Episode three covers the decompensated complications that do not flow primarily through splanchnic vasodilation, starting with two pulmonary syndromes that look related but are physiologically opposite. Hepatopulmonary syndrome is capillary dilation with shunt physiology, recognized by platypnea and orthodeoxia, while portopulmonary hypertension is arteriolar constriction diagnosed by right heart catheterization, and that single distinction picks the therapy and changes the transplant calculus. The episode then works the coagulopathy where the INR misleads because cirrhotic hemostasis is rebalanced rather than impaired, so paracentesis and thoracentesis need no correction. It closes on the vascular liver diseases sorted by anatomic level, Budd-Chiari, sinusoidal obstruction syndrome, portal vein thrombosis, porto-sinusoidal vascular disease, and shock liver. Topics covered Hepatopulmonary syndrome and shunt physiology Platypnea, orthodeoxia, and contrast echocardiography Portopulmonary hypertension and the transplant calculus Hepatic hydrothorax Rebalanced hemostasis and the misleading INR Periprocedural transfusion decisions Budd-Chiari syndrome Sinusoidal obstruction syndrome Portal vein thrombosis and tumor thrombus Key decisions Hepatopulmonary syndrome is diagnosed by contrast echocardiography showing microbubbles in the left atrium three to six cardiac cycles after the right atrium opacifies, and an arterial oxygen below sixty earns transplant-priority exception points with transplant the only cure. Portopulmonary hypertension is confirmed by right heart catheterization with a mean pulmonary arterial pressure of at least twenty-five, a pulmonary vascular resistance over three Wood units, and a wedge of at most fifteen; a mean pressure at or above fifty contraindicates transplant while thirty-five to forty-five is a relative contraindication treatable with vasodilators. Vasodilators help portopulmonary hypertension because the lesion is constriction but do not help hepatopulmonary syndrome because the capillaries are already dilated. Hepatic hydrothorax is managed with sodium restriction, diuretics, therapeutic thoracentesis, and TIPS for refractory cases, while chest tube placement and pleurodesis are contraindicated. The INR does not predict bleeding in cirrhosis because hemostasis is rebalanced, so paracentesis and thoracentesis require no correction and viscoelastic testing captures the real state; high-risk procedures keep platelets above fifty thousand and fibrinogen above a floor. Budd-Chiari mandates a thrombophilia workup with JAK2 the highest-yield test, and treatment escalates stepwise from anticoagulation to angioplasty to TIPS to transplant. In portal vein thrombosis exclude hepatocellular carcinoma with tumor thrombus before anticoagulating, using arterial enhancement as the discriminator, while sinusoidal obstruction syndrome is treated with defibrotide. For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: [email protected]. (00:00) - Introduction and the remaining complications (00:24) - Hepatopulmonary syndrome (01:05) - Platypnea and orthodeoxia (02:39) - Portopulmonary hypertension (04:31) - Hepatic hydrothorax (06:22) - Coagulopathy and the misleading INR (10:16) - Vascular liver disease and Budd-Chiari (12:24) - Sinusoidal obstruction syndrome (13:53) - Portal vein thrombosis

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“What did the council decide on item 42?” — answered with the speaker and the moment.

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