10 Things you Need to Know about TBI by Knight

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10 Things you Need to Know about TBI by Knight

Saúde e medicina

Next Level Neuro Resus
26 June 2015
WilliamA Knight IV, MD, FACEP
University of Cincinnati
Traumatic Brain Injury – 10Things you Need to Know
William.Knight@uc.edu
@waknight4

Epidemiology:TBI in the US
50,000
Deaths
100,000
Hospitalizations
1,111,000
Emergency DepartmentVisits
?? Receiving Other Medical Care or No Care
* Average annual numbers, 1995-2001
2004 CDC Report: TBI in the United States: ED Visits, Hospitalizations, and Deaths
1.5 – 2.0 million
TBIs occur each year.*

Secondary Injury
TBI
Demyelination
Mitochondrial
Uncoupling
Excitotoxic
cascade
Receptor
activation
Reduced
GABA
Inflammatory
Cytokines
Apoptosis
Cerebral
Edema
Cytotoxic
Edema
Vasogenic
Edema
Pro Apoptotic
cascade
Free radicals &
lipid peroxidation

WHATWE HAVE WHATWE NEED

Drug Reversal Method Evidenc
e
Cost
Aspirin (ASA) • Platelets
•Demsopressin (DDAVP)
•rFVIIa (40mcg/kg)
•weak
•$1000 – 12 units
•$1 / mcg
Plavix (Clopidogrel) •Platelets
•Demsopressin (DDAVP)
•rFVIIa (40mcg/kg)
• terrible
•$1000 – 12 units
•$1 / mcg
Warfarin
(Coumadin)
•Vit K
•FFP (250 cc / bag)
•PCC
•Cryoprecipitate
•rFVIIa (40mcg/kg)
• good
•$10 / 10mg
•$60 / bag
•$5000 / dose
•$1200 / 20 bags
•$1 / mcg
TSOACs •PCC (depends)
•Antidotes
•Weak
•???
•$5000 / dose
•???
Heparin •Protamine •solid
NSAIDS •Platelets
•DDAVP
•garbage
•$1000 – 12 units

NEJM 2000

Generalized spike/wave status

Narayan et al, J Nsurg 1981

0%
25%
50%
75%
100%
3 4 5 6 7 8
GR MD SD Veg Dead
Marshall et al, J Nsurg 1991

 DECRA
ProTECT
 Disease definition
 Can what we see contributing to poor or good
outcome be as wrong as these trials suggest or
do we need to define the disease and patients
better?
 Multicenter RCTs can be successfully performed

Adeoye O & Shutter L. Neurotrauma & Critical Care of
the Brain. JalloJ, ed. Thieme; 2009.
CPP?

 Target normal physiologic goals
 Research
 We know how to study
▪ Do we know what to study?
 Early aggressive care is the future
 24 hours of resuscitation prior to prognosis

“It’s not an exceptional case. We
just don’t know how many
exceptions to the rule there are.
So.
I don’t believe in the rule anymore.”
- Joseph Giacino, PhD
http://nymag.com/scienceofus/2015/06/dylan-rizzo-coma.html

10 Things you Need to Know about TBI by Knight

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Precision Medicine in Acute Brain Injury

