This document discusses collateral pathways that develop in portal hypertension. It begins by explaining how portosystemic collateral veins normally exist but increase in flow with portal hypertension. It then discusses the different directions collateral flow can take depending on where the obstruction is located.
The document proceeds to describe various normal and abnormal portosystemic anastomoses, including those connecting the esophagus, stomach, duodenum and other organs. It explains the afferents and efferents of different varices that can form. Images are also included showing various collateral pathways visible on imaging. In summary, the document provides a detailed overview of the venous drainage patterns and collateral vessels that can develop in response to portal hypertension.
This document discusses collateral pathways in portal hypertension. It describes various veins that enlarge to drain blood away from the portal system and into the systemic circulation when portal pressures are elevated. These include esophageal varices, gastric varices, splenorenal shunts, paraumbilical veins, and retroperitoneal varices. The document explains the anatomy and venous drainage patterns of these various collateral pathways and how they develop as alternatives for blood flow.
Circulation of liver & Portosystemic collateralsPratap Tiwari
The document summarizes the circulation of the liver and portosystemic collateral veins. It discusses:
- The dual blood supply to the liver from the hepatic artery (25-30% of flow) and portal vein (70-75% of flow).
- The portal vein is formed by the superior mesenteric vein and splenic vein. It divides within the liver into right and left branches.
- Portosystemic collateral veins develop to bypass portal hypertension and include veins around the falciform ligament, umbilical veins, and abdominal wall veins.
- The presence of dilated umbilical or abdominal wall veins indicates high pressure within the left branch of the portal vein and
Portal Vein and portocaval Anastomosis. Anatomy of portal vein, tributaries, branches and course, formations and relations. Anatomy of portal vein and adjacent structures, their relation to liver and intestine, relation to IVC and Aorta, clinical and applied anatomy for both undergraduates and postgraduates. portal hypertension is an increase in blood pressure, however, rather than being systematic, it's localized to the portal system. Portal hypertension is most commonly caused by liver cirrhosis which in itself can be caused by alcoholism or other liver disease. It can also be caused by blood clots in the portal vein and schistosomiasis amongst other things. This increase in blood pressure can affect areas of anastomosis between the portal vasculature which we just discussed and the caval musculature which are classified as the vessels not relating to the portal system resulting in pressure pushing larger blood volumes into these anastomotic areas. This in turn can cause the vessels to dilate and form varicose veins which can result in potentially fatal hemorrhage. Some of these important porto-caval anastomotic areas are listed below – the first vein being the portal vein and the second vein being the caval vein – the superior rectal and inferior rectal veins, the left gastric and esophageal veins, the colonic veins and the retroperitoneal veins and the para-umbilical and epigastric veins.
In severe cases, the last anastomosis mentioned between the para-umbilical veins which are the small veins that run within the round ligament of the liver and the epigastric veins which are found in the anterior abdominal wall can form large dilations. These dilations can form the clinical presentation caput medusa or the head of the medusa as the dilated veins look like the snakes of the head of the medusa or Gorgon from Greek mythology. In this image on the right, we can only see the beginnings of a presentation of the caput medusa as in a true caput medusa, the veins would be raised and enlarged.
Hello everyone! This is Nicole from Kenhub, and today we're going to talk about the hepatic portal vein.
We are going to discuss the hepatic portal vein and to do so we'll be using this image here which is a ventral view of the portal hepatic vein with the central portion of the liver cut out so we can see the portal vein and other portal vessels. You can also see the aorta just here as well as the inferior vena cava just posterior to the portal hepatic vein. The portal venous system is an important system that has its own unique flow and we'll talk about how this works in tandem with the venous system in the coming slides.
The portal vein is one of the most important vessels in the body.
Its main functions are to direct blood to the liver from the gastrointestinal tract and receive nutrient rich blood from the intestines.
The portal hepatic vein also receives blood from the spleen, the pancreas and the gallbladder which are channels within the vessel.
Varicose veins are dilated, elongated superficial veins caused by venous hypertension. They commonly occur in the legs but can affect other areas. The venous system of the lower limb consists of deep and superficial veins that connect via perforating veins. The long saphenous vein originates in the foot and travels up the medial leg and thigh, connecting to the femoral vein. Short saphenous vein originates laterally and connects to the popliteal vein. Valves in the veins normally prevent backflow but can become incompetent, allowing reflux and varicose vein formation. Color duplex ultrasound can evaluate reflux patterns and valve competence.
Single ventricle physiology involves a heart with only one functional pumping chamber. The document discusses the anatomy, physiology, and surgical management of various types of single ventricle hearts. Key points include: the goal of initial surgery is to provide unobstructed systemic outflow and pulmonary blood flow while limiting pulmonary pressures; manipulation of pulmonary and systemic vascular resistances is important for balancing blood flow; and inotropic support can increase cardiac output while adjusting pulmonary to systemic flow ratios.
Portal hypertension occurs when blood pressure in the portal vein system, which carries blood to the liver, exceeds 10 mm Hg. It is usually caused by cirrhosis or scarring of the liver. Complications include variceal bleeding, ascites, and end-stage liver disease. Diagnosis involves assessing the underlying liver disease through clinical examination, labs, and imaging. Doppler ultrasound and angiography can evaluate the portal venous system. Upper endoscopy is important to identify esophageal or gastric varices which are prone to bleeding in portal hypertension. Treatment depends on the severity but may include pharmacotherapy, endoscopic variceal ligation, TIPS procedure, or liver transplantation.
The pancreas is protected posteriorly by the rib cage and muscles, and anteriorly by surrounding organs that absorb energy. It has relations superiorly, inferiorly, and posteriorly to major blood vessels. Injury can be blunt or penetrating, with indicators including pain, hematoma, and fluid abnormalities. Evaluation involves blood tests, imaging like CT or MRI, and possibly ERCP. Injuries are graded from I to V based on severity. Treatment ranges from observation to surgery like drainage, resection, or reconstruction of the pancreatic duct. Complications can include bleeding, leaks, and long term issues. A high index of suspicion is needed to identify pancreatic trauma.
esophageal varices are the second most common cause of upper GI bleed after PUD.These are actually the dilated veins which occur secondary to increase in the pressure in the portal circulation called as Portal Hypertension..
This document discusses collateral pathways in portal hypertension. It describes various veins that enlarge to drain blood away from the portal system and into the systemic circulation when portal pressures are elevated. These include esophageal varices, gastric varices, splenorenal shunts, paraumbilical veins, and retroperitoneal varices. The document explains the anatomy and venous drainage patterns of these various collateral pathways and how they develop as alternatives for blood flow.
Circulation of liver & Portosystemic collateralsPratap Tiwari
The document summarizes the circulation of the liver and portosystemic collateral veins. It discusses:
- The dual blood supply to the liver from the hepatic artery (25-30% of flow) and portal vein (70-75% of flow).
- The portal vein is formed by the superior mesenteric vein and splenic vein. It divides within the liver into right and left branches.
- Portosystemic collateral veins develop to bypass portal hypertension and include veins around the falciform ligament, umbilical veins, and abdominal wall veins.
- The presence of dilated umbilical or abdominal wall veins indicates high pressure within the left branch of the portal vein and
Portal Vein and portocaval Anastomosis. Anatomy of portal vein, tributaries, branches and course, formations and relations. Anatomy of portal vein and adjacent structures, their relation to liver and intestine, relation to IVC and Aorta, clinical and applied anatomy for both undergraduates and postgraduates. portal hypertension is an increase in blood pressure, however, rather than being systematic, it's localized to the portal system. Portal hypertension is most commonly caused by liver cirrhosis which in itself can be caused by alcoholism or other liver disease. It can also be caused by blood clots in the portal vein and schistosomiasis amongst other things. This increase in blood pressure can affect areas of anastomosis between the portal vasculature which we just discussed and the caval musculature which are classified as the vessels not relating to the portal system resulting in pressure pushing larger blood volumes into these anastomotic areas. This in turn can cause the vessels to dilate and form varicose veins which can result in potentially fatal hemorrhage. Some of these important porto-caval anastomotic areas are listed below – the first vein being the portal vein and the second vein being the caval vein – the superior rectal and inferior rectal veins, the left gastric and esophageal veins, the colonic veins and the retroperitoneal veins and the para-umbilical and epigastric veins.
