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Percutaneous drainage with multiple drains can be curative. It is important to determine the antibiotic sensitivity of the infecting organisms and to administer a full course of antibiotics to reduce the risk of recurrent or persistent infection.

d.Mortality rate for hepatic abscess may be as high as 40% in difficult cases. This high rate is related principally to three factors.

1.Delay in diagnosis. The possibility of an abscess is often overlooked in the critically ill patient. The use of CT scans and ultrasonography should improve this situation.

2.Multiple abscesses. These are more difficult to drain properly, and therefore, the patient may continue to be septic.

3.Malnutrition. Patients with sepsis are very catabolic. Caloric supplementation, either orally or parenterally, is critical for the patient's well-being, wound healing, and immunocompetence.

3.Amebic abscess is the second most common hepatic abscess in the Western world and is more common than bacterial abscesses in third world countries.

a.Etiology. Amebic abscess is due to infection with the protozoan Entamoeba histolytica, which typically reaches the portal vein from intestinal amebiasis.

b.Clinical presentation includes fever, leukocytosis, hepatomegaly, and right upper quadrant pain. Occasionally, liver enzyme levels are elevated.

1.The abscess is usually solitary and affects the right lobe of the liver in 90% of patients.

2.Indirect hemagglutination titers for Entamoeba are elevated in up to 85% of patients with intestinal infestation and in 98% of patients with hepatic abscess.

3.The pus within the abscess is usually sterile and has the appearance of anchovy paste. Trophozoites are occasionally present in the periphery of the abscess.

c.Treatment of choice is parenteral antibiotics, particularly metronidazole. The abscess is aspirated if it is large or adjacent to important structures, but surgical drainage is not usually necessary. Complications include secondary bacterial infection of the cavity and rupture into adjacent structures, such as the pleural, pericardial, or peritoneal spaces.

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4.Hydatid cysts of the liver

a.Etiology. Hydatid cysts result from infection with the parasite Echinococcus granulosus. Dogs are the definitive host, shedding ova in the feces, which infect intermediate hosts, such as man, sheep, and cattle. This infection is endemic in southern Europe, the Middle East, Australia, and South America—all areas where sheep are raised.

b.Clinical presentation

1.Hydatid cysts can develop anywhere in the body, but two thirds occur in the liver.

a.The cyst and cyst lining contain parasites fully capable of spreading the infection.

b.The adjacent compressed liver tissue and scar form the ectocyst, which is not infective and should be retained when evacuating the cyst.

2.Hydatid cysts undergo progressive enlargement and may rupture.

a.Approximately 50% rupture within the hepatic parenchyma to form daughter cysts.

b.Cysts may rupture into bile ducts, where the debris can cause biliary obstruction.

c.Cysts may rupture into the free peritoneal cavity, resulting in urticaria, eosinophilia, or anaphylactic shock and implantation into other viscera.

d.About 30% of patients develop cysts in the lungs or other extrahepatic organs.

3.Symptoms include liver enlargement and right upper quadrant pain in a patient with a history of exposure to an endemic area. Eosinophilia is present in 40% of patients, and serum tests for the parasite antigen

are diagnostic.

a.All symptomatic cysts require surgery.

b.Small cysts deep within the parenchyma should be followed up (for months to years) until they are sufficiently superficial to be removed.

c.When pericystic calcification is visible on an abdominal radiograph, it signifies the death of a parasite, a condition that requires no further treatment.

c.Treatment

1.Because the cyst is quite fragile and easily ruptured, a hydatid cyst can rarely be removed intact. If the scolices spill into the peritoneal cavity, the parasite will multiply and form new cysts.

2.The current method of treatment is controlled rupture of the cyst, followed by its removal.

a.This is accomplished by careful isolation of the operative field to prevent spillage, followed by aspiration of the cyst.

b.Once decompressed, the cyst and its contents are peeled off the ectocyst lining and removed, thus removing all living cyst elements.

c.The residual space is then sterilized with fresh 0.5% silver nitrate solution or hypertonic saline, which are potent scolicide agents and relatively nontoxic. (There is no systemic scolicidal agent currently in use.)

d.The residual cavity is carefully inspected for bile leakage from cyst-biliary communications, and these are sutured closed.

e.If the cyst ruptured into a major bile duct, common bile duct exploration is done to remove all debris.

f.The cyst is closed. No drains are used.

