放射性肺炎如何处理？

我有个病人，食管癌放疗后20月，出现咳嗽咳痰，抗生素使用无效，胸部平片及CT提示：放射性肺炎，小剂量激素使用效不显。本人入行不久，想请教各位前辈，是否可以激素治疗？如何用？有无其他方法？放射性肺炎的治疗原则是足量足够时间的激素的使用，地塞米松可以使用10－20mg／日，时间看病情缓解程度决定，缓慢减量。注意加用抗生素及制酸治疗。当心如果足量抗生素及激素使用后病情仍未得到缓解，需警惕真菌感染。其他对症支持治疗，特别是能过提高呼吸道粘膜抵抗力的药物，如沐舒坦、氨溴索等；可加用H2受体抑制剂如苯海拉明，非甾体抗炎药如消炎痛等以减轻炎性渗。，放射性肺炎的治疗： 1首先是即时的皮质激素治疗。在急性期，及时的激素治疗可降低炎性反应的程度，增加炎性渗出的吸收，对某些因对放射致敏产生的反应效果更佳。同时可促进Ⅱ型细胞内表面活性物质的合成和分泌。 常用的剂量为每日10mg.需注意在症状和体征得到控制后，激素剂量应缓慢减少，过快停药可使症状和体征出现反跳现象，并且更加难以控制。此外，对于后期纤维化过程，激素的应用无益而有害。 2其次，由于放射性肺炎常伴有继发感染，及时大剂量使用抗生素是需要的。抗生素的选择应据感染的菌种和药敏结果而定。 3预防方面，应根据患者的具体情况制定相适易的放疗计划，尽量减少肿块周围正常组织的照射剂量，如条件许可，可采用适形治疗的方法。预防放射性肺炎除了大剂量皮质激素外，放疗同时可以给予氨磷汀。一般来讲急性放射性肺炎往往发生在放疗后3－6个月之间，楼顶的患者在放疗后20个月出现症状，比较少见。放射性肺炎的诊断要点有：1肺部接受过放射性治疗。 2 以发热、咳嗽、呼吸困难等肺部症状为主。 3 肺部病变与照射野一致。尤其第三点是鉴别感染与放射性肺炎的关键。放射性肺炎的预防主要在合理的放疗计划，治疗主要是急性期应用皮质激素，一般为地米10毫克/天 最多可给到40毫克冲击，然后缓慢减量。对于后期因主要是肺纤维化，像本例食道癌放疗后20个月，以隆突区的纤维化较常见，咳嗽症状明显， 激素使用没啥有利之处。由于放射性肺炎往往合并细菌感染，给抗生素是必要的。另外给予一定的支持治疗较好，如对症的止咳药，雾化吸入，低流量吸氧等。总之，放射性肺炎到了后期即纤维化期治疗效果都不是太好。放疗二十个月了比如罗红霉素激素IL-2,IFN等等均无效了放射性肺炎分为：早期的急性放射性肺炎（放疗开始后90天内）和后期的放射性纤维化（放疗开始90天后）。急性放射性肺炎以抗生素和肾上腺激素治疗为主，必要时给予支气管扩张剂和吸氧对症处理。后期放射性肺纤维化尚无有效的治疗方法，重在预防，即在给予肿瘤高剂量照射的同时，尽可能避免和减少对正常肺组织的照射。Pentoxifylline in the Treatment of Radiation-Induced Fibrosis Journal of Clinical Oncology, Vol 22, No 11 (June 1), 2004: pp. 2207-2213Paul Okunieff, Elizabeth Augustine, Jeanne E. Hicks, PURPOSE: Fibrotic sequelae remain the most important dose-limiting toxicity of radiation therapy to soft tissue. Functionally, this is reflected in loss of range of motion and muscle strength and the development of limb edema and pain. Tumor necrosis factor alpha and fibroblast growth factor 2 (FGF2), which are abnormally elevated in irradiated tissues, may mediate radiation fibrovascular injury. PATIENTS AND METHODS: In an open label drug trial, we studied the effects of pentoxifylline (400 mg orally tid for 8 weeks) on 30 patients who displayed late, radiation-induced fibrosis at 1 to 29 years posttreatment (40 to 84 Gy). The primary outcome measurement was change in physical impairments thought to be secondary to radiation, including active and passive range of motion (AROM and PROM), muscle strength, limb edema, and pain. Plasma levels of cytokines (tumor necrosis factor alpha and FGF2) also were measured. Twenty-seven patients completed baseline and 8-week assessments, and 24 patients completed baseline, 8-week, and 16-week assessments. RESULTS: After 8 weeks of pentoxifylline intervention, 20 of 23 patients with impaired AROM and 19 of 22 with impaired PROM improved; 11 of 19 patients with muscle weakness showed improved motor strength; five of seven patients with edema had decreased limb girth; and nine of 20 patients had decreased pain. Pretreatment FGF2 levels dropped from an average of 44.9 