1) The document discusses portal vein thrombosis (PVT), specifically extrahepatic portal vein obstruction (EHPVO). EHPVO is a common cause of portal hypertension and can present from infancy to adulthood.
2) Clinical features depend on whether the PVT is acute or chronic. Acute PVT may cause abdominal pain and infection, while chronic EHPVO often presents with splenomegaly, variceal bleeding, and complications of portal hypertension.
3) Diagnosis involves imaging tests like Doppler ultrasound, CT, or MRI to identify thrombosis, cavernous transformation of the portal vein, and collateral circulation. Treatment depends on whether the PVT is recent or chronic, with recent cases
This document discusses portal hypertension in children. It begins by defining portal hypertension and its causes, which can be prehepatic, intrahepatic, or posthepatic. It then covers the pathophysiology, clinical features such as gastrointestinal bleeding, ascites, and hepatic encephalopathy. It discusses methods of diagnosis including endoscopy, imaging, and labs. Potential complications are outlined as well as approaches to management, including treatment of acute bleeding, reducing portal pressure endoscopically or surgically, and long-term medical therapy to prevent variceal bleeding.
This document discusses cirrhosis and its complications over two parts. Part I covers what cirrhosis is, its etiologies, clinical presentations, physical exam findings, laboratory tests, liver biopsy, and prognosis for different etiologies. Part II covers complications of cirrhosis including portal hypertension, variceal bleeding, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatorenal syndrome, hepatopulmonary syndrome, and hepatocellular carcinoma screening and treatment. Liver transplantation is also discussed as a treatment option.
1) A 35-year old female presented with hematemesis and was found to have signs of portal hypertension including splenomegaly and visible veins on her abdominal wall.
2) Portal hypertension is increased blood pressure in the portal vein, usually caused by cirrhosis of the liver. It can lead to dangerous variceal bleeding from enlarged veins in the esophagus or stomach.
3) Diagnosis involves ultrasound, endoscopy, and liver tests. Treatment focuses on stabilizing any bleeding, identifying its cause via endoscopy, and managing the underlying cause of portal hypertension like cirrhosis.
Portal hypertension in children can be caused by conditions that increase blood flow or resistance through the portal vein, leading to elevated portal venous pressure above 10 mmHg. The main consequences are formation of collateral blood vessels and risk of gastrointestinal bleeding from esophageal or rectal varices. Diagnosis involves blood tests and imaging of the liver and portal vein system. Management focuses on preventing the first bleed through medication or banding, stabilizing acute bleeding episodes, and using banding or medication to prevent further bleeding incidents. Surgical shunting of blood flow may be considered to decrease portal venous pressure in severe cases.
This document provides an overview of ascites, including:
- Ascites is an accumulation of fluid in the peritoneal cavity. It is usually caused by cirrhosis and portal hypertension which increases hydrostatic pressure in blood vessels in the abdomen.
- Diagnosis involves physical exam findings like abdominal distension. Imaging like ultrasound can identify fluid levels. Paracentesis analyzes fluid for causes like spontaneous bacterial peritonitis.
- Treatment depends on the underlying cause but may include dietary sodium restriction, diuretics, large volume paracentesis, TIPSS procedure to lower pressure, or liver transplantation for cirrhosis. Refractory ascites requires more aggressive management.
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,
A 3 month old child presented with neonatal hepatitis and ascites. Initial tests showed liver damage and worsening liver function. Further testing found very high levels of sialic acid in the urine, suggesting Salla disease. Salla disease is a rare lysosomal storage disorder caused by a defect in sialic acid metabolism, characterized by ascites and liver involvement. The child was treated supportively but died from complications within two weeks.
This document discusses portal hypertension in children. It begins by defining portal hypertension and its causes, which can be prehepatic, intrahepatic, or posthepatic. It then covers the pathophysiology, clinical features such as gastrointestinal bleeding, ascites, and hepatic encephalopathy. It discusses methods of diagnosis including endoscopy, imaging, and labs. Potential complications are outlined as well as approaches to management, including treatment of acute bleeding, reducing portal pressure endoscopically or surgically, and long-term medical therapy to prevent variceal bleeding.
This document discusses cirrhosis and its complications over two parts. Part I covers what cirrhosis is, its etiologies, clinical presentations, physical exam findings, laboratory tests, liver biopsy, and prognosis for different etiologies. Part II covers complications of cirrhosis including portal hypertension, variceal bleeding, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatorenal syndrome, hepatopulmonary syndrome, and hepatocellular carcinoma screening and treatment. Liver transplantation is also discussed as a treatment option.
1) A 35-year old female presented with hematemesis and was found to have signs of portal hypertension including splenomegaly and visible veins on her abdominal wall.
2) Portal hypertension is increased blood pressure in the portal vein, usually caused by cirrhosis of the liver. It can lead to dangerous variceal bleeding from enlarged veins in the esophagus or stomach.
3) Diagnosis involves ultrasound, endoscopy, and liver tests. Treatment focuses on stabilizing any bleeding, identifying its cause via endoscopy, and managing the underlying cause of portal hypertension like cirrhosis.
Portal hypertension in children can be caused by conditions that increase blood flow or resistance through the portal vein, leading to elevated portal venous pressure above 10 mmHg. The main consequences are formation of collateral blood vessels and risk of gastrointestinal bleeding from esophageal or rectal varices. Diagnosis involves blood tests and imaging of the liver and portal vein system. Management focuses on preventing the first bleed through medication or banding, stabilizing acute bleeding episodes, and using banding or medication to prevent further bleeding incidents. Surgical shunting of blood flow may be considered to decrease portal venous pressure in severe cases.
This document provides an overview of ascites, including:
- Ascites is an accumulation of fluid in the peritoneal cavity. It is usually caused by cirrhosis and portal hypertension which increases hydrostatic pressure in blood vessels in the abdomen.
- Diagnosis involves physical exam findings like abdominal distension. Imaging like ultrasound can identify fluid levels. Paracentesis analyzes fluid for causes like spontaneous bacterial peritonitis.
- Treatment depends on the underlying cause but may include dietary sodium restriction, diuretics, large volume paracentesis, TIPSS procedure to lower pressure, or liver transplantation for cirrhosis. Refractory ascites requires more aggressive management.
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,
A 3 month old child presented with neonatal hepatitis and ascites. Initial tests showed liver damage and worsening liver function. Further testing found very high levels of sialic acid in the urine, suggesting Salla disease. Salla disease is a rare lysosomal storage disorder caused by a defect in sialic acid metabolism, characterized by ascites and liver involvement. The child was treated supportively but died from complications within two weeks.
This document provides information on ascites including its definition, causes, diagnosis, and management. Ascites is defined as the accumulation of free fluid in the peritoneal cavity, most often caused by liver cirrhosis (75% of cases), malignancy, or heart failure. Diagnosis involves history, physical exam finding shifting dullness or fluid wave, and abdominal ultrasound or paracentesis. Initial ascites management consists of sodium restriction, diuretics, and large volume paracentesis for refractory ascites.
Portal hypertension occurs when blood pressure increases in the portal venous system, which normally carries blood from the gastrointestinal tract to the liver. It is defined as a hepatic venous pressure gradient over 10mm Hg. There are three types - pre-hepatic, intra-hepatic, and post-hepatic - depending on the site of vascular obstruction. Common causes include cirrhosis, schistosomiasis, and portal vein thrombosis. Clinical manifestations involve complications from increased portosystemic shunting and include ascites, esophageal varices, hemorrhoids, and hepatic encephalopathy. Diagnostic evaluations involve blood tests, imaging, and endoscopy. Treatment options include medications, endoscopic therapy, TIPS procedure,
This document discusses portal hypertension (PH), including its definition, classification, pathophysiology, etiology, clinical features, complications, and diagnosis. Some key points:
1. PH is defined as a portal venous pressure gradient above 10 mmHg. It can be pre-sinusoidal, sinusoidal, or post-sinusoidal based on location of blockage.
2. Common causes are cirrhosis, portal or hepatic vein thrombosis, and Budd-Chiari syndrome. Cirrhosis results from fibrosis narrowing hepatic sinusoids.
