Head Trauma: Surgical Management
Sandrine de Ribaupierre MD, FRCSC
Peter Dirks MD, PhD, FRCSC
INTRODUCTION
Pediatric head injury incidence is 2 per 1,000 under 15 years of age, and 3.4 per 1,000 for ages 15 and over.
Neurologic injuries account for 18% of all pediatric injuries and 23% of traumatic deaths.1
Closed head trauma has a fatality risk of 0.5 per 1,000.2
Eight percent to nine percent of patients with a mild head injury (Glasgow Coma Scale 13-15) lacking neurologic symptoms will have an abnormal CT scan, and 1% to 4% will require a neurosurgical intervention.3,4
Children have fewer mass lesions than adults, but more skull fractures.
Severity of head injury is typically assessed with the Glasgow Coma Scale (GCS),
Mild head injury: GCS 13-15.
No or brief loss of consciousness (LOC).
Moderate head injury: GCS 9-12.
LOC from a few minutes to hours, confusion can last a few days.
Severe head injury: GCS ≤8.
Coma is defined by a profound state of unconsciousness.
Comatose patient fails to respond normally to voice, pain or light, does not have sleep-wake cycles, and does not take voluntary actions.
INITIAL MANAGEMENT
Use ATLS protocol for initial evaluation of pediatric head injuries.
DO NOT rush to CT with a unilateral or bilateral mydriasis without completing the ABCs.
Hypoxia, hypoglycemia, and hypotension are associated with much worse outcome following severe head injury.
Establish a secure airway.
Prevent secondary brain injuries by ensuring there are no breathing or circulatory problems in a head-injured child.
If there is evidence of intracranial hypertension/herniation, give mannitol (0.5-1 g/kg) or hypertonic saline (3% NaCl at 3 mL/kg).
Hyperventilation is not routinely recommended, unless clinical signs of acute herniation.
Cervical spine trauma can be associated with significant head injuries.
EVALUATION
History
Determine mechanism of injury as per patient, witness, parents, paramedics:
Acceleration/deceleration mechanism (MVA, falls).
Blunt trauma (falls, blows).
Crush injury.
Penetrating injury (falls, blows, toys, missile).
Children can have bizarre mechanisms of accidental injury.
Determine if loss of consciousness occurred and its duration.
Did patient talk at any time?
Does patient recall the accident?
Determine if there has been a fluctuating level of consciousness or progressive deterioration/amelioration.
Determine amount of time elapsed from time of injury.
Did a seizure occur following the trauma?
Did hypoxia or hypotension occur at any time?
How much bleeding resulted from the head injury (scalp, sinus, carotid, ear, nose)?
Any other injuries?
Physical Exam
Assess pupil size and reactivity to light.
Should occur during primary survey with the GCS.
Check for local signs of trauma, such as contusion/laceration/skin mark above the clavicles.
Use the GCS to record level of consciousness and fluctuations in time (Table 6-1).
Motor assessment is most reliable indicator in infant and younger children (unless associated spinal cord injury).
GCS may be unreliable in young children because different scales can make assessment difficult.
Document each of 3 scores (eyes, motor, verbal) leading to final GCS.
GCS score has not been fully validated in pediatric patients but it is important to document initial GCS and follow trends over time.5
Assess for:
Motor deficits.
Sensory deficits.
Change in reflexes.
Evaluate for signs of basal skull fracture:
Battle sign.
Raccoon eyes
Hemotympanum.
CSF leak (otorrhea, otorrhagia, rhinorrhea).
Monitor heart rate.
Bradycardia may precede decreased level of consciousness in the presence of an expanding mass lesion.
Evaluate for signs of herniation:
Progressive obtundation.
Mydriasis (unilateral, bilateral pupil dilatation). Pupil dilation is a critical lateralizing sign.
Medication (atropine) can be a confounding factor (pupils, HR).
Pupil dilatation can also be from direct trauma or contusions to the optic nerve.
In general, pupil dilatation is more lateralizing than limb weakness.
Contralateral hemiparesis (unilateral hemiparesis = Kernohan notch phenomenon).
Cushing’s triad (bradycardia, hypertension, irregular respirations): Most often late signs.
In infants: Check fontanel when assessing intracranial pressure (sunken, flat, full, bulging, tense).
TABLE 6-1 GCS Scores As Determined by Best Responses by Age | ||||||||||||||||||||
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Laboratory Investigations
Hemoglobin:
Initial hemoglobin level may not reflect intravascular volume status.
In older patients, hypovolemia must be excluded from other sources (abdominal, thoracic, and pelvic).
In older children and teenagers, intracranial bleeding will have mass effect before showing a decrease in hemoglobin.
Infants with intracranial bleeding (or scalp loss) might develop decreased hemoglobin or hypotension.
