Boy, do I have an Excedrin headache managing the head injured patient

1. �Boy, do I have an Excedrin headache!!�managing the head injured patient Leaugeay Webre BS, CCEMT-P, NREMT-P

2. Scenario While descending Mt Hood in Oregon, Bob tumbled head over heels, and came to a stop dangling off a precipice by his Telemark ski at 11,000 ft. On arrival the ski patrol paramedics Bob�s breathing was sonorous and shallow, and he had a GCS of 3-4. The only obvious injuries were to his head. His BP was 87/55, HR 100 and RR 16

3. How should the paramedics treat this patient? Should he be intubated? Should he be fluid resuscitated?

4. Common major trauma 4 million people experience head trauma annually Severe head injury is most frequent cause of trauma death GSW to cranium: 75-80% mortality At Risk population Males 15-24 Infants Young Children Elderly Introduction to Head, Facial, & Neck Injuries

5. 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, Facial, & Neck Injuries

6. Scalp Strong Flexible mass of Skin Fascia Muscular Tissue Highly Vascular Hair provides Insulation Structures Beneath Galea Aponeurotica Between scalp and skull Fibrous connective sheath Subaponeurotica (Areolar) Tissue Permits venous blood flow from the dural sinuses to the venous vessels of scalp Emissary Veins: Potential route for Infection Anatomy & Physiology of the Head

10. Brain Occupies 80% of cranium Comprised of 3 Major Structures Cerebrum Cerebellum Brainstem High metabolic rate Receives 15% of cardiac output Consumes 20% of body�s oxygen Requires constant circulation IF Blood supply stops Unconscious within 10 seconds Death in 4-6 minutes Anatomy & Physiology of the Head

11. Cerebral Perfusion Pressure Pressure within cranium (ICP) resists blood flow and good perfusion to the CNS Pressure usually less than 10 mmHg Mean Arterial Pressure (MAP) Must be at least 50 mmHg to ensure adequate perfusion MAP = DBP + 1/3 Pulse Pressure Cerebral Perfusion Pressure (CPP) Pressure moving blood through the cranium CPP = MAP - ICP Anatomy & Physiology of the Head

12. Calculating MAP (mean arterial pressure) DBP + 1/3 PP PP (pulse pressure) = SBP - DBP SBP + 2(DBP) 3 Calculating CPP (cerebral perfusion pressure) MAP � ICP ICP normally < 10 Anatomy & Physiology of the Head

13. Cerebral Perfusion Pressure Autoregulation Changes in ICP result in compensation Increased ICP = Increased BP This causes ICP to rise higher and BP to rise Brain injury and death become imminent Expanding mass inside cranial vault Displaces CSF If pressure increases, brain tissue is displaced Anatomy & Physiology of the Head

15. Types of Trauma Soft tissue Skull fracture Primary brain injuries Secondary brain injuries

16. The patient presented to the emergency department with the golf cub in his head, which was removed in the operating room

17. Lateral skull x-ray of a patient who presented with a severe intracranial injury produced by a golf club

18. Scalp Injury Contusions Lacerations Avulsions Significant Hemorrhage ALWAYS Reconsider MOI for severe underlying problems

19. 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.� Classification Direct Primary injury caused by forces of trauma Indirect Secondary injury caused by factors resulting from the primary injury

20. Direct Brain Injury Types Coup Injury at site of impact Contrecoup Injury on opposite side from impact

21. Intracranial Perfusion Review 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

22. 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 Dangerous cycle

23. Intracranial Pressure Role of Carbon Dioxide Increase of CO2 in CSF Cerebral Vasodilation Encourage blood flow Reduce hypercarbia Reduce hypoxia Contributes to ? ICP Causes classic Hyperventilation & Hypertension Reduced levels of CO2 in CSF Cerebral vasoconstriction Results in cerebral anoxia

24. Factors Affecting ICP Vasculature Constriction Cerebral Edema Systolic Blood Pressure Low BP = Poor Cerebral Perfusion High BP = Increased ICP Carbon Dioxide Reduced respiratory efficiency

25. Increased pressure Compresses brain tissue Against & around Falx Cerebri Tentorium Cerebelli 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

