ACUTE PANCREATITIS combined.pptx.pptx in kids

PANCREATITIS
Presenter : Dr. Vikas Sharma
Moderator : Dr. Raghvendra Singh

Case Scenerio
• 7 years/ male presented to a private hospital on 31st
July 2019 with
c/o pain in upper abdomen for 1 day, moderate to severe intensity,
associated with nausea and vomiting
Past history – non-significant
Family history – GB calculi in mother
• Examination – Conscious, oriented, vitals – stable
P/A – soft, non-distended, epigastric tenderness+

• Inv – Serum amylase – 632 (normal range 20-80)
Serum lipase – 1935 (normal range 0-160)
CECT abd – Pancreas diffusely bulky and edematous with
heterogenous contrast enhancement, mild
peripancreatic fat stranding, mild- moderate free
fluid in abdomen and pelvis

• SCOPE OF THE SEMINAR
• Pancreas
- Anatomy and Development
- Physiology
- Definition
- Epidemiology
- Classification
- Pathophysiology
- Etiology
- Clinical features
- Diagnosis
- Management
- Complications
- Prognosis
- Pancreatic enzymatic
replacement in chronic
pancreatitis

ANATOMY OF PANCREAS
• The pancreas lies mostly posterior
to the stomach
• Retroperitoneal structure except
for a small part of its tail
• Consists of head, uncinate process,
neck, body and tail
• Head and neck overlies vertebrae

The main pancreatic duct
+
Common bile duct
Hepatopancreatic ampulla
(Ampulla of Vater)
Opens at major duodenal papilla
(2nd
part of duodenum)
• The accessory pancreatic duct opens at
minor duodenal papilla
Accessory pancreatic
duct
Main
pancreatic
duct

DEVELOPMENT
• Dorsal pancreatic bud - invades dorsal
mesentery.
• Ventral pancreatic bud (uncinate process
and inferior part of head) - develops from the
duodenal wall close to the bile duct.
• With the rotation of stomach and the
duodenum, ventral pancreatic bud moves
posterior and inferior to the dorsal pancreatic
bud to fuse with it.
• Ventral pancreatic bud forms main pancreatic
duct (of Wirsung), which opens to major
duodenal papilla.

DEVELOPMENTAL ABNORMALITIES
• Pancreas divisum – 10% individuals, dorsal and
ventral bud duct fail to fuse minor papilla
draining the body and tail risk of recurrent
pancreatitis. Diagnosis – ERCP, MRCP
• Anomalous pancreaticobiliary union
(APBU) – common bile duct and the main
pancreatic duct unite outside duodenal wall
channel more than 15mm in length
increased risk of recurrent pancreatitis and
cholangiocarcinoma.
Pancreas divisum

• Annular pancreas –
The ventral bud becomes misaligned
encircling the second part of
duodenum.
Presentations – Neonatal bowel
obstruction, can be associated with GIT
malformations, chronic pancreatitis (rare)
P

PHYSIOLOGY
• More than 80% of the exocrine pancreas
composed of clusters of acini lobules.
• The basolateral membrane of the acini cells
- receptors for cholecystokinin (CCK),
acetylcholine, vasoactive intestinal peptide
(VIP).
• The acini cells - digestive enzymes
• The centro-acinar cells and the duct cells -
water and bicarbonate.

PANCREATIC SECRETIONS
Pancreatic enzymatic pathways –
1) Proteolytic
(a) Trypsin – cleaves interior peptide bonds involving
basic amino acids.
(b) Carboxypeptidase – cleaves at carboxy
terminals
(c) Chymotrypsin – cleaves interior bonds involving
aromatic amino acids, leucine, glutamine and
methionine
(d) Elastase – cleaves at neutral aliphatic amino
acids.
(Pediatric Gastrointestinal and Liver Disease, Wyllie and
Hyams, 3rd
edition)

