Thirty-two members of staff from the Ear, Nose and Throat Department at Warrington General Hospital were asked to estimate blood loss in commonly encountered epistaxis scenarios. Results showed that once the measured volume was above 100 ml, visual estimation became grossly inaccurate. Comparison of medical and non-medical staff showed under-estimation was more marked in the non-medical group. Comparison of doctors versus nurses showed no difference in estimation, and no difference was found between grades of staff.

Background and objective: Volatile anaesthetic agents are known to influence neutrophil function. The aim was to determine the effect of chronic occupational exposure to volatile anaesthetic agents on the rate of neutrophil apoptosis among anaesthetists. To test this hypothesis, we compared the rate of neutrophil apoptosis in anaesthetists who had been chronically exposed to volatile anaesthetic agents with that in unexposed volunteers.

Methods: Venous blood (20 mL) was withdrawn from 24 ASA I-II volunteers, from which neutrophils were isolated, and maintained in culture. At 1, 12 and 24 h in culture, the percentage of neutrophil apoptosis was assessed by dual staining with annexin V-FITC and propidium iodide.

Results: At 1 h (but not at 12 and 24 h) in culture, the rate of neutrophil apoptosis was significantly less in the anaesthetists – 13.8 (12.9%) versus 34.4 (12.1%) (P = 0.001).

Conclusions: Chronic occupational exposure to volatile anaesthetic agents may inhibit neutrophil apoptosis. This may have implications for anaesthetists and similarly exposed healthcare workers in terms of the adequacy of their inflammatory response.

Patients receiving anticoagulants offer a challenge to anaesthesiologists. The issue of spinal haematoma following central neuraxial block in such patients is a contentious issue. Although rare, with an estimated incidence of <1 : 150 000 for epidural blocks and 1 : 220 000 for spinal anaesthetics in patients with normal coagulation status, this is an emergency situation with a potentially grave prognosis. The review presents cases of spinal haematomata that have occurred in the last 5 years, both spontaneously and after central neuraxial blockade. Of the 60 cases reported in the literature, 33% occurred following central neuraxial block and, of these, 55% were associated with concomitant use of anticoagulants. The pharmacology of the newer and older anticoagulants is also described. The variety of risk factors and diverse recommendations that have been described in these patients are reviewed.

Background and objective: It was previously reported that topical ketamine inhibits albumin extravasation in a rat chemical peritonitis model. Using the same model, the present study investigated whether intravenous ketamine inhibited this extravasation.

Methods: Twenty-four rats anaesthetized with pentobarbital (75 mg kg−1) were randomly assigned to two groups: ketamine and a 0.9% NaCl (saline) group (n = 12 each). Ketamine 1% or saline 0.1 mL kg−1 min−1 was given intravenously for 60 min to the respective group. After the abdomen had been opened, peritonitis was elicited by topically applying a filter paper containing 0.02 M HCl 0.07 mL onto the surface of the appendix or caecum for 5 min. Fifteen minutes after removal of the filter paper, Evans' blue dye (50 mg kg−1) was injected intravenously. The extravasated dye was colorimetrically quantified by a spectrophotometer at 620 nm.

Results: The infusion of ketamine significantly reduced Evans' blue extravasation: 5.26 (range 4.18–6.34) μg per 100 mg tissue compared with the saline group control: 6.81 (5.93−7.69) μg per 100 mg tissue (P < 0.05).

Conclusions: It is suggested that ketamine anaesthesia may reduce albumin extravasation in inflammatory tissues.

Malignant hyperthermia is an autosomal-dominant inherited disorder of the skeletal muscle cell characterized by a hypermetabolic response to all commonly used inhalational anaesthetics and depolarizing muscle relaxants. The clinical syndrome includes muscle rigidity, hypercapnia, tachycardia and myoglobinuria as result of increased carbon dioxide production, oxygen consumption and muscle membrane breakdown. In human beings and animals susceptible to malignant hyperthermia, it is generally accepted that an increase in the level of myoplasmic free calcium is the cause of the syndrome. Various hypotheses have been proposed to account for the increase of intracellular calcium levels, e.g. a defect in the calcium release channel of the sarcoplasmic reticulum (ryanodine receptor), an abnormality of the excitation-contraction coupling mechanisms, or alterations in second messenger systems of skeletal muscles. This review gives an overview of the main features of this disease and recent advances in research including pathophysiology, treatment, diagnosis and genetics as well as association with other disorders.

Background and objective Inflammatory liver dysfunction in rats leads to a prolonged vecuronium-induced neuromuscular blockade due to insufficient metabolism. A coexisting resistance against the drug partly counteracts this prolongation. The present study investigates the pharmacodynamics of atracurium whose metabolism does not depend on liver function.

Methods Male Sprague–Dawley rats (n = 14; 290 ± 30 g) were randomly allocated to either a group in which liver inflammation was induced by intravenous injection of 60 mg kg−1 heat-killed Corynebacterium parvum or to a control group. On day 5 after injection, liver function was assessed using the aminopyrine breath test. Under propofol anaesthesia, duration of action of atracurium (4.8 mg kg−1) was measured by evoked mechanomyography (stimulation of the sciatic nerve; contraction of the gastrocnemius muscle). Nitric oxide concentrations, as variables for the severity of the inflammation, were assessed by measurement of nitrite/nitrate plasma concentrations.

