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Common major trauma
4 million people experience head trauma
annually
 Severe head injury is most frequent cause of trauma death
At Risk population
 Males 15-24 years
 Infants
 Young Children
 Elderly
INTRODUCTION TO HEAD
INJURIES
TIME IS CRITICAL
 Intracranial Hemorrhage
 Progressing Edema
 Increased ICP
 Cerebral Hypoxia
 Permanent Damage
Severity is difficult to recognize
 Subtle signs
 Improve differential diagnosis
 Improves survivability
INTRODUCTION TO HEAD
INJURIES
Mechanism of Injury
 Blunt Injury
 Motor vehicle collisions
 Assaults
 Falls
 Penetrating Injury
 Gunshot wounds
 Stabbing
 Explosions
PATHOPHYSIOLOGY OF
HEAD INJURY
Head Injury
Cranial Injury
Brain Injury
DIFFERENT TYPES OF INJURY
HEAD INJURY
Open
• Skull compromised
and brain exposed
Closed
• Skull not compromised
and brain not exposed
5Head Trauma -
Contusions
Lacerations
Avulsions
Significant Hemorrhage
SCALP INJURY
HEAD INJURIES
Scalp wound
• Highly vascular, bleeds briskly
 Shock: child may develop
 Shock: adult another cause
• Management
 No unstable fracture:
direct pressure, dressings
 Unstable fracture: dressings, avoid direct pressure
7Head Trauma -
Skull fracture
• Linear nondisplaced
• Depressed
• Compound
Suspect fracture
• Large contusion or darkened swelling
Management
• Dressing, avoid excess pressure
HEAD INJURIES
8Head Trauma -
Trauma must be extreme to fracture
 Linear
 Depressed
 Open
 Impaled Object
CRANIAL INJURY
Basal Skull
 Unprotected
 Spaces weaken
structure
 Relatively
easier to fracture
Basal Skull Fracture Signs
 Battle’s Signs
 Retroauricular Ecchymosis
 Associated with fracture of
auditory canal and lower
areas of skull
 Raccoon Eyes
 Bilateral Periorbital
Ecchymosis
 Associated with orbital
fractures
CRANIAL INJURY
BASILAR SKULL FRACTURE
Battle’s sign Raccoon eyes
12Head Trauma -
Basilar Skull Fracture
 May tear dura
 Permit CSF to drain through an
external passageway
 May mediate rise of ICP
 Evaluate for “Target” or “Halo” sign
CRANIAL INJURY
CRAINIAL INJURIES
Penetrating trauma
14Head Trauma -
Bullet fragments
Head Trauma - 15
Forces that cause skull fracture
can also cause brain injury.
As defined by the National Head Injury Foundation
 “a traumatic insult to the brain capable of producing physical,
intellectual, emotional, social and vocational changes.”
BRAIN INJURY
BRAIN INJURY
Response to injury
• Swelling of brain
 Vasodilatation with increased blood volume
 Increased ICP
• Decreased blood flow to brain
 Perfusion decreases
 Cerebral ischemia (hypoxia)
17Head Trauma -
Altered Mental Status
 Altered orientation
 Alteration in personality
 Amnesia
 Retrograde
 Antegrade
Cushing’s Reflex
 Increased BP
 Bradycardia
 Erratic respirations
SIGNS & SYMPTOMS
OF BRAIN INJURY
 Vomiting
 Without nausea
 Projectile
 Body temperature
changes
 Changes in pupil
reactivity
 Decorticate
posturing
Pathophysiology of Changes
 Frontal Lobe Injury
 Alterations in personality
 Occipital Lobe Injury
 Visual disturbances
 Cortical Disruption
 Reduce mental status or Amnesia
 Retrograde
 Unable to recall events before injury
 Antegrade
 Unable to recall events after trauma
 “Repetitive Questioning”
 Focal Deficits
 Hemiplegia, Weakness or Seizures
SIGNS & SYMPTOMS
OF BRAIN INJURY
Classification
Direct
Primary injury caused by forces of trauma
Indirect
Secondary injury caused by factors resulting from the
primary injury
BRAIN INJURY
Direct brain injury
• Immediate damage
due to force
• Coup and contracoup
• Fixed at time of injury
Management
• Directed at prevention
21Head Trauma -
Coup
 Injury at site of impact
Contrecoup
 Injury on opposite side
from impact
DIRECT BRAIN INJURY TYPES
BRAIN INJURY
Indirect brain injury
• Results from hypoxia
or decreased perfusion
• Response to primary injury
• Develops over hours
Management
• Good prehospital care can help prevent
23Head Trauma -
Focal
 Occur at a specific location in brain
 Differentials
 Cerebral Contusion
 Intracranial Hemorrhage
 Epidural hematoma
 Subdural hematoma
 Intracerebral Hemorrhage
Diffuse
 Concussion
 Moderate Diffuse Axonal Injury
 Severe Diffuse Axonal Injury
DIRECT BRAIN INJURY
CATEGORIES
Cerebral Contusion
 Blunt trauma to local brain tissue
 Capillary bleeding into brain tissue
 Common with blunt head trauma
 Confusion
 Neurologic deficit
 Personality changes
 Vision changes
 Speech changes
 Results from
 Coup-contrecoup injury
FOCAL BRAIN INJURY
BRAIN INJURIES
Cerebral contusion
• Bruising of brain tissue
 Swelling may be rapid and severe
• Level of consciousness
 Prolonged unconsciousness,
profound confusion or amnesia
• Associated symptoms
 Focal neurological signs
 May have personality changes
26Head Trauma -
Epidural Hematoma
 Bleeding between dura mater
and skull
 Involves arteries
 Middle meningeal artery most
common
 Rapid bleeding & reduction of
oxygen to tissues
 Herniates brain toward foramen
magnum
FOCAL BRAIN INJURY
INTRACRANIAL HEMORRHAGE
INTRACRANIAL
HEMORRHAGE
Acute epidural hematoma
• Arterial bleed
 Temporal fracture common
 Onset: minutes to hours
• Level of consciousness
 Initial loss of consciousness
 “Lucid interval” follows
• Associated symptoms
 Ipsilateral dilated fixed pupil, signs of increasing ICP, unconsciousness, contralateral
paralysis, death
28Head Trauma -
Subdural Hematoma
 Bleeding within meninges
 Beneath dura mater & within subarachnoid
space
