Linear Skull Fractures

A linear skull fracture is a single fracture line that goes through the entire thickness of the skull.

Management

Linear skull fractures require no stabilization or exploration when the scalp is closed, and when there is no evidence of epidural hematoma or underlying dural or cortical injury. Even when a scalp laceration is present, very seldom is surgical exploration with bone removal necessary. Exceptions would include a machete injury to the skull producing a linear skull fracture with underlying dural laceration and brain damage. The skull fracture does, however, show that significant head trauma has occurred, and a careful assessment of the brain, facial structures, and cervical spine is required. Open linear fractures are débride of foreign material, devitalized soft tissue, and bone fragments; preferably, the damaged soft tissue at the edges of the laceration is excised to healthy, noncontused bleeding tissue (if the tissue excision can be tolerated and will permit primary closure) and the laceration is closed after thorough cleansing. If there is insufficient vascularized soft tissue present to permit excision of the contused devitalized tissue, a rotation flap and skin graft to the donor area may have to be considered (Fig. 22.1).

FIGURE 22.1 Open skull fracture (A) with tissue loss (B) sufficient that an immediate (C) scalp rotation flap had to be performed to achieve scalp closure.

Growing Skull Fractures in Children

A rare complication after linear skull fracture in young children (usually younger than 2 or 3 years) is a “growing” skull defect at the fracture site. In these cases, the dura is torn under the linear skull fracture. The pathogenesis is thought to be an expanding pouch of arachnoid passing through the torn dura and skull fracture, acting as a one-way valve that traps cerebrospinal fluid (CSF) and causes progressive pressure erosion of the fractured edges to enlarge the fracture. Alternatively, the growth of the brain, which produces pulsating, spreading tensile pressure forces on the edges of an unrepaired dural laceration, may also cause a skull defect to enlarge. These vectors of force by the brain may sometimes cause herniation through the skull defect, causing a new neurological deficit (Fig. 22.2). These lesions are surgically repaired with closure of the dura or with a dural patch and replacement or repair of the bone defect. Some surgeons routinely take a skull film at 1 year after linear skull fracture treated nonoperatively to detect such growing skull fractures. For this reason it is worthwhile for the primary care doctor to examine the scalp and skull of any child with a known skull fracture under the age of 2 or 3.

FIGURE 22.2 “Growing”” skull fracture in a child. The mechanism is a closed skull fracture that tears the dura. The pressure of the pulsating brain creates slow erosion of the bone, creating a bone and dural defect. Repair of the dura and cranioplasty is required.

Comminuted Fractures

A comminuted fracture occurs when multiple linear fractures radiate from the point of impact. Some of the fracture lines may involve the suture lines (diastatic fracture) or may stop at them. Around the point of impact there may be free fragments of bone.

Management

If the skin is closed, and no depression of bone fragments greater than the thickness of the skull is demonstrated on CT, management is as that for linear skull fractures. However, in many of these cases, surgery is performed for the underlying intracranial injury, such as an epidural hematoma (Fig. 22.3). After the intracranial injury has been corrected, the bone fragments are primarily replaced as a bone cranioplasty after cleaning.

FIGURE 22.3 Comminuted minimally depressed open skull fracture with underlying epidural hematoma. A, Computed tomography (CT) scan through the center of the depressed region. Note the small amount of air at the anterior edge of the epidural hematoma. B, Intraoperative view of the depressed bone before evaluation. C, The bone was removed, sutured together, and replaced as a cranioplasty. The epidural hematoma was removed after the bone fragments had been removed.

Missing bone can be replaced with a titanium mesh screen. If the skin is open, and free bone fragments are present, cleansing or débridement of the contaminated fragments is performed, before dural and scalp closure (Fig. 22.4). Bone too contaminated may be discarded, and a titanium screen is then used to span the bone defect (Fig. 22.5).

FIGURE 22.4 Comminuted skull fracture involving a diastatic fracture of both coronal sutures and additional fractures of the frontal and parietal bone bilaterally. In this case, the skin was open and cerebrospinal fluid was coming from the wound. A, Lateral radiograph demonstrating the comminuted fracture. B, Computed tomography scan with bone windows near the top of the head showing the comminuted fracture.

