Similar metabolic responses to standardized total parenteral
nutrition of septic and nonseptic critically ill patients1,2
Christian Zauner, Beate I Schuster, and Bruno Schneeweiss
ABSTRACT
Background: Nutritional support is an important link between
the response to injury and recovery in critical illness.
Objective: Our goal was to evaluate energy and substrate metab-
olism in septic and nonseptic critically ill patients in the resting
state and during the administration of standardized total par-
enteral nutrition.
Design: This was a prospective, clinical cohort study of 25 con-
secutively admitted critically ill patients either with (n = 14) or
without (n = 11) sepsis who received total parenteral nutrition.
Resting energy expenditure was measured on days 0, 2, and 7 by
indirect calorimetry. Energy and substrate balances were calcu-
lated on days 2 and 7.
Results: Resting energy expenditure was not significantly differ-
ent between septic and nonseptic patients on day 0 (2.65 ± 0.49
and 2.36 ± 0.56 kJ · min1 · m2, respectively). Energy balances
were positive for both groups on days 2 (0.68 ± 0.4 and 0.74 ± 0.6
kJ · min1 · m2, respectively; NS) and 7 (0.65 ± 0.3 and 0.78 ± 0.5
kJ · min1 · m2, respectively; NS). Substrate balances were not
significantly different between groups on days 0, 2, and 7. Resting
energy expenditure on day 0 was negatively correlated with the
severity of illness in septic patients only (r = 0.58, P < 0.05).
Conclusions: Metabolic changes were not significantly differ-
ent between septic and nonseptic critically ill patients during
the administration of standardized total parenteral nutrition. A
disease-specific macronutrient composition of total parenteral
nutrition formulas does not seem to be necessary in either septic
or nonseptic critically ill patients. Am J Clin Nutr 2001;74:
265–70.
KEY WORDS Body temperature, intensive care, energy
expenditure, sepsis, critically ill patients, severity of illness,
substrate balances, substrate metabolism, total parenteral nutrition,
nutritional support
INTRODUCTION
Nutritional support in critically ill patients is aimed at prevent-
ing the negative effects of starvation during the course of the dis-
ease and at minimizing the negative effects of protein catabolism
(1, 2). Healthy and malnourished nonseptic patients utilize mainly
carbohydrates for energy production and convert excess glucose
into fat (3). In contrast, patients with sepsis show an increase in
oxygen consumption and utilize mainly stored fat to meet their
Am J Clin Nutr 2001;74:265–70. Printed in USA. © 2001 American Society for Clinical Nutrition
See corresponding editorial on page 153.
energy requirements (4–6). The same metabolic changes are found
in nonseptic critically ill patients (7). Consequently, it was recom-
mended that the portion of fat in artificial nutrition be increased for
patients with either sepsis or nonseptic critical illness (5–7).
Although it seems likely that energy and substrate metabolism
are not significantly different between septic and nonseptic criti-
cally ill patients, the 2 groups have not been compared directly. In
addition, the responses of these 2 groups of patients to standardized
nutritional support have not yet been investigated. Thus, we under-
took the present study to evaluate energy and substrate metabolism
in septic and nonseptic critically ill patients and the metabolic
response to standardized total parenteral nutrition (TPN).
SUBJECTS AND METHODS
Subjects
This prospective, clinical cohort study included 25 patients
(10 women, 15 men; –x ± SD age: 56.1 ± 15.1 y) consecutively
admitted to our medical intensive care unit with either sepsis or
a nonseptic critical condition. No patient included in the study
had preexisting diabetes mellitus or a hereditary disturbance of
lipid metabolism. Further exclusion criteria were hemodynamic
shock with serum lactate concentrations > 5 mmol/L, hypertriglyc-
eridemia (ie, triacylglycerol > 5.1 mmol/L, or 450 mg/dL), and
hyperglycemia (ie, glucose > 10 mmol/L, or 180 mg/dL) despite
continuous administration of insulin at a rate of 30 mol/h (5 IU/h)
before the administration of TPN. Patients artificially ventilated
with a fraction of inspired oxygen > 0.55 were also excluded.
Sepsis was diagnosed according to the criteria of the Ameri-
can College of Chest Physicians/Society of Critical Care Medi-
cine Consensus Conference (8). Sepsis was diagnosed if a site of
infection was established and ≥ 2 of the following conditions
were found as a result of infection: temperature > 38 or < 36 C,
heart rate > 90 beats/min, respiratory rate > 20 breaths/min or an
1
From the Department of Internal Medicine IV, University of Vienna.
