1. The pancreas is a retroperitoneal organ that produces enzymes to aid digestion and hormones like insulin and glucagon. 2. Acute pancreatitis is inflammation of the pancreas that ranges from mild to severe, with the most common causes being gallstones and alcohol abuse. 3. Management of acute pancreatitis involves fluid resuscitation, pain control, predicting severity based on criteria like Ranson's or CT severity index, treating any organ failure, and considering ERCP if cholangitis or gallstones are present.

1. Pancreas
rewritten by
Mohammed almohalal
Naseem alsinai
Mohammed alrubaei

2. Pancreas
Anatomy
-It is a retroperitoneal organ lies in an oblique position, sloping upward
to the left from the C-loop of the duodenum to the splenic hilum.
-Its weight is about 80 g (
75
-
150 g )and its length is ( 15
-
20 cm).
-it's divided into:
a- head and neck (30% of the gland )
b- Body and tail (70% of the gland)
-The head lies within the concavity of the doudenum over the IVC ,
Both renal veins and right renal artery at the level of the 2nd lumbar
vertebra.

3. -The neck lies directly anterior to the portal vein.
-Venous branches draining the head and uncinate process enter along
the right lateral and posterior side of portal vein .
Therefore, a plane can be developed between the neck and anterior
aspect of portal vein during pancreatic resection
-The body and tail lie anterior to the aorta, left renal vessels and the
left kidney, in floor of lesser sac behind the posterior wall of the
stomach. (anterior wall of pseudocyst)
-The base of transverse mesocolon attaches to the interior margin of
the body and tail (often forming the inferior wall of pseudocyst(

4. Embryology and duct anomalies :
-the pancreas is formed by the fusion of vertical and dorsal buds .
The ventral bud becomes the inferior portion of the head and uncinate
process, while The larger dorsal bud becomes the superior portion of
the head and the body and the tail of pancreas.
-The duct of ventral bud which arises from the hepatic diverticulum
connects directly with the CBD (called wirsung duct) and drains through
major papilla.

5. -The duct of dorsal bud which arises from the duodenum drains
through the minor papilla (called the duct of sanatorini).
-In upto 30% of cases, the duct of sanatorini ends blindly as a blind
accessory duct (does not empty into the duodenum).
-In about 10% of patients, the duct of wirsung and the duct of
sanatorini fail to fuse and the majority of pancreas drains through the
duct of sanatorini and to To minor papilla while the inferior portion of
head and uncinate process drains through the duct of wirsung and
major papilla this referred to pancreatic divisum
Malrotation of ventral bud results in annular pancreas.

6. Vascular and lymphatic anatomy:
-The blood supply of pancreas comes from multiple branches from
celiac trunk and superior mesenteric artery(SMA)
-Venous drainage follows the pattern of arterial supply and drains into
portal vein
-Lymphatic drainage is diffuse and widespread which explains the high
incidence of lymph nodes metastasis and local recurrence of pancreatic
cancer.

7. Histology and physiology:
1
- Exocrine pancreatic tissues accounts for 85% of gland parenchyma which
secretes 500 to 800ML per day which is enzymes rich ,alkaline fluid in respon
to meal .spontaneous secretion is minimal .
-Secretin hormone which is released from duodenal mucosa stimulates the
bicarbonate and electrolytes secretion.
-CCK Stimulates enzymes rich fluids secretion
-Vagal stimulation increase the volume of secretion.
-Acinar cell secretes the enzymes whereas centriacinar and intercalated cells
secrete electrolyte (Na,k,HCo 3
)lC,
.

8. • Proteases are secreted in inactive form and converts to active form in
duodenum by enterokinase released from mucosa of duodenum
• Tripsinogen remai inactive within pancreas by inhibitor called
pancreatic secretory tripsinogen inhibitor (PSTI) or serine protease
inhibitor kazaf type1
• Insufficient spink1 leads to activation of tripsinogen in pancreas
resulting in recurrent pancreatitis called familial pancreatitis
• Missense mutation of tripsinogen lead to hereditary pancreatitis

9. 2
- Endocrine pancreas accounts for 2% of the gland parenchyma which
secretes glucoregulatory hormones as insulin,
glucagon,somatostastin,ghrelin and pancreatic peptide

10. • Investigation of pancreas
• Estimations of pancreatic enzyme in body fluid:
-Serum amylase level is the most widely used test of pancreatic
damage
-Serum lipase is more sensitive and specific but not widely available
• Pancreatic function test:
a -Direct
-assessment of exocrine secretions in response to standard stimuli
either physiologically as ingested test meal or pharmacological as IV
injection of secretin or cck
-Duodenal intubation has to be performed with triple lumen catheter
so that gastric and duodenal juices can be aspirated

11. b- indirect test
-Nitroblue tetrazolium paraaminobenzoic acid (NBT-PAPA) is
administered orally and degraded in the gut by pancreatic enzyme and
the breakdown product (PAPA) is absorbed and excreted in urine its
urinary level is measured.

