Essential Elements in the Evaluation and Care of the TBI ... · Essential Elements in the Evaluation and Care of the TBI and Concussion Patient . Disclosure • Partner – Benzil

May 3, 2019

Edie E. Zusman, MD, MBAMedical Director

NorthBay Center for Neuroscience

Chief of Neurosurgery

NorthBay Center for Neuroscience “Focus on TBI and Concussion”

Essential Elements in the Evaluation and Care of the TBI and Concussion Patient

Disclosure• Partner

– Benzil Zusman, LLC

– Neuroscience Strategy Consulting

• World Neurosurgery Editorial Board- Section Editor

• Neurosurgery – Editorial Board

• Board of Directors – Epilepsy Foundation of Northern CA and Head Royce

• NorthBay – Foundation Board

• International Advisor, RISE Clinic Anambra , Nigeria

NorthBay Neurosurgery Team• Corey Beausoleil

• Kawanaa Carter

• Bita Joobbani

• Patrick Maloney

• Saint-Aaron Morris

• Phillip Parry

• Atul Patel

• Sherry Taylor

• Edie Zusman

NorthBay State of the Art Neurosurgery OR

Intraoperative CT/O ARM with Computer Guidance

Zeiss Pantera Microscope

NorthBay Hospital – Top Technology Wellness Center – HealthSpring Fitness

o State of the art Operating Roomso NorthBay is completiing 200 million dollar expansiono Zeiss Microscopes and Endoscopeso Minimally Invasive technologyo Stealth Computer Navigation

o State of the art Health Fitness Centero 50,000 square foot wellness centero 4 swimming pools and jogging tracko Mayo Clinic Model – One Stop Shopo Concussion Patients Seen within Dayso Multidisciplinary TBI and Concussion Clinic

IRB Approved Clinical Trial for Chronic TBI

NorthBay Center for Neuroscience “Focus on TBI and Concussion”

Welcome Honored Guests• Diana Lopez Lomeli, MA• Joanne Jacob, RN• Richard Riemer, DO• Mary Mancini, MD

Thank you to our NorthBayCenter for Neuroscience Team

• Kelly Rhoads-Poston

• Sarah Jewel

• Justine Zilliken

• Elnora Cameron

• Shauna Bishop

• Mechelle Levingston

• Wayne Geitz

• Aimee Brewer

High Functioning Trauma Team: Peter Zopfi and Heather Venezio

Neurotrauma – Current CapabilitiesTBI and Concussion

o ACS Certified Level II Trauma Centero Helipado Multidisciplinary TBI and ConcussionClinio Discharge Pathway/Continuum of Care o Trauma Quality and Program Meetingso Trauma CME and Educational Eventso Evidence Based Best Practices

o Clearance of C Spine o TBI Order Set and Pathways of Care

o Building National Reputationo Tracking Metrics and Outomes

NeurotraumaTBI and Concussiono TBI and Concussion Clinic to

Primary Care and ED – Dr. Joshua Kuluvao Link with schools, teams broadly to extend

brand/familiarity – Dr. Neil Pathareo Pediatric concussion collaborations with

Oakland Children’s and NorthBay’s Dr. Michael Ginsberg

o IRB Approved Clinical Trial Dr. Zusman/Omaluo Grant Opportunities – Collaboration with

David Grant Military NeurosurgeonsDr. Morris and Dr. Maloney

Concussion – SportsRemember the Good Old Days?

Vanderbilt SportsConcussion Center 2016

Topics • Focal and Diffuse TBI

• Traumatic Brain Injury Basics – Scalp/Skull

• Glasgow Coma Scale

• Concussion and Mild TBI

• Post-Concussive Syndrome

• Post-Concussive Seizures

• Severe Traumatic Brain Injury – COMA

• Epidural Hematoma

• Subdural Hematoma – acute and chronic

Traumatic Brain InjuryGeneralizedConcussionSDHDiffuse Axonal Injury

FocalEDHContusion

Skull and Scalp - Basics

• Skull Fractures occur when the elastic tolerance of the bone has been

exceeded (temporal areas, thinner bone)

• Intracranial lesions are evident in 2/3 of skull fracture patients..