SMACC Conference

CORTICAL SPREADING DEPOLARISATION IN NEUROLOGICAL DISEASE – AN INTRODUCTION By Toby Jeffcote Cortical spreading depolarization (CSD) is a spreading loss of ion homeostasis, altered vascular response, change in synaptic architecture, and subsequent depression in electrical activity following an inciting neurological injury. It was first described by Leão in 1944, a disturbance in neuronal electrophysiology has since been demonstrated in a number of animal studies, and recently a few human studies that examine the occurrence of this depolarizing phenomenon in the setting of a variety of pathological states, including migraines, cerebrovascular accidents, epilepsy, intracranial hemorrhages, and traumatic brain injuries. The onset of CSD has been demonstrated experimentally following a disruption in the neuronal environment leading to glutamate-induced toxicity. This initial event leads to pathological changes in the activity of ion channels that maintain membrane potential. Recovery mechanisms such as sodium-potassium pumps that aim to restore homeostasis fail, leading to osmolar shifts of fluid, swelling of the neuron, and ultimately a measurable depression in cortical activity that spreads in the order of millimeters per minute. Equally important is the resulting change in vascular response. In healthy tissue, increased electrical activity is coupled with release of vasodilatory factors such as nitric oxide and arachidonic acid metabolites that increase local blood flow to meet increased energy expenditure. In damaged tissue, not only is the restorative vascular response lacking but a vasoconstrictive response is promoted and the ischemia that follows adds to the severity of the initial injury. Tissue threatened by this ischemic response is then at elevated risk for CSD propagation and falls into a vicious cycle of electrical and hemodynamic disturbance. Efforts have been made to halt this spreading cortical depression using N-methyl-D-aspartate receptor antagonists and other ion channel blockers to minimize the damaging effects of CSD that can persist long after the triggering insult.

CSD by Jeffcote Coda 22.pdf

CSD by Jeffcote Coda 22.pdf

CSD by Jeffcote Coda 22.pdf

SMACC Conference

Subdural Haemorrhage and MMA embolisation

Subdural Haemorrhage and MMA embolisation

Subdural Haemorrhage and MMA embolisation

SMACC Conference

Andy Neill - More neuroanatomy pearls for neurocritical care

Andy Neill - More neuroanatomy pearls for neurocritical care

Andy Neill - More neuroanatomy pearls for neurocritical care

SMACC Conference

Andrew Udy talks about Brain Tissue Oxygen Monitoring: It’s Not What You’ve Got It’s What You Do With It The BONANZA Trial Andrew Udy talks about the ongoing BONANZA Trial which is assessing whether an algorithm that incorporates both ICP and brain tissue oxygen (PbTO2) can improve outcomes after traumatic brain injury (TBI). Like with all monitoring, how the PbTO2 is interpreted and managed is critical and the devil is in the detail! More on BONANZA here More on BOOST3 here

The BONANZA Trial and PbTO2 Monitoring

The BONANZA Trial and PbTO2 Monitoring

The BONANZA Trial and PbTO2 Monitoring

SMACC Conference

R. Loch Macdonald, M.D., Ph.D. Community Neurosciences Institute Fresno, California, USA Angiographic vasospasm and more accurately, delayed cerebral ischemia, continue to contribute to morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (SAH). It is known that angiographic vasospasm is common after SAH, occurring in two-thirds of patients. Cerebral infarctions that developed days after the SAH have been attributed to angiographic vasospasm, occuring in about a third of patients, although this has always been controversial. Angiographic vasospasm theoretically can only damage the brain by restricting blood flow but there is no easy, accurate, widely available method to measure cerebral blood flow and this is not the measurement we need. Blood flow depends on metabolic demand so what we need to know to determine if angiographic vasospasm is causing ischemia is oxygen extraction fraction in the brain tissue supplied the the spastic artery. Without this measurement, the attribution of ischemia to vasospasm is subjective. Since angiographic vasospasm is essentially the only detectable delayed phenomenon after SAH, we focus on it and apply tremendous resources to preventing or reversing the vasospasm. Undoubtedly angiographic vasospasm can cause cerebral infarctions, but it has to be severe and flow limiting. But SAH is a complex disease. There are many other causes for cerebral infarctions after SAH, the most common being due to the aneurysm repair procedure. And a given degree of vasospasm may cause infarction in a volume-depleted patient with poor collateral blood supply but not in a patient without these things. There also are hypodense brain lesions after SAH that are due to intracerebral hemorrhages. There can be hypodensities in the brain directly under usually thick SAH where the brain dies. This observation in particular supports a role for cortical spreading depolarizations/ischemia as a cause of infarction after SAH. Other macromolecular processes that are hypothesized to cause brain damage after SAH include microthromboembolism, changes in the microcirculation, delayed brain cell apoptosis and capillary transit time heterogeneity. Determining the importance of these things is hindered by the lack of an easy way to detect them in patients. It is also known that poor grade patients, who presumably have more early brain injury and ischemia than good grade patients, are more prone to delayed cerebral ischemia, suggesting increased sensitivity to secondary insults of the already injured brain. We also assume delayed neurological deterioration when attributed to vasospasm or delayed cerebral ischemia, is purely due to ischemia. While knowledge about what happens pathophysiologically after SAH is increasing, management of delayed cerebral ischemia still focuses on detecting angiographic vasospasm and then augmenting the blood pressure to improve cerebral blood flow or dilating the spastic arteries with balloons or drugs.

