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Trauma Course > Neurotrauma > Flashcards

Neurotrauma Flashcards

1
Q

What are the most common types of traumatic injuries seen in ED?

A

Head injuries

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2
Q

Why is the primary goal of treatment of patients with a suspected TBI is to prevent secondary injury to the brain?

A

Moderate and severe TBIs are associated with significant morbidity and mortality

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3
Q

What does the brain consist of?

A

Cerebrum, brain stem and cerebellum

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4
Q

What is the cerebellum composed of?

A

Right and left hemispheres, separated by the falix cerebri

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5
Q

What does the left hemisphere contain?

A

The language centres

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6
Q

What does the frontal lobe control?

A

Executive function, emotions, motor function and on the dominant side, expression of speech

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7
Q

What does the parietal lobe direct?

A

Sensory function and spatial orientation

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8
Q

What does the temporal lobe regulate?

A

Certain memory functions

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9
Q

What is the occipital lobe responsible for?

A

Vision

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10
Q

What is the brain stem composed of?

A

The midbrain, pons and medulla

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11
Q

What does the midbrain and upper pond contain?

A

The reticular activating system which is responsible for the state of alertness

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12
Q

What resides in the medulla?

A

Vital cardiorespiratory centres

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13
Q

What is the cerebellum responsible for?

A

Coordination and balance, projects posteriorly in the posterior fossa and connects the spinal cord, brain stem and cerebral hemispheres

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14
Q

What are the ventricles in the brain?

A

A system of CFS filled spaces and aqueducts within the brain

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15
Q

Where is CSF constantly produced?

A

The ventricles

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16
Q

What is absorbed over the surface of the brain?

A

CSF

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17
Q

What can impair the reabsorption of CSF in the brain, resulting in increased intracranial pressure?

A

Blood

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18
Q

What separates the brain into regions?

A

Tough meninges partitions

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19
Q

What divides the intracranial cavity into the supratentorial and ifratentorial compartments?

A

Tentorium cerebelli

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20
Q

The mid brain passes through an opening called?

A

The tentorial hiatus or notch

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21
Q

What runs along the edge of the tentorium and may become compressed against it during temporal lobe herniation?

A

The oculomotor nerve / cranial nerve 3

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22
Q

Why does a patient get pupillary dilation or a ‘blown pupil’?

A

Parasympathetic fibres that constrict the pupils lie on the surface of the third cranial nerve and during herniation these fibres can become compressed causing this change, due to unopposed sympathetic activity

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23
Q

What is the tentorial notch?

A

The medial part of the temporal lobe known as the uncus

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24
Q

What is the part of the brain that is most likely to herniate?

A

The uncus/tentorial notch

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25
Q

What is caused by uncal herniation?

A

Compression of the corticospinal tract in the mid brain

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26
Q

What reduces cerebral perfusion causing or exacerbating ischemia?

A

Raised intracranial pressure

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27
Q

What is a normal ICP?

A

Approximately 10 mmHg

28
Q

ICPs greater than 22 mmHg are associated with what?

A

Poor outcomes

29
Q

What is the Monroe-Kellie doctorine?

A

It explains the dynamics of ICP. The total volume of intracranial contents must remain the same because the cranium is rigid that is incapable of expanding. When normal intracranial volume is exceeded ICP rises.

30
Q

Why can ICP remain stable immediately after injury whilst a mass, such as a haematoma, can grow?

A

Venous blood and CFS can be compressed out of the cranium providing some degree of pressure buffering?

31
Q

What happens to a patients ICP once the limit of displacement is reached?

A

It rapidly increases

32
Q

What can diffuse axonal injuries range from?

A

Mild concussions to severe hypoxic, ischemic injuries

33
Q

What are severe diffuse injuries often a result of?

A

A hypoxic ischemic insult on the brain, due to prolonged shock or impact brain apnoea

34
Q

Where are diffuse injuries often seen in a head CT?

A

In the boarders between the great and white matter and are associated with poor outcomes

35
Q

What is a grade 1 category diffuse axonal injury and what is the mortality %?

A

No visible intracranial injury, 10%

36
Q

What is a grade 2 category diffuse axonal injury and what is the mortality %?

A

Cisterns present 0-5 mm midline shift and small, high or mixed density lesions, 14%

37
Q

What is a grade 3 category diffuse axonal injury and what is the mortality %?

A

Cisterns compressed or absent + grade 1 or 2, 34%

38
Q

What is a grade 4 category diffuse axonal injury and what is the mortality %?