2
Address reprint requests to B Schneeweiss, Department of Internal Med-
icine IV, Intensive Care Unit 13 H1, University of Vienna, Währinger-Gürtel
18-20, A-1090 Vienna, Austria. E-mail: bruno.schneeweisz@univie.ac.at.
Received July 3, 2000.
Accepted for publication February 12, 2001.
265
266 ZAUNER ET AL
TABLE 1
Substrates and volumes of total parenteral nutrition administered in each
patient group1
Septic (n = 14) Nonseptic (n = 11)
Volume (mL/h) 79.8 ± 18.6 71.1 ± 21.1
Glucose (g/d) 232 ± 54 207 ± 61
Fat (g/d) 93 ± 22 83 ± 25
Protein (g/d) 68 ± 16 61 ± 18
1–
x ± SD. There were no significant differences between groups.
arterial partial pressure of carbon dioxide < 32 mm Hg, and a
white blood cell count > 12 or < 4  109/L or > 10% immature
band forms (8). The severity of sepsis on day 0 was assessed by
the SOFA (sepsis-related organ failure assessment) score (9).
Critically ill patients not fulfilling the consensus conference cri-
teria for sepsis and with no evidence of infection were included
in a separate group. The severity of illness in all patients was
assessed by the APACHE (acute physiology and chronic health
evaluation) III score (10). The study was approved by the Insti-
tutional Review Board of the University of Vienna.
Metabolic studies
Before TPN was administered, the patients’ resting energy
expenditure (REE) and substrate oxidation rates were measured
by indirect calorimetry after they had fasted overnight (day 0).
Measurements were made by a technician who was not involved
in the treatment and who was not informed of the diagnoses. The
patients’ daily energy supply was 25% above their measured
REE (11) (Table 1). A TPN solution containing 45% glucose,
41% lipids, and 14% amino acids was infused continuously
(Kabi Mix; Fresenius Kabi GmbH, Graz, Austria). TPN was
started immediately after the first measurement at the calculated
infusion rate and the infusion rate remained unchanged during
the whole study period. REE and substrate oxidation rates were
reevaluated on days 2 and 7.
Indirect calorimetry
Respiratory gas exchange was measured by computerized
open-circuit indirect calorimetry (MMC 2900; SensorMedics,
Anaheim, CA) as previously described (5, 12). Oxygen con-
sumption and carbon dioxide production were measured in 1-min
intervals and the average of a 30-min period was calculated. The
system was calibrated at the beginning of each measurement.
Calculations
REE is expressed in kJ · min1 · m2. REE and oxidation rates
for glucose, fat, and protein were calculated according to Ferran-
nini (13). The nonprotein respiratory quotient was calculated by
subtracting the exchange attributable to protein oxidation from
the total gaseous exchange. It was assumed that for each 1 g nitro-
gen produced, 5.923 L oxygen was consumed and 4.754 L carbon
dioxide was produced (respiratory quotient for protein: 0.803)
(14). For calculation of urea nitrogen appearance rates, changes
in plasma urea concentration were taken into account (15). Uri-
nary urea nitrogen was measured colorimetrically (16). The pro-
portion of nonprotein energy derived from carbohydrate and fat
was calculated from the nonprotein respiratory quotient. The pro-
tein oxidation rate (g/d) was calculated as 6.25  24-h urea nitro-
gen production (g/d) (17). Twenty-four–hour carbohydrate, fat,
and protein balances were calculated as 24-h intake minus 24-h
oxidation. Protein balance was corrected for miscellaneous nitro-
gen losses of 4 g/d (18), which is equivalent to a protein intake of
418.4 kJ/d (100 kcal/d). Changes in the free glucose pool were
calculated as follows: change in glucose pool = change in blood
glucose concentration  0.25 L/kg body wt (19).
Statistical analysis
This study was exploratory in nature. Data from the 2 groups
of patients were compared by using the Mann-Whitney U test.
To show differences in values of both groups of patients across
time, a repeated-measures analysis of variance (Greenhouse-
Geisser test) was used. If the results of the repeated-measures
analysis of variance were significant, linear contrasts were used
for post hoc testing. Furthermore, differences in the metabolic
variables between day 2 and day 0, day 7 and day 0, and day 7
and day 2 were calculated. The chi-square test was applied to
compare mortality and the sex distribution between the 2 groups.
