Introduction
Background
Portal hypertension (PH) represents an increase of the hydrostatic pressure within the portal vein or its tributaries. It is defined as an increase in the pressure gradient between the portal vein and hepatic veins or the inferior vena cava (IVC).
Doppler sonogram at the splenic hilum reveals hepatofugal venous flow in a patient with portal hypertension.
Barium swallow in the left lateral decubitus position shows multiple mucosal nodules in the mid to lower esophagus. In a patient with cirrhosis, these are suggestive of esophageal varices.
Most patients with venous PH have intrinsic liver disease. In PH, blood that normally flows through the liver is diverted into systemic veins because of increased resistance to portal venous flow. This diversion of portal venous blood occurs via exiting portosystemic communications (eg, the coronary vein) and the opening of embryonic channels (eg, paraumbilical veins). The most common portosystemic anastomosis is via the coronary-gastroesophageal route; it occurs in 80-90% of patients and gives rise to lower esophageal and gastric varices.
Hematemesis resulting from bleeding esophageal varices is the most common presentation in patients with PH, although some patients seek medical help because of decompensated liver disease. Findings from duplex ultrasonography (US) and color Doppler imaging (CDI), MRI, CT, and endoscopy may support the diagnosis of PH.
Related eMedicine topics:Portal Hypertension (from Gastroenterology)
Esophageal Varices
Pathophysiology
Portal hypertension (PH) is defined as an increase in pressure gradient between the portal vein and the hepatic veins or inferior vena cava (IVC).1 A pressure gradient of 12 mm Hg is regarded as clinically significant for PH. With such an increase in the pressure gradient, portosystemic collaterals develop. These bypass portal venous flow to the liver, diverting blood to the systemic veins.
PH may develop in a variety of clinical circumstances, but by far, most instances are related to cirrhosis.
The causes of PH may be divided into (1) posthepatic, (2) prehepatic, and (3) intrahepatic causes. The major causes of posthepatic causes of PH are right-sided heart failure, constrictive pericarditis, and Budd-Chiari syndrome (BCS). The prehepatic causes of PH include portal vein thrombosis (PVT) and portal compression or occlusion by biliary and pancreatic neoplasms and metastases. PH may be caused by an increase in flow secondary to arterioportal fistula, pancreatic arteriovenous malformations, and massive splenomegaly. The most common intrahepatic cause is cirrhosis. The common feature of all the causes is an increase in resistance to portal venous flow, although in a few cases, increased inflow into the portal venous system is present.
The basis of PH in patients with cirrhosis is an increase in resistance to portal venous flow at the level of the sinusoids as a result of the perisinusoidal deposition of collagen. This deposition results in narrowing and compression of the central veins caused by fibrosis. Pressure from regenerative nodules contributes to this compression. Arteriovenous anastomoses in a fibrous scar also contribute to the increase in portal venous pressure.
Cirrhosis has many causes. In patients with alcoholic liver disease, serious PH may develop in the absence of cirrhosis. In a minority of patients with acute alcoholic hepatitis, progressive obliteration of central veins occurs with resultant centrilobular fibrosis. These changes result in severe outflow obstruction to portal venous flow, which leads to the formation of ascites and esophageal varices. Alcoholism and malnutrition result in nodular or Laennec-type cirrhosis; bile duct obstruction results in biliary cirrhosis; schistosomiasis, prolonged congestive heart failure, and hepatitis cause postnecrotic cirrhosis. Whatever the cause of cirrhosis from a hemodynamic viewpoint, the common denominator is a progressive increase in resistance to portal venous blood flow that results in PH.
Chronic portal vein obstruction is an important cause of PH; it has a variety of causes. Cavernous transformation of the portal vein (ie, development of periportal collaterals) occurs in patients with long-standing PVT as a result of the development of multiple small vessels in and around the recanalizing or occluded main portal vein. A leash of fine or markedly enlarged serpiginous vessels is seen in place of the portal vein. Color Doppler and/or pulsed Doppler imaging shows blood flow in these periportal collaterals that form around the thrombosed portal vein or that replace the vein.
