pancreatitisferencz baranyaysurgical resident

royal melbourne hospital

• 23 y/o M BIBA with epigastric pain is your next patient in the emergency department

• Pt driving along in passenger seat with his mum when began to feel

worsening pain in abdo

• ‘thought I was going to die’, told his mum to stop the car and call an

ambulance…

• After 5 mins of beginning to feel the pain, it hit a crescendo and

stayed until received IV morphine

• Felt pain as stabbing sensation, radiating retrosternally, with slight

nausea and associated shortness of breath

thoughts on diagnoses at this stage?

• No fevers or chills, no unusual bowel or urinary symptoms, no genital issues.

• Previous night he’d had 14-15 drinks, he is an overseas cricketer touring Australia

• Noted a history of GORD symptoms on occasion but is otherwise medically well

examination• o/e stable afebrile• small area of decreased A/E at lung bases• Abdo inspection NAD• ++ epigastric/RUQ tenderness on deep palpation• Murphy’s -ve• No flank tenderness/renal angle tenderness• BS +ve• PR not done and genitals not examined• No peripheral oedema, JVPNE

lab testing• Ix: lipase 230 (60 is upper limit N) • FBE N EUC N AST 87 GGT 227 • Erect CXR NAD• ECG – sinus 96 bpm, no ST/T w abnormalities• FWT: negative

• Pt given lignocaine/mylanta preparation, with PPI and reported no real benefit.

• Dx?

pancreas anatomyMade up of head, neck body and tailRetroperitonealHead lies in the ‘C’ of the duodenum

• also overlies IVC, L2 vertebra, medial aorta and superior mesenteric vessels

Behind the neck splenic veins joins superior mesenteric vein to form portal veinPancreatic duct closely related to common bile duct

Acute pancreatitis

Spectrum of:

mild severe

Mild inflammation of pancreas Extensive pancreatic necrosisMulti-organ failure

75% cases seen in ED 25% cases seen in ED

Mortality 20-30%Mortality <1%

pathophysiology

trypsinogenchymotrypsinogenProelastaseprocarboxypeptidase

active elastases autodigestion of pancreas

trypsin cascade

neutrophils

macrophages and lymphocytes

Acinar cell necrosisPseudocyst formationPossible abscess development with multi-organ failure

causesGallstones (35-40%)

ETOH (2nd most frequent cause)

Tumours•pancreas, ampulla, choledochoceleScorpion sting

Microbiological – infection

Autoimmnune (SLE, crohn’s)

Surgery/trauma (blunt trauma, cardiac surgery, ERCP)

Hyperlipidaemia (<11mmol, 3rd most freq cause), hypocalcemia, hypothermia

Emboli/ischemia

Drugs (carbamazepine, valproate, frusemide, opiates, estrogens, erythromycin, enalapril, rifampicin)

Cause is unknown in 15-20% of cases.

Clinical presentation acute pancreatitisHistory•Any severe acute pain in the abdomen or back should suggest acute pancreatitis. •The diagnosis is usually entertained when a patient presents with

– severe and constant abdominal pain (classically in epigastrium, radiating through to back)– nausea– emesis – fever– tachycardia

Examination•Fever (76%), sinus tachy (65%)•Dehydration•Upper abdo tenderness/epigastric tenderness (68%)

in severe pancreatitis…•Pulmonary signs (effusions, tachypnea secondary to diaphragmatic irritation)•Cullen’s sign (bluish/red discolouration periumbilical wall•Grey-turner’s sign (bluish/red discolouration of flanks)•peritonitis

Cullen’s + Grey Turner’s sign

laboratory testing• No gold standard for diagnosis

(apart from histopathological testing of the pancreas)

• Lipase and amylase– ↑ amylase

• fallopian tubes, ovaries, testes, adipose tissue, small bowel, lung, thyroid, skeletal muscle, and certain neoplasms.

