Recognition of Splenic Vein Occlusion

Transcription

1 Recognition of Splenic Vein Occlusion KYUNG J. CHO1 AND WILLIAM MARTEL1 Radlologic findings and medical records of 27 patients with angiographic documentation of splenic vein occlusion were reviewed. The most common causes were pancreatic cardnoma, pancreatitis, and malignant lymphoma. Radiographic findings which suggest splenic vein occlusion are gastric varices without esophageal varlces and collateral veins In the left upper abdomen during the vascular phase of rapid sequence pyelography. Additional features may be associated with the underlying disease, such as pancreatic calcification and upper abdominal mass lesions. The diagnosis is usually confirmed by high dose cellac or splenic angiography. Examination of the stomach with barium for the detection of gastric varlces is more sensitive than has been previously recognized; features which suggest them are described. Isolated gastric varices may be a clue to isolated splenlc vein occluslon and its underlying causes. Splenic vein occlusion is more common than generally appreciated and usually secondary to pancreatic inflammation or neoplasm [1-3]. This condition is commonly silent clinically but may cause hypersplenism or gastrointestinal hemorrhage due to gastric varices [4, 5]. This form of localized venous hypertension can be controlled by splenectomy. Gastric varices without esophageal varices are associated with splenic vein obstruction, but their recognition by barium studies, in the absence of esophageal varices, can be difficult [6, 7]. This explains why the diagnosis of spienic vein occlusion is rarely made prior to angiography. This study was undertaken to determine whether splenic vein obstruction might be recognized more frequently by simple methods. MaterIals and Methods We reviewed the radiographic findings and medical records of 27 patients at University of Michigan Medical Center from 1970 to 1976 who had splenic vein occlusion diagnosed by celiac, superior mesenteric, or splenic arteriography. Splenoportography was performed in only one patient for the diagnosis. Of the 27 patients, 18 had isolated splenic vein occlusion and nine had additional thrombosis of the superior mesenteric vein. The 15 men and 12 women ranged in age from 20 to 79 years (average, 50 years). The causes of splenic vein occlusion were pancreatic carcinoma, pancreatitis with or without pseudocyst, peripancreatic lymphoma, and unconfirmed (15, seven, one, and four cases, respectively). Clinical symptoms included epigastric or back pain, nausea, vomiting, and weight loss. Three patients had upper gastrointestinal hemorrhage thought to be secondary to gastric varices. Endoscopy was performed in five of the 27 patients. Of these five patients who had gastric varices demonstrated by arteriography, gastric varices were recognized by endoscopy in two. One of these patients had additional esophageal varices which were also evident on esophagogram. Radiographic studies, including gastrointestinal barium examinations, plain abdominal films, and rapid sequence excretory urograms (available in four patients), were reviewed. Special attention was given to the examination of the stomach. In 19 of 27 patients the gastrointestinal examinations with barium were judged adequate for evaluation of gastric varices. Barium studies were not performed in five cases and were madequate in three others. The barium examinations were studied with regard to the presence of gastric varices by one of us (W. Martel) without knowledge of how the cases were selected or whether gastric varices had been demonstrated angiographically. Features of gastric varices on barium studies of the stomach were correlated with varices demonstrated by angiograms. Splenic size was evaluated on plain abdominal radiographs and on angiograms according to the method of Haertel and Beusch [8]. Angiographic Features Results The angiographic diagnosis of splenic vein occlusion was based on (1 ) nonopacification of a segment or entire length of the splenic vein despite visualization of the intrasplenic or hilar veins; (2) demonstration of collateral veins draining the spleen, and (3) opacification of the portal vein via collateral channels from the spleen (figs. 1A, 2B, and 3A). The location of the splenic venous occlusion was variable, ranging from the splenic hilum to the junction with the superior mesenteric vein. The collateral channels were the short gastric-coronary, gastroepiploic, omental, and, occasionally, inferior mesenteric veins. Gastric varices were angiographically demonstrable in 24 of the 27 patients with splenic vein occlusion. None had esophageal varices on angiograms. In three of the patients with both superior mesenteric and splenic yenous occlusion, gastric varices were not present. The short gastric-coronary venous collaterals (i.e., gastric varices) were present in all 18 patients with isolated splenic vein occlusion. The results are summarized in table 1. Radiographic Findings Gastric varices. Gastric varices were diagnosed by barium examinations in 14 of 19 patients (74%) in whom they were angiographically demonstrated. These were most pronounced in the cardia and fundus, and had a variable appearance with a frequent combination of findings. They presented as broad, serpentine redundant Received October 4, 1977; accepted after revision May 30, Presented at the annual meeting of the American Roentgen Ray Society, Boston, September 1977., Department of Radiology, University of Michigan Medical center, Ann Arbor, Michigan Address reprint requests to K. J. cho. Am J Ro.ntg#{149}nol131 : , Sept#{149}mbsr American Roentgen Ray Society X/78/ $00.00

