A 74-year-old man was referred to our hospital and was diagnosed with gastric cancer with para-aortic lymph node metastasis (Fig. 1a–c). We introduced chemotherapy and no newly metastatic lesion was appeared. Curative surgery was proposed, but he declined it. The primary lesion was remarkably shrinking but remaining, and he continued to receive chemotherapy. After the patient received 17 cycles of chemotherapy (S-1 and oxaliplatin), he was admitted to our hospital because of Mallory–Weiss syndrome when he underwent follow-up endoscopic examination. The lesion, which was remarkably shrunk while chemotherapy was introduced, had endoscopically grown. Regular follow-up computed tomography (CT) showed the primary lesion shrank once but gradually increased in size, and the regional and para-aortic lymph nodes slightly shrank (Fig. 1d), and no significant change was observed in diameter after regrowth of the primary lesion. No newly developed metastatic lesions were observed. Gastrectomy and extended lymph node dissection were planned for curative surgery again. He had no history of viral hepatitis, and he did not have drinking habit. Laboratory examination revealed deterioration of liver function after receiving chemotherapy. His serum total bilirubin level was 1.9 mg/dL, a significant increase compared with the previous value of 0.6 g/dL. However, preoperative CT scan did not reveal change suspecting liver cirrhosis including ascites. The patient underwent open total gastrectomy and D2 plus PALN. The patient was allowed oral food intake on postoperative day four. The drain was removed on postoperative day seven. Serous fluid (864 mL) was drained a day before removing the drain. His postoperative course was uneventful, and he was discharged on postoperative day 14. Histological tumour findings were gastric cancer, LM, Post-Less-Ant, ypType 3, 72 × 42 mm, tub1 > pap > tub2, ly1b, v1a, pT1b (SM2), pN0 (0/53), M0, ypStage IA, Grade 1b), according to the Japanese Classification of Gastric Cancer, 15th edition [5].

Fig.1
figure 1

a Esophagogastroduodenoscopy revealed huge ulcerative lesion on the lesser curvature of stomach. b Abdominal CT revealed wall thickness of stomach (arrowhead) and enlarged lymph node along the left gastric artery and its branches. c Abdominal CT revealed enlarged para-aortic lymph node (arrow). d Para-aortic lymph node was slightly shrunk after chemotherapy (arrow)

After discharge, his oral intake was not sufficient. One month after surgery, he presented with bilateral lower extremity oedema and hypoalbuminaemia. Three months after gastrectomy, he was readmitted to our hospital because of insufficient oral intake and dehydration. His abdomen was markedly distended, and severe bilateral lower extremity oedema was observed. On admission, abdominal CT showed a high volume of ascites and no cancer recurrence (Fig. 2a). A drainage catheter placed in the peritoneal cavity drained 7,500 mL of white milky fluid with a high triglyceride level (348 mg/dL). Cytological examination revealed no malignancy. The bacterial culture was negative. The patient was diagnosed as having postoperative CA. We could not identify the sites of lymphatic leakage in the three times of intranodal lymphangiography followed by CT (Fig. 2b). He ingested 250–500 kcal fat restriction food orally and received 1020 kcal parenteral nutrition with intralipid supplementation. Abdominal distension and nutritional status did not improve despite starting a fat-restricted diet, parenteral nutrition support, diuretics, and octreotide (300 μg/day) administration. Almost 1500 mL fluid was drained a day when we performed continuous drainage of his ascites. We performed CART [6] for four times almost each 2 weeks, and approximately 8 L of ascites was drained each time. However, his abdominal distention temporally improved, but he complained of abdominal discomfort in a few days after CART. After one week when he underwent CART, his abdomen was significantly distended. Furthermore, his serum albumin levels progressively decreased for 4 weeks after admission. The postoperative CA was refractory to conservative treatment and lymphangiography. Thus, surgical treatment was considered. However, we suspected surgical approach might not be effective because the several times of lymphangiography could not detect the leakage point. Moreover, his general condition was poor due to loss of lymphatic fluid. After the surgical indications were discussed in detail and the patient was given sufficient informed consent before treatment, we decided to place a PVS.

Fig.2
figure 2

a Abdominal CT showed a large volume of ascites and no sign of cancer recurrence. b Fluoroscopic image showing injection of Lipiodol through the left inguinal lymph nodes (arrow)

The peritoneovenous (Denver) shunt was placed on the 31st day. The first incision was made on a firm, non-compressible rib in the right lower rib cage. A pocket was carved to place the pump as planned. The peritoneal limb of the shunt was inserted into the abdominal cavity through an incision. The venous limb of the shunt was inserted from the subclavian vein into the superior vena cava. A second incision was made on the lateral side of the venous access site. The pump was pushed into the pocket, and the venous limb of the shunt was tunnelled under the skin through the superior aspect of the first incision (Fig. 3). The patient pushed the shunt valve ten times twice a day after PVS placement. His abdominal distension drastically improved after placing the PVS. Although laboratory investigation showed decrease in platelet count (from 10.5 to 4.8 × 104 μL) and in prothrombin time (from 59.5 to 43.5%) in a week, he did not suffer from severe disseminated intravascular coagulation (DIC) and no serious complications were observed. The patient was discharged on the 51st day (20 days after PVS placement) (Fig. 4a). A follow-up examination in the outpatient clinic at 13 months after PVS placement, he remained asymptomatic without recurrence of ascites and cancer (Fig. 5); nutritional status also showed improvement (Fig. 4b).

Fig.3
figure 3

a The venous limb of the peritoneovenous shunt was placed with the tip of the catheter located in the lower end of the superior vena cava (arrowhead). b The peritoneal limb of the shunt was placed at the tip of the catheter within the pelvic region (arrowhead). The pump was placed in front of the right lower rib cage (arrow)

Fig.4
figure 4

Clinical course. a Changes in serum albumin value (Alb) during the second hospitalisation. b Changes in serum albumin value (Alb) and body weight (BW) after initial gastrectomy. CART cell-free and concentrated ascites reinfusion therapy, INL intranodal lymphangiography, PVS peritoneovenous shunt, TG total gastrectomy

Fig.5
figure 5

a Abdominal CT showed a large volume of ascites before peritoneovenous shunt. b Abdominal CT showed no ascites at a follow-up examination in the outpatient clinic. Arrow; the peritoneal limb of the PVS

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