外科-门静脉高压症课件.ppt

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1、Chapter 51PORTAL HYPERTENSION12男 18岁3吴某某 男 43岁4Sections:16ANATOMY,PHYSIOLOGY,AND PATHOPHYSIOLOGY OF PORTAL HYPERTENSION HISTORICAL REVIEWCLASSIFICASION OF PORTAL HYPERTENSIONEVALUATION OF THE PATIENT WITH CIRRHOSISCOMPLICATION OF PORTAL HYPERTENSIONVARICEAL HEMORRHAGE PORTOSYSTEMIC ENCEPHALOPATHYASC

2、ITES6Section 1:ANATOMY,PHYSIOLOGY,AND PATHOPHYSIOLOGY OF PORTAL HYPERTENSIONANATOMY:The liver is a unique organ in that it has a dual blood supply:portal vein and hepatic artery.The portal vein is formed from the confluence of the superior mesenteric and splenic veins781011PHYSIOLOGY:Hepatic blood f

3、low averages 1500 ml/m,which represents approximately 25%of the cardiac output.The portal vein contributes two thirds of the total hepatic blood flow,Hepatic arterial perfusion accounts for over one half of the livers oxygen supply.13Because increased portal venous resistance is usually the initiato

4、r of portal hypertension,classifications of this disorder are generally based on the site of elevated resistance.However,increased portal venous inflow secondary to a hyperdynamic systemic circulation and splanchnic hyperemia is often a major contributor to the maintenance of portal hypertension.15P

5、ATHOPHYSIOLOGYThe most common cause of prehepatic portal hypertension is portal vein thrombosis,it accounts for 50%of cases of portal hypertension in the pediatric age group.The most common cause of intrahepatic,presinusoidal hypertension is virus hepatitis,and schistosomiasis.Postsinusoidal causes

6、of portal hypertension are rare and include the Budd-Chiari syndrome,constrictive pericarditis,and heart failure.1618Sections:15ANATOMY,PHYSIOLOGY,AND PATHOPHYSIOLOGY OF PORTAL HYPERTENSION CLASSIFICASION OF PORTAL HYPERTENSIONEVALUATION OF THE PATIENT WITH CIRRHOSISCOMPLICATION OF PORTAL HYPERTENSI

7、ONVARICEAL HEMORRHAGE PORTOSYSTEMIC ENCEPHALOPATHYASCITES191.In the majority of patients with chronic liver disease and cirrhosis,portal hypertension(PHT)develops as a result of increased resistance to portal venous blood flow within the liver.PHT is defined as portal venous pressure higher than 12

8、mm Hg or a hepatic wedge venous pressure that exceeds the inferior vena cava pressure by more than 5 mm Hg.2.It is classified as prehepatic,hepatic,or posthepatic according to the anatomic site of increased portal venous resistance.Hepatic PHT is further classified according to the functional relati

9、onship to the hepatic sinusoids.Sinusoidal obstruction is more frequently seen with postnecrotic cirrhosis(e.g.,from HCV and HBV infection),whereas postsinusoidal obstruction is more common with alcoholic cirrhosis.3.Prehepatic and posthepatic causes of PHT are less often encountered in patients wit

10、h cirrhosis;Efforts should always be made to rule out such causes,because these conditions all require different therapeutic approaches.20SplenicveinthrombosisPortalveinthrombosisPartialnodulartransformationPrehepatic obstruction21Hepatic obstructionPresinusoidalIdiopathicportalhypertensionSchistoso

11、miasisCongenitalhepaticfibrosisSarcoidosisSinusoidalNodularregenerativehyperplasiaMost forms of cirrhosisViral hepatitisAcutealcoholichepatitisPostsinusoidalAlcoholiccirrhosisVeno-occlusivedisease22Sections:15ANATOMY,PHYSIOLOGY,AND PATHOPHYSIOLOGY OF PORTAL HYPERTENSION CLASSIFICASION OF PORTAL HYPE

