Orbital Complications

Intraorbital Hemorrhages

6.2.1 Iatrogenic Hemorrhage due to Endonasal Surgery of the Sinuses

Intraoperative or postoperative bleeding into the orbit can be caused by sinus surgery. This can result in an orbital compartment syndrome, which, in the worst case, may be associated with a loss of vision (cf. Chapter ▶ 2). Immediate treatment of this complication is always indicated.

According to literature, orbital complications following paranasal sinus surgery (functional endoscopic sinus surgery [FESS]) occur in 0.07% of cases. 1,​ 2 The use of image-guided navigation systems seems to reduce the risk of complications. 3


Intraconal and Retrobulbar Hemorrhage

Intraconal or retrobulbar hemorrhage is usually caused by trauma to the anterior ethmoid artery, rarely also by trauma to the posterior ethmoid artery. The anterior ethmoid artery is particularly at risk in endonasal sinus surgery due to its close position to the ethmoid sinuses. 4,​ 5 An injury to the artery results in its retraction into the orbit, with subsequent acute intraorbital hemorrhage. This increase of intraorbital pressure leads to an orbital compartment syndrome with the risk of blindness due to ischemia of the optic nerve (cf. Chapter ▶ 2.4). 6

Peribulbar Hemorrhage

Peribulbar hemorrhage is usually caused by trauma of the periorbita in the front portion of the orbit. This type of complication is less severe than intraconal or retrobulbar hemorrhage. However, the displacement of the eyeball leads to a secondary increase in pressure, which, in severe cases, is accompanied by traction or pressure to the optic nerve. Clinically, this leads to proptosis and a decrease in visual acuity.


Treatment depends on the location of the hemorrhage. In lighter peribulbar bleedings without a disturbance of eye motility and without visual loss, conservative measures (cooling) can be sufficient. In peribulbar bleeding leading to proptosis, eyeball displacement, or even loss of vision, immediate endonasal orbital decompression is the treatment of choice. Targeted hemostasis by location of the retracted artery is not advisable, since it is rather difficult to find and the manipulation in the orbit leads to a further increase in pressure. Therefore, first a resection of the orbital lamina of the ethmoid bone and then the slitting of the periorbita should be performed in surgery. Necessary pressure relief can be achieved in this way. Lateral canthotomy and cantholysis are emergency procedures for additional pressure relief. 7 In retrobulbar or intraconal bleeding associated with a loss of visual acuity, the measures described are often not sufficient, indicating an additional decompression of the optic nerve.

Orbital Decompression

Resection of the Orbital Lamina of the Ethmoid Bone

First a resection of the ethmoidal cell system and exposure of the skull base is performed via an endonasal, transethmoidal approach. Then the orbital lamina of the ethmoid bone (lamina papyracea) is located in its entire anterior and posterior extension and resected. 8

Slitting of the Periorbita

To achieve further decompression, the periorbita is slit from anterior, leading to a prolapse of orbital adipose tissue. This procedure ensures the endonasal drainage of the hematoma.

Lateral Canthotomy

If sufficient pressure relief cannot be achieved by the measures described above, a lateral canthotomy (widening of the canthus) is indicated. Some authors describe this as an emergency measure ( ▶ Fig. 6.1a). 2,​ 9,​ 10 Here, the soft tissue of the eye angle is transconjunctivally cut down to the bony orbital rim. According to the literature, an intraocular pressure reduction of about 14.2 mm Hg can be achieved with this measure. 11


Fig. 6.1 Emergency procedures to relieve orbital pressure. (Reproduced from Strutz J, Mann W, eds. Praxis der HNO-Heilkunde, Kopf- und Halschirurgie. 2nd ed. Stuttgart: Thieme; 2010:459. Fig. 10:22.) (a) Lateral canthotomy. (b) Inferior cantholysis.


During the subsequent inferior cantholysis the lateral palpebral ligament and the infra-orbital septum are transected to achieve a prolapse of orbital fat. This results in the retraction of the eye, leading to a further pressure reduction of about 30.4 mm Hg. A complementary method in which the upper, stronger proportion of the canthal tendon is cut (“superior cantholysis”; ▶ Fig. 6.1b) to achieve even further pressure relief has been described more recently. Pressure can be decreased by additional 19.2 mm Hg 11,​ 12 using this method.

