(Radiographics. 2000;20:687-698.)
© RSNA, 2000
Diseases of the Hepatopulmonary Axis1
Cris A. Meyer, MD,
Charles S. White, MD and
Kenneth E. Sherman, MD, PhD
1 From the Departments of Radiology (C.A.M.) and Medicine (K.E.S.), University of Cincinnati, 234 Goodman St, ML 0742, Cincinnati, OH 45219-2316; and the Department of Radiology, University of Maryland Medical Center, Baltimore (C.S.W.). Received May 18, 1999; revision requested July 26 and received August 31; accepted September 7. Address reprint requests to C.A.M. (e-mail: meyerca@healthall.com).
 |
Abstract
|
|---|
Hepatopulmonary syndrome is the most widely recognized of the processes associated with end-stage liver disease. Chronic liver dysfunction is associated with pulmonary manifestations due to alterations in the production or clearance of circulating cytokines and other mediators. Hepatopulmonary syndrome results in hypoxemia due to pulmonary vasodilatation with significant arteriovenous shunting and ventilation-perfusion mismatch. Hepatic hydrothorax may develop in patients with cirrhosis and ascites. Rarely, pulmonary hypertension occurs in the setting of portal hypertension. A second group of disorders may primarily affect the lungs and liver (the hepatopulmonary axis). Among these are the congenital conditions 
1-antitrypsin deficiency and cystic fibrosis. Autoimmune liver disease may be associated with lymphocytic interstitial pneumonitis, fibrosing alveolitis, intrapulmonary granulomas, and bronchiolitis obliterans with organizing pneumonia. Sarcoidosis affects the lung and liver in up to 70% of patients. Medications such as amiodarone can result in a characteristic radiologic appearance of pulmonary and hepatic toxic effects. Knowledge of these associations will assist the radiologist in forming a meaningful differential diagnosis and may influence treatment decisions.
Index Terms: Alpha-1-antitrypsin deficiency, 60.7511, 761.69 • Drugs, toxicity, 60.6462, 761.64 • Fibrosis, cystic, 60.252, 761.1496 • Hydrothorax, 60.76 • Hypertension, pulmonary, 564.78 • Liver, cirrhosis, 761.288 • Sarcoidosis, 60.22, 761.22 • Shunts, portosystemic, 94.4539, 94.711 • Telangiectasia, 60.1494
|
Introduction
|
|---|
Pulmonary complications may occur as a result of end-stage liver disease from any cause. These are likely a manifestation of decreased hepatic clearance or increased hepatic production of circulating cytokines and other vascular growth mediators (1). Many circulating factors have been implicated in liver-lung interactions in disease states. These factors are summarized in the Table (2). Mechanical factors may also result in hepatopulmonary complications. For example, translocation of ascites into the pleural space results in hepatic hydrothorax. Relief of portal hypertension occurs through spontaneous intrathoracic portosystemic shunts with some collateral pathways occurring in the chest. Finally, there are congenital disorders, inflammatory processes, and exogenous toxins that primarily affect the liver and the lung.
In this article, we review pulmonary complications of chronic liver disease and specific disorders with hepatic and pulmonary manifestations. The pathophysiologic mechanisms and radiologic manifestations of these entities are discussed.
|
Pulmonary Complications of Chronic Liver Disease
|
|---|
Hepatopulmonary Syndrome
The diagnosis of hepatopulmonary syndrome is established with the following three criteria: chronic liver disease, increased alveolar-arterial gradient on room air, and evidence of intrapulmonary vascular dilatation. Hypoxemia is seen in one-third of decompensated cirrhotic patients (1). The most important mechanism is pulmonary vascular dilatation and consequent ventilation-perfusion mismatch. It is more accurate to describe the intrapulmonary process associated with these vascular dilatations as a diffusion-perfusion abnormality rather than as an intrapulmonary shunt (3). Hypoxia is believed to result from an inability of oxygen to diffuse to the center of massively dilated peripheral vessels. These vessels, which are normally 8–15 mm in diameter, have been demonstrated to dilate to 15–500 mm (4,5). As shown in the Table, the serum concentrations of many circulating mediators are elevated in cirrhotic patients and such elevations are known to cause pulmonary vasodilatation. Because the principal vasoactive substance has not been identified, no effective pharmacologic intervention is available, and treatment consists of supplemental oxygen therapy or liver transplantation (6).
