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TAS Emergencies and Critical Care ✅ > Neurointensive Care and Encephalopathies ✅ > Flashcards

Neurointensive Care and Encephalopathies ✅ Flashcards

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1
Q

What is the purpose of neurointensive care?

A

Prevent further damage (secondary injury) to the brain and allow best possible recovery from primary insult

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2
Q

What is the physiological basis for neurointensive care?

A

Monro-Kellie doctrine

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3
Q

How does the Monro-Kellie doctrine see the head?

A

As a ‘rigid box’ with a fixed volume

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4
Q

What is the fixed volume of the head made up of?

A
  • Brain
  • CSF
  • Arterial and venous blood
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5
Q

What can cause expansion of the brain volume?

A
  • Cerebral oedema

- ‘New matter’ occupying space

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6
Q

What ‘new matter’ can occupy space in the brain?

A
  • Expanding haematoma
  • Tumour
  • Obstructive hydrocephalus
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7
Q

How can raised pressure in the head be compensated for?

A

Reduction in amount of CSF or venous blood

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8
Q

How good is the compensation mechanism of reduction in amount of CSF or venous blood?

A

Limited capacity for compensation, and will still be some increased in ICP towards 20mmHg

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9
Q

What is the normal ICP?

A

5-10mmHg

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10
Q

What happens when the capacity of the head to compensate for increased pressure fails?

A

The system becomes non-compliant and further small increases in volume will produce rapid rises in pressure

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11
Q

What is required due to the rapid increase in ICP when compensation mechanisms fail?

A

Rapid management

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12
Q

What management might be used in raised ICP?

A
  • Osmotherapy

- Definitive surgery

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13
Q

What is the timeframe for performing definitive therapy to manage raised ICP?

A

Within 4-6 hours

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14
Q

What is the aim of definitive surgery to manage raised ICP?

A

Remove expanding intracranial mass lesions, e.g. haematoma

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15
Q

What happens once ICP exceeds mean arterial pressure (MAP)?

A

Cerebral perfusion becomes critically impaired, and hypoxic-brain injury may occur

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16
Q

What can further increases in ICP past MAP lead to?

A
  • Transtentorial herniation

- Uncus or cerebellar tonsillar herniation

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17
Q

What part of the brain is affected in transtentorial herniation?

A

The innermost part of the temporal lobe

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18
Q

What does the uncus or cerebellar tonsillar herniation occur through?

A

The foramen magnum

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19
Q

What does brain herniation (transtentorial, uncus, or cerebellar tonsillar) lead to?

A

Brainstem compression and ultimately brain death

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20
Q

What is tonsillar herniation also known as?

A

Coning

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21
Q

What happens in tonsillar herniation?

A

The cerebellar tonsils move downward through the foramen magnum, causing compression of the lower brainstem and upper cervical spinal cord

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22
Q

What does increased pressure on the brainstem result in?

A

Dysfunction of the centres responsible for controlling respiratory and cardiac function

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23
Q

What investigation is required in all patients with encephalopathy?

A

Neuroimaging

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24
Q

Why do all patients with encephalopathy require neuroimaging?

