Brain Injury
Dr. Shema
Dr. Muyimbo
Case presentation:
• NA
• 18 Y/O
• Muganda
• From Nsambya
• DOA-17/9/2010
• NOK- N B(mother)
PC:
Vomiting
Cut wound on head all 2ry to being knocked by a motorcycle while crossing the
road.
No h/o ENT bleeding
ROS-unremarkable
PMH-index admission, no chronic illnesses, no known drug allergies.
PSH- unremarkable
FSH-un employed,BF a 6/12 baby
O/E:
FGC, mild pallour,not jaundiced, afebrile
CNS: semi comatose, PEARL, GCS-12/15
CVS:PR-72 regular
BP-130/80mmhg
HS-Normal
RS:
RR-18bpm, not in distress, normal air entry
PA:
N fullness, soft, non tender, no organomegally, N bowel sounds
Dx: closed moderate head injury
Inv:
Skull xray
Ct scan-open head injury and cerebral oedema but no increased ICP
Hb gp n xmatch
Mgt:
Sts
T.T 0.5mls stat
Caps ampiclox 500mg qid x5/7
i.V mannitol 100ml 8hrlyx3/7
i.M diclo 75mg stat
Follow up:
2nd day-no photophobia
c/o- severe frontal headache up to date and vomits.
GCS-15/15,BP-110/70mmhg,PR-78bpm
1. Cerebral Trauma
Objectives:
• Define primary and secondary injury
– Discuss types of each
• Discuss evaluation of head injured
patients
• Discuss management of head
injured patients
– Medical
– Surgical
• Understand concept of brain death
Primary vs. secondary injury
1. Primary damage
(at the time of impact)
2. Secondary damage
(after the original incident)
-e.g. hypoxia, brain edema,
hypotension…
Primary injuries
Classification of primary injuries
Skull fractures
A. Linear fracures: Most common type. Heal
expectantly
B. Depressed skull fracture: As with linear skull
fractures, depressed fractures are usually
treated non-operatively. Surgery (to elevate
bone fragments) is indicated if significant
cosmetic deformity or if there is an underlying
hematoma with significant mass effect.
Basal skull fracture
Basal skull fracture: Most commonly extends
through petrous bone. Patients present with
Battle’s sign (bruise at mastoid) or Racoon’s
eyes (periorbital ecchymosis). May have blood
behind tympanic membrane on otoscopy or
bloody discharge from ear. If tympanic
membrane is disrupted, may have CSF
otorrhea. May have hearing loss which is
usually conductive (secondary to blood/CSF in
middle ear) and less often sensorineural (from
disruption of inner ear). Delayed facial palsy
(from swelling of VII in petrous bone) may
occur. Complete resolution with expectant
management in vast majority of cases. Role of
antibiotics controversial.
Brain contusions
Occipital fracture
Contusions: May be “coup” i.e., directly below area of impact on the skull, or
“contra-coup” i.e., opposite side of the brain from area of direct impact. In the above
example, the patient fell backwards, sustaining a linear skull fracture to the occiput.
The brain “bounced” inside the skull, slamming the frontal lobes into the frontal
bones. Thus, the patient has “contra-coup” frontal contusions.
Hematomas
• Extra-axial (i.e., outside of the brain)
– Epidual
– Subdural
• Acute
• Chronic
• Intra-axial (i.e., involves brain paranchyma)
– Intracerebral hematoma
Epidural hematoma
Epidural hematoma: Young patient, often a child or teenager. Classically
caused by a linear fracture of the squamous temporal bone that disrupts
underlying middle meningeal artery. The epidural hematoma is ARTERIAL
in origin, in contrast to subdural hematoma which is venous. Classic
presentation is loss of consciousness, followed by brief “lucid interval”, then
rapid neurological deterioration with localizing deficits (e.g. dilated pupil,
hemiparesis). Excellent outcome if surgical intervention (craniotomy) is
prompt.
