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

Neurointensive Care and Encephalopathies ✅ Flashcards

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
Q

What monitoring should be considered in patients with encephalopathy?

A

ICP monitoring

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26
Q

How is ICP monitoring usually done?

A

Neurosurgical insertion of a fine bore catheter into the substance of the brain through a small burr hole

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27
Q

When is ICP monitoring the standard of care?

A

In traumatic brain injury requiring neurointensive care

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28
Q

What is the advantage of ICP monitoring?

A

Allows accurate assessment of cerebral perfusion pressure (CPP)

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29
Q

How is CPP calculated?

A

MAP - ICP

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30
Q

Why is control of CPP important?

A

To prevent cerebral ischaemia

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31
Q

What is the normal CPP in an infant?

A

> 50mmHg

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32
Q

What is the normal CPP in a child?

A

> 60mmHg

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33
Q

What is the normal CPP in an adolescent?

A

> 70mmHg

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34
Q

What feature of the cerebral vessels does blood flow depend on?

A

Diameter

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35
Q

What is the diameter of cerebral blood vessels affected by?

A

PaCO2

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36
Q

What effect does PaCO2 have on blood vessels?

A

Low levels cause vasoconstriction

High levels cause vasodilation

37
Q

What is the result of PaCO2 having an effect on the diameter of cerebral blood vessels therefore on cerebral blood flow?

A

Maintenance of normocapnia is of critical importance

38
Q

How should normocapnia be maintained in an intubated patient?

A

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
Q

What can hyperventilation lead to in a ventilated patient?

A

Can induce ischaemia

40
Q

What can hypoventilation lead to in an intubated patient?

A

Can lead to increased cerebral blood flow and exacerbation of raised ICP

41
Q

What is the result of CPP being dependent on arterial pressure?

A

It is often necessary to maintain BP at above normal levels

42
Q

What may be required to maintain BP at higher than normal levels?

A

Inotropes

43
Q

What is important for maintaining adequate oxygen delivery in neurointensive care?

A

Ensuring physiologic haemoglobin levels, with transfusion if needed

44
Q

How can cerebral oxygen demand be reduced?

A
  • Sedation

- Seizure control

45
Q

What is the role of hypothermia in reducing cerebral oxygen demand?

A

May have a role, but no definitive trial evidence to support use in children

46
Q

Are steroids used in the treatment of raised ICP?

A

No - limited evidence of beneficial effects, although may have role in meningitis or tumours

47
Q

What is used for osmotherapy in raised ICP?

A

3% saline or mannitol

48
Q

What is the benefit of osmotherapy in raised ICP?

A

May reduce intracranial cellular oedema

49
Q

Should osmotherapy be used in traumatic brain injury?

A

Only on advice of a neurosurgeon

50
Q

What are the other strategies for reducing ICP?

A
  • Fluid restriction

- Maintaining head tilt at 30 degrees upright in midline

51
Q

How does maintaining the head at tilt 30degrees upright help in raised ICP?

A

Improves venous return

52
Q

What are all treatments of raised ICP aimed at?

A

Trying to decrease or limit cerebral oedema, and acutely dropping the ICP by creating more space, hence limiting or preventing secondary brain injury

53
Q

What does uncal herniation commonly cause compression of?

A

Cranial nerve III

54
Q

Where does CN III originate?

A

In anterior aspect of midbrain

55
Q

What does CN III compression result in?

A

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
Q

What often presents first in CN III compression?

A

Pupillary dilatation

57
Q

Why does pupillary dilatation often precede the somatic motor effects of CN III compression?

A

Because the parasympathetic fibres surround the motor fibres of the nerve, and so are compressed first

58
Q

Is the pupillary dilatation unilateral or bilateral in uncal herniation?

A

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
Q

What is acute encephalopathy defined as?

A

A sudden onset of diffuse brain dysfunction, with or without an associated change in level of consciousness

60
Q

Are encephalopathies convulsive or non-convulsive?

A

Can be either

61
Q

What is convulsive status epilepticus (CSE) defined as?

A

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
Q

How might children with non-convulsive acute encephalitis present?

A
  • Reduced conscious level
  • Psychosis
  • Confusion
63
Q

How serious is CSE in childhood?

A

Life threatening condition with serious risk of neurological sequelae

64
Q

What can cause neurological sequelae in CSE?

A
  • Hypoxia due to airway obstruction and hypoventilation

- Neuronal damage due to unmet increased cerebral metabolic demands

65
Q

What is the mortality of CSE in children?

A

Up to 4%

66
Q

What are the neurological sequelae of CSE?

A
  • Epilepsy
  • Motor deficits
  • Learning difficulties
  • Behavioural problems
67
Q

Are neurological sequelae common in CSE?

A

No, they are rare

68
Q

What is the most common cause of CSE in paediatrics?

A

Uncontrolled epilepsy with underlying seizure disorder, or febrile convulsion

69
Q

What age can febrile convulsions occur?

A

Children 6months - 6 years

70
Q

What should be considered when CSE presents in a febrile child?

A

Infective meningoencephalitis

71
Q

What are the most common bacteria causing infective meningoencephalitis?

A

Meningococcus and pneumococcus

72
Q

What are the most common viruses causing infective meningoencephalitis?

A

Herpes simplex

Enteroviridae

73
Q

What causes should be considered in all cases of acute encephalopathy?

A
  • Space occupying lesions
  • Autoimmune disease
  • Vascular occlusion or bleeding
  • Metabolic disorders
  • Poisons and trauma, including NAI
74
Q

What autoimmune diseases can cause acute encephalopathy?

A
  • Acute disseminated encephalomyelitis (ADEM)

- Anti-NMDA receptor antibody encephalitis

75
Q

What should be done in acute resuscitation and stabilisation in CSE?

A
  • High flow oxygen
  • Measure BM
  • Brief history and clinical examination
  • Stabilise airway, breathing, and circulation
  • Assess conscious level (GCS/AVPU)
76
Q

What is the disadvantage of artificial ventilation in acute resuscitation and stabilisation in CSE?

A

Reduces ability to monitor conscious level

77
Q

What anti-microbial management is required in CSE?

A

Until a confirmed microbiological diagnosis has been made, patients should be started on high-dose antibiotic and anti-viral treatment

78
Q

What antimicrobials are often used empirically in CSE?

A
  • Third generation cephalosporin
  • Macrolide
  • Aciclovir
79
Q

What needs to be done prior to taking CSF samples in CSE?

A

Exclude raised ICP

80
Q

Why is it important to exclude raised ICP before taking CSF samples?

A

Because of the risk of coning

81
Q

What will seizures lead to in CSE unless effectively controlled?

A

Further hypoxia and ischaemia

82
Q

Why do seizures lead to further hypoxia and ischaemia in CSE?

A

Due to combination of airway obstruction and neuronal secondary energy failure

83
Q

How can seizure activity be identified in CSE?

A
  • Clinically

- EEG

84
Q

How can brief seizures in CSE be managed?

A

Benzodiazepines, e.g. lorazepam

85
Q

What management is often required for prolonged seizures in CSE?

A
  • IV anticonvulsants, e.g. phenytoin

- Barbiturate infusions, e.g. phenobarbitone, thiopentone

86
Q

When should rapid sequence induction be used in CSE?

A

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
Q

What should be used for rapid sequence induction in CSE?

A

Thiopentoner

88
Q

What kind of agents should be used if neuromuscular paralysis is used in CSE?

A

Short acting

89
Q

Why should neuromuscular paralysis be short acting if used in CSE?

A

To not mask the clinical signs of a convulsion

TAS Emergencies and Critical Care ✅ (8 decks)

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