应用纵隔镜手术诊断Ⅰ期胸部结节病

目的 探讨纵隔镜手术在Ⅰ期胸部结节病诊断和鉴别诊断中的应用价值.方法 回顾性分析1999年11月至2007年6月60例临床拟诊Ⅰ期胸部结节病患者的临床资料.所有患者术前行胸部X线片及CT发现肺门和(或)纵隔淋巴结肿大,肺部未见异常表现.以伴有或不伴有纵隔淋巴结肿大的两侧肺门淋巴结肿大为Ⅰ期胸部结节病的典型表现.结果 本组60例患者术后均获得明确的病理诊断.影像学表现典型者33例,纵隔镜检查术后32例获得病理学证实,诊断准确率97%;1例为纵隔淋巴结反应性增生.27例根据影像学表现考虑不典型Ⅰ期胸部结节病的患者,纵隔镜检查术后病理证实17例(63%),另有纵隔淋巴结结核6例,纵隔淋巴结反应性增生2例,转移性鳞状细胞癌以及小细胞癌各1例.全组手术顺利,无手术死亡及并发症.结论 临床及影像学表现典型的Ⅰ期胸部结节病,其临床诊断准确率高,一般不需要行纵隔镜等有创检查以获得病理学证实.     

小儿甲状腺结核致呼吸困难、术中呼吸停止一例

患儿男,8岁,发现颈两侧肿块半月,经某院诊断颌下淋巴结结核并行抗痨治疗4月余,肿块增大至鸡蛋大,近5天出现呼吸困难于1978年2月28日入院。见左侧肿块5×4.5cm,右侧5×6cm,部份有波动感。肿块表面高低不平,不易推动,质稍硬,有轻度压痛,但不随吞嚥上下移动。甲状腺无明显肿大。呼吸时轻度抬肩,无唇绀;但睡眠时有鼾声、明显三凹征及躁动;吸气时胸骨下段下陷达3～4cm,自醒或被唤醒后症状改善。血沉22mm/小时。胸片:两肺门扩大。细胞学检查报告颈淋巴结结核。入院后继续链霉素及异菸肼治疗,呼吸困难逐渐     

腔镜下腹腔淋巴结活检在疾病诊断中的临床应用

目的:探讨腹腔镜活检在不明原因腹腔淋巴结肿大疾病中的诊断价值。方法:2007年9月至2010年12月为23例临床难以诊断的腹腔淋巴结肿大患者通过腹腔镜检查及活检进行分析诊断,其中男13例,女10例;平均(43.6±21.4)岁。结果:23例分别取出1~4枚0.7~3.0 cm大的淋巴结,病理结果为炎症性淋巴结肿大10例,腹腔、肠系膜淋巴结结核6例,淋巴瘤5例,转移性肿瘤1例,无明确诊断1例。手术时间平均(73.2±47.8)min,术中出血量平均(34.6±11.5)ml,无中转开腹。术后平均住院(3.2±1.7)d。术后1例出现淋巴漏,未出现与腹腔镜检查直接相关的死亡病例。结论:腹腔镜淋巴结活检术具有患者创伤小、安全性高及患者康复快等优点,为不明原因的腹腔内淋巴结肿大提供了安全、有效的诊断手段;尤其对于非特异性淋巴结炎、腹腔淋巴结结核、淋巴瘤、转移性肿瘤等疾病诊断、鉴别困难时,腹腔镜检查、活检可提供正确的诊断,减少误诊。     

纵隔镜诊断成人单纯纵隔淋巴结病变

目的探讨纵隔镜检查在诊断成人单纯纵隔淋巴结病变中的作用。方法对120例纵隔淋巴结肿大患者采用标准颈部纵隔镜检查术或胸骨旁纵隔镜检查术获取可疑组织标本行病理学检查。结果通过纵隔镜检查本组120例患者中有113例获得明确的病理诊断,总确诊率为94.2%(113/120);成人单纯纵隔淋巴结病变以结节病(59.2%)、淋巴滤泡增生(16.7%)、淋巴结结核(11.7%)最为多见。手术时间64.2±21.5min,失血量45.6±26.8ml;穿破左侧胸膜1例,术后死亡1例,死因为药物性血管内溶血。结论纵隔镜检查术是诊断成人单纯纵隔淋巴结病变的一种高效、安全的检查方法。     

