Annual Update in Intensive Care and Emergency Medicine 2011

466 N. Brienza, L. Dalfino, and M.T. Giglio
XI
vanishes, indicating adequate study grouping. Moreover, it is evident that goaldirected
therapy seems really effective only in studies with a control mortality
> 10 %. In the subgroups of lower risk (0–5 % and 5–10 %) patients no significant
difference in mortality is observed. Therefore, these patients may not be ill
enough to clearly benefit from hemodynamic improvement, and the risk to benefit
ratio of perioperative optimization in such patients should be taken into
account.
Goal-directed Therapy and Organ Function
Strategies to maintain DO 2 and minimize splanchnic hypoperfusion have been
advocated to improve postoperative morbidity [40]. Gastrointestinal (GI) dysfunction,
ranging from mild complications (e.g., postoperative ileus and inability
to tolerate enteral nutrition) to more severe surgical complications (ischemic
injury), is a very common complication after major surgery and is associated
with prolonged hospital stay, high mortality, and substantial costs and resource
consumption [41]. Since selective vasoconstriction of mesenteric arterioles, mediated
primarily by the renin–angiotensin system, contributes to the maintenance
of systemic arterial pressure and the perfusion of non-mesenteric organs, episodes
of reduced splanchnic perfusion and oxygenation, related to intraoperative
hypotension or occult hypovolemia, are frequent during major surgery [6, 30].
This response often outlasts the period of the hypovolemic insult or low-flow
state, promoting abdominal organ damage. Strategies to maintain DO 2 and minimize
splanchnic hypoperfusion have been advocated to improve postoperative
morbidity [40] and a recent meta-analysis of 16 RCTs (3410 patients) found that
both major and minor GI complications were significantly reduced by perioperative
goal-directed therapy [42].
Another meta-analysis focused on the protective effect of perioperative goaldirected
therapy on kidney function [22]. Postoperative acute kidney injury (AKI)
is one of the most serious complications in surgical patients, and markedly
increases perioperative morbidity and mortality both in cardiac [43] and non-cardiac
surgery [44]. Most cases of postoperative AKI are related to episodes of renal
hypoperfusion as a consequence of systemic hypotension, hypovolemia, decreased
circulating blood volume, prolonged cardiopulmonary bypass (CPB), and cardiac
dysfunction. The kidney normally receives 20–25 % of total cardiac output resulting
in the highest tissue perfusion in the body and the medullary portion of the
nephrons is especially at risk of hypoperfusion, being physiologically characterized
by low blood flow, and high oxygen demand (due to tubular transport activity) and
extraction (approaching 90 %). Decreased cardiac output not only directly causes
renal hypoperfusion, but also activates neuro-humoral responses which cause renal
vasoconstriction. Maintenance of adequate cardiac output under hemodynamic
monitoring may reduce the risk of postoperative renal injury by assuring adequate
renal blood flow and reducing renal vasoconstriction. The results of this meta-analysis
[22], including 20 studies (4220 patients), substantiate this concept, showing
that postoperative AKI was significantly reduced by goal-directed therapy. The
occurrenceofrenaldysfunctionwasreducedwhentreatmentstartedpreoperatively,
intraoperatively or postoperatively, when performed in high-risk patients
and was obtained by fluids and inotropes. At the moment, perioperative goaldirected
therapy is the only evidence-based strategy shown to reduce kidney injury
in non-cardiac postoperative patients [45].