Mohammad mobasheri

SpR General Surgery

 Exocrine
Acinar cells produce digestive enzymes and
bicarbonate
Endocrine
Islets of Langerhans contain 4 main cell types
Alpha cells glucagon
Beta cells insulin
Delta cells somatostatin
PP cells pancreatic polypeptide
 Retroperitoneal
Lies between the aorta and the stomach
5 parts:
Head
Neck
Body
Tail
Uncinate Process
Head lies in C shape of duodenum
Superior mesenteric artery (arising from aorta
which sits posterior to pancreas) and vein pass
between head and uncinate process of pancreas
and give off branches that enter the small bowel
mesentery
Tail is in contact with the spleen
 Blood supply to the pancreas arises from
coeliac axis (foregut) and superior
mesenteric artery (midgut)
Superior Pancreatico-duodenal artery (arises from
gastroduodenal artery which is a branch of the
common hepatic artery which arises from coeliac
trunk)
Inferior Pancreatico-duodenal artery (arises from
SMA)
Pancreatic branches of splenic artery supply neck,
body and tail: largest of these is called the arteria
pancreatic magna (aka great pancreatic artery).
 Acute pancreatitis
Rapid onset inflammation of the pancreas

Chronic pancreatitis
Long-standing inflammation of the pancreas
 G gallstones
E ethanol (alcohol)
T trauma
S steroids
M mumps and other viruses (EBV, CMV)
A auto-immune (Polyarteritis nodosa, SLE)
S scorpion/snake bite
H hypercalceamia, hypertriglyceridaemia,
hypothermia
E ERCP
D drugs (SAND: steroids and sulphonamides,
azothioprine, NSAIDS, diuretics [loop/thiazide])
 Pancreatic enzymes become activated
within the pancreas
Autolysis
Inflammation/pain/complications
Worst offender is trypsin (protease)

Oedematous pancreatitis heamorrhagic

pancreatitis necrotic pancreatitis (+/-
superceeding infection: aka infected
necrosis)
 Symptoms
Epigastric pain radiating into
the back, often eased by sitting
forward
N&V (vomiting +++)
Fevers
Signs
Haemodynamic instability
(tachycardic, hypotensive)
Peritonism in upper
abdomen/generalised
Grey-turners sign (bruising in
flanks)
Cullens sign (bruising around
umbilicus)
Grey turners and cullens signs
are seen in heamorrhagic
pancreatitis
 Differentials for upper abdominal pain
include:
Gallstone disease and associated complications (E.g.
Biliary colic/acute cholecystitis)
Peptic ulcer disease/perforation
Leaking/ruptured AAA
 Blood tests
Amylase/lipase (other causes of increased amylase include
parotitis, renal failure, macroamylasaemia, bowel perforation,
lung/ovary/pancreas/colonic malignancy can produce ectopic
amylase)

X rays ECXR, AXR (sentinal loop, gallstone)

USS look for gallstones as cause for pancreatitis

CT abdomen (patients not settling with conservative management,

and only after 48hrs of symptom onset)

MRCP If you suspect pancreatitis is due to gallstone that is stuck in

the CBD

ERCP To remove a gallstone in the CBD that has caused panreatitis

 Pancreatitis can be life threatening.
Pancreatitis classified into mild and severe based
on scoring systems:
Modified Glasgow criteria (alternative is Ransons criteria):
P PO2 <8KPa
A age >55yrs
N WCC >15
C calcium <2mmol/L
R renal: urea >16mmol/L
E enzymes: AST >200iu/L, LDH >600iu/L
A Albumin <32g/L
S sugar >10mmol/L
Score of 3 or more within 48hrs of onset suggests
severe pancreatitis
CRP is an independent predictor of severity, and if
>200 is suggestive of severe pancreatitis
 Other scoring systemics include:
Glasgow (non-modified) and Ransons criteria which
measure factors at admission and then after 48
hours.
 ABC
4 Priniciples of management include:
Fluid resuscitation (IVF, catheter, strict FB monitoring)
Analgesia
Pancreatic rest (+/- nutritional support if prolonged
recovery [NJ feeding or TPN])
Determining underlying cause
95% settle with conservative treatment
If severe pancreatitis on scoring HDU
Antibiotics controversial commence if
necrotic pancreatitis/infected necrosis, but not
routinely.
Surgery only very rarely required
 Systemic
Hypocalcaemia (release of lipase results in free fatty
acids which chelate calcium salts reducing serum
levels: this process of calcium chelation is called
saponification)
Hyperglycaemia (diabetes if significant beta cell
damage)
SIRS
ARF
ARDS
DIC
MOF and death
 Local
Pancreatic necrosis (aka necrotic pancreatitis) +/- infection (infected necrosis)

Pancreatic Abscess

Pancreatic Pseudocyst

Haemorrhage: due to bleeding from eroded vessels

Small vessels haemorrhagic pancreatitis with cullens/grey turners sign
Large vessels (e.g. Splenic artery) life threatening bleed (unless forms pseudoaneurysm)

