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23 Nutrition in Acute Liver Failure and Severe Acute Pancreatitis 261
GASTROINTESTINAL
DYSFUNCTION
(A) Disturbances in mobility and absorption
(B) Gap in in mucosal barrier
(C) Changes in microbiome
(D) Increased intra-abdominal pressure
(E) Impaired mesenteric perfusion infections of the GI tract
GRADES OF GASTROINTESTINAL
NO AGI No malfunctioning GI system
GRADE 1 GI symptoms after an insult, self
GRADE 2 GI dysfunction requiring intervention,
GRADE 3 GI failure despite interventions,
GRADE 4 Dramatically worsened GI failure,
INJURY
limiting
not determining deterioration of
general conditions
worsening MODS
immediatly life-threating
1. Stop temporarly NE
2. Consider prokinetics
3. Post piloric feeding
Abdominal distension, absent passage, vomiting,
Small bowel
intolerance
1. Stop temporarly NE
2. Consider measuring IAP
3. Prokinetics or laxatives
NUTRITION
NO CONTROINDICATION NE
Start NE and monitor GI symptoms
Gastrointestinal symptoms: vomiting,
local pain and distension, IAP, large GRV
YES
Increase NE and reassess
Signs of Bowel paralysis
elevated and increasing IAP
1. Keep NE
2. Stop Laxatives
3. Consider infection
NO
Diarrhea
Fig. 23.1 Gastrointestinal dysfunction: Pathophysiology, grading, and nutrition algorithm
intestinal epithelial cell apoptosis and uncontrolled inflammation, leading to intestinal barrier failure [14, 15] (Fig. 23.1).
Acute Liver Failure
Defin
ition
Acute liver failure (ALF), including its most severe form, fulminant hepatic failure,
represents a rare life-threatening disease with a high mortality rate due to subsequent
sepsis and multiple organ failure [16, 17
Clinical manifestations include rapid
].
hepatic injury, coagulopathy derangements, hepatic encephalopathy, and, in some
cases, multiple organ failure, occurring in patients with no history of liver disease.
ALF is rare, with approximately 2000–3000 cases per year in the United States (>10
persons per million). Most affected individuals are young, with a median age of
38, predominantly female and Caucasian. It is crucial to differentiate ALF from
acute on chronic liver failure (ACLF), where patients with preexisting liver disease,
such as cirrhosis, decom pensate with acute injury, as prognosis and treatment
significantly differ. ALF often results from drugs and viruses, less frequently from
causes like Wilson disease, hepatic veno-occlusive disease (or Budd-Chiari syndrome), ischemic liver injury due to cardiopulmonary disease, invasive neoplasms,
and fatty liver pregnancy. The etiology does not correlate with disease severi ty. ALF
is diagnosed in the presence of liver injury onset, hepatic encephalopathy, and
coagulopathy (international normalized ratio >1.5). Hepatic encephalopathy typically develops within 1–4 weeks but may occur within 26 weeks of initial
