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diminishes in-hospital mortality. Pancreatology.
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39. Eckerwall G, Olin H, Andersson B, etal. Fluid resuscitation and nutritional support during severe acute
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JeniferBarrie andDileepN.Lobo
Key Points
1. Patients with severe acute pancreatitis should
be considered to be at moderate to high nutritional risk, because of the catabolic nature of
the disease and the impact of the patient’s
nutritional status for disease development.
2. The majority of patients with acute pancreatitis will experience a mild clinical course with
a short hospital stay and do not need articial
nutritional support unless malnourished.
3. All patients with acute pancreatitis should be
screened for nutritional risk using validated
screening methods. Those found to be at
nutritional risk should have a formal nutritional assessment.
Jenifer Barrie and Dileep N. Lobo contributed equally
with all other contributors.
J. Barrie
Nottingham Digestive Diseases Centre, Division of
Translational Medical Sciences, School of Medicine,
University of Nottingham, Queen’s Medical Centre,
Nottingham, UK
e-mail: j.barrie@nhs.net
4. Enteral nutrition is useful in the treatment or
prevention of malnutrition in patients with
severe acute pancreatitis when the gut is
functional.
5. Parenteral nutrition, including fat, is well tolerated, does not stimulate pancreatic secretion
and can minimise malnutrition when gastrointestinal dysfunction is prolonged.
6. A combination of enteral and parenteral nutrition is a reasonable way to meet metabolic
demands in these patients, and the amount of
nutrients delivered parenterally can be progressively reduced as larger volumes are tolerated enterally.
7. Particular attention should be paid to prevent
refeeding syndrome.
D. N. Lobo (*)
National Institute for Health Research (NIHR)
Nottingham Biomedical Research Centre,
Nottingham University Hospitals NHS Trust and
University of Nottingham, Queen’s Medical Centre,
Nottingham, UK
MRC Versus Arthritis Centre for Musculoskeletal
Ageing Research, School of Life Sciences, University
of Nottingham, Queen’s Medical Centre,
Nottingham, UK
e-mail: Dileep.Lobo@nottingham.ac.uk
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2024
J. A. Windsor et al. (eds.), Acute Pancreatitis, https://doi.org/10.1007/978-981-97-3132-9_11
161
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1 Introduction
Patients with acute pancreatitis, particularly the
severe form, should be considered to be at moderate to high nutritional risk, because of the
catabolic nature of the disease and the impact
of the patient’s nutritional status for disease
development [1, 2]. The principles of nutritional management of patients with acute pancreatitis have evolved over several decades.
Traditionally the concept of ‘pancreatic rest’
(which is perhaps the oldest dogma in the management of acute pancreatitis) was used, and it
was considered that enteral nutrition (EN),
delivered into any part of the upper gastrointestinal tract other than the jejunum, stimulates
pancreatic enzyme secretion, leading to
increased pancreatic autodigestion and, consequently, exacerbation of the severity of acute
pancreatitis [1, 3]. This concept is based on
only physiologic assumption and is not supported by good-quality scientic evidence [1,
4]. Further studies have found that pancreatic
enzyme secretion is signicantly reduced in
acute pancreatitis and the secretion was
inversely related to the severity of pancreatitis
[4]. A lower secretion of trypsin, amylase and
lipase was found in severe pancreatitis [5], and
these data suggest that the injured acinar cells
cannot fully respond to physiologic stimuli, and
may explain why enteral feeding is safe and
does not worsen autodigestion during an attack
of pancreatitis [4]. This chapter outlines the
current principles of nutritional support of
patients with acute pancreatitis.
The majority of patients with acute pancreatitis will experience a mild clinical course with
a short hospital stay, whereas 10–20% of
patients will develop severe acute pancreatitis
with organ failure [6]. In severe acute pancreatitis, with the systemic inammatory response
syndrome (SIRS), the body enters a state of
hypermetabolism and high protein breakdown,
and during the course of the disease, the
patient’s energy and muscle reserves are
depleted rapidly [7].
