1. Bryan E. Bledsoe, DO, FACEP
Neurologic Trauma
Bryan E. Bledsoe, DO, FACEP

2. Neurologic Trauma

3. “Suppose you were an idiot. And suppose you were a member of Congress.
Neurologic Trauma
“Suppose you were an idiot. And suppose you were a member of Congress.
But I repeat myself.”
Mark Twain

4. Traumatic Brain Injury (TBI)
Defined as a blow or jolt to the head or a penetrating head injury that disrupts the function of the brain.

5. Statistics
1.4 million people sustain a TBI each year in the United States:
50,000 die,
235,000 are hospitalized,
1.1 million are treated and released from the ED.

6. Statistics Causes: Falls (28%) MVCs (20%)
Struck by/against events (19%)
Assaults (11%)
 Blasts are the leading cause of TBI for active duty military personnel in war zones.

7. Statistics
Males are about 1.5 times more likely to sustain a TBI as a female.

8. Statistics Highest risk for TBI:
0-4 years
15-19 years
African Americans have the highest death rate from TBI.

9. Statistics
Estimated $60 billion lost from TBI (medical costs and lost productivity).*
* 2000

10. Anatomy

11. Anatomy

12. Anatomy

13. Anatomy

14. Anatomy

15. Anatomy

16. Anatomy

17. Anatomy

18. Anatomy

19. Anatomy

20. Anatomy

21. Anatomy

22. Physiology Brain Metabolism:
Like all tissues, the brain requires a constant supply of oxygen and nutrients.

23. Physiology Brain accounts for 2% of total body mass.
Brain accounts for 15% of total metabolism in the body.
Brain metabolic rate 7.5 times the rate of other neurological tissues.

24. Physiology
Almost all of the brain’s energy needs are supplied by glucose.
Provided by capillaries in the brain.

25. Physiology
Insulin NOT needed for glucose delivery to brain tissues.

26. Physiology
The brain is among the most oxygen dependent organs in the body.
The brain is not capable of much anaerobic metabolism.
Primarily due the high metabolic rate of the neurons.

27. Physiology
Because of this, sudden cessation of blood flow to the brain can cause unconsciousness within 5-10 seconds.

28. Physiology Neuroglobin: Intracellular hemeprotein.
Reversibly binds oxygen with an affinity greater than that of hemoglobin.
Increases oxygen availability to brain tissue and provides protection under hypoxic or ischemic conditions, potentially limiting brain damage.

29. Physiology Brain requires:
Oxygenation
Glucose
Perfusion
Any deficit in these results in immediate dysfunction.

30. Intracranial Pressure
The cranial vault is effectively a closed container.
Largest opening is the foramen magnum.
Limited room for brain swelling.

31. Intracranial Pressure
There is always some pressure in the brain.
Referred to as intracranial pressure (ICP).
Normal ICP:
Children: 0-10 mm Hg
Adults: 0-15 mm Hg

32. Intracranial Pressure
Volume of the cranial vault defined by the Monro-Kellie doctrine:
Intracranial Volume (fixed) =
Brain Volume + CSF Volume + Blood Volume + Mass Lesion Volume

33. Intracranial Pressure
Normally:
Brain = 80% of cranial vault space
Blood = 10% of cranial vault space
CSF = 10% of cranial vault space
Space Available for Blood or MASS = 0%

34. Intracranial Pressure
To perfuse the brain, the pressure of blood delivered to the brain MUST be greater than the intracranial pressure.
CPP = MAP - ICP

35. Intracranial Pressure
Mean Arterial Pressure:
MAP  DP + 1/3 (SP–DP)

36. Intracranial Pressure
Perfusion of the brain is driven by the CPP.
MAP - ICP = CPP
= 40
CPP of 60 is the critical minimum threshold.
CPP of 40 is the critical minimum threshold for children < 8 years of age.

37. Intracranial Pressure
Injury to brain tissue causes:
Swelling
Bleeding
Edema
All cause an increase in the size and mass of the brain.

38. Intracranial Pressure
As the brain swells, it will eventually reach a critical volume where ICP increases to a point that perfusion is compromised.

