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ATLS > Head trauma > Flashcards

Head trauma Flashcards

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
Q

Diffuse intracranial lesion examples

A

Concussion
Multiple contusions
Hypoxic / ischaemic injury
Axonal injury

26
Q

Axonal injury mechanism of injury

A

High velocity impact or deceleration impact
Multiple punctate haemorrhages throughout cerebral hemispheres

Often poor outcome

27
Q

Concussion definition

A

Transient, non-focal neurological disturbance
Often LOC
No CT changes

28
Q

Classic presentation of extra-dural haematome

A

Lucid interval between injury and neurological deterioration

29
Q

Concern with cerebral contusions

A

In hours to days can evolve to form intracerebral haematomas and may require surgery

Repeat CT scans to assess progressive changes

30
Q

Management of mild TBI (traumatic brain injury)

A

Often associated with concussion
Usually make uneventful recovery

31
Q

Indications for CT head

A

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
Q

Management of moderate TBI

A

CT head with follow up scan within 24 hours
D/W neurosurgery
Admit for observation in ITU

33
Q

Management of severe TBI

A

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
Q

Target for systolic BP in TBI

A

Age 50 to 69: SBP > 100 mmHg
Age 15 to 49 or >70: SBP > 110 mmHg

35
Q

Replacement of choice to manage hypovolaemia in TBI and why?

A

Isotonic fluids

Intracranial haemorrhage cannot cause haemorrhagic shock

36
Q

Best prognostic indicator in patients with variable response to stimulation

A

Best motor response

37
Q

Focussed neurological examination in primary survey

A

Level of consciousness
Pupil size and response
Lateralising signs to each limb
Signs of spinal cord injury when pt alert

38
Q

Secondary survey neuro exam

A

Complete neurological examination

39
Q

Reversal of antiplatelets (eg Aspirin, clopidogrel)

A

Platelets

Consider Deamino-Delta-D-Arginine Vasopressin (Desmopressin acetate)

40
Q

Reversal of warfarin

A

FFP
Vitamin K

41
Q

Reversal of unfractionated heparin

A

Protamine sulfate

Monitor APTT

42
Q

Reversal of low molecular weight heparin

A

Protamine sulfate

43
Q

Reversal of direct thrombin inhibitors (Dabigatran)

A

Idarucizumab (Praxbind)

May benefit from prothrombin complex concentrate

44
Q

Reversal of rivaroxaban

A

No reversal agent

May benefit from prothrombin complex concentrate

45
Q

Use of mannitol

A

Reduces raised intracranial pressure in euvolaemic patients with raised ICP

46
Q

Contraindication to mannitol

A

Systemic hypotension SBP < 90

47
Q

Dose of mannitol

A

0.25 - 1 g/kg

Use as bolus

48
Q

Monitoring with mannitol use

A

ICP monitor (unless evidence of herniation)

Maintain serum osmolality <320

Maintain euvolaemia

49
Q

Mechanism of action of mannitol

A

Acts as osmotic diuretic

50
Q

Use of hypertonic saline

A

Reduces raised ICP in euvolaemic patients

51
Q

Concentration of hypertonic saline used

A

3% to 23.4%

52
Q

When is hypertonic saline preferred to mannitol

A

With systemic hypotension

Both provide equivocal effects to reduce ICP in euvolaemic patients

53
Q

When to use anticonvulsants in TBI

A

Only when absolutely necessary to cease seizure activity

Anticonvulsants can inhibit brain recovery

54
Q

Which anticonvulsants are used in TBI and when

A

Phenytoin and Fosphenytoin in acute phase

Benzodiazepines added if necessary until seizure stops

55
Q

Management of intracranial mass lesions

A

Neurosurgery

Rapidly expanding life threatening haematomas may warrant emergency craniotomy

56
Q

Management of penetrating brain injury

A

CT head +/- angiography

Prophylactic abx

Leave partially exteriorised objects in place until definitive neurosurgical management

57
Q

Determination of death by neurological criteria
(Brain death)

A

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
Q

Brainstem reflexes

A

Oculocephalic (Doll’s eyes)
Corneal
Gag reflex

ATLS (14 decks)

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