25-01-2013, 04:46 PM
Traumatic Brain Injury Pathophysiology
Traumatic Brain.ppt (Size: 1.61 MB / Downloads: 65)
Introduction
Traumatic brain injury following the initial insult sets in motion a sequence of pathological events that are delayed and progressive
Initial injury is tear, shear and hemorrhage followed by a delay then onset of secondary insult - The delay suggests that there is room for intervention and modification of the outcome
Focus of today’s discussion on the pathophysiology of Traumatic Brain Injury will primarily be at a “cellular” level
Mechanisms of Primary Injury in TBI
Impact
Extradural, Subdural, Contusion, Intracerebral Hemorrhage, Skull Fracture
Inertial
Concussion syndromes, Diffuse Axonal Injury
Ischemic / Hypoxic
Secondary Injury in TBI tends to follow ischemia precipitated by the initial insult
Global
Hypoxia and ischemia of the brain
Reduced cerebral blood flow can be due to raised intracranial pressure
Focal / local
Impaired cerebral blood flow or change in the extra-cellular environment due to altered/ damaged tissue
While passive damage is instantaneous, secondary brain insults occur from hours to several days after TBI and significantly alters the prognosis
Post-traumatic glucose metabolism
Initial 30 minutes post-injury glucose utilisation increases, followed by drop that remains persistently low for 5 - 10 days
Early hyperglycolysis results from disrupted ionic gradients across neuronal cell membranes and activation of energy-dependent ionic pumps
Evidence shows that there is impairment in oxidative metabolism following trauma, leading to a depletion of ATP with subsequent rise in anaerobic metabolism
Rise in extracellular lactate is thought to be a result of decreased cerebral blood flow in the face of increased energy demand with upto 7x normal lactate concentration
However there is evidence that high lactate levels exist even where blood flow limitations don’t exist - suggests that trauma affects mitochondrial phosphorylation, causing a shift toward anaerobic metabolism
Neuronal dysfunction is thus partly a result of acidosis, but also effected by concurrent membrane damage, ionic flux, disruption of the blood brain barrier and cerebral oedema