Pancreatitis (Acute and Chronic) Flashcards

1
Q

Define AP

A

Acute inflammatory process of the pancreas

  • Self-perpetuating pancreatic inflammation by enzyme-mediated auto-digestion
  • Oedema and fluid shifts → hypovolaemia
  • (Extracellular fluid trapped in gut, peritoneum, retroperitoneum)

Mild: (80%) minimal organ dysfunction and uneventful recovery Severe: (20%) associated with organ failure or local complication such as necrosis, abscess or pseudocyst → life threatening

Progression may be rapid from mild oedema to necrotizing

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2
Q

Causes AP

A

insult results in activation of pancreatic proenzymes within the duct/acini resulting in tissue damage and inflammation

Most common cause:

  • 80% alcohol
  • Gallstones
  • Other: drugs (steroid, azathioprine, thiazides, valproate) Trauma, infection, abdo surgery, ↑lipids, hyperparathyroidism, anatomical, idiopathic

Conventional Causes of Pancreatitis: GET SMASHED

  1. Gallstones
  2. Ethanol
  3. Trauma
  4. Steroids
  5. Mumps/HIV/Coxsackie
  6. Autoimmune
  7. Scorpion Venom
  8. Hypercalcaemia/hypercalcaemia/hypothermia
  9. ERCP
  10. Drugs (e.g. sodium valproate, steroids, thiazides and azathioprine)
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3
Q

Epidemiology AP

A

COMMON

UK Annual Incidence: 10/10,000

Peak age: 60 yrs

Most common cause in:

  • Males = alcohol
  • Females = gallstones
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4
Q

Symptoms AP

A
  • Severe epigastric pain
  • Radiating to the back
  • Relieved by sitting forward
  • Aggravated by movement
  • Associated with anorexia, nausea and vomiting

IMPORTANT: check whether the patient has a history of high alcohol intake or gallstones

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5
Q

Signs AP

A
  • Epigastric tenderness
  • Fever
  • Shock (includes tachycardia and tachypnoea)
  • Decreased bowel sounds (due to ileus)
  • In severe pancreatitis:
  • Cullen’s sign (periumbilical bruising)
  • Grey-Turner sign (flank bruising)
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6
Q

Investigations AP

A

Blood:

  • VERY HIGH SERUM AMYLASE (this does not correlate with severity)
  • High WCC
  • U&Es (to check for dehydration)
  • High glucose
  • High CRP
  • Low Calcium (saponification - calcium binds to digested lipids from the pancreas to form soap)
  • LFTs (may be deranged if gallstone pancreatitis or alcohol)
  • ABG (for hypoxia or metabolic acidosis)

USS: check for evidence of gallstones in biliary tree

Erect CXR: may be pleural effusion. Also to check for bowel perforation

AXR: exclude other causes of acute abdomen

CT Scan: if diagnosis is uncertain or if persisting organ failure

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7
Q

Management AP

A

Assessment of severity has TWO main scales:

  • Modified Glasgow Score (combined with CRP (> 210 mg/L)
  • APACHE-II Score

Medical Management:

  • Fluid and electrolyte resuscitation
  • Urinary catheter and NG tube if vomiting
  • Analgesia
  • Blood sugar control
  • HDU and ITU care
  • Prophylactic antibiotics may be useful in reducing mortality

ERCP and Sphincterotomy:

  • Used for gallstone pancreatitis, cholangitis, jaundice or dilated common bile duct
  • Ideally performed within 72 hours
  • All patients presenting with gallstone pancreatitis should undergo definitive management of gallstones during the same admission or within 2 weeks
  • Early detection and treatment of complications:
  • For example if there are persistent symptoms or > 30% pancreatic necrosis or signs of sepsis –> image guided fine needle aspiration for culture

Surgical:

  • Necrotising pancreatitis should be managed by specialists
  • Necresectomy (drainage and debridement of necrotic tissue) may be necessary
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8
Q

Complications AP

A

Local:

