子宫内膜异位症的诊治规范(20210201142048)

子宫内膜异位症的诊断与治疗规范子宫内膜异位症(内异症)是指子宫内膜组织(腺体和间质)在子宫内膜以外的部位出现、生长、浸润、反复出血，可形成结节及包块，引起疼痛和不育等。

内异症是生育年龄妇女的多发病，发病率有明显上升趋势；其特点表现为(1)症状与体征及疾病的严重性不成比例，(2)病变广泛、形态多样，(3)极具浸润性，可形成广泛而严重的粘连，(4)具有激素依赖性，易于复发。

一、内异症的临床病理类型1．腹膜型内异症：腹膜型内异症(peritoneal endometriosis，PEM)是指发生在盆腹腔腹膜的各种内异症病灶，主要包括红色病变(早期病变)、蓝色病变(典型病变)及白色病变(陈旧病变)。

2．卵巢型内异症：卵巢型内异症(ovarian endometriosis，OEM)可形成囊肿，称为子宫内膜异位囊肿(内异症囊肿)；根据囊肿大小和异位病灶浸润程度分为：I型：囊肿直径<2 cm，囊壁有粘连、解剖层次不清，手术不易剥离。

Ⅱ型：又分为3个亚型，ⅡA：内膜种植灶表浅，累及卵巢皮质，未达卵巢内异症囊肿壁。

常合并功能性囊肿，手术易剥离。

ⅡB：内膜种植灶已累及卵巢内异症囊肿壁，但与卵巢皮质的界限清楚，手术较易剥离。

II C：内膜种植灶穿透卵巢内异症囊肿壁并向周围扩展，囊肿壁与卵巢皮质粘连紧密，并伴有纤维化或多房腔。

囊肿与盆侧壁粘连，体积较大，手术不易剥离。

3．深部浸润型内异症：深部浸润型内异症(deep infiltrating endometriosis，DIE)是指病灶浸润深度I>5 mm，常见于宫骶韧带、子宫直肠陷凹、阴道穹隆、直肠阴道隔等。

其中直肠阴道隔包括两种情况，一种为假性阴道直肠隔内异症，即子宫直肠陷凹的粘连封闭，病灶位于粘连下方；另一种为真性直肠阴道隔内异症，即病灶位于腹膜外，在直肠阴道隔内，子宫直肠陷凹无明显解剖异常。

4．其他部位的内异症：其他部位的内异症(other endometriosis，OtEM)可累及消化、泌尿、呼吸系统，可形成瘢痕内异症及其他少见的远处内异症等。

第二十一章子宫内膜异位症与子宫腺肌病子宫内膜异位症概述：子宫内膜组织(腺体和间质)出现在子宫体以外的部位时，称为子宫内膜异位症，简称内异症。

异位内膜可侵犯全身任何部位，绝大多数位于盆腔脏器和壁腹膜，以卵巢、宫骶韧带最常见，其次为子宫及其他脏腹膜、阴道直肠隔等部位，故有盆腔子宫内膜异位症之称o内异症是激素依赖性疾病，内异症在形态学上呈良性表现，但在临床行为学上具有类似恶性肿瘤的特点：如种植、侵袭及远处转移等。

诊断要点：【病因】1.种植学说，传播途径主要包括：（1）经血逆流:该学说无法解释在多数生育期女性中存在经血逆流，但仅少数(10%〜15%)女性发病，也无法解释盆腔外的内异症。

（2）淋巴及静脉播散:远离盆腔的器官，可能就是内膜通过血行和淋巴播散的结果。

但该学说无法说明子宫内膜如何通过静脉和淋巴系统,而盆腔外内异症的发病率又极低。

（3）医源性种植:剖宫产术后腹壁切口或分娩后会阴切口出现内异症，可能是手术时将子宫内膜带至切口直接种植所致。

2.体腔上皮化生学说卵巢表面上皮、盆腔腹膜均由胚胎期具有高度化生潜能的体腔上皮分化而来，在受到持续卵巢激素或经血及慢性炎症的反复刺激后,能被激活转化为子宫内膜样组织。

3.诱导学说此学说是体腔上皮化生学说的延伸，在兔动物实验中已证实,而在人类尚无证据。

内异症的形成可能还与遗传因素、免疫与炎症因素及其他因素有关。

【病史】生育期女性有继发性痛经且进行性加重、不孕或慢性盆腔痛史。

【临床表现】1.症状（1）下腹痛和痛经:典型症状为继发性痛经、进行性加重。

有患者无痛经，因此痛经不是内异症诊断的必需症状。

（2）不孕:引起不孕的原因复杂。

（3）性交不适:一般表现为深部性交痛,月经来潮前性交痛最明显。

（4）月经异常：经量增多、经期延长或月经淋漓不尽或经前期点滴出血。

（5）其他特殊症状:肠道内异症可出现腹痛、腹泻、便秘或周期性少量便血，严重者出现肠梗阻症状;膀胱内异症常在经期出现尿痛和尿频;异位病灶侵犯和(或)压迫输尿管时，出现腰痛和血尿，甚至形成肾盂积水和继发性肾萎缩;手术瘢痕内异症患者常出现周期性瘢痕处疼痛和包块，并随时间延长而加剧。

子宫内膜异位症的诊断与治疗方案一、引言：子宫内膜异位症（Endometriosis）是一种常见的妇科疾病，其特征是子宫内膜组织在子宫外部器官或盆腔中异位生长。

这种异常生长导致了严重的疼痛、月经不规律及不孕等问题，给患者的身体和心理健康造成了巨大影响。

因此，对于子宫内膜异位症的准确诊断和有效治疗显得尤为重要。

二、子宫内膜异位症的诊断：2.1 病史采集与详细询问：医生应仔细询问患者的月经史、性生活史以及相关疼痛表现等信息，在理解患者主诉和个体情况的基础上，进行初步判断；2.2 体格检查：包括盆腔检查、肛门指检和直肠指检等，通过探测异常灶块和固定感，协助制定进一步的检查计划；2.3 影像学检查：包括超声波检查、核磁共振（MRI）等技术辅助诊断，这些检查可观察盆腔器官的异常情况，确定病变部位和范围；2.4 病理学检查：通过行腹腔镜手术或活检获取患者的组织标本，进行病理学检查以确诊。

