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The purpose of this study was to evaluate the impact of the Glasgow Coma Scale (GCS), Acute Physiology and Chronic Health Evaluation (APACHE) II and Simplified Acute Physiology Score (SAPS) II scoring systems for organophosphate poisoning (OPP) in an intensive care unit (ICU). The following data were collected on all consecutive patients who were admitted to the ICU between June 1999 and December 2004. Demographic data, GCS, APACHE II and SAPS II scoring systems were recorded. Predicted mortality was calculated using original regression formulas. Standardized mortality ratio (SMR) was computed with 95% confidence intervals (CI). The sensitivity and specificity for each scoring system were evaluated by calculating the Area Under the Receiver Operating Characteristic Curves. The actual mortality in OPP was 21.9%. Predicted mortality by all systems was not significantly different from actual mortality [SMR and 95% CI for GCS: 1.00 (0.65-1.35), APACHE II: 0.87 (0.54-1.03), SAPS II: 1.40 (0.98-1.82)]. The area under the ROC curve for APACHE II is largest, but there is no statistically significant difference when compared with SAPS II and GCS (GCS 0.9009 / 0.059, APACHE II 0.9299 / 0.045 and SAPS II 0.8919 / 0.057). In our ICU group of patients, in predicting the mortality rates in OPP, the three scoring systems, which are GCS, APACHE II and SAPS II, had similar impacts; however, GCS system has superiority over the other systems in being easy to perform, and not requiring complex physiologic parameters and laboratory methods.

Background: Low muscle glutamine levels during sepsis are associated with reduced protein synthesis and elevated protein breakdown, in particular myofibrillar protein breakdown. Thus, in a cecal ligation and puncture (CLP)-induced sepsis model in the rat, we hypothesized that glutamine pretreatment would protect the diaphragm muscle function. Methods: Eighty-four male Wistar rats weighing between 180 g and 200 g received standard amino acid solution 1.2 g kg -1 per day intraperitoneally (IP) or standard amino acid solution 1.2 g kg -1 per day plus alanyl-glutamine (GLN) 0.25 g kg -1 per day (IP) during the first 6 days of the experiment. On the seventh day, CLP or sham procedures were applied. The sham and CLP groups were equally divided into 3 subgroups according to the termination of the experiment, which took place at either the 24 th hour, 48 th hour, or 72 nd hour. After the compound muscle action potentials (CMAP) were recorded from the diaphragms of the rats at these selected times, they were decapitated under ketamine/xylazine anesthesia, and diaphragms were harvested for biochemical and histopathological examination. Results: The mean area and amplitude of CMAP were significantly larger in sham+GLN groups when compared with CLP and CLP+GLN groups at all times (p

Although effective analgesia is provided for many patients, some complications may occur due to the catheter delivery system. A rare complication, subcutaneous-epidural connection due to the long-term use of an epidural catheter and subcutaneous injection port in a patient is presented in this paper.

To investigate the effect of N-acetylcysteine on preventing pump-induced oxidoinflammatory response during cardiopulmonary bypass (CPB).Forty patients undergoing coronary artery bypass grafting (CABG) were randomly divided into a study group (n = 20), given 50 mg kg(-1) N-acetylcysteine intravenously for 3 days, and a control group (n = 20) given saline. Serum samples were collected for measurement of myeloperoxidase (MPO), malondialdehyde (MDA), interleukin-6, Alpha1-acid glycoprotein (AAGP), and C-reactive protein (CRP) during surgery and postoperatively.The MPO and MDA values showed a similar pattern during and after CPB in the study group, with significantly less variance than in the control group. Interleukin-6 showed similar patterns in the two groups, but the data from 30 min after the start of CPB and from 6 h post-CPB were significantly different. The AAGP and CRP values were both elevated during CPB in the two groups without a significant difference, but 6 and 24 h post-CPB, the values were significantly higher in the control group than in the study group.N-Acetylcysteine decreased pump-induced oxidoinflammatory response during CPB, suggesting that it could be a novel therapy for assisting in the prevention of CBP-induced oxidoinflammatory damage.

