Sports are a significant source of facial injury. According to published data, 3%-29% of facial injuries occur during sports (39). The complex anatomy of the face makes diagnosis and treatment of these injuries challenging. It is important for those who participate in the care of athletes to understand the wide variety of facial injuries that occur during sports. It is critical for those providing medical coverage on the sidelines at sporting events to be able to recognize and manage facial injuries that require urgent treatment.
Evaluation of the athlete with significant facial injury should begin with the primary survey or "ABCDE" approach outlined in the Advanced Trauma Life Support (ATLS) guidelines. This includes evaluation and maintenance of the airway (with control of the cervical spine), breathing, circulation (with control of hemorrhage), disability (neurologic evaluation), and exposure and environmental control. Next, only after successful resuscitation of the patient when indicated, the secondary survey should be performed. The secondary survey is the "head to toe" evaluation of the patient, including a thorough history and physical examination. If the patient's condition deteriorates, a primary survey should be repeated. The unconscious athlete should be assumed to have a cervical spine injury.
Perry et al. (29) describes facial injuries that result in life-threatening conditions. These include the following:
- Facial injuries resulting in airway compromise (such as panfacial fractures with gross displacement, mobility, or swelling, comminuted mandibular fractures, profuse bleeding, foreign bodes)
- Anterior neck injuries resulting in airway compromise (such as penetrating injuries, laryngeal or tracheal injuries)
- Injuries resulting in profuse blood loss (such as penetrating neck injuries and facial fractures)
Although these are rare, it is important for the sports medicine practitioner to understand the potential worst-case scenarios, particularly in combat sports or extreme sports.
In facial injuries, true emergencies are uncommon (29). Perry et al. described emergency care in facial injury as airway care, control of profuse bleeding, and the management of vision-threatening injuries. A quick assessment of vision can be performed during the primary survey, which may save the athlete's vision. The pupils are assessed during "D" (disability) to assess neurologic status, but this also can reveal presence of a relative afferent pupillary defect (RAPD), which is a sign of optic nerve or retinal injury. The athlete also can be asked quickly whether he or she can see clearly, and the globes can be palpated over closed eyelids. This may reveal a collapsed globe in the case of open globe rupture or a tense, proptosed globe if there is a retrobulbar hemorrhage.
Eye trauma is the leading cause of noncongenital blindness in patients under 20 yr of age and the fourth most common cause of visual loss in those under the age of 46 (12,28,31,48). In the United States, baseball is the most common cause of eye injury in children between the ages of 5 and 15 yr. Racquet sports cause nearly one third of all sports-related eye injuries to those between the ages of 25 and 65 (12,31,48). Protective eyewear can prevent many of these injuries (37).
Ideally, the initial evaluation of a patient with eye trauma should include assessment of visual acuity, gross external examination, funduscopic examination, assessment of optic nerve function, evaluation of the pupils, visual field testing, intraocular pressure measurement, and assessment of extraocular eye movements (44). On the sideline, this often is not practical because of the setting and limited equipment. The following abbreviated examination can be performed as an initial evaluation:
- Palpation of the globes and gross examination for laceration, swelling, orbital rim step off, or any other injury.
- Visual acuity with a handheld eye chart.
- Determine whether light from a penlight is perceived as brighter in one eye versus the other. This is a test for optic nerve injury and is less sensitive than testing for red color saturation and light intensity, but it is more practical on the sideline.
- Determine whether there is RAPD.
- Assess the size of the pupils.
- Test extraocular eye movements.
- Visual field testing. Stand face-to-face with the athlete and slowly bring a finger into the visual field from the periphery. The athlete should see the finger enter the visual field at the same time as the examiner.
