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Year : 2002  |  Volume : 50  |  Issue : 2  |  Page : 83-96

Current approaches to diagnosis and management of ocular lesions in human immunodeficiency virus positive patients

Medical and Vision Research Foundations, Sankara Nethralaya, 18, College Road, Chennai-600 006, India

Correspondence Address:
J Biswas
Medical and Vision Research Foundations, Sankara Nethralaya, 18, College Road, Chennai-600 006
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Source of Support: None, Conflict of Interest: None

PMID: 12194584

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Human immunovirus infection in India is rapidly increasing. Ocular lesions due to highly active antiretroviral therapy have been well recognized. Acquired immunodeficiency syndrome can affect all parts of the eye. However, posterior segment lesions are the most common and of these, Human immunodeficiency virus retinopathy and cytomegalovirus retinitis predominate. Often clinical examination can establish the diagnosis of many ocular lesions in acquired immunodeficiency syndrome; therefore, ophthalmologists need to be aware of the more common ones. Various drugs in different routes can used to treat cytomegalovirus retinitis. Highly active antiretroviral therapy has remarkably reduced systemic and ocular morbidity among acquired immunodeficiency syndrome patients. To facilitate care of these patients aseptic precautions for ophthalmic care personnel are now well established and therefore ophthalmologist should not hesitate to provide ophthalmic care to acquired immunodeficiency syndrome patients.

Keywords: Human immunodeficiency virus, acquired immunodeficiency syndrome, ocular lesions, cytomegalovirus retinitis, highly active antiretroviral therapy, prophylaxis

How to cite this article:
Biswas J, Fogla R, Gopal L, Narayana KM, Banker AS, Kumarasamy N, Madhavan HN. Current approaches to diagnosis and management of ocular lesions in human immunodeficiency virus positive patients. Indian J Ophthalmol 2002;50:83-96

How to cite this URL:
Biswas J, Fogla R, Gopal L, Narayana KM, Banker AS, Kumarasamy N, Madhavan HN. Current approaches to diagnosis and management of ocular lesions in human immunodeficiency virus positive patients. Indian J Ophthalmol [serial online] 2002 [cited 2020 Oct 31];50:83-96. Available from: https://www.ijo.in/text.asp?2002/50/2/83/14793

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Acquired Immunodeficiency Syndrome (AIDS) was first described in 1981,[1] and three years later, the causative virus currently known as Human Immunodeficiency Virus (HIV) was identified.[2],[3] Since then, AIDS has become a global pandemic affecting more than 36.1 million people worldwide and causing enormous human, social and economic burden.[4] In India until, May 2001, a total of 22,912 cases had been reported to the National AIDS Control Organisation. Experts estimated that about 3.86 million people were affected by the end of the year 2000.[5] The Centers for Disease Control (CDC) in 1993 revised its classification of HIV infection and expanded the AIDS survelliance definition to include those individuals with severe immunosuppresion (defined as CD4+, T- lymphocyte count of less than 200 cells/μl)[6] [Table - 1] and [Table - 2]. Since the first description of ocular lesions in 1983,[7] there have been several reports of ocular involvement in AIDS from different parts of the world.[8][9][10][11] We reported the first two cases of eye infection of AIDS from India in 1995.[12] Since then there have been two large series[13][14] and a case report published from different parts of India.[15]

The Human Immunodeficiency virus (HIV) belongs to the lentivirus sub-family of retroviruses. Chronic infection by this virus results in progressive damage to the immune system of the human host. Two major types of HIV, type 1 and type 2, infect humans. Type 1 is the predominant type found throughout the world and type 2 is primarily found in AIDS patients from West Africa, although it has been reported in other parts of the world.[4]

  Detecting HIV infection Top

The main objectives for HIV antibody testing are (1) screening of donated blood for safety, (2) epidemiological surveillance and (3) diagnosis in individuals. These tests include:

  1. 1. Antibody based tests

  2. 2. HIV-1 P 24 antigen testing

  3. 3. Qualitative and quantitative HIV-1 Plasma and Peripheral Blood Monocyte Culture (PBMC) test

  4. 4. Qualitative DNA PCR Test and Quantitative HIV-1 RNA Test.

