Amino acids are the key building blocks required for growth and tissue repair. The majority (98%) are found in existing proteins, and the remainder reside in the free amino acid pool. Proteins are continually degraded into their constituent amino acids and resynthesized through the process of protein turnover. The reutilization of amino acids released by protein breakdown is extensive. Synthesis of proteins from the recycling of amino acids is more than two times greater than from dietary protein intake. An advantage of high protein turnover is that a continuous flow of amino acids is available for the synthesis of new proteins. This allows the body tremendous flexibility in meeting ever-changing physiologic needs. However, the process of protein turnover requires the input of energy to power both protein degradation and synthesis. At baseline, infants are known to have higher rates of protein turnover than adults. Healthy newborns have a protein-turnover rate of 6–12 g/kg/day compared with 3.5 g/kg/day in adults. Even greater rates of protein turnover have been measured in premature infants and those with low birth weight. For example, it has been demonstrated that infants with extremely low birth weight receiving no dietary protein can lose in excess of 1.2 g/kg/day of endogenous protein. At the same time, infants must maintain a positive protein balance to attain normal growth and development, whereas the healthy adult can subsist with a neutral protein balance.

In the metabolically stressed patient, such as the child with severe burn injury, sepsis, or major surgery, protein turnover is increased up to twofold compared with that in normal children, which has been shown to correlate with the duration of the critical illness and severity of injury. ^, This process redistributes amino acids from skeletal muscle to the liver, wound, and tissues taking part in the inflammatory response. The factors required for the inflammatory response (acutely needed enzymes, serum proteins, and glucose) are thereby synthesized from degraded body protein stores. The well-established increase in hepatically derived acute phase proteins (including C-reactive protein, fibrinogen, transferrin, and α-1-acid glycoprotein), along with the concomitant decrease in transport proteins (albumin and retinol-binding protein), is evidence of this protein redistribution. As substrate turnover is increased during the stress response, rates of both whole-body protein degradation and whole-body protein synthesis are accelerated. However, protein breakdown predominates, thereby leading to a hypercatabolic state with an ensuing net negative protein and nitrogen balance.

Protein loss is evident in elevated levels of excreted urinary nitrogen during critical illness. For example, infants with sepsis demonstrate a several-fold increase in the loss of urinary nitrogen that directly correlates with the degree of illness. Clinically, severe protein loss can be manifested by skeletal muscle wasting, growth failure, delayed wound healing, and immune dysfunction. ^, In addition to the reprioritization of protein for tissue repair, healing, and inflammation, the body appears to have an increased need for glucose production during times of metabolic stress. The accelerated rate of gluconeogenesis during illness and injury is seen in both children and adults, and this process appears to be accentuated in infants with low body weight. ^, The increased production of glucose in times of illness is necessary because glucose represents a versatile energy source for tissues taking part in the inflammatory response. For example, it has been shown that glucose utilization by leukocytes is significantly increased during the inflammatory response. Unfortunately, the provision of additional dietary glucose does not suppress the body’s need for increased glucose production. Therefore, net protein breakdown continues to predominate. ^{, ,}

Specific amino acids are transported from muscle to the liver to facilitate hepatic glucose production. The initial step of amino acid catabolism involves removal of the toxic amino group (NH ₃ ). Through transamination, the amino group is transferred to α-ketoglutarate, thereby producing glutamate. The addition of another amino group converts glutamate to glutamine, which is subsequently transported to the liver, where the amino groups are removed from glutamine and detoxified to urea through the urea cycle. The amino acid carbon skeleton can then enter the gluconeogenesis pathway. Alternatively, in skeletal muscle, the amino group can be transferred to pyruvate, thereby forming alanine. When alanine is transported to the liver and detoxified, pyruvate is reformed and can be converted to glucose through gluconeogenesis. The transport of alanine and pyruvate between peripheral muscle tissue and the liver is termed the glucose-alanine cycle. Hence, the transport amino acid systems involving glutamine and alanine provide carbon backbones for gluconeogenesis, while facilitating the hepatic detoxification of ammonia by the urea cycle.

