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Abstract

AIDS-related cryptococcal meningitis can result in significant vision loss, but the risk factors, prognostic features, and optimal management of patients with ocular complications is unknown. We present 2 cases of blindness associated with cryptococcal meningitis and review the literature for associated cases. Twenty-six additional cases of vision deterioration or loss as a result of HIV-associated cryptococcal meningitis were reviewed. Irreversible and complete loss of vision occurred in 14 patients (50%). Permanent vision loss was more likely to occur in patients with ocular symptoms and neurologic signs at presentation. Nearly all patients with permanent visual loss experienced blindness within the first week after hospital admission. Visual complications are not uncommon in cryptococcal meningitis, and once vision loss occurs, it is often irreversible regardless of control of infection or intracranial pressure. Visual complaints in cryptococcal meningitis should be considered a potentially poor prognostic sign.

Keywords

cryptococcus meningitis visual loss blindness

Cryptococcus neoformans is an encapsulated basidiomycetic yeast commonly found in pigeon excreta and rotten wood.¹ Prior to 1981, cryptococcal meningitis was a rare disease with fewer than 500 cases per year in the United States.² It is now the most common central nervous system fungal infection in patients with AIDS and the major etiologic agent of chronic meningitis in this population.³ Infection with C neoformansbegins after inhalation, with hematogenous dissemination following infection in the respiratory tract. For reasons that are unclear, cryptococcus has a propensity to seed the central nervous system during hematogenous dissemination and can result in a severe, chronic form of meningitis.⁴ Occasionally, the resulting meningitis is further complicated by visual loss and even permanent blindness. In undeveloped areas, loss of visual acuity is a relatively common occurrence and is seen in up to 10% of patients with AIDS and cryptococcus infection, often associated with other comorbidities, such as cytomegalovirus (CMV) retinitis.⁵ In contrast, loss of visual acuity is a less common occurrence in developed countries. For example, visual loss was not observed in any patients in a retrospective review of cryptococcal meningitis in San Francisco, California, in the pre–highly active antiretroviral therapy (HAART) era.⁴

The etiology of visual complications associated with cryptococcal meningitis remains unclear. Possible explanations for visual loss with C neoformans meningitis include direct infiltration of the optic nerve or optic tracts by the fungus, inflammatory compression of the optic nerve, adhesive arachnoiditis, amphotericin B toxicity, cerebral vasculitis, and intracranial hypertension among other things.^6
–8 Elevated cerebrospinal fluid (CSF) pressure has long been considered the major risk factor and etiologic agent associated with blindness, and the majority of the medical literature stresses decreasing intracranial pressure (ICP) to both prevent and reverse visual loss. Recently, we encountered 2 patients with cryptococcal meningitis in which the role of ICP as the etiologic agent for blindness was unclear. We present these 2 cases of HIV-positive patients with permanent visual loss complicating cryptococcal meningitis and review the English-language literature with regard to risk factors, presentation, comorbidities, and treatment modalities for this unusual and devastating complication.

Methods

Case reports of C neoformans meningitis in the English-language literature were identified through a computer-generated search with subsequent review of noted references. The search was conducted using the databases PubMed and ScienceDirect with the search criteria “ocular complications [AND] cryptococcal meningitis,” and also “ocular complications [AND] cryptococcal meningitis [AND] HIV” in order to find specific cases of cryptococcal meningitis in HIV-infected patients. A similar search was also performed with the search criteria “blindness [AND] cryptococcal meningitis [AND] HIV,” “vision loss [AND] cryptococcal meningitis [AND] HIV,” and “ophthalmic manifestations [AND] cryptococcal meningitis [AND] HIV.” Once articles were gathered through these search engines, case reports fitting the case definition were isolated and references in all pertinent publications were reviewed for additional cases related to the study.

A case was defined as one in which an adult patient (age ≥18 years old) was identified by the author as HIV positive with confirmed cryptococcal meningitis and ocular manifestations. For the purposes of this review, cryptococcal meningitis was confirmed through either the report of cryptococcal antigen in the CSF or a positive CSF culture. Ocular manifestation was considered relevant if the patient presented with an ocular complaint or an ocular complaint developed after presentation for medical care. Active ocular complications attributable to other etiologies such as CMV infection or central retinal necrosis were not included in the analysis. Cases with visual acuity defined by the authors as no light perception, visual loss, or loss of vision with perception of hand motion only without recovery of vision were defined as permanent blindness. Cases with visual loss (either partial or complete) in which vision returned to normal or near normal were defined as temporary vision loss. Cases were included for analysis if enough demographic information was available to allow identification of individual patients. Two cases observed in our institution where blindness resulted as a complication of cryptococcal meningitis in patients are also included in the analysis and review of the literature.

