2023年脑-肺冲突：重症急性脑损伤合并ARDS管理（全文）.docx

2023年脑肺冲突：重症急性脑损伤合并ARDS管理（全文）文献来源Review>CurrTreatOptionsNeurol.2022:24(9):383-408.doi:10.1007s11940-022-00726-3.Epub2022Aug10.Brain-LungCrosstalk:ManagementofConcomitantSevereAcuteBrainInjuryandAcuteRespiratoryDistressSyndromeNassimMatin1,KasraSarhadi1,CPatrickCrooks1,AbhyitVLele231VasishtSrinivasan4,NicholasJJohnson45,ChiaraRobba67,JamesATown85,SarahWahlster,123Affiliations+expandPMID:35965956PMCID:PMC9363869DOI:10.1007/sl1940-022-00726-3FreePMCarticle背景Fig.1Pathophysiologicalinteractionsbetweenthebrainandlungs图1脑与肺的病理生理交互作用在重症急性脑损伤(severeacutebraininjuryzSABI)中,脑-肺的病理生理交互作用非常复杂。SABI可通过多种途径诱发和加重ARDS,相反,ARDS的低氧血症和全身炎症反应可进一步加速继发性脑损伤。所以处理SABI和ARDS的策略可能存在冲突，而这篇文章的主要目的是回顾治疗SABI和ARDS的关键原则和证据，并根据现有的文献和临床实际考虑提供了处理的指导性意见。SABI患者机械通气目标SABl中需要机械通气是由于意识受损导致的呼吸驱动力下降或气道保护能力降低，或存在继发性呼吸相关事件出现，如吸入性肺炎、肺水肿等，以及患者需要深度镇静。但是SABl患者目前PaO2WPaCO2的最佳目标值是尚未确定的。对于Pao2目标，低氧血症和高氧血症被证明对SABI患者是有潜在危害的。2020年ESICM共识声明建议SABI患者的PaOZ目标为80-120mmHg,并严格避免低氧血症。理想情况下，目标应根据患者脑损伤的类型以及损伤程度来进行个体化选择。PaCO2是影响脑血流的重要因素之一。高碳酸血症可引起脑血管扩张导致ICP增加，通过治疗性过度通气快速降低PaCO2e然而，低碳酸血症可导致ICP峰值反弹，因此治疗性过度通气的使用仍然存在争议，应该是只考虑作为短期抢救的措施。对于大多数的SABI患者，应密切监测PaCO2并避免其剧烈波动。ARDS概述Table3.TheBerlinDefinitionofAcuteRespiratoryDistressSyndromeAcuteRespiratoryDistressSyndromeTimingWithin1weekofaknownclinicalinsultorneworworseningrespiratorysymptomsChestimaging3Bilateralopacitiesnotfullyexplainedbyeffusions,lobarlugcollapse,ornodulesOriginofedemaRespiratoryfailurenotfullyexplainedbycardiacfailureorfluidoverloadNeedobjectiveassessment(eg,echocardiography)toexcludehydrostaticedemaifnoriskfactorpresentOxygenationbMild2mmHg<Pao2F23mmHgwithPEEPorCPAP>5cmH2OcModerate100mmHg<Pao2ZFio2200mmHgwithPEEP5cmH2OSeverePao2ZFio2100mmHgwithPEEP5cmH2OAbbreviations:CPAP1continuouspositiveairwaypressure;Fio2,fractionofinspiredoxygen;Pao2.partialpressureofarterialoxygen;PEEP,positiveend-expiratorypressure.aChestradiographorcomputedtomographyscan.btfaltitudeishigherthan10OOm.thecorrectionfactorshouldbecallatedasfollows:(Pao2TFio2×(barometricpressure/7)J.cThismaybedelivefdnoninvasivelyinthemildacuterespiratorydistresssyndromegroup.2012年柏林定义根据低氧血症严重程度将ARDS分为三类(轻度：P/F比值201-300mmHg、中度：P/F101-200mmHg、重度：PF100mmHg,PEEP5cmH2O)z常见病因是肺炎、非肺脓毒症和胃内容物误吸占85%0合并ARDS患者的脑-肺冲突管理ARDS的标准治疗包括潜在病因治疗，肺保护性通气、高PEEP,神经肌肉阻滞剂、俯卧位、液体管理、皮质类固醇和ECMO,但是跟SABl患者的治疗策略存在一些潜在冲突。一、肺保护性通气(LPV)。小潮气量+PEEP优化来预防肺损伤，是ARDS的标准治疗。LPV下的允许性高碳酸血症可导致SABl患者的ICP升高；此外，对于PaO2>55mmHg的目标值可能不足以满足脑代谢需求，并会加重继发性脑损伤。因此在使用LPV时，需谨慎监测PaCO2,PaOz的目标应该更高(80-120mmHg)o二、呼气末正压（PEEP）。指南推荐中重度ARDS中采用高PEEP的作用是促进肺复张,改善氧合。在SABI患者中，PEEP可增加胸腔和右心房的压力而引起ICP增加，但是多项研究发现，增加PEEP治疗ARDS是合理的，但应根据肺顺应性滴定PEEP,并严格维持MAP水平。