2) Pancreatic triglyceride lipase (PTL) –
secreted in active form, hydrolysis at sn-1
and sn-3 positions, producing fatty acids
and 2- monoacylglycerol
- Bile salts, dietary proteins and phospholipids
inhibits PTL activity
- Pancreatic protein colipase enhances activity
of PTL by forming complex with the PTL
3) Pancreatic alpha amylase – secreted
in active form, hydrolyzes alpha- 1,4
glucose linkages but not alpha- 1,6
(Pediatric Gastrointestinal and Liver Disease, Wyllie and
Hyams, 3rd
edition)

Pancreatic fluid and bicarbonate secretion
- Secretin- induced stimulation can increase HCO3-
concentration to maximum of 140 mEq/L,
creating pH of 8.2 which is necessary for action of
pancreatic enzymes
- Zymogen granules solubilize in alkaline medium
- Pancreatic enzymes are acid sensitive
- In cystic fibrosis, CFTR mutation Cl-
secretion Cl-/HCO3- exchange
HCO3- and Na+,K+, water in duct viscous
fluid duct inspissation chronic
pancreatitis

DEFINITION
• Acute pancreatitis is defined as an acute inflammatory process of the
pancreas with variable involvement of other regional tissues or
remote organ systems
• Clinical definition – at least 2 of the following 3 :
(1) Abdominal pain of pancreatic origin
(2) Amylase and/or lipase at least 3 times upper limits of normal
(3) Imaging findings suggestive/compatible with pancreatic
inflammation
INSPPIRE – International Study Group of
Pediatric Pancreatitis : In Search For a Cure
JPGN 2018; 66: 159-76

EPIDEMIOLOGY
• In children, lesser incidence than adults
• Incidence vary according to the country –
- USA – 13.2 cases/ 1 lac children/ year
(Morinville et al., Pancreas. 2010; 39:5-8)
- Australia – 3.6 cases/ 1 lac children/ year
(Nydegger A et al., J Gastroenterol Hepatol. 2007; 22:1313-6)
- Scarcity of data from India – Estimated 4-7 cases per year per referral
centre

CLASSIFICATION
• Severity in pediatric acute pancreatitis is classified as –
(1) Mild – without organ failure, local or systemic complications, and
usually resolves in the first week
(2) Moderately severe – presence of transient organ failure that
resolves in < 48 hours, or local complications or exacerbation of
comorbid disease
(3) Severe – persistent organ failure that lasts >48 hours and that may
be involving single or multiple organs
INSPPIRE – International Study Group of
Pediatric Pancreatitis : In Search For a Cure

INSPPIRE – International Study Group of Pediatric Pancreatitis : In Search For a Cure

Goldstein B. et al., International Consensus Conference on Pediatrics, 2002

PATHOPHYSIOLOGY
PANCREATIC INJURY
ENZYME ACTIVATION AND
RELEASE
PANCREAS PERITONEUM AND
PERIPANCREATIC TISSUE
WBC ACTIVATION
Edema
Inflammation
Necrosis
Hemorrhage
Trypsinogen
Lipase
Elastase
Chymotrypsinogen
Phospholipase
Abscess
Thrombosis
Peritonitis
Necrosis
Ascites
Fat necrosis
Co- localization
hypothesis

WBC ACTIVATION
LEUKOCYTES AND MONOCYTES
TISSUE DESTRUCTION LEUKOTRIENES
ENDOTHELIAL AND NEUTROPHIL
ACTIVATION
ORGAN FAILURE
Cytokines
TNF- alpha
PAF
Proteases
PMN elastase
Free radicals
Kidney
Lung
Cardiovascular shock

ETIOLOGY
- Infections – Mumps, HIV, Coxsackie B, Hepatitis A,B, Varicella zoster,
Measles, Leptospirosis
- Biliary – Choledochal cysts, Cholelithiasis, Ascariasis, Biliary sludge
- Medications – Valproate, Corticosteroids, L.Asparaginase, Azathioprine,
6- Mercaptopurine
- Idiopathic – Tropical pancreatitis
- Genetic – Hereditary pancreatitis, Trypsinogen gene mutation, SPINK 1
gene mutation
- Structural pancreatic disorders – Annular pancreas, Pancreas divisum,
Sphincter of Oddi dysfunction

- Mechanical – Blunt abdominal trauma
- Metabolic – Hypertriglyceridemia, hypercalcemia
- Systemic disease – Hemolytic uremic syndrome, SLE
- Nutritional – Malnutrition, Vitamin A and D deficiency

