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العنوان
Portal vein consideration in Living Donor Liver Transplantation/
المؤلف
Elbastawesy,Ahmed ElSied Abdelgalil
هيئة الاعداد
باحث / أحمد السعيد عبد الجليل
مشرف / رفعــت رفعــت كامــل
مشرف / محمد محمد بهاء
مشرف / محمد سعيد
الموضوع
Liver Transplantation
تاريخ النشر
2014
عدد الصفحات
140.p:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
جراحة
تاريخ الإجازة
13/4/2014
مكان الإجازة
جامعة عين شمس - كلية الطب - General Surgery
الفهرس
Only 14 pages are availabe for public view

from 140

from 140

Abstract

T
he normal anatomy of the portal vein is defined as a division of the main portal vein into two branches-the left (supplying segments II, III, and IV) and right portal veins; the right dividing secondarily into two branches-the anterior (supplying segments V and VIII) and the posterior (supplying segments VI and VII) portal veins.
Variants are frequent and account for 20 to 35% of the population. The most frequent variants are portal trifurcation with division of the main portal vein into the left, right anterior, and posterior branches, and the early origin of the right posterior branch directly from the portal vein. The presence of portal vein variants increases the risk of bile duct hilar anatomical variation. These variants must be diagnosed before split or living donor transplantation.
PVT is relatively uncommon in the general population, but is more frequent among cirrhotic patients and represents a “milestone” in the natural evolution of liver disease.
Local or systemic pro-thrombotic factors, alone or together, can play an important role in PVT pathogenesis, which is complex and different in each clinical context and in each patient.
The consequent changes in hepatic and splanchnic hemodynamic are responsible for a mild impairment in liver function, in absence of an overt liver disease, or can precipitate a preexistent metastable clinical status in cirrhotic patients.
Moreover, PVT might have indirect effects on other abdominal organs, causing intestinal ischemia and infarction, or predisposition to vascular neoformation and gastrointestinal bleeding.
The identification of protean manifestations of PVT is essential to provide a prompt diagnosis, as the removal of the original trigger factor and an early therapeutic management is crucial to preserve patient health and, sometimes, life.
The history of PVT has been characterized by difficulties in diagnosis and treatment, which, today, have almost been overcome.
In the future, due to innovations in imaging and pharma-ceuticals, clinical attention must be focused on the realization of a scheduled, preemptive, therapeutic approach to the patient, to better define the profile of toxicity and reduce side effects, especially in cirrhotic patients.