In this study, we aimed to determine the risk factors and the incidence of delirium in patients who were followed postoperatively in our surgical intensive care unit for 24 h using the confusion assessment method (CAM). After obtaining approval from the ethics committee, 250 patients were included in the study. Patients who were operated under general anaesthesia or regional anaesthesia and followed in the surgical intensive care unit were evaluated by the Ramsay Sedation Scale on the first postoperative day. CAM was applied to the patients who had a Ramsey Sedation Score of ≤4. Patients' age, gender, American Society of Anesthesiologists (ASA) scores, preoperative risk factors, type of anaesthesia, operation time, intra-operative procedures, pain scores evaluated by the visual analogue scale (VAS) and postoperative analgesia methods were recorded. The incidence of delirium was found to be 18.4%. The average age of patients who developed delirium was greater than the others (68.8±12.7 and 57.6±12, p=0.001, respectively). It was observed that a one-unit increase in the ASA score resulted in a 3.3-fold increase in the risk of delirium. The incidence of delirium in patients undergoing regional anaesthesia was 34.6%, whereas it was 16.5% in patients receiving general anaesthesia (p=0.024). The existence of preoperative diabetes mellitus (DM) and chronic obstructive pulmonary disease (COPD) was shown to improve the development of delirium (p<0.05). Delirium incidence was significantly higher in patients who were administered meperidine for postoperative analgesia (p=0.013). The VAS scores of patients who developed delirium were found to be significantly higher (p=0.006). As a result, we found that older age, high ASA score, preoperative DM and COPD are important risk factors for the development of delirium. Regional anaesthesia, high postoperative pain scores and meperidine use were observed to be associated with the development of delirium. In the postoperative period, addition of CAM, a simple measurement technique, to the daily follow-up forms can provide the early recognition of delirium, which is often underdiagnosed. We think that identification and prevention of effective risk factors have the primary importance for postoperative delirium.

We evaluated the effects of magnesium sulphate infusion on anesthetic requirement, early recovery and postoperative analgesia in desflurane-remifentanil-based, balanced anaesthesia. 60, ASA (American Society of Anesthesiologists) group 1-2 patients who were scheduled for laparoscopic cholecystectomy were randomly divided into two groups. Before anesthesia, the magnesium-treated group (n = 30) received a 15 min infusion of 40 mg/kg of magnesium sulphate followed by 10 mg/kg/h by continuous i.v. infusion during the operation. The same volume of isotonic saline was administered to the control group (n = 30). Anesthesia was induced with propofol, remifentanil and vecuronium, and maintained with desflurane 3-6%, O(2)/air and remifentanil infusion. Desflurane was titrated to maintain BIS (bispectral index) values of 40-60. The times from cessation of anesthesia to spontaneous breathing, eye opening, extubation, reaching BIS 70, and Aldrete scores were recorded. After surgery, patients received a patient-controlled, morphine analgesia device. demographic variables were similar. During the 15 min infusion of magnesium sulphate, the BIS value was significantly lower in the magnesium sulphate-treated group. The amounts of propofol and desflurane used were less in the magnesium sulphate-treated group, by 18% and 22% respectively (p<0.05). The groups did not differ with respect to the time taken to reach BIS 70, spontaneous breathing, eye opening and extubation. Alderete and VAS (visual analogue scale) pain scores, and total morphine consumption were significantly lower in the magnesium sulphate-treated group. There were no differences in side effects, but the rate of re-intubation was higher in the group receiving magnesium sulphate (p = 0.03). perioperative use of magnesium sulphate reduced propofol and desflurane consumption, and the postoperative morphine requirement, while causing a delay in recovery by decreasing the Aldrete score.

