Kuliah Infeksi Imunologi : ENDOPHTALMITIS.pptx

SaniaNadianisa 42 views 39 slides Jul 25, 2024
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About This Presentation

Endophthalmitis


Slide Content

ENDOPHTALMITIS Sania Nadianisa M Source : American Academy of Ophthalmology 2022-2023

INTRODUCTION Endophthalmitis is a clinical diagnosis made when intraocular inflammation involving both the posterior and anterior chambers is attributable to bacterial or fungal infection Post operative Endophthalmitis Posttraumatic Endophthalmitis Chronic Endophthalmitis Endogenous endophthalmitis occurs when bacteria or fungi are hematogenously disseminated into the ocular circulation “Sterile endophthalmitis” describes cases in which infection is suspected but that return negative culture results

Posttraumatic Endophthalmitis Endophthalmitis occurs after 2%–7% of penetrating injuries; the incidence is higher in association with IOFBs and in rural settings marked inflammation featuring hypopyon, fibrin, vitreous infiltration, and corneal opacification A common mechanism is a dirty wire or stick that perforates the cornea, inoculates the anterior chamber or vitreous cavity, and then retracts from the eye. In such cases, there should be a low threshold for intravitreal injection of antibiotics. Fluoroquinolones have acceptable vitreous penetration after systemic (intravenous or oral) administration. Levofloxacin 500 mg daily or moxifloxacin 400 mg daily is a good option for treatment of posttraumatic endophthalmitis in addition to intravitreal antibiotics

Most commonly, B cereus endophthalmitis is associated with injuries caused by soil-contaminated objects, especially in the setting of IOFB. Gram-negative organisms are also frequent pathogens in posttraumatic endophthalmitis. When there is contamination with vegetable matter, posttraumatic fungal infection, most commonly Candida, should be considered.

Postoperative Endophthalmitis classified on the basis of time of onset: acute onset occurs within 6 weeks after surgery, and delayed onset occurs more than 6 weeks after surgery.

Acute-onset postoperative endophthalmitis hypopyon, conjunctival vascular hyperemia, and corneal and eyelid edema. Symptoms include pain and vision loss. coagulase-negative Staphylococcus species, Staphylococcus aureus, Streptococcus species and gram-negative organisms. Intravitreal antibiotic injections should always be administered after culture samples are collected. -- Commonly used agents include ceftazidime and vancomycin. Intravitreal dexamethasone may reduce posttreatment inflammation, but its role in endophthalmitis management remains controversial

In the EVS, patients were randomly assigned to undergo either vitrectomy or vitreous tap/biopsy. Both groups received intravitreal and subconjunctival antibiotics (vancomycin and amikacin). The EVS concluded that vitrectomy was indicated in patients with acute-onset postoperative endophthalmitis (within 6 weeks of cataract extraction) with ight perception vision (Fig 19-8).

Endophthalmitis associated with glaucoma surgery conjunctival vascular hyperemia and noticeable intraocular inflammation, often with hypopyon (occurring months or years after glaucoma filtering surgery) Blebitis without endophthalmitis can be treated with frequent applications of topical and subconjunctival antibiotics and close follow-up. However, if blebitis progresses to bleb-associated endophthalmitis, patients are treated with intravitreal antibiotics with or without vitrectomy

CHRONIC POSTOPERATIVE ENDOPHTHALMITIS has a distinctive clinical course, with multiple recurrences of chronic indolent inflammation in an eye that had previously under gone surgery, typically cataract extraction . General Clinical Finding : Chronic anterior segment inflammation, hypopyon, keratic precipitates, intracapsular plaques, and/or vitritis -– may respond with steroid but often recurs after steroid are tappered

This recurrent indolent inflammation may occur at any point during the postoperative course, but it is often delayed by many months to years . cause corneal decompensation or even iris neovascularization in the most severe cases. Chronic postoperative endophthalmitis can be divided into bacterial and fungal varieties. Common is Propionibacterium acnes -- may sequester itself between an IOL implant and the posterior capsule, Nd:YAG capsulotomy can trigger chronic endophthalmitis by liberating the organism into the vitreous cavity, resulting in a more severe vitreous inflammation and an exacerbation of the under lying infection Additionally, gram- positive bacteria with limited virulence ( eg , Staphylococcus epidermidis and Corynebacterium species), gram- negative bacteria, or Mycobacterium

FUNGAL CHRONIC POSTOPERATIVE ENDOPHTHALMITIS Numerous fungal organisms have been implicated in this chronic inflammatory process, including Candida parapsilosis , Aspergillus flavus, Torulopsis candida , and Paecilomyces lilacinus , as well as Verticillium species. CLINICAL FINDINGS presence of corneal infiltrate or edema, mass in the iris or ciliary body, or development of necrotizing scleritis, vitreous “snowballs” with a “string- of- pearls worsen after topical, periocular, or intraocular steroid therapy

BACTERIAL CHRONIC POSTOPERATIVE ENDOPHTHALMITIS Almost same with Fungal infection