2 Assessment ofNutritional
Requirements
Approximately one-third to two-thirds of patients
with pancreatic diseases are at risk of malnutrition [8], but the incidence of malnutrition in
patients with acute pancreatitis has not been specically quantied. Patients with increased alcohol consumption and those with chronic
substance misuse are more likely to have preexisting malnutrition and, in addition, may be
depleted in micronutrients and vitamins [9].
Although there is no direct evidence that
nutritional screening has an impact on outcome
in acute pancreatitis, it is good clinical practice
to screen all patients for nutritional risk at
admission using validated screening methods
such as the Nutritional Risk Screening 2002
(NRS-2002) [10] or the Malnutrition Universal
Screening Tool (MUST) [11]. However,
patients with predicted severe acute pancreatitis should always be considered at nutritional
risk because of SIRS and the catabolic nature
of the disease [2]. If patients are found to be at
nutritional risk, nutritional assessment can be
done using a variety of approaches, such as
anthropometric and body composition measurements, food and nutrition- related history,
clinical signs, biochemical data and functional
assessment [12]. More recently, the Global
Leadership Initiative on Malnutrition (GLIM)
criteria have been advocated to diagnose malnutrition [13]. The GLIM criteria are a twostep approach for the diagnosis of malnutrition:
rst, screening to identify ‘at risk’ status by the
use of any validated screening tool and, second, assessment for diagnosis and grading the
severity of malnutrition [13]. The current
approach to screening for and diagnosis of
malnutrition is summarised in Fig.1 [14].
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Fig. 1 Current approach to screening and diagnosis.
Approach to screening is according to NRS-2002 [8] and
diagnosis is according to GLIM [11]. BIA bioelectrical
impedance analysis, BMI body mass index, DXA dual-
energy X-ray absorptiometry, GLIM global leadership
initiative on malnutrition, NRS nutritional risk screening.
Reproduced from Schuetz P etal. [14], with permission
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3 Malnutrition inPancreatitis
Resting energy expenditure (REE) in patients
with acute pancreatitis is generally higher than in
healthy individuals [15] because of a combination of inammation-induced hypermetabolism
and septic complications. It is also imperative
that sepsis is dealt with, both to treat the disease
and to achieve nutritional gains [15]. In fact,
almost 60% of patients with severe acute pancreatitis have an increase in resting energy expenditure, and this increases when complicated by
infection. Approximate net nitrogen losses are
20–40g per day, and proteolysis of skeletal muscle can increase by up to 80% [16]. The circulating pool of amino acids decreases to as low as
40% of normal levels, while circulating and skeletal muscle glutamine levels drop to as low as
55% and 15%, respectively [17]. In one study it
was found that muscle mass and function (measured by grip strength and respiratory muscle
strength) rapidly decreased within 5days without
nutritional support in healthy men suffering from
acute pancreatitis [18].
Energy requirements should be estimated with
indirect calorimetry (IC) if possible, or 25kcal/
kg/d can be used as energy goal. A number of
variables affect energy expenditure in severe pancreatitis, such as body temperature, volume status and medications, making predictive equations
inaccurate and of limited value. Nevertheless, IC
remains the gold standard to determine energy
expenditure, helping to prevent over- or
underfeeding [19]. It is recommended that energy
requirements are re-evaluated more than once per
week in order to ensure accurate energy balance
[4].
4 Gut Factors inAcute
Pancreatitis
Micro-organisms responsible for pancreatic
infection and septic complications are generally
common enteric bacteria normally present in the
gut [20]. Gut barrier dysfunction may occur in up
to 60% of patients with acute pancreatitis, mostly
in severe acute pancreatitis. It is thought to lead
to bacterial translocation and infection of necrosis [21]. The mechanisms in gut barrier dysfunction includes microcirculatory injury and
hypovolemia, leading to gut mucosal ischaemia
and reperfusion injury resulting in loss of gut barrier integrity [22]. Vulnerable ischaemic gut is
also subject to the digestive action of activated
pancreatic enzymes in the proximal small bowel
[23], and this is, perhaps, an overlooked mechanism of injury.
