腹股沟疝无张力修补术后慢性疼痛治疗体会

目的 回顾性分析前入路腹股沟疝无张力修补术后患者出现慢性疼痛的原因及应对措施.方法 分析2009年3月至2014年3月在我院普外科行开放性前入路腹股沟疝无张力修补术703例病人中出现慢性疼痛的32例病历及随访资料,对诊治过程及结果进行观察、分析、总结.结果 采用以对症治疗为主的综合治疗方法,均可使患者慢性疼痛症状和生活质量得到不同程度的改善.结论 腹股沟疝无张力修补术后慢性疼痛发生率相对较高,术前难预防,术后难处理,预后难预测,一旦出现,采用个体化、阶梯性、综合性治疗,效果满意.     

腹股沟疝修补术后慢性疼痛的诊治体会

目的报道腹股沟疝修补术后慢性疼痛的诊治体会。方法以我院在2008年10月至2011年3月期间收治的22例腹股沟疝修补术后慢性疼痛的患者为研究对象,将所有的患者随机分为两组,治疗组和对照组均有11例腹股沟疝患者组成,对照组采用传统的治疗方式对患者术后疼痛进行治疗,而治疗组则采用针刀治疗的方式。结果观察两组患者的临床表现、症状及疼痛消失率等,治疗组均明显高于对照组,有统计学差异(P<0.05)。结论采用针刀治疗的方式来治疗腹股沟疝修补术后患者的疼痛症状,是极为安全、有效的,值得在临床中大力推广。     

腹股沟疝患者腹腔镜修补术后慢性疼痛的影响因素

目的：探究腹股沟疝患者腹腔镜修补术后慢性疼痛的影响因素。方法：2019-06～2020-10河南科技大学第二附属医院收治的确诊为腹股沟疝并接受腹腔镜修补手术的124例患者临床以及术后6个月的随访资料,设计基线资料调查表,并根据患者病例资料填写,经单因素与多因素检验,分析患者术后慢性疼痛发生的影响因素。结果：124例腹股沟疝患者中16例术后发生慢性疼痛,占12.90%;发生组是否首次腹腔镜修补术、补片尺寸及术后切口有无感染与未发生组比较,差异有统计学意义(P<0.05);将可能的影响因素纳入,经二分类Logistic回归分析检验结果显示,非首次腹腔镜手术、补片尺寸为大号及术后切口感染是腹股沟疝患者腹腔镜修补术后慢性疼痛发生的危险因素(OR>1,P<0.05)。结论：腹股沟疝患者腹腔镜修补术后慢性疼痛发生的影响因素可能为非首次腹腔镜手术、补片尺寸为大号及术后切口感染。     

腹股沟疝无张力修补术后慢性疼痛的原因及治疗

长期以来,腹股沟疝修补术后慢性疼痛是一常见的并发症,在一定程度上影响了患者术后恢复.绝大多数为腹股沟区疼痛,其发生率为2%～5%,应用无张力疝修补术以来,术后腹股沟区疼痛的发生率已明显降低,但该法同时也引起了新的术后疼痛综合征和其他并发症.目前许多学者对无张力修补术后慢性疼痛的原因作了研究,现就腹股沟疝修补术后慢性疼痛谈几点体会.     

腹腔镜下腹股沟疝修补术治疗成人腹股沟疝的研究

目的:探讨腹腔镜下腹股沟疝修补术治疗成人腹股沟疝的疗效及安全性.方法:157例腹股沟疝患者实施腹腔镜下腹股沟疝修补术,于脐孔处置观察孔,在患侧腹直肌外缘平脐处及脐与髂前上棘连线中点处置5 mm套管针各1个,在镜下切开患侧脐内侧壁根部腹膜,钝、锐性分离腹膜前间隙,暴露耻骨结节,脐孔处置入mesh网片,将网片展平覆盖于腹股沟疝薄弱区,内侧达同侧耻骨结节后,四角用螺旋钉固定,将患侧脐内侧壁牵向患侧,覆盖网片,脐内侧壁边缘用腹壁缝合针固定3针至网片覆盖满意.结果:腹腔镜下腹股沟疝修补术后近期效果良好.且术后患者疼痛轻,无需服用止痛药,康复快,并发症少,不易损伤神经.结论:TAPP与传统手术比较,手术安全且创伤小,术后疼痛小、恢复快.对双侧疝、复发疝效果明显,不需要增加手术切口.     

