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Early Enteral Nutrition in Critically Ill Patients With Hemodynamic Instability: An Evidence-Based Review and Practical Advice Shuofei Yang, Xingjiang Wu, Wenkui Yu and Jieshou Li Nutr Clin Pract 2014 29: 90 DOI: 10.1177/0884533613516167 The online version of this article can be found at: http://ncp.sagepub.com/content/29/1/90

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NCPXXX10.1177/0884533613516167Nutrition in Clinical PracticeYang et al

Review

Early Enteral Nutrition in Critically Ill Patients With Hemodynamic Instability: An Evidence-Based Review and Practical Advice

Nutrition in Clinical Practice Volume 29 Number 1 February 2014 90­–96 © 2014 American Society for Parenteral and Enteral Nutrition DOI: 10.1177/0884533613516167 ncp.sagepub.com hosted at online.sagepub.com

Shuofei Yang, MD; Xingjiang Wu, MD, PhD; Wenkui Yu, MD, PhD; and Jieshou Li, MD, PhD

Abstract Early enteral nutrition (EEN) in critically ill patients is associated with significant benefit as well as elevated risk of complications. Concomitant use of EEN with vasopressors has been associated with nonocclusive bowel necrosis in critically ill patients with hemodynamic instability. The decision when to initiate enteral nutrition in hemodynamically unstable patients that require vasoactive substances remains a clinical dilemma. This review summarizes the effect of EEN and vasoactive agents on gastrointestinal blood flow and perfusion in critically ill patients, based on current evidence. Animal and clinical data involving simultaneous administration of EEN and vasoactive agents for hemodynamic instability are reviewed, and the factors related to the safety and effectiveness of EEN support in this patient population are analyzed. Moreover, practical recommendations are provided. Additional randomized clinical trials are warranted to provide cutting-edge evidence-based guidance about this issue for practitioners of critical care. (Nutr Clin Pract. 2014;29:90-96)

Keywords critical illness; enteral nutrition; vasoconstrictor agents; hemodynamics

Sufficient blood perfusion and adequate motility of the gastrointestinal tract are prerequisite to initiate early enteral nutrition (EEN) safely. However, hemodynamic instability, including high risk of gastrointestinal (GI) hypoperfusion, mesenteric ischemia, and depressed peristalsis, is common in critically ill patients. Initiating EEN while a patient is hemodynamically tenuous will further compromise the splanchnic perfusion. The optimal time to safely and effectively deliver enteral nutrition (EN) in a hemodynamically unstable patient has been a controversy for almost 2 decades. In light of several inconsistent reports of nonocclusive mesenteric ischemia (NOMI) or nonocclusive bowel necrosis (NOBN) during EN among this specific patient population,1-6 clinical recommendations about this issue in guidelines on EN for critically ill patients are unreliable or supported by the lowest level of evidence (Table 1).7-13

GI Blood Flow/Perfusion and EEN in Hemodynamically Unstable Patients of Critical Illness The following 3 subpopulations of hemodynamically unstable patients need vasopressors or inotropes to maintain adequate blood pressure and cardiac output: (1) septic, hemorrhagic, traumatic, or cardiogenic shock; (2) severe or major burns; (3) circulatory compromise or failure after cardiac surgery. In hypotension state, blood is shunted from the gut and other peripheral organs to the central circulation of heart and brain. Vasopressors increase blood pressure by elevating the

sensitivity of the gut to vasoconstriction, thereby increasing the risk of ischemia and associated mortality. Volume resuscitation does not immediately reverse blood flow to gut due to (1) increased levels of endogenous or exogenous vasoconstrictors, such as endothelin I, angiotensin II, and vasopressin; (2) a synchronous decrease in endogenous vasodilators, such as nitric oxide; and (3) ischemia-reperfusion injury to the microcirculation.14 Delivering EEN under these conditions increases mucosal oxygen requirements. Perfusion demand may outstrip supply and thereby lead to NOMI. NOBN is the final event in both severe gut microvascular ischemia and mucosal injury with inflammation. Intraluminal food stimulus, however, augments GI blood flow. Different EN components, especially the protein-rich formula, generate a notable hyperemia effect to

