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Home , Basilar skull fracture, Epidural hematoma, Intracerebral hemorrhage

NorthBay Center for Neuroscience “Focus on TBI and ”

Essential Elements in the Evaluation and Care of the TBI and Concussion Patient May 3, 2019

Edie E. Zusman, MD, MBA Medical Director NorthBay Center for Neuroscience Chief of 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 with Computer Guidance Zeiss Pantera Microscope NorthBay Hospital – Top Technology Wellness Center – HealthSpring Fitness o State of the art Operating Rooms o NorthBay is completiing 200 million dollar expansion o Zeiss Microscopes and Endoscopes o Minimally Invasive technology o Stealth Computer Navigation o State of the art Health Fitness Center o 50,000 square wellness center o 4 swimming pools and jogging track o Mayo Clinic Model – One Stop Shop o Concussion Patients Seen within Days o 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 NorthBay Center for Neuroscience Team • Kelly Rhoads-Poston • Shauna Bishop • Sarah Jewel • Mechelle Levingston • Justine Zilliken • Wayne Geitz • Elnora Cameron • Aimee Brewer High Functioning Trauma Team: Peter Zopfi and Heather Venezio Neurotrauma – Current Capabilities TBI and Concussion o ACS Certified Level II Trauma Center o Helipad o Multidisciplinary TBI and ConcussionClini o Discharge Pathway/Continuum of Care o Trauma Quality and Program Meetings o Trauma CME and Educational Events o Evidence Based Best Practices o Clearance of C Spine o TBI Order Set and Pathways of Care o Building National Reputation o Tracking Metrics and Outomes Neurotrauma TBI and Concussion o TBI and Concussion Clinic to Primary Care and ED – Dr. Joshua Kuluva o Link with schools, teams broadly to extend brand/familiarity – Dr. Neil Pathare o Pediatric concussion collaborations with Oakland Children’s and NorthBay’s Dr. Michael Ginsberg o IRB Approved Clinical Trial Dr. Zusman/Omalu o Grant Opportunities – Collaboration with David Grant Military Neurosurgeons Dr. Morris and Dr. Maloney Concussion – Sports Remember the Good Old Days?

Vanderbilt Sports Concussion Center 2016

Topics • Focal and Diffuse TBI • Traumatic Injury Basics – Scalp/ • Glasgow Scale • Concussion and Mild TBI • Post -Concussive Syndrome • Post -Concussive • Severe – COMA • Epidural • – acute and chronic Traumatic Brain Injury Generalized Concussion SDH

Focal EDH Contusion Skull and Scalp - Basics

• Skull Fractures occur when the elastic tolerance of the has been exceeded (temporal areas, thinner bone)

• Intracranial are evident in 2/3 of patients..

• Clean Staple actively 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 )? 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 – C rosses the – Laceration of Middle Meningial Associated with – Crosses Venous Sinus - Risk of Bleeding - Risk of • 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 • – decreased hearing • Bruising around the eyes – Racoon Eyes • Bruising over the mastoids – Battle Sign • - flattening of face • - Delayed NO Role for Skull XRAYS in 2017 Obtain CT HEAD for any of the above Battle Sign 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. , 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

• 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 level Mild Brain Injury … GCS 13 - 15 Moderate … GCS 9 – 12 Severe … GCS 8 and below Expressed 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 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, or diffuse .

• ‘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 . • Patients with a , 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 caused by rotation of the cerebral hemispheres on the fixed

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 as pallor, , faintness with mild hypotension, or sluggish pupillary reactions

– CT and MRI scans are usually normal, but 3% of patients have 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 TBI Signs Symptoms

• A Glasgow Coma Scale 13-14 o A reported loss of consciousness or post-traumatic • MECHANISM OR EXTERNAL SIGNS OF

TRAUMA o A history of coagulopathy

• Focal neurologic findings o Continued diffuse headache

• Unexplained asymmetric pupils o Amnesia Vomiting • Distracting injuries or intoxication o NO SKULL XRAYS Copyright© 2004 by the McGraw-Hill Companies, Inc. All rights reserved. • 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: Symptoms SOMATIC AFFECTIVE • Headache • Depression • Sleep disturbance • Anxiety • Nausea • Irritability • Sensitivity to photo- • Emotionally labile stimuli COGNITIVE • Dizziness/vertigo • Memory dysfunction • Fatigue • 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 . • 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 Hemorrhage Axonal 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 and swelling -epidural hematomas, subdural hematomas, and subarachnoid bleeds may occur Mechanism and Pathophysiology Contusion– a 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 Cerebral Contusions

Coup and Contracoup Frontal Cerebral Contusions - Contracoup

Opposite direction of impact Facial compress so we see less severe contracoup injury if someone falls forward - think Mercedes Crash Test Quadripolar Contusion – Behavior Severe 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 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 (ICP) – which can further exacerbate the damage.

• Avoid further insults to vulnerable cells by: avoiding hypoxia, , 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, , 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 > 5mm, needs to be surgically evacuated in the context of clinical/GCS

• – 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 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 .

• Most epidurals result from in the temporal or temporoparietal area with an associated skull fracture disrupting the .

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 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 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 . VENOUS but not always – BRIDGING VEINS • Sometimes hard to tell EDH from SDH and maybe BOTH Subdural vs. Epidural

SUBDURAL EPIDURAL Venous Arterial Bleeding likely Stopped Bleeding my be ongoing Diffuse Brain Injury Focal Brain Injury Poorer 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, , and obvious pupillary enlargement 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 , 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 supratentorial to the infratentorial compartments through the tentorial opening, 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 pupil suggests compression of the third nerve from a mass effect • The most extreme finding of bilaterally fixed dilated pupils indicates 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 Families RISE Clinic Adazi-Ani, Nigeria Our Physician TEAM! RISE Clinic International Volunteers Seizures – Emergency Response Team Thank You!

NorthBay Center for Neurocience TBI and Concussion Clinic 707 646 4370 [email protected] Coordinator: Natalie Heckamen, LVN