Subdural hematoma, acute
Acute subdural: Usually an adult with a history of significant trauma. Unlike
epidual hematoma, patient may not have a skull fracture. Presentation is usually
decreased level of consciousness and associated localizing neurological findings
(dilated pupil, hemiparesis). Emergent craniotomy indicated if subdural is large
enough to cause mass effect/neurological deficit. Surgical outcome typically poorer
than epidural hematoma.
Subdural hematoma, chronic
Chronic subdural: Typically elderly
patients with underlying brain atrophy.
Especially at risk are patients on
anticoagulants. Superficial cerebral veins
tethered to inside of skull get “streched”
and leak small amounts of blood
chronically. Often no history of
significant trauma. Often have no
lateralizing findings on clinical exam.
Most chronic SDH’s are able to be
evacuated with simple burr hole drainage
(because chronic blood is liquefied). 82 yo male on warfarrin
for a. fib found on the
Floor at home
Intracerebral hematoma
Intracerebral hematoma:
Traumatic intracerebral
hematomas may be acute or the
result of hemorrhagic conversion
of a brain contusion. Most small
ICH’s are treated non-
operatively. Surgery
(craniotomy) is indicated if
significant mass effect causing
progressive neurologic deficit.
Tiny hemorragic contusions are
called “petechial hemorrhages”
Diffuse brain injury
1. Concussion:
– Brief loss of consciousness or altered level of consciousness
– No focal neurological findings
– Normal CT scan
– Often have “post-concussion syndrome”
• Headache, nausea, malaise that lasts days-weeks
• Symptomatic management
– Avoid sports until symptoms subside. Repeated concussions
require abstinence from sports for period of time.
Diffuse brain injury
2. Diffuse axonal injury
– Severe brain injury resulting from
high speed acceleration-
deceleration.
– Diffuse “shearing of axons” –
changes are at microscopic level,
therefore CT may appear
completely normal
– MRI may disclose small petechial
hemorraghes or contusions,
usually around midline structures
such as corpus callosum
– Very poor prognosis
Secondary injury
Classification of secondary
injuries
Intracranial pressure (ICP)
• Normal = about 10 mm Hg (wide range)
• Abnormal > 20 mm Hg
• Grave > 40 mm Hg
Brain herniation
Cerebral perfusion pressure
(CPP)
• More important than ICP in preventing secondary injury
• CPP is basically the arterial inflow pressure to the brain minus the
venous outflow pressure from the brain
– ICP ~ venous outflow pressure because CSF is absorbed into venous
blood
CPP = Mean arterial pressure – ICP
To prevent secondary injury, neurosurgeons try to keep:
CPP > 70 mm Hg
ICP < 20 mmHg
MAP > 90 mm Hg
Cerebral blood flow (CBF)
• More important than CPP in preventing secondary injury
– However, it is difficult to measure CBF, therefore we use CPP as a
rough guide to CBF
• CBF is normally tightly controlled by a process known as
“autoregulation”
CBF = CPP
CVR *NB: CVR = cerebral vascular resistance
• Normal = 50 ml/100g/min
• EEG fades < 25 ml/100g/min
• Cell death < 10 ml/100g/min
Mechanisms that govern autoregulation
become disturbed in head injured patients
In altered autoregulatory
Normal zone of response, greater CPP is
autoregulation required to maintain the
same CBF
Evaluation and
management of head
injured patients
First thing, remember ABC
Airway, breathing and
circulation, and then…………….
D = deficit or disability, as in
neurological
THIS IS IMPORTANT – YOU NEED TO KNOW THE
GLASGOW COMA SCALE!!!!!!!
Tentorial (uncal) herniation
Classically presents with:
Ipsilateral IIIrd nerve palsy (dilated pupil, deviated “down and out”)
Contralateral hemiparesis (from compression of ipsilateral cerebral peduncle)
False-localizing hemiparesis = Kernohan’s phenomenon (from compression of
contralateral cerebral peduncle against the tentorium)
***Remember, GCS less than (or equal to) 8 = INTUBATE
(for airway protection)
Case example
65 to woman, alcoholic, fell down. Eyes open to pain, best verbal
response is groaning, does not follow commands but localizes pain on
the left. Right hemiparesis and dilated left pupil.
