2016年 · 第39卷第10期

The 2016 edition of the hospital-acquired pneumonia (HAP) guidelines jointly developed by the American Society of Infectious Diseases (IDSA) and ATS explicitly opposes the use of tigecycline to treat HAP caused by Acinetobacter. Although there is low-quality evidence, it is strongly recommended. Given the authority of the American Society of Infectious Diseases and ATS around the world, this concluding opinion will have an immeasurable impact in various countries, and will be followed by fierce debate. Therefore, in the essay column of the editor-in-chief of this issue, Professor Liu Youning, the editor-in-chief of this journal, discussed from two aspects in the article "Can tigecycline be used to treat hospital-acquired pneumonia caused by Acinetobacter": (1) The basis for denying the therapeutic effect of tigecycline on HAP caused by Acinetobacter is insufficient: First of all, it should be explained that tigecycline has not been approved for HAP in the United States. If doctors choose to apply it, it is also an off-label use as in China, but the relevant regulations of American medical regulatory institutions are more loose, giving doctors greater power. In addition, it cannot be ignored that colistins (Polymyxin B and Colistin) are available in the United States. Generally speaking, these two drugs are more sensitive to Acinetobacter than tigecycline. Even so, the reason to completely deny tigecycline in the treatment of HAP caused by Acinetobacter is not sufficient. (2) In China, the combination regimen based on tigecycline is an indispensable and important choice for the treatment of HAP caused by Acinetobacter baumannii: China and the United States have the following four main differences: ① The pathogen of HAP is mainly non-fermenting bacteria (MRSA in the United States is often the first), among which Acinetobacter baumannii is the most common; ② The resistance of Acinetobacter baumannii to carbapenem in China is much more serious than that in the United States; ③ Colistins have not been re-approved in China so far; ④ When treating serious infections of multi-drug resistant gram-negative bacilli such as Acinetobacter, we advocate combined medication, including tigecycline, polymyxin and carbapenems, and try to minimize the use of one of these drugs alone. To learn more, read this article.

The 2016 edition of the guidelines for the diagnosis and treatment of hospital-acquired pneumonia (HAP) jointly developed by the American Society of Infectious Diseases (IDSA) and ATS explicitly opposes the use of tigecycline to treat HAP caused by Acinetobacter, although there is little evidence (low-quality evidence), but it is a strong recommendation (strong recommendation)^[1]。

Many of the alveolar hypopnea syndromes covered in the 3rd edition of the International Classification of Sleep Disorders (ICSD-3) in 2014 are "reluctant to breathe" related to central regulatory dysfunction^[1,2]。 Central regulatory dysfunction and chronic hypoxia and/or high CO₂Stimulation leads to chemoreceptor passivation, brainstem respiratory center lesions, and can also be caused by gene mutation^[3]Among them, the most typical one related to heredity is congenital central alveolar hypopnea syndrome (congenital central hypoventilation syndrome, CCHS). The main manifestations of CCHS are alveolar hypoventilation and autonomic dysfunction. The key to the pathogenesis of CCHS is that the change of PHOX2B (paired-like homeobox 2B) gene function leads to the decrease of sensitivity of chemoreceptors in respiratory center. PHOX2B gene testing has become a necessary examination for the diagnosis of CCHS, which can predict the prognosis of patients, making CCHS a typical case of translational medicine and precision medicine in the field of sleep respiration, which has been transformed from basic research to clinical application^[4]。 As a genetic disease, CCHS mostly starts in infants and young children, but there are more and more reports of late-onset patients in children and adults. The American Thoracic Society (ATS) in 1999 and 2010Am J Respir Crit Care MedPublished guidelines on the diagnosis, treatment, and genetic mechanisms of CCHS^[4,5], greatly strengthening the awareness of the disease; With the development of sleep medicine, the diagnosis and treatment of CCHS have also made great progress. The popularization and application of sleep breathing monitoring with multi-channel physiological recorder can provide objective evidence of alveolar hypopnea in the early stage, and home mechanical ventilation treatment has greatly improved the prognosis of patients.