 Above pia mater
 Slow bleeding
 Superior sagital sinus
 Signs progress over several days
 Slow deterioration of mentation
FOCAL BRAIN INJURY
INTRACRANIAL HEMORRHAGE
INTRACRANIAL
HEMORRHAGE
Acute subdural hematoma
• Venous bleed
 Onset: hours to days
• Level of consciousness
 Fluctuations
• Associated symptoms
 Headache
 Focal neurologic signs
• High-risk
 Alcoholics, elderly, taking anticoagulants
30Head Trauma -
INTRACRANIAL
HEMORRHAGE
Intracerebral hemorrhage
• Arterial or venous
 Surgery is often not helpful
• Level of consciousness
 Alterations common
• Associated symptoms
 Varies with region and degree
 Pattern similar to stroke
 Headache and vomiting
31Head Trauma -
Intracerebral Hemorrhage
 Rupture blood vessel within the brain
 Presentation similar to stroke symptoms
 Signs and symptoms worsen over time
FOCAL BRAIN INJURY
INTRACRANIAL HEMORRHAGE
Due to stretching forces placed on individual nerve cells
Pathology distributed throughout brain
Types
 Concussion
 Moderate Diffuse Axonal Injury
 Severe Diffuse Axonal Injury
DIFFUSE BRAIN INJURY
Mild to moderate form of Diffuse Axonal Injury
(DAI)
 Nerve dysfunction without anatomic damage
Transient episode of
 Confusion, Disorientation, Event amnesia
Suspect if patient has a momentary loss of
consciousness
Management
 Frequent reassessment of mentation
 ABC’s
DIFFUSE BRAIN INJURY
CONCUSSION
BRAIN INJURIES
Concussion
• No structural injury to brain
• Level of consciousness
 Variable period of unconsciousness or confusion
 Followed by return to normal consciousness
• Retrograde short-term amnesia
 May repeat questions over and over
• Associated symptoms
 Dizziness, headache, ringing in ears, and/or nausea
35Head Trauma -
“Classic Concussion”
Same mechanism as concussion
 Additional: Minute bruising of brain tissue
Unconsciousness
May exist with a basilar skull fracture
Signs & Symptoms
 Unconsciousness or Persistent confusion
 Loss of concentration, disorientation
 Retrograde & Antegrade amnesia
 Visual and sensory disturbances
 Mood or Personality changes
DIFFUSE BRAIN INJURY
MODERATE DIFFUSE AXONAL
INJURY
BRAIN INJURIES
Diffuse axonal injury
• Diffuse injury
 Generalized edema
 No structural lesion
 Most common injury from
severe blunt head trauma
• Associated symptoms
 Unconscious
 No focal deficits
37Head Trauma -
Brainstem Injury
Significant mechanical disruption of nerve
cells
 Cerebral hemispheres and brainstem
High mortality rate
Signs & Symptoms
 Prolonged unconsciousness
 Cushing’s reflex
 Decorticate or Decerebrate posturing
DIFFUSE BRAIN INJURY
SEVERE DIFFUSE AXONAL
INJURY
BRAIN ANATOMY
Intracranial volume
• Brain
• CSF
• Blood vessel volume
 Dilatation with high pCO2
 Constriction with low pCO2
 Slight effect on volume
39Head Trauma -
Cranial volume fixed
 80% = Cerebrum, cerebellum & brainstem
 12% = Blood vessels & blood
 8% = CSF
 Increase in size of one component diminishes size of another
 Inability to adjust = increased ICP
INTRACRANIAL PERFUSION
Compensating for Pressure
 Compress venous blood vessels
 Reduction in free CSF
 Pushed into spinal cord
Decompensating for Pressure
 Increase in ICP
 Rise in systemic BP to perfuse brain
 Further increase of ICP
INTRACRANIAL PERFUSION
ICP BP
Vasculature Constriction
Cerebral Edema
Systolic Blood Pressure
 Low BP = Poor Cerebral Perfusion
 High BP = Increased ICP
Carbon Dioxide
Reduced respiratory efficiency
FACTORS AFFECTING ICP
Role of Carbon Dioxide
 Increase of CO2 in CSF
 Cerebral Vasodilation
 Encourage blood flow
 Reduce hypercarbia
 Reduce hypoxia
 Contributes to  ICP
 Reduced levels of CO2 in CSF
 Cerebral vasoconstriction
 Results in cerebral anoxia
INTRACRANIAL PRESSURE
Increased pressure
 Compresses brain tissue
 Herniates brainstem
 Compromises blood supply
 Signs & Symptoms
 Upper Brainstem
 Vomiting
 Altered mental status
 Pupillary dilation
 Medulla Oblongata
 Respiratory
 Cardiovascular
 Blood Pressure disturbances
PRESSURE & STRUCTURAL DISPLACEMENT
Upper Brainstem Compression
 Increasing blood pressure
 Reflex bradycardia
 Vagus nerve stimulation
 Cheyne-Stokes respirations
 Pupils become small and reactive
 Decorticate posturing
 Neural pathway disruption
SIGNS & SYMPTOMS OF BRAIN INJURY
PHYSIOLOGICAL CHANGES
Middle Brainstem Compression
 Widening pulse pressure
 Increasing bradycardia
 CNS Hyperventilation
 Deep and Rapid
 Bilateral pupil sluggishness or inactivity
 Decerebrate posturing
SIGNS & SYMPTOMS OF BRAIN INJURY
PHYSIOLOGICAL CHANGES
Lower Brainstem Injury
 Pupils dilated and unreactive
 Ataxic respirations
 Erratic with no pattern
 Irregular and erratic pulse rate
 ECG Changes
 Hypotension
 Loss of response to painful stimuli
SIGNS & SYMPTOMS OF BRAIN INJURY
PHYSIOLOGICAL CHANGES
Physiological Issues
 Indicate pressure on
 CN-III (Oculomotor Nerve)
 Pressure on nerve causes eyes to be sluggish, then dilated, and finally fixed
 Reduced peripheral blood flow
Pupil Size & Reactivity
 Reduced Pupillary Responsiveness
 Depressant drugs or Cerebral Hypoxia
 Fixed & Dilated
 Extreme Hypoxia
SIGNS & SYMPTOMS OF BRAIN INJURY
EYE SIGNS
HEAD TRAUMA ASSESSMENT
Initial Assessment
Rapid Trauma Exam
Limit patient agitation, straining
• Contributes to elevated ICP
Airway
• Vomiting very common within first hour
• Endotracheal intubation
50Head Trauma -
Head Trauma - 51
Decreased level of consciousness
is an early indicator of
brain injury or rising ICP.
