Category Archives: Neurology

Lessons from Clinical Challenges in Neuro-Critical Care

Traumatic Brain Injury

Traumatic brain injury: integrated approaches to improve prevention, clinical care, and research

Trajectories of early secondary insults correlate to outcomes of traumatic brain injury: results from a large, single centre, observational study

Clinical applications of intracranial pressure monitoring in traumatic brain injury : report of the Milan consensus conference.

 

Intracranial Haemorrhage

Definition: non-traumatic bleeding into the brain parenchyma

2nd most common type of stroke (10-30%)

5.3 million cases worldwide, 3 million deaths (2010 Global Report on Diseases)

Less than 40% of patients regain functional independence

Most important risk factors:

  • hypertension
  • anticoagulation

The critical care management of spontaneous intracranial hemorrhage: a contemporary review

Blood pressure management: BPsys < 140 -160 mmHg

  • Higher systolic pressures may lead to hematoma expansion and increased edema.
  • Prospective trials: INTERACT II, ATACH II

Correction of coagulopathy, if possible… or not?

  • Vitamin-K-antagonists (Phenprocoumon, Marcumar): Yes. Use PCC (prothrombin complex concentrate)
    •  INR-goal: < 1.3
  • DOACs: if specific antidote available and within 2-3 half lifes of substance, probably yes.
  • Heparin: use protamine.
  • Aspirin / Clopidogrel: may depend on hemorrhage size

Summary: intracranial hemorrhage

  • Data: meanwhile useful prospective works available
  • Difficult to estimate who will decompensate
  • Prognosis difficult to estimate, likely to be worse after large ICH.
    No application of score systems for single patients
  • Superficial, cortical hemorrhage: open surgery
  • Large Basal ganglia hemorrhage (> 30 ml): minimally invasive surgery
  • Intraventriular hemorrhage: EVD + Lysis (+ lumbale Drainage)
  • Decompressive surgery: trial ongoing.
  • Massive hemorrhage (> 100 ml): conservative approach
  • ICP monitoring standard in ventilated patients, optionally pbtO2, EEG, eCox, …

Subarachnoid hemorrhage

Transcranial Doppler ultrasound goal-directed therapy for the early management of severe traumatic brain injury.

Calcium antagonists for aneurysmal subarachnoid haemorrhage – Cochrane Review

Transcranial Doppler versus angiography in patients with vasospasm due to a ruptured cerebral aneurysm: A systematic review.

Hyponatraemia: Practical Management

  • Monitor volemia and Natremia after SAH
  • Fluid restriction is not recommended
  • Isotonic saline (0.9%) for drug dilution and fluids (1-3L)
  • We rarely use 3% saline (1 ml/Kg of 3% NaCl increases the PNa by 1mmol/L)
  • Consider hydrocortisone in case of vasopressor use
  • Vaptans are not useful
  • Consider urea (0.5 -1g/Kg/Day) for HypoNa + euvolemia

Summary

  • Late risk: vasospasm
  • Monitoring: depends on severity and risk of vasospasm
  • At least: TCD and ICP, PbtO2 and CMD in tissue at risk
  • HypoNa is frequent: no fluid restriction! NaCl, Steroids, Urea

Acute Management of Status Epilepticus

International League Against Epilepsy (ILAE) task force on classification

SE = Status Epilepticus

◦ condition resulting

  • from the failure of the mechanisms responsible for seizure termination
  • from the initiation of mechanisms which lead to abnormally prolonged seizures

◦Long-term consequences

  • neuronal death, neuronal injury, alteration of neuronal networks, depending on the type and duration of seizures

RSE = Refractory Status Epilepticus

  • SE that persists despite adequate administration of benzodiazepines and at least one antiepileptic drug

SRSE = Super Refractory Status Epilepticus

  • SE that continues or recurs ≥24h after onset of anaesthetic therapy, including recurrence on the reduction or withdrawal of anaesthesia.

Convulsive status epilepticus (CSE)

  • SE with convulsions / seizures / myoclonus

Non-Convulsive Status Epilepticus (NCSE)

  • SE without clinical signs à EEG diagnosis

From theory to practice – ARDS: An old syndrome, new organ interactions #EuAsia18

The lung and the kidneys (Ostermann)

When kidney function lost, –> reduced clearance , fluid overload, acidosis BUT also inflammation, cytokine release and cell death

The distant organ effects of acute kidney injury

AKI causes a higher degree of capillary leakage within the lungs

Ventilator induced kidney injury

IMG_3154

Bench-to-bedside review: Ventilation-induced renal injury through systemic mediator release – just theory or a causal relationship?
Mechanical ventilation as a mediator of multisystem organ failure in acute respiratory distress syndrome.

Fluid management with a simplified conservative protocol for the acute respiratory distress syndrome

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Lung brain interactions (Oddo)

ARDS in the brain-injured patient: what’s different?

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Issues to consider

  • Oxygenation
  • PEEP
  • CO2/TV

Hyperoxia in intensive care, emergency, and peri-operative medicine: Dr. Jekyll or Mr. Hyde? A 2015 update
Cerebro-pulmonary interactions during the application of low levels of positive end-expiratory pressure.

Effect of hyperventilation on cerebral blood flow in traumatic head injury: clinical relevance and monitoring correlates.
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Heart lung interactions (Cecconi)

IMG_3159

Is tidal volume challenge the new PLR? Use of ‘tidal volume challenge’ to improve the reliability of pulse pressure variation

Or end-expiratory hold?
Predicting volume responsiveness by using the end-expiratory occlusion in mechanically ventilated intensive care unit patients.

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#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

IMG_3081 IMG_3082

EUROTHERM Study

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.

IMG_3084

 

New paradigm – quantitative brain function monitoring

Electroencephalography as a Prognostic Tool after Cardiac Arrest.

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Summary

IMG_3090

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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:

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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)

image1

NPi-200 (Neuroptics, USA)

npi200_100x100_72dpi

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