Sepsis/septic shock: participation of the microcirculation: an abbreviated review.

OBJECTIVE

An overview of the importance of understanding mechanisms occurring in the microcirculation during septic and endotoxic shock. The thesis of the paper is to place emphasis on this important vascular network to ultimately benefit the patient.

DATA SOURCES

Early descriptions of vascular reactions to endotoxin which suggest that the microcirculation is a major site of attack during shock. More recent studies were sought out and examined as to their possible impacts on the microcirculation.

STUDY SELECTION

Early comprehensive studies concerning vascular reactions in the microcirculation during shock were selected. Subsequent studies identified from the mainstream scientific medical literature describe the actions of blood, cells, and the emerging significant role of the vascular endothelium among other factors. A consensus view is identified, pointing to the causes of a malfunctioning microcirculation during shock.

DATA EXTRACTION

Data gathered from reports in the mainstream, well-established basic and clinical literature, from reviews and forum reports, from studies by well-established investigators, and from more recent reports of excellent quality.

DATA SYNTHESIS

The microcirculation undergoes massive alterations during sepsis/septic shock. There are numerous changes, including slowing of capillary blood flow due to depressed perfusion pressure as a result of systemic pressure reduction and local arteriolar constriction. Observations suggest that the microcirculation is shut off early in severe sepsis, allowing the effects of hypoperfusion and attacks by microorganisms to prevail in their destructive capabilities. Widespread capillary dilation may ultimately occur. However, with blood flow diverted through some arteriovenous channels, important areas of capillary exchange are bypassed. Decreased capillary blood flow during shock results from failure to allow normal passage of cellular elements, including erythrocytes and neutrophils. This defect occurs, in part, because of decreased perfusion pressure, decreased deformability of red and white cells, constricted arterioles, circulating obstructive fragments (including hemoglobin), and plugging of microvessels with "sludge." Other factors are adherence of cells to capillary and venular epithelial membranes creating increased resistance to flow, loss of fluid through abnormal transcapillary exchange, differential vascular resistance changes between various beds (e.g., intestinal vs. muscle), and the relative absence of regulatory neurohumoral control of small vessel segments of the circulation. During sepsis/septic shock, endothelial cells are reported to modulate vascular tone, control local blood flow, influence the rate of leakage of fluids and plasma proteins into tissues, modulate the accumulation and extravasation of white cells into tissues, and influence white cell activation. As a result of the predominance of many destructive factors, a subsequent round of tissue damage may occur. Because of prolonged capillary vascular stasis, deficient flow, and factors released from injured cells, the microcirculation becomes a trap for uncontrolled bacterial growth enhanced by sustained hypoxemia, acidosis and toxemia. These events may combine to contribute to the loss of normal cell integrity and death of the host.

CONCLUSIONS

The purpose of this review is to draw the readers' attention to the growing list of adverse factors occurring in the microcirculation during sepsis/septic shock. A further aim is to point to the realization of the complexity of factors which may contribute to the importance of a well-functioning microcirculation.