 Reactive: ICP increasing
 Nonreactive (altered LOC):
increased ICP
 Nonreactive (normal LOC): not
from head injury
PUPILS
Both dilated
 Nonreactive: brainstem
 Reactive: often reversible
Unilaterally dilated
52Head Trauma -
Eyelid closure
• Slow: cranial nerve III
• Fluttering: often hysteria
Anisocoria
GLASGOW COMA SCALE
Suspect severe brain injury GCS <9
53Head Trauma -
*Decorticate posturing to pain
**Decerebrate posturing to pain
EXTREMITY POSTURING
Decorticate
• Arms flexed
and legs extended
Decerebrate
• Arms extended
and legs extended
54Head Trauma -
INCREASING ICP
55Head Trauma -
Vital Sign Change with Increasing ICP
Respiration Increase, decrease, irregular
Pulse Decrease
BP Increase, widening pulse
pressure
Cushing’s response
• As ICP increases, systolic BP increases
• As systolic BP increases, pulse rate decreases
Head Trauma - 56
Early efforts
to maintain brain perfusion
can be life-saving.
THE INJURED BRAIN
Hypoxia
• Perfusion decrease causes cerebral ischemia
• Hyperventilation increases hypoxia
significantly more than it decreases ICP
Assist ventilation
• High-flow oxygen
• One breath every 6–8 seconds
• SpO2 >95%
• Maintain EtCO2 at 35 mmHg
57Head Trauma -
THE INJURED BRAIN
Hypotension
• Single instance increases mortality
 Adult (systolic <90 mmHg) 150%
 Child (systolic < age appropriate) worse
Fluid administration for traumatic brain injury, GCS <9
• Titrate to 110–120 mmHg systolic
with or without penetrating hemorrhage
to maintain CPP
58Head Trauma -
THE INJURED BRAIN
Cerebral herniation syndrome
• Brain forced downward
 CSF flow obstructed, pressure on brainstem
• Level of consciousness
 Decreasing, rapid progression to coma
• Associated symptoms
 Ipsilateral pupil dilatation, out-downward deviation
 Contralateral paralysis or decerebrate posturing
 Respiratory arrest, death
59Head Trauma -
CEREBRAL HERNIATION
Is ICP severe enough
to outweigh cerebral ischemia?
60Head Trauma -
HYPERVENTILATION
Cerebral herniation syndrome
• Herniation danger outweighs hypoxia
Indications for hyperventilation
• TBI GCS <9 with decerebrate posturing
• TBI GCS <9 with dilated or nonreactive pupils
• TBI initial GCS <9, then drops >2 points
If signs resolve, stop hyperventilation.
61Head Trauma -
HYPERVENTILATION RATES
Capnography
• Maintain EtCO2 <30 mmHg, but >25 mmHg
62Head Trauma -
Age Group Normal Rate Hyperventilatio
n
Adult 8–10 per minute 20 per minute
Children 15 per minute 25 per minute
Infants 20 per minute 30 per minute
THANK YOU

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Head injuries

  • 1. Common major trauma 4 million people experience head trauma annually  Severe head injury is most frequent cause of trauma death At Risk population  Males 15-24 years  Infants  Young Children  Elderly INTRODUCTION TO HEAD INJURIES
  • 2. TIME IS CRITICAL  Intracranial Hemorrhage  Progressing Edema  Increased ICP  Cerebral Hypoxia  Permanent Damage Severity is difficult to recognize  Subtle signs  Improve differential diagnosis  Improves survivability INTRODUCTION TO HEAD INJURIES
  • 3. Mechanism of Injury  Blunt Injury  Motor vehicle collisions  Assaults  Falls  Penetrating Injury  Gunshot wounds  Stabbing  Explosions PATHOPHYSIOLOGY OF HEAD INJURY
  • 4. Head Injury Cranial Injury Brain Injury DIFFERENT TYPES OF INJURY
  • 5. HEAD INJURY Open • Skull compromised and brain exposed Closed • Skull not compromised and brain not exposed 5Head Trauma -
  • 7. HEAD INJURIES Scalp wound • Highly vascular, bleeds briskly  Shock: child may develop  Shock: adult another cause • Management  No unstable fracture: direct pressure, dressings  Unstable fracture: dressings, avoid direct pressure 7Head Trauma -
  • 8. Skull fracture • Linear nondisplaced • Depressed • Compound Suspect fracture • Large contusion or darkened swelling Management • Dressing, avoid excess pressure HEAD INJURIES 8Head Trauma -
  • 9. Trauma must be extreme to fracture  Linear  Depressed  Open  Impaled Object CRANIAL INJURY
  • 10. Basal Skull  Unprotected  Spaces weaken structure  Relatively easier to fracture
  • 11. Basal Skull Fracture Signs  Battle’s Signs  Retroauricular Ecchymosis  Associated with fracture of auditory canal and lower areas of skull  Raccoon Eyes  Bilateral Periorbital Ecchymosis  Associated with orbital fractures CRANIAL INJURY
  • 12. BASILAR SKULL FRACTURE Battle’s sign Raccoon eyes 12Head Trauma -
  • 13. Basilar Skull Fracture  May tear dura  Permit CSF to drain through an external passageway  May mediate rise of ICP  Evaluate for “Target” or “Halo” sign CRANIAL INJURY
  • 14. CRAINIAL INJURIES Penetrating trauma 14Head Trauma - Bullet fragments
  • 15. Head Trauma - 15 Forces that cause skull fracture can also cause brain injury.