Causes of PVT include the following:
- Idiopathic causes
- Causes secondary to tumor
- Hepatocellular carcinoma
- Cholangiocarcinoma
- Pancreatic carcinoma
- Gastric carcinoma
- Trauma
- Iatrogenic umbilical vein catheterization
- Abdominal sepsis
- Pancreatitis
- Perinatal omphalitis
- Appendicitis
- Diverticulitis
- Ascending cholangitis
- Myeloproliferative disorders
- Clotting disorders (hypercoagulable syndromes)
- Estrogen therapy
- Severe dehydration
- Cirrhosis, especially in the young
- Portal hypertension
Splenic vein thrombosis may be caused by abdominal trauma, tumors, or pancreatitis. Pressure is increased in areas drained by the splenic vein, while pressure in the portal vein remains normal (left-sided PH). The diagnosis is suspected in patients with gastric and/or esophageal varices and normal liver biopsy results. Splenectomy is curative.
BCS is a manifestation of hepatic venous outflow obstruction. The hepatic outflow obstruction usually occurs at the level of the IVC; the hepatic vein; and, depending on the classification and the nomenclature, possibly at the venules. The causes of BCS are numerous. Two types exist: acute and chronic. An acute thrombosis of the main hepatic veins or the IVC causes the acute form. The chronic form is related to fibrosis of the intrahepatic veins, which is presumably related to inflammation. The classical presentation is with ascites, hepatomegaly, and abdominal pain.
Hepatic venous occlusion results in the elevation of sinusoidal pressure, which leads to a delay or reversal of portal venous blood inflow, ascites, and morphologic changes in the liver. The last changes are reflected in abnormal liver function results. Both the acute and chronic forms result in severe centrilobular congestion, hepatocellular necrosis, and atrophy. Two other entities with similar clinical characteristics are severe right-sided heart failure and veno-occlusive disease of the liver. Hepatic veno-occlusive disease is characterized by inflammation of the post-sinusoidal venules, which results in fibrosis and venous occlusion. BCS has been variously classified. Some authors distinguish between primary BCS, which is associated with IVC webs, and secondary BCS, which is ascribed to a myriad of causes, including tumor, thrombosis, and trauma.
Other authors classify the disease according to the location of obstruction as follows:
- Type I disease is defined as occlusion of the IVC with or without secondary hepatic vein occlusion.
- Type II disease involves occlusion of the major hepatic veins.
- Type III disease entails obstruction of the small centrilobular venules (considered as veno-occlusive disease by some authors).
The causes of BCS are numerous. Examples include the following:
- Idiopathic causes: Historically, most cases were considered idiopathic or congenital, although some study results suggest that only one third of the cases have unknown causes.
- Congenital causes: A web, diaphragm, or interruption of the IVC may be observed.
- Venous thrombosis: This condition may be related to polycythemia rubra vera, antiphospholipid syndrome, pregnancy and a postpartum state, oral contraceptive use, sickle cell disease, thrombocytosis, and paroxysmal nocturnal hemoglobinuria.
- Injury and/or inflammation: These may be a result of phlebitis, autoimmune disease (Behçet disease), trauma, radiation injury, immunosuppressive drug use, or exposure to hepatotoxic alkaloids (eg, those in medicinal teas).
- Liver pathology: Fibrosis, hemorrhage, and congestion may be noted.
- Tumor: Renal cell carcinoma, hepatocellular carcinoma, adrenal carcinoma, metastasis, and leiomyosarcoma of the IVC may be present.
In most cases of BCS, the hepatic venous outflow is not completely eliminated, because a variety of accessory hepatic veins drain into the IVC above or below the site of obstruction. The most common of these accessory veins are the accessory inferior hepatic and caudate veins, which drain into the IVC inferior to the major hepatic veins. Vascular communications also exist via the azygos, intercostal, and paravertebral veins, which provide alternative pathways for hepatic venous drainage in BCS. Intrahepatic communication between the hepatic veins and portal veins also reverse flow in some portal venous branches, though flow in the main portal vein tends to remain centripetal.
As in BCS, some hepatic venous drainage is preserved, and the caudate lobe hypertrophies, sometimes massively; this may produce secondary IVC obstruction. Other parts of the liver with preserved venous drainage may also undergo hypertrophy.
