■ Part 2. Operative Technique and Exemplary Repair
Injury to the anterior cranial vault may conveniently be perceived as a cascade, 11 similar to that suggested by Sturla for nasal injuries and by Pollock for palatal fractures. This concept encourages thorough clinical examination and radiographic assessment beyond the zone of apparent trauma because of high incidence of collateral injury ( Fig. 6.23 ).
Preoperative Assessment and Indications for Repair
Widespread injury is often present when load forces of sufficient magnitude reach the cranial base and fractures of the anterior, middle, and/or posterior cranial vault occur.1 , 3 , 19 , 21 – 23 , 31 – 46 The clinical findings are thus often diverse. Central nervous system injury may be present but relatively occult (i.e., cerebral contusion), such that it is apparent only to discerning examination. Lacerations over the frontal boss, temporal fossa, or occipital scalp are more obvious, but in the presence of fracture may violate the dura, creating a conduit that allows CSF leak. By definition, an intracranial injury should be suspected in this setting until proven otherwise.
The passage of blood through intracranial vessels may cause secondary, pulsatile movement of the globe of the eye when fractures of the medial orbital roof (lateral frontal sinus floor) are present. Also, the temporal bone is closely aligned with vascular structures, such as the venous sinuses and jugular bulb. It is thus no surprise that patients with temporal fractures may present with hemotympanum, or venous blood in the external auditory canal.
Consultation with multiple specialties is expected in these patients with diverse injury. Repetitive study of radiographs and serial clinical examination of the patient are advised46 to uncover occult pathology, such as cerebrospinal leak (rhinorrhea and/ or otorrhea), cranial nerve dysfunction, epidural hematoma, or injury to brachial plexus or cervical spine (see Chapters 2 and 9).
The modified Glasgow Coma Scale (GCS) first reported by Teasdale and Jennett47 (15 the best prognosis, and 3 the worst) and the Brain Injury Index described by Jennett and Bond48 (Grade I, loss of consciousness, to Grade IV, brain death) are useful measures that quantify the severity of head injury and the level of consciousness. Although the statistical relationship between the intracranial injury and a specific craniofacial fracture is imprecise,49 most patients with severe head injuries (a score of less than 8 GCS) or major skull fractures (open, depressed, basilar, or compound) usually trigger early neurosurgical intervention.50 , 51
Neurosurgical intervention in patients with combined injuries of the cranium and face is undertaken on average in one of three cases. In the two of three cases, no deviation from routine management of facial fractures is required, despite the additional presence of cranial fractures, because their cranial injuries are solely observed for evidence of increased intracranial pressure.49 , 52 , 53
Medical management is directed toward the resolution of cerebral edema and restoration of cerebral microperfusion50 with high, so-called neurosurgical doses of steroid. An infusion of 1 to 2 g of methylprednisolone every 6 hours is not uncommon for a brief period of time. Maurice-Williams27 has recently urged awareness of temporal lobe contusion (and regional edema) associated with craniofacial injury, such as might occur in the presence of fracture(s) of the greater wing of the sphenoid and posterior displacement (buckling) of the orbital plate of the zygoma.
HRCT has been available for some 30 years, and isolated fractures of the anterior cranial vault and combined injuries of the cranium and face have been a focus of interest for the duration.25 , 35 , 37 , 54 These radiographic studies now offer the radiologist, neurosurgeon, and reconstructive trauma surgeon a clear declaration and record of the extent of combined injury.
Routine radiography and screening computed tomography (used in emergency departments to document expanding subdural or epidural hematoma) do not provide sufficient detail of fractures of this obscure region. Computed tomography sent with patients from regional centers often cannot be used in the presence of severe injury.
HRCT with 1.5- to 2.0-mm cuts offers greater detail of the injury and favor appropriate care and defined surgical intervention.
Frontal Sinus Fractures
Fractures of the frontal sinus may be isolated to either the anterior table or the posterior table or involve both tables.
The injury similarly may traverse the floor of the frontal sinus medially, laterally, or both. In the extreme, the frontal sinus fracture is part of a fault extending to the cribriform plate and the skull base ( Fig. 6.24 ).
