Orbital Cellulitis

Author: John N Harrington, MD, FACS; Chief Editor: Hampton Roy Sr, MD

Background
Orbital cellulitis and preseptal cellulitis are the major infections of the ocular adnexal and orbital tissues. Orbital cellulitis is an infection of the soft tissues of the orbit posterior to the orbital septum, differentiating it from preseptal cellulitis, which is an infection of the soft tissue of the eyelids and periocular region anterior to the orbital septum. (See Presentation.) Orbital cellulitis has various causes and may be associated with serious complications. As many as 11% of cases of orbital cellulitis result in visual loss. Prompt diagnosis and proper management are essential for curing the patient with orbital cellulitis (see the images below). (See Etiology, Prognosis, Presentation, Workup, Treatment, and Medication.)

A male patient with orbital cellulitis with proptosis, ophthalmoplegia, and edema and erythema of the eyelids. The patient also exhibited pain on eye movement, fever, headache, and malaise.

A male patient with orbital cellulitis who demonstrated proptosis, ophthalmoplegia, and edema and erythema of the eyelids. The patient also exhibited chemosis and resistance to retropulsion of the globe.

Anatomy
The orbital septum is a layer of fascia extending vertically from the periosteum of the orbital rim to the levator aponeurosis in the upper eyelid and to the inferior border of the tarsal plate in the lower eyelid.

Patient education
For patient education information, see the Diabetes Center, as well as Cellulitis.

Etiology
Orbital cellulitis occurs in the following 3 situations[1] : Extension of an infection from the periorbital structures - Most commonly from the paranasal sinuses, but also from the face, the globe, and the lacrimal sac Direct inoculation of the orbit from trauma or surgery Hematogenous spread from bacteremia

Extension of infection
Orbital cellulitis can be caused by direct extension of infection from the globe, eyelids, ocular adnexum, and other periocular tissues, as well as from the sinuses. Orbital cellulitis may follow dacryocystitis, osteomyelitis of the orbital bones, phlebitis of the facial veins, and dental infections.

Orbital cellulitis is caused most commonly in all age groups by ethmoid sinusitis, accounting for more than 90% of all cases; aerobic, non-sporeforming bacteria are the organisms that are most frequently responsible. The process involves edema of the sinus mucosa, which leads to narrowing of the ostia and subsequent reduction or cessation of normal sinus drainage. Microflora indigenous to the sinuses and upper respiratory tract proliferate and invade the edematous mucosa, resulting in suppuration. It is enhanced by the reduced oxygen tension within the obstructed sinus cavity. The organisms gain access to the orbit through thin bones of the orbital walls, venous channels, foramina, and dehiscences. Then, subperiorbital and intraorbital abscesses may occur. The resulting elevation of intraorbital pressure results in the typical signs of proptosis, ophthalmoplegia, and chemosis. Orbital cellulitis resulting from infection of the maxillary sinus secondary to dental infections can be caused by microorganisms indigenous to the mouth, including anaerobes, commonly Bacteroides species. Those cases stemming from dacryocystitis most commonly are caused by S aureus, S pneumoniae, Streptococcus pyogenes, and nontypeable H influenzae. Infections spreading from the soft tissues of the eyelids and face are due most commonly to staphylococci and S pyogenes. The initial antibiotic regimen can be modified if the response is inadequate or if the cultures dictate otherwise.

Traumatic causes
Infectious material may be introduced into the orbit directly through accidental (eg, orbital fracture) or surgical trauma. Indeed, orbital cellulitis may be caused by any injury perforating the orbital septum. Orbital inflammation[2] may be noted within 48-72 hours after injury, or, in the case of a retained orbital foreign body, it may be delayed for several months. Surgical procedures, including orbital decompression, dacryocystorhinostomy, eyelid surgery,[3] strabismus surgery, retinal surgery, and intraocular surgery, have been reported as the precipitating cause of orbital cellulitis. Postoperative endophthalmitis can extend to the orbital soft tissues.

Bacterial causes
Streptococcus species, Staphylococcus aureus, and Haemophilus influenzae type B are the most common bacterial causes of orbital cellulitis. Pseudomonas, Klebsiella, Eikenella, and Enterococcus are less common culprits. Polymicrobial infections with aerobic and anaerobic bacteria are more common in patients aged 16 years or older.

