ÖzAmaç: Bu retrospektif çalışmada postoperatif hasta kontrollü analjezi (HKA) uygulanan hastaların demografik özelliklerinin, ağrı durumlarının, kullanılan analjezik ajanların ve yan etkilerin incelenmesi amaçlanmıştır.Gereç ve Yöntem: Hastanemizde yaklaşık 20 aylık periyotta HKA ile postoperatif analjezi tedavisi uygulanan hastalar retrospektif olarak değerlendirildi. Hastaların demografik bilgileri, klinik özellikleri, intravenöz veya epidural uygulama protokolleri kullanılarak servis şartlarında yaklaşık sekiz saat aralıklarla yapılan takip değerlendirme bulguları (ağrı, sedasyon, uykusuzluk, bulantı, kusma, kaşıntı) kaydedildi.Bulgular: Çalışmaya alınan 810 hastanın %57,9’u kadın olup çoğu (%55,8) ortopedik cerrahi uygulanmış olan hastalardı. HKA, 730 (%90,4) hastada intravenöz, 80 (%9,6) hastada epidural yol ile uygulanmıştı. İntravenöz HKA kadınlarda, epidural HKA ise erkeklerde daha fazla tercih edilen bir uygulama idi. En sık tercih edilen analjezik ajan intravenöz uygulamada petidin iken, epidural uygulamada fentanil + bupivakain olarak saptandı. Hastalarda en sık görülen yan etkiler sedasyon/uyku hali, bulantı, kusma ve idrar retansiyonu idi.Sonuç: Hastanemizde HKA uygulamasında intravenöz uygulamanın daha çok tercih edildiği, en sık tercih edilen analjezik ajanın intravenöz uygulamada petidin, epidural uygulamada fentanil + bupivakain olduğu görülmüştür. HKA ile ağrı tedavisi düşük yan etki düzeyleri ile iyi tolere edilmektedir.

AimTo assess the effects of propofol and sevoflurane on the contraction elicited by dopamine, adrenaline and noradrenaline on isolated human umbilical arteries.MethodsUmbilical arteries were cut into endothelium-denuded spiral strips and suspended in organ baths containing Krebs-Henseleit solution bubbled with O-2+CO2 mixture. Control contraction to phenylephrine (10(-5)M) was recorded. Response curves were obtained to 10(-5)M dopamine, 10(-5)M adrenaline or 10(-5)M noradrenaline. Afterwards, either cumulative propofol (10(-6)M, 10(-5)M and 10(-4)M) or cumulative sevoflurane (1.2%, 2.4% and 3.6%) was added to the organ bath, and the responses were recorded. Responses are expressed percentage of phenylephrine-induced contraction (meanstandard deviation) (P<0.05=significance).ResultsPropofol and sevoflurane elicited concentration-dependent relaxations in strips pre-contracted with dopamine, adrenaline and noradrenaline (P<0.05). Highest (10(-4)M) concentration of propofol caused significantly higher relaxation compared with the highest (3.6%) concentration of sevoflurane in the contraction elicited by dopamine. High (10(-5)M) and highest concentrations of propofol caused significantly higher relaxation compared with the high (2.4%) and highest concentrations of sevoflurane on the contraction elicited by adrenaline. High and highest concentrations of sevoflurane caused significantly higher relaxation compared with the high and highest concentrations of propofol on the contraction elicited by noradrenaline.ConclusionDopamine, adrenaline and noradrenaline elicit contractions in human umbilical arteries, and noradrenaline causes the highest contraction. Both propofol and sevoflurane inhibit these contractions in a dose-dependent manner. Propofol caused greater relaxation in the contractions elicited by dopamine and adrenaline while sevoflurane caused greater relaxation in the contraction elicited by noradrenaline.