FIGURE 22.5 A titanium screen can be used to span a bone defect when autologous bone cannot be used because it is contaminated and must be discarded.

Depressed Skull Fractures

In a depressed skull fracture, the greatest bone depression can occur at the interface of fracture and intact skull or near the center of the fracture if several fragments are displaced inward. Impacted fractures may be “wedged” into position by blocked bone edges.

Management

Combined therapy of depressed fractures of the cranial vault extending to involve the frontal sinus or facial bones is covered in the sections on facial fractures. When a depressed skull fracture on the convexity also includes facial fractures, the intracranial injury is typically repaired first with removal of intracerebral hematoma and repair of dural laceration if present (Figs. 22.6 and 22.7).

FIGURE 22.6 Open frontal and facial fracture. A, View of frontal skull fracture under the wound. B, Computed tomography scan showing the epidural hematoma under this open skull fracture.

FIGURE 22.7 Open dressed skull fracture involving the frontal bone with extensive fractures and displacement of bones of the orbit and ethmoid region. A, Presenting scalp laceration. B, Computed tomography scan at the level of the orbit demonstrating extensive orbital and ethmoid fractures with displacement of the bony facial structures.

Although a focal neurological deficit from the cortex directly under a depressed skull fracture is occasionally improved by elevation of the bone fragments (presumably by increasing local cortical blood flow), elevation usually produces no neurological change, implying that the initial impact produces the major cortical damage responsible for the brain deficit. The brain dysfunction usually undergoes a neurological recovery phase of several weeks to months, similar to that after a stroke or head injury without a depressed fracture. Likewise, the incidence of epilepsy after a depressed skull fracture is determined by the cortical damage at the time of impact. Therefore, the treatment of depressed skull fractures is based on relieving pressure on the brain (initiating neurological recovery), minimizing epilepsy, correcting cosmetic deformity, and preventing infection.

In closed, depressed fractures, the major indication for surgery is usually cosmetic, with the procedure performed on an elective basis in the first few days after the trauma, once the patient is cleared for elective anesthesia. The greatest cosmetic deformity occurs in the forehead. Exploration is more urgent for a large, closed depressed fracture when the radiological appearance suggests dural laceration, brain penetration, simultaneous frontal sinus fracture, mass effect, or underlying hematoma. The hematoma is evacuated, the dura is repaired, and the bone fragments are replaced and held in position with small plates and screws.

A compound depressed fracture is a neurosurgical emergency because of the risk of bacterial infection of the cranial cavity. The initial surgery is performed within 24 hours and usually within the first 12 hours. The major objectives are removal of contaminated bone fragment and foreign material; débridement of devitalized scalp, dura, and brain; and provision of a watertight closure of the dura. Often, foreign material or hair wedged between bone fragments cannot be seen through the overlying scalp incision, so simple irrigation and closure may be inadequate for débridement of foreign material. Dural closure is essential to prevent CSF leaks from the wound and brain herniation into the fracture area. Dural closure is essential to prevent CSF leaks from the wound and brain herniation into the fracture area. Dural closure also presents intracranial spread of infection from a scalp wound. Reconstruction of the calvarium is performed during the initial surgery if considered safe: otherwise a cranial defect is left and the cosmetic repair is performed later. The major reasons to consider deferred calvarial reconstruction are to shorten additional anesthesia and blood loss by major head injury or multitrauma, especially with hemorrhage; gross contamination of wounds where the bone fragments cannot be adequately cleaned; and a delay of more than 24 hours for the initial surgery.

The scalp laceration associated with a compound depressed skull fracture is usually stellate and may contain areas of contused/devitalized tissue. These areas require débridement to normal vascularized scalp to allow prompt healing and prevent breakdown of the partially viable scalp covering the fracture site (see Fig. 22.1). Scalp breakdown can many times be treated locally but occasionally will require early flap coverage. If early flap coverage is not successful, the replaced cranial bone may require débridement of any dead or nonviable necrotic bone or portion of the skin flap; a subsequent flap rotation and delayed cranioplasty will be required in stages.