Fungal causes
Fungal causes of orbital cellulitis are most commonly Mucor and Aspergillusspecies. Fungi can enter the orbit. Orbital cellulitis due to fungal infections carries a high mortality rate in patients who are immunosuppressed. Mucormycosis[4, 5, 6] has a wide distribution, while aspergillosis more commonly is seen in warm, humid climates. Mucormycosis has a rapid onset (1-7 days), while aspergillosis is much slower (months to years). Aspergillosis initially results in chronic proptosis and decreased vision, while mucormycosis gives rise to the orbital apex syndrome (involving cranial nerves II, III, IV, V-1, and VI, and orbital sympathetics). More commonly, mucormycosis presents with pain, lid edema, proptosis, and visual loss. While aspergillosis and mucormycosis may each result in nasal and palatal necrosis, mucormycosis also may lead to thrombosing arteritis and ischemic necrosis, while aspergillosis gives rise to chronic fibrosis and a nonnecrotizing granulomatous process.

Path of infection
The medial orbital wall is thin and is perforated not only by numerous valveless blood vessels and nerves but also by numerous defects (Zuckerkandl dehiscences). This combination of thin bone, foramina for neurovascular passage, and naturally occurring defects in the bone allows for easy communication of

infectious material between the ethmoidal air cells and the subperiorbital space in the medial aspect of the orbit. The most common location of a subperiorbital abscess is along the medial orbital wall. The periorbita is adherent relatively loosely to the bone of the medial orbital wall, which allows abscess material to easily move laterally, superiorly, and inferiorly within the subperiorbital space. In addition, the lateral extensions of the sheaths of the extraocular muscles, the intermuscular septa, extend from one rectus muscle to the next and from the insertions of the muscles to their origins at the annulus of Zinn, posteriorly. Posteriorly in the orbit, the fascia between the rectus muscles is thin and often incomplete, allowing easy extension between the extraconal and intraconal orbital spaces. Venous drainage from the middle third of the face, including the paranasal sinuses, is mainly via the orbital veins, which are without valves, allowing the passage of infection anterograde and retrograde.

Epidemiology
An increased incidence of orbital cellulitis occurs in the winter nationally and internationally, because of the increased incidence of sinusitis in cold weather. In the United States, an increase has been noted in the frequency of orbital cellulitis due to communityacquired methicillin-resistant S aureus infections.[7, 8, 9, 10, 11, 12, 13]

Sex- and age-related demographics

In children, orbital cellulitis has been reported as twice as common in males as in females. In adults, however, no difference in the frequency of orbital cellulitis exists between the sexes, except for cases caused by methicillin-resistant Saureus, which are more common in females than in males by a ratio of 4:1. Orbital cellulitis, in general, is more common in children than in adults.[14] The median age range of children hospitalized with orbital cellulitis is 7-12 years.

Prognosis
Prior to the availability of antibiotics, patients with orbital cellulitis had a mortality rate of 17%, and 20% of survivors were blind in the affected eye. As a result of prompt diagnosis and the appropriate use of antibiotics, however, this rate has been reduced significantly, although blindness still occurs in up to 11% of cases. Orbital cellulitis due to methicillin-resistant S aureus can lead to blindness despite antibiotic treatment.

Morbidity and mortality

Orbital cellulitis can result in orbital and intracranial complications. Subperiorbital or orbital abscess formation may occur (7-9%), while permanent vision loss may result from corneal damage secondary to exposure or neurotrophic keratitis, destruction of intraocular tissues, secondary glaucoma, optic neuritis, or central retinal artery occlusion. Blindness also may occur secondary to elevated intraorbital pressure or the direct extension of infection to the optic nerve from the sphenoid sinus. Direct involvement of the ocular motor nerves or the extraocular muscles may lead to decreased ocular motility. Intracranial complications include meningitis (2%), cavernous sinus thrombosis (1%), and intracranial, epidural, or subdural abscess formation. Cavernous sinus thrombosis has a mortality rate of 50% or higher, but it has become relatively rare in industrialized countries with proper treatment. Cavernous sinus thrombosisshould be considered in any patient with orbital cellulitis and should be suspected in the presence of rapid progression of the clinical signs (eg, increasing proptosis, mydriasis, dilation of retinal veins, decreasing visual acuity, development of an afferent pupillary defect).

