Residency · Residency · Critical Care

ICU Nutrition: Enteral and Parenteral

Metabolic Response to Critical Illness

Phases of Metabolic Stress

The metabolic response to critical illness unfolds in a predictable sequence of phases that fundamentally alters substrate utilization and energy expenditure. The initial ebb phase, spanning roughly the first 24 hours after the onset of critical illness, is characterized by a decrease in metabolic rate that occurs in concert with hemodynamic instability and reduced oxygen consumption. During this period, the body prioritizes circulatory stabilization over metabolic demands, and aggressive nutritional support is neither physiologically appropriate nor well-tolerated.

The flow phase begins at approximately 24 to 72 hours and can persist for weeks in patients with ongoing critical illness. This phase represents a hypermetabolic, catabolic state in which resting energy expenditure increases to 120 to 150 percent of predicted values. The profound catabolism that characterizes this phase is driven by counter-regulatory hormones including cortisol, glucagon, and catecholamines, as well as by inflammatory cytokines. The clinical consequence is devastating: patients lose 1 to 2 percent of their skeletal muscle mass per day in the ICU, and the diaphragm is affected within as few as 18 hours of mechanical ventilation. This accelerated proteolysis serves to provide amino acid substrates for hepatic acute-phase protein synthesis, gluconeogenesis, and immune cell proliferation, but the cost to the patient's functional reserve is enormous.

The anabolic recovery phase marks the transition from catabolism to the rebuilding of lean body mass. This process may take months and is highly dependent on adequate nutritional support, rehabilitation, and resolution of the underlying illness. Many ICU survivors never fully recover their pre-illness lean body mass, contributing to the long-term disability that characterizes post-intensive care syndrome.

Metabolic Derangements

Critical illness produces a constellation of metabolic derangements that directly impact nutritional planning and management. Stress hyperglycemia is nearly ubiquitous, arising from insulin resistance at the peripheral tissue level combined with accelerated hepatic gluconeogenesis driven by cortisol and catecholamine release. This hyperglycemia is not merely a marker of disease severity but actively contributes to impaired immune function, endothelial dysfunction, and increased susceptibility to infection.

Protein catabolism in the critically ill patient produces a profoundly negative nitrogen balance, with daily losses of 20 to 30 grams of nitrogen, equivalent to the destruction of 600 to 900 grams of lean tissue per day. This rate of protein breakdown far exceeds what can be fully offset by exogenous protein supplementation, though adequate protein delivery can significantly attenuate the deficit. Lipolysis is accelerated, with enhanced fat oxidation occurring throughout critical illness, though paradoxically, fat utilization is impaired during sepsis, leading to hypertriglyceridemia and hepatic steatosis when lipid-based calories are provided in excess.

Micronutrient depletion occurs rapidly in critical illness, with thiamine, vitamin C, selenium, zinc, and vitamin D being particularly vulnerable to rapid depletion. These micronutrients serve as essential cofactors for immune function, antioxidant defense, and metabolic enzyme activity, and their deficiency may contribute to organ dysfunction and impaired recovery. The role of autophagy, the cellular recycling mechanism that removes damaged organelles and proteins, has received increasing attention. There is an ongoing debate regarding whether early aggressive nutrition may inhibit beneficial autophagy during acute critical illness, providing a potential mechanistic rationale for the observed safety of trophic feeding in the early phase.

Energy Expenditure Assessment

Accurate determination of energy expenditure is essential for appropriate nutritional prescription, yet it remains one of the most challenging aspects of ICU nutrition. Indirect calorimetry is the gold standard for measuring resting energy expenditure and works by measuring oxygen consumption (VO2) and carbon dioxide production (VCO2) at the bedside. The Weir equation, REE = [(3.94 x VO2) + (1.11 x VCO2)] x 1440, converts these gas exchange measurements into kilocalories per day. The respiratory quotient, calculated as the ratio of VCO2 to VO2, provides valuable information about substrate utilization. A normal RQ of 0.8 to 1.0 indicates mixed substrate oxidation, an RQ exceeding 1.0 suggests lipogenesis from carbohydrate overfeeding, and an RQ below 0.7 indicates predominant fat oxidation or ketosis from underfeeding.