Some venous drainage also occurs via the capsular veins, but this drainage is not sufficient to prevent peripheral atrophy in BCS. Parts of the liver with complete obstruction of its venous drainage tend to drain via the portal vein branches, depriving the involved parts of the liver of portal venous blood supply and the trophic effects of hormones. Hepatic hypertrophy and regeneration are always dependent on the trophic effect of portal blood supply. Thus, BCS is typically associated with peripheral atrophy of the liver and caudate and central hypertrophy. On cross-sectional imaging, the porta hepatis may be displaced anteriorly in BCS. Concomitant portal vein thrombosis (PVT) may be present in 9-20% of patients with BCS.
In idiopathic PH (Banti syndrome), no cirrhosis occurs, and the portal vein is patent. Liver biopsy results may be normal or may show fibrosis in the periportal areas and in the space of Disse; dilatation of sinusoids and intimal thickening with eccentric sclerosis of peripheral portal vein walls may be noted. The disease is progressive with increasing PH, and the liver eventually becomes small and fibrotic. A number of exogenous toxins such as copper salts, vinyl chloride, and arsenic may create a similar clinical picture.
Congenital hepatic fibrosis usually appears in childhood in association with autosomal recessive polycystic kidney disease, medullary sponge kidney, or Caroli disease. PH is a major consequence of this form of liver disease. Hepatic function is well maintained. Histologically, fibrous tissue is present within the hepatic parenchyma, with excess numbers of distorted terminal interlobular bile ducts and cysts that do not communicate with the bile ducts. In rare cases, hepatic sarcoidosis leads to hepatic fibrosis and PH.
When deprived of portal venous blood, the liver depends more on hepatic arterial blood. The liver undergoes atrophic changes and shrinks, and its capacity to regenerate is impaired. The changes are related to the lack of hepatotrophic hormones, largely insulin and glucagon, which are responsible for maintaining the normal structure and function of the liver. Vessels in the collateral venous circulation, particularly esophageal varices, are usually not prominent at autopsy because the veins collapse after death.
The spleen is enlarged and firm, with a thickened capsule. Malpighian bodies are inconspicuous. Histologically, sinusoids are dilated and lined by thickened epithelium. Histiocytes proliferate in the sinusoids with occasional erythrophagocytosis. Periarterial hemorrhages may progress to siderofibrotic nodules. The splenic artery and portal vein are enlarged and tortuous; they may be aneurysmal. The portal and splenic veins may show endothelial hemorrhages, mural thrombi, and intimal plaques, which may become calcified. These veins may be unsuitable for portosystemic shunt procedures.
Small, intrasplenic arterial aneurysms are seen in 50% of patients with cirrhosis. Hepatic changes depend on the cause of the PH. The degree of portal venous pressure is poorly correlated with the apparent degree of cirrhosis and fibrosis; a much better correlation is made with the degree of nodule formation.
Frequency
United States
The frequency of portal hypertension is related to the frequency of cirrhosis. Alcohol intake is the most common cause of liver disease in Western nations. Alcoholic cirrhosis is discovered in 1.6 – 9.9% of autopsies in the United States.
International
The exact worldwide incidence of cirrhosis is not known, but large regional variations occur, depending on the frequency of hepatitis B and hepatitis C.
Mortality/Morbidity
Mortality and morbidity of portal hypertension (PH) are related to the underlying cause (eg, cirrhosis, portal vein thrombosis, splenic vein thrombosis, veno-occlusive disease). Hemorrhage caused by esophageal varices is a major complication of PH. Mortality rates in adults with cirrhosis vary; the rate ranges from 30 – 60% for each bleeding episode.
Race
The most common cause of cirrhosis in North America is alcohol intake. In Africa, the Middle East, and the Far East, cirrhosis is virus related. Noncirrhotic idiopathic portal hypertension is more common in India and Japan.
Sex
Alcohol-related cirrhosis frequently affects males, although the incidence in females is increasing. The male-to-female ratio is 2:1. Primary biliary cirrhosis has a female preponderance (>90%).
Age
The incidence of alcoholic cirrhosis peaks in patients 40 – 55 years of age; however, patients 20 – 30 years of age may also have advanced alcoholic liver disease. Primary biliary cirrhosis is found in patients as young as 23 years and as old as 72 years; however, most patients are 40 – 60 years of age.
