Invasive line placement in critically ill patients: do hemostatic defects matter?

BACKGROUND: Blood components are often given prophylactically before the placement of invasive lines in patients with coagulation defects. Little, however, is known about the epidemiology of defects in these patients. The purpose of this study is to ascertain what proportion of intensive care patients who receive invasive lines have hemostatic defects, what actions are taken by physicians to correct these abnormalities before invasive line insertion, and what the incidence is of bleeding complications after invasive line placement. STUDY DESIGN AND METHODS: Charts were retrospectively reviewed for 490 intensive care patients in whom 938 arterial, pulmonary artery, and central venous lines were placed. RESULTS: At least one defect in hemostasis was documented for 388 patients (41%) before line placement, with 253 (27%) of these patients evidencing severe abnormalities. Seventeen percent of patients had no preprocedure laboratory evaluation. Trauma patients showed the highest numbers of abnormalities in hemostatic testing, but medical patients had more-severe defects. The occurrence of isolated abnormal laboratory values did not predict bleeding, but a score derived from a consideration of multiple defects did. Correction of the abnormalities was attempted in 37 percent of patients with hemostatic defects. Sixteen patients had bleeding complications, but only two had complications that were life-threatening. None of the complications were fatal. CONCLUSION: Invasive lines are used frequently in patients with hemostatic defects, often without any attempt to correct the abnormalities. Nevertheless, rates of hemorrhage are low and appear to be closely related to the level of experience of the physician rather than to defects in hemostasis. These findings suggest that the use of blood components for preprocedure correction of hemostatic defects is not necessary, except in those patients who have the most severe hemostatic abnormalities.     

Nonbronchial systemic collateral arteries: significance in percutaneous embolotherapy for hemoptysis

Twenty patients with massive or recurrent hemoptysis underwent percutaneous transcatheter embolotherapy between 1979 and 1986 for the following diseases: cavitary aspergillosis (n = 4); cystic fibrosis (n = 4); tuberculosis (n = 3); bronchogenic carcinoma (n = 3); bronchiectasis (n = 3); small cell lung carcinoma 6 years after irradiation (n = 1); congenital heart disease, after Glenn and Blalock anastomoses (n = 1); and unknown interstitial disease (n = 1). Bronchial arteries were embolized in all but one patient. In nine patients (45%) nonbronchial systemic collateral arteries contributed significantly to areas of pathologic pulmonary tissue and frequently were the major arterial supply. These nonbronchial systemic collaterals included branches of the subclavian and axillary arteries (n = 7), intercostal arteries (n = 5), and phrenic arteries (n = 3) and accounted for 59.5% of the total number of arteries embolized. Recognition and occlusion of nonbronchial systemic collaterals providing blood to hypervascular pulmonary lesions is essential for successful percutaneous embolotherapy of hemoptysis.     

Differentiation of cellular processes involved in the induction and maintenance of stimulated neutrophil adherence

Neutrophil adherence stimulated by phorbol myristate acetate (PMA) was investigated by quantitating the attachment of 51Cr-labeled neutrophils to plastic surfaces and to the endothelium of umbilical veins mounted in compartmentalized Lucite chambers. PMA-induced adherence could be functionally separated into an induction phase requiring cellular metabolism and a Mg++ dependent maintenance phase that was independent of cellular metabolism. Thus, metabolic inhibitors (N-ethylmaleimide, 2- deoxyglucose) blocked adherence when added to neutrophils prior to PMA, but did not cause detachment of cells adhering as a consequence of prior exposure to PMA. PMA failed to induce adherence of neutrophils incubated at low (0.4 degree C) temperature, but temperature reduction, even for prolonged periods, did not cause detachment of adherent cells. Thus, the attractive forces that mediate stimulated adherence persist independently of any sustained metabolic response to the inducing stimulus. However, removal of Mg++ from the media above adherent cells resulted in immediate detachment, indicating that the cation was required for the persistent expression or maintenance of the attractive forces involved. The extent of stimulated adherence correlated well with the extent of degranulation when rates were varied by limiting the incubation time or stimulus concentration. This correlation was not absolute; in the absence of Mg++, PMA induced degranulation normally but failed to enhance adherence. To explain these findings, we investigated the possibility that PMA-stimulated adherence was maintained by Mg++-dependent cellular adherence molecules released during exocytosis. Supernatants of stimulated neutrophils were devoid of adherence-promoting activity, and only weak activity was recovered in supernatants of mechanically disrupted neutrophils. PMA effectively stimulated the tight adherence of degranulated neutrophil cytoplasts to plastic surfaces and did so in the absence of stimulated granule enzyme release. Thus, conditions have been identified under which degranulation occurs in the absence of adherence (removal of Mg++) and adherence occurs without concurrent degranulation. Since neutrophil cytoplasts do contain some granule products and granule material can be identified on cytoplast membranes, it is possible that degranulation or granule products may be involved in the adherent response. However, hyperadherence was shown to develop in the absence of de novo degranulation.(ABSTRACT TRUNCATED AT 400 WORDS)     

