Knuckle pads mimic early psoriatic arthritis.

Knuckle pads or Garrod's nodes are a rare, non-inflammatory condition. They consist of benign, well-circumscribed fibro-adipose tissue over the small joints of hands and feet. Knuckle pads may be under-diagnosed and mistaken for early arthritis. The rheumatologist should perform an accurate differential diagnosis in which he can be helped by ultrasound and by other colleagues, such as the dermatologist. Ultrasound is considered useful in the assessment of the thickening of the subcutaneous tissue, located usually on the extensor site of proximal interphalangeal and metacarpophalangeal hand joints. Dermoscopy may play a role in detecting epidermal and dermal changes. We hereby report the case of a female patient with knuckle pads mimicking psoriatic arthritis.

Plasma cholinesterase correlations in acute surgical and critical illness.

AIM: The properties of plasma cholinesterase (CHE) are partly undiscovered. Equally unknown are the correlations between changes in CHE and other blood variables during the acute phase response related to acute surgical and critical illness. METHODS: Data from 432 measurements of CHE and other variables performed in 92 patients were systematically evaluated and processed by regression analysis. RESULTS: There was a strong direct correlation between CHE and albumin (r=0.77, P<0.0001). CHE was also directly correlated to cholesterol, iron binding capacity, hematocrit, prothrombin activity, and inversely correlated to bilirubin and to presence of sepsis or liver dysfunction (P<0.0001 for all). Postoperatively CHE decreased to about 60% of the preoperative value, remaining directly related to it (r=0.69, P<0.0001), and decreasing further in the presence of sepsis or liver dysfunction, with slow reversal of the decrease during recovery from illness. In parenterally fed septic patients the decrease in CHE was moderated by increasing the amino acid dose (P<0.0001). CONCLUSION: In acute surgical and critical illness CHE mostly behaves as a negative acute phase reactant, independently of the modifications related to other already known factors. This should be taken into account when interpreting the implications of decreased CHE in the clinical setting.

Nail ultrasonography for psoriatic arthritis and psoriasis patients: a systematic literature review.

To systematically review the role of ultrasound (US) in the assessment of the joint-enthesial-nail apparatus in patients with psoriatic arthritis (PsA) or psoriasis (PSO) in terms of prevalence, diagnosis, prognosis, monitoring and treatment. A systematic literature review was conducted through medical databases (PubMed, Embase) and the grey literature up to February 2018. The main areas of application of nail US were first identified, allowing the development of research questions, which were rephrased following the PICOs methodology to develop inclusion criteria. Of the 585 studies produced by PubMed and Embase searches, 17 studies met the criteria for inclusion. Five additional studies were included: 1 from the hand search and 4 from the 2016-2017 ACR and EULAR congresses. The prevalence of nail plate changes varied from < 10 to 97%, for power Doppler signal from 20-30 to 96% and distal interphalangeal joint (DIJ) involvement from 8.9 to 100%. The performance of US nail/DIJ abnormalities in the diagnosis of PsA and PSO elementary lesions was analysed by five studies, with a wide heterogeneity. Reproducibility and reliability of US nil/DIJ were assessed by interclass correlation coefficient or Cohen's k and their values ranged from 0.6 to 0.9. The value of US nail/DIJ in the monitoring of the lesions was analysed only by a single study. The analysis revealed applications for US nail/DIJ in PsA and PSO and highlights limitations. Validation is strongly needed to demonstrate its appropriateness in the clinical practice and to define its diagnostic and prognostic role.

Liver dysfunction and sepsis determine operative mortality after liver resection.

BACKGROUND: Liver failure is the principal cause of death after hepatectomy. Its progression towards death and its relationship with sepsis are unclear. This study analysed predictors of mortality in patients with liver dysfunction and the role of sepsis in the death of these patients. METHODS: The study focused on patients with liver dysfunction, excluding those with vascular thrombosis, after liver resection at one of two centres between 1998 and 2006. RESULTS: Liver dysfunction occurred after 57 (4.5 per cent) of 1271 hepatectomies. Fifty-three patients without vascular thrombosis were included in the analysis, with a mortality rate of 23 per cent. Independent predictors of death were age (odds ratio (OR) 1.18 per year increase; P = 0.017), cirrhosis (OR 54.09; P = 0.004) and postoperative sepsis (OR 37.58; P = 0.005). Sepsis occurred in 15 patients (28 per cent), seven of whom died. Intestinal pathogens were isolated in 12 patients with sepsis. The risk of sepsis was significantly increased in those with surgical complications (11 of 16 versus four of 37; P < 0.001). CONCLUSION: Sepsis plays a key role in the death of patients with liver dysfunction after hepatectomy. Early recognition and aggressive treatment of sepsis may reduce mortality.

