Portal Hypertension and Cirrhosis Complications

• Audio chapter
  Single-voice audio, listen on the commute.
• ABIM-format MCQs
  5-option vignettes with full wrong-answer teaching.
• Study guide
  Tables, decision trees, primary sources.
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What this chapter covers

• Section 23.1: Portal hypertension hemodynamics and Baveno VII

  Portal hypertension begins as increased intrahepatic resistance from sinusoidal architectural distortion, most commonly cirrhosis from any etiology.

• Section 23.2: Variceal screening and primary prophylaxis

  Screening EGD is required in most cirrhotic patients except the Baveno VI exception (liver stiffness under 20 kPa AND platelets over 150,000), where yearly transient elastography and platelet trending substitute for endoscopy until either parameter crosses the threshold.

• Section 23.3: Acute variceal hemorrhage and secondary prophylaxis

  Any GI bleeding in cirrhosis is variceal until proven otherwise.

• Section 23.4: Gastric varices, portal hypertensive gastropathy, and GAVE

  Gastric varices are classified by Sarin: GOV1 (along the lesser curve, extension of esophageal varices, approximately 75 percent of all gastric varices, and behave most like esophageal varices, often controllable with band ligation); GOV2 (cardiofundal extension into the fundus); IGV1 (isolated fundal, often with gastrorenal shunt); IGV2 (isolated ectopic gastric sites).

• Section 23.5: Ascites pathophysiology and diuretic management

  Ascites pathophysiology begins with portal hypertension driving splanchnic vasodilation through nitric oxide and other vasodilator excess.

• Section 23.6: Refractory ascites, TIPS, and hyponatremia

  Refractory ascites is treated with serial large-volume paracentesis plus albumin or with TIPS in carefully selected patients.

• Section 23.7: Spontaneous bacterial peritonitis

  SBP is diagnosed on diagnostic paracentesis with PMN over 250 per mm3 in a patient with cirrhotic ascites, regardless of symptoms or culture result.

• Section 23.8: Hepatorenal syndrome

  HRS terminology has been updated: type 1 HRS is now called HRS-AKI, and type 2 is now HRS-CKD or HRS-NAKI.

• Section 23.9: Hepatic encephalopathy

  Hepatic encephalopathy spans minimal (covert) HE detected only on psychometric testing through grade 4 coma per the West Haven classification.

• Section 23.10: Pulmonary vascular complications: HPS, POPH, hepatic hydrothorax

  Hepatopulmonary syndrome (HPS) and portopulmonary hypertension (POPH) are clinically and physiologically opposite and require very different management.

• Section 23.11: Coagulopathy and periprocedural management

  Cirrhosis produces a state of rebalanced hemostasis: parallel reductions in pro-coagulant factors (II, V, VII, IX, X, XI) and anti-coagulant factors (protein C, protein S, antithrombin) and parallel changes in pro- and anti-fibrinolytic proteins.

• Section 23.12: Vascular liver disease

  Budd-Chiari syndrome (hepatic vein outflow obstruction) presents with abdominal pain, hepatomegaly, ascites, and elevated transaminases.

Podcast episodes

1. 01

   Portal Hypertension and Varices

   Episode one of the Portal Hypertension and Cirrhosis Complications chapter treats portal hypertension as a pressure problem first, then follows that pressure into varices and bleeding. The organizing idea: the hepatic venous pressure gradient is the hemodynamic gold standard, and liver stiffness plus platelets give the noninvasive translation that now drives beta-blocker and screening decisions. Screening thresholds, primary prophylaxis, and the acute variceal hemorrhage bundle all key off the same physiology, with the restrictive transfusion target, mandatory ceftriaxone, and the early-TIPS decision as the cirrhosis-specific layers. It closes on gastric varices, portal hypertensive gastropathy, and GAVE, where anatomy and drainage pick the therapy, not appearance.

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2. 02

   The Splanchnic Vasodilation Cluster

   Episode two follows the splanchnic vasodilation cluster, where one upstream physiology produces four complications, each with its own bundle, threshold, and drug sequence. Portal hypertension drives splanchnic vasodilation, the kidney reads effective hypovolemia and retains sodium, and from that single mismatch flow ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, and hepatic encephalopathy. The episode anchors ascites on the serum-ascites albumin gradient and the fixed spironolactone-to-furosemide ratio, then moves through the TIPS-versus-paracentesis decision, hyponatremia thresholds, the peritonitis antibiotic-plus-albumin bundle, terlipressin for hepatorenal syndrome, and lactulose plus rifaximin for encephalopathy. Every threshold is mechanism-derived rather than arbitrary.

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3. 03

   Pulmonary, Coagulopathy, and Vascular Complications

   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.

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Key topics

• ·Portal hypertension hemodynamics and HVPG thresholds
• ·Beta-blocker response and presinusoidal versus postsinusoidal causes
• ·Noninvasive CSPH detection and the rule of five
• ·Variceal screening and surveillance intervals
• ·Primary prophylaxis: carvedilol versus band ligation
• ·The acute variceal hemorrhage bundle
• ·Early TIPS during the index admission
• ·Gastric varices, portal hypertensive gastropathy, and GAVE
• ·One physiology, four complications
• ·Ascites and the serum-ascites albumin gradient
• ·Diuretic management and the spironolactone-furosemide ratio
• ·Large-volume paracentesis and albumin replacement
• ·Refractory ascites: TIPS versus serial paracentesis
• ·Hyponatremia thresholds
• ·Spontaneous bacterial peritonitis bundle
• ·Hepatorenal syndrome and terlipressin
• ·Hepatic encephalopathy: lactulose plus rifaximin
• ·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