Fig. 8.1
The frontobasilar region: (a–c) Borders of the frontobasilar region. (d) Energy required for different facial segments to fracture [150]
The basilar region is also subdivided into the central and two lateral zones. The superior NOE complex, cribriform plate of the ethmoid bone, and planum sphenoidale form the central zone, and two lateral zones are comprised of the superior and lateral orbital walls and the orbital apex.
8.1 Epidemiology of Frontobasilar Fractures
Injuries involving the frontobasilar region comprise 5–28 % of all facial fractures [3–6]. The main reasons include motor vehicle accidents (55 %) and falls (35 %) [5, 7, 8]. This variety of fracture occurs 95 % of the time in 30–40-year-old men.
8.2 Classification of Frontobasilar Fractures
The classification of frontobasilar fractures proposed by Burstein et al. [2] relies on CT data and is based on the anatomical subdivision of the frontobasilar region (Table 8.1 and Figs. 8.1 and 8.2).
Table 8.1
Classification of frontobasilar fractures
Injured area | Central zone (type 1) | Lateral zone (type 2) | Their combination (type 3) |
|---|---|---|---|
Frontal (F) | Frontal bone | Lateral two-thirds of the supraorbital region | 1F + 2F |
Frontal sinuses; | Squama of the temporal bone | ||
The medial third of the supraorbital region | |||
Basilar (B) | NOE complex | Orbital roof | 1B + 2B |
Cribriform plate | Lateral orbital wall | ||
Planum sphenoidale | Orbital apex | ||
Frontobasilar (FB) | 1F + 1B | 2F + 2B | Any combination of F and B fractures |
Fig. 8.2
Classification of frontobasilar fractures proposed by Burstein et al. [2]: Type I (central) fractures are confined to the superior naso-ethmoidal complex, the midfrontal bone, and the medial third of supraorbital rims medial to the supraorbital notch. The frontal sinus is bilaterally involved (a, 1F type; b, 1B type; c, 1F + 1B type). Type II (unilateral) fractures involve the entire supraorbital rim and the upper portion of the lateral orbital wall. They spread to the squama of the temporal bone and the ipsilateral frontal bone and affect the frontal sinus. The NOE complex remains unaffected (d, 2F type; e, 2B type; f, 2F + 2B type). Type III (bilateral) fractures include fractures of the upper portion of the naso-ethmoid complex, bilateral fractures of the supraorbital rim, fractures of the upper portion of the lateral orbital wall, and bilateral fractures of the frontal bone (g, 1F + 2F type; h, 1B + 2B type; i, F + B type)
Thus, the 1F fracture combines fractures of frontal sinus walls and glabellar fractures, while the 2B fractures include fractures of the orbital roof and apex and local fractures of the orbital roof.
The combined fracture (Type 3) is the most frequent variety.
8.3 Fractures of Walls of the Frontal Sinus
Fractures of walls of the frontal sinus comprise 5–15 % of all facial fractures. They are accompanied by severe head injury 50 % of the time and with other maxillofacial injuries 70–80 % of the time [5, 11, 13]. This variety of fractures is usually a component of multiple traumatic injuries and accounts for the relatively high (5 %) mortality rate among this cohort of patients [5, 8].
Both sinus walls are affected in 70 % of these injuries; the frontonasal duct is involved in ~10 % of patients [7]. Fracture of the posterior wall of the sinus is much more serious because of the higher risk of CSF leak and concomitant brain damage. While the incidence of open and closed fractures is virtually identical, the complication rate accompanying open fractures is three times higher than that for a closed fracture.
Fractures of frontal sinus walls in children typically affect the orbital roof. The NOE complex is involved in 30 % of patients, while nasal bones are affected in 60 % of cases [14]. The injury is accompanied by a higher (60–70 %) risk of CSF leak and intracranial damage, such as hemorrhage to the cranial parenchyma and cranial floor, and pneumocephalus compared to adults [7, 14, 15].
8.3.1 Classification of Fractures of Frontal Sinus Walls
The classification is based on three criteria: conditions of the anterior and posterior walls and the frontonasal duct [5, 7].
Type 1: linear fractures of the anterior wall with minimal displacement of bone fragments or without any displacement.
