308 slide TBI TRAUMATIC BRAIN INJURY Treatment PowerPoint Presentation on CD For Sale

308 slide TBI TRAUMATIC BRAIN INJURY Treatment PowerPoint Presentation on CD


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308 slide TBI TRAUMATIC BRAIN INJURY Treatment PowerPoint Presentation on CD :
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Contains the following key public domain (not copyrighted) U.S. Government publication(s) on one CD-ROM in both Microsoft PowerPoint and Adobe Acrobat PDF file formats:

TITLE: Traumatic Brain Injury, 308 pages (slides)

Partial SLIDE TOPICS, SUBTOPICS and CONTENTS:

TBI 1

Joseph Kamerath

PMR PGY2

TBI 1
In An Instant

Joseph Kamerath

PMR PGY2

TBI 1

Mild/Mod/Severe

Combat TBI

Anatomy

Pathophysiology

Imaging

Next time… Management, treatment etc

(TBI 2: In Several Instances)

TBI

Toronto Bay Initiative – A non-profit, volunteer-based charitable community organization dedicated to a cleaner, greener, healthier, and more accessible Toronto Bay

Total Body Irradiation – When radiation is delivered in a manner that it covers the whole body

Tolerate Bill’s Ignorance – He doesn’t know any better

TBI

National Brain Injury Association

TBI is an insult to the brain, not of a congenital or degenerative nature that may produce a diminished or altered state of consciousness which results in impairment of cognitive abilities or physical functioning. It can also result in the disturbance of cognitive abilities or physical functioning. These impairments may be either temporary or permanent and cause partial or total functional disability or psychosocial impairment.

TBI

Center for Disease Control

Any occurrence of injury to the head that is documented in a medical record, with one of the following conditions attributed to head injury:

Observed or self-reported decreased level of consciousness

Amnesia

Skull fracture

Objective neurological or neuropsychological abnormality

Prevention

airbags

safety belts

motorcycle helmets

motorcycle proficiency

bicycle helmets

violence prevention programs

falls prevention programs for the elderly

following the rules of play in a sport

use of proper sport equipment

Prevention Programs such as “Think First”

Mild TBI

Traumatic head injury with ANY of the following:

LOC: < 30 min

If >30 min; init GCS of 13-15

PTA: < 24 H

AMS: At time of accident

Focal Neuro deficits: Transient or prolonged

No abnormalities on CT scan

No operative lesions

Length of hospital stay < 48 hours

Mild TBI

Nausea

Vomiting

Dizziness

Headache

Blurred vision

Sleep disturbances

Quick fatigue

Lethargy

Some other nondescript sensory loss

Mild TBI: Cognitive Deficits

Decreased:

Attention

Concentration

Perception

Memory

Speech/language abilities

Executive functioning

Mild TBI: Behavioral Changes

Poor emotional responsivity

Emotional lability

Irritability

Quick to anger

Disinhibition

Moderate TBI

Inpt >= 48 hours

GCS score of 9-12 or higher

Operative intracranial lesion

Abnormal CT scan findings

Severe TBI

Occurs with prolonged unconscious state or coma.

Coma no response

Vegetative state sleep-wake cycle/arousal

no interaction

Persistent vegetative state for > one month

Minimally responsive state awareness of environment

prim reflexes, inconsistent

Akinetic mutism dopamine pathway damage

minimal mvmt, eye tracking

Locked in syndrome only eyes move, able to think

Brain Death

Combat TBI

Combat TBI

Blast Injury (1°, 2°, 3°)

Combat TBI

Blast Injury (1°, 2°, 3°)

Polytrauma

Combat TBI

Blast Injury (1°, 2°, 3°)

Polytrauma

Infections

Combat TBI

Blast Injury (1°, 2°, 3°)

Polytrauma

Infections

PTSD

Combat TBI

Blast Injury (1°, 2°, 3°)

Polytrauma

Infections

PTSD

Hippocampus

Prefrontal cortex

amygdala

Primary Injury

Focal

Occur at a specific location in brain

Cerebral Contusion

Intracranial Hemorrhage

Epidural hematoma

Subdural hematoma

Intracerebral Hemorrhage

Subarachnoid Hemorrhage

Diffuse

Diffuse Axonal Injury

Primary Injury

Open/Closed

Cerebral Contusions

Cortical bruising; crests of gyri

Into depths if injury is forceful enough

Gray matter abnormality

Frontal and temporal lobes most effected

Commonly b/l, not nec. symmetrical

Low velocity injury (falls)-usually

Contusion

Frontal

Temporal

Concussion

Deformity of the deep structures of the brain

Widespread neurologic dysfunction

Impaired consciousness or coma

Mild DAI?

Epidural Hematoma

Subdural Hematoma

Subarachnoid Hematoma

Intracerebral hematoma

Intraventricular hemorrhage

Brain herniation:

Supratentorial herniation

Subfalcine herniation:

Most common

Central transtentorial herniation

Uncal herniation

Cerebellar herniation

Diffuse Axonal Injury

Centripetal Model

Disruption at node of Ranvier

Excitotoxicity

Most Vulnerable:

cerebral hemispheres, corpus collosum, midbrain, pons

Diffuse Axonal Injury

Excitatory amino acids:

Glutamate

Aspartate

Glycine

Secondary Brain Injury

Intracranial hemorrhage

Subdural or epidural hematomas

Herniation

Hydrocephalus

Cerebral edema

Cerebral ischemia

Conditions that exacerbate 2º injury:

