Head Trauma

1
Head Trauma

• Mark Bromley PGY2
• Jason Lord FRCPC

2

• Physiology
• Concussion Mild TBI
• Epidural Hematoma
• Subdural Hematoma
• Traumatic SAH
• Contusion
• Skull Fractures
• ED Approach to Head Trauma
• Severe Head Injury Mgmt
• How to Read a Head CT Brain Death

3
Pathophysiology
4
Cerebral Blood Flow

• CBF is maintained _at_ MAP of 60-150 mm Hg
• Hypertension, alkalosis, and hypocarbia promote
  cerebral vasoconstriction
• Hypotension, acidosis, and hypercarbia cause
  cerebral vasodilation

5
Hypotension
6
Cerebral Blood Flow

• In Trauma,
• ? CBF with a disrupted BBB ? vasogenic edema
• CBF a CPP
• CPP MAP ICP
• CBF is constant when CPP is 50-160 mm Hg
• If CPP lt 40 mm Hg
• Øautoregulation of CBF ? ?CBF ? tissue ischemia

7
Monro-Kellie Doctrine

• Cranial vault is a fixed volume
• any change in the contents either
• displaces the normal contents or
• raises the pressure inside the skull
• The cranial vault is normally filled by three
  things
• brain
• blood
• cerebral spinal fluid.
• If a person were to have a brain tumor
• it displaces one of the normal components (i.e.
  ?spinal fluid)
• ?ICP

8
Direct Injury

• head is struck by an object or its motion is
  arrested by another object
• skull initially bends inward at the point of
  contact (coup)
• some energy is transmitted to the brain by shock
  waves that travel distant to the site of impact
  or compression

9
Indirect Injury

• cranial contents are set into motion by forces
  other than the direct contact of the skull with
  another object
• acceleration-deceleration injury
• as brain moves within the skull, bridging
  subdural vessels are strained (subdural
  hematomas)
• shear and strain injuries (diffuse axonal injury
  or concussion)
• intracranial content movement abruptly arrested
  (contrecoup)
• penetrating injury - pressure waves can damage
  structures distal to the path of the missile.

10
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

11
Secondary Brain Injury

• intracellular and extracellular derangements
  (metabolic, ischemic, ion shifting)
• All currently used acute therapies for TBI are
  directed at reversing or preventing secondary
  injury

12
Secondary Brain Injury

• Neurologic outcome is influenced by the extent
  and degree of secondary brain injury
• 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

13
Secondary Brain Injury

• 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

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Case

• 17 ? playing soccer
• was headed by another player
• No LOC
• Pulled from game kept getting beaten
• Progressive confusion
• Amnestic of the event

15

• Now GCS 15
• No Focal Neurologic findings
• ?Imaging
• ?Follow-up

16
Note Minor Head Injury is defined as a witnessed
loss of consciousness, definite amnesia, or
witness disorientation in a patient with a GCS
13-15.
17

• 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.

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Concussion and Mild TBI
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Concussion

• grossly normal structural neuroimaging
• Signs GCS 13-15 at 30 min post injury
• Symptoms confusion and amnesia /- LOC
• ?focus
• ?orientation
• slurred speech / poor coordination
• emotional
• Course resolution of symptoms follows a
  sequential course

20
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

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• His Dad take you aside and says theres a big
  tourney on the weekend with scouts flying in to
  watch.
• can he play?

22
Return to play

• Rest until all symptoms have resolved
• Graded program of exertion
• gt 1 day at each level is needed
• If any symptoms appear, patients drop back to the
  previous asymptomatic level and try again after
  24 h

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.
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Take Home Concussion

• Players should not be allowed to return to play
  in the current game or practice
• Players should not be left alone, and regular
  monitoring for deterioration is essential during
  the initial few hours after injury
• Return to play must follow a medically supervised
  series of steps
• Players should never return to play while
  symptoms persist

25
Case

• 20 year-old ? university student
• presents after a morning game of baseball in
  which he collided with another player
• Brief LOC meanwhile she bled profusely from the
  chin
• When he recovered, she offered him a ride to the
  emergency room, which he declined, saying "it's
  just a bump on the head"
• He returned to his room and told his roommates
  the story, and remained lucid through the
  morning.
• After lunch ? restless with a severe HA ?
  seizure.
• OE ?LOC R pupil dilated

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Epidural Hematoma
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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

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Epidural-Pathophysiology

• Blow to the head fractures the temporal bone and
  ruptures branches of the middle meningeal artery,
  lies outside the dura.
• The ruptured artery then leaks blood between the
  inner skull and the dura.
• The increasing volume of blood strips the dura
  from the inside of the skull, forming, in effect,
  a large blood blister which pushes against the
  brain as it expands.
• The hematoma may strip the dura from the bone as
  far as the sutures of the skull.
• This stripping of the dura from the calvarium may
  be part of the reason for the severe headache.

