case study pulmonary embolism

• 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.

Wolfe TR, Allen TL: Syncope as an emergency department presentation of pulmonary embolism. J Emerg Med. 1998, 16: 27-31. 10.1016/S0736-4679(97)00228-X.

Article   CAS   PubMed   Google Scholar  

Manolis AS, Linzer M, Estes M: Syncope: current diagnostic evaluation and management. Ann Intern Med. 1990, 112: 850-863.

Koutkia P, Wachtel TJ: Pulmonary embolism presenting as syncope: case report and review of the literature. Heart Lung. 1999, 28: 342-347. 10.1053/hl.1999.v28.a99733.

Varon J, Fromm RE: Syncope: the forgotten sign of pulmonary embolism. J Emerg Med. 1998, 16: 117-118. 10.1016/S0736-4679(98)00061-4.

Bell WR, Simon TL, DeMets DS: The clinical features of submassive and massive pulmonary emboli. Am J Med. 1977, 62: 355-360. 10.1016/0002-9343(77)90832-4.

Kapoor WN: Evaluation and management of patients with syncope. J Am Med Assoc. 1992, 268: 2553-2560. 10.1001/jama.268.18.2553.

Article   CAS   Google Scholar  

Edelson G, Reis ND, Hettinger E: Syncope as a premonitory sign of fatal pulmonary embolism. Acta Orthop Scand. 1988, 59: 71-73. 10.3109/17453678809149349.

Thames MD, Alpert JS, Dalen JE: Syncope in patients with pulmonary embolism. JAMA. 1977, 238: 2509-2511. 10.1001/jama.238.23.2509.

Simpson RJ, Podolak R, Mangano CA, Foster JR, Dalldorf FG: Vagal syncope during recurrent pulmonary embolism. JAMA. 1983, 249: 390-393. 10.1001/jama.249.3.390.

Article   PubMed   Google Scholar  

Soloff LA, Rodman T: Acute pulmonary embolism. Am Heart J. 1967, 74: 629-647.

Article   Google Scholar  

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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

Accepted : 06 March 2009

Published : 15 September 2009

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

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• Sujata Devi 1 ,
• Sudipta Mohakud 2 ,
• Nilanjan Kar 1 and
• Divya Muthuvel 2
• 1 General Medicine , All India Institute of Medical Sciences Bhubaneswar , Bhubaneswar , India
• 2 Radiodiagnosis , All India Institute of Medical Sciences Bhubaneswar , Bhubaneswar , India
• Correspondence to Dr Sudipta Mohakud; radiol_sudipta{at}aiimsbhubaneswar.edu.in

A 53-year-old man with diabetes came to the emergency department with fever and dry cough for 5 days, swelling of the left leg for 2 days, shortness of breath and chest pain for 1 hour. He had raised temperature, tachycardia, tachypnoea, reduced oxygen saturation and swollen tender left leg on examination. The frontal chest radiograph showed bilateral ground-glass opacities; he tested positive for COVID-19 with elevated D-dimer. The colour Doppler examination of the left leg revealed acute deep vein thrombosis (DVT) of the common femoral and the popliteal veins. The chest CT showed bilateral diffuse ground-glass opacities predominantly involving peripheral zones and the lower lobes. The CTPA revealed left pulmonary thromboembolism (PTE), treated with low-molecular-weight heparin. COVID-19 predominantly affects the respiratory system. DVT and PTE are common in COVID-19 but lethal. They should be diagnosed early by clinical and radiological examinations and treated promptly with anticoagulants.

• venous thromboembolism
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Contributors SD: primary consultant of the patient, clinical history, follow-up, drafting of the manuscript and manuscript review; SM: radiological diagnosis, drafting of the manuscript and manuscript review; NK: clinical data collection and drafting of the manuscript; DM: collection of radiological data and manuscript editing.

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.

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Approach to pulmonary embolism: A clinical care pathway

El Hussein, Mohamed Toufic RN, PhD, NP (Professor, Adjunct Associate Professor, Acute Care Nurse Practitioner) 1,2,3 ; Bayrouti, Ali (Nursing Student) 4

1 School of Nursing and Midwifery, Faculty of Health, Community & Education, Mount Royal University, Calgary, Alberta, Canada

2 Faculty of Nursing, University of Calgary, Calgary, Alberta, Canada

3 Medical Cardiology, Coronary Care Unit, Rockyview General Hospital, Calgary, Alberta, Canada

4 Mount Royal University, Calgary, Alberta, Canada

Correspondence: Mohamed Toufic El Hussein, RN, PhD, NP, 4825 Mount Royal Gate S.W., Calgary, AB T3E 6K6, Canada. Tel: (403) 440-8633; Fax: (403) 440-6203; E-mail: [email protected]

Competing interests: The authors report no conflicts of interest.

Authors' contributions: Mohamed El Hussein and Ali Bayrouti: conceptualization, writing—original draft, and writing—review and editing.

Acute pulmonary embolism (PE) is a potentially fatal condition that is often underdiagnosed due to its ambiguous and generalized symptoms. As such, nurse practitioners (NPs) may struggle to respond in a timely and accurate manner to clients presenting with acute PE. Given the complexities of diagnosing and managing PE, we propose a visual clinical care pathway to support NPs in recognizing and stratifying clients' risks of PE. The article provides guidance regarding PE diagnostic testing and offers a summary of effective, evidence-based treatment options for adult clients, including those with cancer.

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Pulmonary Embolism: Clinical Case

The following are key points to remember about this clinical case on pulmonary embolism (PE):

• Although approximately 20% of patients who are treated for PE die within 90 days, true short-term mortality attributed to PE is estimated to be <5%. Approximately 50% of the patients who receive a diagnosis of PE have functional and exercise limitations 1 year later (known as post–PE syndrome), and the health-related quality of life for patients with a history of PE is diminished as compared with that of matched controls.
• Newer approaches such as YEARS algorithm and age adjustment for D-dimer thresholds for ruling out PE are recommended.
• Diagnostic chest imaging is reserved for patients in whom PE cannot be ruled out based on clinical decision making.
• After initial diagnosis, clinical risk stratification into high, intermediate high risk, intermediate low risk, and low risk is recommended next. The nomenclature of “massive” and “submassive” in describing PE is confusing, given that clot size does not dictate therapy.
• High risk: Intravenous systemic thrombolysis is the most readily available reperfusion option in high-risk PE patients. Alternative reperfusion approaches include surgical thrombectomy and catheter-directed thrombolysis (with or without thrombectomy). Additional supportive measures include the administration of inotropes and the use of extracorporeal life support.
• Intermediate high risk: When available, catheter-directed thrombus removal remains an option for such. At this time, there is insufficient evidence to support catheter-directed thrombolysis over anticoagulation alone in these patients. Systemic thrombolysis is not typically recommended for these patients.
• Intermediate low risk: Anticoagulation with low molecular weight heparin and close monitoring for 24-48 hours for clinical worsening is recommended.
• Low risk: Outpatient management with direct oral anticoagulants is the preferred strategy.
• All patients with acute PE should receive anticoagulant therapy for ≥3 months. The decision to continue treatment indefinitely depends on whether the associated reduction in the risk of recurrent venous thromboembolism outweighs the increased risk of bleeding and should take into account patient preferences.
• Patients should be followed longitudinally after an acute PE to assess for dyspnea or functional limitation, which may indicate the development of post–PE syndrome or chronic thromboembolic pulmonary hypertension.

Clinical Topics: Anticoagulation Management, Cardiac Surgery, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Prevention, Pulmonary Hypertension and Venous Thromboembolism, Vascular Medicine, Anticoagulation Management and Venothromboembolism, Cardiac Surgery and Arrhythmias, Cardiac Surgery and Heart Failure, Interventions and Imaging, Interventions and Vascular Medicine

Keywords: Anticoagulants, Diagnostic Imaging, Dyspnea, Extracorporeal Membrane Oxygenation, Heparin, Low-Molecular-Weight, Outpatients, Pulmonary Embolism, Quality of Life, Reperfusion, Risk Assessment, Secondary Prevention, Thrombectomy, Thrombolytic Therapy, Thrombosis, Vascular Diseases, Venous Thromboembolism

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• Case report
• Open access
• Published: 06 November 2019

Case report: systolic murmur associated with pulmonary embolism

• Cain M. Dudek   ORCID: orcid.org/0000-0002-0770-3265 1 ,
• Kelly R. McCracken 2 &
• B. James Connolly 2  

International Journal of Emergency Medicine volume  12 , Article number:  32 ( 2019 ) Cite this article

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This case study’s novelty lies in the potential to link a new sign in pulmonary embolism diagnosis which does not increase cost but could lead to more rapid treatment. Early intervention in these cases is vital to decrease morbidity and mortality.

Case presentation

An otherwise healthy 20-year-old female patient presents to the emergency department for evaluation of a syncopal episode which occurred just prior to arriving to the emergency department. Patient also complains of ongoing shortness of breath while performing activities of daily living for 3 weeks. In this patient with no known valvular disease, physical exam revealed a systolic murmur heard only posteriorly. Subsequent emergency department workup revealed bilateral massive pulmonary emboli.

Implications

A new flow murmur heard in atypical locations could be an early sign to aid in the detection and diagnosis of pulmonary embolism. This is especially important in rural community hospitals with limited access to advanced imaging modalities.

Acute pulmonary embolism (PE) is associated with high early mortality rate of up to 30%. Even with pioneering medical advances, this has not substantially changed [ 1 ]. While there are no exact epidemiological studies indicating the prevalence of pulmonary embolism cases, an estimated 300,000 to 600,000 patients are diagnosed per year with a thromboembolic event. Estimates indicate about 80,000 of these patients will die. The first symptom of pulmonary embolism is sudden death in about 25% of patients [ 2 ]. This is especially important in rural or critical access settings where catheter-directed tPA therapy is not readily available. The setting for the case is in a rural community hospital emergency department in the USA during June 2019. This case study is being reported in accordance with the case report (CARE) guidelines.

A 20-year-old Caucasian female presented to the emergency department of a rural community hospital with shortness of breath and a syncopal episode. The patient stated she is a cross-country runner and for the past 4 days has had significant shortness of breath with even mild exertion. The patient had a witnessed syncopal episode at home lasting about one minute. The patient remembered being in the kitchen, but not falling. At that point, her mother brought her to the emergency department for further evaluation.

Upon arrival, the initial set of vital signs were blood pressure 132/78 mmHg; heart rate 109 bpm; regular, respiratory rate of 20; and SpO2 of 89% on room air. The patient appeared well nourished, but mildly anxious. Further assessment revealed no past medical history, no pertinent surgical history, and the only medication she takes daily is birth control. The patient endorsed recent flights from Georgia to Florida to Puerto Rico in the past 4 months. The patient denied ever feeling severe shortness of breath and denies a history of syncope. Patient’s mother denied any congenital defects or pertinent genetic information including family history of clotting disorders or history of blood clot in any first-degree relatives. While talking, the patient’s work of breathing increased as evidenced by accessory muscle use and SpO2 decreases to 89%. When resting, her SpO2 is 95–96% and showed no signs of accessory muscle use or tachypnea.

Physical exam revealed clear and equal lung sounds anteriorly, heart sounds were normal anteriorly, skin was pink, warm, and mildly diaphoretic. Posteriorly lung fields were auscultated as clear, but a low-pitched systolic murmur was heard in the 5th intercostal space in the right scapula region. Lower extremities were normal upon exam. Diagnostic investigation revealed significantly elevated troponin T high sensitivity at 82 ng/L (normal < 14 ng/L). Other lab work was normal. ECG can be seen in Fig.  1 below. Pulmonary embolism was suspected and a diagnostic CT angiogram (CTA) of the chest was obtained. A d-dimer was not included in diagnostic workup because of the high index of suspicion for pulmonary embolism given the other test results.

Twelve lead ECG recording while resting in the bed

The CTA of the chest was read as extensive bilateral pulmonary emboli with evidence of right heart strain, as demonstrated by refluxing of contrast into the right ventricle, see Figs.  2 , 3 , and 4 . The patient was placed on a heparin drip and transferred to a higher acuity facility for catheter-directed thrombolytic therapy and further evaluation.

Large obstruction of right pulmonary artery at the first bifurcation

Large obstruction of the left pulmonary artery at the first bifurcation

Illustrates the extensive bilateral pulmonary emboli present

At the higher acuity facility, echocardiogram showed a mildly dilated right ventricular cavity with moderately reduced function and diffuse hypokinesis. Venous doppler studies of the right and left lower extremities were negative for thrombosis. The patient underwent radiological insertion of a catheter into the pulmonary artery for catheter-directed tPA therapy. After the catheter was removed, an IVC filter was inserted. Patient was anticoagulated and sent home after 4 days in the intensive care unit.

A small number of case reports have reported a systolic murmur in the context of pulmonary embolism with right heart strain [ 3 ]. We present this case report illustrating an otherwise healthy 20-year-old female exhibiting a systolic murmur with confirmed bilateral pulmonary embolism by a CT angiogram of the chest without evidence of valvular disease on echocardiogram. The likely source of the flow murmur, heard only posteriorly, was turbulent pulmonary arterial flow in the posterior segments, caused by clot burden. We believe this case in addition to other previous published cases reinforces the association between massive pulmonary embolism and a systolic murmur. A new murmur such as this could be of critical importance in the presentation of acute pulmonary embolism, especially in the setting of a patient who is unable to undergo diagnostic imaging. Faced with diagnostic uncertainty in an acutely ill patient, this finding may serve as an additional piece of information to aid the clinician in determining whether the patient may be a candidate for thrombolytics for suspected PE, especially in the deteriorating patient whom further diagnostic studies may not be obtainable. Patients presenting with a new systolic murmur and other pulmonary symptoms should have increased suspicion for massive pulmonary emboli. More case studies and further research are needed to determine the efficacy of this murmur for diagnostic purposes.

Limitations

This case report does have some weaknesses. We were unable to record the murmur due to a lack of necessary equipment. Even with these limitations, we believe there is strong evidence to support a link between the systolic murmur and the pulmonary embolism.

Availability of data and materials

The data generated and analyzed for this case study are publicly available and included in the references section of this article.

Abbreviations

Computed tomography

Computed tomography angiogram

• Pulmonary embolism

Bĕlohlávek J, Dytrych V, Linhart A. Pulmonary embolism, part I: epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism. Exp Clin Cardiol. 2013;18(2):129–38.

PubMed   PubMed Central   Google Scholar  

Beckman MG, Hooper WC, Critchley SE, Ortel TL. Venous thromboembolism: a public health concern. Am J Prev Med. 2010;38:S495–501.

Article   Google Scholar  

Jingi AM, Amougou SN, Jemea B, Ouankou CN, Foutko A, Ateba NA, Nkoke C. Low-pitch peripheral systolic murmur associated with pulmonary embolism in the acute phase: a report of two cases. Clinical Case Reports. 2018;6(4):621–5. https://doi.org/10.1002/ccr3.141 .

Article   PubMed   PubMed Central   Google Scholar  

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Acknowledgements

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No funding was provided or solicited for the creation and publication of this case study.

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Temple University, 1801 North Broad Street, Philadelphia, PA, 19122, USA

Cain M. Dudek

Evangelical Community Hospital, 1 Hospital Drive, Lewisburg, 17837, PA, USA

Kelly R. McCracken & B. James Connolly

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KRM was the primary medical clinician and contributed to the patient’s background and hospital timeline. BJC supervised medical decisions and followed the patient’s hospital course after leaving the emergency department. CMD was involved in patient care and a major contributor to the writing of the manuscript. All three authors were heavily involved with reading, reviewing, editing, and approving the final manuscript.

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Dudek, C.M., McCracken, K.R. & Connolly, B.J. Case report: systolic murmur associated with pulmonary embolism. Int J Emerg Med 12 , 32 (2019). https://doi.org/10.1186/s12245-019-0250-y

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Article Contents

Introduction, patient’s perspective, lead author biography, acknowledgements, data availability.

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Expanding outpatient management of low-risk pulmonary embolism to the pregnant population: a case series

Conflict of interest: None declared.

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David R Vinson, Nareg H Roubinian, Ashok P Pai, Jeffrey D Sperling, Expanding outpatient management of low-risk pulmonary embolism to the pregnant population: a case series, European Heart Journal - Case Reports , Volume 8, Issue 9, September 2024, ytae441, https://doi.org/10.1093/ehjcr/ytae441

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Outpatient treatment of pregnant patients with acute pulmonary embolism (PE) is recommended by some obstetric and haematology societies but has not been described in the literature. Little is known about patient selection and clinical outcomes.

