Fig. 4.1
Medial wall fractures: (а) “trap-door” fracture. There is some adipose tissue entrapped in the fracture site (arrow), (b) comminuted fracture of the medial wall, (c) comminuted fracture on axial CT, (d) “punched-out” fracture with single separated bone fragment, (e, f) inferomedial fracture
Sneezing may cause not only a blow-in fracture (which is quite logical) but also a blowout fracture. The possible mechanism underlying bone fragments being displaced into the ethmoidal cells may be explained by the rapid increase in intranasal pressure, passage of air into the orbit, and acute orbital emphysema. Air reflux into paranasal sinuses displaces the fragments of orbital lamina of the ethmoidal bone resulting in a blowout pattern [12]. This fracture type is a good illustration of the hydraulic theory as there is no pressure to on the orbital rim or direct impact of the deformed globe on the medial wall [14].
The majority (90 %) of isolated medial wall injuries occur in the pediatric age group and are linear “trap-door” or tongue-shaped fractures (∩ – formed fractures) [8, 23–25]. This is due to high bone elasticity which allows for transient deformation. While the vast majority of this type of fracture is seen in the pediatric population, it is also possible in adults [4, 26].
The mechanism of “trap-door” fracture is similar to that of the orbital floor injury. Medial wall fragments are pushed outwards (into the ethmoidal cells) and after the impact return to their initial position entrapping less mobile soft tissue [26].
Comminuted fractures or fractures with one detached (“punched-out”) bone fragment are observed in 7 % of cases due to a very low thickness (0.27 mm) and fragility of medial orbital wall in the elderly [8, 23, 24, 27–29].
Thus, the main types of medial wall injuries are isolated (linear or ∩ – formed “trap-door,” comminuted, and “punched-out” fracture), inferomedial, and nasoorbitoethmodial fractures (Figs. 3.4 and 4.1) each with its specific clinical manifestation.
4.1 Isolated “Trap-Door” Fracture
This fracture is clinically characterized by the immediate onset of diplopia and limitation of horizontal globe motion, often accompanied by nausea, minimal edema and hematoma of the eyelids, and absence of enophthalmos [4].
Diplopia during adduction/abduction may be considered the pathognomonic sign of this fracture [6, 9, 30]. One third of the patients complain of diplopia in the primary gaze position, but others develop this sign within 30° from fixation point [31]. One should remember that diplopia with an isolated medial wall fracture may be clinically evident in only 50 % of cases [23], and its absence does not rule out orbital injury.
Occasionally “trap-door” fractures may entrap the medial rectus [25, 26, 32]. Before 1975 only six cases were reported [33], and only six more cases were reported in the following years. Interestingly, all reported patients were black, which may be interpreted as an anatomical predisposition to such injuries due to ethnical differences in midface anatomy [34]. This hypothesis is supported by other case reports on Asian patients, in which medial wall fractures are more commonly seen compared to orbital floor fractures [9, 30, 35]. The incidence of medial wall fractures in patients from Southeast Asia is shown to be higher due to thinner medial wall, weaker nasofrontal suture, lower nasal bridge, and weaker orbital rim compared to Caucasians [4].
Limitation of globe movements is present in 10–25 % of cases and, according to S. Lerman rules, is determined by the site of medial rectus muscle entrapment (preequatorial or postequatorial) [8, 23, 36]. When the anterior portion of the muscle is entrapped, Duane1 pseudosyndrome is observed. Posterior portion entrapment results in exotropia with significant limitation of adduction and normal abduction of the globe2 [3, 4, 25, 37, 38].
Fig. 4.2
Clinical signs of medial wall fracture: (а) esotropia of the left eye in an anterior medial wall fracture; (b–d) exotropia of the left eye (b) with significant limitation of adduction (c) and normal abduction (d), suggesting the entrapment of the posterior part of the medial rectus; (e) eyelid hematoma and subconjunctival hemorrhage, indirect signs of medial wall fracture; (f) orbital emphysema (*) and its drainage technique (g) (see explanation in the text)
Positive duction test (limitation of abduction), sometimes accompanied by nausea and the oculocardiac reflex, confirms muscle or muscle sheath entrapment and rules out other possible causes of globe movement restriction such as injury to the oculomotor nerve and/or contusion of the medial rectus [25].