In severe cases, the last anastomosis mentioned between the para-umbilical veins which are the small veins that run within the round ligament of the liver and the epigastric veins which are found in the anterior abdominal wall can form large dilations. These dilations can form the clinical presentation caput medusa or the head of the medusa as the dilated veins look like the snakes of the head of the medusa or Gorgon from Greek mythology. In this image on the right, we can only see the beginnings of a presentation of the caput medusa as in a true caput medusa, the veins would be raised and enlarged.
Hello everyone! This is Nicole from Kenhub, and today we're going to talk about the hepatic portal vein.
We are going to discuss the hepatic portal vein and to do so we'll be using this image here which is a ventral view of the portal hepatic vein with the central portion of the liver cut out so we can see the portal vein and other portal vessels. You can also see the aorta just here as well as the inferior vena cava just posterior to the portal hepatic vein. The portal venous system is an important system that has its own unique flow and we'll talk about how this works in tandem with the venous system in the coming slides.
The portal vein is one of the most important vessels in the body.
Its main functions are to direct blood to the liver from the gastrointestinal tract and receive nutrient rich blood from the intestines.
The portal hepatic vein also receives blood from the spleen, the pancreas and the gallbladder which are channels within the vessel.
Varicose veins are dilated, elongated superficial veins caused by venous hypertension. They commonly occur in the legs but can affect other areas. The venous system of the lower limb consists of deep and superficial veins that connect via perforating veins. The long saphenous vein originates in the foot and travels up the medial leg and thigh, connecting to the femoral vein. Short saphenous vein originates laterally and connects to the popliteal vein. Valves in the veins normally prevent backflow but can become incompetent, allowing reflux and varicose vein formation. Color duplex ultrasound can evaluate reflux patterns and valve competence.
Single ventricle physiology involves a heart with only one functional pumping chamber. The document discusses the anatomy, physiology, and surgical management of various types of single ventricle hearts. Key points include: the goal of initial surgery is to provide unobstructed systemic outflow and pulmonary blood flow while limiting pulmonary pressures; manipulation of pulmonary and systemic vascular resistances is important for balancing blood flow; and inotropic support can increase cardiac output while adjusting pulmonary to systemic flow ratios.
Portal hypertension occurs when blood pressure in the portal vein system, which carries blood to the liver, exceeds 10 mm Hg. It is usually caused by cirrhosis or scarring of the liver. Complications include variceal bleeding, ascites, and end-stage liver disease. Diagnosis involves assessing the underlying liver disease through clinical examination, labs, and imaging. Doppler ultrasound and angiography can evaluate the portal venous system. Upper endoscopy is important to identify esophageal or gastric varices which are prone to bleeding in portal hypertension. Treatment depends on the severity but may include pharmacotherapy, endoscopic variceal ligation, TIPS procedure, or liver transplantation.
The pancreas is protected posteriorly by the rib cage and muscles, and anteriorly by surrounding organs that absorb energy. It has relations superiorly, inferiorly, and posteriorly to major blood vessels. Injury can be blunt or penetrating, with indicators including pain, hematoma, and fluid abnormalities. Evaluation involves blood tests, imaging like CT or MRI, and possibly ERCP. Injuries are graded from I to V based on severity. Treatment ranges from observation to surgery like drainage, resection, or reconstruction of the pancreatic duct. Complications can include bleeding, leaks, and long term issues. A high index of suspicion is needed to identify pancreatic trauma.
esophageal varices are the second most common cause of upper GI bleed after PUD.These are actually the dilated veins which occur secondary to increase in the pressure in the portal circulation called as Portal Hypertension..
The azygos vein connects the inferior vena cava and the superior vena cava
The thoracic duct is the largest lymph vessel that ultimately drains lymph from all parts of the body into the blood circulation
We shall look at them one at a time
This document discusses liver anatomy, function tests, and imaging. It covers the embryological development of the liver, its lobes and ligament attachments. It describes the dual blood supply, biliary drainage system, and microscopic anatomy. Common liver function tests are outlined including those assessing synthesis, damage, and detoxification. Ultrasound imaging of the liver is also summarized, noting its advantages of being inexpensive and non-invasive but limitations in imaging certain areas.
The liver is the largest organ in the body, located in the right upper quadrant. It has two lobes and is supplied by branches of the hepatic artery and portal vein. Blood drains from the liver through the hepatic veins into the inferior vena cava. The liver has many functions including bile production and detoxification. Tests of liver function include bilirubin, alkaline phosphatase, and transaminases. Imaging of the liver includes ultrasound, CT, MRI, angiography, and nuclear medicine scans to evaluate blood flow, tumors, cysts, and other abnormalities. Biopsies and endoscopic procedures help diagnose and treat conditions of the liver and biliary tract.
The liver is the largest organ in the body, located in the right upper quadrant. It has two lobes and is supplied by branches of the hepatic artery and portal vein. Blood drains from the liver through the hepatic veins into the inferior vena cava. The liver has many functions including producing bile and metabolizing nutrients, toxins, and drugs. There are various imaging modalities used to examine the liver such as ultrasound, CT, MRI, angiography, and nuclear medicine scans which help identify abnormalities in liver structure, blood flow, and function. Biopsy may also be performed to obtain tissue samples for analysis.
The document discusses portal hypertension in children. It covers the anatomy of the portal system, causes/classifications of portal hypertension, clinical manifestations, diagnosis, and treatment. Regarding diagnosis, it describes using endoscopy to identify varices, ultrasound to detect portal vein thrombosis, and CT/MRI/venography to further evaluate vascular anatomy. Treatment of acute variceal bleeding involves stabilizing the patient and reducing portal pressure to stop bleeding.
Imaging and intervention in hemetemesisSindhu Gowdar
This document discusses various imaging modalities for evaluating gastrointestinal bleeding, including hematemesis. It provides details on angiography, computed tomography angiography, and endoscopy. The key points are:
- Endoscopy is the primary initial investigation but additional techniques like CT angiography and catheter angiography may be needed when endoscopy is negative or fails to identify the bleeding source.
- CT angiography has advantages over catheter angiography as it is more widely available, non-invasive, and allows detection of bleeding sources throughout the GI tract.
- Both endoscopy and CT angiography play important roles in evaluating GI bleeding, with endoscopy also allowing for therapeutic interventions when a source is identified.
This document provides information on portal hypertension, including:
1. It defines portal hypertension and describes types such as cirrhotic and non-cirrhotic portal hypertension.
2. It outlines the portal venous system and portosystemic circulation.
3. It discusses causes, clinical features, investigations, and management of portal hypertension including pharmacotherapy, endoscopic therapy, TIPS procedure, and surgeries.
4. Prevention of recurrent variceal hemorrhage is highlighted through long-term pharmacotherapy, endoscopic therapy, interventional procedures like TIPS, or surgical shunts if other options fail.
brief lecture notes for 5th sem MBBS, on portal hypertension and varices. Introduction to portal hypertension and esophageal and gastric varices and management of variceal bleeding.
Sonological features of Pancreatitis.pptxvinodkrish2
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Acute pancreatitis
Last revised by Rohit Sharma on 27 Sep 2023
Citation, DOI, disclosures and article data
Acute pancreatitis (plural: pancreatitides) is an acute inflammation of the pancreas and potentially life-threatening.
On this page:
Article:
Terminology
Epidemiology
Diagnosis
Clinical presentation
Pathology
Radiographic features
Treatment and prognosis
Differential diagnosis
See also
Related articles
References
Images:
Cases and figures
Terminology
Two subtypes of acute pancreatitis are described in the Revised Atlanta Classification 1:
interstitial edematous pancreatitis
the vast majority (90-95%)
most often referred to simply as "acute pancreatitis" or "uncomplicated pancreatitis"
necrotizing pancreatitis
necrosis develops within the pancreas and/or peripancreatic tissue
Epidemiology
The demographics of patients affected by acute pancreatitis reflect the underlying cause, of which there are many (see Pathology below).
Diagnosis
The diagnosis of acute pancreatitis is usually based on clinical criteria or a combination of clinical and radiographic features 1.
Diagnostic criteria
Two of the following three criteria are required for the diagnosis 1:
acute onset of persistent, severe epigastric pain (i.e. pain consistent with acute pancreatitis)
lipase/amylase elevation >3 times the upper limit of normal
characteristic imaging features on contrast-enhanced CT, MRI, or ultrasound
ADVERTISEMENT: Supporters see fewer/no ads
Clinical presentation
Classical clinical features include 3:
acute onset of severe central epigastric pain (over 30-60 min)
poorly localized tenderness and pain
exacerbated by supine positioning
radiates through to the back in 50% of patients
Elevation of serum amylase and lipase are 90-95% specific for the diagnosis 3.