三、子宫内膜异位症的治疗：3.1 保守治疗：3.1.1 非药物治疗：包括调节生活习惯、改善饮食结构、适度锻炼等生活方式干预措施；3.1.2 药物治疗：通过合理应用黄体素、口服避孕药等药物来抑制排卵及月经，缓解盆腔压力和防止异位灶扩散。

3.2 手术治疗：3.2.1 内窥镜手术：通过微创技术，在保护子宫功能的同时剥离异位灶组织，可显著缓解患者的疼痛和不适；3.2.2 子宫切除术：对于无法保留子宫的严重子宫内膜异位症患者，可考虑行子宫切除手术，但需综合考虑患者的年龄、生育要求等。

3.3 中医中药治疗：可选择一些有理论和临床支持的中医中药方剂或针灸疗法进行辅助治疗。

中药有温经活血、调经止痛等作用，能缓解子宫内膜异位引起的疼痛和不适。

四、诊断与治疗方案的制定：4.1 个体化治疗：根据患者的年龄、生育需求、病情严重程度以及伴随性其他疾病等因素，制定符合其个体化特点的治疗方案；4.2 综合治疗策略：结合保守治疗与手术治疗相结合，避免过度依赖某一种方法，并选择最适合该患者的方案；4.3 长期随访管理：对患者在接受任何一种治疗方法后，均应进行长期随访管理，在专业医师指导下进行恰当调整和评估。

子宫内膜异位症的诊断与治疗规范子宫内膜异位症(内异症)是指子宫内膜组织(腺体和间质)在子宫内膜以外的部位出现、生长、浸润、反复出血，可形成结节及包块，引起疼痛和不育等。

内异症是生育年龄妇女的多发病，发病率有明显上升趋势；其特点表现为(1)症状与体征及疾病的严重性不成比例，(2)病变广泛、形态多样，(3)极具浸润性，可形成广泛而严重的粘连，(4)具有激素依赖性，易于复发。

一、内异症的临床病理类型1．腹膜型内异症：腹膜型内异症(peritoneal endometriosis，PEM)是指发生在盆腹腔腹膜的各种内异症病灶，主要包括红色病变(早期病变)、蓝色病变(典型病变)及白色病变(陈旧病变)。

2．卵巢型内异症：卵巢型内异症(ovarian endometriosis，OEM)可形成囊肿，称为子宫内膜异位囊肿(内异症囊肿)；根据囊肿大小和异位病灶浸润程度分为：I型：囊肿直径<2 cm，囊壁有粘连、解剖层次不清，手术不易剥离。

Ⅱ型：又分为3个亚型，ⅡA：内膜种植灶表浅，累及卵巢皮质，未达卵巢内异症囊肿壁。

常合并功能性囊肿，手术易剥离。

ⅡB：内膜种植灶已累及卵巢内异症囊肿壁，但与卵巢皮质的界限清楚，手术较易剥离。

II C：内膜种植灶穿透卵巢内异症囊肿壁并向周围扩展，囊肿壁与卵巢皮质粘连紧密，并伴有纤维化或多房腔。

囊肿与盆侧壁粘连，体积较大，手术不易剥离。

3．深部浸润型内异症：深部浸润型内异症(deep infiltrating endometriosis，DIE)是指病灶浸润深度I>5 mm，常见于宫骶韧带、子宫直肠陷凹、阴道穹隆、直肠阴道隔等。

其中直肠阴道隔包括两种情况，一种为假性阴道直肠隔内异症，即子宫直肠陷凹的粘连封闭，病灶位于粘连下方；另一种为真性直肠阴道隔内异症，即病灶位于腹膜外，在直肠阴道隔内，子宫直肠陷凹无明显解剖异常。

4．其他部位的内异症：其他部位的内异症(other endometriosis，OtEM)可累及消化、泌尿、呼吸系统，可形成瘢痕内异症及其他少见的远处内异症等。

子宫内膜异位症诊断与治疗流程子宫内膜异位症（内异症endometriosis,EMT）是指子宫内膜组织（腺体和间质）在子宫腔被覆内膜及子宫以外的部位出现、生长、浸润，反复出血，继而引发疼痛、不孕及结节或包块等。

内异症是常见的妇产科问题之一，是一组综合征、慢性病，是生育年龄妇女的多发病、常见病。

内异症病变广泛、形态多样、极具侵袭性和复发性，具有性激素依赖的特点。

兼顾各方面的发展，2015年《中华妇产科杂志》发表了《子宫内膜异位症诊治指南》，推动了内异症的规范化诊治，特别是在疼痛、包块和不孕的处理上都有新意，也对手术、深部浸润型内异症（DIE）、恶变及术后管理都有深入的阐述。

本流程是基于2015年指南的基础上制订的子宫内膜异位症的诊疗规范。

一、发病机制以Sampson经血逆流种植为主导理论，逆流至盆腔的子宫内膜需经黏附、侵袭、血管性形成等过程得以种植、生长、发生病变；在位内膜的特质起决定作用，即“在位内膜决定论”；其他发病机制包括体腔上皮化生、血管及淋巴转移学说以及干细胞理论等。

相关基因的表达和调控异常、免疫炎症反应以及性激素受体表达异常等与内异症的发生密切相关。

内异症有家族聚集性。

一级亲属中有内异症患者的妇女发生内异症的风险升高7～10倍。

二、临床病理类型1. 腹膜型内异症或腹膜内异症：腹膜型内异症或腹膜内异症（peritoneal endometriosis）指盆腔腹膜的各种内异症种植病灶，主要包括红色病变（早期病变）、棕色病变（典型病变）以及白色病变（陈旧性病变）。

早期病变发展为典型病灶约需6-24个月，腹腔镜检查可以发现许多微小的腹膜内异症病灶。

2. 卵巢型内异症或卵巢子宫内膜异位囊肿：卵巢型内异症或卵巢子宫内膜异位囊肿（ovarianendometriosis）又根据子宫内膜异位囊肿的大小和粘连情况分为Ⅰ型和Ⅱ型。

Ⅰ型：囊肿直径多<2 cm，囊壁多有粘连、层次不清，手术不易剥离。

Ⅱ型：又分为A、B、C 3种。

子宫内膜异位症的诊断与治疗子宫内膜异位症（Endometriosis），又称子宫内膜异位症候群，是一种常见的妇科疾病，其特点是子宫内膜组织异位到子宫腔以外的其他部位，如盆腔、卵巢、输卵管等处。