  • 16. As defined by the National Head Injury Foundation  “a traumatic insult to the brain capable of producing physical, intellectual, emotional, social and vocational changes.” BRAIN INJURY
  • 17. BRAIN INJURY Response to injury • Swelling of brain  Vasodilatation with increased blood volume  Increased ICP • Decreased blood flow to brain  Perfusion decreases  Cerebral ischemia (hypoxia) 17Head Trauma -
  • 18. Altered Mental Status  Altered orientation  Alteration in personality  Amnesia  Retrograde  Antegrade Cushing’s Reflex  Increased BP  Bradycardia  Erratic respirations SIGNS & SYMPTOMS OF BRAIN INJURY  Vomiting  Without nausea  Projectile  Body temperature changes  Changes in pupil reactivity  Decorticate posturing
  • 19. Pathophysiology of Changes  Frontal Lobe Injury  Alterations in personality  Occipital Lobe Injury  Visual disturbances  Cortical Disruption  Reduce mental status or Amnesia  Retrograde  Unable to recall events before injury  Antegrade  Unable to recall events after trauma  “Repetitive Questioning”  Focal Deficits  Hemiplegia, Weakness or Seizures SIGNS & SYMPTOMS OF BRAIN INJURY
  • 20. Classification Direct Primary injury caused by forces of trauma Indirect Secondary injury caused by factors resulting from the primary injury
  • 21. BRAIN INJURY Direct brain injury • Immediate damage due to force • Coup and contracoup • Fixed at time of injury Management • Directed at prevention 21Head Trauma -
  • 22. Coup  Injury at site of impact Contrecoup  Injury on opposite side from impact DIRECT BRAIN INJURY TYPES
  • 23. BRAIN INJURY Indirect brain injury • Results from hypoxia or decreased perfusion • Response to primary injury • Develops over hours Management • Good prehospital care can help prevent 23Head Trauma -
  • 24. Focal  Occur at a specific location in brain  Differentials  Cerebral Contusion  Intracranial Hemorrhage  Epidural hematoma  Subdural hematoma  Intracerebral Hemorrhage Diffuse  Concussion  Moderate Diffuse Axonal Injury  Severe Diffuse Axonal Injury DIRECT BRAIN INJURY CATEGORIES
  • 25. Cerebral Contusion  Blunt trauma to local brain tissue  Capillary bleeding into brain tissue  Common with blunt head trauma  Confusion  Neurologic deficit  Personality changes  Vision changes  Speech changes  Results from  Coup-contrecoup injury FOCAL BRAIN INJURY
  • 26. BRAIN INJURIES Cerebral contusion • Bruising of brain tissue  Swelling may be rapid and severe • Level of consciousness  Prolonged unconsciousness, profound confusion or amnesia • Associated symptoms  Focal neurological signs  May have personality changes 26Head Trauma -
  • 27. Epidural Hematoma  Bleeding between dura mater and skull  Involves arteries  Middle meningeal artery most common  Rapid bleeding & reduction of oxygen to tissues  Herniates brain toward foramen magnum FOCAL BRAIN INJURY INTRACRANIAL HEMORRHAGE
  • 28. INTRACRANIAL HEMORRHAGE Acute epidural hematoma • Arterial bleed  Temporal fracture common  Onset: minutes to hours • Level of consciousness  Initial loss of consciousness  “Lucid interval” follows • Associated symptoms  Ipsilateral dilated fixed pupil, signs of increasing ICP, unconsciousness, contralateral paralysis, death 28Head Trauma -
  • 29. Subdural Hematoma  Bleeding within meninges  Beneath dura mater & within subarachnoid space  Above pia mater  Slow bleeding  Superior sagital sinus  Signs progress over several days  Slow deterioration of mentation FOCAL BRAIN INJURY INTRACRANIAL HEMORRHAGE
  • 30. INTRACRANIAL HEMORRHAGE Acute subdural hematoma • Venous bleed  Onset: hours to days • Level of consciousness  Fluctuations • Associated symptoms  Headache  Focal neurologic signs • High-risk  Alcoholics, elderly, taking anticoagulants 30Head Trauma -
  • 31. INTRACRANIAL HEMORRHAGE Intracerebral hemorrhage • Arterial or venous  Surgery is often not helpful • Level of consciousness  Alterations common • Associated symptoms  Varies with region and degree  Pattern similar to stroke  Headache and vomiting 31Head Trauma -
  • 32. Intracerebral Hemorrhage  Rupture blood vessel within the brain  Presentation similar to stroke symptoms  Signs and symptoms worsen over time FOCAL BRAIN INJURY INTRACRANIAL HEMORRHAGE
  • 33. Due to stretching forces placed on individual nerve cells Pathology distributed throughout brain Types  Concussion  Moderate Diffuse Axonal Injury  Severe Diffuse Axonal Injury DIFFUSE BRAIN INJURY
  • 34. Mild to moderate form of Diffuse Axonal Injury (DAI)  Nerve dysfunction without anatomic damage Transient episode of  Confusion, Disorientation, Event amnesia Suspect if patient has a momentary loss of consciousness Management  Frequent reassessment of mentation  ABC’s DIFFUSE BRAIN INJURY CONCUSSION
  • 35. BRAIN INJURIES Concussion • No structural injury to brain • Level of consciousness  Variable period of unconsciousness or confusion  Followed by return to normal consciousness • Retrograde short-term amnesia  May repeat questions over and over • Associated symptoms  Dizziness, headache, ringing in ears, and/or nausea 35Head Trauma -
