Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

A transudate is hypointense on T1and hyperintense on T2-weighted images. An exudate has a higher signal intensity on T1weighted images than a transudate. Although the MR signal intensity varies with fluid protein concentration, considerable overlap in the appearance of various ascitic fluids makes this finding of limited significance.

The gallbladder wall is considerably thicker in patients with ascites due to liver cirrhosis than in patients with noncirrhotic ascites. Most malignant ascites is associated with a normal gallbladder wall thickness.

Portal Hypertension–Induced Ascites

Ascites is common in sinusoidal and postsinusoidal portal hypertension. Pathogenesis is multifactorial, consisting of factors favoring efflux of fluid into the peritoneal space, retention of fluid there, and continued replenishment of the intravascular volume. Peripheral vasodilation is common in patients with cirrhosis and ascites and, to a large extent, appears to be secondary to increased vascular production of nitric oxide, which is a potent vasodilator. In these patients ascites is related to a decrease in portal blood flow. Refractory ascites in cirrhosis often leads to accelerated liver decompensation.

Therapy is tailored for those with nonmalignant versus malignant ascites. In patients with nonmalignant ascites, prior enthusiasm for peritoneovenous shunting using Denver or LeVeen shunts has been tempered by shunt occlusions and other complications such as peritoneal fibrosis, and they are little used today.

Transjugular intrahepatic portosystemic shunt (TIPS) was not initially developed to treat ascites, but in a number of patients with portal hypertension and ascites a successful TIPS improved or even resolved their underlying ascites. Some patients with previously refractory ascites respond to medical management following TIPS insertion. Transjugular intrahepatic portosystemic shunt can control ascites in most patients with refractory ascites, with results influenced by the stage of cirrhosis. Ascites tends to improve in stage B cirrhotics but not those with stage C. In some centers TIPS is performed only in those ascitic patients refractory to conventional therapy; major complications in these patients include intraperi-

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toneal hemorrhage, refractory encephalopathy, and progressive liver and renal failure. Some have new onset or worsening of hepatic encephalopathy. In fact, TIPS in patients with advanced liver and renal failure may hasten death.

Malignant Ascites

One aid in distinguishing benign from malignant ascites is gallbladder US; most malignant ascites is associated with a normal gallbladder wall thickness, while the wall is thickened with most benign causes. Also, benign ascites tends to be mostly in the main peritoneal cavity (greater sac) with relative sparing of the lesser sac, while malignant ascites normally involves both.

Therapy for recurrent, symptomatic malignant ascites consists of therapeutic paracenteses to relieve symptoms in these patients with a limited life span. Alternate therapy consists of insertion of a percutaneous tunneled peritoneal catheter to relieve the symptoms.

Pancreatic Ascites

In pancreatitis, ruptured pancreatic ducts usually lead to pseudocyst formation, but occasionally leakage from a pseudocyst or pancreatic duct into the peritoneal cavity incites an exudate secondary to irritation (pancreatic ascites). If pancreatic ascites persists, endoscopic retrograde pancreatography (ERP) is worthwhile to define the pancreatic duct anatomy and identify a possible site of leakage.

Nephrogenic Ascites

The cause of ascites in a setting of nephrotic syndrome is poorly understood. Refractory ascites in patients with end-stage renal disease, called nephrogenic ascites, appears to be either altered peritoneal membrane permeability or impaired resorption due to peritoneal lymphatic obstruction; the ascitic fluid is rich in protein and contains few leukocytes, and the serum-ascites albumin gradient is decreased. In pediatric patients with nephrotic syndrome, ascites is probably due to general fluid retention, while in adults hypoalbuminemia, superimposed liver disease, and congestive heart failure appear to be factors.

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Definitive therapy for nephrogenic ascites is renal transplantation.

Most bilomas are amenable to successful percutaneous catheter drainage.

In Neonates

An unusual cause of ascites in neonates has been termed total parenteral nutrition ascites, developing after infusion through an umbilical vein catheter. These neonates present with ascites, the umbilical vein catheter overlies the liver, and contrast studies through the catheter confirm intraperitoneal extravasation. This complication of total parenteral nutrition is due to liver erosion by the umbilical vein catheter.

Ascitic Hydrothorax

Some patients with ascites develop a hydrothorax, probably due to congenital diaphragmatic defects. At times the hydrothorax predominates, with little evidence of ascites. Most often the peritoneopleural communication is on the right side, although it can be bilateral. Peritoneal communication is confirmed by injecting a Tc- 99m–labeled radioisotope (sulfur colloid or macroaggregated albumin) into the peritoneal cavity and scanning over the chest. A similar approach can be used with CT and MRI after intraperitoneal injection of contrast. Even intraperitoneal air injection and appropriate conventional films are diagnostic if the communication is sufficiently large.

