head injury
DESCRIPTION
surgeryTRANSCRIPT
1. Introduction
Head injury is physical injury to brain tissue that temporarily or permanently impairs
brain function. Loss of consciousness does not need to occur. The severity of head
injuries is most commonly classified by the initial post-resuscitation of Glasgow Coma
Scale (GCS) score, which generates a numerical summed score for eye, motor, and verbal
abilities. Traditionally, a score of 13-15 indicates mild injury, a score of 9-12 indicates
moderate injury, and a score of 8 or less indicates severe injury. Head injury is classified
as either closed or open (penetrating). A closed head injury means you received a hard
blow to the head from striking an object, but the object did not break the skull. While an
open, or penetrating, head injury means you were hit with an object that broke the skull
and entered the brain. This usually happens when you move at high speed, such as going
through the windshield during a car accident. It can also happen from a gunshot to the
head.
2. Classification
2.1 Hematoma
Hematomas (collections of blood in or around the brain) can occur with open or closed
injuries and may be epidural, subdural, or intracerebral. Subarachnoid hemorrhage is
common in head injury, although the appearance on CT scan is not usually the same as
aneurysmal Subarachnoid hemorrhage.
2.2 Subdural hematoma
Subdural hematomas are collections of blood between the dura mater and the pia-
arachnoid mater. Acute subdural hematomas arise from laceration of cortical veins or
avulsion of bridging veins between the cortex and dural sinuses. They often occur with
head trauma from falls and motor vehicle crashes. Compression of the brain by the
hematoma and swelling of the brain due to edema or hyperemia (increased blood flow
due to engorged blood vessels) can increase ICP. When these processes both occur,
mortality and morbidity can be high. A chronic subdural hematoma may appear and
produce symptoms gradually over several weeks after trauma.These hematomas occur
more often in elderly patients (especially in those taking antiplatelet or anticoagulant
drugs, or in those with brain atrophy). Elderly patients may consider the head injury
relatively trivial or may have even forgotten it.
2.3 Epidural hematoma
With an epidural hematoma, the bleeding is located between the dura mater and the skull.
This is often present along the side of the head where the middle meningeal artery runs in
a groove along the temporal bone. This bone is relatively thin and offers less protection
of the skull. As the bleeding continues, the hematoma expands. There is little space in the
skull for the hematoma to grow and as it expands, the adjacent brain tissue is compressed.
As the pressure increases, the whole brain begins to shift and becomes compressed
against the bones of the skull. The pressure tends to build quickly because the septae that
attach the dura to the skull bones create small spaces that trap blood.
2.4 Subarachnoid bleed
Subarachnoid bleeding occurs in the space beneath the arachnoid layer where the CSF is
located. Often there is intense headache and vomiting with subarachnoid bleeding.
Because this space connects with the spinal canal, pressure build-up tends not to occur.
However, this injury often occurs in combination with the other types of bleeding in the
brain, and the symptoms can be compounded.
2.5 Intracerebral bleed
Intracerebral bleeding occurs within the brain tissue itself. Sometimes the amount of
bleeding is small, but like bruising in any other part of the body, swelling or edema may
occur over a period of time, causing a progressive decrease in the level of consciousness
and other symptoms of head injury.
2.6 Skull fracture
The bones of the skull are classified as flat bones, meaning that they do not have an
inside marrow. It takes a significant amount of force to break the skull, and the skull does
not absorb any of that impact. It is often transmitted directly to the brain. Skull fractures
are described by which bone is broken, whether there is an associated laceration of the
scalp, and whether the bone is depressed and potentially pushed into the brain tissue.
2.7 Concussion
Concussion is defined as a transient and reversible post traumatic alteration in mental
status (eg, loss of consciousness or memory) lasting from seconds to minutes and, by
arbitrary definition, < 6 h. Gross structural brain lesions and serious neurologic residual
are not part of concussion, although temporary disability can occur due to symptoms,
such as nausea, headache, dizziness, and memory disturbance (post concussion
syndrome).
2.8 Brain contusions
Contusions (bruises of the brain) can occur with open or closed injuries and can impair a
wide range of brain functions, depending on contusion size and location. Larger
contusions may cause brain edema and increased intracranial pressure (ICP). Contusions
may enlarge in the hours and days following the initial injury and cause neurologic
deterioration.
2.9 Diffuse axonal injury
Diffuse axonal injury (DAI) occurs when deceleration causes shear-type forces that result
in generalized, widespread disruption of axonal fibers and myelin sheaths. A few DAI
lesions may also result from minor head injury. Gross structural lesions are not part of
DAI, but small petechial hemorrhages in the white matter are often observed on CT scan
and on histopathologic examination. DAI is sometimes defined clinically as a loss of
consciousness lasting > 6 h in the absence of a specific focal lesion. Edema from the
injury often increases ICP, leading to various manifestations. DAI is typically the
underlying injury in shaken baby syndrome.
