Pathophysiology and Epidemiology of Traumatic Brain Injury

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Pathophysiology and Epidemiology of Traumatic Brain Injury

  1. 1. We will go through…1 EPIDEMIOLOGY OF TBI BASED ON INDIAN SCENARIO2 PATHOPHYSIOLOGY OF TBI3 CEREBRAL VASCULAR PHYSIOLOGY IN TBI
  2. 2. Definition Traumatic brain injury is a non degenerative, non congenital insult to the brain from an external mechanical force ,possibly leading to permanent or temporary impairment of cognitive, physical and psychosocial functions, with an associated diminished or altered state of consciousness
  3. 3. Severity based on GCS severe= 3-8 Moderate = 9-12 Mild = 13-15
  4. 4. We know all about others ;nothing about ourselves….! At the global level, the annual incidence and mortality from Traumatic Brain Injuries (TBIs) is 200 and 20 per 1,00,000 per year, respectively National level data in India is not available for traumatic brain injuries as in many developed countries.• The only epidemiological study was undertaken in Bangalore by Dr Gururaj et al at NIMHANS during the period March 2000 to March 2003, over a
  5. 5. What it revealed about TBI ININDIA…. the incidence, mortality and case fatality rates were 150/100000, 20/100000 and 10%, respectively At the national level, nearly two million people sustain brain injuries, 0.2 million loose their lives and nearly one million need rehabilitation services every year.
  6. 6. What it revealed about TBI ININDIA…..
  7. 7. What it revealed about TBI ININDIA…. Nearly 10,000 people sustain brain injury every year in the city of Bangalore with more than 1,000 deaths. 20 - 25 patients are registered every day with a head injury at NIMHANS and TBIs constituted 39% of total registration during 2000
  8. 8. How they worked it out?7,164 persons were enrolled into a NeurotraumaRegistry during the year 2000 at NIMHANS.While Phase–1 study focused on identifying andmeasuring all epidemiological correlates in a hospitalsetting,phases–II and III focused on identifying disabilitypatterns, extent of socio-economic burden &measuring quality of life
  9. 9. Various Traumas leading to Brain Injur RTIs Falls (25%) (59%) 1 2 3 4 Violenc e (10%) .
  10. 10. The social picture• majority of these individuals are males, in their early years (5 - 44 years) [male to female ratio of 4:1] Individuals in the age group of 21 - 35 years were represented to the extent of 40% The majority of those injured were with less than collegiate levels of education
  11. 11. Education affects our roadculture also…• ,
  12. 12. Road Traffic InjuriesRTIs occurred predominantly in the age group of 15- 40 years, among men and during evenings andnights (66%).Pedestrians (26%), two-wheeler riders (31%) andpillions (12%) and bicyclists (8%) were representedin higher numbersThe majority of the RTIs took place in midblocks ofroads (70%).
  13. 13. Should I walk or go by avehicle?• .
  14. 14. Injury mechanism among twowheelers• .
  15. 15. Pedestrian TBI- „Hit By‟• .
  16. 16. Our genome always showsperfect inheritance ofdisobedience! Not wearing helmets driving under influence of alcohol over speeding and overtaking crossing in the middle of the road …………………… were the major behavioural factors.
  17. 17. Remain indoor for a prosperouslife! Poor visibility of vehicles and or roads mechanical problems of vehicles ……………….…… were responsible for one-third of injuries Road design and structural issues …………………….. were responsible for another 30% of TBIs.
  18. 18. I am fit…. So unfit for driving• .
  19. 19. A fools‟ adventures in a dirty road….
  20. 20. ROLE OF THE CONDITIONOF ROADS• ,
  21. 21. Other causes Falls were the second-leading cause (25%), with the majority occurring in children and elderly. Amongst them domestic falls (57%) were the leading cause followed by falls in public places (15%). Violence/assault (10%) were the third-leading cause, more frequent among men and associated with use of blunt physical objects.
  22. 22. Prehospital and emergency carewas poor in these areas: availability of First Aid Services high referrals from local hospitals safer transportation longer interval between injury and reaching definitive hospital (only 13% within one hour and 40% in one to three hours)
  23. 23. Severity and patterns In total, 71% of TBIs were mild, 15% moderate and 13% severe in nature based on Glasgow Coma Scale. Concussions (36%), contusion (32%), skull fractures (12%) and brain haemorrhages (13%) were the injury patterns.