Thrombosis of splenic vein, SMV, portal vein (in order of frequency) with
consequent ascites or small bowel venous congestion/ischaemia

Chronic pancreatitis/pancreatic insufficiency (if recurrent attacks)

 At severe end of the spectrum of
pancreatitis is necrotic pancreatitis
This can be complicated by infection of the
necrotic tissue termed infected necrosis
If an infected necrotic area becomes
encapsulated by granulation tissue then it
becomes known as a pancreatic abscess
Infected necrosis is life threatening and has
mortality rate of 50% due to high risk of
SIRS progressing to multi-organ failure
 Management: Antibiotics + Surgery
Infected pancreatic necrosis is the only indication for
surgical intervention in the context of acute
pancreatitis (high mortality if dead infected tissue is
not debrided)

Surgery involves necresectomy (excision of

necrotic tissue)
 Occurs as a complication of infected necrotic pancreatitis

Pancreatic abscess is a collection of pus resulting from pancreatic

tissue necrosis and infection that becomes lined by granulation
tissue (note that infection of necrotic pancreatic tissue in the
absence of abscess formation (i.e. Granulation tissue lining) is
termed infected pancreatic necrosis)

Usually presents 2-4 weeks after initial attack of pancreatitis

Management: Like any abscess it requires antibiotics + drainage:

percutaneous (under CT guidance)
Surgical drainage
 Pseudocyst is a peri-pancreatic fluid collection containing high
concentration of pancreatic enzymes within a fibrous capsule
Usually presents >6 weeks after attack of pancreatitis

95% absorbed spontaneously over 6 months and therefore require

no intervention, unless:
Pseudocyst symptomatic (can cause significant pain)
Pseudocyst causing compression of surrounding structures e.g. CBD (obstructive
jaundice), duodenum (high SBO)
Pseudocyst infected (i.e. has turned into an abscess)

In above three situations the pseudocyst should be drained:

Percutaneously under radiological guidance (CT)
Endoscopically by puncturing posterior wall of stomach and inserting a drain into the cyst
Surgically via laparoscopic/open cystgastrostomy (cyst opened up into stomach allowing
it to drain
 Long-standing inflammation of the pancreas
that alters its structure and function

It can present as:

Acute inflammation in a previously damaged
pancreas (acute on chronic pancreatitis)
Chronic pain
Pancreatic insufficiency (malabsorption/diabetes)
 Chronic upper abdominal pain
Weight loss (secondary to malabsorption)
Steatorrhoea (offensive smelling stools that float due to
high fat content in stool secondary to fat malabsorption)

Differential diagnosis for steatorrhoea

Chronic pancreatitis (exocrine pancreatic insufficiency)
Biliary obstruction (e.g. Pancreatic cancer, cholangiocarcinoma,
choledocholithiasis)
Malabsorption due to small bowel disease (e.g. Crohns, coeliac, short gut
syndrome)
Drugs (e.g. Orlistat weight loss pill)
 Alcohol abuse most common cause
Chronic steroid/NSAID use
No cause found in 25%
Cystic Fibrosis most common cause in
children
Gallstones rarely cause chronic pancreatitis
 Typical triad
Chronic upper abdominal pain
Malabsorption (evidenced by steatorrhoea and weight
loss)
Calcification of pancreas (on AXR/CT)

Investigations:
Amylase/lipase often normal
Faecal elastase
Secretin stimulation test gold standard but rarely used
AXR to look for calcification
CT to look for calcification and structural damage
typical of chronic pancreatitis
 Secretin is a hormone produced in the
duodenum (by S cells)
It is released in response to low pH in
duodenum i.e. When stomach contents
enters duodenum)
It results in:
Release of bicarbonate rich solution from pancreas to
neutralise acid
Excretion of bile from gallbladder and pancreatic
enzymes from pancreas by potentiating effects of
CCK
 Patient starved for 12 hours prior to testing
Triple lumen tube inserted via the nose into the stomach (1 lumen)
and the duodenum (2 lumens)
Gastric lumen used to empty stomach to prevent gastric contents
denaturing secretin which is injected via the duodenal lumen (note
that CCK can be injected as an alternative to secretin)
Over the subsequent 2 hours duodenal fluid is sampled from the tube
to assess its pH, bicarbonate and enzyme content and this is
compared to a control sample taken prior to secretin injection
In pancreatic insufficiency bicarbonate levels and enzyme levels are
lower than expected

90% accuracy for identifying pancreatic exocrine insufficiency

Limitations: length of procedure, NG intubation which is
uncomfortable for patient, radiation exposure to guide placement of
tube into the duodenum
 Elastases protease enzymes that
hydrolyse elastin among many other
proteins

In chronic pancreatitis there is a reduction

in elastase production (due to exocrine
insufficiency)

This results in low levels of elastase in

faeces in patients with chronic pancreatitis
 Mainstay of management is conservative and
medical
Analgesia
Treatment of secondary diabetes
Diet
Oral hypoglycaemics
Insulin
Treatment of malabsorption
Nutritional support
Pancreatic enzyme supplementation (CREON)

Surgical intervention extremely rare

Pancreatic transplants
Questions