We hypothesized that inadequate oxygenation of peripheral tissues may be unrecognized in critically ill patients and may worsen their prognosis. To test this hypothesis, we measured oxygen delivery to tissues, oxygen uptake, and the extraction ratio (uptake/delivery) before and during a 30-minute infusion of a vasodilator, prostacyclin (5 ng per kilogram of body weight per minute), in 27 critically ill patients with acute respiratory failure. Prostacyclin produced an increase in oxygen delivery (median value before vs. during infusion, 375 vs. 492 ml of oxygen per minute per square meter of body-surface area, P less than 0.001) that was similar in the 14 patients who survived and the 13 who died. This increase in oxygen delivery was associated with a significantly greater increase in oxygen uptake in the patients who died as compared with the survivors (median increase, 19 vs. 5 percent, P less than 0.001). In the survivors, the oxygen extraction ratio fell (median change, -17 percent; range, -27 to -6 percent) and the mixed venous oxygen tension increased. In the patients who died, the extraction ratio rose (median change, 11 percent; range -24 to +40 percent) and the mixed venous oxygen tension did not change. These data suggest the presence of a substantial oxygen debt in patients who subsequently die. Inadequate tissue oxygenation, which may be difficult to recognize, appears to be an important mechanism contributing to the development of irreversible multiple organ failure and subsequent death in some patients with acute respiratory failure.
Continuous, high volume, venous-venous haemofiltration was used as renal support in 28 critically ill patients with acute renal failure. Fifteen patients survived and were subsequently discharged from the ITU. Although haemofiltration was highly effective in reducing the blood urea and serum creatinine, only survivors demonstrated a significant increase in arterial pH (medians before and at two days 7.28 and 7.49 respectively, p less than 0.005) with a reduction in severity of their illness (median APACHE II scores before and at two days 23 and 16, p less than 0.005). Patients who died remained severely ill and acidotic (median APACHE II scores before and at two days 26 and 28; median arterial pH values 7.32 and 7.31 respectively) and by day two of treatment, marked differences between the patient groups in APACHE II scores, mean arterial pressure, arterial pH and urine flow rate had developed. Haemofiltration with the correction of acute uraemia alone does not necessarily lead to a reduction in the severity of illness which in the critically ill more frequently reflects other organ dysfunction.
Hydroxyethyl starch (HES 450.000/0.7; Hespan 6.0 g/100 ml) was compared with standard crystalloid solutions in postoperative volume replacement in 20 patients undergoing routine orthopaedic surgery. The HES group showed no clinical evidence of haemorrhage and no laboratory evidence of significant haemostatic defects as assessed by standard coagulation tests, platelet aggregation and fibrinogen concentrations. There was a slight shortening in the thrombin time and a smaller increase in post-operative FVIII RAg and FVIII RCof levels in the HES group. HES is a safe and effective volume expander for postoperative use.
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