22 hours ago cirrhosis is most likely to dilate submucosal esophageal veins, but hemorrhoidal veins occasionally can be affected. Cirrhosis would be rare, however, at this patient's age. A clinical study is performed that includes a group of subjects whose systemic blood pressure … >> Go To The Portal
Ultrasound dilated portal vein (>13 mm): non-specific biphasic or reverse flow in portal vein (late stage): pathognomonic recanalization of paraumbilical vein: pathognomonic portal-systemic collateral pathways (collateral vessels/varices) splenomegaly ascites cause of portal hypertension often identified, most commonly cirrhosis
Increased resistance to portal blood flow, the primary factor in the pathophysiology of portal hypertension, is in part due to morphological changes occurring in chronic liver diseases. This results in rerouting of blood flow away from the liver through collateral pathways to low-pressure systemic veins.
The portal venous system is a unique circulatory system which connects two systems of capillary beds; one in the gastrointestinal tract and splenic parenchyma, and the second in the hepatic sinusoids. The portal vein transports blood from abdominal viscera and ramifies - much like an artery - at the liver, ending into the hepatic sinusoids.
Differential diagnosis. Dilatation of splenic veins at the splenic hilum without splenomegaly may occur in situations such as state of increased perfusion of splenic tissue associated with an immune response 6.
Varices. Varices are varicose veins associated with portal hypertension. Your doctor can view them during an endoscopy (internal viewing of your gastrointestinal tract) or other imaging study. Varices most often occur in the esophagus or stomach as a result of portal hypertension.
A dilated portal vein (diameter of greater than 13 or 15 mm) is a sign of portal hypertension, with a sensitivity estimated at 12.5% or 40%. On Doppler ultrasonography, a slow velocity of <16 cm/s in addition to dilatation in the main portal vein are diagnostic of portal hypertension.
What are the symptoms of portal hypertension?Enlarged liver and spleen.Enlarged veins (varices) of the esophagus and stomach. ... Internal hemorrhoids.Weight loss from malnutrition.Fluid buildup in the belly (ascites)Kidney malfunction.Low platelets.Fluid on the lungs.
Suprahepatic causes of portal hypertension. Cirrhosis is the most common cause of portal hypertension, and chronic viral hepatitis C is the most common cause of cirrhosis in the United States. Alcohol-induced liver disease and cholestatic liver diseases are other common causes of cirrhosis.
An increase in splanchnic blood flow in portal hypertension is the result of a marked vasodilation of arterioles in splanchnic organs, which drain blood into the portal venous system[35].
Variceal hemorrhage is the most common complication associated with portal hypertension. Almost 90% of patients with cirrhosis develop varices, and approximately 30% of varices bleed.
How Is Portal Hypertension Diagnosed? Usually, doctors make the diagnosis of portal hypertension based on the presence of ascites or of dilated veins or varices as seen during a physical exam of the abdomen or the anus. Various lab tests, X-ray tests, and endoscopic exams may also be used.
A recanalized umbilical vein is a sonographic finding that is common in patients with cirrhosis or portal hypertension. The umbilical vein is developed in the fetus and carries oxygenated blood from… Expand. lindseysimon.weebly.com.
The hepatic portal vein is a vessel that moves blood from the spleen and gastrointestinal tract to the liver. It is approximately three to four inches in length and is usually formed by the merging of the superior mesenteric and splenic veins behind the upper edge of the head of the pancreas.
Portal hypertension leads to an increase in the blood pressure inside the veins in the lower esophagus and stomach. These veins were not designed for the higher pressure, and thus they begin to expand, resulting in varices.
Portal hypertension is characterized by a pathologic increase in portal venous pressure that leads to the formation of an extensive network of portosystemic collaterals that divert a large fraction of portal blood to the systemic circulation, bypassing the liver.