ETIOLOGY
• Common causes –
(1) Idiopathic (52.5%)
(2) Trauma (21%)
(3) Biliary (10%) – Gallstones (7%), Choledochal cyst (3%)
(4) Viral infections (7%)
(5) Drugs (5.6%) – L-asparaginase, Valproate, Carbamazepine,
Azathioprine, NSAIDS
(6) Others (4%) – HUS, Macrophage activation syndrome, Post-
ERCP
Poddar et al., SGPGI, 2003-2014

Etiology from various studies
Study Werlin et al., USA Suzuki et al., Japan Das et al., New Delhi Poddar et al.,
Lucknow
Period/ Duration 1996-2001 1985-2011 1994-2001 2003-2014
Number of cases 180 145 28 160
Etiology (%)
Idiopathic 8 8.3 35.7 52.5
Structural 19.5 39.3 10.7 10
Trauma 14 9.6 14.3 21
Drugs 12 13.1 14.3 5.6
Infectious/ viral 8 3.4 7.2 7
Systemic 14 8.9 -------
Metabolic 5.5 -------- -------
Familial 3 2.1 7.2

CLINICAL FEATURES
Symptoms :
More common –
(1) Abdominal pain – epigastric or left
upper quadrant
(2) Nausea and vomiting – increases in
severity in the initial 24-48h along with
pain
(3) Anorexia
Uncommon –
(4) Back pain
(5) Dyspnea
Das et al., AIIMS, New Delhi, 2003

Signs :
More common –
(1) Abdominal tenderness – mid-abdominal,
generalized or epigastric tenderness
(2) Low grade fever
(3) Abdominal distension
(4) Diminished or absent bowel sounds
Uncommon –
(2) Hypotension
(3) Renal failure
(4) Ascites
(5) Pleural effusion, usually left sided
(6) Fluid retention
Das et al., AIIMS, New Delhi, 2003

Pancreatitis
Presenter – Dr. Shefali Yadav
Moderator – Dr. Raghvendra

Learning objectives
• Diagnosis of acute pancreatitis
• Management
• Complications
• Prognosis
• Chronic pancreatitis – pancreatic enzymatic replacement

Diagnosis
• The definition of acute pancreatitis in children is by 2 of the following:
• Abdominal pain
• Elevated amylase or lipase >3 times the upper limit of normal
• Imaging findings of acute pancreatitis
• Initial assessment – history including family history, drug intake and surgical
intervention in the past, if any
• Laboratory investigations –
Serum amylase
Serum lipase
 other tests

Serum amylase
• α-Amylase - hydrolyzes the 1–4 glucosidic linkage in starch
• Synthesized in several organs, majorly in the pancreas and salivary glands
• Levels rise within hours of inflammation of the pancreas and remain increased for 1-2 days
• Specificity of the serum amylase assay is highest when the increase is at least 3-fold
• Serum amylase is of two categories – S-amylase and P- amylase

Serum amylase
• However , 20% of adults with acute pancreatitis - normal serum amylase levels
• A persistent increase - pseudocyst, pancreatic tumor or macroamylasemia
• Levels don’t correlate with degree of severity of pancreatic inflammation

• Pancreatic amylase (P-amylase)
Biliary obstruction
Bowel obstruction
Perforated duodenal ulcer
Acute appendicitis
Mesenteric ischemia or infarction
Peritonitis
Salivary amylase (S-
Amylase)
Salivary: parotitis (mumps),
trauma, surgery, salivary
duct obstruction
Diabetic ketoacidosis
Anorexia nervosa, bulimia
Ovarian: malignancy,
ruptured ectopic pregnancy,
cysts Malignancy
Mixed or unknown
Head trauma
Postoperative
Macroamylasemia
Causes of raised
amylase

Serum lipase
• Sensitivity of serum lipase is between 85% and 95%
• The sensitivity of serum lipase assay is higher than that of serum amylase 24 h after the illness
• As Lipase cleared by the kidney is reabsorbed by the tubules , lipase levels remain raised upto 14
days