Increased muscle protein catabolism is a successful short-term adaptation during critical illness, but it is limited and ultimately harmful to the child with reduced protein stores and elevated protein demands. Unless the inciting stress is eliminated, the progressive breakdown of diaphragmatic, cardiac, and skeletal muscle can lead to respiratory compromise, fatal arrhythmias, and loss of lean body mass. Moreover, a prolonged negative protein balance may have a significant impact on the child’s growth and development. Premature neonates who are gaining weight appropriately have a positive protein balance of nearly 2 g/kg/day. In contrast, critically ill, premature neonates requiring mechanical ventilation have a negative protein balance of 1 g/kg/day. Critically ill neonates who require ECMO have exceedingly high rates of protein loss, with a net negative protein balance of 2.3 g/kg/day, and have protein requirements of up to 3 g/kg/day. ^, It is well established that the extent of protein catabolism correlates with morbidity and mortality in surgical patients.

Fortunately, amino acid supplementation tends to promote increased nitrogen retention and positive protein balance in critically ill patients. ^, The mechanism appears to be an increase in protein synthesis while rates of protein degradation remain constant. ^, Therefore, the provision of dietary protein sufficient to optimize protein synthesis, facilitate wound healing and the inflammatory process, and preserve skeletal muscle mass is one of the most important nutritional interventions in critically ill children. The quantity of protein needed to enhance protein accrual is greater in hospitalized sick children than in healthy children. Table 2.3 lists recommended quantities of dietary protein for hospitalized children. Extreme cases of physiologic stress, including the child with extensive burns or the neonate on ECMO, may necessitate additional protein supplementation to meet metabolic demands. Recent studies of an international cohort concluded that adequate enteral protein intake is associated with a lower 60-day mortality in mechanically ventilated children. ^, In these studies, among critically ill pediatric surgical patients, a majority had inadequate enteral protein intake. Also, greater enteral protein delivery was associated with a dedicated ICU dietician and earlier initiation of enteral nutrition (EN) with fewer interruptions.

The influence of macronutrient intake on protein balance has been explored in several studies. A systematic review of all such studies in mechanically ventilated children showed that a minimum of 1.5 g/kg/day protein and 57 kcal/kg/day energy intake was needed to achieve a positive protein balance in this group. The ASPEN and SCCM guidelines recommend a minimum protein intake of 1.5 g/kg/day for critically ill children between 1 month and 18 years of age. However, it should be noted that toxicity from excessive protein administration can occur, particularly in children with impaired renal and hepatic function. While higher protein provision may improve protein balance, the provision of protein at levels greater than 3 g/kg/day is rarely indicated and can be associated with azotemia. ^, In premature neonates, the possible benefits of early high protein allotments, up to approximately 4 g/kg/day, to replicate intrauterine protein accretion and growth rates, have recently been extensively studied. There is much variability among these studies, but it appears that providing 3.5 g/kg/day is reasonable. Higher amounts, at least given enterally, may be tolerated with associated increased protein balance, though benefits to long-term growth and/or neurodevelopment have yet to be proven. A multicenter randomized controlled trial is ongoing. High-dose amino acid supplementation may lead to alterations in plasma amino acid levels and metabolic disturbances such as elevated ammonia or blood urea nitrogen. ^, Historical studies using protein provisions of 6 g/kg/day in children have demonstrated significant morbidity, including azotemia, pyrexia, strabismus, and lower intelligence quotient (IQ) scores. ^,

Glucose production and availability are a priority in the pediatric metabolic stress response. Glucose is the primary energy source for the brain, erythrocytes, and renal medulla and is used extensively during the inflammatory response. Injured and septic adults demonstrate a twofold increase in glucose turnover, glucose oxidation, and gluconeogenesis. This increase is of particular concern in neonates who have an elevated glucose turnover at baseline. Moreover, glycogen stores provide only a limited endogenous supply of glucose in adults and an even smaller reserve in the neonate. Thus, the critically ill neonate has a greater glucose demand and reduced glucose stores. During illness, the administration of exogenous glucose does not halt the elevated rates of gluconeogenesis and thus net protein catabolism continues unabated. ^, It is clear, however, that appropriate provision of amino acids can effectively improve protein balance during critical illness, primarily through augmentation of protein synthesis.