该疾病会导致盆腔疼痛、月经异常、不孕等一系列临床症状，对女性的生活质量和生育能力造成严重影响。

本文将就子宫内膜异位症的诊断与治疗进行详细阐述，以使读者加深对该疾病的认识和了解。

一、诊断1.1 病史询问与症状描述对于怀疑患有子宫内膜异位症的患者，首先应该详细了解她的病史，包括月经史、性生活史、疼痛史等。

同时，要仔细听取患者对疼痛的描述，包括疼痛的部位、性质、时长、频率等。

1.2 体格检查体格检查对于子宫内膜异位症的诊断非常重要。

通过盆腔检查，可以触及到异常的卵巢、宫颈、子宫等，发现异常质地、大小及疼痛点等。

此外，还需要进行全身检查，以排除其他相关症状。

1.3 影像学检查为了确诊子宫内膜异位症，医生还需要借助各种影像学检查手段，如超声波、MRI等。

这些检查可以帮助医生观察到异常的子宫内膜异位灶，并了解其特点，如大小、数量、位置等。

1.4 病理学检查如果子宫内膜异位症的诊断仍存在疑虑，医生可以选择行手术切除患者的异位灶，并将组织标本送至病理科进行病理学检查。

这里，病理学检查是诊断该病的金标准。

二、治疗2.1 保守治疗对于轻度的子宫内膜异位症患者，可以选择保守治疗。

这主要包括非甾体抗炎药物（NSAIDs）的使用，如布洛芬、止痛痛经片等，以缓解疼痛。

同时，采取规律锻炼、改善饮食，加强免疫力，有助于改善症状。

2.2 药物治疗药物治疗是一种常见的治疗子宫内膜异位症的方法，常用的药物包括口服避孕药、黄体酮和口服雌激素-抗雌激素疗法等。

这些药物可以有效地抑制子宫内膜异位灶的生长，减少疼痛和月经异常。

2.3 手术治疗对于严重症状或伴随不孕的子宫内膜异位症患者，手术治疗是一种有效的方法。

常见的手术方式包括腹腔镜手术、开腹手术和子宫切除术等。

子宫内膜异位诊断与治疗指南引言本指南旨在提供关于子宫内膜异位症的全面诊断与治疗建议。

子宫内膜异位症是一种常见的妇科疾病，患者常常在生殖器官周围出现异常的子宫内膜组织。

以下是诊断与治疗该症的指南。

诊断1. 患者病史- 询问患者相关症状，包括周期性腹痛、月经不规律等。

- 了解患者的月经史和生育史。

2. 临床体检- 对生育期患者进行检查，观察是否存在子宫内膜异位的体征。

- 进行盆腔腹部触诊，检查是否有异常病变存在。

3. 影像学检查- 建议使用超声检查来评估盆腔内异位灶和卵巢囊肿的存在。

- 对于无法确定诊断的病例，可以考虑进行MRI或其他影像学检查。

4. 手术诊断- 对于高度疑似子宫内膜异位症的患者，建议进行腹腔镜手术以明确诊断。

治疗1. 无症状的患者- 对于无症状的患者，观察观察期为6个月至1年。

- 定期随访，了解病情变化。

2. 症状轻微的患者- 非甾体抗炎药物（NSAIDs）用于缓解疼痛症状。

- 给予口服避孕药物，以抑制子宫内膜异位灶的生长。

- 长周期使用黄体酮可以减少月经次数和疼痛程度。

3. 症状严重的患者- 腹腔镜手术用于切除子宫内膜异位灶和囊肿，并改善症状。

- 激素治疗作为手术后的辅助治疗，以预防复发和控制病情。

4. 生育期患者- 考虑手术治疗来清除异位灶和囊肿，以增加生育机会。

- 手术后进行辅助治疗，例如促排卵药物、体外受精等。

结论本指南提供了子宫内膜异位症的诊断与治疗指南，以帮助医师更好地诊断和治疗该病。

请注意，针对每个患者的具体情况可能需要个体化的治疗策略，请在临床实践中综合考虑。

子宫内膜异位症诊治指南疾病简介：当具有生长功能的子宫内膜组织出现在子宫腔被覆粘膜以外的其他部位时，称为子宫内膜异位症(endometriosis，内异症)。

该病最早发现于19世纪中期，最常发生于盆腔腹膜，也见于卵巢、阴道直肠隔，和输尿管，罕见于膀胱、心包膜和胸膜。

内异症虽为良性病变，但具有类似恶性肿瘤的局部种植、浸润生长及远处转移能力。

流行病学特点子宫内膜异位症是激素依赖性疾病，因此主要见于育龄妇女。

近年来，其发病率越来越高，已成为妇科常见病。

育龄妇女中的发病率约为10%,然而，由于它与不孕和盆腔痛的关系，在这些女性人群中，其患病率明显要高。

据报道，其患病率不孕症妇女为25%-35%，盆腔痛的妇女达39-59%。

而内异症患者50%的病人有明显的痛经，30%合并不孕，严重地影响中青年妇女的健康和生活质量。

病因学研究经血逆流子宫内膜种植学说普遍为学者们所接受，在20世纪20年代首次提出，这是最早提出并得到广泛接受的学说。

妇女月经期经血可经输卵管倒流进入腹腔，引起子宫内膜组织在腹腔内播散。

逆流经血中的内膜碎片黏附并侵润腹膜间皮，获得血液供应后持续存活并生长。

近年来，郎景和等发现内异症患者的在位内膜对其发病有重大作用。

但是90%的女性月经期有经血逆流发生，而临床上仅有10%发生EM。

目前的观点认为还有其他多因素参与了EM 的发病，如内膜细胞通过血管或淋巴播散，机械种植机制等。

血行-淋巴播散学说血行-淋巴播散学说 Lymphatic or Vascular Spread：有证据支持子宫内膜异位症起源于子宫内膜组织经淋巴或血管异常播散，子宫内膜异位症发生在一些少见部位如会阴或腹股沟区，更加支持了这一学说。

