Orthopaedi & Traumatologi

Definition
Reperfusion injury : cellular injury
caused by the reperfusion of
physiologic concentration of oxygen
to cells that have been exposed to
injurious but non lethal hypoxic
condition1
Other term : hiperperfusion injury, re-
oxigenation injury
 BRAIN INJURY ISCHEMIA / HAEMORRHAGE
STROKE
GLOBAL ISCHEMIA

TIME
COLLATERAL
SEVERITY OF STENOSIS
ACUTE ISCHEMIA
LEVEL OF ANTIOXIDANT
NECROSIS/
HYPOPERFUSION
APOPTOSIS
REPERFUSION
GOING BETTER
UNPREDICTABLE

REPERFUSION INJURY

MECHANICAL
BIOCHEMICAL
NECROSIS
 Etiology Of Reperfusion
Injury
I. Mechanicals II. CHEMICALS /
Decompression: BIOMOLECULAR
Post Operative 1. Platelet Activating Factor
Recirculation: 2. Inflamation Reaction
Thrombectomy 3. Neurotransmitters
Thrombolytic Therapy 4. Growth Factor
5. Cytokines
6. Free Radicals
7. Epinephirine

NECROSIS
 Model Of Molecular Events During Brain Ischemia And
Reperfusion That Lead to Neuronal Death

ISCHEMIA ATP Depolarization Membrane Damage

-calpain Cystosolic Ca2+ Phospholipase Lipid Peroxidation

activation activation
Fe2+
Calcineurin NOS
eIF4G & spectrin activation activation Peroxynitrite Free Arachidonate
degradation ER Ca2+ Depletion O2
REPERFUSION ATP Inhibited Growth
eIF2 Factor Signaling
kinaseactivation
Epinephrine CHOP
PP1 eIF2 (P) Bad
PP2A Dephosphorylation,
cAMP Inhibited Bad Mitochondria
Inhibited Active Release cytochrome
I1 activation Protein caspase 3 c
PKA Synthesis & caspase 9 to
activation APAF1
Apoptosis
Cells unable to respond to radical and proteolytic injury and DIE
 Reperfusion Injury

Oxygen
Blood
restoratio Inflammatory factor
n ( Interleukin, Free
Radical,
Ischem Leucocyte )
Cell
ia Small
capillary
endotheliu
m

Damage cellular
protein
DNA obstruction
Plasma membrane
Free
radical
 Hypoperfusion
Prolonged
ischemia Hypoxantin
ATP
e Nitric oxide

Xanthine Uric
oxidase react acid
scavenger
Highly reactive
Oxygen superoxide Peroxynitrite
Hydroxyl radicals

Lipid Peroxidation

Membrane cell damage

Apoptosis
In some clinical situation, a substantial
part of the ischemic injury may not have
occurred during the period of ischemia
but during the period of reperfusion.

The secondary consequences of ischemia

are those that occur after the cerebral
circulation has been restored
 Mutimodal to minimize
Reperfusion Injury Effect
Airway secure the patency
Breathing control and let the cell rest
Circulation restore perfusion slowly
Drugs Propofol, Penthotal, Midazolam, COX
Inhibitor, Steroid

Principle
Reduce CMR O2
Minimize Free radical and inflammatory factors production
 Summary
Reperfusion injury is the hidden
danger after successful perfusion
restoration

Reperfusion injury can be minimized

Minimizing reperfusion injury can

improve patients outcome
Thank's