case study of patient with pulmonary embolism

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Case Report

Pulmonary embolism and infarction with a paradoxical thrombus visualised in both atria, hamza zafar.

Cardiology Clinical Academic Group, St Georges University Hospitals NHS Trust, London, UK

Lisa Anderson

Andrew t cox, rachel bastiaenen.

A 59-year-old woman presented with a sudden onset of breathlessness and chest pain. An echocardiography and CT scan showed pulmonary embolism and infarction with a paradoxical thrombus visualised in both atria. For haemodynamically stable patients, the optimal management strategy is poorly defined. Three main strategies were considered: surgical thrombectomy, thrombolysis and anticoagulation. Surgery with reversal of anticoagulation may lead to further coagulation and increased risk of bleeding complications. The significant pulmonary hypertension and right ventricular infarction raised the prospect of difficult weaning from cardiopulmonary bypass following thrombectomy. Thrombolysis, which has significant mortality rate, and systemic embolisation including pulmonary infarction with haemorrhagic transformation were also contraindications. A multidisciplinary approach was adopted and anticoagulation was therefore believed to be the safest and effective approach. Here, the use of anticoagulation alone was fortunately successful but could as easily end in disaster. This approach should be considered the ideal paradigm to yield optimum outcomes.

Paradoxical embolism is a life-threatening condition; unfortunately, its management remains a dilemma with no clear treatment strategies defined. The management of such cases should be patient-specific; that is, early involvement of a multidisciplinary team to define the treatment plan according to the patient’s clinical presentation is the key. In this case, the treatment strategy was formulated according to the patient’s condition and comorbidities, with input from multiple disciplines, which subsequently resulted in an excellent outcome.

Case presentation

A 59-year-old woman was admitted with a 2-week history of worsening shortness of breath and pleuritic chest pain. Doppler ultrasound of the right leg had demonstrated deep vein thrombosis, and the patient had been initiated on warfarin. Medical history included psoriatic arthropathy, for which she was treated with disease-modifying antirheumatic drugs, including methotrexate and prednisolone, and 2 months earlier was started on leflunomide. Leflunomide is an immunosuppressive, pyrimidine synthesis inhibitor that works by blocking dihydroorotate dehydrogenase used in active moderate-to-severe psoriatic arthropathy. The patient was 6 years postmenopause with no history of hormonal therapy, immobilisation, surgery or recent long-distance travel. Her mother had suffered from ‘blood clots’ and her father suffered a stroke after the age of 60 years. The patient was breathless at rest but haemodynamically stable on presentation, with blood pressure of 125/76 mm Hg, heart rate of 78 beats/min and oxygen saturation of 96% on 21% oxygen. Cardiac auscultation revealed no murmur and her chest was normal.

Investigations

Transthoracic echocardiography (TTE) was performed on arrival and demonstrated a serpiginous mass in both the atria and the left ventricle ( figure 1 ) ( video 1 ), with elevated pulmonary artery (PA) pressure (60–65 mm Hg) ( figure 2 ). Colour flow Doppler across the atrial septum was suspicious for a patent foramen ovale (PFO). McConnell’s sign (right ventricular (RV) dysfunction with characteristic sparing of the apex) was evident, suggesting pulmonary thromboembolism 1–3 ( video 2 ). A CT scan of the chest, abdomen and pelvis, including a pulmonary angiogram, demonstrated bilateral pulmonary emboli ( figure 3 ), extending into the segmental arteries, and a right-sided pulmonary infarct ( figure 4 ). There was no evidence of malignancy and a complete thrombophilia screen showed normal results.

Transthoracic echocardiogram: thrombus (arrow) across the right atrium, right ventricle and left atrium.

Apical four-chamber view.

Transthoracic echocardiogram: raised pulmonary artery pressure exhibited by high tricuspid regurgitation velocity jet (arrow).

Parasternal long axis view: thrombus.

CT pulmonary angiogram: right pulmonary emboli (arrow).

CT pulmonary angiogram: right pulmonary infarct (arrow).

The management of this patient was discussed at the departmental multidisciplinary meeting and hence conclusion was reached (see discussion of treatment options below). The clinical team responsible for the patient opted for treatment with unfractionated intravenous heparin as the international normalised ratio was subtherapeutic and warfarin was continued. After discussion with the rheumatology team and on the patient’s request, leflunomide was discontinued. Serial TTEs during the inpatient stay showed a progressive decrease in thrombus size and improving RV function and PA pressure that correlated with the patient’s clinical status. No complications were encountered during the treatment.

Outcome and follow-up

On day 13 there was no evidence of intracardiac thrombus, and the RV size and function and PA pressure had normalised ( video 3 ). The patient was then subsequently discharged from the hospital on warfarin and with long-term follow-up arranged. Follow-up with a transthoracic echocardiogram at 2 months and a year later continued to demonstrate normal RV function and PA pressure.

Complete resolution of the thrombus.

A paradoxical embolus (PDE) is a thrombus that passes from the right to the left side of the heart through an intracardiac defect, such as the patent foramen ovale. The first PDE case was reported in 1877 by Cohnheim, a German pathologist, who followed the path of the emboli through the patent foramen ovale during postmortem studies and found the thrombus of venous origin in the left atrium. 4–6 A PDE may pass into the systemic circulation where it can cause stroke or other serious thromboembolic events. Transthoracic echocardiogram is a quick and effective point-of-care tool to detect PDE and right-sided cardiac effects of pulmonary embolism.

Paradoxical embolisms can be life-threatening, and an optimal treatment strategy commonly poses a dilemma, especially for haemodynamically stable patients at risk of recurrent pulmonary and systemic thromboembolism. Three main strategies were considered to treat this patient: surgical thrombectomy, 7 8 systemic thrombolysis and catheter direct interventions, 9 10 and lastly anticoagulation. 11 Surgery with reversal of anticoagulation may lead to further coagulation, if previously anticoagulated with elevated risk of bleeding complications, transient ischaemic attacks and cardiac tamponade. 12 The significant pulmonary hypertension and RV dysfunction raised the prospect that the patient might not tolerate weaning from cardiopulmonary bypass following thrombectomy. There is increasing evidence that catheter techniques are essential and effective; however, there is no randomised controlled trial comparing their efficacy with systemic thrombolysis and anticoagulation for pulmonary embolism. Furthermore, a potential disadvantage of mechanical thrombectomy includes significant procedure time and risk of injury to the surrounding pulmonary vasculature. 13 The treatment options were therefore limited to anticoagulation or thrombolysis. Thrombolysis has been used in paradoxical embolism with favourable outcomes. 14–16 However, a significant mortality rate (16%–20%) associated with post-treatment systemic embolisation from segments of the large thrombus was considered a contraindication while the patient was clinically stable. 17 The presence of pulmonary infarction and the risk of haemorrhagic transformation with thrombolysis were considered a significant risk. As a result, anticoagulation was selected by the clinical team caring for the patient after departmental multidisciplinary discussion of the case (a consensus between the treatment options, as all were felt to pose a potential risk), as the patient was haemodynamically stable. Thrombosis is not usually a feature of psoriatic arthritis; the patient did not display any additional features of connective tissue disorders. There are case reports of thromboembolism following initiation of leflunomide 18 19 ; hence, for this case, the drug was discontinued on advice of the rheumatology team.

The choice of anticoagulation alone was strongly debated, but in this case it was fortunately successful. Despite numerous case reports and studies, the management of PDE remains a dilemma to which there is no correct solution for all situations.

Learning points

• A multidisciplinary team input from specialists is the key to provide primary care fundamentally in poorly defined management strategies.
• Identification of the triggers of thromboembolism is crucial to prevent disease progression and recurrence.
• In pulmonary embolism with or without infarction in haemodynamically stable patients, anticoagulation should be considered as first-line therapy to yield optimum outcomes.

Contributors: All persons who meet the authorship criteria are listed as authors, and all authors certify that they have participated in the concept, design, interpretation, drafting or revising the work. Furthermore, each author is in agreement to be accountable in ensuring questions leading to the accuracy and integrity of any part of the work were investigated and resolved. Contributions of the authors in each specific category are as follows: Category 1: conception and design of study: HZ and ATC; acquisition of data: HZ; analysis and/or interpretation of data: RB and ATC. Category 2: drafting the manuscript: HZ and ATC. Category 3: approval of the version of the manuscript to be published: HZ, ATC, RB and LA.

Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

Competing interests: None declared.

Patient consent: Obtained.

