Craniofacial Injuries

Published on 13/03/2015 by admin

Filed under Neurosurgery

Last modified 13/03/2015

Print this page

This article have been viewed 1593 times

CHAPTER 339 Craniofacial Injuries

Peter L. Reilly, David J. David

The craniofacial region extends from the coronal suture to the chin. The bony and soft tissue anatomy includes the anterior portion of the skull vault and base, the facial skeleton, and the soft tissue coverings. The viscera include the frontal lobes of the brain, the contents of the orbit, associated cranial nerves, the upper airway, and the upper digestive tract.

Injuries to this anatomically and functionally complex region require the skills of several disciplines and are best managed in a multidisciplinary manner, if not by a formal multidisciplinary team. It follows that the management of craniofacial injuries should be integrated into a regional trauma service that is capable of providing lifesaving emergency and specialist care for extracranial injuries and has a workload sufficient to maintain the skills needed for multidisciplinary assessment and all the disciplines necessary for the treatment of craniofacial injuries in the short and long term.

Epidemiology

The causes of craniofacial trauma reflect the general pattern of neurotrauma but with significant regional variations. Worldwide, modes of transportation are the main cause of neurotrauma and craniofacial trauma. In high-income countries, an overall fall in transport injuries, the use of air bags in motor vehicles, and the use of helmets by motorcyclists have reduced the incidence of maxillofacial injury. Falls in infancy and old age and pedestrian and bicycle accidents have become major causes in some countries.¹ There remains a high incidence in motorbike riders, particularly adolescents. Facial fractures are more common with open face helmets, and the most severe injuries occur in riders with no helmet.² Furthermore, with the development of efficient retrieval systems, more patients with severe injuries survive to reach trauma centers. In developing countries, the continuing rise in the incidence of transport-related neurotrauma³ and the corresponding rise in severe head injuries are accompanied by a parallel increase in craniofacial injury, although these figures are not well documented.

Other causes of craniofacial trauma include falls, assaults,^4,⁵ sporting injuries, industrial accidents, and missile injuries.^1,^2,^6,⁷

Severe craniofacial fractures, typified by panfacial fracture involving all regions of the face, are most often associated with motor vehicle accidents. In this group, major injuries to other systems are common.⁸

In organizing multidisciplinary care and planning preventive strategies, an understanding of the causes and incidences in a particular community is essential.^4,^5,⁹

Functional Anatomy

The Anterior Cranium

The anterior cranial fossa is formed anteriorly and laterally by the frontal bones. The frontal bones are attached to the facial skeleton by the frontonasal, frontomaxillary, and frontozygomatic sutures. The floor of the anterior cranial fossa constitutes the interface between the cranium and the facial skeleton. It is formed laterally by thin supraorbital plates that dip down medially to articulate via the frontoethmoidal sutures with the cribriform plates and crista galli, parts of the ethmoid bone, and posteriorly with the lesser wings of the sphenoid bone via the sphenofrontal sutures. The cribriform plates may be quite narrow and are the lowest points of the anterior fossa floor, on average located 8 mm below the nasion. They form part of the roof of the nose and are related laterally to the anterior and middle ethmoid air cells.

Posteriorly, the ethmoid bone attaches to the body of the sphenoid, which is the roof of the sphenoid sinuses. Laterally, the lesser wings of the sphenoid form the crescentic posterior borders of the anterior fossa. The optic canal is formed by the two roots of the lesser wing of the sphenoid and runs forward and laterally in the superolateral wall of the sphenoid sinus to the orbital apex.¹⁰

The temporal bone forms part of the cranial base. The squamous part articulates with the mandible at the temporomandibular joint.

Fractures of the anterior fossa floor may involve the frontal, ethmoid, or sphenoid sinuses; the cribriform plates; or laterally, the optic canals. In making extradural approaches to this region via a frontal craniotomy, access is greatly increased by removing a bar of bone that includes the supraorbital margins and transects the frontal sinuses.

