Brain MRI

This is a subject that I get asked about a lot by students. MRIs are tougher that CTs to read and yet can offer a lot of diagnostic assistance. I’ll be honest, 99% of the time, I rely on the neurologists or neuroradiologists to read these studies. That works for me because, honestly, we never really get these studies stat at our place. So, almost never is an MRI so important that I have to know right away what it shows. But, I’ve become convinced that that is a sort of lazy attitude. And so, I’m making an effort to learn how to better read Brain MRIs. So, you’re in luck, because as I learn, I’m going to pass that on to you. For now, what I’m passing on are a bunch of good resources.

Radiopaedia is ALWAYS a good place to start when looking for all things radiology. They have a really nice Brain MRI course that was a live event a few years back. You can register for the course still and watch the recordings, but there is a cost. For most of us who just want the basics, there is a pre-course video on YouTube that serves as a nice intro.

Rutgers neurology has another really nice video as well. This Brain Imaging Crash Course covers more than just MRI, they address MRI as well as head CT in a nice case-based format (you know I love case-based learning). It doesn’t go terribly in depth, but I suppose that’s why it’s called a crash course instead of “Everything You Need to Know About Brain Imaging.” Another good starter.

If the written word is more your speed, here are two great resources. The first is an excellent Tweetorial introduction to Brain MRI from Lee Alhilali, MD.

And finally, a great blog post from Tom Lawson called simply, “How to read a Brain MRI.” Simple and straightforward, written by a neurointensivist nurse practitioner, it covers what you need to know in neurocritical care. Incidentally, his blog “neurosciencecriticalcare” is a good site and worth bookmarking if you spend time in the neuro ICU.

There you have a few basic intro resources for reading brain MRIs. Some of you will no doubt want to go deeper, but this is a great starting place. For me, this is what I need to know right now. I’ll let you know if I decide to delve more into all the depths of MRI.

Brain Bleeds on CT

Head CTs are often mysterious to people who don’t practice neurocritical care (or related specialty). But there are some things that are not so subtle and a large hemorrhage is among them. But, there are a few different types that you should be able to differentiate between. It’s critical to be able to differentiate between a subdural hematoma and an epidural hematoma, as one is almost always a medical emergency. Through in subarachnoid hemorrhage and you’ve got three types of hemorrhage to sort out.

Medical Guidelines has a nice Instagram post to help you out.

Spontaneous ICH

Spontaneous Intracranial Hemorrhage (ICH) is one of the more common things we see in the Neuro ICU. This is most commonly caused by hypertension, and so blood pressure management is usually a key part of ICU care in these patients. There is a fine line to walk between proper brain perfusion and increasing further bleeding. The other major pharmacological question involves reversal of oral anticoagulants that the patient may be taking. Although it’s not usually the cause of the bleed (again, hypertension, possibly in concern with anticoagulants is most likely; other causes include aneurysm rupture, vascular malformation, and malignancy), they can certainly exacerbate the bleeding.

@emergencymeded has a great post on Instagram covering the basics of pharmacological management of these patients. They point out that BP targets are controversial. I think controversial may be too strong, the guidelines generally recommend SBP < 140, but they do point out 2 large trials, INTERACT II and ATACH 2 both suggest that there is no increase in negative outcomes by allowing SBP up to 180. For management, labetalol and nicardipine are the mainstays of therapy. I generally start with 10-20mg labetalol IVP q1h PRN. If that is insufficient or if there are contraindications to beta blocker therapy, you can add 10-20mg hydralazine IVP q1h PRN (although this is rarely sufficient). If you’re still not able to get good control, or if you’re having to give lots of PRNs, a nicardipine gtt is the next best step. Although, be aware that due to it’s longer half-life, nicardipine isn’t really truly titratable. Once you get BP in range, it’s a good idea to back off a little on the dose to avoid overshooting. Clevidipine is probably a better option, but it’s pretty expensive so not as readily available. With a half-life of around 1 min, clevidipine is a truly titratable drug. Be aware that it is a lipid emulsion and can easily be confused with propofol in intubated patients.

