Week 6 - Head Injuries

Question 1

Can you see a Moderate diffuse Axonal Injuries divided (DIA) on a CT scan?

Answer 1

NO

Question 2

What is the target temperature range for the initial management of head injuries? Why?

Answer 2

-Target 36-38.3 C

Cerebral metabolic rate increased 5-7% per degree Celsius body temp rises
Brain damage on hypothalamus/inflammation/infection leading to hyperthermia

Question 3

What happens if the brain is deprived of oxygen?

Answer 3

Lack of oxygen to brain is from lack of oxygen in body

Neuron death

Question 4

What is a Intracerebral Hematoma / Haemorrhage? (where is the bleeding occuring? what causes it?)

Answer 4

Focal injury – blunt trauma/penetrating injury/severe acceleration or deceleration

Where is the blood accumulating/what vessel is torn:
-Arteries/veins affected within the brain tissue (beneath pia mater)
-The clot is usually surrounded by an area of edema and ischemia elevated ICP

Question 5

Difference between an acute, subacute, and chronic Subdural hematoma? (S+S)

Answer 5

Acute – within 48 hrs post injury

Subacute – within 2 days – 2 weeks post injury
Slower developing symptomology

Chronic – within 2-4 weeks
Lethargy, absentmindedness, headache, vomiting, pupillary changes
Easy to miss! Mistaken as dementia

Question 6

What do open and closed head injuries have?

Answer 6

Note: “open” head injuries have torn dura and usually broken skin. “Closed” head injuries have intact skin and dura.

Question 7

What is the appropriate range for CPP? (what is the ideal range? What is the dangerous range?)

Answer 7

Normal CPP ranges from 60-100mmhg (50-150mmhg in healthy brains).

Ideal CPP: 60-80mmHg
Values could be from 50-150mmHg and be acceptable depending on the context (injuries, comorbidities, age, etc.)

Dangerous CPP: less than 50mmHg (adults, teens, school children), less than 40mmHg (toddlers, infants)

Question 8

How are diffuse Axonal Injuries divided (DIA)/classified? (what does the servity of the injury depend on?)

Answer 8

Divided into mild (concussion), moderate, and severe

-The amount, severity, and location of axonal damage will determine the clinical severity and outcome of diffuse brain injury

Question 9

What is Chronic Traumatic Encephalopathy (CTE)? (what causes it?)

Answer 9

Repeated concussions – common in athletes - Repeated concussions lead to CTE

Associated with repeated concussions/injuries to the head!!!

Repeating injuries

Progressive degenerative disease of the brain tissue
Tau protein

Question 10

How are TBI classified?

Answer 10

-TBI’s are classified based off of their severity + pathological features!

Question 11

What does Vasoconstriction in brain lead to?

Answer 11

Vasoconstriction in brain  decreased CPP (brain dies)  reduced ICP (no herniation = good)

Question 12

What is the economic significance of a brain injury?

Answer 12

High economic cost
Direct (hospital care, rehabilitation, etc.)
Indirect (lost work/productivity, care burden on

Question 13

Why is a decreased MAP dangerous in brain injuries?

Answer 13

Decrease in MAP = decrease in CPP = neuron death

Question 14

What are our goals in managing secondary brain injuries?

Answer 14

Prevention is key or minimization - Prevention brain injuries from getting worse it key here for prevention of secondary injury

Management is minimizing these secondary injures - hypoxia/hypoxemia, hypotension, anemia, increased ICP, impaired auto regulation, hypo or hyper capnia, hypo or hyper glycemia, biochemical changes, patient’s metabolic demand - by having appropriate cerebral perfusion pressure (50-70 MM), increasing cerebral oxygen delivery to the brain, avoid ischemia to the brain, preventing either systematic (extra cerebral) or neurological (intra cerebral) complications.

Question 15

With basal skull fractures what is an intervention we NEVER do!!

Answer 15

No NGs, packing, or nose blowing!

Question 16

What is a mild diffuse Axonal Injuries (DIA)? What are some S+S? What are some causes of a DIA?

Answer 16

-Transient disturbance of neurological function

-Functional rather than structural

What is DAI?
DAI occurs when the brain rapidly moves within the skull, causing the brain’s long connecting nerve fibers (axons) to shear or tear.

S+S: Besides loss of consciousness and amnesia, other symptoms of moderate DAI can include fatigue, trouble sleeping, difficulty concentrating, headaches, weakness, balance deficits, decreased coordination, and trouble with memory, attention, and processing

Causes:
DAI is often caused by high-speed motor vehicle accidents, falls, sports injuries, or assaults, and can also occur in cases of child abuse like shaken baby syndrome.