Anatomy
The portal venous system includes all veins that carry blood from the abdominal part of the alimentary tract, spleen, pancreas, and gallbladder. The union of the superior mesenteric and splenic veins forms the portal vein posterior to the pancreatic head. The portal vein enters the liver at the porta hepatis and soon divides into left and right portal vein branches. When portal circulation is obstructed, a remarkable collateral circulation develops, redirecting portal venous blood into systemic veins.
Portosystemic collaterals are classified into 4 main groups, as follows:
- Group I has 2 divisions.
- Group Ia: At the cardia of the stomach, the left gastric (coronary) vein and short gastric veins of the portal venous system anastomose with the intercostal veins, diaphragmatic veins, esophageal veins, the azygos vein, and other minor systemic veins of the caval system (such as the lumbar veins). Diversion of blood into these channels leads to the development of submucosal esophageal and gastric varices.
- Group Ib: At the anus, the superior hemorrhoidal vein of the portal system anastomoses with the middle and inferior hemorrhoidal veins of the caval system. Diversion of blood into these channels may lead to the formation of internal hemorrhoids.
- Group II: In the falciform ligament, blood flows through the paraumbilical veins (remnants of umbilical circulation of the fetus).
- Group III: Collaterals occur where intraperitoneal organs are in contact with retroperitoneal tissues or are adherent to the abdominal wall. These collaterals include veins from the liver to the diaphragm; veins in the lienorenal ligament and the omentum; lumbar veins; and veins developing in previous laparotomy scars.
- Group IV: Portal venous blood is carried to the left renal, inferior phrenic, and left adrenal veins directly from the splenic vein or via the diaphragmatic, pancreatic, left adrenal, or gastric veins. Esophageal varices are associated with hepatopulmonary syndrome; anastomoses between the portal veins and pulmonary veins have been found in both animals and humans. With increasing portal venous pressure, the mediastinal veins enlarge, enhancing the likelihood of their draining into the pulmonary veins via the pleural veins. However, direct splenoportography (SP) findings suggest that this shunt pathway is uncommon and small.
Spontaneous splenorenal shunts are seen in 10 – 20% of patients with PH. Blood from gastroesophageal collaterals and retroperitoneal and venous systems of the abdomen ultimately reaches the superior vena cava via the azygos or hemiazygos system. A small volume of blood enters the IVC. Collaterals feeding into the pulmonary veins have been described.
The presence of portosystemic anastomosis usually implies PH, although occasionally, if the collateral circulation is extensive, portal pressure may decrease. Conversely, PH of short duration may exist without demonstrable collateral circulation.
The collateral pathways in extrahepatic venous obstruction depend on the site of obstruction. In the absence of liver disease, with splenic vein occlusion, portal-portal collateral pathways develop over gastric veins (splenic, short gastric, coronary portal veins) and omental veins (splenic, gastroepiploic or arch of Barkow, superior mesenteric portal veins). In superior mesenteric vein obstruction, collaterals develop via the pancreaticoduodenal or cystic veins. In portal vein occlusion, collaterals develop via peribiliary venous plexus, via veins in the hepatoduodenal ligament, and in the hepatic hilus.
Presentation
Etiology of PH
The causes of portal hypertension are many; they may be subdivided into diseases causing prehepatic, hepatic, or posthepatic PH. The causes include alcoholic cirrhosis, schistosomiasis, hepatocellular carcinoma, Budd-Chiari syndrome (BCS), hepatoveno-occlusive disease, hepatitis and other chronic liver diseases, and the many causes of PVT (portal vein thrombosis).
