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The document discusses the proximal splenorenal shunt procedure for patients with liver cirrhosis and portal hypertension combined with hypersplenism. The procedure involves creating a shunt from the splenic vein to the left renal vein to decompress the portal system. It is indicated for select patients as an alternative to other procedures to prevent variceal bleeding while removing the spleen. However, it carries risks of hepatic encephalopathy, worsening liver function, and is not suitable for future transplantation. The authors' experience with 17 patients who underwent this procedure is presented, along with postoperative outcomes.
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Recommended
31
1) The surgical treatment of portal hypertension has evolved significantly in Egypt over the last century, driven by changes in liver pathology and the development of new techniques.
2) Initially, procedures like splenectomy were used but caused only temporary effects. Total portosystemic shunts were then introduced but were later abandoned due to high mortality and morbidity rates.
3) More selective surgeries and techniques were developed like Hassab's operation and mesocaval shunts but still had issues. The distal splenorenal shunt became more widely used as a selective shunt.
33
The document discusses various treatment options for portal hypertension and its complications. It covers surgical procedures like devascularization operations, portosystemic shunts and splenorenal shunts that are aimed at preventing bleeding, stopping active bleeding, and preventing recurrent variceal bleeding. The choice of surgical treatment depends on factors like the severity of bleeding, liver dysfunction, and type of portal hypertension.
Portal hypertension
This document provides information on portal hypertension. It begins by defining portal hypertension and describing the anatomy of the portal vein system. It then discusses the causes of portal hypertension including prehepatic causes like extrahepatic portal vein obstruction (EHPVO) and non-cirrhotic portal fibrosis (NCPF), hepatic causes like cirrhosis and posthepatic causes like sinistral portal hypertension. It describes the clinical presentation of portal hypertension including variceal bleeding. It provides details on the management of acute variceal bleeding and long term treatment options for portal hypertension including pharmacotherapy, TIPS procedure, shunt operations and liver transplantation.
Treatment of portal hypertension
The document summarizes the treatment of portal hypertension and varices. It discusses treatments for variceal bleeding, ascites, and splenomegaly. For varices, it recommends primary prophylaxis with non-selective beta-blockers for medium/large varices without prior bleeding. For acute variceal hemorrhage, it recommends pharmacologic therapy, endoscopic band ligation or sclerotherapy, balloon tamponade, and TIPS or shunt surgery as rescue therapy. It also discusses preventing recurrent bleeding with beta-blockers, repeated endoscopic therapy, and TIPS or shunt surgery.
Non cirrhotic portal fibrosis
Non Cirrhotic Portal Fibrosis (NCPF) is a syndrome of obscure etiology characterized by obliterative portovenopathy leading to portal hypertension and massive splenomegaly in young adults from low socioeconomic backgrounds. The exact cause is unknown but is hypothesized to be related to malnutrition, recurrent infections, exposure to toxins or metals. Pathology shows sclerosis of portal vein branches. Clinical features include gastrointestinal bleeding, splenomegaly, and abdominal pain. Management involves controlling acute bleeding episodes and preventing rebleeding through medications or surgery like portosystemic shunts. Prognosis is generally good if bleeding can be controlled.
Transjugular intrahepatic porto systemic shunt
A transjugular intrahepatic portosystemic shunt (TIPS) is a procedure that creates a connection between the portal and hepatic veins within the liver to decrease portal pressure. It is less invasive than surgery and used to treat complications of portal hypertension like variceal bleeding. The procedure involves placing a stent between the veins under imaging guidance. TIPS can help control bleeding, ascites, and other conditions but carries risks of infection, encephalopathy, and shunt failure over time that require monitoring.
Portal Hypertension
1. Surgery continues to play an important role in the treatment of portal hypertension, both as primary and rescue therapy in select patients.
2. For good risk cirrhotic patients with refractory variceal bleeding, surgical shunts such as distal splenorenal shunt have better long-term outcomes compared to TIPS.
3. TIPS is preferred for poor risk cirrhotic patients, while surgical shunts or devascularization remain the standard treatment for non-cirrhotic portal hypertension. Surgery is not obsolete in managing portal hypertension.
Portal hypertension surgical management
1. Portal hypertension is defined as a portal pressure higher than 5 mm Hg and can lead to variceal bleeding. It is caused by any blockage that impedes portal blood flow.
2. Complications include ascites, encephalopathy, and malnutrition indicating end-stage liver disease. Evaluation involves assessing the underlying liver disease, hepatic function, portal venous anatomy and hemodynamics.
3. Treatment options include pharmacotherapy, endoscopic therapy, TIPS procedure, and liver transplantation for eligible patients. The goal is to reduce portal pressure and prevent further bleeding events.
Recommended
31
1) The surgical treatment of portal hypertension has evolved significantly in Egypt over the last century, driven by changes in liver pathology and the development of new techniques.
2) Initially, procedures like splenectomy were used but caused only temporary effects. Total portosystemic shunts were then introduced but were later abandoned due to high mortality and morbidity rates.
3) More selective surgeries and techniques were developed like Hassab's operation and mesocaval shunts but still had issues. The distal splenorenal shunt became more widely used as a selective shunt.
33
The document discusses various treatment options for portal hypertension and its complications. It covers surgical procedures like devascularization operations, portosystemic shunts and splenorenal shunts that are aimed at preventing bleeding, stopping active bleeding, and preventing recurrent variceal bleeding. The choice of surgical treatment depends on factors like the severity of bleeding, liver dysfunction, and type of portal hypertension.
Portal hypertension
This document provides information on portal hypertension. It begins by defining portal hypertension and describing the anatomy of the portal vein system. It then discusses the causes of portal hypertension including prehepatic causes like extrahepatic portal vein obstruction (EHPVO) and non-cirrhotic portal fibrosis (NCPF), hepatic causes like cirrhosis and posthepatic causes like sinistral portal hypertension. It describes the clinical presentation of portal hypertension including variceal bleeding. It provides details on the management of acute variceal bleeding and long term treatment options for portal hypertension including pharmacotherapy, TIPS procedure, shunt operations and liver transplantation.
