Effects of combined spinal-epidural analgesia on first stage of labor: a cohort study.

Background: Neuraxial anesthesia is considered as the gold standard in the control labor of pain. Its variants are epidural analgesia and combined spinal-epidural analgesia. Few studies, as yet, have investigated the duration of labor as a primary outcome. Some authors have suggested that combined spinal-epidural analgesia may reduce labor duration but at the moment the benefit of shortening labor is uncertain. The main aim of this study was to compare combined spinal-epidural with epidural analgesia in terms of their effect on duration of stage I labor, maternal, and neonatal outcomes. Methods: A prospective cohort study was conducted. Parturients who requested analgesia at cervical dilatation <6 cm were included. Analgesia was either epidural with low concentration levobupivacaine or combined spinal epidural with subarachnoid sufentanil. The primary outcome was the length of stage I labor. Onset and quality of analgesia, mode of delivery, effects on uterine activity and use of oxytocin, fetal heart rate abnormalities and uterine hyperkinesia, maternal, and neonatal complications were also considered. Results: We enrolled 400 patients: 176 in the combined spinal-epidural group and 224 in the epidural group. Patients in the two treatment groups were similar with regard to demographic characteristics, parity, and incidence of obstetric comorbidities, labor induction, oxytocin infusion, Bishop score, and Visual Analogue Score (VAS) at analgesia request. Duration of stage I labor did not differ, at 195 (120-300) minutes for both the groups (p = .7). Combined spinal-epidural was associated with less reduction in uterine contractility after initial administration: 15.34 versus 39.73%, (p < .001) and with delayed need for oxytocin, at dilations of 7 ± 2.5 cm versus 6. ± 2.7, (p = .002). Onset of analgesia was quicker for combined spinal-epidural analgesia: 31 versus 20%, with VAS <4 after 5 minutes, (p < .001); and lower VAS scores after initial analgesia administration. No differences were found in the other outcomes. Conclusions: Combined spinal-epidural with subarachnoid sufentanil may not reduce the duration of stage I labor, but in our study it appeared to affect uterine contractility less. It also had a more rapid onset and was more effective, without any concomitant increase in maternal or neonatal complications.

Outcomes of induced versus spontaneous labor.

PURPOSE: Induced labor is associated with a higher request for analgesia than spontaneous labor. This study compared duration of labor, mode of delivery, quantity of blood loss, type of perineal outcome and neonatal outcomes between women in induced labor and women in spontaneous labor, both on epidural analgesia (administered at cervical dilation ≤ 4 cm). METHODS: In a two-year longitudinal cohort study, data were gathered from nulliparous women with a single cephalic pregnancy of at least 37 weeks attending the labor and delivery ward in Policlinico San Matteo Fundation-Pavia. Data were compared for women with early labor analgesia in (1) spontaneous labor (Robson group 1) and (2) induced labor (dinoprostone - vaginal insert or gel, Robson group 2a). RESULTS: Of the 1104 women who underwent epidural analgesia in the study period, 531 were included: 326 in spontaneous labor and 205 in induced labor. The only significant difference found was duration of the first stage, which lasted 305 (200-390) min in spontaneous labor compared to 205 min (120-345) in induced labor (p <0.001). CONCLUSIONS: In women on early epidural analgesia, induction is associated with a shorter duration of the first stage of labor and does not affect other outcomes.

[D-Ala2,D-Leu5]-enkephalin (DADLE) and morphine-induced postconditioning by inhibition of mitochondrial permeability transition pore, in human myocardium.

The aim of the study was to examine the cardioprotective effect of morphine and Delta 2 opioid D-Ala2-Leu5 enkephalin(DADLE) administered, at early reoxygenation, in isolated human myocardium exposed to hypoxia­reoxygenation. Then,we tested the involvement of mitochondrial permeability transition pore in morphine and DADLE-induced postconditioning.Human right atrial trabeculae were obtained during cardiac surgery (coronary artery bypass and aortic valve replacement).Isometrically contracting isolated human right atrial trabeculae were exposed to 30-min hypoxia and 60-min reoxygenation(control group). In treatment groups, morphine 0.5 mmol, DADLE 10 nmol, DADLE 50 nmol and DADLE 100 nmol were administered during the first 15 min of reoxygenation. In two additional groups, morphine and DADLE 100 nmol were administered in the presence of atractyloside 50 mmol, the mitochondrial permeability transition pore opener. The force of contraction at the end of 60-min reoxygenation period (FoC60 expressed as % of baseline) was compared (mean+standard deviation) between the groups by an analysis of variance. Morphine (FoC60: 81+9% of baseline), DADLE50 nmol (FoC60: 76+11% of baseline) and DADLE 100 nmol (FoC60: 81+4% of baseline) increased significantly (P,0.001) the FoC60 as compared with the control group (FoC60: 53+3% of baseline). DADLE 10 nmol did not modify the FoC60 (50+9% of baseline; P » 0.60 versus control group). The enhanced recovery of FoC60 induced by morphine and DADLE 100 nmol were abolished in the presence of atractyloside (FoC60: respectively 57+6% and 44+7% of baseline;P, 0.001). In conclusion, the administration of morphine and DADLE, in early reoxygenation period, protected human myocardium, in vitro, against hypoxia­reoxygenation injury, at least in part, by the inhibition of mitochondrial permeability transition pore opening.