Case 1

A 39-year-old African American man with AIDS and a history of hypertension and hospitalization 2 weeks earlier for Pneumocystis carinii pneumonia (PCP) presented to the emergency room (ER), complaining of recent onset of headache, dizziness, and syncope. There were no visual complaints at that time. Upon examination he was noted to be awake and alert with no neck stiffness and no focal neurologic deficits or visual loss. Routine blood cultures taken during the recent hospitalization for PCP at an outlying hospital were reported as growing yeast, and a cryptococcal infection was suspected. Lumbar puncture was performed in the ER which revealed an opening pressure of 55 cm/H₂O, protein of 28 mg/dL, glucose of 51 mg/dL, and a white blood cell count of 8 cells/mm³. Cerebrospinal fluid and serum cryptococcal antigen titers were both 1:1024, and CSF cultures grew C neoformans, which was also the yeast identified later from the blood cultures.

The patient was treated with intravenous (IV) amphotericin b and flucytosine beginning on the day of admission. On hospital day 2, the patient had several episodes of sudden, complete loss of vision bilaterally attributed to increased ICP. An ophthalmology consult was obtained, which revealed significant bilateral disc edema with pale, tight optic cups, and tortuous vascularity. There was no vitritis or chorioretinitis seen on examination. Emergent drainage of CSF to decrease ICP resulted in the immediate return of vision. Lumbar punctures to decrease the ICP were performed every 48 hours over the next week with opening pressures always exceeding 55 cm/H₂O and reaching over 70 cm/H₂O on hospital day 6. Vision improved to baseline after each lumbar puncture with transient blurring of vision without complete visual loss occurring prior to each lumbar puncture. A brain computerized tomography (CT) on hospital day 3 was normal, showing no signs of hydrocephalus, but a magnetic resonance imaging (MRI) without contrast on hospital day 9 showed some evidence of optic nerve edema or neuritis. In an effort to relieve symptoms of chronically elevated ICP, an external ventricular drain was placed, which resulted in resolution of symptoms with continued drainage of CSF and return of blurred vision without complete visual loss when the shunt was clamped.

The patient was discharged on hospital day 17 on oral fluconazole 400 mg daily after completing over 2 weeks of IV amphotericin b and flucytosine treatment. A right frontal ventriculoperitoneal shunt placement surgery was performed 2 days after discharge with no complications.

Following discharge and placement of the ventriculoperitoneal (VP) shunt, there was initial relief of symptoms and return of vision to baseline, but over the next 2 months the patient underwent multiple shunt revisions due to recurrent, intermittent decreased visual acuity and blurry vision. The visual changes did not correlate with increases or decreases in measured ICPs. Due to decreasing visual acuity over this time, and lack of response to VP shunt adjustments, the patient underwent a right eye optic nerve sheath fenestration, and a month later underwent the same procedure on the left eye.

Approximately 2 weeks after the left eye optic nerve sheath fenestration, the patient again experienced blurred vision and significant vision loss within a 48-hour period. A brain CT at this time was unremarkable and shunt pressures were within normal limits. Six weeks after the left eye optic nerve fenestration, the patient lost vision bilaterally without elevations in CSF pressures, and vision loss at that time was complete and irreversible. He has had a full immunologic and virologic recovery on antiretroviral therapy at this point and is otherwise well except for the permanent vision loss.

Case 2

A 39-year-old African American female with a history of hypertension, AIDS, and medication nonadherence presented to the ER department complaining of headache, neck pain, and altered mental status developing over a period of 3 days. She did not report any changes in vision. Upon examination, she was febrile to 104.2°F (rectal) with generalized weakness, altered mental status, and thrush. A serum cryptococcal antigen titer of 1:256 was obtained in the ER and a diagnostic lumbar puncture was then performed with an opening pressure of 60 cm/H₂O, protein of 115 mg/dL, glucose of 12 mg/dL, and a white blood cell count of 1344 cells/mm³. The CSF cryptococcal antigen titer was 1:512 and C neoformans subsequently grew out of the CSF cultures. The patient received IV amphotericin b and flucytosine on admission and after the lumbar puncture she experienced improvement in mental status.