4.2 Isolated Comminuted and Punched-Out Fractures
Isolated, comminuted, and punched-out fractures are characterized by a vivid clinical picture. The key diagnostic triad includes diplopia, limitation of horizontal globe motion, and positive abduction test and is commonly accompanied by periorbital edema, ecchymosis, and subconjunctival hemorrhage (Fig. 4.2e) [4, 5, 18, 34, 39].
In one third of patients, the area of the isolated fracture exceeds 4 cm2 which causes mild enophthalmos (up to 2 mm) [8].
Nasal bleeding (epistaxis) is an obvious sign of fracture [21, 40]. The source of bleeding is the anterior ethmoidal artery which is frequently damaged even after minimal displacement of the bone fragments of the medial orbital wall. Small anterior ethmoidal cells are quickly filled with blood, which then flows from the hiatus semilunaris into the middle nasal meatus and obturates it. Difficulties in nasal breathing force a patient to blow his/her nose which leads to orbital emphysema. This characteristic sign of the medial wall injuries [41] was first described by R. Berlin in 1880.
According to radiological findings, emphysema is diagnosed in approximately 50 % of patients with orbital fractures [42] and indicates the involvement of the paranasal sinuses [43]. Orbital emphysema is particularly common in medial wall injuries3 [17, 41, 44].
Emphysema in orbital fractures4 is associated with the communication between orbital cavity and ethmoidal cells, which in 100 % of cases follows the disruption of sinus mucosa. Thus, orbital emphysema is always accompanied by blood in the sinus [17].
Forceful expiratory effort (sneezing, nose blowing, etc.) elevates the intranasal pressure up to 115 mmHg and presses the air into the orbit. If the periosteum is intact, the air can accumulate in the subperiosteal space causing dystopia of the globe and blindness in extreme cases. In most cases, mild emphysema spontaneously resolves in 7–14 days [12, 13].
If the periosteum is ruptured, air passes into the orbit and spreads along the fascia into subconjunctival, preseptal, and postseptal spaces. Generally, it accumulates at the injured orbital wall. Orbital tissues in this case sometimes are pushed against the wall and block the communication, acting as a valve which can lead to the development of tension emphysema [42]. Clinical signs include axial, vertical, or horizontal dystopia. Tension emphysema and valve mechanism are especially characteristic of “trap-door” fractures [45].
Acute increase in intraorbital pressure is usually absorbed by elastic orbital tissues, allowing the displacement of the globe. In the majority of cases, emphysema spontaneously resolves without any sequelae [45, 46].
Rarely, emphysema leads to irreversible loss of vision due to the impairment of vascular supply to the optic nerve or occlusion of the central retinal artery. This clinical scenario is seen predominantly in younger patients whose orbital septum begins to deform at a pressure of only 70–100 mmHg (according to the experimental data of Сh. F. Heerfordt (1904)). This deformation may cause compression of the optic nerve.
Because the perfusion pressure of the retina and optic nerve is only 60–70 mmHg, the increased orbital pressure caused by the deformation of the orbital septum may be greater than the perfusion pressure to the nerve and retina. If that occurs, blood flow to the retina will stop, and if that continues for more than 100 min, it will cause irreversible damage to the retina.
Medical history of recent blunt trauma to the bridge of the nose or orbit or forceful expiratory effort (sneezing and nose blowing) may be helpful in the diagnosis of emphysema. Routine physical examination is also very informative (edema of the eyelids increasing while blowing the nose, crepitus in the periocular soft tissues [35]). Visual acuity and pupil reaction should be a part of the initial evaluation. Other recommended investigations include ophthalmoscopy, intraocular pressure measurement, and CT of the orbit [45].
