HEAD TRAUMA

ATLS 10Th Edition

 INTRODUCTION

HEAD INJURY TRAUMATIC BRAIN INJURY

Head injury is a non-specific and Traumatic brain injury is well defined

antiquated term, which includes as an alteration in brain function
clinically evident external injuries manifest as confusion, altered level
to face, scalp and calvarium, such of consciousness, seizure, coma or
as lacerations, contusions, focal neurological defi cit resulting
abrasions and fractures, and may from blunt or penetrating forces to
or may not be associated with the head.
traumatic brain injury.

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Head injuries are among the most common types
of trauma encountered in emergency
departments (EDs).
Many patients with severe brain injuries die
before reaching a hospital; in fact, nearly 90% of
prehospital trauma-related deaths involve brain
injury.
Approximately 75% of patients with brain injuries
who receive medical attention can be
categorized as having mild injuries, 15% as
moderate, and 10% as severe.
TBI has a preponderance for young males (male
to female ratio 4:1) attributed to interpersonal
violence and motor vehicle accidents in the
“testosterone years”

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 Anatomy Review

A review of cranial anatomy includes :

1. scalp,
2. skull,
3. meninges,
4. brain,
5. ventricular system,
6. intracranial compartments.

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 Anatomy Review
Scalp
Because of the scalp’s generous blood supply, scalp lacerations
can result in major blood loss, hemorrhagic shock, and even death.
Patients who are subject to long transport times are at particular
risk for these complications.

Skull
The base of the skull is irregular, and its surface can contribute to
injury as the brain moves within the skull during the acceleration
and deceleration that occurs during the traumatic event. The
anterior fossa houses the frontal lobes, the middle fossa houses
the temporal lobes, and the posterior fossa contains the lower
brainstem and cerebellum.

Meninges
The meninges cover the brain and consist of three layers: the dura
mater, arachnoid mater, and pia mater

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 Anatomy Review
Brain
The brain consists of the cerebrum, brainstem, and cerebellum.

Ventricular System
The ventricles are a system of CSF-filled spaces and aqueducts within the brain.
Edema and mass lesions (e.g., hematomas) can cause effacement or shifting of the
normally symmetric ventricles, which can readily be identified on brain CT scans.

Intracranial Compartement
compression third cranial nerve during herniation causes pupillary dilation due to
unopposed sympathetic activity, often referred to as a “blown” pupil.
The part of the brain that usually herniates through the tentorial notch is the
medial part of the temporal lobe, known as the uncus. Uncal herniation also causes
compression of the corticospinal (pyramidal) tract in the midbrain. The motor tract
crosses to the opposite side at the foramen magnum, so compression at the level
of the midbrain results in weakness of the opposite side of the body (contralateral
hemiparesis). Ipsilateral pupillary dilation associated with contralateral
hemiparesis is the classic sign of uncal herniation.

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 Physiology Review
Intracranial Pressure
Elevation of intracranial pressure (ICP) can reduce cerebral perfusion
and cause or exacerbate ischemia. The normal ICP for patients in the
resting state is approximately 10 mm Hg. Pressures greater than 22
mm Hg, particularly if sustained and refractory to treatment, are
associated with poor outcomes.

Monro–Kellie Doctrine
Figure 6-6

Cerebral Blood Flow

TBI that is severe enough to cause coma can markedly reduce
cerebral blood flow (CBF) during the first few hours after injury. CBF
usually increases over the next 2 to 3 days, but for patients who
remain comatose, it remains below normal for days or weeks after
injury.
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 Pathophysiology

• Primary brain injury is damage at the time of initial

trauma to the brain, is mechanically irreversible and
includes brain lacerations, contusions, haemorrhages
and avulsions.

• Secondary brain injury is derived from complications

initiated by the primary brain injury and includes
potentially avoidable entities such as hypoxic-
ischaemic injury, cerebral oedema, metabolic
dysfunction, alterations in vascular permeability,
diminished blood flow, inflammation, diffuse axonal
injury and consequences of intracranial hypertension.

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Classification of Head Injuries

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 Severity of Injury

In assessing the GCS score, when there is

right/left or upper/lower asymmetry, be
sure to use the best motor response to
calculate the score, because it is the most
reliable predictor of outcome. However, the
actual responses on both sides of the body,
face, arm, and leg must still be recorded.

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 Morphology
Skull Fractures

Clinical signs of a basilar skull fracture include

periorbital ecchymosis (raccoon eyes),
retroauricular ecchymosis (Battle’s sign), CSF
leakage from the nose (rhinorrhea) or ear (otorrhea),
and dysfunction of cranial nerves VII and VIII (facial
paralysis and hearing loss), which may occur
immediately or a few days after initial injury.

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 Morphology
Intracranial Lession (1)
Focal lesions include :
1. Epidural hematomas (0,5%) : hematomas typically become
biconvex or lenticular in shape, most often located in the
temporal or temporoparietal regions and often result from a
tear of the middle meningeal artery due to fracture, The
classic sign is with a lucid interval between the time of injury
and neurological deterioration.

2. Subdural hematomas : They often develop from the shearing

of small surface or bridging blood vessels of the cerebral
cortex. subdural hematomas often appear to conform to
contours of the brain. subdural hematoma is typically much
more severe than that associated with epidural hematomas
due to the presence of concomitant parenchymal injury.

