Online Module:
Traumatic Brain Injury and increased ICP
Intracranial Hematomas
Spontaneous Subarachnoid Hemorrhage
Herniation Syndromes
Traumatic Brain Injury
and Increased ICP
Practically speaking, the
brain is protected by a
rigid case, within which
there is no “extra” space.
The Cranial Vault

Skull (holds three things)
Brain
 Blood
 Cerebro-Spinal Fluid (CSF)
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An increase in any one of these three
“compartments” displaces the other two.
The principle buffer in the system is CSF.
Only small volume increases can be tolerated
before intracranial pressure (ICP) begins to rise.
The Monroe-Kellie Doctrine

Increase in one constituent necessitates a
compensatory decrease in the volume of
another constituent.
Compliance

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Because the three constituents that take up
residence within the cranial vault are housed
within a relatively rigid container, small increases
in volume can drastically increase the intracranial
pressure
This is the concept of compliance.

Compliance = change in volume/change in pressure
Normal Cerebral Metabolism

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Brain tissue relies on aerobic metabolism – gets
starved for oxygen very quickly because it has
no real backup energy reserve.
Normal cerebral metabolism requires a blood
flow of approximately 50 mL/100g/min.
Serious neurological deficits begin to occur at 20
mL/100g/min.
Prolonged Cerebral Blood Flow > 12
mL/100g/min. results in cerebral infarction.
MAP and ICP

MAP = “Mean Arterial Pressure”
Defined as: [(2 x DBP) + (SBP)]/3
 This is literally the average arterial blood pressure
over a single cardiac cycle.
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ICP = “Intra-Cranial Pressure”
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15 mmHg is getting into the upper limits of normal
in you and me.
MAP – ICP = CPP
Cerebral Perfusion Pressure
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Cerebral Perfusion Pressure is key to brain tissue
survival.
CPP = MAP – ICP
This takes measurable physiologic parameters
into account to determine if the individual is
able to adequately oxygenate brain tissue. It is
the net pressure of blood delivery to the brain.
In a normal adult, CPP is generally regulated
between 70 and 90 mmHg (can be more or less).
Cerebral Metabolism
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In the uninjured brain, the arterioles regulate CBF to
the brain over MAPs ranging from 50-150 mmHg.
Outside of this range, the arterioles lose the ability to
autoregulate, and blood flow becomes dependent upon
blood pressure (this is called pressure-passive flow).
MAPs less than 50 run risk of ischemia due to
decreased blood flow, while MAPs greater than 150
causes excess CBF that can contribute to increased
intracranial pressure.
Autoregulation is impaired in the injured brain.
Cerebral Autoregulation
Summing that up 
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Normal anatomy implies a fixed space in skull
where small increase in volume causes large
increase in pressure.
Perfusion of brain tissue is impaired by anything
that’s taking up space or decreasing blood
delivery to the tissue.
Normal autoregulation processes that help the
brain maintain homeostasis are impaired after
injury.
The TRAUMATIC neuro exam

When dealing with “Emergency” neurological
evaluation, you MUST MUST MUST MUST
MUST KNOW the concept of the Glascow
Coma Scale!!!!!!!
Clinical Assessment: GCS
Diagnostic Imaging
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This is a great way to get past the handicap of
having a relatively inflexible surface to evaluate.
Often provides you the information you need to
ANTICIPATE a problem or PREVENT its
occurrence before it becomes clinically apparent.
Newer diagnostic imaging modalities have
REVOLUTIONIZED management of
intracranial pathology (the benefit to traumatic
brain injury is immeasurable)!
“Reading head films 101”
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#1 – Identify the modality
#2 – Orient yourself
#3 – Describe what you see; don’t just try to
find what’s abnormal
#4 – Pay attention to symmetry!
#5 – Pay attention to proportion
The CT Scan
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The CT scan singlehandedly revolutionized
the landscape for headtrauma.
Allows quick evaluation
of intracranial space (and
skull).
Good for acute eval.
“Fancy X-ray”
Traumatic Brain Injury
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Two general types of injury:
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Primary – represents the direct result of the initial trauma.
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Fracture
Cerebral contusion
Vascular disruption
Secondary – results from the evolution of the initial injury or
complications. (This is what we aim to minimize)
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Hypoxia and ischemia
Cerebral edema
Intracranial hypertension (ICH)
Cerebral Ischemia

