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Home , Annulus of Zinn, Optic disc, Periorbital cellulitis, Sphenoid sinus

YIJOM-3286; No of Pages 10

Int. J. Oral Maxillofac. Surg. 2015; xxx: xxx–xxx

http://dx.doi.org/10.1016/j.ijom.2015.10.014, available online at http://www.sciencedirect.com

Case Reports

Trauma

R. E. Warburton, C. C. D. Brookes,

B. A. Golden, T. A. Turvey

Orbital apex disorders: a case

Department of Oral and Maxillofacial Surgery,

School of Dentistry, University of North

series Carolina at Chapel Hill, Chapel Hill, NC, USA

R. E. Warburton, C. C. D. Brookes, B. A. Golden, T. A. Turvey: Orbital apex

disorders: a case series. Int. J. Oral Maxillofac. Surg. 2015; xxx: xxx–xxx. # 2015

International Association of Oral and Maxillofacial Surgeons. Published by Elsevier

Ltd. All rights reserved.

Abstract. Orbital apex syndrome is an uncommon disorder characterized by

ophthalmoplegia, proptosis, , hypoesthesia of the forehead, and vision loss. It

may be classified as part of a group of orbital apex disorders that includes superior

orbital fissure syndrome and cavernous syndrome. Superior orbital fissure

syndrome presents similarly to orbital apex syndrome without optic

impairment. syndrome includes hypoesthesia of the cheek and

lower in addition to the signs seen in orbital apex syndrome. While

historically described separately, these three disorders share similar causes,

diagnostic course, and management strategies. The purpose of this study was to

report three cases of orbital apex disorders treated recently and to review the

Key words: orbital apex syndrome; superior

literature related to these conditions. Inflammatory and vascular disorders,

orbital fissure syndrome; cavernous sinus

neoplasm, , and trauma are potential causes of orbital apex disorders.

syndrome; orbital compartment syndrome; pto-

Management is directed at the causative process. The cases described represent a

sis; proptosis; ophthalmoplegia; optic neuropa-

rare but important group of conditions seen by the maxillofacial surgeon. A review thy; maxillofacial surgery.

of the clinical presentation, etiology, and management of these conditions may

prompt timely recognition and treatment. Accepted for publication 16 October 2015

1

Orbital apex syndrome (OAS) is an uncom- oculosympathetic paresis, and impairment SOFS developing into OAS or CSS. For

mon disorder characterized by impairment of the ophthalmic and maxillary branches the purpose of discussion OAS, SOFS, and

1

of cranial III, IV, VI, and the oph- of cranial nerve V. CSS presents with CSS can be grouped together as a single

thalmic branch of cranial nerve V, and optic ophthalmoplegia, ptosis, proptosis, de- condition, differentiated chiefly by the

neuropathy. Patients present with ophthal- creased vision, and loss of sensation in anatomical position of the causative pa-

moplegia, proptosis, ptosis, visual im- the ipsilateral forehead, , , thology.

4,5 1

pairment, a fixed dilated , and and cheek. CSS can present bilaterally. Three new cases of orbital apex disor-

hypoesthesia of the ipsilateral forehead, Cranial nerve involvement may be com- ders are reported to illustrate the three

1

upper eyelid, and cornea. Superior orbital plete or incomplete in all three syndromes. syndromes and highlight several key caus-

fissure syndrome (SOFS) presents similarly While frequently described separately ative factors. The relevant anatomy, etiol-

to OAS, without the accompanying optic in the literature, these three orbital apex ogy, and available diagnostic and

2,3

nerve impairment. Cavernous sinus syn- disorders share a similar etiology, diag- treatment modalities are also described.

1,6

drome (CSS) involves palsy of cranial nostic course, and treatment. These syn- This study was reviewed by the Institu-

nerves III, IV, and VI, , dromes can be progressive in nature, with tional Review Board and deemed exempt.

0901-5027/000001+010 # 2015 International Association of Oral and Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved.

Please cite this article in press as: Warburton RE, et al. Orbital apex disorders: a case series, Int J Oral Maxillofac Surg (2015), http:// dx.doi.org/10.1016/j.ijom.2015.10.014

YIJOM-3286; No of Pages 10

2 Warburton et al.

Case series clinic with a 4-day history of right mid-

facial pain and swelling without orbital

Case 1

involvement. He was admitted to the hos-

A 16-year-old Caucasian male with pital with a presumed facial infection of

marked midfacial hypoplasia, retrogenia, unknown cause for further work-up and

and right-sided hemihypoplasia presented intravenous antibiotics. Shortly after ad-

for a Le Fort III osteotomy modified to mission, the patient developed rapid onset

maintain nasal position, right split thick- of ophthalmoplegia, proptosis, ptosis, and

ness parietal harvest with grafting to complete vision loss OD. The right pupil

the bilateral supraorbital rims and mid- was found to be fixed and dilated. Oph-

face, and genioplasty. Preoperative oph- thalmology was consulted and the patient

thalmic evaluation revealed normal vision was found to have an intraocular pressure

(20/20 in the right (OD) and 20/25 in of 57 mmHg OD by handheld tonometry.

