This document discusses portal hypertension and variceal bleeding. It covers the pathophysiology of variceal formation, causes of portal hypertension, detection of varices via endoscopy and other imaging modalities, management of variceal bleeding, and medical therapies to decrease portal pressure including vasopressin analogs, somatostatin analogs, beta-blockers, and other agents. Key points are that variceal bleeding has high mortality, endoscopy is the primary method to detect varices, and drugs like terlipressin and beta-blockers aim to decrease portal pressure and prevent rebleeding.
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.
This document provides an overview of the history, classification, diagnosis, and management of esophageal and gastric varices. It discusses:
1) The timeline of historical discoveries and developments in understanding varices, from early descriptions in the 1500s to advancements in endoscopy in the 1900s.
2) Risk factors for variceal bleeding including portal hypertension levels, varix size, and presence of high-risk signs.
3) Diagnostic tests and classifications used to identify and grade varices, with endoscopy as the gold standard to evaluate location, size, and presence of red signs.
4) Additional sections cover rare ectopic varices that can form in other areas and recommendations for pro
Notes complications of liver cirrhosis Prakash Prakh
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.
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.
This document provides an overview of upper gastrointestinal bleeding (UGIB), including its definition, classification, epidemiology, clinical features, diagnostic evaluation, and management. Some key points:
1. UGIB is more common than lower GI bleeding, with a reported incidence of 170 patients per 100,000 population per year. The most common cause is peptic ulcer disease (40% of cases).
2. Risk of rebleeding is higher in patients on antiplatelet therapy and those with recurrent bleeding within 48-72 hours. Mortality is 5-10% for severe UGIB.
3. Diagnostic evaluation includes endoscopy within 24 hours to identify the source of bleeding, as well as
This document provides an overview of cirrhosis and its complications. It defines cirrhosis as a chronic liver disease characterized by diffuse fibrosis and nodular regeneration. The main causes are chronic viral hepatitis, alcohol, and non-alcoholic fatty liver disease. Complications include portal hypertension, ascites, hepatic encephalopathy, and hepatorenal syndrome. Diagnosis involves clinical evaluation, labs, imaging, and sometimes biopsy. Treatment focuses on managing complications, addressing the underlying cause, and potentially liver transplantation for decompensated cirrhosis.
This document provides an overview of upper gastrointestinal bleeding, including:
- The definition, incidence, mortality, and common causes of upper GI bleeding. The most common causes are gastric and duodenal ulcers, esophagitis, and esophageal varices.
- Principles of management including initial assessment, resuscitation, localization of bleeding site usually through endoscopy, and risk stratification to determine need for inpatient care or intervention.
- Endoscopy is the gold standard for diagnosis and treatment. The Forrest classification guides prognosis and need for endoscopic therapy based on stigmata of recent hemorrhage seen. Proton pump inhibitors are commonly used for prevention of rebleeding.
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.
This document provides an overview of the history, classification, diagnosis, and management of esophageal and gastric varices. It discusses:
1) The timeline of historical discoveries and developments in understanding varices, from early descriptions in the 1500s to advancements in endoscopy in the 1900s.
2) Risk factors for variceal bleeding including portal hypertension levels, varix size, and presence of high-risk signs.
3) Diagnostic tests and classifications used to identify and grade varices, with endoscopy as the gold standard to evaluate location, size, and presence of red signs.
4) Additional sections cover rare ectopic varices that can form in other areas and recommendations for pro
Notes complications of liver cirrhosis Prakash Prakh
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.
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.
This document provides an overview of upper gastrointestinal bleeding (UGIB), including its definition, classification, epidemiology, clinical features, diagnostic evaluation, and management. Some key points:
1. UGIB is more common than lower GI bleeding, with a reported incidence of 170 patients per 100,000 population per year. The most common cause is peptic ulcer disease (40% of cases).
2. Risk of rebleeding is higher in patients on antiplatelet therapy and those with recurrent bleeding within 48-72 hours. Mortality is 5-10% for severe UGIB.
3. Diagnostic evaluation includes endoscopy within 24 hours to identify the source of bleeding, as well as
This document provides an overview of cirrhosis and its complications. It defines cirrhosis as a chronic liver disease characterized by diffuse fibrosis and nodular regeneration. The main causes are chronic viral hepatitis, alcohol, and non-alcoholic fatty liver disease. Complications include portal hypertension, ascites, hepatic encephalopathy, and hepatorenal syndrome. Diagnosis involves clinical evaluation, labs, imaging, and sometimes biopsy. Treatment focuses on managing complications, addressing the underlying cause, and potentially liver transplantation for decompensated cirrhosis.
This document provides an overview of upper gastrointestinal bleeding, including:
- The definition, incidence, mortality, and common causes of upper GI bleeding. The most common causes are gastric and duodenal ulcers, esophagitis, and esophageal varices.
- Principles of management including initial assessment, resuscitation, localization of bleeding site usually through endoscopy, and risk stratification to determine need for inpatient care or intervention.
- Endoscopy is the gold standard for diagnosis and treatment. The Forrest classification guides prognosis and need for endoscopic therapy based on stigmata of recent hemorrhage seen. Proton pump inhibitors are commonly used for prevention of rebleeding.
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.
The document provides information on the role of transjugular intrahepatic portosystemic shunt (TIPS) in treating liver diseases. It discusses how TIPS works to create a channel between the hepatic vein and portal vein using a metal stent to reduce portal pressure. The document outlines guidelines for using TIPS to treat variceal hemorrhaging and describes factors like MELD scores that can help identify high-risk patients who may benefit from early TIPS placement. It also reviews the history of TIPS development and provides details on how to perform the TIPS procedure and assess outcomes.
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.
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
This document discusses the management of variceal bleeding, specifically focusing on esophageal and gastric varices. It provides an overview of endoscopic and medical therapies for controlling acute esophageal variceal bleeding such as endoscopic band ligation, sclerotherapy, and pharmacologic therapies like octreotide. For gastric varices, it describes different classification systems and challenges in managing bleeding, noting endoscopic therapies like sclerotherapy, ligation, and glue injection can control acute bleeding but have high rebleeding risks. It emphasizes a multidisciplinary approach is often needed for gastric variceal 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
MDCT Evaluation of Varices in Portal HypertensionVishwanath R S
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.