单纯在腹膜后发现孤立病变者支持了淋巴扩散学说。

体腔上皮化生(Coelomic Meatplasia)相似的组织。

因为卵巢和苗勒氏管均来源于体腔上皮，因此体腔化生学说可以解释卵巢的子宫内膜异位症。

腹膜间皮同样具有增殖和分化的能力，因此此学说甚至可以扩展至腹膜以解释腹膜子宫内膜异位症。

Norms on the Diagnosis and Treatment of Endometriosis Endometriosis Coordination Group, Gynecology & Obstetrics Society, Chinese Medical AssociationCommunication author:Lang Jinghe, Email: langjh@; Gynecology & Obstetrics Dept., Peking Union Medical College Hospital, Chinese Academy of Medical Sciences (100730)Editor’s note:Endometriosis is a common and frequent disease in the young and middle-aged women. At present, its incidence rate tends to rise evidently, but its diagnosis and treatment still have many problems for solving. In order to normalize the diagnosis/treatment of endometriosis, under the leadership of Prof. Lang Jinghe, the Endometriosis Coordination Group in the Gynecology & Obstetrics Society of Chinese Medical Association prepares this norm through the repeated discussion, protocol drafting and five revisions. This norm aims to better guide the work of clinical doctors.Endometriosis means the occurrence, growth, infiltration and recurrent hemorrhage of endometrial tissues (gland and mesenchyme) at the sites other than endometrium, which can form the nodes and mass and cause the pain and infertility. Endometriosis is frequent in the women of fertility age, and its incidence rate tends to rise evidently. It possesses the following characteristics: (1) Unmatched illness severity with the symptoms and signs; (2) Extensive polymorphic lesion; (3) Extremely infiltrating to form an extensive serious adhesion; and (4) Hormone-dependent, and highly recurrent.I. Clinical Pathological Type1. Peritoneal endometriosis (PEM): It means various endometriosis foci at the pelvic/abdominal peritoneum. Mainly including: Red lesion (early one), blue lesion (typical one) and white lesion (old one).2. Ovarian endometriosis (OEM): It can form a cyst, i.e. endometriotic cyst. According to the size of cyst and the infiltration degree of endometriosis foci, it can be classified into two types. Type I: Cyst diameter of <2cm; and adhesive cyst wall of unclear anatomical layer and difficult surgical stripping. There are three sub-types of Type II. IIA: Superficial endometrial planting foci, involving the ovary cortex but not reaching the OEM cyst wall; often with concomitant functional cyst of very easy surgical stripping; IIB: Endometrial planting foci involving the OEM cyst wall, but at a clear boundary with ovary cortex, and easy surgical stripping; and IIC: Endometrial planting foci penetrating the OEM cyst wall and spreading all around, close adhesion of cyst wall to ovary cortex, with concomitant fibrillation or multiple chambers, larger adhesion of cyst to pelvic wall, difficult surgical stripping.3. Deep infiltrating endometriosis (DIEM): It means a foci infiltration depth of ≥5mm. Including: uterosacral ligament, uterorectal pouch, vaginal fornix and rectovaginal septum. There are two types of rectovaginal septum endometriosis: pseudo one (adhesion and closure of uterorectal pouch, and a foci below this adhesion); and genuine one (foci outside the peritoneum and inside the rectovaginal septum; and uterorectal pouch of no evident anatomical abnormality).4. Other endometriosis (O t EM): It can involve the digestive, urinary and respiratory system. Including: scarry endometriosis and rare distal endometriosis.II. Clinical Manifestations, Gynecological Examination and Auxiliary Examination1. Clinical manifestations: (1) Pain: 70%~80% of endometriosis patients has a pelvic pain of various degrees and incomplete matching with the lesion degree. Including: dysmenorrhea (typically secondary one of progressive aggravation), non-menstrual abdominal pain, chronic pelvic pain (CPP), dyspareunia and dysuria, and acute abdominal pain (in the case of broken OEM cyst); (2) Infertility: About 50% of endometriosis patients has a concomitant infertility. (3) Menstrual disorder. (4) Pelvic mass. In the endometriosis at special sites, there are various symptoms, often with a concomitant cyclic change and following clinical manifestations of pelvic endometriosis. For example: (1) Digestive tract endometriosis: Frequent defecation (or constipation), hemafecia and dysuria; (2) Urinary tract endometriosis: Polyuria, dysuria, hematuria, waist, and even urinary obstruction or renal dysfunction; (3) Respiratory tract endometriosis: Menstrual hemoptysis and pneumothorax; (4) Scarry endometriosis: Nodes at the incision scar of abdominal wall, prolonged menstrual period and aggravated pain after some surgeries (e.g. Caesarean birth); and nodes at the incision or incision scar, prolonged menstrual period and aggravated pain after the perineum surgery.2. Gynecological examination: Typically uterus of retro position and poor mobility; uterosacral ligament, uterorectal pouch or rear fornix tenderness/nodes; and concomitant adnexa cyst and immobile mass.3. Auxiliary examination: (1) CA125: Often mild/moderate rise of serum CA125level; (2) Radiography: Ultrasonic B examination is mainly significant for the diagnosis of OEM cyst. In the typical OEM cyst, there is a mass of no echo and strong light spot at the adnexa site under the ultrasonic B examination. MRI is significant for the diagnosis and assessment of OEM cyst, extra-pelvic endometriosis and deep infiltration foci; and (3) Others: vein/pelvis radiography, cystoscopy and colonoscopy.III. Diagnosis1. Symptoms: Pain (e.g. dysmenorrhea, CPP and dyspareunia) and infertility.2. Gynecological/auxiliary examination: There is an endometriosis foci under both pelvic examination and radiography; and mild/moderate rise of serum CA125 level.3. Laparoscopy: At present, the endometriosis is universally diagnosed through the laparoscopy mainly according to the shape of foci, which can not completely verified by the pathological examination.IV. Clinical StagingAt present, the endometriosis is staged often through the r-AFS method revised by the American Fertility Society in 1985. It is scored mainly according to the size and depth of peritoneal/ovary lesion, the range and degree of ovary-oviduct adhesion, and the closure degree of uterorectal pouch.V. TreatmentThe treatment of endometriosis mainly aims to subside/eliminate the foci, relieve/eliminate the pain, improve/promote the fertility, and reduce/avoid the recurrence. Its treatment should mainly consider the following factors: age, fertility desire, symptom severity, lesion range, past treatmentand patient demand. The treatment measures should be normative and individualized. The pelvic pain, infertility and pelvic mass should be treated separately. Its treatment methods include: surgery, pharmacotherapy, interventional treatment and fertility-assisting treatment.(I) Surgery1. Objective: To excise the foci and resume the anatomy2. Classification: According to the technique, the surgery for endometriosis is classified as follows: (1) Conservative surgery: Retain the fertility function of patients, excise the macroscopic foci and OEM cyst as far as possible, and separate the pelvic adhesion. It is applicable for young patients or those of demanding to retain the fertility function. (2) Semi-radical surgery: Excise the uterus/foci, but retain the ovary. It is mainly applicable for the patients of no fertility desire but demanding to retain the endocrine function of ovary. (3) Radical surgery: Excise the whole uterus, both adnexa and all macroscopic foci. It is applicable for the patients of older age, no fertility desire, serious symptoms or multiple ineffective treatment. (4) Auxiliary surgery: Excise the uterine nerve and anterior uterosacral nerve. It is applicable for the patients with a pain at center-line site.3. Preparation: As the most important contents before the surgery, the severity of illness should be assessed accurately, and the patients or their family members should be fully communicated to obtain their understanding and informed consent. In addition, the risk of surgery should be assessed, and the possibility should be evaluated for the surgical injury (especially the injury of urinary system and intestinal tract) and for the replacement of laparoscopic surgery with laparotomy. The intestinal tract should be fully pre-treated for the DIEM (especially that with a lesion involving the rectovaginal site). In the patients with an evident deep infiltration foci beside the uterus, the ureter and kidney should be examined for abnormality before the surgery, and the assistance should be obtained from the Urinary Surgery and General Surgery if necessary.4. Essential points: The pelvic adhesion should be first separated, so as to resume the anatomy; the PEM foci should be excised or destroyed as far as possible, so as to subside and eliminate it; the smaller and superficial foci can burnt or vaporized; and the deep infiltration foci should be excised.