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 Table of Contents    
ORIGINAL ARTICLE  
Year : 2011  |  Volume : 4  |  Issue : 2  |  Page : 188-193
Role of the maxillofacial surgeon in the management of severe ocular injuries after maxillofacial fractures


1 Head & Neck Department, Division of Maxillofacial Surgery, San Giovanni Battista Hospital, Turin, Italy
2 Department of Clinical Physiopathology, Ophthalmology Institute, Turin, Italy

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Date of Submission20-Apr-2010
Date of Acceptance19-Jul-2010
Date of Web Publication18-Jun-2011
 

   Abstract 

Aim : This study was designed to evaluate the incidence of severe ocular injuries associated to maxillofacial fractures and report their management in the Emergency Department. Patients and Methods : Among the 1779 patients admitted for maxillofacial fractures, those with partial or total loss of vision at the time of emergency consultation were included in the study. Data collected from the patients' medical records included age, gender, mechanism of injury, location and type of facial fractures, type of ocular injuries and cause of blindness, methods of treatment, and days of hospitalization. Results : Forty patients (2.2%), 32 men and 8 women, ranging from 17 to 85 years of age, presented with severely reduced vision or blindness associated to fractures of the facial middle third with involvement of one or more orbital walls, mainly caused by motor vehicle and work accidents. In 18 patients, severe ocular injuries were determined by direct lesion of the globe, in 14 by direct or indirect traumatic optic neuropathy and in 8 by a retrobulbar hematoma. Direct lesion of the eyeball was treated by prompt repair or enucleation of the globe, though no or little recovery of vision was obtained. Ophthalmologic and/or maxillofacial treatment of the anterior compartment lesions of the eye allowed a partial or total recovery of the vision. A partial or total recovery of the vision was observed in almost all the patients with indirect traumatic optic neuropathy after administration of steroids according to NASCIS II protocol. Likewise, an evident improvement of the vision was obtained by immediate drainage of retrobulbar hematoma. Conclusions : Early diagnosis of the nature of the ophthalmic injury and treatment are important, and involvement of the ophthalmologist is mandatory.

Keywords: Blindness, maxillofacial fractures, retrobulbar hematoma, severe ocular injuries

How to cite this article:
Roccia F, Boffano P, Guglielmi V, Forni P, Cassarino E, Nadalin J, Fea A, Gerbino G. Role of the maxillofacial surgeon in the management of severe ocular injuries after maxillofacial fractures. J Emerg Trauma Shock 2011;4:188-93

How to cite this URL:
Roccia F, Boffano P, Guglielmi V, Forni P, Cassarino E, Nadalin J, Fea A, Gerbino G. Role of the maxillofacial surgeon in the management of severe ocular injuries after maxillofacial fractures. J Emerg Trauma Shock [serial online] 2011 [cited 2021 Jan 26];4:188-93. Available from: https://www.onlinejets.org/text.asp?2011/4/2/188/82204



   Introduction Top


The eye represents just 0.1% of the body's total surface. Severe ocular injuries involving partial or total loss of visual acuity, particularly those associated with maxillofacial fractures, are accordingly rare.

While ophthalmologists treat most ocular injuries, maxillofacial surgeons also frequently face severe cases associated with facial fractures in emergency department patients. This is especially true at hospitals lacking ophthalmology divisions; maxillofacial surgeons are often responsible for first ophthalmic assessments at these institutions.

This study presents recommendations based on our experiences, as maxillofacial surgeons, in the management of patients with facial fractures and associated severe ocular injuries.


   Patients and Methods Top


Between January and December 2009, 1779 patients with maxillofacial fractures were admitted to our Division of Maxillofacial Surgery. Patients were selected from this sample population for inclusion in this study. Inclusion criteria were: (1) preoperative coronal and axial computed tomography (CT) scans; and (2) partial or total loss of vision at the time of emergency consultation, determined by a rapid ophthalmological assessment (ROA), according to the guidelines of Hammer [1] and Soparkar and Patrinely. [2] All ocular lesions responsible for the visual damage were classified as Type 3 (severe), based on the severity scale of Rao et al. [3]

Patients with ocular motility deficits and Type 1 and Type 2 [3] ocular injuries, those with incomplete clinical and radiological records, and those who had not completed a maxillofacial and ophthalmologic 6-month follow-up examination were excluded.

Data collected from the patient medical records included age, gender, mechanism of injury, location and type of facial fractures, type of ocular injury and cause of vision loss, method of treatment, and duration of hospitalization (days).