1. Cirrhosis is the most common cause of ascites, accounting for 85% of cases. Other causes include malignancy, tuberculosis, cardiac disease, and nephrotic syndrome.
2. Analysis of ascitic fluid can help determine the cause of ascites. A serum ascites albumin gradient (SAAG) ≥1.1 g/dL suggests portal hypertension while a SAAG <1.1 g/dL suggests a non-cirrhotic cause like malignancy or tuberculosis.
3. Gross appearance, cell count, SAAG, and biochemical properties of ascitic fluid provide clues to diagnose conditions like chylous ascites, spontaneous bacterial peritonitis, or biliary perforation
Upper GI bleeding is a common cause of hospitalization. The most common cause is peptic ulcer disease, which is strongly associated with H. pylori infection. Mortality is 6-10% overall and is usually due to comorbidities rather than bleeding itself. Treatment involves resuscitation, endoscopy, and treating the underlying cause. Endoscopy allows for identification and treatment of the bleeding site. Long term prevention involves treating H. pylori infection, avoiding NSAIDs when possible, and using PPIs for gastroprotection.
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.
1. The document summarizes guidelines for the management of bleeding duodenal ulcers, including the etiology, risk factors, clinical assessment, endoscopic diagnosis and treatment options.
2. Key recommendations include performing early endoscopy within 24 hours, using the Forrest classification system to assess bleeding risk, and employing combination endoscopic therapy with epinephrine injection and thermal coagulation or clipping for high risk stigmata.
3. Doppler ultrasound may help guide endoscopic therapy by identifying persistent blood flow signals requiring further treatment to reduce rebleeding risk.
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.
The document discusses tips for managing ascites, including performing large volume paracentesis with albumin and continuing diuretics if renal sodium excretion is over 30 mmol/day. It also discusses using non-selective beta-blockers and transjugular intrahepatic portosystemic shunts (TIPS) to treat refractory ascites, noting that TIPS significantly reduces hepatic encephalopathy compared to large volume paracentesis alone. TIPS is an effective option for controlling ascites but carries a higher risk of hepatic encephalopathy compared to large volume paracentesis.
Upper Gastrointestinal Bleeding (UGIB) - General ApproachMohamed Badheeb
What does the science & evidence say about UGIB ?
Introduction & Background on Upper GI Bleeding.
- Incidence and Epidemiology
- Etiologies
2. Guidelines on UGIB
- Resuscitation, Risk assessment
- Diagnostic Modalities
- Treatment Options
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.
This document summarizes portal hypertension and its causes. Portal hypertension occurs when there is increased resistance to blood flow through the portal vein, leading to elevated pressure. It can be classified as intrahepatic, prehepatic, or posthepatic based on the location of the increased resistance. Common causes include cirrhosis of the liver, thrombosis of the portal or splenic veins, and cardiac diseases. Complications of portal hypertension include splenomegaly, variceal bleeding, ascites, and hepatic encephalopathy. Treatment depends on the underlying cause and may involve medications, TIPS procedures, surgery such as devascularization or shunts, and liver transplantation.
This document provides information on Budd-Chiari syndrome (BCS), including its definition, epidemiology, etiology, clinical features, diagnosis, pathophysiology, management, and role of medical and minimally invasive treatments. BCS is defined as obstruction of the hepatic veins or inferior vena cava, causing hepatic venous outflow obstruction. Common causes include infections, malignancies, and prothrombotic disorders. Clinical features include abdominal pain, ascites, hepatomegaly, and jaundice. Diagnosis involves imaging like ultrasound, CT, MRI and angiography. Management depends on the cause and includes anticoagulation, thrombolysis, angioplasty, stenting, TIPS, and
Cirrhosis and portal hypertension are defined. Cirrhosis is characterized by fibrosis and nodular regeneration of the liver. Portal hypertension is defined as a portal pressure greater than 5 mmHg and can occur before cirrhosis is established. Complications of cirrhosis and portal hypertension include ascites, variceal hemorrhage, hepatic encephalopathy, and hepatocellular carcinoma. The document discusses the mechanisms, diagnosis, and treatment of these complications.
1. The document discusses conditions other than cirrhosis that can result in diffuse surface nodularity of the liver or portal hypertension such as chronic Budd-Chiari syndrome, chronic portal vein thrombosis, sarcoidosis, and pseudocirrhosis of treated breast cancer metastases or fulminant hepatic failure.
2. It provides imaging examples and characteristics of these non-cirrhotic conditions that can mimic cirrhosis on imaging. For example, pseudocirrhosis of treated breast cancer metastases shows diffuse hepatic nodularity and signs of portal hypertension but the history of breast cancer and prior imaging helps identify the correct diagnosis.
3. Nodular regenerative hyperplasia, congenital hepatic fibrosis, and
This document summarizes ultrasound findings for cirrhosis of the liver. Key findings include coarse echotexture and nodular surface of the liver. Regenerating nodules appear isoechoic or hypoechoic. Portal hypertension is a complication and is evidenced by dilated portal veins, low portal flow, and portosystemic collaterals visible on ultrasound. Doppler ultrasound can detect changes in portal flow from normal hepatopetal to reversed hepatofugal flow in advanced cases.
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.
The document provides information on the role of transjugular intrahepatic portosystemic shunt (TIPS) in treating liver diseases. It discusses how TIPS works to create a channel between the hepatic vein and portal vein using a metal stent to reduce portal pressure. The document outlines guidelines for using TIPS to treat variceal hemorrhaging and describes factors like MELD scores that can help identify high-risk patients who may benefit from early TIPS placement. It also reviews the history of TIPS development and provides details on how to perform the TIPS procedure and assess outcomes.
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.
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
This document discusses the management of variceal bleeding, specifically focusing on esophageal and gastric varices. It provides an overview of endoscopic and medical therapies for controlling acute esophageal variceal bleeding such as endoscopic band ligation, sclerotherapy, and pharmacologic therapies like octreotide. For gastric varices, it describes different classification systems and challenges in managing bleeding, noting endoscopic therapies like sclerotherapy, ligation, and glue injection can control acute bleeding but have high rebleeding risks. It emphasizes a multidisciplinary approach is often needed for gastric variceal 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
MDCT Evaluation of Varices in Portal HypertensionVishwanath R S
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.