Right ventricular failure after left ventricular assist device insertion: preoperative risk factors.

Right ventricular failure after left ventricular assist device placement is the major concern on weaning from cardiopulmonary bypass and it is one of the most serious complications in the postoperative period. This complication has a poor prognosis and is generally unpredictable. The identification of pre-operative risk factor for this serious complication is incomplete yet. In order to determine pre-operative risk for severe right ventricular failure after left ventricular assist device support we analyzed preoperative hemodynamics, laboratory data and characteristics of 48 patients who received Novacor (World Heart Corp., Ottawa, ON, Canada). We compared the data from the patients who developed right ventricular failure and the patients who did not. Right ventricular failure occurred in 16% of the patients. There was no significant difference between the groups in demographic characteristics. We identified as preoperative risk factors the pre-operative low mean pulmonary artery and the impairment of hepatic and renal function on laboratory data. Our results confirm in part the findings of the few previous studies. This information may be useful for the patient selection for isolated left ventricular assist device implantation, but other studies are necessary before establishing criteria for patient selection for univentricular support universally accepted.

The surgical patient with Brugada syndrome: a four-case clinical experience.

Brugada syndrome is characterized by a distinctive electrocardiographic pattern (right bundle branch block and ST segment elevation in precordial leads) and a high risk of cardiac arrest for malignant dysrhythmia. The genetic basis is a molecular defect of the cardiac sodium channel and the pattern of inheritance is autosomal dominant. Many factors during general anesthesia (medications, bradycardia, temperature changes) could precipitate malignant dysrhythmia in these patients. Because criteria to identify the surgical patient at high risk for developing malignant dysrhythmia are lacking, we can only speculate about the available studies on nonsurgical patients. We describe four patients during general anesthesia and propose intraoperative and postoperative monitoring (the first 36 h).

The use of indomethacin in the treatment of plateau waves: effects on cerebral perfusion and oxygenation.

OBJECT: Plateau waves are sudden and steep increases in intracranial pressure (ICP) that can develop in patients with cerebral injuries, reduced pressure-volume compensatory reserve, and preserved autoregulation. They are caused by cerebral vasodilation in response to a reduction in cerebral perfusion and are associated with increased cerebral blood volume and reduced cerebral blood flow. The authors evaluated the hypothesis that administration of indomethacin, a potent cerebral arteriolar vasoconstrictor, could interrupt the vicious cycle that occurs during plateau waves, extinguishing these waves and, ultimately, restoring cerebral perfusion and oxygenation. METHODS: Plateau waves developed in nine patients, seven with severe traumatic brain injury and two with intraparenchymal hemorrhage. One to four episodes of plateau waves per patient were treated with indomethacin (15-20 mg), which was delivered by an intravenous bolus injection. Each patient's mean arterial blood flow (MABP), ICP, cerebral perfusion pressure (CPP), and cerebral tissue PO2 were continuously monitored and the data obtained were stored in a personal computer. Each patient's jugular venous O2 saturation (SjvO2) and venoarterial difference in PCO2 were evaluated by intermittent blood sampling. During five episodes of plateau waves, middle cerebral artery flow velocities were evaluated by transcranial Doppler ultrasonography. Indomethacin extinguished all plateau waves. On average, the ICP decreased from an initial value of 58.9 +/- 11.6 mm Hg to 21.2 +/- 8.6 and 25.8 +/- 13.7 mm Hg after 5 and 10 minutes, respectively (p < 0.01). The MABP did not change significantly. As a consequence the CPP increased by 98 and 81% after 5 and 10 minutes, respectively (p < 0.01). Five and 10 minutes after indomethacin was administered, SjvO2 increased from an initial value of 50 +/- 10.5% to 62 +/- 7.6 and 59.9 +/- 9.3%, respectively (p < 0.01); the cerebral tissue PO2 increased from an initial value of 13.4 +/- 10.6 mm Hg to 23.6 +/- 9.58 and 21.9 +/- 9.2 mm Hg, respectively (p < 0.05); and the venous-arterial PCO2 decreased significantly. The mean and diastolic flow velocities increased significantly, whereas the pulsatility index decreased from 1.39 +/- 0.56 to 1.09 +/- 0.4 at 5 minutes and 1.06 +/- 0.36 at 10 minutes (p < 0.05). CONCLUSIONS: The findings confirm that plateau waves are caused by vasodilation and show that indomethacin, by constricting the cerebral arteries, is effective in extinguishing plateau waves, ultimately restoring cerebral perfusion and oxygenation.