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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
what happens when you have poor brain perfusion?
fainting
26
what ceases to work after brain injury?
autoregualtion
27
what is a concerning ICP?
20+
28
what does it mean if ICP > MAP?
no blood flow to brain — no pressure to push blood to brain
29
how is ICP measured?
- 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
how does a haematoma cause an increased ICP?
obstructs ventricular system — CSF can’t drain — increased pressure — hydrocephalus
31
what can cause a raised ICP?
- oedema - haematoma - hydrocephalus - vasospasm - micro vascular pathology
32
describe cytotoxic oedema
- initial mechanism - fluid retained in cytoplasm - loss of NaK ATPase - glutamate gated Ca channels open - Ca draws water in
33
describe vasogenic oedema
- delayed mechanism (48 hours) - breakdown of BBB - fluid and protein extravasation into parenchyma
34
who is vasogenic oedema esp important for?
patients with stroke or contusions — get ‘flowering’ - gets worse 48 hrs after they 1st happen
35
what are the 3 mechanism of herniation syndromes?
- subfalcine - trans tentorial - tonsillar
36
describe subfalcine herniation
midline shift on ST
37
describe trans tentorial herniation
- pressure on brainstem - uncal herniation - brain herniates down - oculomotor nerve — pupils fixed and dilated (lose pupillary reflex)
38
describe tonsillar herniation
- no skull deficit therefore brain must go down - through foramen magnum - medulla becomes ischaemic — cardiorespiratory centres ischaemic — stop breathing — neurological death
39
in management, what do we aim for to maintain physiology?
- MAP > 90 or CPP > 60 - normocapnia - normothermia - normoglycaemia - avoid hypoxia
40
how do we improve venous drainage?
- head up — if no c-spine injury - no restrictions
41
how do we reverse coagulopathy?
eg. vitamin K to reverse warfarin FFP
42
when would we use anti-epileptics?
if indicted eg if had seizure already if depressed skull fracture or temproal lobe injury
43
hyperventilation in management?
CO2 4-4.5 vasocontriction — reduce ICP
44
osmotherapy?
- hypertonic (30%) sodium chloride — draw H20 out of brain to reduce pressure, by increasing blood Na+ levels - mannitol (glucose)
45
surgical management of head trauma
- 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
what affects prognosis?
- 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
describe glasgow outcome score 1-5
1 = good recovery 5 = death
48
describe an uncal herniation and its effects
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
symptoms of a rise in ICP
- decreased level of consciousness - focal neurological signs - papilloedmea - cushing’s triad — increased BP, irregular breathing, bradycardia
50
common chronic sub dural haematoma symtpoms
- headaches - vision problems - memory loss - slurred speech - unsteady gait
51
what is the pterion?
the area where these meet: - parietal bone - squamous part of temporal bone - frontal bone - greater wing of sphenoid
52
clinical significance of the pterion?
- 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
why can ICP rise rapidly in an extradural haematoma?
dura attached tightly to sutures — blood doesnt cross suture sites and is trapped with no where to go
54
what is the bleeding source of subdural haematomas?
usually bridging veins (connect superficial veins of skull and dural venous sinuses)
55
what are bridging veins vulnerable to?
- rapid acceleration and deceleration (commonly disrupted in car crashes) - the veins get stretched out in the elderly and in chronic alcohol abuse
56
vigorously shaking a child can cause what type of haematoma?
subdural
57
why doesnt pressure build as quickly in subdural haematoma?
blood can cross suture sites — disrupted over larger areas — ICP rises gradually
58
symptoms of extradural vs subdural haematoma
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
how can density on CT help determine the age of a haematoma?
acute = hyperdense (white) chronic = hypodense
60
what type of haematoma has a higher morbiity and mortality rate?
subdural — harder to detect in the early stages
61
what 3 diseases/syndromes can predispose even young invidious to saccular aneurisms, causing subarachnoid haemorrhages?
autosomal dominant polycystic kidney disease, marfan syndrome, and ehlers-danlos syndrome
62
what does a subarachnoid haemorrhage look like on CT scan?
blood in ventricular cisterns, interhemispheric fissures, and within sulci
63
what can cause hydrocephalus and post-traumatic vasospasm?
subarachnoid haemorrhage

PBL SEM 3 (49 decks)

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