Core Curriculum, The: Ultrasound
1st Edition

Localization of tumors to segments of the liver is critical in the planning of surgical resection. The international Couinaud (pronounced “kwee-NO”) system of hepatic nomenclature is currently utilized [4,5,6]. This system is based on the distribution of portal and hepatic veins. The right and left lobes are divided by the main hepatic fissure defined by the middle hepatic vein in the superior portion of the liver and by a line connecting the GB with the IVC in the inferior portion of the liver. Each segment has a branch PV at its center and a hepatic vein at its periphery. Segments are numbered clockwise starting with the caudate lobe (segment 1), left lobe (segments 2-4), and right lobe (segments 5-8) (Table 2.1, Fig. 2.1). The caudate lobe is anatomically distinct, extending between the IVC and the left lobe and separated from the left lobe by the fissure of the ligamentum venosum (Fig. 2.2).

Blood supply to the liver is provided by both the PV (~70%) and the hepatic artery (~30%). This dual blood supply makes infarction rare in the liver. Both enter the liver at the porta hepatis and divide into right and left lobe branches. Doppler documents blood flow direction in both vessels as into the liver (hepatopetal). Spectral Doppler shows a low-resistance, arterial flow pattern for the hepatic artery with forward flow throughout the cardiac
cycle. Diastolic flow velocity increases and resistance index decreases after eating. The PV shows continuous antegrade venous flow with small pulsations that mirror the cardiac cycle. Mean velocity in the PV is 15-18 cm/sec.

Venous drainage of the liver is by three major hepatic veins that enter the IVC just below the diaphragm (Fig. 2.3). The right hepatic vein divides the anterior and posterior segments of the right lobe and enters the IVC separately. The middle and left hepatic veins may join just before entering the IVC. The middle hepatic vein separates the right and left lobe while the left hepatic vein divides the medial and lateral segments of the left lobe. Hepatic veins have no valves and their blood flow reflects the triphasic pulsatility of the IVC and right atrium. Spectral Doppler shows prominent antegrade flow toward the heart during systole reflecting movement of the tricuspid valve toward the cardiac apex. A second antegrade peak is produced in early diastole by opening of the tricuspid valve. In late diastole flow is reversed in the hepatic vein owing to atrial contraction. The caudate lobe drains directly into the IVC via small venous channels.

The liver parenchyma has homogeneous echogenicity equal to or slightly greater than the echogenicity of renal parenchyma (Fig. 2.4). Liver echogenicity is slightly less than that of the spleen. Portal triads are seen as echogenic foci well out into the periphery of the liver
(Fig. 2.4). Fissures and ligaments are usually invested in fat and are highly echogenic (Fig. 2.2). The fissure of the ligamentum teres in the left lobe must not be mistaken for an echogenic mass (Fig. 2.5).

Intrahepatic bile ducts (IHBD) course in the portal triads with the PVs and hepatic arteries. In the portal triads the relationship of the three structures to each other is not constant. The bile ducts may be anterior to, posterior to, or wrap around the PV [7]. Small bile ducts progressively anastomose to form the right and left lobe bile ducts that join in the porta hepatis to form the common hepatic duct. The common hepatic duct becomes the CBD approximately 3 cm distally at the junction of the cystic duct. The common hepatic duct and CBD are approximately 10 cm in length (Figs. 2.6, 2.7). Since they course outside of the liver parenchyma both are considered extrahepatic bile ducts (EHBD). The CBD joins with the main PV and the proper hepatic artery to cross the foramen of Winslow in the hepatoduodenal ligament. In this region the three structures maintain a constant relationship with the larger PV posterior and the smaller CBD and hepatic artery anterior. In cross section the three structures resemble Mickey Mouse with the vein being his face, the CBD his right ear, and the hepatic artery his left ear (Fig. 2.8). Dilatation of the CBD enlarges Mickey’s right ear. The distal CBD passes behind the duodenum to run in a groove formed by the posterior pancreatic head and the medial aspect of the duodenum (see Fig. 2.14). The CBD enters the duodenum opposite the uncinate process of the pancreas.

