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腰椎穿刺检查

时间:2023-03-19 理论教育 版权反馈
【摘要】:2.临床有明显颅内压增高,特别是怀疑有占位性病变者,如视盘水肿、颅骨X线片或CT检查提示颅内占位并有颅内压增高,腰穿可能诱导脑疝发生者,且具有颅脑手术条件的情况下,确实因诊断需要,可慎重进行。8.术毕 最好嘱患者俯卧,或去枕平卧6h左右,以免脑脊液从硬脊膜穿刺孔漏入硬膜外,造成低颅压,引起腰穿后头痛。如脑脊液为红色或粉红色,可用三管试验法予以鉴别。

(一)适应证

1.了解脑脊液成分和压力,进行诊断及鉴别诊断。

2.鉴别脑震荡、脑挫裂伤,有蛛网膜下腔出血者而CT还不能证实的诊断、减压和引流治疗。

3.出血性脑血管病与缺血性血管病的诊断和鉴别诊断,以利于拟定治疗方案。

4.诊断脊髓疾病,进行脑脊液动力学检测,确定有无椎管内蛛网膜下隙梗阻及梗阻程度,还能用于鉴别与多发神经根病变的鉴别诊断。

5.椎管内注射药物。

6.开颅术后了解颅内压动态变化及有无出血和感染,或者放脑脊液减压。

7.造影检查:如脊髓造影、气脑造影和核素脑池扫描等。

8.中枢神经系统炎症病变、脑肿瘤、中枢神经系统血管性病变、脑挫裂伤及转移瘤的诊断和鉴别诊断。

9.某些原因不明的昏迷、抽搐等疾病的鉴别诊断。

(二)禁忌证

1.凡是有脑疝征象者(双侧瞳孔不等大、呼吸抑制、去大脑强直等),属于绝对禁忌证。

2.临床有明显颅内压增高,特别是怀疑有占位性病变者,如视盘水肿、颅骨X线片或CT检查提示颅内占位并有颅内压增高,腰穿可能诱导脑疝发生者,且具有颅脑手术条件的情况下,确实因诊断需要,可慎重进行。

3.腰穿穿刺部位有皮肤和软组织感染者,腰穿易将感染带入椎管内甚至颅内,可行枕大池(C1~2侧方)穿刺术。

4.开放性颅脑损伤或颅底骨折有脑脊液漏者,以免增加逆行感染机会。

5.穿刺部位有腰椎畸形或骨质破坏者。

6.严重全身感染(败血症)、休克、呼吸循环衰竭、躁动不安者,均不宜腰穿。

7.高颈段脊髓压迫性病变、脊髓功能障碍者,腰穿易导致病情恶化,甚至呼吸骤停。

8.怀疑有颅后窝血肿、肿瘤者。

9.血液系统疾病,有出血倾向者,使用肝素等药物抗凝或血小板<50 000/m3者。

10.未做神经系统检查,特别是未行眼底检查者,暂不宜做腰穿。

(三)技术要领及方法

1.体位 穿刺成功与否,体位正确非常重要。一般采取去枕侧卧位,床应平直,躯干与床面垂直,头部向胸前尽量俯屈,膝关节尽量向腹部屈曲,使脊柱弯成弓形,椎间隙增大到最大限度,充分暴露L3~4及L4~5间隙(双侧髂棘最高点连线与背正中线的交点相当于L4棘突)。

2.消毒 消毒前确定好穿刺点。严格无菌操作技术,腰穿包必须经高压消毒后再用,术者戴上无菌手套,局部用碘酊、乙醇消毒皮肤,消毒半径为穿刺点周围15cm,铺无菌巾。

3.穿刺点的确定 摆好体位,先触摸清楚穿刺的椎间隙,一般取L3~4或L4~5间隙为穿刺点。

4.麻醉 2%利多卡因局部浸润麻醉(或用1%~2%普鲁卡因,需要皮试),在该椎间隙正中作一皮丘,然后垂直穿刺,浸润皮下及深部组织,注射麻醉药物的同时,还可探明椎间隙的走行方向。

5.进针 术者左手拇指尖压紧穿刺椎间隙一端皮肤,固定皮肤,右手持7号或9号腰穿针,于椎间隙正中垂直进针,并稍向头侧倾斜进行穿刺,成人进针深度一般为5~7cm,当针尖突破黄韧带和硬脊膜时,均有落空感,即进入蛛网膜下隙,缓慢拔出针芯,可见脑脊液流出,穿刺成功;若无脑脊液流出,可适当调整穿刺针方向和深浅。

