Comparing the efficacy of preemptive intravenous paracetamol on the reducing effect of opioid usage in cholecystectomy.

BACKGROUND: The purpose of the present study was to determine the post-operative analgesic effects of preemptive intravenous (iv) paracetamol and the amount of reduction in tramadol (Contramal(®)) consumption. MATERIALS AND METHODS: Following local research ethics committee approval, ASAI-II, 300 patients were assigned in a randomized manner into three groups: Group I (preemptive) received iv paracetamol 1 g/100 mL 10 min before skin inscision and 100 mL of saline solution at the end of the operation, Group II (post-operative) received 100 mL of saline solution 10 min before skin inscision and iv paracetamol 1 g/100 mL at the end of the operation and Group III (placebo) received 100 mL of saline solution 10 min before skin insicision and 100 mL of saline solution at the end of the operation as well. The time to first analgesic requirement use and 24 h total analgesic consumption were recorded. Visual analog scale (VAS) pain scores were obtained from all patients at 15, 30, min 1, 2, 4, 6, 8, 12 and 24 h after the end of the operation. RESULTS: Time to first analgesic requirement was significantly longer in Group I and Group II, compared to Group III (P < 0.05). Time to first analgesic requirement was significantly longer in Group I compared to Group II (P < 0.05). Total analgesic consumption and postoperative VAS pain scores recorded were significantly lower in Group I and II, compared to Group III. Total analgesic consumption and postoperative VAS pain scores recorded were significantly lower in Group I compared to Group II (P < 0.05). CONCLUSION: In conclusion, preemptive iv paracetamol provided effective and reliable pain control after cholecystectomy surgeries and reduced post-operative pain scores, the need for and use of supplementary opioids and the time to first request of analgesics.

[Comparison of the analgesic effects of intravenous paracetamol and lornoxicam in postoperative pain following thyroidectomies]. / Tiroidektomi sonrasi postoperatif agrida intravenöz parasetamolün analjezik etkinliginin lornoksikamla karsilastirilmasi

OBJECTIVES: The purpose of the present study was to determine the efficacy of intravenous (iv) paracetamol and iv lornoxicam on postoperative analgesia and the reduction in tramadol consumption. METHODS: Sixty patients (ASA class 1-2, age: 18-72 years) undergoing thyroidectomy were enrolled in the study, and were randomized into three groups: Group L received 8 mg of iv lornoxicam, Group P received 1 g iv paracetamol and Group C received 100 cc of iv saline solution. All patients received standard general anesthesia. The postoperative salvage analgesic consumption was recorded at 0-6, 6-12 and 12-24 hour (h) intervals. Pain scores were evaluated with a visual analogue scale at 15 min, and 1, 2, 4, 6, 8, 12, 18, and 24 h postoperatively. RESULTS: The time to first analgesic requirement was approximately 127.5 min in Group L, 162.3 in Group P and 35.5 min in Group C, and the time was found to be significantly prolonged in Group L and Group P. Pain scores were significantly lower in Group P and Group L at 15 min, and 1, 8, 12, and 18 h. Twenty-four hour analgesic consumption was significantly lower in Group P and Group L compared to Group C. Supplemental analgesics requirement was as follows: 100% in Group C, 50% in Group L and 55% in Group P. The degree of satisfaction with postoperative pain management was excellent in 90% in Groups L and P, versus in only 30% in Group C. CONCLUSION: Administration of iv lornoxicam and iv paracetamol following thyroid surgery decreased the postoperative pain scores and opioid requirement, as well as the incidence of nausea and vomiting, while also prolonging the time to the first analgesic supplement.

Preventing postoperative nausea and vomiting after laparoscopic cholecystectomy: a prospective, randomized, double-blind study.

