Profound and complex coagulation disorders are encountered during liver transplantation. They include preoperative coagulation disorders related to the liver disease and haemostatic changes related to the procedure itself. They commonly lead to increased intraoperative bleeding, especially due to increased fibrinolysis, the contribution of which can be demonstrated by the relative efficacy of antifibri-nolytics. Given the multifactorial nature of bleeding in liver transplantation, preoperative coagulation tests cannot predict blood loss even if some statistical relationship is occasionally found.Preoperative correction of coagulation defects has not been shown to be effective in reducing intraoperative bleeding. Throughout the procedure, a rapid and sensitive method for monitoring coagulation is necessary in order to guide the rational use of blood components and pharmacological agents. The usefulness of such a method to assist management of blood loss or blood component requirements is poorly documented and controversial.

Background and objective Volatile anaesthetic effects on altering tone after blocking nitric oxide synthase, cyclo-oxygenase-prostaglandin synthase and KATP channel pathways are controversial. We examined in isolated guinea pig hearts whether anaesthetics alter bradykinin and 5-hydroxytryptamine-induced effects on coronary flow and percentage oxygen extraction after blocking these pathways.

Methods Before and during exposure to sevo-flurane, halothane or isoflurane, hearts were infused with 10−13–10−8 M bradykinin, or 10−8–10−6 M 5-hydroxytryptamine (serotonin), with either L-NAME, indomethacin, or glibenclamide. Bradykinin or 5-hydroxytryptamine alone increased flow and decreased percentage oxygen extraction in a concentration-dependent manner; these effects were largely blocked by L-NAME (nitro-L-arginine methylester), which also decreased basal flow and increased basal percentage oxygen extraction.

Results The anaesthetics restored bradykinin and 5-hydroxytryptamine-induced increases in flow or decreases in percentage oxygen extraction after inhibition by L-NAME. Indomethacin or glibenclamide alone had little effect on basal flow and percentage oxygen extraction. The anaesthetics restored bradykinin and 5-hydroxytryptamine-induced increases in flow or decreases in percentage oxygen extraction after inhibition by L-NAME. Indomethacin or glibenclamide alone had little effect on basal flow and percentage oxygen extraction. Drug-induced increases in flow and decreases in percentage oxygen extraction in the absence or presence of glibenclamide or indomethacin were not altered at either of the two concentrations of anaesthetics.

Conclusions Endothelium-dependent vasodilatation is not affected by blocking prostaglandin release or KATP channels in the intact heart even in the presence of an anaesthetic. However, the diminished responses to vasodilators after nitric oxide synthase inhibition is largely restored or enhanced by anaesthetics.

Background and objective The effect of anaesthesia induced by intrathecal injection of 6.3% MgS04 or 4% lidocaine on intracellular electrolyte homeostasis in spinal cord neurones of a rat model was investigated. Methods Intracellular Ca2+, Mg2+, Na+ and K+ concentrations were determined at different times after intrathecal administration of NaCI (saline, a control group), MgS04 or lidocaine.

Results In both thoracic and lumbar spinal cord segments, Ca2+ concentrations rose significantly 30min and 2 h after 6.3% MgSO4 injection, and after 24 h were still significantly increased compared with the values obtained from the control group which were subjected to sham ‘anaesthesia’ by saline injection (172,121 and 108ngmg−1 protein vs. control 23ngmg−1 protein, respectively, in the thoracic segment and 222, 229 and 176ngmg−1 protein vs. control 43ngmg−1 protein, respectively, in the lumbar segment). Lidocaine injection also produced a significant increase in intracellular Ca2+ in the thoracic and lumbar spinal cord segments (69, 64 and 53ngmg−1 protein vs. control 33.4 ngmg−1 protein and 26, 94 and 46ngmg−1 protein vs. 23ngmg−1 protein respectively). Only a modest rise in intracellular Mg2+ was observed after intrathecal MgS04 or lidocaine injection (27ngmg−1 protein vs. 23ngmg−1 protein). Na+ and K+ concentrations decreased 24 h after MgS04and 1h after lidocaine injection.

