doctor's notes by Claudio Italiano
Clinically the most prominent symptom of cirrhosis of the liver. The
endoperitoneal effusion can be very considerable (even of several liters) and
causes a progressive increase in the volume of the abdomen, which, in the
advanced stages, assumes a characteristic Batracian appearance with a smoothed
or even estroflexed umbilical scar.
The ascitic fluid has the characters of the transudate; clear appearance,
citrus-yellow color, specific weight less than 1015, negative Rivalta reaction,
protein content from 5 to 20%, poor sediment consisting of flaked mesothelium,
lymphocytes and some hams. With the repetition of the paracentesis (which among
other things cause a loss of proteins and electrolytes) the liquid can take on a
cloudy appearance, with an increase in albumins and specific weight, while
Rivalta tends to positive.
The characteristics of the ascitic fluid can also change due to the overlapping
of inflammatory processes, the occurrence of hemorrhages (hemorrhagic ascites),
the presence of kilo, lesions of lymphatic vessels (chylous ascites), or even of
bile pigments, in case of jaundice generalized (biliary ascites).
A rare and serious complication of ascites is spontaneous bacterial peritonitis
(mostly due to gram-positive germs and less frequently to pneumococci or other
germs) that can be explained by the unobstructed passage of germs through the
liver, due to shunts portosystemic.
In the pathogenesis of ascites, in addition to the portal hypertension and the
resulting blood stasis, with consequent transudation in the peritoneal cavity,
other factors are invoked, such as the increased capillary permeability (which
can be linked to toxic phenomena), lymphatic stasis and hypoonchia (ie the
reduced colloid-osmotic plasma pressure) due to hypoalbuminemia due to reduced
hepatic protein synthesis; also the poor inactivation by the liver of the
antidiuretic hormone (whence the oliguria) and of the aldosterone (the
hyperaldosteronism involves a sodium retention which passes in the peritoneal
cavity, dragging water) can come into question.
Another consequence of portal hypertension is the possibility of bleeding at the
level of the venous areas subjected to pressure increase, particularly
esophageal varices and hemorrhoidal veins.
In the pathogenesis of the haemorrhagic phenomenon, in addition to the venous
stasis, the increased vasal fragility and the hemorrhagic diathesis, typical of
cirrhotic with hepatic insufficiency, due to defect of coagulation factors
normally supplied by the liver (prothrombin, factors V, VII, IX and X), a
decrease in fibrinogen and a platelet deficit (thrombocytopenia is present in
50% of the cirrhotic).
A subtle dye of sclera is common in cirrhosis of the liver; On the contrary, it is the pronounced jaundice, which is easier to observe in the terminal phase of the disease, due to the occurrence of extensive hypoxic necrotic lesions of the hepatocytes. It is usually connected to hepatocellular damage, which can be associated with a hyperemolytic component, especially in decurrent cirrhosis with remarkable splenomegaly; an intrahepatic cholestatic component assumes dominant importance in primary biliary cirrhosis.
They depend on various factors, but at the forefront of portal stasis and
hepatic dysfunction. The spleen in about 80% of cases of cirrhosis has increased
in volume, but usually it is a modest tumor of the spleen that does not exceed
the weight of 300-400 g; only in a few cases of cirrhosis there is a real
splenomegaly, up to weights of 1000-1200 g: in these cases we speak of
splenomegalic cirrhosis.
From the pathogenic point of view, the cirrhotic spleen tumor, only partially
represents the consequence of portal stasis, as the conspicuous pulp hyperplasia
(always absent in the stasis spleen due to cardiac decompensation, the volume of
which is usually only moderately increased ) is the expression of a reactive
splenopathy, probably secondary to toxic stimuli, linked to the same harmful
cause that acts on the liver or a product of destruction of the liver tissue.
In the digestive tract, in addition to the previously mentioned venous ectasia
in the submucosa of the lower third of the esophagus, the cardia and the rectum,
there are signs of chronic stasis, with particularly pronounced edema in the
duodenum, punctiform and chronic inflammation (gastropathy and chronic
enteropathy). Frequent peptic ulcers.
The pancreas often presents more or less notable sclerosis phenomena, with
atrophy of the lobular parenchyma, referable to the portal stasis, while not
excluding that the same hepatic agents can act on the pancreas. The islands of
Langerhans (except in the case of hemochromatosic cirrhosis) are generally not
affected, hence the relative rarity of diabetes in cirrhotic.
The lungs can be edematous and congested in hepatopulmonary syndrome. In the
pleural cavity, as already mentioned, it is possible the presence of a bilateral
or more often localized on the right, usually referred to the overflow of the
azygos vein system (or of the vein emiazygos) for the collateral circulation
that is established through the esophageal veins, but certainly favored by
discrete factors.
The kidneys do not show any particular morphological changes. The rare
occurrence of acute renal failure may recognize a "prerenal" cause (severe
dehydration or acute tubular necrosis following massive hemorrhage due to
rupture of esophageal varices), but in many other cases acute or chronic renal
failure is of origin functional.
See also >> epatorenal syndrome. Bones, due to the decreased absorption of
vitamin D by the intestine, caused by the portal stasis and by the altered
biliary secretion, can undergo osteoporosis.
Among the endocrine glands, the testes that appear to be reduced in volume are
particularly affected and they present histologically the hypotrophy of the
seminiferous tubules with reduction of the spermatogensis and thickening of the
basement membrane. It is believed that these lesions (often involving impotence
and decreased libido) depend on the defect in estrogen inactivation by the
injured liver, resulting in hyperestrogenism. The same phenomenon can be
attributed to the frequent appearance, in males, of a hypertrophy of the mammary
gland, mono- or bilateral gynecomastia (the triad of hepatic
cirrhosis-gynecomastia-testicular atrophy is the syndrome of Silvestrini-Corda).
The alterations of the adeno-hypophysis (where the increase of basophilic cells
are frequent) and of the adrenal glands (which more often show pictures of
fascicular hypertrophy) are less significant. The alterations of the central
nervous system, little characteristic, consist in edema and in regressive
lesions of the nerve cells, more marked in those who died in hepatic coma.