1. Sean Caine Stefan Da Silva
Head Trauma
Sean Caine
Stefan Da Silva

2. Objectives Normal Physiology Pathophysiology Concussion Mild TBI
Epidural Hematoma
Subdural Hematoma
Traumatic SAH
Contusion
Skull Fractures
ED Approach to Head Trauma
Severe Head Injury – Mgmt

3. Anatomy
What are the layers of the scalp?
Name the meninges?

4. Normal Physiology Intracranial vault
Fixed internal volume of mL
Contents include:
Brain Parenchyma – 80%
Cerebrospinal fluid – 10%
Blood – 10%

5. Normal Physiology The Brain CSF Intravascular blood
SEMISOLID structure
Weighs 1400 g (3 lbs)
CSF mL
Produced primarily by the choroid plexus at 20mL/hr or 500 mL/day
Resorbed via arachnoid granulations into venous system
Intravascular blood mL
Volume of blood determined by cerebral blood flow (CBF)

6. Monro-Kellie Doctrine
Originally described over 150 yrs ago
Recognizing the skull to be a “rigid box” ICP is a function of the volume of its three components:
Brain
Blood
CSF

7. Monro-Kellie Doctrine
Data from Pathophysiology and management of the intracranial vault. In: Textbook of Pediatric Intensive Care, 3rd ed, Rogers, MC (Ed), Williams and Wilkins p. 646; figure 18.1.

8. Monro-Kellie Doctrine
Smith ER, Sepideh AH. Evaluation and management of intracranial pressure in adults. UpToDate. Last updated October 1, 2008.

9. Cerebral Blood Flow CBF = (CAP – CVP) ÷ CVR ↓CVR and ↑ CBF
Hypotension, acidosis, and hypercarbia cause cerebral vasodilation
↑CVR and ↓CBF
Hypertension, alkalosis, and hypocarbia promote cerebral vasoconstriction

10. Cerebral Blood Flow If CPP < 40 mm Hg Autoregulation
CBF is constant when CPP is mmHg
CPP=MAP-ICP
Normal ICP is 5-15 mmHg
If CPP < 40 mm Hg
Øautoregulation of CBF  ↓CBF  tissue ischemia
In trauma, autoregulation is easily disrupted and warrants tighter control. For example, knowing that

11. Hypertensive Encephelopathy
Cerebral Blood Flow
Hypertensive Encephelopathy
Cerebral Edema
Illustrates autoregulation with MAP of Caveat: curve shifts in presence of chronic hypertension
Ischemia
Smith ER, Sepideh AH. Evaluation and management of intracranial pressure in adults. UpToDate. Last updated October 1, 2008.

12. Pathophysiology

13. Direct Injury “direct” contact of head with object
skull initially bends inward at the point of contact (coup)
Local trauma
Skull fractures
Penetrating trauma
some energy is transmitted to the brain by shock waves that travel distant to the site of impact or compression
VERY RARELY OCCURS IN ISOLATION!
head is struck by an object or its motion is arrested by another object

14. Indirect Injury
acceleration-deceleration injury in absence of direct contact with skull
Concussion (contrecoup)
DAI
subdural hematomas
Injury distal to penetrating head trauma
cranial contents are set into motion by forces without direct contact with skull

15. Primary Injury
mechanical irreversible damage that occurs at the time of head trauma:
brain lacerations, hemorrhages, contusions, and tissue avulsions
mechanical cellular disruption and microvascular injury
No specific intervention exists to repair or reverse primary brain injury
Public health interventions aimed at reducing the occurrence of head trauma

16. Secondary Insults
Complicated series of reactions neurochemical, neuroanatomic, and neurophysioligical initiated at the time of injury
All currently used acute therapies for TBI are directed at reversing or preventing secondary injury
Therefore the cornerstone to ED mngmt of TBI…
Attributed to massive depolarization leading to intracellular and extracellular derangements (metabolic, ischemic, ion shifting, inparticular increased intracellular Calcium), and release of excitatory neurtransmitters glutamate that overwhelm compensatory/protective mechanisms such as free radical scavengers and antioxidants.

17. DEFENCE!!!

18. Secondary Brain Insults
Neurologic outcome is influenced by the extent and degree of secondary brain insults
Hypotension (sBP < 90 mm Hg) reduces cerebral perfusion (ischemia and infarction)
Hypoxia (PO2 < 60 mm Hg)
apnea caused by brainstem compression or injury
partial airway obstruction
injury to the chest wall that interferes with normal respiratory excursion
pulmonary injury that reduces effective oxygenation

19. Secondary Insults
Anemia (reduced oxygen-carrying capacity of the blood)
Increased mortality when Hct < 30%
Other potential reversible causes of secondary injury in head injury include hypercarbia, hyperthermia, coagulopathy, and seizures

20. Case 1
18 yo male presents with headache, nausea, vomiting x 3 over 12 hours
Mother states “there is a virus going around school”
Star player on high school team
At game last night sat out 3rd quarter after getting his “bell rung”
Returned to game for 4th quarter despite not feeling well

21. Case 1 On exam: Vitals Neuro Physical exam otherwise unremarkable
BP: 118/70 HR: 101 RR: 14 T: 36.4
Neuro
GCS: 15
Physical exam otherwise unremarkable
What is the differential diagnosis?
Did he receive a concussion?
Is he at risk for intracranial injury?
Does he need a CT?
Can he return to practice? If not, why? And when can he return to practice?