6.测压及放液 嘱患者缓慢伸腿致半屈位,头稍伸直,接测压表或测压管,然后测初压。如果压力高,避免诱发脑疝,不放脑脊液,将针芯拔出,将测压管内的脑脊液收集送脑脊液常规生化即可,若压力不高,可缓慢释放需要量的脑脊液,然后测末压。收集标本时脑脊液流速不宜过快,以每分钟3滴为宜缓慢释放,量一般不超过10~20ml。

7.拔针 将未污染的针芯插入,拔出穿刺针,亦可直接拔出穿刺针,穿刺点用碘酊消毒,无菌敷料覆盖。

8.术毕 最好嘱患者俯卧,或去枕平卧6h左右,以免脑脊液从硬脊膜穿刺孔漏入硬膜外,造成低颅压,引起腰穿后头痛。

(四)腰穿失败的原因

1.穿刺方向不当、歪斜、太浅或太深。

2.穿刺针选择不合适,成年人用细针,患儿用粗针容易失败。

3.病人过分紧张,乱动可使椎间隙变小。

4.脊柱侧弯畸形,病人过度肥胖。

(五)腰穿并发症

1.腰穿后头痛 最为常见,发生机制通常是脑脊液释放过多,造成低颅压,牵拉三叉神经感觉支支配的脑膜及血管组织所致,大多出现在穿刺后24h,可持续5~8d,头痛以前额和后枕部为著,跳痛或胀痛多见,还可伴颈部和后背部疼痛,咳嗽、打喷嚏或站立时症状加重,严重者还可伴有恶心、呕吐和耳鸣。平卧时症状缓解,应嘱患者大量饮水,必要时可静脉输入生理盐水。

2.出血 大多为损伤蛛网膜或硬脊膜血管所致,出血量通常很少,而且一般不引起明显的临床症状,如果出血量很多时应与蛛网膜下腔出血相鉴别。

3.感染 较少见,如消毒不彻底,或者无菌操作不当,或者局部有感染灶等,可能导致腰穿后感染。

4.脑疝 是腰穿最危险的并发症,易发生于颅内压增高患者,如果颅内压增高患者一定要进行腰穿才能明确诊断,一定要在腰穿前先用脱水药或完善术前准备。

(六)脑脊液压力及动力学检查

1.压力 侧卧位穿刺的正常压力成年人为80~180mmH2O,儿童为50~100mmH2O。超过200mmH2O时提示颅内压增高,低于80mmH2O则为低颅压。为了解椎管是否通畅及通畅程度,常需进一步行压腹试验、压颈试验。

2.压腹试验 压腹时,腹腔深静脉脊髓腔静脉丛受压,引起脊髓脑脊液压力上升,去除压力后,恢复原有水平。具体方法是:用手掌或拳头压迫腹部时,可见脑脊液压力迅速上升,一般约增高1倍;压迫去除后(放手后)压力迅速下降。15~20s恢复致正常水平。如穿刺针未在蛛网膜下隙,不通畅或椎管内完全梗阻,则压腹时压力不升。

3.压颈试验(Queckenstedt test) 当压迫颈静脉时,阻断颅内静脉回流,引起颅内压骤然升高,其压力必然通过脑脊液迅速反应在连接的腰穿测压管或测压表上,正常颅压时亦见相应升高,解除压迫后压力随之下降,借此可帮助了解脑和脊髓蛛网膜下隙是否通畅,颅内静脉窦是否阻塞。

具体操作方法:①手压法:腰穿成功后,接测压管或测压表,然后助手用双手压迫颈静脉10s,记录压力上升情况,解压后10s,再记录压力下降情况。测试侧窦是否梗阻,可先后压迫一侧颈静脉,观察上述压力变化,并将双侧进行比较。②颈部压力表气囊法:用一血压气囊缠于病人颈部,安上血压表,术者腰穿完成后,测定初压,先行压腹试验,确定腰穿针位于蛛网膜下隙,在迅速充气至20mmHg,5s记录上升压力一次,直到压力不能在上升为止,然后迅速放气,除去压颈,5s记录一次压力,直到不能下降为止,随后在分别用同法将血压计气囊充气到40mmHg及60mmHg,测定脑脊液压力变化。以时间为横坐标,压力变化数值为纵坐标,描记出压力-时间曲线。