1. Cirrhosis is the most common cause of ascites, accounting for 85% of cases. Other causes include malignancy, tuberculosis, cardiac disease, and nephrotic syndrome.
2. Analysis of ascitic fluid can help determine the cause of ascites. A serum ascites albumin gradient (SAAG) ≥1.1 g/dL suggests portal hypertension while a SAAG <1.1 g/dL suggests a non-cirrhotic cause like malignancy or tuberculosis.
3. Gross appearance, cell count, SAAG, and biochemical properties of ascitic fluid provide clues to diagnose conditions like chylous ascites, spontaneous bacterial peritonitis, or biliary perforation
Upper GI bleeding is a common cause of hospitalization. The most common cause is peptic ulcer disease, which is strongly associated with H. pylori infection. Mortality is 6-10% overall and is usually due to comorbidities rather than bleeding itself. Treatment involves resuscitation, endoscopy, and treating the underlying cause. Endoscopy allows for identification and treatment of the bleeding site. Long term prevention involves treating H. pylori infection, avoiding NSAIDs when possible, and using PPIs for gastroprotection.
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.
1. The document summarizes guidelines for the management of bleeding duodenal ulcers, including the etiology, risk factors, clinical assessment, endoscopic diagnosis and treatment options.
2. Key recommendations include performing early endoscopy within 24 hours, using the Forrest classification system to assess bleeding risk, and employing combination endoscopic therapy with epinephrine injection and thermal coagulation or clipping for high risk stigmata.
3. Doppler ultrasound may help guide endoscopic therapy by identifying persistent blood flow signals requiring further treatment to reduce rebleeding risk.
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.
The document discusses tips for managing ascites, including performing large volume paracentesis with albumin and continuing diuretics if renal sodium excretion is over 30 mmol/day. It also discusses using non-selective beta-blockers and transjugular intrahepatic portosystemic shunts (TIPS) to treat refractory ascites, noting that TIPS significantly reduces hepatic encephalopathy compared to large volume paracentesis alone. TIPS is an effective option for controlling ascites but carries a higher risk of hepatic encephalopathy compared to large volume paracentesis.
Upper Gastrointestinal Bleeding (UGIB) - General ApproachMohamed Badheeb
What does the science & evidence say about UGIB ?
Introduction & Background on Upper GI Bleeding.
- Incidence and Epidemiology
- Etiologies
2. Guidelines on UGIB
- Resuscitation, Risk assessment
- Diagnostic Modalities
- Treatment Options
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.
This document summarizes portal hypertension and its causes. Portal hypertension occurs when there is increased resistance to blood flow through the portal vein, leading to elevated pressure. It can be classified as intrahepatic, prehepatic, or posthepatic based on the location of the increased resistance. Common causes include cirrhosis of the liver, thrombosis of the portal or splenic veins, and cardiac diseases. Complications of portal hypertension include splenomegaly, variceal bleeding, ascites, and hepatic encephalopathy. Treatment depends on the underlying cause and may involve medications, TIPS procedures, surgery such as devascularization or shunts, and liver transplantation.
This document provides information on Budd-Chiari syndrome (BCS), including its definition, epidemiology, etiology, clinical features, diagnosis, pathophysiology, management, and role of medical and minimally invasive treatments. BCS is defined as obstruction of the hepatic veins or inferior vena cava, causing hepatic venous outflow obstruction. Common causes include infections, malignancies, and prothrombotic disorders. Clinical features include abdominal pain, ascites, hepatomegaly, and jaundice. Diagnosis involves imaging like ultrasound, CT, MRI and angiography. Management depends on the cause and includes anticoagulation, thrombolysis, angioplasty, stenting, TIPS, and
Cirrhosis and portal hypertension are defined. Cirrhosis is characterized by fibrosis and nodular regeneration of the liver. Portal hypertension is defined as a portal pressure greater than 5 mmHg and can occur before cirrhosis is established. Complications of cirrhosis and portal hypertension include ascites, variceal hemorrhage, hepatic encephalopathy, and hepatocellular carcinoma. The document discusses the mechanisms, diagnosis, and treatment of these complications.
1. The document discusses conditions other than cirrhosis that can result in diffuse surface nodularity of the liver or portal hypertension such as chronic Budd-Chiari syndrome, chronic portal vein thrombosis, sarcoidosis, and pseudocirrhosis of treated breast cancer metastases or fulminant hepatic failure.
2. It provides imaging examples and characteristics of these non-cirrhotic conditions that can mimic cirrhosis on imaging. For example, pseudocirrhosis of treated breast cancer metastases shows diffuse hepatic nodularity and signs of portal hypertension but the history of breast cancer and prior imaging helps identify the correct diagnosis.
3. Nodular regenerative hyperplasia, congenital hepatic fibrosis, and
This document summarizes ultrasound findings for cirrhosis of the liver. Key findings include coarse echotexture and nodular surface of the liver. Regenerating nodules appear isoechoic or hypoechoic. Portal hypertension is a complication and is evidenced by dilated portal veins, low portal flow, and portosystemic collaterals visible on ultrasound. Doppler ultrasound can detect changes in portal flow from normal hepatopetal to reversed hepatofugal flow in advanced cases.
1. The document discusses the diagnosis and treatment of acute ischemic stroke. It outlines the time windows for treatment with intravenous thrombolysis, which is most effective within 4.5 hours of symptom onset.
2. Early diagnosis is critical in stroke care due to the concept of "time is brain". Delays in treatment can lead to further neuronal damage and worse outcomes. The goals are to perform a CT scan within 20 minutes of arrival and initiate thrombolysis within 60 minutes.
3. Post-thrombolytic management focuses on monitoring for hemorrhagic complications and providing supportive care to reduce disability from the stroke.
hepaticcoma.pdf is important for medical studentsDrYaqoobBahar
Hepatic coma is an advanced complication of liver failure characterized by reversible decreased neurologic function and loss of consciousness due to the liver's failure to detoxify toxic substances. It is caused by chronic liver disease, fulminant hepatic failure, or portosystemic shunts. Patients experience disturbances in consciousness, neurological signs, and mental changes. Treatment focuses on treating the underlying cause, decreasing ammonia production, and controlling risk factors through supportive care, lactulose, rifaximin, and L-ornithine/L-aspartate supplementation. Complications can include brain herniation, organ failure, and brain edema.
