week 1 brain- traumatic

Question 1

TBI

Answer 1

-Caused by forces of trauma either localized or throughout brain; can be associated with variety of mechanisms

Question 2

primary- focal

Answer 2

occur at specific location in brain. Blunt force. contusion or inter cranial hemorrhage.

Question 3

primary focal-cerebral contusion

Answer 3

Blunt trauma to local brain tissue that produces capillary bleeding into brain tissue
Relatively common with blunt head injuries
Often causes prolonged confusion or other neurologic deficit

-May result from a coup injury (damage at site of force) or injury at several sites in the brain due to coup-contrcoup (Skull and CSF provide protection, but force resulting in bouncing of brain within skull may cause coup-contrecoup injury
Blunt force to head accelerates brain within skull, and then brain decelerates abruptly, hitting inner skull surfaces)

Question 4

Haemorrage

Answer 4

Result from vascular injury & bleeding
Depending on the position of the ruptured vessel, bleeding can occur in any of several compartments, including the epidural, subdural and subarachnoid spaces or into the brain itself (intracerebral haematoma).

Question 5

Focal: Traumatic Intracerebral

Answer 5

-Ruptured blood vessels within substance of brain
Single or multiple; occur in any lobe but typically frontal and temporal.
-Generally minimal blood loss but particularly damaging
-Free blood outside vessels irritates nervous tissue causing tissue oedema
-May occur with severe motion during head injury, or contusion can converge into haematoma
-More common in older adults/those with brittle cerebral vessels

Question 6

Focal: Epidural (Extradural)

Answer 6

Bleeding between the dura mater and skull
Involves arterial vessels, often the middle meningeal artery in the temporal region.
Usually from tear in artery, associated with skull fracture (temporal)
Arterial bleeding so haematoma rapidly expands & compresses brain, increasing ICP
More common in younger people
Dura less firmly attached to skull surface than in older people

Question 7

Focal: Subdural

Answer 7

Develops between dura mater and arachniod layer and bleeds into subarachnoid space.
Usually small venous bleed so develops very slowly; may be subtle presentation- not actually inside the brain on outde put when develops puts pressur eon brain.
Usually due to tear in small bridging vein/s connecting veins on surface of cortex to dural sinuses
Bridging veins pass through CSF-filled subarachnoid space
Readily snapped in injury (sudden brain movement relative to skull)
-acute-fast high mortality
-subacute-loc can be remidied
chronic-presents week later

Question 8

layers of brain

Answer 8

• skull
• dura mater
• subdural space
• arachnoid
• sub arachnoid layer-where csf lives
• pia mater

Question 9

diffuse-concussion

Answer 9

Transient neurogenic dysfunction caused by a mechanical force to the brain
Form of TBI where no injury is detected on CT imaging
Typically due to direct blow to head/face/neck
<10% of concussion injuries involve LoC
Patient has signs/symptoms of altered brain function
-post concusion syndrome involves poor concenttration, memory, insomnia, irratability.

Question 10

diffuse- diffuse axonal injury

Answer 10

Tearing/disruption of axonal fibres in white matter & brain stem
Typically caused by blunt force trauma (MVA etc)
Brain subjected to rotational shearing forces
Stretch &rupture axonal network causing widespread impairment
mild- coma 6-24 hr
moderate 24 +
severe 50% survival chance likely lasting impairment

Question 11

Diffuse: Hypoxic Injury

Answer 11

-Brain receives inadequate oxygen or no oxygen. Result of interrupted circulation, causing global cerebral ischaemia, or lack of oxygenation, resulting in global cerebral hxypoxia
With continued inadequate oxygenation, brain cells become ischaemic and infarct

Question 12

secondary TBI

Answer 12

damage from subsequent swelling
Includes oedema, hypovolemia, hypercarbia & hypocarbia as result of primary insult
Therefore termed the secondary insult
-severeness depends on primary injury

Question 13

common pathway of secondary TBI

Answer 13

Damage involves several common pathways
Ischaemia
Excitatory amino acid injury
Cerebral oedema
Increased intracranial pressure (ICP)

Question 14

mild s TBI

Answer 14

Momentary loss of consciousness
No neurological symptoms/residual damage
Possible residual amnesia
Microscopic changes in neurons & glia within hours, but imaging negative

