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C. Nutrition:
Enteral feeding should be primary therapy in patients with predicted severe AP.
Types of feed:
• Oral/enteral (NG/NJ)
• 25–30kcal/kg with 1.2–2g protein/kg
• Rarely TPN
AGA recommends early feeding (usually within 24h) for all patients with AP
(mild, moderately severe, and severe) as per patient tolerance.
RCTs have shown similar outcomes if feeding is initiated within 24h vs. 72h
(Backer etal., NEJM, 2014).
Enteral feeding is better than parenteral, because
• Less complications
• Less requirement of surgery
• Reduced mortality
• Maintains the structural and functional integrity of GIT
NG feeding is similar to NJ feeding (Meta-analysis Chang et al., Critical
Care, 2013).
However, NJ’s theoretical advantage is that it provides more rest to the pancreas
via the ileal brake mechanism. NG is easier, but many patients don’t tolerate NG
feeding.
NJ is indicated in:
• Critically ill patients with increased risk of aspiration pneumonia
• Gastroparesis
• Intolerant to NG feeding
D. Prophylactic antibiotics:
Meta-analysis showed no benet (Jiang etal., WJG, 2012).
Most patients in India get prophylactic antibiotics (66%) (Talukdar et al.,
IJG, 2014).
Prophylactic antibiotics associated with:
• More resistant infections
• Gram-positive infections
• More fungal infections
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E. Miscellaneous
• Respiratory care
• Cardiovascular care
• Management of metabolic complications (Hyperglycemia, hypocalcemia,
hypomagnesemia)
Diagnosis of (Peri)-Pancreatic Collections and Infected Necrosis:
Pancreatic necrosis
Denition: Lack of enhancement of pancreatic parenchyma on CECT.
Incidence: 5–10% of AP episodes.
Location: Pancreas alone, extrapancreatic tissues alone, or both (most common).
Diagnosis: Presence or absence of pancreatic necrosis is best diagnosed by
CECT after 72h of presentation.
Local complications of AP have been dened in the revised Atlanta classication
There are four types of collections associated with AP.
Interstitial edematous pancreatitis
Necrotizing pancreatitis
<4
weeks
Acute (peri)pancreatic uid collection:
Homogenous uid adjacent to pancreas
without a recognizable wall.
Acute necrotic collection:
Intra- and/or extra-pancreatic necrotic
collection without a well-dened wall.
>4
weeks
Pancreatic pseudocyst
An encapsulated well-dened, usually
extra-pancreatic uid collection with
minimal solids.
Walled-off necrosis
Intra- and/or extra-pancreatic necrotic
collection with a well-dened wall.
Q.What are the indications for intervention in necrotizing pancreatitis?
Ans:
Indications for Intervention in Necrotizing Pancreatitis (Radiological,
Endoscopic, or Surgical):
1. Infected necrotizing pancreatitis (either documented on culture or clinical suspi-
cion) with clinical worsening, preferably after 4 weeks after the necrotic collec-
tion has been well encapsulated.
2. Persistent organ failure for several weeks.
3. Non-infected WON with any one of the following indications:
(a) Gastric outlet obstruction, intestinal obstruction, or CBD obstruction.
(b) Ongoing symptoms (e.g., pain abdomen, “persistent unwellness”) continued
systemic illness, loss of appetite, loss of weight.
(c) Completely disrupted pancreatic duct with ongoing symptoms.
Rare indications for interventions include:
• Abdominal compartment syndrome
• Gastrointestinal bleeding
• Bowel ischemia
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Asymptomatic WON does not warrant any intervention regardless of the size and
extension of the collection as they may spontaneously resolve over time.
Q.Why Is It advisable to intervene after 4 Weeks after onset of symptoms in
case of WON?
Ans:
(a) Allow liquefaction: Predominant solid necrotic component is found initially,
which are poorly demarcated from surrounding viable tissue.
(b) Allow encapsulation: Collection at this stage is not encapsulated. Hence, it is
associated with more complications like pneumoperitoneum, pneumo-
retroperitoneum, and more infective complications.
Q.Indications for emergent intervention
Abdominal compartment syndrome: Life-saving radiological or surgical decom-
pression should be considered once medical management fails.
Other indications for emergency surgery include:
• Hollow viscus perforation
• Severe bleeding refractory to medial, endoscopic, or radiologic (angiographic)
intervention
• Bowel infarction
Q.What are the various strategies for intervention in pancreatic necrotic
collection?
Ans: Minimally invasive endoscopic and surgical step-up techniques have replaced
aggressive treatment modalities like open surgical debridement, which used to be
traditionally employed for infected pancreatic necrosis in the past. Risk of acute
complications like peri-operative stress, organ failure, and chronic ones like exter-
nal pancreatic stulae, pancreatic exocrine and endocrine deciency, and hernias
(incisional) are less commonly seen with newer modalities.
