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. Most recent United States data estimate 1,700,000 traumatic brain injuries (TBIs)
occur annually, including 275,000 hospitalizations and 52,000 deaths.

TBI survivors are often left with neuropsychological impairments that result in disabilities affecting
work and social activity. Every year, an estimated 80,000 to 90,000 people in the United States
experience long-term disability from brain injury. In one average European country (Denmark),
approximately 300 individuals per million inhabitants suffer moderate to severe head injuries
annually, and more than one-third of these individuals require brain injury rehabilitation. Given
these statistics, it is clear that even a small reduction in the mortality and morbidity resulting from
brain injury can have a major impact on public health.

Traumatic brain injury (TBI) is the impairment in brain function after direct or indirect forces to the
brain. The force of an object striking the head or a penetrating injury causes direct injury. Indirect
injuries occur from acceleration/deceleration forces that result in the movement of the brain within
the skull. Traumatic brain injury can be classified as mild, moderate, and severe. Mild TBI includes
patients with a Glasgow Coma Scale (GCS, see Table 160-1) score ≥14. Patients may be
asymptomatic with only a history of head trauma, or may be confused and amnestic of the event.
They may have experienced a brief loss of consciousness and complain of a diffuse headache,
nausea, and vomiting. Patients at high risk in this subgroup include those with a skull fracture, large
subgaleal swelling, focal neurologic findings, coagulopathy, age >60 years, or drug/alcohol
intoxication.

The primary goal of treatment for patients with suspected TBI is to prevent secondary brain injury.
The most important ways to limit secondary brain damage and thereby improve a patient’s outcome
are to ensure adequate oxygenation and maintain blood pressure at a level that is sufficient to
perfuse the brain. After managing the ABCDEs, patients who are determined by clinical examination
to have head trauma and require care at a trauma center should be transferred without delay. If
neurosurgical capabilities exist, it is critical to identify any mass lesion that requires surgical
evacuation, and this objective is best achieved by rapidly obtaining a computed tomographic (CT)
scan of the head. CT scanning should not delay patient transfer to a trauma center that is capable of
immediate and definitive neurosurgical intervention.

The term “head injury” is used to describe all structural damage to the head, including injury to the
skull, brain, or both. The leading causes of head injury are motor vehicle accidents, bicycle crashes,
battle eld trauma, sports injuries, falls, and assaults. Head injury with concussion is becoming
increasingly reconized as a signi cant medical problem with signi cant morbidity and sometimes
devastating complications. High-pro le cases involving athletes and large numbers of returning
armed services personnel with battleeld injuries have brought concussions to the forefront of
concern for school athletic personnel and health care professional

The physical forces associated with head injury may result in skull fractures, brain injury, and
vascular damage, all three of which can coexist. Skull fractures are frequently accompanied by
intracranial lesions, and the presence of skull fracture greatly increases the risk of an underlying
subdural and/or epidural hemorrhage
There are two main stages in the development of brain damage after brain injury: primary and
secondary. Primary injuries, which represent the immediate response to the initial injury, include
focal lesions (contusions and hemorrhage) and diffuse injuries (concussion and diffuse axonal
injuries). Secondary injures involve complicating processes resulting from the initial injury, including
brain swelling, and infection. Ischemia is considered the most common cause of secondary brain
injury. It can result from the hypoxia and hypotension that occur during the resuscitation process or
from the impairment of regulatory mechanisms that control cerebrovascular responses that
maintain blood ow and oxygen supply