Objectives: To examine in a prospective, randomized, double-blind, placebo-controlled study the analgesic effect of periprostatic nerve block and/or intravenous synthetic opioid administration during a 12-core prostate biopsy. Patients and Methods: Patients were prospectively randomized to receive unilateral periprostatic lidocaine administration and/or intravenous synthetic opioid (meperidine or tramadol) administration. Placebo groups received sterile normal saline. Unilateral infiltration was performed and biopsy was begun on this side. The degree of pain was recorded using the visual analog scale/numeric analog scale (VAS/NAS) score before the procedure, during probe introduction into the rectum, during unilateral periprostatic nerve blockade, during the first 6-core biopsy and during the second 6-core biopsy, and 30 min after biopsy completion. Results: Most of the patients had mild or moderate pain (VAS/NAS 0.05). Compared with pain scores, no significant differences existed between the first 6-core (blocked side) and second 6-core biopsies (p > 0.05). Conclusion: Periprostatic lidocaine infiltration and/or intravenous synthetic opioid analgesics are not beneficial in significantly reducing pain during biopsy. We think that most of the patients do have pain during biopsy, however the intensity of pain is tolerable and does not require analgesics.

Objective: To evaluate the efficacy and safety of topical endometrial anaesthesia during endometrial biopsy and compare it with standard paracervical block. Methods: 114 women in reproductive period undergoing endometrial biopsy for abnormal uterine bleeding were enrolled into this study. Women were randomly assigned into four groups to receive different anaesthetics. Group A (placebo group) received intrauterine placebo; Group B received intrauterine lidocaine hydrochloride solution; Group C received paracervical injection of 1 : 1 diluted lidocaine solution alone and Group D received intrauterine topical anaesthesia in addition to paracervical block. All patients were asked by the nurse to rate the intensity of pain on a 0-100 mm scale (VAS) during the application of the anaesthetic (T1), cervical dilation (T2) (if needed), endometrial biopsy (T3) and 15 minutes after the procedure (T4). Results: All groups were similar in medical and demographic characteristics. The mean pain intensity scored ...

Ischemic preconditioning (IPC) was first demonstrated in the heart, but this protective effect has been also recently described in the intestine. The aim of this study was to determine the effects of intestinal ischemic preconditioning on the morphology of intestine and bacterial translocation. Twenty-four male Wistar rats weighting 250 to 300 g were randomized into three groups. A control group of rats (n = 8) were subjected laparotomy. In an ischemic group (n = 8), laparotomy was performed and the superior mesenteric artery was occluded by an atraumatic clamp for 30 min. In the preconditioned group (n = 8), before the ischemia-reperfusion (I/R) period (as in ischemic group), rats were subjected to an initial 10 min of intestinal ischemia and 10 min of reperfusion. Twenty-four hours later, to evaluate whether the I/R induced intestinal injury and bacterial translocation (BT), tissue and blood samples were collected, and liver, spleen, and mesenteric lymph node specimens were obtained under sterile conditions for microbiological analysis. Samples of ileum were removed for both biochemical and histopathological evaluation. In the I/R group, the incidence of bacteria-isolated mesenteric lymph nodes, spleen, liver, and blood was significantly higher than other groups (P < 0.05). IPC prevented I/R-induced BT and it significantly reduced the I/R-induced intestinal injury (P < 0.05). Increased inducible nitric oxide (NO) synthase (iNOS) expression observed on the ileal specimens of the I/R group was found to be prevented by IPC. Our data suggest IPC as a key factor that reduces BT and iNOS activation in intestinal I/R. This is the first study showing that intestinal IPC blocks the cascade of events that causes BT and intestinal injury that may lead to sepsis.