Liver resections for hepatocellular carcinoma in chronic liver disease: experience in an Italian centre.

AIM: Liver resection (LR) and transplantation are the best options for treatment of hepatocellular carcinoma (HCC). We retrospectively analysed the experience obtained with LR for HCC in chronic liver disease patients. METHODS: Up until May 2005, 248 patients with HCC were evaluated, and 113 resected. Of these, 97 with chronic liver disease, who underwent a total of 100 resections, form the basis of this study. Age of the patients was 65.6+/-9.2 years (range 32-81, male/female 76/21). In 77 cases there was unifocal and in 23 multinodular tumour; in 61 the size of the tumours was < or =5 cm and in 39>5 cm. Limited resections were performed in 15 cases, resections of 1-2 segments in 51, and major hepatectomies in 34. RESULTS: Blood transfusions were required in 28 cases. Three patients died postoperatively, from liver failure and/or sepsis. Seventeen patients had nonlethal complications (mostly liver dysfunction, often with signs of amplified inflammatory response, including ARDS, without evident sources of sepsis). The 5- and 10-year survival rates were 44% and 24%, respectively. Decreased survival was significantly related to increasing number of tumour nodules and degree of liver fibrosis/presence of cirrhosis, and with the expression of markers of carcinogenesis in a sub-group who received this assessment. At 5 years the rate of liver HCC recurrence was 46%, however, death was unrelated to recurrence in 41% of non-survivors. CONCLUSIONS: Surgery for HCC achieves acceptable early and long-term results. However, the patterns affecting perioperative outcome must be better understood, and the high recurrence rate warrants further trials to assess preventive treatments after LR.

Total gastrectomy for type 1 gastric carcinoid: an unusual surgical indication?

Gastric carcinoid is a relatively rare neoplasm with peculiar features which differentiate it from the intestinal and pulmonary carcinoid and, obviously, from gastric adenocarcinoma. Gastric carcinoids are divided into three different types: Type 1, associated with gastric atrophy and megaloblastic anemia; Type 2, associated with Zollinger-Ellison syndrome within a type 1 multiple endocrine neoplasia (MEN); and Type 3, sporadic tumor not associated with other lesions, particularly invasive and with poor prognosis. Type 1 carcinoid is usually asymptomatic and casually detected at endoscopy due to aspecific symptoms or to screening in patients with atrophic gastritis. It is generally small, multifocal and located in the gastric fundus, has no tendency for vascular invasion and is associated with a benign course. Therefore, the recommended treatment, for lesions < 10 mm and in a number < 5, is endoscopic resection with strict follow-up. We report a case of a woman with a type 1 gastric carcinoid in which, for the presence of an extended micro-polyposis of the fundus a total gastrectomy was necessary for treatment. Pathology revealed vascular invasion at the level of the major lesion of 8 mm of diameter. In conclusion this finding, unknown before surgery, emphasizes the need for careful assessment also in the presence of apparently less important gastric carcinoid lesions.

Plasma amino acids of the transsulfuration pathway and plasma lactate in septic patients.

OBJECTIVES: In sepsis increasing plasma lactate, even if unrelated to hypoperfusion and hypoxia, is a cause of concern. Among the patterns associated with increasing lactate, several plasma amino acid (AA) abnormalities, more in particular those of sulfur AAs, have remained unexplored, and their assessment has been the purpose of our study. MATERIALS AND METHODS: A systematic and detailed analysis of 183 simultaneous determinations of plasma AA-grams and lactate, from 12 trauma surgery patients who had developed sepsis, was performed. Sepsis severity ranged from moderate to extreme illness. Correlations between changes in lactate and in AA levels were assessed by regression analysis. RESULTS: Increasing lactate was related to increasing alanine, proline, asparagine, tyrosine, cystathionine, histidine, glutamine, citrulline, methionine, phenylalanine and hydroxyproline (r from 0.62 to 0.36, p < 0.001 for all) and to decreasing taurine (r = -0.62, p < 0.001). Furthermore, increasing lactate was strongly related to increasing cystathionine/taurine ratio (r = 0.77, p < 0.001). These correlations were independent of the simultaneous relationship found between increasing lactate and decreasing mixed venous O2 tension. CONCLUSIONS: The overall findings and the correlation with the cystathionine/taurine ratio support the hypothesis that increasing lactate in sepsis may be paralleled by impaired hepatic AA transsulfuration. Because this may disable antioxidant protection by limiting glutathione and taurine availability, the metabolic perturbations associated with septic hyperlactatemia may include enhanced exposure to oxidative stress.