We report two cases of pregnant patients diagnosed with acute PE. The first, at 9 weeks of gestational age, presented to the emergency department with 12 h of pleuritic chest pain and was diagnosed with segmental PE. She was normotensive and tachycardic without evidence of right ventricular dysfunction. She received multispecialty evaluation, was deemed suitable for outpatient management, and, after 12 h of monitoring, was discharged home on enoxaparin with close follow-up. The second case, at 30 weeks of gestational age, presented to obstetrics clinic with 3 days of dyspnoea. Vital signs were normal except for tachycardia. She was referred to labour and delivery, where she was diagnosed with segmental PE. Her vital signs were stable, and she had no evidence of right ventricular dysfunction. After 6 h of monitoring, she was discharged home on enoxaparin with close follow-up. Neither patient developed antenatal complications from their PE or its treatment.

This case series is the first to our knowledge to describe patient and treatment characteristics of pregnant patients with acute PE cared for as outpatients. We propose a definition for this phenomenon and discuss the benefits of and provisional selection criteria for outpatient PE management, while engaging with professional society guidelines and the literature. This understudied practice warrants further research.

Outpatient management of acute pulmonary embolism (PE) in pregnancy can be safe and effective in selected patients.

Professional societies recommend against outpatient antenatal PE care for those with haemodynamic instability, significant comorbidities or clot burden, or lack of home support.

Select non-gravid patients with acute low-risk pulmonary embolism (PE) in the emergency department (ED) and specialty clinics are managed safely and effectively without hospitalization. 1–3 In some settings, primary care physicians diagnose and treat acute PE in outpatient clinics without referral to a specialty clinic, ED, or inpatient ward. 4 Professional society guidelines, including the European Society of Cardiology (ESC) and the American College of Chest Physicians, universally have recommended outpatient PE treatment for non-gravid patients with low-risk characteristics. 5 , 6

Pregnant patients, however, have been systematically excluded from outpatient PE research. 7 Little has been published on outpatient PE management during pregnancy. 8 Society guidelines, therefore, have crafted their site-of-care recommendations for antenatal PE based on expert opinion, inferred from non-gravid research. The American College of Obstetricians and Gynecologists (ACOG), the American Society of Hematology (ASH), and the British Thoracic Society have recommended outpatient PE management for lower-risk pregnant patients ( Table 1 ). 7 , 9 , 10 Several society guidelines do not specifically address the question of site-of-care management. 5 The Hestia study investigators from the Netherlands, on the other hand, cautioned against outpatient management of gravid patients with acute PE, although without providing explanation ( Table 2 ). 11

Contraindications for outpatient management of acute pulmonary embolism in pregnant persons according to US professional society guidelines a

N/A, not applicable.

a These simple, sensible criteria for ambulatory care mirror those of the 2016 guidelines from the American College of Chest Physicians (CHEST), written for non-gravid patients, who should be ‘clinically stable with good cardiopulmonary reserve; no contraindications such as recent bleeding, severe renal or liver disease, or severe thrombocytopenia (i.e. <70 000/mm 3 ); expected to be compliant with treatment; and the patient feels well enough to be treated at home’. 6

Two popular validated risk scores used to guide site-of-care decision-making among non-gravid patients with acute pulmonary embolism

PE, pulmonary embolism.

a Gastrointestinal bleeding or surgery ≤ 2 weeks ago, stroke ≤ 1 month ago, bleeding disorder or platelet count < 75 × 10⁹/L, uncontrolled hypertension (systolic blood pressure > 180 mmHg or diastolic blood pressure > 110 mmHg), or by clinician judgment.

b Systolic blood pressure < 100 mmHg and heart rate > 100 b.p.m., needing intensive care, or by clinician judgment.

c By clinician judgment.

d A total point score for a given patient is obtained by summing the patient’s age in years and the points for each applicable prognostic variable. Point scores correspond with the following classes that estimate escalating risks of 30-day all-cause mortality: ≤65 Class I, very low risk; 66–85 Class II, low risk; 86–105 Class III, intermediate risk; 106–125 Class IV, high risk; >125 Class V, highest risk.

e The most abnormal vital signs in the direction of interest recorded during the diagnostic evaluation and observation period.

f Acute or pre-existing disorientation, lethargy, stupor, or coma.

g With or without supplemental oxygenation.

Outpatient management of acute antenatal PE has not been described in the literature. Here, we report two cases of pregnant patients diagnosed with PE in the first and third trimesters, respectively, who were treated safely as outpatients. We then discuss three questions about outpatient management of antenatal PE: What is it? Why might it be preferable? Who may be eligible ( Figure 1 )?

Three principal questions about outpatient management of antenatal pulmonary embolism.

A healthy 35-year-old woman gravida 2 and para 0 at 9 weeks and 4 days presented to a community-based ED with 12 h of gradual-onset mild-to-moderate pleuritic chest and thoracic back pain. She had no dyspnoea or limb symptoms. Six days earlier, during her first obstetrics appointment, she had been started on prophylactic dose enoxaparin because of two distant, provoked venous thromboembolism (VTE) episodes years prior, the first while taking oestrogen-containing oral contraceptives and the second 4 weeks after COVID-19 ( Tables 3 and 4 ). She had had a prior negative inherited thrombophilia evaluation and no other relevant medical history.

Patient, diagnostic, and treatment characteristics of two pregnant patients with acute pulmonary embolism treated as outpatients

ACOG, American College of Obstetricians and Gynecologists; ASH, American Society of Hematology; ED, emergency department; L&D, labour and delivery; PE, pulmonary embolism.

a Foetal doses of radiation from pulmonary vascular imaging are lower than the background radiation exposure (∼1 mGy) to which a foetus is naturally exposed during pregnancy. The American College of Obstetricians and Gynecologists (2018) explains the radiation exposure as follows: ‘Although the foetal exposure from ventilation–perfusion is low (∼0.32–0.64 mGy), mean foetal doses associated with helical CT are lower (0.0033–0.02 mGy for the first trimester, 0.0079–0.0767 mGy for the second trimester, and 0.0513–0.1308 mGy for the third trimester)’. 9

b Per professional society guidelines. 5–7

Timeline of historical and treatment components of care of two pregnant patients with acute pulmonary embolism treated as outpatients

On admission, the patient’s vital signs were as follows: temperature 36.6°C, blood pressure of 132/69 mmHg, heart rate of 105 b.p.m., respiratory rate of 19 breaths/min, and room-air oxygen saturation of 95%. Her body mass index was 30 kg/m 2 . Physical examination was otherwise normal. Bedside ultrasonography confirmed a singleton intrauterine pregnancy. Twelve-lead electrocardiogram, complete blood count, basic chemistry panel, and troponin were unremarkable. Her D-dimer level was elevated at 1.92 mg/L (normal for non-pregnancy < 0.5 mg/L). B-type natriuretic peptide was not ordered.

The emergency physician consulted the on-call obstetrician, who recommended bilateral lower extremity compression ultrasonography: if positive, treat for deep vein thrombosis with presumptive PE, and if negative, proceed to CTPA. 5 , 13 Ultrasonography was negative. Computed tomography pulmonary angiography identified unilateral segmental PE and absence of right ventricular dilatation ( Figure 2 ). Echocardiography was not indicated. 5 Maternal–foetal medicine (MFM) and haematology were consulted, recommending starting therapeutic dose weight-based enoxaparin (1 mg/kg q12 h) in the ED and continuing it throughout pregnancy, with anticoagulation at least 6-week postpartum. An internal medicine physician specializing in inpatient care was consulted. On re-evaluation, the patient was haemodynamically stable, with improved pain, and able to ambulate without difficulty or desaturation. Her resting heart rate varied from 93 to 109 and increased during ambulation to 113 b.p.m. Her PE Severity Index score 12 (55 points = 35 points for age plus 20 points for tachycardia ≥ 110 b.p.m.) placed her in the lowest risk classification (Class I), although her consultants acknowledged that the index has not been validated in pregnancy ( Table 2 ). The internist documented that the patient reported adequate home support and resources. The patient was discharged home from the ED 12 h after presentation.

Computed tomography pulmonary angiography (axial view) identified right segmental pulmonary artery filling defect (white arrow) characteristic of pulmonary embolism. The heart had a normal ratio (<0.9) of right ventricular to left ventricular diameters, supporting the absence of right ventricular dilatation. LV, left ventricle; RV, right ventricle.

She had close follow-up over the next 10 days ( Table 3 ). At each appointment, she reported symptom improvement. She continued weight-based enoxaparin throughout pregnancy without sequelae. A 39-week delivery was planned for anticoagulation management. She underwent a caesarean delivery for second-stage arrest that was complicated by a delayed postpartum haemorrhage 10 days after delivery. During this episode, her anticoagulation was briefly held, her uterus was evacuated and packed, and she was transfused with multiple blood products. She experienced a quick, complete recovery. She restarted anticoagulation, which she continued for 6-week postpartum before discontinuing ( Tables 3 and 4 ).

A 37-year-old woman gravida 2 and para 1 at 30 weeks and 3 days presented to obstetrics clinic with 3 days of rapid heart rate and moderate dyspnoea on exertion. She had no chest pain or limb symptoms. Her past medical history was remarkable for mild hypertension, diagnosed during the first trimester, managed without pharmacotherapy, and followed serially with periodic laboratory studies and symptom surveillance. She also had mild normocytic anaemia in pregnancy and had been recently diagnosed with cholestasis of pregnancy with elevated bile acids but minimal symptoms and was currently untreated. In the clinic, her heart rate was 130 b.p.m. and a 12-lead electrocardiogram showed only sinus tachycardia. She was referred to labour and delivery (L&D), where her vital signs were as follows: blood pressure of 130/85 mmHg (within her baseline range), heart rate of 126 b.p.m., and room-air oxygen saturation of 98%. Her body mass index was 37.4 kg/m 2 . Physical examination was normal except for a regular tachycardia. Foetal assessment was reassuring. Haematocrit was 29.1%, and platelet count, renal function, liver enzymes, and thyroid stimulating hormone were normal. Troponin and B-type natriuretic peptide were not ordered. Computed tomography pulmonary angiography identified a single segmental PE and absence of right ventricular dilatation. Echocardiography was not ordered. Therapeutic weight-based enoxaparin was begun. Her blood pressure and oxygen saturation remained normal throughout her stay ( Table 3 ). The patient was discharged home 6 h after presentation.

She had reassuring appointments with MFM by telephone the next day and in person 1 week after diagnosis. She continued her regular antepartum testing without incident. She underwent induction of labour at 36 weeks and 4 days for cholestasis and had an uneventful vaginal delivery. She continued enoxaparin for an additional 6-week postpartum without event ( Table 4 ).

This case series is the first to our knowledge to describe patient and treatment characteristics of pregnant patients with acute PE cared for as outpatients. Each received 6–12 h of medical care prior to discharge ( Table 3 ). This allowed confirmation of haemodynamic stability and outpatient eligibility, as well as time for patient education on anticoagulation and indications for seeking medical care ( Figure 1 ). 2 After discharge, both patients received timely follow-up and completed their antenatal course without complications.

What is outpatient management of antenatal pulmonary embolism?

We provisionally defined outpatient antenatal PE care as clinic-only care or discharge home from the ED or L&D within 24 h of registration. For ambulatory non-gravid patients with acute PE, outpatient management has been variously defined. 14 Some definitions are site-of-care specific (e.g. clinic- or ED-only), while others include a temporal component (often <24 h of observation). 1–3 Professional societies have not defined outpatient care for antenatal PE. 7 , 9 , 10 Since L&D is an inpatient unit, an L&D evaluation usually constitutes a hospitalization, except in settings with ED-based or outpatient L&D triage. For this report, we combined site-of-care with duration-of-care parameters to allow a 24-h ED or L&D stay before discharge home, a period of time that serves several important roles, enumerated in Figure 1 .

Why might outpatient care be preferable in eligible patients?

The evidence for the benefits of outpatient PE management is drawn from studies of non-gravid patients. In that population, outpatient treatment is associated with higher patient satisfaction and social functioning without negative impact on outcomes, sparing patients the inconvenience, costs, and risks associated with unnecessary inpatient care. 1 , 15 The benefits of outpatient care extend beyond the participating patients to the larger healthcare system. Avoiding tying up ED and hospital beds helps direct limited healthcare resources to sicker patients who need them ( Figure 1 ). These advantages undergird professional society recommendations for outpatient PE treatment of pregnant and non-pregnant patients with low-risk characteristics. 5–7 , 9

Who may be eligible for outpatient care?

Eligibility criteria for outpatient PE management have not been studied in gravid patients as they have in their non-gravid counterparts. 1 , 2 Given the scarcity of research, eligibility recommendations from society guidelines represent reasonable expert opinion inferred from non-pregnant populations ( Table 1 ). Home-going pregnant patients should have low-risk characteristics and be able to be cared for at home, with ready access to needed pharmacotherapy, timely follow-up care, and availability of emergency care, if needed ( Figure 1 ). 6 , 16

Both cases in this series had low-risk characteristics, lacking nearly all the higher-risk characteristics for non-gravid patients delineated in the PE Severity Index and Hestia criteria, pregnancy excepted ( Tables 2 and 3 ), as well as meeting outpatient eligibility criteria of ACOG ( Tables 1 and 3 ). According to ASH guidelines, both patients also had two contraindications to outpatient care: advanced maternal age and an abnormal vital sign, namely, sinus tachycardia ( Table 1 ). 7 We agree with the treating physicians that advanced age alone (here 35 and 37 years, respectively) was not a sufficient reason to forgo outpatient management. We also agree that isolated tachycardia in an otherwise low-risk patient may not routinely require inpatient care. Heart rates are known to elevate throughout pregnancy, but not normally to the extent illustrated here: up to 113 in the first-trimester case and 133 in the third-trimester case. 17 , 18 Reassuringly, their tachycardia was not accompanied by indications of right heart enlargement or dysfunction on 12-lead electrocardiography, CTPA, or serum biomarkers. In addressing non-gravid patients with acute PE, the ESC guidelines recommended outpatient treatment for low-risk patients, i.e. haemodynamic stable patients in PE Severity Index Classes I–II with the absence of radiologic and biomarker evidence of right ventricular strain ( Table 5 ), 5 criteria that could be adapted for the pregnant population.

European Society of Cardiology classification of pulmonary embolism severity and the risk of early (in-hospital or 30 day) death 5

Copyright Oxford University Press. Used with permission.

BP, blood pressure; CTPA, computed tomography pulmonary angiography; H-FABP, heart-type fatty acid-binding protein; NT-proBNP, N-terminal pro B-type natriuretic peptide; PE, pulmonary embolism; PESI, Pulmonary Embolism Severity Index; RV, right ventricular; sPESI, simplified Pulmonary Embolism Severity Index; TTE, transthoracic echocardiogram.

a One of the following clinical presentations (see table 4 in Konstantinides et al . 5 ): cardiac arrest, obstructive shock (systolic BP < 90 mmHg or vasopressors required to achieve a BP of ≥90 mmHg despite an adequate filling status, in combination with end-organ hypoperfusion), or persistent hypotension (systolic BP < 90 mmHg or a systolic BP drop of ≥40 mmHg for >15 min, not caused by new-onset arrhythmia, hypovolaemia, or sepsis).

b Prognostically relevant imaging (TTE or CTPA) findings in patients with acute PE, and the corresponding cut-off levels, are graphically presented in Figure 3 in Konstantinides et al . 5 , and their prognostic value is summarized in Supplementary Data Table 3 in Konstantinides et al . 5

c Elevation of further laboratory biomarkers, such as NT-proBNP ≥ 600 ng/L, H-FABP ≥ 6 ng/mL, or copeptin ≥ 24 pmol/L, may provide additional prognostic information. These markers have been validated in cohort studies, but they have not yet been used to guide treatment decisions in randomized controlled trials.

d Haemodynamic instability, combined with PE confirmation on CTPA and/or evidence of RV dysfunction on TTE, is sufficient to classify a patient into the high-risk PE category. In these cases, neither calculation of the PESI nor measurement of troponins or other cardiac biomarkers is necessary.

e Signs of RV dysfunction on TTE (or CTPA) or elevated cardiac biomarker levels may be present, despite a calculated PESI of I and II or an sPESI of 0. Until the implications of such discrepancies for the management of PE are fully understood, these patients should be classified into the intermediate-risk category.

Other promising risk scores already designed for the unique physiology of pregnancy are vital sign scoring systems that alert clinicians of impending clinical deterioration among gravid patients, e.g. the new Maternal Early Warning Score (MEWS). 18 These have not been well tested among patients with antenatal PE, but their counterpart scores used in non-gravid populations perform well in predicting early deterioration in acute PE. 19 The absence of worrisome vital sign parameters in MEWS, for example, could objectively corroborate clinical impressions that low-risk patients were eligible for outpatient care.

In both of our cases, outpatient management was a safe course of action. The safety of outpatient care is best assessed by lack of short-term cardiopulmonary decompensation within the first 5–10 days. 3 , 20 A PE-related complication beyond this early treatment period is unlikely to have been prevented or mitigated by 2–3 days of initial hospitalization. Neither patient had an early complication following discharge, nor throughout the remainder of their pregnancy. Case 1 experienced a delayed postpartum haemorrhage, which occurred 5 months after PE diagnosis and was unrelated to initial site-of-care selection.

