pulmonary embolism

肺塞栓症 PE

WordNet

1. an insertion into a calendar (同)intercalation
2. occlusion of a blood vessel by an embolus (a loose clot or air bubble or other particle)

PrepTutorEJDIC

1. 塞栓(そくせん)症(血管に塞栓が詰まること)
2. 肺の;肺を冒す

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/09/17 17:28:23」(JST)

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Pulmonary embolism
Classification and external resources
Chest spiral CT scan with radiocontrast agent showing multiple filling defects both at the bifurcation and in the pulmonary arteries.
ICD-10	I26
ICD-9	415.1
DiseasesDB	10956
MedlinePlus	000132
eMedicine	med/1958 emerg/490 radio/582
MeSH	D011655

A pulmonary embolism (PE) is a blockage of the main artery of the lung or one of its branches by a substance that has travelled from elsewhere in the body through the bloodstream (embolism). PE most commonly results from deep vein thrombosis (a blood clot in the deep veins of the legs or pelvis) that breaks off and migrates to the lung, a process termed venous thromboembolism (VTE). A small proportion of cases are due to the embolization of air, fat, talc in drugs of intravenous drug abusers or amniotic fluid. The obstruction of the blood flow through the lungs and the resultant pressure on the right ventricle of the heart lead to the symptoms and signs of PE. The risk of PE is increased in various situations, such as cancer or prolonged bed rest.

Symptoms of pulmonary embolism include difficulty breathing, chest pain on inspiration, and palpitations. Clinical signs include low blood oxygen saturation and cyanosis, rapid breathing, and a rapid heart rate. Severe cases of PE can lead to collapse, abnormally low blood pressure, and sudden death.

Diagnosis is based on these clinical findings in combination with laboratory tests (such as the D-dimer test) and imaging studies, usually CT pulmonary angiography. Treatment is typically with anticoagulant medication, including heparin and warfarin. Severe cases may require thrombolysis with drugs such as tissue plasminogen activator (tPA) or may require surgical intervention via pulmonary thrombectomy.

Signs and symptoms

Symptoms of PE are sudden-onset dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of a "pleuritic" nature (worsened by breathing), cough and hemoptysis (coughing up blood). More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability due to decreased blood flow through the lungs and into the left side of the heart. About 15% of all cases of sudden death are attributable to PE.

On physical examination, the lungs are usually normal. Occasionally, a pleural friction rub may be audible over the affected area of the lung (mostly in PE with infarct). A pleural effusion is sometimes present that is transudative, detectable by decreased percussion note, audible breath sounds and vocal resonance. Strain on the right ventricle may be detected as a left parasternal heave, a loud pulmonary component of the second heart sound, and raised jugular venous pressure. A low-grade fever may be present, particularly if there is associated pulmonary hemorrhage or infarction.

More rarely, inability of the right ventricle to remove fluid from the tissues leads to fluid accumulation in the legs (peripheral edema), congestion of the liver with mild jaundice and tenderness, and ascites (fluid in the abdominal cavity).^{[citation needed]}

Risk factors

The most common sources of embolism are proximal leg deep venous thrombosis (DVTs) or pelvic vein thromboses. Any risk factor for DVT also increases the risk that the venous clot will dislodge and migrate to the lung circulation, which happens in up to 15% of all DVTs.^{[citation needed]} The conditions are generally regarded as a continuum termed venous thromboembolism (VTE).

The development of thrombosis is classically due to a group of causes named Virchow's triad (alterations in blood flow, factors in the vessel wall and factors affecting the properties of the blood). Often, more than one risk factor is present.

• Alterations in blood flow: immobilization (after surgery, injury, pregnancy (also procoagulant), obesity (also procoagulant), cancer (also procoagulant)
• Factors in the vessel wall: of limited direct relevance in VTE
• Factors affecting the properties of the blood (procoagulant state):
  • Estrogen-containing hormonal contraception
  • Genetic thrombophilia (factor V Leiden, prothrombin mutation G20210A, protein C deficiency, protein S deficiency, antithrombin deficiency, hyperhomocysteinemia and plasminogen/fibrinolysis disorders)
  • Acquired thrombophilia (antiphospholipid syndrome, nephrotic syndrome, paroxysmal nocturnal hemoglobinuria)
  • Cancer (due to secretion of pro-coagulants)

Diagnosis

A Hampton hump in a person with a right lower lobe pulmonary embolism

To diagnose pulmonary embolism, medical societies recommend a review of clinical criteria to determine the need for testing, followed by testing to determine a likelihood of being able to confirm a diagnosis by imaging, followed by imaging if other tests have shown that there is a likelihood of a PE diagnosis.