1) Abdominal tuberculosis poses a diagnostic challenge due to its nonspecific symptoms. It is increasingly common and can involve the gastrointestinal tract, peritoneum, lymph nodes or solid organs.
2) Tubercle bacilli typically spread from the lungs or ingested materials to the abdominal cavity via the bloodstream or lymphatics. This can cause caseating granulomas and lesions in the abdomen.
3) Common presentations include abdominal pain, fever, weight loss, and ascites or abdominal masses. Imaging shows lymphadenopathy, bowel thickening or strictures, and ascites. Diagnosis relies on clinical suspicion plus histology, microbiology or response to antitubercular treatment.
- Abdominal tuberculosis can affect the peritoneum, gastrointestinal tract, abdominal lymph nodes, and solid organs like the liver, pancreas, and spleen. It is most commonly seen in the ileoceal region.
- On imaging, tubercular peritonitis can appear as wet ascites, fibrotic omental thickening, or dry adhesions. Lymphadenopathy often shows peripheral rim enhancement.
- Gastrointestinal tuberculosis frequently involves the terminal ileum and cecum, appearing as thickened valves, contracted cecum, or strictures on barium studies or CT.
Diagnosis and managment of pulmonary embolismDrYaqoobBahar
A pulmonary embolism is a sudden blockage in a lung artery, usually caused by a blood clot breaking off and traveling to the lungs. PE is a common cause of death in hospitalized patients. Risk factors include genetic mutations, cancer, obesity, smoking, and surgery. Symptoms may include dyspnea, chest pain, and cough. Diagnosis involves assessing risk factors, blood tests, imaging like CT scans, and echocardiograms. Treatment involves immediate anticoagulation with blood thinners, potentially thrombolytic therapy for severe cases, and inferior vena cava filters for high-risk patients. Anticoagulation may continue for several months depending on the underlying cause of clotting.
This document discusses peripartum cardiomyopathy, which is a type of dilated cardiomyopathy of unknown origin that presents with left ventricular systolic dysfunction. It can occur in 1 in 4,000 live births in the United States. The precise causes are unclear but may involve viral infection, immune response abnormalities, or prolonged use of tocolytics. Symptoms include dyspnea, chest pain, and edema. Diagnosis involves excluding other potential causes through ECG, echocardiogram, biomarkers and imaging. Treatment focuses on heart failure medications, anticoagulants if needed, and assisted devices. Prognosis is generally good with 50% fully recovering but risks include persistent symptoms or progression to heart failure.
Heart failure is a clinical syndrome where the heart is unable to pump sufficiently to maintain blood flow to meet the body's needs. It can be caused by structural or functional defects in the heart. The most common causes are coronary artery disease, high blood pressure, and diabetes. While it affects about 2% of adults globally, the risk increases to 6-10% for those over age 65. Treatment involves controlling underlying causes, removing precipitating factors, and managing symptoms through diuretics, ACE inhibitors, beta blockers, and other medications.
Pulmonary edema refers to excess fluid accumulation in the lungs. It can be caused by increased hydrostatic pressure, permeability changes, or a mix of both. Common causes include heart failure, fluid overload, near drowning, trauma, and certain drugs. Symptoms include shortness of breath, cough, wheezing, and anxiety. Diagnosis involves physical exam, imaging like chest x-rays, and tests to check for underlying conditions. Treatment focuses on addressing the underlying cause, giving oxygen, diuretics, and other medications to reduce fluid buildup. Ventilatory support may be needed in severe cases.
Pulmonary edema refers to excess fluid accumulation in the lungs. It has four main categories based on pathophysiology: increased hydrostatic pressure, interstitial edema, alveolar flooding, and permeability edema. Causes include heart failure, mitral regurgitation, near-drowning, and renal failure. Symptoms include difficulty breathing, cough, and anxiety. Diagnosis involves clinical exam, BNP levels, chest x-ray, and echocardiogram. Treatment focuses on addressing the underlying cause with oxygen, diuretics, nitrates, and sometimes ventilation support.
1. Acute variceal hemorrhage refers to bleeding from enlarged veins (varices) in the esophagus or stomach that is caused by portal hypertension from liver cirrhosis. Variceal bleeding is a severe complication and is the cause of bleeding in 70% of upper GI bleeds in cirrhotic patients.
2. Varices develop due to increased pressure in the portal vein system from cirrhosis. Once varices form, there is a risk of 15% annual bleeding for large varices. Bleeding can often be controlled with medical and endoscopic therapy but there is a high risk (60%) of rebleeding without intervention.
3. Varices are classified based on location
Hypertension emergencies require rapid reduction of blood pressure to prevent end organ damage. Hypertensive urgency can be managed as an outpatient but emergencies require hospitalization. Initial evaluation assesses for signs of damage to heart, kidneys, brain, or vasculature. Parenteral drugs like nicardipine, labetalol, and esmolol are used to lower blood pressure 10-15% within 1 hour and further to 160/100 mmHg in 2-6 hours, with goals tailored to specific conditions like stroke, heart failure, or aortic dissection. Oral agents like clonidine or nifedipine may be used after initial parenteral treatment to control blood pressure before discharge
Hypertension emergencies require rapid reduction of blood pressure to prevent end organ damage. Hypertensive urgency can be managed as an outpatient with oral medications, while emergencies require hospitalization and intravenous drugs. Initial evaluation assesses for signs of heart, brain, kidney and vascular damage. Parenteral drugs like nicardipine, labetalol and esmolol are used but sodium nitroprusside is no longer first-line due to risks. Treatment goals depend on the specific organ involved and reduce pressure by 10-25% within 1-2 hours.
1) Myxedema coma is a rare life-threatening condition that occurs when a patient with severe, long-standing hypothyroidism experiences physiological decompensation, usually brought on by an external precipitating event like infection.
2) It is characterized by hypothermia, unconsciousness, decreased metabolism and oxygen consumption. Patients often present with symptoms of both the underlying hypothyroidism and the precipitating condition.
3) Treatment involves supportive care, thyroid hormone replacement, glucocorticoids, and treating any underlying infections or precipitating conditions. Patients require intensive monitoring and care due to involvement of multiple organ systems.