2 440 CHO AND MARTEL Fig year-old man with pancreatitis and upper gastrointestinal hemorrhage. A, Splenoportography showing gastric fundal varices filling via coronary vein (arrow) toward portal vein. Note nonfilling of splenic vein. Esophageal varices are not present. B, Double contrast view of gastric fundus showing multiple serpentine and polypoid filling defects, most pronounced in cardia and fundus. C, Mucosal folds of lower esophagus showing no varices. filling defects or clusters of polypoid defects, simulating thickened rugal folds (fig. 1B) Occasionally, they had a characteristic orientation along the circumference of the gastric fundus (fig. 2B). The appearance of the barium collections between varices and adjacent rugal folds was important. These more or less linear collections characteristically varied in thickness due to their continuously undulating margins. Such undulations were irregularly spaced and often subtle (fig. 4). The varices were best demonstrated on double contrast views. Gastric varices were recognized by gastrointestinal examination in 10 of the 11 cases with isolated splenic vein occlusion. In only one of these patients were esophageal varices suspected on barium examination. In three of the patients with additional thrombosis ofthe superior mesenteric vein, esophageal varices were believed present on barium studies of the esophagus. Collateral veins. In four patients venous collaterals in the left upper abdomen were observed during the vascular phase of rapid sequence excretory urography (fig. 3B). The majority of these represented gastric varices arising from the short gastric-coronary and gastroepiploic venous communications, whereas others were collateral venous channels involving omental veins. Splenomegaly. The spleen was moderately enlarged in nine cases, and six of these had isolated splenic vein occlusion. Of the latter, one had lymphoma involving the spleen, three had carcinoma metastatic to the liver, and in the remaining two the splenomegaly was presumably secondary to occlusion of the splenic vein. In three other cases with splenomegaly, venous occlusion was not limited to the splenic vein but involved the superior mesenteric vein as well. Cirrhosis was present in two of these cases. Direct evidence of the causative process. In 11 patients there were abnormalities in the gastrointestinal examinations associated with the underlying disease. These included paraduodenal and perigastric mass lesions and mucosal fixation secondary to mural invasion by pancreatic carcinoma. One of these patients also had pancreatic calcification. Discussion Several authors have described features of gastric varices on barium examination [9, 10], but many emphasize the limitations of the latter examination and endoscopy in detecting gastric varices [6, ii]. Although the detection of gastric varices is admittedly difficult, meticulous examination with small quantities of barium (60-90 ml) and double contrast techniques will often permit a diagnosis even in the absence of esophageal varices. Even though the barium examinations in this study were not tailored for gastric varices, these were believed demonstrable in 14 of 19 patients. Highly redundant serpentine filling defects or linear defects oriented transversely along the circumference of the fundus are suggestive, but the finely undulating margins of the linear collections of barium, causing variations in the thickness of the barium streaks, are distinctive. The recognition of these features will avoid an erroneous diagnosis of gastric neoplasm, particularly inasmuch as varices have been known to produce large polypoid filling defects. Hypotonic agents were not used in these examinations. Although anticholinergic drugs have proved to be valuable in enhancing esophageal varices [12], it is not clear whether they would be helpful in assessing gastric varices, particularly since these are confined largely to the proximal stomach where motility is not a problem. Gastric varices may cause massive gastric hemorrhage; such hemorrhage is a well known complication of pancreatic disease and retroperitoneal fibrosis [13, 14]

3 SPLENIC VEIN OCCLUSION 441 and is occasionally the first clinical manifestation of these diseases. Unlike variceal bleeding associated with cirrhosis or portal vein thrombosis, this type of hemorrhage is easily controlled by splenectomy. Sutton et al. [15] reviewed the English literature regarding splenic vein occlusion from 1900 to They found 53 cases of such occlusion. In the 45 cases with clinical information, 65% had upper gastrointestinal bleeding. The incidence of this complication was lower in our series, probably reflecting differences in how the cases were selected. ltzchak and Glickman [16] noted Fig year-old woman with carcinoma in tail of pancreas. A. Splenic angiogram, arterial phase, showing subtle serrated encasement in proximal splenic artery (arrow). B, Venous phase, subtraction film, showing nonfilling of splenic vein. Gastric varices are more pronounced in cardia and fundus. Varices along circumference of fundus (arrows) correspond to findings in C. C, Prone oblique view of gastric fundus and body showing thin arcuate defects in gastric fundus and linear collections of barium with undulating margins along the circumference of fundus (arrows). Extrinsic impression on lesser curvature is due to tumor. gastrointestinal hemorrhage in only three of 19 patients with splenic vein occlusion. Although we cannot assert on the basis of this retrospective study that gastric varices without esophageal varices warrant a definite diagnosis of splenic vein occlusion, we believe that diagnosis should be highly suspect. In 27 patients with angiographic proof of splenic vein obstruction, 24 had angiographically demonstrated gastric varices; none had esophageal varices. Nineteen of the same patients had adequate barium studies. Gastric varices were demonstrated in 14; of these, four had