The presence of intrapulmonary vascular dilatation can be established with imaging. Chest radiographs demonstrate basilar nodular or reticulonodular areas of increased opacity in 5%–13.8% of patients with chronic liver disease and 46%–100% of patients with hepatopulmonary syndrome (7). Lung volumes are preserved. Intrapulmonary arteriovenous shunting can be established with contrast (microbubble) echocardiography, technetium-99m macroaggregated albumin imaging (Fig 1), right-sided heart catheterization, or pulmonary arteriography. Computed tomography (CT) may demonstrate dilated vessels with an increased number of terminal branches extending to the pleura and can be useful in distinguishing hepatopulmonary syndrome from other causes of hypoxemia such as pulmonary fibrosis (Fig 2).
View larger version (35K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1. Intrapulmonary arteriovenous shunt in a 30-year-old man with cirrhosis and dyspnea. Posterior whole-body image obtained after injection of Tc-99m macroaggregated albumin into the venous circulation shows activity in the brain. The presence of radiotracer on the left side of the circulation confirms that there is a right-to-left shunt bypassing the normal filtering mechanism of the pulmonary capillary beds.
|
|
View larger version (113K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2. Hepatopulmonary syndrome diagnosed with contrast (microbubble) echocardiography in a 48-year-old man with end-stage alcoholic liver disease and hypoxia. Chest CT scan (lung window) shows dilated peripheral pulmonary arterioles (arrow). Note the gynecomastia, which is another manifestation of chronic liver disease.
|
|
Hepatic Hydrothorax
Hepatic hydrothorax is defined as the presence of a large pleural effusion in a cirrhotic patient in the absence of primary pulmonary or cardiac disease (Fig 3). Up to 10% of patients with significant liver disease develop pleural effusions (8). The pressure gradient favors the movement of fluid from the peritoneal cavity to the pleural space through small diaphragmatic defects; for this reason, hydrothorax may be present even in the absence of clinical ascites. Pleural fluid is right sided in 67% of cases, bilateral in 17%, and left sided in 17% (8). Treatment is directed at decreasing the formation of ascitic fluid or obliterating the connections between the peritoneum and the pleural space or pleurodesis. Transjugular intrahepatic portosystemic shunts may be effective in some cases. Spontaneous bacterial empyema has been reported and is presumably due to portosystemic shunting and the impaired reticuloendothelial system inherent in cirrhotic patients (9).
View larger version (114K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 3a. Right-sided hepatic hydrothorax in a 55-year-old woman with primary biliary cirrhosis. Posteroanterior (a) and lateral (b) chest radiographs show blunting of the right costophrenic angle, a finding compatible with effusion.
|
|
View larger version (134K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 3b. Right-sided hepatic hydrothorax in a 55-year-old woman with primary biliary cirrhosis. Posteroanterior (a) and lateral (b) chest radiographs show blunting of the right costophrenic angle, a finding compatible with effusion.
|
|
Pulmonary Hypertension
McDonnell et al (10) reviewed the results of 17,901 autopsies and found that primary pulmonary hypertension occurred in 0.13% of all patients but in 0.73% of patients with cirrhosis. The association occurs almost exclusively in patients with portal hypertension (Fig 4). Causes of pulmonary hypertension may be thromboembolic or plexogenic. It is suggested that a portal venous thrombus may reach the lung through spontaneous or surgically created portosystemic shunts. Plexogenic pulmonary hypertension may result from vasoactive substances such as serotonin, thromboxane, neuropeptide Y, or elastase. It is hypothesized that these substances bypass the liver through portosystemic shunts or are not cleared as effectively by the diseased liver (1). The mean survival of patients with portal hypertension and pulmonary hypertension is 15 months (11). Patients with portal and pulmonary hypertension have high perioperative mortality rates, although improvement after liver or liver-lung transplantation has been reported (11,12).