22. Concussion and Mild TBI

23. Concussion Definition:
“Exposure to a blunt force or acceleration deceleration injury AND any period of transient confusion, disorientation, impaired consciousness, loss of consciousness for less than 30 minutes, and any period of dysfunction of memory (amnesia) associated with the event, neurological or neuropsychological dysfunction”
Practice parameter: The Management of Concussion in Sports (Summary Statement). Report on Quality Standards Subcommittee. Neurology 1997; 48:

24. “Any trauma-induced alteration in mental status”
Concussion
Or more simply put:
“Any trauma-induced alteration in mental status”
What features place a person at high risk for significant findings on CT?
Practice parameter: The Management of Concussion in Sports (Summary Statement). Report on Quality Standards Subcommittee. Neurology 1997; 48:

25. Odds Ratio for Specific Clinical Findings and Positive Head CT
Signs of basilar skull fracture
14 (8-22)
Vomiting
3 (2-4)
Posttraumatic seizure
3 (1-10)
GCS 14
2 (1-3)
Neurological deficits
Anticoagulation
2 (1-4)
Dangerous Mechanism
Loss of consciousness
Odds Ratio for Specific Clinical Findings and Positive Head CT
Smits et al.
OR (95% CI)
Ibanez et al
Fabbri et al.
Signs of basilar skull fracture
14 (8-22)
11 (6-23)
10 (6-16)
Vomiting
3 (2-4)
4 (2-7)
5 (3-8)
Posttraumatic seizure
3 (1-10)
2 ( )
8 (6-12)
GCS 14
2 (1-3)
7 (4-14)
19 (14-26)
Neurological deficits
7 (2-25)
19 (13-28)
Anticoagulation
2 (1-4)
4 (3-7)
8 (3-9)
Dangerous Mechanism
Loss of consciousness
7 (4-11)
2 (2-3)
Posttraumatic amnesia
1.7 (1-2)
3 (2-5)
Headache
1.4 (1-2)
3 (2-6)
Intoxication
1 (0.6-2)
1 (0.3-3)
Age>65
Jagoda AS, Bazarian JJ, Bruns JJ, et al. Clinical Policy: Neuroimaging and ydecisionmaking in adult mild brain injury in the acute setting, in ACEP and CDC Clinical Policy

26. Canadian CT Head Rule
Inclusion Criteria (must have all of the following)
Blunt head trauma resulting in LOC, definite amnesia, or witnessed disorientation
Initial ED GCS = 13-15
Injury occurred within 24 hrs
Exclusion Criteria
<16 yrs old
Minimal head injury
No clear hx of trauma as primary event (ie syncope or seizure)
Penetrating or depressed skull fracture
Acute focal neuro deficit
Seizure prior to being assessed
Bleeding disorder or anticoagulant use
Second assessment
Pregnant

27. Canadian CT Head Rule High Risk (for neurological intervention)
GCS <15 2 h after injury
Suspected open or depressed skull fracture
Any sign of basal skull fracture
hemotympanum, ‘racoon’ eyes, CSF oto/rhinorrhea, Battle’s sign
Vomiting > 2 episodes
Age > 65 years
Medium risk (for brain injury on CT)
Amnesia before impact > 30 min
Dangerous mechanism
Pedestrian vs MVA, ejected from MVA, fall from 3 ft or 5 stairs

28. Design: prospective cohort study ( June 2000-December 2002). 9 EDs
Design: prospective cohort study ( June 2000-December 2002). 9 EDs adults
blunt head trauma → witnessed LOC, disorientation, or definite amnesia and a GCS The CCHR and NOC were compared in a subgroup of 1822 adults with minor head injury and GCS 15.
Outcomes Neurosurgical intervention and clinically important brain injury evaluated by CT and a structured follow-up telephone interview.
Results Among 1822 patients with GCS 15, 8 (0.4%) required neurosurgical intervention and 97 (5.3%) had clinically important brain injury.
NOC and the CCHR both had 100% sensitivity
CCHR was more specific (76.3% vs 12.1%, P.001) (neurosurgical intervention)
↓ CT rates (52.1% vs 88.0%, P.001)
Conclusion For patients with minor head injury and GCS score of 15, the CCHR and the NOC have equivalent high sensitivities for need for neurosurgical intervention and clinically important brain injury, but the CCHR has higher specificity for important clinical outcomes than does the NOC, and its use may result in reduced imaging rates.

29. Case continued…
His Dad takes you aside and mentions that a big game is coming up with US College Scouts.…can he play?

