Digestive Diseases and Sciences, Vol. 36, No. 1 (January 1991), pp. 112-115

CASE REPORT

Abdominal Tuberculosis A Cause of Portal Vein Thrombosis and Portal Hypertension D. R U T T E N B E R G , MD, S. G R A H A M , MD, D. B U R N S , DPhil (Oxon) FCP(SA), D. S O L O M O N , MD, F . R a d (Diag), and P. B O R N M A N , F R C S (Ed) M M e d (Surg) KEY WORDS: abdominal tuberculosis; portal vein thrombosis; portal hypertension.

Abdominal tuberculosis is a rare cause of portal hypertension and obstructive jaundice. We present two cases of tuberculosis with associated portal hypertension: one with segmental splenic vein occlusion caused b y tuberculous l y m p h nodes and a n o t h e r with focal tuberculosis of the pancreas, causing obstructive jaundice and associated thrombosis o f the portal and splenic veins. The aetiology, p a t h o p h y s i o l o g y , diagnosis and m a n a g e m e n t of these unusual manifestations of tuberculosis are discussed. CASE REPORTS

Case 1. A 26-year-old male presented with intermittent dyspepsia of nine years' duration and recent anorexia and weight loss of about 9 kg. There was no history of night sweats, jaundice, hematemesis, melena, or tuberculosis (TB) contacts. Gastroscopy performed three years previously demonstrated mild oesophagitis. Examination revealed a healthy looking man with no icterus, lymphadenopathy, or stigmata of chronic liver disease. Abdominal examination revealed no mass or visceromegaly. The chest x-ray and routine laboratory tests, including full blood count, serum electrolytes, and liver function tests, were noncontributory. Barium meal demonstrated a lobulated mass with an intact mucosa in the gastric fundus (Figure 1). A diagnosis of gastric lymphoma was entertained and the patient underwent endoscopy to confirm this. Gastroscopy showed a normal esophagus and confirmed an irregular fundal submucosal Manuscript received April 10, 1990; revised manuscript received August 9, 1990; accepted August 13, 1990. From the Gastrointestinal Clinic and Surgical Gastroenterology, Groote Schuur Hospital and the Departments of Medicine, Radiology and Surgery, University of Cape Town, Cape Town, South Africa Address for reprint requests: Dr. D. Ruttenberg, Gastrointestinal Clinic, Groote Schuur Hospital, Observatory 7925, Cape Town, South Africa.

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mass. The latter was a 6-cm, light blue lesion, soft in texture, with no evidence of ulceration. Biopsy of the mass caused massive upper gastrointestinal hemorrhage necessitating emergency laparotomy. At laparotomy portal hypertension was evident. The liver was grossly normal. Large lymph nodes occupied the hepatoduodenal ligament and extended to the porta hepatis. Gastrotomy revealed large gastric fundal varices, and the bleeding point was suture ligated. The patient made an uneventful recovery. Lymph node biopsy demonstrated tubercle bacilli, and antituberculous therapy was commenced. A subsequent abdominal ultrasound examination revealed a patent portal vein with no evidence of lympadenopathy, but the splenic vein could not be visualized. Although a follow-up barium meal showed persistent gastric varices, the patient remains asymptomatic one year postoperatively. Case 2. A 42-year-old female presented in 1985 with a three-month history of right upper quadrant pain, recent weight loss, episodic dark urine, and acholic stools. A previous endoscopy in 1983 for abdominal pain had revealed duodenal ulcer disease and incidentally discovered esophageal varices. These had been treated conservatively with antacids and Hz antagonists. There was no history of alcohol abuse. A moderately enlarged hepar was present on abdominal palpation. Special investigations revealed a hemoglobin of 11.7 g/dl, alkaline phosphatase of 487 units (normal 30-115), total bilirubin of 31 ixmol/liter (normal 1-17), conjugated bilirubin 15 ixmol/liter (normal 1-17), lactate dehydrogenase 63 units/liter (normal 5-40), GGT 334 units/liter (normal 0-50), and ALT 317 units/liter (normal 0-53). The hepatitis B surface antigen was negative. Endoscopic retrograde cholangiopancreatography (ERCP) study suggested encasement of the distal common bile duct (Figure 2). The pancreatic duct was not demonstrated. A large mass in the head of pancreas was noted on CT scan (Figure 3). Two fine-needle aspiration biopsies of the pancreatic mass, however, were noncontributory. Laparotomy was undertaken to establish a diagnosis and to bypass the biliary obstruction. This revealed a 5-cm mass in the head of pancreas and Digestive Diseases and Sciences, Vol. 36. No. 1 (January 1991)