肾移植术后并发肺癌伴肺结核1例

患者男,41岁。肾移植术后9年余,发热2周。查体：双肺呼吸音粗,左下胸部叩诊呈实音。胸部增强CT(图1)：右上肺尖后段、左上肺尖段见斑点状、条索状高密度影;左下肺脊柱旁分叶状团块影,密度欠均匀、边界清,约7.0 cm×5.7 cm×8.5 cm,增强后见不均匀强化,未见明显肿大淋巴结。连续3次痰涂片查抗酸杆菌均为阴性,经抗炎对症治疗后体温、血沉控制正常。2010年7月全麻下行左肺下叶切除、左肺上叶楔形切除术和淋巴结清扫术。病理诊断：左下肺高分化腺癌,左肺上叶结核,隆凸下淋巴结结核。术后出现高热,加强抗感染、抗结核治疗,治愈后出院。     

肝移植术后淋巴组织增生性疾病的诊断和治疗(附1例报告及文献复习)

目的探讨肝移植术后淋巴组织增生性疾病(posttransplant lymphoproliferative disease,PTLD)的诊断和治疗。方法回顾性分析1例肝移植后PTLD的临床表现、诊断和治疗过程,并复习相关文献。结果 2003年10月至2011年12月在中山大学附属第三医院肝移植中心随访的336例肝移植术后患者中有1例发生PTLD,发生率为0.3%。该例患者的临床表现不典型,主要表现为反复发热、腹部不适、多处淋巴结肿大和肝脏占位病变等,淋巴结活组织检查提示B细胞源性非霍奇金淋巴瘤淋巴瘤,确诊为PTLD。经减少免疫抑制剂用量、抗炎,对症支持治疗无效后死亡。结论肝移植术后PTLD的临床表现不典型,易被误诊或延误诊断,预后甚差。治疗以减少免疫抑制剂用量、抑制淋巴细胞增殖、对症支持治疗为主。     

腰骶椎结核治疗的方法选择(附65例分析)

[目的]探讨腰椎结核治疗的方法选择。[方法]回顾分析65例腰椎结核患者采用五种不同治疗方法的疗效：A组（14例）单纯病灶清除术;B组（15例）病灶清除并植骨融合术;C组（9例）后路病灶清除植骨融合＋内固定术;D组（12例）后路内固定＋前路病灶清除植骨融合术;E组（15例）前路病灶清除植骨融合＋前路内固定术。术前、术后常规支持和抗结核治疗,并定期随访,观察血沉变化,摄X线平片,CT三维重建评估结核活动、骨块融合和畸形矫正情况。[结果]65例腰椎结核患者术中无大血管、神经、输尿管损伤,随访12～16个月,平均13个月,结核病变无复发,植骨全部融合,愈合时间4～6个月,平均3.8个月。后凸畸形矫正角度无明显丢失,内固定无松动、断裂等并发症。[结论]有效的抗痨是治疗结核的前提,彻底清除病灶是治疗的关键,融合、内固定与否,根据结核破坏的程度、部位而定,合理的选择能提高腰椎结核的治疗效果。     

肠系膜淋巴结结核12例诊断和外科治疗

目的探讨肠系膜淋巴结结核的诊断及手术治疗方法。方法回顾性分析我院2010年1月至2013年9月期间收治的12例肠系膜淋巴结结核患者的临床资料。结果 12例患者均行了手术并明确诊断;所有患者术后均行抗结核治疗并治愈,无死亡病例;术后未出现并发症。术后随访1~2年,无复发。结论肠系膜淋巴结结核的诊断应根据患者病史、症状、体征、影像及实验室资料进行综合分析,手术针对并发症及不能明确诊断的腹部肿块进行处理,选择适当手术方式,手术治疗安全、有效。     

