Chinese expert consensus on the clinical diagnosis and treatment of sepsis induced thrombocytopenia

doi:10.3877/cma.j.issn.2096-1537.2023.03.001

Abstract

Task Force on Chinese expert consensus on the clinical diagnosis and treatment of sepsis induced thrombocytopenia. Chinese expert consensus on the clinical diagnosis and treatment of sepsis induced thrombocytopenia[J]. Chinese Journal of Critical Care & Intensive Care Medicine(Electronic Edition), 2023, 09(03): 225-240.

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References 91

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等级	推荐	证据
Grade 1+	强推荐：“推荐”	高质量的证据
Grade 2+	弱推荐：“建议”	低质量的证据
专家意见	以专家意见形式提出的建议：“专家建议”或“专家不建议”	证据不足
Grade 2-	弱推荐：“不建议”	低质量的证据
Grade 1-	强推荐：“不推荐”	高质量的证据

等级	推荐	证据
Grade 1+	强推荐：“推荐”	高质量的证据
Grade 2+	弱推荐：“建议”	低质量的证据
专家意见	以专家意见形式提出的建议：“专家建议”或“专家不建议”	证据不足
Grade 2-	弱推荐：“不建议”	低质量的证据
Grade 1-	强推荐：“不推荐”	高质量的证据

严重程度	PLT	出血倾向	备注
轻度减少	50×10⁹/L~100×10⁹/L	一般无出血倾向	可以不予治疗，可酌情进行小手术
中度减少	30×10⁹/L~50×10⁹/L	有出血倾向	不推荐进行手术
重度减少	10×10⁹/L~30×10⁹/L	出血倾向增加	对于ITP患者应慎输血小板
极重度减少	<10×10⁹/L	大部分患者有皮肤及黏膜出血症状	可发生颅内出血等危及生命的并发症

严重程度	PLT	出血倾向	备注
轻度减少	50×10⁹/L~100×10⁹/L	一般无出血倾向	可以不予治疗，可酌情进行小手术
中度减少	30×10⁹/L~50×10⁹/L	有出血倾向	不推荐进行手术
重度减少	10×10⁹/L~30×10⁹/L	出血倾向增加	对于ITP患者应慎输血小板
极重度减少	<10×10⁹/L	大部分患者有皮肤及黏膜出血症状	可发生颅内出血等危及生命的并发症

机制类型	病理生理过程
血小板生成减少	血小板由骨髓中的巨核细胞产生，受肝脏所产生的TPO调节。脓毒症导致单核细胞和巨噬细胞对巨核细胞和其他造血细胞的主动吞噬作用，导致血小板生成减少
血小板消耗和破坏增加	脓毒症的病原微生物及其产物通过介导释放多种炎症因子损伤血管内皮、激活血小板。血小板附着在血管内皮细胞上，进而激活凝血系统，刺激纤溶酶原激活物抑制物释放，抑制纤溶系统，造成DIC，进而导致血小板的大量消耗^[1]。细菌及代谢产物通过免疫途径激活补体、破坏血小板，在部分患者体内可出现抗血小板自身抗体，导致血小板与抗体结合，进而免疫识别，使得消耗增加
血小板丢失增加	脓毒症患者发生各种原因的活动性出血，包括手术、消化道应激性溃疡出血，以及女性患者月经期的出血，均可导致血小板减少。体外循环、体外膜肺氧合、血液净化治疗（全血灌流、血液滤过等）治疗过程中损失血液成分，是造成血小板减少的重要因素
血小板在脾脏的集聚	脾脏内储存的血小板占血液中的1/3，输注血小板后，也会有约30%的血小板储存于脾脏中。脓毒症患者的血小板可因通过脾索的速度减慢致使血小板接触脾巨噬细胞的时间延长，加上淤血等因素造成血小板形态改变，脾脏还分泌抑制血小板从骨髓释放的因子，综合造成脾脏对血小板的集聚、扣押和隔离，使得外周血中血小板减少。脓毒症引发的全身炎症状态下，血小板可向肺毛细血管和肝血窦迁移并被扣押和聚集，进一步导致血小板减少

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Chinese expert consensus on the clinical diagnosis and treatment of sepsis induced thrombocytopenia

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类型	风险因素
基础状态	高龄、血清肌酐升高、血清胆红素升高、术前PLT低、入院时高C反应蛋白水平
疾病因素	脓毒症、DIC、非颅脑损伤
检查因素	胃肠道诊断、动脉或中心静脉导管置入、肺动脉导管置入
治疗因素	新鲜冰冻血浆输注、透析治疗、主动脉内球囊反搏术
药物因素	高剂量血管活性药、非甾体抗炎药、化疗药
疾病严重程度	较高的SOFA评分、休克、较高的创伤评分

