Mutation spectrum and prevalence of BRCA1 and BRCA2 genes in patients with familial and early-onset breast/ovarian cancer from Tunisia.

The contribution of BRCA1/BRCA2 mutations to hereditary breast cancer in the Tunisian population has not been accurately estimated. The purpose of our study was to estimate the incidence and spectrum of pathogenic mutations in BRCA1/2 genes in early onset and familial breast/ovarian cancer among Tunisian women. To identify predictive factors for BRCA1/2 mutations, we screened the entire coding sequences and intron/exon boundaries of BRCA1/BRCA2 genes in 48 patients by direct sequencing. Twelve pathogenic mutations were detected (25%); three in BRCA1 (c.211dupA in four families, c.5266dupC in three families and c.1504_1508delTTAAA in one family) and two novel mutations in BRCA2 (c.1313dupT in two families and c.7654dupT in two families). We also identified 23 different polymorphisms and unclassified variants. These results indicate that our population has a spectrum of recurrent BRCA mutations.

Is the diagnostic yield of myocardial stress perfusion MRI impaired by three-vessel coronary artery disease?

BACKGROUND: Three-vessel coronary artery disease (CAD) comes along with globally reduced myocardial perfusion potentially restricting the demarcation of regional hypoperfusion in stress perfusion cardiac magnetic resonance imaging (MRI). PURPOSE: To evaluate whether stress perfusion cardiac MRI is capable of detecting myocardial hypoperfusion in patients with 3-vessel CAD reliably. MATERIAL AND METHODS: Two hundred and five patients with symptoms of CAD were included. The examination protocol comprised imaging of myocardial perfusion at stress (0.14 mg/kg/min adenosine for 4 min) using a 2D saturation recovery gradient echo sequence after administration of gadobutrol (0.1 mmol/kg body weight). Perfusion sequences were assessed qualitatively by two experienced observers. Coronary angiography served as standard of reference. RESULTS: Sensitivity and specificity for hemodynamically relevant stenoses in patients with 0-, 1-, 2-, 3-vessel coronary artery disease were 100%/91%, 91%/73%, 90%/71%, 92%/64%; positive/negative predictive value, 67%/100%, 91%/73%, 83%/81%, 93%/58%; diagnostic accuracy, 93%/87%/83%/87%, respectively. The negative predictive value in patients with 3-vessel CAD was lower than in patients with 0- and 2-vessel CAD and the specificity lower than in patients with no CAD whereas the positive predictive value was higher than in patients with no CAD. The other proportions did not differ significantly between the groups. CONCLUSION: The diagnostic value of stress perfusion cardiac MRI in patients with 3-vessel CAD is comparable to results in patients with 1- or 2-vessel CAD. In the rare event that stress perfusion images do not depict regional hypoperfusion in patients with severe 3-vessel CAD, myocardial ischemia could be identified by reduced semi-quantitative perfusion parameters.

[Cardiac magnetic resonance tomography in the diagnostics of restrictive and unclassified cardiopathies]. / Kardiale Magnetresonanztomographie in der Diagnostik der restriktiven und unklassifizierten Kardiomyopathien.

CLINICAL/METHODICAL ISSUE: Besides ischemic heart disease cardiomyopathies are common causes of heart failure and sudden cardiac death. STANDARD RADIOLOGICAL METHODS: The diagnostic spectrum in cardiomyopathies comprises non-invasive and invasive examination techniques. METHODICAL INNOVATIONS: The exact verification of certain cardiomyopathies necessitates knowledge of the latest classification of cardiomyopathies as well as dedicated examination protocols. PERFORMANCE: Modern imaging modalities, such as echocardiography and cardiac magnetic resonance imaging (MRI) have emerged as useful imaging tools in the investigation of patients suspected of having many different types of cardiomyopathies. ACHIEVEMENTS: Based on a better understanding of the underlying pathophysiology several diagnostic criteria have been defined using cardiac MRI. In particular there is an increasing importance of cardiac MRI in the description of patients with restrictive and unclassified cardiomyopathies. PRACTICAL RECOMMENDATIONS: Echocardiography still remains the modality of choice in the diagnostics of unclear left ventricular heart failure. Further diagnostic work-up should include cardiac MRI in case of any lack of clarity.

Expression of stromal-cell-derived factor-1 (SDF-1): a predictor of ischaemic stroke?