In the past, nutritional support regimens for critically ill patients utilized large amounts of glucose to try to reduce endogenous glucose production. Unfortunately, excess glucose increases CO ₂ production and does not reduce endogenous glucose turnover. Thus, a surplus of carbohydrate may increase the ventilatory burden on the critically ill patient. In one study, adults in the ICU fed with high-glucose PN demonstrated a 30% increase in oxygen consumption, a 57% increase in CO ₂ production, and a 71% elevation in minute ventilation. In critically ill infants, the conversion of excess glucose to fat has also been correlated with an increased CO ₂ production and higher respiratory rates. Finally, data in critically ill neonates have shown that excess caloric allotments of carbohydrate are paradoxically associated with an increased rate of net protein breakdown.

When designing a nutritional regimen for the critically ill child, excessive carbohydrate calories should be avoided. A mixed-fuel system, with both glucose and lipid substrates, should be used to meet the child’s nonprotein caloric requirements. When the postoperative neonate is fed a high-glucose diet, the corresponding RQ is approximately 1.0 and may be higher than 1.0 in selected patients, signifying increased lipogenesis. A mixed dietary regimen of glucose and lipid (at 2–4 g/kg/day) provides the infant with full nutritional supplementation while alleviating an increased ventilatory burden and difficulties with hyperglycemia.

Administration of high caloric (glucose load) diets in the early phase of critical illness may exacerbate hyperglycemia, increase CO ₂ generation with an increased load on the respiratory system, promote hyperlipidemia resulting from increased lipogenesis, and result in a hyperosmolar state. Several reports have linked hyperglycemia with increased mortality in both critically ill children and adults. Overall, multicenter trials in critically ill adults have established that excessive hyperglycemia (>180 mg/dL) should be avoided, though insulin-assisted strict glycemic control (<110 mg/dL) is associated with increased risk of hypoglycemia and possibly decreased survival. Randomized multicenter trials examining tight glucose control in critically ill children have shown no differences in ventilator days, mortality, or ICU stay, and tight glucose control was associated with higher rates of hypoglycemia.

Similar to protein and carbohydrate metabolism, the turnover of lipid is generally increased by critical illness, major surgery, and trauma in the pediatric patient. During the early ebb phase, triglyceride levels may initially increase as the rate of lipid metabolism decreases. However, this process reverses itself during the catabolic flow phase. In one study, endotoxemia induced in adults resulted in significantly increased lipolysis, serum free fatty acid concentration, and fatty acid oxidation. In a pediatric study, critically ill children on mechanical ventilation were shown to have increased rates of fatty acid oxidation. The increased lipid metabolism is thought to be proportional to the overall degree of illness.

RQ values may decline during illness, reflecting an increased utilization of fat as an energy source. This suggests that fatty acids are a prime source of energy in metabolically stressed infants and children. In addition to the rich energy supply from lipid substrate, the glycerol moiety released from triglycerides can be converted to pyruvate and used to manufacture glucose. As seen with the other catabolic changes associated with illness and trauma, the provision of dietary glucose does not decrease fatty acid turnover in times of illness. The increased demand for lipid utilization in critical illness coupled with the limited lipid stores in the neonate puts the metabolically stressed infant or child at high risk for the development of essential fatty acid deficiency. Parenterally fed children receiving inadequate lipid provision develop essential fatty acid deficiency much sooner than adults. Also, preterm infants have been shown to develop biochemical evidence of essential fatty acid deficiency 2 days after the initiation of a fat-free nutritional regimen.