the left eye (OS)) with no afferent pupil- The patient was diagnosed with an OAS

lary defect or . secondary to an orbital compartment syn-

The patient was administered 125 mg of drome, and an emergency lateral canthot-

methylprednisolone and 1 g of cefazolin omy with inferior cantholysis was

intravenously at the start of the procedure performed bedside. Intraocular pressure

and every 4 h subsequently. The midface improved to 38 mmHg OD after the pro-

was mobilized and advanced without dif- cedure. Vision loss and ophthalmoplegia

ficulty. The inner cortex remained intact were unchanged. Brimonidine and dorzo-

during the harvest. The or- lamide/timolol were administered topical-

bital osteotomies were located within ly and an emergency CT of the face was

1 cm of the orbital rim and carried into obtained. Imaging revealed a large cystic

the inferior orbital fissure. No fracture or mass in the right with

Fig. 1. Intraoperative CT scan revealing no

extension of the osteotomies to the orbital erosion of the posterior maxillary sinus

fracture or hematoma involving the right or-

apex was observed. wall and right orbital with poste-

bital apex or . 7

Upon completion of the procedure, the rior tenting (Fig. 2).

right pupil was noted to be fixed and The patient was taken as an emergency

dilated with a 4-mm discrepancy when der of his neurological examination was to the operating room for drainage of the

compared to the left pupil. Bilateral benign. Magnetic resonance imaging right maxillary sinus via a Caldwell–Luc

were non-reactive, which was attributed to (MRI) of the brain and orbits was performed, approach and further orbital decompres-

the depth of anesthesia. The coronal and which revealed no signs of orbital apex sion. Otolaryngology was contacted to

intraoral incisions were reopened and the compression or intracranial pathology. determine the benefit of concomitant en-

right was explored, with no hemato- The patient was diagnosed with a pre- doscopic sinus surgery, but the decision

ma or pulsatile bleeding noted. Ophthal- sumed SOFS. Intravenous methylprednis- was made to defer additional sinus inter-

mology was consulted to help evaluate for olone (125 mg) was continued every 4 h vention at that time. After drainage of the

an intraorbital cause of the patient’s ani- throughout his hospitalization. A formal maxillary sinus, the right intraocular pres-

socoria. Intraocular pressures were found ophthalmic evaluation at less than 24 h sure improved to 16 mmHg by handheld

to be normal at 15 mmHg OD and after surgery found visual acuity to be tonometry and no additional orbital de-

20 mmHg OS by handheld tonometry. 20/40 OD, 20/20 OS. The patient under- compression was pursued. Cultures were

The neurosurgery service was consulted went serial ophthalmic examinations, obtained and the maxillary sinus contents

to rule out any intracranial pathology. An which showed slight improvement in pto- were sent for histopathological evaluation.

emergency computed tomography (CT) of sis and continued ophthalmoplegia. The Postoperative visual acuity improved to

the head and face was obtained, which patient was discharged on postoperative 20/200 OD. The right pupil was sluggishly

revealed no intracranial hemorrhage, mid- day 2 with a 7-day prednisone taper. At the reactive. Ophthalmoplegia was unchanged.

line shift, or brainstem compression. No time of discharge, the patient’s vision was The patient was started on vancomycin and

fracture or hematoma involving the super- 20/30 OD, 20/20 OS with a 2-mm discrep- piperacillin/tazobactam. Maxillary sinus

ior orbital fissure or orbital apex was noted ancy in pupillary size and minimal reac- cultures revealed no growth. The intraop-

(Fig. 1). The patient’s surgical wounds tivity to light OD. erative pathology results returned as sino-

were then closed and he was transferred Three weeks postoperatively, the patient with features consistent with

to the pediatric intensive care unit for showed improved extraocular movements acute on chronic rhinosinusitis. Serial oph-

close neurological monitoring. and ptosis OD. The binocular and thalmic examinations revealed improved

The patient’s postoperative ophthalmic pupillary dilation remained. Five weeks visual acuity and pupillary reactivity, al-

examination revealed complete right postoperatively, the ptosis and ophthalmo- though extraocular motility deficits per-

ophthalmoplegia, mild proptosis, and plegia had improved greatly. The right sisted.

moderate ptosis. The right pupil was pupil remained dilated with some residual The patient was discharged to home on

6 mm and non-reactive to direct light, binocular diplopia. At the 10-week follow- postoperative day 5 with a 7-day course of

although the consensual response was in- up, all symptoms had resolved. amoxicillin/clavulanic acid. Visual acuity

tact. The patient initially reported blurred was 20/25 + 2 OD, 20/20 OS at the time of

vision OD that improved through a pin- discharge. Subsequent fol-

Case 2

hole occluder. Color vision was intact. He low-up at 1 month revealed resolution of

had binocular diplopia as well as antici- A 15-year-old Caucasian male with asth- symptoms except for a persistent right

pated cranial nerve V deficits. The remain- ma and chronic rhinosinusitis presented to inferior arcuate defect. The patient

Please cite this article in press as: Warburton RE, et al. Orbital apex disorders: a case series, Int J Oral Maxillofac Surg (2015), http:// dx.doi.org/10.1016/j.ijom.2015.10.014

YIJOM-3286; No of Pages 10

Orbital apex disorders 3

On postoperative day 3, the patient

returned to clinic with left peri-orbital pain

and swelling, which had started the day

after surgery. Ophthalmology was con-

sulted and reported left orbital proptosis,

partial ophthalmoplegia, and chemosis.