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This is the mechanism that underlies
“secondary” injury to the brain.
It all comes back around to Cerebral Perfusion
Pressure.
Remember that you’ve got two opposing forces –
the mean arterial pressure “pushing” oxygenated
blood into brain tissue, and intracranial pressure
pushing back.
 CPP = MAP - ICP

Bottom Line
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You need adequate CPP to maintain viable brain tissue.
Once past the primary injury, secondary injury sets in as
the volume of any one (or more) of the three
constituents starts to increase and cerebral ischemia
occurs.
ICP begins to rise relatively quickly once the extra
volume increases (especially beyond ~100 cc’s.)
Generally, 60 – 70 mmHG is the target CPP for
patients with TBI.
It is thought that ICP should be treated once it hits a
threshhold of 20 mmHg.
Symptoms and Signs of Elevated
ICP
 Triad

Headache, nausea, vomiting
 Cranial
nerve palsies
 Papilledema

Usually from a more chronic process
 Vital

sign changes
Cushing’s
 Arterial hypertension and bradycardia
 Respiratory
changes
Papilledema
 Swelling
of the optic nerve
head with engorgement of
the retinal veins
 Presence almost always
indicates raised intracranial
pressure.
Management of Elevated ICP:
Airway/ventilator
support
Hypothermia
Maintain adequate Neuromuscular
CPP
blockade
Osmotic diuresis Barbiturate coma
Hypertonic saline Glycemic control
Sedation/analgesiaCSF drainage
Craniectomy
Therapeutic Modalities
for Reduction of ICP
Intracranial
Hematomas
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Epidural Hematoma
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Typically younger patients
Patients may present with alterations in
consciousness, headache, nausea/vomiting, etc.
Evidence of trauma: Contusion, laceration, or
bony step-off may be observed on the head
(should have high clinical suspicion).
Epidural Hematoma
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“Classic presentation”: Impact on side of head
with “lucid interval,” then CT scan
demonstrating biconvex (lenticular – “lens
shaped”) hematoma causing brain compression
and midline shift.
Deterioration can be rapid.
Prognosis is generally excellent if managed
aggressively!!!
Mortality estimated as high as 20%!
Epidural Hematoma
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Epidural Hematomas – 90% seen in head
trauma with a skull fracture that crosses a
portion of the middle meningeal artery/vein.
Middle meningeal artery is torn approximately
2/3rds of the time.
Blood which collects in the epidural space is
limited by the intracranial sutures, where the
dural membrane is closely adherent to the inside
of the calvarium.
Epidural Hematoma
Skull Fracture
Epidural Hematoma
(underneath skull fracture)
Epidural Hematoma
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Generally, treatment is surgical.
Can sometimes manage small EDHs
conservatively if they are asymptomatic (but you
still MUST get these patients to a Neurosurgeon
so that if the EDH evolves or clinical picture
worsens they can receive immediate treatment.
What really hurts these patients is delay in
diagnosis, delay in transfer, i.e. anything that
delays treatment!!!
Epidural Hematoma
Epidural Hematoma
Subdural Hematoma

Come in three different “flavors”:
Acute
 Subacute
 Chronic
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Don’t be fooled!!! Acute to Chronic SDHs are
different clinical entities!
Acute Subdural Hematoma
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About twice as common (or more) as EDHs.
Major difference compared to EDH – magnitude of
primary injury is usually much higher in acute SDH
(mortality is HIGHER!).
Two most common causes of Acute SDH:
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Accumulation of blood around parenchymal laceration
Tearing of surface/bridging vessels from accelerationdeceleration during violent head motion
Mechanism of injury: “brain rattles inside head.”
Much higher risk in patients on anticoagulation!
Acute SDHs
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Typically an older patient who suffers some type
of head injury (or suspected injury) and gets a
CT scan in the ER.
Radiographically, what you typically see is a
HYPER-dense CRESCENT-shaped fluid
collection that CROSSES SUTURE LINES!!!
Associated parenchymal bleeding, even
subarachnoid blood is not an uncommon
finding.
Acute SDH
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30-day mortality is between 50 and 80%!
Dramatic difference between mortality of EDH
and Acute SDH is secondary to the magnitude
of primary brain injury, which is typically much
greater in the setting of Acute SDH than EDH.