The relationship between albumin, other plasma proteins and variables, and age in the acute phase response after liver resection in man.

A large series of plasma albumin (ALB, g/dl) and simultaneous blood and clinical measurements were prospectively performed on 92 liver resection patients, and processed to assess the correlations between ALB, other plasma proteins, additional variables and clinical events. The measurements were performed preoperatively and at postoperative day 1, 3 and 7 in all patients, and subsequently only in those who developed complications or died. In patients who recovered normally ALB was 4.3 +/- 0.4 g/dl (mean +/- SD) preoperatively, 3.7 +/- 0.7 at day 1 and 3, and 3.9 +/- 0.4 at day 7. In patients with complications its decrease was more prolonged. In non-survivors it was 3.4 +/- 0.4 preoperatively, 3.0 +/- 0.4 at day 1, and then decreased further. Regression analysis showed direct correlations between ALB and pseudo-cholinesterase (CHE, U/l, nv 5300-13000), cholesterol (CHOL, mg/dl), iron binding capacity (IBC, mg/dl), prothrombin activity (PA, % of standard reference) and fibrinogen, an inverse correlation with blood urea nitrogen (BUN, mg/dl) for any given creatinine level (CREAT, mg/dl), and weaker direct correlations with hematocrit, other variables and dose of exogenous albumin. An inverse relationship found between ALB and age (AGE, years) became postoperatively (POSTOP) also a function of outcome, showing larger age-related decreases in ALB associated with complications (COMPL: sepsis, liver insufficiency) or death (DEATH). Main overall correlations: CHE = 287.4(2.014)(ALB), r = 0.73; CHOL = 16.5(1.610)(ALB) (1.001)(ALKPH), r = 0.71; IBC = 68.6(1.391)(ALB), r = 0.64; PA = 13.8 + 16.0(ALB), r = 0.51; BUN = 21.3 + 20.2(CREAT) - 6.2(ALB), r = 0.91; ALB = 5.0-0.013(AGE) - {0.5 + 0.003(AGE)( COMPL ) + 0.012(AGE)( DEATH )}( POSTOP ), r = 0.74 [p < 0.001 for each regression and each coefficient; ALKPH = alkaline phosphatase, U/l, nv 98-279, independent determinant of CHOL; discontinuous variables in italics label the change in regression slope or intercept associated with the corresponding condition]. These results suggest that altered albumin synthesis (or altered synthesis unable to compensate for albumin loss, catabolism or redistribution) is an important determinant of hypoalbuminemia after hepatectomy. The correlations with age and postoperative outcome support the concept that hypoalbuminemia is a marker of pathophysiologic frailty associated with increasing age, and amplified by the challenges of postoperative illness.

The relationship between oxygen extraction and venous pH in sepsis.

This study was performed to quantify the impact of Haldane effect (HE) on the relationship between O2 extraction (O2Ex; mL O2/dL blood) and venous pH in 247 measurements performed in 91 septic patients (73 patients with intra-abdominal sepsis, 11 with retroperitoneal abscesses, 6 with severe cholangitis, and 1 with gangrenous fasclitis). The severity of sepsis varied from relatively compensated to extremely diseased conditions. This allowed a detailed assessment of the impact of HE over a wide range of cardiorespiratory and metabolic abnormalities. A recently developed model was used to quantify blood CO2 exchange and Haldane relationships and, in particular, the buffering of venous pH allowed by O2Ex (O2-linked H+ binding) on the basis of arterial and mixed venous blood gas measurements. Arterio-venous pH difference (a-vDpH) was .033 +/- .024 (mean +/- SD). It increased with venoarterial CO2 concentration difference (v-aDCO2; mL CO2/dL blood), but the increase was moderated by a simultaneous increase in O2Ex, as the likely consequence of HE: a-vDpH = .006 + .017 (v-aDCO2) - .009 (O2Ex) [r2 = .96, p < < .001]. To confirm this, the moderation of a-vDpH allowed by the HE (DpH) was calculated. A first component, due to O2-linked H+ binding, had a value of .016 +/- .012, and a second component, due to the Haldane-mediated reduction in venous CO2 tension and plasma carbonic acid concentration, had a value of .019 +/- .006. Their sum (total DpH) was .033 +/- .017 and was related directly and strongly to O2Ex: DpH = -.002 + .009 (O2Ex) [r2 = .85, p < < .001], thus confirming the quantitative impact of HE in moderating the decrease in venous pH relative to arterial pH. The loss of this effect was responsible for the larger decreases in venous pH observed in hypodynamic patients developing impaired O2Ex. These results allow an easy quantification of the Haldane component, separated from the other components affecting pH, and are also useful for assessing the protective role exerted by HE against excessive decreases in venous pH in circulatory failure.

