Mohammad mobasheri
SpR General Surgery
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Exocrine
 Acinar cells – produce digestive enzymes and
bicarbonate
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Endocrine
◦ Islets of Langerhans – contain 4 main cell types
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Alpha cells – glucagon
Beta cells – insulin
Delta cells – somatostatin
PP cells – pancreatic polypeptide
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Retroperitoneal
Lies between the aorta and the stomach
5 parts:
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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
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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).
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Acute pancreatitis
 Rapid onset inflammation of the pancreas
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Chronic pancreatitis
 Long-standing inflammation of the pancreas
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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])
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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)
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Symptoms
 Epigastric pain radiating into the
back, often eased by sitting
forward
 N&V (vomiting +++)
 Fevers
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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
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Differentials for upper abdominal pain
include:
 Gallstone disease and associated complications (E.g.
Biliary colic/acute cholecystitis)
 Peptic ulcer disease/perforation
 Leaking/ruptured AAA
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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)
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X rays – ECXR, AXR (sentinal loop, gallstone)
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USS – look for gallstones as cause for pancreatitis
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CT abdomen (patients not settling with conservative management, and
only after 48hrs of symptom onset)
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MRCP – If you suspect pancreatitis is due to gallstone that is stuck in the
CBD
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ERCP – To remove a gallstone in the CBD that has caused panreatitis
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Pancreatitis can be life threatening.
Pancreatitis classified into mild and severe based on
scoring systems:
◦ Modified Glasgow criteria (alternative is Ransons criteria):
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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
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Other scoring systemics include:
 Glasgow (non-modified) and Ransons criteria which
measure factors at admission and then after 48 hours.
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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
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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
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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
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Acute pancreatitis can be life threatening in severe cases due to SIRS which
can progress to multi-organ failure
SIRS – overzealous inflammatory response resulting in widespread activation
of inflammatory cascades and micro-circulatory dysfunction (believed to be
mediated by TNF-alpha)
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Temp <36oC, >38oC
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HR >90
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RR >20
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WCC >12
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SIRS if 2 or more of the above
SIRS frequently complicated by failure of one or more organ systems
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Acute lung injury (ARDS)
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Acute kidney injury (ARF)
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DIC
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Mutli-organ failure
SIRS may be infective (SIRS + source of infection = sepsis) or non
infective in origin. Non-infective causes include
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Trauma
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Burns
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Acute Pancreatitis
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Ischaemia
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Local
 Pancreatic necrosis (aka necrotic pancreatitis) +/- infection (infected necrosis)
 Pancreatic Abscess
 Pancreatic Pseudocyst
 Haemorrhage: due to bleeding from eroded vessels
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Small vessels  haemorrhagic pancreatitis with cullens/grey turners sign
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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)
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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
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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)
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Surgery involves necresectomy (excision of
necrotic tissue)
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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)
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Usually presents 2-4 weeks after initial attack of pancreatitis
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Management: Like any abscess it requires antibiotics + drainage:
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percutaneous (under CT guidance)
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Surgical drainage
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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:
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Pseudocyst symptomatic (can cause significant pain)
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Pseudocyst causing compression of surrounding structures e.g. CBD (obstructive jaundice),
duodenum (high SBO)
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Pseudocyst infected (i.e. has turned into an abscess)
In above three situations the pseudocyst should be drained:
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Percutaneously under radiological guidance (CT)
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Endoscopically by puncturing posterior wall of stomach and inserting a drain into the cyst
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Surgically via laparoscopic/open cystgastrostomy (cyst opened up into stomach allowing it to
drain
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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)
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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. Crohn’s, coeliac, short gut
syndrome)
 Drugs (e.g. Orlistat – weight loss pill)
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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
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Typical triad
 Chronic upper abdominal pain
 Malabsorption (evidenced by steatorrhoea and weight
loss)
 Calcification of pancreas (on AXR/CT)
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Investigations:
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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
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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
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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
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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
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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)
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Surgical intervention extremely rare
 Pancreatic transplants
Questions