(1) OEM cyst: The surrounding adhesion should be first separated, the dark brown viscous liquid should be sucked out of cyst, and the inner wall of cyst should be rinsed up, the fibrous tissue ring around the cyst breach should be excised, and the inner wall of cyst should be completely stripped, and the normal ovary tissues should be protected as far as possible. In the patients with concomitant infertility, both the uteroscopy and oviduct fluid infusion can be conducted. (2) DIEM: This endometriosis is more difficult to treat. In case of no lesion involvement into the rectal/colonic wall, the foci should be excised as far as possible. In case of intestinal wall infiltration but no intestinal tract stenosis, it was generally recommended not to excise the intestinal wall or segment but to subside and eliminate the foci. If the foci is large enough to cause an intestinal stenosis and even intestinal obstruction, the intestinal segment should be excised and anastomosed according to the actual conditions. (3) Vesical endometriosis: According to the size of foci, the foci or partial vesical wall should be excised. (4) Ureteric endometriosis: According to the state of lesion and the degree of ureteric obstruction, the adhesion should be loosened or the partial ureter should be excised and anastomosed. (5) Scarry endometriosis: It should be treated mainly through the surgery, because it is usually insensitive to the pharmacotherapy. If the endometriosis foci can not be completely excised or if the important organs/tissues may be injured,the gonadotropin releasing hormone agonist (GnRH-a) can be administered for 3~6 months before the surgery. At the time of adhesion separation, uterus excision, uterus blood vessel treatment and ligament treatment, special attention should be paid to the anatomic relation around the ureter, and the ureteral catheter should be laid as the guidance before the surgery if necessary. In addition, relevant drugs can be administered to prevent the adhesion after the surgery.(II) PharmacotherapyThe pharmacotherapy aims to inhibit the function of ovary, retard the progress of endometriosis, decrease the activity of endometriosis foci and reduce the formation of adhesion. Principles of pharmacotherapy: (1) Applicable for the patients of basically-definite diagnosis, and not recommended for long-term tentative treatment; (2) Of yet no standard protocol; (3) Basically same effectiveness but different adverse reactions of various protocols; (4) According to the demand and economic strength. The endometriosis can be treated with four categories of drugs with the following protocol, action mechanism and adverse reactions.1. Oral contraceptive: Administer continuously or cyclically for 6 months. It can inhibit the ovulation. Less adverse reactions: Digestive tract symptoms or liver dysfunction.2. High-performance progestin: Medroxyprogesterone Acetate, 20~30mg/d po, bid or tid, for 6 months. It can cause the decidual change of endometrium tissues and finally cause the atrophy of endometrium; and inhibit the hypothalamus-pituitary-ovary axis in negative feedback. Main adverse reactions: bloated pain rupture hemorrhage, breast swelling pain, body weight gain, digestive tract symptoms and liver dysfunction.3. Androgen derivatives: (1) Danazol: 600~800mg/d po, bid or tid, for 6 months. It can inhibit the peak of luteotropic hormone (LH) at middle menstrual period for ovulation inhibition, inhibit various enzymes participating in the synthesis of steroids, and improve the free testosterone level in blood. Main adverse reactions: Masculine signs (e.g. hypenrichosis, emotional change and voice coarseness), lipoprotein dysbolism, liver functional injury and body weight gain. (2) Ethylnorgestrienone: 2.5mg po, 2~3 times a week, for 6 months. It can antagonize the progestin and estrogen, decrease the level of sex hormone binding globulin, and improve the free testosterone level in blood. Main adverse reactions: Basically same but milder antagonism of estrogen and androgen to that of Danazol.4. GnRH-a: Inject subcutaneously or intramuscularly (according to the medicinal form), monthly administration for 3~6 months. It can down-regulate the function of pituitary to cause a transient medicinal desexuality and a low estrogen level in body. Main adverse reactions: Climacteric symptoms caused by the hypoestrinemia (e.g. hectic fever, vaginal dryness, hyposexuality, insomnia and bone substance loss (at long-term administration).The combined protocol of GnRH-a + Add-back is based on the theory of “Window dose of estrogen”. The sensitivity of estrogen varies with tissues. The estrogen level in body is maintained at 110~146pmol/L estradiol to not stimulate the growth of ectopic endometrium or cause the climacteric symptoms (or bone substance loss) and not affect the effectiveness but relieve the adverse reactions, so as to prolong the treatment time. Add-back protocol: (1) Combined estrogen-progestin protocol: Estrogen (trade name: Premarin) (0.3~0.625mg/d) + Medroxyprogesterone Acetate (2~4mg/d). (2) Tibolone (synonym: Livial): 1.25mg/d.The Add-back protocol at an individualized dose is recommended generally after the administration of GnRH-a for more than 3 months, or begins from the Month 2 of GnRH-aadministration according to the severity of symptoms. The estrogen level should be monitored if possible.(III) Auxiliary treatment of dysmenorrhea and infertility1. Treatment of dysmenorrhea: In the patients with concomitant pelvic nodes or adnexa mass, the surgery is preferred; and otherwise, the pharmacotherapy is preferred. In the patients ineffective to the pharmacotherapy, the surgery can be adopted.Common therapeutic drugs for dysmenorrhea: (1) First-line drugs: Non-steroid anti-inflammatory drugs or oral contraceptives. The oral contraceptives can be administered cyclically or continuously, continue in effective case, but is replaced with the second-line drugs in ineffective case. (2) Second-line drugs: Progestin, androgen derivatives and GnRH-a; preferably the combined protocol of GnRH-a + Add-back to effectively control the adverse reactions at long-term administration; and the surgery can be adopted in ineffective case. (3) Pre-surgical drugs: In the patients with a serious illness, unable complete excision or possible important organ injury, relevant drugs can be temporarily administered for 3 months to reduce the surgical difficulty. (4) Post-surgical drugs: In the patients with milder illness or complete excision, relevant drugs can temporarily not be administered according to the actual conditions. In the patients with serious pelvic lesion or unable complete foci excision, relevant drugs can be administered for 3~6 months according to the existence of pain or not.2. Treatment of infertility: In the infertile endometriosis patients without other infertility factors and ineffective to pure pharmacotherapy as shown by complete examination, the laparoscopy can be conducted to assess the type and stage of endometriosis. In the young patients with mild/moderate endometriosis, the natural pregnancy can be expected half a year after the surgery, and fertility guidance should be offered. In the high-risk patients (aged ≥35 years old, oviduct adhesion and low functional score, infertility duration ≥3 years; and especially primary infertility, moderate/serious endometriosis with concomitant pelvic adhesion, and incomplete foci excision), the fertility-assisting technique should be actively adopted. For infertility treatment, the conservative laparoscopic surgery should excise the foci as completely as possible, separate the adhesion, and resume the anatomy. While