• Clean Staple actively bleeding scalp lacerations vs. pack/local dressing for

delayed formal washout in ED – OK for simple non displaced skull fractures

• Subgaleal Hematoma may help understand the mechanism of impact

• Air Sinuses protect the brain – Think Mercedes

• About 15% of skull fracture pts have a cervical spine fracture

Skull Fractures – DIAGNOSE by CT HEAD

Categorized by:

Location: basilar skull fracture v. convexity

Pattern: linear, depresssed or comminuted

Infection Risk: open or closed

Is there pneumocephalus?

Is there a CSF leak (nose or ear)?

NOTE: No role for skull xrays – go straight to CT

(CT Scout is old fashioned lateral skull xray)

Linear Skull Fractures

• Most have minimal clinical significance • EXCEPTIONS

– Crosses the Temporal Bone – Laceration of Middle Meningial Artery Associated with Epidural Hematoma

– Crosses Venous Sinus- Risk of Bleeding - Risk of Thrombosis

• OK for antibiotic washout and primary closure/staple in the ED

Depressed Skull Fractures

• Trauma was of significant force to drive a segment of skull below

the level of adjacent skull.

• May be open or closed

• Greater than a bone thickness or 1 cm depression associated with

dural laceration

• Cortical lacerations higher association with post traumatic seizures

• Elevate and washout open depressed skull fractures greater than

1 cm depression/skull thickiness in the OR

Evaluation for Basilar Skull Fracture

• Otorrhea or Rhinorrhea• Hemotympanum – decreased hearing• Bruising around the eyes – Racoon Eyes• Bruising over the mastoids – Battle Sign• Facial Nerve - flattening of face • Meningitis - DelayedNO Role for Skull XRAYS in 2017Obtain CT HEAD for any of the above

Battle Sign

Raccoon Eyes

Hemotympanum

Basilar Skull Fractures – Management• Patients diagnosed with a basilar fracture should be admitted for

observation

• If bloody drainage, check for a ‘halo sign’ Most leaks resolve

spontaneously within a few days

• RISK of MENINGITIS– but routine treatment with antibiotics leads to superinfection/resistance – moved away from prophylactic abx

• RISK of DELAYED Cranial Nerve VII palsy - due to swelling from compression, starting 2-3 days after the injury. May use steroids,

obtain ENT consult

‘Halo Sign – Catch on Sterile Gauze

• Collect drops of bloody drainage from the

nose (rhinorrhea), or ear

(otorrhea) is placed on a

white tissue or cloth.

Cerebrospinal fluid, if

present, will separate

beyond the blood.

• Beta 2 Transferrin

Traumatic Brain Injury

• In Football alone, an estimated 10% of US college and 20% of US high school players sustain brain injuries each season.

• The prevalence of long-term disability related to TBI in the U.S. is estimated at between 3 to 5 million, or approximately 1 – 2% of the population.

The Glasgow Coma Scale

• A neurological scale which is aimed at giving a reliable, objective way of recording the conscious state of a person for initial as well as subsequent assessment.

• Was initially only used to evaluate trauma, but is now used for grading and monitoring most neurologically compromised patients.

• The range of scoring is from 3 (deeply unconscious) to 15.

What does it mean when you are called for a GCS of 1?

GCS = Glasgow Coma Score

Interpretation of GCS levelMild Brain Injury … GCS 13 - 15Moderate … GCS 9 – 12Severe … GCS 8 and belowExpressed in the form…

“GCS 9 = E2 V4 M3 in the field at 0730 and currently GCS 12 improving”

PUPIL REACTIVITY – Flashlight or Pupillometer with Speed of Contraction.

Mild Traumatic Brain Injury - Often benign, but carries a high risk of serious

short and long-term sequela- Occurs with a head injury due to contact and/or

acceleration/deceleration forces- Typically defined as ‘mild’ by a Glasgow Coma

Scale (GCS) score of 13 to 15- Concussion – neurologically normal by 24 hours

Mild TBI• Because of a wide variation in outcomes in the ‘mild’ group (which

includes most TBI patients), this group is further divided into “low risk”,

“medium risk” and “high risk” sub-groups.