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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

32
Epidural Hematoma - Imaging

• Head CT fast, simple
• lens-shaped pattern
• collection is limited by dural attachments at
  cranial sutures

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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

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Epidural - ?Surgical

• 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

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Case

• 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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Subdural Hematoma
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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

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Acute SDH

• 24 hours post trauma
• ? LOC
• lucid interval 50 - 70 ? ?mentation

43
Subacute SDH

• symptomatic 24h - 2 wks post injury
• CT hypodense or isodense lesion
• absence of sulci
• shift
• contrast ? detection of isodense lesions

44
Chronic SDH

• gt2 weeks post trauma
• Hemiparesis or Weakness 45
• ?LOC 50

45
Case

• 51 ? MVC single vehicle at highway speeds off
  road and into a tree
• ?LOC
• GCS 8 (scene) 8 (now)

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Subarachnoid Hemorrhage
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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

49
Traumatic SAH

• Øcontrast CT ? density in basilar cisterns
• ? density interhemispheric fissures/sulci
• prognosis reasonable
• cerebral vasospasm ? cerebral ischemia

50
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

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SKULL FRACTURES
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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

53

• 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

54
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.

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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

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?CSF Leak

• Dab fluid on a tissue paper,
• a clear ring of wet tissue beyond the blood
  stain, called a "halo" or "ring" sign

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ED Approach to Head Trauma
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Focused Hx

• Mechanism
• LOC
• Ambulatory at scene
• GCS at scene

59
Focused Physical

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

60
Glasgow Coma Scale

• 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

• Motor response (M)
• 6. Obeys commands
• 5. Localizes pain
• 4. Withdraws from pain
• 3. Abnormal flexion
• 2. Abnormal extension
• 1. None

Developed for evaluation of head trauma 6 hours
post injury Deceased and rocks have GCS 3
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Emergent Management of Closed Head Injury
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Case

• 22 ? bicycle vs truck
• LOC
• Agitated at the scene
• GCS
• Opens eyes to pain
• Withdraws
• Sounds no inteligible words

2
4
2
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Outline

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

64
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

65
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
66
Case

• Paramedics state his GCS was 7 or 8 at the
  scene
• Should they have intubated?

67

• 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.

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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
• Apply cricoid pressure
• Muscle relaxants
• Succinylcholine 1.5 mg/kg IV OR
• Rocuronium 0.6 mg/kg IV

69
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

70
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.
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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.
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Case

• 22 ? with presumed CHI
• Now intubated.
• What are your priorities?

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AVOID HYPOXEMIA
74
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
75

• 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

76

• desaturation occurs rapidly below SpO2 of
  9092

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AVOID HYPOTENSION
78
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
79
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
80
Hypotension
81
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

82
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

83
Case

• Asymetric Pupils L fixed and dilated
• What is happening?
• What would you like to do?

84
Herniation

• 1) The brain squeezes under the falx cerebri in
  cingulate herniation
• 2)The brainstem herniates caudally
• 3) The uncus and the hippocampal gyrus herniate
  into the tentorial notch
• 4)The cerebellar tonsils herniate through the
  foramen magnum in tonsillar herniation.

85

• Uncus can squeeze the third cranial nerve which
  controls ipsilateral parasympathetic input to the
  eye
• pupillary dilatation
• deviation of the eye to "down and out"

86
Brain Specific Therapies
87
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

88
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

89
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
90
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
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Mannitol
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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

94
Mannitol

• Drawbacks
• Osmotic diuresis
• HYPOTENSION
• May accumulate in the brain and result is a
  reverse osmotic shift potentially increasing
  ICP
• Acute renal failure

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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)

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Hypertonic Saline
97
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
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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.
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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?

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Antiepileptic therapy
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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

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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)

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• 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.

105
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.
106
Blood Glucose
107
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

108
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.

109
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

110
Brain Tissue pH and Blood Glucose
Brain pH
111
Steroids
112
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

113
Cooling
114
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

115
Therapeutic HypothermiaExperimental Evidence
116
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

117
NABISH I Outcomes
118
NABISH I Temperature Data
Target Temp 8.4 3 hrs
119
Therapeutic Hypothermia Cardiac Arrest
120
Hypothermia Treatment Window
121
Future Directions
122
ER physicians role in brain death

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

123
Questions?
124
Acknowledgements

• Dr. Jason Lord
• Dr. David Zygun

125
How to Read a Head CT
126
How to Read a Head CT

• Has assumed a critical role in the daily practice
  of Emergency Medicine for evaluating intracranial
  emergencies
• Most practitioners have limited experience with
  interpretation
• In many situations, the Emergency Physician must
  initially interpret and act on the CT without
  specialist assistance

127
Trauma CT

• Is there evidence of hemorrhage?
• Within the ventricles
• Within the subdural space
• Within the subarachnoid space
• Within the epidural space
• Is there mass effect?
• Effacement of sulci
• Is there cerebral edema?
• Small ventricles
• Small basilar cisterns
• General effacement of cortical sulci
• Diffuse loss of grey-white differentiation
• Is there local loss of grey-white
  differentiation?
• Infarction/Inflammation/Tumor
• Is there Hydrocephalus?
• Communicating vs non-communicating
• Have the cisterns been scrutinized for hemorrhage
  and size?
• Is there evidence of infarction?
• Is there calcification?