Several health system characteristics facilitated outpatient care of these two pregnant patients with acute PE. First, the diagnosticians had prognostic testing capabilities and specialists at hand to assist with risk stratification and site-of-care decision-making. Second, patients were health plan members with ready access to necessary pharmacotherapy and timely follow-up care with outpatient clinicians, as well as around-the-clock access to call centre advice nurses and ED care if needed. Moreover, the system had experience with outpatient PE treatment of non-gravid patients from the ED and primary care clinics. 3 , 4 Healthcare settings without these characteristics might not be as prepared for outpatient management of antenatal PE.

Home vital sign monitoring devices might bolster a health system’s ability to ensure their patients’ continued low-risk status in the days following discharge. Although not studied, home monitoring tools could serve as adjuncts to symptom self-surveillance, detecting early changes in pulse oximetry and heart rate, as had been done successfully during home treatment of patients with COVID-19. Device-detected vital sign changes have helped alert diagnosticians to the development of post-operative PE. There may be a similar role for vital sign monitoring devices to help detect PE expansion and recurrence.

Research on outpatient antenatal pulmonary embolism management

The paucity of described cases of outpatient antenatal PE care in the literature prevented us from undertaking comparisons. Little has been published on outpatient treatment in pregnant patients. The 2018 ASH guidelines 7 identified only one peer-reviewed study, a 2007 multicentre prospective UK observational study of 110 gravid patients with acute VTE, 16 of whom were treated as outpatients. 8 The investigators did not specify if any of these 16 outpatients had acute PE. Moreover, characteristics of the outpatient sub-cohort were not presented, precluding an assessment of whether those selected for outpatient care had low-risk characteristics. Treatment was often provided by an obstetrician or haematologist or both. Emergency physicians were not involved, unless they fell in the category of generalists, who saw 26% of the cohort. The nature of follow-up was not reported. None of the 110 patients experienced recurrent VTE or death, although the time course was not described. Besides this one study, the ASH guidelines also identified a short abstract in the literature, a small single-centre Canadian study of 22 pregnant patients with acute VTE, 16 of whom were treated as outpatients. 7 As with the UK study, this also failed to specify the number of patients who had PE and not isolated DVT.

Far more research is needed on this understudied topic of PE management. In light of the dearth of evidence in support of outpatient care of antenatal PE, ASH recommended that ‘studies examining rates of hospital admission after initiation of outpatient therapy in pregnant patients should be undertaken’ to help inform decision-making ‘to identify pregnant patients who require hospital admission for initial management’. 7 We hope this case series is the first of many studies addressing this important gap in the literature and helping expand safe outpatient PE management to the low-risk pregnant population.

I received very thorough care in the ER, including evaluations by several different specialists. The team was careful to make sure I was in good condition and explained everything to me, plus they booked follow-up appointments before letting me go. I’m glad I didn’t have to stay. I was ready to go home and recover where I would be much more comfortable.

David R. Vinson is a senior emergency physician with The Permanente Medical Group, an adjunct investigator with the Kaiser Permanente Division of Research, and a co-chair of the CREST Network in Oakland, California ( https://www.kpcrest.net ). His primary research seeks to improve the care of patients with pulmonary embolism and of patients with atrial fibrillation and flutter. He also enjoys mentoring undergraduates, medical students, residents, and junior faculty via collaborative research projects.

We would like to thank our two patients for their enthusiastic participation and The Permanente Medical Group for their strong support of clinical research.

Consent: The authors confirm, in line with COPE guidance, that written consent for the submission and publication of this case series has been obtained from both patients.

Funding: This work was supported by the Kaiser Permanente Northern California Community Health Programme (2023 #212226).

Additional data underlying this article will be shared on reasonable request to the corresponding author.

Roy PM , Penaloza A , Hugli O , Klok FA , Arnoux A , Elias A , et al.  Triaging acute pulmonary embolism for home treatment by Hestia or simplified PESI criteria: the HOME-PE randomized trial . Eur Heart J 2021 ; 42 : 3146 – 3157 .

Google Scholar

Vinson DR , Aujesky D , Geersing GJ , Roy PM. Comprehensive outpatient management of low-risk pulmonary embolism: can primary care do this? A narrative review . Perm J 2020 ; 24 : 19 . 163 .

Vinson DR , Mark DG , Chettipally UK , Huang J , Rauchwerger AS , Reed ME , et al.  Increasing safe outpatient management of emergency department patients with pulmonary embolism: a controlled pragmatic trial . Ann Intern Med 2018 ; 169 : 855 – 865 .

Vinson DR , Hofmann ER , Johnson EJ , Rangarajan S , Huang J , Isaacs DJ , et al.  Management and outcomes of adults diagnosed with acute pulmonary embolism in primary care: community-based retrospective cohort study . J Gen Intern Med 2022 ; 37 : 3620 – 3629 .

Konstantinides SV , Meyer G , Becattini C , Bueno H , Geersing GJ , Harjola VP , et al.  2019 ESC guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS) . Eur Heart J 2020 ; 41 : 543 – 603 .

Stevens SM , Woller SC , Kreuziger LB , Bounameaux H , Doerschug K , Geersing GJ , et al.  Antithrombotic therapy for VTE disease: second update of the CHEST guideline and expert panel report . Chest 2021 ; 160 : e545 – e608 .

Bates SM , Rajasekhar A , Middeldorp S , McLintock C , Rodger MA , James AH , et al.  American Society of Hematology 2018 guidelines for management of venous thromboembolism: venous thromboembolism in the context of pregnancy . Blood Adv 2018 ; 2 : 3317 – 3359 .

Voke J , Keidan J , Pavord S , Spencer NH , Hunt BJ , British Society for Haematology Obstetric Haematology Group . The management of antenatal venous thromboembolism in the UK and Ireland: a prospective multicentre observational survey . Br J Haematol 2007 ; 139 : 545 – 558 .

American College of Obstetricians and Gynecologists . ACOG practice bulletin no. 196: thromboembolism in pregnancy . Obstet Gynecol 2018 ; 132 : e1 – e17 .

Howard L , Barden S , Condliffe R , Connolly V , Davies CWH , Donaldson J , et al.  British Thoracic Society guideline for the initial outpatient management of pulmonary embolism (PE) . Thorax 2018 ; 73 : ii1 – ii29 .

Zondag W , Mos IC , Creemers-Schild D , Hoogerbrugge AD , Dekkers OM , Dolsma J , et al.  Outpatient treatment in patients with acute pulmonary embolism: the Hestia study . J Thromb Haemost 2011 ; 9 : 1500 – 1507 .

Aujesky D , Roy PM , Verschuren F , Righini M , Osterwalder J , Egloff M , et al.  Outpatient versus inpatient treatment for patients with acute pulmonary embolism: an international, open-label, randomised, non-inferiority trial . Lancet 2011 ; 378 : 41 – 48 .

Leung AN , Bull TM , Jaeschke R , Lockwood CJ , Boiselle PM , Hurwitz LM , et al.  An official American Thoracic Society/Society of Thoracic Radiology clinical practice guideline: evaluation of suspected pulmonary embolism in pregnancy . Am J Respir Crit Care Med 2011 ; 184 : 1200 – 1208 .

Shan J , Isaacs DJ , Bath H , Johnson EJ , Julien D , Vinson DR. “ Outpatient management” of pulmonary embolism defined in the primary literature: a narrative review . Perm J 2021 ; 25 : 20 . 303 .

Roy PM , Corsi DJ , Carrier M , Theogene A , de Wit C , Dennie C , et al.  Net clinical benefit of hospitalization versus outpatient management of patients with acute pulmonary embolism . J Thromb Haemost 2017 ; 15 : 685 – 694 .

Kabrhel C , Vinson DR , Mitchell AM , Rosovsky RP , Chang AM , Hernandez-Nino J , et al.  A clinical decision framework to guide the outpatient treatment of emergency department patients diagnosed with acute pulmonary embolism or deep vein thrombosis: results from a multidisciplinary consensus panel . J Am Coll Emerg Physicians Open 2021 ; 2 : e12588 .

Green LJ , Mackillop LH , Salvi D , Pullon R , Loerup L , Tarassenko L , et al.  Gestation-specific vital sign reference ranges in pregnancy . Obstet Gynecol 2020 ; 135 : 653 – 664 .

Gerry S , Bedford J , Redfern OC , Rutter H , Chester-Jones M , Knight M , et al.  Development of a national maternity early warning score: centile based score development and Delphi informed escalation pathways . BMJ Med 2024 ; 3 : e000748 .

Bavalia R , Stals MAM , Mulder FI , Bistervels IM , Coppens M , Faber LM , et al.  Use of the National Early Warning Score for predicting deterioration of patients with acute pulmonary embolism: a post-hoc analysis of the YEARS study . Emerg Med J 2023 ; 40 : 61 – 66 .

Kabrhel C , Sacco W , Liu S , Hariharan P. Outcomes considered most important by emergency physicians when determining disposition of patients with pulmonary embolism . Int J Emerg Med 2010 ; 3 : 239 – 264 .

Author notes

• pulmonary embolism
• ambulatory care services
• outpatients
• prenatal care

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Pulmonary embolism: update on management and controversies

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• Lisa Duffett , associate scientist , assistant professor 1 2 ,
• Lana A Castellucci , scientist , assistant professor 1 2 ,
• Melissa A Forgie , vice dean of undergraduate medical education and professor of medicine 2
• 1 Clinical Epidemiology Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada
• 2 Department of Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada
• Correspondence to: L A Castellucci lcastellucci{at}toh.ca

Pulmonary embolism is a common and potentially fatal cardiovascular disorder that must be promptly diagnosed and treated. The diagnosis, risk assessment, and management of pulmonary embolism have evolved with a better understanding of efficient use of diagnostic and therapeutic options. The use of either clinical probability adjusted or age adjusted D-dimer interpretation has led to a reduction in diagnostic imaging to exclude pulmonary embolism. Direct oral anticoagulation therapies are safe, effective, and convenient treatments for most patients with acute venous thromboembolism, with a lower risk of bleeding than vitamin K antagonists. These oral therapeutic options have opened up opportunities for safe outpatient management of pulmonary embolism in selected patients. Recent clinical trials exploring the use of systemic thrombolysis in intermediate to high risk pulmonary embolism suggest that this therapy should be reserved for patients with evidence of hemodynamic compromise. The role of low dose systemic or catheter directed thrombolysis in other patient subgroups is uncertain. After a diagnosis of pulmonary embolism, all patients should be assessed for risk of recurrent venous thromboembolism to guide duration of anticoagulation. Patients with a venous thromboembolism associated with a strong, transient, provoking risk factor can safely discontinue anticoagulation after three months of treatment. Patients with an ongoing strong risk factor, such as cancer, or unprovoked events are at increased risk of recurrent events and should be considered for extended treatment. The use of a risk prediction score can help to identify patients with unprovoked venous thromboembolism who can benefit from extended duration therapy. Despite major advances in the management of pulmonary embolism, up to half of patients report chronic functional limitations. Such patients should be screened for chronic thromboembolic pulmonary hypertension, but only a small proportion will have this as the explanation of their symptoms. In the remaining patients, future studies are needed to understand the pathophysiology and explore interventions to improve quality of life.

Series explanation: State of the Art Reviews are commissioned on the basis of their relevance to academics and specialists in the US and internationally. For this reason they are written predominantly by US authors

Contributors: LD and LAC did the primary literature search in collaboration with a health information librarian. LD was the lead author of the manuscript, and LAC wrote the sections on choice of anticoagulation for acute pulmonary embolism, treatment of cancer associated pulmonary embolism, and duration of treatment for pulmonary embolism. MAF guided the writing of the full manuscript. All authors reviewed the full manuscript and contributed to its content and references.

Funding: LAC is supported by Heart and Stroke Foundation of Canada National New Investigator and Ontario Clinician Scientist Phase I award. LD, LAC, and MAF are investigators of the Canadian Venous Thromboembolism Clinical Trials and Outcomes Research (CanVECTOR) Network; the Network receives grant funding from the Canadian Institutes of Health Research (Funding Reference: CDT-142654). CanVECTOR’s Patient Partners platform provided support for patient engagement activities..

Competing interests: We have read and understood the BMJ policy on declaration of interests and declare the following interests: none.

Provenance and peer review: Commissioned; externally peer reviewed.

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Pulmonary Embolism Case Study: Diagnosis and Treatment

by John Landry, BS, RRT | Updated: Sep 24, 2024

A pulmonary embolism is a blockage in the pulmonary artery caused by a blood clot in the lungs. This is a life-threatening condition and results in symptoms that respiratory therapists and medical professionals must be able to identify.

This case study will explore the events leading up to a patient being diagnosed with a pulmonary embolism, as well as the treatment and management of this condition.

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Pulmonary Embolism Clinical Scenario

You are called to the emergency room to treat a 25-year-old, 67 kg female patient. She is experiencing new onset chest pain and shortness of breath. She describes her chest pain as a stabbing sensation that radiates down to her left arm and gets worse during periods of exertion. She also feels lightheaded and highly anxious. In addition, the patient has a history of allergic asthma. Her only home medications are Microgestin Fe 1/20 (i.e., birth control) and albuterol PRN . She has no history of smoking or vaping.

Patient Assessment

• The patient’s pupils are round and reactive.
• She is mildly diaphoretic.
• She is showing signs of nasal flaring without pursed-lip breathing.
• Her trachea is located in the midline.
• She has no jugular venous distention.
• She has been coughing up small amounts of blood-tinged sputum.
• She has bilateral, decreased chest rise.
• Auscultation reveals crackles and a third heart sound.
• Palpation reveals normal tactile fremitus.
• Her percussion findings are normal at the apexes and decreased at the bases.
• She has a normal anterior-posterior chest diameter.
• Her chest is not tender to the touch.
• Her abdomen is soft and not distended.

Extremities:

• She shows no sign of digital clubbing.
• Her capillary refill time is 4 seconds.
• Her fingertips are slightly cyanotic and cool to the touch.
• She shows no signs of pedal edema.
• She has a moderately sized bruise on her right leg that is tender and warm to the touch.

Vital Signs:

• Respiratory rate: 30 breaths/min
• Heart rate: 120 beats/min
• Blood pressure: 100/75 mmHg
• Chest x-ray: Consolidation in both lung bases

Diagnosis and Treatment

Based on the patient’s assessment , history, and vital signs, what condition does the patient have, and why?

The patient is presenting with a pulmonary embolism (PE).

Key Components:

• The use of oral contraceptives is important for the diagnosis because one common side effect is hyper-coagulation.
• A bruise that is accompanied by tenderness and warmth in her leg is a sign of deep vein thrombosis (i.e., blood clot). This is important because blood clots can travel from the legs to the lungs, resulting in a pulmonary embolism.
• Other important signs include hypoxemia (i.e., low SpO2), increased capillary refill, cyanosis, and coolness to the touch. This could be caused by decreased perfusion and/or atelectasis .
• Diaphoresis and anxiety
• The patient has decreased percussion and crackles in the lung bases, which indicates atelectasis. Atelectasis can occur in patients who experience pulmonary infarction due to a pulmonary embolism.
• A third heart sound is sometimes heard in patients with a pulmonary embolism.
• Another important finding is the patient’s chest x-ray, which only shows atelectasis. A pulmonary embolism will not show up on a chest x-ray, but sometimes a wedge-shaped inflate will appear if pulmonary infarction has occurred as a result.

Bonus Point: You should have been able to recognize that, while the patient had a history of allergic asthma , their current presentation did not align with that of an asthma exacerbation. Remember that additional information may be given to you in scenario-based testing. When this happens, take note of the information in case it becomes important later on, but don’t let it distract you from the task at hand.

What tests can confirm the presence of a pulmonary embolism?

• Computed tomography pulmonary angiogram (CTPA): This is the preferred test for confirming a pulmonary embolism. The presence of a blood clot will show as a darkened area.
• V/Q scan: This is the second most preferred radiological test for a suspected pulmonary embolism. It will show a disturbance in gas distribution in the patient’s lungs when a thrombus is present.
• Pulmonary angiogram: This is the least preferred test because it is the most invasive. It involves the insertion of a catheter while dye is injected into the pulmonary artery, which will reveal the presence of an embolism.

You may also wish to recommend specific blood tests, such as D-dimer and platelet count. These will give you clues about the patient’s clotting status. D-dimer is most often used to look for the presence of a blood clot, as it will be increased if a clot is present.

It is important to remember that other factors can cause a patient’s d-dimer and clotting factors to increase; therefore, you should not rely on this test solely to confirm that a pulmonary embolism is present.

Additional Treatment

Let’s assume that you initiated the patient on oxygen therapy via nasal cannula at 2 L/min to try and correct their hypoxemia. After 20 minutes, you decided to incrementally increase the flow to 5 L/min, but there was no improvement in their oxygenation status.

Why is the patient’s SpO2 and PaO2 unresponsive to receiving supplemental oxygen?

