健侧下肢组合血管皮瓣桥携游离（骨）皮瓣转移修复对侧下？…

目的：探讨下肢严重创作需行游离组织移植而患侧下肢无血管可供吻接时的修复方法。方法：健侧小腿胫后血管蒂与带蒂保留真皮下血管网皮且成皮瓣桥,携带皮瓣或骨皮瓣转移修复患肢。结果：６周后经血管造影皮瓣与周围组织血运建立。断蒂后皮瓣与骨皮瓣一期成活,后期复查移植骨成活并且增粗。结论：下肢严重创伤无血管可供吻接时健侧胫后血管皮瓣桥可作为一种理想的供血途径,这为下肢严重创伤提供一种新的修复方法。     

健侧胫后血管皮瓣桥携带游离皮瓣临床应用

目的 探讨下肢大面积软组织缺损采用游离组织移植修复而受区载供血管可以供缝接时的解决办法,方法 在形态学观察及动脉压和血流量测定的实验基础上,设计以健侧胫后血管形成单一顺行皮瓣成桥及顺,逆行两皮瓣桥作为血管蒂而携带游离皮瓣移植修复。结果 采用健侧胫后血管形成顺行皮瓣桥携带游离皮瓣移植修复伤肢一处创面缺损８例,皮瓣全部成活,创面修复,采用健侧胫后血管形成顺－逆行两个皮瓣桥分别携带两个游离皮瓣同时修复伤     

小腿桥式交腿游离皮瓣的临床应用

目的 探讨下肢大面积软组织缺损采用游离组织移植而受区又无可供吻合血管时的解决办法. 方法 采用以健侧胫前或胫后血管为蒂桥式携带游离皮瓣移植修复11例下肢大面积软组织缺损. 结果 采用健侧胫前血管形成顺行皮瓣桥式携带游离皮瓣移植修复患肢创面缺损6例,皮瓣全部成活.采用健侧胫后血管形成顺行皮瓣桥式携带游离皮瓣5例,其中2例皮瓣边缘部分坏死,行清创植皮术后,创面修复良好.其余3例皮瓣全部成活,创面修复.结论 以健侧小腿胫前或胫后血管作为游离组织移植时的供血血管,是解决患侧小腿大面积软组织缺损且受区又无可供吻合血管时的一种理想修复方法.     

小腿火器伤严重组织缺损桥式肌皮瓣移植修复

目的：探讨小腿火器伤严重组织缺损采用游离组织移植修复而受区无供血血管可供缝接时的解决方法。方法：在形态学及动脉压和血流量测定的基础上,设计以健侧胫后血管形成一顺行皮瓣桥作为血管蒂携带游离肌皮瓣移植修复。结果：７例小腿火器伤严重软组织缺损伤者采用皮瓣桥携带的肌皮瓣均成活,创面一期修复;同时有２例伴胫骨缺损,采用对侧游离腓骨移植一期修复,经Ｘ线检查均骨愈合。结论：以健侧胫后血管作为游离组织移植时的供血血管是解决小腿火器伤严重软组织缺损且受区无供血血管可供缝接时的一种理想修复方法;局部软组织条件改善、丰富的血循环是同期游离腓骨移植修复胫骨缺损骨愈合的基础。     

游离股前外侧皮瓣与健侧血管桥接修复下肢严重毁损伤

目的　探讨下肢严重毁损伤造成大面积软组织缺损、骨缺损、骨外露以及胫前、后动脉受损情况下 ,应用游离股前外侧皮瓣健侧胫后血管桥接方式覆盖创面 ,为二期功能重建创造条件 ,从而达到保肢目的。　方法　临床治疗 11例 ,切取股前外侧皮瓣与健侧胫后血管桥接修复下肢大面积皮肤软组织缺损并骨缺损、骨外露巨大创面 ,切取皮瓣最大面积 36cm× 15cm ,双套管活动外固定器固定双下肢 ,术后 4～ 6周断蒂。　结果　 11例皮瓣全部成活 ,3例皮瓣轻度感染 ,其中 2例经换药后愈合 ,另 1例断蒂后愈合。随访 6个月～ 3年 ,皮瓣外观丰满 ,质地均匀 ,保肢成功 ,并最大限度地恢复下肢功能。　结论　应用游离股前外侧皮瓣及健侧胫后血管桥接移植是修复下肢严重毁损伤的有效方法     

