The document provides information on pediatric pancreatitis. It discusses the following key points in 3 sentences: Pancreatitis is uncommon in children but can be caused by trauma, developmental anomalies, infections, drugs/toxins, or hereditary/metabolic factors. It involves inflammation and damage to the pancreas that can lead to complications like pseudocysts, hemorrhage, necrosis, and multi-organ failure. The diagnosis is challenging in children as it requires considering clinical presentation, blood tests showing elevated pancreatic enzymes, and imaging findings on ultrasound, CT, or MRCP to identify abnormalities in the pancreas.

5. PEDIATRIC
PANCREAS
[AC. INFLAM. OF ABDOMINAL TIGER]

6. Background
Pancreatitis (P) is uncommon in children: significant MM
• 13/100k/y children (US). Adult incidence has increased
dramatically past 15y: changing trends in etiology,
increased referral, better Dx
Due to underreporting & underDx incidence in
children (& adults) is unknown
• Evaluate all abdo. pain with HI of suspicion
• P. starts with blockage of ducts & acinar damage 
activation of enzymes  autodigestion (inflam.,
hge., necrosis, pseudocyst (23% of AP; >50% a/with
traumatic P.)
MM. morbidity-mortality, hge. Hemorrhage, Dx. Diagnosis. HI. High index

7. Anatomy
• P. is 6in long & sits across back of abdo, behind stomach;
p. duct joins CBD at ampulla of Vater
• Has indistinct head, body, & tail. Abdo. aorta & IVC cushion
it from vertebrae. Crushing/blunt trauma can injure it
• Numerous cong. anomalies are seen
Pancreas divisum occurs in 5-15% popn.: unsuccessful
fusion of ventral & dorsal buds: accessory Santorini
duct drains majority of p.: smaller, inadequate drainage
may cause chr. pain & rec. P.

8. Development

9. P. divisum with minor papilla stenosis causing rec. P. Note
bulbous shape of duct adjacent to cannula (santorinicele).
Dorsal duct outflow obs. is the probable c/of P.

10. P. is retroperitoneal, except just a part of tail coming through
mesenteric folds. Head is to Rt of L2, body over L1, & tail to Lt of T12

11. Blood supply
of Pancreas

14. Normal histology

16. 50% asymptomatic till adulthood. A/with: GI problems, Down,
polyhydramnios. More risk for p./biliary Ca. CF: due obs. NB may have
complete obs.: not feeding; spits, cries. Adult: fullness after meal, NV.
Dx: USG, AXR, CT, Upper GI & small gut series. Rx. mostly surgery.
Complications. Jaundice, Ca, P. PUD, Perforation, peritonitis

17. Double Bubble
Sign: dilated
stomach &
proximal duo- in
NB, typical in d.
atresia, midgut
volvulus or
annular p.

18. Annular pancreas
A: Upper GI series, oblique v.: narrowing of duo- C-loop (arrows)
B: ERCP: small ducts (arrows) encircling d., consistent with annular p.

19. Ectopic p.: lacks anatomic continuity with main p.; usually in
stomach, duo-, jejunum, Meckel’s. Most are small & asymptomatic.
Incidence at laparotomy is 0.2%. Some develop pseudocyst,
insulinoma, Ca. SS: abdo. pain, bleeding, obs.
Meckel’s
E.P.

20. Functions of the P
Exocrine Function
• Lipase, amylase, trypsin & chymotrypsin, elastase,
kallikrein, phospholipase. Food in stomach: p. juice is
released into duodenum
Endocrine …
• Thousands of islets of Langerhans: (5% wt): 4 cell types: in
order of abundance:
– 1. beta (insulin and amylin)
– 2. alpha (glucagon)
– 3. delta (somatostatin)
– 4. gamma (pancreatic polypeptide)