• ‘Low risk’ = GCS 15 and NO Hx of LOC, amnesia, vomiting or diffuse

headache.

• ‘Medium risk’ = GCS 15, but with a + hx of LOC, amnesia, vomiting or

diffuse headache. These pts have a 1-3% risk of having an intracranial

hematoma requiring surgical evacuation. Option to CT or observe.

Check TOX

• The ‘high risk’ mild head-injury patients are those with a GCS of 14 or 15 with neurological deficits.

• About 10% of these ‘high risk group’ patients will require surgical evacuation of intracranial hematomas.

• Patients with a coagulopathy, drug or alcohol consumption, previous neurosurgical procedures, epilepsy, or age greater than 60 years are included in the high-risk group.

• CT IF ON BLOOD THINNERS

Mild Traumatic Brain Injury• ‘Concussion’ is a term commonly used for

what in the medical literature is now termed ‘mild traumatic brain injury’ (MTBI)

• The American Academy of Neurology defines concussion as “a trauma-induced alteration in mental status that may or may not involve loss of consciousness”

• Length of Anterograde Amnesia – acquisition of new memories

Mechanism

• The CSF cushions the brain from light trauma

• In times of more severe impact, the forces on the brain may be

linear, angular, or rotational

• In rotational movement, the head turns around its center of

gravity – this is the primary mechanism causing concussion

• There is a transient electro-physiologic dysfunction of the

reticular activating system in the upper midbrain caused by

rotation of the cerebral hemispheres on the fixed brainstem

Symptoms of Mild TBI

• Feeling dazed or star struck, often after a blunt forward impact that caused sudden deceleration of the cranium and a movement of the brain within the skull.

• Retrograde Amnesia - if only a few moments of unresponsiveness is reported, then the amnesia will only last for a brief time. It will respond quickly once the patient is alert.

• The memory loss can vary from only moments before the injury, to even several weeks prior to the trauma (retrograde amnesia). Again, this lasts longer, the more severe the injury.

• Anterograde amnesia - This is the inability to form new memories.Ask do you remember the injury and what is the first thing you

remember after the injury?

Symptoms: • Dizziness• Disorientation and confusion• Nausea and vomiting• Loss of balance• Headache – most common symptom• Lack of motor coordination• Light sensitivity• Blurred vision• Tinnitus

Signs of Mild TBI (Concussion)• A vacant stare (befuddled facial expression)

• Delayed verbal expression (slow to answer)

• Inability to focus attention

• Disorientation (e.g. walking in wrong direction)

• Slurred or incoherent speech

• Emotionality out of proportion to situation

• Gross observable uncoordination (stumbling, etc)

• Memory deficits (asking the same questions repeatedly, unable to

recall 3 objects for five minutes)

• Any period of Loss of consciousness

– Hx of a brief convulsion or autonomic signs such aspallor, bradycardia, faintness with mild hypotension,or sluggish pupillary reactions

– CT and MRI scans are usually normal, but 3% of patients have intracranial hemorrhage of some type

• Sequela– A single uncomplicated head injury will only infrequently cause

permanent neurobehavioral changes in those previously free of psychiatric problems and substance abuse

– Minor problems in memory and concentration may be anatomically correlated to small shearing or other microscopic lesions.

Clinical Features• The hallmarks of concussion are confusion and amnesia

-- often without a preceding loss of consciousness.

• The amnesia almost always involves loss of memory for the event, and often includes events just before or just after, as well…[e.g. an athlete may be unable to recall recent plays or recall well-known events in the news].

• Amnesia may be evidenced by the patient repeatedly asking a question that has already been answered]

LOSS OF CONSCIOUSNESS AND/OR AWARENESS

Indications for CT Scanning for Patients with Mild TBISigns

• A Glasgow Coma Scale 13-14

• MECHANISM OR EXTERNAL SIGNS OF

TRAUMA

• Focal neurologic findings

• Unexplained asymmetric pupils

• Distracting injuries or intoxication

•

Symptoms

o A reported loss of consciousness or post-traumatic seizure

o A history of coagulopathy

o Continued diffuse headache

o Amnesia

o Vomiting

Copyright© 2004 by the McGraw-Hill Companies, Inc. All rights reserved.

