ISICEM 2016 Day 4

The final blog from the our man in Brussels: Adrian Wong. Thanks for all the positive feedback over the last week! JS


What we need to know about cerebral metabolism (Helbok)

Increased metabolism can lead to secondary brain damage

Brain injury as a risk factor for fever upon admission to the icu (ref)

Brain main glucose consumer (50%) – neurons intolerant against changes in energy supply

CBF normally coupled with cerebral metabolic rate – metabolic and neuronal hypothesis for neurovascular coupling

Brain can utilize lactate (Cerebral metabolic effects of exogenous lactate supplementation on the injured human brain)

Cerebral metabolism following traumatic brain injury: new discoveries with implications for treatment –

Measuring glucose metabolism

  • PET
  • MR Spectroscopy
  • Jugular bulb catheter

Global cerebal oedema in TBI increase brain glucose utilization at time when supply may be limited

Monitoring glucose metabolism is important but monitors are limited by

  • PET – feasibility
  • Microdialysis catheters – invasive
  • Jugular bulb catheter – technical

Integration of cerebral metabolic function (brain tissue glucose, lactate/pyruvate ratio) may guide clinicians to improve management of pts

Impact of axonal damage after TBI (Stocchetti)

Network dysfunction after TBI (ref)

Axons form extensive networks which have retro and anterograde transport systems

Mechanism of damage

  • Direct axotomy
  • Delayed axotomy – ions flux, cytoskeleton disruption, impeded axonal transport

Biomarkers in traumatic brain injury

EEG monitoring – fancy tool or important device (Oddo)


  • Seizure detection and treatment
  • Altered GCS in general ICU pts
  • Early outcome prognostication
  • Secondary ischaemic insult
  • Depth of sedation

Convulsive status is a clinical diagnosis

Guidelines for the evaluation and management of status epilepticus –

EEG monitor allows us to titrate therapy

  • Clinical termination of SE
  • EEG termination of SE
  • Burst suppression pattern in EEG

EEG is crux of diagnosing of non-convulsive status

Recommendations on the use of EEG monitoring in critically ill patients: consensus statement from the neurointensive care section of the ESICM –

Pic of prognostication flowchart


When to monitor ICP? (Maas)


  • Level 2: all pts with GCS <8 and abnormal CT
  • Level 3: GCS <8 and normal CT if at least 2 of the following; age < 40, SBP < 90mmHg, abnormal extension 

A Trial of Intracranial-Pressure Monitoring in Traumatic Brain Injury BEST:TRIP


  • Both groups received ICP targeted treatment. More aggressive therapy in control group.
  • Power calculation should NOT be based on the total number of patients but on the expected number with raised ICP i.e. IT WAS UNDERPOWERED


  • ICP monitoring should not be abandoned
  • Think in terms of strategy
  • Better characterization aiming for more personalized approaches. Aim for multimodal approach

Goal-directory therapy (pic)


ACS TQIP Best practices in the management of TBI –

Optic nerve sheath diameter (Stocchetti)

Optic nerve sheath diameter is ideal as it is non-invasive

Watanabe – effect of intracranial pressure on the diameter of optic nerve sheath –

Use of T2-weighted magnetic resonance imaging of the optic nerve sheath to detect raised intracranial pressure –

Review –

OND sheath is technically challenging; could use colour Doppler to identify artery 1st 

Non-invasive monitoring (Taccone)


Cerebral oxygenation monitoring –

Conclusion (pic * 2)

Subarachnoid Haemorrhage

When to measure ICP in SAH? (Citerio)

Pathophysiology of high ICP post SAH


300mls/min of CSF turnover in and out of skull

Pt not following commond or WFNS >3 and acute hydrocephalus à EVD set at 10-15cmH2O

Contrast-enhanced echography to detect vasospasm (Duranteau)

 Experimental technique

Compared to traditional TCD better at detecting vessel and velocity. Clinical significance of this is still uncertain.

