- G. V. Volynets added an answer:3Non liver cirrhotic portal hypertension?
A young patient with hemetemesis, OGDS reviewed stigmata of portal hypertension (bleeding esophageal varices and portal hypertensive gastropathy).
USS HBS: no liver cirhosis. CT HBS: no portal vein thrombosis
How are you going to investigate the patient? the etiology?
If there is no cirrhosis Maybe it extrahepatic blockade of the branches of the portal veinFollowing
- Laurence Blendis added an answer:6Chronic hematuria in cirrhosis may be caused by portal hypertension?
Male 45yrs, HBV and D viral cirrhosis following antiviral treatment, listed for LT. Chronic hematuria and anemia since at least one year with need of chronic transfusion. Portal cavernoma associated with trombophylia (homozygous for PAI 1 mutation). No treatment ( platelets 20.000 and INR 2 )
All exams and imaging found no renal disease, cystoscopy only saw mild bilateral blood from both sides . Cryoglobulins are negative.
yes portal hypertension is a rare cause of hematuria from variceal bleeding either from the bladder or from vas deferns. However blood seen coming from both kidneys rule this outFollowing
- Chieng jin yu added an answer:12Why does spider angioma appear only on a skin of the upper part of a trunk in cirrhosis?
Have you seen other location of this sign?
Having more than 3 spider angiomas is likely to be abnormal.
The spider angiomas are found only in the distribution of the superior vena cava, and are thus commonly found on the face, neck, upper part of the trunk and arms.Following
- Amitava Goswami added an answer:3What is the right time to stop non selective beta blocker in portal hypertension?
Left ventricular diastolic dysfunction occurs in 50-70 % of decompensated cirrhosis. However with the development of left ventricular systolic dysfunction or mean arterial pressure < 82mm of hg or Cardiac Index < 1.5 L or refractory ascites; non selective beta blocker should be abandoned.
Window concept for beta blocker is new in portal hypertension. So window period for beta blocker is very short from primary prophylaxis to decompensated cirrhosis without the risk factors (I have already mentioned). Recent studies have shown increased renal failure (HRS) and mortality with beta blocker in refractory ascites, MAP < 82 mm hg, CI < 1.5. In these high risk group endoscopic vareceal ligation is the best alternativeFollowing
- Maher M Al-zaiem added an answer:3Why do patients with diaphragmatic hernia have portal hypertension?Why do patients with diaphragmatic hernia have portal hypertension?what is the percentage of operated patients of diaphragmatic hernia who has portal hypertension?
and if it appears, at what age ?
As pediatric surgeon,i have operated more than 75 cases of different types of diaphragmatic hernia, I have not come across a single case of portal hypertension !Following
- Rustam Zafardjanovich Yuldashev added an answer:4Extrahepatic portal hypertension and congenital heart defect. Which should come first?In management of paediatric patients with extrahepatic portal hypertension and congenital heart defect (ASD, VSD or tetralogy of Fallot) which operation must be done first? Correction of heart defect or portal hypertension?I agree with you to,but on the other hand, Horia and Andreas, usually after correction of congenital heart defects often surgeons use anticoagulants to prevent postoperative complications, which increases the risk of gastroesophageal bleeding.Following
- Mario Romano added an answer:7What is the reason of cyanosis after mesocaval anastomosis in patient with extrahepatic portal hypertension?in 2006 patient operated due to gastroesophageal bleeding. Operation- end to side iliaco mesenterial anastomosis (v. iliaca communis dextra to v/ mesenterica superior). Year after postoperative period patient began to complain on cyanosis, and clubbing of fingers. SpO2 - 66%. Echocardiography-clear. On angiopulmonography also no evidence of arteriovenous fistula in lungs!The increase of NO determines the opening of arteriovenous shunts in the pulmonary vascular bed that are responsible for the onset of hepatopulmonary syndromeFollowing