上海年会专题：围术期严重肺栓塞的诊断和抢救治疗

xyz-cn99

童传耀1
美国北卡路来那州威克森林大学医学院

Objective:
After attending this case, the participants will be able to:
1. Understand the circulatory changes associated with intraoperative acute massive pulmonary embolism.
2. Learn the diagnosis modalities for intraoperative pulmonary embolism.
3. Understand the optimal hemodynamic management, the vasopressors and fluids to maximize the survival possibility.
4. Discuss other treatment options and prevention strategy.
Stem Case:
A 77 years old white female fell 3 days ago and was scheduled for left humeral open reduction and internal fixation (ORIF) and left hip replacement.
PMH: hypertension, type 2 diabetes, hyperlipidemia, hypothyroidism.
SH: living with dementia husband, active and golfing regularly. Nonsmoker.
PE (in ER): BP126/63, HR67, RR22, T95.3, SaO298% in room air.
X-ray remarks: 1) complex humeral head and neck fracture with anterior displacement, and 2) mild displaced left femoral neck fracture.
Labs: HH 13.4/38.9, Platelet 309; electrolytes were normal, Glucose 194. EKG: SR 80, borderline LAD (left axis deviation). Stress echocardiogram was negative in 1997.
Disposition: the patient was admitted to orthopedic floor, continuing her chronic medications, and heparin 5000 u was started, sc bid.
On the day of surgery, a left interscalene brachial plexus catheter and a lumbar plexus block were performed with total of 0.5% bupivacaine 55 ml for postoperative analgesia. General anesthesia was induced by iv propofol (100 mg), fentanyl (150 mcg), and rocuronium (50 mg). The patient’s intubation (7.0 ETT) was confirmed by ETCO2 and equal bilateral breath sounds, and maintained with 0.5% isoflurane in O2/air. Shortly after induction, her blood pressure was trending down to 80/45 mmHg, no changes in heart rate and SaO2, which responded to ephedrine (10 mg) and phenylephrine (120 mcg), then iv hetastarch 500 ml was started.
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Is this common in elderly patient?
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What could be the differential diagnosis?
As planned preoperatively, a 2nd iv and a radial arterial line were placed, the patient was moved from stretcher to OR table, turned to right lateral position (20 min later). Arterial BP was again decreased to 75/40 mmHg with HR 95. This time, it did not respond to ephedrine (35 mg) and phenylephrine (600 mcg). The resident was watching the vital signs, noticed SaO2 was 80% with an ill looking ETCO2 waveform (22-27 mmHg). Immediately gave epinephrine (100 mcg, iv) and started hand bagging with 100% O2…
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What would be the differential diagnosis again?
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Which therapy should be initiated?
Breath sounds and ETT position were re-checked, a chest x-ray ordered immediately, and TEE called. Meanwhile, the patient was turned to a supine position and started neophenylephrine and epinephrine infusion, with both iv fluids wide open. MAP was kept >60 mmHg so as SaO2>90%, but no improvement of ETCO2 waveform.
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What would be the findings from TEE?
TEE showed a significant dilated right atrium and ventricle with decreased contractility (sluggish or hypokinesia), a rather small LV chamber with good contractility (EF 55%), and deviated sepetal wall towards left, moderate to severe tricuspid regurgitation and evident a frail mitral valve prolapsed. Surprisingly, a patent PFO with left to right shunting was found. There was an estimated pulmonary hypertension (~55 mmHg), but no visible clot.
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Do you consider the TEE findings supportive for the diagnosis of PE?
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Was this also possible of acute right heart infarction?
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If TEE were not available, how could ABG, CXR, EKG, PAC, and CVP help for diagnosis?
In next 75 min of continuing resuscitation, the patient’s condition was relatively stabilized, with PaO2>110 mmHg and MAP in range of 70-85 mmHg. Troponin was negative in 2 measurements. EKG later showed junctional tachyarrhythmia (110/min), low voltage QRS (suggesting new pulmonary disease), and new abnormality of nonspecific ST and T changes. At this point, a diagnosis of pulmonary embolism (PE) was made, the original surgery was canceled and the patient was transported to ICU for continue resuscitation and treatments...
Discussion:
1.Risk factors for PE and the differential diagnosis for hypoxia: Bone fracture and bed resting is the most common cause of deep venous thrombosis (DVT) formation in the low extremities, which has a potential risk of PE when the clot dislodged. The differential diagnosis includes fat embolism syndrome (FES) which is manifested by continues release fatty tissue causing pulmonary vasculature inflammatory responses. Others included pneumothorax, tension pneumothorax from multi-rib fracture or interscalene block, pulmonary contusion, endobronchial intubation, anaphylactic reaction to drugs or latex. All of these could cause sudden unstable hemodynamic and hypoxia, and should be rapidly ruled out for effective management.
2.The value of TEE in diagnosis and treatment of PE: a massive PE causes the right ventricle outflow obstruction by its mass and/or inflammatory reaction, results in severe decrease of preload and afterload (hypotension and left heart failure), severe pulmonary hypertension and right ventricle failure, and compromising coronary perfusion; these changes could be instantly characteristically revealed by TEE as dilated right ventricle with impaired contractility and small left chamber volume with preserved function initially. In addition, it may show some unknown preexisting cardiac anomaly, as the finding of a patent PFO with right to left shunt in this patient. The presence of visible clot in the pulmonary arterial confirms the PE diagnosis immediately. TEE is helpful in guiding resuscitation and providing immediately feedbacks concerning the treatments.
3.ACLS (Advance Cardiac Life Support) for managing cardiovascular collapse: When encountered such a scenario, the first is checking the airway to ensure a patent airway (intubation and ventilation with 100% oxygen). The administration of inotropics and volume are aimed to rapidly restore the patient’s cardiovascular function. Two-thirds of the mortality following massive PE occurs within one hour of the onset of hemodynamic instability. Generally, there is no rule regarding the dose range (mcg to mg), drug choice (ephedrine, phenylephrine, epinephrine, or norepinephrine), rather how faster and effectively bring the MAP back to baseline. There is no evidence of the value of steroid (dexamethasone). CPR should be initiated if no response to inotropics in 3-5 min or the presence of PEA (puleless electrical activity). Defibrillation should be delivered immediately if presence of ventricle tachycardia or fibrillation.
4.Prevention and treatment options: the stabilization and fixation of long bone fractures should take place within 72 hrs, the patient should be resuming ambulation early, starting anticoagulation(subcutaneous heparin or lovenox), placing low extremity compression cuff or/and the inferior vena cava filter; all these measures have been shown some effectiveness in decreasing DVT. The definitive emergency treatment is aimed to remove the clot and restore the cardiovascular stability. Medically, thrombolytic therapy is started with administration of thromboplastin activator (tPA) in adjunction with heparinization. Surgically, embolectomy is achieved by extracting the clot through thoracotomy or interventional radiological procedures. Numerous reports showed an immediate ECMO (extracorporeal membrane oxygenation) could be life saving and create an opportunity for definitive therapy.