12、RTENSIONEVALUATION OF THE PATIENT WITH CIRRHOSISCOMPLICATION OF PORTAL HYPERTENSIONVARICEAL HEMORRHAGE PORTOSYSTEMIC ENCEPHALOPATHYASCITES24Section 3:EVALUATION OF THE PATIENT WITH CIRRHOSIS(1)diagnosis of the underlying liver disease,(2)estimation of functional hepatic reserve,(3)definition of port

13、al venous anatomy and hepatic hemodynamic evaluation,(4)identification of the site of upper gastrointestinal hemorrhage,if present.25if upper gastrointestinal hemorrhage present.Precise identification of the site of bleeding is essential because hemorrhage secondary to portal hypertension may be fro

14、m:esophageal varices,gastric varices,portal hypertensive gastropathy and because a significant fraction of patients with portal hypertension bleed from other lesions.26spider angiomas,palmar erythema,testicular atrophygynecomastia.A palpable spleen.hepatic functional decompensation or advanced porta

15、l hypertension:jaundice,ascites,palpation of a firm irregular liver edge,dilated abdominal wall veins,impairment of mental status or the presence of asterixis(liver flap).28Laboratory Tests.Cirrhosis is often accompanied by anemia,leukopenia,and thrombocytopenia.Coagulation may be impaired by a prol

16、onged prothrombin time because many of the coagulation factors are synthesized by the liver and by primary fibrinolysis.29Common serum electrolyte abnormalities in cirrhosis are hyponatremia,hypokalemia,and metabolic alkalosisHepatitic serology should be obtained in most patients with cirrhosis.hepa

17、tocellular carcinoma,which can be diagnosed in approximately 60%of patients by an elevated alpha-fetoprotein level.31Measurement of Hepatic Functional Reserve.The time-honored method of assessing hepatic functional reserve is Childs classification.In most clinical series,operative mortality rates fo

18、r:Childs Class A-0%to 5%,B-10%to 15%,C-greater than 25%.32Section II/Chapter 7-Hepatic FailureTable-Child-Turcotte-Pugh Scoring SystemPoints123EncephalopathyNoneStateIorIIStageIIIorIVAscitesAbsentSlight(orcontrolledbydiuretics)ModeratedespitediuretictreatmentBilirubin(mg/dl)PatientswithPBCorPSC236Al

19、bumin(g/L)3.52.8-3.52.8PT(prolongedsec)INR462.3PBC-primarybiliarycirrhosisPSC-primarysclerosingcholangitis2001WebMDCorp.AllRightsReserved.33Childs classification.34Hepatic Hemodynamic Assessmentportal pressure can be indirectly estimated by measurement of hepatic venous wedge pressure.A complete ang

20、iographic study generally consists of selective injections of radiographic contrast medium into the superior mesenteric and splenic arteries followed by late venous phase films to define splenic,superior mesenteric,and portal veins.35Sections:15ANATOMY,PHYSIOLOGY,AND PATHOPHYSIOLOGY OF PORTAL HYPERT

21、ENSION CLASSIFICASION OF PORTAL HYPERTENSIONEVALUATION OF THE PATIENT WITH CIRRHOSISCOMPLICATION OF PORTAL HYPERTENSIONVARICEAL HEMORRHAGE PORTOSYSTEMIC ENCEPHALOPATHYASCITES36Section 4 COMPLICATION OF PORTAL HYPERTENSIONVariceal bleedingPortalhypertensivegastropathyAscitesSpontaneousbacterialperito

22、nitisSpontaneousshuntsEncephalopathyHypersplenism37Sections:16ANATOMY,PHYSIOLOGY,AND PATHOPHYSIOLOGY OF PORTAL HYPERTENSION HISTORICAL REVIEWCLASSIFICASION OF PORTAL HYPERTENSIONEVALUATION OF THE PATIENT WITH CIRRHOSISCOMPLICATION OF PORTAL HYPERTENSIONVARICEAL HEMORRHAGE PORTOSYSTEMIC ENCEPHALOPATH