Background: Clinical work often encounters cases of multiple pulmonary cystic lesions, but the differential diagnosis of such diseases is challenging. Multidisciplinary discussion between clinical and radiologist is helpful to confirm the diagnosis of this type of disease, especially the findings of chest high-resolution CT have a good role in the differential diagnosis of this type of disease. According to the imaging characteristics of intrapulmonary cystic lesions, this paper introduces the diagnostic process of this kind of diseases. Firstly, pulmonary cystic lesion refers to the round lung containing air cavity, which is clearly demarcated with the surrounding lung tissue, and the wall thickness of the air cavity<2 mm, there are generally no liquid or solid components in the air cavity. It is necessary to differentiate a series of lesions very similar to cystic lesions of the lung, including emphysema, honeycomb lung, cystic bronchiectasis and pulmonary cavities. Secondly, it is necessary to clarify the distribution location of pulmonary cystic lesions in the lungs, subpleural or pulmonary parenchyma: if they are subpleural, emphysema, honeycomb lung and bullae are more common. Third, to determine whether cystic lesions in the lungs are single or multiple? For single intrapulmonary cystic lesions, pulmonary bullae and bronchial cysts are more common. Finally, for diffuse/multiple intrapulmonary vesicles, it is necessary to determine whether there are other pulmonary imaging abnormalities: (1) if there are no other concomitant pulmonary shadows, then lymphangioleiomyomatosis (LAM), middle and late stage of pulmonary Langerhans histiocytosis (PLCH), Birt-Hogg-Dubé syndrome (BHD syndrome), tracheobronchial papillomatosis, bronchopulmonary cancer, intrapulmonary metastatic cancer and certain pulmonary infections, etc.; (2) Combined with multiple pulmonary nodules: common in lymphocytic interstitial pneumonia, early PLCH, pulmonary light chain deposition sign and pulmonary amyloidosis; (3) Combined with pulmonary ground glass shadow: common in pneumocystis pneumonia and desquamative interstitial pneumonia.

According to the data of China's Health Statistics Yearbook in 2013, the peak of pneumonia deaths in China's population is<Among children aged 5 years and adults aged ≥50 years, infants aged 0 to 1 years (more than 20/100,000 in both urban and rural areas) and elderly people aged ≥60 years (more than 5/100,000 in both urban and rural areas) have the highest mortality rate of pneumonia.

Bronchial asthma (asthma) and chronic obstructive pulmonary disease (COPD) are the two most common chronic inflammatory diseases of the lower respiratory tract. With in-depth research on the mechanism of disease, more and more evidence shows that both asthma and COPD patients have different phenotypes. In 2014, the Global Asthma Initiative (GINA)^[1]It has been clearly indicated that asthma is a heterogeneous disease with multiple phenotypes; Similarly, patients with COPD also have different clinical phenotypes. In recent years, it has been found that some patients have both asthma and COPD. Global Chronic Obstructive Pulmonary Disease Initiative (GOLD) 2014^[2]And GINA^[1]This group of patients is defined as asthma-COPD overlap syndrome, or ACOS, and this group of patients also has different phenotypes. The results of several studies have shown that patients have different disease phenotypes and different responses to treatment. For example, subgroups with high eosinophil counts in COPD patients may be more effective for hormone or anti-eosinophil therapy^[3]Asthmatic patients with severe asthma or smoking do not respond well to hormone therapy due to the presence of neutrophil infiltration^[4]Etc. This suggests that specific inflammatory mediators driving airway inflammatory responses play a key role in targeted therapy. Patients may be more beneficial by analyzing the dominant inflammatory mediators in the patient's airway inflammation by bronchoscopic biopsy or induced sputum, or looking for corresponding biomarkers, so as to administer targeted therapy to specific inflammatory mediators. Therefore, this paper analyzes the published research on targeted therapy of airway diseases at home and abroad, so as to provide reference for clinical selection of better treatment options.