Patients were followed up in collaboration with the ophthalmologists of the Ophthalmology Institute.


   Results Top


Among the 1779 admitted patients, 40 (2.2%; 32 male, 8 female) presented with severely reduced vision or blindness caused by Type 3 ocular injuries. These patients were between 17 and 85 years of age (mean=42 years). Severe ocular injuries are associated only with fractures that affect the middle third of the face and involve one or more orbital walls; the 40 patients included in this study constituted 4.1% of the 969 admitted patients with such fractures.

Principal causes of the severe ocular injuries in this sample were workplace accidents (n = 11) and motor vehicle accidents (MVA; n = 11), followed by falls (n = 9), assaults (n=4), and sports injuries (n = 4) [Table 1]. All of the ocular lesions that were secondary to sports related trauma were caused by horse kicks incurred during horseback riding. [Table 2] shows the association between the causes of facial injuries and ocular lesions.
Table 1: Etiology of the severe ocular injuries


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Table 2: Association between causes and type of ocular injuries


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In total, 23 patients exhibited pure orbital fractures (12 floors, 4 medial walls, 3 roofs, 1 lateral wall, and 3 floors plus medial walls), 12 presented with orbito-maxillo-zygomatic (OMZ) complex fractures, and 5 patients suffered other complex facial fracture types, such as naso-orbito-ethmoidal or Le Fort II/III fractures. In total, 23 orbital floors, 16 lateral walls, 11 medial walls, and 3 roofs were involved [Table 3].
Table 3: Summary of patients' parameters


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The severe reduction or loss of vision following these fractures was the result of one or more of the following mechanisms, consistent with Perry and Moutray [4] :

  • Direct lesion of the globe (10 penetrating lesions with successive rupture, 8 lesions of the anterior compartment);
  • Indirect traumatic optic neuropathy (deceleration/shearing forces; 11);
  • Direct traumatic optic neuropathy (two (Nos. 12 and 13) due to intracanalicular bony impingement of the optic nerve, one (No. 14) due to transaction of the optic nerve with traumatic avulsion of the eye);
  • Critical reduction of endorbital tissue perfusion (eight due to orbital compartment syndrome caused by a retrobulbar hematoma).


Of the 10 patients with global rupture, six received retinal assessment, suturing of the globe, and (during the same intervention) treatment of facial fractures within 24 h of arrival in the emergency department. This treatment was conducted in collaboration with consulting ophthalmologists from the Ophthalmology Institute (OI). The severity of the remaining four global ruptures required enucleation, with epithesis placement at least 6 months later.

Two (Nos. 33 and 39) of the eight patients with direct lesions of the anterior compartment were transferred to the OI within 48 h of arrival at the hospital [Figure 1]. The remaining six patients (Nos. 34-38, 40) underwent surgical intervention for orbital and maxillofacial fractures within 48 h, and were subsequently transferred to the OI for management of the ocular injuries. All eight patients with anterior compartment lesions had partial or complete recovery of vision.
Figure 1: Patient No. 33. (a) Clinical image showing post-traumatic cataract of the left eye and (b) coronal CT scan showing a blow-out fracture of the left orbital floor

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Steroids were administered to the 11 indirect neuropathy patients, in accordance with the protocol developed by the second National Acute Spinal Cord Injury Study (NASCIS II; methylprednisolone 30 mg/kg as bolus + 5.4 mg/kg per h/24 h). Nine of these patients experienced partial or complete recovery of vision.

The two patients suffering a direct neuropathy due to intracanalicular bony impingement of the optic nerve received immediate steroid treatment and subsequent surgical decompression of the optic nerve. The surgeries were performed in another hospital 7 and 10 days after the traumatic event. Neither of these patients recovered their vision [Figure 2].
Figure 2: Patient No. 13. (a) Coronal and (b) axial CT scans show lateral wall fracture involving the optic canal

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Seven of the eight patients with retrobulbar hematomas underwent orbital decompression within 24 h of the traumatic event [Figure 3]. The decompressions were performed according to the surgical protocols of our division, [5] and resulted in partial or complete recovery of vision. These patients preoperatively received megadoses of steroids, according to the NASCIS II protocol. One patient (No. 15) with hematoma-associated blindness was referred from another hospital 48 h after the traumatic event. Orbital decompression did not result in recovery of this patient's vision.
Figure 3: Patient No. 22. (a) Coronal and (b) axial CT scans show retrobulbar hematoma of the superior orbital compartment

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The mean length of hospital stay was 9.3 days, and the mean follow-up period was 56 months (range, 12-97). No patient in this study experienced a new-onset of blindness after facial fractures were repaired.