A normal amylase level (normoamylasaemia) in acute pancreatitis is well-recognized, especially when it occurs on the ground of chronic pancreatitis. A normal lipase level has also been reported (<10 case reports) but is extremely rare 16.
(Rare) signs of hemorrhage on the physical exam include:
Cullen sign: periumbilical bruising
Grey-Turner sign: flank bruising
Pathology
There continues to be debate over the precipitating factor leading to acute pancreatitis, with duct occlusion being an important factor, but neither necessary nor sufficient.
Mechanism notwithstanding, activation of pancreatic enzymes within the pancreas rather than the bowel leads to inflammation of the pancreatic tissue, disruption of small pancreatic ducts, and leakage of pancreatic secretions. Because the pancreas lacks a capsule, the pancreatic juices have ready access to surrounding tissues. Pancreatic enzymes digest fascial layers, spreading the inflammatory process to multiple anatomic compartments.
Etiology
gallstone passage/impaction: most common cause of acute pancreatitis (up to 15% develo
Portal hypertension occurs when pressure in the portal venous system rises, usually due to liver cirrhosis or scarring impeding blood flow into the liver. Ultrasound can detect signs of portal hypertension like ascites, splenomegaly, dilated portal veins and collateral vessels that form around the liver. Specific findings include thrombosed or narrowed portal veins, enlarged arteries supplying the liver, and reversed blood flow away from the liver.
Blood supply and lymphatic drainage of stomachMonitoshPaul
The document summarizes the blood supply and lymphatic drainage of the stomach. It discusses the arterial supply from branches like the left gastric, right gastric, and gastroepiploic arteries. It also discusses the venous drainage which parallels the arterial supply. The lymphatic drainage is described through 4 zones that primarily drain to the celiac nodes. The document provides surgical importance for preserving certain vessels and ligating others in procedures like gastrectomy and splenectomy.
The liver, gallbladder, and bile ducts make up the hepatobiliary system. The liver is the largest organ located in the right upper abdomen. It has two surfaces and receives 80% of its blood supply from the portal vein. The gallbladder stores and concentrates bile before it is released into the small intestine. Bile ducts drain bile from the liver and gallbladder and include the right and left hepatic ducts which join to form the common hepatic duct and eventually the common bile duct. Variations can occur in the anatomy of these structures. Ultrasound is useful for evaluating the normal anatomy and identifying any abnormalities.
Ultrasound is useful for evaluating the pancreas and detecting complications of acute and chronic pancreatitis. In acute pancreatitis, ultrasound can identify changes in the pancreas such as areas of hypoechogenicity and peripancreatic inflammation. Complications like pseudocysts and vascular thromboses are also detectable. Chronic pancreatitis is characterized on ultrasound by ductal dilatation, calcifications, and changes in pancreatic echotexture. Differentiating chronic pancreatitis from pancreatic cancer can be challenging. CT or MRI may be needed when ultrasound findings are inconclusive or to further evaluate necrosis in acute pancreatitis.
The portal vein is formed by the superior mesenteric and splenic veins. It drains blood from the intestines, pancreas, colon and rectum. Blood from the portal and hepatic arteries mixes in the liver sinusoids before draining into the hepatic vein and inferior vena cava. Portal hypertension occurs when pressure increases due to increased resistance in the liver from cirrhosis and increased blood flow. It can cause ascites, variceal bleeding, and other complications.
The document provides an overview of sonography of the liver. It discusses liver anatomy, development, lobes and surfaces. It describes the vascular supply including the portal vein and hepatic arteries. Common congenital abnormalities are mentioned such as hepatic cysts, peribiliary cysts, and polycystic liver disease. Imaging findings for these abnormalities on ultrasound are summarized. The document also briefly covers blood supply, nerve supply, lymphatic drainage and Couinaud liver segmentation.
Blood supply and venous drainage of the gastro-intestinal tract and livermeducationdotnet
This document summarizes the blood supply and venous drainage of the gastrointestinal tract and liver. It describes the arterial blood supply from the celiac artery, superior mesenteric artery, and inferior mesenteric artery. It details the embryonic development of the foregut, midgut, and hindgut. It also outlines the venous drainage pattern, with veins generally following the arterial supply and draining via the portal vein to the liver.
Portal hypertension occurs when there is increased resistance to blood flow through the portal vein, causing elevated pressure. It is defined as a hepatic venous pressure gradient over 5 mmHg. Measurement involves catheterization of the hepatic vein. Causes include cirrhosis and other liver diseases. Complications include variceal bleeding, ascites, and encephalopathy. Treatment of acute bleeding involves vasoactive drugs, endoscopic therapy, and TIPS. Secondary prevention uses beta-blockers to reduce portal pressure and risk of rebleeding.
D-Transposition, also known as dextro-Transposition of the great arteries (d-TGA), is a congenital heart defect where the ventricles are connected to the wrong great arteries. Specifically, the aorta arises from the right ventricle while the pulmonary artery arises from the left ventricle. This causes two parallel circulations instead of the normal series circulation. The basic embryological defect is abnormal development of the conus, which prevents normal septal formation between the great arteries. Untreated d-TGA is fatal in infancy due to lack of oxygenated blood to the body. Clinical presentation depends on the degree of mixing between the circulations.
Role of Doppler in Liver Cirrhosis & Portal Hypertensionnishit viradia
Doppler ultrasound is useful for assessing portal hypertension and liver cirrhosis. Key findings include increased portal vein diameter (>13mm), decreased increase in splenic or portal vein diameter with respiration, reversed or biphasic portal flow, increased hepatic artery flow and resistive index, altered hepatic vein waveforms, splenomegaly (>13cm), and presence of portosystemic collateral veins. Together these Doppler ultrasound metrics can diagnose and characterize portal hypertension noninvasively.
The azygos vein connects the inferior vena cava and the superior vena cava
The thoracic duct is the largest lymph vessel that ultimately drains lymph from all parts of the body into the blood circulation
We shall look at them one at a time
This document discusses liver anatomy, function tests, and imaging. It covers the embryological development of the liver, its lobes and ligament attachments. It describes the dual blood supply, biliary drainage system, and microscopic anatomy. Common liver function tests are outlined including those assessing synthesis, damage, and detoxification. Ultrasound imaging of the liver is also summarized, noting its advantages of being inexpensive and non-invasive but limitations in imaging certain areas.
The liver is the largest organ in the body, located in the right upper quadrant. It has two lobes and is supplied by branches of the hepatic artery and portal vein. Blood drains from the liver through the hepatic veins into the inferior vena cava. The liver has many functions including bile production and detoxification. Tests of liver function include bilirubin, alkaline phosphatase, and transaminases. Imaging of the liver includes ultrasound, CT, MRI, angiography, and nuclear medicine scans to evaluate blood flow, tumors, cysts, and other abnormalities. Biopsies and endoscopic procedures help diagnose and treat conditions of the liver and biliary tract.
The liver is the largest organ in the body, located in the right upper quadrant. It has two lobes and is supplied by branches of the hepatic artery and portal vein. Blood drains from the liver through the hepatic veins into the inferior vena cava. The liver has many functions including producing bile and metabolizing nutrients, toxins, and drugs. There are various imaging modalities used to examine the liver such as ultrasound, CT, MRI, angiography, and nuclear medicine scans which help identify abnormalities in liver structure, blood flow, and function. Biopsy may also be performed to obtain tissue samples for analysis.
The document discusses portal hypertension in children. It covers the anatomy of the portal system, causes/classifications of portal hypertension, clinical manifestations, diagnosis, and treatment. Regarding diagnosis, it describes using endoscopy to identify varices, ultrasound to detect portal vein thrombosis, and CT/MRI/venography to further evaluate vascular anatomy. Treatment of acute variceal bleeding involves stabilizing the patient and reducing portal pressure to stop bleeding.
Imaging and intervention in hemetemesisSindhu Gowdar
This document discusses various imaging modalities for evaluating gastrointestinal bleeding, including hematemesis. It provides details on angiography, computed tomography angiography, and endoscopy. The key points are:
- Endoscopy is the primary initial investigation but additional techniques like CT angiography and catheter angiography may be needed when endoscopy is negative or fails to identify the bleeding source.
- CT angiography has advantages over catheter angiography as it is more widely available, non-invasive, and allows detection of bleeding sources throughout the GI tract.