Pulmonary hypertension is a common complication of sarcoidosis, which is more likely in patients with advanced pulmonary sarcoidosis^[1]。 The mortality rate of patients with sarcoidosis-associated pulmonary hypertension (SAPH) increased significantly^[2,3]In recent years, it has gradually attracted attention. Since the pathogenesis of SAPH remains unclear and many different pathogenic pathways are involved, SAPH is classified as category 5 in the World Health Organization (WHO) classification of pulmonary hypertension. The epidemiology, predictors, pathogenesis, diagnosis and treatment of SAPH are reviewed below.

At present, lung cancer is a malignant tumor with the highest morbidity and mortality rate in the world. Distant metastasis is the main cause of death in lung cancer patients. However, many patients have missed the best operation time when diagnosed. Even after early diagnosis and corresponding treatment, some patients still have recurrence of lung cancer within 5 years, which suggests that micrometastasis may occur in the early stage of lung cancer. Early detection, metastasis, efficacy monitoring and prognosis evaluation of lung cancer are of great significance for the treatment of lung cancer patients. circulating tumor cells (CTC) have received more and more attention because hematogenous dissemination is one of the important pathways in lung cancer cell metastasis. The results confirm that CTC can be used to judge the metastasis of colorectal, breast, prostate and lung cancer^[1]。

Tracheal stenosis is an urgent and challenging condition in clinical practice. Tracheal stenosis is divided into benign and malignant. Benign stenosis is generally caused by trauma, tracheal intubation or tracheotomy, inhalation injury, infection and congenital malformation. Malignant stenosis is mostly caused by primary tumor, metastatic tumor or malignant tumor compression of surrounding tissues of the lung trachea. Since Colles proposed the concept of tracheal stenosis in 1886^[1]Clinicians have gradually gained a further understanding of tracheal stenosis. At present, the best treatment for tracheal stenosis is still surgical resection and tracheal reconstruction^[2]。 However, some patients are not suitable for surgery due to severe tracheal stenosis, excessive tracheal damage or systemic complications, or some patients with tracheal stenosis need to recover for a period of time before surgical treatment due to certain conditions (such as central nervous system injury). In this case, it is necessary to maintain the patency of the airway. Tracheostomy is the simplest and more practical method, but because it damages the normal vocal function and changes the pathway of air into the trachea through the oropharynx, there will be many complications, such as chronic cough, increased airway secretions and repeated infections of the lower respiratory tract. In order to solve these problems, Montgomery pioneered the design and introduction of T-tube, which provided a new treatment concept for the treatment of tracheal stenosis.

The study of lung epithelial stem cells is one of the important research hotspots in respiratory system. Basal cells and type 2 alveolar cells have the ability of self-renewal and differentiation, and play an important role in the repair and regeneration of respiratory epithelium. Lung diseases such as bronchial asthma (asthma for short), COPD, lung cancer and influenza are accompanied by damage, proliferation or carcinogenesis of epithelial cells. In recent years, the research on the identification and functional regulation of lung epithelial stem cells has increased rapidly. These research results will speed up the reveal of the mechanism of lung epithelial stem cells in the occurrence and development of major lung diseases. It can be predicted that lung epithelial stem cells will provide new targets for the treatment of major lung diseases such as asthma. Diseases provide new targets.

pyrazinamide (PZA), a nicotinamide analogue, is one of the important drugs for tuberculosis chemotherapy. It can kill MTB in the semi-dormant period, thus reducing the treatment period of tuberculosis from 9 to 12 months to 6 months. Although PZA plays a key role in the treatment of tuberculosis, its target of action and the molecular mechanism of anti-MTB action are not well understood. In recent years, with the emergence and spread of drug-resistant MTB, the molecular resistance mechanism of MTB has received extensive attention. The study of the mechanism of PZA resistance by MTB not only helps to understand the cause of drug resistance, but also helps to establish a molecular diagnostic method for rapid detection of PZA resistance.

