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Head injury management lecture.ppt (1)
- 1. Management of Head Injuries SumitSinha M.S; D.N.B; M.N.A.M.S; M.Ch Asstt. Professor Department of Neurosurgery JPNATC, AIIMS, New Delhi
- 2. ■ Major HealthHazard, 2 million injured and 1 million die/rehab/ year in India ■ 16,000 per year in Delhi. ■ Leading cause of death in multiple injured patient. ■ Tops the list of killers in young ■ Man-made preventable calamity Head Injury
- 3. Large number dieof non- availability of timely treatment. Head Injury
- 4. Head Injury Definition Injury toHEAD AND BRAIN
- 5. Head Injury Etiology ■ Roadtraffic accidents ■ Fall from height ■ Assault
- 6. Head Injury Alcohol involvedin 20% 50% fatal injury occur because of alcohol. ■ Reflexes and reaction time delayed ■ Euphoria
- 7. Classification Skull Fractures FocalBrain Injuries Diffuse Brain Injuries Vault Contusion Concussion Linear Coup Diffuse Axonal Depressed Contrecoup Base Open Hemorrhage / Close Hematoma Epidural Subdural Intracerebral
- 8. Head Injury- Neurological Examination HISTORY ■Careful and precise ■ Time of injury and mechanism- Acceleration/ Impact injuries ■ Accident scene reconstruction ■ H/o LOC or seizures ■ h/o drug or alcohol intake
- 9. Head Injury- Examination VITALSIGNS: ■ Hypertension+ Bradycardia- Intracranial hematoma ■ Hypotension + Bradycardia- Cervical spine Injury ■ Hypotension + Tachycardia- Abdo/ Thoracic Injury
- 10. Head Injury- Examination ■Alternating hyperventilation and apnea- Cheyne Stokes breathing- diffuse b/l cortical dysfunction ■ Ataxic respiration- impaired cyclical rhythm- pontomedullary or medullary injury ■ Apneustic breathing- Prolonged pause at full inspiration- mid-caudal pons injury ■ Cluster Pattern- Lower medullary lesions
- 11. Head Injury- Examination GENERALEXAMINATION ■ Scalp Wounds/ Fractures ■ Nasal/ ear bleeding ■ CSF oto/ rhinorrhoea- skull base fractures ■ Raccoon/ Battle’s sign ■ Facial/mandibular fractures ■ SPINAL INJURY
- 12. Head Injury- Examination LEVELOF CONSCIOUSNESS ■ single most reliable indicator of severity of brain damage (Teasdale and Jennett) ■ COMA- inability to open eyes, speak and follow commands (GCS<8) ■ GCS- introduced in 1974
- 13. Head Injury-GCS Score innormal adults is 15 A. Eye opening Spontaneously 4 ■ To speech 3 ■ To pain 2 ■ None 1 B. Best verbal response ■ Orientated 5 ■ Confused 4 ■ Inappropr words 3 ■ Incompr sounds 2 ■ None 1 C. Best motor response ■ Obeys commands 6 ■ Localisation to pain 5 ■ Withdrawl to pain 4 ■ Spastic flexion to pain 3 ■ Extension to pain 2 ■ None 1
- 14. Head Injury-GCS Drawbacks: ■ Noaccount for pupils, PR, RR and BP ■ EOM, BS reflexes not included ■ b/l eye swelling/ aphasic/ dysphasic- inaccurate
- 15. Head Injury-GCS Condition Self-awarenessMotor function Pain perception Resp function PVS - No purposeful movements - N Locked in syndrome + Quadriplegic + N Akinetic mutism + Less movement + N Brain Death - - - -
- 16. Head Injury Severity basedon GCS Severity GCS Mild (80%) 13-15 Moderate (10%) 9-12 Severe (10%) 3-8
- 17. Head Injury- Examination MEMORY ■Immediate ■ Recent - hippocampal fornicial mamillo- thalamic tracts ■ Remote- cerebral cortex
- 18. Head Injury- Examination ■AGA-inability to lay down new memories following TBI ■ RGA – memory loss to events prior to injury ■ PTA- time from injury to return of memory process- same as RGA ■ PTA- directly related to severity of injury