The complex sphenoid bone is the keystone for the craniofacial skeleton; it contributes to the middle cranial fossa, the anterior cranial fossa, the lateral orbital wall, and the subtemporal fossa.

The Facial Skeleton

The components of the facial skeleton are the nasal bones, ethmoids, zygomas, maxillae, and mandible.

The face is generally described as having an upper, middle, and lower third. The upper third is formed mostly by the frontal bone, which contributes to the orbital roofs. The middle third is formed mostly by the maxillae, zygomatic bones, and nasoseptal complex. These bony elements articulate laterally with processes of the temporal bone, posteriorly with the sphenoid wings to form part of the orbit, and centrally and laterally with the frontal bone. The lower third is formed by the mandible; however, the rami, coronoid processes, and condyles lie within the middle third, and the cranial component of the temporomandibular joint is part of the skull base.

The midfacial skeleton is designed to transmit the powerful forces of mastication to the base of the skull. The strong horizontal elements in the maxillae, the alveoli, and the hard palate make up a foundation to support three paired vertical buttresses. The load path for the distribution of force consists of the two buttresses on the piriform margin, from the region of the lateral incisor to the medial orbital margin, and two buttresses from the region of the molar tooth to the body of the zygoma on each side. It is these buttresses that provide the ideal places for stabilization, particularly with plates and screws (see Fig. 339-11).¹¹

The Orbit

The orbital cavity is in the form of a quadrilateral pyramid and is composed of seven bones. It has a strong orbital rim anteriorly and four thin walls that converge to a strong bony apex. The zygoma contributes to the lateral and inferior orbital margins, the lateral orbital wall, and the orbital floor. The maxillary component of the orbital floor medial to the zygoma is thin and delicate. The anterior orbital floor medial to the infraorbital canal is concave downward, but posterior to the globe it becomes convex upward. Restoration of this orbital floor convexity after injury is essential for the proper forward position of the globe.

The thin medial wall is composed of the lateral plate of the ethmoid bone. The lacrimal bone and the lamina papyracea of the ethmoid bone are the thinnest portion of the medial wall.

The Paranasal Air Sinuses

The size and degree of pneumatization of the paranasal air sinuses (Fig. 339-1) are variable. At birth all the sinuses are rudimentary and do not reach adult proportions until puberty (see Chapter 341).⁸

FIGURE 339-1 Transilluminated skull showing the varying thicknesses of the face and calvaria and indicating the paranasal sinuses. The buttresses supporting the face are demonstrated in the region of the lateral nasal wall and the zygoma.

Frontal Sinuses

The frontal sinuses vary markedly in size and extent and are usually asymmetric. They range from being barely pneumatized to extending superiorly in the frontal bone for a variable distance, sometimes to the lateral margins of the orbit and posteriorly into the anterior roof of the orbit. The frontonasal ducts open inferomedially and drain into the frontal recess of the nasal cavity.

Pneumatization becomes evident during the third year.

Ethmoid Sinuses

The ethmoid air cells vary in number, shape, and size. They constitute an interconnected series of thin-walled cells that lie between the upper lateral nasal cavity and the orbit and are separated from the orbit by the thin lamina papyracea. Their roof forms the floor of the anterior fossa lateral to the cribriform plate. The ethmoid sinuses are related to the maxillary sinuses inferiorly, the frontal sinuses superiorly, and the sphenoid sinuses posteriorly.

They are small at birth and have no direct relationship with the dura of the anterior cranial fossa. By the third year of life they are quite capacious.

Sphenoid Sinuses

The sphenoid sinuses lie within the body of the sphenoid bone. The degree of pneumatization of the body of the sphenoid is quite variable and may sometimes extend into the lesser wing of sphenoid. The sinuses are divided by one or more septa and are frequently asymmetric. They lie beneath the central part of the floor of the anterior fossa (planum sphenoidale) and the pituitary fossa. Medially, they are related to several important structures: the intracavernous internal carotid artery frequently grooving the lateral wall and the optic nerve within the optic canal superolaterally. The sphenoid ostia lie in the anterior wall of the sphenoid sinuses and open into the upper nasal cavity.