From the Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing, China. Financial disclosure: This review was supported by a National Natural Science Foundation (81300278) in China. Drs Shufoei Yang and Xingjiang Wu contributed equally to this work. Received for publication July 10, 2013; accepted for publication November 18, 2013. Corresponding Author: Wenkui Yu, MD, PHD, Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, No. 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, People’s Republic of China, Nanjing, 210002, China. Email: [email protected]

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Table 1.  Recommendations for Early Enteral Nutrition in Critically Ill Patients With Hemodynamic Instability, Based on Current Guidelines. Contributors

Year

Related Suggestions

Evidence Level

European Society for Clinical Nutrition and Metabolism Canadian Critical Care Practice Guidelines Committee

2006 Critically ill patients who were hemodynamically stable should be fed early (< 24 h). 2003 Early EN within 24-48 h from admission to ICU could begin when patients were adequately resuscitated and hemodynamically stable. 2009 Early EN could be applied to all mechanically ventilated patients who were under adequate resuscitation and hemodynamically stable. 2013 The committee noted the results of a large observational study of 1174 critically ill patients on vasopressors that demonstrated that early EN was associated with decreased hospital mortality and that the beneficial effect of early feeding was more evident in patients treated with multiple vasopressors, and the prerequisite that patients were adequately resuscitated and hemodynamically stable was deleted. 2008 None

Nutrition Guidelines Investigators of the ANZICS Clinical Trials Group 2013 Enteral nutrition is considered as a lower Hyunjung Kim, Nancy priority in ICU than interventions for A. Stotts, Erika S. hemodynamic problems. Froelicher, Marguerite M. Engler, and Carol Porter 2009 In the setting of hemodynamic compromise, Society of Critical Care EN should be withheld until the patient is Medicine and American fully resuscitated and/or stable, and EN Society for Parenteral may be provided with caution to patients, and Enteral Nutrition either into the stomach or small bowel on stable low doses of vasopressor agents.

Limitation

Level C

Uncertain about hemodynamically unstable patients

8 level, 2 studies

Uncertain about hemodynamically unstable patients

14 level, 2 studies

Uncertain about hemodynamically unstable patients

16 level, 2 studies

Limitations of this observational study include selection bias where patients with poor ICU course would receive later enteral feedings, inability to control for all factors in an observational study, and no specific analysis of the data on patients who were receiving vasopressors.

None

None

None

Evidence-based interdisciplinary knowledge for high acuity and critical care in adult Korean intensive care patients without systematic evaluation Lowest level of recommendation and, due to individual diversity of drug sensitivity, no precise definition of “low doses” and the shock phase probably lasting for several days

Grade E

EN, enteral nutrition; ICU, intensive care unit.

increase oxygen delivery to the gut.15 It has been proven that this hyperemia effect occurs by shunting systemic blood instead of increasing total cardiac output.16 The mean arterial pressure is likely to decrease with further exacerbation of hemodynamic instability.

Current Research Animal Experiments To determine whether postprandial intestinal hyperemia has beneficial or detrimental effects during gut ischemia, Bortenschlager et al17 found that administration of EN to a hemorrhagic shock model protected the liver function from injury and increased total survival rate without any impacts on GI function. Similarly, GI blood flow was recruited with glutamine or glucose infusion after hemorrhage in another study.18 EEN was able to remarkably improve hepatic and

intestinal mucosal microcirculation and restore tissue oxygenation and hepatic energy storage in a dog model of septic shock with splanchnic ischemia.19 Intestinal microcirculation was also ameliorated by EEN with glucose, and bacterial translocation decreased significantly with oral glutamine or EEN in an animal model of sepsis.20-22 In 1993, Purcell et al23 evaluated the effect of EEN on bowel perfusion during positive end–expiratory pressure ventilation for lung injury. Positive end–expiratory pressure was shown to attenuate intestinal oxygen supply without oxygen consumption alteration, while EEN raised blood circulation in the portal vein as well as hepatic artery and the ratio of oxygen supply/consumption. Perfusion significantly improved within a few minutes as soon as EEN initiated, even in small doses. Early enteral feeding (EEF) increased gut blood flow and mucosal barrier function in a pig model of burn.24 Improved intestinal motility was shown in another study of hemodynamically unstable rat model.25