Correlations were assessed by using Spearman’s rank correlation
coefficient (r). STATISTICA for WINDOWS (release 5.01; Stat-
Soft, Inc, Tulsa, OK) and SAS (release 6.12; SAS Institute Inc,
Cary, NC) were used for the statistical analysis. Results are pre-
sented as means ± SDs. P values < 0.05 were considered to be
statistically significant.
RESULTS
Of the 25 patients studied, 14 were septic and 11 were not.
The 2 groups were not significantly different with respect to
sex, age, height, and weight (Table 2). The underlying dis-
eases, the infectious agents, and the site of infection for the
septic patients are presented in Table 3. The underlying dis-
eases of the nonseptic patients are presented in Table 4. No
positive cultures and no evidence of an infection site were
detectable in nonseptic patients. On day 0, the respiratory rate
was higher in septic patients, whereas there were no significant
differences between the groups in temperature, heart rate, arte-
rial partial pressure of carbon dioxide, and white blood cell
count (Table 5). Laboratory variables measured on days 0, 2,
and 7 are summarized in Table 6.
The severity of illness as assessed by the APACHE III score
was not significantly different between the groups (septic
patients: 70.2 ± 11.1; nonseptic patients: 78.9 ± 24.9; Tables 3
and 4). The APACHE III score correlated negatively with meas-
ured REE in septic patients (r = 0.58, P < 0.05). No such
association was found in nonseptic patients. REE was posi-
tively correlated with body temperature in septic patients only
TABLE 2
Characteristics of the patients in each group1
Septic Nonseptic
(n = 8 M, 6 F) (n = 7 M, 4 F)
Mortality (%) 43 64
Age (y) 57.5 ± 12.92 54.4 ± 18.2
Severe sepsis/septic shock (n) 11/3 —
Weight (kg) 71.4 ± 12.7 65.5 ± 12.9
Height (cm) 172 ± 8.3 173 ± 9.5
BMI (kg/m2) 24.1 ± 4.2 21.8 ± 3.5
Body surface area (m2) 1.84 ± 0.18 1.78 ± 0.21
1
There were no significant differences between groups.
2–
x ± SD.
 NUTRITION IN CRITICAL ILLNESS 267

TABLE 3
Underlying diseases, infection sites, and infectious agents of the septic patients1
APACHE III SOFA
No. Sex Underlying disease Infectious agent Infection site score score
1 M CABG Enterococcus faecalis Infection of CVC 51 5
2 F LTX Candida albicans Pneumonia 76 8
3 F Wegener disease C. albicans Pneumonia 73 11
4 M Burns Escherichia coli, Pseudomonas aeruginosa Wound infection 71 8
5 F LTX Aspergillus fumigatus Pneumonia 86 7
6 F Upper GI tract bleeding Unknown Pneumonia 57 6
7 M Liver cirrhosis Staphylococcus epidermidis Infection of CVC 67 10
8 F Aspiration S. epidermidis Pneumonia 70 8
9 M CPR Enterobacter, S. epidermidis Infection of CVC 82 5
10 M Liver cirrhosis Staphylococcus aureus Infection of CVC 83 15
11 F Vascular surgery S. aureus Pneumonia 74 13
12 M Duodenal ulcer perforation S. epidermidis Pneumonia, peritonitis 57 12
13 M CABG Unknown Pneumonia 57 6
14 M MOF E. faecalis Pneumonia 79 13
1
APACHE, acute physiology and chronic health evaluation (10); CABG, coronary artery bypass grafting; CPR, cardiopulmonary resuscitation; CVC,
central venous catheter; GI, gastrointestinal; LTX, liver transplantation; MOF, multiple organ failure; SOFA, sepsis-related organ failure assessment (9).