Conclusion Intrathecal anaesthesia by MgS04 or lidocaine alters intracellular electrolyte homeostasis in spinal cord neurones of experimental rats. A possible common mechanism of action via Ca2+ ion channels is discussed.

Background and objective We studied the influence of systemic (aortic) blood flow velocity on changes of cerebral blood flow velocity under isoflurane or sevoflurane anaesthesia.

Methods Forty patients (age: isoflurane 24–62 years; sevoflurane 24–61 years; ASA l–lll) requiring general anaesthesia undergoing routine spinal surgery were randomly assigned to either group. Cerebral blood flow velocity was measured in the middle cerebral artery by transcranial Doppler sonography (depth: 50–60 mm). Systemic blood flow velocity was determined by transthoracic Doppler sonography at the aortic valve. Heart rate, arterial pressure, arterial oxygen saturation and body temperature were monitored. After standardized anaesthesia induction (propofol, remifentanil, vecuronium) sevoflurane or isoflurane were used as single agent anaesthetics. Cerebral blood flow velocity and systemic blood flow velocity were measured in the awake patient (baseline) and repeated 5 min after reaching a steady state of inspira-tory and end-expiratory concentrations of 0.75, 1.00, nd 1.25 mean alveolar concentrations of either anaesthetic. To calculate the influence of systemic blood flow velocity on cerebral blood flow velocity, we defined the cerebral-systemic blood flow velocity index (CSvl). CSvl of 100% indicates a 1:1 relationship of changes of cerebral blood flow velocity and systemic blood flow velocity.

Results Isoflurane and sevoflurane reduced both cerebral blood flow velocity and systemic blood flow velocity. The CSvl decreased significantly at all three concentrations vs. 100% (isoflurane/sevoflurane: 0.75 MAC: 85 ± 25%/81 ± 23%, 1.0 MAC: 79 ± 19%/74 ± 16%, 1.25 MAC: 71 ± 16%/79 ± 21%; [mean ±SD] P% 0.0001). Conclusions The reduction of the CSvl vs. 100% indicates a direct reduction of cerebral blood flow velocity caused by isoflurane/sevoflurane, independently of systemic blood flow velocity.

Background and objective The endovascular treatment of abdominal aortic aneurysms has raised great interest amongst vascular surgeons. The aim of this study was to com pare the postoperative morbidity and mortality rates of endovascular treatment with those of open surgery, from the anaesthesiologist's standpoint.

Methods From January 1997 to June 2000, 425 consecutive patients with abdominal aortic aneurysms were referred for regular surgery. Thirty-nine patients who needed a visceral or renal artery revasculariza-tion, or a nephrectomy were excluded. The remaining 386 patients were studied in a prospective manner. Aneurysms were evaluated with spiral computerized tomography scanning and calibrated aortography. After informed consent, only those patients with a suitable vascular anatomy underwent endovascular treatment (n = 193). All other patients underwent open surgery and are considered as a control group n= 193). Endovascular treatment was performed by a femoral or an iliac retroperitoneal route. All stent-grafts were made to measure using auto-expandable stainless-steel stents covered with a standard polyester prosthetic graft.

Results Six patients in the endovascular treatment group needed to be converted to the open surgical technique (during the same operation) because of rupture of the iliac bifurcation (1 patient), a large en-doleak (2 patients), or technical problems (3 patients).

Conclusion The amount of bleeding and the need for blood products were significantly lower in the endovascular treatment group. Despite the absence of significant differences regarding cardiac complications and mortality, there was a lesser incidence of pneumonia, acute respiratory and renal failure. Patients in the endovascular treatment group spent less time in the intensive care unit and in the Hospital.