Intracranial abscess formation is suggested by altered consciousness, signs of central nervous system disturbance, persistent fever despite adequate antibiotic therapy, and resolution of the sinusitis and orbital cellulitis components of the disease. Orbital pseudotumor may cause rapidly developing orbital congestion, proptosis, and limitation of motility, but it typically occurs in older age groups. Orbital echography may be helpful in differentiation. Usually, endocrine orbitopathy may be identified by its typical clinical features. Orbital myositis may produce mild vascular congestion and proptosis. A fast-growing, necrotic retinoblastoma may produce mild vascular congestion, proptosis, and rhabdomyosarcoma. A metastatic orbital tumor, especially breast carcinoma, may produce similar findings.

History
A thorough history and physical examination are critical in establishing a diagnosis of orbital cellulitis. Patients with orbital cellulitis frequently complain of fever, malaise, and a history of recent sinusitis or upper respiratory tract infection. Questioning the patient about any recent facial trauma or surgery, dental work,[15]or infection elsewhere in the body is important. Other common, but variable, signs that accompany orbital cellulitis include the following: Conjunctival chemosis Decreased vision Elevated intraocular pressure Pain on eye movement The above signs may be accompanied by the following: Fever Headache Lid edema Rhinorrhea Increasing malaise

Physical Examination
Proptosis and ophthalmoplegia are the cardinal signs and symptoms of orbital cellulitis. The symptoms advance rapidly at an alarming rate and eventually lead to prostration. (See the images below.)

A male patient with orbital cellulitis with proptosis, ophthalmoplegia, and edema and erythema of the eyelids. The patient also exhibited pain on eye movement, fever, headache, and malaise.

A male patient with orbital cellulitis who demonstrated proptosis, ophthalmoplegia, and edema and erythema of the eyelids. The patient also exhibited chemosis and resistance to retropulsion of the globe.

Proptosis and ophthalmoplegia may be accompanied by the following: Conjunctival chemosis

Decreased vision Elevated intraocular pressure Pain on eye movement Orbital pain and tenderness - Are present early Dark red discoloration of the eyelids, chemosis, hyperemia of the conjunctiva, and resistance to retropulsion of the globe may be present Purulent nasal discharge may be present Vision may be normal early, but it may become difficult to evaluate in very ill children with marked edema.

Diagnostic Considerations
Orbital cellulitis should be suspected in any patient with adnexal, facial, or dental infection when orbital pain, proptosis, limitation of ocular motility, lid edema, or orbital congestion develops. A computed tomography (CT) scan should be obtained, and the patient should be hospitalized and placed on broadspectrum, intravenous (IV) antibiotic therapy as deemed appropriate. Conditions to consider in the differential diagnosis of orbital cellulitis include the following: Infection - Cavernous sinus thrombosis Endocrine dysfunction - Dysthyroid exophthalmos Idiopathic inflammation - Orbital myositis, orbital pseudotumor, Wegener granulomatosis Neoplasm with inflammation - Burkitt lymphoma, histiocytosis X (Letterer-Siwe), leukemia, metastatic carcinoma, retinoblastoma, rhabdomyosarcoma, sarcoidosis Orbital cellulitis resulting from sinusitis usually can be distinguished easily from other causes of acute inflammatory proptosis by clinical signs, computed tomography (CT) scanning, and the assessment of risk factors. Cavernous sinus thrombosis, a serious complication of paranasal sinusitis that most commonly results from the anterograde spread of infection involving the mid-third of the face (eg, orbit, mouth, paranasal sinuses), may be difficult to distinguish from simple orbital cellulitis. (It may also occur with and be caused by orbital cellulitis.) A patient with cavernous sinus thrombosis without orbital cellulitis will show marked restriction of ocular motility out of proportion to the degree of proptosis. A patient also will have normal retropulsion of the globe, hypesthesia in the distribution of the first and second divisions of the trigeminal nerve, dilated retinal veins, orbital congestion, and possibly neurologic defects (eg, altered sensorium). A cranial magnetic resonance imaging (MRI) scan can help to confirm the diagnosis of cavernous sinus thrombosis.

