NUTRITION
From the 42nd Annual Gastroenterology Update, presented by the Cleveland Clinic, Department of
Gastroenterology and Hepatology
| FEEDING THE CRITICALLY ILL PATIENT—Stephen A. McClave, MD, Professor of Medicine, University of Louisville
School of Medicine, Louisville, KY
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| Data on early feeding: between 12 to 24 hr and up to 72 hr to start feeding and change patient outcome; early vs delayed
feeding—cutoff 36 hr; with early feeding, infection reduced by 55%, hospital stay shortened by 2 days, and trend
toward reduced mortality by up to 50%; enteral feeding vs no nutritional support (standard therapy)—early aggressive
efforts at utilizing gut reduce infection by 28% and hospital stay by almost one full day; anastomotic dehiscence favors
aggressive use of enteral route (fewer problems); cumulative caloric balance—patient in intensive care unit (ICU)
expending certain number of calories daily; how quickly feeding and providing calories started determines caloric deficit
developed; European study—showed that overall complications increase as caloric deficit increases; cumulative deficit
correlates to longer hospital stay, more complications, more infections, and longer time on mechanical ventilation
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| Paradigm shift: previously—gut thought to be passive organ, and dysfunction included stress gastropathy and bleeding;
concern about ileus and need to start total parenteral nutrition (TPN); gut considered organ of inconvenience;
currently—gut considered dynamic organ; concerns with increase in permeability, bacteria in gut lumen engaging and
upregulating immune system, providing component to systemic inflammatory response syndrome; gut becomes proinflammatory
organ and part of multiple organ failure syndrome
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| Enteral feeding: supports function of organs at distant sites; not utilizing gut in critical illness leads to increase in gut permeability
and loss of functional and structural integrity; channels between epithelial cells open; when bacteria stick to epithelial
cells in abdominal wall, cells become immunoactive, leading to programmed cell death (apoptosis); phenomenon
time-dependent (window of opportunity 4-6 hr in burns, 24-48 hr in pancreatitis; 48-72 hr with major elective surgery) and
correlates with disease severity; consequences of increased permeability increased risk for infection and for organ failure;
Ziegler study—patients with major burns followed to determine who became infected; looked at markers for gut permeability
(urinary lactulose and mannitol); those who had no infection had no increases in gut permeability; those who became
infected had 3-fold increase in permeability; Canadian study—looked at organ failure and permeability in ICU patients;
results showed that whether participants developed primary or secondary organ failure, number of organs that failed, and degree
of organ failure all correlated to abnormalities of intestinal permeability on admission; previously thought that when
channels opened, bacteria would move across and work way to lungs (bacterial translocation); study—250 participants on
surgical service; cultures from portal vein negative; bacterial translocation phenomenon of laboratory rats; subsequently
learned that action occurs in lymphatic channels (not in portal vein); bacteria do not have to move across; opening of channels
allows bacteria to engage macrophages and neutrophils at surface of gut; cytokines and activated neutrophils released
into lymphatic channels; lymph carries them to distant sites; after leaving gut, first capillary bed encountered in lungs, hence
connection between feeding or not feeding and pneumonia, acute respiratory distress syndrome (ARDS), and respiratory
failure
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| Immune response: innate immune system—acts within 3 to 5 hr and involves macrophages and natural killer T cells;
macrophages activated because channels open and bacteria engage them, or because of reduced blood flow to gut and ischemia
reperfusion; once activated, neutrophils flowing through circulation of gut primed and move to distant sites where
second insult (eg, hypoxemia, hypotension) activates them; diapedesis occurs, organ injured, and level of oxidative stress increases;
increased stress leads to increased complications; acquired immune system—3- to 5-day process; involves proliferation
of lymphocytes (dendritic macrophages) that sample lumen of gut; when patient fed, macrophages sample normal
number of bacteria (commensal bacteria); macrophages do not respond to commensal bacteria (cooling effect on immune
system); food antigen present, and interleukin (IL)-4 released; if patient not fed, macrophages sample bacterial overgrowth
because of reduced contractility; most likely pathogenic bacteria; food antigen absent and IL-12 released; after sampling
bacteria, macrophages migrate back to lamina propria where naive CD4 helper lymphocytes reside; cytokine shower occurs;
if patient not fed—cytokine shower IL-12, causing naive lymphocytes to develop along T-helper type 1 (TH 1) pathway; at
level of gut, this pathway proinflammatory, and cells release interferon and tumor necrosis factor (TNF), which spill over
