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HNN > Head Injury > Flashcards

Head Injury Flashcards

1
Q

What is a primary brain injury? What are the common types.

A

The initial damage to neural tissue.

Focal, polar or diffuse.

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2
Q

Describe focal brain injury?

A

A type of primary brain injury.
Lesions are localised to the site of impact on the skull.
Mechanisms of injury are usually contact (object hitting head, or brain hitting inside of skull), or acceleration-deceleration.
Usually lacerations, contusions and haemorrhage.

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3
Q

What is a contusion?

A

Type of polar brain injury. A ‘bruise’ from multiple microhaemorrhages. Occurs at gyri but extends to subcortical white matter.

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4
Q

Where are contusions most likely to occur?

A

Frontal poles, orbital surface of frontal lobes, temporal poles and lateral sulcus (Sylvian fissure).

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5
Q

What is concussion?

A

A temporary disturbance in brain function as a result of trauma.
A type of polar injury.

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6
Q

What are the signs and symptoms of concussion?

A

Symptoms include head ache, dizziness, memory loss, balance problems.
Signs include loss of consciousness, seizure activity, irritability and poor performance.

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7
Q

What is traumatic axonal injury?

A

A type of diffuse primary injury.
Due to shear and tensile strains after impact.
Axons are disrupted and their membranes become swollen and proteins that normally flow through the axon accumulate at these points, resulting in varicosities.

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8
Q

How can we test for diffuse axonal damage?

A

Using amyloid precursor proteins to detect varicosities as it will accumulate also.

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9
Q

How is diffuse axonal damage graded?

A

1-3.
1 - small haemorrhages around corpus callosum.
3 - usually dead at the scene.

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10
Q

What is secondary brain injury?

Give examples.

A

Changes that evolve as a result of a primary injury.

E.g haematomas, oedema, swelling and ischaemia.

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11
Q

What is a haematoma?

A

A localised collected of blood outside the blood vessels. Results from vascular injury and bleeding.

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12
Q

Where does an epidural haematoma occur?

A

Between the skull bone and the dura.

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13
Q

What artery is most commonly involved in an epidural haematoma and why?

A

Middle meningeal artery.
As it runs under the pterion. The skull is thin here and is a weak area as it is where the frontal, temporal, sphenoidal and parietal bones join.

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14
Q

Who do epidural haematomas most commonly occur in and why?

A

Younger people as the dura is less firmly attached to the skull.

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15
Q

What is the typical pattern of consciousness of a person with an epidural haematoma?

A

Briefly unconscious, lucid period, then unconscious.

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16
Q

What happens if an epidural haematoma is not removed?

A

Raised ICP, tentorial herniation and death can occur.

Good prognosis if removed before loss of consciousness.

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17
Q

Where is a subdural haematoma found?

A

Between dura and arachnoid matter.

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18
Q

What usually causes a subdural haematoma?

A

Rupture of bridge veins which go from the cortex to the dural sinuses.

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19
Q

How does the conciousness level in subdural differ to that of epidural haematomas?

A

No lucid period.

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20
Q

When is an ‘acute’ and ‘chronic’ haematoma?

A

Acute: 2-10 days post injury.
Chronic: Weeks after injury.

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21
Q

What are the 2 types of diffuse cerebral oedema? Describe them.

A

Vasogenic: Due to defective BBB as endothelial junctions break down allowing leaking of water, sodium and proteins. Occurs around contusions and haematomas.

Congestive: Due to swelling of one or both hemispheres.

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22
Q

What could cause ischaemic brain damage?

A

Raised ICP e.g. from a haematoma.

Usually adjacent to contusions or haematomas.

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23
Q

Describe the process of ischaemic brain damage?

A

Hpoperfusion and hypoxamia cause a lack of oxygen and nutrients to cells.
There is decreased ATP production by cells, and energy failure results in a failure of membrane homeostasis and a cascade causes cell damageand sysfunction.
An important event is activation of glutamate receptors causing uncontrolled entry of calcium to neurons, which results in cell death - this is called excitotoxicity.
In ischaemia, cells undergo anaerobic respoiration, leading to lactic acid production. This results in a drop in pH and neuronal damage/death also.
Some vessels and support cells are spared as they are more robust.

24
Q

How is consciousness assessed?

A

Glasgow Coma Scale.
Used for initial and continuous assessment.
Predicts mortality.

25
Q

What is assessed by GCS?

A

Eye opening
Best verbal response
Best motor response

26
Q

How is eye opening in GCS assessed?

A

1 - no opening
2 - opening in response to pain
3 - opening in response to speech
4 - Spontaneous opening

Use a pen to push on their nail tip getting harder to assess pain.
For speech, ask them to open their eyes.

27
Q

How is verbal response assessed on the GCS?

A 
1 - No verbal response 
2 - Incomprehensive speech (sounds only) 
3 - Inappropriate words
4 - Confused speech
5 - Orientated speech

Ask patient name, what month it is.

28
Q

How is motor response assessed on the GCS?