View larger version (109K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 4a. Plexogenic pulmonary hypertension in a 38-year-old woman with primary biliary cirrhosis and end-stage liver disease. (a) Posteroanterior chest radiograph shows enlarged central pulmonary arteries. (b) Coronal T1-weighted fast spoiled gradient-echo magnetic resonance (MR) image shows a cirrhotic liver with splenomegaly, periesophageal varices (arrow), and an enlarged right pulmonary artery (arrowheads).
|
|
View larger version (158K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 4b. Plexogenic pulmonary hypertension in a 38-year-old woman with primary biliary cirrhosis and end-stage liver disease. (a) Posteroanterior chest radiograph shows enlarged central pulmonary arteries. (b) Coronal T1-weighted fast spoiled gradient-echo magnetic resonance (MR) image shows a cirrhotic liver with splenomegaly, periesophageal varices (arrow), and an enlarged right pulmonary artery (arrowheads).
|
|
Respiratory Failure Associated with Fulminant Hepatic Failure
Massive necrosis of the liver from any cause may be associated with acute hypoxic respiratory failure, necessitating ventilatory support (Fig 5). The cause of this association remains unclear but may be related to intrapulmonary vasodilatation or noncardiogenic pulmonary edema (12). Autopsy series have shown vascular dilatation significant enough to result in calculated shunts of up to 39% (13). Noncardiogenic pulmonary edema was seen in 37% of patients with fulminant hepatic failure and had an 81% mortality rate. The mechanism of noncardiogenic pulmonary edema is not well established; it may be related to an imbalance in the level of an Na + ,K + -adenosinetriphosphatase inhibitor, which is elevated in the serum of patients with fulminant hepatic failure. Liver transplantation has resulted in a 1-year survival rate of 55%, which is in marked contrast to the 15% survival rate achieved with standard medical therapy (14).
View larger version (124K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 5. Pulmonary edema in a 32-year-old man with primary sclerosing cholangitis who developed fulminant hepatic failure secondary to hepatitis B. Anteroposterior chest radiograph shows diffuse noncardiogenic pulmonary edema. The patient underwent intubation for respiratory failure. After clearing of the hepatitis B infection, the patient underwent liver transplantation and recovered uneventfully, with resolution of the radiographic findings.
|
|
Chest Manifestations of Portosystemic Shunts
Collateral vascular pathways develop in patients with portal hypertension to allow decompression of the portal vein into the systemic circulation. Intrathoracic manifestations of these spontaneous portosystemic collateral vessels characteristically develop by way of the coronary vein into esophageal or paraesophageal varices. The esophageal varices drain along normal intrinsic esophageal venous channels, whereas the paraesophageal (preaortic esophageal) veins drain into the hemiazygos system (15). On chest radiographs, varices may manifest as focal lateral displacement of the inferior azygoesophageal interface at the level of the gastroesophageal junction (Fig 6). A more unusual manifestation of portosystemic collateral vessels in the chest is varicosity of the left pericardiophrenic vein, resulting in nodularity along the left cardiac border. This collateral pathway is seen when the left portal vein drains into the inferior phrenic vein, the pericardiophrenic vein, and ultimately the systemic venous system via the azygos or supreme intercostal vein (16).
View larger version (156K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 6a. Esophageal varices in a 57-year-old man with cirrhosis and severe portal hypertension. (a) Posteroanterior chest radiograph shows widening of the right paraspinal interface. (b) Contrast material-enhanced chest CT scan shows multiple enhancing periesophageal tubular structures compatible with varices. (Courtesy of H. Page McAdams, MD, Duke University Medical Center, Durham, NC.)
|
|
View larger version (129K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 6b. Esophageal varices in a 57-year-old man with cirrhosis and severe portal hypertension. (a) Posteroanterior chest radiograph shows widening of the right paraspinal interface. (b) Contrast material-enhanced chest CT scan shows multiple enhancing periesophageal tubular structures compatible with varices. (Courtesy of H. Page McAdams, MD, Duke University Medical Center, Durham, NC.)
|
|
Of the surgically performed portosystemic shunts, the one that is visible at chest radiography is splenopneumopexy. In this rarely performed procedure, the diaphragmatic surface of the left lower lobe and the superior surface of the spleen are abraded and approximated through a surgically created diaphragmatic defect (17). This process permits decompression of the portal system into the pulmonary veins. The amount of decompression varies according to the portal pressure. Radiographs of this procedure demonstrate an indistinct diaphragmatic contour and enlarged pulmonary veins in the left lower lobe (Fig 7).