Staging of orbital emphysema:
Stage I—small radiologically diagnosed asymptomatic air mass in the orbit. The treatment is limited to prophylactic oral antibiotics and vasoconstrictive nasal drops for the congestion relief.
Stage II—increase in air mass leads to dystopia and thereby diplopia. In addition to standard treatment, CT scan is recommended to diagnose injuries requiring delayed surgical intervention.
Stage I and stage II are not accompanied by the loss of vision.
Stage III—the increasing air mass causes the failure of the absorbing mechanism of orbital soft tissues. There is an increase in intraocular pressure and obstruction of the blood flow in the smallest vessels of the optic nerve. Severe loss of vision with ophthalmoscopically normal retinal circulation may be observed.
Stage IV—intraocular pressure due to tension emphysema increases up to 60–70 mmHg leading to central retinal artery occlusion and blindness in 100 min. Severe loss of vision with the ophthalmoscopical picture of a central retinal artery occlusion is observed.
Stage III and stage IV cause severe loss of vision5; therefore immediate medical treatment is needed.
In case of emphysema with significant increase in intraocular pressure and loss of vision, orbital decompression should be considered.
After the localization of the air mass on CT scans, drainage of the orbit is performed according to the J. V. Linberg technique (1982). The air mass is drained with a 25-gauge needle attached to a saline-filled syringe with the plunger removed [48]. Proper placement of the needle is confirmed by the appearance of water bubbles in the syringe (Fig. 4.2g). If there is loss of light perception, drainage is combined with canthotomy and cantholysis (Fig. 3.25).
A timely and successful drainage results in rapid return of intraorbital and intraocular pressure to normal and restoration of the blood flow and visual acuity [17, 42, 49, 50].
In the absence of contraindications, single intravenous injection of 30 mg/kg prednisolone is given followed by 15 mg/kg prednisolone every 6 h for 24 h. Symptomatic therapy includes administration of analgesics and antiemetics [45].
Theoretically, emphysema with underlying sinusitis may cause infection of the orbital soft tissues [47]. Therefore broad-spectrum antibiotics in prophylactic doses are indicated, although the necessity and benefit of such treatment is yet to be proved [12].
Emphysema of the face, neck, or mediastinum are uncommon for medial wall fractures, but these complications should be kept in mind, because they may be misleading and interpreted as a clinical sign of thorax or abdominal injury [43, 51, 52].
S. J. Garg et al. (2005) [10] first described the unique case of asymptomatic “blowout” medial orbital wall fracture with a bone fragment penetrating the globe.
4.3 Inferomedial Fracture
If medial wall injury is a part of inferomedial fracture, all patients develop diplopia (Fig. 4.1е, f), and 40 % of patients experience globe movement restriction. If the area of the fracture exceeds 4 cm2 (approximately 80 % of cases), clinically significant enophthalmos (more than 2 mm) is observed.
Nasal congestion causing repetitive nose blowing and orbital emphysema is less common in inferomedial fractures, since blood accumulates in the more spacious maxillary sinus compared to the ethmoidal cells.
Extensive inferomedial fracture is very rarely complicated by globe dislocation into the ethmoidal cells [53, 54]. The first description of the globe dislocation into ethmoidal cells is thought to be published by Raghav et al. [55]. In some cases globe dislocation may still have a favorable functional outcome [56, 57]; however, more commonly it causes irreversible loss of vision and restricted globe mobility in spite of successful globe reposition and reconstruction of muscles and orbital walls [54].
Another rare condition after inferomedial fracture resembles Brown syndrome (superior oblique tendon sheath syndrome with the limitation of globe supraduction during adduction). In this case, the patient experiences diplopia in a primary gaze position and ipsilateral hypotropia. The recommended treatment is the recession of the inferior rectus of the ipsilateral eye [58].
Clinical signs of nasoorbitoethmoidal fracture are discussed in corresponding chapters.
