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14
J. Heard et al.
the enzymes and zymogens that aid in digestion, as well as alkaline uid, which are
produced by the acinar cells and secreted into the ductal system. Initially, the acinar
cells drain into intercalated ducts that come together to form interlobular ducts,
which then join together to form secondary ducts that drain into the main pancreatic
duct, and subsequently the duodenum at the ampulla of Vater.
The composition of pancreatic uid varies depending on whether the body is in
a fasting state or a stimulated phase. When fasting, pancreatic uid has a bicarbonate concentration of 80mEq/L and is rich in protein. However, when the pancreas is
stimulated after a meal, the concentration of bicarbonate increases, and this alkaline
uid enters the duodenum. The uid has a pH of 7.6–9.0 and acts to neutralize gastric acid while delivering digestive enzymes in their inactive state to the duodenum.
Vagal parasympathetic stimulation is largely responsible for the secretion of
enzyme-rich uid, while uid and electrolyte secretion are more hormonally regulated. The main hormones involved are secretin and cholecystokinin. The presence
of acid in the duodenum results in the release of secretin from the duodenal mucosa.
Secretin subsequently stimulates the interlobular duct cells to release bicarbonate
and water. As the bicarbonate concentration increases in the pancreatic uid, chloride concentration decreases in order to maintain isotonicity. CCK, released in the
presence of fat and protein, stimulates the pancreatic acinar cells to release proenzymes. Pancreatic secretion is also inuenced by neuropeptides, which have an
inhibitory effect [13].
Endocrine Physiology
The main endocrine function of the pancreas is regulation of carbohydrate metabolism and glucose homeostasis via insulin and glucagon secretion. While insulin
functions to transport glucose into cells, stimulate protein synthesis, and inhibit
glycogenolysis and fatty acid breakdown, glucagon stimulates glycogenolysis and
gluconeogenesis, increasing blood glucose levels. Pancreatic islet cells of
Langerhans comprise the endocrine structure of the pancreas and are of neural crest
origin. Blood enters the islet cells via an afferent arteriole, which then enters into a
capillary bed within the cell. Hormones secreted as part of the pancreatic endocrine
system are secreted into this capillary bed, and blood then exits via an efferent collecting venule to the portal venous circulation.
The islets of Langerhans are composed of several types of cells, 70% of which
are beta cells, which are mostly found in the core of the islet. These beta cells are
surrounded by alpha cells, delta cells, and pancreatic polypeptide cells, which communicate with each other via extracellular spaces and gap junctions, allowing for
cellular products secreted from one cell type to inuence the function of another.
The four main cell types—A (alpha), B (beta), D cells, and F cells—have varied
distributions and secretory products. While B and D cells are found in the tail of the
pancreas, F cells are primarily located in the head and uncinate process and A cells
are evenly distributed throughout. B cells make up about 70% of the islet cell mass
1 Anatomy andPhysiology
15
and are located centrally in the islet cell. The primary secretory product is insulin
though amylin and cholecystokinin are also secreted by B cells.
Insulin is rst produced as preproinsulin in the ribosomes of the rough endoplasmic reticulum before being cleaved into proinsulin and transported to the Golgi
apparatus, where it is packaged into secretory granules. Proinsulin is then cleaved
into insulin and C-peptide, and the secretory granules fuse with the cell membrane
to secrete insulin. A cells are found more peripherally in the islet cells and comprise
about 10% of islet cell mass. The main secretory product is glucagon. Also found
peripherally within the islets are F cells, which make up 15% of islet cell mass.
These cells secrete pancreatic polypeptide. D cells are distributed evenly within islet
cells and make up 5% of their mass. D cells secrete somatostatin, while D2 cells
secrete VIP.
Glucose is the main regulator of insulin secretion and is taken up by Beta cells
through GLUT2 transporters. Glucokinase then phosphorylates glucose into
glucose- 6-phosphate and subsequently produces ATP in the process of glycolysis.
When the pancreas is unstimulated, insulin is secreted at a basal rate. However,
rapid increases in blood glucose result in a “rst-phase” of insulin release that peaks
within 5min and decreases within 10min. If the concentration of glucose in the
blood remains high, a second phase is entered and insulin secretion is sustained by
the release of both stored and newly synthesized insulin [2, 13].
