eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology
Cholecystitis
Updated: Nov 18, 2008
Introduction
Background
Cholecystitis, which has long been considered an adult disease, is quickly gaining recognition in pediatric practice because of the significant documented increase in nonhemolytic cases over the last 20 years. Gallbladder disease is common throughout the adult population, affecting as many as 25 million Americans and resulting in 500,000-700,000 cholecystectomies per year.
Although gallbladder disease is much rarer in children, with 1.3 pediatric cases occurring per every 1000 adult cases, pediatric patients undergo 4% of all cholecystectomies. In addition, acalculous cholecystitis, uncommon in adults, is not that unusual in children with cholecystitis. Because of the increasing incidence of gallstones and the disproportionate need for surgery in the pediatric population, consider cholecystitis and other gallbladder diseases in the differential diagnosis in any pediatric patient with jaundice or abdominal pain in the right upper quadrant, particularly if the child has a history of hemolysis.
Pathophysiology
Cholecystitis is defined as inflammation of the gallbladder and is traditionally divided into acute and chronic subtypes. These subtypes are considered to be 2 separate disease states; however, evidence suggests that the 2 conditions are closely related, especially in the pediatric population. Most gallbladders that are removed for acute cholecystitis show evidence of chronic inflammation, supporting the concept that acute cholecystitis may actually be an exacerbation of chronic distension and tissue damage. Cholecystitis may also be considered calculous or acalculous, but the inflammatory process remains the same.
Chronic cholecystitis is most often related to gallstone disease but has been documented without gallstones. Its course may be insidious or involve several acute episodes of obstruction. The initiating factor is thought to be the supersaturation of bile, often with cholesterol crystals and/or calcium bilirubinate, which contributes to stone formation and inflammation. These processes lead to chronic obstruction, decreased contractile function, and biliary stasis, which contribute to further inflammation of the gallbladder wall. Biliary stasis also permits the increased growth of bacteria, usually Escherichia coli and enterococci, which may irritate the mucosa and increase inflammatory response. Chronic acalculous cholecystitis is less understood, but it may result from a functional deficiency of the gallbladder, which leads to spasm and an inability to appropriately empty its contents, causing chronic bile stasis.
Acute calculous cholecystitis results from a more sudden obstruction of the cystic duct by gallstones, which results in distension of the sac, edema, and bile stasis with bacterial overgrowth. These events lead to inflammation and a local release of lysolecithins, which further exacerbates the inflammatory process. In addition, edema of the wall and duct reinforces obstruction and may cause ischemia of the local tissue, releasing still more inflammatory mediators. Local lymph node hypertrophy and duct torsion or congenital anomalies may further complicate the obstructive process. As obstruction and inflammatory tissue damage progress, bacteria may proliferate. Bile cultures are positive in 75% of cases, usually with E coli, enterococci, or Klebsiella species. Bacterial infection most likely follows tissue damage, but after colonization, the severity of the disease can dramatically worsen. This cascade of events quickly leads pain and, possibly, a toxic appearance.
Acute acalculous cholecystitis develops in a similar manner but from different etiologic factors than acute calculous cholecystitis. Acute acalculous cholecystitis is most often associated with systemic illness, whether chronic or critical and acute. Increased mucous production, dehydration, and increased pigment load all are factors that increase cholesterol saturation and biliary stasis, whereas hyperalimentation, assisted ventilation, intravenous narcotics, ileus, and prolonged fasting contribute to cholestatic hypofunction.
These conditions allow the formation of biliary sludge and may lead to obstruction. The resulting inflammation and edema lead to compromised blood flow and bacterial infection, as in acute calculous cholecystitis; however, the compromised blood flow appears more central in acute acalculous cholecystitis because acute acalculous cholecystitis can occur in vasculitides (eg, Kawasaki disease, periarteritis nodosa) presumably because of direct vascular compromise.
Frequency
United States
The exact frequency of acute and chronic cholecystitis in children is not known. The overall incidence appears to have increased in the last 3 decades because of the high consumption of fatty foods by young children (ie, Western diet). In children with chronic hemolysis (eg, hemolytic anemias), the incidence of cholecystitis is much more prevalent than in the general population. Biliary sludge and/or gallstones are likely to form in 1 in 5 children with hemolytic anemia before their adolescent years.
Mortality/Morbidity
Most information related to morbidity and mortality in gallstone disease is related to the adult population, although some trends can be extracted and applied to the pediatric population. In general, the mortality rate of cholecystectomy in acute cholecystitis has dropped from 6.6% in 1930 to 1.8% in 1950 to nearly 0% in recent studies. In one study, the overall mortality rate in 42,000 patients receiving open cholecystectomy (OC) was 0.17%; the mortality rate in patients younger than 65 years was 0.03%. Children can be expected to do well, although comorbid conditions are common and may cause complications. Risk factors for morbidity and mortality in the pediatric population include associated conditions, such as cystic fibrosis (CF), obesity, hepatic disease, diabetes mellitus, sickle cell disease, and immunocompromise.