• Other lab tests :
• Complete blood count (CBC),KFT, electrolytes, albumin, glucose, and calcium
• Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase,
gamma-glutamyl transferase (GGT), and total bilirubin
• If clinical features and enzyme elevations favor pancreatitis , imaging is not required to establish
the diagnosis

Conventional radiography
• limited role , non specific findings
• Signs seen on plain abdominal radiography –
 A sentinel loop - distended small bowel loop adjacent to the pancreas
 The colon cutoff sign - air in the splenic or hepatic flexure with a paucity of air
in the distal colon
 Calcifications in the pancreas - chronic pancreatitis
 A barium study - effects of pancreatic enlargement

Sonography
• Advantages - No radiation , no sedation required
• Limitations – user dependent , poor image quality when air is present in the bowel overlying the
pancreas

Sonography
• Findings –
a) diffuse or local enlargement of the pancreas
b) poorly defined borders
c) decreased echogenicity
d) dilated pancreatic ducts
e) pseudocyst
f) Evaluate the gallbladder for cholelithiasis or choledocholithiasis

NORMAL PANCREAS Acute pancreatitis

Computed tomography(CECT)
• Findings include diffuse enlargement of the pancreas, hemorrhage, necrosis, traumatic damage
and complications such as pseudocyst
• However , sedation is required
• A normal CT finding does not exclude pancreatitis

Mild acute pancreatitis
Necrotising pancreatitis

• Non- invasive method, no radiation and has a lower complication rate than ERCP
• Diagnose structural abnormalities of the pancreaticobiliary tract and when ERCP is unsuccessful
• Disadvantage -poor ability to define the peripheral biliary tree
• However , an inflamed pancreas is difficult to delineate on MRCP
Magnetic resonance cholangiopancreatography
(MRCP)

ACUTE PANCREATITIS combined.pptx.pptx in kids

Endoscopic retrograde cholangiopancreatography
• Indications for ERCP:
• Recurrent pancreatitis (more than two discrete episodes of pancreatitis)
• Prolonged episode of pancreatitis (more than 1 month)
• MRCP suggesting structural abnormalities
• First episode of pancreatitis in a child with a family history of pancreatitis
• Pancreatitis following liver transplantation
• Pancreatitis associated with cystic fibrosis
• Pancreatic trauma
• Preoperative evaluation of non-resolving or enlarging

Endoscopic retrograde cholangiopancreatogra
• Complications(in <5%) include
• Pancreatitis, cholangitis
• Post- procedure pain requiring analgesics
• Intramural dye injection
• Perforation, ileus

• Retrospective case record review of pediatric patients (age ≤15 y)
undergoing ERCP between January 2011 to June 2015
• 164 ERCP procedures were done in 126 patients (67 males)
• Indications :
• Choledocholithiasis (50, 30.5%)
• Chronic calcific pancreatitis (38,23.2%)
• Main pancreatic duct injury with leak (21,12.8%)
• Bile leak (12,7.3%)
• The cannulation success rate was 90.4% (114 out of 126), while
procedural success rate was 86% (141 out of 164)
• 8(4.8%) children developed complications:
• Mild pancreatitis (2)
• Retroperitoneal duodenal perforation (2),
• Sphincterotomyrelated bleed (2)
• Hypoxia (2)
Dahale, A.S., Puri, A.S., Sachdeva, S. et al. Indian Pediatr (2019) 56: 196.

Severity grading of acute pancreatitis
• In adults various scoring systems are available –
o Ranson criteria
o Acute Physiology and Chronic Health Evaluation (APACHE)-II
o Computed tomography severity index (CTSI)
However, none of them are validated in pediatric population

Management
Mild AP: AP without organ failure, local or systemic complications, and usually resolving within
the first week
Moderately severe AP : the presence of transient organ failure that resolves in no longer than
48hours, or local complications or exacerbation of co-morbid disease
Severe AP : organ failure that persists for longer than 48 hours
Classification of acute pancreatitis in the pediatric population: clinical report from the NASPGHAN pancre
committee. Abu-El-Haija M, Kumar S, Szabo F, et al. J Pediatr Gastroenterol Nutr 2017;64:984 – 90.