  • Pancreatic necrosis
  • Pseudocyst (peripancreatic fluid collection lasting > 4 weeks)
  • Abscess
  • Ascites
  • Pseudoaneurysm
  • Venous thrombosis

Systemic:

  • Multiorgan dysfunction
  • Sepsis
  • Renal failure
  • ARDS
  • DIC
  • Hypocalcaemia
  • Diabetes

Long-Term: could result in chronic pancreatitis

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9
Q

Prognosis AP

A

20% follow severe fulminating course with high mortality

Infected pancreatic necrosis has a 70% mortality

80% follow a milder course (but this still has 5% mortality)

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10
Q

Define CP

A

Chronic inflammatory disease of the pancreas characterised by irreversible parenchymal atrophy and fibrosis leading to impaired endocrine and exocrine function and recurrent abdominal pain.

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11
Q

Causes CP

A
  • ALCOHOL - 70%
  • Idiopathic - 20%
  • RARE: recurrent acute pancreatitis, ductal obstruction, pancreas divisum, hereditary pancreatitis, tropical pancreatitis, autoimmune pancreatitis, hyperparathyroidism

EXTRA information about pathology/pathogenesis:

Chronic pancreatitis is caused by disruption of normal pancreatic glandular architecture due to chronic inflammation and fibrosis, calcification, parenchymal atrophy, ductal dilation and cyst and stone formation

Pain is associated with raised intraductal pressures

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12
Q

Epidemiology CP

A

Annual UK incidence: 1/100,000

Prevalence: 3/100,000

Mean age: 40-50 yrs (in alcohol-associated disease)

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13
Q

Symptoms CP

A
  • Recurrent severe epigastric pain
  • Pain radiates to the back
  • Pain relieved by sitting forward
  • Pain can be aggravated by eating or drinking alcohol
  • Over many years –> weight loss, bloating and steatorrhoea
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14
Q

Signs CP

A
  • Epigastric tenderness
  • Signs of complications e.g. weight loss, malnutrition
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15
Q

Investigations CP

A

Bloods:

  • High glucose (endocrine dysfunction) - glucose tolerance test may be performed
  • Amylase and lipase usually normal
  • High Ig (especially IgG4 in autoimmune pancreatitis)

Ultrasound

ERCP or MRCP:

  • Early changes that can be seen include main duct dilatation and stumping of branches
  • Late manifestations include duct strictures with alternating dilatation

Abdominal X-Ray:

  • May show pancreatic calcification

CT Scan:

  • May show pancreatic calcification and pancreatic cysts

Tests of pancreatic exocrine function:

  • Faecal elastase (reflects pancreatic exocrine function)
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16
Q

Management CP

A

General:

  • Treatment is mainly symptomatic and supportive (e.g. dietary advice, stop smoking/drinking, treat diabetes, oral pancreatic enzyme replacement, analgesia)
  • Chronic pain management may need specialist input

Endoscopy Therapy:

  • Sphincterotomy
  • Stone extraction
  • Dilatation and stenting of strictures
  • Extracorporial shock-wave lithotripsy (ESWL) is sometimes used to fragment larger pancreatic stones before removal

Surgical:

  • May be indicated if medical management fails
  • Lateral pancreaticojejunal drainage (modified Puestow procedure)
  • Pancreatic resection (pancreaticoduodenectomy or Whipple’s procedure)
  • Limited resection of pancreatic head (Beger procedure)
  • Combining opening of the pancreatic duct and excavation of the pancreatic heaD
17
Q

Complications CP

A

Local:

  • Pseudocysts
  • Biliary duct stricture
  • Duodenal obstruction
  • Pancreatic ascites
  • Pancreatic carcinoma

Systemic:

  • Diabetes
  • Steatorrhoea
  • Chronic pain syndromes
  • Dependence on strong analgesics
18
Q

Prognosis CP

A

Difficult to predict

Surgery improves symptoms in 60-70% but results are often not sustained

Life expectancy may be reduced by 10-20 years