  5. 5. Non-invasive tests.

The summary of the tests are given in [Table - 3].

  Ocular lesions in AIDS Top

Ocular lesions in AIDS are varied and affect almost all structures of the eye. Ocular lesions occur in 40 to 70% of AIDS patients.[16] However, autopsy has shown that as many as 95% of AIDS patients have some form of ocular lesions. Patients can have ophthalmic complaints during the early phase of the AIDS, and ophthalmic manifestation of the disease in fact helps the clinician suspect underlying HIV infection and associated opportunistic infections.

Ocular lesions associated with AIDS can be broadly categorized into four groups:

  1. 1. HIV retinopathy

  2. 2. Opportunistic infections (caused by viruses, bacteria, fungi and protozoa)

  3. 3. Neuro-ophthalmic lesions

  4. 4. Unusual neoplasms.like Kaposi's sarcoma

Ocular lesions can also be categorized by the involvement of ocular structures [Table - 4]. Common manifestations are briefly mentioned below. For detailed description of each lesion the readers are encouraged to read literature listed under the suggested readings.

  Adnexal and anterior segment lesions Top

HIV infections affecting the ocular adnexa and anterior segment have been reported to occur in 50% of cases.[17] Anterior segment lesions may often be the initial ocular presentations of acquired immune deficiency syndrome (AIDS).

Herpes zoster ophthalmicus (HZO) is caused by the varicella-zoster virus and involves the ophthalmic distribution of the trigeminal nerve. Its occurrence in a person below 50 years of age should arouse suspicion of immunosuppression. The reported incidence in HIV population is 5 - 15 %[18] Treatment consists of intravenous acyclovir (10 mg / kg body weight, three times a day for 7 days) followed by oral maintenance regimen (800 mg three to five times daily). Famciclovir can be used in dosage of 500 mg three times daily. Intravenous foscarnet should be considered in case of poor response to acyclovir or famciclovir.

Molluscum contagiosum when manifests, is more severe in HIV positive individuals.[19] Treatment options include cryotherapy, curettage, incision and excision.[20]

Lid infections such as severe blepharitis, stye and lid ulceration may also be the initial manifestation of AIDS.[21] Treatment in these cases with antibiotics along with lid hygiene needs to be continued for a duration longer than needed for normal individuals

Conjunctival squamous cell carcinoma have been associated with HIV infection and AIDS in the sub-Saharan African population.[22]

Keratoconjunctivitis sicca occurs in 10 - 20 % of HIV positive individuals.[23] Treatment is directed towards providing symptomatic relief using artificial tear substitutes and lubricating ointments.

Infectious Keratitis. Viral keratitis is more common, though fungal keratitis is not uncommon.[24] Recurrence is more common in varicella-zoster virus keratitis and herpes simplex keratitis. Treatment is similar in both conditions with oral acyclovir 400 mg five times daily or famciclovir 125 - 500 mg three times daily.

Microsporidia are obligate intracellular parasites known to cause gasteroenteritis, sinusitis, and pneumonitis in HIV infected patients. Ocular involvement manifests as a diffuse superficial punctate keratopathy associated with conjunctivitis.[25] Diagnosis is usually by characteristic staining of the intracellular organism. Treatment is usually with topical fumagillin, propamidine isethionate, and oral itraconazole or albendazole.

Anterior uveitis occurs in 70% to 80% of untreated HIV infected patients. However, it is less common than posterior or panuveitis.[26]

Ophthalmic Kaposi's sarcoma is the most common lesion involving the anterior segment of the eye.[27] However, we did not see this lesion in a large series of 100 HIV positive cases from India.[10] The lesions are purple-red to bright red, highly vascular with surrounding telangiectatic vessels. They may be macular, plaque-like or nodular. Recent reports indicate that human herpes virus 8 have been detected in Kaposi's sarcoma in patients with and without HIV infection.[28]

The rarity of Kaposi's sarcoma in AIDS patients in India could be due to the low prevalence of human herpes virus 8.

