I wanted to post information concerning
different types of physical & mental trauma. These details are slightly deep, but those
who are familiar with experiencing these types of trauma and the mental & physical effects - will be able to understand
it more readily.
Perhaps we all need to be aware of these details because every day we live we are not in total control of what happens to us and the possibilities
that we or someone we love might be faced with these issues isn't that far away from us at any time.
Traumatic Brain Injury
Traumatic brain injury (TBI)
continues to be an enormous public health problem, even with modern medicine in the 21st century. Most patients with TBI (75-80%)
have mild head injuries; the remaining injuries are divided equally between the moderate and severe categories.
The cost to society of TBI
is staggering, from both an economic and an emotional standpoint. Almost 100% of persons with severe head injury and as many
as 2/3 of those with moderate head injury will be permanently disabled and will not return
to their premorbid level of function.
In the United States,
the direct cost of care for patients with TBI, excluding inpatient care, is estimated at more than $25 billion annually. The
impact is even greater when one considers that most severe head injuries occur in adolescents and young adults.
annual incidence of TBI in the United States has been estimated to be 180-220 cases per 100,000 population. In the United
States, with a population of almost 300 million, approximately 600,000 new TBIs occur per year. As many as 10% of these injuries
are fatal, resulting in almost 550,000 persons hospitalized annually in the United States with head injuries.
While various mechanisms may cause TBI, the most common causes include:
- motor vehicle accidents (e.g. collisions between vehicles, pedestrians struck by motor vehicles, bicycle accidents)
- sports-related injuries
- penetrating trauma
Motor vehicle accidents
account for almost 1/2 of the TBI's in the United States, and in suburban/rural settings, they account for most TBIs.
In cities with
populations greater than 100,000, assaults, falls, and penetrating trauma are more common etiologies of head injury. The male-to-female
ratio for TBI is nearly 2:1, and TBI is much more common in persons younger than 35 years.
Appropriate management of TBI requires an understanding of the pathophysiology of head injury. In addition to the obvious
functional differences, the brain has several features that distinguish it from other organ systems.
The most important
of these differences is that the brain is contained within the skull, a rigid and inelastic container. Because the brain is
housed within this inelastic container, only small increases in volume within the intracranial compartment can be tolerated
before pressure within the compartment rises dramatically.
This concept is defined
by the Monro-Kellie doctrine, which states that the total intracranial volume is fixed because of the inelastic nature of
the skull. The intracranial volume (V i/c) is equal to the sum of its components, as follows:
V i/c = V (brain) + V (cerebrospinal fluid) + V (blood)
In the typical adult, the
intracranial volume is approximately 1500 mL, of which the brain accounts for 85-90%, intravascular cerebral blood volume
accounts for 10%, and cerebrospinal fluid (CSF) accounts for the remainder (<3%). When a significant head injury occurs,
cerebral edema often develops, which increases the relative volume of the brain.
Because the intracranial volume is
fixed, the pressure within this compartment rises unless some compensatory action occurs, such as a decrease in the
volume of one of the other intracranial components. This is intimately related to the concept of intracranial compliance,
which is defined as the change in pressure due to changes in volume.
Compliance = Change in volume / change in pressure
Compliance is based on the
pressure volume index (PVI) within the intracranial compartment. The PVI describes the change in intracranial pressure (ICP)
that occurs when a small amount of fluid is added to or withdrawn from the intracranial compartment.
Simply stated, the brain has
very limited compliance and cannot tolerate significant increases in volume that can result from diffuse cerebral edema or
from significant mass lesions such as a hematoma. The rationale for each treatment of head injury is based on the concept
of the Monro-Kellie doctrine and how a particular intervention affects the intracranial compliance. When the volume of any
of the components of the total intracranial volume is decreased, the ICP may be decreased.
A second crucial concept in
TBI pathophysiology is the concept of cerebral perfusion pressure (CPP). CPP is defined as the difference between the mean
arterial pressure (MAP) and the ICP.
CPP = MAP - ICP
In practical terms, CPP is
the net pressure of blood delivery to the brain. In the noninjured brain in individuals without long-standing hypertension,
cerebral blood flow (CBF) is constant in the range of MAPs of 50-150 mm Hg. This is due to autoregulation by the arterioles,
which will constrict or dilate within a specific range of blood pressure to maintain a constant amount of blood flow to the
When the MAP is less than 50 mm Hg
or greater than 150 mm Hg, the arterioles are unable to autoregulate and blood flow becomes entirely dependent on the
blood pressure, a situation defined as pressure-passive flow. The CBF is no longer constant but is dependent on and proportional
to the CPP. Thus, when the MAP falls below 50 mm Hg, the brain is at risk of ischemia due to insufficient blood flow, while
a MAP greater than 160 mm Hg causes excess CBF that may result in increased ICP. While autoregulation works well in the noninjured
brain, it is impaired in the injured brain. As a result, pressure-passive flow occurs within and around injured areas and,
perhaps, globally in the injured brain.
TBI may be divided into 2 categories,
primary brain injury and secondary brain injury. Primary brain injury is defined as the initial injury to the brain as a direct
result of the trauma. This is the initial structural injury caused by the impact on the brain, and, like other forms of neural
injury, patients recover poorly. Secondary brain injury is defined as any subsequent injury to the brain after the initial
insult. Secondary brain injury can result from systemic hypotension, hypoxia, elevated ICP, or as the biochemical result of
a series of physiologic changes initiated by the original trauma. The treatment of head injury is directed at either preventing
or minimizing secondary brain injury.
Elevated ICP may result from
the initial brain trauma or from secondary injury to the brain. In adults, normal ICP is considered 0-15 mm Hg. In young children,
the upper limit of normal ICP is lower, and this limit may be considered 10 mm Hg. Elevations in ICP are deleterious because
they can result in decreased CPP and decreased CBF, which, if severe enough, may result in cerebral ischemia. Severe elevations
of ICP are dangerous because, in addition to creating a significant risk for ischemia, uncontrolled ICP may cause herniation.
Herniation involves the movement of the brain across fixed dural structures, resulting in irreversible and often fatal cerebral
TBI may be divided into 2 broad categories, closed head injury and penetrating head injury. This is not purely a mechanistic
division because some aspects of the treatment of these 2 types of TBIs differ. The clinical presentation of the patient with
TBI varies significantly, from an ambulatory patient complaining of a sports-related head injury to the moribund patient arriving
via helicopter following a high-speed motor vehicle accident. The Glasgow Coma Scale (GCS) developed by Jennett and Teasdale
is used to describe the general level of consciousness of patients with TBI and to define broad categories of head injury.
The GCS is divided into 3 categories, eye opening (E), motor response (M), and verbal response (V). The score is determined
by the sum of the score in each of the 3 categories, with a maximum score of 15 and a minimum score of 3, as follows:
to access the chart
Patients who are intubated
are unable to speak, and their verbal score cannot be assessed. They are evaluated only with eye opening and motor scores,
and the suffix T is added to the their score to indicate that the patient is intubated. In intubated patients, the maximal
GCS score is 10T and the minimum score is 2T. The GCS is often used to help define the severity of TBI. Mild head injuries
are generally defined as those associated with a GCS score of 13-15, and moderate head injuries are those associated with
a GCS score of 9-12. A GCS score of 8 or less defines a severe head injury. These definitions are not rigid and should be
considered as a general guide to the level of injury.
