Head Trauma

Dean Carlo S. Dumalagan M.D.

  Trauma -the leading cause of death in
children and young adults;
 remains a major cause of morbidity and
mortality.
Head Trauma  The three main areas of neurosurgical
focus are:
 traumatic brain injury (TBI)
 spinal cord injury (SCI)
 peripheral nerve injury
  Initial assessment of the trauma patient
includes;
 primary survey
Head Trauma
 resuscitation
 secondary survey
Glasgow Coma  definitive care
Scale Score  Neurosurgical evaluation begins during
the primary survey with the
determination of the GCS for the patient.
  GCS - determined by adding the scores of the
best responses of the patient in each of three
categories.
 motor score from 1 to 6
Head Trauma  verbal from 1 to 5
 eyes from 1 to 4
Glasgow Coma  GCS therefore ranges from 3 to 15.
Scale Score
 Tracheal intubation or severe facial or eye
swelling can impede verbal and eye responses.
 The patient is given the score of 1 with a
modifier, such as verbal “1T” where T = tube.
 MOTOR VERBAL EYE-OPENING
RESPONSE RESPONSE RESPONSE
Obeys 6 Oriented 5 Opens 4
commands spontaneously
Localizes to pain 5 Confused 4 Opens to speech 3

Glasgow Coma Withdraws from 4 Inappropriate 3 Opens to pain 2

Scale Score pain words
Flexor posturing 3 Unintelligible 2 No eye opening 1
sounds
Extensor 2 No sounds 1
posturing
No movement 1
  Blunt or penetrating trauma can cause injury to
the vascularized scalp, thus results a significant
blood loss.
 Direct pressure initially controls the bleeding
Head Trauma  If a simple laceration is found, it should be irrigated
and closed primarily.
 if is short, a single-layer, percutaneous suture
Scalp Injury closure will suffice.
 if long or has multiple arms, may need debridement
and closure in OR
 Reapproximation of the galea will provide a more
secure closure and better hemostasis.
  skull X-rays or head CT- skull fractures
 Closed fracture -covered by intact skin.
 don’t normally require specific treatment
 Open, or compound fracture- associated with
Head Trauma disrupted overlying skin.
 requires repair of the scalp and operative
debridement
Skull Fractures  The fracture lines may be
 single (linear)
 multiple and radiating from a point (stellate)
 or multiple, creating fragments of bone
(comminuted)
  Craniotomy indication;
 depression greater than the cranial thickness
Head Trauma  intracranial hematoma
 and frontal sinus involvement
Skull Fractures  Fractures that cross meningeal arteries can
cause rupture of the underlying vessels and
subsequent epidural hematoma (EDH)
formation.
  Depressed skull fractures- result from a focal injury
of significant force.
 The inner cortex of the bone fragments often has
multiple sharp edges that can lacerate dura, brain,
Head Trauma and vessels.
 Craniotomy is required to
Skull Fractures  elevate the fracture,
 repair dural disruption,
 and obtain hemostasis.
 Fractures overlying dural venous sinuses require
restraint.
  Fractures of the skull base are common in head-
injured patients.
 Aysmptomatic- no treatment.
Head Trauma  Skull base fractures requiring intervention include
those with an associated cranial nerve deficit or
CSF leak.
Skull Fractures
 Fracture of the temporal bone can damage the
facial or vestibulocochlear nerve resulting in
 vertigo,
 ipsilateral deafness,
 or facial paralysis.
  A communication may form between the subarachnoid
space and the middle ear, allowing CSF drainage into the
pharynx via the Eustachian tube or from the ear
(otorrhea).
Head Trauma  Battle’s sign- extravasation of blood results in
ecchymosis behind the ear.
Skull Fractures  A fracture of the anterior skull base can result in
 anosmia (loss of smell from damage to the olfactory
nerve),
 CSF drainage from the nose (rhinorrhea),
 periorbital ecchymosis, known as raccoon eyes.
Head Trauma

Skull Fractures
  Head elevation for several days will heal some of
CSF leaks.
 Head elevation reduces the hydrostatic pressure of
Head Trauma the CSF fluid column in the cranial vault, near the
site of the defect.
Skull Fractures  Lumbar drain can be used to reduce CSF pressure.
 Extraventricular drain should be used for CSF
diversion if there is contraindication to lumbar
drain
Head Trauma