Minimally invasive necrosectomy classication:
A. Method of visualization
1. Open
2. Radiologic
3. Endoscopic
4. Hybrid, or other
B. Route
1. Peroral
(a) Transpapillary
(b) Transmural
2. Percutaneous retroperitoneal
3. Percutaneous transperitoneal, with or without transmural puncture
First-line treatment for infected necrosis:
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Current standard of care for infected necrotizing pancreatitis: Step-up
approach of PCD f/b on-demand necrosectomy in the later phase of illness when the
necrotic collection becomes organized (Based on TENSION trial, Brunschot etal.,
The Lancet, 2018).
Endoscopic transluminal drainage (ETD) or image-guided percutaneous catheter
drainage, preferably via a retroperitoneal approach, followed by endoscopic or min-
imally invasive surgical necrosectomy as needed (IAP/APA guidelines,
Pancreatology, 2013).
Summary of Randomized Controlled Trials Comparing Endoscopic and
Minimally Invasive Surgical Step-Up Approach:
PENGUIN trial TENSION trial MISER trial
Modality Endoscopic Surgical Endoscopic Surgical Endoscopic Surgical
Patients, n 10 10 51 47 34 32
Infected necrosis
(%)
100 90 45 57 91 94
Death % 10 40 18 13 9 6
End-point % 20 80 43 45 12 41
Complications
Bleeding (%) 0 0 22 21 0 9
Perforation (%) 0 20 8 17 0 0
Fistula (%) 10 70 5 32 0 28
Q.What are the various complications of severe AP?
A. Pancreatic stulae.
External pancreatic stulae: Persistent uid drainage via percutaneous drain
(PCD), PCD tract, or surgical wound site, with amylase>3× serum value. Pancreatic
stula usually closes after 10 weeks (median duration).
Management:
Transpapillary stent to bridge the site of leakage [effective in 27% (9–69%)]
(Arvanitakis et al., Endoscopy, 2008). Transpapillary stents may diminish the
chances of recurrent uid collection after resolution.
Endoscopic transpapillary stenting vs. conservative management: Rates of stula
closure same (84 vs. 75 %) but a shorter median time to resolve (71 vs. 120 days)
(Bakker etal., Ann Surg, 2011).
B. Disconnected Pancreatic Duct Syndrome (DPDS)
Important complication of acute necrotizing pancreatitis (ANP).
Forms as a result of necrosis of the MPD, resulting in discontinuation between
viable upstream pancreatic parenchyma and duodenum.
Incidence of DPDS: 16–46.3%
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Most common site: Neck of the pancreas
The diagnostic criteria of DPDS (Rana S, Pancreatology, 2020):
• Necrosis of at least 2cm of the pancreas (<2cm is usually associated with the
development of stricture of PD and not complete disconnection).
• Pancreatic parenchyma distal to the site of necrosis must be viable.
• Free extravasation of contrast agent (dye) on pancreatogram during ERCP with
total cut-off of the MPD.
Complications of DPDS:
1. Recurrent uid collection
Acute and chronic pancreatitis of the distal pancreatic parenchyma: Occurs long
term after resolution of necrotizing pancreatitis. It results due to scarring of the
upstream duct with resultant closed-space obstruction and complications.
2. Diabetes mellitus (More with proximal—head/genu DPD compared to body/tail).
Management:
1. Long-standing indwelling DPSs placed during transmural drainage.
2. Prophylactic trans-papillary PD stenting during transluminal drainage and/or
necrosectomy.
3. For chronic DPDS:
(a) Surgical resection of the upstream gland with or without islet cell autotrans-
plantation to reduce risk of diabetes.
(b) Roux-en-Y PJ: If the upstream PD is amenable for PJ.
(c) EUS-guided pancreaticogastrostomy.
C. Exocrine and endocrine insufciency:
Acute necrotizing pancreatitis is commonly associated with exocrine pancreatic
insufciency. Pooled prevalence: 27.1% at 36 months (Hollemans et al.,
Pancreatology, 2018). Pancreatic enzyme replacement therapy may be benecial
during the early refeeding phase.
Endocrine insufciency:
Pooled prevalence of prediabetes, diabetes mellitus (DM), and insulin require-
ment after acute pancreatitis: 16%, 23%, and 15%, respectively (Das et al.,
Gut, 2014).
The mechanism of endocrine insufciency is unrelated to the severity of pancre-
atitis, reecting pathophysiologic pathways other than necrosis.
D. Splanchnic vein thrombosis (SVT)
Incidence: 16–18% of cases with necrotizing pancreatitis.
