Stasis liver, etiopathogenesis
Notes by dr Claudio Italiano
Etiology
The conditions that can be associated with a stasis liver are the following:
a) Often there is a deficiency of the right and left ventricle (cfr
decompensation) with consequent hepatic congestion. b) Acute myocardial
infarction associated with arrhythmias and cardiogenic shock may complicate
coronary artery disease (see coronary artery disease) resulting in ischemic
hepatitis that overlaps chronic hepatic congestion. c) Rheumatic heart disease
with mitral stenosis and tricuspid regurgitation appears to cause the most
severe form of hepatic congestion d) The sudden appearance of atrial
fibrillation or the appearance of bacterial endocarditis can reduce the left
ventricle range and aggravate the damage hepatic from hypoxia. e) Children with
left-sided hypoplasia and coarctation of the aorta are particularly susceptible
to hepatic necrosis, probably due to the association between reduction of
systemic blood flow, left-right shunt and marked increase in right ventricular
pressure
Pathophysiology
Anterograde heart failure causes a reduction in cardiac output and blood flow in
the liver. Retrograde failure with venous engorgement causes liver congestion.
Both anterograde and retrograde insufficiency cause cell hypoxia and hepatic
damage. Reduction of arterial oxygen saturation also contributes to liver injury.
Conditions of chronic passive congestion
In congestive heart failure with low cardiac output the total hepatic blood flow
is reduced by about one third. The increase in systemic venous pressure is
reflected in hepatic venous hypertension which can cause hepatic cell atrophy
secondary to congestion and sinusoidal expansion. The resulting perisinusoidal
edema may cause a reduction in the spread of oxygen and other metabolites in
hepatocytes. Collagenosis of Disse's space secondary to chronic congestion may
play a minor role in compromising oxygen diffusion. The low cardiac output and
the consequent alterations of the circulation in the intestinal wall can promote
an increase in the diffusion of endotoxins in the portal blood and aggravate the
liver damage. The role of endotoxemia in hepatic damage associated with heart
failure has not been confirmed
Reduction of hepatic blood flow
The increase in the extraction of oxygen by the liver in conditions of reduced
blood flow ensures a constant consumption of oxygen in the hepatic flow within
wide limits. The liver therefore does not suffer from hypoxia as a consequence
of a reduction in hepatic flow under basal conditions. A reduction in hepatic
flow of more than 70% leads to lower oxygen uptake, restores the ability to
eliminate galactose and reduces the concentration of adenosine triphosphate,
while increasing the lactate / pyruvate ratio (an index of tissue hypoxia. The
hepatic artery and the intense selective vasoconstriction of the splanchnic area
under conditions of marked hypoperfusion and of shock cause hypoxic damage in
the liver, characteristically affecting the area adjacent to the terminal
hepatic vein (zone 3 of the acino), because it is the area located more distally
to the supply of blood rich in oxygen (see hepatic circulation) Elevated levels
of aminotransferases (amylated transferase, AST and alanine amino transferase,
ALT cf enzymes) higher than 20 times the upper limit of the value normal
represent the characteristic sign of the necrosis of zone 3. The insufficiency
of the substrates and the accumulation of metetabolites c ontribute to hypoxic
damage. The loss of oxidative phosphorylation in mitochondria, a consequence of
hypoxia, causes alteration of membrane function, impairment of intracellular
omeostasis of the ions and reduction of protein synthesis. In the course of
acute heart failure both the reduction of blood flow of the liver and the
increase in central venous pressure contribute to the appearance of hypoxic
hepatitis.
Pathology
A) Macroscopic
The liver is enlarged and purple with rounded margins. Nodularity is poorly
represented, but nodules can be appreciated in the case of regenerative wave
hyperplasia or cardiac cirrhosis. The section surface shows prominent hepatic
veins that can be thickened. A "nutmeg" appearance is observed due to the
simultaneous presence of central haemorrhagic areas of the lobules and of normal
portals and periportal areas of yellow color.The more intense yellow color
compared to the normal color of the portal area may be due to an increase in fat
in the portal spaces.
B) Microscopic
The histological picture of the liver is generally related to the clinical or
biochemical severity of heart failure and the weight and size of the heart
chambers. Since the beginning of congestive heart failure, the terminal hepatic
veins are engulfed and dilated. Also the sinusoids adjacent to the terminal
hepatic veins dilate and fill with erythrocytes for a variable distance towards
the portal areas. We also observe compression and a variable hepatic cell
atrophy and an apparent increase in the amount of lipofuscin in their cytoplasm.
Moderately severe heart failure can cause necrosis of liver cells belonging to
zone 3. The cellular infiltrate is minimal. In the case of acute severe
hypotension and shock, necrosis of the mid zone can be determined. Necrotic
hepatocytes are often enveloped in a brown pigment likely to correlate with
bilirubin degradation. Necrosis of liver cells moves from zone 3 to portal areas
as heart disease develops. In the most severe form of hepatic congestion
secondary to heart failure only a small area of normal-looking hepatocytes
remains in the periportal space. The reticulin network condenses and can
collapse intron to the terminal hepatic vein following the loss of liver cells.
The formation of bridges that extend and unite adjacent terminal hepatic veins
can be observed; lastly, the non-affected portal areas are surrounded by rings
of fibrous tissue with the formation of inverted lobules. The finding of cardiac
cirrhosis is rare. If present, it is associated with fibrosis of the intima and
thrombosis of the hepatic veins of small and medium size. The resulting ischemia
is responsible for hepatocellular necrosis. the stasis increases the
fibroblastic activation and the deposition of collagen.
Prevalence
Liver involvement in severe heart failure is frequent. With the reduction of the
incidence of rheumatic valvulopathies, diseases of the coronary arteries and
congestive cardiomyopathy are increasingly becoming the main cause of liver
congestion. The total prevalence of hepatic congestion during congestive heart
failure depends on patient selection and the usual criteria for defining liver
involvement (clinical, biochemical, or histological). Among patients with a
cardiac index above 2l / min / m2 only 20-30% of them have a minor increase in
liver enzymes. In contrast, up to 80% of patients with a heart rate of less than
1.5 l / min / m2 have some major biochemical abnormalities.
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Liver from stasis, the clinic
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