**3. Delayed-onset postoperative infectious endophthalmitis**

Delayed-onset postoperative infectious endophthalmitis occurs beyond 6 weeks after the intraocular procedure [3]. It is a synonym that is usually used to describe chronic postoperative endophthalmitis (CPE) [17]. This type of endophthalmitis has a diagnostic and therapeutic dilemma and requires a high index of suspension because other causes may mimic its presentation. Hence, patients with CPE are frequently treated with corticosteroids due to the masquerading presentation of autoimmune intraocular inflammation. CPE was first described in the 1980s and the microorganisms that are responsible for CPE are somewhat different from that of APIE. They are usually low virulent and indolent. Specific groups of bacteria and fungi are considered to be causative pathogens for CPE (**Table 3**) [17–21].

It was observed that CPE has a lower incidence rate than APIE. Its incidence is around 0.017% after cataract surgery [20]. Some studies reported a ratio of acute to chronic postoperative endophthalmitis between 5:1 and 2:1 [17].

Propionibacterium acne, which is a gram-positive, non-spore-forming anaerobic bacillus bacteria, and found usually in skin and hair follicles; is considered to be the most common causative pathogen for CPE. Around two-thirds of the CPE, cases are found to have Propionibacterium acne [21].

The clinical features of CPE are less aggressive than that of APIE. It occurs 6 weeks to months after the intraocular procedure. Usually, the affected eye shows a persistent or recurrent low-grade indolent inflammation [22, 23]. The inflammation is often granulomatous with large keratic precipitates. The ocular pain is usually not severe, but reduced vision is common in almost all patients. Hypopyon is not a frequent


## **Table 3.**

*Microorganisms that are associated with CPE.*

*Infectious Endophthalmitis: Ongoing Challenges and New Prospectives DOI: http://dx.doi.org/10.5772/intechopen.106923*

## **Figure 2.**

*Delayed-onset endophthalmitis due to P. acne. Anterior segment photo shows clear cornea and plaques on the posterior capsule (2a) and intraoperatively photos show moderately inflamed vitreous (2b & 2c) (Courtesy of Dr. Hemant Trehan).*

finding, but microhypopyon may present. Other associated clinical features include conjunctival congestion and photophobia. An important feature in CPE is the presence of white plaques in the capsule. These plaques are associated with a different variety of microorganisms that causes CPE and not only P. acne (**Figure 2**) [20].

Management of CPE is somewhat challenging due to the ambiguous presentation. Many patients with CPE are treated initially with steroids and which may result in a partial response. However; the indolent inflammation persists and recurs after tapering down or discontinuation of the steroids. Furthermore, patients with fungal etiology might get worsening signs if steroid treatment is commenced. There is no standard treatment protocol known for CPE like the one which is known for APIE (i.e., EVS recommendations). However, in real-life practice, treatment may include intravitreal injection of antibiotics alone as an initial treatment or with pars plana vitrectomy (PPV) along with partial or total capsulotomy and removal or exchange of the intraocular lens (IOL) is performed [17]. In addition, sending the IOL with the capsule to a microbiology lab is recommended in the management plan of CPE. The use of empiric intravitreal antibiotics is recommended when treating chronic endophthalmitis. Patients with highly suspected or culture-proven fungal endophthalmitis to be monitored and treated with anti-fungal therapy, such as intraocular amphotericin (5–10 μg in 0.1 ml).

The outcome after treating CPE depends on the causative pathogen. In general, visual acuity of 20/40 or better can be achieved in 29–50% after treatment. Eyes with CPE caused by P. acne or other gram-positive bacteria has a better outcome [17]. However, CPE caused by fungus carries poor visual outcome [20].