Provenance and peer review: Not commissioned; externally peer reviewed.

A 25 year old white female reports to the Emergency Room because of sharp left sided chest pain and shortness of breath of one day duration. The patient was in excellent health until yesterday. She was awakened from her sleep by sharp left sided chest pain. The pain worsened with motion and deep breathing. The pain has been progressively increasing in severity and she now has severe left shoulder pain. She complains of shortness of breath and is very apprehensive about dying. She denies any cough, fever, sputum production or hemoptysis.

She is married and had one normal delivery three years ago. She is currently on birth control pills. She has never been hospitalized except for labor and delivery. Review of systems are negative. She denies any past history of venous problems.

She reveals having a similar transitory minor episode of chest pain approximately one year ago while she was vacationing in Michigan.

She works as a computer programmer. She smokes one pack of cigarettes a day for the past eight years. She considers herself a social drinker.

1 She has pleuritic pain. What are the characteristics of pleuritic pain?

2 Is her pain due to visceral or parietal pleural inflammation?

3 What is the differential diagnosis of pleuritic pain?

4 List diagnoses that could fit the history of this patient as an etiology for pleuritic pain.

Physical Examination

Blood pressure 114/80; pulse 118; temperature 37.0 (oral)

She appears to be in moderate respiratory distress. She is well developed and nourished. Pertinent findings include a respiratory rate of 30 and shallow breathing. There is dullness, decreased chest expansion and decreased breath sounds in the left base. There is egophony in the left base. There were no rales or rubs.

Heart reveals PMI in the 5th intercostal space in MCL. The pulmonic component of the second sound is accentuated.

Abdomen, pelvic and rectal exams are normal.

The extremities reveal no evidence of edema, cyanosis or clubbing.

Patient has negative Homan's Sign.

Joint exam revealed shoulder movements complete in range. No warmth or tenderness noted. The rest of the patient's joints are normal.

5 Which of the diagnoses is supported by the physical exam.

6 What type of process is going on in the chest by evidence of exam.

7 What is Homan's Sign?

The Emergency Room physician orders the following tests:

CBC: Hgb 15.0; Hct 43; WBC 11,500; 83 polys, 1 band and 14 lymphs

SMA-12: Normal

Arterial blood gases: FI02 .21; pH 7.39; PCO2 30; HCO2 20; PO2 80 and SO2 95%

EKG reveals sinus tachycardia and non-specific S-T-T wave changes axis + 80.

CXR reveals a small pleural effusion in the left base. The left diaphragm is elevated.

Shoulder x-ray is normal.

Decubitus reveals a small amount of fluid in the left pleural space.

8 Does the CBC support your diagnosis?

9 Interpret the blood gases.

10 Calculate the A-a gradient.

11 Interpret the CXR.

12 Does the EKG findings support your diagnosis?

13 What is your explanation for her shoulder pain?

14 What is your working diagnosis now, after the screening lab tests?

15 What additional studies would you like to do?

Additional Studies

Lung scan revealed a defect corresponding to the area of pleural effusion.

Pleural tap revealed yellow fluid; protein 3.5 grams; glucose 64 and pH 7.4.

Doppler exam revealed deep vein thrombosis of the left lung.

16 Are you familiar with the way lung scans are reported from a diagnostic consideration of pulmonary embolism?

17 What are the characteristics of pleural effusion of a patient with pulmonary embolism?

18 Why did she develop deep vein thrombosis? Does she have a predisposing factor?

19 Are you surprised by the lack of physical findings for thrombophlebitis in this patient?

20 How often do we have physical findings of thrombophlebitis in patients with proven deep vein thrombosis?

21 Why did she develop deep vein thrombosis? Does she have a predisposing factor?

22 When do you consider pulmonary angiogram in the work-up of a patient suspected to have PE?

The Patient was admitted to the hospital. Repeat lung scan revealed multiple defects.

23 How will you treat her?

24 How long do you want to treat her in the hospital?

25 How long do you want to anticoagulate her as an outpatient and why?

26 Could this problem have been prevented?

• Case report
• Open access
• Published: 15 September 2009

Pulmonary embolism presenting as syncope: a case report

• Ahmet Demircan 1 ,
• Gulbin Aygencel 2 ,
• Ayfer Keles 1 ,
• Ozgur Ozsoylar 3 &
• Fikret Bildik 1  

Journal of Medical Case Reports volume  3 , Article number:  7440 ( 2009 ) Cite this article

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Introduction

Despite the high incidence of pulmonary embolism its diagnosis continues to be difficult, primarily because of the vagaries of symptoms and signs in presentation. Conversely, syncope is a relatively easy clinical symptom to detect, but has varied etiologies that lead to a documented cause in only 58% of syncopal events. Syncope as the presenting symptom of pulmonary embolism has proven to be a difficult clinical correlation to make.

Case presentation

We present the case of a 26-year-old Caucasian man with pulmonary embolism induced-syncope and review the pathophysiology and diagnostic considerations.

Conclusions

Pulmonary embolism should be considered in the differential diagnosis of every syncopal event that presents at an emergency department.

Recognized venous thromboembolism (pulmonary embolism and deep venous thrombosis) is responsible for more than 250,000 hospitalizations and approximately 50,000 deaths per year in the United States. Because it is difficult to diagnose, the true incidence of pulmonary embolism is unknown, but it is estimated that approximately 650,000 cases occur annually [ 1 ].

Despite this high incidence, the diagnosis of pulmonary embolism continues to be difficult primarily because of the notorious vagaries of symptoms and signs in its presentation. Conversely, syncope is a relatively easy clinical symptom to detect, but has varied etiologies that lead to a documented cause in only 58% of syncopal events [ 2 ].

Syncope as the presenting symptom of pulmonary embolism has proven to be a difficult clinical correlation to make. We present the case of a patient with pulmonary embolism-induced syncope and review the pathophysiology and diagnostic considerations.

A 26-year-old Caucasian man with no history of disease was admitted to Gazi University Emergency Department after he had a syncopal episode in his home. The patient was in his usual good state of health until he suddenly collapsed while standing and lost consciousness for approximately five minutes. He recovered spontaneously but was extremely weak and dyspneic. He was also diaphoretic and tachypneic, but denied any associated chest pain or palpitations. No tonic-clonic activity was witnessed, and he experienced no incontinence.

The patient was a computer programmer and he had been working 18 hours a day without rest periods for a month. On admission, physical examination revealed a diaphoretic and dyspneic patient without focal neurologic findings. His heart rate was regular but tachycardic at 128 beats/minute, his blood pressure was 126/72 mmHg without orthostatic changes, and his respiratory rate was 32 breaths/minute. The room air oxygen saturation was 90%, and arterial blood gas analysis in room air revealed hypoxemia (PO 2 = 58 mmHg) with an elevated alveolo-arterial oxygen gradient (A-a O 2 gradient). Examination of his head and neck was normal. The results of chest wall examination revealed reduced breath sounds bilaterally at the lung bases. The findings of heart and abdominal examinations were unremarkable, but on examination of his legs, deep venous thrombosis (DVT) was noted in his left leg, with a positive Homans' sign in the left leg and the left calf measured 3 cm more than the right one.

Levels of serum electrolytes, glucose, blood urea and creatinine, and complete blood counts were normal. Results of a computed tomographic scan of his head were negative for bleeding, aneurysm or an embolic event. Chest X-ray was clear. An electrocardiogram showed a regular rhythm consistent with sinus tachycardia; there were Q and T waves in lead III and an S wave in lead I. A ventilation-perfusion scan demonstrated an unmatched segmental perfusion defect, indicating a high probability of the presence of a pulmonary thromboembolism (PTE) (Figures 1 and 2 ). A transthoracic echocardiogram revealed normal left ventricle function without a patent foramen ovale, an atrial septal defect or a ventricular septal defect, but with mild pulmonary hypertension (42 mmHg). A Doppler scan of the legs revealed an acute DVT in the patient's left leg, in the popliteal vein. Thrombolytic treatment was not given - the patient received standard anticoagulation treatment with unfractionated heparin and an oral anticoagulant. Before treatment, a blood sample was taken to examine the thrombophilia panel. After a 12-day course of hospital treatment, he was discharged on oral warfarin therapy. The patient's long-term follow-up was performed by the Department of Pulmonary Disease, and we learned that the patient was well for four months after that episode without any evidence of recurrent syncope or pulmonary embolism.

Decreased perfusion is seen to the right lung (particularly evident in the right lower lobe on the RPO image) in our case (perfusion scan was performed with Tc-99m MAA) .

