ACUTE PANCREATITIS

• Etiology and Epidemiology

The exocrine pancreas produces numerous proteolytic enzymes,
including trypsin, chymotrypsin, and carboxypeptidase.
• These are produced as inactive proenzymes to protect the
pancreas from autodigestion.
• Trypsin is activated after leaving the pancreas by enterokinase,
an intestinal brush border enzyme.

• After activation, trypsin cleaves other proteolytic proenzymes

into their active states.
• Protease inhibitors found in pancreatic
juice inhibit early activation of trypsin; the
presence of selfdigestion sites on the trypsin
molecule allows for feedback inactivation.
• Pancreatitis occurs when digestive enzymes are
activated inside the pancreas, causing injury.
• Triggers for acute pancreatitis differ between
adults and children.
• In the adult patient, most episodes are related to
alcohol abuse or gallstones.
• In children, most cases are idiopathic or due to
medications.
• Some cases are caused by pancreatic sufficient
cystic fibrosis, hypertriglyceridemia, biliary
microlithiasis, trauma, or viral infection.
• Collagen vascular disorders and parasite
infestations are responsible for the remainder
 Clinical Manifestations

• Acute pancreatitis presents with relatively rapid onset of

pain, usually in the epigastric region.

• The pain may radiate to the back and is nearly always

aggravated by eating.

• The patient moves frequently to find a position of comfort.

• Nausea and vomiting
• Severe pancreatitis can lead to hemorrhage,
visible as ecchymoses in the flanks (Grey
Turner sign) or periumbilical region (Cullen
sign).
• Grey Turner's sign refers to bruising of the flanks, the
part of the body between the last rib and the top of
the hip.
• The bruising appears as a blue discoloration (Goldman
etal ),and is a sign of retroperitoneal hemorrhage, or
bleeding behind the peritoneum, which is a lining of
the abdominal cavity.
• Grey Turner's sign takes 24–48 hours to develop, and
can predict a severe attack of acute pancreatitis
(Bosmann etal 2008)).
• Cullen's sign is the periumbilical ecchymosis
that may be present in severe necrotizing
pancreatitis or other causes of retroperitoneal
hemorrhage.
• With necrosis and fluid collections, patients
experiencing severe pancreatitis are prone
to infectious complications, and the clinician
must be alert for fever and signs of sepsis.
 Laboratory and Imaging Studies
• Acute pancreatitis is based on 2 of the following 3
criteria:
 Abdominal pain consistent with the disease
(severe epigastric pain typically),
 serum amylase and/or lipase greater than 3 time
the upper limit of normal,
 and/ or characteristic findings on imaging.
• As acute pancreatitis progresses, the
amylase level tends to decline faster than lipase, making
the latter a good choice for diagnostic testing late in the
course of
the disease.

• Because enzyme levels are not 100% sensitive or specific,

imaging studies are important for the diagnosis of
pancreatitis.
• Ultrasound is capable of detecting this edema and should be
performed as part of the overall diagnostic approach.

• If overlying bowel gas obscures the pancreas, a computed

tomography (CT) scan allows complete visualization of the
gland.

• It should be done with oral and intravenous (IV) contrast

agents to facilitate interpretation.
• To monitor for the development of Pseudocysts and
for evidence of ductal dilation secondary to
obstruction.

• In the course of pancreatitis is to rule out gallstones,

the liver, gallbladder, and common bile duct all
should be visualized.
 Treatment
• There are no proven specific therapies for
acute pancreatitis.
• If a predisposing etiology is found, such as a
drug reaction or a gallstone obstructing the
sphincter of Oddi, this should be specifically
treated.
• Fluid resuscitation is necessary because of
vomiting and third space losses.
• Pain relief should be provided.

• Antibiotics should be considered if the

patient is febrile, has extensive pancreatic necrosis, or
has laboratory evidence of infection.

• Imipenem, is considered the best choice.

 CHRONIC PANCREATITIS
• Etiology
• Chronic pancreatitis is defined as recurrent or persistent
attacks of pancreatitis, which have resulted in irreversible
morphological changes in pancreatic structure.