This document discusses gastroesophageal varices, which develop in 55% of cirrhotic patients. It covers the risk factors, signs, diagnosis, and treatment of variceal bleeding, including endoscopic band ligation, TIPS procedure, pharmacologic therapies like beta-blockers, and balloon tamponade. The priority in treatment is stabilizing the patient hemodynamically before diagnostic or therapeutic endoscopy. Recurrence of bleeding remains high, so long-term management is also addressed.
This document summarizes adrenal gland function and adrenal insufficiency. It describes:
1) The adrenal glands produce cortisol, aldosterone, and androgens which regulate stress response, electrolyte balance, and sex characteristics.
2) Primary adrenal insufficiency results from adrenal gland dysfunction and causes deficiencies in cortisol, aldosterone, and sex hormones. Secondary adrenal insufficiency is caused by pituitary or hypothalamic disease and causes cortisol deficiency alone.
3) Adrenal crisis is a life-threatening emergency characterized by refractory hypotension that requires aggressive treatment with glucocorticoid replacement such as hydrocortisone.
This document defines hypertensive emergencies and discusses their management. It begins by classifying hypertension and defining hypertensive crises. Hypertensive emergencies are acute severe hypertension with signs of target organ damage, while hypertensive urgencies have severe hypertension without organ damage. The document then covers the epidemiology, etiology, pathophysiology, presentation, investigations, and management of hypertensive emergencies. It discusses treating different organ-specific emergencies like stroke, heart failure, and kidney injury. The management involves rapid blood pressure reduction while monitoring for complications. Various intravenous medications are outlined for treating hypertensive emergencies based on the target organ involved.
This document discusses diffuse parenchymal lung diseases (DPLDs), also called interstitial lung diseases (ILDs). It classifies DPLDs into four main groups and describes some of the most common diseases within each group, including their symptoms, radiologic appearances, and differential diagnoses. Major diseases discussed include sarcoidosis, idiopathic pulmonary fibrosis, hypersensitivity pneumonitis, pneumoconiosis like silicosis, and interstitial lung diseases associated with connective tissue diseases. HRCT is highlighted as a sensitive tool for detecting and characterizing different interstitial lung disease patterns.
This document discusses idiopathic interstitial pneumonias other than idiopathic pulmonary fibrosis. It provides the revised ATS/ERS classification of idiopathic interstitial pneumonias and describes non-specific interstitial pneumonia (NSIP) and cryptogenic organizing pneumonia (COP) in detail. NSIP is characterized by a uniform pattern of interstitial inflammation and fibrosis. It commonly occurs in connective tissue diseases and has a good prognosis with treatment. COP is organizing pneumonia of unknown cause, presenting as patchy consolidation and often resolving with corticosteroid treatment.
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Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
2. • Portal hypertension is directly responsible for the two major
complications of cirrhosis:
- variceal hemorrhage
- ascites.
• Portal hypertension is defined as an increase in hepatic sinusoidal
pressure to 6 mm Hg or greater.
• The development of gastroesophageal varices requires a portal
pressure gradient of at least 10 mm Hg.
• A portal pressure gradient of at least 12 mm Hg is thought to be
required for varices to bleed.
• Portosystemic collaterals decompress the hypertensive hepatic
sinusoids and give rise to varices at different sites.
•
• Variceal hemorrhage is an immediate life-threatening with a 20–
30% mortality rate associated with each episode of bleeding
(Watanabe K, Kimura K, Matsutani S, et al Gastroenterology 1988; 95:434-40)
Sleisenger and Fordtran's Gastrointestinal and Liver Disease Ninth Edition
3. Pathophysiology of variceal formation
• Portal hypertension results from:
- Increase in portal resistance
- Increase in portal inflow.
• Dilated Collateral vessels forms new vascular sprouts that
connects the high-pressure portal venous system with
lower-pressure systemic veins.
• This process of angiogenesis and collateralization is
insufficient for normalizing portal pressure and leading to
portal hypertension and esophageal
varices.(I.wakiri Y, Grisham M, Shah V Hepatology 2008; 47:1754-63)
4. • SPLANCHNIC CIRCULATION:
-Vasodilatation, particularly in the splanchnic bed, permits an
increase in inflow of systemic blood into the portal circulation.
(Sikuler E, Groszmann RJ: ion Hepatology 1986; 6:414-18.)
-Splanchnic vascular endothelial cells are primarily responsible for
- mediating splanchnic vasodilatation and
- enhanced portal venous inflow through excess generation
of NO.(Atucha N, Shah V, Garcia-Cardena G, et al
Gastroenterology 1996; 111:1627-32)
• HEPATIC CIRCULATION
The changes in portal flow and resistance also can be viewed as
originating from mechanical and vascular factors.
- Mechanical factors include the fibrosis and nodularity of the
cirrhotic liver.
- Vascular factors include intrahepatic vasoconstriction.
(Rockey DC, Weisiger RA: Gastroenterology 1998; 114:344-51)
7. The sites of the portal-systemic
collateral circulation in cirrhosis of the liver
8. Variceal pressure
• Measurement of the difference between intravariceal pressure and
pressure within the esophageal lumen (the transmural pressure gradient
across the varices) is potentially a more important indicator of bleeding
risk than measurement of hepatic vein pressure gradient(HVPG).
(Nevens F, Bustami R, Schley SI, et al: Hepatology 1998; 27:15-19)
• A miniature pneumatic pressure sensitivity gauge attached to the tip of an
endoscope allows noninvasive measurement of variceal pressure.( Ruiz del
Arbul L, Martin de Argila C, Vasquez M:Hepatology 1992; 16:147)
• A variceal pressure > 18 mm Hg during a bleeding episode is associated
with failure to control bleeding and predicts early
rebleeding.(Gertsch P, Fischer G, Kleber G:Gastroenterology 1993; 105:1159-66)
• Patients on pharmacologic therapy who show a decrease in variceal
pressure of > 20% from baseline have a low probability of bleeding.
9. DETECTION OF VARICES
Detection of varices can be done by the following techniques:
• A-Upper Gastrointestinal endoscopy
• B-Ultrasound
• C-CT
• D-MRI
• E-Endoscopic ultrasound
• A)-Upper gastrointestinal endoscopy is the most commonly used method to
detect varices.
• The current consensus is that all patients with cirrhosis of the liver should be
screened for esophageal varices by endoscopy.
• In patients in whom no varices are detected on initial endoscopy, endoscopy to
look for varices should be repeated in 2 to 3 years.
