Transcript Head Trauma - Calgary Emergency Medicine

Head Trauma
Sean Caine
Stefan Da Silva
Objectives
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Normal Physiology
Pathophysiology
Concussion Mild TBI
Epidural Hematoma
Subdural Hematoma
Traumatic SAH
Contusion
Skull Fractures
ED Approach to Head Trauma
Severe Head Injury – Mgmt
Anatomy
Normal Physiology
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Intracranial vault
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Fixed internal volume of 1400-1700 mL
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Contents include:
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Brain Parenchyma – 80%
Cerebrospinal fluid – 10%
Blood – 10%
Normal Physiology
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The Brain
 SEMISOLID structure
 Weighs 1400 g (3 lbs)
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CSF
 100-150 mL
 Produced primarily by the choroid plexus at 20mL/hr or 500
mL/day
 Resorbed via arachnoid granulations into venous system
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Intravascular blood
 100-150mL
 Volume of blood determined by cerebral blood flow (CBF)
Monro-Kellie Doctrine
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Originally described over 150 yrs ago
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Recognizing the skull to be a “rigid box” ICP is a
function of the volume of its three components:
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Brain
Blood
CSF
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.
Monro-Kellie Doctrine
Smith ER, Sepideh AH. Evaluation and management of intracranial pressure in adults. UpToDate. Last updated October 1, 2008.
Cerebral Blood Flow
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CBF = (CAP – CVP) ÷ CVR
↓CVR and ↑ CBF
 Hypotension, acidosis, and hypercarbia cause
cerebral vasodilation
↑CVR and ↓CBF
 Hypertension, alkalosis, and hypocarbia promote
cerebral vasoconstriction
Cerebral Blood Flow
Autoregulation
 CBF is constant when CPP is 50-160 mmHg
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CPP=MAP-ICP
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Normal ICP is 5-15 mmHg
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If CPP < 40 mm Hg
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Øautoregulation of CBF  ↓CBF  tissue ischemia
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.
Pathophysiology
Direct Injury
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“direct” contact of head with object
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skull initially bends inward at the point of contact (coup)
 Local trauma
 Skull fractures
 Penetrating trauma
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some energy is transmitted to the brain by shock waves that
travel distant to the site of impact or compression
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VERY RARELY OCCURS IN ISOLATION!
Indirect Injury
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accelerationdeceleration injury in
absence of direct
contact with skull
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Concussion
(contrecoup)
DAI
subdural hematomas
Injury distal to
penetrating head trauma
Primary Injury
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mechanical irreversible damage that occurs at the
time of head trauma:
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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
Secondary Insults
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Complicated series of reactions neurochemical,
neuroanatomic, and neurophysioligical initiated at
the time of injury
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All currently used acute therapies for TBI are
directed at reversing or preventing secondary
injury
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Therefore the cornerstone to ED mngmt of TBI…
DEFENCE!!!
Secondary Brain Insults
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Neurologic outcome is influenced by the extent and
degree of secondary brain insults
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Hypotension (sBP < 90 mm Hg) reduces cerebral
perfusion (ischemia and infarction)
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Hypoxia (PO2 < 60 mm Hg)
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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
Secondary Insults
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Anemia (reduced oxygen-carrying capacity
of the blood)
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Increased mortality when Hct < 30%
Other potential reversible causes of
secondary injury in head injury include
hypercarbia, hyperthermia, coagulopathy,
and seizures
Case 1
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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
Case 1
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On exam:
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Vitals
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Neuro
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BP: 118/70 HR: 101 RR: 14 T: 36.4
GCS: 15
Physical exam otherwise unremarkable
Concussion and Mild TBI
Concussion
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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; 48:581-585.
Concussion
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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; 48:581-585.
Signs of basilar skull
fracture
Vomiting
14 (8-22)
Odds Ratio for Specific Clinical