- Both endoscopy and CT angiography play important roles in evaluating GI bleeding, with endoscopy also allowing for therapeutic interventions when a source is identified.
This document provides information on portal hypertension, including:
1. It defines portal hypertension and describes types such as cirrhotic and non-cirrhotic portal hypertension.
2. It outlines the portal venous system and portosystemic circulation.
3. It discusses causes, clinical features, investigations, and management of portal hypertension including pharmacotherapy, endoscopic therapy, TIPS procedure, and surgeries.
4. Prevention of recurrent variceal hemorrhage is highlighted through long-term pharmacotherapy, endoscopic therapy, interventional procedures like TIPS, or surgical shunts if other options fail.
brief lecture notes for 5th sem MBBS, on portal hypertension and varices. Introduction to portal hypertension and esophageal and gastric varices and management of variceal bleeding.
Sonological features of Pancreatitis.pptxvinodkrish2
MENURadiopaedia.org
SEARCH
ARTICLES
CASES
COURSES
LOG IN
REGISTER NOW
ADVERTISEMENT: Supporters see fewer/no ads
Acute pancreatitis
Last revised by Rohit Sharma on 27 Sep 2023
Citation, DOI, disclosures and article data
Acute pancreatitis (plural: pancreatitides) is an acute inflammation of the pancreas and potentially life-threatening.
On this page:
Article:
Terminology
Epidemiology
Diagnosis
Clinical presentation
Pathology
Radiographic features
Treatment and prognosis
Differential diagnosis
See also
Related articles
References
Images:
Cases and figures
Terminology
Two subtypes of acute pancreatitis are described in the Revised Atlanta Classification 1:
interstitial edematous pancreatitis
the vast majority (90-95%)
most often referred to simply as "acute pancreatitis" or "uncomplicated pancreatitis"
necrotizing pancreatitis
necrosis develops within the pancreas and/or peripancreatic tissue
Epidemiology
The demographics of patients affected by acute pancreatitis reflect the underlying cause, of which there are many (see Pathology below).
Diagnosis
The diagnosis of acute pancreatitis is usually based on clinical criteria or a combination of clinical and radiographic features 1.
Diagnostic criteria
Two of the following three criteria are required for the diagnosis 1:
acute onset of persistent, severe epigastric pain (i.e. pain consistent with acute pancreatitis)
lipase/amylase elevation >3 times the upper limit of normal
characteristic imaging features on contrast-enhanced CT, MRI, or ultrasound
ADVERTISEMENT: Supporters see fewer/no ads
Clinical presentation
Classical clinical features include 3:
acute onset of severe central epigastric pain (over 30-60 min)
poorly localized tenderness and pain
exacerbated by supine positioning
radiates through to the back in 50% of patients
Elevation of serum amylase and lipase are 90-95% specific for the diagnosis 3.
A normal amylase level (normoamylasaemia) in acute pancreatitis is well-recognized, especially when it occurs on the ground of chronic pancreatitis. A normal lipase level has also been reported (<10 case reports) but is extremely rare 16.
(Rare) signs of hemorrhage on the physical exam include:
Cullen sign: periumbilical bruising
Grey-Turner sign: flank bruising
Pathology
There continues to be debate over the precipitating factor leading to acute pancreatitis, with duct occlusion being an important factor, but neither necessary nor sufficient.
Mechanism notwithstanding, activation of pancreatic enzymes within the pancreas rather than the bowel leads to inflammation of the pancreatic tissue, disruption of small pancreatic ducts, and leakage of pancreatic secretions. Because the pancreas lacks a capsule, the pancreatic juices have ready access to surrounding tissues. Pancreatic enzymes digest fascial layers, spreading the inflammatory process to multiple anatomic compartments.
Etiology
gallstone passage/impaction: most common cause of acute pancreatitis (up to 15% develo
Portal hypertension occurs when pressure in the portal venous system rises, usually due to liver cirrhosis or scarring impeding blood flow into the liver. Ultrasound can detect signs of portal hypertension like ascites, splenomegaly, dilated portal veins and collateral vessels that form around the liver. Specific findings include thrombosed or narrowed portal veins, enlarged arteries supplying the liver, and reversed blood flow away from the liver.
Blood supply and lymphatic drainage of stomachMonitoshPaul
The document summarizes the blood supply and lymphatic drainage of the stomach. It discusses the arterial supply from branches like the left gastric, right gastric, and gastroepiploic arteries. It also discusses the venous drainage which parallels the arterial supply. The lymphatic drainage is described through 4 zones that primarily drain to the celiac nodes. The document provides surgical importance for preserving certain vessels and ligating others in procedures like gastrectomy and splenectomy.
The liver, gallbladder, and bile ducts make up the hepatobiliary system. The liver is the largest organ located in the right upper abdomen. It has two surfaces and receives 80% of its blood supply from the portal vein. The gallbladder stores and concentrates bile before it is released into the small intestine. Bile ducts drain bile from the liver and gallbladder and include the right and left hepatic ducts which join to form the common hepatic duct and eventually the common bile duct. Variations can occur in the anatomy of these structures. Ultrasound is useful for evaluating the normal anatomy and identifying any abnormalities.
Ultrasound is useful for evaluating the pancreas and detecting complications of acute and chronic pancreatitis. In acute pancreatitis, ultrasound can identify changes in the pancreas such as areas of hypoechogenicity and peripancreatic inflammation. Complications like pseudocysts and vascular thromboses are also detectable. Chronic pancreatitis is characterized on ultrasound by ductal dilatation, calcifications, and changes in pancreatic echotexture. Differentiating chronic pancreatitis from pancreatic cancer can be challenging. CT or MRI may be needed when ultrasound findings are inconclusive or to further evaluate necrosis in acute pancreatitis.
The portal vein is formed by the superior mesenteric and splenic veins. It drains blood from the intestines, pancreas, colon and rectum. Blood from the portal and hepatic arteries mixes in the liver sinusoids before draining into the hepatic vein and inferior vena cava. Portal hypertension occurs when pressure increases due to increased resistance in the liver from cirrhosis and increased blood flow. It can cause ascites, variceal bleeding, and other complications.
The document provides an overview of sonography of the liver. It discusses liver anatomy, development, lobes and surfaces. It describes the vascular supply including the portal vein and hepatic arteries. Common congenital abnormalities are mentioned such as hepatic cysts, peribiliary cysts, and polycystic liver disease. Imaging findings for these abnormalities on ultrasound are summarized. The document also briefly covers blood supply, nerve supply, lymphatic drainage and Couinaud liver segmentation.
Blood supply and venous drainage of the gastro-intestinal tract and livermeducationdotnet
This document summarizes the blood supply and venous drainage of the gastrointestinal tract and liver. It describes the arterial blood supply from the celiac artery, superior mesenteric artery, and inferior mesenteric artery. It details the embryonic development of the foregut, midgut, and hindgut. It also outlines the venous drainage pattern, with veins generally following the arterial supply and draining via the portal vein to the liver.
Portal hypertension occurs when there is increased resistance to blood flow through the portal vein, causing elevated pressure. It is defined as a hepatic venous pressure gradient over 5 mmHg. Measurement involves catheterization of the hepatic vein. Causes include cirrhosis and other liver diseases. Complications include variceal bleeding, ascites, and encephalopathy. Treatment of acute bleeding involves vasoactive drugs, endoscopic therapy, and TIPS. Secondary prevention uses beta-blockers to reduce portal pressure and risk of rebleeding.
D-Transposition, also known as dextro-Transposition of the great arteries (d-TGA), is a congenital heart defect where the ventricles are connected to the wrong great arteries. Specifically, the aorta arises from the right ventricle while the pulmonary artery arises from the left ventricle. This causes two parallel circulations instead of the normal series circulation. The basic embryological defect is abnormal development of the conus, which prevents normal septal formation between the great arteries. Untreated d-TGA is fatal in infancy due to lack of oxygenated blood to the body. Clinical presentation depends on the degree of mixing between the circulations.
Role of Doppler in Liver Cirrhosis & Portal Hypertensionnishit viradia
Doppler ultrasound is useful for assessing portal hypertension and liver cirrhosis. Key findings include increased portal vein diameter (>13mm), decreased increase in splenic or portal vein diameter with respiration, reversed or biphasic portal flow, increased hepatic artery flow and resistive index, altered hepatic vein waveforms, splenomegaly (>13cm), and presence of portosystemic collateral veins. Together these Doppler ultrasound metrics can diagnose and characterize portal hypertension noninvasively.
