Triggers of portal vein thrombosis.
Slowed portal blood flow, structural changes in the liver, portal vein endothelial injury, plasma fibrinogen FIB, liver transplantation, diabetes, braking, oral contraceptives, history of smoking, tumors, surgery, etc.
Portal vein thrombosis after surgery.
Pre-operative portal vein thrombosis already present in 6-10% of patients, diameter of portal/splenic veins, spleen size, post-operative portal flow velocity, pre- and post-operative portal pressure, post-operative complications, coagulation (platelets) after splenectomy, surgical mechanical damage to blood vessels, blind end of splenic vein, coagulant use, volume deficit, abdominal inflammation or infection.
Morbidity characteristics.
High incidence of 22%-39%, acute onset (1-3 weeks postoperatively, as early as 3 days postoperatively), often lack of clinical specificity, insidious or even asymptomatic onset easily overlooked and missed, slow chronic thrombosis with collateral vessel formation, individual empirical treatment (lack of guideline guidance).
Typing.
I thrombosis is limited to intrahepatic portal branches;
Ⅱ confined to the main portal vein;
Ⅲ limited to portal vein trunk and portal vein branches;
IV limited to superior mesenteric vein and/or splenic vein;
V limited to portal vein trunk, superior mesenteric vein and/or splenic vein;
VI main trunk, branches of portal vein, superior mesenteric vein and/or splenic vein are involved
Yerdel classification.
Grade I: less than 50% of the portal vein lumen, limited without extension to the superior mesenteric vein;
Grade II: portal vein obstruction of 50% to 100%, with or without extension into the superior mesenteric vein;
Grade III: complete obstruction of portal vein and proximal superior mesenteric vein, while the distal superior mesenteric vein is still patent;
Grade IV: complete obstruction of the portal, proximal and distal superior mesenteric veins.
Monitoring: signs and symptoms (abdominal pain, diarrhea, fever), D-dimer, FIB, leukocytes, ascites, ultrasound/CT, liver function
Prevention: reduction of surgical risk, protection from spontaneous shunts, low molecular heparin, enteral aspirin (50 mg qd orally), warfarin. Can prevention reduce portal vein thrombosis?
Treatment aims: in the acute phase to eliminate the thrombus or stop its spread and improve symptoms; in the chronic phase to “recanalize” the portal vein to restore blood flow
Individualized treatment.
In mild cases, no special treatment is needed, expansion treatment and close observation.
If platelets > 800×109/L or fibrinogen Fbg > 4.0g/L, thrombolytic and anticoagulant treatment should be carried out if the diagnosis of grade II or above or grade I clinical symptoms are more severe. Thrombolysis was performed by peripheral intravenous administration of urokinase 200,000-400,000 units/d , or low-molecular dextrose 250-500 mL 2 times/d for 3-5 d.
Heparinization, warfarin maintenance for 2 months
International normalized ratio (INR ) at 2-3 , PT 1.5-2.5 times.
Percutaneous transhepatic therapy (TIPS), indirect method (superior mesenteric artery route), thrombolysis
Conclusion.
Portal vein cavernous degeneration.
If thrombolytic anticoagulation is not effective and intestinal necrosis is suspected, aggressive portal vein dissection for embolization is performed.
If intestinal necrosis has occurred, intestinal resection is performed.