30. Return to Play Graded program of exertion
> 24 hrs at each level is needed
If any symptoms appear starts back to the previous asymptomatic level
Reasonable to use modified return to normal/non-sport activities
McCrory P, Johnston K, Meeuwisse W, Aubry M, Cantu R, Dvorak J, et al. Summary and agreement statement of the 2nd International Conference on Concussion in Sport, Prague Br J Sports Med 2005;39(4):

31. Second Impact Syndrome
Rare event
High mortality rate
Rapid/fulminant cerebral edema from second impact before brain fully recovers

32. Post-concussive syndrome
Prevalence:
80% are symptom free at 6 weeks
15% with symptoms at 1 yr
Common symptoms:
H/A, dizziness, decreased concentration, memory problems, sleep disturbances, irritability, fatigue, visual disturbances, judgement problems, depression, anxiety
Virtually clinically indistinguishable from PTSD
Require F/U with sports med/neuropsych

33. Recurrent Concussions
Strong evidence that recurrent concussions are more significant/severe than initial one
Young age is a risk factor
Associated with diminished cognitive function, slower recovery times, prolonged disability

34. Special Considerations: Mild TBI in presence of coagulopathy
Increased risk for poor outcome
>80% mortality for ICH in pts with elevated INR
Smaller studies suggest that >70% pts with elevated INR deteriorated after a normal CT
Mngmt:
Correct INR with FFP, vitamin K in context of ICH
Admit and observe pts with elevated INR (> 2) and normal CT

35. Observation and disposition
Observation is recommended for 24 hours after a mild TBI because of the risk of intracranial complications
Hospital admission is recommended for patients at risk for immediate complications from head injury
GCS <15
Abnormal CT scan: intracranial bleeding, cerebral edema
Seizures
Abnormal INR PTT
F/U with sports med/urgent neuro with PPCS>3weeks

36. Take Home – Concussion
Players should not be allowed to return to play in the current game or practice
Players should not be left alone to monitor for deterioration
Return to play must follow a medically supervised series of steps
Players should never return to play while symptoms persist

37. Case 2 28 year-old ♂ brought in by EMS Found outside the Cecil Tavern
“I was just standing outside minding my own f***ing business smoking when two a**holes came up asked me for a cigarette and then cracked me across the head with a baseball bat”
Bystanders state the was a brief LOC lasting ~5 min
EMS suspect he is intoxicated. Smells of booze. Slurred speech. Disshevelled. Confused. Often mumbling and eyes drifting close but rousable/

38. Case 2 O/E: Within minutes of sharing his colourful story… AVSS
GCS: 14
Right temporal swelling/boggy scalp
Within minutes of sharing his colourful story…
Difficult to rouse
Right fixed and dilated pupil

40. Epidural Hematoma

41. Epidural Hematoma Usually due to arterial injury
trauma to the skull base → tearing of middle meningeal artery
results in hemorrhage
Occasionally
anterior cranial fossa → rupture of the anterior meningeal artery
vertex → dural arteriovenous fistula
In ~15 % of cases, injury to one of the dural sinuses, or the confluence of sinuses in the posterior cranial fossa, is the source of hemorrhage

42. Epidural-Pathophysiology
Typically fraature of temporal bone ruptures branches of the middle meningeal artery
Expanding hematoma limited by dural attachment at sutures
This stripping of the dura from the calvarium may be part of the reason for the severe headache.

43. Pterion
Pterion

45. Epidural Hematoma - Hx Mean age 20-30 years
Caused by MVC, Falls, Assaults
Skull # present 75-95% of the time
Transient LOC with a “lucid interval”
Symptoms: HA, N/V, drowsiness, confusion, aphasia, seizures, and hemiparesis

46. Epidural Hematoma - Imaging
Head CT – fast, simple
“lens-shaped” pattern
collection is limited by dural attachments at cranial sutures

48. Epidural - Management Neurologic emergency Operative Non-Operative
hematoma expansion
elevated intracranial pressure
brain herniation
Operative
Craniotomy and hematoma evacuation
Burr Hole
Non-Operative
Close observation
serial brain imaging
hematoma enlargement
neurologic deterioration

49. Surgical Indications for EDH
An EDH > 30 cm3 should be surgically evacuated regardless of the patient's GCS
GCS < 9 with anisocoria → evacuation ASAP
An EDH
< 30 cm3
< 15-mm thickness
< 5-mm midline shift (MLS) in patients
with a GCS > 8
w/o focal deficit
…non-operative mgmt with serial CTs and close neurological observation in a neurosurgical center

50. Case 3 83 ♀ presents with confusion
Gradually increasing over the past week
No history of trauma
GCS: 14
CN: ii-xii normal – no focal findings
Urine + nitrates/leuks –epithelials
CT Head

54. Subdural Hematoma

55. Subdural Hematoma SDHs form b/w the dura and the brain
Usually they are caused by the movement of the brain relative to the skull
acceleration-deceleration injuries
Common in patients with brain atrophy (EtOH or elderly)
Superficial bridging vessels traverse greater distances than in patients with no atrophy (more likely to rupture with rapid movement of the head)
Occurs in ~30% of patients with severe head trauma
slow bleeding of venous structures delays clinical signs

56. Acute SDH 24 hours post trauma ↓ LOC;
lucid interval: 50% - 70% → ↓mentation

57. Subacute SDH symptomatic 24h - 2 wks post injury
CT: hypodense or isodense lesion
absence of sulci
shift
contrast  detection of isodense lesions

58. Chronic SDH >2 weeks post trauma Hemiparesis or Weakness: ~45%
↓LOC: ~50%

59. What type of ICH is this? Why?

60. Case 4
51 ♂ MVC – single vehicle at highway speeds off road and into a tree
?LOC
GCS 8 (scene) 8 (now)

62. Traumatic Subarachnoid Haemorrhage

63. Traumatic SAH
TSAH is defined as blood within the CSF and meningeal intima
results from tears of small subarachnoid vessels
detected on the first CT scan in up to 33% of patients with severe TBI (incidence of 44% in all cases of severe head trauma)
 incidence of skull fractures and contusions
↓GCS →  SAH
 SAH → ↓Outcome