Skull Fractures
  Traumatic cranial neuropathies -conservative
management with documentation of the extent of
impairment and signs of recovery.
 Steriod -benefit patients with traumatic facial
Head Trauma nerve palsies.
 Patients with facial nerve palsy of abrupt onset,
Skull Fractures who do not respond to steroids within 48 to 72
hours, may be considered for surgical
decompression of the petrous portion of the facial
nerve.
  Closed head injury (CHI) - the most common type of TBI
 significant cause of morbidity and mortality in the United
States.
 There are two important factors that affect the outcome of
CHI.
 Primary injury- the initial impact
Closed Head  defined as the immediate injury to neurons from
transmission of the force of impact.
Injury (CHI)  the long, delicate axons of the neurons can shear as
they undergo differential acceleration or decelerations.
 Secondary injury- subsequent neuronal damage due to
the sequelae of trauma.
 Hypoxia, hypotension, hydrocephalus, intracranial
hypertension, thrombosis, and intracranial
hemorrhage may all be mechanisms of secondary
injury.
  The Brain Trauma Foundation’s most recent summary
of management recommendations for TBI patients
was published.
 The guidelines standardize the care of these patients
Closed Head with the hope of improving outcomes.
Injury (CHI)  Level I recommendations are based on a body of high-
quality evidence, such as large, well-received
randomized controlled trials.
 Level II and III recommendations are based on
moderate and low quality evidence, respectively.
  The first three elements of the ABCDs of resuscitation—
airway, breathing, and circulation—must be assessed and
stabilized.
Closed Head  Hypoxia and hypotension are known to worsen outcome in
Injury (CHI) TBI (due to secondary injury)
 Patients cant follow commands require intubation for airway
protection and ventilatory control.
Initial  The fourth element, assessment of “D,” for disability, is
Assessment undertaken next.
 Motor activity, speech, and eye opening can be assessed in a
few seconds and a GCS score assigned.
  TBI can be classified as
 mild
 moderate
 severe
Closed Head
 For patients with a history of head trauma,
Injury (CHI) classification is as follows:
 severe head injury if the GCS score is 3 to 8,
Classification  moderate head injury if the GCS score is 9 to 12,
 mild head injury if the GCS score is 13 to 15.
 Many patients present to emergency rooms and
trauma bays with a history of TBI.
  asymptomatic patients who have only headache, dizziness, or
scalp lacerations, and did not lose consciousness, have a low
Closed Head risk for intracranial injury and may be sent home without a
head CT scan.
Injury (CHI)  Printed discharge instructions, which describe monitoring for
confusion, persistent nausea, weakness, or speech difficulty,
Classification should be provided to the caretaker.
 The patient should return to the emergency department for
evaluation of such symptoms
  Patients with a history of the ff have a moderate risk for
intracranial injury and should undergo a prompt head CT.
 altered consciousness,
 amnesia,
Closed Head  progressive headache,
Injury (CHI)  skull or facial fracture,
 vomiting,
 or seizure
Classification  If the CT is normal, and the neurologic examination has
returned to baseline (excluding amnesia of the event), patient
can be discharged .
  Patients with the ff have a high risk for intracranial
injury. These patients should undergo immediate head
CT and admission for observation or intervention as
Closed Head needed.
Injury (CHI)  depressed consciousness,
 focal neurologic deficits,
Classification  penetrating injury,
 depressed skull fracture,
 or changing neurologic examination
  Concussion
Types of  Contusion
Closed Head
 Diffuse Axonal Injury
Injury
 Penetrating Injury
  Concussion -a temporary neuronal dysfunction
following nonpenetrating head trauma.
Types of CHI  If the head CT is normal, and deficits resolve
over minutes to hours.
Concussion  Memory difficulties, especially amnesia of the
event, are very common.
 Concussions may be graded.
  Colorado grading system
 Grade 1-confusion
 Grade 2-amnesia
 Grade 3- lose consciousness
Types of CHI  Studies have shown that the brain remains in a
hypermetabolic state for up to a week after injury.
Concussion  Second-impact syndrome-the brain is also much more
susceptible to injury from even minor head trauma in the
first 1 to 2 weeks after concussion.
 Patients should be informed that, even after mild head
injury, they might experience memory difficulties or
persistent headaches.
  Contusion -bruise of the brain, it happens when the force
from trauma causes breakdown of small vessels and
extravasation of blood into the brain.
 The contused areas appear bright on CT scan.
Types of CHI  The frontal, occipital, and temporal poles are most often
involved.
 Edema may develop around a contusion, causing mass effect.
Contusion  Contusions may enlarge or progress to frank hematoma,
during the first 24 hours.
 Contre-coup injury- contusion occurs in brain tissue opposite
the site of impact.
 These contusions result from deceleration of the brain against
the skull.
Types of CHI