Predictive equations such as the Harris-Benedict, Penn State, and Mifflin-St Jeor formulas attempt to estimate energy expenditure from patient demographics and clinical variables, but they are inaccurate in 40 to 60 percent of ICU patients. This inaccuracy stems from the profound and unpredictable alterations in metabolic rate that critical illness produces. The ASPEN and SCCM guidelines recommend the use of indirect calorimetry when available, and when it is not, suggest using weight-based estimations of 25 to 30 kcal/kg/day for non-obese patients as an imperfect but practical alternative.

Enteral Nutrition (EN)

Benefits and Evidence

Enteral nutrition is the preferred route of nutrient delivery in the critically ill patient for reasons that extend well beyond simple caloric provision. The gut serves as the body's largest immune organ, and enteral feeding maintains gut mucosal integrity and barrier function. By delivering nutrients directly to the intestinal epithelium, enteral feeding preserves the gut-associated lymphoid tissue (GALT), which plays a central role in modulating systemic immune responses. The theoretical reduction in bacterial translocation from the gut lumen to the systemic circulation has been a longstanding rationale for enteral nutrition, though direct human evidence for this mechanism remains limited.

Clinical trials have generally supported early enteral nutrition, with earlier initiation associated with reduced infectious complications and possibly improved mortality. However, the comparison between enteral and parenteral nutrition has been more nuanced than initially believed. The CALORIES trial (2014) compared enteral to parenteral nutrition in ICU patients and found no difference in 30-day mortality, though enteral nutrition was associated with more hypoglycemia and parenteral nutrition with more vomiting. The NUTRIREA-2 trial (2018) specifically examined patients in shock and again found no mortality difference between routes, but importantly demonstrated that enteral nutrition during shock was associated with significantly more gastrointestinal complications, including vomiting, bowel ischemia, and acute colonic pseudo-obstruction. These findings underscore the importance of hemodynamic stability before initiating enteral feeds.

Timing of Initiation

Current evidence supports early enteral nutrition, defined as initiation within 24 to 48 hours of ICU admission, in hemodynamically stable patients who cannot maintain volitional oral intake. The ASPEN/SCCM 2022 guidelines suggest initiating enteral nutrition within 24 to 36 hours in this population. Importantly, early initiation does not imply full-calorie delivery from the outset. Early trophic or hypocaloric feeding at rates of 10 to 20 mL/hr, providing approximately 500 kcal/day, is recommended for the first 48 to 72 hours.

The rationale for trophic feeding was validated by the EDEN trial (2012), which randomized patients with acute lung injury to trophic feeding (approximately 25 percent of caloric goal) versus full enteral feeding for the first six days of mechanical ventilation. The trial found no difference in ventilator-free days, infectious complications, or 60-day mortality between groups, establishing that aggressive early caloric delivery provides no advantage over a more conservative trophic approach. Following the initial trophic period, feeds should be advanced to reach 80 percent of the caloric target by days 3 to 7, with care taken to avoid aggressive early full feeding that may suppress beneficial autophagy and worsen metabolic derangements.

Contraindications to EN

Absolute contraindications to enteral nutrition include mechanical bowel obstruction, high-output intestinal fistula without distal access for feeding, bowel ischemia or infarction, and active gastrointestinal hemorrhage requiring endoscopic or surgical intervention. These conditions represent situations in which luminal nutrient delivery is either physically impossible or poses unacceptable risk of harm.