Also they are usually older patients.
Acute Subdural Hematoma
Acute Subdural
Hematoma
Acute Subdural Hematoma
Acute Subdural Hematoma
Acute Subdural Hematoma
Compare: EDH vs acute SDH
Chronic SDHs
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Generally occur in elderly (avg age of presentation is 63
yrs)
Other risk factors: alcohol abuse, coagulopathies, fall
risk, seizures, etc.
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Anything that impairs blood clotting, coagulation, etc.
Patients can present any of a multitude of different
ways: TIA-type symptoms, headache, confusion,
lethargy, speech trouble, weakness, etc.
Often, no known history of trauma or event.
Chronic SDHs
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Prevailing thought is that Chronic SDHs evolve
from small / asymptomatic acute SDHs.
Blood within the subdural space causes
inflammatory response; fibroblasts invade,
neomembranes form, neovascularization occurs.
Chronic SDHs can be very complex, multilobed structures.
Tend to gradually get larger over time.
Chronic SDHs
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On CT scans, these are CRESCENT-shaped
HYPO-dense lesions that cross suture lines.
Not uncommon to see lobules within the fluid
collection.
Not uncommon to see subacute or even acute
blood within a chronic SDH.
Treatment is surgical when symptomatic or
(generally speaking) once thickness exceeds 1cm.
Chronic SDHs
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Bilateral occurrence as
often as 25% of the time
Acute vs. Chronic SDHs
Radiographic difference between
SDH types: Timeframe
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Acute SDHs – hyperdense (less than one week
old)
Subacute SDHs – isodense (between five days
and three weeks old)
Chronic SDHs – hypodense (between three
weeks and 3-4 months old)
Understand

Acute SDHs, like EDHs, need to be diagnosed
immediately.
If Neurosurgery service is not available, these
patients must be transferred to hospital where it IS
available.
 Delays in diagnosis, transfer, treatment, etc. can
(and do) kill patients!
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Intracerebral hemorrhage
ICH
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In adults, this is the second-most common form of
stroke (~30%) and by far the most deadly.
Typical onset during activity, with headache; also N/V
Age > 55
Hypertension (greatest association)
Drug use
Coagulopathy, liver dysfunction, etc., all associated with
poorer outcomes.
ANY prior CVA increases risk 23 times!
ICH
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Four most common locations:
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Basal Ganglia (Putamen, in particular)
Thalamus
Deep Cerebellar Nuclei
Brainstem (Pons by far)
Despite extensive study, the role of surgery in
management of ICH is largely unclear.
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Surgery never shown to improve long-term outcome over
best medical management (Cerebellar hemorrhage is
exception)
Cerebellar ICH
Other causes of ICH
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Tumor
AVM
Cavernous malformation
Etc.
Angiography should be
done, if at all possible,
whenever you get a
patient younger than 55
with an ICH.
Subarachnoid Hemorrhage
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The most common cause
of Subarachnoid
Hemorrhage (SAH) is
TRAUMA!!!!!!!!
Ruptured intracranial
aneurysms responsible
for 85% of spontaneous
SAH.
Aneurysmal SAH

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Aneurysms tend to occur at bifurcations or
branching points of major cerebral vessels along
the circle of Willis.
As a general rule, 30% in the anterior circulation
(AComm), 30% in the middle circulation (ICA,
MCA branching points), 30% in the posterior
circulation (PComm), and 10% in the basilar
circulation (Basilar bifurcation, PICA, etc).
Spontaneous aneurysmal SAH
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As a general rule, Neurosurgery patients don’t
come any sicker than aneurysm ruptures.
1/3 either don’t make it to the hospital or don’t
survive the first week after rupture.
Of those who survive, half are left with serious
neurological sequelae. Morbidity is high, and
mortality in first six months approaches 50%.
Aneurysmal SAH
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Classic presentation is the sudden onset of the
“worst headache I’ve ever had in my life.”
Nausea, Vomiting.
Decreased mental status
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Can be due to acute hydrocephalus, necessitating
ventriculostomy/EVD placement
Three major complications from
aneurysmal SAH
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An aneurysm can RE-bleed! Greatest risk is
within first 24 hours, then drops exponentially
Vasospasm! This can lead to stroke. Greatest
incidence of symptomatic spasm is between 4
and 10 days after rupture
Hydrocephalus, communicating type. Can
present even months after a bleed.

