Organ Donation Midland Collaborative 7 th May 2015 Birmingham Maria Cartmill Are we able to prognosticate No or not accurately for an individual patient Hippocratic aphorism ID: 619032
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Slide1
Prognostication After Brain Injury
Organ Donation Midland Collaborative
7
th
May 2015 Birmingham
Maria CartmillSlide2
Are
we able
to prognosticate
?
Slide3
NoSlide4
..or not accurately for an individual patient…Slide5
Hippocratic aphorism
“No head injury is so serious that it
should be despaired of nor so
trivial that it
can be ignored”Slide6
Just about rightSlide7
Experienced neurosurgeon
assessed 100 patients;
56% correct prognosis
(Kaufman)
If the initial GCS is reliable,
20% with the worst initial score
will survive; 8-10% with GOS 4-5Slide8
Probabilities not prophecies!Slide9
Glasgow Outcome Scale (GOS)
Unfavourable
1 Death
2 Persistent vegetative state
3 Severe disability (dependent on daily support)
------------------------------------------
Favourable
4 Moderate disability (disabled, independent)
5 Good recovery (resumption of normal life)Slide10
Glasgow Coma Scale (GCS)Slide11
Brain Injuries
Traumatic
Aneurysmal subarachnoid
h
aemorrhage
HypoxiaSlide12
Traumatic
IMPACT/CRASH/TRISS/APACHE 2
Early prognostic indicators
Age
Motor part of GCS
Pupils
Imaging findingsSlide13
Age
P
oor outcome increases with increasing age
Poor outcome increases significantly in patients aged > 60y
Independent of the increased frequency of complications in elderlySlide14
Age vs
outcome
Age (y)
GOS 1 (%)
GOS 5
(%)
1-4
17
17
5-9
22
61
10-14
20
40
15-19
25
40
21-40
35
33
41-60
55
15
61-80
80
5
(
Alberico
. Class
II)Slide15
Age vs
mortality
Age (y)
GOS 1 (%)
11-20
35
21-30
39
31-40
45
41-50
55
51-60
66
61-70
77
71-80
85
81-90
95
(Teasdale. Class I)Slide16
Recent studies
No age threshold
40-50% increase in poor outcome each additional 10y
(
Mukkelhoven
2003, 5600pts)Slide17
Pupils
Post resuscitation responses
“> 4mm is a dilated pupil”
Bilateral absent pupil response > 70% PPV of poor outcomeSlide18
Pupils vs
GOS 1-2 outcome
No of patients in study
Bilat
reactive
%
Unilateral fixed
%
Bilat
fixed
%
600
42
-
95
305
29
54
90
213
36
-
91
746
32
34
74
Ave
35
44
88
(
www.braintrauma.org
)Slide19
GCS (Motor)
The motor component of GCS provides the best predictive value
GCS (M)
GOS 1 (%)
1
88.9
2-4
56.2
5
12.5
6
0.4
(
Colohan
. Class
II)Slide20
Imaging findings
Multiple lesions worse than single
Midline shift > 15 mm worse than < 5 mm
Basal cisterns compressed
Traumatic subarachnoid
haemorrhage
Slide21
Basal cisterns
Compressed basal cisterns x 3 increased
risk of raised ICP
x
2-3 increased risk of mortality
Direct relationship with pupils
Slide22
HerniationSlide23
GOS vs
basal cisterns
Basal cisterns
GOS
%
1
2
3
4
5
Normal
22
6
16
21
35
Compressed
39
7
18
17
19
Absent
77
2
6
4
11
(218
pts
with GCS <8)Slide24
Traumatic subarachnoid haemorrhage
(
TrSAH
)
Present in severe TBI (26-53%)
Mortality increased x2
Extent of
TrSAH
related to outcome
TrSAH
is significant independent prognostic indicatorSlide25
SAH grade
Fisher Grade
Unfavourable
(GOS 1-3)
Favourable
(GOS 4-5)
1
(no blood)
0
14
2
(diffuse/ <1mm)
6
13
3
(clot/ >1mm)
15
6
4
(ICH or IVH)
7
0
(
Harders
. Class II)Slide26
ICP monitoring
Helps manage ICP
Does it alter outcome
?
Useful if ICP > MAP
Pressures can be very high in children with good outcomeSlide27
MRI
Using
conventional imaging, presence of bilateral lesions in the dorsolateral upper brainstem appears to be the factor of greatest adverse prognostic significance.
With MRS, low
NAA/
creatine
ratio in the hemispheres and in the pons predicts a poor outcome
.
(Weiss
et
al,
Crit Care
2007
; 11(5):
230
)Slide28
Neurosurgery registrars’ 3am hopelessness chartSlide29
Aneurysmal subarachnoid h
aemorrhageSlide30
Natural history
Peak incidence 55-60y
10-20% die before reaching medical care
30 day mortality 45%
Overall mortality 51%
1/3 survivors remain dependent
Of the other 2/3 – only 30% patients achieve their previous quality of lifeSlide31
Outcome
Related to grade on admission
Age >70y fare worse for each neurological grade
Amount of blood on CT head (Fisher)
(Drake et al. Report
of World Federation of Neurological Surgeons Committee on a
Universal
Subarachnoid Hemorrhage Grading Scale.