Neuro-ophthalmic complications are known to occur in 10 to 15% of HIV infected patients.[29] Non-viral infections including, toxoplasmosis and cryptococcus are common. Cryptococcal meningitis can present as papilloedema with peripapillary retinal haemorrhages,[30] optic atrophy and ophthalmoplegia.[31]

Posterior segment lesions

Posterior segment lesions involving the retina, choroid and/ or optic nerve are seen in 50% of patients with ocular involvement.[16] Some of these lesions can be vision threatening. Patients are usually asymptomatic, unless the lesions involve the posterior pole. Common ocular symptoms include floaters, flashes of light, visual field defects and dimness of vision. Posterior segment lesions are briefly described below and tabulated in [Table - 4].

HIV retinopathy is a noninfectious microvascular disorder characterised by cotton-wool spots, microaneurysms, retinal haemorrhages, telangiectatic vascular changes, and areas of capillary nonperfusion. Cotton-wool spots occur in approximately 25 to 50 % of patients and are the earliest and most consistent finding in HIV retinopathy. They are distributed along the vascular arcades and may mimic diabetic and hypertensive retinopathy [Figure - 1]. Cotton wool spots in HIV retinopathy disappear in 6 - 12 weeks.[32] The cotton wool spots are not vision threatening, although in advanced HIV disease they can present with corresponding small visual field defects. Haemorrhages are less common than cotton-wool spots and are estimated to occur in about 20% of patients with advanced HIV disease and in approximately 3% of patients with mildly symptomatic HIV disease. HIV-related retinal micro-angiopathy was the most common ocular lesion in patients with AIDS before the introduction of highly active antiretroviral therapy (HAART). With early treatment, the prevalence of HIV retinopathy has reduced.[33]

Cytomegalovirus (CMV) retinitis is the most common infection in HIV-positive subjects. It is seen in 15 to 40% of patients with HIV disease.[34] It usually occurs when the CD4 cell count is less than 100 cells/mm3.[35] Anti-CMV medications have reduced the incidence of bilateral infection.[36] CMV infection of the retina leads to viral invasion of retinal cells with resultant retinal necrosis. The classic description of CMV retinitis is one of scattered yellow-white areas of necrotizing retinitis with variable degree of haemorrhage and mild vitreous inflammation (cottage cheese with catsup or pizza pie retinopathy). Initially presenting as small white, granular patches, these areas continue to enlarge if left untreated. Active lesions show white retinal necrosis usually associated with haemorrhage. Often, the retinitis follows a perivascular distribution. The advancing edge of these lesions is usually very sharp and spreads contiguously. Typically, over several weeks untreated lesions progress to full-thickness necrosis with resultant retinal gliosis and pigment epithelial atrophy. The pathway of expanding lesions can be predicted by the appearance of venous sheathing or white dots distal to the leading edge, indicative of direct cell-to-cell spread of infection. Expanding lesions often take on a brushfire border, with the active edge of whitening spreading from the previously infected area. Since the peripheral retina only is involved, patients either have no subjective complaints, or may complain of floaters. If the retinitis begins in the posterior pole, the patient may notice a visual field deficit. The possible mechanisms for visual loss are direct retinal necrosis by infection, optic nerve involvement, and retinal detachment. CMV retinitis may result in either serous or rhegmatogenous retinal detachment, although the latter is much more common. Rhegmatogenous retinal detachment has been reported in 13.5 to 29% of patients with CMV retinitis and may occur during the active or healed phase of the disease.[37] These detachments are particularly difficult to repair using standard retinal detachment surgery. Other findings associated with CMV retinitis include perivasculitis, vascular attenuation, and vessel closure, as well as anterior uveitis, and papillitis.

Treatment of CMV retinitis can be systemic (intravenous or oral), local (implant or intravitreal injection) or combination of two. A brief summary of the available drugs is provided in [Table - 5].