262 K. Donadello et al.
presentation. ALF can be graded based on encephalopathy development speed:
hyperacute (<7 days), acute (8–28 days), and subacute (>28 days) [2]. ALF pathophysiology involves primary liver injury specific to ALF etiology and secondary
multiple organ failure [11, 17]. Primary insult drugs like acetam inophen and ethanol
cause oxidative stress damage, depleting glutathione (GSH), and worsening with
fasting and malnutrition. Secondary multiple organ failure shares features with
18]. T
sepsis [
now recognized for its key role in immunologic homeostasis, receiving blood supply
from both portal and systemic veins, rich in nutrients and bacterial products,
maintaining antigenic stimulation balance through inflammatory and antiinflammatory mechanisms [19, 20
nutrition includes energy metabolism, protein synthesis, fat synthesis, and glycemic
control. During fasting, glycogen hydrolysis produces glucose; prolonged fasting
initiates gluconeogenesis using lactate, pyruvate, glycerol, and amino acids. Gluconeogenesis is inhibited by insulin and promoted by glucagon. The liver synthesizes
nonessential amino acids, plasma proteins, and ammonia, metabolizes amino acid
and fats, and converts glucose to fatty acids [17]. In ALF, hypercatabolism leads to
proteolysis, resulting in negative nitrogen balance, muscle breakdown, and lean
body mass loss. Hepatic encephalopathy results from prolonged proteolysis, where
released amino acids convert to ammonia due to the failing liver’s inability to
transform ammonia into urea. Hyperammonemia causes brain cell swelling. Zinc
deficiency affects the urea cycle, impairing ammonia detoxification [21]. Tissue
ischemia/infarction, renal failure, and respiratory failure can dysregulate phosphate,
magnesium, and potassium levels. Electrolytes should be monitored frequently, with
correction protocols initiated for acid-base disturbances. Progressive renal failure
may require renal replacement therapy (CRRT) [
hypoglycemia due to increased hepatic glucose extraction, glycolysis, and impaired
gluconeogenesis, along with rapidly depleted glycogen stores [16]. Short-chain fatty
acids (SCFAs), by-products of bacterial colonic carbohydrate fermentation, play
roles in intestinal health, reducing luminal pH, stimulating mucin production, and
maintaining enterocyte viability and tight junction integrity. SCFAs condition intestinal epithelial cells to respond to bacterial products, modulate immune responses,
and shape T-cell repertoire [
he liver, once considered minimally involved in immune function, is
]. The liver’s crucial role in metabolism and
16]. ALF often presents with
19].
s
Nutrition in ALF
The feeding way of choice depends on patients’ encephalopathy. Patients suffering
from only mild encephalopathy can be fed orally as long as swallowing and cough
reflexes are intact, implementing with oral nutrition supplements in case of insufficient food oral intake. A switch to enteral nutrition via nasogastric or nasojejunal
tube should be considered in case of cough or swallowing reflexes failure [22]. Caloric goals for enteral feeding in patients with ALF are driven by increased resting
energy expenditure (between 18% and 30%) [
23].
23 Nutrition in Acute Liver Failure and Severe Acute Pancreatitis 263
In general, decisions on when to initiate nutrition support and which route to use
are made in accordance with the recommendations for nutrition support in other ICU
patient groups [24]. In “hyperacute” liver failure, due to the short duration of illness
in most patients, nutrition support is thought to play a relatively minor role and
prognosis is more favorable in this subtype. In “acute” liver failure and in “subacute”
liver failure, early nutrition support is often necessary and might influence patient’s
prognosis. According to ESICM guidelines [9], low-dose EN should be started as
soon as acute, immediately life-threatening metabolic derangements have been
controlled, with or without liver support strategies, independent from the grade of
encephalopathy. Arterial ammonia levels should be strictly monitored, as patients
with hyperacute ALF and elevated and sustained arterial ammonia levels
(>150 μMol/l) may be at increased risk of cerebral edema and development of
intracranial hypertension. In this specific setting, protein administration may indeed
further elevate ammonia levels and increase the risk of cerebral edema. Protein
administration should be thus deferred for a short period of time (24–48 h), waiting
for liver function improvement and arterial ammonia should be monitored when
protein is then introduced in patient’s daily diet.
There are
no published studies comparing enteral formulas in patients with ALF.
In other critically ill patients with liver disease, no evidence supports the use of
BCAA-enriched EN compared to standard whole-protein formulations, and they are
seldom used in the care of ALF patients [22]. Protein should rarely be restricted, and
ESPEN guidelines recommend 1.2–1.5 g/kg/day of protein intake. Hospitalized
patients or those unable to tolerate PO intake should have supplemental feedings
to reach these targets [
In most patients with ALF, it is practical and safe to use
21].
EN, and formulas can be delivered in amounts comparable to other critical illnesses.
