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Year 3 > Acute pancreatitis (GI) > Flashcards

Acute pancreatitis (GI) Flashcards

1
Q

Define acute pancreatitis.

A

Autodigestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis

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2
Q

What are the causes of acute pancreatitis?

A

I GET SMASHED

  • Idiopathic (10-20%)
  • Gallstones (F>M)
  • Ethanol (most common worldwide, M>F)
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune disease e.g. collagen vascular diseases / Ascaris infection
  • Scorpion venom
  • Hypertriglyceridaemia, hypercalcaemia, hyperchylomicronaemia, hypothermia
  • ERCP
  • Drugs (mesalazine, azathioprine, sodium valproate, furosemide, bendroflumethiazide, pentamidine, didanosine)
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3
Q

What drugs can cause acute pancreatitis? (7)

A
  • mesalazine
  • azathioprine
  • sodium valproate
  • furosemide
  • bendroflumethiazide
  • pentamidine
  • didanosine
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4
Q

How can acute pancreatitis be classified? (3)

A
  • mild (80%) - no organ failure, no complications
  • moderate - no/transient (<48h) organ failure, possible complications
  • severe - persistent (>48h) organ failure, possible complications
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5
Q

Describe the pathophysiology of acute pancreatitis.

A
  • local inflammation of pancreas –> enzyme release –> autodigestion
  • abnormal intracellular calcium accumulation –> potentiate colocalization of zymogen and lysosome granules –> premature enzymatic activation
    • proteases and inflammatory response can cause leaks in blood vessels and rupture –> excess fluid and pancreatic swelling and bleeding
    • activated lipases can destroy peripancreatic fat
    • digestion and bleeding can liquify tissue –> liquefactive haemorrhagic necrosis
  • ethanol: direct toxic insult to acinar cell –> inflammation and membrane destruction
    • causes increase in ductal Pa secondary to protein deposition within the pancreatic duct favouring retrograde flow and intra-pancreatic enzymatic activation
  • sphincter of Oddi dysfunction
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6
Q

What is the most likely cause of chronic pancreatitis?

A

Alcohol

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7
Q

What are the clinical features of acute pancreatitis? (7)

A
  • epigastric pain radiating to the back - constant, severe, sudden, worse with movement
  • tender, distended abdomen with voluntary guarding
  • nausea and vomiting –> dehydration, electrolyte abnormalities, hypokalaemic metabolic acidosis
  • signs of shock - hypovolaemia (dry mucous membranes, decreased skin turgor, sweating), hypotension, tachycardia
  • anorexia
  • fever
  • signs of pleural effusion - ARDS, reduced air entry, stony dullness on percussion
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8
Q

What can nausea and vomiting in acute pancreatitis lead to? (3)

A
  • dehydration
  • electrolyte abnormalities
  • hypokalaemic metabolic alkalosis
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9
Q

What signs of shock are seen in acute pancreatitis? (3)

A
  • hypovolaemia - dry mucous membranes, decreased skin turgor, sweating
  • hypotension
  • tachycardia
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10
Q

What signs of pleural effusion might be seen in acute pancreatitis? (3)

A
  • ARDS
  • reduced air entry
  • stony dullness on percussion (more commonly on left)
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11
Q

What do we see in severe pancreatitis? (2)

A
  • Cullen’s sign: periumbilical bruising
  • Grey-Turner sign: bruising of flanks
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12
Q

What might you see on examination of acute pancreatitis? (5)

A
  • signs of hypovolaemia - oliguria, hypotension, dry mucous membranes, decreased skin turgor, sweating, tachycardia, tachypnoea
  • signs of pleural effusion - ARDS, reduced air entry, stony dullness on percussion
  • jaundice (severe gallstone pancreatitis)
  • signs of hypercalcaemia (Chvostek’s or Trousseau’s sign)
  • ecchymotic bruising and discolouration (Cullen’s, Grey Turner’s, Fox’s sign) if haemorrhagic
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13
Q

What are the risk factors for acute pancreatitis?