26. Altered Mental Status Altered orientation Alteration in personality Amnesia Retrograde Antegrade Cushing�s Reflex Increased BP Bradycardia Erratic respirations Signs & Symptoms of Brain Injury

27. 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

28. 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 InjuryPhysiological Changes

29. Middle Brainstem Compression Widening pulse pressure Increasing bradycardia CNS Hyperventilation Deep and Rapid Bilateral pupil sluggishness or inactivity Decerebrate posturing Signs & Symptoms of Brain InjuryPhysiological Changes

30. 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 InjuryPhysiological Changes

31. Different pathology than older patients Skull can distort due to anterior and posterior fontanelles Bulging Slows progression of increasing ICP Intracranial hemorrhage contributes to hypovolemia Decreased blood volume in ped�s General Management Avoid hyperextension of head Tongue pushes soft pallet closed Ventilate through mouth and nose Signs & Symptoms of Brain InjuryPediatric Head Trauma

32. Signs & Symptoms of Brain InjuryGlasgow Coma Scale

33. Physiological Issues Indicate pressure on CN-II, CN-III, CN-IV, & CN-VI 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 InjuryEye Signs

34. Skull Fractures The skull will not fracture without extreme force Closed/ open linear depressed comminuted basilar impaled object Depressed skull fx requires surgery if =/ > skull thicknessDepressed skull fx requires surgery if =/ > skull thickness

35. Cranial Injury Trauma must be extreme to fracture Linear Depressed Open Impaled Object Basal Skull Unprotected Spaces weakenstructure Relatively easier to fracture

36. Cranial Injury 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

37. Cranial Injury 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

38. Basilar Skull Fracture Cribiform plate fracture Battle�s sign Periorbital ecchymosis CSF leakage Resulting in torn dura and 7th cranial n. palsy 2ndary to torn tympanic membraneResulting in torn dura and 7th cranial n. palsy 2ndary to torn tympanic membrane

39. Primary Brain Injury Results from direct trauma Focal Diffuse

40. Direct Brain Injury Categories Focal Occur at a specific location in brain Differentials Cerebral Contusion Intracranial Hemorrhage Epidural hematoma Subdural hematoma Intracerebral Hemorrhage Subarachnoid Hemorrhage Diffuse Concussion Moderate Diffuse Axonal Injury Severe Diffuse Axonal Injury

41. Focal Contusions Intracerebral hematoma Subdural hematoma Subarachnoid hematoma Epidural hematoma

42. Contusions LOC with resultant cellular damage �bruising� Temporal injury often presents with repetitive questioning

43. A young male arrived in the emergency department after experiencing a gunshot wound to the brain. The entrance was on the left occipital region. A CT scan shows the skull fracture and a large underlying cerebral contusion. The patient was taken to the operating room for debridement of the wound and skull fracture, with repair of the dura mater

44. Focal Brain Injury 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

45. Epidural Hematoma Located between skull and dura mater Usually involves arterial bleeding- middle meningeal artery Sharply defined edges on CT Usually no underlying brain injury Classical presentation is �lucid interval� May quickly evolve into herniation Bleeding from MMA occurs from hi pressure vessel, ICP builds rapidly compressing cerebrum. Bleeding may displace brain away from injury site towards foramen magnum Surgery often reverses processBleeding from MMA occurs from hi pressure vessel, ICP builds rapidly compressing cerebrum. Bleeding may displace brain away from injury site towards foramen magnum Surgery often reverses process

46. Lucid Interval transient LOC followed by a lucid period where patient is neurologically intact followed by a secondary onset of HA and decreasing LOC Result of initial LOC due to a concussion/ traumatic tearing of meningeal A. Spasm and clotting occurs and bleeding subsides then slowly begins to leak and form hematoma Once HA and decreasing LOC occur secondary ICP has occurredResult of initial LOC due to a concussion/ traumatic tearing of meningeal A. Spasm and clotting occurs and bleeding subsides then slowly begins to leak and form hematoma Once HA and decreasing LOC occur secondary ICP has occurred

47. 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 InjuryIntracranial Hemorrhage

48. CT scan of an acute left-sided epidural hematoma. Note the typical convex or lens-shaped appearance. The hematoma takes this shape as the dura strips from the undersurface of the cranium, limited by the suture lines. A midline shift of the ventricular system exists.

