EMS Management of Traumatic head injury.pptx

EMS CME lecture on field management of traumatic head injury including pathophysiology

1. Traumatic Head Injury 1

2. Traumatic Head Injury 1.4 million affected Approximately 64,000 deaths in 2020 223,135 hospitalized in 2019 2,274 pediatric Head Injury Deaths in 2020 2% population live with TBI disabilities Most prevalent in the South, lowest in the Midwest and Northeast

3. Traumatic Head Injury Age groups at highest risk 0-4 year old Young adults 16-30 years old More likely to die or be hospitalized if over 75 Leading causes Falls: 28% MVC: 20% Struck/against: 19% Assaults: 11%

4. 4 Important points The importance of a proper, thorough and accurate patient assessment The necessity of maintaining a high degree of suspicion for any patient exhibiting signs of an alerted mental status, or other signs or symptoms (including vomiting) of a serious head injury

5. 5 Important points The importance of relaying all pertinent information, including all signs and symptoms and suspicion of serious injuries, when transferring care

6. A Little Anatomy… Enclosed in protective box Skin Muscle Bone Meninges Cerebrospinal Fluid 6

7. Meninges Three layers of tissue enclosing brain, spinal cord Dura mater Arachnoid Pia mater 7

8. Cerebrospinal Fluid (CSF) Surrounds brain, spinal cord in space between arachnoid and pia mater (subarachnoid space) Acts as a shock absorber Protects brain from jolts, shocks 8

9. 9 Brain Functions localized to specific areas Cerebrum Cerebellum Brainstem

10. Cerebrum Frontal lobe Foresight, planning, judgment Movement Parietal lobe Sensation from body surface Temporal lobe Hearing Speech Occipital lobe Vision Center for conscious perception and response

11. 11 Cerebellum Posture Balance Equilibrium Fine motor skills

12. 12 Brain Stem Automatic functions below level of consciousness Heart rate Respirations Blood pressure Body temperature

13. Traumatic Injuries to Scalp and Skull 13

14. Injuries to Scalp and Skull Scalp Lacerations 14

15. 15 Scalp Lacerations VERY vascular area Can distract from possible underlying injuries Care for laceration, but ask, “did anything happen to the underlying brain?”

16. 16 Scalp Lacerations Bleeding usually NOT severe enough to produce hypovolemic shock If shock present, think about other injuries Exceptions Laceration that involves a large artery

17. 17 Skull Fractures Injury to rigid box around brain Indicates significant force What happened to underlying brain?

18. Types of Skull Fracture Linear Most common “Crack” in skull Most commonly around parietal region of skull. 18

19. Types of Skull Fracture Comminuted Multiple cracks radiate from impact point In this case, frontal comminuted fracture 19

20. Types of Skull Fracture Depressed Bone fragments pressed inward Places pressure on brain Brain tissue may be exposed through injury 20

21. Types of Skull Fracture Basilar Fractures in floor of skull Signs and symptoms Periorbital ecchymosis (Raccoon eyes) Battle’s sign CSF drainage from nose, ears 21

22. 22 Basilar Skull Fracture Signs

23. 23 Basilar Skull Fracture Signs

24. 24 Basilar Skull Fracture Signs

25. 25 Basilar Skull Fracture Signs

26. 26 Basilar Skull Fracture Signs If possible basilar skull fracture, DO NOT put anything in nose…right??? Not so fast… There has only been three documented cases of nasopharyngeal airway going through cribriform plate into brain Emphasize PROPER placement! Nasogastric tube is another story…

27. 27 Basilar Skull Fracture Signs

28. Traumatic Injuries to Brain 28

29. Traumatic Brain Injury Definitions Minimal injury (+/- mild concussion) No LOC or any other alteration in neurologic function No vomiting +/- minimal headache Effects clear without residual effects As a whole, no imaging or emergent care needed for these patients Can be managed at home with observation by family or friends

30. Traumatic Brain Injury Definitions Minor TBI (concussion) Temporary alteration in mental state at the time of the accident (dazed, disoriented, confused) GCS >12 after 30 minutes Brief LOC <30 seconds Residual mild to moderate headache Amnesia Any loss of memory for events immediately before or after the incident (but not more than 24 hours of memory loss) Requires emergent ED evaluation +/- imaging

31. Traumatic Brain Injury Definitions Moderate TBI GCS 9-13 after 30 minutes LOC > 30sec < 24 hours Amnesia > 1 day < 7 days +/- Neurologic deficit Requires emergent imaging and hospitalization 31

32. Traumatic Brain Injury Definitions Severe TBI LOC > 24 hours Amnesia > 7days Significant neurologic injury and deficit Abnormal neuroimaging Requires neurosurgery evaluation and ICU admission 32

33. Post-Concussive Syndrome 33 Physical symptoms Cognitive symptoms Behavioral symptoms Headaches Dizziness/Balance problems Sensitivity light/noise Changes in vision/hearing Fatigue/sleep disturbance Forgetting Poor concentration Changes in speech Slowed thinking and behavior Poor organizing/follow-through Personality changes Mood swings Apathy Irritability Impulsivity

