Emmy Yuen-mei Li
Dr. Emmy Li graduated from the University of Hong Kong in 2004 with First Class Honor. She was admitted as fellow of the Royal College of Surgeons of Edinburgh in 2010 and fellow of the College of Ophthalmologists of Hong Kong in 2011. She is currently an Honorary Clinical Assistant Professor at the Department of Ophthalmology and Visual Sciences of the Chinese University of Hong Kong and an Associate Consultant of the Hong Kong Eye Hospital.
Hunter Kwok-Lai Yuen
Dr. Hunter Kwok-Lai Yuen is the consultant ophthalmologist and head of the Oculoplastic & Orbital Surgery Service at Hong Kong Eye Hospital. Dr. Yuen was awarded as one of Ten Outstanding Youth Persons in 2007. Subsequently, he received The Fourth Hong Kong Volunteer Award in year 2011. He received Achievement Award and Distinguished Service Award from the Asian Pacific Academy of Ophthalmology in 2012. Moreover, he is the present first Vice President of Asia Pacific Society of Ophthalmic Plastic and Reconstructive Surgery (APSORPS), President of the Hong Kong Society of Ophthalmic Plastic and Reconstructive Surgery, Honorary Secretary of Asia-Pacific Society of Ocular Oncology and Pathology (APSOOP), and editorial member and reviewer of several journals.
Non-necrotizing
Introduction
Acute bacterial infection of the orbit is associated with diffuse edema of the orbital tissues with infiltration of inflammatory cells. There are usually cardinal signs of inflammation including pain, redness, swelling, and warmth. Since the orbit is a confined space, tissue edema secondary to the inflammatory process may lead to proptosis, as well as compression of the structures within the orbit causing conjunctival injection, ophthalmoplegia, and, in severe case, compressive optic neuropathy resulting in visual loss.
Conventionally, in the Chandler classification, orbital cellulitis was grouped into five different stages [1]:
Stage 1 – Preseptal cellulitis, with inflammation localized anterior to the orbital septum. There are eyelid swelling, erythema, and tenderness yet no orbital signs.
Stage 2 – Orbital cellulitis, where infection extends posterior to the orbital septum leading to diffuse orbital edema yet without discrete abscess. There are eyelid edema and erythema, proptosis, and chemosis with limited or normal extraocular movement and normal visual acuity.
Stage 3 – Subperiosteal abscess. There is pus collection between periorbital and orbital bones, which can displace the orbital contents, causing proptosis and ophthalmoplegia.
Stage 4 – Intraorbital abscess, with pus collection within orbital tissues. There are severe exophthalmos, chemosis, complete ophthalmoplegia, and visual impairment.
Stage 5 – Cavernous sinus thrombosis, caused by extension of infection posterior to the orbit. There are bilateral orbital pain, chemosis, proptosis, and ophthalmoplegia. It can be associated with meningitis, intracranial abscess formation, and sepsis.
A more practical and commonly used approach is to divide orbital infections into preseptal or postseptal cellulitis. Preseptal cellulitis refers to those infections localized to the eyelids and periocular structures anterior to the orbital septum where postseptal cellulitis describes an infection involving the soft tissues posterior to the orbital septum. In general, postseptal cellulitis is more severe and may be associated with sight and life-threatening complications [2, 3].
Preseptal Cellulitis
Preseptal cellulitis occurs more commonly than orbital cellulitis and is generally associated with a more favorable prognosis. Preseptal cellulitis can occur alone or as a spread of infection from adjacent soft tissues of the face, ocular adnexa, and paranasal sinuses. There may be a history of trauma, insect bites, foreign bodies, chalazion or hordeola, dacryocystitis, skin infection like impetigo, sinusitis, upper respiratory tract infection, or recent periocular/oral procedures [3].
The typical presentations of preseptal cellulitis are eyelid edema and erythema. As the infection is superficial, patients have no orbital signs. Evaluation should start with relevant history to identify predisposing factors like trauma, surgery, or adjacent infection. A comprehensive ophthalmic examination, including assessment of visual acuity, pupillary response, extraocular movement, intraocular pressure, anterior segment biomicroscopy, and dilated fundal examination, is recommended. The distinctive features to differentiate preseptal cellulitis from orbital cellulitis are normal vision, absence of proptosis, absence of afferent pupillary defect, and absence of pain and limitation on extraocular movement. Care should be taken to identify any wound suggestive of trauma, especially perforating injuries that may affect the globe integrity or suggestive of a possible foreign body [4, 5].
The primary strategy in the treatment of preseptal cellulitis is the prompt initiation of appropriate antibiotic therapy. Given the predisposing factors of preseptal cellulitis, the choice of antibiotics should target towards causative agents of sinusitis and upper respiratory tract infection, in particular Staphylococcus and Streptococcus species. In cases with history of local trauma, coverage for Staphylococcus aureus is mandatory. Mild preseptal cellulitis in adults and children over 1 year old can be treated with empiric broad-spectrum oral antibiotics in outpatient setting. Those who require hospital admission for intravenous antibiotics are children less than 1 year of age, immunocompromised individuals, and patients who fail to respond to oral treatment and with development of more severe infection or systemic toxicity [4, 6–10]. A negative immunization history against Haemophilus influenzae and Streptococcus pneumoniae is considered a relative indication for early admission. Surgical interventions are usually not required in preseptal cellulitis, unless associated with the development of eyelid abscess or in the presence of foreign body [9]. Percutaneous drainage and debridement of an eyelid abscess can be performed through a direct incision over the area of fluctuance under local anesthesia. Loculation in the cavity should be broken with a curette and the wound packed with ribbon gauze to promote further drainage. Expressed material should be sent for microbiological evaluation, especially culture and sensitivity to guide subsequent antibiotic therapy. Any concurrent sinusitis should be treated and appropriate referral arranged [6].