64. Traumatic SAH Øcontrast CT:  density in basilar cisterns
 density interhemispheric fissures/sulci
prognosis reasonable
cerebral vasospasm → cerebral ischemia

65. Chicken vs Egg
Did this patient lose consciousness while driving because of spontaneous SAH and subsequently crash his car, or did the patient sustain head injury from the motor vehicle accident causing traumatic SAH?
cerebral angiogram to exclude an underlying aneurysm or vascular malformation

66. Diffuse Axonal Injury

67. Diffuse Axonal Injury
Definition: prolonged traumatic coma not caused by mass lesions, ischemic insults, or nontraumatic etiologies
Typically coma persisting > 6h
CT often normal
classic finding are small petechial hemorrhages adjacent to third ventricle, within the corpus collosum, or internal capsule
Most common CT finding in severe head injury

68. Diffuse Axonal Injury Mild DAI Mod DAI Severe DAI Coma 6-24 h
1/3 will demonstrate decorticate or decerebrate posturing
15% mortality
Most recover with mild or no permanent deficits
Mod DAI
Coma > 24h
Abnormal posturing
Severe posttraumatic amnesia
Moderate cognitive deficit
25% mortality
Severe DAI
Majority due to MVA
Autonomic dysfunction (tachycardia, HTN, irreg resps)
Majority die
Others are severely disabled or persistent vegetative satate

69. SKULL FRACTURES

70. Linear skull fracture
low-energy blunt trauma over a wide surface area of the skull.
Full thickness through bone
…of little significance except
when it runs through a vascular channel,
venous sinus groove
suture
Then, it may cause
epidural hematoma
venous sinus thrombosis and occlusion
sutural diastasis

71. Fractures Sutures Less than 2 mm in width Same width throughout
Greater than 3 mm in width
Widest at the center and narrow at the ends
Runs through both the outer and the inner lamina of bone, hence appears darker
Usually over temporoparietal area
Usually runs in a straight line
Angular turns
Sutures
Less than 2 mm in width
Same width throughout
Lighter on x-rays compared with fracture lines
At specific anatomic sites
Does not run in a straight line
Curvaceous

72. Basilar skull fracture
Petrous temporal bone: CSF otorrhea and bruising over mastoids (Battle sign)
Anterior cranial fossa: CSF rhinorrhea and bruising below eyes (raccoon eyes)
Longitudinal temporal bone → ossicular chain disruption and conductive deafness Facial palsy, nystagmus, and facial numbness are 2’ to VII, VI, and V CN palsy
Transverse temporal bone: VIII CN palsy and labyrinth injury → nystagmus, ataxia, and permanent neural hearing loss
Occipital condylar fracture: coma and have other associated c-spine injuries
Vernet syndrome or jugular foramen syndrome is involvement of IX, X, and XI CN → difficulty in phonation, aspiration and ipsilateral motor paralysis of the vocal cord, soft palate (curtain sign), superior pharyngeal constrictor, sternocleidomastoid, and trapezius.

73. Depressed Skull Fracture
Elevation
depressed segment is > 5mm below inner table
gross contamination,
dural tear with pneumocephalus
underlying hematoma
Craniectomy
underlying brain is damaged and swollen

74. CSF Oto/rhinorrhea Dab fluid on a tissue paper,
a clear ring of wet tissue beyond the blood stain, called a "halo" or "ring" sign

75. ED Approach to Head Trauma

76. Focused Hx
Mechanism
LOC
Seizure?
Ambulatory at scene
GCS at scene

77. Focused Physical ABC’s ATLS protocol GCS Signs of external injury
Pupils
Check Ears/Nose
Extremities - movement

78. Glasgow Coma Scale* Motor response (M) Eye Opening (E)
6. Obeys commands
5. Localizes pain
4. Withdraws from pain
3. Abnormal flexion
2. Abnormal extension
1. None
Eye Opening (E)
4. Spontaneous
3. To voice
2. To pain
1. None
Verbal Responses (V)
5. Oriented
4. Confused
3. Inappropriate words
2. Incomprehensible sounds
*Developed for evaluation of head trauma 6 hours post injury
Deceased and rocks have GCS 3

79. Emergent Management of Closed Head Injury

80. Case 6 22 ♀ bicycle vs truck LOC Agitated at the scene GCS
Opens eyes to pain
Withdraws on left and localizes on right
Sounds – no inteligible words 2 5 2

81. Outline Airway Avoid Hypoxia Avoid Hypotension
Brain Specific Therapies
Position
Hyperventilation
Mannitol
Hypertonic Saline
Cooling
Indications for ICP Monitoring
Surgical Management

82. Airway
Capture it!
How you do it probably does not have a great effect on neurological outcome unless you cause hypoxemia or hypotension
There is little evidence-based medicine to guide the choice of agents

83. Intubation – Indications*
Coma (i.e. GCS 8) or significantly deteriorating LOC
Loss of protective laryngeal reflexes
Copious bleeding into mouth
Respiratory arrhythmia
Ventilatory insufficiency
clinical decision - not necessarily requiring ABG
Bilateral mandibular fracture
Any facial injury compromising airway
Seizures
Any other injury that requires ventilation/intubation
Agitated patient requiring CT scan
*Eastern Association For The Surgery of Trauma, 2003; NICE guidelines, 2003