23、YASCITES38Section 5:VARICEAL HEMORRHAGEBleeding from esophagogastric varices is the single most life-threatening complication of portal hypertension,responsible for one third of all deaths in patients with cirrhosis.The risk of death from bleeding in any individual patient is mainly related to the u

24、nderlying hepatic functional reserve.The greatest risk of death from variceal bleeding is within the first few days and declines rapidly between then and 6 weeks.39PathogenesisVarices in the distal esophagus and proximal stomach are a component of the collateral network that diverts high pressure po

25、rtal venous flow through the left and right gastric veins and the short gastric veins to the azygous system.Esophagogastric varices do not develop until portal pressure exceeds 12 mm Hg and,once present,bleed in only one third to one half of patients.40The pathogenesis of variceal rupture is incompl

26、etely understood but is most likely multifactorial.endoscopic classification schemes that consider size of varices and characteristics such as cherry-red spots and red wale markings,which are related to the thickness of the overlying epithelium,have improved the predictability of variceal hemorrhage

27、.These prognostic indices are especially important when considering prophylactic therapy.41Diagnosis of BleedingThe key procedure for diagnosing the site of upper gastrointestinal hemorrhage in a patient with portal hypertension is endoscopy.Portal hypertensive bleeding is most commonly from esophag

28、ogastric varices (esophageal varices=90%;gastric varices=10%).The only nonvariceal cause of portal hypertensive bleeding is portal hypertensive gastropathy42TreatmentTherapy for portal hypertension and variceal bleeding has evolved over the past 100 years.The many treatment modalities available sugg

29、est that no single therapy is entirely satisfactory for all patients or for all clinical situations.4344Resuscitation and DiagnosisInitial resuscitation is usually with isotonic crystalloid solutions,a minimum of six units of blood should be typed and crossmatched for most patients with variceal ble

30、eding.If the prothrombin time is prolonged more than 3 seconds,fresh frozen plasma(FFP)should be a component of the resuscitation volume.If the platelet count is less than 50,000 per cu.Mm,platelet transfusions are necessary.45Endoscopy to determine the cause of bleeding should be performed as soon

31、as the patient is stabilized.Sclerotherapy should be performed during the initial endoscopy if the expertise is available.Bleeding from gastric varices or from portal hypertensive gastropathy should be initially treated with pharmacotherapy.Because these lesions are often incompletely controlled by

32、nonoperative means,such patients frequently require either insertion of a TIPS or early surgical intervention.46Pharmacotherapy(Drug)Vasopressin has been the most commonly used drug in the acute setting and controls hemorrhage in approximately 50%of patients.Vasopressin is usually administered intra

33、venously as a bolus dose of 20 units over 20 minutes and then as a continuous infusion of 0.4 units per minute,Somatostatin is administered as a 250-ug.intravenous bolus,followed by a continuous infusion of 250 ug.per hour for 2 to 4 days.Octreotide is given as an intravenous infusion of 25 to 50 mg

34、.per hour for a similar length of time.47Balloon TamponadeThe major advantages of variceal tamponade with the Sengstaken-Blakemore tube are immediate cessation of bleeding in more than 85%of patientsSignificant disadvantages of balloon tamponade are frequent recurrent hemorrhage after balloon deflat

35、ion,considerable discomfort for the patient,and a high incidence of serious complications such as esophageal perforation,ischemic necrosis of the esophagus.48Endoscopic TreatmentEndoscopic treatment(variceal sclerosis or ligation)is the most commonly used therapy for both management of the acute ble

36、eding episode and prevention of recurrent hemorrhage.The most commonly used sclerosants are sodium morrhuate and sodium tetradecyl sulfate.Alternatively,each varix can be ligated with a rubber band.A subsequent treatment session is planned for 4 to 6 days later.Rubber band ligation of varices may be