into systemic circulation; if patient fed—cytokine shower IL-4 and naive lymphocytes develop along TH 2 pathway, which
directly opposes TH 1 pathway; T regulatory type 1 (TR 1) and TH 3 pathways involved in oral tolerance also activated; net
clinical effect of these pathways to reduce inflammation and calm immune system
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| Enteral nutrition in ICU: study—at speaker’s institution, residents and staff ordering only 65% of daily caloric requirements;
problems with delivery (only 15% of patients got to goal within 3 days; ideally, goal reached in 36 to 48 hr); combined
defects of underordering and underdelivery meant patients received only 50% of caloric requirements; effect of enteral
feeding dose-dependent; speaker’s conclusion—providing 55% to 60% of goal caloric requirement necessary for gut integrity
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| Permissive underfeeding: obese patients given 60% of goal calories lose weight and do well, provided enough protein
given for wound healing; for patients on TPN, if 80% of requirements provided, insulin sensitivity improves; application to
nonobese patients on enteral feeding worrisome; Krishnan study—25 cal/kg per day caloric goal; middle tertile had higher
survival and off ventilator earlier than lowest tertile; top tertile had lower survival and stayed on ventilator longer than lowest
tertile; Ibrahim study—only 27% of calories infused in group supposed to get 100%; group supposed to get 20% of
goal calories got only 7%; group that received lesser feedings did better; became basis for statement that early enteral feeding
ineffective and permissive underfeeding good idea; study too flawed to be useful; meta-analysis by Heyland—studies
looked at mortality with enteral feeding alone vs supplemental TPN with enteral feeding; trend towards improved mortality
with enteral feeding alone ); no difference in infection, hospital length of stay, and days on ventilator; adding TPN may
worsen mortality; evidence that TPN suppressing immune function; concept of permissive underfeeding shaky
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| Providing expertise on gut function and tolerance: help nutrition team in ICU evaluate gut and segmental contractility;
based on assessment, select tube and determine location of tube and need for decompression of stomach; correct electrolytes
and modulate sedation and analgesia to promote contractility; can give naloxone (Narcan) through feeding tube
(removes effects of narcotic at level of gut and does not affect central nervous system sedation); minimize periods of ileus by
being aggressive in early placement of tubes; develop concept of feeding ileus (no need to wait for bowel sounds); study—
looked at use of Narcan to reverse effects of fentanyl at level of gut; amount of enteral feeding patients received increased,
gastric residual volumes decreased significantly, and incidence of pneumonia reduced from 56% to 34%; encourage use of
immune formulas— adding immune stimulants, substituting fish oil for traditional omega-6 fats, and adding cocktail of
antioxidants results in greater impact on outcome than with standard enteral feeding formula; meta-analysis—immune formula
vs standard formula; using immune formula reduced infections from 55% to 75%, organ failures by 80%; amount of
time on ventilator, in ICU, and in hospital reduced by 1.5 to 3.5 days
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| Monitors for aspiration: deterrent to delivery of enteral feeding and do not prevent aspiration; 2 studies looked at how
often aspiration occurs; evidence of aspiration seen 22% to 30% of time if patient checked at bedside every 4 hr; affects
nearly all patients (75%-89%); frequent unwitnessed aspiration events; aspiration does not mean patient will get pneumonia;
depends on host factors, (eg, patient’s age, comorbidities) and on aspirate (eg, volume, bacterial contamination, presence
of acid); pneumonia more linked to aspiration of colonized oropharyngeal secretions than to infected gastric
contents; monitors insensitive, inaccurate, and impede enteral feeding
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| Reassessing monitors: study looking at aspiration events showed that as patient remains in hospital, aspiration events
increase, increasing risk for pneumonia; number of accumulated aspiration events higher in group who got pneumonia;
those with highest frequency of aspirations stayed in hospital or ICU 2 days longer and on ventilator 3 days longer
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| Residual volumes: 5000 mL of salivary and gastric secretions daily added to enteral feeding of 25 to 125 mL/hr; assume
normal gastric emptying of 35% to 50% per hour; expect that up to 464 mL/hr go through normal stomach; 2 studies randomized
patients to 2 different gastric residual volume cutoffs; incidence of aspiration no different; incidence of aspiration
does not change across range of residual volumes; refractometry improves accuracy of measuring and analyzing residual
volumes
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| Reducing risk for aspiration: move level of feeding farther down gastrointestinal tract; Canadian study showed that