Decompression of the Optic Nerve

Endonasal decompression of the optic nerve can be performed with the aid of a microscope or an endoscope. After ethmoid and sphenoid sinus surgery, the bone shell of the optic nerve is located in the lateral sphenoid sinus wall and resected round a circumference of 180°. Afterwards, the nerve sheath is slit in order to relieve pressure. During sphenoid sinus surgery, attention should be paid to the internal carotid artery in the area of the lateral sphenoid sinus wall. The optic canal is located craniolateral to the internal carotid artery. Both structures are characterized by protrusions in the lateral sphenoid sinus wall. A triangular depression, usually found between the optic nerve channel and the internal carotid artery, can provide guidance (see Chapter ▶ 1). If possible, the decompression of the optic nerve should be performed using a computer-assisted navigation system.


If intraocular pressure is increased, relief within 24 hours is recommended. Due to a correlation between the duration of nerve injury and postoperative increase of visual acuity, pressure relieve within 8 hours is even better. The more quickly decompression occurs, the better the expected postoperative visual results. 8 With consistently combined conservative and surgical treatment, visual recovery is expected to range between 68% and 80%. 13,​ 14


With a rate of 0.07%, iatrogenic hemorrhage in the course of sinus surgery is rare. Due to the anatomical location, bleeding of the anterior ethmoid artery occur more frequently than bleeding of the posterior ethmoid artery. This may result in an intraconal/retrobulbar or a peribulbar hematoma, while the first is considered to be the more serious complication. Prompt initiation of therapy possibly with surgical procedures (resection of the orbital lamina of the ethmoid bone, slitting of the periorbita, lateral canthotomy, cantholysis, or decompression of the optic nerve) is essential to counteract a permanent loss of vision and blindness.

6.2.2 Bleeding into the Orbit as a Result of Trauma

A cranial or craniocerebral trauma combined with fractures of the bony orbital walls that are associated with an additional injury of arteries can result in severe bleeding into the orbit.


In pathogenic terms there are basically two ways of posttraumatic hemorrhage into the orbit:

  • The ruptured blood vessels (e.g., anterior/posterior ethmoid artery) retract into the eye socket and quickly cause an increase in intraorbital pressure due to acute bleeding.

  • Fracture lines crossing arteries that run in bone canaliculi (e.g., the infra-orbital artery) can cause direct bleeding from the bone fragment into the orbit.

The compression of the optic nerve leads to nerve damage, which may be associated with loss of vision or even blindness (= orbital compartment syndrome) (see Chapter ▶ 2.3).

Bleedings from the supra-orbital artery can result from a fracture of the orbital roof. It arises from the ophthalmic artery, runs through the orbit, and exits through the supra-orbital rim via the supra-orbital foramen.

As part of a zygomatic fracture, the infra-orbital artery, a branch of the maxillary artery, can be injured in its course. The artery runs from the pterygopalatine fossa through the maxillary foramen and infra-orbital canal, to exit via the infra-orbital foramen. Le Fort II and III fractures as well as skull base fractures can also damage the infra-orbital artery, especially in the superior and inferior orbital fissures.

The ophthalmic artery may be injured in skull base fractures that run through the optic canal.

Escher III and IV fractures (skull base fractures) can result in injury of the anterior or posterior ethmoid artery. The anterior ethmoid artery arises from the ophthalmic artery and passes through the anterior ethmoidal foramen from the orbit into the cranial cavity. The posterior ethmoid artery is also a branch of the ophthalmic artery and runs through the posterior ethmoidal foramen from the orbit into the cranial cavity.

Clinical Symptoms

Clinically, the acute condition presents a rapidly progressing, hard swelling (on palpation) of the upper and/or lower eyelid with progressive exophthalmos. Ocular motility is initially unimpeded, but then quickly limited. The lid seems to be retracted due to the exophthalmos. After a while, a reddish-bluish tissue discoloration can be observed (monocular hematoma) ( ▶ Fig. 6.2). Visual acuity may decrease rapidly in acute hemorrhage.


Fig. 6.2 Monocular hematoma (left).


Like iatrogenic bleedings, traumatic bleeding into the orbit requires immediate endonasal orbital decompression, possibly also a decompression of the optic nerve by resection of the orbital lamina of the ethmoid bone, slotting of the periorbita, and where necessary also lateral canthotomy and cantholysis as well as decompression of the optic nerve (see “Therapy” in Chapter ▶ 6.2.1).

