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Septic shock and chemotherapy-induced cytopenia: effects on microcirculation
T. Karvunidis, J. Chvojka, D. Lysak, R. Sykora, A. Krouzecky, J. Radej, I. Novak, M. Matejovic,
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
ProQuest Central
from 1997-01-01 to 1 year ago
Medline Complete (EBSCOhost)
from 2000-01-01 to 1 year ago
Nursing & Allied Health Database (ProQuest)
from 1997-01-01 to 1 year ago
Health & Medicine (ProQuest)
from 1997-01-01 to 1 year ago
- MeSH
- Blood Vessels physiology MeSH
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Microcirculation physiology MeSH
- Neutropenia chemically induced physiopathology MeSH
- Pancytopenia chemically induced physiopathology MeSH
- Antineoplastic Agents adverse effects MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Shock, Septic physiopathology MeSH
- Case-Control Studies MeSH
- Mouth Mucosa blood supply MeSH
- Mouth Floor blood supply MeSH
- Microscopy, Video MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
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.
References provided by Crossref.org
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- $a 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.
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