A critical problem
Organ hypoperfusion and reduced tissue oxygenation represent a common state in a wide range of diseases, in both intensive care medicine and high-risk surgery. In particular, all forms of shocks are usually characterized by an inadequacy between oxygen transport to parenchyma cells, and their need in oxygen to sustain normal organ function. This oxygen debt, if not corrected, is associated with increased organ dysfunction and greater morbidity and mortality.
Septic shock notably, is distinctive from other types of shock because of its high mortality rate. With huge impact on hospital costs and a growing incidence over the past 40 years, it is a significant public health problem.
To prevent complications associated with organ ischemia, clinicians pay a careful attention in monitoring and restoring optimal hemodynamic conditions for their patients.
Traditionally, the treatment strategy to ensure better oxygen delivery to cells consists in correcting macrohemodynamics derangements by administrating fluids and/or vasopressors, upon pressure-based resuscitation targets. Keeping track of cardiac output and preload-dependency, as well as monitoring of systemic hypoperfusion signals such as hyperlactatemia and/or central venous oxygen saturation, are common means to guide the therapeutic manoeuvers and assess the response of patient to treatment.
Despite an increase of systemic blood flow within satisfactory levels and arterial blood pressure normalization after resuscitation, microvascular alterations sometimes persist and contribute to cellular hypoxia.
During septic shock, notably, at an advanced stage, different mechanisms, linked to endothelial inflammation and coagulopathy, may lead to a reduction of perfused capillaries, a heterogenous blood flow distribution and dissociation between macro- and microcirculation. Recent studies have shown that microvascular alterations could also be observed in conditions like severe heart failure or among patients undergoing high-risk surgery. As microcirculation is the site of oxygen and substrate exchange, its deficiency during circulatory shock can subsequently result in multiple organ dysfunction, often associated with prolonged periods of morbidity and even death. Therefore, macro- and microcirculation dissociation represents a peculiarly risky situation, in which physician could over emphasize the importance of arterial blood pressure and be falsely reassured that the patient is clinically stable. Furthermore, targeting merely systemic hemodynamics could even carry the risk of overusing vasoactive drugs that would worsen tissue perfusion.
Up to now, continuous and real-time assessment of microcirculation at bedside was still challenging. Available devices like Laser Doppler or Sidestream Dark Field imaging were used for research purposes and could render “snapshots” of capillary perfusion, but cannot be considered as genuine monitoring solutions. Moreover, the sublingual site of measurement, the most widely studied nowadays, is still considered controversial to faithfully provide an accurate picture of microcirculatory alterations of patients.
The splanchnic circulation irrigates a territory composed of stomach, small intestine, colon, liver, pancreas and spleen.
During low systemic blood flow or hemorrhage, perfusion of vital organs (brain, heart…) is maintained at the expense of visceral organs perfusion. A number of studies have demonstrated disproportionately impaired perfusion of gut and colon in low-flow states.
As a consequence of splanchnic ischemia, the gut mucosa may become permeable, and allows endotoxin and other bacterial products to pass through blood vessels (a phenomena known as “bacterial translocation”), thereby causing additional injury to local and distant organs.
Due to its high sensitivity to ischemia when low-flow states occur, the guts is one of the most clinically relevant organs to monitor microcirculation and local perfusion. The duodenum is particularly prone to ischemia and necrosis because of anatomical specificity of villous circulation.
(upstream diffusion of oxygen within villi when mesenteric blood flow decreases).
Last update : 07/09/2017