Head injury (2)

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Head injury (2)

  1. 1. HEAD INJURIES Mizan Kidanu April 03/2013
  2. 2. OUTLINE Introduction Epidemiology Anatomy Causes Classification Diagnosis Management Complication
  3. 3. INTRODUCTION A head injury is any trauma that leads to injury of the scalp, skull, or brain The injuries can range from a minor bump on the skull to severe brain injury
  4. 4. EPIDEMIOLOGY Number one killer in trauma 25% of all trauma deaths 50% of all deaths from MVA 200,000 people in the world live with the disability caused by these injuries 50% in ages b/n 15 and 35
  5. 5. ANATOMY  Anatomy of the ’’SCALP’’ Skin firmly bound to the 3rd layer by perpendicular fibers Connective tissue contain blood vessels of the scalp Aponeurosis  fibrous sheet, found over much of the vertex attaches occipitalis to frontalis m
  6. 6. Loose connective tissue accounts for the mobility of the scalp blood tracks freely in this layer bilateral orbital edema following sever head injury or cranial operation Periosteum adheres to the suture lines of the skull collection of blood beneath this layer  outlines the affected bone  cephalohematoma (children)
  7. 7. Anatomy of the meninges Dura endosteum and true meningeal layer forms falx, tentorium, diaphragm Arachinoid vascular membrane arachinoid granulations Pia highly vascular dips into sulci and fissures carries cortical vessels
  8. 8. CAUSES OF HEAD INJURY Road traffic accident 65% of deaths following severe head injury Falls Injuries at work place, during sport, or at home Assaults
  9. 9. CLASSIFICATIONS OF HEAD INJURY 1. Blunt Vs Penetrating 2. Primary Vs Secondary 3. Mild, Moderate, or Severe
  10. 10. PRIMARY INJURY TO SCALP Hematoma - Usually do not require Rx - If large aspiration when it liquefies Wounds Abrasions - Cleaned & exposed - Dressed - if hemorrhagic or serous exudates Lacerations - Cleaned & sutured( LA or GA) - LA infiltrated into scalp - Wound closure without tension
  11. 11. PRIMARY INJURY TO SKULL Linear fractures - Do not require Rx - At temporal area  tear MMAEDH Depressed #s - Simple Vs Open Surgery indicated in: ocompression (large plate of bone) ocosmetic area o compound/open wound:  wound debridement  elevate the depression  suture dural laceration
  12. 12.  Fractures of the skull base Diagnosis oHistory - nasal bleeding,… oPhysical examination Raccoon eyes Battle sign Rhinorrhea,...... Management: conservative, advise on danger Sn closure of dura - persistent CSF leak
  13. 13. PRIMARY BRAIN INJURY The damage caused to the brain at the moment of impact Concussion  temporary neuronal dysfunction after blunt head trauma  head CT is normal, & deficits resolve over minutes to hours Contusion/laceration  bruise of the brain  breakdown of small vessels and extravasation of blood into the brain Diffuse axonal injury  damage to axons throughout the brain  most frequent finding in patients who die from severe head injury
  14. 14. Mechanisms Coup & counter-coup injuries  Common sites:- undersurface of frontal lobe tip of temporal lobe
  15. 15. SECONDARY BRAIN INJURY Extracranial  hypoxia  hypotension Intracranial     hematoma brain edema raised ICP infection
  16. 16. DIAGNOSIS History  Age  Loss of consciousness  Cause, circumstance and mechanism of injury  Presence of headache & vomiting  Seizures  Anticoagulant use,….
  17. 17. ASSESSMENT OF NEUROLOGICAL FUNCTION AND OF CONCIOUS LEVEL Glasgow Coma Score Best Eye Response (4) No eye opening……………………………1 Eye opening to pain..…………………….2 Eye opening to verbal command.……...3 Eyes open spontaneously…...………….4 Best Verbal Response (5) No verbal response ………………………1 Incomprehensible sounds. ……………..2 Inappropriate words. …………………….3 Confused …………………………………..4 Orientated  …………………………………5 Best Motor Response (6) No motor response.…………………..…..1 Extension to pain.…………………….…..2 Flexion to pain.……………………….…...3 Withdrawal from pain..……………….…..4
  18. 18. Classification of head injury Mild: GCS = 13-15 Moderate: GCS = 9-12 Severe: GCS = 3-8
  19. 19. Exclude other causes of depressed conscious level (causes of coma) No focal signs drugs (alcohol, opiate) circulatory collapse hypothermia / hyperthermia concussion meningitis, encephalitis subarachinoid hemorrhage Focal signs present cerebral abscess ,infarction, tumor intracranial hemorrhage
  20. 20. Investigations Skull radiograph CXR and X-ray of cervical spines CT-Scan - first line investigation
  21. 21. Indication for CT-scan  GCS<13 at any stage  GCS =13 or 14 at 2 hours following injury  Suspected open or depressed #  Any sign of basal skull #  Post-traumatic seizures  Focal neurologic deficit  Post-traumatic amnesia of >30 minutes  Persistent vomiting  Coagulopathy  Significant mechanism of injury
  22. 22. GENERAL MANAGEMENT OF HEAD INJURY ABC rule stabilization of airway, breathing and circulation IV access - maintain normovolemia - hypotonic/glucose containing fluids should not be used endotracheal intubation (e.g: GCS ≤ 8, hypoxia,…) Head end elevation - 300 Treat co-existing injuries chest drain - tension pneumothorax cervical collar - # of cervical spine,….
