Traumatic Brain Injury


Published on

A synopsis on Head injury and management

Published in: Education
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide
  • Vasogenic edema arises from transvascular leakage caused by mechanical failure of the tight endothelial junctions of the BBB. Vasogenic edema accumulates in white matter and is frequently associated with focal contusions or hematomas. Vasogenic edema eventually resolves as edema fluid is reabsorbed into the vascular space or the ventricular system.
    Cytotoxic edema is an intracellular process that results from membrane pump failure when CBF is reduced to 40% or less of baseline. If CBF drops to 25% of baseline, membrane pumps fail and cells begin to die. It is associated with post-traumatic ischemia and tissue hypoxia.
  • Traumatic Brain Injury

    1. 1. Traumatic Brain Injury Dr. Abimanyu Sakthivelu MD Assistant Professor Department of Accident, Emergency & Critical care. Vinayaka Mission University Salem, Tamil nadu, India
    2. 2. Cerebral Hemodynamics Brain Blood Artery Arteriole Capillary The blood-brain barrier (BBB) maintains the microenvironment of the brain tissue Introduction
    3. 3. Movement across BBB regulates extracellular ion and neurotransmitter concentrations Prolonged disruption of the BBB contributes to the development of post-traumatic vasogenic cerebral edema
    4. 4. The brain has an extremely high metabolic rate Uses up to 20% of oxygen volume consumed by the body The brain requires approximately 15% of the total cardiac output Optimal regional CBF is maintained by altering cerebral vessel diameter in response to changing physiologic conditions
    5. 5. Cerebral Blood vessel Cerebral vasoconstricti on Cerebral vasodilatio n Hypertension Alkalosis Hypocarbia Hypotension Acidosis Hypercarbia Hypoxia Ischemia Increased ICP
    6. 6. Cerebral Perfusion Pressure  The cerebral perfusion pressure (CPP) is the pressure gradient required to perfuse the cerebral tissue  CPP is calculated as the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP): MAP – ICP = CPP MAP = DBP + [(SBP – DBP)/3]  The local adjustment of cerebral blood flow within the brain microcirculation is termed autoregulation.
    7. 7. Cerebral autoregulation  Cerebral autoregulation is a homeostatic mechanism that minimizes deviations in cerebral blood flow (CBF) when cerebral perfusion pressure (CPP) changes.  CBF is 50 to 55 ml per 100g of brain tissue per minute CBF is maintained at constant levels MAP of 60 to 150 mm Hg CPP of 50 to 160 mm Hg
    8. 8. Biomechanics of Head Trauma
    9. 9. Direct impactCompression Energy applied Cranium absorbs Shock waves Travel distant to the site of impact or compression Distort and disrupt intracranial contents Alter regional ICP
    10. 10. Prolonged application Ability of the skull to absorb the force is overwhelmed Multiple linear skull fractures High-energy rapid compression force to a small area of the skull. Depressed fractures Compressio n
    11. 11. Cranial contents are set into vigorous motion Bridging subdural vessels are strained Indirect brain injury DAI/Concussio n SDH Differential acceleration – one brain region slides past another Shear and strain injuries results in diffuse injuries Abrupt arrest of intracranial contents Contrecoup contusions
    12. 12. Primary brain injury  It is mechanical irreversible damage that occurs at the time of head trauma and includes brain lacerations, hemorrhages, contusions, and tissue avulsions Secondary brain injury  It results from intracellular and extracellular derangements that are probably initiated at the time of trauma by a massive depolarization of brain cells and subsequent ionic shifts