A variety of eye injuries can occur in sport, but the most important to understand are the vision-threatening injuries. These include globe injuries, retrobulbar hemorrhage, traumatic optic neuropathy, and eyelid laceration (29). Other eye injuries, such as retinal detachment or lens dislocation, generally do not threaten rapid irreversible loss of vision but should be evaluated by an ophthalmologist as soon as possible. In the unconscious athlete, the key factors to assess on examination are pupillary size, pupillary reaction to light, and globe tension with gentle palpation (29). The presence of RAPD is a sensitive indicator of visual impairment. Presence of RAPD indicates asymmetrical damage to the retina, optic nerve, chiasm, or optic tract (9). RAPD is called "relative" because the examiner is comparing the pupillary reaction to light of one pupil relative to the other. The swinging flashlight test, in which the examiner alternates shining light in one eye then the other, can be used to detect RAPD. When light is shined in the unaffected eye, both eyes will constrict, and when the light is moved rapidly to the affected eye, both eyes will appear to dilate. This is because, in the case of RAPD, the affected eye constricts less than the unaffected eye and the ocular reflex (efferent response) is consensual. A patient with either anisocoria or dilation of both pupils after facial trauma may have increased intracranial pressure and must be evaluated in the emergency department immediately.
Blunt trauma to the eye may cause either an open or closed globe rupture. An open globe rupture has a full-thickness tear through the cornea and sclera, and a closed globe rupture does not. Globe rupture is a common cause of blindness in trauma and may not be obvious on exam, requiring a high index of suspicion in blunt eye trauma (3). Signs and symptoms include decreased visual acuity, severe subconjunctival hemorrhage involving 360° of the conjunctiva, and limitation of extraocular movements (9,26). Pressure must not be placed on the eye during examination because it can cause the further expulsion of intraocular contents if the patient has an open globe rupture (3).
In an open globe rupture, the globe looks collapsed and the intraocular pressure is low. Intraocular contents such as vitreous gel or uveal tissue may be seen extruding from the eye (3). A hyphema often is present, as well. In closed globe rupture, the globe looks well formed, and intraocular pressure is often high (9,29).
A plastic shield should be taped over the eye if globe rupture is suspected. Tetanus prophylaxis should be given if not current. For open globe rupture, surgical repair must be done as soon as possible and no later than 24 h after the injury (29).
Close follow-up is necessary because retinal membrane formation, cataract, glaucoma, retinal detachment, and endophthalmitis can occur.
This condition essentially is a compartment syndrome of the eye. Irreversible damage has been shown to occur after only 60 min of ischemia (17). In retrobulbar hemorrhage, bleeding and edema in the orbit lead to increased pressure and compression of the optic nerve and ophthalmic and retinal vessels, which causes ischemia of the optic nerve and retina. The important signs to look for are proptosis, loss of vision, pain, and an afferent pupillary defect. In an unconscious patient, a tense, proptotic globe and a dilated pupil may be the only signs of a retrobulbar hemorrhage. It is important to note that a dilated pupil also may be a sign of brain injury causing increased intracranial pressure. Lateral canthotomy and inferior cantholysis can be performed to help relieve pressure while the patient is waiting for surgery. Definitive treatment is surgical decompression (5,29).
Traumatic Optic Neuropathy
Traumatic optic neuropathy occurs when the forces involved in an injury are transmitted to the optic canal. These forces can be shearing, contusion, or stretching forces, and they cause injury to the optic nerve. Injury to the optic nerve causes inflammation leading to optic nerve compression and vaso-occlusion, which is reversible initially. Eventually, the condition progresses to arterial obstruction and irreversible infarction (29). Loss of vision usually is severe and almost immediate, but it can be partial and delayed. Immediate evaluation by an ophthalmologist is needed. Steroids are the mainstay of treatment, but surgical decompression also is used.
The most important consideration if an eyelid laceration is present is that it may be a sign of a more serious ocular injury. Assessment of the globe for penetrating globe injury or foreign body is more important initially than the eyelid laceration itself (3).
Eyelid lacerations threaten vision because drying of the cornea occurs when the eyelids cannot be closed properly. Even small eyelid lacerations can threaten vision loss in this manner (29). Medial lacerations can damage the lacrimal system. Upper eyelid lacerations can injure the levator palpebrae muscle, resulting in ptosis (43).
The eye must be protected by a generous application of antibiotic ointment or artificial tears and covering the entire eye with wet gauze to prevent drying of the cornea. Surgical repair must be performed as soon as possible because drying of the cornea occurs rapidly.