changing level from stomach to third portion of duodenum reduced incidence of aspiration significantly; unknown
whether risk for pneumonia reduced; using mouthwash twice daily reduces risk for pneumonia by 70%
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| Conclusion: results of speaker’s study of targeted education to promote enteral feeding show near elimination of clear liquids,
reduction of caloric deficit by 23%, trend towards reduction of days in ICU (2 days) and multiple organ failure
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| NUTRITION ISSUES IN CHRONIC PANCREATITIS—Darwin Conwell, MD, Director of Pancreas Clinic, Department of
Gastroenterology and Hepatology, Cleveland Clinic Foundation, Cleveland, OH
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| Chronic pancreatitis: results in pain and steatorrhea; if patients report visible droplets of oil in stool, definitely evidence
of pancreatic insufficiency or at least malabsorption; usually see increased volume of stool, light-colored stool, and
foul odor; most of pain due to complications; in late-stage disease, may have maldigestion; latency of pancreatic insufficiency
and steatorrhea different, depending on whether etiology from alcohol or idiopathic; depletion of nutrients, increased
metabolic activity in pancreas, weight loss, and postprandial pain present; up to 90% pancreatic exocrine
function loss required for clinical steatorrhea; expect deficiency in fat-soluble vitamins (A, D, E, and K) but often normal
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| Physiology: secretin stimulates pancreatic duct cells; cholecystokinin (CCK) stimulates acinar cells; cholinergic stimulation
and regulation of pancreatic secretions; secretin stimulates basolateral surface (secondary mediator cyclic adenosine
monophosphate [cAMP]), resulting in bicarbonate and water secretion into ducts; chloride also involved; cystic fibrosis
(CF) transmembrane regulator mutated in patients with CF; in CCK pancreatic function testing, stimulating primarily acinar
cells and secondary messengers results in exocytosis of protein-rich thick tenacious fluid that gets into pancreatic acinus
(secretion of duct cells thin this for entry into duodenum); tri-glycerides digested with lipase and colipase from
pancreas, with resulting formation of dimonoglycerides and fatty acids; steatorrhea—>100 droplets of fat on qualitative
fat stain (Sudan stain) strongly suggestive of pancreatic steatorrhea; mechanism includes decreased concentrations of lipase
and colipase; pancreatic lipase inactive if duodenal pH <4.5; problem of bile salt precipitation with low duodenal
pH; while healthy people have high bicarbonate concentration in duodenum, patients with chronic pancreatitis have low
bicarbonate (acidic fluid in duodenum; inactive enzymes); no difference between coated and uncoated enzymes when
given for steatorrhea; may have to add proton pump inhibitor (PPI) to protect lipase in stomach from destruction by acid
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| Terminology: basal energy expenditure (BEE)—amount of energy required for essential body functions; resting energy
expenditure (REE)—amount of energy required when body at rest; total energy expenditure—combination of
REE and BEE and includes diet-induced thermogenesis and shivering as well as physical activity; indirect calorimetry assesses
energy expenditure based on O2 consumption and CO2 production during respiratory gas exchange; study—looked
at REE in patients with chronic pancreatitis; group 1, 13 patients with alcohol-related chronic pancreatitis and normal
weight; group 2, 20 underweight patients with alcohol-related pancreatitis; group 3, undernourished patients without identifiable
disease; found group 2 patients hypermetabolic; REE >110% of predicted; when adjusted for fat-free mass, REE statistically
significantly higher in group 2 patients; concluded that in chronic pancreatitis, weight loss accompanied by
hypermetabolism (should be considered during nutritional support); patients on enzyme therapy had higher albumin and percentage
of ideal body weight
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| Metabolic bone disease in early and late chronic pancreatitis
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 | CF: benefits of long-term enzyme therapy well documented; multiorgan system disease; have longstanding pancreatic insufficiency;
bone mineralization 20% less in CF than in normal patients; accelerated bone loss in CF; 30% of patients
with CF have significant reduction in bone mineral density; 80% of adults with CF have osteoporosis
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| Chronic inflammatory bowel disease: more bone disease in Crohn’s disease (CD) than in ulcerative colitis (UC); effect of
chronic inflammation on bone metabolism—cytokines play role; TNF decreases osteoblast activity and increases
osteoclast activity; increased osteoclast survival and decreased osteoblast apoptosis; IL-1 and IL-6 stimulate osteoclast
activity; in chronic pancreatitis, risk factors for metabolic bone disease similar to those in CD and UC; include age,
presence of chronic inflammatory condition, physical inactivity, smoking, female sex, alcohol abuse, and maldigestion;
speaker’s case series found that older women with chronic pancreatitis who smoke and abuse alcohol have even