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10. Türkvatan A, Erden A, Türkoğlu MA, Yener Ö. Congenital variants and anomalies of the pan-
creas and pancreatic duct: imaging by magnetic resonance cholangiopancreaticography and
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11. Tol JAMG, Gouma DJ, Bassi C, Dervenis C, Montorsi M, Adham M, et al. Denition of
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14. Yap CH, Coupland D, Au J, Raju S.Duodenum inversum: a rare cause of nausea and epigastric
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of pancreaticobiliary maljunction and clinical features in children. J Hepato-Biliary-Pancreat
Sci. 2017;24(8):449–55.
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19. Chen JJ, Lee HC, Yeung CY, Chan WT, Jiang CB, Sheu JC.Meta-analysis: the clinical features
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radiologic considerations. Radiographics. 1993;13:1063–80. https://doi.org/10.1148/
radiographics.13.5.8210590.
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26. Schubert ML.Gastric acid secretion. Curr Opin Gastroenterol. 2016;32(6):452–60.
27. Field BCT.Neuroendocrinology of obesity. Br Med Bull. 2014;109(1):73–82.
28. Cakir M, Dworakowska D, Grossman A. Somatostatin receptor biology in neuroendocrine
and pituitary tumours: part 1—molecular pathways. J Cell Mol Med. 2010;14(11):2570–84.
29. Villar HV, Fender HR, Rayford PL, Bloom SR, Ramus NI, Thompson JC. Suppression of
gastrin release and gastric secretion by gastric inhibitory polypeptide (GIP) and vasoactive
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J. Heard et al.
Part II
Acute Pancreatitis
Chapter 2
Diagnosis andMedical Management
ofAcute Pancreatitis
CarlosTheodoreHuerta, JodieAdamBarkin, andOnurC.Kutlu
Etiology
Acute pancreatitis is a major source of economic burden with an estimated cost of
AP-related hospitalizations exceeding 2 billion dollars to the US healthcare system.
[1, 2] The incidence of AP has been reported ranging between 15 and 45 cases per
100,000 patients in the United States and 5 and 73 cases per 100,000 patients globally,
with an increase observed in recent years [3]. However, the two most frequent etiologies in the US patient population include gallstones and excess alcohol consumption,
which are estimated to occur between 40–70% and 25–35% of cases, respectively
[4–6]. Given the importance of early diagnosis and recognition of the etiology of AP
to prevent future recurrent episodes, abdominal ultrasound should be used to screen
for the presence of cholelithiasis in all patients with AP [7, 8, 9]. Should the presence
of cholelithiasis be conrmed in the setting of AP, these patients should be referred for
consideration of interval cholecystectomy to prevent future episodes of disease.
Regarding pancreatitis secondary to alcohol consumption, symptoms can manifest along the entire disease spectrum ranging from individual, acute episodes to
recurrent, chronic pancreatic dysfunction. Although multifactorial in nature due to
other sensitizing factors such as smoking and genetic factors, patients with
C. T. Huerta
DeWitt Daughtry Family Department of Surgery, University of Miami Miller School of
Medicine, Miami, FL, USA
J. A. Barkin
Pancreas Center, Division of Gastroenterology, University of Miami Miller School of
Medicine, Miami, FL, USA
O. C. Kutlu (
DeWitt Daughtry Department of Surgery, University of Miami Miller School of Medicine,
Miami, FL, USA
e-mail: okutlu@med.miami.edu
Switzerland AG 2025
E. P. Ceppa et al. (eds.), The SAGES Manual of Evolving Techniques in
Pancreatic Surgery, https://doi.org/10.1007/978-3-031-78409-5_2
*)
19© The Author(s), under exclusive license to Springer Nature
20
C. T. Huerta et al.
alcohol- induced AP may have a history of excess alcohol intake more than 50g per
day for more than 5years [6, 9–14].
Although alcohol and cholelithiasis-related AP predominate as the most commonly encountered cases in patients, the remaining differential includes a broad list
of potential etiologies that should be carefully evaluated. While only estimated to
constitute less than 4% of cases, hypertriglyceridemia is a well-studied cause of
AP. Serum levels of triglycerides are often >1000 mg/dL in patients with either
primary or secondary hypertriglyceridemia-induced pancreatitis, and a fasting
serum triglyceride taken 30days after discharge is often recommended in this population to conrm the diagnosis [15–18]. Electrolyte disturbances including hypercalcemia in isolation, or as a result of another medical cause such as
hyperparathyroidism, have been documented as a causative factor in some patients.
Pharmacologic insults from drugs known to cause AP such as azathioprine and
6-mercaptopurine are capable of eliciting disease episodes [6, 19]. Although uncommon, polymicrobial infections and toxins have also been shown to induce AP.