The two main parts of the tooth are the root and the crown. The crown is the portion visible above the gums, and the root is below the gumline. The superficial layer of the crown is the enamel, which is whitish in color. Below the enamel is the dentin, which is a yellowish color. Neither the enamel nor the dentin are able to regenerate themselves (18). The pulp of the tooth underlies the dentin and contains the neurovascular bundle. The root of the tooth lies in a socket of alveolar bone, which is present in the mandible and maxilla. The root attaches to the socket by the periodontal ligament. The preservation of the periodontal ligament on the avulsed tooth is critical to the possibility of successful reimplantation of the tooth (32).
For tooth fractures, luxations, or avulsions, the course of action at the time of injury is rather straightforward. Replace the avulsed tooth in its socket whenever possible, having the athlete bite down gently on gauze or cloth to keep the tooth in place. If this is not possible, place the tooth or tooth fragment in Hank's solution to preserve it (13,14,23). Handle the tooth only by the crown to avoid damaging the root and the periodontal ligament. If the tooth is not clean, wash it gently with sterile saline before placing it in the socket. The athlete must be evaluated by a dentist immediately. Reimplantation of a tooth within 30 min results in a greater than 90% chance of saving the tooth. Delay of more than 2 h results in only a 5% chance of survival of the tooth (18,22). Tetanus prophylaxis should be given if not up-to-date for tooth avulsions if the tooth contacts soil or if intraoral lacerations are present (14,32).
There are a few exceptions to the guidelines listed above. Avulsions of primary teeth should not be placed back into the socket. Intrusive luxations, in which the tooth is driven into the alveolar socket causing the tooth to look shorter than surrounding teeth, should not be repositioned in the field. Tooth fractures of only the enamel do not require urgent dental evaluation (18). A tooth fracture that is air-sensitive requires urgent dental referral. Consider the use of a temporary filling such as dental wax until a dentist can evaluate the athlete.
With any dental injury, a concussion or other head or neck injury may be present, and the athlete must be evaluated for these conditions as well. Mouthguards have been shown to decrease the occurrence of dental injury and should be recommended to athletes (32).
Facial lacerations should be irrigated with sterile saline and explored for the presence of foreign bodies or damage to underlying structures. Pressure should be applied to control bleeding. Closure can be achieved using either tissue adhesive or sutures. Tetanus prophylaxis should be given if not current. Treatment of human bite wounds should include administration of an appropriate antibiotic regimen.
Use of tissue adhesive such as octyl-2-cyanoacrylate (Dermabond™, Ethicon Inc., Somerville, NJ) can provide several advantages over the use of sutures in the closure of facial lacerations. Tissue adhesive generally is recommended for closure of simple lacerations less than 4 cm in length that are not at points of high skin tension. A randomized, controlled trial of 111 patients showed Dermabond use in facial plastic surgery patients to have a superior cosmetic outcome at 1 yr compared with sutures, with no increase in complications such as infection or wound dehiscence (46). Application of tissue adhesives generally can be accomplished more quickly than the application of sutures, does not require the use of anesthetic, prevents permanent suture tracks when sutures are not removed in a timely fashion, and avoids the pain of suturing, which is especially important in pediatric patients. Wounds should be evaluated for placement of subcutaneous sutures before tissue adhesive is applied. Absorbable subcutaneous sutures should be placed before skin closure for facial wounds that have separation of deep tissues. Otherwise, a depressed scar may result. If the laceration overlies an area with a higher level of underlying muscle contraction (forehead, perioral region, or over the mandible), subcutaneous sutures should be placed before skin closure to decrease wound tension and allow for proper skin eversion (46,47). Lack of proper skin eversion results in a widened, depressed scar from tension on the wound as it heals. Closure with sutures instead of tissue adhesive may be preferable for wounds over 4 cm in length or at points of high skin tension. If tissue adhesive is used for a laceration anywhere near the eye, be sure to place a drape to prevent dripping of the adhesive into the eye.