A

GET SMASHED

  • gallstones
  • alcohol (F 50-70 or young/middle-aged men)
  • trauma
  • steroids
  • mumps
  • autoimmune conditions (SLE, Sjogren’s)
  • scorpion venom
  • hypertriglyceridaemia and hypercalcaemia
  • ERCP (use of contrast –> pancreatic inflammation)
  • drugs
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14
Q

What are the main factors indicating severe pancreatitis? (6)

A
  • age >55
  • hypocalcaemia (<2mmol/L)
  • hyperglycaemia (>10mmol)
  • hypoxia (<7.9kPa)
  • neutrophilia
  • elevated LDH and AST
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15
Q

What criteria is used to determine severity of pancreatitis?

A

Glasgow score: 3+ means severe pancreatitis

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16
Q

What is the Glasgow score for severity of pancreatitis?

A

PANCREAS: 3+ –> severe pancreatitis

  • PaO2 <7.9kPa
  • Age >55
  • Neutrophilia
  • Calcium <2mmol/L
  • Renal function: urea >16mmol/L
  • Enzymes –> elevated LDH & AST
  • Albumin <32g/L
  • Sugar: glucose >10mmol
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17
Q

What are the first-line investigations for acute pancreatitis? (4)

A
  • serum lipase or amylase
  • FBC with differential
  • CRP
  • urea/creatinine
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18
Q

What are serum amylase/lipase like in acute pancreatitis?

A

Serum lipase or amylase >3x upper limit of normal (in 1000s) - confirms the diagnosis of acute pancreatitis in a patient with acute upper abdominal pain

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19
Q

Which out of serum amylase and lipase is more useful?

A

Serum lipase:

  • lipase levels remain elevated for longer (14d vs 5d for amylase) –> better for diagnosis in delayed presentation
  • more sensitive and specific than amylase
20
Q

What does FBC show in acute pancreatitis? (3)

A
  • leukocytosis with left shift (more immature neutrophils)
  • neutrophilia
  • elevated haematocrit is predictor of poor prognosis due to increased risk of necrotising pancreatitis
21
Q

What does urea/creatinine show in acute pancreatitis?

A

Elevated - suggests dehydration or hypovolaemia

22
Q

What might LFTs show in acute pancreatitis?

A

Elevated LFTs suggest gallstones are the cause

23
Q

What might serum calcium show in acute pancreatitis?

A
  • high
  • causative
  • whilst hypercalcaemia can cause pancreatitis, hypocalcaemia is an indicator of pancreatitis severity
24
Q

What imaging is done in acute pancreatitis and why? (4)

A
  • early abdominal US to assess aetiology as this affects management
  • contrast-enhanced CT (CECT) - investigating differentials, may also show pseudocyst, inflammation, necrosis
  • erect CXR - rule out perforation, may show pleural effusion or elevated hemidiaphragm, atelectasis
  • ERCP/MRCP - if gallstones suspected
25
Q

When can acute pancreatitis be diagnosed without imaging?

A

Characteristic pain + serum amylase/lipase 3x upper limit of normal

26
Q

What could a CRP >200 units/L mean in acute pancreatitis?

A

High risk of developing pancreatic necrosis

27
Q

What investigation can indicate severity in acute pancreatitis?

A

Hypocalcaemia on bloods

28
Q

Describe the diagnostic criteria for acute pancreatitis.

A

2/3 of the following must be met for diagnosis:

  • clinical (upper abdominal pain)
  • laboratory (serum lipase or amylase >3x upper limit of normal)
  • imaging (CT, MRI, US) criteria
29
Q

What are signs of systemic inflammatory response syndrome (SIRS) in acute pancreatitis?

A

At least 2 of:

  • heart rate >90bpm
  • respiratory rate >20/min (or PaCO2<32mmHg)
  • temperature >38C or <36C
  • WCC >12x10^9/L or <4x10^9/L
30
Q

What are some differential diagnoses for acute pancreatitis? (12)

A
  • peptic ulcer disease
  • perforated viscus (acute abdomen, peritoneal signs, elevated lipase)
  • oesophageal spasm (dysphagia, odynophagia, weight loss)
  • intestinal obstruction
  • AAA
  • choledocholithiasis
  • cholecystitis
  • cholangitis
  • viral gastroenteritis
  • hepatitis (jaundice, RUQ pain, anorexia, malaise)
  • mesenteric ischaemia (Hx AF and risk factors for PVD)
  • MI
31
Q

What are the key aspects of acute pancreatitis management? (3+1)

A
  • fluid resuscitation
  • analgesia with IV opioids
  • nutrition
  • (consider antiemetic)
32
Q

How do we fluid resuscitate patients with acute pancreatitis?

