中华普通外科杂志
2023年 · 第38卷第04期
中华普通外科杂志
In recent years, although the overall incidence of gastric cancer has decreased, the incidence of proximal gastric adenocarcinoma such as adenocarcinoma of esophago-gastric junction (AEG) and cardia cancer has increased significantly[1]。 It was found that proximal gastric cancer was different from distal gastric cancer in many aspects such as clinicopathological characteristics[2]However, there is still a lack of clear consensus on the diagnosis of proximal gastric cancer. This article combs the research progress of the definition, diagnosis and multidisciplinary treatment of proximal gastric cancer.
Gastric cancer is one of the most common causes of cancer death in the world, and its morbidity and mortality rank among the top five in the world[1]。 However, traditional clinical treatment methods have limited efficacy, and the prognosis of advanced gastric cancer is poor. Chemotherapy is a conventional treatment for advanced gastric cancer. Commonly used chemotherapy drugs include fluorouracil/capecitabine, paclitaxel and platinum, but the median over survival (OS) of conventional chemotherapy drugs is only 8 months[2]。 Tumor cells have multiple mechanisms to escape the host immune response. Co-suppressive signaling pathways mediated by immunosuppressive checkpoints, such as programmed death receptor-1 (PD-1) /programmed death ligand-1 (PD-L1) and cytotoxic T lymphocyte-associated antigen-4 (CTLA-4), play an important role in tumor-induced immunosuppression[3]。 PD-1 is expressed on the surface of T, B cells and myeloid cells, and its binding to the ligand PD-L1 activates the immunosuppressive pathway, thus forming immune escape[4]。 PD-1 blockade relieves partially suppressed immune function, thereby inducing an antitumor response. CTLA-4 binds to B7 on the surface of antigen-presenting cells and prevents its binding to costimulatory CD28 receptors on CD4-positive T cells. Thus, CTLA-4 deprives T cells of the costimulatory signal of CD28, and anti-CTLA-4 antibodies specifically bind CTLA-4 and release T cells from inhibition[4]。
A 76-year-old female was admitted to the hospital for "lower abdominal pain with changes in defecation habits for more than 1 month". Colonoscopy in external hospital showed that one sigmoid colon (20 cm away from the anal margin) occupied the full circumference and showed a bulging growth new organism. Biopsy pathology revealed poorly differentiated malignancy. After admission, abdominal enhanced CT examination showed that the pelvic sigmoid wall was significantly thickened with the formation of a mixed density mass, about 10 cm in size
A 50-year-old male was admitted to the hospital with "abdominal distension after closed abdominal injury with abnormal defecation for more than 5 months". physical examination : BMI 18.29 kg/m2Moderate anemia, frog-like abdomen, soft abdominal muscles, deep tenderness in the left middle abdomen, no rebound pain, hyperactive intestinal sound, 6 times/min, and the sound of air passing through water can be audible. Colonoscopy showed that the mucosa was congested and swollen at 20 cm from the anal margin, partially nodular bulge, and the lumen was narrow, so the endoscope could not pass. Abdominal enhanced CT examination showed that the pelvic small intestine and sigmoid colon were collected, and the adhesions were petal-shaped, considering the possibility of enteral fistula formation (Figure 1). The transanal inflation test was performed, and the rectum and lower sigmoid colon were developed at the beginning of inflation (Figure 2A). With the increase of gas, a large segment of small intestine in the abdominal cavity was developed, while the remaining colon was not developed (Figure 2B), indicating that the gas directly entered the small intestine through the lower sigmoid colon, and the sigmoid colon communicated with the small intestine, with a sinus tract between them. The diagnosis of intestinal colic fistula was clear, and laparoscopic exploration was performed. During the operation, the sigmoid colon formed dense adhesion with multiple segments of the small intestine, and formed an adhesion band with the lateral abdominal wall (Figure 3), which compressed the intestinal tube, resulting in stenosis of the sigmoid colon and small intestine there, and obvious dilatation of the descending colon and upper small intestine. The small intestine and the sigmoid colon formed dense adhesions at 3.6 m and 5.0 m away from the Trigger's ligament, which could not be separated. According to the principle of preserving as much intestinal tube as possible, two segments of small intestine were removed for lateral anastomosis, and the diseased sigmoid colon was removed, and descending colon + rectal anastomosis was performed. The fistula was about 0.5 cm in size and 1.0 cm in length. Exhaust occurred on the 4th postoperative day, and gradual feeding occurred on the 5th day. He was cured and discharged at 2 weeks, and his body weight increased by 20 kg at 6 months after operation compared with that before operation.
A 57-year-old male was admitted to the emergency department with "abdominal pain for 10 h" and had a history of diabetes and hypertension. Physical examination: abdominal swelling, slightly tight abdominal muscles, tenderness in the upper abdomen and periumbilical area (+), suspected rebound pain, and weak intestinal sounds. Laboratory test: White blood cell count: 12.50×109/L, percentage of neutrophils: 79.80%, rapid C-reactive protein: 38.61 mg/L. Abdominal CT scan: gas accumulation in the intestinal wall of the small intestine, extensive gas accumulation in the hepatic portal vein and its branches, and superior mesenteric vein, which did not exclude the possibility of necrotizing enteritis; A small amount of ascites (Figure 1). Diagnosis: necrotizing enteritis with portal pneumatosis. Exploratory laparotomy was performed in the emergency department. About 300 ml of peritoneal blood effusion was seen during the operation, and necrotic small intestine was visible 15-85 cm away from the ileocecal region (Figure 2). Necrotic small intestine resection + intestinal anastomosis was performed. After operation, the patient developed wound infection, and was subjected to enhanced dressing change, debridement and suture. Postoperative pathology: Local intestinal mucosa and intestinal wall tissue necrosis, accompanied by edema, hemorrhage and more acute and chronic inflammatory cell infiltration, consistent with intestinal hemorrhagic infarction. Two weeks after operation, CT examination showed basic absorption of gas accumulation in the original hepatic portal vein and its branches, mesenteric space and intestinal wall. The patient recovered well with no obvious discomfort after 1 month of follow-up.
