SYMPTO.MS REFERABLE TO DISTURB ANCES OF THE CIRCULATIO.N.—So long as there is a well-established collateral cir culation, for so long will there be no symptoms referable to obstruction. It is only when this collateral circulation be comes inadequate to carry the portal blood to the heart that ascites and other obstructive disturbances supervene. Thus, not infrequently we meet with ex tensive portal cirrhosis without a sign of ascites. Very frequently, however, the nature of this collateral circulation is the direct cause of death; more especially is this the case with the plexus of submit cons veins at the lower end of the cesoph agus which plays a prominent part in this collateral circulation. These veins, being practically unsupported toward the free surface of the cesophagus, become varicosed and relatively enormous; the patient may appear in very fair health and the liver be performing its functions satisfactorily with but a thirty-second of an inch or less intervening between life and death; for it is these varicosed sub cesophageal veins which are especially liable to rupture and to produce so ex treme a hamorrhage that death follows in the course of a few hours.
The best account of this collateral cir culation is given by Osler and we here recapitulate it:— "The compensatory circulation is usu ally readily demonstrated. It is carried out by the following set of vessels: 1. The accessory portal system of Sappey, of which important branches pass in the round and suspensory ligaments and unite with the epigastric and mammary systems. These vessels are numerous and small. Occasionally a large single vein, which may attain the size of the little finger, passes from the hilus of the liver in the round ligament and joins the epi gastric veins at the navel. Although this has the position of the umbilical vein, it is usually, as Sappey showed, a para-mnbilical vein; that is, an enlarged vein by the side of the obliterated um bilical vessel. There may be produced about the navel a large bunch of varices: the so-called caput Medusm. Other branches of this system occur in the gastro-epiploic omentum, about the gall bladder, and, most important of all, in the suspensory ligament. These latter form large branches, which anastomosc freely with the diaphragmatic veins, and so unite with the vena azygos. 2. By the anastomosis between the cesophageal and gastric veins. The veins at the lower end of the cesophagus may be enormously enlarged, producing varices which pro ject on the mucous membrane. 3. The
communications between the luemor rhoidal and the inferior mesenteric veins. The freedom of coramunication in this direction is very variable, and in some instances the hwmorrhoidal veins are not much enlarged. 4. The veins of Retzius, which unite the radicles of the portal branches in the intestines and mesentery with the inferior vena cava and its branches. To this system belong the whole group of retroperitoneal veins, which are, in most instances, enormously enlarged, particularly about the kidneys, and which serve to carry- off a consider able proportion of the blood." But in addition to the disturbance in the portal circulation, there appears to be also a frequent accompanying disturb ance in the general circulation. It may here be more correct—inasmuch as this disturbance seems to be largely associ ated with alterations in the blood brought about by the hepatic disturbance —to refer to this under a later heading.
Case of alcoholic cinthosis in which there were present enlargement of the liver, dilatation of the subcutaneous ab dominal veins and ascites (necessitating four punctures in the course of a year).
Small, erectile, venous tumors appeared on the face, in the pharynx, and on the internal surface of the last phalanx of the ring-finger of the left hand. The lat ter became the source of a quite-active Inemorrhage. Bouchard Plarseille-m6d., Oct. 15, '91).
ascites of portal cir rhosis develops gradually, and in this way is to be distinguished from that follow ing thrombosis of the portal vein. While it is a very prominent and characteristic symptom of the condition, it must be remembered that it is far from being constantly present. Indeed, I may go further and point out that much of the failure of clinicians to recognize portal cirrhosis is due to the erroneous belief that ascites ahnost constantly de velops. It does not by any means; only in advanced atrophic cases is it the rule. The older writers speak of it as being present in about SO per cent. of the cases; more recent careful observers give a lower proportion, thus: Rolleston and Fenton (Birmingham Med. Review, Oct., '96) find, from the post-mortem records at St. George's Hospital in London, that of 114 cases only 36, or a little over 30 per cent., showed ascites. Iielynack in 121 examples (ibid., Feb., '97) of com mon hepatic cirrhosis, as he terms it, coming to the post-mortem room at the Manchester Royal Infirmary, found as cites in 56 per cent.