Background and objective In a randomized, placebo-controlled, double-blind trial, we compared the efficacy of dolasetron and metoclopramide in preventing postoperative nausea and vomiting in women undergoing hysterectomy.

Methods Patients were allocated randomly to one of three groups: group A (n =50) received 50 mg dolasetron orally, group B (n =50) received 20 mg metoclopramide intravenously and placebo orally, group C (n =50) received placebo orally. If patients complained of retching or vomiting, or if patients demanded an antiemetic, 1.25 mg droperidol was administrated intravenously. To quantify postoperative nausea and vomiting the following score was used: 0 =no nausea, 1 =nausea, 2 =retching, 3 =single vomiting, 4 =multiple vomiting. The Raatz test was used to analyse postoperative nausea and vomiting (PONV) scores.

Results Dolasetron reduced the postoperative nausea and vomiting score significantly (P <0.02 vs. metoclopramide; P <0.0001 vs. placebo). Metoclopramide also reduced the postoperative nausea and vomiting score (P <0.02 vs. placebo). Fisher's exact test showed a significant reduction of vomiting in the dolasetron group compared with metoclo-pramide-treated patients (P <0.007) and placebo-treated patients (P <0.000006) and a significantly lower rate of nausea in comparison to the placebo group (P <0.009). There were no significant differences between the metoclopramide and the placebo groups (in Fisher's exact test). The use of postoperative droperidol per patient was significantly lower in the dolasetron group (P <0.04 vs. metoclopramide; P <0.0001 vs. placebo) than in the metoclopramide (P <0.02 vs. placebo) and in the placebo groups.

Conclusions Oral dolasetron is more effective than either metoclopramide given intravenously or placebo for preventing vomiting after hysterectomy. It also was significantly superior to either metoclopramide or placebo concerning the PONV score and the need for droperidol rescue.

Background and objective We have assessed the analgesic efficacy and side-effects of neostigmine when added to lidocaine for axillary brachial plexus block, in a prospective, randomized, double-blind, placebo-controlled study.

Methods We studied 34 ASA I or II patients undergoing elective ambulatory carpal tunnel release. Axillary brachial plexus block was performed using a peripheral nerve stimulator to locate the median nerve. All patients were administered 1.5% lidocaine 450 mg and epinephrine 5 μg mL−1. Patients were allocated randomly to one of two groups. Neostigmine 500|ig was added in group N, and saline 1 mL in group S.

Results The duration of analgesia did not significantly differ between groups [mean (SD)]: 812.5 (456.9) for group S vs. 746.7 (474.1) min for group N (P >0.05). The need for supplementary analgesia did not significantly differ between groups: 4.4 (1.5) extra doses for group S vs. 3.8 (2.2) extra doses for group N (P>0.05). Visual analogue pain scores and occurrence of side-effects did not significantly differ between groups.

Conclusion Neostigmine does not seem to be of clinical value for peripheral nerve blocks.

A 6-months pregnant woman suffering from severe tetanus was successfully treated with intrathecal baclofen. She delivered a premature but healthy neo-nate, and was safely discharged home 40 days after the onset of symptoms of tetanus. Specific aspects of intrathecal baclofen therapy in the pregnant woman are discussed.

The cuffed oropharyngeal airway is a modified Guedel airway and is recommended for anaesthesia in spontaneously breathing patients. To our knowledge this is the first report of transient unilateral lingual nerve palsy after the use of a cuffed oropharyngeal airway to maintain anaesthesia during arthroscopy of an ankle. The aetiology of lingual nerve damage is multi-factorial. The possible mechanisms involved include anterior displacement of the mandible during insertion of the cuffed oropharyngeal airway (as in the jaw hrust manoeuvre), compression of the nerve against the mandible, or stretching of the nerve over the hyoglossus by the cuff of the cuffed oropharyngeal airway. We recommend gentle airway manipulation with the use of the cuffed oropharyngeal airway, avoidance of excessive cuff inflation and early recognition of such a complication if it occurs.