类别	参数	0分	1分	2分
PT	PT-INR	≤1.2	>1.2~1.4	>1.4
凝固物	PLT（×10⁹/L）	≥150	100~<150	<100
SOFA总分	SOFA 4项	0	1	≥2

出血风险因素	得分
中度肾功能衰竭，GFR 30~59 ml/（min·m²）	1.0
男性	1.0
年龄40~84岁	1.5
近期癌症	2.0
风湿免疫疾病	2.0
中心静脉置管	2.0
ICU/CCU	2.5
重度肾功能衰竭，GFR<30 ml/（min·m²）	2.5
肝衰竭（INR>1.5）	2.5
年龄≥85岁	3.5
PLT<50×10⁹/L	4.0
入院前3个月内的出血	4.0
活动性胃十二指肠溃疡	4.5

血小板减少症发生机制	病史/临床诊断思路
假性血小板减少
EDTA抗凝血中血小板聚集；接受GPⅡbⅢa拮抗剂治疗	非预计或无法解释的血小板减少且无出血症状；既往使用过GPⅡbⅢa受体拮抗剂
血液稀释
输注液体和（或）血浆	大量输液/输血
血小板耗竭
失血	出血或凝血因子丢失
严重创伤	病史、体格检查及放射学检查
DIC	各种原因的休克、严重感染、产科并发症或其他的潜在因素表现为凝血时间延长，纤维蛋白分解产物增多，识别出有核红细胞
脓毒症	脓毒症相关标准及病原学指标
体外血管通路	治疗需要使用体外血管通路
血小板滞留（扣押）
肝脾肿大	病史、特有的伴随疾病（如肝硬化或骨髓纤维瘤），以及超声或放射学诊断
血小板生成减少
中毒	滥用或服用药物史；可进行毒物鉴定
病毒感染（EBV、CMV、COVID-19）	病毒感染的相关依据
骨髓浸润（白血病、肿瘤）	骨髓检查、血涂片发现相应疾病改变
辐射	相应病史
化疗	相应病史
血小板破坏
ITP	血清或血小板表面有IgG抗体，脾脏无明显肿大，骨髓中巨核细胞正常或增加；糖皮质激素治疗有效
药物依赖性血小板减少性紫癜	药物史（发病前7~14 d使用过新的药物）、PLT<20×10⁹/L、停用可疑或检测到的药物后PLT增加、确认存在药物依赖性证据
肝素诱导性血小板减少	使用肝素治疗后5~14 d PLT减少50%（最低可达20×10⁹/L~80×10⁹/L），PF4抗体/肝素抗体阳性
血栓性微血管病（TTP、HUS、HELLP综合征）	溶血且直接抗球蛋白试验阴性、血涂片可见碎裂红细胞、通常PLT低至10×10⁹/L~30×10⁹/L、血栓事件伴随神经（TTP）或肾（HUS）症状、妊娠（HELLP综合征）、乳酸脱氢酶升高
输血后紫癜	输血史、PLT低至<10×10⁹/L、出血症状、高滴度HPA-1a抗体
被动同种免疫性血小板减少	输入（尤其是经产献血者的）含血制品后（被动传递同种血小板抗体）血小板突然、迅速下降

