Pancreas

• Objectives:
• The Basics anatomy and physiology
• Congenital anomalies
• Trauma ( blunt , penetrating)
• Pancreatitis ( acute , chronic) .
Anatomy
retropertointorgan radiation pain to back
vesselshigh go we needagresivefluid
 exo y to ya
physiology endo T Ed La
we

• Weight = 80 grams. Of this, 80–90 per cent is composed of exocrine

acinar tissue, which is organized into lobules.
• The main pancreatic duct branches into interlobular and intralobular
ducts, ductules and, finally, acini.
• The main duct is lined by columnar epithelium, which becomes
cuboidal in the ductules. Acinar cells are clumped around a central
lumen, which communicates with the duct system.

o
• Clusters of endocrine cells, known as islets of Langerhans, are
distributed throughout the pancreas. Islets consist of different cell
types: 75 per cent are B cells (producing insulin); 20 per cent are A
cells (producing glucagon); and the remainder are D cells (producing
somatostatin) and a small number of pancreatic polypeptide cells.
 Cont-
• The pancreas secretes digestive enzymes in an
alkaline (pH 8.4) bicarbonate-rich fluid.
• The hormone secretin, which is released from the
duodenal mucosa, evokes a bicarbonate-rich fluid.
• Cholecystokinin (CCK) (synonym: pancreozymin) is
wtf
released from the duodenal mucosa in response to
food. CCK is responsible for enzyme release.
• Vagal stimulation increases the volume of secretion.
During this phase, the proteolytic enzymes ( e.g
amylase, lipase, trypsin, elastase and chymotrypsin )
are in an inactive form, the maintenance of which is
important in preventing pancreatitis.
 Investigations:
• Serum levels of proteolytic enzymes like
amylase, lipase, trypsin, elastase and
chymotrypsin
• directly measuring pancreatic secretion in
response to a standardized stimulus. The
stimulus to secretion can be physiological,
e.g. ingestion of a test meal, as in the
Lundh test, or pharmacological, e.g.
intravenous injection of a hormone, such
as secretin or CCK
 Imaging
• Ultrasound.
• C.T scan. ( Computerized tomography)
• MRI ( MRCP) ( magnetic resonance
cholangiopancreatography)
• ERCP. ( endoscopic retrograde
cholangiopancreatography)
• Endoscopic ultrasound.
 Congenital diseases
• Cystic fibrosis
8
• Pancreas divisum : embryological ventral and dorsal
000
parts of the pancreas fail to fuse. Usually asymptomatic
but have a higher incidence of acute , chronic
pancreatitis and pancreatic pain.
• Treatment:
• Endoscopic sphincterotomy and stenting Surgical
intervention can take the form of phincteroplasty,
pancreatojejunostomy or even resection of the
pancreatic head
• Annular pancreas
• This is the result of a failure of complete rotation of the
ventral pancreatic bud during development, so that a
ring of pancreatic tissue surrounds the second or third
part of the duodenum.
• It is most often seen in association with congenital
duodenal stenosis or atresia and is therefore more
e
prevalent in children with Down’s syndrome. Duodenal
obstruction typically causes vomiting in the neonate .
• The usual treatment is bypass
(duodenoduodenostomy).
a
• Ectopic pancreas.
q
• Congenital cystic disease of the pancreas
 INJURIES TO THE
PANCREAS
in sea 58 Yoo
Ii
• BLUNT
• not frequent…… why????
• If there is damage to the pancreas, it is often
concomitant with injuries to other viscera, especially the
liver, the spleen and the duodenum.
• Occasionally, a forceful blow to the epigastrium may
crush the body of the pancreas against the vertebral
column.
 Diagnosis:
• Blunt pancreatic trauma usually presents with epigastric
pain, which may be minor at first, with the progressive
development of more severe pain due to the sequelae of
leakage of pancreatic fluid into the surrounding tissues.
35 236 I
• The clinical presentation can be quite deceptive; careful
serial assessments and a high index of suspicion are
threquired.
e
A rise in serum amylase occurs in most cases.
A CT scan of the pancreas will delineate the damage that
has occurred to the pancreas. If there is doubt about
duct disruption, ERCP and MRCP.
 Treatment of blunt injuries.
• The most important factor that determines treatment is