A
  • aggressive early hydration with crystalloids
  • aim for urine output of >0.5mls/kg/hr
  • may help reduce pain by reducing lactic acidosis
33
Q

What type of nutrition do we give to patients with acute pancreatitis?

A
  • NBM not routinely unless there is a clear reason
  • enteral > parenteral
  • enteral nutrition normally offered for anyone with moderately-severe or severe acute pancreatitis within 72h of presentation
  • parenteral nutrition is used only when EN has failed or is CI
34
Q

What is the role of Abx in acute pancreatitis?

A
  • there is none
  • empirical IV Abx only if infection confirmed or strongly suspected - infected pancreatic necrosis
35
Q

How can we treat the underlying causes in acute pancreatitis? (6)

A
  • calcium and magnesium replacement therapy
  • ERCP: for gallstone pancreatitis with cholangitis
  • cholecystectomy: for gallstone pancreatitis without cholangitis
  • endoscopic biliary sphincterotomy: if unfit for surgery
  • vitamin replacement for alcohol-related pancreatitis: thiamine, folic acid and vitamin B
  • admit to ICU
36
Q

How do we manage patients with acute pancreatitis due to gallstones?

A

ERCP for gallstone pancreatitis with cholangitis

Cholecystectomy if no cholangitis

37
Q

When is debridement done for acute pancreatitis?

A

Patients who fail to settle with necrosis and have worsening organ dysfunction

38
Q

What do we do in all patients with infected necrosis in acute pancreatitis?

A

Radiological drainage or surgical necrosectomy

39
Q

What are some complications of acute pancreatitis? (11)

A
  • acute renal failure
  • sepsis
  • ARDS/acute lung injury (bilateral pulmonary infiltrates and hypoxaemia)
  • pseudocysts - occur 4 weeks after, persistently raised amylase
  • pancreatic necrosis
  • pancreatic abscess
  • abdominal compartment syndrome
  • enteric fistulas
  • pancreatic ascites/pleural effusion
  • haemorrhage
  • chronic pancreatitis
40
Q

What are pancreatic pseudocysts (complication of acute pancreatitis)?

A
  • fibrous tissue surrounds liquefactive necrotic tissue and fills with pancreatic juice
  • leads to abdominal pain, anorexia and palpable mass
  • infected –> pancreatic abscess (fever, WCC)
  • percutaneously drained with endoscopic ultrasound, can be visualised with CT
41
Q

Describe the prognosis of acute pancreatitis.

A
  • majority of patients improve in 3-7 days of conservative management
  • mortality increases in severe pancreatitis
42
Q

What causes chronic pancreatitis?

A

Alcohol (mostly)

43
Q

When is pain worse in chronic pancreatitis?

A

15-30 mins after meals

44
Q

What are the symptoms of chronic pancreatitis? (3)

A
  • steatorrhoea (foul-smelling, greasy stool) due to pancreatic insufficiency
  • pain
  • weight loss
45
Q

What other condition develops in most patients with chronic pancreatitis?

A
  • DM (>20 years after Sx begin) due to loss of endocrine function
  • patients with chronic pancreatitis require HbA1c monitoring every 6 months
46
Q

What are the main investigations for chronic pancreatitis? (3)

A
  • CT pancreas with IV contrast most sensitive at detecting pancreatic calcification (CECT)
  • faecal elastase (low) can also be used to assess exocrine function
  • normal amylase
47
Q

How do we manage chronic pancreatitis? (2 + 5)

A

Pancreatic enzyme supplements and analgesia

  • coeliac plexus block (pain)
  • endoscopic/surgical pseudocyst decompression
  • pancreatic ductal compression
  • extracorporeal shock wave lithotripsy (stones)
  • distal pancreatectomy

Year 3 (148 decks)

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