epidural hematoma case report
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Angeles University Foundation
College of Nursing
CASE REPORT:
EPIDURAL HEMATOMA
Submitted to:
Maria Aileen Chanco-Bondoc RN, MN
Submitted by:
Gamboa, Christine G.
BSN IV-9
Group 36
I. INTRODUCTION
Head injuries are caused by a sudden impact or force to the head or inertial
forces within the skull. It is the trauma that leads to the potential injury to the scalp, skull,
or brain in which it can range from a simple bump to the skull to serious brain injury.
Head injuries can cause traumatic brain injury which is an insult to the brain that is
capable of producing intellectual, emotional, social, and vocational changes.
Motor-vehicle accidents are the leading cause of head injuries. Clients admitted
to the emergency department, most are males younger than 30 years and 50% have
evidence of ingestion of alcohol or other substances of abuse. Alcohol slows down the
reflexes and alters cognitive processes and perception. These physiologic changes
increase the chances of being involved in an accident or altercation. A second risk factor
is driving without seatbelts. Peak occurrence is during evenings, nights, and weekends.
Other causes are assaults, falls, and sports related injury.
In the United States, a head injury is experienced approximately every 15
seconds. Head injuries occur in about 7 million Americans every year. Among these
head-injured people, more than 500,000 are hospitalized, 100,000 experience chronic
disability, and about 2000 are left persistent vegetative state (Black, 2008).
Adding to that, Traumatic brain injury is a major cause of death and disability
worldwide, especially in children and young adults. Causes include falls, vehicle
accidents, and violence. Prevention measures include use of technology to protect those
who are in accidents, such as seat belts and sports or motorcycle helmets, as well as
efforts to reduce the number of accidents, such as safety education programs and
enforcement of traffic laws.
Brain trauma can be caused by a direct impact or by acceleration alone. In
addition to the damage caused at the moment of injury, brain trauma causes secondary
injury, a variety of events that take place in the minutes and days following the injury.
These processes, which include alterations in cerebral blood flow and the pressure
within the skull, contribute substantially to the damage from the initial injury.
Traumatic Brain Injury can cause a host of physical, cognitive, social, emotional,
and behavioral effects, and outcome can range from complete recovery to
permanent disability or death.
Epidural hematoma, a type of focal injury caused by traumatic head trauma, also
called as extradural hematoma, which forms between the skull and the dura mater. It
occurs in about 10% of severe head injuries and is usually associated with a skull
fracture. An epidural hematoma occurs from injury to the cerebral blood vessels, most
often the middle meningeal artery. Bleeding is usually continuous, and a large clot forms,
which separates the dura from the skull.
Epidural hematoma (ie, accumulation of blood in the potential space between
dura and bone) may be intracranial or spinal. Intracranial epidural hematoma occurs in
approximately 2% of patients with head injuries and 5-15% of patients with fatal head
injuries. Intracranial epidural hematoma is considered to be the most serious
complication of head injury, requiring immediate diagnosis and surgical intervention.
Intracranial epidural hematoma may be acute (58%), subacute (31%), or chronic (11%).
Spinal epidural hematoma may also be traumatic, though it may occur spontaneously.
In the United States, epidural hematoma complicates 2% of cases of head
trauma (approximately 40,000 cases per year). Spinal epidural hematoma affects 1 per
1,000,000 people annually. Alcohol and other forms of intoxication have been associated
with a higher incidence of epidural hematoma. International frequency is unknown,
though it is likely to parallel the frequency in the United States. Mortality rate associated
with epidural hematoma has been estimated to be 5-50%. No racial predilection has
been reported. Intracranial and spinal epidural hematomas are more frequent in men,
with a male-to-female ratio of 4:1. Intracranial epidural hematoma is rare in individuals
younger than 2 years it is also rare in individuals older than 60 years because the dura is
tightly adherent to the calvaria and Spinal epidural hematoma has a bimodal distribution
with peaks during childhood and during the fifth and sixth decades of life. Increasing age
has been noted as a risk factor for postoperative spinal epidural hematoma.
Manifestations are usually acute in onset because the bleeding is often arterial.
With an epidural hematoma, the following sequence of events may occur: (1) the client is
unconscious immediately after head trauma, (2) the client awakens and is quite lucid, (3)
loss of consciousness occurs and pupil dilation response rapidly deteriorates, with onset
of eye movement paralysis, on the same side as that of the hematoma, (4) the client
lapses into a coma, (5) blood behind the tympanic membrane, (6) periorbital
ecchymoses (bruises around the eyes), and (7) later, a bruise over the mastoid process
or battle’s sign.
Because the underlying brain has usually been minimally injured, prognosis is
excellent if treated aggressively. Outcome from surgical decompression and repair is
related directly to patient's preoperative neurologic condition.
Objectives
Broaden the knowledge about the disease process.
To know the precipitating and predisposing factors that contributed to the
development of the disease.
To know each nursing responsibility that the group of student-nurse
researchers would perform with each abnormality the client may manifest.
To be familiar with the treatment of the disease such as its medications to
be given, laboratory test/s to be performed and the health teachings to be
given to the significant others of the client.
Be able to make three nursing care plan
Completion of case report
Determine the nursing responsibilities (prior, during and after) of all the
medical management given to the patient.
Search the current trends and statistics regarding the disease condition.
Analyze and interpret the different diagnostic and laboratory procedures,
its purpose and its essential relationship to patient’s disease condition.
Current Trends
According to Medscape’s article: Intravascular Temperature Modulation as an
Adjunct to Secondary Brain Injury Prevention in a Patient with an Epidural Hematoma,
Epidural hematoma can result in long-term neurological deficits, prompt surgical
intervention and prevention of secondary brain injury can enable a full recovery.
Maintaining normothermia has been shown to be associated with improved
neurological outcomes (Lasater, 2005). Despite two temperature spikes associated
with coagulase-negative staphylococcus infection and one fever episode
associated with temporary suspension of cooling therapy for a catheter change, a
temperature of 36.5 °C was maintained for 13 days during the acute phase of the
case study patient's hospitalization. Neurological changes such as right-sided
weakness, along with hyperthermia (defined in our institution as a temperature of
>38.5 °C), resolved within several days of thermoregulation. This is an anecdotal
finding with implications for further studies to evaluate the role of
thermoregulation in ameliorating neurological changes in patients with traumatic
brain injuries.
II. ANATOMY AND PHYSIOLOGY
The human cranium and the facial bones are the foundation for the soft tissues of
the face and head. Thus, much of the visible appearance of the human face depends
upon the shapes and qualities of these bones. The cranium is that part of the skull that
holds and protects the brain in a large cavity, called the cranial vault. Eight plate-like
bones form the human cranium by fitting together at joints called sutures. The most
important of these cranial bones for the appearance of the face is the frontal bone,
which underlies the top of the face above the eyeballs. The human skull also includes
14 facial bones that form the lower front of the skull and provide the framework for most
of the face that is important to psychological research. These 22 skull bones form other,
smaller cavities besides the cranial vault, including those for the eyes, the internal ear,
the nose, and the mouth. The important facial bones include the jaw bone or mandible,
the maxilla or upper jaw, the zygomatic or cheek bone, and the nasal bone.
The skull base forms the floor of the cranial cavity and separates the brain from other
facial structures. This anatomic region is complex and poses surgical challenges for
otolaryngologists and neurosurgeons alike. Working knowledge of the normal and
variant anatomy of the skull base is essential for effective surgical treatment of disease
in this area.
The 5 bones that make up the skull base are the ethmoid, sphenoid, occipital, paired
frontal, and paired parietal bones. The skull base can be subdivided into 3 regions: the
anterior, middle, and posterior cranial fossae. (See the image below.) The petro-occipital
fissure subdivides the middle cranial fossa into 1 central component and 2 lateral
components. This article discusses each region, with attention to the surrounding
structures, nerves, vascular supply, and clinically relevant surgical landmarks.
Anterior Skull Base
The anterior limit of the anterior skull base is the posterior wall of the frontal
sinus. The anterior clinoid processes and the planum sphenoidale, which forms the roof
of the sphenoid sinus, mark the posterior limit. The frontal bone forms the lateral
boundaries. The frontal bone houses the supraorbital foramina, which, along with the
frontal sinuses, form 2 important surgical landmarks during approaches involving the
anterior skull base.
