scholarly journals HEMATOGENOUS AND OBSTRUCTIVE ICTERUS

1913 ◽  
Vol 17 (6) ◽  
pp. 593-611 ◽  
Author(s):  
G. H. Whiffle ◽  
C. W. Hooper

Normal and Eck fistula dogs react in a similar manner to the intravenous injection of hemoglobin obtained from laked red cells of the same animal. Hemoglobin appears in the urine after a few minutes and bile pigments in one to one and one half hours. In this simple type of hematogenous jaundice the reaction is in no way influenced by shutting out the portal blood from the liver and cutting down its blood supply to about 25 per cent. of normal. In a second type of hematogenous jaundice produced by chloroform anesthesia, which produces central liver necrosis, there is no essential difference between the normal and Eck fistula dog. The Eck fistula dog, as a rule, is more resistant to this poison, but, given a definite liver necrosis, the jaundice developing will reach its maximum on the second day as in the normal animal. This jaundice must be explained in part by capillary biliary obstruction, but in part by a hemolysin formed in the injured liver cells (Joannovics and Pick). Simple obstruction of the common duct when combined with an Eck fistula gives rise to a definite low grade icterus with bile pigment constantly present in the urine. Under these conditions after doubly ligating and cutting the common duct with separation of the cut ends, the lumen of the duct may be established and bile may enter the intestine by means of a fistulous tract between the cut ends of the bile duct. The formation of bile and bile pigments is much less in an Eck fistula dog than in a normal animal and consequently the icterus is much less intense. This is probably due to a lessened activity of the liver cells because of decreased blood supply. This observation does not harmonize with the current view that bile pigments are formed solely from hemoglobin, as there is no evidence of more hemolysis in a normal than in an Eck fistula dog. This suggests that the bile pigment may be formed in part, at least, from other substances than hemoglobin, and, further, that bile pigment formation normally may depend in part upon the functional activity of the liver cell rather than upon the amount of hemoglobin supplied to it.

1911 ◽  
Vol 13 (1) ◽  
pp. 115-135 ◽  
Author(s):  
G. H. Whipple ◽  
J. H. King

These experiments indicate that, in obstructive jaundice, the bile which escapes from the liver is absorbed by the hepatic capillaries and carried by the blood to the kidneys. The presence of a thoracic duct fistula influences in no way the development of icterus after total obstruction of the common bile duct. Bile pigments, sufficient to give a Salkowski test, may or may not appear in the lymph of the thoracic duct in such experiments, their appearance possibly depending upon the rapidity of bile secretion and the amount of lymph flow. Chronic icterus developing in an animal with a thoracic duct fistula gives an interesting distribution of bile pigments in the body fluids. The lymph and pericardial fluid contain the same amount, which is much less than the content of bile pigment in the blood serum and urine. It seems clear that in both acute and chronic obstructive jaundice the lymphatic apparatus takes no essential or active part in the absorption of bile pigments from the liver. At best, the lymphatic system is a secondary factor in the mechanism of jaundice.


1925 ◽  
Vol 41 (5) ◽  
pp. 601-609 ◽  
Author(s):  
Peyton Rous ◽  
D. R. Drury

The jaundice that develops after obstruction of the common duct in the absence of complications, expresses the physiological wastage of corpuscles occurring from day to day; and the intensity of the bilirubinemia varies as does the total of functioning hemoglobin-containing tissue from which this wastage takes place. There is to be observed a constantly readjusted direct relationship between hemoglobin percentage, bilirubinemia, and, by corollary, bilirubinuria. Induced losses of red cells find expression at once in a lessened accumulation and excretion of bile pigment; and as the regeneration of hemoglobin takes place the amount of bile pigment increases pari passu both in plasma and urine. The jaundice of bile retention is far less pronounced during secondary anemia than when the individual is full blooded, other things being equal. During uncomplicated obstructive jaundice the intercurrent changes in bilirubinemia correspond closely with those in circulating hemoglobin even when tissue icterus is of long standing. The fact indicates the presence of a barrier to the distribution of bile pigment from the blood, and such a barrier is to be found in the walls of the vessels. Its influence is at once evident on comparing lymph specimens and blood specimens from the long jaundiced animal. The amount of bile pigment in the lymph is then seen to be negligible, relatively speaking. Tissue icterus should be thought of as, ordinarily, the highly imperfect secondary expression of a condition which tends to be localized to the blood pool. On occasion more pigment than usual may escape from this pool, as for example into the wheats of the yellow urticaria described by clinicians.