Treatment of portal hypertension
The document summarizes the treatment of portal hypertension and varices. It discusses treatments for variceal bleeding, ascites, and splenomegaly. For varices, it recommends primary prophylaxis with non-selective beta-blockers for medium/large varices without prior bleeding. For acute variceal hemorrhage, it recommends pharmacologic therapy, endoscopic band ligation or sclerotherapy, balloon tamponade, and TIPS or shunt surgery as rescue therapy. It also discusses preventing recurrent bleeding with beta-blockers, repeated endoscopic therapy, and TIPS or shunt surgery.
Non cirrhotic portal fibrosis
Non Cirrhotic Portal Fibrosis (NCPF) is a syndrome of obscure etiology characterized by obliterative portovenopathy leading to portal hypertension and massive splenomegaly in young adults from low socioeconomic backgrounds. The exact cause is unknown but is hypothesized to be related to malnutrition, recurrent infections, exposure to toxins or metals. Pathology shows sclerosis of portal vein branches. Clinical features include gastrointestinal bleeding, splenomegaly, and abdominal pain. Management involves controlling acute bleeding episodes and preventing rebleeding through medications or surgery like portosystemic shunts. Prognosis is generally good if bleeding can be controlled.
Transjugular intrahepatic porto systemic shunt
A transjugular intrahepatic portosystemic shunt (TIPS) is a procedure that creates a connection between the portal and hepatic veins within the liver to decrease portal pressure. It is less invasive than surgery and used to treat complications of portal hypertension like variceal bleeding. The procedure involves placing a stent between the veins under imaging guidance. TIPS can help control bleeding, ascites, and other conditions but carries risks of infection, encephalopathy, and shunt failure over time that require monitoring.
Portal Hypertension
1. Surgery continues to play an important role in the treatment of portal hypertension, both as primary and rescue therapy in select patients.
2. For good risk cirrhotic patients with refractory variceal bleeding, surgical shunts such as distal splenorenal shunt have better long-term outcomes compared to TIPS.
3. TIPS is preferred for poor risk cirrhotic patients, while surgical shunts or devascularization remain the standard treatment for non-cirrhotic portal hypertension. Surgery is not obsolete in managing portal hypertension.
Portal hypertension surgical management
1. Portal hypertension is defined as a portal pressure higher than 5 mm Hg and can lead to variceal bleeding. It is caused by any blockage that impedes portal blood flow.
2. Complications include ascites, encephalopathy, and malnutrition indicating end-stage liver disease. Evaluation involves assessing the underlying liver disease, hepatic function, portal venous anatomy and hemodynamics.
3. Treatment options include pharmacotherapy, endoscopic therapy, TIPS procedure, and liver transplantation for eligible patients. The goal is to reduce portal pressure and prevent further bleeding events.
Portal Hypertension
Portal hypertension occurs when blood pressure in the portal vein system leading to the liver is elevated above normal levels. It has many potential causes but is most commonly caused by cirrhosis of the liver. Diagnosis involves blood tests, imaging like ultrasound and endoscopy. Management depends on the underlying cause but often involves endoscopic procedures to treat variceal bleeding and may progress to surgical shunts, TIPSS, or liver transplantation in advanced cirrhosis.
Devascularization in portal hypertension.dr quiyum
role of surgery in portal hypertension is promising. Devascularization is one of the procedure of choice in unshuntable portal vein. Though LT is treatment of choice
Portal hypertension & management
Portal Hypertension and its Management is discussed. Key points include:
- Portal hypertension results from increased resistance to portal blood flow from liver fibrosis and vasoconstriction.
- Clinical presentation includes variceal bleeding, ascites, and encephalopathy. Imaging helps evaluate portal vein anatomy and pressure.
- Treatment depends on severity but includes medications, endoscopic therapies like banding, transjugular intrahepatic portosystemic shunt (TIPS), and surgeries like shunts.
- Selective shunts like distal splenorenal shunt aim to decompress varices while maintaining some portal blood flow to the liver, reducing risks of encephalopathy and
Portal Hypertension
This document summarizes information about portal hypertension and variceal bleeding. It discusses the causes of portal hypertension including pre-sinusoidal, sinusoidal and post-sinusoidal factors. It also describes treatments for acute variceal bleeding such as pharmacologic therapies, endoscopic therapies like band ligation, balloon tamponade and TIPS. It notes that prevention of recurrent bleeding involves pharmacotherapy, endoscopic therapy, TIPS or surgical options like portosystemic shunts or liver transplantation.
Acs0510 Portal Hypertension 2004
1) Portal hypertension results from increased resistance to blood flow through the portal vein, most commonly due to cirrhosis.
2) Management of acute variceal bleeding from portal hypertension involves airway protection, volume resuscitation, antibiotics, pharmacotherapy with octreotide or vasopressin, and endoscopic ligation or sclerotherapy of the varices.
3) The mortality of variceal hemorrhage depends on the severity of liver disease and ranges from 5% for mild cirrhosis to over 50% for decompensated cirrhosis.
Portal hypertension
The document summarizes portal hypertension and portal vein system. It describes that the portal vein is formed by the union of the splenic and superior mesenteric veins, running within the lesser omentum and posterior to the common bile duct and hepatic artery. Portal hypertension is defined as a hepatic venous pressure gradient greater than 5 mmHg and can be caused by pre-hepatic, intra-hepatic, or post-hepatic issues. Complications of portal hypertension include splenomegaly, ascites, and esophageal varices. Treatment involves pharmacological therapy, endoscopic procedures like band ligation, and transjugular intrahepatic portosystemic shunt placement.