21. Pancreas Disorders
• Pancreatitis
• Diabetes type 1 (autoimmune) & type 2
• CF: affects multiple systems
• Tumors: different cells. The commonest is from p. duct &
is often advanced at Dx. Islet cell: benign/Ca
(Gastrinomas, glucagonomas, insulinomas)
• Pseudocyst
• Enlarged p: may mean nothing, or, it can be due to an
anatomic defect. But other c/of an enlarged p. may
exist & require treatment

22. Ac. P: Requires 2:
1. Suggestive abdo. pain: acute, esp. in epigastrium
2. S. amylase and/or lipase activity x3
3. Compatible imaging
Rec. P.: 2 distinct episodes of AP. Interval with:
• Resolution of pain (≥1mo). Normal s. enzymes
Chr. P.: 1 of:
1. Abdo. pain of p. origin & imaging of p. damage
2. Evidence of exocrine p. insufficiency & imaging findings
3. ... endocrine ... & imaging …
4. Surgical/biopsy: features compatible with CP
PANCREATITIS

23. AC. PANCREATITIS IN CHILDREN
Etiology (30% idiopathic). Many are a/with a systemic
illness. Some affect multiple organs
• Common: trauma (23%), dev. anomalies (15%),
multisystem d. (14%), drugs/toxins (12%):
• Less common
• Inf. (10%): MR, coxsackie B, EBV, CMV & HBV (primarily in organ
transplants); HIV, campylobacter, HAV, salmonella, mycoplasma.
Ascaris is a recognized c/of AP
• Hereditary/metabolic (4%):
• Biliary: rare
Most adult AP are c/by alcohol or g. stone

24. –Trauma: RTA, abuse, bicycle handlebars
–Cong.: p. divisum, malunion/maljunction, sphincter
anomaly, CD cysts, FAP
–Drugs/toxin: TPN, tetracycline, valproate,
immunosuppressants
–Hereditary: 2nd commonest cong. P. following CF.
AD. 20% no P. (variable penetrance)
–Metabolic: hyperTG, hyperCa
–Multisystem: Hypotension, ischemia. SLE, HSP, IBD,
(rarely) Kawasaki, Reye's
FAP. Familial adenomatous polyposis. CD choledochal
Etiology …

25. (Adults)
(3rd commonest)
No alcohol AP in children
(Adults)

26. Pathophysiology
• AP: Inciters are unclear: acinar injury  disruption of
ducts. Enzymes are activated: autodigestion
• Inflam. May be local/diffuse: ac., chr., necrotic, hgeic.
Interstitial edema. Severe P.  necrosis, BV blockage
 hge., & SIRS with MOF. Secretions often are walled
off by gr. tissue (pseudocyst; 10-23% in AP, 50% after
traumatic P. Mainly in lesser sac behind stomach).
Stomach, small gut, etc. may form part of capsule
CP: Chr. inflam. cell infiltration & irreversible fibrosis  loss
of exocrine & endocrine functions seen when ≥90%
cells are destroyed
MOF. Multiorgan failure

29. p. in CT : enlarged (blue arrow) with indistinct shaggy borders.
Peripancreatic fluid (red a.) and extensive infiltration of surrounding
fat (black a.)

30. Modified Glasgow Criteria (severe P.)
Score >/= 3 indicates severe pancreatitis
PaO2 <8kPa (60mmhg)
Age >55years
Neutrophils: WBC >15 x109/l
Calcium <2mmol/l
Renal F. : Urea >16 mmol/l
Enzymes: AST/ALT >200 iu/L or LDH > 600 iu/L
Albumin <32g/l
Sugar: Glucose >10mmol/L
(‘PANCREAS’)

31. Histologic features
• AP: Focal fat necrosis interspersed with interstitial hge.
• CP: fibrosis, acinar destruction, lymphocytic infiltration, &
duct obstruction

32. CF
Classical AP in adults: midepigastric pain radiating to back
• Children: quite varied; mostly: abdo. pain (90%), F. (76%)
NV (73%), tenderness (85%), guarding (68%), jaundice
(28%), distention (18%), SoB (10%), H&M (5%). Others:
HR, pallor, low BP (10%), rebound tenderness, & less
BS, diaphoresis, pulmo. Edema
These are nonspecific. Eating may exacerbate pain
• An acutely ill child may lie on his side with hips
& knees flexed. Pain typically increases for 24-
48h. Clinical course is variable
Typical posture of AP