压颈压力-时间曲线分析:①蛛网膜下隙无阻塞时,脑脊液压力在15s左右上升至最高点,减压后15s左右降至初压水平,加压至60mmHg可使颅内压升高至500mmH2O左右;②蛛网膜下隙部分阻塞时,颈部加压后脑脊液压力上升及下降均较为缓慢,或上升迅速而下降缓慢,或减压后压力不能降至初压水平;③蛛网膜下隙完全阻塞时,颈部加压后脑脊液压力不上升,甚至加压至60mmHg仍不上升;④当一侧乙状窦血栓形成时,压迫病灶侧颈静脉,脑脊液压力可不上升,压迫健侧颈静脉则脑脊液压力上升正常;⑤腰椎椎管内肿瘤时,压腹试验可不上升或上升很慢,甚至为“干性”穿刺。

(七)脑脊液检查

1.脑脊液常规

(1)性状:正常脑脊液是无色透明的液体。当脑脊液红细胞数<360/m3时,外观可无明显改变;当红细胞>1 000/m3时为肉眼血性脑脊液。如脑脊液为红色或粉红色,可用三管试验法予以鉴别。具体方法是:用3根试管连续接取脑脊液,前后各管为均匀一致的红色为新鲜出血,可见于蛛网膜下腔出血,前后各管颜色依次变淡,为穿刺道损伤。血性脑脊液离心后颜色变为无色,可能为新鲜出血或穿刺道副损伤;若变为黄色,提示为陈旧性出血;若为烟雾状,通常是细菌感染引起的细胞数增多,见于各种化脓性脑膜炎,严重者可为米汤状;放置后有纤维蛋白膜形成,见于结核性脑膜炎,该现象称为蛛网样凝固(cobweb-like coagulation);脑脊液呈黄色,离体后不久自动凝固为胶冻样,称为弗洛因综合征(Frion syndrome),是因为脑脊液蛋白质过多所致,常见于椎管梗阻。

(2)细胞数:正常脑脊液细胞数为(0~5)×106/L,多为单核细胞。白细胞增多见于脑脊髓炎或脑实质炎性病变,涂片检查如发现致病菌(细菌、真菌)及脱落的瘤细胞等,有助于病因诊断。

(3)潘氏试验(Pandy test):是一种脑脊液蛋白定性试验方法。利用脑脊液中球蛋白能和饱和石炭酸结合形成不溶性蛋白盐的原理,球蛋白含量越高反应反而越明显,通常作为蛋白定性的参考试验,可出现假阳性反应。

2.脑脊液生化检查

(1)蛋白:正常人(腰穿)脑脊液蛋白含量为0.15~0.45g/L,脑池液位0.1~0.25g/L,脑室液为0.05~0.15g/L,蛋白质增高见于中枢神经系统感染、脑肿瘤、脑出血、脊髓压迫症、吉兰-巴雷综合征、糖尿病性神经根神经病、黏液性水肿及全身感染等;蛋白降低见于腰穿或硬膜损伤脑脊液丢失,身体极度虚弱和营养不良者。

(2)糖:脑脊液糖含量取决于血糖水平,正常值为2.5~4.4mmol/L,为血糖的50%~70%。通常脑脊液糖低于2.25mmol/L为异常,见于化脓性脑膜炎,轻至中度减少见于结核性或真菌性脑膜炎(特别是隐球菌性脑膜炎)以及脑膜癌病;糖含量增高见于糖尿病。

(3)氯化物:正常脑脊液含氯化物120~130mmol/L,较血氯水平高,细菌性或真菌性脑膜炎均可使氯化物含量降低,尤其以结核性脑膜炎最为明显,氯化物降低还可见于全身性疾病引起的电解质紊乱等。

3.特殊检查 其他较为特殊的检查包括细胞学检查、蛋白电泳、免疫球蛋白、寡克隆区带、酶、病毒学检测、囊虫特异性抗体检测、抗酸染色、墨汁染色、细菌及真菌培养等,外伤合并颅内感染,抗酸染色、墨汁染色、细菌及真菌培养往往是常用的脑脊液检查,明确感染原因,以利于对症下药。

(吴国材 李明荣 杨 慧  陈 鹏 张世彬 张 弦 高伯元 张礼均)

参考文献

[1] Williams BR,Lazic SE,Ogilvie RD.Polysomnographic and quantitative EEG analysis of subjects with long-term insomnia complaints associated with mild traumatic brain injury.Clin Neurophysiol,2008,119:(2):429-438.

[2] Korngut L,Young GB,Lee DH,et al.Irreversible brain injury following status epilepticus.Epilepsy Behav,2007,11(2):235-240.