Portal hypertension and gastrointestinal bleeding
These slides describe the pathophysiology and the management of patients with liver cirrhosis and portal hypertension. The slides are at the level of post-graduate students
TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPS)
Transjugular intrahepatic portosystemic shunt (TIPS) is a procedure that creates a connection between the hepatic vein and a branch of the portal vein to allow portal blood flow to bypass the liver and lower portal hypertension. TIPS is indicated for acute variceal bleeding unresponsive to other treatments, recurrent variceal bleeding, refractory ascites, and other complications of portal hypertension. The procedure involves accessing the hepatic vein via the jugular vein, puncturing the liver to access a portal vein branch, dilating the tract, and placing a stent to form the shunt. The goal is to reduce the portosystemic gradient to less than 12 mmHg to relieve portal hypertension.
Esophageal varix surgical treatment
1. This document presents the case of a 44-year-old female patient with a history of HCV liver cirrhosis and esophageal variceal bleeding who was admitted for nausea.
2. The patient underwent a Kobayashi operation to treat her esophageal varices. This involves devascularization of the esophagus and stomach, truncal vagotomy, esophageal resection and anastomosis, and pyloroplasty.
3. Follow up after 2-4 weeks showed complete resolution of varices in 12 cases, marked decrease in 9 cases, and some change in 2 cases. Recurrence risks are lower with this non-shunt operation compared to shunt operations.
Surgical shunts
Surgical shunts are procedures to treat portal hypertension by creating bypass routes to circumvent blocked liver vessels and reduce high blood pressure in the portal venous system. A portacaval shunt directly connects the portal and hepatic veins but risks hepatic encephalopathy and has a poor 2-year survival rate. TIPS (transjugular intrahepatic portosystemic shunt) is non-invasive and has a low mortality rate, reducing hypertension while allowing possible future liver transplantation, though infections and allergies can occur. The meso-cavo jugular shunt also reduces hypertension non-invasively while enabling potential liver transplantation, but long-term outcomes are not well known.
Portal hypertension by Dr mohammed Hussien
This document discusses portal hypertension and bleeding varices. It begins by describing the physiology of the portal system and defining portal hypertension. It then discusses the causes of portal hypertension including morphological alterations in the liver from cirrhosis and fibrosis. It also discusses the hyperdynamic circulation seen in portal hypertension which involves increased vasodilators and reduced sensitivity to vasoconstrictors. Risk factors for bleeding varices include portal pressure, variceal size, wall structure, and hepatic function. The document concludes by covering the history, physical exam, classifications, and laboratory evaluation of portal hypertension.
New consensus on ncpf
NCPF is a condition characterized by portal fibrosis and involvement of small and medium portal veins, leading to portal hypertension and splenomegaly despite normal liver function and structure. It commonly affects individuals in the Indian subcontinent aged 25-35 years from low socioeconomic backgrounds. Diagnosis involves evidence of portal hypertension and varices with normal liver function tests and histology showing obliteration of small portal veins without cirrhosis or injury. Management focuses on treatment and prevention of variceal bleeding through endoscopic therapies and beta blockers, with an otherwise excellent prognosis.
VARICEAL HAEMORRHAGE WITH SPECIAL ATTENTION TO PORTAL HYPERTENSION
Portal hypertension occurs when blood flow through the liver is blocked, increasing pressure in the portal vein and spleen. This causes collateral veins to develop like esophageal varices, which can bleed if ruptured. Diagnosis involves blood tests, ultrasound, and endoscopy. Treatment depends on severity but may include medications, band ligation, TIPS procedure, or liver transplant. Managing variceal bleeding quickly through fluid resuscitation, medications, and endoscopic therapy can help prevent complications from progressive liver disease.
Portal Hypertension
A presentation on the pathology and current management (with Especial emphasis on surgical management) of Portal Hypertension; a common complication of liver cirrhosis among other liver diseases. Being a copy of seminar presentation I for the HepatoPancreaticoBiliary Unit of the Division of General Surgery, Ahmadu Belllo University Teaching Hospital, Zaria.
portal hypertension and upper G I bleeding
This document discusses portal hypertension (PHT), including its definition, classification, etiology, pathophysiology, clinical features, diagnosis and management. PHT is defined as a pathological increase in portal pressure above 5 mmHg. It can be classified based on the location of obstruction as pre-sinusoidal, sinusoidal, or post-sinusoidal. The etiology includes pre-hepatic causes such as portal vein thrombosis, intra-hepatic causes like cirrhosis, and post-hepatic causes like Budd-Chiari syndrome. Clinical features include upper GI bleeding, splenomegaly, ascites, and varices. Diagnosis involves clinical evaluation, endoscopy, imaging like ultrasound, and treatment depends
Portal hypertension
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.
Anesthetic Management of Nasopharyngeal Angiofibroma Resection with Carotid I...
This document describes the anesthetic management of a 13-year-old patient undergoing resection of a nasopharyngeal angiofibroma tumor invading the carotid artery and facial sinuses. Key aspects included:
1) Preoperative embolization of feeding arteries to reduce bleeding risk.
2) Intraoperative profuse bleeding requiring massive transfusion during tumor resection near the ethmoid cells.
3) A long 9-hour procedure with careful hemodynamic management and volume resuscitation.
4) Postoperative tracheostomy to protect the airway given risk of edema from surgical manipulation.
Notes complications of liver cirrhosis
Portal hypertension is a major complication of liver cirrhosis that can lead to serious issues like variceal hemorrhage and ascites. It is caused by increased resistance to blood flow within the liver and increased blood flow into the portal vein system. Variceal hemorrhage has a high mortality rate and ascites can become refractory to treatment, requiring interventions like TIPS or transplantation. Managing the complications of portal hypertension is challenging and important for patient outcomes.
Variceal bleeding management
This document summarizes guidelines for managing varices and variceal hemorrhage in patients with cirrhosis. It discusses risk factors for variceal bleeding, methods for risk stratification, and recommendations for primary prevention of bleeding in patients with and without varices. Key points include using nonselective beta-blockers or endoscopic variceal ligation for primary prevention in patients with medium or large varices, monitoring patients without varices for development of varices, and using the hepatic venous pressure gradient to further stratify risk and guide treatment decisions.
