Orbital complications of paranasal sinusitis in Taiwan, 1988 through 2015: Acute ophthalmological manifestations, diagnosis, and management

Abstract

PurposeParanasal sinusitis is widespread and can lead to orbital complications, blindness, and death. However, the correlation between ophthalmological findings and disease staging remains unclear. This study aimed to investigate the staging, acute ophthalmological manifestations, diagnosis, management, and outcomes of orbital complications of paranasal sinusitis during a 27-year period.MethodsWe retrospectively reviewed the medical records of all patients with orbital complications of paranasal sinusitis hospitalized at the National Cheng Kung University Hospital, a medical center in Taiwan during 1988–2015. Sex, age, symptoms, history, ophthalmological findings, laboratory and imaging findings, treatments, and outcomes were analyzed by staging.ResultsEighty-three patients aged 9 days to 80 years had stage I (preseptal cellulitis, n = 39 patients), II (postseptal orbital cellulitis, n = 8), III (subperiosteal abscess, n = 16), IV (orbital abscess, n = 8), or V (intracranial involvement, n = 12) complications. Peak incidences occurred in patients aged 0–19 and 60–69 years. Chronic sinusitis and diabetes mellitus were common preexisting diseases. Extraocular movement limitation and proptosis predicted postseptal (stage II or more) involvement. The likelihood of elevated intraocular pressure increased with stage. Reduced visual acuity and presence of relative afferent pupillary defect indicated consideration of magnetic resonance imaging to investigate possible intracranial extension. Ipsilateral maxillary (81.7%) and ethmoidal (75.6%) sinuses were the most common sources of infection, and the most frequently implicated pathogens were coagulase-negative Staphylococcus spp. (25.3%) and Staphylococcus aureus (20.5%). All patients received intravenous antimicrobial therapy (multi-drug therapy in 88.0%), and 55.4% underwent surgery, most commonly endoscopic sinus surgery. One (1.2%) diabetic man with stage V complications died of fungal sinusitis with intracranial invasion. Five (6.0%) patients, all stage V, lost vision despite intensive treatment. The average length of hospital stay was 13.8 days (range 2–72 days), and significantly longer stays were associated with stages II–V as compared to stage I.ConclusionsOrbital infection originating from paranasal sinusitis can cause vision loss and death due to intracranial extension. Acute ophthalmological findings predict staging and prognosis. Cooperative consultation between ophthalmologists, otorhinolaryngologists, and neurologists is essential. Urgent diagnostic studies and aggressive antimicrobial therapy are indicated, and surgery should be considered.

The Development of Dry Eye Disease after Surgery-Indicated Chronic Rhinosinusitis: A Population-Based Cohort Study

“…Other diseases that correlated to the occurrence of DED, including keratopathy, uveitis, glaucoma and AMD, showed a significant correlation to DED in the current study. Because the persistent DED may cause damage in the ocular surface including the cornea [12], it is reasonable for the correlation between the two diseases in the current study. In addition, the preservatives in anti-glaucomatous medications may cause further damage of ocular surface and lead to inflammation of the ocular surface and DED [28].…”

“…In addition, tissue from patients with CRS demonstrated inflammatory cell infiltration, thus suggesting an inflammatory nature of CRS [18]. On the other hand, the vicious cycle in developing DED includes components such as meibomian gland dysfunction (MGD), aqueous deficiency, exposure-related damage and goblet cell deficiency [12]. Among them, both the MGD and goblet cell deficiency are related to the increment inflammatory reaction [12,19], in which MGD will lead to the evaporative excess subtype of DED and affects about 50 percent of patients with DED [20].…”

“…On the other hand, the vicious cycle in developing DED includes components such as meibomian gland dysfunction (MGD), aqueous deficiency, exposure-related damage and goblet cell deficiency [12]. Among them, both the MGD and goblet cell deficiency are related to the increment inflammatory reaction [12,19], in which MGD will lead to the evaporative excess subtype of DED and affects about 50 percent of patients with DED [20]. Besides, several inflammatory mediators-like interleukin and matrix metalloproteinases-are elevated in those individuals with DED [12,21].…”

“…Among them, both the MGD and goblet cell deficiency are related to the increment inflammatory reaction [12,19], in which MGD will lead to the evaporative excess subtype of DED and affects about 50 percent of patients with DED [20]. Besides, several inflammatory mediators-like interleukin and matrix metalloproteinases-are elevated in those individuals with DED [12,21]. As a consequence, the persistent inflammatory process in prolonged CRS may activate the inflammatory reaction in the DED cycle.…”

“…Symptoms of dry eye disease (DED) can include a sensation of dryness, irritation resulting from evaporative excess, aqueous deficiency, ocular surface damage, or all of these symptoms [11]. Recently, the major pathophysiology of DED is speculated as a multi-factorial vicious cycle that leads to inflammatory processes [12]. Since the etiology of CRS is usually related to inflammation [13], a certain association may exist between these two disorders, which has rarely been reported elsewhere.…”