Contusion
  Diffuse axonal injury (DAI)- is caused by damage to axons
due to rotational acceleration and then deceleration.
 Axons may be completely disrupted and then retract,
Types of CHI forming axon balls.
 Small hemorrhages can be seen in more severe cases,
Diffuse Axonal especially on MRI.
Injury  DAI can be considered to be a severe form of a concussion,
often with irreversible consequence.
 It can often explain a poor neurological examination (such
as impaired arousal) in cases without clear radiographic
signs of global bran injury.
  Two main subtypes are
 missile (e.g., due to bullets or fragmentation
devices)
Types of CHI  nonmissile (e.g., due to knives or ice picks).
 skull X-rays and CT scans are useful
Penetrating
 Cerebral angiography must be considered if the object
Injury passes near a major artery or dural venous sinus.
 Operative exploration is necessary to remove any
object extending out of the cranium
  Traumatic intracranial hematomas-
contribute to death and disability secondary to
head injury; they can expand and cause brain
shift and subsequent herniation.
Traumatic
Intracranial Epidural Hematoma
Hematomas Acute Subdural Hematoma
Chronic Subdural Hematoma
Intraparenchymal Hemorrhage
Pneumocephalus
  EDH- is the accumulation of blood between the skull
Traumatic and the dura.
 usually results from arterial disruption, especially of
Intracranial the middle meningeal artery.
Hematomas  Dura is adherent to bone, and some pressure is required
to dissect between the two.
Epidural  Head CT- the blood clot is bright, biconvex in shape
Hematoma (lentiform), and well-defined border that usually
respects cranial suture lines.
  EDH has a classic three-stage clinical presentation.
1. The patient is initially unconscious from the
concussive aspect of the head trauma.
Traumatic 2. Then awakens and has a “lucid interval,” while
Intracranial the hematoma subclinically expands.
Hematomas 3. As the volume of the hematoma grows, the
decompensated region of the pressure volume
curve is reached, ICP increases, and the patient
Epidural rapidly becomes lethargic and herniates.
Hematoma  Uncal herniation from an EDH classically causes
ipsilateral third nerve palsy and contralateral
hemiparesis.
  Craniectomy for evacuation of clot and hemostasis is
indicated for EDH.
Traumatic
 Patients who meet all of the following criteria may
Intracranial be managed conservatively:
Hematomas  clot volume: < 30cm3
 maximum thickness < 1.5cm
Epidural  GCS score >8
Hematoma  Prognosis after successful evacuation is better for
EDH than subdural hematoma (SDH).
Traumatic
Intracranial
Hematomas

Epidural
Hematoma
 Acute SDH -result of an accumulation of blood
Traumatic between the arachnoid membrane and the dura.
Intracranial - results from venous bleeding, from tearing of a
Hematomas bridging vein running from the cerebral cortex to the
dural sinuses.
Acute Bridging veins - subject to stretching and tearing
Subdural during acceleration/deceleration of the head because
the brain shifts in relation to the dura.
Hematoma
Elderly and alcoholic patients are at higher risk for
acute SDH formation
  Head CT scan- the clot is bright or mixed-density,
Traumatic  crescent-shaped (lunate)
Intracranial  less distinct border
Hematomas  does not cross the midline
 Craniotomy for evacuation of acute SDH is indicated
Acute for any of the following:
 thickness >1 cm,
Subdural  midline shift >5 mm,
Hematoma  or GCS drop by two or more points from the time
of injury to hospitalization.
Traumatic
Intracranial
Hematomas

Acute
Subdural
Hematoma
  Chronic SDH- a collection of blood breakdown
products that is at least 2 to 3 weeks old.
Traumatic  Acute hematoma- bright white (hyperdense) on CT
Intracranial scan for approximately 3 days, after which they fade to
Hematomas isodensity with brain, and then to hypodensity after 2
to 3 weeks.
 Chronic SDH will be nearly as dark as CSF on CT.
Chronic
 Traces of white are often seen due to small, recurrent
Subdural hemorrhages into the collection, may expand the
Hematoma collection enough to make it symptomatic.
 This phenomenon is referred to as an acute-on-chronic
SDH.
  Higher risk for developing chronic SDH
 Alcoholics
 Elderly
Traumatic  Patients on anticoagulation
Intracranial  Patients may present with
Hematomas  headache,
 seizure,
Chronic  confusion,
Subdural  contralateral hemiparesis,
 or coma
Hematoma
 Chronic SDH >1 cm or any symptomatic SDH should
be surgically drained.
Traumatic  A simple burr hole can drain most chronic SDHs.
Intracranial  Single burr hole placed over the dependent edge of the
Hematomas collection can be made, and the space is copiously
irrigated until the fluid is clear.
Chronic  A second, more anterior burr hole can then be placed if
Subdural the collection does not drain satisfactorily due to
containment by membranes.
Hematoma
Traumatic
Intracranial
Hematomas

