A system of practical medicine. By American authors. Vol. 2

by Unknown

IV. DISEASES OF THE PORTAL VEIN.

Thrombosis and Embolism of the Portal Vein; Stenosis; Pylephlebitis.

DEFINITION.—By the terms at the head of this section are meant the various pathological processes which induce coagulation of the blood in some part of the portal system. As the portal vein is made up of many branches coming from the various organs of the abdominal cavity except the kidneys, and as it empties, so to speak, into the liver, it is obvious that various and complex derangements will ensue on the formation of thrombi.

CAUSES.—Thrombosis of the portal vein occurs under three general conditions: the blood is in a readily coagulable state; the action of the heart is weak and the blood-current sluggish; the circulation through the vein is impeded by external pressure. The coagulability of the blood is increased in diseases characterized by an excess of its fibrin-producing constituents, of which cirrhosis of the liver may be mentioned as one having this peculiarity. In chronic maladies of a depressing kind there may be simply a weak action of the heart, or the muscular tissue of the organ may be affected by a fatty and atrophic degeneration. The external pressure by which the blood-current through the vein is impeded may be caused by the newly-formed connective tissue of Glisson's capsule, by enlarged lymphatics in the hilus of the liver, or by tumors of various kinds. The first named of these causes of compression—atrophic cirrhosis—is most frequently acting. Very rarely, organized exudations of the peritoneum may be so situated as to compress the portal vein. This result can only happen when the hepatic portion of the peritoneum is involved.

Pylephlebitis exists in two forms: the adhesive and suppurative. The former results in changes not unlike those of simple thrombosis. The blood coagulates in the affected part of the vessel, the clot is organized, and the vessel ultimately forms a solid rounded cord which is permanently occluded. The suppurative variety is so different in its origin and in its results that it requires separate treatment, and I therefore postpone the consideration of it to the next section.

SYMPTOMS OF THROMBOSIS AND ADHESIVE PYLEPHLEBITIS.—It is a remarkable fact that the biliary function of the liver is not necessarily affected in cases of occlusion of the portal vein. It is true, in advanced cases of cirrhosis, when the interlobular veins are obliterated by the pressure of the contracting newly-formed connective tissue, the functions of the liver are arrested in so far as the damage thus caused extends. Notwithstanding the blocking of the portal, sufficient blood reaches the hepatic cells by the anastomosis between the hepatic artery and the interlobular veins—an anatomical connection demonstrated by Cohnheim and Litten.²⁰⁹ So long as this anastomosis continues bile will be formed, although the portal vein is occluded.

²⁰⁹ Virchow's Archiv, Band lxvii. p. 153, "Ueber Circulationsstörungen in der Leber."

The most significant symptoms of thrombosis of the portal vein are the sudden formation of ascites, which quickly assumes a very high grade, and equally sudden passive congestion of the gastro-intestinal mucous membrane, enlargement of the spleen, and distension of the superficial veins of the abdominal parietes. When these symptoms succeed to cirrhosis of the liver, or appear after the formation of a tumor in the hepatic region, or come on in the course of phthisis or chronic inflammation of the hepatic peritoneum, the existence of thrombus of the portal vein may be reasonably suspected.

Coincidently with the occlusion of the portal vein the gastro-intestinal mucous membrane becomes the seat of a catarrhal process, and to the fluid thus produced is added a much more abundant transudation from the distended capillaries. Nausea, vomiting, and diarrhoea result, the rejected matters being serous, watery, and in many cases tinged with blood. Now and then quite a severe hemorrhage takes place, and the blood is brought up by vomiting (hæmatemesis) or is discharged by stool. Hemorrhoids form, and, in large masses protruding, much pain is experienced, and free bleeding may result from rupture of a distended vein.

The veins of the abdominal parietes, which in the normal state are invisible or at least not prominent, and which form anastomoses with the portal, when the obstruction occurs dilate, sometimes to a remarkable extent. The most important anastomosis is that between the femoral and saphena and internal mammary and epigastric veins. When the hepatic branches of the portal are closed, but the trunk remains pervious, the parumbilical vein enlarges greatly, and, communicating with the superficial veins of the anterior part of the abdominal walls, forms a radiating network of tortuous veins to which is given the striking title of caput Medusæ.