BACKGROUND AND PURPOSE: Platelet stromal-cell-derived factor-1 (SDF-1) plays a pivotal role in angiogenesis and the regeneration of ischaemic tissue through the regulation of haematopoietic progenitor cells and is upregulated at the sites of vascular injury and platelet activation. Thus, SDF-1 has recently been discussed as a predictor in ischaemic diseases such as acute myocardial infarction. However, no clinical data pertinent to the investigation of the platelet SDF-1 expression in patients with stroke are available. METHODS: We consecutively evaluated 196 patients who were admitted to the stroke unit with symptoms suspected for stroke. Surface expression of the platelet activation markers (P-selectin and GPIb) and the expression of platelet-bound SDF-1 were determined by two-colour whole blood flow cytometry. RESULTS: Patients with transient ischaemic attack (TIA) as well as with ischaemic stroke showed similar levels of SDF-1 expression on hospital admission compared with patients with non-ischaemic (NI) events and with 30 healthy controls (TIA (mean fluorescence intensity±SD): 31.5±18.2 vs. NI: 26.4±15.7; P=0.361; stroke: 28.7±19.8 vs. NI; P=0.943; control: 26.1±11.3; P>0.05 compared with all). Platelet SDF-1 expression showed a trend with the severity of stroke according to National Institute of Health Stroke Scale score (r=0.125; P=0.085), but significantly correlated with the peak levels of C-reactive protein (r=0.218; P=0.002) and with the levels of platelet activation (P-selectin: r=0.389; P=0.001). Multifactorial analysis of covariance revealed a significant influence on platelet SDF-1 expression by smoking (P=0.019). CONCLUSIONS: Platelet SDF-1 surface expression did not show any significant difference in patients with TIA and ischaemic stroke compared with patients with NI events. Thus, single biomarker evaluation of platelet SDF-1 surface expression is not helpful to predict ischaemic stroke.

Urokinase receptor: a molecular organizer in cellular communication.

In a variety of cell types, the glycolipid-anchored urokinase receptor (uPAR) is colocalized pericellularly with components of the plasminogen activation system and endocytosis receptors. uPAR is also coexpressed with caveolin and members of the integrin adhesion receptor superfamily. The formation of functional units with these various proteins allows the uPAR to mediate the focused proteolysis required for cell migration and invasion and to contribute both directly and indirectly to cell adhesive processes in a non-proteolytic fashion. This dual activity, together with the initiation of signal transduction pathways by uPAR, is believed to influence cellular behaviour in angiogenesis, inflammation, wound repair and tumor progression/metastasis and open up the way for uPAR-based therapeutic approaches.

Urokinase receptor (CD87) regulates leukocyte recruitment via beta 2 integrins in vivo.

The urokinase receptor (CD87; uPAR) is found in close association with beta 2 integrins on leukocytes. We studied the functional consequence of this association for leukocyte adhesion and migration. In vivo, the beta 2 integrin-dependent recruitment of leukocytes to the inflamed peritoneum of uPAR-deficient mice was significantly reduced as compared with wild-type animals. In vitro, beta 2 integrin-mediated adhesion of leukocytes to endothelium was lost upon removal of uPAR from the leukocyte surface by phosphatidyl-inositol-specific phospholipase C. Leukocyte adhesion was reconstituted when soluble intact uPAR, but not a truncated form lacking the uPA-binding domain, was allowed to reassociate with the cell surface. uPAR ligation with a monoclonal antibody induced adhesion of monocytic cells and neutrophils to vascular endothelium by six- to eightfold, whereas ligation with inactivated uPA significantly reduced cell-to-cell adhesion irrespective of the beta 2 integrin-stimulating pathway. These data indicate that beta 2 integrin-mediated leukocyte-endothelial cell interactions and recruitment to inflamed areas require the presence of uPAR and define a new phenotype for uPAR-deficient mice. Moreover, uPAR ligation differentially modulates leukocyte adhesion to endothelium and provides novel targets for therapeutic strategies in inflammation-related vascular pathologies.

Expression of platelet glycoprotein VI is associated with transient ischemic attack and stroke.