A small subgroup of hyperacute patients may be at transient risk of worsening
hyperammonemia at high protein loads and thus may be intolerant to full-dose EN
in the early phase of their illness. As for other critically ill patients who require
nutrition support therapy, PN carries no clear advantage over EN and may increase
the risk for infectious complications. Furthermore, the decision to start total PN is
not recommended prior to days 5–7 post critical care presentation, as data suggest no
significant benefit [
Moreover, PN is accounted as a cause of parenteral nutrition-
16].
associated liver disease (PNALD), due to disturbances of the enterohepatic bile acid
cycling, systemic infection, bacterial overgrowth, absence of enteral nutrients, and
PN composition. In case of PNALD, limiting soybean-based lipids to ≤1.0 g/kg/die
has been suggested also in adults, and the exchange of soybean-based lipids by a
100% fish-oil emulsion has been reported to be effective [22]. In the rare cases in
which the parenteral route of administration must be used, lipid emulsions are safe.
Interestingly, SMOF lipids (SMOF) are newer preparations containing ω-3 and
medium-chain triglycerides with higher patient performance compared to
soy-based lipids. Indeed, fat metabolism is actively regulated by mitochondrial
function, avoiding their potential accumulation and further liver damage. Unfortunately, solid evidence in patients with ALF is lacking. Lipidic metabolism (triglycerides target >3 mmol/L or 265 mg/dL) has thus to be controlled along with
creatinine kinase [
23].
264 K. Donadello et al.
The maintenance of euglycemia is warranted, glycemia should be strictly monitored (at least every 2 h), and ideal blood glucose targets range between 150 and
180 mg/dL, though higher goals may be acceptable [24]. Administration of 1.5 – 2g/
kg/d of glucose is recommended, and hypoglycemia can be managed with continuous glucose infusions in the intensive care unit [16]. Enteral nutrition should be
prioritized in patients with ALF, but the presence of severe shock or gut dysfunction
may affect the ability to provide nutrition enterally. Hyperglycemia can exacerbate
intracranial hypertension (ICH) and should thus be avoided.
Hypertonic sodium chloride can be administered to induce mild hypernatremia
(145–155 mEq/L) to lower the incidence/degree of ICH. Patients at the highest risk
for developing cerebral edema (high-serum ammonia, high-grade hepatic encephalopathy, acute renal failure, and/or requirement of vasopressor) should be given a
trial of hypertonic saline [16]. Microbial ecological agents include at least three
classes: probiotics, prebiotics, and synbiotics [26]. Probiotics are live organisms
which provide direct and indirect host benefits after ingestion and have been shown
to favorably impact the production of SCFAs, gut barrier integrity, and alter colonic
pH and immune system modulation [19]. Fiber-containing supplements are also
considered as probi otic due to the increase in normal gut flora associated with their
administration [
21]. Probiotics have been demonstrated to have a beneficial impact
on patients with cirrho sis and hepatic encephalopathy and are associated with
improvements in symptom burden, blood ammonia levels, and infection rates, but
robust data are lacking on ALF [19].
Prebiotics are nondigestible food ingredients that exert effects on the intestinal
microbiome with secondary beneficial effectson host homoeostasis [
19, 26]. Through
the selective GI bacteria growth stimulation, prebiotics have been shown to improve
mucosal barrier function, to stimulate regulatory T cells, and to reduce
pro-inflammatory cytokines [26]. Lactulose has a well-established role in the treatment of hepatic encephalopathy in chronic liver disease [27]: it is metabolized by
colonic bacteria, and it therefore exerts positive selection pressure promoting
bifidobacterial population expansion [19, 28]; more over, it acidifies colonic microenvironment and leads to an absorption reduction of the ammonium salts that derive
from intestinal bacterial metabolism [19].
Synbioti
cs a
re combinations of both prebiotics and probiotics, with synergistic
properties, and have shown some interesting effects in patients with inflammatory
bowel diseases. These agents can increase the intestinal tract physiological activity,
increase favorable bacterial strain levels, prevent pathogen grow th, improve mucosal
layer function, and preserve intestinal epithelial cells, thereby reducing BT and LPS
release [26].