– ↑ lipase• more specific, but still in small

intestine

• Rule out all valid differentials From Tintinalli’s Emergency Medicine 18th edition

differentials for upper abdo pain and tenderness

• perforated viscus, especially peptic ulcer– Erect CXR

• acute cholecystitis and biliary colic– LFTs, liver/biliary ultrasound, ERCP

• acute intestinal obstruction– Abdo XR

• mesenteric vascular occlusion– CT angiogram of intestinal vessels

• renal colic– Urinanalysis, hourly urine output,

serum creatinine, CT ureters

• myocardial infarction– ECG, troponin

• dissecting aortic aneurysm– CT angiogram

• connective tissue disorders with vasculitis– ESR

• Pneumonia– CXR

• diabetic ketoacidosis– serum glucose, ABG

Assessing severity

Ranson’s criteria

At admission•age in years > 55 years•white blood cell count > 16000 cells/mm3•blood glucose > 10 mmol/L (> 200 mg/dL)•serum AST > 250 IU/L•serum LDH > 350 IU/L

At 48 hours•Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL)•Hematocrit fall > 10%•Oxygen (hypoxemia PO2 < 60 mmHg)•BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration•Base deficit (negative base excess) > 4 mEq/L•Sequestration of fluids > 6 L

...many severity scores

Score 0 to 2 : 2% mortality Score 3 to 4 : 15% mortality Score 5 to 6 : 40% mortality Score 7 to 8 : 100% mortality

Radiology of acute pancreatitis

U/S useful for biliary pathology, 70-80% sensitive for pancreatitis

CT more useful for judging severity and regional effectsTry to wait >12 hours as early CT is usually unhelpful

treating acute pancreatitismild to moderate pancreatitis:• usually requires treatment with IV fluids and fasting. • clear liquid diet is frequently started on the third to sixth day • regular diet by the fifth to seventh day• The decision to reintroduce oral intake is usually based on the following criteria:

– a decrease in or resolution of abdominal pain; – the patient is hungry; and – Organ dysfunction, if present, has resolved– (don’t use lipase or amylase! Not indicative of resolution if normal levels)

Antibiotics – controversial, but currently recommended

unremitting fulminant pancreatitis:• usually requires inordinate amounts of fluid• close attention to complications

– cardiovascular collapse, respiratory insufficiency, and pancreatic infection, as well as possible surgical debridement or drainage.

Chronic pancreatitis

• Inflammatory disease of pancreas

• irreversible morphological changes in the pancreatic duct, acinar cell destruction and fibrosis

• Four clinical manifestations include abdominal pain, steatorrhoea, diabetes, and calcification of pancreas

Etiology of chronic pancreatitis

• Mostly due to ETOH in the Western World– Increases viscosity of pancreatic juice– Decreased local secretion of ‘lithostatin’ which usu

makes calcium salts soluable• Precipitation of calcium within gland

– Direct toxic effect on acinar cells– Cytokines recruit stellate cells, causing fibrosis

• Other unusual causes such as cystic fibrosis, severe malnutrition, hereditary or idiopathic

Investigations

• AXR• U/S• CT abdo• Secretin test

complications of chronic pancreatitis

• Narcotic addiction • Gastrointestinal bleeding• Impaired glucose tolerance • Jaundice• Gastroparesis • Cholangitis and/or biliary cirrhosis• Effusions with high amylase content • Pancreatic cancer

Medical treatment of chronic pancreatitis

• Enzyme replacement (lipase, protease, somatostatin)

• Often require insulin• Behaviour modification • Analgesia, often difficult

Surgical treatment• Pseudocyst drainage

Surgical treatment• Pseudocyst drainage

Surgical treatment• Whipple’s procedure

Chronic pancreatitisHead of pancreas Ca

Duodenal CaCholangiocarcinoma

Ampullary Ca

In summary

• In the patient with an acute abdomen, all possible differentials should be considered

• Diagnosis of acute pancreatitis should rule out other differentials, can be life threatening, and should be carefully managed

• Management of chronic pancreatitis requires consideration of medical and surgical therapies