Endogenous endophthalmitis


Endogenous endophthalmitis

Description, Causes and Risk Factors:

Endogenous endophthalmitis is a severe inflammation of intraocular structures. Although is not a common occurrence, it is considered one of the most severe vision threatening ocular condition. It is most frequently caused by microbial organisms and much less commonly results from direct physical or chemical tissue injury or from immunologic or neoplastic processes. In clinical practice the term endophthalmitis generally refers to microbial causes.

The clinical presentation of endogenous endophthalmitis can be extremely variable and led Greenwald to propose a system of classification for bacterial (reasonably useful also for fungal) endophthalmitis into several clinical presentations (types).

    Focal endophthalmitis: localized inflammatory nodules are present in the iris,ciliary body, retina and choroid. The inflammation in the anterior chamber can be associated with hypopyon but never obscure the view of the fundus. Lesions involving the choroid and retina are white or yellowish accompanied by moderate vitreous haze. The intraocular pressure is usually normal. The prognosis in these cases is good.

  • Diffuse anterior endophthalmitis: it is a severe anterior segment inflammation characterized by conjunctival chemosis, marked anterior chamber reaction with fibrin clots and significant hypopyon that hampers the view of the retina. Intraocular pressure is typically elevated. It is an ocular emergency and if not promptly and adequately treated the infection can spread to the entire eye. The visual prognosis is excellent with aggressive and appropriate treatment. Blindness usually results from delay in treatment.

  • Diffuse posterior endophthalmitis: the vitreous inflammation is so intense that it obscures retinal details. Nevertheless, during the early stages of the disease whitish emboli and perivascular hemorrhages can be noted. As the infection progresses, the retina becomes totally necrotic and vitreous abscess frequently occur. The anterior segment remains moderately involved. The intraocular pressure is low. The poor visual prognosis is most likely due to retinal ischemia as a result of occlusion of the central retinal artery by a septic embolus.

  • Panophthalmitis: it is a severe involvement of either anterior and posterior segment presenting with marked lid edema, proptosis and limitation of ocular movements. All details of anterior as well as posterior chamber are lost because of the prominent hypopyon. Typically the intraocular pressure is high. It is a disastrous and rapidly developing infection that destroys the globe and invades the orbit, resulting in blindness, phthisis or enucleation. Depending of the virulence of the pathogen, progression of a panophthalmitis may be life threatening.

In endogenous bacterial endophtalmitis the microrganisms enter into the uveal tract or retinal circulation as scattered organisms or in a bolus, and lodge in small capillaries. To invade ocular tissues and produce infection these bacteria must cross the blood-ocular barrier and establish a septic focus that can develop in the retina prior to breaking into the vitreous. The infectious embolus is usually in proximity to the retinal vessels. If a large septic embolus pass through the central retinal artery and disseminates throughout the retina, retinal necrosis and ischemia may occur,allowing the microrganism to quickly invade the vitreous and further the anterior segment. Similarly, in cases of fungal endophthalmitis a localized inflammatory reaction surrounding a small nidus of fungi forms in the inner choroid, breaks through Bruch's membrane into the retina forming a microabscess and spreads into the vitreous cavity.

Endogenous endophthalmitis rarely occurs in healthy patients. Since the disease occurs secondary to the hematogenous spread of microrganisms to the eye from a site of infection in the body, any disease process that produces septicemia can lead to development of endophthalmitis. Well known predisposing factors are active foci of infection in the body (even occult), debilitating conditions like diabetes, malignancies, alcoholism and liver diseases, heart abnormalities (valve abnormalities and endocarditis), recent surgery, long postoperative course, intravenous catheters and hyperalimentation, intravenous drug abuse, prolonged use of corticosteroids and, in case of fungal endophthalmitis, broad spectrum antibiotic therapies.