Question 17

What is the normal range for ICP? At what range do we treat ICP?

Answer 17

Intracranial pressure is normally between 0-20mmHg

-We treat any patient with an ICP of 20mmHg or above

Question 18

Metabolic Demand - what can increase a patient’s metabolic demand? (3 main things) (what does it put our tissue at risk for?)

Answer 18

Seizures, hyperthermia, agitation increases our metabolic demand and put tissue at risk for ischemia

Question 19

S+S for a subdural hematoma? How do we diagnose them?

Answer 19

depends on acute, subacute, or chronic - S+S depends on the speed/how fast the bleed is occurring!!!!! We differentiate between the 3 different types of bleed based on the S+S

Pupil abnormalities, motor deficits, altered LOC

Acute – within 48 hrs post injury
Subacute – within 2 days – 2 weeks post injury
Slower developing symptomology
Chronic – within 2-4 weeks
Lethargy, absentmindedness, headache, vomiting, pupillary changes
Easy to miss! Mistaken as dementia

Dx: CT or MRI

Question 20

How can a TBI occur?

Answer 20

A traumatic brain injury (TBI) can occur due to a blow to the head, skull
penetration, or oxygen deprivation.

Question 21

What are Subdural hematomas more common than?

Answer 21

6 times more common than epidural hematomas, and 60-90% are fatal

Question 22

S+S for a mild diffuse Axonal Injuries (DIA)? How long do these S+S last for? (What is it?) How long does it take for them to typically resolve/get better?

Answer 22

S/S: coma 6-24 hrs max
Amnesia (severity/length is a good indicator of injury severity), Headache, Drowsy, disoriented, Confusion, Staggered gait / slurred speech, Visual disturbances (seeing stars – occipital lobe), Personality/behavioural changes, Memory difficulties (difficulty concentrating), Vertigo, (paresthesia, paralysis, weakness), Apathy, irritability, insomnia

resolve in 7-10 days - You will go back to your baseline

Question 23

What is a primary brain injury? What does it result in?

Answer 23

This is the initial injury!!! (MVA, Blunt force, etc.) -this results in a focal and/or diffuse injury

Question 24

What is normal MAP?

Answer 24

Normal value for an adult: 70-100mmHg

Question 25

Difference between a primary and secondary brain injury?

Answer 25

Primary – occur at time of initial injury (baseball bat into head  Cerebral Contusion) Secondary – cascading effects (hypoxia, ischemia, hypotension, edema, increased ICP) of the primary injury that cause further damage hours to days later

Question 26

What is a secondary brain injury a result of (think of 5 different reasons/causes)? What can/do they occur? (What is something else that they can occur from that you normally wouldn't think of?)

Answer 26

Secondary injury is the resulting hypoxia, ischemia, hypotension, edema, or increased ICP that follows the primary injury. Secondary injuries can also occur from injuries to the body that cause hypoxia (such as strangulation) Secondary injuries occur several hours to days after the initial injury

Question 27

Difference between a focal and diffuse brain injury?

Answer 27

Focal brain injury: Symptoms that are related to damage to a specific area/part of the brain Diffuse brain injury: Widespread injury that is spread out all over/across the brain!

Question 28

Causes of primary brain injury?

Answer 28

occur at the initial time of the injury – MVC, blunt force, that results in displacement, bruising, or damage to the three components (CSF, Blood, Brain tissue) – which results in a focal or diffuse or both injury

Question 29

S+S of a Moderate diffuse Axonal inury (DAI)? Where is the impairment/damage occuring? (Will the patient recover to their baseline?)

Answer 29

Coma for 24 hours to a few days Tearing of axons in both hemispheres - impairment to cerebral cortex and diencephalon Incomplete recovery to patient’s baseline (DAI occurs when the brain rapidly moves within the skull, causing the brain's long connecting nerve fibers (axons) to shear or tear - DAI is often caused by high-speed motor vehicle accidents, falls, sports injuries, or assaults, and can also occur in cases of child abuse like shaken baby syndrome)

Question 30

What is CPP? (What is it different b/w), What does it represent?

Answer 30

Cerebral Blood Flow (CPP) = Difference b/w arterial input pressure and venous output pressure CPP represents the pressure difference between the blood pressure pushing blood into the brain and the pressure within the skull that resists that flow *Cerebral perfusion pressure (CPP) is the net pressure gradient that drives blood flow and oxygen delivery to the brain, calculated as the difference between mean arterial pressure (MAP) and intracranial pressure (ICP).

