Ascites & Portal Hypertension
(Hepatology 2004;39:1-16)
DEFINITION:
Accumulation of fluid within the peritoneal cavity
EPIDEMIOLOGY:
More than 30% of patients with ascites have an ascitic fluid infection at the time of admission or during hospitalization; Therefore tap ‘em!
ETIOLOGIES:
More than 80% of patients with ascites have decompensated chronic liver disease (cirrhosis)
Peritoneal carcinomatosis is the second most common cause (10%)
Other causes: heart failure (5%), acute alcoholic hepatitis, fulminant or subacute hepatic failure, pancreatic disease, dialysis ascites, nephrotic syndrome, hepatic vein obstruction, chylous ascites, bile ascites
PATHOPHYSIOLOGY:
Bottom line is sodium retention!
Cirrhosis:
Portal/Sinusoidal HTN » Lymph formation >> Absorption = Ascites (i.e. movement of extra fluid into the peritoneal space)
Systemic vasodilation via nitric oxide (probably) » Arterial underfilling » Release of hormones:
Aldosterone: Na/Water retention » Expanded plasma volume leads to Portal/Sinusoidal HTN (See above)
Antidiuretic hormone: Free water retention » Hyponatremia
Norepinephrine/Angiotensin: Renal vasoconstriction » Hepatorenal syndrome
Cirrhotics have low protein ascites because the now fibrotic sinusoids no longer allow proteins (albumin, compliment) to escape to space of disse
CLINICAL MANIFESTATIONS/PHYSICAL EXAM:
Shifting dullness and Fluid wave has 60% sensitivity
LABORATORY STUDIES:
Paracentesis technique: Am J Gastroenterol 2006;101:1954-55
Send fluid for: albumin, total protein, cell count, gram stain & culture; Others: amylase, cytology, LDH
Serum-ascites albumin gradient (SAAG); 95% accuracy
Subtract albumin concentration of ascites from albumin concentration of serum (obtained on same day)
Physiologically based on oncotic-hydrostatic balance and is related directly to portal pressure
≥ 1.1 g/dl: Portal HTN “Transudate”
Pre Sinusoidal
Portal or Splenic vein thrombosis
Schistosomiasis (pHTN without cirrhosis)
Sinusoidal
Cirrhosis (81%), including SBP
Note: most SBP occurs with pHTN & Cirrhosis
Reason: Ascites with dilute proteins have ↓ concentration of opsonins and ↑ SBP risk
Acute hepatitis
Extensive malignancy (HCC or mets)
Congenital hepatic fibrosis (pHTN without cirrhosis)
Partial nodular transformation (Nodular regenerative hyperplasia)
Sarcoidosis (pHTN if large enough granulomatous burden, pHTN without cirrhosis)
Idiopathic (thought to be arsenic toxicity as one of the causes)
Post Sinusoidal
Right-sided heart failure (including RV dysfunction, constrictive pericarditis and tricuspid regurgitation)Related posts:
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