Differential Diagnoses
Exophthalmos Mucormycosis Retinoblastoma Sarcoidosis Spider Bites Thyroid Ophthalmopathy

Pharmacologic Therapy
Medical care of orbital cellulitis consists of the proper use of the appropriate antibiotics. Broad-spectrum IV antibiotics should be started immediately and continued until the choice of antibiotics can be tailored for specifically identified pathogens identified on cultures. Typically, IV antibiotic therapy should be continued for 1-2 weeks and then followed by oral antibiotics for an additional 2-3 weeks. Fungal infection requires IV antifungal therapy along with surgical debridement. Regarding pediatric care, a study by Emmett et al found that the length of IV therapy associated with successful nonsurgical management of children with subperiosteal abscess was considerably shorter

than the length of time normally recommended in pediatric infectious disease literature. This result suggested that clinical judgment regarding each patients initial CT scan findings and evolving signs, symptoms, and laboratory profile should be taken into account when scheduling IV intervals. [19]

Indications for Surgical Drainage

Surgical drainage of an orbital abscess is indicated in any of the following instances: A decrease in vision occurs An afferent pupillary defect develops Proptosis progresses despite appropriate antibiotic therapy The size of the abscess does not reduce on CT scan within 48-72 hours after appropriate antibiotics have been administered; if brain abscesses develop and do not respond to antibiotic therapy, craniotomy is indicated. The presence of a drainable fluid collection is evident on CT scan in patients older than 16 years

Medication Summary
Prompt administration of appropriate antibiotics is key to successful treatment of orbital cellulitis. Most cases of orbital cellulitis result from ethmoid sinusitis; in such cases, the initial antibiotics are chosen based on the most likely sinus pathogens, primarily Streptococcus pneumoniae and other streptococci, S aureus,H influenzae, and non-sporeforming anaerobes. The occurrence of methicillin-resistant S aureus in orbital cellulitis is increasing, and empiric antimicrobial therapy should be directed against this organism if it is prevalent in the community. Infection due to methicillin-resistant S aureus is best treated with vancomycin, cefotaxime, and clindamycin. Fungal orbital cellulitis also occurs and is primarily due to Mucor and Aspergillusspecies. Fungal infection requires antifungals, such as amphotericin. Corticosteroids may be helpful, but they should not be started until after any surgery is performed and until the patient has been on appropriate antibiotics for 2-3 days. If glaucoma develops secondary to orbital cellulitis, ocular antihypertensives should be administered promptly. In cases of posttraumatic orbital cellulitis, tetanus prophylaxis should be given according to standard protocol.

Antibiotics, Other
Class Summary
Appropriate antibiotics may include nafcillin (for Staphylococcus andStreptococcus species), cefotaxime (for gram-negative organisms, nontypeable H influenzae, Moraxella, and resistant pneumococci), and metronidazole (for anaerobes). Ticarcillin-clavulanate would cover most gram-positive and gram-negative organisms and most anaerobes. Nafcillin in combination with ceftazidime is also appropriate, although chloramphenicol may be substituted for ceftazidime. Cefazolin can be used in place of nafcillin in cases of mild allergy to penicillin and vancomycin can be used in cases of severe penicillin allergy. Vancomycin, cefotaxime, clindamycin, and trimethoprim/sulfamethoxazole double-strength would be appropriate for susceptible penicillinase- and non-penicillinase-producing strains of methicillin-resistant S aureus.
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Vancomycin

Vancomycin is a tricyclic glycopeptide antibiotic for IV administration. It is indicated for the treatment of susceptible strains of methicillin-resistant (beta-lactam resistant) staphylococci in penicillin-allergic patients.
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Clindamycin (Cleocin)
Clindamycin inhibits bacterial protein synthesis at the bacterial ribosomal lever, binding with preference to the 50S ribosomal subunit and affecting the peptide chain initiation process.
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Cefotaxime (Claforan)
Cefotaxime is a semisynthetic, broad-spectrum antibiotic for parenteral use. It is effective against grampositive aerobes, such as S aureus, including penicillinase- and non-penicillinase-producing strains (but it does not cover methicillin-resistant strains) and S pyogenes; gram-negative aerobes (eg, H influenzae); and anaerobes (eg, Bacteroides species).
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Nafcillin
Nafcillin is a semisynthetic penicillin that is effective against a wide gram-positive spectrum, including Staphylococcus, pneumococci, and group A beta-hemolytic streptococci.
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Ceftazidime (Fortaz, Tazicef)