MDCT Evaluation of Varices in Portal Hypertension
MDCT is useful for identifying portosystemic collateral vessels in patients with portal hypertension. It can accurately demonstrate the majority of collateral channels. Dynamic CT with contrast allows visualization of varices in the esophagus, stomach, rectum, and other locations. Precise mapping of collateral vessels is important before surgical or interventional procedures to avoid blood loss. MDCT plays an invaluable role in managing portal hypertension.
portalhypertension
This document discusses portal hypertension, its causes, signs, symptoms, diagnosis, and management. It provides an overview of normal portal circulation and defines portal hypertension as a portal pressure greater than 12 mmHg. It describes various etiologies of portal hypertension including presinusoidal, sinusoidal, postsinusoidal, and posthepatic causes. Complications of portal hypertension like variceal bleeding, ascites, and hepatic encephalopathy are discussed. The management of portal hypertension and its complications is also summarized.
Portal Hypertension.pptx
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.
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Portal Hypertension
Portal hypertension occurs when blood pressure in the portal vein system leading to the liver is elevated above normal levels. It has many potential causes but is most commonly caused by cirrhosis of the liver. Diagnosis involves blood tests, imaging like ultrasound and endoscopy. Management depends on the underlying cause but often involves endoscopic procedures to treat variceal bleeding and may progress to surgical shunts, TIPSS, or liver transplantation in advanced cirrhosis.
Devascularization in portal hypertension.dr quiyum
role of surgery in portal hypertension is promising. Devascularization is one of the procedure of choice in unshuntable portal vein. Though LT is treatment of choice
Portal hypertension & management
Portal Hypertension and its Management is discussed. Key points include:
- Portal hypertension results from increased resistance to portal blood flow from liver fibrosis and vasoconstriction.
- Clinical presentation includes variceal bleeding, ascites, and encephalopathy. Imaging helps evaluate portal vein anatomy and pressure.
- Treatment depends on severity but includes medications, endoscopic therapies like banding, transjugular intrahepatic portosystemic shunt (TIPS), and surgeries like shunts.
- Selective shunts like distal splenorenal shunt aim to decompress varices while maintaining some portal blood flow to the liver, reducing risks of encephalopathy and
Portal Hypertension
This document summarizes information about portal hypertension and variceal bleeding. It discusses the causes of portal hypertension including pre-sinusoidal, sinusoidal and post-sinusoidal factors. It also describes treatments for acute variceal bleeding such as pharmacologic therapies, endoscopic therapies like band ligation, balloon tamponade and TIPS. It notes that prevention of recurrent bleeding involves pharmacotherapy, endoscopic therapy, TIPS or surgical options like portosystemic shunts or liver transplantation.
Acs0510 Portal Hypertension 2004
1) Portal hypertension results from increased resistance to blood flow through the portal vein, most commonly due to cirrhosis.
2) Management of acute variceal bleeding from portal hypertension involves airway protection, volume resuscitation, antibiotics, pharmacotherapy with octreotide or vasopressin, and endoscopic ligation or sclerotherapy of the varices.
3) The mortality of variceal hemorrhage depends on the severity of liver disease and ranges from 5% for mild cirrhosis to over 50% for decompensated cirrhosis.
Portal hypertension
The document summarizes portal hypertension and portal vein system. It describes that the portal vein is formed by the union of the splenic and superior mesenteric veins, running within the lesser omentum and posterior to the common bile duct and hepatic artery. Portal hypertension is defined as a hepatic venous pressure gradient greater than 5 mmHg and can be caused by pre-hepatic, intra-hepatic, or post-hepatic issues. Complications of portal hypertension include splenomegaly, ascites, and esophageal varices. Treatment involves pharmacological therapy, endoscopic procedures like band ligation, and transjugular intrahepatic portosystemic shunt placement.
Portal hypertension and gastrointestinal bleeding
These slides describe the pathophysiology and the management of patients with liver cirrhosis and portal hypertension. The slides are at the level of post-graduate students
TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPS)
Transjugular intrahepatic portosystemic shunt (TIPS) is a procedure that creates a connection between the hepatic vein and a branch of the portal vein to allow portal blood flow to bypass the liver and lower portal hypertension. TIPS is indicated for acute variceal bleeding unresponsive to other treatments, recurrent variceal bleeding, refractory ascites, and other complications of portal hypertension. The procedure involves accessing the hepatic vein via the jugular vein, puncturing the liver to access a portal vein branch, dilating the tract, and placing a stent to form the shunt. The goal is to reduce the portosystemic gradient to less than 12 mmHg to relieve portal hypertension.
Esophageal varix surgical treatment
1. This document presents the case of a 44-year-old female patient with a history of HCV liver cirrhosis and esophageal variceal bleeding who was admitted for nausea.
2. The patient underwent a Kobayashi operation to treat her esophageal varices. This involves devascularization of the esophagus and stomach, truncal vagotomy, esophageal resection and anastomosis, and pyloroplasty.
3. Follow up after 2-4 weeks showed complete resolution of varices in 12 cases, marked decrease in 9 cases, and some change in 2 cases. Recurrence risks are lower with this non-shunt operation compared to shunt operations.
Surgical shunts
Surgical shunts are procedures to treat portal hypertension by creating bypass routes to circumvent blocked liver vessels and reduce high blood pressure in the portal venous system. A portacaval shunt directly connects the portal and hepatic veins but risks hepatic encephalopathy and has a poor 2-year survival rate. TIPS (transjugular intrahepatic portosystemic shunt) is non-invasive and has a low mortality rate, reducing hypertension while allowing possible future liver transplantation, though infections and allergies can occur. The meso-cavo jugular shunt also reduces hypertension non-invasively while enabling potential liver transplantation, but long-term outcomes are not well known.