Type 2: comminuted or blow-in fractures of the anterior wall involving or not involving the frontonasal duct. Approximately 30 % of all injuries are type I and type II fractures [16].
Type 3: comminuted fractures of both walls of the frontal sinus.
Type 4: comminuted fractures of both walls with injury to the dura mater and CSF leak. Type 4 comprises almost 40 % of all the injuries [7].
Type 5: the same with damage to soft tissues and/or bones (Fig. 8.3).
Fig. 8.3
Fractures of frontal sinus walls (frontal and lateral view): (a, b) A linear fracture of the anterior sinus wall with or without the minimal displacement of bone fragments (type I). The posterior wall and the cribriform plate were not affected (shown with arrows). (c, d) A comminuted fracture of the anterior wall, while the posterior wall and the cribriform plate were not affected (type 2). (e–h) A fracture of both sinus walls (type 3). The absence of a CSF leak is caused by the fracture of the posterior sinus wall without displacement of bone fragments (shown with arrows) (Cited from Bell et al. [5]; Montovani et al. [7]). (i, j) A comminuted fracture of both sinus walls with CSF leak (shown with arrows) through the damaged posterior wall and the cribriform plate (type 4). (k–n) A comminuted fracture of both sinus walls with CSF leak and the concomitant defect of soft tissues and bones (type 5) (shown with arrows) (citation from Bell et al. [5]; Montovani et al. [7]). (o, p) An isolated fracture of the posterior wall of the frontal sinus
One should bear in mind that:
There have been anecdotal reports of isolated fractures of the posterior wall of the frontal sinus (less than 1 % of cases) (Fig. 8.3o, p).
Fractures of both sinus walls, as well as involvement of the NOE complex or the medial orbital rim into the fracture, explicitly indicate that the frontonasal duct is injured.
The traumatic impact is sometimes confined to wavelike deformation of the anterior wall with the energy transmission to the frontonasal duct, thus affecting its function of aeration. The force may also be transmitted to the optic canal or the superior orbital fissure, resulting in the superior orbital fissure syndrome or the orbital apex syndrome.
8.3.2 Clinical Presentation of Fractures of Frontal Sinus Walls
Eighty-two percent of conscious patients complain of pain in the fracture area. Fifty percent of patients have skin defects in this area; 25 % of them have an obvious depression [17] (Fig. 8.4).
Fig. 8.4
Clinical presentation of the fracture of frontal sinus walls: (a) Skin wound in the frontal region. (b) Depression of the frontal region (shown with arrows along its perimeter). (c) A comminuted fracture of the anterior wall (type 3); the supraorbital neurovascular bundle is shown with an arrow. (d) Orbital emphysema (shown with arrows) causing hypoglobus and exophthalmos. (e) A CT scan of a glabellar (type 1F) fracture. (f) Appearance of a female patient with a glabellar defect; its borders are shown with arrows (Reproduced with permission of professor G.A. Khatskevich)
Approximately half of patients have neurological findings. These may be secondary to brain concussions or sub- and epidural hematomas requiring emergency drainage in 10 % of cases. The most severe fractures (2.5–13 % of all sinus injuries) are complicated by open head injury.
A third of the fractures of frontal sinus walls are accompanied by leakage of CSF from the skin wound [18]. Leak of CSF fluid from only one naris usually, but not always, indicates the side of rupture in the dura mater. A CSF leak is sometimes disguised as lacrimation1 or massive edema of the upper eyelid that is disproportional to the “minimal” injury to the frontal region. This is a sign that CSF has accumulated in soft tissues [19–22]. One should bear in mind that a nasal CSF leak can be absent within the first several hours or even days after trauma because of occlusion of the rupture of the dura mater by swollen brain tissue or obstruction of the ethmoidal labyrinth by a blood clot [1, 11].
CT cisternography and/or nasal endoscopy with preliminary intrathecal (subarachnoidal) injection of fluorescein may be required in patients with the minimal trauma of the sinus to diagnose a CSF leak [11]. Concomitant anosmia indicates that the defect of the dura mater fused to the cribriform plate of the ethmoid bone is the most likely source of CSF leak. Injury to the posterior wall of the frontal sinus is a source of a leak much less often. The olfactory ability remains unaffected in this case.