excising the OEM cyst, the normal ovary tissues should be protected, the oviduct fluid infusion test should be conducted to know the smoothness of oviduct, and the uteroscopy should be made to grasp the conditions of uterine cavity. The following fertility-assisting technique should be selected according to the actual conditions of patients. (1) controlled ovarian hyperstimulation and/or artificial fertilization: Mainly applicable for the infertility patients with mild/moderate endometriosis, masculine factor (mild oligospermia and asthenospermia), cervical factor and unknown cause. The artificial fertilization has a single-cycle pregnancy rate of about 15%. If the pregnancy fails after 3~4 treatment courses, the fertility-assisting technique should be adjusted. (2) In vitro fertilization-embryo transplantation (IVF-ET): Mainly applicable for the infertility patients with serious endometriosis, long illness duration, old age or ineffective to other therapeutic methods (e.g. natural pregnancy, induced ovulation, artificial fertilization and surgery). Before the IVF-ET, GnRH-a is preferably administered for 2~3 months, so as to better improve the success rate of fertility assistance. The duration pharmacotherapy should be adjusted according to the severity of endometriosis and the storage conditions of ovary.Fig.1: Diagnosis and treatment of endometriosisVI. Problems of Hormone TreatmentAfter the menopause or radical surgery, the endometriosis patients can receive the hormone treatment, so as to improve their quality of life. The hormone treatment should be individualized according to the symptoms. Even after the hysterectomy, the combined estrogen with progestin had better be administered in case of residual endometriosis foci. Without the residual endometriosis foci, the single estrogen can also be administered. When possible, the estradiol level should be monitored, so that the estrogen level is high enough to not cause the symptoms or recurrence of endometriosis and is low enough not to cause the loss of bone substance.VII. RecurrenceThe recurrence of endometriosis means the re-appearance of clinical symptoms and their restoration to the degree before the treatment (or their aggravation) or the re-appearance of endometriosis foci after the subsidence/disappearance of foci and the relief of symptoms throughthe surgery or normative pharmacotherapy. It should be treated basically through the original treatment measures of endometriosis, and in the following individualized ways. OEM cyst: surgery or ultrasonic puncture, with subsequent pharmacotherapy. Dysmenorrheal: surgery for its recurrence after the pharmacotherapy; first pharmacotherapy and then surgery at ineffective pharmacotherapy for its recurrence after the surgery; and radical surgery for the patients of old age, serious symptoms but no fertility desire. Infertility patients with concomitant OEM cyst: surgery or ultrasonic puncture, with subsequent first GnRH-a administration for 3 months and then IVF-ET. Infertility patient without concomitant OEM cyst: first GnRH-a administration for 3 months and then IVF-ET.VIII. CancerationThe canceration of endometriosis has an incidence rate of about 1%. Under the following conditions, the canceration should be alerted: (1) Cyst diameter >10cm, or evident cyst enlargement within a short time; (2) Recurrence after the menopause; (3) Change of pain pace or continuation of dysmenorrhea; (4) Solid or papillary structure of cyst (radiography); and abundant blood flow and low resistance index at the foci (color Doppler ultrasonic examination); (5) Evident rise of serum CA125 level (>200kU/L).Diagnostic criteria for atypical endometriosis: (1) Cancer tissues and endometriosis tissues coexist at the same foci; (2) Both above tissues are histologically correlated just as the endometrial mesenchyme and gland; or there is a remote hemorrhage; (3) Other primary tumors are excluded; or the cancer tissues appear at the endometriosis foci, but do not metastasize from other sites; (4) There is a morphological evidence for the transformation of endometriosis lesion to malignant lesion; or the benign endometriosis lesion is mutually infiltrated with the malignant tumor tissues. The atypical endometriosis is a histopathologically-diagnosed atypic or nucleus atypia change of ectopic endometrium glandular epithelium, which does not break through the basal membrane. It has the following histopathological signs: deep/light staining of ectopic endometrium glandular epithelium, with concomitant moderate/serious nucleus atypia, increase of nuclear/cytoplasm proportion, and dense cells of multiple layers or clustery protrusion. The atypical endometriosis is regarded as a precancerous lesion or boundary tumor state.The canceration of endometriosis occurs mainly at the ovary, but less at other sites (e.g. rectovaginal septum and belly/perineum incision). It is treated according to the treatment principles for oophoroma.IX. AdenomyosisIn the myometrium, there are endometrium gland and mesenchyme. Under the action of hormones, there will be a hemorrhage and hyperplasia of muscular fibers and connective tissues, to cause a diffuse/local lesion or endometrioma.1. Etiology: At present, there is yet unknown cause for adenomyosis, including: invasion of endometrium (primary cause), diffusion of blood/lymph vessel, metaplasia of epithelium, and influence of hormone.2. Clinical manifestations: (1) Dysmenorrhea: More than half of patients have a secondary dysmenorrhea and its progressive aggravation; (2) Menstrual disorder: Hypermenorrhea, prolonged menstrual period and irregular hemorrhage; (3) Infertility; (4) Uterus enlargement:Generally uniform spherical enlargement, and sometimes uneven protrusion and hard texture.3. Diagnosis: The preliminary diagnosis can be obtained according to the symptoms, pelvic examination and following auxiliary examinations: (1) Ultrasonic scanning: uterus enlargement, myometrium thickening, more evident posterior uterus wall, and forward shifting of endometrium equal or enhanced echo at the foci, intermittent punctual low echo between the foci, and no evident boundary between the foci and its periphery. (2) MRI: foci of unclear boundary and low signal intensity. T2 enhanced scanning: foci of high signal intensity, and widening bonding area between endometrium and myometrium (>12mm). (3) Serum CA125level: generally rise. (4) Pathological examination: golden diagnostic criteria.4. Treatment: (1) Temporization: Regularly observe the patients of no symptoms or no fertility desire. (2) Surgery: Main treatment method (including the radical surgery of uterus excision). In the young patients requiring to retain the fertility function, the foci can be excised and the uterus is wedge uterectomy; or the auxiliary surgery should be conducted (i.e. uterus nerve excision, anterior uterosacral nerve excision or uterus artery blockage). In the patients with concomitant hypermenorrhea and of no fertility desire, the endometrium can be excised. (3) Pharmacotherapy: Same as endometriosis. (4) Intervention treatment. (5) Fertility-assisting treatment: after the GnRH-a administration for 3~6 months in the infertility patients; and after the combined protocol of surgery + GnRH-a in the patients with a local lesion or adenomyosis.Members of Endometriosis Coordination Group:Peking Union Medical College Hospital, Medical University, Chinese Academy of Medical Sciences (Lang Jinghe, Y u Qi, Leng Jinhua, Zhu Lan); People’s Hospital of Peking University (Wei Lihi, Cui Heng); First Hospital of Peking University (Zhou Yingfang); Affiliated Beijing Chaoyang Hospital of Capital Medical University (Zhang Zhenyu); China-Japan Friendship Hospital (Bian Meilu); Affiliated Gynecology & Obstetrics Hospital of Medical College of Fudan University (Cao Binrong); Second Affiliated Hospital of Sun Yat-Sen University (Yang Dongzi); Affiliated Union Hospital of Huazhong University of Science and Technology (Gu Meijiao); First Affiliated Hospital of Medical College of Zhejiang University (Zhang Xinmei); Second Xiangya Hospital of Central South University (Xiao Hongmei); First Affiliated Hospital of Jinan University (Luo Xin); Maternity and Child Health Hospital for women & children of Fujian Province (Chen Jie)。