Dilating the Dogma of Vasospasm

Dilating the Dogma of Vasospasm

Dilating the Dogma of Vasospasm

SMACC Conference

EVD Tips and Tricks

EVD Tips and Tricks

EVD Tips and Tricks

SMACC Conference

Part 2 of a debate over the classification of TBI. Andrew Udy then argues that this classification is fundamentally flawed. He discusses the issues with the Glasgow Coma Scale, and therefore the follow-on issues in TBI classification, including all the confounders to the GCS, the issues with timing of the score as well as GCS not taking baseline function or specifics subtypes of TBI into account. He makes teh argument that biomarkers may better categorise the diffuse entity we call TBI.

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

SMACC Conference

Andrew Chow, Intensivist with a neurosurgical background, argues that the current categorisation system for traumatic brain injury (TBI) works, and makes sense! He tackles us through the history of this system, and why it’s important to differentiate different types of TBI. The arguments in favour of this categorisation include the consistency and benefits of a universal language, the implications for triage and management, and the fact that this system has been endorsed by all major organisations

TBI Debate - Mild, moderate and severe categories work

TBI Debate - Mild, moderate and severe categories work

TBI Debate - Mild, moderate and severe categories work

SMACC Conference

Dr Nick Little is an experienced Neurosurgeon who's looked after patients with traumatic brain injury for his whole career. Here he discusses the difficulties of prognostication following traumatic brain injury (TBI). He talks about the statistics of outcomes following mild, moderate and severe TBI and then goes on to tackle the harder topic of how we try to work out what an individual would want if they knew the spectrum of outcomes that they may face. The issues with the clinical examination findings we use to prognosticate are covered, as well as which imaging findings he finds most helpful. He also mentions the difficulties with current prognostic calculators.

TBI: when to stop and when to give time

TBI: when to stop and when to give time

TBI: when to stop and when to give time

SMACC Conference

Historically, when it came to brain injury, ketamine had a bad rap. Much of that dogma was dispelled in the last decade, and ketamine is now frequently used as an induction agent in acute brain injury, especially traumatic brain injury, due to it’s favorable effects on haemodynamics. However a new application of ketamine is now being explored - whether ketamine may be able to reduce secondary brain injury.

Ketamine in Brain Injury by Toby Jeffcote

Ketamine in Brain Injury by Toby Jeffcote

Ketamine in Brain Injury by Toby Jeffcote

SMACC Conference

20 million people around the world are living with a spinal cord injury (SCI). The medical issues they develop over the years differ to any other patient cohort. These complications include autonomic dysreflexia, management of pressure areas, specific infections, nuanced peri-operative care and highly specific issues such as baclofen pump management and syringomyelia Do look at the NeuroResus section on this and listen to Spinal Rehab Specialist Bonne Lee talk about this side of SCI care. Keywords SCI, spinal, spinal cord injury, autonomic dysreflexia, pressure areas, infection, peri-operative care, baclofen pump, syringomyelia, chronic SCI, spinal trauma, spinal rehab, incomplete SCI