Causes of PH include the following:
- Prehepatic causes
- Splenic vein thrombosis
- PVT
- Periportal venous collaterals in the presence of chronic portal vein occlusion (usually secondary to PVT)
- Hepatic causes
- Focal nodular hyperplasia
- Congenital hepatic fibrosis
- Peliosis hepatis
- Polycystic disease
- Idiopathic
- Hypervitaminosis A
- Arsenic, copper sulfate, and vinyl chloride monomer intoxication
- Sarcoidosis
- Tuberculosis
- Primary biliary cirrhosis
- Schistosomiasis
- Amyloidosis
- Mastocytosis
- Rendu-Osler disease
- Hematologic liver disease
- Acute fatty liver of pregnancy
- Severe viral hepatitis
- Chronic active hepatitis
- Hepatocellular carcinoma
- Nonalcoholic liver cirrhosis
- Alcoholic liver cirrhosis
- Acute alcoholic hepatitis
- Veno-occlusive disease
- Posthepatic causes
- BCS
- Congenital malformation (web, diaphragm, and interruption) and thrombosis of the IVC
- Constrictive pericarditis
- Tricuspid valve disease
- Miscellaneous causes such as arteriovenous fistulae; massive splenomegaly; and splenic, aortomesenteric, aortoportal, hepatic artery-portal, or pancreatic arteriovenous malformations
Clinical presentation
PH may be accompanied by the following 3 major complications:
- Gastrointestinal tract hemorrhage
- Ascites
- Encephalopathy
Hepatic encephalopathy is devastating and usually results from gastrointestinal bleeding, which is life threatening. The development of hepatic encephalopathy in patients with portal hypertension is most often related to the size of the portosystemic anastomosis. Splenoportal shunts are usually large. Cirrhosis of the liver is the most common cause of PH. Stigmata of cirrhosis, including jaundice, spider nevi, caput medusae, and palmar erythema, may be associated with signs of PH.
Preferred Examination
Plain radiographs are not often obtained in cases of portal hypertension, but because most hospitalized patients undergo chest radiography, radiologists need to be aware of abnormalities that may be found in patients with PH. The appearance of calcification in the distribution of the portal vein on a plain abdominal radiograph may indicate PH. An upper GI tract barium series is often performed for the detection of esophageal varices (see Images 1-4).
Barium swallow in the left lateral decubitus position shows multiple mucosal nodules in the mid to lower esophagus. In a patient with cirrhosis, these are suggestive of esophageal varices.
Barium swallow in a 56-year-old man with known cirrhosis who had a recent episode of hematemesis shows thickened mucosal folds and multiple polypoid filling defects at the lower end of the esophagus. These are suggestive of varices.
Endoscopic findings in a 47-year-old man with a history of polycythemia rubra vera who had a recent episode of hematemesis. Endoscopy showed a normal esophagus, but multiple polypoid submucosal lesions were seen in the fundus and body of the stomach (same patient as in Images 4-6 in Multimedia). The final diagnosis was left-sided portal hypertension secondary to splenic vein thrombosis.
Part of an upper gastrointestinal tract barium series (same patient as in Images 3-6 in Multimedia) shows multiple polypoid filling defects within the fundus of the stomach. The final diagnosis was a left-sided portal hypertension secondary to splenic vein thrombosis.
US techniques such as duplex US or spectral Doppler imaging and CDI or power Doppler imaging are the modalities of choice in the evaluation of the liver and PH. These techniques are noninvasive, rapid, and highly sensitive and specific.
Angiographic techniques such as splenosportography (SP), transhepatic portography, transumbilical catheterization, transjugular catheterization, wedge hepatic venography, and arterial portography are invasive. However, they are much more specific for the evaluation of PH hypertension; they are indicated when definitive surgery or radiologic intervention is contemplated.
The use of angiographic techniques is declining because noninvasive imaging techniques such as US, CT, computed tomographic angiography (CTA), and magnetic resonance angiography (MRA) are now available. These techniques are quickly improving, and this will lead to further decline in the use of angiographic methods.
Splenoportography and transumbilical catheterization are rarely performed. Arterial portography (indirect portography) and wedge hepatic venography with manometry is indicated before surgical portacaval shunt placement.
Carbon dioxide wedge hepatic venography is the most commonly used method for visualizing the portal vein before portal vein puncture for a transjugular intrahepatic portosystemic shunt (TIPS) procedure. TIPS is a radiology-guided creation of a shunt between the portal and hepatic veins in the liver by use of a percutaneous transjugular approach. Because of its proven safety and effectiveness, TIPS has largely replaced surgical decompressive shunt procedures.2,3,4
Limitations of Techniques
Plain radiographs are usually not indicated for patients with portal hypertension. Most plain radiographs are obtained for other reasons, and signs of PH are detected incidentally. Therefore, plain radiographs are of limited value.
Duplex US is a sensitive technique for the detection of PH in addition to other important features. When respiratory variation in the size of the portal, splenic, and superior mesenteric veins does not occur or when it is less than 20%, PH may be diagnosed with a sensitivity of 80% and a specificity of 100%.
