Summary

Background and objective: It is important to provide good postoperative analgesia after discharge from day case surgery. The usefulness of intra-articular morphine for analgesia after day case knee arthroscopy remains controversial. A large dose of morphine intra-articularly may provide a good long-lasting analgesia, but its efficacy and pharmacokinetics are not known and may be no better than intramuscular morphine. We compared the effect of 10 mg intra-articular and intramuscular morphine for 24 h post-injection in a randomized double-blind study.

Methods: Forty adults undergoing knee arthroscopy were recruited and received either 10 mg morphine intra-articularly or intramuscularly. Our primary outcome was overall visual analogue assessment of pain (0–100 mm scale where 0 is no pain and 100 is worst possible pain) between 4 h (on discharge) and 24 h (postoperatively). Plasma morphine concentrations were measured at 15 min, and 1, 2, 4 and 24 h. The use of additional analgesia was noted.

Results: The assessment of pain experienced between discharge (4 h) and 24 h was significantly better in the intra-articular (n = 20; mean ± SD: 18 ± 19) than the intramuscular (n = 19; mean ± SD: 34 ± 20) group (P = 0.027). The number of patients consuming any additional analgesia between discharge and 24 h was significantly lower in the intra-articular morphine group (P = 0.038), with 4 (20%) patients in the intra-articular group and 11 (60%) patients in the intramuscular group consuming supplementary analgesia. There were no differences in plasma morphine concentrations between the groups.

Conclusions: A large dose of intra-articular morphine provided better analgesia than the same dose of intramuscular morphine, low plasma morphine levels suggesting a peripheral mechanism.

Summary

Background and objective: The aim of this study was to test the efficacy of positive end-expiratory pressure (PEEP) to the dependent lung during one-lung ventilation, taking into consideration underlying lung function in order to select responders to PEEP.

Methods: Forty-six patients undergoing open-chest thoracic surgical procedures were studied in an operating room of a university hospital. Patients were randomized to receive zero end-expiratory pressure (ZEEP) or 10 cmH2O of PEEP to the dependent lung during one-lung ventilation in lateral decubitus. The patients were stratified according to preoperative forced expiratory volume in 1 s (FEV1) as an indicator of lung function (below or above 72%). Oxygenation was measured in the supine position, in the lateral decubitus with an open chest, and after 20 min of ZEEP or PEEP. The respiratory system pressure–volume curve of the dependent hemithorax was measured in supine and open-chest lateral decubitus positions with a super-syringe.

Results: Application of 10 cmH2O of PEEP resulted in a significant increase in PaO2 (P < 0.05). This did not occur in ZEEP group, considered as a time matched control. PEEP improved oxygenation only in patients with high FEV1 (from 11.6 ± 4.8 to 15.3 ± 7.1 kPa, P < 0.05). There was no significant change in the low FEV1 group. Dependent hemithorax compliance decreased in lateral decubitus, more in patients with high FEV1 (P < 0.05). PEEP improved compliance to a greater extent in patients with high FEV1 (from 33.6 ± 3.6 to 48.4 ± 3.9 mL cmH2O−1, P < 0.05).

Conclusions: During one-lung ventilation in lateral decubitus, PEEP applied to the dependent lung significantly improves oxygenation and respiratory mechanics in patients with rather normal lungs as assessed by high FEV1.

Summary

Background and objective: This prospective observational study analyses cardiovascular changes in adult patients with acute respiratory distress syndrome (ARDS) during transition from pressure-controlled ventilation to high-frequency oscillatory ventilation (HFOV), using transoesophageal echocardiography (TOE) and invasive haemodynamic monitoring.

Methods: Nine patients (median age 65 years; range 42–70) with ARDS were studied. HFOV was started and maintained with an adjusted mean airway pressure of 5 cmH2O above the last measured mean airway pressure during pressure-controlled ventilation. Haemodynamic and TOE measurements were performed in end-expiration during baseline pressure-controlled ventilation, and again 5 and 30 min after the start of during uninterrupted HFOV.