View larger version (111K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 7a. Enlarged pulmonary veins in a 36-year-old woman with protein C deficiency who underwent splenopneumopexy for portal hypertension. (a) Posteroanterior chest radiograph shows enlarged pulmonary vessels in the left lower lobe (arrow). (b) CT scan (lung window) obtained just above the diaphragm shows multiple tortuous vascular structures in the left lower lobe, which are engorged pulmonary veins due to the surgically created portosystemic shunt.
|
|
View larger version (110K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 7b. Enlarged pulmonary veins in a 36-year-old woman with protein C deficiency who underwent splenopneumopexy for portal hypertension. (a) Posteroanterior chest radiograph shows enlarged pulmonary vessels in the left lower lobe (arrow). (b) CT scan (lung window) obtained just above the diaphragm shows multiple tortuous vascular structures in the left lower lobe, which are engorged pulmonary veins due to the surgically created portosystemic shunt.
|
|
|
Specific Disorders with Hepatic and Pulmonary Manifestations
|
|---|
There are also disease processes that can primarily affect the liver and lung. These include congenital disorders such as 1-antitrypsin deficiency, cystic fibrosis, and hereditary hemorrhagic telangiectasia; inflammatory processes such as primary biliary cirrhosis and sarcoidosis; and reactions to exogenous toxins such as drugs.
1-Antitrypsin Deficiency
1-Antitrypsin deficiency is the most common metabolic liver disease in children (18). Over 90% of the 1-antitrypsin protein is produced in hepatocytes by codominant gene expression on chromosome 14. There are over 100 known genetic variants of the protein (19). The most severe hepatopulmonary manifestations result from the homozygous PiZZ phenotype. The 1-antitrypsin protein inhibits neutrophil elastase; in patients with severe deficiency, the neutrophil elastase acts unopposed. The unopposed elastase is damaging to the lower respiratory tract and the lung bases, which are more seriously affected due to gravitational distribution of pulmonary blood flow.
The classic presentation of the disease is dyspnea in the 4th or 5th decade of life, although up to 20% of homozygous 1-antitrypsin–deficient individuals never develop clinically apparent emphysema. Hepatic manifestations of this disease are those of cirrhosis with the concomitant increased risk of hepatocellular carcinoma. Chest imaging findings include panacinar emphysema, bronchiectasis (Fig 8), and hepatopulmonary syndrome (1,19). Survival is substantially worse in smokers, who have a 15–20-year decrease in longevity relative to nonsmokers (20).
View larger version (140K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 8a. Emphysema and bronchiectasis in a 52-year-old woman with 1-antitrypsin deficiency. (a) Posteroanterior chest radiograph shows findings consistent with diffuse emphysema. (b) High-resolution CT scan (lung window) shows basilar predominant panlobular emphysema and fusiform bronchiectasis (arrow).
|
|
View larger version (73K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 8b. Emphysema and bronchiectasis in a 52-year-old woman with 1-antitrypsin deficiency. (a) Posteroanterior chest radiograph shows findings consistent with diffuse emphysema. (b) High-resolution CT scan (lung window) shows basilar predominant panlobular emphysema and fusiform bronchiectasis (arrow).
|
|
Cystic Fibrosis
Cystic fibrosis is the most common lethal inherited disorder in the white population. The disease has an autosomal recessive inheritance pattern and an overall gene frequency in the U.S. population of one in 25. The overall defect is in transmembrane conduction of chloride by the cystic fibrosis transmembrane regulator (21). Viscous secretions obstruct the lower respiratory tract and peripheral airways, and superinfection, particularly by Pseudomonas species, results in progressive parenchymal destruction and bronchiectasis (Fig 9). Liver disease is a minor contributor to the overall morbidity from cystic fibrosis. Hepatic abnormalities include diffuse fatty infiltration, which may be the initial manifestation in infants. Up to 40% of cystic fibrosis patients have focal biliary cirrhosis, and 5%–12% develop multilobular biliary cirrhosis (22). The latter group may progress to portal hypertension with varices and splenomegaly.