  23. 23. Anticonvulsants may decrease early posttrauma seizures but no benefit in long term epilepsy prevention Phenytoin  Loading dose = 18 - 20 mg/kg  Maintenance dose = 100 mg q 8 hrly
  24. 24. Regular observation at half hourly interval: GCS BP, HR, RR, and Temperature oxygen saturation pupil size & reactivity limb movement
  25. 25. EPIDURAL HEMATOMA Usually from torn middle meningeal artery and/or vein Other causes: torn dural sinuses(e.g: saggital sinus) oozing from diploe bone & stripped dura Uncommon but serious,1- 4% of TBI Highest among adolescents and young adults Skull fractures in 75-95%
  26. 26. Clinical presentation lucid interval (in 1/3 of cases) associated with headache vomiting, drowsiness, confusion, aphasia, seizures and hemiparesis epidural hematoma due to venous bleeding neurologic decline is slower posterior fossa EDH - elevated ICP
  27. 27. Diagnostic evaluation  CT scan - lens shaped collection - hematoma volume estimation Management  craniotomy / ?burr hole Prognosis-mortality -10%
  28. 28. SUBDURAL HEMATOMA Pathophysiology result from the tearing of bridging veins crossing the subdural space or hemorrhage from severe cerebral contusions Spread more diffusely over the hemisphere than extradural and are often associated with diffuse swelling of the underlying hemisphere Clinical manifestations - depends on type
  29. 29. ACUTE SUBDURAL HEMATOMA 1-2 days after onset coma in (56%) lucid interval (12-38%) posterior fossa SDH - signs of increased ICP Result from: torn bridging veins cortical lacerations torn dural sinuses
  30. 30. CT SCAN FEATURES clot is bright or mixed-density crescent-shaped (lunate) may have a less distinct border does not cross the midline due to the presence of falx Signs of mass effect: ventricular compression, midline shift and reduction in the size of the basal cisterns
  31. 31. SUBACUTE SUBDURAL HEMATOMA After approximately 1-2 weeks the subdural collection become isodense to grey matter detection may be challenging & recognized when:  effacement of cortical sulci  deviation of lateral ventricle  midline shift Contrast enhancement will often define cortical- subdural interface
  32. 32. CHRONIC SUBDURAL HEMATOMA after 2 weeks usually post trivial injury due to injury of small bridging veins headache, cognitive impairment, apathy, seizures and focal deficits symptoms are transient and fluctuating proximal, painless and intermittent paraparesis
  33. 33. CT features  After 2 weeks, hypodense crescentic collections  Acute-on-chronic SDHs can further complicate the images, with hyperdense fresh haemorrhage intermixed, or layering posteriorly, within the chronic collection  Do not cross the midline
  34. 34. Management Acute SDH - Surgery for symptomatic & unstable pt  Surgery burr hole craniotomy  Nonoperative Mx clinically stable clot thickness <10mm no clinical or CT signs of herniation repeat CT scans 6-8 hrs after initial scan
  35. 35. Chronic SDH Surgery - burr hole signs of increased ICP clot thickness >10mm cognitive impairment motor impairment
  36. 36. RAISED INTRACRANIAL PRESSURE The three normal contents of the cranial vault are brain tissue (80%), blood (10%), and CSF (10%) Normal state - ICP normal 4-14 mmHg - normal >20mmHg – abnormal
  37. 37. The Monro-Kellie doctrine states that ’’the cranial vault is a rigid structure, and therefore, the total volume of the contents determines ICP ’’ Cerebral Perfusion Pressure (CPP) can be determined by the following formula: CPP = MAP – ICP
  38. 38. Symptoms & Signs of increased ICP  Diminishing level of consciousness  Headache, vomiting, seizures  Cushing’s Triad:  bradycardia  hypertension  abnormal respiration  Pupillary changes  Papilledema
  39. 39. Effects of raised ICP: brain herniation 1. subfalcine herniation 2. uncal herniation 3. central transtentorial herniation 4. tonsillar herniation reduced cerebral perfusion
  40. 40. Management of raised ICP includes airway protection and adequate ventilation (intubation may be required) a bolus of Mannitol 0.25-1g/kg causes: free water diuresis increased serum osmolality and extraction of water from the brain require rapid neurosurgical evaluation ventriculostomy or craniotomy may be needed for definitive decompression
  41. 41. COMPLICATIONS HEAD INJURY Meningitis & brain abscess CSF rhinorrhea and otorrhea Epilepsy - about 80% arise in 2yrs Hydrocephalus- usually due to atrophied white matter Amnesia (PTA) Postconcussional Sx Posttraumatic encephalopathy Cranial nerve injury - in up to 30% pts
  42. 42. REFERENCES Mark S. Greenberg: Hand Book of Neurosurgery; 6th ed Bailey & Love’s: Short Practice of Surgery; 24th ed, 2004 Peter J Morris: Oxford Text Book of Surgery; 2nd ed, 2002 Schwartz's: Principles of Surgery; 9th ed, 2010

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