Relative contraindications require careful clinical judgment. High vasopressor requirements, defined in the NUTRIREA-2 trial as norepinephrine doses exceeding 0.14 mcg/kg/min, are associated with increased risk of bowel ischemia during enteral feeding. Paralytic ileus with persistently high gastric residual volumes and recent bowel anastomoses, where surgeon preference often dictates the timing of enteral feeding, represent additional relative contraindications. Regarding hemodynamic instability, the current consensus is that enteral nutrition should be initiated once patients are being actively resuscitated and mean arterial pressure is stable on vasopressor support, but feeding should be avoided during periods of active titration or hemodynamic deterioration.

Caloric and Protein Targets

Caloric targets for the critically ill patient should be calculated using ideal body weight for non-obese patients, with a goal of 25 to 30 kcal/kg/day. For obese patients with a BMI exceeding 30, a hypocaloric strategy using 11 to 14 kcal/kg of actual body weight or 22 to 25 kcal/kg of ideal body weight is recommended. Overfeeding must be assiduously avoided, as it is associated with hyperglycemia, hepatic steatosis, increased carbon dioxide production that can complicate ventilator weaning, and lipogenesis.

Protein delivery has emerged as arguably the most important macronutrient target in critical illness, receiving even greater emphasis than total caloric delivery. The ASPEN/SCCM 2022 guidelines recommend 1.2 to 2.0 g/kg/day of protein, with the higher end of this range (2.0 g/kg/day) reserved for patients with burns, major trauma, and surgical critical illness, and the lower end (1.2 g/kg/day) appropriate for medical ICU patients and those with hepatic encephalopathy. Despite these clear recommendations, protein delivery remains consistently inadequate in clinical practice, with the average ICU patient receiving less than 60 percent of their protein target. Nitrogen balance, calculated as (protein intake/6.25) minus (urinary urea nitrogen + 4), should be monitored with the goal of achieving positive nitrogen balance.

Formulations

A wide range of enteral formulations is available for the critically ill patient, each designed to address specific clinical needs. Standard polymeric formulas provide 1.0 to 1.5 kcal/mL and contain intact proteins, complex carbohydrates, and long-chain triglycerides, making them appropriate for the majority of ICU patients with normal digestive and absorptive capacity. High-protein formulas are enriched with additional protein to meet the elevated requirements of catabolic states.

Semi-elemental or peptide-based formulas contain partially hydrolyzed proteins that require less digestive processing and may be better tolerated in patients with malabsorption, short bowel syndrome, or pancreatic insufficiency. Renal formulas are concentrated at 2 kcal/mL to minimize fluid delivery and contain reduced potassium and phosphate, though protein should be less restricted in patients receiving continuous renal replacement therapy given the significant amino acid losses in the effluent. Diabetic formulas utilize a lower glycemic index with higher fat content and may reduce insulin requirements. Fiber-containing formulas can help regulate bowel function but should be avoided in hemodynamically unstable patients due to the risk of bowel ischemia with fiber. Immunonutrition formulations containing arginine, glutamine, and omega-3 fatty acids are not recommended for routine use in critically ill patients, as the evidence for benefit has been inconsistent and some studies have suggested potential harm.

<image>Enteral nutrition decision algorithm for ICU patients. Starting point: "ICU admission — nutritional assessment within 24-48 hours." First decision: "Can patient eat?" Yes → oral diet with monitoring. No → "Is there a contraindication to EN?" (list contraindications). If contraindicated → parenteral nutrition. If EN appropriate → "Is patient hemodynamically stable?" (MAP stable on vasopressors, lactate trending down). If unstable → hold EN, reassess q6h. If stable → initiate trophic EN (10-20 mL/hr) within 24-48 hours. Advance to goal rate by day 3-5. Monitoring pathway: check gastric residual volumes (hold if >500 mL), assess for intolerance (vomiting, abdominal distension, diarrhea). If intolerant → prokinetics (metoclopramide, erythromycin), consider post-pyloric tube, switch to peptide-based formula. If still intolerant after 5-7 days → supplemental or total PN. Include caloric and protein targets at each step with IBW-based calculations.</image>