34. Cerebral Contusion Bruising and swelling of brain tissue No collection of blood outside brain Results from brain hitting skull’s inside Coup- contracoup pattern Rotational forces!! Since brain is in closed box, pressure increases as brain swells, blood flow to brain decreases 34

35. Coup- Contrecoup Pattern 35

36. Normal Brain CT 36

37. Cerebral Contusions

38. Cerebral Contusion Signs and Symptoms Altered level of consciousness Paralysis (one-sided or total) or stroke-like symptoms Unequal pupils Seizures Vomiting 38

39. Epidural Hematoma Usually associated with skull fracture in temporal area Uncommon – only ~5% of injuries Fracture damages middle meningeal artery on inside of skull Blood collects in epidural space between skull and dura mater Since skull is closed box, intracranial pressure rises as blood collects 39

40. Epidural Hematoma Signs and Symptoms “Classic”- Loss of consciousness followed lucid interval x minutes to hours then gradual decline Occurs in ~1/3 of cases Headache, confusion, amnesia Dilated pupil on side of injury +/- Weakness, paralysis on side of body opposite injury +/- Seizures 40

41. Epidural Hematoma 41

42. Subdural Hematoma Usually results from tearing of large bridging veins between dura mater and arachnoid layer Mostly low pressure venous bleed so can accumulate slowly Signs and symptoms may not develop for days to weeks Worse prognosis than epidural – often has underlying brain injury 42

43. Subdural Hematoma Signs and Symptoms Deterioration of consciousness Change in personality or behavior Dilated pupil on side of injury Weakness, paralysis on side of body opposite injury Seizures 43 Because of slow or delayed onset, may be mistaken for stroke

44. Subdural Hematoma 44

45. Subdural Hematoma

46. Cerebral Laceration Crushing and tearing of brain tissue Mostly result from penetrating injury Low velocity – knives, arrows, sticks, etc High velocity – gunshot wounds Can cause: Massive destruction of brain tissue Bleeding into cranial cavity with increased intracranial pressure 46

47. This is not good Cerebral Lacerati on

48. Assessment and Management of Traumatic Head Injury 48

49. Assessment of Head Injury Mechanism of Injury History of LOC and seizure activity Primary assessment including Glasgow Coma Scale C-spine precautions Secondary assessment PMH, medications, ingestions, ETOH, Toxicology Accucheck !!

50. Assessment of Head Injury Assessing the level of consciousness is the most important first step in the exam Any decrease in the level of consciousness implies possible presence of brain injury Other (perhaps concurrent or additional) causes of decreased level of consciousness: Hypoxia, alcohol, drugs, hypoglycemia, cerebrovascular accident, hypo-/hyperthermia….. 50

51. Glasgow Coma Scale Eye Opening Spontaneous = 4 To Voice = 3 To Pain = 2 None = 1 51 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 Score each response then total scores Maximum Score = 15 Minimum Score = 3

52. Decorticate Posturing - FLEX 52

53. Decerebrate Posturing - EXTEND 53

54. Assessment of Pupils Measurement difference of 1 mm or more is defined as asymmetry ‘Fixed’ pupil shows no response to bright light Loss of pupil motor functions most likely due to an expanding intracranial lesion, edema, hemorrhage Gaze, pupillary reaction, accommodation, extraocular movements, corneal reflexes

55. Assessment of Pupils Dilation + fixation of one pupil = herniation Bilateral fixed + dilated = brain stem injury Remember: Hypoxia and hypothermia are associated with abnormal pupil size and reactivity 55

56. Assessment of Pupils “An unconscious head trauma patient with a unilaterally dilated pupil or with bilaterally fixed and dilated pupils is presumed to have cerebral herniation and in need of emergent interventions to lower the ICP.” - Brain Trauma Foundation 1999

57. Assessment of Scalp and Ears Palpate scalp for wounds and swelling Occiput can be deferred until cspine protected and pt log-rolled Check ears for Battle’s sign and drainage Halo sign Check nose for drainage Accucheck 57

58. Halo Sign 58

59. Assessment of Head Injury Vital Signs 59 Isolated head injury does not cause hypotension or tachycardia! Signs of shock in head injured patient indicate other injuries are present!

60. Vital Signs Comparison of Vital Signs in Shock and Head Injury 60 Vital Signs Shock Head Injury Pulse Increased Decreased BP Decreased Increased Respirations Increased Decreased LOC Decreased Decreased

61. Assessment of Head Injury Vital Signs Body responds to increasing intracranial pressure by raising BP in attempt to maintain cerebral blood flow CPP = MAP – ICP Heart rate falls in response to rising BP 61

62. Cushing’s Triad Classic pattern Increased systolic and decreasing diastolic pressure (widening pulse pressure) Bradypnea or altered respirations ( Cheyne -Stokes) Bradycardia

63. Cushing’s Triad 63 Increased BP Slow Pulse Altered Breathing

64. Prehospital Management Goals Establishment of airway Protect c -spine Oxygen administration Minimizing secondary injury Maintain and improve cerebral perfusion