Relevant Anatomy: Several aspects
of neuroanatomy and neurophysiology require review in a discussion of TBI. Although a comprehensive review of neuroanatomy
is beyond the scope of this discussion, a few key concepts are reviewed.
The brain essentially floats within the CSF; as a result, the
brain can undergo significant translation and deformation when the head is subjected to significant forces. In a deceleration
injury, in which the head impacts a stationary object such as the windshield of a car, the skull stops moving almost instantly.
However, the brain continues to move within the skull toward the direction of the impact for a very brief period after the
head has stopped moving. This results in significant forces acting on the brain as it undergoes both translation and deformation.
In an acceleration injury, as in a direct blow to the head,
the force applied to the skull causes the skull to move away from the applied force. The brain does not move with the skull,
and the skull impacts the brain, causing translation and deformation of the brain. The forces that result from either deceleration
or acceleration of the brain can cause injury by direct mechanical effects on the various cellular components of the brain
or by shear-type forces on axons. In addition to the translational forces, the brain can experience significant rotational
forces, which can also lead to shear injuries.
The intracranial compartment is divided into 3 compartments
by 2 major dural structures, the falx cerebri and the tentorium cerebelli. The tentorium cerebelli divides the posterior fossa
or infratentorial compartment (the cerebellum and the brainstem) from the supratentorial compartment (cerebral hemispheres).
The falx cerebri divides the supratentorial compartment into 2 halves and separates the left and right hemispheres of the
brain. Both the falx and the tentorium have central openings and prominent edges at the borders of each of these openings.
When a significant increase in ICP occurs, caused by either a large mass lesion or significant cerebral edema, the brain can
slide through these openings within the falx or the tentorium, a phenomenon known as herniation. As the brain slides over
the free dural edges of the tentorium or the falx, it is frequently injured by the dural edge.
Several types of herniation exist, as follows: (1) transtentorial
herniation, (2) subfalcine herniation, (3) central herniation, (4) upward herniation, and (5) tonsillar herniation.
Transtentorial herniation occurs when the medial aspect of the
temporal lobe (uncus) migrates across the free edge of the tentorium. This causes pressure on the third cranial nerve, interrupting
parasympathetic input to the eye and resulting in a dilated pupil. This unilateral dilated pupil is the classic sign of transtentorial
herniation and usually (80%) occurs ipsilateral to the side of the transtentorial herniation. In addition to pressure on the
third cranial nerve, transtentorial herniation compresses the brainstem.
Subfalcine herniation occurs when the cingulate gyrus on the
medial aspect of the frontal lobe is displaced across the midline under the free edge of the falx. This may compromise the
blood flow through the anterior cerebral artery complexes, which are located on the medial side of each frontal lobe. Subfalcine
herniation does not cause the same brainstem effects as those caused by transtentorial herniation.
Central herniation occurs when a diffuse increase in ICP occurs
and each of the cerebral hemispheres is displaced through the tentorium, resulting in significant pressure on the upper brainstem.
Upward, or cerebellar, herniation occurs when either a large
mass or increased pressure in the posterior fossa is present and the cerebellum is displaced in an upward direction through
the tentorial opening. This also causes significant upper brainstem compression.
Tonsillar herniation occurs when increased pressure develops
in the posterior fossa. In this form of herniation, the cerebellar tonsils are displaced in a downward direction through the
foramen magnum, causing compression on the lower brainstem and upper cervical spinal cord as they pass through the foramen
Another aspect of the intracranial anatomy that has a significant
role in TBI is the irregular surface of the skull underlying the frontal and temporal lobes. These surfaces contain numerous
ridges that can cause injury to the inferior aspect of the frontal lobes and the temporal lobes as the brain glides over these
irregular ridges following impact. Typically, these ridges cause cerebral contusions. The roof of the orbit has many ridges,
and, as a result, the inferior frontal lobe is one of the most common sites of traumatic cerebral contusions.
- After the patient has been stabilized and an appropriate neurologic
examination has been conducted, the diagnostic evaluation may begin. Patients with TBI do not require any additional blood
tests beyond the standard panel of tests obtained in all trauma patients. A urine toxicology screen and an assessment of the
blood alcohol level are important for any patient who has an altered level of consciousness because any central nervous system
depressant can impair consciousness.
- Once an important part of the head injury evaluation, skull
radiographs have been replaced by CT scans and are rarely used in patients with closed head injury.
- Skull radiographs are occasionally used in the evaluation of
penetrating head trauma, and they can help provide a rapid assessment of the degree of foreign body penetration in nonmissile
penetrating head injuries (eg, stab wounds).
- Skull radiographs are sometimes used in patients with gunshot
wounds to the head to screen for retained intracranial bullet fragments.
- A CT scan is the diagnostic study of choice in the evaluation
of TBI because it has a rapid acquisition time, is universally available, is easy to interpret, and is reliable.
- When first introduced more than 25 years ago, CT scans of the
brain required almost 30 minutes to complete. This acquisition time has decreased steadily; the current generation of ultrafast
CT scanners can perform a head CT scan in less than 1 minute, faster than the time required to enter patient's demographic
data into the scanner.
- The standard CT scan for the evaluation of acute head injury
is a noncontrast scan that spans from the base of the occiput to the top of the vertex in 5-mm increments.
- Three data sets are obtained from the primary scan, (1) bone
windows, (2) tissue windows, and (3) subdural windows. These different types of exposure are necessary because of the significant
difference in exposure necessary to visualize various intracranial structures. The bone windows allow for a detailed survey
of the bony anatomy of the skull, and the tissue windows allow for a detailed survey of the brain and its contents. The subdural
windows provide better visualization of intracranial hemorrhage, especially those hemorrhages adjacent to the brain (eg, subdural
- Each intracranial structure has a characteristic density, which
is expressed in Hounsfield units. These units are defined according to a scale that ranges from (-) 1000 units to (+) 1000
units. Air is assigned a density of (-) 1000 units, water is assigned a density of 0 units, and bone has a density of (+)
1000 units. On this scale, CSF has a density of (+) 4 to (+) 10 units, white matter has a density of (+) 22 to (+) 36 units,
and gray matter has a density of (+) 32 to (+) 46 units. Extravascular blood has a density of (+) 50 to (+) 90 units, and
calcified tissue and bone have a density of (+) 800 to (+) 1000 units.
- When reviewing a CT scan, using a systematic approach and following
this same protocol each time are important. Consistency is much more important than the specific order used.
- First, examine the bone windows for fractures, beginning with
the cranial vault and then examining the skull base and the facial bones.
- Next, examine the tissue windows for the presence of (1) extra-axial
hematomas (eg, epidural hematomas, subdural hematomas), (2) intraparenchymal hematomas, or (3) contusions.
- Next, survey the brain for any evidence of pneumocephalus,
hydrocephalus, cerebral edema, midline shift, or compression of the subarachnoid cisterns at the base of the brain.
- Finally, examine the subdural windows for any hemorrhage that
may not be visualized easily on the tissue windows.