  • 36. “Classic Concussion” Same mechanism as concussion  Additional: Minute bruising of brain tissue Unconsciousness May exist with a basilar skull fracture Signs & Symptoms  Unconsciousness or Persistent confusion  Loss of concentration, disorientation  Retrograde & Antegrade amnesia  Visual and sensory disturbances  Mood or Personality changes DIFFUSE BRAIN INJURY MODERATE DIFFUSE AXONAL INJURY
  • 37. BRAIN INJURIES Diffuse axonal injury • Diffuse injury  Generalized edema  No structural lesion  Most common injury from severe blunt head trauma • Associated symptoms  Unconscious  No focal deficits 37Head Trauma -
  • 38. Brainstem Injury Significant mechanical disruption of nerve cells  Cerebral hemispheres and brainstem High mortality rate Signs & Symptoms  Prolonged unconsciousness  Cushing’s reflex  Decorticate or Decerebrate posturing DIFFUSE BRAIN INJURY SEVERE DIFFUSE AXONAL INJURY
  • 39. BRAIN ANATOMY Intracranial volume • Brain • CSF • Blood vessel volume  Dilatation with high pCO2  Constriction with low pCO2  Slight effect on volume 39Head Trauma -
  • 40. Cranial volume fixed  80% = Cerebrum, cerebellum & brainstem  12% = Blood vessels & blood  8% = CSF  Increase in size of one component diminishes size of another  Inability to adjust = increased ICP INTRACRANIAL PERFUSION
  • 41. Compensating for Pressure  Compress venous blood vessels  Reduction in free CSF  Pushed into spinal cord Decompensating for Pressure  Increase in ICP  Rise in systemic BP to perfuse brain  Further increase of ICP INTRACRANIAL PERFUSION ICP BP
  • 42. Vasculature Constriction Cerebral Edema Systolic Blood Pressure  Low BP = Poor Cerebral Perfusion  High BP = Increased ICP Carbon Dioxide Reduced respiratory efficiency FACTORS AFFECTING ICP
  • 43. Role of Carbon Dioxide  Increase of CO2 in CSF  Cerebral Vasodilation  Encourage blood flow  Reduce hypercarbia  Reduce hypoxia  Contributes to  ICP  Reduced levels of CO2 in CSF  Cerebral vasoconstriction  Results in cerebral anoxia INTRACRANIAL PRESSURE
  • 44.
  • 45. Increased pressure  Compresses brain tissue  Herniates brainstem  Compromises blood supply  Signs & Symptoms  Upper Brainstem  Vomiting  Altered mental status  Pupillary dilation  Medulla Oblongata  Respiratory  Cardiovascular  Blood Pressure disturbances PRESSURE & STRUCTURAL DISPLACEMENT
  • 46. Upper Brainstem Compression  Increasing blood pressure  Reflex bradycardia  Vagus nerve stimulation  Cheyne-Stokes respirations  Pupils become small and reactive  Decorticate posturing  Neural pathway disruption SIGNS & SYMPTOMS OF BRAIN INJURY PHYSIOLOGICAL CHANGES
  • 47. Middle Brainstem Compression  Widening pulse pressure  Increasing bradycardia  CNS Hyperventilation  Deep and Rapid  Bilateral pupil sluggishness or inactivity  Decerebrate posturing SIGNS & SYMPTOMS OF BRAIN INJURY PHYSIOLOGICAL CHANGES
  • 48. Lower Brainstem Injury  Pupils dilated and unreactive  Ataxic respirations  Erratic with no pattern  Irregular and erratic pulse rate  ECG Changes  Hypotension  Loss of response to painful stimuli SIGNS & SYMPTOMS OF BRAIN INJURY PHYSIOLOGICAL CHANGES
  • 49. Physiological Issues  Indicate pressure on  CN-III (Oculomotor Nerve)  Pressure on nerve causes eyes to be sluggish, then dilated, and finally fixed  Reduced peripheral blood flow Pupil Size & Reactivity  Reduced Pupillary Responsiveness  Depressant drugs or Cerebral Hypoxia  Fixed & Dilated  Extreme Hypoxia SIGNS & SYMPTOMS OF BRAIN INJURY EYE SIGNS
  • 50. HEAD TRAUMA ASSESSMENT Initial Assessment Rapid Trauma Exam Limit patient agitation, straining • Contributes to elevated ICP Airway • Vomiting very common within first hour • Endotracheal intubation 50Head Trauma -
  • 51. Head Trauma - 51 Decreased level of consciousness is an early indicator of brain injury or rising ICP.
  • 52.  Reactive: ICP increasing  Nonreactive (altered LOC): increased ICP  Nonreactive (normal LOC): not from head injury PUPILS Both dilated  Nonreactive: brainstem  Reactive: often reversible Unilaterally dilated 52Head Trauma - Eyelid closure • Slow: cranial nerve III • Fluttering: often hysteria Anisocoria
  • 53. GLASGOW COMA SCALE Suspect severe brain injury GCS <9 53Head Trauma - *Decorticate posturing to pain **Decerebrate posturing to pain
  • 54. EXTREMITY POSTURING Decorticate • Arms flexed and legs extended Decerebrate • Arms extended and legs extended 54Head Trauma -
  • 55. INCREASING ICP 55Head Trauma - Vital Sign Change with Increasing ICP Respiration Increase, decrease, irregular Pulse Decrease BP Increase, widening pulse pressure Cushing’s response • As ICP increases, systolic BP increases • As systolic BP increases, pulse rate decreases
  • 56. Head Trauma - 56 Early efforts to maintain brain perfusion can be life-saving.
