Portasystemic Shunt, Transjugular Intrahepatic
Cranial Fossa, Posterior
Cerebrospinal Fluid Pressure
Metabolic Syndrome X
Vena Cava, Inferior
Exudates and Transudates
Vena Cava, Superior
Managing Budd-Chiari syndrome: a retrospective review of percutaneous hepatic vein angioplasty and surgical shunting. (1/234)BACKGROUND: The role of percutaneous hepatic vein angioplasty in the management of Budd-Chiari syndrome has not been well defined. Over a 10 year period at our unit, we have often used this technique in cases of short length hepatic vein stenosis or occlusion, reserving surgical mesocaval shunting for cases of diffuse hepatic vein occlusion or failed angioplasty. AIMS: To review the outcome of angioplasty and surgical shunting to define their respective roles. PATIENTS: All patients treated by angioplasty or surgical shunting for non-malignant hepatic vein obstruction over a ten year period from 1987 to 1996. METHODS: A case note review of pretreatment features and clinical outcome. RESULTS: Angioplasty was attempted in 21 patients with patent hepatic vein branches and was successful in 18; in three patients treatment was unsuccessful and these patients had surgical shunts. Fifteen patients were treated by surgical shunting only. Mortality according to definitive treatment was 3/18 following angioplasty and 8/18 following surgery; in most cases this reflected high risk status prior to treatment. Venous or shunt reocclusion rates were similar for both groups and were associated with subtherapeutic warfarin in half of these cases. Most surviving patients in both groups are asymptomatic although one surgical patient has chronic hepatic encephalopathy. CONCLUSION: With appropriate case selection, many patients with Budd-Chiari syndrome caused by short length hepatic vein stenosis or occlusion may be managed successfully by angioplasty alone. Medium term outcome is good following this procedure provided that anticoagulation is maintained. Further follow up is required to assess for definitive benefits but we suggest that this should be included as a valid initial approach in the algorithm for management of Budd-Chiari syndrome. (+info)
Results of surgical treatment (modified Sugiura-Futagawa operation) of portal hypertension associated to complete splenomesoportal thrombosis and cirrhosis. (2/234)BACKGROUND: Hemorrhagic portal hypertension, secondary to both intrahepatic and extrahepatic portal hypertension, is an uncommon entity. In this condition, the extrahepatic and the intrahepatic obstruction of the portal vein, due to chronic liver disease, produce a more severe form of hemorrhagic portal hypertension that is more difficult to control. The results of surgical treatment (modified Sugiura-Futagawa operation) in this subset of patients is analyzed. METHODS: Among 714 patients with a history of hemorrhagic portal hypertension, 14 cases were found with histologically proven liver cirrhosis and complete splenomesoportal thrombosis demonstrated by means of preoperative angiography. Patients with incomplete (partial) splenomesoportal thrombosis were excluded. There were nine males and 5 females with a mean age of 51 years. Alcoholic cirrhosis was demonstrated in 50% of the cases, post hepatitic cirrhosis in 28%, primary biliary cirrhosis in 7%, and cryptogenic cirrhosis in 14%. There were nine Child-Pugh A and 5 B cases. All cases were treated by means of our modified Sugiura-Futagawa procedure. RESULTS: Bleeding recurrence from esophagogastric varices was shown in one case, colonic varices in one case and hypertensive gastropathy in another of the survivors. Post operative encephalopathy was shown in 3 of the cases. The thirty-six month survival rate was 30% (Kaplan-Meier). CONCLUSIONS: The combination of intrahepatic plus extrahepatic portal hypertension has a worse prognosis. Treatment options are limited (sclerotherapy and/or devascularization), because shunt surgery, TIPS and liver transplantation have a very restricted role and postoperative outcome is poor. (+info)
Successful twin pregnancy in a dual-transplant couple resulting from in-vitro fertilization and intracytoplasmic sperm injection: case report. (3/234)There are numerous reports of successful pregnancy following liver transplantation. Little information is available regarding the incidence and management of infertility in transplant recipients, particularly the use of artificial reproductive technologies. We present a case of a successful twin pregnancy resulting from in-vitro fertilization with intracytoplasmic sperm injection (IVF/ICSI) in a liver transplant recipient, whose partner was a renal transplant recipient with severe oligozoospermia. With careful evaluation and monitoring, and the involvement of appropriate consultants, artificial reproductive technologies can be safely used in transplant recipient couples experiencing infertility. (+info)
