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Pancreatitis

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Acute pancreatitis

Updated by Charles Gomersall June 2008

Aetiology

4 main categories:

  • biliary tract disease,
  • excessive alcohol ingestion over many years,
  • idiopathic
  • miscellaneous

Biliary disease and alcohol account for 70% of cases although the relative incidence of these two causes varies according to country

Miscellaneous group include the following:

  • Metabolic: hyperlipidaemia, hyperparathyroidism, DKA, end-stage renal failure, pregnancy, post renal transplant
  • Mechanical disorders: post traumatic, post-operative, post ERCP, penetrating duodenal ulcer, duodenal obstruction
  • Infections: mumps, EBV, HIV, mycoplasma, hepatitis, Campylobacter, Legionella, ascariasis
  • Vascular: necrotizing vasculitis (SLE, TTP), atheroma, shock
  • Drugs: Definite: azathioprine, thiazides, frusemide, tetracyclines, oestrogens, sulphonamides, valproate, metronidazole, pentamidine, nitrofurantoin, erythromycin, methyldopa, cimetidine, ranitidine, salicylates, paracetamol
  • Toxins: scorpion venom, methyl alcohol, organophosphates
  • Associations: hypothermia, histocompatibility antigens, a 1-antitrypsin deficiency, hereditary

Pathophysiology

  • pancreas contains enzymes which have potential to cause extensive tissue damage
  • under normal circumstances several mechanisms protect the pancreas from damage by these enzymes
  • inappropriate activation of the enzyme systems leads to extensive damage by autodigestion
  • trypsin, chymotrypsin and elastase previously considered to be main destructive agents but there is increasing evidence that phospholipase A2 may be important. This is also implicated in extrapancreatic complications.
  • proposed mechanisms by which autodigestion begins:
    - reflux of duodenal contents (evidence in humans inconclusive)
    - reflux of bile into pancreatic duct when CBD blocked
    - activation of complement system and overstimulation of pancreatic secretions (eg from scorpion stings and hyperPTH)
  • coincidental release of vasoactive substances (eg bradykinin) into circulation may explain the increased vascular permeability, hypotension and organ dysfunction which accompany some episodes of acute pancreatitis
  • transition from acute oedematous pancreatitis to necrotizing pancreatitis may be due to pancreatic ischaemia

Clinical features

Symptoms

  • alcoholic pancreatitis usually < 40 years and M>F
  • biliary pancreatitis occurs in middle to later life, 3 times more common in women
  • onset of pain relatively quick, classically central, radiating to back and eased by sitting forward
  • nausea and vomiting in 90%

Signs

  • agitation and restlessness
  • generalized abdominal tenderness and guarding
  • marked rigidity may occur: may simulate ruptured viscus
  • fever common. Usually <39° . Hypothermia has been described
  • basal wheezes or pleural effusions in 10-20%
  • severe cases: shock, acute respiratory failure
  • erythematous nodules due to fat necrosis
  • retroperitoneal haemorrhage: brown discolouration in flanks (Grey Turner) or around umbilicus (Cullen)
  • abdominal usually distended due to associated ileus or presence of complications

Differential diagnosis

  • perforated viscus, cholecystitis, bowel obstruction, vascular occlusions, renal colic, MI, pneumonia, DKA

Severe pancreatitis

  • pancreatitis associated with organ failure and/or local complications
  • 2 phases:
    • first 2 weeks: SIRS due to release of proinflammatory mediators from pancreas. Most patients with significant organ dysfunction have pancreatic necrosis
    • 2-3 weeks after onset: deterioration in organ function usually due to secondary infection of pancreatic or peripancreatic necrosis

Investigations

Biochemistry

  • amylase 2-3 times normal usually diagnostic. Concentrations rise within 2-3 h and return to normal in 3-10 days. Quicker changes seen in mild oedematous forms and in severe necrotizing cases. In the latter enzyme concentrations decline rapidly because of extensive damage to pancreas. Amylase levels also rise in patients with perforated or infarcted bowel, in conditions which affect other organs which secrete amylase (salivary glands and ovaries). Absolute values of amylase are not prognostic
  • serum lipase parallels amylase but may remain higher for longer and is not increased by extra-pancreatic disorders
  • transient elevations in bilirubin in 10%. Concentrations return to normal within 4 days. May also be increases in alk phos and transaminases. Threefold or greater rise in serum ALT may be best indicator of biliary aetiology
  • hyperglycaemia in 25-75%
  • calcium falls in 25%. Usually due to concomitant hypoalbuminaemia. However ionized Ca may decrease, possibly due to intraperitoneal saponification. Occasionally requires treatment.
  • hypomagnesaemia may occur

Haematology

  • WCC typically raised to 15-20 with neutrophilia and L shift
  • ± haemoconcentration

Ultrasound

  • in general definition of gland more difficult than with CT and it is not seen in up to 40% of patients
  • particularly useful in demonstrating gallstones but only 60-70% sensitive
  • collections such as cysts and pseudocysts not reliably found

Contrast CT

  • imaging method of choice for delineating pancreas as well as demonstrating necrotizing pancreatitis and many of the complications of acute pancreatitis (eg pancreatic pseudocyst)
  • accuracy of contrast CT >90% when there is more than 30% glandular necrosis
  • presence of pancreatic necrosis good marker of prognosis. In one series necrosis associated with 82% morbidity and 23% mortality while those without necrosis had 6% morbidity and 0% mortality
  • however in early stages routine contrast CT is of little value in the critically ill
    • most patients with organ failure will have necrosis
    • risk of infected necrosis and local complications, other than ascites, is low
    • administration of contrast may increase risk of renal failure

ECG

  • widespread ST-T changes may simulate acute MI
  • arrhythmias have been observed in pericarditis associated with pancreatitis

