The document discusses acute pancreatitis (AP) in children. It defines AP as a reversible inflammatory process of the pancreas that can involve other nearby tissues or organs. A diagnosis requires abdominal pain compatible with AP as well as serum amylase and/or lipase levels at least 3 times above normal. Common causes include infections, biliary issues, medications, and unknown factors. Clinical features are typically abdominal pain, fever, vomiting, and jaundice. Severity can range from mild to severe based on organ dysfunction. Treatment involves fluid resuscitation, pain management, nutritional support, and antibiotics for infected necrosis in severe cases. Complications can be systemic or local.

1. Acute Pancreatitis
Presenter: Dr. Basant Kumar Pandey
Moderator: Dr. Rishi Bolia, Assistant Professor
Dr.Pooja Semwal, SR (Paediatric Gastroenterology)

2. Definition
Acute pancreatitis (AP) is an acute reversible inflammatory process of the
pancreas with variable involvement of other regional tissues or remote
organ systems.
The INSPPIRE (International Study Group of Pediatric Pancreatitis: In search
for a cure) 2012 has recommended at least 2 of the following 3 criteria for
the diagnosis of AP:
1. Abdominal pain suggestive of, or compatible with AP (i.e., abdominal pain
of acute onset, especially in the epigastric region).
2. Serum amylase and/or lipase activity at least three times greater than the
upper limit of normal (IU/L).
3. Imaging findings characteristic of, compatible with AP.

3. ETIOLOGY
 Infections: Mumps, HIV, Coxsackie B, Hepatitis A,B, Varicella zoster,Measles
 Biliary: Choledochal cysts, Cholelithiasis, Biliary sludge, Ascariasis
 Medications: Valproic acid, Corticosteroids, L. Asparginase,Azathioprinea, 6 MP
 Idiopathic
 Structural pancreatic disorders: Annular pancreas, Pancreas divisum, Sphincter of Oddi
dysfunction
 Mechanical: Blunt abdominal trauma
 Metabolic: Hypertriglyceridemia, Hypercalcemia
 Systemic disease: Hemolytic Uremic syndrome, Systemic Lupus Erythematosus
 Nutritional :Malnutrition, Vitamin A and D deficiency

4. referen
ces
n Etiology
sytemic Biliary Anatomic Trauma Familial Metabolic Drugs Idiopathic
De
Banto
et al
(2002)
301 3.5 10.5 1.5 13.5 5.5 4 11 34
Suzuki
et al
(2008)
135 8.9 30.4 29.5 9.6 NA NA 11.1 10.4
Vybhav
et al
(2020)
101 12 14 - 15 1 - 7 50
Sathiya
sekara
n
(2015)
48 21.8 17.3 - 17.4 -- - 23 17

6. Clinical features
Abdominal pain 85.9 % (n-116)
Fever 38.5 % (n-52)
Vomiting 37.8 % (n-51)
Jaundice 8.1 % (n-11)
Back pain 4.4 % (n-6)
Pale stool 3% (n-4)
Diarrhea 2.2% (n-2)
Reference: Suzuki, M. (2014). Acute pancreatitis in children and adolescents. World
Journal of Gastrointestinal Pathophysiology

7. Clinical manifestation
1.Mild Acute pancreatitis
2.Moderately Severe Acute pancreatitis
3.Severe Acute Pancreatitis

8. Mild Acute Pancreatitis
 Not a/w organ failure,local or systemic complications
 Resolves within the 1st week after presentation
 Most common form of AP
 Moderate to severe abdominal pain
 The pain increases in intensity for 24–48 hr, during which time vomiting may increase
 The prognosis for complete recovery in the acute uncomplicated case is excellent

9. Moderately Severe Acute pancreatitis
Transient organ failure/dysfunction lasting < 48 hours or development
of local or systemic complication
Imaging may reveal sterile peri-pancreatic necrosis
Prognosis is excellent but recovery may be prolonged.

10. Severe acute pancreatitis is rare in children:
 Development of organ dysfunction that persists more than 48 hours
 Uncommon in children
 A bluish discoloration may be seen around the umbilicus (Cullen sign) or in the flanks (Grey
Turner sign).
 The pancreas is necrotic and can be transformed into an inflammatory hemorrhagic mass.
 The mortality rate, which is ≈20%
 Has a poor prognosis.

