76
ABSTRACTS
Complement
Sprung 14525,
Activation
CL, Schultz 1986.
in
OR, Marcia1
Septic
Shock
E, et al. Crit
Patients.
Care
Med
To evaluate the status of the complement system and to determine the effects of corticosteroids on complement component levels in septic shock, C3, C4, and Factor B were measured in 42 patients with severe late septic shock. Serum levels of C4 and Factor B correlated with C3 levels (r = 0.48 and 0.64, respectively; p < .Ol) in patients in shock for more than 4 h, but only Factor B correlated with C3 (r = 0.85; p < .01) in patients in shock for 4 h or less. C3 and Factor B levels were significantly (p < .OS) lower in patients who died (12,174 + 1,524 CHSo U/ml and 14 + 1 mg/dl, respectively) than in patients who survived (18,418 + 2,833 CHSo U/ml and 21 + 2 mg/dl, respectively). Corticosteroids did not alter complement component levels. The alternative pathway appears to be activated early in septic shock, whereas the classical pathway is activated later. C3 and Factor B levels may predict survival of patients in septic shock. In this study, corticosteroids did not change the complement component levels of patients in late severe septic shock. (Reprinted with permission.) Serial
Changes
Multiple
in Cellular
Organ-System
J, Hosotsubo
Immunity
of Septic
Patients
With
Nishijima MK, Takezawa Care Med 14:87, 1986.
Failure.
KK. et al. Crit
Total lymphocyte count, lymphocyte cell-surface markers (OKT3,OKT4,OKT8, and B-l), serum complement factors (C3 and C4), immunoglobulins (IgG, IgA, and IgM), ceruloplasmin (Crl), and transferrin (Trf) were determined weekly for nine septic postoperative patients, all of whom had multiple organ-system failure. The peripheral blood total lymphocyte count, its subpopulation, T-cell subset, and proliferative responses of lymphocyte to phytohemagglutinin (PHA) and concanavalin A (Con A) decreased in all patients. OKT3 and B-l decreased progressively in the four nonsurvivors compared with the five survivors. Although immunoglobulin levels were within the normal range in both groups, they tended to increase in survivors and decrease in nonsurvivors. Serial levels of C3, C4, Crl, and Trf increased in survivors but did not change in nonsurvivors. T-cell function and antibody-producing activity diminished progressively in nonsurvivors. These changes in cellular immunity may represent another manifestation of multiple organsystem failure during sepsis. (Reprinted with permission.) Cellular Depression
and
Y-H.
Care
Crit
Humoral of Lymphocyte
Med
14:81,
Bases of Function.
Hemorrhage-Induced
Abraham
E, Chang
1986.
Bacterial infection often occurs after trauma and hemorrhage and is believed to be a reflection of a compromised host defense system. In the present study, the effect of hemorrhage on phytohemagglutinin-induced lymphocyte prohferation was investigated. Lymphocytes obtained from rats 2 h after blood withdrawal in an amount equivalent to 30% of total blood volume showed a 48% reduction in proliferative response as compared to cells obtained from the same animal before bleeding. This depression in lymphocyte proliferative capacity appeared to be due to a serum factor or factors induced by hemorrhage. The hemorrhage-induced serum
factor(s) is heat-stable, dialyzable, and has an apparent molecular weight between 13,000 and 23,000 on gel filtration chromatography. The hemorrhage-induced factor seems to suppress lymphocyte proliferation in a rapid and irreversible manner. This abnormality in host defense mechanisms may contribute to the increased incidence of sepsis present after trauma and hemorrhage. (Reprinted with permission.) Variability of Resting teers During Fasting
F, Schutz 1986.
Energy Expenditure in Healthy and Continuous Enteral Feeding.
Y, Frascarolo
P, et al. Crit
Care
Med
VolunZurlo
14535,
The magnitude of variability in resting energy expenditure (REE) during the day was assessed in nine healthy young subjects under two nutritional conditions: 1) mixed nutrient (53% carbohydrate, 30% fat, 17% protein) enteral feeding at an energy level corresponding to 1.44 REE; and 2) enteral fasting, with only water allowed. In each subject, six 30-min measurements of REE were performed using indirect calorimetry (hood system) at 90-min intervals from 9 AM to 5 PM. The mean REE and respiratory quotient were significantly (p < .Ol) greater during feeding than during fasting (1.08 + 0.07 [SEMI vs. 1.00 + 0.06 kcal/min and 0.874 k 0.007 vs. 0.829 t 0.008 kcal/min, respectively). Mean postprandial thermogenesis was 4.9 + 0.4% of metabolizable energy administered. The intraindividual variability of REE throughout the day, expressed as the coefficient of variation, ranged from 0.7% to 2.0% in the fasting condition and from 1.2% to 4.1% in the feeding condition. There was no significant difference between the REE measured in the morning and that determined in the afternoon. (Reprinted with permission.) Resting sured
Metabolic v Predicted.
al. Anesthesiology
Critically
Ill Patient:
Weissman C, Kemper 64:673, 1986.
Rate
of the
M, Askanazi
Mea-
J, et
Critically ill patients requiring mechanical ventilation are particularly susceptible to malnutrition. A knowledge of the energy requirements of these patients is essential in designing nutritional regimens. This study examines 45 resting energyexpenditure measurements performed in a group (n = 40) of postoperative, critically ill patients who were hemodynamitally stable, noncomatose, and receiving mechanical ventilation. It examines in particular to what degree the resting energy expenditure of such patients can be predicted using the Harris-Benedict and Aub-Dubois formulae. Resting energy expenditure was measured using indirect calorimetry. There was only a moderate correlation between measured resting energy expenditure and that predicted using the Harris-Benedict (r = 0.57) and Aub-Dubois (r = 0.59) formulae. There was little correlation between the ratio of the measured to the predicted (Harris-Benedict) resting energy expenditure and age, or the ratio of actual to ideal body weight and body weight. The measured resting energy expenditure differed widely (70-140%) from predicted, reflecting the many complex factors that influence these patients’ metabolic rate. The role of standard predictive formulae in such patients is as an arbitrary reference point to be used to define hypermetabolism (measured greater than predicted) and hypometabolism (predicted greater than measured). (Reprinted with permission.)