Anatomy

Location and relation

Ducts
Blood supply

Anatomy
Location:

- Retroperitoneal

(posterior to stomach, transverse mesocolon and lesser

omentum)

- At the level of the body of L2

Divided into:
1. Head: includes uncinate process and abuts the second part of the
duodenum.
2. Neck: portion anterior to superior mesenteric vein.
3. Body: lies to the left of the neck, forms posterior floor of lesser sac.
4. Tail: enters splenorenal ligament, adjacent to splenic hilum*
*susceptible to injury during splenectomy.

Anatomy
Ducts:
1. Wirsung duct:
The main duct; runs entire length of pancreas. It joins the
common bile duct and empties into the second part of the
duodenum at the ampulla of Vater.

1. Santorini duct:
(Small duct) is an accessory duct often joining the
duodenum more proximally than the ampulla of Vater

Anatomy
Blood supply:
Head:

Anterior and posterior superior pancreaticoduodenal

arteriesbranches of the gastroduodenal artery.

Anterior and posterior inferior pancreaticoduodenal

arteries branches of the superior mesenteric artery.

Neck, body and tail:

Splenic artery and branches (dorsal pancreatic artery).

Anatomy
Nerve supply:
Sympathetics: Pain sensation is provided by the celiac

plexus (via the splanchnic nerves).

Parasympathetics: Islets, acini, and ducts are innervated

by branches of the vagus.

*Clinical note: Celiac plexus block can be done for pain control
in pancreatic disease.

Physiology
Exocrine vs. Endocrine

Physiology
Exocrine:
1. Acinar cells: secrete enzymes (e.g. chymotrypsin,

trypsin, carboxypeptidase, amylase, lipase).

2. Centroacinar & ductal cells: secrete water &
electrolytes (e.g. Na , K , HCO , Cl ).
+

Endocrine:
1. Insulin: From beta cells in islets of Langerhans.
2. Glucagon: From alpha cells in islets of Langerhans.
3. Somatostatin: From delta cells in islets of Langerhans.

 Control of the exocrine function of the pancreas is via the

hormones gastrin, cholecystokinin & secretin which are secreted

by cells in the stomach and duodenum, in response to distension
and/or food and which cause secretion of pancreatic juices.
The precursor enzymes (termed zymogens or proenzymes) are

inactive variants of the enzymes; thus autodegradation, which

can lead to pancreatitis, is avoided.
Once released in the intestine, the enzyme enteropeptidase

present in the intestinal mucosa activates trypsinogen by cleaving

it to form trypsin. The free trypsin then cleaves the rest of the
trypsinogen, as well as chymotrypsinogen to its active form
chymotrypsin.

Acute pancreatitis
Inflammation (NOT infection) of the pancreas due

to parenchymal autodigestion by proteolytic

enzymes

Has a significant mortality and morbidity rates.

Acute pancreatitis
(causes)
1. Gallstones.
2. Alcohol.
3. Iatrogenic.
4. Metabolic.
5. Infection.
6. Drugs.
7. Tumors.
8. Ischemia.
9. Congenital anomalies.

Pathophysiology
Gallstone:
when a migrating gallstone obstructs the ampulla of Vater.

Alcohol:
- At the cellular level, ethanol leads to intracellular accumulation
of digestive enzymes and their premature activation and
release.
- At the ductal level, it increases the permeability of ductules,
allowing enzymes to reach the parenchyma and cause
pancreatic damage.

Pathophysiology
The underlying mechanism of injury in pancreatitis is thought to

be 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 (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

Severity
Mild acute pancreatitis
Characterized by interstitial edema & minimal organ dysfunction.
80% of patients will have a mild attack of pancreatitis, the

mortality from which is around 1%.

Severe acute pancreatitis

Characterized by pancreatic necrosis, a severe systemic

inflammatory response and often multi-organ failure.

Acute pancreatitis
(approach)
Case study
A 50-year-old man, presents to the ER

complaining of severe epigastric pain for 3

hours duration.

Acute pancreatitis
(approach)

History:

History of present illness:

The pain was sudden, constant, epigastric, radiates to the back, deep
dull in nature, he gave it 8.5/10. It improves when leaning forward,
worsens with deep inspiration and movement. The patient vomited a
large amount of undigested food but the pain is not relieved.
Systemic review: free
Past medical history: recurrent attacks of colicky RUQ pain.
Past surgical history: clear
Family history: DM and HTN and PUD (mother)
Social history: smoker (1pack/day), drink alcohol only in the weekends!

Acute pancreatitis
(approach)
Physical Examination:
General:
Patient is in pain, looks ill and jaundiced
Vital signs: T= 38.8, BP= 110/60, HR= 110, RR= 28

Abdominal exam:
The abdomen was rigid and tender in the epigastric and

periumbilibal area.
Mild abdominal distension was noticed.