The greater portion of the anterior floor is convex and grooved by the frontal lobe
gyri. This portion of the skull base consists of the orbital portion of the frontal bone. The
ethmoid bone forms the central part of the floor, which is the deepest area of the anterior
cranial fossa. In the center of this region is the cribriform plate, through which the
olfactory tracts pass. The fovea ethmoidalis, or the roof of the ethmoid cavity, continues
laterally from the cribriform plate. The cribriform plate may be more than 1 cm lower than
the roof of the ethmoid cavity (fovea ethmoidalis), and it is made of extremely thin bone
compared with the relatively thick bone of the lateral fovea ethmoidalis. During
transethmoidal approaches to the anterior skull base, this relationship is extremely
important to remember.
The foramen cecum sits between the frontal crest and the prominent crista galli
and is a site of communication between the draining veins of the nasal cavity and the
superior sagittal sinus. The crista galli, which projects up centrally between the cerebral
hemispheres, serves as the site of attachment for the falx cerebri.
The optic chiasm, or chiasmatic sulcus, sits slightly posteriorly in the midline. The
anterior clinoid processes form the posterolateral segment and help form the roof of the
optic canal. In the medial aspect, the lesser wing of the sphenoid forms the anterior
clinoid process, an important landmark for the optic nerve and supracavernous internal
carotid artery (ICA).
Inferior relationships — extracranial aspects
The most important anatomic structures below the anterior cranial fossa are the
orbits and the paranasal sinuses. A thorough description is beyond the scope of this
article, but important anatomy and relationships are discussed.
The bony orbit is often a route for intracranial and extracranial spread of infection
and tumors because of its direct proximity to the anterior fossa. The posterior wall is thin
and adjacent to the superior sagittal sinus and frontal lobe dura. The posterior aspect
includes the optic canal, the superior orbital fissure (SOF), and the inferior orbital fissure
(IOF). The SOF conveys the oculomotor, trochlear, abducens, and ophthalmic nerves
(cranial nerves [CN] III, IV, VI, and V1, respectively), as well as the ophthalmic veins.
The IOF transmits the maxillary nerve (CN V2) and infraorbital vessels, and it
communicates with the infratemporal and pterygomaxillary fossae. The lateral portion of
the IOF is an important surgical landmark for positioning lateral orbital osteotomies
during anterior skull base resections. The optic canal transmits the optic nerve (CN II)
and the ophthalmic artery.
The image below demonstrates the relationship of the openings described
above. The medial wall is closest to the apex and is formed by the orbital process of the
frontal, lacrimal, ethmoid, and sphenoid bones. The medial wall transmits the anterior
and posterior ethmoid arteries through their respective foramina. These foramina help in
identifying the frontoethmoid suture line, which marks the inferior extent of the anterior
cranial fossa. The posterior ethmoid artery foramen is also an important surgical marker
for the location of the optic canal and nerve, which lies about 0.5 cm posterior to it.
The lesser wings of the sphenoid and the frontal process of the maxilla form the
lateral walls. The posteriormost segment of the lateral orbital wall forms the anterior wall
of the middle cranial fossa and is discussed in greater detail in the next section.
The ethmoid sinuses can be found inferior to the anterior cranial fossa and
medial to the orbits. The frontal sinuses arise as evaginations of ethmoid air cells into
the frontal bone and have a thick anterior and thinner posterior wall. The posterior wall is
adjacent to the superior sagittal sinus and the frontal lobe dura. As a result, the frontal
sinus can be used as a route of surgical entry into the anterior cranial fossa. Infectious
processes and tumors can exploit this relationship as well, to gain intracranial access.
Contents
The dura mater attaches anteriorly at the frontal crest and crista galli to form the
falx cerebri, which transmits the superior and inferior sagittal sinuses. The superior
sagittal sinus drains the superior cerebral and frontal diploic veins of Breschet. These
veins form a potential pathway for infection to spread intracranially, causing
complications such as sagittal sinus thrombosis, empyema, and abscess.
The foramen cecum, found anterior to the crista galli, usually ends blindly, though
it may transmit a vein from the nasal mucosa to the superior sagittal sinus. Its patency
may lead to the formation of developmental anomalies, such as nasal dermoid cysts,
nasal gliomas, encephaloceles, and meningoencephaloceles.
The frontal lobes occupy the anterior fossa and sit superior to the orbits and sinonasal
tract. The major structures in this area are the olfactory bulb and tract. The olfactory bulb
lies along the medial edge of the frontal orbital plate and connects with the olfactory
tract, which courses above the cribriform plate and planum sphenoidale.
Middle Skull Base
Boundaries — intracranial aspects
The greater wing of the sphenoid helps form the anterior limit of the middle skull
base. The posterior limit is the clivus, which is formed from the sphenoid and occipital
bones. The greater wing of the sphenoid forms the lateral limit as it extends laterally and
upward from the sphenoid body to meet the squamous portion of the temporal bone and
the anteroinferior portion of the parietal bone. The greater wing of the sphenoid forms
the anterior floor of the fossa. The anterior aspect of the petrous temporal bone forms
the posterior floor of the middle cranial fossa.
The body of the sphenoid makes up the central portion of the middle fossa and
houses the sella turcica. The sella turcica can be found between the anterior and
posterior clinoid processes and is composed of 3 sections. The tuberculum sellae is an
olive-shaped swelling and sits on the anterior slope between the chiasmal sulcus and
the sella turcica. The hypophyseal or pituitary fossa lies immediately posterior to the
tuberculum sellae. The dorsum sellae is the furthest posterior. In this region lies the
sigmoid groove for the ICA as it traverses the petrous apex through the cavernous sinus.
The floor and the lateral walls are grooved for the middle meningeal artery, which
courses anterolaterally from the foramen spinosum and which divides into frontal and
parietal branches. The former ascends across to the pterion, where it courses
posteriorly. The pterion is an H -shaped suture, where the frontal bone, the greater wing
of the sphenoid bone, the squamous temporal bone, and the parietal bone meet. This
suture is approximately 3.5 cm behind the zygomaticofrontal suture and 4 cm above the
zygomatic arch.
The pterion is made up of thin bone and can be easily fractured during trauma. If
fractured, it can result in injury to the anterior branches of the middle meningeal artery,
with eventual formation of an epidural hematoma.
The petrous portion of the temporal bone forms the posteromedial limit of the
middle cranial fossa. The superior petrosal sinus creates a longitudinal groove in the
petrous ridge. The anteromedial petrous tip houses the trigeminal or gasserian ganglion
in a region known as Meckel cave. This area is superior to the point at which the ICA
enters the cavernous sinus just above the foramen lacerum. Along the superomedial
surface of the petrous temporal bone, the roof of the carotid canal is frequently
dehiscent, a feature that makes dural elevation risky.
The arcuate eminence is the superior extent of the superior semicircular canal. It
can be appreciated on the superior aspect of the midpetrous ridge. The eminence is an
important landmark during the middle fossa approach for localization of the internal
auditory canal (IAC). Lateral to the arcuate eminence, the thin tegmen tympani and
tegmen mastoideum cover the middle ear and mastoid, respectively. The tegmen is a
thin plate of bone that separates the dura of the middle lobe from the middle ear and the
mastoid cavity. The bone of the floor of the middle fossa may be dehiscent over the
geniculate ganglion of the facial nerve.
Foramina — intracranial aspects
The SOF, foramen rotundum, foramen ovale, and foramen spinosum lie in an
anteroposterior and mediolateral plane. (See the image below.) Beginning lateral to the
clinoid process anteriorly, the SOF extends inferomedially and toward the orbital apex
and transmits the oculomotor nerve (CN III); the trochlear nerve (CN IV); the lacrimal,
frontal, and nasociliary branches of CN V1; and the abducens nerve (CN VI). It also
transmits the superior ophthalmic vein.
The foramen rotundum lies posteroinferior to the base of the SOF, at the level of
the sella turcica. It transmits the maxillary division (CN V2) of the trigeminal nerve into
the pterygopalatine fossa. The foramen sits near the lateral wall of the sphenoid sinus.
