Pancreatitis is an inflammatory condition of the pancreas. Two major forms : acute pancreatitis (is reversible) and chronic pancreatitis(is irreversible).

1. PANCREATITIS
By Dr NDAYISABACORNEILLE

2. INTRODUCTION
■ Pancreatitis is an inflammatory condition of the pancreas. Two major forms : acute pancreatitis (is
reversible) and chronic pancreatitis(is irreversible).
■ Acute pancreatitis is more prevalent, and most patients have a single episode of pancreatitis. A small
number of patients have recurrent episodes of acute pancreatitis and are at risk of developing Chronic
Pancreatitis.
■ Research demonstrated differences between pancreatitis in children and adults, particularly in
presentation, etiology, prognosis, and nature of acute recurrent pancreatitis (ARP).
11/5/2019 Dr NDAYISABA CORNEILLE

3. Pancreas
■ The healthy pancreas is protected by:
 Pancreatic proteases that are synthesized as
inactive proenzymes;
 Digestive enzymes that are segregated into
secretory granules at pH 6.2 with low calcium
concentration, which minimizes trypsin activity;
 The presence of protease inhibitors both in the
cytoplasm and zymogen granules;
 enzymes that are secreted directly into the ducts.
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4. ACUTE PANCREATITIS
Acute pancreatitis, the most common
pancreatic disease in children .Acute
pancreatitis can occur in mild and
severe forms. in general, mild
pancreatitis is limited to the pancreas
and the peripancreatic fat, whereas
severe
disease includes pancreatic necrosis,
involvement of other organs,
cardiovascular collapse, infection, or
fluid collections
11/5/2019 Dr NDAYISABA CORNEILLE