Currently, there are six FDA-approved treatments for CMV retinitis: intravenous and oral ganciclovir (Cytovene), intravenous foscarnet (Foscavir), intravenous cidofovir (Vistide), the ganciclovir implant (Vitrasert), and fomivirsen (Vitravene ). Description of details of treatment is out of scope of this articles. Investigational agents used for treatment of viral retinitis include Valganciclovir, GN 1263 W94 - a halogenated benzamidazole, Valacyclovir and Adefovir dipivoxil.

  Surgical management of viral retinitis Top

The surgical management includes intervention for diagnostic and therapeutic purposes. Cases of atypical manifestation may need support from microbiological and molecular biologic study of the ocular tissue specimen. In such relatively rare situations, a vitreous biopsy is warranted.

Therapeutic surgical intervention is needed either for intraocular implant of slow release device or a complex vitreoretinal surgery for rhegmatogenous or combined rhegmatogenous / tractional detachment. Two distinct clinical settings are retinal detachment secondary to CMV retinitis and retinal detachment secondary to acute retinal necrosis.

Retinal detachment secondary to CMV retinitis is the most common situation in AIDS patients. The areas of necrotic retina can harbour fine holes that may not be obvious. Vitreous detachment may or may not be present. Proliferative vitreoretinopathy is not very common. The areas of retinal necrosis usually involve mid equatorial region. However, posterior pole can also be affected. Hence, the retinal breaks are likely to be multiple and can be significantly posterior. Scleral buckling alone would be difficult in a majority of cases. Pars plana vitrectomy with silicone oil tamponade may be needed in most cases.[38] Since removal of silicone oil is difficult in these patients, it is preferable to use 5000 cst oil. However, with the increasing longivity of these patients due to use of HAART treatment this may become an issue in the future.

Acute retinal necrosis (ARN) may be insidious in onset, with the initial presentation of a mild anterior uveitis accompanied by blurred vision; patients may also have severe ocular pain. The retinitis is often seen first in the peripheral fundus but within days to weeks, may progress to dramatic whitening of the peripheral retina and retinal pigment epithelium in multifocal and coalescents patches. [Figure - 2] Vasculitis involving both arteries and veins is a prominent feature, usually with associated areas of haemorrhage and vascular occlusion. With evolution of necrotizing retinitis, there may be an increase in vitreous turbidity associated with vitreous organization and development of retinal traction. Acute swelling of the optic nerve head and macular oedema are often present during the active phase of the disease. If the second eye becomes involved, the clinical course is similar.

Subsequently, retinal lesions regress with whitening, followed by mild pigmentary scarring of the retina with sharp demarcation lines between normal and affected areas. Regression begins at the outer margin of the lesions and moves centrally, sometime quite rapidly, taking only 2-3 weeks. A late sequelae is the development of vitreoretinal traction due to organization of the vitreous. This traction leads to retinal tears, and rhegmatogenous detachment. Clinical differentiation between the retinitis caused by Herpes simplex virus (HSV) and Varicella zoster virus is often not possible. However, there are indications that retinitis due to HSV-2 begins at the posterior pole. The American Uveitis Society (1994) laid down standard diagnostic criteria for ARN. Treatment of ARN includes intravenous acyclovir (1500 mg/sq, meter/day in three divided doses) for 7 to 10 days follwed by oral acyclovir (800 mg five times daily) for 6 weeks. Prophylactic laser photocoagulation is considered beneficial following resolution of retinitis.[39] Retinal detachment in ARN requires vitrectomy, intravitreal silicone oil tamponade and endolaser photocoagulation.[40]

Progressive outer retinal necrosis (PORN) is a recently recognized variant of necrotizing herpetic retinopathy representing a distinct form of ARN, developing in patients with AIDS or conditions compromising the immune status.[41] It is characterized by early macular retinitis in presence of a little or no intraocular inflammation. There is rapid progression with development of lesions in the mid and peripheral retina with no consistent direction of disease spread. Unlike ARN and typical CMV retinitis, which involve full thickness of the retina, PORN is characterized by deep retinal opacification without granular borders, giving the impression of an "outer retinitis". [Figure - 3] With progression there is clearing of areas around retinal vessels, described as a "cracked mud" appearance. These are regions of perivascular retinal sparing or represent early removal of necrotic debris and oedema from retinal tissue adjacent to the vasculature. As infected areas of retina become necrotic, large retinal breaks occur leading to rhegmatogenous retinal detachment in the majority of affected eyes, contributing to the overall poor prognosis. Diagnosis of PORN is always clinical. It closely mimics ARN and CMV retinitis. The differential features between ARN, PORN and CMV retinitis are given in the [Table - 6].