• Supportive care includes careful monitoring of vital signs, ensuring bedrest and correcting
intravascular fluid depletion and acidosis.
• Pain management - Intravenous morphine or other opioid should be used for acute pancreatitis
pain not responding to acetaminophen or NSAIDs
• Look for complications
• Mild disease - The treatment is mainly supportive and includes intravenous fluid resuscitation and
pain management
• Severe pancreatitis- address local, systemic and septic complications while providing supportive
care
OVERVIEW OF MANAGEMENT

Fluid resuscitation in AP
Purpose of effective fluid resuscitation - replenish the blood volume, stabilize the
capillary permeability, modulate the inflammatory reaction, and sustain intestinal
barrier function
Colloids and/or crystalloids: Among crystalloids, lactate Ringer’s better than
normal saline. Use colloids especially when albumin < 2.0 g/dL or hematocrit <
35%
A “controlled” resuscitation aimed at reversing hypotension, and being able to
maintain effective mean arterial pressure (MAP) and urine output > 0.5 mL/kg/hr
Aggarwal A, Manrai M, Kochhar R. Fluid resuscitation in acute
pancreatitis. World J Gastroenterol. 2014;20(48):18092–18103

Children with diagnosis of acute pancreatitis should be provided 1.5–2x maintenance IV
fluids with monitoring of urine output over the next 24–48h
Based on assessment of hydration status/hemodynamic status, if evidence of
hemodynamic compromise, a bolus of 10–20mL/kg is recommended
The IAP/APA guidelines recommend that patients receive 5–10 ml/kg/hr until
resuscitation goals are achieved with regards to improvements in heart rate, urine
output, mean arterial pressure and/or hematocrit
Abu-El-Haija M, Kumar S, Quiros JA, et al. Management of Acute Pancreatitis in the Pediatric Population: A Clinical Report
From the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition Pancreas Committee. J Pediatr
Gastroenterol Nutr. 2018;66(1):159–176

Monitoring
• Vitals should be strictly monitored to decide both the rate of hydration as well as the early
detection of complications, if any :
Cardiovascular Monitoring - HR, Bp, urine output
Pulmonary Monitoring - ABG (PaO2), CXR
Renal Monitoring – KFT, Urine ouput

Nutrition During Acute Pancreatitis
Enteral Nutrition (Oral, Gastric, Jejunal) During an Episode of Acute Pancreatitis
Enteral Versus Parenteral Nutrition in Acute Pancreatitis
Timing of Initiation of Enteral Feedings in Acute Pancreatitis
Gastric Versus Jejunal Feeding in Acute Pancreatitis
Diet/Formula Composition in Acute Pancreatitis
“Nutritional Considerations in Pediatric Pancreatitis: A Position Paper from the NASPGHAN Pancreas Committ
ESPGHAN Cystic Fibrosis/Pancreas Working Group.” Abu-El-Haija, Maisam et al. Journal of pediatric
gastroenterology and nutrition vol. 67,1 (2018): 131-143.

• Mild AP
• Should be started on a general (regular) diet and advanced as tolerated
• Should be nourished preferably via mouth as compared to nasogastric route
• EN(enteral nutrition) is favored over PN(parenteral nutrition) when possible
• Jejunal tube feedings should be reserved for those unable to tolerate oral or nasogastric tube
• Parenteral mode of nutrition should be used when oral/ NG/NJ feeds are not tolerated
• Combination of EN and PN, rather than PN alone, should be used in children who do not meet
caloric goals with EN alone
“Nutritional Considerations in Pediatric Pancreatitis: A Position Paper from the NASPGHAN Pancreas
Committee and ESPGHAN Cystic Fibrosis/Pancreas Working Group.” Abu-El-Haija, Maisam et al. Journal of
pediatric gastroenterology and nutrition vol. 67,1 (2018): 131-143.