5. Acute Pancreatitis Pathophysiology
■ Acute pancreatitis results from injury of the pancreas and a subsequent inflammatory response that
may involve adjacent and distant tissues and organs. an event that initiates a process of acinar cell
injury such as Pancreatic duct obstruction(Due to the effect of lipase, any obstruction will cause fat
necrosis and produce an inflammatory response). Primary acinar cell injury (it can be damaged by
ischemia, viral infections (e.g., mumps) ,Drugs ,Direct trauma to the pancreas.). Defective
intracellular transport of proenzymes within acinar cells.
■ The cell injury produces pancreatic edema and a local inflammatory response, with release of
inflammatory mediators.
The production of cytokines and chemokines provoke a systemic inflammatory response. The magnitude
of this inflammatory response determines the clinical severity of acute pancreatitis and can lead to
complications such as pancreatic necrosis, shock, and distant organ failure.
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6. ■ Calcium signals initiate the premature
intracellular activation of trypsinogen to
trypsin . Trypsin, in turn, activates other
digestive proenzymes(zymogens most
notably trypsinogen) Normally,
trypsinogen is converted into trypsin (in
duodenum ) where it assists in the
digestion of proteins. Then trypsinogen
meet with lysosomal enzymes
(specifically cathepsin), which activate
trypsinogen to trypsin.This lead to
inflammation, edema, vascular injury,
and even cellular death
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7. etiology of acute pancreatitis in children
■ 1.Common: a.Biliary disorders such as sepsis, shock (alone or with sepsis), hemolytic uremic syndrome, and systemic lupus
erythematosus
b. Systemic conditions such as Brain tumor, DM, Malnutrition, Peptic ulcer, Renal failure
c. Medications such as valproic acid, Acetaminophen (overdose), Cimetidine, Erythromycin, Methyldopa,
Tetracycline, Metronidazole, Isoniazid,…
d. Traumatic such as Blunt injury, Burns, Hypothermia, Surgical trauma,…..
e. Idiopathic
■ 2.Less common: a.Infection such as Hepatitis A, B; Influenza A, B; Malaria, Measles,Rubelle,mumps
b. Genetic/hereditary disorders such as Cationic trypsinogen gene, Cystic fibrosis gene, SPINK-1 gene(serine
protease inhibitor Kazal type 1)
■ 3.Rare: a.Autoimmune pancreatitis occurs in two forms (types 1 and 2) type 2 associated with Inflammatory bowel disease,type 1
no elevation of immunoglobulin G4 (IgG4) this respond to corticosteroid therapy
b. Anatomic pancreaticobiliary abnormalities such as pancreas divisum , abnormal junction of the common bile duct and
main pancreatic duct (common channel syndrome),choledochal cysts, …
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8. CLINICAL MANIFESTATIONS.
■ severe abdominal pain (87%)
■ persistent vomiting (64%) and fever.
■ The pain is epigastric or in either upper quadrant and steady
■ . The abdomen may be distended and tender(77%)[lead to abdominal guarding,rebound
tenderness]. A mass may be palpable.
■ The pain increases in intensity for 24–48 hr, during which time vomiting may increase
■ the patient may require hospitalization for dehydration and may need fluid and
electrolyte therapy.
■ The prognosis for complete recovery in the acute uncomplicated case is excellent
Mild acute pancreatitis
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9. Severe acute pancreatitis
■ Severe acute pancreatitis is rare in children .Patient present with :
 severe nausea, vomiting, and abdominal pain.
 Shock, high fever, jaundice, ascites, hypocalcemia, and pleural effusions can occur.
 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 ≈25%, is related to the systemic inflammatory response syndrome with
multiple organ dysfunction (MOD): shock, renal failure, acute respiratory distress syndrome,
disseminated intravascular coagulation, massive gastrointestinal bleeding, and systemic or intra-
abdominal infection.
 Has a poor prognosis.
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10. DIAGNOSIS
■ Most children (≥90%) have mild disease.
■ Acute pancreatitis in pediatric patients requires at least two of three criteria:
(1) abdominal pain (ie, abdominal pain of acute onset, especially in the epigastric region);
(2) serum amylase or lipase activity at least three times greater than
the upper limit of normal;
(3) imaging findings compatible with acute pancreatitis . use computed tomography (CT) of the
abdomen gives information about the presence or absence of pancreatic necrosis, pancreatic
enlargement, a pancreatic masses, fluid collections, and abscesses
Use of Endoscopic ultrasonography (EUS) and magnetic resonance cholangiopancreatography (MRCP)
magnetic resonance imaging of the biliary tree and surrounding structures (pancreas and liver) but are
very expensive .
Other laboratory abnormalities that may be present in acute pancreatitis include
hemoconcentration(increased concebtration of cell and solids in the blood usually result from loss of fluid to tissue),
coagulopathy,hypocalcemia,hyperglycemia
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11. TREATMENT
Mild acute pancreatitis
■ Fluid replacement (first 12-24h)
Aggressive hydration at a rate of 5 to 10 mL/kg
per hour of isotonic crystalloid solution (e.g.,
normal saline or lactated Ringer’s solution)
In severe volume depletion that manifests as
hypotension and tachycardia, more rapid
repletion with 20 mL/kg of intravenous fluid given
over 30 minutes followed by 3 mL/kg/hour for 8 to
12 hours
■ Pain control such as Acetamophin
■ Nutritional support (within 48h of
admission): oral intake in mild disease and in
absence of nausea/vomiting and abdominal
pain
The treatment of severe acute pancreatitis
may involve :
■ enteral or total parenteral nutrition,
antibiotics, gastric acid suppression and
peritoneal lavage to reduce the risk of
secondary infection.
■ Endoscopic therapy may be of benefit when
pancreatitis is caused by anatomic
abnormalities, such as strictures or stones.
■ Surgical therapy of acute pancreatitis is rarely
required, but may include drainage of necrotic
material or abscesses.
■ management of a patient with acute pancreatitis consists of supportive care with fluid resuscitation,
antiemetics, pain control, nothing by mouth, and nutritional support. (basic RX)
{MildACUTE PANCREATITIS (use basic RX)Then on Severe acute pancreatitis(use Basic Rx +ICU)}
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12. Clinical manifestation
Biochemical examination Imaging studies
Diagnosis
Physical findings
.abdominal pain,vomiting,
Cullen sign,Grey Turner sign.
Chest & abdominal x-ray
Ultrasonography,CT,MRCP
Serum amylase,lipase leval
Other pancreatic enzyme
Laboratory findings
coagulopathy,hyperglyc
emia
Severity assesment severe
<basic RX+ICU>
Mgt of multiorgan failure
Prevention & RX of infection
Surgical therapy
Non severe
<Basic RX>
fluid
resuscitation,
antiemetics, pain
control
nutritional
support
Recovery period
Reduction of
drug,Oral intake
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13. Acute Recurrent Pancreatitis
■ Acute Recurrent Pancreatitis defined as at least two
episodes of acute pancreatitis per year, or more than
three episodes over a lifetime, in a patient without CP
or a pancreatic pseudocyst.
■ Etiology :including biliary disease, anatomic
pancreaticobiliary abnormalities, inflammatory bowel
disease, and autoimmune pancreatitis,..
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14. Chronic Pancreatitis
■ Chronic Pancreatitis is defined as a
process leading to irreversible
destruction of the pancreatic
parenchyma and ducts and loss of
exocrine function. Many of these
patients have a history of ARP before
the irreversible changes in pancreatic
anatomy and function become
apparent.
The cause of Chronic Pancreatitis is
usually idiopathic or associated with
mutations in PRSS-1, SPINK-1,
CFTR, or CTRC genes, alone or in
combination.
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15. DIAGNOSIS
■ The diagnosis of CP is clinical and based on a combination of symptoms, imaging
studies, and functional insufficiency.
■ It is important to consider all of these parameters when CP is suspected in a patient,
because diagnosis often is delayed.With advanced disease, amylase and lipase
levels will not be elevated, even in the presence of disabling pain.
■ imaging such as CT,..
■ functional insufficiency :this identify pancreatic insufficiency and support
the diagnosis ofCP
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16. TREATMENT
■ pain control :acetaminophen may be effective
■ Endoscopic treatment for CP should be considered only when
ductal strictures or pancreatic duct stones are present or for
symptomatic pseudocysts.
■ Total pancreatectomy with islet cell autotransplant is currently
offered to patients who have genetic causes of pancreatitis
■ Pancreatic insufficiency is treated with pancreatic enzyme
replacement therapy. The goal is to restore digestive function and
maintain weight gain and growth
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17. REFERENCE
■ 1.
■ .2 American academy of peadiatric accessed on http://pedsinreview.aappublications.org/
Kliegman: Nelson Textbook of Pediatrics, 18th ed.
11/5/2019 Dr NDAYISABA CORNEILLE