General complications, such as pulmonary, cardiac, thromboembolic, hepatic, and renal insufficiency, account for most deaths. Procedure-related complications mainly contribute to morbidity and occur with higher frequency in acute cholecystitis in which symptoms of gallstone disease have been present longer than 1 year. The most common procedure-related complications are wound infections, abscess, cholangitis or pancreatitis, ileus, hemorrhage, and bile duct complications.
Although OC is still commonly performed, the laparoscopic approach has become much more common and is now the new criterion standard. In 1994, approximately 80% of all cholecystectomies were performed laparoscopically. This approach reduces the morbidity associated with length of recovery. Patients report less pain, a shortened hospital stay, and a faster return to productivity. In addition, cosmetic results are improved. Lugo-Vicente found that the length of stay, days that pain medication is taken, and time before a regular diet can be resumed were all reduced by one half.1
Laparoscopic cholecystectomy (LC) is associated with risks as well. Major complications include bleeding, pancreatitis, leakage from the duct stump, and major bile duct injury. The risk of ductal injury increases from 0.1-0.2% in OC to 0.5-1% in LC; however, Holcomb et al reported no iatrogenic injuries with LC in their first 100 patients.2 They believe that with conscientious surgical care, morbidity related to the laparoscopic approach can be minimized.
Acalculous cholecystitis has its own statistics for mortality and morbidity. Mortality in the adult population has been reported to be as high as 10% and, in patients with critical illness, up to 50%. The mortality rate in patients with critical illness is most likely related to the close association with severe systemic illness. Surrounding illness and risk factors should be considered when predicting morbidity and mortality in children.
Other procedures used in cholecystitis carry risks. Choledochotomy and endoscopic papillotomy may be performed independently or in conjunction with cholecystectomy to aid in the treatment of choledocholithiasis. The overall mortality rate from choledochotomy (also applied to papillotomy) was determined to be 2.1%; however, by excluding patients with preexisting cholangitis or pancreatitis, the mortality rate decreased to 1.2%. The morbidity rate with these exclusions rests at 6-8%. The most serious complications resulting from these procedures have been hemorrhage, cholangitis, and pancreatitis.
Although controversy still surrounds the use of cholecystectomy versus medical management, the morbidity and mortality rates have been the same in patients receiving early surgery as in those in whom surgery was delayed more than 48 hours for stabilization of inflammation. However, because symptoms continued in 24% of patients in whom surgery was delayed, if surgery is the goal of treatment, no advantage to delaying surgery is noted. In general, the complication rates of cholecystitis and cholecystectomy are low in the absence of critical illness. The ability to tolerate general anesthesia and operative conditions for cholecystectomy has become the most significant indicator of outcome in cholecystitis. As a rule, children recover well once appropriate operative treatment has been established.
Race
Racial and genetic influences in the adolescent age group are similar to those of adults. African Americans (without hemolytic disease) and the African Masai are less prone to cholelithiasis, whereas Chilean women, Pimas, and whites are more predisposed to this disease. Two contributing diseases in particular have a genetic component and racial distribution. Hemolytic diseases, including sickle cell disease and hemoglobin C disease, occur almost exclusively in the black population, although thalassemia also has a Mediterranean distribution. CF, which occurs mainly in whites, may also contribute to the formation of biliary sludge and, possibly, acalculous cholecystitis.
Sex
No sex predilection is observed in children. In adult patients, the disease is more prevalent in females than in males.
Age
The incidence of cholecystitis in the pediatric population varies mostly according to age, with some racial and cultural influences. In a review of 693 cases of cholelithiasis, 10% of gallstones were found in children younger than 6 months, 21% were found in children aged 6 months to 10 years, and 69% were found in persons aged 11-21 years.3 In general, the infants who had cholelithiasis tended to be patients who were ill, were receiving hyperalimentation, and had prematurity, congenital anomalies, and necrotizing enterocolitis as compounding risk factors. Children aged 1-5 years most frequently had hemolysis as the underlying condition. Adolescent risk factors included menarche, pregnancy, and use of birth control pills; sex, race, and genetic influences also contributed to risk.
Cholelithiasis in infancy is most often related to acute and chronic illness and hyperalimentation. Risk factors include abdominal surgery, sepsis, bronchopulmonary dysplasia, hemolytic disease, malabsorption, necrotizing enterocolitis, and hepatobiliary disease. Other factors implicated include CF, polycythemia, phototherapy, and distal ileal resection. The immature hepatobiliary system of infants may predispose them to stone formation. Decreased hepatobiliary flow and immature bilirubin conjugation both contribute to stasis and sludge formation. Interestingly, as much as one half of infantile gallstones, especially those associated with hyperalimentation, may spontaneously resolve.
