Critical illness is associated with a systemic inflammatory response and catabolic state that leads to increased infections, multiorgan dysfunction, prolonged hospitalization, and death. The individual’s adaptive response aims to increase energy provision to vital organs by increasing release of pituitary hormones, increasing sympathetic nervous system stimulation, and increasing peripheral resistance to anabolic hormones. Society of Critical Care Medicine (SCCM) and American Society of Parenteral and Enteral Nutrition (ASPEN)’s approach to nutritional is designed to preserve lean body mass, attenuate stress response, prevent oxidative injury, and modulate immune response.¹ The current nutritional bundle includes (1) assess patients for nutritional risk and calculate energy and protein requirements to determine goals; (2) initiate enteral nutrition (EN) within 24 to 48 hours after the onset of critical illness and admission to the intensive care unit (ICU) and increase to goal within the first week of the ICU stay; (3) reduce the risk of aspiration or improve tolerance to gastric feeding with the use of prokinetic agents, continuous infusion, chlorhexidine mouthwash, elevation of the head of the bed, and diverted level of feeding in the gastrointestinal (GI) tract; (4) implement enteral feeding protocols with institution-specific strategies to promote delivery of enteral nutrition; (5) do not use gastric residual volumes as part of routine care to monitor ICU patients on EN; and (6) start parenteral nutrition (PN) early when EN is not feasible or sufficient in high-risk poorly nourished patients.¹

The patient population in the ICU is heterogeneous, and objective markers such as albumin, prealbumin, transferrin, and retinol binding protein participate in the acute phase response and do not accurately reflect the nutritional status of a critically ill patient.¹ Other markers are still under investigation; these include calcitonin, C-reactive protein, interleukin-1, interleukin-6, citrulline, ultrasound with measurement of muscle mass, and computed tomography.¹ Nutritional risk assessment such as the Nutritional Risk Score (NRS-2002) helps to identify patients who will likely benefit from early enteral therapy because they will reduce nosocomial infection, complications, and mortality risk.¹ Patients with an NRS-2002 greater than 3 are at risk, and those with scores of 5 or greater are at high nutritional risk.^1-4

Energy needs are determined via indirect calorimetry (low evidence), but when this is unavailable, a weight-based equation of 25 to 30 kcal/kg/d can be used.¹ The accuracy of this equation varies from 40% to 75% and becomes less accurate with obese and underweight patients.¹ Other considerations for this calculation include using dry weight and including energy provided by dextrose-containing fluids and lipid-based medications.¹ Because of protein’s role in wound healing, immune function, and maintaining lean body mass, protein requirements are higher in critically ill patients, and most EN has a high ratio of nonprotein calorie to nitrogen.¹ When nitrogen balance studies are not available, 1.2 to 2 g/kg/d can be used to monitor adequate protein provision, although requirements maybe higher in patients with burns or trauma.¹ There is low-level evidence suggesting that protein provision is more closely linked to better outcomes than total energy provision, although two subsequent small randomized controlled trials (RCTs) showed no difference.^1,5-9

Early Initiation of Enteral Nutrition

Although the quality of evidence is poor, it is recommended that EN be initiated within 24 to 48 hours of critical illness in patients who are unable to maintain volitional intake because it is believed that EN maintains gut functional integrity via maintaining blood flow; releases trophic endogenous agents such as cholecystokinin, gastrin, bombesin, and bile salts; and maintains tight junctions and structural integrity via maintaining villous height and support IgA producing immunocytes that make up gut-associated tissue and in turn mucosal-associated lymphoid tissue.^1-4,10-16 Heyland and colleagues¹⁴ showed a trend toward reduced mortality (relative risk [RR] = 0.52; 95% confidence interval [CI] 0.25–1.09; P = 0.08), Mark and coworkers¹⁵ showed a reduction in infectious morbidity (RR = 0.45; 95% CI 0.30–0.66; P = 0.00006), and Doig and colleagues¹⁶ showed reductions in pneumonia (odds ratio [OR] = 0.31; 95% CI 0.12–0.78; P = 0.02) and mortality (OR = 0.34; 95% CI 0.14–0.85; P = 0.02) but no difference in multiorgan failure (MOF).

Enteral nutrition is generally preferred over PN because of reduced infectious and noninfectious complications and hospital length of stay.^1,14-20 Although assessment of contractility should not be a prerequisite for initiating EN, reduced or absent bowel sounds are associated with greater symptoms of intolerance and higher mortality rates (11.3% vs 22.6% vs 36.0%).^21-23 Although in most critically ill patients, EN is safely initiated in the stomach, there is a moderate to high level of evidence for diverting EN lower in the GI tract for those who are at high risk of aspiration or have intolerance.¹ Davies and coworkers²⁴ found no difference in clinical outcomes such as length of stay, mortality rate, nutrient delivery, or pneumonia between gastric and small bowel EN, but aggregates of the RCTs showed improved nutrient delivery with small bowel feeding and reduced risk of pneuomonia.^1,24-35

Patients with low nutrition risk with normal baseline nutrition status (NRS-2000 ≤ 3 or Nutrition Risk in the Critically Ill [NUTRIC] score ≤ 5) do not need specialized nutritional therapy over the first ICU week because it does not improve mortality rates. Those who are at high nutrition risk (NRS-2000 > 5 or NUTRIC score ≥ 5 or severely malnourished) should be advanced toward goal within 24 to 48 hours and should receive more than 80% of estimated goal within 48 to 72 hours to achieve clinical benefit.¹ Fewer than 50% of critically ill patients meet their nutritional goal, and it is recommended to limit NPO (nothing by mouth) status, avoid using gastric residual volume (GRV) less than 500 mL in the absence of other signs of intolerance as a limiting factor to EN, use enteral feeding protocols, and use top-down or volume-based feeding protocols.¹ Volume-based feeding use 24-hour volume targets instead of hourly targets. Top-down protocols use a volume-based strategy, prokinetics, and postpyloric tube feeding.

