Acute and chronic pancreatitis in three pages.

1. Pancreatitis
Pancreatitis is the inflammation of
pancrease. It can be in the setting of the
acute or chronic.
Acute
Acute pancreatitis in children has been
previously defined as having the presence of
at least 2 of the following 3 criteria:
abdominal pain compatible with pancreatic
origin, amylase and/or lipase at least 3 times
upper limits of normal, and imaging findings
suggestive/ compatible with pancreatic
inflammation.
Etiology:
 Multisystem diseases:
 HUS
 IBD
 Biliary stones
 Microlothiasis
 Drugs and toxins
 Valporic acid
 L-asparaginase
 Azathioprine
 Infections
 Metabolic disorder
 Blunt abdominal injuries
Pathophysiology
The initial insult such as ductal
disruption or obstruction causes the
premature activation of tyrpsinogen to
trypsin inside the acinar cell. Trypsin
activates other enzymes within the
pancrease causing autodigestion. This
also causes further activation of other
enzymes and the release of active
proteases. Continues production of
pancreatic enzymes causes pancreastasis.
These enzymes also cause the release of
cytokines and pro-inflammatory
mediators which may further complicate
the problem.
Clinical features
Mild acute pancreatitis
 Severe abdominal pain
 Persistent vomiting
 Fever
 Abdominal destenstion
 Abdominal tenderness
Sever acute pancreatitis (rare)
 Severe nausea and vomiting
 Abdominal pain
 High fever
 Shock
 Jaundice
 Ascites
 Hypoglycemia
 Pleural effusion

2. On examination
 Abdomen is distended
 Abdominal tenderness
 Bluish discoloration around the
umbilicus (Cullen sign) due to
bruising and edema
 Bluish discoloration of the flanks
(grey turner sign) due to bruising.
Diagnosis
With history and clinical features persistent
with acute pancreatitis established,
measurement of amylase and lipase is the
next step. Of these two, serum lipase is
considered the test of choice for it’s more
specific than amylase. Serum lipase remains
elevated for longer than amylase. Other
laboratory abnormalities that may be present
in acute pancreatitis include
hemoconcentration, coagulopathy,
leukocytosis, hyperglycemia, glucosuria,
hypocalcemia, elevated γ-glutamyl
transpeptidase, and hyperbilirubinemia. X-
rays including those of the chest may show
complications like pleural effusion,
pericardial effusion and pulmonary edema.
Abdominal x-rays might demonstrate a
sentinel loop, dilation ofnthe transverse
colon (cutoff sign), ileus, pancreatic
calcification (if recurrent), blurring of the
left psoas margin, a pseudocyst, diffuse
abdominal haziness (ascites), and
peripancreatic extraluminal gas bubbles. CT
scan may show enlarged pancrease
edematous pancreas, pancreatic masses,
fluid collections, and abscesses.
Ultrasonography is sensitive for the
diagnosis of biliary stones.
Treatment
The intention of medical management is to
relieve pain and restore metabolic
homeostasis. Analgesia should be given in
adequate doses. Fluid, electrolyte, and
mineral balance should be restored and
maintained. Nasogastric suction is useful in
patients who are vomiting. While vomiting,
the patient should be kept NPO. Anti-biotic
are not used for prophylactic but only when
infection is established. PPI is used for
suppression of gastric acids. Endoscopy is
recommended is if the pancreatitis is due to
anatomical abnormalities.
Prognosis
Children with uncomplicated acute
pancreatitis do well and recover within 4-5
days. When pancreatitis is associated with
trauma or systemic disease, the prognosis is
typically related to the associated medical
conditions.
Chronic pancreatitis
Chronic pancreatitis in children is by far
caused by genetic mutations or the

3. congenital anomalies of the pancreatic of
biliary ductal system. Mutation in cationic
trypsinogen, pancreatic typsin inhibitor and
chymotropsin c genes as well as cystic
fibrosis can all lead to chronic pancreatitis.
Other conditions associated with chronic
pancreatitis include: Autoimmune
pancreatitis, Juvenile tropical pancreatitis,
hyperlipidemia and ascariasis.
Clinical features
 Frequent or chronic abdominal pain
 Nausea and vomiting
 Vomiting
 Diarrhea
 Weight loss
 Jaundice
 Steatorrhea
 Poor growth (if it effects younger
age)
 Diabetes ( many years after the first
episode)
Diagnosis
The diagnostic evaluation include; Serum
lipid, calcium, and phosphorus levels is
discovered. Stool analysis for the presence
of ascaris. Sweat test to exclude or include
the presence of cystic fibrosis. Plain
abdominal x-ray may show the calcification
of the pancrease. Ultrasound and CT scan is
used for the detection of pseudocyst.
Ultrasound is also used for the detection of
stones in the biliary tract. If available,
genetic evaluate on is carried out. For
through analysis of the anatomy of the gland
and before surgery, if considered, Magnetic
resonance cholangiopancreatography and
endoscopic retrograde cholangio-pancreato-
graphy are used.
Treatment
If there is an anatomic abnormality, then
surgery, often performed through an
endoscope, can be curative. Metabolic
abnormalities such as high serum
calcium or serum fat (triglycerides) can
also be treated. Pills containing
pancreatic digestive enzymes are
prescribed to patients who experience
chronic pain. Draining of pseudocysts, and
insertion of pancreatic orbiliary
endoprosthetic stents also is carried.
Sources:
1. NelsonTEXTBOOK of
PEDIATRICS ( 20th edition)
2. https://pancreasfoundation.org/pati
ent-information/childrenpediatric-
pancreatitis/chronic-pancreatitis-in-
children/
3. https://www.naspghan.org/files/Clas
sification_of_Acute_Pancreatitis_in
_the.32(2).pdf