How will you proceed with management of pancreatitis?

Case History:

A 45 year old lady comes to your clinic with complaints of severe pain in epigastric region for 6 hours duration. The pain is sharp stabbing type with radiation to the back. There is slight relief of her pain on leaning forward. She also has vomited twice since her pain began. She gives you a history of incidental diagnosis of cholelithiasis two years back. On examination, she looks very distressed. Her pulse is 100bpm, BP is 100/60mmHg, RR is 24/min. There is significant tenderness in epigastric region with rigidity and guarding. What is your provisional diagnosis? How will you proceed with management of this case?  


Pancreatic inflammatory disease may be

    classified as (1) acute pancreatitis and (2) chronic pancreatitis.

Acute Pancreatitis

The pathologic spectrum of acute pancreatitis varies from edematous pancreatitis, which is usually a mild and self-limited disorder, to life threatening necrotizing pancreatitis.
The incidence of pancreatitis varies in different countries and depends on cause, e.g., alcohol, gallstones, metabolic factors, and drugs.

Causes of Ac. Pancreatitis

Common Causes
  • Gallstones (including microlithiasis): 30-60%
  • Alcohol (acute and chronic alcoholism): 15-30%
  • Hypertriglyceridemia
  • Endoscopic retrograde cholangiopancreatography (ERCP), especially after biliary manometry
  • Trauma (especially blunt abdominal trauma)
  • Postoperative (abdominal and nonabdominal operations)
  • Drugs (azathioprine, 6-mercaptopurine, sulfonamides, estrogens, tetracycline, valproic acid, anti-HIV medications)
  • Sphincter of Oddi dysfunction
Uncommon causes
  • Vascular causes and vasculitis (ischemic-hypoperfusion states after cardiac surgery)
  • Connective tissue disorders and thrombotic thrombocytopenic purpura (TTP)
  • Cancer of the pancreas
  • Hypercalcemia
  • Periampullary diverticulum
  • Pancreas divisum
  • Cystic fibrosis
  • Renal failure
Rare causes
  • Infections (mumps, coxsackievirus, cytomegalovirus, echovirus)
  • Autoimmune (e.g., Sjo¨gren’s syndrome)

Causes to consider in patients with recurrent bouts of acute pancreatitis without an obvious etiology
  • Occult disease of the biliary tree or pancreatic ducts, especially microlithiasis, sludge
  • Drugs
  • Hypertriglyceridemia
  • Pancreas divisum
  • Pancreatic cancer
  • Sphincter of Oddi dysfunction
  • Cystic fibrosis
  • Idiopathic

  • Acute pancreatitis occurs as a consequence of premature activation of zymogen granules,  releasing proteases which digest the pancreas and surrounding tissue 
  • The severity of acute pancreatitis is dependent upon the balance between activity of released proteolytic enzymes and antiproteolytic factors. The latter comprise an intracellular pancreatic trypsin inhibitor protein and circulating β2-macroglobulin, α1-antitrypsin and Cl-esterase inhibitors.
  • Usually mild and self-limiting with minimal organ involvement however in some cases, it is severe with local complications such as necrosis, pseudocyst or abscess, and systemic complications leading to multi-organ failure. 
  • The mortality in this severe group is approximately 30%. 

Clinical Features

  • upper abdominal pain and the pain usually begins in the epigastrium accompanied by nausea and vomiting.
  •  As inflammation spreads throughout the peritoneal cavity the pain becomes more intense.
  • There is radiation of the pain to the back with relief on bending forward because of involvement of the retro-peritoneum. 
  • Only upper abdominal tenderness in mild cases
  • In more severe disease, the patient may have a tachycardia, hypotension and be oliguric.
  • Abdominal examination may show widespread tenderness with guarding as well as reduced or absent bowel sounds.
  • Specific clinical signs that support a diagnosis of severe necrotizing pancreatitis include periumbilical (Cullen's sign) and flank bruising (Grey Turner's sign).

  • Serum amylase – within 24 hours, the rise is   > 3 times normal, the level falls down over next 3-5 days; persistent elevation is suggestive of pseudocyst formation
  • Serum lipase – also raises in early period but its level remains elevated for 7 – 15 days, so important in cases of late presentation
  • Other baseline investigations
  • a full blood count , CRP, urea and electrolytes, blood glucose, liver biochemistry, plasma calcium and arterial blood gases
  • These are documented at presentation and then repeated at 24 and 48 hours and provide a basis for assessing the severity of an attack and prognosis.