49. Subdural Hematoma Located between the dura mater and pia mater All venous bleeds, usually present with slow onset Indistinct on CT Underlying brain injury May not present with Sx for hours or days ICH may present as stroke- HTNICH may present as stroke- HTN

50. 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 InjuryIntracranial Hemorrhage

51. Acute subdural hematoma: note the bright (white) image properties of the blood on this noncontrast cranial CT scan. Note also the midline shift.

52. Subacute subdural hematoma: the crescent-shaped clot is less white than on CT scan of acute subdural hematoma

53. Intracerebral Hemorrhage Rupture blood vessel within the brain Presentation similar to stroke symptoms Signs and symptoms worsen over time Focal Brain InjuryIntracranial Hemorrhage

54. Intracerebral Hematoma Located in the brain parenchyma Difficult to distinguish from contusion

55. Intracranial hemorrhage. CT scan of right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.

56. Subarachnoid Hemorrhage May not present with physical findings HA stiff neck nuchal rigidity Blood in CSF @ndary injury may be hydrocephalus because CSF is unable to drain properly@ndary injury may be hydrocephalus because CSF is unable to drain properly

57. Brain CT scan shows subtle finding of blood at the area of the circle of Willis consistent with acute subarachnoid hemorrhage.

58. Diffuse Brain Injury Due to stretching forces placed on axons Pathology distributed throughout brain Types Concussion Moderate Diffuse Axonal Injury Severe Diffuse Axonal Injury

59. Concussion Transient LOC Usually complete recovery Mild form of diffuse injury Often presents with a brief period of confusion Pt may exhibit retrograde or posttraumatic amnesia

60. Diffuse Axonal Injury Rapid, profound, prolonged unconsciousness Often leads to increased ICP

61. 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 InjuryConcussion

62. �Classic Concussion� Same mechanism as concussion Additional: Minute bruising of brain tissue Unconsciousness If cerebral cortex and RAS involved 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 InjuryModerate Diffuse Axonal Injury

63. Brainstem Injury Significant mechanical disruption of axons Cerebral hemispheres and brainstem High mortality rate Signs & Symptoms Prolonged unconsciousness Cushing�s reflex Decorticate or Decerebrate posturing Diffuse Brain InjurySevere Diffuse Axonal Injury

65. Pathway of Deterioration Cranial insult Tissue edema Increasing ICP Compression of arteries Decreased cerebral blood flow Decreased O2 with cellular death Edema around necrotic tissue

66. Con�t Increasing ICP with compression of brainstem and respiratory center Accumulation of CO2 resulting in vasodilation Increasing blood volume further increasing ICP Death

67. Any swelling or bleeding decreases the circulating blood volume and cerebral blood flow Decreased cerebral blood flow results in hypoxia and CO2 rises Hypercarbia dilates cerebral blood vessels causing increasing BP Attempts to perfuse brain resulting in increased ICP

68. Herniation Depression of 3rd cranial nerve results in pupillary dilation- aniscoria Lateral paresis Cushing�s triad Decorticate posturing Decerebrate posturing

69. Decorticate Posturing Results from lesions of internal capsules, basal ganglia, thalamus or cerebral hemisphere Interrupts corticospinal pathways Presents with flexed arms and extended lower extremities

70. Decerebrate Posturing Results from injury to midbrain and pons Indicative of brainstem dysfunction Presents with extended upper extremities and pronation Extended lower extremities Usually indicative of graver injury

71. Cushing�s Reflex Late sign of increasing ICP Bradycardia Widening pulse pressure/ increasing BP Changes in respiratory patterns

72. Respiratory Patterns May be indicative of injury location in the brain Cheyne - Stokes Central Neurogenic hyperventilation Apneustic Cluster breathing Ataxic breathing

73. Cheyne- Stokes Respirations Periodic breathing in which depth of each breath increases to peak then decreases to a period of apnea Hyperpneic stage usually lasts longer than apneic phase Bilateral lesions in cerebral hemispheres