Visual acuity was 20/40-1 OD, 20/60-1

OS and intraocular pressure was

12 mmHg OD, 21 mmHg OS by handheld

tonometry. The patient’s pupils remained

symmetric and reactive, with no afferent

pupillary defect. No changes in color vi-

sion or hypoesthesia of the left forehead,

eyelids, or cheek were noted.

The patient was sent to the emergency

department for a CT of the head and face

with a presumed . She was

administered a dose of intravenous clin-

damycin and dexamethasone, as well as

topical brimonidine and dorzolamide/ti-

molol. Imaging confirmed prior fractures

and additionally revealed a minimally dis-

placed left orbital floor fracture. No he-

Fig. 3. (A) CT scan demonstrating left orbital

matoma, cellulitis, or entrapment was

Fig. 2. (A) CT scan demonstrating a large proptosis and enlargement of the left orbital

noted. Mild dilation of the left superior

right maxillary cystic mass with erosion of the vasculature (arrow). (B) CT angiography re-

ophthalmic vein was observed. Detection

posterior maxillary sinus wall extending into vealing an enlarged left cavernous sinus (ar-

the right infratemporal fossa. (B) CT scan of a temporal bruit by the maxillofacial row), mild enlargement of the left extraocular

demonstrating right orbital cellulitis and par- surgery team prompted further investiga- musculature, and engorgement of the left

tial opacification of the right ethmoid and tion with CT angiography, which revealed superior ophthalmic vein indicative of a ca-

sphenoid sinuses. Right posterior globe tent- a left carotid–cavernous fistula (Fig. 3). rotid–cavernous fistula.

ing is present, signifying an acute increase in

The patient underwent transarterial coil

intraorbital pressure with stretching of the 9

7 embolization of the left carotid–cavernous 13–17 mm of the orbit. The superior or-

.

fistula by interventional radiology without bital fissure follows the junction of the

event. The patient was monitored over- roof and the lateral wall and is formed

underwent right-sided functional endo- night in the neurosurgical intensive care medially by the lesser wing of the sphe-

scopic sinus surgery with right maxillary unit. Serial ophthalmic examinations dem- noid and laterally by the greater wing of

antrostomy and right anterior ethmoidect- onstrated marked improvement in propto- the sphenoid. The optic canal is located in

omy approximately 3 months after his ini- sis, ptosis, chemosis, and extraocular the superomedial corner of the orbital

tial presentation. motility. The patient was transferred to apex and is formed by the two roots of

9

the ward after 24 h and was discharged the lesser wing of the sphenoid.

to home on hospital day 3 with dorzola- The , from which four of

Case 3

mide/timolol eye drops and erythromycin the six attach,

A 44-year-old Caucasian female presented ointment. encloses the optic foramen and the medial

to clinic 4 days after a motor vehicle The patient was evaluated by ophthal- portion of the superior orbital fissure

accident. She had been seen initially by mology 12 days after discharge. She (Fig. 4). The annulus of Zinn contains

an outside emergency department where reported mild blurred vision at a distance the optic nerve, ophthalmic artery, cranial

her head and cervical spine had been and diplopia with left gaze. Examination nerves III and VI, and the nasociliary

9

cleared. Upon evaluation she was found revealed a left consistent with nerve. These structures are at greater risk

to have a right mandibular body and left left abducens palsy. The patient was seen 6 of compression or shear injury as a result

mandibular angle fracture. A left cheek weeks after discharge for a follow-up of their confinement within the annulus of

3

laceration had been closed at the outside arteriogram, which showed no residual Zinn. The lateral portion of the superior

emergency department. Only axial cuts arteriovenous shunting. Further ophthal- orbital fissure contains cranial nerve IV,

from the outside hospital CT scans were mic evaluation at 11 weeks noted a re- the , the , and

9

available; these demonstrated a minimally solved left esotropia and no residual the superior ophthalmic vein. Cranial

displaced left lateral maxillary sinus wall defects. nerve IV is less frequently involved in

fracture in addition to the fractures de- SOFS and OAS secondary to its anatomi-

scribed above. cal location outside the annulus of

3,10

The patient was taken to the operating Discussion Zinn.

room for open reduction and internal fixa- The cavernous sinuses are located lat-

Anatomy

tion of her bilateral mandible fractures eral to the and posterior to the

with wire maxillomandibular fixation. The orbit is pyramidal in shape, consisting superior orbital fissure. The ophthalmic

8

The patient did well postoperatively and of four walls, an apex, and a base. The and maxillary branches of cranial nerve

was discharged home with oral antibiotics orbit is approximately 40–50 mm deep, V and cranial nerves III and IV pass

following the procedure. with the apex encompassing the posterior through the lateral wall of the cavernous

Please cite this article in press as: Warburton RE, et al. Orbital apex disorders: a case series, Int J Oral Maxillofac Surg (2015), http:// dx.doi.org/10.1016/j.ijom.2015.10.014

YIJOM-3286; No of Pages 10

4 Warburton et al.

22

carcinoma can involve the orbital apex

via perineural spread, local invasion, or

metastasis. Rhabdomyosarcoma is one of

the most common orbital tumors of child-

hood, and can cause an OAS via mass effect

23

or direct invasion. Lymphoma affecting

the orbital apex can arise from localized

invasion from the ,

base, or from distant metastasis. Primary

lymphoma of the orbital apex has also been

24

reported. Metastatic melanoma, breast,

kidney, or lung cancer can also result in

1

an orbital apex disorder.