84. Case Paramedics state his GCS “…was 7 or 8 at the scene”
Should they have intubated?

85. Methods: Before–After system wide controlled clinical trial conducted in 17 cities. Adult patients who had experienced major trauma in a BLS phase and a subsequent ALS phase (during which paramedics were able to perform intubation and administer fluids and drugs intravenously). The primary outcome was survival to hospital discharge.
Results:
Survival did not differ overall (81.1% ALS v. 81.8% among those in the BLS; p=0.65)
Among patients with GCS < 9, survival was ↓ with ALS (50.9% v. 60.0%; p=0.02)
The adjusted odds of death for the advanced life-support v. basic life-support phases were non-significant (1.2, 95% confidence interval 0.9–1.7; p=0.16)
Interpretation: The OPALS Major Trauma Study showed that systemwide implementation of full advanced life-support programs did not decrease mortality or morbidity for major trauma patients. We also found that during the ALS phase, mortality was greater among patients with GCS < 9.
These patients are sensitive to Hypoxia and Hypotension

86. Airway Preparation and Preoxygenation Prevent ICP rise
Lidocaine mg/kg IV
Rocuronium mg/kg (defasciculating dose)
Fentanyl 3 ug/kg IVP
Prevent Vagally stimulated bradycardia
Atropine 0.01 mg/kg IV (Minimum dose: 0.1 mg)
Sedation
Etomidate 0.3 mg/kg IVP OR
Thiopental (Pentothal) 4 mg/kg IVP (IF BP stable) OR
Propofol 2mg/kg IVP OR
Midazolam 0.1mg/kg (max 5mg) IVP
Ketamine (2 mg/kg) IV
Muscle relaxants
Succinylcholine 1.5 mg/kg IV OR
Rocuronium 0.6 mg/kg IV

87. Airway - Intubation Lidocaine (1.5 to 2 mg/kg IV push)
…may ↓ cough reflex, HTN response, ICP
Succinylcholine – fasciculations ↑ICP
premedicate w a subparalytic dose of a nondepolarizing agent
Etomidate (0.3 mg/kg IV)
good effect on ICP ↓CBF and metabolism
minimal adverse effects on BP
Minimal respiratory depressant effects
Ketamine
May increase ICP
Anaes and animal studies indicate no increased ICP

88. Methods: Medline literature search was undertaken for evidence of the effect of succinylcholine (SCH) on the intracranial pressure (ICP) of patients with acute brain injury and whether pretreatment with a defasciculating dose of competitive neuromuscular blocker is beneficial in this patient group.
Conclusions: Studies were weak and small
For those patients suffering acute TBI the authors could find no studies that investigated the issue of pretreatment with defasciculating doses of competitive neuromuscular blockers and their effect on ICP in patients given SCH.
SCH caused ↑ ICP for patients undergoing neurosurgery for brain tumours with elective anaesthesia and that pretreatment with defasciculating doses of neuromuscular blockers reduced such increases. ?impact on outcome.

89. Background: laryngeal instrumentation and intubation is associated with a marked, transient rise in ICP.
Methods: A literature search was carried out to identify studies in which intravenous lidocaine was used as a pretreatment for RSI in major head injury. Any link to an improved neurological outcome was also sought.
Results: No evidence was found to support the use of intravenous lidocaine as a pretreatment for RSI in patients with head injury and its use should only occur in clinical trials.

90. Case 7
22 ♀ with presumed CHI
Now intubated.
What are your priorities?

91. AVOID HYPOXEMIA

92. Hypoxemia and Arterial Hypotension at the Accident Scene in Head Injury
Stocchetti, Nino MD; Furlan, Adriano MD; Volta, Franco MD
Design: Prospective, observational study.
Materials and Methods: Arterial Hbo2 was measured before tracheal intubation
at the accident scene in 49 consecutive patients with head injuries. Arterial
pressure was measured using a sphygmomanometer.
Main Results: Mean arterial saturation was 81% (SD 24.24); mean arterial systolic
pressure was 112 mm Hg (SD 37.25). Airway obstruction was detected in 22
cases. Twenty-seven patients showed an arterial saturation lower than 90% on
the scene, and 12 had a systolic arterial pressure of less than 100 mm Hg. The
outcome was significantly worse in cases of hypotension, desaturation, or both.
Conclusions: Hypoxemia and shock are frequent findings on patients at the
accident scene. Hypoxemia is more frequently detected and promptly corrected,
while arterial hypotension is more difficult to control. Both insults may have a
significant impact on outcome
Volume 40(5) May 1996 pp

93. Methods: 846 cases of severe TBI (GCS ≤ 8) were analyzed retrospectively to clarify the effects of multiple factors on the prognosis of patients.
Results:
Worse outcomes were strongly correlated (p < 0.05) with GCS score, age, pupillary response and size, hypoxia, hyperthermia, and high intracranial pressure (ICP).
Even a single O2 sat reading < 90% was associated with a significantly worse outcome
Conclusions: These findings indicate that prevention of hypoxia, control of high ICP, and prevention of hyperthermia may improve outcome in patients with TBI

