A gallbladder septum may result from a congenital mucosal diaphragm, adenomyomatosis, or a combination of the two. Although a gallbladder septum may be an incidental finding during an otherwise normal examination, stasis of bile in the distal segment predisposes to calculus formation.¹² A single septum appears as a thin linear echo separating the gallbladder into compartments. Simple junctional folds may mimic a septum.

The multiseptated gallbladder is one of the rarest congenital gallbladder malformations. This anomaly may be associated with biliary colic or cholelithiasis or may be entirely asymptomatic without associated cholelithiasis.¹³

A multiseptated gallbladder can have variable sonographic appearances. There can be fine linear septa or a honeycomb pattern of clustered septations resulting in multiple communicating cyst-like compartments. Septa may cluster in the neck and body region of the gallbladder. Differential diagnoses include desquamated gallbladder mucosa (an unusual finding in acute cholecystitis) and hyperplastic cholecystoses (such as polypoid cholesterolosis or adenomyomatosis). Desquamated gallbladder mucosa appears as multiple, haphazardly arranged, linear, nonshadowing densities within the gallbladder lumen, which does not consistently arise from the gallbladder wall because they do in multiseptated gallbladder. Polypoid cholesterolosis may more often resemble multiseptated gallbladder, although the nonshadowing polypoid densities are more bulbous, and there is no bridging of the lumen by septa as in the multiseptated gallbladder. In adenomyomatosis, Rokitansky-Aschoff sinuses could be confused with the honeycomb pattern, but cyst-like Rokitansky-Aschoff sinuses are smaller and are actually within the thickened gallbladder wall; there is no bridging of the lumen itself to form cyst-like compartments.^13,14

Childhood jaundice is usual. Although interposition of the gallbladder (the absence of the CHD and cystic duct) is a rare anomaly, its diagnosis is important because it is surgically correctable. Normally, the right and left main hepatic ducts join to form the CHD, which are entered by the cystic duct to form the CBD. In interposition, the main hepatic ducts drain, separately or together, directly into the gallbladder. The gallbladder then drains directly into the CBD, although variants can also occur (Fig. 8-15). The cause of interposition of the gallbladder is unknown.¹¹

A patient with interposition of the gallbladder presents with jaundice, which may be intermittent, abdominal
pain, and sometimes an enlarged gallbladder. Sonography may show enlarged intrahepatic ducts with a normal CBD, mimicking Caroli disease, or the ducts may appear to enter a cystic mass in the porta hepatis, mimicking a choledochal cyst. Although sonography may be difficult to interpret in this situation, it is still a good initial step, indicating that jaundice is caused by an anatomic biliary abnormality.¹¹

Biliary atresia is the most common type of obstructive biliary disease in infants and young children.¹⁵ Destruction of the extrahepatic biliary system occurs because of inflammation and sclerosing cholangiopathy.¹⁶ Progressive obliteration of the extrahepatic ducts and, in many instances, the gallbladder takes place. This obliteration extends into the proximal intrahepatic duct system, which usually remains patent in the first few weeks of life. The severity varies with the duration of involvement. Fibrosis and obliteration of the biliary tree progress distal to proximal.¹⁷

More than 50% of neonates have transient jaundice characterized by mild elevation of serum bilirubin, which resolves spontaneously. Persistent or sudden-onset jaundice after the 1st and 2nd week of life may indicate a more serious abnormality, most commonly, biliary atresia or neonatal hepatitis. Less common causes include choledochal cysts, inspissated bile syndrome, enzyme deficiencies, metabolic abnormalities, hemolysis, hyperalimentation, and other congenital biliary anomalies.^11,17

Biliary atresia is twice as common in males, whereas neonatal hepatitis is four times more common in females. It is important to distinguish biliary atresia from neonatal hepatitis because atresia may be treated surgically with a liver transplant or the Kasai procedure. The outcome is better with early surgical intervention. If surgical correction is not possible, death usually occurs within months; however, a few children survive several years.^4,17 Complications of untreated biliary atresia are cirrhosis, cholangitis, portal hypertension, malabsorption, and failure of biliary drainage.^16,17

In normal neonates, the CHD is generally visible sonographically and measures no more than 1 mm. Intrahepatic duct dilatation combined with inability to visualize the CHD is suggestive of biliary atresia.¹⁷ If only the cystic duct is obstructed, a hydropic gallbladder will develop.⁴ Detection of both intrahepatic and extrahepatic dilatations excludes atresia and indicates obstruction (choledochal cyst, inspissated bile, and biliary calculi).¹⁷

There are five types of choledochal cysts, the most common being Type I, a fusiform dilatation of the CBD. Along with Type IV, Type I, has an abnormally long channel between the bile duct and pancreatic duct. The less common Type II is seen as true diverticula extending off the CBD. Type III is a duodenal choledochocele and Type IV is characterized by multiple cystic dilatations of the intrahepatic and extrahepatic ducts. Type V, Caroli disease (communicating cavernous ectasia), is a nonobstructive, saccular dilatation of communicating intrahepatic ducts.² Different causes of choledochal cysts have been cited, including congenital weakness of the duct wall, which results in the formation of a cystic structure, and angulation of the CBD, causing partial obstruction leading to dilatation and cyst formation.⁴

