Sequential changes in the metabolic response in severely septic patients during the first 23 days after the onset of peritonitis.
OBJECTIVE
To quantify the sequential changes in metabolic response occurring in patients with severe sepsis after the onset of peritonitis.


BACKGROUND
Understanding the changes in energy expenditure and body composition is essential for the optimal management of severely septic patients; however, they have not been quantified in the context of modern surgical care.


METHODS
Twelve patients with severe sepsis secondary to peritonitis (median APACHE II score = 21.5) had measurements of energy expenditure and body composition as soon as they were hemodynamically stable and 5, 10, and 21 days later. Sequential measurements of acute-phase proteins and cytokine responses were also made.


RESULTS
Resting energy expenditure rose to 49% above predicted and remained elevated throughout the study period. Total energy expenditure was 1.25 x resting energy expenditure. Body fat was oxidized when energy intake was insufficient to achieve energy balance. There was a positive fluid balance of 12.5 1 over the first 2 days after onset of sepsis; thereafter, body water changes closely paralleled body weight changes 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 from viscera. Intracellular potassium levels were low but did not deteriorate further after hemodynamic stability had been reached. There was a reprioritization of hepatic protein synthesis that was obligatory and independent of changes in total body protein. The cytokine responses demonstrated the complexity, redundancy, and overlap of mediators.


CONCLUSIONS
The period of hypermetabolism in severely septic patients is similar to that previously described, but the fluid changes are larger and the protein loss is greater. Protein loss early on is predominantly from muscle, thereafter from viscera. Fat loss can be prevented and cell function preserved once hemodynamic stability is achieved.
Plank
L D
LD
University Department of Surgery, Auckland Hospital, New Zealand.
Connolly
A B
AB
Hill
G L
GL
D018806:APACHE; D000328:Adult; D000368:Aged; D001798:Blood Proteins / Q000378:metabolism; D001823:Body Composition; D001834:Body Water; D001835:Body Weight; D016207:Cytokines / Q000097:blood; D004734:Energy Metabolism; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009132:Muscles / Q000378:metabolism; D010538:Peritonitis / Q000150:complications / Q000378:metabolism*; D011506:Proteins / Q000378:metabolism*; D018805:Sepsis / Q000209:etiology / Q000378:metabolism*; D013997:Time Factors; D014781:Viscera / Q000378:metabolism
D001798:Blood Proteins; D016207:Cytokines; D011506:Proteins