Location: splenic vein (most common), portal vein, superior mesenteric vein.
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Clinical features:
• Mainly asymptomatic (with isolated splenic vein involvement)
• Torrential upper GI variceal bleeding
• Ascites
Management: Symptomatic treatment of complications to be considered.
Role of anticoagulation: Controversial data exist in literature. Recanalization
rate not statistically signicant in patients treated with anticoagulants. Not recom-
mended in patients with isolated splenic vein involvement.
E. Pseudoaneurysm.
Arterial pseudoaneurysm results from erosion of walls of surrounding arteries by
necrotic collection. Direct injury to adjacent vessels can also be caused by percuta-
neous drains, LAMS, and during endoscopic or surgical necrosectomy.
Peripancreatic pseudoaneurysm classication:
Type of artery
Communication with
GIT
Exposure to pancreatic
juice
I.Minor artery >5mm away from a
major artery
A.No communication 1. No exposure
II.Major artery which may be sacriced B.Communication + 2. Exposure +
III.Major artery which cannot be
sacriced
Most common location of pseudoaneurysms:
• Splenic artery (most common) (35–50%)
• Gastroduodenal
• Pancreaticoduodenal (20–25%).
Risk of rupture of pseudoaneurysm is much higher compared to aneurysm of
comparable size due to poor support of the aneurysm wall, and are associated with
signicant morbidity and mortality.
Management:
Trans-arterial embolization ± pseudoaneurysm stenting. Cyanoacrylate glue,
ethiodized oil, gel foam, thrombin, polyvinyl alcohol injection, or coil can also be
placed for better hemostasis.
Further Reading
Dijk V, et al. Acute pancreatitis: recent advances through randomised trials. Gut.
2017;66(11):2024–32.
Crockett SD, etal. American Gastroenterological Association Institute guideline on initial man-
agement of acute pancreatitis. Gastroenterology. 2018;154(4):1096–101.
P. Debnath et al.
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© The Author(s), under exclusive license to Springer Nature Singapore Pte
Ltd. 2022
V. Singh, A. Roy (eds.), Clinical Rounds in Hepatology,
https://doi.org/10.1007/978-981-16-8448-7_23
B. L. Meena · A. Roy · V. Singh (*)
Department of Hepatology, Post Graduate Institute of Medical Education and Research,
Chandigarh, Punjab, India
23
Chronic Pancreatitis
BabuLalMeena, AkashRoy, andVirendraSingh
Q.What are the commonly used definitions for Chronic Pancreatitis (CP)?
The classical denition of CP was the “Cambridge denition” (1984) which dened
CP as a continuing inammatory disease of the pancreas, characterized by irrevers-
ible morphological change, and typically causing pain and permanent loss of
function.
In 2016, a Mechanistic denition was incorporated which has characters of both
end-stage pancreatic disease (pancreatic atrophy, brosis, pain syndromes, stric-
tures, calcications, exocrine, and endocrine insufciency) as well as the mecha-
nisms of disease pathogenesis in individuals with genetic, environmental, and/or
other risk factors.
The central concept of the mechanistic denition involves an algorithm in a sus-
picious case of CP based on three features:
• Clinical features: Family history, characteristic pain, and features of pancreatic
insufciency.
• Risk: As per the TIGAR-0 risk assessment system (detailed below).
• Biomarkers: High amylase, lipase, triglycerides, vitamin deciency (A, D, E,
K), and exocrine function test.
Q.What are the components of the TIGAR-O checklist for the etiology of
Chronic Pancreatitis?
The components of the TIGAR-O system can be enumerated as:
• T: Toxic or metabolic (Alcohol, smoking, hypertriglyceridemia, drugs)
• I: Idiopathic (Subclassied as early-onset <35 years and late-onset >35 years)
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• G: Genetic (PRSS-1, CFTR, SPINK-1)
• A: Autoimmune Pancreatitis Type 1 and 2
• R: Recurrent acute or severe pancreatitis
• O: Obstructive lesions
Q.What are the common genetic polymorphisms that are implicated in CP?
In patients with Idiopathic Pancreatitis, what are the essential genetic
evaluations that should be done?
Acinar cell dysfunction polymorphisms
• PRSS1 (cationic trypsinogen gene)
• CPA1 (carboxypeptidase A1 gene)
• CEL (carboxyl ester lipase) A
• SPINK1 (serine protein inhibitor Kazal type 1)
• CTRC (chymotrypsin C)
Ductal cell dysfunction polymorphisms
• CFTR (cystic brosis transmembrane conductance regulator)
Disease-modifying genes polymorphisms
• CASR (calcium-sensing receptor gene)
• CTRC (chymotrypsin C)
• CLDN2 locus (Claudin-2 gene locus)
Although extensive panels can be ordered in resourceful centers, however, the
essential mutations that should be looked for are PRSS1, SPINK1, CFTR,
and CTRC.