When it comes to reversing oral anticoagulation drugs, the first question to ask is, “should we reverse?” Patients are on these drugs for a reason, after all. This is a decision that needs to be made after a careful risk:benefit assessment. In most cases though, you’ll end up reversing these drugs to prevent worsening of the bleed. There are 2 different strategies to reverse these drugs, targeted and non-targeted. Targeted involves giving an “antidote,” that is a specific reversal agent. Vitamin K for warfarin (although it doesn’t work fast enough and you’ll want to give FFP or 4-PCC as well), idarucizamab for dabigitran, and andexanet for the Xa inhibitors. Andexanet is not widely available due to cost and questions of efficacy. Non-targeted involves giving clotting factors that reverse all drugs. This is predominately 4-factor prothrombin complex concentrate (4-PCC) as FFP won’t reverse the Xa inhibitors and 4-PCC has been shown to do a better job of reversing warfarin than FFP. I’ll do a whole post soon on reversing anti-coagulation drugs.

Melatonin for the Prevention of ICU Delirium

Delirium is a common problem in the ICU. The reason is usually multi-modal, but sleep deprivation and alterations in the sleep-wake cycle are often a big part of it. so, if we ensure that patients get good sleep, that should prevent delirium, or at least SOME cases, right? to that end, we often will start patients who we deem at-risk for ICU delirium on melatonin in order to help them sleep and thereby prevent delirium. But does it actually work?

Pharmacy Joe looks at a recent study examining the efficacy of melatonin as a preventative strategy for ICU delirium and the results were not what I was hoping to see. The study was a multi-center RCT of around 800 patients in ICUs across Australia. Patients in the study group were all given 4mg of melatonin every night during their ICU stay. All patients were assessed twice daily using the CAM-ICU for delirium. There was no significant differences between the study group and the control group in terms of delirium.

One thing that isn’t clear is if 4mg might not be enough. Although I typically start with 3mg, I will often escalate it to 6mg pretty quickly if 3mg doesn’t seem to effective. I also typically don’t start melatonin until either the patient or the nurse complains of poor sleep. Further study is needed to determine if melatonin plays any role in delirium prevention.

For right now, it seems that the best strategy to prevent delirium (and we know that prevention is superior to treatment) is to focus on the nonpharmacological interventions. Maintaining a normal sleep-wake cycle is key. I encourage lights on during the day and having the TV on if there are no visitors to converse with the patient. It’s ok for patients to nap, but they shouldn’t be sleeping all day. If able, ambulation in the hallway or at least being up to the chair are beneficial as well.

Likewise, minimizing disturbances at night are important. Often patients are very ill and staff need to be in and out of the room frequently, but if possible, minimize these disturbances. Lights should be left off or low as much as possible. Don’t leave the TV on all night in the room. And, remember that sedation does not = sleep. I was a night shift ICU nurse for 10 years and often saw that the same care not to disturb day/night cycle was not observed in patients who were sedated.

The biggest pharmacological therapy you can do for prevention is to avoid the use of drugs known to cause or exacerbate delirium. The big offenders here are benzodiazepines. Benzo drips should almost never be used except in the case of status epilepticus. They were also found to be helpful in some cases of COVID back in 2020-2021 when nothing else would keep patients sedated, but they should be avoided in most cases.

The Critical Illness, Brain Dysfunction, and Survivorship (SIBS) Center has some great resources on delirium prevention and treatment.


I want to talk about Paroxysmal Sympathetic Hyperactivity (PSH), or brainstorming as it’s sometimes called. This is something we see not uncommonly in neurocritical care, but I feel like it’s often misunderstood. I sometimes hear, “I think they’re brainstorming,” thrown around as a possible explanation to any number of symptoms in a patient with any kind of brain injury. But, not so fast. PSH has specific ways that it presents and is much less common in stroke and anoxic injuries than in TBI. So, let’s don’t be so quick to write those symptoms off.

TBI is the most common condition leading to PSH, with 80% of PSH cases happening in TBI patients. 10% in anoxic injury and 5% each in stroke and “other.” There is also no definitive test for PSH, so it’s largely a diagnosis of exclusion. the other thing to keep in mind is that PSH correlates at least somewhat with the degree of brain injury. So, if you have a patient with a relatively minor ICH but symptoms suggestive of severe acute PSH, that deserves some further investigation.