In this lipopolysaccharide (LPS)-induced endotoxemia model, the effects of 3-aminobenzamide (3-AB), a poly(ADP-ribose) synthetase (PARS) inhibitor, on ileal apoptosis were evaluated by light microscopy and M30 cell death staining. Moreover, the relationship between Bcl-2, iNOS expression, and serum nitrate (NO(3)(-)) levels were investigated. Thirty-two male Wistar rats, weighing 180-220g were randomly divided into four groups. The group I (control; n=8) received saline and group II (sepsis; n=8) received 10 mg kg(-1) LPS intraperitoneally. 3-AB was given to the group IV (S+3-AB; n=8) 20 min before giving LPS and to the group III (C+3-AB; n=8) 20 min before giving saline. Six hours later, blood and ileum samples were taken. Endotoxemic group exhibited significant apoptosis in intestinal epithelial cells and the immunohistochemical examination with M30 was demonstrated that the 3-AB reduced the LPS-induced intestinal apoptosis. Serum NO(3)(-) level was increased in endotoxemic group, whereas the elevation of NO(3)(-) level was prevented in LPS+3-AB group (P0.05). The increased iNOS expression observed in the LPS group was also prevented by 3-AB. Compared with the endotoxemic group, ileal epithelial columnar cells from LPS+3-AB group had a dense Bcl-2 staining which was almost identical with control. In conclusion, 3-AB decreases LPS-induced apoptosis in ileum by preventing LPS-induced depletion of Bcl-2 and blocking iNOS gene. Modification of Bcl-2 expression by PARS inhibitors should further be investigated as a new therapeutic alternatives in septic states.

Tissue subjected to a period of ischemia undergoes functional and morphological damage that increases during the reperfusion phase. In this study, the protective effect of aprotinin, which is a protease inhibitor, was assessed in a rabbit unilateral renal ischemia-reperfusion (I/R) model. New Zealand rabbits, weighing 1.5-2 kg, were randomized to receive either aprotinin 30.000 KIU x kg(-1) and 10.000 KIU x kg(-1) x h(-1) i.v. infusion (group I, n= 7) or equivalent volumes of 0.09% sodium chloride (SF) (group II, control, n= 7) i.v. 15 minutes before a 45 minutes interruption of left renal artery blood flow and then 45 minutes of reperfusion. Blood samples were obtained before and after the ischemia-reperfusion period for measurement of nitric oxide serum (NO) levels with the nitrite/nitrate colorimetric method. Histological changes were evaluated by quantitative measurements using a numerical score (0-4) and immunohistochemical analysis of inducible nitric oxide synthase (iNOS) expression was determined. A Wilcoxon W -test was used for statistical analysis of biochemical measurements and mean values were expressed as +/-sd. Histological examination revealed the distinctive pattern of ischemic renal tissue injury with obvious signs of epithelial necrosis. The intensity of epithelial necrosis was more extensive in the SF group. Immunohistochemical analysis showed that there was severe immunostaining in the tubular epithelium in both cortical and medullary regions and iNOS expression was more intense in SF-only cases. The staining results for aprotinin cases did not differ much from the non-ischemic kidney. Biochemical analysis revealed an increase in serum NO levels in both groups (P0.05), but this was more evident in the SF group (mean NO levels were 38.63 +/- 19.03 micromol x L(-1) in group I, 50.63 +/- 24.28 micromol x L(-1) in group II). No statistically important difference was observed between the two groups. These results suggest that aprotinin may be beneficial in the prevention of systemic inflammation after transient renal ischemia.

Introduction and Objective. Paradoxical embolism through a patent foramen ovale (PFO) is a frequent cause of cerebral embolim on young patients. In this report, we describe a young woman who presen...

