Preservation of blood volume during edema removal in nephrotic subjects

Preservation of blood volume during edema removal in nephrotic subjects. During the gradual removal of edema with diuretics in 21 edematous patients with the nephrotic syndrome (NS) we monitored blood volume. For comparison, nine healthy subjects were studied after equilibration on diets containing 20, 200, and 1138mEq sodium. The initial extracellular fluid volume (ECFV) in the patients exceeded the final ECFV by 63.4 ± 8.4%. In 10 patients with a very low plasma oncotic pressure (8.2 ± 0.4mm Hg, Group 1), the blood volume changed little. In Group 2 (plasma oncotic pressure 13.4 ± 1.0mm Hg), it was 11.0 ± 2.5% higher at entry than after edema withdrawal. In the normal volunteers, the highest sodium intake raised the ECFV by 21.4 ± 4.1%. The accompanying rise in blood volume, 11.2 ± 3.0%, was larger than in the patients of Group 1 (2.4 ± 1.9%, P < 0.04), but not of Group 2 (8.1 ± 1.9%, NS) at similar degrees of expansion. There was no difference in blood volume between the edema-free patients and the normal subjects at low-sodium diet. The course of blood pressure and creatinine clearance during edema removal gave no evidence that functional hypovolemia was induced, but the plasma renin activity was higher than in the normal subjects at similar degrees of expansion. We conclude that the blood volume to ECFV relationship curve is flattened in the presence of hypoalbuminemia. Thus, the increase in blood volume that normally follows ECFV expansion is less in patients with the NS, but a drop below normal upon removal of edema is absent also

Functional relationships in the nephrotic syndrome

Functional relationships in the nephrotic syndrome. An analysis of 70 observations in patients with the nephrotic syndrome (NS) on a low sodium diet is presented. The following parameters were determined: plasma volume, plasma renin activity, plasma aldosterone concentration, serum albumin, urinary sodium and protein excretion, and creatinine clearance. In 41 instances glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were determined on the basis of 51Cr-EDTA and 125I-hippuran clearances, and the filtration fraction (FF) was calculated. The results in patients with minimal lesions (ML) and those with histological glomerular lesions (HL) were compared to determine whether these groups can be separated on the basis of signs of hypovolemia and primary renal sodium retention. Although a higher proportion of the ML patients showed extreme sodium retention and elevated plasma renin and aldosterone levels, these values tended to overlap and no differences were found for blood volume, blood pressure, and overall renal function between the groups. FF was markedly and equally depressed in both groups: 13.5 ± 1.6% in the ML and 14.2 ± 1.1% SEM in the HL group (NS). Analysis of the within-group relationships between the parameters under study revealed relatively few correlations, which supports the hypothesis that primary impairment of renal water and salt excretion is an important if not overruling factor in patients with the NS.Relations fonctionnelles au cours du syndrome néphrotique. Une analyse de 70 observations de malades atteintes de syndrome néphrotique (NS) en régime pauvre en sodium est présentée. Les paramètres suivants ont été déterminés: volume plasmatique, activité rénine plasmatique, aldostéronémie, albuminémie, natriurèse et protéinurie, et clearance de la créatinine. Dans 41 fois, le débit de filtration glomérulaire (GFR) et le débit plasmatique rénal efficace (ERPF) ont été déterminés par des clearances au 51Cr-EDTA et au 125I-hippuran, et on a calculé la fraction de filtration (FF). Les résultats des groupes de malades atteints de lésions minimes (ML) et de ceux atteints de lésions glomérulaires histologiques (HL) ont été comparés pour savoir s'il est possible de séparer ces groupes sur la base des signes d'hypovolémie et de rétention sodée d'origine rénale. Bien qu'une plus forte proportion de malades ML ait présenté une réntention sodée et une élévation des niveaux de rénine et d'aldostérone plasmatiques extrêmes, ces valeurs tendaient à se chevaucher et il n'a pas été trouvé de différence dans le volume sanguin, la pression artérielle et la fonction rénale globale entre les groupes. FF était diminuée de façon marquée et identique dans les deux groupes: 13,5 ± 1,6% dans le groupe ML et 14,2 ± 1,1% SEM dans le groupe HL (NS). Une analyse des interrelations à l'intérieur des groupes entre les paramètres étudiés a révélé relativement peu de corrélations, ce qui est en faveur de l'hypothèse que l'altération primitive de l'excrétion rénale d'eau et de sel est un facteur important, sinon capital chez les malades atteints de NS

Occurrence and impact of delayed cerebral ischemia after coiling and after clipping in the International Subarachnoid Aneurysm Trial (ISAT)