三、俯卧位通气。PROSEVA试验证明当氧合15OmmHg的患者，俯卧位时间16h,绝对死亡率降低17%;但是在SABI患者中，PP对于ICP.CPP和神经预后的影响尚不完全清楚，但在大多数研究中，PP对氧合和血流动力学的益处似乎大于ICP的短暂升高。四、神经肌肉阻滞剂的使用。ARDS患者通常需要深度镇静或神经肌肉阻滞剂，以促进人机同步和降低全身的氧耗。对于SABl患者来说，深度镇静可能会带来低血压或低心排，影响脑灌注压，因此建议首选短效药物（如丙泊酚）进行间歇性神经学评估。五、吸入性肺血管扩张剂。虽然已被证明是可改善氧合和降低肺动脉压，但是尚未被证实对ARDS的生存获益，因此不常规推荐用于ARDS治疗，而是选择性作为真正难治性低氧血症或特定人群中的一种补充方式。六、体外膜肺氧合（ECMO）。ECMO为严重心肺衰竭患者提供循环支持和气体交换，是严重ARDS患者地有效抢救治疗手段。但在高度选择患者时，应首先考虑其神经功能预后。七、液体和血流动力学管理。对于合并ARDS的患者，不断以多模式监测和评估循环容量状态制定个体化液体管理策略，以正常血管内容量为目标。八、糖皮质激素应用：对于皮质类固醇尚未被证明对SABl有效，甚至可能是有害的。目前尚需要更多的数据来确定激素对各种ARDS和SABI亚型的总体获益或危害。TBlr ICF EDM. SDH. contusion hydrocephaiu vas09enk. and cy<o<ox>c edew impaired autocegulatk>nEdmawithin A9*bsd BP Urgets IHfl： 7dft>SBP i 1 mmHg for age 503 SBP 工Bimodal dtruticn 110 mmH9 Ior a9e 15-49 or > 70Early (< 72 h): peak atda/4largeRCT (MRC CRASH) 48h methylprednisolone infusion ! in death at 2 weeks and 6 months.Etiology of increased mortality remains UnCZrMemdnaIySiS of RCTsaIso showed T in modality (driven by large number of patients in MRC CRASH)ICrbrl prfusion tmpa<ed MJtOCcguldtkxx BCVlLau(> 72 h)： peak at day 7Blossoming of contusions majority within 24-48 h mot within < 7dCPP60-70 mmHg. ICP < ZO mmHgAvoid hypovolemiaBTF9uMlifs do not recommend high-dose steroids due to harm!ICP: mass CfIeet from SAH1PH, hydrocephalus, ischemic infarcts cylo<ooDC edem< retraction ede<na after dippingRb¼din94% day 1 then 1-2%perday u(i aneurysm securedlCrbral prfuslon: vasospasm. DCI Acute hydrocephalus distal mkothfombi. neurogenic first 3 days (subacute 4- CafdiomyO(Xathy and card>gef)ic14 <1 late > 2 weeks)SbockCSWUnsecuredvascular lesion dvod extreme HTN to prevent re rupture. maintain CPP. ideal qcmI not established, consider p<e morbid basdtne BP, guidelines suggest S8P 90A < 160 mmH9Scurd vascular IMiOn: duhng Ibe vasospasm period, avoid hypotension PermISSAe HTN. consider BP augmentation case by case maiuin strict intravascular euvolemiaTwosystematic reviews and fneU*nlyes 1S4 IiZ): limited W hefogecity. overall inc<iusivc I in natnures Cnd hypovoletnia. Trend towards I in symptomatic vasospasm overall no significant cha9e in neurological outcomesPre-admission use: T EoaaiityVMoSPMm3 21 dy PeAk 5 7-10. only < 5% after day 14NCSguidelines ne t recommended (lack of evidence、nd harm in other SAB4 and SCI trials)1ICF: »CH expansion intra pefihemstoml (vas09eic > cytotxk) edema. hydrocepliA (IVK extewi ventricular dtstoion)Edmat within 24 h.PMk days 2T decreases > day 7Second peak cn occur days 10-14 (often coupled with I in Na)Exacttar9et unckr, avoid Cxtrrfne HTN end large