A 27-year experience with surgical treatment of Budd-Chiari syndrome. (4/234)OBJECTIVE: To determine the effects of surgical portal decompression in Budd-Chiari syndrome (BCS) on survival, quality of life, shunt patency, liver function, portal hemodynamics, and hepatic morphology during periods ranging from 3.5 to 27 years. SUMMARY BACKGROUND DATA: Experiments in the authors' laboratory showed that surgical portal decompression reversed the deleterious effects of BCS on the liver. This study was aimed at determining whether similar benefit could be obtained in patients with BCS. METHODS: From 1972 to 1999, the authors conducted prospective studies of the treatment of 60 patients with BCS who were divided into three groups: the first had occlusion confined to the hepatic veins treated by direct side-to-side portacaval shunt (SSPCS); the second had occlusion involving the inferior vena cava (IVC) treated by a portal decompressive procedure that bypassed the obstructed IVC; and the third group, who had advanced cirrhosis and hepatic decompensation and were referred too late for treatment by portal decompression, required orthotopic liver transplantation. RESULTS: In the 32 patients with BCS resulting from hepatic vein occlusion alone, SSPCS had a surgical death rate of 3%, and 94% of the patients were alive 3.5 to 27 years after surgery. All 31 survivors remained free of ascites and almost all had normal liver function. No patient with a patent shunt had encephalopathy. The SSPCS remained patent in all but one patient. Liver biopsies showed no evidence of congestion or necrosis, and 48% of the biopsies were diagnosed as normal. Mesoatrial shunt was performed in eight patients with BCS caused by IVC thrombosis. All patients survived surgery, but five subsequently developed thrombosis of the synthetic graft and died. Because of the poor results, mesoatrial shunt was abandoned. Instead, a high-flow combination shunt was introduced, consisting of SSPCS combined with a cavoatrial shunt (CAS) through a Gore-Tex graft. There were no surgical or long-term deaths among 10 patients who underwent combined SSPCS and CAS, and the shunts functioned effectively during 4 to 16 years of follow-up. Ten patients with advanced cirrhosis were referred too late to benefit from surgical portal decompression, and they were approved and listed for orthotopic liver transplantation. Three patients died of liver failure while awaiting a transplant, and four patients died after the transplant. The 1- and 5-year survival rates were 40% and 30%, respectively. CONCLUSIONS: SSPCS in BCS with hepatic vein occlusion alone results in reversal of liver damage, correction of hemodynamic disturbances, prolonged survival, and good quality of life when performed early in the course of BCS. Similarly good results are obtained with combined SSPCS and CAS in patients with BCS resulting from IVC occlusion. In contrast, mesoatrial shunt has been discontinued in the authors' program because of an unacceptable incidence of graft thrombosis and death. In patients with advanced cirrhosis from long-standing, untreated BCS, orthotopic liver transplantation is the only hope of relief and results in the salvage of some patients. The key to long survival in BCS is prompt diagnosis and treatment by portal decompression. (+info)
Successful liver transplantation in a patient with Budd-Chiari syndrome caused by homozygous factor V Leiden. (5/234)Budd-Chiari syndrome (BCS) is a rare form of portal hypertension characterized by hepatic venous outflow obstruction. Although hematologic disorders are the most common cause of this syndrome, to date, 30% of the cases have been classified as idiopathic. Resistance to activated protein C caused by factor V Leiden is the most common cause of thrombophilia; its role in the pathogenesis of BCS is now becoming apparent. We report successful liver transplantation in a patient with BCS caused by homozygous factor V Leiden. The patient was administered standard heparin anticoagulation until activated protein C resistance was normalized by the liver allograft. Liver transplantation corrected the thrombophilic state. The patient has excellent graft function, is not on anticoagulation therapy, and has had no recurrent venous thrombosis at 5 months posttransplantation. Activated protein C resistance caused by the factor V Leiden mutation may be responsible for idiopathic cases of BCS. To avoid unnecessary long-term anticoagulation after liver transplantation, factor V Leiden should be considered as a pathogenic factor in BCS. In addition, because of the high prevalence of factor V Leiden in the world population, cadaveric organ donors with a history of venous thrombosis should be screened for activated protein C resistance lest thrombophilia be transmitted to the recipient. (+info)
Factor V Leiden mutation, prothrombin gene mutation, and deficiencies in coagulation inhibitors associated with Budd-Chiari syndrome and portal vein thrombosis: results of a case-control study. (6/234)In a collaborative multicenter case-control study, we investigated the effect of factor V Leiden mutation, prothrombin gene mutation, and inherited deficiencies of protein C, protein S, and antithrombin on the risk of Budd-Chiari syndrome (BCS) and portal vein thrombosis (PVT). We compared 43 BCS patients and 92 PVT patients with 474 population-based controls. The relative risk of BCS was 11.3 (95% CI 4.8-26.5) for individuals with factor V Leiden mutation, 2.1(95% CI 0.4-9.6) for those with prothrombin gene mutation, and 6.8 (95% CI 1.9-24.4) for those with protein C deficiency. The relative risk of PVT was 2.7 (95% CI 1.1-6.9) for individuals with factor V Leiden mutation, 1.4 (95% CI 0.4-5.2) for those with prothrombin gene mutation, and 4.6 (95% CI 1.5-14.1) for those with protein C deficiency. The relative risk of BCS or PVT was not increased in the presence of inherited protein S or antithrombin deficiency. Concurrence of either acquired or inherited thrombotic risk factors was observed in 26% of the BCS patients and 37% of the PVT patients. We conclude that factor V Leiden mutation and hereditary protein C deficiency appear to be important risk factors for BCS and PVT. Although the prevalence of the prothrombin gene mutation was increased, it was not found to be a significant risk factor for BCS and PVT. The coexistence of thrombogenic risk factors in many patients indicates that BCS and PVT can be the result of a combined effect of different pathogenetic mechanisms. (+info)
Successful outcome of orthotopic liver transplantation in patients with preexisting malignant states. (7/234)Preexisting malignancy is considered a relative contraindication to orthotopic liver transplantation (OLT) because of the risk of tumor recurrence. The purpose of this study is to assess the outcome of OLT in patients with a preexistent malignant state. Of 1,097 OLTs performed between 1989 and 1999 at King's College Hospital (London, UK), 18 patients had a pretransplantation malignant state, including 6 cases of myeloproliferative disorder (MPD) presenting as Budd-Chiari syndrome. Those patients with solid-organ malignancies had their tumor detected at an early stage and underwent curative treatment before or during OLT. Patients were followed up for a median of 71 months (range, 1 to 119 months) post-OLT, and the rates of rejection and malignancy were compared with those of transplant recipients without preexisting malignancy during the same period. One patient had a recurrence of his primary malignancy (non-Hodgkin's lymphoma) after 27 months, whereas another patient developed a de novo posttransplant lymphoproliferative disorder after 57 months. One patient with MPD developed acute leukemia 72 months after OLT. In comparison, of 1,079 OLTs performed in patients without preexisting malignancy during the same period, there were 34 cases of de novo malignancies. The rate of rejection in patients with and without preexisting malignancy was similar. Successful medium-term outcome after OLT can be achieved in carefully selected patients with preexisting malignancy providing the malignancy is amenable to curative treatment before or at OLT. Primary MPDs responsible for Budd-Chiari syndrome should not be considered a contraindication to OLT. (+info)
Factor V Leiden related Budd-Chiari syndrome. (8/234)BACKGROUND: The role of factor V Leiden as a cause of Budd-Chiari syndrome has only recently been described. AIMS: To assess the specific features of factor V Leiden related Budd-Chiari syndrome. PATIENTS: Sixty three consecutive patients with hepatic vein or terminal inferior vena cava thrombosis. METHODS: Standardised chart review. RESULTS: Factor V Leiden was found in 20 patients (31% (95% CI 20-43)). In the subgroup of patients with, compared with the subgroup without, factor V Leiden, a combination of prothrombotic states was more common (70% (95% CI 50-90) v 14% (95% CI 3-24)); inferior vena cava thrombosis was more frequent (40% (95% CI 19-61) v 7% (95% CI 0-14)); and distribution of initial alanine aminotransferase values was bimodal (almost normal or extremely increased) versus unimodal (p=0.003). Factor V Leiden accounted for four of five cases of massive ischaemic necrosis (transaminases >50-fold the upper limit of normal values) (p=0.014), and also for all three cases developing during pregnancy. Patients with and without factor V Leiden did not differ with regard to mortality, portosytemic shunting, or listing for liver transplantation. Hepatocellular carcinoma developed in two patients; both had factor V Leiden and indolent obstruction of the inferior vena cava. CONCLUSIONS: In patients with Budd-Chiari syndrome, factor V Leiden (a) is common; (b) precipitates thrombosis mostly when combined with another risk factor; (c) is associated with one of two contrasting clinical pictures: indolent thrombosis-particularly of the inferior vena cava-or massive ischaemic necrosis; and (d) is a major cofactor of Budd-Chiari syndrome developing during pregnancy. (+info)
Budd-Chiari Syndrome is a rare but serious medical condition that occurs when there is a blockage in the veins that carry blood from the liver to the heart. This blockage can be caused by a variety of factors, including blood clots, cancer, or scarring of the veins. The condition is named after the two doctors who first described it, Dr. Takeo Budd and Dr. Takeo Chiari. Symptoms of Budd-Chiari Syndrome can include abdominal pain, swelling in the abdomen or legs, yellowing of the skin and eyes (jaundice), and dark urine. In severe cases, the condition can lead to liver failure and even death. Treatment for Budd-Chiari Syndrome depends on the underlying cause of the blockage. In some cases, medications may be used to dissolve blood clots or reduce inflammation. In more severe cases, surgery may be necessary to remove the blockage or repair damaged veins. In some cases, a liver transplant may be necessary if the liver has been severely damaged by the condition.
