99% Sure He had a Subarachnoid Hemorrhage.

"We're back here!" I heard a shout coming from the back of the house.

We made our way back to the kitchen and found the patient lying on the ground with his wife standing over him, frantic.

"He was just sitting there. He was just sitting there, eating dinner, and then - poof - he complained of this massive headache out of nowhere... I kept asking if he was okay, but he just kinda doubled over... I called 911, and then he started vomiting. Is he okay?"

Spoiler alert: No. He was not okay.

He was somnolent and just kind of staring at the wall. There was vomit in the back of his mouth - a sure way to buy a tube, for the record. He was breathing but irregularly. He had bounding radial pulses and diaphoresis.

I looked at my partner and the firefighters who had just arrived to help us, "Time to go."

I then directed my attention to his wife, "when was he last seen normal?"

"Like 10 minutes ago, he was fine 10 minutes ago."

"Does he have any medical problems?"

She handed me a File of Life record on him, "here."

He had a history of hypertension, hyperlipidemia, and probably an MI in the past, given his meds. He was seventy-five and looked relatively in shape, to be honest.

We got him out to the truck and my partner put him on the monitor and got some vitals.

His HR was 55 and his BP was 220/136. His SpO2 was 100% on the non-rebreather we placed on him as we extricated. His glucose was normal and so was his temp.

Then... he vomited again.

"We need to intubate him," my partner said as I got an IV.

"Yup, let's set up."

The guy was having a massive stroke... More specifically,

I was 99% sure he had a subarachnoid hemorrhage.

Remember, there are two types of strokes: Ischemic and hemorrhagic. The vast majority of strokes are ischemic-- around 85% or so. The rest, then, are hemorrhagic. The concept is the same, but the pathophysiology and treatment are different.

A stroke is the sudden loss of brain function due to a disruption of blood flow. This disruption can be from a blockage, like in an ischemic stroke, or a ruptured vessel, like in a hemorrhagic stroke. There are two main categories of hemorrhagic stroke: Intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). ICH happens within the brain tissue itself, whereas SAH happens in the subarachnoid space.

SAH happens between the arachnoid mater and the pia mater. 75-80% of the time this is from a ruptured aneurysm and it usually occurs in the circle of Willis at the base of the skull.

SAH classically presents with a "thunderclap" headache (around 80% of patients will describe this) that happens instantly and reaches maximal intensity within minutes. SAH can also be associated with neck stiffness, limb paralysis, pupillary changes, altered mental status, loss of consciousness, nausea, vomiting, and photophobia. Our patient here had this presentation and was frankly altered, and thus, a poor historian... But this guy is having a massive head bleed and already has signs of devastating consequences.

Blood in the cranial vault is bad for a few reasons.

Number one, intracranial bleeding can increase the intracranial pressure (ICP). The skull is a fixed space with a fixed volume inside - there is no room for anything else. The cranium essentially contains three things: Brain, blood, and CSF. The stuff takes up 100% of the volume in the skull and exerts pressure against it. This is called the intracranial pressure. You ALWAYS have intracranial pressure - it's around 5-15 mmHg and varies depending on position, activity, etc. Anything >20 is considered "raised" and can lead to badness.

Here, this guy popped a vessel and is actively bleeding into this space... This wants to take up room in the cranial vault too - and it does. For a while, your body can compensate for this, but not very long. Eventually, this blood takes up more and more room, and suddenly your ICP spikes. This puts pressure on things and can lead to herniation, decreased brain perfusion, etc.

In this guy, this happened VERY quickly. He reached critical mass within minutes... The sudden rise of ICP led to a complete cessation of the cerebral circulation and rapid LOC. This cerebral hypoxia led to the development of cerebral edema and acute ischemic injury (stroke). His brain is tight, and his body is trying to keep blooded headed up there - which is why his BP is so high…

I wrote a TBI post where I go into all of this stuff more, so check that one out for more details!

Anyway, the second big jam here is that blood is pretty caustic. It is meant to be inside your blood vessels and when it leaks out, it's very irritating to the tissues - this can actually cause cell death, edema, etc. by itself. The big deal with it though, is seizures.

So this guy is left with this scenario where his head is tight, full of edema, and he is getting worse and worse by the minute. He is altered, has lost his ability to protect his airway, and is only getting worse.

The treatment goals in SAH are to support the patient's ABCs, decrease the ICP, and reduce the risk of re-rupture!

Re-rupture? Yup! Re-rupture. Up to 20% of aneurysmal patients will have a recurrent hemorrhage within the first 72 hours. These carry a mortality rate of over 75% - so it's important to prevent it!