Risk factors in children include hepatobiliary disease, abdominal surgery, artificial heart valves, and malabsorption. Gallstones usually contain a mixture of calcium bilirubinate and cholesterol. Hemolysis and prolonged hyperalimentation are significant influences in this age group. In adolescents, the epidemiology more closely resembles that of adults. Major risk factors include pregnancy, hemolytic disease, obesity, abdominal surgery, hepatobiliary disease, hyperalimentation, and malabsorption. In addition, differences based on race, genetics, and sex become more evident. Adolescent girls are much more at risk than boys. The female-to-male ratio in white adults is 4:1; in adolescents, the ratio is estimated to be 14-22:1.
Pregnancy, birth control pills, dehydration, and obesity have contributory roles. Early menarche has been shown to significantly increase incidence, perhaps because of the lithogenic effect of estrogen on bile. Racial and genetic influences in the adolescent age group are similar to those in adults (see Race).
Clinical
History
Symptoms of cholelithiasis often precede those of cholecystitis, although patients may have acute cholecystitis on initial presentation. Cholelithiasis causes biliary colic. Patients may complain of intermittent abdominal pain of inconsistent severity in the right upper quadrant, with possible radiation to the scapular region of the back, or pain may be diffuse or localized to the epigastrium. Discomfort is more likely to be nonspecific in infants and younger children. Patients of this age group often present with irritability, jaundice, and acholic stools. The classic history of patients with gallstones is postprandial right upper quadrant pain associated with nausea and vomiting, but this is usually observed only in older children. Jaundice in pediatric cholelithiasis is much more frequent than in adults and can occur in the absence of gallstone obstruction of the common bile duct. Most likely, the stone causes inflammation of the ductal tissue, creating an edematous obstruction to bile flow.
- Patients with chronic cholecystitis usually present similarly to patients with biliary colic, with an intermittent and indolent history of pain. Therefore, differentiation must be made on the basis of findings from the physical examination and diagnostic tests.
- Acute cholecystitis pain resembles biliary colic but is usually more severe and constant, lasting for several days. The pain may begin as a vague discomfort; however, as inflammation spreads and affects the surrounding peritoneum, the pain localizes to the right upper quadrant. Patients often report a recent history of nausea, vomiting, anorexia, and a low-grade fever. Onset of symptoms usually occurs approximately 1 week prior to presentation, although the patient may report years of the less severe symptoms of biliary colic and chronic cholecystitis.
Physical
The physical examination in acute cholecystitis usually reveals right upper quadrant tenderness. The classic triad is right upper quadrant pain, fever, and leukocytosis. The patient may have abdominal guarding and a positive Murphy sign (ie, arrest of inspiration on deep palpation of the gallbladder in the right upper quadrant of the abdomen). Omental adherence to the inflamed gallbladder combined with distension may create a palpable mass between the 9th and 10th costal cartilages. The ductal system may become inflamed, causing cholangitis. In 50% of these cases, the examiner may find a Charcot triad.
- Charcot triad: This combination of right upper quadrant pain, fever, and jaundice is indicative of obstruction to the common bile duct and the presence of acute cholangitis. The Charcot triad is considered a medical emergency, and patients require immediate intervention.
- Biliary colic versus chronic cholecystitis: Performing a physical examination may be the only way to distinguish biliary colic from chronic cholecystitis. In chronic cholecystitis, the patient usually complains of tenderness to palpation in the right upper quadrant; however, the differentiation may be trivial given the high likelihood of chronic cholecystitis in the presence of recurring biliary colic.
Causes
Cholelithiasis is the most common cause of acute or chronic cholecystitis in adults and children. Three major types of gallstones may form, although most gallstones have components of more than one type. Cholesterol gallstones are radiolucent and are composed of cholesterol (>50%), calcium salts, and glycoproteins. They form within the gallbladder and migrate to the bile duct. Pigment gallstones are black, often radiopaque, and usually associated with hemolytic diseases. Radiopacity and color are related to an increased concentration of calcium bilirubinate, which interacts with mucin glycoproteins to form gallstones. These gallstones also form within the gallbladder and migrate to the ductal system. Brown gallstones, in contrast, form within the ductal system and are orange, soft, and greasy. They are composed of calcium salts of bilirubin, stearic acid, lecithin, and palmitic acid. These gallstones are more often associated with infection.