Same patient, comparing pre- and postop
Mannitol
• Indications for mannitol
– Signs of herniation (e.g., fixed or dilated pupil, hemiparesis)
– Progressive neurological deterioration
– ICP > 20mmHg
• Intermittent boluses more effective than continuous
infusion
• Effective doses: 0.25-1 gm/kg
• Hypovolemia should be avoided by fluid replacement
with normal saline
Hypertonic (3%) saline
• Head injured patients often develop hyponatremia,
usually not secondary to SIADH
• An increase in serum sodium concentration significantly
decreases ICP and increases CPP
• Many centers now using hypertonic saline in patients
with an exhausted response to mannitol.
– Some studies claim hypertonic saline is more effective than
mannitol at lowering ICP
Hyperventilation
• Chronic prolonged hyperventilation therapy (PaCO2 of
25 mm Hg or less) is discouraged in current practice
– Has negative effect on autoregulation curve, and ultimately,
cerebral blood flow
• Mild hyperventilation (PaCO2 30-35 mm Hg) may be
necessary for
– brief periods when there is acute neurological deterioration
– longer periods if there is high ICP refractory to sedation,
paralysis, CSF drainage, and osmotic diuretics (see “second teir”
therapies)
Glucocorticoids
• Not recommended for head injury on the basis of randomized controlled
trials (Class I evidence)
Anti-Seizure Prophylaxis
• Phenytoin or carbamazepine
• May be used to prevent early post-traumatic seizure (i.e., seizures
occuring up to 7 days post-injury) in “high-risk” patients:
– e.g. GCS < 10, cortical contusion, depressed skull fracture, hematoma,
penetrating head injury, seizure within 24 hrs after injury
ICP monitoring
• Requires surgical placement of either an external ventricular drain or a
parenchymal device
• Indicated for most patients with severe head injury (GCS 3-8), especially if
CT scan shows an abnormality such as a hematoma, contusion, edema or
compressed basal cisterns
General measures to control ICP
• Avoid hypotonic intravenous fluids (hypotonic fluids
contribute to cerebral edema)
• Control body temperature (prevent hyperthermia)
• Seizure prophylaxis
• Elevate head of bed
• Avoid jugular venous outflow obstruction (e.g. tight
spine collar)
• Sedation +/- pharmacological paralysis
• Adequate O2
• Maintain adequate blood pressure (CPP > 70 mm Hg)
Treatment algorithm for
elevated ICP
• 1st tier therapies:
– CSF drainage (if external ventricular drain in place)
– Mannitol and/or hypertonic saline
• 2nd tier therapies
– Barbiturates (if pt is hemodynamically stable)
– Hypothermia
– Hyperventilation
– Decompressive craniectomy (controversial)
Brain death
• Heart continues to beat, but patient is legally dead
• Must pass a rigorous clinical protocol to make this diagnosis, including:
– Fixed dilated pupils, no corneal response, negative doll’s eyes,
negative calorics, no response to pain, no spontaneous respirations,
no drugs that depress the central nervous system, no metabolic
disturbance, no hypothermia, positive apnea test (no respirations
despite PaCO2 > 60mmHg)
– Requires independent assessment by 2 physicians to make the
diagnosis (usually a neurosurgeon or neurologist + the ICU attending)
• Questionable cases require ancillary testing (e.g. Angiogram, cerebral
blood flow studies, EEG)
• Patients that meet criteria for brain death are candidates for organ
donation
– Requires consent of patient (e.g., organ donor card) and/or next-of-
kin
And finally….
An example of the “Saskatoon epidemic”!
27 yo man stabbed in the head with a knife. The knife
handle was removed.
Postop – mild hemiparesis (resolved by 6 weeks)
Thank you for listening!
Any comments?