  24. 24. Hospital stay• .
  25. 25. We are just observers in manysituations… Severe polytrauma was noticed in 22% of total injuries. 5.5% died in hospital and 4% were discharged in a persistent vegetative state. Severe and moderate disabilities were observed in 15% and 37%, respectively. Various types of disabilities affecting activities of daily living, memory, communication, social interaction and ability to work were seen in 52% of the patients at hospital discharge time.
  26. 26. Disabilities…• .
  27. 27. Quality of life @ 1 year• .
  28. 28. In 1 sec, life is turned upsidedown… 35% had problems in health, social, economic dimensions of life at 1-year follow-up more than 50% of them continued to have problems in similar areas at second year follow up The quality of life was poor in nearly 30% of brain- injured persons at two years post discharge.
  29. 29. Income wise….• .
  30. 30. When we treat him/her for umptyno: of days, we should be awareof…. major economic burden on individuals and families to meet costs of hospitalization and rehabilitation affected families had to spend resources [ their own or borrowed ] to reach definitive hospitals, to take care of injured person during hospital stay and after discharge. The indirect costs due to loss of work and income are substantial
  31. 31. Foundation for gathering all these data is a……a neurotrauma registerprovidesdetailed description of all individuals sustaining aTBIduring a given period (beginning with a date)in a defined population,the major demographic features of which are
  32. 32. CRITERIA• The criteria of a neurotrauma registry are:- . 1) Uniform definition 2) Inclusion of all subjects with a TBI in a defined area 3) Case identification from multiple sources 4) Case evaluation by a trained team 5) Consistency in diagnosis 6) Established classification methods.
  33. 33. HOW IT IS VITAL IN EPIDEMIOLOGY OF TBIThe registry can identify major causes, pattern andmode of injury occurrence in subcategories ofinjured persons, thus identifying "Population at risk”It improves diagnostic accuracy as all subjects areweighed in comparison with gold standard.Registry helps in in establishing cause-effectassociations over a period of time (e.g.: Epilepsyand TBIs).
  34. 34. HOW IT IS VITAL IN EPIDEMIOLOGY OF TBIThe registry reveal vital data on morbidity, mortalityand disability rates (Incidence,fatality and disabilityrates)will reveal temporal changes in occurrence andpattern of neurotraumait can serve as a basic ground tool for clinical andintervention trials. It would highlight how muchchange has been brought about by an intervention
  35. 35. HOW IT IS VITAL IN EPIDEMIOLOGY OF TBIhelps in developing and understanding prognosis inneurotrauma management and in anticipatingfuture risks.reveal the socioeconomic burden and health needsof a communitythis will help in creating awareness among policymakers and public to place neurotrauma preventionhigh on the public health agenda
  36. 36. .PATHOPHYSIOLOG Y PRIMARY INJURY
  37. 37. TBI Traumatic brain injury (TBI) is the result of an external mechanical force applied to the cranium and the intracranial contents, leading to temporary or permanent impairments, functional disability, or psychosocial maladjustment
  38. 38. Injuries are divided into 2subcategories (1) primary injury, which occurs at the moment of trauma, and (2) secondary injury, which occurs immediately after trauma and produces effects that may continue for a long time.
  39. 39. Primary injury-Physical mechanisms Impact loading - Collision of the head with a solid object at a tangible speed [through a combination of contact forces and inertial forces] Impulsive loading - Sudden motion without significant physical contact Static or quasistatic loading :occurs when a slowly moving object traps the head against a fixed rigid structure and gradually squeezes the skull, causing many comminuted fractures and deforms the brain
  40. 40. 3 basic types of tissuedeformation Compressive - Tissue compression Tensile - Tissue stretching Shear - Tissue distortion produced when tissue slides over other tissue
  41. 41. Types of Primary Injuries focal injuries (eg, skull fractures, intracranial hematomas, lacerations, contusions, penetrating wounds) diffuse (as in diffuse axonal injury).