Experimental
observational studies found that intestinal flora modifications can
improve the survival rate of patients with liver failure [26]; therefore, ESPEN GL
recommend using nutritional supplements containing selected probiotics or
synbiotics to improve liver enzymes in NAFL/NASH patients [22]. Patient’s medical history should be always investigated to identify potential vitamin deficiencies.
Patients presenting with a history of alcohol or illicit drug abuse may present thiamin
23 Nutrition in Acute Liver Failure and Severe Acute Pancreatitis 265
and B12 vitamin deficit, while pancreatitis or pancreatic atrophy may impact fat
soluble vitamins such as vitamins A, D, E, and K [16].
In patients
with ALF, clotting tests should be performed to investigate contingent
imbalance in procoagulant and anticoagulant factors, such as prolonged INR,
prolonged thromboplastin time, and abnormal factor V [16, 29]. Newer data suggest
that procoagulant disarrangements verify more frequently than anticoagulant ones,
causing hypercoagulable states [16, 29]. Bleeding is indeed uncommon unless a very
low platelet count coexists. Routine vitamin K determination lacks robust evidence,
but in case of bleeding, empiric management with vitamin K supplementation can be
considered, though strong supportive data are still missing [30]. Vitamin D helps in
maintaining the integrity of the intestinal barrier and mitigates inflammation pathways. It is still unknown whether vitamin D deficiency is frequent in ALF patients,
but supplementation may be beneficial in patients with low vitamin levels
[16]. Moreover, ESPEN guidelines suggest the supplementation of water- and
fat-soluble vitamins as well as daily trace elements administration in patients with
ALF receiving PN nutrition [
22]. In this high-risk patient group, it seems prudent to
administer a first dose of thiamine before starting PN to prevent both Wernicke’s
encephalopathy and refeeding syndrome, even if deficiency may not have been
documented [
On the other hand, considering the high prevalence of micronu-
22].
trient deficiency and its correlation with physiological responses to stress and
infection, vitamins A, D, and K should be administered along with thiamine, folate,
and pyridoxine to correct their deficiency [
22]. Leucine, isoleucine, and valine,
branched-chain amino acids (BCAA), are necessary amino acids that work not
only as protein building blocks but also as physiological stimulants (especially for
leucine) for protein synthesis [31]. Almost 40% of the amino acids needed by
mammals are represented by BCAAs. BCAAs altogether or leucine alone can
sustain protein synthesis and inhibit protein breakdown [
32
Although BCAA
].
supplementation is crucial for the management of hepatic encephalopathy and
sarcopenia, L-leucine has been described to be mostly involved in protein turnover,
being able to reverse proteolytic processes towards protein synthesis. BCAA administration improves albumin production in the cirrhotic liver. On the other hand,
excess BCAAs are immediately catabolized in cells, as amino acids are little stored
in free form in animal bodies. Two enzymes are critically important in the catabolism/storage of BCAAs: branched-chain aminotransferase (BCAT) and branchedchain-keto acid dehydrogenase (BCKDH) complex. In humans, skeletal muscles are
considered the major site for BCAA catabolism, whereas other amino acids are
subjected to liver catabolism. The BCKDH complex has extremely low activity
within the human liver, compared to other animals, having instead greater activity
within muscle tissues as skeletal muscles represent about 40% of body weight
[
During liver failure in humans, the molar ratio of BCAAs to aromatic amino
31].
acids (AAAs), called Fisher’s ratio, can be an important marker of failure degree.