Hepatic resections in normothermic ischemia.

BACKGROUND: Reduction of operative blood transfusions is a primary goal in resective surgery of the liver. Temporary vascular inflow occlusion is an effective method to decrease hemorrhage during hepatic resection. This study was performed to assess the impact of normothermic ischemia on intraoperative bleeding and outcome after hepatic resection. METHODS: Sixty-one hepatic resections were performed by using pedicle clamping alone or associated with total vascular exclusion of the liver. The mean duration of normothermic ischemia was 40 +/- 18 minutes (range, 7 to 98 minutes). Major resections were performed in 32 cases (52.5%). RESULTS: Operative mortality was nil. Major complications occurred in 11.5% of cases. Twenty-five patients (41%) received intraoperative blood transfusions; mean +/- SD of transfused blood units was 2.4 +/- 1.3. Twelve major resections (37.5%) did not require any transfusion. Postoperative changes in liver function test results were moderate and transient. CONCLUSIONS: The results of this study confirm the benefit of vascular occlusion techniques in reducing intraoperative bleeding and postoperative complications. The routine use of these techniques during hepatic resections, if applied properly and with the necessary precautions, is not associated with severe adverse effects on liver function.

Pathophysiologic correlates of hypocholesterolemia in critically ill surgical patients.

OBJECTIVE: To assess correlates of hypocholesterolemia in moderate to critical surgical illness. DESIGN: Prospective analysis of laboratory and clinical data. SETTING: Department of surgery in a university hospital. PATIENTS: 135 patients undergoing uncomplicated abdominal surgery or with sepsis, liver failure, hemorrhage, severe cholestasis, or multiple organ dysfunction syndrome (MODS). INTERVENTIONS: Surgical and/or medical therapy according to clinical status. MEASUREMENTS AND MAIN RESULTS: Determinations of total cholesterol, additional variables, and clinical data. Cholesterol decreased after surgery, in sepsis, liver failure, acute hemorrhage, and MODS and increased in cholestasis. Hypocholesterolemia correlated with decreases in plasma proteins and indices of hepatic protein synthetic adequacy, with hemodilution from blood loss, and was moderated or prevented by cholestasis. CONCLUSIONS: These results help to explain the dynamics of the development, clinical relevance, and negative prognostic value of hypocholesterolemia in critical illness.

Physiological and metabolic correlations in human sepsis. Invited commentary.

The septic response in man appears to be a disease in which the infecting agent induces a state of disordered metabolic control in the host. The abnormal regulation of metabolic pathways causes a diversion of substrate utilization toward gluconeogenesis and ketone body formation and a reduction in oxidative energy-producing metabolism. This state of metabolic insufficiency is reflected in the pattern of cardiorespiratory, vascular, and physiological compensation. The precise magnitude of the resultant physiological compensation and its rate and direction of change can be quantified by the use of physiological state trajectories which also reflect the magnitude of underlying metabolic derrangements. The prognostic and therapeutic implications of these changes are discussed.

Quantitative assessment of changes in blood CO(2) tension mediated by the haldane effect.

