The objective was to carry out a retrospective study of changes in regional cerebral oxygen saturation (rSO2) using the Somanetics Invos Cerebral Oximeter (SICO) in older patients undergoing prolonged major abdominal surgery. Since evidence is accumulating that detection and correction of falls in rSO2 may be associated with a reduced incidence of postoperative cognitive dysfunction, the study assessed the incidence and possible predisposing factors for significant falls in rSO2 and strategies for correction.

Data from 46 consecutive patients aged 55 yr or above undergoing major abdominal surgery were collected and studied. A SICO electrode was placed over the right forehead prior to commencement of anaesthesia and values of rSO2 were recorded automatically on a floppy disk at 20 s intervals throughout the procedure and until transfer of the patient to the postanaesthesia care unit. Anaesthesia and physiological data were routinely collected by the author on an anaesthetic record computer and transferred to an Excel spreadsheet for analysis.

Average duration of the surgery exceeded 7 h. Average blood loss was 1363 mL (interquartile range 500–2000). In 11 of the 46 patients the rSO2 drop exceeded 20%, and in six, there was a significant temporal association of rSO2 drop with ongoing major haemorrhage. In 23 of the 46 patients, a maximum drop in rSO2 occurred, which was about 15% or more. Fall in rSO2 in the 46 patients significantly correlated with blood loss (P < 0.05) and percentage fall in haemoglobin (Hb) (P = 0.01) but not with lowest Hb. Despite maintenance of conventional haemodynamic parameters such as systolic blood pressure (BP) in most patients, the fall in rSO2 seemed only reversible by blood transfusion. In five of the six patients who experienced the greatest decline in rSO2 during haemorrhage, there was no correlation between fall in rSO2 and systolic BP.

This retrospective study confirms that a significant reduction in rSO2 is a common accompaniment to prolonged major abdominal surgery in elderly patients, especially if associated with blood loss, and is correctable by blood transfusion. In most cases, these changes would have gone unnoticed with conventional monitoring.

Pain on injection is still a problem with propofol. The purpose of the study was to compare the effectiveness of diphenhydramine and lidocaine on pain caused by propofol at the site of injection.

One hundred and eighty ASA I–II adults undergoing elective surgery were randomly assigned into three groups of 60 each. Group I (placebo) received 2 mL normal saline, Group II received 2 mL (40 mg) 2% lidocaine and Group III received 2 mL (20 mg) diphenhydramine intravenously (i.v.) during a 1-min venous occlusion, followed by propofol into a cephalic forearm vein of the antecubital fossa. Pain assessment was made immediately after propofol injection.

In the placebo group 25 (41.7%) patients experienced pain during propofol injection as compared to 2 (3.3%) and 3 (5.0%) in the lidocaine and diphenhydramine groups, respectively. The prevalence of pain and pain score were significantly less in both the lidocaine and diphenhydramine groups than in the placebo group (P= 0.00). No difference was found between the diphenhydramine and lidocaine groups (P = 0.60).

Previous injection of diphenhydramine with venous occlusion can be considered as an alternative to lidocaine for reducing the prevalence of pain caused by injection of propofol into peripheral veins.

The objective of the study was to assess the safety of training fibre-optic intubation performed under propofol light general anaesthesia in patients with an anticipated difficult intubation.

Patients with ear, nose and throat cancer having at least two criteria for anticipated difficult intubation and scheduled for fibre-optic intubation were included prospectively. In 26 patients, intubation was performed by an anaesthesia resident (under senior supervision), whereas in 20 patients, it was performed by a senior anaesthesiologist. All patients received propofol light general anaesthesia adjusted to maintain both loss of consciousness and spontaneous ventilation.

Of the 46 patients, 45 had successful fibre-optic intubation, and one needed a rescue procedure because of hypoxaemia. Residents failed to intubate four patients, who were easily intubated by the senior. Episodic hypoxaemia (SPO2 < 90%) occurred in three patients in each group. No statistically significant difference was found between junior and senior neither on the duration of the procedure (9.3 ± 4.9 vs. 7.5 ± 4.0 min) nor on the propofol consumption (197 ± 130 vs. 193 ± 103 mg) or the ETCO2 at the end of the procedure (36 ± 6 vs. 38 ± 6 mmHg), respectively.

Teaching fibre-optic tracheal intubation in patients with anticipated difficult intubation and sedated with propofol did not increase morbidity significantly compared with an experienced anaesthesiologist. Fibre-optic intubation under propofol light general anaesthesia could be safely performed by a resident as long as a senior anaesthesiologist is permanently present, spontaneous ventilation is maintained and a rescue oxygenation technique is immediately available.

Respiratory variations in pulse oximetry plethysmographic waveform amplitude (ΔPOP) are related to respiratory variations in arterial pulse pressure (ΔPP) in the critical care setting. The aims of this study were to test the hypothesis that in mechanically ventilated patients undergoing general anaesthesia, ΔPOP calculation is feasible and can detect changes in preload.