The sphenoid sinuses are present at birth. They enlarge slowly and are the last of the sinuses to establish a relationship with the anterior cranial fossa. Much of their development takes place after puberty.

Maxillary Sinuses

The maxillary sinuses usually fill the entire body of the maxilla and may extend into the zygomatic arch and below the floor of the nose. They have fragile walls and are easily fractured.

As with all the paranasal sinuses, they are rudimentary at birth.

Pathophysiology

The Cranial Cavity

The dura of the anterior fossa floor is firmly adherent to the cribriform plate, where it is penetrated by filaments of the olfactory nerves accompanied by sheaths of arachnoid. Fractures of the anterior fossa floor may lacerate the dura. A dural arachnoid tear with a fracture that communicates with the nose or paranasal sinuses will lead to a cerebrospinal fluid (CSF) fistula ¹² (see Chapter 341).

The Brain

Any part of the brain may be injured with trauma to the craniofacial region, but the frontal lobes are particularly vulnerable to the effects of blunt frontal impact and to contrecoup injury. The frontal orbital cortex may be damaged by shearing movement across the anterior fossa floor or by anterior fossa fractures when the orbital plates are shattered and buckled. Bilateral frontal lobe injury can result in a wide range of neuropsychological impairments (see the later section “Impairments and Disabilities”).

Olfactory Nerve

The olfactory nerve filaments may by avulsed by the shearing forces of a frontal or occipital impact or be torn by fractures crossing the cribriform plates. Stripping dura from the cribriform plate will lead to anosmia and sometimes to a CSF leak.

Optic Nerve

Traumatic injury to the optic nerve is indicated by a dilated, sometimes irregular pupil with hippus; the pupil does not show a direct or consensual light reaction but does react to contralateral light. With a partial injury, some light reactions may be seen.¹³ Flash evoked potentials may help diagnose early injury in unconscious patients and children.¹⁴

The optic nerve may be compressed by a displaced fracture through the optic canal, by contusion or hematoma within the canal without a fracture, or by direct injury to the orbit.^15,¹⁶

The Globe and Orbit

The orbit may be fractured directly or indirectly as part of frontal, nasoethmoid, midface, or zygomatic fractures. Orbital fractures may be indicated by diplopia, enophthalmos, impaired globe elevation because of entrapment of soft tissues, and paresthesia of the cheek or upper incisor teeth. The orbital signs may become apparent only after the edema has subsided.

Early marked exophthalmos suggests a significant reduction in bony orbital volume and requires urgent ophthalmologic and radiologic examination.

Orbital wall fractures may be “blow-out” or “blow-in” (outward on inward buckling of the orbital wall). A pure blow-in or blow-out fracture is one in which the orbital rim is intact; those often inaccurately referred to as “impure” fractures are extensions of fractures involving the orbital rim. Isolated medial wall defects in the middle third of the orbit increase orbital volume posterior to the axis of the globe and may cause enophthalmos. Until the advent of computed tomography (CT), these fractures were not easily recognized.

The globe can be injured by direct penetration or by blunt force. The globe is robust and cushioned by the surrounding soft tissue and will resist a blunt force sufficient to cause a blow-out fracture of the floor or medial wall.¹⁷ Nonetheless, the incidence of ocular injury with an orbital fracture is about 20%.¹⁸ Blunt injuries to the globe include corneal abrasions, hyphema, vitreous hemorrhage, and retinal detachment.

Penetration injury may damage any part of the globe and cause immediate or delayed loss of vision. The patient’s visual acuity is the best guide to the likelihood of visual recovery. If there is no perception of light, recovery of useful vision is highly unlikely.