  42. 42. Skull fractures vault fractures or basilar fractures. stellate, closed, or open fractures depressed or nondepressed simple fracture and compound fracture Vault fractures may extend into the sinuses Basal skull fractures may be associated with injuries to the cranial nerves and discharges from the ear,
  43. 43. Auditory/vestibular dysfunction conductive or sensorineural hearing loss. Benign paroxysmal positional vertigo
  44. 44. Intracranial hemorrhages Epidural hematoma Subdural hematoma Intracerebral hemorrhages Intraventricular hemorrhage Subarachnoid hemorrhage
  45. 45. Intracranial hemorrhages Epidural hematoma Subdural hematoma Intracerebral hemorrhages Intraventricular hemorrhage Subarachnoid hemorrhage
  46. 46. Epidural hematoma laceration of the dural arteries or veins, or by diploic veins in the skulls marrow a tear in the middle meningeal artery when hematoma occurs from laceration of an artery, blood collection can cause rapid neurologic deterioration.
  47. 47. Intracerebral hemorrhages Due to injury to larger, deeper cerebral vessels occurring with extensive cortical contusion. Intraventricular hemorrhage tends to occur in the presence of very severe TBI and is, therefore, associated with an unfavorable prognosis.
  48. 48. Subarachnoid hemorrhage by lacerations of the superficial microvessels in the subarachnoid space. If not associated with another brain pathology, this type of hemorrhage could be benign. may lead to a communicating / noncommunicating hydrocephalus if blood products obstruct the arachnoid villi / the third or fourth ventricle.
  49. 49. Coup and contrecoupcontusions Coup contusions occur at the area of direct impact to the skull and occur because of the creation of negative pressure when the skull, distorted at the site of impact, returns to its normal shape.
  50. 50. Coup and contrecoupcontusions Contrecoup contusions are are located opposite the site of direct impact. Cavitation in the brain, from negative pressure due to translational acceleration impacts as the skull and dura matter start to accelerate before the brain on initial impact.
  51. 51. contusion is coup orcontrecoup type? impact from a small, hard object tends to dissipate at the impact site, leading to a coup contusion. In contrast, impact from a larger object causes less injury at the impact site, because energy is dissipated at the beginning or end of the head motion, leading to a contrecoup contusion
  52. 52. Concussions caused by deformity of the deep structures of the brain leading to widespread neurologic dysfunction that can result in impaired consciousness or coma Concussion is considered a mild form of diffuse axonal injury.
  53. 53. Diffuse axonal injury characterized by extensive, generalized damage to the white matter of the brain. Strains of the tentorium and falx during high-speed acceleration/deceleration produced by lateral motions of the head may cause the injuries. also could occur as a result of ischemia
  54. 54. Neuropathologic findings inpatients with diffuse axonalinjury Grade 1 - Axonal injury mainly in parasagittal white matter of the cerebral hemispheres Grade 2 - As in Grade 1, plus lesions in the corpus callosum Grade 3 - As in Grade 2, plus a focal lesion in the cerebral peduncle...........Gennarelli and colleagues
  55. 55. .PATHOPHYSIOLOG YSECONDARY
  56. 56. Secondary injuries Due to further cellular damage from the effects of primary injuries. develop over a period of hours or days following the initial traumatic assault. mediated through the following neurochemical mediators..
  57. 57. Excitatory amino acids glutamate and aspartate influx of Cl,Na and Ca, leading to acute neuronal swelling., vacuolization, and neuronal death ↓high-energy phosphate stores or ↑ free radical production... cause astrocytic swellings via volume-activated anion channels (VRACs). Tamoxifen is a potent inhibitor of
  58. 58. Endogenous opioid peptides modulating the presynaptic release of EAA neurotransmitters. Heightened metabolism in the injured brain is stimulated by an increase in the circulating levels of catecholamines from TBI-induced stimulation of the
  59. 59. First stage.. .
  60. 60. Second stage.. .
  61. 61. Oxidative stress excessive production of reactive oxygen species due to excitotoxicity and exhaustion of the endogenous antioxidant system induces peroxidation of cellular and vascular structures.These mechanisms can cause.... immediate cell death inflammatory processes and
  62. 62. Endogenous opioid peptides .