Q.What are the areas for scoring for assessing the severity of Chronic
Pancreatitis as per the M-ANNHEIM System?
The acronym M-ANNHEIM has been used for pancreatitis with Multiple risk
factors- Alcohol consumption, Nicotine consumption, Nutritional factors, Hereditary
factors, Efferent duct factors, Immunological factors, Miscellaneous, and rare met-
abolic factors. It is used scoring system for the grading of chronic pancreatitis sever-
ity by using the following factors:
• Patient report of pain
• Pain control
• Surgical intervention
• Exocrine insufciency
• Endocrine insufciency
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• Severe organ complications
• Morphologic status on pancreatic imaging (according to the Cambridge
classication)
The severity is graded as:
• M-ANNHEIM A Minor 0–5 points
• M-ANNHEIM B Increased 6–10 points
• M-ANNHEIM C Advanced 11–15 points
• M-ANNHEIM D Marked 16–20 points
• M-ANNHEIM E Exacerbated .20 points
Q.Describe in brief the natural history of CP?
The evolution of CP is thought to be subsequent to a series of acute pancreatic inju-
ries at the acinar level or ductal level. These events are labeled as the Sentinel Acute
Pancreatitis Event (SAPE), which do not necessarily translate into clinical events.
The transition into chronicity occurs in phases, although the spatial distribution is
not homogenous, and there can be signicant overlaps between the phases:
• Early: First 5 years characterized by recurrent episodes of pain.
• Intermediate: 5–10 years characterized by morphological changes such as pan-
creatic calculi, ductal strictures, and pseudocysts.
• Late stages: Usually after 10 years characterized by pancreatic exocrine insuf-
ciency and diabetes.
Q.What is Type 3c Diabetes?
Diabetes secondary to CP is termed Type 3c diabetes, which occurs due to islet cell
loss. Patients with advanced CP usually have a low body mass index compared to
the classical obese type 2 diabetes phenotype. The duration of CP is the primary risk
factor for the development of endocrine failure. Western literature shows that diabe-
tes in CP occurs around 10 years after disease onset; however, Indian literature sug-
gests an earlier onset (Talukdar R etal. Pancreatology 2013).
Q.What are the causes of pain in CP, and what are its options for
management?
Causes of pain in CP include:
• Ongoing disease process
• Pancreatic pseudocyst
• Duodenal obstruction
• Biliary obstruction and cholangitis
• Development of pancreatic cancer
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The options for management of pain are multiple, and the approach should be
based on the WHO (World Health Organisation) Step ladder approach for pain
control:
• Analgesics: NSAIDs, Opioids.
• Antioxidants: Methionine, beta carotene, selenium, vitamin C.
• Neuromodulators: Pregabalin.
• Pancreatic enzyme replacement therapy: Although frequently used in the clin-
ical setting, a recent meta-analysis has shown a lack of efcacy with regard to
analgesia with pancreatic enzyme supplementation (Yaghoobi M etal. 2016).
However, PERT should be considered in patients with exocrine insufciency to
improve the complications of malnutrition.
• Endoscopic management: Extracorporeal shock wave lithotripsy (ESWL) with
or without endoscopic retrograde cholangiopancreatography (ERCP) and stent-
ing is currently recommended for large obstructive pancreatic ductal stones,
especially those located in the head and body region. According to one study
with a follow up of 2–5 years, there was complete pain relief in 68.7% of patients
(Tandan etal. GIE 2013).
• Surgical intervention: For long-term relief of pain after rst-line endoscopic
approaches have been exhausted or unsuccessful.
• TPIAT: (Total pancreatectomy with islet auto-transplant) Should be considered
only in cases of refractory pain when all other resources of pain control have
been exhausted.
Q.What are the characteristics of biliary obstruction in CP?
Ans: CBD stricture may be seen in 3–46% of cases of CP (Abdullah etal., HPBS
2007) and is more commonly seen with calcic CP.
Clinical presentation:
• Incidental in 17%
• Jaundice 30–50%
• Cholangitis 10%
• Secondary biliary cirrhosis: 7.3%
Biochemical marker: ALP>2× ULN: specic for CBD stricture
Radiological ndings
Five types of bile duct stricture:
• Type I: Long retro-pancreatic stenosis (Common)
• Type II: Spincter of oddi stricture with dilated common bile duct (Common)
• Type III: Hourglass CBD stricture
• Type IV: Symptomatic of cyst/cancer
• Type V: Carcinoma of the pancreas
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