Clinically, the signs and symptoms include intermittent jaundice associated with colicky pain, failure to thrive, and sometimes a palpable subhepatic mass displacing the stomach and the duodenum.^4,18 Choledochal cysts are three to four times more common in females than in males, and often present early in life. Surgical management is recommended because of the increased incidence of malignant transformation that may occur later in life.²

Sonographically, choledochal cysts appear as a localized cystic mass separate from the gallbladder in the region of the porta hepatis or intrahepatically depending on the type (Fig. 8-16). To avoid mistaking a fluid-filled bowel loop for a choledochal cyst, the examiner should verify peristalsis.

Sludge represents precipitates formed in the bile. It consists of a collection of calcium bilirubinate, mucus, and lesser amounts of cholesterol crystals within viscous bile that contains high concentrations of mucus and other proteins.¹⁹

The pathogenesis, clinical significance, and ultimate prognosis of sludge remain uncertain. Sludge alone can produce biliary symptoms such as the classic pain of gallstones, and it can also be associated with other complications. Therefore, sludge associated with biliary pain can be a significant finding. The presence of sludge implies the formation of a precipitate and should not be regarded as normal. Sludge is sometimes a precursor to gallstone disease.^2,19

Sludge may be caused by conditions such as prolonged fasting, total parenteral nutrition (TPN), bile stasis, pregnancy, rapid weight loss and recent surgery and in critically ill patients.^2,19

Sonographically, sludge produces a homogeneous, low-amplitude, nonshadowing echo pattern that tends to layer dependently (Figs. 8-17A-D and 8-18A, B). True sludge often forms a fluid-fluid level that remains constant in longitudinal and transverse images. Sludge slowly moves with changes in patient position. Sludge can disappear and
reappear over time. Scattered brighter echoes within sludge may represent larger cholesterol crystals. If sludge completely fills the gallbladder (total bile sludging or hepatization of bile), it may be difficult to distinguish the echo-filled gallbladder from adjacent liver parenchyma (Fig. 8-19). Sludge may also lead to gallstones.^2,19

Tumefactive sludge from long-standing biliary obstruction frequently does not layer but often resembles a polypoid mass that can mimic a gallbladder neoplasm (Fig. 8-20A, B). Color Doppler sonography can be useful in determining tumefactive sludge from a neoplasm.²⁰ Occasionally, mobile, round, echogenic, nonshadowing masses known as sludge balls are seen within the gallbladder.¹⁹ Also, sludge may be found in conjunction with gallstones (Fig. 8-21).

Using excessively high-gain settings fills the gallbladder with artifactual echoes, giving a false appearance of sludge. This artifactual pattern has a snowflake appearance, whereas true sludge has a defined, low-level pattern. Increased echogenicity of surrounding organs is another clue of too much gain. It is also important to distinguish sludge from the “false debris” echo pattern of slice thickness artifacts.

Gallstones can be large or small, single or multiple, symptomatic or silent. Gallstones are common worldwide with 2% to 10% of the population affected, with North America being near the 10% mark. The prevalence of gallstones is higher in females than in males.² Gallstones are occasionally seen in fetuses and children (Fig. 8-22A, B).^15,21

The majority of stones contain a mixture of cholesterol, bilirubin, and calcium. Approximately 75% of the gallstones in the United States are primarily cholesterol, with black or brown pigment stones accounting for 25% to 30% (Fig. 8-23). Many factors are associated with gallstone formation. Supersaturation of bile with cholesterol, abnormal gallbladder emptying, and altered absorption contributes to cholesterol stone formation.^22,23

The most common risk factors for cholelithiasis are female gender, obesity, age, pregnancy, and diabetes.² Other associated risks include ethnicity, genetics, diet, TPN, cirrhosis, rapid weight loss, ileal disorders (Crohn), and various medications.²¹

The majority of patients with gallstones are asymptomatic, with most found during routine abdominal scanning. Patients with symptoms, however, generally present with right upper quadrant (RUQ) pain that is steady, occurs after meals, or radiates to the upper back, shoulder, or epigastric area. The patient may also have nausea or vomiting.²⁴ Pertinent laboratory values may include an elevated alkaline phosphatase and mildly elevated AST and ALT levels, when the cystic duct or CBD is obstructed.⁸

Prognosis and treatment of cholelithiasis can vary depending on the frequency and severity of the attacks as well as the size of the stones. Small calculi tend to be more troublesome because they may exit the gallbladder and cause ductal obstruction.²⁴ Cholelithiasis may take a benign course, and a low-fat diet may be sufficient treatment in some cases. Persistent symptoms may require surgical intervention, either laparoscopic or open cholecystectomy, to provide definitive treatment of gallstones.²¹ Percutaneous cholecystostomy may assume a limited role in elderly patients and patients at high risk. Surgical cholecystostomy to remove stones has been performed, but cholecystectomy is often necessary subsequently because of the high recurrence rate.²⁵ Sonography is the modality of choice for monitoring stones in these patients.²