In some cases the only sign of penetrating head trauma is pneumocephalus, an accumulation of air in the epidural, subdural, subarachnoidal, or intraventricular spaces. This is caused by a combination of a valve effect in the fracture area and the negative intracranial pressure in patients with a profound CSF leak. Unlike a CSF leak which involves the frontal sinus, the presence of pneumocephalus only indicates that there is a cranial fracture but does not necessarily localize it to the frontal sinus [23]. Furthermore, presence of pneumocephalus does not predict a prolonged leak. Since there are no characteristic clinical signs, pneumocephalus is typically diagnosed radiologically [24].
At least of 25 % of injured patients have defects of the visual system, such as traumatic optic neuropathy, damage in the optic chiasm, oculomotor nerves palsy, or, less frequently, scleral rupture, intraocular hemorrhage, and retinal detachment.
Infrequently the fracture may spread along the floor of the anterior cranial fossa to the middle fossa and have corresponding symptoms, or it may spread along the squama of the temporal bone, accompanied by dysfunction of the facial and vestibulocochlear nerves.
8.3.3 Radiological Diagnosis
Extensive injuries to frontal sinus walls, such as composite or comminuted fractures, are seen quite easily in panoramic X-ray images or seen in more detail in images in the nasomental view. Isolated injuries to the supraorbital rim are imaged as an angular stepwise deformity or fragmentation; shadowing of the sinus is usually seen because of blood in the sinus. Pneumocephalus is sometimes detected. A fracture of the posterior wall of the frontal sinus, in particular a linear one, may not be visible by plain radiological examination. Hence, plain radiological examination should be used for diagnosis only if computed tomography is unavailable2. Otherwise, CT scanning of all cranial segments should be carried out.
Coronal CT scanning allows the surgeon to diagnose an injury to the frontal recess. Axial CT scanning is indispensable for verifying fractures of sinus walls. Sagittal CT scanning is the most informative method as it shows all the signs of frontal sinus injury listed above (Fig. 8.3) [25]. Multiplanar reconstructions are used to assess the spatial arrangement of the dislocated bone fragments.
Neurological symptoms and ophthalmic disorders are indications for examining the brain, orbital apex, optic canals, and sella turcica [20, 26–28].
Since the treatment strategy largely depends on the extent of damage to the frontonasal duct, special attention should paid to such radiological signs as destruction of the anterior ethmoidal air cells and fracture of the floor of the frontal sinus when analyzing X-rays.
One should bear in mind that only 80 % of frontobasilar fractures can be visualized by neuroradiological methods.
8.3.4 Treatment of Fractures of Frontal Sinus Walls
There are four treatment regimens: (1) the watch-and-wait approach, (2) open reposition and rigid fixation of the fracture without obliteration/cranialization of the frontal sinus, (3) obliteration, and (4) cranialization. The choice for the specific treatment strategy relies on two criteria: damage to the nasofrontal duct and presence of persisting CSF leak.
Sixty percent of the time, the watch-and-wait approach is appropriate because there is minimal, less than 2 mm, displacement of bone fragments (type 1) [1, 5, 6, 29]. Surgical intervention is required in all other cases.
Surgical management of frontal sinus fractures aims at:
Preventing immediate or early cerebral complications of trauma (CSF leak, meningitis)
Restoring nasofrontal duct patency
Preventing late complications, such as osteomyelitis of the frontal bone, chronic frontal sinusitis, mucocele, mucopyocele, and cerebral abscess
Restoration of the frontal contour
8.3.4.1 Optimal Surgery Time
Selecting the optimal surgery time can be rather challenging, especially if the frontobasilar fracture is accompanied by other head and midfacial injuries [7, 30]. In this situation, the brain injury can be life-threatening, and it is extremely important not to aggravate patient’s condition by early surgical management of the facial injury. On the other hand, taking into account the suboptimal outcomes of secondary reconstructions, frontobasilar fractures should be operated on as early as possible. It is important to use the individualized and multidisciplinary approach in this case, which would allow the surgeons to choose the optimal strategy in each particular case [14, 15, 27].