NO SKULL XRAYS

Post-concussion Syndrome• Primary features include: fatigue, dizziness, headache, and difficulty in

concentration. Difficulty with attention, memory and other cognitive deficits are

also present AFTER 6 WEEKS

• Seen to some degree in 30-80% of pts with mild to moderate brain injury. Does not

correlate with severity.

• Theorized to be secondary to subtle axonal shearing lesions and/or biochemical

changes.

• Test scores tend to improve rapidly during the first 6 months of recovery, then

much more slowly for years. Improve over 1-2 years.

Post-concussion Syndrome: SymptomsSOMATIC

• Headache

• Sleep disturbance

• Nausea

• Sensitivity to photo-

stimuli

• Dizziness/vertigo

• Fatigue

AFFECTIVE

• Depression

• Anxiety

• Irritability

• Emotionally labile

COGNITIVE

• Memory dysfunction

• Concentration difficulty

• Attention deficit

Copyright© 2004 by the McGraw-Hill

Post-concussion Syndrome - Treatment

• Identify and treat: depression, sleeplessness, anxiety, persistent headache, and dizziness

• Clearly explain the syndrome INCLUDING FAMILY

• Avoid prolonged use of habituating drugs• Vestibular exercises +/- phenergan if dizzy• Serial neuropsychological testing to

document improvement

‘Second-impact’ Syndrome• Occurs when a person suffers a second concussion

before an earlier concussion has healed.• May occur within minutes, or days, or weeks of the

first injury.• Often fatal, or severely damaging at the least.• Thought to be due to arterioles loosing their ability to

auto-regulate following the first injury, leading to brain edema.

• Often seen in younger athletes.

Prevention of Second-Impact Syndrome

Any athlete who has suffered a concussion should avoid contact sports and return to play until cleared by a trained clinician. (Patel/Ginsberg/Pathare)

Repeated concussion in football, soccer, and boxing is associated with mild, cumulative cognitive deficits -dementia pugilistica

CHRONIC TRAUMATIC ENCEPHALOPATHY –Defined by Dr. Bennet Omalu

In the brain tissue…

Contusions HemorrhageAxonal Shearing

TBI - Pathophysiology• Divided into two separate but related categories:

primary brain injury and secondary brain injury

• Primary Brain Injury:

- occurs at the time of the trauma

- damage results from multiple focal contusions, hematomas,

axonal shearing injuries, and the resulting cerebral edema and swelling

-epidural hematomas, subdural hematomas, and

subarachnoid bleeds may occur

Mechanism and PathophysiologyContusion– a bruise on the surface of the brain. Often

it is the result of blunt deceleration impact.

For example, a victim’s head hitting the car dashboard, or a drunk falling forward might cause contusions to the orbital

surfaces of the frontal lobes and the anterior and basal portions of the temporal lobes – COUP Contusion

The coup-contracoup mechanism – Falling backwards

Coup and Contracoup

Cerebral Contusions

Frontal Cerebral Contusions -Contracoup

Opposite direction of impactFacial bones compress so we see less severe contracoup injury if someone falls forward - think Mercedes Crash TestQuadripolar Contusion – BehaviorSevere Cerebral Edema – ICP

Monitoring and repeat CT

Axonal Shearing Injuries - DAI• Axonal rupture may occur at the time of impact from

shearing forces, but milder degrees of axonal damage play a role as well, resulting in impaired axonal transport.

• Intermediate Coup Contusions

• Other neuro-imaging techniques (PET, SPECT, functional MRI) show structural and physiologic changes not appreciated on routine CT scan

• When widespread bilaterally, called diffuse axonal injury and may cause persistent coma

• High OR low ICP is possible – when to monitor?

