British journal of anaesthesia
-
Off-label use of medications in paediatric anaesthesia is common practice, owing to the relative paucity of evidence-based dosing regimens in children. Well-performed dose-finding studies, especially in infants, are rare and urgently needed. ⋯ We discuss the problems of off-label medication use and the lack of evidence for various definitions of hypotension and associated treatment strategies in paediatric anaesthesia. What is the aim of treating hypotension associated with anaesthesia induction: restoring the MAP to awake baseline values or elevating it above a provisional hypotension threshold?
-
Editorial Comment
Diagnosing nociplastic pain in cancer survivors: a major step forward.
Nociplastic pain syndromes include particular fibromyalgia, irritable bowel syndrome, headache, complex regional pain syndrome, and idiopathic orofacial pain. Several mechanisms have been proposed to account for nociplastic pain including central sensitisation, alterations of pain modulatory controls, epigenetic changes, and peripheral mechanisms. Importantly, nociplastic pain might also be present in patients with cancer pain, particularly those with pain related to complications of cancer treatment. Increased awareness of nociplastic pain associated with cancer should have important implications for monitoring and managing such patients.
-
Sepsis-associated encephalopathy is characterised by cognitive dysfunction, and might be mediated by deficits in neurotransmission. Reduced cholinergic neurotransmission in the hippocampus impairs memory function. We assessed real-time alterations of acetylcholine neurotransmission from the medial septal nucleus to the hippocampus, and explored whether sepsis-induced cognitive deficits can be relieved by activating upstream cholinergic projections. ⋯ Systemic or local LPS reduced cholinergic neurotransmission from the medial septum to hippocampal pyramidal neurones, and their selective activation alleviated defects in hippocampal neuronal function and synaptic plasticity and ameliorated memory deficits in sepsis model mice through enhanced cholinergic neurotransmission. This provides a basis for targeting cholinergic signalling to the hippocampus in sepsis-induced encephalopathy.