Clinical examination may show chemosis, subconjunctival swelling, and poor visual acuity. During preoperative assessment it is important to avoid causing additional damage by placing pressure on the globe.

Oculomotor Nerves

Swelling of the orbit from direct injury may limit ocular movements and make early assessment of individual oculomotor nerve function difficult. Pupillary asymmetry or nonreactivity may be caused by direct injury to cranial nerve III by a fracture through the superior orbital fissure, often combined with injury to the ophthalmic nerve. Traumatic mydriasis from a blunt injury to the globe results from temporary sphincter paralysis. However, in an unconscious patient, pupillary asymmetry should always be regarded as a probable sign of brainstem injury or tentorial herniation.

Other Cranial Nerves

Any of the cranial nerves can be injured by fractures of the skull base or in their extracranial course. The most commonly injured nerves are the olfactory (see earlier) and the facial nerves (Kruse, 1998).

The Nerves of the Face

Trigeminal Nerve

The ophthalmic branch may be injured with orbital injuries, the infraorbital nerve with zygomatic fractures, and the inferior dental nerve with fractures through the mandibular canal.

Facial Nerve

The main trunk of the facial nerve may be injured by fractures of the temporal bone, and any of its branches may be injured with facial lacerations.

Mechanisms of Injury

Frontal Impact

The most common mechanism of craniofacial injury is blunt frontal impact. Blunt impact to the cranium may result in linear fractures, and focal impact may result in depressed fractures. Fractures of the anterior skull base may be caused by forces impacting on the cranial vault and transmitted to the skull base or by impact to the facial skeleton.

Fractures of the skull base are rarely significant in themselves; however, the force required to fracture the skull base is considerable and frequently injures the soft tissues, brain, cranial nerves, major vessels, orbit, and inner and middle ear. Dural tears may lead to fistulous communication with the nose, paranasal sinuses, or middle ear. The skin of the face or scalp may be lacerated or perforated by the impact.

Fracture lines caused by blunt trauma to the facial skeleton or skull follow points of weakness and avoid the bony buttresses. Hence, the fracture patterns of the facial skeleton are determined by the facial struts and buttresses and the honeycomb nature of the facial skeleton and paranasal air sinuses. The facial fracture pattern is generally described in terms of the upper, middle, and lower third divisions of Le Fort. Middle third fractures include orbital blow-in and blow-out fractures. The lower third comprises mandibular fractures.

However, fracture patterns rarely conform to this simple plan, and most injuries combine various components of these basic patterns.

Penetrating and Missile Wounds

Penetrating injuries follow no pattern. The tissue damage incurred by low-velocity penetration is confined to the pathway of the penetrating agent.

Gunshot wounds may be penetrating, perforating, or ablative, depending on the velocity and nature of the projectile. A low-velocity missile typically causes a penetrating injury. The missile remains embedded in the tissue and will cause little damage unless it strikes a vital structure. The facial bones are fractured and the skin lacerated without tissue loss. Most civilian gunshot wounds are of low to medium velocity, and the tissue damage is restricted to the path of the projectile. Penetrating brain injuries carry high mortality, nearly 70% in a recent report.¹⁹

Higher velocity missiles cause perforating injuries. There is an entry wound, which is often small, a larger exit wound, and a core of damaged tissue between.

High-velocity missiles cause massive avulsion with loss of bone and soft tissue, which is often more extensive than immediately apparent because tissues may be devitalized or injured by the traction of the avulsion. The eyes and brain may be injured either directly or by vascular injury, which may be immediate or delayed.

Crushing Injury

Crushing wounds may result in extensive fracturing of the skull base along with cranial nerve palsies and CSF leaks through the ear or the anterior skull base.

Associated Injuries

Severe frontal impact may also cause hyperextension injuries such as brainstem lacerations, cervical fracture-dislocation, and cervical carotid artery dissection.²⁰

Initial Management

Severe craniofacial injuries often pose an immediate threat to life. Airway obstruction caused by massive shattering of the facial skeleton, dislodged dentures, or collapse of the mandibular arch with retrodisplacement of the tongue may result in severe hypoxia.