- 19. Duration of PTASeverity 0-1 hr Mild 1-24 hrs moderate 1-7 days Severe > 7 days Very Severe Head Injury- Examination Classification using PTA
- 20. Head Injury- Examination PUPILS UNILATERALNONREACIVE DILATATION- TRANSTENTORIAL HERNIATION HUTCHINSON’S PUPILS
- 21. Head Injury- Examination PUPILS Pupillarysize Light response Interpretation U/L dilated Sluggish/fixed TT herniation (III n. palsy) B/l dilated Sluggish/fixed B/l III n. Palsy Brain death U/l dilated Marcus Gunn II n. injury B/l miotic Difficult to assess Opiates, metabolic encephalopathy, pos lesion U/l miotic normal Sympathetic injury
- 22. Head Injury- Examination EYEMOVEMENTS Resting eye position ■ Destructive Frontal lobe lesion (ICH)- conjugate eye deviation towards the lesion ■ Deep thalamic lesions- conjugate deviation away from lesion ■ U/l Pontine lesions- conjugate deviation away from lesion ■ Spontaneous slow roving eye movements- intact brainstem
- 23. Head Injury- Examination EYEMOVEMENTS ■ Thalamic/ Tectal lesions- Forced downgaze ■ Cerebellar/ Brainstem lesions- skew deviation/ vertical divergence ■ Pontine tegmental lesions- Ocular bobbing ■ Oculocephalic reflex (Doll’s Eye movements)- if BS intact- eyes lag behind and rolls to opposite side, with head turning (ABSENT IN ALERT PTS AND IN BS INJURY) ■ Oculovestibular reflex (caloric testing)
- 24. Treatment Basis ■ Primaryinjury Initial damage at impact Irreversible damaged neurones Partially injured –can recover Particularly susceptible to hypoxia and ischemia Initiates cascade of metabolic changes 10 days ↓ ■ Secondary neuronal damage
- 25. AIM Provide optimum circumstancesfor recovery from damage already sustained. Prevent Secondary injury Head Injury Management
- 26. Head Injury Management ■Secondary Injury ■ (Golden hour) – Hypoxia – Hypotension – ischaemia – hematoma
- 27. Early episodes ofhypotension or hypoxia greatly increase morbidity and mortality from severe head injury Head Injury Management
- 28. Impaired consciousness withALCOHOL intake -- manage along head injury lines -- rather than assuming due to alcohol Head Injury Management
- 29. Initial Management ■ A.Airway ■ B. Breathing ■ C. Circulation ■ D. Diagnosis
- 30. Head Injury Management AIRWAY Protectionof airway patency from vomit, blood FB, loose teeth Intubate if ■ Airway or ventilation is inadequate ■ Patient remains unresponsive (cannot protect airway) ■ Soft tissue swelling of face/neck Aspirated /lung contusion/ pneumo/ hemothorax Suspect cervical spine injury – careful during intubation
- 31. Head Injury Management BREATHING Controlledventilation (PCO 2 : 30 to 35) – Ensures normal O2 supply to brain – Prevents atelact. – expands collapsed alveoli – Combats restlessness – ↓ exhaust. resp. work. – IV Midazolam / Synchronizes Resp. with vent. – CT without artifact
- 32. Head Injury Management ■At least two IV lines – 0.9% NS – Maintain BP> 100 ■ Shock is usually not related to head injury Infants Terminal situations Suspect Cervical spine injury ■ Look for other injury- viscera, # femur CIRCULATION
- 33. Head Injury Management InitialAssessment in < 2 mts. Define problems requiring urgent diagnostic / therapeutic action ■ Level of Consciousness (GCS) ■ Pupillary size, reaction ■ Focal Neurologic Deficits
- 34. Head Injury Management ■Transportation- Cont. ABC ■ Treatment of life threatening emergency- pneumothorax etc. ■ Goal of emergency room T/T- prevent secondary insult from systemic abnormality or primary CNS injury.