3

Fig. 4. Schematic of the right orbital apex contents (from Chen et al. ). Infection

25

Chandler et al. classified orbital infec-

sinus. The internal carotid artery and post- and lateral canthal tendons. Rapidly pro- tions into five groups: preseptal cellulitis,

ganglionic sympathetic fibers pass gressive intraorbital pressure can result in orbital cellulitis, sub-periosteal abscess, or-

through the medial portion of the sinus. an orbital compartment syndrome, leading bital abscess, and cavernous sinus throm-

Cranial nerve VI travels within the sinus to ischemic damage to the and optic bosis.

between the internal carotid artery and the nerve, potentially resulting in permanent Preseptal cellulitis can occur as a result

11 14

lateral wall. vision loss. of acute , upper respiratory infec-

26

The clinical features of OAS, SOFS, tion, peri-orbital trauma, or otitis media.

and CSS are based on the anatomical Due to the acting as a

Etiology

position of the pathological process. Im- barrier, preseptal cellulitis rarely pro-

pairment of cranial nerves III, IV, and VI gresses into the orbit and can be differen-

3 Inflammatory disorders

results in ophthalmoplegia. Proptosis tiated from other forms of orbital infection

occurs due to the loss of extraocular mus- Multiple granulomatous inflammatory by the absence of visual or extraocular

26,27

cle tension on the globe, retrobulbar swell- diseases have been implicated in orbital movement impairment.

2

ing, or venous congestion. Ptosis can be apex disorders. Granulomatosis with poly- Sinusitis is the most common cause of

caused by impaired cranial nerve III in- angiitis, Churg–Strauss syndrome, and orbital cellulitis, sub-periosteal and orbital

1,5,15

nervation to the levator palpebrae super- sarcoidosis have all been described. abscesses, and septic cavernous sinus

27,28

ioris muscle or by loss of sympathetic Tolosa–Hunt syndrome is a rare disorder thrombosis. Children are more com-

8 27

innervation to the superior tarsal muscle. caused by granulomatous inflammation of monly affected than adults. Infection

Mydriasis occurs as a result of impaired the orbital apex or cavernous sinus in may be transmitted directly via the lamina

parasympathetic innervation from cranial which patients present with unilateral or- papyracea of the , which is

2

nerve III. Loss of corneal reflex is caused bital pain and ophthalmoplegia that typi- thin with multiple dehiscences that can

by involvement of the . cally resolves within 72 h of corticosteroid allow for communication between the eth-

1,16 27

Damage to the optic nerve can occur at therapy. Optic neuropathy is rare and moid sinuses and the orbit. Infection can

the , or along the intraorbital, symptoms can be recurrent. also be spread from the maxillary or fron-

intracanalicular, or intracranial portions of Extraocular myositis can be idiopathic or tal sinuses through bony erosion or pre-

12 15

the nerve. Most traumatic injury occurs secondary to Graves’ ophthalmopathy. existing dehiscence of the sinus walls.

at the intracanalicular portion of the optic Clinical features of Graves’ ophthalmopa- Indirect transmission of bacteria between

12,13

nerve. This is due to the periosteum of thy include , eyelid retraction the paranasal sinuses, orbit, and the cav-

the optic canal being continuous with the with , chemosis, and con- ernous sinus can also occur through the

dural covering of the optic nerve as it junctival injection. Restrictive ophthalmo- venous system that drains this anatomical

29

passes through the canal, causing the optic plegia and can occur in region. Case patient 2 presented with a

17

nerve to be more susceptible to compres- advanced cases. Graves’ ophthalmopathy maxillary sinus infection with erosion of

3,9

sion, tension, or shear injury. typically consists of an active inflammatory the posterior maxillary sinus wall and

18

CSS can involve both the ophthalmic phase and an inactive fibrotic phase. involvement of the pterygopalatine fossa,

and maxillary branches of cranial nerve V, Symptoms are a result of autoimmune-me- potentially allowing for infection to prog-

reflecting their position along the lateral diated extraocular muscle enlargement and ress into the orbit via the inferior orbital

5

wall of the cavernous sinus. Cranial nerve adipogenesis, which increases intraorbital fissure.

19

VI is more frequently involved in CSS pressure and impedes venous drainage. ,

when compared to cranial nerve III and pneumoniae, and anaerobic Gram-nega-

cranial nerve IV, due to its location within tive bacilli such as Prevotella, Porphyr-

4 Neoplasms

the sinus. Communication via the inter- omonas, and Fusobacterium have been

1,28,30

cavernous sinuses can result in bilateral Primary neural tumors affecting the orbital noted frequently upon culture.

cavernous sinus involvement. apex include neurofibroma, schwannoma, Mucormycosis and aspergillosis have

The orbit is functionally a closed com- , glioma, and meningio- been implicated in immunocompromised

1,19 20 1,31

partment, with anterior expansion limited ma. cystic carcinoma, squa- hosts. As seen in case patient 2, an