    13. 13.  Hyperpyrexia (core body temperature >38.5 °C) – The mechanism involves stimulation of metabolism in injured areas of the brain, thus recruiting blood flow with a resultant increase in ICP  Anemia (hematocrit <30%) – reduces the oxygen-carrying capacity of the blood, thus reducing the amount of necessary substrate delivered to the injured brain tissue. Secondary Systemic Insults
    14. 14. Secondary Systemic Insults  Hypoxia (Po2 less than 60 mm Hg) – cerebral vessels dilate to ensure adequate oxygen delivery to brain tissue Brainstem compression or injury – transient or prolonged apnea Partial airway obstruction Chest wall injury interfering with expansion Pulmonary injury reducing effective oxygenation Ineffective airway management, The overall mortality from severe head injury may double or quadruple
    15. 15. Secondary Systemic Insults  Hypercarbia  Hyperthermia  Coagulopathy  Seizures
    16. 16. Pathophysiology
    17. 17. Increased Intracranial Pressure  It is defined as CSF pressure greater than 15 mm Hg (or 195 mm H2O) and is a frequent consequence of severe head injury.  ICP represents a balance of the pressures exerted by the contents of the cranial cavity.  This relationship is explained by the Monro-Kellie doctrine
    18. 18. Monro-Kellie doctrine Total intra cranial volume remains constant as the cranial vault is a rigid non expansile container
    19. 19. Hayreh SS, Br J Ophthalmol, 1964;48:522–43. FUNDOSCOPY ** CT BRAIN Clinical signs *ONSD or invasive monitoring
    20. 20. Traumatic mass lesion or edema increases ICP CSF displaced from cranial vault to spinal canal Compromise of compensatory mechanism Accommodat es volume of 50 to 100 ml Vasodilation, CSF obstruction, or small areas of focal edema Compromise of CPP, vasoparalysis & Loss of autoregulation Offsets increased blood or brain volume Brain tissue compression compensates the increase in ICP
    21. 21. The CBF directly depends on systemic MAP Loss of autoregulation cause massive cerebral vasodilation Systemic pressure is transmitted to the capillaries Outpouring of fluids into the extravascular space Vasogenic edema further increase ICP ICP rises to the level of the systemic arterial pressure, CBF ceases and brain death occurs
    22. 22. Cerebral edema  Cerebral edema is an increase in brain volume caused by an absolute increase in cerebral tissue water content. On computed tomography scans Bilateral compression of the ventricles Loss of definition of the cortical sulci Effacement of the basal cisterns Vasogenic edema arises from transvascular leakage caused by mechanical failure of the tight endothelial junctions of the BBB Cytotoxic edema is an intracellular process resulting from membrane pump failure when CBF ≤ 40% of baseline
    23. 23. Cushing's Reflex
    24. 24. Cerebral Herniation
    25. 25. New Orleans and Canadian CT Clinical Decision Rules New Orleans Criteria—GCS 15* Canadian CT Head Rule—GCS 13–15* Headache GCS <15 at 2 h Vomiting Suspected open or depressed skull fracture Age >60 y Any sign of basal skull fracture Intoxication More than one episode of vomiting Persistent antegrade amnesia Retrograde amnesia >30 min Evidence of trauma above the clavicles Dangerous mechanism (fall >3 ft or struck as pedestrian) Seizure Age 65 y Identification of patients who have an intracranial lesion on CT 100% sensitive, 5% specific 83% sensitive, 38% specific Identification of patients who will need neurosurgical intervention 100% sensitive, 5% specific 100% sensitive, 37% specific *Presence of any one finding indicates need for CT scan. Limitations: Not applicable for children and patients on anticoagulation
    26. 26. Classification Of Head injury Morphology Severity Mechanism