Other less common posterior segment infections are summarized in [Table - 7].

  Opportunistic infections Top

An expanding list of infections of the retina and choroid has been reported to affect individuals with advanced HIV disease. Clinical presentation in these patients is different from immunocompetent individuals. Lesions tend to be multifocal and often involve the other eye. There is a higher chance of recurrence. Finally, new, as yet undescribed infections of the retina and choroid are likely to be encountered in the setting of HIV infection in future. A strong correlation exists between the level of immunosuppression (CD4 count) and the appearance of particular opportunistic infections [Table - 8].[42]

  Management of HIV and opportunistic infections Top

A detailed account on antiretroviral therapy is beyond the scope of the current discussion.

The currently available anti-retroviral drugs disrupt the HIV life cycle by inhibiting the enzyme reverse transcriptase, thus thwarting HIV genes before they can proceed to integrate into helper T lymphocyte nucleus. There are two classes of reverse transcriptase inhibitor drugs, in addtion to protease inhibitors.

A. Nucleoside Analogue Reverse Transcriptase inhibitors (NRTIS): These are drugs that resemble nucleosides, the basic components of DNA. A nucleoside analogue therefore acts as a decoy. When this is added into the developing DNA, the entire process is disrupted. These include zidovudine, stavudine, zalcitabine and didanosine

B. Non-nucleoside reverse transcriptase inhibitors (NNRTIS): These are drugs composed of other substances; they also disrupt the function of reverse transcriptase.

Protease Inhibitors (PIs): Newly produced HIV protein in the host cell is a long molecule which is split into smaller pieces by the enzyme protease. These smaller pieces are then used in assembly of the new viruses. Inhibiting protease thwarts the formation of new copies of HIV proteins. The drugs in this group include saquinavir, ritonavir, indinavir, nelfinavir and abacavir. The list of currently available antiretroviral drugs are given in the [Table - 9].

  HAART (Highly Active Antiretroviral Therapy Top

This is an acronym for the regimen of combinations of antiretroviral drugs which make them more potent and probably reduce or postpone the occurrence of drug resistance. The advent of the HAART has brought enormous changes in AIDS treatment.[43] The drugs include either combination of 2 NRTIs and 1 NNRTIs or combination of 2NRTIs and 1 PI.

  Therapeutic Decision Making Top

Decisions regarding the initiation of antiretroviral therapy should be guided by laboratory parameters of plasma HIV RNA (viral load) and CD-4 cell count, in addition to the clinical condition of the patient. Viral load testing is essential for decisions to initiate or change antiretrovial therapy.

Recent advances in management of the HIV-infected patient in developed countries have led to an improved longevity and quality of life in these patients. However, these advances have had little impact on patients in the developing countries like India, where the vast majority of infected individuals have no access to new therapies due to high cost.[44] As estimated by UNAIDS, the impact of the AIDS epidemic in the developing world continues to increase at a rate of over 16,000 new infections per day, representing 90% of all new infections worldwide. Provision for HAART is well beyond the available health resources of much of the developing world. In India the cost of HAART ranges from Rs. 1,800 to 9,900 per month depending on the choice of combination of drugs. Therefore, the approach to the management of the HIV-infected patient in developing countries should be based on a holistic, cost-effective approach. It should take into account the number of infected people, the spectrum of HIV disease and the available resources in each country. The use of single antiretroviral drug is now almost out of practice as dual therapy is superior than monotherapy, but still resistance develops.

