Acute Pancreatitis

Presentation

Sudden-onset abdominal pain radiating to the back
Nausea
Vomiting
Anorexia
Abdominal pain
Tachycardia

History

Pain

  • Onset - sudden, which becomes continuous
  • Precipitating and alleviating factors - pain may worsen with movement and can be alleviated by adopting the foetal position
  • Location - epigastric region radiating to the back
  • Pain may be generalized with peritonism if peritonitis is present.
  • If caused by gallstones, the pain may be sudden and knife-like. Pain is often initiated by a large meal
  • If caused by alcohol, pain may less abrupt in onset and poorly localized

Assess risk factors:

  • Gallstones
  • Alcohol
  • Trauma
  • Idiopathic - previous MRCP, ERCP
  • Steroids
  • Autoimmune conditions - SLE, Sjogren's syndrome
  • Scorpion stings/spider bites
  • Metabolic disorders - Hyperlipidaemia/hypercalcaemia/hyperparathyroidism
  • ERCP
  • Mumps

Examination

Abdominal examination

  • Abdominal tenderness — can vary from mild tenderness in the epigastrium to generalized peritonitis, rebound tenderness, and guarding
  • Abdominal distension - caused by leakage of fluid into the retroperitoneum in an effort to dilute pancreatic enzymes, causing the abdominal contents to be pushed forward.

Signs indicating haemorrhagic pancreatitis

  • Cullen's sign: Peri-umbilical blue discoloration
  • Grey Turner's sign: Blue discolouration in the flanks bilaterally

Bedside investigations

Temperature - pyrexia
Heart rate - tachycardia due to shock
Blood pressure - hypotension due to shock
Oxygen saturation

Laboratory investigations

Lipase or amylase levels 3 times the upper limit of the normal range

  • Levels peak early, and decline over 3–4 day

FBC and differential - leukocytosis
AST/ALT - can indicate gallstone disease if >3 times the upper limit of normal
CRP - indicator of severity and progression of inflammation. Levels >200 units/L are associated with pancreatic necrosis
Haematocrit - an indicator of pancreatic necrosis if >44% on admission
ABG - hypoxaemia and disturbances in acid-base balance

Imaging

  • Abdominal X-ray - sentinel loop adjacent to the pancreas (isolated dilatation of a segment of gut), calcifications
  • Abdominal ultrasound if a biliary aetiology is suspected
  • CXR - may show pleural effusion, especially on the left hand side
  • MRCP - may detect stones, enlargement of the pancreas with irregular contour, pancreatic necrosis, or pseudocysts

Differential Diagnosis

  • Perforated peptic ulcer
  • Bowel obstruction
  • Ischaemic bowel
  • Ruptured abdominal aortic aneurysm
  • Myocardial infarction
  • Biliary colic, acute cholecystitis, or cholangitis
  • Viral hepatitis
  • Gastroenteritis

Clinical features (abdominal pain and vomiting) together with elevation of plasma concentrations of pancreatic enzymes are the cornerstones of diagnosis.

Management

Assess severity of pancreatitis using the Glasgow criteria. Scores range from 0 to 8. >2 indicates severe pancreatitis. <3 indicates severe pancreatitis is unlikely:

  • Age >55 years = 1 point
  • Serum albumin <32 g/L (3.2 g/dL) = 1 point
  • Arterial PO2 on room air <8 kPa (60 mmHg) = 1 point
  • Serum calcium <2 mmols/L (8 mg/dL) = 1 point
  • Blood glucose >10.0 mmols/L (180 mg/dL) = 1 point
  • Serum LDH >600 units/L = 1 point
  • Serum urea nitrogen >16.1 mmols/L (45 mg/dL) = 1 point
  • WBC count >15 x 10^9/L (15 x 10^3/microlitre) = 1 point.

Initial treatment

  • Resuscitation with intravenous fluid
  • Early nutritional support - Patient should be kept nil-by-mouth initially. Enteral feeding is preferable, but oral feeding can commence in cases of mild acute pancreatitis if there is no nausea, vomiting, or abdominal pain
  • Oxygen therapy (to maintain oxygenation of vital organs).
  • Pain relief
  • Anti-emetics e.g ondansetron
  • Calcium and magnesium replacement therapy if levels are low
  • Antibiotics for treatment of associated cholangitis or acute infections, such as chest infections or UTIs

Complications

Local:

  • Pancreatic necrosis with or without infection.
    • Inflammatory mediators released in acute pancreatitis induce thrombosis and haemorrhage, leading to pancreatic necrosis.
    • Infected pancreatic necrosis responsible for majority of deaths from acute pancreatitis.
  • Pseudocyst
    • Pseudocysts can be complicated by infection, rupture, or haemorrhage.
  • Pancreatic abscess
    • Collection of pus within the abdomen that sometimes contains gas. It follows an infection of peri-pancreatic fluid
  • Fistulae caused by disruption of the pancreatic ducts
  • Vascular complications
    • Pre-hepatic portal hypertension, usually involving the splenic vein and causing subsequent segmental portal hypertension.

Systemic:

  • Acute renal failure.
  • Multiple organ dysfunction.
  • Acute respiratory distress syndrome.
  • Disseminated intravascular coagulation.
  • Sepsis

Prognosis

  • Mild acute pancreatitis has a mortality rate of 1%.
  • Severe acute pancreatitis has a mortality rate of 10% with sterile pancreatic necrosis and 25% with infected pancreatic necrosis.
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