TOPIC OF DISCUSSION: CENTRIFUGATION SLIDESHARE.pptxshubhijain836
Centrifugation is a powerful technique used in laboratories to separate components of a heterogeneous mixture based on their density. This process utilizes centrifugal force to rapidly spin samples, causing denser particles to migrate outward more quickly than lighter ones. As a result, distinct layers form within the sample tube, allowing for easy isolation and purification of target substances.
Anti-Universe And Emergent Gravity and the Dark UniverseSérgio Sacani
Recent theoretical progress indicates that spacetime and gravity emerge together from the entanglement structure of an underlying microscopic theory. These ideas are best understood in Anti-de Sitter space, where they rely on the area law for entanglement entropy. The extension to de Sitter space requires taking into account the entropy and temperature associated with the cosmological horizon. Using insights from string theory, black hole physics and quantum information theory we argue that the positive dark energy leads to a thermal volume law contribution to the entropy that overtakes the area law precisely at the cosmological horizon. Due to the competition between area and volume law entanglement the microscopic de Sitter states do not thermalise at sub-Hubble scales: they exhibit memory effects in the form of an entropy displacement caused by matter. The emergent laws of gravity contain an additional ‘dark’ gravitational force describing the ‘elastic’ response due to the entropy displacement. We derive an estimate of the strength of this extra force in terms of the baryonic mass, Newton’s constant and the Hubble acceleration scale a0 = cH0, and provide evidence for the fact that this additional ‘dark gravity force’ explains the observed phenomena in galaxies and clusters currently attributed to dark matter.
Embracing Deep Variability For Reproducibility and Replicability
Abstract: Reproducibility (aka determinism in some cases) constitutes a fundamental aspect in various fields of computer science, such as floating-point computations in numerical analysis and simulation, concurrency models in parallelism, reproducible builds for third parties integration and packaging, and containerization for execution environments. These concepts, while pervasive across diverse concerns, often exhibit intricate inter-dependencies, making it challenging to achieve a comprehensive understanding. In this short and vision paper we delve into the application of software engineering techniques, specifically variability management, to systematically identify and explicit points of variability that may give rise to reproducibility issues (eg language, libraries, compiler, virtual machine, OS, environment variables, etc). The primary objectives are: i) gaining insights into the variability layers and their possible interactions, ii) capturing and documenting configurations for the sake of reproducibility, and iii) exploring diverse configurations to replicate, and hence validate and ensure the robustness of results. By adopting these methodologies, we aim to address the complexities associated with reproducibility and replicability in modern software systems and environments, facilitating a more comprehensive and nuanced perspective on these critical aspects.
https://hal.science/hal-04582287
BIRDS DIVERSITY OF SOOTEA BISWANATH ASSAM.ppt.pptxgoluk9330
Ahota Beel, nestled in Sootea Biswanath Assam , is celebrated for its extraordinary diversity of bird species. This wetland sanctuary supports a myriad of avian residents and migrants alike. Visitors can admire the elegant flights of migratory species such as the Northern Pintail and Eurasian Wigeon, alongside resident birds including the Asian Openbill and Pheasant-tailed Jacana. With its tranquil scenery and varied habitats, Ahota Beel offers a perfect haven for birdwatchers to appreciate and study the vibrant birdlife that thrives in this natural refuge.
Sexuality - Issues, Attitude and Behaviour - Applied Social Psychology - Psyc...PsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
Compositions of iron-meteorite parent bodies constrainthe structure of the pr...Sérgio Sacani
Magmatic iron-meteorite parent bodies are the earliest planetesimals in the Solar System,and they preserve information about conditions and planet-forming processes in thesolar nebula. In this study, we include comprehensive elemental compositions andfractional-crystallization modeling for iron meteorites from the cores of five differenti-ated asteroids from the inner Solar System. Together with previous results of metalliccores from the outer Solar System, we conclude that asteroidal cores from the outerSolar System have smaller sizes, elevated siderophile-element abundances, and simplercrystallization processes than those from the inner Solar System. These differences arerelated to the formation locations of the parent asteroids because the solar protoplane-tary disk varied in redox conditions, elemental distributions, and dynamics at differentheliocentric distances. Using highly siderophile-element data from iron meteorites, wereconstruct the distribution of calcium-aluminum-rich inclusions (CAIs) across theprotoplanetary disk within the first million years of Solar-System history. CAIs, the firstsolids to condense in the Solar System, formed close to the Sun. They were, however,concentrated within the outer disk and depleted within the inner disk. Future modelsof the structure and evolution of the protoplanetary disk should account for this dis-tribution pattern of CAIs.
Candidate young stellar objects in the S-cluster: Kinematic analysis of a sub...Sérgio Sacani
Context. The observation of several L-band emission sources in the S cluster has led to a rich discussion of their nature. However, a definitive answer to the classification of the dusty objects requires an explanation for the detection of compact Doppler-shifted Brγ emission. The ionized hydrogen in combination with the observation of mid-infrared L-band continuum emission suggests that most of these sources are embedded in a dusty envelope. These embedded sources are part of the S-cluster, and their relationship to the S-stars is still under debate. To date, the question of the origin of these two populations has been vague, although all explanations favor migration processes for the individual cluster members. Aims. This work revisits the S-cluster and its dusty members orbiting the supermassive black hole SgrA* on bound Keplerian orbits from a kinematic perspective. The aim is to explore the Keplerian parameters for patterns that might imply a nonrandom distribution of the sample. Additionally, various analytical aspects are considered to address the nature of the dusty sources. Methods. Based on the photometric analysis, we estimated the individual H−K and K−L colors for the source sample and compared the results to known cluster members. The classification revealed a noticeable contrast between the S-stars and the dusty sources. To fit the flux-density distribution, we utilized the radiative transfer code HYPERION and implemented a young stellar object Class I model. We obtained the position angle from the Keplerian fit results; additionally, we analyzed the distribution of the inclinations and the longitudes of the ascending node. Results. The colors of the dusty sources suggest a stellar nature consistent with the spectral energy distribution in the near and midinfrared domains. Furthermore, the evaporation timescales of dusty and gaseous clumps in the vicinity of SgrA* are much shorter ( 2yr) than the epochs covered by the observations (≈15yr). In addition to the strong evidence for the stellar classification of the D-sources, we also find a clear disk-like pattern following the arrangements of S-stars proposed in the literature. Furthermore, we find a global intrinsic inclination for all dusty sources of 60 ± 20◦, implying a common formation process. Conclusions. The pattern of the dusty sources manifested in the distribution of the position angles, inclinations, and longitudes of the ascending node strongly suggests two different scenarios: the main-sequence stars and the dusty stellar S-cluster sources share a common formation history or migrated with a similar formation channel in the vicinity of SgrA*. Alternatively, the gravitational influence of SgrA* in combination with a massive perturber, such as a putative intermediate mass black hole in the IRS 13 cluster, forces the dusty objects and S-stars to follow a particular orbital arrangement. Key words. stars: black holes– stars: formation– Galaxy: center– galaxies: star formation
SDSS1335+0728: The awakening of a ∼ 106M⊙ black hole⋆Sérgio Sacani
Context. The early-type galaxy SDSS J133519.91+072807.4 (hereafter SDSS1335+0728), which had exhibited no prior optical variations during the preceding two decades, began showing significant nuclear variability in the Zwicky Transient Facility (ZTF) alert stream from December 2019 (as ZTF19acnskyy). This variability behaviour, coupled with the host-galaxy properties, suggests that SDSS1335+0728 hosts a ∼ 106M⊙ black hole (BH) that is currently in the process of ‘turning on’. Aims. We present a multi-wavelength photometric analysis and spectroscopic follow-up performed with the aim of better understanding the origin of the nuclear variations detected in SDSS1335+0728. Methods. We used archival photometry (from WISE, 2MASS, SDSS, GALEX, eROSITA) and spectroscopic data (from SDSS and LAMOST) to study the state of SDSS1335+0728 prior to December 2019, and new observations from Swift, SOAR/Goodman, VLT/X-shooter, and Keck/LRIS taken after its turn-on to characterise its current state. We analysed the variability of SDSS1335+0728 in the X-ray/UV/optical/mid-infrared range, modelled its spectral energy distribution prior to and after December 2019, and studied the evolution of its UV/optical spectra. Results. From our multi-wavelength photometric analysis, we find that: (a) since 2021, the UV flux (from Swift/UVOT observations) is four times brighter than the flux reported by GALEX in 2004; (b) since June 2022, the mid-infrared flux has risen more than two times, and the W1−W2 WISE colour has become redder; and (c) since February 2024, the source has begun showing X-ray emission. From our spectroscopic follow-up, we see that (i) the narrow emission line ratios are now consistent with a more energetic ionising continuum; (ii) broad emission lines are not detected; and (iii) the [OIII] line increased its flux ∼ 3.6 years after the first ZTF alert, which implies a relatively compact narrow-line-emitting region. Conclusions. We conclude that the variations observed in SDSS1335+0728 could be either explained by a ∼ 106M⊙ AGN that is just turning on or by an exotic tidal disruption event (TDE). If the former is true, SDSS1335+0728 is one of the strongest cases of an AGNobserved in the process of activating. If the latter were found to be the case, it would correspond to the longest and faintest TDE ever observed (or another class of still unknown nuclear transient). Future observations of SDSS1335+0728 are crucial to further understand its behaviour. Key words. galaxies: active– accretion, accretion discs– galaxies: individual: SDSS J133519.91+072807.4
2. • Presence of portosystemic collateral veins
(PSCV) is common in portal hypertension due to
cirrhosis.
