Pancreatitis (acute + chronic) Flashcards
What is the epidemiology of acute pancreatitis?
150-420 cases/million and rising
80% have mild disease and recover without complications
- 30% mortality in severe cases
What is the aetiology of acute pancreatitis? (mnemonic)
IGETSMASHED:
- Idiopathic
- Gall stones* (blocking the bile duct and cause back pressure in the main pancreatic duct)
- Ethanol*
- Trauma
- Steroids
- Mumps (also hepatitis, and coxackie B), malignancy
- Autoimmune i.e. SLE
- Scorpion stings
- Hypothermia, hypercalcaemia, hyperparathyroidism, hyperlipidaemia (also uraemia, anorexia)
- ERCP/surgery
- Drugs e.g. thiazides, valproate, azathioprin (all rare)
What is the pathophysiology of acute pancreatitis?
Increase in intracellular calcium - activation of intracellular proteases (trypsin) - autolysis -necrosis - extravasation of enzymes - breakdown of:
- Surfactant (atelectasis, pleural effusion, pulmonary failure)
- BBB
- Cardiac cells
Also:
- Pseudocyst formation
- Systemic inflammatory response
- Haemorrhage
- Peritonitis
- Sepsis
How does acute pancreatitis present?
Pain:
- Upper abdominal pain starting in epigastrium
- May radiate to the back
- May be relieved upon sitting forward
- Widespread tenderness with guarding
- Usually decreases slowly over 72hrs
Nausea and vomiting
Reduced/absent bowel sounds as a result of paralytic ileus
Possible stigmata indicating underlying cause:
- Jaundice
- Alcoholic liver disease
Severe presentation:
- Periumbilical bruising (Cullen’s sign) and flank bruising (Grey-Turner’s sign) - both indicate severe necrotising pancreatitis
- Signs of shock (tachycardia, hypotension, oliguria)
- Left sided pleural effusion
How do you investigate acute pancreatitis?
Bloods:
- Serum amylase 3+ times normal is the traditional way of diagnosing acute pancreatitis
- Serum lipase levels are more sensitive and more specific, but may not rise until 8hrs after symptom onset
- CRP, FBC, U+E, glucose - all useful to measure prognosis
- LFTs - gallstones? Alcohol?
ABG for oxygenation and acid-base balance
Plain erect AXR (+/-CXR):
- To exclude SBO, perforation etc.
- May show calcification of pancreas
CT + contrast:
- Identify swelling, fluid collection and density change of pancreas
- CT severity index (CTSI) can be used to classify findings
- Useful to predict need for surgery
USS:
- Generally not as accurate but might be useful to detect presence of gallstones
- Endoscopic USS = more accurate
MRCP
- Magnetic resonance cholangiopancreatography = lots of detail
What is the Glasgow Prognostic Score for acute pancreatitis?
PANCREAS:
- pO2 <8kPa
- Age >55yrs
- Neutrophilia = WCC >15 x 10^9/L
- Calcium <2mmol/L
- Renal urea >16mmol/L
- Enzymes – LDH >600iu/L, AST >200iu/L
- Albumin >32g/L
- Sugar – glucose >10mmol/L
3+ score = severe, with a higher mortality
Other Scales include APACHE II (>8), Ranson (>3)
How do you manage mild acute pancreatitis?
- Admit to general ward
- NBM; NG tube if severe vomiting
- Possible oxygen
- IV fluids + catheter
- Pain relief - titrate from bottom of analgesic ladder
- Abx if specific infections
When pain and other symptoms have resolved and bloods normal:
- Start oral fluids then solids
- If gallstones cause - consider cholecystectomy during admission
How do you manage severe acute pancreatitis?
Admit to ITU/HDU
If significant necrosis:
- Abx, preferably following percutaneous aspiration of peritoneal fluid for culture
NG feed:
- Tube placed after ligament of Treitz (connecting duodenum to diaphragm) - if no ileus
- Reduces morbidity and mortality
Hyperbaric oxygen therapy:
- 100% O2 at 2.5 atmospheres
ERCP:
- Endoscopic retrograde cholangiopancreatography
- To treat co-existing cholangitis or biliary obstruction
Surgery:
- Indicated when there is an infection and necrosis
- Open or transgastric endoscopy
What are some complications of acute pancreatitis?