Splenic vein occlusion results in back pressure which is transmitted through its anastomoses with the short gastric and gastroepiploic veins and subsequently via the coronary vein into the portal system. This results in reversal of flow in these veins and the formation of gastric varices.
b) includes all arteries but the veins are part of the pulmonary circulation pathway.
d) are blood vessels that directly connect arteries to veins.
a) The tunica intima is the innermost layer of a blood vessel wall.
d) Capillaries have both a tunica intima and a tunica media.
d) from the right ventricle through the body to the right atrium.
c) Blood pressure is lower in arteries than in veins.
c) Veins have a tunica media while arteries do not.
Portal hypertension is defined as hepatic venous pressure gradient (HVPG) greater than 5 mmHg. HVPG is a surrogate for the portosystemic pressure gradient. Clinically significant portal hypertension is defined as a gradient greater than 10 mmHg and variceal bleeding may occur at a gradient greater than 12 mmHg.
Generally, management options include: lifestyle modifications: dietary sodium restriction (e.g. for ascites) medications: propranolol (e.g. for varices), diuretics (e.g. for ascites) interventional procedures.
Gastric varices, along with esophageal varices, are by far the most common portosystemic pathways seen in portal hypertension[21]. The reported prevalence of gastric varices ranges from 2% to 70%. Esophageal and gastric varices frequently coexist, as noted in the widely used Sarin endoscopic grading classification for gastric varices (Table (Table11)[28]. Esophageal varices are more likely to be supplied by the left gastric or the coronary vein, whereas gastric varices are more likely to be supplied by the short gastric and posterior gastric veins[29]. Dilated short gastric veins appear as a tangle of vessels along the medial aspect of the spleen near the hilum, making it often difficult to distinguish between the gastric fundus and individual vessels (Figure (Figure7).7). Gastric varices are known to simulate tumors or thickened rugae at endoscopy or barium radiography (Figure (Figure88).
Portal hypertension is a common clinical syndrome, defined by a pathologic increase in the portal venous pressure. Increased resistance to portal blood flow, the primary factor in the pathophysiology of portal hypertension, is in part due to morphological changes occurring in chronic liver diseases. This results in rerouting of blood flow away from the liver through collateral pathways to low-pressure systemic veins. Through a variety of computed tomographic, sonographic, magnetic resonance imaging and angiographic examples, this article discusses the appearances and prevalence of both common and less common portosystemic collateral channels in the thorax and abdomen. A brief overview of established interventional radiologic techniques for treatment of portal hypertension will also be provided. Awareness of the various imaging manifestations of portal hypertension can be helpful for assessing overall prognosis and planning proper management.
Portosystemic collateral pathways and direction of blood flow in portal hypertension. Progressive resistance to hepatopetal flow results in slowed and eventually reversed flow in the main portal vein (MPV). Portal venous system decompresses by recruiting several pre-exiting collateral pathways, the selection of which is partly dictated by the location of the portal venous resistance. Paraumbilical (PUVar), abdominal wall varices (AWVar), esophageal (EVar), paraesophageal (PEVar), gastric (GVar), cardiophrenic (CPVar), mesenteric (MVar) and rectal (RVar) varices may be created in order to allow the passage the portal venous blood into systemic circulation. LGV: Left gastric vein; SV: Splenic vein; IMV: Inferior mesenteric vein; IVC: Inferior vena cava; SRS: Splenorenal shunt; GRS: Gastrorenal shunt.
To ensure consistency in terminology, it should be noted that varices are dilated end-organ veins that have the propensity to bleed whereas shunts are dilated collateral channels that simply connect the portal and systemic vascular beds. The portosystemic collateral channels that can develop in portal hypertension are numerous, widespread and varied in appearance. Intrathoracic manifestations of portosystemic collateral vessels characteristically develop by way of the coronary vein into esophageal or paraesophageal (22%-38%) varices and cardiophrenic varices (18%)[10,18,19]. Other common pathways of portosystemic shunting involve gastroesophageal, paraumbilical, splenorenal, and inferior mesenteric collateral vessels. Pleuro-pericardial-peritoneal, pancreaticoduodenal, splenoazygos and mesocaval collaterals are less common pathways for decompression of portal vein (Figure (Figure22).