View larger version (132K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 9a. Bronchiectasis and biliary cirrhosis in a 17-year-old boy with cystic fibrosis. (a) Posteroanterior chest radiograph shows irregular tubular and nodular markings, findings consistent with bronchiectasis and enlarged pulmonary arteries. (b) Contrast-enhanced abdominal CT scan shows a nodular contour of the liver with adjacent gastric varices (arrow), findings consistent with multilobular biliary cirrhosis. (c) Contrast-enhanced abdominal CT scan shows small-bowel fold thickening (arrowhead) and fatty atrophy of the pancreas (arrow).
|
|
View larger version (142K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 9b. Bronchiectasis and biliary cirrhosis in a 17-year-old boy with cystic fibrosis. (a) Posteroanterior chest radiograph shows irregular tubular and nodular markings, findings consistent with bronchiectasis and enlarged pulmonary arteries. (b) Contrast-enhanced abdominal CT scan shows a nodular contour of the liver with adjacent gastric varices (arrow), findings consistent with multilobular biliary cirrhosis. (c) Contrast-enhanced abdominal CT scan shows small-bowel fold thickening (arrowhead) and fatty atrophy of the pancreas (arrow).
|
|
View larger version (143K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 9c. Bronchiectasis and biliary cirrhosis in a 17-year-old boy with cystic fibrosis. (a) Posteroanterior chest radiograph shows irregular tubular and nodular markings, findings consistent with bronchiectasis and enlarged pulmonary arteries. (b) Contrast-enhanced abdominal CT scan shows a nodular contour of the liver with adjacent gastric varices (arrow), findings consistent with multilobular biliary cirrhosis. (c) Contrast-enhanced abdominal CT scan shows small-bowel fold thickening (arrowhead) and fatty atrophy of the pancreas (arrow).
|
|
Hereditary Hemorrhagic Telangiectasia
Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease) is a group of autosomal dominant inherited disorders that result in a range of vascular abnormalities. In one form, the disease is caused by a gene that encodes transforming growth factor binding protein (23). Vascular abnormalities of the mucous membranes, skin, lung, brain, and gastrointestinal tract characterize this disorder. Up to 60% of patients with pulmonary arteriovenous malformations have hereditary hemorrhagic telangiectasia, and 5%–15% of patients with hereditary hemorrhagic telangiectasia have pulmonary arteriovenous malformations (23). These are well demonstrated at helical CT as tortuous tubular lesions with feeding arteries and draining veins (Fig 10) (24,25). The liver is affected in 8%–31% of patients. Multiple hepatic vascular malformations are well demonstrated with color Doppler ultrasonography, CT, MR imaging, or angiography (Fig 11) (26).
View larger version (122K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 10a. Pulmonary arteriovenous malformation in a 33-year-old woman with orthodeoxia. (a) Posteroanterior chest radiograph shows bibasilar well-defined nodules (arrows). (b) CT scan (lung window) shows the feeding artery and large draining vein of a pulmonary arteriovenous malformation.
|
|
View larger version (80K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 10b. Pulmonary arteriovenous malformation in a 33-year-old woman with orthodeoxia. (a) Posteroanterior chest radiograph shows bibasilar well-defined nodules (arrows). (b) CT scan (lung window) shows the feeding artery and large draining vein of a pulmonary arteriovenous malformation.
|
|
View larger version (164K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 11. Hepatic telangiectases in a 79-year-old patient with hereditary hemorrhagic telangiectasia. Contrast-enhanced abdominal CT scan shows multiple intrahepatic telangiectases.