- Skull fractures may be classified as either linear or comminuted
fractures. Linear skull fractures are sometimes difficult to visualize on the individual axial images of a CT scan. The scout
film of the CT scan, which is the equivalent of a lateral skull x-ray film, often demonstrates linear fractures. The intracranial
sutures are easily mistaken for small linear fractures. However, the sutures have characteristic locations in the skull and
have a symmetric suture line on the opposite side. Small diploic veins, which traverse the skull, may also be interpreted
as fractures. Comminuted fractures are complex fractures with multiple components. Comminuted fractures may be displaced inwardly;
this is defined as a depressed skull fracture.
- Extra-axial hematomas include epidural and subdural hematomas.
Epidural hematomas are located between the inner table of the skull and the dura. They are typically biconvex in shape because
their outer border follows the inner table of the skull and their inner border is limited by locations at which the dura is
firmly adherent to the skull. Epidural hematomas are usually caused by injury to an artery, although 10% of epidural hematomas
may be venous in origin. The most common cause of an epidural hematoma is a linear skull fracture that passes through an arterial
channel in the bone. The classic example of this is the temporal epidural hematoma caused by a fracture through the course
of the middle meningeal artery. Epidural hematomas, especially those of arterial origin, tend to enlarge rapidly.
- Subdural hematomas are located between the dura and the brain.
Their outer edge is convex, while their inner border is usually irregularly concave. Subdural hematomas are not limited by
the intracranial suture lines; this is an important feature that aids in their differentiation from epidural hematomas. Subdural
hematomas are usually venous in origin, although some subdural hematomas are caused by arterial injuries. The classic cause
of a posttraumatic subdural hematoma is an injury to one of the bridging veins that travel from the cerebral cortex to the
dura. As the brain atrophies over time, the bridging veins become more exposed and, as a result, are more easily injured.
Occasionally, the distinction between a subdural and an epidural hematoma can be difficult. The size of an extra-axial hematoma
is a more important factor than whether the blood is epidural or subdural in location. In addition, a mixed hematoma with
both a subdural and an epidural component is not uncommon.
- Intra-axial hematomas are defined as hemorrhages within the
brain parenchyma. These hematomas include intraparenchymal hematomas, intraventricular hemorrhages, and subarachnoid hemorrhages.
Subarachnoid hemorrhages that occur because of trauma are typically located over gyri on the convexity of the brain. The subarachnoid
hemorrhages that result from a ruptured cerebral aneurysm are usually located in the subarachnoid cisterns at the base of
the brain. Cerebral contusions are posttraumatic lesions in the brain that appear as irregular regions, in which high-density
changes (ie, blood) and low-density changes (ie, edema) are present. Frequently, 1 of these 2 types of changes predominates
within a particular contusion. Contusions are most often caused by the brain gliding over rough surfaces, such as the rough
portions of the skull that are present under the frontal and temporal lobes.
- CT scans may be used for classification and for diagnostic
purposes. Marshall et al published a classification scheme that classifies head injuries according to the changes demonstrated
on CT scan images. This system defines 4 categories of injury, from diffuse injury I to diffuse injury IV.
- In diffuse injury I, evidence of any significant brain injury
- In diffuse injury II, either no midline shift or a shift of
less than 5 mm is present and the CSF cisterns at the base of the brain are widely patent. In addition, no high-density or
mixed-density lesions (contusions) of greater than 25 mL in volume are present.
- In diffuse injury III, a midline shift of less than 5 mm is
present, with partial compression or absence of the basal cisterns. No high- or mixed-density lesions with a volume greater
than 25 mL are present.
- Diffuse injury IV is defined as midline shift greater than
5 mm with compression or absence of the basal cisterns and no lesions of high or mixed density greater than 25 mL.
- MRI has a limited role in the evaluation of acute head injury.
Although MRI provides extraordinary anatomic detail, it is not commonly used to evaluate acute head injuries because of its
long acquisition times and the difficulty in obtaining MRIs in persons who are critically ill. However, MRI is used in the
subacute setting to evaluate patients with unexplained neurologic deficits.
- MRI is superior to CT scan for helping identify diffuse axonal
injury (DAI) and small intraparenchymal contusions. DAI is defined as neuronal injury in the subcortical gray matter or the
brainstem as a result of severe rotation or deceleration. DAI is often the reason for a severely depressed level of consciousness
in patients who lack evidence of significant injury on CT scan images and have an ICP that is within the reference range.
- Magnetic resonance angiography may be used in some patients
with TBI to assess for arterial injury or venous sinus occlusion.
- Once a common diagnostic study in persons with acute head injury,
angiography is rarely used in the evaluation of acute head injury today.
- Prior to the development of the CT scan, cerebral angiography
provided a reliable means for demonstrating the presence of an intracranial mass lesion.
- Currently, angiography in used in acute head injury only when
a vascular injury may be present. This includes patients with unexplained neurologic deficits, especially in the setting of
temporal bone fractures, and patients with clinical evidence of a potential carotid injury (eg, hemiparesis, Horner syndrome).
- The initial evaluation of patients with TBI involves a thorough
systemic trauma evaluation according to the advanced trauma life support (ATLS) guidelines. Once this has been completed and
the patient is stable from a cardiopulmonary standpoint, attention may be directed to a focused head injury evaluation.
- The evaluation of the spine for potential injury is critically
important in patients with TBI because approximately 10% of those with severe head injuries have a concomitant spine injury.
Many of these injuries are cervical spine injuries.
- Attempt to obtain a thorough history of the mechanism of the
trauma and the events immediately preceding the trauma. Specific information, such as the occurrence of syncope or the onset
of a seizure prior to a fall or a motor vehicle accident, prompts a more extended evaluation of the etiology of such an event.
Because many patients with TBI have altered levels of consciousness, the history is often provided by family members, police
officers, paramedics, or witnesses.
- After sufficient information has been obtained regarding patient
history, appropriate physical and neurologic examinations are performed.
- The neurologic assessment begins with ascertaining the GCS
score. This is a screening examination and does not substitute for a thorough neurologic examination.
- In addition to determining the GCS score, the neurologic assessment
of patients with TBI should include the following:
- Brainstem examination - Pupillary examination, ocular movement
examination, corneal reflex, gag reflex
- Motor examination
- Sensory examination
- Reflex examination
- Many patients with TBI have significant alterations of consciousness
and/or pharmaceuticals present that limit the scope of the neurologic examination. When such factors limit the neurologic
examination, noting their presence is important.
- A careful pupillary examination is a critical part of the evaluation
of patients with TBI, especially in patients with severe injuries. When muscle relaxants have been administered to a patient,
the only aspect of the neurologic examination that may be evaluated is the pupillary examination.
- Several factors can alter the pupillary examination results.
Narcotics cause pupillary constriction (meiosis), and medications or drugs that have sympathomimetic properties cause pupillary
dilation (mydriasis). These effects are often strong enough to blunt or practically eliminate pupillary responses. Prior eye
surgery, such as cataract surgery, can also alter or eliminate pupillary reactivity.
- Proper assessment of the pupillary response requires the use
of a strong light source to override any of the potential factors that may affect pupillary reaction. Each pupil must be assessed
individually, with at least 10 seconds between assessment of each eye to allow consensual responses to fade prior to stimulating
the opposite eye.