Fractures of the frontal sinus are arbitrarily and conveniently divided into four components,11 based on radio-graphic assessment by HRCT:
The anterior table
Medial sinus floor, FSOFT, and nasoethmoid complex (anterior and middle ethmoid cells)
Lateral sinus floor and anteromedial orbital roof
The posterior table and dura (particularly in the area of the crista gall)
Fractures of the anterior table are dependent on the pneumatization of the frontal sinus. Lacerations over the frontal boss are common and may extend upward as a scalping avulsion or may descend to involve the nasal and nasomaxillary regions.
Displaced fractures of the posterior table of the frontal sinus imply rents in the dura and suggest the need for neurosurgical consultation and surgical intervention. Fractures of the posterior table on occasion occur without fractures of the frontal sinus floor or anterior table; in our experience, this occurs with trauma to the back of the head (occipital impact, leading to occipital-frontobasilar fracture). The incidence of posterior table or anterior- and-posterior table fractures has progressively increased since the mandated use of seatbelts and the ensuing increased rates of survival ( Fig. 6.26 ).
Isolated fractures of the ethmoid and sphenoid roof are obscure and best referred to simply as basilar. In their presence, “coned down” views of the optic strut and optic canal (see Chapter 8) and the wings of the sphenoid are taken. Most frontobasilar fractures deviate laterally when reaching the roof of the sphenoid sinus, to end at the foramen ovale, foramen lacerum, foramen spinosum (OLS), or carotid canal.
Fractures of the floor of the frontal sinus and posterior table may extend through the base of the crista galli, cribriform plate (ethmoid), and roof of the sphenoid sinus. In this instance, the fracture is said to be frontobasilar.21 , 37 , 54 Like isolated basilar fractures, the frontobasilar fracture ends among the cluster of foramina (OLS) in the posterolateral sphenoid ( Fig. 6.27 ).
Temporobasilar Bone Fractures
Fractures of the temporal bone are seldom isolated. More often, a fracture sufficient to extend through the dense bone of the petrous pyramid also involves paratempo-ral bone. In a large majority, the fault also reaches the nearby cluster of foramina (OLS) in the greater wing of the sphenoid. Thus, it follows in many cases, temporal bone fractures are in fact temporobasilar . The term is more inclusive and more descriptive of the extent of injury, and we have long encouraged its use when appropriate.
Temporobasilar fractures are parallel, transverse, or oblique to the long axis of the petrous pyramid.55 – 72 The incidence of these categories varies greatly between surviving patients and postmortem cohorts,58 – 62 , 64 , 66 , 71 creating controversy.
Eighty percent of temporobasilar fractures are said to be longitudinal because they parallel the architecture of the pyramid. They usually follow a blow to the side of the head. The fracture begins in the bony ear canal (at the posterior root of the zygomatic process), traverses the tympanic membrane, crosses the notably thin attic (roof) and tegument tympani of the middle ear cavity, skirts the roof of the glenoid fossa and the labyrinth (otic capsule), and runs near the margin of the carotid canal, ending in the cluster of foramina (OLS) nearby ( Fig. 6.28 ).
Some one in five patients with longitudinal tem-porobasilar fractures suffer facial nerve paralysis and, when present, it tends to be incomplete.56,59 , 60 Most facial nerve injury associated with longitudinal fracture occurs in the area of the geniculate ganglion . Some authors suggest that traction on the facial nerve by the greater petrosal nerve, in the area of the ganglion, plays a role in the etiology of this injury.69
When the longitudinal fault crosses the middle ear cavity, there is usually tympanic disruption and perhaps ossicular derangement.60,61,70 , 71 Hough suggests a specific incidence, in decreasing order, when such is the case: incudostapedial separation >>> incus dislocation (“incu-do-toss”) >> fracture of the stapedial arch > fracture of the handle of the malleus.61
Upon disruption of the ossicular chain, the “molar tooth” sign, created by the outline of the malleus and the incus in the lateral HRCT projection, is obscured. The “crown of the tooth” is formed by the head of the malleus and the body of the incus, the “anterior root” by the handle of the malleus, and the “posterior root” by the long process of the incus,73 and these normal features are disrupted after trauma. Middle ear exploration/reconstruction may be required to reconstitute the displaced ossicular chain ( Fig. 6.29 ).
Twenty percent of temporobasilar fractures are transverse or mixed fractures of the temporal bone68 and often are part of occipitobasilar fractures.