|
|
Inflammatory or Autoimmune Diseases
Primary biliary cirrhosis is a chronic granulomatous inflammatory process of the hepatic bile ducts that causes cholestasis. Associated autoimmune disorders include rheumatoid arthritis, Hashimoto thyroiditis, Sjögren syndrome, scleroderma, and sarcoidosis. There is a clear association between primary biliary cirrhosis and Sjögren syndrome: 66%–100% of patients with primary biliary cirrhosis have signs of the sicca complex, whereas 6% of patients with Sjögren syndrome have mitochondrial antibodies (27). The pulmonary manifestations reported include lymphocytic interstitial pneumonitis, usual interstitial pneumonitis, intrapulmonary granulomas, bronchiolitis obliterans with organizing pneumonia, obstructive airways disease, pulmonary hypertension, hepatopulmonary syndrome, and pulmonary hemorrhage (18).
Sarcoidosis is a systemic granulomatous disease of unknown origin. The chest manifestations are well known and include bulky mediastinal adenopathy, parenchymal granulomas, fibrosis, and honeycomb lung. Although autopsy series report liver granulomas in up to 70% of patients, CT detection of hepatic lesions and splenic lesions is considerably less common, occurring in 5% and 15% of cases, respectively (28). Patterns of involvement described include diffuse organomegaly or a nodular pattern of organ involvement (Fig 12). Abdominal adenopathy may be seen in up to 10% of patients (29). Abdominal involvement appears to be unrelated to chest radiographic stage or disease duration but does correlate with serum levels of angiotensin-converting enzyme (29,30).
View larger version (78K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 12a. Nodular organ involvement in a 38-year-old woman with sarcoidosis. (a) CT scan (lung window) obtained at the level of the right upper lobe bronchus shows multiple pulmonary nodules and peribronchovascular nodular thickening. (b) Contrast-enhanced CT scan of the upper abdomen shows multiple hypoattenuating nodules in the liver and spleen secondary to sarcoidosis.
|
|
View larger version (108K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 12b. Nodular organ involvement in a 38-year-old woman with sarcoidosis. (a) CT scan (lung window) obtained at the level of the right upper lobe bronchus shows multiple pulmonary nodules and peribronchovascular nodular thickening. (b) Contrast-enhanced CT scan of the upper abdomen shows multiple hypoattenuating nodules in the liver and spleen secondary to sarcoidosis.
|
|
Drug Reactions
Many drugs are known to have toxic effects on the lung and liver. Among them are methotrexate, phenytoin, and amiodarone. Amiodarone is a triiodinated benzofuran used as an antiarrhythmic with characteristic radiologic findings in the lung and liver (Fig 13). Amiodarone toxicity is dose related. The acute presentation is characterized by high-opacity areas of consolidation, whereas the chronic variety more frequently manifests as diffuse interstitial infiltrates (31). Alveolar macrophages contain abnormal cytoplasmic inclusions due to abnormal phospholipid storage in pneumocyte lysosomes. Hepatic phospholipidosis can develop; it is similar to alcoholic hepatitis at histopathologic analysis and is characterized by Mallory bodies, steatosis, and cellular fibrosis (32). CT of the liver reveals increased attenuation relative to that of the spleen; normally, the liver has slightly higher attenuation than the spleen. The predominant hepatocyte uptake helps distinguish amiodarone liver from other causes of increased attenuation of the liver and spleen that have a more even distribution in the reticuloendothelial system (eg, thorium dioxide [Thorotrast] or hemochromatosis).
