TRAUMATIC BRAIN INJURY

with INITIAL MANAGEMENT IN ED

DR. MUNAWARUZZAMAN BIN

MANAN
PAKAR PERUBATAN KECEMASAN
JABATAN KECEMASAN
HOSP QUEEN ELIZABETH
KOTA KINABALU
SABAH

ABDUL

Classification
TBI

is classified based on the clinical

assessment of a patient's level of consciousness
with little or no regard to the actual underlying
injury

severe (GCS score of 3 to 8)

moderate (GCS score of 9 to 13)
mild (GCS score of 14 or 15)

Pathophysiology
Brain

consumes 20% of the body's total oxygen

requirement
and 15% of total cardiac output
sensitive to ischemia and low-oxygen states
Vasoconstriction occurs with

Hypertension
Hypocarbia
alkalosis

CBF
Flow

= 750 mls/min
CMRO2 = 50mls O2/min
Control

CBF = CPP/CVR

CBF
CPP

CPP = MAP ICP

Normal ICP < 15
mmHg

CVR

Metabolic
autoregulation
Pressure
autoregulation
Chemical (pO2 &
pCO2)
Nervous system

Monro-Kellie Doctrine

Skull is a rigid box

Fluid is incompressible
Any increase in intracranial content will
result in a large increase in pressure

However,

pressure does not rise initially

because of translocation of csf into
extracranial subarachnoid space

Primary brain injury

Contusion
Hematoma

(SDH, EDH, SAH,

Intraparenchymal, Intraventricular)
DAI
Tearing, shearing
irreversible

Secondary brain injury

damage caused by a series of
deleterious cellular and subcellular
events that follows the primary injury
and leads to an expansion of the original
injury
AKA Secondary cascade
calcium and ion shifts, mitochondrial
damage, production of free radicals, and
enzyme activity that lead to cell death

Secondary insult
hypotension,

hypoxemia, elevated ICP

Worsen the outcome of TBI

ED Management

History

Mechanism of injury

Fall from height, impact area, speed, seat belt,

airbag

Patient condition before and after injury

Medical cond on anticoagulation
Intoxication
Nausea, Vomitting, Headache

The goal of ED resuscitation is to

prevent secondary insult and potentially
slow the expansion of the underlying
injury

Airway and Breathing

Hypoxia

increases mortality
Patients with severe TBI (GCS score of 8)
require prompt airway control
Induction

Etomidate Favourable hemodynamic/ rapid

onset/ short duration (0.3 mg/kg)
Propofol rapid onset and recovery/ strong
anti seizure/ cautious in labile BP (12mg/kg)

Paralysis

- Scoline

Circulation

the most important secondary insult is hypotension

Hypotension and subsequent ischemia of vulnerable
and injured neuronal tissue can dramatically
exacerbate the underlying secondary cascade and lead
to an expansion of the injury and worse outcomes
In severe TBI, a single episode of hypotension doubles
mortality
aggressive fluid resuscitation may be required to
prevent hypotension and secondary brain injury

Does not increase ICP

Maintain SBP >90 mmHg (BTF 3rd ed 2007)

Disability
Moderate

and severe CT
Mild Head injury

Canadian
New Orlean

The Canadian CT Head

Rule

Ian G Stiell, George A Wells, Katherine Vandemheen, Catherine Clement, Howard Lesiuk,
1.GCS
<15 two hours after injury
Andreas Laupacis,
R Douglas McKnight, Richard Verbeek, Robert Brison, Daniel Cass, Mary A Eisenhauer, Gary H
2.Suspected
open or depressed skull fracture
Greenberg, James
Worthington,
for the
CCC Studyskull
Group.Lancet
2001; 357:
139196
3. Any
sign of
basilar
fracture:
hemotympanum,raccoon
eyes
(intraorbital bruising), Battle's sign(retroauricular bruising),
orCSF leak, oto- or rhinorrhea
4.2 episodes of vomiting
5. 65 years or older
6. Amnesia before impact of 30 or more minutes
7. Dangerous mechanism (pedestrian struck by motor
vehicle,occupant ejected from motor vehicle, fall from 3 feet or
5 stairs)
Patients < 16 yrs old, GCS < 13 ,those with neurologic deficit,
seizure, obvious open skull # , presence of bleeding diathesis,
or oral anticoagulant use were excluded

The New Orleans Criteria

Haydel MJ et al. Indications for computed tomography in patients with minor
head injury. N Engl J Med 2000 Jul 13 343 100-105.

