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Background: The creatinine height index (CHI) is an estimate of lean body mass. We hypothesize that a modified CHI estimate using serum creatinine (sCr) levels in patients with normal renal function when performed soon after injury would reflect preinjury protein nutrition status., Methods: The urine CHI (uCHI) was calculated using the 24-h urine sample. The serum-derived estimated CHI (sCHI) was calculated using the sCr on admission. Correlation between abdominal computed tomography images at specific lumbar vertebral levels and total body fat and muscle content was used for comparison as an independent measurement of nutrition status unlikely to be substantially altered by trauma., Results: A total of 45 patients were enrolled, all with a significant injury burden (median injury severity score [ISS] = 25; interquartile range, 17-35). The calculated sCHI on admission was 71.0% (SD = 26.9%) and likely underestimates the CHI when compared with uCHI (mean = 112.5%, SD = 32.6%). Stratifying by degree of stress demonstrated that in a group of 23 moderately and severely stressed patients, uCHI (mean = 112.7%, SD = 5.7%) and sCHI (mean = 60.8%, SD = 1.9%) were significantly different and without correlation (r = -0.26, P = 0.91). In patients without stress, there was a significant negative correlation between sCHI and psoas muscle area (r = -0.869, P = 0.03), and in patients with severe stress there was a significant positive correlation between uCHI and psoas muscle area (r = 0.733, P = 0.016)., Conclusion: The CHI calculated from the initial sCr is not an appropriate estimate of uCHI in critically ill trauma patients and is not a valid measure of psoas muscle mass in this setting., (© 2023 American Society for Parenteral and Enteral Nutrition.)

It is now generally accepted that early feeding post injury exerts a positive effect on outcome in the critically ill, despite the fact that many of these patients are well nourished or even overnourished on admission. One possible mechanism is that early feeding post injury may have a positive influence on the duration and intensity of the systemic inflammatory response, especially when coupled with intensive insulin therapy to maintain normoglycemia at <150 mg/dL. Current clinical nutrition guidelines recommend early enteral nutrition providing full nutrition requirements in the critically ill patient; however, in the first week post injury, exclusive enteral feeding is typically inadequate, particularly in protein. A potentially new and different therapeutic goal to modulate the systemic inflammatory response might be more effectively accomplished for the first week post injury by hypocaloric feedings (~9-18 kcal/kg or 50%-75% resting metabolic expenditure) principally as intravenous dextrose but with at least 1 g/kg protein as intravenous amino acids to provide early metabolic support. This proposed regime, along with intensive insulin therapy to maintain glucose homeostasis, should promote the protein synthetic component of the postinjury inflammatory response while reducing net protein catabolism. A formal trial of early metabolic support in the acutely injured should be safe, easy to execute, and potentially efficacious, with subsequent improvement in the inflammatory state and, it is hoped, clinical outcomes.

Background: Certain patients receiving home total parenteral nutrition (HPN) are likely to develop iron-deficiency anemia because of inadequate absorption or chronic iron loss from gastrointestinal lesions. The objective of this study was to examine the incidence and prevalence of iron deficiency anemia in patients on long-term HPN (>6 months) and to investigate both the efficacy of and rate of adverse reactions to parenteral iron dextran therapy., Methods: The records of 55 patients treated with HPN for >6 months between January 1, 1994 and December 31, 1999 were examined., Results: Thirty patients (55%) had evidence of iron-deficiency anemia. Ten patients were diagnosed at the initiation of HPN, and in 20 patients, iron deficiency developed after receiving HPN. The time between initiation of HPN and development of anemia ranged from 2 to 97 months (mean 28.8+/-26.2 months). Mild iron loss from the gastrointestinal tract seemed to be the predominant reason for iron deficiency. Regular treatment with small amounts of iron in HPN appeared to be safe and efficacious, with no reported side effects. Total dose infusion of iron was associated with adverse reactions in as many as 25% of these patients, although all reactions were mild and self-limited., Conclusions: Iron-deficiency anemia is common in patients receiving chronic HPN. Regular small doses of iron in HPN formula, rather than total dose infusion, is the preferred treatment.

Background: End stage liver disease (ESLD) is a devastating illness. Its protean manifestations involve many different aspects of disturbed hepatic function. One consequence of ESLD is a decrease in plasma levels of very long chain polyunsaturated fatty acids (VL-PUFAs), particularly arachidonic acid (AA) and docosahexaenoic acid (DHA), the former important for eicosanoid metabolism and the latter for retinal and brain membrane structure. The purpose of this study was to define the VL-PUFA changes in liver disease by comparing plasma and tissue levels of VL-PUFAs in controls to patients with ESLD., Methods: Fatty acid profiles from plasma, red blood cell (RBC) membranes, muscle, liver, and fat tissue from ESLD patients undergoing liver transplants were measured and compared with control patients undergoing elective liver resection., Results: Fatty acid profiles from plasma and RBC membranes showed significant decreases in AA and DHA levels in patients with ESLD compared with controls. However, there were no significant differences in tissue fatty acid composition between ESLD patients and controls., Conclusions: ESLD affects the liver's ability to maintain circulating levels of AA and DHA, and thereby presumably RBC membrane levels. However, solid tissues appear not to be affected by ESLD. Although the mechanism for these changes remains to be defined, it is consistent with hepatic impairment of elongation and desaturation to produce VL-PUFA for transport. The present results also suggest that dietary interventions to include preformed VL-PUFA rather than their precursors, linoleic and alpha linolenic acid, would be needed to normalize plasma VL-PUFA levels in patients with ESLD.