[3] Hebb MO,McArthur DL,Alger J,et al.Impaired percent alpha variability on continuous electroencephalography is associated with thalamic injury and predicts poor long-term outcome after human traumatic brain injury.J Neurotrauma,2007,24(4):579-590.

[4] Fossi S,Amantini A,Grippo A,et al.Continuous EEG-SEP monitoring of severely brain injured patients in NICU:methods and feasibility.Neurophysiol Clin,2006,36(4):195-205.

[5] Dan W,Tang W.Clinical study and electroencephalogram(EEG)monitoring of early post-traumatic seizures on acute moderate and severe head injuries.Chin J Clin Rehab,2003,7(2):300-301.

[6] Kroppenstedt S-N,Sakowitz OW,Thomale U-W,et al.Influence of norepinephrine and dopamine on cortical perfusion,EEG activity,extracellular glutamate,and brain edema in rats after controlled cortical impact injury J Neurotrauma,2002,19(11):1421-1432.

[7] Pointinger H,Sarahrudi K,Poeschl G,et al.Electroencephalography in primary diagnosis of mild head trauma.Brain Inj,2002,16(9):799-805.

[8] Vespa PM,Boscardin WJ,Hovda DA,et al.Early and persistent impaired percent alpha variability on continuous electroencephalography monitoring as predictive of poor outcome after traumatic brain injury.J Neurosurg,2002,97(1):84-92.

[9] Wallace BE,Wagner AK,Wagner EP,et al.A history and review of quantitative electroencephalography in traumaticbrain injury.J Head Trauma Rehabil,2001,16(2):165-190.

[10] Letizia M,Fabrizio PM,Assimo Zetal.Somatosensory and motor evoked potentials at different stages of recovery from severe traum atic brain injury.Arch PhysMed Rehabil,1999,80:33.

[11] 4Sibel OD,MufteA,Fusun GU,et al.Postacute predictors of functional and cognitive progress in traum atic brain injury:somatosensory evoked potentials Arch Phys Medrehabil,1999,80:252.

[12] Di Russo F,Aprile T,Spitoni G,et al.Impaired visual processing of contralesional stimuli in neglect patients:A visual-evoked potential study.Brain,2008,131(3):842-854.

[13] Kaplan PW Electrophysiological prognostication and brain injury from cardiac arrest.Semin Neurol,2006,26(4):403-412.

[14] Guérit J-M.Evoked potentials in severe brain injury.Prog Brain Res,2005,150:415-426.

[15] Schalamon J,Singer G,Kurschel S,et al.Somatosensory evoked potentials in children with severe head trauma.Eur J Pediatr,2005,164(7):417-420.

[16] Amantini A,Grippo A,Fossi S,et al.Prediction of‘awakening’and outcome in prolonged acute coma from severe traumatic brain injury:Evidence for validity of short latency SEPs.Clin Neurophysiol,2005,116(1):229-235.

[17] Schalow G.Surface EMG-and coordination dynamics measurements-assited cerebellar diagnosis in a patient with cerebellar injury.Electromyogr.Clin Neurophysiol,2006,46(6):371-384.

[18] Schalow G,Jaigma P.Improvement after severe traumatic brain injury induced by coordination dynamics therapy:Comparison with physiologic CNS development.Electromyogr Clin Neurophysiol,2006,46(4):195-209.

[19] Cosan TE,Adapinar B,Cakli H,et al.Peripheral seventh nerve palsy due to transorbital intracranial penetrating pontine injury.Eur Arch Oto-Rhino-Laryngol,2006,263(4):327-330.

[20] Zhang F-S,Yan C-X,Zhang W-B,et al.Evaluation on brain functional and prognosis of patients with diffuse axonal injury by neurophysiology examination.J Clin Rehab,2004,8(7):1222-1223.

[21] Mayer NH.Choosing Upper Limb Muscles for Focal Intervention after Traumatic Brain Injury.J Head Trauma Rehabil,2004,19(2):119-142.

[22] Hamalainen M,Hari R.Magnetoencephalographic characterization of dynamic brain activation:Basic principles and methods of data collection and source analysis,in Mazziotta J(ed):Brain Mapping:The methods.London,Elsevier,2002,227-253.

[23] Murakami S,Zhang T,Hirose A,et al.Physiological origins of evoked magnetic fields and extracellular field potentials produced by guinea-pig CA3hippocampal slices.J Physiol,2002,544:237-251.

[24] Eliashiv DS,Elsas SM,Squires K,et al.Ictal magnetic source imaging as a localizing tool in partial epilepsy.Neurology,2002,59:1600-1610.