    27. 27. Mechanism Blunt Penetrating High Velocity Low velocity Gun shot Automobile collision Falls & assault Stab wounds Severity Moderate - GCS 9-13Mild - GCS 14-15 Severe - GCS 3-8 Morphology Skull fractures Vault Basilar Linear/stellate Depressed/non depressed Open/closed ±CSF leak ±7th -nerve palsy Intracranial lesions Epi Dural Hematoma Sub Dural Hematoma Intra Cerebral Hematoma Focal Diffuse Concussion Multiple contusion Hypoxic/ischemic injury
    28. 28. Pre-Hospital Care
    29. 29. Airway Airway interventions to prevent hypoxia Unsuccessful attempts at field intubations delays IN – HOSPITAL CARE and increase the risk for aspiration or hypoxia Unintentional hyperventilation of intubated patients
    30. 30. Outcome of Out – Of – Hospital Endotracheal intubations in TBI
    31. 31. Prehospital hyperventilation
    32. 32. Circulation Compression of the brainstem and medulla have profound effects on the cardiovascular system - cardiac dysrhythmia Establishing intravenous (IV) access Cardiac monitor during transport Scalp lacerations should be secured with less bulky dressing and firm constant manual pressure should be applied to avoid excessive blood loss
    33. 33. Neurologic assessment Should focus on GCS Pupillary responsiveness and size Level of consciousness Motor strength and symmetry Determine the subsequent effectiveness of treatment
    34. 34. Need for sedation Agitated patients Exacerbate physical injury Cause an increase in ICP Interfere with appropriate stabilization and management Lorazepam Diazepam Midazolam Haloperidol Droperidol Tripardol
    35. 35. Emergency Department management
    36. 36. Management Of Mild Head Injury (GCS14 -15) History General Examination to exclude systemic injuries Limited Neurologic Examination C-spine and other X-rays as indicated Blood alcohol level and urine toxicology screening CT scan is indicated if criteria for high or moderate risk of neurosurgical intervention are present Observe or admit to hospital Discharge from hospital
    37. 37. Observe or admit to hospital No CT scanner available Abnormal CT scan All penetrating head injuries H/O prolonged loss of consciousness Deteriorating level of consciousness Moderate to severe headache Significant alcohol / drug intoxication Skull fracture CSF leak – rhinorrhea or otorrhea Significant associated injuries No reliable companion at home Abnormal GCS score (<15) Focal neurological deficits
    38. 38. Discharge from hospital Patient does not meet any of the criteria for admission Discuss need to return if any problems develop and issue a “warning sheet” Schedule a follow – up visit
    39. 39. Management of moderate head injury (GCS 9-13) Initial Examination Same as for mild head injury plus baseline blood work CT scan brain – obtained in all cases Admit to a facility capable of definitive neurosurgical care After Admission Frequent Neurologic Checks Follow up CT if condition deteriorates or preferably before discharge Improves (90%) Deteriorates (10%) Discharge when appropriate Follow up in clinic If the patient stops following simple commands repeat CT scan Manage as per severe head injury protocol
    40. 40. Management of severe head injury(3 - 8 ) ABCDEs Primary Survey and Resuscitation Secondary Survey and ‘AMPLE’ history Admit to facility – neurosurgical care Neurologic Re-evaluation Eye opening Motor response Verbal response Pupillary reaction Therapeutic agents (administered after Neurosurgical consult) Mannitol Moderate hyperventilation (Pco2 ~ 35 mmHg) Anti convulsants CT Brain
    41. 41. Airway Attention must be given to the increased ICP that can potentially occur with any physical stimulation of the respiratory tract Lidocaine (1.5–2 mg/kg IV push) Suppresses Cough reflex Hypertensive response Increased ICP associated with intubation Etomidate (0.3 mg/kg IV) Short-acting sedative-hypnotic agent Beneficial effects on ICP by reducing CBF and metabolism. Has minimal adverse effects on blood pressure and cardiac output Fewer respiratory depressant effects than other agents.