Syringomyelia is a medical condition characterized by the formation of fluid-filled cysts (syringes) within the spinal cord. These cysts can cause damage to the spinal cord and lead to a range of symptoms, including pain, weakness, numbness, and tingling in the arms and legs. Syringomyelia can be caused by a variety of factors, including trauma to the spine, spinal cord infections, and inherited conditions such as Chiari malformation. The condition can also be idiopathic, meaning its cause is unknown. Diagnosis of syringomyelia typically involves imaging tests such as MRI or CT scans, which can show the presence of the cysts within the spinal cord. Treatment options for syringomyelia depend on the severity of the symptoms and the underlying cause of the condition. In some cases, surgery may be necessary to remove the cysts or relieve pressure on the spinal cord. Other treatment options may include medication, physical therapy, and lifestyle changes.
In the medical field, a syndrome is a set of symptoms and signs that occur together and suggest the presence of a particular disease or condition. A syndrome is often defined by a specific pattern of symptoms that are not caused by a single underlying disease, but rather by a combination of factors, such as genetic, environmental, or hormonal. For example, Down syndrome is a genetic disorder that is characterized by a specific set of physical and intellectual characteristics, such as a flattened facial profile, short stature, and intellectual disability. Similarly, the flu syndrome is a set of symptoms that occur together, such as fever, cough, sore throat, and body aches, that suggest the presence of an influenza virus infection. Diagnosing a syndrome involves identifying the specific set of symptoms and signs that are present, as well as ruling out other possible causes of those symptoms. Once a syndrome is diagnosed, it can help guide treatment and management of the underlying condition.
Encephalocele is a medical condition in which a portion of the brain or spinal cord extends through a defect in the skull or vertebral column. This can occur when the neural tube, which forms the brain and spinal cord, fails to close properly during fetal development. Encephaloceles can be classified based on the location of the defect and the extent of the brain or spinal cord that is exposed. They can be present at birth or may not be diagnosed until later in life. Encephaloceles can cause a range of symptoms, depending on the size and location of the defect and the extent of brain or spinal cord involvement. Treatment typically involves surgical repair of the defect to reduce the risk of complications and improve the quality of life for the affected individual.
Platybasia is a medical term that refers to a condition in which the occipital bone (the bone at the back of the skull) is flat or flattened. This can be caused by a variety of factors, including genetic factors, head injuries, and certain medical conditions such as Down syndrome or achondroplasia. Platybasia can cause a number of symptoms, including headaches, dizziness, and balance problems. In some cases, it may also lead to structural problems in the skull, such as an increased risk of fractures or pressure on the brain. Treatment for platybasia typically depends on the underlying cause and the severity of the symptoms. In some cases, no treatment may be necessary, while in others, surgery may be recommended to correct the flattened occipital bone.
The cranial fossa, posterior refers to the posterior part of one of the four main cavities or spaces within the skull. The skull is composed of several bones that fit together to form a protective structure around the brain. The cranial fossae are the main cavities within the skull that house the brain. There are four main cranial fossae: the anterior cranial fossa, the middle cranial fossa, the posterior cranial fossa, and the temporal fossa. The posterior cranial fossa is located at the back of the skull, behind the middle cranial fossa. It is the largest of the four cranial fossae and contains several important structures, including the cerebellum, the brainstem, and the occipital lobe of the cerebrum. The posterior cranial fossa is bounded by several bones, including the occipital bone, the cerebellar peduncles, and the tentorium cerebelli. The tentorium cerebelli is a thin, translucent membrane that separates the cerebellum from the brainstem. The cerebellar peduncles are the two thickened areas of the brainstem that connect the cerebellum to the rest of the brain. The posterior cranial fossa is an important part of the skull and plays a crucial role in protecting the brain. Any damage to the bones that form the posterior cranial fossa can potentially cause serious injury to the brain.