Anatomic causes resulting in hepatobiliary obstruction can similarly result in
AP.Both benign and malignant masses of the hepatobiliary and pancreatic system as
well as the duodenum that impact the main pancreatic duct have been recognized as
less common causes of AP.Previous series have identied up to 14% of patients with
idiopathic AP (IAP) may have underlying pancreatic or biliary malignancies [20–22].
Given the increasing incidence of pancreatic malignancy, a high degree of clinical
suspicion for neoplastic etiologies associated with AP should be maintained particularly in younger patients and those with recurrent or prolonged episodes with no
clearly identied etiology on routine workup [23–25]. Focused cross-sectional
imaging of the pancreas through abdominal contrast-enhanced CT or MRI/MRCP as
well as endoscopic ultrasound (EUS) can be considered in these patients [6, 26, 27].
Aberrant pancreatic anatomy and function can further predispose patients to
develop AP.Congenital anomalies such as pancreas divisum can result in ampullary
stenosis or obstruction impeding outow of the main pancreatic duct [28, 29].
Physiologic outow obstruction secondary to functional biliary dysfunction syndrome is also a rare physiologic cause of AP [30]. Instrumentation procedures of the
ampulla such as endoscopic radiographic cholangiopancreatography (ERCP) for
these and other conditions can further precipitate AP episodes [31]. Newer genetic
targets including mutations and polymorphisms in genes such as SPINK1, CFTR,
and PRSS1 have been implicated in the development AP, and the role of testing for
these allelic defects in patients with a signicant family history of AP and pancreatic disease is still to be fully determined in future work [28, 32]. Patients with more
than one family member with pancreatic disease may benet from formal genetic
counseling. Together, these native genetic defects can further worsen the risk of
disease in patients with the aforementioned anatomic and environmental factors
contributing to a tissue milieu highly predisposed to inammation.
IAP occurs in patients without these aforementioned risk factors and in whom no
clear etiology is elucidated on diagnostic laboratory workup and imaging tests [33,
34]. In these patients without a structural cause identied on abdominal cross-
sectional imaging, EUS may be considered to interrogate for the presence of
microlithiasis.
2 Diagnosis andMedical Management ofAcute Pancreatitis
Etiology ofAcute Pancreatitis
A Alcohol, autoimmune
B Biliary, including gallstones, microlithiasis, and sludge
C Congenital—Pancreas divisum associated with genetic abnormality and pancreas, Crohn’s
disease via inammation, ampulla, or duodenal obstruction
D Drugs, toxins (including, smoking, tobacco, and marijuana use)
E Post-ERCP pancreatitis, eosinophilic pancreatitis
F Formations—Primary cancers (pancreatic ductal adenocarcinoma, especially in patients
>50years, lymphomas, carcinoids, metastatic cancers, small cell of lungs, renal, melanoma
G Genetic mutations and polymorphisms—cystic brosis, transmembrane conductance
regulator [CFTR], cationic trypsinogen (PRSS1), serine protease inhibitor Kayal type 1
(SPINK1) and claudin-2 (CTRC)
H Hypertriglyceridemia, hypercalcemia, hypertriglyceridemia may be associated with
metabolic pancreatitis, i.e., elevated glucose, obesity, hypercalcemia associated with
hyperparathyroidism or iatrogenic infusion
I Infection—Including viruses, CMV, mumps and EBV (Forsmark NEJM), ascariasis and
Clonorchis sinensis, bacteria tuberculosis
J Juxta ampullary diverticula—Likely mechanism obstruction
K Kinetic injury and other trauma, including seat belt injuries
Ref. Barkin JS, Barkin JA
21
Pathophysiology
The pathophysiology of AP is incompletely understood. However, the clinical and
pathologic features appear similar regardless of the etiology. Inciting physiologic
insults from the aforementioned etiological factors are thought to result in the loss
of intracellular and extracellular compartmentalization and lead to aberrant activation of pancreatic enzymes within the pancreatic acinar cells [6–9]. This may subsequently result in autodigestive injury to the pancreas. Under normal conditions,
the exocrine pancreas synthesizes and secretes several inactive digestive enzymes
that are released into the duodenum via the pancreatic ducts and activated by trypsin. Under physiologic conditions, small amounts of these zymogens are activated
spontaneously within the pancreas but are offset by natural inhibitory factors including pancreatic secretory trypsin inhibitor (PSTI or SPINK1), mesotrypsin, and
enzyme Y which inactivate and lyse trypsin [10, 11, 35]. Nonspecic antiproteases
in the pancreatic parenchyma such as alpha-1-antitrypsin and alpha-2- macroglobulin
also help to prevent damage from inappropriate trypsin activation [10, 11]. During
AP episodes, an overabundant pool of trypsin is activated within the pancreas and
overwhelms these native defenses. Pathologic autodigestion develops from the
colocalization of lysosomal enzymes including cathepsin B and trypsinogen in the
22
acinar cells as well as subsequent activation of trypsinogen and other glandular
enzymes such as chymotrypsin, phospholipase A, and elastase within the pancreas
[10, 13]. Elastase overactivity may result in the breakdown of the elastic bers
within the vasculature wall and lead to hemorrhage. Phospholipase A among other
factors has been implicated in fat necrosis observed in AP [14, 27]. This cascade of
pathological enzymatic-induced degradation spreads throughout the pancreatic
gland propagating further intrapancreatic enzyme activation and cell damage in a
positive loop. The resultant activation of the systemic inammatory response syndrome (SIRS) is responsible for driving systemic complications including extrapancreatic end organ damage and failure [36].