Adequate assessment of circulatory and gas-exchange interactions may involve the quantification of the Haldane effect (HE) and of the changes in blood PCO(2) mediated by changes in Hb-O(2) saturation and O(2)-linked CO(2) binding. This is commonly prevented by the complexity of the involved calculations. To simplify the task, a large series of patient measurements has been processed by regression analysis, thus developing an accurate fit for this quantification (v-a) PCO(2)HE + 0.460 [(a-v) HbO(2)]0.999e0.015(PvCO(2))-0.852(Hct) (n = 247, r(2) = 0. 99, P << 0.001), where (v-a)PCO(2 HE) is the reduction in venous PCO(2) (Pv(CO(2)), Torr) allowed by the chemical binding of CO(2) in blood due to the HE (Torr), (a-v)HbO(2) is the arteriovenous difference in Hb-bound O(2) (ml/dl), and Hct is hematocrit fraction. Values of (v-a)PCO(2 HE) estimated by this expression compared well with the results of previously published experiments. This formula is useful in assessing the impact of HE on Pv(CO(2)) and venoarterial PCO(2) gradient and the survival advantage offered by HE in extreme conditions. Use may be extended to all investigative and clinical settings in which changes in blood O(2) saturation and O(2)-linked CO(2) binding must be converted into the corresponding changes in dissolved CO(2) and PCO(2).

Calculation of venoarterial CO2 concentration difference.

Quantitative relationships in CO2 transport and exchange processes were combined for use as the basic components of an original mathematical model for the calculation of venoarterial blood CO2 concentration difference (v-aDCO2). This is calculated as the sum of the increment in CO2 concentration (CCO2) related to the increase in CO2 tension (delta P) from arterial to venous value at constant O2 saturation (delta CCO2/delta P) and of the increment in CO2 concentration related to the decrease in O2 saturation (delta S) from arterial to venous value at constant CO2 tension (delta CCO2/delta S). The newly developed relationships correlated well with the experimental data from which they were derived (r2 = 0.94-0.99). The results provided by the model compared remarkably well with the results of previously published measurements (r2 = 0.96-0.99). This new model allows one to overcome some of the limitations implicit in previously available methods and provides a useful tool for the assessment and monitoring of hemodynamic, metabolic, and O2-CO2 exchange patterns in whole body and regional vascular beds.

Death after portal decompressive surgery. Physiologic state, metabolic adequacy, and the sequence of development of the physiologic determinants of survival.

Detailed serial cardiovascular and respiratory physiologic studies were carried out in 80 patients with cirrhotic liver disease, including 45 cirrhotic patients who underwent portal decompressive surgery on an urgent or elective basis. In surgical cases, death could be predicted from the first postoperative day's pattern of response. Predictors of death were an increase in percent of pulmonary shunt due to a redistribution of the increased pulmonary blood flow, and a disproportionate fall in vascular tone, which permits an increased cardiac ejection fraction even when significant myocardial depression occurs. The etiology of the vascular tone defect seems related to the rise in levels of the false neurotransmitter octopamine, which are shown to increase as oxygen consumption falls in the patho-physiologic hyperdynamic B state, presumably due to a block in the oxidative metabolism of aromatic amino acids.

Pathologic synergy in cardiovascular and respiratory compensation with cirrhosis and sepsis. A manifestation of a common metabolic defect?

Multivariable physiologic studies of cardiovascular, respiratory, and metabolic functions were performed in 341 patients (884 studies). Eighty patients had cirrhotic liver disease, 64 had sepsis, 87 had nonseptic cariogenic syndromes, and 110 had nonseptic general surgical or traumatic injury. The group with cirrhosis had the highest cardiac index and ejection fraction. When compared with the group with nonseptic surgery or trauma, vascular tone was reduced in the patients with cirrhosis or sepsis and was lowest in patients with both conditions. Ventricular function was good in the groups with cirrhosis or sepsis, due to the additive effect in reducing vascular tone that allowed ejection fraction to increase, but caused the ratio of alveolar ventilation to perfusion (VA/QT) to fall, resulting in a greater perfusion of a decreased pulmonary vascular bed. The falls in vascular tone and VA/QT in patients with cirrhosis or sepsis result from the reduced oxygen consumption that occurs due to metabolic imbalance (B state). This B state seems to reflect a hepatic inability to metabolize aromatic amino acids, so that levels of tyrosine, phenylalanine, and the false neurotransmitter octopamine increase. These mechanisms are pathologically synergistic when sepsis and cirrhosis occur together.

Liver resections with or without pedicle clamping.

