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Transcript of Perioperative cerebral protection Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab.DCA, Dip....
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Perioperative cerebral protection Dr. S. Parthasarathy
MD., DA., DNB, MD (Acu), Dip. Diab.DCA, Dip. Software
statistics,Phd (physio)Mahatma Gandhi Medical college and research
institute , puducherry , India
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What is it ??
• Neuroprotection • Before the ischemic insult
• Neuro resuscitation – • After the ischemic insult
• Planning an insult = perioperative
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After the primary insult
• We have restored perfusion but ??
• apoptosis and inflammation, inhibition of protein synthesis, sustained oxidative stress, and neurogenesis continues !!
• Post ischemic interventions !!
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Why should the insult occur ??
Deprivation of oxygen, glucose or both
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Some physiology
• CBF = CPP/CVR
• CPP = MAP – ICP • Brain + blood + CSF = same =
MK doctrine
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Who needs ??
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Indications
1. SOL with or without increased ICP – Neuro surgery
2. Intracranial vascular procedures,
3. extracranial vascular procedures including carotid
endarterectomy (CEA) and superficial temporal
artery to middle cerebral artery (STA-MCA) bypass,
which involve temporary vessel occlusion and the
possibility of focal ischemia.
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– for the clipping or coiling of giant or complex
basilar artery aneurysms,
– deep hypothermic circulatory arrest (DHCA).
– Cardiac bypass patients
– Patients who have had a cardiac arrest with
circulation reestablished within 2 hours.
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Pharmacological nonpharmacological
Clinical therapies
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Nonpharmacological
• Temperature • Hypothermia has been proposed to offer
therapeutic benefit for more than 60 yr• But later put into disuse by studies • But those studies did not induce hypothermia
early • Till further studies , use hypothermia
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Hypothermia
• neurosurgical procedures in which the brain is at risk for
ischemic insult, a goal temperature of 35 to 36°C is
reasonable.
• Mild hypothermia (33 to 35°C) may be appropriate in many
patients, even recognizing that there may be no benefit to
this therapy.
• Finally, deep hypothermia (<20°C) is appropriate in any
situation in which a prolonged cardiac arrest is required.
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Glucose • No glucose worsens brain injury in the presence of oxygen
• glucose without oxygen is more dangerous ??
• May be due to anaerobic metabolism and intracellular
acidosis
• Hyperglycemia and cerebral ischemia combination deadly
• Maintain normoglycemia
• around 150 – frequent measurement
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Hyperventilation
• Hypocapnia can reduce CBF, CBV, and intracranial
pressure (ICP)
• Previously thought useful.
• Probable ischemic insult because of decreased CBF??
• Refractory cerebral edema – may be helpful
• Otherwise not useful
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Seizure prophylaxis
• Seizures commonly occur in patients with intracranial pathology.
• Seizure activity is associated with increased neuronal activity, increased CBF and CBV (and consequently increased ICP), and cerebral acidosis
• Prevent and treat seizures aggressively.
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Arterial oxygen partial pressure• Normobaric hyperoxia • May be useful in early resuscitation times • But questions ?? • Do you need to remember this picture ??• NO
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But- we need to remember this
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Pharmacological
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Influence of Anesthetics on an Ischemic Brain
• Barbiturates• Propofol• Ketamine• Etomidate• Volatile Anesthetics
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What we want ??
• Decrease cerebral metabolism
• Cerebral blood flow increase
• Many agents do !!
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Barbiturates
• In humans, thiopental loading has been demonstrated in
a single study to reduce post–cardiopulmonary bypass
neurologic deficits
• Setting of focal ischemia , barbiturates better than in
global ischemia setting
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Barbiturates
• anti-oxidant or free radical scavenging actions
• reduce ischaemia induced neurotransmitter release.
• Inhibition of the release of excitatory neurotransmitters
(aspartate, taurine, glutamate & GABA) has been
demonstrated.- (reperfusion)
• Reduce CMRO2 and ICP
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Thiopentone
• Loading dose consists of 25 to 50 mg/kg.
followed by an infusion 2 to 10 mg/kg/1hr to give plasma
concentration of 10 to 50 mg/L.
High dose may benefit focal ischemia
There are doses of 3- 5mg /kg doses and barbiturate induced EEG
burst suppression is maintained
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Thiopentone
• Low dose in three minutes 1 mg /kg for ICP reduction
• Small bolus dose for short term protection• A dose of 4 mg/kg over 3 minutes• Temporary clamping and focal ischemia• Ten minutes prior start – 24 hours post insult
acceptable • Duration controversial 72 hours !!
