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Elderly acute pulmonary thromboembolism initially presenting as syncope: a case report

(Department of Geriatrics, First Hospital, China Medical University, Shenyang 110001, China)

Case presentation

Yao, 80-year-old female, was admitted to the hospital due to the reduplicated disturbance of consciousness. One day before admission, the patient suddenly collapsed and lost consciousness for approximately 1 minute after oral hypotensor and micturition, without tic, incontinence, or bite injury of tongue. She came to Emergency Depart-ment of our hospital after her consciousness recovered spontaneously, as she felt weakness, diaphoretic and short of breath. Electrocar-diogram (ECG) (emergency) and cardiac enzymes of serum were found normal. The patient refused to stay in Emergency Department for further observation before finishing intravenous nitrogly-cerine. The similar episode attacked 5 times after she went home.

Past medical history: the patient had hypertension and chest oppression for 30 years. The highest blood pressure was 17-180/80-90mmHg (1 mmHg = 0.133 kPa), and she is using Valsartan to keep blood pressure between 130-140/70-80mmHg. She also had phlebeur-ysma of lower extremities for about 50 years.

Physical examination: T, 35.8℃, HR, 72 beats/min, BP: 80/0 mmHg. The patient’s consciousness was clear, the face and palpehra coniunetiva was pale, with cold extremities syndromes. There were no obvious rales. The superficial veins of lower shanks were bulgy. An ECG (Figure 1) showed ST segment in lead V1-V3lower 0.05 mV. cTnI: 1.22mg/L. Initial diagnosis: acute non-ST elevated myocardial infarction Killip I, cardiac syncope.

Providing rescue therapy such as oxygen, dilatation, elevating blood pressure, anticoagulant (subcutaneous low-molecular-weight heparin 4000IU once a day, total 7 days), antiplatelet (oral asprin 100mg once a day, oral clopidogrel 75mg once a day), stabilizing plaque (statin), protecting gastric mucosa and anti-inflammatory,, the patient’s life signs were recovered gradually.

Figure 1 ECG on 23rdJun

Sinus rhythm, HR: 75beats/min, Axis:-26°, ST segment in lead V1-V3lower 0.05mV, T waves in lead Ⅱ, Ⅲ, AVF and V1-V3were inverted 0.1-0.3 mV

On the 12th day of hospitalization, the patient suddenly felt chest oppression, shortness of breath and pericardial discomfort when she changed position. BP: 63/34mmHg, and ECG indicated multifocal atrial tachycardia (the most fast heart rate was 160 beats/min). Arterial blood gas: PaO2: 61.1mmHg, PaCO2: 36.3mmHg, PH: 7.373; D-D:＞20mg/L; cTnI: 0.22ng/ml; CK: 82U/L, CK-MB: 26U/L, LDH: 1085U/L. It was considered to be acute pulmonary thromboembolism. Except for haemo-dynamic and respiratory support, the patient was asked to lie in bed, and anticoagulant was strengthened (oral warfarin 2.5mg once a day＋subcutaneous low-molecular- weight heparin 4000IU once a day). Seventeen days later, the administration of low-molecular-weight heparin was stopped, and warfarin was modulated by 0.125mg to keep INR between 1.6-2.4.

Thirty days after hospitalization, the patient’s condition was stable and auxiliary examinations were accomplished. Echocardiogram showed pulmonary arterial pressure elevated (60mmHg), echo of endocardium of left ventricular inferior wall enhanced, EF 57%. Color ultrasound of deep vein of both lower limbs showed plexus venosus leg muscle thrombosis. Pulmonary artery CT scan showed artery embolism of superior lobe, lobusmedius of right lung, and part branch arteries of superior lobe of left lung (Figure 2). Coronary artery CT showed no obvious abnormity in bilateral coronary arteries. Ventilation-perfusion scintigraphy was also performed: right pulmonary, developer of posterior segment of superior lobe and lobusmedius were deficient. Left pulmonary, developer of partial posterior segments of superior lobe apex, partial dorsal segments of inferior lobe, anterior basal segments were attenuated and filling-defect. Pulmonary blood ratio: left lung/total lung=59.10%, right lung/total lung=40.90% (Figure 3).