Radiological investigations
  • Erect chest X-ray- to exclude gastro-duodenal perforation which may also raise amylase
  • Abdominal USG- to exclude cholelithiasis and choledocholithiasis
  • Contrast-enhanced spiral CT scanning - essential in all except for mild attacks of pancreatitis. Carried out within 2-3 days of presentation, it allows the extent of pancreatic necrosis to be assessed.
  • MRI or MRCP – particularly useful in differentiating solid and fluid inflammatory masses

Assessment of severity

Factors during the first 48 hours that indicate severe pancreatitis and a poor prognosis (three or more factors present predict a severe episode)
  • Age  >55 yrs
  • WBC  > 15,000/cmm
  • Blood glucose >10mmol/l
  • Serum urea  >16mmol/l
  • Serum albumin <30g/dl
  • Serum aminotransferase >200U/l 
  • Serum calcium <2mmol/l
  • Serum LDH >600U/l
  • PaO2 <60mmHg
In addition, serial assessment of C-reactive protein (CRP) is a useful indicator of progress. A peak CRP > 210 mg/l in the first 4 days predicts severe acute pancreatitis with 80% accuracy.

Complications of Acute Pancreatitis

  • Necrosis
  • Sterile
  • Infected
  • Pancreatic fluid collections
  • Pancreatic abscess
  • Pancreatic pseudocyst
  • Pain
  • Rupture
  • Hemorrhage
  • Infection
  • Obstruction of gastrointestinal tract (stomach, duodenum, colon)
  • Pancreatic ascites
  • Disruption of main pancreatic duct
  • Leaking pseudocyst
  • Involvement of contiguous organs by necrotizing pancreatitis
  • Massive intraperitoneal hemorrhage
  • Thrombosis of blood vessels (splenic vein, portal vein)
  • Bowel infarction
  • Obstructive jaundice


  • Pleural effusion
  • Atelectasis
  • Mediastinal abscess
  • Pneumonitis
  • Adult respiratory distress syndrome
  • Hypotension
  • Hypovolemia
  • Sudden death
  • Nonspecific ST-T changes in electrocardiogram simulating myocardial infarction
  • Pericardial effusion
  • Disseminated intravascular coagulation
  • Gastrointestinal hemorrhage
  • Peptic ulcer disease
  • Erosive gastritis
  • Hemorrhagic pancreatic necrosis with erosion into major blood vessels
  • Portal vein thrombosis, variceal hemorrhage

  • Oliguria
  • Azotemia
  • Renal artery and/or renal vein thrombosis
  • Acute tubular necrosis
  • Hyperglycemia
  • Hypertriglyceridemia
  • Hypocalcemia
  • Encephalopathy
Central nervous system
  • Psychosis
  • Fat emboli
  • Fat necrosis
    • Early fluid losses in acute pancreatitis may be large, requiring well-maintained intravenous access as well as a central line and urinary catheter to monitor circulating volume and renal function.
    • Nasogastric suction: to prevent aspiration pneumonia
    • Baseline arterial blood gases determine the need for continuous oxygen administration.
    • Prophylactic antibiotics: cefuroxime or aztreonam
    • Analgesia requirements. Pethidine and tramadol are the drugs of choice. The morphine derivatives should be avoided because they can cause sphincter of Oddi contraction.
    • Feeding. In patients with a severe episode there is little likelihood of oral nutrition for a number of weeks. Total parenteral nutrition has been associated with a high risk of infection and has been replaced by enteral nutrition. This is administered via a nasojejunal tube, which is well tolerated and can maintain adequate nutritional input.
    • In a small proportion of patients, multiorgan failure will develop in the first few days after presentation reflecting the extent of pancreatic necrosis. Such patients will require positive-pressure ventilation and often renal support. 
    • These patients may also need surgical debridement of necrotic pancreatic tissue.
    • The mortality in this group is extremely high (in excess of 80%).

    Treatment of gallstone related pancreatitis
    • In patients with gallstone-related pancreatitis and associated cholangitis, endoscopic intervention with sphincterotomy and stone extraction is of proven benefit and is the treatment of choice. 
    • In the absence of cholangitis, sphincterotomy and stone extraction is only of proven benefit when the episode of pancreatitis is predicted as severe.
    • In less severe cases of gallstone-related pancreatitis intervention for gallstone can be deferred until full recovery is obtained (an approximate 6-week period).


    Mortality: 10-15%
    One-third occur within the first week, usually from multi-organ failure. After this time the majority of deaths result from sepsis, especially that complicating infected necrosis.