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Albumin has a number of important physiologic functions, which include maintaining oncotic pressure, transporting various agents (fatty acids, bile acids, cholesterol, metal ions, and drugs), scavenging free oxygen radicals, acting as an antioxidant, and exerting an antiplatelet effect. Hypoalbuminemia in adults, defined by an intravascular albumin level of <3.5 g/dL, is associated with poor postoperative outcomes in patients undergoing surgical intervention. Although the relationship of hypoalbuminemia and poor surgical outcome has been known for many years, the pathophysiology behind the relationship is unclear. Three theoretical constructs might explain this relationship. First, albumin might serve as a nutritional marker, such that hypoalbuminemia represents poor nutritional status in patients who go on to experience poor postoperative outcomes. Second, albumin has its own pharmacologic characteristics as an antioxidant or transporter, and therefore, the lack of albumin might result in a deficiency of those functions, resulting in poor postoperative outcomes. Or third, albumin is known to be a negative acute phase protein, and as such hypoalbuminemia might represent an increased inflammatory status of the patient, potentially leading to poor outcomes. A thorough review of the literature reveals the fallacy of these arguments and fails to show a direct cause and effect between low albumin levels per se and adverse outcomes. Interventions designed solely to correct preoperative hypoalbuminemia, in particular intravenous albumin infusion, do little to change the patient's course of hospitalization. While surgeons may use albumin levels on admission for their prognostic value, they should avoid therapeutic strategies whose main endpoint is correction of this abnormality.

Personalization of ICU nutrition is essential to future of critical care. Recommendations from American/European guidelines and practice suggestions incorporating recent literature are presented. Low-dose enteral nutrition (EN) or parenteral nutrition (PN) can be started within 48 h of admission. While EN is preferred route of delivery, new data highlight PN can be given safely without increased risk; thus, when early EN is not feasible, provision of isocaloric PN is effective and results in similar outcomes. Indirect calorimetry (IC) measurement of energy expenditure (EE) is recommended by both European/American guidelines after stabilization post-ICU admission. Below-measured EE (~ 70%) targets should be used during early phase and increased to match EE later in stay. Low-dose protein delivery can be used early (~ D1-2) (< 0.8 g/kg/d) and progressed to ≥ 1.2 g/kg/d as patients stabilize, with consideration of avoiding higher protein in unstable patients and in acute kidney injury not on CRRT. Intermittent-feeding schedules hold promise for further research. Clinicians must be aware of delivered energy/protein and what percentage of targets delivered nutrition represents. Computerized nutrition monitoring systems/platforms have become widely available. In patients at risk of micronutrient/vitamin losses (i.e., CRRT), evaluation of micronutrient levels should be considered post-ICU days 5–7 with repletion of deficiencies where indicated. In future, we hope use of muscle monitors such as ultrasound, CT scan, and/or BIA will be utilized to assess nutrition risk and monitor response to nutrition. Use of specialized anabolic nutrients such as HMB, creatine, and leucine to improve strength/muscle mass is promising in other populations and deserves future study. In post-ICU setting, continued use of IC measurement and other muscle measures should be considered to guide nutrition. Research on using rehabilitation interventions such as cardiopulmonary exercise testing (CPET) to guide post-ICU exercise/rehabilitation prescription and using anabolic agents such as testosterone/oxandrolone to promote post-ICU recovery is needed.

Strategies for providing optimal nutritional therapy have evolved over time, with the emphasis on specific directives (such as route, use of immunonutrition, high protein, organ-specific formulas, etc.), achieving variable degrees of success for improving outcomes in the intensive care unit. As the largest immune organ in the body comprising the largest interface between the host and the external environment, the gut can have an amplifying effect on a pattern of dysbiosis, immune dysregulation, and multiple organ failure seen in the critically ill patient. Conversely, maintenance of gut integrity can serve to restore a pattern of homeostasis, appropriate immune responses, symbiosis, and clinical recovery. Simply providing refined polymeric formulas as enteral nutrition may not take full advantage of the potential for optimal outcome that could be derived by giving therapy designed to directly stimulate gut defenses and support the intestinal microbiota. This article describes a series of strategies (such as use of intact whole food formulas, soluble fiber, fecal microbial transplantation, serum bovine immunoglobulin, or agents to promote commensal behavior) that should modulate the gut microbiome and shift the critically ill patient toward a pattern of health and recovery. •While providing early enteral nutrition is an appropriate first strategy, this form of nutritional therapy by itself may be suboptimal in supporting gut defenses and the microbiome.•Provision of fermentable fiber (with its production of butyrate) and probiotic organisms help maintain the growth of commensal bacteria in the gut.•Critical illness promotes increases in gut permeability, immune dysregulation, and emergence of a virulent pathobiome.•The process of quorum sensing and virulent phenotypic expression by gut pathogens is a reversible phenomenon, depending on changes in the luminal environment.•A number of clinical nutritional strategies in the ICU are described which may help refaunate the gut with commensal organisms, restore appropriate immune responses, and re-establish gut integrity.