Findings and Positive Head 3CT
(2-4)
Smits et al.
Posttraumatic seizure
OR (95% CI)
Signs of basilar skull
fracture
Ibanez et al
OR (95% CI)
Fabbri et al.
3 (1-10)
OR (95% CI)
14 (8-22)
11 (6-23)
3 (2-4)
4 (2-7)
Posttraumatic seizure
3 (1-10)
2 (0.25-17)
8 (6-12)
GCS 14
2 (1-3)
7 (4-14)
19 (14-26)
2 (1-3)
7 (2-25)
Anticoagulation
2 (1-4)
4 (3-7)
Dangerous Mechanism
2 (1-4)
Vomiting
GCS
14
Neurological
deficits
Neurological deficits
Anticoagulation
Loss of consciousness
2 (1-3)
7 (4-11)
1.7 (1-2)
3 (2-5)
Headache
1.4 (1-2)
Dangerous
Mechanism
3 (2-6)
Posttraumatic amnesia
Intoxication
1 (0.6-2)
Age>65
Loss of consciousness
10 (6-16)
2 (1-3)
2 (1-3)
5 (3-8)
19 (13-28)
8 (3-9)
2 (1-4)
3 (2-4)
2 (2-3)
8 (6-12)
2 (1-4)
1 (0.3-3)
2 (1-3)
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.
Canadian CT Head Rule
Inclusion Criteria (must have all of the following)
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Blunt head trauma resulting in LOC, definite amnesia, or witnessed disorientation
Initial ED GCS = 13-15
Injury occurred within 24 hrs
Exclusion Criteria
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<16 yrs old
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Minimal head injury
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No clear hx of trauma as primary event (ie syncope or seizure)
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Penetrating or depressed skull fracture
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Acute focal neuro deficit
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Seizure prior to being assessed
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Bleeding disorder or anticoagulant use
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Second assessment
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Pregnant
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
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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
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Pedestrian vs MVA, ejected from MVA, fall from 3 ft or 5 stairs
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.
Case continued…
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His Dad takes you aside and mentions that
a big game is coming up with US College
Scouts.…can he play?
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
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 2005;39(4):196-204.
Second Impact Syndrome
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Rare event
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High mortality rate
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Rapid/fulminant cerebral edema from
second impact before brain fully recovers
Post-concussive syndrome
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Prevalence:
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80% are symptom free at 6 weeks
15% with symptoms at 1 yr
Common symptoms:
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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
Recurrent Concussions
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Strong evidence that recurrent concussions
are more significant/severe than initial one
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Young age is a risk factor
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Associated with diminished cognitive
function, slower recovery times, prolonged
disability
Special Considerations: Mild TBI in
presence of coagulopathy
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Increased risk for poor outcome
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>80% mortality for ICH in pts with elevated INR
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Smaller studies suggest that >70% pts with elevated INR
deteriorated after a normal CT
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Mngmt:
 Correct INR with FFP, vitamin K in context of ICH
 Admit and observe pts with elevated INR (> 2) and normal
CT
Observation and disposition
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Observation is recommended for 24 hours after a mild TBI
because of the risk of intracranial complications
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Hospital admission is recommended for patients at risk for
immediate complications from head injury
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GCS <15
Abnormal CT scan: intracranial bleeding, cerebral edema
Seizures
Abnormal INR PTT
F/U with sports med/urgent neuro with PPCS>3weeks
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
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Case 2
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28 year-old ♂ brought in by EMS
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Found outside the Cecil Tavern
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“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”
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Bystanders state the was a brief LOC lasting ~5 min
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EMS suspect he is intoxicated. Smells of booze. Slurred speech.
Disshevelled. Confused. Often mumbling and eyes drifting close but
rousable/
Case 2
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O/E:
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AVSS
GCS: 14
Right temporal swelling/boggy scalp
Within minutes of sharing his colourful story…
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Difficult to rouse
Right fixed and dilated pupil
Epidural Hematoma
Epidural Hematoma