GCS = 15 and require CT scanning if..

Headache
Vomiting
Age >60 years of age
Drug or alcohol intoxication
Persistent anterograde amnesia
Visible trauma above the clavicle

Extra/Epidural Hematoma
(EDH)
traumatic

accumulation of blood
between the inner table of the skull and
the stripped-off dural membrane
Blunt trauma to the temporal or
temporoparietal area with an associated
skull fracture and middle meningeal
arterial disruption is the primary
mechanism of injury

EDH

prognosis is excellent if treated aggressively

Classic history Lucid interval

temporary improvement in a patient's

condition after a traumatic brain injury, after
which the condition deteriorates

The high-pressure arterial bleeding of an

epidural hematoma can lead to herniation
within hours after an injury
1/3 venous bleed

EDH
Expanding

high-volume epidural hematomas

can produce a midline shift and subfalcine
herniation of the brain.
Compressed cerebral tissue can impinge on
the third cranial nerve, resulting in ipsilateral
pupillary dilation and contralateral hemiparesis

Mx
Resus
RSI

if necessary
Reduce ICP

Elevate head 300

Mannitol 0.25 1 g/kg

200 cc of 20% over 20 min (40g of mannitol)

Hyperventilation

Phenytoin

- reduces the incidence of early

posttraumatic seizures, not affect late-onset
seizures
Refer for evacuation

Subdural Hematoma

collection of blood below the inner layer of the dura

but external to the brain and arachnoid membrane
acute subdural hematomas

subacute phase

begins 3-7 days after acute injury

isodense or hypodense

Chronic subdural hematomas

are less than 72 hours

Hyperdense

21 days (3 wk) or older

Hypodense

Tinti acute <14/7, chronic > 2/52

SDH
caused

by sudden acceleration-deceleration of
brain parenchyma with subsequent tearing of
the bridging veins
Brains with extensive atrophy, as in the elderly
and in alcoholics, are more susceptible to acute
subdural hematoma

Mx
Medical

management similar to EDH

Surgical decomp

associated with a midline shift greater than or equal

to 5 mm
exceeding 1 cm in thickness
comatose patient with an acute subdural hematoma
less than 1 cm in thickness causing a midline shift of
less than 5 mm if any of the following criteria are
met
The

GCS score decreases by 2 or more points between

the time of injury and hospital evaluation
The patient presents with fixed and dilated pupils
The intracranial pressure (ICP) exceeds 20 mm Hg

Diffuse Axonal Injury

disruption

of axonal fibers in the white matter

and brainstem
Shearing forces on the neurons generated by
sudden deceleration cause diffuse axonal injury
edema can develop rapidly
result in devastating and often irreversible
neurologic deficits

DAI
A

CT scan of a patient with diffuse axonal injury

may show normal findings, but the classic CT
demonstrates punctuate hemorrhagic injury
along the grey-white junction of the cerebral
cortex and within the deep structures of the
brain

Subarachnoid hemorrhage
extravasation

of blood into the subarachnoid

space between the pial and arachnoid
membranes
Patients with isolated traumatic subarachnoid
hemorrhage may present with headache,
photophobia, and meningeal signs
Patients who show early development of
traumatic subarachnoid hemorrhage have a
threefold higher mortality risk than those without
traumatic subarachnoid hemorrhage

SAH
Some

traumatic subarachnoid hemorrhages can

be missed on early CT scans.
Generally, CT scans performed 6 to 8 hours after
injury are more sensitive for detecting traumatic
subarachnoid hemorrhage

Hunt & Hess

Intraparenchymal
hematoma / contussion
bleeding

into the tissue of the brain caused by

trauma to the head
most commonly occur in the subfrontal cortex, in
the frontal and temporal lobes, and,
occasionally, in the occipital lobes
Contusions may occur at the site of the blunt
trauma or on the opposite site of the brain,
known as a contrecoup injury

THANK YOU