This is an abnormal fullness of the blood-vessels of the liver,
followed by an enlargement of that organ. It is active when there is
abnormal pressure in the portal veins (afferent vessels); passive when
there is excessive pressure in the sublobular veins (efferent vessels).
=Osteopathic Etiology= and =Pathology.=—=Active hyperemia= is usually
due to indiscretions in diet. After each meal a physiological hyperemia
of the liver occurs, which is greatly increased by habitually
overeating and overdrinking. This condition may lead to functional
disturbance and possibly to organic change. Traumatism and lesions of
the vertebræ and ribs, irritating vasomotor nerves, are important.
Habitual constipation, malaria, heat, and arrested menstrual epoch, and
infectious fevers are also causes of the active form. Enteroptosis is
not a rare cause.
=Passive hyperemia= is due to obstructions of the efferent circulation.
Valvular heart disease is the most common cause. Lung diseases, as
emphysema or cirrhosis; obstruction to the vena cava or interference
with the flow of blood through the liver; and diseases of the pleura,
are among the causes.
Most cases of congestion of the liver present lesions to the vasomotor
nerves of the liver, fifth to ninth dorsal. Especially are the ribs
over the liver apt to become displaced and affect the organ.
=Pathologically=, the liver is enlarged and engorged with blood. The
appearance of the organ depends upon the duration of the hyperemia.
In passive hyperemia the central portion of the lobule and the area
of the hepatic vein are deeply colored. The periphery and the area of
the portal vein are pale. This alternation of the dark and light color
gives rise to the nutmeg liver, which is so noticeable upon section. In
cases of long standing, atrophy of the liver cells and overgrowth of
connective tissue result.
=Symptoms.=—=Active Hyperemia.=—Dull aching and a sense of fullness in
the right hypochondrium, aching of the limbs, coated tongue, nausea,
vomiting, constipation, highly colored urine, and slight jaundice.
In =passive hyperemia= the symptoms are the same, but less marked. The
onset is gradual and the liver may attain considerable size. In severe
cases following tricuspid regurgitation the liver may pulsate. In
severe cases dropsy takes place.
=Diagnosis.=—Active hyperemia is occasionally confounded with catarrhal
jaundice. Usually congestion of the liver is easily diagnosed.
=Prognosis.=—In active hyperemia the prognosis is good, unless repeated
attacks lead to atrophic degeneration. In passive hyperemia the
prognosis depends entirely upon the cause.
=Treatment.=—=Active hyperemia.=—The treatment consists of measures
which tend to diminish the congestion, principally a thorough, direct
manipulation over the liver by raising and spreading the ribs. Careful
and thorough treatment to the dorsal splanchnics of the liver is also
indicated. The substitution of a scanty for a heavy diet is essential.
The foods given should be such as are easily digested, as milk and
broths; fats and sugars are to be avoided.
In =passive hyperemia= the treatment consists of correcting the
disorder causing it. Often heart diseases are the cause. A thorough
depletion of the bowels will aid largely in relieving ascites that may
follow passive congestion (See ascites).
In liver congestions it is well to pay attention to the intestinal
condition in order that the circulatory mechanism here may be
thoroughly coordinated with the hepatic.