Facial injuries

The frontal sinuses are paired structures that begin to be detected at 3 years of age. Significant pneumatic expansion does not begin to occur until approximately 7 years, with full sinus development complete by the age of 18–20.

The frontal sinuses are lined with respiratory epithelium, which consists of a ciliated membrane with mucus-secreting glands. A blanket of mucin is essential for normal function, and the cilia beat this mucin in the direction of the nasofrontal ducts.

When injured, they serve as a focus for infection, especially if duct function is impaired.

One-third of fractures involve the anterior table alone, and 60% involve the anterior table and posterior table and/or ducts.

Forty percent of frontal sinus fractures have an accompanying dural laceration.

Lacerations, bruises, hematomas, and contusions constitute the most frequent signs of frontal bone or sinus fractures.

Occasionally, the first presentation of a frontal sinus fracture may be an infection or symptom of frontal sinus obstruction, such as mucocele or abscess formation. Infection in the frontal sinus may produce serious complications because of its location.

Frontal sinus fractures should be characterized by describing both the anatomic location of the fracture, including involvement of the anterior table, posterior table, or both, and their degree of displacement.

Indications for operative management include:

Depression of the anterior table.

Radiographic demonstration of involvement of the nasofrontal duct with presumed future non-function.

Obstruction of the nasofrontal duct with persistent air fluid levels.

Mucocele formation.

Fractures of the posterior table that are displaced and presumably have lacerated the dura resulting in a cerebrospinal fluid leak.

While some authors recommend exploration of any posterior table fracture or any fracture in which an air fluid level is visible, most explore posterior wall fractures only if their displacement exceeds the width of the posterior table.

The nasofrontal duct passes through the anterior ethmoidal air cells to exit adjacent to the ethmoidal infundibulum beneath the middle meatus.

Blockage prevents adequate drainage of normal mucous secretions and predisposes to the development of mucoceles.

The reported average interval between the primary injury and development of frontal sinus mucocele is 7½ years.

The best technique of exposure is the coronal incision. Occasionally, a laceration may be used.

Any depressed frontal sinus fracture of the anterior wall potentially requires exploration and wall replacement in an anatomic position to prevent contour deformity.

If the nasofrontal duct is compromised, obliteration of the sinus is required and commonly involves stripping of the mucosa, burring of the bone, and occlusion with well-designed “formed-to-fit” calvarial bone plugs or soft tissue ( Fig. 9.2A–C ) .

If most of the posterior bony wall is intact, the entire frontal sinus cavity may be filled either with fat or cancellous bone.

If the posterior table is missing, or significantly displaced, the sinus should be “cranialized”. In cranialization, the posterior wall of the frontal sinus is removed, effectively making the frontal sinus a part of the intracranial cavity. The “dead space” may be filled with cancellous bone or left open. Any communication with the nose by the nasofrontal duct or with the ethmoid sinuses should be sealed.

A galeal flap with a pedicle of the superficial temporal artery can be a useful method for vascularized soft tissue obliteration of frontal bone problems.

Complications of frontal bone and sinus fractures include:

• Cerebrospinal fluid (CSF) fluid rhinorrhea.

• Pneumocephalus and orbital emphysema.

• Absence of orbital roof and pulsating exophthalmos.

• Carotid–cavernous sinus fistula.

Orbital fractures may occur as isolated fractures of the internal orbit or may involve both the internal orbit and the orbital rim.

An orbital blow-out fracture is caused by the application of a traumatic force to the rim, globe, or soft tissues of the orbit accompanied by sudden increase in intraorbital pressure and subsequent fracture through the orbital floor ( Fig. 9.3 ) .

In children, the mechanism is more frequently like that of a trapdoor, rather than the “blow-out” fracture seen in adults ( Fig. 9.4 ) .

As opposed to incarceration of fat adjacent to the inferior rectus muscle, children more frequently “scissor” or capture the muscle directly in the fracture site.

Muscle incarceration is an urgent situation that demands immediate release of the incarcerated muscle.

The patient with true muscle entrapment may experience pain on attempted eye motion as well as nausea, vomiting, and an oculocardiac reflex (nausea, bradycardia, and hypotension).