33. Age 0-2y 3-10 11-20 Total
Cohort
Abdo. pain 42.9% 93.2% 93.4% 90%
Epigastric
tenderness
57.1% 86.4% 87.2% 85%
N/vomiting 28.6% 69.5% 78.1% 73%
Age group with presenting complaints

35. Acute hemorrhagic pancreatitis
Rare in children
• Life-threatening; MR ~50% (shock, SIRS with MOF, ARDS,
DIC, massive GI hge., & systemic or peritoneal inf.
• PE: a bluish discoloration of flanks (Grey Turner sign) or
periumbilical region (Cullen) due to blood pooling in
fascial planes
Others: pleural e., H&M, coma

37. Cullen’s and Grey Turner’s Signs in AP
63y M, no h/of alcohol abuse had ac., severe epig. pain. S. lipase was 1380U/l (22-51). US: g.
stones. He needed ICU. PE: jaundice and distention with ecchymosis (periumbilical and flank).
These are due to free enzymes causing fat necrosis and inflam. with retroperitoneal /abdo. hge.
that diffuses from retroperitoneum to umbilicus via round lig. and to subcut. tissues of flanks.
These, although nonsp., are a/with severe AP and high MR. CT confirmed necrotizing P. with
several ac. peripancreatic fluid collections (Balthazar grade E). He died of MO failure

39. Dx
Pediatric P. is a Dx challenge!
• No single test! Mainly clinical.
• CF, blood tests, imaging
• Dx needs 2 or more of:
– Amylase & lipase
most common: levels rise; but, do not correlate with
severity. Other d. can also raise; so nonsp.
US & CT
most common imaging; to look for inflam. & are
preferred both for Dx & FU
Importantly, P. can sometimes appear normal

40. •  s. amylase peaks at 48h, may be normal in 10-15%
Typically stay raised x4d. Amylase can rise in other
abdo. d., but not typically as high as in AP
• S. lipase is more specific than amylase in AP, & typically,
stay raised x8-14d
It can also rise in other d.; so, all lab. data are assessed
in cl. setting

41. Imaging
Imaging may be normal in 20% children with AP
• US: ducts, stones, margins. Primary screening (no IR/
sedation): a focally/diffusely enlarged, hypoechoic,
sonolucent, p.; dilated ducts; p. mass; peripancreatic
fluid; abscess; pseudocyst. Sensitivity is 50-80%;
specificity 90%
• ERCP is gold standard; also therapeutic (g. stones,
stenting, sphinterectomy). Essential for p. & biliary
anomalies Sens. & spec. 90-100%. Has substantial
observer variability, & may confuse AP for CP

42. Imaging …
• MRCP: non-invasive alternative to ERCP; no Rx option, no
IR: for g. stones, T, inf., inflam., ducts, c/of P
Secretin can enhance image
• CT is both highly sensitive and specific, risk of IR. Findings:
ductal/parenchymal calcifications, dilatation of main
ducts, pseudocyst & p. atrophy
 contrast, it is better for CP, complications, trauma, T.
Often used to FU: an enlarged p.; ill-defined margins;
peripancreatic fluid; pseudocysts

44. MRCP showing changes consistent
with chronic pancreatitis.

45. Comparison of EUS of normal p. and EUS of CP.
Endoscopic ultrasound showed agreement with ERCP,
the gold standard, in 75% of cases

46. Radiography
• XR: nonsp. distended loop of small gut (sentinel loop), g.
stones, dilatation of t. colon (cutoff sign), ascites,
peripancreatic gas bubbles, ileus, L basal pleural e., &
blurring of L psoas margin
Histology
• AP: necrosis & inflam., hge. If severe: large, blue-black
hgeic. foci among yellow-white chalky areas of fat
necrosis
• CP: parenchymal damage & fibrosis; acinar destruction,
lymphocytic infiltration, & p. duct obs. Ducts are dilated
& obstructed with protein plugs

