Head injury


Published on

created with much hard work

Published in: Health & Medicine
  • Be the first to comment

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

No notes for slide

Head injury

  1. 1. Dr.Sumit S. HadgaonkarModerator : Dr.Th. Gojen
  2. 2. EpidemologyHead injury Number One Killer in Trauma 25% of all trauma deaths 50% of all deaths from MVC 200,000 people every year inthe world live with thedisability caused by theseinjuries
  3. 3. Indian Head Injury Foundation India – highest rate of head injuries in the world Yearly 1,00,000 lives lost with 1 million suffering fromsevere head injury 1 out off 6 trauma victim dies in India ; in USA thefigure is 1 out off 200 RTA (road traffic accidents) most common causefollowed by falls and assault Motorcylist and pedesticians most common victims ofRTAs
  4. 4.  In the year 2050India will have the highest number of automobiles onthe planet , overtaking USA
  5. 5. Etiology Road traffic accidents (RTA) – most common cause Falls Sports injury Assault Gun shot wounds to head
  6. 6. Basic Anatomy Scalp Skull Meninges Dura Mater Arachnoid Pia Mater Brain Tissue CSF and Blood
  7. 7. Skull
  8. 8. Dura-mater
  9. 9. Venoussinuses
  10. 10. Arachnoidmater
  11. 11. Pia-mater
  12. 12. CSF
  13. 13. Greymatter
  14. 14. Whitematter
  15. 15. Ventricles
  16. 16. Intracranial Volume 80%Brain Matter 10%Blood 10%CSF
  17. 17. Dictates that “the total volume ofthe intracranial contents MUSTremain constant”The MONROE KELLIE doctrine
  18. 18. Brain Physiology Brain Metabolism :1.Brain oxygen consumption (CMRO2, cerebralmetabolic rate for oxygen) – 3.5 ml per 100 g per min2.90% of energy from blood glucose Cerebral blood flow (CBF) :CBF is 55 ml per 100g per minautoregulated over mean arterial pressure range of 50 -150 mm of Hg
  19. 19. Intracranial Pressure The pressure of the brain contents within the skull isintracranial pressure (ICP) The pressure of the blood flowing through the brain isreferred to as the cerebral perfusion pressure (CPP) The pressure of the blood in the body is the mean arterialpressure (MAP) Cerebral Perfusion Pressure (CPP) can be determined bythe following formula:CPP = MAP - ICP
  20. 20. Normal state- ICP normal
  21. 21. Compensated state- ICP normal
  22. 22. Uncompensated state- ICP Elevated
  23. 23. Volume-Pressure Curve
  24. 24.  Primary Brain Injury :-occurs at the time of impact- mechanical damage which is irreversible- causes permanent mechanical cellular disruptionand microvascular injury.-includes 1) cerebral contusions2) diffuse axonal injuries (DAI)3) cerebral lacerationsPATHOPHYSIOLOGY
  25. 25. Secondary Brain Injury occurs at some time after the moment of impact often preventable Prevention of secondary brain injury results inimproved neurological outcome after head injury may make the difference between independentsurvival and dependent survival/death.
  26. 26. Brain suffers from traumaticinjuryBrain swelling or bleedingincreases intracranial volumeRigid cranium allows no room forexpansion of contents so ICPincreasesPressure on blood vessels withinthe brain causes blood flow to thebrain slowlyCerebral hypoxia and ischemiaoccursIntracranial pressure continuesto rise. Brain may herniateCerebral blood flow decreases
  27. 27. CLASSIFICATIONmorphologyseveritymechanism
  28. 28. MECHANISM BLUNT INJURY High Velocity Low Velocity PENETRATING INJURY Gunshot Sharp instruments
  29. 29. Morphology Scalp injury Skull fractures : a) vault fractureb) base of skull fracture Intracranial injury : a) focal lesions– extradural hematoma- subdural hematoma- subarachnoid hematoma- intracranial hematomab)diffuse lesions-contusions (multiple)- DAI
  30. 30. MORPHOLOGY SCALP INJURYCephal HematomaSubgaleal HematomaScalp laceration
