Dr. Imad El Sadek Presents

Cerebral protection & Neuroresuscitation

1

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.

2

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

3

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

Cerebral edemaPost myocardial infarctionPost cranial surgerySeizuresHead injuryCerebral hypoxiaPost cardiorespiratory arrestBrain infectionSpace occupying lesion

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