Question 31

When does brain ischemia develop? (when are we worried?) (When does irreversible brain damage start to occur?)

Answer 31

Brain ischemia develops at CPP levels below 60 and irreversible brain damage occurs with CPPs less than 50mmHg -We are worries Less then 60 CPP brain damage occurs , less than 50, brain damage IS occurring

Question 32

What are the 4 different types of skull fractures? Are they focal or diffuse injuries?

Answer 32

Describe the different types of skull fractures (focal injuries) 1.) Linear – single fracture line or crack 2.) Comminuted – splintered/shattered skull fraction 3.) Depressed skull fracture – bone fragments inwardly compressed into the brain tissue (open or closed) 4.) Basilar skull fracture – linear fracture along the base of the skull (periorbital echymosis/racoon eyes or battle signs)

Question 33

What systemic factors (extra cerebral) can lead to a secondary brain injury? (what does it ultimately lead to?)

Answer 33

Hypoxia! = Low levels of O2 in the blood = not enough O2 is available for tissue perfusion (can’t “officially” test for hypoxia but we gage this off of O2 stats!) -If the brain is deprived of O2 due to lack of O2 in the body it will lead to neuron death

Question 34

S+S for a Intracerebral Hematoma / Haemorrhage (4 of them? when do they typically occur? How do we diagnose them? When do symptoms typically begin to appear?

Answer 34

S+S: Majority of neurological deterioration occurs in the first 48-72 hrs (up to 7-10 days post injury) -Headache, progressive deterioration in level of consciousness, motor deficits (contralateral hemiplegia) and pupil abnormalities Dx: CT or MRI

Question 35

What are 5 interventions we want to do for out initial managament of head injuries?

Answer 35

1.) Airway remains first priority! Low GCS can’t protect airway – consider c-spine 2.) Oxygen to prevent hypoxia/hypoxemia, possibly hyperventilation Less co2 = less vasodilation, but can lead to ischemia/vasoconstriction  hyperventilation only to avoid herniation 3.) Maintain cerebral perfusion pressure AVOID HYPOTENSION, but avoid Hypertension MAP >90 ; ICP < 20; CPP 60-80 4.) Frequent GCS Changes in LOC occur first 5.) Temperature control Cerebral metabolic rate increased 5-7% per degree Celsius body temp rises Brain damage on hypothalamus/inflammation/infection leading to hyperthermia Target 36-38.3 C

Question 36

What is cushing triad/what does it indicate? What are its S+S?

Answer 36

Cushing’s Triad: set of three physiological responses indicating increasing ICP and brain herniation 1.) Hypertension (widening pulse pressure) - Increasing systolic pressure with normal or low diastolic pressure 2.)Bradycardia 3.) Irregular breathing pattern/Bradypnea

Question 37

What is a cerebral contusion? What is it's MOI? (think back to Patho!!)

Answer 37

Bruising to brain tissue, most often frontal or temporal lobes - Bruising to the brain tissue (frontal/temporal lobe) Coup - Site of impact Contrecoup – Opposite site of impact

Question 38

Complications of a TBI?

Answer 38

These may include memory impairment, changes in behavior or personality, movement disorders, paralysis, vision and hearing loss, persistent headaches, seizures, difficulty with anger and impulse control, impaired motor function, speech difficulties, loss of consciousness, and even death.

Question 39

What do cerebral contusions have the potential for?

Answer 39

Potential for haemorrhage and edema  increased ICP

Question 40

What is the secondary brain injury a result of? What does it damage?

Answer 40

It is a result of the primary injury!!! - Primary injury leads to a secondary cascades which extend the damage to cells that are not initially irreversibly damaged.

Question 41

What are 4 medical management/interventions we can do for head injuries? (what can one of the meds cause?)

Answer 41

1.) Patient positioning – low fowlers (HOB 15-30 degrees) 2.)Meds: Sedation – impairs reliability of neuro assessments, but pain/cough/suction/repositioning on ventilator increase ICP -Analgesia – can reduce BP and lower demands on brain Seizure prophylaxis – important! -Paralytics - ventilation -Diuretics/hypertonic saline – mannitol! (osmotic diuretic) Reduces ICP in 30 minutes – given in repetitive boluses (May cause electrolyte/osmolarity disturbances) 3.)Fluid restriction – avoid hypo/hypertension/prevent fluid overload orcerebral volume 4.) Glucose control – prevent anaerobic metabolism/maintain osmotic gradient

Question 42

What is the leading cause of all trauma related deaths + Permanent Disability?