  31. 31.  SKULL FRACTURES Vault : linear/stellatedepressed/non depressedopen/closed
  32. 32. Basilar skull fractures Usually diagnosed on CT imaging or on clinicalevidences Clinical signs include Battle sign ,Raccoon Eyes andCSF leak. May or may not be associated with seventh and eighthcranial nerve injury
  33. 33. Battle signRaccoon eyesCSF rhinorrhea
  34. 34. INTRACRANIAL LESIONSEpidural hematoma Collection of blood & clot b/n dura mater and bones ofthe skull Source Middle Meningeal ArteryDural Venous Sinuses C/F Brief loss of consciousness, headache,drowsiness, dizziness ,nausea, vomitting Rapid clinical deterioration
  35. 35.  Classical presentation seen only in 1/3 rd cases On CT scan lentiform hyper dense lesion betweenskull and brain Associated with mass effect on underlying brain withor without midline shift. Overall mortality rate 18% in all cases but only 2% inisolated EDH
  36. 36. Acute subdural Hematoma Accumulates in space between dura and arachnoid Disruption of cortical vessels or brain lacerationproduces hematoma A/w significant primary injury- patients present withimpaired conscious level from the time of injury CT scan –hyperdense concave lesion spreading acrossbrainmidline shift disproportionate to size of lesion Mortality rate as high as 40% in some series
  37. 37. Subarachnoid Hemorrhage Trauma is most common cause followed by Aneurysms Rarely aneurysmal hemorrhage immediately precedestrauma. Most can be managed conservatively
  38. 38. Chronic subdural Hemorrhage Usually occurs in elderly on anti coagulant or antiplatelet agents h/o minor head injury in weeks or months prior topresentation Small bridging veins tear and cause small clinicallysilent ASDH ,when hematoma breaks down andincreases in size mass effect is produced c/f- headache, cognitive impairment, focalneurological deficit and seizures. CT scan – acute blood (0-10 days) = hyperdense- sub acute blood (10-14 days) = isodense- chronic blood (>2 weeks) =hypodense
  39. 39. Acute on chronic SDH Chronic SDH will more recent hemorrhage independant (posterior) areas. Treatment is Burr hole evacuation rather thancraniotomy
  40. 40. Cerebral contusions Coup and counter coup injuries Most commonly affecting inf frontal fossa andtemporal lobes CT appears heterogeneous with mixed areas of highand low density Rarely require immediate surgery Observation for 48-72 hrs
  41. 41. Concussion Temporary & brief interruption of neurological functionafter minor head injury Due to shearing / stretching of white matter fibres at thetime of impact or temporary neuronal dysfunction C/o headache, confusion, amnesia CT/MRI cannot detect 3 grades (Colorado Grading)grade I- symptoms for 15 mins no LOC , only confusiongrade II-symptoms for > 15 mins ,no LOC, amnesiagradeIII- LOC present Medical opinion should be sought in Grade II and III
  42. 42. DAI Diffuse Axonal Injury Disruption of axons in white matter and brainstem Injury occurs immediately and is irreversible Seen after MVC or shaken baby syndrome Usually have persistent sequlae e.g. cognitiveimpairment, spasticity etc. 90% pts with severe DAI will be vegetative CT usually normal MRI with multiple, diffuse abnormalities Hemorrhagic spots classically seen over corpuscallosum, dorsolateral midbrain.
  43. 43. Brain Herniation
  44. 44. APPROACH TO A PATIENT WITH HEADINJURY History Initial Assessment Primary Survey Secondary Survey
  45. 45. History
  46. 46.  This is early triage mostly done by paramedics Core of ATLS system and constitutes ABCDE of traumacarePRIMARY SURVEY
  47. 47.  Airway maintenance with cervical spine protection
  48. 48. Intubation with Cervical inline stabilization Breathing and ventilation : Intubation precautionsPre-medicate with Lidocaine, 1mg/kg IV 2 minutesprior to attempt Laryngoscopy produces an ICP Spike