The diagnosis of PE is based primarily on validated clinical criteria combined with selective testing because the typical clinical presentation (shortness of breath, chest pain) cannot be definitively differentiated from other causes of chest pain and shortness of breath. The decision to do medical imaging is usually based on clinical grounds, i.e. the medical history, symptoms and findings on physical examination, followed by an assessment of clinical probability.

The most commonly used method to predict clinical probability, the Wells score, is a clinical prediction rule, whose use is complicated by multiple versions being available. In 1995, Wells et al. initially developed a prediction rule (based on a literature search) to predict the likelihood of PE, based on clinical criteria. The prediction rule was revised in 1998 This prediction rule was further revised when simplified during a validation by Wells et al. in 2000. In the 2000 publication, Wells proposed two different scoring systems using cutoffs of 2 or 4 with the same prediction rule. In 2001, Wells published results using the more conservative cutoff of 2 to create three categories. An additional version, the "modified extended version", using the more recent cutoff of 2 but including findings from Wells's initial studies were proposed. Most recently, a further study reverted to Wells's earlier use of a cutoff of 4 points to create only two categories.

There are additional prediction rules for PE, such as the Geneva rule. More importantly, the use of any rule is associated with reduction in recurrent thromboembolism.

The Wells score:

• clinically suspected DVT — 3.0 points
• alternative diagnosis is less likely than PE — 3.0 points
• tachycardia (heart rate > 100) — 1.5 points
• immobilization (≥ 3d)/surgery in previous four weeks — 1.5 points
• history of DVT or PE — 1.5 points
• hemoptysis — 1.0 points
• malignancy (with treatment within 6 months) or palliative — 1.0 points

Traditional interpretation

• Score >6.0 — High (probability 59% based on pooled data)
• Score 2.0 to 6.0 — Moderate (probability 29% based on pooled data)
• Score <2.0 — Low (probability 15% based on pooled data)

Alternative interpretation

• Score > 4 — PE likely. Consider diagnostic imaging.
• Score 4 or less — PE unlikely. Consider D-dimer to rule out PE.

Blood tests

Early primary research has shown that in low/moderate suspicion of PE, a normal D-dimer level (shown in a blood test) is enough to exclude the possibility of thrombotic PE. This has been corroborated by a recent systematic review of studies of patients with low pre-test probability (PTP) of PE and negative D-dimer results that found the three month risk of thromboembolic events in patients excluded in this manner was 0.14%, with 95% confidence intervals from 0.05 to 0.41%, though this review was limited by its use of only one randomized-controlled clinical trial, the remainder of studies being prospective cohorts. D-dimer is highly sensitive but not very specific (specificity around 50%). In other words, a positive D-dimer is not synonymous with PE, but a negative D-dimer is, with a good degree of certainty, an indication of absence of a PE.

When a PE is being suspected, a number of blood tests are done, in order to exclude important secondary causes of PE. This includes a full blood count, clotting status (PT, aPTT, TT), and some screening tests (erythrocyte sedimentation rate, renal function, liver enzymes, electrolytes). If one of these is abnormal, further investigations might be warranted.^{[citation needed]}

Imaging

Selective pulmonary angiogram revealing significant thrombus (labelled A) causing a central obstruction in the left main pulmonary artery. ECG tracing shown at bottom.

CT pulmonary angiography (CTPA) showing a saddle embolus and substantial thrombus burden in the lobar branches of both main pulmonary arteries.

Ventilation-perfusion scintigraphy in a woman taking hormonal contraceptives and valdecoxib.
(A) After inhalation of 20.1 mCi of Xenon-133 gas, scintigraphic images were obtained in the posterior projection, showing uniform ventilation to lungs.

(B) After intravenous injection of 4.1 mCi of Technetium-99m-labeled macroaggregated albumin, scintigraphic images were obtained, shown here in the posterior projection. This and other views showed decreased activity in multiple regions.

In typical patients who are not known to be at high risk of PE, imaging is helpful to confirm or exclude a diagnosis of PE after simpler first-line tests are used. Medical societies recommend tests such as the D-dimer to first provide supporting evidence for the need for imaging, and imaging would be done if other tests confirmed a moderate or high probability of finding evidence to support a diagnosis of PE.