4.4 Radiological Signs
X-ray gives a clear view of the medial wall fracture only in 15 % of cases [44] due to superimposition of multiple anatomical structures in the nasoorbitoethmoidal region [59]. Generally, the diagnosis of medial wall fracture is based on indirect clinical signs including orbital emphysema and ethmoidal cells opacification [60].
Introduction of high-sensitive CT scanners brought the diagnosis of medial wall fractures to a higher level [21, 59]. Thus, the number of medial wall surgical procedures has doubled in the past decade [61].
Axial and coronal views are especially useful in this pathology [34]. CT signs of medial orbital wall fracture besides obvious displacement of bone fragments include [9]:
Entrapment of the orbital fat in the ethmoidal cells (Fig. 4.1а)
Orbital emphysema and hemosinus (Fig. 4.3а)
Fig. 4.3
CT signs of medial orbital wall fracture: (а) air mass under the roof of the orbit and blood in the ethmoidal cells (arrows) on coronal CT indicate medial orbital wall fracture regardless of the seemingly intact medial wall contour. (b) Medial wall fracture with thickening and dislocation of medial rectus belly (arrow). (c) Displacement of medial rectus into ethmoidal sinus, the muscle seems to be absent both in the orbit and in the sinus. Arrow shows contralateral medial rectus. (d) Entrapment of the posterior portion of the medial rectus (arrow). (e) Bone fragment. (f) Extensive blowout fracture of the medial wall
4.5 Treatment of the Medial Wall Fractures
Surgical treatment of the “blowout” medial orbital wall fracture is aimed at the restoration of a normal orbital wall, reconstruction of the initial orbital shape and volume, and normalization of ethmoidal ventilation [23].
It should be remembered that not all patients with medial orbital wall fractures need surgical treatment [1, 2, 29, 63].
Indications for medial orbital wall reconstruction [28, 63] are:
Enophthalmos > 2 mm
Globe movement restriction
Persistent horizontal diplopia
Bone defect >2 cm2 with fragment displacement ≥3 mm
Accompanying orbital floor fracture
“Rounding” of medial rectus (height to width ratio >0.7 according to coronal CT) which is a sign of late enophthalmos
Surgical Timing. “Trap-door” fracture of the orbital wall is a medical emergency [4]6; other medial wall injuries should be surgically treated 7–14 days after acute symptoms are controlled [23].
Surgery should be carried out under endotracheal or intravenous anesthesia.
The surgical approach to the medial orbital wall is determined by the localization and extent of the fracture. The different approaches are transcutaneous, transconjunctival, microscopic transnasal, and endoscopic [23, 64].
Transcutaneous approaches include subciliary, upper lid, medial eyebrow, medial canthal, and bicoronal incisions.
The subciliary incision is described in detail in the previous chapter and is considered the optimal transcutaneous approach [9, 38, 39] but gives a suboptimal view of the upper third of the medial wall.
In contrast, the bicoronal approach (Fig. 4.4а) exposes the whole medial wall leaving the medial canthal ligament intact but requires extensive dissection and may cause a significant bleeding. Postoperatively this incision may be complicated by persisting forehead skin anesthesia.