Portal hypertension by Dr mohammed Hussien
This document discusses portal hypertension and bleeding varices. It begins by describing the physiology of the portal system and defining portal hypertension. It then discusses the causes of portal hypertension including morphological alterations in the liver from cirrhosis and fibrosis. It also discusses the hyperdynamic circulation seen in portal hypertension which involves increased vasodilators and reduced sensitivity to vasoconstrictors. Risk factors for bleeding varices include portal pressure, variceal size, wall structure, and hepatic function. The document concludes by covering the history, physical exam, classifications, and laboratory evaluation of portal hypertension.
New consensus on ncpf
NCPF is a condition characterized by portal fibrosis and involvement of small and medium portal veins, leading to portal hypertension and splenomegaly despite normal liver function and structure. It commonly affects individuals in the Indian subcontinent aged 25-35 years from low socioeconomic backgrounds. Diagnosis involves evidence of portal hypertension and varices with normal liver function tests and histology showing obliteration of small portal veins without cirrhosis or injury. Management focuses on treatment and prevention of variceal bleeding through endoscopic therapies and beta blockers, with an otherwise excellent prognosis.
VARICEAL HAEMORRHAGE WITH SPECIAL ATTENTION TO PORTAL HYPERTENSION
Portal hypertension occurs when blood flow through the liver is blocked, increasing pressure in the portal vein and spleen. This causes collateral veins to develop like esophageal varices, which can bleed if ruptured. Diagnosis involves blood tests, ultrasound, and endoscopy. Treatment depends on severity but may include medications, band ligation, TIPS procedure, or liver transplant. Managing variceal bleeding quickly through fluid resuscitation, medications, and endoscopic therapy can help prevent complications from progressive liver disease.
Portal Hypertension
A presentation on the pathology and current management (with Especial emphasis on surgical management) of Portal Hypertension; a common complication of liver cirrhosis among other liver diseases. Being a copy of seminar presentation I for the HepatoPancreaticoBiliary Unit of the Division of General Surgery, Ahmadu Belllo University Teaching Hospital, Zaria.
portal hypertension and upper G I bleeding
This document discusses portal hypertension (PHT), including its definition, classification, etiology, pathophysiology, clinical features, diagnosis and management. PHT is defined as a pathological increase in portal pressure above 5 mmHg. It can be classified based on the location of obstruction as pre-sinusoidal, sinusoidal, or post-sinusoidal. The etiology includes pre-hepatic causes such as portal vein thrombosis, intra-hepatic causes like cirrhosis, and post-hepatic causes like Budd-Chiari syndrome. Clinical features include upper GI bleeding, splenomegaly, ascites, and varices. Diagnosis involves clinical evaluation, endoscopy, imaging like ultrasound, and treatment depends
Portal hypertension
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.
Anesthetic Management of Nasopharyngeal Angiofibroma Resection with Carotid I...
This document describes the anesthetic management of a 13-year-old patient undergoing resection of a nasopharyngeal angiofibroma tumor invading the carotid artery and facial sinuses. Key aspects included:
1) Preoperative embolization of feeding arteries to reduce bleeding risk.
2) Intraoperative profuse bleeding requiring massive transfusion during tumor resection near the ethmoid cells.
3) A long 9-hour procedure with careful hemodynamic management and volume resuscitation.
4) Postoperative tracheostomy to protect the airway given risk of edema from surgical manipulation.
Notes complications of liver cirrhosis
Portal hypertension is a major complication of liver cirrhosis that can lead to serious issues like variceal hemorrhage and ascites. It is caused by increased resistance to blood flow within the liver and increased blood flow into the portal vein system. Variceal hemorrhage has a high mortality rate and ascites can become refractory to treatment, requiring interventions like TIPS or transplantation. Managing the complications of portal hypertension is challenging and important for patient outcomes.
Variceal bleeding management
This document summarizes guidelines for managing varices and variceal hemorrhage in patients with cirrhosis. It discusses risk factors for variceal bleeding, methods for risk stratification, and recommendations for primary prevention of bleeding in patients with and without varices. Key points include using nonselective beta-blockers or endoscopic variceal ligation for primary prevention in patients with medium or large varices, monitoring patients without varices for development of varices, and using the hepatic venous pressure gradient to further stratify risk and guide treatment decisions.
MDCT Evaluation of Varices in Portal Hypertension
MDCT is useful for identifying portosystemic collateral vessels in patients with portal hypertension. It can accurately demonstrate the majority of collateral channels. Dynamic CT with contrast allows visualization of varices in the esophagus, stomach, rectum, and other locations. Precise mapping of collateral vessels is important before surgical or interventional procedures to avoid blood loss. MDCT plays an invaluable role in managing portal hypertension.
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portalhypertension
This document discusses portal hypertension, its causes, signs, symptoms, diagnosis, and management. It provides an overview of normal portal circulation and defines portal hypertension as a portal pressure greater than 12 mmHg. It describes various etiologies of portal hypertension including presinusoidal, sinusoidal, postsinusoidal, and posthepatic causes. Complications of portal hypertension like variceal bleeding, ascites, and hepatic encephalopathy are discussed. The management of portal hypertension and its complications is also summarized.
Portal Hypertension.pptx
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.
PORTAL HTN spleno renal shunt.ppt
This document discusses portal hypertension and anesthetic concerns for lienorenal shunt surgery. It begins by defining portal hypertension as an increase in pressure gradient between the portal vein and hepatic veins/inferior vena cava. Common causes include increased resistance to hepatic blood flow from cirrhosis and increased splanchnic blood flow from splanchnic vasodilation. Major consequences include ascites, portosystemic shunts/varices, splenomegaly, and hepatic encephalopathy. Management of acute variceal bleeding and procedures like TIPS and surgery are discussed. Anesthetic considerations include aspiration prophylaxis, hemodynamic monitoring, and managing complications of variceal bleeding and procedures.
Portal+Hypertension.ppt hepatobiliary system
The document discusses portal hypertension, including:
- Anatomy of the portal vein and causes of increased portal pressure.
