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Head injury by Dr. sumit sinha

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Head injuries can be caused by various reasons but it can be easily treated by Dr. Sumit Sinha.

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Head injury by Dr. sumit sinha

  1. 1. HEAD INJURY Dr Sumit Sinha MBBS, MS, DNB, MCh Faculty, AO Spine Faculty, Advanced Trauma Life Support Associate Professor, Deptt of Neurosurgery, AIIMS and JPNATC, New Delhi
  2. 2. Objectives • Anatomy and Pathophysiology of CNS trauma. • Assessment and treatment • Identify indications for spinal immobilization.
  3. 3. Head and Brain Trauma • Worldwide, there are approximately: – 200 to 300 cases of TBI per 100,000 population – 25 cases of severe TBI per 100,000 population • In the US: – 4 million head injuries/ year – 1.4 million treated in hospitals – 300,000 admitted/ year – 90,000 with residual neurologic deficit
  4. 4. Anatomy: Skull and Brain Skull Periosteum Dura mater } One functional layer Arachnoid membrane Pia mater Vessels in subarachnoid space Epidural space Subdural space Subarachnoid space
  5. 5. Anatomy: The Brain • Frontal lobe – Foresight, planning, judgment, movement • Parietal lobe – Sensation from body surface • Temporal lobe – Hearing – Speech • Occipital lobe – Vision
  6. 6. Pathophysiology of CNS Injury • Primary injury – Damage that occurs at the moment of impact • Secondary injury – Damage that occurs subsequent to the initial impact • Systemic causes • Intrinsic causes
  7. 7. Brain Metabolism and Perfusion • Perfusion of the brain depends on maintaining Cerebral Blood Flow (CBF). • Flow requires pressure gradient, referred to as Cerebral Perfusion Pressure (CPP). – CPP is the pressure that keeps blood moving through the brain. • Autoregulation allows BP changes to maintain CPP. • CPP = Mean Arterial Pressure (MAP) – Intracranial Pressure (ICP) • ICP is usually 10 to 15 mm Hg
  8. 8. Intracranial Pressure • Intracranial contents include: – 80% brain tissue – 10% blood – 10% cerebrospinal fluid • Intracranial volume or space is fixed.
  9. 9. Intracranial Pressure • An increase in the volume of any of the three contents may cause increased ICP. – Swelling – Bleeding – CSF accumulation
  10. 10. Intracranial Pressure • As ICP increases, everything in the skull is compressed: – Blood vessels – CSF – Brain • You can displace a small amount of blood; • You can displace a small amount of CSF; • But…
  11. 11. Pathophysiology of Brain Injury • Hypercarbia (hypoventilation) causes cerebral vasodilation. – Results in ↑ blood volume ⇨ ↑ ICP ⇨ ↓ CPP • Hypotension results in ↓ CPP ⇨ cerebral vasodilation. – Results in ↑ blood volume ⇨ ↑ ICP ⇨ ↓ CPP
  12. 12. Pathophysiology of Brain Injury • As ICP ↑ and approaches MAP, CBF ↓ ⇨ ↓ CPP. – Compensatory mechanisms attempt to ↑ MAP. – As CPP ↓, cerebral vasodilation occurs to ↑ blood volume, and the body tries to ↑ CBF. – This leads to further ↑ ICP, ↓ CPP, and so on. – If pressure inside the skull exceeds mean arterial pressure, blood flow to brain stops (CPP = MAP – ICP).
  13. 13. The Endless Cycle… • In the case of EDH or SDH, we can also add the effect of the expanding hematoma.
  14. 14. Clinical Effects of ↑ ICP • Pressure exerted down on the brain – Cerebral cortex and RAS • Altered level of consciousness – Hypothalamus • Vomiting
  15. 15. Clinical Effects of ↑ ICP • Pressure exerted down on the brain – Brain stem • ↑ BP to force blood into the brain against ↑ ICP • Bradycardia 2° vagal stimulation and ↑ BP • Irregular respirations (↑ CO2) or tachypnea (↓ CO2) • Unequal/unreactive pupils 2° cranial nerve III compression • Abnormal posturing (flexion or extension) • Seizures – Herniation of the brain
  16. 16. Patient Assessment • Primary Survey – Determine the mechanism of injury and the need to consider possible spine injury. – Airway compromise? – Ventilatory compromise? – Adequate oxygenation? – Adequate circulation and perfusion? • Neurologic Assessment for Disability
  17. 17. Patient Assessment • The complete neurological exam consists of six components: – Mental status (MS) – Cranial nerves – Motor response – Sensory response – Coordination – Reflexes
  18. 18. Mental Status–AVPU • Initial Impression–how sick is this patient? – Alert – Responds to Verbal stimulus – Responds to Painful stimulus – Unresponsive
  19. 19. Glasgow Coma Scale Eye Opening Spontaneous = 4 To Voice = 3 To Pain = 2 None = 1 Verbal Response Oriented = 5 Confused = 4 Inappropriate Words = 3 Incomprehensible Sounds = 1 None = 1 Motor Response Follows Commands = 6 Localizes Pain = 5 Withdraws = 4 Flexion = 3 Extension = 2 None = 1 • Use the modified GCS for pediatrics. • WHEN do you score the GCS? AFTER the correctible causes of altered mental status have been addressed
  20. 20. Traumatic Head and Brain Injury • Mechanism of Injury – Blunt – Penetrating • Type of Injury – Closed – Open