Fig. 4.4
Surgical approaches to the medial orbital wall (transcutaneous): (а) coronal (1), along the inner half of the fold of the upper eyelid (2), and medial eyebrow approach (3). The course of supratrochlear nerve is shown with the dashed line. (b) Lynch approach (2.5-cm curvilinear skin incision made 10 mm medial to the insertion of medial canthal ligament, followed by the division and blunt dissection of the periosteum of the medial orbital wall up to the middle third of the lamina papyracea). (c) Upper medial Z-formed approach. Arrows show the location of the medial canthal ligament and trochlea of superior oblique that should be avoided during skin incision. (d) Upper medial W-formed approach (see description in text). (e) (1) Inferior (preseptal and postseptal) transconjunctival approach without lateral canthal ligament dissection; (2) medial transconjunctival (transcaruncular or retrocaruncular) approach. The incision is begun in the sulcus between the lacrimal caruncle and plica semilunaris and continued up to 20 mm along the inferior conjunctival fornix. Subconjunctival dissection to the posterior lacrimal crest is made in the avascular zone parallel to the medial wall behind Horner’s muscle. Division of periosteum is made behind the posterior lacrimal crest; (3) inferior transconjunctival approach with the division of lateral canthal ligament; combinations of inferior and medial approaches, with dissection of lateral palpebral ligament if necessary, are also used. (f) The line of transcaruncular incision. (g) Transcaruncular approach in coronal plane. (h) Orbital zones exposed by different methods (1) coronal approach, (2) approach along the upper eyelid, (3) medial eyebrow approach (Illustration materials from www.aofoundation.org)
The incision along the medial half of the fold of the upper eyelid poorly exposes deep parts of the orbit and does not allow the placement of a large implant. The medial eyebrow approach may also lead to the permanent numbness of the forehead skin due to the supratrochlear nerve injury (Fig. 4.4а).
The ethmoidal Lynch incision provides a good view of all areas of the medial wall (Fig. 4.4b), but it is made perpendicular to the Langer’s skin tension lines. This leads to excessive scarring and deformation of the medial canthus [23, 65]. To avoid this complication, not only the well-known medial and upper medial Z incisions can be used (Fig. 4.4c) [68] but also the W modification of this incision as proposed by Burns et al. [23].
Upper Medial W-Formed Approach. After temporary tarsorrhaphy, the 3-cm-long W-formed incision is made along the upper medial edge of the orbit, starting 1 cm medial from the insertion of medial canthal ligament to the lower medial edge of the eyebrow (Fig. 4.4d). The angles between the cuts are approximately 110–120°. Because all four cuts run parallel or at an acute angle to the Langer’s skin tension lines, this incision results in a very cosmetic scar. The lateral part of the W-formed incision may be continued laterally along the lower edge of the medial third of the eyebrow, if necessary, providing good view of the whole medial wall and a placement of larger implant (up to 3 cm in length) to close total wall defect.
A careful splitting (parallel to the orbital edge) of the orbicularis oculi is then performed to avoid supratrochlear nerve injury.
Division of the periosteum is made at the upper edge of palpebral canthal ligament (partially cutting it off, if necessary) and carried out to the upper medial orbital edge 3–4 mm from the rim. It is important to preserve the inferior part of the medial canthal ligament to avoid the subsequent telecanthus formation. Periosteum is then separated from the medial wall up to the lacrimal bone.
To avoid injuries to the trochlea which will result in diplopia due to acquired Brown’s syndrome and injuries of the lacrimal sac, adjacent periosteum is not dissected. After the dissection of periosteum from the medial orbital wall and inner part of the orbital roof, the fracture, entrapped soft tissues, and anterior ethmoidal neurovascular bundle become clearly visible. Anterior ethmoidal vessels should be cauterized to prevent profuse bleeding. Dissection is generally extended up to the middle third of the lamina papyracea. When the posterior ethmoidal artery becomes exposed, further dissection should be immediately stopped due to high risk of optic nerve injury.
Transconjunctival approaches include inferior and medial incisions [40, 69], extended transcaruncular approach [70], and a combination of transcaruncular and inferior transconjunctival approaches (Fig. 4.4е, f) [31, 71].
Inferior conjunctival incision was already described in detail in previous chapter(s). The main disadvantage of this approach is poor exposure of upper areas of the medial wall [22].
Medial Conjunctival (Retrocaruncular) Approach (Fig. 4.4f–h). In this approach the 10–14-mm-long incision is made behind the lacrimal caruncle followed by blunt dissection to reach the suture between the lacrimal and ethmoidal bones. After the dissection of the periosteum, the fracture zone becomes visible and the anterior ethmoidal artery is cauterized if necessary [66].
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