Common Types of Traumatic Brain Injury
Disorder Clinical Findings Diagnosis
Acute subdural hematoma Typically, acute neurologic
dysfunction, which may be
focal, nonfocal, or both
Patients with small
hematomas may have normal
function
CT: Hyperdensity in subdural
space, classically crescent-
shaped
Degree of midline shift
important
Basilar skull fracture Leakage of CSF from the nose
or ear
Blood behind the tympanic
membrane (hemotympanum)
or in the external ear
Ecchymosis behind the ear
(Battle's sign) or around the
eye (raccoon eyes)
CT: Usually visible
Brain contusion Widely variable degrees of
neurologic dysfunction or
normal function
CT: Hyperdensities resulting
from punctate hemorrhages
of varied sizes
Concussion Transient mental status
alteration (eg, loss of
consciousness or memory)
lasting < 6 h
Based on clinical findings
CT or MRI: Clinical
abnormalities not explained
by lesions in brain
parenchyma
Chronic subdural hematoma Gradual headache,
somnolence, confusion,
sometimes with focal deficits
or seizures
CT: Hypodensity in subdural
space (abnormality is
isodense during subacute
transition from hyperdense to
hypodense)
Diffuse axonal injury Loss of consciousness lasting
> 6 h but may not have focal
deficits or motor posturing
Based on clinical findings
CT: At first, may be normal or
show small hyperdensities
(microhemorrhages) in corpus
callosum, centrum semiovale,
basal ganglia, or brain stem
MRI: Often abnormal
Epidural hematoma Headache, impaired
consciousness within hours,
sometimes with a lucid
interval
Herniation typically causing
contralateral hemiparesis and
ipsilateral pupillary dilation
CT: Hyperdensity in epidural
space, classically lenticular-
shaped and located over the
middle meningeal artery
(temporal fossa) due to a
temporal bone fracture
Subarachnoid hemorrhage Typically, normal function
Occasionally, acute neurologic
dysfunction
CT: Hyperdensity within
subarachnoid space on the
surface of the brain; often
outlining sulci
3. Etiology
By definition, trauma is required to cause a head injury, but that trauma does not
necessarily need to be violent. Falling down a few steps or falling into a hard object may
be enough to cause damage. Motor vehicle crashes account for more than 50% of
traumatic brain injuries, with sports related injuries mostly football adding another 20%.
Almost 80% of head injuries occur in males.
3.1 Penetrating trauma
Missiles such as bullets or sharp instruments (such as knives, screwdrivers, or ice picks)
may penetrate the skull. The result is called a penetrating head injury. Penetrating injuries
often require surgery to remove debris from the brain tissue. The initial injury itself may
cause immediate death, especially if from a high-energy missile such as a bullet.
3.2 Blunt head trauma
These injuries may be from a direct blow (a club or large missile) or from a rapid
deceleration force (a fall or striking the windshield in a car accident).
4. Pathophysiology
Brain function may be immediately impaired by direct damage (crush, laceration) of
brain tissue. Further damage may occur shortly from the cascade of events triggered by
the initial injury. Head injury of any sort can produce cerebral edema and decrease brain
blood flow. The cranial vault is fixed in size (constrained by the skull) and filled by CSF
and minimally compressible brain tissue, consequently, any swelling from edema or an
intracranial hematoma has nowhere to expand and thus increases ICP. Cerebral blood
flow is proportional to the cerebral perfusion pressure (CPP), which is the difference
between mean arterial pressure (MAP) and mean ICP. Thus, as ICP increases, CPP
decreases. When CCP falls below 50 mm Hg, the brain may become ischemic. Ischemia
and edema may trigger various secondary mechanisms of injury (eg, release of excitatory
neurotransmitters, intracellular Ca, free radicals, and cytokines), causing further cell
damage, further edema, and further increases in ICP. Systemic complications from
trauma (eg, hypotension, hypoxia) can also contribute to cerebral ischemia and are often
called secondary brain insults. Excessive ICP initially causes global cerebral dysfunction.
If excessive ICP is unrelieved, it can push brain tissue across the tentorium or through the
foramen magnum, causing herniation and increased morbidity and mortality.
5. Symptoms
Signs and symptoms of head injuries vary with the type and severity of the injury.