Meningomyelocele is a birth defect that occurs when the spinal cord and the protective membranes surrounding it (the meninges) protrude through a weak spot in the baby's spine (vertebrae). This can result in a sac-like structure containing the spinal cord and meninges, which is usually located at the base of the spine or the lower back. Meningomyelocele can cause a range of symptoms, depending on the severity of the defect and the extent of the spinal cord damage. Some common symptoms include weakness or paralysis in the legs, difficulty walking or standing, loss of sensation in the lower body, and problems with bladder and bowel control. Treatment for meningomyelocele typically involves surgery to repair the spinal defect and close the sac. In some cases, additional surgery may be necessary to address complications such as hydrocephalus (an accumulation of fluid in the brain) or tethered spinal cord (a condition in which the spinal cord is attached to surrounding tissues, causing it to stretch and damage nerve fibers). Overall, meningomyelocele is a serious condition that requires prompt medical attention and ongoing management to ensure the best possible outcomes for affected individuals.
Decompression, surgical refers to a surgical procedure in which pressure is relieved from a compressed or trapped body part or tissue. This can be done to treat a variety of medical conditions, including: 1. Herniated discs: A herniated disc occurs when the soft tissue inside a spinal disc bulges out through a tear in the outer layer. This can put pressure on the spinal cord or nerves, causing pain, numbness, or weakness. A surgical decompression may be performed to remove the herniated disc material and relieve pressure on the affected nerves. 2. Carpal tunnel syndrome: Carpal tunnel syndrome is a condition in which the median nerve, which runs from the forearm to the hand, becomes compressed or trapped in the wrist. This can cause pain, numbness, or weakness in the hand. A surgical decompression may be performed to release the pressure on the median nerve and relieve symptoms. 3. Sciatica: Sciatica is a type of pain that travels down the leg from the lower back. It can be caused by a herniated disc or other spinal condition that compresses the sciatic nerve. A surgical decompression may be performed to relieve pressure on the sciatic nerve and alleviate symptoms. 4. Tarsal tunnel syndrome: Tarsal tunnel syndrome is a condition in which the posterior tibial nerve, which runs from the calf to the foot, becomes compressed or trapped in the ankle. This can cause pain, numbness, or weakness in the foot. A surgical decompression may be performed to release the pressure on the posterior tibial nerve and relieve symptoms. Surgical decompression is typically performed under general anesthesia and may involve making a small incision in the skin to access the affected area. The surgeon will then use specialized instruments to remove any tissue or bone that is compressing the affected nerve or body part. After the procedure, the incision will be closed with stitches or staples, and the patient will be monitored for any complications.
Decompressive craniectomy is a surgical procedure in which a portion of the skull is removed to relieve pressure on the brain. This is typically done when the brain is swelling rapidly and the skull is not able to expand enough to accommodate the increased size of the brain. The goal of the surgery is to reduce intracranial pressure and prevent further damage to the brain. The removed bone is typically replaced with a synthetic material or the patient's own bone at a later date. The procedure is typically performed as an emergency treatment for severe head injuries or brain swelling caused by conditions such as stroke, brain tumor, or head trauma.
Down syndrome, also known as trisomy 21, is a genetic disorder caused by the presence of an extra copy of chromosome 21. This extra genetic material affects the development and function of the body, leading to a range of physical, cognitive, and medical characteristics. Individuals with Down syndrome typically have distinct facial features, such as a flattened face, small ears, and a short neck. They may also have intellectual disabilities, ranging from mild to moderate, and may experience delays in speech and language development. Other common features include an increased risk of certain medical conditions, such as heart defects, respiratory problems, and hearing loss. Down syndrome is caused by a random event during the formation of reproductive cells, and the risk of having a child with the condition increases with the age of the mother. There is currently no cure for Down syndrome, but early intervention and support can help individuals with the condition to reach their full potential and lead fulfilling lives.
Cerebrospinal fluid pressure (CSFP) is the pressure exerted by the cerebrospinal fluid (CSF) within the spinal canal and the ventricles of the brain. It is an important parameter in the diagnosis and management of various neurological conditions, including hydrocephalus, meningitis, and intracranial hypertension. CSFP is typically measured using a device called a lumbar puncture, which involves inserting a needle into the lower back and withdrawing a small amount of CSF for analysis. The pressure is then measured using a manometer. Normal CSFP ranges from 5 to 15 mmHg, although this can vary depending on the individual and the specific circumstances. Abnormal CSFP can be caused by a variety of factors, including increased production of CSF, decreased absorption of CSF, or blockage of the flow of CSF. High CSFP can lead to symptoms such as headache, nausea, vomiting, and confusion, while low CSFP can cause symptoms such as dizziness, weakness, and loss of consciousness.