3. Clinical features include splenomegaly, abdominal collaterals, ascites, gastrointestinal bleeding from varices, and hepatic encephalopathy.
This document discusses complications that can arise in patients with cirrhosis, including portal hypertension, ascites, hepatic encephalopathy, and hepatorenal syndrome. It provides details on the pathophysiology, clinical presentation, diagnosis, and treatment of these complications. Specifically, it focuses on portal hypertension and the development of varices, describing the risks of variceal bleeding and approaches to prevention and management. It also covers ascites extensively, explaining how and why it develops in cirrhosis and its treatment with diuretics and sodium restriction.
Portal hypertension in children is usually caused by cirrhosis blocking blood flow in the liver. This raises pressure in the portal vein, leading to complications like splenomegaly, portosystemic shunts and varices. Varices are abnormal enlarged veins that can bleed, occurring in the esophagus, stomach, anus and other locations. Diagnosis involves detecting signs of chronic liver disease, encephalopathy, ascites and varices through tests like ultrasound and endoscopy. Treatment focuses on managing complications and underlying causes.
Cirrhosis is the end stage of chronic liver disease caused by various chronic stress factors that damage the liver over time. This results in progressive fibrosis that destroys the liver's normal structure and function. Common causes include alcohol, hepatitis B/C, toxins, and unknown factors. Complications arise from portal hypertension and liver dysfunction, such as ascites, hepatic encephalopathy, and bleeding disorders. Management focuses on treating complications, slowing fibrosis, and preventing further liver damage through lifestyle changes and medications.
This document discusses various types of cirrhosis including alcoholic cirrhosis, cirrhosis due to viral hepatitis, autoimmune hepatitis, nonalcoholic fatty liver disease, biliary cirrhosis, and cardiac cirrhosis. It covers the pathogenesis, clinical features, diagnosis, and treatment of alcoholic cirrhosis in detail. For other types of cirrhosis, it focuses on their causes and management of complications, which are generally similar regardless of the underlying etiology of cirrhosis. The main complications discussed are ascites, variceal bleeding, and hepatic encephalopathy.
Presentation by Dr. Mishal Saleem on the topic of Extra hepatic manifestation of hep C, which is a grey area nut very important topic for FCPS Residents.
The document discusses portal hypertension in children. It covers the anatomy of the portal system, causes/classifications of portal hypertension, clinical manifestations, diagnosis, and treatment. Regarding diagnosis, it describes using endoscopy to identify varices, ultrasound to detect portal vein thrombosis, and CT/MRI/venography to further evaluate vascular anatomy. Treatment of acute variceal bleeding involves stabilizing the patient and reducing portal pressure to stop bleeding.
Portal hypertension is caused by increased vascular resistance and blood flow and can result from cirrhosis, vascular diseases, or other conditions. It leads to complications like ascites, variceal bleeding, and hepatic encephalopathy. Treatment involves general measures, variceal treatment including banding, TIPS procedure, and in some cases transplantation. Ascites is treated with paracentesis and diuretics along with albumin to prevent renal failure.
portal hypertension UG class by Prof. Ajay Khanna, IMS, BHU, Varanasi, IndiaDivya Khanna
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.
Portal hypertension is high blood pressure in the portal vein system that supplies blood to the liver. It has various clinical manifestations that may require surgical management. The surgical approach depends on factors like the underlying liver disease severity and venous anatomy. The main goals of surgery are to decrease portal pressure and prevent complications by bypassing resistance sites or directly treating complications. Procedures include devascularization to reduce variceal blood flow or decompression procedures to reduce portal pressure while maintaining hepatic blood flow. Selective shunts only decompress the variceal compartment while non-selective or partial shunts provide complete or incomplete decompression of the entire portal system. The distal splenorenal shunt is a commonly used selective shunt that
Cirrhosis is a disease where the liver transforms into regenerating nodules surrounded by fibrous bands. Common causes include alcoholism, viral hepatitis, and non-alcoholic steatohepatitis. Complications include portal hypertension, ascites, hepatic encephalopathy, and hepatorenal syndrome. Portal hypertension is defined as a hepatic venous pressure gradient over 5 mmHg and can cause variceal bleeding, ascites, and hypersplenism. Ascites is treated initially with sodium restriction and diuretics, while refractory ascites may require paracentesis, TIPS, or liver transplant. Hepatic encephalopathy is caused by increased ammonia and treated with lactulose and rifaxim
Portal hypertension:A disease better controlled than cured.KETAN VAGHOLKAR
Portal hypertension is one of the common causes of upper gastrointestinal bleeding. It is a very lethal condition. Prompt diagnosis and commencement of early medical treatment can help keeping the disease under control. Surgery is a very useful adjunct in uncontrollable bleeding and in long term prevention in certain selected cases.
This document discusses oesophageal varices, which are dilated and tortuous veins in the oesophageal wall caused by increased venous pressure. Varices are prone to rupture and bleeding. The document defines portal hypertension and discusses the epidemiology, etiology, risk factors, pathophysiology, clinical manifestations, diagnostic evaluations, medical and surgical management, nursing care, and conclusions regarding oesophageal varices. It also summarizes two research articles on using capsule endoscopy to diagnose varices and using blood ammonia levels to predict variceal presence and bleeding risk.
Portal hypertension can be caused by conditions that block the portal vein (precirrhotic) or damage the liver (cirrhotic). It leads to complications like ascites, esophageal varices, and bleeding. Symptoms include abdominal swelling and pain, bleeding, and fatigue. Treatment focuses on reducing portal pressure through dietary changes, diuretics, banding or sclerotherapy of varices, transjugular intrahepatic portosystemic shunting (TIPS), or surgery in severe cases.
Portal hypertension is elevation of portal venous pressure
above 10-12 mm Hg (normal 5-10 mm Hg). Portal
hypertension results from (a) increased resistance to portal
blood flow and (b) high portal blood flow.
Portal vein thrombosis can occur with or without underlying liver disease. It refers to the development of a thrombus in the portal vein or its branches.
Acute portal vein thrombosis presents with abdominal pain and may lead to complications like intestinal ischemia or infarction if not treated promptly with anticoagulation. Chronic portal vein thrombosis results in the formation of collateral vessels and portal hypertension over time. Common complications include bleeding from esophageal varices, recurrent thrombosis, and portal cavernoma cholangiopathy. Imaging plays an important role in the diagnosis and management of both acute and chronic portal vein thrombosis.
1. Chronic cholestasis can be caused by intrahepatic or extrahepatic conditions. Common intrahepatic causes include primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and drug-induced liver injury (DILI).
2. PBC is an autoimmune disease characterized by progressive destruction of intrahepatic bile ducts, presence of antimitochondrial antibodies (AMA), and histologic findings of florid duct lesions on liver biopsy. PBC diagnosis requires two of three criteria: cholestatic liver enzymes, AMA positivity, or liver biopsy consistent with PBC.
3. PSC is a chronic inflammatory condition of
This document provides information on ascites including its definition, causes, diagnosis, and management. Ascites is defined as the accumulation of free fluid in the peritoneal cavity, most often caused by liver cirrhosis (75% of cases), malignancy, or heart failure. Diagnosis involves history, physical exam finding shifting dullness or fluid wave, and abdominal ultrasound or paracentesis. Initial ascites management consists of sodium restriction, diuretics, and large volume paracentesis for refractory ascites.
Portal hypertension occurs when blood pressure increases in the portal venous system, which normally carries blood from the gastrointestinal tract to the liver. It is defined as a hepatic venous pressure gradient over 10mm Hg. There are three types - pre-hepatic, intra-hepatic, and post-hepatic - depending on the site of vascular obstruction. Common causes include cirrhosis, schistosomiasis, and portal vein thrombosis. Clinical manifestations involve complications from increased portosystemic shunting and include ascites, esophageal varices, hemorrhoids, and hepatic encephalopathy. Diagnostic evaluations involve blood tests, imaging, and endoscopy. Treatment options include medications, endoscopic therapy, TIPS procedure,
This document discusses portal hypertension (PH), including its definition, classification, pathophysiology, etiology, clinical features, complications, and diagnosis. Some key points:
1. PH is defined as a portal venous pressure gradient above 10 mmHg. It can be pre-sinusoidal, sinusoidal, or post-sinusoidal based on location of blockage.
