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Yr 4 - ACC > Head Injury > Flashcards

Head Injury Flashcards

1
Q

What is a diffuse axonal injury (DAI)?

A

The shearing of the brain’s long connecting nerve fibers (axons) that happens when the brain is injured as it shifts and rotates inside the bony skull.

This is considered one of the most common and detrimental forms of traumatic brain injury (TBI).

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2
Q

What is a brain contusion?

A

A bruise to the brain: causes bleeding and swelling inside of the brain around the area where the head was struck.

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3
Q

When does 2ary brain injury occur?

A

This occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury.

The normal cerebral auto regulatory processes are disrupted following trauma rendering the brain more susceptible to blood flow changes and hypoxia.

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4
Q

What happens in DAI?

A

The resistant inertia that occurs to the brain at the time of injury, preceding and following its sudden acceleration against the solid skull, causes shearing of the axonal tracts of the white matter.

Axonal disconnection and mechanical disruption to axonal cytoskeletal structure results in immediate severe brain injury.

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5
Q

What is the most frequent cause of DAI?

A

Road traffic accidents (RTAs)

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6
Q

Causes of DAI?

A

1) RTAs

2) Assault

3) Falls

4) Child abuse e.g. shaken baby syndrome and abusive head trauma.

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7
Q

DAIs can be classified into what 3 categories?

A

Grade I

Grade II

Grade III

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8
Q

What occurs in Grade I DAI?

What is the effect on consciousness?

A

What –> Diffuse axonal damage within the white matter of the cerebral hemispheres and grey-white matter interfaces.

Effect –> Brief loss of consciousness

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9
Q

What occurs in Grade II DAI?

What is the effect on consciousness?

A

What –> Tissue tear haemorrhages present; axonal damage of the white matter including grade 1 regions and the territory of the corpus callosum.

Effect –> Variable recovery process, coma of unclear duration.

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10
Q

What occurs in Grade III DAI?

What is the effect on consciousness?

A

What –> Grade 2 findings in addition to tissue tear haemorrhages within the brainstem

Effect –> Instant coma with posturing and incomplete recovery

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11
Q

What are the 2 pathognomonic histological findings of axons with DAI?

A

1) Axonal varicosities – periodic swelling along the axonal length at the site of injury, secondary to the interrupted axonal transport

2) Axonal bulb – Single large swellings at the site of disconnection, following complete axonal severance

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12
Q

Clinical features of DAI?

A

1) LOC at time of injury

2) Prolonged post-traumatic coma (often attributed to co-existent injury, e.g. acute haemorrhage or cerebral contusions)

3) The diagnosis is often only suspected when patients do not make a neurological recovery

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13
Q

What is the main differential for DAI?

A

The main differential in cases of head injury are cortical contusions, typically found superficially at the cortical level, not concentrated to the grey-white matter junction.

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14
Q

1st line imaging following head injury?

A

CT within contrast

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15
Q

1st line imaging for DAI detection?

A

MRI

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16
Q

Management of DAI?

A

Following any trauma, patients should be appropriately resuscitated and stabilised, prior to transfer to a neuro-trauma centre.

Therapeutic interventions for DAI are limited. Options are all aimed to preventing secondary effects such as cerebral oedema or haemorrhage.

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17
Q

Prognosis of DAI?

A

A spectrum of clinical consequences may follow DAI, dependent on the severity of the pathology ranging from very minor to extensively diffuse damage.

Long-term vegetative state appears at the severe end of the spectrum. There is a predictive correlation between the extent of brainstem DAI and likelihood of persistent vegetative state.

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18
Q

What is the Cushing’s reflex?

A

A triad of signs that are indicative of raised ICP.

1) Bradycardia

2) Irregular respirations

3) Widened pulse pressure (increasing systolic, decreasing diastolic)

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19
Q

What does the Cushing’s reflex indicate?

A

often occurs late and is usually a pre terminal event

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20
Q

What are the 4 types of intracranial haemorrhage?