  21. 21. Traumatic Head and Brain Injury Primary brain injury – Skull fracture – Concussion – Brain contusion – Intracranial hemorrhage • Epidural • Subdural • Subarachnoid • Intracerebral – Cerebral laceration – Diffuse axonal injury (DAI) Secondary brain injury • Systemic causes – Hypotension – Hypoxia – Cerebral edema – Increased ICP – Intracranial infection – Seizure • Intrinsic causes – Seizures – Edema – Hematomas – Increased intracranial pressure (ICP)
  22. 22. Primary Brain Injury • Skull fracture – Injury to the brain’s protective case – Indicates significant force, • So you have to ask… “What happened to the brain (and neck)?” – Presence increases suspicion for intracranial hematoma and TBI – Types of skull fractures • Linear (80%) • Depressed • Open/closed • Basilar
  23. 23. Primary Brain Injury • Concussion – Temporary period of abnormal neurological function that returns to normal without visible structural damage to the brain.
  24. 24. Primary Brain Injury • Brain contusion – Bruising of brain tissue – Signs and symptoms • Altered mental status • Loss of consciousness • Vomiting • Focal neurologic abnormalities – Depending on the area of the brain injured – May be associated with cerebral edema causing increased ICP
  25. 25. Primary Brain Injury • Intracranial hematomas – Epidural – Subdural – Intracerebral
  26. 26. Subarachnoid Hemorrhage • The most common post-traumatic intracranial bleed • Signs and symptoms – Headache – Nausea, vomiting • May cause increased ICP, vasospasm, impaired cerebral circulation
  27. 27. Cerebral Laceration • Tearing of brain tissue • Can result from penetrating or blunt injury
  28. 28. Diffuse Axonal Injury • Widespread damage to the nerve axons • Symptoms – Diffuse cerebral edema – Loss of consciousness – Increased ICP
  29. 29. The Bottom Line… • So… how do you know, in the field, what brain injury your patient has? • Most of the bad TBI stuff presents about the same way: • Headache • Vomiting • Altered mentation • Neurologic deficits
  30. 30. Assessment of Head Injury • Change in LOC- earliest and best indicator of patient’s ICP. – Evaluation methods • AVPU system • GCS score • Early detection of increasing ICP is critical– before herniation has occurred. Assess and re-assess
  31. 31. Intracranial Hypertension • Warning signs of possible increasing ICP and impending herniation – Decline in GCS score of 2 points or more – Development of sluggish or nonreactive pupil – Development of hemiplegia or hemiparesis – Cushing’s phenomenon
  32. 32. Intracranial Hypertension • Signs of intracranial hypertension – Cushing’s phenomenon (triad) • Bradycardia • Hypertension • Alterations in ventilatory patterns (e.g., Cheyne– Stokes) – Abnormal motor posturing • Decorticate • Decerebrate
  33. 33. Prehospital Care of CNS Trauma • ABCs • Spinal motion restriction • Initial resuscitation • Rapid transport
  34. 34. Management of CNS Trauma – Open it. • Maintain spinal motion restriction • Jaw thrust – Clear it. • Use suction as needed. – Maintain it • GCS 9 or more ? Able to maintain patency? – If not, use airway management. Airway MONITOR: Oxygen saturation (95% or higher) Blood pressure ETCO2
  35. 35. Management of CNS Trauma • Studies have shown that prehospital intubation and RSI have been associated with worse patient outcomes. • RSI has been associated with: – Hypoxia – Hypercarbia – Hypocarbia – Hypotension
  36. 36. Management of CNS Trauma Breathing – Provide oxygen (100%) – Assist ventilations (as needed) • Maintain normal EtCO2 35 to 40 mm Hg • Rate: – Adults: 10 to 12 breaths per min – Peds: 12 to 20 breaths per min NO ROUTINE hyperventilation
  37. 37. Management of CNS Trauma • Hyperventilation indicated for: – Bilateral dilated and unresponsive pupils – Unequal pupils (with altered LOC) – Abnormal posturing – Neurologic deterioration (decrease in GCS of two or more points in patient with initial GCS <9) Target – EtCO2 30 to 35 mm Hg
  38. 38. Management of CNS Trauma Circulation – Prevent anemia: control hemorrhage. EVERY RBC COUNTS! – Maintain adequate BP and perfusion. – If BP is normal or elevated: • IV of LR/NS – If BP is decreased: • IV of LR/NS bolus, titrate BP to a minimum of 90 mm Hg
  39. 39. Intracranial Hypertension: Management Additional management options –Treatment of seizures –Sedation –Chemical paralysis –Osmotherapy (mannitol)
  40. 40. Summary • Identify the mechanism of injury. • Primary survey: identify and treat life- threatening conditions first. • Shock is a late finding in patients with TBI; consider the possibility of internal hemorrhage.
  41. 41. Summary • Assess indications for immobilization. – When in doubt, immobilize. • The most important sign of TBI is a change in mental status. • Key aspect is to determine if baseline assessment findings are changing and in which direction (better or worse).
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