Although most patients typically experience minimum to mild organ dysfunction
as a result of pancreatitis, approximately 10–20% develop SIRS [36–38]. This is
dened by the presence of at least two of the following features: temperature below
36°C or above 38°C; heart rate above 90 beats per minute; respiratory rate above
20 breaths per minute or PaCO2 below 32 torr; white blood cell count above
12,000 cells/mm3, below 4000cells/mm3, or above 10% immature cells (bands)
[12]. Pancreatic inammation can trigger SIRS via the activation of an inammatory cascade mediated by cytokines, immunologic cells, and the complement system. These inammatory cytokines cause dispersion and trafcking of macrophages
and migration distant from the pancreas such as the lungs and kidneys. SIRS can
lead to a fulminant course with multiorgan failure in addition to the development of
local or systemic complications [3, 15, 31].
C. T. Huerta et al.
Diagnosis
The diagnosis of AP is established by the presence of two or more of the three following criteria: (i) abdominal pain consistent with the disease (acute onset of a
persistent, severe, epigastric pain often radiating to the back), (ii) serum amylase
and/or lipase greater than three times the upper limit of normal, and/or (iii) characteristic ndings from abdominal imaging [39].
Clinical Presentation
Physical exam ndings in AP vary based on the severity of disease presentation. As
a result, the nonspecic nature of AP symptomatology may lead to misdiagnosis
based on physical examination alone. Patients with mild AP may present only with
minimal tenderness to palpation in the epigastrium, while those with severe pancreatitis may have signicant tenderness diffusely throughout the abdomen and associated fever, tachypnea, hypoxemia, and hypotension [40, 41].
The most common presentation is signicant abdominal pain, which may be so
severe that the patient is reluctant to initiate deep respiratory efforts. This may
2 Diagnosis andMedical Management ofAcute Pancreatitis
23
subsequently result in hypoventilation and contribute to the increased incidence of
respiratory complications observed in these patients, such as atelectasis and pulmonary consolidation [42, 43]. Given these patients’ abdominal pain and associated
nausea and/or emesis, they may present with profound dehydration resulting in
tachycardia, orthostatic hypotension, and even shock physiology. Sequestration of
uid outside of the intravascular space in the retroperitoneum and other anatomic
compartments due to inammatory mediators can further compound extrapancreatic organ system failure such as in the renal system [36, 41].
Abdominal distention precipitated by the extravasation of uid into the retroperitoneum is common. Fulminant peritonitis may evolve as a rare, late nding associated with severe AP and is associated with a worse prognosis [44, 45]. Although
uncommon, palpation of abdominal masses in the epigastrium or upper abdomen
may suggest the presence of a pancreatic pseudocyst. Cullen’s sign (bruising of the
periumbilical area) and Grey Turner’s sign (bruising of the ank) are consistent with
retroperitoneal bleeding that can manifest in severe AP.These signs are rare and are
associated with increased mortality [44, 45]. Signs of hepatobiliary obstruction
including jaundice may be present on exam and should raise concern for an obstructive process due to neoplastic lesions or anatomic causes.