Delayed cerebral ischemia (DCI) is an important cause of poor outcome after aneurysmal subarachnoid hemorrhage (SAH). We studied differences in incidence and impact of DCI as defined clinically after coiling and after clipping in the International Subarachnoid Aneurysm Trial. We calculated odds ratios (OR) for DCI for clipping versus coiling with logistic regression analysis. With coiled patients without DCI as the reference group, we calculated ORs for poor outcome at 2 months and 1 year for coiled patients with DCI and for clipped patients without, and with DCI. With these ORs, we calculated relative excess risk due to Interaction (RERI). Clipping increased the risk of DCI compared to coiling in the 2,143 patients OR 1.24, 95% confidence interval (95% CI 1.01–1.51). Coiled patients with DCI, clipped patients without DCI, and clipped patients with DCI all had higher risks of poor outcome than coiled patients without DCI. Clipping and DCI showed no interaction for poor outcome at 2 months: RERI 0.12 (95% CI −1.16 to 1.40) or 1 year: RERI −0.48 (95% CI −1.69 to 0.74). Only for patients treated within 4 days, coiling and DCI was associated with a poorer outcome at 1 year than clipping and DCI (RERI −2.02, 95% CI −3.97 to −0.08). DCI was more common after clipping than after coiling in SAH patients in ISAT. Impact of DCI on poor outcome did not differ between clipped and coiled patients, except for patients treated within 4 days, in whom DCI resulted more often in poor outcome after coiling than after clipping

The relationship between the time of cerebral desaturation episodes and outcome in aneurysmal subarachnoid haemorrhage: a preliminary study.

In this preliminary study we investigated the relationship between the time of cerebral desaturation episodes (CDEs), the severity of the haemorrhage, and the short-term outcome in patients with aneurysmal subarachnoid haemorrhage (aSAH). Thirty eight patents diagnosed with aneurysmal subarachnoid haemorrhage were analysed in this study. Regional cerebral oxygenation (rSO2) was assessed using near infrared spectroscopy (NIRS). A CDE was defined as rSO2 < 60% with a duration of at least 30 min. The severity of the aSAH was assessed using the Hunt and Hess scale and the short-term outcome was evaluated utilizing the Glasgow Outcome Scale. CDEs were found in 44% of the group. The total time of the CDEs and the time of the longest CDE on the contralateral side were longer in patients with severe versus moderate aSAH [h:min]: 8:15 (6:26-8:55) versus 1:24 (1:18-4:18), p = 0.038 and 2:05 (2:00-5:19) versus 0:48 (0:44-2:12), p = 0.038. The time of the longest CDE on the ipsilateral side was longer in patients with poor versus good short-term outcome [h:min]: 5:43 (3:05-9:36) versus 1:47 (0:42-2:10), p = 0.018. The logistic regression model for poor short-term outcome included median ABP, the extent of the haemorrhage in the Fisher scale and the time of the longest CDE. We have demonstrated that the time of a CDE is associated with the severity of haemorrhage and short-term outcome in aSAH patients. A NIRS measurement may provide valuable predictive information and could be considered as additional method of neuromonitoring of patients with aSAH

Optimizing the Definitions of Stroke, TIA and Infarction for Research and Application in Clinical Practice

Background and purposeUntil now, stroke and transient ischemic attack (TIA) have been clinically based terms which describe the presence and duration of characteristic neurological deficits attributable to intrinsic disorders of particular arteries supplying the brain, retina, or (sometimes) the spinal cord. Further, infarction has been pathologically defined as death of neural tissue due to reduced blood supply. Recently, it has been proposed we shift to definitions of stroke and TIA determined by neuroimaging results alone and that neuroimaging findings be equated with infarction.MethodsWe examined the scientific validity and clinical implications of these proposals using the existing published literature and our own experience in research and clinical practice.ResultsWe found that the proposals to change to imaging-dominant definitions, as published, are ambiguous and inconsistent. Therefore, they cannot provide the standardization required in research or its application in clinical practice. Further, we found that the proposals are scientifically incorrect because neuroimaging findings do not always correlate with the clinical status or the presence of infarction. In addition, we found that attempts to use the proposals are disrupting research, are otherwise clinically unhelpful and do not solve the problems they were proposed to solve.ConclusionWe advise that the proposals must not be accepted. In particular, we explain why the clinical focus of the definitions of stroke and TIA should be retained with continued sub-classification of these syndromes depending neuroimaging results (with or without other information) and that infarction should remain a pathological term. We outline ways the established clinically based definitions of stroke and TIA, and use of them, may be improved to encourage better patient outcomes in the modern era

Pharmacological treatment of delayed cerebral ischemia and vasospasm in subarachnoid hemorrhage

Subarachnoid hemorrhage after the rupture of a cerebral aneurysm is the cause of 6% to 8% of all cerebrovascular accidents involving 10 of 100,000 people each year. Despite effective treatment of the aneurysm, delayed cerebral ischemia (DCI) is observed in 30% of patients, with a peak on the tenth day, resulting in significant infirmity and mortality. Cerebral vasospasm occurs in more than half of all patients and is recognized as the main cause of delayed cerebral ischemia after subarachnoid hemorrhage. Its treatment comprises hemodynamic management and endovascular procedures. To date, the only drug shown to be efficacious on both the incidence of vasospasm and poor outcome is nimodipine. Given its modest effects, new pharmacological treatments are being developed to prevent and treat DCI. We review the different drugs currently being tested