pg/mL to 24.0 pg/mL after 8 weeks of treatment. CONCLUSION: Patients receiving pentoxifylline demonstrated improved AROM, PROM, and muscle strength and decreased limb edema and pain. Reversal of these delayed radiation effects was associated with a decrease in circulating FGF2Background: Radiation pneumonitis is an interstitial pulmonary inflammation that can develop in as many as 5-15% of patients with thoracic irradiation, most often due to lung cancer, breast cancer, lymphoma, or thymoma. Acute radiation pneumonitis occurs within 1-6 months following treatment. Symptoms can include low-grade fever, cough, and fullness in the chest. Severe reactions can result in dyspnea, pleuritic chest pain, hemoptysis, acute respiratory distress, and death. Fibrosis can occur without previous pneumonitis but once pneumonitis occurs, fibrosis is almost certain to take place. The radiographic hallmark of radiation pneumonitis is a diffuse infiltrate corresponding to a previous radiation treatment field.Pathophysiology: Two separate and distinct mechanisms are involved in the pathogenesis of acute radiation pneumonitis. The first, classical radiation pneumonitis, involves direct toxic injury to endothelial and epithelial cells from the radiation, resulting initially in an acute alveolitis. This process leads to an accumulation of inflammatory and immune effector cells within the alveolar walls and spaces. The accumulation of leukocytes distorts the normal alveolar structures and results in the release of lymphokines and monokines. The alveolar macrophage is thought to play a central role in the subsequent development of chronic inflammation (fibrosis). The second mechanism, sporadic radiation pneumonitis, results in an "out-of-field" response. This is thought to be an immunologically mediated process resulting in bilateral lymphocytic alveolitis. In contrast to acute radiation pneumonitis, permanent changes of radiation fibrosis can take months to years to evolve but normally stabilize within 1-2 years. Pulmonary fibrosis is the repair process that follows the acute inflammatory response and is characterized by progressive fibrosis of the alveolar septa thickened by bundles of elastic fibers. The process is not fully understood but believed to be a function of activation on cells to produce cytokines and growth factors, which orchestrate most aspects of the inflammatory response. Current research focuses on chemotactic factors for fibroblasts, including transforming growth factor-beta (TGF-B, a cytokine known to promote connective tissue formation), fibronectin, and platelet-derived growth factor (PDGF). The most important stimulator of collagen synthesis is believed to be TGF-B, for which the alveolar macrophage is