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Toronto Notes 2019 Liver Gastroenterology G39
Treatment
• treatunderlyingprecipitatingfactors
• decreasegenerationofnitrogenouscompounds
■ routine protein restriction is no longer recommended given patients generally have concurrent malnutrition and muscle wasting; however, vegetable protein is better tolerated than animal protein
■ lactulose: titrated to achieve 2-3 soft stools/d
◆ prevents diffusion of NH3 (ammonia) from the colon into blood by lowering pH and forming
non-diffusible NH4 (ammonium)
◆ serves as a substrate for incorporation of ammonia by bacteria, promotes growth in bowel lumen
of bacteria which produce minimal ammonia
◆ also acts as a laxative to eliminate nitrogen-producing bacteria from colon
• oralrifaximinforbothacutetreatmentandmaintenancetherapyhashighlevelevidenceforefficacy • bestacutetreatmentincomatosepatientislactuloseenemas
Ascites
Definition
• accumulationofexcessfluidintheperitonealcavity
Etiology
Table 19. Serum-Ascites Albumin Gradient in the Evaluation of Ascites
Serum [Alb] – Ascitic [Alb] >11 g/L (1.1 g/dL) Portal Hypertension Related
Cirrhosis/severe hepatitis
Chronic hepatic congestion (right heart failure, Budd-Chiari) Massive liver metastases
Myxedema
Serum [Alb] – Ascitic [Alb] <11 g/L (1.1 g/dL) Non-Portal Hypertension Related
Peritoneal carcinomatosis TB
Pancreatic disease Serositis
Nephrotic syndrome* * In nephrotic syndrome: decreased serum [Alb] to begin with therefore gradient not helpful
Pathophysiology
• keyfactorinpathogenesisisincreasedsodium(andwater)retentionbythekidneyforreasonsnotfully understood. Theories include:
■ underfillhypothesis:firststepinascitesformationisincreasedportalpressureandlowoncoticpressure (e.g. low serum albumin) driving water out of the splanchnic portal circulation into abdominal cavity; the resulting decreased circulating volume causes secondary sodium retention by the kidney
■ overfill hypothesis: cirrhosis directly causes increased sodium retention by the kidney in the absence of hypovolemia and ascites arises secondarily
■ peripheral arterial vasodilation theory (most popular): as portal hypertension develops in cirrhosis, production of local mediators such as nitric oxide lead to splanchnic arterial vasodilation which ultimately results in reduction of effective arterial volume and compensatory sodium and fluid retention by the kidneys (i.e. circulation volume is increased, as per overflow hypothesis, but relatively underfilled, as per underfill hypothesis)
Diagnosis
• abdominalultrasound
• physicalexam(clinicallydetectablewhen>500mL)
■ bulging flanks, shifting dullness, fluid-wave test positive ■ most sensitive symptom: ankle swelling
Investigations
• diagnosticparacentesis
■ 1st aliquot: cell count and differential
■ 2nd aliquot: chemistry (especially albumin, but also total protein; amylase if pancreatitis; TG and
chylomicrons if turbid and suspect chylous ascites)
■ 3rd aliquot: C&S, Gram stain
■ 4th aliquot: cytology (usually positive in peritoneal carcinomatosis)
Treatment
• diuretic-sensitiveascites
■ Na+ restriction (daily sodium intake <2 g)
■ diuretics: spironolactone, furosemide
■ aim for weight loss 0.5-1 kg/d, more if concomitant peripheral edema (which is mobilized quicker
than ascitic fluid); overly rapid weight loss increases risk of renal failure
■ if target weight loss is not achieved and there are no complications, increase dose to achieve target
while monitoring for complications
• refractoryascites(diureticsareinadequateornottolerated)
■ therapeutic paracentesis with intravenous albumin
■ TIPS in an appropriate patient (no contraindications) with potential transplant-free survival
advantage
■ liver transplantation should be considered in every case, since development of ascites in patients
with cirrhosis is associated with 50% 2 yr mortality