12. • Imaging investigation
-US is investigation of patients with jaundice and
suspicion of pancreatic pathology but obesity and
overlying gas ofen make interpretation of pancreas
unsatisfactory
-CT : high quality CT scan (three dimensional
reconstructions) is useful in :
a- Confirm the acute pancreatitis
b- Identify tumor 1
-
2 CM

13. d- Therapeutic and diagnostic CT guided intervention
-MRI: pancreas can clearly identified and detecting
pancreatic and bile duct together with fluid collection.
-MRCP: may replace the diagnostic endoscopic
cholepancreatography and ERCP as it is non invasive
and less expensive .

14. Acute pancreatitis (AP)
• Defined as an acute inflammation condition presenting with acute
abdominal pain consistent with acute pancreatitis (epigastric pain
radiating to the back, relieved by Leaning forward), a three fold or
greater rise of pancreatic enzymes (amylase and lipase) in serum
levels and/or characteristic findings of pancreatic inflammation on
contrast enhanced CT-scan.
The incidence and epidemiology:
• Acute pancreatitis accounts for 2% of all cases of acute abdominal
admitted into hospital in UK.
• Worldwide the incidence ranges 5
-
80/100000 population with the
highest rate being in finland and USA.
• Acut pancreatitis is the most common gastrointestinal discharge
diagnosis in the USA.

15. • The crude mortality rate of 1/100000 ranks it as the 14th most fatal
illness overall and the ninth most common non-concer
gastrointestinal death .
• The incidence of acute pancreatitis (AP) also shows significant
variation related to the prevalence of etiological factors and ethnicity
typically alcohol and drug induced acute pancreatitis presents in the
third and forth decades compared with gallstones and trauma
induced disease in the sixth decade.
• Pathenogenesis:
• Multiple factors triggering the premature activation of the pancreatic
enzymes within the pancreas leading to process of
autodigestion,acinar cell injury and inflammatory process which may

16. • Etiology:
• Other most common causes are gallstones and alcohol accounting for
upto 80% of cases .
• Other causes : hyperlipidemia, hypercalcemia and hereditary
pancreas trauma, ductal obstruction, ischemia, infection and drug
• The drugs e.x thiazides,furosemide, steroids, …………
dna dica cirpolav,
,negortse
……… and propofol.

17. Clinical features
• The cardinal symptom of AP is abdominal pain in the epigastrium but
may be localized to upper quadrant or diffuse involve the whole
abdomen
-The pain is rapid in onset progressive reaching maximal intensity
within hours and become severe consistent aching pain radiating to
back (46% of cases)
-Refractory to usual analgesic but may relieved by leaning forward in
some cases
-Associated with nausea ,frequent vomiting and retching which may
persist despite the stomach being kept empty by NGT decompression
-Hiccup may persist due to gastric distension or diaphragmatic

18. • The patient may appear gravely ill with profound shock, toxicity,
confusion, tachycardia, tachypnea
• Hypotension and respiratory distress
• The abdomen may be distended with diffuse tenderness
quarding,and rigidity
• Epigastric mass may be palpable
• Grey turner sign and gullen sign may present
• Chest exam may reveal pleural effusion

19. Management
• intial investigation: CBC,RFT,LFT,amylase level, electrolyte, CXR
• admission into ward or ICU(fluid resuscitation, pain relief(..
• Establishment the correct diagnosis:
diagnostic criteria with or without CE CT
serum amylase level does not correlate with severity of AP
Normal amylase level does not exclude the diagnosis
• Contrast enhanced CT scan is indicated if:
Diagnosis uncertainty, or deterioration of clinical features, or
assessment of severity

20. • predicating the severity of AP :
Various scoring systems have been used to assess the severity and risk
of mortality to provide the patient adequate high quality supportive
care , monitoring and treatment the complications.

21. Diagnosis criteria
a- Revised Atlanta criteria
• Mild AP: no local or systemic complications
• Moderately severe:local complications with transient organ failure
resolve within 48 hours
• Severe AP: local complications with organ failure either single or
multiple
b- Ransoni criteria at admissions and 48 hours.
c - CT scan : CT abdomen not performed before the first 12 hours of
onset of symptoms as early CT may result normal finding.