Postoperative nausea and vomiting (PONV) are some of the most-common and undesirable adverse effects after surgery performed under general anesthesia. We investigated the prophylactic value of dexamethasone as an alternate to ondansetron or metoclopramide to prevent PONV after gynecologic surgery.One hundred sixty ASA I-II patients scheduled for elective gynecologic surgery were enrolled. Before induction of anesthesia, patients were randomly allocated to receive intravenously dexamethasone (8 mg) in group D, ondansetron (4 mg) in group O, metoclopramide (10 mg) in group M, and saline (2 mL) in group P. Total incidence of nausea and vomiting, rescue antiemetic requirement, pain scores, and any adverse effects were recorded at 3 observational periods (0-2 hours, 2-12 hours, and 12-24 hours).Total rates of PON, POV, and PONV were significantly higher in group P at 0-2 hours and 2-12 hours compared with group D, O, and M (P.05). There was no difference in PON, POV, and PONV among D, O, and M groups. None of the groups differed in PONV in the subsequent 12-24 hours. Number of patients requiring rescue antiemetic was significantly higher in group P than the other groups at 0-2 hours (10%, 10%, 15%, and 45% in group D, O, M, and P) (P.05).Prophylactic IV dexamethasone 8 mg significantly reduces the incidence of PONV in gynecologic surgery. At this dosage, dexamethasone is as effective as ondansetron 4 mg and metoclopramide 10 mg, and is more-effective than placebo.

BACKGROUND Intrathecal morphine has been used in hopes of providing long-lasting postoperative analgesia in patients after cardiac surgery. The aim of this study was to evaluate the effects of 7 micro/kg intrathecal morphine administration in coronary bypass surgery in the postoperative period. METHODS We conducted a prospective, randomized, blinded, and controlled study. Twenty-three patients, who underwent primary elective coronary bypass surgery, were randomly allocated to receive morphine 7 micro/kg intrathecally, before the induction of general anesthesia (Group M, n = 12) or no intrathecal injection (Group C, n = 11). Pain scores, determined by visual analogue scale (VAS), were recorded immediately after extubation upon admission to the intensive care unit (ICU), at the 2nd, 4th, 6th, and 18th hour after extubation. Pethidine was administered if the patient's VAS > or = 4 and consumption was recorded. Extubation time and ICU length of stay were also recorded. RESULTS VAS scores were lower in the Group M at each measured time than the control group (p = 0.016, 0.023, 0.004, 0.0001, and 0.001, respectively). According to the VAS scores, pethidine requirement was lower in the Group M than the control (p = 0.001). Extubation time (3.58 +/- 1.57 vs. 4.86 +/- 1.38 hours, p = 0.045) and ICU length of stay (16.25 +/- 2.70 vs. 19.30 +/- 2.45 hours, p = 0.014) were also significantly shorter in the Group M than the control group. No significant complications were seen in this group of patients. CONCLUSIONS Intrathecal morphine provided effective analgesia, earlier tracheal extubation and less ICU length stay after on-pump coronary bypass surgery. The influence on ICU length of stay requires further evaluations.

In this study, histopathological and biochemical changes due to chronic usage of morphine or tramadol in liver and kidney were assessed in rats. Thirty male Wistar rats (180–220 g) were included and divided into three groups. Normal saline (1 ml) was given intraperitoneally as placebo in the control group (n = 10). Morphine group (n = 10) received morphine intraperitoneally at a dose of 4, 8, 10 mg/kg/day in the first, second and the third ten days of the study, respectively. Tramadol group (n = 10), received the drug intraperitoneally at doses of 20, 40 and 80 mg/kg/day in the first, second and the third ten days of the study, respectively. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatinin, blood urea nitrogen (BUN) and malondialdehyde (MDA) levels were measured in the serum. Liver and kidney specimens were evaluated by light microscopy. Serum ALT, AST, LDH, BUN and creatinin levels were significantly higher in morphine group compared to the control group. Serum LDH, BUN and creatinin levels were significantly increased in the morphine group compared to the tramadol group. The mean MDA level was significantly higher in morphine group compared to the tramadol and control groups (P