74. Central Neurogenic Respirations Sustained regular, rapid and deep breathing Midbrain and upper pons injury

75. Apneustic Respirations Breathing with a long pause at full inspiration or full expiration Respiratory function present at brainstem level only

76. Cluster Breathing Gasping breaths with irregular pauses Lesion high medulla or low pons

77. Ataxic Breathing Totally irregular consisting of both deep and shallow breaths associated with irregular pauses Consistent with medulla injury since the inspiratory and expiratory centers are located here

78. Glascow Coma Scale Widely used to measure severity of injury in a patient and prognosis Use best possible response Most predictive subsequent to resuscitation

79. GCS Eye opening 1- 4 Verbal response 1-5 Motor response 1- 6 Total 8 generally indicated intubation necessary for airway protection Dead person score? Motor response best predictor prior to sedation and paralysisTotal 8 generally indicated intubation necessary for airway protection Dead person score? Motor response best predictor prior to sedation and paralysis

80. Trauma Score Respiratory rate Blood pressure May be incorporated into the GCS

81. Secondary Brain Injury HYPOXIA HYPOTENSION Anemia Hyperglycemia Hypoglycemia Hyperthermia Intracranial mass

82. Significance Surviving the initial injury is a small part of the battle for the traumatic brain injured person Secondary injury may have a greater influence over the final outcome than the primary injury Two most common hypoxia and hypotension and may be as devastating as the primary injury

83. Hypotension Single most prognostic factor A single episode of decreased BP has been correlated with poorer outcome Brain requires blood flow for perfusion Keep BP > 90 systolic CPP= MAP- ICP Most important to keep MAP =/ > 70

84. Hypotension in the face of cerebral edema results in decreased CPP (cerebral perfusion pressure)

85. MAP (2) DBP + SBP 3 Normal (70- 100)

86. Hypoxia Defined as SpO2 < 90% Leads to cell damage and resultant swelling Closely follows hypotension in influence RSI faster and more reliable Less than 8 intubate

87. Treatment Provide adequate ventilation Provide adequate fluid resuscitation Continually monitor VS HOB@ 30 degrees and head midline Consider mannitol and hyperventilation if herniation imminent Prophylactic seizure medication is not indicated

88. Ventilation RSI and ventilate at a rate to maintain EtCo2 between 35- 45 mmHg Lidocaine 1mg/ kg prior to any intubation attempt

89. Hyperventilation Has become very controversial recently and is no longer automatically recommended May exacerbate brain injury in all but the herniating patient Receptors respond to increased O2 with vasoconstriction Injured tissue is no longer perfused Results in increased edema and necrosis

90. Fluid Resuscitation Initiate IV infusion to maintain SBP =/ > 90 Preferably Map > 70 mm HG Fluid of choice LR or NS Glucose causes fluid to be pulled into cells resulting in cerebral edema

91. Monitor Continuously monitor VS for Sx of rising ICP Changes in breathing patterns Increasing BP Decreasing HR Unequal pupils Posturing

92. Position Elevated HOB Midline head placement Assists with venous drainage from the head which decreases ICP

93. Hyperthermia Causes an increase in ICP and should be regulated Head injured patients often suffer from increased body temperatures and should be monitored Acetaminophen and other cooling techniques may be used Do not induce hypothermia which may lead to shivering which results in increased ICP

94. Seizures In the event of seizures treatment should be initiated immediately due to resultant hypoxia and increased ICP Treatment may include the use of Valium and Cerebyx Valium does not terminate abnormal electrical discharge as fosphenytoin does Patients may need to be in an induced barbiturate coma

95. Treatment in Herniation Hyperventilate to EtCo2 of no < 30 mmHg Mannitol- osmotic diuretic which may be useful in decreasing ICP 1- 1.5 mg/ kg Lasix is a loop diuretic and not useful Purpose is to keep the patient alive for definitive treatment surgical evacuation drain placed

96. Medications: Oxygen Primary 1st line drug Administer high flow Hyperventilation is contraindicated Reduces circulating CO2 levels NRB: 15 LPM BVM: 12-20 times per minute Keep SaO2 > 95%