View larger version (106K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 13a. Drug reaction in a 68-year-old woman receiving amiodarone for dilated cardiomyopathy and severe arrhythmias. (a) Anteroposterior chest radiograph shows multifocal peripheral consolidations of high opacity. (b) Chest CT scan (mediastinal window) shows a hyperattenuating peripheral consolidation in the right upper lobe. (c) Nonenhanced abdominal CT scan shows high attenuation of the liver (78 HU) relative to that of the spleen (44 HU).
|
|
View larger version (139K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 13b. Drug reaction in a 68-year-old woman receiving amiodarone for dilated cardiomyopathy and severe arrhythmias. (a) Anteroposterior chest radiograph shows multifocal peripheral consolidations of high opacity. (b) Chest CT scan (mediastinal window) shows a hyperattenuating peripheral consolidation in the right upper lobe. (c) Nonenhanced abdominal CT scan shows high attenuation of the liver (78 HU) relative to that of the spleen (44 HU).
|
|
View larger version (168K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 13c. Drug reaction in a 68-year-old woman receiving amiodarone for dilated cardiomyopathy and severe arrhythmias. (a) Anteroposterior chest radiograph shows multifocal peripheral consolidations of high opacity. (b) Chest CT scan (mediastinal window) shows a hyperattenuating peripheral consolidation in the right upper lobe. (c) Nonenhanced abdominal CT scan shows high attenuation of the liver (78 HU) relative to that of the spleen (44 HU).
|
|
|
Conclusions
|
|---|
Thoracic manifestations of chronic liver disease may be visible on conventional chest radiographs and thoracic CT scans. These manifestations include hepatopulmonary syndrome, hepatic hydrothorax, pulmonary hypertension, and varices. There are also disease processes that can primarily affect the liver and lung, including congenital disorders, inflammatory processes, and drug reactions. Knowledge of the spectrum of diseases involving the hepatopulmonary axis assists the radiologist in forming a meaningful differential diagnosis.
|
References
|
|---|
-
King PD, Rumbaut R, Sanchez C. Pulmonary manifestations of chronic liver disease. Dig Dis 1996; 14:73-82.[Medline]
-
Panos RJ, Baker SK. Mediators, cytokines, and growth factors in liver-lung interactions. Clin Chest Med 1996; 17:151-169.[Medline]
-
Krowka MJ, Cortese DA. Hepatopulmonary syndrome: current concepts in diagnostic and therapeutic considerations. Chest 1994; 105:1528-1537.[Free Full Text]
-
Castro M, Krowka MJ. Hepatopulmonary syndrome: a pulmonary vascular complication of liver disease. Clin Chest Med 1996; 17:35-48.[Medline]
-
Rodriguez-Roisin R, Agusti A, Roca J. The hepatopulmonary syndrome: new name, old complexities. Thorax 1992; 47:897-902.[Abstract]
-
Lange PA, Stoller JK. The hepatopulmonary syndrome. Ann Intern Med 1995; 122:521-529.[Abstract/Free Full Text]
-
McAdams HP, Erasmus J, Crockett R, Mitchell J, Godwin JD, McDermott VG. The hepatopulmonary syndrome: radiologic findings in 10 patients. AJR Am J Roentgenol 1996; 166:1379-1385.[Abstract/Free Full Text]
-
Alberts WM, Salem AJ, Solomon DA, Boyce G. Hepatic hydrothorax: cause and management. Arch Intern Med 1991; 151:2383-2386.[Abstract]
-
Xiol X, Castellote J, Baliellas C, et al. Spontaneous bacterial empyema in cirrhotic patients: analysis of 11 cases. Hepatology 1990; 11:365-370.[Medline]
-
McDonnell PJ, Toye PA, Hutchins GM. Primary pulmonary hypertension and cirrhosis: are they related?. Am Rev Respir Dis 1983; 127:437-441.[Medline]
-
Mandell MS, Groves BM. Pulmonary hypertension in chronic liver disease. Clin Chest Med 1996; 17:17-33.[Medline]
-
Krowka MJ, Cortese DA. Pulmonary aspects of liver disease and liver transplantation. Clin Chest Med 1989; 10:593-616.[Medline]
-
Williams A, Trewby P, Williams R, Reid L. Structural alterations to the pulmonary circulation in fulminant hepatic failure. Thorax 1979; 34:447-453.[Abstract]
-
Peleman RR, Gavaler JS, Van Thiel DH. Orthotopic liver transplantation for acute and subacute hepatic failure in adults. Hepatology 1987; 7:484-489.[Medline]
-
Ibukuro K, Tsukiyama T, Mori K, Inoue Y. Preaortic esophageal veins: CT appearance. AJR Am J Roentgenol 1998; 170:1535-1538.[Abstract/Free Full Text]
-
Minami M, Kawauchi N, Itai Y, Kokubo T, Sadaki Y. Transdiaphragmatic portosystemic shunt to the pericardiophrenic vein. AJR Am J Roentgenol 1993; 161:569-571.[Free Full Text]
-
Sakoda K, Ono J, Kawada T, Katsuki T, Akita H. Portopulmonary shunt by splenopneumopexy for portal hypertension in children. J Pediatr Surg 1998; 23:323-327.
