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pbl y2 s3 > C10 - Head Trauma > Flashcards

C10 - Head Trauma Flashcards

1
Q

What is the blood supply to the scalp? Where are these branches derived from?

A

‘Some Scary Sharks Overeat People’
- Supraorbital = ICA
- Supratrochlear = ICA
- Superficial temporal = ECA
- Occipital = ECA
- Posterior auricular = ECA

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2
Q

What signs may be present upon examination if a patient has a skull fracture?

A
  • ‘Racoon eyes’ = bilateral eye bruising
  • ‘Battle sign’ = bleeding behind the ear
  • Haemotympanum = bleeding behind ear drum in canal
  • CSF leak = clear fluid dripping from nasal passages
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3
Q

How does the Glasgow Coma Scale assess a patient on their eye opening response?

A

1: None = no opening at any time
2: To pressure = after finger tip stimulus
3: To sound = after spoken or shouted request
4: Spontaneous = open before stimulus

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4
Q

How does the Glasgow Coma Scale assess a patient on their verbal response?

A

1: None = no audible response
2: Sounds = only moans/ groans
3: Words = intelligible single words
4: Confused = not orientated but communicates coherently
5: Orientated = correctly gives name, place and date

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5
Q

How does the Glasgow Coma Scale assess a patient on their motor response?

A

1: None = no movement in arms/ legs
2: Extension = extends arms at elbow
3: Abnormal flexion = bends arm at elbow, but clearly abnormal
4: Normal flexion = bends arm at elbow, features not abnormal
5: Localising = brings hand above clavicle to stimulus on head neck
6: Obeys commands = obeys a 2-part request

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6
Q

How is the Glasgow Coma Scale score rated?

A

13-15 = mild
9-12 = moderate
3-8 = severe

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7
Q

What is the normal value of intracranial pressure?

A

5-12 mmHg (anything >20 is concerning)

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8
Q

What is cerebral pefusion pressure and how is it calculated?

A

Net pressure gradient causing cerebral blood flow to the brain
CPP = MAP - ICP

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9
Q

How is the brain injured following a blow to the head? (step process)

A

1: Impact - blow sends shockwaves through brain, damaging patches of neurons
2: Deceleration - swings cerebrum on brainstem, tears reticular formation and corticospinal tracts
3: Rotation: stretches connections (axons) between the 2 hemispheres
4: Vibration: resonance after impact bruises the underlying cortex

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10
Q

What is the final common pathway of acute brain injury?

A

Ca2+ enters cell, leading to swelling.
Increases intracranial pressure
Decreases cerebral perfusion pressure
Cerebral ischaemia
Provokes further acidosis, glutamate and free radical release

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11
Q

What NT is responsible for acute epilepsy?

A

Glutamate

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12
Q

What is prosopagnosia? What can it be caused by?

A

Difficulty recognising faces (interpreting visual information)
Can be caused by damage to the temporal lobe

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13
Q

What is temporal lobe epilepsy and what symptoms may present?

A

Focal seizure in the temporal lobe
De ja vu, unprovoked fear, visual distortions

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14
Q

What is cytotoxic oedema?

A

Initial oedema, refers to cellular swelling. Gluid is retained in the cytoplasm and theres a loss of Na+-K+ ATPase. Glutamate-gated Ca2+ channels are open and Ca2+ draws water in. This raises ICP

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15
Q

What is vasogenic oedema?

A

Delayed oedema (48hr). Breakdown of blood brain barrier leads to protein and fluid extravasation into the parenchyma

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16
Q

How would oedema (and thus raised ICP) be treated/ managed?

A
  • Elevate head to 30 degrees
  • Intubate and hyperventilate (short periods)
  • IV mannitol
  • Ventricular drainage
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17
Q

Why would you intubate and hyperventilate a patient that had raised ICP? Why is it only performed for short periods?

A

Causes vasoconstriction so can lower cerebral blood flow = thus lower ICP
For short periods to avoid causing cerebral ischaemia

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18
Q

What can raise ICP?

A

Oedema
Hydrocephalus
Vasospasm
Microvascular pathology
Idiopathic intracranial hypertension

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19
Q

What are some signs of raised ICP?

A
  • Headache: straining, worse on bending over and worse in the morning
  • Vomiting
  • Loss of consciousness
  • Papilloedema - swelling of disc at back of eye
  • Cushing’s triad: wide pulse pressure, irregular breathing, bradycardia
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20
Q

What is the point of decompensation?

A

TO maintain ICP at an appropriate level, the brain can lose extra CSF and blood. The point that this works up to is ‘the point of decompensation’, above which the pressure in the skull increases exponentially

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21
Q

How can a patient lose their pupillary response with raised ICP?

