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:

http://www.sciencedirect.com/science/article/pii/S1474442216000156

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: https://www.ncbi.nlm.nih.gov/pubmed/26381281

Good inter-rater reliability for pupillometry. Big difference between standard assessment v pupillometry: https://t.co/MSwD9JG7RI

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: https://www.ncbi.nlm.nih.gov/pubmed/22659054

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: https://www.ncbi.nlm.nih.gov/pubmed/12546375

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? https://www.ncbi.nlm.nih.gov/pubmed/17325503

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: https://www.ncbi.nlm.nih.gov/pubmed/22343469

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: https://www.ncbi.nlm.nih.gov/pubmed/25005878

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

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

Intervention

• 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