  • 57. THE INJURED BRAIN Hypoxia • Perfusion decrease causes cerebral ischemia • Hyperventilation increases hypoxia significantly more than it decreases ICP Assist ventilation • High-flow oxygen • One breath every 6–8 seconds • SpO2 >95% • Maintain EtCO2 at 35 mmHg 57Head Trauma -
  • 58. THE INJURED BRAIN Hypotension • Single instance increases mortality  Adult (systolic <90 mmHg) 150%  Child (systolic < age appropriate) worse Fluid administration for traumatic brain injury, GCS <9 • Titrate to 110–120 mmHg systolic with or without penetrating hemorrhage to maintain CPP 58Head Trauma -
  • 59. THE INJURED BRAIN Cerebral herniation syndrome • Brain forced downward  CSF flow obstructed, pressure on brainstem • Level of consciousness  Decreasing, rapid progression to coma • Associated symptoms  Ipsilateral pupil dilatation, out-downward deviation  Contralateral paralysis or decerebrate posturing  Respiratory arrest, death 59Head Trauma -
  • 60. CEREBRAL HERNIATION Is ICP severe enough to outweigh cerebral ischemia? 60Head Trauma -
  • 61. HYPERVENTILATION Cerebral herniation syndrome • Herniation danger outweighs hypoxia Indications for hyperventilation • TBI GCS <9 with decerebrate posturing • TBI GCS <9 with dilated or nonreactive pupils • TBI initial GCS <9, then drops >2 points If signs resolve, stop hyperventilation. 61Head Trauma -
  • 62. HYPERVENTILATION RATES Capnography • Maintain EtCO2 <30 mmHg, but >25 mmHg 62Head Trauma - Age Group Normal Rate Hyperventilatio n Adult 8–10 per minute 20 per minute Children 15 per minute 25 per minute Infants 20 per minute 30 per minute

Editor's Notes

  1. Scalp is very vascular and bleeds freely when lacerated. Children may develop shock from briskly bleeding scalp wound. Head injuries are common in child abuse. Suspect abuse when no clear explanation of cause, if story is inconsistent with injury, or suggests child performed activity not age-appropriate. Pay attention to setting. If abuse suspected, follow procedures for your area. As a general rule, if you have an adult patient with a scalp injury who is in shock, look for another cause for shock (such as internal bleeding). However, do not underestimate blood loss from a scalp wound. Most bleeding from scalp can be easily controlled in field with direct pressure if your exam reveals no unstable fractures under wound.
  2. IMAGE: Scalp laceration. Notice linear fracture on visible skull. Skull injuries can be linear nondisplaced fractures, depressed fractures, or compound fractures. Suspect an underlying skull fracture in adults who have a large contusion or darkened swelling of scalp. Very little can be done for skull fractures in field except to avoid placing direct pressure upon an obvious depressed or compound skull fracture. Open skull fractures should have wound dressed, but avoid excess pressure when controlling bleeding.
  3. Basilar skull fracture indicated by any of following: Bleeding from ear or nose Clear or serosanguineous fluid running from nose or ear Swelling and/or discoloration behind ear (Battle’s sign) Swelling and discoloration around both eyes (raccoon eyes) Battle’s sign can occur from immediately following injury to within 1–2 hours postinjury. Raccoon eyes are a sign of anterior basilar skull fracture. Through thin cribriform plate in upper nasal cavity and allow spinal fluid and/or blood to leak out. Raccoon eyes with or without drainage from nose are an absolute contraindication to inserting a nasogastric tube or nasotracheal intubation.
  4. IMAGE: Knife impaled in skull. IMAGE: X-ray of gunshot to head. Tissue destruction is seen in light area. NOTE: Reference to Mechanism of Injury (from Scene Size-up lecture). Remember: Velocity injuries (missiles) cause additional damage due to the shock wave of expanding tissues (temporary cavity). Penetrating objects in skull should be secured in place (impaled object) and patient transported immediately. Unless there is a clear entrance and exit wound in a perfectly linear path, assume that bullet may have ricocheted and is lodged in neck near spinal cord.
  5. Forces that can cause a skull fracture can also cause a brain injury. Treat brain injury with adequate oxygenation and maintain perfusion.
  6. Initial response of injured brain is to swell. Bruising or injury causes vasodilatation with increased blood flow to injured area, and thus an accumulation of blood that takes up space and exerts pressure on surrounding brain tissue. There is no extra space inside skull. Swelling of injured area increases intracerebral pressure and eventually decreases blood flow to brain that causes further brain injury. Increase in cerebral water (edema) does not occur immediately, but develops over hours. Only significant opening through which pressure can be released is foramen magnum at base, where brain stem becomes spinal cord.
  7. Primary brain injury is immediate damage to brain tissue as direct result of injury force and is essentially fixed at time of injury. Most primary injuries are from blunt trauma or from movement of brain inside skull. In deceleration injuries, head strikes object such as windshield, causing sudden deceleration of skull. Brain continues to move forward, impacting first against skull in original direction of motion (“coup”) and then rebounding to hit (fourth collision) opposite side of inner surface of skull (“contracoup”). Interior base of skull is rough, and movement of brain over this area may cause various degrees of injury to brain tissue or to blood vessels supporting brain. Management of primary brain injury is best directed at prevention with such measures as better occupant restraint systems in autos, use of helmets in sports and cycling, firearms education, and so forth.