In humans, the polyunsaturated fatty acids linoleic and linolenic acid are considered essential fatty acids because the body cannot manufacture them by desaturating other fatty acids. Linoleic acid is used by the body to synthesize arachidonic acid, an important intermediary in prostaglandin synthesis. The prostaglandin family includes the leukotrienes and thromboxanes, all of which serve as mediators in wide-ranging processes such as vascular permeability, smooth muscle reactivity, and platelet aggregation. If an individual lacks dietary linoleic acid, the formation of arachidonic acid (a tetraene) cannot occur. Instead, the desaturation of oleic acid, a nonessential fatty acid, increases and eicosatrienoic acid (a triene) accumulates. Clinically, a fatty acid profile can be performed on human serum, and an elevated triene-to-tetraene ratio greater than 0.2 is indicative of biochemical EFAD (Essential Fatty Acid Deficiency) with clinically observed EFAD not occurring until >0.4., though this cutoff is somewhat variable and depends on the specific laboratory assay utilized. ^, Signs of fatty acid deficiencies include dermatitis, alopecia, thrombocytopenia, increased susceptibility to infection, and overall failure to thrive. To avoid essential fatty acid deficiency in infants, the allotment of linoleic and linolenic acid is recommended at concentrations of 3.0%–4.5% and 0.5% of total calories, respectively. In addition, evidence exists that the long-chain fatty acid docosahexaenoic acid (DHA), a derivative of linolenic acid important for neurodevelopment, may also be deficient in preterm and formula-fed infants. Clinical trials thus far have not reached consensus on whether supplementation with long-chain polyunsaturated fatty acids (i.e., DHA) is of clinical benefit in this population because most have shown neither benefit nor harm. ^,

Parenterally delivered lipid solutions also limit the need for excessive glucose intake as lipid emulsions provide a higher quantity of energy per gram than does glucose (9 kcal/g vs. 4 kcal/g). This reduces the overall rate of CO ₂ production and the RQ value. There are risks when starting a patient on intravenous lipid administration, including hypertriglyceridemia, a possible increased risk of infection, hematologic abnormalities, and decreased alveolar oxygen-diffusion capacity. Therefore, most institutions initiate lipid provisions in children at 0.5–1.0 g/kg/day and advance over a period of days to 2–4 g/kg/day. During this time, triglyceride levels are monitored closely. Lipid administration is generally restricted to 30%–40% of total caloric intake in ill children in an effort to obviate immune dysfunction, ^, although this practice has not been validated in a formal clinical trial.

In settings of prolonged fasting or uncontrolled diabetes mellitus, the accelerated production of glucose depletes the hepatocyte of needed intermediaries in the citric acid cycle. When this occurs, the acetyl-coenzyme A (CoA) generated from the breakdown of fatty acids cannot enter the citric acid cycle and instead forms ketone bodies, acetoacetate, and β-hydroxybutyrate. These ketone bodies are released by the liver to extrahepatic tissues, particularly skeletal muscle and the brain, where they can be used for energy production instead of glucose. However, during surgical illness ketone body formation is relatively inhibited secondary to elevated serum insulin levels. Thus, compared with starvation, ketone bodies do not significantly supplant the need for glucose in surgical patients and do not play a major role in the metabolic management of the pediatric stress response.

In addition to their nutritional role, fatty acids profoundly influence inflammatory and immune events by changing lipid mediators as well as inflammatory protein and coagulation protein expression. After ingestion, n-6 and n-3 fats are metabolized by an alternating series of desaturase and elongase enzymes, transforming them into the membrane-associated lipids arachidonic acid, eicosapentaenoic acid (EPA), and DHA ( Fig. 2.2 ). In PN, substitution of conventional soybean oil–based lipid emulsion (Intralipid), which is rich in proinflammatory omega-6 fatty acids, with a fish oil–based lipid emulsion (Omegaven), which has antiinflammatory omega-3 fatty acids, has been successful at reversing cholestasis in pediatric intestinal failure–associated liver disease (IFALD) across several studies. ^, More recently, a lipid emulsion containing soybean oil, medium-chain triglycerides, olive oil, and fish oil (SMOflipid) was approved by the US Food and Drug Administration for pediatric patients. In a pilot multicenter blinded randomized controlled trial comparing soybean oil (30%), medium-chain triglycerides (MCTs) (30%), olive oil (25%), and fish oil (15%) with a soy-based lipid emulsion, infants who received the combination lipid product had significantly lower conjugated bilirubin than those who received a soy-based lipid emulsion. In a single-center, retrospective analysis of neonates with IFALD on SMOflipid, liver disease was reversed by switching to Omegaven monotherapy.