Managing Complications of Chronic SCI by Bonne Lee

Managing Complications of Chronic SCI by Bonne Lee

Managing Complications of Chronic SCI by Bonne Lee

SMACC Conference

Tania is a neurologist and epileptologist with expertise in continuous EEG (cEEG) and status epilepticus (SE). This talk covers what a seizure is, what status is, including focal and generalised status epilepticus. So why do we do cEEGs for patients with suspected SE? To confirm the diagnosis To see if patient just post ictal or still seizing To establish that the clinical and electric seizures have stopped To see if burst suppression is achieved To exclude other differential diagnoses She makes a good argument for why cEEG is such an important tool in managing SE. In the questions after the talk, the issue of availability of cEEG in the Australian setting was discussed. Limited montage EEGs are discussed including their pros and cons.

EEG and Status Eplilepticus by Tania Farrar

EEG and Status Eplilepticus by Tania Farrar

EEG and Status Eplilepticus by Tania Farrar

SMACC Conference

Stuart Browne is a Neuro Rehab specialist from Sydney. These slides accompany a talk he gave at the Brian Symposium in 2023. He discusses what "severe disability" really means. Severe disability is more common than many realise - about 6% of the Australian population. Stuart discusses how health is more than simply physical recovery and how it is a multidimensional construct. He covers how permanent disability doesn't necessarily equate to a poor quality of life. He also discusses the long timespan of recovery, which is often much longer than appreciated. He specifically discusses "Locked-in Syndrome" and how the survivors have surprisingly positive self-reported health-related quality of life and well-being. Stuart also covers how severely disabled people face various forms of discrimination.

Browne Neuro symposium.pptx

Browne Neuro symposium.pptx

Browne Neuro symposium.pptx

SMACC Conference

Paediatric Stroke by Shree Basu

Paediatric Stroke by Shree Basu

Paediatric Stroke by Shree Basu

SMACC Conference

After spinal cord injury (SCI), there aren’t many interventions we have available that actually make a difference. Augmenting blood pressure to increase spinal cord perfusion pressure is an attractive concept that may improve neurological outcomes following SCI. We know that hypotension can make SCI worse. Clinical studies looking at blood pressure augmentation are mostly old, retrospective and flawed in various ways. Aiming for a MAP of > 85 for 5-7 days is recommended by guidelines but why this pressure and duration are good questions. Hypertensive therapy is relatively safe and easy to implement but not without risk. Tessa discusses the pros and cons, how this is managed practically and what the future may hold in this area.

Hypertensing Spinal Cord Injury - gold standard or wacky?

Hypertensing Spinal Cord Injury - gold standard or wacky?

Hypertensing Spinal Cord Injury - gold standard or wacky?

SMACC Conference

Mark Weedon takes us through the increasingly utilised concept of an optimal cerebral perfusion pressure (CPPopt) for each unique patient. He discusses the background to CPPopt, including intrcranial pressure (ICP), the Monroe Kelly hypothesis, neurovascular coupling, and cerebral autoregulation in health and following brain injury. He shows how intracranial pressure is affected by intracranial compliance and how this affects ICP waveforms. Cerebral perfusion pressure in relation to the Brain Trauma Foundation guidelines is covered including management of elevated ICP (EICP). The currently recommended tiered approach to managing cerebral perfusion pressure and EICP is mentioned citing recent guidelines. He uses a clinical case of a TBI to illustrate how the CPPopt can be ascertained and used to guide therapy, including the easy to perform “MAP Challenge”. Mark also describes the Pressure Reactivity Index (PRx) and how it can be used as a target for therapy. Finally, he covers the exciting results of the preliminary COGiTATE pilot study.