DIAGNOSIS aerobic, anaerobic, and fungal cultures of the aqueous, capsular plaques (if present), and vitreous at the time of pars plana vitrectomy--slow Polymerase chain reaction (PCR) studies of primers for P acnes or pan- fungal and pan- bacterial primers are helpful if available – immedietly

DIFFERENTIAL DIAGNOSIS noninfectious causes such as lens- induced uveitis from retained cortical material or retained intravitreal lens fragments, intraocular inflammation from iris chafing resulting from IOL malposition, uveitis- glaucoma- hyphema syndrome, and intraocular lymphoma masquerade syndrome

TREATMENT Pars plana vitrectomy and injection of intravitreal and endocapsular vancomycin are therapeutic in many cases of chronic postoperative bacterial endophthalmitis – May not completely eradicate IOL explantation , complete capsulectomy, and intravitreal vancomycin injection is curative Chronic fungal endophthalmitis treatment is more difficult and requires the use of weekly intravitreal antifungal injections (amphotericin or voriconazole) and, possibly, systemic antifungal drugs in the most severe cases. In vitrectomized eyes, antifungals are often injected twice a week –may necessary multiple vitrectomies

ENDOGEN BACTERIAL ENDOPHTHALMITIS caused by hematogenous dissemination of bacterial organisms, resulting in intraocular infection. Immnuocompromised : diabetes mellitus, systemic malignancy, sickle cell anemia, systemic lupus erythematosus, and HIV infection Possible infection sources to be considered are tooth abscess, pneumonia, endocarditis, urinary tract infection, bacterial meningitis, and liver abscess . There may be a history of an indwelling line or port

The most common gram- positive organisms are Streptococcus species (endocarditis), Staphylococcus aureus (cutaneous infections), Bacillus species (from intravenous drug use), and Nocardia species (in immunocompromised patients). The most common gram- negative organisms are Neisseria meningitidis, Haemophilus influenzae, and enteric organisms such as Escherichia coli and Klebsiella species. In Asia , infection from Klebsiella species in liver abscesses is the most common cause of endogenous endophthalmitis

Clinical Finding and Symptoms suggestive of an ongoing systemic infection and may include fever greater than 101.5°F, elevated peripheral leukocyte count, and positive bacterial cultures from extraocular sites (blood, urine, sputum). Clinical symptoms include acute onset of pain, photophobia, and blurred vision . Examination usually reveals severely reduced visual acuity , and fibrin in the anterior chamber ; hypopyon may be pres ent ; very rarely there may be periorbital and eyelid edema . There may be significant vitreous inflammation and vitreous cells . Small microabscesses in the ret ina or choroid and white-centered reti nal hemorrhages (Roth spots) may also be present

DIAGNOSIS Diagnosis is based on anterior chamber paracentesis and vitrectomy with vitreous and aqueous cultures and appropriate stains. PCR evaluation of ocular fluids with pan- bacterial or pan- fungal primers is extremely useful Blood and other body fluid cultures should be used along with ocular culture results to confirm the diagnosis and establish therapy

Treatment Bacterial Endogenous Antibiotic Intravitreal and systemic depend on severity. If it is not clear that fungal organisms may be involved, treatment of both fungal and bacterial causes is indicated at the time of vitrectomy. systemic antifungal therapy may be warranted for 6 weeks or more. Initial antimicrobial choices may be empiric and subsequently tailored to culture results

Complications If the diagnosis of systemic infection is missed, the patient may develop sepsis and even die complications such as cataract development, retinal detachment, suprachoroidal hemorrhage, vitreous hemorrhage, macular scar, hypotony, and phthisis bulbi can occur in the most severe cases.

Endogenous Fungal Endophthalmitis Endophthalmitis develops slowly as focal or multifocal areas of chorioretinitis There ara granulomatous and non granulomatous Observed with keratic precipitates, hypopyon, and vitritis with cellular aggregates. Begins in the choroid, appearing as yellow- white lesions with indistinct borders that range in size from small cotton- wool spots to several disc diameters. It can subsequently break through into the vitreous, producing localized cellular and fungal aggregates overlying the original site(s). Iris nodules and rubeosis may also be noted in severe fungal endophthalmitis

Endogenous fungal endophthalmitis caused by Histoplasma capsulatum, Cryptococcus neoformans, Sporothrix schenckii , and Blastomyces dermatitidis is less common than that caused by Candida and Aspergillus species

Candida Endophthalmitis Important cause of nosocomial infections and are the most common fungal organisms, causing endogenous endophthalmitis in both pediatric and adult populations. In patients with candidemia, the reported prevalence rates of intraocular candidiasis vary widely, ranging between 9% and 78% Predisposing conditions associated with candidemia and the development of intraocular infection include: hospitalization with a history of recent major gastrointestinal surgery, bacterial sepsis, systemic antibiotic use, use of indwelling catheters, hyperalimentation, debilitating diseases ( eg , diabetes mellitus), immunomodulatory therapy, prolonged neutropenia, organ transplantation, Hospitalized neonates and intravenous drug users , HIV