There may be profuse bleeding, hypovolemic shock, and hypotension. They are often associated with injuries elsewhere in the body. Consequently, less severe craniofacial injuries may be overlooked in the urgency to manage severe injuries elsewhere in the body.²¹

Emergency Assessment and Resuscitation

The primary survey, resuscitation, secondary survey, and stabilization are followed by determination of the priorities of management. It is most important to be aware of the specific problems that may arise in craniofacial injuries, particularly during initial resuscitation.

Specific Acute Problems with Craniofacial Injuries

Breathing

Breathing may be impaired by head or chest injuries. Cough and swallowing reflexes may be impaired both by the direct injury and by brain injury.

Securing the Airway

Intubation may be very difficult and requires a highly experienced anesthetist. Endotracheal intubation is contraindicated by fracture of the larynx. Nasal intubation should be undertaken with great care because of the possibility of anterior fossa fracturing.

The airway may be secured in the following ways:

1 Intubation with light sedation or without anesthesia if the patient is unconscious from a head injury. Laryngoscopy often allows damaged tissues to be lifted away from the larynx and posterior pharyngeal wall to gain an adequate view for intubation.

2 Intubation with anesthesia, which provides good conditions but is potentially disastrous if the paralyzed patient cannot be ventilated.

3 Gaseous induction, which is safer because there is no paralysis but is not possible if bleeding or a disrupted face precludes containment of the gas within a facemask. Use of the fiberscope is handicapped by the presence of bleeding, which can readily obscure vision.

4 Tracheostomy under local anesthesia in an awake patient, which may be the first choice in those with panfacial fractures, even though neck swelling can make this very difficult.²²

5 Cricothyroidotomy, which is useful when it is not possible to pass an endotracheal tube.

6 Blind nasal intubation, which is potentially dangerous when the anterior cranial fossa may be fractured.

Circulation

Craniofacial injuries, especially those of the midface, may result in severe bleeding from superficial facial or temporal arteries and deep bleeding from the external carotid artery, usually the maxillary branch. Superficial arterial bleeding may be controlled by direct pressure or by exploring the wound and ligating the bleeding point.

Epistaxis or oropharyngeal bleeding may be controlled by packing. The nasal cavity and nasopharynx should be examined endoscopically if this is available, bleeding points cauterized, and packs placed. In the rare and difficult situation in which deep hemorrhage cannot be controlled, arterial ligation may be considered. If the bleeding is thought to come from the lower half of the nasal cavity, the pterygopalatine segment of the maxillary artery can be ligated via a transantral approach.

If the bleeding appears to come from higher in the nasal cavity, it may be necessary to ligate the anterior ethmoidal artery, a branch of the internal carotid system. Interventional radiologic techniques are proving useful in arresting deep bleeding in the maxillofacial region.

Clinical Assessment

Neurological

The conscious state is assessed early with the Glasgow Coma Scale, pupils, and localizing signs and repeated regularly.

Evidence of specific cranial nerve injury is sought. Anosmia should be identified when possible. Careful ophthalmologic assessment should be undertaken, with additional notation of pupillary symmetry and reactions, evidence of orbital injury, visual acuity, and as far as possible, visual fields. Evidence of direct injury to the orbit or globe or impaired vision requires urgent assessment by an ophthalmologist. Facial sensory nerve function is identified by assessing perception of light touch in the relevant zones. To assess sensation in the teeth (superior and inferior alveolar nerves), the patient is instructed to palpate them with a sweeping action of the tongue. The corneal reflex should be tested.

Facial nerve function can be assessed by observation and by the response to painful stimuli.

The Face

Bruising, lacerations, and contour deformities should be noted and recorded. Periorbital bruising (raccoon eyes) indicates a possible anterior fossa fracture. The mastoid region may show bruising (Battle’s sign) from a temporal bone fracture.