Symptoms can vary from almost none to loss of consciousness and coma. As well, the
symptoms may not necessarily occur immediately at the time of injury. While a brain
injury occurs at the time of trauma, it may take time for enough swelling or bleeding to
occur to cause symptoms that are recognizable. Minor blunt head injuries may involve
only symptoms of being "dazed" or brief loss of consciousness. They may result in
headaches or blurring of vision or nausea and vomiting.There may be longer lasting
subtle symptoms including, irritability, difficulty concentrating, insomnia, and difficulty
tolerating bright light and loud sounds. These post concussion symptoms may last for a
prolonged period of time. Severe blunt head trauma involves a loss of consciousness
lasting from several minutes to many days or longer. Seizures may result. The person
may suffer from severe and sometimes permanent neurological deficits or may die.
Neurological deficits from head trauma resemble those seen in stroke and
include paralysis, seizures, or difficulty with speaking, seeing, hearing, walking, or
understanding. While in penetrating trauma may cause immediate, severe symptoms or
only minor symptoms despite a potentially life-threatening injury. Death may follow
from the initial injury. Any of the signs of serious blunt head trauma may result.
6. Diagnosis
The physician or health care practitioner will take a history of the events. The
information may be provided by the patient, people who witnessed the event, emergency
medical personnel, and if applicable, the police. The circumstances are very important
since it is important to find out the severity and intensity of the trauma sustained by the
head. If the patient is not fully awake, the examination will initially try to determine the
level of coma using the Glasgow Coma Scale (GCS) which number is useful in tracking
whether the patient is improving or declining in function over time. If no other injuries
are found on examining the body, attention will be paid to the head and the neurologic
exam. The health care practitioner will examine the patient for evidence of a basilar
skull fracture, in which an injury has occurred to the bones that support the brain. Signs
of this type of fracture include bruising of around the eyes (called raccoon eyes), bruising
behind the ear (Battle's sign), bleeding from the ear canal, or CSF leaking from the ear or
nose. The neurologic exam may include evaluation of the cranial nerves. If the neck is
not injured, the exam may include evaluation of muscle tone and strength of the arms and
legs; sensation in the extremities including light touch, pain, and vibration; coordination;
and walking. It is important to remember that injuries to other parts of the body may also
be present, and the evaluation of the head injury may occur at the same time as the
evaluation of other injuries.
Imaging should always be done in patients with more than transiently impaired
consciousness, GCS score < 15, focal neurologic findings, persistent vomiting, seizures, a
history of loss of consciousness or clinically suspected fractures. However, a case can be
made for obtaining a CT scan of the head in all patients with more than a trivial head
injury, because the clinical and medicolegal consequences of missing a hematoma are
severe. MRI may be useful later in the clinical course to detect more subtle contusions
and DAI. It is usually more sensitive than CT for the diagnosis of very small acute or
isodense subacute and isodense chronic subdural hematomas. Preliminary, unconfirmed
evidence suggests that certain MRI findings predict prognosis.
7. Treatment
Multiple noncranial injuries, which are likely with motor vehicle crashes and falls, often
require simultaneous treatment. At the injury scene, a clear airway is secured and external
bleeding is controlled before the patient is moved. Particular care is taken to avoid
displacement of the spine or other bones to protect the spinal cord and blood vessels.
Proper immobilization should be maintained with a cervical collar and long spine board
until stability of the entire spine has been established by appropriate examination and
imaging. After the initial rapid neurologic assessment, pain should be relieved with a
short-acting opioid. In the hospital, after quick initial evaluation, neurologic findings
(GCS and pupillary reaction), BP, pulse, and temperature should be recorded frequently
for several hours because any deterioration demands prompt attention. Serial GCS and CT
results stratify injury severity.
7.1 Mild injury
Injury is mild (by GCS score) in 80% of patients who have head injury and present to an
emergency department. If there is brief or no loss of consciousness and if patients have
stable vital signs, a normal head CT scan, and normal mental and neurologic function,
they may be discharged home provided family members or friends can observe them
closely for an additional 24 h. These observers are instructed to return patients to the
hospital if any of the following develop: decreased level of consciousness, focal
neurologic deficits, worsening headache, vomiting, or deterioration of mental function.
Patients who have had loss of consciousness or have any abnormalities in mental or
neurologic function and cannot be observed closely after discharge are generally
observed in the emergency department or overnight in the hospital and follow-up CT is
done in 4 to 8 h. Patients who have no neurologic changes but minor abnormalities on
head CT (eg, small contusions, small subdural hematomas with no mass effect, or
punctuate or small traumatic subarachnoid hemorrhage) may need only a follow-up CT
within 24 h. With a stable CT and normal neurologic examination results, these patients
may be discharged home.