Enteral Nutrition Management

Gastric vs. Post-Pyloric Feeding

Gastric feeding via nasogastric or orogastric tube is the standard first-line approach for enteral nutrition in the ICU due to its ease of placement and accessibility. Tube position can be confirmed by pH testing of aspirates or radiographic verification. Post-pyloric feeding via nasojejunal tube is reserved for patients who demonstrate intolerance to gastric feeding, including those with persistently high gastric residual volumes, recurrent aspiration, or gastroparesis. The ASPEN guidelines recommend post-pyloric feeding for patients at high risk of aspiration.

Placement of post-pyloric feeding tubes can be achieved through fluoroscopic guidance, endoscopic placement, or electromagnetic-guided systems such as the Cortrak device. Despite theoretical advantages in reducing aspiration risk, meta-analyses have not demonstrated a clear mortality difference between gastric and post-pyloric feeding, suggesting that the choice should be individualized based on clinical tolerance and aspiration risk assessment.

Gastric Residual Volume (GRV) Monitoring

Monitoring of gastric residual volumes has been a traditional practice in ICU enteral nutrition management, with the ASPEN 2016 guidelines establishing a threshold of 500 mL as the level at which enteral feeds should be held. However, the utility of GRV monitoring has been increasingly questioned. The NUTRIREA-3 trial approach and practices at some centers have moved toward eliminating routine GRV monitoring entirely, recognizing that GRV is an imperfect marker of aspiration risk that correlates poorly with actual aspiration events.

When GRV monitoring is employed and volumes exceed 500 mL, the appropriate response is to temporarily hold feeds, consider initiating prokinetic agents, and reassess. It is critically important to recognize that a single elevated GRV should not mandate permanent discontinuation of enteral nutrition, as this leads to unnecessary caloric and protein deficits that worsen patient outcomes.

Prokinetics

Prokinetic agents play an important role in managing gastroparesis and feed intolerance in the ICU. Metoclopramide, a dopamine antagonist, is administered at 10 mg IV every 6 to 8 hours and enhances gastric motility, though it carries risks of tardive dyskinesia with prolonged use and QT prolongation. Erythromycin, given at a low dose of 250 mg IV every 8 hours, acts as a motilin receptor agonist and is often the most effective single prokinetic agent, though its efficacy diminishes due to tachyphylaxis within 3 to 4 days of continuous use. The combination of metoclopramide and erythromycin may provide synergistic benefit when either agent alone is insufficient. Methylnaltrexone, a peripherally acting mu-opioid receptor antagonist that does not cross the blood-brain barrier, is useful specifically for opioid-induced ileus, allowing treatment of the gastrointestinal effects of opioids without reversing centrally mediated analgesia.

Complications of EN

Diarrhea is the most common complication of enteral feeding, affecting 30 to 40 percent of tube-fed ICU patients. The differential diagnosis includes hyperosmolar formula, medications containing sorbitol as an excipient, Clostridioides difficile infection, and malabsorption. Management involves excluding C. difficile infection, reducing formula osmolality, considering the addition of fiber, reviewing medication formulations for osmotic contributors, and transitioning to a peptide-based formula if standard formulations are not tolerated.

Aspiration occurs in 5 to 10 percent of enterally fed patients, though much aspiration is subclinical. Risk reduction strategies include maintaining head of bed elevation at 30 degrees or greater, post-pyloric tube placement in high-risk patients, and avoidance of excessive sedation. Refeeding syndrome is a potentially fatal complication that occurs when nutrition is initiated in patients who have been malnourished or fasting for prolonged periods. The pathophysiology involves rapid intracellular shifts of phosphate, potassium, and magnesium upon refeeding, leading to dangerous depletion of these electrolytes. Patients at highest risk include those with a BMI below 16, weight loss exceeding 15 percent over 3 to 6 months, minimal nutritional intake for more than 10 days, or low baseline electrolyte levels. Prevention requires starting feeding at 10 to 15 kcal/kg/day, advancing slowly over 4 to 7 days, aggressively replacing electrolytes, and administering thiamine 200 to 300 mg IV daily for 3 days before initiating feeding.