primary pulmonary artery sarcoma (PPAS) is a rare malignant tumor of the pulmonary vascular system, which originates from endothelial cells of the pulmonary artery^[1]The symptoms and signs lack specificity, and the diagnosis is difficult. It is easy to be misdiagnosed as pulmonary thromboembolism (PTE) and the prognosis is poor. At present, the literature on PPAS is mostly case reports or small-scale retrospective clinical studies. In order to improve the understanding of PPAS and reduce misdiagnosis and missed diagnosis, the diagnosis and treatment status of primary pulmonary artery sarcoma in recent years is introduced as follows.

Oxygen inhalation is an important treatment for many diseases such as respiratory distress syndrome, circulatory shock, severe infection and multiple organ failure in newborns or adults. However, inflammatory exudation caused by acute diffuse alveolar injury and pulmonary fibrosis may occur during long-term high concentration oxygen inhalation, which lacks effective treatment and is life-threatening^[1,2]。 The results indicate that the activation of lung myofibroblasts expressing α-SMA and collagen-Ⅰ as molecular markers plays an important role in the formation of pulmonary fibrosis^[3]。 Because that cell hyperproliferate, decrease apoptosis, and secrete and synthesize large amounts of extracellular matrix in the fibrous foci and surrounding tissues, the lung tissue is remodeled, and ultimately structural changes and loss of function in the lung^[4]。 Hyperoxia induces the phenotypic transformation of lung fibroblasts into contractile lung myofibroblasts and increases collagen synthesis^[5]。

A 19-year-old male developed distended pain in the upper abdomen and dull pain in the back without obvious trigger for 2 weeks, aggravated with radiating pain in the right shoulder for 3 days. No symptoms such as cough, fever, jaundice, nausea, vomiting, diarrhea and melena. There was no history of tuberculosis and contact with tuberculosis patients, and no history of tumor family members. Physical examination: No positive signs were found. Laboratory tests: 182 U/L for amylase, 125 U/L for pancreatic amylase and 198 U/L for lipase. Irregular antibody test negative; MTB antibody negative; Five indexes of tumor were normal. Blood image and biochemical examination were normal. Ultrasound examination showed solid hypoechoic nodules in the neck of the pancreas with clear boundaries and uniform echoes (Figure 1)。 Clinically, he was admitted to the hospital with "pancreatic tumor". Imaging examination: Chest CT normal. Upper abdominal CT showed solid low-density nodules in the pancreatic neck, about 18 mm ×18 mm in size, with clear boundaries. The enhanced scan showed annular enhancement, uneven liver perfusion in the early artery, and obvious enhancement in the left lobe (Figure 2)。 MRI pancreatic neck showed rounded and slightly longer T₁, etc. T₂Signal nodule, approximately 19 mm ×16 mm ×15 mm in size, with lower T visible inside₂Signal, nodule inverse phase signal did not decrease significantly, diffusion-weighted imaging showed high signal, apparent diffusion coefficient value 0.001 2 (b =500), enhanced scan showed annular enhancement, clear boundary with pancreatic peripheral parenchyma, uneven liver perfusion in early artery, and obvious enhancement in left lobe (Figure 3,Figure 4,Figure 5,Figure 6)。 Surgical findings: About 30 mm ×30 mm mass in the neck of the pancreas, gray-white, high tension, local fluctuation sensation, cystic changes in the tumor after incision, and a small amount of yellow-white liquid and caseous necrosis in the sac content. No enlarged lymph nodes were observed in the abdominal cavity. The pathological results showed epithelial-like granulomatous lesions, consistent with tuberculosis, and acid-fast bacilli were found by acid-fast staining (Figure 7)。 The patient recovered well after six months, one year and two years of follow-up.