BACKGROUND: Postoperative nausea and vomiting (PONV) are potential complications in patients after laparoscopic cholecystectomy (LC). Combination antiemetic therapy often is effective for preventing PONV in patients undergoing LC, and combinations of antiemetics targeting different sites of activity may be more effective than monotherapy. OBJECTIVE: The aim of this study was to compare the administration of a subhypnotic dose of propofol combined with dexamethasone with one of propofol combined with metoclopramide to prevent PONV after LC. METHODS: Sixty adult patients scheduled for LC were randomly assigned to 1 of 2 treatment groups. The patients in group 1 received 0.5 mg/kg propofol plus 8 mg dexamethasone, and those in group 2 received 0.5 mg/kg propofol plus 0.2 mg/kg metoclopramide. The number of patients experiencing nausea and vomiting at 0 to 4, 4 to 12, and 12 to 24 hours postoperatively and as well as additional use of rescue antiemetics were recorded. RESULTS: The total PONV rates up to 24 hours postanesthesia were 23.3% and 50% for group 1 and group 2, respectively. Comparisons of the data revealed that at 0 to 4 hours, the number of patients experiencing vomiting was 6 (20%) in group 1 and14 (46.7%) in group 2 (P = 0.028). The frequency of vomiting in group 1 was significantly lower than that for group 2 (P = 0.028), and the rate of rescue antiemetic use in group 2 was higher than that in group 1 (20% vs 46.7%; P = 0.028). In the evaluation of PONV based on the nausea and vomiting scale scores, the mean PONV score was 0.4 (0.2) in group 1 compared with 1.0 (0.2) in group 2 (P = 0.017). There were no significant differences between the values at 4 to 12 hours and at 12 to 24 hours. The frequency of adverse reactions (respiratory depression: 1.3%, 1.3%; laryngospasm: 1.3%, 0%; cough: 1.3%, 0%; hiccup: 1.3%, 0%;) was not significantly different in the 2 groups. CONCLUSIONS: Administration of a subhypnotic dose of 0.5 mg/kg propofol plus 8 mg dexamethasone at the end of surgery was more effective than administration of 0.5 mg/kg propofol plus metoclopramide in preventing PONV in the early postoperative period in adult patients undergoing LC.

[A case of acute abdomen due to ventriculo-peritoneal shunt infection]. / Ventrikülo-peritoneal sant enfeksiyonu nedeniyle gelisen akut batin olgusu.

Peritonitis is a rare complication of ventriculoperitoneal shunt. Shunt infection may be the cause in patients with ventriculoperitoneal shunt, who have acute abdomen. Specific clues taken from patient's history, physical examination and some further investigations may clarify the diagnosis. This case is a 25-years-old male with a ventriculoperitoneal shunt who presented symptoms of acute abdomen. The patient was admitted with complaints of abdominal pain. There were no neurologic signs or symptoms. Physical examination on admission revealed a mass in the right lower abdomen and abdominal muscular guarding with rebound tenderness. Laboratory studies showed leukocytosis of the peripheral blood. Abdominal ultrasound demonstrated a mass and the preoperative diagnosis was appendicitis. On abdominal exploration, appendix was found to be normal but a catheter infection related omental necrosis was present. Surgical therapy was carried out by withdrawal of the catheter and segmental resection of the omentum. The patient was discharged on seventh day postoperatively.

Effects of methoctramine on bladder overactivity in a rat model.

OBJECTIVES: To determine the functional effects of methoctramine as an M(2) muscarinic receptor antagonist on isolated detrusor strips in vitro and bladder overactivity in vivo in rats. METHODS: A total of 114 Sprague-Dawley rats were used in the present study. Isolated rat detrusor strips were contracted by depolarizing the preparations with carbachol. Methoctramine was added to the tissue bath in increasing concentrations, and contraction inhibition was assessed. Isovolumetric contractions were evoked by electrical stimulation using a bipolar electrode. Efficacy against bladder instability was evaluated using the obstructed hypertrophied bladder model in the rat. The acetic acid bladder cystometry model was used to assess the efficacy of methoctramine in neurogenic detrusor overactivity. RESULTS: Methoctramine inhibited carbachol-induced bladder contractions significantly in isolated rat detrusor strips in a concentration-dependent manner. The amplitude of electrically evoked isovolumetric contractions was decreased significantly after methoctramine exposure. In vivo methoctramine administered intravenously significantly increased the voiding interval and bladder compliance. In addition, a decrease occurred in the number of spontaneous contractions during the filling phase in a model of neurogenic and obstruction-induced detrusor overactivity. CONCLUSIONS: M(2) antagonists in general may represent a new useful class of drug worth considering in the treatment of bladder overactivity.