BACKGROUND AND PURPOSE: Platelet collagen receptor glycoprotein VI (GPVI) contributes significantly to platelet adhesion and thrombus formation. We aimed to investigate GPVI in patients presenting with symptoms of acute cerebrovascular disease and to define GPVI as biomarker for acute stroke. METHODS: We consecutively evaluated 205 patients, who admitted the stroke unit with symptoms for stroke. Surface expression of the platelet activation markers (GPVI, CD62P, GPIb) was determined by two-color whole blood flow cytometry. RESULTS: Patients with transient ischemic attack (TIA) (n = 18; 8.8%) as well as with stroke (n = 133; 64.9%) showed a significantly enhanced GPVI expression (mean fluorescence intensity +/- SD) on admission compared to patients with non-ischemic (NI) events (n = 54; 26.3%) (TIA: 20.9 +/- 7.1 vs. NI: 16.2 +/- 3.9; P = 0.002; stroke: 20.4 +/- 5.7 vs. NI; P = 0.002). Neither CD62P nor GPIb surface expression showed a significant difference. Logistic regression analysis revealed that on admission GPVI was associated with stroke independent of conventional laboratory markers such as C-reactive protein, blood glucose, and creatine kinase. Using a receiver operating characteristic curve on GPVI, we have determined the cut off value of 18.2 for stroke. Thus, patients with enhanced GPVI expression levels (>or=18.2) had a 2.4-fold relative risk for stroke. Patients with elevated platelet GPVI expression level had a poorer clinical outcome in cumulative event-free survival for stroke, myocardial infarction, and cerebro-/cardiovascular death at 3-month follow-up (log rank; P = 0.045). CONCLUSIONS: These findings indicate that platelet GPVI surface expression is significantly enhanced in patients with TIA and stroke compared to patients with NI events. Determination of platelet-specific GPVI may be useful as an early biomarker for cerebral ischemia.

[Cardiac MRI in addition to MR angiography: a longitudinal study in vascular risk patients]. / Kardiale MRT als ergänzung zur MR-angiografie: eine longitudinale studie bei vaskulären risikopatienten.

PURPOSE: The aim of the study was to assess the feasibility and additional diagnostic information of cardiac MRI as a supplement to state-of-the-art MR angiography (MRA) in the case of vascular risk patients. Therefore, the prevalence of delayed myocardial enhancement (DE) was determined in patients suffering from peripheral artery disease (PAD) and a clinical follow-up was evaluated after 2 years. MATERIALS AND METHOD: 87 consecutive patients (ages 66 +/- 10 years, 67 males) with symptomatic peripheral arterial occlusive disease (n = 68) or abdominal aortic aneurysm (n = 19) were examined using delayed cardiac enhancement (DE) within the clinical indication of MRA at a 1.5T system. A follow-up examination was carried out two years later (24 months +/- 4 months) with regards to cardiac events (cardiac death, myocardial infarction or acute coronary syndrome, heart insufficiency, coronary revascularization). RESULTS: In total, 40 / 87 patients had myocardial infarctions shown in MRI (46 %). In 25 patients (29 %), the myocardial infarction was already known, while in 15 patients (17 %) an occult progressing infarction was diagnosed (38 % of the myocardial infarcts). Follow-up data was able to be obtained after 2 years for 82 patients. 15 patients had a major cardiac event during the follow-up period, and 10 (67 %) of them already showed DE in the MRI. In the group with occult progressing infarctions, cardiac events occurred in 40 % (6 / 15 patients, cardiac death n = 1, ischemia n = 4, heart insufficiency n = 1, bypass n = 1), in patients with known infarction in 17 % (4 / 23 patients, cardiac death n = 1, ischemia n = 3, bypass n = 2) and in 11 % of patients without myocardial scars (5 / 44 patients, cardiac death n = 1, ischemia n = 2, heart insufficiency n = 2). CONCLUSION: Cardiac MRI in combination with MRA was feasible and showed a high prevalence of known and unexpected myocardial infarctions. This was of prognostic relevance in the follow-up 2 years later. Therefore, this enables important additional information regarding to the risk stratification and eventually targeted therapy in risk patients with PAD.

[MR stress perfusion for the detection of flow-limiting stenoses in symptomatic patients with known coronary artery disease and history of stent implantation]. / MR-Stressperfusion zur Vorhersage flusslimitierender Stenosen bei symptomatischen Patienten mit bekannter KHK nach Stentimplantation.