子宫内膜异位症诊疗规范一、概述子宫内膜异位症（endometriosis）简称内异症，是指子宫内膜组织（腺体和间质）在子宫腔被覆内膜及子宫肌层以外的部位出现、生长、浸润、反复出血，可形成结节及包块，引起疼痛、不孕等，是生育年龄妇女的常见病。

其发病率有明显上升趋势，但发病机制至今未明。

子宫内膜异位症病变广泛、形态表现多样、极具浸润性，可形成广泛、严重的粘连，而症状、体征与疾病的严重程度不成比例，且由于其激素依赖性，治疗后易于复发。

二、流行病学特点目前报道子宫内膜异位症的发病率为1∙4%〜10%,而在痛经、性交痛、经量多和不孕的人群中其发病率可增加5倍。

事实上，内异症在普通人群中的发病率尚不清楚，除非找到一种可靠的、无创的、可应用于大样本非选择性人群的检查方法。

内异症的高发年龄为25〜34岁，而其严重程度则与年龄无关。

流行病学研究提示，初潮年龄早（W11岁）、月经周期短（≤27d）＞经量大、生育少、哺乳时间短、BMI低等，均会增加内异症发生的风险，而口服避孕药是否会增加内异症的风险则是有争议的，宫内节育器与内异症的发生发展无关。

免疫系统异常增加罹患内异症的风险，研究表明，在类风湿关节炎、系统性红斑狼疮、多发性硬化症、甲状腺功能异常的患者中，内异症的发病风险明显增加。

同时有癌症家族史，特别是乳腺癌家族史的人群，内异症的风险也明显高于普通人群。

内异症患者的一级亲属发生内异症的风险是正常人的4〜8倍，中隔子宫等苗勒管发育异常的患者，内异症的发生风险增加，这说明内异症的发生有其基因及分子基础。

环境和生活饮食习惯也与内异症的发生发展密切相关。

胎儿期暴露于高雌激素环境会导致成年后内异症发生风险增加，摄入酒精、咖啡、不饱和脂肪酸，会增加患内异症的风险，适当运动可以降低风险，而高强度运动则明显增加患子宫内膜异位症的风险。

三、病因学研究子宫内膜异位症的具体病因及发病机制仍不详。

"经血逆流”是发病机制之一，但90%的女性均有经血逆流，内异症的发病率却仅为10%,异位子宫内膜要能生存、生长并引起病变和症状，必须通过黏附、侵袭、血管生成三步曲才能完成，因此，盆腹腔环境的改变与内异症的发生发展密切相关。

子宫内膜异位症诊治原则概述子宫内膜异位症（EMT）简称内异症，是指子宫内膜组织（腺体和间质）出现在子宫体以外的部位。

病灶分布范围以卵巢、宫骶韧带最常见，其次为子宫及其他脏腹膜、直肠阴道膈等部位。

组织学上，内异症是良性疾病，临床表现上具有种植、侵袭及远处转移等类似恶性肿瘤的特点。

内异症是激素依赖性疾病，是生育年龄妇女的多发病、常见病。

持续加重的盆腔粘连、疼痛、不孕是其典型的临床表现。

特点如下：①生育年龄妇女的多发病，主要引起疼痛及不育；②发病率有明显上升趋势；③症状与体征及疾病的严重性不成正比例；④病变广泛、形态多样；⑤极具浸润性，可形成广泛、严重的粘连；⑥有激素依赖性，易复发。

