Category Archives: Neurology

#EuAsia18 Keynote: Caring for the Injured Brain

Mauro Oddo

Championing individualised neurointensive care

  • Neurological examination
  • Imaging
  • Monitoring

The RCTs of therapies in Neuro ICU have shown no effect on pt prognosis

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A Trial of Intracranial-Pressure Monitoring in Traumatic Brain Injury

So what do you do??

Evidence for Health Decision Making — Beyond Randomized, Controlled Trials

Severe traumatic brain injury: targeted management in the intensive care unit.

Fluid therapy in neurointensive care patients: ESICM consensus and clinical practice recommendations.


But it may be that we are not finding the solution/therapy due to the heterogeneity of TBI

Diverse effects of hypothermia therapy in patients with severe traumatic brain injury based on the computed tomography classification of the traumatic coma data bank.

A response to the Chestnut trial –

A Method of Managing Severe Traumatic Brain Injury in the Absence of Intracranial Pressure Monitoring: The Imaging and Clinical Examination Protocol.


There is therefore an unsurprising degree of variation in how TBIs are managed.

Variation in monitoring and treatment policies for intracranial hypertension in traumatic brain injury: a survey in 66 neurotrauma centers participating in the CENTER-TBI study.

  • Outcome was more favourable in pts treated in aggressive centres


Multi Modal Monitoring (MMM)

Multimodal monitoring approach improves ability to detect hypoperfusion in the injured brain

Accuracy of brain multimodal monitoring to detect cerebral hypoperfusion after traumatic brain injury.



New paradigm – quantitative brain function monitoring

Electroencephalography as a Prognostic Tool after Cardiac Arrest.

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LIVES 2016: Neuromonitoring in acute brain injury

Interesting session on current and future neuromonitoring in acute brain injury – mainly focused on bedside monitoring but also some imaging

Excellent introductory slide from Giuseppe Citerio about options currently available for monitoring so have bumped it to the top:


Also worth looking at – nice review on neurological prognostication after cardiac arrest:

Automated infrared pupillometry – Mauro Oddo

Infrared video pupillometry: infrafred camera, processor and LED calibrated light source in simple handheld device

Two main options:

Neurolight Algi-scan (ID-MED France)


NPi-200 (Neuroptics, USA)


Only moderate inter-rater reliability in pupillary assessments using standard clinical approach i.e. torch and subjective assessment:

Good inter-rater reliability for pupillometry. Big difference between standard assessment v pupillometry:

Quantitative devices also much better at diagnosing pupillary asymmetry (L v R) and therefore highlighting deterioration quicker

In cardiac arrest, during CPR – possible to detect recovery of light reflex with pupillometry. Linked to survival v no reflex:

Awaiting larger cohort study post-arrest – 288 patients included and hoping to present next year at LIVES 2017

Also of potential benefit in acute TBI – predicting uncal herniation:

Non invasive assessment of brain oxygenation – Pierre Bouzat

Firstly NIRS – what exactly are we measuring and how?

Early discussion of limitations. Light scattering by tissues. A fair number of estimations so no actual value for cerebral oxygenation e.g. variation in diffusion path-length factor (DPF) between patients and injuries may affect values .

What anatomical and physiological factors affect NIRS?

  1. Hb
  2. Skull thickness
  3. Area of CSF layer

Caution using NIRS with subdural haemorrahge – may not be able to exclude that you are measuring oxygenation of clot

Extracranial contamination – significantly affect NIRS measurements of cerebral oxygen saturation:

NIRS in subarachnoid haemorrhage: no relationship between absolute rSO2 values and DCI

Tissue oxygen saturation monitoring using MRI – may be a future technique for prognostication:

Question: Could NIRS be more useful as a dynamic variable rather than static number? Overwhelming take home from talk was a lot of concern about use of NIRS outside operating room. Potentially of use post-cardiac arrest and in ECMO

Quantitative EEG: Ready for use by general intensivists? – Giuseppe Citerio

Continuous EEG gives us more information than we had before and as a consequence can potentially do things differently e.g. intervene earlier

Caution though: James Cash Penney – “Theory is splendid but until put into practice, it is valueless”

Options for ICU EEG:

  1. Spot EEG (one occasion)
  2. Continuous EEG
  3. Quantitative EEG

But substantial barriers to adopting routine clinical EEG services on intensive care:

  1. Lack of uniform terminology
  2. No consensus on clinical significance
  3. Infrastructure
  4. Need to simplify complex info so clinicians can quickly ID issues
  5. Personnel – to apply the EEG and interpret results

Important to fully engage neurophysiology services to set up critical care EEG

Also – role of mobile app technology to help adoption on ICU

Potential is huge though


A number of injuries can produce a GCS 3 and interventions are multiple with varying evidence of efficacy

Pragmatic, multicentre multinational RCT

Open-label with blinded follow-up

Could be randomised up to 10/7 post injury and must have had first-level interventions to treat it (head up, CSF drainage, etc)

If could not be controlled with hypothermia had barbiturates or hypertonic

Screen 2498 patients, 387 randomised

  • 188 randomised and analysed in hypothermia
  • 187 randomised and analysed in controls

No significant differences in baseline characteristics including age, severity of injury, APACHE, etc AND neurosurgical intervention prior to randomisation

Hypothermia did control ICP more than standard interventions in control group

Stopped early as greater incidence of unfavourable outcome (poor GOSE score) in hypothermia compared with controls

Unadjusted hazard ratio for mortality 1.45 (1.01,2.10) at 6/12

No difference in pneumonia rate between two groups


Conclusion: Titrated hypothermia to reduce raised ICP in addition to standard care did not improve outcomes but and increased mortality

Hypothermia for Intracranial Hypertension after Traumatic Brain Injury


EPO has a long history: EPO-2 EPO-3 may reduce mortality in trauma but concerns about thromboembolic events and efficacy have limited application.

EPO is a pleiotropic cytokine and receptors exist in the blood-brain barrier. In response to hypoxia EPO is produced within the brain. Hence worthy of investigation:

Double-blind, placebo-controlled multi-centre trial

  • GCS < 13
  • Non-penetrating TBI
  • Hb < = normal
  • < 24 h since traumatic injury
  • Valid consent


  • EPO 40 000 IU or placebo SC
    • First dose was administered within 24 h of the estimated time of traumatic brain injury
    • Then weekly for a maximum of three dose
  • Baseline screening USS < = 7 of lower limbs for DVT

Main outcome GOS-E at 6 months

  • GOS-E of 1–4 (death, vegetative state, and severe disability)
  • GOS-E of 5–8 (moderate disability and good recovery)

606 randomised after inclusion / exclusion

Populations well matched

  • Mean age 35
  • Majority male
  • Mainly RTC
  • Most had severe TBI (GCS 3-8)

No effect on proportion with severe disability at 6/12

No increase in thrombotic events (including VTE and MI)

May reduce mortality – 5% ARR at 6/12 but does not achieve statistical significance


Becomes significant after sensitivity testing but this is exploratory

Rates of proximal DVT in TBI 17%

Conclusion: Following moderate or severe traumatic brain injury, erythropoietin did not reduce the number of patients with severe neurological dysfunction (GOS-E level 1–4) or increase the incidence of deep venous thrombosis of the lower limbs. The effect of erythropoietin on mortality remains uncertain.

Erythropoietin in traumatic brain injury (EPO-TBI): a double-blind randomised controlled trial