The use of probiotics containing live microorganisms of healthy gut ora has been shown to
be detrimental in acute pancreatitis [24], and
until an acceptable safety prole can be proven,
their use should be avoided [25]. However, it is
possible that the increased intestinal ischaemic
events in the PROPATRIA study [24] had little to
do with probiotics themselves but the aggressive
approach to EN in patients who still had splanchnic vasoconstriction and were
under-resuscitated.
Acute pancreatitis is also associated with deciency of various vitamins and micronutrients
including vitamins B1, B2, B3, B12, C, A, folic acid
and zinc [26]. This could be pre-existing (as in
the case of some patients with alcohol-induced
pancreatitis) or could develop during the course
of the disease. This may be both a cause and
effect of gut dysfunction.
5 Obesity
Obesity has long been considered a risk factor for
mortality in pancreatitis, as well as a risk factor
for local and systemic complications [27, 28].
Excessive proinammatory cytokines derived
from visceral adipose tissue can promote the
development of SIRS, which is thought to progress to organ failure and lead to death in patients
with severe acute pancreatitis [29]. Obese patients
have increased intra-pancreatic fat [30], and evidence suggests that the release of nonesteried
fatty acids from pancreatic adipocytes may
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165
potentiate local pancreatic injury during acute
pancreatitis [31]. Emerging evidence suggests
that an obesity paradox also exists in patients
with acute pancreatitis [32] and the presence of
obesity may be protective.
At present there is a paucity of literature on
feeding in obese patients with acute pancreatitis.
However, in one recent study, it took longer for
class III obese (BMI>40kg/m2) patients to reach
goal rate of jejunal feeding than non-class III
obese patients, and this correlated with mortality
[33]. It has been found in the laboratory that obesity aggravates acute pancreatitis via damage to
the intestinal mucosal barrier and changing the
composition of microbiota [34]. It is, thus,
thought that obese patients have altered intestinal
mucosal reactions to EN [33].
6 Evolution ofNutritional
Support inAcute
Pancreatitis
The contemporary evidence for nutritional support in patients with acute pancreatitis has been
summarised in Table1 [35–38], and an overview
of the twentieth-century literature can be found
here [1].
6.1 Oral Nutrition
The European Society of Parenteral and Enteral
Nutrition (ESPEN) recommends that oral feeding
with low-fat diet may be offered as soon as it is
clinically tolerated in patients with predicted
mild acute pancreatitis, independent of serum
lipase (or amylase) concentrations [2]. The
proven benets of early oral feeding in patients
with mild to moderate acute pancreatitis are now
well recognised and have been translated into
clinical practice. Patients are able to tolerate this,
and it correlates with a shorter length of stay
when compared with conventional oral feeding
practices (traditionally introduced after resolution of symptoms or decrease in serum lipase or
amylase) [39]. It is acceptable to start an oral diet
without waiting for abdominal pain to abate,
peristalsis to begin or appetite to recover. There is
no benet to applying restrictions based on biochemical results such as serum lipase or amylase
concentrations, leukocyte counts or C-reactive
protein concentrations in order to commence diet
in patients with mild or moderate acute pancreatitis [40]. Oral feeding in the literature has classically been dened as immediate and early.
More recently, immediate oral feeding and
hunger- based feeding [41] have been studied.
Table 1 Contemporary evidence for current management of nutritional support in patients with acute pancreatitis
Author Year Type of study Clinical question Conclusions
Al-Omran
etal. [35]
Bakker
etal. [36]
Dutta etal.
[37]
Jiang etal.