Diffuse axonal shearing

Hemorrhages• Torsion, or shearing forces within the brain cause

hemorrhages in the basal ganglia and other deep structures

• For unknown reasons, deep cerebral hemorrhages may not develop until several days after injury.

• Any sudden neurologic deterioration in a comatose patient should prompt an investigation (CT scan)

Secondary Brain Injury – EDEMA and ISCHEMIA

• A cascade of molecular injury mechanisms that are initiated by the initial

trauma, but continue for hours or days.

• Includes: electrolyte imbalances; mitochondrial dysfunction; inflammatory

responses; apoptosis; and secondary ischemia from vasospasm, focal micro-

vascular occlusion, and vascular injury.

• All lead to neuronal cell death and cerebral edema and increased intracranial

pressure (ICP) – which can further exacerbate the damage.

• Avoid further insults to vulnerable cells by: avoiding hypoxia, fever, seizures,

and hyperglycemia

Severe Traumatic Brain Injury

Severe Traumatic Brain Injury

• The development of standardized approaches to care has been a major advance in the past 20 years

• Better patient outcomes result from being treated in neurological intensive-care units

• Patients with head trauma also often have multiple additional trauma – and are best cared for at a trauma center

Severe TBI – ED Care• Neuro exam with GCS = 8 or less -> severe TBI

• Continuous re-assessments are required as deterioration is common in initial hours and assess for other trauma

• Labs: include coagulation parameters, blood alcohol level, and urine toxicology screen

• Must recognize increased ICP and possible impending herniation (unilateral or bilateral fixed pupil, decorticate or decerebrate posturing, bradycardia, hypertension, and/or respiratory depression) -> treat with head elevation, hyperosmolar therapy and MAP/ICP management

Severe TBI – Prehospital Care• The primary pre-hospital goal is to prevent hypotension

(systolic BP < 90 mm Hg) and hypoxia (PaO2 < 60 mm Hg) which can cause secondary injury after severe TBI.

• Intubation is recommended for pts with GCS = 8 or less. Bag-mask ventilation if expert intubation not available.

[neck protection and basilar skull fracture)

• IV – Normal saline or Hypertonic Saline

• Must assume the cervical spine is fractured and take precautions using stabilization and immobiliziation

Require Neurosurgery:• EPIDURAL HEMATOMA – larger than 30 temporal or 60 cc frontal/parietal in

the context of clinical/GCS

• SUBDURAL HEMATOMA – if acute subdural is > 10 mm in thickness or

associated with a midline shift > 5mm, needs to be surgically evacuated in the

context of clinical/GCS

• INTRACEREBRAL HEMORRHAGE – if elevated ICP

• PENETRATING INJURY – debride and close. Need antibiotics. GSW –

Bihemispheric in coma is not operative

• DEPRESSED SKULL FXT – if depressed greater than the thickness of the

cranium or contaminated, or sinus involved, or cosmetic deformity,

pneumocephalus.

Principles of Neuro Intensive-Care Management:• BP and oxygen support, as stated earlier

• Prevention of DVT (deep vein thrombosis)

• Nutritional support

• ICP monitoring (increased ICP is associated with higher morbidity and worse

outcomes) KEEP MAP GREATER THAN 60 at all times

1) head of bed elevated to 30 degrees

MILD REVERSE TRENDELENBERG OK in SPINE PRECAUTIONS

2) optimize venous drainage from the head

Post-traumatic seizures (PTS)

• About 6% of people hospitalized with TBI have at least one seizure.

• Early PTS occur within a week of the injury; late seizures occur more than a

week after.

• IMMEDIATE Post Traumatic seizures are provoked by the direct trauma

• Late seizures are more epileptic, with the re-wiring of the brain leading to a

more easily excited state.

• TREAT SEIZURES when they occur

• Prophylaxis for seizures if would impact outcome – GCS 8 or less/Mass

Intracranial Hematomas

Epidural Hematoma

• Epidural hematomas result from blood collecting in the potential space between the skull and the dura mater.

• Most epidurals result from blunt trauma in the temporal or temporoparietal area with an associated skull fracture disrupting the middle meningeal artery.

