Dr. Imad El Sadek… Presents CEREBRAL PROTECTION & NEURORESUSCITATION
Sep 28, 2015
Dr. Imad El Sadek Presents
Cerebral protection & Neuroresuscitation
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Cerebral Protection
Brain Resuscitation
Definitions
Neuroprotection was defined as treatment initiated before onset of ischaemia, intended to modify intra-ischaemic cellular and vascular biological responses to deprivation of energy supply so as to increase tolerance of tissue to ischaemia resulting in improved outcome.
Neuroresuscitation, in contrast, implied treatment begun after the ischaemic insult had occurred with the intent of optimizing reperfusion.
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Brain & Energy
CMRO2= 5.5 mL / 100 g / min
Function= 3.3 mL / 100 g /min
Integrity= 2.2 mL /100 g /min
Cerebral Protection
CMRO2
Function
Integrity
= 5.5 mL 100 g 1 min 1
= 3.3 mL 100 g 1 min 1
= 2.2 mL 100 g 1 min 1
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CMRO2
CMRO2
[CATEGORY NAME][PERCENTAGE][CATEGORY NAME][PERCENTAGE]FunctionIntegrity0.60.4
Brain Ischemia
Global
Focal
Region one: like global ischemia
Region Two: Penumbra, collateral flow
Region Three: normal flow
Brain Ischemia
Primary insult
Vascular insufficiency/disruption
Infection/Inflammation
Tumor
Metabolic & Nutiritional derangement
Cerebral Insult
Secondary insult
Reduction in CBF and metabolism
Hydrocephalus
Shift vital structures and axonal disruption
Pressure effect to underlying brain region
Neuronal Injury is worsened by:
Hypoxia
Hypercapnia
Prolonged hypocapnea
Hyperglycemia
Hypotension
Hyperthermia
Anemia
Electrolyte imbalance
Seizure
Cerebral Insult
Indications for Cerebral Protection/ Neuroresuscitation
To prevent of minimize pathological sequele of inadequate cerebral perfusion, regardless of cause.
To reverse cerebral damage
Management directed towards prevention of secondary insult
Aim of Cerebral Protection/ Neuroresuscitation
Physiological Manipulation
Pharmacological
Physical Manipulation
Methods of Cerebral Protection
Mechanical Ventilation
Maintain PCO2 30-40 mmHg, PaO2 100
Cerebral vasculature is reactive to CO2 levels
ICP reduced by 30% per 10mmHg reduction in CO2
Rise in PCO2 in TBI with increased ICP with result in general cerebral vasodilatation & increased CBV
Further increase in ICP and reduced cerebral perfusion
Physiological Manipulation
Hyperventilation vasoconstriction of normal cerebral vessels shunting blood from normal tissue to ischemic area (Robin Hood Steal Phenomena)
Avoid hypoxia cytotoxic cerebral edema
Hyperventilation for how long? 24-48 hrs
Acute changes return to normal value due to normalization of CSF pH & compensatory to CSF volume
Each 1 C reduction can reduce CMRO2 by 7%
Decreases both metabolic and functional activities of brain
Provides protection to ischemic brain due to diminished gap between demand and supply
Aim for mild to moderate hypothermia or DHCA
Small decrease results in significant reduction in the damage from cerebral ischemia
Avoid shivering : incrases CMRO2 and CBF
Physiological Manipulation- Hypothermia
Aim
Limit ischemia by increasing rCBF
To overcome regional vasospasm
Requires vasopressors
Maintain MAP 70-90mmHg
Maintain adequate CPP
During ischemia
Auroregulation is impaired
CBF is pressure dependent
Maintain CPP 70-80 mmHg
Physiological Manipulation- Hypertension
Sedation and Neuromuscular blockage
IV anesthetics CMRO2 and CBF
Opioids has minimal effect of cerebral metabolism and CBF
Routine use NMB should be avoided
Prevents raise in ICP during straining & coughing
Long term polyneuropathy & myopathy
Volatile Anesthetic Agents have been shown to have neuroprotective effects.
Ischemic preconditioning & anesthetic preconditioning
Pharmacological Manipulation
Aim fluid management to provide adequate hydration
Hypotonic fluid (dextrose) may exacerbate brain edema
Aim for sugar level 6-10 mmol/L
High plasma levels of glucose are associated with poor outcome in TBI
Fluid Management glycemic control
Causes reduction of ICP after 20-30 minutes
May result in hypovolemia thus should not be given until volume is replaced.
Hypertonic Saline
Reduces brain water by establishing osmotic gradient across BBB
Osmotic diuretic: mannitol
Thank you