Head Trauma

1
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
4
Normal Physiology

• Intracranial vault
• Fixed internal volume of 1400-1700 mL
• Contents include
• Brain Parenchyma 80
• Cerebrospinal fluid 10
• Blood 10

5
Normal Physiology

• The Brain
• SEMISOLID structure
• Weighs 1400 g (3 lbs)
• CSF
• 100-150 mL
• Produced primarily by the choroid plexus at
  20mL/hr or 500 mL/day
• Resorbed via arachnoid granulations into venous
  system
• Intravascular blood
• 100-150mL
• 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 1996. 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

• Autoregulation
• CBF is constant when CPP is 50-160 mmHg
• CPPMAP-ICP
• Normal ICP is 5-15 mmHg
• If CPP lt 40 mm Hg
• Øautoregulation of CBF ? ?CBF ? tissue ischemia

11
Cerebral Blood Flow
Hypertensive Encephelopathy Cerebral Edema
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!

14
Indirect Injury

• acceleration-deceleration injury in absence of
  direct contact with skull
• Concussion (contrecoup)
• DAI
• subdural hematomas
• Injury distal to penetrating head trauma

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

17
DEFENCE!!!
18
Secondary Brain Insults

• Neurologic outcome is influenced by the extent
  and degree of secondary brain insults
• Hypotension (sBP lt 90 mm Hg) reduces cerebral
  perfusion (ischemia and infarction)
• Hypoxia (PO2 lt 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 lt 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
• BP 118/70 HR 101 RR 14 T 36.4
• Neuro
• GCS 15
• Physical exam otherwise unremarkable

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
48581-585.
24
Concussion

• Or more simply put
• Any trauma-induced alteration in mental status

Practice parameter The Management of Concussion
in Sports (Summary Statement). Report on Quality
Standards Subcommittee. Neurology 1997
48581-585.
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 2 (1-3)
Anticoagulation 2 (1-4)
Dangerous Mechanism 2 (1-4)
Loss of consciousness 2 (1-3)
Smits et al. OR (95 CI) Ibanez et al OR (95 CI) Fabbri et al. OR (95 CI)
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 (0.25-17) 8 (6-12)
GCS 14 2 (1-3) 7 (4-14) 19 (14-26)
Neurological deficits 2 (1-3) 7 (2-25) 19 (13-28)
Anticoagulation 2 (1-4) 4 (3-7) 8 (3-9)
Dangerous Mechanism 2 (1-4) 3 (2-4)
Loss of consciousness 2 (1-3) 7 (4-11) 2 (2-3)
Posttraumatic amnesia 1.7 (1-2) 3 (2-5) 8 (6-12)
Headache 1.4 (1-2) 3 (2-6)
Intoxication 1 (0.6-2) 1 (0.3-3)
Agegt65 2 (1-3) 2 (1-3)
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. 2008.
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
• lt16 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 lt15 2 h after injury
• Suspected open or depressed skull fracture
• Any sign of basal skull fracture
• hemotympanum, racoon eyes, CSF oto/rhinorrhea,
  Battles sign
• Vomiting gt 2 episodes
• Age gt 65 years
• Medium risk (for brain injury on CT)
• Amnesia before impact gt 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. 2707 adults
• blunt head trauma ? witnessed LOC,
  disorientation, or definite amnesia and a GCS
  13-15. 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
• gt 24 hrs at each level is needed
• If any symptoms appear starts back to the
  previous asymptomatic level

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 2004. Br J Sports Med
200539(4)196-204.
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
• gt80 mortality for ICH in pts with elevated INR
• Smaller studies suggest that gt70 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 (gt 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 lt15
• Abnormal CT scan intracranial bleeding, cerebral
  edema
• Seizures
• Abnormal INR PTT
• F/U with sports med/urgent neuro with PPCSgt3weeks

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
  fing business smoking when two aholes 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
• AVSS
• GCS 14
• Right temporal swelling/boggy scalp
• Within minutes of sharing his colourful story
• Difficult to rouse
• Right fixed and dilated pupil

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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
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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

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48
Epidural - Management

• Neurologic emergency
• 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 gt 30 cm3 should be surgically evacuated
  regardless of the patient's GCS
• GCS lt 9 with anisocoria ? evacuation ASAP
• An EDH
• lt 30 cm3
• lt 15-mm thickness
• lt 5-mm midline shift (MLS) in patients
• with a GCS gt 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

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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

• gt2 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)

61
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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 gt 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
• 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 gt 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
• 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 gt 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

• ABCs
• ATLS protocol
• GCS
• Signs of external injury
• Pupils
• Check Ears/Nose
• Extremities - movement

78
Glasgow Coma Scale

• Motor response (M)
• 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
• 1. None

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/intubat
  ion

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 BeforeAfter 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 p0.65)
• Among patients with GCS lt 9, survival was ? with
  ALS (50.9 v. 60.0 p0.02)
• The adjusted odds of death for the advanced
  life-support v. basic life-support phases were
  non-significant (1.2, 95 confidence interval
  0.91.7 p0.16)
• 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 lt
  9.