0163-2116/91/0100-0112506.50/0 ,~ 1991 Plenum Publishing Corporation

ABDOMINAL TUBERCULOSIS

Fig 1. Double-contrast barium meal showing lobulated filling defects in gastric fundus.

adenopathy along the common bile duct. Frozen-section biopsies of the pancreas and lymph nodes were nondiagnostic, but a clinical diagnosis of advanced pancreatic cancer was made and a Roux-en-Y cholecystoenterostomy done. Final histology of the lymph nodes, however, revealed tuberculosis and antituberculous treatment was commenced. The patient made a remarkable recovery, but presented again at the beginning of 1988 (four years later) with signs and symptoms of obstructive jaundice. It was assumed that the patient had relapsed, and a second course of anti-TB therapy was commenced. In February 1989, while still on treatment, the patient presented again with abdominal pain. An ERCP and abdominal ultrasound revealed persistent bile duct stenosis with common bile duct stones (Figure 4). Further surgery was considered in view of the unsatisfactory biliary drainage by the cholecystojejunostomy. The earlier finding of esophageal varices, however, prompted angiography and delayed portography to assess the feasibility of biliary surgery in the presence of portal hypertension. This demonstrated portal and splenic vein thrombosis, encasement of the splenic and hepatic arteries and extensive collaterals in the porta hepatis. It was decided that surgery would be too hazardous, and endoscopic papillotomy was carried out, and the stones were removed. This effectively decomPressed the biliary system. The patient remains well one year later. Digestive Diseases and Sciences, Vol. 36, No. 1 (January. 1991)

Fig 2. Encasement of distal common bile duct demonstrated on endoscopic retrograde cholangiogram.

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RUTTENBERG

Fig 3. Right side down decubitus CT scan demonstrating pancreatic head mass.

DISCUSSION Compression of the porta hepatis by tuberculous lymph nodes was first observed by Knight in 1845 and has been reported as an unusual cause of either portal hypertension or obstructive jaundice. In 1956 Caroli and Puraf, using splenoportography, made the first preoperative diagnosis of portal vein compression and portal hypertension in a patient with abdominal tuberculosis (1). Bruno in 1977 reported the second case of obstructive jaundice caused by tuberculous lymphadenopathy in the porta hepatis

Fig 4. Calculus (arrow) in main bile duct demonstrated on endoscopic retrograde cholangiogram.

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ET AL

(2). Although both of our patients had portal hypertension, in only one case (case 2) could portal vein and splenic vein thrombosis be documented. The other patient (case 1) had a patent portal vein, and in view of his isolated gastric varices and a patent portal vein, it is presumed that splenic vein occlusion and subsequent thrombosis was responsible for the segmental portal hypertension (4, 5). Patients with bleeding gastric varices due to splenic vein occlusion are best treated by splenectomy (4, 6). Whether our patient requires a splenectomy for the persistent gastric varices remains uncertain considering the iatrogenic cause of the previous bleed. On balance, close follow-up would seem appropriate, bearing in mind the possible implications of splenectomy in a patient who is at risk of recurrent tuberculosis. Obstructive jaundice caused by pancreatic tuberculosis is uncommon. Crowson et al (7) in 1984 reported the first case in the English literature. Direct invasion of the pancreas is uncommon, even in the presence of miliary TB with splenic and hepatic involvement. In a review of miliary tuberculosis from 1891-1961, Paraf et al found pancreatic or peripancreatic involvement in 2% of the 526 cases studied (8). In another autopsy series, pancreatic involvement was found in 4.7% of the 297 cases of miliary tuberculosis (9). Focal tuberculosis of the pancreas is even more unusual (10). In the majority of cases of pancreatic TB, infection is the result of direct extension from tuberculous abdominal lymph nodes. It is also possible that haematogenous spread to the splanchnic lymph nodes occurs after pulmonary tuberculosis. Previous surgery and prior treatment with steroids are also thought to predispose to reactivation of TB peritonitis (11, 12). While caseation predominates, epithelioid cells and Langhans giant cells are often not found (12). Diagnosis is difficult as the CXR, sputum analysis, and culture of biopsy material are often negative. Abdominal calcification on x-ray is also uncommon. Untreated pancreatic TB may progress to pancreatic fibrosis and changes of chronic pancreatitis (13). A laparotomy is mandatory to establish the diagnosis. A biliary bypass for the obstructive jaundice may be indicated on clinical grounds, but the mainstay of treatment remains antituberculous therapy (7). The surgical management of biliary calculi in the presence of portal vein thrombosis is hazardous. Subtotal cholecystectomy has, to a certain extent, resolved the problem of removal of the Digestive Diseases and Sciences, Vol. 36, No. 1 (January 19911