There is no significant ventilation defect in our case (ventilation scan was performed with Xe-133 gas) .

Pulmonary embolism is a frequent cause of death in the United States. Nevertheless, it remains difficult to diagnose. Pulmonary emboli differ considerably in size and number, and the underlying disorders, including malignancy, trauma, and protein C or S deficiency, are numerous [ 1 ]. The classic triad of pleuritic chest pain, dyspnea, and hemoptysis is rare, and clinically apparent DVT is present in only 11% of confirmed cases of pulmonary embolism in patients without underlying cardiopulmonary disease [ 3 ].

However, the clinical picture of pulmonary embolism is variable and most patients suffering from acute pulmonary embolism present with one of three different clinical syndromes. These clinical syndromes are pulmonary infarction, acute unexplained dyspnea, and acute cor pulmonale. The pulmonary infarct syndrome usually occurs with a submassive embolism that completely occludes a distal branch of the pulmonary circulation. Patients with this condition have pleuritic chest pain, hemoptysis, rales, and abnormal findings on chest X-ray. The acute, unexplained dyspnea pattern may also be the result of submassive pulmonary embolism without pulmonary infarction. Results of a chest X-ray and electrocardiogram are usually normal, but pulse oxygen saturation is often depressed. The third pattern, acute cor pulmonale syndrome, is caused by the complete obstruction of 60 to 75% of pulmonary circulation. Patients with this pattern experience shock, syncope, or sudden death [ 4 , 5 ].

Syncope, in contrast to pulmonary embolism, is relatively easy to detect, but can be a difficult symptom from which to determine the etiology. In as many as 50% of patients with syncope, no specific cause is found despite extensive evaluation. Syncope has been classified as cardiovascular (reflex and cardiac syncope), noncardiovascular (including neurologic and metabolic disorders) and unexplained [ 2 , 6 ]. It occurs in approximately 10% of patients with acute pulmonary embolism and is commonly ascribed to a massive, hemodynamically unstable acute pulmonary embolism. Although the prognostic value of syncope has not been specifically addressed, it has generally been considered a poor indicator in diagnosing pulmonary embolism [ 7 ].

Syncope in the setting of pulmonary embolism can be the result of three possible mechanisms. First, greater than 50% occlusion of the pulmonary vascular tree causes right ventricular failure and impaired left ventricular filling, leading to a reduction in cardiac output, arterial hypotension, reduced cerebral blood flow, and ultimately syncope. The second mechanism of syncope associated with pulmonary embolism is the appearance of arrhythmias associated with right ventricular overload. In the third mechanism, the embolism can trigger a vasovagal reflex that leads to neurogenic syncope. However, the contribution of hypoxemia secondary to ventilation or perfusion abnormalities must also be considered and may play an important role in the development of syncope. Moreover, acute pulmonary hypertension may also lead to right-to-left flow across a patent foramen ovale, and thus exacerbate hypoxemia [ 8 , 9 ].

The clinician should seek the following clues to the diagnosis of pulmonary embolism in patients who have had a syncopal episode: (a) hypotension and tachycardia or transient bradyarrhythmia; (b) acute cor pulmonale according to electrocardiogram criteria or physical examination; and (c) other signs and symptoms indicative of pulmonary embolism. The presence of any of these findings without other obvious causes of syncope should lead to further work-up, including arterial blood gas analysis, ventilation-perfusion scanning, lower extremity duplex sonogram, echocardiography, multislice computed tomography and angiography, if necessary. Although oxygen saturation levels are inadequate for screening purposes, respiratory alkalosis with hypoxia and increased A-a O 2 gradient are typically seen. However, results of blood gas analysis are normal in 10% of cases [ 4 , 10 ].

In our case, the patient presented to the emergency department with complaints of dyspnea, tachypnea and tachycardia, following a syncopal episode. He had experienced immobilization for one month, hypoxemia in room air, and DVT according to the ultrasonographic results. PTE was initially considered and all of the diagnostic procedures were carried out to prove this presumptive diagnosis. Because DVT and PTE developed in this young patient with no history of any underlying diseases or disorders, he was referred for thrombophilia panel testing (including protein C or S deficiency and Factor V mutation) before treatment; however, as his long-term follow-up was performed by the Department of Pulmonary Diseases, we do not have any further detailed results from these examinations. This case is interesting because the patient did not experience a massive embolism but did develop syncope.

Pulmonary embolism presenting with syncope is difficult to diagnose. Physicians and other health care professionals must be vigilant with patients who have syncope, because this symptom may be a 'forgotten sign' of life-threatening pulmonary embolism.

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

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Department of Emergency Medicine, Gazi University Faculty of Medicine, Ankara, Turkey

Ahmet Demircan, Ayfer Keles & Fikret Bildik

Department of Internal Medicine, Gazi University Faculty of Medicine, Ankara, Turkey

Gulbin Aygencel

Department of Anesthesiology and Reanimation, Gazi University Faculty of Medicine, Ankara, Turkey

Ozgur Ozsoylar

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Correspondence to Gulbin Aygencel .

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The authors declare that they have no competing interests.

Authors' contributions

AD, AK and FB analyzed and interpreted the patient data regarding the syncope and the pulmonary embolism. GA and OO performed the acute treatment of the patient, and were major contributors in writing the manuscript. All authors read and approved the final manuscript.

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Demircan, A., Aygencel, G., Keles, A. et al. Pulmonary embolism presenting as syncope: a case report. J Med Case Reports 3 , 7440 (2009). https://doi.org/10.4076/1752-1947-3-7440

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Received : 17 January 2008

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Published : 15 September 2009

DOI : https://doi.org/10.4076/1752-1947-3-7440

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• Acute Pulmonary Embolism
• Syncopic Episode
• Pleuritic Chest Pain

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• Patient 4: Shortness of Breath in a Young Woman
• Things Are Not What They Appear to Be
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A 34-year-old woman presented to the ED with dyspnea that began three hours earlier.

The ambulance call report clearly captures the essence of the patient’s clinical presentation ( Figure 1 ).

Her chief complaint was: “I can’t breathe.” She had dull substernal chest pain. The ambulance crew noted that she was “hysterical and hyperventilating” and that she was taking birth control pills. During the previous month, she had had episodes of shortness of breath and dull chest pain.

She appeared ill, and the presumptive diagnosis was “rule-out myocardial infarction.”

On arrival in the ED, she was anxious and in mild respiratory distress. Her vital signs were: blood pressure 120/80 mm Hg, pulse 104 beats/min, respiratory rate 24 breaths/min, and she was afebrile. Her oxygen saturation by pulse oxymetry was 88% on room air and 94% on 4 L/min oxygen administered by nasal cannula.

On examination, her lungs were clear to auscultation and her heart was rapid and regular without murmur, pericardial friction rub, or gallop. Her abdomen was not tender and there was no lower extremity edema or tenderness. She was overweight.

Blood tests, EKG, and chest radiographs were obtained. The EKG revealed sinus tachycardia and nonspecific T-wave flattening.

The chest radiographs were interpreted as being “normal” ( Figure 2 ).

A bolus and infusion of heparin was administered by intravenous catheter.

• Should you order a chest radiograph in this patient?
• What are you looking for?

(There are three significant radiographic findings.)

See patient outcome .

Pulmonary embolism (PE) was the primary diagnostic consideration in this patient . Although the radiograph was initially interpreted as normal, there are three significant findings: (1) blunting of the right costophrenic sulcus; (2) relatively increased opacity at the left lung base; and (3) an enlarged left hilum ( Figure 3 ).

Patient 4—AP view (see text for explanation).

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• Vol 11, No 8 (April 28, 2023) /

Acute pulmonary embolism with loss of consciousness as the first manifestation: a case report

Zhongyi Chai, Rong Hu, Changsheng Ma

Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University , National Clinical Research Center for Cardiovascular Diseases , Beijing , China

Contributions: (I) Conception and design: C Ma; (II) Administrative support: R Hu; (III) Provision of study materials or patients: Z Chai; (IV) Collection and assembly of data: Z Chai; (V) Data analysis and interpretation: Z Chai; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Background: The clinical manifestations of pulmonary embolism are varied, and atypical pulmonary embolism can easily be missed in some patients, resulting in serious clinical consequences and injuries.