the main source.Frequency: In the US: Asymptomatic radiologic findings are observed in as many as 50% of treated patients. Clinical radiation pneumonitis can develop in 5-15% of patients undergoing radiation treatment to the thorax. The clinical pathologic course is biphasic and is dependent upon the dose and volume of lung exposed and the use of chemotherapy agents. Mortality/Morbidity: Morbidity and mortality vary greatly based on the volume of lung irradiated, dose per fraction of radiation delivered, use of concomitant chemotherapy, total dose of radiation delivered, and performance status of the patient. Predisposing factors such as smoking history, collagen vascular disease, and steroid withdrawal also affect the frequency of symptoms. Moderate-to-severe radiation pneumonitis occurs in an estimated 2-9% of patients treated for lung cancer with combination chemotherapy and irradiation. This represents the high-risk group. Even in this high-risk group, mortality is estimated to be 1-2%. Race: No race predilection exists. Sex: Women tend to have higher rates of moderate-to-severe radiation pneumonitis. This may reflect that most women have smaller lung volumes and smaller forced expiratory volume in 1 second (FEV1) values. Thus, given similar radiation field sizes, a greater proportion of lung may be at risk. This also may represent an autoimmune predisposition to injury. Many autoimmune diseases, such as systemic lupus erythematosus, are more common in women than in men and are a known risk factor for increasing the chance of subsequent radiation-induced lung damage. Age: No direct link to age exists. However, rates do increase as performance status decreases, which is indirectly related to age. Clinical Details: Classic radiation pneumonitis has 3 main phases. Early phase (first month): This represents a latent period of pneumonitis. During this phase, loss of both type I and type II pneumonocytes occurs. Type II pneumonocytes produce surfactant, and decreased amounts result in transudation of serum proteins into the alveoli. This leads to edema of the intersitial spaces. Intermediate phase (1-6 months): This is characterized by dose-dependent leakage of proteins into the alveolar space, thickening of the alveolar septa, and development of clinical symptoms. Common clinical symptoms include nonproductive cough, low-grade fever, tachycardia, and dyspnea. Late phase (6 months and later): This is characterized by a loss of capillaries and increased collagen deposition. This results in restrictive changes within the lung characterized by reductions in vital capacity, lung volumes, diffusing capacity of lung for carbon monoxide (DLCO), and total lung capacity.Preferred Examination: Chest radiography is