Bowel ischemia, though rare at 1 to 2 percent, is a devastating complication with high mortality. The risk is substantially elevated in patients receiving vasopressors, particularly at norepinephrine doses exceeding 0.14 mcg/kg/min, as splanchnic vasoconstriction compromises intestinal blood flow during a period of increased metabolic demand from nutrient absorption.

Parenteral Nutrition (PN)

Indications

Parenteral nutrition is indicated when enteral nutrition is contraindicated or cannot be feasibly delivered for a duration expected to exceed 7 days, as recommended by ASPEN. In patients identified as being at high nutritional risk, defined by a Nutritional Risk Screening score of 5 or greater or a NUTRIC score of 5 or greater, supplemental parenteral nutrition should be considered earlier, at days 3 to 4, if enteral nutrition targets are not being met. Specific conditions mandating parenteral nutrition include short bowel syndrome, high-output fistula, complete bowel obstruction, and severe ileus unresponsive to prokinetic therapy.

Timing

The timing of parenteral nutrition initiation in the ICU has been a subject of considerable investigation. The ASPEN/SCCM 2022 guidelines recommend against initiating parenteral nutrition within the first 7 days if any level of enteral nutrition is tolerable. This recommendation is strongly supported by the EPaNIC trial (2011), which randomized critically ill patients to late parenteral nutrition (initiated on day 8) versus early parenteral nutrition (initiated on day 3). Late initiation was associated with fewer infections, shorter ICU length of stay, and shorter duration of mechanical ventilation, establishing that withholding parenteral nutrition in the first week is not only safe but superior to early supplementation.

The EAT-ICU trial (2017) evaluated an even more aggressive approach using early goal-directed nutrition guided by indirect calorimetry with parenteral supplementation and found no benefit compared to standard care, with more hyperglycemia in the intervention group. The current consensus is clear: low-calorie nutrition is acceptable and likely preferable during the first week of critical illness, and early aggressive parenteral supplementation should be avoided.

Composition

Parenteral nutrition is formulated as a three-in-one admixture containing dextrose, amino acids, and lipid emulsion. Dextrose provides 3.4 kcal/g and is typically delivered at 150 to 250 g/day, with serum glucose monitored to maintain levels below 180 mg/dL. Amino acids are provided at 1.2 to 2.0 g/kg/day protein equivalent, available in standard or branched-chain formulations.

Lipid emulsions deserve particular attention in the ICU setting. Traditional soybean-based emulsions (Intralipid) are available as a 20 percent solution providing 2 kcal/mL but contain high concentrations of omega-6 fatty acids that may promote inflammation. Olive oil-based emulsions (ClinOleic) are less pro-inflammatory than soybean-based products. Fish oil-based emulsions (Omegaven) provide anti-inflammatory omega-3 fatty acids and are particularly valuable in intestinal failure-associated liver disease. Mixed lipid emulsions (SMOF), containing soybean oil, medium-chain triglycerides, olive oil, and fish oil, offer a balanced fatty acid profile and are the preferred formulation in the ICU setting. Regardless of the emulsion used, IV lipid should be limited to 1 g/kg/day and should not exceed 30 percent of total calories.

Electrolytes including sodium, potassium, chloride, calcium, magnesium, and phosphate are added to the parenteral nutrition solution and must be adjusted daily based on serum levels. Standard multivitamin and trace element preparations are added daily. The typical total volume of parenteral nutrition is 1.5 to 2.5 liters per day delivered as a three-in-one admixture.