  • Supra-orbital artery: fracture of the orbital roof.

  • Infra-orbital artery: zygomatic fracture, skull base fracture.

  • Ophthalmic artery: skull base fracture through the optic canal.

  • Anterior or posterior ethmoid artery: skull base fracture.

6.3 Orbital Complications of Acute Sinusitis

6.3.1 Pathogenesis

Orbital and intracranial complications can occur alongside acute sinusitis. Due to the close anatomical proximity, orbital complications are usually caused by an ethmoidal or frontal sinusitis (75%). Maxillary or sphenoid sinusitis is comparatively rare as a cause. 6 As the pathogenesis of sinogenic orbital complications is different in children, this topic will be discussed separately in Chapter ▶ 6.6.

A bacterial sinusitis episode is usually precipitated by an upper respiratory tract infection/rhinitis accompanied by sinusitis. Viral sinusitis are mostly caused by rhinoviruses (30–40%), less often also by coronaviruses, human parainfluenza viruses, human respiratory syncytial viruses, influenza viruses, adenoviruses, coxsackieviruses/echo viruses, and other viruses. 6 Bacterial sinusitis is usually a superinfection of a viral infection. The most common causative pathogens are Streptococcus pneumoniae (31%) and Haemophilus influenzae (21%). Anaerobes, Staphylococcus aureus, Streptococcus pyogenes, Moraxella catarrhalis, and gram-negative bacteria are found less frequently ( ▶ Table 6.1). 6,​ 15

Table 6.1 Pathogens of acute bacterial sinusitis 6


Frequency (%)

Streptococcus pneumoniae


Haemophilus influenzae


(e.g., Bacteroides, Peptostreptococcus, Fusobacterium)


Staphylococcus aureus


Streptococcus pyogenes


Moraxella catarrhalis


Gram-negative bacteria
(e.g., Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli)


Acute sinusitis has a multifactorial etiology but in most cases it is based on a ventilation disturbance of the sinuses due to a narrowing around the osteomeatal unit of the middle nasal meatus. Viral rhinitis leads to an edematous swelling of the mucosa around the sinus ostium with resultant secretion. It results in a local inflammatory response of the nasal sinuses and consecutive shift of the ostia. 6

The inflammation can be transferred to the orbit via bone gaps and blood vessels, especially through veins. Veins of the paranasal sinuses and the nasal cavity are closely associated with the veins of the orbit. For example, the ethmoidal vein of the ethmoid cells anastomose with the superior ophthalmic vein and the pterygoid plexus in the area of the maxillary sinus with the inferior ophthalmic vein. Orbital veins do not contain venous valves, enabling blood to flow in both directions between the ethmoid sinuses and the orbit dependent on the pressure gradient within the veins. During inflammations in the ethmoid sinuses, the venous pressure gradient increases, causing the venous blood to flow towards the orbit (see Chapter ▶ 1.5.2). 16 The orbital lamina of the ethmoid bone, the frontal sinus floor, and the superior, and inferior orbital fissure are bony areas of predilection for inflammatory progression ( ▶ Fig. 6.3). The activation of an inflammatory cascade causes pressure to increase within the retrobulbar compartment, which might quickly be accompanied by optic nerve damage and amaurosis. On the other hand, bacterial toxins lead to direct nerve or dural sheath damage (optic neuritis) requiring immediate surgical source control (see Chapter ▶ 2).


Fig. 6.3 Sinogenic genesis of orbital complication with swelling and redness of the upper lid.

6.3.2 Phases of Orbital Complications

The transfer of a sinogenic inflammation onto the orbit can result in various stages of orbital complications, while these stages can gradually evolve into each other or skip certain phases. Any orbital complication indicates an ophthalmological examination.

A number of different phase classifications for orbital complications can be found in the literature. ▶ Table 6.2 outlines three different classifications that are commonly used.