The foramen ovale is posterior and lateral and transmits the mandibular division (CN V3)
of the trigeminal nerve, the accessory meningeal artery, the lesser superficial petrosal
nerve (LSPN), and emissary veins to the pterygoid plexus into the infratemporal fossa.
The foramen spinosum lies further posterolaterally and transmits the middle
meningeal artery, as well as the meningeal branch of the facial nerve (CN VII).
The carotid canal forms where the petrous apex articulates with the sphenoid
and occipital bone. It continues into the foramen lacerum on the undersurface of the
skull base. The jagged foramen lacerum lies posteromedial to the foramen ovale. Two
inconsistent foramina are the innominate foramen, which may be found medial to the
foramen spinosum, and the foramen of Vesalius, found medial to foramen ovale. The
foramen of Vesalius is found in 40% of individuals and transmits an emissary vein from
the cavernous sinus.
Of note, the petro-occipital fissure, a gap between the medial border of the
petrous temporal bone and the lateral border of the clivus, is an important radiographic
and preoperative surgical landmark, because it lies in close proximity to various middle
cranial fossa foramina. It also serves to anatomically divide the middle skull base into a
central compartment and 2 lateral compartments.
Contents
Important structures in the middle fossa include but, are not limited to, the
temporal lobe, the pituitary gland, the trigeminal or gasserian ganglion, the greater
superficial petrosal nerve (GSPN), the intracranial portion of the ICA, and the cavernous
sinus and its contents. In the middle fossa, the dura strongly adheres to the clinoid
processes, the petrous and sphenoid ridges, and the basal foramina. In the midline, it
forms the diaphragma sellae—a circular dural plate—which covers the pituitary gland.
The pituitary stalk or infundibulum and the hypophyseal veins perforate this structure.
The cavernous sinus resides on both sides of the sella turcica and the body of the
sphenoid bone. Details of cavernous sinus anatomy are discussed further in following
sections of this article.
The temporal lobe takes up most of the space of the middle fossa and extends to
the inferior portion of the anterior fossa. The GSPN branches from the geniculate
ganglion and passes through a small hiatus into the middle fossa before coursing
parallel to the petrous ridge of the temporal bone and entering the foramen lacerum. The
GSPN, which is composed of parasympathetic fibers from the facial nerve to the lacrimal
gland, is an important surgical landmark. It is easily identified and can be followed back
medially to the foramen lacerum and the petrous ICA.
The GSPN and rostral LSPN run along the floor beneath the dura and parallel
the anterior edge of the petrous bone into foramen lacerum. Here, the GSPN joins with
the deep petrosal nerve to form the vidian nerve or the nerve of the pterygoid canal. This
area is also a landmark for the ICA, which lies deep and parallel to the temporal bone
and medial to the styloid process.
The facial nerve (CN VII) and vestibulocochlear nerve (CN VIII) originate from the
caudal pons. They course through the subarachnoid space and enter the porus
acusticus and IAC. CN VII continues through the temporal bone, the middle ear, and the
mastoid bone to exit at the stylomastoid foramen and innervate the facial nerve
musculature. The eustachian tube originates at the protympanum and runs
anteromedially and inferiorly. The bone directly medial to the eustachian tube may be
dehiscent, and the ICA may be seen. This feature is clinically relevant during surgical
exploration of the middle fossa, because the eustachian tube must be traversed before
the ICA is reached in this area.
Cavernous sinus
The cavernous sinus is a complex plexus of veins in the dura that can be found
lateral to the sphenoid sinus. It extends from the SOF to the apex of the petrous
temporal bone. The anterior and posterior petroclinoid folds serve as the lateral borders.
Along the lateral wall runs the ICA, which gives off 2-6 caroticocavernous branches that
supply the hypophysis and that join branches from the middle meningeal artery.
Running lateral to the ICA, the abducens nerve (CN VI) enters the dura superior
to the clivus and enters the Dorello canal. Infection of the petrous apex classically
manifests as abducens palsy due to inflammation in the Dorello canal. The petroclinoid
and petrosphenoidal ligaments of Gruber form the roof of the canal; the roof lies in close
proximity to the trigeminal ganglion and within 3 mm of the sphenoid sinus.
Running superoinferiorly in the lateral wall are the oculomotor nerve (CN III), the
trochlear nerve (CN IV), the ophthalmic nerve (CN V1), and the maxillary nerve (CN V2).
The oculomotor nerve divides into superior and inferior divisions at the most anterior
portion of the cavernous sinus. The trochlear nerve enters at the angle between the
anterior and posterior petroclinoid folds and courses the lateral wall.
The 3 divisions of the trigeminal traverse inferior to the tentorium cerebelli into
the Meckel cave, within the subarachnoid space. From here, V1, V2, and V3 pass into
the lateral wall of the cavernous sinus.
The cavernous sinus has complex venous drainage. It connects anteriorly to the
superior ophthalmic vein and the sphenoparietal sinus and drains posteriorly into the
superior and inferior petrosal sinuses en route to the basilar plexus. The superior and
inferior petrosal sinuses emerge from the posterior aspect of the cavernous sinus and
eventually drain into the sigmoid sinus and the internal jugular vein. The superficial,
middle, and inferior cerebral veins drain into the cavernous sinus from above, and the
emissary veins drain into the pterygoid plexus below the sinus. Interruption of the
anastomotic branch of the superficial middle cerebral vein as it connects to the
transverse sinus is likely to cause an infarction.
Knowledge of these complex relationships is necessary for recognizing the
manifestations of carotid-cavernous fistulas, which are reported to occur with basilar
skull fractures. In the case of such fistulas, traumatic tears of the intracavernous carotid
result in high-pressure arterial blood flooding the cavernous sinus. Clinically significant
backflow in the low-pressure superior ophthalmic veins draining into the cavernous sinus
then leads to venous engorgement, proptosis, and chemosis. In severe cases, pulsating
exophthalmos can be observed.
In rare cases, infections may enter the skull base from the facial venous system
and travel retrograde through the valveless ophthalmic veins into the anterior portion of
the cavernous sinus. The result is cavernous sinus thrombosis. Pimples and pustules,
which occur in the medial canthal, nasal, and labial areas (danger zone of the face), may
pass through the valveless angular and facial veins and drain superiorly into the
ophthalmic veins. They may eventually seed the cavernous sinus. Dental infections may
spread into the cavernous sinus by means of the pterygoid plexus.
Internal carotid artery
The course of the ICA is complex, and landmarks must be recognized during
skull base surgery. The course can be divided into 4 parts: cervical, intratemporal,
cavernous, and supracavernous.
The cervical portion passes near the third and fourth cervical vertebrae. At this
point, it is deep to the posterior digastric muscle and styloid process and superior and
posteromedial to the external carotid artery. The cervical ICA can be distinguished from
the external carotid because it has no branches. This feature is clinically important,
because the relationship with the external carotid may be aberrant. The ICA enters the
petrous bone through the carotid foramen and runs cranially into the foramen lacerum.
The intratemporal segment is difficult to mobilize because of an adherent fibrous
ring. This vertical portion ascends 5 mm and turns anteromedially into the horizontal
portion. At this point, it is medial to the eustachian tube and anterolateral and inferior to
the cochlea. At times, the carotid artery can be dehiscent in this area and extend into the
middle ear cleft. In these cases, the artery is at great risk during surgery involving the
middle ear. A dehiscent or aberrant ICA can appear as a pinkish or white-blue mass
filling the inferior portion of the middle ear. A pulsatile tympanic membrane is sometimes
observed.
In the normal case, the temporal carotid artery runs forward along the petrous
bone at a 45° angle to the midsagittal plane, giving off the caroticotympanic and
pterygoid branches. At this point, the artery is superior and lateral to the sphenoid bone
in an area referred to as the carotid siphon. The artery then enters the cavernous sinus
medial to the abducens nerve (CN VI).
On traversing the roof of the cavernous sinus medial to the anterior clinoid
process, the ICA enters the supracavernous portion. The last segment turns backward
under the optic nerve to the anterior perforated substance, where it joins the circle of
Willis through its terminal anterior and middle cerebral arteries.
Lateral relationships — extracranial aspects
As previously discussed, the petro-occipital fissure divides the middle cranial
fossae into central and lateral components.