Optimal Cerebral Perfusion Pressure

Optimal Cerebral Perfusion Pressure

Optimal Cerebral Perfusion Pressure

SMACC Conference

The Power of Words - Death and Language.ppt

The Power of Words - Death and Language.ppt

The Power of Words - Death and Language.ppt

SMACC Conference

Appropriate use of antimicrobials is primarily a patient safety issue, and is the key aim of an effective antimicrobial stewardship program. We discuss the challenges in the management of a patient with sepsis, and how decision-making is usually done in the absence of effective diagnostics. Time dependent protocols and the knowledge that undertreatment of a patient with sepsis will lead to poor outcomes will lead to prescribing that may be driven by fear. Antimicrobial resistance is associated with over-use of antimicrobials but is usually not the immediate concern. Antimicrobial stewardship programs should work closely with sepsis teams to ensure that sepsis pathways are implemented across the whole hospital, and that key principles of judicious use are embedded within the clinical pathway.

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

SMACC Conference

Being able to prognosticate in the aftermath of a traumatic brain injury (TBI) is important as it assists with counselling patients and families. Moreover, it helps rationally allocate healthcare resources. However, due to the heterogenous nature of TBI and variable pre brain injury patient factors and post brain injury course, this has proven to be a difficult task. Large cohort studies have enabled improved accuracy in the prediction of 6 month mortality and unfavourable outcome. Furthermore, many of the factors that contribute to long-term outcome have also emerged. However, it is not yet possible to use them in prediction algorithms or mathematical models. There is emerging evidence that pre injury psychosocial and demographic factors may be of more relevance than injury severity. Moreover, that 'outcome' becomes increasingly subjective and complex as the post injury duration increases. We end with three brief vignettes which highlight the fraught nature of long term outcome prediction.

Brain injury outcomes and predictors

Brain injury outcomes and predictors

Brain injury outcomes and predictors

SMACC Conference

Mais de SMACC Conference (20)

Precision Medicine in Acute Brain Injury

Precision Medicine in Acute Brain Injury

Precision Medicine in Acute Brain Injury

CSD by Jeffcote Coda 22.pdf

CSD by Jeffcote Coda 22.pdf

CSD by Jeffcote Coda 22.pdf

Subdural Haemorrhage and MMA embolisation

Subdural Haemorrhage and MMA embolisation

Subdural Haemorrhage and MMA embolisation

Andy Neill - More neuroanatomy pearls for neurocritical care

Andy Neill - More neuroanatomy pearls for neurocritical care

Andy Neill - More neuroanatomy pearls for neurocritical care

The BONANZA Trial and PbTO2 Monitoring

The BONANZA Trial and PbTO2 Monitoring

The BONANZA Trial and PbTO2 Monitoring

Dilating the Dogma of Vasospasm

Dilating the Dogma of Vasospasm

Dilating the Dogma of Vasospasm

EVD Tips and Tricks

EVD Tips and Tricks

EVD Tips and Tricks

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

TBI Debate - Mild, moderate and severe categories work

TBI Debate - Mild, moderate and severe categories work

TBI Debate - Mild, moderate and severe categories work

TBI: when to stop and when to give time

TBI: when to stop and when to give time

TBI: when to stop and when to give time

Ketamine in Brain Injury by Toby Jeffcote

Ketamine in Brain Injury by Toby Jeffcote

Ketamine in Brain Injury by Toby Jeffcote

Managing Complications of Chronic SCI by Bonne Lee

Managing Complications of Chronic SCI by Bonne Lee

Managing Complications of Chronic SCI by Bonne Lee

EEG and Status Eplilepticus by Tania Farrar

EEG and Status Eplilepticus by Tania Farrar

EEG and Status Eplilepticus by Tania Farrar

Browne Neuro symposium.pptx

Browne Neuro symposium.pptx

Browne Neuro symposium.pptx

Paediatric Stroke by Shree Basu

Paediatric Stroke by Shree Basu

Paediatric Stroke by Shree Basu

Hypertensing Spinal Cord Injury - gold standard or wacky?

Hypertensing Spinal Cord Injury - gold standard or wacky?

Hypertensing Spinal Cord Injury - gold standard or wacky?