On hospital day 2, the patient complained of sudden complete loss of vision bilaterally. An ophthalmology consult was obtained which revealed retinol microvasculopathy without chorioretinitis or papilledema and consistent with retrobulbar pathology of the optic nerve, brain, and optic tract. Both MRI and CT scan were unremarkable and a repeat lumbar puncture opening pressure was only 10 cm/H₂O. The patient was given acetazolamide without improvement in vision, but became progressively acidotic with altered mental status and was intubated due to respiratory failure on hospital day 6. An MRI performed on hospital day 8 revealed scattered parenchymal ischemic lesions without abscesses, masses, or evidence of increased ICP. The patient recovered consciousness and was extubated but developed right-sided hemiparesis with continued bilateral visual loss. The retinal examination showed retinal microvasculopathy consistent with cryptococcal infection without chorioretinitis or papilledema. After completing 2 weeks of IV amphotericin B and flucytosine, she was switched to oral fluconazole 400 mg daily. She was discharged on hospital day 30 to an extended-care facility in stable condition with right-sided hemiparesis and complete visual loss. She experienced respiratory arrest in the extended care facility and died acutely 4 days postdischarge.

Results

Demographics and Past Medical History

A total of 28 cases of ocular complications of HIV-associated cryptococcal meningitis were compiled for this study,^{6,7,9

–23} including 26 obtained from a review of the literature from 1985 to 2011 and 2 cases presented in this report (Table 1). Twenty of these patients (71%) had total loss of sight, which resulted in permanent blindness in 14 (50%). Of the total cases, 25 were men (89%) and 3 were women (11%). Of the 14 patients with permanent blindness, 11 were men (78%) and 3 women (22%). The average age of all patients was 35.4 years (range 20-58 years). Of the 14 patients who experienced permanent blindness, the average age was 31.3 years (range, 26-45 years). Race was indicated in 15 cases (5 caucasians, 8 African Americans, and 2 Asian). Only 3 patients with permanent blindness had a prior history of an AIDS-defining illness including 1 from the current case reports. None of the 3 had prior cryptococcal meningitis. Seven patients with temporary vision loss had a prior AIDS-defining illness, and 5 of these had prior cryptococcal meningitis.

Table 1.

Demographics and Past Medical History of Patients with Visual Loss Secondary to Cryptococcal Meningitis

Visual loss	28
Temporary vision loss	14
Permanent blindness	14
Male	25
Female	3
Average age total	35.4
Race
Caucasian	5 (2 with permanent blindness)
African American	8 (3 with permanent blindness)
Asian	2 (1 with permanent blindness)
Partial or temporary visual loss/prior or AIDS-defining illness	7 (5 with prior cryptococcal meningitis)
Permanent visual loss prior AIDS-defining illness	3 (10 with prior cryptococcal meningitis)

Symptoms and Signs

Initial signs and symptoms at presentation are shown in Table 2. For the 14 patients with permanent blindness, signs and symptoms at presentation were available for 11. Of the 11 patients, 10 (91%) presented with headache, and 5 (45%) of 11 patients presented with visual complaints. For 6 (54%) of 11 patients, ocular or neurologic abnormalities were recorded in the initial physical examination (2 with cranial nerve palsies, 2 with papilledema, and 2 with abnormal pupil responses to light). For the 14 patients with temporary vision loss, 10 had symptoms recorded at presentation. Nine (90%) of 10 had headache, and 1 (10%) complained of acute visual loss. Only 4 patients had neurologic or ocular signs at presentation. Three were reported as within normal limits and 1 had papilledema with decreased hearing as well.

Table 2.

Signs and Symptoms of Patients at Presentation with Temporary Vision Loss Compared to Patients with Permanent Blindness

	Temporary Vision Loss, n = Number of Cases	Permanent Blindness, n = Number of Cases
Symptoms	10	11
Headache	9	10
Visual complaint	1	5
Signs
CN palsy	0	3
Papilledema	1	6
Abnormal/pup./reactions	0	3