J
Neurosurg
. Jun 1988;68(6):985-
6
)
WFNS grade
GCS score
Major
deficit
1
15
-
2
13-14
-
3
13-14
+
4
7-12
+ or -
5
3-6
+ or -Slide32
Physiology
Average blood loss < 10mls
Rapid increase in ICP to > blood pressure
Cerebral
stand
still
Lose consciousness/ vomit/ severe headache
Possible seizure
Permanent
vs
transient effect upon brain
Cerebral Stunning
- “TIA of the midbrain”Slide33
When to prognosticate?
Recommendation is to wait 6 hours to test
If diabetes
insipidus
/ hypothermia then likely permanent
Keep assessing
Support
in the
interim
Allows for re-perfusion of central structuresSlide34
HypoxiaSlide35
Pre-hospital
Poor outcome associated with:
Type of
arrhythmia:
shockable
>> non-
shockable
Age > 70 years
Anoxia / no-flow time (witnessed) >25
mins
Duration of CPR
Co-morbidities
Variable, with poor sensitivity / specificity
Cannot be used to reliably prognosticateSlide36
Clinical
Affected by therapeutic hypothermia (sedation)
GCS
Motor response to pain
Corneal reflexes
Unaffected
Pupillary reflexes
Seizures / early myoclonus
(
Cronberg
et al. Recommendations
from the Swedish Resuscitation Council.
Resuscitation
. 2013; 84(7): 867–
72)Slide37
Imaging
MRI
4 stages
MRI sensitive but non-specific
as single prognosticator
Grey-white-matter ratio (GWR)
Recent data suggests GWR <1.16 predicts poor outcome (100% specific / 38% sensitive)
(
Scheel
et al.
Scandinavian
Journal of Trauma, Resuscitation and Emergency Medicine
. 2013; 21(1):
23)Slide38
Biomarkers
S-100B: calcium-binding
astroglial
protein
Neuron-specific
enolase
(NSE): isomer of
enolase
, located in neurones
Ammonia & lactate
References
Intensive
Care Society.
Standards for the management of patients
a
fter
ca
rdiac
a
rrest.
2008 Oct.
http
://www.ics.ac.uk/ics-homepage/guidelines-standards/ (accessed 12/09/2013)
Huntgeburth
et al. Changes in
neuron-specific
e
nola
se
are
more suitable
t
han
i
ts
a
bsolute
s
erum
l
evels
for
the
p
rediction
of
neurologic
o
utcome
in
hypothermia-treated
p
atients
with
out
-of
-hospital
c
ardiac
a
rrest
. Neurocritical Care. 2014;20(3):358-366 Shinozaki et al. Blood ammonia and lactate levels on hospital arrival as a predictive biomarker in patients with out-of-hospitalcardiac arrest. Resuscitation. 2011; 82(4): 404–9. Slide39
Neurophysiology
SSEPs
Bilateral median nerve stimulation
Measure cortical (N20) or shoulder (N9) potentials
Reliable specific test of neurological outcome (even with hypothermia)
EEG
Burst suppression / generalised
epileptiform
discharge predict poor outcome
Issues of accuracy (not recommended)Slide40Slide41
Seizures
Seizures / myoclonus post-arrest + during cooling associated with poor outcome
Myoclonic
jerks on day 3, or after warming, do not
predict poor outcome
Lance-Adams, action-induced myoclonus without LOC
(
Yadavmali
et al
.
The Lance-Adams syndrome: helpful or just hopeful, after cardiopulmonary arrest.
Journal
of the Intensive Care Society. 2011; 12(4): 324 –
328
)Slide42
Can we prognosticate?
Good
Bad
Early
Reaction to pain (GCS M ≥ 5)
Normal CT
Reactive
EEG
Myoclonic status (+/- EEG)
Reduced GWR
Increase
in biomarkers
Late
Reaction
to pain
(GCS M ≥ 5)
Normal CT
Low biomarkers
Reactive EEG
GCS
M 1 – 2
Pupils / cornea unreactive
SSEP: bilateral lack of N20
Abnormal CT / MRI
High levels of biomarker
(Recommendations
from the Swedish Resuscitation Council.
Resuscitation
. 2013; 84(7): 867–
72)Slide43
When to prognosticate?
Traditional guidance
72 hours after
arrest
/event
If cooled
72 hours
after
reaching
normothermia
(
Wijdickset
al.
Neurology
. 2006; 67(2): 203–
10)Slide44
Are we able to prognosticate in patients with brain injury
?Slide45
Conclusion
Not early
We can give an early probability
MDT approach recommended
Time