Presentation1 part one - TBI and the work up

Traumatic Brain Injury and the
Neurosurgical Patient
Edward J Skicki, DO
Trauma Surgeon
Department of Surgery
Division of Trauma and Acute Care Surgery
Lancaster General Hospital
Edward.Skicki2@pennmedicine.upenn.edu
Last Updated Jan 2024

Disclosure Statement
 I have no financial interest with manufacturers or any
commercial products related to this presentation
material
 Unlabeled/unapproved use of drugs and/or devices will
not be discussed in this presentation
 Some of the educational material used in this
presentation is derived from other sources. Resources,
as best as possible, are cited throughout and at the end
of this presentation

Evidence Based Practice
 Medicine is an evolving art that practices using
evidence and expert opinion. As a result, this following
presentation is based on evidence based medicine
(with citations included) and experience regarding best
practices.
 All evidence based recommendations in this
presentation are up-to-date as of the cited date on the
title slide. Always consult current medical references in
your patient care.

Educational Use Disclaimer
 The following is for use in medical education and training.
 If reuse qualifies as medical education, material may be
reused under the condition:
– You must cite the author as a reference
– Do not modify the slide content
– If repeating recommendations from published
guidelines, do not modify the recommendation wording
– The author is notified of any erratum so that it may be
corrected

Education Objectives
1. Define Traumatic Brain Injury (TBI) and Discuss Its
Prevalence
2. Review the Pathophysiology of TBI
3. Review the Symptoms/Manifestations of TBI
4. Review a Focused Evaluation of the TBI Patient
5. Describe the Acute Management of the TBI Patient
6. Describe the Indications for Increased
Monitoring/Consultation for Surgical Intervention
7. Describe the Post-Op Management of the
Neurosurgical Patient

Before We Begin, Some Context:
Aug 8, 2017 – While driving home from work, Dylan was T-boned by
another car at 80mph only a few miles from his home.
The above photograph is not from Dylan’s accident. It and his case are used as part of this didactic reconstruction.
Source: https://triblive.com/local/pittsburgh-allegheny/1-injured-when-car-crashes-into-fence-in-front-of-troy-hill-elementary-school/

He was rushed to a nearby hospital where he was hypotensive with a
small head laceration. He was taken emergently to the OR.
Source: https://www.inquirer.com/health/a/gun-violence-shot-hospital-emergency-room-trauma-bay-penn-medicine-20190805.html

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His spleen was shattered, requiring removal. After resuscitation, he was
brought to the recovery room pending transfer to the ICU.
Source: https://www.inquirer.com/health/a/gun-violence-shot-hospital-emergency-room-trauma-bay-penn-medicine-20190805.html

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While in PACU, he did not emerge from anesthesia as expected, so he
was brought the ICU where completion CT scans were done.
Source: https://www.alfredhealth.org.au/events/basic-assessment-support-in-intensive-care-november-2018/

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He had a number of underlying cervical fractures and a yet undiagnosed
cerebral bleed requiring a return to the OR with Neurosurgery.
Source: https://radiopaedia.org/articles/cervical-spine-fractures?lang=us
Source: https://radiopaedia.org/articles/cerebral-haemorrhagic-contusion?lang=us

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Dylan survived his injuries and spent a
year and a half in recovery including
traumatic brain injury rehabilitation.
Today, he is an advocate for seat belts
and transportation safety. He and other
survivors created a photo-series for the
New Zealand Transport Agency for the
a social awareness campaign: “Belt up.
Live on.” They don makeup to recreate
their injuries and tell their stories as
trauma survivors.
The above photograph is Dylan Chirnside in makeup by PROFX for “Belt up. Live on.”
Source: https://beltedsurvivors.nz/survivor/dylan-chirnside

1
Objective 1
Define Traumatic Brain Injury (TBI) and Discuss Its
Prevalence

1
Traumatic Brain Injury (TBI)
Several definitions (CDC, DoD, etc) exist, but there is a
general consensus:
“Traumatic brain injury (TBI) is a non-degenerative,
non-congenital insult to the brain from an external
mechanical force, possibly leading to permanent or
temporary impairment of cognitive, physical, and
psychosocial functions, with an associated
diminished or altered state of consciousness.”
aka. a “concussion”

1
A Note about “Traumatic Brain Injury”
 The “silent epidemic”
 In the trauma patient, TBI is presumed until proven
otherwise, NOT vice-versa
• Falls under Disability in ATLS (Airway, Breathing, Circulation,
Disability, Exposure)
• Often overshadowed by the ABCs
• Few overt symptoms, subtle/non-specific manifestations
 Any head injury is still a traumatic brain injury
 TBI is underdiagnosed in the United States,
especially with concomitant life threatening injury

1
The “Silent Epidemic” (2013 incidence)
https://www.cohenveteransbioscience.org/traumatic-brain-injury/

1

2
https://thejns.org/view/journals/j-neurosurg/130/4/article-p1080.xml

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https://biacolorado.org/brain-injury-facts-figures/
Many people are
concerned about
sports and the
prevalence of TBI

2
https://www.cdc.gov/traumaticbraininjury/data/dist_death.html
The most common
causes of TBI change
with age (NB: Sports
are Other and Struck
by/Against)