A 71-year-old female was admitted to hospital for "intermittent right upper abdominal distension and pain with skin and sclera yellowing for 1 month". Physical examination: skin and sclera yellowing, abdominal swelling, right upper abdomen tenderness. Abdominal circumference 86 cm. Laboratory tests: urinalysis suggested bilirubin (+ + +), protein (+); Liver function suggests cholestasis and liver function damage; CA19-9: 183.4 U/ml. Imaging examination: Both abdominal enhanced CT and abdominal ultrasound showed a huge cystic mass in the liver, about 22 cm ×20 cm ×20 cm in size, and intrahepatic bile duct dilatation (Figure 1). Percutaneous transhepatic liver cyst puncture drainage was performed, and the cyst discharged reddish-brown serous. After drainage, the symptoms of jaundice were significantly reduced and the abdominal circumference was reduced to 80 cm. Considering that the patient's hepatic cyst has a large cyst cavity, simple puncture and drainage cannot destroy the mucosal secretion function, and the cyst is located in the hepatic hilar area, and the risk of collateral injury is high after sclerotherapy, laparoscopic hepatic cyst fenestration is decided. The resected specimens were pathologically confirmed to be hepatic cyst (Figure 2). The patient was discharged on the 4th postoperative day. Daily drainage volume after discharge<50 ml. Three weeks after the operation, CT examination showed no obvious dilatation of intrahepatic bile duct, no recurrence of cyst (Figure 3), and the level of liver enzyme was close to normal. The internal drainage tube of liver cyst was removed.
A 49-year-old male was admitted to hospital for more than 2 months due to intermittent claudication of his right lower limb. The patient had no obvious trigger 2 months ago. After walking or running exercises, he developed pain and numbness in his right calf, which can be relieved after rest. The symptoms appeared repeatedly. He now has a claudication distance of about 200 m and no resting pain. Admission physical examination: the femoral artery pulsation of the right lower limb was normal, and the popliteal, dorsal foot and posterior tibial arteries could not palpate the pulsation. Ultrasonography before admission: Right superficial femoral, popliteal, posterior tibial and peroneal artery flow velocity decreased, spectral morphology changed, and three-phase wave disappeared. Three-dimensional CT angiography showed severe stenosis of the P1 segment of the right popliteal artery and posterolateral compression of the popliteal artery. MRI of knee joint showed a circular abnormal signal shadow on the posterolateral side of popliteal artery, with clear boundaries and high T2WI signal, 1.7 cm ×2.5 cm in size and about 3.1 cm in length (Figure 1). Preliminary diagnosis: popliteal artery entrapment syndrome (PAES), ganglion cyst (GC). Right popliteal artery decompression + cystectomy under epidural anesthesia. During the operation, the popliteal artery was compressed by an intramuscular cyst on the medial side of the long head of the biceps femoris tendon. The surface of the cyst wall was smooth and tough, and the contents were pale yellow jelly-like. After cyst resection, intraoperative ultrasound showed that the popliteal artery flow velocity and three-phase wave returned to normal, and the operation was ended. The postoperative pathology was consistent with the pathological characteristics of tendon sheath cyst. After 4 months of follow-up, the right femoral, popliteal, dorsal foot and posterior tibial artery pulsation were normal, and there was no obvious abnormality in the lower extremity vascular ultrasound.
The patient, a 68-year-old female, was admitted to hospital for "finding a left hip mass for more than 1 year". Physical examination: A mass about 30 mm ×20 mm in size can be palpable on the left hip, which is tough in texture, poor in mobility, clear in boundary, and no tenderness. Serum tumor indexes: carbohydrate antigen 72-4 20.07 U/ml, human epididymal secreted protein 91.24 pmol/L. The B-ultrasound examination results suggest a mass on the body surface, see Figure 1. The erythrocyte sedimentation rate was 61 mm/h. Subcutaneous massectomy of left hip under local anesthesia: A white cystic-solid mass with a size of about 4 cm ×3 cm in the subcutaneous fat layer was seen, with clear boundaries, no invasion of surrounding tissues, clear boundaries with surrounding tissues, and intact envelope. Postoperative pathological examination showed: (left hip mass) gray-white skin and subcutaneous tissue, located in the subcutaneous tissue, immediately adjacent to the basal margin, 3.7 cm ×2.6 cm ×1.2 cm in size, fusiform flap, 3.5 cm ×1 cm in size, and a gray-white nodule, 3.5 cm ×2.5 cm ×1.2 cm in size, with clear boundaries, gray-white incision, solid and delicate texture. Postoperative pathological examination showed a mixture of spindle cells and polymorphic cells (Figure 2). Immunohistochemical results: S100 (weak +), CD34 (+), Ki67 index ~20% (Fig. 3), CD10 (+), Vimentin (+) (Fig. 4), P16 (+). Pleomorphic undifferentiated sarcoma is considered. No distant metastasis of sarcoma was found by PET-CT and other examinations after operation. The TNM stage was T1N0M0G3Ⅱ, and adjuvant chemotherapy with AIM regimen (doxorubicin liposome + ifosfamide + mesna) was performed. After 2 cycles of chemotherapy, the patient improved and was discharged from hospital. After 1 and 2 years of follow-up, the patient did not relapse.
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