Histopathologic changes in rat brain due to chronic use of morphine and/or tramadol in progressively increased doses were investigated in this study. Thirty male Wistar rats (180-220 g) were included and divided into three groups. Normal saline (1 ml/kg) was given intraperitoneally as placebo in the control group (n = 10). Morphine group (n = 10) received morphine intraperitoneally at a dose of 4 mg/kg/day for the first 10 days, 8 mg/kg/day between 11-20 days, and 12 mg/kg/day between 21-30 days. The tramadol group (n = 10) received the drug intraperitoneally at doses of 20, 40, and 80 mg/kg/day in the first, second, and the third 10 days of the study, respectively. All rats were decapitated on the 30th day and the brain was removed intact for histology. The presence and the number of red neurons, which are a histologic marker of apoptosis, were investigated in the parietal, frontal, temporal, occipital, entorhinal, pyriform, and hippocampal CA1, CA2, CA3 regions. Red neurons were found in morphine and tramadol groups but not in the control group. The total number of red neurons was not different in morphine and tramadol groups, but the numbers of red neurons were significantly higher in the temporal and occipital regions in tramadol group as compared with the morphine group (p < .05). In conclusion, chronic use of morphine and/or tramadol in increasing doses is found to cause red neuron degeneration in the rat brain, which probably contributes to cerebral dysfunction. These findings should be taken into consideration when chrome use of opioids is indicated.

Since oleic acid (OA) induces morphologic and cellular changes similar to those observed in human acute lung injury (ALI) and acute respiratory distress syndrome, it has become a widely used model to investigate the effects of several agents on pathogenesis of lung injury. The antioxidant and anti-inflammatory properties of N-acetylcysteine (NAC) has been documented in many lung injury models. In this study, we evaluated the role of NAC in an OA-induced lung injury model by measuring myeloperoxidase (MPO) activity, malondialdehyde (MDA) and 3-nitrotyrosine (3-NT) levels in lung tissue. Five groups labelled Sham, NAC, OA, Pre-OA-NAC and Post-OA-NAC were determined. ALI was induced by intravenous administration of OA. The pre-OA-NAC group received iv NAC 15 min before OA infusion and the post-OA-NAC group received iv NAC 2 h after OA infusion. In both of the NAC treatment groups' blood and tissue samples were collected 4 h after OA infusion, independent from the time of NAC infusion. The MPO activity, MDA and 3-NT levels in lung homogenates were found to be increased in OA group and the administration of NAC significantly reduced tissue MPO, MDA and 3-NT levels (p = 0.0001) Lung histopathology was also affected by NAC in this OA-induced experimental lung injury model.

Recent experimental studies have described protective effect of ischemic preconditioning (IPC) on ischemia-reperfusion (I/R) injury of the intestine. We hypothesize that to reach a new point of view on the effect of IPC in intestinal barrier function, the relationship between I/R-induced mucosal injury and apoptosis must first be clarified. The present study was undertaken to investigate the role of IPC on intestinal apoptosis and probable contributions of bcl-2 expression to this process. We also investigated the effect of intestinal IPC on ileal malondyaldihyde levels. Forty-four male Wistar rats were randomized into four groups each consisting of 11 rats: sham-operated control, I/R group (30 min of superior mesenteric artery occlusion), IPC-I/R group (10 min of temporary artery occlusion prior before an ischemic insult of 30 min), and IPC alone group (10 min of preconditioning). Twenty-four hours later, ileum samples were obtained. Ileal malondyaldihyde levels were increased in the I/R group (31.9 +/- 18.8 vs. 106.8 +/- 39.8) but not in the IPC alone and IPC-I/R groups (38.1 +/- 13.6 and 44.7 +/- 12.7; P < 0.01). The number of apoptotic cells was significantly lower in IPC-I/R group than that of I/R group, and these findings were further supported by DNA laddering and M30 findings. Diminished bcl-2 expression observed in the ileal specimens of I/R group was prevented by IPC. Our results indicate that IPC may provide a protective effect on ileal epithelium and that this effect is probably the result of a significant increase in the expression of bcl-2 after the insult. The reversal of apoptosis by IPC might help preserving the vitality of intestinal structures that have a critical function, cessation of which often leads to multiorgan dysfunction syndrome.