成人腹股沟疝无张力修补术后并发症的防治

目的：总结并提高成人腹股沟疝无张力修补术并发症的防治水平。方法：对本院2002年1月-2009年7月386例成人腹股沟疝无张力修补术治疗的临床资料进行回顾性分析。结果：治愈384例（99．48％），术后65例出现各种并发症，其中，术后尿潴留26例，补片周围积液3例，伤口深部感染1例，网塞感染脱出1例，切口、阴囊血肿8例，腹股沟区异物感16例，慢性腹股沟疼痛9例，复发1例。结论：无张力疝修补术具有手术创伤小、恢复快的特点，但若处理不当，可出现各种并发症，须重视其防治。     

传统疝修补术与无张力腹股沟疝修补术后慢性疼痛原因分析及治疗

目的探讨传统疝修补术与无张力疝修补术后慢性疼痛的原因及治疗。方法对我院自2002年2月至2010年9月426例实施传统疝修补术与无张力疝修补术患者的临床资料进行回顾性地分析。结果所有患者根据手术方式分为两组：传统疝修补术组（n=210）和无张力疝修补术组（n=216）。术后疼痛发生率,传统疝修补术组为9.0%（19/210）,无张力疝修补术组为4.2%（9/216）,两者差异有统计学意义（P〈0.05）。结论聚丙烯平片无张力疝修补术可减少腹股沟疝修补术后慢性疼痛的发生,传统疝修补术与无张力疝修补术后慢性疼痛引起的原因不同治疗方法基本相同。     

成人腹股沟疝58例无张力性修补术体会

对我院2007年5月～2008年9月58例患者采用无张力性疝修补术治疗，全部治愈。随诊6～24月无复发。现报道如下：     

无张力疝修补术治疗成人腹股沟疝的临床分析

腹股沟疝是普外科常见病,多发病,腹股沟疝最有效的治疗手段是手术治疗,但传统的手术方法并发症较多,复发率高达10%～15%[1].     

无张力疝修补术治疗成人腹股沟疝152例

目的 回顾分析西华县人民医院成人腹股沟疝治疗的手术方式及术后并发症的处理.方法 对西华县人民医院2007年2月至2010年2月采用无张力疝修补术治疗成人腹股沟疝152例的回顾分析总结.结果 本组152例全部治愈,不良反应为2例出现尿潴留,2例出现阴囊积液,1例切口感染,1例疼痛,术后疝复发0例.结论 无张力疝修补术创伤...     

Tapentadol extended release: in adults with chronic pain

The extended release (ER; as ascribed in the US) or prolonged release (PR; as ascribed in Europe) formulation (hereafter referred to as ER) of the oral analgesic tapentadol is believed to exert its analgesic effects via μ-opioid receptor agonistic and norepinephrine reuptake inhibitory activity. Direct conversion between tapentadol immediate release and tapentadol ER is permissible utilizing approximately equivalent total daily doses. For the most part, shorter-term (15 weeks) therapy with tapentadol ER 100-250?mg twice daily provided more effective pain relief and significantly improved functional and health status outcomes compared with placebo in four well designed studies in adult patients with moderate to severe chronic pain associated with knee osteoarthritis, the lower back or diabetic neuropathy. Moreover, longer-term (≤24 months) therapy with tapentadol ER provided sustained analgesic effects in two multinational tolerability studies in patients with moderate to severe chronic pain associated with knee or hip osteoarthritis or the lower back. The development of tolerance was not observed in clinical studies of tapentadol ER, with the mean total daily dose and the analgesic (mean pain intensity) scores remaining relatively stable over ≤24 months' therapy. Oral tapentadol ER therapy for up to 24 months was generally well tolerated, with the nature of treatment-emergent adverse events generally similar across the clinical studies.     

