Surgery and Chronic Pancreatitis

Chronic pancreatitis is characterized by irreversible and continued destruction of pancreatic acinar and duct cells. These cells are replaced by fibrous tissue and deposition of extracellular matrix.¹⁵ Chronic pancreatitis is a spectrum of a disease that ranges from mild, with occasional attacks; to moderate, with frequent attacks and more irreversible glandular changes; to severe, with disabling sequelae, such as intractable pain, diabetes, and pancreatic insufficiency (Fig. 1). Until recently, surgeons were referred only patients with severe chronic pancreatitis who were malnourished, often abusers of alcohol or narcotics, and who had end-stage glandular disease. Pancreatic function did not improve after surgery, and improvement of pain and diminished frequency and severity of attacks were the sole determinant of a successful surgical procedure. Much has changed in the past decade. Today, earlier diagnosis of chronic pancreatitis by endoscopy and axial imaging and intervention for mild symptoms may delay the progressive changes in secretory function and exocrine and endocrine malfunction.40, 42

Objective complications of chronic pancreatitis warrant surgery; however, at present, these account for a minority of the procedures used to treat chronic pancreatitis. In contrast, the most common indications for surgery are the subjective complaints of intractability, interference with lifestyle, and pain. These issues create a dilemma in the selection of procedures and patients for treatment, akin to deciding jury awards for pain and suffering. In both, it is difficult to reach a wise judgment or a happy outcome.

This article reviews the current surgical treatment of chronic pancreatitis. Lessons learned from a 25-year experience are included to caution surgeons that unbridled enthusiasm is best replaced by tempered judgments.

The prevalence of chronic pancreatitis (as with pancreatic cancer) is low, at 8 to 10 cases per 100,000 population. Long-term consumption of alcohol is the cause of the disease in 75% of patients worldwide. Primary duct obstruction as a cause of chronic pancreatitis is present in only 5% of patients.⁴² Depending on hospital population and surgical referral practice, the causes of pancreatitis vary widely. Idiopathic pancreatitis, a diagnosis of exclusion, is more common in tertiary centers than in urban hospitals and accounts for nearly 40% of the cases referred to the author's institution. The cause of chronic pancreatitis is important only in preventing ongoing glandular insult by removing an exogenous stimulus, if identified. The choice of surgical procedure is dependent on anatomic findings and not on the cause.

Complications of chronic pancreatitis occur secondary to healing and fibrosis of the pancreas or deposition of inspissated proteinaceous material in the pancreatic duct, leading to duct obstruction and calculi. Tissue samples from patients undergoing pancreatic resection for chronic pancreatitis demonstrate an increased tissue level of connective tissue growth factor (CTGF; 25-fold) and transforming growth factor (TGF-B₁; increased in 50% of chronic pancreatitis tissue samples). CTGF is a cysteine-rich peptide that belongs to a family of genes needed for the coordination of tissue repair.¹⁵ The overexpression of CTGF and TGF-B₁ in chronic pancreatitis suggests that these proteins may contribute to the enhanced extracellular matrix synthesis, leading to fibrin and collagen deposition in chronic pancreatitis.¹⁵ As a result of pancreatic fibrosis, complications that develop include:

• Bile duct obstruction (from cicatrix or a mass in the head of the pancreas)

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  Figure 4. An endoscopic retrograde cholangiopancreatography (ERCP) showing a dilated bile duct (BD) and pancreatic duct (PD).

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  Figure 5. The author's approach to all pancreatic surgery begins with an upper midline incision. The incision in this case was 3 inches long. (See also Color Plate 1, Fig. 1.)

• Duodenal obstruction (from extrinsic compression of a fibrosed pancreas)
• Gastric varices (from splenic vein entrapment and obstruction)
• Obstruction of the pancreatic duct (from calculi, fibrotic parenchymal strictures, or duct strictures)
• Pancreatic ascites (from a leaking pancreatic duct or pseudocyst)
• Pancreatic pseudocyst formation (discussed elsewhere in this issue)