We investigated whether early enteral nutrition alone may be sufficient prophylaxis against stress-related gastrointestinal (GI) bleeding in mechanically ventilated patients. Prospective, double blind, randomized, placebo-controlled, exploratory study that included mechanically ventilated patients in medical ICUs of two academic hospitals. Intravenous pantoprazole and early enteral nutrition were compared to placebo and early enteral nutrition as stress-ulcer prophylaxis. The incidences of clinically significant and overt GI bleeding were compared in the two groups. 124 patients were enrolled in the study. After exclusion of 22 patients, 102 patients were included in analysis: 55 patients in the treatment group and 47 patients in the placebo group. Two patients (one from each group) showed signs of overt GI bleeding (overall incidence 1.96%), and both patients experienced a drop of >3 points in hematocrit in a 24-hour period indicating a clinically significant GI bleed. There was no statistical significant difference in the incidence of overt or significant GI bleeding between groups (p=0.99). We found no benefit when pantoprazole is added to early enteral nutrition in mechanically ventilated critically ill patients. The routine prescription of acid-suppressive therapy in critically ill patients who tolerate early enteral nutrition warrants further evaluation. •GI bleeding has low incidence in the critically ill mechanically ventilated patients.•Adding PPI to enteral nutrition may not offer an added prophylaxis against stress-related GI bleeding.•Our study supports the protective role of enteral nutrition in ICU.

Background: Failure to use the gastrointestinal (GI) tract in patients with acute pancreatitis may exacerbate the stress response and disease severity, leading to greater incidence of complications and prolonged hospitalization. The objectives of this study were to determine the optimum route for nutrition support, whether nutrition therapy is better than no artificial nutrition support, whether specific additives to enteral or parenteral therapy can further enhance their efficacy, and whether methodologic differences in delivery of enteral nutrition (EN) influence tolerance. Methods: A computerized search was performed of MEDLINE, Cochrane database, EMBASE, and reference lists of pertinent review articles for prospective randomized trials in adult patients with acute pancreatitis that evaluated interventions with nutrition therapy. Primary outcome data and surrogate endpoint parameters (for nutrition indices, stress markers, and measures of the inflammatory/immune response) were extracted in duplicate independently. Where appropriate, meta-analysis was performed by random-effects model. Results: From 119 articles screened, 27 randomized controlled trials were included and analyzed. In patients admitted for acute pancreatitis, meta-analysis of 7 trials showed that use of EN was associated with a significant reduction in infectious morbidity (risk ratio [RR] = 0.46; 95% confidence interval [CI], 0.29 – 0.74; p = .001) and hospital length of stay (LOS; weighted mean difference [WMD] =– 3.94; 95% CI, –5.86 to –2.02; p < .0001), a trend toward reduced organ failure (RR = 0.59; 95% CI, 0.28–1.27; p = .18), with no effect on mortality (RR = 0.88; 95% CI, 0.43–1.79; p = .72) when compared with use of parenteral nutrition (PN). Results from individual studies suggest that EN in comparison to PN reduces oxidative stress, hastens resolution of the disease process, and costs less. Insufficient data exist to determine whether EN improves outcome over standard therapy (no artificial nutrition support) in patients admitted for acute pancreatitis. However, in those patients requiring surgery for complications of acute pancreatitis, meta-analysis of 2 trials indicates that provision of EN postoperatively may reduce mortality (RR = 0.26; 95% CI, 0.06– 1.09; p = .06) compared with standard therapy. PN provided early within 24 hours of admission was shown to worsen outcome, whereas PN provided later after full-volume resuscitation appeared to improve outcome when compared with standard therapy. In early individual studies, specific supplements added to EN, such as arginine, glutamine, ω-3 polyunsaturated fatty acids, and probiotics, may be associated with a positive impact on patient outcome in acute pancreatitis, compared with EN alone without the supplements, but studies are too few to make strong treatment recommendations. Supplementation of PN with parenteral glutamine was shown to reduce oxidative stress and improve patient outcome (reduced duration of nutrition therapy and decreased hospital LOS) compared with PN alone in patients with acute pancreatis. A wide range of tolerance to EN exists, irrespective of known influences such as mode (continuous vs bolus) and level of infusion within the GI tract (gastric vs postpyloric). Conclusions: Patients with acute severe pancreatitis should begin EN early because such therapy modulates the stress response, promotes more rapid resolution of the disease process, and results in better outcome. In this sense, EN is the preferred route and has eclipsed PN as the new “gold standard” of nutrition therapy. When PN is used, it should be initiated after 5 days. The favorable effect of both EN and PN on patient outcome may be further enhanced by supplementation with modulators of inflammation and systemic immunity. Individual variability allows for a wide range of tolerance to EN, even in severe pancreatitis. The route, timing, and content of nutrition support affect its efficacy and impact on outcome in patients with acute pancreatitis. Although enteral nutrition is the preferred route, standard therapy (no nutrition support) may be preferred over parenteral nutrition in certain circumstances. Specific strategies may be used to enhance tolerance to enteral feeding.