- A normal pupillary examination result consists of bilaterally
reactive pupils that react to both direct and consensual stimuli. Bilateral small pupils can be caused by narcotics, pontine
injury (due to disruption of sympathetic centers in the pons), or early central herniation (mass effect on the pons).
- Bilateral fixed and dilated pupils are secondary to inadequate
cerebral perfusion. This can result from diffuse cerebral hypoxia or severe elevations of ICP preventing adequate blood flow
into the brain.
- Pupils that are fixed and dilated usually indicate an irreversible
injury. If due to systemic hypoxia, the pupils sometimes recover reactivity when adequate oxygenation is restored.
- A unilateral fixed (unresponsive) and dilated pupil has many
potential causes. A pupil that does not constrict when light is directed at the pupil but constricts when light is directed
into the contralateral pupil (intact consensual response) is indicative of a traumatic optic nerve injury.
- A unilateral dilated pupil that does not respond to either
direct or consensual stimulation usually indicates transtentorial herniation.
- Unilateral constriction of a pupil is usually secondary to
Horner syndrome, in which the sympathetic input to the eye is disrupted and the pupil constricts due to more parasympathetic
than sympathetic stimulation. In patients with TBI, Horner syndrome may be caused by an injury to the sympathetic chain at
the apex of the lung or a carotid artery injury. A unilateral constricted pupil can be caused by a unilateral brainstem injury,
but this is quite rare.
- A core optic pupil is a pupil that appears irregular in shape.
This is caused by a lack of coordination of contraction of the muscle fibers of the iris and is associated with midbrain injuries.
- Ocular movement examination
- When the patient's level of consciousness is altered significantly,
a loss of voluntary eye movements often occurs and abnormalities in ocular movements are frequently present. These abnormalities
can provide specific clues to the extent and location of injury.
- Ocular movements involve the coordination of multiple centers
in the brain, including the frontal eye fields, the paramedian pontine reticular formation (PPRF), the medial longitudinal
fasciculus (MLF), and the nuclei of the third and sixth cranial nerves. In patients in whom voluntary eye movements cannot
be assessed, oculocephalic and oculovestibular testing may be performed.
- Oculocephalic testing (doll's eyes) involves observation of
eye movements when the head is turned from side to side. This maneuver helps assess the integrity of the horizontal gaze centers.
- Before performing oculocephalic testing, the status of the
cervical spine must be established. If a cervical spine injury has not been excluded reliably, oculocephalic testing should
not be performed.
- When assessing oculocephalic movements, the head is elevated
to 30° from horizontal and is rotated briskly from side to side.
- A normal response is for the eyes to turn away from the direction
of the movement as if they are fixating on a target that is straight ahead. This is similar to the way a doll's eyes move
when the head is turned; this is the origin of the term doll's eyes.
- If the eyes remain fixed in position and do not rotate with
the head, this is indicative of dysfunction in the lateral gaze centers and is referred to as negative doll's eyes. Some patients
may have negative doll's eyes and normal oculovestibular reflexes.
- Oculovestibular testing, also known as cold calorics, is another
method for assessment of the integrity of the gaze centers. Oculovestibular testing is performed with the head elevated to
30° from horizontal to bring the horizontal semicircular canal into the vertical position.
- Oculovestibular testing requires the presence of an intact
tympanic membrane; this must be assessed before beginning the test.
- In oculovestibular testing, 20 mL of ice-cold water is instilled
slowly into the auditory canal. If is no response occurs within 60 seconds, the test is repeated with 40 mL of cold water.
- When cold water is irrigated into the external auditory canal,
the temperature of the endolymph falls and the fluid begins to settle. This causes an imbalance in the vestibular signals
and initiates a compensatory response.
- Cold-water irrigation in the ear of an alert patient results
in a fast nystagmus away from the irrigated ear and a slow compensatory nystagmus toward the irrigated side. If warm water
is used, the opposite will occur; the fast component of nystagmus will be toward the irrigated side, and the slow component
will be away from the irrigated side. This is the basis for the acronym COWS, which stands for cold opposite, warm same. This
refers to the direction of the fast component of nystagmus.
- As the level of consciousness declines, the fast component
of nystagmus fades gradually. Thus, in unconscious patients, only the slow phase of nystagmus may be evaluated.
- A normal oculocephalic response to cold-water calorics (ie,
eye deviation toward the side of irrigation) indicates that the injury spares the PPRF, the MLF, and third and sixth cranial
nerve nuclei. This means that the level of injury must be rostral to the reticular activating system in the upper brainstem.
- If a unilateral frontal lobe injury is present, the eyes are
deviated toward the side of injury prior to caloric testing. Cold-water irrigation of the opposite ear results in a normal
response to caloric testing (ie, eye deviation toward the irrigated side) because the injury is in the frontal region and
spares the pontine gaze centers.
- When a pontine injury is present, the eyes often deviate away
from the side of injury. In this situation, cold-water irrigation of the contralateral ear does not cause the gaze to deviate
toward the irrigated ear because an injury has occurred at the level of the pons and the pontine gaze centers are compromised.
- A dysconjugate response to caloric testing suggests an injury
to either the third or sixth cranial nerves or an injury to the MLF, resulting in an internuclear ophthalmoplegia.
- If caloric testing causes a skew deviation, in which the eyes
are dysconjugate in the vertical direction, this indicates a lesion in the brainstem. The exact location of injury that results
in skew deviation is not known.
- After completing the brainstem examination, a motor examination
should be performed. A thorough motor or sensory examination is difficult to perform in any patient with an altered level
- When a patient is not alert enough to cooperate with strength
testing, the motor examination is limited to an assessment of asymmetry in the motor examination findings. This may be demonstrated
by an asymmetric response to central pain stimulation or a difference in muscle tone between the left and right sides. A finding
of significant asymmetry during the motor examination may be indicative of a hemispheric injury and raises the possibility
of a mass lesion.
- Performing a useful sensory examination in patients with TBI
is often difficult.
- Patients with altered levels of consciousness are unable to
cooperate with sensory testing, and findings from a sensory examination are not reliable in patients who are intoxicated or
- Peripheral reflex examination
- A peripheral reflex examination can be useful to help identify
gross asymmetry in the neurologic examination.
- This may indicate the presence of a hemispheric mass lesion.
Medical therapy: The treatment
of head injury may be divided into the treatment of closed head injury and the treatment of penetrating head injury. While
significant overlap exists between the treatments of these 2 types of injury, some important differences are discussed. Closed
head injury treatment is divided further into the treatment of mild, moderate, and severe head injuries.
Closed head injury
Mild head injury
Most head injuries are mild head injuries. Most people presenting
with mild head injuries will not have any progression of their head injury; however, up to 3% of mild head injuries progress
to more serious injuries. Mild head injuries may be separated into low-risk and moderate-risk groups. Patients with mild-to-moderate
headaches, dizziness, and nausea are considered to have low-risk injuries. Many of these patients require only minimal observation
after they are assessed carefully, and many do not require radiographic evaluation. These patients may be discharged if a
reliable individual can monitor them.