   Discussion Top


Every victim of midfacial trauma should ideally be assessed by an ophthalmologist. This is unfortunately not always possible, particularly in hospitals like ours that lack ophthalmology divisions.

The literature displays a consensus that an accurate ocular assessment must precede the surgical treatment of midfacial ocular fractures. [6-18] Identification of the ocular lesion is important because its management may take precedence over the treatment of midfacial and orbital fractures. For example, the repair of an orbital fracture may exacerbate a misdiagnosed ocular rupture or laceration, resulting in permanent damage to the vision. [9],[18] Jamal et al. [18] reported that preoperative diagnosis of an ocular lesion is also a crucial medicolegal issue, so that responsibility for a permanent loss of vision is not ascribed to the treatment of maxillofacial fractures.

Maxillofacial surgeons are important components of emergency department teams, because they can manage the airways, oral and maxillofacial bleeding, and craniofacial fractures, as well as perform ocular assessments. [4] The early identification of ocular lesions causing partial or complete loss of vision allows the maxillofacial surgeon to request an early ophthalmological consultation or referral (if the patient's condition permits), to plan the eventual treatment of facial fractures.

We use the ROA to investigate ocular injuries in conscious and aware patients, especially when midfacial fractures are present. [1] The ROA consists of inspection (e.g., for redness or laceration), and testing of visual acuity, red and brightness saturation, pupillary functions, and double vision. When an accurate anamnesis cannot be obtained (e.g., patient is intoxicated, unconscious, sedated, or intubated), pupillary dimensions and light reactivity must be clinically assessed. [13] It is also essential to know the timing of vision loss; several authors [8],[11],[13],[14],[18] have demonstrated that better prognoses for vision recovery when the loss was slow and progressive after the traumatic event.

We found a 2.2% incidence of severe ocular injuries among the 1779 emergency department patients with maxillofacial fractures who were admitted to the Division of Maxillofacial Surgery. This incidence increased to 4.1% when only patients with middle third facial fractures were considered. These results fall within reported ranges among midfacial fracture patients, which vary from 0.32% described by Zachariades et al. [7] and 0.8% by MacKinnon et al. [12] to 10.6% by Ugboko et al. [15] and 22% by Ansari et al., [13] that only considered patients with midfacial fractures.

Pelletier et al. [9] and Brown et al. [10] have suggested that such wide variation in occurrence may reflect ophthalmologists' participation in the assessment of facial trauma patients; such participation increases the incidence of ocular injuries identified.

The literature reflects widespread agreement about the causes and sites of the facial fractures most frequently associated with severe ocular injuries. [6],[10],[11],[13],[16],[17],[18] As we found in this study, MVAs and workplace accidents are the principal causes of ocular lesions. The fracture sites most frequently associated with severe ocular injuries are orbital (mainly involving the orbital floor, followed by the lateral wall), as demonstrated in this study and in previously published research.

Although magnetic resonance imaging (MRI) can provide detailed information about the orbital soft tissues, the additional resolution is not a significant factor in surgical planning decisions. CT scans are routinely used to diagnose facial fractures (including those involving the optic canal), optic nerve lesions, and intraorbital hematomas; they are also used to exclude the presence of intracranial lesions that might impact visual acuity.

Patients presenting at the emergency department of our hospital with severe loss of vision caused by severe ocular injuries associated with maxillofacial fractures were managed by a maxillofacial surgeon alone or, more rarely, with an OI ophthalmologist providing emergency consultation. Such consultations were performed for 18 patients with facial fractures associated with direct global lesions, the most frequent cause of partial or total vision loss in our sample. A ruptured globe should undergo prompt surgical repair if the patient's condition allows. An ophthalmologist successfully repaired six of the 10 global ruptures in this sample, but none of these patients recovered vision. Following ophthalmological intervention, a maxillofacial surgeon repaired the middle third facial fractures during the same surgical session. Enucleation was necessary for the remaining four patients.

An ophthalmologist diagnosed anterior compartment lesions of the eye in the eight patients with partial global lesions. He performed immediate surgical treatment in only two of these cases; six patients first underwent maxillofacial fracture repair.

