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PBL SEM 3 > 10 - acute head trauma > Flashcards

10 - acute head trauma Flashcards

1
Q

risk factors for head trauma

A
  • male
  • young (15-30) and old (65+)
  • urban areas
  • substance misuse, esp alcohol
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2
Q

what does primary prevention of head injury include?

A
  • seat belts
  • helmets
  • alcohol prevention/limits
  • health and safety (in industry and community)
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3
Q

what is included in the history of a head trauma assessment?

A
  • from patient (if able to talk) and collateral (witnesses, friends, family, paramedics etc)
  • time
  • mechanism
  • conscious level (at worst)
  • seizures
  • PMHx/DHx
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4
Q

describe the ABCDE assessment

A

A = airway - patency
B = breathing - other injuries, apnoea, hypoxia
C = circulation - other injuries, hypotension, heart rate
D = disability - GCS, pupils, C-spine (10% of head injuries also have c-spine injury)
E = entire body - primary survey

also check glucose (hypoglycaemia can mimic head injury as brain needs glucose to function), temperature

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5
Q

what are some specific signs of a base of skull fracture?

A
  • raccoon eyes (bilateral eye bruising)
  • battle sign (bleeding behind ear)
  • haemotympanum (blood behind ear drum)
  • CSF leak (get clear fluid leaking from nasal passages)
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6
Q

what are components of the GCS

A

eye opening = /4

verbal response = /5

best motor response = /6

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7
Q

when would a CT be performed within 1 hour?

A
  • GCS less than 13 on initial assessment in the emergency department
  • GCS less than 15 at 2 hours after injury
  • suspected open or depressed skull fracture
  • any sign of basal skull fracture
  • post-traumatic seizure
  • focal neurological deficit
  • more than 1 episode of vomiting
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8
Q

when would a CT be performed within 8 hours of the head injury for adults who have experienced some loss of consciousness or amnesia since the injury?

A
  • age 65+
  • any history of bleeding or clotting disorders
  • dangerous mechanisms of injury
  • more than 30 minutes’ retrograde amnesia of events immediately before the head injury
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9
Q

primary vs secondary brain injury

A

> primary = the original insult

> secondary = the damage caused after which worsens the brain injury

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10
Q

what can secondary brain injury be caused by?

A
  • hypoxia
  • hypotension/hypertension
  • raised ICP
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11
Q

what do each of these CT scans show?

A
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12
Q
A
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13
Q

describe a diffuse axonal injury

A
  • brain ricochets forwards and backwards
  • seen more in the young
  • has a bad outcome
  • may not be too noticeable on initial CT scan — MR more likely to pick up changes
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14
Q

where in an extradural haematoma?

A

in potential space between the skull and the dura

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15
Q

an extra dural haematoma is normally bleeding from what artery?

A

middle meningeal

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16
Q

extradural haematoma on CT scan?

A
  • extradural therefore normally doesn’t cross the surgical suture sites
  • lentiform shape
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17
Q

extradural vs sub dural haematoma events

A

extradural:
- impact to head
- lose consciousness immediately
- regain consciousness
- then get drowsy and lose consciousness again

sub dural :
- follows trauma, most frequently caused by falls
- gradual loss of consciousness
- bleeding from bridging veins

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18
Q

what kind of haematoma does cross the suture sites?

A

subdural

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19
Q

what are the effects of secondary insults in terms of favourable outcome, severely disabled and dead?

A
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20
Q

what are normally in equilibrium in a fixed vault?

A

blood, brain and CSF

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21
Q

equation for mean arterial pressure (MAP)

A

CO x SVR (systemic vascular resistance)

DBP + 1/3 (SBP - DBP)

= pressure pushing blood to brain

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22
Q

pressure which MAP has to overcome to get into brain = ?

A

intracranial pressure (ICP)

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23
Q

what is the pressure of blood going through the brain? how is it worked out?

A

= cerebral perfusion pressure (CPP)

MAP - ICP

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24
Q

what should ICP be in mmHg?

A

5-12mmHg

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25
Q

what happens when you have poor brain perfusion?

A

fainting

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26
Q

what ceases to work after brain injury?

A

autoregualtion

27
Q

what is a concerning ICP?

A

20+

28
Q

what does it mean if ICP > MAP?

A

no blood flow to brain — no pressure to push blood to brain

29
Q

how is ICP measured?

A
  • in neurointensive care unit
  • neurosurgeons put intracranial pressure wires into the intraparenchymal (normal), intraventricular, subarachnoid or epidural area
  • gives pressure in that localised area (not the whole brain)
30
Q

how does a haematoma cause an increased ICP?

A

obstructs ventricular system — CSF can’t drain — increased pressure — hydrocephalus

31
Q

what can cause a raised ICP?

A
  • oedema
  • haematoma
  • hydrocephalus
  • vasospasm
  • micro vascular pathology
32
Q

describe cytotoxic oedema

A
  • initial mechanism
  • fluid retained in cytoplasm
  • loss of NaK ATPase
  • glutamate gated Ca channels open
  • Ca draws water in
33
Q

describe vasogenic oedema

A
  • delayed mechanism (48 hours)
  • breakdown of BBB
  • fluid and protein extravasation into parenchyma
34
Q

who is vasogenic oedema esp important for?

A

patients with stroke or contusions — get ‘flowering’ - gets worse 48 hrs after they 1st happen

35
Q

what are the 3 mechanism of herniation syndromes?