The GB is a pear-shaped, bile-filled sac nestled in a concave fossa on the visceral surface of the liver (Figs. 2.6, 2.9). The fundus usually projects beyond the edge of the liver while the body and neck extend dorsally toward the porta hepatis. The hepatic surface of the GB is attached to the liver by blood vessels and connective tissue whereas the inferior surface and fundus of the GB are covered by visceral peritoneum. Occasionally the GB is suspended on a mesentery and is not closely applied to the liver. The GB wall is made up of three layers of tissue. The inner mucosa is redundant and loosely connected to the fibromuscular layer. The mucosa is mucin-secreting columnar epithelium and is continuous with the epithelium of the cystic duct and biliary tree. The fibromuscular layer provides the framework of the sac with interlaced fibrous tissue and smooth muscle. The external coat is the covering peritoneum. The cystic duct is 4 cm long extending from the GB neck to the hepatic duct which it joins to form the CBD. The mucosal lining of the cystic duct forms 5-12 folds that constitute the spiral valve of Heister. These folds may cast acoustic shadows and mimic small stones lodged in the cystic dust. After a fast of 4 or more hours the normal GB is well distended and easily visualized by US as a gourd-shaped sac of fluid. Normal bile is echo-free. The normal GB does not exceed 5 cm in transverse diameter. In 4% of patients the fundus
folds back on itself forming a “Phrygian cap.” Additional normal folds may be seen near the neck of the GB. The GB wall is visualized as a thin echogenic line at the GB interface with the liver. Wall thickness is measured between the liver parenchyma and the GB lumen. This measurement, which includes the liver capsule, the entire GB wall, and intervening tissue, is normally less than 3 mm.

The pancreas is identified on US by recognition of the blood vessels within and around the pancreatic parenchyma (Figs. 2.10, 2.11, 2.12, 2.13 and 2.14). The neck, body, and tail of the pancreas course anterior and parallel to the SV. The total length of the pancreas from head to tail is 12-15 cm. The neck of the pancreas is anterior to the confluence of the SV and the SMV that forms the PV. The SV is of uniform diameter (<10 mm) until its junction with the SMV where the combined veins form a teardrop-shaped dilatation (Figs. 2.12, 2.13 and 2.14). The SMV courses in sagittal plane just to the right and usually slightly anterior to the superior mesenteric artery (SMA). The uncinate process of the pancreas extends leftward beneath the SMV to form a
tapered projection. Blunting of the normally tapered uncinate process is a sensitive sign of pancreatic enlargement or tumor. The SMA arises anteriorly from the aorta at or near the level of the crossing SV (Fig. 2.10). The SMA is surrounded by a collar of echogenic fat and appears, on transverse section, as the hole in a doughnut (Figs. 2.12, 2.14). The left renal vein and the transverse portion of the duodenum course underneath the SMV and SMA caudal to the level of the pancreas. The celiac axis arises from the aorta just cephalad to the pancreas (Fig. 2.10). In transverse plane the bifurcation into the hepatic and splenic arteries resembles a seagull in flight. The left gastric artery origin off the celiac axis may be seen in longitudinal plane.

The CBD extends caudally in the posterior aspect of the pancreatic head where it is commonly visualized as a tubular structure that ends at the major papilla entering the descending duodenum (Fig. 2.14). The pancreatic duct courses centrally within the pancreatic parenchyma from the tail to the head (Fig. 2.15). It joins the CBD to drain into the major papilla in 80% of individuals. In the remaining 20% the pancreatic duct enters the duodenum separately at the minor papilla. The hypoechoic muscular wall of the stomach should not be mistaken for the pancreatic duct (Fig. 2.16). The gastroduodenal artery courses anterior and parallel to the CBD. Doppler US confirms its identification.

The normal echogenicity of the pancreatic parenchyma depends upon the amount of fatty infiltration. The pancreas has no distinct capsule and, with aging, fat infiltrates between the lobules of parenchyma and increases the echogenicity. In children and younger adults the pancreas resembles a slab of meat and has well-defined margins with echogenicity

approximately equal to liver parenchyma. In older patients the pancreas resembles a dust mop and has poorly defined margins with echogenicity just slightly less than fat.

