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NSB236 > Week 2: Acute Neuro Injury > Flashcards

Week 2: Acute Neuro Injury Flashcards

1
Q

What is Intracranial Pressure?

A

ICP is the pressure excreted by the cerebrospinal fluid within the ventricles of the brain.

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2
Q

What state is ICP?

A

Dynamic state

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3
Q

What is the normal range of ICP?

A

0-15mmHg

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4
Q

What is the benefit of monitoring ICP?

A

Indicated to prevent cerebral ischemia and maximise cerebral oxygenation.
Provides early detection of cerebral oedema in sedated patients.

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5
Q

What factors impact ICP under normal circumstances?

A
  1. Arterial pressure
  2. Venous pressure
  3. Intra-abdominal and intrathoracic pressure (valsalva manouvre)
  4. Posture (30 deg incline to decrease ICP)
  5. Temperature
  6. Blood gases - specifically CO2 (vasodilation/constriction can be caused by alteration in CO2)
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6
Q

What is the Munroe-Kellie doctrine/hypothesis?

A

Cranial cavity is filled with “3 non-compressible elements: the brain 78%, CSF 10% and blood 12%”

If one increases, the others must decrease.

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7
Q

What is the compensatory processes involved in the Munroe-Kellie hypothesis?

A

a) Displacement of CSF
b) Compression of the low pressure venous system
c) Decrease the production of CSF
d) Vasoconstriction of cerebral vessels

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8
Q

What is ICP compliance?

A

It is a measure of the adaptive capacity of the brain to maintain intracranial equilibrium in response to changes?

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9
Q

What factors influence compliance?

A
  1. Volume increases
  2. Time frame for accommodation of volume
  3. Size on intracranial compartment

Alcohol abuse causes the brain to shrink, meaning they’ll have more space for ICP.
Paediatric’s skull may be a bit more compliant due to the lack of fusion of their fontenelles.

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10
Q

What is the average mL/min of cerebral blood flow through the brain?

A

750-800mL/min, primarily located in the low pressure venous system.

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11
Q

What is autoregulation?

A

Is the capacity of the brain to regulate its own CBF to meet the needs of the brain despite the variation in the systemic arterial pressure. I.e. adjusts the diameter of the blood vessels.

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12
Q

Define Cerebral Perfusion Pressure

A

The BP gradient across the brain.

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13
Q

How is CPP calculated?

A

MAP - ICP = CPP

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14
Q

What is the normal CPP range?

A

70-100mmHg

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15
Q

What is the minimum range of CPP required for adequate cerebral perfusion?

A

50-60mmHg

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16
Q

What is associated with CPP <50mmHg?

A

Ischaemia and neuronal death

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17
Q

What is the result of CPP <30mmHg?

A

Cellular ischaemia and is incompatible with life

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18
Q

What is the normal range for MAP?

A

60-150mmHg

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19
Q

what is the ideal range for MAP?

A

70-90mmHg

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20
Q

T/F

Autoregulation operates within limited parameters

A

True

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21
Q

T/F

Patients with a high MAP are more likely to be hypertensive

A

False

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22
Q

T/F

If autoregulation fails then CBF and Cerebral Blood Volume becomes massively dependent on changes in systemic BP

A

True

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23
Q

What are some Signs and Symptoms of raised ICP?

A
  1. Decreased LOC
  2. Headache
  3. Vomiting
  4. Pupillary abnormalities
  5. Visual disturbances
  6. Motor dysfunction
  7. Speech disturbances
  8. Changes in vital signs

Cushings triad is late stage

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24
Q

What is the incidence of an acquired brain injury?

A

1 in 50

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25
Q

How many with an acquired brain injury have a severe disability?

A

47%

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26
Q

What is the biomechanics of a traumatic brain injury?

A

Traumatically induced structural injury or physiological disruption of brain function as a result of an external force.

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27
Q

What is involved/occurs with a TBI?

