Traumatic Skull and Facial Fractures

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Chapter 22 Traumatic Skull and Facial Fractures

Clinical Pearls

Linear skull fractures do not require stabilization or treatment when the scalp is closed. Depressed skull fractures may need exploration depending on the extent of the injury to the underlying brain, frontal sinus, or facial bones. Closed depressed fractures are usually repaired for cosmetic reasons. Compound depressed skull fractures with brain involvement are often neurosurgical emergencies. It becomes an emergency to treat the underlying brain injury, perform a watertight closure of the dura, and débride the devitalized scalp.

Growing skull fractures, although rare, occur in children under 2 to 3 years of age and require surgical repair. If there is a tear in the dura accompanying a skull fracture after trauma, the pressure of the brain pulsations in a growing brain may enlarge the fracture and dural opening. The brain can herniate through this skull defect, causing a pulsatile mass under the scalp.

Basilar skull fractures may present with periorbital ecchymoses, hemotympanum, or ecchymosis over the mastoid. The management of these fractures is usually conservative unless a cerebrospinal fluid (CSF) leak is present. Many traumatic CSF leaks will spontaneously resolve in a week. Those that do not may be managed by CSF drainage, or in some cases surgical repair to avoid infection, once the location of the leak is identified.

Frontal sinus fractures can be diagnosed on computed tomography (CT) and are managed differently depending on whether the frontal or posterior wall is disrupted. Orbital fractures are managed based on the extent of the injury to the globe, optic nerve, and orbital contents. Patients with a fluctuating or worsening visual acuity will require decompression of their optic nerve and relief of globe pressure. There are two indications for surgery of orbital “blow-out” fractures: (1) muscle or ligament entrapment with diplopia or (2) enophthalmus (backward dislocation of the globe) caused by prolapse of the orbital contents through the fracture. Le Fort fractures are often injuries to the entire midface region. Their surgical management depends on the extent and stability of the maxillary fracture.

Skull Fractures

Skull fractures are classified in three ways: by pattern (linear, comminuted, depressed), by anatomical location (vault convexity, base), and by skin integrity (open, closed). The pattern of a skull fracture is affected by two factors. The first factor is the force of impact. A linear fracture results first at a point of weakness when the skull structure fails to undergo further elastic deformation as a response to impact; the fracture typically starts at the point of weakness in response to the maximal stress (the point of weakness is often remote from the actual impact point) and then extends to the point of impact. A comminuted fracture results when the impact force is sufficient to break the bone into multiple pieces under the point of impact and further through areas of weakness. Comminution absorbs the force of the injury. With even larger impact energies, the comminuted pieces can be driven inward to create a depressed fracture and may penetrate the dura and cortical surface of the brain.

The second factor is the ratio of the impact force to the impact area. If the impact, even one of high energy, is dispersed over a large area, as in a blunt head injury to an individual wearing a motorcycle helmet, it often produces no skull fracture, even though the brain may be severely injured. Parenthetically, it should be noted that some helmets, by the efficiency of their very force-transferring protection, have created basal skull fractures by transferred energy absorbed from protection of the vault and face and then transmitted through the mandible via the chin strap to the skull base. However, if the impact, even one of low energy, is concentrated in a small area, such as from a hammer blow, it often produces a small depressed fracture with multiple linear skull fractures radiating from the site of impact.

The location of a skull fracture is classified by its geography in two distinct areas: the skull convexity (generally termed skull vault fracture) or the base of the skull (generally termed basilar fracture). Any of the two areas can occur singly or in combination. The pattern may also become more comminuted with increasing energy forces. A skull fracture can be further classified as “open” or “closed” by the presence or absence, respectively, of an overlying scalp laceration. In addition, a fracture extending into the skull base with violation of the paranasal sinuses, the nose, middle ear, or mastoid structures is also considered an “open” fracture.

Linear Skull Fractures

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

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.

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.


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.

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).

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.


Some patients with depressed skull fractures experience initial loss of consciousness and neurological damage owing to the force transferred from the impact through the skull and into the brain. However, 25% of patients experience neither loss of consciousness nor neurological deficit. Another 25% of patients experience only brief loss of consciousness. Although the diagnosis of a depressed skull fracture is often indicated on routine skull radiographs by an area of double density (overlying bone fragments) or by multiple or circular fractures, the full extent and depth of injury are rarely appreciated with a CT scan. Physical examination is more difficult in the presence of scalp mobility and swelling. Scalp mobility can result in nonalignment of the sheared layers of the scalp or a scalp laceration and can therefore simulate, under palpation, the sense of a skull fracture; normal skull under a scalp laceration also does not exclude a depressed fracture 1 or 2 cm from one edge of the laceration. Furthermore, post-traumatic swelling of the scalp minimizes the palpable and visual appearance of the step-off at the bony edges, preventing accurate clinical assessment of the extent of a skull deformity or displacement for the first few days.

CT is the diagnostic method of choice. When image display windows are adjusted to optimize bony detail, they display the position, extent, and number of fractures as well as the presence and depth of depression. With the imaging windows set to optimize intracranial contents, the same CT scan also allows assessment of the underlying brain for contusion or hematoma, small bone fragments, or foreign bodies as well as other intracranial trauma. Occasionally, coronal CT images through fractures near the vertex of the head or extending into the skull base are used to supplement the standard CT images, because the depth of a depression is more accurately measured on CT images perpendicular to the depression.