Twenty-five mechanically ventilated patients were studied immediately after induction of general anaesthesia. Haemodynamic data (mean arterial pressure [MAP], central venous pressure [CVP], ΔPP and ΔPOP) were recorded at baseline, before and after tilting the patient from anti-Trendelenburg to Trendelenburg position in order to induce preload changes.

Change from anti-Trendelenburg to Trendelenburg position induced changes in MAP (58 ± 9 to 67 ± 10 mmHg, P < 0.05), CVP (4 ± 4 to 13 ± 5 mmHg, P < 0.05), ΔPP (14 ± 8 to 7 ± 5%, P < 0.05) and ΔPOP (17 ± 12 to 9 ± 5%, P < 0.05). There was a significant relationship between ΔPOP in anti-Trendelenburg position and percent change in MAP after volume expansion (r = 0.82; P < 0.05).

ΔPOP can be determined in the operating room and is influenced by changes in preload. This new index has potential clinical applications for the prediction of fluid responsiveness.

The A-Line® auditory evoked potential index (AAI) (AEP Monitor/2, Danmeter A/S, Odense, Denmark) is a newly developed composite parameter representing the degree of hypnosis. We conducted a prospective, observational study to explore the performance and validity of the AAI during conventional sedation for gastrointestinal (GI) endoscopy.

Thirty adults of either sex, age <65, scheduled for combined oesophagogastroduodenoscopy (OGD) and colonoscopy under sedation with intravenous (i.v.) midazolam and alfentanil were enrolled. The sedative end-point was set at the Observer’s Assessment of Alertness/Sedation (OAA/S) score less than 4. An AEP Monitor/2 was used in all patients. AAI, sedation scores, heart rate (HR), blood pressure (BP) and SPO2 were recorded every 2 min up to the end of the procedure. Receiver operator characteristic analysis was used to test validity and to select optimal sedation.

There was a significantly positive correlation between AAI and OAA/S scores (ρ = 0.886; P < 0.001). The AAI also showed significant differences between subsequent levels of sedation scores (P < 0.001). AAI greater than 54 indicated fully awake or minimal sedation and values between 54 and 42 were suggestive of moderate sedation. Values between 42 and 34 were associated with moderate to deep sedation and readings below 34 were associated with deep sedation. The relative risk of SPO2 < 95% for OAA/S = 2 compared with 3 was 15.98 (95% confidence interval (CI): 3.94–64.81).

AAI is an effective tool for monitoring sedation during GI endoscopy induced by i.v. midazolam and alfentanil.

Tissue depletion of adenosine during endotoxaemia has previously been described in the lung. Therapeutic approaches to prevent adenosine depletion and the role of A1 and A2 receptor agonists, however, have not been investigated until now.

In isolated and ventilated rabbit lungs, it was tested whether pretreatment with adenosine A1 agonist 2-chloro-N6-cyclopentyladenosine (CCPA; 10−7 mol, n = 6) or A2 receptor agonist 5′-(N-cyclopropyl)-carboxyamido adenosine (CPCA; 10−7 mol, n = 6) prior to injection of lipopolysaccharide (LPS) (500 pg mL−1) influenced pulmonary artery pressure (PAP), pulmonary energy content and oedema formation as compared with controls, solely infused with LPS (n = 6). Release rates of adenosine and uric acid were determined by high-performance liquid chromatography. Pulmonary tissue concentrations of high-energy phosphates were measured and the adenine nucleotide pool, adenosine 5′-triphosphate (ATP)/adenosine 5′-diphosphate (ADP) ratio and adenylate energy charge of the pulmonary tissue were calculated.

Administration of LPS induced increases in PAP within 2 h up to 20.8 ± 2.9 mmHg (P < 0.01). While pretreatment with the A1 agonist merely decelerated pressure increase (13.8 ± 1.1 mmHg, P < 0.05), the A2 agonist completely suppressed the pulmonary pressure reaction (9.6 ± 1.0 mmHg, P < 0.01). Emergence of lung oedema after exclusive injection of LPS up to 12.0 ± 2.9 g was absent after A1 (0.6 ± 0.5 g) and A2 (−0.3 ± 0.2 g) agonists. These observations were paralleled by increased adenosine release rates compared with LPS controls (P < 0.05). Moreover, tissue concentrations of ADP, ATP, guanosine 5′-diphosphate, guanosine 5′-triphosphate, nicotinamide-adenine-dinucleotide and creatine phosphate were significantly reduced after LPS. Consequently, the calculated tissue adenine nucleotide pool and the adenylate energy charge increased after adenosine receptor stimulation (P = 0.001).

Adenosine A1- and A2-receptor agonists reduced LPS-induced vasoconstriction and oedema formation by maintenance of tissue energy content. Thus, adenosine receptor stimulation, in particular of the A2 receptor, might be beneficial during acute lung injury.

The kind of fluid for correcting hypovolaemia is still a focus of debate. In a prospective, randomized, controlled and double-blind study in patients undergoing major abdominal surgery, a total balanced volume replacement strategy including a new balanced hydroxyethyl starch (HES) solution was compared with a conventional, non-balanced fluid regimen.