The classic sonographic appearance of a gallstone is a mobile, gravity-dependent, echogenic foci within the gallbladder lumen that casts a posterior acoustic shadow (Fig. 8-24A-F).⁵ If the proper technique and transducer are used, virtually all calculi over 5 mm can be accurately diagnosed. If less than 2 to 3 mm, stones can be more difficult to visualize. However, small stones are typically multiple and described as “gravel,” thereby making detection easier (Fig. 8-25A, B).¹⁹ Small gallstones that are located within the cystic duct or in the neck of the gallbladder can be more difficult to visualize.⁵ The majority of gallstones produce “clean” shadows with distinct margins because they are highly reflective. The visualization of a clean shadow is dependent on gain settings, transducer position and frequency, harmonics, focusing, and compound imaging.² Cholesterol stones or polyps can demonstrate reverberations and comet tail artifacts because of the rigidity and physical characteristics of cholesterol. Other causes of echogenic foci with reverberation and comet tail artifacts within the RUQ include air in the biliary tree, surgical clips in the gallbladder bed, gas in an intrahepatic abscess, drainage catheters, emphysematous cholecystitis, lead pellets, focal hepatic calcifications, and scars.

As the patient changes position, gallstones should roll to the most dependent portion of the gallbladder (Fig. 8-26A, B). Stones that do not demonstrate mobility may be polyps, stones impacted in the gallbladder neck, or stones adherent to the gallbladder wall (Fig. 8-27A, B).

There are many possible technical, anatomic, and diagnostic pitfalls of cholelithiasis (Table 8-1). Again, meticulous scanning in multiple planes using a variety of techniques, patient positions, and transducer frequencies is crucial for accurate diagnosis and proper patient management.

With careful technique, the wall-echo-shadow (WES) triad or double-arc shadow sign may be seen (Fig. 8-28A, B). The first arc or curved echogenic line represents the thickened gallbladder wall. The second arc is from the surface of the stone followed by posterior acoustic shadowing.^1,2 With chronic disease, the gallbladder may be so contracted that it is difficult to visualize sonographically. Air-filled bowel loops in the RUQ may create shadowing, which can be mistaken for a contracted gallbladder with stones. The differential diagnosis for chronic cholecystitis is adenomyomatosis and gallbladder carcinoma.²⁶

In up to 95% of cases, acute cholecystitis or inflammation of the gallbladder results from impacted stones within the neck of the gallbladder or the cystic duct.^5,19,20,27 It is the most common inflammatory condition of the gallbladder.²⁷ Inflammation may result in necrosis, ulceration, swelling, and edema.⁵ Various degrees of bacterial infection occur with acute cholecystitis, leading to potential complications.⁸

Clinically, the signs and symptoms of cholecystitis are indistinguishable and somewhat nonspecific. Patients present with RUQ pain, positive Murphy sign, nausea, vomiting, distention, fever, a palpable RUQ mass, and/or jaundice.^8,20,28 These symptoms can be confused with acute pancreatitis, perforated peptic ulcer, liver abscess, or acute alcoholic hepatitis.⁸ Laboratory results can also be nonspecific, possibly showing serum liver transaminase, leukocytosis, hyperbilirubinemia, or elevated alkaline phosphatase.²⁹ Approximately 20% of patients with cholelithiasis will develop acute cholecystitis; however, only 20% to 35% of patients with RUQ pain will have acute cholecystitis.^5,20

On sonogram, a positive sonographic Murphy sign, wall thickening, and gallstones are signs of acute cholecystitis. Pericholecystic fluid and, at times, a hydropic gallbladder can also be seen.^5,20 Together, the findings of cholelithiasis and a positive sonographic Murphy sign are highly suggestive of acute cholelithiasis. Gallbladder wall thickening and pericholecystic fluid are considered secondary signs.²⁷ Color or power Doppler imaging may also be helpful in diagnosing acute cholecystitis by detecting hyperemia and an enlarged cystic artery (Fig. 8-29A-F).²

One thought is to manage the patient medically because 60% of acute cases resolve spontaneously, and surgery should be saved until the acute attack has subsided. The preferred approach is to perform a cholecystectomy within the first several days of the onset of symptoms because early surgical intervention results in fewer complications and lower costs.^20,30 In patients with severe acute cholecystitis who are poor surgical candidates, are very ill, or are elderly, sonographically guided aspiration and percutaneous drainage of the gallbladder or antibiotic therapy is an alternative.²⁹ The pathophysiologic events of acute cholecystitis represent a dynamic process. Time is needed for these changes to occur. As a result, the clinical onset may precede the appearance of sonographic signs by as much as 12 to 24 hours.³¹