The spleen is normally visualized in the left upper quadrant of the abdomen between the diaphragm and the fundus of the stomach (Fig. 2.17). The spleen is soft and pliable allowing it to conform to the shape of the structures around it. Its diaphragmatic surface is smooth and convex, matching the concavity of the diaphragm. Its visceral surface is rounded and smooth with concavities for the stomach, left kidney, and the splenic flexure of the colon. Usual dimensions in adults are 12 cm in length, 7 cm in breadth, and 3-4 cm in thickness.

The spleen parenchyma is a network of lymphatic follicles (the white pulp) surrounded by vascular lakes filled with blood (the red pulp). On US the splenic parenchyma is extremely homogeneous with mid-to-low-level echogenicity slightly greater than that of the liver. The SV runs a relatively straight course rightward from the splenic hilum to the commencement of the PV dorsal to the neck of the pancreas. The SV receives the small inferior mesenteric vein in the region of the distal body of the pancreas and joins with the larger SMV to form the PV. The splenic artery is tortuous as it courses from the celiac axis to the splenic hilum. As the splenic artery enters the hilum it divides into six or more branches which ramify throughout the parenchyma. The capsule of the spleen is covered by closely applied visceral peritoneum except at the hilum and a small “bare area” at the posterior dome of the diaphragm. The spleen is anchored by phrenicolienal, lienorenal, and gastrolienal ligaments that converge at the hilum.

The peritoneal cavity is that portion of the abdominal cavity that is bounded by the parietal peritoneum. It consists of numerous recesses formed by organs, ligaments, and peritoneal reflections [8]. The lesser sac is the large potential space behind the stomach. It communicates with the remainder of the peritoneal cavity only by the small opening of the foramen of Winslow. Fluid in the lesser sac usually occurs only as a result of disease in structures bordering the lesser sac [9]. The major recesses of the greater peritoneal cavity are the right
and left subdiaphragmatic spaces, the hepatorenal recess (Morison’s pouch) (Fig. 2.18), the paracolic gutters, and the pelvic cul-de-sac. These recesses are most apparent when fluid is present in the peritoneal cavity.

US is approximately 90% accurate in differentiating obstructive from non-obstructive jaundice by depicting the presence of biliary dilatation. The 10% inaccuracy arises from the fact that biliary obstruction is not always accompanied by biliary dilatation and that biliary dilatation does not always mean biliary obstruction (Box 2.3). US accurately determines the
level of obstruction in 92-95% of cases and the cause of obstruction in 71-88% of cases (Table 2.3) [57].

Common duct stones are the most common cause of obstructive jaundice (36-50% of cases). Stones are found in the bile ducts in 12% of patients undergoing cholecystectomy. The fact that 4% of patients in autopsy series have biliary stones is evidence that biliary stones may be relatively asymptomatic and pass spontaneously. Sensitivity of US in the diagnosis of stones in the CBD is only approximately 55-75%. Careful scanning technique is required.

Pneumobilia is most often caused by sphincterotomy or surgical biliary-enteric anastomosis. Other causes include incompetence of the sphincter of Oddi or fistulas between the biliary tree and intestine. Air may be mistaken for stones in the biliary tree.

Ascariasis is the most common parasitic infection worldwide. The roundworm usually lives in the intestine but may migrate through the ampulla of Vater and gain access to the biliary tree and pancreatic duct resulting in cholangitis, acute cholecystitis, or, often fatal pancreatitis.

Choledochal cysts are uncommon congenital anomalies of the bile ducts characterized by cystic dilatation of portions of the intra- or extrahepatic biliary tree [62,63]. Choledochal cysts are usually discovered in infancy or childhood (60%). However, diagnosis may be delayed until adulthood. Patients are usually female (70-84%) and present with abdominal mass, jaundice, pain, or pancreatitis. Biliary stasis results in an increased incidence of gallstones and carcinoma of the bile ducts or GB. The Todani classification is commonly used (Fig. 2.55) [64].

