Link To And Excerpts From First10EM’s “The Crashing Brain: Approach to the first 10 minutes”

Today, I review, link to, and excerpt from First10EM‘s outstanding The Crashing Brain: Approach to the first 10 minutes.*

*Lin, K. The Crashing Brain: Approach to the first 10 minutes, First10EM, August 28, 2023. Available at:

All that follows is from the above resource.

This is a guest post by Dr. Katie Lin.

Dr. Katie Lin is an Assistant Professor of Emergency Medicine at the University of Calgary, a Stroke Attending with the Calgary Stroke Program, and a critical care Flight Transport Physician with STARS Air Ambulance in Alberta. She completed her residency training and stroke fellowship in Calgary and a Masters of Public Health through Harvard. She loves med ed, simulation, brains, and interdisciplinary collaboration.


You are called into resuscitation, where EMS has just transferred a 63-year-old male onto the ED stretcher. According to collateral history from family, the patient had a sudden witnessed onset of severe headache and vomiting, followed moments later by decreased level of consciousness. His current GCS is 6, O2 sats are 88% on RA, and his BP is 220/160…


Aside from status epilepticus, acute spontaneous (ie. non-traumatic) neurologic disasters generally come in one of two flavours:

  • Thromboembolic event (80%): acute ischemic stroke (AIS), cerebral venous sinus thrombosis
  • Hemorrhagic event (20%): intracranial hemorrhage (ICH), subarachnoid hemorrhage (SAH)

Unfortunately, when faced with an undifferentiated crashing brain, clinical features alone are NOT reliable for distinguishing between ischemic vs. hemorrhagic pathologies (Runchey 2010). Definitive diagnosis and management requires expedited neuroimaging, but we are often forced to empirically resuscitate before an imaging diagnosis can be established. So how do we tackle the first 10 minutes when we know we have a sick brain on our hands, but we don’t yet know exactly what kind of sick brain we’re dealing with?

Priorities in the Undifferentiated Crashing Brain

You likely already have a solid approach to immediate ABC priorities, so I won’t dwell on those here. However, I do want to focus on neuro-specific critical action items to integrate into your initial approach when faced with an undifferentiated neurological catastrophe.

A crashing brain can deteriorate quickly, and you never know where/when the tipping point is, so it’s imperative to identify impending and evolving neurological disasters early and to act fast.

The ultimate goal is to safely expedite neuroimaging (most often CT +/- CTA) in order to establish the diagnosis and arrange for definitive therapy. However, in order to safely package the patient for neuroimaging (and avoid the dreaded resuscitation in the CT scanner), we must first neuro-resuscitate.

The three most critical initial priorities in the crashing brain include:

  1. Check the glucose
  2. Perform a rapid neuro exam to identify signs of herniation and/or MAJOR deficits
  3. Avoid hypotension and hypoxia at all costs while targeting neuroprotective vital signs & airway management

Check the Glucose

Hypoglycemia can mimic many neurological disasters, including decreased level of consciousness/coma and focal neurological deficits. Thankfully, it’s a relatively straightforward problem to address. Make sure to get a blood glucose check as part of the initial ABC assessment, and if for whatever reason a glucose check is not possible or will be delayed, treat empirically with one amp (50cc) of D50W.

The 10-Second Rapid Neuro Screening Exam

Leave your reflex hammers and tuning forks behind, this is not the neuro exam you learned in med school.

When faced with a crashing brain, we need to rapidly recognize, resuscitate, and expedite imaging. All we REALLY care about in the first few moments are:

  1. Are there signs of herniation (impending or evolving)?
  2. Are there MAJOR focal deficits present? (speech/motor)

We don’t need to get fancy with it – almost all of the information that matters most to our stroke, neurosurgery, and ICU colleagues is captured in a simple 3-step approach: GCS + pupils + lateralizing motor response:

  • GCS: What is the level of consciousness and is it deteriorating?
  • Pupils: What do the pupils look like? Are they even and reactive?
  • Lateralizing Motor Response: What kind of motor response are we seeing and have we seen with our own eyes movements that are purposeful and equal bilaterally? Or is there asymmetry/posturing present?

