Publications

SCOPUS: no.j

Sepsis is physiologically viewed as a proinflammatory and procoagulant response to invading pathogens. There are three recognized stages in the inflammatory response with progressively increased risk of end-organ failure and death: sepsis, severe sepsis, and septic shock. Patients with cirrhosis are prone to develop sepsis, sepsis-induced organ failure, and death. There is evidence that in cirrhosis, sepsis is accompanied by a markedly imbalanced cytokine response ("cytokine storm"), which converts responses that are normally beneficial for fighting infections into excessive, damaging inflammation. Molecular mechanisms for this excessive proinflammatory response are poorly understood. In patients with cirrhosis and severe sepsis, high production of proinflammatory cytokines seems to play a role in the worsening of liver function and the development of organ/system failures such as shock, renal failure, acute lung injury or acute respiratory distress syndrome, coagulopathy, or hepatic encephalopathy. In addition, these patients may have sepsis-induced hyperglycemia, defective arginine-vasopressin secretion, adrenal insufficiency, or compartmental syndrome. In patients with cirrhosis and spontaneous bacterial peritonitis (SBP), early use of antibiotics and intravenous albumin administration decreases the risk for developing renal failure and improves survival. There are no randomized studies that have been specifically performed in patients with cirrhosis and severe sepsis to evaluate treatments that have been shown to improve outcome in patients without cirrhosis who have severe sepsis or septic shock. These treatments include recombinant human activated C protein and protective-ventilation strategy for respiratory failure. Other treatments should be evaluated in the cirrhotic population with severe sepsis including the early use of antibiotics in "non-SBP" infections, vasopressor therapy, hydrocortisone, renal-replacement therapy and liver support systems, and selective decontamination of the digestive tract or oropharynx.

info:eu-repo/semantics/published

Introduction: Cardiac surgery can be complicated by organ dysfunction resulting in increased hospital length of stay and mortality rates. Several studies have reported microvascular alterations after cardiac surgery but none has investigated the time course of these alterations. Near-infrared spectroscopy (NIRS) associated with a vascular occlusion test (VOT) may provide a reliable qualitative evaluation of the microcirculation. Hypothesis: To evaluate of the microvascular alterations occurring during cardiac surgery using NIRS. Methods: Seventeen patients undergoing elective cardiac surgery with cardiopulmonary bypass (CPB) were included. Measurements were performed the day before surgery, after anesthesia induction, immediately after surgery on admission to the ICU, and 24 hours after surgery. The NIRS probe was placed on the thenar eminence. After stabilization of the signal (StO2baseline), we performed a 3-min VOT.We calculated the decrease in the StO2 (descending slope) during VOTand the NirVO2 (the reverse descending slope multiplied by the average tissue hemoglobin index [THI]) during the first min of the VOT to estimate muscle oxygen consumption. We also calculated the ascending slope after deflation of the pneumatic cuff to assess reactive hyperemia as a marker of microvascular reactivity. Results: The mean age of the studied population was 64+12 years; the mean preoperative left ventricular ejection fraction was 56+8%. Anesthesia was standardized and corticosteroids were administered to all patients prior to CPB. The median duration of CPB was 113 (101-145)min. At ICU admission, 7 patients were receiving dobutamine (median dose 5 mcg/kg/min [3.9-5.7]) and 8 norepinephrine (0.04 mcg/kg/min [0.01- 0.035]). Baseline StO2values increased after induction (from 80+7.6 to 85.2+5.9, p=0.49) and decreased after CPB (to 77.5+8.7, p=0.001). The descending slope and the NirVO2 decreased after induction (p=0.03 and p=0.001), did not change during CPB, and had returned to baseline values by day 1 (p=0.068 and p=0.019).The ascending slope decreased after anesthesia induction (p=0.008) and remained stable thereafter. Conclusions: Cardiac surgery is associated with microvascular dysfunction. These abnormalities seem to be primarily related to the anesthesia, rather than the CPB, and had reversed by the first day after surgery.