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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
Objectives
• Anatomy and Pathophysiology of CNS trauma.
• Assessment and treatment
• Identify indications for spinal immobilization.
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
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
Anatomy: The Brain
• Frontal lobe
– Foresight, planning,
judgment,
movement
• Parietal lobe
– Sensation from body
surface
• Temporal lobe
– Hearing
– Speech
• Occipital lobe
– Vision
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
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
Intracranial Pressure
• Intracranial contents include:
– 80% brain tissue
– 10% blood
– 10% cerebrospinal fluid
• Intracranial volume or space is fixed.
Intracranial Pressure
• An increase in the volume of any of the three
contents may cause increased ICP.
– Swelling
– Bleeding
– CSF accumulation
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…
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
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).
The Endless Cycle…
• In the case of EDH or SDH, we can also add
the effect of the expanding hematoma.
Clinical Effects of ↑ ICP
• Pressure exerted down on the brain
– Cerebral cortex and RAS
• Altered level of consciousness
– Hypothalamus
• Vomiting
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
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
Patient Assessment
• The complete neurological exam consists of
six components:
– Mental status (MS)
– Cranial nerves
– Motor response
– Sensory response
– Coordination
– Reflexes
Mental Status–AVPU
• Initial Impression–how sick is this patient?
– Alert
– Responds to Verbal stimulus
– Responds to Painful stimulus
– Unresponsive
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
Traumatic Head and Brain Injury
• Mechanism of Injury
– Blunt
– Penetrating
• Type of Injury
– Closed
– Open
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)
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
Primary Brain Injury
• Concussion
– Temporary period of abnormal neurological
function that returns to normal without visible
structural damage to the brain.
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
Primary Brain Injury
• Intracranial
hematomas
– Epidural
– Subdural
– Intracerebral
Subarachnoid Hemorrhage
• The most common post-traumatic intracranial
bleed
• Signs and symptoms
– Headache
– Nausea, vomiting
• May cause increased ICP, vasospasm,
impaired cerebral circulation
Cerebral Laceration
• Tearing of brain tissue
• Can result from penetrating or blunt injury
Diffuse Axonal Injury
• Widespread damage to the nerve axons
• Symptoms
– Diffuse cerebral edema
– Loss of consciousness
– Increased ICP
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
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
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
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
Prehospital Care of CNS Trauma
• ABCs
• Spinal motion restriction
• Initial resuscitation
• Rapid transport
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
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
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
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
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
Intracranial Hypertension: Management
Additional management options
–Treatment of seizures
–Sedation
–Chemical paralysis
–Osmotherapy (mannitol)
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.
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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Head injury by Dr. sumit sinha

  • 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. Objectives • Anatomy and Pathophysiology of CNS trauma. • Assessment and treatment • Identify indications for spinal immobilization.
  • 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. 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. Anatomy: The Brain • Frontal lobe – Foresight, planning, judgment, movement • Parietal lobe – Sensation from body surface • Temporal lobe – Hearing – Speech • Occipital lobe – Vision
  • 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. 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. Intracranial Pressure • Intracranial contents include: – 80% brain tissue – 10% blood – 10% cerebrospinal fluid • Intracranial volume or space is fixed.
  • 9. Intracranial Pressure • An increase in the volume of any of the three contents may cause increased ICP. – Swelling – Bleeding – CSF accumulation
  • 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. 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. 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. The Endless Cycle… • In the case of EDH or SDH, we can also add the effect of the expanding hematoma.
  • 14. Clinical Effects of ↑ ICP • Pressure exerted down on the brain – Cerebral cortex and RAS • Altered level of consciousness – Hypothalamus • Vomiting
  • 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. 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. Patient Assessment • The complete neurological exam consists of six components: – Mental status (MS) – Cranial nerves – Motor response – Sensory response – Coordination – Reflexes
  • 18. Mental Status–AVPU • Initial Impression–how sick is this patient? – Alert – Responds to Verbal stimulus – Responds to Painful stimulus – Unresponsive
  • 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. Traumatic Head and Brain Injury • Mechanism of Injury – Blunt – Penetrating • Type of Injury – Closed – Open
  • 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. 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. Primary Brain Injury • Concussion – Temporary period of abnormal neurological function that returns to normal without visible structural damage to the brain.
  • 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. Primary Brain Injury • Intracranial hematomas – Epidural – Subdural – Intracerebral
  • 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. Cerebral Laceration • Tearing of brain tissue • Can result from penetrating or blunt injury
  • 28. Diffuse Axonal Injury • Widespread damage to the nerve axons • Symptoms – Diffuse cerebral edema – Loss of consciousness – Increased ICP
  • 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. 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. 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. 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. Prehospital Care of CNS Trauma • ABCs • Spinal motion restriction • Initial resuscitation • Rapid transport
  • 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. 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. 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. 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. 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. Intracranial Hypertension: Management Additional management options –Treatment of seizures –Sedation –Chemical paralysis –Osmotherapy (mannitol)
  • 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. 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).
  • 42. ?