A

To make an assessment of ICP

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25
What monitoring should be considered in patients with encephalopathy?
ICP monitoring
26
How is ICP monitoring usually done?
Neurosurgical insertion of a fine bore catheter into the substance of the brain through a small burr hole
27
When is ICP monitoring the standard of care?
In traumatic brain injury requiring neurointensive care
28
What is the advantage of ICP monitoring?
Allows accurate assessment of cerebral perfusion pressure (CPP)
29
How is CPP calculated?
MAP - ICP
30
Why is control of CPP important?
To prevent cerebral ischaemia
31
What is the normal CPP in an infant?
>50mmHg
32
What is the normal CPP in a child?
>60mmHg
33
What is the normal CPP in an adolescent?
>70mmHg
34
What feature of the cerebral vessels does blood flow depend on?
Diameter
35
What is the diameter of cerebral blood vessels affected by?
PaCO2
36
What effect does PaCO2 have on blood vessels?
Low levels cause vasoconstriction | High levels cause vasodilation
37
What is the result of PaCO2 having an effect on the diameter of cerebral blood vessels therefore on cerebral blood flow?
Maintenance of normocapnia is of critical importance
38
How should normocapnia be maintained in an intubated patient?
Once the patient is intubated, a formal blood gas should be measured to determine PaCO2. This should be correlated to end-tidal CO2 measurement, allowing adjustment of the ventilation constantly to avoid hyperventilation or hypoventilation
39
What can hyperventilation lead to in a ventilated patient?
Can induce ischaemia
40
What can hypoventilation lead to in an intubated patient?
Can lead to increased cerebral blood flow and exacerbation of raised ICP
41
What is the result of CPP being dependent on arterial pressure?
It is often necessary to maintain BP at above normal levels
42
What may be required to maintain BP at higher than normal levels?
Inotropes
43
What is important for maintaining adequate oxygen delivery in neurointensive care?
Ensuring physiologic haemoglobin levels, with transfusion if needed
44
How can cerebral oxygen demand be reduced?
- Sedation | - Seizure control
45
What is the role of hypothermia in reducing cerebral oxygen demand?
May have a role, but no definitive trial evidence to support use in children
46
Are steroids used in the treatment of raised ICP?
No - limited evidence of beneficial effects, although may have role in meningitis or tumours
47
What is used for osmotherapy in raised ICP?
3% saline or mannitol
48
What is the benefit of osmotherapy in raised ICP?
May reduce intracranial cellular oedema
49
Should osmotherapy be used in traumatic brain injury?
Only on advice of a neurosurgeon
50
What are the other strategies for reducing ICP?
- Fluid restriction | - Maintaining head tilt at 30 degrees upright in midline
51
How does maintaining the head at tilt 30degrees upright help in raised ICP?
Improves venous return
52
What are all treatments of raised ICP aimed at?
Trying to decrease or limit cerebral oedema, and acutely dropping the ICP by creating more space, hence limiting or preventing secondary brain injury
53
What does uncal herniation commonly cause compression of?
Cranial nerve III
54
Where does CN III originate?
In anterior aspect of midbrain
55
What does CN III compression result in?
Q- Parasympathetic paralysis and pupillary dilation of the eye on the affected side - Loss of innervation of all ocular motility muscles except for lateral rectus and superior oblique, resulting in deviation of eye to ‘down and out’ position
56
What often presents first in CN III compression?
Pupillary dilatation
57
Why does pupillary dilatation often precede the somatic motor effects of CN III compression?
Because the parasympathetic fibres surround the motor fibres of the nerve, and so are compressed first
58
Is the pupillary dilatation unilateral or bilateral in uncal herniation?
Initially ipsilateral to side of lesion, but as ICP continues to rise, contralateral CN III is also compressed and bilaterally ‘fixed and dilated’ pupils seen
59
What is acute encephalopathy defined as?
A sudden onset of diffuse brain dysfunction, with or without an associated change in level of consciousness
60
Are encephalopathies convulsive or non-convulsive?
Can be either
61
What is convulsive status epilepticus (CSE) defined as?
Generalised convulsion lasting 30 minutes or longer, or repeated tonic-clonic convulsions occurring over a 30 minute period without recovery of consciousness between each convulsion
62
How might children with non-convulsive acute encephalitis present?
- Reduced conscious level - Psychosis - Confusion
63
How serious is CSE in childhood?
Life threatening condition with serious risk of neurological sequelae
64
What can cause neurological sequelae in CSE?
- Hypoxia due to airway obstruction and hypoventilation | - Neuronal damage due to unmet increased cerebral metabolic demands
65
What is the mortality of CSE in children?
Up to 4%
66
What are the neurological sequelae of CSE?
- Epilepsy - Motor deficits - Learning difficulties - Behavioural problems
67
Are neurological sequelae common in CSE?
No, they are rare
68
What is the most common cause of CSE in paediatrics?
Uncontrolled epilepsy with underlying seizure disorder, or febrile convulsion
69
What age can febrile convulsions occur?
Children 6months - 6 years
70
What should be considered when CSE presents in a febrile child?
Infective meningoencephalitis
71
What are the most common bacteria causing infective meningoencephalitis?
Meningococcus and pneumococcus
72
What are the most common viruses causing infective meningoencephalitis?
Herpes simplex | Enteroviridae
73
What causes should be considered in all cases of acute encephalopathy?
- Space occupying lesions - Autoimmune disease - Vascular occlusion or bleeding - Metabolic disorders - Poisons and trauma, including NAI
74
What autoimmune diseases can cause acute encephalopathy?
- Acute disseminated encephalomyelitis (ADEM) | - Anti-NMDA receptor antibody encephalitis
75
What should be done in acute resuscitation and stabilisation in CSE?
- High flow oxygen - Measure BM - Brief history and clinical examination - Stabilise airway, breathing, and circulation - Assess conscious level (GCS/AVPU)
76
What is the disadvantage of artificial ventilation in acute resuscitation and stabilisation in CSE?
Reduces ability to monitor conscious level
77
What anti-microbial management is required in CSE?
Until a confirmed microbiological diagnosis has been made, patients should be started on high-dose antibiotic and anti-viral treatment
78
What antimicrobials are often used empirically in CSE?
- Third generation cephalosporin - Macrolide - Aciclovir
79
What needs to be done prior to taking CSF samples in CSE?
Exclude raised ICP
80
Why is it important to exclude raised ICP before taking CSF samples?
Because of the risk of coning
81
What will seizures lead to in CSE unless effectively controlled?
Further hypoxia and ischaemia
82
Why do seizures lead to further hypoxia and ischaemia in CSE?
Due to combination of airway obstruction and neuronal secondary energy failure
83
How can seizure activity be identified in CSE?
- Clinically | - EEG
84
How can brief seizures in CSE be managed?
Benzodiazepines, e.g. lorazepam
85
What management is often required for prolonged seizures in CSE?
- IV anticonvulsants, e.g. phenytoin | - Barbiturate infusions, e.g. phenobarbitone, thiopentone
86
When should rapid sequence induction be used in CSE?
If 20 mins after IV phenytoin or phenobarbitone has commenced, the child remains in CSE, or if the airway is not protected because of reduced conscious level
87
What should be used for rapid sequence induction in CSE?
Thiopentoner
88
What kind of agents should be used if neuromuscular paralysis is used in CSE?
Short acting
89
Why should neuromuscular paralysis be short acting if used in CSE?
To not mask the clinical signs of a convulsion

TAS Emergencies and Critical Care ✅ (8 decks)

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