AUTHOR AND EDITOR INFORMATION

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• Introduction
• Clinical
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• Workup
• Treatment
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• Follow-up
• Miscellaneous
• Multimedia
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INTRODUCTION

Section 2 of 11  

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• Follow-up
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Background

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. 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. Orbital cellulitis has various causes and may be associated with serious complications. Up to 11% of cases of orbital cellulitis result in visual loss. Prompt diagnosis and proper management are essential for curing the patient with orbital cellulitis.

Pathophysiology

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; (2) direct inoculation of the orbit from trauma or surgery; and (3) hematogenous spread from bacteremia.

The medial orbital wall is thin and perforated not only by numerous blood valveless vessels and nerves but also by numerous other 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 subperiorbitalspace.

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 both anterograde and retrograde.

Infectious material may be introduced into the orbit directly from accidental or surgical trauma.

Ethmoid sinusitis is the most common cause of orbital cellulitis in all age groups and aerobic non-spore–forming bacteria are the organisms most frequently responsible.

Frequency

United States

Orbital cellulitis is more common, both nationally and internationally, in winter because of the increased prevalence of sinusitis when the weather is cold.

Mortality/Morbidity

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. However, with prompt diagnosis and appropriate use of antibiotics, this rate has been reduced significantly; blindness occurs in up to 11% of cases. Orbital cellulitis due to methicillin-resistant Staphylococcus aureus can lead to blindness despite antibiotic treatment.

Race

No racial predilection exists for orbital cellulitis.

Sex

No frequency difference exists between the sexes in adults. However, in children, orbital cellulitis has been reported as twice as common in males than in females.

Age

Orbital cellulitis is more common in children than in adults. Median age of children hospitalized with orbital cellulitis is 7-12 years.

CLINICAL

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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, or infection elsewhere in the body is important.

• Other common but variable accompanying signs 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

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.

• 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.
  • Vision may be normal early, but it may become difficult to evaluate in very ill children with marked edema.
  • 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.

Causes

Orbital cellulitis is caused by infection of the orbital soft tissues by extension of infection from periorbital structures, direct inoculation from accidental trauma or surgery, or hematogenous spread of infection.

• Orbital cellulitis is caused most commonly by ethmoid sinusitis, accounting for more than 90% of all cases. 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 can be caused by direct extension of infection from the globe, eyelids, ocular adnexum, and other periocular tissues, as well as the sinuses. Orbital cellulitis may follow dacryocystitis, osteomyelitis of the orbital bones, phlebitis of the facial veins, and dental infections.
• Orbital cellulitis may be caused by any injury perforating the orbital septum. Orbital inflammation 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. Orbital fractures may result in orbital cellulitis.
• Surgical procedures, including orbital decompression, dacryocystorhinostomy, eyelid surgery, 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 of orbital cellulitis are most commonly Streptococcus species, S aureus, and Haemophilus influenzae type B. 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 of orbital cellulitis are most commonly Mucor and Aspergillus species. Orbital cellulitis due to fungal infections carries a high mortality rate in patients who are immunosuppressed. Fungi can enter the orbit, most commonly Mucor and Aspergillus species. Mucormycosis is widespread in 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 gives chronic proptosis and decreased visions, while mucormycosis gives the orbital apex syndrome (involving cranial nerves II, III, IV, V-1, and VI, and orbital sympathetics), and, more commonly, it presents with pain, lid edema, proptosis, and visual loss. While both may result in nasal and palatal necrosis, mucormycosis also may give thrombosing arteritis and ischemic necrosis, while aspergillosis gives chronic fibrosis and a nonnecrotizing granulomatous process.

DIFFERENTIALS

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Other Problems to be Considered

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)

WORKUP

Section 5 of 11  

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Lab Studies

• Laboratory evaluation should include the following:
• • A complete blood count: Leukocytosis greater than 15,000 with a shift to the left commonly is seen.
  • Obtain blood cultures prior to the administration of any antibiotics, although they are unlikely to reveal the responsible organism.
  • Collect purulent material from the nose with a cotton or calcium alginate swab, smear for Gram stain, and culture on both aerobic and anaerobic media. Assess any material obtained from the sinuses or directly from an orbital abscess in the same manner.
  • Needle aspiration of the orbit is contraindicated.

Imaging Studies

• High-resolution CT scan with contrast infusion, including axial and coronal views, is essential.
• • Axial views should include low narrow cuts of the frontal lobes to rule out peridural and parenchymal brain abscess formation.
  • Coronal views are helpful in determining the presence and extent of any subperiorbital abscesses. However, coronal views, which require hyperflexion or hyperextension of the neck, may be difficult in uncooperative children and in patients who are acutely ill.
• MRI may be helpful in defining orbital abscesses and in evaluating the possibility of cavernous sinus disease.

Other Tests

• Lumbar puncture is advisable if cerebral or meningeal signs develop.

TREATMENT

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Medical Care

The patient with orbital cellulitis should be promptly hospitalized for treatment. Hospitalization should be continued until the patient is afebrile and is clearly improved clinically. Historically, the presence of subperiosteal or intraorbital abscess was an indication for surgical drainage in addition to antibiotic therapy; however, medical management alone is successful in many cases. Medical care of orbital cellulitis consists of the proper use of the appropriate antibiotics. Intravenous broad-spectrum antibiotics should be started immediately until the choice of antibiotics can be tailored for specifically identified pathogens identified on cultures. Typically, intravenous antibiotic therapy should be continued for 1-2 weeks and then followed by oral antibiotics for an additional 2-3 weeks. Fungal infection requires intravenous antifungal therapy along with surgical debridement.