2. Common causes are cirrhosis, portal or hepatic vein thrombosis, and Budd-Chiari syndrome. Cirrhosis results from fibrosis narrowing hepatic sinusoids.
3. Clinical features include splenomegaly, abdominal collaterals, ascites, gastrointestinal bleeding from varices, and hepatic encephalopathy.
This document discusses complications that can arise in patients with cirrhosis, including portal hypertension, ascites, hepatic encephalopathy, and hepatorenal syndrome. It provides details on the pathophysiology, clinical presentation, diagnosis, and treatment of these complications. Specifically, it focuses on portal hypertension and the development of varices, describing the risks of variceal bleeding and approaches to prevention and management. It also covers ascites extensively, explaining how and why it develops in cirrhosis and its treatment with diuretics and sodium restriction.
Portal hypertension in children is usually caused by cirrhosis blocking blood flow in the liver. This raises pressure in the portal vein, leading to complications like splenomegaly, portosystemic shunts and varices. Varices are abnormal enlarged veins that can bleed, occurring in the esophagus, stomach, anus and other locations. Diagnosis involves detecting signs of chronic liver disease, encephalopathy, ascites and varices through tests like ultrasound and endoscopy. Treatment focuses on managing complications and underlying causes.
Cirrhosis is the end stage of chronic liver disease caused by various chronic stress factors that damage the liver over time. This results in progressive fibrosis that destroys the liver's normal structure and function. Common causes include alcohol, hepatitis B/C, toxins, and unknown factors. Complications arise from portal hypertension and liver dysfunction, such as ascites, hepatic encephalopathy, and bleeding disorders. Management focuses on treating complications, slowing fibrosis, and preventing further liver damage through lifestyle changes and medications.
This document discusses various types of cirrhosis including alcoholic cirrhosis, cirrhosis due to viral hepatitis, autoimmune hepatitis, nonalcoholic fatty liver disease, biliary cirrhosis, and cardiac cirrhosis. It covers the pathogenesis, clinical features, diagnosis, and treatment of alcoholic cirrhosis in detail. For other types of cirrhosis, it focuses on their causes and management of complications, which are generally similar regardless of the underlying etiology of cirrhosis. The main complications discussed are ascites, variceal bleeding, and hepatic encephalopathy.
Presentation by Dr. Mishal Saleem on the topic of Extra hepatic manifestation of hep C, which is a grey area nut very important topic for FCPS Residents.
The document discusses portal hypertension in children. It covers the anatomy of the portal system, causes/classifications of portal hypertension, clinical manifestations, diagnosis, and treatment. Regarding diagnosis, it describes using endoscopy to identify varices, ultrasound to detect portal vein thrombosis, and CT/MRI/venography to further evaluate vascular anatomy. Treatment of acute variceal bleeding involves stabilizing the patient and reducing portal pressure to stop bleeding.
Portal hypertension is caused by increased vascular resistance and blood flow and can result from cirrhosis, vascular diseases, or other conditions. It leads to complications like ascites, variceal bleeding, and hepatic encephalopathy. Treatment involves general measures, variceal treatment including banding, TIPS procedure, and in some cases transplantation. Ascites is treated with paracentesis and diuretics along with albumin to prevent renal failure.
portal hypertension UG class by Prof. Ajay Khanna, IMS, BHU, Varanasi, IndiaDivya Khanna
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.
Portal hypertension is high blood pressure in the portal vein system that supplies blood to the liver. It has various clinical manifestations that may require surgical management. The surgical approach depends on factors like the underlying liver disease severity and venous anatomy. The main goals of surgery are to decrease portal pressure and prevent complications by bypassing resistance sites or directly treating complications. Procedures include devascularization to reduce variceal blood flow or decompression procedures to reduce portal pressure while maintaining hepatic blood flow. Selective shunts only decompress the variceal compartment while non-selective or partial shunts provide complete or incomplete decompression of the entire portal system. The distal splenorenal shunt is a commonly used selective shunt that
Cirrhosis is a disease where the liver transforms into regenerating nodules surrounded by fibrous bands. Common causes include alcoholism, viral hepatitis, and non-alcoholic steatohepatitis. Complications include portal hypertension, ascites, hepatic encephalopathy, and hepatorenal syndrome. Portal hypertension is defined as a hepatic venous pressure gradient over 5 mmHg and can cause variceal bleeding, ascites, and hypersplenism. Ascites is treated initially with sodium restriction and diuretics, while refractory ascites may require paracentesis, TIPS, or liver transplant. Hepatic encephalopathy is caused by increased ammonia and treated with lactulose and rifaxim
Portal hypertension:A disease better controlled than cured.KETAN VAGHOLKAR
Portal hypertension is one of the common causes of upper gastrointestinal bleeding. It is a very lethal condition. Prompt diagnosis and commencement of early medical treatment can help keeping the disease under control. Surgery is a very useful adjunct in uncontrollable bleeding and in long term prevention in certain selected cases.
This document discusses oesophageal varices, which are dilated and tortuous veins in the oesophageal wall caused by increased venous pressure. Varices are prone to rupture and bleeding. The document defines portal hypertension and discusses the epidemiology, etiology, risk factors, pathophysiology, clinical manifestations, diagnostic evaluations, medical and surgical management, nursing care, and conclusions regarding oesophageal varices. It also summarizes two research articles on using capsule endoscopy to diagnose varices and using blood ammonia levels to predict variceal presence and bleeding risk.
Portal hypertension can be caused by conditions that block the portal vein (precirrhotic) or damage the liver (cirrhotic). It leads to complications like ascites, esophageal varices, and bleeding. Symptoms include abdominal swelling and pain, bleeding, and fatigue. Treatment focuses on reducing portal pressure through dietary changes, diuretics, banding or sclerotherapy of varices, transjugular intrahepatic portosystemic shunting (TIPS), or surgery in severe cases.
Portal hypertension is elevation of portal venous pressure
above 10-12 mm Hg (normal 5-10 mm Hg). Portal
hypertension results from (a) increased resistance to portal
blood flow and (b) high portal blood flow.
Portal vein thrombosis can occur with or without underlying liver disease. It refers to the development of a thrombus in the portal vein or its branches.
Acute portal vein thrombosis presents with abdominal pain and may lead to complications like intestinal ischemia or infarction if not treated promptly with anticoagulation. Chronic portal vein thrombosis results in the formation of collateral vessels and portal hypertension over time. Common complications include bleeding from esophageal varices, recurrent thrombosis, and portal cavernoma cholangiopathy. Imaging plays an important role in the diagnosis and management of both acute and chronic portal vein thrombosis.
1. Chronic cholestasis can be caused by intrahepatic or extrahepatic conditions. Common intrahepatic causes include primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and drug-induced liver injury (DILI).
2. PBC is an autoimmune disease characterized by progressive destruction of intrahepatic bile ducts, presence of antimitochondrial antibodies (AMA), and histologic findings of florid duct lesions on liver biopsy. PBC diagnosis requires two of three criteria: cholestatic liver enzymes, AMA positivity, or liver biopsy consistent with PBC.
3. PSC is a chronic inflammatory condition of
This document discusses the approach to evaluating and treating bleeding in neonates. It notes that the neonatal coagulation system is different from adults, with lower levels of several coagulation factors at birth. A clinical approach is outlined, examining factors like the baby's health status and risk factors. Common causes of bleeding include coagulation defects, platelet issues, fibrinolytic dysfunction, and vascular abnormalities. Tests like complete blood count, coagulation studies, and peripheral smear can help identify the underlying cause. Treatment depends on the diagnosis but may include vitamin K, fresh frozen plasma, or specific coagulation factor replacements.
