Minimizing secondary brain injury at the bedside #ISICEM19

Minimizing secondary brain injury at the bedside #ISICEM19

Secondary brain injury is a frequent event

Minimizing secondary brain injury at the bedside #ISICEM19

Victoria McCredie, University of Toronto

Presentation slides

 

Take Home messages:

Importance of neuroprotection

  • The overall aim of our intensive care management has also been to protect the brain, to ensure perfusion to the brain and meet its metabolic demands.
  • We should always be thinking about how to ANTICIPATE, PREVENT, or HALT secondary brain insults regardless of whether we are looking after a specific neurocritical patient, or a septic patient!

Importance of dierential pathophysiological mechanisms

STRUCTURE

  • The concept of different pathophysiological mechanisms cannot be overstressed.
  • Following the primary cerebral insult, a cascade of events amplifies the initial damage regardless of the etiology of the precipitating event.
  • Cerebral hemorrhage, edema, and axonal injury can present similarly, but have drastically different clinical trajectories.
  • If we look at structural changes, here at a macroscopic level we might see damage includes shearing of white-matter tracts, focal contusions, hematomas (intracerebral and extracerebral) or diffuse swelling.
  • Each type of head injury might initiate VERY different pathophysiological mechanisms, with variable extent and duration.
  • These mechanisms (acting concurrently and often with synergising effects) and the intensity of systemic insults determine the extent of secondary brain damage.
  • The contributions of each of these pathways to the secondary brain injury vary depending on the specific TBI lesion; for example, inflammation-mediated brain injury seems predominant in contusion while calcium-mediated injury predominates in diffuse axonal injury

TIME

  • Dynamic and PROGRESSIVE process following injury
  • Secondary brain injury processes develop over hours and days, and include neurotransmitter release, free-radical generation, calcium-mediated damage, gene activation, mitochondrial dysfunction, and inflammatory responses.

Neuroprotective agents

  • Neuroprotective strategies that limit secondary tissue loss and improve functional outcomes have always been an important goal
  • Over the past 20 years, research has focused on the possibility of early pharmacological agents to improve outcomes in brain injured patients
  • Over 30 clinical trials have failed to translate a therapeutic agent for clinical use and numerous explanations for this failure have been postulated
  • Has this deflected attention from the development of neuroprotective strategies and trials addressing everyday ICU management such as optimal hemodynamic management

Outcomes improving over time

  • Despite repeated failures in pharmacological neuroprotection, outcomes for TBI patients have improved.
  • Likely that the organization of intensive treatment has contributed, offering a different kind of neuroprotection based on careful prevention and limitation of intracranial and systemic threats.

Secondary brain injury targets

  • Neurophysiologic targets: Hypoxemia/hyperoxemia, hypotension, intracranial hypertension, hypoglycemia, fever
  • Neurophysiologic concepts:
    • Secondary insult ‘dose
    • ICP dose
    • Pressure*time burden of intracranial hypertension
    • We always talk about a THRESHOLD, but the burden of time really appears to affect longer term outcome
    • Individualized thresholds
    • Towards individualized thresholds in Neurocritical Care with neuromonitoring
    • Cerebral perfusion pressure thresholds- may depend upon the patient’s autoregulatory status
    • Ability to tolerate burden of intracranial hypertension dependent on CA
    • Trajectory
    • Think about dynamic assessments of patients at the bedside, incorporating trajectory over minutes to hours

Neuroprotection at the bedside

  • Detection of secondary insults at the bedside
    • Integrated neurophysiologic monitoring
    • Up to 40% of TBI patients show a clinically relevant neurological worsening within the first 48 hours
    • How do we detect secondary brain insults in a comatose patient?
    • The role of an integrated neuromonitoring approach
    • With mounting evidence that a single neuro-monitor cannot comprehensively detect all instances of cerebral compromise, multimodal neuromonitoring allows an individualized approach to patient management based on monitored physiologic variables rather than a generic one-size-fits-all approach targeting predetermined and often empirical thresholds.
    • We are seeing a change from pure neurological clinical evaluation to an era of structural definition, associated with monitoring of cerebral hemodynamics, oxygenation, metabolism, and electrophysiology.
    • It remains to be demonstrated whether multimodal monitoring-guided therapy is able to improve outcome.
  • Translation of neuroprotective strategies at the bedside
    • Standardized management protocol
    • How can protocols improve patient care?
      • Facilitate communication
      • Reduce cognitive load
      • Coordinate the interdisciplinary team
      • Increase the adoption of evidence-based interventions and improve adherence to guidelines

Summary:

  • Secondary brain injury is a frequent event in TBI patients.
  • These events greatly influence prognosis and are potentially preventable.
  • Our understanding of secondary brain injury mechanisms and physiologic responses to treatment is evolving.

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