86
Airway

• Preparation and Preoxygenation
• Prevent ICP rise
• Lidocaine 1.5-2 mg/kg IV
• Rocuronium 0.06 - 0.1 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 764-767
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 lt
  0.05) with GCS score, age, pupillary response and
  size, hypoxia, hyperthermia, and high
  intracranial pressure (ICP).
• Even a single O2 sat reading lt 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
100
Favourable outcome
90
Unfavourable outcome
80
70
60
50
of patients in outcome group
40
30
20
10
0
none
early
late
both
Timing of hypotension (SBP lt 90 mmHg)
Traumatic Coma Data Bank 1991
96
Hypotension

• Single occurrence of ?BP (SBPlt90mmHg)
• 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 60-150 mmHg and ICP 10 mmHg)
• CPP is normally between 70 and 90 mmHg
• lt70 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 CPPgt60 mmHg
• pressors can be used safely without further ? ICP
• in the setting of sedation ? ?iatrogenic
  ?BP
• Hypertension should generally not be treated
• Avoid CPP lt60 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 Babinskis
• 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
Herniation Syndromes

• Kernohans 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
Herniation Syndromes

• Central Transtentorial
• Bilateral rostrocaudal deterioration
• Early
• Bilateral motor weakness
• Pinpoint pupils (lt2mm)
• Increased muscle tone
• Bilateral Babinskis
• Later
• Midpoint fixed pupils
• Decorticate ? decerebrate
• Irregular resps

http//download.imaging.consult.com/ic/images/S193
3033208702313/gr8-midi.jpg (Accessed May 12, 2009)
104
Herniation Syndromes

• Cerebellotonsillar
• 70 mortality
• Medullary compression by cerebellar tonsils
• Sudden respiratory and CV collapse
• Pinpoint pupils
• Flaccid quadriplegia

http//scielo.isciii.es/img/revistas/neuro/v18n3/5
_img_1ab.jpg (Accessed May 12, 2009)
105
Herniation Syndromes

• Upward Transtentorial
• Expanding posterior fossa lesion
• Pinpoint pupils
• Downward conjugate gaze

http//download.imaging.consult.com/ic/images/S193
3033208702313/gr10-midi.jpg
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

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 lt 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
111
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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

• 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 2000. 1741-51.
• Horn et al. Neurol Res 199921 758-64
• Quereshi et al. J Trauma 199947659-65.
• Simma et al. Crit Care Med 1998261265-70.
• Clark Kochanek. Crit Care Med 1998261161-2.
• Doyle et al. J Trauma 2001 50 367-383.
• Petersen et al. Crit Care Med 2000281136-1143

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 23.4 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 0.001) or an absolute serum
sodium of 145 mmol/L (p 0.007) 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 (0.05-0.15 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

• 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
  (95CI) were calculated
• Main results
• 10 eligible RCTs, 2036 participants
• (RR) for early seizure prevention was 0.34 (95CI
  0.21, 0.54)
• ? risk of early seizures by 66
• Seizure control in the acute phase did not show
  ? mortality (RR 1.15 95CI 0.89, 1.51)
• 
  ?
  death/disability (RR 1.28 95CI 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
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

125
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126
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127
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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

• O/E
• HR 90 RR10 BP105/72 T36.6
• GCS 10 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
  babinskis.
• CT scanner is 1 h E. NeuroSx is 3 h NW. No
  general surgeon in town.

130
ED Burr Hole - Preparation

1. Type and screen, PTT, INR
2. Administer IV antiobiotics (ie ceftriaxone)
3. Shave and prep patient
4. 2 lido with epi to reduce scalp bleeding
5. 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

1. 4 cm vertical incision 3cm (2 finger breadths)
   anterior to tragus and 2cm above zygoma
2. Divide temporalis muscle and lift it off the
   skull with scalpel handle
3. Insert self-retaining retractor

132
ED Burr Holes - Decompression

1. Triangular-shaped perforator to penetrate to
   inner table of skull

133
ED Burr Holes - Decompression

1. Switch to burr bit to produce cylindrical hole
2. Leave fine rim of inner table
3. Separate dura from inner table with elevator
4. Rangeur rim
5. If epidural suction our blood/clot
6. If subdural, elevate dura with hook and incise
   with 15 blade
7. DO NOT SUCTION THE BRAIN TISSUE
8. Place drain in small pocket of temporalis muscle
   and close scalp
9. Consider frontal, parietal and then contralateral
   holes if no hematoma found

134
ED Burr Holes
135
ED Burr Holes

• Relative Indications
• GCS lt 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

136
Questions?
137
Acknowledgements

• Dr. Mark Bromley
• Dr. Stefan Da Silva
• Dr. David Zygun

138
Brain Tissue pH and Blood Glucose
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.

142
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143
Therapeutic HypothermiaExperimental Evidence
144
NABISH I Outcomes
145
NABISH I Temperature Data
Target Temp 8.4 3 hrs
146
NABISH 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 physicians role in brain death

• Hope Program
• http//iweb.calgaryhealthregion.ca/hope

148
Hypothermia Treatment Window
149
Therapeutic Hypothermia Cardiac Arrest