A suture larger than 6-0 rarely is used on the face, especially in children. The only time a 5-0 suture should be used is for a scalp laceration or for a nonvisible soft tissue surface (43). Ideally, facial lacerations should be closed using a subcuticular closure with a 7-0 monofilament nylon suture. Facial lacerations have important cosmetic, social, and psychological implications for patients, and this should be considered when repair is undertaken (43). If the laceration is too complex, it should be referred to a surgical subspecialist. Lacerations associated with underlying pathology such as facial fractures or severed nerves should not be closed and should be kept moist with saline soaked gauze to prevent drying and eschar formation. Lacerations involving the lacrimal apparatus, parotid gland, facial nerve, or anatomic borders require special consideration and should be referred for surgical repair.
Lacerations across structural or functional borders such as the vermilion border of the lip, eyelid, nasal alar rims, or helical rims of the ear require precise repair to prevent poor cosmetic results. These wounds should be closed only by highly experienced practitioners or referred for repair to a surgical subspecialist. A mistake that commonly is made in repair of lip lacerations is closure using too much tension because surrounding tissue swelling from the initial injury or infiltration of local anesthetic is not taken into account. This can be minimized by using infraorbital nerve block for upper lip repairs or mental nerve block for repairs of the lower lip (41).
Lacerations involving the facial nerve present with facial droop or asymmetry. Early diagnosis is important because earlier repair improves the chance of nerve regeneration. Also, the distal end of peripheral nerve can be stimulated for up to 72 h, which allows for accurate identification of the distal portion of the severed nerve during the repair process (43).
With any deep cheek laceration, injury to the parotid duct should be suspected. The parotid duct exits the parotid gland near the lateral border of the masseter, travels across the masseter, and enters the oral cavity lateral to the second upper molar. Although transection of the parotid duct is not common, missing this injury can result in an infected sialocele or salivary fistula. Concomitant injury to a buccal branch of the facial nerve usually occurs because it is adjacent to the parotid duct. Drainage of saliva from the wound is the most common sign of injury to the parotid duct (20).
Lacerations involving the medial one third of the eyelids may damage the lacrimal apparatus. Epiphora results with laceration of the lacrimal apparatus, and this may not be obvious at the time of injury. These injuries should be referred for surgical repair.
If the athlete suffers a facial abrasion, it initially should be cleaned with antimicrobial soap and water, followed by irrigation with sterile saline. Application of topical anesthetic such as LET (lidocaine 4%, epinephrine 0.1225%, and tetracaine 0.5%) gel or EMLA (eutectic mixture of local anesthetics; lidocaine and prilocaine in an emulsion base) cream is appropriate before cleansing larger abrasions that may be more painful. Tetanus prophylaxis should be given if not up-to-date. All debris must be removed carefully as "tattooing" of the skin can occur if the skin heals over embedded debris (10). It is crucial to remove any debris at the time of injury because it is extremely difficult to remove after the abrasion has healed. If there is too much debris or the debris is deep in the skin, the athlete should be taken to a medical facility where it can be removed.
According to recent studies, facial fractures account for 4%-18% of all sports injuries and 6%-33% of all facial bone fractures (2,8,27). Midface and mandibular fractures are notable because they may threaten the airway or cause profuse bleeding. Orbital fractures and zygomatic fractures can threaten vision.
Orbital Blowout Fractures
Orbital blowout fractures occur when blunt trauma to the eye results in collapse of the inferior orbital wall. The medial orbital wall commonly is involved, as well. Entrapment of the medial and lateral rectus muscles may occur, resulting in decreased range of extraocular movements on examination. Collapse of the inferior wall of the orbit helps to decrease the amount of pressure absorbed directly by the globe in blunt eye trauma. This may explain why blowout fractures are much more common than globe ruptures (20).
Common signs and symptoms of orbital blowout fracture include diplopia, enophthalmos, and infraorbital hypoesthesia, a result of damage to the infraorbital nerve that runs through the inferior wall of the orbit (4,30). If limitation of the extent of extraocular movements occurs with a suspected blowout fracture, urgent computed tomography (CT) scanning with coronal and axial cuts is indicated to rule out strangulation of the extraocular muscles, which will lead to muscle necrosis.
Orbital fracture can lead to superior orbital fissure syndrome. In this condition, increased intraorbital pressure leads to injury or compression of cranial nerves III, IV, ophthalmic division of V, and VI as they pass through the superior orbital fissure to enter the orbit. The result is limitation of extraocular movements, paresthesias of the forehead and brow, and pupillary dilation. This condition requires emergent surgical intervention (7).