Clinical manifestation blurred or decreased vision resulting from macular chorioret i nal involvement or pain arising from anterior uveitis , which may be severe. Typically, Candida chorioretinitis is characterized by multiple, bilateral, white, wellcircumscribed lesions less than 1 mm in dia meter. These lesions are distributed throughout the postequatorial fundus and associated with overlying vitreous cellular inflammation The chorioretinal lesions may be associated with vascular sheathing and intraretinal hemorrhages . The vitreous exudates may assume a string- of- pearls appearance. Fungi may then break through the Bruch membrane , form subretinal abscesses, and secondarily involve the retina and vitreous

Diagnosis positive results on either blood or vitreous cultures. Fungal stains and cultures, and PCR for Candida species, should be obtained on undiluted vitreous fluid samples vitreous snowballs

Treatment systemic and intravitreal administration of antifungal drugs oral triazole antifungal drugs fluconazole or voriconazole (200 mg, twice daily, for 2–4 weeks) When the vitreous body is involved, intravitreal injection of antifungal drugs (amphotericin B, 5–10 µg/0.1 mL, or voriconazole, 100 µg/0.1 mL) More severe infections may require intravenous amphotericin B with or without flucytosine. intravenously administered caspofungin , an antifungal drug in the echinocandin class (drugs that inhibit synthesis of glucan in the cell wall) -- less toxic than amphotericin B

Cryptococcosis Endophthalmitis Cryptococcus neoformans is a yeast found in high concentrations worldwide in contaminated soil and pigeon feces. predilection for the central ner vous system common cause of fungal meningitis, as well as the most frequent fungal eye infection in patients with HIV infection or AIDS. direct extension from the optic nerve.

Manifestations cryptococcal meningitis include mainly papilledema followed by optic atrophy and cranial nerve palsies. diplopia, nystagmus, ptosis, and ophthalmoplegia. variable degrees of vitritis , vascular sheathing, exudative ret i nal detachment, papilledema, and granulomatous anterior chamber inflammation.

Diagnosis and Treatment culture of the fungus from cerebrospinal fluid. Intravenous amphotericin B and oral flucytosine required to halt disease progression. With optic nerve or macular involvement, the prognosis is poor for recovery of vision.

Aspergilus Endophthalmitis associated with disseminated aspergillosis among patients with severe chronic pulmonary diseases, cancer, endocarditis, severe immunocompromise, or intravenous drug abuse The spores of these ubiquitous saprophytic molds become airborne and seed the lungs and paranasal sinuses of humans.

Manifestation A confluent yellowish infiltrate is often pres ent in the macula, beginning in the choroid and subret i nal space. A hypopyon can develop in the subret i nal or subhyaloidal space Retinal hemorrhages, retinal vascular occlusions, and full- thickness retinal necrosis larger and more likely to be hemorrhagic, and they commonly invade the retinal and choroidal vessels, which may result in broad areas of ischemic infarction. Fundus photograph showing a large chorioretinal infiltrate with surrounding hemorrhage

Diagnosis positive results from pars plana vitreous biopsy and cultures as well as results from Gram and fungal stains. In Aspergillus endophthalmitis, the principal foci are ret i nal and choroidal vessels and the subret i nal or subret i nal pigment epithelial space.

Treatment intravitreal injection of amphotericin B or voriconazole; intravitreal corticosteroids may be used in conjunction with these drugs. Because most patients with this condition have disseminated aspergillosis, systemic treatment with oral voriconazole, intravenous amphotericin B, or caspofungin is often required. Other systemic antifungal drugs, such as itraconazole, miconazole, fluconazole, and ketoconazole, may also be used

Coccidioidomycosis Endophthalmitis dimorphic soil fungus Coccidioides immitis inhalation of dust- borne arthrospores , most commonly resulting in pulmonary infection and secondary dissemination to the central ner vous system, skin, skeleton, and eyes. Mild upper respiratory tract infection or pneumonitis approximately 3 weeks after exposure to the organism. Erythema nodosum or multiforme may appear from 3 days to 3 weeks after the onset of symptoms

Manifestation causes blepharitis, keratoconjunctivitis, phlyctenular and granulomatous conjunctivitis, episcleritis and scleritis, and extraocular nerve palsies and orbital infection. multifocal chorioretinitis characterized by multiple, discrete, yellowwhite lesions usually less than 1 disc dia meter in size located in the postequatorial fundus. Vitreous cellular infiltration, vascular sheathing, ret i nal hemorrhage, serous ret inal detachment, and involvement of the optic nerve have also been reported.

Diagnosis Positive results of serologic testing for anticoccidioidal antibodies in the serum, cerebrospinal fluid, vitreous, and aqueous,

Treatment oral azole antifungal drug such as fluconazole or itraconazole. Surgical debulking of anterior chamber granulomas, pars plana vitrectomy, and intraocular injections of amphotericin and voriconazole may be required Despite aggressive treatment, ocular coccidioidomycosis carries a poor visual prognosis, and most eyes require enucleation because of pain and blindness
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