Hypoxemia

Hypercarbia

Hypotension

Acidosis

Cerebral edema: Causes

Neurochemical transmitters

Increased ICP

Disruption of the blood brain barrier

Impairment of vasomotor autoregulation

Dilatation of cerebral blood vessels

Progression of injury

Cranial insult

Tissue edema

Increasing ICP

Compression of arteries

Decreased cerebral blood flow

Decreased O2 with cellular death

Edema around necrotic tissue

Progression

Increasing ICP with compression of brainstem and respiratory center

Accumulation of CO2 resulting in vasodilation

Increasing blood volume further increasing ICP

Death

Cerebral Physiology

AutoRegulation

CVR maintain CPP despite MAP

Responsive to pCO2

CBF=CPP/CVR

CPP=MAP-ICP

MAP= 2DP+SBP/3

NL= 50-150

Hypotension

Most prognostic factor

Episode of decreased BP correlated with poor outcome

MAP> 90

CPP= MAP- ICP

Most important to keep CPP > 70

Hydration, Pressors

Future Physiology…

Biomarkers

S100B

Neuron-specific enolase

Myelin basic protein

Glial fibrillary acid protein

Frontal Lobe

Paralysis

Sequencing

Perseveration

Attending

Lability

Social behavior

Personality

Problem solving

Expressive (Broca's) aphasia

Parietal Lobe

Inability to attend to more than one object at a time.

Anomia

Agraphia

Alexia

Left/Right confusion

Dyscalculia

Apraxia

Inability to focus visual attention

Hand-eye coordination

Occipital Lobe

Visual field cuts

Difficulty with locating objects in environment

Difficulty in recognizing drawn objects

Color Agnosia

Hallucinations

Visual illusions

Movement Agnosia

Temporal Lobes

Prosopagnosia (faces)

Wernicke's aphasia

Short/long term memory

Decreased interest in sex

Inability to catagorize objects (Categorization).

Right lobe damage can cause

persistent talking

Aggression

Brain Stem

Decreased respiratory vital capacity (speech)

Dysphagia

Balance/movement

Vertigo

Insomnia, sleep apnea

Endocrine abnormalities

Cerebellum

Coordination/balance

Inability to reach out and grab objects.

Tremor

Vertigo

Slurred Speech (Scanning Speech).

Rapid movements

Imaging

CT

Imaging

CT

MRI

Imaging

CT

MRI

D-MRI (Diffusion MRI)

Diffusion Weighted Imaging

Imaging

CT

MRI

D-MRI

DTI (Diffusion Tension Imaging)

Diffusion Tensor Imaging (DTI)

Imaging

CT

MRI

D-MRI

DTI

BOLD fMRI (Blood Oxygen Level Dependant)

BOLD fMRI

Imaging

CT

MRI

D-MRI

DTI

BOLD fMRI

PW-MRI (Perfusion Weighted)

Imaging

CT

MRI

D-MRI

DTI

BOLD fMRI

PW-MRI

MRS (Magnetic Resonance Spectroscopy)

Imaging

CT

MRI

D-MRI

DTI

BOLD fMRI

PW-MRI

MRS

SWI (Susceptibility-Weighted Imaging)

SWI

Imaging

CT

MRI

D-MRI

DTI

BOLD fMRI

PW-MRI

MRS

SWI

PET

PET

TBI 2

Joseph Kamerath

PGY2

TBI Complications/Mgmt etc…

TBI Rehab State of Science 2006

Pharmcologic neuroprotection

Nonpharmacologic acute treatment

Seizure

HO

DVT

Spasticity

Dysautonomia

Hydrocephalus

Cognitive Rehab

Pharm tx of cognitive deficits

TBI Complications/Mgmt etc…

Posttraumatic agitation

Cranial Neuropathy

Endocrine

Headache

Depression

Pharmacologic Neuroprotection

Corticosteroids: bad

Pharmacologic Neuroprotection

Corticosteroids: bad

NMDA receptor antagonists?

Gacyclidine: maybe

Pharmacologic Neuroprotection

Corticosteroids bad

NMDA receptor antagonists?

Cannabiniod

Dexabinol: no benefit

Pharmacologic Neuroprotection

Corticosteroids bad

NMDA receptor antagonists?

Cannabiniod

Dexabinol

Magnesium, Progesterone, Cyclosporine, Citicoline effective in preclinical models

NIH trials now underway

Nonpharm acute tx

Hypertonic saline

Nonpharm acute tx

Hypertonic saline

Nutrition

Nonpharm acute tx

Hypertonic saline

Nutrition

Therapeutic hypothermia

Nonpharm acute tx

Hypertonic saline

Nutrition

Therapeutic hypothermia

Early decompressive craniectomy

Posttraumatic Seizures

Immediate – within 1 day post injury

Early – within 1-7 days

Late – after 1st week

Proposed mechanism of PTS

Posttraumatic Seizures

Most occur within 1-3 months

50-66% within 1 yr

75-80% within 2 yr

Mild TBI – 1.5%

Mod TBI – 2.9%

Severe TBI – 17%

Overall – 3.1%

Risk Factors for late PTS

Penetrating head injury (33-50%)

Intracranial hematoma (25-30%)

Early Sz (25%)

Depressed skull fracture (3-70%)

Prolonged coma/PTA >24hrs (35%)

Others – Dural tearing, Presence of FB, Age, ETOH, TCAs, focal signs (aphasia/hemiplegia)

Prophylactic Anticonvulsants

Valproic acid, carbamazepine less sedating

All anticonvulsants - Sedating, cognitive deficits

Duration of treatment.

Phenytoin – Effective at preventing early PTS (Temkin ’90)

No proof of improved outcome

Withdrawal of anticonvulsants




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