Optimizing Pain Management in Cardiac Surgery: A Review of Analgesic Adjuvants.

PURPOSE OF REVIEW: Pain management following cardiac surgery is a critical component in optimizing both short- and long-term patient outcomes, with poor pain management associated with significant acute and chronic opioid use, opioid dependence and a significant rate of opioid related adverse drug events. The significant burden of both acute and chronic pain following cardiac surgery has given rise to the need for multimodel analgesic strategies, to optimize outcomes and minimize side effects. RECENT FINDINGS: While significant research has focused recently on the additive value of peripheral nerve blocks, less emphasis has been given to the value of non-opioid based analgesics in preference to traditional opioid based anesthetic and analgesic strategies. In this review, we examine the evidence for several common analgesics, highlighting the evidence supporting efficacy following cardiac surgery, as well as the safety concerns with each agent. We demonstrate the value of a multimodal analgesic strategy to reduce pain scores and improve patient-centered outcomes, and highlight the need for further studies of combination analgesic strategies.

Neurovascular toxicity of N-methyl-d-aspartate is markedly enhanced in the developing mouse central nervous system.

Penumbral perfusion is critical to brain viability. Proximal arterial occlusion and deep brain stroke has variable effect on cortical dysfunction. Cortical microvessel collaterals may be recruited and at times sufficient for partial parenchymal perfusion. Postnatal neural and endothelial cells are markedly vulnerable to glutamate excitotoxicity. Early vascular cell stress may promote partial protective neural preconditioning though postnatally a developmental window of the cerebral microvasculature may be particularly vulnerable to injury. We tested the hypothesis that postnatal NMDA excitotoxic injury, when cerebral endothelial cells' central energy source is via glycolysis, is age specific. Neurovascular responses of cortical viability were directly identified with diffuse reflectance patterns of perfusion properties in a non-invasive manner, over time. Histological evaluation for neural and vascular cytoarchitectonic abnormalities were evaluated 4- 7days post injury. Optical diffuse reflectance recordings were obtained at the injection site prior to, immediately after and 48h post injury. Extent of neurovascular injury at the infarct zone was greatest at PND 5 and cortical perfusion responses identified with recordings of pattern change. These data further suggest excitotoxic injury to both neural and vascular cells, in vivo, can enhance CNS injury in the young and neuroprotective strategies may benefit from vascular directed therapies.