• These include scarring of the ducts with irregular areas of

narrowing and dilation (beading), fibrosis of parenchyma,
and loss of acinar and islet tissue.

• Pancreatic exocrine insufficiency and diabetes

mellitus may result from unremitting chronic pancreatitis.
• Most patients have discrete attacks of acute
symptoms occurring repeatedly, but chronic pain may
be present.
• The causes of chronic pancreatitis include hereditary
pancreatitis and milder phenotypes of cystic fibrosis
associated with pancreatic sufficiency.

• Familial disease is caused by one of several known

mutations in the trypsinogen gene.
• These mutations obliterate autodigestion sites
on the trypsin molecule, inhibiting feedback
inhibition of trypsin digestion.
 Clinical Manifestations

• Children with chronic pancreatitis initially present

with recurring attacks of acute pancreatitis.

• Injury to the pancreatic ducts predisposes these

children to continued attacks owing to scarring
of small and large pancreatic ducts, stasis of
pancreatic secretions, stone formation, and
inflammation.
• Loss of pancreatic exocrine and endocrine tissue over
time can lead to exocrine and endocrine deficiency.
• More than 90% of the pancreatic mass must be
destroyed before exocrine deficiency becomes
clinically apparent; this is a late complication that does
not occur in all cases.
• Chronic pain is a serious problem in most
affected individuals.
• These patients have many episodes; many
do not require hospitalization.
 Laboratory and Imaging Studies

• Chronic pancreatitis is similar to acute

pancreatitis, but with more severe loss of
pancreatic tissue, it becomes less likely that
the patient presents with elevation of
amylase or lipase.
•
 Pancreatic and biliary imaging:
• Endoscopic retrograde
cholangiopancreatography (ERCP).

 ERCP offers the possibility of therapeutic

intervention to remove gallstones, dilate
strictures, and place stents to enhance flow of
pancreatic juice.
• Plain abdominal x-rays may show pancreatic
calcifications.
• Genetic testing– such as cystic fibrosis
 Treatment
• AIMS:
• Supportive medical therapy
-intravenous hydration
-pain control
-Bowel rest
• DIET
- Low fat diet
• Surgical management: only needed if the
symptoms are severe and prolonged with
complications.
 Peritonitis

• The peritoneum consists of a single layer of

mesothelial cells that covers all intraabdominal
organs.
• The portion that covers the abdominal wall is
derived from the underlying somatic
structures and is innervated by somatic nerves.
• The portion covering the viscera is derived from
visceral mesoderm and is innervated by
nonmyelinated visceral afferents.
• Inflammation of the peritoneal lining of the abdominal
cavity can result from infectious, autoimmune, neoplastic,
and chemical processes.
• Infectious peritonitis is usually defined as primary
(spontaneous) or secondary.

• In primary peritonitis, the source of infection

originates outside the abdomen and seeds the peritoneal
cavity via hematogenous, lymphatic, or transmural spread.
• Secondary peritonitis arises from the abdominal
cavity itself through extension from or rupture
of an intraabdominal viscus or an abscess
within an organ.
• Tertiary peritonitis refers to recurrent diffuse or
localized disease and is associated with poorer
outcomes than secondary peritonitis.
• Clinically, patients have abdominal pain,
abdominal tenderness, and rigidity on exam..
 AcutePrimaryPeritonitis

• ETIOLOGY
 Primary peritonitis usually refers to bacterial infection
of the peritoneal cavity without a demonstrable
intraabdominal source.

 Most cases occur in children with ascites resulting from

cirrhosis and nephrotic
syndrome.
 Infection can result from translocation of gut
bacteria as well as immune dysfunction.

 Pneumococci (most common), group A

streptococci, enterococci, staphylococci, and Gram-
negative enteric bacteria, especially Escherichia coli
and Klebsiella pneumoniae, are most commonly
found.
 CLINICAL MANIFESTATIONS
• Onset may be insidious or rapid and is
characterized by fever, abdominal pain and a
toxic appearance.

