Minerva anestesiologica
-
Minerva anestesiologica · Jun 2010
ReviewBiomarkers of acute kidney injury in anesthesia, intensive care and major surgery: from the bench to clinical research to clinical practice.
Acute kidney injury (AKI) is common after major surgery and reportedly occurs in approximately 36% of ICU patients (RIFLE Risk/Injury/ Failure categories). It is associated with increased mortality, greater cost, and prolonged Intensive Care Unit (ICU) and hospital stay, despite attempts to develop therapies to prevent or attenuate AKI, which have had limited success. One major reason for this lack of success may be the result of delayed implementation due to the inability to detect AKI early. ⋯ They can be used to evaluate the effect of new techniques and therapies on kidney function, as safety markers to monitor toxicity and as measures of treatment effect. For example, NGAL and cystatin C have been used in a safety monitoring trial of hydroxyethylstarch therapy and to detect AKI early, during or immediately after cardiac surgery. Clinical use beyond research settings is rapidly expanding.
-
Minerva anestesiologica · Jun 2010
Risk factors for inadequate emergence after anesthesia: emergence delirium and hypoactive emergence.
Inadequate emergence after anesthesia in the adult patient may be distinguished by the patients' activity level into two subtypes: emergence delirium and hypoactive emergence. The aim of this study was to determine the incidence of inadequate emergence in its different forms, to identify causative factors and to examine the possible influence on postoperative length of stay in the recovery room and in the hospital. ⋯ Inadequate emergence after anesthesia is a frequent complication. Preventable risk factors for emergence delirium were induction of anesthesia with etomidate, premedication with benzodiazepines and higher postoperative pain scores. Hypoactive emergence was less frequent than emergence delirium and was associated with a longer postoperative hospital stay.
-
Minerva anestesiologica · Jun 2010
Nitrous oxide discretely up-regulates nNOS and p53 in neonatal rat brain.
Animal studies suggest that neuronal cell death often results from anesthetic administration during synaptogenesis. Volatile anesthetics are strongly involved in triggering neuronal apoptosis, whereas other inhalational agents (xenon) demonstrate protective effects. Nitrous oxide (N2O) has modest pro-apoptotic effects on its own and potent, synergistic toxic effects when combined with volatile agents. Recent findings suggest that, during periods of rapid brain development, the enhanced neurodegeneration triggered by anesthetic drugs may be caused by a compensatory increase in intracellular free calcium, a potent activator of neuronal nitric oxide synthase (nNOS). Anesthesia-induced neuro-apoptosis is also activated via the intrinsic and the extrinsic apoptotic pathways because both pathways involve p53, a key regulatory gene. The molecular events related to neuronal cell apoptosis are not completely understood. To gain further insight into the events underlying neuro-apoptosis, we analyzed the transcriptional consequences of N2O exposure on nNOS, iNOS and p53 mRNA levels. ⋯ Our preliminary data show that N2O induced a selective increase in nNOS and p53 transcription. These new findings provide evidence of pro-apoptotic action by N2O and may shed new insight on its toxic effects; however, further investigations are necessary.
-
Minerva anestesiologica · May 2010
Randomized Controlled TrialTime course of endogenous nitric oxide inhibitors in severe sepsis in humans.
Asymmetric and symmetric dimethylarginines (ADMA and SDMA, respectively) are protein breakdown markers; both compete with arginine for cellular transport and both are excreted in urine. Moreover, ADMA is a non-selective inhibitor of nitric oxide (NO) synthase that is metabolized by a specific hydrolase in which the activity during stress remains controversial. While an increase in ADMA is known to be associated with adverse events, little is known about SDMA. We investigated plasma ADMA and SDMA levels during ICU stay to reveal the time course of endogenous NO inhibition in patients with sepsis. ⋯ ADMA catabolism appears to be activated by inflammation; its increase during the advanced septic phase in surviving patients may suggest an endogenous inhibition of NO synthesis during the full-blown septic phase. In severe sepsis, SDMA, but not ADMA, appears to be a marker of alterations in vital functions and mortality.