Fatty acid synthesis from omega-3, omega-6, and omega-9 fats.

From Lee S, Gura KM, Kim S et al. Current clinical applications of omega-6 and omega-3 fatty acids. Nutr Clin Pract . 2006;21:323–341.

The vitamin and micronutrient (trace element) needs of healthy children and neonates are relatively well defined in the literature, and guidelines have been published. In the neonate and child, required vitamins include the fat-soluble vitamins (A, D, E, and K) and the water-soluble vitamins ascorbic acid, thiamine, riboflavin, pyridoxine, niacin, pantothenate, biotin, folate, and vitamin B ₁₂ . Because vitamins are not consumed stoichiometrically in biochemical reactions but instead act as catalysts, the administration of large amounts of vitamin supplements in metabolically stressed states is not logical from a nutritional standpoint. The trace elements required for normal growth and development include zinc, iron, copper, selenium, manganese, iodide, molybdenum, and chromium. Trace elements are needed for the synthesis of a ubiquitous and extraordinarily important class of enzymes called metalloenzymes. More than 200 zinc metalloenzymes alone exist, and both DNA and RNA polymerase are included in this group. As with vitamins, these metalloenzymes act as catalytic agents.

In addition to inadequate macronutrient intake, postsurgical and critically ill children are also at risk for micronutrient deficiencies. Table 2.4 lists symptoms, risk factors, and laboratory assessments for common pertinent micronutrient deficiencies in the pediatric surgical population. Special attention should be paid to children with loss of functional bowel, high gastrointestinal losses, malabsorption, and/or chronic malnutrition, such as in short bowel syndrome, cystic fibrosis, and cholestatic liver disease. Altered plasma levels of a variety of vitamins and trace minerals (vitamin A, C, 25-OH D, E, selenium, zinc) have been described in critical illness, with some studies showing that the degree of deficiency correlates with the severity of illness and outcomes. The driving force behind alterations in micronutrient plasma levels has not been fully elucidated, and no clear causal relationships have been systematically described. Levels may be altered due to increased losses, increased demand, fluid shifts, altered protein binding, dialysis, or redistribution into tissues. A majority of children in the pediatric intensive care unit (PICU) also do not receive their dietary recommended intake of micronutrients. Trials of vitamin and trace mineral supplementation during critical illness have yielded mixed results. ^,

Following the estimation of energy expenditure and macronutrient requirement in the hospitalized child, the next challenge is to facilitate the provision of this nutritional support. In most pediatric patients with a functioning gastrointestinal tract, the enteral route of nutrient administration is preferable to PN, particularly oral nutrition if able. EN is physiologic and has been shown to be more cost effective without the added risk of nosocomial infection inherent in PN. Early EN has been shown to be associated with decreased mortality in critically ill children. ^, Based on adult critical care literature, the European Society of Intensive Care Medicine and the ASPEN guidelines recommend the use of early enteral feeding in critical illness (within 24–48 hours after ICU admission), except in patients with bowel ischemia or hemodynamic instability requiring significant vasopressor support. ^, The ASPEN and SCCM joint guidelines for critically ill children also recommend EN as the preferred mode of nutrient delivery, starting within 24–48 hours after PICU admission if able and aiming to achieve up to two-thirds of nutrient goal in the first week. Traditionally, enteral feeding after intestinal surgery would be delayed due to expected postoperative ileus and the presence of a fresh intestinal anastomosis. However, recent experimental data suggest that early enteral feeding (within 24 hours) after intestinal surgery, proximal to an anastomosis, does not negatively affect mortality or anastomotic integrity and instead could decrease length of hospitalization. In addition, early EN may promote more collagen deposition at the anastomosis. Nevertheless, the timing of starting EN initiation should be tailored to each patient based on clinical judgment. In current practice, PN is used to supplement or replace EN in those patients in whom EN alone is unable to meet the nutritional goals.

