Focal Changes

4

Focal Changes

4

Pancreas

pseudocysts may resolve and vanish. The rate of regression after acute pancreatitis is 50% within 6 weeks. The classification of pancreatic pseudocysts is shown in Table 4.5.

Ultrasound findings. Some pseudocysts are extremely large, filling most of the abdomen, and ultrasound may not be able to retrace them to the pancreas with certainty. Anechoic pseudocysts are rare; in most cases, they are filled with hyperechoic irregular intrinsic structures that (in infection, incidence 5%) are rooted in pus and detritus or necrosis and blood clots (Figs. 4.23, 4.24, 4.25).

In the differential diagnosis pseudocysts have to be considered separately from cystic tumors; distinctive features are listed in 4.3

(see Table 4.8).

Fig. 4.23 Symptomatic macro-pseudocyst (PZ) with sediment, compressing the main bile duct (DHC). VC = vena cava.

Fig. 4.24

a Microcyst (z) and macrocyst (Z) type II after an acute episode of chronic pancreatitis: anechoic mass in the body and tail of the pancreas. GB = gallbladder.

b Same patient as in a. After 5 months, spontaneous resolution of the pseudocysts; hyperechoic calcification, shadowing (arrows). L = liver; MA = stomach; P = pancreas; VL = splenic vein.

Fig. 4.25 Differential diagnosis: pseudocyst or cystic tumor?

a Power Doppler sonography: no vessels inside.

b CEUS: no enhancement, so a neoplasm can be ruled out (cf. Fig. 4.59).

Fluid Collections/Necrosis

As the term implies, the severe course of acute (“hemorrhagic necrotizing”) pancreatitis will produce necrosis within a few days of the onset of the disease. Frequently, it is accompanied by collections of peripancreatic fluid, especially in the lesser sac as circumscribed anechoic masses; peripancreatic hyperechoic masses correspond most likely to fatty necroses, ascites (around spleen, liver, kidney, and in the lower abdomen/rectouterine pouch), and pleural effusion of the left lung (Figs. 4.26, 4.27, 4.28).

The Atlanta classification proposes another classification of cystic lesions in acute and

acute relapsing pancreatitis with regard to the complications:

1.Acute fluid collections (intrapancreatic or peripancreatic)

2.Pancreatic necroses

3.Infected necroses

4.Acute pseudocyst (after 4 weeks)

5.Chronic pseudocyst (in chronic pancreatitis; high enzyme level)

6.Pancreatic or peripancreatic abscess

The differentiation between acute edematous and hemorrhagic necrotizing pancreatitis is based on histopathological criteria. However, native ultrasound or, better, CEUS (as also in

CT angiography) can differentiate the structures that indicate whether tissue is vital or nonvital. In the early stages CT studies may therefore be useful as a second imaging procedure for staging and in obtaining the baseline status when an intervention or surgical operation may be an option.

Abscess. Most abscesses arise from infected necrosis; early fine-needle aspiration cytology and culturing of the necroses are necessary in order to decide on possible interventions or surgery. Fever and septic temperature course are indicative of abscess formation (Fig. 4.29).

4

Focal Changes

b CDS: thrombosis of the splenic vein (VL); pseudocyst (PZ) without color coding. CF = venous confluence, AO = aorta, VC = vena cava, WS = vertebral column.

Fig. 4.28 CDS: severe necrotizing pancreatitis, peripancreatic extended, fluid collection (bursa omentalis), incipient pseudocyst.

Fig. 4.29 Peripancreatic abscess after pancreatitis (patient hospitalized because of septic temperatures, no clinical sign of previous pancreatitis): irregularly defined hypoechoic abscess formation (A) below the liver with adjacent inflammatory lymphadenopathy (LK); paracaval (VC) view high in the epigastrium; evacuated by ultrasoundguided fine-needle aspiration.

will visualize them as round cystic structures. CDS identifies them as ducts and not blood vessels.

Dilated segments of the pancreatic duct due to ductal obstruction in chronic pancreatitis may mimic cysts and be easily misdiagnosed ( 4.1h, Fig. 4.32).

Fig. 4.30 Anechoic cystic structures in the body of the pancreas (arrow).

Fig. 4.31 Color-flow Doppler scan demonstrates the splenic artery.

Fig. 4.32 Dilated prepapillary CBD (arrow) within the head of the pancreas in chronic pancreatitis. Borderline pancreatic duct (3.2 mm).

Hypoechoic Lesion

Neuroendocrine Tumors

Pancreatic Cancer

Metastasis, Malignant Lymphoma, Inflammatory Lymph Node

Abscess

Hemorrhagic/Infected Cyst/Pseudocyst

Focal (Segmental) Pancreatitis/Ventral Anlage

round, and smoothly delineated, and in contrast to metastases and other tumors they demonstrate marked hypervascularity in CDS and hyperenhancement in CEUS.9 The pancreatic duct is not obstructed (Fig. 4.33b,c).10 EUS is the most sensitive imaging modality in the diagnosis of neuroendocrine tumors, but further differentiation by ultrasonography is not possible.