2
What Conditions Co-Occur with TBI?

2
Cost of TBI (CDC data, 2010)
 $76.3 billion direct/indirect costs
 Approximately 100,000 are on
long-term disability due to TBI
• Accounts for 51.6% of mortality amongst
trauma patients (Dutton. J Trauma. 2010.)
 Progression of Intracranial
Hemorrhagic Injury (IHI)
(Thomas. J Am Coll Surg. 2010.)
• Longer hospitalizations (14.4 d vs. 9.7 d, p
<0.01)
• Increased mortality (24% vs. 3%, p <0.01)

2
Objective 2
Review the Pathophysiology of TBI

2
A Note on Micro to Macro Pathophysiology
 Changes at the
microscopic level are
always in flux
 An accumulation of
microscopic injury
leads to macroscopic
manifestations
• Cellular injury adds
up in an organ
• “Second hits” worsen
outcomes/survival
https://medicineforidiots.wordpress.com/2018/04/02/what-happens-in-a-reversible-cell-injury/

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Pathophysiology of Injury
 Primary Injury
• Direct trauma and damage to neural tissue
• Irreversible
 Secondary Injury
• injury to adjacent tissue due to
– decreased perfusion
– lipid peroxidation
– free radical / cytokines
– cell apoptosis
• Mechanism similar to a stroke from impaired blood flow, compression, and local injury

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https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-016-0555-1

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Mechanisms that Worsen TBI
 Hypoperfusion
 Hypoxia
 This is why Disability comes after the ABCs in ATLS

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Importance of Intracranial Pressure
 MAP is the DRIVING FORCE
 ICP is the RESISTANCE
 Cerebral Perfusion Pressure (CPP)
CPP = MAP – ICP
• <50mmHg = cerebral ischemia
• <30mmHg = brain death
 Autoregulation is limited by the body; fails if
BP and/or ICP rises

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Affects of Local Injury
https://smw.ch/article/doi/smw.2017.14538
Bleeding and Injury creates an infarct core. The surrounding “in-danger” tissue is called the
penumbra. After the injury, the core is lost and we try to preserve the penumbra.
• Seizures after TBI cause
hypoxia which worsen
the penumbra/cause
more infarct
• Overlapping oligemia areas are
functionally penumbra and
overlapping penumbra have a high
chance of dying
• After hemorrhage, the
brain clots off bleeding
areas leading to
physiology that
resembles strokes

3
Manifestations of Pressure and Poor Blood Flow
 Cerebral Edema, Midline shift
 Compression of ventricles (blocks/impairs CSF)
 New/developing infarcts (can bleed into infarcts)
https://neupsykey.com/cerebral-edema-state-of-the-art/

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Objective 3
Review the Types, Symptoms and Manifestations of TBI
and its Sequela

3
Types of Traumatic Brain Injury
 Contusion
 Chronic Traumatic Encephalopathy (CTE)
 Epidural Hematoma
 Subdural Hematoma
 Subarachnoid Hematoma
 Intra-parenchymal (Intra-cerebral) Hemorrhage
 Intraventricular Hemorrhage
 Shear Injury/Diffuse Axonal Injury (DAI)

3
TBI is Combined Bleeding, Shear & Axonal Injury
• In its simplest form, TBI
is an accumulation of
microscopic brain
damage that manifests
itself as bleeding, shear
or axonal injury
• If tissue survives, it can
partially heal but there is
always some residual
damage
• Young, plastic brain can
learn to function/adapt to
these deficits but not
always back to baseline

3
Contusions from Coup/Contrecoup Injury

4
Intracranial Bleeding
Usually diagnosed
on non-contrast CT
scans
Commonly seen
following trauma

4
Diffuse Axonal/Shear Injury
 Usually occur with sudden rotation of
the head
 Shearing forces “stretch” axons
 If axon injured but not severed, may
recover without secondary injury
 Presents with impulsivity, confusion
https://radiopaedia.org/cases/diffuse-axonal-injury-3?lang=gb

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Long Term Sequela
 The scary thing about TBI is that once the damage is done,
recovery is long, arduous, and may not occur at all

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 Overstimulation and lack of relief of stress on the brain’s
capacity leads to permanent brain injury

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Repeated/Accumulated Injuries
CHRONIC TRAUMATIC ENCEPHALOPATHY (CTE)
Progressive degenerative neurological process found in
some athletes who sustain multiple concussions and sub-
concussive blows. This early degenerative process is
characterized by cerebral atrophy and increased levels of tau
protein, as well as cognitive impairment (dementia) and, in
some cases, depression.
LOW-MOD INCIDENCE – HIGH POTENTIAL CHRONIC IMPACT
McKee/Cantu, 2009; Omalu/DeKosky 2005

4
Owen Thomas – UPenn Football Player
 Played football for
years without
symptoms
 Developed headaches
and trouble focusing
 Straight-A student
suddenly failing
 Sudden and
uncharacteristic
emotional collapse

4
CHRONIC TRAUMATIC ENCEPHALOPATHY
Tau Protein: Amygdala (McKee et al. 2009)
Healthy Brain Football Player Boxer

Presentation1 part one - TBI and the work up

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