The gold standard for diagnosing pulmonary embolism (PE) is pulmonary angiography. Pulmonary angiography is used less often due to wider acceptance of CT scans, which are non-invasive. CT pulmonary angiography is the recommended first line diagnostic imaging test in most people.^{[citation needed]}

Non-invasive imaging

CT pulmonary angiography (CTPA) is a pulmonary angiogram obtained using computed tomography (CT) with radiocontrast rather than right heart catheterization. Its advantages are clinical equivalence, its non-invasive nature, its greater availability to people, and the possibility of identifying other lung disorders from the differential diagnosis in case there is no pulmonary embolism. Assessing the accuracy of CT pulmonary angiography is hindered by the rapid changes in the number of rows of detectors available in multidetector CT (MDCT) machines. According to a cohort study, single-slice spiral CT may help diagnose detection among people with suspected pulmonary embolism. In this study, the sensitivity was 69% and specificity was 84%. In this study which had a prevalence of detection was 32%, the positive predictive value of 67.0% and negative predictive value of 85.2% (click here to adjust these results for people at higher or lower risk of detection). However, this study's results may be biased due to possible incorporation bias, since the CT scan was the final diagnostic tool in people with pulmonary embolism. The authors noted that a negative single slice CT scan is insufficient to rule out pulmonary embolism on its own. A separate study with a mixture of 4 slice and 16 slice scanners reported a sensitivity of 83% and a specificity of 96%. This study noted that additional testing is necessary when the clinical probability is inconsistent with the imaging results. CTPA is non-inferior to VQ scanning, and identifies more emboli (without necessarily improving the outcome) compared to VQ scanning.

Ventilation/perfusion scan (or V/Q scan or lung scintigraphy), which shows that some areas of the lung are being ventilated but not perfused with blood (due to obstruction by a clot). This type of examination is as accurate as multislice CT but is often used less because of the more widespread availability of CT technology. It is particularly useful in people who have an allergy to iodinated contrast,impaired renal function, or in pregnancy due to lower radiation exposure than CT.. The test can be performed with planar two-dimensional imaging, or single photon emission tomography (SPECT) which enables three-dimensional imaging. Hybrid devices combining SPECT and CT (SPECT/CT) further enable anatomic characterization of any abnormality.

Low probability diagnostic tests/non-diagnostic tests

Tests that are frequently done that are not sensitive for PE, but can be diagnostic.

• Chest X-rays are often done on patients with shortness of breath to help rule-out other causes, such as congestive heart failure and rib fracture. Chest X-rays in PE are rarely normal, but usually lack signs that suggest the diagnosis of PE (e.g. Westermark sign, Hampton's hump).
• Ultrasonography of the legs, also known as leg doppler, in search of deep venous thrombosis (DVT). The presence of DVT, as shown on ultrasonography of the legs, is in itself enough to warrant anticoagulation, without requiring the V/Q or spiral CT scans (because of the strong association between DVT and PE). This may be valid approach in pregnancy, in which the other modalities would increase the risk of birth defects in the unborn child. However, a negative scan does not rule out PE, and low-radiation dose scanning may be required if the mother is deemed at high risk of having pulmonary embolism.^{[citation needed]}

Electrocardiogram

Electrocardiogram of a patient with pulmonary embolism showing sinus tachycardia of approximately 150 beats per minute and right bundle branch block.

An electrocardiogram (ECG) is routinely done on patients with chest pain to quickly diagnose myocardial infarctions (heart attacks). An ECG may show signs of right heart strain or acute cor pulmonale in cases of large PEs — the classic signs are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III (S1Q3T3). This is occasionally (up to 20%) present, but may also occur in other acute lung conditions and has therefore limited diagnostic value. The most commonly seen signs in the ECG is sinus tachycardia, right axis deviation and right bundle branch block. Sinus tachycardia was however still only found in 8–69% of people with PE.

Echocardiography

In massive and submassive PE, dysfunction of the right side of the heart can be seen on echocardiography, an indication that the pulmonary artery is severely obstructed and the heart is unable to match the pressure. Some studies (see below) suggest that this finding may be an indication for thrombolysis. Not every patient with a (suspected) pulmonary embolism requires an echocardiogram, but elevations in cardiac troponins or brain natriuretic peptide may indicate heart strain and warrant an echocardiogram.