A 59-year-old male was admitted to the hospital on January 12, 2014 due to "repeated cough and expectoration for more than 2 years, aggravated with hemoptysis for 2 days". In December, 2012, he was diagnosed as "double lung tuberculosis" in the respiratory tuberculosis department of our hospital. After anti-tuberculosis treatment according to the course of treatment, he still had repeated cough and yellow phlegm, and did not perform regular outpatient chest CT examination. 2 days ago, cough and expectoration were worse than before, and bright red blood was poured once, about 200 ml, so I came to our department for treatment. Chest CT examination performed in our outpatient department showed increased pulmonary field transparency, patchy high-density blurred shadows in both upper lungs, punctate calcification in the interior, cavity formation in the left upper lung, swollen lymph nodes about 1.5 cm ×1.4 cm in size in the mediastinum, right pleural effusion, calcification of the aorta and bilateral coronary arteries (Figure 1)。 Laboratory test: 4.89×10 white blood cells⁹/L, neutrophils were 3.34×10⁹/L, lymphocytes were 1.05×10⁹/L, procalcitonin was 0.07 μ g/L, ESR was 66 mm/1 h, no acid-fast bacilli were found in the acid-fast staining of sputum smear, and anti-MTB antibody was positive. Strong positive PPD skin test. Diagnosis: Secondary tuberculosis of both lungs with left upper lung cavity, negative sputum smear. After admission, the treatment effect of Yunnan Baiyao, carosulfonate sodium, carbamic toluic acid, hemostatic sensitivity and hemagglutinase promoting coagulation of white-eyebrown snake venom was not good, and hemoptysis was still repeated. Considering the poor hemostatic effect of internal medicine, selective bronchial artery embolization was performed with the consent of the patient and family members. The procedure went smoothly, the hemoptysis stopped gradually after the operation, and no mobility impairment of both lower limbs was found at the end of the operation. After 3 h, the patient complained that both lower limbs could not move. Physical examination: Pain and temperature perception in the plane below the third vertebral body of the sternum were significantly reduced, abdominal wall reflex was normal, muscle strength of both lower limbs was reduced, muscle strength grade 0, tendon reflex of both lower limbs disappeared, bilateral Papanicolaou sign, Chadock sign and Oppenheim sign were all positive, deep sensation was not impaired, and bladder sphincter dysfunction. Magnetic resonance examination showed mild edema of the spinal cord at the level of the third vertebral body of the sternum (Figure 2)。 Angiography showed left 3, 4, right 2~4 intercostal arteries were not shown (Figure 3)。 Please consider anterior spinal artery syndrome after multidisciplinary consultation in the whole hospital. Spinal arteriography showed that the left 3rd and 4th intercostal arteries were common, the distal branch arteries were sparse, and the blood supply of the spinal arteries was insufficient. Methylprednisolone pulse therapy, circulation improvement and nerve nutrition were given, and the therapeutic effect was poor.

follicular dendritic cell sarcoma (FDCS), also known as dendritic reticular cell sarcoma, is a rare malignant tumor originating from follicular dendritic cells in the germinal center. FDCS mostly occurs in cervical and axillary lymph nodes, and about one third of cases occur in tonsils, thyroid gland, palate, nasopharynx, parotid gland, lung, breast gland, liver, spleen, pancreas, gastrointestinal tract and intracranial tract other than lymph nodes^[1]But lesions originating in the lungs are rare. A case of primary pulmonary FDCS admitted to Enze Medical Center in Taizhou, Zhejiang Province is reported as follows.

On the basis of interpretation of mechanical ventilation pressure and breathing patterns, interpretation of ventilation patterns, first of all, basic ventilation patterns^[1,2]。

The basic ventilation mode has been developing and evolving, and a series of new modes have appeared^[1,2]。