1. Mohammad mobasheri SpR General Surgery
Acute Pancreatitis
Mohammad mobasheri
SpR General Surgery

2. Pancreas: Functions Exocrine Endocrine
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

3. Pancreas Anatomy 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

4. Pancreas: Anatomy

5. Pancreas: Anatomy
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).

6. Pancreas: Vasculature

7. Pancreatitis Acute pancreatitis Chronic pancreatitis
Rapid onset inflammation of the pancreas
Chronic pancreatitis
Long-standing inflammation of the pancreas

8. Acute Pancreatitis: Aetiology
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])

9. Acute Pancreatitis: Pathogenesis
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)

10. Acute Pancreatitis: Clinical Features
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

11. Acute Pancreatitis: Differential Diagnosis
Differentials for upper abdominal pain include:
Gallstone disease and associated complications (E.g. Biliary colic/acute cholecystitis)
Peptic ulcer disease/perforation
Leaking/ruptured AAA

12. Acute Pancreatitis: Investigations
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

13. Acute Pancreatitis: Assessing Severity
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

14. Acute Pancreatitis: Scoring
Other scoring systemics include:
Glasgow (non-modified) and Ransons criteria which measure factors at admission and then after 48 hours.

15. Acute Pancreatitis: Management
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

16. Acute Pancreatitis: Complications
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

17. Acute Pancreatitis: Complications – SIRS overview
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)
Temp <36oC, >38oC
HR >90
RR >20
WCC >12
SIRS if 2 or more of the above
SIRS frequently complicated by failure of one or more organ systems
Acute lung injury (ARDS)
Acute kidney injury (ARF)
DIC
Mutli-organ failure
SIRS may be infective (SIRS + source of infection = sepsis) or non infective in origin. Non-infective causes include
Trauma
Burns
Acute Pancreatitis
Ischaemia

18. Acute Pancreatitis: Complications
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)

19. Acute Pancreatitis: Infected necrosis
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

20. Acute Pancreatitis: Infected necrosis
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)

21. Pancreatic Abscess
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

22. Pancreatic Pseudocyst
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

23. Acute Pancreatitis: Peri-pancreatic fluid collections

24. Chonic Pancreatitis
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)

25. Chronic Pancreatitis: Clinical Features
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)

26. Chronic Pancreatitis: Causes
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

27. Chronic Pancreatitis: Diagnosis
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

28. Secretin 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

29. Secretin stimulation Test
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

30. Faecal Elastase
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

31. Chronic Pancreatitis: Management
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

32. The End
Questions