Especially if we are pushed to rapidly intubate this patient for airway concerns, quickly taking note of these important initial findings can be invaluable for guiding decisions around definitive management later in the case when the neuro exam may be hampered by intubated status or medication effects. It could mean the difference between a “go” or “no-go” treatment decision by the neurosurgeon or stroke consultant.

A few quick notes on identifying herniation:

  • Herniation is a dynamic process, and serial assessments are critical for early detection of deterioration. The clinical trend over time is often more important than a single static assessment.
  • Early herniation is all about recognizing symptoms of rising ICP:
    • Worsening headache
    • Escalating/refractory nausea or vomiting
    • Evolving focal deficits (Cranial nerve, motor, speach)
    • Dropping GCS
  • Late herniation is all about recognizing the Cushing response and watching for pupillary changes:
    • Cushing Response Triad: ­BP, ¯HR, irregular respiration
    • Uneven pupils AND/OR non-reactive pupils

Remember that the Cushing response is a triad of vital sign derangements, and dysregulated breathing is an important sign to watch for. Respiratory patterns seen in the setting of herniation include:

It’s also important to note that NOT all herniation comes with a blown pupil:

  • Subfalcine herniation often doesn’t have ANY overt pupillary changes
  • Central hernia manifests as small, pinpoint pupils that can easily be mistaken for opioid toxidrome in the setting of low GCS
  • Uncal herniation is associated with the classic blown pupil that we’re familiar with
  • Tonsillar herniation can show up as mid-fixed, non-reactive pupils

We need to look for pupils PLUS clinical signs of herniation – symptoms or rising ICP or the labile vital signs of the Cushing Response Triad.

Avoiding the Deadly Duo of Hypoxia and Hypotension

Mortality is high in the setting of both ischemic and hemorrhagic stroke, with an estimated 30-day mortality of up to 23% in ischemic stroke and 52% in hemorrhagic stroke (Grysiewicz 2008). Within this high-mortality setting, hypoxia and hypotension have been shown to independently double the risk of death in neurocritical patients when present (Ferdinand 2016, Besmertis 2018).

Therefore, early neuroprotective resuscitation and prevention of secondary neurologic injury begins with the immediate correction of any existing hypoxia or hypotension and avoiding it at all costs throughout the resuscitation process. This means prioritizing IV access for early fluid and/or vasopressor support, as well as aggressive escalation of supplemental oxygen and preparation for intubation where needed.

Neuroprotective Vital Signs

Cerebral autoregulation functions best within certain parameters of oxygenation, blood pressure, PaCO2, temperature, and glucose. In the setting of an acute neurologic insult, the mechanisms of autoregulation are disrupted, leading to an even narrower window of neuroprotection.

The optimal targets are different for ischemic vs hemorrhagic causes:

  • AIS: BP needs to be higher to drive perfusion past the point of occlusion (ie. around a partial occlusion or via collateral blood flow)
  • ICH/SAH: BP needs to be lower to reduce hematoma expansion

BP targets in the setting of AIS or ICH/SAH are a challenging subject of ongoing research and numbers will vary depending on which guideline is being referenced.

My simplified pragmatic recommendation*: until you obtain an imaging diagnosis and can target your definitive hemodynamic goals, I would suggest aiming for the following in an undifferentiated neurocritical patient:

  • If HYPOtensive: target MAP >80 mmHg
  • If HYPERtensive: target SBP <180 mmHg

*Note that these are pragmatic recommended BP targets based on my consideration of the existing literature and guidelines on AIS/ICH/SAH management, rather than any specific guideline recommendation. 

Why these targets?

Because they represent a generally safe middle ground between the opposing needs of a potential AIS vs a potential ICH/SAH. Not too low (risk of hypoperfusion), and not too high (risk of bleed/hematoma expansion). If the patient turns out to have an AIS (80% of acute stroke cases), reperfusion therapy can immediately be initiated as the BP will be within guideline treatment range (whether for IV thrombolysis or mechanical EVT). If the patient turns out to have ICH (20% of acute stroke cases), then you have already started to lower the BP to minimize ongoing risk for hematoma expansion.