39. Brain Injury Etiology of TBI: Primary injury:
Damage to the brain from mechanical effects of trauma causing:
Ischemia
Anoxia/hypoxia
Shear injury

40. Brain Injury Secondary Injury:
Results from a traumatic event and changes in the brain or in the brain vasculature.
Hypoxia
Hypotension ( cerebral blood flow)
 ICP
Hyperglycemia/Hypoglycemia
Metabolic disturbances
Seizures

41. Brain Injury 12-24 hours post-injury:
Hypoperfusion and decrease in CBF.
Results from increases in distal microvascular resistance and intravascular clot formation.

42. Brain Injury 1-5 days post injury: Increased CBF > CMRO2.
Vascular engorgement
Swelling
Increased ICP
Induction of free radicals and oxidative stress.

43. Brain Injury 5/6-14 days post injury: CBF slows due to vasospasm
Brain vulnerable to changes in ICP.

44. Brain Injury Secondary Injury: Impaired autoregulation:
Autoregulation is the ability of the brain to maintain CBF in light of changes in BP and CPP.
Impaired autoregulation causes:
 O2 delivery to the brain and cerebral ischemia.
Cerebral metabolism altered due to loss of, or a decrease in, CBF.
Conversion from aerobic to anaerobic metabolism.

45. Brain Injury Secondary Injury (extracranial causes):
Hypotension (SBP < 90 worsens outcomes)
Hypoxia (significantly associated with increased morbidity and mortality)
Hypocapnia:
Low CO2 causes vasoconstriction
1 mm Hg decrease on CO2 = 3% decrease in CBF.
Anemia
Hyperthermia

46. Brain Injury

47. Brain Injury Compensatory mechanisms: Brain shifts or is compressed.
Venous blood is shunted to heart.
CSP shunted to spinal SAS.

48. Vegetative- Severe Disability
Secondary Injury
Secondary Insults
No. of Patients
Good-Moderate
Disability
Vegetative- Severe Disability
Dead
Hypoxia 78
45%
22%
33%
Hypotension
113
26%
14%
60%
Both 52 6%
19%
75%

49. Signs and Symptoms Early ( ICP): Altered mental status Agitation
Nausea and/or vomiting
Hemiparesis

50. Signs and Symptoms Late ( ICP): Coma Hemiplegia Posturing
Cushing’s Triad:
Widening pulse pressure
Bradycardia
Respiratory abnormalities

51. Brain Herniation
Results when ICP increases beyond the capability of physiologic and limited physical compensation mechanisms.

52. Brain Herniation Major areas of brain herniation syndrome:
Subfalcial (a)
Uncal (b)
Central transtentorial (c)
External (d)
Cerebellotonsillar (e)

53. TBI Mild (GCS = 14-15) Moderate (GCS = 9-13) Severe (GCS < 9)
~ 80% of patients
Moderate (GCS = 9-13)
~ 10% of patients
Severe (GCS < 9)
~ 10 of patients

54. Trauma Types Scalp Laceration: Highly vascular
Can lead to massive blood loss

55. Trauma Types Skull Fracture: Classified by:
Location
Pattern
Open/closed
Up to 50% of patients with skull fracture will NOT have LOC or neurologic symptoms.

56. Trauma Types Concussion:
Brief and temporary loss of neurologic function following head trauma.
May occur with or without LOC.
Symptoms:
Amnesia
Duration of amnesia predictive of injury severity.
Confusion

57. Concussion Grade 1: No LOC Confusion without amnesia Treatment:
Remove from event and examine immediately and every 5 minutes for the development of amnesia.
If asymptomatic > 20 minutes, can return to game.
2 Grade 1 concussions:
No sports for the day
3 or more Grade 1 concussions:
Out for season and no contact sports for 3 months

58. Concussion Grade 2: No LOC Confusion and amnesia Treatment:
Remove from event for the day.
Refer for exam the next day.
May return in 1 week if asymptomatic with rest/exertion.
2 Grade 2 concussions:
No play for 1 season
3 Grade 2 concussions:
Season terminated.