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Usually due to arterial injury
 trauma to the skull base → tearing of middle meningeal
artery
 results in hemorrhage
Occasionally
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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
Epidural-Pathophysiology
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Typically fraature of temporal bone ruptures
branches of the middle meningeal artery
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Expanding hematoma limited by dural attachment
at sutures
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This stripping of the dura from the calvarium may
be part of the reason for the severe headache.
Pterion
Epidural Hematoma - Hx
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Mean age 20-30 years
Caused by MVC, Falls, Assaults
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Skull # present 75-95% of the time
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Transient LOC with a “lucid interval”
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Symptoms: HA, N/V, drowsiness,
confusion, aphasia, seizures, and
hemiparesis
Epidural Hematoma - Imaging
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Head CT – fast, simple
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“lens-shaped” pattern
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collection is limited by dural attachments at
cranial sutures
Epidural - Management
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Neurologic emergency
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Operative
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hematoma expansion
elevated intracranial pressure
brain herniation
Craniotomy and hematoma evacuation
Burr Hole
Non-Operative
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Close observation
serial brain imaging
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hematoma enlargement
neurologic deterioration
Surgical Indications for EDH
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An EDH > 30 cm3 should be surgically evacuated
regardless of the patient's GCS
GCS < 9 with anisocoria → evacuation ASAP
An EDH
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< 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
Case 3
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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
Subdural Hematoma
Subdural Hematoma
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SDHs form b/w the dura and the brain
Usually they are caused by the movement of the brain
relative to the skull
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acceleration-deceleration injuries
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Common in patients with brain atrophy (EtOH or elderly)
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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
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24 hours post trauma
↓ LOC;
lucid interval: 50% - 70% → ↓mentation
Subacute SDH
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symptomatic 24h - 2 wks post injury
CT: hypodense or isodense lesion
absence of sulci
shift
contrast  detection of isodense lesions
Chronic SDH
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>2 weeks post trauma
Hemiparesis or Weakness: ~45%
↓LOC: ~50%
What type of ICH is this? Why?
Case 4
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51 ♂ MVC – single vehicle at highway
speeds off road and into a tree
?LOC
GCS 8 (scene) 8 (now)
Traumatic Subarachnoid
Haemorrhage
Traumatic SAH
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TSAH is defined as blood within the CSF and
meningeal intima
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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
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↓GCS →  SAH
 SAH → ↓Outcome
Traumatic SAH
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Øcontrast CT:  density in basilar cisterns
 density interhemispheric fissures/sulci
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prognosis reasonable
cerebral vasospasm → cerebral ischemia
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Chicken vs Egg
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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?
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cerebral angiogram to exclude an underlying
aneurysm or vascular malformation
Diffuse Axonal Injury
Diffuse Axonal Injury
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Definition: prolonged traumatic coma not caused by mass
lesions, ischemic insults, or nontraumatic etiologies
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Typically coma persisting > 6h
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CT often normal
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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
Diffuse Axonal Injury
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Mild DAI
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Coma 6-24 h
1/3 will demonstrate
decorticate or decerebrate
posturing
15% mortality
Most recover with mild or no
permanent deficits
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Mod DAI
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Coma > 24h
Abnormal posturing
Severe posttraumatic
amnesia
Moderate cognitive deficit
25% mortality
Severe DAI
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Majority due to MVA
Autonomic dysfunction
(tachycardia, HTN, irreg
resps)
Majority die