• Physiologically, normal portosystemic
anastomoses exist which exhibit hepatofugal
flow.
• With the development of portal hypertension,
transmission of backpressure leads to increased
flow in these patent normal portosystemic
anastomoses.
• In extrahepatic portal vein obstruction collateral
circulation develops in a hepatopetal direction
and portoportal pathways are frequently found.
• The objective is to illustrate the various PSCV
3. • When blood flow through a vessel or a vascular
bed is obstructed due to occlusion, as in EHPVO,
or distortion, as in liver cirrhosis
• Collateral pathways open up as blood bypasses
the occlusion or obstruction
• Always flowing down a pressure gradient from a
high pressure to a low-pressure vessel or bed.
• The formation of portosystemic pathways occurs
due to reopening of collapsed embryonic
channels or reversal of the flow within existing
adult veins.
4.
5. • The left gastric vein (LGV) anastomoses with the
esophageal veins, which in turn drain into the
azygos vein (AV).
• The superior rectal vein (SRV) anastomoses with
the middle and inferior rectal veins (IRV), which are,
respectively, tributaries of the internal iliac and the
pudendal veins.
• The paraumbilical vein (PUV) anastomoses with
subcutaneous veins in the anterior abdominal wall.
NORMAL PORTOSYSTEMIC ANASTOMOSE
6. • In the retroperitoneal region, tributaries of the
splenic and pancreatic veins anastomose with the
left renal vein.
• Short veins also connect the splenic and colic veins
to the lumbar veins of the posterior abdominalwall.
• The veins of the bare area of the liver also
communicate with those of the diaphragm, as well
as the right internal thoracic vein.
8. bare area of the
liver
diaphragm, aswell
asthe right internal
thoracic vein
Tributaries of the
splenic and
pancreatic veins
left
renal vein
9. THE DIRECTION OF COLLATERAL FLO
• When vascular obstruction is intrahepatic,
collateral vessels drain away from the liver
(hepatofugal collateral circulation).
• When the obstruction is extrahepatic, the
collateral circulation usually develops toward the
portal vein beyond the site of obstruction and thus
drains toward the liver
(hepatopetal collateral circulation).
10. • There are intraepithelial channels, a superficial
venous plexus and deep submucosal and
adventitial veins.
• In addition, perforating veins connect the
adventitial and deep submucosal veins.
• Backpressure transmitted through the tributaries
of the portal vein results in the engorgement of
the collaterals outside the gut wall in a
paraesophageal, para-gastric para-rectal or
paracholedochal location.
• The backwaters of the gut wall results in the
formation of varices in a submucosal or subepithelial
location.
ORDER OF APPEARANCE OF COLLAT
11. • In patients with oesophageal varices dilated deep
intrinsic veins displace the superficial venous
plexus, assume a subepithelial position.
• And are easily seen on endoscopy as the red
color sign on varices i.e. telangiectasiae, cherry
red spots, hemocystic spots and red wale
markings or as the varices themselves.
• Veins on the mucosal aspect can cause gastrointestinal
luminal bleeding and those outside the wall may cause
extraluminal i.e. pleural or peritoneal bleeding.
• Submucous veins are the first sites of ‘bloodlogging’
and become varicose before those upon the outer
surface of esophagus in portal hypertension.
12. The varices
outside the
wall are called
para-in location
and varices
adjacent to the
muscular layer are
called peri-in
location.
The hematocystic
spots represent focal
weakness on the
varicea lwall.
13. CLASSIFICATIONOFCOLLATERAL
PATHWAYS
• Simplest classification of PSCVputs
esophagogastric varices into one group andall
other varices asectopic varices.
• Someauthors describe PSCVaccording to
their drainage into either the superior vena
cava(SVC)or the inferior vena cava(IVC)
14. CollateralVesselsDraininginto the SuperiorVenaCava
• left gastricveinlarger than 5–6 mm in diameter at
Doppler ultrasonography is considered abnormal and is
an indicator of portal hypertension
• Shortgastricveinscourse along the lateral aspect of the
gastric wall and descendalong the medial aspectof the
spleen . These veins drain the gastric fundus and the left
side of the greater curvature .
• Dilated short gastric veins appear asacomplextangle of
vessels in theregion ofthesplenichilum
• EsophagealandParaesophagealVarices-Thesevarices are
supplied primarily by the left gastric vein , which divides
into anterior and posterior branches. Theanterior
branch supplies the esophagealvarices,and the
posterior branch forms the paraesophagealvarices.
15. CollateralVesselsDrainingintotheIVC
• Splenorenal and Gastrorenal Shunts- The splenoportal
vein axis and the left renal vein communicate through
the coronary vein, short gastric vein (gastrorenal shunt),
or other veins that normally drain into the splenic vein
(splenorenal shunt)
• Splenorenal or gastrorenal shunts are seen aslarge,
tortuous veins in the region of the splenic and left renal
hila and drain into an enlarged left renal vein.
• Paraumbilical Veinand Abdominal Wall Veins-The umbilical
vein never opens after closure . Rather, patent portal veins
in the ligamentum teres and falciform ligament are actually
enlarged paraumbilical veins.
16. • Paraumbilical vessels may anastomose with the superior
epigastric or internal thoracic veins and drain into the
superior vena.
• Mesenteric collateral vesselsusually appear asdilated and
tortuous branches of the superior mesenteric veinwithin
the mesenteric fat.
• Mesenteric collateral vessels may arise from the superior
and inferior mesenteric veins and may ultimately drain
into the systemic venous system via the retroperitoneal
or pelvic veins .
17. • Aretroperitoneal shunt maybepresent between the
mesenteric vesselsandthe renal vein or inferior venacava.
• Retroperitoneal varicesinclude various pathways between
the intestinal or retroperitoneal tributaries of the superior
or inferior mesenteric veinsandsystemicveins.
• Their communications with the inferior venacavaareknown
as the veinsof Retzius.
18. ESOPHAGEAL VARICES
• VenousDrainageof Esophagus
• eightto ten veins,whichdrainfrom right border of
esophagusto join the medialaspectof AV
• veinson left sideof esophagusdraininto
hemiazygosveins.
19. venousdrainageof abdominal esophagus
• predominantlyto the left gastricvein (LGV)atributary of
the portal venoussystem
• LGVhastwo branches- Theanterior branch of LGVdrains
the cardiacregion andthe posterior branch terminates
by joining the AV
.
• Paraesophagealveinsarepresent on the sideof
esophagus andareconnected with the posterior branch
of the LGV
.
20. • TheAfferent to EsophagealVarices
• LGVisthe afferent to esophagealvarices(EV)
• TheEfferentfromEsophagealVarices
• In 78%of cases,the LGVconnectsto the AVesophagealand
para-esophagealvarices.
21.
22. • VenousDrainageof Stomach
• Gastric varices (GV) are generally defined as cardiac or
fundic according to their location. This location is
consistent with the boundary line of portosystemic
shunting.
• Thisareaof shunting ismainly in posteriorwall of the cardiac
or the fundic area, which isfixed to the retroperitoneum
and isthe closest site to the systemiccirculation.
