Portal Hypertension Dr. Basim Rassam Al-Madena copy

Portal Hypertension Normal portal venous pressure is 80 -120 mm H2O and depends on splanchnic blood flow, resistance to outflow from the liver and pressure in the Inferior vena cava. In portal hypertension it reaches 400 mm H2O or more. Bleeding from oesophageal varices starts when portal pressure exceeds 250 – 300 mm H2O. The portal vein is formed of two main vessels- the Superior mesentieric and splenic veins. It has no valves .As a result of portal hypertension, extrahepatic portasystemic anastomotic channels become engorged and dilated ( i.e. oesphageal varices with profuse painless heamatmesis, caput medusae around umbilicus and haemorrhoids). Hypersplenisim with pancytopaenia, stasis in the portal circulation with portal vein thrombosis and infarction of the intestine, as well as ascites , also results.

Causes of Portal Hypertension . Prehepatic presinusoidal (liver is normal) include umbilical sepsis (neonatal), clotting diathesis (polycythaemia), malignant portal vein obstruction and idiopathic causes. . Intrahepatic presinusoidal (liver is diseased) include schistosomiasis, congenital hepatic fibrosis, sarcoidosis and liver intoxication. . Intrahepatic postsinusoidal group includes cirrhosis. . Posthepatic postsinusoidal include hepatic vein obstruction (Budd-Chiari syndrome) and constrictive pericarditis. Schistosomiasis and cirrhosis are the commonest causes of portal hypertension worl-wide. Al-Madena copy

Between the supperior and inferior rectal veins: forming haemorrhoids There are four main areas of portosystemic anastomosis that become developed in portal obstruction. These are: Between the left vein and the oesophageal veins: forming oesophageal varices Between the supperior and inferior rectal veins: forming haemorrhoids Along the obliterated umblical vein to the superior and inferior epigastric veins: forming a caput medusae Retroperitoneal and diaphragmatic anastomoses: which may cause intraoperative hazards Oesophageal varices and resulting gastrointestinal haemorrhage are the most serious complication of portal hypertension. Splenomegaly occurs because of: Portal congestion Leucopenia and thromobocytopenia causing hypertrophy of the splenic substance itself Ascites is due to a combination of: Raised portal pressure (not enough to cause ascites on its own) Low serum albumin Al-Madena copy

↑ Aldosterone activity with sodium retention ↑ Lymphatic pressure in the cirrhotic liver resulting in lymph transudation. Clinical features of portal hypertension Because of its range of effects, portal hypertension can present in many ways: Haemorrhage from bleeding oesphageal varices or haemorrhoids With signs hepatic failure: jaundice; CNS effects; stigmata of liver disease A cause of splenomegaly A cause of hepatomegaly Because of its catastrophic effect, haemorrhage from bleeding oesphageal varices is the most significant surgical presentation of portal hypertension. Haemorrhage from oesophageal varices Oesophageal varices account from 50% of deaths from upper gastrointestinal bleeding, although they cause only 10% of cases. Whilst the patient is being resuscitated, certain investigations should take place- others should be delayed until the patient’s condition stabilizes (see the shaded box below). Al-Madena copy

Diagnosis and assessment of portal hypertension Liver function tests; chest X-ray; barium swallow (soap-bubble appearance of varices); barium meal; i.v. urography to evaluate left renal function (for lienorenal shunt); splenoportography and ultrasound (may show patent or obstructed portal vein); transhepatic venography and endoscopy especially in emergency bleeding to confirm the site of bleeding from chronic peptic ulcer or erosive gastritis which may account for %40 of misdiagnosed bleeding varices. Peptic ulcer is more common in cirrhotics and the presence of varices does not necessarily mean that they are source of upper gastrointestinal tract bleeding. The severity of liver disease is graded according to Child’s classification into A, B and C and modified into a flexible system using points. Serum bilirubin (mg/100ml) < 2 (1), 2-3 (2), > 3 (3) (μmol/1) < 34 (1), 34-51 (2), >51 (3) Serum albumin (g/100ml) > 3.5 (1), 3-3.5 (2), <3 (3) Prothrombin time (seconds prolonged) <2 (1), 3-5 (2), >5 (3) Al-Madena copy

Ascites None (1), Mild/moderate (2), Gross (3) Encephalopathy None (1), Minimal (2), Moderate/severe (3) The added points are classified as follows: A= 5-7 points B= 8-9 points C= 10-15 points A liver biopsy is essential and liver scan may be required to exclude hepatomas. The ideal patient for a shunt operation should be under 45 years of age, category A or B, with inactive liver disease and should look and feel well. The four important effects of portal hypertension are: Development of a collateral portosystemic circulation Splenomegaly Ascites Hepatic failure and its sequelae. Al-Madena copy

The management should be carried out in high-dependency units with specialized teams. The principles are: Control the acute bleeding Prevent recurrent bleeding Treat underlying Control of variceal haemorrahge Immediate resuscitation takes priority. The airway should be protected. Central venous access is often indicated. Blood, fresh frozen plasma and platelets are usually needed. Catheterization to monitor urine output. Over-expansion of the circulation may cause a dangerous increase in portal venous pressure. Prevention od complication or the early recognition and treatment of these is important. Al-Madena copy