• Severe AP
• Enteral nutrition (oral, NG or NJ as tolerated) should be attempted in children with
SAP within 72 hours from presentation to medical care, once deemed
hemodynamically stable
• Jejunal tube feeding should be reserved for those unable to tolerate oral or NG tube
feeding
• The use of specialized formulas or immunonutrition is not necessary
“Nutritional Considerations in Pediatric Pancreatitis: A Position Paper from the NASPGHAN Pancreas Committee
and ESPGHAN Cystic Fibrosis/Pancreas Working Group.” Abu-El-Haija, Maisam et al. Journal of pediatric
gastroenterology and nutrition vol. 67,1 (2018): 131-143.

Complications of pancreatitis
• Local complications :
Pseudo cyst-
• localized collection in the lesser sac
• Clinical features - vomiting, pain abdomen, mass palpable per abdomen
• Imaging – Usg, ct will help define the problem
• Complications include – hemorrhage, infection or rupture
• Management - <4cm usually resolve spontaneously, some may drain on its
own into stomach or colon, others require intervention – endoscopic or
surgical

Complications of pancreatitis
• Other local complications :
Abscess
Necrosis

Systemic Complications of pancreatitis
Respiratory
Pleural effusion
Adult respiratory distress syndrome
Cardiovascular
Shock
Fluid loss/ sequestration
Bleeding
Pericarditis
Myocardial
depression
Renal failure
Hypovolemia
Shock
DIC
Central nervous system
Psychosis or coma
Dermatologic
Fat necrosis
Hematologic
Disseminated intravascular coagulation
Hemolysis
Thrombocytopenia
Metabolic
Hypocalcemia
Acidosis
Hyperlipidemia
Hyperkalemia
Gastrointestinal
Paralytic ileus
Hemorrhage
Stress ulcers
Colonic obstruction/ fistula/ wall erosion Splenic
hematoma/ rupture

Recurrent pancreatitis
• Definition : ≥ 2 discrete episodes of AP , failure to meet AP criteria for a period after first episode
and absence of evidence of irreversible structural changes in pancreas
• Pancreatitis-associated gene mutations are the most common risk factors - PRSS1 ,SPINK1
• PERT should not be routinely used in children diagnosed with ARP, who do not have exocrine
pancreatic insufficiency

• From January 2003 to December 2015, 93 consecutive children (≤18
years of age) diagnosed to have ARP were included in this study
• A baseline Magnetic resonance cholangiopancreatography (MRCP)
done in all cases
• Serum calcium, lipid profile, blood sugar and stool fat (Sudan stain)
were done in all cases
• Genetic markers (PRSS1, SPINK1, and CFTR) were studied in a group
of 22 idiopathic ARP casesdiagnosed to have ARP were included in
this study
• Etiology wise – MC- IDIOPATHIC, f/b biliopancreatic structural causes
• ARP, especially in those with idiopathic and genetic mutations, is a
precursor of chronic pancreatitis(CP) and acts as a transition phase
between AP and CP
Poddar, Ujjal & Yachha, Surender & Borkar, Vibhor & Srivastava, Anshu. (2017). Is acute recurrent
pancreatitis in children a precursor of chronic pancreatitis? A long-term follow-up study of 93
cases. Digestive and Liver Disease. 49. 10.1016/j.dld.2017.02.019.

Pathophysiology
• Continuous destruction of the pancreatic gland resulting in irreversible scarring of the acinar and
ductal cells
• About 90% of the gland must be destroyed before clinical signs of pancreatic dysfunction occur
• There is infiltration of the glandular tissue by lym- phocytes, plasma cells and macrophages
• Each flare results in further damage and eventually leads to exocrine and endocrine dysfunction
• Pancreatic ducts show fibrosis, stricture and dilation. Calcification within the gland may be seen

Causes
Obstructive
● Congenital ductal anomalies-
Pancreas divisum Choledochal cyst
Stricture
● Trauma
● Sclerosing cholangitis
● Idiopathic fibrosing cholangitis
● Autoimmune pancreatitis
● Secondary to other autoimmune
disorders
Calcific
• Hereditary causes:
• PRSS1
SPINK1
CFTR mutations
?Mesotrypsin mutation
?Anionic trypsin mutation
● Tropical pancreatitis
● Hyperlipidemia
● Hypercalcemia
● Organic acidemias
Miscellaneous
● Idiopathic
● Mitochondrial cytopathy
● Inflammatory bowel
disease

