Case information [Case 1] Male, 88 years old. He was admitted to our hospital on July 27, 2011 due to epigastric pain with nausea for 20 days. The patient had epigastric pain after meals with nausea and vomiting after eating for 20 days before admission. After anti-inflammatory treatment at the local hospital, the abdominal pain was relieved, but the pain started after eating. Ten days after the onset of the disease, the epigastric pain worsened and there was fever with a temperature of 38.9 0C, accompanied by chills, coughing and coughing of yellow mucous-like sputum. Ultrasonography performed at the local hospital showed strong echogenicity with acoustic shadowing in the gallbladder and no echogenic area around the gallbladder, and the diagnosis was “cholecystitis, gallbladder stones and peri-gallbladder fluid”. After symptomatic treatment, his condition gradually worsened and he was transferred to our hospital. Body check: temperature 37.8 0C, pulse 103 times/min, respiration 20 times/min, blood pressure 113/80 mmHg. skin and sclera were not yellowish. The right upper lung breath sounds were weak with wet rales. The abdomen was flat, no gastrointestinal pattern or peristaltic waves were seen; the liver and spleen were not detected under the ribs, the whole abdomen was painful with pressure, mainly in the right upper abdomen, Murphy’s sign was positive, the whole abdomen had mild rebound pain and muscle tension, no mass was palpated; mobile turbid sounds were negative. Laboratory findings: leukocytes 10.5´109/L, granulocyte percentage 89.1%; glutamate transaminase 11 U/L, total bilirubin 23.4 mmol/L, direct bilirubin 11.2 mmol/L, g-glutamyl transpeptidase 105 U/L, alkaline phosphatase 87 U/L, albumin 25.6 g/L; amylase normal. Ultrasound showed a 7.9´5.2 cm cystic anechoic liver lobe with a 0.5 cm thick cyst wall, dotted echogenicity and striated separation, and several strong echogenic clusters with acoustic shadowing in the gallbladder and common bile duct. Ultrasound diagnosis: 1, hepatic cyst; 2, dilated common bile duct with stones; 3, gallbladder stones and cholecystitis. CT diagnosis: 1, cystic low-density shadow in the liver, considering cyst; 2, cholecystitis and gallbladder stones; 3, dilated common bile duct and lower stones; 4, right lung infection and a small amount of pleural effusion on the right side. Magnetic resonance cholangiography (MRCP) showed that the right and left hepatic ducts, common hepatic duct and common bile duct were significantly widened with a diameter of about 1.7 cm, and 1.7 ´ 1.6 cm ovoid low signal shadow was seen in the middle duct of the common bile duct; 1.6 ´ 0.9 cm filling defect in the gallbladder floor. T2 high signal effusion was seen around the gallbladder, splenic hilar region and around the liver and spleen.MRCP diagnosis: 1, low biliary obstruction, common bile duct stones and gallbladder stones; 2, peritonitis and peritoneal effusion. The clinical diagnoses were: 1, gallbladder stones, cholecystitis; 2, common bile duct stones, cholangitis; 3, left hepatic cyst; 4, right lower pneumonia. Intraoperatively, he saw wrapped adhesions between the left outer lobe of the liver and the lesser curvature of the stomach, and after separating the adhesions, he saw a large amount of pus flowing out, and the lesser curvature of the stomach saw an open ulcer, about 1.5 cm in size, and there was hard scar tissue in the stomach wall on the side of the lesser curvature, and no obvious enlarged lymph nodes were seen around. Intraoperative diagnosis was gastric ulcer perforation, repair operation was performed, gallbladder was removed, common bile duct was explored, stones were removed, and common bile duct was sutured in one stage. After the operation, the family complained that he had a history of “gastric ulcer” for 20 years and a small amount of food each time. He was discharged from the hospital with good recovery after postoperative anti-inflammation, acid control, nutritional support, and control of pulmonary infection. [Case 2] Male, 95 years old, monk. He was admitted to our hospital on August 14, 2011 due to epigastric pain for 10 days. The patient had epigastric pain after meals for 10 days prior to admission and vomited several times, with stomach contents. He was diagnosed with “intra- and extra-hepatic bile duct stones” by ultrasonography at the local hospital, and was treated with anti-infection, antispasmodic and other symptomatic treatments, but his symptoms were not significantly relieved, so he was transferred to our hospital. 15 years ago, he had undergone cholecystectomy and choledocholithiasis in our hospital for gallbladder stones and common bile duct stones, and 9 years ago, he underwent femoral head replacement for right femoral neck fracture. Body temperature was 36.6°C, pulse 92 beats/min, respiration 19 beats/min, blood pressure 131/84 mmHg. skin and sclera were mildly yellowish. Breath sounds in both lower lungs were weak. The abdomen was flat, no gastrointestinal type or peristaltic wave was seen; epigastric pressure pain, no rebound pain throughout the abdomen, no mass was palpated; mobile turbid sounds were negative. Laboratory findings: leukocytes 6.53´109 / L, granulocyte percentage 78.5%; glutamate transaminase 46 U / L, total bilirubin 44.4 mmol / L, direct bilirubin 24.7 mmol / L, g-glutamyl transpeptidase 213 U / L, alkaline phosphatase 350 U / L, albumin 24.1 g / L. Amylase was normal. Ultrasound examination showed an 8.9´7.6 cm anechoic area in the left lobe of the liver with fibrous separated echogenic floating, dilated intra- and extrahepatic bile ducts and multiple strong echogenicity. CT showed that the intrahepatic bile ducts and common bile ducts were significantly thickened, and multiple nodule-like dense shadows were seen inside. The left lobe of the liver showed a huge cystic low-density shadow, about 9.1×9.7 M. Fluid was seen in the abdominal cavity. CT diagnosis: 1, “post cholecystectomy and common bile duct exploration” changes; 2, multiple stones and dilatation of intra- and extra-hepatic bile ducts and common bile duct; 3, giant cystic hypodense shadow in the left lobe of the liver; 4, fluid in