Optimal Cerebral Perfusion Pressure

Optimal Cerebral Perfusion Pressure

Optimal Cerebral Perfusion Pressure

The Power of Words - Death and Language.ppt

The Power of Words - Death and Language.ppt

The Power of Words - Death and Language.ppt

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Brain injury outcomes and predictors

Brain injury outcomes and predictors

Brain injury outcomes and predictors

Último

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These are simplified slides discussing the regulation of cardiac output and venous return. Learning objectives: 1. Comprehend the determinants of cardiac output and factors affecting cardiac output 2. Comprehend the factors affecting stroke volume and heart rate and total peripheral resistance 3. Identify the factors regulating venous return 4. Discuss the causes of high and low output cardiac failure 5. Enlist the functions of veins and recognise the significance of venous reservoirs Study Resources: 1. Chapter 20, Guyton and Hall Textbook of Medical Physiology, 14th edition 2. Chapter 30 and 32, Ganong’s Review of Medical Physiology, 26th edition 3. Chapter 10, Human Physiology by Lauralee Sherwood, 9th edition 4. Physiology, Cardiac Output - StatPearls https://www.ncbi.nlm.nih.gov/books/NBK470455/

Cardiac Output, Venous Return, and Their Regulation

Cardiac Output, Venous Return, and Their Regulation

Cardiac Output, Venous Return, and Their Regulation

MedicoseAcademics

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Dr. Faiza delivers an insightful lecture on the distinguishing characteristics of skeletal, smooth, and cardiac muscles, offering a comprehensive understanding of their histology, physiological anatomy, electrophysiological properties, and contractile mechanisms. Through meticulous tabulation and comparison, she aims to equip learners with a detailed comprehension of the unique features and functionalities of each muscle type. Beginning with a detailed exploration of histological differences, Dr. Faiza outlines key distinctions such as multinucleation in skeletal muscle, mononucleation in smooth and cardiac muscles, and the presence of striations in skeletal and cardiac muscles. She meticulously elucidates the structural arrangement of each muscle type, highlighting their cellular morphology and organization within tissues. Transitioning to physiological anatomy, Dr. Faiza navigates through various aspects including innervation, level of control, initiation of contraction, and modification by hormones. By delineating the role of the somatic nervous system in skeletal muscle control, and contrasting it with the autonomic nervous system's influence on smooth and cardiac muscles, she offers a nuanced understanding of neural regulation in muscle physiology. Furthermore, Dr. Faiza delves into electrophysiological properties, elucidating the mechanisms underlying action potential generation, duration, and ionic basis in each muscle type. Through insightful analysis, she reveals how differences in action potential characteristics contribute to variations in muscle contraction speed, duration, and resistance to fatigue. Finally, Dr. Faiza meticulously examines the contractile mechanisms of skeletal, smooth, and cardiac muscles, shedding light on the sliding filament theory, mechanisms of calcium action, and speed of contraction. By comprehensively comparing these mechanisms, she provides learners with a deep understanding of the intricate processes governing muscle contraction and function. Through engaging presentation and meticulous analysis, Dr. Faiza's lecture serves as a valuable resource for students seeking a thorough understanding of the fundamental differences between skeletal, smooth, and cardiac muscles.