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Nevertheless, some other studies demonstrated that EEN has the potential to exacerbate gut ischemia. For instance, one study investigating total occlusion of the superior mesenteric artery in a rat model revealed that the degree of tissue hypoxemia and mucosal permeability worsened when metabolic nutrients were infused into the gut.26 However, total superior mesenteric artery occlusion is an extreme case of GI hypoperfusion with no possibility of EN-induced hyperemia. Despite several animal experiments supporting the notion that EEN can ameliorate GI blood perfusion and function, a lot of unsolved problems from current animal experiments still exist. For example, in most studies, EN follows fluid resuscitation alone without consideration of the vasopressor response, whereas fluid resuscitation and vasopressor always go hand in hand to treat shock and hypotension. Furthermore, current studies focus on blood flow and bowel motility exclusively, with no examination to the induced dysfunction of GI mucosal barrier and bacterial translocation. In addition, systemic hemodynamic changes and related dose fluctuation of vasoactive agents by EEN in hemodynamically unstable status were never analyzed. Therefore, more practical and comprehensive experimental designs are warranted in the future.

Clinical Studies Berger et al27 in 2000 reported clinical tolerance of EEN with delayed rather than suppressed intestinal absorption in patients with hemodynamic failure after cardiac surgery. Five years later, the same research group studied EEN in 70 critically ill patients with severe hemodynamic failure after cardiopulmonary bypass without any abdominal complications.28 They found that EN delivery was negatively affected by increased doses of dopamine and norepinephrine. Administration of EEN via a postpyloric tube in postoperative cardiac surgery patients with circulatory compromise increased cardiac index and splanchnic blood flow.29 EEN in cardiac surgery patients with hemodynamic compromise is feasible, safe, and not associated with serious complications.30 In severely burned patients of the first 48 hours, during the shock phase, early high caloric duodenal feeding did not increase the CO2 gap, reflecting good tolerance to EEF in spite of hemodynamic instability.31 In major burned patients, EEN was associated with good maintenance of GI motility and splanchnic perfusion.32 In patients with septic shock, hemodynamic instability is frequently considered as a contraindication to EEF. In a retrospective cohort study, Rai et al33 found that despite delayed gastric emptying, protocol-directed EEF was feasible. Simultaneous administration of vasoactive agents for hemodynamic support and EEN was found safe and effective in another retrospective study.34 Tolerability was linked to the maximum cumulative vasopressor dose and the specific vasopressor used. In 2010, prospectively collected EEN data were analyzed retrospectively in a multi-institutional medical intensive care

unit (ICU) database of 1174 critically ill patients who were treated with vasopressors and mechanical ventilation.35 In this study, patients in the EEN group had a lower hospital mortality, and EEN was administered within 48 hours after onset of mechanical ventilation if the patient had a functional gut. However, this observational study had a selection bias when patients with poor ICU status received delayed enteral feedings. The study also failed to analyze the data of patients who were receiving vasopressors. In a study by Moore et al,36 half the patients following severe traumatic shock had fast intestinal migrating motility complex, which required intact neural and motor function and was associated with good tolerance to EEN. Several clinical studies have reported good tolerance to EEN in critically ill patients of hemodynamic instability, with notable bowel hyperemia and mucosal barrier maintenance. It was a common practice to withhold enteral feeding in patients on ECMO (extracorporeal membrane oxygenation), based on the resulting hemodynamic alterations and risk of splanchnic ischemia leading to loss of intestinal integrity, predisposing to bacterial translocation and sepsis.37 In recent studies, EEF was well tolerated by patients on ECMO under appropriate supervision, whether in venovenous or venoarterial mode, and intolerance did not differ between ECMO modes.38-40 It was suggested that feeding be withheld during initiation of ECMO until the subjects had stable hemodynamics and gas exchange (typically 12 to 24 hours) and that EEF be initiated as continuous intragastric feeding at 20 mL per hour, increasing the rate of delivery every 4 hours over 24 to 36 hours to the target rate.38 However, there was limited information from these retrospective observational studies. More studies are clearly warranted to confirm these findings. However, these studies are all small-scale, retrospective, descriptive, or case series and heterogeneous in EN dosage and observational patient population or items without adequate randomization and control. Formulating systematic evidencebased guidelines therefore remains difficult at present.

