Head trauma Flashcards

(58 cards)

1
Q

Primary goal of treatment for patients with suspected traumatic brain injury

A

Prevent secondary brain injury

Via ABCDE and controlling BP etc

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2
Q

Cushing’s triad

(Aka Cushing’s response)

A

Hypertension
Bradycardia
Irregular breathing

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3
Q

Implication of Cushing’s triad

A

Impending uncal herniation (coning)

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4
Q

Uncus

A

Medial part of temporal lobe

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5
Q

Compartments of the intracranial cavity

A

Supratentorial compartment
Infratentorial compartment

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6
Q

Through which structure does the uncus herniate

A

Tentorial notch

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7
Q

Consequence of uncal herniation

A

Compression of midbrain
Compression of CN III
Contralateral hemiparesis

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8
Q

Implication of a blown pupil

A

Midline shift and impeding uncal herniation
eg from subdural haematoma

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9
Q

Classical signs of (impending) uncal herniation

A

Ipsilateral blown pupil
Contralateral hemiparesis

Cushing’s response

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10
Q

Monro-Kellie Doctrine

A

Total volume of intracranial contents must remain constant as it is a closed space

When intracranial volume increases, ICP rises

CSF and venous blood compressed out first
Once this compression has reached capacity, brain matter becomes compressed
Leads to herniation / hemispheric shift

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11
Q

Cerebral perfusion pressure

A

Cerebral perfusion pressure = Mean arterial pressure - Intracranial pressure

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12
Q

Intracranial consequence of low MAP

A

Ischaemia / infarct of brain tissue

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13
Q

Intracranial consequence of high MAP

A

Brain swelling

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14
Q

Layers of the meninges including vessels

A

Skull
Meningeal arteries
Dura mater (encloses large venous sinuses)
Arachnoid mater
Blood vessels and CSF
Pia mater
Grey matter
White matter

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15
Q

Parts of the brainstem

A

Midbrain
Pons
Medulla

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16
Q

Ventricular system in brain

A

Filled with and constantly produce CSF

CSF absorbed over brain surface

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17
Q

Consequence of blood in CSF

A

Can impair reabsorption of CSF and increase intracranial pressure

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18
Q

Normal intracranial pressure

A

10 mmHg

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19
Q

Raised intracranial pressure associated with poor outcomes

A

20 mmHg

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20
Q

Methods of classifying Traumatic brain injury

A

Severity

Morphology

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21
Q

Severity of traumatic brain injury classification

A

Mild = GCS 13 - 15
Moderate = GCS 9 - 12
Severe (/ coma)= GCS 8 or less

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22
Q

Morphology of traumatic brain injury classification

A

Skull fractures:
- Vault
- Basilar

Intracranial lesions:
- Focal
- Diffuse

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23
Q

Signs of basilar skull fracture

A

Panda eyes
Battle’s sign
Oto/rhinorrhoea of blood or CSF
Facial paralysis
Hearing loss

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24
Q

Focal intracranial lesion examples

A

Epidural haemorrhage
Subdural haemorrhage
Intracranial haemorrhage

25
Diffuse intracranial lesion examples
Concussion Multiple contusions Hypoxic / ischaemic injury Axonal injury
26
Axonal injury mechanism of injury
High velocity impact or deceleration impact Multiple punctate haemorrhages throughout cerebral hemispheres Often poor outcome
27
Concussion definition
Transient, non-focal neurological disturbance Often LOC No CT changes
28
Classic presentation of extra-dural haematome
Lucid interval between injury and neurological deterioration
29
Concern with cerebral contusions
In hours to days can evolve to form intracerebral haematomas and may require surgery Repeat CT scans to assess progressive changes
30
Management of mild TBI (traumatic brain injury)
Often associated with concussion Usually make uneventful recovery
31
Indications for CT head
Initial GCS <13 GCS <15 after 2 hours Suspected open or depressed skull fracture Sign of basilar skull fracture Vomiting > 2 episodes LOC / amnesia and >65 yrs age LOC > 5 mins Amnesia > 30 mins prior to HI Anticoagulant use Dangerous mechanism of injury
32
Management of moderate TBI
CT head with follow up scan within 24 hours D/W neurosurgery Admit for observation in ITU
33
Management of severe TBI
Urgent Neurosurgical consult Intubate Treat hypotension and hypoxia Maintain pCO2 around 4.7 kPa (35 mmHg) Consider mannitol, pCO2 28-32 for deterioration Avoid pCO2 <28
34
Target for systolic BP in TBI
Age 50 to 69: SBP > 100 mmHg Age 15 to 49 or >70: SBP > 110 mmHg
35
Replacement of choice to manage hypovolaemia in TBI and why?
Isotonic fluids Intracranial haemorrhage cannot cause haemorrhagic shock
36
Best prognostic indicator in patients with variable response to stimulation
Best motor response
37
Focussed neurological examination in primary survey
Level of consciousness Pupil size and response Lateralising signs to each limb Signs of spinal cord injury when pt alert
38
Secondary survey neuro exam
Complete neurological examination
39
Reversal of antiplatelets (eg Aspirin, clopidogrel)
Platelets Consider Deamino-Delta-D-Arginine Vasopressin (Desmopressin acetate)
40
Reversal of warfarin
FFP Vitamin K
41
Reversal of unfractionated heparin
Protamine sulfate Monitor APTT
42
Reversal of low molecular weight heparin
Protamine sulfate
43
Reversal of direct thrombin inhibitors (Dabigatran)
Idarucizumab (Praxbind) May benefit from prothrombin complex concentrate
44
Reversal of rivaroxaban
No reversal agent May benefit from prothrombin complex concentrate
45
Use of mannitol
Reduces raised intracranial pressure in euvolaemic patients with raised ICP
46
Contraindication to mannitol
Systemic hypotension SBP < 90
47
Dose of mannitol
0.25 - 1 g/kg Use as bolus
48
Monitoring with mannitol use
ICP monitor (unless evidence of herniation) Maintain serum osmolality <320 Maintain euvolaemia
49
Mechanism of action of mannitol
Acts as osmotic diuretic
50
Use of hypertonic saline
Reduces raised ICP in euvolaemic patients
51
Concentration of hypertonic saline used
3% to 23.4%
52
When is hypertonic saline preferred to mannitol
With systemic hypotension Both provide equivocal effects to reduce ICP in euvolaemic patients
53
When to use anticonvulsants in TBI
Only when absolutely necessary to cease seizure activity Anticonvulsants can inhibit brain recovery
54
Which anticonvulsants are used in TBI and when
Phenytoin and Fosphenytoin in acute phase Benzodiazepines added if necessary until seizure stops
55
Management of intracranial mass lesions
Neurosurgery Rapidly expanding life threatening haematomas may warrant emergency craniotomy
56
Management of penetrating brain injury
CT head +/- angiography Prophylactic abx Leave partially exteriorised objects in place until definitive neurosurgical management
57
Determination of death by neurological criteria (Brain death)
1) GCS 3 2) Non reactive pupils 3) Absent brainstem reflexes 4) No spontaneous ventilatory effort on formal apnoea testing 5) No confounding factors eg EtOH, drugs, hypothermia
58
Brainstem reflexes
Oculocephalic (Doll's eyes) Corneal Gag reflex