Orbital Cellulitis Clinical Presentation

  • Author: John N Harrington, MD, FACS; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Feb 9, 2012
 

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[9] , 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
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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, andresistance to retropulsion of the globe may be present.
  • Purulent nasal discharge may be present.
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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.[10]

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[11] 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,[12] 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[13, 14, 15] 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.

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Contributor Information and Disclosures
Author

John N Harrington, MD, FACS  Director of Ophthalmic Plastic and Reconstructive Surgery, Department of Ophthalmology, Baylor University Medical Center; Clinical Professor Emeritus, Department of Ophthalmology, University of Texas Southwestern Medical Center at Dallas, Southwestern Medical School

John N Harrington, MD, FACS is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, American Medical Association, American Society of Ophthalmic Plastic and Reconstructive Surgery, and Texas Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Brian A Phillpotts, MD  Former Vitreo-Retinal Service Director, Former Program Director, Clinical Assistant Professor, Department of Ophthalmology, Howard University College of Medicine

Brian A Phillpotts, MD is a member of the following medical societies: American Academy of Ophthalmology, American Diabetes Association, American Medical Association, and National Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mark T Duffy, MD, PhD  Consulting Staff, Division of Oculoplastic, Orbito-facial, Lacrimal and Reconstructive Surgery, Green Bay Eye Clinic, BayCare Clinic; Medical Director, Advanced Cosmetic Solutions, A BayCare Clinic

Mark T Duffy, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, American Society of Ophthalmic Plastic and Reconstructive Surgery, Sigma Xi, and Society for Neuroscience

Disclosure: Allergan - Botox Cosmetic Honoraria Speaking and teaching

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

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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 with proptosis, ophthalmoplegia, and edema and erythema of the eyelids. The patient also exhibited chemosis and resistance to retropulsion of the globe.
 
 
 
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