AIM:Definitive abdominal closure may not be possible for several days or weeks after laparotomy in damage-control surgery, abdominal compartment syndrome and intraabdominal sepsis, until the patient has stabilized. Vacuum-assisted closure (VAC therapy(®), KCI, San Antonio, TX, USA) and abdominal re-approximation anchor system (ABRA, Canica, Almonte, Ontario, Canada) are novel techniques in delayed closure of open abdomen. Our aim is to present the use of these strategies in the management of 7 patients with open abdomen.METHODS:Between August 2010 and December 2011, 7 patients with severe peritonitis were stabilized by laparotomy and treated with either ABRA system or ABRA system in conjunction with VAC dressing. VAC dressing applied to 4 patients initially and followed by ABRA. ABRA was applied alone to remaining 3 patients. Demographic data and patient characteristics, timing of VAC dressing and ABRA system were recorded. ICU and hospital stay and development of incisional hernia were also recorded. Stage of open abdomen, width of abdominal defect, extent to damage to fascia, and pressure sores were staged.RESULTS:The mean duration with VAC dressing before ABRA application was 18 days. The mean duration of ABRA application was 53 days. The average width of the abdominal defect was 18 cm. The average length of defect was 20.8 cm. Delayed primary abdominal closure was accomplished in 6 patients without further surgery. Incisional hernia with a small abdominal defect developed in 2 patients.CONCLUSION:Abdominal re-approximation anchor system and VAC dressing can be used separately or in conjunction with each other for closure of delayed open abdomen successfully.