Results In C. parvum-injected rats, nitrite/nitrate plasma concentrations were increased (972 ± 597 vs. 25 ± 7 μmol L−1), the aminopyrine turnover was depressed (1.7 ± 0.4% vs. 3.5 ± 0.5%), and the atracurium-induced neuromuscular blockade was shortened (372 ± 128 s vs. 1081 ± 234 s).

Conclusions A systemic inflammatory response syndrome with liver dysfunction results in decreased sensitivity to atracurium. Further investigations are needed regarding a possible up-regulation of acetylcholine receptors or an increased protein binding of atracurium during sepsis to clarify reasons behind this phenomenon.

Background and objective Laboratory stress studies found that acute psychological stresses may elicit changes in leukocyte numbers similar to those occurring in physical stresses. Both types of stress evoke – mainly by release of catecholamines – leukocytosis resulting from a release of natural killer cells (NK-cells), of CD8+ T-cells, of monocytes and of neutrophils. However, there is little proof that laboratory stress models can be applied to daily clinical routines. As a likely inductor of an immunological stress response the setting of retrobulbar anaesthesia prior to intraocular surgery permits the study of a short-term painful anaesthetic procedure under highly standardized conditions. This was examined in 16 female patients.

Methods Counts of leukocyte subsets, serum cortisol and cardiovascular variables were measured 30 min and 1 min prior to retrobulbar anaesthesia as well as 2, 15 and 45 min afterwards.

Results The setting of retrobulbar anaesthesia induced an increase in total leukocytes [+380 cells μL−1; P < 0.01 (means; significance level)] mainly due to rising counts of neutrophils (+241 cells μL−1, P < 0.01). Of all lymphocyte subpopulations, natural killer cells increased most markedly (+64 cells μL−1; P < 0.01). Furthermore, the retrobulbar block induced an increase in systolic arterial pressure (+15.2 mmHg; P < 0.01).

Conclusion These changes in immunological and cardiovascular variables are considered to be elements of a sympatho-adrenal stress reaction; catecholamines are considered to induce a demargination of leukocytes by binding to β2-adrenoceptors and by modifying the avidity state of adhesion molecules.

Diabetes mellitus is the most common metabolic disease and its incidence is increasing. New classifications have been recently proposed based upon a better knowledge of pathogenesis, mechanisms of glucose transport and insulin resistance. The perioperative care of diabetic patients is less dependent on blood-glucose control, which needs to be exceptionally tight, and is usually easily obtained thanks to pharmacological improvements, human insulins and analogues, technical progress with blood-glucose monitoring at the bedside and infusion with constant flow rates. More important is the influence of end-organ pathology, often clinically silent, which must be carefully assessed during the preoperative evaluation. The organ impairments concern especially the heart, but also all those organs that were modified by abnormal glycosylated proteins. The pre-existing pathology has many consequences on anaesthesia management; the anaesthetic technique depends essentially on their existence. A better long-term control of diabetes both for Type 1 and Type 2 by insulins, and the new oral anti-diabetic drugs reduce the incidence of the end-organ pathology and the risk linked to organ failures in the perioperative period.

The elimination of procalcitonin and the course of plasma concentrations during continuous veno-venous haemodiafiltration were measured in patients with sepsis or multiple organ dysfunction syndrome, because these patients are a main target group for the measurement of procalcitonin and often require renal replacement therapy. Procalcitonin was measured in the prefilter plasma and the filtrate at 5 min, 15 min and 1, 2, 4, 6, 12, 24 h after set-up of continuous veno-venous haemodiafiltration. In a prospective study, 19 patients with plasma levels of procalcitonin >3ng mL−1 and acute oliguric renal failure treated with continuous veno-venous haemodiafiltration using a polysulphone membrane, were evaluated for the study of clearance. Twenty-one control patients (procalcitonin <2ng mL−1) were studied to determine whether filtration itself induced a procalcitonin response. No interventions were required. In patients with low procalcitonin concentrations (procalcitonin <2ng mL−1) continuous veno-venous haemodiafltration did not cause a rise in procalcitonin. In patients with increased procalcitonin plasma concentrations (>3ng mL−1), the protein was removed through the polysulphone membrane, with a final clearance of 4 mL min−1 after the initial adsorption period (clearance 0.4–0.9mL min−1 during the first hour of continuous veno-venous haemodiafiltration). Thus, on the average, approximately 10% of plasma concentrations were measurable in the filtrate ultimately. However, procalcitonin plasma levels were not significantly altered during continuous veno-venous haemodiafiltration (86% of the initial concentration after 24 h). Although procalcitonin is removed from the plasma during continuous veno-venous haemodiafiltration in measurable amounts plasma procalcitonin concentrations did not change significantly during haemodiafiltration. Procalcitonin thus can also be used as a diagnostic parameter in patients undergoing continuous veno-venous haemodiafiltration.