疾病名称	引起血小板减少的机制	诊断与鉴别要点
TTP	主要以终末小动脉与毛细血管形成透明血栓为发病机制，血小板消耗性减少	好发年龄为10~40岁，临床上表现为三联征（微血管病溶血性贫血、血小板减少、神经精神异常）或五联征（三联征+发热、肾脏损害）
自身免疫性疾病
系统性红斑狼疮	主要因血清中存在抗血小板抗体以及抗磷脂抗体和骨髓巨核细胞成熟障碍有关	好发于青年女性，临床主要表现为面部蝶形红斑，可伴发热、关节痛、肾脏及心血管系统损害，也可表现为间质性肺炎。血清学检查、皮肤及肾活检有助于诊断
抗磷脂综合征	反复动脉或者静脉血栓形成引起血小板消耗性减少	女性发病多见，主要临床表现为反复动脉、静脉血栓形成、习惯性流产及血小板减少；抗心磷脂或狼疮抗凝物实验持续阳性。依据临床表现及实验室检查可诊断
自身免疫性甲亢	甲亢代谢旺盛，能量物消耗过多，铁、维生素、叶酸产生不足，使血小板生成减少；亦可因过多的甲状腺素损伤干细胞，影响血小板生成	好发年龄为20~40岁，常伴弥漫性、对称性甲状腺肿大；有心慌、多汗、眼球突出、舌手震颤等表现，依据临床表现、甲状腺功能检测及TSAb检测可明确诊断
HIT	抗体-肝素-PF4形成的免疫复合物激活血小板，产生促凝物质，血小板消耗性减少	有应用肝素的药物史，停用肝素后数日血小板及凝血变化可得到纠正；肝素依赖性抗血小板抗体检测阳性。结合病史及实验室检查可诊断
HELLP综合征	血管内皮细胞受损，激活血小板，使血小板消耗性减少；PGⅠ2合成减少与血小板激活释放TXA2，使血管进一步痉挛和血小板聚集消耗	为妊娠期高血压疾病的严重并发症，临床上以溶血、肝酶升高和血小板减少为特点；早期应用糖皮质激素及配合应用血制品为主要治疗手段。可依据病史及临床表现诊断
嗜血综合征	感染、肿瘤、免疫介导性疾病等引起嗜血细胞增多，加速血细胞破坏，使血小板破坏性减少	该病的特征为：发热、肝脾肿大伴全血细胞减少、骨髓及脾脏或者淋巴结可见嗜血细胞但无恶性表现、NK细胞活性降低或缺乏、高铁蛋白血症、可溶性白介素受体水平升高
成人原发免疫性血小板减少症	患者对自身抗原的免疫失耐受，导致免疫介导的血小板破坏增多和免疫介导的巨核细胞产生血小板不足	60岁以上人群为高发群体，临床表现为皮肤黏膜出血，严重者有内脏出血甚至颅内出血。诊断为排除性诊断，血小板抗体及TPO检测有助于鉴别诊断

药物类型	作用机制	代表药物
抗肿瘤药及免疫抑制剂	骨髓抑制	吉西他滨、柔红霉素、多柔比星、博来霉素、甲氨蝶呤、环磷酰胺、氮芥、环孢素等
抗菌药	免疫抑制和骨髓抑制	万古霉素、利奈唑胺、氟康唑、卡泊芬净、两性霉素B脂质体、利福平、庆大霉素、链霉素、氯霉素、青霉素、头孢菌素类、氟喹诺酮类及磺胺类等
解热镇痛药	抑制血小板聚集	阿司匹林、对乙酰氨基酚、水杨酸钠、布洛芬、保泰松等
抗癫痫药	骨髓抑制	苯妥英钠、卡马西平、三甲双酮等，丙戊酸钠
血小板抑制剂	免疫机制	阿昔单抗、替罗非班、依替巴肽、噻氯匹定、西洛他唑、氯吡格雷、阿司匹林、曲克芦丁等
中药制剂	机制不详	鱼腥草注射液、穿琥宁注射剂、苍耳子、复方丹参片、六神丸、牛黄解毒片等
雌激素	机制不详	己烯雌酚
疫苗	机制不详	百日咳疫苗、狂犬病疫苗、流感疫苗、乙肝疫苗、乙型脑炎疫苗、破伤风类毒素、脊髓灰质炎糖丸等
其他药物	机制不详	氯磺丙脲、格列本脲、呋塞米、氯噻嗪、地高辛、洋地黄毒苷、地西泮、雷尼替丁、维拉帕米、甲硝唑、氯丙嗪、乙胺嘧啶、辛伐他汀、阿托伐他汀、卡托普利等，奎尼丁

等级	出血类型
1级	（1）瘀点、瘀斑、稀疏、分散分布；（2）口咽、鼻出血持续<30 min
2级	（1）消化道、呼吸道、肌肉骨骼或软组织出血，未引起血流动力学紊乱，在24 h内不需要输注红细胞；（2）鼻或口咽出血持续>30 min；（3）有症状的口腔黏膜血疱；（4）弥散分布的瘀点或瘀斑；（5）血尿；（6）侵入性或手术部位异常渗血；（7）非月经期的阴道出血；（8）浆膜腔出血；（9）视网膜出血
3级	（1）需要红细胞输注的出血（尤其是发生在24 h内），但未出现血流动力学紊乱；（2）严重的浆膜腔出血；（3）CT发现的无症状性颅内出血
4级	（1）视网膜出血和视野缺损；（2）有症状性非致命性脑出血；（3）有血流动力学紊乱（低血压，收缩压或舒张压降低>30 mmHg）的出血；（4）任何原因引起的致命性出血

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Chinese expert consensus on the clinical diagnosis and treatment of sepsis induced thrombocytopenia

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