健侧隐神经营养血管皮瓣桥携带游离皮瓣修复小腿软组织缺损

目的 报道受区无供血血管时修复小腿软组织缺损的方法及其疗效.方法 对受区无可供吻合血管的小腿软组织缺损16例,选择隐神经营养血管皮瓣作为皮瓣桥,供血血管均选择健侧胫后血管,均为顺行皮瓣桥接.其中携带胸脐皮瓣6例、背阔肌皮瓣6例、股前外侧皮瓣4例.结果 术后1例背阔肌皮瓣由于患者突发心梗出现血管危象,皮瓣坏死,余15例(肌)皮瓣均顺利成活.术后4～6周断蒂,皮瓣质地好、外形满意.结论 健侧隐神经营养血管皮瓣桥携带游离皮瓣移植是修复小腿软组织缺损的有效方法.     

健侧胫后血管皮管桥接游离皮瓣在小腿骨折合并软组织缺损及血管损伤的修复应用

[目的]探讨和评价胫腓骨骨折合并血管损伤及软组织缺损的修复方法。[方法]以健侧小腿内侧皮瓣设计成皮管，桥接游离皮瓣移植修复创面，两小腿用外固定架平行可靠固定。断蒂后重新恢复健侧胫后血管的通畅性。[结果]游离皮瓣全部成活，患肢功能恢复满意。健侧小腿内侧仅有线形瘢痕，足部无畏寒表现。[结论]应用健侧小腿内侧皮瓣皮管桥接游离皮瓣移植是修复小腿骨折合并血管损伤及软组织缺损的一种较理想的方法。     

健侧跨区供血骨(膜)皮瓣交腿桥式修复小腿皮肤及骨缺损

目的 探讨健侧胫后动脉穿支与膝降动脉隐支联合跨区供血骨(膜)皮瓣交腿桥式转移修复患侧胫骨缺损并大面积皮肤软组织缺损的临床疗效. 方法 采用以健侧胫后血管远端为蒂切取跨区供血胫骨骨(膜)皮瓣,皮瓣切取范围可为健侧胫后动脉供血区皮瓣和膝降动脉隐支供血区皮瓣之和,携带胫骨骨膜支血管,交腿桥式转移修复患侧胫骨长段骨缺损并小腿大面积皮肤软组织缺损.骨(膜)切取面积7 cm×12 cm～10 cm×16cm.皮瓣切取面积:10 cm ×25 cm ～20 c m ×41 cm. 结果 本组17例,12例获得随访.所有骨皮瓣均成活,分别于术后14 ～ 55 d伤口愈合,4～12个月骨折线消失,骨折全部愈合. 结论 健侧跨区供血骨皮瓣交腿桥式转移修复术式,不需吻合血管,手术成功率高,疗效肯定,是一种较理想的治疗方法.     