Patients who are discharged after mild head injury should be
given an instruction sheet for head injury care. The sheet should explain that the person with the head injury should be awakened
every 2 hours and assessed neurologically. Caregivers should be instructed to seek medical attention if patients develop severe
headaches, persistent nausea and vomiting, seizures, confusion or unusual behavior, or watery discharge from either the nose
or the ear.
Patients with mild head injuries typically have concussions.
A concussion is defined as physiologic injury to the brain without any evidence of structural alteration. Concussions are
graded on a scale of I-V. A grade I concussion is one in which a person is confused temporarily but does not display any memory
changes. In a grade II concussion, brief disorientation and anterograde amnesia of less than 5 minutes' duration are present.
In a grade III concussion, retrograde amnesia and loss of consciousness for less than 5 minutes are present, in addition to
the 2 criteria for a grade II concussion. Grade IV and grade V concussions are similar to a grade III, except that in a grade
IV concussion, the duration of loss of consciousness is 5-10 minutes, and in a grade V concussion, the loss of consciousness
is longer than 10 minutes.
As many as 30% of patients who experience a concussion develop
postconcussive syndrome (PCS). PCS consists of a persistence of any combination of the following after a head injury: headache,
nausea, emesis, memory loss, dizziness, diplopia, blurred vision, emotional lability, or sleep disturbances. Fixed neurologic
deficits are not part of PCS, and any patient with a fixed deficit requires careful evaluation. PCS usually lasts 2-4 months.
Typically, the symptoms peak 4-6 weeks following the injury. On occasion, the symptoms of PCS last for a year or longer. Approximately
20% of adults with PCS will not have returned to full-time work 1 year after the initial injury, and some are disabled permanently
by PCS. PCS tends to be more severe in children than in adults. When PCS is severe or persistent, a multidisciplinary approach
to treatment may be necessary. This includes social services, mental health services, occupational therapy, and pharmaceutical
After a mild head injury, those displaying persistent emesis,
severe headache, anterograde amnesia, loss of consciousness, or signs of intoxication by drugs or alcohol are considered to
have a moderate-risk head injury. These patients should be evaluated with a head CT scan. Patients with moderate-risk mild
head injuries can be discharged if their CT scan findings reveal no pathology, their intoxication is cleared, and they have
been observed for at least 8 hours.
Moderate and severe head injury
The treatment of moderate and severe head injuries begins with
initial cardiopulmonary stabilization by ATLS guidelines. The initial resuscitation of a patient with a head injury is of
critical importance to prevent hypoxia and hypotension. In the Traumatic Coma Data Bank study, patients with head injury who
presented to the hospital with hypotension had twice the mortality rate of patients who did not present with hypotension.
The combination of hypoxia and hypotension resulted in a mortality rate 2.5 times greater than if neither of these factors
Once a patient has been stabilized from the cardiopulmonary
standpoint, evaluation of their neurologic status may begin. The initial GCS score provides a classification system for patients
with head injuries but does not substitute for a neurologic examination. After assessment of the coma score, a neurologic
examination should be performed. If a patient has received muscle relaxants, the only neurologic response that may be evaluated
is the pupillary response.
After a thorough neurologic assessment has been performed, a
CT scan of the head is obtained. The results of the CT scan help determine the next step. If a surgical lesion is present,
arrangements are made for immediate transport to the operating room. Fewer than 10% of patients with TBI have an initial surgical
Although no strict guidelines exist for defining surgical lesions
in persons with head injury, most neurosurgeons consider any of the following to represent indications for surgery in patients
with head injuries: extra-axial hematoma with midline shift greater than 5 mm, intra-axial hematoma with volume greater than
30 mL, an open skull fracture, or a depressed skull fracture with more than 1 cm of inward displacement. In addition, any
temporal or cerebellar hematoma that is larger than 3 cm in diameter is considered a high-risk hematoma because these regions
of the brain are smaller and do not tolerate additional mass as well as the frontal, parietal, and occipital lobes. These
high-risk temporal and cerebellar hematomas are usually evacuated immediately
If no surgical lesion is present on the CT scan image, or following
surgery if one is present, treatment of the head injury begins. The first phase of treatment is to institute general measures.
Once appropriate fluid resuscitation has been completed and the volume status is determined to be normal, intravenous fluids
are administered to maintain the patient in a state of euvolemia or mild hypervolemia. A previous tenet of head injury treatment
was fluid restriction, which was believed to limit the development of cerebral edema and increased ICP. Fluid restriction
decreases intravascular volume and, therefore, decreases cardiac output. A decrease in cardiac output often results in decreased
cerebral flow, which results in decreased brain perfusion and may cause an increase in cerebral edema and ICP. Thus, fluid
restriction is contraindicated in patients with TBI.
Another supportive measure used to treat patients with head
injuries is elevation of the head. When the head of the bed is elevated to 20-30°, the venous outflow from the brain is improved,
thus helping to reduce ICP. If a patient is hypovolemic, elevation of the head may cause a drop in cardiac output and CBF;
therefore, the head of the bed is not elevated in hypovolemic patients. In addition, the head should not be elevated (1) in
patients in whom a spine injury is a possibility or (2) until an unstable spine has been stabilized.
Sedation is often necessary in patients with traumatic injury.
Some patients with moderate head injuries have significant agitation and require sedation. In addition, patients with multisystem
trauma often have painful systemic injuries that require pain medication, and many intubated patients require sedation. Short-acting
sedatives and analgesics should be used to accomplish proper sedation without eliminating the ability to perform periodic
neurologic assessments. This requires careful titration of medication doses and periodic weaning or withholding of sedation
to allow periodic neurologic assessment.
The use of anticonvulsants in patients with TBI is a controversial
issue. No evidence exists that the use of anticonvulsants decreases the incidence of late-onset seizures in patients with
either closed head injury or TBI. Temkin et al demonstrated that the routine use of Dilantin in the first week following TBI
decreases the incidence of early-onset (within 7 d of injury) seizures but does not change the incidence of late-onset seizures.
In addition, the prevention of early posttraumatic seizures does not improve the outcome following TBI. Therefore, the prophylactic
use of anticonvulsants is not recommended for more than 7 days following TBI and is considered optional in the first week
After instituting general supportive measures, the issue of
ICP monitoring is addressed. ICP monitoring has consistently been shown to improve outcome in patients with head injuries.
ICP monitoring is indicated for any patient with a GCS score less than 9, any patient with a head injury who requires prolonged
deep sedation or pharmacologic relaxants for a systemic condition, or any patient with an acute head injury who is undergoing
extended general anesthesia for a nonneurosurgical procedure.
ICP monitoring involves placement of an invasive probe to measure
the ICP. Unfortunately, noninvasive means of monitoring ICP do not exist, although they are under development. ICP may be
monitored by means of an intraparenchymal monitor, an intraventricular monitor (ventriculostomy), or an epidural monitor.
These devices measure ICP by fluid manometry, strain-gauge technology, or fiberoptic technology.
Intraparenchymal ICP monitors are devices that are placed into
the brain parenchyma to measure ICP by means of fiberoptic, strain-gauge, or other technologies. The intraparenchymal monitors
are very accurate; however, they do not allow for drainage of CSF. Epidural devices measure ICP via a strain-gauge device
placed through the skull into the epidural space. This is an older form of ICP measurement and is rarely used today because
the other technologies available are more accurate and more reliable.
