Chronic pancreatitis is a recurrent pancreatitis resulting from the progression of acute pancreatitis. It is a pathological process characterized by chronic progressive inflammation, destruction, and fibrosis of pancreatic acini and ducts, often accompanied by calcification, pseudocysts, and reduction or atrophy of islet cells. Clinically, it can be classified into two types: chronic relapsing pancreatitis and chronic persistent pancreatitis.

bubble_chart Etiology

In Western countries, long-term alcohol consumption is the primary disease cause, accounting for 68–82% of CP. Alcohol can lead to protein precipitation and calcification within the pancreas, resulting in chronic inflammation. It causes pain and impairs both the endocrine and exocrine functions of the pancreas. In China, biliary system diseases are the main disease cause of CP. The mechanism may involve biliary stones causing spasms and inflammation of the Vater ampulla, leading to mechanical obstruction and gall fel reflux into the pancreatic duct, thereby triggering pancreatic inflammatory reactions.

Currently, some also believe that severe acute pancreatitis, if improperly treated during its course, can result in pancreatic tissue necrosis, fibrosis, scarring, and ultimately CP. Other disease causes mentioned in the literature include anatomical variations of the cystic duct, duodenal obstruction, pancreatic trauma, pancreatic duct ascariasis, genetic factors, and certain medications.

bubble_chart Pathological Changes

The fundamental pathological changes involve continuous destruction of the pancreas and its replacement by fibrous tissue, leading to gradual hardening and thinning of the pancreas or irregular nodular sclerosis. There may be pseudocysts of varying sizes, dilation of the pancreatic duct, and calcification or stone formation in the pancreatic duct. Modern perspectives classify CP into two categories based on pathological manifestations: alcoholic and obstructive chronic pancreatitis.

Abdominal pain is the main symptom of this disease, which may be related to factors such as stimulation of nerves in pancreatic tissue by inflammatory products (e.g., kinins), inflammatory reactions of the abdominal membrane, and increased pressure in the pancreatic duct due to obstruction. Nausea and vomiting are also common symptoms, especially during the stage of attack, but abdominal pain does not significantly improve after vomiting. Steatorrhea is a late-stage [third stage] manifestation of CP, caused by severe impairment of pancreatic exocrine function; when islet cell function is damaged, symptoms of hyperglycemia may occur. Additionally, clinical manifestations such as weight loss, refractory ascites, and jaundice may also be present.

Recurrent or persistent abdominal pain, weight loss, diarrhea, or steatorrhea may occur, and late-stage [third stage] manifestations may include abdominal cystic masses, jaundice, and diabetes. The primary causes are the long-term presence of biliary tract diseases (e.g., stones, inflammation, or parasites).

It is more common in men over 40 years old, with a disease course lasting several years or over a decade.

Abdominal pain is more common in the early stages, often located in the upper middle abdomen or the left or right upper abdomen. It is related to changes in body position and is often triggered by factors such as fatigue, emotional stress, or dietary indiscretion. Pancreatic insufficiency manifests as exocrine dysfunction, indigestion, intolerance to fatty foods, malabsorption of fat-soluble vitamins, abdominal masses or ascites, and jaundice. Endocrine insufficiency may lead to latent diabetes or abnormal glucose tolerance.

1. Stool examination: Observe fat droplets and undigested muscle fibers in the stool.
2. Blood and urine amylase levels may only increase during acute episodes.
3. Blood glucose and glucose tolerance tests often show positive results.
4. Other methods to assess pancreatic exocrine function include quantitative analysis of fat intake and excretion, urinary para-aminobenzoic acid excretion test, and secretin-pancreozymin test.
5. Additionally, experimental studies reported in the literature indicate that phospholipase A2 (PLA2) is elevated in most CP specimens and is primarily distributed in immunoreactive acinar and ductal cells.
6. Elevated PLA2-II and PLA2-IV in acinar and ductal cells of chronic pancreatitis patients suggest pancreatic injury and are directly or indirectly related to pancreatic structural changes.
7. Imaging studies: For patients clinically suspected of CP, ultrasound screening is the first choice. If no positive findings are detected, CT may be considered. Patients with pancreatic duct dilation may undergo ERCP or magnetic resonance cholangiopancreatography (MRCP). MRCP is a non-invasive examination; calcifications in the pancreatic duct lumen in chronic pancreatitis appear as low-signal defects on MRCP. Intraoperative ultrasound and pancreatic ductography have definitive diagnostic value. Other methods include abdominal plain films, selective stirred pulse imaging, and cholangiography.

bubble_chart Treatment Measures

1. Indications

1. Recurrent intractable pain despite strict dietary control or medical treatment, combined with biliary tract disorders.
2. Palpable mass in the upper abdomen.
3. Severe digestive tract malabsorption accompanied by jaundice.
4. Pancreatic duct obstruction, suspicious lesions, pancreatic stone formation, pancreatic pseudocysts, etc.

2. Surgical Principles

Eliminate the disease cause, relieve obstruction, and remove lesions. Preoperative selective stirred pulse angiography, ERCP, or intraoperative cholangiopancreatography should be performed to determine the surgical approach. With thorough and adequate preparation, the surgical success rate can reach 80–100%.

3. Surgical Methods

Based on pancreatic pathological changes:

1. For biliary tract or Oddi's sphincter lesions, common bile duct incision for stone (or parasite) removal, Oddi's sphincteroplasty, or biliary-enteric anastomosis may be performed.
2. For pancreatic duct stones or strictures localized to the body or tail of the pancreas, distal pancreatectomy may be performed; if located in the pancreatic head, the pancreatic tail may be resected followed by Roux-Y pancreaticojejunostomy. For multiple strictures in the pancreatic duct, a longitudinal incision of the entire pancreatic duct may be performed for stone removal followed by pancreaticojejunostomy.
3. For pancreatic fibrosis, calcification, or loss of function, total pancreatectomy may be performed.
4. For intractable cases, visceral neurectomy or anhydrous alcohol blockade may be considered.