European journal of pain : EJP
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Clinical Trial Controlled Clinical Trial
Improving the quality of postoperative pain relief.
A review of the literature shows a constant need to improve the quality of postoperative pain management. The objective of this study was to decrease the intensity and variation of postoperative pain by developing a nurse-based pain service on the ward. An acute pain nurse was appointed and an educational programme with detailed algorithms was started. ⋯ On an average, inadequate pain relief (retrospective average pain > 3/10) on the first postoperative day was more frequent on the ward before than after the reform (47 vs. 21%; 95% CI for differences 15-35%; p<0.001 for pain scores). The incidence of side-effects was similar in both groups (p> 0.05). The intensity and variation of postoperative pain on the ward decreased by developing a nurse-based pain service with an acute pain nurse, an educational programme and regular pain intensity measurements.
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Clinical Trial
Relationship between mechanical sensitivity and postamputation pain: a prospective study.
Limb amputation is followed by stump and phantom pain in a large proportion of amputees and postamputation pain may be associated with signs of hyperexcitability such as hyperalgesia to mechanical stimulation. The present study examined the possible relationship between mechanical pain threshold of the limb and early (after 1 week) and late (after 6 months) phantom pain. Thirty-five patients scheduled for amputation of the lower limb were examined before, 1 week and 6 months after amputation. ⋯ One week after amputation there was a significant and inverse relationship between mechanical thresholds and phantom pain but no relationship was found after 6 months. The findings suggest that although tenderness of the limb before and after amputation is related to early stump and phantom pain, the relationship is weak. Neuronal sensitization peripherally or centrally may play a role in the development of phantom pain.
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Subcutaneous (s.c.) administration of bee venom into the plantar surface of one hind paw in rats has been found to produce an immediate single phase of persistent spontaneous nociceptive responses (continuously flinching, licking or lifting the injected paw) for 1-2 h accompanied by a 72-96 hour period of primary heat and mechanical hyperalgesia in the injection site and a spread of heat, but not mechanical, hyperalgesia in the non-injected hind paw (Chen et al., 1999b). To gain insight into the underlying mechanisms of the bee venom-induced hyperalgesia in particular, we further identified a heat, but not mechanical, hyperalgesia in an area (paw pad) distant from the injection site induced by s.c. injection of bee venom into the posterior leg 0.8-1.2 cm proximal to the heel measured by paw withdrawal reflex to radiant heat or von Frey monofilament stimuli in conscious rats. ⋯ Moreover, pre- or post-treatment with a single dose of MK-801 (0.01 mg/kg, i.p.), a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, completely blocked the occurrence, and reversed the established process of the heat hyperalgesia identified in either the bee venom-treated or non-treated paw pads, while the same treatments with the drug did not produce any influence upon the development and maintaining of the heat and mechanical hyperalgesia identified in the heel of the injected hind limb. Taken together with our previous results following s.c. intraplantar bee venom injection, we conclude that: (1) in addition to the well-identified primary heat and mechanical hyperalgesia in the injection site and its adjacent area, s.c. bee venom is also able to produce a secondary heat hyperalgesia in a region distant from the injection site which has a similar characteristic to the contralateral heat hyperalgesia; (2) NMDA receptors are involved in either development or maintenance of the secondary and the contralateral heat hyperalgesia, but without any role in those processes of the primary heat and mechanical hyperalgesia; (3) the secondary heat hyperalgesia seen in the injected hind limb is likely to share the same neural mechanisms with that identified in the non-injected side via co-activation of NMDA receptors.