Others are severely disabled
or persistent vegetative satate
SKULL FRACTURES
Linear skull fracture
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low-energy blunt trauma over a wide surface area
of the skull.
Full thickness through bone
…of little significance except
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when it runs through a vascular channel,
venous sinus groove
suture
Then, it may cause
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epidural hematoma
venous sinus thrombosis and occlusion
sutural diastasis
Fractures
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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
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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
Basilar skull fracture
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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.
Depressed Skull Fracture
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Elevation
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depressed segment is > 5mm below inner table
gross contamination,
dural tear with pneumocephalus
underlying hematoma
Craniectomy
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underlying brain is damaged and swollen
CSF Oto/rhinorrhea
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Dab fluid on a tissue paper,
a clear ring of wet tissue beyond the blood
stain, called a "halo" or "ring" sign
ED Approach to Head Trauma
Focused Hx
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Mechanism
LOC
Seizure?
Ambulatory at scene
GCS at scene
Focused Physical
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ABC’s
ATLS protocol
GCS
Signs of external injury
Pupils
Check Ears/Nose
Extremities - movement
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
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
Emergent Management of
Closed Head Injury
Case 6
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22 ♀ bicycle vs truck
LOC
Agitated at the scene
GCS
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Opens eyes to pain 2
Withdraws on left and localizes on right
2
Sounds – no inteligible words
5
Outline
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Airway
Avoid Hypoxia
Avoid Hypotension
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Brain Specific Therapies
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Position
Hyperventilation
Mannitol
Hypertonic Saline
Cooling
Indications for ICP Monitoring
Surgical Management
Airway
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Capture it!
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How you do it probably does not have a great
effect on neurological outcome unless you
cause hypoxemia or hypotension
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There is little evidence-based medicine to guide
the choice of agents
Intubation – Indications*
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Coma (i.e. GCS 8) or significantly deteriorating LOC
Loss of protective laryngeal reflexes
Copious bleeding into mouth
Respiratory arrhythmia
Ventilatory insufficiency
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clinical decision - not necessarily requiring ABG
Bilateral mandibular fracture
Any facial injury compromising airway
Seizures
Any other injury that requires ventilation/intubation
*Eastern Association For The Surgery of Trauma, 2003; NICE guidelines, 2003
Case
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Paramedics state his GCS “…was 7 or 8 at
the scene”
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Should they have intubated?
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:
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Survival did not differ overall (81.1% ALS v. 81.8% among those in the BLS; p=0.65)
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Among patients with GCS < 9, survival was ↓ with ALS (50.9% v. 60.0%; p=0.02)
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The adjusted odds of death for the advanced life-support v. basic life-support phases were nonsignificant (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.
Airway
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Preparation and Preoxygenation
Prevent ICP rise
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Prevent Vagally stimulated bradycardia
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Atropine 0.01 mg/kg IV (Minimum dose: 0.1 mg)
Sedation
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Lidocaine 1.5-2 mg/kg IV
Rocuronium 0.06 - 0.1 mg/kg (defasciculating dose)
Fentanyl 3 ug/kg IVP
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
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Succinylcholine 1.5 mg/kg IV OR
Rocuronium 0.6 mg/kg IV
Airway - Intubation
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Lidocaine (1.5 to 2 mg/kg IV push)
…may ↓ cough reflex, HTN response, ICP
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Succinylcholine – fasciculations ↑ICP
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Etomidate (0.3 mg/kg IV)
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premedicate w a subparalytic dose of a nondepolarizing agent
good effect on ICP ↓CBF and metabolism
minimal adverse effects on BP
Minimal respiratory depressant effects
Ketamine
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
May increase ICP
Anaes and animal studies indicate no increased ICP
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.
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.
Case 7