Besides forming the malar eminence, or cheekbone, the zygoma forms a portion of the orbit and orbital rim, provides an attachment point for the superior portion of the masseter muscle, and forms the outer facial frame. Thus, zygomatic fractures can affect the vision, function of the jaw, and cosmetically, the width of the face (19,20).
Zygomatic fractures generally are from blunt trauma, presenting with flattening of the cheekbone. Other signs and symptoms of zygomatic fracture include subconjunctival hemorrhage, periorbital ecchymosis, infraorbital hypoesthesia, palpable step-off in the upper lateral orbital rim, inferior orbital rim, and upper buccal sulcus, emphysema in the orbit or overlying soft tissues of the cheek, trismus, malposition of the globe, and diplopia. Involvement of the zygomatic arch is important for cosmetic reasons because the arch forms the outer facial frame, which determines the width and anterior projection of the midface (19). Additionally, the zygoma forms the lateral orbital rim, part of the inferior orbital rim, and the lateral orbital wall, explaining the ophthalmic involvement in zygomatic fractures.
For displaced or comminuted fractures, internal fixation must be done within 2 wk (15,19). It is important to explain this to the patient, who may not be able to see the full extent of the deformities, which may be masked by overlying soft tissue swelling still present 2 wk after injury (19).
Classification of maxillary fractures is based upon fracture patterns described by René Le Fort in 1901 (24,45). The Le Fort classification system is based on the most superior level of the fracture site (Fig. 1) (25). Clinically, many fractures do not follow the pattern of Le Fort I, II, and III fractures exactly. Le Fort fractures occur with very high-impact injuries. Le Fort I fractures are least severe, and Le Fort III fractures are most severe. It is important to note that Le Fort II and III fractures are more serious fractures, which commonly cause airway obstruction and generally require hospital admission (6). Reduction of these fractures can help to control bleeding and compromise of the airway (29).
A Le Fort I fracture is a transverse fracture through the maxilla only. The fracture line runs horizontally above the roots of the teeth and just below the nose, causing separation of the tooth-bearing part of the maxilla from the rest of the maxilla (6,11). In other words, the palate is separated from the rest of the face (11). On examination, there may be a step-off deformity of the palate, or when grasping the upper teeth, the palate may be loose in an anterior-posterior direction or in an inferior-superior direction as with a loose denture (6). The posterior portion of the palate may drop inferiorly, resulting in an open bite (40). Radiographically, Le Fort I fracture is the only of the three to involve the nasal fossa (33).
A Le Fort II fracture, roughly speaking, separates a pyramid-shaped central segment containing the maxilla and nose from the orbits and zygomatic bones (7). Specifically, the superior fracture line crosses the nasal bridge, maxilla, lacrimal bones, medial and lateral orbital walls, and orbital rim. The maxilla and nasal complex will move as a unit when the upper teeth are grasped and rocked. Radiographically, a Le Fort II fracture is the only one of the Le Fort fractures to involve the inferior orbital rim (33).
A Le Fort III fracture separates the bones of the midface from the base of the cranium (craniofacial dysjunction). The fracture line runs through the bridge of the nose and extends along the medial wall of the orbit, across the floor of the orbit, through the lateral orbital wall, and finally breaks through the zygomatic arch. Manipulation of the palate will result in movement of the zygomatic bones. Radiographically, a Le Fort III fracture is the only Le Fort fracture to involve the zygomatic arch (33).
The nose is the most prominent facial structure and is the most commonly fractured bone in the adult face (16). The bones of the nose include the frontal process of the maxilla, the nasal process of the frontal bone, the ethmoid, the vomer, and the nasal bones. The cartilaginous structures of the nose include the two lower lateral cartilages, two upper lateral cartilages, and the septum. The blood supply to the nose is extensive, and epistaxis frequently is encountered in nasal fractures. Epistaxis generally originates from Kiesselbach's plexus in the anteroinferior septum. This generally can be managed by applying pressure with the fingers distal to the nasal bones for 15 min and by using nasal packing and nasal decongestant spray such as oxymetolazone or phenylephrine (21). Bleeding from posterior nasal sources usually originates from a branch of the sphenopalatine artery and may require posterior packing. In either case, if these measures do not control bleeding, the athlete must be seen by a specialist for arterial ligation or, in severe cases, interventional arterial embolization.
