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Portal hypertension is present when portal venous pressure exceeds 10 mm Hg. This chapter addresses the causes, evaluation, and treatment options for patients with portal hypertension. While the emphasis is on surgical aspects, this group of patients requires a multidisciplinary approach and surgical therapy must inevitably be viewed in this context. The major clinical presentations that will be addressed are variceal bleeding, ascites, end-stage liver disease, and the pulmonary syndromes. Whatever the presentation of portal hypertension, be it an incidental finding or one of the above clinical presentations, it demands full investigation. In the United States, the etiology is most commonly cirrhosis, but other etiologies such as prehepatic portal or splenic vein thrombosis or other intraparenchymal liver disease such as schistosomiasis or hepatic fibrosis should be considered. Definition of the cause is important as prognosis depends on the underlying liver disease, and a full evaluation to allow development of a treatment plan for variceal bleeding, ascites, or end-stage liver disease is paramount at initial presentation. The focus of this chapter is on emphasizing the role of a multidisciplinary team approach to managing patients with portal hypertension.


Portal hypertension was recognized by the Greeks1,2, was highlighted by Shakespeare in his character of Falstaff, and has played a role through much of history. The evolution of the treatment of portal hypertension was driven by surgeons until the 1980s. Nicolai Eck, a Russian Army surgeon, performed an end-to-side portacaval shunt in 1883 in an animal model. Pavlov, the great Russian physiologist, conducted animal studies that showed the detrimental effect of diverting portal flow, describing meat intoxication (encephalopathy) and liver failure. Vidal, a French surgeon is credited with performing the first portal systemic shunt in a human in 1903. Morison and Talma operated on patients with portal hypertension with procedures such as omentopexy and splenic transposition, but their failure to recognize cirrhosis as the cause of portal hypertension led to poor results.


In the 1940s, Whipple and the Columbia Presbyterian group in New York initiated an era of success for portal decompression.3 The next 40 years saw many refinements to decompressive shunts, Drapanas with mesocaval shunts,4 Warren and Inochuchi with selective variceal decompression,5,6 and Sarfeh with partial shunts.7 This era saw many randomized trials documenting efficacy of shunts.


Endoscopic therapy was the next major advance in managing variceal bleeding, being first done by surgeons with rigid esophagoscopes.8 In the 1980s, three surgeons, Johnston, Terblanche,9 and Paquet,10 bridged the gap from rigid to flexible variceal sclerotherapy. Another surgeon, Steigmann,11 moved the field forward by introducing variceal band ligation.


Over the last three decades, the more recent advances have been made by nonsurgeons. A better understanding of the pathophysiology, the ability to better evaluate liver diseases, the introduction of pharmacologic therapy, development of the radiologic shunt, and coming of age of liver transplantation are the main contributors to this progress. Lebrec and ...

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