1925 ◽  
Vol 42 (1) ◽  
pp. 99-122 ◽  
Author(s):  
Robert Elman ◽  
Philip D. McMaster

A variety of evidence is presented, all of which supports the view that in the uninfected animal the intestinal tract is the only place of origin of urobilin, not merely under normal circumstances, but when there is biliary obstruction. Animals rendered urobilin-free by collection of all of the bile from the intubated common duct remain urobilin-free even after severe hepatic injury. In our experiments urobilinuria was never found after liver damage except when bile pigment was present in the intestine. Thus, for example, it appeared during the first days after Ugation of the common duct, but disappeared as the stools became acholic. When this had happened a small amount of urobilin-free bile, given by mouth, precipitated a prompt urobilinuria. After obstruction of the duct from one-third of the liver, mild urobilinuria was found, but no bilirubinuria. In animals intubated for the collection of a part of the bile only, while the rest flowed to the duodenum through the ordinary channels, liver injury caused urobilinuria, unless indeed it was so severe as to lead to bile suppression, when almost at once the urobilinuria ceased, though the organism became jaundiced. The evidence here presented, when taken with that of our previous papers, clearly proves that urobilinuria is an expression of the inability of the liver cells to remove from circulation the urobilin brought by the portal stream, with result that the pigment passes on to kidney and urine. Urobilinuria occurs with a far less degree of liver injury than does bilirubinuria. Our work has, for the most part, been carried out with animals having uninfected livers and bile passages. But the influence of cholangitis with infection has been briefly discussed in the light of some preliminary observations. The influence of infection on the place of formation of urobilin and on the occurrence of urobilinuria will form the subject of another communication.


2015 ◽  
Vol 57 (1) ◽  
pp. e5-e8
Author(s):  
M. Simon ◽  
M. D. Stockholm
Keyword(s):  
X Ray ◽  

1960 ◽  
Vol 151 (2) ◽  
pp. 255-260 ◽  
Author(s):  
WILLIAM FRANCIS RIENHOFF

2006 ◽  
Vol 130 (9) ◽  
pp. 1358-1360 ◽  
Author(s):  
Stephen E. Vernon ◽  
Pablo A. Bejarano

Abstract Low-grade fibromyxoid sarcomas are uncommon deep soft tissue neoplasms first described by Evans in 1987. They exhibit a deceptively benign appearance, with a whorled or linear arrangement of spindle-shaped cells showing few to absent mitoses. A characteristic, but not specific, feature is the presence of areas of myxoid stroma. Recurrences are common, and late metastases have been recorded. A closely related but morphologically distinct tumor, the so-called hyalinizing spindle cell tumor with giant rosettes, has also been described; both neoplasms share the same cytogenetic abnormality, a balanced translocation resulting in a FUS/CREB3L2 fusion gene. Because of similar clinical behavior and the common cytogenetic abnormality, some authors prefer to consider both lesions as a single entity within the spectrum of low-grade sarcomas.


1973 ◽  
Vol 8 (12) ◽  
pp. 80B-80D
Author(s):  
William B. Seaman
Keyword(s):  

JAMA ◽  
1965 ◽  
Vol 191 (6) ◽  
pp. 470 ◽  
Author(s):  
Frank Glenn
Keyword(s):  

1966 ◽  
Vol 3 (4) ◽  
pp. 379-400 ◽  
Author(s):  
Glen C. Todd ◽  
Lennart Krook

A histologic examination of spontaneous cases of sawdust livers in cattle indicated that the focal liver necrosis was an expression of vitamin E-selenium deficiency. The condition was reproduced in Hereford steers by feeding a diet rich in polyunsaturated fatty acids and poor in protein, vitamin E. and selenium. Lesions also occurred in the kidney, heart, skeletal muscled and pylorus. Addition of dictary protein or injection of selenium partially prevented the condition. Cellular anoxia with formation of hyalinc bodies in the liver and kidney was considered to be the common denominator of the degenerative changes. Due to the relatively mild tissue changes, plasma GOT and OCT determinations were found to be of no diagnostic value.


2015 ◽  
Vol 88 (3) ◽  
pp. 420-423
Author(s):  
Ivan Maslarski

Vascular variations are significant for liver transplantations, radiological procedures, laparoscopic method of operation and for the healing of penetrating injuries, including the space closer to the hepatic area. This variants are very common in the abdominal region, and their description will be useful. During a routine dissection of 73 year old female cadaver, we found on subhepatic region that the blood supply of the liver differed from a normal one. The difference was found in the absence of the right liver branch and the cystic artery, which normally arises from the common hepatic artery. After a detailed dissection of the superior mesenteric artery we distinguished a branch, which is routed to the right lobe of the liver. The diameter of this vessel is 3.7 mm and the length is 8.2 cm. In the artery pathway, three consecutive branches were observed. The first branch was found about 2.02 cm before the portal region of the liver. The second one became visible after another millimeter and finally the artery made one little curve and became a cystic artery.


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