Figure 2 CTPA images on 29thJuly

A: Artery embolism of superior lobe, lobusmedius of left lung;B: part branch arteries of superior lobe of right lung

Figure 3 Ventilation-perfusion scintigraphy on 9thAug

Right pulmonary: developer of posterior segment of superior lobe and lobusmedius were deficiency. Left pulmonary: developer of partial posterior segments of superior lobe apex, partial dorsal segments of inferior lobe, anterior basal segments were attenuated and filling-defect. Pulmonary blood ratio: Left lung/Total lung=59.10%, Right lung/Total lung= 40.90%

Sixty days after hospitalization, an intravenous filter was placed in the inferior vena cava to prevent further pulmonary thrombosis.

Definite diagnosis: (1) acute pulmonary embolism; (2) phlebeurysma of lower extremities (hibateral); (3) post-intravenous filter plantation; (4) hypertension degree 3 (extremely high risk).

Clinical Discussion

In this case, acute pulmonary thromboembolism initially presented as syncope, but not common dyspnoea, tachyphoea, or chest pain. Emer-gency ECG showed moving down of ST segment instead of right axis deviation or typical change of SⅠQⅢTⅢ. In addition, cardiac troponins and cardiac enzymes in serum were slightly elevated, which mislead to be acute cardiac infraction. Moreover, hypoxemia and plasma D-dimer could also be the result of cardiac infraction which makes initial differential diagnosis more difficult. The diagnosis was defined by pulmonary artery CT scan, coronary artery CT and color ultrasound of deep vein of both lower limbs after hospitalization. Although the indication for permanent inferior vena cava filter is classⅢ for patients with peripheral type of deep vein thrombosis who are undergoing antigoagulation therapy[1], color Doppler indicated her thrombosis was fresh enough to drop at anytime, associated with the history of reduplicated syncope and shock, permanent inferior vena cava filter was chosen.

This patient initially presented as syncope. Syncope is common in the general population, especially in the elderly who are over 65 years. The incidence of syncope shows a sharp rise after the age of 70 years, from 5.7 events per 1000 person-years to 11.1 events. Syncope in the elderly have its own specificities. (1) In the elderly, syncope occurring in the morning favors orthostatic hypotensor. (2) One-third of individuals over 65 years are taking three or more prescribed medications, which may cause or contribute to syncope. Withdrawal of these medications may reduce recurrences of syncope. (3) Cognitive impairment is present in 5% of 65 years old and 20% of 80 years old. This may attenuate the patients’ memory of syncope and falls. So, when the elderly were suspected to be cognitive impairment, the Mini-Mental State Examination should be performed except evaluation of neurological and locomotor systems[2].

The most common causes of syncope in the elderly are orthostatic hypotension, reflex syncope (especially carotid sinus syncope), and cardiac syncope (such as arrhythmia, acute myocardiac infarction, pulmonary embolism). Moreover, different causes often co-exist in a patient. Though rigorous steps and methods for syncope were established, only 58% of syncope events’ causes can be determined[3]. The incidence of syncope is less than 20% in acute pulmonary thromboembolism; however, it cannot be ignored because it is the sign of illness getting worse. There are 3 possible mechanisms of syncope in the setting of pulmonary throm-boembolism. First, massive pulmonary thromboembolism can cause acute right ventricular failure, impaired left ventricular filling, tachycardia, hypotension, and result in the reduced cerebral perfusion. In some cases, this situation progresses to cardiac arrest. However, one must distinguish between 2 possible causes for systemic hypotension. The impaction of an embolus in a major pulmonary artery may elicit a Bezold-Jarisch type of reflex with hypotension and, perhaps, bradycardia and slow respiratory rate. This syncope is transient, lasting no more than 15 minutes after the onset of a massive pulmonary embolism. Prognosis during that period is difficult to evaluate because of the reflex hypotension and the tendency to spontaneous recovery. If hypotension persists, it is more likely to be the result of mechanical occlusion of pulmonary artery system which is an extremely prognosis sign. Second, pulmonary thromboembolism causes rapid or slow arrhythmias which results in hemodynamic instability, and might be due to reduction of cardiac diastolic function caused by pulmonary thromboembolism. Third, the pulmonary thromboembolism can trigger a vasovagal reflex and lead to syncope on a neurogenic basis[3].These three mechanisms can exist independently, and can also play a role together.