  63. 63. Increased intracranialpressure The severity increase due to heightened ICP [esp if the pressure exceeds 40 mm Hg.] also can lead to cerebral hypoxia, cerebral ischemia, cerebral edema, hydrocephalus, and brain herniation
  64. 64. Hydrocephalus communicating type of hydrocephalus is more common The noncommunicating type of hydrocephalus is often caused by blood clot obstruction of blood flow at the interventricular foramen, third ventricle, cerebral aqueduct, or fourth ventricle.
  65. 65. Cerebral edema-contributors neurochemical transmitters increased ICP. Disruption of the blood-brain barrier impairment of vasomotor autoregulation leading to dilatation of cerebral blood vessels
  66. 66. Brain herniation Supratentorial herniation is attributable to direct mechanical compression by an accumulating mass or to increased intracranial pressure. Types :
  67. 67. Subfalcine herniation The cingulate gyrus of the frontal lobe is pushed beneath the falx cerebri when an expanding mass lesion causes a medial shift of the ipsilateral hemisphere. This is the most common type of herniation.
  68. 68. Central transtentorialherniation characterized by the displacement of the basal nuclei and cerebral hemispheres downward while the diencephalon and adjacent midbrain are pushed through the tentorial notch.
  69. 69. Cerebellar herniation involves the displacement of the medial edge of the uncus and the hippocampal gyrus medially and over the ipsilateral edge of the tentorium cerebelli foramen, causing compression of the midbrain; the ipsilateral or contralateral third nerve may be stretched or compressed.
  70. 70. Cerebellar herniation This injury is marked by an infratentorial herniation in which the tonsil of the cerebellum is pushed through the foramen magnum and compresses the medulla, leading to bradycardia and respiratory arrest.
  71. 71. Cerebellar herniation .
  72. 72. .CEREBROVASCULAR PHYSIOLOGY AFTER TBI
  73. 73. Altered Cerebral Blood Flowand Metabolism can cause flow-metabolism uncoupling, resulting in cerebral ischemia or cerebral hyperemia; Hyperemia is as bad as ischemia [vasoparalysis↑CBV ↑ICP] show 3 phases FIRST[6-12 HRS]: brain may suffer poor perfusion and cerebral ischemia SECOND phase of hyperemia[CBF>55ml/100g/min]: With luxury perfusion & ↑ ICP THIRD: vasospasm and poor perfusion
  74. 74. Altered Cerebral Blood Flowand Metabolism Focal/global ischemia occurs frequently & is a a major causative factor for poor outcome the critical threshold of CBF for the development of irreversible tissue damage is 15 ml 100 g21 min21 in patients with TBI
  75. 75. How TBI causes ischemia? Morphological injury (e.g. vessel distortion) hypotension in the presence of autoregulatory failure inadequate availability of nitric oxide or cholinergic neurotransmitters potentiation of prostaglandin-induced vasoconstriction
  76. 76. Altered CO2 Vasoreactivity During the early period, CO2 vasoreactivity can be transiently impaired, but generally recovers after 4 to 7 days may be associated with cerebral hyperemia, cerebral ischemia, or intracranial hypertension CO2 vasoreactivity is less in patients with lower baseline CBF
  77. 77. Altered CO2 Vasoreactivity Cerebrovascular CO2-reactivity seems to be a more robust phenomenon. It is in patients with severe brain injury and poor outcome, where CO2-reactivity is found to be impaired in the early stages ; it was intact in most other patients with lesser insults
  78. 78. Altered CO2 Vasoreactivity hyperventilation to induce cerebral vasoconstriction and reduce CBF, ICP and cerebral blood volume may unintentionally lead to secondary ischemic damage after TBI hyperventilation may not be effective in TBI if CO2 vasoreactivity is decreased.
  79. 79. Altered CO2 Vasoreactivity hyperventilation to induce cerebral vasoconstriction and reduce CBF, ICP and cerebral blood volume may unintentionally lead to secondary ischemic damage after TBI hyperventilation may not be effective in TBI if CO2 vasoreactivity is decreased.
