Acute Pancreatitis

Question 1

Definition

Answer 1

Acute inflammatory process of the pancreas with varying involvement of local tissues or more remote organ systems.

Question 2

Levels of severity of pancreatitis?

Answer 2

Mild – absence of complications or organ dysfunction, usually uneventful recovery
Moderate – local complications and/or transient organ dysfunction which resolves within 48 hrs.
Severe – persistent organ dysfunction (failure to resolve in 48hrs) often leading to local complications: pancreatic, abscess and pseudocyst formation.

Question 3

Prevalence & patient demographics

Answer 3

30 per 100,000. 80% have mild pancreatitis.Gallstone pancreatitis- white women >60yrs
Alcoholic pancreatitis- Men

Question 4

Pathophysiology

Answer 4

Processes lead to intra-pancreatic zymogen activation & auto-immune digestion with destruction of acinar cells. Pancreatic ductal obstruction & hypersecretion contribute to the inititation of the inflammatory process. Intra-acinar activation of trypsinogen results in activation of proteases causing cell damage.

Question 5

Causes

Answer 5

I GET SMASHED

Question 6

Risk factors

Answer 6

Middle aged women
Gallstones
Alcohol
HIV/AIDS
Hypertriglyceridaemia
trauma
SLE
Sjogren’s

Question 7

Clinical presentation

Answer 7

Acute upper or generalised abdo pain
Hx of gallstones and –OH misuse.
Pain – severe pain and sudden onset, which become continuous in the epigastric region and may radiate to the back. Worsens with movement and alleviated assuming the foetal position.

Other: nausea, anorexia and vomiting.

Question 8

Signs

Answer 8

Abdo tenderness, distension, generalised peritonitis, rebound tenderness and guarding.
Leakage of fluid into the retroperitoneum in an effort to dilute pancreatic enzymes, causing abdo contents to be pushed forward.
Bluish discolouration around umbilicus (cullen’s)
Flank discolouration (Grey-Turner’s sign) sometimes associated with haemorrhagic pancreatitis
Tachycardia and hypotension if in shock.

Question 9

Differentials

Answer 9

Perforated peptic ulcer
Bowel obstruction
Ischaemic bowel
Ruptured AAA
Biliary colic, cholecystitis,cholangitis
MI
Viral hepatitis
Gastroenteritis

Question 10

Investigations

Answer 10

Lipase or amylase levels
Assessment of prognostic feature to identify those at risk of severe attack
CT, MRI or USS

Question 11

Management

Answer 11

Admit urgently
Initial: resuscitation with IV fluids, O2, pain relief, ATX, early nutritional support.
Manage in HDU or intensive therapy unit.
If caused by suspected or proven gallstones: endoscopic retrograde cholangiopancreatography to relieve obstruction within 72 hrs of onset of pain. Cholecystectomy during admission

Question 12

Prognosis

Answer 12

Mild – 1% mortality
Severe – 10% with sterile pancreatic necrosis, 25% with infected pancreatic necrosis.
Mortality is higher.

Question 13

Complications

Answer 13

Pancreatic necrosis ± infection. Becomes infectious when the sterility is broken i.e. when the bacterial gut flora enters. Inflammatory mediators induce thrombosis and haemorrhage. Infected pancreatic necrosis is responsible for 80% of deaths.
Pseudocyst – block pancreatic duct.
Pancreatic abscess – collection of pus within abdo that contains gas.
Fistulae – caused by disruption of pancreatic ducts. Can track from pancreatic duct to the abdo cavity (causing ascites), pleural cavity (causing pleural effusions) or pericardial cavity (pericardial effusions).
Vascular – pre-hepatic portal HTN, usually involving splenic vein.
Systemic: acute renal failure, multiple organ dysfunction, acute resp. distress, DIC, sepsis.