A

1) Extradural (epidural) haemorrhage

2) Subdural haemorrhage

3) Subarachnoid haemorrhage (SAH)

4) Intracerebral haemorrhage

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21
Q

What is an extradural (epidural) haemorrhage?

A

Bleeding into the space between the dura mater and the skull.

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22
Q

Risk factors for an intracranial haemorrhage?

A
  • Head injuries
  • Hypertension
  • Aneurysms
  • Ischaemic strokes (progressing to bleeding)
  • Brain tumours
  • Thrombocytopenia (low platelets)
  • Bleeding disorders (e.g., haemophilia)
  • Anticoagulants (e.g., DOACs or warfarin)
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23
Q

An extradural haemorrhage is usually caused by rupture of what artery?

A

The middle meningeal artery in the temporoparietal region.

This is vulnerable to injury as the thin skull at the pterion overlies the middle meningeal artery.

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24
Q

What is an extradural haemorrhage often caused by?

A

It is almost always caused by trauma and most typically by ‘low-impact’ trauma (e.g. a blow to the head or a fall).

A typical history is a young patient with a traumatic head injury and an ongoing headache.

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25
How do patient with an extradural haemorrhage typically present?
1) Patient has period of improved neurological symptoms and consciousness 2) Followed by a rapid decline over hours as the haematoma gets large enough to compress the intracranial contents 3) Develops fixed and dilated pupil due to the compression of the parasympathetic fibers of the 3rd cranial nerve.
26
How does an extradural haemorrhage appear on a CT?
- Biconvex, hyperdense collection - Limited by the cranial sutures (they do not cross the sutures, which are the points where the skull bones join together).
27
Where does a subdural haemorrhage occur?
Between the dura and the arachnoid mater.
28
Subdural haemorrhage is the result of the rupture of which vessel?
Caused by a rupture of the bridging veins in the outermost meningeal layer.
29
Who are subdural haemorrhages more common in?
Elderly & alcoholic patients --> have more atrophy in their brains, making the vessels more prone to rupture.
30
What is an ACUTE subdural haemorrhage usually the result of?
High-impact trauma
31
What is a CHRONIC subdural haemorrhage?
A collection of blood within the subdural space that has been present for weeks to months.
32
Presentation of a chronic subdural haemorrhage?
Typically a several week to month progressive history of either confusion, reduced consciousness or neurological deficit.
33
What will a subdural haemorrhage look like on a CT?
They have a crescent shape and are not limited by the cranial sutures (they can cross over the sutures).
34
How can a subdural haemorrhage be classified?
Acute: <3 days Subacute: 3-21 days Chronic: >21 days
35
What time period defines an acute subdural haemorrhage?
<3 days
36
What are the most common causes of a subdural haemorrhage?
1) Trauma (typically a blow to the temporal side of the head, rupturing the bridging cranial veins) 2) Rupture of a cerebral aneurysm 3) Rupture of an arteriovenous malformation (AVM) 4) Cerebral hypotension 5) Malignancy (rare)
37
Typical symptoms of a SDH?
Headache Nausea/vomiting Confusion Drowsiness Poor balance Weakness Paraesthesia or numbness
38
Presentation of an acute vs chronic SDH on CT?
Acute: typically has a hyperdense appearance (bright white) Chronic: typically has a hypodense appearance (black/dark grey)
39
What does the hyperdense appearance on a head CT indicate?
The hyperdense appearance represents recently coagulated blood.
40
What does the hypodense appearance on a head CT indicate in SDH?
The hypodense appearance of chronic SDH represents the dissolution of cellular elements into liquified blood.
41
Risk factors for a SDH?
1) old age 2) alcoholism 3) anticoagulants
42
Describe onset of symptoms between epidural and subdural haemorrhage
