C. G. Olthof

Non-invasive conductivity technique to detect changes in haematocrit: in vitro validation.

An on-line haematocrit measurement in extracorporeal circuits might be useful under some clinical circumstances (e.g. haemodialysis or cardiac surgery). As no such measurement exists, a device has been developed that makes it possible to detect haematocrit (Ht) continuously without a loss of blood. It is a multi-frequency system for the detection of electrical conductivities. The aim of this study was to investigate whether this device can measure Ht alterations properly. Ht alterations were induced by adding pure mannitol and 20% mannitol to fresh human blood. Furthermore, the effect of both mannitol substances on the intracellular ion content, intracellular conductivity and Ht were investigated. Alternations in Ht were established by the addition of 1000, 800, 600, 400, 200 and 0 mg of pure mannitol to 10 ml of fresh human blood, and 3.0, 2.5, 2.0, 2.0, 1.5, 1.0, 0.5 and 0 ml of 20% mannitol to fresh human blood until a total volume of 10 ml was achieved. Although their effects were significantly different, pure mannitol and 20% mannitol both caused a reduction in mean cellular volume, and thus in Ht. A highly significant correlation was found between Ht and intracellular conductivity (r=0.90, p<0.001). In addition to these effects, addition of pure mannitol and 20% mannitol had different effects on the intracellular ion content. Pure mannitol caused an increase in intracellular ion content due to a transcellular ion shift, whereas 20% mannitol induced a decrease. From this study, it can be concluded that the multi-frequency conductivity method observes changes in Ht (and intracellular fluid volume) in an accurate manner. Changes in intracellular ion content of erythrocytes depend on the sort of mannitol substance that is added. The intracellular ion concentration can be calculated from measured intracellular conductivity and Ht. The total number of intracellular ions can be derived from intracellular conductivity and the number of erythrocytes.

Determination of capillary leakage due to recombinant interleukin-2 by means of noninvasive conductivity measurements

SummaryOne of the most common side effects of treatment with recombinant interleukin-2 (IL-2) is capillary leakage. Its genesis is not completely understood. The aim of the study was to determine whether capillary leakage can be monitored by means of a non-invasive conductivity technique and to study its starting point. Eight patients with advanced renal cell cancer were studied in a medium care section of the Department of Medical Oncology, University Hospital over 4 days during treatment sessions of continuous, intravenously administered IL-2 (mean dose of 15.6 × 106 IU · m−2 · day −1). The fluid shift from the intravascular to the extra- and intracellular compartments was monitored by means of noninvasive conductivity measurements. Changes in blood volume were calculated from serial erythrocyte counts. The clinical parameters of capillary leakage (oliguria, positive fluid balance, and gain in mass) were recorded. The mean gain in mass was 9% after 4 days of IL-2 treatment. The extracellular fluid volume increased significantly [46 (SD 23.2)%; P < 0.01], whereas the intracellular fluid volume did not change. The increase in blood volume (BV) amounted to 7% (P < 0.05). The decline in albumin concentration was significantly more than the increase in BV [38 (SD 4.3) %; P < 0.01], indicating capillary albumin leakage. The main changes were observed after the 2nd day of treatment. From this study, it is suggested that conductivity measurements are a suitable method to monitor capillary leakage induced by IL-2, and could be used to detect the exact onset and severity of this leakage. The leakage started within the first 24 h of treatment and was detected as a fluid shift from the intravascular to the extracellular space, while the intracellular compartment remained stable. These measurements could be useful during intervention studies with the aim of preventing this adverse effect of IL-2.