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Side effects of barbiturates
• Depression of cardiac output & cerebral perfusion pressure,
& even frank cardiovascular collapse in poorly hydrated
patients.
• Depression of respiration – ventilators and ICU ready
• Metabolized by liver – note liver function
• Immune depression and lung infections
• Neuro evaluation ??
High Medium and low
doses
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Etomidate
• etomidate produces EEG burst suppression and reduces CMR
for glucose and oxygen.
• Clinically, etomidate decreases CBF, CMRO2 and ICP
• But no hemodynamic compromise
• Steroid suppression is insignificant because we use high dose
steroids BUT ??
• injury-enhancing effect of etomidate has been attributed to its
ability to reduce nitric oxide levels in ischemic brain tissue.
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Propofol
• The metabolic changes resulting from propofol
anaesthesia closely resemble the homogenous
depression of CMR caused by barbiturates and
etomidate
• But CVS depression and hypotension and CPP
• Overall !!
• Improved cerebral perfusion and better maintenance
of autoregulation
•
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Ketamine ??
• Mechanism of action of ketamine ??
• Some of the neurotransmitters is NMDA
• Hence offer protection • But not much used instead of established
agents ??
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Benzodiazepines
No adverse intracranial effects • No adverse cardiopulmonary effects • Decrease CMRO2, CBF and ICP • Anesthetic sparing • Reversal
Anti seizures effect
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Inhalational agents
• Isoflurane offers a similar level of metabolic
depression as barbiturates at a concentration less
likely (than barbiturates) to be accompanied by
severe cardiovascular depression or prolonged
recovery
• < 2 MAC
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Inhalational agents
• GABA effects • Inhibit ischemia induced calcium influx• Inhibit glutamate induced activation. • Ischemic threshold less than with enflurane or
halothane • Both sevoflurane and desflurane decreased
cerebral insult after focal ischemia
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nitrous oxide
• Some forms of cerebral protection may be adversely affected by the presence of nitrous oxide.
• Decreased barbiturate’s efficacy • Nitrous oxide decreases isoflurane’s efficacy as
a neuro protectant
No nitrous oxide
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Other agents
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Glucocorticoids
• High dose methyl prednisolone ( 30 mg/kg) • Inhibit lipid peroxidation • Possible uses • Spinal injury • Head injury • Cerebral vasospasm • Dangers • Infection, GI bleeding , hyperglycemia
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Tirilazad mesylate
• Aminosteroid • Inhibit lipid peroxidation • Decrease vasospasms
• 6 mg /kg in divided doses • SAH and ischemic strokes
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Superoxide dismutase• Superoxide anion is generated on reperfusion of post
ischaemic tissues. • It is capable of producing significant biological injury.• Superoxide dismutase (SOD) is a specific scavenger of
superoxide anion. • Because, superoxide dismutase (SOD) has a biological
half-life of only 5 minutes, it has been conjugated with polyethylene glycol (PEG-SOD) for use in humans.
• Head injury use- less vegetative states, less mannitol requirements
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Nimodipine
• Calcium influx blocked • Use of nimodipine – prior to surgeries• Brain retraction
• Increases CBF as a vasodilator
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Lignocaine
• Prophylactic infusion of lidocaine, substantially improved neuropsychologic outcome at 10 days, 10 weeks, and 6 months after cardiac surgeries
• 1 mg / kg • 240 mg / first hour • 120 mg/ second hour • 60 mg/ 3rd Hour and thereon
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Mannitol
• Mannitol can scavenge free radicals & thus reduce tissue damage caused by superoxide radicals.
• 0.25 gm – 1 gm/kg bolus infusions • Cerebral edema decrease and ICP reduction
• Beware of sodium levels and hypovolumia
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Miscellaneous drugs
• Alpha2-agonists • Aprotinin • Insulin • Papaverine • Acadesine• Tromethamine • Perflurocarbons
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Chemical brain retractor concept
• This concept includes the use of a total IV
anaesthesia technique, mild hypocapnia &
mannitol with strict monitoring & maintenance
of the global cerebral homeostasis
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To know ??
• Our ability to protect the brain is limited. By
contrast, our capacity to exacerbate ischemic
brain damage is limitless.
• Emphasis should be placed on maintenance of
physiologic homeostasis rather than on reliance
on pharmacologic agents to protect the brain.
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The essence • Mild hypothermia • Maintain PCO2 and glucose • Barbiturates • Any agent • Maintain CPP• Don’t allow seizures
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Thank you all