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G38 Gastroenterology
Portal Hypertension
Signs
• Esophageal varices • Melena
• Splenomegaly
• Ascites
• Hemorrhoids
Management
• β-blockers
• Nitrates
• Shunts (e.g. TIPS)
Liver Toronto Notes 2019 Portal Hypertension
Definition
• pressuregradientbetweenhepaticveinpressureandwedgedhepaticveinpressure(correctedsinusoidal pressure) >5 mmHg
Pathophysiology
• 3sitesofincreasedresistance(rememberpressure=flowxresistance)
■ pre-sinusoidal (e.g. portal vein thrombosis, schistosomiasis, sarcoidosis)
■ sinusoidal (e.g. cirrhosis, alcoholic hepatitis)
■ post-sinusoidal (e.g. right-sided heart failure, hepatic vein thrombosis, veno-occlusive disease,
constrictive pericarditis)
Complications
• GI bleeding from varices in esophagus, less commonly in stomach, even less frequently from portal hypertensive gastropathy
• ascites
• hepaticencephalopathy • thrombocytopenia
• renaldysfunction
• sepsis
• arterialhypoxemia
Treatment
• non-selectiveβ-blockers(propanolol,nadolol,carvedilol)decreaseriskofbleedingfromvarices
• TIPS:todecreaseportalvenouspressure
■ radiologically inserted stent between portal and hepatic vein via transjugular vein catheterization and percutaneous puncture of portal vein
■ can be used to stop acute bleeding or prevent rebleeding or treat ascites
■ complications: hepatic encephalopathy, deterioration of hepatic function
■ contraindicated with severe liver dysfunction, uncontrolled hepatic encephalopathy, and congestive
heart failure
■ most commonly used as a “bridge” to liver transplant
• othersurgicallycreatedshunts:portacaval,distalspleno-renal(Warrenshunt)-allusedonlyrarelyin the modern era
Hepatic Encephalopathy
Definition
• spectrumofpotentiallyreversibleneuropsychiatricsyndromessecondarytoliverdiseasediagnosed after ruling out other causes for symptoms (e.g. structural/metabolic)
Pathophysiology
• portosystemicshuntaroundhepatocytesanddecreasedhepatocellularfunctionincreaselevelof systemic toxins (believed to be ammonia from gut, mercaptans, fatty acids, amino acids) which go to the brain
Precipitating Factors
• nitrogenload(GIbleed,proteinloadfromfoodintake,renalfailure,constipation) • drugs(narcotics,CNSdepressants)
• electrolytedisturbance(hypokalemia,alkalosis,hypoxia,hypovolemia)
• infection(spontaneousbacterialperitonitis)
• deteriorationinhepaticfunctionorsuperimposedliverdisease
Stages
• I:apathy,restlessness,reversalofsleep-wakecycle,slowedintellect,impairedcomputationalabilities, impaired handwriting
• II: asterixis, lethargy, drowsiness, disorientation
• III: stupor (rousable), hyperactive reflexes, extensor plantar response (upgoing Babinski) • IV: coma (response to painful stimuli only)
Investigations
• clinicaldiagnosis:supportedbylaboratoryfindingsandexclusionofotherneuropsychiatricdiseases • ruleout
■ non-liver-related neuropsychiatric disease in a patient with liver problems (e.g. alcohol withdrawal or intoxication, sedatives, subdural hematoma, metabolic encephalopathy)
■ causes of metabolic encephalopathy (e.g. renal failure, respiratory failure, severe hyponatremia, hypoglycemia)
• characteristicEEGfindings:diffuse(non-focal),slow,highamplitudewaves
• serumammonialevelsincreased,butnotoftennecessarytomeasureinroutineclinicaluse
Precipitating Factors for Hepatic Encephalopathy
Hepatics
Hemorrhage in GI tract/Hypokalemia Excess dietary protein
Paracentesis
Alkalosis/AAnemia
Trauma
Infection
Colon surgery
Sedatives
A Randomized, Double-Blind, Controlled Trial Comparing Rifaximin Plus Lactulose With Lactulose Alone in Treatment of Overt Hepatic Encephalopathy
American J Gastroenterol 2013;108:1458-1463
Study: prospective double-blind RCT.
Objectives: Efficacy and safety of rifaximin plus lactulose vs. lactulose alone for treatment of overt HE.
Results: Of the patients, 48 (76%) in group A (lactulose plus rifaximin 1,200 mg/day; n=63) compared with 29 (50.8%) in group B (lactulose (n=57) plus placebo) had complete reversal of HE (P<0.004). There was a significant decrease in mortality after treatment with lactulose plus rifaximin vs. lactulose and placebo (23.8% vs. 49.1%, P<0.05). There were significantly more deaths in group B because of sepsis (group A vs. group B: 7:17, P=0.01), whereas there were no differences because of gastrointestinal bleed (group A vs. group B: 4:4, P=nonsignificant (NS)) and hepatorenal syndrome (group A vs. group B: 4:7, P=NS). Patients in
the lactulose plus rifaximin group had shorter hospital stay (5.8±3.4 vs. 8.2±4.6 d, P=0.001).
Conclusion: Combination of lactulose plus rifaximin is more effective than lactulose alone in the treatment of overt HE.