First and foremost, neurosurgical management of penetrating head injuries with extensive tissue damage and exposure of the brain parenchyma or other life-threatening injuries or other injuries with a high risk of neurological deficit is performed [31, 32]. It is followed by surgical management of open-globe injury and optic nerve decompression. The frontal sinus walls are reconstructed only after 10–14 days.
Delayed surgical intervention is significantly complicated by the formation of granulation tissue between bone fragments, development of persistent soft tissue swelling, and high risk of infectious complications caused by inadequate drainage of the injured paranasal sinuses [1, 20].
Hence, a tendency toward early one-stage and thorough surgical management of frontobasilar and orbitofacial fractures has recently been described [31]. The practice has demonstrated that early one-stage surgeries are technically simpler, have less complications, and have better aesthetic outcomes. Contrary to what one might expect, if the multidisciplinary approach is used, the one-stage surgery may not aggravate preexisting neurological deficits [33, 35, 36].
8.3.4.2 The Main Surgical Stages
Approaches to the frontal sinus. The choice of an approach depends on fracture length and the degree of involvement of the brain and meninges in the traumatic process.
The approach through the wound, as well as the superciliary, trans-superciliary and superior supratarsal incisions, can be used in patients with an isolated fracture of the anterior wall not affecting the frontonasal duct and/or the medial orbital rim and having no concomitant craniofacial pathologies (type 2) (Fig. 8.5) [37–40]. The endoscopic approach can be used in some cases [41–45]. The bicoronal or vertex approaches that provide good overview of the entire frontobasilar region are recommended for all other types of frontal sinus fractures [15, 46].
Fig. 8.5
Some approaches to the frontal sinus: (a) Approach through the existing wound. (b) The superior supratarsal approach. (c) The superciliary approach. (d) Skin incisions to place an endoscope and an elevator. (e) Visualization of the fracture area. (f) The suture running through all the layers of external soft tissues (skin, mimic muscles, and periosteum) that improves the view (Materials from www.aofoundation.org were used for this illustration)
Reposition of bone fragments without frontal sinus obliteration is recommended only for type 2 fractures that do not affect the frontonasal duct. This situation is found in about 25 % of patients [5]. The surgery in this case consists in mobilization and reposition of fragments of the anterior sinus wall followed by rigid fixation with low-profile titanium constructs and keeping the mucous membrane intact (Fig. 8.6) [5, 47]. Closed repositioning proposed by Piccolino et al. [6] can be used in some cases of type 2 fractures. Using CT guidance, a percutaneous screw is placed into the center of a depressed bone fragment which is then used to lift the fragment to its original position (Fig. 8.6d).
Fig. 8.6
Management of the isolated fracture of the anterior frontal sinus wall: (a) Schematic view of the fracture. (b, c) Bone fragment repositioning with an elevator. (d) Distraction of the bone fragment using a screw placed in it. (e) Intraoperative evaluation of the integrity of sinus floor. (f) Rigid fixation of bone fragments with low-profile titanium constructs (Materials from www.aofoundation.org were used for this illustration)
Type 2 fractures involving the NOE complex and/or the superomedial orbital rim explicitly indicate that the frontonasal duct has been injured and there is a need for sinus obliteration [31, 48]. Sinus obliteration is also required for all type 3–5 fractures. The borders of the frontal sinus should be meticulously identified at the first stage of the surgery using one of the four methods: (1) bayonet forceps can be used as a probe determining the borders of the sinus cavity; (2) direct observation can be done using endoscopic illumination; (3) an unmagnified X-ray of the frontal sinus can be displayed to compare with the surgical field; and (4) a tele-imaging system can also be utilized (Fig. 8.7a–e). The frontal wall is removed with a drill and bone-cutting forceps; the mucous membrane is then detached (Fig. 8.7f–i). The mucosa and periosteum are then removed from all the sinus segments using a drill and various burs (Fig. 8.7j, k) [49]. If a fracture of the posterior sinus wall is less than 25 % of its surface area, the fragments are removed and the dura mater is inspected to find any lesions that require meticulous closure (Fig. 8.7l–p).