This occurs because blood clots reduce or entirely prevent blood from flowing past a clot. Therefore, any alveoli distal to the clot will receive little to no perfusion. This decrease in perfusion prevents carbon dioxide and oxygen from effectively being exchanged at the alveolar-capillary membrane, even when the patient is ventilating normally.

This prevention of effective gas exchange due to low perfusion is part of what causes patients with a pulmonary embolism to be unresponsive to supplemental oxygen. The development of atelectasis due to pulmonary infarction secondary to a pulmonary embolism can further reduce the patient’s responsiveness to oxygen.

What other treatment methods would you recommend?

• Anticoagulants: The administration of a fast-acting anticoagulant, like heparin, and a slow-acting anticoagulant, like Warfarin should be recommended. This can help stop the existing clot from growing and to prevent new clots from forming. Patients who are prescribed Warfarin will need to have their other medications, dietary supplements, and nutrition plan reviewed. That is because medications, supplements, or food can impact the blood’s ability to clot while potentially negatively impacting the drug.
• Thrombolytic agents: The administration of thrombolytic drugs, such as altepase, streptokinase, or urokinase, can help break down the embolism. Patients who are prescribed a thrombolytic should be monitored for an increased risk of bleeding. This is especially true when prescribed heparin alongside a thrombolytic agent.
• Analgesics: These drugs can be administered for any pain the patient may be experiencing.
• Preventative actions: Ensuring the patient stays active, moves their limbs, is well-hydrated, and wears compression socks can help prevent another clot from forming.
• Pneumatic compression cuffs: These should be placed on the patient’s legs while they’re bedridden to decrease the risk of more blood clots forming.
• Surgical interventions: A pulmonary embolectomy can be performed to remove an existing clot that is not dissolved by medications. The placement of an inferior vena cava filter can also be used to prevent future clots from reaching the patient’s lungs. These filters are usually reserved for patients who are at high risk for developing further embolisms despite receiving pharmaceutical interventions.

Final Thoughts

A pulmonary embolism is a serious medical condition that can be difficult to diagnose. Respiratory therapists must be aware of the risk factors and symptoms to properly assess and treat their patients. A few key things to remember about patients with a pulmonary embolism include:

• They often present with radiating chest pain.
• They need radiological testing that is more extensive than a simple chest x-ray.
• They are often unresponsive to supplemental oxygen.

Treatment for a pulmonary embolism should be aimed at dissolving existing clots while preventing future clots from forming. Thanks for reading, and, as always, breathe easy, my friend.

Written by:

John Landry is a registered respiratory therapist from Memphis, TN, and has a bachelor's degree in kinesiology. He enjoys using evidence-based research to help others breathe easier and live a healthier life.

• Egan’s Fundamentals of Respiratory Care. 12th ed., Mosby, 2020.
• Wilkins’ Clinical Assessment in Respiratory Care. 8th ed., Mosby, 2017.
• Clinical Manifestations and Assessment of Respiratory Disease. 8th ed., Mosby, 2019.
• Tarbox, Abigail K., and Mamta Swaroop. “Pulmonary Embolism.” National Library of Medicine, Int J Crit Illn Inj Sci, Jan. 2013, www.ncbi.nlm.nih.gov/pmc/articles/PMC3665123 .
• Turetz, Meredith, et al. “Epidemiology, Pathophysiology, and Natural History of Pulmonary Embolism.” National Library of Medicine, Semin Intervent Radiol, Jan. 2018, www.ncbi.nlm.nih.gov/pmc/articles/PMC5986574 .
• Morrone, Doralisa, and Vincenzo Morrone. “Acute Pulmonary Embolism: Focus on the Clinical Picture.” National Library of Medicine, Korean Circ J., May 2018, www.ncbi.nlm.nih.gov/pmc/articles/PMC5940642 .
• Lavorini, Federico, et al. “Diagnosis and Treatment of Pulmonary Embolism: A Multidisciplinary Approach.” National Library of Medicine, Multidiscip Respir Med, 2013, www.ncbi.nlm.nih.gov/pmc/articles/PMC3878229 .

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Faqs about the clinical simulation exam (cse), pulmonary embolism: overview and practice questions, copd: overview and practice questions, pulmonary edema: overview and practice questions, pleural effusion: overview and practice questions, myocardial infarction: overview and practice questions, what is the recovery time for blood clots in the lungs, 7+ mistakes to avoid on the clinical simulation exam (cse), the 50+ diseases to learn for the clinical sims exam (cse).

Episode 21: Pulmonary Embolism

In this episode on Pulmonary Embolism we have the triumphant return of Dr. Anil Chopra, the Head of the Divisions of Emergency Medicine at University of Toronto, and Dr. John Foote the CCFP(EM) residency program director at the University of Toronto. We kick it off with Dr. Foote’s  approach to undifferentiated dyspnea and explanation of Medically Unexplained Dyspea (‘MUD’) and go on to discuss how best to develop a clinical pretest probability for the diagnosis of pulmonary embolism using risk factors, the value of the PERC rule, Well’s criteria and how clinical gestalt plays into pre-test probability. Dr. Chopra tells about the appropriate use of D-dimer to improve our diagnostic accuracy without leading to over-investigation and unwarranted anticoagulation. We then discuss the value of V/Q scan in the workup of PE, and the pitfalls of CT angiography. A discussion of anticoagulation choices follows and the controversies around thrombolysis for submassive PE closes the podcast. Dr. Chopra & Dr. Foote answer such questions as: What are the most important under-recognized risk factors for pulmonary embolism, and how does the absence of risk factors change the pre-test probability of PE? Should we be using D-dimer in pregnant patients? How does the D-dimer value change with age and how can we incorporate this into our work-up? How does an experienced doctor’s clinical gestalt compare to clinical desicion rules in working up PE? In what situations is V/Q scan preferred over CT angiogram for the diagnosis of PE? How should we manage patients with subsegmental PE found on CTA? What is the danger of aggressive fluid resuscitation in patients with massive PE? Which patients can be sent home from the ED with PE? Should we thrombolyse patients with submassive PE? What is Medically Unexplained Dyspnea (MUD) and how can we identify these patients and avoid lengthy work-ups?

Podcast: Play in new window | Download (Duration: 1:24:18 — 67.6MB)

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Written summary and blog post prepared by Claire Heslop, edited by Anton Helman March 2012

Cite this podcast as:  Chopra, A, Foote, J, Helman, A. Pulmonary Embolism. Emergency Medicine Cases. March, 2012. https://emergencymedicinecases.com/episode-21-respiratory-emergencies-1-pulmonary-embolism/. Accessed [date].

APPROACH TO THE PATIENT WITH DYSPNEA

Big Categories to Consider

• Respiratory
• The most common presentation of MI in patients >85 y.o. is dyspnea
• Effusion and tamponade may also present as dyspnea
• Anemia (Hb < 80)
• Neuromuscular (E.g. Guillan Barre)
• Metabolic acidosis of any cause

COPD patients are at higher risk than the general population for PE, CHF, pneumonia, tamponade, pneumothorax, and MI

• Rizkallah and colleagues found 20% of COPD exacerbation admissions had PE
• Suspect other processes if your patient with COPD presents atypically from their usual episodes, or if they are not improving with medical therapies for their exacerbation

Medically Unexplained Dyspnea (‘MUD’)

A condition characterized by a sensation of a need to take a deep inspiration or the feeling of an ‘oppressive’ chest plus symptoms of anxiety, in the absence of wheeze, cough, or sputum, ECG, CXR, or peak flow abnormalities, and without cardiopulmonary explanations for their dyspnea.  It has been called “the IBS of respiratory”.  Patients are often over-investigated without significant findings.  A diagnosis of MUD should not be made on a single ED visit, but should be considered in patients who have had extensive previous work-up for the same symptoms in the past.

PULMONARY EMBOLISM WORK-UP & MANAGEMENT

Risk factors and symptoms for pulmonary embolism.

Classic Risk Factors for PE:  “THROMBOSIS” T rauma/ T ravel H ypercoagulable state/ H RT R ecreational drugs (IVDU) O lder M alignancy B irth Control O besity/ O bstetrical (The risk of Pulmonary Embolism is highest in the first 6 weeks postpartum) S urgery I mmobilization S ickness

Chronic illnesses such as Lupus, CAD, CHF & COPD contribute to risk.

Varicose veins are a risk factor for Pulmonary Embolism, but when they generate clots, they may be less likely to embolize

Note: 20% of Pulmonary Embolism patients will have no identifiable risk factors at presentation.

Suspect PE when you see RAPID onset of symptoms, dyspnea+/- tachypnea, and pleuritic chest pain. Always be alert to older patients who present atypically.

D-dimer in the work-up of Pulmonary  Embolism

Overuse of the D-dimer can lead to over-investigation and anticoagulation, unless used wisely and in the correct clinical context.

Tips for using D-Dimer wisely:

• use a high sensitivity assay,
• test low risk patients,
• test when you expect it will be negative (to rule out PE),
• don’t test D-dimer if you plan to order a CT regardless

Is D-dimer useful in pregnancy?

• The American Thoracic Society Guidelines state D-dimer should not be used to rule out Pulmonary Embolism in pregnancy.
• D-dimer rises in the 2nd and 3rd trimester, and stays high post-partum.
• Cutoffs of 1.5x, 2x and 2.2x the local threshold per trimester have been suggested. **However, our experts suggest that only in the first trimester a negative D-dimer may be useful to rule out PE.**
• Guidelines for investigating for Pulmonary Embolism in pregnancy start with evaluation for signs & symptoms of DVT. If these are found, a leg doppler is done.
• If no DVT is suspected or found, order a CXR:
• *V/Q scan exposes pregnant women to less radiation than a CT scan for PE (V/Q and CT expose the fetus to similar radiation dosages; both dosages are low and well below background levels.)

What about the elderly?

• Consider adjusting the upper limit cutoff for negative D-dimer in patients older than 50
• Adjusted upper limit = age x 10

What about a patient on Warfarin?

• D-dimer can be falsely negative due to anticoagulation

Well’s criteria for pretest probability of pulmonary embolism

Use Well’s criteria (3) to assess pretest probability for Pulmonary Embolism:

Clinical signs of symptoms of DVT +3 points PE is #1 Diagnosis or equally likely +3 points Heart rate > 100 +1.5 points Immobilization at least 3 days, or surgery in the previous 4 weeks +1.5 points Previous, objectively diagnosed PE or DVT +1.5 points Hemoptysis +1 point Malignancy with treatment within 6 months, or palliative +1 point

If the patient is determined to be low risk (

Alternatively consider a rule-out criteria such as PERC (see below).

If the D-dimer is negative consider stopping the workup.

If the D-dimer is positive consider chest CTA.

If the patient is determined to be moderate risk (score 2-6 points, 16.2% incidence of PE), consider high sensitivity D-dimer testing or chest CTA.

If the D-dimer is negative consider stopping workup.If the D-dimer is positive consider chest CTA.

If the patient is determined to be high risk (score >6 points: 37.5% incidence of PE) consider chest CTA. D-dimer testing is not recommended.

Calculate Well’s Score on MD Calc

PERC Rule to help decide which low risk patients need a work-up for pulmonary embolism

The “Pulmonary Embolism Rule-Out Criteria” (PERC) is a step 2 decision support for excluding PE. If none of the eight PERC features are present in a patient that has been deemed low risk by Well’s criteria or by clinical gestalt, then no further tests are indicated.

PERC RULE: “HAD CLOTS”

H ormones (estrogen) A ge >50 D VT or PE history C oughing up blood (hemoptysis) L ower extremity swelling O 2 <95% T achycardia S urgery or trauma in past 4 weeks

The PERC rule is only accurate when applied to LOW risk patients.

Calculate PERC score on MD Calc

Update 2022: A post hoc analysis of two European prospective cohorts including 2968 patients presenting to the ED with low clinical probability of pulmonary embolism found that the removal of hemoptysis from the PERC, YEARS and PEGeD clinical decision tools did not significantly alter the the performance of these clinical decision tools or lead to a clinically significant reduction in diagnostic imaging. Abstract

What are the Chest X-Ray Findings for Pulmonary Embolism?

Although the CXR may appear unremarkable, about 75% of patients with Pulmonary Embolism have findings resulting from the clot, such as an elevated hemi-diaphragm , a unilateral pleural effusion , enlarged pulmonary arteries, and even infiltrates .

In young patients with pleuritic chest pain, a pleural effusion increases the likelihood of PE.

Uncommon findings of Pulmonary Embolism (see below) have low sensitivity for detecting PE.

Uncommon findings for Pulmonary Embolism include:

• “Westermark’s Sign” representing a region of oligemia
• Wedge shaped consolidation aka “Hampton’s Hump”

Westermark Sign

Hampton hump

ECG Findings in Pulmonary Embolism

ECG is useful to rule out other diseases, and~30% will be normal. ECG findings that may suggest PE include:

• sinus tachycardia
• RV strain pattern
• incomplete RBBB
• flipped T waves in anterior leads
• S1Q3T3 (poor sensitivity & specificity)
• flipped T waves in anterior and inferior leads, an uncommon finding which has been shown to be highly specific for PE

Do all patients with Pulmonary Embolism patients require admission?

Aujesky and colleagues reported outpatient management for PE was not inferior to management in hospital, for hemodynamically stable patients with no significant comorbidity, who could be safely anticoagulated, and closely followed as outpatients.

Once diagnosed, PE therapy begins with anticoagulation . LMWH (Fragmin or Enoxaparin) or Fondaparinux for at least 5 days and the INR=2.0-3.0, plus Warfarin

NOACs: Dabigatran (Pradaxa®), Rivaroxaban (Xarelto®), Apixaban (Eliquis®) These NOACs have been shown in large studies to be effeictive for the initial (rivaroxaban, apixaban), acute (all agents) and extended (all agents) treatment of PE. Dosages of NOACs for Pulmonary Embolism Rivaroxaban 15 mg bid x 21 days, followed by 20 mg once daily for at least 3 months Apixaban 10 mg bid x 7 days, followed by 5 mg bid Note that 5 days of therapeutic LMWH should be administered prior to the initiation of Dabigatran when this anticoagulant is used for the treatment of PE.

Massive and Submassive Pulmonary Embolism

Massive Pulmonary Embolism: acute PE with sustained hypotension (systolic blood pressure 15 minutes or requiring inotropic support, not due to another cause), pulselessness, or profound bradycardia.

Thrombolysis is indicated in massive PE .

Submassive Pulmonary Embolism: no sustained hypotension, but either RV dysfunction (based on echocardiography, CT, BNP, Tropinin or ECG evidence) and/or myocardial necrosis (based on troponin elevation).

Finally: Fluid resuscitation in Pulmonary Embolism with shock is indicated as first line support, but *resuscitate judiciously* as volume expansion may impair RV function.

For Dr. Joel Yaphe’s interpretation of the literature on submassive pulmonary see Episode Episode 61 Whislter’s Update in EM Conference Highlights 2015

For Salim Rezaie’s Best Case Ever on PE see Best Case Ever 44 Low Risk Pulmonary Embolism

Dr. Helman, Dr. Chopra and Dr. Foote have no conflicts of interest to declare

Key References

Aujesky et al. Lancet. 2011;378: 21. www.ncbi.nlm.nih.gov/pubmed/21703676

Douma et al. BMJ. 2010; 340: c1475. www.ncbi.nlm.nih.gov/pubmed/20354012

Jaff et al. Circulation. 2011; 123; 1788. www.ncbi.nlm.nih.gov/pubmed/21422387

Leung et al.Am J Respir Crit Care. 2010;184:1200. www.ncbi.nlm.nih.gov/pubmed/22086989

Rizkallah et al. Chest. 2009;135:786. www.ncbi.nlm.nih.gov/pubmed/18812453

Tillie-Leblond et al.Ann Intern Med. 2006;144:390. www.ncbi.nlm.nih.gov/pubmed/16549851

Wells et al.Thromb Haemos. 2000; 83:416. www.ncbi.nlm.nih.gov/pubmed/10744147

Witting MD, Mattu A, Rogers R, Halvorson C. Simultaneous T-wave inversions in anterior and inferior leads: an uncommon sign of pulmonary embolism. J Emerg Med. 2012;43(2):228-35.  http://www.ncbi.nlm.nih.gov/pubmed/22142671

More FOAMed Resources on Pulmonary Embolism

Scott Weingart discusses Pulmonary Embolism Treatment Options on EMCrit

Brit Long blogs on Pulmonary Embolism: Management of the Unstable Patient on emDocs

About the Author: Anton Helman

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Pulmonary embolism - saddle embolus

• Report problem with case

Citation, DOI, disclosures and case data

At the time the case was submitted for publication Jeremy Jones had no recorded disclosures.

Presentation

Shortness of breath and pleuritic chest pain.

Patient Data

Note:  This case has been tagged as "legacy" as it no longer meets image preparation and/or other case publication guidelines.

Large non-occlusive pulmonary embolus draped over the bifurcation of the main pulmonary artery; a saddle pulmonary embolus.