Metabolic Syndrome X, also known as Syndrome X or Insulin Resistance Syndrome, is a cluster of conditions that increase the risk of developing heart disease, stroke, and type 2 diabetes. The five key components of Metabolic Syndrome X are: 1. Abdominal obesity: A waist circumference of 102 cm (40 inches) or more in men and 88 cm (35 inches) or more in women. 2. High blood pressure: A systolic blood pressure of 130 mmHg or higher, or a diastolic blood pressure of 85 mmHg or higher. 3. High fasting blood sugar: A fasting blood sugar level of 100 mg/dL or higher. 4. High triglyceride levels: A triglyceride level of 150 mg/dL or higher. 5. Low HDL cholesterol levels: An HDL cholesterol level of less than 40 mg/dL in men and less than 50 mg/dL in women. These conditions are often found together and can be caused by a variety of factors, including genetics, lifestyle, and certain medical conditions. Treatment for Metabolic Syndrome X typically involves lifestyle changes, such as diet and exercise, and may also include medication to manage blood pressure, blood sugar, and cholesterol levels.
In the medical field, the term "cattle" refers to large domesticated animals that are raised for their meat, milk, or other products. Cattle are a common source of food and are also used for labor in agriculture, such as plowing fields or pulling carts. In veterinary medicine, cattle are often referred to as "livestock" and may be treated for a variety of medical conditions, including diseases, injuries, and parasites. Some common medical issues that may affect cattle include respiratory infections, digestive problems, and musculoskeletal disorders. Cattle may also be used in medical research, particularly in the fields of genetics and agriculture. For example, scientists may study the genetics of cattle to develop new breeds with desirable traits, such as increased milk production or resistance to disease.
In the medical field, "cats" typically refers to Felis catus, which is the scientific name for the domestic cat. Cats are commonly kept as pets and are known for their agility, playful behavior, and affectionate nature. In veterinary medicine, cats are commonly treated for a variety of health conditions, including respiratory infections, urinary tract infections, gastrointestinal issues, and dental problems. Cats can also be used in medical research to study various diseases and conditions, such as cancer, heart disease, and neurological disorders. In some cases, the term "cats" may also refer to a group of animals used in medical research or testing. For example, cats may be used to study the effects of certain drugs or treatments on the immune system or to test new vaccines.
Side effects of cyproterone acetate
Lourdes Medical Bureau
Ernesto Pompeo Molmenti
List of pathologists
Portal vein thrombosis
Hepatic veno-occlusive disease
Serum-ascites albumin gradient
Mamun Al Mahtab (Shwapnil)
UCL Medical School
Liver support system
Budd-Chiari syndrome - Wikipedia
Budd-Chiari syndrome - Wikipedia
Budd-Chiari Syndrome: Practice Essentials, Background, Pathophysiology
Budd-Chiari Syndrome: Practice Essentials, Background, Pathophysiology
Budd-Chiari Syndrome - Hepatic and Biliary Disorders - MSD Manual Professional Edition
Placement of a caudal vena cava stent for treatment of Budd-Chiari-like syndrome in a 4-month-old Ragdoll cat | Advanced...
Hepatic vein obstruction (Budd-Chiari): MedlinePlus Medical Encyclopedia
Budd-Chiari Syndrome Differential Diagnoses
Budd-Chiari syndrome CT - wikidoc
Budd-Chiari Syndrome: Practice Essentials, Background, Pathophysiology
The Diagnosis and Management of Budd-Chiari Syndrome
Budd-Chiari Syndrome | 5-Minute Clinical Consult
Budd-Chiari syndrome-UKMLA PLAB AMC USMLE Prometric MCQ
Budd-Chiari Syndrome as A Manifestation of Right Atrium Myxoma
Pregnancy Outcomes in Women with Budd Chiari Syndrome or Portal Hypertension - ISTH Congress Abstracts
Imaging of Liver Transplantation Complications: Practice Essentials, Complications, Postoperative Fluid Collections
Cirrhosis: Practice Essentials, Overview, Etiology
Current knowledge in pathophysiology and management of Budd-Chiari syndrome and non-cirrhotic non-tumoral splanchnic vein...
JPM | Free Full-Text | Hepatic Venous Occlusion Type of Budd–Chiari Syndrome versus Pyrrolizidine Alkaloid-Induced...