Fig. 4.33

a Metastasizing neuroendocrine tumor (T) of the head of the pancreas. AO = aorta; L = liver; P = pancreas; VC = vena cava; VL = splenic vein.

4

Focal Changes

Pancreatic carcinoma of the body: tumor attitude in CDS and CEUS

Infiltrative growth, metastases

a Pancreatic carcinoma in the head (uncinate process,T), with obstruction of the pancreatic duct (DP). VL = splenic vein.

d hypoechoic structure, in CDS no vascularization.

g Pancreatic carcinoma of the tail, infiltration of the splenic artery with prestenotic dilatation and partly chromatic spots (blue).

b Pancreatic carcinoma in the head with duct dilatation, CDS: blurred defined polycyclic tumor (T), no intratumoral vessels detectable. KO = venous confluence, P = pancreatic body.

e CEUS, early phase, hypoenhancement in contrast to the rest of the organ.

h Pancreatic carcinoma of the head (T; see 4.2b), infiltration into the CBD (DC) and obstruction of the cystic duct (clinically Courvoisier’s sign) infiltrated celiac trunk; consequently inoperable.

c Pancreatic carcinoma of the tail, polycyclic contours, hypoechoic structure. Infiltration into the splenic vein (CDS).

f In the late phase, accentuated hypoenhancement.

i Pancreatic carcinoma, EUS: multiple hypoechoic lymph nodes the largest with cursors. EUS is the best procedure for the detection of small tumors as well as the evaluation of operability.

4

Pancreas

Abscess

Abscess occurs as an anechoic or, more commonly, hypoechoic mass; frequently, it demonstrates intrinsic structures and may then appear as a hypoechoic inhomogeneous lesion (Fig. 4.29). In CEUS, abcesses can be well differentiated by peripheral hypervascularization and absence of central enhancement.

Hemorrhagic/Infected Cyst/Pseudocyst

Pancreatic pseudocysts may display a variety of textures, but normally they are anechoic. Bleeding or calcification in the wall will result in a rather hypoechoic mass, even resembling a tumor or abscess (Fig. 4.37).

4

Focal Changes

Fig. 4.37

a Intracystic hemorrhage of a pancreatic pseudocyst, smooth margin, hypoechoic to complex structured mass.

b Infection of a pseudocyst. Fine echoes caused by bacterial gas with gas-related reverberations.

Focal pancreatitis of the head/tail of the pancreas resembles a tumor, making differentiation from true malignancy difficult. The suspected diagnosis of focal pancreatitis is based on the patient’s history and clinical symptoms, but it should be remembered that pancreatic cancer may also trigger acute pancreatitis. A special form is “groove pancreatitis”, a focal pancreatitis affecting the head of the pancreas around the intrapancreatic CBD. In this case, any increased tumor marker will subside after resolution of the acute symptoms, while in pancreatic cancer the marker will increase steadily. Fine-needle aspiration biopsy is of differential diagnostic value only if it is positive.

Compared to standard US, CEUS seems to increase diagnostic confidence in the differential diagnosis between mass-forming pancreatitis and pancreatic carcinoma.5

Undulating pancreatic duct, calcification, and fibrosis in the residual pancreas support the diagnosis of focal chronic pancreatitis; ductal cut-off and well-defined dilated duct support pancreatic carcinoma (see section “Dilatation of the Pancreatic Duct”). Further diagnostics are endoscopic ultrasound fine-needle aspiration (EUS-FNP), and, if indicated, exploratory laparotomy; elastography may be helpful in the differential diagnosis. In general, the older the patient, the more often a cancer is to be found.

A ventral anlage often presents as a hypoechoic mass in the caudal–dorsal parts of the pancreatic head, including the uncinate process, and may be mistaken as focal pancreatitis (Figs. 4.17b, 4.38, 4.39, 4.40, 4.41, Table 4.7).

Fig. 4.38

a Focal pancreatitis in the head of the pancreas (P): hypoechoic, swollen, well-defined head with calcifications, probably intraductal calculi (arrow): the swelling in the pancreatic head is almost impossible to differentiate from cancer. L = liver; AO = aorta; VL = splenic vein.

c Focal pancreatitis in the pancreatic head, “groove pancreatitis” with a duct stone, extracted endoscopically. Hypoechoic area in the uncinate process around the common bile duct (DC). VL = splenic vein.

b Left-sided pancreatitis in the tail. Hypoechoic mass, undisturbed course of the splenic vein (CDS).

d Stenosis of the intrapancreatic common bile duct (arrow); inflammatory wall thickening (calipers).