Ceftazidime is a semisynthetic, broad-spectrum, beta-lactam antibiotic for parenteral injection. It has a broad spectrum of effectiveness against gram-negative aerobes, such as H influenzae; gram-positive aerobes, such as S aureus (including penicillinase and non-penicillinase-producing strains) and S pyogenes; and anaerobes, including Bacteroides species.
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Chloramphenicol
Chloramphenicol exerts a bacteriostatic effect on a wide range of gram-negative and gram-positive bacteria and is particularly effective against H influenzae.
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Ticarcillin and clavulanate potassium (Timentin)

Ticarcillin is a semisynthetic, injectable penicillin that is bactericidal against gram-positive and gramnegative organisms, including H influenzae, S aureus (non-penicillinase producing), beta-hemolytic streptococci (group A), S pneumoniae, and anaerobic organisms, such as Bacteroides and Clostridium species. Clavulanate potassium is a beta-lactamase inhibitor that protects against resistance by betalactamase producing enzymes.
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Cefazolin
Cefazolin is a semisynthetic cephalosporin for intramuscular (IM) or IV administration. It has a bactericidal effect against S aureus (including penicillinase-producing strains), group A beta-hemolytic streptococci, and H influenzae.
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Trimethoprim and sulfamethoxazole (Bactrim, Bactrim DS, Septra DS)

Trimethoprim/sulfamethoxazole inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid. The antibacterial activity of trimethoprim/sulfamethoxazole includes common urinary tract pathogens, except Pseudomonas aeruginosa.

Antifungals, Systemic
Class Summary
Fungal orbital cellulitis is a potentially lethal condition, and the principal organisms involved, Mucor and Aspergillus, require the use of antifungals.
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Amphotericin B deoxycholate (AmBisome)

This is a lipid preparation consisting of amphotericin B within unilamellar liposomes. It delivers higher concentrations of the drug, with a theoretical increase in therapeutic potential and decreased nephrotoxicity. Amphotericin is the antifungal medication of choice in the treatment of fungal orbital cellulitis. It is administered intravenously and, in cases of severe infection, may be appropriately provided before laboratory confirmation of fungal infection.

Decongestants, Intranasal
Class Summary
Nasal decongestants may help to open the sinus ostia and aid with drainage in cases of orbital cellulitis secondary to sinusitis.
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Phenylephrine nasal (Neo-Synephrine)

This agent is beneficial in the treatment of nasal congestion that may cause blockage of the ostia of the sinus, interfering with sinus drainage.
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Oxymetazoline (Afrin, Dristan, Duramist Plus)

Oxymetazoline is applied directly to mucous membranes, where it stimulates alpha-adrenergic receptors and causes vasoconstriction. Decongestion occurs without drastic changes in blood pressure, vascular redistribution, or cardiac stimulation.

Antiglaucoma, Carbonic Anhydrase Inhibitors

Class Summary
These agents reduce intraocular pressure (IOP).
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Acetazolamide (Diamox Sequels)

Acetazolamide inhibits the enzyme carbonic anhydrase, reducing IOP by reducing the rate of aqueous humor formation. It is used for the adjunctive treatment of chronic simple (open-angle) glaucoma and secondary glaucoma and is employed preoperatively in acute angle-closure glaucoma when there is a desire to delay surgery in order to lower IOP.

Corticosteroids
Class Summary
Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. These agents modify the body's immune response to diverse stimuli. Corticosteroids may be helpful, but they should not be started until after any surgery is performed and until the patient has been on appropriate antibiotics for 2-3 days.
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Prednisone
Prednisone inhibits phagocytosis of platelets and may improve RBC survival.
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Prednisolone (Orapred ODT, Prelone, Millipred)

Prednisolone decreases autoimmune reactions, possibly by suppressing key components of the immune system. This agent does not need to undergo hepatic metabolism.

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