BP drops, consider pre-morbid BP and rerul failureUpper BP Kmit < 140-180 mmHgPoOlCd.zlysc showed no difference in mort4ftty or neurological OUtCOE. but higher dvme effect rate, one RCT terminated early due to【Kfectbra HifiJPre admission use: I )rulityICrbrl prfusion VdSCUur compression by ICHAHA9uiddins not recommended due to Iddc o( evidence of Mfkacy nd risk of adverse events1KP: CytOtOXk > VaSO9enic CdemA (malignant MCA)I hydrocephalus (vetfacuM compression), hemorrhagic uans4ofmation. repeduson ifryd<naf w<tm 24 h. peak days J-5. decreases > &y 7 (younger patents tend to swell eader than Cwef PatientS)BPgoals: ideal 90ab unknown and very C4se-by Ge, consider presence, degree nd chron>y of OCdUSiOnSk StenaSeSl coHa<eral2a<ion and reonaiizatk>n status, bemoagk CofWerSion and reperfusionMetaanatyse (8 RCTs of Cortkost erods within 48 h) showed no difference in rxxt3iity or neurological outcome, inconsistent results between tria*s, SmM numbers a GS 155JPre-AdfTMsston use: f morulity1Ccbrlrfusion: LVO. cervical SIenoSis/0CdUSk>r KudaaM ather。SCleroSk dissectionHm0ra9kAvoidhypotension after acute stroke, msted AHA gudHn 他 recommended due to tack oftransformation 2-permissive HTN. No evidence in favor ofevidence of efficacy aM potential complications14 ctoy mostly within induced HTN1 CJn consider CMe by eASe 7 days (more common inIar9er inUrcts)PeHusIondpn<hnc Rost M < 185/110 mmHg, pos< MT < ISO 241>-7 daysmmH or< UO mmHg if successfulreperfusion Qr h(tnorrhagk traslOrTnMi0。 Volume StAtUs avoid -QravascuUc hypovolemiaPCA 11CP Vasogenk and cytotoxic edew Ed<na within 24 KBP goals: AVoid hypotension:Vsopressin epinephrine and me<hy>redntwloncBIpeak days 2-5. decreasedduring CPR and stress dose hydrocortisone for*ys7-10S8P >90 mmHg. MAP >6S mmHgport rwuitotic>n shock npfowd su<v*l Iodecharge with tavoab*e neurologkal outcome compared to epephrine alone (1591Crbcal prfuslo<r shock, decreased cardic output, right shifted or narrow cerebral ut0re9uUti0r mkrovascuUr dysfunction Vdmient hyperemia delayed hypoperfusionIRk of herniation Volume status based on presence and type during rew4rmiog from of shock therapeutic hypothermiaBrain tiuue hypoxia nadirM 13-40 h post arrestMethylpfedntsoloneand vatoprein during CPR 1 ROSG o change in survival and neur009ic4l outcome 116Q)Systematicreview: no benefit foe corticosteroids ak>ne Ufil lfi2图2SABI亚型的具体注意事项总结Dragimagetoreposition.DoubleCIkktomagnifyfurther.图3SABI中ARDS管理原则的冲突。红框：潜在冲突，绿框：管理策略图4SABI合并ARDS的治疗流程ARDS在SABI中很常见，与较高的死亡率和较差神经系统预后相关。ARDS和SABl的管理策略可能会发生冲突。SABl合并ARDS的治疗需要特别注意氧合和通气、血流动力学和容量状态、体温管理和神经系统检查。