Fractures of the orbital floor and medial wall

The indirect, "blowout" fracture of the orbital floor occurs when a major blunt blow is applied across the anterior orbital entrance, the fracture resulting from hydraulic collapse of the orbital floor and possibly by transmission of energy from a transient deformation of the inferior orbital rim. Typically one edge of the fracture involves the infraorbital nerve canal and a transient neuropraxia of this nerve is extremely common, with hypoaesthesia of the ipsilateral cheek, side of nose and upper gum.

Unlike most direct fractures of the orbital floor, the blowout fracture occurs without breach of the orbital rim. The rise in orbital pressure during the blow causes a herniation of orbital tissues through the floor defect, the extremes being either a large prolapse of tissues through an extensive bone defect or a "pinch" of tissues through a tiny crack in the floor. Direct entrapment of the inferior rectus in the fracture line is extremely rare, but diplopia probably results from a combination of contusion of orbital tissues and from entrapment of the fascial planes around inferior rectus muscle.

Comminuted blowout fractures of the medial orbital wall can occur in isolation, but are generally part of an orbital floor blowout fracture. Orbital emphysema, usually the result of nose-blowing, is commoner with ethmoid fractures and the ophthalmic circulation may be embarrassed if the entrapped air causes an undue rise in the orbital pressures; this ophthalmic emergency should be treated urgently by aspiration of air or incision and drainage of the orbital spaces, or an irreversible loss of vision may result. Direct medial wall fractures from blunt trauma also involve the nasal bones, the lacrimal bone and the frontal process of the maxilla, being commonly manifest as a depressed nasal bridge and telecanthus.


Any patient with major orbital trauma is likely to have a fracture of the orbital wall or ocular injury. Specific features suggestive of blowout fracture include vertical diplopia with restriction of up or down gaze, pain on extremes of eye movement, hypoaesthesia in the infraorbital nerve territory, periocular emphysema, or enophthalmos and hypoglobus. Forced duction testing will confirm that the restriction of eye movement is of mechanical origin.

Unless there is marked dental artefact, direct coronal CT scans at a bone-imaging window are the investigation of choice (Figure 14.1); not only is the orbital floor better shown than that after reformatting of axial scans, but the orbital apex and the other orbital walls are also well shown.

Most orbital floor blowout fractures do not require surgery and eye movements will often return to normal over several weeks to months. Orthoptics assessment, with sequential Hess charts and fields of binocular single vision, is useful for following the course of recovery and detecting those who are unlikely to return to normal ocular balance.

Blowout Fracture Medial
Figure 14.1 Coronal CT scan showing blowout fracture of the medial part of the orbital floor and inferior part of the ethmoid lamina papyracea.

Typically the small, linear fracture causes the greatest disturbance of ocular motility, whereas large fractures with comminution of the orbital floor tend to recover full eye movements. Persistent diplopia within 30° of the primary position is the main indication for surgery and, for most, diplopia on down-gaze is particularly troublesome as it interferes with reading and negotiating stairs. Certain occupations, however, demand frequent use of up-gaze as, for example, with decorators, plasterers, certain sportsmen and pilots.

Cosmetically evident if greater than about 2mm, this degree of enophthalmos generally indicates a significant displacement of bone that merits orbital wall repair. Enophthalmos may not be evident for many weeks until post-traumatic orbital oedema has settled but, if manifest is early, it suggests a major fracture justifying early intervention at 7-14 days after injury - when much of the acute haemorrhage and oedema has settled, but before fibrosis has occurred.

Apart from the presence of marked enophthalmos that justifies early intervention, the timing of surgery remains controversial. There is no good evidence that recovery of ocular motility is improved by early surgery, although the gross restriction of movement due to fascial entrapment in hairline fractures


Figure 14.2 Gross restriction of up (a) and down (b) gaze after a "hairline" blowout fracture of the orbital floor with entrapment of fascia around inferior retus muscle.

(Figure 14.2) may recover better with the release of entrapped tissues within a day or two of injury.


The assessment and treatment of systemic, facial and cranial injury takes precedence over the repair of orbital fractures. The patient with acute orbital fracture involving the paranasal sinuses should be instructed not to blow his/her nose for 10 days and, in view of the sight-threatening nature of acute orbital cellulitis, a short course of systemic antibiotics should be considered. Oral anti-inflammatory medications may be given after injury to accelerate the resolution of orbital inflammation and oedema.

Orbital floor repair

If surgical repair is indicated, then the orbital floor is readily approached through a lower eyelid swinging flap (Chapter 11) or a subciliary skin-muscle blepharoplasty flap (Chapter 8). Using one of these routes, the orbital rim is exposed and the periosteum incised about 5mm outside the rim, to leave a margin of periosteum for adequate closure in front of any orbital floor implant. The periosteum is raised into the orbit, across the orbital floor until the site of fracture is located and then the periosteum around the sides of the fracture site is raised to define the extent of tissue incarceration; particular care must be taken laterally, as this area is liable to major haemorrhage from the infraorbital neurovascular bundle in the area of the inferior orbital fissure. There should be a clinically evident improvement in the forced duction test after the incarcerated orbital tissues are released completely from the fracture site and the whole of the fracture edge should be visible; typically there is a ledge of normal orbital floor at the posterior edge of the fracture site. Although often not possible, the sinus mucosa should be kept intact to avoid formation of sino-orbital fistula.