Table 6.2 Overview of different classifications of orbital complications


Chandler (1970) 17

Kastenbauer (1992) 18

Stammberger (1993) 19


Preseptal cellulitis

Orbital edema

Inflammatory eyelid edema


Orbital cellulitis

Orbital periostitis

Periorbital osteitis/edema


Subperiostal abscess

Subperiosteal abscess

Subperiosteal abscess


Orbital abscess

Orbital apex syndrome

Intraorbital infiltration/ abscess


Cavernosus sinus thrombosis

Orbital cellulitis

Cavernosus sinus thombosis

From the author’s own experience, the following classification of orbital complications has proved to be useful. 6,​ 8

Stage I: Orbital edema

An orbital edema manifests clinically as an inflammatory, usually unilateral, upper and/or lower lid swelling during frontal or ethmoidal sinusitis. Soft tissue inflammation is limited to the anterior orbit (“preseptal cellulitis”). Ocular motility is unimpaired and visual acuity is not reduced. The eye can usually be actively opened.

Stage II: Periostitis of the orbit

Periostitis is characterized by a transfer of the inflammation to the periosteum of the orbit, resulting in a soft tissue edema behind the orbital septum (postseptal cellulitis; synonym, orbital cellulitis), which may lead to proptosis. Ocular motility may be painful yet not restricted. At this stage, visual impairment is not yet present. The eye can usually only be opened passively.

Stage III: Subperiosteal abscess

A subperiosteal abscess is defined as a withdrawal of the periorbita from the orbital lamina of the ethmoid bone due to an inflammatory infiltration. Displacement of the periorbita accompanies the abscess. The resulting motility disorder leads to double vision. Periostitis and a subperiosteal abscess are often clinically indistinguishable. Usually, the abscess becomes visible through computed tomography or magnetic resonance imaging ( ▶ Fig. 6.4).


Fig. 6.4 CT scans of a subperiosteal abscess at the medial orbital wall on the right side, based on an adjacent ethmoid sinusitis. Air inclusions suggest gas-forming bacteria. (a) The coronal view presents the medial rectus muscle and the trochlear displaced laterally. A fine tissue lamella between the abscess and orbital content might indicate an intact periorbita. (b) The axial view presents the exophthalmos.

Stage IV: Orbital abscess

Should a subperiosteal abscess spread to the periorbita it causes an orbital abscess, including motility disorders, diplopia, and visual loss. An orbital abscess can occur at multiple sites, both preseptal and postseptal (medial orbital wall, cranial to the eyelids, in the upper and/or lower eyelid, and in the lacrimal gland). The diagnosis of an orbital abscess requires a CT or MRI scan.

Stage V: Orbital cellulitis with orbital apex syndrome

An orbital abscess can transform into orbital cellulitis, leading to ophthalmoplegia due to paralysis of the cranial nerves II, III, IV, and VI, and can cause amaurosis. In pathogenic terms, this stage presents a breakthrough of the pus through the periorbita as a result of the subperiosteal orbital abscess. The inflammation then spreads very quickly to the orbital adipose tissue, muscles, and nervous structures ( ▶ Fig. 6.5).


Fig. 6.5 Phases of orbital complication. (Reproduced from Strutz J, Mann W, eds. Praxis der HNO-Heilkunde, Kopf- und Halschirurgie. 2nd ed. Stuttgart: Thieme: 2010:439. Fig.10:14.)


Orbital complications

Stage I: Orbital edema

Stage II: Periostitis of the orbit

Stage III: Subperiosteal abscess

Stage IV: Orbital abscess

Stage V: Orbital cellulitis with orbital apex syndrome (= ophthalmoplegia, amaurosis)

6.3.3 Therapy

Initiation of inpatient treatment is necessary as soon as any sinusitis causes orbital complications. Depending on the clinical symptoms, a conservative approach might be sufficient; otherwise, surgical procedures are indicated.

Conservative Treatment Measures

Conservative treatment includes mainly the treatment of the sinusitis itself with decongestant agents and intravenous antibiotic therapy.

Decongestion of nasal mucous membranes is achieved by inhalation with saline (3 times daily), 0.1% xylometazoline-containing nasal spray or gel (3 times daily), or the insertion of decongestant strips into the middle nasal meatus (2 times daily). Mucolytics such as acetylcysteine can be added for dissolution of mucus.

Intravenous antibiotic therapy uses broad-spectrum penicillin (i.e., ampicillin + sulbactam) or—in patients with allergy to penicillin—with clindamycin as it reacts well with soft tissue and bony structures. (Caution: cross-reactivity between penicillins and cephalosporins is possible).