The purpose of orbital floor reconstruction/replacement in this scenario, whether a bone graft or an inorganic implant, is to re-establish the size and the shape of the orbital cavity. This replaces the orbital soft tissue contents and allows scar tissue to form in an anatomic position.

A forced duction test is performed by grasping the orbital conjunctiva with forceps and testing the range of motion of the globe ( Fig. 9.5 ) .

• Limitation of forced rotation or motion is a positive test for entrapment of extraocular muscles. This test should be performed:

• Before dissection.

• After dissection.

• After the insertion of each material used to reconstruct the orbital wall.

• Just prior to closure of the incisions.

Indications for surgical treatment of orbital fractures:

Diplopia caused by incarceration of muscle or the fine ligament system, documented by forced duction examination and suggested by CT scans.

Radiographic evidence of extensive fracture, such that enophthalmos would occur.

Enophthalmos or exophthalmos produced by an orbital volume change.

Visual acuity deficit, increasing and not responsive to medical dose steroids, implying that optic canal decompression would be indicated.

“Blow-in” orbital fractures that involve the medial or lateral walls of the orbit, and severely constrict orbital volume, creating increased intraorbital pressure.

Goals of surgical management:

Disengage entrapped structures and restore ocular rotatory function.

Replace orbital contents into the usual confines of the normal bony orbital cavity, including restoration of both orbital volume and shape.

Restore orbital cavity walls, which, in effect, replaces the tissues into their proper position and dictates the shape into which the soft tissue can scar.

The orbits are conceptualized in thirds progressing from anterior to posterior.

Anteriorly, the orbital rims consist of thick bone.

The middle third of the orbit consists of thin bone, while the bone structure thickens again in the posterior third.

The orbital bone structure is thus analogous to a “shock-absorbing” device in which the middle portion of the orbit breaks first, followed by the rim.

The optic foramen is situated at the junction of the lateral and medial walls of the orbit posteriorly and is well above the horizontal plane of the orbital floor. The foramen is located 40–45 mm behind the inferior orbital rim.

Exposure considerations:

• Endoscopic approaches through the maxillary sinus permit direct visualization and repair of the orbital floor and manipulation of the soft tissues without an eyelid incision ( Fig. 9.6 ) .

  

• Lower eyelid incisions have the least incidence of ectropion of any lid incision location but tend to be the most noticeable.

• Subciliary incisions near the upper margin of the lid leave the least conspicuous cutaneous scar, although they have the highest incidence of lid retraction.

• Transconjunctival incisions can be performed in the preseptal or retroseptal plane and avoid external scars. Occasionally, a lateral canthotomy or caruncular extension is necessary to widen exposure to the lateral and medial orbit, respectively.

Diplopia: usually the result of muscle contusion, but can be the result of incarceration of muscle, soft tissue adjacent to the muscles, or nerve damage to cranial nerve III, IV, and VI.

Enophthalmos: second major complication of blow-out fractures, usually due to enlargement of the orbital volume.

Retrobulbar hematoma: signaled by globe proptosis, congestion, and prolapse of the edematous conjunctiva. Diagnosis is confirmed by a CT scan imaged with soft tissue windows. It is usually not possible to drain retrobulbar hematomas.

Ocular (globe) injuries and blindness.

Implant migration, late hemorrhage around implants, and implant fixation.

Ptosis of the upper lid: true ptosis of the upper lid should be differentiated from “pseudoptosis” resulting from the downward displacement of the eyeball in enophthalmos.

Scleral show, ectropion and entropion – vertical shortening of the lower eyelid.

Infraorbital nerve anesthesia.

The “superior orbital fissure” syndrome: when a roof fracture extends posteriorly to involve the superior orbital fissure and its contents (CN III, IV, V, VI). Signaled by: restricted gaze and numbness of the forehead, brow, medial portion of upper lid, and medial upper nose.

The “orbital apex” syndrome: when a roof fracture extends posteriorly to involve the superior orbital fissure and optic foramen and their contents (CN II, III, IV, V, VI). Signaled by: all symptoms of the superior orbital fissure syndrome with visual acuity change or blindness.