Acute Pancreatitis

Overview
Objectives Anatomy review Physiology review Pathology Aetiology Clinical Features Investigations Management Prognosis and complications

Objectives
To revise anatomy and physiology of the pancreas To learn the commonest causes of pancreatitis To learn how to predict the severity of pancreatitis with examination and investigations To learn the importance of aggressive fluid management

Anatomy
Crura of the diaphragm

IVC

Left adrenal gland

Splenic artery
CBD Duodenum Main pancreatic duct (of Wirsung) Superior mesenteric artery Superior mesenteric vein Ampulla of Varter Coeliac plexus Left kidney

ccessory pancreatic duct

Anatomy

Splenic vein

Anatomy

Hepatic Right gastroepiploic

Left Gastric Coeliac axis

Lymphatics into superior mesenteric nodes.

Physiology
Exocrine 98% of volume of pancreas Acinar Cells Digestive enzymes Endocrine 2% of volume of pancreas Islets of Lnagerhans Insulin, glucagon, somatostatin, polypeptide

Exocrine Pancreas

Physiology
Enzymes secreted as inactive proenzymes Vagus and sympathetic nerves

Physiology
Enterokinase Trypsinogen Chymotrypsinogen Procarboxypolypeptidase Trypsin Chymotrypsin Carboxypolypeptidase

Polypeptides

Peptides

Pancreatitis
Pancreatic enzymes released and activated prematurely

Hyper-secretion and ductal obstruction or reflux of small bowel contents Vicious cycle
Leading to autodigestion of pancreas

Pathology
Proteolytic enzymes damage blood vessles
Ischaemia and haemorrhage.

Main enzymes trypsin, lipase and amylase 4 stages

Stage 1
Oedema Fluid shift Leading to hypovolaemia Compounded by vomiting

Stage 2
Autodigestion affects blood vessles Leading to haemorrhage Into retroperitoneal space Grey Turners and Cullens sign

Grey Turners sign

Cullens sign

Stage 3
Inflammation progresses to necrosis Affecting all or part of pancreas

Stage 4
Necrosis becomes infected Associated with high mortality

Pancreatitis
Acute
Acute onset abdo pain Raised enzymes in blood and urine Returns to anatomical and functional normality

Chronic
Irreversible abnormalities Fibrosis and pancreatic insufficiency

Aetiology
GET SMASHIN Gallstones and alcohol account for 80% of cases in the UK

Gallstones

Gallstones

Gallstones

Gallstones

Gallstones

Aetiology
G Gallstones/biliary tract disease 40% E Ethanol related 40% T Toxins and drugs (eg. Steroids, thiazides) S Surgery or trauma (inc ERCP) M Mumps/Metabolic A Autoimmune S Snake bite, scorpion stings H Hypothermia I - Idiopathic N Neoplasia

Classification
Oedematous (70%) simple or associated phlegmon Severe/necrotising (25%)
Sterile or infected Peripancreatic fluid collections (pseudocysts)

Haemorrhagic (5%)

History - Pain
Site Epigastrium, Either hypochondrium, diffuse (peritonitic) Onset Sudden/Gradual Character Constant Radiation to back Associated Symptoms Fever, Nausea, vomiting, Retching Time Course Exacerbating / Relieving factors Severity Severe

History
Typical presentation is an acute abdomen in a systemically unwell patient. Differential diagnosis
Acute cholecystitis Peritonitis Peptic ulcer disease High intestinal obstruction M.I

Clinical Features
Clinical features Systemic and local Local
Pain Grey-Turners Cullens signs

Clinical features
Systemic
Fever Shock retroperitoneal fluid loss, vasoactive sustances Respiratory faliure ARDS and effusions Renal faliure due to hypolulaemia

Investigations
Serum amylase - >1000u is diagnostic Other bloods
FBC (WCC), U&Es, LFTs(Alb, AST, LDH), Ca, Glucose

Urinary amylase ABG (PaO2) Erect CXR and AXR

Amylase
Most useful Can be normal in up to 30% If greater than 3x the upper limit of normal usually diagnostic Degree of elevation not correlated to severity If normal consider urinary amylase or serum lipase

Investigations
USS gallstones
Within first 24 h If confirmed urgent ERCP and spincterotomy

Contrast enhanced CT
Shows pancreas more clearly Can determine % necrosed

Scoring system
Glasgow Criteria
PO2 Age Neutrophils (WCC) Calcium Renal function (Urea) Enzymes (LDH) Albumin Sugar (blood glucose) < 8.0 > 55 yrs >15 <2.0 >16 > 600 <32 >10

Assessed within 48 hours of admission. 3 or more = Severe pancreatitis predicted Involve HDU/ITU

Management
Resuscitation
Oxygen IV fluid Analgesia

Oral/NG/NJ feeding
Need not be kept NBM NG if vomiting

Catherisation and fluid balance

Management
Consider sliding scale Consider antibiotics in sever cases
7 days Meropenem/Imipenem etc. follow local guidelines

Reduce gastric acid secreation

PPI

USS within 24 h ERCP if gallstones present

Consider definitive management

CT

CT

Prognosis
Majority settle with conservative management in a few days However severe pancreatitis may lead to multi organ failure Infected pancreatic necrosis may require
CT guided aspiration Necrosectomy Postoperative cavity irrigation

Complications
Pseudocyst
collection of fluid in lesser sac May become infected

Abscess
Does not contain necrotic tissue

Necrosis Haemorrhage splenic artery / vein Splenic vein thrombosis Systemic complications
ARDS SIRS / MODS

Summary
Inflammation of the pancreas caused by autodigestion Incidence increasing Main causes gallstones ethanol idiopathic Epigastric pain radiating to the back Pyrexia, tachycardia, hypotension Shock, renal failure, diabetes, ARDS, SIRS, MODS Severity score Imaging to identify cause Supportive management Surgical treatment for necrosis, haemorrhage, pseudocyst

Objectives revisited
To revise anatomy and physiology of the pancreas To learn the commonest causes of pancreatitis To learn how to predict the severity of pancreatitis with examination and investigations To learn the importance of aggressive fluid management