Pancreatitis

Function

Exocrine
Acinar cells make up the parenchyma.
Secrete digestive proteolytic enzymes such as trypsinogen, lipase and amylase in a high SID alkaline juice (1500mls/day).
Secreted into a tubular system which joins to form pancreatic duct.
Joins common bile duct to from ampulla of vata which opens into duodenum.
Endocrine
Islets of Langerhans
α – glucagon
ß – insulin
D – somatostatin
These hormones secreted into portal circulation

Pathogenesis

Inappropriate release and activation of pancreatic proteases pancreatic autodigestion and inflammation and SIRS.
80% mild and self limiting.
20% severe (SAP) with either organ dysfunction or local/regional complications.
50% with SAP develop necrosis.
25% with SAP will develop shock, pancreatic necrosis and MOF.

Complications

Local
Necrosis
Haemorrhage
Pseudocyst (walled-off pancreatic fluid)
Abscess
Regional
Fluid collections – abdominal, pleural (usually L)
Massive haemorrhage (retroperitoneal, peritoneal, GI tract)
Venous thrombosis - portal (portal hypertension) and systemic
Pseudoaneurysm – aorta, splenic, gastroduodenal)
Systemic
RS - ARDS, diaphragm splinting (abdo pain, fluid collections, oedema), effusions
AbdoCS - Surgical decompression if contributing to MOF
Shock -
plasma volume (capillary leak, albumin, vomiting, fever), SIRS
AKI, ALF (obstruction, cholangitis)

Causes

Most common causes are gallstones and alcohol (70%)
Idiopathic (20%)
Obstructive
Gallstones or biliary sludge
Thick pancreatic secretions – alcoholism, CF
CA
Parenchymal
Trauma
Autoimmune
α1 antitrypsin deficiency
Systemic
Hypoxia
Hypothermia
Viruses/drugs/toxins
Hypercalcaemia

Diagnosis

Clinical
Abdo pain/peritonitis
Vomiting
Discolouration flanks, umbilicus, ileoinguinal ligament (retroperitoneal haemorrhage).
Systemic organ involvement – ARF, ARDS, jaundice, confusion.

Investigations
Amylase >300u/ml (1000 in some texts) but can be normal.
Can also measure lipase (more sensitive and specific) and trysinogen.
Deranged LFTs, anaemia,
WBC, DIC.

Severity scoring
Severity scoring is currently poor.
Ransom and Glasgow scores not as good as APACHE.
Serum markers such as CRP, ILs, pro-calcitonin or trypsinogen inadequate.
CT scoring systems.
Glasgow score

  • WBC, glucose, LDH, AST, urea, Ca, albumin, PaO2
Imaging
US biliary tract in all
CT – diagnosis unsure, rule out other intra-abdominal pathology, detect and stage regional complications.
If diagnosis clear delay CT for 48-72 hours to allow necrosis to develop.

Nutrition

Traditional concerns that enteral feeding could exacerbate SAP by stimulating enzyme release but good evidence that EN better than PN in SAP
. Meta-analysis in 2008 showed reduced mortality and infectious complications in EN vs PN.
Gastric feeding often fails because of ileus in which case try jejunal feeding.
Parenteral if enteral not established in 5 days.
Some evidence that glutamine supplementation modifies the inflammatory response.
Probiotics increase mortality via bowel ischaemia.

ABX

Low incidence of infection if no necrosis.
50% necrosis in SAP. 40% of these become infected by week 3-4.
Infection thought to come from bowel translocation of gram –ve organisms.
Prophylactic ABX
infection of necrotic pancreas in some studies but may infection with resistant bacteria or fungi.
Therefore insufficient evidence to support prophylactic ABX, antifungals or selective gut decontamination with or without necrosis.
Must rigorously try to detect infection:
  • Blood cultures
  • FNA (radiologically guided) of pancreatic or peripancreatic collections
  • CT may show retroperitoneal gas
  • Temp >39 suggestive
Broad spectrum (carbapenems ideal as excellent pancreatic penetration) if infection suspected and very unwell.
The treatment for infected necrosis is surgical debridement, not just antibiotics.

Surgery

Relief of biliary obstruction.
ERCP +/- sphincterotomy in 1st 72h if obstructive jaundice or acute cholangitis.
Necrosis
Mortality very high if surgery in 1st 2 weeks.
Infection of necrosis develops by week 3-4.
Without debridement mortality is very high if infected.
By week 3-4 necrosis is also well demarcated allowing a single procedure with good pancreatic preservation
May need repeated laparotomies for washouts or a laparostomy.