Electrolytes:
Sodium: Hyponatremia might cause neurologic findings in patients with decreased level of consciousness and unclear traumatic history.
Platelets and coagulation studies:
Brain injury and blood loss might lead to disseminated intravascular coagulation (DIC).
Patient may require surgery; therefore check coagulation status, and type and cross-match the blood.
Imaging
Role of Plain Radiographs
Except in a center where a CT-scan is unavailable, skull x-rays are not indicated.
When no CT is available:
Check for linear fractures going through the temporal region (middle meningeal artery: risk of epidural bleeding).
29% of linear fractures are associated with intracranial lesions.4
Check for depressed fractures.
Check for pneumocephalus.
Role of Computed Tomography (CT)
Any trauma with a persistent GCS below 15.
GCS = 15 but:
More than brief LOC or LOC of uncertain duration (persistent LOC is more important than a fracture for predicting intracranial hematoma).
Bradycardia.
Mechanism of injury especially concerning (fall from significant height, high-speed MVA).
Abnormal neurologic exam.
LOC with lucid interval but progressive worsening headaches.
Signs of important local trauma or skull base fracture.
All penetrating injuries.
Skull fracture (seen on x-ray, or for infants with falls, an obvious scalp abnormality may be a clue for a skull fracture).
What to look for on CT-head:
Contusions, subdural or epidural hematomas, subarachnoid blood.
Lesion leading to a mass effect, midline shift, herniation.
Disappearance of basal cisterns, shape of ventricles (indirect signs of edema), loss of sulci.
Gray/white matter differentiation.
Skull fractures (basal skull fracture: integrity of vessels).
Pneumocephalus.
Petechial hemorrhages indicating diffuse axonal injury.
Subdurals may be difficult to see; thin but diffuse subdurals can be massive.
Indications for CT-venogram:
Evidence of trauma near a venous sinus (occipital fracture), to ensure patency of the sinus and rule out a tear.
Indications for CT-arteriogram:
Basal skull fracture crossing the carotid canal, or evidence of blood in sphenoid sinus.
Any motor deficit unexplained by CT scan (suspect early infarction).
Beware of carotid dissection.
Unclear history of LOC before trauma and evidence of subarachnoid blood.
Crush injury to the head.
See Chapter 4 on Diagnostic Imaging for details.
Role of Magnetic Resonance Imaging (MRI)
MRI is not part of the primary survey.
MRI should be reserved for the trauma center.
Can be useful if CT does not explain a depressed consciousness level or to assess diffuse axonal injuries.
Unexplained neurologic deficit (check for parenchymal, brainstem or spinal cord lesions).
SPECIFIC INJURIES
Skull Fractures
Linear Skull Fracture
Definition: Linear fracture running through the entire thickness of bone without significant displacement.
Simple linear fracture: Most common type of fracture, especially in children <5 years old. Linear fractures increase risk of intracranial hematoma, but risk of hematoma is less in children compared to adults.
Basilar skull fractures represent 19% to 21% of all skull fractures.
Specific Types of Skull Fractures:
Longitudinal temporal bone fractures:
Conductive deafness (ossicular chain disruption); facial palsy, nystagmus, and facial numbness.
Transverse temporal bone fractures:
Nystagmus, ataxia (labyrinth), and permanent neural hearing loss (VIII).
Occipital condylar fracture:
Rare but serious injury.9
Associated with cervical spinal injuries, lower cranial nerve injuries, and hemiplegia or quadriplegia (needs CT/MRI evaluation).
Mechanism: Result from blunt trauma, usually low-energy over wide surface area.
Falls are more common cause than motor vehicle accidents.
Presentation: No clinical signs by itself, if not associated with other injuries—except in basal skull fracture (see below) and tempoparietal fracture that involve the cochlea and labyrinth.
A large, boggy, scalp contusion may predict a fracture.
CT findings: Linear fracture with no, or minimal, displacement (rule out epidural and subdural hematoma).
Management:
Admit infants with simple linear fractures for overnight observation regardless of neurologic status.
Treat neurologically intact patients with linear basilar fractures conservatively, without antibiotics.
Initially manage temporal bone skull base fractures conservatively. Tympanic membrane ruptures usually heal on their own.
Complex linear fractures may raise suspicion for nonaccidental injury.
Depressed Skull Fracture
Definition: Fracture with misalignment of the fragments, which are pushed inwards, usually caused by a greater impact injury than the linear fracture. Significant when the displacement is greater than the thickness of the skull.
More frequently associated with intracranial findings than linear fractures.
Depressed fractures are:
75% frontoparietal.
10% temporal.
5% occipital.
10% other.
Most depressed fractures are open fractures (75-90%).
Comminuted fragments.Related posts:
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