• Vomiting and diarrhea may be present.

• Hypotension and tachycardia are common

along with shallow, rapid respirations because
of discomfort associated with breathing.
• Abdominal palpation might demonstrate rebound
tenderness and rigidity.
• Bowel sounds are hypoactive or absent.

• However, signs and symptoms may be subtle at times

and increase vigilance is needed in cirrhotic
patients who have ascites and present with
unexplained leukocytosis, azotemia, or metabolic
acidosis.
 DIAGNOSIS AND TREATMENT
• Peripheral leukocytosis with a marked predominance
of polymorphonuclear cells is common, although the
white blood cell (WBC) count can be affected by
preexisting hypersplenism in patients with cirrhosis.

• Patients with nephrotic syndrome generally have

proteinuria, and low serum albumin in these patients
is associated with increased risk of
peritonitis.
• X-ray examination of the abdomen -reveals dilation of the
large and small intestines, with increased separation of
loops secondary to bowel wall thickening.
• the diagnosis of primary peritonitis is made by CT scan,
laparoscopy, or laparotomy.
• In a child with known renal or hepatic disease and ascites,
the presence of peritoneal signs should prompt diagnostic
paracentesis.
• Infected fluid usually reveals a WBC count of ≥250
cells/mm3, with >50% polymorphonuclear cells.
• Inoculation of ascitic fluid obtained at paracentesis
directly into blood culture bottles increases the yield
of positive cultures.
• TREATMENT: broad spectrum coverage,
such as cefotaxime, should be started promptly, with
subsequent changes dependent on sensitivity
testing for 10-14 days
 Acute Secondary Peritonitis

• Acute secondary peritonitis most often results

from entry of enteric bacteria into the
peritoneal cavity through a necrotic defect in
the wall of the intestines or other viscus as a
result of obstruction or infarction or after
rupture of an intraabdominal visceral abscess.

• It most commonly follows perforation of the

appendix.
• Other causes include incarcerated hernias,
rupture of a Meckel diverticulum, midgut
volvulus, intussusception, hemolytic uremic
syndrome, peptic ulceration, inflammatory
bowel disease, necrotizing cholecystitis,
necrotizing enterocolitis, typhlitis, and
traumatic perforation.
• Peritonitis in the neonatal period most often occurs as
a complication of necrotizing enterocolitis but may be
associated with meconium ileus

• In postpubertal girls, bacteria from the genital

tract (Neisseria gonorrhoeae, Chlamydia trachomatis)
can gain access to the peritoneal cavity via the
fallopian tubes, causing secondary peritonitis.
• The presence of a foreign body, such as a
ventriculoperitoneal catheter or peritoneal
dialysis catheter, can predispose to peritonitis,
with skin microorganisms, such as
Staphylococcus epidermidis, Staphylococcus
aureus, and Candida albicans, contaminating
the shunt.
• CLINICAL MANIFESTATIONS
Similar to primary peritonitis, characteristic
symptoms include fever, diffuse abdominal pain,
nausea, and vomiting.
• Physical findings of peritoneal inflammation include
rebound tenderness, abdominal wall
rigidity, a paucity of body motion (lying still), and
decreased or absent bowel sounds from paralytic
ileus.
• Massive exudation of fluid into the
peritoneal cavity, along with the systemic release of
vasodilative substances, can lead to the rapid
development of shock.

• A toxic appearance, irritability, and restlessness are

common.

• Basilar atelectasis as well as intrapulmonary shunting can

develop, with progression to
acute respiratory distress syndrome.
• a peripheral WBC count >12,000 cells/
mm3, with a marked predominance of
polymorphonuclear forms.

• X-rays of the abdomen can reveal free air in the

peritoneal cavity, evidence of ileus or
obstruction, peritoneal fluid, and obliteration of
the psoas shadow.
• Fluid findings may reveal elevated total protein (>1
g/dL), low glucose (<50 mg/dL).

• TREATMENT
Aggressive fluid resuscitation and support of
cardiovascular function should begin immediately.
• Stabilization of the patient before surgical
intervention is mandatory.