The most significant symptom of portal thrombosis is a quickly-forming ascites. It is true, ascites is a common symptom in advanced cirrhosis, but the rapid accumulation of fluid and the prompt filling of the cavity after tapping distinguish that which arises from portal thrombosis from all others. Besides its excessive extent, the ascites presents the usual symptoms.
Due to the same cause as the enlargement of the superficial veins, the hemorrhages, the ascites, etc., there occurs considerable hypertrophy of the spleen in many of the cases. It sometimes happens that the new compensatory circulation and the hemorrhages from some part in the usual route of the portal so dispose of the blood that the spleen does not enlarge sufficiently to be readily made out.
COURSE AND TERMINATION.—It is obvious that a condition such as that induced by thrombosis of the portal must be comparatively quickly fatal; but the cases vary in duration as the compensatory circulation is more or less complete. Whilst the majority of cases terminate within two weeks, instances of several months' duration are not unknown, but a fatal termination, sooner or later, is inevitable in all cases.
Coming on in the course of some chronic affection of the liver or some obstructing cause exterior to the organ, there soon follow ascites, nausea and vomiting, hæmatemesis, bloody stools of a liquid character, enlargement of the spleen, distension of the abdominal veins, and the distressing symptoms produced by an excessive accumulation of fluid in the peritoneal cavity.
DIAGNOSIS.—As there is no symptom of thrombosis of the portal which may not be caused by advanced cirrhosis, the diagnosis rests on the rapid production of the attendant phenomena and their conjoint appearance.
TREATMENT.—A symptomatic treatment is alone possible. The highly irritable and congested intestinal mucous membrane precludes the employment of hydragogue cathartics. Salines which cause outward diffusion from the vessels are the only cathartics which can be used with propriety. Action of the kidneys and of the skin must be maintained. To this end the resin of copaiba in pilular form and pilocarpine subcutaneously may be used. If the strength of the patient will permit, leeches around the anus can be applied, and much relief may be expected from free bleeding. It is probable that opening a swollen hemorrhoid would give the same kind of relief as that caused by a free hemorrhage. In any case the benefit derived from treatment must be merely palliative and temporary.
Suppurative Pylephlebitis.
PATHOGENY.—Primary pylephlebitis rarely if ever occurs. On the other hand, the secondary form is by no means uncommon; it succeeds to ulcerative or purulent inflammation at some point in the circuit of origin of the portal radicles. The most frequently-occurring cause is ulceration and suppuration of some part of the intestinal tube, and hence the most common result is multiple abscess of the liver. Pylephlebitis has often resulted from typhlitis; from ulcers of the large intestine, as in dysentery; from such traumatic injuries as tying hemorrhoids; from proctitis; from ulcers of the stomach and similar morbid processes elsewhere within the range of origin of the portal system. The pathogeny is clear. The inflammatory or ulcerative action extends to and involves the walls of the veins, or some morbid material diffuses through the vein walls. In either case coagulation of the blood in the vessel ensues, and the clot undergoes a series of changes resulting in the formation of emboli, which, carried into the main current, are subsequently lodged in the hepatic capillaries.
There are three steps in the morbid process: the changes in the vein wall; the production and transformation of the thrombus; and the formation of secondary suppurating foci in the liver.
The appearance of the tunics of the inflamed vessels varies with the stage at which they are examined. At first the walls of the vessels are reddish from congestion, succulent, and swollen, infiltrated by leucocytes and inflammatory exudation and the cellular elements undergoing proliferation. The intima especially is much altered in its appearance and structure, becoming thick, opaque, grayish or yellowish in color, and having adherent to it a thrombus passing through its characteristic changes. Ulceration of the intima then occurs, and the purulent elements, with shreds of tissue, mingle with the degenerating blood-clot, and ultimately there remains a purulent dépôt lined with sloughing, even gangrenous, contents. Emboli detached from such decomposing thrombus are arrested in the vessels of the liver, and there set up a suppurating phlebitis, ending in an abscess formation, or a quantity of pus from the original point of ulcerative phlebitis passes into the portal vein, and is generally distributed through the hepatic branches, here and there foci of suppuration being established by the deposit of decomposing emboli. There may be numerous small abscesses irregularly distributed through the liver, or there may be one or two larger collections of pus. Very often the vessel whose occlusion by a suppurating embolus has caused the mischief is destroyed, and hence no communication with the abscess-cavity can then be traced. These abscesses are not limited by a line of inflammatory demarcation or by a limiting membrane, but the hepatic tissue adjacent is congested and infiltrated with pus.