Boundaries — extracranial aspects
The anterior boundary of the middle cranial fossa is the posterolateral wall of the
maxillary sinuses; the petro-occipital sutures form its posterior boundary. The lateral
margin consists of primarily the squamous and petrous portions of the temporal bone.
Many surgical approaches in the lateral skull base involve the infratemporal
fossa. Working knowledge of this area is imperative for the surgeon. The anterior
boundary of the infratemporal fossa is the posterior wall of the maxillary sinus. The
posteroinferior boundary is the parapharyngeal space. The lateral pterygoid plate forms
the medial boundary, whereas the mandibular ramus and condyle create the lateral
boundary. Finally, the greater wing of the sphenoid bone forms the superior border of the
infratemporal fossa.
Contents — extracranial aspects
When viewed from the extracranial lateral aspect, the infratemporal fossa lies below the
temporal bone, inferomedial to the zygomatic arch, and posterior to the maxilla.
Structures first identified in the infratemporal fossa include the muscles of mastication,
namely, the temporalis, masseter, and medial and lateral pterygoid muscles. The
internal maxillary artery, one of the terminal branches of the external carotid artery,
provides blood to these muscles and should be preserved in case a temporalis flap is
necessary to reconstruct skull base defects.
The medial and lateral pterygoid muscles take up most of the space of the infratemporal
fossa. Dissecting further in a medial direction reveals the cartilaginous eustachian tube
and the tensor and levator veli palatini muscles.
Moving anteriorly past the pterygoid process, one finds the pterygomaxillary fissure,
which transmits the maxillary artery to the pterygomaxillary fossa. (See the image
below.) The greater petrosal nerve joins the deep petrosal nerve to form the vidian
nerve, which enters the fossa through the vidian or pterygoid canal en route to the
pterygopalatine ganglion. The maxillary nerve enters through the foramen rotundum and
branches thereafter to supply sensory information from regions of the face. Both nerves
send branches to the parasympathetic sphenopalatine ganglion. The IOF is at the most
anterior limit of the pterygomaxillary fossa and is continuous with the infratemporal
fossa.
Two important bony surgical landmarks may be identified in the infratemporal
fossa. The first is the root of the lateral pterygoid plate. This plate serves as a marker for
the foramen rotundum, which lies immediately anterior to it, as well as for the foramen
ovale, which lies immediately posterior. Once the foramen ovale is identified, the
foramen spinosum is easily identifiable immediately posterior to the foramen. The
second landmark is the sphenoid spine, which helps in identifying the highest portion of
the cervical ICA and the carotid canal. The sphenoid spine is just medial to the condylar
or glenoid fossa and posterolateral to the foramen spinosum.
Drainage of the external lateral skull base involves the internal and external
jugular venous system and the retromandibular vein. The mastoid and occipital emissary
veins can link the intracranial dural sinus system with the external circulation, namely,
with branches of the occipital, postauricular, or retrofacial veins. The pterygoid venous
system can be highly variable in this region.
The facial, superficial temporal, and occipital and postauricular branches of the
external carotid artery provide arterial supply to the lateral skull base. The internal
maxillary artery, with its deep temporal and middle meningeal branches, can be
identified in the infratemporal fossa as well. The cervical portion of the ICA ascends
vertically to enter the middle fossa medial to the sphenoid spine.
The deep lobe of the parotid gland and the accompanying facial nerve (CN VII)
and its branches may be encountered in the lateral aspect of the extracranial skull base.
The facial nerve exits the mastoid through the stylomastoid foramen and enters
the substance of the parotid gland. Before exiting, the postauricular branch of the facial
nerve branches off and gives rise to the occipital, auricular, digastric, and stylohyoid
branches, as well as to a communicating branch that joins the glossopharyngeal nerve.
The chorda tympani nerve arises from the temporal segment of the facial nerve and
eventually joins the lingual nerve to supply taste to the anterior two thirds of the tongue.
The jugular foramen, which transports CNs IX, X, and XI, is a large, bony gap
between the jugular process of the occipital bone and the jugular process of the petrous
bone. In the extracranial aspect, its anterior border is the carotid canal, its lateral border
is the styloid process sheath, and its medial borders are the hypoglossal foramen and
canal. It lies posterolaterally in the lateral skull base and anteromedially to the mastoid
tip. The jugular foramen can be divided into the pars nervosa anteriorly and the pars
venosa posteriorly. Intracranial details of the jugular foramen are discussed in the
Posterior Skull Base section.
Medial relationships
The sphenoid sinus can serve as an access route to the pituitary and the clivus.
Sellar pneumatization of the sinus facilitates entry during transsphenoidal approaches. It
is important to avoid disrupting the lateral wall during instrumentation, because the ICA
and optic nerve are just lateral to a thin margin of bone. Dehiscence may be present in
the lateral wall of the sphenoid, resulting in exposure of the carotid artery, optic nerve, or
vidian nerve.
The nasopharynx lies posterior and inferior to the sphenoid sinus along the
midline. Mucosa covers the medial surface of the medial pterygoid plate. Along with the
investing pharyngobasilar fascia and the superior pharyngeal constrictor muscle, it helps
to form the lateral portion of the choana and part of the lateral portion of the
nasopharynx.
The sinus of Morgagni is a weak point in the superolateral nasopharyngeal wall.
It is created by the passage of the levator veli palatini and the cartilaginous eustachian
tube through the superior constrictor muscle. This is a region for infections or tumor to
potentially invade the skull base. Directly superior to the nasopharynx is the foramen
lacerum and the ICA, just before its entry point into the cavernous sinus.
The investing fascia of the nasopharynx, also known as the pharyngobasilar fascia, is
suspended from the skull base and clivus, located superiorly. The vertebrobasilar artery
and the brainstem lie posterior to the clivus.
Posterior Skull Base
Boundaries
The posterior skull base consists of primarily the occipital bone, with
contributions from the sphenoid and temporal bones. The basal portion of the occipital
bone (the basiocciput) and the basisphenoid form the anterior portion of the posterior
skull base. These 2 regions combine to form the midline clivus.
The posterior surface of the petrous temporal bone and the lateral aspect of the
occipital bone form the lateral wall. The occipital bone also fuses with the mastoid
portion of the temporal bone to form the occipitomastoid suture. The petrous portion of
the temporal bone and the greater wings of the sphenoid bone are particularly important
for identifying structures. The overlying tentorium cerebelli separates the cerebellum
from the cerebral hemispheres above, whereas the occipital bone forms the lateral walls
and floor.
The floor is grooved for the cerebellar hemispheres, and the midline internal
occipital crest runs from the foramen magnum to the internal occipital protuberance. The
crest serves as an attachment for the falx cerebelli, which contains the occipital sinus.
Grooves for the superior sagittal sinus are superior to the internal occipital protuberance.
The horizontal grooves for the paired transverse sinuses can be found lateral to the
internal occipital protuberance. They descend to the mastoid angle of the parietal bone
to become continuous with the sigmoid sulcus.
The sigmoid sulcus can be found in the lateral aspect of the posterior cranial
fossa in the mastoid portion of the temporal bone. It ends at the jugular foramen. The
sulcus for the inferior petrosal sinus sits posterior to the clivus and anterior to the petrous
apex.
Foramina
The porus acusticus is the opening of the IAC. Found on the posterior surface of
the petrous bone, it transmits the CNs VII and VIII, the nervus intermedius, and the
labyrinthine vessels (branches of the anterior inferior cerebellar artery en route to the
inner ear). The vestibular aqueduct is posteroinferior to the IAC. It transmits the
endolymphatic duct.
The jugular foramen extends laterally from the posterior aspect of the occipital
condyle. It is formed by the anterior processus jugularis of the petrous bone and the
occipital bone in its posterior aspect, and it lies at the posterior end of the petro-occipital
fissure. The sigmoid sinus and the jugular bulb enter the foramen at its smooth posterior
end (pars venosa). CNs IX, X, and XI enter its rough anterior end (pars nervosa). The
inferior petrosal sinus usually enters this portion of the jugular foramen between CNs IX
and X, but its path is highly variable. It may even enter the internal jugular vein below the
skull base.