PURPOSE: The aim of the present study was to determine the correlation of myocardial perfusion MR imaging (MPMRI) and coronary angiography for the detection of flow-limiting stenosis in symptomatic patients with known coronary artery disease and a history of intervention. MATERIALS AND METHODS: MPMRI was performed in 51 symptomatic patients (44 male, 64.7 +/- 9.5 years) with known coronary artery disease and a history of stent implantation (between 5 years and 2 weeks prior to MRI). Malperfused myocardial regions were correlated with findings of coronary angiography. A stenosis of > 70% was regarded as hemodynamically significant. RESULTS: In MPMRI 37 patients (73%) showed a stress induced perfusion deficit. In 35 of these patients coronary angiography revealed a stenosis of > 70 %. A total of 38 patients (75%) showed stenoses of > 70%. MPMRI yielded a sensitivity of 92% with a specificity of 85 %. The positive predictive value was 95 % and negative predictive value was 79%. The assignment of malperfused segments to coronary artery territories was carried out according to the standardized myocardial model of the American Heart Association (sensitivity/specificity was 59/85% for RCA, 79/81% for LAD and 54/68 % for LCX). CONCLUSION: MPMRI is a suitable non-invasive method for detecting flow-limiting coronary artery stenoses in patients with a history of stent implantation.

Uncorrected total anomalous pulmonary venous drainage in pregnancy.

Total anomalous pulmonary venous drainage is a rare form of congenital heart disease. It usually presents in the neonatal period, although later presentation, including in adulthood, is known to occur. We could not find any accounts of adult survivors with the undiagnosed disease becoming pregnant. We describe the case of a 19-year-old Bengali primiparous woman who arrived in the UK at 27 weeks' gestation and needed an urgent caesarean section for intrauterine growth restriction at 34 weeks' gestation. Uncorrected congenital heart disease was diagnosed at this time although the exact nature of the pathology was not clear. She underwent an uncomplicated caesarean section using a combined spinal-epidural technique with invasive monitoring. Intrathecal 0.5% hyperbaric bupivacaine 0.7 mL and fentanyl 25 microg were sufficient for surgery. She remained cardiovascularly stable throughout the procedure and a female infant was successfully delivered. She underwent corrective cardiac surgery 14 months after delivery. To our knowledge, this is the first report of caesarean section in a patient with uncorrected total anomalous pulmonary venous drainage. In this case, regional anaesthesia was successfully used.

Regulation of leukocyte recruitment by polypeptides derived from high molecular weight kininogen.

Proteolytic cleavage of single-chain, high molecular weight kininogen (HK) by kallikrein releases the short-lived vasodilator bradykinin and leaves behind a two-chain, high molecular weight kininogen (HKa) reported to bind to the beta2-integrin Mac-1 (CR3, CD11b/CD18, alphaMbeta2) on neutrophils and exert antiadhesive properties by binding to the urokinase receptor (uPAR) and vitronectin. We define the molecular mechanisms for the antiadhesive effects of HK related to disruption of beta2-integrin-mediated cellular interactions in vitro and in vivo. In a purified system, HK and HKa inhibited the binding of soluble fibrinogen and ICAM-1 to immobilized Mac-1, but not the binding of ICAM-1 to immobilized LFA-1 (CD11a/CD18, alphaLbeta2). This inhibitory effect could be attributed to HK domain 5 and to a lesser degree to HK domain 3, consistent with the requirement of both domains for binding to Mac-1. Accordingly, HK, HKa, and domain 5 inhibited the adhesion of Mac-1 but not LFA-1-transfected K562 human erythroleukemic cells to ICAM-1. Moreover, adhesion of human monocytic cells to fibrinogen and to human endothelial cells was blocked by HK, HKa, and domain 5. By using peptides derived from HK domain 5, the sequences including amino acids H475-G497 (and to a lesser extent, G440-H455) were identified as responsible for the antiadhesive effect, which was independent of uPAR. Finally, administration of domain 5 into mice, followed by induction of thioglycollate-provoked peritonitis, decreased the recruitment of neutrophils by approximately 70% in this model of acute inflammation. Taken together, HKa (and particularly domain 5) specifically interacts with Mac-1 but not with LFA-1, thereby blocking Mac-1-dependent leukocyte adhesion to fibrinogen and endothelial cells in vitro and in vivo and serving as a novel endogenous regulator of leukocyte recruitment into the inflamed tissue.

Transient interaction of activated platelets with endothelial cells induces expression of monocyte-chemoattractant protein-1 via a p38 mitogen-activated protein kinase mediated pathway. Implications for atherogenesis.