the preferred initial examination. Further imaging can be performed with CT scans, which are more sensitive. Nuclear medicine imaging with ventilation/perfusion scans and, more recently, fluorine 18 fluorodeoxyglucose-positron emission tomography (FDG-PET) may provide additional information in clinically and radiographically equivocal cases.Limitations of Techniques: Chest radiography :Low sensitivity in detecting small volumes Cannot quantitate the volume of affected lung versus the total lung volume Low sensitivity in detecting small areas close to the chest wall, as is the case in tangential field irradiation for breast cancer DIFFERENTIALS Idiopathic Pulmonary Fibrosis Lung, Drug-induced Disease Scleroderma, Thoracic Other Problems to be Considered: Recurrent cancer X-RAY Findings: Chest radiographic findings vary from normal or subtle hazy ground glass density to marked patchy or homogenous consolidation. Air bronchograms are commonly present and volume loss of the affected portion of the lung may be observed. There is usually a sharp boundary crossing the normal anatomic structures without segmental or lobar distribution. Rarely, an entire lung or both lungs are involved (adult respiratory distress syndrome [ARDS]).Degree of Confidence: Chest radiographs occasionally are normal.False Positives/Negatives: False positives include recurrent disease, infection/pneumonia, cardiac disease, and lymphangitic carcinomatosis. CAT SCAN Findings: Acute radiation pneumonitis changes, especially the subtle ground glass opacity (GGO), are seen earlier on CT than on radiographs. Different patterns of radiation-induced damage observed on chest radiographs are seen to better advantage with CT and vary from early homogenous, slight increase in radiodensity (GGO), to patchy or homogenous consolidation. Small pleural and pericardial effusions are not uncommon. CT is useful in detecting recurrent tumor in an irradiated area. This is suggested by the presence of a masslike lesion or development of focal air space opacity without air bronchogram. CT scans can be used to detect and calculate volumes of lung affected as a percentage of the total lung volume.Degree of Confidence: CT scans are more sensitive that chest radiographs and detect abnormalities in as many as 50% of patients. NUCLEAR MEDICINE Findings: Nuclear medicine ventilation/perfusion scans are frequently abnormal following radiation treatment for lung cancer, breast cancer, or lymphoma involving the mediastinum. Perfusion defects are more common than ventilation defects. This process is thought to be the result of abnormal shunts occurring after radiation treatment, with some irradiated areas remaining ventilated but not adequately perfused. During the