47. CP: destruction of acini replaced
by extensive fibrosis & relative
sparing of islets; with calculi
AP: Hemorrhage, necrosis, fat necrosis, neutrophils

48. Colon Cut off signSentinel Loop Sign

49. Enzymatic Fat Necrosis

50. Other lab. tests:
• Coagulopathies, leukocytosis, hypoCa, hyperglycemia, 
bilirubin & GGT, Hct. & CRP (prognosis)
• Urinary trypsin activator peptide (TAP) may show severity
• A high s. lipase (>19 above upper normal) & a low albumin
& TLC have more morbidity. These 3 identify most at
risk of severe P. & can direct a more aggressive Rx
• Sweat chloride: in CF
• Genetic testing: for CF

51. No single drug. Mainly supportive. Admission may be needed
Uncomplicated AP usually resolve within 2-4d
Severe AP occur in 20% AP in children: more MM, longer
stay, aggressive Rx. Mn. children are more likely to have
comorbidities (CP & encephalopathy). Mn. can mask
typical early CF
Goal: to achieve FEB, analgesia, p. rest, meta. homeostasis
• Intractable V or ileus: NG suction for intestinal-pancreatic
rest (gastric contents in duodenum are the most potent
activator of p. enzymes). FEB
• ABT in inf., severe P.:
• Rx of complications
Management

52. • Analgesics: Tramadol is a central analgesic. Meperidine is
opioid (severe pain): risk of ampullary spasm
• AB: Imipenem & cilastatin in combination
Ceftriaxone has BS G-ve activity; lower efficacy against
G+ve; & higher against resistant MO
• Chr. relapsing P.: enzyme supplement, insulin, &
elemental or low-fat diets are useful

53. Nutrition
• Intractable V/ileus: bowel rest. Stomach content in duo- is
the most potent activator of p. enzymes
• Mild AP
– If pt. feels hungry; can start eating in a day or 2 if no NV,
& symptoms have resolved (amylase now normal)
– feeding small & slowly increasing low-fat, low-protein
soft diet appears safe, more calories; no transition
• Severe AP
– Severe P.: NPO & parenteral nutrition (avoid catabolism)
– Parenteral nutrition should be avoided, unless enteral
route is N/A, not tolerated, or not meeting calories

54. RATIONALE OF EARLY ENTERAL
NUTRITION
• The need to place p. at rest until complete
resolution of AP no longer seem imperative
– Bowel rest is a/with intestinal mucosal atrophy &
bacterial translocation: more inf. &complications
• Early enteral feeding maintains gut mucosal barrier,
prevents disruption, & prevents translocation of
bacteria that seed p. necrosis: less inf.
complications, organ failure & mortality

55. Route of enteral Nutrition
• Traditionally nasojejunal route has been preferred
to avoid the gastric phase of stimulation BUT
– Nasogastric route appears comparable in efficacy &
safety
MERITS OF NG ROUTE DEMERITS OF NG ROUTE
NGT placement is far easier than
NJ tube placement (requiring
interventional radiology or
endoscopy: expensive)
Slight increased risk of aspiration
(overcome by placing pt upright &
be placed on aspiration
precautions)

56. Surgery
• Generally, surgery is not needed in children; mostly done in
intractable pain in chr./relapsing P. (failed Rx, Mn., &
narcotic addiction), diffuse necrosis, hge., cong. defects
(p. divisum), ductal fistulae & AP induced ascites,
abscess, pseudocyst
• Goal: to alleviate pain & preserve functions:
– Distal pancreatectomy with Roux-en-Y pancreaticojejunostomy
(Duval procedure)
– Lateral pancreaticojejunostomy (Puestow procedure)
– Decompression of p. ducts, repair of p. divisum, sphincteroplasty
• A few cases benefitted with total pancreatectomy & ICT
ICT: islet cell transplantation