Results: Right atrial pressure increased immediately (P = 0.004). After 30 min, pulmonary arterial occlusion pressure increased (P = 0.008), cardiac index decreased (P = 0.01), stroke volume index decreased (P = 0.02) and both left ventricular end-diastolic and end-systolic area indices decreased (P = 0.02). Fractional area change, left ventricular end-systolic wall stress, heart rate, mean arterial pressure and mean pulmonary artery pressure remained unchanged.

Conclusions: Transition to HFOV at a mean airway pressure of 5 cmH2O above that during pressure-controlled ventilation induced significant, but clinically minor, haemodynamic effects, which are most probably due to airway pressure-related preload reduction.

Summary

Background and objectives: To evaluate the effects of cardiopulmonary bypass (CPB) on platelet function in children undergoing open-heart surgery.

Methods: Data from 16 consecutive children undergoing cardiac surgery with CPB were prospectively collected. Blood samples of 10 mL were collected via the central venous line immediately before and after CPB for CD62 measurements by flow cytometry.

Results: Ten children had acyanotic heart disease (median age 3 yr, range 1.8–14) and six had a cyanotic defect (median age 4 yr, range 2–14). The platelet count decreased significantly with CPB in both groups: from 163.5 (130–201) to 93.5 (57–186) × 103 μL−1 in acyanotic children and from 139.5 (77–212) to 75 (43–99) × 103 μL−1 in cyanotic children (P < 0.0001). The percentage of activated platelets was significantly lower in acyanotic children at baseline: 1% (0–23%) vs. 5% (3–8%) (P = 0.07). CPB increased the percentage of activated platelets significantly in both groups: post-bypass the values were 10% (range 1–17%) in acyanotic children and 7% (range 1–30%) in cyanotic children (P = 0.03). The increase in the percentage of activated platelets did not differ between the two study groups (P = 0.11).

Conclusion: CPB induces significant platelet activation in children undergoing open-heart surgery.

Summary

Background and objective: The beta-adrenergic blocker esmolol and the alpha 2-adrenergic agonist dexmedetomidine have the potential to decrease perioperative myocardial ischaemia. The pathophysiological mechanisms involved in these anti-ischaemic properties have not been thoroughly studied. We compared the effects of esmolol and dexmedetomidine on two indices of overall myocardial oxygen demand and on directly measured myocardial oxygen consumption of the left anterior coronary artery territory.

Methods: Eleven mongrel dogs were instrumented to measure aortic and left ventricular pressure, aortic and left anterior coronary artery flow and myocardial wall thickening. Variables related to myocardial oxygen metabolism were also determined. Measurements were performed during four sequential experimental conditions in each dog (Control 1: esmolol; Control 2: dexmedetomidine).

Results: Esmolol and dexmedetomidine decreased haemodynamic indices of myocardial oxygen demand to a similar extent: esmolol decreased the rate–pressure product by 16 ± 3% and the pressure–work index (PWI) by 16 ± 3%, dexmedetomidine decreased the rate–pressure product by 26 ± 3% and the PWI by 16 ± 7%. However, these similar decreases resulted from different haemodynamic effects of the two study drugs. Dexmedetomidine had a more pronounced bradycardic effect than esmolol (P = 0.01) and increased systolic aortic pressure (SAP) by 15 ± 4% while esmolol decreased SAP by 8 ± 2% (P < 0.01). dP/dtmax and regional myocardial area decrease were lower after esmolol than after dexmedetomidine. Neither drug had an effect on myocardial oxygen consumption.

Conclusions: Esmolol and dexmedetomidine decreased two haemodynamic indices of overall myocardial oxygen demand to a similar extent but neither drug decreased directly measured myocardial oxygen consumption in the territory of the left anterior descending artery.

Summary

Background: Lidocaine has actions potentially of benefit during ischaemia–reperfusion. Neutrophils and endothelial cells have an important role in ischaemia–reperfusion injury.