acute phase of radiation pneumonitis, perfusion defects begin approximately 25 days following the radiation exposure and reach a maximum within 150 days. Three-dimensional single photon emission computed tomography (3-D SPECT) perfusion scans more recently have been shown to provide a 3-D map of functioning vascular/alveolar subunits within the lung. Pulmonary perfusion is often not uniformly distributed. Pretreatment SPECT scans can be useful in designing treatment beams that minimize the physiologic impact of thoracic irradiation. More recently, researchers have demonstrated that the acute phase of radiation pneumonitis results in increased uptake of FDG in regions of lung affected by radiation pneumonitis. FDG imaging with either a dedicated PET or dual-head coincidence gamma camera system can be used. This may become useful in the setting of clinically and radiographically equivocal cases. INTERVENTION Intervention: Corticosteroids remain the treatment of choice for radiation pneumonitis. Prophylactically administered corticosteroids have been shown to decrease the physiologic effects of radiation in mice. However, in human studies, this approach has failed to prevent the development of clinical pneumonitis. TGF-B has been the target of more recent studies. Angiotensin-converting enzyme (ACE) inhibitors have been shown to decrease the expression of TGF-B1 in animals and recently have been tested in human trials. Researchers at Duke University recently reviewed the records of 213 patients receiving thoracic irradiation for lung cancer with curative intent. Of these patients, 12% were on ACE inhibitors for hypertension. Initial results revealed that at the dose used for the treatment of hypertension, ACE inhibitors had no protective effect. Future trials will evaluate larger doses. The recommended treatment is to begin prednisone at 1 mg/kg as soon as the diagnosis is reasonably certain. The initial dose is maintained for several weeks and then reduced slowly. If steroids are tapered too soon or too quickly, exacerbation of symptoms has been reported, requiring higher doses and longer treatment with steroids. Antibiotics and anticoagulants have been evaluated as treatment options but neither has been found to be clinically beneficial. Pentoxifylline has been shown to decrease late effects from radiation damage but clinical trials in humans have shown no benefit.Special Concerns: Differentiating radiation pneumonitis from recurrent cancer is important >延伸一下。放射性肺炎的预防：严格掌握放射野、时间与剂量。乳腺癌做放疗，最好做切线放射，尽量避免损伤肺部。放疗过程中，应严密观察患者有无呼吸道症状及体温升高。x线检查发现放射性肺炎，应及时停止放射治疗。scf wrote:x线检查发现放射性肺炎，应及时停止放射治疗。scf君其他谈的都很好。还是要继续完成放射治疗的，除非病人症状明显；放射性肺炎是不可避免的；另外，使用平阳霉素类药的病人要多注意。多交流！非常感谢各位仁兄对我的关心，我将及时将治疗体会与大家交流，衷心希望大家继续关注!!!楼上各位也已讲得很明了，　很透彻了．　