TBI - Medical Management Flashcards
Definition
Blow or jolt to the head or a penetrating head injury
Disrupts function of the brain
What is the leading cause of TBI
Falls (47% resulting in ED visit, hospitalization, or death
What age group is most common for TBI
Children 0-14 (54%)
Adulta over 65 (79%)
TBI - M vs. F
M 3 x more likely to die from TBI than women
Mechanisms of brain injury
Acc-Dec Direct blow to head Blow to other body part Blast waves Shaking Head rotation Penetrating injury
Assessment TBI
GCS
Pupillary response
S/S with early vs. late signs
Glascow Coma Scale is used to measure what
Gold standard to assess LOC
What is the most useful clinical sign of deterioration
Change in LOC
Using the GCS
GCS - unable to use if
Hypoglycemic
Hypothermia
Shock
Alcohol/Drug
Pupillary Response - only important when
there are changes or deterioration in LOC
Not necessary with a GCS of 15
Pupillary response - if adverse response means what
Oculomotor nerve 3 - something is compressing the nerve and causing an adverse response to light
GCS scores range from
15 to 3
Lowest 3
GCS what is considered a coma
Less than 8
GCS - T or F - A person identified as brain dead can still have a GCS score of 3
TRUE
GCS - start with what
least invasive to the most invasive (4) observe if they have their eyes open spontaneously If not, then try speech (3) pain (2) no EO (1)
GCS - verbal response
5 oriented 4 confused 3 inappropriate words 2 incomprehensible words 1 no verbal response (on vent can be 1)
GCS - Motor Response
6 obeys commands
5 localizes pain
4 withdrawal to pain
3 abnormal flexion - decorticate posturing
2 abnormal extension - decelerate posturing
1 no motor response
What is typically the most important component of the GCS
Motor response
Pupil Response can be
Brisk
Sluggish
No rxn
Pupil Response - size
Pupil dilation is ___ to injury
Varies
Pupil dilation is ipsilateral to injury
Early s/s neuro deterioration
HA Drowsiness Disorientation Agitation N/V Irritability
Late s/s neuro deterioration
Posturing Seizing Pupil dilation Asymmetrical pupil response Cushings triad
Late s/s neuro deterioration - cushing’s triad
Bradycardia
Irregular respirations
HTN, wide pulse pressure
Classification of brain injury is based on what
GCS score
Duration of amnesia
Classification of brain injury - Mild - what GCS score and how long amnesia
More then or equal to 13
Less than 24 hours
Classification of brain injury - Mild - Clinical presentation
Awake, EO, Confusion, Memory and attn deficits, HA, Bx problems
Classification of brain injury - Moderate - what GCS score and how long amnesia
9-12 GCS
1-7 days amnesia
Classification of brain injury - Moderate - clinical presentation
Lethargic, EO to stimulation, Sleepy, Arousable
Classification of brain injury - Severe - GCS score and how long amnesia
Less than or equal to 8
1-4 wks (can last 1-2 months too though)
Classification of brain injury - Severe - Clinical Presentation
Coma, EC even with stimulation
Classification of brain injury - which ones are hospitalized
Moderate to Severe
Diagnostic Evaluation includes what
CT scan
MRI
EEG
Patterns of brain injury - Primary injury
Immediate result of direct cellular damage from a traumatic event
Unable to reverse the injury
Types - focal and diffuse
Patterns of brain injury - Secondary injury
Occurs hrs to days after initial injury
Disruption of blood flow and oxygen to brain
Focus tx on preventing this second injury
It is the damage occuring as a result of the body’s response to the first injury
Categories of Primary Injury - Diffuse (global)
Concussion - blow to head
Directly impacts consciousness
Diffuse axonal injury
Categories of Primary Injury - Focal (local)
Skull fractures
Intracranial hemorrhages
Contusion
Indirectly affect consciousness
Skull fractures - Types - Linear Basilar
Raccoon eyes (ant fossa) Battle signs (middle) CSF otorrhea (middle)
Skull Fractures - Types - Depressed Skull Fracture
Will have injury underneath - contusion
Intracranial hematomas - Epidural