The specific appearance of the right ventricle on echocardiography is referred to as the McConnell's sign. This is the finding of akinesia of the mid-free wall but normal motion of the apex. This phenomenon has a 77% sensitivity and a 94% specificity for the diagnosis of acute pulmonary embolism in the setting of right ventricular dysfunction.

Algorithms

Recent recommendations for a diagnostic algorithm have been published by the PIOPED investigators; however, these recommendations do not reflect research using 64 slice MDCT. These investigators recommended:

• Low clinical probability. If negative D-dimer, PE is excluded. If positive D-dimer, obtain MDCT and based treatment on results.
• Moderate clinical probability. If negative D-dimer, PE is excluded. However, the authors were not concerned that a negative MDCT with negative D-dimer in this setting has an 5% probability of being false. Presumably, the 5% error rate will fall as 64 slice MDCT is more commonly used. If positive D-dimer, obtain MDCT and based treatment on results.
• High clinical probability. Proceed to MDCT. If positive, treat, if negative, additional tests are needed to exclude PE.

Pulmonary Embolism Rule-out Criteria

The Pulmonary Embolism Rule-out Criteria, or PERC rule, helps assess people in whom pulmonary embolism is suspected, but unlikely. Unlike the Wells Score and Geneva score, which are clinical prediction rules intended to risk stratify patients with suspected PE, the PERC rule is designed to rule out risk of PE in patients when the physician has already stratified them into a low-risk category.

Patients in this low risk category without any of these criteria may undergo no further diagnostic testing for PE: Hypoxia — Sa_O2 <95%, unilateral leg swelling, hemoptysis, prior DVT or PE, recent surgery or trauma, age >50, hormone use, tachycardia. The rationale behind this decision is that further testing (specifically CT angiogram of the chest) may cause more harm (from radiation exposure and contrast dye) than the risk of PE. The PERC rule has a sensitivity of 97.4% and specificity of 21.9% with a false negative rate of 1.0% (16/1666).

Treatment

In most cases, anticoagulant therapy is the mainstay of treatment. Acutely, supportive treatments, such as oxygen or analgesia, are often required.

Anticoagulation

Main article: Anticoagulant

In most cases, anticoagulant therapy is the mainstay of treatment. Unfractionated heparin, low molecular weight heparin (LMWH), or fondaparinux is administered initially, while warfarin, acenocoumarol, or phenprocoumon therapy is commenced (this may take several days, usually while the patient is in the hospital). LMWH may reduce bleeding among patients with pulmonary embolism as compared to heparin according to a systematic review of randomized controlled trials by the Cochrane Collaboration. The relative risk reduction was 40%. For patients at similar risk to those in this study (2.0% had bleeding when not treated with low molecular weight heparin), this leads to an absolute risk reduction of 0.8%. 125 patients must be treated for one to benefit.

It is possible to treat low risk patients (risk class I or class II) as outpatients. A randomised trial of 344 patients (171 outpatients and 168 inpatients) found that outcomes were equivalent whether patients were treated in hospital or at home (there was one death at 90 days in each group). This confirms the findings of an earlier systematic review of observational studies.

Warfarin therapy often requires frequent dose adjustment and monitoring of the international normalized ratio (INR). In PE, INRs between 2.0 and 3.0 are generally considered ideal. If another episode of PE occurs under warfarin treatment, the INR window may be increased to e.g. 2.5–3.5 (unless there are contraindications) or anticoagulation may be changed to a different anticoagulant e.g. LMWH. In patients with an underlying malignancy, therapy with a course of LMWH may be favored over warfarin based on the results of the CLOT trial.

Similarly, pregnant women are often maintained on low molecular weight heparin to avoid the known teratogenic effects of warfarin, especially in the early stages of pregnancy.^{[citation needed]}

People are usually admitted to hospital in the early stages of treatment, and tend to remain under inpatient care until INR has reached therapeutic levels. Increasingly, low-risk cases are managed on an outpatient basis in a fashion already common in the treatment of DVT.

Warfarin therapy is usually continued for 3–6 months, or "lifelong" if there have been previous DVTs or PEs, or none of the usual risk factors is present. An abnormal D-dimer level at the end of treatment might signal the need for continued treatment among patients with a first unprovoked pulmonary embolus.

Thrombolysis

Main article: Thrombolysis

Massive PE causing hemodynamic instability (shock and/or hypotension, defined as a systolic blood pressure <90 mmHg or a pressure drop of 40 mmHg for >15 min if not caused by new-onset arrhythmia, hypovolemia or sepsis) is an indication for thrombolysis, the enzymatic destruction of the clot with medication. It is the best available medical treatment in this situation and is supported by clinical guidelines.

