Patient, female, 75 years old. She was admitted to the gastroenterology department with epigastric distension and pain for 1 week with increased coughing and wheezing for 1 day. On admission, her symptoms were: weakness, nausea, epigastric distention and discomfort, occasional vague pain, wheezing and coughing with a small amount of white sputum that was not easily excreted, mild edema of both lower extremities, lying down at night, poor appetite, fair sleep, little urine and one stool for 3 days. He has a history of hypertension for more than 10 years, with a maximum blood pressure of 160/100mmHg, which has been controlled at 130/90mmHg with long-term antihypertensive medication. In 2002, when he was hospitalized for rheumatoid arthritis, his fasting blood glucose was 6.27 mmol/L and triacylglycerol was 2.09 mmol/L. In 2003, he started to take glucocorticosteroid therapy and gradually reduced the dosage from 30 mg per day to 5 mg per day and stopped taking it for one month before admission. He had a history of peptic ulcer. On admission, T380C, P96 times/min, R20 times/min, BP120/80 mmHg. He was clear and had centripetal obesity. A large area of light red irregular ringworm was seen in the chest and left forearm, the lips were cyanotic, barrel-shaped chest, and the right lower lung could be heard as a wet stadium. The right lower lung can be smelled as a wet mask, TP53.6g/L,TG2.07mmol/L,HBDH258U/L,LDH295U/L,Urea6.1 mmol/L. Blood cortisol(F):1.5ug/dl(6am),ACTH＜1.00pg/ml,24hUFC124ug/24h. Ultrasound:fatty liver,hepatomegaly . ECG: sinus rhythm with non-specific T-wave changes. Echocardiogram: aortic sclerosis, lightly enlarged left atrium, thickened septum, reduced left ventricular diastolic function. x-ray chest film (2007-11-29) right pleural thickening, small amount of pleural effusion possible. The right lung had increased density shadow, multiple fractures of thoracic vertebrae, multiple fractures of ribs and other parts, and enlarged heart. Subsequent repeated X-ray chest films suggested old lesions in both lungs and right lung atelectasis. Chest CT (2007-12-15): scattered patchy blurred shadows, multiple fibrous cord shadows, pleural thickening on both sides, more fatty density shadows in the mediastinum, multiple lymph node shadows visible within them, and enlarged heart shadows were seen in both lungs. On admission, pulmonary infection was considered, and the patient was transferred to ICU on December 12, 2007 after anti-inflammatory treatment but no significant improvement in pulmonary infection. 11:30PM on December 12, 2007, the patient was in a drowsy state and his blood pressure dropped. Respiration was shallow and fast, R30-40 times/min, HR115 times/min. Respiratory failure was considered and the patient was immediately ventilated with assisted breathing. The patient’s temperature rose to 38.2℃ on the night of December 13, and gradually decreased after physical cooling, According to the opinion of the whole hospital consultation, the treatment plan was adjusted as follows: 1. according to the sputum culture results, the antibiotics were adjusted to ceftazidime + vancomycin + amphotericin B liposome combination anti-infection; 2. additional gammaglobulin was added to target the current severe infection causing multivisceral failure; 3. hormones continued to be applied and acid suppressant was added at the same time; 4. continued to be intubated via trachea The sputum culture results showed that the pathogenic organism was Flavobacterium, but the drug sensitivity indicated full drug resistance, so all antibiotics were stopped and supportive treatment was given, with the addition of raw pulse to benefit qi and nourish yin, and tonics to clear heat and resolve phlegm. intermittent offline exercise was given on 09/01/2008. After gradual discontinuation of dopamine, blood pressure was stabilized in the normal range. The pulmonary infection was basically absorbed, with occasional cough and no fever. Condition at discharge: He complained of pain in the ribs, sternum and thoracic spine at times, and was given morphine analgesia and treated with local injection, and the pain was relieved. After discharge from the hospital, the patient took 2.5 mg of prednisone daily, but gradually developed symptoms such as loss of appetite and nausea, and then went to the hospital to recheck the low sodium chloride. Discussion: The patient had been taking prednisone for more than 4 years before admission for rheumatoid arthritis, and after admission, the blood cortisol (F): 1.5ug/dl (6am), adrenocorticotropic hormone (ACTH) <1.00pg/ml. 24hUFC 124ug/24h, according to these data, the diagnosis of secondary hyperalgesia can be made. It would be more convincing if an ACTH excitation test could be performed. In addition, the symptoms of these patients are atypical, so they are easily misdiagnosed as gastrointestinal disorders or respiratory tract infections, which delays the resuscitation time and results in a high mortality rate. Long-term oral administration of exogenous adrenocorticotropic hormone such as prednisone can suppress the function of hypothalamic-pituitary-adrenocortical axis, causing the atrophied adrenal cortex to fail to respond to stress when the patient encounters various kinds of stress such as infection or sudden discontinuation of the drug. This patient has been taking prednisone orally for a long time and has experienced all the side effects: ①, Cushing's syndrome; ②, induced infection aggravation; ③, peptic ulcer; ④, elevated blood glucose and lipids, atherosclerosis and hypertension; ⑤, osteoporosis, multiple fractures, hormone secretion and negative nitrogen balance. Discontinuation of hormones for one month prior to admission, the presence of secondary hyperalgesia, and a high risk of adrenocortical crisis when emergency situations such as infection arise. The patient had gastrointestinal and respiratory symptoms a week before admission. On admission, the blood potassium, sodium, chloride and albumin were all low. The patient's mediastinum was widened, her body shape was obese, and her diaphragm was elevated due to the accumulation of pericardial fat caused by the long-term application of glucocorticosteroids, which seriously compressed the chest cavity and obviously affected her breathing. The use of glucocorticosteroids causes pericardial fat accumulation, which is easily misdiagnosed as pericardial effusion or heart enlargement, and has been rarely reported in the past. The patient's long-term use of hormones caused immunosuppression of the body, which made him more prone to atypical infections on top of common bacterial infections. The patient was able to be discharged from the hospital in a stable condition, thanks to the combined diagnosis and treatment of Chinese and Western medicine. When the patient developed resistance to all pathogenic bacteria, all antibiotics were discontinued and Chinese medicine was used to clear the heat and detoxify the body and support the symptomatic and systematic and regular application of glucocorticoids.