An important part of the history is identification of previous nasal deformities or surgery. Old pictures or the patient's driver's license can provide a means of comparison. After repair, the nose tends to return to its previously deformed state if there is a previous untreated nasal injury, making treatment of an acute nasal fracture difficult (16).
Before examination of the nose, it is important to make sure the athlete has an adequate airway. Nasal fractures generally will present with a visible deformity, tenderness, and epistaxis (Fig. 2). X-rays are not useful in detecting the presence of a nasal fracture.
Clear rhinorrhea or any fluid drainage from the nose should raise suspicions for cerebrospinal fluid leakage, which indicates fracture of the cribriform plate and puts the athlete at risk for meningitis (34). The athlete may note a sweet taste or complain of postnasal drip, as the fluid preferentially drains down the throat (16,35). Referral to an otolaryngologist should be made as soon as possible, and treatment with antibiotics will be needed because of the risk of meningitis.
The athlete with suspected nasal fracture should be evaluated carefully for signs and symptoms of naso-orbito-ethmoid fractures such as telecanthus or midface fractures. If these are present, the patient should be referred for evaluation by a specialist (21).
The septum should be examined for a septal hematoma, which is a purple or blue area of swelling. If present, it must be drained to prevent abscess formation and development of a saddle nose deformity. The athlete should be seen in follow-up because the hematoma can recur.
The best time to examine the nose is within the first few hours of the injury, before significant edema occurs. At this time, the injury can be visualized clearly and closed reduction performed. After closed reduction, the incidence of nasal deformities requiring subsequent rhinoplasty ranges from 14% to 50% (38). The athlete should understand that it is unlikely the nasal deformity will be corrected completely with closed reduction, and he or she may desire open reduction and rhinoplasty in the future.
If the athlete presents after significant edema has occurred, after assessing the patient, give pain medication and antibiotics for open wounds, instruct the athlete to ice the area and keep the head elevated, and arrange an appointment with a specialist in 5-7 d (16). At this time, edema will be resolved, and a definitive treatment plan can be made.
Mandibular fractures present with swelling, malocclusion, numbness in the distribution of the inferior alveolar nerve (lower lip), and intraoral lacerations. Malocclusion may be noted and can be checked by asking the athlete to bite a tongue blade. Over 50% of mandible fractures are multiple. The presence of one mandibular fracture should prompt the search for an additional fracture, often located contralaterally. Mandible fractures of the body, condyle, and angle occur with nearly the same frequency, while fractures of the ramus and coronoid process are less common (Fig. 3). It is imperative to be aware of possible airway obstruction, which may occur because of intraoral bleeding or tooth avulsion. Airway obstruction also can occur after bilateral mandibular angle or body fractures because of the posterior displacement of the tongue (1,42). A Barton's Bandage can be placed to stabilize the mandible until the athlete is evaluated at a medical facility.
CT or Panorex are the radiographic studies ordered for mandibular fractures. These fractures require referral to an oral maxillofacial surgeon for reduction and fixation.
RETURN TO PLAY
There is a lack of evidence-based studies on return to play after facial trauma. Currently, no specific guidelines exist. Recently, recommendations for return to play after facial fracture were published in a study by Roccia et al. in 2009 (36). The study states that the bone healing process begins with an inflammatory reaction hematoma stage for up to 5 d after fracture, followed by a callus formation stage 4-40 d after fracture, and finally, a remodeling phase, which occurs between day 25 and 50 after fracture. Based upon the timing of this healing process, the authors recommend return to play in a stepwise fashion. The authors recommend no activity for the first 20 d after fracture, light aerobic exercise only during days 21-30, noncontact training drills during days 31-40, and finally, full-contact training and game play after day 41. Advancement from one step to the next should be allowed only if the athlete is asymptomatic at the current step. The exception is for facial fractures in an athlete who participates in combat sports. In this case, return to activity is recommended no sooner than 3 months.