greater increased risk of developing metabolic bone disease
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| Recommendations: nutritional assessment of patients with chronic pancreatitis; stratify patients based on pancreatic
function tests; determine risk for bone density loss and which patient should have bone density measurement; pancreatic
enzyme therapy—assess effects on absorption of vitamin D and calcium; should be administered early in chronic pancreatitis;
may retard bone density loss; utility of modifying fat intake unknown, although patients feel better and have less
steatorrhea; medium-chain triglycerides given if patient has severe insufficiency; dietary recommendations—include
abstinence from alcohol, 30% to 40% fat in diet well tolerated; frequent meals (4-5) daily; 1 to 1.5 g of protein and carbohydrate-rich
meals; pancreatic enzyme therapy (6 to 8 pills per meal); enteral nutrition rarely needed, unless patient undergoing
surgery
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Suggested Reading
Bodoky G et al: Effect of enteral nutrition o.exocrine pancreatic function. Am J Surg 161:144, 1991; Chang WK et
al: Use of the refractometer as a tool to monitor dietary formula concentration in gastric juice. Clin Nutr 21:521, 2002;
Herndon DN et al: Increased mortality with intravenous supplemental feeding in severely burned patients. J Burn Care
Rehabil 10:309, 1989; Heyland DK et al: Canadian clinical practice guidelines for nutrition support in mechanically
ventilated, critically ill adult patients. 27:355, 2003; JPEN; Heyland DK et al: Effect of postpyloric feeding on gastroesophageal
regurgitation and pulmonary microaspiration: results of a randomized controlled trial. Crit Care Med 29:1495,
2001; Lewis SJ et al: Early enteral feeding versus "nil by mouth" after gastrointestinal surgery: systematic review and
meta-analysis of controlled trials. BMJ 323:773, 2001; Marik PE et al: Early enteral nutrition in acutely ill patients: a
systematic review. Crit Care Med 29:2264, 2001; Erratum in: Crit Care Med 2002; Marik PE et al: Meta-analysis of
parenteral nutrition versus enteral nutrition in patients with acute pancreatitis. BMJ 328:1407, 2004; Marik PE: Aspiration
pneumonitis and aspiration pneumonia. N Engl J Med 344:665, 2001; McClave SA et al: Enteral tube feeding in
the intensive care unit: factors impeding adequate delivery. Crit Care Med 27:1252, 1999; McClave SA et al: Nutritional
management in acute and chronic pancreatitis. Gastroenterol Clin North Am 27:421, 1998; McClave SA et al:
Poor validity of residual volumes as a marker for risk of aspiration in critically ill patients. Crit Care Med 33:324, 2005;
Meissner W et al: Enteral naloxone reduces gastric tube reflux and frequency of pneumonia in critical care patients during
opioid analgesia. Crit Care Med 31:776, 2003; Neumann DA et al: Gastric versus small-bowel tube feeding in the
intensive care unit: a prospective comparison of efficacy. Crit Care Med 30:1436, 2002; Stanga Z et al: Effect of jejunal
long-term feeding in chronic pancreatitis. JPEN J Parenter Enteral Nutr 29:12, 2005; Taylor SJ et al: Prospective,
randomized, controlled trial to determine the effect of early enhanced enteral nutrition on clinical outcome in mechanically
ventilated patients suffering head injury. Crit Care Med 27:2525, 1999; Trolli PA et al: Pancreatic enzyme therapy and
nutritional status of outpatients with chronic pancreatitis. Gastroenterol Nurs 24:84, 2001; Ziegler TR et al: Increased
intestinal permeability associated with infection in burn patients. Arch Surg 123:1313, 1988
Educational Objectives
| The goal of this program is to improve nutritional management of critically ill patients and patients with chronic pancreatitis.
After hearing and assimilating this program, the clinician will be better able to:
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| Recognize the advantages of early feeding in the critically ill patient.
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| Describe the concept of permissive underfeeding
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| Utilize methods that reduce the risk for aspiration.
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| Recognize and prevent metabolic bone disease in patients with chronic pancreatitis.
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| Propose dietary recommendations for patients with chronic pancreatitis.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members to disclose
relevant financial relationships within the past 12 months that might create any personal conflicts of interest. Any
identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary
business or commercial interest. For this program, the following has been disclosed: Dr. McClave has received
research support from Nestle and is on the Speakers’ Bureaus of Ross, Nestle, Novartis, and Coram.
Acknowledgements
Drs. McClave and Conwell were recorded at the 42nd Annual Gastroenterology Update, held November 16-17,
2006, in Cleveland, OH, and sponsored by the Cleveland Clinic, Department of Gastroenterology and Hepatology.
The Audio-Digest Foundation thanks the speakers and the sponsor for their cooperation in the production of this program.
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