Acutely, you can have obstructive hydrocephalus.
Aneurysms
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Much more common in
the population than you
might think
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Some estimates as high as
10%.
Outpatient f/u for
incidental aneurysms is
appropriate.
Risk of rupture at any
given time is LOW
“Triple-H therapy”
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Hypertension
Hemodilution
Hypervolemia
Also, Nimotop 60mg PO q4h is started
immediately (for vasospasm prophylaxis) and
continued through post-bleed day #21.
Treatment of Aneurysms
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Incidentally found aneurysms do not necessitate
treatment; patients may choose to seek
treatment or not.
Ruptured aneurysms must be treated
Craniotomy and clipping
 Endovascular treatment (newer treatment modality)
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What you can do

In any suspected intracranial hemorrhage,
traumatic brain injury, etc., there are some
principles you can remember and things you can
do…
Labs
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In addition to all of the “normal” labs that are
drawn in the ER setting, make sure you order
coags (PT, INR, PTT) and start to correct any
existing coagulopathy appropriately.
FFP
 Vitamin K
 Platelets

Blood Pressure

Take care not to “bottom out” blood pressure
just because it’s high. Remember, the body is
trying to maintain CPP.
In the setting of an EDH or SDH, blindly reducing
a patient’s BP can accelerate neural injury.
 In the setting of intraparenchymal hemorrhage,
shoot for a BP between 140 and 160 systolic; the
idea is drawing a balance between decreasing BP to
help stop the bleeding, and protecting the ischemic
penumbra.

Blood Pressure (cont’d)

In the setting of a ruptured aneurysm, allowing
a patient to be extremely hypertensive can
predispose to re-rupture of the aneurysm.
Herniation Syndromes
Remembering the “Box”

Increased ICP contributes to cerebral ischemia,
but remember that an expanding mass lesion
displaces its surrounding constituents. Since the
intracranial volume is generally considered to be
“fixed,” past a certain point that extra volume
has to go somewhere.
Pertinent Anatomy considering
herniation syndromes

The intracranial compartment is divided into 3
compartments by 2 major dural structures, the
falx cerebri and the tentorium cerebelli. The
tentorium cerebelli divides the posterior fossa or
infratentorial compartment (the cerebellum and
the brainstem) from the supratentorial
compartment (cerebral hemispheres).
Pertinent Anatomy considering
herniation syndromes

Both the falx and the tentorium have central
openings and prominent edges at the borders of
each of these openings. When a significant
increase in ICP occurs, caused by either a large
mass lesion or significant cerebral edema, the
brain can slide through these openings, a
phenomenon known as herniation. As the brain
slides over the free dural edges of the tentorium
or the falx, it can sustain injuies caused by the
dural edge.
Herniation Syndromes
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Uncal
Subfalcine
Tonsillar
Uncal Herniation
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When people talk “herniation”, this is it.
The uncus of the hippocampus is pushed across
the tentorial notch into the posterior fossa.
Clinical Presentation
Ipsilateral “blown pupil.”
 Compression of ipsilateral cerebral peduncle
(Contralateral hemiparesis).
 Compression of ipsilateral PCA (Occipital
infarction).

Uncal Herniation
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Uncal herniation is
generally an acute
process.
Earliest consistent sign:
unilaterally dilating pupil!
Once brainstem
involvement occurs (i.e.
contralateral hemiparesis,
respiratory compromise),
damage may be
irreversible!
Uncal herniation

Preventing uncal herniation is the general idea
behind rapid diagnosis of EDHs and aggressive
management.
Subfalcine herniation
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Occurs when there is
herniation of the cingulate
gyrus beneath the falx.
Usually asymptomatic unless
causes ipsilateral (or
sometimes bilateral) ACA
occlusion (contralateral leg
weakness can be a warning
that transtentorial herniation
is about to occur!).
MOST COMMON
HERNIATION!
Tonsillar herniation
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In an acute setting, the
cerebellar tonsils “cone”
through the foramen
magnum, causing
compression of the
medulla.
Leads to respiratory
arrest.
Typically rapidly fatal.
INFRATENTORIAL
Tonsillar herniation
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Can occur with either supra or infra-tentorial
lesions, or with elevated ICP.
Can be precipitated by Lumbar Puncture!
Same type of anatomical finding demonstrated
in patients with Chiari malformation (but
chronic rather than acute).
Summary

This online module contained information from
four of your “topics.”
Traumatic Brain Injury and increased ICP
 Intracranial hematomas
 Spontaneous Subarachnoid Hemorrhage
 Herniation Syndromes
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