The document discusses the approach to evaluating and diagnosing bleeding in neonates. It notes that while the neonatal coagulation system is immature compared to adults, healthy term infants do not typically have bleeding issues. A bleeding neonate should first be assessed for general health and vitamin K administration history. Screening tests include a complete blood count, coagulation tests, and peripheral smear. Abnormal results can indicate disorders like disseminated intravascular coagulation, infection, liver disease, immune thrombocytopenia, or inherited coagulation factor deficiencies. The causes, patterns, and management of various bleeding disorders seen in neonates are described.
HVOTO (Hepatic Venous Outflow Tract Obstruction), also known as Budd-Chiari syndrome, is caused by obstruction of the hepatic veins or inferior vena cava. It has a variable presentation ranging from acute liver failure to chronic liver disease manifestations. Investigations include Doppler ultrasonography, CT/MRI scans, and hepatic venography. Treatment depends on the severity and includes anticoagulation, thrombolysis, TIPS, and liver transplantation in severe cases.
This document provides an overview of cholestatic liver diseases in adults. It defines cholestasis as a disruption of bile flow that can occur within hepatocytes or in intrahepatic or extrahepatic bile ducts. Cholestatic diseases are classified as intrahepatic or extrahepatic based on imaging findings. Examples of intrahepatic and extrahepatic causes are provided. The document then discusses primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) in detail, including their definitions, pathophysiology, presentations, diagnostic criteria, management, and comparisons. It also briefly covers drug-induced cholestasis, hepatitis, and post-liver transplantation chole
1. Primary sclerosing cholangitis (PSC) is a chronic, progressive cholestatic liver disease characterized by inflammation and fibrosis of both intrahepatic and extrahepatic bile ducts, leading to multifocal bile duct strictures.
2. PSC is diagnosed based on cholangiography showing characteristic bile duct changes along with elevated cholestatic liver enzymes and exclusion of secondary causes.
3. There is no established medical treatment for PSC, but ursodeoxycholic acid and immunosuppressants have been used to limited benefit. Endoscopic retrograde cholangiography can help relieve symptoms from dominant strictures.
Presentation by DR. MISHAL on the topic of NON CIRRHOTIC PORTAL HYPERTENSION. Its a grey area but very important topic particularly for FCPS residents .
EHPVO ( Extra Hepatic Portal Vein Obstruction)drmanojkurmana
This document provides an overview of extra-hepatic portal vein obstruction (EHPVO). It discusses the prevalence, etiology, clinical features, diagnosis, management, and prognosis of EHPVO. Key points include that EHPVO is characterized by obstruction of the portal vein outside the liver, it is more common in India than Western countries, causes include thrombosis and hypercoagulable states, clinical features include variceal bleeding and splenomegaly, management involves preventing complications through anticoagulation and procedures like TIPS, and prognosis depends on the underlying cause and presence of complications.
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.
Hepatic cysts are abnormal fluid-filled spaces in the hepatic parenchyma and biliary tree
They are categorized into 3 main types:
fibrocystic diseases of the liver
cystadenomas and cystadenocarcinomas
and hydatid cysts
This document discusses polycythemia, a blood disorder characterized by the overproduction of red blood cells. It defines polycythemia and classifies it as either relative, absolute primary, or absolute secondary. Primary polycythemia, also called polycythemia vera, is caused by a mutation in the JAK2 gene that results in excessive blood cell production. Signs and symptoms include headache, dizziness, itching and red skin. Treatment focuses on phlebotomy to reduce red blood cell counts as well as medications to suppress bone marrow activity.
This document discusses coagulopathy in patients with cirrhosis. It notes that cirrhosis was traditionally viewed as a hypocoagulable state, but patients also have a high risk of thrombosis. Coagulation is complexly altered in cirrhosis through effects on platelets, coagulation factors, natural anticoagulants, fibrinolysis and inflammation. Prevention of bleeding focuses on vitamin K, fresh frozen plasma, platelets and new thrombopoietin receptor agonists which may increase platelet counts before procedures.
This document discusses the management of coagulopathy and bleeding risk in a patient with chronic liver disease undergoing surgery. It notes that the patient has mildly abnormal coagulation tests including an INR of 2.2, but that such tests do not reliably predict bleeding risk. It emphasizes that prophylactic transfusions are not recommended and that bleeding is best managed by addressing its underlying cause rather than by correcting coagulation parameters. Active bleeding should be treated with vasoconstrictors, endoscopic therapies, and restrictive transfusions as needed while avoiding volume overload.
- The document provides an overview of gastrointestinal bleeding (GIB), including causes, evaluation, and management.
- Common causes of upper GI bleeding (UGIB) include peptic ulcer disease, esophageal varices, esophagitis, and malignancy. Evaluation involves history, physical exam, and laboratory tests to assess severity and risk of rebleeding.
- Initial management of UGIB includes IV fluids, blood transfusions if needed, and upper endoscopy within 24 hours to identify the source of bleeding and guide treatment. Management depends on the cause and risk of rebleeding.
Biliary atresia is a rare disease where the bile ducts outside and inside the liver are destroyed, preventing bile from draining from the liver to the intestines. This leads to jaundice, liver damage, and life-threatening cirrhosis if left untreated. The cause is unknown but may involve a viral infection. Affected infants show prolonged jaundice beyond 14 days of age. Diagnosis involves blood tests, imaging like ultrasound and MRCP, and liver biopsy to examine duct proliferation and fibrosis. The definitive diagnosis is made during surgery using intraoperative cholangiography. Early diagnosis is important so the bile ducts can be surgically reconstructed to drain bile before irreversible liver damage occurs.
Biliary atresia is a progressive disease affecting the bile ducts in infants. It is the most common cause of liver transplantation in children. The Kasai procedure involves removing the damaged bile ducts and connecting the liver to the intestine to restore bile flow, but only half of patients achieve long-term native liver survival. Even after a successful Kasai procedure, patients remain at risk of complications like cholangitis, portal hypertension, and hepatopulmonary syndrome that may eventually require liver transplantation.
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.
This document summarizes infectious diseases of the liver, focusing on pyogenic liver abscess and amebic liver abscess. Pyogenic liver abscess is usually polymicrobial, with risk factors including biliary tract disease, cirrhosis, and diabetes. Clinical features include fever, right upper quadrant pain, and jaundice. Treatment involves antibiotics and drainage of large abscesses. Amebic liver abscess is caused by Entamoeba histolytica and presents with nonspecific symptoms. Serology and imaging can help with diagnosis, and metronidazole is the treatment. Complications of liver abscesses include rupture, fistula formation, and spread to other organs.
This document summarizes information about liver abscesses, including pyogenic and amebic types. It discusses the epidemiology, causes, clinical presentation, diagnosis, and management of both types of liver abscesses. For pyogenic liver abscesses, it notes that they are usually polymicrobial infections most commonly caused by E. coli or Klebsiella. Cryptogenic cases may indicate underlying malignancy. Diabetes is a major risk factor. Ultrasound and CT are important diagnostic tools. Treatment involves drainage and antibiotics. For amebic liver abscesses, it indicates they are endemic in India and usually caused by Entamoeba histolytica infection following travel to endemic areas. Clinical features, ultrasound and serology can aid
Similar to Kurdistan Boar GEH J Club: PVT From Saudi J Gastroenterology. (20)
Dietary fiber from whole foods like grains, legumes, vegetables, and fruits has demonstrated benefits for gastrointestinal (GIT) health. Isolated and extracted fibers also show promising regulatory effects on the gut and microbiome. However, fibers have varying physicochemical properties depending on their origin and processing that influence their functional characteristics and clinical applications. More research is needed, including well-designed randomized controlled trials, to determine which fiber sources, characteristics, doses and durations optimize GIT health benefits and manage gastrointestinal disorders. Combining fibers with different physiological effects may be a promising therapeutic strategy.
- Coronaviruses typically cause common colds but SARS-CoV and MERS-CoV can cause pneumonia, respiratory failure, and death. A novel coronavirus, SARS-CoV-2, emerged in Wuhan, China in late 2019 and caused a global pandemic.
- SARS-CoV-2 spreads mainly through respiratory droplets when people cough, sneeze or talk within 6 feet of each other. Asymptomatic and pre-symptomatic people are highly infectious.
- COVID-19 symptoms range from mild to critical illness. The elderly and those with pre-existing conditions are at higher risk for severe disease. Diagnosis involves PCR testing of respiratory samples.