In cases involving bleeding varices that are unresponsive to endoscopic sclerotherapy or when intractable ascites are present, a TIPS procedure is indicated. TIPS is performed after portal vein patency is documented at duplex US.
Differential Diagnoses
Budd-Chiari Syndrome
Cirrhosis
Congestive Heart Failure
Constrictive Pericarditis
Portal Vein Thrombosis
Other Problems to Be Considered
Veno-occlusive disease
Splenic vein thrombosis
Splenomegaly not resulting from liver disease
Arteriovenous fistula
Web lesion or thrombosis of the IVC
Idiopathic PH
More on Portal Hypertension |
 Overview: Portal Hypertension |
| Imaging: Portal Hypertension |
| Follow-up: Portal Hypertension |
| Multimedia: Portal Hypertension |
| References |
| Further Reading |
| Next Page » |
References
Bosch J, Pizcueta P, Feu F, et al. Pathophysiology of portal hypertension. Gastroenterol Clin North Am. Mar 1992;21(1):1-14. [Medline].
Mergo PJ, Ros PR. Imaging of diffuse liver disease. Radiol Clin North Am. Mar 1998;36(2):365-75. [Medline].
Murakami T, Mochizuki K, Nakamura H. Imaging evaluation of the cirrhotic liver. Semin Liver Dis. May 2001;21(2):213-24. [Medline].
Parvey HR, Raval B, Sandler CM. Portal vein thrombosis: imaging findings. AJR Am J Roentgenol. Jan 1994;162(1):77-81. [Medline].
Henseler KP, Pozniak MA, Lee FT Jr, Winter TC 3rd. Three-dimensional CT angiography of spontaneous portosystemic shunts. Radiographics. May-Jun 2001;21(3):691-704. [Medline].
Mitchell DG, Nazarian LN. Hepatic vascular diseases: CT and MRI. Semin Ultrasound CT MR. Feb 1995;16(1):49-68. [Medline].
Winter TC 3rd, Nghiem HV, Schmiedl UP, Freeny PC. CT angiography of the visceral vessels. Semin Ultrasound CT MR. Aug 1996;17(4):339-51. [Medline].
Zhao LQ, He W, Chen G. Characteristics of paraesophageal varices: A study with 64-row multidetector computed tomograghy portal venography. World J Gastroenterol. Sep 14 2008;14(34):5331-5. [Medline].
Ulu EM, Kirbas I, Emiroglu FK, Cakir B, Harman A, Bakar C, et al. Multidetector CT findings of splenic artery aneurysm in children with chronic liver disease. Pediatr Radiol. Oct 2008;38(10):1095-8. [Medline].
Kim M, Mitchell DG, Ito K. Portosystemic collaterals of the upper abdomen: review of anatomy and demonstration on MR imaging. Abdom Imaging. Sep-Oct 2000;25(5):462-70. [Medline].
Nghiem HV, Winter TC, Schmiedl UP, Freeny PC. MR angiography of the portal venous system. Semin Ultrasound CT MR. Aug 1996;17(4):360-73. [Medline].
Spritzer CE. Vascular diseases and MR angiography of the liver. Magn Reson Imaging Clin N Am. May 1997;5(2):377-96. [Medline].
Bolognesi M, Sacerdoti D, Merkel C, et al. Noninvasive grading of the severity of portal hypertension in cirrhotic patients by echo-color-Doppler. Ultrasound Med Biol. Jul 2001;27(7):901-7. [Medline].
Colli A, Cocciolo M, Riva C, et al. Abnormalities of Doppler waveform of the hepatic veins in patients with chronic liver disease: correlation with histologic findings. AJR Am J Roentgenol. Apr 1994;162(4):833-7. [Medline].
Grant EG. Doppler imaging of the liver. Ultrasound Q. 1992;10:117-54.
Kedar RP, Merchant SA, Malde HH, Patel VH. Multiple reflective channels in the spleen: a sonographic sign of portal hypertension. Abdom Imaging. Sep-Oct 1994;19(5):453-8. [Medline].
Koslin DB, Mulligan SA, Berland LL. Duplex assessment of the portal venous system. Semin Ultrasound CT MR. Feb 1992;13(1):22-33. [Medline].