94. AVOID HYPOTENSION

95. Trauma Coma Data Bank 100 Favourable outcome 90 Unfavourable outcome80 70 60 50
% of patients in outcome group 40 30 20 10
Trauma Coma Data Bank
none
early
late
both
Timing of hypotension (SBP < 90 mmHg)
Traumatic Coma Data Bank 1991

96. Hypotension Single occurrence of ↓BP (SBP<90mmHg)
doubles mortality*
↑ disability in survivors of head injury*
↑duration and ↑ frequency = ↓ prognosis**
*Chesnut et al., 1993; Management and Prognosis of Severe Traumatic Brain Injury, 2000
**Schierhout and Roberts, 2000

97. Hypotension

98. Mean Arterial Pressure
What is adequate?
Enough to maintain CBF
Normally (MAP mmHg and ICP ~10 mmHg)
CPP is normally between 70 and 90 mmHg
<70 mmHg for a sustained period → ischemic injury
Outside of the limits of autoregulation
↑ MAP raises CPP
↑ ICP lowers CPP

99. Blood pressure control
BP should maintain CPP>60 mmHg
pressors can be used safely without further ↑ ICP
…in the setting of sedation → ?iatrogenic ↓BP
Hypertension should generally not be treated
Avoid CPP <60 mmHg or
normalization of BP in chronic HTN
…the autoregulatory curve has shifted to the right

100. Case 8 Asymetric Pupils – L fixed and dilated What is happening?
What would you like to do?

101. Herniation Syndromes Uncal Most common
Temporal lobe uncus forced through tentorial hiatus
Compression of CN III causing ipsilateral:
Anisocoria
Impaired EOM
Sluggish pupil (EARLY)
Fixed and dilated (LATE)
Contralateral Babinski’s
Bilateral decorticate posturing (LATE)
Anterior view of transtentorial herniation caused by large epidural hematoma. Skull fracture overlies hematoma. (From Rockswold GL: Head injury. In Tintinalli JE et al [eds]: Emergency Medicine. New York, McGraw-Hill, 1992, p 915.)

102. Kernohan’s notch syndrome
Herniation Syndromes
Kernohan’s notch syndrome
Contralateral cerebral peduncal forced against opposite endge of tentorium
~25% of uncal herniations
Motor signs ipsilateral to the dilated pupil
Anterior view of transtentorial herniation caused by large epidural hematoma. Skull fracture overlies hematoma. (From Rockswold GL: Head injury. In Tintinalli JE et al [eds]: Emergency Medicine. New York, McGraw-Hill, 1992, p 915.)

103. Central Transtentorial
Herniation Syndromes
Central Transtentorial
Bilateral rostrocaudal deterioration
Early
Bilateral motor weakness
Pinpoint pupils (<2mm)
Increased muscle tone
Bilateral Babinski’s
Later
Midpoint fixed pupils
Decorticate → decerebrate
Irregular resps
Expanding lesion at the vertex, frontal or occipital pole
Diencephalon compression – small reactive pupils
Midpoint fixed due to midbrain compression
(Accessed May 12, 2009)

104. Herniation Syndromes Cerebellotonsillar 70% mortality
Medullary compression by cerebellar tonsils
Sudden respiratory and CV collapse
Pinpoint pupils
Flaccid quadriplegia
Cerebellar tonsils herniate downwards through foramen magnum. Compress medulla.Also caused by cerebellar mass or central vertex mass lesion.
Flaccid paralysis from bilateral compression of corticospinal tracts
Pictured is T2 MR image cerebellotonsillar herniation from a posterior fossa subarachnoid cyst
(Accessed May 12, 2009)

105. Upward Transtentorial
Herniation Syndromes
Upward Transtentorial
Expanding posterior fossa lesion
Pinpoint pupils
Downward conjugate gaze
Figure 10 : Ascending transtentorial herniation in a 13-year-old boy. Sagittal FLAIR MRI demonstrates upward bulging of the vermis (arrowheads) and downward displacement of the cerebellar tonsils (arrow). Callosal diffuse axonal injury is also seen.

106. Brain Specific Therapies

107. Position Maximize venous outflow from the head
↓ excessive flexion or rotation of the neck
avoid restrictive neck taping
minimize stimuli that could induce Valsalva
(i.e. suctioning)
Position the head above the heart (30o)
head elevation may lower CPP

108. Hyperventilation Once a mainstay for treatment of ↑ICP
Concerns about cerebral ischemia
difficult to demonstrate
Outcome worse with hyperventilation in some studies of head injury
The theoretical advantages of hyperventilation are cerebral vasoconstriction for intracranial pressure (ICP) control and reversal of brain and cerebrospinal fluid (CSF) acidosis. Possible disadvantages include cerebral vasoconstriction to such an extent that cerebral ischemia ensues, and only a short-lived effect on CSF pH with a loss of HCO3-buffer from CSF.

109. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial
Methods: RCT
normal ventilation PaCO2 35Hg
hyperventilation PaCO2 25Hg
hyperventilation plus THAM
Outcome: GCS at 3/6/12 months
Results:
Those in the 25 mm Hg group did worse
Muizelaar et. al. 1991

110. Acute head injury (6 hrs post impact)
Areas in red show regions with rCBF < 20 ml/100g/min)
(Coles et al. Crit Care Med 2002)
0 ml/100g/min 60
0 ml/100g/min 60
PaCO2: 38 mmHg
PaCO2: 25 mmHg

112. Mannitol Benefits: Plasma expanding effect
Reduces hematocrit and viscosity
↑ cerebral blood flow
Osmotic effect creates a fluid gradient out of cells. This osmotic effect initially decreases intracellular edema, thus decreases ICP

113. Mannitol Drawbacks: Osmotic diuresis HYPOTENSION
May accumulate in the brain and result is a “reverse osmotic shift” potentially increasing ICP
Acute renal failure

114. Mannitol Indications: (prior to ICP monitoring)
Signs of transtentorial herniation
Progressive neurological deterioration
not attributable to extra-crainal complications
Dose: 0.25 – 1g/kg IV bolus
Avoid hypovolemia
(foley recommended)

115. Hyperosmotic agents Dose: 2-4 ml/Kg 5% NaCl Max Na+ ~ 160 mmol/l
Mannitol effective through non- osmotic effects
Problems with big fluid shifts from diuresis
Increasing interest in use of hypertonic saline (3-24%)
? more effective with fewer side effects.
Outcome  with  Na+; survival with Na+ 180 mmol/l!
Munar et al. J Neurotrauma :41-51.
Horn et al. Neurol Res 1999;21:
Quereshi et al. J Trauma 1999;47:
Simma et al. Crit Care Med 1998;26:
Clark & Kochanek. Crit Care Med 1998;26:
Doyle et al. J Trauma 2001; 50:
Petersen et al. Crit Care Med 2000;28:
Dose: 2-4 ml/Kg 5% NaCl
Max Na+ ~ 160 mmol/l
Max osmol ~ 325 mOsm/l

116. Methods: Consecutive patients with clinical TTH treated with 23
Methods: Consecutive patients with clinical TTH treated with 23.4% saline (30 to 60mL) were included in a retrospective cohort. Factors associated with successful reversal of TTH were determined.
Results: 76 TTH events. In addition to 23.4% saline, TTH management included hyperventilation (70% of events), mannitol (57%), propofol (62%), pentobarbital (15%), ventriculostomy drainage (27%), and decompressive hemicraniectomy (18%).
Reversal of TTH occurred in 57/76 events (75%).
Reversal of TTH was predicted by a 5 mmol/L rise in serum sodium concentration (p ) or an absolute serum sodium of 145 mmol/L (p ) 1 hour after 23.4% saline.
Adverse effects included transient hypotension in 13 events (17%); no evidence of central pontine myelinolysis was detected on post-herniation MRI (n 18). Twenty-two patients (32%) survived to discharge, with severe disability in 17 and mild to moderate disability in 5.
Conclusion: Treatment with 23.4% saline was associated with rapid reversal of transtentorial herniation (TTH) and reduced intracranial pressure, and had few adverse effects. Outcomes of TTH were poor, but medical reversal may extend the window for adjunctive treatments.

117. Case
The R2 ER resident on NSx asks what you think his chances are of putting in a EVD?
What are the indications for ICP monitoring?

118. Antiepileptic therapy

119. Antiepileptic therapy
Seizure incidence
12% blunt trauma
50% penetrating head injury
Seizures can contribute to
Hypoxia, Hypercarbia
Release of excitatory neurotransmitters
↑ICP
Anticonvulsant therapy → if seizing
Prophylaxis
There are no clear guidelines
? high-risk mass lesions

120. Anti-epileptic Acute Treatment
Lorazepam ( mg/kg IV, over 2-5 min - max 4 mg)
Diazepam (0.1 mg/kg, up to 5 mg IV, Q10 min - max20 mg)
Prophylaxis
phenytoin (13 to 18 mg/kg IV)
fosphenytoin (13 to 18 phenytoin equivalents/kg)

121. Data collection and analysis
Selection criteria
All randomised trials of anti-epileptic agents, in which study participants had a clinically defined acute traumatic head injury of any severity. Trials in which the intervention was started more than eight weeks after injury were excluded.
Data collection and analysis
Two reviewers
Relative risks and 95% confidence intervals (95%CI) were calculated
Main results
10 eligible RCTs, 2036 participants
(RR) for early seizure prevention was 0.34 (95%CI 0.21, 0.54)
↓ risk of early seizures by 66%
Seizure control in the acute phase did not show ↓ mortality (RR = 1.15; 95%CI 0.89, 1.51)
↓ death/disability (RR = 1.28; 95%CI 0.90, 1.81)
Authors' conclusions
Prophylactic anti-epileptics reduce early seizures
No reduction in late seizures
No effect on death and neurological disability
Insufficient evidence is available to establish the net benefit of prophylactic treatment at any time after injury.

122. Seizure Prophylaxis in Severe Head Trauma
Indications*
Depressed skull fracture   
Paralyzed and intubated patient   
Seizure at the time of injury   
Seizure at ED presentation   
Penetrating brain injury   
Severe head injury (GCS ≤8)   
Acute subdural hematoma   
Acute epidural hematoma   
Acute intracranial hemorrhage   
Prior Hx of seizures
*Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed.