EDITOR: Tramadol is a synthetic centrally acting analgesic drug with opioid agonist activity selectively on μ receptors and weakly on κ and σ receptors. It also inhibits re-uptake of norepinephrine and increases extraneuronal serotonin concentrations. Nitric oxide (NO), produced from L-arginine by the enzyme nitric oxide synthase (NOS) increases the intracellular content of cyclic GMP. The activation of the L-arginine-NO-c-GMP pathway is involved in the modulation of pain perception and in the nociceptive transmission at spinal and supraspinal levels [1]. NG-nitro-L-arginine methyl ester (L-NAME) is a non-selective antagonist that inhibits the activity of both endothelial NOS (eNOS) and neuronal NOS (nNOS), while 7-nitro indazole (7-NI) has been described as a nNOS inhibitor in vivo [2]. The role of NOS inhibitors on the systemic analgesic effect of tramadol has not been studied previously. We aimed to investigate the interaction of NOS inhibitors L-NAME and 7-NI with tramadol by using thermal and chemical pain models. After local animal Ethics Committee approval, 108 adult female Swiss-Webster mice 25-45 g served as the subjects. Hot-plate and acetic acid induced writhing tests were used in order to assess nociception. All drugs were injected intraperitoneally, in a volume of 10 mL kg−1, by the same person and from the same side. Control animals received saline, 36 mice were randomly assigned into six equal groups for the hot-plate test. The first injection was saline, L-NAME 10 mg kg−1 or 7-NI 3 mg kg−1. Twenty minutes after the first intraperitoneal injection, the mice received either saline or Tramadol 40 mg kg−1. Each mouse was placed on a hot-plate, at 55°C 20 min after the second injection. A cut off latency period of 40 s was used in order to prevent tissue damage. Measurements were repeated at the 50th and 80th minutes of injection. Seventy-two mice were randomly allocated into three groups to receive intraperitoneal saline, L-NAME 10 mg kg−1, or 7-NI 3 mg kg−1. Each main group was divided into four subgroups to make 12 groups. Twenty minutes after the first injection another injection of saline, tramadol 10 mg kg−1, tramadol 20 mg kg−1, tramadol 40 mg kg−1 were applied to the subgroups of these three main groups. Writhing was induced by an intraperitoneal injection of 3% acetic acid at a dose of 300 mg kg−1 20 min after the second injections. The number of writhes per animal was counted during a 15 min test period, starting at the 5th minute after injection of acetic acid. Constriction of abdomen, turning of trunk to one side, and extension of hind legs were accepted as one writhing. Friedman test was used for analysing time effect in hot-plate latencies. Kruskal-Wallis test was used for comparing groups and U-test was used with correction of significance for post-hoc multiple comparisons. P < 0.05 values were accepted as statistically significant (Fig. 1).Figure 1.: Hot-plate latencies in the study groups. *P < 0.05 compared to all other groups. #P < 0.05 compared to Saline group. †P < 0.05 compared to L-Name group. ‡P < 0.05 compared to 7-NI + Tramadol group.Although 7-NI did not show any increase in hot-plate latencies by itself, it increased the analgesic effect of tramadol significantly in the hot-plate tests performed at the 20th and the 50th minutes after injections. 7-NI pretreatment lead to significantly longer hot-plate latencies compared to tramadol alone, the effect was emphasized in the 50th minute after injections. L-NAME pretreatment followed by tramadol administration did not show a significant change in hot-plate latencies compared to tramadol alone. 7-NI or L-NAME pretreatments did not possess an analgesic effect solely on writhing tests (Table 1). No statistically significant differences were observed when the pretreatments were compared in the three doses of tramadol used in the study.Table 1: Number of writhes observed.Systemic pretreatment with 7-NI, augmented the analgesic effect of tramadol in the hot-plate test in mice. The same dose of 7-NI itself administered alone, demonstrated no analgesic effect on its own. In contrast to systemic interaction of tramadol with 7-NI in hot-plate test, no interaction between tramadol and L-NAME in both hot-plate and acetic acid induced writhing was observed. 7-NI increased the analgesic effect of tramadol in thermal pain model, not in acetic acid induced writhing test. L-NAME pretreatment did not increase the analgesic effect of tramadol both in hot-plate and acetic acid induced writhing tests. Our results emphasize the possible involvement of different mechanisms, other than those that have been identified, taking part in the analgesic effect of tramadol. It has been proposed that some non-steroidal anti-inflammatory drugs stimulate NO production, which results in increased c-GMP levels and antinociception [3]. Inhibition of NOS activity also attenuates ketamine antinociception [4]. NO-c-GMP pathway is also involved in the mechanism of benzodiazepine induced antinociception in the writhing test in mice [2]. On the other hand there are several observations indicating that NO-c-GMP pathway plays a hyperalgesic rather than antinociceptive role [5]. Neuronal NOS inhibitors, inhibit hyperalgesia in the rat regardless of the type of noxious stimuli [6]. L-NAME has a synergistic antinociceptive interaction with morphine in response to thermal stimulation when given intrathecally, epidurally or intravenously in rats but it inhibits the analgesic effect of ketamine in rats [4]. L-NAME potentiates the antinociception induced by sumatriptan and buspiron but does not alter the pain threshold itself in the acetic acid writhing assay at a dose of 20 mg kg−1 [7]. In mice, a 94% inhibition of cortical NOS activity has been reported following administration of L-NAME [4]. So we assumed that this used dose in our study would be enough to inhibit the brain NOS activity. We could not find an increase in the analgesic effect of tramadol when the mice were pretreated with L-NAME. The mechanism of antinociception in the writhing test in mice involves NO-c-GMP pathway [2]. NOS inhibitors fail to alter acute thermal and mechanical pain, whereas persistent chemical pain associated with writhing or the second phase of formalin assay are very sensitive to inhibition by these drugs [2]. Writhing reflects nociception that unlike the tail-flick and hot-plate tests, is mediated by NMDA receptor activity known to be associated with NO synthesis. Writhing assay is somewhat unique as it involves a noxious stimulus and behavioural responses that persist for a sufficient time interval to reflect sensitivity to the relatively slow generation of NO. We found that systemic pretreatment with the NOS inhibitor 7-NI augmented the analgesic effect of tramadol in the hot-plate test even though it did not exhibit an analgesic effect by itself. No effects of pretreatments with 7-NI or L-NAME were observed in acetic acid induced writhing. The potentiation of analgesic effect of tramadol by 7-NI might be an indicator of the involvement of NO in the antinociceptive effect of tramadol. This is a preliminary study which suggests that NOS inhibitors may interfere with the analgesic effect of tramadol for the first time. It is also possible that 7-NI may increase the analgesic effect of tramadol other than the inhibition of neuronal NOS inhibition with some indistinct mechanism. In order to find out the overall aspects of this synergism, further studies are required. Acknowledgement This study has been presented at the Turkish Anaesthesiology and Reanimation Congress on November 28th 2003 in Antalya, Turkey and XXII Annual European Society of Regional Anaesthesia & Pain Therapy Congress on September 12th 2003 in St Julian, Malta. Alper B. Iskit has been supported by the Turkish Academy of Sciences, in the framework of the Young Scientist Award Program (EA-TUBA-GEBIP/2001-2-11). D. Dal M. A. Salman A. E. Salman A. B. Iskit Ü. Aypar *Department of Anaesthesiology and Reanimation, Hacettepe University Faculty of Medicine Hacettepe, Ankara, Turkey †Department of Pharmacology Hacettepe University Faculty of Medicine Hacettepe, Ankara, Turkey ¶Department of Anaesthesiology and Reanimation, Hacettepe University Faculty of Medicine Hacettepe, Ankara, Turkey

