Base deficit does not predict mortality when secondary to XXXX .

@entity1 @entity8193 @entity520 @entity51 @entity519 @entity204
Base deficit has been established as a predictor of mortality and endpoint of resuscitation. We hypothesized that in a significant subset of surgical intensive care @entity1 , base deficit is secondary to @entity520 , and that these @entity1 experience lower mortality than those @entity1 whose base deficits are secondary to other causes. Seventy-five consecutive surgical intensive care @entity1 with base deficits greater than 2.0 were prospectively studied. The etiology of the @entity1 ' base deficits was determined by admission laboratory data. @entity1 were divided into those with @entity520 , and those with @entity520 from other causes. Mortality within these groups was compared by Fisher's exact test. Thirty-seven @entity1 (49.3%) had @entity520 . Thirty-three @entity1 (46.7%) had @entity8193 . Three @entity1 (4%) had base @entity51 , and two @entity1 (2.6%) had base @entity51 . There were no significant differences in age, APACHE II scores, or volumes of resuscitation between the hyperchloremic group and the remaining @entity1 . There were four @entity204 (10.8%) in the hyperchloremic group and thirteen @entity204 (34.2%) in the remaining @entity1 (P = 0.03). @entity520 resulted from resuscitation with lactated Ringer's solution in 18 (48.6%) of the hyperchloremic @entity1 . @entity520 is a common etiology of base deficit in the surgical intensive care unit. It is associated with lower mortality than base deficit secondary to other causes. Moreover, it is frequently induced following resuscitation with lactated Ringer's solution. Failure to properly diagnose this subset of acidotic @entity1 may result in inappropriate clinical interventions due to the erroneous presumption of ongoing tissue @entity519 .