Finally, the ascending pharyngeal artery may send a posterior meningeal branch
through the jugular foramen. The jugular tubercle may be medial to the lower aspect of
the jugular foramen, and it serves as a landmark for the hypoglossal foramen.
The hypoglossal foramen is inferomedial to the jugular foramen and near the
jugular tubercle. It transmits the hypoglossal nerve (CN XII), a meningeal branch of the
ascending pharyngeal artery, and the hypoglossal venous plexus. Emissary veins in
connection with the sigmoid sinus may leave the posterior fossa through mastoid
foramina.
The brainstem communicates with the vertebral canal through the foramen
magnum. The structures that pass through are the medulla oblongata, the spinal
accessory nerve, the vertebral and posterior spinal arteries, and the apical ligament of
the dens and membrane tectoria.
Contents
The midbrain, the pons, the medulla, and the cerebral and cerebellar
hemispheres lie in the posterior fossa. Dura and the tentorium cerebelli enclose the
various aforementioned venous sinuses. CNs VII-XII exit through the posterior fossa.
CNs VII and VIII and the nervus intermedius exit through the porus acusticus, and
nerves IX, X, and XI traverse the jugular foramen. CN XII exits through the hypoglossal
canal.[8]
On entering the posterior fossa through the foramen magnum, the vertebral
arteries ascend ventral to the roots of CNs IX, X, and XI. The posterior inferior cerebellar
arteries usually branch off from the vertebral arteries before forming the midline basilar
artery at the base of the pons. The basilar artery then branches into the anterior inferior
cerebellar arteries, which travel to the cerebellopontine angle in close relationship to
CNs VII and VIII. The basilar artery then branches into the labyrinthine artery, numerous
long and short pontine arteries, and, finally, the superior cerebellar arteries, which make
up the posterior portion of the circle of Willis. (See the image below.)
Inferior relationships — extracranial aspects
A surgeon must have knowledge of the outer regions of the skull base, because
these regions often serve as access points during surgery.
Suboccipital region
The mastoid tip serves as the origin for the sternocleidomastoid, while the
posterior digastric muscle originates deep to this area. In the posterior aspect, the
trapezius muscle is most superficial. Immediately deep lies the splenius capitis and
cervicis muscles and the semispinalis capitis muscle. On reflection of these muscles
from the superior nuchal line, the suboccipital triangle is exposed. (See the image
below.)
The suboccipital triangle is superficial to the ligaments connecting the atlas to the
axis and contains the occipital artery, the vertebral artery, a complex of veins, the
greater occipital nerve, and the C1 nerve. The occipital artery courses posteriorly deep
to the mastoid tip. Surgical approaches in this area allow mobilization of the vertebral
artery and access to the foramen magnum.
Vertebral artery
The vertebral artery originates from the subclavian artery and has 4 parts:
cervical, foraminal, atlantic, and subarachnoid. The atlantic portion is encountered in the
suboccipital triangle of the nuchal region and is covered by the semispinalis capitis
muscle.
The atlantic portion exits the atlas at the transverse foramen medial to the lateral
rectus capitis muscle and curves posteriorly behind the lateral mass of the atlas. It then
passes medially along the groove on the posterior arch of the atlas and pierces the
atlantooccipital membrane to enter the vertebral canal and subarachnoid space. The
subarachnoid portion of the artery is considered to lie in the posterior cranial fossa
proper.
III. PATHOPHYSIOLOGY
Schematic Diagram
MODIFIABLE FACTORS:
Alcohol Drinking
Substance Abuse
Motor-Vehicular
Accident
Assaults
Falls
Sport-related injuries
NON-MODIFIABLE FACTORS:
AGE
GENDER
Brief contact force
Severe head injuries or skull fracture
Injury to the cerebral blood vessels (Middle Meningeal Artery)
Rapid continuous bleeding
Rupture of the outer surface of the dura mater and the skul
Synthesis of the disease
Definition of the disease
Epidural hematoma is a mass of blood in the space between the inner
table of the skull and the dura mater (the leathery outer covering of the brain). Typically
caused by traumatic brain injury, the bleeding into the epidural space can cause
pressure on the brain which can lead to neurological symptoms including coma and
death if severe enough.
Leaking of blood between dura mater and the skull
Collection of blood
Mass or Clot Formation
Pressure on the brain
Rapid increase of the pressure inside the head (Increase Intracranial pressure)
Additional brain injury
Coma Confusion Drowsiness or Altered level of awareness
Enlarged Pupil in one eye
Severe headache
DeathPermanent brain damage
This can occur with more severe head injury, they can also occur with
relatively mild injuries, particularly if they are in the temporal area and cause a fracture of
the bone of the skull. The fracture can tear blood vessels in this area, leading to the
hematoma.
Modifiable/Non-Modifiable Factors
Modifiable factors
Alcohol Drinking – Alcohol slows the reflexes and alters
cognitive processes and perception that could lead potential
accident due to decrease alertness.
Substance Abuse – contributes to injuries among adolescents
and young adults because it has negative effects on perception,
judgment, and reaction time
Motor-Vehicular Accident – leading cause of death from injury
and sometimes associated with alcohol drinking causes slight to
severe physical injuries.
Assaults – physical assaults that are caused by an object that
causes a strong impact on a certain body part that could lead to
minor or to even severe injury.
Falls – most common cause of non-fatal injuries sometimes
associated with alcohol drinking.
Sport-related injuries – injuries that happen accidentally that is
acquired during falling, slipping, etc.
Non-Modifiable factors
Age – any age group is affected and can have the potential of
acquiring injuries. In children, due to increase activity could
engage in dangerous activities such as climbing, which can cause
injury if they accidentally fall. In older persons, due to the increase
age, there could be degeneration of certain abilities, problems in
vision and ambulation is sometimes the cause of injuries to the
elderly.
Sign and symptoms with rationale
The clinical manifestations of an epidural hematoma are increase ICP,
permanent brain damage, coma, confusion, enlarged pupil in one eye,
drowsiness or altered level of consciousness and even death. Not all of these
clinical manifestations are present in every epidural hematoma. The diagnosis of
an epidural hematoma is based on the patient symptoms, the physical signs and
the CT scan and MRI findings.
Increase ICP – increase in ICP is brought about the accumulation
of blood that causes compression, thus causing an increase
pressure on the brain.
Permanent brain damage – due to the increase pressure in the
brain, this causes additional damage on the brain and permanent
brain damage could occur if it is not immediately manage.
Coma, Confusion, and Drowsiness or altered level of
consciousness – due to the pressure caused in the brain, this
causes depressed level of consciousness, leading to confusion
and even coma.
Enlarged pupil in one eye - pressure on one side of the brain,
causing shift of the brain from one side to the other, can often
cause changes in the pupils of the eyes
Death – due to the permanent brain damaged caused by the
increased pressure, this can sometimes lead to irreversible brain
damage that in long run could cause dysfunction of the brain
leading to death.
IV. CLINICAL INTERVENTION AND MANAGEMENT
Diagnostic Procedures
CT scan
Plain radiography of the head (skull radiography) may reveal skull
fractures, though CT scanning has largely replaced the use of skull
radiography because the diagnostic information is so much greater with CT.
Cervical spine radiographs with anteroposterior, lateral, and odontoid views
are useful to identify associated traumatic fractures. Plain radiographs of the
vertebral column may identify a cavernous angioma.
Myelography outlines the epidural space and may illustrate a space-
occupying mass. CT myelography may be used when MRI is unavailable or if
the patient cannot tolerate MRI.
Noncontrast CT scanning of the head not only visualizes skull fractures
but also directly images an epidural hematoma.
o Acute epidural hematoma may appear as a hyperdense
lenticular-shaped mass situated between the brain and the
skull, though regions of hypodensity may be seen with serum
or fresh blood. On rare occasion, an acute epidural may
appear completely isointense with respect to brain.
Planoconvex or crescent-shaped epidural hematoma must be
differentiated from subdural hemorrhage. Subdural
hematomas may rarely appear convex and mimic epidural
hematomas. Subacute lesions are homogenously hyperdense.
o Chronic epidural hematoma may have a heterogeneous
appearance due to neovascularization and granulation, with
peripheral enhancement on contrast administration.
o CT scanning may also depict air collections and displacement
of brain parenchyma.
o Clinical deterioration should prompt repeat imaging with CT
scanning.
