Complications
This condition can arise in any situation associated with a rapid change in immune status, and is thus not limited to HIV and therapy with antiretroviral therapy (ART).[27] It has been reported in 30% to 35% of HIV-positive patients receiving ART and in 5% undergoing solid-organ transplantation.[77][78] Time to onset of IRIS is usually 5 to 8 weeks after the initiation of ART, and it tends to disproportionately affect those who are antiretroviral-naive and have less cerebrospinal fluid inflammation on initial presentation.[20][79]
IRIS should be considered when worsening of the clinical status occurs despite microbiological evidence of effective antifungal therapy.[20] Although new or worsening clinical or radiographical manifestations occur, biomarkers and cultures are usually negative.
Short-term treatment with corticosteroids or anti-inflammatory agents may be considered in severe cases, but evidence-based management strategies are lacking.[1][20][55]
Use of amphotericin-B is associated with hypokalaemia, nephrotoxicity, and anaemia.[23] The World Health Organization guidelines for cryptococcal meningitis provide recommendations for preventing, monitoring, and managing toxicity, including protocols for monitoring of potassium, magnesium, creatinine, and haemoglobin.[23] They also recommend pre-hydration and electrolyte replacement prior to each amphotericin-B infusion, as this can substantially reduce toxicity.[23]
The single dose liposomal amphotericin-B and the seven-day amphotericin-B deoxycholate regimens are better tolerated than a 14-day amphotericin deoxycholate regimen, but the shorter regimens still require careful monitoring.[23]
One study found that 18% of patients receiving amphotericin-B deoxycholate for the treatment of HIV-related cryptococcal meningitis developed amphotericin-induced phlebitis.[81]
Clinicians should be aware the paradoxical development of meningeal cryptococcosis or intracranial cryptococcoma after the institution of antiretroviral therapy.[52]
May arise via direct extension or haematogenous spread. Nuchal rigidity, and Kernig and Brudzinski signs in the presence of neurological deficits are suggestive of intracranial infection.
Typical radiological finding in patients with brain abscess (on either computed tomography or magnetic resonance imaging) is that of one or more ring-enhancing lesions. Intracranial cryptococcomas appear very similar to toxoplasmosis. In people with prior cryptococcosis on effective antiretroviral therapy, paradoxical immune reconstitution inflammatory syndrome manifestations of cryptococcomas are common, whereas breakthrough unmasking of toxoplasmosis is exceedingly rare in people receiving appropriately dosed trimethoprim-sulfamethoxazole prophylaxis.[35][75]
Treatment requires aggressive antifungal therapy, support in an intensive care unit, and possible surgical evacuation.
The incidence of secondary bacterial infection due to lumbar puncture is low but not negligible, and prolonged external lumbar drainage carries the risk of bacterial infection. Ventriculoperitoneal shunts may uncommonly become secondarily infected with bacteria. If antifungal therapy has been instituted, secondary infection of the shunt with Cryptococcus neoformans generally does not occur.[55]
More than one quarter of patients with meningitis may have ocular signs or symptoms.[80]
Use of this content is subject to our disclaimer