  Opportunistic infections due to AIDS Top

Systemic opportunistic infections in AIDS patient in India is different from the other countries. In a series of 2010 HIV positive patients treated between June 1996 and September 2000, at an AIDS care centre (YRG Centre for AIDS Research and Education, Chennai) the spectrum of opportunistic infections included oropharyngeal candidiasis (45%), pulmonary tuberculosis (37.6%), herpes zoster (14.1%), extrapulmonary tuberculosis (8.8%), dermatophyte infection (8%), herpes simplex (7.7%), Pneumocystis carinii pneumonia (5%), Cryptococcal meningitis (2.7%), Toxoplasmosis (2.5%) and Cryptosporidial diarrohea (1.5%). The other less opportunistic infections were oral hairy leukoplakia, CMV retinitis, recurrent bacterial pneumonia, extensive molluscum contagiosum, Aspergillosis, Penicilliosis and Nocardiosis. Approximately 85% of infected individuals had multiple opportunitistic infections. High plasma viral load and lower CD4 cell counts were seen in persons with multiple opportunistic infections. Multidrug resistant tuberculosis, Candidiasis resistant to antifungal drugs and unusual clinical presentation of various microorganisms were also observed.[44]

  Ocular manifestations of HIV in the era of HAART Top

The advent of potent antiretroviral has had a profound impact on the ophthalmological manifestations of AIDS patients. As these drugs lead to improved immune function, patients have fewer opportunitistic infections.[16]

Patients who had never received potent antiretroviral therapy, should be placed on a combination of agents to improve immune function. Control of CMV retinitis is relatively easier in patients with evidence of immune reconstitution (elevated CD4+ T-lymphocyte counts, lower HIV blood levels), and in many cases it is possible to discontinue specific anti-CMV therapy altogether. Immune reconstitution can take 8 weeks or longer. Thus, aggressive anti-CMV therapy may be needed during the period immediately after diagnosis. There are no well-established criteria for identifying patients with sufficient immune recovery to allow withdrawal of specific anti-CMV therapy.

An emerging problem among patients with CMV retinitis is "immune recovery uveitis". As immune function improves following the initiation of potent antiretroviral therapy, some patients develop heightened intraocular inflammatory responses, presumably to CMV antigens. Immune recovery uveitis is characterized by anterior chamber cells and vitreous haze. This is likely to lead to persistent macular oedema, epiretinal membranes, and decreased vision.[45],[46] Inflammation and macular oedema may respond to corticosteroid therapy, and possibly to nonsteroidal anti-inflammatory agents, but improvement tends to be short lasting. Recovery of normal vision is less likely in patients with macular oedema. The frequency of immune recovery uveitis ranges from 20 to 60% of patients.

  Aseptic Precautions for Health-care Personnel Top

Universal precautions is the most significant preventive measure against AIDS infection. There is no consensus on mandatory HIV screening, in all patients undergoing surgery. We suggest the following precautions in providing ophthalmic care of HIV and suspected HIV positive patients.[47]

These precautions are applicable to all health personal coming in direct contact with the patents. They include ophthalmologists, surgical assistants, nurses laboratory technicians, operating room technicians, secretaries and other staff.

Major risks include needle stick injury, cut from sharp instruments contaminated with an infected patient's blood.

Maximum risk in ophthalmic set up include blood collection in laboratory, fundus fluorescein angiography (FFA), intraocular injection, and ophthalmic surgery.

The known actual risks are needle stick 1 in 300 (0.3%), exposure of eye, nose, mouth to HIV infected blood: 1 in 1000 (0.1%) and exposure of skin to HIV infected blood: <0.1%. However, 99.7% of needle stick injury do not lead to infection. Hollow large bore needle filled with blood caries the maximum risk.[48]

  Precautions at various levels Top

A ) Reception and secretary

  • Receptionist and secretaries are advised to go through the referral letter and check whether it mentions that patient is HIV positive.

  • They should indicate in the front page of the case sheet that the patient is HIV positive and inform the optometrists, ophthalmologists and other health care personnel.

B) Optometrists and ophthalmologists

  • If the optometrists or ophthalmologists have open wound or cut, they should wear gloves.

