Indications for Surgical Exploration in the Diagnosis of Intrahepatic Obstructive Jaundice

1952 ◽  
Vol 22 (2) ◽  
pp. 232-243
Author(s):  
Leonard A. Stine ◽  
Richard M. Bendix ◽  
Jerome M. Swarts
PEDIATRICS ◽  
1955 ◽  
Vol 16 (1) ◽  
pp. 135-137
Author(s):  
Orvar Swenson ◽  
John Herbert Fisher

IN THE care of infants with prolonged jaundice, the surgeon is particularly concerned with those suspected of having obstruction of the extrahepatic ducts. In 1927, Ladd was the first to correct successfully congenital atresia of the bile duct system. At that time, and for some time afterwards, there was great enthusiasm and hope that a considerable number of infants with signs of obstructive jaundice could be helped. Unfortunately, events have not proved this to be so. According to various reports, only 2 to 3 per cent of infants with clinical obstructive jaundice prove to have an atresia of the extrahepatic duct system which is amenable to surgery. To select these few patients who have atresia of the extrahepatic duct out of the large number of jaundiced infants is a difficult task. Formerly, it was common practice to subject all these infants to extensive surgical exploration at 6 to 8 weeks of age to be sure that no correctable lesion was overlooked. Gellis was the first to call attention to the fact that these explorations, particularly in infants under 3 months, were not without hazard. Among the cases he reviewed there were some deaths directly attributable to the diagnostic explorations. Consequently, it has become common practice to delay exploration on these infants until they are 5 to 6 months of age. This practice seems reasonable to circumvent the problem of deaths after exploration, for this hazard is a great deal less after the infants are 6 months or more of age.


PEDIATRICS ◽  
1960 ◽  
Vol 26 (1) ◽  
pp. 27-35
Author(s):  
Thomas V. Santulli ◽  
Ruth C. Harris ◽  
Keith Reemtsma

From a review of 71 cases and an evaluation of frozen-section examinations of liver biopsies, the authors propose the following method of management of infants with prolonged obstructive jaundice. All patients are carefully selected on the basis of history, clinical findings and appropriate laboratory investigation. Laboratory studies found to aid in the differential diagnosis are: serial determinations of bilirubin (conjugated and unconjugated) in the serum, zinc sulfate turbidity test, cholesterol and cholesterol esters in serum, estimation of bile pigment in urine and stool, studies of the maternal and infant blood factors and erythrocyte fragility. Determinations that have not been useful in the differential diagnosis are: cholesterol esterase, alkaline phosphatase and cephalin fiocculation.19 The activity of transaminases in the serum may prove helpful and are currently under study. The measurement of the prothrombin time should be included in the preoperative studies. If the diagnosis is impossible by the age of 7 weeks, then surgical exploration is carried out. This consists of exposing the liver, taking a biopsy for frozen-section examination and performing a cholangiogram, if possible. With increasing experience, confidence has been acquired in interpretation of the frozen-section of the liver biopsy at this age. The authors are convinced of its value in helping the surgeon establish the diagnosis before proceeding with further exploration of the bile ducts. By this method of management, surgical exploration need not be delayed beyond 7 weeks of age. Thus a patient with congenital atresia of the bile ducts, who may be fortunate enough to have a correctable lesion, will not be deprived of the only possible chance of cure. At this age it is unlikely that biliary cirrhosis will have progressed to a severe degree. Admittedly, it would be preferable to explore such a case earlier, but more experience is needed in diagnosis by frozen-section examination at an earlier age. It does not appear that any patient with hepatitis or other non-surgical condition has been harmed either by the anesthesia or surgical trauma attendant on this limited procedure. One of the greatest advantages of the frozen-section examination has been the information provided to the surgeon at a crucial time during the exploration. With this information the surgeon should be able to avoid unnecessary exploration of the bile ducts and possible injury to patent ducts, as well as unnecessary biliary-intestinal anastomoses which have been performed in the past because of mistaken diagnoses.


PEDIATRICS ◽  
1978 ◽  
Vol 62 (2) ◽  
pp. 235-237
Author(s):  
Vivian J. Harris ◽  
John Kahler

Obstructive jaundice in young infants represents a clinical situation whose diagnostic evaluation has changed dramatically over the past few years.1-3 Biliary atresia and some forms of neonatal hepatitis are the most common diseases to be differentiated. Emphasis has shifted in recent years toward early surgical exploration for the possibility of performing some form of portoenterostomy. Among surgically correctible lesions, the choledochal cyst, although a rare cause of obstructive jaundice during the newborn period, should be considered and actively pursued since irreversible cirrhosis is a major sequela in untreated cases.4 We describe a patient who was considered to have biliary atresia but on whom a choledochal cyst was discovered at 5½ months of age.


PEDIATRICS ◽  
1969 ◽  
Vol 43 (2) ◽  
pp. 273-276
Author(s):  
Jay Bernstein ◽  
Raul Braylan ◽  
A. Joseph Brough

Conjugated hyperbilirubinemia in the newborn period and early infancy can result from choledochal obstruction or hepatocellular damage. Examples of the former include biliary atresia, choledochal cyst, and choledochal bile plugs. The recognition of these conditions and their differentiation are of importance in determining the best and most effective course of therapy. Choledochal cysts and bile plugs can be corrected surgically, and the presence of these two conditions is best determined by surgical exploration and transcholecystic cholangiography. Previous liver biopsy is helpful in establishing the presence of an obstructive lesion; but, because of the similarity of histopathological effects on the liver, it will be of little help in differentiating the causes of obstruction.


1988 ◽  
Vol 60 (01) ◽  
pp. 025-029 ◽  
Author(s):  
M Colucci ◽  
D F Altomare ◽  
G Chetta ◽  
R Triggiani ◽  
L G Cavallo ◽  
...  

SummaryMicrovascular thrombosis is considered an important pathogenetic factor in renal failure associated with obstructive jaundice but the mechanisms leading to fibrin deposition are still unknown. The plasma levels of plasminogen activator inhibitor (PAI) in 29 patients with obstructive jaundice were found significantly increased as compared to 20 nonjaundiced patients. Fibrin autography of plasma supplemented with tissue plasminogen activator (t-PA) revealed that in icteric samples most of the added activator migrated with an apparent Mr of 100 kDa, corresponding to t-PA-PAI complex, whereas in control samples virtually all t-PA migrated as free enzyme. PAI activity detected in icteric samples is similar to the endothelial type PAI since it is neutralized by a monoclonal antibody against PAI-1.Venous stasis in jaundiced patients was neither associated with an increase in blood fibrinolytic activity nor with a decrease in PAI activity. Immunologic assay showed that t-PA release was impaired in 3 out of 4 patients. In controls, venous occlusion induced an increase in both fibrinolytic activity and t-PA antigen and a reduction in PAI activity. Bile duct recanalization in jaundiced patients subjected to surgery was accompanied by a decrease in plasma PAI activity which paralleled the decrease in serum bilirubin levels. In nonjaundiced patients, surgical treatment did not cause significant changes in either parameter. Rabbits made icteric by bile duct ligation showed an early and progressive increase in plasma PAI activity indicating that obstructive jaundice itself causes the elevation of circulating PAI. It is concluded that obstructive jaundice is associated with a severe impairment of fibrinolysis which might contribute to microvascular thrombosis and renal failure.


2002 ◽  
Vol 46 (6) ◽  
pp. 593 ◽  
Author(s):  
Dong Kyun Yoo ◽  
June Sik Cho ◽  
Kyung Sook Shin ◽  
Dae Young Kang

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