Difference Between Skeletal Smooth and Cardiac Muscles

Difference Between Skeletal Smooth and Cardiac Muscles

Difference Between Skeletal Smooth and Cardiac Muscles

MedicoseAcademics

ANATOMY AND PHYSIOLOGY OF REPRODUCTIVE SYSTEM.pptx

ANATOMY AND PHYSIOLOGY OF REPRODUCTIVE SYSTEM.pptx

ANATOMY AND PHYSIOLOGY OF REPRODUCTIVE SYSTEM.pptx

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In this lecture on circulatory shock, Dr. Faiza, an Assistant Professor of Physiology, delves into the profound implications of inadequate blood flow throughout the body, leading to tissue damage. The session begins by defining circulatory shock and elucidating its physiological causes, including decreased cardiac output, diminished blood volume, decreased vascular tone, obstruction to blood flow, excess metabolic rate, and abnormal perfusion patterns. Dr. Faiza categorizes shock into various types, such as cardiogenic shock, hypovolemic shock, neurogenic shock, obstructive shock, anaphylactic shock, and septic shock, and explores the pathophysiological basis of each. Furthermore, the lecture examines the stages of shock, from the non-progressive phase where compensatory mechanisms aim for full recovery to the progressive phase where shock worsens steadily without intervention, potentially leading to irreversible damage. Dr. Faiza discusses therapeutic interventions for shock, including replacement therapy, blood and plasma transfusion, sympathomimetic drugs, and other adjunctive treatments like head-down positioning, oxygen therapy, and glucocorticoids.

Circulatory Shock, types and stages, compensatory mechanisms

Circulatory Shock, types and stages, compensatory mechanisms

Circulatory Shock, types and stages, compensatory mechanisms

MedicoseAcademics

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10 Things you Need to Know about TBI by Knight

1. Next Level Neuro Resus 26 June 2015 WilliamA Knight IV, MD, FACEP University of Cincinnati Traumatic Brain Injury – 10Things you Need to Know William.Knight@uc.edu @waknight4

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7. Epidemiology:TBI in the US 50,000 Deaths 100,000 Hospitalizations 1,111,000 Emergency DepartmentVisits ?? Receiving Other Medical Care or No Care * Average annual numbers, 1995-2001 2004 CDC Report: TBI in the United States: ED Visits, Hospitalizations, and Deaths 1.5 – 2.0 million TBIs occur each year.*

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10. Secondary Injury TBI Demyelination Mitochondrial Uncoupling Excitotoxic cascade Receptor activation Reduced GABA Inflammatory Cytokines Apoptosis Cerebral Edema Cytotoxic Edema Vasogenic Edema Pro Apoptotic cascade Free radicals & lipid peroxidation

11. WHATWE HAVE WHATWE NEED

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20. Drug Reversal Method Evidenc e Cost Aspirin (ASA) • Platelets •Demsopressin (DDAVP) •rFVIIa (40mcg/kg) •weak •$1000 – 12 units •$1 / mcg Plavix (Clopidogrel) •Platelets •Demsopressin (DDAVP) •rFVIIa (40mcg/kg) • terrible •$1000 – 12 units •$1 / mcg Warfarin (Coumadin) •Vit K •FFP (250 cc / bag) •PCC •Cryoprecipitate •rFVIIa (40mcg/kg) • good •$10 / 10mg •$60 / bag •$5000 / dose •$1200 / 20 bags •$1 / mcg TSOACs •PCC (depends) •Antidotes •Weak •??? •$5000 / dose •??? Heparin •Protamine •solid NSAIDS •Platelets •DDAVP •garbage •$1000 – 12 units

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32. Generalized spike/wave status

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37. Narayan et al, J Nsurg 1981

38. 0% 25% 50% 75% 100% 3 4 5 6 7 8 GR MD SD Veg Dead Marshall et al, J Nsurg 1991

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40.  DECRA ProTECT  Disease definition  Can what we see contributing to poor or good outcome be as wrong as these trials suggest or do we need to define the disease and patients better?  Multicenter RCTs can be successfully performed

41. Adeoye O & Shutter L. Neurotrauma & Critical Care of the Brain. JalloJ, ed. Thieme; 2009. CPP?

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44.  Target normal physiologic goals  Research  We know how to study ▪ Do we know what to study?  Early aggressive care is the future  24 hours of resuscitation prior to prognosis

45. “It’s not an exceptional case. We just don’t know how many exceptions to the rule there are. So. I don’t believe in the rule anymore.” - Joseph Giacino, PhD http://nymag.com/scienceofus/2015/06/dylan-rizzo-coma.html