Background: Temporary occlusion of blood flow is used during arthroscopic knee surgery in order to provide a bloodless surgical field. The resulting ischaemia‐reperfusion causes lipid peroxidation, which contributes to tissue injury. The aim of the study was to investigate the effect of low‐dose n‐acetyl cysteine (NAC) infusion on oxidative stress by determining malondialdehyde (MDA) levels during arthroscopic knee surgery.Methods: Thirty patients, ASA I – II, undergoing arthroscopic knee debridement under a tourniquet were divided into NAC and control groups. Anaesthesia was induced with propofol, fentanyl and vecuronium bromide and maintained with desflurane in an equal parts O2‐N2O mixture. In the NAC group, an infusion of NAC, 5 mg kg−1.h−1, was started after intubation, and continued until extubation. An equal volume of saline was infused to the control group. Duration of ischaemia, anaesthesia time, total dose of NAC infused were also recorded. Venous blood and synovial membrane tissue samples were obtained 10 min after the onset of NAC infusion but before tourniquet inflation (t1), after 30 min of ischaemia (t2), and after 5 min of reperfusion following tourniquet release (t3).Results: Plasma MDA levels were significantly lower in the NAC group on reperfusion. There were no differences between the groups in tissue MDA levels at ischaemia and reperfusion times.Conclusion: Low‐dose n‐acetyl cysteine infusion attenuates lipid peroxidation and ischaemia‐reperfusion injury in arthroscopic knee surgery requiring tourniquet application.

Previous studies suggest a correlation of central venous pressure (CVP) with peripheral venous pressure (PVP) in different clinical settings. The effect of body temperature on PVP and its agreement with CVP in patients under general anesthesia are investigated in this study. Fifteen American Society of Anesthesiologists I-II patients undergoing elective craniotomy were included in the study. CVP, PVP, and core (Tc) and peripheral (Tp) temperatures were monitored throughout the study. A total of 950 simultaneous measurements of CVP, PVP, Tc, and Tp from 15 subjects were recorded at 5-minute intervals. The measurements were divided into low- and high-Tc and -Tp groups by medians as cutoff points. Bland-Altman assessment for agreement was used for CVP and PVP in all groups. PVP measurements were within range of +/-2 mm Hg of CVP values in 94% of the measurements. Considering all measurements, mean bias was 0.064 mm Hg (95% confidence interval -0.018-0.146). Corrected bias for repeated measurements was 0.173 +/- 3.567 mm Hg (mean +/- SD(corrected)). All of the measurements were within mean +/- 2 SD of bias, which means that PVP and CVP are interchangeable in our setting. As all the measurements were within 1 SD of bias when Tc was > or = 35.8 degrees C, even a better agreement of PVP and CVP was evident. The effect of peripheral hypothermia was not as prominent as core hypothermia. PVP measurement may be a noninvasive alternative for estimating CVP. Body temperature affects the agreement of CVP and PVP, which deteriorates at lower temperatures.

We studied the effect of ketamine sedation on oxidative stress during arthroscopic knee surgery with tourniquet application by determining blood and tissue malonyldialdehyde (MDA) and hypoxanthine (HPX) levels. Thirty ASA I-II patients undergoing arthroscopic knee surgery with tourniquet were randomly divided into two groups. Spinal anesthesia induced with 12.5 mg bupivacaine was administered to all patients. In the ketamine group, after IV administration of 0.01 mg/kg midazolam, a continuous infusion of ketamine (0.5 mg . kg(-1) . h(-1)) was used until the end of surgery whereas the placebo group received a volume-equivalent placebo infusion. Ramsey Sedation Scale (RSS) was used for assessing the sedation level. Venous blood and synovial membrane tissue samples were obtained before ketamine infusion, at 30 min of tourniquet ischemia, and at 5 min after tourniquet deflation for MDA and HPX measurements. Tissue MDA and HPX levels were significantly less in the ketamine group than the control group after reperfusion. RSS scores were higher in the ketamine group without any adverse effect. We conclude that ketamine sedation attenuates lipid peroxidation markers in arthroscopic knee surgery with tourniquet application.