A ventriculostomy is a catheter placed through a small twist
drill hole into the lateral ventricle. The ICP is measured by transducing the pressure in a fluid column. Ventriculostomies
allow for drainage of CSF, which can be effective in decreasing the ICP.
Once an ICP monitor has been placed, ICP is monitored continuously.
No absolute value of ICP exists for which treatment is implemented automatically. In adults, the reference range of ICP is
0-15 mm Hg. The normal ICP waveform is a triphasic wave, in which the first peak is the largest peak and the second and third
peaks are progressively smaller. When intracranial compliance is abnormal, the second and third peaks are usually larger than
the first peak. In addition, when intracranial compliance is abnormal and ICP is elevated, pathologic waves may appear.
Lundberg described 3 types of abnormal ICP waves, A, B, and
C waves. Lundberg A waves, known as plateau waves, have a duration of 5-20 minutes and an amplitude of 50 mm Hg over the baseline
ICP. After an episode of A waves dissipates, the ICP is reset to a baseline level that is higher than when the waves began.
Lundberg A waves are a sign of severely compromised intracranial compliance. The rapid increase in ICP caused by these waves
can result in a significant decrease in CPP and may lead to herniation.
Lundberg B waves have a duration of less than 2 minutes, and
they have an amplitude of 10-20 mm Hg above the baseline ICP. B waves are also related to abnormal intracranial compliance.
Because of their smaller amplitude and shorter duration, B waves are not as deleterious as A waves.
C waves, known as Hering-Traube waves, are low-amplitude waves
that may be superimposed on other waves. They may be related to increased ICP; however, C waves can also occur in the setting
of normal ICP and compliance.
When treating elevated ICP, remember that the goal of treatment
is to optimize conditions within the brain to prevent secondary injury and to allow the brain to recover from the initial
insult. Maintaining ICP within the reference range is part of an approach designed to optimize both CBF and the metabolic
state of the brain. Treatment of elevated ICP is a complex process that should be tailored to each particular patient's situation
and should not be approached in a “cookbook” manner. Many potential interventions are used to lower ICP, and each
of these is designed to improve intracranial compliance, which results in improved CBF and decreased ICP.
The Monro-Kellie doctrine provides the framework for understanding
and organizing the various treatments for elevated ICP. In patients with head injuries, the total intracranial volume is composed
of the total volume of the brain, the CSF, intravascular blood volume, and any intracranial mass lesions. The volume of one
of these components must be reduced to improve intracranial compliance and to decrease ICP. The discussion of the different
treatments for elevated ICP is organized according to which component of intracranial volume they affect.
The first component of total intracranial volume to consider
is the blood component. This includes all intravascular blood, both venous and arterial, and comprises approximately 10% of
total intracranial volume. Elevation of the head increases venous outflow and decreases the volume of venous blood within
the brain. This results in a small improvement in intracranial compliance and, therefore, has only a modest effect on ICP.
The second component of intracranial vascular volume is the
arterial blood volume. This may be reduced by mild-to-moderate hyperventilation, in which the PCO2 is reduced to
30-35 mm Hg. This decrease in PCO2 causes vasoconstriction at the level of the arteriole, which decreases blood
volume enough to reduce ICP. The effects of hyperventilation have a duration of action of approximately 48-72 hours, at which
point the brain resets to the reduced level of PCO2. This is an important point because once hyperventilation is
used, the PCO2 should not be returned to normal rapidly. This may cause rebound vasodilatation, which can result
in increased ICP.
At one time, severe hyperventilation was an important component
of the treatment of increased ICP. Reducing PCO2 to less than 25 mm Hg has been shown to cause enough vasoconstriction
that CBF is reduced to the point at which a high probability exists of developing cerebral ischemia. Therefore, prolonged
severe hyperventilation is not used routinely to treat elevated ICP. Brief periods of severe hyperventilation may be used
to treat patients with transient ICP elevations due to pressure waves or in the initial treatment of patients in neurologic
distress until other measures can be instituted.
CSF represents the next component of total intracranial volume
and accounts for 2-3% of total intracranial volume. In adults, total CSF production is approximately 20 mL/h or 500 mL/d.
In many patients with TBI who have elevated ICP, a ventriculostomy may be placed and CSF may be drained. Removal of small
amounts of CSF hourly can result in improvements in compliance that result in significant improvements in ICP.
The third and largest component of total intracranial volume
is the brain or tissue component, which comprises 85-90% of the total intracranial volume. When significant brain edema is
present, it causes an increase in the tissue component of the total intracranial volume and results in decreased compliance
and increased ICP. Treatments for elevated ICP that reduce total brain volume include diuretics, perfusion augmentation (CPP
strategies), metabolic suppression, and decompressive procedures.
Diuretics are powerful in their ability to decrease brain volume
and, therefore, decrease ICP. Mannitol, an osmotic diuretic, is the most common diuretic used. Mannitol is a sugar alcohol
that draws water out from the brain into the intravascular compartment. It has a rapid onset of action and a duration of action
of 2-8 hours. Mannitol is usually administered as a bolus because it is much more effective when given in intermittent boluses
than when used as a continuous infusion. The standard dose ranges from 0.25-1 g/kg, administered every 4-6 hours. Because
mannitol causes significant diuresis, electrolytes and serum osmolality must be monitored carefully during its use. In addition,
careful attention must be given to providing sufficient hydration to maintain euvolemia. The limit for mannitol is 4 g/kg/d.
At daily doses higher than this, mannitol can cause renal toxicity. Mannitol should not be given if the patient's serum sodium
level is greater than 145 or serum osmolality is greater than 315 mOsm.
Other diuretics that sometimes are used in patients with TBI
include furosemide, glycerol, and urea. Mannitol is preferred over furosemide because it tends to cause less severe electrolyte
imbalances than a loop diuretic. Interestingly, mannitol and furosemide have a synergistic effect when combined; however,
this combination tends to cause severe electrolyte disturbances. Urea and glycerol have also been used as osmotic diuretics.
Both of these compounds are smaller molecules than mannitol and, as a result, tend to equilibrate within the brain sooner
than mannitol; therefore, they have a shorter duration of action than mannitol. Urea has the additional problem that it can
cause severe skin sloughing if it infiltrates into the skin.
CPP management involves artificially elevating the blood pressure
to increase the MAP and the CPP. Because autoregulation is impaired in the injured brain, pressure-passive CBF develops within
these injured areas. As a result, these injured areas of the brain often have insufficient blood flow, and tissue acidosis
and lactate accumulation occur. This causes vasodilation, which increases cerebral edema and ICP. When the CPP is raised to
greater than 65-70 mm Hg, the ICP is often lowered because increased blood flow to injured areas of the brain decreases the
tissue acidosis. This often results in a significant decrease in ICP.
Metabolic therapies are designed to decrease the cerebral metabolic
rate, which decreases ICP. Metabolic therapies are powerful means of reducing ICP, but they are reserved for situations in
which other therapies have failed to control ICP. This is because metabolic therapies have diffuse systemic effects and often
result in severe adverse effects, including hypotension, immunosuppression, coagulopathies, arrhythmias, and myocardial suppression.