Live births after management of severe OHSS by GnRH antagonist administration in the luteal phase

Ovarian hyperstimulation syndrome (OHSS) is a serious complication of ovarian stimulation protocols. Currently, no curative therapy exists and the main preventive option is cycle cancellation. Gonadotrophin-releasing hormone (GnRH) antagonist administration in the luteal phase was recently proposed as a new approach for the management of patients with established severe OHSS. Three polycystic ovarian syndrome patients undergoing IVF treatment developed severe OHSS, diagnosed 6 days after oocyte retrieval. On day 6, the patients underwent blastocyst transfer and received GnRH antagonist for 4 days, combined with luteal phase support using exogenous oestradiol and progesterone. Two patients had successful pregnancies that resulted in births of healthy infants, while one patient had a biochemical pregnancy. In all patients, established severe OHSS regressed to a moderate form of the syndrome, no pregnancy-induced life-threatening OHSS was observed, while a short monitoring period was required at an outpatient level, avoiding the need for patient hospitalization. This is the first report in the literature on GnRH antagonist administration in the luteal phase, combined with embryo transfer and exogenous oestradiol and progesterone supplementation. This novel treatment was effective in the regression of established severe OHSS, and resulted in the birth of healthy infants.     

颈动脉支架置入术和内膜剥脱术治疗颈动脉狭窄的随机对照研究

背景:颈动脉狭窄是脑卒中的重要原因.颈动脉支架置入术(carotid-artery stenting,CAS)和颈动脉内膜剥脱术(carotid endarterectomy,CEA)是治疗颈动脉狭窄的可选择手段,但以往对比研究,如症状性重度颈动脉狭窄患者动脉内膜剥脱术与血管成形术比较(EVA-3S)、保护性支架血管成形术与颈动脉内膜剥脱术比较(SPACE)及国际颈动脉支架研究(ICSS)关于CAS和CEA孰优孰劣的报道存在矛盾.     

Prenatal express-diagnosis by the method of QF-PCR and automatic microelectroforesis with microarrays

The modern molecular-genetic methods have been implementing actively into the medical practiee.They improve diagnostic accuracy,help to prognosticate the course of oncological diseases,optimize the res...     

An introduction to QT interval prolongation and non-clinical approaches to assessing and reducing risk

Owing to its association with Torsades de Pointes, drug-induced QT interval prolongation has been and remains a significant hurdle to the development of safe, effective medicines. Genetic and pharmacological evidence highlighting the pivotal role the human ether-a-go-go-related gene (hERG) channel was a critical step in understanding how to start addressing this issue. It led to the development of hERG assays with the rapid throughput needed for the short timescales required in early drug discovery. The resulting volume of hERG data has fostered in silico models to help chemists design compounds with reduced hERG potency. In early drug discovery, a pragmatic approach based on exceeding a given potency value has been required to decide when a compound is likely to carry a low QT risk, to support its progression to late-stage discovery. At this point, the in vivo efficacy and metabolism characteristics of the potential drug are generally defined, as well its safety profile, which includes usually a dog study to assess QT interval prolongation risk. The hERG and in vivo QT data, combined with the likely indication and the estimated free drug level for efficacy, are put together to assess the risk that the potential drug will prolong QT in man. Further data may be required to refine the risk assessment before making the major investment decisions for full development. The non-clinical data are essential to inform decisions about compound progression and to optimize the design of clinical QT studies.This article is commented on by Guth and Rast, pp. 22–24 of this issue and is part of a themed section on QT safety. To view this issue visit http://www3.interscience.wiley.com/journal/121548564/issueyear?year=2010