Ascitic hydrothorax can be life threatening. Therapy is difficult; chest tube drainage leads to loss of fluids and electrolytes, creates a fistula, and generally is unsatisfactory in these sick patients. Therapy of the underlying cause of ascites should be considered, including TIPS or even liver transplantation, if appropriate.

Biliary Ascites/Biloma

Although bile may leak into the peritoneal cavity and result in bile ascites and bile peritonitis, more often an induced inflammatory response to the intraperitoneal bile results in bile being walled-off, forming a biloma. Most bilomas have a CT attenuation close to water, unless bleeding or infection supervenes.

Magnetic resonance bile signal should be similar to that obtained from gallbladder bile. Bile ranges from hypoto hyperintense on T1and hyperintense on T2-weighted images.

Chylous Ascites/Lymphocele

Chylous ascites, or chyloperitoneum, is the presence of chyle in the peritoneal cavity, while a lymphocele is a localized collection. Aside from trauma, including injury to the cisterna chyli, chylous ascites develops secondary to major occlusion of intraabdominal lymphatics. Thus thoracic duct ligation during esophagectomy or surgery on the pancreas, aorta, or other major structures leads to postoperative chylous ascites. Some cirrhotic patients develop chylous ascites. Even occlusion of a portosystemic shunt on rare occasion results in chylous ascites. It is a rare complication of severe pancreatic necrosis. Massive chylous ascites can develop secondary to pancreatic transection. In children chylous ascites is found in a setting of small bowel obstruction or a lymphangioma.

Chylous ascites is a rare initial presentation of an abdominal malignancy, presumably secondary to lymphatic obstruction. Chylous ascites is associated with lymphoma and Kaposi’s sarcoma in patients with AIDS; it has also developed with Mycobacterium infection.

Imaging studies of most patients with chylous ascites are nonspecific. Lymph contains fat and occasionally CT reveals chylous ascites to have a density of negative Hounsfield units— a highly suggestive finding. Likewise, a fluid– fluid level within the peritoneal cavity with the patient recumbent should suggest chylous ascites or a lymphocele.

One of the few indications for lymphangiography or lymphoscintigraphy is suspected chylous ascites. The study identifies a site of leakage or obstruction of extraperitoneal lymphatics. It does not define mesenteric or hepatic lymphatic leakage.

Incidentally, MRCP can define some cisterna chyli, especially if they are dilated.

Most lymphoceles develop after lymphatic disruption due to surgery or other type of trauma. They are relatively common after lymphadenectomy. Most are extraperitoneal in location; intraperitoneal lymph leakage usually results in chylous ascites rather than a lymphocele. They range from a unilocular collection mimicking a simple cyst to a multiseptated, irregular cystic structure containing necrotic

material. Hemorrhage or infection modifies their CT and US appearance. At times imaging differentiation from a urinoma or hematoma is not possible. Some lymphoceles mimic an abscess; also, a lymphocele may become infected. In general, aspiration is required to confirm the underlying condition.

Small lymphoceles tend to resolve spontaneously while larger ones generally require drainage. Simple percutaneous catheter drainage appears to be effective in treating postoperative lymphoceles. Thus percutaneous catheter drainage of symptomatic lymphoceles after radical pelvic lymphadenectomy led to resolution of most lymphoceles (37). If necessary, drainage catheters are inserted using imaging guidance, and lymphocele sclerosis is performed with such sclerotic agents as absolute alcohol. although doxycycline, povidone iodine and bleomycin have been used. Presence of a catheter allows repeat lymphocele ablation as needed. Few complications are associated with this procedure.

At times lymphangiectasia, regardless of cause, results in leakage of chyle percutaneously or into a hollow viscus. Computed tomographic lymphography and MRI are worthwhile in an attempt to define chylous enteric or other drainage. After initial lymphographic opacification for guidance, several patients with uncontrolled postoperative chyle fistulas underwent percutaneous transabdominal puncture and catheterization of the cisterna chyli or lymphatic ducts (38); the thoracic duct could be catheterized in some patients, the fistulas identified with aqueous contrast, and a thoracic duct fistula embolized with coils, leading to resolution of the patient’s chylothorax. No morbidity was encountered.

An interesting percutaneous translymphatic thoracic duct embolization in a patient with postoperative chylothorax was started by first performing unilateral lymphangiography, then an abdominal lymph vessel was punctured with a fine needle using fluoroscopic guidance and a 4-French catheter introduced to establish lymph system access (39); the thoracic duct was then embolized with coils and tissue adhesive.

Urinoma

Most localized collections of urine, or urinomas, are extraperitoneal in location. Less often

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leakage from the urinary tract results in the accumulation of urine in the peritoneal cavity either as single or multiple urinomas or as urinary ascites. The most common cause of urine spill is trauma to the urinary tract, especially bladder dome injury. A cystogram should be diagnostic of a bladder perforation, but may miss the occasional more proximal perforation. Contrast-enhanced CT should detect these. Some urinomas eventually lose their communication with the urinary tract. An occasional urinoma extends through the aortic hiatus into the mediastinum.