Case Description: This report describes a rare case of acute pulmonary embolism with loss of consciousness as the first manifestation. A 50-year-old male was admitted with loss of consciousness and difficulty breathing. Acute coronary syndromes and neurological disorders such as seizures were excluded by clinical history and electrocardiogram dynamic changes. Multiple clues such as coagulation function and myocardial enzymes are highly suggestive of pulmonary embolism, after the completion of computed tomography pulmonary angiogram (CTPA) diagnosis, the severity of the acute pulmonary embolism was evaluated, after which the patient was given low-molecular-weight heparin sequentially overlapping with oral warfarin as the anticoagulation treatment. Following this, the life signs of the patient were stable, and there were no special complaints; thus, this patient was discharged smoothly. As of this writing, the patient is still being followed up clinically with no recurrent embolism or deterioration occurred.

Conclusions: This case is of guiding significance for the early detection and rapid diagnosis and treatment of such patients with pulmonary embolism. It is necessary to acquire the vital signs, including those related to heart rate, electrocardiography, respiration, and blood oxygen saturation in the first clinical contact for patients with syncope as soon as possible. Patients with problems related to the above-mentioned basic vital signs should be highly suspected of cardiopulmonary diseases, and CTPA should be performed as soon as possible after the evaluation of the clinical possibility of pulmonary embolism and D-dimer screening. Moreover, the critical degree of pulmonary embolism should be evaluated, and then reperfusion or anticoagulation treatment should be performed appropriately. This should be followed by etiology screening. To avoid recurrence or aggravation of pulmonary embolism, the cause of the disease should be determined and treated.

Keywords: Loss of consciousness; pulmonary embolism; clinical possibility; etiology screening; case report

Submitted Feb 02, 2023. Accepted for publication Apr 06, 2023. Published online Apr 17, 2023.

doi: 10.21037/atm-23-656

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Key findings

• Patients admitted with the primary clinical presentation of loss of consciousness alone may have pulmonary embolism without the typical signs.

What is known and what is new?

• The clinical manifestations of pulmonary embolism are varied.

• Loss of consciousness may also be an atypical clinical manifestation of pulmonary embolism.

What is the implication, and what should change now?

• For patients admitted to hospital due to loss of consciousness, attention should be paid first to the exclusion of life-threatening diseases, as the clinical manifestations may be obscure and easily missed.

Introduction

Pulmonary embolism is a common thromboembolic disease in clinic. Its typical clinical manifestations include dyspnea (more than 50%), pleural pain (39%), cough (23%), retrosternal pain (15%), fever (10%), hemoptysis (8%), syncope (less than 5%), unilateral limb swelling (24%), and unilateral limb pain (6%) ( 1 ). Acute pulmonary embolism is a clinical and pathophysiological syndrome of pulmonary circulation obstruction caused by endogenous or exogenous emboli blocking the main artery or branches of the pulmonary artery. It is a critical and severe disease with a high mortality rate. However, due to the lack of sufficient attention to the prevention and treatment of the disease for a long time, doctors often miss the diagnosis. The vast majority of these patients have disease causes, such as lower limb or pelvic vein thrombosis, long-term bedridden or inactive, chronic cardiopulmonary disease, surgery, trauma, malignant tumors, pregnancy and oral contraceptives. Treatment methods include anticoagulation, thrombolysis and interventional therapy ( 2 ).

Syncope can be the only first symptom of pulmonary embolism, but fewer than 1% of patients with pulmonary embolism have syncope or loss of consciousness as the main symptom ( 2 ). Pulmonary embolism is not a routine screening item in the differential diagnosis of syncope in our region. The patient described in this report was a rare case of clearly diagnosed acute pulmonary embolism with loss of consciousness as the first manifestation. If such patients are not detected in time and continue to undergo a series of screening and examination on the cause of syncope in the outpatient clinic according to the general syncope patients, it will lead to a series of serious consequences such as deterioration of the condition of such patients and even death. We present the following article in accordance with the CARE reporting checklist (available at https://atm.amegroups.com/article/view/10.21037/atm-23-656/rc ).

Case presentation

The patient was 50-year-old male, who 2 days before admission, had difficulty breathing when standing at home after bending over and working, which was accompanied by shortness of breath and amaurosis. He subsequently fell to the ground unconsciousness, but experience no fall injuries. After being unconscious on the ground for 10 seconds, the patient regained consciousness and had experienced no convulsion when falling, no rolling up of the eyes, and no incontinence. There was no dizziness, headache, chest tightness, chest pain, nausea or vomiting, palpitation, or sweating before the onset of loss of consciousness. After waking up, the patient continued to have dyspnea, general fatigue, intermittent shortness of breath, and chest pain. After that, the patient developed intermittent dry cough but no fever or expectoration, no dizziness or headache, no palpitation or back pain, and no residual neurological symptoms and was able to walk. He complained that when he went up the stage, he had increased shortness of breath and amaurosis but no chest pain or fainting. Moreover, the patient had no history of chest distress, chest pain, or asthma. He could lie down quietly and sleep at night. For further diagnosis and treatment, he visited to the cardiology department of Beijing Anzhen Hospital. From the onset of the disease, the patient had a clear mind, good spirits, normal stool and urine, and no significant change in weight. He had a history of gout for about 3 years. Before admission, he had experienced gout attacks and swollen and painful feet. The patient had oral administration of Celebrex and sodium bicarbonate 1 month before admission which reduced the activity of both his lower limbs. He had a history of varicose veins of the lower limbs for 20 years and a history of fatty liver for 10 years. The patient underwent radiofrequency ablation for paroxysmal atrial fibrillation 3 years prior in our hospital, and there was no recurrence during postoperative follow-up. His father had a history of high blood pressure, diabetes, and pulmonary embolism, while his mother had coronary heart disease. Physical examination results on admission were the following: temperature, 36.5 ℃; pulse, 82 times/minute; respiration, 16 times/minute; and blood pressure, 131/74 mmHg. The superficial lymph nodes of the whole body were not palpable or swollen. The breath sounds in both lungs were clear, no dry or wet rales were heard, the heart boundary was normal, the heart rhythm was regular, and no pathological murmur could be heard in the auscultation area of each valve. P2 showed no hyperactivity, the abdomen was flat and soft with no tenderness, there was no rebound pain or muscle tension, and bowel sounds were normal. The patient had mild edema in both the lower limbs but was negative for gastrocnemius gripping pain. Other physical examinations showed no obvious abnormalities.

The complete results of laboratory examination after admission are described below. (I) The results of routine laboratory examinations were the following: blood gas analysis (without oxygen inhalation) indicated PH 7.442, CO 2 partial pressure 28.2 mmHg↓, O 2 partial pressure 95.4 mmHg, and oxygen saturation 98.1%; no abnormalities were found in routine blood or urine tests. Liver and kidney function results were the following: alanine aminotransferase, 8 U/L↓; aspartate aminotransferase, 16 U/L; α-hydroxybutyrate dehydrogenase; 205 U/L↑; albumin, 38.0 g/L↓; uric acid, 598 µmol/L↑; triglyceride, 1.84 mmol/L↑; creatinine, 75 µmol/L; estimated glomerular filtration rate (eGFR) 102 mL/min ×1.73 m 2 ; and blood electrolytes, normal. B-type natriuretic peptide (BNP) levels were 136 pg/mL↑. Myocardial injury marker results were as follows: troponin I (TNI), 0.053 ng/mL↑; tumor markers (−); and thyroid functions (−). (II) Results for coagulation markers were the following: fibrin degradation product, 49.3 ug/mL↑; and D-dimer, 5,366 ng/mL↑. (III) Screening results for pulmonary embolism etiology and thrombophilia were the following: lupus anticoagulant factor test, 1.33↑; β-2 determination of glycoprotein I, 34.16 RU/mL↑; autoantibody spectrum, antinuclear antibody negative; immune index: complement 3:1.540 G/L↑; no abnormality in immunoglobulin determination; protein C activity, 148.0%↑; protein S activity, negative; blood M protein, negative; antithrombin III activity measurement, (−); blood homocysteine (−); anticardiolipin antibody, 5.7 U/mL; anti-nucleosome antibody, 0.67 RU/mL; and anti-double-stranded DNA antibody, 7.3 IU/mL.