Monitoring

Monitoring during parenteral nutrition requires attention to both short-term metabolic parameters and longer-term complications. Daily monitoring includes blood glucose (every 4 to 6 hours during insulin infusion adjustment), serum electrolytes, and triglyceride levels, which should be maintained below 400 mg/dL. Weekly monitoring encompasses liver function tests, as parenteral nutrition-associated cholestasis is a common complication, and prealbumin, which has a short half-life of approximately 2 days and therefore reflects recent protein status, though its value is confounded by its behavior as a negative acute-phase reactant that decreases during active inflammation. During the initial 3 to 5 days of parenteral nutrition, daily monitoring of phosphate, potassium, and magnesium is essential to detect and treat refeeding syndrome.

Complications of PN

Parenteral nutrition carries a distinct complication profile that requires vigilant monitoring and prevention. Central line-associated bloodstream infection (CLABSI) is a significant concern, as parenteral nutrition is an independent risk factor for catheter-related infections, necessitating strict adherence to central line care bundles. Hyperglycemia is managed with insulin infusion protocols, and dextrose infusion rates should not exceed 4 to 5 mg/kg/min to minimize this risk.

Hypertriglyceridemia requires monitoring and management, with lipid emulsions held if triglyceride levels exceed 400 mg/dL. Clinicians must also account for the lipid calories provided by propofol infusions, which deliver 1.1 kcal/mL and can contribute substantial unintended caloric load. Parenteral nutrition-associated liver disease, manifesting as cholestasis and steatosis, can be prevented by cycling parenteral nutrition with 10 to 12 hours off per day, limiting dextrose delivery, and transitioning to enteral nutrition as early as possible. Refeeding syndrome carries the same risks as with enteral nutrition and requires identical monitoring and gradual advancement strategies. Finally, the significant volume contribution of parenteral nutrition must be factored into daily fluid balance calculations, as fluid overload is an increasingly recognized contributor to morbidity in critical illness.

<image>Parenteral nutrition composition diagram showing a TPN bag with labeled components and their caloric contributions. Central 3-in-1 admixture bag connected to a central venous catheter via infusion pump. Three input streams into the bag: (1) Dextrose (D70W) with concentration, calories per gram (3.4 kcal/g), and daily dose range; (2) Amino acids (10-15%) with protein equivalent calculation and daily targets; (3) Lipid emulsion (20% SMOF) with caloric density (2 kcal/mL), types of fatty acids, and maximum dose. Side panel showing added components: electrolytes (Na, K, Ca, Mg, PO4 with daily ranges), multivitamins, trace elements (Zn, Cu, Mn, Se, Cr), and insulin. Below: monitoring checklist (glucose, electrolytes, triglycerides, LFTs, prealbumin) with frequency recommendations. Warning boxes for complications: hyperglycemia threshold, hypertriglyceridemia threshold, refeeding syndrome risk criteria.</image>

Special Populations

Obesity

Nutritional management of the obese critically ill patient requires a specific approach that differs substantially from standard practice. A hypocaloric, high-protein strategy is recommended, providing 11 to 14 kcal/kg of actual body weight while delivering protein at 2.0 to 2.5 g/kg of ideal body weight. The rationale is that obese patients have substantial endogenous energy reserves in the form of adipose tissue and do not require exogenous caloric provision at the same rate as normal-weight patients. Excessive caloric delivery in obese patients risks worsening hyperglycemia, hepatic steatosis, and other metabolic complications. For calculation purposes, ideal body weight should be used for protein targets and adjusted body weight, calculated as IBW plus 0.25 times the difference between actual and ideal body weight, should be used for caloric calculations.