MRI
Demonstrates the evolution of an epidural hematoma, though this imaging modality may not be appropriate for patients in unstable
condition. Spinal MRI may delineate the location of an epidural hematoma
and identify an associated vascular malformation. Spinal cord enhancement may be apparent and should be
distinguished from inflammation or neoplasia. Diffusion-weighted imaging with the use of periodically rotated
overlapping parallel lines with enhanced reconstruction (PROPELLER) MRI may be used for improved detection of acute spinal epidural hematoma.
Gadolinium-enhanced magnetic resonance arteriography (MRA) may further define the extent of an arteriovenous malformation.
Surgical Procedure
Although several recent reports have described successful conservative
management of epidural hematoma, surgical evacuation constitutes definitive treatment
of this condition. Craniotomy or laminectomy is followed by evacuation of the hematoma,
coagulation of bleeding sites, and inspection of the dura. The dura is then tented to the
bone and, occasionally, epidural drains are employed for as long as 24 hours.
Minimally invasive surgical procedures, including the use of burr holes and negative
pressure drainage, may be used in selected cases.
Craniotomy
Craniotomy is the surgical removal of a section of bone (bone flap) from the skull
for the purpose of operating on the underlying tissues, usually the brain. The bone flap is
replaced at the end of the procedure. If the bone flap is not replaced, the procedure is
called a craniectomy. A craniotomy is used for many different procedures within the
head, for trauma, tumor, infection, aneurysm, etc.
Procedure
The craniotomy is labeled by which part of the skull is opened. A frontal
craniotomy indicates the opening is in the frontal bone while a parietal
craniotomy involves opening the parietal bone. If part of two adjacent bones is
opened, then both bones are mentioned, for example, fronto-temporal
craniotomy (Figure 10)
1. In the temporal areas, which are covered by muscle, the neurosurgeon
may carry out a craniectomy in which the bone is not replaced
2. Surgery on the back part of the brain beneath the tentorium is usually
carried out by removal of the lower part of the occipital bone. This is
called a suboccipital craniectomy. The craniectomy may be in the midline
or to one side or the other. When the bone removal is more to the side and
just behind the mastoid bone it may be called a retromastoid craniectomy.
Occasionally an abnormality is situated in the low brainstem or cerebellum
and may extend to the upper spinal cord. In these instances a cervical
laminectomy may also accompany the suboccipital craniectomy
Outline of
a fronto-
temporal
craniotom
y. The
small
circles
indicate
bur holes.
Outline of
a midline
suboccipit
al
craniecto
my. Note
the bur
holes that
are used
The
darker
blue area
indicates
where
bone is
removed
and not
replaced.
The dark
blue line
indicates
where the
bone is
cut. The
light blue
area is
replaced
after the
surgery.
to start
the bone
removal.
The blue
area
indicates
the bone
removed.
The incision in the scalp is designed to expose the skull over the lesion to be
removed
Removal of the bone flap is done in the following manner:
1. A series of small holes (bur holes) are made in the skull. The holes are
positioned around the periphery of the proposed bone flap. Making the
holes may be accomplished in one of three ways at the discretion of the
surgeon
The oldest method, which is still used by many surgeons, involves
a set of three drill bits and a hand drill. The first bit has a point and
is used to just penetrate the bone. The second and third bits,
which have more of a curvature, widen the hole without cutting the
underlying dura, which lines the inner surface of the skull
Another method is by using a special air powered drill. The drill bit
is made so that as soon as the center of the drill bit penetrates the
bone, the drill stops
The last method uses an air driven burr to gradually remove bone
until the dura is seen. This method allows the smallest holes, and
the holes can also be tailored in shape.
2. The skull is cut between each two adjacent burr holes in a progressive
manner until the bone flap is separated from the surrounding skull. This is
accomplished in one of two ways
The oldest method involves the passage of a thin metal strip (saw
guide) between two adjacent holes. The strip is placed between
the skull and the dura. A small hook on saw guide allows a wire
saw (Gigli saw) to be drawn under the skull in the same path as
the guide. The saw driven by hand then cuts the bone from inside
out
The air driven craniotome has for the most part replaced the
manual method. The craniotome resembles an air drill with a
protective footplate. Cuts are then made with the craniotome from
hole to hole until the bone flap is free
Photograph
of an air drill
making a bur
Wire Gigli
saw for
hole. cutting bone.
Operative
photograph
showing the
Gigli saw
being used.
Air
craniotome
being used
in surgery.
3. After the bone flap is removed, the underlying dura is cut to expose the
lesion. The dura is then cut within the margins of the skull opening. If the
lesion is a meningioma that is attached to the dura, the dura is cut around
the tumor leaving a margin of normal dura. When there is a loss of dura,
various substitutes can be used such as bovine pericardium (covering of
the heart), banked human dura, Gortex plastic or an absorbable collagen
matrix
4. What occurs next depends on the specific lesion that is found. When the
surgery is for a malignant brain tumor, the surgeon may wish to line the
cavity left by removal of the tumor with an absorbable wafer impregnated
with an anticancer drug. This has been shown to extend life by two to four
months.
The
cut
bone
is
elev
ated.
MRI
obtain
ed
after
partial
remo
val of
a
malig
nant
brain
tumor
(gliobl
astom
a
multif
orme)
in
which
the
tumor
was
treate
d with
absor
bable
wafer
s
(arro
ws)
impre
gnate
d with
an
antica
ncer
drug.
Court
esy
A.
Sloan
, M.D.
5. Following removal of the lesion, all bleeding is secured, the dura is
sutured closed and the bone flap restored to the skull with wire sutures or
titanium miniplates and screws. Burr holes in cosmetically exposed areas
are covered with small titanium plates. If the bone cannot be replaced
(infected or invaded by tumor) a prosthesis can be used. These are
usually made of titanium mesh or plastic. The scalp is then sutured closed
Titanium
mesh
cranioplast
y used for
replaceme
nt of an
infected
bone flap.
There are several instruments that have improved the ease and accuracy of a
craniotomy:
1. Operating Microscope. The human hand can make very small and
accurate movements as long as the eye can see it. The magnification
provided by the operating microscope has added another dimension to
operating. The magnification varies between 4 and 16x. This allows
magnification of small brain structures particularly the blood vessels and
nerves at the base of the brain. The microscope has markedly improved
the surgery of aneurysms of the brain arteries and tumors at the brain
base
2. Ultrasonic Aspirator. The ultrasonic aspirator is used to remove tumors
from the brain with a minimum of brain movement. The small tip of the
instrument vibrates back and forth at thousands of times per second, thus
liquefying the tumor tissue and allowing it to be easily sucked away with a
minimum of injury to the surrounding brain
3. Intraoperative Doppler Ultrasound. The intraoperative ultrasound is used
for localizing a lesion below the surface of the brain. It is similar to the
ultrasound used by an obstetrician to image a fetus in the womb. Sound
waves are sent out from the instrument (transducer) that strike the target
lesion and bounce back to the recording portion of the transducer. A
picture is thus produced which can guide the surgeon to the lesion
4. Stereotaxic Image Guided Craniotomy in the last few years, a significant
improvement in brain surgery is made possible by the marriage of modern
imaging studies (CT and MRI) and computer graphics. This frameless
stereotaxic (three dimensional) image guided surgery is a major advance
in the removal of lesions inside the skull, particularly small lesions and
lesions beneath the surface of the brain. It has only slightly affected large
lesions, diffuse brain lesions and surgery for ruptured cerebral aneurysm
Prior to surgery, small markers (feducials) that show up on CT or
in the MRI are applied to the head of the patient. The patient is
then placed in the CT or MRI unit and a series of images are
obtained. The electronic data that are the source of the images
are transferred to a computer in the operating room. This
computer reconstructs the CT or MRI images and produces a
three dimensional picture of the head containing the lesion as well
as a reconstruction of the head and lesion in three planes
After the patient is anesthetized, the head is pinned in a head
holder to rigidly hold it in place. The feducials are registered on
the CT or MRI are matched to the corresponding feducials on the
patient's head. The latter is accomplished with a pointer containing
an array of light emitting diodes. A receiver positioned near the
operating table registers the position of the diodes and thus the
position of the head feducials. This information is transferred
directly to the computer. The pointer or any other instrument
containing the diode array can then be used to direct the surgeon
to the lesion with no more than a 1-2 mm. error
Using this technique, the surgical trauma to the brain is reduced
and the size of the craniotomy is minimized. This is translated into
a faster and better recovery with discharge from hospital frequently
occurring in 24 hours
a. MRI
of
left
fron
tal
met
ast
atic
brai
n
tum
or
(arr
ow)
.