It should be noted that athletes have returned to play after facial fracture with protective face masks much sooner than these guidelines recommend. This is one measure that can be taken to protect athletes after facial injury, but no guidelines have been established that specify how quickly return should be allowed after specific facial injuries with or without protective devices. At this point most decisions regarding return to play after facial injury are based upon expert opinion.
A variety of facial injuries occur in sports. These can be serious injuries that cause profuse bleeding, threaten the vision, compromise the airway, or cause other disability. Proper understanding of the diagnosis and treatment of facial injuries will help to ensure the safety and good health of athletes. Use of protective equipment is key in the prevention of facial injury in sports. Development and use of safety equipment as well as guidelines for return to play after facial injury are topics for future study that can help to improve the safety of participation in sport.
The author thanks Douglas B. McKeag, M.D., FACSM, David Peck, M.D., FACSM, Vickram S. Reehal, M.D., and Umang Mehta, M.D., for their much-valued input in the preparation of this article.
1. Bavitz JB, Collicott PE. Bilateral mandibular fractures contributing to airway obstruction. Int. J. Oral Maxillofac. Surg
. 1995; 24:273-5.
2. Bayliss T, Bedi R. Oral, maxillofacial and general injuries in gymnasts. Injury
. 1996; 27:353-4.
3. Bord SP, Linden J. Trauma to the globe and orbit. Emerg. Med. Clin. North Am
. 2008; 26:97-123.
4. Brady SM, McMann MA, Mazzoli RA, et al. The diagnosis and management of orbital blowout fractures: update 2001. Am. J. Emerg. Med
. 2001; 19:148-54.
5. Brunette DD. Ophthalmology. In: Marx JA, Hockberger RS, Walls RM, et al., editors. Rosen's Emergency Medicine
, 7th ed. Mosby Elsevier; 2009.
7. Cappuccino GJ, Rhee ST, Granick MS. Maxillofacial Injuries. In: Asensio JA, Trunkey DD, editors. Current Therapy of Trauma and Surgical Critical Care
, 1st ed. Mosby Elsevier; 2008.
8. Carroll SM, Jawad MA, West M, O'Connor TP. One hundred and ten sports related facial fractures. Br. J. Sports Med
. 1995; 29:194-5.
9. Corbett JJ. The bedside and office neuro-ophthalmology examination. Semin. Neurol
. 2003; 23:63-76.
10. Echlin P, McKeag DB. Maxillofacial injuries in sport. Curr. Sports Med. Rep
. 2004; 3:25-32.
12. Ferrari LR. The injured eye. Anesthes. Clin. N. Am
. 1996; 14:125.
13. Flores MT, Andersson L, Andreasen JO, et al. Guidelines for the management of traumatic dental injuries. I. Fractures and luxations of permanent teeth. Dental Traumatology: Official Publication of International Association for Dental Traumatology
. 2007; 23:66-71.
14. Flores MT, Andersson L, Andreasen JO, et al. Guidelines for the management of traumatic dental injuries. II. Avulsion of permanent teeth. Dental Traumatology: Official Publication of International Association for Dental Traumatology
. 2007; 23:130-6.
15. Fraioli RE, Branstetter BF 4th, Deleyiannis FW. Facial fractures: beyond Le Fort. Otolaryngol. Clin. North Am
. 2008; 41:51-76.
16. Higuera S, Lee EI, Cole P, et al. Nasal trauma and the deviated nose. Plast. Reconstr. Surg
. 2007; 120.
17. Hislop WS, Dutton GN, Douglas PS. Treatment of retrobulbar haemorrhage in accident and emergency departments. Br. J. Oral Maxillofac. Surg
. 1996; 34:289-92.
18. Howe AS. Craniomaxillofacial injuries. In: Seidenberg PH, Beutler AI, editors. The Sports Medicine Resource Manual
. Philadephia: Saunders Elsevier; 2008. p. 253-71.
19. Kelley P, Hopper R, Gruss J. Evaluation and treatment of zygomatic fractures. Plast. Reconstr. Surg
. 2007; 120(Suppl. 2):5S-15S.
21. Kucik CJ, Clenney T, Phelan J. Management of acute nasal fractures. Am. Fam. Phys
. 2004; 70:1315-20.
