ALTERED MICROCIRCULATION IN SEPTIC SHOCK
L Ratiani1, M Gamkrelidze1, E Khuchua1
1Tbilisi State Medical University; Elizabeth Blackwell Hospital, Tbilisi, Georgia.
Georgian Medical News
|July 16, 2015
Summary
Severe sepsis causes microvascular dysfunction that persists despite treatment, leading to organ failure. This microcirculatory impairment, not just hemodynamics, strongly predicts patient outcomes in septic shock.
Area of Science:
- Critical Care Medicine
- Vascular Biology
- Pathophysiology
Background:
- Sepsis is a life-threatening organ dysfunction caused by dysregulated host response to infection.
- Severe sepsis involves significant microvascular dysfunction that persists even after hemodynamic stabilization.
- This persistent microcirculatory impairment is a key factor in multi-organ failure.
Purpose of the Study:
- To analyze the characteristics and implications of microcirculatory dysfunction in septic shock.
- To highlight the role of microvascular alterations as predictors of outcome in sepsis.
- To explore the multifaceted mechanisms contributing to microcirculatory failure in septic shock.
Main Methods:
- Retrospective data analysis of microcirculation in patients with septic shock.
- Review of existing clinical studies correlating microcirculatory variables with patient outcomes.
- Examination of factors contributing to endothelial barrier dysfunction and capillary perfusion deficits.
Main Results:
- Microcirculatory alterations are more potent predictors of outcome in severe sepsis than global hemodynamic variables.
- Persistent microvascular dysfunction occurs despite fluid resuscitation, vasopressors, and infection treatment.
- Mechanisms include increased capillary permeability, arteriolar hyporesponsiveness, and reduced capillary density.
Conclusions:
- Microvascular dysfunction is a critical determinant of outcome in septic shock.
- Addressing microcirculatory derangements is essential for improving sepsis management.
- Understanding the pathophysiology of microcirculatory failure can guide future therapeutic strategies.


