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 battles 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 patients disease condition. Current Trends

According to Medscapes 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 sellaea circular dural platewhich 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:

NON-MODIFIABLE FACTORS: AGE GENDER

Alcohol Drinking Substance Abuse Motor-Vehicular Accident Assaults Falls Sport-related injuries

Brief contact force

Severe head injuries or skull fracture

Injury to the cerebral blood vessels (Middle Meningeal Artery)

Rupture of the outer surface of the dura mater and the skul

Rapid continuous bleeding

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

Permanent brain damage

Coma

Confusion

Drowsiness or Altered level of awareness

Enlarged Pupil in one eye

Severe headache

Death

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.

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 spaceoccupying 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 from isointense subdural with respect to brain. Planoconvex or crescent-shaped epidural hematoma must be differentiated 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.

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 bur holes. The darker blue area not replaced. The dark blue line indicates where the bone is cut. The

Outline of a midline suboccipital used to start the bone removal. The blue

craniotomy. The small circles indicate craniectomy. Note the bur holes that are indicates where bone is removed and area indicates the bone removed.

light blue area is replaced after the surgery. 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 hole.

Wire Gigli saw for cutting bone.

Operative photograph showing the Gigli saw being Air craniotome being used in surgery. used.

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 elevated.

MRI obtained after partial removal of a malignant brain tumor (glioblastoma multiforme) in which the tumor was treated with absorbable wafers (arrows) impregnated with an anticancer drug.

Courtesy 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 cranioplasty used for

replacement 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 frontal metastatic brain tumor (arrow). Note: MRI images show the left side to the viewer's right b. Computer screen as seen by the neurosurgeon during image guided surgery. Note the images have been flipped from side to side so that the surgeon has a left sided image to his own left side. The arrows point to a yellow line that represents the direction of 'attack' chosen by the surgeon. The red 'cross hairs' is the position of the instrument being used by the surgeon. The right lower image shows the skin surface of the patient with multiple donut shaped feducials on the surface. The red asterisk lies on the tumor imaged in blue c. Post-operative MRI showing complete removal of the

tumor 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 o

Endovascular embolization to minimize bleeding during the acute stage 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 Close monitoring of the neurological status, observing for signs of increased 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

course since that time intracranial pressure

pain, and steroids such as dexamethasone according to physicians 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 Monitor pupillary dilation and response to light. Note precisely the size of the

the side opposite the injury. 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 Maintain fluid restriction. These patients need to be kept a little dry to help control Position the patient to maintain venous outflow from the brain. Elevate the HOB

suctioning, doing blood gases, monitoring ventilator settings, providing O2 therapy. ICP. 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, Provide emotional support to the family. Allow them to spend as much time as

or oral mucous membranes. 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 S> O > The patient manifests: -immobility -destruction in skin integrity -redness on the area -trauma -pain -surgical incision/wound >The patient may manifest: -edema -swelling NURSING DIAGNOSIS Impaired skin integrity related to surgery AEB destruction of skin layers and surface and invasion of body structures 20 open reduction internal fixation. After 7 days of NI, the patient will exhibit improved skin lesions or wounds. >Use a foam mattress, bed cradle, >To minimize >Maintain proper environmental conditions. >To promote patients sense of wellbeing. After 7 days of NI, the patient shall have exhibited improved skin SCIENTIFIC EXPLANATION 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. Long term: After 2 days of NI, the patient will achieve timely wound healing. >Assist with general hygiene and comfort measures. >To promote comfort and sense of wellbeing. Long term: OBJECTIVES Short term: NURSING INTERVENTIONS >Inspect skin every shift, describe and document skin condition, and report changes. RATIONALE > To provide evidence of the effectiveness of the skin care regimen. After 2 days of NI, the patient shall have achieved timely wound healing. EXPECTED OUTCOME Short term:

-itching

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.

skin breakdown.

lesions or wounds.

>To reduce potential for infection.

>To reduce pressure, promote circulation and minimize skin breakdown.

>To >Perform prescribed treatment regimen for the skin condition involved; monitor progress. >To maintain or modify encourage compliance.

current >Administer pain medication and monitor its effectiveness. >To relieve the patient of pain. therapy.

Risk for Infection ASSESSMENT NURSING SCIENTIFIC OBJECTIVES NURSING RATIONALE EXPECTED

S> 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 -seizures

DIAGNOSIS Risk for infection related to tissue destruction 20 to open reduction internal fixation.

EXPLANATION 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 will arise.

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.

INTERVENTIONS >Observe for localized signs of infection at sutures or surgical incision wound. >Note signs and symptoms of sepsis; fever, chills, diaphoresis.

>To check for any signs of infection.

OUTCOME Short term: After 2 days of NI, the patient shall have identified

>To check for the presence of infection and give necessary interventions.

interventions to prevent/reduce risk of infection. Long term: After 5 days of

>Change surgical/wound dressings, as indicated, using proper technique for changing/disposing of contaminated materials.

>To facilitate wound healing and prevent infection by minimizing growth and spread of microorganisms.

NI, the patient shall have manifested absence of infection.

>Teach family how to clean incision site daily and remind them to change dressings as needed. >Note and report laboratory values. >To provide a global view of the patients immune function and nutritional >Administer/monitor medication regimen and note patients response. status. >To determine effectiveness of therapy. > To educate the family about the right procedure to clean and change dressings.

Risk for Disuse Syndrome ASSESSMENT NURSING SCIENTIFIC OBJECTIVES NURSING RATIONALE EXPECTED

S> O > The patient manifests: -coma -prolonged inactivity or immobility -pain -changes in integumentary and musculoskeletal status -presence of surgical wound >The patient may manifest: -changes in cardiovascular status,

DIAGNOSIS Risk for disuse syndrome related immobilization due to being comatose secondary to epidural hematoma

EXPLANATION 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, ability to move about and decrease risk

INTERVENTIONS > Avoid positions that put prolonged pressure on body parts and compress blood vessels.

> To enhance circulation and help prevent tissue or skin breakdown. >To prevent or

OUTCOME Short term: After 3 days of NI, the patient shall have demonstrated a decrease in significant changes in cardiovascular status,

>Inspect skin every shift and protect areas subject to irritation.

mitigate skin breakdown.

> To assess > Monitor temperature, blood pressure, pulse and respirations at least every 4 hours. >Perform passive ROM exercises at least once per >To prevent joint contractures, for indications of infection or other complications.

respiratory status, GI status, nutritional status and genitourinary status AEB decrease fatigability, ability to move about and

respiratory status, GI status, nutritional status and genitourinary status

for muscle atrophy. Long term: After 5 days of NI, the patient will maintain muscle strength and tone and joint ROM.

shift.

muscle atrophy, and other complications of prolonged inactivity.

decrease risk for muscle atrophy. Long term: After 5 days of NI, the patient shall have maintained muscle strength and tone and joint ROM.

>Provide or help with daily hygiene; keep skin dry and lubricated.

> To prevent cracking and possible infection.

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