Although oral nutrition is preferred, when possible, its safety needs to be ensured. Particularly pertinent to neonates or in the setting of neurologic impairment, prolonged intubation, or airway and/or upper gastrointestinal malformations, attention must be paid to identifying swallowing difficulties when providing EN. If impaired swallowing with aspiration is suspected, formal bedside swallowing evaluation and/or radiographic contrast studies are warranted. If aspiration is suspected or at high risk of occurring, EN should be delivered through alternative enteral access, or the food consistencies modified based on recommendations from a feeding therapist. Critically ill neonates are often deprived of oral nutrition due to a series of interacting factors including impaired feeding skills, prolonged hospitalization, multiple operative procedures, and prolonged intubation. As a result, critical oral motor skills, which have a key window of development during the first 6 months of life, may fail to develop normally and the child may develop oral aversion. Data on prevention of oral aversion are lacking, though conventional practice involves introduction of oral stimulation as early in life as safely possible through nonnutritive sucking or oral feeding. For patients who go on to develop oral aversion, investigating modifiable etiologies such as abdominal pain or vomiting is essential. Once that has been ruled out, behavior techniques such as exposing children to the sensation of a utensil to their lips and exploring various textures of foods should be utilized. ^, Including feeding therapists in multidisciplinary nutritional support teams seems beneficial.

In children on EN, data are insufficient to make recommendations regarding the site of the enteral feeding (gastric vs. postpyloric). Both enteral routes have been successfully used for nutritional support of the critically ill child. In a study examining the role of small bowel feeding in 74 critically ill children randomized to receive either gastric or postpyloric feeds, no significant difference was observed in microaspiration, tube displacement, and/or feeding intolerance between the two groups. Although caloric goals were met in only a small percentage of the population studied and enteral feeds were interrupted in a large number of patients, a higher percentage of subjects in the small bowel fed group achieved their daily caloric goal when compared with the gastric fed group. A prospective observational study found that early (<24 hours after ICU admission) postpyloric feeding was well tolerated in critically ill children, with less abdominal distention. A more recent randomized trial of mechanically ventilated adults found no differences in energy delivery, mortality, pneumonia, or diarrhea between early nasojejunal feeding and continued nasogastric feeding, though the nasojejunal feeding group had higher rates of minor gastrointestinal bleeding. It may be prudent to consider postpyloric feeds in patients who do not tolerate gastric feeding or those who are at high risk of aspiration. Transpyloric feeding may be limited by an inability to obtain small bowel access, variable ICU expertise and resources, and concern for dumping. Operative placement of gastrostomy or jejunostomy tubes allows long-term enteral feeding and drug administration in the ICU and after discharge. A gastrostomy tube can also be exchanged for a gastrojejunostomy tube under fluoroscopic guidance in patients who do not tolerate intragastric feeding. Gastrojejunostomy tubes allow for simultaneous gastric decompression while feeding distally ( Fig. 2.3 ). Stoma site infection, obstruction, and tube dislodgement are common complications and must be identified and managed early. Gastrojejunostomy tubes can also be associated with small bowel–to–small bowel intussusception. Malposition of the tube is frequently encountered with any of these devices either at placement or during its use. Methods to identify tip position range from auscultation during air insufflation to ultrasound-guided localization. Feedings should be held when malposition of the tip is suspected. When in doubt, a contrast study may be needed to confirm tip position before recommencing feeds.

(A) This gastrojejunostomy tube has been placed in a child with a history of short bowel syndrome who has not tolerated gastric feedings. (G marks the gastric port for decompression, and J marks the jejunal port for feeding.) (B) A gastrojejunostomy tube contrast study is seen through the jejunal port in the same child.