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).

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.

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).


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.

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.


Basal skull fractures are managed depending on whether a CSF leak is present. A patient with a basal skull fracture but no leak is observed for 2 to 3 days. During this time, repeated checks for rhinorrhea and otorrhea are made to verify the absence of a CSF leak. Otorrhea is more likely than rhinorrhea to resolve spontaneously. Because antibiotics are not effective in preventing meningitis over a prolonged interval and select for resistant organisms if an infection occurs, “prophylactic” antibiotics are not used on a prolonged basis in patients with basal skull fractures. When definitive closure of a leak is performed, perioperative antibiotics are utilized.

A CSF leak is managed initially by observing the amount of leakage and monitoring for signs of infection: change in temperature, altered mental status, or increased white blood cell count. Radiographic or imaging studies may indicate the area and size of the defect, which may suggest the likelihood of spontaneous closure. Most traumatic CSF leaks resolve spontaneously within the first week. If the leak persists beyond 5 to 7 days, lumbar punctures are performed daily for 3 days, removing 30 to 50 mL of spinal fluid each time, attempting to decrease the CSF pressure.

If spinal taps fail to stop the leak, spinal drainage can be used for 72 hours with the patient in a 30-degree head-up position. Should pneumocephalus develop during the course of the CSF drainage, the drainage procedure is terminated and the dural leak is surgically closed. CSF leaks refractory to spinal fluid drainage require surgical closure; the exact site of the leak is determined preoperatively from a CT scan with water-soluble intrathecal contrast or from a nuclear cisternogram with nasal pledgets for small or questionable leaks. A CT scan of the base of the skull can provide additional details of the pattern and size of the bone spicules in the fracture.

CSF otorrhea usually occurs through a fracture in the petrous bone with perforation of the tympanic membrane, although it can occasionally take place through a laceration of the external canal via fractured mastoid air cells. If the tympanic membrane remains intact, CSF that has gained access to the middle ear can flow through the eustachian tube and present as rhinorrhea. In these cases, the CT scan typically images a fracture in the temporal bone and fluid in the mastoid air cells and middle ear. Blood from the ear canal or a tympanic canal laceration may also be caused by a temporomandibular joint injury or dislocation, either of which may produce some of the same symptoms (bloody fluid from the ear canal).

A patient with CSF otorrhea often presents with hearing loss from blood in the external ear canal. Irrigation and probing of the ear in cases of suspected otorrhea are not indicated initially because they increase the risk of infection. Such a patient is managed by placing a loose-fitting sterile gauze pad over the ear; the pad is changed every nursing shift and saved as an indicator of the amount of drainage from the ear. Most cases of otorrhea stop spontaneously within the first few days. A detailed auditory, vestibular, and facial nerve function examination is performed initially and 6 to 8 weeks after trauma to diagnose abnormalities and determine treatment or sequence progress.

Patients with basilar skull fracture who have immediate complete facial nerve paralysis and temporal bone fracture are considered for high-dose steroid treatment or surgical exploration to decompress or graft the nerve. Patients with delayed onset of the facial paralysis or those who initially have only facial paresis are treated with steroids, and observed, because some spontaneous recovery frequently occurs.

Maxillofacial Injuries

Skull and maxillofacial fractures often coexist after head trauma. For instance, fractures of the frontal bone or basilar skull commonly extend into the orbit, and midfacial fractures frequently accompany frontal skull, frontal sinus, or orbital fractures. In addition, fractures through the skull into the nasal sinuses can cause dural lacerations with CSF leak or pneumocephalus. When maxillofacial injury is suspected on physical examination, a CT scan of the face is the most useful diagnostic test and should be obtained at the time of the initial radiographic survey. Facial CT scans should consist of bone and soft tissue windows and axial and coronal sections.


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.

Associated Conditions

Profuse Hemorrhage

Cutaneous bleeding that accompanies facial lacerations is usually controlled with digital pressure, which allows precise identification of the bleeding vessel for control or ligature. Blind probing in facial tissue or unselective cautery or ligature placement can damage branches of the facial nerve and should be avoided.

Bleeding from closed maxillofacial injuries usually results from fractures involving the sinuses. Bleeding from the nose (epistaxis) occurs with nasal, zygomatic, orbital, frontal sinus, nasoethmoidal, maxillary, and cranial base fractures. Although profuse nasopharyngeal hemorrhage usually accompanies Le Fort maxillary fractures, epistaxis is a nonspecific indication of many types of midfacial fractures. Usually the hemorrhage is self-limiting. Several maneuvers control the hemorrhage when required, including anteroposterior nasal packing, manual repositioning of the maxilla, the application of intermaxillary fixation (rest position of the maxilla), or an external facial compression (Barton) dressing.

If profuse nasopharyngeal hemorrhage from closed fractures does not respond to the preceding measures, arterial embolization or arterial ligation can be performed. An angiogram is obtained to determine the major source of bleeding. In Le Fort fractures bleeding usually involves the branches of the internal maxillary artery. This artery can be embolized or selectively ligated directly through the back wall of the maxillary sinus, or arterial ligation of the external carotid and superficial temporal arteries (both) on the ipsilateral side usually reduces such bleeding substantially. Arterial ligation is rarely necessary.

Because bleeding abnormalities are noted early in patients with cerebral injuries and facial fractures, replacement of depleted coagulation factors is based on assessment of coagulation factors in hemorrhaging patients.

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

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