A
  1. Loss/decreased or ALOC
  2. Amnesia
  3. Neurological deficit
  4. Intracranial deficit
  5. Severe TBI defined as GCS <8
  6. Penetrating or closed
  7. Damage related to MOI, type and location
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28
Q

What age group is more at risk of a TBI?

A

15-44 year olds

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29
Q

What is a primary head injury?

A

Moment of impact

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30
Q

What is a secondary head injury?

A

Evolves hours/days later

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31
Q

What is commonly involved with secondary head injuries?

A
  • Cerebral oedema
  • Hypoxia
  • Hypotension
  • Hypercapnia
  • Hyperthermia
  • Sustained increase in ICP
  • Anaemia
  • Electrolyte disturbances
  • Vasospasm
  • Hydrocephalus
  • Seizures
  • Infection
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32
Q

What type of energy was used to cause the injury?

A

Transfer of energy from the environment to tissue above the amount that be absorbed without dysfunction.

Dynamic or Angular loads

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33
Q

What are the 4 mechanisms of a TBI?

A
  1. Acceleration
  2. Deceleration
  3. Acceleration - deceleration
  4. Rotational forces
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34
Q

What is an example of acceleration (mechanism of TBI)?

A

Whiplash style injury

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35
Q

What is an example of deceleration (mechanism of TBI)?

A

blow to the head

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36
Q

What is an example of acceleration-deceleration (mechanism of TBI)?

A

Brain rebounds in the skull = coup-contracoup

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37
Q

What does the mechanisms of a TBI often result in?

A

Haematoma, skull fracture, and traumatic shearing

38
Q

What is a diffuse axonal head injury?

A

Sudden acceleration-deceleration forces cause injury to the brain.
Tensile forces related to trauma - shaken baby syndrome.
Shearing of the axons. Axonal disconnection.
Neurotransmitters leaking and in contact with the brain tissue.

39
Q

What is the most likely outcome of a diffuse axonal head injury?

A

Poor outcomes - 90% of patients remain in a permanent vegetative state.

40
Q

What is pathophysiology of mechanical damage in a TBI?

A

a) Rupture of cellular and vascular membranes
b) Release of intracellular contents
c) Ultrastructural damage of axons
d) Changes in cerebral blood flow

41
Q

What is the pathophysiology of metabolic derangement in a TBI?

A

a) Release of excitatory neurotransmitters
b) Dysregulation of Ca homeostasis
c) Energy failure
d) Free radical generation
e) Cell death

42
Q

What is the pathophysiology of global consequences?

A

a) increased ICP
b) decreased CBF
c) Tissue ischaemia
d) Cerebral oedema
e) Dyfunction of the blood-brain barrier (BBB)

43
Q

What % of O2 does the brain use of the total uptake in the body?

A

20%

44
Q

T/F

Brain capillaries have a high permeability

A

False

45
Q

T/F

BBB allows lipids, glucose, essential amino acids, H20, CO2 and O2 to cross

A

True

46
Q

T/F

Insulin is NOT needed for glucose delivery to brain tissues

A

True

47
Q

T/F

The brain is not capable of much anaerobic metabolism

A

True

Primarily due to the high metabolic rate of the neurons

48
Q

What is the physiology of Neuroglobin?

A
  • Intracellular hemeprotein
  • Reversibly binds oxygen with an affinity greater than that of haemoglobin
  • Increases oxygen availability to brain tissue and provides protection under hypoxic or ischemic conditions, potentially limiting brain damage
49
Q

What needs to be considered neurologically in infants?

A
  • Cranial sutures are not fused until 18-24 months
  • Congenital hydrocephalus = increased volume of CSF
  • Can have ineffective thermoregulation
  • Seizures can be caused by febrile illness & development disorders
50
Q

What is the normal CPP range for a neonate?

A

> 30mmHg

51
Q

What is the normal CPP range for a 1month - 6month old?

A

> 35mmHg

52
Q

What is the normal CPP range for a 6month - 11month old?