Unless complicated by bleeding or infection, most urinomas have a CT attenuation close to that of water.

Technetium-99m–mercaptoacetylglycilgly- cilglycine (MAG3) renal scintigraphy appears useful to detect urinary leakage into the peritoneal cavity or a more localized collection.

Hemoperitoneum

Bleeding due to trauma has already been discussed in an earlier section (see Trauma).

Common causes of a spontaneous hemoperitoneum are gynecologic diseases and spontaneous rupture of a liver hemangioma or hepatocellular carcinoma. Other reported tumoral causes of hemoperitoneum include bleeding from an enteric sarcoma or even a carcinoid.

At times portal hypertension evolves into unusual variceal formations, rupture of a varix, and intraabdominal hemorrhage. Most esophageal varices bleed intraluminally, but rarely they bleed intraperitoneally. Thus largevolume paracentesis in a setting of portal hypertension can lead to rupture of esophageal or mesenteric varices and an acute hemoperitoneum, a condition having a high mortality rate.

Anticoagulant therapy can lead to a spontaneous intraabdominal hemorrhage and an acute abdomen. Bleeding can occur into the peritoneal cavity, extraperitoneally, into the anterior abdominal wall, or even into bowel wall or lumen.

The most common spontaneous ruptured visceral aneurysm involves the splenic artery. Computed tomography should detect most of these aneurysms.

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Spontaneous hemoperitoneum in the pediatric age group is rare. An occasional vascular malformation or ovarian cyst ruptures and bleeds. Hemoperitoneum in a newborn is generally secondary to antenatal hemorrhage.

Loculated blood can mimic a complex cyst or neoplasm, with loculations ranging from single to multiple. Depending on location, some appearances suggest a bowel origin. Computed tomography attenuation of blood in the peritoneal cavity or a hematoma varies with time. An immediate bleed has an attenuation similar to that of intravascular blood, unless it is mixed with other fluid. The hematoma attenuation increases up to 90HU due to clot formation and red blood cell concentration, and then gradually begins to decrease with clot lysis, reaching water density or slightly higher within several weeks. Bleeding may be intermittent and clot formation and lysis extend for some time, resulting in a heterogeneous CT appearance. Eventual resorption may lead to a normal appearance or evolve into residual fibrosis. A similar change with hematoma age is found with MRI. An acute hematoma is isointense on T1and hyperintense on T2-weighted images. Within several days the signal gradually becomes hyperintense on T1-weighted images and a hematoma then is hyperintense on both T1and T2-weighted images.

Presence of hyperechoic pelvic fluid detected with transvaginal US, usually performed for suspected gynecological disease, suggests a hemoperitoneum.

Hematoma

Extraperitoneal Hematoma

Hematomas range from discrete collections to a diffuse infiltrate throughout the involved tissues. The most common site is in the rectus abdominis muscle, with other muscles, such as the internal oblique and gluteus muscles, less often involved.

Conventional radiography cannot identify even an extensive extraperitoneal hematoma, although an abnormality is suggested if the usual fatty tissue planes are obliterated. Computed tomography is generally preferred over US in evaluating suspected extraperitoneal hemorrhage.

Figure 14.11. Psoas hematoma. Transverse CT image reveals an enlarged, hyperdense psoas muscle. (Source: Paley M, Sidhu PS, Evans RA, Karani JB. Retroperitoneal collections—aetiology and radiological implications. Clin Radiol 1997;52:290–294, with permission from the Royal Collage of Radiologists.)

As already discussed, CT findings depend on hematoma age, and they range from hyperdense fresh blood, typically >50HU, to a fluid–fluid level (Fig. 14.11). Ultrasonography findings vary: an inhomogeneous cystic and hyperechoic appearance is common. With some hematomas a hemorrhagic neoplasm is in the differential diagnosis, although rapid onset should suggest the correct diagnosis.

A resolving hematoma has a hyperintense rim on precontrast T1-weighted images.

Spontaneous muscle hematomas are often associated with anticoagulation therapy; if necessary, they are amenable to being percutaneously decompressed.

Abdominal Wall Hematoma

The most common rectus abdominis muscle and sheath tumors consist of desmoids and hematomas. Rectus sheath hematomas occur spontaneously or are traumatic in origin (Table 14.1). Clinically, these hematomas are difficult to detect. A typical hematoma develops in the lower third of the abdominal wall. In the upper abdomen the rectus sheath limits spread, while inferiorly this sheath is incomplete and a hematoma spreads medially and laterally. Also, inferiorly the rectus muscle is separated from the peritoneum and properitoneal fat only by