A

Increased ICP can lead to transtentorial herniation, where the brain herniates downwards and places pressure on the brainstem. As the oculomotor nerve sits near here, it can lead to fixed dilated pupils

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22
Q

What is the investigation of choice for raised ICP?

A
  • CT scan
  • Invasive ICP monitoring: catheter in lateral ventricle of brain to monitor pressure
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23
Q

How can CSF be removed?

A
  • Repeated lumbar puncture
  • Drain from intraventricular monitor
  • Ventroperitoneal shunt (hydrocephalus)
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24
Q

What is an extradural haematoma? What is its common cause/ location?

A

Collection of blood between the dura mater and the skull.
Common cause = trauma, collection of blood often found in temporal region at pterion (overlying middle meningeal artery) as bone is very thin here

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25
Q

How does an extradural haematoma present?

A

Patient intially loses consciousness, then briefly regains it (lucid), then loses consciousness again

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26
Q

How is an extradural haematoma treated?

A

Craniotomy - evacuation of haematoma

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27
Q

What is a subdural haematoma?

A

Collection of blood deep to the dural layer of the meninges, due to rupture of bridging veins

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28
Q

What are some symptoms of a subdural haematoma?

A

headache, nausea, vomiting, confusion, drowsiness, poor balance

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29
Q

How do subdural and extradural haematomas present on a CT scan?

A

Extradural = lemon shape
Subdural = crescent shape

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30
Q

What is a subarachnoid haemorrhage and how can it be caused?

A

Collection of blood within the subarachnoid space, deep to the subarachnoid meninges
Most common cause = head injury, or brain aneurysm (usually secondary to HTN)

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31
Q

How might a patient present with a subarachnoid haemorrhage?

A

Headache: ‘thunderclap’, occipital region, sudden onset
Nausea and vomiting
Meningism - photophobia (sensitive to light), neck stiffness
Coma
Seizures

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32
Q

If you suspect a subarachnoid haemorrhage but the CT is negative, what test might you perform and why?

A

Lumbar puncture - test for RBC’s to see if blood has leaked into CSF

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33
Q

What is a seizure? What 2 processes can lead to one?

A

Sudden uncontrolled electrical disturbance in the brain
- Increased glutamate activity at NMDA receptors
- Reduced GABA or GABA receptor expression
= uncontrolled action potentials in the brain

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34
Q

What can cause seizures?

A

Epilepsy, infections, electrolyte imbalance, toxins, drugs, febrile seizures (in children when they have a temperature)

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35
Q

What are the 2 types of seizures?

A

Generalised = involves both cerebral hemispheres, typically lose consciousness
Focal = limited area of cortex (usually temporal), level of awareness can vary

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36
Q

What can a focal seizure lead to?

A

If in an area of the motor cortex = clonic movement of limb
If sensory cortex = triggers abnormal sensation

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37
Q

What investigations might be done for a seizure?

A

EEG
MRI

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38
Q

How would generalised seizures be treated?

A

Sodium valproate - males only
Lamotrigine

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39
Q

How would focal seizures be treated?

A

Lamotrigine
Carbomazepine

40
Q

What is sodium valproates mode of action?

A

Thought to be either:
- Valproic acid (active form) binding to GABA transaminase and inhibiting it = increasing GABA levels
- Inhibiting voltage-dependent Na+ channels, suppressing firing

41
Q

How does lamotrigine exert its anti-seizure effects?

A

Bind to voltage-gated sodium channels, inhibiting release of aspartate and glutamate

42
Q

What is a linear cranial fracture?

A

When the area that is impacted bends inwards, causing the area around it to bend outwards. There’s a break in the bone but it doesn’t move

43
Q

What is a diastatic cranial fracture?

A

Fracture line traverses one or more sutures of the skull, causing a widening of the suture. This is common in infants

44
Q

What is a depressed cranial fracture?

A

Broken bones are displaced inwards, which carries a high risk of increasing ICP and crushing delicate tissues.

45
Q

How is a depressed cranial fracture typically treated?

A
  • Immediate CT scan (within 1hr)
  • Anti-epileptics to avoid seizures
  • Raise head by 30 degrees
  • Surgery to lift pieces of bone off the brain if its placing pressure
46
Q

What is a basilar/ basal cranial fracture?

A

Breaks in bones at the base of skull. This has characteristics signs: racoon eyes, CSF leak, blood in sinuses etc.
(most serious cranial fracture)

47
Q

Define consciousness

A

Alert cognitive state in which you are continually aware of your internal and external environment, both past and present, as well as the emotions arising from it

48
Q

What needs to be intact for someone to be considered fully conscious?

A

Need to be awake and aware:
- Intact ascending Reticular Activating System (awake)
- Functioning cerebral cortex (aware)

49
Q

Give some characteristics a patient may show if in a confusional state

A

Disorientation, bewilderment, difficulty following demands

50
Q

What is the difference between comatose and stupor?