whether the pancreatic duct has been disrupted.
f
• Support with intravenous fluids and a nil by mouth
regimen should be instituted while these investigations
are performed. There is no need to rush to a laparotomy
if the patient is haemodynamically stable, without
peritonitis. It is preferable to manage conservatively at
first, investigate and, once the extent of the damage has
been ascertained, undertake appropriate action.
• Operation is indicated if there is disruption of the main
pancreatic duct; in almost all other cases, the patient will
recover with conservative management.
 Penetrating injury
• Need urgent surgery. Haemostasis and closed
drainage is adequate for minor parenchymal
Id i n't
injuries. If the gland is transected in the body or
tail, a distal pancreatectomy should be
performed, with or without splenectomy.
we a É
However, if the plane of transection is flat and
clean, it may be possible to anastomose the
stump of the distal pancreas to a Roux loop of
jejenum as an end-to-side pancreatojejunostomy.
 I
I of the
• If damage is purely confined to the head
pancreas, haemostasis and external drainage is
normally effective.
• However, if there is severe injury to the
pancreatic head and duodenum, then a
pancreatoduodenectomy may be necessary
I
 Iatrogenic injury ( VERY
IMPORTANT)
• Injury to the tail of the pancreas during
splenectomy, resulting in a pancreatic fistula.
• • Injury to the accessory pancreatic duct
(Santorini), which is the main duct in 7 per cent
of patients, during Billroth II gastrectomy.
Ow
• • Enucleation of islet cell tumors of the pancreas
can result in fistulae.
• • Duodenal or ampullary bleeding following
sphincterotomy. This injury may require
duodenotomy to control the bleeding.
Pancreatic fistula (IMPORTANT)
• Causes: Trauma. Acute and chronic pancreatitis.
• It is important to define the site of the fistula and the
epithelial structure with which it communicates (e.g.
externally to skin or internally to bowel).
• Diagnosis: measurement of the amylase in the fistula
content.
• Management: correction of metabolic and electrolyte
disturbances and adequate drainage of the fistula into
a stoma bag with protection of the skin . When there is
obstruction within the pancreatic duct, stenting the
duct endoscopically.
• parenteral or nasojejunal nutritional support . The use
of octreotide will also suppress pancreatic secretion
 Suggested questions????
Mcl acidosis Holy
• 1- what are the fluid and electrolytes
disturbances associated with pancreatic
fistula?
 Acute pancreatitis
• defined as an acute condition presenting with abdominal pain and is
usually associated with raised pancreatic enzyme levels in the blood or
urine as a result of pancreatic inflammation. Acute pancreatitis may
ormove
recur.
• Due to premature activation of pancreatic enzymes within the
pancreas, leading to a process of autodigestion.
• Anything that injures the acinar cell and impairs the secretion of
zymogen granules, or damages the duct epithelium and thus delays
enzymatic secretion, can trigger acute pancreatitis. Once cellular injury
has been initiated, the inflammatory process can lead to pancreatic
oedema, haemorrhage and, eventually, necrosis. As inflammatory
mediators are released into the circulation, systemic complications can
arise, such as haemodynamic instability, bacteraemia (due to
translocation of gut flora), acute respiratory distress syndrome and
pleural effusions, gastrointestinal haemorrhage, renal failure and
disseminated intravascular coagulation (DIC).
 classification
• Mild acute pancreatitis is characterised by interstitial
oedema of the gland and minimal organ dysfunction.
80% . Mortality 1%.
• Severe acute pancreatitis is characterised by pancreatic
necrosis, a severe systemic inflammatory response and
often multi-organ failure. In those who have a severe
attack of pancreatitis, the mortality varies from 20 to 50
per cent. About one-third of deaths occur in the early
phase of the attack, from multiple organ failure, while
deaths occurring after the first week of onset are due to
septic complications