Case Discussion

The large embolus draped over the pulmonary artery bifurcation is non-occlusive. However, the distal pulmonary artery branches were full of occlusive thrombus and right heart pressures were high.

The decision was made to thrombolyse based on radiological burden of clot, evidence of right heart strain and her clinical signs and symptoms.

She made a complete recovery following appropriate resuscitation and thrombolysis. Follow up confirmed a Factor V Leiden deficiency.

4 articles feature images from this case

• Pulmonary embolism
• Saddle pulmonary embolism
• Factor V Leiden
• Filling defect

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• Published: 23 September 2024

Pulmonary embolism and intracardiac foreign bodies caused by bone cement leakage: a case report and literature review

• Zihan Zhao 1 , 2 ,
• Ranran Wang 1 , 2 ,
• Lihua Gao 1 , 2 &
• Meijing Zhang 1 , 2 , 3  

Journal of Cardiothoracic Surgery volume  19 , Article number:  544 ( 2024 ) Cite this article

43 Accesses

Metrics details

Percutaneous vertebroplasty (PVP) is a surgical procedure that involves injecting polymethylmethacrylate (PMMA) bone cement into the diseased vertebrae to rapidly relieve pain and strengthen the vertebrae. We reported a 73-year-old patient who underwent percutaneous vertebroplasty (PVP) surgery for thoracolumbar vertebral compression fracture. After the surgery, the patient experienced symptoms such as chest tightness and dyspnea. Further examination revealed multiple high-density foreign bodies in the blood vessels/heart and concomitant multi-organ dysfunction. It was considered that the multi-organ embolism was caused by bone cement leakage. The patient improved after undergoing surgical treatment and anticoagulant therapy.

Peer Review reports

Introduction

Percutaneous vertebroplasty (PVP) is a surgical procedure that involves injecting polymethylmethacrylate (PMMA) bone cement into the diseased vertebrae to rapidly relieve pain and strengthen the vertebrae. Complications of PVP include pain, infection, bleeding, and damage to nerve roots or adjacent organs, with the main risk often related to cement leakage [ 1 ]. This case report presents a case of multi-organ embolism after PVP surgery and describes the diagnosis and treatment process, providing reference for the diagnosis and treatment of similar patients.

Case description

A 73-year-old female was admitted to the hospital due to “chest tightness and shortness of breath for 5 days.” The patient had intermittent chest tightness and shortness of breath without obvious cause 5 days ago, accompanied by palpitations, without chest pain, radiating pain, dizziness, syncope, nausea, or vomiting. Symptoms could be relieved after resting for a few minutes. Complete laboratory tests at an outside hospital showed elevated inflammatory markers, and symptomatic anti-infective treatment was administered. However, the symptoms recurred, and upon emergency department admission to our hospital, laboratory tests showed elevated inflammatory markers, significantly elevated D-dimer and liver enzymes, and echocardiography revealed a large amount of pericardial effusion. The patient was admitted to our department for further diagnosis and treatment. Past surgical history includes appendectomy 40 years ago, PVP for compression fracture of the thoracic vertebra 1 year ago, and a repeat procedure for lumbar vertebra 10 days ago. The patient was diagnosed with pulmonary tuberculosis 50 years ago, which improved with medication. There is no history of hypertension, diabetes, renal insufficiency, hyperlipidemia, other surgeries, blood transfusions, trauma, smoking, alcohol consumption, or family hereditary diseases. On admission, vital signs were as follows: temperature 36.5 °C, heart rate 121 beats/minute, respiratory rate 20 breaths/minute, blood pressure 130/82 mmHg, and no abnormal findings on examination of the heart, lungs, and abdomen. Laboratory tests showed: white blood cell count 13.29 × 10^9/L, neutrophil percentage 78%, hemoglobin 107 g/L, platelets 160 × 10^9/L, potassium 4.42mmol/L, sodium 131.4mmol/L, urea 15.1mmol/L, creatinine 91.2 µmol/L, ALT 517.6U/L, AST 646U/L, amylase 209.8U/L, lipase 71.7U/L, D-dimer 4306 µg/L, FDP 35.86 mg/L, BNP 72.9pg/ml, TnI 0.03ng/ml, CK-MB 0.63ng/ml. Blood gas analysis did not show hypoxemia. Urine and stool routine tests and thyroid function tests were generally normal. PPD test and tuberculosis antibody were negative. ECG did not show any abnormalities. Echocardiography revealed a fluid collection in the pericardial sac, with approximate depths of 10 mm in the posterior wall of the left ventricle, 11 mm in the lateral wall of the left ventricle, 14 mm in the inferior wall of the left ventricle, 10 mm in the anterior wall of the right ventricle, and 15 mm in the free wall of the right ventricle. Lower extremity venous Doppler ultrasound did not show any abnormalities. Head CT showed lacunar infarction. The CT scan of the chest showed bilateral old changes in the lungs, bilateral pleural effusion, pericardial effusion, coronary artery calcification, high-density shadow in the right ventricle (Fig.  1 ), and high-density shadows in the bilateral pulmonary arteries (Fig.  2 ). The abdominal CT scan showed slight thickening of the left adrenal gland, duodenal diverticulum, compression fracture of the 12th thoracic and 1st lumbar vertebrae with postoperative changes, and a tubular shadow in the inferior vena cava and on the right side of the spine (Fig.  3 ).

High density shadows visible in the right ventricle

High density shadows of bilateral pulmonary arteries visible in the mediastinal window of chest CT

Tubular shadows in the inferior vena cava and on the right side of the spine

Diagnosis and treatment process

The patient was admitted to the hospital due to chest tightness and dyspnea accompanied by a large amount of pericardial effusion. Considering the emergency laboratory results of “pericardial effusion, liver dysfunction, elevated D-dimer,” combined with the patient’s history of previous tuberculosis, tuberculosis pericardial effusion was initially considered. However, the completed PPD test and tuberculosis antibody detection were both negative. Further check in chest-abdomen-pelvis CT examination suggested dense shadows in the right ventricle, high-density shadows in the bilateral pulmonary arteries, compression fractures of the 12th thoracic and 1st lumbar vertebrae with postoperative changes, intravascular and tube-shaped shadows on the right side of the spine. Based on the recent history of the patient undergoing percutaneous vertebral body augmentation, reviewing the pre-hospital imaging data (Fig.  4 ), it was clear that the symptoms of the patient were caused by multiple embolisms (inferior vena cava embolism, pulmonary embolism, hepatic embolism, pancreatic embolism, and foreign body in the heart) resulting from the fracture of bone cement after the percutaneous vertebral body augmentation procedure. Subsequent thrombosis occurred. After treatment with anticoagulants, hepatoprotective agents, diuretics, and anti-infective therapy, the above abnormal indicators improved compared to before. The patient underwent the removal of the foreign body from the heart and cardiac repair under cardiopulmonary bypass, and postoperatively, the patient’s vital signs were stable, and the condition improved. Follow-up examinations showed no abnormalities in various indicators.

A Abdominal CT sagittal map after bone cement surgery; B Follow up abdominal CT sagittal map after admission

The PVP procedure involves injecting PMMA bone cement into the diseased vertebra to rapidly relieve pain and strengthen the vertebra. It is commonly used to treat osteoporotic vertebral compression fractures, vertebral metastases, multiple myeloma and vertebral hemangiomas [ 1 ]. With advancements in technology, new techniques such as percutaneous kyphoplasty (PKP) [ 2 ] and bone cement augmented pedicle screw fixation (BCAPSF) [ 3 ] have been developed to achieve better therapeutic effects and lower postoperative complications. Complications associated with PVP and related procedures primarily include pain, infection, bleeding, and damage to nerve roots or adjacent organs. The main risks are often related to cement leakage. PMMA, being a foreign body, is not absorbed by the body and is considered to have potential thrombogenicity due to its irregular shape and porous surface. While in most patients, the cement particles are small and dispersed, leading to clinically inconspicuous symptoms in case of embolism, there have been reported cases of fatal complications such as pulmonary embolism, paradoxical cerebral embolism, right ventricular perforation, renal artery embolism, and acute respiratory distress syndrome [ 4 ].

Pulmonary Cement Embolism (PCE) is a relatively rare postoperative complication of percutaneous vertebroplasty (PVP), mainly associated with cement leakage. The vast majority of cases do not present with obvious clinical symptoms. However, some patients may exhibit non-life-threatening clinical symptoms such as chest pain, dyspnea, tachypnea, tachycardia, cough, hemoptysis, palpitations, and dizziness. These symptoms may be transient or persistent. The most severe manifestation of PCE involves embolism-induced hemodynamic abnormalities, leading to symptoms such as pulmonary hypertension, heart failure, and potentially progressing to respiratory or cardiac arrest, shock, or even death. The pathway for bone cement pulmonary embolism leakage involves the cement initially entering the paravertebral venous plexus, then entering the vertebral venous system, and ultimately reaching the pulmonary artery and its branches [ 5 ]. Common risk factors include the location of the fracture, the number of segments (more common in thoracic vertebrae [ 6 ]), the type of fracture or bone destruction (more common in tumor-related fractures [ 7 ]), the amount of bone cement, the mixing ratio, viscosity, state of the bone cement [ 8 ] and the surgical approach [ 9 ].Some studies [ 6 , 10 ] have confirmed that the number of affected vertebrae, the location of the lesion, the puncture pathway, the duration of surgery, and the amount of PMMA injected are independent risk factors for PCE. If cement leaks into the paravertebral venous plexus of the thoracic vertebrae, the incidence of PCE is significantly higher. The most commonly used imaging examinations are chest X-ray (1-6.8%) or CT (2.1-26%). The imaging features show tubular or branching high-density opacities corresponding to the distribution of arteries [ 11 ], and cement emboli can often be found in the paravertebral veins and the azygos venous system. In recent years, the selection of some emerging surgical methods has reduced the incidence of complications for preventing cement leakage, such as low-dose cement injection [ 12 ], the use of high-viscosity bone cement [ 8 ], the application of other materials (special screws [ 3 ], etc.), the selection of different surgical approaches (midline approach, Wiltse approach, unilateral approach [ 13 ]), and the use of some special techniques (pre-filling technique [ 14 ]). Due to the unpredictable nature of this complication, it is recommended to conduct postoperative chest X-ray examinations to exclude this diagnosis, even in asymptomatic patients. Currently, there are no standard guidelines for the treatment of PCE patients. Treatment plans often depend on the severity of symptoms and the location of the cement embolus. For patients with mild or no symptoms, observation or continuous anticoagulant therapy for 3–6 months may be considered. For patients with severe symptoms or hemodynamically unstable conditions, most studies still recommend surgical removal as the treatment of choice [ 15 ].

The intracardiac cement embolism (ICE) is a relatively rare but potentially life-threatening complication, with a reported low incidence rate (3.9%) in a single-center retrospective analysis, most of which coexist with PCE, and ICE-related symptoms and complications (0.3%) are even rarer [ 16 ]. After bone cement enters the ventricle, it can lead to tricuspid regurgitation [ 17 ], heart failure, cardiac perforation, and can further migrate to the pulmonary artery, causing symptoms such as chest pain, dyspnea, and shock, posing a life-threatening risk. Intracardiac bone cement embolism often occurs when the venous system cement embolism ruptures and circulates to the heart, and due to the presence of broken ends, there is a relatively high risk of perforation or valve dysfunction. Currently, most studies [ 18 , 19 ] recommend intervention or open surgery to remove the cement for treatment, but a small number of studies [ 20 ] also suggest that anticoagulant therapy may be considered for asymptomatic intracardiac embolism to promote encapsulation and reduce potential thrombus formation. Ziad et al. [ 21 ] found through a literature review that at present, intracardiac cement embolism is a rare complication after vertebroplasty or kyphoplasty. Most cases were diagnosed during surgery or in a short time after surgery, and in most cases, open-heart surgery was chosen to remove the embolism, while a few chose to use catheter technology. The safety and superiority of conservative treatment remain unclear.

In this case, the patient presented with pericardial effusion as the initial symptom. Based on the patient’s history of previous surgeries and laboratory test results, it was ultimately considered that the patient had bone cement leakage into the heart and lungs after PVP, leading to secondary liver dysfunction, thrombosis, and cardiac perforation. The patient was treated conservatively with medication, followed by removal of the foreign body from the heart and cardiac repair surgery. The patient had a good prognosis after the surgery. The purpose of reporting this case of multi-organ dysfunction after PVP is to raise awareness among clinical doctors about the potential complications of PVP, in order to achieve early diagnosis, treatment, and prevention of serious complications. It also calls for the development of new technologies or methods to reduce the occurrence of related surgical complications, or to treat complications through non-invasive means.

Data availability

No datasets were generated or analysed during the current study.

Buchbinder R, Johnston RV, Rischin KJ, et al. Percutaneous vertebroplasty for osteoporotic vertebral compression fracture. Cochrane Database Syst Rev. 2018;4(4):Cd006349.

PubMed   Google Scholar  

Jindal V, Binyala S, Kohli SS. Balloon kyphoplasty versus percutaneous vertebroplasty for osteoporotic vertebral body compression fractures: clinical and radiological outcomes. Spine Journal: Official J North Am Spine Soc. 2023;23(4):579–84.

Article   Google Scholar  

Han F, Chen H, Zhao H. Comparing percutaneous kyphoplasty with bone cement augmented pedicle screw fixation in severe thoracolumbar osteoporotic vertebral compression fracture. Asian J Surg. 2024;47(1):558–9.

Article   PubMed   Google Scholar  

Radcliff KE, Reitman CA, Delasotta LA, et al. Pulmonary cement embolization after kyphoplasty: a case report and review of the literature. Spine Journal: Official J North Am Spine Soc. 2010;10(10):e1–5.

Groen RJ, du Toit DF, Phillips FM, et al. Anatomical and pathological considerations in percutaneous vertebroplasty and kyphoplasty: a reappraisal of the vertebral venous system. Spine. 2004;29(13):1465–71.

Wang L, Lu M, Zhang X, et al. Risk factors for pulmonary cement embolism after percutaneous vertebroplasty and radiofrequency ablation for spinal metastases. Front Oncol. 2023;13:1129658.

Article   CAS   PubMed   PubMed Central   Google Scholar  

Mansour A, Abdel-Razeq N, Abuali H, et al. Cement pulmonary embolism as a complication of percutaneous vertebroplasty in cancer patients. Cancer Imaging: Official Publication Int Cancer Imaging Soc. 2018;18(1):5.

Luo AJ, Liao JC, Chen LH, Lai PL. High viscosity bone cement vertebroplasty versus low viscosity bone cement vertebroplasty in the treatment of mid-high thoracic vertebral compression fractures. Spine Journal: Official J North Am Spine Soc. 2022;22(4):524–34.

Guo H, Huang H, Shao Y, et al. Risk factors for pulmonary cement embolism (PCE) after polymethylmethacrylate augmentation: analysis of 32 PCE cases. Neurospine. 2021;18(4):806–15.

Article   PubMed   PubMed Central   Google Scholar  

Zou D, Dong S, Du W, Sun B, Wu X. Risk factor analysis of pulmonary cement embolism during percutaneous vertebroplasty or kyphoplasty for osteoporotic vertebral compression fractures. J Orthop Surg Res. 2021;16(1):312.

Ku L, Lv H, Ma X. Pulmonary artery bone cement embolization resulting from percutaneous vertebroplasty. Eur Heart J. 2023;44(1):72.

Lu LM, Ni XH, Ni JP, et al. Clinical effect of unilateral balloon infusion of low dose bone cement in PKP for osteoporotic thoracolumbar compression fractures in the elderly. Eur Rev Med Pharmacol Sci. 2022;26(10):3642–7.

Wu W, Zhang X, Li X, Yu S. Can the Unipedicular Approach Replace Bipedicular Percutaneous Balloon Kyphoplasty for the management of metastatic vertebral lesions? Acad Radiol. 2023;30(10):2147–55.

Chen LH, Tai CL, Lee DM, et al. Pullout strength of pedicle screws with cement augmentation in severe osteoporosis: a comparative study between cannulated screws with cement injection and solid screws with cement pre-filling. BMC Musculoskelet Disord. 2011;12:33.

Sun HB, Jing XS, Shan JL, Bao L, Wang DC, Tang H. Risk factors for pulmonary cement embolism associated with percutaneous vertebral augmentation: a systematic review and meta-analysis. Int J Surg (London England). 2022;101:106632.

Fadili Hassani S, Cormier E, Shotar E, et al. Intracardiac cement embolism during percutaneous vertebroplasty: incidence, risk factors and clinical management. Eur Radiol. 2019;29(2):663–73.

Duijvelshoff R, Anthonissen NFM, Morshuis WJ, Van Garsse L. Intracardiac cement embolism resulting in tricuspid regurgitation. Eur J cardio-thoracic Surgery: Official J Eur Association Cardio-thoracic Surg. 2019;55(2):366–8.

