PubMed · 5757547
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A Seoane de Lucas. 1968. [Anesthesia in hyperthyroid goiter].. https://pubmed.ncbi.nlm.nih.gov/5757547/
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BACKGROUND: Children generally lie still enough for magnetic resonance imaging (MRI) only if they are asleep, either under sedation, which is deeper than conscious sedation, or under anaesthesia. Anaesthesia resources, however, are limited, and non-anaesthetists must use sedation frequently. Demand for MRI has increased and the failure of our sedation regimen led to an impractical demand for anaesthesia and unacceptable waiting times for scanning. We have therefore developed a nurse-led sedation service in a designated unit next to the scanner. This study assessed the safety and efficacy of this approach. METHODS: Children who required MRI were sedated in the unit by designated sedationist nurses, who used an oral drug regimen (according to weight and age from conception: weight <5 kg, 50 mg/kg chloral hydrate; 5-10 kg, 100 mg/kg chloral hydrate; 10-20 kg, 1 mg/kg temazepam plus 0.25 mg/kg droperidol; >20 kg temazepam and droperidol as directed by radiologist, maximum doses 20 mg and 5 mg respectively). Nurses checked patients for their suitability, charted and administered the drugs according to a protocol, and monitored the children throughout the sedation. We prospectively audited failure and complications of sedation. FINDINGS: During the 30 month study, there were 1155 sedations. 61 (5%) were unsuccessful, and there were no adverse events relating to the airway or breathing. After scanning had finished all children, in response to gently pinching the nose, could open their mouths to maintain their airway. INTERPRETATION: This study suggests that it is possible to have a nurse-led sedation service for MRI of children that is both successful and safe.
1. Experiments were performed on anaesthetized cats to investigate the receptive properties of regenerated cutaneous tibial nerve nociceptors, and to obtain evidence for coupling between them and other afferent fibres as being possible peripheral mechanisms involved in neuropathic pain. These properties were studied 6-7 months after nerve section and repair. 2. Recordings were made from 25 regenerated nociceptors; 14 were A fibres and the remainder were C fibres. Their receptive field sizes and conduction velocities were similar to controls. There was no significant difference between their mechanical thresholds and those of a control population of nociceptors. 3. Regenerated nociceptors were significantly more responsive to suprathreshold mechanical stimuli than were uninjured control fibres. This increase in mechanical sensitivity occurred in both A and C fibres, although A fibres showed a greater increase in mechano-sensitivity than C fibres. Over half of the regenerated nociceptors (13/25) showed after-discharge to mechanical stimuli which was never seen in controls; the mean firing rate during this period of after-discharge was significantly related to both stimulus intensity and stimulus area. 4. There was no significant difference between the heat encoding properties of regenerated nociceptors and control nociceptors. Cold sensitivity was similarly unchanged. Thus, abnormal peripheral sprouting was unlikely to account for the increased mechanical sensitivity of the regenerated fibres. None of the regenerated nociceptors were found to be coupled to other fibres. 5. These results suggest that the clinical observation of mechanical hyperalgesia in patients after nerve injury may have a peripheral basis. Based on this model, other signs of neuropathic pain (i.e. tactile or thermal allodynia) are more likely to be due to altered central processing.
1. This study describes a novel vagal respiratory reflex in anaesthetized rabbits. In contrast to the well-known inspiratory (I) off-switching by vagal afferent excitation, this vagal reflex initiates and maintains the central I activity of phrenic nerve discharges in rabbits pre-treated with antagonists of N-methyl-D-aspartate-type excitatory amino acid receptors (NMDA-Rs). 2. Under NMDA-R blockade with either dizocilpine (0.025-0.3 mg kg-1), D-2-amino-5-phosphonopentanoic acid (AP5, 0.5-1 mg, i.c.v.) or ketamine (10 mg kg-1), vagal stimulation at low frequencies (5-40 Hz) during the I phase prevented or markedly delayed the spontaneous I termination. In contrast, stimulation of the same vagal afferent at the same intensity but at a higher frequency (100-160 Hz) during the I phase immediately terminated the I phase. 3. In non-vagotomized rabbits, maintaining the tidal volume at end-expiratory levels during the I phase prevented spontaneous I termination and maintained apneusis after NMDA-R blockade with dizocilpine. 4. Brief stimulation of vagal afferents at low frequency (5-40 Hz) during the expiratory (E) phase constantly initiated phrenic I discharge after NMDA-R block. 5. We conclude that low-frequency discharge of vagal pulmonary stretch receptor afferents, as when lung volume is near functional residual capacity, promotes central I activity under NMDA-R blockade.