3. Contusions and Intracerebral Hematomas (20-30%) : Most

contusions are in the frontal and temporal lobes. In a period
of hours or days, contusions can evolve to form an
intracerebral hematome. Patients with contusions generally
undergo repeat CT scanning to evaluate for changes in the
pattern of injury within 24 hours of the initial scan.

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 Morphology
Intracranial Lession (2)

Diffuse Brain Injuries

Diffuse brain injuries range from mild concussions, in which the head CT is normal, to severe
hypoxic, ischemic injuries.
With a concussion, the patient has a transient, nonfocal neurological disturbance that often
includes loss of consciousness.
Severe diffuse injuries often result from a hypoxic, ischemic insult to the brain from
prolonged shock or apnea occurring immediately after the trauma. In such cases, the CT
may initially appear normal, or the brain may appear diffusely swollen, and the normal gray-
white distinction is absent.

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Management of Brain Injury

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 Management of
Brain Injury

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Management of
Brain Injury
cont.

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 Algorithm for Management of Mild
Brain Injury

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 Algorithm for Management of
Moderate Brain Injury

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 Algorithm for Management of
Severe Brain Injury

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 Algorithm for Management of
Severe Brain Injury
cont.

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 PRIMARY SURVEY AND RESUSCITATION
a. Airway and Breathing
• Perform early endotracheal intubation in
comatose patients
• Ventilate the patient with 100% oxygen and
oxygen saturations of > 98% are desirable

b. Circulation
• Hypotension usually is not due to the brain injury
itself, except in the terminal stages when
medullary failure supervenes or there is a
concomitant spinal cord injury.
• Intracranial hemorrhage cannot cause
hemorrhagic shock. establish euvolemia as soon
as possible using blood products, or isotonic
fluids as needed.

c. Neurogical Examination
• GCS score, pupillary light response, and focal
neurological deficit.

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 SECONDARY SURVEY

1. Brief or Focused Neurological Examination

Examine Pupils, Determine New GCS Score, Evaluate for Any Evidence of
Lateralizing Signs
2. Evaluation of Cervical Spine
3. Transfer Communication
4. Helmet Removal
5. Detailed Neurological Exam
7. Removal of Spine Board
8. Evaluation of Head CT Scans
9. Evaluation of Cervical Spine Images

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DIAGNOSTIC PROCEDURES
• CT scan as soon as possible after hemodynamic normalization

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MEDICAL THERAPIES FOR BRAIN INJURY
1. Intravenous Fluids 6. Barbiturates
Ringer’s lactate solution or normal saline is thus "Highdose barbiturate administration is
recommended for resuscitation. recommended to control elevated ICP refractory
to maximum standard medical and surgical
2. Correction of Anticoagulation treatment. (IIB)."

3. Hyperventilation 7. Anticonvulsants
Prophylactic hyperventilation (pCO2 < 25 mm Prophylactic use of phenytoin (Dilantin) or
Hg) is not recommended (IIB). valproate (Depakote) is not recommended for
preventing late posttraumatic seizures (PTS).
4. Mannitol Phenytoin is recommended to decrease the
Use 0.25–1 g/kg to control elevated ICP ; arterial incidence of early PTS (within 7 days of injury),
hypotension (systolic blood pressure when the overall benefit is felt to outweigh the
complications associated with such treatment.
5. Hypertonic Saline (IIA).
Hypertonic saline is also used to reduce elevated
ICP, in concentrations of 3% to 23.4%;

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 SURGICAL MANAGEMENT

1. Scalp Wounds

2. Depressed Skull Fractures

3. Intracranial Mass Lesions

4. Penetrating Brain Injuries

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 PROGNOSIS

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Predictors of outcome:
• Age: Severe TBI older patients have worse outcomes than young adults, and young
children still have neuronal plasticity.
• Glasgow Coma Scale (GCS): Lower total score is associated with poor outcome.
Intoxication can also hamper outcome prediction.
• Pupillary response and eye movement: Unilateral dilated pupil suggests a mass
lesion and abnormally dilated and non-reactive pupils are strongly associated with
poor neurological outcome. The absences of oculocephalic and oculovestibular
responses are poor prognostic signs.
• Type of brain lesion on imaging studies: Marshall classification has prognostic signifi
cance with progressive mortality increasing from I to IV and good to moderate
outcomes in 62 % of Grade I and 6 % in Grade IV.

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 TAKE HOME MESSAGE
• Patients with head and brain injuries must be evaluated efficiently. In a comatose
patient, secure and maintain the airway by endotracheal intubation. Perform a
neurological examination before paralyzing the patient. Search for associated
injuries, and remember that hypotension can affect the neurological examination.

• Trauma team members should become familiar with the GCS and practice its use,
as well as performance of rapid, focused neurological examinations. Frequently
reassess the patient’s neurological status.

• Adequate resuscitation is important in limiting secondary brain injury. Prevent

hypovolemia and hypoxemia. Treat shock aggressively and look for its cause.
Resuscitate with Ringer’s lactate solution, normal saline, or similar isotonic
solutions without dextrose. Do not use hypotonic solutions. The goal in
resuscitating the patient with brain injuries is to prevent secondary brain injury.

• Determine the need for transfer, admission, consultation, or discharge. Contact a

neurosurgeon as early as possible. If a neurosurgeon is not available at the facility,
29 transfer all patients with moderate or severe head injuries.
THANK YOU!

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