- Sexual dysfunction and infertility are more prevalent in men with IBD compared to the general population.
- Depression is the most consistent negative predictive factor of sexual function among men with IBD.
- Sulfasalazine can reversibly reduce male fertility, so it is recommended to discontinue 3-4 months prior to conception. Most other IBD medications do not significantly impact fertility.
- Men with IBD have an increased risk of prostate cancer and prostate cancer screening guidelines for higher risk patients should be followed.
The document summarizes a consensus clinical care pathway for women with inflammatory bowel disease (IBD) who are considering pregnancy or are pregnant. The pathway was created by an expert multidisciplinary team representing multiple societies to provide standardized, evidence-based recommendations for gastroenterology and obstetric providers to ensure healthy pregnancies for women with IBD. It addresses the lack of consistent advice available previously by compiling available data on therapeutic options for IBD that have increased over the last 15 years and putting them into an easily accessible format for clinical practice.
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Upper and lower GI endoscopies have diagnostic, therapeutic, and screening indications. For upper endoscopy, common diagnostic indications include dyspepsia in patients over age 60 or with red flags, upper GI bleeding, and dysphagia. Therapeutic uses include treatment of bleeding, removal of foreign bodies, dilation of strictures, and stenting. Screening is done for portal hypertension, Barrett's esophagus, eosinophilic esophagitis, and cancers. Lower endoscopy indications involve diagnostic evaluation of bleeding, abdominal pain, diarrhea, and screening of average-risk adults over 50 and high-risk groups. Therapeutic colonoscopy is used for polypectomy, bleeding treatment, and stricture dilation
Dr. Hiwa Abubakir and Dr. Mohamed Alshekhani discuss the management of nonvariceal gastrointestinal bleeding. They recommend endoscopy within 24 hours, or earlier for high-risk patients, to identify and treat the bleeding source. A variety of endoscopic tools can be used for hemostasis, including injection of adrenaline combined with clips, bands, electrocautery, or laser coagulation. Newer tools like over-the-scope clips are best for high-risk or recurrent bleeders. Doppler probes help ensure complete vessel occlusion. Additional prothrombotic agents or interventions may be needed in some cases.
The document discusses antithrombotic strategies for patients with diabetes who are at risk of cardiovascular events. It proposes strategies for primary prevention, stable coronary artery disease, acute coronary syndromes, ischemic stroke, peripheral artery disease, atrial fibrillation, and venous thromboembolism. More aggressive antithrombotic therapies are associated with greater reduction in recurrent cardiovascular events for patients with diabetes. However, these strategies must be weighed against the risk of bleeding. Further clinical trials are still needed to better understand optimal antithrombotic treatment for cardiovascular patients with diabetes.
1) Gastric carcinoma is the third leading cause of cancer death worldwide, with highest incidence in East Asia and parts of South America.
2) Risk factors include H. pylori infection, smoking, diet high in salted/preserved foods, and family history of gastric cancer.
3) Early detection through endoscopy in dyspeptic patients over 50 years old or with red flags can improve outcomes, as resection allows for potential cure in early gastric cancer confined to mucosa or submucosa.
This document summarizes guidelines for the diagnosis and management of irritable bowel syndrome (IBS). It defines IBS and its subtypes based on the Rome IV criteria. It recommends diagnosing IBS based on symptoms in the absence of alarm features or abnormal test results. Limited testing like fecal calprotectin can help distinguish IBS from inflammatory bowel disease. Treatment involves dietary changes, probiotics, antispasmodics, antidepressants, and targeted therapies depending on IBS subtype and predominant symptoms. For refractory cases, a multidisciplinary approach including psychological support may help manage persistent symptoms.
GIT 4th indication for upper GI endoscopy.Shaikhani.
Upper gastrointestinal endoscopy has diagnostic, therapeutic, and screening indications. Diagnostically, it is used to detect diseases causing dyspepsia like gastric cancer, investigate upper GI bleeding, diagnose dysphagia, remove foreign bodies, assess GERD, detect esophageal varices, and diagnose celiac disease. Therapeutically, it treats upper GI bleeding, removes foreign bodies, dilates strictures, treats achalasia, places stents, treats GERD, eradicates Barrett's esophagus, inserts feeding tubes, and performs bariatric procedures. Screening indications include detecting Barrett's esophagus, portal hypertension, and cancers of the esophagus and stomach in high-risk patients
The document discusses various autoimmune and cholestatic liver diseases including primary biliary cholangitis, primary sclerosing cholangitis, and intrahepatic cholestasis of pregnancy. It provides details on the epidemiology, clinical features, diagnosis, and management of these conditions. It also includes several multiple choice questions to test understanding of topics covered in the document.
1. The document outlines 19 potential mistakes that can occur during colonoscopy procedures. These include doing colonoscopies without proper indications or patient evaluation, failing to adequately prepare the colon, misdiagnosing conditions like ulcerative colitis or hemorrhoids, not performing important parts of the exam like ileal intubation or biopsies, and not adhering to quality standards. Addressing these issues can help improve safety, accuracy of diagnoses, and overall quality of colonoscopy.
This document provides an overview of inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease. It discusses risk factors, clinical manifestations, diagnostic testing, and treatment approaches. The main points are:
- IBD is characterized by idiopathic inflammation of the gastrointestinal tract. The two main types are ulcerative colitis and Crohn's disease.
- Genetic and environmental factors contribute to risk. Smoking increases risk for Crohn's but decreases risk for ulcerative colitis.
- Symptoms vary based on disease location but may include abdominal pain, diarrhea, bleeding, weight loss, and nutritional deficiencies. Extraintestinal manifestations are more common with Crohn's.
This document provides information on irritable bowel syndrome (IBS), including its definition, diagnostic criteria, subtypes, differential diagnosis, evaluation, and management approaches. Some key points:
- IBS is a common functional gastrointestinal disorder characterized by abdominal pain and altered bowel habits. It affects 10-15% of the population.
- Diagnosis is based on fulfilling the Rome symptom criteria, with subtyping based on predominant stool pattern. Additional testing is usually not needed in absence of alarm features.
- Treatment involves reassurance, dietary modifications, antispasmodics, laxatives/antidiarrheals based on subtype, and tricyclic antidepressants/SSRIs for refractory cases.
This document discusses the classical and long-term indications for PPI use, including GERD, Barrett's esophagus, use with NSAIDs, use with anti-platelets, and non-ulcer dyspepsia. For GERD, guidelines recommend daily PPI for erosive esophagitis but intermittent PPI courses may be sufficient for many patients. For Barrett's esophagus, the absolute cancer risk reduction with daily PPI is low. For NSAID and anti-platelet users at high risk of bleeding, the benefits of daily PPI are well documented. Intermittent PPI courses are often sufficient for non-ulcer dyspepsia, though some patients may require long-
This document discusses potential long-term side effects of PPI use including increased risk of dementia, chronic kidney disease, and fractures. It notes that the evidence for associations between PPI use and these conditions is not conclusive. The document advises using the lowest effective dose of PPIs for indicated conditions and avoiding long-term daily use when possible. It also stresses the importance of only prescribing PPIs for appropriate indications and discontinuing them when no clear benefit exists.
The document summarizes short-term side effects of PPIs (proton pump inhibitors), which are generally well tolerated. The most common side effects are headache, diarrhea, abdominal pain and nausea. Diarrhea appears to be related to acid suppression and the overall incidence is less than 5%, though it may be dosage and age related. PPIs are considered safe for short-term use and have similar safety profiles to H2 blockers. PPIs should be used cautiously in patients with liver disease.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
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1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
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Osteoporosis is an increasing cause of morbidity among the elderly.
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Mercurius is named after the roman god mercurius, the god of trade and science. The planet mercurius is named after the same god. Mercurius is sometimes called hydrargyrum, means ‘watery silver’. Its shine and colour are very similar to silver, but mercury is a fluid at room temperatures. The name quick silver is a translation of hydrargyrum, where the word quick describes its tendency to scatter away in all directions.