A
  • subfalcine
  • trans tentorial
  • tonsillar
36
Q

describe subfalcine herniation

A

midline shift on ST

37
Q

describe trans tentorial herniation

A
  • pressure on brainstem
  • uncal herniation - brain herniates down
  • oculomotor nerve — pupils fixed and dilated (lose pupillary reflex)
38
Q

describe tonsillar herniation

A
  • no skull deficit therefore brain must go down
  • through foramen magnum
  • medulla becomes ischaemic — cardiorespiratory centres ischaemic — stop breathing — neurological death
39
Q

in management, what do we aim for to maintain physiology?

A
  • MAP > 90 or CPP > 60
  • normocapnia
  • normothermia
  • normoglycaemia
  • avoid hypoxia
40
Q

how do we improve venous drainage?

A
  • head up — if no c-spine injury
  • no restrictions
41
Q

how do we reverse coagulopathy?

A

eg. vitamin K to reverse warfarin

FFP

42
Q

when would we use anti-epileptics?

A

if indicted

eg if had seizure already

if depressed skull fracture or temproal lobe injury

43
Q

hyperventilation in management?

A

CO2 4-4.5

vasocontriction — reduce ICP

44
Q

osmotherapy?

A
  • hypertonic (30%) sodium chloride — draw H20 out of brain to reduce pressure, by increasing blood Na+ levels
  • mannitol (glucose)
45
Q

surgical management of head trauma

A
  • remove the mass — haematoma/contusion, Burr Hole (drain blood)
  • remove the CSF (hydrocephalus) — external ventricular drain
  • remove the skull — decompressive craniectomy (allows brain to swell outside skull, avoiding herniation). improves survival BUT significant neurological impairments
46
Q

what affects prognosis?

A
  • age (younger = better regeneration of brain)
  • presenting GCS
  • co-morbidities
  • episodes of hypoxia or hypotension
  • pupillary response — fixed dilated pupils = already got transtentorial herniation and occlusion of oculomotor nerve
  • duration ICP > 20
  • country (high economic = better)
47
Q

describe glasgow outcome score 1-5

A

1 = good recovery
5 = death

48
Q

describe an uncal herniation and its effects

A

a type of transtentorial herniation

  • innermost part of temporal lobe (uncus) herniated down towards tentorium and puts pressure on brainstem
  • can compress oculomotor nerve — eye looks down and out
  • dilated pupil that doesn’t respond to light
  • posterior cerebral artery can be compressed — homonymous hemianopia (contralateral to artery affected). macula sparing as centre also receives blood supply from MCA (as well as PCA)
49
Q

symptoms of a rise in ICP

A
  • decreased level of consciousness
  • focal neurological signs
  • papilloedmea
  • cushing’s triad — increased BP, irregular breathing, bradycardia
50
Q

common chronic sub dural haematoma symtpoms

A
  • headaches
  • vision problems
  • memory loss
  • slurred speech
  • unsteady gait
51
Q

what is the pterion?

A

the area where these meet:

  • parietal bone
  • squamous part of temporal bone
  • frontal bone
  • greater wing of sphenoid
52
Q

clinical significance of the pterion?

A
  • skull is very weak at this point so more easily broken
  • overlies anteiror division of MCA
  • fracture here can lead to an extradural haematoma
53
Q

why can ICP rise rapidly in an extradural haematoma?

A

dura attached tightly to sutures — blood doesnt cross suture sites and is trapped with no where to go

54
Q

what is the bleeding source of subdural haematomas?

A

usually bridging veins (connect superficial veins of skull and dural venous sinuses)

55
Q

what are bridging veins vulnerable to?

A
  • rapid acceleration and deceleration (commonly disrupted in car crashes)
  • the veins get stretched out in the elderly and in chronic alcohol abuse
56
Q

vigorously shaking a child can cause what type of haematoma?

A

subdural

57
Q

why doesnt pressure build as quickly in subdural haematoma?

A

blood can cross suture sites — disrupted over larger areas — ICP rises gradually

58
Q

symptoms of extradural vs subdural haematoma

A

extradural haematoma
- impact to head, lose consciousness immediately, regain consciousness, headache over hours, then get drowsier and lose consciousness again
- headaches, nausea, vomiting, focal neurological symptoms (weakness, numbness, vision and auditory problems). cerebral oedema —> brain herniation —> loss of consciousness, coma, death

subdural haematoma:
- worsening headaches, nausea or vomiting, visual problems, slurred speech, dizziness, unsteady gait, confusion, cognitive impairment, seizures, hemiparesis

59
Q

how can density on CT help determine the age of a haematoma?

A

acute = hyperdense (white)
chronic = hypodense

60
Q

what type of haematoma has a higher morbiity and mortality rate?

A

subdural — harder to detect in the early stages

61
Q

what 3 diseases/syndromes can predispose even young invidious to saccular aneurisms, causing subarachnoid haemorrhages?

A

autosomal dominant polycystic kidney disease, marfan syndrome, and ehlers-danlos syndrome

62
Q

what does a subarachnoid haemorrhage look like on CT scan?

A

blood in ventricular cisterns, interhemispheric fissures, and within sulci

63
Q

what can cause hydrocephalus and post-traumatic vasospasm?

A

subarachnoid haemorrhage

PBL SEM 3 (49 decks)

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