  49. 49. Circulation Maintain MAP >90mmhg- adequate Hematocrit >30%
  50. 50.  Isolated intracranial injuries do not cause hypotension LOOK FOR THE CAUSE OF HYPOTENSION
  51. 51.  Pupillary size and reaction GCS (Glasgow Coma Scale) Motor function Injury levelDisability
  52. 52. Assessment Findings Constricted? narcotics? Sluggish/dilated? mid brain ICP Unilateral dilation? pressure on CNIII Fixed and Dilated? herniation
  53. 53. SECONDARY SURVEY AMPLE history Examination of Head to toe Glasgow Coma Scale Detailed Neurological Examination
  54. 54. SYMPTOMS & SIGNS OF INCREASED ICP Diminishing level of consciousness Headache, vomiting, seizures Cushing’s Triad – bradycardia hypertension abnormal respiration Pupillary changes Papilloedema
  55. 55. Severity of Head Injury
  56. 56. MANAGEMENT OFMILD HEAD INJURY (GCS14 -15) History General Examination Limited Neurologic Examination C-spine and other X-rays as indicated CT scan?? Discharge with advice
  57. 57.  Patient can be discharged if following criteria are metbefore discharge1.GCS must be 15/152.no focal neurological deficit3.accompanied by responsible adult4.verbal and written advice given
  58. 58.  Aim is prevention of secondary brain injury Achieved by avoidance of hypoxia and hypotension CT scan after complete stabilization of patient. Early neurosurgery consult if intracranial hematomaseen Measures to reduce ICP (reverse Trendelenburg) i.e.head up position by 20-30 degrees ? ICP monitoring Mannitol during transport.MANAGEMENT OF MODERATE HEADINJURY(GCS 9-12)
  59. 59. MANAGEMENT OF SEVERE HEAD INJURY(3 -8 ) 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
  60. 60.  CT scan only after hemodynamic stabilization Medical therapy for raised ICP Immediate neurosurgeon opinion If needed surgical management
  61. 61. MEDICAL THERAPIES FOR HEAD INJURY Head end elevation – 30 deg Intravenous fluids: Maintain normovolemia Hypotonic/glucose containing fluidsshould not be used Serum sodium levels monitored daily
  62. 62. Mannitol 0.25-1g/kg Osmotic agent- dec ICP, maintains CBF,CPP and brainmetabolism Dec ICP within 6 hrs. Expands volume, O2 carrying capacity. Diuretic effect- net intravascular volume is reduced.
  63. 63. Furosemide To reduce ICT in conjunction with mannitol Dose 0.3 to 0.5 mg/kg Never use in Hypovolemia
  64. 64.  Hypertonic Saline Improves CPP and brain tissue O2 levels Decreased ICP by 35% (8-10 mm HG) CPP increased by 14% MAP remained stable Greatest benefit in those with higher ICP and lower CPP Repeated doses were not associated with rebound,hypovolemia or HTN 30 mL of 23.4% over 15 minutes
  65. 65. HYPERVENTILATION No role as prophylaxis in 24 hrs. Reducing PaCO2 cerebral vasoconstriction Maintain PaCo2 25 – 35 mmhg Last resort for reducing ICP TEMPORARY MEASURE ONLY.
  66. 66. Barbiturates Effective in reducing ICP – refactory to other measures Not used in presence of hypotension/hypovolemia
  67. 67. Anticonvulsants Phenytoin-Loading dose - 18 – 20 mg/kgMaintenance dose - 100 mg q 8 hrly
  68. 68. Surgical Management of SpecificHead injuries Various guideline followed Guidelines For Surgical Management of TraumaticBrain Injury Published in 2001 All new reports and literature regularly updatedthrough Neurosurgical Evidence Based MedicineCentre ,University Of Washington.
  69. 69. Depressed skull Freacture Indications of operative treatment1.gross wound contamination2.significant intracranial hematoma3.gross cosmetic deformity4.frontal sinus involvement5.dural penetration6.depression > 1cm7.wound infection8.pneumocephalus Elevation and debridement – method of choice