Endogenous endophthalmitis

The visual outcome is usually good in the anterior form of endophthalmitis, differently from posterior diffuse and panophthalmitis forms. Ultrasonography negative prognostic factors are vitreous and subhyaloid opacities, choroidal and retinal detachment. Other factors that are associated with a poor visual outcome are the patogenicity of organism, delay in time between the diagnosis and treatment, low intraocular pressure, initial visual acuity of light perception, severe hypopyon and absent red reflex.

Symptoms:

The most common ocular symptoms referred from a patient with endogenous endophthalmitis areblurred vision, pain, redness and external discharge. Associated systemic symptoms may bepresent such fever, malaise, weight loss especially when the disease is advanced, these aremore severe in sepsis.

Ocular signs may include ciliary and conjunctival injection, hypopyon, corneal edema, posteriorsynechia with bombe' iris, cells in the anterior chamber and vitreous cavity, and retinal and choroidallesions.

Diagnosis:

The high incidence of misdiagnosis of endogenous endophthalmitis ranging from conjunctivitis,acute glaucoma or other ocular conditions should alert the ophthalmologist to make a correctdiagnosis of this insidious entity. The possibility of endogenous endophthalmitis should beconsidered in any patient who manifests a pronounced anterior reaction that is refractory tosteroid treatment. The appropriate diagnosis is necessary to start the appropriate treatment andinfluence dramatically the visual outcome as well as reduce the incidence of systemiccomplications, sometime fatal. Therefore the crucial point is diagnostic suspicion.

    Accurate ocular and systemic history.

  • Investigation of risk factors.

  • Search source of infection: cooperation with internal medicine and infectious disease.

  • B and A scan: to exclude posterior involvement, during the follow-up to monitor the adequacy oftreatment.

  • Intraocular fluids: anterior aqueous tap, vitreous tap or vitrectomy.

  • Non-ocular fluids: blood, urine, CSF, all suspicious source of infection, others.

  • Culture of fluids.

In cases when there is no suspicion for endogenous (and this can happen especially if the clinical setting is negative or the patient is healthy), other common causes of uveitis must be excluded with the usual serologic tests.

    Autoimmune causes.

  • Other infectious diseases: viral, protozoal, fungal.

  • Malignancies, masquerade,metastatic tumors.

  • Whether, a negative response is obtained after a carefully exclusion of these causes, ocular and non ocular fluids culture must be considered.

Treatment:

Bacterial: prompt and intensive intravenous antibiotic treatment continued for 3 weeks or longer is imperative. Initial doses should be those recommended for systemic infections. The selection of antibiotics prior to define identification of the causative agent reflects the characteristics of the patient and the likely source of bacteriemia. In other cases, broad spectrum coverage is indicated. Vancomycin is used for Gram positive bacteria, while gentamicin, amikacin or ceftazidime are indicated in cases of Gram negative infection. Intraocular and intravitreous injections are effective. Generally gentamicin and amikacin are now less commonly used because of associated risk of retinal toxicity and macular infarction; ceftazidime has been preferentially used more recently. Subconjunctival and topical antibiotics are also employed as well as intravitreal and oral steroids. The role of systemic antibiotic analyzed by the endophthalmitis vitrectomy study group (EVS) is not applicable for the endogenous forms.

Fungal: intravitreal and intravenous amphotericin B is currently the drug of choice. Treatment duration and total dose of intravenous drug are determined by the clinical response and the degree of systemic or non-ocular involvement. Toxic side effects, including renal and hepatic toxicity, must be carefully monitored. Flucytosine can be used in combination with amphotericin B in cases of macular involvement and extensive inflammatory response, but its use alone is not recommended because of the frequent occurrence of drug resistance.

Surgical Treatment: Surgical treatment is controversial and moreover criteria formulated from the EVS regarding the benefits of vitrectomy versus vitreous tap are not applicable. In general vitrectomy is indicated in cases of prominent vitreous involvement showing progressive disease despite intensive medical treatment. In these cases vitrectomy is effective in clearing the vitreous of inflammatory debris. Other advantages include the possibility to have larger sample to make the diagnosis and also to deliver a therapeutic level of drug in the vitreous.

NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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