Enskyce™(desogestrel and ethinyl estradiol tablets USP)0.15 mg/0.03 mg
Polycythemia Vera Treatment & Management: Approach Considerations, Medical Care, Phlebotomy
Nicholas Endrulat | CaringBridge
Liver Care Center
Demulen (Ethinyl Estradiol and Ethynodiol Diacetate): Uses, Dosage, Side Effects, Interactions, Warning
Classifications for Combined Hormonal Contraceptives | CDC
CT and MRI of the Abdomen and Pelvis: A Teaching File, Second edition, edited by Pablo R. Ros and Koenraad J. Mortele with...
Pathology Outlines - Drug / toxin induced hepatitis (DILI)-general
Liver Blood Tests (Normal, High, and Low Levels): Symptoms & Causes
Chronic cerebrospinal venous insufficiency in patients with multiple sclerosis | Journal of Neurology, Neurosurgery & Psychiatry
World Journal of Clinical Cases - Baishideng Publishing Group
-   Other acquired hypercoagulable disorders that may result in Budd-Chiari syndrome include antiphospholipid syndrome and paroxysmal nocturnal hemoglobinuria , which are responsible for 10-12% and 7-12% of Budd-Chiari syndrome cases, respectively. (wikipedia.org)
- Underlying prothrombotic disorders included myeloproliferative neoplasms (N=4), protein C deficiency (N=2), antiphospholipid syndrome (N=1) and cirrhosis (N=5) [Table 1]. (isth.org)
- Nick has Antiphospholipid Syndrome and Budd Chiari. (caringbridge.org)
- Primary Budd-Chiari syndrome occurs due to thrombosis of the hepatic vein. (wikipedia.org)
-  Inherited disorders of hypercoagulability may lead to thrombosis of the hepatic vein and Budd-Chiari syndrome. (wikipedia.org)
- Alternatively, this syndrome is characterized by occlusion due to hepatic vein thrombosis or mechanical venous obstruction. (fortunejournals.com)
- Complications include iron deficiency (from chronic haemoglobinuria), progressive renal impairment (from haemoglobinuria), and the Budd Chiari syndrome (hepatic vein thrombosis). (lu.se)
Obstruction of hepatic venous2
- Budd-Chiari syndrome is obstruction of hepatic venous outflow that originates anywhere from the small hepatic veins inside the liver to the inferior vena cava and right atrium. (msdmanuals.com)
- Budd-Chiari syndrome is characterized by obstruction of hepatic venous flow at the level of right atrium, inferior vena cava, large hepatic veins, or hepatic venules . (fortunejournals.com)
- The prognosis is poor in patients with Budd-Chiari syndrome who remain untreated, with death resulting from progressive liver failure in 3 months to 3 years from the time of the diagnosis. (medscape.com)
- A diagnosis of Budd-Chiari-like syndrome secondary to a membranous obstruction of the caudal vena cava was made. (avmi.net)
- Aydinli M, Bayraktar Y. Budd-Chiari syndrome: etiology, pathogenesis and diagnosis. (medscape.com)
- CT scan may be helpful in the diagnosis of Budd-Chiari syndrome. (wikidoc.org)
- The diagnosis, initial management and long-term follow-up of patients with Budd-Chiari syndrome is reviewed. (medscape.com)
- Budd-Chiari syndrome is also seen in tuberculosis , congenital venous webs and occasionally in inferior vena caval stenosis . (wikipedia.org)
- up to 39% develop venous thromboses,  and 12% may acquire Budd-Chiari. (wikipedia.org)
- Any obstruction of the venous vasculature of the liver is referred to as Budd-Chiari syndrome, from the venules to the right atrium . (wikipedia.org)
- Budd-Chiari syndrome is an uncommon condition induced by thrombotic or nonthrombotic obstruction of the hepatic venous outflow and is characterized by hepatomegaly, ascites, and abdominal pain. (medscape.com)
- Tian ZL, Jia GL, Xi HL, Feng S, Wang XK, Li R. Investigation on etiology of hepatic venous obstruction Budd-Chiari syndrome. (medscape.com)
- Budd-Chiari syndrome is a rare disorder caused by hepatic venous outflow obstruction and resulting hepatic dysfunction. (medscape.com)
- Budd-Chiari syndrome (BCS) is a rare condition marked by a number of symptoms due to hepatic venous obstruction. (fortunejournals.com)
- Cutaneous manifestations of cirrhosis include jaundice, spider angiomata, skin telangiectasias ("paper money skin"), palmar erythema, white nails, disappearance of lunulae, and finger clubbing, especially in the setting of hepatopulmonary syndrome. (medscape.com)
-   Budd-Chiari syndrome may be the presenting sign of these hypercoagulable disorders. (wikipedia.org)