59. Concussion Grade 3: LOC Treatment: Transport to ED for evaluation
Return to sport in 1 month if asymptomatic for a 2-week period.
2 Grade 3 concussions:
Season terminated.

60. Trauma Types Cerebral contusion: Most frequent type of TBI
Most common in:
Subfrontal cortex
Frontal lobe
Temporal lobe
Occipital (less common)
Often associated with SAH.

61. Trauma Types

62. Contusion

63. Trauma Types Subarachnoid hemorrhage:
Disruption of subarachnoid vessels.
1/3 of all patients with moderate to severe TBI have traumatic SAH.

64. Trauma Types Epidural hematoma:
Collection of blood between the dura and the skull.
Arterial bleed.
Incidence:
% of all head-injured patients.
<10% of head-injured patients who are comatose.
Almost all associated with skull fracture.
80% will progress to uncal herniation.

65. Epidural Hematoma

66. Epidural Hematoma Signs and Symptoms:
Classis syndrome (<20% of cases):
Immediate LOC.
Patient awakens and has a “lucid interval.”
Loses consciousness as hematoma expands.
Most commonly:
Most patients either never lose consciousness or never regain consciousness.

67. Trauma Types Subdural hematoma:
Collection of blood between the dura and the SAM.
Venous bleed.
Associated with sudden acceleration and/or deceleration.
Tears bridging veins.

68. Subdural Hematoma

69. Subdural Hematoma
Usually more brain parenchymal injury than epidurals.
Classified as:
Acute (< 3 days)
Subacute (3-14 days)
Chronic (> 14 days)

70. Trauma Types Diffuse Axonal Injury (DAI):
Interruption of axonal fibers in the white matter and brain stem.
Shearing forces (usually deceleration) cause injury.
Adults: MVCs
Babies: “Shaken baby” syndrome
Injury occurs immediately and is usually irreversible.

71. Diffuse Axonal Injury

72. Trauma Types Intracerebral Hemorrhage:
Usually caused by shearing forces.
Severity depends upon location and size.
Secondary injury common.

73. Trauma Types Penetrating Injury: Severity of injury related to:
Kinetic energy of injury
Location of injury
Infection a common complication.

74. Trauma Types
Probably mortal.

75. TBI Signs and Symptoms Anxiety/nervousness Behavioral changes:
Disinhibition
Impulsiveness
Inappropriate laughter
Irritability
Diplopia
Depression
Trouble concentrating
Aphasia
Dysphagia
Dizziness
Headache
Uncoordination of movements
Lightheadedness
Ataxia
Amnesia

76. TBI Signs and Symptoms Muscle stiffness/spasm Seizures Sleep disorders
Slurred or slowed speech
Tingling
Numbness
Pain
Vertigo
Localized weakness
Nausea
Vomiting
Body temperature changes
Coma
Posturing
Pupillary abnormality

77. ARE EXTREMELY VARIABLE
TBI Signs and Symptoms
SIGNS AND SYMPTOMS
IN TBI
ARE EXTREMELY VARIABLE

78. Assessment/Treatment
Airway (with c-spine control)
Breathing
Circulation
Disability
Exposure

79. Assessment/Treatment
Palpate skull, facial bones and neck
Assess rate, depth and quality of respirations.
Consider tachypnea at the following rates a sign of deterioration:
Infant: 40 breaths per minute
Child: 30 breaths per minute
Adult: 20 breaths per minute

80. Assessment/Treatment
Assess pupils carefully:
Pupil size
Symmetry
Reactivity to light

81. Assessment/Treatment
Pupillary assessment:
Bilateral symmetry (asymmetric pupils differ more than 1 mm).
Reactivity to light (a fixed pupil shows <1mm change in response to bright light).
Dilation (greater than or equal to 4mm diameter in adults)

82. Assessment/Treatment
Single fixed and dilated pupil:
45% poor outcome
Bilateral fixed and dilated pupils:
82% poor outcome

83. Assessment/Treatment
Mid-position fixed and dilated pupil:
Suggests brain stem herniation.
Indicative of mass on same side.
Treat hypoxia and hypotension, if present.
Treat increased ICP per practice parameters.