Back to the scenario:

You have an elderly guy who has a sudden headache and essentially collapses. He's minimally responsive and is vomiting into his airway... He's profoundly hypertensive and at high risk of re-bleeding... We need to address all of these things.

For us, we decided to intubate him first. We pre-oxygenated with both an NC and NRB until his SpO2 was 100% and then left it there to continue to provide nitrogen washout. We then gave our meds, including a sympatholytic dose of fentanyl, and performed a neuro-protective intubation with his head of bed elevated. The tube passed quickly, and the procedure was done very gently so as not to worsen his hypertension.

I have a whole FB post about neuro-protective intubations too, so check that out!

Once he was intubated, we ventilated him with a BVM with the goal of normoxia and avoiding hypoxia by all means necessary - something that nearly doubles mortality in head bleed patients, and we kept a goal of normocarbia.

The next big things to consider are BP control and post-intubation sedation. Now, if this guy was on blood thinners, that would be a thing to consider too - but he's not so we won't get into that. The goal now is to limit the risk of rebleeding and preventing secondary brain injury.

Now, this is all protocol dependent, etc. and most services aren't in the business of lowering BPs - they generally try to raise them - so the following is more of an ED/CC transport thing and less of an EMS thing…

This guy is hypertensive. He is bleeding into his brain, and a BP of >160 is associated with an increased risk of re-rupture - we desperately need to avoid that - which is counterintuitive if you've learned anything about BP management in TBI. The goal is to keep the SBP <160 or <140  or keep the MAP <110 - the neuro folk will argue one vs the other. This reduces the risk of re-rupture.

TXA can be considered in these bleeds, but the jam in EMS is that we don't know it's a bleed because it hasn't been confirmed by CT yet. Plus the evidence to support this is... eh... at best.

So what are some things WE can do to reduce ICP? Because this is well within the realm of EMS actions.

First, keep the head of the bed >30 degrees. This is important for several reasons, but specifically in neuro patients. Don't lay neuro patients flat. We can also keep their neck midline to allow venous drainage, ensure normothermia, ensure euvolemia, treat seizures if they occur (very aggressively), and, really importantly, we can treat pain and nausea - both of which can significantly increase ICP and BP and put the patient at an increased risk of rupture. Really, treat their pain aggressively. If they are intubated we can induce a deep sedation and, if your protocols allow, we can give things like hypertonic saline or mannitol. Lastly, we can avoid obnoxious stimuli - but this may be kinda hard in the back of a moving box.

Some other things to consider, depending on your protocols could be things like fever prophylaxis, seizure prophylaxis, and the treatment of cardiopulmonary complications of SAH like stress cardiomyopathy and neurogenic pulmonary edema - both of which are bad signs.

These patients can also have ECG changes, so get a 12-lead if you have time, but this is obviously not the highest priority. Look for things like QT prolongation, a high R-wave, deep, symmetric T-waves, and peaked P waves - these can all be signs of neuro-badness.

So, for this guy, what did we do?

Well, he got intubated, placed an OGT - WHICH EVERY INTUBATED PATIENT SHOULD HAVE (I will die on this hill), we sat him up, put some towel rolls next to his head to keep him in line, and kept him nice and sleepy with some fentanyl and midazolam post-intubation. We kept his EtCO2 around 40 as best we could without a vent and a gas and did an ECG while calling into the closest appropriate facility.

Our closest appropriate facility was a tertiary care center about 15 minutes away, thankfully! But this is an important thing to consider too.

What are your thoughts? Have you ever treated a patient like this? How'd it go? Do you have any questions? Let me know below! If you have ideas for other topics/calls for these kinds of posts, let me know that, too. I am always looking for ideas!

-Dean Stockley

References:

Ajiboye N, Au, YK, Shah, OS. Ch. 4: Cerebrovascular Emergencies: Aneurysmal Subarachnoid Hemorrhage (SAH). The Jefferson Manual for Neurocritical Care. King Printing Company, 2021.

Nelson, AM, Mase, CA, and Ma, OJ. Ch. 166: Spontaneous Subarachnoid and Intracerebral Hemorrhage. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill Education, 2020.

Singer, RJ, Ogilvy, CS, and Rordorf, G. Aneurysmal subarachnoid hemorrhage: Treatment and prognosis. UpToDate. 2023. Accessed from: https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis?search=subarachnoid%20hemorrhage%20treatment&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H1332326243.

Wartenberg, KE & Mayer, SA. Ch. 14: Subarachnoid Hemorrhage in the Neurocritical Care Unit. Neurocritical Care, 2nd ed. Cambridge University Press, 2019.