Other auxiliary examination results after admission were conducted. (I) Electrocardiogram (ECG) results were the following: sinus rhythm, typical SIQIIITIII manifestation on electrocardiogram, V1–V3 lead T wave inversion (in Figure 1 ), and no dynamic changes in the recheck. (II) Chest radiography revealed heavier bilateral lung markings and possibly a small amount of pleural effusion on the left side. (III) Echocardiogram indicated a slightly increased pulmonary artery systolic pressure (41 mmHg). The echocardiogram of this patient did not show the characteristic features of pulmonary embolism, and only mild to moderate tricuspid regurgitation was observed. (IV) Colored Doppler ultrasound of lower limb veins revealed no vein thrombosis in the left superficial femoral vein, popliteal vein, posterior tibial vein, or lower leg soleus muscle, but there was bilateral great saphenous vein inflow segment reflux (severe). (V) Computed tomography pulmonary angiogram (CTPA) revealed the following (see Figure 2 ): multiple pulmonary embolisms at the bifurcation of left and right pulmonary arteries and at each segment of the pulmonary artery, high density shadow at the dorsal side of the lower lobes of both lungs. Before discharge, CTPA reexamination showed that the multiple pulmonary embolism at the bifurcation of the left and right pulmonary arteries and at each segment of the pulmonary artery had basically disappeared, while a slight embolism might have remained at the residual left upper lobe and lower lingual segment of the pulmonary artery. (VI) Abdominal ultrasound showed no obvious abnormalities in liver, spleen, or kidney.

After admission, the relevant examinations were completed, the diagnosis of pulmonary embolism was confirmed. Since the patient’s vital signs were stable upon admission, no recurrent syncope episodes were observed, and no significant right ventricular dysfunction was observed on echocardiography, we chose conventional anticoagulant therapy over thrombolytic therapy. Immediate anticoagulation was administered with 6,000 IU q12h (based on the patient’s body weight (body weight ×100 U), this patient weighed about 60 kg) via a subcutaneous injection of enoxaparin sodium. After this, the patient did not complain of dyspnea, chest pain, or shortness of breath and did not experience a loss of consciousness. The current examination results of this patient could not confirm the diagnosis of thrombophilia, so the treatment plan after discharge was to review CTPA and other items after anticoagulation for 3–6 months to determine the discontinuation of medication and follow-up. We decided to use warfarin instead of the new oral anticoagulant for health insurance and financial reasons. Subsequently, administration for oral warfarin and heparin were overlapped for anticoagulation. The international normalized ratio (INR) was 1.22 on admission. After warfarin was added, the INR was 2.38 and heparin was stopped. After discharge, the CTPA reexamination showed that the multiple pulmonary embolisms at the left and right pulmonary artery bifurcation and at each segment of the pulmonary artery had basically disappeared. Therefore, the patient was arranged to leave the hospital, and the patient was ordered to have regular outpatient follow-up, monitor the INR, and be alert to bleeding. The patient was additionally instructed to adjust the dose of warfarin as appropriate. As of this writing, this patient is still in the process of clinical follow-up (see Figure 3 for a summary of the case).

The latest European guidelines classify syncope as reflex syncope, postural hypotension and cardiogenic syncope. Due to the clinical manifestations of the patient's characteristic dyspnea and a series of subsequent auxiliary examination results that clearly indicated embolism, the syncope was considered to be caused by acute pulmonary embolism and no further screening was conducted for other syncope causes.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki (as revised in 2013). Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

This patient was a middle-aged male who experienced a sudden loss of consciousness as the first symptom of pulmonary embolism, which was followed by continuous dyspnea, shortness of breath, and chest pain. After admission, ECG, echocardiography, D-dimer, blood gas analysis, BNP, TNI and other relevant examinations suggested the possibility of pulmonary thromboembolism. The patient had high blood pressure and normal oxygen saturation when he was admitted. After the diagnosis of pulmonary embolism was confirmed with CTPA, low-molecular-weight heparin overlapped with warfarin anticoagulantion therapy was administered to the patient. After anticoagulantion therapy, the patient did not complain of any dyspnea, shortness of breath, chest pain, or other discomfort, and thus warfarin was taken via oral administration, INR was monitored, and the patient was discharged according to the doctor’s advice.

In this case, the patient may have been bedridden for a short time due to recent gout attacks, and venous thrombosis was formed after lower limb immobility, which eventually led to the occurrence of pulmonary embolism. At the same time, the first clinical manifestation of pulmonary embolism in this patient was the transient disorder of cerebral blood supply resulting in loss of consciousness due to the sudden restricted pulmonary gas exchange.

Therefore, this is a rare case of acute pulmonary embolism with sudden loss of consciousness as the first symptom. The possibility of pulmonary embolism should be considered in patients with syncope and dyspnea. Examination should be improved in time to assist in the diagnosis, anticoagulation and reperfusion therapy should be given in time.

The pathophysiological mechanism of pulmonary embolism causing syncope

Acute pulmonary embolism can lead to increased pulmonary circulation resistance, increased pulmonary artery pressure, and decreased pulmonary vascular bed area. When the pulmonary vascular bed area is reduced by 30% to 40%, the mean pulmonary artery pressure can reach more than 30 mmHg; when the pulmonary vascular bed area is reduced by 40% to 50%, the mean pulmonary artery pressure can reach 40 mmHg; when the pulmonary vascular bed area is reduced by 50% to 70%, persistent pulmonary hypertension can occur; when the pulmonary vascular bed area is reduced by more than 85%, sudden death can occur ( 2 ). As pulmonary vascular resistance increases, the pressure and volume of the right ventricle increase, the right ventricle dilates, and wall tension increases to maintain blood flow in the blocked pulmonary vascular bed, while systemic vascular constriction stabilizes systemic blood pressure. However, the degree of this immediate compensation is limited, and right cardiac insufficiency eventually occurs, resulting in reduced left cardiac return blood volume and thus reduced cardiac output. The cerebral cortex is unable to meet the demand for blood supply, and hypoxemia caused by the imbalance of the ventilation: blood flow ratio in the clogged capillary bed also affects the oxygen demand of the cerebral cortex. The normal functioning of the higher nervous system mainly in the cerebral cortex depends on the continuous provision of a sufficiently large blood supply and oxygen demand. As the demand for adequate blood and oxygen supply cannot be met during acute pulmonary embolism, amaurosis, fainting, and loss of consciousness may result, which explains the patient’s clinical symptoms ( 2 ). However, our center has also admitted patients who were only clinically suspected of pulmonary embolism, but in whom timely CTPA examination and anticoagulation-related treatment were not implemented. The patients’ ischemic and anoxic state could not be corrected accordingly for a long period of time. During hospitalization, these patients might present various nonspecific clinical manifestations, such as continuous disturbance of consciousness and even shallow coma, compared with syncope alone. These patients could have acute chest pain with corresponding ST segment elevation in the thoracic leads, which is similar to the symptoms of acute myocardial infarction or variable angina pectoris.

Differential diagnosis of syncope or loss of consciousness in clinic

The diagnosis and differential diagnosis of syncope or loss of consciousness is an area of intense research focus. In the modern era, clinicians cardiology departments are required to quickly and accurately identify the causes of a patients’ loss of consciousness in order to quickly ascertain critical factors of this syncope. The causes of syncope can be divided into several categories: (I) hypotensive syncope; (II) hypoglycemia, in which, before the onset of hypoglycemic syncope, people usually experience hunger, sweating, and prolonged disturbance of consciousness, which can be significantly improved with eating; (III) hypoxia, which is more common in syncope caused by pulmonary embolism, such as the syncope in this case; (IV) cerebrovascular diseases, including transient ischemic attack of the vertebrobasilar artery system or severe stenosis of the corresponding vessels, subclavian steal syndrome, and rare cerebrovascular diseases (e.g., moyamoya disease); (V) abnormal electrical activity in the cerebral cortex, including seizures; and (VI) hystericus insultus, which includes states of anxiety and hysterical syncope. Among these, syncope caused by hypotension is still the most common ( 3 - 5 ). Syncope caused by hypotension can be subdivided into 5 types: (I) poor ventricular filling, including dehydration, bleeding, severe pulmonary hypertension, pericardial tamponade, and atrial myxoma; (II) poor ventricular emptying, including aortic coarctation, hypertrophic obstructive cardiomyopathy, and severe systolic heart failure; (III) abnormal heart rhythm, including various types of tachycardia and bradycardia, vasovagal syncope (cardiac inhibitory), and carotid sinus syncope (cardiac inhibitory); (IV) reduced peripheral resistance, including vasovagal syncope (vascular inhibitory type), postural hypotension, carotid sinus allergy (vascular inhibitory type), and drug-related hypotension (nitrates, alpha-blockers, tricyclic antidepressants, etc.); and (V) syncope with other specific causes, including cough-related syncope, urination-related syncope, etc. ( 6 ). Our center has a complete examination procedure for patients with loss of consciousness whose condition is stable. In addition to routine hospital-related examinations, routine blood tests (including myocardial injury markers, BNP, coagulation analysis and D-dimer, routine biochemical indicators and blood gas analysis, and long-term dynamic ECG monitoring for 24–72 hours), echocardiography, blood pressure detection in different positions, and ultrasonography of the carotid artery, subclavicular artery, and peripheral artery should be completed. The upright tilt test, head magnetic resonance imaging (MRI) and transcranial Doppler examination, and the further monitoring of the intracranial artery via magnetic resonance (MR) angiography and electroencephalogram are evaluated according to the consultation opinions of neurology department, and then a further examination and treatment plan are made according to the patient’s clinical data and the results of the corresponding examinations described above ( 7 ).