  • They should wash hands with soap and water after examination and dry with a disposable paper towel.

  • It is advised that the next patient is examined only when the hands are dry.

  • The Schiotz or applanation tonometer tip should be cleaned with 70 % alcohol soaked sponge.

C) Ophthalmologists and anaesthesiologists

  • Necessary precautions for minor out-patient procedures like anterior chamber tap / vitreous tap and intravitreal injections.

  • Anticipate and avoid needle sick Injury

  • Supervise the disposal of the sharps to avoid risk to other staff.

  • Protective goggles for the surgeons and anaesthesiologist (in case of general anaesthesia).

  • To use hard soled shoes in operating room.

D) Laboratory technicians

  • Wear disposable gloves

  • Use disposable needles and syringes

  • Anticipate and avoid needle stick injury

  • Avoid recapping / bending disposable needle

  Recommendations during ophthalmic surgery in HIV Positive Patients. Top

  • Double gloving

  • Avoid or limit passage of needles or sharp instruments; recap the needles

  • Use blunt tipped scissors

  • Use disposable instruments, and incinerate at the end of surgery

  • Never reload the same suture needle

  • Never leave the needles dangling in surgical field

  • Handling of instruments between surgeon and nurse through neutral zone

  • All intraocular and periocular fluid should be isolated

  • Appropriate labeling (infection hazard) must be done on the specimens sent for laboratory examination

  • Sample should be placed in a sturdy container

  • All items used on patients that need to be disposed should be kept in a separate container

Waste Disposal method is summarized in [Figure - 4].

  Post Exposure Prophylaxis Top

The term 'post-exposure prophylaxis' (PEP) refers to treatment antiretroviral therapy immediately following occupational exposure to HIV. Post exposure prophylaxis if initiated immediately after the exposure is likely to prevent HIV infection.[48]

  Current guidelines for PEP: Top

  • Therapy should be recommended after exposure.

  • All regimens must include zidovudine.

  • Therapy should be initiated within 1-2 hours of exposure.

  • If the source patient's HIV status is unknown, one has to decide whether to give PEP on a case-to-case basis.

  • Follow-up counseling and HIV testing should be carried out periodically for atleast 6 months (i.e. at baseline, 6 weeks, 12 weeks and 6 months). It is estimated that 95% of health care workers seroconvert within 6 months of exposure.

  Recommended regimen of PEP: Top

There are two types of regimen for PEP- the Basic and the Expanded regimens [Table - 10] and [Figure - 5]. The appropriate regimen is selected depending on the type and severity of exposure.

In case the exposed health care worker is pregnant, the potential effect of antiretrovirals on the pregnant woman and on foetus needs consideration. There are limited data on the pharmacokinetics, safety and side-effects of antiretrovirals in pregnancy. Current data suggests that zidovudine is safe and well-tolerated when used after 14 weeks of gestation in HIV-infected women. Limited data on the use of lamivudine alone or in combination with zidovudine indicate that lamivudine is safe during pregnancy for women and infants, although long-term safety is not known.

AIDS is now more than two decades old. Systemic and ocular lesions of this disease are now well understood. The diagnosis of various ocular lesions in AIDS can now be made fairly accurately. 40 to 70% of HIV positive patients may develop ocular lesions. The ophthalmologists should be able to recognise the common ocular lesions. HIV testing should be obtained when atypical or unusual ocular lesions are seen. Highly active antiretroviral therapy can prolong the life of AIDS patients. It can also reduce the systemic and ocular morbidity. However, financial constraint in the developing country remains the main obstacle in the management of AIDS patients. Ophthalmic care of an AIDS patient is no longer dangerous as aseptic precautions are well established. Ophthalmologists can make early diagnosis and improve the quality of life of these patients.

