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Biomedical subjects

R R Nelson

Publications and source records attributed to R R Nelson.

At least 19 recordsLinked to original sources
PubMed2000

Isolation and characterization of glycopeptide-resistant enterococci from hospitalized patients over a 30-month period.

In February 1996, a Hospital Infection Control Practices Advisory Committee-style screening program was commenced to isolate and subsequently characterize glycopeptide-resistant enterococci (GRE) from patients at a hospital trust in Glasgow, Scotland. Over the next 30 months, GRE were isolated from 154 patients. GRE were isolated from patients in traditionally high-risk areas such as the renal unit and intensive care unit and also in areas considered to be lower risk, including medical wards and associated long-stay geriatric hospitals. The majority (90%) of isolates were Enterococcus faecium vanB. The remaining isolates consisted of seven E. faecalis (vanA), three E. gallinarum (vanC), and a further six E. faecium (five vanA, one both vanA and vanB) isolates. Analysis of SmaI-digested DNA by pulsed-field gel electrophoresis revealed that 34 of 40 (85%) VanB E. faecium isolates were identical or closely related, while 11 of 13 (85%) VanA GRE were distinct. High-level aminoglycoside resistance was seen in less than 8% of isolates. VanB E. faecium isolates were almost uniformly resistant to ampicillin and tetracycline. In this study, GRE have been isolated over a prolonged period from a broad range of patients. Glycopeptide resistance within the study hospital trust appeared to be mainly due to the clonal dissemination of a single strain of E. faecium VanB.

Aminoglycosides↗
PubMed1999

Intrinsically vancomycin-resistant gram-positive organisms: clinical relevance and implications for infection control.

Intrinsic resistance to vancomycin in gram-positive bacteria presumably predates acquired vancomycin resistance in enterococci but it has only recently generated interest. Intrinsically resistant enterococci possessing the vanC gene and the non-enterococcal genera Leuconostoc, Lactobacillus, Pediococcus and Erysipelothrix are known to cause human infection. This review examines the available data on their identification, resistance mechanisms, epidemiology, clinical infections and antimicrobial susceptibility. Intrinsically vancomycin-resistant gram-positives are usually opportunistic pathogens. Although serious infections may occur, treatment options remain available. No additional infection control measures for the intrinsically resistant genera appear justified with currently available evidence, although vigilance should be maintained to detect future changes in susceptibility patterns.

Anti-Bacterial Agents↗
PubMed1998

Selective isolation of vancomycin-resistant enterococci.

Many laboratories are likely to be or to become involved in screening patients for the carriage of vancomycin-resistant enterococci (VRE). A choice has to be made from the numerous formulations described and decisions made on the degree of vancomycin supplementation and the need for an enrichment phase. Few comparative trials and little critical evaluation has been performed to date and there is as yet no clear choice as to the optimal formulation. Laboratories must choose the formulation that most suits their particular requirements and circumstances.

Bacteriological Techniques↗
PubMed1996

An audit of peripheral catheter care in a teaching hospital.

Post-insertion care of peripheral venous catheters (PVCs) in 100 patients on general medical and surgical wards of a teaching hospital was audited. A variety of methods were used to attach the PVC to the patients' skin including 'Vecafix' dressings, bandages and adhesive tape. Sixty-eight PVC were incorrectly attached, and of these 49 (71%) were associated with two or more symptoms or signs of inflammation at the insertion site. Of those PVC that were correctly attached only five out of 32 (16%) were associated with inflammation. There was a significant association between incorrect dressing application and inflammation (P < 0 center dot 01). Similarly, there was a direct relationship between inflammation and PVCs that had been in situ for greater than 48 h (P < 0 center dot 01). The results suggest that a significant reduction in the incidence of inflammation associated with PVC use may be achieved by correct application of dressings and replacing the catheters after 48 h in situ.

Bandages↗
PubMed1982

Detection of left ventricular aneurysm on two dimensional echocardiography.