(12.2% rise in REE/C rise in body temperature; Figure 1). No DISCUSSION

association between body temperature and APACHE III score Our results suggest that no significant differences in measured
was found in either group. REE and substrate oxidation rates after an overnight fast existed
REE was not significantly different between groups on day 0, between septic and nonseptic critically ill patients. Infusion of a
and no significant differences in REE were detected between standardized TPN formula resulted in no significant changes in
groups during the study period. Furthermore, REE did not REE between or within groups during the study period. Thus, the
change within groups during the study period (Tables 7 and 8). metabolic response to TPN might not differ between septic and
The respiratory quotient increased significantly in both groups nonseptic critically ill patients. In septic patients, REE was neg-
on day 2 compared with day 0 and remained high on day 7. No atively correlated with the severity of illness. Although it has
significant differences in respiratory quotient between groups been shown that enteral nutrition is preferable in critically ill
were observed on days 0, 2, and 7. patients, we chose to use the parenteral route in this study to
Substrate balances were not significantly different between groups avoid enteral substrate losses that might be difficult to assess and
during the study period (Table 7). Energy balances became positive because it remains unclear whether macronutrients provided
in both groups on day 2 (septic patients: 0.68 ± 0.4 kJ · min1 · m2; enterally are satisfactorily absorbed because of a possible
nonseptic patients: 0.74 ± 0.6 kJ · min1 · m2; NS) and day 7 exocrine pancreatic insufficiency in critically ill patients (20).
(septic patients: 0.65 ± 0.3 kJ·min1 ·m2; nonseptic patients: Nutritional support is indicated to prevent or correct protein-
0.78 ± 0.5 kJ·min1 ·m2; NS). There was no significant difference energy malnutrition when adequate food intake is not possible
within the groups between days 2 and 7. for long periods of time (1). For providing energy, many differ-
ent TPN solutions with different macronutrient compositions are
available. Metabolic changes in critically ill patients are the
TABLE 4 result of systemic actions of mediators released in response to
Underlying diseases of the nonseptic patients1
trauma, injury, or infection (2). The concentration of these medi-
APACHE III ators is associated with the severity of illness (21) and it was
No. Sex Underlying disease score
1 M Ventricular fibrillation, CPR 72
2 M Guillain-Barré syndrome, 68 TABLE 5
respiratory insufficiency Sepsis criteria of both patient groups on day 01
3 M Surgery for pharyngeal cancer, ARF 126 Septic (n = 14) Nonseptic (n = 11)
4 M Multiple trauma 65
Temperature (°C) 37.3 ± 1.2 37 ± 0.7
5 F Upper GI tract bleeding 80
Heart rate (beats/min) 108 ± 21 95 ± 18
6 M CABG 110
RF (breaths/min) 27 ± 10 16 ± 22
7 M Dilative CMP 63 PaCO2 (mm Hg) 32.6 ± 9.8 33.1 ± 5.1
8 F NTX 87 WBC (1  109/L) 17.1 ± 12.3 13 ± 5.2
9 M Whipple disease 31 MAP (mm Hg) 84 ± 13 79 ± 19
10 F Respiratory insufficiency, CPR 82 SOFA score 9±3 —
11 F COPD, respiratory insufficiency 84 1–
x ± SD. MAP, mean arterial pressure; PaCO2, arterial partial pressure
1 of carbon dioxide; RF, respiratory frequency; SOFA, sepsis-related organ
APACHE, acute physiology and chronic health evaluation (10); ARF,
acute renal failure; CABG, coronary artery bypass grafting; CMP, cardiomy- failure assessment (9); WBC, white blood cell count.
2
opathy; COPD, chronic obstructive pulmonary disease; CPR, cardiopul- Significantly different from septic group, P < 0.0005 (Mann-Whitney
monary resuscitation; GI, gastrointestinal; NTX, kidney transplantation. U test).