Answer 42

Head injuries = leading cause of all trauma related deaths + Permanent Disability

Question 43

Why do we want to administer O2 as an inital management/intervention for head injuries? (think about what it prevents)

Answer 43

Oxygen to prevent hypoxia/hypoxemia, possibly hyperventilation -Less co2 = less vasodilation, but can lead to ischemia/vasoconstriction  hyperventilation only to avoid herniation

Question 44

What are the S+S for a cerbrbal contusion? How do we dignose it?

Answer 44

S+S: delayed loss of consciousness (associated with DAI), depend on the location of the contusion, headaches, nausea and vomiting, diplopia, or seizures Dx: CT – Xray not enough detail

Question 45

For secondary brain injuries what is it a result of? (what is there ultimaltey a lock of?

Answer 45

Secondary – resulting hypoxia, ischemia, hypotension, edema, or increased ICP occurring several hours to days after primary injury result of cerebral blood flow and cerebral metabolism mismatch (ultimately there is a lack of oxygen, glucose, or both at the cellular level)

Question 46

What is the personal significance of a brain injury? (think 2 main/big ones)

Answer 46

High personal cost Physical suffering (long term disabilities are not uncommon with severe brain injuries) Psychosocial suffering (sudden loss of function and abilities can cause stress and emotional trauma to the patient and their family)

Question 47

What is the ideal range for CPP? (when *could* different values be acceptable?) What is the dangerous range for CPP?

Answer 47

Ideal CPP: 60-80mmHg Values *could* be from 50-150mmHg and be acceptable depending on the context (injuries, comorbidities, age, etc.) Dangerous CPP: less than 50mmHg (adults, teens, school children), less than 40mmHg (toddlers, infants) We are worries Less then 60 CPP brain damage occurs , less than 50, brain damage IS occurring

Question 48

What do Electrolyte imbalances/metabolic changes lead to?

Answer 48

Electrolyte imbalances, metabolic changes, hypotension, seizures, ischemia, oxygen (hypoxia/hypoxemia), CO2, glucose  lead to secondary brain damage/cascading effects

Question 49

What Systemic Factors (Extra Cerebral) constitutes a major predictor of brain death? (think vital signs) (What is the value that constitutes a major predictor of brain death)

Answer 49

*Hypotension* Systemic hypotension (<90mmHg) constitutes a major predictor of brain death No blood to brain = unconsciousness and neuron death in minutes

Question 50

What are the ranges for CPP? (normal, when damage occurs, when Imminent brain death occurs)

Answer 50

Cerebral Perfusion Pressure (CPP): Normal: 60-100; Healthy 60-80; Damage occurs < 60; Imminent brain death < 50mmHg. Too low  death

Question 51

What is the overall goal of managing brain injuries?

Answer 51

Goal: balancing act of above MAP, CPP, ICP pressures

Question 52

What is a brain herniation?

Answer 52

Distortion and displacement of the brain from one intracranial compartment to another

Question 53

What is Monro-Kellie hypothesis? What are its components?

Answer 53

Monro-Kellie hypothesis: -An increase in any one of the components that make up volume and pressure, causes a change in the volume of the others brain tissue (80%), Blood (10%) and CSF (10%)

Question 54

Difference between head and brain injury?

Answer 54

What is the difference between head injuries and brain injuries? Head = skull / Brain = Brain (often synonymous)

Question 55

What type of hhead injury is an epidural hematoma? Where is the bleed occurring? What patients are they more common with?

Answer 55

Focal Injury – blunt trauma to temporal frontal or occipital areas Meningeal artery between the skull and dura mater More common in younger patients

Question 56

What is a subdural hematoma? Where is the bleeding occuring? What causes it?

Answer 56

Focal injury – rapid acceleration/deceleration Where is the blood accumulating/what vessel is torn: Bridging veins b/w dura and arachnoid mater

Question 57

What is the first priority for the initial management of head injuries?

Answer 57

Airway remains first priority! Low GCS can’t protect airway – consider c-spine

Question 58

What are the S+S for a epidural hematoma? How do we diagnose it?

Answer 58

S+S: history of head injury and a brief period of unconsciousness, followed by a lucid period in which consciousness is regained, followed by rapid progression to unconsciousness. *They are often associated with someone losing conscious then they become lucid and saying they’re okay and then decomp very quickly (artierial bleed)!!!!!!* Dx: CT or MRI (X-ray not enough to diagnose!)