  70. 70. Fracture Skull Base With CSF leaksno acute surgery required for CSF leakfor first 72 hrs observation (elevation of head)if leak persiststemporary CSF diversion (lumbar drainage orventriculostomy)Still leak persists surgery to be done Exploration of floor of frontal fossa with closure ofdural defect
  71. 71. EDH Absolute indications of surgery (regardless of GCS)1. > 30 ml vol of hematoma2. > 15 ml thickness of blood clot3. midline shift >5 mm4. anisocoria ( > 1mm) If GCS <8 = immediate surgery If GCS > 8 = as soon as possible If size less than above but GCS <8 = surgery If size less than above but GCS >8 =nonoperativemanagement can be done Mean time of EDH for reexpansion is 8 hrs -36 hrs.
  72. 72. SDH Absolute indication of surgery1. > 10 mm thickness of blot clot2.Midline shift > 5mm If size less than above but GCS <8 along with1. GCS decreased by 2 from time of injury toadmission2. Pt. with asymmetric or fixed dilated pupils3.ICP >20 mm of Hg If size less than above and GCS >8 = non operativetreatment. If planned surgery should be within first 4 hrs Craniotomy with duraplasty with or without bone flapremoval
  73. 73. Posterior Fossa Lesions No monitoring possible because of location Guidelines for evacuation1. > 3cm clot on CT scan2. any size of clot with ASDH or EDH
  74. 74. Penetrating Brain Injury Meningitis and abscess most common complicationsfollowed by Seizures If grossly contaminated wound then craniotomy anddebridement required Small clean wounds with no scalp devitalization can bemanaged conservatively If open sinus suspected repair should be done If dural injury suspected repair should be done.
  75. 75. Burr hole Pentrator Burr hole bit Bone rongeur Scalpel
  76. 76. ProcedureA burr hole is placed onthe side of the dilatingpupil.In the absence of a CTscan, the burr hole isplaced 2 finger widthsanterior to the tragus ofthe ear and 3 finger widthsabove the tragus of the ear.
  77. 77. A vertical incision is made approximately 3cm long, centered over the entry point allthe way down to the temporalis muscledividing the fibers of the muscle vertically.The periosteum is then cut in the samemanner.
  78. 78. The outer table of the skull is drilled with thepenetrator
  79. 79. If there continues to be excessive bleedingthrough the hole, packing the wound shouldbe tried with Gel foam or by cutting off a pieceof temporalis muscle and stuffing it into thehole.
  80. 80. Decompressive Craniectomy Controversial Used in patients without focal lesion and raised ICPwho are refractory to maximum medical management The operation involves removing a large section ofskull and opening the dura, allowing the swollen brainto expand underneath the scalp The bone flap is stored and can be replaced 3–6months later when the patient has made a goodneurological recovery and the brain swelling hasresolved
  81. 81. Long term sequelae of Head Injury Neurorehabilitation Neuropsychology – after minor head injuries such asheadache, dizziness, impaired short term memory,concentration etc. Seizures –prophylactic anticonvulsants cant prevent longterm seizures Delayed CSF leak –CT cisternography or CT isotope studiescan be done
  82. 82.  Seizure Disorder 2% Early post-traumatic incidence Increased to 30% in children, alcoholics and withintracranial hematoma Prophylactic antiepileptics reduce early occurrence Use not supported by the literature Concussion- Brief LOC - Vertigo - Nausea- Dizziness - Headache - Vomiting- Photophobia - Cognitive/Memory dysfunction
  83. 83.  Concussion Up to 80% may have symptoms at 3 months 15% may have symptoms at 1 year Persistence of these symptoms is termed PostconcussiveSyndrome 85-90% recover after 1 year Risk factors:- Female - Litigation - Low socioeconomic status
  84. 84. Outcome
  85. 85. Pheneas Gage – most popularpatient in Neurosurgery
  86. 86. THANK YOU