4 442 CHO AND MARTEL t Fig year-old man with splenic vein occlusion and gastric varices secondary to chronic pancreatitis. A, Venous phase of splenic angiogram showing occlusion of splenic vein at hilum with numerous gastric varices. Spleen is normal size. B, Vascular phase of rapid sequence excretory urogram showing tortuous venous collaterals (arrows) in left upper abdomen. TABLE 1 Results of Angiographic and Barium Examinations Isolated Splenic Vein Thrombosis Splenic and 5uperior Mesenteric Thrombosis Angiography: No. patients Gastric varices Esophageal varices Barium examination: No. patients Gastric varices Esophageal varices Note-Data on 27 patients with splenic vein occlusion. Total Fig year-old man with cirrhosis and portal hypertension. Gastroesophageal varices demonstrated at endoscopy. Venous phase of supenor mesenteric angiogram showed retrograde filling of dilated left gastric vein (not shown). Barium collections (A and B ) adjacent to varices have somewhat linear configuration with characteristic, gently undulating margins. These cause slight variations in thickness of barium collections. suspected esophageal varices (table 1). This evidence indicates the preferential route of venous flow in isolated splenic vein occlusion is toward the portal vein. Hence, the splenoportal collaterals (short gastric-coronary and gastroepiploic veins) feed the gastric varices; esophageal veins are a less frequent collateral route. Itzchak and Glickman [16] reported that isolated gastric varices were angiographically demonstrated in 18 of their 19 patients with splenic vein occlusion. One of their patients who had esophageal varices had associated cirrhosis. In reporting four cases of splenic vein occlusion, Rice et al. [11] emphasized the importance of preendoscopic diagnosis of gastric varices without esophageal varices because they often presented as fundal mass.

5 SPLENIC VEIN OCCLUSION 443 This study indicates that splenic vein occlusion can be suggested from simple radiographic examinations prior to angiographic studies. The features are gastric varices without esophageal varices, collateral veins in the left upper abdomen during the vascular phase of rapid sequence intravenous pyelography, and direct evidence of the causative process on gastrointestinal examinations or plain abdominal films. REFERENCES 1. Salam AA, Warren WD, Tyras DH: Splenic vein thrombosis: a diagnosable and curable form of portal hypertension. Surgery 74 : , Yale CE, Crummy AB: Splenic vein thrombosis and bleeding esophageal varices. JAMA 217: , Cho KJ, Aeuter SA: Angiographic assessment of pancreatic pseudocyst: a reappraisal.j Can Assoc Radiol 27: , Goldstein GB: Splenic vein thrombosis causing gastric varices and bleeding.amj Gastroenterol 58: , Marks U, Weingarten B, Gerst GA: Carcinoma of the tail of the pancreas associated with bleeding gastric varices and hypersplenism.ann Intern Med 37: , Gabrielsson N: Diagnosis of gastric varices by conventional roentgenography as compared with splenoportal phlebography. Acta Radiol [Diagn] (Stockh) ii : , Belgrad A, Carlson HC, Payne WS, Cain JC: Pseudotumoral gastric varices. Am J Roentgenol 91 : , Haertel M, Beusch HA: The normal angiographic anatomy of the spleen. Fortschr Rontgenstr 1 20 : , Samuel E: Gastric varices. BrJ Radiol 21 : , Evans JA, Delany F: Gastric varices. Radiology 60:46-51, Rice AP, Thompson WM, Kelvin FM, KrinerAF, GarbuttJT: Gastric varices without esophageal varices. JAMA 237: , Ghahremani GG, Port RB, Winans CS, Williams JA: Esophageal varices: enhanced radiologic visualization by anticholinergic drugs. Am J Dig Dis 17 : , Lavender 5, Lloyd-Davies AW, Lea Thomas M: Aetroperitoneal fibrosis causing localized portal hypertension. Br MedJ 3: , Walter J, Chuang VP, Bookstein JJ, Reuter SA, Cho KJ, Pulmano CM: Angiography of massive hemorrhage secondary to pancreatic disease. Radiology 124: , Sutton JP, Yarborough DY, Richards JT: Isolated splenic vein occlusion.arch Surg 100: , ltzchak W, Glickman M: Splenic vein thrombosis in patients with a normal size spleen. Invest Radiol 12: , 1977