How portal hypertension is tested on Step 1

Expect a cirrhotic patient with hematemesis, ascites, or new confusion, or a question about venous anatomy.

Portal hypertensionPrehepaticPortal vein thrombosisIntrahepaticCirrhosis, schistosomiasisPosthepaticBudd-Chiari, right heartfailure
Where is the block? Posthepatic causes congest the liver ("nutmeg liver"); prehepatic causes spare liver function.
SitePortal vein tributarySystemic veinClinical sign
EsophagusLeft gastricEsophageal → azygosEsophageal varices
UmbilicusParaumbilicalSuperficial and inferior epigastricCaput medusae
RectumSuperior rectalMiddle and inferior rectalAnorectal varices

Anorectal varices are distinct from internal hemorrhoids, which are vascular cushions.

Ascites and the SAAG

Portal hypertension, low albumin, and sodium retention drive ascites in cirrhosis.

SAAG ≥ 1.1 g/dLPortal hypertensionCirrhosisHeart failure (high ascitic protein)Budd-Chiari syndromeTransudate patternSAAG < 1.1 g/dLPeritoneal carcinomatosisTuberculous peritonitisNephrotic syndromePancreatitisNot portal hypertensionvs
SAAG = serum albumin − ascitic albumin. It reflects the hydrostatic pressure gradient across the peritoneum.

Complications

Each is a classic cause of decompensation.

Variceal bleedHematemesis, shock; octreotide, antibiotics, bandligationSBPFever, pain, confusion; ascitic PMNs ≥ 250/mm³HepatorenalSplanchnic vasodilation → renal vasoconstrictionEncephalopathyAmmonia bypasses the liver; lactulose, rifaximinHypersplenismSplenomegaly → thrombocytopenia
Complications. Hepatorenal syndrome looks prerenal (very low urine sodium) but does not improve with fluid.

Treatment principles

Lower portal pressure and treat each complication.

  • Nonselective β-blockers (propranolol, nadolol, carvedilol): β₁ blockade lowers cardiac output; β₂ blockade leaves α-mediated splanchnic vasoconstriction unopposed, reducing portal inflow.
  • Acute variceal bleeding: octreotide (splanchnic vasoconstriction), prophylactic antibiotics such as ceftriaxone, and endoscopic band ligation.
  • TIPS: stent from the portal vein to a hepatic vein; lowers pressure but shunts ammonia past the liver.
  • Ascites: sodium restriction, spironolactone (counters secondary hyperaldosteronism) plus furosemide, and large-volume paracentesis with albumin.
  • Spontaneous bacterial peritonitis: ceftriaxone or cefotaxime plus albumin; secondary prophylaxis afterward.

Worked example

Use the SAAG and cell count together.

functions Worked example — fever in a patient with ascites

A man with alcohol-related cirrhosis has fever, diffuse abdominal tenderness, and new confusion. Serum albumin is 2.8 g/dL; ascitic albumin 1.0 g/dL; ascitic neutrophils 420/mm³. Interpret the results.

  1. SAAG = 2.8 − 1.0 = 1.8 g/dL (≥ 1.1), consistent with portal hypertension.
  2. Ascitic neutrophils ≥ 250/mm³ define spontaneous bacterial peritonitis.
  3. Likely organisms are gram-negative enteric bacteria such as E. coli and Klebsiella.
  4. Infection can precipitate hepatic encephalopathy and hepatorenal syndrome.

Answer. Spontaneous bacterial peritonitis in portal hypertensive ascites; treat with a third-generation cephalosporin and albumin.