Orbital Cellulitis
Orbital cellulitis refers to infections that involve the tissues posterior to the orbital septum, including the extraocular muscles and orbital fat within the bony orbit. In contrast to preseptal cellulitis, it may result in more significant complications. Permanent visual loss has been reported in the range of 11–26 % of cases, as results of compressive optic neuropathy, toxic optic neuritis, panophthalmitis, or exposure keratopathy due to proptosis. Intracranial complications, though rare, include cavernous thrombosis, meningitis, brain abscess, and subdural empyema. Therefore accurate diagnosis, close observation, and expeditious treatment are of paramount importance [11–13].
Orbital cellulitis can affect all age groups yet it occurs more commonly in the pediatric population (Fig. 33.1). The most common cause is a direct extension of infection from the adjacent paranasal sinuses, in particular the ethmoid sinus through the thin lamina papyracea. The inflamed mucosa in sinusitis leads to closure of ostia and blocks the sinus drainage, which promotes proliferation and accumulation of bacteria, resulting in suppuration and extension to the orbit through the thin bones of orbital walls, foramina, and venous and lymphatic channels. Other predisposing factors include trauma, especially those associated with orbital fracture or foreign bodies, dacryocystitis, untreated preseptal cellulitis, endophthalmitis, and dental infections or procedures [14–16]. Orbital cellulitis following ophthalmic surgery is uncommon, but has been reported after strabismus surgery, eyelid surgery, lacrimal surgery, cataract extraction, scleral buckling, and peribulbar injection [17–20]. Though uncommon, it can be the presenting feature of retinoblastoma in children [21]. Hematogenous spread in the setting of bacteremia is also possible.
Fig. 33.1
Orbital cellulitis in the left eye with periorbital swelling and erythema
Patients with orbital cellulitis typically present with more severe edema and erythema of periorbital tissues and may be associated with decreased vision, proptosis, pain with eye movement, and ophthalmoplegia with or without diplopia. The presence of fever is variable. Apart from identifying predisposing factors, like history of sinusitis, trauma, or surgery, a thorough ophthalmic examination is required, especially to identify any complications from the disease, e.g., the presence of relative afferent pupillary defect signifying compressive optic neuropathy, exposure keratopathy secondary to proptosis, elevated intraocular pressure, venous stasis, or even central retinal artery occlusion due to raised intraorbital pressure [22]. Systemic examination including assessment of vital signs should be performed. Blood cultures should be taken, and a lumbar puncture may be necessary if signs of meningitis are present. Urgent imaging is indicated to assess the anatomic extent of disease, to identify subperiosteal or orbital abscess that requires exploration and drainage, to look for sources of contiguous spread like sinusitis, and to rule out intracranial extension.
Before the introduction of the Haemophilus influenzae type B (HiB) vaccine, H. influenzae was one of the most commonly reported organisms associated with orbital infections [9]. In a more recent study on microbiology of pediatric orbital cellulitis, Staphylococcus aureus was the most common species isolated (one-third being methicillin-resistant S. aureus (MRSA)), followed by Streptococcus species. Anaerobic bacteria, including Peptococcus, Peptostreptococcus, and Bacteroides, are less common causes and are associated with infections following animal bites [10]. Blood cultures are usually negative. Cultures from ocular secretions and nasal swab can be performed, but there may be normal flora contaminants; thus organisms recovered from abscess or nasal drainage are the most reliable source of causative agents.
Medical Management
Early diagnosis and aggressive proper management of orbital cellulitis are essential to avoid vision- or life-threatening complications. Intravenous antibiotics should be started promptly based on empiric coverage for the common causative microorganisms, typically the gram-positive Staphylococcus and Streptococcus species. Vancomycin should be considered early if the local resistance profile suggests high prevalence of methicillin-resistant staphylococcal infection. Second- or third-generation cephalosporin, clindamycin, or metronidazole is often added to provide coverage of gram-negative and anaerobic organisms [23, 24]. Treatment should be modified based on clinical response as well as culture and sensitivity results. Consultation with the infectious disease/microbiology team may be helpful. For patients with concurrent sinusitis, nasal decongestant and nasal irrigation can promote drainage of the sinus [25]. Intranasal corticosteroid can also be considered to facilitate drainage by reducing mucosal edema [26]. The use of systemic corticosteroids is still debatable. Although suppression of the immune system may lead to worsening of the infection, there are multiple theoretical advantages. Firstly, the reduction of tissue edema and cell migration may decrease compression on orbital structures to avoid irreversible visual loss and may facilitate drainage to accelerate recovery from sinusitis. Secondly, by inhibiting fibroblast proliferation, corticosteroids can reduce scarring of orbital tissues and potential long-term sequelae. In a retrospective study by Yen, it was concluded that the use of intravenous corticosteroids in the acute management of pediatric orbital cellulitis with subperiosteal abscess did not adversely affect clinical outcome [27]. In a prospective trial by Pushker, oral corticosteroids were offered after initial response to intravenous antibiotics, and it was observed that such adjunct hastened resolution of inflammation with a low risk of exacerbating infection [28].
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