[25] Stefan H,Scheler G,Hummel C,et al.Magnetoencephalography(MEG)predicts focal epileptogenicity in cavernomas.J Neurol Neurosurg Psychiatry,2004,75(9):1309-1313.

[26] Assaf BA,Karkar KM,Laxer KD,et al.Magnetoencephalography source localization and surgical outcome in temporal lobe epilepsy.Clin Neurophysiol,2004,115:2066-2076.

[27] Jannin P,Morandi X,Fleig OJ,et al.Intergration of sulcal and functional information for multimodal neuronavigation.J Neurosurg,2002,96:713-723.

[28] Firsching R,Bondar I,Heinze HJ,et al.Practicability of Magnetoencephalography-guided neuronavigation.Neurosurg Rev,2002,25:73-78.

[29] Bittar RG,Oliver A,Sadikt AF,et al.Localization of somatosensory function by using positron emission tomography scanning:A comparison with intraoperative cortical stimulation.J Neurosurg,1999,90:478-483.

[30] Lehericy S,Duffay H,Cornu P,et al.Correspondence between functional magnetic resonance imaging somatotopy and individual brain anatomy of the central region:Comparison with intraoperative stimulation in patients with brain tumors.J Neurosurg,2000,92:589-598.

[31] Makela JP,Kirveskari E,Seppa M,et al.Three-dimensional integration of brain anatomy and function to facilitate intraoperative navigation around the sensorimotor strip.Hum Brain Mapp,2001,12:180-193.

[32] Duffay H.Lessons from brain mapping in surgery for low-grade glioma:Insights into associates between tumor and brain plasticity.Lancet Neurol,2005,4:476-485.

[33] Towle VL,Khorasani L,Uftring S,et al.Noninvasive identification of human central sulcus:A comparison of gyral morphology,functional MRI,dipole localization,and direct cortical mapping.Neuroimage,2003,19:684-697.

[34] Papanicolaou AC,Simos PG,Castillo EM,et al.Magnetoencephalography:A noninvisive alternative to the Wada procedure.J Neurosurg,2004,100:867-876.

[35] Szymanski MD,Perry DW,Cage NM,et al.Magnetic source imaging of late evoked field response to vowel:Toward an assesment of hemispheric dominance for language.J Neurosurg,2001,94:445-453.

[36] Lewine JD,Davis JT,Sloan JH,et al.Neuromagnetic assessment of pathophysiologic brain activity induced by minor head trauma.AmJ Neurordiol,1999,20(5):857-866.

[37] Bigler ED.Neuroimaging in pediatric traumatic head injury:diagnostic considerations and relationships to neurobehavioral outcome,.J HeadTrauna Rehabil,1999,1(4):406-423.

[38] Gatez M,Bemstein DM.The current status of electophysiologic procedures for the assessment of mild traumatic brain injury.J Head Trauma Rehabil.2001,16(4):386-405.

[39] Iwasaki M,Nakasato N,Kanno A,et al..Somatosensory evoked fields in comatose survivors after severe traumatic brain injury.Clin Neurophysiol,2001,112(1):205-211.

[40] Schiff ND,Ribary U,Moreno DR,et al.Resiaual cerebral activity and behavioural fragments can remain in the persistently vegetative brain,Brain,2002,125(pt6):1210-1234.

[41] Plum F,Schiff N,Ribary U,et al.Coordinated expression in chronicailly unconscious persons.Philos Trans R Soc Lond B Biol Sci,1998,353(1377):1929-1933.

[42] Jaffres P,Francony G,Bouzat P,et al.Use of transcranial doppler at the emergency room for head-injured patients.Reanimation,2007,16(7-8):665-672.

[43] Martin NA,patwardhan RV,Alexander MJ,et al.Characterization of cerebral hemodynamic phases following severe head trauma:hypoperfusion,hyperemia,and vasopasm[J].Neuroury,1997,87(1):9-19.

[44] Homar J,Abadal JMa,Llompart-Pou JA,et al.Cerebral hemodynamics in patients with traumatic brain injury evaluated by transcranial doppler and transcranial color coded sonography.A comparison study.Neurocirugia,2007,18(3):221-226.

[45] Ract C,Le Moigno S,Bruder N,et al.Transcranial Doppler ultrasound goal-directed therapy for the early management of severe traumatic brain injury.Intensive Care Med,2007,33(4):645-651.

[46] Scott W,Marc M,Robert A,et al.Transcranial Doppler ultrasound criteria for recanalization thrombolysis for minddle cerebral artery strok,2000,31:1128-1132.

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