Patient Hematocrit, % g/I 1 41 62 0.22 1.9 1.7 2 32 44 1.56 4.7 3.2 3 32 30 1.83 6.2 4.4 4 22 32 3.50 7.6 4.2 5 17 19 2.00 3.8 1.8 6 38 52 0.008 3.9 3.9 7 35 32 1.02 4.8 3.8 8 8 11 1.94 3.8 1.9 9 29 37 0.30 3.8 3.5 10 28 34 0.75 4.3 3.5 11 12 16 2.22 3.7 1.4 12 29 42 0.85 6.2 5.4 13 33 24 0.73 3.1 2.3 Mean 27 33 1.30 4.4 3.1 SD 10 14 0.99 1.5 1.2 SE 3 4 0.27 0.4 0.3 Clinical Chemistry 42, No. 5, 1996 779 Plasma Dextran Concentrations in Trauma Patients Administered Hypertonic Saline-Dextran-70 To the Editor: A hypertonic/hyperoncotic solution [75 g/L NaCI in 60 g/L dextran-70: hyper- tonic saline-dextran (HSD)] has recently been introduced for resuscitation of trauma patients who are hypotensive ow- ing to hemorrhage [1-3]. Concern has been raised as to the degree of hyper- natremia and hypokalemia induced by HSD administration /4, 5] as well as whether the dextran administered could induce adverse effects or adversely affect blood typing or blood clotting in these patients [6-8]. Previous human trials re- ported that HSD infusion in trauma pa- tients raised serum sodium and chloride concentrations by -10 nirnol/L in most cases, but without adverse effects [2, 3, 9, 10]; none of these studies, how- ever, reported dextran concentrations. We obtained blood samples from 13 patients who were treated with 250 mL of HSD (Pharmacia AB, Uppsala, Swe- den) as a part of a larger prospective, randomized, double-blinded placebo- controlled study evaluating the efficacy of the solution [3,9,10]. The patients enrolled in our study were selected blindly from the larger test population. This study was approved by the Human Subjects Review Board at the University of California, Davis. Patients were transported to the hos- pital by a Life Flight helicopter system, and all had hypotension (systolic blood pressure <90 mmHg) upon enrollment in the study. HSD (250 mL) was admin- istered intravenously, usually via percu- taneously inserted catheters, over 2-5 mm while en route to the hospital. The delivered dose of HSD was 3.6 ± 0.2 mL/kg of body weight (range: 2.5-5.0 mL/kg). All other aspects of the patients’ care were those used routinely. Addi- tional fluid (lactated Ringer’s solution) was administered as clinically indicated. The time of administration of the HSD was noted, and the volumes of all addi- tional fluids given were recorded. Upon patients’ arrival in the emer- gency room, 26.7 ± 4.5 mm (range: 6-63 mm) from initiation of the HSD dose, a venous blood sample was taken for measurement of hematocrit and plasma total protein, glucose, total car- bohydrate, sodium, and potassium. Total carbohydrate concentrations in plasma were determined in duplicate by the an- throne reaction, with serial dilutions of HSD as calibrator, after the precipitation of plasma protein with 100 g/L trichlo- roacetic acid [11].Plasma glucose was determined by an automated glucose- hexokinase enzymatic method on a Co- bas-Fara II analyzer (Roche Analytical Instruments, Belleville, NJ). Dextran concentrations were calculated as the dif- ference between plasma total carbohy- drate and glucose concentrations. Data are presented as mean ± SE. At the time of initial examination in the emergency room, the patients were all hemodiluted, as indicated by low he- matocrit (27.4% ± 2.8%) and total plasma protein (33 ± 4 g/L; Table 1) (reference intervals: 34-50% and 60-80 g/L, respectively). Plasma concentrations of sodium were significantly increased (155 ± 1 mmol/L; P <0.05, Student’s t-test) from normal values (135-145 mmol/L), whereas plasma potassium (4.0 ± 0.1 mmol/L) tended to be normal (3.5-5 mmnollL). These data are consis- tent with the larger multicenter trial re- sults for serum electrolytes [2, 3, 9, 10]. In the current study, plasma dextran con- centrations ranged from 1.4 to 5.4 g/L (mean ± SE, 3.15 ± 0.34 g/L) (Table I). The hemodilution observed upon ad- mission to the emergency room reflects not only the infusion of crystalloid fluids but also the transcapillary influx of fluid into the vascular space after hemorrhage and the facilitation of this process by HSD administration [1-3, 12, 13]. These processes resulted in a decrease in hemat- Table 1. Plasma values Totai protein ocrit and concentrations of total plasma protein by simple dilution. The mean plasma dextran (3.15 g/L) was considerably less than expected. In a 70 kg euvolemic man, plasma volume is assumed to be -2250 mL. Adding 250 mL of HSD containing 60 g/L dextran (15 g) to this volume should give a final dextran concentration of 6.7 g/L. Given the hemodilution effect of dextran, this concentration might actually reach 5 g/L. However, because the study patients experienced significant hemorrhage, consequently reducing their plasma vol- ume, the concentration of dextran should have been >5 g/L. The low plasma dex- iran concentrations observed in this study suggest a rapid clearance, seques- tration (or binding) of dextran, a larger volume of distribution, or hemodilution. The time to clearance of half of the dextran is 7-10 h [14-16]. Since the blood samples were obtained within 0.5 h of HSD administration, the clearance of dextran would be minimal. Fibrmnogen, an acute-phase protein, can increase in response to tissue injury and traumatic stress [17]. Previous stud- ies have reported that dextrans may react with fibrinogen /7, 18]. If this conjugate forms in vivo after HSD infusion, any dextran bound would be removed by the precipitation with trichloroacetic acid, rendering this dextran unavailable for assay. However, subsequent studies in experimented animals have detected no significant differences between serum or plasma dextran concentrations after HSD infusion and have found no detect- in patients given HSD. Giucose Totai carbohydrate Dextran Downloaded from https://academic.oup.com/clinchem/article/42/5/779/5646601 by guest on 25 November 2021