Background: An increase in the level of intracellular calcium activates the calcium-dependent neutral protease calpain, which in turn leads to cellular dysfunction and cell death after an insult to the central nervous system. In this study, we evaluated the effect of a calpain inhibitor, AK 295, on spinal cord structure, neurologic function, and apoptosis after spinal cord injury (SCI) in a murine model. Methods: Thirty albino Wistar rats were divided into 3 groups of 10 each: the sham-operated control group (group 1), the spinal cord trauma group (group 2), and the spinal cord trauma plus AK 295 treatment group (group 3). After having received a combination of ketamine 60 mg/kg and xylazine 9 mg/kg to induce anesthesia, the rats in groups 2 and 3 were subjected to thoracic trauma by the weight drop technique (40 g-cm). One hour after having been subjected to that trauma, the rats in groups 2 and 3 were treated with an intraperitoneal injection of either dimethyl sulfoxide 2 mg/kg or AK 295 2 mg/kg. The effects of the injury and the efficacy of AK 295 were determined by an assessment of the TUNEL technique and the results of examination with a light microscope. The neurologic performance of 5 rats from group 2 and 5 from group 3 was assessed by means of the inclined plane technique and the modified Tarlov's motor grading scale 1, 3, and 5 days after spinal cord trauma. Findings: Light-microscopic examination of spinal cord specimens from group 2 revealed hemorrhage, edema, necrosis, and vascular thrombi 24 hours after trauma. Similar (but less prominent) features were seen in specimens obtained from group 3 rats. Twenty-four hours after injury, the mean apoptotic cell numbers in groups 1 and 2 were zero and 4.57 ± 0.37 cells, respectively. In group 3, the mean apoptotic cell number was 2.30 ± 0.34 cells, a value significantly lower than that in group 2 (P < .05). Five days after trauma, the injured rats in group 2 demonstrated significant motor dysfunction (P < .05). In comparison, the motor scores exhibited by group 3 rats were markedly better (P < .05). Conclusions: AK 295 inhibited apoptosis via calpaindependent pathways and provided neuroprotection and improved neurologic function in a rat model of SCI. To our knowledge, this is the first study to evaluate the use of AK 295, a calpain inhibitor, after SCI. Our data suggest that AK 295 might be a novel therapeutic compound for the neuroprotection of tissue and the recovery of function in patients with a SCI. Introducción: Una lesión en el sistema nervioso central origina un incremento en los niveles de calcio intracelular que activa la proteasa neutral calciodependiente calpaina, que a su vez conduce a la producción de disfunción y muerte celular. En este estudio evaluamos el efecto de un inhibidor de la calpaina, AK 295, sobre la estructura de la médula espinal, la función neurológica y apoptosis tras lesión medular en un modelo murino. Métodos: Treinta ratas Wistar se dividieron en tres grupos de 10 ratas cada uno: Un grupo control (grupo 1), un grupo sometido a trauma espinal (grupo 2) y un grupo de ratas a las que se sometió a trauma medular y tratamiento con AK 295 (grupo 3). Después de recibir una combinación de ketamina 60 mg/kg y xylazina 8 mg/kg para la inducción anestésica, las ratas del grupo 2 y 3 fueron sometidas a trauma medular torácico mediante la técnica de caída de peso (40 g-cm). Una hora después de haber sufrido el traumatismo, las ratas del grupo 2 y 3 fueron tratadas mediante una inyección intraperitoneal bien de dimetil-sulfóxido 2 mg/kg o de AK 295 2 mg/kg. Los efectos del traumatismo y la eficacia de AK 295 fueron determinados mediante la estimación de la técnica TUNEL y los resultados del examen del tejido mediante microscopía óptica. La función neurológica de 5 ratas del grupo 2 y 5 del grupo 3 fue estimada mediante la técnica del plano inclinado y la escala motora de Tarlov modificada a 1, 3 y 5 días desde el traumatismo medular. Resultados: El estudio mediante microscopía óptica de las preparaciones de médula espinal del grupo 2 demostró la existencia de hemorragia, edema, necrosis y trombosis vascular 24 horas tras el traumatismo. Hallazgos similares pero menos importantes se encontraron en las preparaciones procedentes del grupo 3. Veinticuatro horas tras el trauma, el número medio de células apoptóticas en los grupos 1 y 2 fueron cero y 4.57 ± 0.37 células respectivamente. En el grupo 3, el número medio de células apoptóticas fue de 2.30 ± 0.34 células, un valor significativamente menor que en el grupo 2 (p < 0.05). Cinco días tras el traumatismo, las ratas lesionadas en el grupo 2 demostraron una significativamente mayor disfunción neurológica (p<0.05). En comparación, la puntuación motora que exhibieron las ratas del grupo 3 fue marcadamente mejor (p < 0.05). Conclusión: AK 295 inhibe la apoptosis a través de vías calpain-dependientes y provee neuroprotección y consigue una mejor función neurológica en el modelo de lesión medular traumática en la rata. En nuestro conocimiento, este es el primer estudio en evaluar el uso de AK 295, un inhibidor de la calpaina, tras lesión medular traumática. Nuestros datos sugieren que AK 295 podría ser un nuevo compuesto terapéutico capaz de ofrecer neuroprotección tisular y recuperación funcional en pacientes con lesión medular traumática.