Surgical Care

Consider surgical drainage if the response to appropriate antibiotic therapy is poor within 48-72 hours or if the CT scan shows the sinuses to be completely opacified. If the presence of a drainable fluid collection is evident on CT scan, surgical drainage should be considered in patients older than 16 years. Consider orbital surgery, with or without sinusotomy, in every case of subperiosteal or intraorbital abscess formation. In cases of fungal infection, surgical debridement of the orbit is indicated and may require exenteration of the orbit and the sinuses. Canthotomy and cantholysis should be performed on an emergency basis if an orbital compartment syndrome is diagnosed at any point in the course of the disease.

Surgical drainage of an orbital abscess is indicated if any of the following occurs:

• A decrease in vision
• 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.

Consultations

Consult other specialties as indicated.

• Generally, obtain consultation with a pediatrician, an internist, or a family physician, and an infectious disease specialist, in any case of orbital cellulitis.
• Ear, nose, and throat (ENT) consultation is appropriate for cases of orbital cellulitis arising from sinus disease.
• Neurosurgical consultation is indicated if brain abscesses appear.

Diet

No special diet requirements are indicated other than adequate hydration of the patient.

Activity

Hospitalization with intravenous antibiotic therapy is indicated.

MEDICATION

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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-spore–forming anaerobes.

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. Those spreading from infections of 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.

Ampicillin-sulbactam is a good initial choice for broad-spectrum coverage.

Infection due to methicillin-resistant S aureus, which statistically is increasingly prevalent, is best treated with vancomycin, cefotaxime, and clindamycin.

Fungal orbital cellulitis also occurs and is primarily due to Mucor and Aspergillus species. Fungal infection requires antifungals, such as amphotericin.

Corticosteroids may be helpful.

If secondary glaucoma develops secondary to orbital cellulitis, ocular antihypertensives should be instigated promptly. In cases of posttraumatic orbital cellulitis, tetanus prophylaxis should be given according to standard protocol.

Drug Category: Antibiotics

Appropriate antibiotics may include nafcillin (for Staphylococcus or Streptococcus 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 in cases of severe allergy to penicillin.

Drug Category: Antifungals

Fungal orbital cellulitis is a potentially lethal condition, and the principal organisms involved, Mucor and Aspergillus, require the use of antifungals.

Drug Category: Nasal decongestants

Nasal decongestants may help open the sinus ostia and aid with drainage in cases of orbital cellulitis secondary to sinusitis.

Drug Category: Diuretics

These agents reduce IOP.

FOLLOW-UP

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Further Inpatient Care

• Closely monitor the patient (at least daily), with vision reevaluated by standardized vision testing, as appropriate, and preferably by the same examiner. Evaluate the antibiotic coverage daily and change as needed depending on the results of cultures and the patient's clinical course. Repeat CT scans if the patient's condition worsens or does not respond to appropriate antibiotics.
• Once the patient is clearly improving and has been afebrile for at least 48 hours, the patient can be changed from intravenous antibiotics to oral antibiotics (eg, ampicillin, cefpodoxime, cefuroxime, cefprozil) for aerobic infections or metronidazole for anaerobic infections.

In/Out Patient Meds

• See Medication.

Transfer

• The patient may be transferred if necessary for further diagnostic evaluation or surgical intervention if necessary.

Deterrence/Prevention

• No foolproof method for the prevention of orbital cellulitis exists; however, proper treatment of conditions that may precipitate orbital cellulitis (eg, preseptal cellulitis, sinusitis, dental disease) is the best deterrent.

Complications

• Either orbital or intracranial complications of orbital cellulitis may occur. Subperiorbital or orbital abscess formation may occur (7-9%) or permanent vision loss may occur 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 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. Although cavernous sinus thrombosis has become relatively rare in developed countries with proper treatment, it has a mortality rate of 50% or higher. Cavernous sinus should be considered in any patient with orbital cellulitis and 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 cellulitis resulting from sinusitis usually can be distinguished easily from other causes of acute inflammatory proptosis by clinical signs, CT scans, and assessment of risk factors.
• Cavernous sinus thrombosis, a serious complication of paranasal sinusitis that most commonly results from anterograde spread from infection involving the mid third of the face (eg, orbit, mouth, paranasal sinuses), may be difficult to distinguish from simple orbital cellulitis. It may 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 MRI can help confirm the diagnosis of cavernous sinus thrombosis.
• 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. Metastatic orbital tumor, especially breast carcinoma, may give similar findings.

Patient Education

• For excellent patient education resources, see eMedicine's Diabetes Center. Also, visit eMedicine's patient education article Cellulitis.

MISCELLANEOUS

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Medical/Legal Pitfalls

• 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 CT scan should be obtained, and the patient should be hospitalized and placed on broad-spectrum intravenous antibiotic therapy as deemed appropriate.

MULTIMEDIA

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Media file 1:  A male 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.
	View Full Size Image
Media type:  Photo

Media file 2:  The same patient exhibited chemosis and resistance to retropulsion of the globe.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

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• Differentials
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Article Last Updated: Nov 3, 2006