However, the dynamics of BCAA and AAA serum levels appear to differ between
ALF and chronic liver failure (CLF). Inconsistent data are available on serum
BCAAs during ALF, as they can be decreased, similar, and increased in comparison
to normal concentrations, although markedly increased serum AAA concentrations
266 K. Donadello et al.
ACUTE LIVER FAILURE
• Onset of liver injury
. Presence of hepatic encephalopathy (HE)
. Coagulopathy (INR >1.5)
NUTRITION
Increased resting energy expenditure
► ORAL: intact cough and swallow reflexes
► ENTERAL: start low dose
► PARENTERAL: not
. ESPEN recommends 1.2–1.5 g/kg/day
. BCAAs not suggested in ALF tolerating EN (risk of
increasing nitrogen overload and accelerate
hyperammoniemia, worsening encephalopathy)
. Suggested doses: L-leucine 2500 mg, L-isoleucine
1250 mg, L-valine 1250 mg
( +18-30%)
threatening derangements are controlled (no
preferred formula)
prefer SMOF with ω-3 and MCT
when acute life-
indicated prior to 5-7 days;
PROTEIN INTAKE
. GRADE 1 OR HYPERACUTE: within 7 days
. GRADE 2 OR ACUTE: 8-28 days
. GRADE 3 OR SUBACUTE: >28 days
GLUCOSE CONTROL
. Monitor every 2h
. Provide 1.5–2 g/kg/d of glucose
. Maintain 150-180mg/dl target
. Manage hypoglicemia with continuous glucose
infusion
. Hyperglicemia exacerbates intracranial pressure
HEPATIC ENCEPHALOPATHY
3 grades differentiation according to
speediness of encephalopathy
development
Fig. 23.2 Acute liver failure: Definition criteria, grading according to encephalopathy, indications
on feeding route, protein intake management, and glucose control
have often been reported. In contrast, decreased serum BCAA and slightly increased
serum AAA concentrations have been consistently reported in CLF. Administration
of BCAA to patients with ALF should be cautious as it can cause nitrogen overload,
accelerating hyperammonemia and hepatic encephalopathy [
20]. Therefore, with
respect to BCAA metabolism, the two liver failure conditions may differ, and it is
not suggested to use BCAAs in critically ill patients hospitalized with ALF or ACLF
who are tolerating EN [
33]. Focusing on ALF protein supplementation, according to
the European Association for the Study of the Liver, the recommended nutritional
support in liver failure is L-leucine 2500 mg, L-isoleucine 1250 mg, L-valine
1250 mg, HMB 1500 mg (namely, the therapeutic dosage), vitamin D 40 mcg
(therapeutic dosage) or 1600 I.U., and vitamin K 60 and 400 mcg; 25 mg of vitamins
B1, B2, and B6 and niacin; 400–800 mcg of folic acid; and 25 mcg of vitamin B12
[
23] (Fig. 23.2).
Acute Pancreatitis
Acute pancreatitis (AP) is a common pancreatic inflammatory disease with an
estimated annual incidence of 34 per 10,000 person-years in high-income countries;
it represents the gastrointestinal disease most frequently requiring hospital admission
[13, 34]. AP presentation includes epigastric and acute abdominal pain (80–95%),
nausea and vomiting (40–80%), abdominal distension, dyspnea, and fever, and in
almost 10% of cases, it can evolve into severe forms requiring intensive care
treatment [
saturation must be prioritized, and first emergency care should be assur ed even prior
34].
As for any sick patient, the assessment of vital signs and oxygen
23 Nutrition in Acute Liver Failure and Severe Acute Pancreatitis 267
to diagnosis; thus, oxygen, intravenous fluid resuscitation, and pain relief are usually
indicated, as this does not impair the accurate differential diagnosis of abdominal
pain [34].
The diagnosis of
AP is based on the fulfillment of two of three criteria: (1) upper
abdominal pain, (2) increased serum amylase or lipase (or both) to at least three times
the upper normal limit, or (3) acute pancreatitis consistent findings on imaging
(contrast-enhanced computer tomography [CECT], magnetic resonance imaging
[MRI], or abdominal ultrasound [US]) [13]. Therefore, the initial investigations for
acute pancreatitis should include serum amylase and lipase, triglyceride and lipid
panel, full blood count, renal and liver function tests, glucose, HbA1c, calcium, and
transabdominal US. Chest X-ray or US should be performed to identify pleural
effusion, as this is an indicator of more severe AP forms [
34]. If the diagnosis still
remains unclear, abdominal MRI or CT is indicated to identify specific features of
acute pancreatitis such as pancreatic swelling, inflammatory fat stranding, or
peripancreatic fluid collections; moreover, imaging should be performed as early
as possible also to identify the etiology, as recommended [13]. Necrotizing pancreatitis can commonly be detected on imaging only after 72–96 h after symptom
onset [13].