65. Secondary Injuries Delayed secondary injury at the cellular level is a major contributor to the ultimate tissue loss that occurs after brain injury. This secondary tissue damage is the root of the most severe, long-term deficits a person with brain injury may experience ***Key to improving survival is preventing secondary TBI***

66. Secondary Intracranial Insults Expanding Hematoma Epidural, subdural and/or intracerebral Brain swelling/edema Increased intracranial pressure Cerebral vasospasm Hypoxia Hypotension causing hypoperfusion

67. Pre-hospital prevention of secondary systemic insults Airway management - if available, utilize RSI protocol to intubate patients if the airway cannot be adequately managed less invasively Generally GCS <8 but controversial Monitor ETCO2/SaO2 levels continuously!! Administer sedation and paralytics if necessary Prevent hypotension & hypothermia

68. Preventing secondary injury  ICP, cerebral edema, cerebral dysautoregulation & metabolism Preventing hypotension Single episode of hypotension in the field(<90 mm Hg) doubles mortality. 8-13% of civilian brain trauma are associated with hypotension in the field Prevention and/or prompt treatment of hypotension is crucial 68

69. Pre-Hospital Prevention of hypotension in TBI patients Evidence of head injury in the multi-trauma patient dictates the resuscitation No head injury = damage control resuscitation Remember?? Radial pulse and mentation… Evidence of head injury = goal SBP 100mmHg to maintain cerebral perfusion

70. Preventing secondary injury  ICP, cerebral edema, cerebral dysautoregulation & metabolism Preventing hypoxia pO2<60% (Sat <90%) correlates with poor outcome In civilian community 50% present with sat <90%, this is associated with a 50% mortality and 50% severe disability in survivors . 70

71. Prehospital Prevention of Hypoxia Keep airway clear and patent 100% O2 via NRB or via vent Suction no longer than 15 seconds – extended suctioning can decrease the CO2 level in the blood, causing vasoconstriction of the cerebral arteries.

72. Ventilatory management Avoid over-ventilation with BVM during transport of patient One breath every 4-5 seconds at most! Monitor ETCO2 values on all head injury patients to keep values around 40

73. Preventing secondary injury  ICP, cerebral edema, cerebral dysautoregulation & metabolism Detecting increasing ICP Development of asymmetric irregular pupil Pupil asymmetry > 1mm, dilated pupil(s) Decerebrate (extensor) posture Drop of 2 points in GCS from an initial GCS 8 or less 73

74. Prehospital Management of ICP Elevate the patient’s head between 15 -30 ° to improve cerebral venous outflow For every 10 ° of head elevation, the mean ICP decreases by 1 mm Hg Cervical/TL spine should be cleared or stabilized Longboard can be elevated and secured on stretcher. Maintain neutral alignment of head and neck – avoid tight cervical collars and tight taping of ETT

75. Prehospital Management of ICP What about hyperventilation?? Lowers blood CO2 levels which causes cerebral vasoconstriction and quickly lowers ICP HOWEVER… Research shows that decreased perfusion to brain (and subsequent decreased oxygen to brain) is damaging to brain and may further increase swelling 75

76. Prehospital Management of ICP Hyperventilation no longer recommended BUT… If signs of imminent herniation, consider controlled hyperventilation with GREAT CAUTION Must be done with EtCO2 monitoring with goal EtCO2 of ~35 76

77. Controlled Hyperventilation Normal ventilation Adults: 10-12/bpm Children: 12-16/bpm Infants: 16-20/bpm Hyperventilation Adults: 16-20/bpm Children: 20-24/bpm Infants: 24-28/bpm

78. Prehospital Management of ICP Hypertonic saline can be used to reverse imminent herniation Mechanism: Osmotic effect on cells Decreases free fluid in brain tissue Increases circulating blood volume Increased microvascular circulation 78

79. Hypertonic Saline If signs of herniation are present (Unilateral or Bilateral dilation of pupils, Posturing decorticate/decerebrate: Adult: 30ml of 23.4% NaCl given through IO over 5-10 minutes.

80. To transport or not to transport Are there patients that can safely be diverted to Treatment in Place or Urgent Care? Mild headache, dizziness, scalp lacerations (w/o exposed brain!!), scalp contusions, and scalp abrasions are not considered high risk Tele-providers can utilize clinical decision rules Canadian Head CT rule New Orleans CT rule 80

81. High-risk patients Anyone on coumadin or blood thinners ( plavix , etc ) needs a CT scan! Pediatrics Overall high risk population Will probably transport all but the most minor of these BUT may need to set expectations for parents 81

82. Pediatric Head Injury GCS <14, other signs of altered mental status*, or palpable skull fracture = Peds Trauma center Occipital/parietal/temporal scalp hematoma, LOC >5s, severe mechanism of injury, not acting normal per parent = Peds Trauma or VHC for possible CT scan If none of above, no CT scan needed but should be evaluated and observed in ED 82 *Agitation, somnolence, slow response to verbal or other stimulation

83. Questions?