97. Medications: Diuretics Mannitol (osmotrol) MOA Large glucose molecule Does not leave blood stream Osmotic Diuretic Effective in drawing fluid from brain Contraindication Hypovolemia & Hypotension CHF Dose 1gm/kg CAUTION Forms crystals at low temperatures Reconstitute with rewarming & gentle agitation USE IN-LINE filter & PREFLUSH line

98. Medications: Diuretics Furosemide (Lasix) MOA Loop Diuretic Inhibits reabsorption of Na+ in Kidneys Increased secretion of water and electrolytes Na+, Cl�, Mg++, Ca++. Venous dilation & Reduces cardiac preload May be given in combination with Mannitol Not effective in reducing cerebral edema Contraindication Pregnancy: fetal abnormalities Dose Slow IVP or IM over 1-2 minutes 0.5-1 mg/kg: Commonly 40 or 80 mg

99. Medications: Paralytics Succinylcholine (Anectine) MOA Depolarizing Medication Causes Fasciculations Onset & Duration Onset: 30-60 seconds Duration: 2-3 minutes Precaution Paralyzes ALL muscles including those of respiration Increases intraoccular eye pressure Contraindication Penetrating eye injury & Digitalis Dose 1-1.5 mg/kg IV Consider administration of defasiculating dose of paralytic Use with lidocaine 1mg/kg in head injured patients

100. Medications: Paralytics Pancuronium (Pavulon) MOA Non-depolarizing agent Does not affect LOC Onset & Duration Onset: 3-5 min Duration: 30-60 min Dose Must premed with sedative 0.04-0.1 mg/kg

101. Medications: Sedatives Diazepam (Valium) MOA Benzodiazepine Anti-anxiety Muscle relaxant Onset & Duration Onset: 1-15 min Duration: 15-60 min Dose 5-10 mg

102. Medications: Sedative Morphine MOA Opium alkaloid Analgesic Sedation Anti-anxiety Reduces vascular volume & cardiac preload Increases venous capacitance Side Effects Respiratory depression Hypovolemia Dose 5-10 mg IVP Consider using promethezine with to reduce nausea Naloxone (Narcan) is antagonist

103. Medications: Atropine MOA Anticholinergic Reduces parasympatholyic stimulation Reduce oral and airway secretions Reduce fasciculations Pupillary dilation Dose 0.5-1 mg rapid IVP

104. Medications: Dextrose Consider if patient is hypoglycemic Only if VERIFIED by GLUCOMETER Cause increased cerebral edema Dose 25 gm IVP Consider Thiamine if known alcoholic 100 mg Thiamine

105. Medications: Thiamine Vitamin B1 Essential for the processing of glucose through Kreb�s cycle Chronic alcoholics can have B1 depletion Dose 100 mg IV or IM

106. Transport Considerations Limit external stimulation Can increase ICP Can induce seizures Cautious about Air Transport Seizures

107. Transport Patients with increased ICP for greater than 4 hours show an increasingly poor outcome Should be quickly transported to definitive facility

108. controversy exists as to whether elevated ICP or decreased CPP is a more important prognostic factor. This is an important distinction because it directs the main goals of therapy in severely injured patients. If ICP elevations are considered a more important factor, then efforts may be directed at lowering ICP as a primary goal and improving CPP as a secondary goal. If one considers CPP to be the more important factor, then the primary goal of treatment should be to maintain an appropriate CPP.

109. Summary Bob was fortunate enough to be in the 3- 4% of patients with initial GCS 3 that recover with nearly complete neurological recovery He was removed from the mountain with the help of five EMS entities and Life Flighted out.

110. He was diagnosed with a diffuse axonal injury and remained in a coma for two weeks He was later discharged to a SNF for two months and underwent two years of rehabilitation Bob has returned to work and won multiple engineering awards and recently placed 11th in the Nike World Masters Games in the mountain bike competition

111. Conclusion We have the opportunity to make a substantial difference in the outcome of our patients with traumatic brain injuries if we follow scientifically validated guidelines Our two main adversaries are hypotension and hypoxia Maintain Map > 70 or SBP >90 Orally intubate patients with GCS <8 Hyperventilate only herniating injuries to EtCO2 to 30mmHG