Metabolic suppression may be achieved through drug therapies or induced hypothermia.
Barbiturates are the most common class of drugs used to suppress
cerebral metabolism. Barbiturate coma is typically induced with pentobarbital. A loading dose of 10 mg/kg is administered
over 30 minutes, and then 5 mg/kg/h is administered for 3 hours. A maintenance infusion of 1-2 mg/kg/h is begun after loading
is completed. The infusion is titrated to provide burst suppression on continuous electroencephalogram monitoring and a serum
level of 3-4 mg/dL. Typically, the barbiturate infusion is continued for 48 hours, and then the patient is weaned off the
barbiturates. If the ICP again escapes control, the patient may be reloaded with pentobarbital and weaned again in several
Hypothermia may also be used to suppress cerebral metabolism.
The use of mild hypothermia involves decreasing the core temperature to 34-35°C for 24-48 hours and then slowly rewarming
the patient over 2-3 days. Patients with hypothermia are also at risk for hypotension and systemic infections.
Another treatment that may be used in patients with TBI with
refractory ICP elevation is decompressive craniectomy. In this surgical procedure, a large section of the skull is removed
and the dura is expanded. This increases the total intracranial volume and, therefore, decreases ICP. Which patients benefit
from decompressive craniectomy has not been established. Some believe that patients with refractory ICP elevation who have
diffuse injury but do not have significant contusions or infarctions will benefit from decompressive craniectomy.
Management of elevated ICP involves using a combination of treatments.
Each patient represents a slightly different set of circumstances, and treatment must be tailored to each patient. Although
no rigid protocols have been established for the treatment of head injury, many published algorithms provide treatment schemas.
The American Association of Neurologic Surgeons published a
comprehensive evidence-based review of the treatment of TBI, called the "Guidelines for the Management of Severe Head Injury."
In these guidelines, 3 different categories of treatments, standards, guidelines, and options are outlined. Standards are
the accepted principles of management that reflect a high degree of clinical certainty. Guidelines are a particular strategy
or a range of management options that reflect a high degree of clinical certainty. Options are strategies for patient management
for which clinical certainty is unclear.
The treatment of penetrating brain injuries involves 2 main
aspects. The first is the treatment of the TBI caused by a penetrating object. Penetrating brain injuries, especially from
high-velocity missiles, frequently result in severe ICP elevations. This aspect of penetrating brain injury treatment is identical
to the treatment of closed head injuries.
The second aspect of penetrating head injury treatment involves
debridement and removal of the penetrating objects. Penetrating injuries require careful debridement because these wounds
are frequently dirty. When objects penetrate the brain, they introduce pathogens into the brain from the scalp surface and
from the surface of the penetrating object.
Penetrating injuries may be caused by high-velocity missiles
(eg, bullets), penetrating objects (eg, knives, tools), or fragments of bone driven into the brain. Bullet wounds are treated
with debridement of as much of the bullet tract as possible, dural closure, and reconstruction of the skull as needed. If
the bullet can be removed without significant risk of neurologic injury, it should be removed to decrease the risk of subsequent
infection. Penetrating objects such as knives require removal to prevent further injury and infection. If the penetrating
object either is near or traverses a major vascular structure, an angiogram is necessary to assess for potential vascular
injury. When the risk of vascular injury is present, penetrating objects should be removed only after appropriate access has
been obtained to ensure that vascular control is easily achieved.
Penetrating brain injuries are associated with a high rate of
infection, both early infections and delayed abscesses. Appropriate debridement and irrigation of wounds helps to decrease
the infection rate. Some of the risk factors for infection following penetrating brain injury include extensive bony destruction,
persistent CSF leak, and an injury pathway that violates an air sinus.
Late-onset epilepsy is a common consequence of penetrating brain
injuries and can occur in up to 50% of patients with penetrating brain injuries. No evidence exists that prophylactic anticonvulsants
decrease the development of late-onset epilepsy. During the Vietnam War, prophylactic anticonvulsants were used, and the rate
of late-onset epilepsy was not different from that of previous wars, when prophylactic anticonvulsants were not used.
Head injury in children
Head injuries in children differ from head injuries in adults
in several ways. Children tend to have more diffuse injuries than adults, and traumatic intracerebral hematomas are less common
in children than in adults. In addition, early posttraumatic seizures are more common in children than in adults. Overall,
children have much lower morbidity and mortality rates from traumatic head injury compared to adults.
When a child with a head injury is being evaluated, nonaccidental
trauma must be excluded. In the United States, as many as 1 million cases of nonaccidental trauma in children may occur annually.
TBI is the most common cause of morbidity and mortality in nonaccidental trauma in children.
Radiographic signs of nonaccidental trauma include unexplained
multiple or bilateral skull fractures, subdural hematomas of different ages, cortical contusions and shearing injures, cerebral
ischemia, and retinal hemorrhages. If any of these are present, the case should be referred to the proper child welfare agency.
Follow-up care: For excellent patient
education resources, visit eMedicine's Back, Ribs, Neck, and Head Center, Back, Neck, and Head Injury Center, and Eye and Vision Center. Also, see eMedicine's patient education articles Concussion, Bicycle and Motorcycle Helmets, and Black Eye.
Complications resulting from TBI
are common and can be divided into 2 categories:
complications. The systemic complications of TBI are typical
of any severe injury and depend on the types of intensive treatments used.
Be aware of the complications of intensive care treatment when considering systemic complications
of head injury. The neurologic complications of TBI include:
- focal neurological deficits
- global neurological deficits
- CSF fistulae
- vascular injuries
- brain death
Focal neurological deficits
neurological deficits are quite common following TBI. Cranial nerves are affected often because of their anatomic
location at the base of the brain.
When the brain shifts within the skull as it undergoes either acceleration or deceleration forces, significant
force is often placed on the entire brain and the cranial nerves.
nerves are tethered at their exit sites from the skull, and, as a result, they may be stretched when the brain
shifts as a result of acceleration or deceleration forces.
In addition, the cranial nerves are very susceptible to injury as they course through narrow
bony canals and grooves. The cranial nerves that are injured most commonly in patients with TBI are cranial nerves I, IV,
VII, and VIII.
Anosmia caused by traumatic injury to the first cranial nerve occurs in 2-38% of patients with TBI. It's more common in those
with frontal fractures and in those with posttraumatic rhinorrhea.
Posttraumatic anosmia improves
slowly, and as many as 1/3 of patients do not show any improvement in olfaction.
Injuries to the fourth cranial nerve, the trochlear nerve, are also quite common. This nerve is often injured
in patients with head trauma because it has the longest intracranial course of the cranial
to the trochlear nerve causes a positional diplopia, in which those affected experience diplopia when they look
down and toward the eye in which the trochlear nerve is injured. As a result, to compensate, the head is tilted up and away
from the side of the injury. Trochlear nerve injuries resolve fully in approximately 2/3 of those with unilateral injury and
in 1/4 of those with bilateral injuries.
injuries often occur with head injuries in which the temporal bone is fractured. From 10-30% of persons with
longitudinal fractures of the temporal bone and 30-50% of those with transverse fractures of the temporal bone have either
acute or delayed facial nerve injury.