1. Contusions
Contusions represent a bruising on the brain surface or a lacerations or tearing of brain
tissue. Contusions can result from direct force, a depressed skull fracture, or a closed
acceleration-deceleration injury. Closed injury contusions are often distributed along the
rough, irregular inner surface of the brain and are more likely to occur in the frontal or
temporal lobes, resulting in cognitive and motor de cits. The clinical effects of a contusion
depend on its size and related cerebral edema. Small, unilateral, frontal lesions may be
asymptomatic; whereas larger lesions may result in neurological defects. They can cause
secondary mass effects from edema resulting in an increased ICF, and possible herniation
syndromes. Persons suffering from cerebral contusions are usually managed medically with
emphasis toward prevention of secondary injuries
2. Hematomas
Hematomas result from vascular injury and bleeding. Depending on the anatomic position of
the ruptured vessel, bleeding can occur in any of several compartments, including the
epidural, subdural, and subarachnoid spaces, or into the brain itself (intracerebral
hematoma).
1) Epidural Hematoma.
- tulang cranium dan lapisan duramater, pecahnya middle meningeal artery yang
letaknya nempel di kranium (lapisan periosteum tulang kranium)
- pecahnya arteri tsb menyebabkan epidural hemorrhage
- disertai dengan adanya fraktur, karena pembuluh darah yang pecah disebabkan
karena fraktur
- progresivitas perdarahan parah menyebabkan peningkatan tekanan intrakranial
An epidural hematoma is one that develops between the inner side of the skull and the
dura. It usually results from a tear in an artery, most often the middle meningeal, usually
in association with a head injury in which the skull is fractured. Because bleeding is
arterial in origin, rapid expansion of the hematoma compresses the brain. Epidural
hematoma is more common in a young person because the dura is less rmly attached to
the skull surface than in an older person; as a cosequence, the dura can be easily
separated from the inner surface of the skull, allowing the hematoma to grow
Typically, a person with an epidural hematoma presents with a history of head injury
and a brief period of unconsciousness followed by a lucid period in which consciousness
is regained. There is then a rapid progression to unconsciousness. The lucid interval does
not always occur, but when it does, it is of great diagnostic value. With rapidly
developing unconsciousness, there are focal symptoms related to the area of the brain
involved. These symptoms can include ipsilateral pupil dilation and contralateral
(opposite side) hemiparesis from uncal herniation. If the hematoma is not removed, the
condition progresses, with increased ICP, tentorial herniation, and death. The prognosis
is excellent, however, if the hematoma is removed before loss of consciousness occurs.
 2) Subdural Hematoma
- Duramater dan arachnoid mater
- Disebabkan rupturenya bridging vein karena menjembatani bagian duramater ke
arachnoid mater
- Ketika benturan arah kanan hingga bridging vein sebelah kiri ruptur
- Tekanan vena lebih rendah hingga kalau pendarahan bentuknya akan crescent
shaped
A subdural hematoma develops in the area between the dura and the arachnoid
(subdural space) and usually is the result of a tear in the small bridging veins that
connect veins on the surface of the cortex to dural sinuses. The bridging veins pass from
the pial vessels through the CSF filled subarachnoid space, penetrate the arachnoid and
the dura, and empty into the intradural sinuses. These veins are readily snapped in head
injury when the brain moves suddenly in relation to the cranium (Fig. 37-8). Bleeding can
occur between the dura and arachnoid (i.e., subdural hematoma) or into the CSF filled
subarachnoid space (i.e., subarachnoid hematoma). The venous source of bleeding in a
subdural hematoma develops more slowly than the arterial bleeding in an epidural
hematoma. Subdural hematomas are classified as acute, subacute, or chronic. This
classification system is based on the approximate time before the appearance of
symptoms. Symptoms of acute hematoma are seen within 24 hours of the injury,
whereas subacute hematoma does not produce symptoms until 2 to 10 days after injury.
Symptoms of chronic subdural hematoma may not arise until several weeks after the
injury.
3) Intracerebral Hematomas.
- Pecah PD namun tidak spesifik tergantung lokasi didalam parenkim otak
Traumatic intracerebral hematomas may be single or multiple. They can occur in any
lobe of the brain but are most common in the frontal or temporal lobes, related to the
bony prominences on the inner skull surface (Fig. 37-9). They may occur in association
with the severe motion that the brain undergoes during head injury, or a contusion can
coalesce into a hematoma. Intracerebral hematomas occur more frequently in older
persons and alcoholics, whose cerebral vessels are more friable
3. Concussions
A cerebral concussion can be de ned as a transient neurogenic dysfunction caused by
mechanical force to the brain. Acceleration–deceleration is the mechanism of injury, usually
due to a nonpenetrating force such as a sudden blow to the head. There may be a
momentary loss of consciousness without demonstrable symptoms, except for residual
amnesia. Microscopic changes can often be detected in neurons and neuroglia within hours
of injury, but brain imaging is usually negative. Although recovery usually takes place within
24 hours, mild symptoms, such as headache, irritability, insomnia, and poor concentration
and memory, may persist for months. This is known as the postconcussion syndrome. The
amnesia or memory loss usually includes an interval of time preceding the injury (retrograde
amnesia) and following the injury (anterograde amnesia). The duration of retrograde
amnesia correlates with the severity of the brain injury. Traditionally, the diagnosis and
management of concussion has relied heavily on the person’s self-reporting of symptoms.
Because symptom resolution often precedes cognitive recovery and because many persons
don’t report symptoms in an effort to return to their normal activities, additional
neurophysiologic testing and monitoring can be useful. Neurophysiologic tests commonly
evaluate decision-making ability, reaction time, attention, memory, and cognitive processing
speed in an objective fashion. CT or MRI imaging is usually reserved for cases in which
 intracranial bleeding is suspected. Treatment, which is largely supportive, includes both
physical and mental rest. Once symptoms have resolved, the person may begin shortened
work days with decreased work demands. Students may bene t from short periods of
reading and studying with frequent breaks. Athletes are advised to follow a slow stepwise
return to play. The complications of concussion, although rare, are potentially serious.
Currently, the clinical and neuropathic consequences of repeated mild head injury are
known as chronic traumatic encephalopathy. The disorders often manifests years or decades
after the inciting head injuries with effects on behavior, cognition, and movement. Cognitive
changes may occur early in the disease course and include loss of executive function and
poor memory. A widely feared complication of concussion is the second-impact syndrome. It
is thought to occur when someone who is still recovering from a recent concussion suffers a
second head trauma. Signi cant morbidity and even death can result from edema caused by
cerebral congestion that occurs
4. Diffuse Axonal Injury
Diffuse axonal injury is caused by shearing of fragile axons by acceleration-deceleration
forces at the time of trauma. The difference in acceleration–deceleration gradient on certain
areas of the brain, permits generation of rotational forces that cause axonal shearing injury.
It is characterized by distinct and microscopic ndings, including axonal swelling, that are
widely distributed in the cerebral hemispheric white matter, corpus callosum, and upper
brain stem. Diffuse axonal injury is characterized clinically by functional cerebral impairment,
which may range from confusion to coma and death. The clinical diagnosis of diffuse axonal
injury is based on immediate onset of unconsciousness in a person with signi cant cerebral
trauma and no intracranial lesion noted on CT scan. Current treatment modalities focus on
supportive care, especially for the unconscious person. Studies indicate that axonal injury
evolves over a period of hours or days, suggesting that there may be an opportunity to
arrest its progression and preserve axonal integrity