EN in critically ill children is often interrupted for a variety of reasons, some of which may be avoidable. Children with frequent interruptions have a higher reliance on PN. Intolerance to enteral feeds may be a limiting factor, and supplementation with PN in this group of patients allows for improved nutritional intake. Enteral feeds are held for a period before procedures such as elective endotracheal intubation, general anesthesia, procedural sedation, extubation, and other such interventions to lower the corresponding risk of aspiration. Most centers do not use enteral feeding with patients who are on multiple vasopressor drugs for hypotension or who have evidence of bowel ischemia to limit the risk of exacerbating intestinal ischemia. In a subgroup of critically ill patients, PN may be required for a period before initiation of enteral feeds.

Prospective cohort studies and retrospective chart reviews have reported the inability to achieve the daily caloric goal in many critically ill children. In an international multicenter prospective cohort study of mechanically ventilated children, energy and protein intake were found to be grossly inadequate. A subsequent recent multicenter study of pediatric surgical patients found that two-thirds of the patients examined had inadequate enteral protein intake (<60% prescribed goal) during their PICU stay, and the entire surgical cohort had much lower total and enteral delivery of calories and protein compared with their medical counterparts. A majority of patients in both studies had interruptions in EN delivery during their ICU stay. A previous single-center study of PICU patients found that many EN interruptions were potentially avoidable. Overall, 158 patients with EN interruptions took longer and were less likely to reach caloric goals. Aside from EN interruptions, delay in starting EN is another significant contributor to inadequate EN delivery. Finally, a recent retrospective multicenter review found positive-pressure ventilation, illness severity, procedures, and gastrointestinal disturbances to be risk factors for delayed initiation of EN in critically ill children.

Addressing preventable interruptions and delays in enteral feeding in critically ill children is essential to attaining goal feeds. A multidisciplinary nutrition team that includes a dedicated dietician can be invaluable in tailoring nutritional delivery that is optimized for the goals of individual patients. A stepwise EN algorithm may also be of benefit. A single-center study showed significantly improved EN delivery with implementation of a stepwise EN algorithm. However, a multicenter study found that percentage adequacy of EN delivery was not associated with the use of algorithms, although less than one-third of the centers examined had an EN algorithm, and there was variability in agreement with national guidelines. Many feeding algorithms also use gastric residual volumes (GRVs) to assess for EN intolerance when providing gastric feeds, though whether GRV accurately reflects gastric emptying has been questioned. In fact, measurement of GRV is no longer recommended as part of routine care to monitor EN tolerance in recent adult critical care nutrition guidelines. Use of transpyloric feeding tubes and changing from bolus to continuous feeds during brief periods of intolerance are strategies that may help achieve nutrition goals in this population. Randomized studies comparing enteral feeds administered by bolus or continuously in children are not strong enough to recommend one feeding method over the other. In one randomized controlled trial, 60 children aged 5–17 years old were separated into continuous or bolus feeding groups. The mean time to reach goal calories was higher in the continuously fed group; however, they had better outcomes with a decreased percentage of patients experiencing enteral intolerance. In contradistinction, a more recent randomized controlled trial performed on 158 children aged 1 month to 12 years in the PICU found that the bolus fed group reached goal feeds faster, which improved calorie and protein intake. Currently, there is not enough evidence to recommend the routine use of prokinetic medications, motility agents (for feeding intolerance or to facilitate enteral tube placement), probiotics, or prebiotics in critically ill children.

In summary, EN must be initiated early in hospitalized children with bowel activity. Postpyloric EN may be utilized in children with a high risk of aspiration or when gastric feeding is either contraindicated or has failed. Enterally administered feeds can meet nutritional requirements in critically ill children with a functional gastrointestinal system and have the advantages of low cost, manageability, safety, and preservation of hepatic and other gastrointestinal function. Early introduction of enteral feeds in critically ill patients helps achieve positive protein and energy balance and restores nitrogen balance during the acute state of illness. EN maintains gut integrity and elicits release of growth factors and hormones that maintain gut integrity and function. However, inadequate delivery of EN seems prevalent across most PICUs. Fig. 2.4 offers an algorithm for initiating and advancing EN in children, based on practices in the multidisciplinary PICU at Boston Children’s Hospital.

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