A 
1 - No response to pain 
2 - Extensor response
3 - Abnormal flexion
4 - Withdrawal (normal flexion)
5 - Localising response 
6 - Obeying commands

Ask patient to open mouth and stick out tongue, or grip your hand then let go.
Check pain response using trapezius pinch or pressing on the supraorbital notch if they dont response to trapezius.

29
Q

What local factors could affect using the GCS accurately?

A 
Hearing impairment (all)
Tracheal tube (verbal)
Swelling of eyes (eyes)
Injury to arm or face (motor)
Paralysis (motor)
30
Q

What is the normal range of ICP supine at rest?

A

7-15mmHg.

31
Q

What determines ICP?

A
  1. Pressure-volume relationships between brain tissue, CSF and blood in the intracranial cavity.
  2. The Monro-Kellie hypothesis.
  3. Compliance of the brain and its ability to buffer chance in intracranial volume.
32
Q

Explain the Monro-Kellie Hypothesis?

A

If any of the 3 components (tissue, CSF or blood) change, there is a compensatory response.

33
Q

What does ‘compliance’ refer to in terms of ICP?

A

The ability to accommodate changes in volume without significant changes in pressure.

34
Q

What changes can occur in compliance?

A

It is limited by the rigidity of the skull.
Cerbebral vessels can change volume e.g. vasoconstriction.
Venous compression also decreases blood volume.
CSF can be displaced from the ventricles/subarachnoid space to the spinal subarachnoid space.

35
Q

How is compliance calculated?

A

change in volume/change in pressure.

36
Q

What is Cerebral Perfusion Pressure?

A

The net pressure gradient causing cerebral blood flow to the brain.

37
Q

What CPP is needed for adequate cerebral function?

A

70mmHg

38
Q

How is CPP calculated?

A

MAP - ICP

39
Q

Describe clinical features of raised ICP?

A

Headache: worse in the morning, aggravated by stopping/bending.
Vomiting: Due to acute rise in ICP.
Papilloedema: Swelling of optic disc and retina, may result in disc haemorrhage.

40
Q

What is the function of the falx cerebri?

A

Separates the cerebral hemispheres. Helps protect the brain.

41
Q

What is the function of the tentorium cerebelli?

A

Divides the cranial cavity to anterior and posterior fossae. Separates the cerebellum from the occipital lobes. Protects the brain.

42
Q

What is brain herniation?

A

When one brain compartment has an elevated ICP, causing displacement of tissue to an area of lower pressure.

43
Q

Describe the 2 broad categories of brain herniation?

A

Supratentorial: Herniation of structures above the tentorial notch inferiorally.
E.g. Uncal and central herniation.

Infratentorial: Structures below the tentorial notch herniating e.g. upward cerebellar and tonsillar.

44
Q

List 2 causes of hypoxic brain damage?

A

Extracranial blood loss due to injury.

Seizures

45
Q

How would the brain compensate for a drop in BP?

A

Cerebral vasodilation would occur to maintain cerebral perfusion via cerebrovascular autoregulation.

46
Q

What happens if cerebrovascular autoregulation is impaired after head injury?

A

Brain more likely to get hypotension and hypoxia.

47
Q

How is a head injury managed?

A

Cardiopulmonary stabilisation (ABC) - Attention to airway is vital due to damage of respiratory centres in the medulla.
Check D for Disability - Neurological exam using GCS.
Imagine - CT/MRI to assess damage.
Surgical Intervention - For fractures, bleeding vessels, and large haematomas, or increased ICP.

48
Q

How is raised ICP surgically managed?

A

Craniectomy

CSF fluid drainage.

49
Q

Compare regeneration capacity of central and peripheral neurons?

A

Adult CNS neurons have limited regeneration compared to PNS neurons.
This is due to a lack of growth factors, and presence of factors which inhibit growth in the PNS.

50
Q

How could neurons recover if they cant regenerate?

A

Due to neuronal plasticity - the adaptation of undamaged tissue to undertake the damaged nerve’s functions.
Exposure to a stimulus prompts the brain to dedicate more neurons to that stimulus.
So behavioural adaptation plays a large part of compensating for disability.

51
Q

List some long-term problems that may occur after head injury?

A

Cognitive impairment
Hemiparesis - one sided weakenss.
Epilepsy
Post-traumatic syndrome - headache, malaise, depression.
Chronic subdural haematoma.
‘Punch-drunk’ syndrome - from repeated injury. Cognitive impairment.

52
Q

Describe an uncal herniation?

A

Uncus is part of the medial temporal lobe. IT goes down through tentorum cereblli.
This can damage the occulomotor nerve and get pupil dilation. As it worsens also get paralysis of extraoccular muscles.
Then get contralateral hemiplegia as crus cerebri are compressed.
Can then affect respiratory and CV centres in the brainstem.

53
Q

Describe a cingulate herniation?

A

Cingulate gets displaces under falx cerebri and affects other cingulate gyrus. Get contralateral hemiplegia and confusion.

54
Q

What happens i the cerebellum herniates superiorly?

A

Can get hydrocephalus as the cerebral aqueduct is compressed.

55
Q

What happened if the cerebellum herniates inferiorly?

A

Can get CV and resp centre failure due to brainstem compression.

HNN (18 decks)

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