Caroli’s disease is a rare congenital malformation of the IHBD characterized by non-obstructing saccular or fusiform dilatation of the IHBD. The condition presents in childhood and has an autosomal recessive inheritance pattern. Complications include biliary stones, recurrent bacterial cholangitis, hepatic fibrosis, portal hypertension, and hepatic failure [65].

Sclerosing cholangitis is characterized by intra- and extrahepatic biliary fibrosis with progressive obliteration of the bile ducts. Primary sclerosing cholangitis is idiopathic but associated with ulcerative colitis, Crohn’s disease, and retroperitoneal fibrosis. It eventually leads to biliary cirrhosis and hepatic failure [66].

Also called Oriental cholangiohepatitis in the literature, recurrent pyogenic cholangitis is related to infestation with Clonorchis sinensis and other parasites. Bacterial superinfection by Escherichia coli and other enteric pathogens is nearly always present. It is one of the most common diseases of the biliary tract in Southeast Asia and Hong Kong, and is seen in the United States primarily in Asian immigrants [68].

Acquired immunodeficiency syndrome (AIDS)-related cholangiopathy encompasses several types of biliary diseases encountered in patients with AIDS. Opportunistic infection plays a role in the illness with cytomegalovirus, Cryptosporidium species, and Enterocytozoon bieneusi organisms cultured from the bile. Patients present with abdominal pain and markedly elevated serum alkaline phosphatase [69].

Cholangiocarcinoma arising in small bile ducts in the periphery of the liver is the second most common primary hepatic malignancy. Approximately 10% of cholangiocarcinomas are peripheral. Intrahepatic cholelithiasis, Caroli’s disease, Clonorchis infestation, and Thorium exposure are predisposing factors. The tumor is an adenocarcinoma and is rare before age 40 [71,72].

Cholangiocarcinoma that arises in the hilum of the liver (the porta hepatis) is commonly called a Klatskin tumor. The tumor occurs at the confluence of the right and left bile ducts. Approximately 25% of cholangiocarcinomas are hilar [74].

Distal cholangiocarcinoma occurs in the EHBD and presents early with biliary obstruction and jaundice. The prognosis is better than with peripheral or hilar cholangiocarcinoma because the tumors are small and more often resectable.

Thickening of the GB wall is a non-specific finding caused by diseases of the GB as well as by extrinsic conditions (see Box 2.4 for differential diagnosis).

Sludge refers to bile that appears echogenic due to the presence of calcium bilirubinate granules and cholesterol crystals mixed with mucus. Sludge is commonly an incidental finding that is related to the lack of bile turnover in patients who are fasting for prolonged periods of time. Sludge is especially common in hospitalized patients. However, sludge may also be seen in patients with obstruction of the cystic duct or more distal bile ducts. Sludge
requires 5-7 days to form and is not caused by routine overnight fasting requested in preparation for GB US. Sludge may fill the entire GB, layer below anechoic bile, or form into balls or masses (tumefactive sludge). Sludge may become viscous and thicken to the consistency of toothpaste (see Fig. 2.62).

Gallstones affect 10-15% of the population and are a major cause of GB morbidity (Box 2.5). Most gallstones are mixtures of cholesterol, calcium bilirubinate, and calcium carbonate. Key US findings are

A GB filled with gallstones may be difficult to differentiate from a gas-filled bowel loop. Characteristic findings have been described as the wall-echo-shadow sign (WES triad) or the double-arc-shadow sign [78].

Acute cholecystitis is most commonly caused by impaction of a gallstone in the GB neck obstructing the GB and resulting in inflammation of the GB wall. Ischemia and bacterial infection are contributing and inciting factors. Patients present with pain, right upper quadrant tenderness, and leukocytosis. The differential diagnosis of patients with this set of symptoms is extensive and US is usually the first imaging study performed. No US finding is pathognomonic. The more findings that are present, the greater the likelihood of the diagnosis. The obstructing stone may spontaneously disimpact resulting in resolution of symptoms.