Methods: Isolated human neutrophil CD11b and CD18, and human umbilical vein endothelial cell (HUVEC) ICAM-1 expression and supernatant IL-1β concentrations in response to hypoxia–reoxygenation were studied in the presence or absence of different concentrations of lidocaine (0.005, 0.05 and 0.5 mg mL−1). Adhesion molecule expression was quantified by flow cytometry and IL-1β concentrations by ELISA. Differences were assessed with analysis of variance and Student–Newman–Keuls as appropriate. Data are presented as mean ± SD.

Results: Exposure to hypoxia–reoxygenation increased neutrophil CD11b (94.33 ± 40.65 vs. 34.32 ± 6.83 mean channel fluorescence (MCF), P = 0.02), CD18 (109.84 ± 35.44 vs. 59.05 ± 6.71 MCF, P = 0.03) and endothelial ICAM-1 (146.62 ± 16.78 vs. 47.29 ± 9.85 MCF, P < 0.001) expression compared to normoxia. Neutrophil CD18 expression on exposure to hypoxia–reoxygenation was less in lidocaine (0.005 mg mL−1) treated cells compared to control (71.07 ± 10.14 vs. 109.84 ± 35.44 MCF, P = 0.03). Endothelial ICAM-1 expression on exposure to hypoxia–reoxygenation was less in lidocaine (0.005 mg mL−1) treated cells compared to control (133.25 ± 16.05 vs. 146.62 ± 16.78 MCF, P = 0.03). Hypoxia–reoxygenation increased HUVEC supernatant IL-1β concentrations compared to normoxia (3.41 ± 0.36 vs. 2.65 ± 0.21 pg mL−1, P = 0.02). Endothelial supernatant IL-1β concentrations in lidocaine-treated HUVECs were similar to controls.

Conclusions: Lidocaine at clinically relevant concentrations decreased neutrophil CD18 and endothelial ICAM-1 expression but not endothelial IL-1β concentrations.

Summary

Background and objective: An acute inflammatory response associated with cerebral ischaemia–reperfusion contributes to the development of brain injury. Aprotinin has potential, though unexplained, neuroprotective effects in patients undergoing cardiac surgery.

Methods: Human neutrophil CD11b/CD18, endothelial cell intercellular adhesion molecule-1 (ICAM-1) expression and endothelial interleukin (IL)-1β supernatant concentrations in response to in vitro hypoxia–reoxygenation was studied in the presence or absence of aprotinin (1600 KIU mL−1). Adhesion molecule expression was quantified using flow cytometry and IL-1β concentrations by enzyme-linked immunosorbent assay. Data were analysed using ANOVA and post hoc Student–Newman–Keuls test as appropriate.

Results: Exposure to 60-min hypoxia increased neutrophil CD11b expression compared to normoxia (170 ± 46% vs. 91 ± 27%, P = 0.001) (percent intensity of fluorescence compared to time 0) (n = 8). Hypoxia (60 min) produced greater upregulation of CD11b expression in controls compared to aprotinin-treated neutrophils [(170 ± 46 % vs. 129 ± 40%) (P = 0.04)] (n = 8). Hypoxia–reoxygenation increased endothelial cell ICAM-1 expression (155 ± 3.7 vs. 43 ± 21 mean channel fluorescence, P = 0.0003) and IL-1β supernatant concentrations compared to normoxia (3.4 ± 0.4 vs. 2.6 ± 0.2, P = 0.02) (n = 3). Hypoxia–reoxygenation produced greater upregulation of ICAM-1 expression [(155 ± 3.3 vs. 116 ± 0.7) (P = 0.001)] and IL-1β supernatant concentrations [(3.4 ± 0.3 vs. 2.6 ± 0.1) (P = 0.01)] in controls compared to aprotinin-treated endothelial cell preparation (n = 3).

Conclusions: Hypoxia–reoxygenation-induced upregulation of neutrophil CD11b, endothelial cell ICAM-1 expression and IL-1β concentrations is decreased by aprotinin at clinically relevant concentrations.