Microvascular alteration is a key physiological feature of sepsis and a determinant of multiple organ failure. OPS imaging allows non-invasive visualization of microvascular network of mucosal surfaces. We used OPS to assess microcirculation impairment in our porcine model of septic shock.
Sublingual microvascular flow and density were investigated in 6 pigs (26.5±3.6kg), by OPS imaging. Basal data were collected in healthy animals, before surgery for implantation of hemodynamic monitoring probes. After recovery, an E. coli laden fibrin clot was implanted intraperitoneally. OPS data were acquired for 6 hours following implant or until animals died. In survivors data were then acquired every 24 hours. At each time 2-4 sequences were captured for off-line analysis. Microvascular flow was graded semi-quantitatively by independent observer as 0:no-flow, 1:intermittent or sluggish, 2:continuous slow-moving and 3:brisk continuous. Density for perfused vessels (DPV) <20mm was assessed as number of vessels intersecting a grid superimposed on the analyzed field. Data are expressed as mean±SD. Two-way ANOVA and Pearson Correlation were used as statistical tests.
3 animals expired prior to 6 hours, 3 survived over 24 hours. Microvascular Flow Score (MFS) was 2.62±0.41 for basal and 1.22±0.48 for sepsis (p=0.0002, 53.4% decrease). MFS improved markedly in animals that survived, to 2.11±0.20. Concomitantly DPV decreased from 14.12±1.93 to 12.35±2.09 vessels/mm (12.5% reduction), and increased subsequently to 14.37±1.32 vessels/mm. No correlation was found between cardiac output (CO) and either MFS or DPV (p=0.12 and p=0.13 respectively).
OPS provides a reliable method to investigate microvascular impairment. We demonstrated deterioration of microvascular flow and DPV from the onset of sepsis and showed recovery in survivors. The poor correlation between CO and MFS or DPV may suggest that microvascular abnormalities persist despite normalization of systemic hemodynamic parameters (“cryptic shock”).
OPS may have clinical utility to quantify microvascular perturbation in sepsis and to evaluate its time course.
M. Guglielmi, None.