Millener P, Grant EG, Rose S, et al. Color Doppler imaging findings in patients with Budd-Chiari syndrome: correlation with venographic findings. AJR Am J Roentgenol. Aug 1993;161(2):307-12. [Medline].
Nelson RC, Sherbourne GM, Spencer HB, Chezmar JL. Splenic venous flow exceeding portal venous flow at Doppler sonography: relationship to portosystemic varices. AJR Am J Roentgenol. Sep 1993;161(3):563-7. [Medline].
Piscaglia F, Donati G, Serra C, et al. Value of splanchnic Doppler ultrasound in the diagnosis of portal hypertension. Ultrasound Med Biol. Jul 2001;27(7):893-9. [Medline].
Ralls PW. Color Doppler sonography of the hepatic artery and portal venous system. AJR Am J Roentgenol. Sep 1990;155(3):517-25. [Medline].
Ralls PW, Mack LA. Spectral and color Doppler sonography. Semin Ultrasound CT MR. Oct 1992;13(5):355-66. [Medline].
Restrepo-Schafer I, Wollenberg B, Riera-Knorrenschild J, Gorg C. Partially reversed intrasplenic venous blood flow detected by color Doppler sonography in two patients with hematologic diseases and splenomegaly. J Clin Ultrasound. Jun 2001;29(5):294-7. [Medline].
Tessler FN, Mitchell E, Siskin T. Sonography of the transjugular intrahepatic portosystemic shunt. Ultrasound Q. 1998;14(3):165-70.
Zwiebel WJ. Sonographic diagnosis of hepatic vascular disorders. Semin Ultrasound CT MR. Feb 1995;16(1):34-48. [Medline].
McKiernan PJ, Sharif K, Gupte GL. The role of endoscopic ultrasound for evaluating portal hypertension in children being assessed for intestinal transplantation. Transplantation. Nov 27 2008;86(10):1470-3. [Medline].
Pan JJ, Chen C, Geller B, Firpi R, Machicao VI, Caridi JG, et al. Is sonographic surveillance of polytetrafluoroethylene-covered transjugular intrahepatic portosystemic shunts (TIPS) necessary? A single centre experience comparing both types of stents. Clin Radiol. Oct 2008;63(10):1142-8. [Medline].
Morgan J, Sadler MA, Siegel S. US, CT, and MR imaging of hepatic masses in Alström syndrome: a case report. Clin Imaging. Sep-Oct 2008;32(5):393-5. [Medline].
Superina RA, Alonso EM. Medical and Surgical Management of Portal Hypertension in Children. Curr Treat Options Gastroenterol. Sep 2006;9(5):432-443. [Medline].
Habib SF, Muhammad R, Koulaouzidis A, Gasem J. Pulmonary embolism after sclerotherapy treatment of bleeding varices. Ann Hepatol. Jan-Mar 2008;7(1):91-3. [Medline].
Goyal AK, Pokharna DS, Sharma SK. Ultrasonic measurements of portal vasculature in diagnosis of portal hypertension. A controversial subject reviewed. J Ultrasound Med. Jan 1990;9(1):45-8. [Medline].
Schraufnagel DE, Kay JM. Structural and pathologic changes in the lung vasculature in chronic liver disease. Clin Chest Med. Mar 1996;17(1):1-15. [Medline].
Further Reading
Guidelines and clinical studies:
The role of transjugular intrahepatic portosystemic shunt in the management of portal hypertension. American Association for the Study of Liver Diseases - Private Nonprofit Research Organization. 2005 Feb. 15 pages. NGC:004222
Peginterferon Alpha-2a Maintenance Therapy for Portal Hypertension in Patients With Hepatitis C
Use of Sanvar® With Endoscopic Treatment for the Control of Acute Variceal Bleeding
Efficacy and Safety of Simvastatin in the Treatment of Portal Hypertension
Efficacy and Safety of Cobiprostone in Patients With Portal Hypertension
Evaluation of Probiotics in the Treatment of Portal Hypertension
Keywords
portal hypertension, PH, portal HTN, portal venous pressure, hepatic venous pressure, portal venous flow, hematemesis, bleeding esophageal varices, portosystemic collateral vessels, portosystemic collaterals, cirrhosis, splenoportography
