Chronic pancreatitis

Causes and mechanism of development

The etiology of the disease is highly diverse. The development of inflammation can be triggered by gastroenterological issues, such as a prior history of acute pancreatitis or concomitant pathologies of the hepatobiliary system and upper gastrointestinal tract. Important roles are played by infectious diseases (both viral and bacterial) as well as genetic factors, including hereditary predisposition and various congenital enzymopathies. Among external factors, alimentary disorders (regular dietary indiscretions) and blunt abdominal trauma are of the greatest significance.

The pathogenetic mechanism of inflammation boils down to the fact that pancreatic enzymes are activated earlier than intended—not in the intestinal lumen, but directly inside the ductal system and parenchyma of the pancreas itself. This process triggers autoaggression, leading to pronounced tissue edema and significantly increasing the risk of the inflammation progressing to a destructive form—necrosis.

Clinical syndromes

The clinical presentation during an acute flare-up is complex and consists of several leading syndromes:

• Pain syndrome. This is the leading clinical feature. Pain attacks are usually triggered by dietary indiscretions (consumption of fatty, coarse, fried, sweet, or cold foods, as well as juices and fermented milk products). The pain is localized predominantly in the epigastric region, less frequently in isolation in the left or right hypochondrium. Radiation to the back, and the right or left halves of the chest (often taking a girdle-like character) is typical. The duration of the attack varies from 4–5 hours to several days. The patient attempts to assume a forced position to relieve the condition and reduce tension on the pancreatic capsule: sitting with the torso leaning forward, lying on the abdomen, or assuming the knee-chest position.
• Dyspeptic syndrome. Manifests as decreased appetite, dry mouth, and heartburn. Persistent nausea progresses to repeated vomiting which (unlike in gastric pathologies) does not bring the patient relief — this is a critical differential diagnostic sign. Intestinal symptoms include marked flatulence and stool instability (characterized by alternating constipation and diarrhea).
• Asthenoneurotic syndrome. Develops due to exhaustion of the nervous system against the background of constant chronic pain and intoxication. The patient exhibits emotional lability: tearfulness, irritability, aggressiveness, or hyperexcitability. In some cases, depressive episodes occur with general suppression and withdrawal.

Physical examination findings

Upon general inspection, pallor of the skin is notable, often acquiring a specific grayish or earthy tint. Hyperhidrosis (excessive skin moisture) is frequently recorded, indicating severe pain stress and bodily intoxication. The abdomen is usually soft, and peritoneal signs (symptoms of peritoneal irritation) are absent.

Physical examination reveals a number of specific signs of organ involvement:

• Superficial abdominal palpation: zones of pronounced cutaneous hyperesthesia (Zakharyin–Head zones) are determined, along with local protective tension of the abdominal muscles (muscle guarding) — predominantly the left rectus abdominis muscle at the level of the umbilicus.
• Deep palpation: marked local tenderness is noted at characteristic pancreatic points. Pain at Desjardins' point indicates involvement of the pancreatic head, tenderness at Mayo-Robson's point indicates involvement of its tail. Tenderness is also elicited at Kach's point and the Chauffeur choledochopancreatic zone.

Diagnostics and management

Diagnostic evaluation for suspected chronic pancreatitis is based on laboratory and instrumental data. The key laboratory indicator is moderate or pronounced hyperamylasemia (elevated activity of the enzyme amylase in blood and urine). The functional capacity of the organ is also assessed:

1. Exocrine insufficiency: confirmed by the presence of steatorrhea (fatty stools) and a decreased concentration of fecal pancreatic elastase.
2. Endocrine insufficiency: involvement of the islet apparatus of the gland may manifest as fasting hyperglycemia.

To visualize structural changes in the parenchyma, ultrasonography (US), computed tomography (CT), and, if necessary, diagnostic laparoscopy are used. Additionally, upper endoscopy (FEGDS), intragastric pH-metry, and ELISA for viral hepatitis markers may be prescribed.

Management tactics during a flare-up aim to provide functional rest for the damaged organ (maximal reduction of pancreatic and gastric secretion) and symptom relief. Non-pharmacologic treatment is based on the classical rule of "cold, hunger, and rest": the patient is prescribed strict bed rest, therapeutic fasting or a strict low-calorie diet, as well as local hypothermia (an ice pack to the abdomen). Following discharge from the hospital, dispensary follow-up, scheduled courses of anti-relapse therapy, and sanatorium-resort treatment in specialized facilities with mineral waters (Essentuki, Borjomi, Zheleznovodsk) are mandatory.

Class and exam questions

What else to study on this topic

• Topography of specific pancreatic points (Desjardins, Mayo-Robson, Kach) and the Chauffard zone.
• Differential diagnosis of pain syndrome with acute surgical abdominal conditions.
• The relationship between chronic pancreatitis and hepatobiliary system pathologies.
• The role of 24-hour intragastric pH-metry and FEGDS in the complex diagnosis of flare-ups.

Other topics in "Chapter 7. Digestive System Diseases"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.