Screening of patients at risk for pulmonary embolism

The most common clinical manifestation in patients with pulmonary embolism is dyspnea, while the most common sign is increased respiratory rate (>20 beats/min). Dyspnea, syncope, cyanosis, and hypotension tend to indicate a large pulmonary embolism near the main pulmonary artery, whereas pleural pain, cough, and hemoptysis tend to indicate a small pulmonary embolism near the pleura. Therefore, routine D-dimer screening should be performed for a patient with loss of consciousness, and the possibility of pulmonary embolism should be vigilantly monitored for patients with dyspnea. For patients suspected of pulmonary embolism clinically, the following should be considered for clinical possibility assessment: (I) previous history of pulmonary embolism or lower limb venous thrombosis; (II) a heart rate increase of more than 20% compared with the normal base value; (III) history of surgery, fracture, or breaking within the last 1 month; (IV) hemoptysis; (V) tumor activity stage; (VI) age over 65 years; (VII) unilateral lower limb swelling and pain; and (VIII) gastrocnemius muscle grip pain, deep vein tenderness of lower limb, and unilateral swelling of lower limb. If 3 or more of the above 8 criteria are met, the possibility of pulmonary embolism is high. At this time, CTPA should be able to confirm or exclude the diagnosis of pulmonary embolism regardless of the results of D-dimer. If only 0–2 of the 8 criteria meet, D-dimer screening should be further improved; if D-dimer is elevated, further CTPA examination can be considered for definite diagnosis; if D-dimer is not high, pulmonary embolism can be basically excluded ( 7 ).

Formulation of the subsequent treatment plan after definite diagnosis

Risk stratification should be performed simultaneously for patients with suspected acute pulmonary embolism to guide the subsequent diagnosis and treatment measures. There are multiple different criteria and scores for the risk stratification of pulmonary embolism, and the clinical indicators observed by the corresponding criteria and scores are not the same. A comprehensive assessment of risk stratification as recommended by the earliest guidelines for the diagnosis, treatment, and prevention of pulmonary thromboembolism was previously performed ( 8 ), with patients being classified into a high-risk group (with shock or hypotension), middle-high-risk group (stable hemodynamics but positive laboratory indicators and imaging), medium-low risk group (stable hemodynamics, with single positive laboratory indicators or imaging), and low-risk group (stable hemodynamics but no laboratory indicators or imaging abnormalities). There are also several other kinds of complicated scores for assessment of pulmonary embolism used at present ( 9 , 10 ). The scoring indicators are as follows: older age (over 65-year-old), male sex, tumor presence, chronic heart failure, chronic lung disease, pulse greater than 110 beats/min, systolic blood pressure less than 100 mmHg, respiratory rate greater than 30 beats/min, arterial oxygen saturation less than 90%, new characteristic ECG changes, hypothermia and changes in mental state, ultrasound changes in right ventricular shape, positive findings of deep venous thrombosis of lower extremities, and abnormal increase of cardiac TNI and BNP, etc. However, in clinical practice, no significant clinical benefit has been observed when thrombolytic therapy is actively applied to certain patients with high risk scores or grades compared with conventional anticoagulant therapy. Pulmonary embolism patients with syncope as the first symptom are not necessarily high-risk patients, nor do they necessarily need reperfusion therapy, but the presence of shock or persistent hypotension is suspected to be high-risk acute pulmonary embolism. Shock or persistent hypotension refers to systolic blood pressure <90 mmHg and/or a decrease to >40 mmHg for more than 15 minutes, except in cases of new arrhythmias, decreased blood volume, sepsis, etc. ( 11 ). These patients can be directly treated with reperfusion. In the absence of shock or persistent hypotension, conventional anticoagulant therapy can be used, and remedial reperfusion therapy can be used as appropriate in patients with elevated troponin combined with changes in right ventricular morphology and function ( 12 , 13 ).

Etiology screening of pulmonary embolism

In view of the etiology of pulmonary embolism in this patient, relevant risk factors of pulmonary embolism should be identified first, including major trauma, surgery, lower limb fracture, spinal cord injury, autoimmune disease, hereditary hypercoagulability, thromboembolism, inflammatory bowel disease, tumor, oral contraceptives and hormone replacement therapy, arteriovenous catheterization, stroke paralysis, chronic heart failure and respiratory failure, pregnancy, long-term bed immobilization, sedentary, aging, varicose veins, risk factors associated with atherosclerosis, history of use of chemotherapy drugs [e.g., erythropoietin (EPO) (hemopoietin) and some non-steroid anti-inflammatory drugs (NSAIDs)] ( 14 - 17 ). This patient had a clear history of varicose veins of the lower limbs and a family history of pulmonary embolism. One month before admission, he had taken NSAIDs orally and had relative immobilization due to gout attack and increased bed rest and thus belonged to the population prone to pulmonary embolism. In addition, the improvement of the screening related to thrombolysis after admission was demonstrated by the following results: lupus anticoagulant factor test, 1.33↑; and β2 glycoprotein I, 34.16 RU/mL↑. The possibility of antiphospholipid antibody syndrome was not excluded. The patient was asked to undergo review for the indicators related to the thrombolysis in the outpatient department of rheumatology and immunology 2 months later to confirm whether the diagnosis of antiphospholipid antibody syndrome could be established and to continue to follow up.

Conclusions

The possibility of pulmonary embolism should be considered particularly in patients with syncope complicated with dyspnea. Vital signs, heart rate, electrocardiogram, respiration, and blood oxygen saturation of patients with syncope should be determined immediately, and appropriate respiratory support and blood pressure support should be given to high-risk patients as soon as is needed. Patients with the above basic vital signs should be highly suspected of loss of consciousness caused by cardiopulmonary diseases. After finishing the clinical possibility assessment for pulmonary embolism and D-dimer screening are completed, CTPA should be performed according to the circumstances to help clarify or exclude the diagnosis of pulmonary embolism. Meanwhile, the severity of pulmonary embolism should be evaluated, and then reperfusion or anticoagulation therapy should be administered accordingly. Following this, etiological screening and medical history should be conducted to identify the risk factors related to pulmonary embolism, and corresponding treatments and disease guidance should be provided accordingly to avoid recurrence or aggravation of pulmonary embolism.

Acknowledgments

Funding: None.

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at  https://atm.amegroups.com/article/view/10.21037/atm-23-656/rc

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Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://atm.amegroups.com/article/view/10.21037/atm-23-656/coif ). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki (as revised in 2013). Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/ .

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The Portuguese Journal of Cardiology, the official journal of the Portuguese Society of Cardiology, was founded in 1982 with the aim of keeping Portuguese cardiologists informed through the publication of scientific articles on areas such as arrhythmology and electrophysiology, cardiovascular surgery, intensive care, coronary artery disease, cardiovascular imaging, hypertension, heart failure and cardiovascular prevention. The Journal is a monthly publication with high standards of quality in terms of scientific content and production. Since 1999 it has been published in English as well as Portuguese, which has widened its readership abroad. It is distributed to all members of the Portuguese Societies of Cardiology, Internal Medicine, Pneumology and Cardiothoracic Surgery, as well as to leading non-Portuguese cardiologists and to virtually all cardiology societies worldwide. It has been referred in Medline since 1987.

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• Palavras-chave
• Introduction
• Case report
• Venous thromboembolism
• Venous thromboembolism during pregnancy
• Imaging studies
• Acute treatment
• Maintenance treatment
• Conclusions
• Conflict of interest
• Bibliography

We describe the case of a 37-year-old pregnant woman who presented at 29 weeks of gestation with syncope and shortness of breath caused by pulmonary embolism. Due to persistent hypotension thrombolytic therapy with tenecteplase was administered and the clinical and hemodynamic response was excellent, with no maternal or fetal hemorrhagic complications.