7.2 Moderate and severe injury
Injury is moderate in 10% of patients who have head injury and present to an emergency
department. They often do not require intubation and mechanical ventilation (unless other
injuries are present) or ICP monitoring. However, because deterioration is possible, these
patients should be admitted and observed even if head CT is normal.
Injury is severe in 10% of patients who have head injury and present to an emergency
department. They are admitted to a critical care unit. Because airway protective reflexes
are usually impaired and ICP may be increased, patients are intubated endotracheally
while measures are taken to avoid increasing ICP. Close monitoring using the GCS and
pupillary response should continue, and CT scan is repeated, particularly if there is an
unexplained ICP rise. Osmotic diuretics (eg, mannitol) may be given IV to lower ICP and
maintain serum osmolality.
7.3 Surgery
Intracranial hematomas may require urgent surgical evacuation to prevent or treat brain
shift, compression, and herniation; hence, early neurosurgical consultation is mandatory.
However, not all hematomas require surgical removal. Small intracerebral hematomas
rarely require surgery. Patients with small subdural hematomas can often be treated
without surgery. Factors that suggest a need for surgery include a midline brain shift
of > 5 mm, compression of the basal cisterns, and worsening neurologic examination
findings. Chronic subdural hematomas may require surgical drainage but much less
urgently than acute subdural hematomas. Large or arterial epidural hematomas are treated
surgically, but small epidural hematomas that are thought to be venous in origin can be
followed with serial CT scans.
7.4 Rehabilitation
When neurologic deficits persist, rehabilitation is needed. Rehabilitation is best provided
through a team approach that combines physical, occupational, and speech therapy, skill-
building activities, and counseling to meet the patient's social and emotional needs. Brain
injury support groups may provide assistance to the families of brain-injured patients.
8. Prognosis
Adults with severe head injury who are treated have a mortality rate of about 25 to 33%.
Mortality is lower with higher GCS scores. Mortality rates are lower in children ≥ 5 yr
(≤10% with a GCS score of 5 to 7). Children overall do better than adults with a
comparable injury. The vast majority of patients with mild head injury retain good
neurologic function. With moderate or severe head injury, the prognosis is not as good
but is much better than is generally believed. There are indications for head injury
outcome:
Good recovery (return to previous level of function)
Moderate disability (capable of self-care)
Severe disability (incapable of self-care)
Vegetative (no cognitive function)
Death
Over 50% of adults with severe head injury have a good recovery or moderate disability.
Occurrence and duration of coma after a head injury are strong predictors of disability.
Of patients whose coma exceeds 24 h, 50% have major persistent neurologic sequelae,
and 2 to 6% remain in a persistent vegetative state at 6 mo. In adults with severe head
injury, recovery occurs most rapidly within the initial 6 mo. Smaller improvements
continue for perhaps as long as several years. Children have a better immediate recovery
from head injury regardless of severity and continue to improve for a longer period of
time. Cognitive deficits, with impaired concentration, attention, and memory, and various
personality changes are a more common cause of disability in social relations and
employment than are focal motor or sensory impairments. Posttraumatic anosmia and
acute traumatic blindness seldom resolve after 3 to 4 mo. Hemiparesis and aphasia
usually resolve at least partially, except in the elderly.
9. Prevention
In sporting activities, the use of a helmet may help minimize the risk of injury; similarly,
wearing a helmet while riding a motorcycle or bicycle helps minimize the risk of brain
injury. Seatbelts can help prevent a head injury during a car crash. Since alcohol is a risk
factor for falls and other injuries, it should be used responsibly. Falls are a concern in the
elderly. Homes can be made less fall-prone by installing assist devices on walls and in
bathrooms. Loose floor coverings such as area rugs should be avoided, since walking
from one floor covering to another increases the risk of falls. If needed, canes and
walkers may be helpful as walking assistive devices.
References
Brain Traumatic Injury. The Merck Manual of Diagnosis and Therapy website. Available
from:http://www.merckmanuals.com/professional/sec21/ch310/ch310a.html
[Accessed 10 April 2011]
Benjamin, C. 2010. Head Injury, Medicinenet website, Available from :
http://www.medicinenet.com/head_injury/article.htm [Accessed 11 April 2011]
David , A. 2009. Head Injury, Emedicine website, Avalaible from :
http://emedicine.medscape.com/article/1163653-overview
[Accessed 11 April 2011]
Kumar P, Clark M. 2002. Clinical Medicine 5th Edition. Head Injury.
WB Saunders. P 1175-1176
Tortora G, Derrickson B. 2006. Principles of Anatomy and physiology 11th Edition.
The Brain and Cranial Nerves. John Wiley & sons,Inc. P 496