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Accidental hepatic artery ligation in humans
Authors
Alessandri
Andreassen
+68 more
Bakes
Behrend
Behrend
Berman
Bertrand
Bianchi
Bradley
Breton
Browning
Brunschwig
Cameron
Chaw
Child
Edgecomb
Eiselberg
Elias
Fahmy
Ford
Frieson
From
G. Hermann
Goldsmith
Graham
Grube
Guynn
Hansbrough
Healey
Hofmeister
Holst
Horvath
Huggins
Jefferson
Kausch
Kehr
Klose
Lewis
Loeffler
Markowitz
Markowitz
McFadzean
Michels
Misnik
Palacia-Ranam
Popper
Popper
R.S. Brittain
Restrepo
Rienhoff
Ritter
Schenk
Segall
Shann
Smith
Socin
Spector
Sprengel
T.E. Starzl
T.L. Marchioro
Tanturi
Tichau
Tuffier
Tygstrup
von Haberer
W.R. Waddell
Wendel
Wilms
Wolbach
Woolling
Publication date
1 January 1964
Publisher
'Elsevier BV'
Doi
View
on
PubMed
Abstract
Despite the vast amount of information from experimental animals, it has been difficult to obtain a clear-cut picture of the effects of ligation of the hepatic artery in humans with relatively normal livers. The last complete review of this subject in 1933 indicated that a mortality in excess of 50 per cent could be expected in non-cirrhotic patients with injury of the hepatic artery or its principal branches. Five cases of dearterialization of the normal human liver have been observed. These were due to accidental interruption of the right hepatic artery in four and the proper hepatic artery in one. The injured vessel was repaired in one case and ligated in the others. In four of the five patients the vascular disruption was the sole injury. In the other the common bile duct was also lacerated. There was no evidence of hepatic necrosis in any case although one patient died from complications of common duct repair. Transient changes in SGOT and temporary low grade bilirubinemia were commonly noted. In addition, all cases of ligation of the hepatic artery reported since 1933 have been compiled. On the basis of reviewed, as well as the presently reported cases, it is concluded that ligation of the hepatic artery or one of its branches in the patient with relatively normal hepatic function is not ordinarily fatal in the otherwise uncomplicated case. Adequate perfusion of the liver can usually be provided by the remaining portal venous flow and whatever arterial collaterals are present, unless additional factors further reduce the portal venous flow or increase hepatic oxygen need. These factors include fever, shock and anoxia. The key to therapy in unreconstructed injuries to the hepatic artery is avoidance of these secondary influences. © 1964
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