A 32-year-old man presented to our hospital with a sudden onset of vomiting blood with no apparent cause. On admission, the vomiting of blood increased and was accompanied by black stools. The patient had no history of hepatitis, cardiac disease, tuberculosis or any surgical history. On physical examination, the patient had no fever, a heart rate of 86 beats per minute, a blood pressure of 130/80 mmHg and a respiratory rate of 20 breaths per minute. The patient was well developed and conscious with vague epigastric pain. All cardiopulmonary examinations were negative, there was no yellowing of the skin or sclera, no spider nevus, the liver and spleen were not palpable under the ribs, there was no percussion pain in liver and spleen, Murphy’s sign was negative, shifting dullness was negative, there was no edema in both lower limbs, bowel sounds were 5/min, there was no vascular murmur and all neurological investigations were normal.
Routine blood tests showed a significant decrease in hemoglobin concentration and red blood cell count. Laboratory investigations showed a prothrombin time of 14.1S, D-Dimer of 9.87 mg/L, hemoglobin of 86 g/L,blood urea nitrogen of 12.40 mmol/L, creatinine of 87.3 umol/L,
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normal liver and renal function, normal electrolytes, negative hepatitis serology, normal autoimmune liver antibodies and negative for 9 tumor markers (male). ECG showed normal electrocardiographic changes. Ultrasonography showed splenomegaly. Enhanced CT of the whole abdomen showed varices of the lower oesophagogastric fundus; multiple intra-abdominal lymph nodes were calcified, with the larger lymph nodes located in the hepatic hilar region and compressing the main portal vein; and the spleen was enlarged (Fig. 1). No significant abnormalities were found on cranial and chest CT. Medication was given on admission to stop the bleeding, but there was no improvement. The morning of the next day, there was recurrent vomiting of blood, heavy bleeding and a significant drop in hemoglobin. Digital subtraction angiography (DSA) was then given and intraoperative arteriography showed no significant abnormalities; venography showed severe stenosis of the junction of left and right branches of the portal vein, with a stenosis of approximately 80%. A small amount of portal blood entered the liver through the stenotic portion and most of it flowed backwards into the splenic vein. Multiple side branches of the splenic and superior mesenteric veins formed and flowed into the gastro-Esophagus fundic plexus, and contrast spillage was seen in the fundic plexus (Fig. 2). Then, an appropriate amount of tissue glue and embolization coil was injected into the above-mentioned side branches for embolization, and portal vein stenting was performed at the portal vein stenosis (Fig. 3). The portal vein pressure below the stenotic segment was measured with a glass manometer at 34 cm H2O prior to embolisation. A combined whole abdomen enhanced CT and DSA angiogram showed lymph node calcification in the hepatic hilar region compressing the portal trunk, the same location as the DSA angiogram showed for the portal stenosis, so portal stenosis and portal hypertension were considered to be due to lymph node calcification compression. The night of the next day, the patient continued to vomit blood postoperatively. Emergency gastroscopy showed varices in the lower esophagus with multiple red signs; active bleeding was seen and was treated with local sclerotherapy with polidocanol under gastroscopy. However, there was still active hemorrhage after treatment, so laparoscopic splenectomy with perisoph-agogastric devascularization was performed in the early morning of the third day. Intraoperatively, there were multiple caseous nodules in the greater omentum and abdominal wall, and approximately 3 × 5 cm caseous nodules in the left abdominal wall. The greater omentum was clearly adherent to the abdominal wall and the liver and spleen, and the gastrointestinal tract was clearly dilated with dark red bloody material. There were no obvious cirrhotic changes in the liver, the spleen was markedly enlarged and the lower esophagus and perigastric fundus veins were markedly stagnant and dilated. The spleen and the caseous nodule in the left upper abdomen were excised and sent for pathological examination.Intraoperative diagnosis: EVB, hemorrhagic shock, abdominal tuberculosis and portal vein stenosis. Postoperative pathological examination of the spleen was consistent with chronic hematopoietic splenomegaly; the caseous mass of the abdominal wall showed a cystic wall-like structure microscopically, a large amount of necrotic material within the cyst, and vascular proliferation within the cystic wall with lymphocytic histiocytic infiltration (Fig. 4). Because of the intraoperative diagnosis of abdominal tuberculosis, postoperative culture of sputum acid-fast bacilli, ascites antacid cultures and tuberculosis DNA (sputum) tests were negative and combined with pathological examination suggested that calcification of the abdominal lymph nodes was not related to tuberculosis. Postoperatively, the patient’s vital signs were stable, no significant drop in hemoglobin, no bleeding symptoms, bleeding stopped and he was discharged with symptomatic supportive treatment. Follow-up after discharge was good, with no complaints of bleeding (Fig. 5).
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