22 ♀ with presumed CHI
Now intubated.

What are your priorities?

AVOID HYPOXEMIA
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
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
AVOID HYPOTENSION
% of patients in outcome group
100
90
80
70
60
50
40
30
20
10
0
Favourable outcome
Unfavourable outcome
none
early
late
both
Timing of hypotension (SBP < 90 mmHg)
Traumatic Coma Data Bank 1991
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
Hypotension
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
 <70 mmHg for a sustained period → ischemic injury

Outside of the limits of autoregulation
 ↑ MAP raises CPP
 ↑ ICP lowers CPP
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

Case 8

Asymetric Pupils – L fixed and dilated

What is happening?
What would you like to do?

Herniation Syndromes



Uncal
Most common
Temporal lobe uncus forced
through tentorial hiatus
Compression of CN III causing
ipsilateral:






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, McGrawHill, 1992, p 915.)
Anisocoria
Impaired EOM
Sluggish pupil (EARLY)
Fixed and dilated (LATE)
Contralateral Babinski’s
Bilateral decorticate posturing
(LATE)
Herniation Syndromes
Kernohan’s notch syndrome
 Contralateral cerebral
peduncal forced against
opposite endge of
tentorium
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, McGrawHill, 1992, p 915.)

~25% of uncal herniations

Motor signs ipsilateral to
the dilated pupil
Herniation Syndromes


Central Transtentorial
Bilateral rostrocaudal
deterioration
Early





Later



http://download.imaging.consult.com/ic/images/S1933033208702313/gr8midi.jpg (Accessed May 12, 2009)
Bilateral motor weakness
Pinpoint pupils (<2mm)
Increased muscle tone
Bilateral Babinski’s
Midpoint fixed pupils
Decorticate → decerebrate
Irregular resps
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)
Herniation Syndromes
Upward Transtentorial

Expanding posterior
fossa lesion


http://download.imaging.consult.com/ic/images/S1933033208702313/gr10midi.jpg
Pinpoint pupils
Downward conjugate
gaze
Brain Specific Therapies
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
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
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
Acute head injury (6 hrs post impact)
Areas in red show regions with rCBF < 20 ml/100g/min)
ml/100g/min
ml/100g/min
60
60
(Coles et al. Crit Care Med 2002)
PaCO2: 25 mmHg
0
0
PaCO2: 38 mmHg
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
Mannitol

Drawbacks:




Osmotic diuresis
HYPOTENSION
May accumulate in the brain and result is a
“reverse osmotic shift” potentially increasing ICP
Acute renal failure
Mannitol
Indications: (prior to ICP monitoring)
Signs of transtentorial herniation
Progressive neurological deterioration
1.
2.

not attributable to extra-crainal complications
Dose: 0.25 – 1g/kg IV bolus
Avoid hypovolemia
(foley recommended)
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!
Dose: 2-4 ml/Kg 5% NaCl
Max Na+ ~ 160 mmol/l
Max osmol ~ 325 mOsm/l
Munar et al. J Neurotrauma 2000. 17:41-51.
Horn et al. Neurol Res 1999;21: 758-64
Quereshi et al. J Trauma 1999;47:659-65.
Simma et al. Crit Care Med 1998;26:1265-70.
Clark & Kochanek. Crit Care Med 1998;26:1161-2.
Doyle et al. J Trauma 2001; 50: 367-383.
Petersen et al. Crit Care Med 2000;28:1136-1143
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.
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?
Antiepileptic therapy
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
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)

Selection criteria


Data collection and analysis



Two reviewers
Relative risks and 95% confidence intervals (95%CI) were calculated
Main results





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.
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.
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.
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
“…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
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

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 babinski’s.
CT scanner is 1 h E. NeuroSx is 3 h NW. No
general surgeon in town.
ED Burr Hole - Preparation
1.
2.
3.
4.
5.
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
6.
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
ED Burr Hole - Exposure
1.
2.
3.
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
ED Burr Holes - Decompression
1.
Triangular-shaped
perforator to
penetrate to inner
table of skull
ED Burr Holes - Decompression
2.
3.
4.
5.
6.
7.
8.
9.
10.
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
ED Burr Holes
ED Burr Holes

Relative Indications






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
Questions?
Acknowledgements
Dr. Mark Bromley
Dr. Stefan Da Silva
Dr. David Zygun
Brain Tissue pH and Blood Glucose
7
Brain pH
Brain pH
7.5
6.5
6
0
5
10
Glucose
15
20
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
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
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.
Therapeutic Hypothermia:
Experimental Evidence
NABIS:H I
Outcomes
60
% of Patients
50
56.85
56.01
40
30
27.92
20
26.59
10
0
Poor Outcome
Hypothermia
Mortality
Normothermia
NABIS:H I
Temperature Data
Temperature (C)
40
38
36
34
32
Target Temp
8.4 + 3 hrs
30
0
8
16
hypo mean
24
32
40
48
56
64
Hours from Hospital Arrival
+1 SD
-1 SD
normo mean
72
80
+1 SD
88
-1 SD
96
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
ER physician’s role in brain death

Hope Program
http://iweb.calgaryhealthregion.ca/hope
Hypothermia Treatment Window
Therapeutic Hypothermia: Cardiac Arrest