12. Investigations
1.Biochemical Test
Lipase
Amylase
2.Abdominal ultrasound
3.CT

13. Amylase
 After 3-7 days normalises even if inflammation
continues.
 Hence normal levels doesn’t exclude the disease

14.  High Amylase levels seen in:
Pancreatic disorder
Salivary disorders
Renal failure
Intestinal diseases- gut infarction perforation ,peritonitis, obstruction
Ectopic production : cancers of pancreas, thymus, breast, lung ,ovary.
DKA and other acidotic conditions

15. S.Lipase
 More specific
 Stays even upto 8 to 14 days
 Half life about 10 to 14hrs
 Level of lipase can’t predict disease severity and outcome

18.  Diffuse Decrease in Pancreatic Echogenicity (than liver)
 Free fluid
 Increased volume of Pancreas i.e, Bulky Pancreas
 Gall stones
 Parenchymal inhomogenicty may correlate with necrosis
 Pseudocysts
 Splenic vein thrombosis

19. Indication of CT
Not routinely indicated
Diagnosis of AP uncertain
Severe clinical pancreatitis , abdominal distension and tenderness, high
grade fever
No improvement after 72 hour of conservative treatment
Acute changes in clinical status (new onset fever, pain and shock after
successful initial medical therapy

20. Severity Assesment
De Banto Score
Age (<7 yr)
weight (<23 kg)
 Admission WBC (>18,500)
Admission LDH (>2,000)
48-h trough Ca2+ (<8.3 mg/dl)
48-h trough albumin (<2.6 g/dl)
48-h fluid sequestration (>75 ml/ kg/48 h)
48-h rise in BUN (>5 mg/dl).
cut-off for predicting a severe outcome is three criteria.

21. CTSI BALTHAZAR SCORE

23. Grading
:Mild
:Moderate
 0-3
 4-6
 7-10 : severe

24. Etiological workup
Serum alanine aminotransferase (ALT) activity and GGTP
Fasting blood triglycerides
Serum calcium
Viral antibodies

25. MANAGEMENT
Reference: Management of Acute Pancreatitis in Pediatric population: A Clinical report
from North America Society for Pediatric Gastroenterology, Hepatology and Nutrition
Pancreas Committee (NASPHAGAN), January 2018

26. 1.FLUID RECUSCITATION
Main stay of therapy
Should be initially resuscitated with crystalloids (RL>NS)
If severe vomiting insert NG tube
PPI should be started in all patient
If evidence of hemodynamic compromise, a bolus of 10 to 20 mL/kg is
recommended.
1.5 to 2 times maintenance IV fluids should be given with monitoring of
urine output over the next 24 to 48 hours
Serial evaluations done to assess fluid status clinically and by
measuring BUN & Hematocrit every 8-12 hrs.

27. 2. Pain Management
1st line of pain management is NSAIDS
IV morphine or other opioid should be used for acute pancreatitis pain
not responding to acetaminophen or NSAIDs

28. 3.Nutrition
children with mild AP may benefit from early (within 48–72 hours of presentation)
oral/enteral nutrition (EN).If child not abe to take by mouth then consider NG feeding.
Children with mild AP should be started on regular diet
Parenteral nutrition (PN) should be considered in cases when EN is not possible for a
prolonged period (longer than 5–7 days).
Enteral nutrition should commence as soon as feasible, with a combination of EN
and PN being superior to sole PN.

29. 4.Role of Antibiotics
 Prophylactic therapy has no role
 Mild disease doesn’t needs antibiotics at all
 For severe pancreatitis i.e, with necrosis may benefit
 Definitive role is seen with proven cases of infected Necrosis
 Antibiotics of choice are CARBAPENAMS

30. Complications:
Systemic
 Pleural effusion
 ARDS
 Atelectasis
 Hypotension
 arrythmias
 Pericardial effusion
 DIC
 ATN
 Renal vein /artery thrombosis
 Hyperglycemia
 Encephalopathy
 Subcutaneous fat necrosis

31. Ref: Banks PA, Bollen TL, Dervenis C, et al Classification of acute pancreatitis—2012: revision
of the Atlanta classification and definitions by international consensus

32. Clinical manifestation of AP
Biochemical
test Imaging
Diagnosis
Severity
assesment
Non-severe Severe
Recovery
Adbominal pain,vomiting,medical
history,Etiology
S.Amylase ,lipase USG,CT
Fluid resuscitation
Pain management
Nuritional support
Basic treatment and intensive care
Circulatory and respiratory
management
Follow up if any systemic or local
complication

33. THANK YOU