Management

  • supportive treatment. Large volumes of fluid may need to be infused to replace large volumes sequestered in retroperitoneal and peritoneal spaces
  • traditionally patients have been kept nil by mouth but there is no evidence to support this practice and there is a move towards early enteric feeding, backed by preliminary data.
  • no effect on clinical course demonstrated from use of NG drainage but can provide symptomatic relief for patients with ileus or protracted nausea or vomiting
  • treatment to decrease pancreatic secretion: several drugs have been tried in humans (H2 blockers, glucagon, somatostatin or its analogue octreotide, calcitonin, fluorouracil) but all have been disappointing. However none of the trials have been big enough to exclude a therapeutic effect. Meta-analysis of trials of somatostatin showed significant improvement in mortality.
  • TPN. Only randomized study showed no benefit but patients were only moderately ill. Retrospective study of severely ill patients given TPN early suggested a significant decrease in morbidity and mortality. Two recent trials of TPN vs enteral feeding beyond ligament of Treitz showed that enteral feeding was associated with lower incidence of total and infectious complications.
  • peritoneal lavage. No good evidence to support this treatment
  • early endoscopic removal of bile duct stones. Recent meta-analysis suggests that early ERCP does not reduce morbidity or mortality in patients with predicted severe acute biliary pancreatitis in the absence of acute cholangitis, although it is recommended in some guidelines.
  • surgery is not indicated for sterile acute necrotizing pancreatitis
  • -prophylactic antibiotic treatment is controversial. A recent meta-analysis suggests that it does not reduce incidence of infected necrosis or mortality, but a different meta-analysis concluded that it reduces mortality but not the incidence of infected necrosis.

     

Complications

Systemic

CVS

  • hypotension & shock
  • pericardial effusion & tamponade

RS

  • hypoxia
  • atelectasis, pneumonia
  • acute lung injury
  • pleural effusion

Abdominal

  • acute renal failure
  • renal artery or vein thrombosis
  • GI bleeding
  • abdominal compartment syndrome

Metabolic

  • hypocalcaemia
  • hyperglycaemia
  • hyperlipidaemia
  • metabolic acidosis
  • hypomagnesaemia

Haematologic

  • vascular thrombosis
  • DIC

GI

  • bleeding

Local

  • phlegmon or swelling of pancreatitis seen on US or CT in 30-50%. Palpable in 15-20%
  • pancreatic abscesses usually develop after 5th week
  • pseudocysts usually occur after 2-3 weeks. May cause compression of adjacent structures. May resolve spontaneously
  • surrounding inflammation may lead to fistula formation, haemorrhage and infection. More common with severe necrotizing disease
  • ascites
  • involvement of contiguous organs with massive intraperitoneal bleeding, vascular thrombosis and infaction of bowel

Management of pancreatic infection

- fever > 39°C, tachycardia, WCC > 20 or evidence of clinical deterioration
– risk of infected necrosis increases with the amount of pancreatic glandular necrosis and time from onset of infection with a peak incidence at 3 weeks
- CT investigation of choice. Can demonstrate areas of necrosis, fluid collections or gas in pancreatic parenchyma or a fluid collection; all suggestive of possible pancreatic infection. CT guided aspiration and gram staining and culture of aspirate should be used to identify organisms responsible. Gm stain remains positive even in patients treated with systemic antibiotics. Aspiration indicated in patients with acute necrotizing pancreatitis who deteriorate or fail to improve despite aggressive supportive care
- broad spectrum antibiotics for patients with suspected pancreatic infection. Imipenem, ciprofloxacin and ofloxacin attain high levels in pancreatic tissue
- definitive treatment requires debridement of devitalized and infected tissue. Optimal method is controversial

Treatment of pancreatic fluid collections and pseudocysts

- asymptomatic pseudocysts of < 6 cm diameter can be followed with little risk of serious complication. Resolution may occur over several months
- symptomatic non-infected: can be drained percutaneously but many recur. Octreotide may decrease recurrence
- large or complicated: usually surgical drainage but catheter drainage can be used for pseudocyst infection

Prognosis

Overall mortality in severe acute pancreatitis ~30%. Mortality and morbidity closely linked to presence of necrosis.

APACHE II score probably best guide to severity

Modified Glasgow criteria

Within 48 hours:
- age > 55
- WCC > 15
- glucose >
- urea >
- LDH >
- albumin <
- calcium <
- PaO2 < 60 mmHg

 Ranson criteria

Criteria

Alcoholic

Gallstone

On admission to hospital

 

 

Age

>55

>70

WCC

>16

>18

Glucose (mmol/l)

>10

>10

LDH

>350

>400

AST

>250

>250

Within 48h of hospital admission

 

 

Decrease in Hct

>0.1

 

Increase in urea

>>0.9

 

Calcium

<2

 

PaO2 (mm Hg)

<60

 

Base deficit

>4

>5

Estimated fluid deficit

>6 L

>4 L

Both systems have a high false positive rate. 25-50% predicted to have severe pancreatitis and develop complications or die have an uncomplicated course

Most deaths occur in patients with > 4 criteria and mortality rises sharply in patients with > 6. In patients with score 3-5 mortality is 15%

Further reading

Werner J et al. Management of acute pancreatitis: from surgery to interventional intensive care. Gut, 2005; 54:426-36

Maher MM et al. Acute pancreatitis: the role of imaging and interventional radiology. Cardiovasc Intervent Radiol, 2004; 27:208-225

Segal D et al. Acute necrotizing pancreatitis: role of CT-guided percutaneous catheter drainage. Abdom Imaging, 2007; 32:351-361


© Charles Gomersall December 1999, June 2008

 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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