Not
e:
MRI
ima
ges
sho
w
the
left
side
to
the
vie
wer'
s
righ
t
b. Co
mp
uter
scr
een
as
see
n
by
the
neu
ros
urg
eon
duri
ng
ima
ge
gui
ded
sur
ger
y.
Not
e
the
ima
ges
hav
e
bee
n
flipp
ed
fro
m
side
to
side
so
that
the
sur
geo
n
has
a
left
side
d
ima
ge
to
his
own
left
side
.
The
arro
ws
poi
nt
to a
yell
ow
line
that
repr
ese
nts
the
dire
ctio
n of
'att
ack'
cho
sen
by
the
sur
geo
n.
The
red
'cro
ss
hair
s' is
the
posi
tion
of
the
inst
rum
ent
bei
ng
use
d
by
the
sur
geo
n.
The
righ
t
low
er
ima
ge
sho
ws
the
skin
surf
ace
of
the
pati
ent
with
mul
tiple
don
ut
sha
ped
fed
ucia
ls
on
the
surf
ace
.
The
red
ast
eris
k
lies
on
the
tum
or
ima
ged
in
blu
e
c. Pos
t-
ope
rati
ve
MRI
sho
win
g
co
mpl
ete
rem
oval
of
the
tum
or
Complications
Complications following craniotomy are primarily related to involvement of the brain and
its coverings. Some of the complications are:
Complications of anesthesia (see Anesthesia)
Infection
Hemorrhage and/or post-operative hematoma
Leak of cerebrospinal fluid
Brain swelling
Raised intracranial pressure (pressure inside the head)
Paralysis
Hydrocephalus (see Shunt for Hydrocephalus)
Loss of sensation
Loss of vision
Loss of speech
Memory loss
Recovery
Following surgery the patient is usually admitted to the intensive care unit
Level of consciousness is carefully observed for any change
Blood pressure is carefully monitored along with the pulse. A catheter inserted in
an artery may be used to continuously monitor the blood pressure
Intracranial pressure may be monitored through a small catheter placed within
the head and connected to a pressure gauge
Blood may be drawn to determine to determine the level of red blood cells, and to
determine the concentration of sodium and potassium
In some cases, a tube may be left in the windpipe to control respiration.
Antibiotics are usually given to prevent infection
Medication is frequently given to suppress the possibility of seizures
If there are no serious problems, the patient may be discharged the following
day, however, hospitalization may be considerably longer depending on the
lesion and the difficulty of the procedure
If there are problems such as weakness, loss of speech, hospitalization may be
delayed
Transfer to a rehabilitation unit may be necessary
Further care
The patient returns to the surgeon's office 7-10 days following discharge. At this
time sutures or staples may have to be removed. Continued care depends on the
lesion. Prolonged follow up is usually required for infection and tumor
Infections. A craniotomy for an infection is usually for a brain abscess. Frequently
the patient must be kept on specific antibiotics for the infectious agent causing
the abscess. On occasion antibiotics may be necessary for several months.
Brain tumors. The after care for a brain tumor differs depending on whether it is
benign or malignant
1. Patient with benign tumors usually have to be followed for several years
to be sure there is no recurrence. If there is recurrence, the alternatives
are usually repeat surgery or radiation therapy
2. Malignant tumors of the brain usually have a gloomy outlook. Additional
therapies include
Radiation therapy is usually given following removal of both
metastatic tumors and tumors that originate in the brain such as a
glioblastoma multiforme. Survival following surgery doubles if
radiation therapy is given
Chemotherapy has been used for glioblastoma but often helps
only slightly and frequently has unwanted side-effects
Immunotherapy involves stimulating the patient's own immune
system to fight the tumor. The patient's tumor (glioblastoma
multiforme) taken at the time of surgery is used to make a vaccine
(like the polio vaccine). The vaccine is given to the patient, which
stimulates blood cells to create lymphocytes that will find and
attack the tumor. Early trials have shown that immunotherapy
improves survival in some patients with minimal side-effects
Novel therapeutic approaches
o Endovascular embolization to minimize bleeding during the acute stage
o Thrombolytic evacuation using closed suction drain
Medication Regimen
Osmotic diuretics, such as mannitol or hypertonic saline, may be used to
diminish intracranial pressure. As hyperthermia may exacerbate neurological injury,
acetaminophen may be given to reduce fevers. Anticonvulsants are used routinely to
avoid seizures that may be induced by cortical damage. Patients with spinal epidural
hematoma may require high-dose methylprednisolone when spinal cord compression is
involved. Immobilized patients may require heparin for prevention of venous thrombosis,
whereas vitamin K and protamine may be administered to restore normal coagulation
parameters. Antacids are used to prevent gastric ulcers associated with traumatic brain
injury and spinal cord damage.
Nursing Management
Obtaining an accurate history, especially the mechanism of injury and clinical
course since that time
Close monitoring of the neurological status, observing for signs of increased
intracranial pressure
Physical examination against a baseline neurological assessment
Elevation of the head of the bed 300 to reduce the intracranial pressure
Administration of diuretics such as mannitol, mild analgesics or codeine to control
pain, and steroids such as dexamethasone according to physician’s prescriptions. In
some cases, the nurse may also need to provide seizure precautions, including the
administration of prophylactic anticonvulsants
Monitor LOC using the Glasgow scale or some other objective scale.
Assess motor responses bilaterally, check for positive Babinski
Assess for decreased sensory response bilaterally but with special emphases on
the side opposite the injury.
Monitor pupillary dilation and response to light. Note precisely the size of the
pupils in mm. Notify the physician immediately if dilation of pupils occurs.
Monitor vital signs. Notify physician if any deviation from parameters.
Provide nursing measures related to respiratory care. That would include
suctioning, doing blood gases, monitoring ventilator settings, providing O2 therapy.
Maintain fluid restriction. These patients need to be kept a little dry to help control
ICP.
Position the patient to maintain venous outflow from the brain. Elevate the HOB
to 30 degrees (except for a dural tear). Do not put a pillow under the head as it may
flex the head forward and could impede venous outflow. Turn by logrolling every 1 -
2 hours.
Administer prescribed medications. (will be discussed later)
Control noise and stimulation from the environment. It is very important to
separate stimuli such as turning, bathing, suctioning, injection, dressing changes,
and changing the bed. Allow a rest period between each activity as
the continued stimuli will cause the ICP to rise.
Maintain a desired temperature range either with the use of antipyretics or a
hypothermia blanket. If the patient has a hypothalamic injury, the fever will not
respond to antipyretics so a hypothermia blanket will be necessary.
Provide nursing care to prevent complications such as damage to the eyes, skin,
or oral mucous membranes.
Provide emotional support to the family. Allow them to spend as much time as
possible with the patient. Involve them in the care of the patient if they wish to
participate. Always encourage them to talk to and touch the patient. Answer
questions for them when possible or refer them to the MD
ICP monitoring device-Monitor ICP via the Epidural catheter if present. EC is a
transducer that is placed between the skull and the dura, leaving the
dura intact. A similar device is the subdural catheter - a transducer that is placed
under the dura mater.
V. NURSING CARE PLAN
Impaired Skin Integrity
ASSESSMENT NURSING
DIAGNOSIS
SCIENTIFIC
EXPLANATION
OBJECTIVES NURSING
INTERVENTIONS
RATIONALE EXPECTED
OUTCOME
S > ø
O > The patient
manifests:
-immobility
-destruction in
skin integrity
-redness on the
area
-trauma
-pain
-surgical
incision/wound
>The patient
may manifest:
-edema
Impaired skin
integrity related
to surgery
AEB
destruction of
skin layers and
surface and
invasion of
body structures
20 open
reduction
internal
fixation.