57. Pseudocysts
• CF: ANV from obs. of stomach/gut, F (inf). Rarely, hge. into
abdo./gut. Pain, tender epigas. mass or abdo. fullness.
Jaundice, chest pain, wt. loss, ascites. Post-traumatic: 60%
need surgery. If size is
<5cm: observe x4-6w as most resolve
>5cm: supportive x4-6w (cyst wall to mature) surgery
>10cm has risk for rupture
Chr. pseudocysts (>3mo): best Rx by internal drainage
– Cystogastrostomy: if adherent to back of stomach
– Cystoduodenostomy: if present in the head of p.
– Distal pancreatectomy: when it is in tail of p.
– Cystojejunostomy: other than above

58. A Large Pseudocyst
Compressing The
Duodenum

59. Contrast CT: upper abdomen: a well-defined p. pseudocyst

61. FAPsyn.withpersistentP.duetoapartially
obstructingampullaryadenoma.Seeav.prominent
ductalsys.Aspt.hadseveralop.,sheoptedforan
endoscopicampullectomy

62. Same pt., stents
were placed
following
ampullectomy.
P. resolved in
1w. Stents were
later removed

63. • Total pancreatectomy with ICT is being evaluated for CP.
ICT has no v. serious SE ("brittle diabetes,") (pt’s BGL
often swings quickly from high ~ low ~ high
CP need multispecialty care (gastroenterologists, surgeons,
nutritionists, psychologists, etc)
How long will AP last?
• Usually a week
• S/he needs not stay for that whole period. SS do improve
over time. A few have more severe d. & may end up
admitted for a month or more

64. Complications of AP
Immediate common
• Hypovolemic/septic shock a/with dysfunction of MOs
• Renal dysfunction
• Ascites, pleural e, ARDS, hypoCa, hge
Late common
• P. necrosis
• Infection
• Pseudocysts (homogeneous collection of amylase-rich
p. fluid that lacks an epithelium). 10-20% of AP

65. LOCAL COMPLICATIONS (Ps)
• Peripancreatic fluid collections
• (Peri)Pancreatic necrosis (sterile ± infected)
• Pancreatic abscess (Phlegmon)
• Pseudocyst
• Pancreatic ascites
• Pseudoaneurysm
• Adjacent organs: bleed, thrombosis, obs. jaundice, bowel
infarction, fistula, mechanical obs.
CP: Complications: pseudocyst, pseudoaneurysm, splenic
vein thrombosis, CBD obs, duodenal obs, p. fistula, adenoCa

66. SYSTEMIC COMPLICATIONS
• CVS
– Shock: hypovolemic & septic
– Arrhythmias/pericardial e./sudden death
– ST-T nonspecific changes
• Pulmonary
– Respiratory failure, pn., atelectasis, pleural e., ARDS
• Renal
– Oliguria, azotemia, renal artery/vein thrombosis
• Hematological
– Hemoconcentation, DIC

67. SYSTEMIC COMPLICATIONS …
• Metabolic: HypoCa, hyperglycemia, hyperlipidemia,
hypermetabolic state
• GIT: PU/Erosive gastritis, ileus, portal -/splenic vein
thrombosis with varices
• Neurological
– Visual (Sudden blindness: Purtscher’s retinopathy)
– Confusion, irritability, psychosis, fat emboli
– Alcohol withdrawal syn., encephalopathy
• Misc.: subcut. fat necrosis, Intra-abdominal saponification,
Arthralgia

68. Typical fundus in Purtscher retinopathy: multiple cotton-wool spots surround disc
after blunt thoracic trauma

69. Subcutaneous Fat necrosis in
AP (nodules of panniculitis)
Pancreatic fat necrosis with ghost
cells

70. Fat embolism: Fat can enter blood from BM due to trauma, & if fat is
released by enzymatic digestion (AP). Common causes: 1. Fractures of
long bones &/or operative manipulation of fractures; 2. trauma to fat
or fatty liver; 3. AP. Fat emboli tend to be small and often cause small
infarcts adjacent to capillaries at the sites of blockage