A

> 40mmHg

53
Q

What is the normal CPP range for a 1yr - 4yr old?

A

> 45mmHg

54
Q

What is the normal CPP range for a 5yr - 9yr old?

A

> 50mmHg

55
Q

What needs to be considered neurologically in the elderly?

A
  • Cerebral atrophy, loss of grey matter, decreased volume & weight
  • Decline in memory
  • Impairment in gait, vision, proprioception
  • Incidence of dementia increases
  • Slower nerve conduction
  • More easily distracted
  • 7% of people over 75yrs are reported to have epilepsy
56
Q

Go through a Primary Survey for someone with an acute neurological injury

A 
D = Danger to you and them
R = GCS assessment, need to consider the impact of confounding factors
A = Secured/nonsecured/at risk?, vomitus, how to confirm position, what support is in place
B = rate, rhythm (?# ribs, pneumothorax), efficiency
C = neuro-haemo dynamics
D = diagnostics: CT, cerebral angiogram, MRI, PET, EEG, LP
E = Environment &amp; electrolytes
F = Follow up investigations, family
57
Q

What is a piece of pertinent information to gather in the secondary survey?

A

Hx of presenting complaint, and determining the persons previous level of functioning by asking family / friends

58
Q

What does alterations in consciousness stem from?

A
  1. Disorders affecting in reticular formation
  2. Disorders affecting both cerebral hemispheres
  3. Disorders affecting the connections between the brainstem and the hemisphere
59
Q

What are you assessing with GCS?

A
  1. Consciousness requires Arousal = from the brainstem reticular formation (e.g. response to noxious stimuli)
  2. Content = time, person, place (awareness), from the cerebral hemispheres
60
Q

In GCS what does AEIOU stand for?

A 
A = alcohol
E = epilepsy
I = insulin
O = opiates
U = urea
61
Q

Which cranial nerve is associated with fixed enlarged bilateral eyes?

A

Cranial nerve 3

62
Q

What does the cranial nerve 3 control?

A

Oculomotor nerve

63
Q

What is the function and origin of the oculomotor nerve?

A

Origin = midbrain
Function =
- Eye movement inward (medially), up, down, and outward
- Pupil constriction, shape, and equality
- Elevates upper eyelid
- Accommodation reflex

64
Q

What is the dysfunction of the oculomotor nerve?

A
  • Unable to look up/down/L/R = dysconjugate gaze
  • ptosis, pupil dilation = bilateral or ipsilateral
  • Loss of accommodation reflex
65
Q

What is cushings triad?

A

Hypertension
Bradycardia
Diminished respiratory effort

66
Q

What is cushings reflex?

A

Increased ICP

67
Q

What happens when the brain is squeezed through the foramen magnum?

A

Herniation occurs, the brainstem is compressed, the patient stops breathing and the patient dies. Altered ICP

68
Q

What are the 2 types of intracranial haemorrhage?

A
  1. Subarachnoid

2. Incracerebral

69
Q

What are 2 common features of a skull fracture?

A
  1. Battles sign

2. Racoon eyes

70
Q

What would be the location of the fracture if the patient had the clinical feature Battle Sign?

A

Indicator of basilar fracture, otorrhoea (CSF will come through the ears)

71
Q

What would be the location of the fracture if the patient had the clinical feature of raccoon eyes?

A

Indicator of orbital fracture, rhinorrhoea (CSF will from through their nose)

72
Q

What is a skull fracture?

A

A break in the continuity of the skull

73
Q

What is the most common type of skull fracture?

A

Linear = fracture from impact to base of skull, low risk of CSF leak

74
Q

What are the 3 types of skull fracture?

A
  1. Linear
  2. Comminuted/depressed fractures (increased risk of direct brain injury - contusions/bone fragments)
  3. Basilar (at base of the skull, may be either of the above)
75
Q

T/F

You do not insert a NGT if there is a suspect or known base of skull fracture

A

True

76
Q

T/F

There is an infection risk if there is a CSF leak

A

True

As there is communication with external environment to the brain

77
Q

How to determine if it is CSF?