Clinical features
Chronic abdominal pain with episodic exacerbation
Eventually pain improves- burning out of pancreas- exocrine and endocrine pancreatic
insufficiency
Exocrine insufficiency - hyperphagia to compensate for the gastrointestinal malabsorptive
losses ,secondary growth failure, stools – malodorous and features of protein and fat
malabsorption
Endocrine insufficiency – adulthood diabetes(3c)
Children with chronic pancreatitis should be screened for pancreatic exocrine insufficiency every
6 to 12 months

• Children <19 years of age were considered eligible for inclusion in the study if
they met criteria for ARP and/or CP
• Those patients who had total pancreatectomy (TP) with or without islet
autotransplantation (IAT)-were excluded
• 6% of children diagnosed with DM
• 40% of children in the registry with a diagnosis of DM having a diagnosis of CP
and 60%, having ARP
• 5 children with DM also had beta cell antibodies(38%)
• DM was more common in those children who also had hypertriglyceridemia
and other autoimmune disorders
• Thus,a multitude of risk factors were present and not just pancreatitis
Bellin MD et al. Diabetes Mellitus in Children with Acute Recurrent and Chronic Pancreatitis: Data From the
INternational Study Group of Pediatric Pancreatitis: In Search for a CuRE Cohort. J Pediatr Gastroenterol Nutr.
2019 Nov;69(5) 599-606.

Diagnosis
• Serum amylase and lipase are raised – eventually decrease once pancreatic destruction occurs
• Calcifications in the pancreas on CT or plain radiography
• ERCP/MRCP- beading of ducts (narrowing and dilation)
• Genetic testing – PRSS1, SPINK 1, CTRC,CFTR

Diagnosis
• Fecal elastase-1 (FE-1)on formed stool - used for the diagnosis of Exocrine Pancreatic
Insufficiency - a value less than 100 μg/g is diagnostic
• 72-h fecal fat test - coefficient of fat absorption [CFA: (grams of fat ingested-grams of fat
excreted)/(grams of fat ingested) x100] can be calculated - absorption value of <85% of fat intake
is considered abnormal in children younger than 6 months of age, and < 93% is abnormal for
children older than 6 months of age
• Direct pancreatic secretion testing (collection of pancreatic/intestinal fluid) is considered invasive
and not commonly used

Management
• Exacerbations – treated like acute pancreatitis
• PAIN – multimodal treatment
Non-medication therapies - distraction, visual imaging
Integrative pain strategies such as aromatherapy, acupuncture
Non-opioid medications
Opioids
Hospitalization with inpatient pain management

PAIN MANAGEMENT
• No specific pediatric guidelines exist
• Medical therapies include acetaminophen, nonsteroidal anti-inflammatory
drugs and narcotic analgesics
• Non-narcotic analgesics should be the first line of therapy for pain, and
narcotics reserved for uncontrollable pain
• Surgical therapies - drainage procedures to decompress obstructed ducts,
resection of strictures and removal of pancreatic stones .
• Total pancreatectomy and islet auto transplantation may be indicated in
children with CP and intractable pain, unresponsive to other measures
Párniczky, Andrea & Abu-El-Haija, Maisam & Husain, Sohail & Lowe, Mark & Oracz, Grzegorz & Sahin-Tóth, Miklós & Szabo,
Flora & Uc, Aliye & Wilschanski, Michael & Witt, Heiko & Czakó, László & Grammatikopoulos, Tassos & Rasmussen, Ib &
Sutton, Robert & Hegyi, Peter. (2018). EPC/HPSG evidence-based guidelines for the management of pediatric pancreatitis.
Pancreatology. 18. 10.1016/j.pan.2018.01.001.

