The Role of the Liver in Surgery

Boyce, Frederick Fitzherbert; Thomas, Charles C.

doi:10.1097/00000441-194105000-00025

Cited by 21 publications

(3 citation statements)

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“…The term hepatorenal syndrome was coined by Heyd in 1924 to describe the deterioration in renal function during the course of liver disease. Since then a great variety of papers have appeared supporting or challenging the concept of hepatorenal syndrome (for a review see [6,27]). While the high occurrence of defective renal function in patients with liver disease remains unquestioned, the search for a unique pathophysiological mechanism causing hepatorenal syndrome has failed.…”

Section: Discussionmentioning

confidence: 99%

New clues to the pathophysiology of hepatorenal failure

1993

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In patients with advanced liver disease, decreases in renal blood flow, glomerular filtration rate, and urinary output are frequently observed. The deterioration in renal function is usually not due to a unique cause but is the result of the concerted action of several mechanisms operating in parallel; decreased plasma protein formation and increased intrahepatic vascular resistance lead to sequestration of blood volume, favoring hypovolemia and reduction in cardiac output. At the same time enhanced formation of nitroxide leads to peripheral vasodilation; bacterial endotoxin escaping clearance by the diseased liver stimulates the expression of a long-acting nitroxide synthase. Furthermore, vasodilating intestinal mediators such as substance P escape inactivation by the liver. In the face of peripheral vasodilation the maintenance of blood pressure requires an increase in cardiac output, which is achieved by activation of sympathetic nervous tone, renal vasoconstriction, enhanced release of renin, angiotensin, aldosterone, and antidiuretic hormone, leading to renal retention of sodium and water. Renal vasoconstriction is opposed by vasodilatatory prostaglandins, and renal failure may be triggered by inhibition of prostaglandin formation. On the other hand, vasoconstrictive eicosanoids, such as thromboxane B2 and leukotriene E2, which escape hepatic inactivation, may contribute to renal vasoconstriction. Beyond these mechanisms disturbed hepatic regulation of renal function may participate in the generation of hepatorenal syndrome. The liver regulates renal function via both a hepatorenal reflex decreasing renal blood flow and a hypothetical liver-borne diuretic factor increasing renal blood flow. Both enhanced hepatorenal reflex activity and decreased formation of the liver-borne diuretic factor could participate in the pathogenesis of hepatorenal syndrome.

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Section: Discussionmentioning

confidence: 99%

New clues to the pathophysiology of hepatorenal failure

1993

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“…While the "hepato-renal" syndrome clinically suggests that disastrous disturbances in water balance may occur under combined hepatic and renal control, biochemical and metabolic studies of this state have failed to disclose what fundamental mechanisms are aberrant (46,47).…”

Section: Discussionmentioning

confidence: 99%

Water Storage and the Movements of Body Fluids and Chlorides During Acute Liver Disease

Labby¹,

Hoagland²

1947

J. Clin. Invest.

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“…death" syndrome has been described as an important cause of death in surgery of the biliary tract as well as in thyroid disease and an occasional cause of death after other operations (Sutton, 1943;Boyce, 1941;Wilensky, 1939). A recent investigation by Reichmann and Wohlgemuth (1964) indicates that advances in anaesthetic and surgical techniques have not eliminated this syndrome.…”

Section: Direct Traumamentioning

confidence: 99%

Liver Injury in the Surgical Patient: A Critical Review

Johnstone¹

1964

British Journal of Anaesthesia

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This is a critical review of the reports of postoperative jaundice and liver necrosis that have been published during the past twenty-five years. Postoperative liver damage has the following causes: transmitted, provoked, or coincidental viral infections; acute sepsis and septicaemic states; blood transfusion; widespread vasoconstriction with hypotension lasting more than twenty-four hours; allergic reactions to antigenic substances; alleged "hypersensitivity" to drugs to which antibodies cannot be identified; the direct effects of certain therapeutic agents on the liver; surgical trauma to the liver and its appendages; and postoperative pancreatitis. Several of these factors may operate simultaneously in the patient recovering from a surgical operation and in these circumstances it is impossible to dissociate one particular cause from the others. The syndromes of viral hepatitis and drug "hypersensitivity" are indistinguishable. Both are associated with fever, skin rashes, leucopenia, arthralgia, cholestatic jaundice, and liver necrosis with a mononuclear infiltration of the liver. Both are peculiar to man and the time interval between the exposure to risk and the appearance of jaundice varies from less than seven days to more than three months. The development of immunity to the one or desensitization from the other is not universal. There is no inhalational anaesthetic agent in common use which comes within the definitions of directly or indirectly hepatotoxic substances. The pharmacological methods of screening inhalational anaesthetic agents for hepatotoxidty have always been reliable and there is no reason to doubt their efficacy at the present time.

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The Role of the Liver in Surgery

Cited by 21 publications

References 0 publications

New clues to the pathophysiology of hepatorenal failure

New clues to the pathophysiology of hepatorenal failure

Water Storage and the Movements of Body Fluids and Chlorides During Acute Liver Disease

Liver Injury in the Surgical Patient: A Critical Review

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