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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
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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.
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.
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  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,  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.
A 44-years-old men was admitted in 1985 because of recurrent swelling of the right upper eyelid. At the time of admission he showed a latero-caudal displacement and protrusion of the right eye and complained of double images. The visus of the right eye was not impaired. Clinical investigation showed a livid tumor in the right nose. The conventional tomography of the paranasal sinuses (no CT-scan available at this time) showed a tumor of the right paranasal sinuses, which infiltrated the skull base around the posterior wall of the frontal sinus and the roof of the ethmoid sinus. The tumor had also invaded the orbita. A surgical approach was chosen for therapy including a resection of the right upper jaw and exenteration of the right orbita. During surgery a broad infiltration of the orbita and the skull base with an infiltration of dura mater on an area of 4x5 cm and an endocranial tumorinfiltration were found. After interim closure of the dura mater the endocranial part of the tumor was neurosurgically resected in a second operation. The pathohistological investigation of both tumor parts showed a hemangiopericytoma with an aggressive and bone-destructive growth. Radiotherapy was given in a dose of 60 Gy postoperatively. In 1999 an MRI showed an endocranial tumor in the opposite frontal lobe. This recurrence was treated neurosurgically again in January 2000 and postoperatively irradiated with 54 Gy. By the end of 2001 the patient was in a good general condition without signs of a tumor recurrences.
Tumour-like lesions are very rare entity among orbital diseases. Between 1996 and 2007, 83 patients with orbital disorders were treated and three of them complained about different tumour-like lesions: giant cell granuloma, eosinophilic granuloma and fibrous dysplasia. Because of the considerable increase of functional disorders and tumour growth, all of the patients underwent surgical treatment. In this paper we describe the clinical symptoms, diagnostics and the methods of therapy for each of the lesions. The results shows that the preoperative neuro-ophthalmological examination as well as radiological imaging are necessary to assess the motility, visual field, vision, eye ball dislocation and to plan the surgical strategy. In terms of this descriptive character of the paper, we hope to submit some relevant information in order to improve the diagnostics and therapeutic procedures for tumour-like lesions of the orbit. 041b061a72