268 ZAUNER ET AL

TABLE 6
Laboratory variables assessed during the study period1
Day 0 Day 2 Day 7 P2
Septic patients (n = 14)
Serum urea (mmol/L) 27 ± 14 27 ± 14 28 ± 18 NS
Glucose (mmol/L) 6.8 ± 2.7 8.8 ± 2.23 7.1 ± 1.24 < 0.05
Lactate (mmol/L) 1.4 ± 0.7 1.9 ± 1 1.2 ± 0.7 NS
Triacylglycerol (mmol/L) 2.2 ± 1.1 2.3 ± 1.8 2.2 ± 1.8 NS
Cholesterol (mmol/L) 3.1 ± 1.8 3.5 ± 1.9 3 ± 1.5 NS
Creatinine (mol/L) 209 ± 152 201 ± 163 178 ± 115 NS
UNP (g/d) 12.6 ± 6.7 10.8 ± 5.4 11.3 ± 6.3 NS
Nonseptic patients (n = 11)
Serum urea (mmol/L) 19 ± 15 13 ± 135 12 ± 8 < 0.05
Glucose (mmol/L) 6.5 ± 1.4 7.8 ± 1.65 6.8 ± 1.2 < 0.05
Lactate (mmol/L) 1.2 ± 0.8 0.8 ± 0.56 1 ± 0.3 NS
Triacylglycerol (mmol/L) 2.1 ± 1.4 2 ± 1.1 1.8 ± 0.9 NS
Cholesterol (mmol/L) 2.6 ± 0.7 2.7 ± 0.9 3.3 ± 0.5 NS
Creatinine (mol/L) 249 ± 218 164 ± 1805 157 ± 165 < 0.05
UNP (g/d) 13.9 ± 11.9 8.9 ± 6.8 8.3 ± 4.5 NS
1–
x ± SD. UNP, urea nitrogen appearance rate.
2
Test for time effect by repeated-measures ANOVA.
3,5
Significantly different from day 0: 3 P < 0.01, 5 P < 0.05.
4
Significantly different from day 2, P < 0.05.
6
Significantly different from septic patients, P < 0.05.

shown that REE correlates positively with different severity adaptation of macronutrient composition in feeding of septic and
scoring systems (22, 23). Although it was not the aim of this nonseptic critically ill patients is necessary. An alternative expla-
study to compare the REE of critically ill patients and healthy nation for our data is that the methods used were not sufficiently
control subjects, our measurements of REE were in the range of sensitive or the statistical power to find differences between the
values published by other authors for critically ill septic and non- 2 groups of patients was too low (ie, type I error).
septic patients (4, 5, 24). Surprisingly, we found a negative asso- In contrast with the case in healthy subjects and nutritionally
ciation between the APACHE III score and REE in the septic depleted patients (3), the respiratory quotient in the subjects in
patients but not in the nonseptic patients. This negative associa- our study never exceeded 1.0, indicating that no net de novo lipo-
tion between the severity of illness and REE agrees with results genesis was present (ie, total lipid oxidation was higher than
reported by Kreymann et al (24), who also found that REE total lipid synthesis) in our critically ill patients despite positive
decreased with the severity of sepsis. Kreymann et al argued that energy and substrate balances. Protein oxidation rates remained
this negative association is a mediator-related effect. Experimen- unchanged during the administration of TPN in all patients and
tal data support these clinical findings; it was shown that com- protein balances were not significantly different from zero after
bined infusion of interleukin 1 and tumor necrosis factor the administration of TPN. However, because protein oxidation
decrease mitochondrial oxygen consumption in vitro (25). rates were calculated from the urea nitrogen appearance rate
In our study body temperature was positively correlated with only, we cannot make conclusions concerning protein metabo-
REE in the septic patients. This agrees with the findings of lism in critically ill patients (18).
Frankenfeld et al (26), who showed that febrile patients with
systemic inflammatory response syndrome were significantly
more hypermetabolic than were afebrile patients with systemic
inflammatory response syndrome. The amount of the increase in
our patients (12%/°C) corresponds to that found by DuBois (27)
and Wallace et al (28). No such association was found in our
nonseptic patients. This may have been due to the smaller sam-
ple size of the nonseptic patient group, or the association itself
may not exist. Energy balances were positive in both groups
during the administration of TPN in an amount 25% above the
REE measured on day 0.
In accordance with the findings of earlier studies (5–7), fat was
the main substrate for oxidation, and glucose oxidation was
depressed in all our patients after an overnight fast. The respira-
tory quotient rose in both groups after the initiation of TPN. Sub-
strate balances for carbohydrate and fat became positive in both
septic and nonseptic patients. This might reflect that the same FIGURE 1. Relation between body temperature and resting energy
metabolic derangement is manifest in both groups of critically ill expenditure (REE) in septic (, solid line; r = 0.63, P < 0.05) and non-
patients and that metabolic adaptation to substrate administration septic (X, dotted line; r = 0.46, NS) patients. For septic patients,
does not seem to differ. Thus, our data suggest that no specific y = 0.3273x  9.4325; for nonseptic patients, y = 0.4275x  13.462.