SAH: Medical management (Oddo)

Target SBP < 160mmHg with IV agent eg nircardipine or labetolol

Optimise CPP

Management of hyponatremia and volume contraction. –

Other drugs – Statins, Magnesium, ET-1 Receptor blocker and Intrathecal thrombolysis ALL DO NOT WORK

Critical Care Management of Patients Following Aneurysmal Subarachnoid Hemorrhage: Recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference –

Delayed neurological deterioration after subarachnoid haemorrhage –

Summary pic

Heart-Brain Injury (Mayer)


  • Minimise early brain injury and ICP
  • Prevent rebleeding
  • Minimise delayed ischaemia and vasospasm

Trop > 2ng/ml is associated with poor outcome in SAH

Left ventricular dysfunction and cerebral infarction from vasospasm after subarachnoid hemorrhage. –

Diastolic dysfunction is common after SAH (70%)

Cardiac injury after SAH exacerbates early brain injury and increase risk of vasospasm

Neurogenic stunned myocardium – takasubo on echo

QTc prolonged and inverted T waves – ECG changes following SAH


  • Fluids are not beneficial if not hypovolaemia
  • Pressor choice – guided by PiCCO. Usually start with NorAd and can consider milrinone

When do you need a neurosurgeon? (Le Roux)



International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial –

Predictors of Rehemorrhage After Treatment of Ruptured Intracranial Aneurysms

The Cerebral Aneurysm Rerupture After Treatment (CARAT) Study –

Combined approach of surgical and endovascular for some SAH

Blood pressure management (Reuter)



MAP does not equal perfusion or flow

BUT need to consider right and left heart; Normally COleft = COright

Hemodynamic variables related to outcome in septic shock –

MAP < 65mmHg BAD

For effective filtration to occur in the kidney, renal perfusion pressure of 50mmHg is required

Classically, sepsis was thought to be distributive shock. This is clearly not solely the case. Cardiac dysfunction is very common.

High versus Low Blood-Pressure Target in Patients with Septic Shock –


Managing the airway during cardiac arrest (J Nolan)


  • Improve ROSC and improve survival
  • Improve oxygenation and ventilation
  • Protect airway

ETT regarded as gold standard BUT skill of operator

Intubation learning curve –

  • Need at least 50
  • Skill maintenance is also an issue

Waveform capnography is recommended to confirm and continuously monitor the position of a ETT. ERC Guidelines – MUST have capnography

Endotracheal intubation versus supraglottic airway placement in out-of-hospital cardiac arrest: A meta-analysis –

Randomised comparison of the effectiveness of the laryngeal mask airway supreme, i-gel and current practice in the initial airway management of out of hospital cardiac arrest: a feasibility study

Revisiting ventilation during CPR (Richard)

Ventilation during CPR interrupts chest compression and causes a drop in perfusion pressure

Too much ventilation i.e. above FRC is bad for circulation

Quality metric of CPR (Morrison)

Ensure high quality chest compression

  • 100-120bpm
  • 40-55mm depth

Keep pre-shock pause short –

EtCO2 can be used a marker of quality of CPR; increased in ETCO2 favours ROSC

Hemodynamic Directed CPR Improves Short-term Survival from Ventricular Fibrillation Cardiac Arrest

Still a place for epinephrine? (Nolan)

Adrenaline used to increase coronary perfusion pressure

Trial suggest that it does but most recent studies suggest that EtCO2 and cerebral oximetry doesn’t improve

Hagihara JAMA 2012 307 1161-1168 – propensity matched; adrenaline = better ROSC but much worse survival outcome –

Intravenous Drug Administration During Out-of-Hospital Cardiac Arrest –

Data suggest that there might be harm in the long run – large placebo-controlled trial essential.

PARAMEDIC2 trial ongoing –

Do we need any drugs at all? (Sunde)

ALS guidelines – adrenaline every 3-5min, amiodarone after 3rd shock

Vasopressin also showed no difference in favourable outcomes compared to adrenaline

Vasopressin, Steroids, and Epinephrine and Neurologically Favorable Survival After In-Hospital Cardiac Arrest –

New Strategies (Fries)

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