[38]
EN enteral nutrition, PN parenteral nutrition, NJ nasojejunal, NG nasogastric
2010 Cochrane
2014 Multicentre,
2020 Cochrane
2020 Systematic
systematic
review
randomised
clinical trial
systematic
review
review and
meta-analysis
PN vs. EN effect on
mortality, morbidity and
length of hospital stay in
patients with acute
pancreatitis
Early nasoenteral tube
feeding vs. oral diet at 72h
after presentation with acute
pancreatitis
NJ vs. NG in severe acute
pancreatitis effect on
mortality, morbidity and
nutritional status
Clinical benet of
glutamine-supported early
EN in patients with severe
acute pancreatitis
Enteral nutrition signicantly reduced
mortality, multiple organ failure, systemic
infections and the need for operative
interventions compared to those who received
PN
Early nasoenteral tube feeding was not
superior to oral diet in patients with acute
pancreatitis at high risk for complications
Insufcient evidence to conclude that there is
superiority, inferiority or equivalence between
the nasogastric and nasojejunal mode of
enteral tube feeding in people with severe
acute pancreatitis
Glutamine-supported early EN is benecial in
severe acute pancreatitis management
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Fig. 2 Suggested algorithm for nutritional support in patients with acute pancreatitis
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Hunger-based feeding is established on the physiology of hunger and the fact that experiencing
hunger in acute pancreatitis demonstrates recovery of the gut [41]. The ESPEN guidelines recommend using low-fat, oral diet when reinitiating
oral feeding in patients with mild acute pancreatitis [2]. Figure2 demonstrates the role of oral
feeding in acute pancreatitis.
Around 16% of patients with mild or moderate acute pancreatitis may have intolerance to
oral feeding [25]. Oral feeding intolerance (OFI)
is characterised by recurrent gastrointestinal
symptoms on resuming an oral diet, such as
abdominal pain, nausea and vomiting [42]. This
is often accompanied by biochemical abnormalities and increased opioid requirements [42].
Relapse of pain can occur in 20% of patients after
oral refeeding, which may, in turn, suggest severe
acute pancreatitis [43]. Risk factors for OFI are
summarised in Table 2. The timing of initiation
of an oral diet does not appear to be related with
the development of OFI, but OFI has been found
to be associated with worse clinical outcomes
including longer hospital length of stay and
increased risk of admission to intensive care [42].
Oral food intake in patients undergoing minimally invasive necrosectomy is safe and feasible
and may be initiated in the rst 24h after the procedure, if the clinical state (haemodynamic stability, septic parameters, gastric emptying) of the
patients allows it [2]. Patients with acute pancreatitis who are discharged with gastrointestinal
symptoms, or without having tolerated solid diet
during their hospital stay, are at higher risk of
early readmission [44]. Nausea and vomiting
Table 2 Risk factors associated with oral feeding intolerance (OFI) in patients with acute pancreatitis
Risk factors
Younger age
Male sex
Smoking
Active alcohol use
Elevated admission blood urea nitrogen
High admission haematocrit
Non-biliary pathology
Systemic inammatory response at 48h after
admission
Pancreatic necrosis
may be due to gut dysmotility. Strategies to
reduce this include the use of prokinetic agents
and, in a recent study, soluble dietary bre [45].
6.2 Enteral Nutrition
Oral feeding is sometimes not appropriate in
patients with acute pancreatitis due to OFI often
associated with signicant symptoms of pain,
nausea and vomiting, gastrointestinal dysmotility
and severe or necrotising disease. The severity of
pancreatitis is in itself not a contraindication to
oral feeding. The preferred primary feeding route
in patients with severe acute pancreatitis is
enteral, as there are benets over parenteral feeding [2]. For example, recent studies have found
more than a twofold reduction in rates of multiorgan failure and almost a fourfold reduction in
pancreatic necrosis with EN compared with parenteral nutrition (PN) across all severities of
acute pancreatitis [46]. According to the ESPEN
guidelines, EN should be started early, within
24–72h of admission, in case of intolerance to
oral feeding [2]. EN carries a lower potential for
hyperglycaemia than PN [47]. The benets of
enteral over PN are most observable when EN is
started within 48h of admission [48].