Atypical forms and complications of acute cholecystitis include the following:

Acalculous cholecystitis refers to acute cholecystitis developing in the absence of gallstones. In children, approximately one-half of the cases of acute cholecystitis are acalculous. Adults rarely develop acalculous cholecystitis unless they have a predisposing condition. Most cases occur in adult patients, who are hospitalized because of recent major surgery, trauma, burns, or debilitating diseases, are immunocompromised, or who are receiving intravenous hyperalimentation. Most cases are related to prolonged biliary stasis,
ischemia, and biliary infection. Outpatients who develop acalculous cholecystitis are usually elderly males with advanced arterial disease.

Gangrenous cholecystitis refers to necrosis, hemorrhage, ulceration, and microabscess formation in the GB wall. Gangrenous changes complicate 20-30% of cases of acute cholecystitis. Patients are at high risk for perforation and mortality is in the 5-10% range. Findings that suggest gangrene in acute cholecystitis include:

Emphysematous cholecystitis is characterized by the presence of gas in the GB wall and lumen. It is associated with gangrene (75%), early GB perforation (20%), and high mortality (15%). Gas-producing bacteria are causative. Most patients are elderly and up to 50% have diabetes [81].

Chronic cholecystitis occurs as a result of continued irritation by gallstones. Patients have recurring symptoms of biliary colic. The cystic duct is usually chronically obstructed.

Calcification of the GB wall in chronic cholecystitis is referred to as porcelain GB. Porcelain GB is associated with an increased risk of GB carcinoma (11-22%) [84].

GB polyps are quite common being present in 4-6% of the population [85]. Most (90%) are cholesterol polyps, which are abnormal deposits of cholesterol in a polypoid mass. Cholesterol polyps have no neoplastic potential and are incidental findings. The remainder (10%) are adenomatous polyps that have potential for malignant transformation.

Adenomyomatosis is a benign hyperplasia of the epithelium and smooth muscle of the GB wall with herniations of mucosa forming tiny pockets in the wall called Rokitansky-Aschoff sinuses [86]. The condition is entirely benign with no malignant potential, although the findings may mimic GB carcinoma [87].

GB carcinoma affects primarily older individuals (>60 years). Pathologic types are adenocarcinoma (90%) and squamous cell carcinoma (10%). GB carcinoma has a variety of appearances [88].

Acute pancreatitis is most commonly caused by alcohol abuse or a gallstone impacted in the distal CBD. Additional causes include trauma, surgery, endoscopic pancreatography, and drugs. Inflammatory changes vary from mild interstitial edema to extensive necrosis with hemorrhage. Contrast-enhanced CT is used for initial evaluation to detect necrosis [91]. US is utilized for follow-up, to detect complications, and to guide intervention.

Chronic pancreatitis is a chronic inflammatory disease of the pancreas characterized by progressive pancreatic damage with irreversible fibrosis. This process results in major structural abnormalities in varying combination including parenchymal atrophy, calcifications, stricture and dilatation of the pancreatic duct, fluid collections, pseudomass formation, and alteration of peripancreatic fat [94,96]. Although many patients with chronic pancreatitis have recurrent episodes of acute pancreatitis, chronic pancreatitis appears to be a separate entity. Patients with chronic pancreatitis average 13 years younger than those with acute pancreatitis. Acute pancreatitis seldom results in the development of chronic pancreatitis. Causes of chronic pancreatitis include alcoholism (70%), autoimmune disease, tropical pancreatitis [97], and non-alcoholic duct-destructive pancreatitis [98].

Pancreatic carcinoma is an aggressive and usually fatal tumor. The only realistic hope for cure is early detection and aggressive surgery (Whipple procedure). US is highly accurate in the detection of the pancreatic carcinoma with reported sensitivity of 88-94% [100]. Color Doppler is used to assess vascular involvement by tumor [101]. Approximately 70% of tumors occur in the pancreatic head.

Islet cell tumors may function and secrete hormones (insulin, gastrin, glucagon), or be non-functional and grow to large size prior to detection. Tumors may be benign or malignant but are characteristically slow growing.