• If small varices are detected on the initial endoscopy, endoscopy should be
repeated in 1 to 2 years.[93],[94]
10. Reporting of esophageal varices
• Various criteria have been used to try to standardize the reporting of esophageal
varices.
• The best known of these criteria are those compiled by the Japanese Research
Society for Portal Hypertension.
The descriptors include :
a) Red color signs (OMINOUS SIGNS) include
- red “wale” markings, which are longitudinal whip-like marks on the varix;
- cherry-red spots, which usually are 2 to 3 mm or less in diameter;
- hematocystic spots, which are blood-filled blisters 4 mm in diameter.
b) Color of the varix can be white or blue.
c) Form(size) of the varix at endoscopy is described most commonly.
Grade I - Esophageal varices may be small and straight;
Grade II - Tortuous and occupying less than one third of the esophageal lumen;
Grade III - Large and occupying more than one third of the esophageal lumen.
11. d) Location- Varices can be in the lower third, middle third, or upper third of
the esophagus.
• Of all of the aforementioned descriptors:
The size of the varices in the lower third of the esophagus is the most
important.
• Highest risk of variceal bleeding within 1 year is in patients with:
- large esophageal varices,
- Child (or Child-Pugh) class C cirrhosis and
- red color signs on varices.
12. • B)-Ultrasound examination of the liver with Doppler study of the vessels has been
used widely to assess patients with portal hypertension.
• Features suggestive of portal hypertension on ultrasonography include
- splenomegaly,
- portosystemic collateral vessels, and
- reversal of the direction of flow in the portal vein (hepatofugal flow).
• Some studies have demonstrated that:
- a portal vein diameter greater than 13 mm and
- the absence of respiratory variations in the splenic and mesenteric veins
are sensitive but nonspecific markers of portal hypertension.
These criteria are not used routinely in clinical practice in most centers.
• Transient elastography may be useful in detecting portal hypertension but is not
sufficiently sensitive to recommend as a modality to monitor decreases in portal
pressure in patients on pharmacotherapy.
(The North Italian Endoscopic Club (NIEC) for the Study and Treatment of Esophageal Varices: A
prospective multicenter study. N Engl J Med 1988; 319:983-9)
13. E)- Endoscopic ultrasound examination (endosonography) is done using
* radial or linear array echo-endoscopes
or
* endoscopic ultrasound mini-probes passed through the working
channel of a diagnostic endoscope
• Endoscopic ultrasonography has been used to study several aspects of esophageal
varices including:
* the cross-sectional area of varices to identify patients at increased
risk of bleeding.(Escorsell A, Gines A, Llach J, et al:Hepatology 2002; 36:936-4o)
* size of and flow in the left gastric vein, azygous vein, and paraesophageal
collaterals;
*changes after endoscopic therapy; and
*recurrence of esophageal varices following variceal ligation.
• Endosonography can be combined with endoscopic measurement of transmural
variceal pressure to allow estimation of variceal wall tension, which is a predictor of
variceal bleeding.(Leung VK, Sung JJ, Ahuja AT, et al:Gastroenterology 1997; 112:1811-6)
14. • C)- Computed tomography (CT) is :
useful for demonstrating many features of portal hypertension,
including abnormal configuration of the liver, ascites, splenomegaly, and
collateral vessels.
helpful in distinguishing submucosal from perigastric fundal varices
less invasive alternative to conventional angiographic portography.
is not a recommended screening method for detecting large esophageal
varices.(Kumar S, Sarr MG, Kamath PS:N Engl J Med 2001; 345:1683-8)
• Detection of varices may be an emerging indication for CT.
• Diagnosis of fundal varices by multidetector row CT (MDCT) is at least as
accurate as endoscopic ultrasonography.
15. • D)- Gadolinium-enhanced magnetic resonance imaging (MRI) is becoming
recognized as a potentially useful method of detecting esophageal
varices.(Matsuo M, Kanematsu M, Kim T, et al:Am J Roentgenol 2003; 180:461-6)
• MRI :
can be used to measure portal and azygous blood flow
provides excellent detail of the vascular structures of the liver
can detect portal venous thrombosis and spleen stiffness
can accurately assess the stiffness of even fatty livers.
(Talwalkar JA, Yin M, Fidler JL, et al: Hepatology 2008; 47:332-42)
• The role of MRI in the assessment of portal hypertension requires further study.
16. Management of UGIB
GENERAL MEDICAL
MANAGEMENT
TYPE OF BLEEDING
VARICEAL BLEEDING
NON VARICEAL
BLEEDING
MEDICAL ENDOTHERAPY
SURGICAL
INERVENTION
PRESSURE
TECHNIQUES
17. A. Medical Therapy
The pharmacologic agents used in the treatment of portal hypertension are
divided into two groups:
(a) Those that decrease splanchnic blood flow
eg. Vasopressin & their analogs , somatostatin & their analogs , β-adrenergic
blocking agents(propranolol)
(b) Those that decrease intrahepatic vascular resistance.
eg. α-adrenergic blocking agents(prazosin), angiotensin receptor blocking
agents and nitrates
(but only nitrates are now considered for clinical use).
* Diuretics, by decreasing plasma volume, may reduce portal pressure but are not
recommended as sole agents for the treatment of portal hypertension.
* Metoclopramide and other gastric prokinetic agents may decrease intravariceal
pressure by contracting the lower esophageal sphincter, but these agents have not
been evaluated in clinical trials and are not recommended.
18. • Vasopressin and Its Analogs
• Vasopressin(0.1 0.5 units/minute for 4 to 12hrs(up to 48hrs) is an endogenous
peptide hormone that causes splanchnic vasoconstriction, reduces portal venous
inflow, and reduces portal pressure.
It is associated with serious systemic side effects:
* vasopressin may result in necrosis of the bowel.
* It has direct negative inotropic and chronotropic effects on the
myocardium that lead to reduced cardiac output and bradycardia,
respectively.
* antidiuresis can result in hyponatremia.
• Terlipressin(2mg bolus followed by 1mg every 4-6 hrly for 3- 5 days) is a
semisynthetic analog of vasopressin that is cleaved by endothelial peptidases to
release lysine vasopressin.
*Compared with vasopressin, terlipressin results in lower circulatory levels of
the vasopressin analog and a lower rate of systemic side effects.