Complications of vericeal haemorrhage Aspiration * Pneumonia Hepatic encephalopathy * Hypoxia Ascites * Renal failure Infections from enteric organisms * Alcohol withdrawal Drug treatment of oesophageal varices Somatostation is a hormone that reduces splanchnic and hepatic flow. Octreotide and lanreotide are longer-acting synthetic analogues of somatostatin. Vasopressin causes generalized vasoconstriction but its use is controversial. It is given in combination with glyceryltrinitrate under close cardiac monitoring. Terlipressin is an analogue of vasopressin which has a longer action and fewer systemic effects. Ballon tamonade Insertion of a double-ballooned Sengstaken-Blakemore or Minnisota tube into the oesophagus controls variceal bleeding temporarily by direct compression at the bleeding site. Use of balloon tamponade is recommended in: Massive bleeding preventing endoscopy Stabilizing patients awaiting definitive therapy Patients being transferred to a specialist unit. It should not be used in patients with a large hiatus hernia. Al-Madena copy

Sclerotherapy of varices Injecting sclerosant, such as ethanolamine, into bleeding varices is usually undertaken at the initial emergency endoscopy to control acute bleeding. Successful in 70-90% of cases, and may be repeated the following week to prevent re-bleeding. If two attempts of sclerotherapy fail, a more major intervention is indicated. Complications include: Fever Retrosternal discomfort Dysphagia Ulceration Stricture Local perforation Variceal banding Banding produces better control of bleeding than sclerotherapy with lower morbidity and reduced re-bleeding. Not as suitable for the acutely bleeding patient, due to technical limitations. Banding is therefore recommended for second or subsequent endoscopy sessions to eradicate varices initially treated by sclerotherapy. Al-Madena copy

Intrahepatic shunt Trans-jagular intrahepatic porto-systemic shunt (TIPSS) is a radiological technique for creating a porto-systemic shunt via the trans-jagular route. Indications for TIPSS Uncontrolled acute varical bleeding Recurrent varical bleeding Failed endoscopic therapy Patient intolerant of endoscopic therapy Surgery contraindicated by poor hepatic function or general condition Patients awaiting liver transplants. Under local or general anaesthetic, the right hepatic-hepatic vein is cannulated by a percutaneous jagular route and the liver punctured to gain access to the portal vein The track is then dilated with a balloon catheter and a stent of 8-12mm diameter is placed to maintain patency The principle is to reduce the portal pressure gradient by short circuiting the liver. TIPSS is contraindicated in: Right-sided heart failure with an elevated central venous pressure Polycystic liver disease Severe acute progressive hepatic failure. Al-Madena copy

Extrahepatic shunt In long-term elective treatment, extrahepatic shunt or oesophageal transection are the alternatives to repeated sclerotherapy. The aim of extrahepatic shunt is to decompress the whole or part of the portal venous circulation. These shunts require a surgical procedure and are indicated in patients with failed endoscopic treatment. The three main extrahepatic shunts are: Total shunt (portocaval): the whole of the portal venous circulation is fully decompressed. In total shunts, there is no portal vein flow into the liver. The incidence of encephalopathy is high. Partial shunt (narrow diameter portocaval): the whole of the portal venous circulation is partly decompressed with a narrow (8-10mm) non-expansile graft. Some portal flow continues so post-operative encephalopathy is reduced. This procedure can be done without extensive dissection and so is preferable to a total shunt for both uncontrolled acute and recurrent bleeding. Selective shunt (distal splenorenal): an isolated part of the portal circulation is fully decompressed. This is not advocated in an acute situation because of its technical complexity. Al-Madena copy

Mesocaval graft interpostion Al-Madena copy

Oesophageal transection The aim of oesophageal transection is to interrupt the gastric oesophageal porto-systemic anastomosis. Early oesophageal transection has compared favourably with injection sclerotherapy, but it requires a laparotomy and disseration in the presence of established portal hypertension and opening of the stomach, all of which may be hazardous in the acutely bleeding patient. Anterior gastrotomy Stabling gun passed up into the oesophagus Vagus nerve identified and excluded Lower oesophageal wall tied into stapling line Gun fired to transect and re-anastomose the oesphagus simultaneously Problems include: Bleeding gastric varices require further devascularization May be more hazardous than simple partial shunt Chances od sepsis are increased by opening stomach Recurrent bleeding is more likely than with shunts Indication for elective surgery in portal hypertension Bleeding oesophageal varices (once they have bled they will bleed again) is an absolute indication. Hypersplenism and ascites are relative indications. Al-Madena copy

Liver transplantation Liver transplantation may be the preferable option for intractable portal hypertension. It is not suitable in cases of pre-hepatic obstruction with good liver function or in cases with a persisting underlying cause. Al-Madena copy

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