Gallstones a
he major cause of acute pancreatitis worldwide, accounting for
re t
20–70% of all cases in the West, with incre ased prevalence with age and female sex;
thus, ultrasonography should be included within the initial workup to eventually
identify gallbladder stones [13, 34]. Alcohol abuse is the second leading cause,
responsible for 2% (Latin America) to 70% (Finland) of total acute pancreatitis,
depending on the prevalence of alcohol abuse [34]; however, only a minority of
heavy drinkers develop identifiable episodes of AP, indicating the presence of
cofactors such as genetic risk, hypertriglyceridemia, and smoking [34]
. T
he third
most common cause of AP is endoscopic retrograde cholangiopancreatography
(ERCP), due to a strong association with the procedure, and proved to determine
AP in up to 14% of high-risk patients; effective stra tegies are described to reduce this
risk as prolonged procedures or repeated attempts at bile duct cannulation or
unintended pancreatic duct cannulation increase the risk of post-ERCP pancreatitis
[34]. Other causes of AP include hypertriglyceridemia, drugs, hypercalcemia, infection, genetics, autoimmune diseases, and (surgical) trauma
[13]
ypertriglyceridemia is on e of the peculiar causes of AP because it is directly
. H
associated with the pathology, and there is an approximate 4% increase in the
incidence of acute pancreatitis for every 100 mg/dl rise in serum triglyceride levels
above 1000 mg/dl, a level frequently used to define hypertriglyceridemia as the
cause of acute pancreatitis [
35]. Hypertriglyceridemia should be identified upon
admission, as it infers a worse prognosis, both as a unique cause or as a cofactor,
being hypertriglyceridemia-associated AP more frequently severe than other
forms [34]
.
Severe AP
occurs in 20–25% of cases and is often characterized by two distinct
phases: an early phase (within the first week), in which systemic inflammation may
lead to multiple organ failure, and a late phase (after the first week), in which organ
failures may become persistent and local complications may arise [36]. AP severity
268 K. Donadello et al.
is determined based on the revised Atlanta criteria. Mild AP is defined by the
absence of organ failure or local complications; moderately severe AP is defined
by transient organ failure (less than 48 h) and/or local complications; severe AP is
defined by persistent organ failure (greater than 48 h) [
34]. Organ failure is typically
defined using the Modified Marshall scoring system for organ dysfunction, which
considers cardiovascular, respiratory, and renal impairments [
37]. The pancreatitis
activity scoring system (PASS) serves a similar function to monitor patients’ progression and may be more accurate without the inclusion of pain medication
[34, 38], but further studies are needed to assess proper cutoff values [39]. The
prediction of severity should be made as early as possible to distinguish those
patients who are likely to develop local and/or systemic complications and may
thus benefit from early intensive management. Worse outcomes are associated with
advanced age, multiple comorbidities, elevated body mass index, presence of systemic inflammation, elevated BUN and/or hematocrit, pleural effusion/s and/or
infiltrates, and altered mental status [
37]. Inflammation of, and damage to, the
gastrointestinal tract results in bacterial translocation, endotoxemia and portal bacteremia, infected pancreatic necrosis, and exacerbating systemic inflammation, all of
which may result in multi-organ failure and death [34, 40].