  80. 80. Impaired Cerebral PressureAutoregulation incidence is 28% after moderate and 67% after severe TBI a recent study of severe pediatric TBI reported that cerebral autoregulation often changed and worsened during the first 9 days after injury
  81. 81. The vicious cycle “vasodilatorcascade” . ↓CPP ↓MAP cerebral vasodilatio ↓CPP&C n, BF ↑in CBV
  82. 82. Impaired Cerebral PressureAutoregulation autoregulatory vasoconstriction seems to be more resistant compared with autoregulatory vasodilation indicates that patients are more sensitive to damage from low rather than high CPPs.16
  83. 83. Secondary Insults and Injuries Secondary insults, include systemic causes such as hypotension, hypocarbia, hypercarbia, hypoxia, hyperthermia, and hyperglycemia result in secondary injuries
  84. 84. Cerebral vasospasm occurs in more than one-third of patients with TBI and indicates severe damage to the brain.• onset varies from post-traumatic day 2 to 15 and hypoperfusion• (haemodynamically significant vasospasm) occurs• in 50% of all patients developing vasospasm
  85. 85. The mechanisms behindCerebral vasospasm chronic depolarization of vascular smooth muscle due to reduced potassium channel activity release of endothelin along with reduced availability of nitric oxide cyclic GMP depletion of vascular smooth muscle potentiation of prostaglandin-induced vasoconstriction
  86. 86. Cerebral metabolicdysfunction Cerebral metabolism and cerebral energy state are frequentlyreduced after TBI outcome is worse in patients with lower metabolic rates compared with those with minor or no metabolic dysfunction.
  87. 87. Mechanisms-metabolicdysfunction mitochondrial dysfunction with reduced respiratory rates and ATP-production a reduced availability of the nicotinic co-enzyme pool intramitochondrial Ca2-overload …… may not be associated with matching decreases in CBF. reflects uncoupling of CBF and metabolism, probably
  88. 88. Cerebral oxygenation imbalance between cerebral oxygen delivery and cerebral oxygen consumption leading to brain tissue hypoxia. have identified the critical threshold of brain tissue oxygen pressure in patients suffering from TBI 15– 10 mm Hg PtO2 below which infarction of neuronal tissue occurs. oxygen deprivation of the brain with consecutive
  89. 89. Oedema - vasogenic caused by breakdown of the endothelial cell layer of brain vessels allows for uncontrolled ion and protein transfer from the intravascular to the extracellular (interstitial) brain compartments Anatomically, this pathology increases the volume of the extracellular space
  90. 90. Oedema - vasogenic caused by breakdown of the endothelial cell layer of brain vessels allows for uncontrolled ion and protein transfer from the intravascular to the extracellular (interstitial) brain compartments Anatomically, this pathology increases the volume of the extracellular space
  91. 91. Oedema - Cytotoxic• Caused by intracellular water accumulation due to an increased cell membrane permeability for ions, ionic pump failure due to energy depletion, and cellular reabsorption of osmotically active solutes• irrespective of the integrity of the vascular endothelial wall.• more frequent than vasogenic oedema in TBI
  92. 92. Inflammation Both primary and secondary insults activate the release of cellular mediators including proinflammatory cytokines, prostaglandins, free radicals, and complement  induce chemokines and adhesion molecules and in turn mobilize immune and glial cells injured and adjacent tissue is replaced astrocytes produce microfilaments and neutropines ultimately to
  93. 93. Inflammation The additional release of vasoconstrictors (prostaglandins and leucotrienes)• the obliteration of microvasculature through adhesion of leucocytes and platelets,• the blood–brain barrier lesion,• and the oedema formation• further reduce tissue perfusion and consequently aggravate secondary brain damage
  94. 94. Necrosis vs apoptosis Two different types of cell death may occur after TBI Necrosis occurs in response to severe mechanical or ischaemic/hypoxic tissue damage neurons undergoing apoptosis are morphologically intact The clinical relevance of apoptosis relates to the delayed onset of cellular deterioration, potentially offering a more realistic window of opportunity for
  95. 95. Outcome of the last hour shouldbe…..Understanding the multidimensional cascade ofinjury offers therapeutic options including the managementof CPP, mechanical (hyper-) ventilation, kinetic therapy to improve oxygenation and to reduce ICP, and pharmacological intervention to reduce excitotoxicity and ICP
  96. 96. THANK YOU

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