Objective
Sepsis and septic shock are a common cause of mortality in critically ill patients. Many substances have been implicated in the pathophysiology of these syndromes. We postulated that adenosine may be implicated in the sepsis- or septic shock-induced blood pressure failure. Indeed, this nucleoside is a strong endogenous vasodilating agent released by endothelial cells and myocytes under circumstances of metabolic stress, such as during critical illness.
Design
A prospective, comparative observational study.
Setting
The adult intensive care unit of a tertiary care university hospital.
Patients
We measured adenosine plasma concentration (APC) in patients with severe sepsis (n = 11), in patients with septic shock (n = 14), in patients with hemorrhagic traumatic shock (n = 14), and in 12 healthy volunteers. APC was evaluated every 12 hrs over 3 days.
Interventions
None.
Measurements and Main Results
At study entry, we found that APC was higher in patients with septic shock (mean ± sd = 8.4 ± 3.5 μmol/L) than in patients with hemorrhagic traumatic shock (1.1 ± 0.6 μmol/L) and controls (0.8 ± 0.3 μmol/L). Intermediate values (3.9 ± 1.9 μmol/L) were found in patients with severe sepsis. APC in patients with traumatic shock did not differ from controls. In the course of the hospitalization, for both sepsis and septic shock patients, APC decreased significantly but remained higher than controls 72 hrs after entry into the study. In the septic shock group, APC was significantly higher in the nonsurvivor group (n = 6) than in the survivor group (n = 8), whatever the time of sample collection and assay.
Conclusions
High adenosine plasma concentrations are found in patients with septic shock but not during traumatic shock, or in healthy volunteers. Intermediate values of circulating adenosine are found in patients with severe sepsis. APC may be a prognostic index for outcome in septic patients, with much higher values being found in nonsurvivors.