Mucinous cystic neoplasm (macrocystic tumor) occurs as a malignant tumor (mucinous cystadenocarcinoma) or as a benign tumor with malignant potential (mucinous cystadenoma).
Tumors are characterized by copious mucin production that may result in multicystic masses, striking dilatation of the pancreatic duct, or diffuse multicystic enlargement of the pancreas [102,103,104]. Tumors that arise in peripheral pancreatic ducts are mucinous cystadenomas/carcinomas. Tumors that arise in the main pancreatic duct are called intraductal papillary mucinous tumors [103].

Serous cystadenoma (microcystic tumor) is a benign cystic neoplasm without malignant potential. The tumor grows slowly and is commonly large at presentation.

True pancreatic cysts are rare and are seen far less frequently than pancreatic pseudocysts. Congenital epithelial lined cysts are usually solitary. Multiple pancreatic cysts are seen with von Hippel-Lindau syndrome and autosomal dominant polycystic disease.

Pancreatic or peripancreatic lymphoma may be difficult to differentiate from primary pancreatic malignancy.

Metastases to the pancreas are uncommon; they are reported in autopsy series in only 3-11% of patients with known malignancy. Common primary tumors are melanoma, breast, lung, and renal carcinoma [106].

Cystic fibrosis is a genetic disease characterized by increased volume of abnormally viscous mucous secretions from exocrine glands. The pancreas is a major site of involvement. Secretions precipitate within the pancreatic ducts and result in obstruction, dilatation, and creation of small cysts. Patients develop exocrine pancreatic insufficiency and malabsorption [107].

Isolated nodules of functioning splenic tissue are found separated from the spleen in 10% of the population. They vary in size from a few millimeters up to several centimeters. They must be recognized as normal splenic tissue to avoid mistaking them for pathological masses [108].

Splenosis refers to the implantation of ectopic splenic tissue on peritoneal surfaces resulting from trauma with fragmentation of the spleen. Severe traumatic injury to the spleen commonly results in splenectomy. The residual implanted splenic tissue then hypertrophies and assumes the function of the parent spleen. A clinical clue to this condition is the absence of Howell-Jolly bodies in the peripheral blood in a patient with a history of splenectomy. Howell-Jolly bodies are fragments of nuclear material within red blood cells. When functioning splenic tissue is present, these red blood cells are filtered from the blood.

US measurement of the maximum splenic dimension shows good correlation with the volume and weight of the spleen [109]. Splenomegaly may be the only sign of disease. The causes of splenomegaly are many. Unfortunately, US is unable to differentiate the various etiologies in the majority of cases because the echotexture of the spleen remains normal despite the presence of disease. Causes of splenomegaly include portal hypertension, lymphoproliferative disorders (lymphoma, leukemia, polycythemia vera, hereditary spherocytosis, etc.), infiltrative disorders (Gaucher’s disease, amyloidosis), infections (malaria, infectious mononucleosis, AIDS), and vascular disorders (acute SV thrombosis) [110].

In rare cases the spleen lacks its normal attachments and has a long vascular pedicle that allows the spleen to move freely within the abdomen. The misplaced spleen may present as an abdominal mass or may cause abdominal pain because of torsion.

In some individuals the left lobe of the liver is exceptionally elongated and partially envelops the spleen simulating a subcapsular splenic hematoma or fluid collection. This wraparound portion of the liver is often thin and not obviously part of the liver on initial inspection.

Calcifications reflect previous granulomatous disease, most commonly histoplasmosis or tuberculosis. Splenic artery calcifications are a common manifestation of atherosclerotic disease. Splenic artery aneurysm is the most common visceral artery aneurysm.

Posttraumatic cysts are the most common cystic lesion of the spleen [112]. They occur as the end result of an intrasplenic hematoma.

Fluid associated with acute pancreatitis may dissect along the splenic vessels to the splenic hilum and subcapsular locations in the spleen.

True splenic cysts are congenital lesions that are lined by epithelium. These are often discovered in utero or in early childhood.

Pyogenic splenic abscesses are caused by hematogenous infection (75%), penetrating trauma (15%), or as a complication of splenic infarction (10%) [112]. Fever, chills, and pain may be pronounced, or the patient may be relatively asymptomatic.