21

by the orbital septum, tarsi, and medial mous cell carcinoma, or mucoepidermoid acute orbital compartment syndrome can

Please cite this article in press as: Warburton RE, et al. Orbital apex disorders: a case series, Int J Oral Maxillofac Surg (2015), http:// dx.doi.org/10.1016/j.ijom.2015.10.014

YIJOM-3286; No of Pages 10

Orbital apex disorders 5

43

result from a rapidly progressive orbital maxillary disjunction. In case patient 1, growth of a cavernous carotid aneurysm

infection. no fracture of the superior orbital fissure or can result in compression of the optic

optic canal was noted in postoperative nerve or superior orbital fissure, leading

imaging. There was an air-fluid level in to an OAS or SOFS. CSS can occur as a

Trauma 53

the , possibly indicating a result of lateral aneurysm growth. Cav-

Orbital apex disorders can occur as a result non-displaced sphenoid fracture. Indirect ernous carotid aneurysms in rare instances

of craniomaxillofacial trauma. Limited transmission of sheer or concussive forces, can result in intracranial hemorrhage, ca-

data are available regarding the incidence or swelling of the orbital apex in the rotid–cavernous fistula formation, or

of OAS or CSS; however retrospective setting of hypotensive anesthesia, result- thromboembolism causing distal cerebral

51

studies have found the incidence of SOFS ing in ischemic neuropathy, can also not infarction.

after facial trauma to range from 0.3% to be excluded as a potential cause of the

10,32

0.8%. Fractures associated with the patient’s SOFS.

orbital apex include skull base, high Le

Diagnosis

Fort, orbital, nasoorbitoethmoidal, and

Vascular disorders

zygomaticomaxillary complex frac- An orbital apex disorder is diagnosed

9,10,32

tures. Carotid–cavernous fistulas, cavernous si- clinically. A detailed history and physical

Direct and indirect mechanisms of inju- nus thrombosis, and cavernous carotid examination should be performed on any

33

ry can occur. Direct injury can be a result aneurysms can result in an orbital apex patient in whom an orbital apex pathology

of penetrating trauma or impingement of disorder. Carotid–cavernous fistulas are is suspected. This must include a com-

the orbital apex by displaced bony frag- traditionally classified as direct or indirect plete ophthalmic evaluation, followed by

ments. Indirect injury occurs by transmis- lesions. Direct carotid–cavernous fistulas serial examinations, ideally by the same

sion of shear forces to the superior orbital arise from a communication between the provider.

fissure or optic canal from the surrounding internal carotid artery and the cavernous Imaging is important in discerning the

34,35 44

facial skeleton. This can result in or- sinus. They are typically high-flow causative etiology. MRI or fine-cut CT

bital axonal damage and injury to the pial lesions that are most commonly associated imaging of the head and face is helpful

11

vessels supplying the optic nerve, result- with trauma. Injury to the carotid artery in characterizing neoplastic, infectious, or

ing in ischemic necrosis or compressive can be the result of penetrating trauma or inflammatory disorders. The non-contrast

12,34

hematoma formation. Post-traumatic laceration secondary to bony fracture. fine-cut CT scan of the head and face is the

intracanalicular optic nerve swelling and Transmission of traumatic forces to the study of choice to evaluate for orbital apex

9

vasospasm can result in further dam- arterial wall, or an abrupt increase in fractures in craniomaxillofacial trauma.

34,36

age. Reperfusion of neuronal tissue intraluminal pressure can potentially lead Magnetic resonance angiography or CT

11,45

can result in the formation of free radicals, to rupture. Carotid–cavernous fistulas angiography can help identify vascular

1

leading to lipid peroxidation and cell give rise to venous hypertension and con- causes. Laboratory tests are ordered as

13

membrane damage. gestion, resulting in the characteristic triad indicated by the history, physical exami-

Trauma is a well-known cause of orbital of acute onset pulsatile exophthalmos, nation, and imaging findings. Biopsy can

46

compartment syndrome. It is generally a chemosis, and bruit. Venous hyperten- be obtained in cases of orbital apex

result of retrobulbar hemorrhage, orbital sion can lead to intracranial hemorrhage, masses.

emphysema, or retrobulbar edema. The massive epistaxis, and cerebral or retinal Orbital compartment syndrome is an

11,47

incidence of retrobulbar hemorrhage ischemia. emergency condition differentiated clini-

resulting in orbital compression ranges Indirect carotid–cavernous fistulas are cally from other orbital apex disorders by

37 38

from 0.45% to 3.6%, with most cases caused by communication between the a rapidly progressive loss of vision and

14

associated with fractures of the orbit or cavernous sinus and dural branches of tense proptosis. Intraorbital pressure

zygomaticomaxillary complex. Orbital the internal carotid artery, the external can be estimated by digital palpation of

44

emphysema is typically a benign condition carotid artery, or both. They are largely the globe or more precisely approximated

39 40

associated with 50% to 60% of orbital low-flow, spontaneous in nature, and less by measurement of intraocular pressure

11

fractures. In rare cases, an orbital com- commonly associated with trauma. Clin- by tonometry. Cadaveric models have

partment syndrome can occur when the ical symptoms are generally less severe. found a close correlation between intraor-