However, aggressive EN in critically ill
patients is not without risk. Abdominal distension
caused by aggressive enteral feeding can compromise ventilation and respiratory function [49] and
can also lead to an increase in intra- abdominal
pressure and compartment syndrome. A multicentre study in critically ill patients showed that one
or more gastrointestinal complications occurred
in 62.8% of patients receiving EN, necessitating
the withdrawal in 15.2% of patients [50]. Patients
with gastrointestinal complications had a longer
hospital stay (20.6 vs. 15.2days, P<0.01) and a
higher mortality rate (31 vs. 16.1%, P < 0.001)
than those without gastrointestinal complications
[50]. The metabolic stress of aggressive enteral
feeding in the under- resuscitated patient and in
some critically ill patients can increase the risk of
non-occlusive mesenteric ischaemia or enteral
feeding intolerance (EFI) [51].
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EN comprises nutritional preparations in liquid form, which are absorbed by the intestines.
Typically, it involves the administration of nutrients directly into the stomach or small intestine.
This can be done with either a nasogastric tube
(NG) or a nasojejunal tube (NJ). NG feeding carries the advantages of ease of commencement
due to the simplicity of bedside placement compared with the need for uoroscopic or endoscopic placement of a NJ tube. There is a known
aspiration risk with NG feeding, particularly in
patients with a reduced Glasgow Coma Score.
Any degree of gastroparesis or gastric outlet or
duodenal obstruction resulting from retroperitoneal inammation in severe pancreatitis is a contraindication to nasogastric feeding [37]. These
patients will have early satiety, nausea and vomiting. In this case, insertion of a NJ tube should be
considered, and a NG tube may be left in situ for
gastric decompression. In a recent meta-analysis,
post-pyloric feeding had a lower incidence rate of
pulmonary aspiration, gastric reux and pneumonia. It has also been attributed with a reduced
incidence of gastrointestinal complications such
as vomiting, nausea, diarrhoea, abdominal distension, high gastric residual volume and constipation. It has been associated with more optimal
nutrition as measured by the percentage of total
nutrition provided to the patient, the time to tolerate EN and the time required to reach nutritional
targets. Shorter length of mechanical ventilation,
critical care and hospital stay have also been
attributed to post-pyloric feeding [52]. However,
in an up-to-date Cochrane systematic review
looking at severe acute pancreatitis, there was not
sufcient evidence to conclude that there is superiority, inferiority or equivalence between the NG
and NJ mode of enteral tube feeding [37]. In
practical terms it would be benecial to insert the
NG and start feeding into the stomach and then
change to post-pyloric feeding if there were any
early signs of gastric outlet obstruction or
impaired gastric emptying.
In patients who need tube feeding, current
guidelines recommend continuous feeding over
bolus feeding [53]. Better feeding tolerance and
fewer interruptions of delivery of EN due to ele-
vated residuals and vomiting were found with
continuous infusion of feed [54].
A wide range of supplemental feeds are available, but the main categories of feed are broadly
subdivided into oligomeric feeds, polymeric
feeds and immunonutrition [25]. EN can also be
given orally, most often as a supplement to oral
intake (oral nutritional supplements—ONS) [20].
Oligomeric, also termed semi-elemental, formulations contain small peptides, medium chain
fatty acids and simple polysaccharides. Polymeric
feeds contain full proteins, complex lipids and
carbohydrates. Oligomeric formulations do not
require digestion by pancreatic enzymes, so, in
theory, these offer a greater degree of pancreatic
rest than the polymeric feeds [25] and, although
more expensive, they are better tolerated in
patients with acute pancreatitis. Having said that,
there has been no demonstrable clinical advantage with the use of oligomeric formulations, so
relatively inexpensive polymeric formulations
should be used [25]. Other specialised formulations are also available for clinical use.
Immunonutrition refers to specialised formulations composed of immunomodulatory supplements that are believed to enhance the immune
response. These formulations are enhanced by
specic amino acids such as glutamine or arginine, ω3FAs and nucleotides with the potential to
modify the immune response [37]. Data from
experimental studies have demonstrated that
marine ω-3 polyunsaturated fatty acids (ω3FAs)
have anti-inammatory properties [55]. ω3FA
administration in the early phase of acute pancreatitis and sepsis appears safe and has the potential
to reduce the incidence of acute organ dysfunction, infectious complications and mortality [56].