Question 15

moderate s TBI

Answer 15

Many small haemorrhages & some brain tissue swelling

• More likely in frontal & temporal lobes causing cognitive & motor deficits
• period of unconsciousness
• Hemiparesis, aphasia, cranial nerve palsy
• Contusions often visualised on CT

Question 16

severe s TBI

Answer 16

-Extensive primary &; secondary injury to brain structures
Primary injury: instantaneous and irreversible
-Shearing &pressure forces that cause dai, disruption of blood vessels, and tissue damage
-evident on CT
-Often accompanied by severe neurological deficits
Coma, hemiplegia, elevated ICP
-GCS of less than 8

Question 17

Monro-Kellie Hypothesis:

Answer 17

an increase in one compartment is offset by a change or decrease in another compartment
Should the blood vessels dilate, the volume of the other two compartments will decrease and their pressure increase: normal:80% brain tissue: 10% blood: 10% csf

Question 18

(CPP) Cerebral Perfusion Pressure

Answer 18

The pressure gradient driving cerebral blood flow (CBF) and hence oxygen and metabolite delivery is Cerebral Perfusion Pressure (CPP).
Normal range 70 – 100mmHg

Question 19

spiral of death

Answer 19

cranial insult-tissue endema-increase icp-compression of arteries-decrease cerebral blood flow-decrease oxygen so death of brain cells-endema around necrotic (dead) tissue-increase icp with compression of brainstem and respiratory center-CO2 acculmulates, vasodilation-increae icp due to increase blood volume- death

Question 20

Excitotoxic Brain Injury

Answer 20

excessive activity of excitatory neurotransmitters &their receptor-mediated effects

-Glutamate: principle excitatory neurotransmitter
In ischaemia, glutamate transport mechanisms immobilised  extracellular glutamate increases
Intracellular glutamate released form damaged cells
Causes uncontrolled opening of NMDA receptor-operated channels  increased calcium

Question 21

The Cushing reflex,

Answer 21

The Cushing reflex, consisting of an increase in sympathetic outflow to the heart as an attempt to increase arterial blood pressure and total peripheral resistance and that is conflicting with the baroreceptor attempt to apply vagal tone and decrease heart rate, is a hypothalamic response to ischaemia, usually due to poor perfusion in the brain.
The ischaemia activates the sympathetic nervous system, causing an increase in the heart’s output via increased rate and contractility along with peripheral constriction of the blood vessels. This accounts for the rise in blood pressure, ensuring blood delivery to the brain.
The increased blood pressure also stimulates the baroreceptors (pressure sensitive receptors) in the carotids, leading to an activation of the parasympathetic nervous system, which slows down the heart rate, causing the bradycardia. The Cushing reflex is usually seen in the terminal stages of acute head injury.

Question 22

Cushing’s triad

Answer 22

is a triad of hypertension (progressively increasing systolic blood pressure), bradycardia and irregular respirations. It is sign of increased intracranial pressure. Other sources state that the triad is hypertension, bradycardia and widening pulse pressure (an increase in the difference between systolic and diastolic pressure over time).

Question 23

why DAI so damaging

Answer 23

DAI normally occurs when the brain experiences a rotational/shearing force, and the grey and white matter of the brain moves dramatically, placing huge stretching force on these axons, so they are stretched hugely, and/or shorn.
The axonal network allows the brain to complete cognitive tasks, and therefore DAI will lead to non-communication between the two hemispheres.

Question 24

what is hypoxic brain injury

emma

Answer 24

When the brain receives inadequate oxygen, most commonly secondary to reduced or lack of blood flow. If the circulation is impaired, then oxygen delivery will be impaired, and anaerobic metabolism will commence. As a result, the brain cells become ischaemic (lack of oxygen) and infarct (die).

Question 25

What is a secondary traumatic brain injury, and how may a primary injury result in this?
emma

Answer 25

The damage that occurs from brain swelling (which occurs with primary injury), often secondary to diffuse injury. Secondary brain injury includes oedema, hypovolaemia, hypercarbia, and hypocarbia. Typically is caused by ischaemia (often due to hypotension and hypoxia).
The significance of a secondary injury depends on the extent of the primary injury, and how well we (as paramedics) manage the injury.