Many came
8 ME
differentialdiagnosis
Many
 Pancreatitis
most ion 5 T
o ut
 Clinical presentation to Gisplexus
81 seat a
• Pain is the cardinal symptom.
• develops quickly, reaching maximum intensity within
minutes and persists for hours or even days.
• The pain is frequently severe, constant and refractory to
the usual doses of analgesics. Pain is usually
experienced first in the epigastrium but may be localized
to either upper quadrant or felt diffusely throughout the
abdomen.
• There is radiation to the back in about 50 per cent of
patients, and some patients may gain relief by sitting or
leaning forwards.
• In fact, acute pancreatitis can mimic most causes of the
acute abdomen
 Cont-
• Nausea, repeated vomiting and retching
• Why ? Hiccough.
• on examination: the appearance may be that of
a patient who is well or, at the other extreme,
one who is gravely ill with profound shock,
toxicity and confusion.
• Tachypnea is common, tachycardia is usual,
and hypotension may be present. The body
temperature is often normal or even subnormal,
but frequently rises as inflammation develops
 early hypo volmic shock
late septic shock

Jundice
• Mild icterus can be caused by biliary obstruction in gallstone
pancreatitis, and an acute swinging pyrexia suggests cholangitis.
Bleeding into the facial planes can produce bluish discoloration of
the flanks (Grey Turner’s sign) or umbilicus (Cullen’s sign)
• Subcutaneous fat necrosis may produce small, red, tender nodules
on the skin of the legs.
• Abdominal examination may reveal distension due to ileus or, more
rarely, ascites with shifting dullness. A mass can develop in the
epigastrium due to inflammation. There is usually muscle guarding
in the upper abdomen, although marked rigidity is unusual. A pleural
effusion is present in 10–20 per cent of patients. Pulmonary oedema
and pneumonitis are also described and may give rise to the
differential diagnosis of pneumonia or myocardial infarction. The
patient may be confused and exhibit
• the signs of metabolic derangement together with hypoxaemia.
• Grey Turner sign • Cullen’s sign
 Differential

• Not all inclusive, but may include:

§ Biliary disease
§ Intestinal obstruction
§ Mesenteric Ischemia
§ MI (inferior)
§ AAA ( abdominal aortic aneurism)
§ Distal aortic dissection
§ PUD peptic irked
 Evaluation
•  amylase…Nonspecific !!!
§ Amylase levels > 3x normal very suggestive of
pancreatitis
• May be normal in chronic pancreatitis!!!
§ Enzyme level  severity
§ False (-): acute on chronic alcoholism ; HyperTG
§ False (+): renal failure, other abdominal or salivary
gland process, acidemia
•  lipase
§ More sensitive & specific than amylase
 Evaluation
• Other inflammatory markers will be elevated
§ CRP, IL-6, IL-8 (studies hoping to use these markers
to aid in detecting severity of disease)
• ALT > 3x normal  gallstone pancreatitis
§ (96% specific, but only 48% sensitive)
• Depending on severity may see:
§  Ca
§ WBC
§ BUN Bloodu rin nitrogen
§  Hct hematocrit
§  glucose usalincrosesysteme
 Radiographic Evaluation
• AXR - “sentinel loop” or small bowel ileus
• US or CT may show enlarged pancreas with stranding,
abscess, fluid collections, hemorrhage, necrosis or
pseudocyst
• MRI/MRCP Better visualization of fluid collections
§ MRCP allows visualization of bile ducts for stones
§ Does not allow stone extraction or stent
insertion
CT Scan of acute pancreatitis
• CT shows
• significant
• swelling
• and
• inflammation
• of the
• pancreas
Gall stone pancreatitis by
ERCP
 Acute Pancreatitis

• Morbidity and mortality highest if necrosis

present (especially if necroctic area
infected)
§ Dual phase CT scan useful for initial eval to
look for necrosis
• However, necrosis may not be present for 48-72
hours
 Prognosis
• Many different scoring systems
§ Ranson (most popular & always taught in med-school)
• No association found with score, and mortality or length of
hospitalization
• GLASCOW scale :
§ APACHE II
§ CT severity Index
• Recent studies show this to be most predictive of adverse
outcomes
§ Imrie Score.
 Ranson Criteria
• Admission it • During first 48 hours
§ Age > 55 § Hematocrit drop > 10%
§ WBC > 16,000 § Serum calcium < 8
§ Glucose > 200 § Base deficit > 4.0
§ LDH > 350 § Increase in BUN > 5
§ AST > 250 § Fluid sequestration >
6L
§ Arterial PO2 < 60
5% mortality risk with <2 signs
15-20% mortality risk with 3-4 signs
40% mortality risk with 5-6 signs
99% mortality risk with >7 signs
 CT Severity Index
• CT Grade • Necrosis score
§ A is normal (0 points)
§ None (0 points)
§ B is edematous pancreas
(1 point) § < 1/3 (2 points)
§ C is B plus extrapancreatic § > 1/3, < 1/2 (4 points)
changes (2 points)
§ > 1/2 (6 points)
§ D is severe extrapancreatic
changes plus one fluid • TOTAL SCORE =
collection (3 points)
§ CT grade + Necrosis
§ E is multiple or extensive
fluid collections (4 points)
0-1 = 0% mortality
2-3 = 3% mortality
4-6 = 6% mortality
7-10 = 17% mortality
 Therapy

• Remove offending agent (if possible)

• Supportive !!!
• #1- NPO (until pain free)
§ NG suction for patients with ileus or emesis
§ TPN may be needed
• #2- Aggressive volume repletion with IVF
§ Keep an eye on fluid balance/sequestration
and electrolyte disturbances
 Therapy continued