- 35. Head Injury Management ■Quick re-assessment ■ CT Scan – Conservative – Surgery
- 36. Indications for Surgery ■Open compound wounds – CSF leak, brain come out ■ ↑ICP -in conjunction with clinical condition hematoma EDH SDH craniotomy ICH contusion refractory edema- decompressive craniotomy
- 37. Avoided or Corrected ■Hypoxia ■ Hypovolemia ■ Hypotension ■ Acidosis ■ ↑ ICP ■ Seizures ■ Edema ■ Pyrexia ■ Hypo/hypernatremia ■ Hyperglycemia ■ Anaemia
- 38. Head Injury Management GeneralTreatment ■ Normothermia / Mild hypothermia (340C) ■ Correct anemia – low Hb raises CBF ■ Control serum glucose ■ Maintain normal BP ■ Correct electrolyte – Hyponatremia
- 39. Conservative Treatment incases with no hematoma or post op. ■ Prevention of infection – antibiotics ■ Control of pain and restlessness ■ Bladder and bowel care ■ Control of ↑ ICP ■ Anticonvulsants Head Injury Treatment
- 40. Sedation/ Narcotics in restlesspatients Can be given after CT Scan has ruled out any sizeable lesion in the brain Head Injury Management
- 41. •History •G/E •Neurological examination •Skull X-Ray •Cervical spineX-Ray •Blood Alcohol levels CT HEAD - ideally in all but completely asymptomatic pts ADMI T DISCHARGE •Amnesia •H/o LOC •Deteriorating consciousness •Moderate-severe headache •Alcohol/drug intoxication •Skull fracture •CSF leak •Significant ass injuries •Abnormal CT scan •Does not meet criterion for admssion •Discuss need to return if problem
- 42. •Initial w/u •CT SCANIN ALL CASES ADMIT even if CT is normal Frequent neurological examinations FU CT Scan if deteriorates/before discharge If pt improves (90%) Discharge when stable If pt deteriorates (10%) Repeat CT Scan Manage as per severe HI
- 43. •History •Rescuscitation- ABC •Catheters •X-Rays- Cx/Chest/Skull/Abdomen/Pelvis/Extremities •G/E Emergency measuresfor ass injuries: •Tracheostomy •Chest tubes •Neck stabilization •Abdominal paracentesis Neurological examination
- 44. Intubate, Hyperventilate, Sedate,Mannitol (1g/kg) CT Scan Diffuse lesion Not Available Exploratory burr holes ICU •Monitor ICP •Elevate Head end •Sedate •Maintain Pao2 100 mm Hg •Maintain PaCo2 27-30 mm Hg ICP still high Treat ICP Surgical Lesion → OT
- 45. Monitor ICP ICP<20 ICP>20Check PaO2,PacO2 Head/ Neck position Treat pain, Fever Recalibrate ICP system Repeat CT Surgical Mass Lesion Craniotom y No Surgical mass lesion •Mannitol •Hyperventilate •Barbiturate Coma •DC
- 47. Head Injury Management SPECIFICHEAD INJURIES
- 48. Extradural Haematoma Biconvex hyperdense Management ■A surgical emergency ■ Evacuated as soon as possible ■ Excellent recovery
- 49. Acute Subdural Haematoma ■Concavo- convex ■ Injuries to the cortical veins or pial artery ■ Severe TBI. ■ mortality rate very high, 60%-80%. ■ High speed ground impact injury
- 50.
- 51. Chronic Subdural Haematoma ■Presents several weeks after a trivial trauma. ■ A simple burr hole evacuation curative. ■ May present to physician as stroke ■ May be B/L isodense
- 52. Intracerebral contusion/h’ge ■ Ifdeep, small or multiple observation ICP monitoring surgery for the largest lesion ■ If large surgical evacuation. ■ May deteriorate after several days because of increase in the size / edema
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- 55.
- 56. PRIMARY BRAIN STEMINJURY ■ 5-10% of all serious HI ■ True (Primary)/As part of DAI ■ Rent/tear/laceration/ Transection- Spinomedullary junction Pontomedullary junction Mesencephalo – pontine junction
- 57. PRIMARY BRAIN STEMINJURY ■ Clinical features – – Low GCS at admission – Immediate unconsciousness after accident – Persistant vegetative state – ICP < 20 ■ CT – Hemorrhage in ambient cistern – Blood along tent
- 58. Conclusion ■ Treatment shouldbe PROMPT (within golden hour) so that secondary brain damage can be avoided. ■ Doctors in periphery have a responsible job.
- 59. Conclusion ■ Management shouldbe done by a dedicated neurosurgical team with inputs from other specialities if required. ■ The best management plan would be a goal towards avoiding head injury.
- 60. Conclusion – Enforcement oftraffic rules and laws – Improved illumination, vehicle design, road conditions – Not mixing drink and driving – delays reflexes and judgment