Fig. 8.7
Obliteration of the frontal sinus. Its borders are identified at the first stage: (a) Using a bayonet forceps. (b) Using endoscopic illumination. (c, d) Using a template made of the unmagnified X-ray of the frontal sinus. (e) Using a tele-imaging system. (f) Drilling multiple perforations in the bone. (g, h) The frontal sinus with anterior wall is removed. (i–k) The mucosa and inner osteal layer are meticulously removed. (l) Treatment of a small defect in the posterior sinus wall. (m, n) The posterior wall of the frontal sinus is removed. (o) Nibbling away at fracture edges with bone-cutting forceps; the brain parenchyma is protected by retractors. (p) Occlusion of the frontonasal duct. (q) Filling the sinus lumen with autologous fat tissue. (r) Rigid fixation of fragments of the anterior sinus walls with titanium constructs (Materials from www.aofoundation.org were used for this illustration)
The next stage is obliteration of the frontonasal duct to prevent contamination from the nasal cavity and to prevent the ingrowth of the mucous membrane of the ethmoidal labyrinth into the frontal sinus. The duct is broadened by carefully destructing the upper ethmoidal air cells, the mucosal remnants are removed, and the duct is tightly plugged with autologous fascia or muscle (Fig. 8.7q).
The sinus cavity can be left empty relying on subsequent osteogenesis. However, it is usually filled with autologous fascia or adipose tissue, pericranium, muscular tissue, milled bone, hydroxyapatite, or carbon (Fig. 8.7r) [50, 51].
Cranialization of the frontal sinus has been described especially for extensive fractures of its posterior wall occupying over 25 % of its surface area and accompanied by a CSF leak and/or soft tissue and bone defect (types 4 and 5). The procedure is identical to obliteration but there is one exception: the posterior wall of the frontal sinus is completely removed during the surgery for injuries to the brain [52]. Treatment of the rupture of the dura mater and obliteration of the frontonasal duct is then performed. The final stage of the surgery includes repositioning and rigid fixation of anterior wall fragments performed according to the conventional procedures.
The CAD/CAM method provides precise reconstruction of the supraorbital rim and the anterior sinus wall with a titanium implant that is a mirror reflection of the contralateral healthy orbit. It renders invaluable help in patients with unilateral comminuted fractures [53]. In much more severe bilateral injuries, meticulous repositioning of bone fragments, which can be put together both on the operating field and on an instrument tray holder, is the only practical solution [15]. Reconstruction of an extensive defect of the anterior wall is performed if needed.
The fragments of NOE and other orbital fractures are anchored to the stabilized frontal bone at the final stage of the surgery.
Postoperative treatment includes a 2-week antibiotic therapy [34].
8.3.5 Complications of Fractures of Frontal Sinus Walls
Complications of fractures of frontal sinus walls can be caused by either the injury itself or through the surgical manipulation. Traumatic complications include obstruction of the frontonasal duct, CSF leak, or infections secondary to a contaminated wound. Possible complications include an inappropriate surgical approach, untimely and/or inadequate range of surgical repair, the graft material used, etc. [8, 17]. According to the time of onset, the complications can be subdivided into early, within the first month after trauma, and late, after 1 month.
The reported incidence of early complications of a fracture of frontal sinus walls is 2.5–24 % [11, 13]. Such a high discrepancy between the figures is because some authors have reported transient complications such as hypoesthesia of the supraorbital nerve or transient vertical diplopia that spontaneously resolve within 2–3 weeks.
Since the injuries requiring surgical management are severe, the risk of complications among these patients is 15–16 % [5, 8].
CSF leak is the most serious early complication of a frontal sinus fracture. Fifty to eighty percent of the time, the leak can be managed by nonoperative measures which aim to reduce the risk of increased intracranial pressure (e.g., bed rest, elevated head position, prevention of coughing and sneezing, normalization of stool frequency and consistency, the use of diuretics and antibiotics, lumbar drainage placement) [54, 55].
The watch-and-wait approach is justified if the CT shows that the degree of displacement of fragments of the posterior sinus wall is less than its thickness. However, one should bear in mind that persistent CSF leak for 7 days increases the risk of meningitis two- to eightfold, thus necessitating surgical intervention. Emergency surgery is needed when the degree of displacement of the posterior wall fragments is higher than its thickness, because a CSF leak does not stop spontaneously in these cases [11].