The clinical presentation of pulmonary embolism is sometimes camouflaged by the physiological changes that occur in pregnancy and diagnosis is often delayed by reluctance to expose the fetus to ionizing radiation. Systemic thrombolysis is considered a high-risk treatment in pregnancy and very few women have received it. However, the complication rates of thrombolytic therapy are acceptable in the light of the underlying disease.

Grávida de 37 anos de idade com 29 semanas de idade gestacional recorre ao serviço de urgência por síncope e dispneia causadas por tromboembolismo pulmonar com repercussão hemodinâmica. Por hipotensão persistente foi-lhe administrada terapêutica trombolítica com tenecteplase com excelente resposta hemodinâmica e clínica, sem intercorrências hemorrágicas maternas ou fetais.

A apresentação clínica do tromboembolismo pulmonar é por vezes camuflada pelas transformações fisiológicas que ocorrem na gravidez e o diagnóstico é muitas vezes atrasado pela relutância em expor o feto a radiação ionizante. A trombólise é um tratamento de alto risco na grávida e há poucos casos descritos da sua utilização; porém, as taxas de complicações com a terapia trombolítica são aceitáveis em relação à doença subjacente.

It is estimated that 0.2–4% of pregnancies in the Western world are complicated by cardiovascular disease, and this figure is increasing. There is frequently a need for diagnostic and/or therapeutic cardiological intervention in pregnant women, and this is always a challenge, both because most cardiologists lack experience with this patient group and because few cardiological interventions have been thoroughly validated in this population.

The recently published ESC guidelines on the management of cardiovascular diseases during pregnancy were developed more by extrapolating the evidence for non-pregnant patients than on the basis of the limited data available, and most of their recommendations are level of evidence C (consensus of opinion of the experts and/or small studies, retrospective studies, registries). 1

A 37-year-old pregnant woman at 29 weeks of gestation (gravida 2 para 1), with a history of overweight, no relevant family history and not taking any regular medication, presented with fatigue and pain in the side and back of the left thigh 24 hours after a short flight of about 3 hours. The clinical setting was interpreted as a possible herniated disc with inflammation of the left sciatic nerve, and she was medicated with analgesics and anti-inflammatory agents. Her fatigue worsened, with shortness of breath on successively less exertion; on the ninth day she suffered brief loss of consciousness at home and oppressive chest pain, and went to the emergency department.

On physical examination she was agitated, hypotensive (73/35 mmHg), tachycardic (115 bpm), hypoxemic (oxygen saturation in room air 80%) and tachypneic (50 cpm). No signs of deep vein thrombosis (DVT) were observed. Laboratory tests revealed hemoglobin 12.3 g/dl; platelets 170 × 10 9 /l; D-dimers 2962 ng/ml; and troponin I 0.43 ng/ml (reference value ng/ml). Arterial blood gas analysis (with the patient on 5 l/min supplementary oxygen) showed respiratory alkalosis (pH 7.49); pO 2 105 mmHg; pCO 2 28 mmHg, HCO 3 − 20.9 mmol/l; and O 2 saturation 98%. The electrocardiogram (ECG) showed sinus tachycardia and signs of right ventricular (RV) overload ( Fig. 1 ), confirmed by bedside transthoracic echocardiography (TTE) ( Fig. 2 ).

ECG showing sinus tachycardia, S1Q3T3 pattern and T-wave inversion in V1–V4, probably related to ischemia and/or overload in the right ventricle and the ventricular septal region.

Transthoracic echocardiography: (A) end-diastolic apical 4-chamber view showing right ventricular dilatation, paradoxical septal wall motion and pulmonary artery systolic pressure of 65 mmHg; (B) parasternal short-axis view showing diastolic flattening of the ventricular septum due to pulmonary hypertension; (C) preserved right ventricular systolic function (tricuspid annular plane systolic excursion 23 mm).

The fetus was in transverse position, with good vital signs; the cardiotocogram was reactive, with good variability and no uterine contraction. The ultrasound scan showed concordant fetal growth.

Doppler ultrasound of the lower limbs excluded DVT.

According to the Wells score, the patient's clinical probability of acute pulmonary thromboembolism (PTE) was intermediate ( Table 1 ). She was medicated with subcutaneous enoxaparin 1 mg/kg and fluid therapy was initiated. It was decided to perform thoracic computed tomography (CT) with administration of intravenous contrast in the pulmonary arterial phase, the fetus being protected from radiation by lead shielding. CT angiography confirmed acute bilateral PTE ( Fig. 3 ).

The Wells scoring system for diagnosis of PTE.

Clinical probability:

2–6, intermediate;

DVT: deep vein thrombosis; PTE: pulmonary thromboembolism.

(A) Occlusive thrombus in the right pulmonary artery extending to the lobar branches. An occlusive thrombus can be seen on the left in the superior lobar artery extending to the left pulmonary artery. Another thrombus is visible in the inferior lobar artery, not completely occlusive, extending into the segmental branches; (B) right ventricle measuring 57 mm and left ventricle measuring 29 mm; (C) coronal plane reconstruction with a thick slice (24 mm) in maximum intensity projection, showing thrombus in the right pulmonary artery (red arrow).

The patient was transferred to the coronary care unit, where after four hours she was still agitated, hypotensive (80/45 mmHg), tachycardic (115 bpm) and tachypneic (60 cpm). After weighing the hemorrhagic risk against the greater risk of irreversible clinical decompensation, it was decided to administer thrombolytic therapy with tenecteplase (40-mg bolus over 5 minutes). Within three hours clear clinical and hemodynamic improvement was seen, with blood pressure 95/65 mmHg, heart rate 100 bpm, breathing rate 25 cpm, and decreasing need for supplementary oxygen therapy.

She was discharged from the coronary care unit on the fourth day and transferred to the Obstetrics and Gynecology Department. She remained hemodynamically stable throughout her hospital stay, with 96% oxygen saturation in room air. No maternal or fetal hemorrhagic complications occurred.

On the fifth day ECG and TTE ( Fig. 4 ) were performed, which showed a normal-sized RV and no signs of pulmonary hypertension. She was discharged home on the 17th day, medicated with subcutaneous enoxaparin 60 mg twice a day.

(A) ECG showing sinus bradycardia of 58 bpm, absence of S wave in DI and T-wave inversion in V1–V4. (B) Transthoracic echocardiography in end-diastolic apical 4-chamber view showing right/left ventricle ratio mmHg.

On the 30th day after diagnosis, obstetric ultrasound ( Fig. 5 ) showed fetal growth in the same percentile curve and normal morphology, amniotic fluid volume and flowmetry in the umbilical and middle cerebral arteries. Investigation of maternal thrombophilia revealed her to be heterozygous for factor V Leiden.

(A) Doppler flowmetry of the right middle cerebral artery; (B) parasagittal cranial image; (C) estimated fetal weight.

The most feared manifestation of venous thromboembolism (VTE) is PTE, a common entity with a mortality of 30% if untreated, mainly due to recurrence. Oral anticoagulation (OAC) at therapeutic doses within 24 hours reduces mortality to 2–8%. 2,3 In-hospital mortality is 5–17% in patients who present evidence of RV dysfunction at diagnosis 4 and 20–30% in those with hemodynamic compromise. 5

VTE, which includes DVT and PTE, is the leading cause of maternal death (20%) in developed countries, accounting for 1.2–4.7 deaths per 100 000 pregnancies. 6 The precise incidence of VTE is unknown but is estimated at 0.5–2 cases per 1000 pregnancies. 7 The risk is greatest in the first three weeks after birth by cesarean section, 2 but the risk is still high between the third and sixth week after delivery and is the same as during pregnancy. From the sixth week the risk is the same as for non-pregnant women. 8

Venous stasis : This begins in the first trimester and reaches a maximum at 36 weeks. It is caused by progesterone-induced venodilation, compression of the pelvis by the gravid uterus, and pulsatile compression by any of the iliac arteries on the left iliac vein (which explains why 80% of cases of DVT in pregnancy are on the left, a phenomenon known as May-Thurner syndrome) 10 ;

Vascular injury : During childbirth the veins of the pelvic region may be distended and/or traumatized, especially when a cesarean section is performed (which explains the greater risk described above);