桥式游离背阔肌肌皮瓣在下肢软组织缺损中的应用

目的　观察应用桥式游离背阔肌肌皮瓣修复下肢软组织缺损的效果。　方法　采用桥式游离背阔肌肌皮瓣修复7例下肢严重软组织损伤患者。术前对拟行移植的背阔肌肌皮瓣血管和健肢血管行超声多普勒检查,以确认皮瓣及健肢血管循环良好。清创后,根据创面大小、深度设计皮瓣,用作携带桥的皮瓣长度较双下肢手术部位之间距离长10%左右;供区面积较受区大20%,形成皮管部位的皮肤设计应宽大,避免张力过大对血管造成压迫。然后行皮瓣修复术。观察皮瓣成活情况,总结手术指征及应注意的问题。　结果　7例患者手术后皮瓣均成活。除2例患者因皮瓣较为臃肿行皮瓣修薄术外,其余患者术后外形良好,功能恢复满意。手术指征:患侧肢体一条主要的动脉(胫前或胫后动脉)受损,不宜用另一条动脉作吻合血管行游离皮瓣移植术者;患侧肢体受伤严重,深层组织结构破坏,血管损伤情况不明或估计难以找到受区血管者;对侧健肢的重要血管无损伤者。注意点:术前应考虑桥式皮瓣的血运及断蒂后皮瓣是否能够成活。术后注意皮瓣血运,术区妥善固定。　结论　桥式游离背阔肌肌皮瓣修复下肢软组织缺损效果满意。恰当的创面处理、宽大的皮瓣、稳妥的固定是手术成功的关键。     

桥式交叉皮瓣修复小腿软组织缺损

目的探讨应用桥式交叉皮瓣修复受区缺乏可利用血管的小腿软组织缺损创面的临床应用。方法2002年5月～2004年9月19例小腿软组织缺损患者胫前及胫后血管损伤严重,无法利用。急诊清创并处理骨折后,将游离皮瓣血管与健侧胫后动静脉吻合,建立皮桥,双下肢固定,健侧踝及大腿悬吊。结果6～8周后断蒂,19例皮瓣均成活良好。结论采用桥式交叉皮瓣修复患侧缺乏可供吻合的血管的小腿创面是一个较好的方法。     

Burdened by training not by anaesthesia

Editor—Larsson and colleagues¹ have investigated importantbut often ignored aspects of anaesthetic practice. However,they imply that specialist anaesthetists experience reducedlevels of stress when compared with trainees because they havedeveloped successful coping mechanisms over the years. Thisconclusion cannot be drawn because the specialists' attitudesto work were identified at a particular time and cannot showa progression in learned coping abilities. To demonstrate thedevelopment of these skills, the specialists would have hadto be interviewed     

Treatment of hemospermia caused by dilated seminal vesicles by direct drug injection guided by ultrasonography

Bilateral seminal vesicle puncture and injection of drugs with ultrasound guidance were performed in patients with hemospermia resistant to conservative therapy and with dilated seminal vesicles. Of 7 patients 6 had resolution of hemospermia for 2 to 3 months and then relapse. No side effect was noted.     

Amplification by hyperoxia of coronary vasodilation induced by propofol

We tested the hypothesis that in vitro coronary and myocardial effects of propofol (10-300 microM) should be significantly modified in an isolated and erythrocyte-perfused rabbit heart model in the absence (PaO(2) = 137 +/- 16 mm Hg, n = 12) or in the presence (PaO(2) = 541 +/- 138 mm Hg, n = 12) of hyperoxia. The induction of hyperoxia provoked a significant coronary vasoconstriction (-13% +/- 7%). Propofol induced increased coronary vasodilation in the presence of hyperoxia. Because high oxygen tension has been reported to induce a coronary vasoconstriction mediated by the closure of adenosine triphosphate-sensitive potassium channels, we studied the effects of propofol in 2 additional groups of hearts (n = 6 in each group) pretreated by glibenclamide (0.6 microM) and cromakalim (0.5 microM) in the absence and presence of hyperoxia, respectively. The pretreatment by glibenclamide induced a coronary vasoconstriction (-16% +/- 7%) which did not affect propofol coronary vasodilation. The pretreatment by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. Propofol induced a significant decrease in myocardial performance for a concentration >100 micro M both in the absence and presence of hyperoxia. We conclude that propofol coronary vasodilation is amplified in the presence of hyperoxia. This phenomenon is not explained by the previous coronary vasoconstriction induced by glibenclamide. However, the pretreatment of hearts by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. The myocardial effects of propofol were not affected by the presence of hyperoxia. IMPLICATIONS: Propofol induced a coronary vasodilation that was amplified in the presence of hyperoxia. This phenomenon does not seem to be related to previous coronary vasoconstriction. The myocardial effects of propofol were not significantly modified in the presence of hyperoxia.     