G Trauma

Due to its large size, the liver is frequently injured by both blunt and penetrating trauma.

1.Mortality. Due to its high blood flow, proximity to the inferior vena cava, nearby vital structures, and propensity to develop infections, the overall mortality of liver trauma remains about 10%–20%. Injury to the hepatic veins and retrohepatic inferior vena cava has a mortality of over 50%, regardless of the method used to obtain control of the bleeding.

2.Diagnosis is usually related to intraperitoneal bleeding. Ongoing bleeding mandates surgery.

3.Nonsurgical management. In a hemodynamically stable patient, some trauma centers angiographically visualize the liver and occlude disrupted arteries with thrombus in an attempt to control hemorrhage and avoid surgery. The safety of this approach is being evaluated, but the approach seems to be safe in many patients.

4.Surgical management. At surgery, hemostasis is usually obtained via packing and the Pringle maneuver (control and compression of the porta hepatis). Further exposure and ligation of individual

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parenchymal bleeders is not typically necessary. Less common methods to control bleeding include:

a.Tractotomy or opening of a missile tract or fracture to expose bleeding parenchyma

b.Resectional debridement, the removal of nonviable parenchyma without an anatomic (i.e., segmental or lobar) resection

c.Anatomic resection has a high mortality (about 50%) when done as an emergency procedure.

d.Hepatic artery ligation may control arterial bleeding but is associated with infectious complications in the compromised parenchyma.

e.Definitive packing can be useful when other methods are unavailable or fail. Ideally, it provides time (24–48

hours) to restore normothermia and clotting factors.

5.Late complications are common.

a.Subcapsular and intrahepatic hematomas can be carefully observed, but many ultimately require drainage.

b.Perihepatic collections, whether of blood or bile, usually become infected and must be drained.

c.Biliary fistulas may track to the skin or into the chest (biliary-pleural, bronchobiliary fistula). Treatment is similar to the treatment for gastrointestinal fistulas (see Chapter 2, VII).

d.Traumatic arteriovenous fistulas may result from penetrating trauma. Large fistulas are best treated by arterial embolization.

e.Hemobilia is due to arteriobiliary fistula formation.

1.Patients present late (more than 1 month after injury) with gastrointestinal bleeding (hematemesis or melena), jaundice, biliary colic, or fever.

2.Diagnosis and treatment are via arteriography and embolization.

IIPortal Hypertension

A Anatomy

(see I A 2 b; Fig. 14-2)

B Pathophysiology

Portal hypertension is an abnormal elevation in portal venous pressure (normal is 5–6 mm Hg).

1.The increase in pressure stimulates the development of venous collaterals, which attempt to decompress the portal system into the systemic venous system.

2.The collateral veins are very fragile. They form portosystemic connections between the portal system and the inferior vena cava or the superior vena cava via the azygos system.

3.When portal pressure exceeds 20 mm Hg, dilated veins or varices are likely to develop. When the varices form in a submucosal location, such as at the gastroesophageal junction, they are subject to rupture and hemorrhage.

CEtiology

1.Intrahepatic causes are most common.

a.Cirrhosis causes 85% of portal hypertension in the United States. The most common etiology of cirrhosis is alcohol abuse, followed by hepatitis C.

1.Pathologically, cirrhosis produces:

a.Progressive narrowing of sinusoidal and postsinusoidal vessels due to centrilobular collagen deposition

b.Distortion of the sinusoidal anatomy by cirrhotic regenerative nodules

2.The resultant sinusoidal block increases resistance to portal blood flow through the liver and increases portal pressure.

b.Schistosomiasis is a common cause worldwide. Portal hypertension develops when parasitic ova in small portal venules cause a presinusoidal block.

c.Wilson's disease, hepatic fibrosis, and hemochromatosis are occasional causes of portal hypertension.