Shamekhi J, Düsing P, Sedaghat A, Kütting D, Nickenig G, Sinning JM. Healing a heart of Stone: percutaneous extraction of Cardiopulmonary Cement Embolism. JACC Cardiovasc Interventions. 2020;13(4):532–3.

Liu X, Chu P, Miao Q. Case report: open-heart removal for a cement embolism formed 10 years ago in the right ventricle and pulmonary artery. Front Cardiovasc Med. 2023;10:1221525.

Hatzantonis C, Czyz M, Pyzik R, Boszczyk BM. Intracardiac bone cement embolism as a complication of vertebroplasty: management strategy.

Audat ZA, Alfawareh MD, Darwish FT, Alomari AA. Intracardiac Leakage of Cement during Kyphoplasty and Vertebroplasty: a Case Report. Am J case Rep. 2016;17:326–30.

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Zihan Zhao, Ranran Wang, Lihua Gao & Meijing Zhang

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Zihan Zhao-Conceptualization, data curation, writing (original draft). Ranran Wang- Formal analysis, methodology, validation. Lihua Gao- Formal analysis, methodology, validation. Meijing Zhang- Conceptualization, methodology, writing (review & editing).

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Zhao, Z., Wang, R., Gao, L. et al. Pulmonary embolism and intracardiac foreign bodies caused by bone cement leakage: a case report and literature review. J Cardiothorac Surg 19 , 544 (2024). https://doi.org/10.1186/s13019-024-03049-3

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Risk stratification and management of intermediate- and high-risk pulmonary embolism.

1. Introduction

2. risk factors for pulmonary embolism, 3. pathophysiology, 4. risk stratification, 5. long-term complications, 6. management strategies, 6.1. systemic thrombolysis, 6.2. catheter-directed thrombolysis, 6.3. catheter-directed embolectomy, 6.4. surgical thrombectomy, 6.5. mechanical circulatory support, 7. selection of therapy, 8. future directions, 9. conclusions, acknowledgments, conflicts of interest.

• Wendelboe, A.M.; Raskob, G.E. Global Burden of Thrombosis: Epidemiologic Aspects. Circ. Res. 2016 , 118 , 1340–1347. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Silver, M.J.; Giri, J.; Duffy, Á.; Jaber, W.A.; Khandhar, S.; Ouriel, K.; Toma, C.; Tu, T.; Horowitz, J.M. Incidence of Mortality and Complications in High-Risk Pulmonary Embolism: A Systematic Review and Meta-Analysis. J. Soc. Cardiovasc. Angiogr. Interv. 2023 , 2 , 100548. [ Google Scholar ] [ CrossRef ]
• Martin, K.A.; Molsberry, R.; Cuttica, M.J.; Desai, K.R.; Schimmel, D.R.; Khan, S.S. Time Trends in Pulmonary Embolism Mortality Rates in the United States, 1999 to 2018. J. Am. Heart Assoc. 2020 , 9 , e016784. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Konstantinides, S.V.; Meyer, G.; Becattini, C.; Bueno, H.; Geersing, G.-J.; Harjola, V.-P.; Huisman, M.V.; Humbert, M.; Jennings, C.S.; Jiménez, D.; et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Eur. Heart J. 2020 , 41 , 543–603. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Anderson, F.A.; Spencer, F.A. Risk factors for venous thromboembolism. Circulation 2003 , 107 , I9–I16. [ Google Scholar ] [ CrossRef ]
• Rogers, M.A.M.; Levine, D.A.; Blumberg, N.; Flanders, S.A.; Chopra, V.; Langa, K.M. Triggers of hospitalization for venous thromboembolism. Circulation 2012 , 125 , 2092–2099. [ Google Scholar ] [ CrossRef ]
• Iorio, A.; Kearon, C.; Filippucci, E.; Marcucci, M.; Macura, A.; Pengo, V.; Siragusa, S.; Palareti, G. Risk of Recurrence After a First Episode of Symptomatic Venous Thromboembolism Provoked by a Transient Risk Factor: A Systematic Review. Arch. Intern. Med. 2010 , 170 , 1710–1716. [ Google Scholar ] [ CrossRef ]
• Prandoni, P.; Lensing, A.W.A.; Piccioli, A.; Bernardi, E.; Simioni, P.; Girolami, B.; Marchiori, A.; Sabbion, P.; Prins, M.H.; Noventa, F.; et al. Recurrent venous thromboembolism and bleeding complications during anticoagulant treatment in patients with cancer and venous thrombosis. Blood 2002 , 100 , 3484–3488. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Heit, J.A.; O’Fallon, W.M.; Petterson, T.M.; Lohse, C.M.; Silverstein, M.D.; Mohr, D.N.; Melton, L.J., III. Relative Impact of Risk Factors for Deep Vein Thrombosis and Pulmonary Embolism: A Population-Based Study. Arch. Intern. Med. 2002 , 162 , 1245–1248. [ Google Scholar ] [ CrossRef ]
• Marques, M.A.; Panico, M.D.B.; Porto, C.L.L.; Milhomens, A.L.M.; Vieira, J.M. Venous thromboembolism prophylaxis on flights. J. Vasc. Bras. 2018 , 17 , 215–219. [ Google Scholar ] [ CrossRef ]
• Stein, P.D.; Beemath, A.; Matta, F.; Weg, J.G.; Yusen, R.D.; Hales, C.A.; Hull, R.D.; Leeper, K.V.; Sostman, H.D.; Tapson, V.F.; et al. Clinical Characteristics of Patients with Acute Pulmonary Embolism. Am. J. Med. 2007 , 120 , 871–879. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Zöller, B.; Svensson, P.J.; Dahlbäck, B.; Lind-Hallden, C.; Hallden, C.; Elf, J. Genetic risk factors for venous thromboembolism. Expert Rev. Hematol. 2020 , 13 , 971–981. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Geerts, W.H.; Heit, J.A.; Clagett, G.P.; Pineo, G.F.; Colwell, C.W.; Anderson, F.A.; Wheeler, H.B. Prevention of venous thromboembolism. Chest 2001 , 119 , 132S–175S. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Chopard, R.; Behr, J.; Vidoni, C.; Ecarnot, F.; Meneveau, N. An Update on the Management of Acute High-Risk Pulmonary Embolism. J. Clin. Med. 2022 , 11 , 4807. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Coutance, G.; Cauderlier, E.; Ehtisham, J.; Hamon, M.; Hamon, M. The prognostic value of markers of right ventricular dysfunction in pulmonary embolism: A meta-analysis. Crit. Care 2011 , 15 , R103. [ Google Scholar ] [ CrossRef ]
• Zhang, R.Z.; Rhee, A.R.; Grossman, K.G.; Singh, A.S.A.; Nayar, A.N.; Elbaum, L.E.; Greco, A.G.; Postelnicu, R.P.; Alviar, C.A.; Bangalore, S.B. McConnell’s sign predicts normotensive shock in patients with acute pulmonary embolism. Eur. Heart J. Acute Cardiovasc. Care , 2024; in press. [ Google Scholar ] [ CrossRef ]
• Aujesky, D.; Obrosky, D.S.; Stone, R.A.; Auble, T.E.; Perrier, A.; Cornuz, J.; Roy, P.M.; Fine, M.J. Derivation and validation of a prognostic model for pulmonary embolism. Am. J. Respir. Crit. Care Med. 2005 , 172 , 10411046. [ Google Scholar ] [ CrossRef ]
• Jiménez, D.; Aujesky, D.; Moores, L.; Gómez, V.; Lobo, J.L.; Uresandi, F.; Otero, R.; Monreal, M.; Muriel, A.; Yusen, R.D.; et al. Simplification of the Pulmonary Embolism Severity Index for Prognostication in Patients With Acute Symptomatic Pulmonary Embolism. Arch. Intern. Med. 2010 , 170 , 1383–1389. [ Google Scholar ] [ CrossRef ]
• Zhou, X.-Y.; Ben, S.-Q.; Chen, H.-L.; Ni, S.-S. The prognostic value of pulmonary embolism severity index in acute pulmonary embolism: A meta-analysis. Respir. Res. 2012 , 13 , 111. [ Google Scholar ] [ CrossRef ]
• Bangalore, S.; Horowitz, J.M.; Beam, D.; Jaber, W.A.; Khandhar, S.; Toma, C.; Weinberg, M.D.; Mina, B. Prevalence and Predictors of Cardiogenic Shock in Intermediate-Risk Pulmonary Embolism. JACC Cardiovasc. Interv. 2023 , 16 , 958–972. [ Google Scholar ] [ CrossRef ]
• Zhang, R.S.; Yuriditsky, E.; Zhang, P.; Maqsood, M.H.; Amoroso, N.E.; Maldonado, T.S.; Xia, Y.; Horowitz, J.M.; Bangalore, S. Composite Pulmonary Embolism Shock Score and Risk of Adverse Outcomes in Patients with Pulmonary Embolism. Circ. Cardiovasc. Interv. 2024 , 17 , e014088. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• den Exter, P.L.; van Es, J.; Kroft, L.J.M.; Erkens, P.M.G.; Douma, R.A.; Mos, I.C.M.; Jonkers, G.; Hovens, M.M.C.; Durian, M.F.; ten Cate, H.; et al. Thromboembolic resolution assessed by CT pulmonary angiography after treatment for acute pulmonary embolism. Thromb. Haemost. 2015 , 114 , 26–34. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Sista, A.K.; Horowitz, J.M.; Tapson, V.F.; Rosenberg, M.; Elder, M.D.; Schiro, B.J.; Dohad, S.; Amoroso, N.E.; Dexter, D.J.; Loh, C.T.; et al. Indigo Aspiration System for Treatment of Pulmonary Embolism: Results of the EXTRACT-PE Trial. JACC Cardiovasc. Interv. 2021 , 14 , 319–329. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Kahn, S.R.; Hirsch, A.M.; Akaberi, A.; Hernandez, P.; Anderson, D.R.; Wells, P.S.; Rodger, M.A.; Solymoss, S.; Kovacs, M.J.; Rudski, L.; et al. Functional and Exercise Limitations After a First Episode of Pulmonary Embolism: Results of the ELOPE Prospective Cohort Study. Chest 2017 , 151 , 1058–1068. [ Google Scholar ] [ CrossRef ]
• Kahn, S.R.; Akaberi, A.; Granton, J.T.; Anderson, D.R.; Wells, P.S.; Rodger, M.A.; Solymoss, S.; Kovacs, M.J.; Rudski, L.; Shimony, A.; et al. Quality of Life, Dyspnea, and Functional Exercise Capacity Following a First Episode of Pulmonary Embolism: Results of the ELOPE Cohort Study. Am. J. Med. 2017 , 130 , 990.e9–990.e21. [ Google Scholar ] [ CrossRef ]
• Albaghdadi, M.S.; Dudzinski, D.M.; Giordano, N.; Kabrhel, C.; Ghoshhajra, B.; Jaff, M.R.; Weinberg, I.; Baggish, A. Cardiopulmonary Exercise Testing in Patients Following Massive and Submassive Pulmonary Embolism. J. Am. Heart Assoc. 2018 , 7 , e006841. [ Google Scholar ] [ CrossRef ]
• Chatterjee, S.; Chakraborty, A.; Weinberg, I.; Kadakia, M.; Wilensky, R.L.; Sardar, P.; Kumbhani, D.J.; Mukherjee, D.; Jaff, M.R.; Giri, J. Thrombolysis for pulmonary embolism and risk of all-cause mortality, major bleeding, and intracranial hemorrhage: A meta-analysis. JAMA 2014 , 311 , 2414–2421. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Meyer, G.; Vicaut, E.; Danays, T.; Agnelli, G.; Becattini, C.; Beyer-Westendorf, J.; Bluhmki, E.; Bouvaist, H.; Brenner, B.; Couturaud, F.; et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N. Engl. J. Med. 2014 , 370 , 1402–1411. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Brown, K.N.; Devarapally, S.R.; Lee, L.S.; Gupta, N. Catheter-Directed Thrombolysis of Pulmonary Embolism. In StatPearls [Internet] ; StatPearls Publishing: Treasure Island, FL, USA, 2024. Available online: http://www.ncbi.nlm.nih.gov/books/NBK536918/ (accessed on 26 April 2024).
• Kucher, N.; Boekstegers, P.; Müller, O.J.; Kupatt, C.; Beyer-Westendorf, J.; Heitzer, T.; Tebbe, U.; Horstkotte, J.; Müller, R.; Blessing, E.; et al. Randomized, Controlled Trial of Ultrasound-Assisted Catheter-Directed Thrombolysis for Acute Intermediate-Risk Pulmonary Embolism. Circulation 2014 , 129 , 479–486. [ Google Scholar ] [ CrossRef ]
• Piazza, G.; Hohlfelder, B.; Jaff, M.R.; Ouriel, K.; Engelhardt, T.C.; Sterling, K.M.; Jones, N.J.; Gurley, J.C.; Bhatheja, R.; Kennedy, R.J.; et al. A Prospective, Single-Arm, Multicenter Trial of Ultrasound-Facilitated, Catheter-Directed, Low-Dose Fibrinolysis for Acute Massive and Submassive Pulmonary Embolism: The SEATTLE II Study. JACC Cardiovasc. Interv. 2015 , 8 , 1382–1392. [ Google Scholar ] [ CrossRef ]
• Management of PE [Internet]. Am. Coll. Cardiol . Available online: https://www.acc.org/Latest-in-Cardiology/Articles/2020/01/27/07/42/Management-of-PE (accessed on 25 June 2024).
• Tapson, V.F.; Sterling, K.; Jones, N.; Elder, M.; Tripathy, U.; Brower, J.; Maholic, R.L.; Ross, C.B.; Natarajan, K.; Fong, P.; et al. A Randomized Trial of the Optimum Duration of Acoustic Pulse Thrombolysis Procedure in Acute Intermediate-Risk Pulmonary Embolism: The OPTALYSE PE Trial. JACC Cardiovasc. Interv. 2018 , 11 , 1401–1410. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Avgerinos, E.D.; Jaber, W.; Lacomis, J.; Markel, K.; McDaniel, M.; Rivera-Lebron, B.N.; Ross, C.B.; Sechrist, J.; Toma, C.; Chaer, R.; et al. Randomized Trial Comparing Standard Versus Ultrasound-Assisted Thrombolysis for Submassive Pulmonary Embolism. JACC Cardiovasc. Interv. 2021 , 14 , 1364–1373. [ Google Scholar ] [ CrossRef ]
• Shatla, I.; Iskandarani, M.E.; Khan, M.Z.; Elkaryoni, A.; Elbadawi, A.; Goel, S.S.; Saad, M.; Balla, S.; Darki, A.; Elgendy, I.Y. Ultrasound-Assisted Versus Standard Catheter-Directed Thrombolysis for Acute Pulmonary Embolism: Insights From National Inpatient Sample. J. Soc. Cardiovasc. Angiogr. Interv. 2024 , 35 , 101360. [ Google Scholar ] [ CrossRef ]
• Zhang, R.S.; Maqsood, M.H.; Sharp, A.S.P.; Postelnicu, R.; Sethi, S.S.; Greco, A.; Alviar, C.; Bangalore, S. Efficacy and Safety of Anticoagulation, Catheter-Directed Thrombolysis, or Systemic Thrombolysis in Acute Pulmonary Embolism. JACC Cardiovasc. Interv. 2023 , 16 , 2644–2651. [ Google Scholar ] [ CrossRef ]
• Tu, T.; Toma, C.; Tapson, V.F.; Adams, C.; Jaber, W.A.; Silver, M.; Khandhar, S.; Amin, R.; Weinberg, M.; Engelhardt, T.; et al. A Prospective, Single-Arm, Multicenter Trial of Catheter-Directed Mechanical Thrombectomy for Intermediate-Risk Acute Pulmonary Embolism: The FLARE Study. JACC Cardiovasc. Interv. 2019 , 12 , 859–869. [ Google Scholar ] [ CrossRef ]
• Toma, C.; Jaber, W.A.; Weinberg, M.D.; Bunte, M.C.; Khandhar, S.; Stegman, B.; Gondi, S.; Chambers, J.; Amin, R.; Leung, D.A.; et al. Acute outcomes for the full US cohort of the FLASH mechanical thrombectomy registry in pulmonary embolism. EuroIntervention J. Eur. Collab. Work. Group Interv. Cardiol. Eur. Soc. Cardiol. 2023 , 18 , 1201–1212. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Sedhom, R.; Elbadawi, A.; Megaly, M.; Athar, A.; Bharadwaj, A.S.; Prasad, V.; Cameron, S.J.; Weinberg, I.; Mamas, M.A.; Messerli, A.W.; et al. Outcomes with catheter-directed thrombolysis vs. catheter-directed embolectomy among patients with high-risk pulmonary embolism: A nationwide analysis. Eur. Heart J. Acute Cardiovasc. Care 2023 , 12 , 224–231. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Sedhom, R.; Elbadawi, A.; Megaly, M.; Jaber, W.A.; Cameron, S.J.; Weinberg, I.; Mamas, M.A.; Elgendy, I.Y. Hospital procedural volume and outcomes with catheter-directed intervention for pulmonary embolism: A nationwide analysis. Eur. Heart J. Acute Cardiovasc. Care 2022 , 11 , 684–692. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Monteleone, P.; Ahern, R.; Banerjee, S.; Desai, K.R.; Kadian-Dodov, D.; Webber, E.; Omidvar, S.; Troy, P.; Parikh, S.A. Modern Treatment of Pulmonary Embolism (USCDT vs MT): Results from a Real-World, Big Data Analysis (REAL-PE). J. Soc. Cardiovasc. Angiogr. Interv. 2023 , 3 , 101192. [ Google Scholar ] [ CrossRef ]
• Stulz, P.; Schläpfer, R.; Feer, R.; Habicht, J.; Grädel, E. Decision making in the surgical treatment of massive pulmonary embolism. Eur. J. Cardio-Thorac. Surg. Off. J. Eur. Assoc. Cardio-Thorac. Surg. 1994 , 8 , 188–193. [ Google Scholar ] [ CrossRef ]
• Aklog, L.; Williams, C.S.; Byrne, J.G.; Goldhaber, S.Z. Acute pulmonary embolectomy: A contemporary approach. Circulation 2002 , 105 , 1416–1419. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Osborne, Z.J.; Rossi, P.; Aucar, J.; Dharamsy, S.; Cook, S.; Wheatley, B. Surgical pulmonary embolectomy in a community hospital. Am. J. Surg. 2014 , 207 , 337–341. [ Google Scholar ] [ CrossRef ]
• Ismayl, M.; Ismayl, A.; Hamadi, D.; Aboeata, A.; Goldsweig, A.M. Catheter-directed thrombolysis versus thrombectomy for submassive and massive pulmonary embolism: A systematic review and meta-analysis. Cardiovasc. Revasc. Med. 2024 , 60 , 43–52. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Al-Bawardy, R.; Rosenfield, K.; Borges, J.; Young, M.N.; Albaghdadi, M.; Rosovsky, R.; Kabrhel, C. Extracorporeal membrane oxygenation in acute massive pulmonary embolism: A case series and review of the literature. Perfusion 2019 , 34 , 22–28. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• George, B.; Parazino, M.; Omar, H.R.; Davis, G.; Guglin, M.; Gurley, J.; Smyth, S. A retrospective comparison of survivors and non-survivors of massive pulmonary embolism receiving veno-arterial extracorporeal membrane oxygenation support. Resuscitation 2018 , 122 , 1–5. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Zieliński, D.; Dyk, W.; Wróbel, K.; Biederman, A. Surgical pulmonary embolectomy: State of the art. Kardiochirurgia Torakochirurgia Pol./Pol. J. Cardio-Thorac. Surg. 2023 , 20 , 111–117. [ Google Scholar ] [ CrossRef ]
• Pandya, V.; Chandra, A.A.; Scotti, A.; Assafin, M.; Schenone, A.L.; Latib, A.; Slipczuk, L.; Khaliq, A. Evolution of Pulmonary Embolism Response Teams in the United States: A Review of the Literature. J. Clin. Med. 2024 , 13 , 3984. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Chaudhury, P.; Gadre, S.K.; Schneider, E.; Renapurkar, R.D.; Gomes, M.; Haddadin, I.; Heresi, G.A.; Tong, M.Z.; Bartholomew, J.R. Impact of Multidisciplinary Pulmonary Embolism Response Team Availability on Management and Outcomes. Am. J. Cardiol. 2019 , 124 , 1465–1469. [ Google Scholar ] [ CrossRef ]
• Wright, C.; Goldenberg, I.; Schleede, S.; McNitt, S.; Gosev, I.; Elbadawi, A.; Pietropaoli, A.; Barrus, B.; Chen, Y.L.; Mazzillo, J.; et al. Effect of a Multidisciplinary Pulmonary Embolism Response Team on Patient Mortality. Am. J. Cardiol. 2021 , 161 , 102–107. [ Google Scholar ] [ CrossRef ]
• Rosovsky, R.; Chang, Y.; Rosenfield, K.; Channick, R.; Jaff, M.R.; Weinberg, I.; Sundt, T.; Witkin, A.; Rodriguez-Lopez, J.; Parry, B.A.; et al. Changes in treatment and outcomes after creation of a pulmonary embolism response team (PERT), a 10-year analysis. J. Thromb. Thrombolysis 2019 , 47 , 31–40. [ Google Scholar ] [ CrossRef ]
• Jaff, M.R.; McMurtry, M.S.; Archer, S.L.; Cushman, M.; Goldenberg, N.; Goldhaber, S.Z.; Jenkins, J.S.; Kline, J.A.; Michaels, A.D.; Thistlethwaite, P.; et al. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension. Circulation 2011 , 123 , 1788–1830. [ Google Scholar ] [ CrossRef ] [ PubMed ]
• Rivera-Lebron, B.; McDaniel, M.; Ahrar, K.; Alrifai, A.; Dudzinski, D.M.; Fanola, C.; Blais, D.; Janicke, D.; Melamed, R.; Mohrien, K.; et al. Diagnosis, Treatment and Follow Up of Acute Pulmonary Embolism: Consensus Practice from the PERT Consortium. Clin. Appl. Thromb. 2019 , 25 , 1076029619853037. [ Google Scholar ] [ CrossRef ] [ PubMed ]

