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Drs. Varon and Fromm are from the Sections of Cardiology, Pulmonary and Critical Care, Department of Medicine, Baylor College of Medicine; and Department of Emergency Services, The Methodist Hospital, Houston, TX.
Correspondence to: Joseph Varon, MD, FCCP, Department of Emergency Services, The Methodist Hospital, 6565 Fannin St, MS M-196, Houston, TX 77030; e-mail: jvaron{at}bcm.tmc.edu
In recent decades, the incidence of the sepsis syndrome has increased dramatically, largely due to an increased number of invasive procedures being performed, immunosuppressive therapy, and the advancing age of the population. Statistics from the Centers for Disease Control and Prevention have shown that mortality from sepsis has increased 13-fold from 1950 to 1991.1 2 In the United States, it has been estimated that there are approximately 500,000 new episodes of sepsis each year, with an associated 35% crude mortality rate.1 3 4 5 6
The management of patients with sepsis is based largely on treating or eliminating the source of infection, the use of appropriate antimicrobial agents, and hemodynamic and other physiologic supportive measures, as noted by Alsous et al in this issue of CHEST (see page 1749). It is well recognized that sepsis results in a systemic microcapillary injury with increased capillary permeability, tissue edema, and relative intravascular volume depletion.7 8 Therapy of this syndrome includes the administration of relatively large amounts of fluid in an attempt to replete the intravascular space. However, this task tends to be quite difficult due to the hemodynamic derangements of sepsis.
Parker and others9 have demonstrated that these cardiovascular responses of sepsis can be predictive of survival. Sufredinni et al10 have shown that similar hemodynamic derangements are induced by endotoxin in normal volunteers and are associated with cytokine production. These types of studies make prognostication in sepsis less than perfect. Typically, the number and degree of organ dysfunction form the basis of risk assessment.
In this issue of CHEST, Alsous et al report on a small cohort of patients from a medical ICU in the community setting. They examined the impact of overall fluid balance to survival of these critically ill patient. The mean APACHE (acute physiology and chronic health evaluation) II score for patients admitted to their study was 25.4. In addition, patients with chronic renal failure were excluded from the cohort. These authors demonstrated that the relative risk of mortality for patients who achieved > 500 mL of negative fluid balance by the third day of treatment was 5.0.
In essence, Alsous et al showed, based on their retrospective data, that patients who have a resolution of the physiologic aberrations associated with sepsis have a better prognosis. This, of course, sounds intuitively obvious, but it is useful to see confirmation even in a small cohort of patients. However, one must be careful in applying these data to clinical practice. This study was not a trial of therapy aimed at producing negative fluid balance, but rather an observational study demonstrating that its occurrence is associated with improved outcomes.
Sepsis remains a common and major clinical challenge for clinicians of all specialties. Therapy of sepsis must be aimed at correcting the underlying illness while supporting the physiology of the patients. The association of a particular physiologic state with better outcomes does not necessarily imply that therapy aimed at producing a similar physiologic state will be advantageous to the patient. Specifically, fluid management should continue with the aim of repleting the intravascular space, and a goal of inducing negative fluid balance is not warranted at this time.
References
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