The effects of somatostatin on the microperfusion of the pancreas during acute necrotizing pancreatitis in rats.

BACKGROUND/AIMS: Autodigestion and impairment of microcirculation of the pancreas play an important role in the pathogenesis of acute pancreatitis. Somatostatin with the reducing effect on the hepato-splanchnic blood flow decreases exocrine pancreatic secretion. Microcirculatory changes are central to the pathogenesis of acute pancreatitis. However, little is known about the effects of somatostatin on the pancreatic tissue oxygen pressure and acinar cell injury during acute pancreatitis. The aim was to evaluate somatostatin by measuring its effect on the pancreatic tissue oxygen pressure and acinar injury in acute pancreatitis. METHODOLOGY: Acute necrotizing pancreatitis was induced in rats by standardized intraductal bile acid infusion and cerulein hyperstimulation. Serum trypsinogen activation peptide was measured to verify comparable disease severity. After the induction of acute necrotizing pancreatitis, animals randomly received either ringer lactate or somatostatin. Monitoring included cardiorespiratory parameters, hematocrit, amylase, pancreatic tissue oxygen pressure, and trypsinogen activation peptide levels. At the end of the experiments the pancreas was removed for evaluation of acinar cell injury. RESULTS: The two study groups were comparable with regard to mean arterial pressure, heart rate, arterial blood gases, hematocrit, and serum amylase. The induction of pancreatitis resulted in the significant decrease of pancreatic tissue oxygen pressure in both groups. The use of somatostatin did not increase pancreatic tissue oxygen pressure. There were no significant differences in plasma trypsinogen activation peptide and serum amylase levels in the animals of two treatment groups. Only somatostatin decreased pancreatic damage significantly. CONCLUSIONS: The use of somatostatin did not improve pancreatic microcirculation or trypsinogen activation peptide level in acute necrotizing pancreatitis; however, it reduced pancreatic damage. Therefore, it has a limited value in the treatment of the acute pancreatitis.

Effects of the tyrosine kinase inhibitor tyrphostin AG 556 on acute necrotising pancreatitis in rats.

OBJECTIVE: To investigate the effects of the tyrosine kinase inhibitor tyrphostin AG 556 on the course of acute necrotising pancreatitis in rats. DESIGN: Laboratory study. SETTING: Medical school, Turkey. ANIMALS: 72 Sprague Dawley rats, 12 in the sham operated (control) group and 20 in each of the three others. MAIN OUTCOME MEASURES: Cardiorespiratory measurements, mortality, effect on the activities of various enzymes in serum and tissue of pancreas and lung, and the histological picture. RESULTS: The four study groups were sham + Ringer's lactate, acute necrotising pancreatitis with Ringer's lactate, tryphostin AG 556, and dimethylsulfoxide (DMSO). There were 12 animals in the first group and 20 in each of the other groups. The induction of pancreatitis increased mortality from 0/12 in the control to 6/20 (30%), 7/20 (35%), 8/20 (40%) in the three experimental groups, respectively. Heart rate, packed cell volume (PCV), serum activities of amylase and alanine aspartate transferase, tissue activity of myeloperoxidase (MPO) and malondialdehyde (MDA) in the pancreas and lung, serum concentrations of urea and calcium, volume of ascites, degree of pancreatic damage, blood pressure, and urine production did no differ between the pancreatitis groups. CONCLUSIONS: Treatment with the tyrphostin kinase inhibitor did not improve the course of acute pancreatitis or reduce the extent of acinar cell injury and is therefore unlikely to be of benefit in patients with pancreatitis.