Normal portal venous pressure is between 5 to 10 mmHg, while the normal pressure gradient between the portal vein and the inferior vena cava, known as the hepatovenous pressure gradient (HVPG), is typically 1 to 5 mmHg[1]. Pathologic increase in portal venous pressure is primarily caused by resistance to portal inflow, which can occur either at the level of the portal vein, hepatic sinusoids or hepatovenous outflow. In addition to an increase in hepatic vascular resistance to portal blood flow, there is progressive splanchnic vasodilatation that aggravates the portal hypertension syndrome by augmenting portal blood flow[2]. Recent updates in pathophysiologic understanding of portal hypertension have also highlighted the contribution of hepatic sinusoidal endothelial dysfunction elevating portal pressure[1]. Ongoing portal hypertension eventually leads to formation of collateral circulation that directly connects the portal blood vessels to systemic circulation, bypassing the liver and thus constituting the clinical syndrome of portal hypertension[3-5]. Clinically significant portal hypertension is defined as an increase in HVPG to ≥ 10 mmHg; above this threshold, the complications of portal hypertension may begin to appear[6]. Formation of portosystemic collaterals is a complex process involving the opening, dilatation and hypertrophy of pre-existing vascular channels in order to decompress the portal system[2,4,5,7,8]. Some have also postulated that a component of angiogenesis is also involved in collateral formation[9].
Axial enhanced computed tomography of the upper abdomen in portal venous phase demonstrates multiple large tubular and serpiginous esophageal (white arrow) and paraesophageal (black arrow) varices at the level of the esophageal hiatus of the diaphragm.
Esophageal vari ces, the most common and clinically important collateral vessels, consist of dilated subepithelial and submucosal veins in the wall of the lower esophagus (Figure (Figure4).4). They usually drain into the azygos or the hemiazygos system[20]. The reported rate of variceal hemorrhage in patients with esophageal varices is estimated at 10%-30% per year, with the mortality from variceal hemorrhage high at 20%-35%[26]. CT is useful for detection and grading of esophageal varices , with a detection rate of more than 92% of large varices which have an elevated risk of bleeding[18]. Typical CT appearance is nodular thickening of the esophageal wall and enhancing nodular intraluminal protrusions with scalloped borders[18].
Since blood passes through the larger vessels relatively quickly, there is limited opportunity for blood in the lumen of the vessel to provide nourishment to or remove waste from the vessel’s cells. Further, the walls of the larger vessels are too thick for nutrients to diffuse through to all of the cells.
Arteries and arterioles have thicker walls than veins and venules because they are closer to the heart and receive blood that is surging at a far greater pressure ( Figure 20.1.2 ). Each type of vessel has a lumen —a hollow passageway through which blood flows. Arteries have smaller lumens than veins, a characteristic that helps to maintain the pressure of blood moving through the system. Together, their thicker walls and smaller diameters give arterial lumens a more rounded appearance in cross section than the lumens of veins.
network of 10–100 capillaries connecting arterioles to venules
Both arteries and veins have the same three distinct tissue layers, called tunics (from the Latin term tunica), for the garments first worn by ancient Romans. From the most interior layer to the outer, these tunics are the tunica intima, the tunica media, and the tunica externa (see Figure 20.1.2 ).
Precapillary sphincters located at the junction of a metarteriole with a capillary regulate blood flow. A thoroughfare channel connects the metarteriole to a venule. An arteriovenous anastomosis, which directly connects the arteriole with the venule, is shown at the bottom.
Since the pressure within arteries is relatively high, the vasa vasorum must function in the outer layers of the vessel (see Figure 20.1.2) or the pressure exerted by the blood passing through the vessel would collapse it, preventing any exchange from occurring.
Eventually, the smallest arteries, vessels called arterioles, further branch into tiny capillaries, where nutrients and wastes are exchanged. Capillaries come together to form venules, small blood vessels that carry blood to a vein, a larger blood vessel that returns blood to the heart.