Minerva anestesiologica
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Minerva anestesiologica · Feb 2021
Randomized Controlled TrialThe aerosol box for tracheal intubation by a junior operator in patients with COVID-19.
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Minerva anestesiologica · Feb 2021
Chronic cancer and non cancer pain and opioid-induced hyperalgesia share common mechanisms: neuroinflammation and central sensitization.
Neuroinflammation, a peculiar form of inflammation that occurs in response to noxious stimuli in peripheral and central nervous system (CNS), consists in altered vascular permeability followed by leukocyte recruitment and activation in the inflamed tissue, release of inflammatory mediators including cytokines and chemokines, and finally in the activation of microglia and astrocytes in the spinal cord and CNS. This phenomenon mediates and even worsen the inflammatory pain in many painful states and is responsible for central sensitization leading to pain chronicity. We describe the major neuroinflammatory mechanisms shared by cancer and non-cancer pain. ⋯ We also hypothesize that one type of cancer pain, the breakthrough pain, can be attributable to receptor-mediated interaction of opioids with tumor cells and intratumoral leukocytes. Surprisingly, long-term opioid treatment shares the same neuroinflammatory potential responsible for the chronicity of both cancer and non-cancer pain; thus, resulting in paradoxical worsening rather than relieving pain. This paradox has upset the world of pain therapy, with neuroinflammation now being a main target of emerging therapies.