A

Comatose= unconscious and unable to respond to verbal command. May be able to show motor response to painful stimuli
Stupor = unconscious but roused by verbal command or painful stimuli for short periods, and produce verbal responses

51
Q

What is the Grady Coma Scale?

A

Grades a coma from I (confusion) to V (coma): based on the state of awareness and response to stimuli, i.e. name being called, light pain, deep pain etc.

52
Q

What state is ‘sleep’?

A

Sleep = state of unconsciousness from which a person can be aroused, therefore external stimuli have no effect. The brain is more responsive to internal stimuli than external

53
Q

How can brain activity be assessed during sleep?

A

Electroencephalogram (EEG)
Eye movements (EOG)
Muscle tone (EMG)

54
Q

What stages occur in a sleep cycle?

A

Non-rapid eye movement sleep (NREM): N1, N2, N3 = then followed by an episode of REM sleep

55
Q

How long is a sleep cycle and how many do we have a night?

A

90-110 minutes
4-5x a night

56
Q

What proportion is REM sleep of total sleep time?

A

20-25%

57
Q

How long can an episode of REM sleep be?

A

The first may be <10 minutes, but the last of the night might be >60 minutes

58
Q

How does deep sleep differ from sleep?

A

Sleep = consciousness fades in and out
Deep sleep = State of physiological reversible unconsciousness

59
Q

What mediates the transition from deep sleep to wakefulness?

A

Reticular Activating System

60
Q

What mediates the transition from wakefulness to sleep?

A

Arousal inhibitory mechanism of a partial blockade of the thalamus and upper brainstem (inc thalamic sleep spindles)

61
Q

What is a feature of dreaming?

A

We don’t experience our environment - we’re disconnected

62
Q

What are the key goals of anaesthesia?

A

As well as inducing behavioural unresponsiveness; aim to prevent experience of surgery by inducing unconsciousness or disconnecting consciousness from the environment

63
Q

What happens during REM sleep?

A
  • Associated with dreaming
  • Eyeballs move rapidly, breathing becomes rapid and irregular, blood pressure rises
  • Brain is highly active: metabolism can increase by 20%
64
Q

What signal is sent before you enter REM sleep?

A

Brainstem sends a signal down spinal cord to alpha motor neurones to enter a state of paralysis

65
Q

Which nucleus controls swallowing?

A

Nucleus ambiguus: IX, X, XI

66
Q

Where do most muscle relaxants have their action?

A

Motor end plate - on acetylcholine nicotinic receptors

67
Q

What is the aim of each step in the triad of general anaesthesia?

A

1: Hypnosis: make the patient unconscious
2: Muscle relaxant: blocks NMJ, relaxing and paralysing muscles by inhibiting ACh (makes intubation easier)
3: Analgesia: pain relief

68
Q

What drugs might be used for hypnosis of general anaesthesia? Give their mode of administration

A

IV agents: propofol, ketamine, thiopental sodium (IV = usually for induction)
Inhaled: sevoflurane, desflurane, isoflurane, nitrous oxide (inhaled= for maintenance)

69
Q

What are volatile anaesthetic agents? Give some examples

A

Volatile = liquid at room temperature. Need to be vaporised into gas to be inhaled - concentration can be altered to modify depth of anaesthesia
Examples = sevoflurane, desflurane, isoflurane

70
Q

Why are IV agents used for inducing hypnosis over intravenous?

A

Inhaled medications diffuse across the lung tissue so takes a while to reach an effective concentration, whereas IV agents are infused directly into the blood so is quicker

71
Q

What is ‘Total Intravenous Anaesthesia’ (TIA)? What drug does it commonly use?

A

When IV medication is used for both induction and maintenance - gives a nicer recovery.
Propofol is typically used (sometimes with remifentanyl)

72
Q

What are the 2 types of muscle relaxants used for general anaesthesia?

A

Depolarising drugs = produces the same action as ACh (I.e. influx of Na+, K+ and release of Ca2+), i.e. suxamethonium

Non-depolarising drugs= just antagonistic at the receptor, i.e. atracurium, rocuronium

73
Q

What drug can reverse the effects of muscle relaxants?

A

Cholinesterase inhibitors, i.e. neostigmine

74
Q

What drugs are used for analgesia within general anaesthesia?

A

Opiates mainly used (bind to u or delta receptors): i.e. fentanyl, afentanyl, remifentanyl, morphine

75
Q

Which receptor targeted by opiates is responsible for analgesia?

A

u1

76
Q

What drug is typically used for maintenence of anaesthesia?

A

Desflurane

77
Q

Describes steps that are done before a patient is put under general anaesthetics

A
  • Fasting: 6h no food, 2h no liquids
  • Pre-oxygenation: inspire 100% for a few minutes to create an oxygen reserve for when they lost consciousness and are intubated
  • Pre-medication to relax, reduce anxiety and pain
78
Q

Why is it important a patient is fasted before put under general anaesthetic?