• #3- Narcotic analgesics usually necessary

for pain relief…
• NO conclusive evidence that morphine has
deleterious effect on sphincter of Oddi
pressure
• #4- Urgent ERCP and biliary
sphincterotomy within 72 hours improves
outcome of severe gallstone pancreatitis
§ Reduced biliary sepsis, not actual
improvement of pancreatic inflammation
summary
 Complications
• Necrotizing pancreatitis
§ Significantly increases morbidity & mortality
§ Usually found on CT with IV contrast
• Pseudocysts
§ Suggested by persistent pain or continued high
amylase levels (may be present for 4-6 wks afterward)
§ Cyst may become infected, rupture, hemorrhage or
obstruct adjacent structures
• Asymptomatic, non-enlarging pseudocysts can be
watched and followed with imaging
• Symptomatic, rapidly enlarging or complicated
pseudocysts need to be decompressed
 Complications continued #2
• Infection
§ Many areas for concern: abscess, pancreatic necrosis,
infected pseudocyst, cholangitis, and aspiration
pneumonia -> SEPSIS may occur
§ If concerned, obtain cultures and start broad-spectrum
antimicrobials (appropriate for bowel flora)
§ In the absence of fever or other clinical evidence for
infection, prophylactic antibiotics is not indicated
• Renal failure
§ Severe intravascular volume depletion or acute tubular
necrosis may lead to ARF
 Complications continued #3

• Pulmonary
§ Atelectasis, pleural effusion, pneumonia and
ARDS can develop in severe cases
• Other
§ Metabolic disturbances
• hypocalcemia, hypomagnesemia, hyperglycemia
§ GI bleeds
• Stress gastritis
§ Fistula formation
 Prognosis

• 85-90% mild, self-limited

§ Usually resolves in 3-7 days
• 10-15% severe requiring ICU admission
§ Mortality may approach 50% in severe cases
 Chronic pancreatitis
• Pathophys - irreversible parenchymal destruction leading to pancreatic
dysfunction andloss of exocrine acinar cells and a marked increase in
interstitial fibrous connective tissue. The islets of Langerhans are preserved
and constitute a relatively greater proportion of the pancreatic tissue.
Hyperplasia of islet cells is also seen. The sizes and number of nerves are
increased, but the protective perineural sheath is damaged, and nerves are
found in proximity to inflammatory foci. There appear to be selective
increases in certain peptidergic nerves. These histologic observations may
be related to the cause of pain in chronic pancreatitis

gauge eto
fibrosis end
dust
herbee
 Chronic pancreatitis
• #1- etiology is chronic alcohol abuse (90%) 70 4

• Gallstones
• Hyperparathyroidism
• Congenital malformation
• (pancreas divisum)
• Idiopathic
 Presentations

• Pain .Why? Persistent, recurrent episodes

of severe pain
• Anorexia, nausea
• Constipation, flatulence
• lipid
Steatorrheatexocrainedangesmalabsorption notabsorbtion
• Diabetes endocrinedanger
 Evaluation

•  or normal amylase and lipase

• Plain AXR / CT may show calcified
pancreas
CT - chronic pancreatitis
 Complications

• Exocrine insufficiency typically manifests

as weight loss and steatorrhea
§ If steatorrhea present, a trypsinogen level < 10
is diagnostic for chronic pancreatitis
§ Manage with low-fat diet and pancreatic
enzyme supplements (Pancrease, Creon)
• Endocrine insufficiency may result from
islet cell destruction which leads to
diabetes
 management
• No cure . Symptomatic treatment.
• Alcohol cessation may improve pain
• Pain management critical but Narcotic
dependency is common
• Steatorrhea: Therapy involves limitation of fat
intake and administration of adequate amounts
of exogenous pancreatic enzyme preparations to
provide at least 10% of normal lipolytic activity in
the duodenum at the time that the food substrate
is present
 Management. surgery
• Pain is the primary indication for surgery. Selection of the best
operation for a particular patient must include consideration of the
anatomy of the gland, preexisting endocrine or exocrine dysfunction,
compliance and the rehabilitative capacity of the patient,
postoperative endocrine or exocrine deficiency, and the likelihood of
postoperative pain relief.
• Patients with a dilated duct (>6 mm) are candidates for ductal
drainage, with lateral pancreaticojejunostomy being the best choice
of these procedures. It is important to achieve adequate
decompression of the enlarged pancreatic head and uncinate
• process during drainage procedures
 Conclusion

• Pancreatitis is common
§ YOU WILL SEE IT!!!
• 10-15% are severe = ICU admission
§ Mortality may approach 50% in severe cases
• These are the cases where knowing future
complications would be great (ie finding a marker
that correlates with severity…and that’s what the
clinical researchers are attempting to do)
 Suggested questions???? disease complication
of
Fort
dgnogicidegree

• The aims in investigating patients with suspected

acute pancreatitis.
• Enumerates three therapeutic differences
between the management of mild and severe
forms of acute pancreatitis .
• Causes of renal failure in acute pancreatitis.
seven
mild
antibuaticnutantucated antibioticanticated

not hospitalneed hospital

panel
NG tube shoutpond NGTubelong