84. Assessment/Treatment
Indications of herniation:
Unilateral or bilateral dilated, nonreactive pupils.
Asymmetric pupils.
Decerebrate posturing.
No motor response to painful stimuli.

85. Assessment/Treatment
Monitor SpO2 and ETCO2.
Maintain SpO2 > 90%
Maintain ETCO2 between mm Hg
Initiate IV line with saline:
Maintain adult systolic BP > 90 mm Hg
Pediatric values are lower.
Utilize Glasgow Coma Scale

86. Glasgow Coma Scale (Adult)
Eye Opening (E)
Verbal Response (V)
Motor Response (M)
Obeys (6)
Oriented (5)
Localizes (5)
Spontaneous (4)
Confused (4)
Withdraws (4)
Reaction to Speech (3)
Inappropriate Words (3)
Decorticate (3)
Reaction to Pain (2)
Incomprehensible
Sounds (2)
Decerebrate (2)
No Response (1)
TOTAL = E + V + M

87. Glasgow Coma Scale (Infant)
Eye Opening (E)
Verbal Response (V)
Motor Response (M)
Obeys (6)
Coos, Babbles (5)
Localizes (5)
Spontaneous (4)
Irritable Cry (4)
Withdraws (4)
Reaction to Speech (3)
Cries to Pain (3)
Decorticate (3)
Reaction to Pain (2)
Mans, Grunts (2)
Decerebrate (2)
No Response (1)
TOTAL = E + V + M

88. Assessment/Treatment
Assess blood glucose level.

89. Treat Airway Protect C-spine alignment, consider facial trauma.
Airway support per scope of practice.
Intubate severe TBI patients.
Correct hypoxia.

90. When to Intubate GCS < 9 (severe TBI).
All patients with respiratory failure of apnea.

91. Treat Breathing Oxygenation. Ventilation.
Administer supplemental oxygen by non-rebreather or BVM as appropriate.
Ventilation.
Assess rate, depth, quality, to determine the effectiveness of respirations.
As necessary, assist ventilations with BVM and supplemental O2.

92. Adult normal Ventilation rate = 10-12 per minute
Treat Breathing
Adult normal
Ventilation rate =
10-12 per minute

93. Hyperventilation? Hyperventilation:
Rapid  PaCO2
Cerebral vasoconstriction
Decreased CBF
 ICP
But, hyperventilation can  CBF to the point of ischemia.
Monitor ETCO2!

94. Hyperventilation?
Potential harm in patients without evidence of brain herniation.
Short-term measure used in specific TBI patients (herniation) until definitive diagnostic or therapeutic can be provided.

95. Hyperventilation? Rates: Ages 9-Adult: 20 breaths per minute:
(ETCO2 ~ 35 mm Hg).
Ages 1-8 years: 30 breaths per minute:
(ETCO2 ~ mm Hg).
Ages < 1 year: 40 breaths per minute:

96. Fluids Fluids to maintain SBP> 90 mm Hg. Normal saline
Hypertonic saline?

97. Brain-Targeted Therapies
Glucose for hypoglycemia
Sedatives for agitation
Analgesics for pain
Paralytics for ET intubation
Controversial:
Mannitol
Lidocaine
Hypertonic Saline

98. Destinations Mild (GCS 14-15): Emergency Department
Moderate (GCS 9-13): Trauma Center
Severe (GCS < 9): Trauma Center with severe TBI management capabilities.

99. Take Home Messages Clinical practice should be evidence-based.
Do early and repeated neurological assessments.
Identify patients with severe TBI (GCS < 9).

100. Take Home Messages Avoid hypoxia, keep SpO2 > 90%.
Avoid hypotension, keep SBP > 90 mm Hg.
Hyperventilate only for clinical signs of herniation.
Triage and transport TBI to appropriate facilities based on severity.

101. The Future Therapies to protect against secondary injury: Hypothermia.
Sedative-induced coma.
Metabolic therapies.
Antioxidant therapies.