the abdominal cavity; 5, fluid in the chest cavity on both sides. Main clinical diagnosis: 1, intrahepatic bile duct and common bile duct stones, cholangitis; 2, hepatic cyst; 3, bilateral pleuropleural effusion; 4, post cholecystectomy; 5, post right femoral head replacement. After symptomatic treatment with anti-infection and nutritional support, the abdominal pain symptoms were relieved. However, after the condition was stabilized, the patient had symptoms of epigastric pain again when eating a liquid diet. During the case discussion, it was considered that the cystic mass in the left outer lobe of the liver might be caused by gastric perforation, and ultrasound-guided puncture was performed on August 21, 2011 to extract the cloudy fluid, and an 8F drainage tube was placed to drain the fluid. A small amount of Melan was administered orally and the drainage tube was stained with Melan. Additional diagnosis of gastric perforation was made. The patient was treated with anti-infection, acid control, nutritional support and keeping the drainage open. The drainage flow was 500ml on the first day after the puncture, and then gradually decreased. 2 weeks later, there was no fluid outflow, and the patient’s symptoms improved significantly and the gastric perforation was cured and discharged. Reasons for misdiagnosis Gastric and duodenal perforation in elderly patients is easy to be misdiagnosed and missed: j In elderly patients, physiological function is reduced, response to pain is slow, abdominal wall muscles are atrophied, when gastric and duodenal perforation, clinical symptoms are atypical, pain is lighter, and “plate-like abdomen” signs are not easily seen. Some authors reported 89 cases of gastroduodenal ulcer perforation in the elderly, and only 35.9% of patients had obvious plate-like abdominal signs. k In elderly patients, the body’s reaction ability is poor, and indicators such as white blood cell count and body temperature do not reflect the inflammatory changes in the body in time when gastric perforation occurs. In this group, the leukocytes were mildly elevated in patient 1 and not significantly elevated in patient 2. However, the granulocyte percentage was significantly higher than normal in both patients. l Difficulties exist in history taking and comprehensive ancillary examinations in elderly patients. The history of the elderly patients was not accurately described at the time of consultation, and their mobility was limited, so the clinical ancillary examinations were not easily completed. The two patients in this group had hearing impairment and had difficulty in communication; when they were referred to our hospital, they only had ultrasound findings, and no X-ray abdominal examination was performed, and the presence or absence of subdiaphragmatic free gas at the early stage of the disease was unknown. No careful analysis of imaging features: in this group of 2 patients, after gastric perforation, an encapsulated effusion between the stomach and the left lobe of the liver was formed, and both ultrasound and CT suggested a cystic mass in the left lobe of the liver, but careful analysis led to imaging features different from those of hepatic cysts: j The cystic mass had an extremely irregular morphology (Figures 1 and 2), and in case 2, the cystic mass even reached the lower part of the transverse colon, which was obviously different from simple hepatic cysts that were round or oval in the liver The cysts in case 2 even reached the lower part of the transverse colon, which is obviously different from the simple hepatic cysts which are round or oval with no echogenic dark areas. k Simple hepatic cysts can be one or several, varying in size, with thin and smooth walls and clear demarcation from the surrounding tissues, unlike the cysts with thick walls, dotted echogenicity and separation seen on ultrasound in our patients. Limitations in diagnostic thinking: Satisfied with the diagnosis of cholelithiasis, the patient’s symptoms were all attributed to cholecystitis and/or cholangitis. No deeper investigation was made as to why the bilirubin was not significantly elevated, the symptoms were not relieved by prolonged use of antibiotics, and the pain throughout the right upper abdomen after eating rather than primarily in the right upper abdomen were different features from those of cholelithiasis. In addition, history taking and review were not comprehensive, such as ignoring the history of gastric ulcer in case 1 and not reviewing the history of previous surgery without liver cyst in case 2. Prevention of misdiagnosis and treatment measures. With the aging of our social population, the incidence of gastric and duodenal ulcer perforation in the elderly is on the rise. Therefore, for elderly patients with cholelithiasis, detailed medical history, symptoms and signs should be understood to avoid gastric perforation symptoms being masked by cholelithiasis symptoms, and abdominal standing X-ray should be performed at the early stage of the disease to understand whether there is free gas under the diaphragm; some patients with negative X-ray examination can be positive after re-examination by gastric tube injection. In case of senior gallstone patients with cystic masses in the left lobe of the liver, the possibility of gastric perforation should be considered, instead of just satisfying the diagnosis of hepatic cysts, ultrasound-guided abdominal puncture is feasible to confirm the diagnosis if necessary. Treatment measures: As long as the patient’s physical condition permits, surgery should be preferred. At present, the simple repair plus postoperative comprehensive treatment is advocated for gastric perforation in the elderly. Surgery should be simple and effective. In our case 2, the treatment purpose was also achieved by puncture and drainage plus comprehensive treatment, which indicates that for patients with ultra-high-aged gastric perforation who cannot tolerate surgery, comprehensive treatment measures such as puncture and drainage to relieve symptoms + nutritional support + proton pump antagonist (omeprazole) for gastric wall cells can also achieve satisfactory results.