 NUTRITION IN CRITICAL ILLNESS 269

TABLE 7
Metabolic variables assessed during the study period1
Day 0 Day 2 Day 7 P2
Septic patients (n = 14)
·
VO2 (mL·min1 ·m2) 135 ± 26 134 ± 25 127 ± 32 NS
·
VCO2 (mL·min1 ·m2) 103 ± 18 112 ± 21 108 ± 27 NS
RQ 0.77 ± 0.05 0.84 ± 0.053 0.86 ± 0.053 < 0.01
Nonprotein RQ 0.75 ± 0.07 0.85 ± 0.073 0.87 ± 0.073 < 0.01
REE (kJ·min1 ·m2) 2.65 ± 0.5 2.69 ± 0.5 2.55 ± 0.7 NS
CHO (kJ·min1 ·m2) 0.23 ± 0.8 0.42 ± 0.44 0.28 ± 0.53 < 0.05
FAT (kJ·min1 ·m2) 1.89 ± 1 0.24 ± 0.53 0.39 ± 0.53 < 0.0001
PRO (kJ·min1 ·m2) 0.53 ± 0.3 0.01 ± 0.33 0.04 ± 0.23 < 0.0001
Nonseptic patients (n = 11)
·
VO2 (mL·min1 ·m2) 122 ± 31 119 ± 25 108 ± 24 NS
·
VCO2 (mL·min1 ·m2) 90 ± 19 99 ± 21 88 ± 18 NS
RQ 0.75 ± 0.05 0.84 ± 0.044 0.82 ± 0.044 < 0.01
Nonprotein RQ 0.72 ± 0.1 0.85 ± 0.07 4
0.83 ± 0.064 < 0.05
REE (kJ·min1 ·m2) 2.36 ± 0.6 2.38 ± 0.5 2.15 ± 0.5 NS
CHO (kJ·min1 ·m2) 0.08 ± 0.7 0.5 ± 0.43 0.59 ± 0.63 < 0.005
FAT (kJ·min1 ·m2) 1.69 ± 0.7 0.22 ± 0.63 0.12 ± 0.43 < 0.0001
1 2
PRO (kJ·min ·m ) 0.59 ± 0.5 0.3 ± 0.23
0.1 ± 0.13 < 0.005
1– ·
x ± SD. CHO, carbohydrate balance; FAT, fat balance; PRO, protein balance; REE, resting energy expenditure; RQ, respiratory quotient; VCO2, carbon
·
dioxide production; VO2, oxygen consumption.
2
Test for time effect by repeated-measures ANOVA.
3,4
Significantly different from day 0: 3 P < 0.01, 4 P < 0.05.

TABLE 8
Differences in metabolic variables over time in both groups1
Day 2  day 0 Day 7  day 0 Day 7  day 2
Septic Nonseptic Septic Nonseptic Septic Nonseptic
·
VO2 (mL·min1 ·m2) 1.3 ± 16.1 3 ± 23.7 3.3 ± 19 3.1 ± 16.8 0.7 ± 23.5 9.4 ± 17.6
·
VCO2 (mL·min1 ·m2) 9 ± 11.2 9 ± 18.1 8.6 ± 17.4 3.1 ± 17.3 1.2 ± 19 8.1 ± 11.3
RQ 0.07 ± 0.06 0.09 ± 0.07 0.09 ± 0.06 0.06 ± 0.04 0.01 ± 0.05 0.01 ± 0.04
Nonprotein RQ 0.11 ± 0.09 0.17 ± 0.18 0.13 ± 0.09 0.1 ± 0.1 0.03 ± 0.07 0.01 ± 0.06
REE (kJ·min1 ·m2) 0.03 ± 0.3 0.02 ± 0.4 0 ± 0.4 0.02 ± 0.3 0.01 ± 0.5 0.2 ± 0.3
1– · ·
x ± SD. REE, resting energy expenditure; RQ, respiratory quotient; VCO2, carbon dioxide production; VO2, oxygen consumption. There were no signi-
ficant differences within the groups over time.

In conclusion, septic and nonseptic critically ill patients seem to
show the same alterations in energy and substrate metabolism. The
metabolic responses during the administration of standardized TPN
are comparable in these patients. Therefore, a disease-specific
macronutrient composition of a TPN formula does not seem to be
necessary for septic or nonseptic critically ill patients.
We thank Barbara Schneider for her statistical assistance and Katrin Kornfell
for her thoughtful revision of the manuscript.
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