Tetrastarch sustains pulmonary microvascular perfusion and gas exchange during systemic inflammation.

OBJECTIVE: According to Fick's law of diffusion, gas exchange depends on the size and thickness of the blood perfused alveolocapillary membrane. Impairment of either one is tenuous. No data are available concerning the impact of hydroxyethyl starches and saline on pulmonary microperfusion and gas exchange during systemic inflammation. DESIGN: Prospective, randomized, controlled experimental study. SETTING: University research laboratory. SUBJECTS: Thirty-two anesthetized rabbits assigned to four groups (n = 8). INTERVENTIONS: Except for the control group, systemic inflammation was induced by lipopolysaccharide. Fluid resuscitation was performed with saline alone or in conjunction with tetrastarch or pentastarch. Pulmonary microcirculation was analyzed at 0 hr and 2 hrs using intravital microscopy. Thickness of the alveolocapillary membrane was measured using electron microscopy. MEASUREMENTS AND MAIN RESULTS: Macrohemodynamics were stable in all groups. In pulmonary arterioles, lipopolysaccharide reduced the erythrocyte velocity and impeded the microvascular decrease of the hematocrit in the saline and pentastarch group. In contrast, infusion of tetrastarch normalized these perfusion parameters. In capillaries, lipopolysaccharide decreased the functional capillary segment density and the capillary perfusion index, which was prevented by both starches. However, compared with saline and pentastarch, treatment with tetrastarch prevented the lipopolysaccharide-induced reduction of the capillary erythrocyte flux and inversely reduced the erythrocyte capillary transit time. Thickening of alveolocapillary septae after lipopolysaccharide application was solely observed in the saline and pentastarch group. In contrast to pentastarch and saline, the application of tetrastarch prevented the lipopolysaccharide-induced increase of the alveoloarterial oxygen difference. CONCLUSIONS: Tetrastarch sustains pulmonary gas exchange during experimental systemic inflammation more effectively than saline and pentastarch by protecting the diffusion distance and the size of the microvascular gas exchange surface. Improved capillary perfusion resulting from tetrastarch therapy, which is typically applied to increase blood pressure, may according to the Ohm's law locally decrease hydrostatic perfusion pressures in the pulmonary microvasculature during systemic inflammation.

Syndecan-1 as a biomarker for sepsis survival after major abdominal surgery.

AIM: Sepsis is a serious complication following surgery and identification of patients at risk is of high importance. Syndecan-1 (sSDC1) levels are known to be elevated during sepsis. MATERIALS & METHODS: Fifty-five patients scheduled for major abdominal surgery were prospectively included and sSDC1 concentrations were measured during hospital stay. RESULTS: Patients with postoperative sepsis showed a continued increase of sSDC1 levels and exhibited higher median sSDC1 concentrations at day 1 compared with nonseptic patients 90.3 versus 16.5 ng/ml. A significant association of sSDC1 levels with the incidence of sepsis and death was demonstrated. CONCLUSION: This study identifies sSDC1 as potential biomarker for sepsis and survival after abdominal surgery.

Perioperative fluid therapy: defining a clinical algorithm between insufficient and excessive.

In the perioperative scenario, adequate fluid and volume therapy is a challenging task. Despite improved knowledge on the physiology of the vascular barrier function and its respective pathophysiologic disturbances during the perioperative process, clear-cut therapeutic principles are difficult to implement. Neglecting the physiologic basis of the vascular barrier and the cardiovascular system, numerous studies proclaiming different approaches to fluid and volume therapy do not provide a rationale, as various surgical and patient risk groups, and different fluid regimens combined with varying hemodynamic measures and variable algorithms led to conflicting results. This review refers to the physiologic basis and answers questions inseparably conjoined to a rational approach to perioperative fluid and volume therapy: Why does fluid get lost from the vasculature perioperatively? Whereto does it get lost? Based on current findings and rationale considerations, which fluid replacement algorithm could be implemented into clinical routine?

Perioperative fluid and volume management: physiological basis, tools and strategies.

Fluid and volume therapy is an important cornerstone of treating critically ill patients in the intensive care unit and in the operating room. New findings concerning the vascular barrier, its physiological functions, and its role regarding vascular leakage have lead to a new view of fluid and volume administration. Avoiding hypervolemia, as well as hypovolemia, plays a pivotal role when treating patients both perioperatively and in the intensive care unit. The various studies comparing restrictive vs. liberal fluid and volume management are not directly comparable, do not differ (in most instances) between colloid and crystalloid administration, and mostly do not refer to the vascular barrier's physiologic basis. In addition, very few studies have analyzed the use of advanced hemodynamic monitoring for volume management.This article summarizes the current literature on the relevant physiology of the endothelial surface layer, discusses fluid shifting, reviews available research on fluid management strategies and the commonly used fluids, and identifies suitable variables for hemodynamic monitoring and their goal-directed use.