Finn P J, Plank L D, Clark M A, Connolly A B, Hill G L
University Department of Surgery, Auckland Hospital, New Zealand.
Lancet. 1996 Mar 9;347(9002):654-6. doi: 10.1016/s0140-6736(96)91204-0.
According to a recent hypothesis, the profound loss of body protein that occurs in critically ill patients is triggered and maintained by cell shrinkage secondary to cellular dehydration. We tested this hypothesis by studying sequential changes in intracellular water, total body protein, total body potassium, and intracellular potassium in patients receiving intensive care for blunt trauma or sepsis.
Nine patients with multiple blunt trauma and 11 with severe sepsis were studied in an intensive care unit for 21 days. Intracellular water was measured in two ways--by subtraction of extracellular water (bromide dilution) from total body water (tritium dilution), and by bioimpedance spectroscopy. Total body protein was measured by whole-body neutron activation analysis and total body potassium by whole-body counting.
Over the study period intracellular water decreased by 15-20%, total body protein by 15%, and total body potassium by about 20%. Intracellular potassium concentration did not change, and was similar to that in healthy adult volunteers. In the trauma patients, sequential measurements of the ratio of potassium to protein in lost tissue indicated that cells were losing water in quantities greater than would be expected from protein losses.
The loss of protein and potassium from body stores in major trauma or sepsis is accompanied by progressive cellular dehydration. This insight opens up new therapeutic options for limiting the loss of body protein in critically ill patients.