- Several factors predispose to the development of Budd-Chiari syndrome, including hypercoagulable, inherited, and acquired conditions, as well as a variety of other causes, can be identified in approximately 75% of patients. (fortunejournals.com)
- Etiology, management, and outcome of the Budd-Chiari syndrome. (medscape.com)
- Budd-Chiari syndrome: long-term effect on outcome with transjugular intrahepatic portosystemic shunt. (medscape.com)
- Overt Budd-Chiari syndrome generally requires the occlusion of at least 2 hepatic veins. (medscape.com)
- In 1899, Chiari described an "obliterating endophlebitis of the hepatic veins" and its association with hepatomegaly, ascites and abdominal pain. (medscape.com)
- Budd-Chiari syndrome is an uncommon disorder resulting from obstruction of the large hepatic veins or inferior vena cava at the suprahepatic level. (fortunejournals.com)
- These cases are known as idiopathic Budd-Chiari syndrome. (wikipedia.org)
- Budd-Chiari syndrome should be considered separate from veno-occlusive disease (VOD), also known as sinusoidal obstruction syndrome, which is characterized by toxin-induced, nonthrombotic obstruction of prehepatic veins (see the images below). (medscape.com)
- Outflow obstruction caused by the sinusoidal obstruction syndrome (formerly 'veno-occlusive disease') and cardiac disorders is excluded. (medscape.com)
- We searched PubMed without time restriction using key words: bone marrow and fibrosis as the main stem against the terms: growth factors, cytokines and chemokines, morphology, megakaryocytes and platelets, myeloproliferative disorders, myelodysplastic syndrome, collagen biosynthesis, mesenchymal stem cells, vitamins and minerals and hormones, and mechanism of tissue fibrosis. (bvsalud.org)
- Budd-Chiari syndrome in Sweden: epidemiology, clinical characteristics and survival - an 18-year experience. (medscape.com)
- Herein, our authors present a case of a 40-year-old female patient with Budd-Chiari syndrome in whom the right atrium myxoma was manifested with worsening of clinical symptoms despite medical treatment therapy. (fortunejournals.com)
-  The syndrome can be fulminant , acute, chronic, or asymptomatic. (wikipedia.org)
- The acute syndrome presents with rapidly progressive severe upper abdominal pain , yellow discoloration of the skin and whites of the eyes , liver enlargement , enlargement of the spleen , fluid accumulation within the peritoneal cavity , elevated liver enzymes , and eventually encephalopathy . (wikipedia.org)
- The fulminant syndrome presents early with encephalopathy and ascites. (wikipedia.org)
- Hamulyák EN, Wiegers HMG, van Duuren JR, Middeldorp S, Ganzevoort W. Pregnancy Outcomes in Women with Budd Chiari Syndrome or Portal Hypertension [abstract]. (isth.org)
- Pregnancy in women with known and treated Budd-Chiari syndrome: maternal and fetal outcomes. (medscape.com)
- Secondary Budd-Chiari syndrome, which is very rare compared to the primary variant, is due to compression of the hepatic vein by an outside structure (such as a tumor or polycystic kidney disease ). (wikipedia.org)
- Sometimes Budd-Chiari syndrome begins during pregnancy and unmasks a previously asymptomatic hypercoagulability disorder. (msdmanuals.com)
- CLINICAL RELEVANCE: Budd-Chiari-like syndrome is a rare phenomenon in veterinary medicine, and congenital malformations should be considered in young feline patients with ascites. (avmi.net)
- Rotterdam score predicts early mortality in Budd-Chiari syndrome, and surgical shunting prolongs transplant-free survival. (medscape.com)
- Intracardiac tumors have rarely been reported as a predisposing cause for the development of Budd-Chiari syndrome, and surgical removal of these tumors is generally a curative treatment for this syndrome [1, 3-6]. (fortunejournals.com)
- The description of the clinical features of hepatic vein outflow obstruction is generally attributed to a pathologist, Hans Chiari (although he was not the first). (medscape.com)
- Qi X, Ren W, Wang Y, Guo X, Fan D. Survival and prognostic indicators of Budd-Chiari syndrome: a systematic review of 79 studies. (medscape.com)
- The classic form of CD manifests as a malabsorption syndrome associated with chronic diarrhea, mineral deficiencies, failure to thrive, and weight loss. (hindawi.com)
- Hepatic vein blockage is the most common cause of Budd-Chiari syndrome. (medlineplus.gov)