The use of thrombolysis in non-massive PEs is still debated. The aim of the therapy is to dissolve the clot, but there is an attendant risk of bleeding or stroke. The main indication for thrombolysis is in submassive PE where right ventricular dysfunction can be demonstrated on echocardiography, and the presence of visible thrombus in the atrium.

Surgery

Used inferior vena cava filter.

Surgical management of acute pulmonary embolism (pulmonary thrombectomy) is uncommon and has largely been abandoned because of poor long-term outcomes. However, recently, it has gone through a resurgence with the revision of the surgical technique and is thought to benefit selected patients.

Chronic pulmonary embolism leading to pulmonary hypertension (known as chronic thromboembolic hypertension) is treated with a surgical procedure known as a pulmonary thromboendarterectomy.

Inferior vena cava filter

Main article: Inferior vena cava filter

If anticoagulant therapy is contraindicated and/or ineffective, or to prevent new emboli from entering the pulmonary artery and combining with an existing blockage, an IVC filter may be implanted.

Epidemiology

Pulmonary embolism occur in more than 0.6 million people in the United States each year. It results in between 50,000 200,000 deaths per year in the United States. The risk in those who are hospitalized is around 1%. The rate of fatal pulmonary emboli has declined from 6% to 2% over the last 25 years in the United States.

Prognosis

Large saddle embolus seen at PA.

Mortality from untreated PE is said to be 26%. This figure comes from a trial published in 1960 by Barrit and Jordan, which compared anticoagulation against placebo for the management of PE. Barritt and Jordan performed their study in the Bristol Royal Infirmary in 1957. This study is the only placebo controlled trial ever to examine the place of anticoagulants in the treatment of PE, the results of which were so convincing that the trial has never been repeated as to do so would be considered unethical. That said, the reported mortality rate of 26% in the placebo group is probably an overstatement, given that the technology of the day may have detected only severe PEs.

Prognosis depends on the amount of lung that is affected and on the co-existence of other medical conditions; chronic embolisation to the lung can lead to pulmonary hypertension. After a massive PE, the embolus must be resolved somehow if the patient is to survive. In thrombotic PE, the blood clot may be broken down by fibrinolysis, or it may be organized and recanalized so that a new channel forms through the clot. Blood flow is restored most rapidly in the first day or two after a PE. Improvement slows thereafter and some deficits may be permanent. There is controversy over whether or not small subsegmental PEs need to be treated at all and some evidence exists that patients with subsegmental PEs may do well without treatment.

Once anticoagulation is stopped, the risk of a fatal pulmonary embolism is 0.5% per year.

Predicting mortality

The PESI and Geneva prediction rules can estimate mortality and so may guide selection of patients who can be considered for outpatient therapy.

Underlying causes

After a first PE, the search for secondary causes is usually brief. Only when a second PE occurs, and especially when this happens while still under anticoagulant therapy, a further search for underlying conditions is undertaken. This will include testing ("thrombophilia screen") for Factor V Leiden mutation, antiphospholipid antibodies, protein C and S and antithrombin levels, and later prothrombin mutation, MTHFR mutation, Factor VIII concentration and rarer inherited coagulation abnormalities.^{[citation needed]}

References

UpToDate Contents

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• 1. 成人における急性肺塞栓症の概要 overview of acute pulmonary embolism in adults
• 2. 急性肺塞栓症の臨床像、評価、および診断 clinical presentation evaluation and diagnosis of the adult with suspected acute pulmonary embolism
• 3. 成人における急性肺塞栓症に対する治療、予後、および経過観察の概要 overview of the treatment prognosis and follow up of acute pulmonary embolism in adults
• 4. 静脈血栓塞栓症の患者における理論的根拠と無期限の抗凝固の適応 rationale and indications for indefinite anticoagulation in patients with venous thromboembolism
• 5. Fibrinolytic (thrombolytic) therapy in acute pulmonary embolism and lower extremity deep vein thrombosis

English Journal

• Approach to Adult Patients with Acute Dyspnea.