Depressed Fractures over Dural Sinuses

Depressed skull fractures over a venous sinus require special handling. Surgical elevation of these fractures may involve massive blood loss if a depressed fragment has been plugging a sinus tear. There are two strategies for management. The fracture can be carefully elevated, attempting to gain control of the venous sinus as soon as possible, preparing for significant transfusion requirements. If the fracture site is not grossly contaminated with foreign material, or will not cause a major cosmetic or functional deformity, or not cause intracranial hypertension secondary to sinus occlusion, such fractures are managed with scalp débridement alone and irrigation, followed by serial CT scans for signs of brain abscess for at least a year. A delayed cranioplasty may then be required for contour. The management of these fractures requires both judgment and experience as no definite rules apply to the variation of presentations.

Basilar Skull Fractures

Fractures of the base of the skull occur in 3.5% to 24% of head-injured patients. This wide variation results from differences in study populations and the difficulty in obtaining radiographic verification of the fractures. Linear fractures in the skull base carry a risk of meningitis, whereas this risk is extremely low in fractures of the convexity unless the scalp, bone, and dura are all violated. The dura is easily torn in a basal skull fracture; this places the subarachnoid space in direct contact with the paranasal sinuses or middle ear structures, providing a pathway for infection. For example, a persistent fistula allows a continuous CSF leak, and bacterial colonization of the meninges will eventually develop.

Petrous bone fractures can either be either longitudinal or transverse, relative to the long axis of the petrous pyramid. Longitudinal fractures are more common and usually involve the tympanic membrane or external ear canal, thereby producing otorrhea. Transverse fractures result from higher-energy impacts and can damage middle ear ossicles or the facial nerve. These fractures occur with or in continuity with linear, comminuted, or depressed skull fractures and not infrequently are large linear extensions of vault fractures, crossing the base of the anterior and middle cranial fossae (Fig. 22.8).

FIGURE 22.8 Type III frontobasilar fracture involves both the lateral and the central segments of the anterior skull.

Diagnosis

Clinical signs of basal skull fractures include bilateral periorbital ecchymoses (spectacle hematoma) (Fig. 22.9), anosmia, or CSF rhinorrhea for anterior skull base fractures, as well as hemotympanum, blood in the external auditory canal, seventh or eighth cranial nerve palsies, ecchymoses over the mastoids (Battle’s sign), or CSF otorrhea for temporal bone fractures (Fig. 22.10). Frequently, the CSF leak is first detected several days or weeks after the trauma. This delay often occurs because the CSF leak was hidden in bloody nasal discharge from facial fractures, or less frequently, it is the result of delayed development of hydrocephalus with rupture of the arachnoid at the fracture site. A larger clear ring surrounding a central blood-tinged clot when a few drops of bloody discharge are placed on a paper towel indicates that CSF is probably mixed with the blood. This sign (the “double ring”) can also be noted on the patient’s pillow during rounds.

FIGURE 22.9 Bilateral spectacle hematoma from an open frontal sinus anterior skull base fracture.

FIGURE 22.10 Cerebrospinal fluid leaks from the ear canal and a hematoma is visible in the postauricular area. These are signs of a fracture at the junction of the middle and posterior cranial fossa.

Basal skull fracture with CSF rhinorrhea is common after head injury and has an estimated incidence in the United States of 150,000 cases per year. A clear, watery nasal discharge containing glucose indicates CSF rhinorrhea. An intermittent CSF leak from the paranasal sinuses can often be demonstrated by having the patient sit on the edge of the bed with the head close to the knees for 2 minutes and watching for clear fluid to drip from the nose. CSF mixed with blood may form a halo on a piece of gauze it touches. Testing for beta-2 transferrin presence in the fluid confirms the protein found almost uniquely in CSF.

Assessment

The events of the injury should be ascertained and a complete history of the accident or injury should be reached as described by the emergency medical technician, patient, or family members. A thorough facial physical examination is performed in sequence, concentrating on functional deficits in areas of injury. Consultations from specific specialists, such as an ophthalmologist, are also obtained. Cranial nerve abnormalities may also accompany facial fractures; oculomotor deficit, facial sensory deficit, and visual deficit are some common symptoms.

Soft tissue injury implies the possibility of damage to deeper structures, which should be presumed until appropriate examination excludes them. Hematomas are usually diffuse, and not amenable to aspiration, but localized hematomas can be aspirated or removed to facilitate healing. Lacerations should be carefully debrided and repaired after damage to bones and deep soft tissue structures has been determined.