Once the orbital contents have been completely freed from the fracture site, an implant may be shaped and positioned across the defect in the orbital floor and medial wall (Figure 14.3). Where the repair is for release of entrapped tissues (rather than volume enhancement), it is essential to place the rear of the implant on the intact fragment of orbital floor at the orbital apex, behind the point of emergence of the infraorbital nerve from the inferior orbital fissure. Bulky implants should be avoided within 1cm of the orbital apex, as thick materials may bear upon the optic nerve or ophthalmic artery and lead to blindness, and any materials should be inserted gently and not forced into place. Likewise, when placing the material it is very important to avoid snagging of the orbital fat with the back edge of the implant, or motility disorders will result. The most useful implant materials include porous polyethylene and silicone sheeting, although silicone is

Figure 14.3 Implant material placed across an orbital floor fracture, approached through a lower eyelid swinging flap: (a) orbital floor pre- and (b) post insertion of implant.

Figure 14.3 Implant material placed across an orbital floor fracture, approached through a lower eyelid swinging flap: (a) orbital floor pre- and (b) post insertion of implant.

inadvisable where there has been a breach of sinus mucosa; whilst still widely used, bone grafts have the disadvantage of reabsorption and donor-site morbidity. Microplate fixation may be necessary where there has been extensive damage to the orbital walls or fracture of the orbital rim, although treatment of such facial fractures is outside the realm of the ophthalmic surgeon.

The anterior edge of the orbital periosteum is closed with a 5/0 absorbable suture, the lower eyelid approach repaired in layers with a 6/0 absorbable suture and the eyelid placed on upward traction with a 4/0 nylon suture. The site is padded with a firm elastic dressing.

Fractures of the medial orbital wall can be readily repaired during orbital floor repair, with extension of the flexible implant upwards alongside the medial defect. For isolated fractures of the medial wall, however, it is possible to use either the extended post-caruncular incision, directed postero-medially onto the orbital wall, or the aesthetically less desirable Lynch incision, through the skin of the nasal part of the upper eyelid and medial to the inner canthus.

The patient should be nursed head-up after surgery and it is important that any severe or increasing pain is reported. Where pain is severe or increasing, the vision in the affected eye and the state of the orbit should be checked; a very tense orbit with markedly decreased vision, a relative afferent pupillary defect and loss of eye movements, suggests accumulation of orbital haemorrhage and this may lead to irreversible visual loss. If this emergency appears to be developing, the operative site should be reopened at the "bedside", without delay, and any accumulation of blood allowed to drain.

The patient should refrain from nose blowing for 10 days after orbital floor repair and should be prescribed a course of systemic antibiotics and anti-inflammatory medications. It is possible that eye movement exercises performed several times daily, with forced ductions to the extremes of range, may increase the recovery of tissue compliance and speed the resolution of post operative diplopia; if, however, diplopia persists at several months after repair then squint surgery may be of value when the Hess charts are stable.


Post operative haemorrhage, with threat to vision, is the most feared complication and should be recognised and treated promptly.

The risk of this major complication may be reduced by recognition of the various arterial branches that cross between the orbit and the walls (the branches to the infraorbital nerve and the anterior ethmoidal vessels being the most troublesome in this context) and appropriate coagulation of the vessels.

Increased infraorbital nerve hypoaesthesia is fairly common and generally recovers. Transient alteration in muscle balance is almost inevitable, this typically settling over a week or two, but capture of the released orbital tissues by an edge of the implant should be avoided as it may permanently worsen motility.

Infection, more common with entrance into the sinus cavity, may occur soon after surgery (Figure 14.4) and necessitates removal of the implant with later repair after the infection has settled on systemic therapy. Late infection may occur where maxillary sinusitis spreads through a thin interface into the site of orbital repair.

Migration of the implant is less common with integrating implants, such as porous polyethylene, and frank extrusion from the operative site (Figure 14.5) is almost unknown with avoidance of direct incision over the inferior orbital rim - an unsightly surgical approach used widely in the past. Formation of a pneumatocoele around non-integrating implants such as silicone (Figure 14.6), lined by respiratory epithelium that has migrated through an sino-orbital fistula, may be avoided

Figure 14.4 Patient referred with acute infection of an orbital floor implant.

Que Necrose Pele Apos Peeling
Figure 14.5 Late extrusion of a silicone implant through a direct incision over the orbital rim.
Figure 14.6 Air-filled cavity (in communication with the maxillary sinus) that has formed around a silicone sheet implant for repair of an orbital fracture.

by using integrating implants where there is a defect into the sinuses at the time of surgery; where a pneumatocoele forms, it can later be excised and the defect repaired, if necessary, with an integrating implant material.

Surgical approaches through the lower eyelid may rarely lead to a cicatricial retraction of the lower lid, with secondary entropion or ectropion.

Damage to the lacrimal drainage system, either during exposure of a fracture site or due to bearing of the implant on the nasolacrimal duct, may lead to epiphora that may require dacryocystorhinostomy. Likewise, surgery on the medial orbital wall carries a very minor risk of cerebro-spinal fluid leak or intracranial damage.

Figure 14.4 Patient referred with acute infection of an orbital floor implant.

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