- Cirrhosis of the liver is a leading cause of portal hypertension due to obstruction of blood flow through the liver.
- Consequences of portal hypertension include splenomegaly, variceal bleeding, and ascites.
- Investigations involve assessing liver function and imaging tests to identify varices.
- Treatment depends on severity but may include band ligation, sclerotherapy, drugs, or shunt surgery to reduce portal pressure.
Portal hypertension
This document discusses portal hypertension and its management. It defines portal hypertension as increased portal pressure and describes how hepatic venous pressure gradient (HVPG) is used to measure it noninvasively. The main causes of portal hypertension are discussed as pre-hepatic, intra-hepatic, and post-hepatic. Clinical features include gastroesophageal varices, ascites, and splenomegaly. Management involves screening and treatment of varices, diuretics for ascites, and splenectomy in rare cases. Transjugular intrahepatic portosystemic shunt (TIPS) or surgical shunts are considered if medication fails or is not available.
Hepatectomy anaesthesia
1) Liver resection procedures carry significant risks including major blood loss, coagulopathy, and postoperative liver failure.
2) Anesthesia aims to limit intraoperative blood loss through low central venous pressure, intermittent hepatic inflow occlusion, and avoidance of positive pressure ventilation during resection.
3) Close monitoring of hemodynamics, blood loss, and liver and renal function is needed due to the risks of hypotension, arrhythmias, and multi-organ dysfunction in the postoperative period.
Portal+Hypertension.pptx
This document discusses portal hypertension, including its causes, clinical presentation, investigations, and treatments. Key points:
- Portal hypertension occurs when portal vein pressure exceeds 12 mmHg. It can be caused by increased resistance (e.g. cirrhosis) or increased blood flow (e.g. arterio-portal fistula).
- Clinical sequelae include portosystemic collaterals, splenomegaly, gastrointestinal congestion, variceal bleeding, and ascites.
- Investigations include liver function tests, endoscopy to detect varices, and tests to identify the underlying cause such as hepatitis markers or biopsy.
- Treatment depends on severity but may include endoscopic var
portal hypertension UG class by Prof. Ajay Khanna, IMS, BHU, Varanasi, India
This document provides information on portal hypertension, including its definition, anatomy, pathophysiology, etiology, clinical features, investigations, treatment of variceal bleeding, ascites, encephalopathy, Budd-Chiari syndrome, and various surgical procedures. Portal hypertension is defined as a portal venous pressure greater than 12 mmHg and is characterized by the development of portosystemic collaterals. Common causes include liver cirrhosis, portal vein thrombosis, and Budd-Chiari syndrome. Treatment involves reducing portal pressure, treating complications, and addressing the underlying liver disease.
3255739dwe43ew234eds34ew96-GI-Bleed-ppt.ppt
This document discusses gastrointestinal bleeding, which can be divided into upper and lower GI bleed. It provides details on the causes, clinical presentation, risk factors, examination findings, emergency management, and treatment approaches for non-variceal and variceal upper GI bleeding. For non-variceal bleeds, endoscopy is the main diagnostic and therapeutic tool, while variceal bleeds in cirrhotic patients require vasoconstrictor drugs, antibiotics, endoscopic band ligation, and may necessitate TIPS or surgical shunting. Patient prognosis depends on the severity of underlying liver disease.
Portal Hypertension Surgical MANagement.pptx
Portal hypertension can be treated with shunt operations to lower portal pressure and reduce variceal bleeding by shunting blood away from the liver. Selective shunts like the distal splenorenal shunt are preferred as they do not divert all blood flow and have a lower risk of hepatic encephalopathy. Non-selective shunts effectively lower pressure but carry higher risks of encephalopathy. Investigation with angiography and ultrasound is needed before surgery to assess anatomy. Complications include bleeding, shunt thrombosis and encephalopathy.
Ugi bleeding
Upper gastrointestinal bleeding occurs above the ligament of Treitz and can be classified as variceal or non-variceal, acute or chronic. The most common causes are peptic ulcer disease, esophageal varices, and gastritis. Evaluation involves history, physical exam, and testing to identify the source and severity of bleeding. Treatment depends on risk level and may include medications, endoscopic therapies, angiography, or surgery. The goal is to control bleeding and prevent rebleeding through appropriate medical, endoscopic, radiologic, or surgical interventions.
Portal hypertension
This document discusses portal hypertension and variceal bleeding. It begins by describing portal hemodynamics and defining clinically significant portal hypertension as a hepatic venous pressure gradient (HVPG) greater than 10-12 mm Hg.
The etiology of portal hypertension is categorized as prehepatic, hepatic, or posthepatic. Prehepatic causes include portal/splenic vein thrombosis. Hepatic causes include cirrhosis, which leads to fibrosis and increased production of vasoconstrictors. Posthepatic causes include Budd-Chiari syndrome.
Complications of portal hypertension include variceal bleeding, ascites, hepatic encephalopathy, and hepatorenal syndrome. Investigations for diagnosis include ultrasound Doppler,
Dynamic Renal scan lecture (2.pdf
Renal scintigraphy can be used to evaluate renal infection in several ways. It can detect acute renal involvement in a urinary tract infection using tracers like Tc-99m DMSA that identify areas of reduced renal uptake, indicating infection. It can also detect cortical scarring from a prior or chronic infection. Following treatment, renal scintigraphy can monitor for resolution of the infection or scarring. The test provides important clinical information about renal involvement that cannot be reliably determined through other means. It allows for early diagnosis and treatment of infection or scarring to prevent long-term kidney damage.
Portal hypertension by kiran maindale
Portal hypertension occurs when blood pressure in the portal vein system, which drains blood from the gastrointestinal tract to the liver, increases above normal levels. It is defined as a hepatic venous pressure gradient greater than 15 mmHg. Two key factors that contribute to portal hypertension are increased vascular resistance and increased blood flow. Investigation may include blood tests and imaging of the liver, portal system, and varices. Complications include variceal bleeding, ascites, and hepatic encephalopathy. Treatment depends on severity but may involve medication, endoscopic procedures, transjugular intrahepatic portosystemic shunt placement, or surgical shunting of blood flow to reduce portal pressure.