在这里补充两点．第一：　有学者认为，　放射性肺炎可以分为典型性和偶发性，　两者的发病机制不同．　前者是放射损伤有关,　与放射剂量, 照射面积和照射分割方式有关．后者机制仍不很清楚，可能与免疫反应有关，是一种淋巴细胞性肺泡炎（或是超敏反应)． 肺纤维化是肺组织损伤修复的结果．　第二：　治疗方面我没有经验，　但是今天看到一篇文章，　说中用普米克吸入疗法来预防放射性肺炎．　可以减少激素副作用．　似乎有一定道理．　另外附一篇review，很不错，　大家看看 Cancer treatment-related pneumonitis.pdf (30.63k)很奇怪，为何无人谈到使用高压氧治疗放射性肺炎？我们对于恶性淋巴瘤或肺癌的病人行斗篷野或纵隔照射后出现放射性肺炎，除了激素、抗生素等外，同时加高压氧治疗10次/疗程×2个疗程，病情多可以得到有效控制；在放疗同时进行高压氧治疗，可以预防或减轻放射性肺炎的发生；个家之言，互相学习。楼上任兄提到使用高压氧治疗放射性肺炎，我想不失为一良法，是否可以提供更详细的发生机制如病理生理等方面的内容？经典 不过能否更详细点啊今看到一则短讯：中医中药对放射性肺炎有效，中西结合是治疗的趋向，哪位能提供些这方面的资料？今查找相关中药资料，与大家共同讨论。中医认为，射线是热渡之邪，可损伤人体正气和阴血。根据中药现代药理研究，女贞子 当归 川芎能对抗辐射损伤；香附 桃仁 赤芍 丹参能非特异性抗炎；女贞子 当归 生地 黄芪 提高免疫刺激骨髓造血；桃仁 红花 当归 川芎 赤芍 丹参能活血化淤抗纤维化；瓜蒌 杏仁 百部 紫金牛止咳化痰。方中重用香附，其非特异性抗炎作用强于氢化可的松的8倍。不仅取代激素的抗炎抗纤维化作用又避免了激素的副作用，符合本病疗程长恢复慢的治疗需要，更重要的是避免了激素长期使用而至肿瘤复发转移的弊端。放射性肺炎治疗原则 1.肾上腺皮质激素控制炎症。 2.抗凝疗法对防止小血管栓塞有效。 3.高浓度氧疗以改善低氧血症。 4.适当应用抗生素以预防继发感染。 放射性肺炎用药原则 1.一般放射性肺炎患者可选用口服强的松或地塞米松。 2.重症者静滴地塞米松。 3.合并肺部感染时，加用抗生素。 本例放射性肺炎的治疗主要是：改用大剂量的抗生素及肾上腺皮质激素，尤其是大剂量使用肾上腺皮质激素,可用地塞米松10－20mg／d，或甲基强的松龙80-160mg/d连续数周。其他可给予支气管扩张剂、祛痰剂沐舒坦等对症治疗。试试阿米福丁阿米福汀是冷战时期美国陆军研究所研制的4000余种放射保护剂中最有效的一种。也是美国食品与药物监督管理局（FDA）按一类优 先批准上市的第一个泛细胞保护剂。该药已于1995年在德国和美国上市，受到广大患者和医务界的欢迎。它之所以被选为肿瘤放射治疗保护剂，是因为阿米福汀只对正常细胞起保护作用，对肿瘤细胞不保护。阿米福汀对正常组织放射保护机制表现在如下几方面：1. 正常组织中细胞膜结合碱性磷酸酶含量明显高于肿瘤组织，而阿米福汀需要在碱性磷酸酶的作用下才产生作用。2. 正常组织周围的中性环境较肿瘤组织的中性环境更接近碱性磷酸酶的最适PH值，更利于碱性磷酸酶发挥作用。3. 正常组织通过浓度依赖的载体介导扩散方式转运阿米福汀，转运速度快。而肿瘤组织只通过被动扩散转运阿米福汀，速度极慢。4. 正常组织血液供应好，肿瘤组织生长快，中间常常缺血，因此正常组织摄取的阿米福汀多于肿瘤组织。 与放射增敏剂相反，放射保护剂就是可以减少放射线对细胞的损伤作用。放射保护剂也是中外放射工作人员梦寐以求的物质。冷战时代，苏美两个超级大国大搞核武器，企图通过应用放射保护剂来战胜一方；在当代，人们开发太空，宇航员在太空受到射线特别是一些重粒子的辐射，需要放射保护剂。目前科学家通过几个途径开发放射保护剂，一是清除放疗中产生的自由基，减少自由基对DNA的损伤，这一类以阿米福汀为代表。一是阻止辐射后细胞的分裂，使细胞停留在有丝分裂期前，不至于出现分裂后细胞死亡，让细胞有足够的时间进行损伤再修复，目前已初步清楚细胞分裂的调控基因和某些蛋白，但这些蛋白经静脉用药，未进入细胞就被分解，因此这方面的研究未明显突破。>zjy1973 wrote:楼上任兄提到使用高压氧治疗放射性肺炎，我想不失为一良法，是否可以提供更详细的发生机制如病理生理等方面的内容？非常抱歉，具体机制不祥，使用高压氧治疗放射性肺炎是我们与高压氧科咨询后所作的工作，目前仍处于病例积累阶段，考虑可能与高压氧改善肺换气功能有关；最近查询清华全文期刊，未查到专门就此问题做过研究的文章，但我找到有关放射性肺炎及高压氧治疗肺间质纤维化的文章，仅供大家参考。由于软盘故障问题，只能提高两篇文章，其余文章我尽快上传。非常抱歉！ 新建文件夹.rar (44.39k)chenyanfmmu wrote:试试阿米福丁阿米福丁一般在放疗前应用，预防放疗的副反应，包括放射性肺炎、放射性食管炎、放疗后口干等。另外也能预防化疗药物对肾脏等功能的损害。此患者放射性纤维化也已形成再用阿米福丁似无用处。当务之急是用激素抑制纤维化的加重和扩散蔓延，预防感染，减轻缺氧。本人孤陋寡闻，见过病例不多，目前尚未见过肺纤维化治疗后能够消失者。我也觉得楼上仁兄意见，阿米福丁在放疗前应用可预防放疗的副反应，yaobin斑竹也讲解了该药的来源，不知价格如何？可能很贵，非常感谢大家的群策群力。我那病人现在该用的也上了，症状略有好转，（未摄片证实）我也想用用高压养试试，请yujd多关心，谢谢！！！下面我写了一篇关于放射性肺炎的文章，请参考放射性肺炎是正常肺组织受到大剂量放射线照射而产生的无菌性肺炎，放疗是肿瘤治疗的三大手段之一，随着放疗技术的普遍应用，放射性肺炎的发生率不断增高，它限制了肿瘤放射治疗的剂量，从某种意义上说也就限制了放疗的疗效，严重影响了患者的生存质量。因此，积极地预防、逆转和治疗这些并发症是非常重要的课题。1．发病因素放射性肺炎的发生及严重性与肺受照体积、放射剂量、剂量率、分割方式、放射部位、治疗前肺原发疾病和放射时使用化疗药物等因素有关。其中肺照射体积是肺损伤发生的决定因素。30.0Gy时1/4肺照射体积很少有症状性肺损伤发生，而同样剂量的双肺照射有可能致命[1]，Cax等分析了超分割放射间隔时间与放射性损伤的关系，显示间隔时间越短损伤越重，有人认为肺门或纵隔放射易发生放射性肺损伤，可能与纵隔淋巴管阻塞有关。第2次进行放射时，放射性肺损伤的发病率为首次放疗的3倍以上，且起病早，同样剂量的条件下，肺底部照射敏感性高于肺尖部[2]。