Glutamine improves lymphocyte function and
contributes to antioxidative defences. It can also
support the intestinal integrity and decrease bacterial translocation, hence reducing systemic
inammatory responses and sepsis, which are
important in critical illnesses such as acute pancreatitis [57]. Glutamine-supplemented EN has
been shown to improve outcomes in pancreatitis
in terms of mortality, multi-organ failure and
length of hospital stay in initial studies. It has
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also been found that supplementing PN but not
EN with glutamine may be of value [58].
Additional high-quality, large-scale RCTs or
multi-centre collaborative research is required to
conrm these ndings [38].
When EN is not feasible (EFI) or contraindicated and PN is indicated, parenteral glutamine
should be supplemented at 0.20 g/kg/day of
L-glutamine [2]. The advantages of glutamine
supplementation include reduced mortality [59],
rate of infections and length of hospital stay
[59–61], but large-scale high-quality trials are
necessary before glutamine can be recommended
in routine clinical practice.
Other specialised formulations include breenhanced formulations that can stimulate the
growth of normal enteral micro-organisms,
probiotic- enhanced formulations containing live
bacteria or yeasts and symbiotic formulations that
contain probiotics and prebiotic bres. There is
not enough evidence to support any of these formulations as a preferred feeding method [37, 62].
EN can be given safely even in severe acute
pancreatitis complicated by stulae, ascites or
pseudocysts [63] unless there is EFI.In cases of
ileus, it is still suggested to administer EN in
reduced amounts [63]. Common complications
in patients receiving EN include EFI, abdominal
distension, diarrhoea and tube displacement or
blockage [7]. In the event of EFI, patients should
be started on PN within 72h [64]. Trophic feeding, dened as a small volume of balanced EN
insufcient for the patient’s nutritional needs, has
been recommended as it may help maintain gastrointestinal mucosal integrity and produce some
positive gastrointestinal or systemic benet [65].
There is, however, no specic evidence for the
benet of trophic feeding in patients with severe
acute pancreatitis.
In patients who require nasoenteral tube feeding for an extended period (typically beyond
30days), other feeding options should be considered. Complications of prolonged duration of NG
or NJ feeding include sinusitis and nasal passage
trauma, malpositioning or inadvertent removal of
the tube [66]. Complications of EN are listed in
Table 3. In these patients, a percutaneous endoscopic gastrostomy, surgical jejunostomy or gastrojejunostomy (by an endoscopic, laparoscopic
or open approach) should be considered. There is
a paucity of literature regarding extended enteral
feeding and further studies are required to clarify
the optimal method for long-term EN.
6.3 Parenteral Nutrition
PN is the intravenous administration of nutrients
that a patient receives via a catheter inserted
directly into a major central or via a smaller
peripheral vein [20]. PN is indicated in patients
with severe acute pancreatitis who do not tolerate
EN over 72h, where a NG or NJ tube cannot be
placed, or patients who are unable to achieve targeted requirements (Fig.2).
Increased mortality has been demonstrated in
a subset of patients with severe acute pancreatitis
receiving PN.This is thought to reect the severity of disease rather than due to a complication of
PN, including catheter-related infections, sepsis,
metabolic derangements and gut barrier dysfunction (Table3). The lack of stimulus for peristalsis
can result in hypomotility of the gut, and stagnant
bowel contents can lead to signicant changes in
the intestinal microora, including bacterial
overgrowth and dysbiosis [63]. Patients receiving
PN have been shown to require a signicantly
higher dose of insulin in order to achieve normoglycaemia than those having EN [47]. It is worth
noting that it is believed that hyperglycaemia
inuences the risk of infectious complications
and mortality [47] through a number of potential
mechanisms including oxidative stress, cytokine
activation and hypercoagulability [47].
In some patients, a combination of EN and PN
is a reasonable way to meet metabolic and nutrient demands, and the amount of nutrients delivered parenterally can be progressively reduced as
larger volumes are tolerated enterally.
Complications of EN are listed in Table 3.
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