• DeVos E1, Jacobson L2.
• Emergency medicine clinics of North America.Emerg Med Clin North Am.2016 Feb;34(1):129-49. doi: 10.1016/j.emc.2015.08.008.
• Undifferentiated patients in respiratory distress require immediate attention in the emergency department. Using a thorough history and clinical examination, clinicians can determine the most likely causes of dyspnea. Understanding the pathophysiology of the most common diseases contributing to dysp
• PMID 26614245

• Treatment Options in Massive and Submassive Pulmonary Embolism.

• Wadhera RK1, Piazza G.
• Cardiology in review.Cardiol Rev.2016 Jan-Feb;24(1):19-25. doi: 10.1097/CRD.0000000000000084.
• Pulmonary embolism (PE) is a common cardiovascular condition that represents a spectrum of disorders with a gradient of increased risk of adverse outcomes. The U.S. Surgeon General estimated that approximately 100,000 to 180,000 PE-related deaths occur in the United States annually, and that PE is t
• PMID 26274535

• Thromboembolism as an important complication of inflammatory bowel disease.

• Bollen L1, Vande Casteele N, Ballet V, van Assche G, Ferrante M, Vermeire S, Gils A.
• European journal of gastroenterology & hepatology.Eur J Gastroenterol Hepatol.2016 Jan;28(1):1-7. doi: 10.1097/MEG.0000000000000495.
• BACKGROUND: Patients with inflammatory bowel disease (IBD) have a higher risk of developing thromboembolic events (TE) compared with the healthy population.AIM: This study aimed to describe a cohort of IBD patients with a history of TE focusing on recurrence of TE, disease activity and IBD medicatio
• PMID 26513610

Japanese Journal

• 胸腔鏡下手術により診断した肺梗塞の4例

• 片岡 和彦,藤原 俊哉,松浦 求樹
• 気管支学 : 日本気管支研究会雑誌 33(5), 337-341, 2011-09-25
• 背景. 近年,肺梗塞の症例が増加している.症例. 腫瘤影を呈し,胸腔鏡下手術で診断した肺梗塞の4例を報告する.症例1は39歳男性で,胸痛と血痰を認めた.CTで左下葉にスリガラス影を認めたが,3週間後に側方の膨隆した台形の腫瘤影に変化した.他の3例は無症状であった.CTでは,症例2と症例3で側方の膨隆した台形の腫瘤影を呈し,症例4で類円形の結節影を呈していた.4例とも胸腔鏡下に肺部分切除を施行し,切 …
• NAID 110008750376

• Epidemiology and Predictors of Short-Term Mortality in Symptomatic Venous Thromboembolism : A Nationwide Population-Based Study

• LEE Cheng-Han,CHENG Ching-Lan,LIN Li-Jen,TSAI Liang-Miin,YANG Yea-Huei Kao
• Circulation journal : official journal of the Japanese Circulation Society 75(8), 1998-2004, 2011-07-25
• … The overall 1-month mortality rate was 8.8%, with 7.1% in deep venous thrombosis and 12.9% in pulmonary embolism. … Multivariate analysis demonstrated that pulmonary embolism, cancer, neurologic disease with extremity paresis or paralysis, older age, longer hospital stay, and major abdominal and thoracic surgery in the 3 months preceding VTE were independent predictors of 1-month death. …
• NAID 10029128322

• 奇静脈瘤に対して胸腔鏡下手術を施行した1例

• 捶井 達也,小田 誠,田村 昌也,早稲田 龍一,松本 勲,渡邊 剛
• 日本呼吸器外科学会雑誌 = The journal of the Japanese Association for Chest Surgery 25(5), 505-508, 2011-07-15
• 症例は32歳，女性．乳房痛を自覚し，精査のため胸部造影CTを施行したところ後縦隔に均一な造影効果を伴う径3.1cmの腫瘤を認めた．右上肢からの静脈造影では造影剤が上大静脈から奇静脈弓へ逆行性に流入し，腫瘤が濃染した．これにより腫瘤を静脈瘤と診断した．血栓による肺血栓塞栓症や瘤の破裂の可能性を考え外科的切除の方針とした．手術は胸腔鏡下にて施行した．まず血栓の流出を防止するため奇静脈弓の上大静脈合流部 …
• NAID 10029125703

Related Links

• Pulmonary embolismとは - goo Wikipedia (ウィキペディア)

To diagnose pulmonary embolism, medical societies recommend a review of clinical criteria to determine the need for testing, followed by testing to determine a likelihood of being able to confirm a diagnosis by imaging, followed by ...

• Pulmonary embolism | definition of pulmonary embolism by ...