37、 more effective and associated with fewer complications than sclerosis.The technique has been generally unsuccessful for bleeding gastric varices.495051Transjugular Intrahepatic Portosystemic Shunt.(TIPS)Access is gained to a major intrahepatic portal venous branch through puncture through a hepatic

38、 vein.A parenchymal tract between hepatic and portal veins is then created with a balloon catheter and a 10-mm.expandable metal stent is inserted,thereby creating the shunt TIPS is a technique that accomplishes portal decompression without an operation.5253the success rate of TIPS has been over 90%,

39、TIPS in the emergency setting revealed an in-hospital mortality of 56%and incomplete control of bleeding in 26%of patients.TIPS should not be recommended as initial therapy for acute variceal hemorrhage but should be used only after less invasive treatments such as endoscopic therapy and pharmacothe

40、rapy have failed to control bleeding.One clear indication for TIPS is as a short-term bridge to liver transplantation for patients in whom endoscopic treatment has failed,or patients with advanced hepatic functional decompensation(Childs Class C),who are not transplant candidates.54Emergency Surgery

41、emergency operation should be promptly done when less invasive measures fail to control hemorrhage or are not indicated,such as failure of acute endoscopic treatment,failure of long-term endoscopic therapy,and hemorrhage from gastric varices or portal hypertensive gastropathy.Esophageal transection

42、with a stapling device is rapid and relatively simple.The most commonly performed shunt operation in the emergency setting is the portacaval shunt.The major disadvantage of emergency surgery is that operative mortality rates exceed 25%.55For prevention of bleedingNonselective ShuntsInclude the end-t

43、o-side portacaval shunt(Eck fistula),the side-to-side portacaval shunt,large-diameter interposition shunts,and the conventional splenorenal shunt.The most common causes of death in medically treated and shunted patients were rebleeding and accelerated hepatic failure,respectively.Nonselective shunts

44、 effectively decompress varices.However,because of complete portal flow diversion,they are complicated by frequent postoperative encephalopathy and accelerated hepatic failure.Side-to-side nonselective shunts effectively relieve ascites as well as prevent variceal hemorrhage.56Partial ShuntsThe obje

45、ctives of partial and selective shunts are the same:(1)effective decompression of varices,(2)preservation of hepatic portal perfusion,and(3)maintenance of some residual portal hypertension.A small-diameter interposition portacaval shunt using a polytetrafluoroethylene graft,combined with ligation of

46、 the coronary vein and other collateral vessels,A lower frequency of encephalopathy after the partial shunt but similar survival as nonselective shunts.575859Nonshunt OperationsThe simplest nonshunt operation is transection and reanastomosis of the distal esophagus with a stapling device.The most ef

47、fective nonshunt operation is extensive esophagogastric devascularization combined with esophageal transection and splenectomy.In China,the results with this operation have been excellent.However,extensive devascularization procedures have generally been less successful in North American patients wi

48、th alcoholic cirrhosis.6061Hepatic TransplantationOf the numerous therapeutic options for prevention of recurrent variceal hemorrhage,hepatic transplantation is the only one that addresses the underlying liver disease in addition to providing reliable portal decompression.Patients with variceal blee

49、ding who are transplant candidates include nonalcoholic cirrhotics and abstinent alcoholic cirrhotics with either limited hepatic functional reserve(Childs Class C)or a poor quality of life secondary to their disease(e.g.,encephalopathy,fatigue,or bone pain).6263Sections:15ANATOMY,PHYSIOLOGY,AND PATHOPHYSIOLOGY OF PORTAL HYPERTENSION CLASSIFICASION OF PORTAL HYPERTENSIONEVALUATION OF THE PATIENT WITH CIRRHOSISCOMPLICATION OF PORTAL HYPERTENSIONVARICEAL HEMORRHAGE PORTOSYSTEMIC ENCEPHALOPATHYASCITES6465