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Share and Cite

Mojaddedi, S.; Jamil, J.; Bishev, D.; Essilfie-Quaye, K.; Elgendy, I.Y. Risk Stratification and Management of Intermediate- and High-Risk Pulmonary Embolism. J. Clin. Med. 2024 , 13 , 5583. https://doi.org/10.3390/jcm13185583

Mojaddedi S, Jamil J, Bishev D, Essilfie-Quaye K, Elgendy IY. Risk Stratification and Management of Intermediate- and High-Risk Pulmonary Embolism. Journal of Clinical Medicine . 2024; 13(18):5583. https://doi.org/10.3390/jcm13185583

Mojaddedi, Sanaullah, Javairia Jamil, Daniel Bishev, Kobina Essilfie-Quaye, and Islam Y. Elgendy. 2024. "Risk Stratification and Management of Intermediate- and High-Risk Pulmonary Embolism" Journal of Clinical Medicine 13, no. 18: 5583. https://doi.org/10.3390/jcm13185583

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• SCCM Pod-526 CCM: Alteplase Dosing in Pulmonary Embolism

Host Samantha Gambles Farr, MSN, AG-ACNP, FNP-C, RNFA, is joined by Roman Melamed, MD, to discuss the comparative effectiveness of reduced-dose versus full-dose alteplase for acute pulmonary embolism, focusing on patient outcomes and complications. They will highlight study findings on significant improvements in hemodynamic and respiratory parameters in both groups, with a lower rate of hemorrhagic complications in the reduced-dose group ( Melamed R, et al. Crit Care Med . 2024;52:729-742 ). Dr. Melamed is a critical care intensivist and director of the Pulmonary Embolism Program at Abbott Northwestern Hospital in Minneapolis, Minnesota, USA, and an adjunct associate professor at the University of Minnesota.

*If you are unable to play the podcast please click here to download the file .

Category: CCM Podcast

Transcript:

Dr. Gambles-Farr: Hello and welcome to the Society of Critical Care Medicine Podcast. I’m your host, Samantha Gambles-Farr. Today I’ll be speaking with Dr. Roman Melamed, MD, about the article, “Safety and Efficacy of Reduced-Dose Versus Full-Dose Alteplase for Acute Pulmonary Embolism: A Multicenter Observational Comparative Effectiveness Study,” published in the May 2024 issue of Critical Care Medicine . Dr. Melamed is a practicing critical care physician with over 20 years of experience. He currently serves as an adjunct associate professor at University of Minnesota. He is also a fellow of the American College of Chest Physicians. He is currently the director of the Pulmonary Embolism Program at Abbott Northwestern Hospital, and he also serves as the director of critical care research in the same facility. Dr. Melamed, thank you so much for being here. Before we start, do you have any disclosures to report? Dr. Melamed: No disclosures. Dr. Gambles-Farr: I’m so happy you’re here today. You are so well versed to speak to this conversation. Reading your article, I was very intrigued about something that we all, as critical care clinicians, have to manage at some point or another in our practice. We all know that pulmonary embolism is a significant cause of morbidity and mortality in critically ill patients and that patients can present with multiple signs of shock. They can require CPR, and all these things lead to long-term mortality if not treated quickly and appropriately. I feel like, with your background, this is the exact study that needed to be done and the exact person, along with your other colleagues who are listed on this paper, to take on this study. I’m very happy to have you here as an expert to discuss your findings of this paper. Could you speak a little bit to past research that we’ve seen as it relates to PEs and the utilization of alteplase historically? Dr. Melamed: Yes, thank you. And thank you for asking me to comment on this paper. The field of pulmonary embolism is quite complicated, and we’ll start with just a reminder that we deal with several types of pulmonary embolism, including massive or high-risk PE, which is associated with hypotension or shock; submassive or intermediate-risk pulmonary embolism that is not associated with hypotension but has some high-risk features such as right ventricular dysfunction, positive biomarkers, or signs of altered gas exchange; and low-risk PE. For each of these types there are treatments. The common treatment accepted for all of them is systemic anticoagulation, typically with unfractionated or low-molecular-weight heparin in a hospitalized patient. In patients with massive or high-risk PE, systemic thrombolysis has been shown to improve outcomes, including mortality. In patients with intermediate-risk PE, it’s less well established. The majority of them can be treated with systemic anticoagulation alone, but there is a subset of these patients who are right on the verge of decompensation, still not being hypotensive but having significant RV dysfunction, evidence of some hemodynamic instability presenting significant tachycardia or altered gas exchange that prompts physicians to look for additional interventions in addition to the anticoagulation. This is where the systemic thrombolysis comes in. In general, we have two regimens for the thrombolysis. The full-dose regimen is 100 mg of alteplase administered over two hours. It’s an FDA-approved regimen based on a fairly old study that compared alteplase to urokinase in patients who were getting angiograms and showed improved outcomes. However, there is no dose titration study for the alteplase. And, while systemic thrombolysis can improve outcomes, it can be associated with hemorrhagic complications. A randomized controlled study published in 2002 showed that systemic thrombolysis in patients with high-risk submassive PE reduced the risk of clinical decompensation. In this study, there wasn’t any significant increase in hemorrhagic complications. However, a more recent randomized controlled trial called the PEITHO study also confirmed that thrombolysis reduces the risk of clinical decompensation. However, there were a significant number of hemorrhagic complications. There is also some evidence that a lower dose of alteplase, such as 50 mg as opposed to 100 mg, may result in similar outcomes but less complications. That’s the reason that we wanted to look at the real-world outcomes in large health systems and try to compare full- and the reduced-dose alteplase. Dr. Gambles-Farr: Right, because we understand that having papers like this is so important as the next phase because of all the work that, as you mentioned, has been done before. But there have not been a lot of studies looking into that phase two, comparing the amount of medication that’s being given and how that can impact complications such as hemorrhagic complications. In doing the study, you had some inclusion criteria that included some propensity scores. Can you speak a little bit to that? Dr. Melamed: Yes. The cohorts who received full- versus reduced-dose thrombolysis, as expected, were somewhat different at baseline. In general, as clinicians, we instinctively tend to give higher-dose alteplase to patients with higher disease severity, especially those who have massive PE with hypertension or shock. Therefore, in order for us to compare the two dose regimens, in addition to just comparing the groups at baseline, we had to balance the groups. This was done by propensity score weighting that took into account multiple variables in patients in both groups, and balanced the reduced- and full-dose alteplase quite nicely, allowing us to compare the outcomes. Dr. Gambles-Farr: There was a large amount of detail that you guys put in your data research in comparing and looking at medical records using the EMRs to look at comorbidities, the issues that the patients had prior to them presenting, the issues that they had while they were hospitalized. That information I felt was very detailed to really give a good idea of not just the number of patients but what the patients actually had as chronic illnesses prior to their PE. I felt like that was a very detailed aspect, and it’s very well detailed in all of the tables that you have within the paper. Moving on to kind of shifting the findings, we’ve talked a lot about research in the past, why you felt like this was so important, but then also talking about your inclusion criteria. Maybe discussing some of the findings, which we’ve kind of already alluded to, but giving those specific findings that you guys had as a result of your paper. Dr. Melamed: Yes. We were able to include 284 patients, 98 treated with a full-dose and 186 treated with a reduced-dose alteplase regimen. About a third of the patients had massive PE and the rest had high-risk submassive PE. In general, the baseline characteristics in Table 1 show just a reflection of our practices. Who gets what dose regimen? As I mentioned, as expected, patients with massive PE tended to receive a full-dose regimen more often. But in the weighted cohorts, after the balancing by the propensity scoring, there was no significant difference. Overall, we looked at the abnormalities in the troponin and lactate levels. We looked at the anticoagulation or antiplatelet agents prior to the administration of systemic thrombolysis, trying to see if those were somehow factored into the development of the complications. So, overall, we felt that the propensity scoring was successful. We were able to achieve a fairly balanced group of patients for comparison. Dr. Gambles-Farr: I think that that’s an important aspect to think about in critical care when we’re managing these patients is that sometimes the medication that we’re actually giving them may not be the main reason why they may have these complications. Sometimes it’s the timing of the medications they were on before or the medications that they may be on after that medication that could increase their complications as well, particularly with like alteplase, heparin, and all those other medications that we utilize in the ICU. As with any type of research paper, there are always limitations to our studies that we perform. What were some of the limitations that you found as you moved forward in your study? Dr. Melamed: The main limitation was the retrospective observational study design, that we were limited to what we had in the charts. The study was done over a fairly long time period, about nine years. Over this time period, the electronic health records have evolved so we were limited in terms of getting all the comprehensive data in some cases. We were specifically limited in echocardiographic data, just because of how things get reported. We certainly wanted to have more echocardiographic data but had to limit our reporting to what we had. Therefore, this wasn’t the main aspect of the paper. All the potential confounders that come with the retrospective design, manual chart review, which we had to do a fair amount, just because it is almost impossible to figure out all the complications from the ICD coding, because many times they are not coded at all. We tried to do as good a job as possible, and every complication was reviewed by two researchers. In case of disagreements, they were discussed, and we tried to come to a solution. But those were limitations. Dr. Gambles-Farr: The interesting part that I found in reading this is that your study went all the way into December 31, 2020, and we know that we were in the depths of COVID during that time. So I wonder, during COVID, we did have an increase of DVTs, and I wonder if that had any impact. And that could be another study that could potentially come later on as an adjunctive thing, because a lot of our patients were having DVTs and some PEs as a result of COVID. That’s something that could also be looked at perhaps as a retrospective study as well. Dr. Melamed: This is a good point. We did not collect COVID data for this study, but it is a good point, and we noticed increased VTEs during the COVID epidemic. Dr. Gambles-Farr: Yeah, that was just me. You know, just what you see in clinical practice a lot of times will affect kind of what we think of could be the next gap that we have in research, right? So that just popped into my mind just now, thinking about, that was a whole year, well, not quite a whole year of COVID, because in the United States, we kind of started in March. But definitely pursuing and continuing this research article, as you are more than likely dealing with actively sick patients among multiple institutions, such large-scale data mining and looking into charts, that’s commendable to have been able to do that and gather so much information, despite your limitations, of course. I think, finally, and just kind of talking about everything that we’ve discussed here, you know, everything that we do, we’re trying to improve patient outcomes and give the best evidence-based medicine. What do you think overall needs to happen and how can we invest the findings that you have into our everyday practice of what we’re doing? Then what can we do moving forward to help improve patient outcomes as they relate to alteplase and acute pulmonary embolisms? Dr. Melamed: The study provides information on the way systemic thrombolysis works. I think one of the important messages is that alteplase does work. We were happy to find that our clinical bedside impression was confirmed with the data analysis. What we found at the eight-hour time mark after alteplase administration, we measured blood pressures, and heart rate, and shock index, and respiratory rate, and all these parameters improved in both full- and reduced-dose alteplase regimens and in propensity-weighted cohorts as well. That’s good news that just confirms that this treatment works in the appropriate patient population. The other message I would say from the paper is that both regimens work pretty similarly. This is based on our finding that the mortality and discharge outcomes were pretty much similar in both groups in reduced- and full-dose alteplase. This was, in a way, good news to us because we have a little more ground to using the reduced-dose alteplase if we feel that it is a safer regimen. We also found that it basically confirmed the previous research that mortality mostly happens in patients with massive PE. If we look at the differences in mortality in massive and submassive PE in our studies, they’re pretty striking. The majority of deaths happen in massive PE, so we know our high-risk patient population and can be probably a little bit more selective in submassive or intermediate-risk patients. One of the main findings that we feel is of value to our practice is the analysis of hemorrhagic complications. We noticed that hemorrhagic complications happen more often with full-dose alteplase as compared to reduced-dose. This was statistically significant in the unweighted cohorts, especially for major extracranial complications. Once we looked at the weighted cohorts, the differences were still pretty significant. For major complications, it was 7.1% for full-dose, 1.3% in reduced-dose. Because the number of events wasn’t that high, it didn’t reach statistical significance. The number of intracranial hemorrhages luckily was not that high. We had three. Two of them happened in a setting of extra-supratherapeutic anticoagulation. It’s not an inconsequential number but provides some important information of what to expect. And the finding that there are some other factors associated with complications will probably give us some guidance in terms of what are the ways to reduce them. We found that about a third of patients who develop complications had an invasive procedure. It was either a vascular access procedure or some kind of surgery. So, understandably, these patients are at higher risk and probably need extra attention to minimize the complications. Also, the vast majority of patients who develop complications were on systemic anticoagulation with heparin. And over a third of them had heparin in supratherapeutic levels. That points to another direction to reduce complications, such as being cautious with heparin titration in these patients who receive alteplase and trying to avoid high levels of anticoagulation. We all know that the half-life of alteplase is very short but it can leave behind a post-thrombolysis coagulopathy affecting our ability to clot, thrombocytopenia, low fibrinogen levels. These are things that could potentially be monitored and also direct us to ways to potentially reduce the complications. Dr. Gambles-Farr: Just hearing your descriptions, I’m hearing what we’ve been talking about this entire time. But then also, and just knowing that you are the director of the pulmonary embolism program there, it sounds like there are at least two additional papers that could come out of just this paper by itself. You know, phase two, looking at the different dosing of alteplase in a more applicable way in patients who are moving forward but then also looking at adjunctive anticoagulants that are used and how they’re monitored, associated with alteplase as well. It’s such an important thing for us to have these important discussions about risk stratification when it comes to these patients as they’re receiving these medications because of the complications. But like you said, three is not a high number, but it’s still significant because the patients can have really bad outcomes as a result of it. Dr. Melamed, thank you so much for coming on the podcast today and discussing your paper. I feel like it’s very on par with the things that we need to be thinking about in critical care medicine. Is there anything that you wanted to end our discussion on? Dr. Melamed: Thank you for inviting me to this podcast. It’s been a pleasure. I’ll just summarize our findings that, to us, it feels like the alteplase is an effective method of reperfusion therapy in pulmonary embolism patients who need reperfusion. However, patient selection is the key because, as we know, especially in a group of submassive or intermediate-risk patients, the majority of them will not decompensate and will do well just with anticoagulation. Finding this small group of patients who benefit from reperfusion and whose benefits substantially overweigh their risk is the challenge. So patient selection is the key, and ways to reduce potential complications such as cautious heparin titration therapies afterward, avoiding invasive procedures, and probably additional studies that focus more on the optimal dose regimens and ideally prospective studies that would not have the limitations of the retrospective analysis. Dr. Gambles-Farr: Excellent thoughts, and thank you for that powerful ending. Dr. Melamed, thank you so much for joining us again. This concludes another episode of the Society of Critical Care Medicine podcast. If you’re listening on your favorite podcast app and you like what you heard, consider rating and leaving a review. For the Society of Critical Care Medicine Podcast, I’m Samantha Gambles-Farr. Announcer: Samantha Gambles-Farr, MSN, AG-ACNP, FNP-C, RNFA, is a nurse practitioner intensivist in the Department of Trauma, Surgical Critical Care, Burns and Acute Care Surgery at University of California San Diego Health. She is also adjunct faculty at University of San Diego Hahn School of Nursing and Health Science in its nurse practitioner program. Join or renew your membership with SCCM, the only multiprofessional society dedicated exclusively to the advancement of critical care. Contact a customer service representative at +1 847 827-6888 or visit sccm.org/membership for more information. The SCCM Podcast is the copyrighted material of the Society of Critical Care Medicine, and all rights are reserved. 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Large-bore Aspiration Thrombectomy with the FlowTriever System for the Treatment of Pulmonary Embolism: A Large Single-Center Retrospective Analysis