2.Prehepatic causes of portal hypertension are rare but are more common in children. Examples of prehepatic causes are portal vein obstruction due to either thrombosis, congenital atresia, or stenosis caused by extrinsic compression,

such as occurs with tumors.

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3.Posthepatic causes of portal hypertension are also rare.

a.Budd-Chiari syndrome is characterized by hepatic vein thrombosis, which causes a postsinusoidal block with resultant hepatomegaly and ascites. This syndrome may be idiopathic or due to a hypercoagulable state as occurs with tumors, hematologic disorders, oral contraceptive use, and trauma. In Asia, inferior vena caval webs are the most common cause of hepatic vein obstruction. Oddly, this syndrome is not uncommon after bone marrow transplantation.

b.Constrictive pericarditis produces a markedly elevated inferior vena cava pressure, resulting in resistance to hepatic venous outflow. It should be suspected when calcification of the pericardium is present.

4.Increased portal venous flow may result in portal hypertension. This is due to primary splenic disease and splenic arteriovenous fistulas or shunts.

5.Splenic vein thrombosis may cause left-sided portal hypertension, resulting in varices confined to the gastric fundus. This is usually due to pancreatitis or a pancreatic tumor (see II K 2 c).

D Clinical presentation

The following are common findings in portal hypertension:

1.Encephalopathy

a.This is secondary to portosystemic collaterals (with shunting of portal blood around the liver) and hepatic insufficiency.

b.It may be related to elevated serum levels of ammonia in some patients, but the correlation is unreliable.

2.Gastrointestinal hemorrhage, frequently from gastroesophageal varices and complicated by impaired coagulation

3.Malnutrition, particularly in alcoholic cirrhosis

4.Ascites (see II L) secondary to hepatic sinusoidal hypertension, hypoalbuminemia, and hyperaldosteronism

5.Other manifestations of collateral venous development, such as a periumbilical caput medusae or hemorrhoids

6.Splenomegaly, which may be associated with hypersplenism (see II K)

E Medical management of acute variceal hemorrhage

Variceal hemorrhage is life threatening and is the principal complication of portal hypertension that requires emergency intervention.

1.The management of acute upper gastrointestinal (UGI) hemorrhage is described in Chapter 9, III F.

2.Gastroesophagoscopy should be performed as soon as possible to find the site of bleeding and determine the presence of varices.

a.The cause of an UGI hemorrhage in cirrhotic patients is varices in 20%–50%, erosive gastritis in 20%–60%, peptic ulcer disease in 6%–19%, and esophageal tears (Mallory-Weiss syndrome) in 5%–18%.

b.Up to 8% of patients have two bleeding sites.

3.Measures for controlling acute variceal bleeding (Fig. 14-4) include the following:

a.Variceal banding with small rubber bands is the treatment of choice for bleeding varices. This procedure is performed endoscopically. It is at least as effective as sclerotherapy and is safer (Fig. 14-5).

b.Injection sclerotherapy

1.Injection of a sclerosing agent is currently the preferred method of managing acute variceal bleeding. The injection into a varix results in thrombosis of the vein.

2.The procedure is done endoscopically and controls bleeding temporarily in 80%–90% of patients; it is associated with a mortality rate of 1%–2%.

3.Injection sclerotherapy has a complication rate of approximately 20%–40%, which includes esophageal perforation, worsening of hemorrhage, and more minor complications such as esophageal ulceration, fever, retrosternal chest pain, and pleural effusions.

c.Pharmacotherapy

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FIGURE 14-4 Treatment plan for acute variceal hemorrhage.

1.Vasopressin and nitroglycerin

a.Vasopressin, a potent vasoconstrictor, lowers portal pressure by splanchnic vasoconstriction, which results in diminished mesenteric blood flow. Vasopressin is useful only for short-term hemorrhage control; it does not improve patient survival rates.

b.Nitroglycerin lowers portal pressure independently and helps to counteract some of the systemic side effects of vasopressin (e.g., myocardial ischemia, limb ischemia, and bowel necrosis).