As most cases of orbital cellulitis are related to acute sinusitis, optimal management of orbital infections requires appropriate treatment for the underlying or associated sinus infection. For most cases, management of sinusitis will entail use of saline nasal sprays, nasal decongestants, and nasal corticosteroids in addition to systemic antibiotics and anti-inflammatories. In some cases, surgical drainage of the sinuses is necessary. A more detailed discussion of sinusitis management is provided in the subsequent chapter.

This rise in community-acquired MRSA (CA-MRSA) demands physicians to differentiate between the hospital-acquired MRSA (HA-MRSA) version of the organism, which is perhaps more familiar to healthcare practitioners. The CA-MRSA is known to be more virulent than its HA-MRSA counterpart due to cytotoxin Panton-Valentine leukocidin secretion. However, the CA-MRSA is more susceptible to tetracyclines, trimethoprim-sulfamethoxazole, clindamycin, and fluoroquinolones than the nosocomial strain. For this reason, some guidelines suggest non-beta-lactam antibiotics where CA-MRSA prevalence is greater than 15% [22]. Despite this consideration, a 2011 review of 94 children with orbital infections in Colorado showed two-thirds of patients were discharged on antibiotics not effective against MRSA, despite being on intravenous drug regimens covering MRSA while inpatient [23].

Antibiotic regimens differ by geography, reflecting both differences in microbiology and susceptibilities as well as economic differences that can dictate available treatment options [24–27]. Modern treatment recommendations include intravenous therapy with a variety of antibiotic combinations. Some empiric regimens include vancomycin, ampicillin-sulbactam, and/or piperacillin-tazobactam [16] and a third-generation cephalosporin with good central nervous system penetration such as ceftriaxone, clindamycin, or ampicillin-sulbactam depending on suspicion for MRSA [28, 29]. The National Health Service in the United Kingdom published guidelines in 2013 recommending intravenous co-amoxicillin, ceftriaxone, and metronidazole [30]. All treatment regimens also included nasal decongestants during treatment. Intravenous antibiotics are recommended for at least 2–3 days, followed by a course of oral antibiotics [16, 31]. Of consideration, in third-world countries where cost can be a prohibitive issue and patients must pay for medication out of pocket as well as obtain the medications themselves, the recommendations include Ampiclox, gentamicin, and metronidazole [27].

Indeed, medical therapy has become markedly more effective in treating orbital cellulitis. In a 2016 survey of the UK National Health Service database, 87.9% of the 14,149 cases of orbital cellulitis between 2002 and 2010 were managed without surgical intervention. Surgery was least likely to be needed in the youngest patients, with 5.1% of patients under 5 years of age requiring surgical intervention [32].

In the 1970s, corticosteroid therapy was discouraged in orbital cellulitis treatment, as it was associated with poorer outcomes. It was felt to delay patients’ antibiotic response and failed to show improvement in edema [7]. There continued to be a thought that steroids may be beneficial in orbital cellulitis patients by decreasing edema, decreasing cell migration and inflammatory mediators, and decreasing fibroblast proliferation to limit scarring. In a 2005 retrospective study of patients with subperiosteal abscesses receiving steroid therapy on admission, Yen et al. showed steroids combined with antibiotic therapy decreased duration of hospitalization from 10 to 6.5 days. Additionally, only 2 of 12 patients receiving steroids required intravenous antibiotics after discharge compared to 7 of 11 patients not receiving steroids [33].

In a 2013 prospective study by Pushker et al., patients were placed on a standardized antibiotic regimen of intravenous vancomycin and ceftriaxone with the addition of metronidazole if no improvement was seen in 2 days or if anaerobic infection was suspected. Following 3 days of antibiotic therapy, patients in the test group were dosed with oral prednisolone 1.5 mg/kg/day for 3 days and then 1 mg/kg/day for 3 days. Steroids were tapered over the course of 1–2 weeks. The steroid group exhibited several beneficial effects over the control group: quicker resolution of fever, less pain, faster edema and proptosis resolution, and faster return of normal ocular motility. Patients receiving steroids reached maximal vision improvement at 10 days compared to 12 weeks in the control group. No subjects in the test group had return or spread of infection. Steroid treatment was also shown to decrease hospital stay from 14.1 to 18.4 days and decrease the duration of intravenous antibiotic therapy. Of note, due to ethical concerns, no patients under 10 years of age were included in the study [34].

