Pathophysiology of traumatic brain injury.pptx

This describes the pathophysiology of traumatic brain injury (TBI).

1. PATHOPHYSIOLOGY OF TRAUMATIC BRAIN INJURY

2. Pathophysiologic Classification of Traumatic brain injury Primary TBI Secondary TBI Sustained during the traumatic event Mechanical focal damage (contusions/hemorrhages) Diffuse Axonal Injury (Shear mechanism) Delayed by hours/months/days Alterations in Neurochemical Metabolic Cellular changes

3. Mechanistic hypostheses Injury impulse travels from surface to core Primary damage to cortical/sub-cortical strcutures Core (rostral brainstem) injury follows cortical –subcortical injury Unconsciousness and memory disturbances possible without brain stem injury Converse not possible

4. UNDERSTANDING TRAUMATIC FORCE VECTORS Axial forces directed along long axis of body Stretching/ compression and axial rotation Lateral forces Lateral bending and rotation Sagittal forces Antero-posterior rotation Physical processes Contact forces Inertial loading (producing movement sans contact) Compressive/static forces

5. Physical processes and primary injury patterns Contact forces Coup and contrecoup/ bone fractures Inertial loading Subdural hematomas/ contusions (translational) Diffuse atonal injury (rotational) Static forces Crush injury to skull and brain

6. Manifestations of primary injury Acute Subdural hematoma Commonest focal lesion (1/4 th of severe head injuries) Injury to cortical bridging veins/rarely superficial arteries Fronto -parietal bridging veins most commonly torn Underlying brain injury common

7. Manifestations of primary injury Acute Epidural hematoma Occurs in upto 10% of the cases of severe TBI- mostly fracture hematomas More common in younger patients due to robust dural vascularity Lucid interval seen in only 1/5 th of cases EDH due to venous injury typically cross midline and the tentorial line Excellent prognosis in patients without coma/ intradural injury.

8. Manifestations of primary injury Contusions Focal areas of subpial hemorrhage and cortical injury Laceration – in presence of pial disruption Coup/ contre-coup , Fronto-temporal poles, inferolateral temporal lobe , perisylvian regions common Significant source of secondary injury

9. Manifestations of primary injury Diffuse axonal injury Most common lesion in TBI Caused by stress due to rapid angular acceleration/deceleration to rapid angular acceleration/deceleration Axonal disruption/Interruption of axoplasmic flow Small punctate hemorrhages in corona radiata /ganglionic structures/fornix /corpus callosum / DWI/GRE/DTI MR sequences more sensitive for detection Jallo and Loftus, Neurotrauma and Critical Care of the Brain, 2nd Ed.

10. Manifestations of primary injury Intracerebral hematomas About 20-30 % of all traumatic intracranial hematomas Can be formed from coalescence of contusions Parenchyma lesion must be containing 2/3 rd volume blood on imaging to be called a contusion Usually result from disruption of small blood vessels Deep ganglionic bleeds (2%) have a poorer prognosis Deranged coagulation (iatrogenic/pathological) predisposes

11. Manifestations of primary injury Intraventricular hemorrhage (IVH) Less than 10% of severe TBI cases Typically large forces required Damage to deep structures (septum pellucidum , choroid plexus, forniceal ,sub-ependymal veins) Acute obstructive hydrocephalus uncommon

12. Secondary Injury

13. Disturbances of cerebral blood flow and autoregulation Disturbances of cerebral metabolism Alterations in ion hemostasis Elevated intracranial pressure Neuroinflammation Secondary brain shifts and herniation Mechanisms of Secondary Injury

14. DISTURBANCES OF CEREBRAL BLOOD FLOW Brain perfusion tightly coupled to CMRO 2 (N- 3.2ml/100gm/min) Low CMRO 2 in comatose patients CBF doesn’t decline proportionately CMRO 2 ~ 1.2 ml/100gm/min after severe TBI and coma TBI , CBF > 33 ml/100gm/min Luxury Perfusion/hyperemia

15. Disturbances of cerebral METABOLISM Traumatic disruption of microcirculation Critical ischemia threshold (20 ml/100mg/min) is higher than in uninjured brain Traumatic disruption of microcirculation Impaired oxygenation and perfusion Failure of mitochondrial oxidative metabolism Hyperglycolysis , lactic acidosis (transient), increased glucose requirement

16. Alterations in cerebral autoregulation Cerebral autoregulation – responsive to blood pressure and metabolism Pressure vasoreactivity dysregulated (>60 % cases) Vasoconstrictive response better retained as compared to vasodilatory Hence fall in CPP immediately translates into low CBF Metabolic vasoreactivity (response to PaCO 2 ) more robust

17. Alterations in Ion/neurotransmitter hemostasis Calcium hemostasis Dramatic increase in intracellular calcium “ Mechanoporation ” Intracellular calcium impairs oxidative metabolism in mitochondria Calcium dependent enzymes activated ( caspases,proteaseas , endonucleases) Glutamate dysregulation