Immediate facial nerve injury suggests direct injury to the nerve, while delayed injury suggests progressive edema within the
nerve. In severely injured patients, a delay in the diagnosis of facial nerve injuries occurs frequently because facial nerve
function is difficult to assess in obtunded patients.
Cochlear nerve injury (cranial nerve VIII) is also a common occurrence in patients with head injury, especially in
patients with temporal bone fractures. In addition, vestibular disorders, including vertigo, dizziness, and tinnitus, are
extremely common in patients with head injuries.
Hydrocephalus is a common
late complication of TBI. Posttraumatic hydrocephalus may present as either ventriculomegaly with increased ICP or as normal
In patients with increased ICP secondary to posttraumatic hydrocephalus, the typical signs of hydrocephalus
are often observed and include:
Normal pressure hydrocephalus
usually manifests as memory problems, gait ataxia, and urinary incontinence.
The diagnosis of normal pressure hydrocephalus may be difficult to make in patients with TBI because they
often have memory difficulties and gait abnormalities secondary to their head injury.
addition, as many as 86% of patients with TBI demonstrate some degree of ventriculomegaly on follow-up CT scan
images. This ventriculomegaly is often secondary to diffuse brain atrophy, and radiographic features rarely help make the
distinction between atrophy and normal pressure hydrocephalus.
patient who develops neurologic deterioration weeks to months following TBI should be evaluated for the possibility
of normal pressure hydrocephalus.
When CT scan findings cannot help distinguish between normal pressure hydrocephalus and ventriculomegaly
secondary to brain atrophy, a high-volume lumbar puncture tap test is performed to ascertain if CSF drainage would improve
the patient's neurologic condition.
Posttraumatic seizures are
a frequent complication of TBI and are divided into 3 categories. Early seizures occur within 24 hours of the initial injury,
intermediate seizures occur 1-7 days following injury, and late seizures occur more than 7 days after the initial injury.
Posttraumatic seizures are
very common in those with a penetrating cerebral injury, and late seizures occur in as many as half of these patients.
Cerebrospinal fluid fistulae
Cerebrospinal fistulae, either
in the form of rhinorrhea or otorrhea, may occur in as many as 5-10% of patients with TBI. They may present either immediately
or in a delayed fashion and are more frequent in patients with basilar skull fractures. Approximately 80% of acute cases of
CSF rhinorrhea resolve spontaneously within 1 week. A 17% risk of meningitis exists when CSF rhinorrhea is present. Prophylactic
antibiotics have not been demonstrated to decrease this meningitis risk, although very few studies have examined this issue.
More than 95% of acute episodes of CSF otorrhea resolve spontaneously within 1 week, and CSF otorrhea is complicated by meningitis
in fewer than 4% of cases.
When acute CSF fistulae do
not resolve spontaneously, a lumbar subarachnoid drain may be placed for several days in an attempt to divert CSF and allow
the fistula to close. If this fails, radiographic dye is introduced into the subarachnoid space via lumbar puncture (metrizamide
cisternogram), and a high-resolution CT scan is performed in an attempt to identify the origin of the CSF fistula. A craniotomy
is performed, and the fistula site is repaired. Delayed CSF fistulae may occur from 1 week after the initial injury to years
later. These delayed fistulae are more difficult to treat and frequently require surgical intervention.
Vascular injuries are uncommon
sequelae of TBIs. Arterial injuries that may occur following head trauma include arterial transactions, thromboembolic phenomena,
posttraumatic aneurysms, dissections, and carotid-cavernous fistulae (CCF).
Arterial occlusions secondary
to transactions or thromboembolism following closed head injuries are uncommon occurrences.
Posttraumatic intracranial aneurysms,
which are also rare, differ from congenital aneurysms because the posttraumatic aneurysms tend to be located distally, as
opposed to the congenital aneurysms, which are typically proximal in location.
Arterial dissections are more
common than the aforementioned arterial injuries and should be considered if significant injury has occurred to the petrous
portion of the temporal bone, through which the carotid artery passes, or when an unexplained neurologic deficit is present.
A cerebral angiogram is often necessary to help exclude arterial injury in these cases.
Posttraumatic CCF occur when
the internal carotid artery is injured within the cavernous sinus, resulting in a direct connection between the carotid artery
and the veins of the cavernous sinus. This overloads the venous system and results in chemosis and proptosis on the affected
side. Other signs of CCF include diplopia, ophthalmoplegia, visual disturbances, and headaches. Some high-risk fistulae may
cause intracerebral hemorrhage. CCF are treated with endovascular balloon occlusion of the fistula origin.
Specific intracranial venous
injuries are uncommon following TBI if one excludes the injury to the bridging veins, which are the most common source of
subdural hematomas. Depressed skull fractures overlying any of the major intracranial venous sinuses may cause injury to the
sinus. When these venous sinus injuries require treatment, substantial, and sometimes life-threatening, blood loss can occur.
A second type of venous injury
following TBI involves venous sinus thrombosis. Although very rare following head injury, this is a potentially life-threatening
injury because the impaired venous drainage often causes severe ICP elevations and venous infarction. The treatment for venous
sinus thrombosis is anticoagulation, which presents significant risk in those with acute head injuries. If the thrombosis
progresses despite systemic anticoagulation, direct intracranial intravenous thrombolysis is necessary.
Intracranial infections are
another potential complication of TBI. In uncomplicated closed head injury, infection is uncommon. When basilar skull fractures
and/or CSF fistulae are present, the risk of infection is increased. In addition, if a patient has had a ventriculostomy for
ICP monitoring, the risk of infection is also increased, for either a ventriculitis or meningitis.
Other intracranial infections
such as subdural or epidural empyema and intraparenchymal abscesses are rare following closed head injury. As one would expect,
the incidence of infection in penetrating cerebral injuries and open depressed skull fractures increases.
Brain death can result from either massive initial injury or
as the result of prolonged severe elevations of ICP. Brain death is defined as the absence of brain function. A rigid protocol
is necessary to prove that brain death has occurred. It must be established that no sedating medications or neuromuscular
blocking agents are present. The patient's electrolyte levels, blood count, body temperature, and arterial blood gas values
must be within the reference ranges. The neurologic examination should demonstrate fixed nonreactive pupils, lack of corneal
and gag reflexes, fixed position of the eyes during rotation of the head (ie, negative doll's eyes), no response to supraorbital
pain, and no movement of the eyes to cold-water calorics.
A lack of any neurologic response is not sufficient to establish
brain death, and confirmatory testing must be performed. One of these tests is an apnea test, which involves removing a patient
from the ventilator for a brief period to assess any sign of spontaneous respiration. This is performed after a 30-minute
preoxygenation period with 100% oxygen. At the conclusion of the testing period, if the patient has not had any spontaneous
respirations and the arterial blood gas measurements demonstrate a PCO2 of greater than 65 mm Hg, the test results
are consistent with brain death. Two neurologic examinations and 2 apnea tests 12 hours apart are sufficient for determining
brain death. A nuclear blood flow study or a cerebral angiogram may be performed instead of one of the apnea tests for brain
death determination. The results of these studies demonstrate the absence of CBF when brain death has occurred. In most states,
brain death is considered to be death.