Manifestasi Klinis

Diffuse (global) brain injury, whether due to head trauma or other pathologic processes, is
manifested by alterations in sensory, motor, and cognitive function and by changes in the level of
consciousness. In contrast to a localized injury, which causes focal neurologic deficits without altered
consciousness, global injury nearly always results in altered levels of consciousness, ranging from
inattention to stupor or coma. Severe injury that seriously compromises brain function may result in
brain death

Klasifikasi
Intracranial lesions are classified as diffuse or focal, although these two forms frequently coexist.

1. 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.
Another diffuse pattern, often seen in high-velocity impact or deceleration injuries, may
produce multiple punctate hemorrhages throughout the cerebral hemispheres. These
“shearing injuries,” often seen in the border between the gray matter and white matter, are
referred to as diffuse axonal injury (DAI) and define a clinical syndrome of severe brain injury
with variable but often poor outcome.
2. Focal Brain Injuries
Focal lesions include epidural hematomas, subdural hematomas, contusions, and
intracerebral hematoma
1) Epidural hematoma
Epidural hematomas are relatively uncommon, occurring in about 0.5% of patients with
brain injuries and 9% of patients with TBI who are comatose. These hematomas typically
become biconvex or lenticular in shape as they push the adherent dura away from the
inner table of the skull. They are most often located in the temporal or temporoparietal
regions and often result from a tear of the middle meningeal artery due to fracture.
These clots are classically arterial in origin; however, they also may result from
disruption of a major venous sinus or bleeding from a skull fracture. The classic
presentation of an epidural hematoma is with a lucid interval between the time of injury
and neurological deterioration.
2) Subdural hematoma
Subdural hematomas are more common than epidural hematomas, occurring in
approximately 30% of patients with severe brain injuries. They often develop from the
shearing of small surface or bridging blood vessels of the cerebral cortex. In contrast to
the lenticular shape of an epidural hematoma on a CT scan, subdural hematomas often
appear to conform to contours of the brain. Damage underlying an acute 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
Cerebral contusions are fairly common; they occur in approximately 20% to 30% of
patients with severe brain injuries. Most contusions are in the frontal and temporal
lobes, although they may be in any part of the brain. In a period of hours or days,
contusions can evolve to form an intracerebral hematoma or a coalescent contusion
with enough mass effect to require immediate surgical evacuation. This condition occurs
in as many as 20% of patients presenting with contusions on initial CT scan of the head.
For this reason, patients with contusions generally undergo repeat CT scanning to
evaluate for changes in the pattern of injury within 24 hours of the initial scan