RESUMO
The adverse events of antiviral drugs are dose-dependent and often reversible. The nervous system is often affected and to date, many studies have been published regarding the central nervous system toxicity of antiviral agents. They may cause significant neuropsychiatric complications, which range from mild symptoms such as irritability and difficulty sleeping to severe complications such as depression, psychosis, and painful peripheral neuropathy, side effects which may necessitate discontinuation of treatment. The pathogenetic mechanisms may involve molecular targets common to other centrally active drugs, including human monoamine oxidase-A (MAO-A), serotonin receptors, gamma-aminobutyric acid (GABA) GABA-A receptors, 5-HT2A and 5-HT2C receptors and others. Notable examples include oseltamivir which may act as MAO inhibitor and efavirenz, which has an affinity for serotonin 5-HT2 and GABA-A receptors, the serotonin transporter, the MAO enzyme, and the vesicular monoamine transporter, with subjective effects which may be similar to those of the psychedelic hallucinogen lysergic acid diethylamide (LSD). Other antiviral drugs with prominent nervous system effects include nucleoside reverse transcriptase inhibitors, which are associated with the development of peripheral neuropathy after prolonged use (an effect strongly associated with older drugs which have since fallen into disfavor such as stavudine) and interferons, which may cause depression. Clinicians should be familiar with such adverse effects in order to recognise them promptly once they occur and manage them appropriately.
RESUMO
BACKGROUND: Sepsis and multi-organ failure remain a major clinical problem with high morbidity and mortality worldwide. Lactate measurement remains part of the initial assessment and management of patients with sepsis. Although arterial blood is most commonly used for lactate measurement, there is increasing use of peripheral venous lactate for initial assessment and for monitoring of response to treatment in patients with sepsis. The aim of this study was to evaluate the relation between lactate levels measured from central line, peripheral vein and arterial line in patients treated for sepsis in the emergency department (ED). METHODS: This prospective study enrolled 31 patients with diagnosis of sepsis who were evaluated and treated in the ED of a university hospital. During initial resuscitation, blood samples from the artery, peripheral vein and central vein (when available) were collected and lactate concentrations were measured. Correlation between lactate values from the three different locations was assessed using Pearson correlation. Bland-Altman plots were used to evaluate agreement between lactate measurements in different sampling locations. All patients were eventually admitted to the Internal Medicine Department ward or to the intensive care unit (ICU) for further treatment. RESULTS: Our data showed strong, highly significant correlation between arterial and peripheral venous lactate levels (r = 0.880, P < 0.0001), between arterial and central venous blood lactate (r = 0.898, P < 0.0001) and between central and peripheral venous blood lactate (r = 0.941, P < 0.0001). CONCLUSIONS: In this study we observed strong correlation between arterial, central vein and peripheral vein lactate concentrations in 31 patients assessed and treated for sepsis. We suggest that lactate measurement in peripheral venous blood could be used for screening and for monitoring response to therapy in sepsis patients. However, because this is a small study in only 31 patients and published data are limited, larger studies are needed in order to confirm the validity of our findings.