Epidural History and Clinical Course• The ‘classic’ history is one of head trauma with

LOC, followed by a lucent period after which the patient again loses consciousness.

• TALK AND DIE PHENOMENON• The diagnosis is made by CT and physical findings.• The arterial bleeding can be high-pressure and

lead to brain herniation within hours unless the bleeding vessel (usually middle meningeal artery) is coagulated

Epidural Hematoma

Trepanation (‘Burr holes’)

Subdural Hematoma

• Acute SDH is usually caused by tearing of the bridging veins that drain from the surface of the brain to the dural sinuses

• But -- 20-30% of SDH are caused by arterial ruptures

• Venous bleeding is usually arrested by the rising ICP or by direct compression by the clot itself.

• FALSE – All Subdural Hematomas are Venous

• FALSE – All Epidural Hematomas are Arterial

CT Assessment – NON Contrast

• Differences between SDH and epidural hematoma are made evident by NON CONTRAST CT:

• Epidural hematoma does not cross sutures - therefore, it has a lens-shaped appearance on CT. ARTERIAL but not always – MIDDLE MENINGEAL

• SDH does cross suture lines, and conforms to the surface of the brrain making it a crescent-shaped extra-axial lesion. VENOUS but not always – BRIDGING VEINS

• Sometimes hard to tell EDH from SDH and maybe BOTH

Subdural vs. Epidural

SUBDURAL VenousBleeding likely StoppedDiffuse Brain InjuryPoorer Prognosis

EPIDURALArterialBleeding my be ongoing Focal Brain Injury Better Prognosis

Acute Subdural Hematoma

• Or, the trauma may have been only minor, or there may be no history of trauma, especially in older people and those on anti-coagulants.

• Some pts report a unilateral headache and have a slightly enlarged pupil unilaterally.

• Large subdurals, however, are likely to result in coma, hemiparesis, and obvious pupillaryenlargement

Chronic Subdurals• The patient may or may not have a hx of trauma (20-

30% do not recall any head injury)

• May develop headache, slow thinking, a vague personality change, possibly have a seizure.

• The headache may fluctuate with head position changes

• Provider may initially suspect stroke, associated with atrophy and aging brain –

Dr. Maziyar Kalani from Mayo will discuss his research in minimally invasive treatment of Chronic

SDH

Cerebral Herniations• Recall that the cerebral hemispheres are separated by the

falx, while the anterior and posterior fossa are separated by the tentorium.

• Herniation refers to the displacement of brain tissue into a compartment that it normally does not occupy.

• The most common herniations are from the supratentorialto the infratentorial compartments through the tentorialopening, and so they are referred to as transtentorial.

• Compression of different portions of brain result in differing signs

Pupillary Signs – FIXED AND DILATED PUPILS

• Normally reactive and round midsize pupils

(2.5 – 5 mm) exclude midbrain damage

An unreactive and enlarged pupil (>6mm), or a poorly reactive pupilsuggests compression of the third nerve from a mass effect

• The most extreme finding of bilaterally fixed dilated pupilsindicates severe midbrain damage, often from compression by a supratentorial mass

• Must rule out drugs with anticholinergic activity and direct ocular trauma

Coma: Outcome• Outcome can be associated with a patient’s best response in the

first 24 hours after injury.

• Using the GCS, if the best score is:

- 3-4 after 24 hrs, then 87% will die or remain vegitative

- 5-7, then 53% will die or remain vegetative, and 34% will have a moderate disability and/or good recovery

- if GCS 8-10. then 27% will die or remain vegetative

- if GCS 11-15, then only 7% will die or remain vegetative

Trauma and Infection Causes of Epilepsy in Anambra, Nigeria

Patients and FamiliesRISE Clinic Adazi-Ani, Nigeria

Our Physician TEAM!

RISE Clinic International Volunteers

Seizures – Emergency Response Team

Thank You!

NorthBay Center for NeurocienceTBI and Concussion Clinic

707 646 [email protected]

Coordinator: Natalie Heckamen, LVN