• Terlipressin is the first choice in many countries because it is the only drug that
has been associated with improved survival.(Levacher S, Letoumelin P, Pateron D, et al
Lancet 1995; 346:865-8)
19. • Somatostatin and Its Analogs
Somatostatin is a 14-amino-acid peptide.
Half-life: Following intravenous injection,it has a half-life of 1 to 3
minutes; therefore, longer-acting analogs of somatostatin have been
synthesized.
Analogs: octreotide(t1/2 80-120 min), lanreotide, and vapreotide.
Action: It decreases portal pressure and collateral blood flow by
inhibiting release of glucagon.
• Dose: Following a infusion 250mg followed by an infusion of
6mg/24h for 120 h .(Avgerinos A, Nevens F, Raptis S et al. Lancet 1997; 350: 1495)
• Mostly treatment with somatostatin or octreotide is combined with
endoscopic management of variceal bleeding.
20. β-Adrenergic Blocking Agents
• Nonselective β-adrenergic blocking agents have been used extensively in
preventing variceal rebleeding.(Lebrec D, Poynard T, Hillon P, et al: N Engl J Med 1981; 305:1371-4. )
• Nonselective beta blockers such as propranolol or nadolol are preferred.
• The usual method of monitoring the efficacy of beta blockers is to observe a
decrease in the heart rate .
• The dose of propranolol or nadolol can be increased gradually every three to five
days until the target heart rate of 25% below baseline or 55 to 60 beats per minute
or the maximum tolerated dose is reached, provided that the systolic blood
pressure remains above 90 mm Hg.
• The usual starting dose of long-acting propranolol is 40 mg once daily and that of
nadolol is 20 mg once daily.
• Because the risk of bleeding is greatest at night, the beta blocker should probably
be administered in the evening.(Sugan OS, Yamamoto K, Sasao K, et al: Hepatol 2001; 34:26-31)
21. • The side effects of beta-blocker treatment are probably
overemphasized because only approximately 15% of patients need to
discontinue the drug.(Escorsell A, Ferayomi L, Bosch J, et alGastroenterology 1997; 112:2012-16)
• Pts on ß- blocker, in whom the HVPG has decreased to less than
12 mm Hg, the risk of bleeding is virtually eliminated.
• only 30% to 40% of patients respond to a beta blocker, those with better liver
function show the best response.(Escorsell A, Ferayomi L, Bosch J, et al: Gastroenterology 1997; 112:2012-
16)
• In patients who are intolerant of or who have contraindications to beta blockers,
isosorbide mononitrate has been tried but is not better than placebo in preventing
variceal bleeding.(Garcia-Pagan JC, Villanueve C, Vila MC, et al: Gastroenterology 2001; 121:908-14)
• patients who do not achieve a decrease in the HVPG to less than 12 mm Hg, or
greater than 20%, on beta blocker may not respond well to endoscopic variceal
ligation either. (Bureau C, Peron JM, Alric L, et al Hepatology 2002; 36:1361-6)
• Nitrates are no longer recommended, either alone or in combination with a beta
blocker, for primary prophylaxis to prevent first variceal bleeds.
• For secondary prophylaxis (to prevent variceal rebleeding), isosorbide
mononitrate may be added to a beta blocker.
(Garci Pagan JC, Villanueve C, Vila MC, et al: Gastroenterology 2001; 121:908-14)
22. • The ideal agent for treatment of portal hypertension would be a drug that decreases
intrahepatic vascular resistance.
• A desirable drug would be one that selectively decreases intrahepatic vascular resistance
without worsening systemic vasodilatation.
• long-term administration of prazosin causes worsening of the systemic hyperdynamic
circulation associated with portal hypertension and consequent sodium retention and
ascites.(Albillos A, Lledo JL, Rossi I, et al:Gastroenterology 1995; 109:1257-65)
• In randomized, controlled trials of losartan or another angiotensin II receptor antagonist,
irbesartan, portal pressure was not reduced significantly.
(Schepke M, Werner E, Biecker E, et al:Gastroenterology 2001; 121:389-95.
• Renal function has worsened in patients given losartan or irbesartan.
(Gonzalez-Abraldes J, Albillos A, Banares R, et alGastroenterology 2001; 121:382-8. )
• ET-receptor blockers and liver-selective NO donors are promising investigational agents
for therapies that target intrahepatic vascular resistance.(Failli P, DeFranco R, Caligiuri A, et
al:Gastroenterology 2000; 119:479-92)
• Studies suggest that simvastatin may decrease intrahepatic resistance and maintain
hepatic blood flow while decreasing portal pressure. This effect probably results from
simvastatin-mediated NO release.(Zafra C, Abraldes JG, Turnes J, et
al:Gastroenterology 2004; 126:749-55)
23. B.Pressure techniques
• Esophageal balloon
• Sengstaken blakemore tube,
• Minnesota tube
• Linton Nicholas tube(only gastric
balloon with gastric aspiration)
• Balloon should be inflated for less than 24 hrs.
75% rebleeding rate after balloon deflation.
• Most reports suggest that balloon tamponade provides
initial control of bleeding in 85% to 98% of cases.
Sleisenger and Fordtran's Gastrointestinal and Liver Disease Ninth Edition
24. • variceal rebleeding recurs soon after the balloon is deflated in
21% to 60% of patients.
• The major problem with tamponade balloons is a 30% rate of
serious complications, such as aspiration pneumonia,
esophageal rupture, and airway obstruction.
• Clinical studies have not shown a significant difference in
efficacy between vasopressin administration and balloon
tamponade.(Pitcher JL: Safety and effectiveness of the modified Sengstaken-Blakemore tube: A
prospective study. Gastroenterology 1971 Sep;61(3):291–298 )
Sleisenger and Fordtran's Gastrointestinal and Liver Disease Ninth Edition
25. ENDOSCOPIC THERAPY
Esophageal varices Gastric varices Ectopic varices
A. Sclerotherapy
B. Band Ligation
-Sclerotherapy-
( Cyanoacrylate
injection )
Duodenal Stomal Colonic
A.Endoscopic
glue injection
B. Band ligation
A. Hemostatic clips
B. Band Ligation
Embolization of
varices
26. Esophageal varices
(a) Sclerotherapy
* Endoscopic sclerotherapy has largely been supplanted by endoscopic band
ligation, except when poor visualization precludes effective band ligation of
bleeding varices.