Pulmonary Embolism Definition Pulmonary embolism is an obstruction of a blood vessel in the lungs, usually due to a blood clot, which blocks a coronary artery. Description Pulmonary embolism is a fairly common condition that can ...

Related Pictures

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★リンクテーブル★

リンク元	「肺塞栓症」「静脈血栓塞栓症」「PE」「venous thrombosis」
関連記事	「emboli」「pulmonary」

「肺塞栓症」

　　[★]

英

pulmonary embolism PE

同

肺梗塞, 肺動脈塞栓症

• 静脈系を経由して血栓、脂肪、腫瘍、空気、異物が肺動脈を閉塞したもの。総称

• 肺血栓塞栓症

症状

• 呼吸困難、胸痛、血痰、失神、咳

身体所見 SPU.380

• 多呼吸、頻脈
• ときに、発熱、チアノーゼ
• 胸部聴診：約半数に湿性ラ音・乾性ラ音
• 肺高血圧が著明な場合IIp音の増強

検査

血算

• 白血球：1万/ul　→　肺組織の壊死を示唆

血液生化学

• LDH：上昇
• 総ビリルビン：上昇
• AST：正常

LDH、総ビリルビンは半分の症例で上昇。心筋梗塞ではASTが上昇する。

凝固線溶系検査

• FDP、D-ダイマー、TAT：(血栓塞栓症の急性期)上昇

動脈血ガス

• 低酸素血症、低炭酸ガス血症、A-aDO2が開大(換気血流不均衡のため)

• 呼吸性アルカローシス

血清学検査

• IgE：上昇(250 U/ml以上)(50%の症例)

心電図 HIM.1653

• 洞性頻脈
• SI,QIII,TIII：I誘導でS波、III誘導でQ波が見られる。III誘導で陰性T波　←　特性は高いが、感度は低い
• 前胸部誘導(V1～V4)で陰性T波がよく見られる。
• 右軸偏位　←　右室負荷のため
• 一過性の右脚ブロック、心房細動

心エコー

• The specific appearance of the right ventricle on echocardiography is referred to as the McConnell's sign. This is the finding of akinesia of the mid-free wall but normal motion of the apex. This phenomenon has a 77% sensitivity and a 94% specificity for the diagnosis of acute pulmonary embolism.(wikipedia enより)

参考

• wiki ja

• http://ja.wikipedia.org/wiki/%E8%82%BA%E5%A1%9E%E6%A0%93%E7%97%87

「静脈血栓塞栓症」

　　[★]

英

venous thromboembolism、VTE

静脈血栓塞栓症 WMM.529

• 深部静脈血栓症 deep vein thrombosis DVT
• 肺塞栓症 pulmonary embolism PE

静脈血栓症発症の原因

uptodate

• 遺伝性血栓性素因

• 第V因子ライデン変異
• プロトロンビン遺伝子突然変異
• プロテインS欠乏症
• プロテインC欠乏症

• アンチトロンビン欠乏症

• (稀)異常フィブリノゲン血症

• 後天性

• 悪性腫瘍
• 中心静脈カテーテルの存在
• 手術、特に整形外科
• 外傷
• 妊娠
• 経口避妊薬
• ホルモン補充療法
• タモキシフェン、サリドマイド、レナリドマイド
• 固定化
• うっ血性心不全
• 抗リン脂質抗体症候群
• 骨髄増殖性疾患
• 真性赤血球増加症
• 本態性血小板血症
• 発作性夜間血色素尿症
• 炎症性腸疾患
• ネフローゼ症候群

<rad> http://www.uptodate.com/contents/image?imageKey=HEME%2F59759&topicKey=PULM%2F1363&source=see_link&utdPopup=true <rad>

「PE」

　　[★]

• pulmonary emphysema 肺気腫
• pulmonary embolism 肺塞栓症
• pericardial effusion 心嚢液 心膜液
• preeclampsia 妊娠高血圧腎症
• pulmonary eosinophilia 肺好酸球増多症
• polyethylene ポリエチレン
• phosphatidylethanolamine ホスファチジルエタノールアミン
• phycoerythrin フィコエリスリン

「venous thrombosis」

　　[★] 静脈血栓症

関

deep vein thrombosis, pulmonary embolism

「emboli」

　　[★] 塞栓, 栓子

関

embolic、embolization、embolus、plug

「pulmonary」

　　[★]

• adj.

• 肺の、肺性の

関

lung、pneumo