Chronic
Subdural
Hematoma
Traumatic
Intracranial
Hematomas

Chronic
Subdural
Hematoma
  Isolated hematomas within the brain parenchyma are
most often associated with hypertensive hemorrhage
or arteriovenous malformations (AVMs).
Traumatic  Mass effect from developing hematomas may present
as a delayed neurologic deficit.
Intracranial
Hematomas  Delayed traumatic intracerebral hemorrhage- most
likely to occur within the first 24 hours.
 Indications for craniotomy include:
Intraparenchymal  any clot volume >50 cm3
Hemorrhage  or a clot volume >20 cm3 with referable neurologic
deterioration (GCS 6–8)
 and associated midline shift >5 mm or basal cistern
compression.
Traumatic
Intracranial
Hematomas

Intraparenchymal
Hemorrhage
  Pneumocephalus- seen in neurosurgical patients
following head trauma or following intracranial surgery.
Traumatic
 Pneumocephalus requires a defect in the skull that
Intracranial allows air to enter the intracranial cavity.
Hematomas  66% of postcraniotomy CT scans demonstrate some
extent of pneumocephalus.
Pneumocephalus  In rare cases, pneumocephalus can also be seen in
association with skull based tumors or infections.
  Tension pneumocephalus - when the intracranial air
pocket is under tension which can result herniation.
 - a neurosurgical emergency
Traumatic
 Two radiographic features have been associated with a
Intracranial tension pneumocephalus.
Hematomas 1. the “Mount Fuji” sign-the air pocket separates
the frontal lobes and widens the inter-hemispheric
Pneumocephalus fissure, mimicking the silhouette of Mount Fuji.
2. the “air bubble” sign- there are multi-focal
pockets of air throughout the subarachnoid
cisterns within the subarachnoid space.
  Two major mechanisms by which pneumocephalus
develops.
1. “ball valve” mechanism- involves the passage of
Traumatic air into the intracranial cavity during periods of
positive pressure, whereby the defect in the skull
Intracranial acts as a one-way valve.
Hematomas 2. “inverted bottle” mechanism- involves air
entering the intracranial space due to a negative
Pneumocephalus pressure gradient created by the drainage of CSF.
 In most cases, drainage occurs through a traumatic or
iatrogenic CSF leak, but it may also occur through
ventricular or lumbar drainage.

Traumatic  If the CSF leak is at the skull base- the head of bed must be
elevated so as to reduce hydrostatic pressure in the ventricular
Intracranial CSF fluid column, and controlled CSF diversion can be performed
Hematomas using an extraventricular or lumbar drain .
 Definitive repair of the skull based defect can also be considered,
but this is often done on an elective basis.
Pneumocephalus  nontension pneumocephalus will resolve on its own with time
as it is resorbed into the blood stream.
Traumatic
Intracranial
Hematomas

Pneumocephalus
  Patients with CHI and evidence of intracranial
Management hemorrhage or a depressed skull fracture should
of Traumatic receive a 1 g Keppra loading dose, followed by 1 week
Brain Injury of therapeutic maintenance Keppra 500 mg twice a
day.
General  Antiseizure prophylaxis has been shown to decrease
the incidence of early posttraumatic seizures.
Medical
 Blood glucose levels should be closely monitored by
Management and controlled.
  Fevers also should be controlled with antipyretics
Management
 Hyperglycemia and hyperthermia are toxic to injured
of Traumatic neurons and contribute to secondary injury.
Brain Injury  Head-injured patients have an increased prevalence of peptic
ulceration and GI bleeding.
General  Cushing’s ulcers- Peptic ulcers occurring in patients with head
injury or high ICP.
Medical  Ulcer prophylaxis should be used.
Management  Compression stockings or athrombic pumps should be used
  Steroids- not recommended for the management of
Management TBI or reduction of elevated ICP.
of Traumatic  High-dose methylprednisolone - contraindicated in
Brain Injury severe TBI.
 Blood pressure management in TBI is a complex
issue.
Steroids and  hypotension results in hypoperfusion that may
Traumatic worsen brain injury that occurs following TBI.
Brain Injury  hypertension may result in expansion of
intracranial hematomas that are often seen in TBI.
  Anticoagulation reversal - important to reduce
Management the risk of hematoma expansion.
of Traumatic  Anticoagulant reversal is also associated with
Brain Injury thrombotic cardiovascular complications.
 Level III (low-quality) recommendation of Brain
Trauma Foundation Guidelines-anticoagulation
Anticoagulation prophylaxis with low-molecular weight heparin or
Reversal and low-dose unfractionated heparin may be used to
Prophylaxis reduce the risk of venous thrombosis.
Management
of Traumatic
Brain Injury  Decompressive craniectomy - can be performed to
relieve intracranial pressure associated with diffuse
cerebral edema in cases of severe TBI without mass
Decompressive lesions (e.g., extra-axial hematoma).
Craniectomy for
Severe TBI