A

To reduce risk of stomach contents refluxing into the oropharynx, and then aspirated into the trachea.
Gastric contents in lungs can lead to aspirated pneumonitis = major cause of morbidity of anaesthetics

79
Q

What drugs may be given before GA?

A

Benzodiazepines: i.e. medazalam, relax muscles and reduce anxiety, some amnesia

Opiates: i.e. fentanyl, to reduce pain and hypertensive response to laryngoscope

a2-adrenergic agonists: i.e. clonadine, helps with sedation and pain

80
Q

What is rapid sequence induction (RSI)?

A

When you gain control of the airway quickly, i.e. patient is intubated without pre-planning = high risk of aspiration. bed is positioned to be mroe upright, possibly use cricoid pressure
Usually done in an emergency but may be done in patients where airway has to be secured quickly, i.e. pregnancy or patients with gastroesophageal reflux.

81
Q

What are the 5 steps to the process of anaesthesia? Give the most common drug for each one

A

1: Preparation - ‘optimising’, i.e. stop smoking, lose weight, improve exercise tolerance, info and anticipation
2: Induction - usually IV and propofol
3: Maintenance - usually desflurane but can use any volatile agent (‘_fluranes)
4: Short term recovery - give Neostigmine to remove muscle relaxant effects before gain consciousness, usually given with glycopyrulate
5: Long term recovery - early mobilisation (reduce DVT risk), physiotherapy etc.

82
Q

Why is glycopyrulate given with neostigmine?

A

Neostigmine can cause bradycardia so glycopyrulate is given to increase BP

83
Q

How are patient responses during emergence usually assessed to prevent awareness under anaesthesia?

A

Nerve stimulators are rsed to test muscle response to stimulation, either:
- Ulnar nerve in wrist- look for thumb movement
- Facial nerve in temple -look for obicularis oculi muscle around eye

‘Rule of 4’ = test 4x to see if muscle response remains strong (relaxant is worn off) or if it gets weaker (not fully worn off)

84
Q

What post-op medications may be given after general anaesthetic procedures?

A

Anti-emetics: prevent post-operative nausea and vomiting
Prophylaxis drugs: dexamethosone, cylozone

85
Q

What are the risks of general anaesthesia?

A
  • Sore throat, post-operative nausea and vomiting = common adverse effects
  • Dental injury from laryngoscope
  • Malignant hyperthermia
  • Anaphylaxis
86
Q

What is malignant hyperthermia? What is the risk highest with?

A

Rare but potentially fatal hypermetabolic response to anaesthesia. Causes high body temperature, high Co2 exhalation, tachycardia, rigidity, acidosis and hyperkalaemia. Can lead to rhabdomyolysis and cardiac arrest due to using up all ATP

Risk is highest with volatile anaesthetics and suxamethonium.

87
Q

What is an antagonist for opiates?

A

Naloxone

88
Q

What is the mechanism of action of propofol?

A

Binds to a specific site on GABA-A receptors to increase GABA in the CNS

89
Q

What are some contraindications of propofol?

A

Asthma
Bleeding disorders

90
Q

What is the mechanism of action of isoflurane?

A

Multiple theories:
- Disrupts synaptic transmission
- Direct action on plasma neuronal membrane
- Meyer-Overton theory: lipid solubiity and anaesthetic potency

91
Q

What is the mechanism of action of suxamethonium? What is its duration of action?

A

Depolarising neuromuscular blocker, i.e. mimics ACh without being rapidly depolarised by ACE
Duration = 3-5 minutes

92
Q

What is the mechanism of action of fentanyl?

A

Similar action to morphine but more rapid onset and shorter duration of action. Strongly binds to u opioid receptors and inhibits adenylate cyclase = inhibits substance P, GABA and dopamine

93
Q

What are the different types of social support?

A
  • Esteem = other people increase one’s own self-esteem
  • Support = others offer advice
  • Companionship = support through activities
  • Instrumental = involves physical health
94
Q

Compare structural and functional support?

A

Structural support = refers to type, size, density and frequency of contact with the network of people available to an individual
Functional support = perceived benefit provided by this structure

95
Q

What is the ‘main effect hypothesis’ for how social support influences health?

A

Suggests social support itself is beneficial and its absence is stressful, therefore modulates the stress-illness link
(presence reduces stressor, and absence acting as a stressor)

96
Q

What is the ‘stress buffering hypothesis’ for how social support influences health?

A

Social support helps an individual cope with stress, and influences their appraisal of the stressor

97
Q

What is the social support reactivity hypothesis?

A

Social support reduces physiological responses to stress, i.e. CV reactivity

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