A
  • Dextrostix or test tape
  • Halo test
  • Formal pathology test = beta 2 transferrin
78
Q

What do you NOT do if there is a suspected basal skull fracture?

A
  • Do not insert a dressing
  • Do not suction
  • Do not insert NGT
79
Q

In Neuro-haemodynamics, the objective is to limit ….?

A

Secondary injury

  • results from a traumatic event and changes in the brain or the brain vasculature
  • Hypoxia
  • Hypotension (decreased cerebral blood flow)
  • Increased ICP
  • Hyper/hypoglycaemia
  • Metabolic disturbances
  • Seizures
80
Q

What is an example of a secondary injury? (neurohaemodynamics)

A

Impaired autroregulation (autoregulation is the ability of the brain to maintain CBF in light of changes in BP and CPP)

81
Q

What does impaired autoregulation cause in brain injuries? (neuro-haemodynamics)

A
  • Decreased O2 delivery to the brain and cerebral ischaemia
  • Cerebral metabolism altered due to loss of or a decrease in CBF
  • Conversion from aerobic to anaerobic metabolism
82
Q

What are some extracranial causes of secondary brain injury? (neuro-haemodynamics)

A
  • Hypotension (SBP <90 worsens outcome)
  • Hypoxia (significantly associated with increased morbidity and mortality)
  • Hypocapnia (low CO2 causes vasoconstriction, 1mmHg decrease on CO2 = 3% decrease in CBF)
  • Anemia
  • Hyperthermia
83
Q

What are the treatment parameters for acute neurological care? (BP, ICP, CPP, Temp, Oxygen, SpO2, PaCO2, pH, Na)

A 
BP = specifically MAP, 70-90
ICP = <20mmHg
CPP = proxy for CBF, >60
Temp = normathermic
Oxygen = PaO2 80-100
SpO2 = >95%
PaCO2 = 35-40
pH = 7.35-7.45
Na = 135-140
84
Q

What needs to be considered when caring for patients with a brain injury?

A
  • External stimuli (limit bedside conversation, cluster care, and education/support of family)
  • Management of altered ICP
  • Positioning (elevate to 30 deg)
  • Sedation, analgesics
85
Q

What 3 clinical cares need to be considered to optimise haemodynamic stability?

A
  1. BP = MAP 70-90
  2. ICP = <20mmHg
  3. CPP = proxy for CBF >60
86
Q

What clinical cares must be addressed in patients with a brain injury?

A
  1. Temperature = aim is normothermia
  2. Oxygenation = important to ensure oxygenation to support neuronal cells and limit ischaemia, avoid acidosis, vasoconstriction/dilation
  3. Osmolarity
  4. Seizures = use anticonvulsants and barbituates (reduce cerebral metabolic demand and blood flow) (Phenytoin - common side effect is fever, causes cerebral hypermetabolism)
  5. Renal & GIT = urinary output min: 0.5mL/Kg/Hr, pituitary damage, ensure meeting of nutritional needs
  6. Delirium = 83-87% incident of delirium in all admitted ICU patients
  7. General = DVT risk, mouth & eye care, pressure area care, circadian rhythms
87
Q

What level of PaCO2 causes vasoconstriction?

A

<35

88
Q

What level of PaCO2 causes vasodilation?

A

> 45

89
Q

How is delirium characterised?

A
  • inattention
  • ALOC
  • disorganised thinking
90
Q

How is ICP monitored in hospital?

A
  1. Codmans device (only measures pressure)

2. EVD (measures pressure an allows for drainage of CSF)

91
Q

What is the benefit/use of decrompressive craniotomy?

A
  • Managment of significant ICP
  • Manipulate the Monroe-Kellie hypothesis
  • Reduce duration of mechanical ventilation and time in ICU
  • Improved survival, however with poor functional outcomes

NSB236 (5 decks)

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