Signs of acute
pancreatitis
GENERAL SIGNS:
Fever (76%)
tachycardia (65%) & hypotension
Abdominal tenderness(68%) & distention (65%)
Jaundice (28%)
Dyspnea (10%); tachypnea
In severe cases, hemodynamic instability (10%) and

hematemesis or melena (5%).

Local Late Signs:

1- These signs are not specific for acute pancreatitis; they can occur in any
retroperitoneal bleeding
2- These are uncommon physical findings and they are associated with
severe necrotizing pancreatitis

Acute pancreatitis (approach)

Diagnosis is clinical, but laboratory tests are usually
obtained:
To confirm the diagnosis
To define an etiology, look for complications & determine the

prognosis

Investigations (labs)
CBC:
For leukocytosis and anemia is severe cases

Serum amylase and lipase

Typically elevated in patients with acute pancreatitis

Lipase level remains high for 12 day
Increase 3 times in amylase suggests Acute pancreatitis.
The elevated amylase is less specific for pancreas than lipase*

*Lipase Only found in gastric, intestinal mucosa and liver. While Amylase
apart from intestine found also in salivary glands, ovaries, testes, and
skeletal muscle.
*High amylase levels are seen in intestinal disease, perforated ulcer,
ruptured ectopic pregnancy, salpingitis, salivary gland disorders, renal
failure & DKA.

Investigations (labs)
Liver enzymes:
Alkaline phosphatase, total bilirubin, AST and ALT levels to search for

evidence of gallstone pancreatitis.

Serum electrolytes, BUN, creatinine, glucose,

cholesterol and triglycerides.

C-reactive protein (CRP).
LDH and bicarbonate.

Investigations (imaging)
I. X-ray
Sentinel loop sign

localized ileus from

nearby inflammation

Colon cut-off sign

Gaseous distension of the right

and transverse colon with or
absent air beyond the splenic

Investigations (imaging)
II. Ultrasonography:
It is the most useful initial test in determining the etiology of

pancreatitis.
pseudocysts, phlegmon, abscesses or cholelithiasis.

III. ERCP
Should be used with extreme caution in patients with acute

pancreatitis and should never be used as a first-line diagnostic

tool in this disease.
Diagnostic and therapeutic (in biliary pancreatitis)

IV. Abdominal CT:

Diagnostic test of choice (90% sensitive and 100% specific)

Can differentiate between mild and severe pancreatitis.
Demonstrates pseudocysts, phlegmon, abscesses or pancreatic

necrosis

What are the indications to use the CT scan ?

1.

If diagnosis is uncertain,

2.

To distinguish INTERSTITIAL from NECROTISING pancreatitis,

3.

If there are organ failure & clinical worsening,

4.

When a localized complication is suspected.

Lab results:
CBC:
WBC= 19.000, Hb= 17 g/dl, Hct= 47 %

Back to our case

LFT:
Bilirubin= 3.2 mg/dl, AST= 435 U/l, LDH= 300U/L , Amylase=
6800 IU/L

CT Abdomen

Management:
In acute pancreatitis always stabilization of the

patient is the most important step.

Then classify your patient according to:

Glasgow
Ransons Criteria
APACHE II score
CT severity index
CRP level

Glasgow criteria
One form of the Glasgow criteria suggests that a case be

considered severe if at least three of the following are true:

Age > 55 years

Blood levels:
P02 Oxygen < 60mmHg
White blood cells > 15
Calcium < 2mmol/L
Urea > 16mmol/L
Lactate dehydrogenase (LDH) > 600iu/L
Aspartate transaminase (AST) > 100iu/L
Albumin < 32g/L
Glucose > 10mmol/L in the absence of diabetes

Ransons criteria

Evaluation of severity of
pancreatitis
Severe pancreatitis is suspected if:
Ranson >= 3 (or) Glasgow >=3

Mortality in mild pancreatitis is less than 1%, while in

severe pancreatitis is 10-30%.

R-Regimen
(except pancreatic
1. Rest the pain by pethidine NOT morphine (?)
necrosis)
2. Rest the bowel NPO, nasogastric tube
3. Resuscitation IVF & electrolytes
4. Resist infection Antibiotics (controversial)
5. Repeated examination (every 2 hrs)
6. Repeated serum tests (WBC, Ca, albumin)
7. Respiratory support (O2, assisted ventilation if needed)

Nutrition
TPN in early period of disease
Post-pyloric enteral feeding (in which a feeding tube is endoscopically or

radiographically introduced to the third portion of the duodenum)

The advantage of enteral feeding is that it is more physiological,

prevents gut mucosal atrophy, and is free of the side effects of TPN
(such as fungemia).
The additional advantages of post-pyloric feeding are the inverse

relationship of pancreatic exocrine secretions and distance of nutrient

delivery from the pylorus, as well as reduced risk of aspiration.