Portal hypertension
Portal hypertension is defined as elevated portal pressure above 10-12 mm Hg. It is classified as pre-hepatic, intra-hepatic, or post-hepatic based on the location of blockage. Common causes include liver cirrhosis and blockages in the portal vein. Clinical features include upper GI bleeding, splenomegaly, ascites, and hepatic encephalopathy. Management involves treating acute bleeding episodes endoscopically and use of beta-blockers for prevention, along with diuretics and paracentesis for ascites. More advanced treatments include TIPSS, surgical shunting, and liver transplantation.
Upper gi bleeding
This document summarizes the presentation, evaluation, and management of a 70-year-old man with upper gastrointestinal bleeding due to esophageal varices from liver cirrhosis. Key points include: the patient presented with blood vomiting and black stools; examination found dehydration and signs of liver disease; endoscopy revealed esophageal varices that were banded to stop the bleeding. Variceal bleeding is a complication of portal hypertension in cirrhosis and has high rebleeding risks. Initial stabilization is followed by endoscopic treatment, vasoactive drugs, and antibiotics to prevent rebleeding.
2 portal hypertension
The document discusses portal hypertension, which occurs when portal venous blood pressure is greater than 12 mmHg. It outlines the causes of portal hypertension as pre-hepatic, hepatic, or post-hepatic. Cirrhosis is the most common hepatic cause. Complications of portal hypertension include esophageal and gastric varices, which can bleed severely. Treatment involves beta-blockers, sclerotherapy or banding of varices, and sometimes transjugular intrahepatic portosystemic shunt placement or liver transplant. Management of acute variceal bleeding requires fluid resuscitation and blood transfusion, with potential use of balloon tamponade or vasoactive drugs.
Portal Hypertension
The document discusses portal hypertension, which occurs when portal venous blood pressure is greater than 12 mmHg. It can be caused by conditions that affect blood flow pre-hepatically, hepatically, or post-hepatically. Complications include esophageal and gastric variceal bleeding. Management involves treating the underlying cause, reducing portal pressure with medications, banding or sclerotherapy of varices, and shunt procedures or transplant for severe cases.
4th-liver.pptx
The document discusses the anatomy, blood supply, drainage, and ligaments of the liver. It describes the internal segmentation of the liver into right and left lobes and lists the main functions of the liver, including metabolism, protein synthesis, and detoxification. Common liver diseases mentioned include liver failure, trauma, esophageal varices, hydatid cysts, and tumors such as hepatocellular carcinoma. Imaging modalities and treatments for various liver conditions are also summarized.
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portal hypertension UG class by Prof. Ajay Khanna, IMS, BHU, Varanasi, India
portal hypertension UG class by Prof. Ajay Khanna, IMS, BHU, Varanasi, India
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This document discusses endoscopic therapies for the management of variceal hemorrhage, specifically endoscopic sclerotherapy (EST) and endoscopic variceal ligation (EVL). It provides background on variceal bleeding and survival rates over time. It then describes the modalities and techniques of EST and EVL, including injection methods, sclerosing agents used, risks, and indications. Randomized controlled trials comparing EST and EVL are summarized, showing higher eradication rates with EVL. In conclusion, endoscopic therapies like EST and EVL are effective for controlling acute variceal bleeding and reducing recurrence when used for primary or secondary prophylaxis.
25
This document discusses chemotherapy options for biliary tree carcinoma. It begins by outlining the increasing mortality rates and poor prognosis of the disease. It then provides detailed information on the anatomical classification, histological classification, definition, risk factors, and problems associated with diagnosis and treatment. The document discusses surgery as the only potentially curative option but notes that most patients present with advanced, unresectable disease. It reviews several palliative chemotherapy regimens and their response rates and survival benefits, with various gemcitabine-based combinations showing the most promise. The challenges of treating this rare cancer are also summarized.
22
This document discusses the multimodal treatment of hepatocellular carcinoma. It begins by noting that 70% of HCC occurs in patients with cirrhosis. Available treatment methods include surgical resection, liver transplantation, transarterial embolization, chemotherapy, and various ablation techniques. Surgical resection has improved and offers the best chance of cure for non-cirrhotic patients, though recurrence rates are high. Liver transplantation offers the best disease-free survival for selected cirrhotic patients meeting criteria such as tumor size and number, but organ shortage is a major limitation. Other treatments such as arterial embolization and chemotherapy have limited or debated efficacy.
20
This document summarizes a study comparing outcomes of surgical treatment for intrahepatic cholangiocarcinoma (ICC) and hilar cholangiocarcinoma (Klatskin tumor). 59 patients who underwent liver resection for these tumors were analyzed. Klatskin tumors required more extensive resections and had higher postoperative morbidity. 5-year survival was similar for both tumor types at around 35%. Expression of the p27 protein was associated with lower recurrence rates and better survival outcomes. Surgical resection remains the primary treatment when possible but molecular markers may help guide future adjuvant therapies.
32
The document discusses different surgical treatments for portal hypertension between 1877-2003. It lists various types of shunt procedures that were developed over time to reduce portal pressure, including Eck-Pavlov-Vidal shunt in 1967, Warren shunt in 1967, and Starzl auxiliary liver transplantation in 1973. The document also discusses surgical treatments for Budd-Chiari syndrome and ascites, such as portocaval shunts, mesenterico-caval shunts, and LeVeen shunts. It concludes by providing data on the types of shunt procedures performed between 1997-2003 for portal hypertension treatment and their results.