经验性治疗肝移植术后非结核分枝杆菌感染1例附文献复习

目的总结肝移植术后非结核分枝杆菌(NTM)感染的诊疗经验。方法对第二军医大学附属长征医院收治的1例肝移植术后NTM成功经验性治疗病例进行研究分析,并对相关文献进行回顾。结果 1例肝移植术后7个月NTM感染患者,临床表现以午后发热为主,动态CT检查提示病情进展时右肺下叶基底段内病灶扩大融合且出现薄壁空洞。采用纤维支气管镜检查(刷检或灌洗)、结核分枝杆菌感染T细胞免疫斑点试验(T-SPOT.TB)、多次痰培养及经验性抗结核治疗支持NTM感染的诊断。该患者诊断性四联抗结核治疗有效,治愈后出院。随访持续至投稿日,患者病情平稳,无再次出现发热、咳喘症状,肝功能正常。结论肝移植术后NTM感染罕见但不可忽视,纤维支气管镜刷检或灌洗可提高阳性发现率,诊断性四联抗结核治疗有效。     

肾移植术后结核的发病特点及诊断和治疗经验

目的 探讨肾移植受者术后结核的发病特点及诊断和治疗经验.方法 1991年1月至2007年4月间的2333例肾移植受者中有37例术后发生结核病,回顾性分析术后发生结核病受者的临床资料,总结肾移植术后结核的发病特点及其诊断和治疗经验.结果 肾移植受者术后结核的发病率为1.59%,发病时间为术后1～91个月,中位时间为术后7个月,22例集中在肾移植术后1年内;29例为肺部结核或肺部结核合并有肺外病灶,其他为肺外结核.肾移植受者术后结核病的表现以发热、咳嗽和咳痰为主;所有受者结核菌素纯化蛋白衍生物(PPD)皮试均为阴性;29例受者X线胸片检查有典型的结核表现;6例痰涂片查抗酸杆菌阳性,16例经病原学和/或病理学确诊.7例确诊合并有其它感染.抗结核治疗采用一线抗结核药物并调整或停用免疫抑制剂和激素,28例受者经治疗后好转,9例因治疗无效死亡.结论 肾移植受者术后早期结核的发病风险较高;X线胸片结合病原学和/或病理学检查是主要的确诊手段;抗结核治疗时,应加强对免疫抑制剂的监测,及时调整抗结核药和采取免疫抑制剂的个体化治疗方案.     

超声对移植肝肝门部淋巴结反应性增生的诊断和随访价值

目的探讨超声对移植肝肝门部淋巴结反应性增生的诊断和随访价值。 方法回顾性分析2006年2月至2016年2月在浙江大学医学院附属第一医院肝移植中心行肝移植术并接受超声常规随访1年以上1 019例受者的超声资料,分析和总结87例符合移植后肝门部淋巴结反应性增生受者的临床资料和超声影像特征。 结果肝移植术后1年,肝门部淋巴结反应性增生发生率为8.54% (87/1 019),超声发现淋巴结肿大时间中位数为移植术后55 d (7～270 d);肝门部淋巴结增大单发57例,多发30例;淋巴结平均长径(24.6±6.2) mm,横径(17.4±2.9) mm;内部回声均匀,彩色血流信号不丰富。伴发门静脉受压2例,轻、中度狭窄;包绕肝门血管生长并伴有肝内胆管轻度扩张3例。肝门部肿大淋巴结平均消失或缩小时间为(82±57) d。 结论对肝门部淋巴结反应性增生超声特征的认识可以减少一部分移植肝穿刺活检。超声可以作为肝移植术后辅助诊断和监测肝门部淋巴结反应性增生的有效影像手段。     

78例肝硬化患者肠道细菌易位及其相关性研究

目的了解肝硬化患者肠道细菌易位（BT）的发生率及其相关危险因素,分析BT与术后感染的关系。方法对77例肝移植和1例未行肝移植的肝硬化患者进行术中采样,取外周血、门脉血及肠系膜淋巴结（MLN）,分别进行需氧及厌氧培养,了解BT的发生率。结合术前、术后各种临床资料分析发生BT的危险因素及BT的临床意义。结果78例肝硬化患者中BT的发生率为10．3％（8／78）;细菌易位的部位以MLN为主,占5／8,发生BT的细菌主要是肠道G-兼性厌氧杆菌（55．6％）,其次为G^＋兼性厌氧球菌（22．2％）。BT组患者术前胆红素总量显著高于无BT组（P=0．022）;发生BT的患者其术后感染的风险是无BT患者的1．3倍。结论高胆红素血症是促发BT的独立危险因素,发生BT的肝移植患者术后感染的风险明显升高。     

Antituberculous therapy-induced fulminant hepatic failure: successful treatment with liver transplantation and nonstandard antituberculous therapy.