Tracheal constriction by morphine and by fentanyl in man

The effects of morphine and fentanyl on tracheal smooth muscle tone were studied in 38 patients during induction of anesthesia. Endotracheal tube cuff pressure was used to measure tracheal tone. Anesthesia was maintained with nitrous oxide, 70 per cent in oxygen, and pancuronium and ventilation was controlled with a respirator. Morphine, 0.5 mg/kg, produced a biphasic response, initially causing tracheal dilatation and then tracheal constriction. Ten minutes after morphine injection, cuff pressure increased to significantly (21 +/- 8 per cent) above control. Morphine-induced tracheal constriction could be completely blocked by the prior administration of atropine, 0.5 mg. Fentanyl, 0.006 mg/kg, also produced significant tracheal constriction, cuff pressures increasing to 44 +/- 11 per cent above control at 10 min. Fentanyl-induced tracheal constriction could be blocked by pretreatment with droperidol, 0.25 mg/kg. At equianalgesic doses, morphine and fentanyl produced similar tracheal constriction.     

Reversal by nalbuphine of respiratory depression caused by fentanyl

In 60 ASA class I or II patients given intravenous fentanyl for elective operations in doses large enough to produce postoperative respiratory depression, the intravenous administration of 20 mg nalbuphine resulted in prompt reversal of respiratory depression without loss of analgesia.     

Lavage by laparoscopy fares better than lavage by laparotomy

Background: Although carbon dioxide (CO2) pneumoperitoneum is proposed increasingly for treatment of secondary peritonitis, associated deleterious effects have been reported in experimental models, with the hypothesis that increased intraperitoneal pressure might facilitate bacterial translocation. The purpose of this study was to compare the outcome (and qualitative microbiologic analysis) from peritonitis in rats after lavage by laparoscopy with the outcome after lavage by laparotomy. Methods: After determination of the standard innoculum for this study in 30 animals, 120 male Wistar rats received 1 ml of Escherichi coli 106 colony-forming unit (CFU), Bacteroides fragilis 107 CFU, Enterococcus faecalis 107 CFU in a sterile rat feces-barium sulfate suspension adjuvant, were anesthetized with intramuscular ketamine, and then underwent peritoneal lavage by either laparotomy (n = 60) or laparoscopy (n = 60). The duration of peritonitis defined two groups: group A: duration less than 3 h (n = 20) and group B: duration 3 h or more (n = 40). Both groups underwent successive lavage with 10-ml aliquots (total, 50 ml) of 0.9% saline solution at 37°C. Five 2-ml samples of liquid lavage were drawn for culture and microbiologic analysis. Blood (0.2 ml) and peritoneal liquid lavage samples were incubated 48 h at 37°C and cultured. Results: All the animals survived. Mean duration of peritoneal lavage was 13.2 min (range, 6-25 min) for laparoscopy and 9.7 min (range, 6-15 min) and for laparotomy. The difference was not statistically significant. The mean duration of operation was significantly longer with laparoscopy than with laparotomy: 44.5 min (range, 35-62 min) and 25 min (range, 16-40 min), respectively (p = 0.0001). The collected lavage volumes were not statistically different: 48.5 ml (range, 40-54 ml) and 46.7 ml (range, 37-56 ml), respectively. No statistically significant differences were found between the laparoscopy and laparotomy groups in terms of E. coli bacteremia, irrespective of peritonitis duration. The rates of positive blood culture for B. fragilis and E. faecalis were signficantly lower after laparoscopy than after laparotomy, both in the overall group (p = 0.025 and p = 0.045, respectively) and when duration of peritonitis exceeded 3 h (p = 0.001 and p = 0.044, respectively). Conclusions: In this animal model of secondary peritonitis, lavage by laparoscopy was associated with less bacteremia for B. fragilis and E. faecalis than peritoneal lavage by laparotomy.