In the ICU, we mainly use 2 strategies to deal with PSH, stopping the episodes and preventing further ones. In terms of stopping or controlling episodes, propofol, opioids, and benzos are the mainstay. If you have a patient with severe storming, its likely that they’re intubated, so a propofol infusion can help to control the episodes along with providing sedation. Morphine is the commonly used opioid for stopping a storm, but fentanyl may work faster.

In addition to stopping storms, you want to prevent future ones. Propranolol is my first go to drug here, but you have to be careful in people with reasons to avoid beta-blockade(bradycardia, hypotension, heart blocks). Gabapentin can also be helpful, with the added benefit of helping in patients with neuropathic pain. If you don’t need to big gun sedation of propofol to stop a storm, dexmedetomidine can provide some lighter sedation and serve to prevent storms.

Bottom line, the most important take home message is, be sure that you’ve excluded other pathologies before settling in on PSH as the cause of your problems. Josh Farkas has a great article over at the IBCC on PSH. Check it out here.

TXA for SAH?

Tranexamic acid (TXA) is an antifibrinolytic drug that stabilizes clots and helps to control bleeding. It is often used in acute trauma and of cases of massive hemorrhage. It is not prothrombotic, so it can help to control bleeding while not increasing clotting like some other drugs. So, is there a place for it in the initial management of aneurysmal subarachnoid hemorrhage?

Endovascular coiling or surgical clipping is the preferred management of bleeding cerebral aneurysms, but could TXA be useful in situations where surgical management is not readily available? Pharmacy Joe looks at a new study by Long and Gottlieb in Academic Emergency Medicine that seeks to answer that question.

The review of the literature included 13 studies of nearly 3000 patients and essentially concluded that there was no real benefit. Although there was no difference in adverse events between placebo and TXA, there was no difference in mortality or functional outcomes either. There did appear to be a benefit when it came to rebleeding. The study found 8.7% reduction in rebleeding among patients treated with TXA. So, there may be some benefit in reducing further complications, but more study is needed.

Check out Pharmacy Joe’s episode for all the details and links to the relevant evidence.

Neuroradiology for Intensivists

I have a particular bias towards neurocritical care. Even though I practice surgical critical care as well, I have an interest in neuro and I think that my practice in neurocritical care has really helped make me a better surgical intensivist as well. Neuro is a weird niche that scares lots of people who don’t do neurocritical care. So, another one of my favorite things is teaching on neurocritical care aimed specifically at non-neurointensivists.

So, I really like this video posted by Dr Casey Albin. Dr Albin is a neurointensivist who is one half of the NeuroEMCrit team and has been a guest on an upcoming episode of our Critical Care Scenarios podcast. She recently did a nice talk covering the basics of neuroimaging aimed specifically at non-neuro intensivists. She covers the basics of reading a head CT (which we’ve covered in detail before, here), CT Perfusion scans, thrombectomy scoring (TICI), how to identify liking cause of intracerebral hemorrhage, and more. I highly recommend it for anyone who wants a good overview of neuroradiology stuff.

Best Vasopressor in TBI?

What vasopressor do you routinely use in the management of traumatic brain injury patients? Admittedly, in my neurocritical care practice, I don’t manage a lot of true TBI patients. In our system, the only neurotrauma patients that come to the neuro ICU are isolated neurotrauma (brain and/or spine without other major trauma). Polytrauma patients go to the trauma service and are comanaged in the TICU along with neurosurgery.

But, in my limited experience, I typically use norepinephrine. I might have formerly said phenylephrine, as that used to be the vasopressor of choice in the neuro ICU. This was mostly due to the fact that at one point, we were mostly using vasopressors to augment BP in order to increase perfusion to the brain or spine, a practice that has largely fallen out of favor. In these cases, the patients often just needed short runs of low dose pressor and so phenylephrine was considered safer to run without a central line, making it appealing in this subset.

But, in the past few years, we’ve gradually shifted away from this to favoring norepinephrine. I think this is largely because we’ve seen a steady increase in the overall acuity of the patients and now those who need pressors typically need them for actual shock, not just to drive MAPs. In that case, central access is typically needed anyway, eliminating the one benefit of phenylephrine.

In this episode of the Elective Rotation podcast, Pharmacy Joe covers a recent study in Anesthesia and Analgesia that seems to favor the use of phenylephrine as the first line vasopressor in TBI patients. It was a rather large retrospective study that showed a statistically significant increase in in-hospital mortality in patients who received norepinephrine as compared to those who received phenylephrine. The study found that norepinephrine was much more common in sicker patients (higher ISS, use of ICP monitoring, comorbidities, etc.), but the authors used propensity-matching statistical analysis to account for this.