22. CT scan severity index (balthazar criteria(
a- degree of pancreatitis
normal CT=0 point
Diffuse enlargement of pancreas =1 point
peripancreatic inflammation =2 point
single fluid collection=3 point
multiple fluid collection =4 point
b- Degree of necrosis
no necrosis =0 point
lower than 30%
=
2 point
30
_
50
% necrosis =4 point

23. Risk of mortality reflects the spectrum of
severity
• mild disease lower than 1%mortality =0 to 2
• Moderate up to 10%
=
3 to 4
• Severe 20 to 40%
=
5 to 6
• Critical more than 50%
=
7 to 8

24. Clasgo score is valid for both alcohol and
gallstones induced AP(pancreas)
P: Pao 2
<
60 MMHg
A: Age>55years
N: neutrophils WBC>15000
C: calcium <2mmol/L
R: renal urea >16mmol/l no response to fluid resuscitation
E: enzymes LDH>600unit/L
A: Albumin <3.2gL
S: sugar blood glucose >10mmol/L no history of DM

25. a logarithm for evaluation and management
of acute pancreatitis
1
- Diagnosis :
a- history of abdominal pain consistent with acute pancreatitis .
b- three times elevation of pancreatic enzymes (amylase , ligase) above
the upper limit.
c- CT scan of required to confirm diagnosis.
2
- initial assessment / management (first four hours( :
a- Analgesia IV fluid resuscitation
b- predict severity of pancreatitis reasons criteria, Glasqo , BisAps
c- Assess synthetic response SIRS score , SOFA

26. 3
- Reassessment/ management :
a- Assess response to fluid resuscitation (MAP , HR, UOP, HT)
b- Determine etiology by ultrasonography, laboratory tests
c- MRCP and/ or urgent ERCP (jaundice , gall stone , dilated CBD)
d- Admission into ICU or transfer to special centers of:
- deterioration of failure to respond to initial management
- intensive support for
organ failure
e- Consider EN and no probiotics

27. 4
- Conservative management and monitoring (at least daily)
a-clinical elevation (Cvs, respiratory, and renal function.
b- daily CRP
c- classify severity based on local and systemic complications. local
complications based on CT severity index
5
- indication for pancreatic protocol CT scan:
a- clinical deterioration and elevated CRP
b- suspicion of local complications
c- suspected bowel ischemia
d- abdominal compartment syndrome

28. 6
- invasive intervention:
a- step up approach with in initial drain guided by CT
b- video assisted retroperitoneal debridement
c- endoscopic transluminal debridement
d- ongoing large bore drainage and............
7
- indication for laparotomy
a- failed step up approach for further debridement/ drainage
b- acute abdomen (perforation ischemia)
c- sever abdominal compartment syndrome (rarely required)

29. Further management
• If after intial assessment of patients is considered to have mild attack
of pancreatitis conservative approach is indicated with fluid
resuscitation, pain relief and non invasive observations
Brief period of fasting
antibiotic isn’t indicated
CT scan unnecessary unless there is evidence of deterioration

30. • If severe attack is predicted we should:
1
- admission into ICU or high dependency
2
- aggressive fluid resuscitation guided by vital signs UOP and CVP
3
- prophylactic antibiotics and antisecretery (H2 blockers,somatostatin
4
- Ct scan if clinical deterioration or complications
5
- ERCP if cholangitis with CBD stones within hours
6
- supportive treatment for organs failure

31. Management of local complications
• Once acute phase has been survived usually at end of first weak and
major organ failure is under control the local complications can
manage conservatively but surgery restricted to situations in which
conservative management failed
• 1
- Acute peripancreatic fluid collection (APFC)
• 2
- sterile and infected pancreatic necrosis (non viable
parenchyma):pancreatic necrosis is associated with lysis of
peripancreatic fat leading to acute necrotic collection (ANC) <4 weeks
but > 4 weeks called walledof necrosis (WON) collection with necrotic
material encapsulated with granulation tiisue

32. 3
- pancreatic abscess:WON becomes infected
4
- pancreatic ascites;generalized peritoneal enzyme rich effusion
usually associated with pancreatic duct disruption. Paracentesis will
reveal turbid fluid with high amylase level
ttt,: adequate drainage with wide borne drain placed under imaging
quide is essential
5
- pancreatic effusion
6
- hemorrhage may occur in to gut ,retroperitoneal, or intraperitoneal
7
- portal vein or splenic vein thrombosis may develop silently
8
- pseudocyst