Hypercoagulability : The production of several coagulation factors (I, II, VII, VIII, IX and X) increases in pregnancy, while protein S production and the activity of the inhibitors of fibrinolysis PAI-1 and PAI-2 are reduced. These physiological changes are crucial to the hemodynamic challenges of birth (peripartum bleeding is the leading cause of maternal death in developing countries 11 ). This prothrombotic state will be further exacerbated by the presence of hereditary thrombophilia such as factor V Leiden, the G20210A mutation in the prothrombin gene, antithrombin III or protein C or S deficiency, or the presence of antiphospholipid antibodies. 12

The clinical features of VTE can be frustratingly difficult to evaluate, since most healthy pregnant women have lower limb edema and up to 70% suffer from shortness of breath during pregnancy. 13 Diagnosis of VTE, and particularly PTE, requires a high index of clinical suspicion, based on predisposing conditions and risk factors (in the case presented, these included overweight, pregnancy at age over 35, thrombophilia, immobility during a flight, and initial symptoms in the left leg compatible with DVT). 1,2

Based on risk factors and physical examination, the clinical probability of PTE can be calculated using the Wells or Geneva score. This then guides the choice of diagnostic exams ( Table 1 ). 2 These tools have not been validated in the pregnant patient, although one study has found three variables that appear to predict DVT in pregnant women: left leg symptoms, >2 cm difference in thigh circumference, and first trimester. 14

Laboratory results such as respiratory alkalosis or elevated fibrin degradation products are also commonly found in healthy pregnant women; levels of the latter increase with gestational age and reach a maximum at the time of birth, but such tests should be performed due to their ability to exclude disease and to avoid unnecessary exposure to ionizing radiation. 1,15

The deep venous system of the lower limbs is difficult to assess by physical examination, and when DVT and/or PTE are suspected the techniques used are B-mode echocardiography and compression venous ultrasonography together with color Doppler in transverse view. 1,2 Magnetic resonance imaging has 100% sensitivity in diagnosing DVT and appears to be safe in pregnancy. 16 Documented DVT in a hemodynamically stable pregnant woman is sufficient motive to begin OAC without needing to exclude or confirm PTE, although at least 70% of patients with PTE do not have DVT at the time of diagnosis. 17

Exams using ionizing radiation in women of childbearing age should be performed during the first 10 days after a menstrual cycle, and if there is a possibility that the woman is pregnant, this must be excluded first. Exposure of the ovaries to radiation pre-conception has no measurable effects on future gestations, and the risk from ionizing radiation to pregnant women is the same as to those who are not pregnant. However, for the fetus, ionizing radiation can cause death, malformations (particular ocular), growth retardation and mutagenic and carcinogenic effects, which depend mainly on gestational age (the most vulnerable period is between the second and eighth week) and the absorbed radiation dose.

A major problem with diagnosis of PTE is clinicians’ reluctance to expose the fetus to ionizing radiation, often due to overestimation of the risk of harm. When faced with the clinical probability of PTE, the primary diagnostic modalities are pulmonary ventilation-perfusion scintigraphy (VPS) and thoracic CT. The estimated radiation dose from CT absorbed by the fetus is 0.003–0.13 mGy, while from VPS it is 0.2 mGy. There is no evidence that doses of up to 50 mGy lead to fetal abnormalities, low IQ, growth restriction or miscarriage. Less radiation is absorbed by the mother's mammary and pulmonary tissue with VPS than with CT. 18,19 Although VPS and CT appear to be safe for the fetus, it should be noted that some studies suggest that exposure to low radiation doses in utero can increase the risk of childhood leukemia (1 in 2000 compared to the baseline risk of 1 in 2800), which does not compare with the risk of maternal death from undiagnosed and untreated PTE (15%). 20

In a pregnant woman with normal chest X-ray, VPS may be more valuable in diagnosing PTE than CT, since in the latter exam the contrast material can be interrupted by unopacified blood from the inferior vena cava. Conversely, CT should be used when the chest X-ray is abnormal, since it can diagnose other conditions such as pneumonia or other lung disease. Pulmonary angiography should not be used in pregnancy. 1,21

Iodinated contrast agents may lead to fetal thyroid dysfunction (although this has never been reported with isolated use), and this should be assessed in the first week after birth.

All women should be routinely assessed for risk of VTE before conception or in the first weeks of pregnancy. The most important risk factors are history of unprovoked DVT, recurrent VTE, PTE or thrombophilias (for which a family history of VTE is an important factor). Half of the women with VTE during pregnancy have either a thrombophilic disorder or a previous thrombotic event, and there are thought to be identifiable risk factors in around 80% of cases of death from PTE in pregnancy. 1,22 Prevention of VTE in pregnancy is without doubt better than cure and prophylactic measures (OAC with enoxaparin 0.5 mg/kg and compression stockings) should be taken when the risk is considered to be high or even moderate. 1

OAC, together with unfractionated or low molecular weight heparin, should be administered to achieve therapeutic doses within 24 hours. This reduces mortality by preventing recurrence of PTE and improving RV function. There is no evidence of differences in mortality between OAC alone or in combination with thrombolytics, although in patients with signs of RV dysfunction thrombolysis is associated with less clinical deterioration (10% vs. 25%), 23 more rapid resolution of hemodynamic alterations, and probable long-term improvement in pulmonary artery pressure and pulmonary vascular resistance. 24 Thrombolysis is indicated in PTE when there is severe clinical instability (i.e. with shock or systolic blood pressure mmHg or a fall of >40 mmHg in 15 minutes not caused by new-onset arrhythmia, hypovolemia or sepsis), a situation associated with high early mortality (>15%). Although it may be considered in other situations such as severe hypoxemia, severe scintigraphic perfusion defects, RV dysfunction, massive PTE on CT, free-floating thrombus in the right atrium or RV, and patent foramen ovale, there is general agreement on the use of thrombolysis only in the case of persistent hypotension. 2 Current thinking is to prescribe thrombolysis not on the basis of the extent or severity of PTE but solely to counteract its hemodynamic repercussions. Pregnancy is a relative contraindication to the use of thrombolytics 2 , but successful thrombolysis has been reported in at least 200 pregnant women. 1 The reported risks are 1% for maternal death, 6% for fetal loss and 8% for hemorrhage, mostly from the genital tract. At the time of delivery, thrombolytic treatment should not be used except in extremely severe cases and if surgical embolectomy is not immediately available. The thrombolytics most commonly used in pregnancy are streptokinase, urokinase and recombinant tissue plasminogen activator (rt-PA). If OAC is absolutely contraindicated, as in the immediate postoperative or postpartum period, possible treatments include an inferior vena cava filter, thrombus fragmentation with or without local thrombolysis, or surgical embolectomy. The use of fluid challenge in PTE-induced hemodynamic compromise is controversial; it should not exceed correction of 500–1000 cm 3 . 2

Warfarin should not be used in pregnancy, particularly in the first trimester due to the risk of embryopathy and in the third trimester due to the risk of placental abruption or fetal and neonatal hemorrhage, but can be used after delivery and during breastfeeding. Vaginal delivery is preferable to cesarean section, which should be reserved for specific fetal or maternal indications. It is safe to begin OAC 12 hours after delivery; it should be continued for at least three months. 1,2

Tenecteplase (TNKase) is a genetically engineered glycoprotein derived from rt-PA by substituting three amino acids, which confers slower plasma clearance, longer half-life, greater fibrin binding, less fibrinogenolysis and coagulopathy, and greater resistance to inactivation by PAI-1. Tenecteplase does not cross the blood-placenta barrier, and single-bolus administration results in more rapid plasmin formation and hence to resolution of the clinical setting. 25

A search in PubMed for the keywords “pregnancy” and “tenecteplase” reveals that this is the fifth report of the use of this thrombolytic in pregnancy and the first in the context of PTE (of the previous four cases, two were of myocardial infarction and two of mechanical valve thrombosis).

Pulmonary thromboembolism is common in pregnancy and is associated with significant maternal morbidity and mortality. It should always be considered in the presence of suspicious symptoms and signs and confirmed by appropriate diagnostic exams, including VPS or CT. Oral anticoagulation should be begun immediately, and thrombolysis should be considered in cases of hemodynamic instability as it has been shown to be effective in the few cases described in the literature and in the case presented here.

The authors have no conflict of interest to declare.

Please cite this article as: Santos, L, et al. Imagem Tromboembolismo pulmonar agudo na gravidez: A propósito de um caso clínico. Rev Port Cardiol. 2012. doi:10.1016/j.repc.2011.11.007 .

Joint authors.

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