in Stroke some months ago) With the advent of the new oral (and unantagonisable) anticoagulants, what… Read more »
Patrick,
Welcome aboard. Can’t say I agree with your contention on reversal of warfarin. I’ve yet to meet a dissenter on the reversal of that drug, despite the absence of a RCT. If you read the discussion of Dowlatshahi’s paper (PMID: 22556194) you will see that his cohort, which didn’t even have very good reversal protocols or success had a 20% lower mortality than non-reversed cohorts.
As to dabigatran, you may want to see the page on this blog for that one, but the short answer is nobody knows. Rivaroxaban will reverse with PCCs.
Are their specific criteria and preferred pharmacology for managing both hypotension and hypertension in TBI patients?
Definitely, you can find some of it in my SAH cast, but all will be in the Neurocritical Care Society’s ENLS course coming very soon at <http://enls.neurocriticalcare.org>.
Hello, I am new to the emcrit podcasts and I am a Paramedic Student. In this podcast it was stated that Sodium Bicarb can be used to reduce ICP. Working in rural EMS, transport times can have a negative effect on patient outcome. In this unique situation, If my patient was presenting with obvious signs of increased ICP and I was worried about herniation, would I be wrong to call medical control and request bicarb?
Hi Scott, I know that this podcast is over 5 years old but it’s still mostly up to date. I had a question about central venous access in patients with elevated ICP. All the evidence I have found says that it’s fine to use the IJV, but colleagues in my neuro-ICU disagree and always go for the femoral veins. Any thought? Who’s right? Thanks for all your great work.
nobody knows. theoretical worry is that you are occluding venous drainage by blocking the IJ, esp. if you go for a dominant IJ. I go subclavian as my primary line in these pts, but will fall back on IJ when I need to.
Would love to see some “Brain Code” scenarios….like ACLS. These could he sent to our training staff/Unit Educators to train RT,RN,Provider teams.