In Group A (n = 15), a new balanced 6% HES 130/0.42 was given along with a balanced crystalloid solution; in Group B (n = 15), an unbalanced conventional HES 130/0.42 plus an unbalanced crystalloid (saline solution) were administered. Volume was given when mean arterial pressure (MAP) was <65 mmHg and central venous pressure (CVP) minus positive end-expiratoric pressure (PEEP) level was <10 mmHg. Haemodynamics, acid–base status, coagulation (thrombelastography (TEG)) and kidney function (including kidney-specific proteins, N-acetyl-beta-d-glucosaminidase (beta-NAG) and alpha-1-microglobulin) were measured after induction of anaesthesia, at the end of surgery, 5 and 24 h after surgery.

Group A received 3533 ± 1302 mL of HES and 5333 ± 1063 mL of crystalloids, in Group B, 3866 ± 1674 mL of HES and 5966 ± 1202 mL of crystalloids were given. Haemodynamics, laboratory data, TEG data and kidney function were without significant differences between the groups. Cl− concentration and base excess (−5 ± 2.4 mmol L−1 vs. 0.4 ± 2.4 mmol L−1) were significantly higher in patients of Group B than of Group A.

A complete balanced volume replacement strategy including a new balanced HES preparation resulted in significantly less derangement in acid–base status compared with a non-balanced volume replacement regimen. The new HES preparation showed no negative effects on coagulation and kidney function.

Alfentanil was reported to relax the rat aorta by direct action on the vascular smooth muscle. The aims of this in vitro study were to examine the effect of alfentanil on phenylephrine-induced contractions in the rat aorta and to determine the cellular mechanism associated with this process.

Endothelium-denuded aortic rings were suspended in order to record isometric tension. In the rings with or without 10−6 mol naloxone or 10−5 mol verapamil, the concentration–response curves for phenylephrine and potassium chloride were generated in the presence or absence of alfentanil (10−6, 5 × 10−5, 10−4 mol). In the rings exposed to a calcium-free isotonic depolarizing solution, the contractile response induced by the addition of calcium was assessed in the presence or absence of alfentanil (5 × 10−5, 10−4 mol).

Alfentanil (5 × 10−5, 10−4 mol) attenuated (P < 0.05) the phenylephrine-induced contraction in the ring with or without 10−6 mol naloxone but had no effect on the phenylephrine-induced contraction in the rings pretreated with verapamil. Alfentanil (5 × 10−5, 10−4 mol) produced a significant rightward shift (P < 0.01) in the potassium chloride dose–response curve, and attenuated the contractile response (P < 0.001) induced by calcium in the calcium-free isotonic depolarizing solution in a dose-dependent manner.

A supraclinical dose of alfentanil attenuates the phenylephrine-induced contraction via an inhibitory effect on calcium influx by blocking the l-type calcium channels in the rat aortic vascular smooth muscle.

Arterial oxygenation may be compromised in morbidly obese patients undergoing bariatric surgery. The aim of this study was to evaluate the effect of a vital capacity manoeuvre (VCM), followed by ventilation with positive end-expiratory pressure (PEEP), on arterial oxygenation in morbidly obese patients undergoing open bariatric surgery.

Fifty-two morbidly obese patients (body mass index >40 kg m−2) undergoing open bariatric surgery were enrolled in this prospective and randomized study. Anaesthesia and surgical techniques were standardized. Patients were ventilated with a tidal volume of 10 mL kg−1 of ideal body weight, a mixture of oxygen and nitrous oxide (FiO2 = 40%) and respiratory rate was adjusted to maintain end-tidal carbon dioxide at a level of 30–35 mmHg. After abdominal opening, patients in Group 1 had a PEEP of 8 cm H2O applied and patients in Group 2 had a VCM followed by PEEP of 8 cm H2O. This manoeuvre was defined as lung inflation by a positive inspiratory pressure of 40 cm H2O maintained for 15 s. PEEP was maintained until extubation in the two groups. Haemodynamics, ventilatory and arterial oxygenation parameters were measured at the following times: T0 = before application of VCM and/or PEEP, T1 = 5 min after VCM and/or PEEP and T2 = before abdominal closure.

Patients in the two groups were comparable regarding patient characteristics, surgical, haemodynamic and ventilatory parameters. In Group 1, arterial oxygen partial pressure (PaO2) and arterial haemoglobin oxygen saturation (SaO2) were significantly increased and alveolar-arterial oxygen pressure gradient (A-aDO2) decreased at T2 when compared with T0 and T1. In Group 2, PaO2 and SaO2 were significantly increased and A-aDO2 decreased at T1 and T2 when compared with T0. Arterial oxygenation parameters at T1 and T2 were significantly improved in Group 2 when compared with Group 1.

The addition of VCM to PEEP improves intraoperative arterial oxygenation in morbidly obese patients undergoing open bariatric surgery.