In stages I and II of orbital complications, conservative therapy can be sufficient at first. Since most of the stage I and II complications improve within 24 hours of consistent therapy, conservative management is justified. However, if progression of clinical symptoms including visual and/or motility loss and increased exophthalmos is observed after 24 hours, CT scanning of the paranasal sinus system and the optic nerve canal (axial and coronal planes) should be performed and surgical intervention is mandatory. 6

In addition, intravenous cortisone therapy for additional detumescence and inflammatory reduction and application of heparin to prevent venous sinus thrombosis are recommended in stages III to V.

Surgical Treatment

The following clinical symptoms are an indication for surgical intervention:

  • Deterioration of clinical findings within 24 hours.

  • Visual loss.

  • Impairment of eye motility.

Surgical procedures include sinus surgery as source control; abscess relief in cases of subperiostal or orbital abscess; and orbital decompression in cases of orbital cellulitis ( ▶ Table 6.3).

Table 6.3 Therapeutic management of orbital complications due to an acute sinusitis according to stage of the disease


Conservative therapy

Surgical procedures


Decongestant agents

Progression at 24 hours despite conservative therapy:
surgical source control

Intravenous antibiotic therapy


Decongestant agents

Progression at 24 hours despite conservative therapy:
surgical source control

Intravenous antibiotic therapy


Intravenous antibiotic therapy

Indication of immediate surgical procedure:
surgical source control


Intravenous corticoid therapy


Intravenous antibiotic therapy

Indication of immediate surgical procedure:
endonasal orbital relief, eventually with additional transfacial access depending on abscess localization


Intravenous corticoid therapy


Intravenous antibiotic therapy

Indication of immediate surgical procedure:
endonasal orbital relief, eventually with additional transfacial access depending on abscess localization


Intravenous corticoid therapy


The prognosis in terms of postoperative visual improvement seems to be dependent on the following factors: initial blindness (complete loss of vision) indicates a negative prognosis; also a long interval before surgical intervention (>48 hours) is associated with significant deterioration of visual recovery, a fact that is explained by the pathophysiological processes that take place during an inflammatory response of the optic nerve (see Chapter ▶ 2). With timely diagnosis and consistent treatment (intravenous antibiotic therapy and possibly surgical measures) the prognosis of visual loss in the context of an orbital abscess or orbital cellulitis is as high as a 68 to 100% recovery rate. 20,​ 21,​ 22,​ 23,​ 24

6.4 Orbital Complications of Other Cause

Orbital complication can have other causes than traumatic, iatrogenic, or sinogenic ones. Knowledge of the genesis is crucial in order to be able to initiate appropriate therapeutic strategies.

6.4.1 Orbital Emphysema

Orbital emphysema describes an abnormal intraorbital accumulation of air. Due to the relatively loose tissue texture and numerous fascial spaces, air can spread throughout the entire orbit. The extent of emphysema, particularly retrobulbar and intraconal, is only visible via CT scan or MRI scan of the orbit.


A precondition for the emergence of orbital emphysema is a physical connection between intraorbital soft tissues and the air-filled spaces. The most common cause is a fracture of the bony medial and cranial orbital wall or of the orbital floor with subsequent opening to the sinus system. 25 Forceful nose blowing increases pressure into the sinuses, pushing air into orbital soft tissue. Hence, about 33% of skull base and craniocerebral trauma are accompanied by soft tissue emphysema. 26 Sporting activity is the second most common cause for the development of orbital emphysema. Weight training considerably tightens abdominal muscles 27: this leads to pressure in the sinus system. Energy exceeding 2.08 J exerted on the orbital lamina of the ethmoid bone during this pressure increase cause to a fracture that allows air to enter into the orbit. 28 A similar mechanism is the cause for orbital emphysema resulting from heavy nose blowing or diving with hyperbaric breathing gas bottles, which can also trigger a fracture of the lamina papyracea. 29,​ 30,​ 31,​ 32 Finally, accidents can also facilitate air entering into the orbit through the conjunctiva, for example, when working with machines that produce a strong air pressure (such as high-pressure air jets). 28 In those cases, however, lesions of the conjunctiva and the eyeball usually predominate.

Clinical Symptoms

Clinically, a soft and resilient swelling of the upper and lower lid is usually present. Palpation is mostly accompanied by typical tissue crepitation. Eyelid motility may be limited in cases with significant accumulations of air in the soft tissue of the eyelids, while ocular motility is generally neither obstructed nor painful. Invading air can have space-occupying effects, but the pressure generated in this way is often not sufficient to decrease visual acuity. In the context of emphysema this has been described only in case reports. 30,​ 33,​ 34 Key et al report three cases of orbital emphysema triggered by trauma that led to rapidly progressive visual loss and required immediate surgical decompression. Nonetheless, patients presenting with orbital emphysema should receive thorough clinical ophthalmologic examination.