-
Krowka MJ. Recent pulmonary observations in 1-antitrypsin deficiency, primary biliary cirrhosis, chronic hepatitis C, and other hepatic problems. Clin Chest Med 1996; 17:67-82.[Medline]
-
King MA, Stone JA, Diaz PT, Mueller CF, Becker WJ, Gadek JE. 1-antitrypsin deficiency: evaluation of bronchiectasis with CT. Radiology 1996; 199:137-141.[Abstract/Free Full Text]
-
American Thoracic Society. Guidelines for the approach to the patient with severe hereditary 1-antitrypsin deficiency. Am Rev Respir Dis 1989; 140:1494-1497.[Medline]
-
Ruzal-Shapiro C. Cystic fibrosis. Radiol Clin North Am 1998; 36:143-161.[Medline]
-
Agrons GA, Corse WR, Markowitz RI, Suarez ES, Perry DR. Gastrointestinal manifestations of cystic fibrosis: radiologic-pathologic correlation. RadioGraphics 1996; 16:871-893.[Abstract]
-
Guttmacher AE, Marchuk DA, White RI. Hereditary hemorrhagic telangiectasia. N Engl J Med 1995; 333:918-924.[Free Full Text]
-
Remy J, Remy-Jardin M, Giraud F, Wattinne L. Angioarchitecture of pulmonary arteriovenous malformations: clinical utility of three-dimensional helical CT. Radiology 1994; 191:657-664.[Abstract/Free Full Text]
-
Remy J, Remy-Jardin M, Wattinne L, Deffontaines C. Pulmonary arteriovenous malformations: evaluation with CT of the chest before and after treatment. Radiology 1992; 182:809-816.[Abstract/Free Full Text]
-
Buscarini E, Buscarini L, Civardi G, Arruzzoli S, Bossalini G, Piantianida M. Hepatic vascular malformations in hereditary hemorrhagic telangiectasia: imaging findings. AJR Am J Roentgenol 1994; 163:1105-1110.[Abstract/Free Full Text]
-
Wallace JG, Tong MJ, Ueki BN, Quismorio FP. Pulmonary involvement in primary biliary cirrhosis. J Clin Gastroenterol 1987; 9:431-435.[Medline]
-
Scott GC, Berman JM, Higgins JL. CT patterns of nodular hepatic and splenic sarcoidosis: a review of the literature. J Comput Assist Tomogr 1997; 21:369-372.[Medline]
-
Warshauer DM, Dumbleton SA, Molina PL, Yankaskas BC, Parker LA, Woosley JT. Abdominal CT findings in sarcoidosis: radiologic and clinical correlation. Radiology 1994; 192:93-98.[Abstract/Free Full Text]
-
Britt AR, Francis IR, Glazer GM, Ellis JH. Sarcoidosis: abdominal manifestations at CT. Radiology 1991; 178:91-94.[Abstract/Free Full Text]
-
Jones WP, Shin MS, Stanley RJ, et al. Dense liver in a 72-year-old woman with congestive heart failure. Invest Radiol 1985; 20:911-915.[Medline]
-
Gefter WB, Aronchick JM, Miller WT, Jr, Pietra GG, Hatabu H, Miller WT. Drug-induced chest disorders. In: Greene R, Muhm JR, eds. Syllabus: a diagnostic categorical course in chest radiology. Oak Brook, Ill: Radiological Society of North America, 1992; 167-180.
Top
Abstract
Introduction