Pulmonary thromboembolism is a relatively common cardiovascular emergency. The death rates of acute pulmonary thromboembolism were as high as 7%-11%. The mean age of patients with acute pulmonary embolism is 62 years old, and the incidence increases exponentially with age and there is similar case for both idiopathic and secondary pulmonary thrombo-embolism. The patients with shock and hypotension are thought to be high-risk, as the in-hospital or 30-day mortality is over 15%[4]. The principle of treatment of acute pulmonary embolism is initially promising haemodynamic and respiratory support until it allows to choose thrombolysis, surgical pulmonary embolectomy, percutaneous catheter embolectomy and fragmentation. No matter what other therapy will be combined, anticoagulant should be used as soon as possible for highly suspected or diagnosed acute pulmonary thromboe-mbolism except for patients at high risk of bleeding or with severe renal dysfunction. Thrombolysis can significantly reduce death or recurrence of patients with high risk acute pulmonary thromboembolism. In patients with absolute contraindications to thrombolysis, surgical embolectomy is the second choice and catheter embolectomy or thrombus fragmentation is the following consideration, though the safety and efficacy of such interventions has not been adequately documented. Intravenous unfractionated heparin should be the preferred mode of initial anticoagulation in patients with acute pulmonary thromboembolism at high risk, as low molecular weight heparin and fondaparinux have not been tested in the setting of hypotension and shock. The patient with shock and hypotension in this case was at high risk, but safer low molecular weight heparin is better for her according to HAS-BLED risk scores: ＞65 years, hypertension, history with anticoagulation administration. Long-term follow-up is recommended to this patient for better management of chronic disease.

(Translator: JIN Bo)

以暈厥為首發(fā)癥狀的老年急性肺栓塞1例

1 病例摘要

姚某某, 女, 80歲, 因“反復(fù)發(fā)作意識障礙1天”入院, 入院前1天, 患者口服降壓藥并排尿后突發(fā)意識不清, 近1 min, 無抽搐、排尿、排便失禁及舌咬傷, 神志自行恢復(fù)。但自覺乏力、冷汗、胸悶氣短, 遂就診于我院急診科。急診心電圖、心肌酶正常。予硝酸酯類藥物治療, 患者拒絕急診留觀?；丶液笊鲜霭Y狀再發(fā)5次?；颊呒韧懈哐獕? 胸悶30年, 血壓最高達(dá)170～180/80～90 mmHg（1 mmHg = 0.133 kPa）, 平素應(yīng)用纈沙坦維持血壓于130～140/70～80 mmHg; 雙下肢靜脈曲張50余年。入院查體: 體溫35.8℃, 心率72次/min,血壓80/0 mmHg; 神志尚清, 面色及瞼結(jié)膜蒼白, 四肢發(fā)涼, 雙肺未聞及干濕啰音, 雙小腿淺表靜脈突出于皮膚表面; 心電圖: V1～V3導(dǎo)聯(lián)ST段下移0.05 mV（圖1）; cTnI 1.22 μg/L。初步診斷: 急性非ST段抬高性心肌梗死Killip I級, 心源性休克。給予吸氧、擴(kuò)容、升壓、抗凝（低分子肝素4000 IU, 每日1次皮下注射, 療程7 d）、抗血小板聚集（阿司匹林0.1 g, 每日1次口服, 氯吡格雷75 mg, 每日1次口服）、穩(wěn)定斑塊（他汀類藥物）、抗炎、保護(hù)胃黏膜等搶救措施后, 患者各項(xiàng)生命指征平穩(wěn)。

入院第12 d, 患者被動改變體位時突發(fā)胸悶氣短、心前區(qū)不適, 血壓63/34 mmHg, 心電圖示紊亂性房性心律失常（最高心率160次/min）。急檢動脈血?dú)? PaO261.1 mmHg, PaCO236.3 mmHg, pH 7.373; D-二聚體＞20 mg/L; cTnI 0.22 μg/L; CK 82 U/L, CK-MB 26 U/L, LDH 1085 U/L, 考慮為急性肺栓塞, 除給予呼吸道和血流動力學(xué)支持外, 囑患者絕對臥床, 并加強(qiáng)抗凝治療（華法林2.5 mg, 每日1次口服＋低分子肝素4000 IU, 每日1次皮下注射）。17d后停用低分子肝素, 以0.125 mg為單位調(diào)整華法林的劑量, 維持國際標(biāo)準(zhǔn)化比值于1.6～2.4。