  References Top

Pneumocystic pneumonia - Los Angeles, MMWR Mort Wkly Rep 1981;30:150-252.  Back to cited text no. 1
Barre-Sinoussi F, Chermann J-C, Rey F, Nugeyre MT, Chamant S, Gruest J et al: Isolation of a T- lymphotropic Retrovirus from a patient at risk for acquired immunodeficiency syndrome (AIDS). Science 1983;220:868-71.  Back to cited text no. 2
Gallo RC, Salahuddin SZ, Popovic M, Shearer Gm, Kaplan M, Haynes BF et al: Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk for AIDS. Science 1984;224:500-03.  Back to cited text no. 3
Fauci AS. The AIDS epidemic. New Engl J. Med. 1999;341:1046-50.  Back to cited text no. 4
National AIDS Control Organisation, Ministry of Health and family affairs, Government of India. Surveillance for HIV infection / AIDS cases in India. May 2001.  Back to cited text no. 5
Centers for Disease Control and Prevention, "1993 Revised Classification System for HIV Infection and Expanded Surveillance Definition for AIDS Among Adolescents and Adults," Morbidity and Mortality Weekly Report 1992;41:1-19.  Back to cited text no. 6
Holland GN, Pepose JS, Pettit TH, Gottlieb MS, Yee RD, Foos RY. Acquired immune deficiency syndrome, ocular manifestations. Ophthalmology 1983;90:859-73.  Back to cited text no. 7
Freeman WR, Lerner CW, Mines JA, Lash RS, Nadel AJ, Starr MB Tapper ML. A prospective study of the ophthalmologic findings in the acquired immune deficiency syndrome. Am J Ophthalmol 1984;97:133-42.  Back to cited text no. 8
Jabs DA, Green WR, Fox R, Polk BF and Bartlett JG: Ocular manifestations of acquired immune deficiency syndrome. Ophthalmology 1989;96:1092-99  Back to cited text no. 9
Biswas J, Madhavan HN, George AE, Kumarasamy N, Solomon S. Ocular lesions associated with HIV infection in India: A series of 100 consecutive patients evaluated at a referral center. Am J Ophthalmol 2000;129:9-15.  Back to cited text no. 10
Kestelyn P, Van de Penre P, Rouvroy D, Lepage P, Bugaerts J, Nizaramba D et al. A prospective study of the ophthalmic findings in the acquired immunodeficiency syndrome in Africa. Am J Ophthalmol 1985;100:230-38.  Back to cited text no. 11
Biswas J, Madhavan HN, Badrinath SS. Ocular lesions in AIDS: a report of first two cases in India. Indian J Ophthalmol 1995;43:69-72.  Back to cited text no. 12
Biswas J, Joseph AE, Raizada S, Kumarasamy N and Solomon S. Ophthalmic manifestations of acquired immunodeficiency syndrome in India. Indian J Ophthalmol 1999;47:87-93.  Back to cited text no. 13
Sahu DK, Namperumalsamy P, Walimbe P, Rajalakshmi C. Ocular manifestations of HIV infection/AIDS in South Indian patients. Indian J Ophthalmol 1999;47:79-85.  Back to cited text no. 14
Jalali S, Rao UR, Laxmi V. Acute retinal necrosis syndrome in an HIV positive case: the first case reported from India. Indian J Ophthalmol 1996;44:95-97.  Back to cited text no. 15
Cunningham ET, Margolis TP. Ocular manifestations of HIV infection. N Eng J Med 1998;339:236-44.  Back to cited text no. 16
Akduman L, Pepose JS. Anterior segment manifestations of acquired immunodeficiency syndrome. Semin Ophthalmol 1995;10:111-18.  Back to cited text no. 17
Jabs DA, Quinn TC. Acquired immunodeficiency syndrome. In: Pepose JS, Holland GN, Wilhemus KR, eds. Ocular infection & immunity. St Louis: Mosby-Year Book, 1996:289-310.  Back to cited text no. 18
Biswas J, Therese L, Kumarasamy N, Solomon S, Yesudian P. Lid abscess with extensive molluscum contagiosum in a patient with acquired immunodeficiency syndrome. Indian J Ophthalmol 1997;45:234-36.  Back to cited text no. 19
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  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5]

  [Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6], [Table - 7], [Table - 8], [Table - 9], [Table - 10]

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