For other vital sign parameters, target as close to normal as possible to prevent secondary injury:

  • SpO2 >94%
  • Temperature <38C
  • PaCO2 35-40 mmHg
  • BGL 4-10 mmol/L*

*Links to Conversion Table (mmol/L to mg/dl)  for Blood Glucose Monitoring from the Joslin Diabetes Center.

Neuroprotective Airway Management

Is your patient:

  • Actively vomiting?
  • Too agitated to lie still?
  • Rapidly dropping their GCS?
  • Having apneic spells?

If so, it’s time to think about airway capture BEFORE you send the patient to neuroimaging, or you might find yourself getting called to tube in the scanner. The threshold to intubate in the setting of a suspected intracranial disaster is lower to ensure that time-critical neuroimaging can be completed quickly and safely.

But HOW are you going to safely capture this neurocritical airway without worsening the neurological outcome?

In the crashing brain, when things are going downhill fast, choose RSI. There is no single “Right Way”, but rather the best approach is the approach you know well and wield often. Choose the tools YOU are most comfortable with and don’t complicate things by adding unfamiliar elements under stress. Bonus points if your routine approach is hemodynamically sound.

For me, this looks like:

  • Preoxygenation with NRB over HFNC at flush
  • Pretreatment with antiemetic (if vomiting) or vasopressor (if hypotensive) while setting up the rest of my equipment
  • Head of the bed at 15-30o
  • Ketamine or Etomidate induction (BP can drop precipitously during induction when cerebral autoregulation is compromised, even in initially hypertensive patients)
  • Rocuronium paralytic
  • Propofol + Fentanyl post-intubation sedation
  • Neuroprotective ventilation settings (target PCO2 30-35 and O2 sats >94%)

It all comes back to avoiding HYPOXIA and HYPOTENSION at all costs.

If I have a few additional minutes to prepare in advance, I might consider optimizing by including a few finesse items, but only if I and my team have the bandwidth to do so (these are “nice-to-have”, not “need-to-have”):

  • Pre-treatment with analgesic and/or antihypertensive (if hypertensive – fentanyl should be first line)
  • Fentanyl 3-5 mcg/kg IV (3 minutes prior to intubation)
  • Lidocaine spray for the cords (to reduce the ICP spike that can occur with laryngeal stimulation)

Final Thoughts & Key Take-Homes

The next time you’re faced with a neurocritical disaster, remember:

  1. Early recognition hinges on serial rapid neuro assessments to identify signs of herniation (­ICP symptoms, pupils, Cushing Response triad) and major neurologic deficits (speech/motor/level of consciousness).
  2. A rapid neuro exam for critical findings can be accomplished quickly and simply with the 3-step approach of: GCS + pupils + lateralizing motor response.
  3. Focus on avoiding and correcting HYPOXIA and HYPOTENSION aggressively throughout all phases of resuscitation and airway capture.


  • Runchey and McGee. Does this patient have a hemorrhagic stroke?: clinical findings distinguishing hemorrhagic stroke from ischemic stroke. JAMA. 2010;303(22):2280-6. Doi: 10.1001/jama.2010.754.
  • Grysiewicz, Thomas, and Pandey. Epidemiology of Ischemic and Hemorrhagic Stroke: Incidence, Prevalence, Mortality, and Risk Factors. Neurol Clin. 2008;26:871-895.
  • Ferdinand and Roffe. Hypoxia after stroke: a review of experimental and clinical evidence. Exp Transl Stroke Med. 2016;8:9. Doi:10.1186/s13231-016-0023-0.
  • Besmertis, Bonovich, and Hemphill. The role of hypotension in secondary brain injury after intracerebral hemorrhage. Stroke. 2000;32:358.
  • Yartsev, A. Brain Herniation. Deranged Physiology. 2023. URL: Retrieved Aug 1, 2023.


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