In rural Asia, infections with Opisthorchis sinensis or Ascaris lumbricoides are predisposing conditions. In the United States, these gallstones are more rare, although they have been found after cholecystectomy in which the bile was infected (most often by E coli) and in infants and children infected with Staphylococcus, Enterobacter, Citrobacter, and Salmonella species. In addition, chronic urinary tract infections may predispose individuals to the formation of these gallstones, and isolated gallstones associated with Ascaris have been recorded in the United States.
All gallstones require similar conditions to form. First, the bile must be supersaturated either by cholesterol or bilirubin. Second, chemical kinetics must favor nucleation of cholesterol. This occurs when cholesterol is no longer soluble in bile. Finally, stasis of the gallbladder allows cholesterol or calcium bilirubinate crystals to remain long enough to aggregate to form gallstones.
Many disease processes can precipitate or foster these events. Infection induces the deconjugation of bilirubin glucuronide, thereby increasing the concentration of unconjugated bilirubin in the bile. Hemolysis overwhelms the conjugation abilities of the liver, increasing the amount of unconjugated bilirubin in the bile. Hemolytic diseases include hereditary spherocytosis, sickle cell disease, thalassemia major, hemoglobin C disease, and possible uncontrolled glucose-6-phosphate dehydrogenase (G-6-PD) deficiency. Multiple blood transfusions also increase the pigment load, which predisposes the bile to the formation of biliary sludge.
Dehydration concentrates the bile, thereby increasing viscosity and stone formation. Cystic fibrosis (CF) is associated with increased mucous production and may cause a similar scenario. Gallstones remain the most common cause of cholecystitis. Although acalculous cases significantly contribute to incidence of cholecystitis, most acalculous cases are related to systemic illness and risk factors rather than epidemiologic determinants. Therefore, the discussion of epidemiology focuses on the development of cholelithiasis.
- Acalculous cholecystitis
- The aforementioned diseases may also contribute to the development of acalculous cholecystitis because the formation of gallstones is not necessary for the obstruction of the bile duct. In addition, acalculous cholecystitis has been heavily associated with local inflammation, endocarditis, vasculitides, and systemic infection. Implicated infections include those occurring in typhoid fever, scarlet fever, measles, and acquired immunodeficiency syndrome (AIDS) and those caused by mycoplasma, Streptococcus (groups A and B), and gram-negative organisms, such as Shigella and E coli.
- Acalculous cholecystitis may also occur postoperatively. Tsakayannis et al observed acute cholecystitis occurring after open-heart surgery in 4 of their patients, although it is more commonly observed in other nonbiliary surgeries and trauma.4 Shock, sepsis, hyperalimentation, prolonged fasting, intravenous narcotics, and multiple transfusions were the most common risk factors for the development of acute acalculous cholecystitis. The presence of 4 or more of these risk factors is highly predisposing.
- Other unusual causes
- Gallstones may also be caused by medications. Furosemide,5 octreotide, ceftriaxone,6,7 and cyclosporine8 have all been associated with gallstone disease. Ceftriaxone causes a reversible pseudolithiasis through several mechanisms. Ceftriaxone displaces bilirubin on albumin, thereby increasing the blood concentration of unconjugated bilirubin. Ceftriaxone is also secreted in bile, and calcium salts of ceftriaxone have been found in biliary sludge.
- Risk factors associated with gallstone formation include prolonged fasting and age older than 24 months. Lasix has also been implicated in gallbladder disease, but it usually is only a compounding factor in the presence of prematurity, sepsis, or small-bowel disease. Cyclosporine may be lithogenic, but it seems to require high drug levels and hepatotoxicity. Finally, ileal disease or resection has been correlated with cholelithiasis in adults and children, although the risks associated with resection seem to be highest after puberty. These patients have an increased cholesterol secretion and a lowered bile acid secretion, which leads to cholesterol supersaturation.
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Further Reading
Keywords
cholecystitis, acute cholecystitis, chronic cholecystitis, acalculous cholecystitis, calculous cholecystitis, gallbladder inflammation, gall bladder inflammation, gallstones, gall stones, gallbladder disease, Escherichia coli, Klebsiella, Kawasaki disease, periarteritis nodosa, chronic bile stasis, lymph node hypertrophy, biliary sludge, hemolytic anemia, cystic fibrosis, CF, obesity, hepatic disease, diabetes mellitus, sickle cell disease, immunocompromise, sickle cell disease, hemoglobin C disease, thalassemia, prematurity, congenital anomalies, necrotizing enterocolitis, abdominal surgery, sepsis, bronchopulmonary dysplasia, hemolytic disease, malabsorption, hepatobiliary disease, Charcot triad, glucose-6-phosphate dehydrogenase deficiency, G-6-PD deficiency, typhoid fever, scarlet fever, measles
