Clots



Clots





VASCULAR ANATOMY OF LIVER



  • Liver constitutes 5% of body weight and receives 20% of cardiac output via hepatic artery (Ha) and portal vein (Pv)



    • Hepatic artery is a branch of hepaticoduodenal artery from celiac axis and carries 30% of total flow, but >50% of needed oxygen; Under high pressure, highly variable, dependant upon systemic blood pressure, regulated by adenosine concentration


    • Portal vein is valveless (formed from splenic & SMV), carries 70-80% of total liver blood flow and delivers <50% of needed oxygen; Under low pressure, not affected by systemic circulation, not regulated


    • Both Ha and Pv defined into Right & Left branches and eventually become arterioles and venules that drain into the sinusoids



      • At this level, hepatic arteries and sinusoids have sphincters that dynamically regulate blood flow i.e. a reduction of Pv flow leads to an immediate increase in Ha flow (total sinusoidal blood flow maintained constant; However, Pv flow is relatively constant and is not influenced by Ha flow)


    • At the end of sinusoid, blood enters the central venule forming the hepatic venule; Three major hepatic veins(Hv): Right/Middle/Left



      • The veins have different blood distributions from Ha and Pv, influencing surgical intervention


    • The liver is divided into eight segments, each having own afferent and efferent blood supply



      • Note: the Caudate lobe is drained by small veins directly into the IVC, hence the compensatory hypertrophy in BCS


  • Microarchitecture: See also Liver- Histopathology of Liver (Chapter 4.19)



    • Basic element of liver structure is liver cell plate, consisting of 15-20 hepatocytes lined up between the portal area and hepatic veins


    • Perivenular (Zone III) hepatocytes are subject to more hypoxia because they are at end of unidirectional sinusoidal blood flow


    • Zone II and III are involved in drug metabolism and are rich in cytochrome P450 enzymes









    Pv (portal vein)
    Ha (hepatic artery)
    Hv (hepatic venules)
    E (fenestrated epithelium) (contain Kupffer cells)

    Blood from Pv and Ha, join and traverse sinusoids, leaving the liver from Hv; Low pressure circulation in sinusoids allows plasma to pass through E, and reach D, where via direct contact with hepatocytes, exchange of nutrients and metabolites takes place


    D (space of Disse) (contain Stellate cells)
    Bd (bile duct)

    Note: Stellate cells when activated take on characteristics of fibroblasts and cause fibrosis or cirrhosis; Kupffer cells are phagocytic cells



  • Note: a sick liver can produce a misbalance of clotting/anticlotting factors, hence a cirrhotic can form clots if more clotting factors produced






Modified with permission from McNally P. GI/Liver Secrets. 3rd ed. New York: Elsevier/Mosby, 2006:237.



BUDD-CHIARI SYNDROME (BCS)


Definition:



  • Thrombosis/occlusion of the hepatic veins (small venules, large hepatic veins), IVC or even the right atrium


Etiologies:



  • Hypercoagulable: Myeloproliferative syndromes, Paroxysmal nocturnal hemoglobinuria, SLE, Protein C & S or antithrombin-III deficiency, Pregnancy/OCP


  • Tumor invasion: HCC, Renal, Adrenal, Pancreas


  • Inferior vena cava membranous web


  • Trauma


  • Postpartum


  • Idiopathic (Factor V Leiden may be responsible for 25% of BCS considered ‘idiopathic’)


Pathophysiology:



  • Increased sinusoidal pressure caused by obstructed hepatic venous outflow: hypoxic damage to hepatocytes and increased portal pressure



    • Continued obstruction leads to further hepatic necrosis and ultimately cirrhosis


Clinical Manifestations/Physical Exam:

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Aug 24, 2016 | Posted by in GASTROENTEROLOGY | Comments Off on Clots

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