Total pancreatectomy and islet auto
transplantation
• INDICATIONS :
1.Pain or debilitation for >6 months, as demonstrated by one of the following:
a. Chronic opioid dependence for >6 months
b. Severely impaired quality of life (frequent school absence and/or hospitalizations)
2. Failure of maximal medical and endoscopic therapies
3. Absence of reversible cause of CP or ARP
4. Absence of physiologic or psychosocial contraindication
5. Willingness to accept risk of lifelong diabetes
6. Adequate islet function (absence of C-peptide negative diabetes)
Párniczky, Andrea & Abu-El-Haija, Maisam & Husain, Sohail & Lowe, Mark & Oracz, Grzegorz & Sahin-Tóth,
Miklós & Szabo, Flora & Uc, Aliye & Wilschanski, Michael & Witt, Heiko & Czakó, László & Grammatikopoulos,
Tassos & Rasmussen, Ib & Sutton, Robert & Hegyi, Peter. (2018). EPC/HPSG evidence-based guidelines for the
management of pediatric pancreatitis. Pancreatology. 18. 10.1016/j.pan.2018.01.001.

Dosing of PERT
• Not known for children with Chronic pancreatitis
• However doses well defined for children with Cystic Fibrosis- 1000 to 2500 lipase units/kg per
meal in < 4 years of age and 500–2500 lipase units/kg per meal are used for those > 4 years of
age
• Lipase may also be based on grams of fat ingested : 500–4000 units lipase per gram fat . For
snacks, half the dose is recommended
• Infants - 2,000 to 4,000 units per 120 mL of infant formula or per breast- feeding.
• Doses are adjusted based on effect (clinical, stool, growth)
“Nutritional Considerations in Pediatric Pancreatitis: A Position Paper from the NASPGHAN Pancreas Committee and
ESPGHAN Cystic Fibrosis/Pancreas Working Group.” Abu-El-Haija, Maisam et al. Journal of pediatric gastroenterology
and nutrition vol. 67,1 (2018): 131-143.

DRUG COMPANY CONTENTS PRICE(INR)
Creon Solvay Lipase-10000 IU,
amylase – 8000 IU,
protease – 600 IU
205.5
Leno - EZ Bestochem Alpha galactosidase A
200mg, lactase 7mg,
protease 25mg ,
amylase 50mg,lipase
3mg
57
Digemax Shreya Lipase 20000 u,
amylase 62250 u,
protease 93750 u
145
Pan lipase Sun Lipase 10000 USP u,
protease 37000 USP
u, amylase 33200 USP
u
120.80

FOLLOW UP
• Growth and nutritional status
• Fat soluble vitamin levels – vit D, PT-INR
• Development of exocrine and endocrine pancreatic insufficiency
• Psychosocial assessment – missed school days, pain control

Ministry of Health, Labour and Welfare of
Japan (JPN) scoring
1. Base excess ≤ -3 mEq or shock (systolic blood pressure cutoffs according to age group);
2. PaO2 ≤ 60 mmHg (room air) or respiratory failure;
3. Blood urea nitrogen ≥ 40 mg/dL [or creatinine (Cr) ≥ 2.0 mg/dL] or oliguria (< 0.5 mL/kg per h);
4. Lactate dehydrogenase ≥ 2 × the value of the upper limits;
5. Platelet count ≤ 1 × 105
/mm3
;
6. Calcium ≤ 7.5 mg/dL;
7. C-reactive protein ≥ 15 mg/dL;
8. Number of positive measures in pediatric SIRS score ≥ 3;
9. Age < 7 years old or/and weight < 23 kg
• The cutoff for predicting a severe outcome was set at three criteria
• Sensitivity - 80% & specificity - 96%
Suzuki, Mitsuyoshi et al. “Scoring system for the prediction of severe acute pancreatitis
in children.” Pediatrics international : official journal of the Japan Pediatric Society 57 1
(2015): 113-8

CT SEVERITY INDEX (CTSI)
• Grading of pancreatitis (Balthazar score)
• A: normal pancreas: 0
• B: enlargement of pancreas: 1
• C: inflammatory changes in pancreas and peripancreatic fat: 2
• D: ill-defined single peripancreatic fluid collection: 3
• E: two or more poorly defined peripancreatic fluid collections: 4
• Pancreatic necrosis
• none: 0
• ≤30%: 2
• >30-50%: 4
• >50%: 6
• Scoring : 0-3: mild acute pancreatitis
• 4-6: moderate acute pancreatitis
• 7-10: severe acute pancreatitis

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