There is a slower onset of symptoms in SDH compared to an epidural haematoma. There may be fluctuating confusion/consciousness.
43
What is a SAH?
Subarachnoid haemorrhage involves bleeding in the subarachnoid space, where the cerebrospinal fluid is located, between the pia mater and the arachnoid membrane.
44
What is the most common cause of SAH?
This is usually the result of a ruptured cerebral (berry) aneurysm.
45
What are the 2 types of SAH?
Traumatic & spontaneous
46
What is a traumatic SAH caused by?
Head injury
47
What are the causes of a spontaneous SAH?
1) intracranial aneurysm (saccular ‘berry’ aneurysms) 2) arteriovenous malformation 3) pituitary apoplexy 4) mycotic (infective) aneurysms
48
What conditions are associated with berry aneurysms?
1) HTN 2) Adult polycystic kidney disease 3) Ehlers-Danlos syndrome 4) Coarctation of the aorta
49
Clinical presentation of SAH?
1) Occipital headache: - usually of sudden-onset (‘thunderclap’ or ‘hit with a baseball bat’) - severe (‘worst of my life’) 2) N&V 3) Meningism (photophobia, neck stiffness) 4) Focal neuro signs etc
50
Which type of intracerebral haemorrhage can cause neck stiffness?
SAH
51
How does a SAH present on CT?
Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.
52
Risk factors for spontanoeus SAH?
- Hypertension - Smoking - Family history - Autosomal dominant polycystic kidney disease (ADPKD) - Age over 50 years - Female sex (approximately 1.5x baseline risk)
53
1st line investigation in SAH?
Non-contrast CT head
54
In which time frame is a non-contrast head CT sufficient to rule out SAH in most patients?
Within 6 hours
55
If CT head is done within 6 hours of symptom onset and is normal in SAH, what is next step?
consider an alternative diagnosis
56
If CT head is done more than 6 hours after symptom onset in SAH and is normal, what is next step?
Do a lumbar puncture
57
When should a LP be performed in an SAH?
LP should be performed at least 12 hours following the onset of symptoms.
58
Why should a LP be performed at least 12 hours after onest of symptoms in SAH?
to allow the development of xanthochromia (the result of red blood cell breakdown).
59
LP findings in SAH?
- xanthochromia - normal or raised opening pressure
60
If the CT scan (or LP) shows evidence of SAH, what is next step?
Referral to neurosurgery
61
Management of SAH?
1) supportive 2) vasospasm is prevented using a course of oral nimodipine 3) intracranial aneurysms are at risk of rebleeding and therefore require prompt intervention, preferably within 24 hours
62
what class of drug is nimodipine?
CCB
63
Role of nimodipine in SAH?
Used to prevent vasospasm (works by relaxing blood vessels in the brain to allow more blood to flow to damaged area).
64
Complications of SAH?
1) rebleeding 2) hydrocephalus 3) vasospasm 4) hyponatraemia 5) seizures
65
How can SAH cause hyponatraemia?
Due to SIADH
66
What are 3 important prognostic factors in SAH?
1) conscious level on admission 2) age 3) amount of blood visible on CT head
67
What is an intracerebral haemorrhage?
a collection of blood within the substance of the brain.
68
How does an intracerebral haemorrhage present?
Very similarly to ischaemic stroke
69
What investigation is key in differentiating between intracerebrael haemorrhage and ischaemic stroke?
Non-contrast CT scan
70
How will an intracerebral haemorrhage present on CT?
CT imaging will show a hyperdensity (bright lesion) within the substance of the brain.
71
Management of intracerebral haemorrhage?
Treatment is often conservative under the care of stroke physicians, but large clots in patients with impaired consciousness may warrant surgical evacuation.
72
What are the 2 surgical options for treating an extradural or subdural haematoma?
1) Craniotomy (open surgery by removing a section of the skull) 2) Burr holes (small holes drilled in the skull to drain the blood)
73
Head injury vs TBI?
Head Injury = a patient who has sustained any form of trauma to the head, regardless of whether they have any symptoms of neurological damage Traumatic Brain Injury = evidence of damage to the brain as a result from trauma to the head, represented with a reduced Glasgow Coma Scale or presence of a focal neurological deficit