Available evidence does not support emergency sclerotherapy as first-line
treatment of variceal bleeding.
(D’Amico G, Pietras G, Tarantino I, Pagliaro L:Gastroenterology 2003; 124:1277-91).
* The technique involves injection of a sclerosant into (intravariceal) or adjacent to
(paravariceal) a varix.
* The sclerosants used :
• sodium tetradecyl sulfate, (Sotradecol).
• sodium morrhuate,( Scleromate)
• ethanolamine oleate( Ethamolin)
• Polidocanol(3%) {lauromacrogol}
• absolute alcohol
• the choice of a sclerosant is based on availability, rather than on superior efficacy
of one agent over another.
27. • (b)Endoscopic variceal ligation
* is the preferred endoscopic modality
* the utility of band ligation in the treatment of gastric varices is
limited.
* Variceal ligation is simpler to perform than injection sclerotherapy.
* Endoscopic variceal ligation is associated with fewer complications
than sclerotherapy.
-Varices at the gastroesophageal junction are banded initially, and then more
proximal varices are banded in a spiral manner at intervals of approximately 2 cm;
the endoscope is then withdrawn.
-The procedure involves suctioning of the varix into the channel of an endoscope
and deploying a band around the varix.
-The band strangulates the varix, thereby causing thrombosis.
-Multi-band devices can be used to apply several bands without requiring
withdrawal and reinsertion of the endoscope.
-.
30. Algorithm for the prevention of
recurrent variceal bleeding (secondary
prophylaxis).
31. Gastric varices
• 25% of patients with portal hypertension have gastric varices,
• Preferred endoscopic therapy for fundal gastric variceal bleeding is
injection of polymers of cyanoacrylate( N-butyl-2-cyanoacrylate).
(Lo G, Lai K, Cheng J, et al Hepatology 2001; 33:1060-4)
Sarin classificatiion
Type 1 gastroesophageal varices (GOV1)-2 to 5 cm below the
gastroesophageal junction and are in continuity with esophageal varices.
• Type 2 gastroesophageal varices (GOV2) -in the cardia and fundus of the
stomach and in continuity with esophageal varices.
• Type 1 (IGV1)-varices that occur in the fundus of the stomach in the
absence of esophageal varices are called isolated gastric varices.
• Type 2 (IGV2)- varices that occur in the gastric body, antrum, or pylorus
are called isolated gastric varices.
Sarin SK, Lahoti D, Saxena SP Hepatology 1992; 16:1343-9., et al
34. ectopic varices
• Varices that occur at a site other than the gastroesophageal junction are
termed ectopic varices
• less than 5% of all varix-related bleeding episodes.
• Ectopic varices most commonly manifest with melena or hematemesis.
• The duodenum is a most common site of ectopic varices.
• in patients with inflammatory bowel disease and primary sclerosing
cholangitis who have undergone a proctocolectomy with creation of an
ileostomy varices may develop at junction & termed as stomal varices.
.
• Anorectal varices are reported in 10% to 40% of cirrhotic pts.
38. TRANSJUGULAR INTRAHEPATIC
PORTOSYSTEMIC SHUNT(TIPS)
• TIPS reduces elevated portal pressure by creating a communication
between the hepatic vein and an intrahepatic branch of the portal vein.
TIPS is used to treat complications of portal hypertension, mainly
* mainly refactory variceal bleeding and refractory ascites,
* as well as Budd-Chiari syndrome,
* hepatic hydrothorax, and
* hepatorenal syndrome.
• Procedure, the hepatic vein is cannulated through a transjugular
approach, and by using a Rosch needle, the portal vein is cannulated,then
a guidewire is passed to connect the hepatic vein and a branch of the
portal vein. Dilate the tract and a metallic stent is placed.
• Dilate the tract at the confluence of the hepatic vein if required to reduce
the portacaval pressure gradient (the pressure difference between the
portal vein and the inferior vena cava) to below 12 mm Hg
39. Child-Turcotte-Pugh Scoring System
and Classification
PARAMETER NUMERICAL SCORE
1 2 3
Ascites None Slight Moderate/severe
Encephalopathy none Slight/Mod Mod/severe
Bilirubin(mg/dl) <2 2-3 >3
Albumin(g/dl) >3.5 2.8-3.5 <2.8
Prothrombin time(sec
increased)
1-3 4-6 >6
Total numerical score Child class
5-6 A
7-9 B
10-15 C
40. MELD score
• The MELD score was created originally to predict survival in patients with cirrhosis and
portal hypertension undergoing placement of a transjugular intrahepatic portosystemic
shunt (TIPS).(Kamath PS, Kim WR: Hepatology 2007; 45:797-805)
• The MELD score incorporates three objective variables into a mathematical formula:
9.57 loge(creatinine) + 3.78 loge(total bilirubin) + 11.2 loge(INR) + 6.43.
• The working range is 6 to 40.
• MELD is used most often for prioritizing the allocation of donor organs for liver
transplantation.
• Before 2002, organs were allocated by the United Network for Organ Sharing (UNOS) on the
basis of the CTP score and time on the wait list.
• In this system were raised in light of subjective variables in the CTP score (specifically, the
amount of ascites and grade of encephalopathy)
• The MELD score eliminating wait time as a criterion for organ allocation.
• Since implementation of the MELD score for prioritizing organ allocation, the number of
deaths among patients on the wait list has decreased
• In interpreting the MELD Score in hospitalized patients, the 3 month mortality is:
40 or more — 71.3% mortality
30–39 — 52.6% mortality
20–29 — 19.6% mortality
10–19 — 6.0% mortality
<9 — 1.9% mortality (Wiesner et al.. Gastroenterology (2003) vol. 124 (1).
41. Selection of patients-TIPS
• TIPS may worsen liver function & increase the risk of hepatic
encephalopathy.
• Factors associated with a poor prognosis include a
* Emergency TIPS
* Serum alanine aminotransferase (ALT) level
greater than 100 U/L,
* Serum bilirubin level greater than 3 mg/dL
* Pre-TIPS hepatic encephalopathy unrelated to
bleeding.
* Patients with a high CTP(class B & C) or MELD
score.
(Chalasani N, Clark WS, Martin LG, et al:Gastroenterology 2000; 118:138-44).