  8. Good prehospital care can help prevent development of secondary brain injury. Secondary brain injury is result of hypoxia or decreased perfusion of brain tissue as result of brain’s response to primary injury, swelling.
  9. Cerebral contusion is bruised brain tissue. Presents with a history of prolonged unconsciousness or serious alteration in level of consciousness. Example: profound confusion, persistent amnesia, abnormal behavior. May still be unconscious on arrival. May have focal neurological signs (weakness, speech problems) and appear to have suffered a cerebrovascular accident (stroke). Depending upon location of cerebral contusion, patient may have personality changes such as inappropriately rude behavior or agitation. Brain swelling may be rapid and severe.
  10. IMAGE: Figure 10-4: Epidural hematoma (on page 149). Acute epidural hematoma is most often due to a tear in middle meningeal artery that runs along inside of skull in temporal region. Temporal bone (temple) quite thin and easily fractured. Arterial bleeding, so rise in ICP can occur rapidly, and death may occur quickly. History of head trauma with initial loss of consciousness often followed by a period during which patient is conscious and coherent (“lucid interval”). Symptoms: After a few minutes to several hours, develops signs of increasing ICP (vomiting, headache, altered mental status), lapses into unconsciousness, and develops body paralysis on side opposite of head injury. Often a dilated and fixed (no response to bright light) pupil on side of head injury. EMS may be called to evaluate after initial loss of consciousness while in lucid interval. Be suspicious of possibility of a developing epidural hematoma.
  11. IMAGE: Figure 10-5: Subdural hematoma (on page 149). Acute subdural hematoma is result of bleeding between dura and arachnoid and is associated with injury to underlying brain tissue. Because bleeding is venous, intracranial pressure increases more slowly, and diagnosis often is not apparent until hours or days after injury. Signs and symptoms include headache, fluctuations in level of consciousness, and focal neurologic signs (e.g., weakness of one extremity or one side of body, altered deep tendon reflexes, and slurred speech). Due to underlying brain tissue injury, prognosis is often poor. Mortality is very high (60%–90%) in patients who are comatose when found. Always suspect a subdural hematoma in an alcoholic with any degree of altered mental status following a fall. Elderly patients and those taking anticoagulants are also at high risk for this injury.
  12. IMAGE: Figure 10-6: Intracerebral hemorrhage (on page 149). Intracerebral hemorrhage is bleeding within brain tissue. Traumatic intracerebral hemorrhage may result from blunt or penetrating injuries of head. Unfortunately, surgery is often not helpful. Signs and symptoms depend upon regions involved and degree of injury. They occur in patterns similar to those that accompany a stroke; spontaneous hemorrhages of this type may be seen in patients with severe hypertension. Alteration in level of consciousness is commonly seen, though awake patients may complain of headache and vomiting.
  13. A concussion implies no structural injury to brain that can be demonstrated by current imaging techniques. There is a brief disruption of neural function that often results in loss of consciousness, but many people will have a concussion without a loss of consciousness. Classically there is a history of trauma to head with a variable period of unconsciousness or confusion and then a return to normal consciousness. There may be amnesia following injury. This amnesia usually extends to some point before injury (retrograde short-term amnesia), so often patient will not remember events leading to injury. Short-term memory is often affected, and patient may repeat questions over and over as if he hasn’t been paying attention to your answers. Patients may also report dizziness, headache, ringing in ears, and/or nausea.
  14. Diffuse axonal injury: Most common type of injury as a result of severe blunt head trauma. Brain is injured so diffusely that there is generalized edema. Usually, there is no evidence of a structural lesion. In most cases patient presents unconscious, without focal deficits.
  15. NOTE: Briefly review key issues of anatomy. NOTE: Point out brain stem (respiratory center) at area of foramen magnum. NOTE: Point out optic nerves would come directly from brain to pupils (pupil evaluation).   Increased volume of any one of these components has to result in decrease of another component. Vasoconstriction or vasodilation influence intracranial volume. Brain normally adjusts blood flow in response to metabolic needs based on level of carbon dioxide in blood (pCO2). Normal level of pCO2 is around 40 mmHg (also commonly listed as 35 to 45 mmHg). Increased pCO2 (hypoventilation) promotes cerebral vasodilatation, which increases ICP. Lowering pCO2 (hyperventilation) causes vasoconstriction and decreases blood flow. Hyperventilation has only minimal effect on ICP. NOT, as previously thought, that hyperventilation improved cerebral blood flow by causing vasoconstriction and decreasing ICP.
  16. Initial Assessment in head-trauma patient is to determine quickly if patient is brain injured and, if so, if patient’s condition is deteriorating. All observations must be recorded because later treatment is often dictated by detection of deterioration of clinical stability. Determining exact type of TBI or hemorrhage cannot be done in field. It is more important presence of brain injury be recognized and supportive measures be provided during transport. TBI patients may be difficult to manage because they are often uncooperative and may be under influence of alcohol or drugs. Remember to check blood glucose in all altered mental status. Limit patient agitation, when possible: Avoid excessive movement or jostling of patient. Limit lights and noise to the necessary. Evaluate if extra rescue personnel not directly involved in patient care in a closed environment are necessary. Consider sedation. IV lidocaine is no longer recommended. Topical lidocaine is acceptable.
  17. Initial Assessment neurological exam is limited to level of consciousness and any obvious paralysis. History of head trauma, or if Initial Assessment reveals altered mental status, then Rapid Trauma Survey will include a more complete neurological exam. Treatment of Decreased LOC is: Establish/maintain an adequate airway. Establish adequate ventilation and oxygenation. Establish adequate perfusion. Check blood glucose. Look for and correct any complicating factors. Level of consciousness is most sensitive indicator of brain function. Evaluate and monitor patient closely for change in condition.