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- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
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Kurdistan Boar GEH J Club: PVT From Saudi J Gastroenterology.
1. Kurdistab Board GEH J Club:
Dr. Mohamed Alshekhani
Professor in Medicine.
MBChB-CABM-FRCP-EBGH.
2015
From Saudi J Gastroenterology 2015.
1
2. Introduction:
• (NCPH), a heterogeneous group due to intrahepatic or extrahepatic
etiologies.
• The lesions are vascular in nature classified based on the site of
resistance to blood flow as “prehepatic,” “hepatic,” &“posthepatic.”
• The “hepatic” causes of NCPH can be subdivided into
“presinusoidal,” “sinusoidal,” &“postsinusoidal”
• PVT was first seen in the late 1860s in a patient with splenomegaly,
ascites&variceal dilatation,termed cavernoma to describe spongy
appearance of portal vein (PV).
• Generally a hypercoagulable state, intra-abdominal
infection/peritonitis&PV anomaly (PV stenosis &atresia) are
considered important predisposing factors of EHPVO; but thr vast
majority are due to primary thrombosis of the PV, often with more
than one cause.
2
3. Introduction:
• 0.05- 0.5% population prevalence.
• On autopsy 1%.
• PVT is responsible for 5%–10% of PHT., 40% in developing Cs. In
children,80%.
• Incidence of PVT among liver cirrhotics 0.6-64.1%.
• After cirrhosis, EHPVO is the most common cause of portal
hypertension globally.
• In the India 20–30% of all variceal bleeds are due to EHPVO.
• In Japan, 10–20% of variceal bleeds& in the west, 2–5% of variceal
bleeds are due to EHPVO.
3
5. PVT: Clinical presentation
• Different in acute &chronic thrombosis.
• This depends on development&extent of collateral
circulation.
• Acute PVT:
• Intestinal congestion&ischemia with abdominal
pain, fever, diarrhea, rectal bleeding, distension,
sepsis&lactic acidosis with or without splenomegaly
are common.
• Chronic PVT:
• Can be asymptomatic or could be characterized by
splenomegaly, pancytopenia, varices&rarely ascites.
5
6. PVT: Pathophysiology
• PV obstruction is usually well tolerated &often asymptomatic.
• 2 important mechanisms play a role in Pvobstruction:
• Arterial vasodilationor rescue, can preserve the liver function in
acute settings&allows a second mechanism to operate the venous
rescue.
• Venous rescue allows several collaterals to develop, which try to
bypass portal vein obstruction, takes around 4–6 weeks&
obstructed portal vein is replaced by collateral network called
cavernoma.,bypasses the obstructed portal vein &a thrombosed
portal vein turns into a fibrotic cord.
• The network is seen around structures near the obstructed PV as
bile duct, GB, pancreas, gastric antrum & duodenum.
• The bile duct may be difficult to locate within the network of
collaterals on abdominal ultrasonography.
6
7. PVT: Pathophysiology
• Biopsy of liver is usually normal except hemosiderosis related to
porto systemic shunt.
• In much advanced states of PVT, hypoperfused cells of the liver die
by apoptosis as a result of increased apoptotic signals & enhanced
mitotic activity in normally perfused cells,finally leads to reduced
synthetic function of the liver in later stages of EHPVO.
7
8. PVT: Epidemiology
• Most with PVT are cirrhotics with primary or metastatic cancer.
• Nontumoral /noncirrhotic PVT is the second most frequent cause
of portal hypertension, worldwide,5–10% in the western world,
40% in the India.
• Acute PVT: 10–25% of all PVTs
• Chronic PVT/EHPVO: 75–90% of all PVTs
• Overall EHPVO: 5–10% of portal hypertension
• • In developing countries EHPVO: 35–40% of portal HT.
• • In India: 20–30% of all variceal bleeds are due to PVT
• • In Japan: 10–20% of all variceal bleeds are due to PVT
• • In the West: 2–5% of all variceal bleeds are due to PVT
• • In children, 70% of all variceal bleeds are due to EHPVO from the
India.
8
9. PVT: Epidemiology
• A prevalence of 0.6–26% of PVT in cirrhotics& highest in orthoptic
liver transplants.
• A 6.5% PVT is seen in patients with hepatocellular carcinoma (HCC)
at the time of diagnosis, which increases in later stages of HCC.
• The etiology of liver disease has an influence on prevalence of
PVT, being 3.6% in primary sclerosing cholangitis (PSC), 8% in
primary biliary cirrhosis (PBC), 16% each in acute liver disease
(ALD), hepatitis B virus (HBV)-related cirrhosis& 35% in HCC.
• The risk of PVT is independently associated with severity of
cirrhosis.
• Cirrhosis listed for liver transplantation, 7.4- 16% of PVT reported
in with 12 months prospective follow up.
9
10. PVT: Etiopathogenesis
• Thrombophilic conditions are seen in 60% of PVT, while local
predisposing factors account for 30%.
• Usually there is > 1 factor responsible for PVT.
• Idiopathic 30% of PVT.
12. PVT:Ethiopathogesis
• Factor V Leiden mutation is the most common thrombophilia predisposing
factor to PVT followed by PC deficiency.
• The role of protein S &antithrombin (AT) III deficiency has not yet been
confirmed
• A simple method of screening deficiency of natural anticoagulants in
patients with liver disease comprises of the ratio of PS or PC or AT to
[(Factor II + Factor X/2)],If <70%, a genetic cause needs to be evaluated.
• To evaluate the role of thrombophilia, laboratory screening should
include functional tests for activated PC resistance, genotyping of Factor V
to search for G1691A mutation & prothrombin gene to search for
G20210A mutation.
• Factor VIII &antiphospholipid assays should also be done.
• Screening should include measurements of naturally occurring
anticoagulant proteins such as AT, PC&PS.
• Genetic variations in thrombin activatable fibrinolysis inhibitor (TAFI)
gene, recently described as a risk factor for PVT.
• Much less commonly acquired disorders are APS,PNH.
13. Ethiopathogesis: infants & children
• In most cases the cause could not be identified.
• If cause found majority showed direct injury to the umbilical
vascular system (oomphalites, umbilical vein catheterization) or
intrabdominal & umbilical sepsis,but seemed to be a coexistent
prothrombotic state.
• Risk factors in umbilical catheterization causing PVT:
• Later insertion
• Catheter dwell time >3 days
• Catheter misplacement
• Trauma on catheter insertion site
• Type of solution infused.
• Abdominal sepsis has been identified as a risk factor in 11% of PVT
with strong association between Bacteroides fragilis infection with
PVT
• The transient development of anticardiolipin antibodies has been
suggested as a pathophysiological link between this infection and
PVT.
14. Ethiopathogesis:MPD
• Among the thrombophilic states, primary MPD are more common ,
frequently occult MPD.
• 50% of presumed idiopathic PVT suffered from primary MPD,not
detected from conventional testing but by spontaneous formation of
erythroid colonies in bone marrow culture.
• An acquired mutation (JAK 2/V617F) testing associated with MPD yields a
higher rate of diagnosis, presently considered among the major criteria.
• Individuals with occult MPD are very often younger than those with full
blown MPD who conversely have a relatively low incidence of splanchnic
vein thrombosis in their postdiagnosis follow up.
• These findings reflect that MPD presenting as splanchnic thrombosis has
often atypical phenotype, that is, juvenile disorder with high thrombotic
risk &typical MPD is less likely to develop in these patients.
• The diagnosis of occult MPD is not straight forward,requires endogenous
erythroid colony assessment.
• Endogenous erythroid colony assessment (EEC) is spontaneous growth of
erythroid colonies in cultures of bone marrow in absence of added
erythropoietin, demonstrated in up to 78% of patients of Budd–Chiari
syndrome & 48% of patients with EHPVO.
15. Ethiopathogesis:MPD
• Bone marrow morphology is currently included in
WHO criteria of MPD &clusters of enlarged, mature,
pleiomorphic megakaryocytes is considered to be a
diagnostic hallmark of Philadelphia negative MPD.
• By using bone marrow, underlying MPD
demonstrated in 30% of EHPVO.