OBJECTIVE: Activated platelets induce alterations of chemotactic and adhesive properties of endothelial cells, a critical initial step in atherogenesis. We investigated the effect of transient interaction of activated platelets with cultured human umbilical vein endothelial cells (HUVECs) on secretion of monocyte chemoattractant protein-1 (MCP-1), a key molecule in monocyte chemotaxis and transmigration. METHODS AND RESULTS: Transient interaction of alpha-thrombin-activated platelets with endothelial cells for 10-120 min substantially induced endothelial secretion of MCP-1, monocyte chemotaxis and adhesion to HUVECs. Platelet-induced secretion of MCP-1 and monocyte-endothelium adhesion was reduced by the MAP kinase p38-specific inhibitor SB203580, but not by other kinase inhibitors including PD98059, wortmannin, or rapamycin. In addition, activated platelets induced transcription of a luciferase reporter construct containing a MCP-1 promotor, an effect that could be inhibited by SB203580. Overexpression of dominant-negative mutants of MAP kinase p38, CSBP2-(D168A) and CSBP2-(T180E,Y182E) reduced platelet-induced expression of MCP-1. CONCLUSIONS: Activation of the p38 MAP kinase and consecutive endothelial secretion of MCP-1 induced through transient interaction of activated platelets might play an important role in atherogenesis.

Lipodermatosclerosis is characterized by elevated expression and activation of matrix metalloproteinases: implications for venous ulcer formation.

Lipodermatosclerosis refers to skin induration of the lower extremities and is associated with patients preceding venous ulcerations. To better understand the pathogenesis of ulcer formation we investigated the expression of matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) in lipodermatosclerosis. By preparing biopsies from healthy skin and liposclerotic lesions, MMP-1, MMP-2, MMP-9, TIMP-1, and TIMP-2 were analyzed by using reverse transcriptase-polymerase chain reaction, western blot, zymography, hydrolysis of [3H]labeled collagens, and immunohistochemistry. Our investigations provide evidence that mRNA and protein expression of MMP-1, MMP-2, and TIMP-1 were significantly increased in lipodermatosclerosis, whereas the total amount of MMP-9 and TIMP-2 mRNA and protein was not altered. Western blot of liposclerotic lesions revealed an inactive proMMP-1-TIMP-1 complex, whereas MMP-2 was prominent as an active 66 kDa band. Increased proteolytic activity of MMP-2 could be proven in lesional in comparison with healthy skin by zymography and [3H] collagen degradation. Increased diffuse staining was found for MMP-1 in the epidermis and dermis in comparison with controls. In lipodermatosclerosis, MMP-2 was predominantly localized in the basal and suprabasal layers of the epidermis, in perivascular regions, and in the reticular part of the dermis. Furthermore, MMP-2 was imbalanced by locally reduced expression of TIMP-2 in the basement membrane zone of lesional skin. Our findings indicate lipodermatosclerosis to be characterized by elevated matrix turnover.

The relevance of blood cell-vessel wall adhesive interactions for vascular thrombotic disease.

Activation and signaling of circulating blood and vessel wall cells, as well as their direct adhesive interactions, are critical for the regulation of vascular homeostasis related to vasomotor responses, inflammation, hemostasis, and wound repair. Under conditions of stress, inflammation, or infection the targeting and anchoring of leukocytic cells to the vascular endothelium is mediated by specific pairs of adhesion receptors and their counter-ligands that may induce juxtacrine signaling resulting in the expression of prothrombotic agonists such as tissue factor. Concomitant action of inflammatory cytokines may down-regulate thromboprotective mechanisms of the endothelium. Through similar intercellular interactions, the platelets recruited to these inflamed sites may aggregate and modulate leukocyte function. In addition, leukocytes can influence coagulation by their ability to produce pro- and anticoagulant factors as well as by providing specific receptors (such as Mac-1 or EPR-1) that serve as direct molecular links between inflammation and hemostasis. The initiation and amplification of blood clotting reactions on the leukocyte surface has consequences on other vascular cell functions and involves (cytokine) activation and signaling pathways that contribute to pathophysiological aspects of inflammatory responses. As a consequence, the diverse cell-to-cell interactions, as well as different inflammatory mediators or bidirectional signaling pathways, appear to be promising targets for the treatment of thrombotic complications in the context of inflammation-dependent vascular diseases.

Molecular crosstalk between adhesion receptors and proteolytic cascades in vascular remodelling.