Building on this data, Davies et al. examined the effect of initiating steroid therapy earlier in the treatment course. Patients were started on 1 mg/kg/day prednisone treatment once C-reactive protein levels fell below 4, which was 2.9 days on average. This study also showed a significant decrease in hospital stay with patients receiving steroids hospitalized an average of 3.96 days compared to 7.17 days in the control group. All patients enjoyed a full recovery with no permanent disability [35].

Based on these results, there is a strong consideration for including steroid therapy in the medical management of orbital cellulitis.

While bacteria are the most common cause for orbital infection, fungal pathogens can cause devastating disease. Fungal orbital cellulitis is most often found in immunocompromised patients. This state is commonly due to diabetes mellitus, acquired immunodeficiency syndrome, hematologic or lymphoproliferative malignancy, congenital immunodeficiency, and iatrogenic causes such as chemotherapy, antirejection medication, or treatment for autoimmune inflammatory disorders. These infections may occur secondary to hematogenous spread in fungemic patients or from adjacent spread of the fungus, either along tissue planes or through angioinvasive routes. Due to severity of underlying fungal infection and markedly reduced host response, fungal orbital infections carry a high mortality rate with case series showing 71–85% mortality [36, 37].

Orbital-cerebral phycomycosis was first clinically described in 1943 by Gregory et al. [38]. This type of infection is commonly due to spores of Rhizopus, Mucor, or other organisms entering the nose of the patient. These patients almost always have underlying acid-base imbalance, commonly due to diabetic ketoacidosis or dehydration accompanying metabolic acidosis secondary to diarrhea in the pediatric population. Patients tend to develop rapid facial swelling, proptosis, ptosis, orbital cellulitis, and vision loss. There is commonly a necrotic ulcer on the palate. Histologic exam of affected tissue shows broad, nonseptate hyphae that stain well with hematoxylin-eosin occluding the vasculature and extending into adjacent tissue [1]. This aggressive disease has a high mortality and must be treated promptly with antifungal therapy and surgical debridement [39].

While phycomycosis can be heralded by a marked inflammatory response and proptosis, the immunocompromised nature of most patients can result in few if any symptoms in patients with rampant orbital fungal infection. This paucity of initial symptoms demands the clinician to have a heightened clinical suspicion for fungal orbital infection in immunocompromised patients with periorbital edema, headache, and facial pain. As the disease progresses, cranial neuropathies can develop resulting in extraocular motility disorders, vision loss, paresthesias, and paralysis [1].

McCarty et al. recommended MRI to evaluate the extent of infection and early multidrug antifungal therapy combined with surgical debridement and hyperbaric oxygen therapy. The underlying metabolic and/or immunologic disturbance should also be promptly rectified. Frequently, sinus washings were inadequate to make the diagnosis, and biopsy was required [37].

Aspergillus is another common fungal cause of orbital cellulitis. The disseminated, fulminant orbital aspergillosis is almost always found in severely immunocompromised patients. The fungus can invade and destroy adjacent structures as well as proliferate within vessel walls in a vaso-occlusive pattern. The initial symptoms are similar to those encountered in Mucor infections: proptosis and decreased vision. However, due to immune status of the patient, more severe signs of inflammation are rare until the later stages of the disease, if they manifest at all [1].

Commonly, direct biopsy or fine needle aspiration of the affected area is required to make the diagnosis. Histology of aspergillosis tends to show small branching hyphae branching at acute angles. The organism preferentially stains with methenamine silver and periodic acid-Schiff [1].

Kronish et al. described a case series of invasive aspergillosis in HIV patients in which all patients had adjacent ethmoid and maxillary sinus involvement. The patients were treated with surgical debridement and intravenous amphotericin B dosed at 0.5–0.6 mg/kg/day. In some of these chronic cases, local injection or irrigation of amphotericin B was employed and felt to be beneficial [40]. Modern treatment azole antifungal medications combined with aggressive surgical excision perhaps provide a more effective means for combating Aspergillus orbital cellulitis [1].