• Molecular markers of clonal disease are useful in
the diagnostic workup of MPD such as JAK2
(V617F), rare (<1%) in general population.
17. Clinical features:
• EHPVO can present as early as 6 weeks after birth as well as manifest in
adulthood.
• Clinical presentation depends on recent or chronic onset of clinical
disease &age of presentation.
• The most common clinical features are hemetemesis; often massive &
usually not associated with hepatocellular dysfunction.
• Gastrointestinal bleed is usually recurrent before a patient seeks medical
attention.
• There is no firm data to support that recurrence of variceal bleeding
decreases after puberty.
• Patients can present with hemetemesis& malena from conventional
esophageal gastric varices &can also bleed from ectopic varices or may
present with obscure GI bleeding or bleeding from the biliary tract.
• Anemia &splenomegaly are other common features of EHPVO with
reduction in cell lines, but hypersplenism is only in 5–10% of patients.
• Massive splenomegaly can give a dragging sensation or left upper
quadrant pain due to splenic infarct or perisplenitis.
18. Clinical features:
• Ascites can present transiently in 10–20% of children following
surgery or GI bleed.
• It is seen > in adults with long-standing disease &declining LFs.
function.
• Jaundice result from BD compression because of dilated venous
collaterals due to portal biliopathy.
• Portal biliopathy(abns of extr& intrahepatic BDs with or without
abns of the GB wall,includes indentation of paracholedochal
collaterals on bile ducts, strictures,angulations, focal narrowing,
stones, irregular walls.
• GB varices are common,but GB contractibility remains intact.
• Frequency of cholelithiasis is higher in EHPVO.
• Biliopathy seen in 90–100% ; but only few are symptomatic ,
usually in adult s& reflects advance disease&complicated by GSs,
CBD stones, cholangitis, secondary biliary cirrhosis& hemobilia.
19. Clinical features:
• Clinical features can be summarized:
• Recent PVT
• • Asymptomatic
• • Symptomatic
• • Severe nonalcoholic abdominal pain, distention, fever, systemic
inflammatory (SIRS)
• • Persistent pain, ascites; ileus should raise suspicion of intestinal
infarction
• • Portal pylephlebitis should be suspected if spiky fevers,
tenderness, shock, and sepsis-related cholestasis is seen
• • Associated thrombosis in other regions to be investigated.
20. Clinical features:
• Clinical features can be summarized:
• Chronic PVT/EHPVO
• • With portal hypertension
• • Variceal bleed well tolerated
• • Splenomegaly moderate
• • Hypersplenism.
• • Growth retardation in children
• • Jaundice, biliopathy, mild hepatic dysfunction.
22. EHPVO DIAGNOSIS:
• • Liver function test (LFT): Normal
• • Endoscopy: Esophageal varices, gastric varices, anorectal varices
• • Doppler: PVT & portal vein cavernoma
• • CECT &CT :angiocollaterals
• • Liver biopsy: Normal but not mandatory.
• EHPVO imaging characteristic&pattern of obstruction:
• • Color Doppler ultrasound
• • Recent: No color flow or Doppler signal within portal vein,
distention of portal vein, absence of cavernoma.
• Contrast EUS is useful to confirm portal vein thrombosis
• • Chronic: No color flow in portal vein and hepatopetal signal within
the cavernoma or varices at gall bladder wall &signs of portal
hypertension.
22
23. EHPVO DIAGNOSIS:
• Contrast-enhanced CT/MR
• Recent
• Nonenhancing material within portal vein & increased hepatic enhancement in
arterial phase.
• Enhancement of thrombus suggests malignant thrombus.
• CT/MR angiography are more useful.
• Chronic
• Cavernomatus transformation of portal vein with splenomegaly, collaterals, and/or no
opacification of intrahepatic portal vein.
• Chronic venous thrombus can manifest as linear areas of calcification within
thrombus.
• Rim enhancement of vessel wall may also be seen &presumed to be due to normal
flow in vasa vasorum.
• Care must be taken to avoid confusion between “pseudo thrombus image” with true
portal vein thrombus.
• Pseudothrombus appearance occurs during HAP in main portal vein lumen due to
mixed flow from enhanced splenic vein return & nonenhanced superior mesentric
vein return.
• Newly proposed Baveno classification (yet to be published) for EHPVO; Site of PVT
(TYPE 1, 2a, 2b, 3).
• TYPE 1: Only trunk.
• TYPE 2: Only branch 2a (one), 2b (both branches).
• TYPE 3: Trunk & branches. 23
24. EHPVO DIAGNOSIS:Definitions
• Presentations:
• R (Recent)
• Ch (Chronic) with portal cavernoma and PHT
• TYPE of underlying liver disease
• C: Cirrhotic
• N: Noncirrhotic liver disease
• H: HCC and local malignancy
• L: Post–liver transplant
• A: Absence of liver disease.
• Degree of portal venous system occlusion
• • Incomplete: Flow visible in PV lumen through imaging
• • Total: No flow visible in PV lumen on imaging
• • Extent of portal vein system occlusion
• • Splenic vein• Mesentric • Or both. 24
26. Treatment:
• RECENT EHPVO
• • This rarely resolves spontaneously in noncirrhotic patients with
symptomatic recent EHPVO
• • Low molecular weight heparin should be started immediately
followed by oral anticoagulant therapy.
• In asymptomatic patients, anticoagulation should be considered
• • Anticoagulation should be given for at least 3 months,unless an
underlying persistent pro-thrombotic state has been documented in
which case anticoagulation is recommended
• • Antibiotic therapy should be given if there is any evidence of SIRS
or infection.
26
27. Treatment:
• TREATMENT OF CHRONIC EHPVO:
• No consensus on anticoagulants, but in patients with a persistent
prothrombotic state, anticoagulants can be considered.
• There is insufficient evidence in favor of interventional therapy such
as TIPS or local thromobolysis.
• TREATMENT OF BLEEDING
• For primary prophylaxis of variceal bleeding, insufficient data on
whether beta-blocker or endoscopic therapy should be preferred.
• For control of acute variceal bleed, endoscopic therapy is effective.
• For secondary prophylaxis, endoscopic therapy is effective&
beta-blockers are as effective as EVL.
• Decompressive surgery or interventional radiology should be
considered for patients with failure of endoscopic therapy.
• Mesenteric left PV bypass (REX Shunt) is preferred in bleeding from
pediatric patients with chronic EHPVO if feasible.
28. Treatment:
• PORTAL BILIOPATHY
• Asymptomatic: No treatment.
• Symptomatic :
• • Stones need endoscopic treatment
• • CBD stricture
• • Endoscopic stenting should be considered whenever possible if
not treated by the above treatment, hepaticojejunostomy is
preferred.
• • ERCP is only recommended if therapeutic is contemplated,
otherwise MRCP is the first line of investigation.
31. Treatment:
• CHRONIC EHPVO IN CHILDREN
• Mesentric: Left PV bypass (REX Shunt) should be considered in all
children with complications of chronic EHPVO
32. Treatment:
• SHUNT SURGERIES IN EHPVO
• Medical&endoscopic management is usually recommended for
EHPVO&various surgical shunts are used for refractory or
complicated cases, surgery is primarily indicated when endotherapy
fails to control bleeding, in the presence of gastric or ectopic varices
not amenable to endoscopic management& with delayed sequelae
such as portal biliopathy /rectal varices.
• Emergency shunt surgeries is rare in the era of endoscopic trt.
• Other indications of shunt surgery include symptomatic
hypersplenism, growth retardation,portal biliopathy, massive
splenomegaly affecting the quality of life, rare blood group&
remote area of residence.
• Shunt patency in 85–98% with long-term survival in >95% with
conventional portosystemic shunts, proximal splenorenal shunt,
central splenorenal shunt, side to side lienorenal shunt& mesocaval
shunt.
34. Treatment:
• INDICATIONS/CONTRAINDICATIONS TO TREATMENT:
• The indication of medical or surgical treatment in EHPVO patient,
especially garden variety group idiopathic EHPVO
• in Asian children without underlying liver disease or HCC is not well
settled.