74
Head injuries can be classified according to the GCS scale as minimal, mild, moderate, or severe. What is the GCS score for each?
Minimal: 15, with no loss of consciousness Mild: 13-15 Moderate: 9-12 Severe: 3-8
75
Any patients presenting to A&E with evidence of head injury should be examined how quickly?
Within 15 minutes of arrival
76
How should all patients with had injury be managed?
ABCDE
77
What is the most common cause of death and disability in those under the age of 40 in the UK?
Head injuries
78
What is the Monro-Kellie hypothesis?
This describes the relationship between the contents of the skull and ICP. In the skull there are 3 main substances: brain tissue, CSF & blood. If the volume of one of these substances increases, to maintain a constant ICP, the volume of one of the others must decrease. Initially, this can be achieved through a process referred to as compliance e.g. an increase in the amount of blood in the skull leads to a compensatory decrease in the amount of CSF and normal ICP is maintained. However, one the compensatory compliance mechanism is overwhelmed, small increases in the volume of any one of the three substances will lead to dramatic increases in ICP.
79
If left untreated, what cause rising ICP cause?
- reduced cerebral perfusion - herniation of brainstem - death
80
Clinical features of a raised ICP?
1) headache 2) N&V 3) restlessness, agitation or drowsiness 4) slow slurred speech 5) papilloedema 6) Ipsilateral sluggish dilated pupil which then becomes fixed (“blown pupil”) 7) Cranial nerve palsy (e.g. CN III palsy with ‘down and out’ pupil) 8) Seizures 9) Reduced GCS 10) Abnormal respiratory pattern 11) Abnormal posturing, initially decorticate and then decerebrate
81
Palsy to which cranial nerve causes a 'down and out' pupil?
CN III
82
What is cerebral perfusion pressure (CPP)?
The pressure driving blood through the brain tissue, allowing the delivery of oxygen and nutrients.
83
How can CPP be calculated?
CPP = Mean Arterial Pressure (MAP) – ICP
84
How will a rise in ICP affect CPP?
Will reduce it. If CPP drops too low for a significant amount of time, ischaemia occurs.
85
What is herniation?
Herniation can be defined as the movement of brain structures from one cranial compartment to another. Herniation of different brain structures leads to different clinical features.
86
What will the cerebellar tonsils herniate through in raised ICP?
The foramen magnum - 'coning'
87
Effect of herniation of the cerebellar tonsils through the foramen magnum?
Compression of the brainstem and respiratory arrest.
88
What will the uncus of the temporal lobe herniate through in raised ICP?
Tentorial notch
89
Effect of herniation of the uncus of the temporal lobe through the tentorial notch?
Compression of CN III (oculomotor) --> leading to the classical “blown pupil” that is often assessed for in TBI patients.
90
What are some factors that may contribute to 2ary brain injury (indirect damage to brain tissue that that occurs after the primary insult)?
1) Hypoxia & hypercapnia 2) Hypovolaemia & hypotension 3) Cerebral oedema & raised ICP 4) Expanding haematoma 5) Hypoglycaemia or hyperglycaemia 6) Increased metabolic demand (e.g. hyperthermia or seizures)
91
What interventions can limit hypoxia and hypercapnia causing 2ary brain injury?
1) O2 to maintain sats 94-98% 2) Intubation in patients unable to protect their airway or with poor respiratory effort
92
What interventions can limit hypovolaemia and hypotension causing 2ary brain injury?
1) Resuscitate with intravenous fluids or blood products 2) Vasopressors
93
What interventions can limit cerebral oedema & raised ICP causing 2ary brain injury?
1) Avoid tight C-spine collars 2) Position the patient at 30° to aid venous drainage 3) Mannitol or hypertonic saline to reduce ICP 4) Intubation and hyperventilation strategies
94
What interventions can limit an expanding haemotoma causing 2ary brain injury?
