SEQUENTIAL-CHANGES IN THE METABOLIC RESPONSE IN SEVERELY SEPTIC PATIENTS DURING THE FIRST 23 DAYS AFTER THE INSET OF PERITONITIS

Objective To quantify the sequential changes in metabolic responses oc curring in patients with severe sepsis after the onset of peritonitis. Summary Background Data Understanding the changes in energy expenditu re and body composition is essential for the optimal management of sev erely septic patients; however, they have not been quantified in the c ontext of modern surgical care. Methods Twelve patients with severe se psis secondary to peritonitis (median APACHE II score = 21.5) had meas urements of energy expenditure and body composition as soon as they we re hemodynamically stable and 5, 10, and 21 days later. Sequential mea surements of acute-phase protein and cytokine responses were also made . Results Resting energy expenditure rose to 49% above predicted and r emained elevated throughout the study period. Total energy expenditure was 1.25 x resting energy expenditure. Body fat was oxidized when ene rgy intake was insufficient to achieve energy balance. There was a pos itive fluid balance of 12.5 l over the first 2 days after onset of sep sis; thereafter, body water changes closely paralleled body weight cha nges and were largely accounted for by changes in extracellular water. During the 21-day study period, there was a loss of 1.21 kg (13%) of total body protein. During the first 10 days, 67% of the protein lost came from skeletal muscle, but after this time it was predominantly fr om viscera. Intracellular potassium levels were low but did not deteri orate further after hemodynamic stability had been reached. There was a reprioritization of hepatic protein synthesis that was obligatory an d independent of changes in total body protein. The cytokine responses demonstrated the complexity, redundancy, and the overlap of mediators . Conclusions The period of hypermetabolism in severely septic patient is similar to that previously described, but the fluid changes are la rger and the protein loss is greater. Protein loss early on is predomi nantly from muscle, thereafter from viscera. Fat loss can be prevented and cell function preserved once hemodynamic stability is achieved.