Prognostication After Brain

InjuryOrgan Donation Midland Collaborative

7th May 2015 Birmingham Maria Cartmill

Are we able to prognosticate?

No

..or not accurately for an individual patient…

Hippocratic aphorism

“No head injury is so serious that it

should be despaired of nor so trivial that it can be

ignored”

Inappropriately ambiguous

Unduly optimistic

Unnecessarily pessimistic

Just about right

• 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 4-5

Probabilities not prophecies!

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)

Glasgow Coma Scale (GCS)

Brain Injuries• Traumatic • Aneurysmal subarachnoid haemorrhage• Hypoxia

Traumatic• IMPACT/CRASH/TRISS/APACHE 2• Early prognostic indicators• Age• Motor part of GCS• Pupils• Imaging findings

Age• Poor outcome increases with increasing age • Poor outcome increases significantly in patients

aged > 60y• Independent of the increased frequency of

complications in elderly

Age vs outcomeAge (y) GOS 1 (%) GOS 5 (%)1-4 17 175-9 22 6110-14 20 4015-19 25 4021-40 35 3341-60 55 1561-80 80 5

(Alberico. Class II)

Age vs mortalityAge (y) GOS 1 (%)11-20 3521-30 3931-40 4541-50 5551-60 6661-70 7771-80 8581-90 95

(Teasdale. Class I)

Recent studies

• No age threshold• 40-50% increase in poor outcome each additional

10y (Mukkelhoven 2003, 5600pts)

Pupils

• Post resuscitation responses• “> 4mm is a dilated pupil”• Bilateral absent pupil response > 70% PPV of

poor outcome

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)

GCS (Motor)• The motor component of GCS provides the best

predictive value

GCS (M)

GOS 1 (%)

1 88.92-4 56.25 12.56 0.4

(Colohan. Class II)

Imaging findings• Multiple lesions worse than single• Midline shift > 15 mm worse than < 5 mm• Basal cisterns compressed• Traumatic subarachnoid haemorrhage

Basal cisterns• Compressed basal cisterns x 3 increased risk of raised ICP• x 2-3 increased risk of mortality• Direct relationship with pupils

Herniation

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)

Traumatic subarachnoid haemorrhage (TrSAH)

• Present in severe TBI (26-53%)• Mortality increased x2• Extent of TrSAH related to outcome• TrSAH is significant independent prognostic

indicator

SAH gradeFisher Grade Unfavourabl

e (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)

ICP monitoring• Helps manage ICP• Does it alter outcome?• Useful if ICP > MAP• Pressures can be very high in children with good

outcome

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)

Neurosurger

y registrars’

3am

hopelessnes

s chart

Aneurysmal subarachnoid haemorrhage

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 life

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 -

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”

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 structures

Hypoxia

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 prognosticate

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)

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)

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 after cardiac arrest. 2008 Oct. http://www.ics.ac.uk/ics-homepage/guidelines-standards/ (accessed 12/09/2013)

Huntgeburth et al. Changes in neuron-specific enolase are more suitable than its absolute serum levels for the prediction of neurologic outcome in hypothermia-treated patients with out-of-hospital cardiac arrest. 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.

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)

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)

Can we prognosticate?

Good Bad

EarlyReaction to pain (GCS M ≥ 5)Normal CTReactive EEG

Myoclonic status (+/- EEG)Reduced GWRIncrease in biomarkers

Late

Reaction to pain (GCS M ≥ 5)Normal CTLow biomarkersReactive EEG

GCS M 1 – 2Pupils / cornea unreactiveSSEP: bilateral lack of N20Abnormal CT / MRIHigh levels of biomarker

(Recommendations from the Swedish Resuscitation Council. Resuscitation. 2013; 84(7): 867–72)

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)

Are we able to prognosticate in patients with brain injury?

Conclusion• Not early

• We can give an early probability

• MDT approach recommended

• Time