Diagnostic ultrasound ( PDFDrive )

96 PART II Abdominal and Pelvic Sonography
samples from the generation of shear waves in the liver within
a small region of interest with utilization of acoustic radiation
force impulse (ARFI) imaging. Results are expressed in either
kPa or meters per second, and in North America, seemingly the
latter are preferred. here are published data giving the range
of values for each technique and equipment used. 79 he introduction
of these techniques is invaluable to reduce the requirement
for liver biopsy, to allow for follow-up of patients undergoing
new antiviral therapy with chronic liver disease, and to allow
for preoperative assessment of those with liver cancer for optimal
selection of therapy options. he current status of this technique
was recently published in a special report by the Society of
Radiologists in Ultrasound. 80
VASCULAR ABNORMALITIES
Portal Hypertension
Normal portal vein pressure is 5 to 10 mm Hg (14 cm H 2 O).
Portal hypertension is deined by (1) wedge hepatic vein pressure
or direct portal vein pressure more than 5 mm Hg greater than
IVC pressure, (2) splenic vein pressure greater than 15 mm Hg,
or (3) portal vein pressure (measured surgically) greater than
30 cm H 2 O. Pathophysiologically, portal hypertension can be
divided into presinusoidal and intrahepatic groups, depending
on whether the hepatic vein wedge pressure is normal (presinusoidal)
or elevated (intrahepatic).
Presinusoidal portal hypertension can be subdivided into
extrahepatic and intrahepatic forms. he causes of extrahepatic
presinusoidal portal hypertension include thrombosis of the
portal or splenic veins. his should be suspected in any patient
who presents with clinical signs of portal hypertension (ascites,
splenomegaly, and varices) and a normal liver biopsy. hrombosis
of the portal venous system occurs in children secondary to
umbilical vein catheterization, omphalitis, and neonatal sepsis.
In adults the causes of portal vein thrombosis include trauma,
sepsis, HCC, pancreatic carcinoma, pancreatitis, portacaval
shunts, splenectomy, and hypercoagulable states. he intrahepatic
presinusoidal causes of portal hypertension are the result
of diseases afecting the portal zones of the liver, notably schistosomiasis,
primary biliary cirrhosis, congenital hepatic
ibrosis, and toxic substances, such as polyvinyl chloride and
methotrexate.
Cirrhosis is the most common cause of intrahepatic portal
hypertension and accounts for greater than 90% of all cases of
portal hypertension in the West. In cirrhosis the distorted vascular
channels increase resistance to portal venous blood low and
obstruct hepatic venous outlow. Difuse metastatic liver disease
also produces portal hypertension by the same mechanism. Over
time, thrombotic diseases of the IVC and hepatic veins, as well
as constrictive pericarditis and other causes of severe right-sided
heart failure, will lead to centrilobular ibrosis, hepatic regeneration,
cirrhosis, and inally portal hypertension.
Sonographic indings of portal hypertension include the
secondary signs of splenomegaly, ascites, and portosystemic
venous collaterals (Figs. 4.30 and 4.31). When the resistance to
blood low in the portal vessels exceeds the resistance to low
in the small communicating channels between the portal and
systemic circulations, portosystemic collaterals form. hus
although the caliber of the portal vein initially may be increased
Coronary v.
L. portal v.
Gastroesophageal vv.
Para-umbilical v.
Portal v.
Splenic v.
Gastrorenalsplenorenal
vv.
Inferior
vena cava
Inferior
mesenteric v.
Pancreaticoduodenal
vv.
Retroperitoneal
paravertebral vv.
Superior
mesenteric v.
Superior-middle/
inferior rectal vv.
FIG. 4.30 Portal Hypertension. Major sites of portosystemic venous collaterals.