Microabscesses occur in the setting of an immunocompromised patient with an opportunistic infection [113]. Common causative organisms include Mycobacterium tuberculosis and M. avium-intracellulare, Pneumocystis carinii, candidiasis, and other fungal infections. Kaposi’s sarcoma may produce similar lesions. Tiny lesions are best visualized with higher-frequency transducers (5 MHz).

Involvement of the spleen is seen in only 2% of human infestations with Echinococcus [114].

As the major organ of the lymphatic system the spleen is commonly affected by lymphoma and leukemia [115]. Patterns of disease involvement include infiltrative without discrete masses, miliary with numerous tiny lesions (<2 cm), and massive with extensive replacement of spleen parenchyma [112].

Metastases to the spleen are usually a late manifestation of disseminated malignancy in terminal patients. The most common primary tumors are melanoma and breast, lung, or ovary carcinoma. Isolated metastases (without mets seen elsewhere) are rare but are reported with colon and renal carcinomas and gynecologic malignancies [116].

Infarction occurs as a result of occlusion of branches of the splenic artery, or of thrombosis of venous sinusoids when the spleen is massively enlarged [112]. Arterial occlusion is associated with hemolytic anemias, endocarditis, arteritis, and pancreatic carcinoma. Most patients present with pain, but up to 40% are asymptomatic [117].

Hemangiomas are found much less commonly in the spleen than in the liver. Although scarce, hemangiomas are the most common primary neoplasm of the spleen. Multiple splenic hemangiomas are seen with Klippel-Trenaunay-Weber syndrome [118].

Lymphangiomas are similar to hemangiomas except that the vascular spaces are filled with lymph rather than blood [112]. The lesions may be solitary or multiple.

Angiosarcomas of the spleen are rare lesions, accounting for less than 2% of all soft tissue sarcomas [119]. Exposure to thorium dioxide (Thorotrast), vinyl chloride, and arsenic are predisposing factors.

Splenic peliosis is a rare cause of spontaneous splenic rupture [120]. Peliosis refers to the presence of multiple blood-filled cystic spaces (1-10-mm size) in the spleen or liver parenchyma. Both organs are usually affected. The etiology is unknown. Most patients are asymptomatic and the lesion is discovered incidentally.

The spleen parenchyma is injured and bleeding occurs, but the splenic capsule remains intact.

Injury lacerates the splenic parenchyma and the splenic capsule resulting in fragmentation of the spleen and blood in the peritoneal cavity.

Ascites is an accumulation of fluid within the peritoneal cavity. Ascites may be a transudate or exudate, blood, pus, bile, urine, pancreatic juice, or lymphatic fluid. US is highly sensitive in detecting intraperitoneal fluid and demonstrates as little as a few mL of fluid.

US is currently frequently used to detect the presence of hemoperitoneum in the setting of abdominal trauma [121]. Detection of even a tiny amount of fluid is used to triage patients urgently to CT or laparotomy. Fluid in the abdominal cavity in this setting is considered evidence of organ injury. US detection of solid organ injury is insensitive and clearly inferior to contrast-enhanced CT [122,123]. In addition, hemoperitoneum is absent in 17-34% of patients with abdominal visceral injuries, most commonly in patients with bowel and mesenteric injury [124,125].

Implants of mucin-producing cells on peritoneal surfaces results in a gelatinous form of ascites that tends to loculate and produce cystic pseudomasses. Causes include mucinous cystadenomas and cystadenocarcinomas of the appendix, colon, and ovary.

Peritoneal implantation of metastatic tumor nodules occurs most commonly with ovarian, gastric, colon, and pancreas carcinomas.

US is an excellent screening method for the detection of intraperitoneal abscesses; however, abdominal wounds, surgical dressings, drainage tubes, and bowel gas limit its use to a small subset of patients. Interloop abscesses, between loops of small bowel, are better demonstrated by CT. Abscesses are caused by spillage of contaminated fluid into the peritoneal cavity as a result of trauma, surgery, pancreatitis, bowel perforation, or by infection elsewhere.

Lymphoceles are cystic collections of lymphatic fluid that occur as a result of surgical or traumatic disruption of lymphatic vessels. They are seen commonly after lymphadenectomy in the retroperitoneum or pelvis and following renal transplantation.