Standard antituberculous therapy including isoniazid, rifampin, ethambutol, and pyrazinamide is widely used for the treatment of active tuberculosis. Its most important side effect is hepatotoxicity, ranging from asymptomatic transaminitis to fulminant hepatic failure. A 19-year-old woman was admitted to our unit due to jaundice and unconsciousness. According to her past medical history, she was diagnosed as having extrapulmonary tuberculosis and had been prescribed standard antituberculous therapy. The patient became icteric and unconscious on the fourth day after therapy initiation. She was diagnosed with drug-induced acute fulminant hepatic failure and underwent living-related liver transplantation. Nonhepatotoxic antituberculous therapy (cycloserine, ciprofloxacin, streptomycin, and ethambutol) and low-dose immunosuppressive therapy were started after transplantation. Currently the patient is very well with normal graft function 42 months after transplantation. Here we report a case of a patient with acute fulminant hepatic failure caused by isoniazid, rifampicin, or both, who was successfully treated with living-related liver transplantation and a relatively less hepatotoxic antituberculous therapy. In conclusion, liver transplantation is a feasible therapy for individuals with standard antituberculous therapy-induced hepatic failure. Nonhepatotoxic antituberculous therapy may achieve control of active tuberculosis in such individuals after transplantation.     

Recurrent hepatic sarcoidosis post-liver transplantation manifesting with severe hypercalcemia: a case report and review of the literature.

Sarcoidosis is a systemic granulomatous disease primarily involving the lungs, lymph nodes, skin, eyes and nervous system; liver involvement is asymptomatic in most cases. However, once the patient develops clinical symptoms liver disease is usually progressive and may necessitate orthotopic liver transplantation. There are a few reports of asymptomatic recurrent sarcoidosis developing within the liver allograft. We report a case of early recurrence of sarcoidosis in the liver allograft diagnosed on biopsy in a patient who presented with severe hypercalcemia, kidney dysfunction, and increase in size of abdominal lymph nodes. The liver chemistry tests were within normal limits. The patient responded well to steroid treatment by normalizing serum calcium and creatinine levels and reducing lymph node size. To date, there has been no report in the literature of symptomatic recurrence of hepatic sarcoidosis following orthotopic liver transplantation.     

Plasmacytic hyperplasia--the early form of posttransplant lymphoproliferative disorder--with atypical morphology and clinical course in patient after liver transplantation: a case report

This case report describes an early lesion of posttransplant lymphoproliferative disorder (PLTD)--plasmacytic hyperplasia with atypical morphology. The 54-year-old patient was 4 months after liver transplantation due to alcoholic cirrhosis. The postoperative course had been uneventful without graft rejection episodes. Primary immunosuppressive therapy included tacrolimus and prednisone. On admission to the hospital the patient showed rapidly increasing jaundice, hepatomegaly, anemia, thrombocytopenia, and significant leukocytosis. A biopsy suggested generalized infection. Acute Epstein-Barr virus (EBV) infection was confirmed using serological methods. Despite treatment the patient died. On autopsy we found features of generalized infection. Histological examination of the enlarged lymph nodes showed plasmacytic hyperplasia despite lymph node atrophy. Plasmacytic hyperplasia, an early lesion of PTLD despite usually a good prognosis with multifactor therapy may display a rapid course that leads to death through intensified immunosuppression. In accordance with other reports we confirmed reactivation of EBV infection as the probable cause of plasmacytic hyperplasia. The lymph node morphology of plasmacytic hyperplasia may be atypical with atrophy of lymphoid components accompanying plasma cell proliferation.     

<Emphasis Type="Italic">Stenotrophomonas maltophilia</Emphasis> bacteremia after living donor liver transplantation: Report of a case

Stenotrophomonas maltophilia (previously named Xanthomonas maltophilia) is an aerobic, nonfermentive, Gram-negative bacillus that is widespread in the environment. It is considered to be an organism with a limited pathogenic potential, which is rarely capable of causing diseases in humans other than in those who are in an immunocompromised state. In this study, we outline the case of a patient with Stenotrophomonas maltophilia bacteremia after living donor liver transplantation, which showed the clinical signs of severe sepsis and was resistant to almost all antibiotics. However, we successfully treated the patient with the antibiotics trimethoprim-sulfamethoxazole (TMP/SMX) and minocycline hydrochloride (MINO), and performed endotoxin-absorbing therapy using polymyxin B (PMX) to remove the endotoxin from Gramnegative bacillus as well as continuous hemodiafiltration (CHDF) to remove inflammatory cytokines. To the best of our knowledge, this is the first report on the treatment of Stenotrophomonas maltophilia bacteremia after living donor liver transplantation.     