128
Head CT

• Blood Can Be Very Bad

129
Blood Can Be Very Bad

• Blood
• Cisterns
• Brain
• Ventricles
• Bone

130
Blood Can Be Very Bad

• Blood
• Cisterns
• Brain
• Ventricles
• Bone

131
Blood Can Be Very Bad

• Blood
• Cisterns
• Brain
• Ventricles
• Bone

132
Blood Can Be Very Bad

• Blood
• Cisterns
• Brain
• Ventricles
• Bone

133
Blood Can Be Very Bad

• Blood
• Cisterns
• Brain
• Ventricles
• Bone

134
CT Scan Basics

• A CT image is a computer-generated picture based
  on multiple x-ray exposures taken around the
  periphery of the subject
• X-rays are passed through the subject, and a
  scanning device measures the transmitted
  radiation
• The denser the object, the more the beam is
  attenuated, and hence fewer x-rays make it to the
  sensor

135
CT Scan Basics

• The denser the object, the whiter it is on CT
• Bone is most dense 1000 Hounsfield U
• Air is the least dense - 1000 Hounsfield U

136
CT Scan Basics Windowing
Focuses the spectrum of gray-scale used on a
particular image
137
Posterior Fossa

• Brainstem
• Cerebellum
• Skull Base
• Clinoids
• Petrosal bone
• Sphenoid bone
• Sella turcica
• Sinuses

138
Sagittal View
139
Cisterns
140
CT Scan
141
Brainstem Lateral View
142
2nd Key Level Sagittal View
2nd Key Level
2nd Key Level
143
Cisterns at Cerebral Peduncles Level
144
CT Scan
145
CT Scan
146
3rd Key Level
147
Cisterns at High Mid-Brain Level
148
CT Scan
149
Ventricles
150
CSF Production

• Produced in choroid plexus in the lateral
  Ventricles ? Foramen of Monroe ? IIIrd Ventricle
  ? Acqueduct of Sylvius ? IVth Ventricle ?
  Lushka/Magendie
• 0.5-1 cc/min
• Adult CSF volume is approx. 150 ccs
• Adult CSF production is 500-700 cc/day

151
B is for Blood

• Is blood present?
• If so, where is it?
• If so, what effect is it having?

152
Acute blood is bright white on CT (once it clots)
Blood becomes isodense at approx 1 week

• Blood becomes hypodense at approx 2 weeks

153
Acute blood is bright white on CT (once it clots)
Blood becomes isodense at approx 1 week

• Blood becomes hypodense at approximately 2 weeks

154
Acute blood is bright white on CT (once it clots)
Blood becomes isodense at approximately 1 week

• Blood becomes hypodense at approximately 2 weeks

155
Epidural Hematoma

• Lens shaped
• Does not cross sutures
• Classically described with injury to middle
  meningeal artery
• ? mortality if treated prior to unconsciousness
  (lt 20)

156
CT Scan
157
CT Scans
158
Subdural Hematoma

• Typically falx or sickle-shaped
• Crosses sutures
• Does not cross midline
• Acute subdural is a marker for severe head injury
  (Mortality 80)
• Chronic subdural usually slow venous bleed and
  well tolerated

159
CT Scan
160
CT Scan
161
Subarachnoid Hemorrhage
162
Subarachnoid Hemorrhage

• Blood in the cisterns/cortical gyral surface
• Aneurysms responsible for 75-80 of SAH
• AVMs responsible for 4-5
• Vasculitis accounts for small proportion (lt1)
• No cause is found in 10-15
• 20 will have associated acute hydrocephalus

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166
C is for CISTERNS
(Blood Can Be Very Bad)

• 4 key cisterns
• Circummesencephalic
• Suprasellar
• Quadrigeminal
• Sylvian

167
Cisterns

• 2 Key questions to answer regarding cisterns
• Is there blood?
• Are the cisterns open?

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B is for BRAIN
(Blood Can Be Very Bad)
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Tumor
174
Atrophy
175
Abscess
176
Hemorrhagic Contusion
177
Mass Effect
178
Stroke
179
Intracranial Air
180
Intracranial Air
181
Intracranial Air
182
V is for VENTRICLES
(Blood Can Be Very Bad)
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BONE
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No Worries

• If
• No blood is seen
• All cisterns are present/open
• The brain is symmetric
• with Normal gray-white diff
• The ventricles are symmetric
• without dilation
• There is no fractured bone

192
Practice CT
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