With the number of individuals older than 65 years expected to rise significantly over the next few decades, dramatic changes to our society and health care system will need to take place to meet their needs. Age-related changes in muscle mass and body composition along with medical comorbidities including stroke, dementia, and depression place elderly adults at high risk for developing malnutrition and frailty. This loss of function and decline in muscle mass (ie, sarcopenia) can be associated with reduced mobility and ability to perform the task of daily living, placing the elderly at an increased risk for falls, fractures, and subsequent institutionalization, leading to a decline in the quality of life and increased mortality. There are a number of modifiable factors that can mitigate some of the muscle loss elderly experience especially when hospitalized. Due to this, it is paramount for providers to understand the pathophysiology behind malnutrition and sarcopenia, be able to assess risk factors for malnutrition, and provide appropriate nutrition support. The present review describes the pathophysiology of malnutrition, identifies contributing factors to this condition, discusses tools to assess nutritional status, and proposes key strategies for optimizing enteral nutrition therapy for the elderly.

The value of nutrition therapy for the adult hospitalized patient is derived from the outcome benefits achieved by the delivery of early enteral feeding. Nutritional assessment should identify those patients at high nutritional risk, determined by both disease severity and nutritional status. For such patients if they are unable to maintain volitional intake, enteral access should be attained and enteral nutrition (EN) initiated within 24-48 h of admission. Orogastric or nasogastric feeding is most appropriate when starting EN, switching to post-pyloric or deep jejunal feeding only in those patients who are intolerant of gastric feeds or at high risk for aspiration. Percutaneous access should be used for those patients anticipated to require EN for >4 weeks. Patients receiving EN should be monitored for risk of aspiration, tolerance, and adequacy of feeding (determined by percent of goal calories and protein delivered). Intentional permissive underfeeding (and even trophic feeding) is appropriate temporarily for certain subsets of hospitalized patients. Although a standard polymeric formula should be used routinely in most patients, an immune-modulating formula (with arginine and fish oil) should be reserved for patients who have had major surgery in a surgical ICU setting. Adequacy of nutrition therapy is enhanced by establishing nurse-driven enteral feeding protocols, increasing delivery by volume-based or top-down feeding strategies, minimizing interruptions, and eliminating the practice of gastric residual volumes. Parenteral nutrition should be used in patients at high nutritional risk when EN is not feasible or after the first week of hospitalization if EN is not sufficient. Because of their knowledge base and skill set, the gastroenterologist endoscopist is an asset to the Nutrition Support Team and should participate in providing optimal nutrition therapy to the hospitalized adult patient.

To the Editor: Cederholm and Bosaeus (July 11 issue) 1 propose three causal subtypes of malnutrition: disease-related with and without underlying inflammation and “starvation due to inadequate access to food (i.e., food insecurity).” In the Summary, they write that treatment consists of dietary interventions such as “individualized nutritional counseling combined with energy- and protein-fortified oral nutritional supplements. Interventions may still not reverse the condition because of the inflammatory nature of the underlying disease.” Could a cleaner definition of malnutrition be “a condition for which there is good evidence that this patient will benefit from modification of nutrient intake”? Nutrition support may . . .