在肺照射前、中、后使用博来霉素、白消安、丝裂霉素、阿霉素、长春新碱等化疗药可增加放射性肺毒性，亦有人报道同时使用干扰素也可能加重放射性肺损伤。年龄和照射前的肺功能情况也影响肺的耐受性，儿童肺的放射耐受性比成人差，亦有人认为吸烟也是不利因素[1，3]。2．发病机理对放射性肺损伤发病机理的研究始于20世纪50年代，当时多为病理形态学观察。80年代集中于“关键靶细胞”的研究。归纳起来有几种学说：肺泡上皮损伤、肺血管内皮细胞损伤；肺胞巨细胞生长因子；免疫反应；淋巴管受累；巨细胞参与。目前比较推崇的观点是细胞生长因子参与放射性肺损伤的发生和发展[4，5]。近几年来，有作者认为在放射性肺损伤的发生过程中，除了放射性肺炎和纤维化外，尚存在着一种由免疫介导引起的双侧淋巴细胞性肺泡炎，称之为散发性放射性肺炎(sporadic radiation pneumonitis)，临床上已有散在报告。目前认为引起这种特发性肺炎改变的病理机理是由于大量T淋巴细胞受到激活，发生免疫应答反应所致[6]。3．病理改变根据尸解情况[7]，可将放射性肺炎的病理改变大致分成早期和晚期两个阶段。早期（急性期）表现为肺泡细胞肿胀、破坏、II型上皮细胞增殖或脱屑，肺泡腔内富有纤维蛋白之沉积物和透明膜形成，肺泡隔水肿，有单核细胞浸润，嗜中性细胞显著缺乏，毛细血管内皮细胞肿胀及血栓形成，内膜增生，内膜下可见含有脂肪的巨噬细胞积聚，动脉壁玻璃样变，支气管粘膜局灶性坏死，鳞状上皮化生，偶尔能见到胸膜反应。晚期（慢性期）肺泡壁广泛纤维化，血管壁增厚，内腔狭窄，血管减少。许多学者指出，在同一肺组织标本上，可同时存在着不同阶段的病理改变，这是放射性肺炎的一个重要的病理特征。4．临床表现临床上将肺的放射性损伤分为急性放射性肺炎和后期放射性肺纤维化。典型者多发生于放疗开始1～3个月，放射性肺纤维化发生于放疗后9个月或更晚[8]，放射性肺病症状的严重决定于肺受累的程度。4.1 急性放射性肺炎的症状和体征与一般肺炎无特殊，可能有低热、刺激激性咳嗽、咳少量白色粘液样痰、胸痛、气短等非特异性呼吸道症状。严重病例有高热、胸闷、呼吸困难、不平能卧、剧烈咳嗽、咯血痰。胸部体征可有局部实变征、湿性罗音、胸膜摩擦音和胸水体征。晚期有杵状指和慢性肺心病体征，严重病例可并发急性心功能衰竭而致死。急性症状性肺病持续时间相对较短，急性期过后可表现为潜伏期，后期放射性纤维化一般由急性放射性肺炎发展而来，一小部分患者也可无急性放射性肺病症状而由隐性肺损伤发展为放射性肺纤维化。临床表现为进行性呼吸困难，严重患者可发展为慢性呼吸衰竭。4.2 “散发型放射性肺炎”出现于少数病人，在放射性肺炎病人中只占5%～10%，临床表现为呼吸困难的程度与肺照射体积不符，症状消退后常常不继发纤维化为特征，此类病人类似于过敏性肺炎，对皮质激素敏感[6]。5．诊断依据[9]（1）患者具有一侧或整个肺部受射线照射史，剂量达到20GY以上；（2）患者接受放疗前，无上呼吸道和肺部感染史，X线检查两肺正常。（3）患者放疗过程中，或放疗结束后的一定时间内，出现不同程度的呼吸系统的临床表现，或无表现，肺平片显示，在受照范围内的肺实质发生炎症；（4）患者在停止放疗的一段时间内，经过适当处理，炎症可以吸收消散，或间有肺纤维变。6．治疗6.1 对症治疗 当病人出现放射性肺炎症状时应适时停止放射治疗，卧床休息。出现呼吸急促和发绀时，及时吸氧，防止心力衰竭。适当应用支气管扩张剂和镇咳药，症状明显者可选用下列治疗方法。6.2 西医治疗 肾上腺皮质激素仍是目前治疗放射性肺炎最常用而有效的药物，特别在早期能减轻实质细胞的损害和微血管的改变，减轻肺泡内水肿从而能改善症状。常用强的松60～100mg/d口服。应用皮质激素时应注意，开始时间量稍大，以后逐渐减量并注意防止诱发或扩散感染[10]，消炎痛、阿斯匹林等药物可有效地降低放射性引起的血管内皮细胞损伤，使血管渗透性表面区域产物的产生减少，阻断放射性肺炎（RP）的发生，后者在放射性损伤中亦起到一定作用[11]。D•青霉胺是一种鳌合剂，在体内能阻止盐溶性的胶原向不溶性胶原的成熟过程，对肺组织有显著亲和作用。对放疗后的肺纤维化患者的主观症状、X张改变和肺功能均有改善作用，抗凝治疗[12]旨在减轻血管的阻塞和纤维化；抗组织胺药物可以降低放疗后肺血管通透性。对合并在感染而致白细胞升高者，先控制感染，使白细胞下降后再放疗为佳，如发现有CMV或HSV感染的表现，应及时抗病毒治疗，如阿糖腺甙、无环乌苷，但干扰素对造血重建有一定抑制作用，可用复方新诺明防之，有人用脉通治疗，可使纤维化减轻[13]。6.3 中医中药 放射性肺炎症状大致类属于中医“肺痿”范畴。从中医观点看，电离辐射（放射治疗）是一种热性杀伤物质，此热可化火灼津而造成阴虚证候，电离辐射之“火”与癌毒相博，伤败之物与热互结，瘀积成毒，“阴虚”与“热毒”是放射治疗的最常见的副反应，故中医药治疗重点放在养阴及清热解毒两个方面，两者并重，不可偏废，李氏报道[14]，临床养阴生津常选用：沙参15～20g，生地20～30g，麦冬10～15g，石斛10～15g，玉竹10～15g，天花粉20～30g消热解毒选用金银花15～30g，鱼腥草20～30g，生石膏20～40g，野菊花10～20g。刘氏认为[15]肺气虚是该病久治难愈的原因，自拟益气补肺汤：冬虫夏草9g，黄芪20g，茯苓10g，白术12g，陈皮10g，麦冬10g，木蝴蝶10g，西洋参9g，五味子6g，炙百合10g，沙参10g，甘草3g，20天为1疗程，治疗20例，总有效率85%。蒋氏[16]应用百合固金汤加减：生地12g，热地黄12g，麦冬15g，北沙参15g，白芍15g，百合12g，玄参12g，桔梗12g，川贝母12g，当归12g，甘草6g。每日服强的松20mg，每日3次，连用10～14天。62例中药治疗组30例，总有效率86.6%；对照组32例，总有效率59.4%。何氏报道[17]应用消燥救肺汤加减（桑叶、石膏、太子参、麦冬、沙参、杏仁、杷叶、桔梗、白术、茯苓、黄芩、火炉林仁、阿胶、生甘草），每日1剂，1个月为1疗程，治疗26例，总有效率85%。张氏[18]应用清热解毒，养阴清肺兼顾脾胃，佐以活血化瘀止痛法，药用金银花30g，黄连6g，沙参30g，天冬12g，芦根30g，杷叶30g，橘皮10g，百合12g，生薏仁30g，焦三仙各9g，生甘草6g，三七粉30g（另包冲服），临床疗效显著。陈氏[19]以补气养阴、清肺活血、止咳平喘，自拟“放射性性肺炎方”，药用黄芪、女贞子、当归、香附、红花、丹参、生地、赤芍、川芎、桃仁、瓜蒌、百部、杏仁、紫金牛治疗，治疗组肿瘤复发，转移率低于对照组。