A CSF leak, and a persistent CSF leak in particular, is closely associated with infectious complications [1, 34] that affect both the frontal sinus (frontal sinusitis and mucopyocele) and the brain. The incidence of meningitis, encephalitis, or frontal lobe abscess can be up to 6 % [33, 56].
The symptoms of meningitis include high fever, pronounced headache caused by intracranial hypertension, nuchal rigidity, the Kernig’s sign, and upper and lower Brudziński’s sign, secondary to meningeal irritation and progressive depression of consciousness. If a patient has high intracranial pressure, during a lumbar puncture, CSF quickly trickles or there may be a sudden rush of fluid. Pleocytosis and high CSF protein level are reliable laboratory signs of meningitis. MRI reveals meningeal thickening.
Treatment of meningitis includes intravenous, or sometimes intrathecal, injection of antibiotics, depending on the results of CSF culture and the patient’s symptoms.
Encephalitis occurs when the process affects the brain parenchyma and cranial nerves. Focal symptoms—cranial nerve III, IV, VI, and VII palsy, hemiparesis or generalized muscle weakness, and aphasia—are observed in addition to meningitis signs.
Infection spread through the area of the fracture of the posterior frontal sinus wall has a high risk of developing subperiosteal (Pott’s puffy tumor) and/or epidural abscess located between the bone and the dura mater. The abscess manifests itself as infection-induced encephalopathy with headache, fever, and abnormal blood tests. The treatment includes immediate lavage of the frontal sinus and abscess drainage simultaneously with targeted antibiotic therapy.
The subdural empyema develops in the space between the dura mater and the arachnoid mater as infection is spread through the perforant veins in the frontal sinus. Because the clinical presentation is very nonspecific, the diagnosis is based on CT and MRI findings. These findings reveal the low-density crescent or ribbon-shaped contents along the cranial bones. Therapy is performed in accordance with the principles listed above. Subdural empyema has a rather serious prognosis, since the disease is characterized by a severe torpid course and high mortality rate.
Frontal lobe abscess is a rare but potentially fatal complication accompanied by nonspecific symptoms: persistent headache, fever, psychic changes, and hypersomnia. The concomitant brain injury makes the neurological signs not so evident; hence, CSF analysis and timely CT scanning and MRI are very important.
Intravenous contrast-enhanced CT scans show the abscess as a low-density round focus (0–30 HU) with an unclear contour surrounded by a narrow zone (capsule) intensively accumulating the contrast.
T1-weighted MRI images show a ring-shaped structure whose central portion generates a hypointense signal, while the peripheral portion generates a hyper- or an isointense signal. T2-weighted MRI images show the abscess as a focus with a hyperintense signal in its central portion and a hypointense signal from its peripheral portion.
Treatment of a frontal lobe abscess at early stages is confined to the timely parenteral administration of antibiotics that can easily penetrate through the blood–brain barrier and selection of the appropriate antibiotic based on the CSF culture results. The third- and fourth-generation cephalosporins, carbapenems (ceftriaxone, cefotaxime, cefepime, meropenem), and vancomycin are typically used.
Surgical management of an abscess with a dense capsule is indicated in addition to medical treatment.
The treatment regimen should be continually monitored by evaluating clinical signs, laboratory test results, and CT and MRI findings. The duration of treatment often ranges from 3 to 9 months. The osteoplastic surgery is postponed until the patient fully recovers. The prognosis depends on early diagnosis and timely onset of treatment.
Late complications of mucocele and/or mucopyocele result after fractures located medial to the supraorbital notch affecting the NOE complex lead to obstruction of the frontonasal duct. Although they are rare, they progress very slowly and are accompanied by few symptoms. These complications are very severe as they damage the orbital walls, sinuses, and the skull [11, 57]. Treatment includes complete excision of pathological tissues and reconstruction of bone defects.
Complications caused by the surgical approach. Incisions along the lower edge of the eyebrow extending medially are associated with a high risk of rough scar formation.
An incorrect coronal incision is complicated by transection of the frontal branches of the facial nerve and devascularization of the temporal fat pad. This may result in an aesthetically unappealing depression in this region. Finally, even with a perfectly performed coronal approach, alopecia may also lead to a poor aesthetic appearance.
