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Essay: Discussing Anatomical Study of Orbital Blowout Fracture and Its Impact on Ocular Health

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  • Published: 1 April 2019*
  • Last Modified: 23 July 2024
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Anatomical Study of A Blowout Fracture

An orbital blowout fracture is a consequential outcome of trauma to the orbital bones. Orbital blowout fractures are differentiated based on their anatomical location. Floor blowout fractures are the most common and are often associated with radiating force rippling through the orbital rim.  Superior and lateral walls are typically strong enough to withstand such forces. Many hypotheses have been proposed regarding the pathophysiology of the blowout fracture. Bone Conduction Theory proposes that a force, not strong enough to fracture the rim upon impact, transfers energy throughout the orbit. The orbital floor is weak and susceptible to collapse in the presence of excess strain. Globe-to-Wall Theory model suggests that a force pushes the globe into the orbit and causes a collision fracture based on a ricochet effect. The Hydraulic Mechanism states that the colliding stimulus causes an increase in intraocular pressure exerting a force upon the orbit. It is likely that the etiological mechanism of an orbital fracture is the accumulation of multiple theories.1 Orbital blowout fractures are influenced by geographic location, local demographics, and social behaviors. Reviewed literature studies found males to be more likely to sustain fractures to the orbital floor with a peak incidence between ages 20-29.2 Orbital fractures often present with symptoms such as ptosis, enophthalmos, corneal abrasion, hyphema, iritis, acute glaucoma, hemorrhaging, retinal detachments, or optic neuropathy.3 Throughout a case study, an evaluation of the structural anatomy of the orbit and periorbital region is assessed in order to further understand the etiology and treatment of a blowout fracture to the orbit floor.

During the assessment of a 22-year-old male case-study patient, a subject presents complaining of moderate pain around his left eye after being hit in the face with a softball earlier that same day. Observations of the left eye reveal ecchymosis, significant swelling, and inflammation. Evaluation of EOMs reveals a possible restriction of gaze upon elevation. Fundal examination of the posterior pole established no obvious damage or detachments. The patient is educated on the findings and referred to the ER for a CT scan. The CT scan returned imaging a left eye floor fracture into the maxillary sinus. Imaging discloses the displacement of the floor of the orbit and indicates a compromised maxillary sinus. The patient returns for a follow-up appointment expressing concern about intermittent diplopia with enopthalmos. The periorbital tissue of the left eye has lost sensation. The EOMs reveal superior restriction of the inferior rectus. The patient is placed on a prophylactic antibiotic and scheduled for a consultation with an oculoplastic surgeon.

An anatomical overview of the orbit and periorbital region helps further understand the case-study. The orbit is the bony cavity that contains the eye, extraocular muscles, nerves and blood vessels. The orbit is strong and provides protection and support from the external environment. The globe is posteriorly surrounded by the orbital cavity of the skull lined in connective tissue. The orbit is composed of seven bones: (1) frontal, (2) maxillary, (3) zygomatic, (4) sphenoid, (5) ethmoid, (6) palatine, and (7) lacrimal. The frontal bone, zygomatic bone, maxillary bone form the orbital rim. The orbital bones vary in thickness. The lateral wall and orbital apex are the strongest due to their enduring exposure to the external elements, whereas the medial wall and inferior floor make up the weakest bones making them particularly vulnerable to fracture by propagating forces. Fractures to the orbital floor can cause ocular complications such as enophthalmos which is caused by the displacement of the globe into the maxillary sinus. Dislocation can cause a secondary subjective pseudoptosis observation due to the loss of structural support.4

Paranasal sinuses are sets of paired mucosa-lined, air filled spaces that surround the nasal cavity and are located in four of the orbital bones. The frontal sinus is located superiorly to the orbit, the ethmoid and sphenoid sinuses are medial, and the maxillary sinuses are located under the eyes. Of these structures, the maxillary sinus is separated from the ocular tissue by 0.5 to 1mm thick orbital plate. The thin wall of the sinus is a poor barrier for the restriction of bacteria and pathogens. Orbital infections such as orbital cellulitis or orbital emphysema are possible ramifications of blowout fracture because of the pathologic pathway between the sinus and orbit cavities.  Patients dealing with blowout fractures, like the case-study subject, should be warned not to blow their nose and to avoid sneezing as a preventative measure. Nose blowing can propel bacterial sinus contents into the orbit resulting in orbital emphysema. Orbital emphysema can corrupt the ocular tissue and may include complications such as a loss of vision, increased intraocular pressure, or central retinal artery occlusion.5  Many studies suggest the use of prophylactic antibiotics such as Azithromycin to prevent a secondary pathological infection.6