• Regarding medical treatment of patients who have no varices but
have EHPVO on imaging, there is no consensus regarding use of
beta-blockers for prevention of variceal formation.
• Patients who have nonbleeding varices but have EHPVO there is
only limited evidence of treating them with beta-blockers.
• Current guidelines justify use of such modalities for large&high-risk
varices, especially for patients who belong to far flung areas but for
others such modality is not indicated.
35. Treatment:
• INDICATIONS/CONTRAINDICATIONS TO TREATMENT:
• Patients who are not bleeders & who have no symptoms of
hypersplenism, growth retardation, decreased quality of life with
massive splenomegaly&who have only asymptomatic biliopathy
should not go for shunt surgery as shunt surgery has its own
problems such as postoperative complications, shunt thrombosis, &
so on.
• FOLLOW UP
• In children, follow up of growth retardation especially in Indian
setting is done every 3–6 months.
• Endoscopic surveillance should be done 1–2 yearly for varices.
• In asymptomatic biliopathy, follow-up algorithm is shown as
Flowchart
36. Treatment:
• PORTAL VEIN THROMBOSIS IN SPECIAL SITUATIONS
(POSTOPERATIVE/LIVER TRANSPLANTATION)
• 5% of acute (less than 30 days) postoperative PVT rate in patients
who underwent portal vein reconstruction during
pancreaticoduodenectomy.
• Low incidence of acute vein portal vein thrombosis may be
secondary to lack of detection until chronic changes have
occurred.
• Certainly mortality rates are higher in cases with associated
mesenteric ischemia.
• Early diagnosis&ability to treat is very important.
• Use of Doppler ultrasound& CT/MRA helps in reaching diagnosis.
• Site-directed thrombolytic therapy can be indirect via SMA
catheter placement or directly via catheter in portal vein. With
excellent response from 75-100% Partial/complete
recanalization.
38. Treatment:
• PORTAL VEIN THROMBOSIS IN LIVER TRANSPLANT
• Enoxaprin given prophylactically to chronic liver disease patients
with a CTP score of 7–10 revealed significantly reduced
decompensation events.
• Due to liver injury in CLD patients, more thrombin is generated,
which causes intrahepatic thrombosis,in turn causes stimulation of
PAR-1 on HSC that can lead to further fibrosis.
38
39. Treatment:
• PORTAL VEIN THROMBOSIS IN LIVER TRANSPLANT:
• PVT seen in 2–6% post-transplant
• Pre-transplant PVT no longer contraindication for transplant &can
represent itself as an indication for liver transplant.
• Terminal to terminal PV anastomosis with or without
thrombectomy is usually done in low-grade PVT, that is, <50% PV
occlusion& portocaval hemitransposition, mandatory in Grade IV
Yerdel’s.
• Transplant of Grade 1 Yerdel’s postoperative PVT is similar to
non-PVT patients undergoing transplantation.
• The rate of thrombosis recurrence is 9–-42% or lower.
• After liver transplantation,PVT is rare (1–2%) in the early period
with preferential localization to the anastomotic site:
• Technical problems, small diameter of PV are risk factors for PVT.
• Prophylactic anticoagulants in CLD with PVT waiting for transplant
40. Conclusion:
• EHPVO is a vascular disorder of liver, which results in
obstruction&cavernomatous transformation of PV with or without
the involvement of intrahepatic portal vein, splenic vein, or
superior mesenteric vein.
• Portal vein obstruction due to chronic liver disease, neoplasm, or
postsurgery is a separate entity ¬ the same as extrahepatic
portal vein obstruction.
• Patients with EHPVO are generally young&belong mostly to Asian
countries.
• It is very important to define PVT as acute or chronic from
management point of view.
• Portal vein thrombosis in certain situations such as liver transplant
& postsurgical/liver transplant period is an evolving area& needs
extensive research.
• There is a need for a new classification, which includes all areas of
the entity
41. Conclusion:
• It is equally important to identify cirrhosis, HCC, or any other
malignancy in cases of PVT.
• In cases of idiopathic MPD, occult MPD should be investigated.
• Mutations such as JAK2 and TAFI should be ruled out in addition to
conventional testing for inherited& acquired coagulation
disorders.
• In the modern era, CT / MR angiography as tools have made the
diagnosis of PVT more accurate.
• Adopting newer methods of treatment for acute portal vein
thrombosis in the setting of postoperative & liver transplantation
is rational.
42. PVT In Liver cirrhosis
Dr. Mohamed Alshekhani
Professor in Medicine.
MBChB-CABM-FRCP-EBGH.
2015
42
43. Coagulation in chronic liver diseases:
• The liver plays a central role in maintaining the critical balance
between bleeding & thrombotic events.
• Liver cirrhosis (LC) is characterized by a complex picture of impaired
coagulation, thrombocytopenia, decreased pro/anticoagulant factors
produced by the liver, increased VWF, factor VIII& decreased pro- &
antifibrinolytic factors, with a low tendency to hyperfibrinolysis.
• Despite clear evidence of an increased tendency for bleeding in
patients with liver cirrhosis, in some circumstances these patients are
characterized by a hypercoagulable state.
43
44. PVT in chronic liver diseases:
• Incidence of PVT in compensated LC is 0.6- 5%&15–25% in decomp.
• There are no data regarding the difference in the prevalence
between partial & total PVT in cirrhotic patients.
• PVT is a serious complication of cirrhosis due to further increase in
portal venous pressure &decreased blood flow to the liver, with the
risk of variceal bleeding &worsening of the liver function.
• The impact of PVT on the natural history of cirrhosis remains
unclear&natural course of PVT in patients with LC is not well known.
• There are many asymptomatic cirrhotics in whom PVT is detected
incidentally on abd U/S¬ established whether such patients need
anticoagulant therapy.
• There is no consensus nor guidelines for using anticoagulants
duration, &monitoring of cirrhotics with PVT.
• Spontaneous recanalization of the portal vein in the absence of any
specific therapy is unusual, especially in total PVT. 44
45. PVT in chronic liver diseases:
• Nonmalignant partial PVT remained stable/improved in>50% of
cirrhotics & aggravated in >1/4 in whom it negatively influenced the
survival & decompensation rates.
• Natural Course of Nonmalignant PVT in Cirrhotics
• Irina Girleanu Carol Stanciu, Camelia Cojocariu, Lucian Boiculese,
Ana-Maria Singeap,Anca Trifan.
• The Saudi Journal of Gastroenterology 2014.
45
46. PVT in chronic liver diseases:
• Anticoagulation, a widely available option for VT, is also employed
for the PVT in cirrhotics.
• There is a relatively low risk of anticoagulation-related bleeding & a
high rate of PV recanalization after anticoagulation, providing the
support for the use of anticoagulation in cirrhosis with PVT.
• Whether or not anticoagulants should be used, the natural history
of PVT in cirrhosis in the absence of any interventions should be
known.
• Spontaneous recanalization varies from 30-50% in cirrhotics.
• This recent article found that partial PVT could be spontaneously
recanalized or unchanged in 72.7% (16/22) &worsened in only
27.3% (6/22)& the study showed a significantly higher incidence of
hepatic decompensation&mortality in the cirrhotics with worsened
PVT than in those with recanalized or unchanged PVT.
47. PVT in chronic liver diseases:
• Anticoagulation should be selectively performed in patients who
would develop the thrombus extension, thereby improving survival;
by contrast, it is unnecessary in those who would develop the
spontaneous thrombus resolution.
• The severity of liver function (i.e. MELD score) was the only
independent predictor for the survival&hepatic decompensation.
• Worsened PVT &deteriorated liver function jointly incr mortality.
• There is a vicious cycle bet PVT & deterioration of liver functions.
• The portal vein flow velocity decreases with worsening liver fibrosis
/function& a decreased portal vein flow velocity predicts a higher
risk of developing PVT&PV flow velocity decreases with worsening
liver fibrosis& liver function.
48. PVT in chronic liver diseases:
• Collectively, spontaneous PV recanalization can be frequently
observed in patients with partial PVT,attributed to the
improvement of liver function.
• Further work should focus on identifying the candidates who will
develop the thrombus extension suitable for anticoagulation.