SOFA Score, Hemodynamics and Body Temperature Allow Early Discrimination between Porcine Peritonitis-Induced Sepsis and Peritonitis-Induced Septic Shock

Abstract

Porcine model of peritonitis-induced sepsis is a well-established clinically relevant model of human disease. Interindividual variability of the response often complicates the interpretation of findings. To better understand the biological basis of the disease variability, the progression of the disease was compared between animals with sepsis and septic shock. Peritonitis was induced by inoculation of autologous feces in fifteen anesthetized, mechanically ventilated and surgically instrumented pigs and continued for 24 h. Cardiovascular and biochemical parameters were collected at baseline (just before peritonitis induction), 12 h, 18 h and 24 h (end of the experiment) after induction of peritonitis. Analysis of multiple parameters revealed the earliest significant differences between sepsis and septic shock groups in the sequential organ failure assessment (SOFA) score, systemic vascular resistance, partial pressure of oxygen in mixed venous blood and body temperature. Other significant functional differences developed later in the course of the disease. The data indicate that SOFA score, hemodynamical parameters and body temperature discriminate early between sepsis and septic shock in a clinically relevant porcine model. Early pronounced alterations of these parameters may herald a progression of the disease toward irreversible septic shock.

Keywords: SOFA score; pig; sepsis; septic shock.

Figure 1

Sequential organ failure assessment (SOFA) score, lactate, cytokines and body temperature. Open columns, sepsis; filled columns, septic shock. *, p < 0.05 vs. baseline (TP1); #, p < 0.05 vs. sepsis. (a) SOFA score in sepsis and septic shock; (b) plasma levels of lactate in sepsis and septic shock; (c) plasma levels of IL-6 in sepsis and septic shock; (d) plasma levels of TNF-α in sepsis and septic shock; (e) body temperature in sepsis and septic shock.

Figure 2

Hemodynamics and vasopressors. Open columns, sepsis; filled columns, septic shock. *, p < 0.05 vs. baseline (TP1); #, p < 0.05 vs. sepsis. (a) Cardiac output in sepsis and septic shock; (b) heart rate in sepsis and septic shock; (c) systemic vascular resistance in sepsis and septic shock; (d) mean arterial pressure in sepsis and septic shock; (e) norepinephrine dose in sepsis and septic shock. (f) low-frequency (LF) and high-frequency (HF) bands in sepsis and septic shock. Open symbols, HF. Filled symbols, LF.

Figure 3

Respiratory gases and acid-base balance. Open columns, sepsis; filled columns, septic shock. *, p < 0.05 vs. baseline (TP1); #, p < 0.05 vs. sepsis. (a) PaO₂/FiO₂ ratio in sepsis and septic shock; (b) arterial pCO₂ in sepsis and septic shock; (c) arterial bicarbonate in sepsis and septic shock; (d) arterial pH in sepsis and septic shock; (e) mixed venous (pulmonary artery, PA) pO₂ in sepsis and septic shock; (f) mixed venous (pulmonary artery) O₂ saturation (SvO₂) in sepsis and septic shock.

Figure 4

Renal functions. Open columns, sepsis; filled columns, septic shock. *, p < 0.05 vs. baseline (TP1); #, p < 0.05 vs. sepsis. (a) Creatinine plasma levels in sepsis and septic shock; (b) Urea plasma levels in sepsis and septic shock; (c) Renal blood flow in sepsis and septic shock; (d) Oxygen consumption by mitochondrial complexes I, I+II and IV measured by ultrasensitive oxygraphy. Group of sepsis at baseline and at the end of the experiment. Group of septic shock at baseline and at the end of the experiment.