Haemophagocytic syndrome after liver transplantation in adults

The haemophagocytic syndrome is defined as a proliferation of phagocytic macrophages in the bone marrow, lymph nodes and spleen. Clinically, it is characterised by fever and pancytopenia. We present here a case of haemophagocytic syndrome after liver transplantation in a 63-year-old man who had undergone transplantation for autoimmune hepatitis. One month after liver transplantation, he developed ascites, fever and progressive pancytopenia. Bone marrow biopsy showed proliferation of non-neoplastic histiocytes, demonstrating phagocytosis of haemopoietic cells. No infectious or neoplasm-associated disease was found. Several kinds of treatment were attempted, but the course was fatal. The haemophagocytic syndrome is uncommon after liver transplantation, but this diagnosis has to be kept in mind in cases of pancytopenia of unknown origin.     

Tuberculosis nearly preventing a curative resection for colorectal liver metastasis: A case report

Perihepatic lymph node involvement portends a poor prognosis, and is reported to be the most important prognostic factor following R0 resection of colorectal liver metastases. Tuberculous lymphadenitis is one of the common presentations of tuberculosis and is often diagnosed only after histopathological confirmation. In this patient, a frozen section revealing tuberculosis in the perihepatic nodes allowed us to proceed with the curative liver resection.     

Langerhans' cell histiocytosis after living donor liver transplantation: report of a case.

We report a case of Langerhans' cell histiocytosis (LCH) occurring after a living donor liver transplantation (LDLT) for fulminant hepatitis. A 9-month-old girl underwent an LDLT for fulminant hepatitis of an unknown cause. The histology of the native liver did not show any findings of LCH. On postoperative day 42, her Epstein-Barr virus (EBV)-DNA and cytomegalovirus antigenemia were both found to be positive. As a result, she was treated with antiviral agents and a reduction of the immunosuppression dosage. On postoperative day 98, acute rejection occurred, and she was treated with FK506, methylprednisolone, and finally, anti-CD3 murine monoclonal antibody was added. Subsequently, the EBV was re-activated. Thereafter, skin eruptions, swelling of the systemic lymph nodes, and pancytopenia appeared on postoperative day 127. LCH was diagnosed based on the typical histological findings as LCH, CD1a, and S-100-positive cells in her skin and a lymph nodes biopsy. She was treated by chemotherapy. The symptoms disappeared a few weeks after the start of the chemotherapy, and a clinical remission of LCH was obtained. We could not detect any evidence of EBV infection in the tumor cells. In spite of the fact that her LCH lesions thereafter remained in remission, she died of hepatic failure at 22 months after undergoing the liver transplantation. In conclusion, we discuss the factors influencing the occurrence of LCH in our patient after LDLT, while also evaluating the relationship between LCH and the immunosuppressive therapy administered to this patient.     

Tuberculoma of the mediastinal lymph nodes with spinal caries

A 65-year-old male presented with a chief complaint of back pain. Chest computed tomography (CT) demonstrated partially calcified enlargements of the anterior mediastinal lymph nodes and pleural effusion in both lungs. His spondylous lesion rapidly progressed and developed into quadriparesis approximately 2 months after he noticed the back pain. We could not determine whether the lesion was an invasion of the spinal cord by a carcinoma of unknown primary or malignant lymphomas. Therefore, we performed a lymph node biopsy using a thoracoscope for a definitive diagnosis. Histopathology showed tuberculoma with epithelioid cell growth and images of previous scars. However, the staining method for tubercle bacillus did not reveal the presence of tubercle bacillus. As in this case, not all cases of tuberculoma present tubercle bacillus. Therefore, even with poor, suspicious findings for tuberculosis, we should always consider tuberculosis. Old tuberculoma may relapse and rapidly progress. Therefore, we concluded that a biopsy should be performed when tuberculoma is suspected.