Academic Day Seminars

ADS – Complications of Liver Disease

This was a complicated but interesting lecture on the complications of liver disease. My co-residents Alex and Nina did a great job explaining all the different sequale of liver disease! Below is my summary of the conditions discussed.

Cirrhosis: chronic hepatocellular injury leading to progressive fibrosis

  • Decompensated cirrhosis: presence of any major complication:
    • Variceal hemorrhage
    • Ascites
    • Spontaneous Bacterial Peritonitis
    • Hepatic Encephalopathy

Prognosticating cirrhosis:

  • Child-Pugh Classification is based on encephalopahy, ascites, bilirubin, albumin and PTT – the higher the score the worse the grade (e.g. Class A, B, C) the higher the one-year survival in non-surgical patients.
  • Model for End-stage Liver Disease (MELD): used to prioritize liver allocation for transplant. Higher MELD score is associated with inc severity of hepatic dysfunction and inc 3 month mortality risk

Pathophys of ascites: a series of positive feedback loops

  • the cirrhosis changes the architecture in the liver which causes portal hypertension
  • Portal HTN results in inc NO which results in systemic/splanchinc vasodilation
  • This results in dec effective arterial blood volume which activated the RAS system
  • This results in hyperdynamic circulation, sodium and water retention, renal vasoconstriction as compensatory mechanisms
  • However the area that supplies the spleen in non-reactive to the RAS system so positive feedback ensues resulting in fluid collection in the peritoneal cavity = ascites
Spontaneous Bacterial Peritonitis:
  • Primary mechanism is bacterial translocation from gut: low-protein ascites has diminished antimicrobial activity, failure of immune system to destroy bacteria.
  • Most commonly gram-negative enteric bacilli: E.coli, Klebsiella species, Pneumococci
  • Inpatient non–infection-related mortality rates are 20% to 40%
  • If the patient survives that hospitalization, one-year and two-year mortality rates for those with SBP are approximately 70% and 80%, respectively
  • Empiric tx: cefotax 2g IV Q8H or similar 3rd gen cep
    • Alt: ciprofloxacin (if they haven’t been receiving cipro for prophylaxis)
    • Albumin: 1.5g alb/kg w/in 6 hrs of detection and 1.0 g/kg on day 3
    • DoT = 5 days (or longer if clinically unwell)
  • Prophylaxis tx: (recurrence is up to 69% in one year)
    • Septra DS i tab daily
    • Cipro 500mg po daily (or potentially norfloxacin)
  • Secondary ≠ Spontaneous Bacterial Peritonitis
    • Secondary = ascitic infection from an intraabdominal source (e.g. periappendiceal abscess)
    • requires antibiotics and surgery usually – less than 5% of ascitic infections
Esophageal varices:
  • Most important clinical sequale of portal HTN, correlated with Child-Pugh score (40% & 85% in class A & C respectively)
  • Endoscopy is gold standard for diagnosis
  • Risk factors: large >5 mm varcies, hepatic veous portal gradient is >12 mmHg, Child-Pugh B/C, red wale marks
  • Guidelines for treatment:
    • Pre-primary prophylaxis (have cirrhosis but no varices): no b-blockers, repeat esophagogastrduodenoscopy (EGD) in 3 years
    • Primary prophylaxis (no hx of history, small varices): shoulde use non-selective b-blockers in pts who are at high risk for bleeding, can use in low risk too. Rpt EGD in 2 yrs in those who do not take b-blockers.
    • Primary prophylaxis (medium/large varices): Non-selective B-blockers or endoscopic variceal ligation are recommended in patients with high risk for bleeding, while B-blockers preferred first-line in patients not high risk for bleeding
    • Acute variceal bleed: hemodynamic resuscitation (IVF, PRBCs +/- platelets), prevent infection (prophylactic antibiotics – norfloxacin, ciprofloxacin, ceftriaxone), control of bleeding (vasoactive meds, endoscopic variceal ligation, balloon tamponade)
    • Secondary prophylaxis: non-selective b-blocker + EVL is best option, TIPS should be considered for recurrent variceal bleeds despite combo pharmacological therapy

Hepatic Encephalopathy:

  • Multifactorial: ammonia, amino acid balance, GABA involvement
  • Treatment:
    • Control precipitating factors (e.g. PUD, excess dietary protein, constipation, electrolyte abnormalities, drug-induced CNS depression)
    • Treat only overt hepatic encephalopathy
    • Primary prevention for overt HE not required – unless cirrhosis pt w/ high risk
    • Secondary prevention of overt HE is recommended
    • Treatment: lactulose 25mL po q1-2h until 2 soft/loose BMs/day
    • Other options: rifaximin (antibiotic..$$$$)
    • No ammonia levels – doesn’t correlated w/ staging or level of severity of sx
  • Secondary prevention: lactulose titrate to 2-3 BMs/day

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