30
TIPSS is a procedure that creates a permanent connection between the portal and hepatic veins to reduce portal hypertension. It has several indications including uncontrolled variceal bleeding and refractory ascites. The procedure involves catheterization of the jugular vein and placement of a stent. Complications can include thrombosis, hemorrhage, and encephalopathy. Success rates are over 80% for variceal bleeding and 50% for ascites, but secondary dysfunction occurs in 40% after 1 year often requiring revision. TIPSS provides immediate reduction in portal pressure and is less invasive than surgical shunting.
28
The document discusses pathogenesis and management of portal hypertension. It covers hemodynamic assessment of portal hypertension, causes of non-cirrhotic portal hypertension including nodular regenerative hyperplasia. Animal models of portal hypertension are described. The role of nitric oxide and endothelin in regulating vascular tone is discussed. Clinical consequences of cirrhotic portal hypertension include variceal bleeding. Management of acute variceal bleeding involves vasoactive drugs and endoscopic therapy. Secondary prophylaxis to prevent rebleeding involves non-selective beta-blockers or band ligation.
24
The document discusses guidelines for evaluating and treating hepatic metastases from colorectal cancer. It recommends investigations like CT, MRI, and ultrasound to evaluate metastases. Metastases are considered immediately resectable if the surgery is technically possible and leaves at least 40% of liver volume. Resection may be possible but risky if it requires complex procedures. Factors like number, size and location of metastases impact prognosis but are not absolute contraindications to resection. Repeat resection of recurrent metastases can provide long-term survival.
23
This document summarizes various radiation therapy modalities for treating hepatic malignant tumors. It discusses external beam radiotherapy techniques like conventional radiotherapy, 3D conformal radiotherapy, stereotactic radiotherapy, and proton radiotherapy. It also covers internal radiotherapy techniques like selective internal radiotherapy using yttrium microspheres, metabolic radiotherapy with iodine-131 lipiodol, and brachytherapy. The document provides details on each technique's dosimetry, efficacy, and safety considerations.
21
1. The document discusses the history and mechanisms of radiofrequency ablation (RFA) for treating hepatic tumors. RFA uses alternating current within 200-1200 MHz to generate heat and coagulate tissue.
2. RFA can be performed percutaneously, laparoscopically, or during open surgery. Different ablation schemes and needle types are used depending on tumor size and location.
3. Complications of RFA include wound infection, bleeding, and abscesses. Studies show high rates of initial tumor necrosis but frequent recurrence within a year.
19
This document discusses the management of cholangiocarcinoma based on the author's experience at the Mansoura University Gastroenterology Surgical Center in Egypt. Some key points include:
- Cholangiocarcinoma is the second most common malignant liver tumor after hepatocellular carcinoma.
- Surgical resection remains the main treatment when possible but many cases are unresectable due to advanced stage at presentation.
- Of 385 patients treated between 1995-2002, 216 had central cholangiocarcinoma and most (79%) of these were unresectable.
- For unresectable cases, various palliative treatments were used with a mean survival of 5.8
18
The document discusses classification and surgical treatment options for extrahepatic bile duct cancer. It examines preoperative biliary drainage and portal embolization. Surgical techniques discussed include laparoscopy, posterior approach, tumor resection, hepatectomy, and caudate lobe resection. Operative procedures and mortality are analyzed according to tumor location, TNM classification, and staging. Long-term survival outcomes are presented for different patient groups and surgical approaches.
11
1) This document discusses liver surgery for hepatocellular carcinoma (HCC), with a focus on techniques and outcomes in Japan.
2) The use of intraoperative ultrasound during liver surgery has enabled more limited and precise resections, such as subsegmentectomies, while preserving important vascular structures.
3) Hepatic resection for HCC has become much safer over time, with mortality rates decreasing to less than 1% at specialized centers due to techniques like intermittent inflow occlusion and precise limited resections guided by intraoperative ultrasound.
8
This document discusses antiviral therapy peri-liver transplantation. It provides data on primary liver disease in adult transplant recipients, with chronic hepatitis C being the most common at 20.7-40%. It also shows survival rates after transplantation by diagnosis. Therapeutic strategies for patients with HBV, HDV, and HCV undergoing liver transplantation aim to prevent recurrent infection of the graft. Recurrence of HBV infection is related to liver disease and HBV replicative status pre-transplant. Combination therapy with hepatitis B immune globulin and antiviral drugs like lamivudine is most effective for preventing HBV recurrence post-transplant according to various studies cited. Guidelines are provided for HBV prophylaxis and treatment of recurrence after
6
This document discusses liver transplantation for hepatitis C virus (HCV) disease. It outlines that HCV reinfection is common after transplantation, occurring in 87-97% of cases. There are different patterns of HCV recurrence post-transplant, including minimal liver injury, chronic HCV, and cholestatic HCV. Factors associated with increased rates of fibrosis post-transplant include older recipient age, bolus steroid use for rejection, induction with mycophenolic acid, and short duration of prednisone use. High pre-transplant HCV RNA levels are also associated with worse patient and graft survival outcomes.
5
- Liver resection (LR) and liver transplantation (LTx) are two treatment options for hepatocellular carcinoma (HCC). This study compares outcomes of 282 patients receiving LR and 187 receiving LTx.
- Patients who received LTx had a higher perioperative mortality rate compared to LR patients (18.1% vs 4.5%), mainly due to sepsis, multiple organ failure, and vascular complications. Late mortality was higher in LR patients and mainly due to tumor recurrence.
- Recurrence rates were significantly higher after LR (47.4% vs 9%), and survival after recurrence was also lower with LR. Factors associated with recurrence and survival included tumor characteristics such as α-fetoprotein levels,
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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- 1. PROXIMAL SPLENORENAL SHUNT FOR PORTAL HYPERTENSION COMBINED WITH HYPERSPLENISM IN LIVER CIRRHOSIS Authors: I.Timaru, I.P.Oprea, C.Musat, M.Tanase, A.Zaciu, N.Tudor, C.Dutu, R.Nica THE CENTRAL CLINICAL EMERGENCY MILITARY HOSPITAL The 2 nd Surgical Clinic