The injection of small doses of local anesthetic solutions through pencil-point directional needles and maintaining the lateral decubitus position for 15 to 30 minutes after the injection have been suggested to facilitate the unilateral distribution of spinal anesthesia. We evaluated the effects of hypobaric and hyperbaric bupivacaine in attempting to achieve unilateral spinal anesthesia for patients undergoing lower limb orthopedic surgery. Fifty patients were randomly allocated into 2 groups to receive either 1.5 mL hyperbaric bupivacaine 0.5% (7.5 mg; n = 25) or 4.2 mL hypobaric bupivacaine 0.18% (7.5 mg; n = 25). Drugs were administered at the L3–4 interspace with the patient in the lateral position. Patients remained in this position for 15 minutes before turning supine for the operation. Spinal block was assessed by pinprick and modified Bromage scale on both sides. Unilateral spinal block was observed in 20 patients in the hyperbaric group (80%) and in 19 patients in the hypobaric group (76%) while in the lateral position. However, 15 minutes after patients were turned supine, unilateral spinal anesthesia decreased to 68% of cases in the hyperbaric group and 24% of cases in the hypobaric group (P < .05). The motor block was more intense during the first 5 and 10 minutes (P < .05), but at the end of operation there was no difference between the groups. The hemodynamic changes were similar between the groups. As a result, unilateral spinal anesthesia with hyperbaric and hypobaric bupivacaine provided a rapid motor and sensory recovery and good hemodynamic stability, but more unilateral spinal block was achieved in patients in the hyperbaric group when compared with patients in the hypobaric group.

The aim of this study was to compare the analgesic efficacy and side effects of continuous epidural infusions of ropivacaine and ropivacaine-sufentanil mixtures after thoracotomy. Sixty-two patients scheduled for thoracic surgery were allocated in this prospective double-blinded randomised study. They received an epidural catheter inserted from thoracic 5-6 (Th(5-6)) interspace a day before surgery and were randomly assigned into two groups, sufentanil-ropivacaine group (Group SR, n=31) and ropivacaine group (Group R, n=31). Bolus dose of the study drugs, ropivacaine 0.2% or ropivacaine 0.2% and sufentanil 0.75 microg/ml calculated in ml according to the patient's height was given through the epidural catheter before surgery. One hour after anaesthesia induction, another bolus was given and the epidural infusion was started (4.5-8 ml). Whenever visual analogue scale (VAS) scores were > or =4 during function, the patients received additional boluses and the infusion rate was increased by 1 ml/h. If the pain was not relieved after administration of two boluses, the patient was excluded from the study. VAS at rest and during function was lower in ropivacaine-sufentanil group and the need for additional boluses and infusion rate increase was high in ropivacaine group (P<0.05). Ropivacaine-sufentanil infusion rate was decreased due to nausea and vomiting in two patients and due to CO(2) retention in one patient. There was no statistically significant difference between the incidences of side effects except pruritus significantly higher in Group SR. The total epidural solution volume was more in Group R (P<0.05). The continuous epidural infusion of ropivacaine with sufentanil provided superior pain relief than ropivacaine alone without causing any severe side effect or post-operative pulmonary impairment.