Apoptotic loss of parenchymal cells may lead to organ dysfunctions in critically ill patients with septic states. As an antioxidant, the protective effects of N-acetylcysteine (NAC) are documented in many experimental and clinical studies. In this experimental study, we investigated the role of chronically used NAC in septic lung injury on a cecal ligation and puncture (CLP) model. To evaluate this, 30 male Wistar rats were randomly divided into four groups as sham (n = 7), CLP (n = 8), sham + NAC (n = 7) and CLP + NAC (n = 8) groups. NAC was administered 150 mg kg(-1) day through intramuscular route beginning 6 h after the operations and lasting for a period of 1 week. One week later, histopathology and epithelial apoptosis were assessed by hematoxylin-eosin and immunohistochemically by M30 and caspase 3 staining to demonstrate septic lung injury. Additionally, lung tissue myeloperoxidase (MPO) activity, malondialdehyde (MDA), and nitrite/nitrate levels were measured. The MPO activity and MDA levels in lung homogenates were found to be increased in CLP group and the administration of NAC prevented their increase significantly (P < 0.05). However, there were no significant differences among the groups regarding nitrite/nitrate levels. The number of apoptotic cells was significantly lower in CLP+NAC group than CLP group, and this finding was supported by M30 and caspase 3 expression in lung (P < 0.05). Lung histopathology was also protected by NAC in CLP-induced sepsis. In conclusion, the chronic use of NAC inhibited MPO activity and lipid peroxidation, which resulted in reduction of apoptosis in lung in this CLP model. Because lung tissue nitrite/nitrate levels did not change significantly, organs other than the lungs may be responsible for producing the increased nitric oxide during sepsis. The chronic use of NAC needs further investigation for its possible antiapoptotic potential in septic states besides its documented antioxidant and antiinflammatory effects.

Apoptosis of tissues may contribute to ischaemia-reperfusion injury. The aim of the present study was to determine whether administration of a colloid solution would prevent apoptosis after liver ischaemia-reperfusion. New Zealand rabbits, weighing 1.5-2 kg, were randomized to receive either 4% SG (20 ml kg (-1)h(-1) ) by 30 min of intravenous (i.v.) infusion (Group I, n= 7) or equivalent volumes of 0.9% sodium chloride (Group II, n= 6) i.v. before a 45 min interruption of the portal vein blood flow and then 45 min of reperfusion. The animals were killed following the reperfusion period. Their livers were processed for histopathological examination and paraffin sections of these tissues were examined. The expression of Bcl-2, Bax and caspase 3 were analysed by immunohistochemistry. ANOVA and the Wilcoxon W -test were used for statistical analysis, and mean values were expressed +/-sd. Histologically, the foci of ischaemic necrosis were observed in liver specimens of the periportal area in one of the animals in Group I and in two in Group II. Immunhistochemical analysis demonstrated an increase in Bcl-2 protein levels in Group I compared to Group II ( P0.05). Bax expression was lower in Group I than in Group II. Immunoreactivity for caspase 3 did not differ significantly between the two groups (47.0 +/- 35.93 in Group I, 32.83 +/- 23.63 in Group II). Our results indicate that gelofusine did not protect the liver tissue against ischaemia-reperfusion-induced apoptosis.

PubMedID: 8902871 The antinociceptive effect of dipyrone, a nonsteroidal anti-inflammatory drug, was studied in a series of experiments employing tail-flick and hot-plate models and the abdominal constrictor test. The drug was given via intracerebroventricular (ICV), intrathecal (IT) or subcutaneous (SC) routes. Dipyrone exhibited no analgesic activity in the tail-flick and hotplate tests while it inhibited the number of stretches in a dose-dependent manner. The antinociceptive effect of dipyrone administered by the ICV and IT routes was almost completely reversed by naloxone treatment. The same procedure attenuated but not completely inhibited the dipyrone action induced by SC administration. Histopathological examination revealed that IT dipyrone application produces no significant lesion in the spinal cord. The results suggest that dipyrone may exert a central antinociceptive action reversed by naloxone. © 1996 S. Karger AG, Basel.