    42. 42. Hypotension A cause other than the head injury should be sought Scalp lacerations can cause hypovolemic hypotension Hemorrhage into an epidural or subgaleal hematoma (children) Neurogenic hypotension in concomitant high spinal cord injury Fluids should never be withheld in the head trauma patient with hypovolemic hypotension for fear of increasing cerebral edema and ICP
    43. 43. Hyperventilation Acute hyperventilation prevents or delays herniation in the patient with severe TBI Goal is to reduce the pco2 to the range of 30 to 35 mm hg The onset of effect is within 30 seconds and peaks within 8 minutes Hyperventilation lowers the ICP by 25%
    44. 44. Osmotic Agents Mannitol is the mainstay for control of elevated ICP acute severe TBI. Mannitol (0.25–1 g/kg) Hypertonic saline (HTS) Preclinical studies have demonstrated that HTS can significantly reduce ICP Adverse events - Renal Failure, Central Pontine Myelinoysis, Rebound ICP elevation
    45. 45. Brain cell VesselMannitol Expands vessel volume in hypovolemic shock Decrease ICP (6 to 8 hrs) provides space for expansion of hematoma Reduces blood viscosity & microcirculator y resistance & promotes CBF Free radical scavenger In large doses Renal failure & Hypotension Induce a paradoxical effect
    46. 46. Crystalloids Vs Colloids
    47. 47. Role of Albumin in TBI
    48. 48. Mannitol Vs 7.45% Hypertonic Saline Solution (HSS)
    49. 49. Barbiturates Reduce cerebral metabolic demands of the injured brain tissue Affect vascular tone and inhibit free radical-mediated cell membrane lipid peroxidation
    50. 50. Role of Barbiturates
    51. 51. Furosemide  To reduce ICT in conjunction with mannitol  Dose 0.3 to 0.5 mg/kg  Never use in Hypovolemia
    52. 52. Biomarkers for TBI
    53. 53. Admission serum albumin levels – Effective indicator of outcome of TBI
    54. 54. Role of Hypothermia TBI
    55. 55. Role of hyperglycemia in TBI
    56. 56. Seizure Prophylaxis INDICATIONS FOR ACUTE SEIZURE PROPHYLAXIS IN SEVERE HEAD TRAUMA Depressed skull fracture Paralyzed and intubated patient Seizure at the time of injury Seizure at emergency department presentation Penetrating brain injury Severe head injury (GCS score ≤8) Acute subdural hematoma Acute epidural hematoma Acute intracranial hemorrhage Prior history of seizures Early seizures can cause hypoxia, hypercarbia, release of excitatory neurotransmitters, and increased ICP, which can worsen secondary brain injury Lorazepam (0.05– 0.15 mg/kg IV over 2–5 minutes up to a total of 4 mg) Diazepam (0.1 mg/kg, up to 5 mg IV, every 10 minutes up to a total of 20 mg) Phenytoin (18–20 mg/kg IV) Fosphenytoin (15–18 phenytoin equivalents/kg) IV or IM can be given
    57. 57. Recombinant factor VIIa (rFVIIa)
    58. 58. Role of steroids in TBI
    59. 59. Cranial Decompression Emergency trephination Signs of herniation Refractory rise of ICP Rapid detoriation Blind invasive procedure Chances of localizing the expanding lesions are uncertain May temporarily reverse or arrest the herniation syndrome Provides time formal craniotomy
    60. 60. Specific indications for craniotomy  Clinical deterioration  Size > 1cm thick extracerebral clot. Volume > 25 – 30 ml in intracerebral hematomas.  Midline shift > 5 mm.  Enlargement of contralateral ventricle (temporal horn).  Obliteration of basal cisterns or third ventricle.  Raised or increasing ICP
    61. 61. EDH Need surgical evacuation  Timing – Any patient with EDH in coma or Any EDH with >30cm3 irrespective of the GCS Can wait  EDH<30cm3  <15mm thickness  <5mm midline shift  GCS> 8 Ref:-neurosurg-58,2006
    62. 62. When to operate in Acute SDH Acute SDH >10mm or midline shift >5mm on CT regardless of GCS If GCS is decreased in hospital from time of injury to Admission by >2, Anisocoria or ICP>20mmhg Ref:-neurosurg-58,2006
    63. 63.  Operations definitely indicated only if it is a compound (open) fracture (not over sagittal sinus) or if the fracture is so extensive that it causes mass effect.  Closed depressed skull fractures are usually treated conservatively, but operation may be appropriate in selected cases to reduce mass effect or correct defigurement.
    64. 64. Role of probiotics and early entral nutrition in TBI
    65. 65. Researches and ongoing trials
    66. 66. ACHIEVE To explore the efficacy of albumin as a neuroprotective agent for TBI in humans, a randomized controlled trial, Albumin for Intracerebral Hemorrhage Intervention (ACHIEVE), is currently underway
    67. 67. THANK YOU