根据临床病理类型可分为：①腹膜型内异症；②卵巢型内异症；③深部浸润型内异症（DIE，指病灶浸润深度≥5mm），病灶分布范围包括宫骶韧带、阴道直肠窝、直肠结肠壁、阴道穹隆等；④其他部位的内异症（瘢痕内异症以及其他少见的远处如肺、胸膜等部位内异症）。

诊断1. 症状（1）疼痛：70%～80%的患者有不同程度的盆腔疼痛，与病变程度不完全平行。

①痛经：典型者为继发性，并渐进性加重。

②非经期痛经：慢性盆腔痛。

③性交痛以及排便疼痛等。

④卵巢内异症囊肿破裂，可引起急性腹痛。

（2）不孕：40%～50%的患者合并不孕。

（3）月经异常。

（4）盆腔结节及包块。

（5）特殊部位内异症。

各种症状常有周期性变化，可合并盆腔内异症的临床表现：①消化道内异症，如大便次数增多或便秘、便血、排便痛等症状。

②泌尿道内异症，如尿频、尿痛、血尿及腰痛，甚至出现泌尿系统梗阻及肾功能障碍。

③呼吸道内异症，如经期咯血及气胸等。

④瘢痕内异症，如腹部剖宫产等手术切口或伤口瘢痕结节。

2.体征典型盆腔内异症妇科检查可发现子宫后倾固定，直肠子宫陷凹、宫骶韧带或子宫后壁下方可扪及触痛性结节，一侧或双侧附件处触及囊实性包块，活动度差。

病变累及直肠阴道间隙时，可在阴道后穹降触及或者直接看到局部隆起的小结节或紫蓝色斑点。

2021《子宫内膜异位症管理指南》解读（全文）子宫内膜异位症(简称内异症) 为育龄期女性常见病、疑难病, 常与不孕症密切相关。

作为一种慢性疾病, 具有迁延难愈的特点, 临床医师在诊疗过程中需坚持长期管理原则, 同时注意医源性内异症的防治。

2018年法国妇产科医师协会(CNGOF) 及法国国家卫生管理局(HAS) 颁布了新版指南即《子宫内膜异位症的管理指南》[1], 用来替代2006年的临床实践指南, 新版指南在原指南的基础上详细介绍了腹膜、卵巢及深部内异症的诊断和管理, 本文就该指南推荐意见进行简要解读。

1 发病率及流行病学普通人群内异症的患病率难以预估[2], 据报道15~49岁的女性中内异症年发病率为0.1%。

急性盆腔痛者超过33%伴发内异症, 慢性盆腔痛女性流行病学研究结果异质性较大, 从2%~74%不等。

2 子宫内膜异位症自然演变史内异症是一种涉及遗传、环境和月经的多因素疾病。

高危因素包括:月经初潮早、经量增多、周期缩短、一级亲属内异症病史。

已有数据显示内异症与卵巢癌无因果关系[证据水平(level of evidence, LoE) 2], 故指南不建议对内异症患者行卵巢癌筛查(B级) 。

内异症并不一定合并疼痛(LoE2) , 该指南不建议因遗传(与内异症相关) 或月经高危因素(经量增多、周期缩短) 对无症状的患者行系统性筛查, 亦不建议对普通人群行内异症筛查(专家共识) 。

3 诊断3.1 临床表现内异症临床表现呈多样性, 其中痛经(以10分制为准, 疼痛评分≥8分) , 慢性盆腔痛、深部性交痛(LoE2) 、经期合并泌尿系统症状(LoE2) 、不孕(LoE2) 较为常见[3,4]。

3.2 辅助检查3.2.1 一线辅助检查子宫内膜异位症一线诊断依据为妇科查体及超声, 其中经阴超声对子宫腺肌病具独特诊断价值。

绝经后女性应注意鉴别恶性肿病(LoE2) , 若影像学发现性质不明确的卵巢肿块, 建议重复超声检查(A级) 。

2021子宫内膜异位症的诊治指南专家解读（下）五、内异症的药物治疗内异症药物治疗的目标是缓解疼痛症状，改善生育能力，术后长期管理，延缓症状复发。

目前可供选择的药物主要有非甾体类抗炎药、复方口服避孕药、高效孕激素、雄激素衍生物及GnRH-a 共五大类。

非甾体类抗炎药，可以抑制前列腺素的合成，直接作用于伤害性感受器，阻止致痛物质的形成和释放。

给药时机掌握良好有助于加强疗效，如月经来潮前24～48 h前给药，止痛效果明显增强。

如果疼痛仍未缓解，或者效果不满意，应该予进一步的治疗。

该类药物的不良反应主要为胃肠道反应，偶有肝肾功能异常。

长期应用要警惕胃溃疡的可能。

复方口服避孕药是治疗内异症相关疼痛的一线用药，疗效明确、安全性好、费用低，适合长期使用，控制轻～中度痛经的疗效明显。

观察性研究显示，口服避孕药治疗内异症相关疼痛的疗效明确，可以明显提高患者痛经、性交痛、非经期疼痛、大便痛等的缓解率。

对于年龄<16岁的青少年内异症患者，口服避孕药也是安全和有效的，常与非甾体类抗炎药联合应用，以便更好地控制内异症相关疼痛。

对青少年的身高、体质量及近期体脂百分比无明显影响。

因此，对于青少年和暂时没有生育要求的育龄期年轻女性，复方口服避孕药是较为理想的药物治疗方式。

孕三烯酮是合成的19-去甲睾酮衍生物，是1种抗孕激素的甾体激素，为临床治疗内异症的主要药物之一。

其使用方式为口服，使用方便。

一般疗程为6个月，疗效显著，作用稳定。

孕三烯酮的不良反应主要表现为高雄激素症状，如多毛、痤疮、脂溢性皮炎和嗓音变粗等，还有体质量增加、血脂异常、肝功能异常、不规则出血和情绪变化等，不利于患者的耐受及长期使用。

GnRH-a对治疗内异症的近期疗效已经得到公认，被认为是内异症药物治疗的“金标准”药物。

GnRH-a可以有效缓解疼痛，特别是中～重度疼痛，也可以用于延缓术后疼痛及囊肿的复发。

同时，GnRH-a 的预处理可以使接受IVF治疗的内异症不孕患者受益。