Septic shock and chemotherapy-induced cytopenia: effects on microcirculation

Abstract

Purpose: Neutrophil and platelet activation and their interactions with endothelial cells are considered central features of sepsis-induced microcirculatory alterations. However, no study has evaluated the microvascular pattern of septic shock patients with chemotherapy-induced severe cytopenia.

Methods: Demographic and hemodynamic variables together with sublingual microcirculation recording [orthogonal polarization spectral imaging enhanced by sidestream dark-field technology (OPS-SDF) videomicroscopy] were collected in four groups of subjects: septic shock (SS, N = 9), septic shock in cytopenic patients (NSS, N = 8), cytopenia without infection (NEUTR, N = 7), and healthy controls (CTRL, N = 13). Except for controls, all measurements were repeated after complete resolution of septic shock and/or neutropenia. Video files were processed using appropriate software tool and semiquantitatively evaluated [total vascular density (TVD, mm/mm(2)), perfused vessel density (PVD, mm/mm(2)), proportion of perfused vessels (PPV, %), mean flow index (MFI), and flow heterogeneity index (FHI)].

Results: Compared with controls, there were statistically significant microcirculatory alterations within all tested groups of patients (TVD: SS = 8.8, NSS = 8.8, NEUTR = 9.1 versus CTRL = 12.6, p < 0.001; PVD: SS = 6.3, NSS = 6.1, NEUTR = 6.9 versus CTRL = 12.5, p < 0.001; PPV: SS = 71.6, NSS = 68.9, NEUTR = 73.3 versus CTRL = 98.7, p < 0.001; MFI: SS = 2.1, NSS = 1.9, NEUTR = 2.1 versus CTRL = 3.0, p < 0.05; FHI: SS = 1.0, NSS = 0.9, NEUTR = 0.6 versus CTRL = 0.0, p < 0.001). No significant differences were detected between SS, NSS, and NEUTR groups at baseline. Incomplete restoration of microcirculatory perfusion was observed after septic shock and/or neutropenia resolution with a trend towards better recovery in MFI and FHI variables in NSS as compared with SS patients.

Conclusions: Microvascular derangements in septic shock did not differ between noncytopenic and cytopenic patients. Our data might suggest that profound neutropenia and thrombocytopenia do not render microcirculation more resistant to sepsis-induced microvascular alterations. The role and mechanisms of microvascular alterations associated with chemotherapy-induced cytopenia warrant further investigation.