1) Reverse clotting abnormalities 2) Consider the use of tranexamic acid if < 3 hours since injury 3) Neurosurgical intervention
95
What interventions can limit hypoglycaemia or hyperglycaemia causing 2ary brain injury?
Maintain blood glucose within normal range with insulin or dextrose as required
96
What interventions can limit increased metabolic demand (e.g. hyperthermia or seizures) causing 2ary brain injury?
1) Maintain normothermia 2) Anti-convulsant medications if seizure activity 3) Neuroprotective anaesthesia
97
What areas in the history is it important to cover in a head injury? Note - taking a history should not delay performing an urgent ABCDE assessment.
1) Accurate history of injury itself 2) Collateral history 3) Description of the scene from the paramedics. 4) Establishing if the patient has any neurological symptoms e.g. seizure activity, weakness, sensory or visual changes. 5) Any LOC or amnesia 6) Symptoms due to raised ICP 7) DH & allergies (especially anticoagulants) 8) Focused PMH e.g. bleeding disorder, previous brain surgery 9) Focused SH & baseline 10) Other injuries: especially pain in cervical spine
98
In a patient suffering with head injury, what should you always consider?
If cervical spine has been injured. At the start of the assessment* consider whether the cervical spine requires immobilisation via a semi-rigid collar, blocks, and tape (this may already be in place if the patient was brought in by ambulance)
99
What GCS indicates that a patient may not be able to maintain their own airway?
≤8 --> call the on-call anaesthetic team immediately to assist with airway management.
100
Which airway manouevre is most appropriate in traumatic head injuries?
A jaw thrust (NOT a head-tilt chin-lift manoeuvre).
101
A nasopharyngeal airway is contraindicated in a basal skull fracture. What are some signs suggestive of a basal skull fracture?
1) CSF (clear fluid) leaking from nose or ear 2) Raccoon eyes: bruising around the eyes 3) Battle sign: bruising behind the ear over the mastoid process 4) Haemotympanum: blood noted behind the tympanic membrane on otoscopy
102
What is key in 'breathing' part of ABCDE in TBI?
Ensure adequate ventilation (with a secure airway) and oxygenation is particularly important following head injury to limit further brain damage from hypoxia.
103
What is key in 'circulation' part of ABCDE in TBI?
Ensure adequate tissue perfusion to prevent any further secondary ischaemic damage to the brain. Ensure a good circulating volume is maintained from resuscitation with appropriate fluids.
104
What is intervention in hypovolaemic patients with TBI?
Administer a 500ml bolus Hartmann’s solution or 0.9% sodium chloride (warmed if available) over less than 15 mins.
105
What is intervention in hypovolaemic patients with TBI at risk of fluid overload?
Administer 250ml bolus Hartmann’s solution or 0.9% sodium chloride (warmed if available).
106
How many times can administration of fluid boluses be repeated for hypovolaemia in TBI?
Up to four times (e.g. 2000ml or 1000ml in patients at increased risk of fluid overload), reassessing the patient each time.
107
How may a pupil present in a raised ICP or herniation?
An oval-shaped pupil, sluggish reaction to light, “blown pupil” or deviated pupil
108
What is the Glasgow Coma Scale (GCS)?
The Glasgow Coma Scale (GCS) is a universal assessment tool for the level of consciousness. It is scored based on eyes, verbal response and motor response.
109
What is the maximum GCS score?
15/15
110
What is the minimum GCS score?
3/15
111
What GCS score indicates the need for airway support?
≤8
112
Describe the different modalities & scores of the GCS
Motor: 6. Obeys commands 5. Localises to pain 4. Withdraws from pain (normal flexion) 3. Abnormal flexion to pain (decorticate posture) 2. Extending to pain 1. None Verbal: 5. Orientated 4. Confused 3. Inappropriate words 2. Incomprehensible sounds 1. None Eye opening: 4. Spontaneous 3. To speech 2. To pain 1. None
113

Yr 4 - ACC (73 decks)

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