Burns

Burn patients represent the population with the highest caloric requirements of any ICU patient cohort. The Curreri formula, which calculates requirements as 25 kcal/kg plus 40 kcal per percent TBSA burned, was historically used but overestimates needs in patients with large burns. The Toronto formula or indirect calorimetry is preferred for accuracy. Protein requirements are markedly elevated at 1.5 to 2.0 g/kg/day, driven by massive protein losses through wound exudate and the intense hypermetabolic response. Enteral nutrition should be initiated within 4 to 6 hours of burn injury, as early feeding has been shown to attenuate the hypermetabolic response. Glutamine supplementation is recommended by ESPEN specifically for burn patients, though its use remains controversial in other critically ill populations.

Renal Failure

Nutritional management in renal failure must balance the need for adequate protein delivery against the metabolic consequences of impaired renal clearance. In patients without renal replacement therapy, protein should be provided at 0.8 to 1.0 g/kg/day, with a critical caveat that protein restriction below 0.8 g/kg/day should be avoided as it worsens catabolism without meaningful clinical benefit. In patients receiving continuous renal replacement therapy, protein requirements increase substantially to 1.5 to 2.5 g/kg/day to account for the significant amino acid losses in the dialysis effluent, which can reach 10 to 15 g/day. Fluid restriction often necessitates the use of concentrated enteral formulas at 2 kcal/mL. Electrolyte management requires formulas with reduced potassium and phosphate content, unless the patient is on continuous renal replacement therapy, which provides ongoing electrolyte clearance.

Hepatic Failure

A critically important paradigm shift in the management of nutrition in hepatic failure has been the recognition that protein restriction is not only unnecessary but actively harmful. Protein should be provided at 1.2 to 1.5 g/kg/day, as restriction worsens sarcopenia and paradoxically exacerbates hepatic encephalopathy by reducing the substrate available for hepatic urea cycle function. Branched-chain amino acid supplementation may provide modest improvement in hepatic encephalopathy, though the evidence remains limited. Patients with hepatic failure benefit from small, frequent feedings to avoid prolonged fasting, as impaired gluconeogenesis predisposes them to hypoglycemia. A late evening snack is specifically recommended to prevent overnight catabolism, which is accelerated in the setting of liver disease.

Key Clinical Pearls

• Early trophic enteral nutrition (10-20 mL/hr) within 24-48 hours is preferred over full caloric delivery in the first week of critical illness
• Protein delivery is consistently more important than caloric delivery — prioritize reaching 1.2-2.0 g/kg/day protein target
• Avoid parenteral nutrition in the first 7 days if any enteral nutrition is tolerated (EPaNIC trial)
• Refeeding syndrome is under-recognized and potentially fatal — screen all malnourished patients and replace thiamine, phosphate, potassium, and magnesium proactively
• Indirect calorimetry is the gold standard for energy expenditure assessment; predictive equations are inaccurate in 40-60% of ICU patients
• GRV monitoring is an imperfect tool — a single elevated GRV should not lead to permanent discontinuation of EN
• Do NOT restrict protein in liver failure patients — this worsens outcomes and hepatic encephalopathy
• Account for propofol lipid calories (1.1 kcal/mL) in the nutritional prescription — at 30 mL/hr, propofol provides ~800 kcal/day

References

1. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: SCCM and ASPEN. JPEN. 2016;40(2):159-211.
2. Casaer MP, Mesotten D, Hermans G, et al. Early versus late parenteral nutrition in critically ill adults. N Engl J Med. 2011;365(6):506-517.
3. Rice TW, Wheeler AP, Thompson BT, et al. Initial trophic vs full enteral feeding in patients with acute lung injury: the EDEN randomized trial. JAMA. 2012;307(8):795-803.
4. Reignier J, Boisrame-Helms J, Brisard L, et al. Enteral versus parenteral early nutrition in ventilated adults with shock: a randomised, controlled, multicentre, open-label, parallel-group study (NUTRIREA-2). Lancet. 2018;391(10116):133-143.
5. Harvey SE, Parrott F, Harrison DA, et al. Trial of the route of early nutritional support in critically ill adults. N Engl J Med. 2014;371(18):1673-1684.

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