Orbital cellulitis is an infection of the fat and muscles around the eye. It affects the eyelids, eyebrows, and cheeks. It may begin suddenly or be a result of an infection that gradually becomes worse.
processing.... Drugs & Diseases > Ophthalmology Orbital Cellulitis Updated: Jan 11, 2023 Author: Anna G Gushchin, MD; Chief Editor: Edsel B Ing, MD, PhD, MBA, MEd, MPH, MA, FRCSC more... Share Print Feedback Close Facebook Twitter LinkedIn WhatsApp Email webmd.ads2.defineAd({id: 'ads-pos-421-sfp',pos: 421}); Sections Orbital Cellulitis Sections Orbital Cellulitis Overview Background Etiology Epidemiology Prognosis Show All Presentation History Physical Examination Show All DDx Workup Laboratory Studies Imaging Studies Procedures Show All Treatment Approach Considerations Inpatient Care Pharmacologic Therapy Indications for Surgical Drainage Show All Medication Medication Summary Antibiotics, Other Antifungals, Systemic Decongestants, Intranasal Antiglaucoma, Carbonic Anhydrase Inhibitors Corticosteroids Show All Questions & Answers Media Gallery References Overview 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. Preseptal cellulitis is an infection of the soft tissue of the eyelids and periocular region anterior to the orbital septum. (See Presentation.) Orbital cellulitis and preseptal cellulitis can sometimes be a continuum.
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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.)
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 is commonly associated with sinus infection and can be caused by direct extension of infection from the globe, eyelids, ocular adnexa, and other periocular tissues. Orbital cellulitis may follow dacryocystitis, osteomyelitis of the orbital bones, phlebitis of the facial veins, and dental infections.
The organisms gain access to the orbit through thin bones of the orbital walls, venous channels, foramina, and dehiscences. Then, subperiosteal 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.
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.
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 of orbital cellulitis are most commonly Mucor and Aspergillus species. Fungi can enter the orbit. Orbital cellulitis due to fungal infections carries a high mortality rate in patients who are immunosuppressed.
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 each may result in nasal and palatal necrosis, mucormycosis also may lead to thrombosing arteritis and ischemic necrosis, whereas aspergillosis gives rise to chronic fibrosis and a nonnecrotizing granulomatous process.
The medial orbital wall is thin and is perforated by numerous valveless blood vessels and nerves, as well as by numerous defects (lamina papyracea/Zuckerkandl dehiscences). This combination of thin bone, foramina for neurovascular passages, 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 subperiosteal 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, mainly is via the orbital veins, which are without valves, allowing the passage of infection anterograde and retrograde.
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.
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 caused by methicillin-resistant S aureus can lead to blindness despite antibiotic treatment.
Orbital cellulitis can result in orbital and intracranial complications. Subperiosteal or orbital abscess formation may occur (7-9%), whereas 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.
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 thrombosis should 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 cellulitis is defined as a serious infection that involves the muscle and fat located within the orbit. It is also sometimes referred to as postseptal cellulitis. Orbital cellulitis does not involve the globe itself. Although orbital cellulitis can occur at any age, it is more common in the pediatric population.The causative organisms of orbital cellulitis are commonly bacterial but can also be polymicrobial, often including aerobic and anaerobic bacteria and even fungal or mycobacteria. Orbital cellulitis is primarily diagnosed clinically by objective findings on physical examination combined with presenting signs and symptoms. The most important distinguishing feature of orbital cellulitis is the presence of ophthalmoplegia, the presence of pain with eye movement, and/or proptosis. Orbital cellulitis also typically cause eyelid swelling with or without erythema; however, these findings are also seen in another less serious condition called preseptal cellulitis. This activity reviews the cause, pathophysiology and presentation of orbital cellulitis and highlights the role of the interprofessional team in its management.
Objectives:Describe the pathophysiology of orbital cellulitisRecall the causes of orbital cellulitisList the treatment and management options available for orbital cellulitisDiscuss interprofessional team strategies for improving care coordination and communication to advance the treatment of orbital cellulitis and improve outcomes.Access free multiple choice questions on this topic. 2351a5e196