Ocular Signs and Symptoms

The tempo of ocular symptoms from preadmission presentation to worst ocular symptoms were recorded for 12 out of 14 patients with temporary vision loss and for 11 out of 14 patients with permanent blindness. For cases with extensive information about prior HIV-related admissions without cryptococcal meningitis, the timing of ocular complaints was evaluated from information recorded about the admission in which cryptococcus was first diagnosed. For the 14 patients with temporary vision loss, the initial symptoms were recorded in 12 cases and were diplopia and/or decreased vision in 11 out of 12 cases. The first recorded ocular abnormalities in 11 out of 12 cases consisted of acute visual loss (2 cases including presenting with acute visual loss prior to admission), CN palsies (3 cases), and papilledema (4 cases), and abnormal pupil reactions to light (2 cases). The onset of ocular symptoms began prior to admission in 1 case, with late onset (>1 week after admission) in 6 cases. Five cases had onset of ocular complaints within the first week after admission. For the 14 patients with permanent blindness, 11 patients had information recorded about initial ocular complaints. Five of 11 patients had ocular complaints at the time of admission and the remaining 6 had ocular complaints within 1 week after admission. The initial ocular complaints were decreased vision (acute or subacute) or diplopia in all cases. The first recorded ocular findings were cranial nerve palsies (3 cases), papilledema or optic nerve edema (6 cases), abnormal pupil response to light (3 cases), and microvasculopathy (1 case).

The first recorded ocular complaint either at admission or during hospitalization was listed for 12 out of 14 patients with temporary vision loss, and 12 of 14 patients with permanent blindness. For 6 patients with permanent blindness, the first visual complaint was sudden catastrophic visual loss. Only in 2 patients with temporary vision loss, sudden loss of vision was the first complaint. For the majority of patients with temporary vision loss, the initial complaint was bilateral gradual visual loss (10 patients).

Diagnostics

Cryptococcus neoformans meningitis was confirmed by culture or antigen in all cases, according to the case definition. In 11 (69%) of the 16 cases where an antigen level was reported, the level was 1:1024 or greater. Cryptococcal CSF antigen was ≥1:1024 in 4 cases with permanent blindness and 7 cases with temporary vision loss. Opening pressure with lumbar puncture was documented in 18 cases (78%) with a numerical or description notation (Table 3). Of the 9 patients who experienced permanent blindness, 7 had elevated opening pressures on examination as did 7 of 9 patients with temporary vision loss. A cranial CT scan or MRI was performed in 27 cases and was without hydrocephalus in 24 out of 27 cases. Three cases had mild or “equivocal” hydrocephalus (2 cases with temporary vision loss and 1 with permanent blindness).

Table 3.

Diagnostic Studies

	Temporary Vision Loss	Permanent Blindness
CSF opening pressure	n = 9	n = 9
≤20 cm H₂O	2 (22%)	2 (22%)
>20 cm H₂O	7 (78%)	7 (78%)
CSF antigens
<1:1024	2 (22%)	3 (43%)
≥1:1024	7 (78%)	4 (57%)
CT scans	n = 14	n = 13
No hydrocephalus	12 (86%)	12 (92%)
Hydrocephalus	2 (14%)	1 (8%)

Treatment

Information about treatment was reported in all 28 cases. Twenty-seven patients received amphotericin B with or without 5-flucytosine as initial therapy. One patient who had temporary vision loss received itraconazole. Cerebrospinal fluid draining was performed via repeat lumbar puncture (LP) or shunts in 15 patients including 5 with permanent blindness. Optic nerve decompression was used in 2 cases, both of which resulted in permanent blindness.

Discussion

Cryptococcus neoformans is an encapsulated, basidiomycete yeast that has become more prevalent as an opportunistic infection since the advent of human immunodeficiency virus. Although commonly associated with neurological complications and intracranial hypertension, the ocular complications of cryptococcal meningitis in patients with HIV are relatively uncommon. In a review of cryptococcal meningitis in the pre-HAART era in the United States, there were no reported cases of visual loss.⁴ In a review of cryptococcal meningitis in Rwanda in the pre-HAART era, papilledema occurred in 32.5% of patients, and bilateral visual loss occurred in 5% of patients (4 patients total), most of whom had other concurrent opportunistic infections such as CMV retinitis.²⁴ In a review of AIDS associated ocular findings in a group of over 1000 patients enrolled in the Multicenter AIDS cohort study (MACS) study, ocular findings associated with cryptococcal infection were rare, consisting of cryptococcal choroiditis in 2 patients.²⁵ Visual loss has been reported in non–HIV-associated meningitis and may actually occur at a higher frequency. In a 12-year review of cryptococcal meningitis in Australia from 1968 to 1980, 10% of patients developed permanent blindness due to chronic increased ICP.²⁶

Two patterns of visual loss appear to occur in HIV-infected patients—rapid onset of visual loss and gradual visual deterioration. Traditionally, the rapid onset of vision loss (<3 days) and the vision loss after an extended period of time (>3 days) have been thought to have different etiologic mechanisms. The first is thought to result from direct infiltration of the optic nerves or adhesive or inflammatory arachnoiditis,^7,9 while the second occurs from uncontrollable long-term intracranial hypertension.¹⁹