Even though the i
mportance of nutritional support in AP patients was recognized
back in the 1970s, parenteral nutrition (PN) had been preferred over enteral nutrition
(EN), embracing the hypothesis of “pancreatic rest,” with the aim of preventing the
stimulation of exocrine function and reducing the release of proteolytic enzymes,
thus not increasing autodigestion [41]. This paradigm dramatically shifted over the
last decade as great evidence suggested that early feeding does not exacerbate
pancreatic parenchymal inflammation, but is actually beneficial [34]
. R
ecent studies
demonstrate that gastrointestinal dysfunction does not represent a “per se” damage,
but it has an important role in stepping up organ failure, and RCT comparing EN and
PN demonstrated that patients’ outcome is worsened by the lack of luminal stimulation [ 37, 41]; in addition, EN prote cts the gut mucosal barrier better than PN, with
the latter being also accountable for catheter-related infection, electrolyte and metabolic disturbances, increased intestinal permeability, and gut barrier failure [41]
Patients
with AP should be considered at moderate to high nutritional risk,
.
because of both the catabolic nature of the disease and the impact of nutritional
status on disease development [42]; being the pancreatic gland deeply involved in
digestion and glucose control, its malfunction leads to enzyme production and
secretion deficiencies, resulting in maldigestion, malabsorption, malnutrition, and
glucose control impairment [
43]. All patients with mild to moderate AP should thus
be screened using validated screening methods such as the Nutritional Risk Screening 2002 (NRS 2002), while those with predicted severe AP should always be
considered at nutritional risk [
42].
According to the growing evidence suggesting
that in AP patients the gut should be dealt with as a vital organ MODS, nutrition
assessment is mandatory to determine the presence and degree of malnutrition and to
allow
a nutrition
plan of care to be prepared [43]. For those patients admitted to the
ICU, the calculation of a Nutritional Risk in Critically Ill (NUTRIC) score to
determine nutritional risk can assist in determining the appropriate nutrition therapy:
23 Nutrition in Acute Liver Failure and Severe Acute Pancreatitis 269
patients with a NUTRIC score of equal to or greater than 5 should start EN and meet
the energy and protein goal within 24–48 h. In addition, a malnutrition diagnosis can
be confirmed by the presence of two or more of the following criteria: insufficient
energy intake, weight loss, loss of muscle mass, loss of subcutaneous fat, presence of
edema or fluid accumulation, and diminished functional status as measured by
handgrip strength or reduction in activities of daily living [
44]. Indirect calorimetry
is the gold standard for measuring the resting metabolic rate of critically ill adults.
When indirect calorimetry is not available, weight-based nomograms can be used to
estimate energy and protein needs [44].
The pancreas plays a central role in diges
tion and glucose homeostasis and is
composed of two major types of tissues: the acini, representing the exocrine tissue
responsible for digestive secretion released into the duodenum, and the islets of
Langerhans, which secrete the hormones insulin, glucagon, and somatostatin [44,
45]. Exocrine pancreatic function includes carbohydrate, protein, and fat digestion,
which are carried out by amylase, proteolytic enzymes, and lipase, respectively.
Enzyme secretion begins during the cephalic and gastric phases, stimulated by the
vagal nerve and nerve reflexes. It continues during the intestinal phase when the
acidic chyme enters the duodenum, simultaneously stimulating bicarbonates, cholecystokinin, and secretin secretion. Bicarbonates alkalize the duodenal contents and
activate the enzymes, while cholecystokinin promotes zymogen secretion within the
lumen. The “interdigestive phase,” characterized by a deep interconnection between
pancreatic secretion and the migrating motor complex, acts as a housekeeper,
cleaning the small bowel from bacterial overgrowth and other detrimental collections within the lumen [43, 44, 46].
All pancreatic functions, both digestive and interdigestive, as well as the endocrine function, are heavily affected by inflammatory diseases [
43].
The clinical picture of pancreatic exocrine insufficiency is dominated by the
consequences of deficient lipase activity resulting in steatorrhea, which becomes
apparent when pancreatic lipase output is reduced to 5–10% of its normal values.
Weight loss, bloating, abdominal discomfort, and complications of malnutrition (i.e.,
deficiency in lipid-soluble vitamins with consequences such as osteoporosis) are
other clinical manifestations of pancreatic maldigestion [43].