入院30 d后, 患者病情平穩(wěn), 開始進(jìn)行相關(guān)檢查。經(jīng)胸超聲心動圖示: 肺動脈壓力升高（60 mmHg）, 左室下壁心內(nèi)膜回聲增強(qiáng), 射血分?jǐn)?shù)57%; 雙下肢深靜脈彩超示: 雙小腿肌間靜脈可見血栓形成; 肺動脈CT血管造影示: 右肺上葉、中葉肺動脈栓塞, 左肺上葉肺動脈局部分支栓塞（圖2）; 冠脈CT示: 兩側(cè)冠狀動脈未見明顯異常; 肺通氣-血流灌注顯像示: 右肺上葉后段、中葉見顯像劑分布缺損, 左肺部分上葉尖后段、部分下葉背段、前底段見顯像劑分布稀疏缺損區(qū), 肺血流比異常, 左肺/全肺= 59.10%, 右肺/全肺= 40.90%（圖3）。

入院60 d后, 為防止再次發(fā)生肺栓塞, 患者接受了下腔靜脈濾器植入術(shù)。

出院診斷:（1）急性肺栓塞;（2）下肢靜脈曲張（雙側(cè)）, 深靜脈血栓（雙小腿肌間靜脈）;（3）下腔靜脈濾器植入術(shù)后;（4）高血壓病3級（極高危險組）。

2 臨床病例討論

金博住院醫(yī)師: 本例急性肺血栓栓塞癥的臨床表現(xiàn)并非常見的胸痛、氣促、呼吸困難, 而表現(xiàn)為暈厥, 心電圖無電軸右偏、SIQⅢTⅢ的典型改變, 而表現(xiàn)為ST段下移, 同時血清肌鈣蛋白和心肌酶輕度升高, 極易與心肌梗死混淆, 而低氧血癥、血漿D-二聚體升高也可由心肌梗死造成, 更使二者的初步鑒別異常艱難。入院后完善肺動脈CT血管造影、冠狀動脈CT、雙下肢深靜脈彩超等檢查才明確診斷。需指出, 下肢遠(yuǎn)端靜脈血栓植入永久性下腔靜脈濾器為Ⅲ類推薦[1], 但超聲顯示該患者的下肢血栓較為新鮮, 隨時有脫落的可能, 結(jié)合患者有反復(fù)暈厥及休克的病史, 遂為患者植入了永久性下腔靜脈濾器。

于凱主治醫(yī)師: 該患者以暈厥為首發(fā)癥狀。暈厥在人群中, 特別是在65歲以上的老年人中發(fā)生很普遍, 當(dāng)年齡超過70歲時, 暈厥的發(fā)生率會從每年的5.7‰上升至11.1‰, 而且老年人的暈厥具有自身的特點(diǎn):（1）在老年人中, 發(fā)生于清晨的暈厥多為直立性低血壓型; （2）在65歲以上的老年人中, 有超過1/3的患者應(yīng)用3種或3種以上的處方藥, 暫停這些藥物可能會減少暈厥的發(fā)生; （3）有5%＞65歲老年人和20%＞80歲老年人存在認(rèn)知功能障礙, 有時他們并不能區(qū)分暈厥和跌倒。因此對于老年人, 除了評價神經(jīng)、運(yùn)動系統(tǒng)外, 對懷疑有認(rèn)知障礙者, 應(yīng)進(jìn)行簡易精神狀態(tài)檢查[2]。