The procedure is
invasive in nature
since it will require
an incision and the
use of mechanical
implants. There is
destruction on the
skin layers of the
affected part.
Short term:
After 2 days of
NI, the patient
will achieve
timely wound
healing.
Long term:
After 7 days of
NI, the patient
will exhibit
improved skin
lesions or
wounds.
>Inspect skin every
shift, describe and
document skin
condition, and report
changes.
>Assist with general
hygiene and comfort
measures.
>Maintain proper
environmental
conditions.
>Use a foam
> To provide
evidence of
the
effectiveness
of the skin
care regimen.
>To promote
comfort and
sense of well-
being.
>To promote
patient’s
sense of well-
being.
Short term:
After 2 days
of NI, the
patient shall
have
achieved
timely wound
healing.
Long term:
After 7 days
of NI, the
patient shall
have
exhibited
-swelling
-itching
mattress, bed cradle,
or other devices.
>Warn against
tampering with the
wound or dressings.
>Position patient for
comfort and minimal
pressure on bony
prominences and
change his position
at least every 2
hours.
>Instruct family
members in a skin
care regimen.
>Perform prescribed
treatment regimen
for the skin condition
involved; monitor
>To minimize
skin
breakdown.
>To reduce
potential for
infection.
>To reduce
pressure,
promote
circulation and
minimize skin
breakdown.
>To
encourage
compliance.
>To maintain
improved skin
lesions or
wounds.
progress.
>Administer pain
medication and
monitor its
effectiveness.
or modify
current
therapy.
>To relieve the
patient of pain.
Risk for Infection
ASSESSMENT NURSING
DIAGNOSIS
SCIENTIFIC
EXPLANATION
OBJECTIVES NURSING
INTERVENTIONS
RATIONALE EXPECTED
OUTCOME
S> ø
O>The patient
manifests:
-presence of
surgical
incision/wound
>The patient
may manifest:
The pt. may
manifest:
-hyperthermia
-chills
-diaphoresis
-increase WBC
-pain and
swelling on the
surgical site
-alteration in
VS
Risk for
infection
related to
tissue
destruction
20 to open
reduction
internal
fixation.
The surgical wound
is at risk for
infection since
there is destruction
in the first line of
defense of the body
which is the skin.
This entitles
different pathogenic
organisms to
invade the surgical
wound. If it is not
properly taken
cared of like proper
cleaning and
changing of
dressings, there
can be growth and
spread of infectious
microorganisms
and so an infection
Short term:
After 2 days of
NI, the patient
will identify
interventions to
prevent/reduce
risk of infection.
Long term:
After 5 days of
NI, the patient
will manifest
absence of
infection.
>Observe for
localized signs of
infection at
sutures or surgical
incision wound.
>Note signs and
symptoms of
sepsis; fever,
chills, diaphoresis.
>Change
surgical/wound
dressings, as
indicated, using
proper technique for
changing/disposing
of contaminated
>To check for
any
signs of
infection.
>To check for
the presence of
infection and
give
necessary
interventions.
>To facilitate
wound healing
and prevent
infection by
minimizing
growth
and spread of
Short term:
After 2 days of
NI, the patient
shall have
identified
interventions to
prevent/reduce
risk of infection.
Long term:
After 5 days of
NI, the patient
shall have
manifested
absence of
infection.
-seizures will arise. materials.
>Teach family how to
clean incision
site daily and
remind them to
change dressings
as needed.
>Note and report
laboratory values.
>Administer/monitor
medication regimen
and note patient’s
response.
microorganisms.
> To educate the
family about the
right procedure
to clean and
change
dressings.
>To provide a
global view of
the patient’s
immune function
and nutritional
status.
>To determine
effectiveness of
therapy.
Risk for Disuse Syndrome
ASSESSMENT NURSING
DIAGNOSIS
SCIENTIFIC
EXPLANATION
OBJECTIVES NURSING
INTERVENTIONS
RATIONALE EXPECTED
OUTCOME
S > ø
O > The patient
manifests:
-coma
-prolonged
inactivity or
immobility
-pain
-changes in
integumentary
and
musculoskeletal
status
-presence of
surgical wound
>The patient
may manifest:
Risk for disuse
syndrome
related
immobilization
due to being
comatose
secondary to
epidural
hematoma
After the surgery,
immobilization of
the affected part is
prescribed for a
few days.
Prolonged
immobilization
may lead to
muscle atrophy,
impeded blood
circulation and
ineffective tissue
perfusion which
arises to the
occurrence of
disuse syndrome.
Short term:
After 3 days of
NI, the patient
will demonstrate
a decrease in
significant
changes in
cardiovascular
status,
respiratory
status, GI
status,
nutritional status
and
genitourinary
status
AEB decrease
fatigability,
> Avoid positions
that put prolonged
pressure on body
parts and
compress blood
vessels.
>Inspect skin
every shift and
protect areas
subject to irritation.
> Monitor
temperature, blood
pressure, pulse
and respirations at
least every 4
hours.
> To enhance
circulation and
help prevent
tissue or skin
breakdown.
>To prevent or
mitigate skin
breakdown.
> To assess
for indications
of infection or
other
complications.
Short term:
After 3 days of
NI, the patient
shall have
demonstrated a
decrease in
significant
changes in
cardiovascular
status,
respiratory
status, GI
status,
nutritional status
and
genitourinary
status
AEB decrease
-changes in
cardiovascular
status,
respiratory
status, GI status,
nutritional status
and
genitourinary
status
ability to move
about and
decrease risk
for muscle
atrophy.
Long term:
After 5 days of
NI, the patient
will maintain
muscle strength
and tone and
joint ROM.
>Perform passive
ROM exercises at
least once per
shift.
>Provide or help
with daily hygiene;
keep skin dry and
lubricated.
>To prevent
joint
contractures,
muscle
atrophy, and
other
complications
of prolonged
inactivity.
> To prevent
cracking and
possible
infection.
fatigability,
ability to move
about and
decrease risk for
muscle atrophy.
Long term:
After 5 days of
NI, the patient
shall have
maintained
muscle strength
and tone and
joint ROM.
VI. CONCLUSION
An Epidural hematoma is a mass of blood in the space between the inner table of
the skull and the dura mater (the leathery outer covering of the brain). Typically caused
by traumatic brain injury, the bleeding into the epidural space can cause pressure on the
brain which can lead to neurological symptoms including coma and death if severe
enough. This can occur with more severe head injury, they can also occur with relatively
mild injuries, particularly if they are in the temporal area and cause a fracture of the bone
of the skull. The fracture can tear blood vessels in this area, leading to the hematoma.
The surgical management most widely used is craniotomy which is indicated to evacuate
the hematoma, prevent and manage coagulation of bleeding sites, and inspection of the
dura. In this case report, the main focus is to broaden the knowledge about epidural
hematoma, its manifestations, risk factors and causes, possible diagnostic procedures or
test, surgical management, and nursing management. Also, the nurse must be aware of
her responsibilities to provide quality care to the patient. She must provide her health
teachings like the proper management of the surgical wound, the benefits of the surgery
and the complications that may occur. The nurse must provide adequate knowledge to
the patient and also to the SO to rule out anxiety and misconceptions. And, the nurse
must help the patient to achieve timely wound healing and to increase the level of
wellness and prevent the occurrence of complications.
VII. BIBLIOGRAPHY
Modern Medical Guide, Revised Edition, 2002
Medical Surgical Nursing, Eight Edition, 2009
http://www.blogtopsites.com/outpost/51b3b6303a2d9b8b95c8ddae04460e4a
http://hematomatreatment.com/nursing-care-of-subdural-and-epidural-hematomas/
http://emedicine.medscape.com/article/824029-followup
http://www.nursing-lectures.com/2011/02/head-trauma-and-nursing-intervention.html
http://health.nytimes.com/health/guides/disease/extradural-hemorrhage/overview.html
http://www.yoursurgery.com/ProcedureDetails.cfm?Proc=19scape.com/viewarticle/
580271_5
http://hematomatreatment.com/nursing-care-of-subdural-and-epidural-hematomas/
http://emedicine.medscape.com/article/882627-overview#a1
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002385/
http://en.wikipedia.org/wiki/Epidural_hematoma
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