Causes and mechanisms of development
The development of the disease is caused by a combination of various adverse factors. Most often, the chronic process is a consequence of a prior acute inflammation, with persistence of similar pathogenic microflora in the biliary tract.
An important role is played by congenital anomalies of the biliary tract (e.g., Caroli syndrome or choledochal cyst), as well as allergic reactions. Key predispositions include:
- Family history of the disease.
- Dietary disorders (systematic overeating, poor-quality food).
- Physical inactivity and obesity.
- Concomitant pathologies of the gastroduodenal zone (stomach and duodenum).
The main link in pathogenesis lies in a persistent disturbance of bile production processes and its adequate passage.
Clinical presentation
The disease has a wave-like course, with periods of remission alternating with exacerbations.
During the exacerbation phase, which is often triggered by stress, excessive physical exertion, or dietary indiscretions (consumption of fatty, fried foods, sodas, canned goods), the child develops intense paroxysmal pain. The pain syndrome can last up to one hour. Concurrently, dyspeptic symptoms develop: heartburn, nausea, eructation, and vomiting.
In the fading phase, the character of the pain changes: it becomes dull, aching, and pressing, gradually turning into a constant sensation of heaviness in the right upper quadrant. Children exhibit a very pronounced asthenovegetative syndrome — rapid fatigability, emotional lability (lethargy alternating with irritability), headaches, and weakness.
On physical examination, skin pallor and periorbital shadows are noted, while body temperature may remain normal. Functional cardiac disorders are possible (blood pressure changes, arrhythmias, brady- or tachycardia). Specific gallbladder signs (Kerr, Murphy, Ortner, Mussy) have low diagnostic value in children, and hepatomegaly is rare.
Diagnostics and complications
Establishing a diagnosis requires a comprehensive approach, as symptoms necessitate differentiation from peptic ulcer disease, chronic gastroduodenitis, and chronic pancreatitis.
- Laboratory data: blood tests reveal markers of inflammation (pronounced leukocytosis, left shift, accelerated ESR, elevated CRP, prealbumin, haptoglobin) and signs of cholestasis syndrome (elevated bilirubin, GGT, alkaline phosphatase levels).
- Instrumental methods: Ultrasound and CT visualize gallbladder wall thickening (from 2–3 mm), presence of polyps, anomalies, or calculi. Dynamic hepatobiliary scintigraphy is used to assess functional state (uptake and excretion capacity).
- Surgical diagnostics: diagnostic laparoscopy is indicated in unclear situations.
Without adequate treatment, severe complications develop: local ones (hydrops, empyema), inflammation of adjacent structures (cholangitis, pericholecystitis), and purulent processes (subhepatic or subphrenic abscesses). Pericholecystitis is particularly dangerous because it disrupts bile outflow, provoking pancreatitis and promoting stone formation.
Principles of treatment and prognosis
Patient management tactics during an exacerbation are similar to the treatment of an acute process. Bed rest is prescribed, the duration of which depends on the severity of intoxication and fever.
The mainstay of therapy is diet: therapeutic nutrition tables No. 5 and 5a according to Pevzner. In the acute phase, daily caloric intake is reduced, and food is taken in fractional meals (5–6 times a day) in small portions. Diet No. 5 is maintained during the remission phase.
Medical treatment is based on drugs capable of accumulating in the biliary tract:
- Antibacterial agents whose concentration in bile exceeds that in serum.
- Nitrofuran derivatives (nifuratel, furazolidone) eliminated with bile.
- In the calculous form, litholytic therapy (ursodeoxycholic acid) is prescribed.
It is strictly forbidden to prescribe cholekinetics and choleretics in the presence of stones due to the high risk of their impaction and acute duct obstruction.
The prognosis of the disease is serious due to the prolonged recurrent course. The gallbladder becomes a chronic focus of infection. Disturbances in the enterohepatic circulation of bile lead to maldigestion. A vicious circle is formed: the pathologies sustain endogenous intoxication and create ideal conditions for further stone formation.
To remember the triggers of cholecystitis exacerbation, use the "Three S" rule: Stress, Sport (excessive physical exertion), Sustenance (fatty and fried foods).
Class and exam questions
Why are cholagogues contraindicated in calculous cholecystitis?
Cholekinetics and choleretics stimulate gallbladder contraction and bile production. This can lead to stone movement, its impaction in the duct, and the development of acute biliary obstruction.
Which form of cholecystitis is more common in children?
In pediatric practice, the non-calculous (acalculous) variant of the disease absolutely dominates, which usually begins with inflammation of the gallbladder neck.
What diseases require differential diagnosis?
Chronic cholecystitis must be differentiated from other gastrointestinal diseases with a prolonged wave-like course: chronic gastroduodenitis and chronic pancreatitis.
What else to study on this topic
- Mechanism of dyscholia and lithogenesis development
- Features of asthenovegetative syndrome in gastrointestinal pathologies in children
- Dynamic hepatobiliary scintigraphy: principles of the method
- Biochemical markers of cholestasis syndrome
- Pevzner diet: differences between tables No. 5 and No. 5a
Master the entire topic in the Pediatrics course
This is a summary. The course covers everything tested in classes and exams.
- Complete guidelines on "Chronic cholecystitis in children" and 3,738 more pages on the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 71 video lessons on the subject
Other topics in "Chapter 7. Digestive System Diseases"
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