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GCS

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Title: PowerPoint Presentation Author: Mason Last modified by: JFREEMAN Created Date: 3/27/2006 11:13:35 AM Document presentation format: On-screen Show – PowerPoint PPT presentation

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Title: GCS


1
GCS 1. Best eye response - (max 4) 2. Best
verbal response - (max 5) 3. Best motor response
- (max 6) GCS- 13 mild H I 9-12- moderate H I 8
or less severe H I
2
  • HI
  • May result in LOC
  • Longer unconscious and deeper coma gt
  • likelihood that pt has suffered severe HI
  • 60 good recovery
  • Based on US, UK and Netherland figures
  • for every 100 HI, 5 VS, 15 severely disabled, 20
    minor problems, 60 full recovery

3
  • Nature of lesions in HI
  • Non - missile- RTA
  • Missile
  • Distribution of lesions
  • Focal
  • Diffuse

4
  • Primary damage
  • scalp laceration
  • skull fracture
  • cerebral contusions
  • ICH
  • DAI

TIME COURSE
Immediate
Delayed
  • Secondary damage
  • ischemia
  • hypoxia
  • cerebral oedema
  • infection

5
Pattern of damage in non -missile
HI Focal Scalp- contusion, laceration Skull -
fracture Meninges - haemorrhage, infection Brain
- contusions, laceration, infection Diffuse
damage Brain, DAI, DVI, HIE, Cerebral oedema
6
ICH is a complication of 66 of cases of
non-missile head injury
7
Haemorrhage May be EXTRADURALINTRADURAL -
subdural, subarachnoid
intracerebral
8
  • EDH
  • Found in 2 HI
  • Usually associated
  • with skull fracture
  • Arterial bleed -
  • usually meningeal
  • vessels

9
  • Subdural haemorrhage
  • Usually venous
  • Rupture of bridging
  • veins

10
Subdural haematoma classification 48-72 hours
acute composed of clotted blood 3-20 dys
subacute mixture of clotted and fluid
blood 3 weeks - chronic encapsulated haematoma
11
  • Traumatic SAH
  • may result from severe contusions
  • Fracture of skull can rupture vessels
  • IVH may enter SAS
  • RULE OUT ANEURYSM

12
  • Cerebral contusions
  • Superficial bruises of the brain
  • Frequent but not inevitable after
  • head injury

13
Various types of surface contusions and
lacerations
Coup at point of impact Contrecoup-
diametrically opposite point of impact
Herniation at point of impact between
hernia Fracture related to of skull
14
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15
  • Sites of cerebral contusions
  • Frontal poles
  • Orbital surfaces of the frontal
  • poles
  • Temporal poles
  • lateral and inferior surfaces of
  • occipital poles
  • cortex adjacent to sylvian fissure

16
  • Uncommon types of focal brain damage
  • Ischaemic brain damage due to traumatic
  • dissection and thrombosis of vertebral or carotid
  • arteries by hyperextension of the neck
  • Infarction of pituitary - due to transection
  • of pituitary stalk
  • pontomedullary rent

17
  • Infection
  • complication of skull fracture
  • Open HI
  • Incidence is increased even after closed
  • HI as devitalised tissue prone to infection

18
  • Diffuse damage
  • DAI - widespread damage to axons in the
  • CNS due to acceleration/deceleration of the
  • head
  • Pts usually unconscious from moment of
  • impact
  • Lesser degrees compatible with recovey of
  • consciousness

19
  • Brain swelling and raised ICP
  • Results from
  • cerebral vasodilation - inc cerebral blood vol
  • damage to BV - escape of fluid through BBB
  • inc water content of neurones and glia-
    cytotoxic
  • cerebral oedema

20
ICH herniation
Subfalcine herniation
Tentorial herniation
Tonsillar herniation
21
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22
End result of herniation is compression and Duret
haemorrhages as seen in the pons
23
The pathologist and CNS neoplasms Clinical
details of importance Age Sex F/X
Site of neoplasm
24
INCIDENCE Second commonest form of cancer in
children Accounts for 3.5 of all deaths in the
1-14 year age group Sixth commonest cause of
cancer deaths in adults 25 of all tumors in
adults are in the brain and 35 are
neurectodermal and 40 are metastatic
25
Most primary tumors are sporadic and of
unknown aetiology Secondary tumors vary
greatly between 14-40 Fewer than 5 are
associated with hereditary syndromes that
predispose to neoplasia
26
CNS neoplasms present with epilepsy (focal
or generalised) focal neurologic deficits
symptoms and signs of raised ICP symptoms and
signs of hydrocephalus
27
SSites of cerebral tumors
Sites of cerebral tumors ADULTS Supratentorial
tumors account for 90 Therefore increased
incidence of epilepsy and decreased incidence of
headache Posterior fossa tumours cause headache
and vomiting as early features
28
CHILDREN Cerebellum Pons Optic nerve/chiasm SUPRA
TENTORIAL TUMORS ARE RARE Therefore Headache,
vomiting, visual disturbances common Epilepsy -
unusual
29
  • Diagnosis
  • 1. Clinical picture
  • 2. CT or MRI scan
  • Biopsy
  • smear
  • Frozen section
  • paraffin section