A maxillofacial surgeon performed emergency decompression on the eight patients with orbital compartment syndrome due to increased endorbital pressure caused by a retrobulbar hematoma. This procedure resulted in the partial or complete recovery of vision in all but one case (No. 15). This patient was referred from another hospital 48 h after the traumatic event, causing delays in diagnosis and treatment that led to the failure of vision recovery. Ophthalmologic assessment was requested within 12 h after surgical decompression, if the patient's condition allowed.

Megadoses of steroids were preoperatively administered to seven hematoma patients, according to the NASCIS II protocol. [19] The use of megadose steroid therapy in patients with severe visual deficits following traumatic optic neuropathy has been extensively discussed. [20],[21],[22],[23],[24] In 1999, the International Optic Nerve Trauma Study found "sufficient evidence to conclude that neither corticosteroids nor optic canal surgery should be considered the standard of care for patients with traumatic optic neuropathy." [25] Given their beneficial effects on spinal cord injuries, however, physicians are reluctant to not use megadose steroid therapy to treat traumatic optic neuropathies. [24]

The mechanism of compartment syndrome following an orbital hemorrhage is well defined. The orbital contents are enclosed in a fascial sheath and surrounded by rigid bony walls, except for the semi-flexible anterior border created by the orbital septum and eyelids. Increased volume from even minimal bleeding in this space may increase the orbital pressure. Perfusion pressure to the retina is thereby reduced, resulting in compression of the long and short ciliary vessels and successive ischemic damage to the retina. Gerbino et al., [5] therefore, stated that "the most critical aspect of orbital hematoma treatment is the rapidity of the diagnosis and the decision to perform surgical drainage." Drainage was performed in the patients in our study with the same surgical approach used to treat orbital wall fractures. A marginotomy allowed better exposition for drainage of the hematoma.

The role of surgery in the management of ocular injuries is controversial; some centers routinely explore all causes of traumatic vision loss, while others perform only selective exploration. Postsurgical improvements have been reported among many ocular injury patients, including those with no initial light perception and those operated upon several months after injury. [26],[27],[28],[29],[30] Spontaneous improvement without medical or surgical intervention has also been reported. [31],[32]

The 11 patients in our study with indirect traumatic optic neuropathy received megadoses of steroids within 8 h after the traumatic event. Steroid therapy was associated with the surgical treatment of facial fractures in seven of these patients, and partial or complete recovery of vision was achieved in nine patients. In contrast, megadose steroid therapy had no apparent effect in two patients with direct traumatic optic neuropathy.


   Conclusions Top


The maxillofacial surgeon may encounter severe ocular injuries during the emergency assessment of patients with facial fractures. More subtle ocular injuries, however, may be missed by a nonophthalmologist. The maxillofacial surgeon must, therefore, be able to perform an ROA and to evaluate the severity of ocular lesions.

The ophthalmic assessment of an unconscious patient should minimally include observation of the pupils, ocular structures, and changes in global pressure, even in the presence of significant post-traumatic eyelid swelling. A conscious patient is able to provide an accurate anamnesis, alerting the physician to previous ocular pathologies or ophthalmologic surgical interventions that may contribute to the diagnosis.

The ROA should be performed as soon as the patient's condition allows, quickly assessing pupillary reactions and the patient's ability to count fingers. In cases of severe vision loss, knowledge of the timing can allow the surgeon to distinguish among retinal damage, optic nerve damage, and other causes. The vision should be monitored for several hours, because further deterioration may suggest an indirect traumatic optic neuropathy or a compartment syndrome.

The cause and site of the lesion are important factors; previously reported data and our results show a higher frequency of severe ocular injuries associated with fractures of one or more orbital walls, following a workplace accident or MVA. CT scans should be used to assess the risks presented by the ocular lesion by confirming the orbital fracture, identifying potential fracture extensions to the bony canal of the optic nerve, and excluding the presence of endorbital hematomas.

In consultation with an ophthalmologist, the maxillofacial surgeon will be able to plan the treatment of skeletal and ocular lesions. Some ocular injuries may require management before repair of the bony lesions, whereas other lesions of the ocular adnexa may be treated simultaneously or following the repair of maxillofacial fractures.

 
   References Top

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Correspondence Address:
Paolo Boffano
Head & Neck Department, Division of Maxillofacial Surgery, San Giovanni Battista Hospital, Turin
Italy
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-2700.82204

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    Figures

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    Tables

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