 Endoscopic (ERCP)
If gall stone is strongly suspected as the cause of

pancreatitis, the stones should be removed through

endoscopic sphincterotomy.
If there is severe pancreatitis, or cholangitis, both

sphinterotomy and ERCP is done

Surgery indicated in:

i) Infected pancreatic necrosis.
ii) Diagnostic uncertainty.
iii) Complications.

What are the

complications of
?acute pancreatitis

Acute pseudocyst
Is a collection of pancreatic fluid that is walled off by

granulation tissue after an episode of acute pancreatitis,

It requires 4 or more weeks to develop
If after 6 weeks they have not resolved and are > 6 cm in

size, internal drainage of the mature cyst is indicated via

cyst gastrostomy or Roux-en-Y cyst jejunostomy.

Intra-abdominal infection
It is common.
Within the first 1-3 weeks, fluid collection or

pancreatic necrosis can become infected and

jeopardize clinical outcome.
From 3 to 6 weeks, pseudocysts may become infected

or a pancreatic abscess may develop.

Pancreatic necrosis
It is a nonviable area of pancreatic parenchyma that

is often associated with peripancreatic fat necrosis

and is principally diagnosed with the aid of dynamic
spiral CT scan.

No enhancement of pancreas with IV contrast

Pancreatic fat necrosis

Fat necrosis is a consequence of enzyme damage to the

membranes of the adipocytes near the affected pancreatic

tissue.
The term "saponification" has been used to describe this

lesion in fat, due to the "soap-like" alteration of the

triglycerides released from the adipocytes.

Treatment
Minimally invasive management: necrosectomy

through small incision in skin (left flank) or stomach

Conventional management: necrosectomy with simple
drainage
Closed management: necrosectomy with closed
continuous postoperative lavage
Open management: necrosectomy with planned staged
reoperations at definite intervals (up to 20+
reoperations in some cases)

:Definition
Chronic inflammation or recurrent acute pancreatitis
that causes irreversible parenchymal fibrosis,
destruction and calcification, leading to loss of
endocrine and exocrine function.

Etiology
Alcohol abuse (70%).
Idiopathic (20%).
Other (10%): Hyperparathyroidism,

hypertriglyceridemia, congenital
Pancreatic anomalies, hereditary, obstruction.

Typical Hx of chronic pancereatitis

A 41-year-old alcoholic patient, has a 6-year

history of recurrent attacks of pancreatitis

characterized by epigastric pain radiating to the
back. Recently developed evidence of diabetes
and steatorrhoea. CT imaging shows pancreatic
calcifications but no cystic or mass lesions.

Clinically
Recurrent or constant epigastric and/or

back pain.
Malabsorption/malnutrition (exocrine
dysfunction).
Steatorrhea (exocrine dysfunction), fatsoluble vitamin deficiency.
DM (endocrine dysfunction).

Diagnosis
Serum amylase and lipase levels may be slightly

elevated
Fecal fat analysis.
Abdominal X-ray
CT scan
ERCP

X-ray (kidneys, ureters &

bladder): Pancreatic
calcifications

CT: Pseudocysts, Gland enlargement/

atrophy, calcifications, masses

ERCP: Chain-of-lakes pattern

ductal irregularities with dilation
.and stenosis

Treatment
Nonoperative:
Includes control of abdominal pain, endocrine and
exocrine insufficiency (insulin and pancreatic enzymes
therapy).

Operative:
(must do preop. ERCP to evaluate the anatomy)
Persistent pain
Gastrointestinal or biliary obstruction
Pseudocyst infection, hemorrhage, rupture or enlarging

Surgical methods
Pain relief: Celiac plexus block.
Ampullary procedures: ERCP with endoscopic

sphincterotomy
Ductal decompression procedures:
Puestow procedure (longitudinal pancreaticojejunostomy)

for segmental ductal dilation.

Duval procedure (retrograde drainage with distal resection
and end-to-end pancreaticojejunostomy).

Ablative procedures (resection of portions of pancreas):

Frey procedure (longitudinal pancreaticojejunostomy with partial

resection of the pancreatic head).

Whipple procedure (pancreaticoduodenectomy with

choledochojejunostomy, pancreaticojejunostomy and

gastrojejunostomy).
Near-total pancreatectomy.

Thank you :)
Mai Mazin & Hanan Al-Fayyomi