• Isolated GVare related to gastroepiploic (GEV)veinsand
are located in bodyofstomach
GASTRIC VARICES
23. • Stomachdrainseither directly orindirectlyintothe portalvein
asfollows
• Short gastric veinsdrain from the fundus to the splenic vein
• Left gastroepiploic vein (LGEV)movesalong greater
curvature to splenic vein
• Rightgastroepiploic (RGEV)movesfrom the right end of
greater curvature to superior mesentericvein
• Left gastric vein movesfrom the lessercurvature of the
stomach to the portalvein
• Rightgastric vein movesfrom the lessercurvature ofthe
stomach to the portalvein
24. portal and systemic venous
pathways that are potentially
involved in gastric varices.ADV
=adrenal vein, AZV=azygos
vein, EV=esophageal vein,
HAZV=hemiazygos vein, ICV=
intercostal vein, ITV=internal
thoracic vein, LGV=left gastric
vein, LIPV=left IPV,LRV=left
renal vein, PGV=posterior
gastric vein, PPV=
pericardiophrenic vein, RIPV=
right IPV,SGV=short gastric
vein, 1 =precaval interphrenic
anastomotic vein, 2 =
anastomotic vein to the renal
capsular vein and adrenal vein,
3 =paravertebral anastomotic
veins, * =termination of the
LIPVinto the inferior venacava
(IVC),* =termination of the
LIPVinto the left renalvein.
25. Afferents to GastricVarices
• leftgastric vein - Thesecardiac varices are
contiguous with submucosal varices of thelower
part of theesophagus
• short gastric veins - course along the greater
curvature on the medial side of the spleen to
empty into the splenicvein
• posterior gastric vein - localized between theleft
and short gastric veins, which runs superiorly in
the retroperitoneum and gastrophrenicligament
and joins GV
26. Efferents from GastricVarices
• Gastric varices drain into the systemic vein via the esophageal-
paraesophageal varices (gastroesophageal venous system), the
inferior phrenic vein (IPV) (gastrophrenic venous system).
• The left IPVterminates either (a) inferiorly into the left renal
vein (forming a gastrorenal shunt)
• Majority of GVform the gastrorenal shunt (80–85% ofcases)
while 10–15% form the gastrocaval shunt.
27. • The gastrorenal shuntis formed mainly by lower branch of
inferior phrenic vein, which can open into the renal vein
directly (spleno-gastro-phreno-renal shunt) or via left
adrenal vein.
28. Afferents to gastric
varices. Theafferents to
GVcome from left
gastric vein, shortgastric
veins and posterior gastric
vein the left gastric
vein mainly contributes to
formation of cardiac
varices whereas the short
gastric vein and posterior
gastric vein contribute to
formation of fundal
varices. Isolated gastric
varices are more likely to
be related to
gastroepiploeic
veins
29. • GOVsdraining via the
gastroesophagealvenous
system.Thegastric varices
(GV)aresupplied bythe
left gastric vein (LGV)and
drain via the esophageal
varices(EV) andazygosand
hemiazygosveins (AZV and
HAZV)into the superior
venacava(SVC). Redline
with arrowheads
=blood flow from theleft
gastric vein through the
gastroesophagealvarices
into the azygosvein
30. • IGVsdraining viathe
gastrophrenic venous
system.Gastric varices (GV)
aresuppliedbythe
posterior gastric vein (PGV)
andthe short gastric vein
(SGV),which drain viathe IPV
into the left renal vein (LRV)
(forming agastrorenal shunt
[GRS])or IVC(gastrocaval
shunt [GCS]).Redlines with
arrowheads =blood flow
from the posterior and
short gastric veins through
the gastric varicesinto the
gastrorenaland gastrocaval
shunts.PPV
=pericardiophrenic
vein.
32. contrast- enhanced CTimage shows gastric
varices (GV) draining through the multiple
channels of agastrorenal shunt (arrows) into
the left renalvein
Coronal contrast-enhanced CTimage
shows the varices (arrows) draining
through agastrorenal shunt (arrowheads)
into the left renal vein(LRV).
33. PericardiophrenicVein
• Theleft pericardiophrenic vein anastomoseswith the
left IPVat the cardiacapex.
• It runs superiorly alongthe pericardium andin the left
superior mediastinum, then terminates into the left
brachiocephalic vein.
• Theleft pericardiophrenic vein isoften seenwith a
gastrorenalshunt at multidetector CTasanaccessory
drainageveinfrom gastric varices.
• In afew cases(5%),it canserveasa main drainageroute of
gastricvarices
34. Gastric varices with accessory drainage via the
pericardiophrenic vein in apatient with liver
cirrhosis. Coronal contrast-enhanced MIP CTimage
shows gastric varices (GV)draining via a
gastrorenal shunt (black arrows) and the
pericardiophrenic vein (white arrows). LRV=left
renalvein.
Coronal contrast-enhanced CTimage
shows gastric varices (GV) draining mainly
via the leftIPV (arrowheads) and the
pericardiophrenic vein (arrows) into the
left innominatevein.
35. • VenousDrainageof Duodenum
• Four small pancreatico duodenal veins drain the head ofthe
pancreasand the adjacent secondand third portions of the
duodenum.
• Thefour veins regularly form ananterior and sometimes a
posterior arcade through anastomosesbetween the superior
and inferior veins.
• Thepancreatico duodenal veins joins SMV.
• Thetwo major tributaries of the SMVare the gastrocolic
trunk and the first jejunal trunk which join the SMVroughly
at the samelevel but on opposite sides.
ECTOPIC VARICES IN DUODENUM
36. Afferents to DuodenalVarices
• pancreatico duodenal venous arcades,which
are in communication with portal venous
system.
37. Efferentsfrom DuodenalVarices
• Theefferents from DV
• In cirrhosis, they areformed in the descending or transverse
parts of the duodenum and flow hepatofugallyvia
retroperitoneal shunts (alsocalled veinsof Retzius)into the IVC
via the following veins:
1.Rightrenal vein (mesenterorenalshunt)
2.Lumbarveins
38. Portoportal Efferents of Duodenal
Varices
• In extrahepatic portal veinobstruction
(EHPVO)
• Efferents of DVare formed in the
duodenal bulbwhich flow
hepatopetally via portoportal
collaterals into theliver
40. paraumbilical vein (solid arrows) as it extends superiorly and inferiorly to
the anterior abdominal wall to anastomose with the superior and inferior
epigastric veins
41. Retroperitoneal shunt. (a) AxialCT
scanshows tortuous dilated
vessels(arrows) in the medial
portion of theleft
kidney. (b) Coronal MIP CT
portal venogram demonstrates
atortuous, dilated
retroperitoneal shunt (arrows)
that communicates with the
inferior vena cava(I) through
the left renal vein(R).
42. VenousDrainageof JejunoilealVarices
• Mesenteric collateral vesselsmayarise from the superior
(SMV)and inferior mesenteric veins (IMV) ultimately drain
into the IVCvia the retroperitonealor pelvic veins
• Veinsof Retziusare various veins in the dorsal wall of the
abdomen forming anastomoses between the inferior vena
cavaand the superior and inferior mesenteric veins.
• Suchanastomoses between the portal and the systemic
venous systemcanexist even under normal conditions.
ECTOPIC VARICES IN SMALL INTESTIN
43. Afferentsto JejunalandIleal Varices
• Jejunal and ileal veins (tributaries of SMV).
EfferentsfromJejunalandIleal Varices
• Small bowel varices generally drain into abdominal
wall. Theymay also drain into veins of Retzius
44. Applied Anatomyof ColonicandRectalVarices
• Colonicvarices,areusually located in the cecum,and
rectosigmoid region. Theyareoften associatedwith
cirrhosis or portal veinobstruction.
• Lesscommoncausesof colonic varicesarecongestiveheart
failure, mesenteric vein thrombosis, pancreatitis with
splenic vein thrombosis, adhesionsandmesenteric vein
compression
• Theright colon isdrained by three tributaries of SMV,
which include the ileocolic, right colic andmiddle colic
veins. Tributaries joining inferior mesenteric vein drainthe
rest of thecolon
ECTOPIC VARICES IN LARGE INTESTIN
45. Afferentsto ColonicVarices
1.Ileocolic vein
2.Right colic vein
3.Middle colic vein
4.Sigmoid colonic vein
Efferentsfrom Colonic Varices
Efferents candrain into veins of Retzius, whichinclude:
1.Right gonadalvein
2.Right renal vein
3.Systemiclumbar veins
Rectal Varices
Afferents to RectalVarices
Inferior mesenteric vein (IMV) continues asthe superior
rectal vein and acts as afferent to rectalvarices
46.