Orbital emphysema usually requires conservative therapy. Since there is a very high probability that fractures are followed by bacterial dissemination from intranasal sites via the sinuses into the orbit, treatment is recommended to include broad-spectrum antibiotics (e.g., aminopenicillins, cephalosporins, clindamycin) for 5 to 7 days, accompanied by cooling measures and the administration of a nonsteroidal, anti-inflammatory drugs such as ibuprofen (4 × 600 mg/day). 25,​ 27,​ 35 Orbital decompression is indicated only in exceptional circumstances, namely in the course of a rapid deterioration of vision. 32,​ 34 The procedure corresponds to that described under “Therapy” in Chapter ▶ 6.2.1.

As an emergency procedure for immediate relief, some authors suggest the transpalpebral insertion of a large-caliber needle through which excess air can escape. 31

The overall prognosis is positive. In most cases the resorption of excessive air takes up to a week. Loss of vision that initially necessitated surgical decompression is usually completely regressed with a full recovery of visual acuity. 34

6.4.2 Dysthyroid Optic Neuropathy

A special form of orbital complication is dysthyroid optic neuropathy (DON), which can occur in course of active thyroid orbitopathy and may lead to a rapid loss of vision requiring immediate surgical treatment. The loss of vision often represents the most serious symptom for patients. 36


Endocrine orbitopathy is an autoimmune disease characterized by the proliferation of retrobulbar adipose tissue and a thickening of the extraocular muscles due to myositis. A detailed discussion of the disease’s pathogenesis is given in Chapter ▶ 7, so it is only briefly mentioned here. The consequence of these mechanisms is a massive increase in intrabulbar and intraocular pressure. At the same time, the venous pressure in the superior ophthalmic vein increases, which may contribute to a further elevation of intraocular pressure. 37 All the elevated pressure gradients act on the optic nerve and this results in proptosis-induced stress on the nerve. 38 In about 5% of cases, this leads to the development of dysthyroid optic neuropathy characterized by a rapid loss of vision, among other things. 38 From a pathogenetic view, the two factors—pressure increase and autoimmunologically triggered inflammatory response—act on the optic nerve during the deterioration of visual acuity.

Clinical Symptoms

The prominent clinical symptoms of active Graves’s ophthalmopathy include chemosis, upper lid retraction, proptosis, and ocular motility disorders. The intraocular pressure is increased. Within only a few days, deterioration of visual acuity or even blindness may also occur.


High-dose corticosteroids are administered over a period of 3 to 4 days. 39 Additionally, orbital decompression is indicated for improvement or recovery of visual acuity if no significant improvement is achieved by corticosteroid treatment within 1 to 2 weeks. 38 This reduces pressure on the nerve and leads to almost normal blood flow in the superior ophthalmic vein. 37 Despite these therapeutic procedures, the prognosis regarding visual recovery is uncertain. If there has been a loss of vision during DON prior to the initiation of therapy, the rate of complete remission is about 40%. 39

6.4.3 Dentogenic Abscesses


After sinogenic causes, dentogenic processes are the second most common cause of orbital complications. Most of these abscesses are triggered by the following 40:

  • Mouth–antrum connection after dental procedures.

  • Periapical periodontitis (acute apical inflammation).

  • Deep marginal periodontitis (chronic apical inflammation).

  • Alveolitis (inflammation of bony tooth socket) after tooth extraction in the upper jaw.

  • Submucosal abscess.

  • Infected implants.

  • Over pressed filling material after a dental root canal treatment.

  • Iatrogenic origin from excessive pushing of instruments in dental root canal treatment.

  • Traumatic damage to the front teeth of the upper jaw.

  • Dentogenic maxillary sinusitis.

  • Infected odontogenic maxillary cysts that have grown in the maxillary sinus (radicular, follicular, or occlusion cysts).

  • Odontogenic tumors.