Reports of EEN-Associated NOMI or NOBN In 1995, Myers et al41 published their 16-year study results involving 1938 patients who were administered EN via catheter jejunostomy. All 3 NOBN patients used vasopressors for septic shock and variceal bleeding. Marvin et al1 reported 13 cases of bowel necrosis in 4311 traumatic patients with EEN. Four were related to vasopressor, and 11 were associated with inotrope. However, in this study, more than 60% of the patients did not receive vasoactive medications until the appearance of acute abdominal symptoms, which suggested that vasoactive medications may not contribute to most cases of NOBI or NOBN. In a study by Scaife et al,42 3 severely burned patients with hemodynamic instability had EN via catheter jejunostomy along with vasopressors. They developed ileus, followed by bowel necrosis 11-14 days after admission.

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Table 2.  Clinical Symptoms and Radiographic Signs of NOMI or NOBN.

agents, risk of intolerance and complication increases severalfold anyhow.

Clinical Symptoms •• •• •• •• ••

Sudden massive abdominal distention, bloating, or cramps Ileus, cessation of stooling or passing gas High nasogastric tube output Oliguria Shock

Radiographic Signs •• 25% to 30% of NOMI or NOBN patients may have normal radiographic images •• Dilated thickened loops of bowel with thumbprinting •• Air in the wall of the gastrointestinal tract •• Portal venous gas •• Air in the peritoneal space NOBN, nonocclusive bowel necrosis; NOMI, nonocclusive mesenteric ischemia.

Bowel ischemia may have been precipitated by increased mesenteric blood flow requirement in combination with metabolic stress. Clinical symptoms and radiographic signs of NOMI or NOBN should be continuously monitored in patients with EEN on vasopressors (Table 2).

Possible Factors Associated With Safety Outcomes Route of EEN No direct evidence of EEN leading to NOBN is currently available. Jejunal tube or catheter jejunostomy feeding is the regular route of EN. However, a series of case reports and retrospective studies show that when EEN and vasoactive agents are administered together to critically ill patients, jejunal feeding has the highest incidence of NOBN of 0.29% to 1.14%.2-6,43 Presumably, under conditions of bowel hypoperfusion and depressed peristalsis, when gastric or duodenal retention develops, the stomach could act as a buffering chamber. Whereas retention occurs on jejunal feeding, there is no buffering, and aggressive intraluminal tension will aggravate the bowel ischemia further. Therefore, EEN by jejunal route should be carefully monitored. Rapid increase of gastric residual volume, diarrhea, and abdominal distention are all signs of aggravated intestinal ischemia.11 EEN should be discontinued upon worsening of hemodynamic instability or systemic inflammatory response, followed by reevaluation of GI perfusion, even by laparotomy. Current reports suggest that postoperative, traumatic, and burned patients are high-risk groups for NOBN, with no data of NOBN involving nonoperative patients in ICU so far.1-6 Therefore, EEN by nasogastric tube in nonoperative patients is possibly a relatively low risk approach. Under hemodynamic support with vasoactive

EEN Dosage and Formula In hemodynamically unstable patients, EEN is administered primarily to maintain the intestinal mucosal barrier function rather than serve energy supplement. “Trophic” EN at the rate of 10 to 20 mL per hour is utilized in patients with increased risk, and most of their nutritional demand is provided parenterally.44 Immunonutrition with glutamine is not supported by evidence, especially in septic patients. A randomized trial recently showed that early intervention with glutamine and antioxidants in critically ill patients did not improve clinical outcomes. Instead, glutamine was associated with an increase in mortality among critically ill patients with multiorgan failure.45 Energy deficiency is often covered by parenteral nutrition (PN) supplementation. However, early supplemental PN in critically ill adults increases infection, length of ICU stay, and total cost.46 Trauma patients that receive EEN with PN supplementation have increased nosocomial infections compared to EN alone.47 Additional trials are warranted to identify critically ill populations that may benefit from combined EN and PN support under conditions of hemodynamic compromise. Hypertonic (>700 mOsm) or fiber-rich enteral solutions have been hypothesized to draw fluid into the gut, predisposing the patient to decreased GI tract perfusion as well as dysmotility.1 As there is no clinical evidence currently available supporting specific EEN dosage or formulation for hemodynamically unstable patients of critical illness, it is still controversial whether any of the supplements will benefit this specific patient population or exacerbate the GI ischemia.