123. Steroids Beneficial in tumors Decreases cerebral edema
Many reasonable sized RCTs that have failed to show benefit.
Some have shown mild benefits in subgroup analysis
Not recomended

124. On Injuries of the Head 400 B.C.E
“…a man will survive longer in winter than in summer, whatever be the part of the head in which the wound is situated.”
On Injuries of the Head 400 B.C.E
Hippocrates

128. Case You are doing a summer locum in Nelson, BC
Cyclist brought in by EMS
Fell off 20 ft ledge while mountain biking
No Helmet
GCS 12 on the scene

129. CT scanner is 1 h E. NeuroSx is 3 h NW. No general surgeon in town.
O/E
HR RR10 BP105/72 T36.6
GCS Pupils 2 mm and reactive
Left temporal scalp bogginess
Obvious deformity to left wrist
Cspine collar, intubated, 2 large bore IVs
GCS declines to 5 despite medical therapy. Right pupil becomes fixed and dilated. Left sided babinski’s.
CT scanner is 1 h E. NeuroSx is 3 h NW. No general surgeon in town.

130. ED Burr Hole - Preparation
Type and screen, PTT, INR
Administer IV antiobiotics (ie ceftriaxone)
Shave and prep patient
2% lido with epi to reduce scalp bleeding
Place sandbag/pillow under ipsilateral shoulder to optimize venous return from head
Get equipment
Scalpel with 15 blade
Self-retaining retractor
Suction
Penetrator and burr drill bit
Rangeur
Hook
Elevator
Drain (ie Jackson-Pratt)
Suture tray
Bone wax

131. ED Burr Hole - Exposure
4 cm vertical incision 3cm (2 finger breadths) anterior to tragus and 2cm above zygoma
Divide temporalis muscle and lift it off the skull with scalpel handle
Insert self-retaining retractor
Avoid superficial temporal artery. Remaining above zygoma protects the facial nerve.

132. ED Burr Holes - Decompression
Triangular-shaped perforator to penetrate to inner table of skull
Saline, suction to clear field

133. ED Burr Holes - Decompression
Switch to burr bit to produce cylindrical hole
Leave fine rim of inner table
Separate dura from inner table with elevator
Rangeur rim
If epidural – suction our blood/clot
If subdural, elevate dura with hook and incise with 15 blade
DO NOT SUCTION THE BRAIN TISSUE
Place drain in small pocket of temporalis muscle and close scalp
Consider frontal, parietal and then contralateral holes if no hematoma found

134. ED Burr Holes

135. ED Burr Holes Relative Indications Contraindications Complications
GCS < 8
Lateralizing signs (anisocaria, hemiparesis)
Autonomic dysfunction (tachycardia, hypertension, irregular resps)
Refractor to medical tx
Delay to surgery
Phone consult and NSx agrees
Contraindications
Lack of training
Coagulopathy
Complications
CN Injury (ie CN VII)
Infection
Bleeding
Unable to identify lesion
Duration of decerebrate 70% < 2h. 40% if 4-6 h, 0%<6
Delay to sx for acute SDH 30-90% if >4h

136. Questions?

137. Acknowledgements
Dr. Mark Bromley
Dr. Stefan Da Silva
Dr. David Zygun

138. Brain Tissue pH and Blood Glucose
Brain pH
Glucose 5 10 15 20 6
6.5 7
7.5
Brain pH

139. Hyperglycemia-Induced Neuronal Injury
Intracellular acidosis triggers calcium entry into the cell, lipolytic release of cytotoxic free fatty acids and glutamate and eventually cell death
↓ glucose available to the glycolytic pathway, treatment of hyperglycemia could theoretically ↓ lactate production, ↑ pH, result in less neuronal damage, and improve patient outcome

140. Blood Glucose
Lam et al found 43% of patients with severe brain injury to have admission blood glucose levels above 11.1 mM
Rovlias and Kotsou showed postoperative glucose levels, independent of their relationship with GCS, significantly contributed to the prediction of the patients’ prognosis

141. Hyperglycemia-Induced Neuronal Injury
? increased tissue lactic acidosis
Brain tissue acidosis is associated with mortality following head injury
↑ glucose supply during incomplete ischemia may allow continuation of anaerobic glycolysis, which would lead to accumulation of lactate and subsequently to tissue acidosis
Injured brain cells may not be able to metabolize excess or even normal levels of glucose through the oxidative pathway.

143. Therapeutic Hypothermia: Experimental Evidence

144. NABIS:H I Outcomes

145. NABIS:H I Temperature Data
Target Temp
hrs
The cardiac arrest protocols differed from the brain injury protocols, however, in that hypothermia induction was begun within 60 minutes of cardiac arrest. The earliest that hypothermia induction was begun in brain injury studies was 4 hours after injury in the multicenter trial with induction 8–24 hours after injury in other trials. This may be important in explaining the variance in results of the two diseases. In the laboratory, hypothermia must be induced in less than 1 hour after experimental brain injury to have any neuroprotective effect. The treatment window is like a trigger. The effect is present and strong if hypothermia is rendered within 60 minutes in rats, and there is no effect whatsoever after that

146. NABIS:H I
AIM
To determine whether surface-induced moderate hypothermia (33.0o C), begun rapidly after severe traumatic brain injury (GCS 3-8) and maintained for 48 hours will improve outcome with low toxicity

147. ER physician’s role in brain death
Hope Program

148. Hypothermia Treatment Window

149. Therapeutic Hypothermia: Cardiac Arrest