22. Howe AS. Craniomaxillofacial injuries. In: Seidenberg PH, Beutler AI, editors. The Sports Medicine Resource Manual
. Philadephia: Saunders Elsevier; 2008. p. 253-71.
23. Kerr IL, Bigsby GA, Haeseler GA. Prevention and emergency first-aid treatment for sports-related dentofacial injuries. Compendium
. 1993; 14:1142-56.
24. Le Fort R. Experimental study of fractures of the upper jaw. Rev. Chir. Paris
. 1901; 23:208-227, 360-79 (Reprinted in Plast. Reconstr. Surg
. 1972; 50:497-506).
25. Manson PN, Hoopes JE, Su CT. Structural pillars of the facial skeleton: an approach to the management of Le Fort fractures. Plast. Recontr. Surg
. 1980; 66:54-61.
27. Mourouzis C, Koumoura F. Sports-related maxillofacial fractures: a retrospective study of 125 patients. Int. J. Oral Maxillofac. Surg
. 2005; 34:635-8.
28. National Society for the Prevention of Blindness. Vision Problems in the US
. New York, National Society for the Prevention of Blindness, 1980.
29. Perry M, Dancey A, Mireskandari K, et al. Emergency care in facial trauma-a maxillofacial and ophthalmic perspective. Injury
. 2005; 36:875-96.
30. Petrigliano FA, Williams RJ 3rd. Orbital fractures in sport: a review. Sports Med
. 2003; 33:317-22.
31. Pizzarello LD, Haik BG, editors. Sports Ophthalmology
. Springfield, IL: Thomas Books; 1987.
32. Ranalli DN. Dental injuries in sports. Curr. Sports Med. Rep
. 2005; 4:12-17.
33. Rhea JT, Novelline RA. How to simplify the CT diagnosis of Le Fort fractures. Am. J. Roentgenol
. 2005; 184:1700-5.
34. Rice DH. Cerebrospinal fluid rhinorrhea: diagnosis and treatment. Curr. Opin. Otolaryngol. Head Neck Surg
. 2003; 11:19-22.
35. Rice DH. Cerebrospinal fluid rhinorrhea: diagnosis and treatment. Curr. Opin. Otolaryngol. Head Neck Surg
. 2003; 11:19-22.
36. Roccia F, Diaspro A, Nasi A, Berrone S. Management of sport-related maxillofacial injuries. J. Craniofacial Surg
. 2008; 19:377.
37. Rodriguez JO, Lavina AM, Agarwal A. Prevention and treatment of common eye injuries in sports. Am. Fam. Phys
. 2003; 67:1481-8.
38. Rohrich RJ, Adams Jr WP. Nasal fracture management: minimizing secondary nasal deformities. Plast. Reconstruct. Surg
. 2000; 106:266.
39. Romeo SJ, Hawley CJ, Romeo MW, Romeo JP, Honsik KA. Sideline management of facial injuries. Curr. Sports Med. Rep
. 2007; 6:155-61.
41. Sagerman PJ. Wounds. Pediatr. Rev
. 2005; 26:43-9.
42. Seshul MB, Sinn DP, Gerlock Jr AJ. The Andy Gump fracture of the mandible: a cause of respiratory obstruction or distress. J. Trauma
. 1978; 18:611-2.
44. Stewart MG. Head, Face, and Neck Trauma: Comprehensive Management
. New York: Thieme; 2005.
45. Tessier P. The classic reprint. Experimental study of fractures of the upper jaw. I and II. René Le Fort, M.D. Plast. Reconstr. Surg
. 1972; 50:497-506.
46. Toriumi DM, O'Grady K, Desai D, Bagal A. Use of octyl-2-cyanoacrylate for skin closure in facial plastic surgery. Plast. Reconstr. Surg
. 1998; 102:2209-19.
47. Trott A. Wounds and Lacerations: Emergency Care and Closure
. Philadelphia: Mosby; 2005. p160-164.
48. Vinger PF. The eye and sports medicine. In: Tasman W, Jaeger WEM, editors. Duanes Clinical Ophthalmology
, Vol. 5. Philadelphia: JB Lippincott; 1992. p. 1-51.