The mechanism of ascites

Hyatt, Robert E.; Smith, John R. Lindsay

doi:10.1016/0002-9343(54)90359-9

Cited by 77 publications

(3 citation statements)

References 76 publications

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“…Most forms of ascites are post sinusoidal, consisting of a modified transudate originating from beyond (cranial to) the hepatic sinusoids. In animals with hypoproteinemia, all types of ascites will be recognised as transudates regardless of their origin (Hyatt andSmith 1954, Greene 1979).…”

Section: Discussionmentioning

confidence: 99%

Cor triatrium dexter with Budd‐Chiari syndrome and a review of ascites in young dogs

Otto

Mahaffey

Jacobs

et al. 1990

J of Small Animal Practice

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Ascites with accumulation of a true or modified transudate, is relatively uncommon in young dogs. When it does occur, congenital defects of the cardiovascular, gastrointestinal, or renal systems, infectious diseases and trauma must be considered. Cor triatrium dexter, an abnormal membrane obstructing the caudal vena cava at the level of the right atrium, was diagnosed in an eight‐month‐old cocker spaniel presented with ascites.

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Section: Discussionmentioning

confidence: 99%

Cor triatrium dexter with Budd‐Chiari syndrome and a review of ascites in young dogs

Otto

Mahaffey

Jacobs

et al. 1990

J of Small Animal Practice

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“…Blakemore, Rousselot, Linton, and others [22][23][24] reported large series of patients treated with some type of portacaval shunt or by splenectomy and proximal splenorenal shunt. For about 10 years it appeared that the problem had been resolved until the recognition of portal systemic encephalopathy [25][26][27][28] and the existence of the portaprival metabolic syndrome raised serious doubts about the validity of this approach. During a subsequent decade, incidence of reported encephalopathy ranged from 12% to as high as 45%, although careful analyses of the data available showed that the occurrence of serious and uncontrollable encephalopathy was probably in the range of 5 to 10% as more effective medical (intestinal antibiotics, lactulose, restriction of protein, etc.)…”

Section: Elective Portal Systemic Shuntsmentioning

confidence: 99%

Bleeding esophageal varices

McDermott

1984

World j. surg.

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Bleeding esophageal varices remain a major problem which has not been solved despite the number of ingenious and imaginative efforts to control and prevent hemorrhage through a variety of surgical, radiologic, pharmacologic, and endoscopic techniques.A surgically constructed portal systemic shunt still remains the most effective method of permanent control, but the high morbidity and mortality rates have led to efforts to explore other types of therapy. Variations of shunt surgery, such as the selective procedure described by Warren, are promising as are types of portal azygous disconnections and transections.There has been a revival of endoscopic sclerosis of varices stimulated by the development of more sophisticated equipment. Radiologic obliteration of the coronary vein and other portal systemic collaterals is under evaluation.In the face of the catastrophic emergency of exsanguinating hemorrhage, balloon tamponade is the most effective means of temporary control prior to definitive therapy in those patients who have not responded to other conservative approaches such as vasopressin or pituitrin. Success is primarily determined by the degree of hepatocellular function, and biochemical evaluations such as amino‐acid tolerance appear to be more predictive than the simpler and widely used Child's classification which has been the yardstick for 3 decades.In short, the multiplicity of recommended methods of therapy indicates the lack of unanimity and thus the absence of a single universally accepted algorithm for management of this difficult and multifactorial clinical problem.

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“…Animal experiments of hepatic vascular outflow restriction show increased hepatic lymph production. When the hepatic vein is ligated in a dog and the liver is placed within the thorax, pleural fluid accumulates instead of ascites; when it is placed within a bag, fluid accumulates in the bag (5,6). In cirrhotic ascites, however, the protein concentration of the ascitic fluid more closely resembles intestinal lymph than hepatic lymph.…”

mentioning

confidence: 99%

Pathophysiology, Diagnosis, and Management of Pediatric Ascites

Giefer

Murray

Colletti

2011

J. pediatr. gastroenterol. nutr.

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The pediatric population has a number of unique considerations related to the diagnosis and treatment of ascites. This review summarizes the physiologic mechanisms for cirrhotic and noncirrhotic ascites and provides a comprehensive list of reported etiologies stratified by the patient's age. Characteristic findings on physical examination, diagnostic imaging, and abdominal paracentesis are also reviewed, with particular attention to those aspects that are unique to children. Medical and surgical treatments of ascites are discussed. Both prompt diagnosis and appropriate management of ascites are required to avoid associated morbidity and mortality.

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The mechanism of ascites

Cited by 77 publications

References 76 publications

Cor triatrium dexter with Budd‐Chiari syndrome and a review of ascites in young dogs

Cor triatrium dexter with Budd‐Chiari syndrome and a review of ascites in young dogs

Bleeding esophageal varices

Pathophysiology, Diagnosis, and Management of Pediatric Ascites

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