  18. IMAGE: Abnormally dilated pupils (mydriasis). IMAGE: Anisocoria with unevenly sized pupils. IMAGE: Unilaterally dilated pupil. IMAGE: Cranial nerve III damage may cause eyelid to droop (ptosis) or close slowly. Outward and slightly downward deviation of the eye also reflects damage to cranial nerve III. NOTE: Asymmetry (unequal) is defined as 1 mm (or more) difference in size of pupil. NOTE: Fixed (nonreactive) is defined as no response (&amp;lt;1 mm) to bright light. NOTE: Anisocoria is a common condition characterized by unequal pupils, however there is less than a 1 mm difference in the size of the pupils. 20% of population has a mild form of anisocoria. Pupils are controlled in part by third cranial nerve, which is easily compressed by brain swelling, and thus may be affected by increasing ICP. Development of a unilaterally dilated, nonreactive pupil (“blown pupil”) while you are observing comatose patient is an extreme emergency and mandates rapid transport and hyperventilation. Other causes of dilated pupils that may or may not react to light include hypothermia, lightning strike, anoxia, optic nerve injury, drug effect (e.g., atropine), or direct trauma to eye. Fixed and dilated pupils signify increased intracranial pressure only in patients with a decreased level of consciousness. If patient has a normal level of consciousness, dilated pupil is not from head injury (more likely due to eye trauma or drugs such as atropine). Fluttering eyelids are often seen with hysteria. Slow lid closure (like a curtain falling) is rarely seen with hysteria.
  19. IMAGE: Table 10-2: Glasgow Coma Scale (on page 154). NOTE: See also Appendix F: Trauma Scoring in the Prehospital Care Setting. In TBI patient, a Glasgow Coma Scale score of 8 or less is considered evidence of a severe brain injury. GCS score that is determined in field serves as baseline for patient; be sure to record it. Record score for each part of GCS, not just total score. Perform a finger-stick glucose on all patients with altered mental status.
  20. IMAGE: Figure 10-10: Decorticate and decerebrate posturing (on page 153). Extremities should include evaluation of sensation and motor function. If patient is unconscious, note response to pain stimulus. Withdrawal or localization to pinching of fingers and toes indicates grossly intact sensation and motor function, which indicates that there is normal or only minimally impaired cortical function. Decorticate posturing or rigidity and decerebrate posturing or rigidity are ominous signs of deep cerebral hemispheric or upper brain stem injury. Decerebrate posturing is worse and usually signifies cerebral herniation. It is one of indications for hyperventilation. Flaccid paralysis usually denotes spinal-cord injury.
  21. Frequent vital signs measurement is extremely important in head trauma. They can indicate changes in ICP. Reassess frequently. Unusual respiratory patterns may reflect level of brain or brain stem injury. Just before death, patient may develop a rapid, noisy respiratory pattern called central neurogenic hyperventilation. However, it is not as useful an indicator as are other vital signs in monitoring course of head injury. Abnormal respiratory patterns may indicate a chest injury or other problem that could lead to hypoxia if untreated. Cushing’s response (reflex)—When ICP increases, systemic blood pressure increases to try to preserve blood flow to brain. The rise in systemic blood pressure triggers a drop in pulse rate as body tries to lower blood pressure. This hypertension is usually associated with a widening of pulse pressure (systolic minus diastolic pressure). Other causes of hypertension include fear and pain. Hypotension due only to head injury is rare. If hypotensive, look for hemorrhage.
  22. Goal is good oxygenation and good perfusion.
  23. Significant decrease in cerebral perfusion from vasoconstriction, which results in cerebral hypoxia. The injured brain does not tolerate hypoxia. Thus, both hyperventilation and hypoventilation can cause cerebral ischemia and increased mortality in TBI patient. Maintaining good ventilation (not hyperventilation) at a rate of about one breath every 6 to 8 seconds (8 to 10 per minute) with high-flow oxygen is very important. Prophylactic hyperventilation for head injury is no longer recommended.
  24. NOTE: GCS &amp;lt;9 is same as GCS of 8 or less. NOTE: Cerebral perfusion pressure (CPP). Usually pediatric patients have a better recovery from TBI. Hypoxia and hypotension appear to eliminate any neuroprotective mechanism normally afforded by age. If child with a serious brain injury is allowed to become hypoxic or hypotensive, chance of recovery is even worse than in an adult with same injury.
  25. Sudden rise in ICP may force portions of brain downward, obstructing flow of cerebrospinal fluid and applying great pressure to brain stem. Classic findings on exam are a decreasing level of consciousness (LOC) that rapidly progresses to coma, dilation of pupil and an outward–downward deviation of eye on side of injury, paralysis of arm and leg on side opposite injury, or decerebrate posturing. This syndrome often follows an acute epidural or subdural hemorrhage.
  26. NOTE: Emphasize that hyperventilation is only to be performed with cerebral herniation.
  27. If cerebral herniation is imminent, aggressive therapy is needed. Cerebral herniation syndrome is only situation in which hyperventilation is still indicated. Hyperventilation will decrease size of blood vessels in brain and briefly decrease ICP. Danger of immediate herniation outweighs risk of cerebral ischemia that can follow hyperventilation. Clinical signs of cerebral herniation in patient who has had hypoxemia and hypotension corrected are any one (or more) of following: TBI GCS &amp;lt;9 with extensor posturing (decerebrate posturing). TBI GCS &amp;lt;9 with asymmetric (or bilateral), dilated, or nonreactive pupils. TBI patient with initial GCS &amp;lt;9 who then drops his or her GCS by more than 2 points. If patient has signs of herniation as listed above, and signs resolve with hyperventilation, you should discontinue hyperventilation.
  28. NOTE: Assisted ventilation should be with high-flow oxygen. NOTE: No studies prove the efficacy of mannitol in prehospital setting.