54,55

orbital adnexa occludes a traumatic com- Aseptic cavernous sinus thrombosis can bital and intraocular pressures. Nor-

munication between orbit and paranasal potentially occur in patients predisposed mal intraocular pressures range from 10 to

56

sinuses, creating a one-way valve that to a hypercoagulable state. Trauma, ma- 20 mmHg. An acute change in intraoc-

allows air to enter the orbit but not es- lignancy, post-surgical status, inflamma- ular pressure exceeding 40 mmHg can

39,41 48

cape. Sneezing, vomiting, or nose tory bowel disease, polycythemia vera, result in compromised blood flow to the

57,58

blowing can drive air into the orbit result- acquired and hereditary coagulopathies, optic disc, resulting in ischemia. In-

ing in an acute increase in retrobulbar pregnancy, and oral contraceptives can traocular pressure above 40 mmHg via

41 49,50

pressure. The use of a high-speed air- result in thrombus formation. tonometry in the setting of a suspected

cooled dental drill during dentoalveolar Cavernous carotid aneurysms can occur orbital compartment syndrome is an

surgery has also been implicated in the as a result of trauma, infection, atheroscle- indication for emergency surgical decom-

59,60

development of a compressive orbital em- rosis, or congenital weakening of the arte- pression. Measurement of intraocular

42 51 52

physema. rial wall. Approximately 18% to pressure is also necessary to provide a

53

Orbital apex disorders have also been 34% of cavernous carotid aneurysms starting point by which the efficacy of

reported during Le Fort osteotomies. This are asymptomatic and are typically dis- any treatment can be compared. Care

has been attributed to atypical fracture covered incidentally on imaging studies. should be taken when interpreting intra-

propagation or indirect transmission of The most commonly reported symptoms ocular pressures in the patient,

52

forces to the skull base during pterygo- are orbital pain and diplopia. Anterior as they may be chronically elevated.

Please cite this article in press as: Warburton RE, et al. Orbital apex disorders: a case series, Int J Oral Maxillofac Surg (2015), http:// dx.doi.org/10.1016/j.ijom.2015.10.014

YIJOM-3286; No of Pages 10

6 Warburton et al.

Treatment impairment should undergo surgical drai- Trauma

nage.27,64

Inflammatory disorders There is no current consensus on the man-

There have been many different surgi-

agement of traumatic orbital apex disor-

Granulomatous inflammatory disorders cal approaches described in the literature.

ders. Corticosteroid therapy, surgical

are managed in a multidisciplinary setting The medial orbit can be approached via a

decompression, the combination of corti-

with systemic immunomodulatory agents, Lynch–Howarth or transcaruncular inci-

27 costeroids and surgery, and observation

including corticosteroids, cyclophospha- sion. This allows for surgical access to

19,61 have all been described as potential treat-

mide, methotrexate, and azathioprine. the ethmoid sinuses via the lamina papyr- 3,36,70

ment modalities.

The treatment of Graves’ ophthalmopathy acea, as well as the medial aspect of the

is dependent on the clinical phase of the superior orbit. A transconjunctival ap-

disease. In the acute phase, management proach allows for access to the inferior

65 Corticosteroids

consists of immunosuppression with cor- orbit. A Caldwell–Luc approach, as uti-

ticosteroids or external beam radiothera- lized in case patient 2, can be used for Corticosteroid use in the treatment of

py. Surgical decompression of the orbit if involving the maxillary sinus. traumatic orbital apex disorders has been

71

indicated is recommended during the in- A transnasal endoscopic approach is advocated since the early 1990s. The use

18,19

active phase. often preferred in the management of me- of corticosteroids was reinforced by the

65,66

dial sub-periosteal abscesses. This ap- results of the National Acute Spinal Cord

72

proach allows for improved cosmesis, Injury Study II (NASCIS II), a multicen-

Neoplasms

reduced postoperative edema, and short- ter randomized double-blind study that

The management of neoplasms of the ened hospitalization times compared to evaluated patient response to intravenous

66

orbital apex is dictated by the causative traditional external approaches. Super- methylprednisolone after acute spinal cord

pathology. Surgical resection, radiation ior or inferior extension of the sub-perios- injury. Patients were administered a meth-

therapy, and chemotherapy are all poten- teal abscess can require a combined ylprednisolone bolus of 30 mg/kg fol-

tial treatment modalities. external and endoscopic approach. lowed by an infusion of 5.4 mg/kg/h for

Case patient 2 presented with a maxil- 23 h. Patients who received this high-dose

lary sinus infection that rapidly progressed methylprednisolone protocol within 8 h of

Infection

into the orbit, resulting in an acute orbital injury showed a significant improvement

Orbital cellulitis, orbital abscesses, and compartment syndrome. Management of in motor and sensory function at 6

72

sub-periosteal abscesses should be treated this emergency condition requires prompt months and improved motor function

73

aggressively with broad-spectrum intrave- recognition and treatment to avoid perma- after 1 year compared to those who

nous antibiotics that cover staphylococci nent vision loss. The decision to treat received placebo. High-dose corticoster-

and streptococci. Anaerobes are found in should be decided based on clinical pre- oid therapy has been suggested to improve

24% of post-septal orbital infections and sentation and not delayed to obtain imag- microvascular circulation in injured neural

67,68

should also be considered when selecting ing studies. Hayreh et al., in studies tissue and inhibit lipid peroxidation, there-