Impact of Vasoactive Agents on Splanchnic Blood Flow In humans, disturbances in GI motility are directly related to the dose of dopamine and norepinephrine, as indicated by the reduced migration of feeding tubes in patients on high doses.48 The effects of vasoactive agents on the gut that are associated with EEN in hemodynamic instability have been discussed in detail in another review.49 Dopamine, norepinephrine, epinephrine, and vasopressin have shown ambiguous effects in splanchnic mucosal perfusion under different conditions of hemodynamic compromise experimentally and clinically.50-55 In general, dopamine, epinephrine, and vasopressin negatively regulate GI blood flow, which is minimally affected by norepinephrine. Inotropes such as dobutamine and milrinone, when used alone, increase cardiac index and GI blood flow.56 In clinical practice, multidrug combinations, individual drug susceptibility variations, and dose-dependent effects of vasoactive agents are common phenomena. Based on current evidence, it is really hard to estimate the risk of intestinal ischemia with different types of vasoactive agents.

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Table 3.  Current Controversies and Consensus of EEN in Hemodynamically Unstable Patients. Controversy •• Whether it is safe to deliver early enteral nutrition to patients with hemodynamic instability—if yes, how early is the best (< 6, 6-12, or 24-48 h?) •• Whether EEN in this patient population will induce gastrointestinal mucosal barrier dysfunction with bacterial translocation and systemic hemodynamic fluctuation or demand augment of vasoactive agent •• Current clinical studies are all small-scale, retrospective, descriptive, or case-series study and heterogeneous in patient population, enteral nutrition dosage, and observational items, without adequate randomization and control. •• Influence of EEN route, formula, and vasoactive agent in this patient population is uncertain.  

Consensus •• The degree of risk for NOBN is difficult to determine based solely on the absolute dose of vasoactive agents. •• EEN ought to start up when the patient is on stable or declining doses of vasopressors. •• Volume resuscitation is always the priority to EEN. •• Trophic feeding or nutrition (10-20 mL/h) with step-up progression is probably the best strategy for this patient population. •• Any radiographic or laboratory monitoring cannot take the place of tight observation of clinical symptoms and complaints.

EEN, early enteral nutrition; NOBN, nonocclusive bowel necrosis.

Summary According to current evidence, EEN in critically ill patients with hemodynamic instability is still a clinical controversy. Although available data indicate that EEN is able to safely restore splanchnic perfusion/oxygenation in hemodynamically unstable patients, the consensus is that vasopressors are not a contraindication in carefully monitored EEN. It seems imprudent to jump to conclusions given that NOBN is a serious complication with mortality as high as 80%.57 The casual relation between EEN and NOBN has yet to be clearly established in hemodynamic instability. The indications for EEN in specific subgroups of critically ill patients with hemodynamic instability need to be defined. The role of EEN, either alone or combined with PN, the safety, and the tolerability need to be determined as well. Existing studies are mostly limited to cardiac surgery. Additional investigation is warranted in patients with septic or traumatic shock, which is more common in ICU (Table 3). Unfortunately, no large randomized studies are available that address these issues authoritatively. Turza et al44 suggested a clinical guideline on EEN in 2009 along with vasoactive agents for critically ill patients on the basis of limited evidence available from case series, reviews, short-term randomized studies, and clinical experience. This article delineates a 4-tiered approach for EN in vasoactive agent–dependent patients. It emphasizes the significance of patient evaluation for premorbid medical and nutritional history, current physiologic status, and postinitiation clinical monitoring of clinical as well as radiographic signs and symptoms of NOMI. The indications for dosage of different vasopressors for EN are also listed. In the absence of all the details, a consensus is desirable (Table 3).

In conclusion, current knowledge of EEN in critically ill patients with hemodynamic instability is still incomplete. Additional randomized clinical trials are warranted to provide appropriate clinical guidance for practitioners of critical care.

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Nutrition in Clinical Practice 29(1)

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Early enteral nutrition in critically ill patients with hemodynamic instability: an evidence-based review and practical advice.

Early enteral nutrition (EEN) in critically ill patients is associated with significant benefit as well as elevated risk of complications. Concomitant...
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