Department of Anesthesiology and Reanimation, Hacettepe University Faculty of Medicine, Ankara, Turkey

Background and objective: The aim of this study was to investigate any possible protective effect of ketamine in acute muscular ischaemia and reperfusion injury by measuring malondialdehyde using thiobarbituric acid assay in rats. Methods: Twelve female Wistar albino rats were anaesthetized with chloral hydrate and randomly assigned into two groups to receive ketamine 1 mg kg min(-1) or saline infusion. Blood and gastrocnemius muscle samples were obtained 10 min after onset of infusion, before ischaemia. Then, femoral arteries were clamped for 30 min. Blood and muscle samples were obtained at the 30th minute of ischaemia and 10 min after reperfusion. Results: Muscle malondialdehyde concentrations were 27.88 +/- 2.45, 27.62 +/- 3.98 before ischaemia, 32.10 +/- 4.19, 30.77 +/- 2.73 in the 30th minute of ischaernia and 44.34 +/- 2.45, 34.83 +/- 2.78 after reperfusion in saline and ketamine-treated rats, respectively (nmol g(-1), mean +/- SD). The muscle malondialdehyde level after reperfusion was lower in ketamine-treated rats compared to saline group (P < 0.002). Plasma malondialdehyde levels were 3.77 +/- 0.16, 3.78 +/- 0.18 before ischaemia, 3.81 +/- 0.25, 4.00 +/- 0.86 at the 30th minute of ischaemia and 4.00 +/- 0.53, 3.94 +/- 0.95 after reperfusion, respectively, in saline and ketamine-treated rats (mu mol L-1, mean +/- SD). The effect of ketamine on muscular malondialdehyde was not observed in concurrent plasma malondialdehyde levels. Conclusion: Ketamine was found to attenuate acute ischaemia-reperfusion injury in muscle tissue in rats (muscular protective). Ketamine may attenuate lipid peroxidation in muscle tissue in tourniquet-requiring manoeuvres.

Department of Anesthesiology and Reanimation, Hacettepe University Faculty of Medicine, Ankara, Turkey

Department of Anesthesiology and Reanimation, Hacettepe University Faculty of Medicine, Department of Pharmacology, Ankara, Turkey

Study Objective: Previous studies suggest a correlation of central venous pressure (CVP) with peripheral venous pressure (PVP) in different clinical setups. The aim of this study was to investigate the effect of measurement site on PVP and its agreement with CVP in patients undergoing general anesthesia.Design: Prospective randomized study.Settings: University hospital.Patients: Thirty patients of American. Society of Anesthesiologists physical status I and 11 undergoing elective craniotomy.Interventions: Patients were randomly assigned into Group A (antecubital; n = 15) and Group D (dorsum hand; n = 15) for antecubital and hand dorsum catheterization sites, respectively. Central venous pressure and PVT were monitored throughout the study. A total of 1925 simultaneous measurements were recorded at 5-minute intervals. Bland-Altman assessment for agreement was used for CVP and PVP in 2 groups.]Measurements: Peripheral venous pressure measurements were within the range of +/- 2 mm Hg of CVP values, in 93.9% of the measurements in Group A, and in 91.2% of the measurements in Group D. Considering all measurements, mean bias was -0.072 mm Hg (95% Cl, -0.134 to -0.010). Group A measurements showed a bias (CVP-PVP) of 0.173 +/- 3.557 mm Hg, whereas the bias was -0.122 +/- 4.322 mm Hg (mean +/- SD(corrected) for repeated measurements) in Group D. All of the measurements were within mean +/- 2SD of bias, which means that PVP and CVP are interchangeable in our clinical setting.Conclusion: Peripheral venous pressure measurement may be a noninvasive alternative for estimating CVP in patients undergoing elective neurosurgical operations. Measuring PVP from hand dorsum does not interfere with the agreement of CVP and PVP. (c) 2005 Elsevier Inc. All rights reserved.

s and Programme: European Society of Anaesthesiologists; 9th Annual Meeting with the Swedish Society of Anaesthesiology; Gothenburg, Sweden, 7-10 April 2001: Local and Regional Anaesthesia

s and Programme: European Society of Anaesthesiologists; 9th Annual Meeting with the Swedish Society of Anaesthesiology; Gothenburg, Sweden, 7-10 April 2001: Neurosciences: Monitoring Equipment and Computers