Noninvasive intracranial pressure monitoring for HIV-associated cryptococcal meningitis

Mortality and adverse neurologic sequelae from HIV-associated cryptococcal meningitis (HIV-CM) remains high due to raised intracranial pressure (ICP) complications. Cerebrospinal fluid (CSF) high opening pressure occurs in more than 50% of HIV-CM patients. Repeated lumbar puncture with CSF drainage and external lumbar drainage might be required in the management of these patients. Usually, there is a high grade of uncertainty and the basis for clinical decisions regarding ICP hypertension tends to be from clinical findings (headache, nausea and vomiting), a low Glasgow coma scale score, and/or fundoscopic papilledema. Significant neurological decline can occur if elevated CSF pressures are inadequately managed. Various treatment strategies to address intracranial hypertension in this setting have been described, including: medical management, serial lumbar punctures, external lumbar and ventricular drain placement, and either ventricular or lumbar shunting. This study aims to evaluate the role of a non-invasive intracranial pressure (ICP-NI) monitoring in a critically ill HIV-CM patient.

Late emergence of A594V and L595W mutations related to ganciclovir resistance in a patient with HCMV retinitis and long-term HIV progression

The emergence of ganciclovir (GCV) resistance during the treatment of human cytomegalovirus (HCMV) infection is a serious clinical challenge, and is associated with high morbidity and mortality. In this case report, we describe the emergence of two consecutive mutations (A594V and L595W) related to GCV resistance in a patient with HCMV retinitis and long-term HIV progression after approximately 240 days of GCV use. Following the diagnosis of retinitis, the introduction of GCV did not result in viral load reduction. The detected mutations appeared late in the treatment, and we propose that other factors (high initial HCMV load, previous GCV exposure, low CD4+ cell count), in addition to the presence of resistance mutations, may have contributed to the treatment failure of HCMV infection in this patient.