Effects of a brief pain and smoking cessation intervention in adults with chronic pain: A randomized controlled trial

Tobacco cigarette smokers with comorbid chronic pain experience greater difficulty quitting smoking relative to those without chronic pain. A brief smoking cessation intervention was developed to address smoking in the context of chronic pain to increase the intention to engage in smoking cessation treatment. The primary aim of this randomized controlled trial was to investigate the effects of a brief pain and smoking (BPS) cessation intervention on the willingness to consider quitting smoking in adults with chronic pain seeking treatment in a pain specialty outpatient clinic. Subjects randomized to the BPS intervention were 7.5 times more likely to endorse willingness to consider quitting smoking. Subjects who received the BPS intervention were also greater than 2.5 times more likely to report an interest in learning about cessation programs, and nearly 5 times more likely to endorse willingness to consider participating in an intensive smoking cessation program. Moreover, subjects who received the BPS intervention evinced a trend-level reduction in perceived difficulty of quitting smoking. These results contribute to a growing multidisciplinary literature examining pain-smoking interrelations and suggest that smokers with chronic pain may become more willing to consider engaging a cessation attempt as awareness increases about how continued smoking may interfere with the clinical outcomes of pain treatment. These results are also consistent with clinical practice guidelines for promoting intention to quit among smokers currently unwilling to engage a quit attempt by incorporating strategies aimed at identifying ambivalence about the continued use of tobacco.     

Opioids in chronic pain.

The advance in our understanding of the biogenesis of various endogenous opioid peptides, their anatomical distribution, and the characteristics of the multiple receptors with which they interact open a new avenue for understanding the role of opioid peptide systems in chronic pain. The main groups of opioid peptides: enkephalins, dynorphins and beta-endorphin derive from proenkephalin, prodynorphin and proopiomelanocortin, respectively. Recently, a novel group of peptides has been discovered in the brain and named endomorphins, endomorphin-1 and -2. They are unique in comparison with other opioid peptides by atypical structure and high selectivity towards the mu-opioid receptor. Another group, which joined the endogenous opioid peptide family in the last few years is the pronociceptin system comprising the peptides derived from this prohormone, acting at ORL1 receptors. Three members of the opioid receptor family were cloned in the early 1990s, beginning with the mouse delta-opioid receptor (DOR1) and followed by cloning of mu-opioid receptor (MOR1) and kappa-opioid receptor (KOR1). These three receptors belong to the family of seven transmembrane G-protein coupled receptors, and share extensive structural homologies. These opioid receptor and peptide systems are significantly implicated in antinociceptive processes. They were found to be represented in the regions involved in nociception and pain. The effects of opioids in animal models of inflammatory pain have been studied in great detail. Inflammation in the periphery influences the central sites and changes the opioid action. Inflammation increased spinal potency of various opioid receptor agonists. In general, the antinociceptive potency of opioids is greater against various noxious stimuli in animals with peripheral inflammation than in control animals. Inflammation-induced enhancement of opioid antinociceptive potency is characteristic predominantly for mu opioid receptors, since morphine elicits a greater increase in spinal potency of mu- than of delta- and kappa-opioid receptor agonists. Enhancement of the potency of mu-opioid receptor agonists during inflammation could arise from the changes occurring in opioid receptors, predominantly in affinity or number of the mu-opioid receptors. Inflammation has been shown to alter the expression of several genes in the spinal cord dorsal horn. Several studies have demonstrated profound alterations in the spinal PDYN system when there is peripheral inflammation or chronic arthritis. Endogenous dynorphin biosynthesis also increases under various conditions associated with neuropathic pain following damage to the spinal cord and injury of peripheral nerves. Interestingly, morphine lacks potent analgesic efficacy in neuropathic pain. A vast body of clinical evidence suggests that neuropathic pain is not opioid-resistant but only that reduced sensitivity to systemic opioids is observed in this condition, and an increase in their dose is necessary in order to obtain adequate analgesia. Reduction of morphine antinociceptive potency was postulated to be due to the fact that nerve injury reduced the activity of spinal opioid receptors or opioid signal transduction. Our recent study with endogenous ligands of the mu-opioid receptor, endomorphins, further complicates the issue, since endomorphins appear to be effective in neuropathic pain. Identification of the involved differences may be of importance to the understanding of the molecular mechanism of opioid action in neuropathic pain, as well as to the development of better and more effective drugs for the treatment of neuropathic pain in humans.     

Antidepressants in chronic neuropathic pain

This review presents available clinical studies and new insights into mechanisms of analgesic effect and possible new routes of administration of antidepressant drugs. Older TCAs continue to be superior treatments. We focused on recent findings on newer antidepressants as analgesics. Their use should be supported by further controlled trials.