Although fasting was thought to decrease pancreatic exocrine output, emerging
knowledge of the role played by an intact gut barrier in critical illness, especially in
severe acute pancreatitis, added to studies showing that early EN start improves
morbidity and mortality in severe AP, provides no justification to keep patients with
AP fasting during the first days [44].
ents with predicted mild AP, ESPEN guidelines recommend offering oral
In pati
feeding as soon as clinically tolerated and independently from serum lipase concentrations [36, 42]. This strategy is related to a shorter length of stay compared to
conventional delayed oral feeding. Moreover, oral nutrition should include soft diet
elements because they seem more beneficial regarding caloric intake and are equally
tolerated compared with clear liquid diets. Approximately 16% of these patients can
develop subsequent oral feeding intolerance, with predictive factors being the
presence of pleural effusions and/or collections and severity [
42].
270 K. Donadello et al.
The only exception to early oral feeding should be hypertriglyceridemiaassociated acute pancreatitis because its treatment aims to reduce serum triglyceride
levels, which may include gut rest with no oral inta ke to expedite circulating
triglyceride clearance. The metabolic/endocrine team should be involved, with
choices including intravenous insulin alongside fluid resuscitation or plasmapheresis
for more severe or obstinate HTG, monitoring high triglyceride levels. Resumption
of oral/enteral intake should include fibrates and, if not possible, parenteral nutrition
with minimal lipid content [34]. In patients with AP and inability to feed orally, EN
should be preferred to parenteral nutrition (PN) because it significantly decreases
complication rates, multiorgan failure, and mortality. Furthermore, EN is preferable
to PN even if complications such as fistulas, ascites, and pseudocysts are present. EN
is feasible and recommended even after surgery for pancreatitis, by intraoperative
jejunostomy. Enteral tube feeding provides safe nutritional support in AP, even in
cases of gastric outlet obstruction [36]. In severe AP, ESPEN guidelines recommend
providing an energy supply of 25–35 kcal/kg/day, with 1.2–1.5 g/kg of protein/day
(unless concomitant presence of renal and/or severe hepatic failure), 3–6 g/kg of
carbohydrates/day, and up to 2 g/kg of lipid/day. Plasma glucose and triglyceride
concentrations should not exceed 10 mmol/l (180 mg/dl) and 3–4 mmol/l (266 mg/
dl), respectively [36].
The effi
cacy
of EN is clear in patients in whom nutrition is started early (within
24 or 48 h after admission); nevertheless, enteral tube feeding initiated too early
(within the first 24 h from admission) might be suboptimal. Indeed, fluid resuscitation is required to restore blood volume and overcome reflex splanchnic vasoconstriction before enteral feeding can increase the demand for splanchnic perfusion. It
is therefore recommended to start enteral tube feeding early, but not too early, and
preferably after initial fluid resuscitation/optimization [24, 41].
Enteral t
ube f
eeding, however, should be limited to patients who are hemodynamically unstable, display gastrointestinal intolerance, or have frequent
intervention-related interruptions. Attempts to maximize enteral nutrition should
be avoided in patients who are not volume optimized due to the risk of inducing
gut injury through nonocclusive mesenteric ischemia [
34]. PN should be adminis-
tered in patients with AP who do not tolerate EN or who are unable to tolerate
targeted nutritional requirements, or if contraindications for EN exist. Complications
of severe AP, which may occur and represent a contraindication for EN, include
bowel obstruction, abdominal compartment syndrome, prolonged paralytic ileus,
and mesenteric ischemia. Similarly, to critically ill patients with other diseases,
approximately 20% of patients with severe AP have complications, which are
associated with absolute or relative contraindications for EN [42]
Inadequate
nutrition has prompted the use of combined enteral and parenteral
.
nutrition, the latter to be started before, during, or after enteral intake when this is
considered insufficient. However, current trials and meta-analyses do not provide
definitive evidence of superiority for this combined approach [34]. Multiple EN
formulations exist and can be classified into two categories: polymeric and semielemental. Semi-elemental formulations are proposed to have improved absorption
rates from the intestine, cause less pancreatic stimulation, and be better tolerated.