Fluid management based on the assessment of heart filling pressures (CVP, PCWP) to reach hemodynamic stability is an important point in management of the critically ill patient. In the case of impaired permeability induced by inflammation, this strategy usually results in excessive interstitial fluid sequestration. In this situation, consequent hemodynamic stability is often at the expense of positive fluid balance and oedema formation, which can cause tissue oxygenation to deteriorate resulting in organ failure progression. The aim of our study was to analyse the relationship between fluid intake and fluid balance together with development of organ dysfunction in surviving and nonsurviving critically ill patients over the course of ten consecutive days.
Materials and methods
117 critically ill patients admitted to our department from 1996 to 1998 were included in this retrospective study. Criterion for inclusion was hospitalisation longer than 3 days. Patients were divided in two groups: survivors (n=70, average age 49±16 years, 54% multiple trauma, 24% elective surgery, 26% medical, average duration of ICU stay 15±8 days) and nonsurvivors (n=47, average age 51±17 years., 48% multiple trauma., 20% elective surgery, 32% medical, average duration of ICU stay 17±11 days). In both groups, fluid intake and fluid balance were evaluated during a ten day interval (from 3rd until 13th day of ICU stay, Fig. 1, Fig. 2) together with intensity of inflammatory response (average CRP value during whole period of evaluation) and organ dysfunction development (sum of SOFA score on 3rd and 13th day of ICU stay, Fig. 3).
In the nonsurvivors group a much more positive fluid balance was found within the interval from 3rd until 13th day of ICU stay, together with increasing extent of the organ dysfunction. The stronger correlation between fluid intake and fluid balance in nonsurviving patients compared to survivors (Fig. 1) points to the need for careful fluid management in critically ill patients, especially in those with an intensive inflammatory response.
Figure 1. Relationship between fluid intake and fluid balance in nonsurvivors (average fluid intake, 5810±1800 ml; average fluid balance, 1580±1900 ml; average value of CRP, 125±62 mg/l).
Figure 2. Relationship between fluid intake and fluid balance in survivors (average fluid intake, 5539±1160 ml, not significant compared to nonsurvivors; average fluid balance, 523±1480 ml, P<0.05 compared to nonsurvivors; average value of CRP, 92±60 mg/l, P<0.05 compared to nonsurvivors).
Figure 3. Organ dysfunction development.