Antoni Jurkiewicz

A Comparison of Predictive Outcomes of APACHE II and SAPS II in a Surgical Intensive Care Unit

The Acute Physiologic Score and Chronic Health Evaluation (APACHE) II and the Simplified Acute Physiologic Scale (SAPS) II are two of the more commonly employed predictors of outcome and performance in the intensive care unit setting. However, controversy persists about whether the scores generated by these systems have similar predictive value. This study compared the predicted mortalities derived from APACHE II and SAPS II and contrasted them to the actual mortality in a surgical intensive care unit (SICU). Data for 1665 patients admitted to the SICU between July 1994 and August 1997 were entered into an SICU computerized database. From recorded demographic, hemodynamic, and laboratory data, APACHE II and SAPS II scores were obtained with corresponding predicted mortalities. Patients were stratified by age into categories of less than and greater than 65 years old. Predicted mortalities by APACHE II and SAPS II were compared for each group. An additional analysis included a comparison of survivors and nonsurvivors. There was no significant difference in predicted mortality between APACHE II and SAPS II in any of the groups. Actual mortality was 30 of 486 (6.2%) in patients less than 65 years of age and 73 of 1179 (6.2%) in patients 65 years of age or greater. The APACHE II and SAPS LI predicted mortalities (mean ± SD) for patients less than 65 years of age were 10.5% ± 10.6% and 10.9% ± 13.3%, respectively (P > .05). The APACHE II and SAPS II predicted mortalities in patients 65 years of age or greater were 19.1% ± 17.8% and 18.7% ± 21.0%, respectively (P > .05). Similarly, when patients were stratified by survival status, no significant difference was present between groups. However, in individual patients, a difference between APACHE II and SAPS II scores was often present. We conclude that although disparities between APACHE II and SAPS II predicted mortalities in individual patients may be significant, APACHE II and SAPS II have similar predictive value in a large SICU patient population. However, both APACHE II and SAPS II systems overestimate mortality in SICU patients. Based on our results, we conclude that either system can be used to measure quality of care in the SICU; however, neither system can be reliably applied to a single patient.

Effect of hematocrit on regional oxygen delivery and extraction in an adult respiratory distress syndrome animal model

BACKGROUND The purpose of this prospective, randomized, controlled study was to investigate the effects of hematocrit (Hct) on regional oxygen delivery and extraction following induction of adult respiratory distress syndrome (ARDS) in an animal model. METHODS Animals were instrumented to monitor central venous pressure (CVP), systemic mean arterial pressure (MAP), pulmonary artery occlusion pressure (PAOP), and cardiac output (CO) and to measure blood flow in the renal, hepatic, and superior mesenteric arteries and portal vein. ARDS was induced, positive end expiratory pressure (PEEP) applied and CO was maximized with volume loading and epinephrine infusion. Data were acquired at baseline (BL) and at Hct levels ranging from 25% to 50%. RESULTS Systemic DO(2) increased steadily and significantly with increased Hct. Systemic O(2) extraction ratio (O(2)ER) decreased significantly with increasing Hct until a threshold value of 40%, after which further increases in Hct did not cause a statistically significant decrease in O(2)ER. Similarly, renal and hepatic DO(2) increased and O(2)ER decreased in a statistical significant manner with transfusions up to a Hct of 35%. In the splanchnic circulation blood transfusions did not cause any statistically significant increase in DO(2), and O(2)ER showed no decrease after an Hct of 35%. Systemic, renal, hepatic, and splanchnic VO(2) were not affected by changes in Hct. Blood viscosity decreased from a baseline value of 2.9+/-0.2 centipoise at a Hct of 38% to 2.3+/-0.1 centipoise at a Hct of 25% (P<0.05). Viscosity increased progressively with increasing hematocrits and reached the value of 4.2+/-0.2 centipoise at an Hct of 50% (P<0.05 versus Hct 30%, 35%, 40%, 45%). CONCLUSIONS Based on the results of this non-supply-dependent animal model we conclude that a progressive increase in Hct up to 40% causes a corresponding increase in systemic DO(2) associated with a decrease in O(2)ER. However, there is no improvement in renal, hepatic, and splanchnic DO(2) and O(2)ER after a threshold Hct of 35%. All other factors being the same, an Hct greater than 35% may in fact cause a decrease in blood flow rate and change in blood flow characteristics as a consequence of increased blood kinematic viscosity, which may alter and compromise cellular oxygen transfer.