ABDOMINAL TUBERCULOSIS gallbladder stones (14), but exploration of the bile duct in the presence of cavernous transformation around the bile duct remains a formidable procedure and may lead to life-threatening bleeding. Since portal decompression is not feasible in this situation, endoscopic removal of calculi in our patient was deemed the only safe option. In the presence of bile duct stenosis and the inadequate biliary enteric bypass via the gallbladder (15), the patient, however, remains at risk of recurrent stone formation. Regular follow-up and ERCP is therefore required. In neither of our cases was tuberculosis entertained as a possible explanation for obstructive jaundice or gastric varices. Tuberculosis of the pancreas can be simulated by carcinoma of the head of the pancreas (16), and therefore, in endemic areas, a tissue diagnosis is essential to detect this eminently treatable condition. Once identified, institution of antituberculous therapy is mandatory and carries an excellent prognosis. Our one patient also highlights the difficulties of differentiating gastric varices from mitotic lesions in the fundic area of the stomach and cautions against indiscriminate biopsying of such lesions before the possibility of varices is excluded. REFERENCES 1. Caroli J, Paraf A: Pylephlebites tuberculeuses. Rev Meal Chir Mal Foie 31:73-77, 1956 2. Bruno MS: Obstructive jaundice. NY State J Med 77:174551, 1977

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3. Brown KM. Kaplan MM, Donowitz M: Extrahepatic portal venous thrombosis: Frequent recognition of associated diseases. J Clin Gastroenterol 7(2):153-159, 1985 4. Muhletaler C, Gerlock AJ Jr, Goncharenko V, Avant GR, Flexner JM: Gastric varices secondary to splenic vein occlusion: radiographic diagnosis and clinical significance. Radiology 132:593--598, 1979 5. Salam AA, Warren WD, Tyras DH: Splenic vein thrombosis: A diagnosable and curable form of portal hypertension. Surgery 74:961-972, 1973 6. Marshall JP (II), Smith PD, Hoyumpa AN: Gastric varices. Problem in diagnosis. Am J Dig Dis 22:947-955, 1977 7. Crowson MC, Perry M. Burden E: Tuberculosis of the pancreas: A rare cause of obstructive jaundice. Br J Surg 71:239, 1984 8. Paraf A, Menanger C, Texier J: La tuberculose du pancreas et la tuberculose des ganglions de l'etage superieur de l'abdomen. Rev Med Chir Mal Foie 41:101-26, 1966 9. Auerbach O: Acute generalised miliary tuberculosis. Am J Opthalmol 20:121-136, 1944 10. Stambler JB, Klibaner MI, Bliss CM, Lamont JT: Tuberculous abscess of the pancreas. Gastroenterology 83:922-925, 1982 11. Rafoth R, Morse R, Edwards LD, Jupa J, Levin S: Tuberculous peritonitis after laparotomy. Scand J Infect Dis 4:139-142. 1972 12. Doerr W, Seifert, U: Spezielle pathologische Anatomie. Band 6. Berlin, Springer-Verlag 1973, pp 225-257 13. Stock KP, Riemann JF, Stadler W, Rosch W: Tuberculosis of the pancreas. Endoscopy 13:178-180, t981 14. Bornman PC, Terblanche J: Subtotal cholecystectomy: For the difficult gallbladder in portal hypertension and cholecystitis. Surgery 98(1):1-6, 1985 15. Carter DC: Pancreatitis and the biliary tree: The continuing problem. Am J Surg 155:10-17, 1988 16. Chandrasekhara KL, Iyer SK, Stanek AE, Herbstman H: Pancreatic tuberculosis mimicking carcinoma. Gastrointest Endosc 31(6):386-388, 1985

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Abdominal tuberculosis--a cause of portal vein thrombosis and portal hypertension.

Digestive Diseases and Sciences, Vol. 36, No. 1 (January 1991), pp. 112-115 CASE REPORT Abdominal Tuberculosis A Cause of Portal Vein Thrombosis and...
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