The outcomes of fronto-orbital fractures depend on the degree of brain damage and cerebral complications [31].
8.4 Orbital Roof Fractures
Second only to the lateral wall, the orbital roof is the strongest orbital wall. It is formed by the orbital lamina of the frontal bone and the lesser wing of the sphenoid3 [58]. The additional factors reinforcing the orbital roof include its arc-shaped profile, the dura mater that is significantly thick and tightly fused with the bone, and the cerebrospinal fluid and the medullary substance counteracting the intraorbital pressure that increases in the moment of trauma [59]. The frontal sinus also plays a crucial role in the clinical presentation and treatment strategy of orbital roof fractures.
8.4.1 Epidemiology of Orbital Roof Fractures
Orbital roof fractures are the least common orbital fractures [60]. A meta-analysis of the English-language literature published from 1970 to 2000 revealed that orbital roof fractures are observed in 1–9 % of all facial traumas but 60–93 % of other craniofacial injuries [54, 55, 61, 62]. A typical adult patient is a 30-year-old man (89–93 %) who has experienced a high-energy blow and has multiple concomitant injuries to other organs and systems (57–77 %) [63], including fractures of long bones (26–30 %) and spine (12 %), and non-penetrating injuries to the thoracic, abdominal, and pelvic organs. The high mortality rate of 12 % is attributable to these accompanying injuries [54, 55].
The major causes of trauma include motor vehicle accidents, falls, blows to the face with heavy objects, or penetrating orbital injuries [63].
An almost equal sex distribution is observed in the pediatric population. In 53–93 % of patients, the orbital roof fracture is a component of a frontobasilar fracture without or with an insignificant displacement of bone fragments and accompanied by multiple other trauma sites. Bilateral fractures are observed in 5–10 % of cases [54, 64]. The pediatric traumas are caused by falls and motor vehicle accidents in half and third of cases, respectively [54].
Orbital roof fractures, both as an independent entity and as a component of a more extensive craniofacial trauma, typically occur in young children, which is due to the specific features of their skull anatomy [65].
The anthropometric parameters of a newborn’s head are a balance between the size of the maternal passages, the disproportionately large brain, and a comparatively small face. The ratio between the face and skull size is 1:8; hence, fractures of facial bones in infants are tenfold less frequent than in adults (0.6–1.2 % and 10 %, respectively) [66, 67]. On the contrary, the protruding orbital roof is injured much more frequently compared to adults because a newborn’s skull does not reach 80 % of its final dimension until the age of 2 and does not reach its final size until the age of 7. The situation is worsened by physiological hypoplasia of the frontal sinus that does not have the ability to dampen blows.
As opposed to the skull, the facial skeleton continues to grow during the second decade of one’s life. The “face/skull” ratio eventually decreases to 1:2, thus increasing the incidence rate of fractures of facial bones, including the inferior orbital wall. Furthermore, pneumatization of the frontal sinus reduces the incidence rate of orbital roof fractures [68].
As a result, the orbital roof fractures, both isolated and combined with injuries to the other wall, in 3–7-year-old children comprise 60 % of all orbital injuries, while the orbital floor fractures comprise less than 25 % of fractures. Six- to eight-year-old children have an equal risk of fracturing the orbital floor and roof. In 12-year-old children, the distribution of the different types of orbital fractures does not differ from the adult population, since growth of facial bones and pneumatization of paranasal sinuses makes inferomedial fractures the most common type [65, 68, 69].
8.4.2 Classification of Fractures
Messinger et al. [54] used the CT findings to subdivide orbital roof fractures into three types:
1.
Nondisplaced fractures (Fig. 8.8a–e) comprise 40 % of all fractures [55].
Fig. 8.8
Types of orbital roof fractures: (a–d) Without displacement of bone fragments. (e) 3D reconstruction of a comminuted fracture (white box) shown in Fig. 8.8c (top view, view from the anterior cranial fossa). (f–h) A blow-out fracture of the orbital roof (shown with an arrow). (i–l) Blow-in fracture. The bone fragment displaces the globe downward (k)
2.