Necrosis:
- Rising CRP suggests necrosis and is confirmed by dynamic CT
- Can be infected too, quite common (3x mortality risk)
- If infected needs IV Abx and aggressive surgical debridement
Acute fluid collections:
- Common
- Most will resolve spontaneously and patient is stable, will not require treatment
Pancreatic abscess:
- Collection of pus adjacent to pancreas that persists
- Requires surgery
Acute pseduocyst:
- Contains pancreatic juice in a wall of fibrous or granulation tissue
- Arises 4/52 after episode
- Can rupture or haemorrhage
- Needs surgery
Systemically:
- Pulmonary oedema, pleural effusions, ARDS
- Hypovolaemia, shock
- DIC
- Renal dysfunction
- Metabolic disturbances
What is the epidemiology of chronic pancreatitis?
3/100,000 but rising in parallel in relation to other alcohol-related diseases
M>F
What is the aetiology of chronic pancreatitis?
Similar causes to acute pancreatitis
- IGETSMASHED
- Most cases caused by alcohol (c.6-12yr Hx of alcohol abuse)
Smoking
Genetic risk factors
- Including cystic fibrosis
Rarer causes:
Hereditary pancreatitis:
- Mutations in trypsinogen genes leading to increases in their autoactivation within the pancreas
- Presents at a younger age
- Endocrine and exocrine dysfunction
- High incidence of pancreatic carcinoma
Tropical pancreatitis:
- Gene mutations + possible malnourishment/dietary toxins
- Higher prevalence in Japan
Autoimmune pancreatitis:
- High levels of IgG autoantibodies (also possible ANA, RF etc)
- Higher prevalence in Japan
- Steroid and immunomodulator responsive
What is the pathophysiology of chronic pancreatitis?
Unclear, possible:
- Obstruction of/reduction in bicarbonate secretion leading to an activation of pancreatic enzymes, destruction of tissue with eventual necrosis and fibrosis
- Toxic effects of alcohol including excessive free radical formation
Process progresses to fibrosis over several years
Large duct vs small duct pancreatitis:
- Large = dilatation and dysfunction of the large tracts, easily seen on imaging; along with diffuse calcification; more common in men; steatorrhoea = common and replacement of pancreatic enzyme does not reduce pain; surgery usually required
- Small duct = more common in women; no calcification, imaging normal = difficult Dx; steatorrhoea rare; pain responsive to pancreatic enzymes
How does chronic pancreatitis present?
Pain:
- Epigastric, radiating to back
- Episodic or continuous
- Very severe - usually requiring opiates in acute (+/- chronic) flares
- Tenderness on palpation
Nausea + vomiting
Decreased appetite
Exocrine dysfunction:
- Malabsorption
- Weight loss
- Diarrhoea, steatorrhoea
- Protein deficiency
How do you investigate chronic pancreatitis?
Early Dx is difficult:
- No specific biomarkers, radiology may be normal
FBC, U+E, creatinine, LFT, Ca, amylase, Glu, HBa1c:
- Should all be done but results may be all be un informative
Secretin stimulation test:
- +ve if >60% exocrine function is damaged
- Can be combined with MRI
Imaging:
- CT - any calcification?
- Secretin-enhanced MRI or MRCP
- Endoscopic USS
Pancreatic biopsy:
- Usually chronic inflammation + irregularly placed fibrosis
- But is risky and so is rarely performed
How do you manage chronic pancreatitis?
Pain:
- Start at the bottom of the analgesic ladder
- Opiates are often required in the acute stages and possibly long term
Malabsorption:
- Give high dose pancreatic enzymes (proteases, lipases, amylase) PO e.g. pancreatin (as lots are degraded in the stomach) - reduces pain too, possibly through -ve feedback to pancreas
- 1 month trial then if successful, 6/12 follow up then stopped - 50% will have long term cessation of pain
- Also cholecystokinin (CCK) and octreotide can be used
- Vitamin ADEK supplementaion
ECRP:
- May reduce pain by dilating pancreatic ducts; also stenting is possible but may require regular changing
Surgery:
- If any complications e.g. pseduocyst, intractable pain
Counselling/screeening:
- CAGE + illicit drug intake
- Mental health
- Neoplastic disease
- Smoking cessation
- Diet advice - high protein, low carb
- Assess for opiate dependence