Assessment of the extraocular muscles following trauma may limit movement of the globe due to entrapment of the muscles or perimuscular fascia into the fractured site. The six extrinsic extraocular muscles of the eye dictate ocular movement and are enclosed within the orbit. Confined at the apex of the orbit is the common tendinous ring of Zinn, which stems the four rectus muscles. The superior, inferior, lateral, and medial rectus muscles primary actions include elevation, depression, abduction, and adduction respectfully. The superior oblique muscle originates on the lesser wing of the sphenoid bone coursing through the trochlea. The inferior oblique muscle originates on the maxillary bone.7 In blowout fractures, it is a common to detect the entrapment of the inferior rectus muscle which restricts superior gaze and may cause diplopia in its vertical restriction of motility. It is essential to differentiate limitations of muscle entrapment from traumatic neurological palsy in order to effectively diagnose and treat. Forced duction testing can help clarify the etiology by forcibly moving the anesthetized globe through a full range of motion. Restrictive movement indicates a mechanical restriction whereas passive movement indicates a neurological disorder.8

The eyelids, or ocular adnexa, surround the eye and have four functions that help protect, produce, drain, and spread tears across the anterior surface of the eye. The eyelids are separated superiorly and inferiorly and meet at the corners of the lateral and medial canthi. The upper and lower eyelids are subdivided into tarsal and orbital regions. The tarsal portion lies closest to the margin and rest against the globe. The orbital portion extends from the superior sulcus to the eyebrow in the upper lid, and from the inferior sulcus onto the cheek in the lower lid. The eyelids are made up of six distinct layers. From anterior to posterior, the layers include: (1) skin, (2) subcutaneous connective tissue, (3) orbicularis oculi muscle, (4) submuscluar areolar layer, (5) tarsal plate and muscle of Muller, and (6) the palpebral conjunctiva.4

The blood vessels surrounding the periorbital tissue are located within the submuscluar areolar layer of the eyelids arranged in a series of arcades. The marginal palpebral arcades lies near the lid margin and peripheral arcade lies near the orbital portion of the tarsal plate. The arteries forming theses arcades originate from the ophthalmic and lacrimal arteries. These arteries branch into the medial and lateral palpebral arteries which make-up the arcades.  Periorbital ecchymosis is the result of localized trauma to the eye or orbit. Hemorrhaged blood pools in the subcutaneous tissue of the eyelid and is commonly characterized by red, blue, or purple discoloration of the eyelids and associated swelling.9 Swelling, heat, pain, and redness are cardinal signs of acute inflammation. The inflammatory response is triggered when the body’s tissues are injured or irritated. The response releases local extracellular inflammatory chemicals such as histamine, complement, kinins, and prostaglandings through the bloodstream to dilate local vessels and increases permeability to the area of injury.  Leukocytosis, margination, diapedesis, and chemoteaxis summarize the inflammatory infiltration process and counteract the response mechanism of the injury so that the inflamed tissue can be repaired.10

Neither red blood cells nor white blood cells are normally found in the anterior chamber of the eye and typically indicate damage, inflammation, or infection. Examination of anomalous cells in the anterior chamber can be accomplished using a reflective beam which disperses light in a Tyndall phenomenon.  A separation to the tight junctions between nonpigmented ciliary cells causes a breakdown to the blood brain barrier and can cause the inflammatory response to release leukocytes and immune factors into the eye resulting in a condition known as ‘cells and flare’.  Accumulation of settling lymphocytes in the inferior anterior chamber is known as a hypopyon whereas the accumulation of blood cells is known as a hyphema. Trauma involving head injuries or whiplash, which may lead to blowout fractures, can cause a tear or a rupture in one or more blood vessels. This will cause blood to enter the anterior chamber.11

Computed tomography (CT) is the best imaging modality in evaluation of orbital trauma. CT scans evaluate the injury, location of fractures, degree of fragment dislocation, and expands on secondary sources of complications. CT assessment includes evaluation of morphology, positioning, density, and thickness of the orbital wall. Other imaging modalities that may be used in the initial evaluation of the ocular anatomy include radiographs. MRI, and ultrasonography. Each imaging process has it’s limitations, Radiographs cannot evaluate soft tissue, complex fractures, or uncompressed foreign bodies. MRI is limited to a long scan time and patient cooperation, yet it offers excellent anatomical detail of soft tissue. Ultrasonography offers no information on bones, sinuses, or intracranial structures. Additionally it requires orbital contact and may be challenging on uncooperative patients or penetrating injuries.12

CT’s volume rendering techniques allow 3D reconstructions and help surgeons evaluate and treat patients as appropriate.  Surgical management is a controversial factor in the evaluation of blowout fractures. Indications for surgical treatment are subdivided into mechanical and aesthetic reasons. Mechanical problems are caused by encroachment of the periorbital soft tissue, EOMs, nerves, and vessels. Most restrictions are provoked by the entrapment of the inferior rectus muscle which can cause diplopia, nausea, and arrhythmia. Aesthetic indications are associated with cosmetic encounters such as enopthalmos. Most surgeons agree that defects larger than 50% of the orbital floor are candidates for surgical repair. In comparison, if there is motility, minimal diplopia, and no significant pseudoptosis or enophthalmos, surgeons prefer to deflect to more conservative means.8 Management of a blowout fracture is based on collaborative clinical findings, imaging, and assessment of risks.

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