lzdb00

楼主题可能要帮忙翻译一下

winnerxiao

是的，谢谢，的确是今年的主题，我们今年已经在围术期碰到两例了，真倒霉，都是骨科手术，其中一例还没做麻醉与手术前，在搬动病人体位发生的，最后抢救过来，入住icu后，最后还是挂了。

胜哥

:):):):):):):)

cbx1955

我英文不好,看起来很慢,那只能慢慢看啦

chexuehua1972

患者存在的房缺对当时的临床状况和处置有何影响呢

树上

恩，我实习的时候也遇到过一例，抢救了好长时间，送到icu，咱们的条件哪有TEE啊，只有依靠经验，我感觉老外处理的简单又得当。

zcyuan1958

干了15年临床麻醉，今年遇到一例剖宫产肺栓塞，症状比较典型，发现及时，抢救成功，现在想起都害怕。

adam01

哇，全是英文啊！！如何能够理解其精髓呢？？？

cbx1955

有的看不懂,下了慢慢看

zhangyougao

怎么不用中文版。

心超

1# xyz-cn99

祥子：这个病例要好好挖掘一下：

比如：

low voltage QRS (suggesting new pulmonary disease),

QRS 低电压 提示 新出现的肺部疾病？

肺性P波 和 QRS 低电压 哪个更有意义？

右房负荷过重。急性肺部实变性疾病、肺梗塞等可使右心室负荷过重间接引起右房负荷过重，常可见到肺型P波；各种原因使血液回流过快过多均可使右房负荷增加P波电压增高。如运动试验当心率达到110次/分左右时，部分人可出现肺型P波，输液过快也可出现肺型P波。


QRS波电压降低及意义：肢导联各导QRS电压算术和均＜0.5mV，即∑QRSI+II+III＜1.5mV，称肢导联低电压；胸导联各导QRS电压算术和均＜1.0mV（有用＜0.7mV）称胸导联低电压。V4-V6导联QRS电压低称左胸导联低电压。I、aVL、V5-V6导联QRS电压低称左侧导联低电压。
肢导联低电压或胸导联低电压的意义：
①部分见于正常人，特别肥胖者。
②四肢及胸壁皮肤水肿、胸腔积液、胸腔积气、心包积液或肺气肿时常见肢导联低电压。大量胸腔积液或积气时可表现出左胸或左侧导联显著低电压，QRS电压常＜0.5mV。
③心包炎、心肌炎、心肌梗死等。急性心肌炎及心肌梗死时出现明显低电压是预后不良的重要判断指标。
④其它：水电解质紊乱、心力衰竭也可导致低电压。
右胸导联R波递增不足、R波递减及其意义：V4导联呈Rs型时，RV3＜0.3mV，称右胸导联R波递增不足，但需除外顺钟向转位。当RV1＞RV2＞RV3时称右胸导联R波递减（逆递增）或R波丢失。
右胸导联R波递增不足或右胸导联R波递减，应考虑有无不典型的局限性陈旧性前间壁心肌梗死，如伴ST段抬高与有症状时，可能为急性不典型的局限性前间壁心肌梗死，别忘了复查心电图与跟踪心电图演变。右胸导联R波递增不足有时与电极放置位置有关，打图时发现此情况应及时确认电极放置是否正确。
左胸导联低电压伴胸导联R波递减或R波丢失意义：当左侧胸腔积液或积气时常见到此现象。其中左胸+V2V3导联显著低电压多为左侧胸腔大量积液。左胸或左侧导联低电压伴胸导联R波递减多见于左胸液气胸或单纯气胸。无明显左侧导联低电压，仅胸导联R波递减（RV3>RV4.RV5>RV6）多为悬垂位心。

zjgyms

晕，全英文。看不懂。有中文版下载吗？

Angel@天堂

{:2_42:}{:2_35:}收下了啦，谢谢

wudawu

全英文。看不懂。有中文版下载吗