王春雷副主任醫(yī)師: 老年人暈厥的病因多為體位性低血壓、反射性暈厥（尤其是頸動脈竇綜合征）和心源性暈厥（如心律失常、急性心肌梗死、肺栓塞等）, 而且同一個患者可能同時存在幾種病因。雖然人們?yōu)闀炟手贫藝?yán)謹(jǐn)?shù)脑u價步驟和方法, 但僅有58%的暈厥事件能夠找到確切的病因[3]。暈厥在肺栓塞中的發(fā)生率不足20%, 但其預(yù)示著病情的危重, 在明確病因時不可忽視。肺栓塞導(dǎo)致暈厥的機(jī)制有以下3點(diǎn): （1）大塊肺動脈栓塞引起急性右心衰竭、左室充盈減少、心動過速、血壓下降, 從而導(dǎo)致腦供血不足。在某些病例中, 這種情況可出現(xiàn)心臟停搏。在這種機(jī)制中包含兩種導(dǎo)致系統(tǒng)性低血壓的原因: 肺動脈主干被栓子壓迫引起B(yǎng)ezold- Jarisch反射和肺動脈系統(tǒng)閉塞。Bezold-Jarisch反射導(dǎo)致低血壓, 可伴有心動過緩和呼吸節(jié)律緩慢, 此類暈厥是短暫的, 持續(xù)時間不超過發(fā)生大塊肺栓塞后的15 min, 在這期間很難判斷患者的預(yù)后, 因?yàn)榇藭r的低血壓為反射性的, 并有自主恢復(fù)的趨勢; 如果低血壓狀態(tài)持續(xù)存在, 則更像是肺動脈系統(tǒng)閉塞所致。（2）肺動脈栓子引起快速型或緩慢型心律失常, 導(dǎo)致血流動力學(xué)不穩(wěn)定, 這種情況被認(rèn)為是由肺動脈栓子降低了心臟的舒張性所致。（3）肺動脈的栓子引起了某種血管反射, 從而導(dǎo)致了神經(jīng)源性暈厥[3]。3種機(jī)制可以單獨(dú)存在, 也可以聯(lián)合發(fā)揮作用。

白小涓主任醫(yī)師: 肺栓塞是一種相對高發(fā)的心血管急癥。急性肺栓塞的病死率高達(dá)7%～11%, 發(fā)病的平均年齡為62歲, 而且隨著年齡的增長, 原發(fā)性和繼發(fā)性肺栓塞的發(fā)病率均呈指數(shù)級上升。伴有休克和低血壓的肺栓塞患者, 危險分層為高危組, 即在住院期間或30 d內(nèi)因肺栓塞死亡的概率大于15%[4]。急性肺栓塞的治療原則是在提供呼吸和血流動力學(xué)支持的基礎(chǔ)上, 選擇溶栓、外科栓子清除術(shù)、經(jīng)皮導(dǎo)管栓子清除和碎裂術(shù)。對于高度懷疑或確診的急性肺栓塞患者, 無論是否合并其他治療策略, 都應(yīng)立即進(jìn)行抗凝治療, 除非患者是出血的高危人群或存在嚴(yán)重的腎功能不全。溶栓術(shù)可明顯減少高危患者的死亡率和栓塞再發(fā)率, 當(dāng)存在溶栓的絕對禁忌時, 依次選擇外科栓子清除術(shù)和經(jīng)皮導(dǎo)管栓子清除和碎裂術(shù), 但后者的安全性和有效性還缺乏足夠的文獻(xiàn)證實(shí)。因?yàn)樯腥狈Φ头肿痈嗡睾突沁_(dá)肝癸鈉在此類人群中的實(shí)驗(yàn)數(shù)據(jù), 高危患者的抗凝推薦使用普通肝素。本例急性肺栓塞患者, 伴有休克和低血壓, 危險分層為高危組, 但其年齡＞65歲, 有高血壓病史, 有抗凝藥使用史, 根據(jù)HAS-BLED出血風(fēng)險評分[5], 為出血的高危人群, 因此使用出血風(fēng)險低的低分子肝素單純抗凝更適合該患者。建議對該患者進(jìn)行長期隨訪, 做好慢病管理。

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[2] Moya A, Sutton R, Ammirati F,Guidelines for the diagnosis and management of syncope (version 2009)[J]. Eur Heart J, 2009, 30(21): 2631-2671.

[3] Koutkia P, Wachtel TJ. Pulmonary embolism presenting as syncope: case report and review of the literature[J]. Heart Lung, 1999, 28(5): 342-347.

[4] Torbicki A, Perrier A, Konstantinides S,Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC)[J]. Eur Heart J, 2008, 29(18): 2276-2315.

[5] Camm AJ, Kirchhof P, Lip GY,. Guidelines for the management of atrial fibrillation: the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC)[J]. Eur Heart J, 2010, 31(19): 2369-3429.

（參與討論醫(yī)師: 金 博, 于 凱, 王春雷, 白小涓）

（金 博整理）

（編輯: 任開環(huán)）

2011-11-03;

2012-01-14

白小涓, Tel: 024-83282770, E-mail: xjuanbai@hotmail.com

R543.2

A

10.3724/SP.J.1264.2012.00058