71. Prognosis usually in children is excellent
Death is quite rare. But can happen. 1% in mild AP
• 20-50% in severe AP. More with underlying d. 1/3rd die in
1w (MOF); 2/3rd later (MOF & sepsis)
Recurrence
• Yes, it can occur in 10%. Even fewer will have multiple.
Another episode warrants additional testing to search
for known c/of recurrent AP
Prevention
• Some treatable c/of AP: gallstone d, hyperCa, high TG, &
abnormalities of ducts

72. CHR. PANCREATITIS IN CHILDREN
SS
• Frequent or chr. Abdo. Pain is the most common; can be
constant or come & go unpredictably
• Others: NV, wt. loss, D (oily motions). Some have trouble
digesting & may have poor growth, especially if quite
young at first episode of P
• DM generally takes many years to appear, but this, too, is
highly variable; some will DM in adolescence

73. Etiology of Chr. P in children
Some are life-long, not often Dx until adulthood
• Fibrosing P./TCP commonest in tropics
• CF
• Chr. Hereditary P. (usually Dx at adulthood)
– Hyperlipidemias
– Partial lipodystrophy
– Wilson's disease
– hemochromatosis
– Alpha-1 antitrypsin deficiency
• IEM: (esp. branched chain aminoacidemias)
• Idiopathic

74. CP: Dx
• As biopsy is impractical & potentially risky in many pts.,
clinical, lab., & radiologic criteria are essential for Dx.
• Lab. Direct: small gut intubation, using secretin, CCK or
nutrient stimulants to measure secretion: highly
sensitive and specific, but time-consuming and invasive
• Lab. Indirect: stool fat globules & assays for faecal
elastase, as well as other stool, breath, & urine/plasma
tests. They tend to lack sensitivity & specificity &
cannot DD between mild and moderate exocrine
dysfunction. Faecal elastase & a 72h faecal fat is
adequate

76. CP: Management
Goals:
1. Dx and etiology
2. Analgesia
3. Long-term FU to monitor & Rx exocrine insufficiency, DM
4. No smoking and alcohol (risk of p. adenoCa)
Others: antioxidants, enzyme, octreotide, pancreatic
protease inhibitors. But, currently insufficient evidence
to recommend these
• Surgery is only indicated when there is chr., unremitting
pain unresponsive to medical Rx. Goal: adequate
drainage of p. ducts. This can be endoscopic or surgical.
Pancreatic resections have high MM & rarely required

77. DD: Ac. vs. Chr. Pancreatitis
Trait Ac. P Chr. P
Duration 2w Life long
Emergency May be life threatening; an
emergency (hge, shock)
Slowly developing
Etiologies Trauma (23%), dev.
anomalies (15%), sys. d.
(14%), drugs/toxins (12%),
viral (10%), etc. 25% is
unknown
Trauma, sys. d., cong.
anomalies
Pathogenesis Morphological changes are
reversible with good support
Calcifications and
destruction of architecture
Complications Permanent DM almost never
follows a single attack
DM , malabsorption
Lab High s amylase, lipase within
1-2d
Requires proof of irreversible
damage to P, loss of digestive
F or DM: by
CT/MRI, ERCP, endoscopic US

78. Peculiarities Of Pancreas
• Mixed gland
• Develops from 2 primordial buds
• Congenital anomalies can cause malignancy
• Minimally infected
• Disorders causes autodigestion
• Chronic pancreatitis is life-long

79. MCQ
• HyperCa is common in AP
• Imaging may be normal in AP
• Lipase is more specific than amylase
• DM is more common in AP
• 25% AP are idiopathic

80. • Inf. is a common c/of AP in children
• ERCP is a common cause of AP
• Most p. pseudocysts require drainage
• Gall stone pancreatitis is common in children
• An enlarged pancreas is always significant
MCQ

84. THANK YOU……….