A

Midline shift greater than 5 mm and grade 1,2 or 3, 56%

39
Q

Where are extradural haematomas commonly located?

A

The temporal or temporoparietal regions

40
Q

What are extradural haematomas often a result of?

A

A tear in the middle meningeal artery due to a fracture, disruption of a major venous sinus or bleeding from a skull fracture

41
Q

How do patients who have a extradural haematoma typically present?

A

Following a period of lucidity post injury with rapid deterioration later on

42
Q

What are subdural haematomas commonly a result of?

A

Shearing of small surface or bridging vessels of the cerebral cortex

43
Q

Why is the damage underlying a subdural haematoma more severe than that of an extradural haematoma?

A

The presence of concomitant parenchymal injury

44
Q

Can the primary injury/initial insult that has caused a TBI be reversed?

A

No

45
Q

What is the management of a TBI aimed at?

A

Avoiding secondary injury caused by hypoxia and hypotension through the maintenance of adequate cerebral blood flow and the prevention of hypoxia

46
Q

What do patient who have had a severe TBI require and why?

A

Mechanical ventilation to maintain arterial PO2 to about 11kP and PCO2 between 4.5 and 5 kPa

47
Q

Why is it important to make sure that patients who have TBI have adequate sedation?

A

It minimises pain, anxiety and agitation
Reduces cerebral metabolic rate of oxygen consumption
Facilitates mechanical ventilation

48
Q

Why is midazolam a commonly used sedation drug for patients with TBI and what is it’s downside?

A

It’s used due to its effectiveness as a sedative and anticonvulsant but accumulation may be an issue

49
Q

Why is propofol a commonly used sedation drug for patients with TBI and what is it’s downside?

A

It’s superior metabolic suppressive effects and short half life however in hypothermic patients it has a tendency to accumulate and precipitate hyperlipidaemia. It has also been associated with cardiovascular collapse and the propofol infusion syndrome

50
Q

What is the propofol infusion syndrome?

A

Acidosis, rhabdomyolysis and bradycardia

51
Q

Why are neuromuscular blocks utilized for TBI patients?

A

To minimise coughing and straining

52
Q

What drug is administered to provide neuromuscular block?

A

Rocuronium or atracurium

53
Q

What does a reduction or PaCO2 cause?

A

Cerebral vasoconstriction, reducing cerebral blood volume and consequently ICP

54
Q

If hyperventilation is utilised for TBI patients, what must be maintained?

A

A balance between the beneficial effects of ICP and potentially deleterious effects of cerebral blood flow

55
Q

Following a TBI what can compound cerebral ischemia in the first 24 hours?

A

Induced hyperventilation

56
Q

Why are TBI patients prone to haemodynamic instability?

A

Associated injuries may lead to intravascular volume depletion and trauma to the myocardium which can result in pump failure

57
Q

What can brain stem injuries directly effect?

A

Cardiovascular stability

58
Q

Why must hypotension be avoided at all costs for TBI patients?

A

It causes a reduction in cerebral blood flow and is likely a result of cerebral ischemia

59
Q

Intravascular volume for TBI patients should be maintained with a target central venous pressure of 5-10 mmHg using what?

A

Isotonic crystalloids

60
Q

What is a key intervention in the management of cerebral oedema and raised ICP?

A

Hyperosmolar therapy, such as mannitol or hypertonic saline

61
Q

How does mannitol work?

A
  • plasma expanding effect and improved blood rheology due to a reduction of haemocrit
  • establishes an osmotic gradient between plasma and brain cells, reducing cerebral oedema by drawing water across areas of intact blood brain barrier into the vascular compartment
62
Q

Why does repeated administration of mannitol become problematic?

A

It’s effect on serum osmolarity
Severe intravascular volume depletion
Hypotension
Hyperkalaemia
Rebound increase in ICP

63
Q

How does hypertonic saline work?

A

It produces a reduction in cerebral oedema by moving water out of cells, reducing tissue pressure and cell size, resulting in a decrease in ICP

64
Q

What drug improves cerebral blood flow, independently of ICP, by decreasing endothelial cell volume, increasing diameter of capillary lumen and reducing erythrocyte size thereby improving blood rheology?

A

Hypertonic saline

65
Q

Why is hypertonic saline preferred over mannitol for patients with TBI?

A

Has proven efficacy in controlling ICP in patients refractory to mannitol and is also effective as a volume expander without causing hyperkalaemia and impaired renal function

Trauma Course (17 decks)

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