The facial bones should be examined in a methodical sequence from top to bottom. Symptoms that imply bone injury include soft tissue injury (contusion, laceration, hematoma), bone movement, crepitation, localized tenderness, discomfort, numbness in the distribution of a cranial sensory nerve, paralysis in the distribution of a cranial motor nerve, malocclusion, visual acuity disturbance, diplopia, facial deformity or asymmetry, intraoral lacerations, fractured or avulsed teeth, air in soft tissues, and bleeding from the nose or mouth. The examiner should palpate the symmetry of the facial bones, comparing both sides. In all cases reference to old photographs (such as a driver’s license) are valuable aids in documenting a preexisting facial deformity or in establishing a change from previous appearance. Dental malalignment (malocclusion) is an index of bone or tooth fracture, edema, or temporomandibular joint injury.

Facial sensation is noted in the supraorbital, supratrochlear, infratrochlear, infraorbital, and mental nerve regions of the trigeminal nerve distribution for both pinprick and light touch sensation. Diminished sensation in the distribution of a specific sensory nerve indicates injury from transaction, impact, or continued compression of the nerve as the result of a fracture. The facial nerve is tested by comparing facial expression bilaterally. Extraocular movements and pupil response are compared, evaluating symmetry, pupil size, and the speed of pupil reaction bilaterally to both direct and consensual responses to light.

Emergency treatment is immediately directed toward life-threatening events such as (1) airway obstruction, (2) bleeding (major hemorrhage from the scalp or face), and (3) aspiration (prevented when the airway is maintained by orotracheal intubation, although occasionally an emergency cricothyroidotomy is required). The stability of the cervical spine is assessed in every patient with head trauma during this phase.

The early management of maxillofacial injuries is based entirely on a good clinical examination and facial CT scans (Fig. 22.11). Soft tissue windows are necessary on the CT scan to evaluate the brain and orbital soft tissue fully. Axial (Fig. 22.12) and coronal CT bone windows (direct or reformatted) are crucial to reveal details of fractures of the upper face and orbit. Coronal sections (Fig. 22.13) begin with the nasal pyramid and continue posteriorly through the orbital apex. Axial scans begin at the superior aspect of the skull and progress through the brain with standard axial brain imaging. The size and spacing of the cuts at the level of the frontal sinus are reduced to 5 mm or less to obtain the required detail. When a mandible fracture is suspected, the axial CT scanning is continued through the entire mandible and temporomandibular joints, visualizing both the horizontal and vertical portions of the mandible and the temporomandibular joints. Although three-dimensional reconstruction with shading (Fig. 22.14) adds spatial information, it does not provide the detail of two-dimensional axial and coronal images. In some cases, special reconstructions, as one performed in the longitudinal axis of the optic nerve in orbital injury, provide additional information.

FIGURE 22.11 Two-dimensional facial computed tomography (CT) scans are essential in facial fracture evaluation. They can be rapidly obtained after the CT evaluation of the brain. Axial and coronal windows should be obtained through the entire area of the injury. Here, coronal CT scans demonstrate reduction of a zygomatic fracture by plate and screw fixation and orbital floor bone grafting.

FIGURE 22.12 Axial window of an orbital fracture. The globe is prolapsing into the floor defect.

FIGURE 22.13 Direct coronal windows are preferable for evaluation of the orbit, sinuses, and palate. Both soft tissue (A) and bone (B) windows should be obtained for the orbit. Two blow-out fractures are seen. In A the inferior rectus muscle is adjacent to the fracture. In B soft tissue windows clearly show the inferior meatus muscle adjacent to the fracture. C, Reformatted images may be obtained where the direct coronal image is not possible. Their clarity depends on the axial cuts.

FIGURE 22.14 Three-dimensional computed tomography (CT) scans add spatial perspective, but they do not replace two-dimensional CT scans and are not essential for fracture repair. A depressed zygomatic and orbital fracture is seen.

Associated Conditions

Facial Fracture Classification by Anatomical Region

The treatment of maxillofacial fractures is organized by anatomical region (Fig. 22.15). The frontal bone region includes the frontal bone, the supraorbital rims bilaterally, and the frontal sinus (Fig. 22.16