47. • Theblood from superior rectal vein goesto extrinsic rectal
venous plexus (ERVP),which lies outside rectum below the
level of peritoneal reflection.
• From the ERVPthe blood flows by perforators through the
muscularis propria into intrinsic rectal venous plexus (IRVP)
which consists of two groups of veins – the superior group
lying in the rectal submucosaand the inferior group lying in
the corresponding anal subcutaneous tissue.
• The rectal varices are formed from this superior group of
upper submucosal veins of IRVP
.
• Theinferior group of IRVPlying in the anal subcutaneous
tissue passesdown to form the inferior rectal vein and
contribute to formation of externalhaemorrhoids.
48. Efferents from RectalVarices
Fromboth ERVPandIRVPthe portal hemorrhoidal blood worksinto systemiccirculation
through two portosystemicshunts (recto genital andinter-rectal).
1.rectal venousplexuswith vesico-prostatic or vaginalvenousplexus
2.Theinter-rectal communicationsoccurbetween the three rectal
veins both in ERVPandIRVP
49. Afferents to OmentalVarices
1. Superior or inferior mesentericveins
Efferentsfrom Omental Varices
1. Theretroperitoneal or pelvicveins.
2. Omental veins may also drain into GEV
.
ECTOPIC VARICES: OMENTAL
COLLATERAL VESSELS
50. • In 1883, Sappeydescribed accessoryportal veins entering
the livercapsule from different locations.
• Thesevesselsplay arole in the origin of transhepatic
portosystemic shunts and are sometimes the only PSCV
capableof transporting portal blood into the liver in
EHPVO.
ECTOPIC VARICES: VEINS OF SAPPEY
51. • Thedifferent locationsare:
1.Upper part of falciform ligament -superior veins of Sappey,
2.Lowerpart of falciform ligament–inferior veins of Sappey
3.Ligamentumteres in the central part of falciform
ligament-the recanalized umbilical vein
4.Left triangular ligament–left inferior phrenic vein and
intercostalvein
5.Right triangular ligament–right inferior phrenicvein
6.Gastrohepatic omentum (cystic veins and branches of left
gastric veins)
7.Diaphragmatic veins (bare area of liver)
8.Ligamentum venosum–patent ductus venosusif present
52. • Theparaumbilical veinsarealsocalledinferior veinsof
Sappey.
• Theyaccompanyligamentum teres (obliterated left
umbilical vein) in the falciform ligament andconnect
superior andinferior epigastricveins in the rectus
sheathat umbilicus with left branch of portal vein
• Afferentto UmbilicalVarices
• Left branch of portal vein receivesthe umbilical and
paraumbilical veinsto form umbilical varicesby the
recanalisedligamentum teres in the falciform
ligament.
53. • EfferentsfromUmbilicalVarices
• Superior and inferior epigastric veinsare the
efferents of umbilical varices.
• Themost common path of drainage of
paraumbilical veins isthrough the inferior
epigastricveins, which follow the posterior faceof
the rectus abdominis musclesto finally reachthe
external iliac veins.
• Paraumbilical vesselsmayalsoanastomosewith
internal thoracic veinsand drain into the superior
venacava.
54. • Vesicalvarices are rare in patients withportal
hypertension becausethe bladder wall is an
unusual collateral route for the venous
splanchnic blood. Generally reported casesof
vesical varices haveahistory of abdominal
surgery.
ECTOPIC VARICES: VESICAL VARIC
55. • VenousDrainageof Vaginaand Uterus
• Theanatomyof the vaginaand uterus makesthem unlikely
locations to develop varicesasthe uterus hasanextensive
extensive venousplexus,which primarily drains into the
uterine veinsand later into the internal iliac vein (part of
systemic circulation).
• Thevaginaalsohasavenous plexus,which similarly drains
into the internal iliac vein via bilateral vaginal veins.
• The plexusesare in communication with eachother and
with thevesical and hemorrhoidal plexuses.
ECTOPIC VARICES: VAGINAL AND UTERINE
VARICES
56. Afferentto VaginalandUterine Varices
• Superior portion of the hemorrhoidalplexus
EfferentfromVaginalandUterine Varices
• Venousplexusesof uterus and vagina,internal iliac vein and
uterine veins.
57. • Gallbladder varicesarepresent in 12%of patientswith
portal hypertension but aremore frequent in those with
extrahepatic portal hypertension(30%).
• TheGBwall varicesrefer to presenceof varicesin or
outside the wall of GBin apericholecysticlocation.
• Afferentsto GallbladderVarices
• Cysticvein, branch of the right portalvein.
• EfferentsfromGallbladder Varices
• Theymaydrain to hepatic vein
ECTOPIC VARICES: GALLBLADDER VARI
58. • These collateral veins are related to 2 preformed venous
systems near the extrahepatic bile ducts: the paracholedochal
(PACD) veins of Petren, and the epicholedochal (ECD) venous
plexusof Saint.
• The PACDvenous plexus of Petren runs parallel to the CBD, and
the ECD plexus of Saint veins form a reticular mesh on the
surfaceof the CBD.
• The PACD collaterals, if dilated, may cause extrinsic
compression and protrusion into the thin and pliable CBD.
• And the ECD collaterals, if dilated, may make the normally
smooth intraluminal surface of theCBDirregular.
ECTOPIC VARICES: BILIARY VARICES
59. • Saint's anatomic studies suggestthat dilatation of the
PACDveinswill occurfirst in portal hypertension.
• PortoportalConnectionsof BiliaryVarices
• Theright-sided plexus cancommunicate with
pancreatico duodenal vein to the cystic vein.
• The left sided plexus can communicate with left and
right gastric vein (LGV and RGV) and with the left portal
vein (LPV).
• Generally the flow occurs toward the branches of portal
vein in the liver.
61. • Surgeryinvolving apposition of abdominal structures
(drained bysystemic veins) to the bowel (drained by portal
tributaries) mayresult in the formation of collaterals at
unusualsites.
• Transcapsularcollaterals are especially common in
patients whohad undergone hepatobiliary surgery and
who had chronicPVT.
• 50%of patients with surgical digestive stoma in acontext
of portal hypertension havestomal varices.
ECTOPIC VARICES: ANASTOMOTIC AND
STOMAL VARICES
62. • VenousDrainageof Diaphragm
• Superior surface of diaphragm isdrained by pericardiophrenic
and musculophrenic veins, which drain into the internal
thoracic vein.
• Inferior phrenic veinsdrain the inferior surface.
• Theright inferior phrenic vein usually opensinto the inferior
venacavawhereasthe left inferior phrenic vein joins the IVC
and or left renal or suprarenal vein.
• Cardiophrenic varicesparticularly on the right side are usually
located at acardiophrenic angle, and rupture israre.
ECTOPIC VARICES: DIAPHRAGM
64. • Theword interportal communication isdifferent from
portoportal communications.
• Theconceptual difference between portoportal and
interportal collateral isthat aportoportalcollateral will be
connectedto the portalveinonentryand/or exit .
• Whereas an interportal collateral goesfromonepart of
portalvenoussystem intoanother part of portal venous
system.
INTERPORTAL COMMUNICATIONS
65. • Interportal communication indicates flow of blood that
bypassesan obstructedsegmentof the portalvenous
system.
• Thisoccurs mainly in EHPVOwhere the collaterals havea
tendency to go toward the portal venoussystemafter
bypassing the site of obstruction.
66. COLLATERAL PATHWAYS IN BUDD–CHIARI
SYNDROME
• Three types of obstruction can occur in Budd–Chiari
syndrome(BCS) which include
• obstruction to the major hepatic veins alone (Type I)
• obstruction to the suprahepatic IVC alone (Type II)
• and combined obstruction to the major hepatic veins
and IVC (Type III)
• Development of collateral pathways depends on the
type and location of obstruction in BCS and can occur
in intra and extrahepatic locations.
67. •Twoforms of intrahepatic collaterals maydevelop:
1.Those that communicate withsystemicveinsviathe
subcapsularvessels–
• Thesubcapsularvesselsoriginate asintrahepatic collaterals
but becomeextrahepatic after goingthrough the capsule
of liver and communicatewith leftinferior phrenic vein.
2. Those that shunt blood from the occludedto the non-
occludedsegmentsof the hepatic vein.
• Intrahepatic collaterals, which remain inside liver, develop
as commashapedcollateralsbetween the adjacentright
andleft hepaticvein.