Often the third molar of the mandible or maxilla (37.5%), the first molar of the maxilla (12.5%), or the second molar of the lower jaw (12.5%) is the origin of infection. 41 The root tip of the maxillary canine extends almost up to the orbit (which is why it is also called the “eye tooth”) and is often the focus of an orbital complication. 41

The infection is usually a secondary infection that is transferred to the orbit either hematogenously, lymphogenously, or by continuity through bone gaps on the maxillary sinus and the orbital floor (see Chapter ▶ 6.2.1). 41

The polymicrobial bacterial spectrum of odontogenic inflammation usually differs from the spectrum of sinogenic orbital abscesses. It comprises aerobic bacteria such as streptococci and staphylococci and anaerobic bacteria, predominantly oral pathogenic anaerobes such as Peptostreptococcus, Fusobacterium, and Prevotella species. 40,​ 42

Clinical Symptoms

Typical symptoms are toothache and headache as well as increased body temperature. Clinically, usually swelling and reddening of the cheek and/or the lower lid is observed with the possibility of upper lid edema. Affected teeth are touch-sensitive and cause headaches. Depending on the inflammatory stage, the development of chemosis, proptosis, dysmotility or even amaurosis and ophthalmoplegia is possible.


Axial and coronal CT scans of the paranasal sinus system are essential for assessing the anatomy and the extent of the complication,. Intravenous antibiotic therapy should be initiated using aminopenicillin with a β-lactamase inhibitor, possibly combined with metronidazole. Lincosamides (e.g., clindamycin) can be used as an alternative. 40,​ 41,​ 42 Surgical therapy includes elimination of the focus of infection with tooth extraction or root resection and abscess drainage performed by a dental surgeon or an oral and maxillofacial surgeon. 40,​ 41 In cases where the inflammation leads to the formation of an abscess in the orbit or to orbital cellulitis, procedures referred to under “Surgical treatment” in Chapter ▶ 6.3.3 are to be carried out as well.

6.4.4 Infection of the Cheek Skin


An infection in the facial area (skin injury, furuncle, atheroma, etc.) can act as an access point for the transmission of an inflammation to the internal structure of the orbit and cause swelling around the eye. Bacteria such as staphylococci and streptococci are usually detectable. The inflammation is transmitted through the bloodstream, usually venous, to the internal structures of the orbit, where it can cause orbital complications. It should be noted that the transition of inflammations through the angular vein can cause venous sinus thrombosis and thrombophlebitic sepsis. 43

Clinical Symptoms

The clinical picture shows classical signs of inflammation, such as pain, swelling, redness, and warmth in the access area as well as swelling of the affected eyelids, which can be associated with chemosis. In advanced stages, the inflammation can manifest itself in erysipelas or abscess formation. 43


The focus of therapeutic procedures is on intravenous antibiotic therapy with a broad-spectrum penicillin (e.g., ampicillin + sulbactam) or alternatively with clindamycin. Incision for pus drainage is necessary in treating abscesses.

6.4.5 Dacryoadenitis


Dacryoadenitis is an inflammation of the lacrimal gland. Two different types are distinguished 44:

  • Acute dacryoadenitis: acute, infectious, usually unilateral (exception: infection with mumps).

  • Chronic dacryoadenitis: chronic, noninfectious, usually bilateral.

Acute dacryoadenitis is often associated with a common cold or flu, but it might also be predisposed by a preexisting immune deficiency. Acute inflammation is usually of bacterial origin. Typical bacteria are staphylococci, streptococci, and pneumococci. Viruses, such as mumps and measles virus, influenza virus, herpes simplex/zoster, and the Epstein–Barr virus are less common. 44

Systemic diseases (e.g., sarcoidosis, Wegener’s granulomatosis, Sjögren’s syndrome, amyloidosis) in the course of tuberculosis or leukemia or triggered by an orbital pseudotumor are examples of causes of chronic dacryoadenitis. 44

Clinical Symptoms

The main symptoms of dacryoadenitis are epiphora and often conjunctivitis. Pressure-sensitivity and redness and swelling of the upper eyelid are common, the latter presenting the typical paragraph form ( ▶ Fig. 6.6). Motility disorders and proptosis are also possible. A fulminant course may lead to orbital cellulitis. Differential diagnosis should also consider a phlegmon of the upper lid, for example, after superficial skin injuries. 44,​ 45


Fig. 6.6 Dacryoadenitis on the left eye. (a) Paragraph form of the upper lid due to a dacryoadenitis. (b) CT scan of paranasal sinuses in axial plane with visible swelling in the left lacrimal gland.

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