CSF leakage should be sought, although it may be hard to identify with certainty in the presence of blood and mucus. Secretion of saliva in the wounds may indicate injury to the salivary glands. Jaw movements and the muscles of facial expression are tested. The cervical spine is palpated for tenderness or deformity and the scalp for lacerations and hematomas.

By standing behind the patient with the head held back, any asymmetry of the facial prominences or deviations from the midline will be apparent.

Each facial region should be palpated systematically from the frontal bone to the mandible to specifically seek evidence of deformity or abnormal movement. Palpation of the inferior orbital margin may help differentiate isolated fractures of the zygoma (where the lateral part of the inferior rim is usually depressed) from midface pyramidal fractures or nasomaxillary fractures (where the medial aspect of the rim is depressed).

The mandible is examined with the patient’s mouth slightly open; the posterior rami, angles, lower border, and symphyseal regions are first palpated externally. Condylar movements are palpated by placing an examining finger in the external auditory meatus with the pulp directed anteriorly during active mandibular excursions. An intraoral examination is performed with a gloved finger to palpate the alveolar ridges and the hard palate. Dentoalveolar injuries are recorded on a dental chart. The anterior wall of the maxilla and the zygomaticomaxillary junctions are also palpated intraorally. Abnormal movements of the midface are elicited by grasping the maxillary alveolar ridge or pressing on the anterior hard palate (but not the incisor teeth) and applying a rocking movement while palpating the face with the free hand.

Abnormalities in dental occlusion must be noted.

Investigations

Early Imaging

Computed Tomography

A cranial CT scan is performed after initial resuscitation to assess for possible brain injury. This scan may be combined with scans of the cervical spine, thorax, and abdomen as indicated. Fractures of the anterior fossa floor can be visualised by fine-cut bone windows in the axial and coronal planes; however, at this initial stage it is inadvisable to spend time on investigations except for emergency management.

Angiography

Angiography is indicated for penetrating injuries in the region of major vessels or blunt injuries where there is suspicion of vascular injury.

Later Imaging

In general, detailed diagnostic imaging of the craniofacial injury should not be performed until a full clinical examination has been completed and a plan of investigation has been formulated. The principle investigation is CT.

Standard Radiographic Projections

1 Lateral view—brow-up standard.

2 Caldwell’s view—posteroanterior with 15-degree x-ray beam angulation caudal to the canthomeatal line (from the center of the external auditory meatus to the outer canthus of the eye). The orbital floor can be seen projected above or at the level of the petrous bones.

3 Waters’ view—posterior view with 37-degree x-ray beam angulation caudally. The petrous bones are projected below the floors of the antra to permit clear visualization of the sinuses, midface (including the maxilla), zygoma, and orbital rim and floor.

4 Submentovertical (basal axial) view—an anteroposterior view taken with the canthomeatal line vertical and parallel to the film and the x-ray beam angled 5 degrees. Cervical spine injury must be excluded before this view is obtained. This view shows the walls and posterior surface of the maxillary sinuses, lateral orbital wall, zygomatic arches, arch of the mandible, temporomandibular joints, ethmoid sinuses, and mastoid air cells.

5 Towne’s view—an anteroposterior view taken with the canthomeatal line at right angles to the film and the interpupillary plane parallel to the film. The x-ray beam is angled 30 degrees in a caudal direction. This view shows the zygomatic arches, the mandibular rami, the condylar necks, and the lower parts of the occipital bones.

6 Orthopantogram—a panoramic radiograph that shows the mandible, temporomandibular joints, and teeth. Different areas can be highlighted by centering the radiograph, but there is tomographic blurring in the region of the incisor teeth, which may hide a fracture (Fig. 339-2).

FIGURE 339-2 Orthopantogram (OPG). Because of the nature of the OPG image, there is blurring, particularly at the symphysis of the mandible. Undisplaced fractures in this area and in the condylar processes can be missed. The state of the alveolar bone and the relationship of the maxillary teeth to the maxillary sinuses are well shown.