In case 2 of this report, the patient lost her eyesight within 5 days of her initial symptoms. Although this is slightly longer than the previously defined rapid onset of vision loss, the relatively normal ICP observed in this patient suggests that the mechanism for vision loss may have been direct infiltration of the optic nerve or damage to the pathway. Optic nerve infiltration by cryptococcus without elevated ICP or papilledema has been reported but only evaluated by autopsy in 1 case.⁷ Additionally, direct infection of the optic nerve with cryptococcus can result in rapidly progressing optic neuropathy and permanent damage to the optic nerve.^12,15

Vision loss over an extended period of ≥4 weeks has often been attributed to long-term intracranial hypertension.^{9,12,18,21,23} No patients in this review who had permanent blindness had a prolonged course of visual complaints. In addition, patients who eventually developed permanent visual loss did not appear to be more debilitated or chronically ill than those with temporary decreases in vision but presented more acutely. Additional comorbidities such as opportunistic infections including prior cryptococcal meningitis did not appear to be a major factor associated with permanent blindness. However, the patients with permanent blindness presented with more visual complaints and more objective evidence of neurologic involvement than those with only temporary vision loss. The majority of patients in this report had elevated ICP, which has been linked to a poor prognosis in HIV patients with cryptococcal meningitis even in the absence of vision loss.^12,27,28 Case 1 of this report reflects a case of late-onset vision loss, and intermittently elevated ICP postinfection The irreversible optic nerve damage associated with prolonged ICP was the most probable cause of eventual blindness.

Subacute vision loss has also been attributed to arachnoiditis.²⁸ While traditional arachnoiditis brought on by an inflammatory response is uncommon in immunodeficient patients, polysaccharide sheaths discarded by cryptococcal proteins or cryptococcal fungi can infiltrate and clog the arachnoid villi, preventing CSF reabsorption.⁹ Possible outcomes of this arachnoiditis are cranial or optic nerve compression, elevated ICP, and an increased risk of optic nerve infiltration by the fungi, all of which can cause visual loss in the short or long term.¹²

The ocular complications reported in this article were relatively uncommon but were not reversed in all cases even with early detection of infection or aggressive treatment. In the majority of cases seen in this report, CT and MR scans were normal or rarely showed nonspecific signs of very mild hydrocephalus despite the documented presence of elevated CSF pressure. It has been previously noted that CT scans may not be the most effective diagnostic tools for intracranial hypertension as a result of cryptococcal meningitis.²⁹ In patients that show signs of elevated ICP, such as cranial nerve palsies, papilledema, or altered mental status, lumbar puncture should be performed emergently and the opening pressure measured.³⁰ Lumbar puncture is also the most useful diagnostic tool for determining whether further invasive measures to lower ICP should be undertaken. Although papilledema might be an expected indicator of ocular involvement or intracranial hypertension, a significant number of cases showed no signs of papilledema on fundoscopic examination despite relatively long-standing increased ICP. The MRI of the optic nerves can be a useful indicator of optic nerve infiltration, however, and compression of the optic nerve without other signs of hydrocephalus can be observed in some cases.¹⁵ While this article focused on cryptococcal meningitis and intraocular complications that lead to vision loss (temporary and permanent), other ocular etiologies of vision loss include endophthalmitis and retinal and vitreal inflammation. Similar to the patients in this case series, the majority of patients did not have significant underlying complications or a history of cryptococcal infections. Additionally, vision loss was often permanent as well.³¹

Vision loss can be a presenting feature or complication of cryptococcal meningitis. In cases where visual loss is permanent, patients tend to have the vision loss as the initial complaint associated with other neurologic complications early in presentation without additional or prior comorbidities. Multiple treatment strategies have been tried to reverse visual loss when it occurs, but this symptom is a poor prognostic sign. Finally, cryptococcal meningitis should be considered as a potential cause of acute or subacute vision loss in patients known to have HIV.

Footnotes

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

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Ocular Complications of Cryptococcal Meningitis in Patients with HIV

Abstract

Keywords

Methods

Case 1

Case 2

Results

Demographics and Past Medical History

Symptoms and Signs

Ocular Signs and Symptoms

Diagnostics

Treatment

Discussion

Footnotes

Declaration of Conflicting Interests

Funding

References