BACKGROUND: Decreasing operative bleeding during liver resection, and thus extent of transfusions, has become a main criterion to evaluate operative results of hepatectomies. Hepatic pedicle clamping (HPC) is widely used for this purpose. The aim of the study was to evaluate safety, efficacy, technique, and contraindications of HPC during liver resections, comparing results of resections performed with or without HPC. METHODS: Data from 245 liver resections were analyzed. In all, 125 resections were performed with HPC (group A), continuous in 100 cases and intermittent in 25 cases. The average duration of ischemia in group A was 39 +/- 20 minutes (range 7 to 107). In 20 cases (16%) ischemia was prolonged for 60 minutes or more. A total of 120 resections were performed without HPC (group B). Major resections were 53.6% in group A (67 cases) and 38.3% in group B (46 cases). Cirrhosis was present in 36 cases, 19 in group A and 17 in group B. RESULTS: Operative mortality was nil. Postoperative mortality was 2.9%, morbidity 22.4%. Percentage of transfused cases (34.4% versus 60.0%; P <0.001) and number of blood units per transfused case (2 +/- 1 versus 4 +/- 3; P <0.001) were lower in group A versus group B. Similar figures were found by considering only major resections. Postoperative blood chemistries did not show important differences between the two groups, and postoperative alterations were related more to extent and complexity of the operation than to length of HPC. CONCLUSIONS: HPC during liver resection is a safe and effective technique. This is demonstrated in a context where HPC is used continuously in most cases, intermittently in cases with impaired liver function and for more prolonged ischemia, and avoided in cases with limited bleeding, jaundice, and simultaneous bowel anastomoses.

Substrate supply as determinant of O2 extraction in sepsis and nonseptic trauma.

Metabolic and hemodynamic measurements performed in 72 septic (S) and 40 nonseptic (NS) surgical patients undergoing total parenteral nutrition were analyzed to assess the role of substrate supply as a determinant of O2 extraction (O2Ex). In S, O2Ex was inversely related to cardiac index (CI); at any given CI, significant increases in O2Ex with simultaneous increases in O2 consumption (VO2) were related to increasing doses of amino acids, with a less remarkable effect of fat and no effect of glucose dose. In NS, O2Ex was also inversely related to CI; however, at any given CI, there was no evident substrate-supply dependency of O2Ex, which was more normally related to P50. The increase in VO2 per gram of administered amino acids, at any CI and O2 transport index, was 817 ml in S and 267 ml in NS. These results suggest that the impaired O2Ex and VO2 in S may at least partly reflect abnormalities in substrate utilization and that amino acid support may have a role in modulating these abnormal O2Ex patterns by providing preferential substrate for oxidative metabolism.

Impact of fat and glucose administration on metabolic and respiratory interactions in sepsis.

Metabolic and respiratory interactions were analyzed in a large group of septic patients (S) and in a reference group of nonseptics (NS) during the iv administration of glucose and fat. In spite of a moderate increase in CO2 production (VCO2) observed during the administration of fat in S, a VCO2-sparing effect of fat, with respect to equicaloric amounts of glucose, was reconfirmed. The relevance of the therapeutic modulation of CO2 production during parenteral nutrition, and the relative impact on the abnormal septic respiratory patterns, were emphasized by analyzing the physiological relationships and mechanisms responsible for the increase in respiratory work in sepsis.

Respiratory quotient and patterns of substrate utilization in human sepsis and trauma.

Three hundred measurements of indirect calorimetric and hemodynamic variables were performed in 99 critically ill septic and nonseptic surgical patients. Septics manifested, with respect to nonseptics, higher O2 consumption, metabolic rate and cardiac index, and lower respiratory quotient in the presence of higher glucose infusion rates and glucose infusion rate/metabolic rate ratios. Among septics there was a group of more severely ill patients with signs of multiple organ failure who manifested a dissociated pattern characterized by a tendency to decreased O2 consumption in the presence of increasing cardiac index and central venous O2 partial pressure: they had higher respiratory quotients, with respect to the other septics, for a given glucose infusion rate/metabolic rate ratio. The lower mean respiratory quotient of septics indicates that they depend generally more than nonseptic trauma patients on fat as an energy substrate and confirms a previously obtained evidence of limited hepatic lipogenesis in sepsis. At the same time, however, it is suggested that fat utilization becomes impaired (and hepatic lipogenesis becomes prominent) in sepsis at a stage in which signs of impaired oxidative metabolism and major metabolic abnormalities also develop.