Computed Tomography

Axial CT scanning is indispensable in managing severe craniocerebral injury and is the major form of imaging for presurgical planning and evaluation of the craniomaxillofacial injury.

Fine-cut two-dimensional CT is the best available method for assessing craniofacial fractures, particularly those of the middle third of the face. A fracture is seen most clearly on a scan at right angles to the bony plane that contains the fracture. Alternatively, the acquired slice data may be reformatted into the desired plane, but this will degrade the image to some extent. The thinner the slices, the better the reformatting.

Three-Dimensional Computed Tomography Reconstructions

The acquired CT slices, usually axial, can be used to produce three-dimensional representations of the skeleton, soft tissue, or both. These representations can be viewed from any direction and greatly facilitate an understanding of the anatomy of facial fractures.²³^–²⁶ These data can also be used to produce solid nylon models for planning surgical reconstruction and as a template on which a prosthesis can be manufactured.

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) is rarely used in the initial assessment. Specific later indications are as follows:

1 To identify sites of CSF leakage (see Chapter 341).

2 To identify intracranial wood and other nonmetallic foreign bodies in penetrating injuries.²⁷ Wood may show up more readily on MRI.²⁸

3 As a later assessment of brain damage for prognosis

4 To assess ocular injury

Management

Brain Injury

Craniocerebral injuries may be classified into five main clinical groups:

1 Externally compound frontal fractures and penetrating wounds with varying degrees of local cerebral damage

2 Internally compound fractures of the anterior cranial fossa, often associated with some form of craniofacial fistula

3 Closed primary brain injuries resulting from impact-induced acceleration or deceleration

4 Secondary injury such as intracranial hemorrhage, cerebral swelling, hypoxia, and metabolic disorders

5 Complications such as CSF leakage or intracranial aerocele (or both), intracranial infection, carotid-cavernous fistula, or posttraumatic epilepsy

At all stages of care the possibility of a primary brain injury needs to be kept in mind and steps taken to minimize the risk for secondary injury:

1 Early resuscitation to prevent hypoxia and hypotension

2 Early recognition and treatment of cerebral compression from intracranial hematoma

3 Control of raised intracranial pressure

4 Prevention of infection

Orbital Injury

Injury to the Globe

The status of the globe must be assessed urgently in all cases of injury about the orbit and the urgency of treatment determined.

Optic Nerve Injury

Management of traumatic optic nerve injury remains controversial, and the debate whether observation alone is better than steroids, surgical decompression, or a combination of the two remains unresolved.²⁹^–³⁶ A regimen of megadose methylprednisolone (loading dose of up to 30 mg/kg; maintenance dose of up to 5 mg/kg per hour for 72 hours) followed by a gradual reduction has been recommended³⁷; however, the International Optic Nerve Trauma Study found no benefit from either corticosteroid therapy or optic nerve decompression.³² A Cochrane review published in 2005 noted a high rate of spontaneous recovery and concluded that traumatic optic nerve injury initially seen more than 8 hours after injury should not be treated with steroids; for those seen within 8 hours, the evidence of benefit was weak.³⁸ Several papers have reported some good results after endoscopic decompression.^33,^39,⁴⁰ A small study reported better results in those operated early³⁰; however, a further Cochrane review in 2007 was unable to find sufficient evidence from the small retrospective series available and noted the risk for complications.⁴¹

Definitive Repair

Once the necessary assessments have been completed, a treatment plan is devised by all the specialties involved. Isolated injuries rarely give rise to conflicting treatment priorities, whereas multiple injuries and complex craniofacial injuries require a clear assessment of priorities based on the degrees of urgency.

In deciding on the appropriateness of early versus delayed surgery,⁴²^–⁴⁴ the following principles need to be observed:

Buy Membership for Neurosurgery Category to continue reading. Learn more here

Related

Youmans Neurological Surgery