The differentiation of left ventricular aneurysm from diffuse left ventricular dilation and hypokinesia may have important therapeutic consequences. Thus the diagnostic accuracy of wide angle two dimensional echocardiography for the detection of left ventricular aneurysm was evaluated in a prospective study of 26 consecutive patients with the clinical suspicion of left ventricular aneurysm referred over a 10 month period. Every patients was examined with two dimensional echocardiography and left ventricular cineangiography, and findings were interpreted by two independent observers. A dilated hypokinetic left ventricle without aneurysm formation on cineangiography in nine patients was identified in all with two dimensional echocardiography. A left ventricular aneurysm on cineangiography in 17 patients was correctly identified in 14 with the two dimensional study, as were the site and extent of the lesion (apical in 12, anterior in 1 and inferior in 1). One apical aneurysm was interpreted on the two dimensional study as apical dyskinesia; one anterior and one posterobasal aneurysm were missed with this technique. Mural thrombi were correctly identified with two dimensional echocardiography in seven of seven patients. It is concluded that two dimensional echocardiography is an accurate noninvasive method that allows differentiation of left ventricular aneurysm from diffuse left ventricular dilation in the majority of patients. It provides information regarding the resectability of the aneurysm and may obviate cineangiography in many cases.

Coronary Disease↗
PubMed1982

The pathophysiology of angina pectoris and the effect of lidoflazine.

Angina pectoris results from a deficiency in myocardial oxygen supply. The rate-pressure product is an important predictor of myocardial oxygen requirements in patients with ischemic heart disease and in normal persons. The rate-pressure product at the onset of angina pectoris is reproducible under a variety of circumstances with a suitable protocol. In some patients, coronary artery spasm may reduce myocardial blood flow and contribute to the development of angina pectoris. Lidoflazine is a synthetic drug that appears to be a calcium-entry blocker and results in symptomatic improvement in patients with angina pectoris. Lidoflazine reduces the exercising rate-pressure product by its effect on heart rate and by decreasing systemic vascular resistance. It decreases coronary vascular resistance and antagonizes processes leading to an increase in coronary vasomotor tone.

Angina Pectoris↗
PubMed1981

Site of premature ventricular contractions demonstrated by echocardiography.

Abnormal ventricular activation in Wolff-Parkinson-White Syndrome (WPW) can be identified by echocardiography, but the effects of premature ventricular contractions have been demonstrated. We examined motion of the interventricular septum (IVS) and left ventricular posterior wall (LVPW) by surface echocardiography in 12 awake dogs using a method developed and validated in our laboratory. Premature ventricular contractions (PVCs) were induced by right (RV) and left ventricular (LV) pacing (6 dogs), injection of dopamine (2 dogs) and phenylephrine (2 dogs), and posterior myocardial infarction (MI) caused by embolization of the circumflex coronary artery (2 dogs), and posterior myocardial infarction (MI) caused by embolization of the circumflex coronary artery (2 dogs). PVCs induced by RV and LV septal pacing showed early IVS systolic posterior motion beginning 40.0 msec (range 26--48 msec) after the pacing impulse, while LVPW showed normal motion beginning 78.8 msec (range 63--116 msec) after the pacing impulse and accompanied by decreased posterior IVS motion. PVCs induced by LVPW pacing demonstrated early LVPW systolic anterior motion beginning 43.3 msec (range 31--68 msec) after the pacing impulse, while IVS showed a normal motion which began 97.3 msec (range 76--130 msec) after the pacing impulse and was accompanied by reduced anterior motion of the LVPW. PVCs induced by dopamine and phenylephrine showed a similar echocardiographic pattern to RV and LV septal pacing, while PVCs induced by MI exhibited a pattern similar to LVPW pacing. This study demonstrates that early IVS or LVPW contraction can be demonstrated by echocardiogram, and also indicates where the site of early excitation after PVCs is.

Animals↗
PubMed1978

Left and right ventricular dimensions during ventricular fibrillation in the dog.

Ventricular dimensions by surface echocardiography and intraventricular pressures were monitored in 27 dogs before and during ventricular fibrillation (VF) induced by coronary embolization (nine dogs), potassium infusion (nine dogs) and calcium infusion (nine dogs). Left ventricular diameter (LVD) fell by an average of 10.3 mm during the first 30 s after the onset of VF induced by ischemia or potassium and remained smaller than the prefibrillation end-diastolic LVD during the ensuing 10 min. LVD fell during calcium infusion, and after the onset of VF it remained only slightly larger than the preinfusion end-systolic LVD. Right ventricular (RV) diameter increased progressively for the first 2 min during VF an average of 15.9 mm. The failure of LV size to increase during VF was explained by a pressure gradient inhibiting LV filling during the early phase of VF. Despite progressive RV filling, pressure in the more compliant RV remained lower than in the LV, which exhibited reduced compliance during VF. Therefore, cardiac dilation during VF appears to be confined to the RV, and inhibition to LV filling is an important feature of the syndrome.

Animals↗