在中成药的研究方面，尹强等报道[20]生脉注射液能降低放射性肺炎的发生率，刘尔车报道[21]丹参可减轻放射性肺损伤。据报道[18]应用双黄连粉剂（哈尔滨中药二厂产）治疗RP，效果满意。据抑菌试验发现：双黄连对金黄色葡萄球菌等多种细菌有不同程度的抑制作用，抑菌力随浓度降低而减弱。有学者认为[22]双黄连气道吸入治疗呼吸系统疾病，优于其他给药途径。呼吸系统具有毛血管床丰富，弥散功能强的生理特点，加之双黄连对免疫功能的刺激作用，使机体的NK细胞、α-干扰素具有增强作用，直接对病毒、细菌加以抑制而达到早期控制症状、缩短病程的疗效，尤其对病毒性急性呼吸道感染（ARI）的疗效更有优势，已引起世界卫生组织的广泛重视[23]。7．预防已产生放射性肺纤维化是不可逆的，严重影响着患者的生命质量，所以重要的是预防。放射性肺炎是肺部放疗中不易控制的并发症，放疗中应根据个体特点使用正确的放疗技术，尽量避免或减少不利因素[24]。对肺部有慢性疾病患者及时缩野照射野，调整剂量，兼采用中医扶正治疗，密切注意病人变化，及时对症处理，以减少放射性肺炎的发生[25]。8．结语放射性肺炎是胸部放疗中一种不易控制的并发症。目前西医常用抗菌素、激素、抗凝血及抗组织胺制剂治疗虽有一定疗效，但这些疗法多停留在探索和实验阶段，故其疗效多不理想。资料表明，根据中医清热解毒、养阴清肺、健脾和胃、活血化瘀等四大治则进行辨证治疗获得较好的临床疗效。笔者认为，放射性肺炎的急性期用西药控制病情，慢性期用中药调理，无疑能进一步提高疗效；在放射治疗前和放射治疗过程中用中药预防，并不断改进放疗技术，这对预防放射性肺炎的发生无疑是有益的。目前，中医药配合化疗治疗肿瘤的增敏、减毒研究很多，其规模大、比较系统和规范。而中医药配合放疗治疗肿瘤的研究则很少，且不系统也不规范。故中医有必要对放射性肺炎进行系统的、规范的研究，从基础的证侯学入手，进行系统的观察研究，辨证论治，为大规模开展中医药早期预防、治疗放射性损伤作准备。参考文献：1. Zhong xing Liao. Damage and morbidity from pneumonitis after irraiation of partial vofumes of mouse fung [J] Inf Radial Oncol Biol Phys, 1995, 32(5): 13592. 吴开良，李艳如. 放射性肺损伤[J]. 实用癌症杂志, 2001, 169(1): 111.3. 王明臣, 刘洪明, 刘杰, 等. 放射性肺炎影响因素的多元回归分析[M]. 中华放射肿瘤学杂志, 2003, 2(12): 增刊49—51.4. Loatefaris A, penny R, Breit SN. M itotic activity in the elerm is of mice during gratf versus bost disease: the role of fibrobfast replication in dermal fibrosis [J]. J lnvest Dermatol, 1992, 99 : 7795. Thornton SC, Rabbins JM, Sheffey L, et al, Fibrobfast growth factor inconnective tissue disease associated interstitial fung disease: association with disease activity and identification as TNFa， PDGF and fibronection[J]. Clin exp Immunol, 1992, 90(3): 447.6. 王迎选, 王所亭主编. 现代立体放射治疗学[M]. 北京: 人民军医出版社, 1999, 305.7. 潼岛任. 临床呼吸器病讲座. 东京: 金原出版株式会社, 1977, 2: 167.有以下事实，1、有吸烟史的患者发生放射性肺炎的概率较正常人低。 2、放射性肺炎有时可能发生在放射野外。所以有人认为放射性肺炎的发生的机制之一是体内的自身免疫作用，吸烟病人由于造成肺局部的免疫功能下降，所以可能会降低放射性肺炎的发生率。另外由于某些体液因子的作用，肺的损伤可能会在野外发生。具体的文章来源我记不清楚了，有兴趣的可以查一下。之于治疗没有什么争议的：大剂量的激素、抗感染和对症处理。有一个病人的个例，是一年前我收治的放射性肺炎病人，治疗过程中出现MRDS，经过积极抢救脱离危险。不知大家有没有碰到过？另附：放射性肺炎的诊断被专家认为不妥，现在已有使用放射性肺损伤或放射性肺病来代替的趋势。胜读十年书不知zjy1973的那位食道癌患者目前病情如何？现补充所查的全文高压氧医学论坛> 高压氧.rar (127.55k)我试用高压氧治疗，做了六次，激素 抗生素 沐舒坦，继续在用，患者咳嗽咳痰有好转，DXM 10mg x15d ，现已减为5mg ，好像有点激素依赖，目前无明显感染症状，只一组抗生素在用。非常感谢yujd 的关心。高压氧治疗可以继续否？DXM是否可继续减量？zjy1973 wrote:高压氧治疗可以继续否？DXM是否可继续减量？既然目前治疗有效，可以继续高压氧治疗，前几日我科刚完成一例霍奇金淋巴瘤患者斗篷野照射后出现憋气、咳嗽咳痰，经高压氧治疗10次后明显好转。DXM可以继续减量，尽早撤下激素。目前DXM已减为2.5mg，又作了几次高压氧，病人家境不好，高压氧治疗次数有无一个相对标准？在激素、抗炎、抗真菌疗效均不佳的情况下，还有第三种可能：肿瘤复发。可依据既往化疗，考虑用二线或者三线联合化疗方案。在激素、抗炎、抗真菌疗效均不佳的情况下，还有第三种可能：肿瘤复发和转移。可依据既往化疗，考虑用二线或者三线联合化疗方案。zjy1973 wrote:目前DXM已减为2.5mg，又作了几次高压氧，病人家境不好，高压氧治疗次数有无一个相对标准？我院是10次/疗程×2疗程，大约40元人民币/次。晓禾 wrote:放射性肺炎的治疗原则是足量足够时间的激素的使用，地塞米松可以使用10－20mg／日，时间看病情缓解程度决定，缓慢减量。注意加用抗生素及制酸治疗。当心如果足量抗生素及激素使用后病情仍未得到缓解，需警惕真菌感染。其他对症支持治疗，特别是能过提高呼吸道粘膜抵抗力的药物，如沐舒坦、氨溴索等；可加用H2受体抑制剂如苯海拉明，非甾体抗炎药如消炎痛等以减轻炎性渗。，你是南通医学院毕业的吗？