This third-spacing of extracellular uid may further precipitate hemoconcentration evidenced by elevated hematocrit and leukocytosis on serologic laboratory testing [42, 46]. Electrolyte abnormalities, elevated blood urea nitrogen, hypocalcemia,
and hyperglycemia are also seen. Elevated bilirubin and alkaline phosphatase, with
or without the presence of elevated aminotransferases, should raise the suspicion for
biliary obstruction—a common presentation of biliary pancreatitis [42, 46].
Laboratory Tests
Serum amylase and lipase are the most common laboratory tests used to diagnose
AP [47, 48]. Early during AP, there is blockage of pancreatic digestive enzymes
secretion while synthesis continues. Digestive enzymes leak from acinar cells
through the basolateral membrane and into the interstitial space eventually entering
systemic circulation. Serum amylase levels may rise 6–12h after the onset of symptoms and usually return to normal within 3–5days in uncomplicated cases [49].
Serum amylase elevation is considered a nonspecic nding with sensitivity and
specicity for the diagnosis of AP of 67–83% and 85–98%, respectively [48]. Serum
amylase may be elevated in other conditions with an extra-pancreatic cause, such as
diseases of the salivary glands, which also produce amylase. Patients with alcoholic
pancreatitis may have an inability to produce sufcient amylase levels to meet criteria for pancreatitis in as high as 20% of cases and elevated triglyceride levels in
hypertriglyceridemia-associated pancreatitis may interfere with accuracy of the
amylase assay in up to 50% of patients [50, 51]. Furthermore, mild elevations in
amylase or lipase in the setting of multiorgan failure and shock may be incidental
ndings of systemic hypoperfusion and not true acute pancreatitis. A threefold
24
C. T. Huerta et al.
elevation of serum lipase level is more diagnostic, especially in patients seen several
days after the acute attack, and serum lipase is elevated in both alcoholic and nonalcoholic pancreatitis [48]. Serum lipase has a sensitivity of 82–100% for the diagnosis of acute pancreatitis, often rising within 4–8h after symptom onset and peaking
at 24h. Lipase levels remain elevated longer than amylase, generally returning to
normal within 8–14days after an episode of acute pancreatitis [48, 50, 51]. Trending
of amylase and lipase levels in an acute episode is not indicated, and once a diagnosis of acute pancreatitis is made, management should be driven only by symptomatology. The only utility to repeating enzyme levels is when a patient has initially
improved, then clinically declines with concern for complication such as a collection (necrotic or inammatory) or recurrent episode of acute pancreatitis [39].
Imaging
At presentation, abdominal radiographs are useful in the exclusion of other causes
of abdominal pain, such as bowel obstruction, ileus, or perforated bowel, but are not
diagnostic for AP.Chest X-ray studies may show inltrates, left lower lobe atelectasis, or effusion [52, 53]. Abdominal lms may be unremarkable or show localized
ileus of the small intestine, paucity of air in the distal colon to the splenic exure
due to functional spasm of the descending colon, or ground glass appearance indicating an acute peripancreatic uid collection [52, 53].
On abdominal ultrasonography, the pancreas may appear diffusely enlarged and
hypoechoic in AP [53]. Peripancreatic uid collections can be seen as anechoic
areas that may contain internal echoes if pancreatic necrosis is present. Sensitivity
of abdominal ultrasonography is as high as 95% in diagnosing uncomplicated cholelithiasis though its sensitivity decreases in the setting of biliary pancreatitis due to
concurrent bowel distention [52, 53]. Up to 25–35% of patients have a limited
radiologic exam on abdominal ultrasonography due to ileus or bowel gas that precludes adequate visualization of the gland or the bile duct [54]. Nonetheless,
abdominal ultrasonography is recommended to be performed in all patients with
acute pancreatitis to evaluate for biliary etiologies and gallstones [53, 55]. Additional
imaging should be used only when the diagnosis is not conclusive from the history,
physical examination, and laboratory ndings or when a complicated course is
anticipated.
CT imaging is not routinely indicated as the diagnosis is obvious in many cases,
and many patients may have a mild and uncomplicated course. Despite this, intravenous contrast-enhanced CT scanning is a useful imaging technique not only for
diagnosis of acute pancreatitis but also for detection of local complications of pancreatitis. This should be delayed until the patient is rehydrated if there is uncertainty
of diagnosis because impairment of pancreatic perfusion and signs of pancreatic
necrosis, recognized by the lack of enhancement on contrast-enhanced CT, can take
several days [52]. After this time contrasted CT has been demonstrated to reliably
identify the presence and extent of necrosis as well as local complications. If a