There are three complications from EN: bowel ischemia, aspiration, and diarrhea. Bowel ischemia is a rare complication, and EN is generally avoided in patients who have a mean arterial pressure of less than 50 mmHg, those in whom pressors are being initiated, and those who require escalating pressor doses.¹ If a patient has been initiated on EN and has signs of intolerance such as abdominal distention, increasing nasogastric output, decreased stool or flatus, hypoactive bowel sounds, or increasing metabolic acidosis, EN should be held because these can be early signs of bowel ischemia.¹

Aspiration is another complication, and the patient population at high risk includes those who have an inability to protect their airways, nasoenteric enteral access devices, mechanical ventilation, altered mental status, gastroesophageal reflux disease, or poor oral care; who are older than 70 years of age or are supine; who undergoing bolus feeding; or who are in facilities with inadequate nurse-to-patient ratios.^1,36 Efforts to attenuate this risk include postpyloric feeding if the patient is at high risk for aspiration with a moderate to high level of evidence, continuous infusion rather than bolus feeding, prokinetics such as metoclopramide or erythromycin, keeping the head of the bed elevated by 30 to 45 degrees, use of chlorhexidine mouthwash twice a day, reducing sedation, and minimizing transport out of the ICU.^1,36-56

Diarrhea is defined as two to three liquid stools or more than 250 g of liquid stool per day, and contributing factors include fiber; osmolality of EN; high content of fermentable oligosaccharides, disaccharides, and monosaccharides and polyols (FODMAPS); delivery mode; contamination; medications such as antibiotics, proton pump inhibitors, oral hypoglycemics, nonsteroidal anti-inflammatory drugs, and sorbitol; and infections.¹

Adjunctive Therapy

There are three types of adjunctive therapy: prebiotic fiber, probiotics, and multivitamins. A total of 10 to 20 mg in divided doses of prebiotic fiber or fermentable soluble fiber, such as fructo-oligosaccharides, is given over 24 hours in patients with diarrhea because they are fermented in the colon into short-chain fatty acids, which provide nutrition to colonocytes, increase blood flow and stimulate pancreatic secretions, allow colonocytes to absorb water and electrolytes, and stimulate growth of healthy bacteria such as bifidobacteria and lactobacillus.^1,56-61 Small RCTs showed reduced diarrhea but no difference in ventilator days, ICU length of stay, or multiorgan failure.^1,62-65 Probiotics inhibit pathogenic bacteria and help eliminate pathogenic toxins, enhance the intestinal barrier, and can modulate immune responses, but consistent outcome benefit has not been shown.¹ This may be because of the heterogeneous ICU population and probiotics. However, some studies suggest that Lactobacillus GG decreases the incidence of ventilator-associated pneumonia (VAP). Synbiotic Forte with Pediococcus pentoseceus, Leuconostoc mesenteroides, Leuconostoc paracasei subsp paracasei, and Leuconostoc plantarum showed reduced infectious complications when begun 1 hour after surgery (40% vs 12.5%; P < 0.05), and probiotics decrease VAP, colitis, and diarrhea in patients with liver transplants, trauma, and pancreatectomy.^1,66-77 Antioxidant vitamins and trace minerals are believed to improve patient outcomes with a significant reduction in overall mortality but do not affect infectious complications, length of stay, or duration of mechanical ventilation.¹

Parenteral Nutrition

Parenteral nutrition is not recommend for patients with low nutritional risk in the first 7 days even if volitional intake or early EN is not possible because of infectious morbidity and minimal benefit over standard therapy in which no nutrition is provided.^1,78-80 Heyland and coworkers’ aggregate analysis of four studies showed an increased mortality rate with PN (RR = 0.178l; 95% CI 1.11–2.85; P < 0.05) and trend toward greater complications (RR = 2.40; 95% CI 0.88–6.58) compared with no nutrition.⁸¹ Regardless of nutritional risk, PN should be considered for more than 7 to 10 days if unable to meet more than 60% of energy and protein by EN.¹ When more than 60% of target energy has been delivered with EN, PN can be discontinued. Hypocaloric PN (≤ 20 kcal/kg/d or 80% estimated energy needs) with adequate protein ≥ 1.2 g/kg/d) should be considered in high-risk or severely malnourished patients in the first 7 days of the ICU stay; it has not been shown to reduce infectious complications or morbidity but is associated with a decreased incidence of hyperglycemia.^1,82-84 Table 32-1 provides a list of recommendations per disease.¹