OVERVIEW
Acquired Immunodeficiency Syndrome (AIDS), also known as AIDS, is a new viral infectious disease that gained worldwide attention in the 1980s. It is a serious disease caused by the human immunodeficiency virus and is characterized by cellular immunodeficiency. And as a result, difficult-to-control conditionally pathogenic microbial infections occur, often combined with malignant tumors, such as Kaposi’s sarcoma and Burkitt’s lymphoma. Patients die within a relatively short period of time. It is now non-rare in China and has a tendency to increase rapidly. Fundus and other ocular lesions often occur in AIDS patients, which is a very important topic for ophthalmologists.
Etiology
Caused by the human immunodeficiency virus (HIV).
Symptoms
The incubation period after infection varies from 1 year to several years or even more than 10 years (average 4.5 years). There is persistent fever, night sweats, diarrhea, wasting, enlarged lymph nodes, TH cell reduction, and inverted TH cell to TS cell ratio throughout the body. Due to cellular immune deficiency, patients are highly susceptible to harmless conditionally pathogenic microorganisms and develop multiple organ and systemic infections with malignancy.
Fundus damage can occur as a result of HIV infection itself or as a result of secondary infection with conditionally pathogenic microorganisms.
In HIV infection itself, the main manifestation is a cotton-wool spot, mostly located in the posterior part of the fundus near the vascular arch or in the superficial retina around the optic disc, which appears quietly in one or more places, disappears within 4-6 weeks, and then reappears as a new lesion in a different place. Absorbent cotton spots are formed by inflammatory obstruction of the anterior retinal capillary arteries, causing focal ischemia, hypoxia, axial plasma flow blockage in the nerve fiber layer, and edematous degeneration of the nerve fibers. Fundus fluorescence angiography (FFA) shows areas of no perfusion at the corresponding sites of the white spot (including the vanished sites). Sometimes flame-like hemorrhage in the posterior pole of the fundus and hemorrhagic spots with white centers can also be seen. Peripapillary occlusion around the macular pits can also lead to macular edema and exudation, with radial microcystic folds and stellate patches along Henle’s fibers.
HIV invades and destroys TH cells, which are the core of the immune system, resulting in irreversible immunodeficiency, which leads to a variety of conditionally pathogenic microorganisms (viruses, bacteria, fungi, protozoa) that cause infectious diseases of the fundus, such as cytomegalovirus retinitis, toxoplasma chorioretinitis, fungal (Candida cryptococcus, etc.) choroidal retinitis, and Mycobacterium avium choroidal retinitis.
The prevalence of cytomegalovirus retinitis is as high as 12% to 46% in patients with AIDS (in addition to patients with malignant tumors and immunosuppressive drugs after organ transplantation). It is usually seen late in the course of the disease, but may precede the appearance of other systemic pathologies. It starts slowly, with no significant impairment of central vision, and patients often have no sensation or only mosquitoes. On ophthalmoscopy, there is a blurred, yellowish-white, scattered granular or grayish-white flocculent turbidity in the peripheral fundus or near the posterior pole vascular arch, which gradually enlarges and fuses. Extensive retinal edema, exudation, and flame hemorrhages, and macular stellate hard exudation give the fundus a crumbly cheese and ketchup appearance.
Toxoplasma retinal choroiditis is caused by Toxoplasma gondii protozoa entering the choroidal retina via the short posterior ciliary artery or reaching the vicinity of the optic disk from the cerebrospinal fluid. The fundus manifestations are the same as those of generalized acquired Toxoplasma gondii choroidal retinitis. However, the inflammatory response is rapid, and the fundus is often not visualized because of atrial fluid and vitreous clouding.
Examination
1. Laboratory tests
Laboratory immunologic tests are very important to determine the diagnosis, including absolute peripheral blood lymphocyte values, TH and TS cell values and their ratios; HIV isolation, detection of HIV antigen and nucleic acid or reverse transcriptase.
2. Other auxiliary tests
In the case of concurrent cytomegalovirus retinitis, there is a large area of nonperfusion in the retina on FFA examination, and the walls of the arteriolar and venular ducts have a large amount of leakage. If the lesion continues to intensify, the optic disc becomes congested and edematous, retinal exudative detachment occurs, and vision is completely lost.
Diagnosis
Clinical diagnosis of AIDS can be made on the basis of history, at-risk groups, systemic multisystemic symptoms and signs, recurrent, multiple or one conditionally pathogenic microbial infections, and rare cases of Kaposi’s sarcoma and Pneumocystis carinii pneumonia.
Treatment
There is no effective treatment, and the emphasis is on prevention.
Acquired immunodeficiency syndrome (AIDS) cytomegalovirus infection causing giant cell retinitis can be treated with propoxyguanosine added to saline in a slow intravenous drip for several months or even years. In the acute stage, intravitreal injection of propoxyguanosine can also be used. It can prolong the patient’s life and relieve retinal inflammation.