Etiology and mechanism of development
The development or exacerbation of the disease is triggered by a complex of causes. The most frequent etiological factor is alimentary-toxic. Typically, an acute attack occurs the day after a feast with alcohol abuse combined with fatty food. The second most important cause is pathologies of the biliary system, primarily cholelithiasis. In addition, inflammation can be caused by traumatic impact (abdominal trauma, iatrogenic injuries during surgery), penetration of a duodenal ulcer, the use of certain medications (nonsteroidal anti-inflammatory drugs, diuretics, antibiotics), as well as infections and systemic vasculitis.
The key link in the pathogenesis is the phenomenon of "self-digestion" of the gland. Under the influence of triggers, proteolytic enzymes (trypsin, elastase) are activated inside the organ tissue. If bile enters the pancreatic duct, it causes its obstruction, disrupts the outflow of secretion, and worsens the condition. The process is accompanied by the release of vasoactive mediators such as histamine and bradykinin. As a result, vascular permeability sharply increases, leading to the classical morphological triad in the organ:
- Massive edema.
- Phenomena of necrosis.
- Hemorrhages.
Clinical presentation
The leading clinical symptom is a specific pain syndrome. Patients experience constant pain in the epigastrium, umbilical region, or hypochondrium, which often acquires a girdle character radiating to the back. Body position critically affects well-being: in the supine position, the pain intensifies, so the patient assumes a forced posture (sitting leaning forward) that brings relief.
Digestive function is impaired due to the development of intestinal paresis (atony of the stomach and small intestine). This is accompanied by nausea, vomiting, and pronounced abdominal distension (meteorism).
Systemic reactions include fever, tachycardia, and a drop in blood pressure. The pathogenesis of the shock state in pancreatitis consists of hypovolemia and the toxic effect of kinins, which cause powerful vasodilation and secondarily reduce myocardial contractility.
Objective examination reveals weakened bowel sounds and signs of an "acute abdomen" (peritoneal irritation). Pronounced edema of the pancreatic head can compress the biliary tract, leading to obstructive jaundice. A specific skin symptom is subcutaneous nodules with erythema—a consequence of focal fat necrosis of the adipose tissue.
Diagnosis, prognosis, and treatment
To confirm the diagnosis, physicians use the classical diagnostic triad:
- Persistent pain syndrome of characteristic localization.
- Clinical signs of the inflammatory process.
- Laboratory confirmation of elevated blood amylase levels.
The prognosis depends on the severity of the process. The risk of death increases sharply in pancreatic necrosis, which can be complicated by acute kidney injury and refractory shock.
The main goal of conservative therapy is to provide the organ with "functional rest" and suppress its secretory activity.
- Regimen and diet: Strict fasting is prescribed.
- Decompression: Placement of a nasogastric tube for continuous aspiration. This prevents acidic gastric contents from entering the small intestine and stimulating pancreatic secretion.
- Infusion therapy: Active administration of plasma-substituting solutions to combat hypovolemia.
- Suppression of secretion: Octreotide (a synthetic somatostatin analog) and atropine-like drugs are used.
- Antibiotic therapy: Broad-spectrum agents (gentamicin, clindamycin) are prescribed for the prevention of infections.
- Pain relief: Narcotic analgesics are used. The use of morphine is strictly excluded, as it provokes spasm of the sphincter of Oddi and disrupts the outflow of secretion.
Briefly: answers to topical questions
What specific eponymic skin symptoms (e.g., Cullen, Grey Turner) are detected in destructive pancreatitis?
The sources mention the following specific symptoms, including skin manifestations detected in pancreatitis:
- Grey Turner sign
- Cullen sign
- Kacha sign — a zone of cutaneous hyperesthesia along the left hypochondrium.
Subcutaneous nodules with erythema are also noted as a consequence of fat necrosis of the adipose tissue.
What abdominal palpation symptoms (Mayo-Robson, Voskresensky) are characteristic of acute pancreatitis?
In acute pancreatitis, the sources indicate the following palpation and abdominal signs:
- Mayo-Robson sign — pronounced tenderness on palpation in the left costovertebral angle.
- Korte sign — tenderness and resistance of the abdominal wall in the epigastric region.
- In destructive forms — increasing tenderness and muscular defense in the upper half of the abdomen.
- The Shchetkin-Blumberg sign is also mentioned as a sign of peritoneal irritation.
Voskresensky sign in the cited sources is indicated for typical appendicitis, rather than as a sign of acute pancreatitis.
What laboratory markers, in addition to blood amylase, are used to diagnose acute pancreatitis?
To diagnose pancreatitis, in addition to blood amylase, the following laboratory markers are used:
- Blood lipase.
- Urinary amylase.
- Nonspecific inflammatory markers: neutrophilic leukocytosis, accelerated ESR.
To memorize the first-line therapy tactics, use the "Fasting and Tube" rule. Strict fasting and gastric content aspiration reliably shut down secretion stimulation, providing the gland with the necessary functional rest.
Class and exam questions
Why is the use of morphine for pain relief prohibited in acute pancreatitis?
Morphine causes spasm of the sphincter of Oddi. This mechanically impedes the outflow of pancreatic secretion into the intestine, significantly enhancing the process of self-digestion of the gland tissue.
What is the mechanism of shock development in severe pancreatitis?
Shock occurs due to a critical combination of hypovolemia and the release of vasoactive kinins. Kinins provoke systemic vasodilation and secondarily suppress myocardial contractility.
What causes obstructive jaundice in pancreatitis?
Jaundice develops due to massive edema of the pancreatic head. The enlarged tissue physically compresses the adjacent common bile duct.
What else to study on this topic
- Pathophysiology of the development of disseminated intravascular coagulation (DIC) syndrome and acute respiratory distress syndrome (ARDS) in pancreatic necrosis.
- Mechanisms of formation of local complications: abscesses, pseudocysts, and pancreatogenic ascites.
- Features of the clinical presentation and intensive care of acute kidney injury (AKI) against the background of pancreatic necrosis.
- Neurological complications: causes of psychosis in systemic pancreatic damage.
- Renal artery and vein thrombosis as a severe vascular complication of acute pancreatitis.
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