Question 59

When does Chronic Traumatic Encephalopathy (CTE) occur? What does it lead to/its S+S? ( 8 main ones)

Answer 59

Occurs months, years, or decades after repeated head injuries Leads to memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, and eventually, progressive dementia

Question 60

What are some surgical interventions we can use for the management of head inuries?

Answer 60

CSF Drainage – external ventricular drain (reduce ICP) Craniotomy / Craniectomy

Question 61

What medications can we administer for the meical management of head injuries? ( 5 main ones)

Answer 61

Diuretics/hypertonic saline – mannitol! (osmotic diuretic) -Reduces ICP in 30 minutes – given in repetitive boluses!!May cause electrolyte/osmolarity disturbances Sedation – impairs reliability of neuro assessments, but pain/cough/suction/repositioning on ventilator increase ICP Analgesia – can reduce BP and lower demands on brain Seizure prophylaxis – important! Paralytics - ventilation

Question 62

What do Seizures and/or hyperthermia increase and put us at risk for?

Answer 62

Seizures, hyperthermia, agitation increases our metabolic demand and put tissue at risk for ischemia

Question 63

Due to hypotentsion (Systemic Factors (Extra Cerebral): Blood Pressure) what does no blood to the brain lead to?

Answer 63

No blood to brain = unconsciousness and neuron death in minutes

Question 64

Why do we do a frequent GCS as part of our inital management for head injuries?

Answer 64

4.) Frequent GCS Changes in LOC occur first

Question 65

What can excessive ICP lead to/obstruct?

Answer 65

Sustained pressures greater than 20mmHg constitute increased intracranial pressure or intracranial hypertension. Excessive ICP can obstruct blood flow, destroy brain cells, displace brain tissue and damage delicate brain structures (brain herniation = dead)

Question 66

How can the scalp be injured? (3 things/ways)

Answer 66

How can the scalp be injured? Abrasion (top layer of skin removed), contusion (hematoma), laceration (scalp is torn).

Question 67

What should the patient bed position be if they have a head injury?

Answer 67

Patient positioning – low fowlers (HOB 15-30 degrees)

Question 68

What does Vasodilation in brain lead to?

Answer 68

Vasodilation/blood flow in brain  increased CPP (brain wants this)  increased ICP (brain dead/herniation

Question 69

What is the normal range for MAP? (what does it determine? what happens when its to low?)

Answer 69

Mean Arterial Pressure (MAP): Normal: 70-100mmHg. Determines CPP. Too low  death

Question 70

S+S of a Traumatic Subarachnoid hemorrhage (6 main ones) ? How do we diagnose them?

Answer 70

S+S: decreased level of consciousness, motor deficits (hemiparesis), pupil abnormalities, and possible evidence of meningeal irritation such as headache, photophobia, and nuchal rigidity Dx: CT (bleeding in ventricles) or MRI

Question 71

What is a Traumatic Subarachnoid hemorrhage? Where is the bleeding occuring? (what kind of injury is it?

Answer 71

Focal injury – severe head trauma Where is the blood accumulating/what vessel is torn: Artery b/w arachnoid and pia mater - This is fed by arteries (fast bleed + progress quicker)

Question 72

What is a diffuse Axonal Injury (DIA)? (what are they caused by?, how much of the brain is affected?)

Answer 72

Diffuse injury – blunt trauma from acceleration/deceleration or rotational forces (MVCs most common). Does not need direct hit on head Entire brain is effected Definition: -Effect entire brain -Axons are strained and torn or disrupted/transected (Trauma causes the axon to twist and tear/chear) -They are the worst kind of brain injury -Functionally impaired

Question 73

What specific diuretic can we administer for the medical management of a head injury? (how is it given? what might it cause?)

Answer 73

Diuretics/hypertonic saline – mannitol! (osmotic diuretic) -Reduces ICP in 30 minutes – given in repetitive boluses -May cause electrolyte/osmolarity disturbances

Question 74

Treatment for a Traumatic Subarachnoid hemorrhage?

Answer 74

Treatment: NEEDS a drain

Question 75

S+S for a severe diffuse Axonal Injuries(DIA)? what impairment/damage occuring? What is the treatment?

Answer 75

Coma for days to months Extensive white matter dysfunction Small tears visible on CT or MRI Treatment is supportive care Poor prognosis, major cognitive and neuro deficits (vegetative state)