The multifunctionality of adhesion receptor ligands as well as the promiscuous nature of vascular integrins and nonintegrin-dependent adhesive interactions allow ligand-receptor binding of variable strength. The cooperation with pericellular proteolysis cascades is required for vascular remodelling during angiogenesis, atherogenesis or inflammatory processes. In particular, integrin-dependent cell contact, spreading and (trans-)migration can be modulated by ECM-associated PAI-1 and uPA-receptor driven reactions that are intimately linked to the invasive potential of cells. Recently, mechanisms of molecular crosstalk between these receptor systems have been recognized: (a) uPA-receptor may directly interact with beta 1- and beta 2-integrins on circulating blood cells; (b) av beta 3-integrin-directly binds to a matrix metalloproteinase; (c) uPA and PAI-1 balance the high affinity binding of vitronectin to uPA-receptor; (d) vitronectin-dependent cell adhesion and migration involving alpha v-integrins or uPA-receptor are blocked by active PAI-1 independent of its role as protease inhibitor. These results are compatible with vascular injury studies in uPA- and PAI-1 knock-out mice and provide new targets for the treatment of diseases associated with imbalanced vascular remodelling.

Spinal analgesia for transvaginal oocyte retrieval.

Day case transvaginal ultrasound-guided needle puncture is currently the method of choice for oocyte retrieval. The risk of morbidity from this procedure increases with sudden patient movement in response to needle manipulation. The provision of effective pain relief can limit this risk, but is complicated by the need to balance efficacy with day case compatibility. The aim of this pilot study was to establish whether spinal analgesia using a mixture of bupivacaine and fentanyl could be useful in this context. The results identify several advantages of this technique over current clinical practice, and merit further comparative investigation.

Epidural anaesthesia and neural tube defects.

This is a retrospective record of the analgesic management during labour of 16 patients with spina bifida seen at Leicester Royal Infirmary Maternity Hospital between March 1994 and February 1996. The information highlights the potential difficulties in providing epidural analgesia for this patient group, and demonstrates how an antenatal pre-anaesthetic clinic can help to optimize pain management by providing the opportunity to formulate a realistic analgesic plan, which can be documented in the notes.

Retrosternal goitre: a cause of dyspnoea in pregnancy.

During pregnancy, the thyroid undergoes several changes including altered function and gland enlargement. We describe the management of a 38-week pregnant woman presenting with cough and increasing breathlessness. She gave a 5-year history of asthma which initially obscured the final diagnosis of upper-airway obstruction secondary to tracheal compression by a large retrosternal goitre. Once this was recognized, management was straightforward. Delivery by caesarean section was carried out under epidural anaesthesia, following which her symptoms rapidly resolved. A subtotal thyroidectomy was performed 4 weeks later under general anaesthesia, again without incident. We outline the normal physiological changes that occur to the thyroid gland during pregnancy and also highlight the value of the flow volume loop in the evaluation of airway obstruction.

Does midwifery-led intrapartum care require anaesthetic services?

The report of the Expert Maternity Group 'Changing Childbirth' (The Cumberlege Report) advocates a greater role for midwives in the care of the low risk pregnant woman, and has promoted much discussion about the future development of maternity services in the UK. At Leicester Royal Infirmary NHS Trust the 'Home from Home' delivery scheme provides midwifery-led antenatal and intrapartum care of women with uncomplicated pregnancies. We have performed a retrospective review of the requirements for anaesthetic services in this unit. During the 12 month review period 1610 women were admitted to the 'Home from Home' delivery scheme in labour. One hundred and eighty one women subsequently received anaesthetic intervention. Of this group, 137 (77.0%) required an epidural, 17 (9.6%) a spinal, 18 (10.1%) a general anaesthetic, 5 (2.8%) an epidural and a general anaesthetic and 1 (0.6%) an epidural and a spinal. Our results demonstrate that low risk pregnant women in labour being cared for in a midwifery led unit have a considerable need for anaesthesia and analgesia.

Acid aspiration prophylaxis in 202 obstetric anaesthetic units in the UK.

A postal survey of obstetric anaesthetic units in the UK was conducted by questionnaire to gain information about current acid aspiration prophylaxis. Information regarding the delivery rate and the caesarean section rate under regional techniques was also requested. Replies were received from 202 obstetric anaesthetic units in the UK, a 75% response rate. The results are compared to similar surveys carried out in 1984 and 1988. Sodium citrate and the H(2) antagonist ranitidine remain the drugs most commonly used for acid aspiration prophylaxis. However, the number of departments carrying out routine prophylaxis for patients in active labour has fallen from 75% in 1988 to 57% in the current survey.