Isolated blow-out fractures with one or several bone fragments displaced upward, into the frontal cranial fossa, along with the orbital adipose tissue. The dura mater and medullary substance can be either unaffected or affected (Fig. 8.8f–h) [70–72]. The bone fragments may also be displaced into the large frontal sinus, which illustrates the dampening effect of the sinus in such injuries [54, 73]. The large expanse of the frontal sinus contributes to an anatomically weak orbital roof [74]. A blow-out fracture of the orbital roof is caused by a sudden and abrupt increase in intraorbital pressure or, less frequently, by a penetrating orbital injury.
3.
Isolated blow-in fractures can occur with one or several bone fragments displaced downward into the orbit, either with or without periosteal damage. The bone fragments in this type of fracture may be forced into the orbital adipose tissue (Fig. 8.8i–k). This type of fracture results from a high-energy impact to the supraorbital region of the frontal bone followed by deformation and fracture of the thin orbital roof [26, 59, 75]. A more unusual mechanism of a blow-in fracture is a remote cranial injury that transmits increased intracranial pressure to the orbital roof with a resulting fracture [76]. Isolated blow-in fractures occur more often than the blow-out types in the adult population and are typically accompanied by brain injury [77].
Furthermore, each of these fracture varieties may involve the supraorbital rim.
Isolated supraorbital rim fractures are extremely rare (Fig. 8.9). A literature search found only one report of a supraorbital rim fracture with a bone fragment displaced under the scalp as a consequence of a motor vehicle accident [78]. The fracture line usually spreads from the orbital rim to the orbital roof or the squamous part of the frontal bone. This injury pattern is typical of patients with undeveloped frontal sinuses [54].
Fig. 8.9
Supraorbital rim fracture: (a) Schematic view of an isolated fracture. (b) A much more common type: the supraorbital rim fracture as a component of a more extensive injury. (c, d) Blow-in fracture of the supraorbital rim
8.4.3 Clinical Presentation of Orbital Roof Fractures
In addition to massive swelling of the eyelids and ecchymosis, the clinical presentation of a typical orbital roof fracture includes several signs and symptoms.
These include a subperiosteal hematoma, with a bone fragment, or a leptomeningeal cyst in the upper orbital area [77, 79–81]. Hypoglobus is observed in a third of patients and indicates that the orbital roof fracture has an anterior localization and is a blow-in type (Fig. 8.10). Proptosis is typical of a posterior blow-in fracture and is found in 60–65 % of patients [54].
Fig. 8.10
Clinical presentation of a subperiosteal hematoma in a patient with a fracture of the left orbital roof: (a, b) Small palpebral hematoma (a, patient’s appearance before surgery; b, after drainage of the hematoma narrowing of the orbital fissure caused by ptosis and downward displacement of the globe). (c, d) MRI scans before treatment was started (the hematoma is shown with an arrow)
Ocular motility disorders (17 %) and ptosis of the upper eyelid (25 %). In the case of an anterior fracture, the mechanical effect of a bone fragment or subperiosteal hematoma on the superior muscle complex is the main reason for motility disorders and ptosis [44, 79, 82, 83]. In patients with posterior blow-in orbital wall fractures, the ocular motility disorders may be a sign of the superior orbital fissure or orbital apex syndromes [54, 84]. In these cases, the external and internal ophthalmoplegia is accompanied by dysesthesia in the innervation zone of the first branch of the trigeminal nerve. One should be aware that brain stem injuries can also lead to limited ocular motility in these patients as well [84].
Limited vertical movements of the globe in patients with orbital roof fracture should be differentiated from supraduction deficit in patients with Brown’s syndrome. This syndrome is caused by a restriction of the tendon of the superior oblique muscle, usually in the region of the trochlear notch, and is most notable during adduction4 [85].
The triad of nasal CSF leak, pneumocephalus, and pulsating exophthalmos is caused by combined injury to the orbital roof and dura mater and occurs in 3–9 % of cases [55]. A number of factors contribute to this triad:
The relatively thin orbital plate can be easily fractured under mechanical impact. This leads to a traumatic communication between the frontal sinus and ethmoidal labyrinth cavities with the anterior cranial fossa.
Nasal bone fractures, which are often associated with the orbital injury, displace the perpendicular plate of the ethmoidal bone upward, damage the cribriform plate, and rupture the dura mater which is tightly fused with the crista galli.
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