Arterial in origin Rapid onset Hx of immediate LOC, awake, and then LOC Immediate surgery needed Better outcome if caught early
Intracranial hematomas - Subdural
Venous in origin
Acute or chronic onset
Worst outcome
Supportive or Surgical evacuation
Intracranial hematomas - Intraparenchymal
Bleeding in brain tissue, small large, single or multipl
Edema is pronounced
Supportive management
Monitoring
CR
Arterial line
Central venous pressure
ICP and cerebral profusion pressure
Indication for ICP monitoring
GCS score less than 8 AND an abnormal CT scan
Two of the following:
Symptomatic with bilateral motor posturing
Syst BP less than 90
Age over 40
Pathophysiology - Intracranial vault consists of what components
Brain tissue (80%)
Blood (10%)
CSF (10%)
Pathophysiology - Monroe Kellie Hypothesis
If volume in any component changes, the other areas have to compensate
If unable to compensate, the ICP will inc
ICP measures what
Pressure exerted by brain tissue, blood, and CSF within the cranial vault
ICP measures - normal
0 to 10 mmHg
ICP measures - abnormal
Greater than 20 for more than 5 minutes
You will initiate tx if greater than 20
Cerebral perfusion pressure - is what
Pressure at which the brain is perfused
Regulates cerebral blood flow - indirect measure of cerebral blood flow
Cerebral perfusion pressure - how to calculate
CPP = MAP minus ICP
CPP - normal range
Adult over 70
CPP - what level will lead to hypoperfursion of the brain and lead to ischemia
Less than 40
Cerebral blood flow - is regulated why
to supply brain with oxygen and glucose
If not maintained, ischemia occurs to the brain
Factors for regulating CBF
CPP ICP BP (MAP) Autoregulation to changes in BP Chemoregulation responst of BVs to hypoxia, CO2
CBF - if you have high carbon dioxide what happens
Vasodilate - inc CBF - inc ICP
CBF - if low carbon dioxide what happens
Vasoconstrict - dec CBF
Tx goal of TBI
Focus on factors that cause further injury
Intervention to reduce risk of secondary injury
Early management
Airway/Cervical Spine precautions Breathing Circulation Disability (GCS) Exposure
TBI management - Airway/Breathing
Intubate if GCS less than 8
We want SaO2 95% or higher
Maintain PaCO2 35-40
TBI management - Circulation
Control bleeding
Maintain adequate BP (IV fluids, Blood administration, Vasopressor)
Normovolemia - maintain CVP between 5 and 10
TBI management - optimize positioning to improve venous return
Head of bed raised 30 degrees
Neutral head position
Ensure C collar is not too tight
Avoid extreme hip flexion
TBI management - decrease metabolic rate
Reduce environmental stimulation Sedation meds Analgesia meds for pain NM blockade (paralytics) Normothermia
TBI management - Lowering ICP
External ventricular drain
Hyperosmolar therapy
TBI management - Lowering ICP - External ventricular drain
Drains CSF to reduce intracranial volume
Measures ICP at same time too
TBI management - Lowering ICP - Hyperosmolar Therapy
Dec cerebral edema
Meds - mannitol, hypertonic saline
These meds pull extra fluid from the brain down to decrease ICP
TBI Management - surgical management
Evacuate hematoma
Decompressive craniotomy
TBI management - surgical management - tier 2 is what
Decompressive craniotomoy - Remove part of cranium to allow brain to swell - place bone flap once edema resolved
Usually not done unless all other measures fail
TBI management - max swelling usually occurs when
72 hours is usually when it peaks and it can last 1 to 2 weeks
TBI management - Reduce cerebral metabolic demands
Tier 2
Induced hypothermia
Barbituate coma to reduce brain activity
Systems management
Stable electrolytes and blood sugar Stress ulcer prophylaxis Anticonvulsants to prevent seizures Venous thrombosis prophylaxis Nutrition Skin breakdown prevention Bowel and bladder regime Tracheostomy Social
Complication
Sepsis
Renal failure
Pulmonary failure
Predicting outcome
Duration of unconsciousness Initial GCS CT scan results ICP results Pupillary response Age of patient
Long term neurobehavioral sequela
Cog deficits
Bx and personality changes
Psychiatric disorders