27 36,74

antibiotic coverage. Final antibiotic involving rhesus monkeys in which a tran- by reducing neural cell damage.

therapy should be dictated by culture sient central retinal artery occlusion was Evidence supporting corticosteroid ad-

and susceptibility test results. induced, found that the retina can tolerate ministration in the treatment of traumatic

There has been little investigation into approximately 100 min of ischemia before orbital apex disorders has come from mul-

the effects of corticosteroids on orbital irreversible damage occurs. Medical treat- tiple small retrospective case series, often

infections. A retrospective study of 23 ments such as topical dorzolamide, timo- lacking uniformity in corticosteroid dose

2,3,71,75

patients with a sub-periosteal abscess lol, and brimonidine, and systemic agents or implementation of controls.

70

reported no adverse outcomes in patients such as acetazolamide, corticosteroids, Acartu¨rk et al., in a recent retrospective

who received corticosteroids in addition to and mannitol can be beneficial if not con- case series of 11 patients, evaluated the

62

routine treatment. A prospective, single- traindicated, but are not a substitute for efficacy of corticosteroid treatment in

14

blind study of 21 patients treated for an surgical intervention. SOFS and OAS. Patients were treated with

orbital infection showed improvement of A lateral canthotomy and inferior a similar high-dose methylprednisolone

ptosis, proptosis, visual acuity, and extrao- cantholysis is the treatment of choice for protocol to that employed in the NASCIS

14

cular movements when corticosteroids rapid decompression of the orbit. Suc- II trial. Each patient showed clinical im-

were administered starting on hospital cessful decompression is accompanied by provement within 48 h, with complete

63 70

day 4 compared to antibiotics alone. a decrease in intraocular pressure and resolution of symptoms by 6 months.

This study, however, excluded pediatric improvement in visual function. A super- Other evidence suggests that cortico-

patients under 10 years old. ior cantholysis or orbital septolysis can be steroid administration may have little ef-

In addition to broad-spectrum antibiotic completed if no improvement occurs after fect on post-traumatic visual acuity. The

55

coverage, surgical intervention is indicat- a brief period. Insufficient inferior International Optic Nerve Trauma Study

76

ed in the presence of an orbital or sub- cantholysis should also be considered. If (IONTS) was a prospective non-ran-

periosteal abscess. The management of surgical decompression remains inade- domized interventional study that evalu-

sub-periosteal abscesses is somewhat con- quate, emergency imaging should be ated the effects of observation,

troversial. Some authors suggest a trial of obtained and further intervention under corticosteroids, or surgery on visual acuity

14

antibiotic therapy with close ophthalmic general anesthesia pursued. Additional in 133 patients with indirect traumatic

observation in patients less than 9 years orbital decompression can be achieved optic neuropathy. Patients were initially

old with no visual impairment and a small with careful blunt intraorbital dissection examined within 3 days of injury and

69

medially located abscess. Patients who are via an inferolateral anterior orbitotomy, treatment was initiated within 7 days of

over 9 years old, fail to improve with or removal of the orbital floor, medial or injury. Eighty-five of the enrolled patients

14

antibiotic therapy, or present with visual lateral walls. received intravenous methylprednisolone

Please cite this article in press as: Warburton RE, et al. Orbital apex disorders: a case series, Int J Oral Maxillofac Surg (2015), http:// dx.doi.org/10.1016/j.ijom.2015.10.014

YIJOM-3286; No of Pages 10

Orbital apex disorders 7

or equivalent in dosages ranging from less Based on the existing evidence, high- nerve decompression, found that cortico-

than 100 mg per day to greater than dose corticosteroids have not been shown steroids offer no significant improvement

5400 mg per day. The authors found no to provide a proven benefit in the treat- in visual acuity. Thirty-two of 33 patients

significant improvement in visual acuity in ment of traumatic orbital apex disorders. in the IONTS who underwent surgery also

subjects treated with corticosteroids at any The decision to administer corticosteroids received corticosteroids, with no signifi-

76

dose compared to untreated patients. should be based on the circumstances of cant benefit when compared to observa-

76

These results were further supported in the individual patient after an appropriate tion alone.

a subsequent randomized, double-blind discussion of the risks and benefits. Pro-

placebo-controlled trial involving 31 viders should exercise caution when con-

Observation

patients that evaluated the benefit of cor- sidering high-dose corticosteroids in

ticosteroids in the treatment of traumatic patients with a traumatic head injury. Complicating any evaluation of the effi-

77

optic neuropathy. Patients with a trau- cacy of available medical and surgical

matic injury less than 7 days old were treatments is the relatively high rate of

Surgical decompression

started on 250 mg intravenous methyl- spontaneous improvement in visual acuity

prednisolone every 6 h for 3 days, fol- Surgical decompression of the optic canal and cranial nerve function seen in patients

lowed by 1 mg/kg prednisone for 14 or superior orbital fissure has been pro- with traumatic orbital apex disorders.