Overall, it is an interesting study but there are number of issues including incomplete data regarding shock states. Despite the propensity-matching analysis, I think it’s reasonable to assume that there is probably some bias with patients receiving norepinephrine instead of phenylephrine being sicker at baseline which may account for the difference to a greater degree than is appreciated.

What about you? What is your practice regarding vasopressors in TBI? After reading this study and/or listening to the podcast episode, will you change your practice?

Reading EEGs

A few days ago, I wrote a post on the use of continuous EEG in the ICU. I mentioned that intensivists should know some of the basics of reading EEGs. I am far from an expert in this. I have learned a few basic things. Mostly what we’re doing at this level with EEG is looking for seizures, specifically subclinical seizures. I think a good way to think of the EEG in this regard is similar to what I first learned about neurocritical care in general. Having come from a cardiac surgery background, an intensivist I worked with said, “think of everything we do in the CTICU, then do the opposite.” Not completely true, but it helped me!

I do something similar with EEGs. I compare them to ECGs. And if they look anything like ECGs, that’s bad. Brain wave activity should be much more random than cardiac electrical activity. So, an EEG that is rhythmic like an ECG is likely to be seizures. At the very least, it’s abnormal. Likewise, flat lines on ECGs represent asystole (bad) and flat lines on EEGs represent the absence of brain activity. Now, sometimes, we want this, as in when we’ve induced burst suppression to help deal with ICP crisis. But, absent that, flat lines on EEGs are usually a bad thing.

Now, of course you can learn a lot more from an EEG than that. If you’re interested in learning more about of EEGs work and the basics of how to read them, Nizam Ahmed has a really nice series of YouTube videos. I think there are about 10 of them in total, but they’re each pretty short and great for microlearning. So, check them out and delve a little more into what the EEG means. And, if you don’t really feel the need to read the squiggly lines yourself, but need some help making heads or tails out of the EEG report, Casey Albin and Neha Dangayach have you covered.

Continuous EEG in the ICU

When I first started in neurocritical care several years ago, I heard Stephan Mayer give a talk on neuromonitoring in the ICU at a conference where he talked about how continuous EEG should be as ubiquitous in the NSICU as continuous ECG monitoring is in the CCU. It made a lot of sense. After all, we don’t manage arrhythmias by looking once and then not again. We don’t assume that because the patient isn’t in a-fib at that exact moment that they won’t be in a-fib at some point (umm…Holter monitors?). But, that’s pretty much what we do with EEG.

At the time, we hardly had any continuous EEG monitoring in our NSICU. Mayer was at Columbia at the time and he proudly proclaimed that their NSICU had the capability to do continuous EEG as part of the bedside monitor package. A few years later, we still don’t have that sort of setup, but we do have a lot of more continuous EEG monitoring. The problem isn’t actually lack of neurologists (although there is a serious lack of neurologists, especially in smaller areas) but a shortage of the technologists and equipment.

In this episode of the CODA Change Critical Care Podcast, Terry O’Brien, a neurologist from Australia makes the case for greater use of continuous EEG use in the ICU and discusses briefly where he thinks this sort of thing is headed. He makes the comparison with echocardiography. A few years ago, it took an echosonographer or cardiologist to get an echo in the ICU. And, while those formal studies are still available and helpful, plenty of us do bedside echos every day in the ICU and are able to get the information that we need. I think that it’s only a matter of time before the ICU nurses are trained to apply EEG electrodes (at least some basic sort of setup) and intensivists are trained to read them (again, in some sort of basic way).

In this way, its comparable to 12-lead ECGs. Any intensivist worth their salt can read a 12-lead ECG. Now, a cardiologist, and especially an electrophysiologist, can obviously get much more information from that ECG than I can. And I think that’s where EEGs are headed. The average intensivist will be able to read an EEG for seizures and maybe some other basics, while an epileptologist can glean much more and could be formally consulted for more info. Speaking of reading EEGs, I’m working on a post about that, so if that interests you, stay tuned.

In the meantime, listen to Terry O’Brien’s talk on continuous EEG in the ICU here.