30
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31
Epidemiological aspects of stroke In the USA
stroke is the third commonest cause of death
Incidence increases with age Major risk
factors for stroke are hypertension, cardiac
disease, smoking, hyperlipidemia, and diabetes
Other causes OCP, sickle cell, coagulation
disorders In USA - brain infarction 10 times
commoner than haemorrhage
32
Blood supply to the brain Human brain approx
2 of body weight Receives 15 of total
cardiac output O2 consumption approximately 20
of whole body (i.e high metabolic rate) How
long would the brain survive if blood flow
interrupted
33
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34
Terminology Ischaemia - arterial stenosis
or occlusion Infarction - perfusion territory of
the affected vessel Global brain ischaemia -
lt CPP below the threshold for autoregulation i.e
when systemic blood pressure falls very low e.g
cardiac tamponade, heroin overdose, or ICP rises
to a level that compromises cerebral
perfusion Resultant brain damage or infarction
is accentuated in the WATERSHED REGIONS
35
CPP SAP - ICP CPP gt 40 mmHg - necessary for
autoregulation If CPP lt 40 mmHg CBF falls
dramatically
36
Selectively vulnerable zones Hippocampus -
CA1 Laminae 3 and 5 of cortex Purkinje
cells cerebellum
37

HYPOXIA - blood flow to the CNS may be normal or
increased Damage occurs in selectively
vulnerable neurones
38
CIRCLE OF WILLIS
39
  • Berry aneurysms
  • Congenital
  • Risk of bleeding inc
  • Hypertension
  • AVM
  • systemic vascular
  • disease
  • defects collagen
  • polcystic renal disease

40
  • ICH causes
  • Hypertension
  • Trauma
  • CAA
  • Berry aneurysm
  • AVM
  • Bleeding diathesis
  • Vasculitides
  • Drugs
  • Neoplasm
  • Infective

41
CNS INFECTION Development and outcome depends
on Organism nature route of
entry dose Host Anatomical defenses - skull,
meninges Physiological - immune defense
mechanisms
42
Bacteria Entry into the cranial
cavity Haematogenous - distant foci e.g
lung Local spread - Skull - middle ear, nasal
sinus, osteomyelitis Abnormal routes -
Trauma -fractures
Surgery - shunts Congenital
sinus
43
  • BACTERIAL INFECTIONSDepending on their
    virulence/pathogenicity bacteria can induce
  • Purulent lesions
  • Cellular inflammatory reactions with giant cells
  • Inflammatory oedema caused by toxins and other
    inflammatory
  • substances released by bacterial secretions
    or lysis, in the absence of bacterial replication

44
  • PYOGENIC INFECTION1. BONE EPIDURAL usually
    spinal sec to osteomyelitis
  • DURA MATER - SUB DURAL - sec to sinusitis,
    otitis etc.
  • ARACHNOID SUBARACHNOID sec to haematogenous
    spread of bacteria
  • 4. PIA - INTRAPARENCHYMAL - abscess

45
SUBDURAL
46
  • Three organisms responsible for acute
  • meningitis in childhood or adult life
  • Meningococcus
  • Haemophilus influenza
  • Pneumococcus

47
Bacterial meningitis
48
  • Complications of acute meningitis
  • in the neonate
  • Obstructive hydrocephalus
  • Cavitating lesions in the white matter

49
CSF
50
  • Complications of bacterial meningitis
  • Acute inflammation of adjacent structures
  • Organisation of inflammatory structures

51
Organisation of inflammatory exudate
Impedes flow of CSF into venous sinuses
Obstructs CSF outflow from IV ventricle
52
Cerebral abscess Mean age 35.2 P/C
headaches, pyrexia, altered mental state
(depends on site, number, and /- secondary
cerebral lesion) Site frontal lobe
commonest Majority associated with
sinusitis, mastoiditis 20 no source
Bacteria isolated from 73. Polymicrobial
17.7 Anaerobes 13.6 9.8 died 11
developed epilepsy
53
Cerebral abscess Predisposing conditions Local
otitis media, sinusitis, trauma Systemic
chronic lung disease cyanotic congenital
heart disease transplants
immunosupression
54
Parenchymal abscess formation Early
cerebritis (days 1-3) Late cerebritis (days
4-9) Early capsule formation (days 10-13)
Late capsule formation (days 14 onward)
55
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56
AIMS OF TREATMENT Eliminate infectious
process Reduce mass effect within cranial
cavity thus reduce secondary injury
Treat infections
57
Tuberculous meningitis Usually M
Tuberculosis More commonly associated with
documented history of tuberculosis exposure in
children than adults

58
CSF
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