Ascitic fluid samples are frequently sent to the laboratory for analysis. Although the underlying cause of the ascites is often thought to be clinically obvious, it is important to establish a definitive diagnosis. The value of a cell count and bacterial culture of the ascitic fluid is not disputed, but the role of biochemical testing is less clear. The use of ascitic fluid total protein to try to classify ascitic fluids as either an exudate or a transudate has contributed to this. The use of the physiologically based serum ascites albumin gradient to differentiate ascites caused by portal hypertension from other causes provides a better diagnostic approach. We recommend that the serum ascites albumin gradient is performed by laboratories as the first-line test and that interpretative reports are provided. Additional testing should be restricted to specific diagnostic queries and requires close collaboration between the laboratory and the clinician.

SUMMARY There have been considerable advances in understanding the metabolic role of the endothelial lining cells of the blood vessels. Angiotensin-converting enzyme activity is concentrated in these cells, especially those lining the pulmonary circulation. The enzyme exerts control over systemic vascular tone indirectly through the powerful pressor effect of angiotensin II. A number of therapeutic agents are now available which directly inhibit converting enzyme activity and thereby effect a reduction in blood pressure.Macrophages are the source of increased angiotensin-converting enzyme activity commonly found in association with active sarcoidosis. A better understanding of this phenomenon may give fresh insight into this puzzling condition. Pulmonary endothelial metabolism is affected by lung injury and it is likely that in this situation changing activities of serum angiotensin converting enzyme may indicate the extent of damage and the response to therapy. The full clinical significance of serum ACE measurements has yet to be established. However, raised activities have been reported in a number of other conditions and diabetes mellitus and hyperthyroidism are of particular current interest.The numerous methods and reference ranges described in the literature for the measurement of serum ACE activity require further assessment, and there is a clear need for an accepted reference method.Angiotensin I, a decapeptide generated by action of the enzyme renin on a glycoprotein substrate angiotensinogen, is converted to the pressor octapeptide angiotensin II. The exopeptidase responsible for this conversion was first identified and isolated in plasma by Skeggs et al,'2 who named it angiotensinconverting enzyme. This enzyme is a halideactivated, EDTA-sensitive, peptidase that catalyses the cleavage of dipeptidyl residues from the COOH termini of peptide substrates,3 and releases His-Leu from the COOH terminus of the decapeptide angiotensin I.The ready conversion of angiotensin I to angiotensin II was assumed to take place in the circulation until Ng and Vane4 recognised that the enzyme activity present in plasma was insufficient to account for the rapidity of "in vivo" conversion, and demonstrated most conversion of circulating angiotensin I to angiotensin II occurred during passage through the lungs. Stanley and Biron' confirmed the importance *Present address: Harefield Hospital, Harefield, Middlesex...Accepted for publication 17 January 1983 of lung as a site of angiotensin-converting enzyme activity by demonstrating reduced angiotensin I conversion in dogs on cardiopulmonary bypass; the lowered rate of conversion, however, was still higher than that in blood alone.The pulmonary vascular bed is uniquely placed to modify levels of circulating vasoactive substances, being immediately up stream of the high pressure systemic circulation and receiving virtually the whole cardiac output. However, the fact that blood pressure control is maintained, albeit at a lower level, during cardiopulmonary bypass indicates th...

Biochemical examination of pleural fluid is usually done to try to identify the cause of a pleural effusion. The various analytes that have been suggested for this are reviewed and evaluated. Distinguishing whether the effusion is an exudate or transudate is a pragmatic first step. with further investigations dictated by the clinical features and these results. Total protein and lactate dehydrogenase were used first; Light's criteria were published in 1972 and since then additional markers including cholesterol, bilirubin and albumin gradient plus combinations of these have been proposed. Although combination testing does improve the sensitivity for diagnosis of an exudate. this is at the expense of specificity. Measurement of fluid to serum ratios appears to confer no advantage, and if a single test is required total protein performs as well as any. Additional tests may be useful in specific circumstances: pleural fluid pH may aid decisions over drainage of a parapneumonic effusion; glucose may indicate an effusion associated with rheumatoid arthritis; and adenosine deaminase may help with the diagnosis of tuberculous effusions.

SUMMARY. Blunders which occurred over a 1 year period in the clinical chemistry departments of two health districts were recorded and categorized according to type and detection stage. A blunder was defined as an incident leading to an incorrect result/set of results either being reported or detected at the final checking-out stage in the laboratory. Of the total of 120 blunders-which is a blunder rate of less than 0'1 % of requests-53 (440/0) were detected at the final checking-out stage. Blunders detected after the report had left the laboratory were divided into those subsequently picked up by laboratory personnel (23); those detected by clinicians (19); and those by external quality assessment schemes (21). The types of blunder were fairly equally distributed between the booking-in (36), analysis (38), and reporting (35) stages of the laboratory process. A formal review of blunders detected in laboratories is a valuable aid to overall performance. Additional key phrases: quality assurance; errors; analysisDespite passing interest during each of the three last decades in 'blunders' occurring in clinical chemistry laboratories, the situation remains as Northam! described it in 1977, namely 'that although much effort and expense is being devoted to the assessment of analytical variation, little attention has been directed to the detection of laboratory blunders'.That seriously addressing the issue of laboratory blunders has not occurred is surprising, because the most recent study-reported a rate of O' 3% in a large laboratory. Although this figure represented a significant improvement over the rate of 2'3% found by McSwiney and Woodrow;' it does imply that at least two serious errors occur each working day in large laboratories.To investigate the current situation, the South East Thames Quality Assurance Group decided to monitor the number, type and detection stage of blunders which were picked-up over a 1 year period in each of two health districts.Correspondence: Mrs R Lapworth. METHODA blunder was defined as an incident leading to an incorrect result/set of results either being reported or detected at the final checking-out stage in the laboratory. Errors detected before or during analysis, or before the final validation stage were not included. The staff in each laboratory were informed that the study was being carried out and agreed to bring any blunders that occurred to our attention. Details of these, and at what stage the blunder was detected were recorded by ourselves or occasionally by other senior laboratory staff. The blunders were then categorized according to type and detection stage.Blunders which affected samples distributed by the external quality assessment schemes (EQAS) during the period of this study were included if the results were more than three standard deviations (SD) from the method mean. The blunder rate affecting EQAS samples was also calculated separately as they may give a better estimate of the true detection rate.?Users of the service were not specifically asked to bring blun...

1. The effects of low dose infusion of atrial natriuretic peptide (ANP) were observed in double-blind, placebo-controlled study in six fluid-loaded volunteers. After baseline observations, hourly increments of 0.4, 2 and 10 pmol min-1 kg-1 were infused with continuous observation of heart rate, blood pressure and cardiac output. Plasma ANP, aldosterone, and catecholamines, and urinary volume and sodium excretion, were estimated at half-hourly intervals. 2. ANP infusion resulted in an increase of 35, 98 and 207% in urinary sodium excretion and of 10, 20 and 71% in urinary volume when compared with placebo. Plasma ANP was markedly elevated above placebo levels only during infusion of 10 pmol of ANP min-1 kg-1. 3. No change in heart rate of blood pressure was noted during the study, but a significant fall in stroke volume index was observed during active treatment. Plasma levels of aldosterone and catecholamines were not significantly different on the 2 treatment days. 4. The potent natriuretic and diuretic effects of this peptide at plasma concentrations not significantly elevated from physiological suggest a hormonal role for ANP in the homoeostasis of salt and water balance.