3

days. No significant improvement in visu- posed in cases of bony impingement, optic Chen et al. reviewed 19 previously de-

al acuity was found in patients treated with nerve sheath hematoma, or to relieve optic scribed case reports of SOFS and found

3,10,78

corticosteroids compared to placebo at the nerve swelling. Surgical techniques that eight (42%) had complete resolution

77

3-month follow-up. to access the orbital apex include a trans- of symptoms with no intervention other

84

High-dose corticosteroids have also maxillary approach, orbitozygomatic than reduction of concomitant facial frac-

3

been associated with negative out- approach, transethmoidal approach, and tures. The literature on traumatic optic

74,78 85

comes. Patients enrolled in NASCIS transcranial pterional approach. The re- neuropathy reports spontaneous improve-

12,33,76

II treated with high-dose corticosteroids duction of surrounding maxillofacial frac- ment in 0–57% of patients. This

had significantly worse motor and sensory tures has also been suggested by some wide distribution is in part a result of

2,75

outcomes compared to placebo when authors to provide additional benefit. differences in the timing of the initial

33,36

treatment was started at more than 8 h Evidence supporting surgical decom- clinical evaluation across case series.

79

after injury. The Medical Research pression is limited to primarily small,

Council Corticosteroid Randomization retrospective case series. Wohlrab

86 Vascular disorders

After Significant Head Injury (MRC et al. reported improvement in visual

CRASH) study was a prospective, ran- acuity in eight of 19 patients (42%) with The treatment of choice for direct carotid–

domized, double-blind, placebo-con- traumatic optic neuropathy who under- cavernous fistulas is endovascular embo-

11

trolled trial investigating the effect of went surgical decompression of the optic lization. Transarterial or transvenous

87

high-dose corticosteroids after head inju- canal. Fujitani et al. reported visual im- approaches may be employed using metal

80

ry. Subjects suffering from traumatic provement in 34 of 70 (47.7%) that coils, detachable balloons, or liquid adhe-

11,91

head injury with a Glasgow Coma Scale underwent transethmoidal surgical de- sives. Covered stent grafts have also

10 92

score of 14 or less were assigned to a 48-h compression. Chen et al. reported a sim- been described. More than 80% of

methylprednisolone protocol or placebo ilar level of recovery of cranial nerve III, patients treated with endovascular embo-

within 8 h of the initial trauma. The meth- IV, and VI function in six patients with lization experience complete resolution of

11

ylprednisolone protocol consisted of a 2-g SOFS after surgical decompression when symptoms. Surgical intervention may be

infusion over 1 h, followed by a 0.4-g/h compared to 27 patients who did not un- considered if endovascular embolization

maintenance infusion for 48 h. The study dergo decompression, despite worse initial has failed or is otherwise not feasible.

was stopped after enrolling 10,008 sub- cranial nerve function in the surgical Techniques described include clipping

jects due to increased mortality in subjects group. or suturing of the fistula, packing of the

80

treated with high-dose corticosteroids. cavernous sinus, or ligation of the internal

Animal studies have also cast doubt on carotid artery with an intracranial by-

Corticosteroids and surgery 11,93

the benefits of corticosteroid treatment. pass.

81

Ohlsson et al. reported no difference There is no strong evidence to suggest that Indirect carotid–cavernous fistulas can

in visual evoked potentials, retinal cell a combined approach involving cortico- often be managed conservatively, as 20–

11

survival, or axonal degeneration or regen- steroids and surgical decompression has 60% will resolve spontaneously. Regu-

eration after optic nerve crush injury in greater efficacy when compared to other lar follow-up is requisite to monitor for

88

rats treated with high-dose methylprednis- treatment modalities. Li et al., in a non- changes in visual acuity, fundoscopic ex-

82

olone compared to controls. Huang et al. randomized study of 237 patients with amination, or a significant increase in

94

found that neither intraocular triamcino- traumatic optic neuropathy, found no sig- intraocular pressure. Patients with sig-

lone nor systemic methylprednisolone nificant difference between those patients nificant ocular pain, headache, progressive

provided any additional benefit compared treated with corticosteroids and endoscop- vision loss, or elevated intraocular pres-

to placebo in the preservation of retinal ic optic nerve decompression and those sure not responsive to medical therapy

cells after optic nerve crush in- treated with corticosteroids alone. Yang may require endovascular emboliza-

83 89 11,94

jury in a rat model. Steinsapir et al. et al., in a retrospective case series of 96 tion. Transvenous approaches are of-

reported a dose-dependent increase in op- patients who underwent endoscopic optic ten necessary secondary to the complex

tic nerve axonal loss with the administra- nerve decompression, found no additional vascular anatomy associated with indirect

91

tion of intravenous methylprednisolone benefit from corticosteroid administration. carotid–cavernous fistulas. Stereotactic

90

when compared to intravenous saline in Similarly, Ropposch et al., in a study of radiotherapy can result in occlusion of a

rats after optic nerve crush injury. 42 patients treated with endoscopic optic carotid–cavernous fistula over the course

Please cite this article in press as: Warburton RE, et al. Orbital apex disorders: a case series, Int J Oral Maxillofac Surg (2015), http:// dx.doi.org/10.1016/j.ijom.2015.10.014

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are not available or are unsuccessful.

Bussone G, International Headache Society.

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Not required.

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149 Brauer Hall

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Please cite this article in press as: Warburton RE, et al. Orbital apex disorders: a case series, Int J Oral Maxillofac Surg (2015), http:// dx.doi.org/10.1016/j.ijom.2015.10.014