Travis pebror.

1 Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN USA

Adam William Schmitz

Andrew gauger, reid masterson, sabah david butty.

2 Indiana University Health Radiology, 714 N Senate Ave, Indianapolis, IN 46202 USA

Evaluate the outcomes of patients undergoing large-bore aspiration thrombectomy for the treatment of pulmonary embolism at a large university medical center.

Materials and methods

All patients treated for pulmonary embolism with the FlowTriever System (Inari Medical, Irvine, CA) between September 2019 and January 2023 were retrospectively analyzed. The primary safety and effectiveness outcomes included 7- and 30-day all-cause mortality, major bleeding, procedure-associated clinical decompensation, pulmonary vascular or cardiac injury, and pulmonary artery pressure reduction. Additional outcomes included technical success (completing thrombectomy with the device as intended), changes in hemodynamics and supplemental oxygen requirements, and postprocedural intensive care unit stay.

A total of 286 patients were identified. The mean age was 60.5 years, and 90.9% of patients presented with intermediate-risk pulmonary embolism. Technical success was achieved in 96.9% ( n  = 277) of cases. The average reduction in mean pulmonary arterial pressure was 6.8 mmHg, from 28.7 ± 9.0 to 21.9 ± 8.0 mmHg ( p  < 0.0001). Two major bleeds (0.7%), 2 pulmonary vascular injuries (0.7%), and 4 (1.4%) procedure-associated decompensations were reported, but no device-related deaths occurred. The mean post-procedure intensive care unit stay was 2.0 ± 4.1 days, and 49.3% of patients had no postprocedural intensive care unit admittance. The overall 7-day and 30-day all-cause mortality rates were 2.4% and 6.7%, respectively, with a 30-day pulmonary embolism-related mortality rate of 3.5%.

This non-industry-sponsored single-center analysis of large-bore aspiration thrombectomy in a large population corroborates the findings of other studies and confirms that this approach is safe and effective for the treatment high- and intermediate-risk pulmonary embolism.

Level of Evidence IV

Retrospective observational study.

Graphical Abstract

Introduction

Pulmonary embolism (PE) is associated with significant mortality, representing the third leading cause of cardiovascular death. In-hospital mortality for high-risk PE is often reported above 25% [ 1 – 4 ], while 30-day mortality in intermediate-risk PE is reported near 10% [ 1 , 2 ]. Current treatment guidelines recommend reperfusion treatment with systemic thrombolytic therapy for high-risk PE and front-line anticoagulation therapy for intermediate-risk PE, escalating to reperfusion treatment in the event of hemodynamic deterioration [ 5 ]. However, updated consensus suggests a Pulmonary Embolism Response Team (PERT) also convenes as soon as possible to consider reperfusion treatment, including via catheter-directed therapies, for intermediate-risk PE patients who fail to improve after 24–48 h of therapeutic-dose anticoagulation [ 6 ].

The FlowTriever System (Inari Medical, Irvine, CA) is a large-bore aspiration thrombectomy (LBAT) device used for percutaneous PE treatment without thrombolytics. It is the most investigated mechanical thrombectomy treatment for PE, having been evaluated in the industry-sponsored FLARE, FLASH, and FLAME studies with outcomes reported from nearly 1,000 total patients with intermediate- and high-risk PE [ 7 – 10 ]. However, many non-industry-sponsored evaluations of this LBAT device are of modest size [ 11 – 14 ]. Considering the large number of PE patients treated with LBAT at our center, we aimed to evaluate the safety and effectiveness of LBAT in routine clinical practice at our institution through a retrospective review of patients treated with this approach.

Materials and Methods

Study design and population.

Electronic health records of patients treated for PE at a large university medical center between September 2019 and January 2023 were retrospectively analyzed. By September 2019, LBAT had largely supplanted catheter-directed thrombolysis (CDT) as the primary interventional PE treatment method at our institution due to immediacy of clinical improvement following a single-session procedure without the need to administer thrombolytics. To assess outcomes with this updated approach, all patients treated with LBAT using the FlowTriever System were included in this analysis, and those treated with CDT were excluded. No other criteria were applied. Patients were treated using an institutional PE treatment protocol which included: 1) imaging via CT, 2) treatment determination by a multidisciplinary Pulmonary Embolism Response Team (PERT) composed of an emergency medicine physician, interventional radiologist, and pulmonary critical care physician, 3) interventional reperfusion with LBAT in appropriate patients per PERT decision, and 4) admission to the progressive care unit following LBAT unless intensive care unit (ICU) admission was needed.

PE risk stratification was performed using the current European Society of Cardiology (ESC) guidelines [ 5 ]. Generally, the PERT recommended intermediate-risk PE patients with central bulky thrombus to be treated via an interventional approach, and patients with low-risk or peripheral PE to receive anticoagulation. Risk stratification markers like troponin, brain natriuretic peptide (BNP), and right heart strain, determined independently by diagnostic radiologists using commonly defined imaging findings such as right ventricular-to-left ventricular (RV/LV) ratio > 0.9, were also considered by the PERT in making treatment determinations.

Procedure Description

At our institution, a typical LBAT procedure course is as follows. The patient is on anticoagulation before arrival to the procedure room. Additional heparin is given to achieve activated clotting time of 250–300 s, and the patient is placed under conscious sedation. LBAT is initiated by gaining vascular access through the femoral vein. A balloon-tipped or pigtail catheter is navigated through the heart into the pulmonary arteries, and pressure measurements may be taken. Once the pulmonary vasculature has been accessed, the catheter is removed over a stiff guidewire to allow for insertion of the Triever aspiration catheter (16 Fr, 20 Fr or 24 Fr). This is positioned immediately proximal to the embolic debris and aspiration is initiated with a 60 mL syringe attached to the Triever catheter side port. Aspiration is repeated as needed. Mechanical disruption of embolic debris with the FlowTriever disks is not used at our institution. Once it became available (August 2021), the FlowSaver blood return system (Inari Medical) was implemented in the majority of LBAT procedures to filter aspirated blood in the syringe and return it to the patient through the access site. The decision of when to terminate the LBAT procedure is left to the discretion of the interventional radiologist performing the procedure based on thrombus removal and observed improvement in clinical status. At the conclusion of the procedure, hemostasis is achieved using a pre-close technique with two Perclose ProGlide devices (Abbott, Plymouth, MN) or a purse-string suture technique.

The primary safety and effectiveness outcomes assessed included 7- and 30-day all-cause mortality, major bleeding, procedure-associated clinical decompensation, pulmonary vascular or cardiac injury, and pulmonary artery pressure (PAP) reductions. Major bleeding was determined using the Society of Interventional Radiology (SIR) reporting standards, i.e., intracranial, intraocular, or retroperitoneal hemorrhage or any hemorrhage requiring transfusion and/or resulting in a hematocrit decrease ≥ 15% or hemoglobin decrease ≥ 5 g/dL [ 15 ]. All clinical decompensation events, defined as an acute physiological worsening of clinical status that posed an immediate increased risk of serious harm or death [ 16 ], occurring during hospitalization whether before, during, or after the thrombectomy procedure were recorded. PAPs were measured immediately prior to and following thrombectomy via standard invasive hemodynamic assessment techniques. Additional outcomes included technical success per the SIR reporting standards, i.e., the ability to deliver the device into the pulmonary artery, operate the device to aspirate thrombus, and remove the device at the end of the procedure [ 15 ], change in hemodynamic measurements, and postprocedural hospital length of stay (LOS).

Statistical Analysis

Data values are reported as counts (%) for categorical variables and mean ± standard deviation (SD) or median [interquartile range (IQR)] for continuous variables. For comparative analysis of changes in hemodynamics and oxygenation status following thrombectomy, p -values were calculated using two-sided paired Student t tests for continuous data and McNemar tests for categorical data. Change in PAP following thrombectomy was analyzed in patients with paired pre-procedure and post-procedure measurements, and p -values were calculated using one-sided paired Student t tests. A p -value < 0.05 was considered statistically significant. Statistical analysis was performed in R, version 4.3.2.

Ethics Statement

This research activity was granted exemption from full Institutional Review Board review and waived informed consent by a qualified staff member of the Human Research Protection Program of the affiliated university in accordance with 45 CFR 164.512(i)(2)(ii).

Patient Characteristics and PE Presentation

During the study period, 319 PE patients were treated with catheter-directed therapy, including 33 who underwent CDT and 286 who underwent LBAT. All 286 patients treated with LBAT were included in the analysis population, while the 33 CDT patients were excluded. As depicted in Table  1 , the analysis population was 53.5% male, with a mean age of 60.5 ± 16.2 years and a mean BMI of 35.2 ± 10.6 kg/m 2 . Concurrent deep vein thrombosis was present in 62.9% of patients, 18.9% had a history of malignancy, and 16.1% were diagnosed with PE within 3 months of having surgery. Intermediate-high-risk PE was diagnosed in 75.2% of patients, while 15.7% presented with intermediate-low-risk PE, 8.0% with high-risk PE, and 1.0% with low-risk PE. Right ventricle dilatation on CT was identified in 87.4% of the cohort, while 95.5% had elevated cardiac biomarkers.

Table 1

Baseline characteristics and pulmonary embolism presentation

Values are mean ± standard deviation or n (%)

BMI body mass index; BNP brain natriuretic peptide; DVT deep vein thrombosis; PE pulmonary embolism; RV / LV right ventricle-to-left ventricle diameter ratio

Procedural Characteristics, Outcomes, and LOS

Table ​ Table2 2 shows the procedural characteristics and LOS data for the cohort. The mean total procedure time from pre-procedure time out to access site closure was 90.5 ± 32.3 min. No patients were treated with thrombolytic therapy intraprocedurally, but 4.5% ( n  = 13) received thrombolytic therapy at an outside hospital prior to the procedure. The mean post-procedural hospital LOS was 7.3 ± 9.1 days and the mean post-procedural ICU LOS was 2.0 ± 4.1 days, with 49.3% of patients not requiring ICU admittance. Among 145 (50.7%) patients with post-procedure ICU admittance, the mean LOS was 3.9 ± 5.1 days.

Table 2

Procedural characteristics and length of stay

ICU intensive care unit; IQR interquartile range; SD standard deviation

a n  = 285

b Technical success defined as the ability to deliver the device into the pulmonary artery, operate the device to aspirate thrombus, and remove the device at the end of the procedure

c Mean ± SD and median [IQR] reported for 145 patients admitted to ICU post-procedure

Technical success was achieved in 277 (96.9%) cases. Of the 9 technical failures, 7 involved emboli that could not be aspirated, 1 procedure could not be completed for undocumented reasons, and 1 procedure was terminated due to a pulmonary artery pseudoaneurysm, details of which are described below. In the 7 cases involving emboli that could not be aspirated, 6 were due to intractable chronic thrombus and 1 was due to very large central thrombus size. Of the 6 patients with intractable chronic thrombus, 1 expired during the procedure and 5 continued medical management with anticoagulation and survived through 30 days. The patient with central thrombus that was too large to aspirate died of uterine hemorrhage in the setting of endometrial cancer 18 days following the procedure.

Hemodynamics and oxygen supplementation

Table ​ Table3 3 shows changes in hemodynamics and oxygenation status at presentation and post-procedure. Prior to thrombectomy, 183 (64.0%) of patients were tachycardiac (heart rate ≥ 100 beats per minute [bpm]). Of these tachycardiac patients, 54.1% experienced resolution of their tachycardia immediately following the procedure. The mean reduction in heart rate among the entire cohort was 13.5 bpm ( p  < 0.0001). There was not a statistically significant change in the number of patients who required supplemental oxygen prior to and immediately following thrombectomy ( n  = 180 [62.9%] vs n  = 165 [57.7%]; p  = 0.0997), though 27.2% of patients with supplemental oxygen requirements at presentation no longer required oxygen support following the procedure.

Table 3

Changes in patient hemodynamics and oxygenation status following thrombectomy

Bpm beats per minute

a p -values calculated using McNemar tests for categorical data and two-sided paired t tests for continuous data

b Post-procedure value and mean change calculated for n = 285

c Percentage reported out of 183 patients with tachycardia at presentation

d Percentage reported out of 180 patients requiring oxygen supplementation at presentation

Figure  1 depicts the change in PAPs among patients with paired pre- and post-thrombectomy measurements. The mean reduction in mean and systolic PAP immediately following thrombectomy was 6.8 mmHg (28.7 ± 9.0 to 21.9 ± 8.0 mmHg; p  < 0.0001) and 11.7 mmHg (46.0 ± 14.0 to 34.3 ± 12.0; p  < 0.0001), respectively.

Change in mean pulmonary arterial pressure (PAP), systolic PAP, and diastolic PAP following thrombectomy. Plots and statistics are based on patients with paired pre-procedure and post-procedure measurements ( n  = 247–252). Boxes represent IQR (Q1, Q3) with horizontal bars representing the median and the whiskers representing 1.5 × IQR. Outliers are shown as individual points. The mean is indicated on each box by a “ + ” sign, with numeric mean ± SD data reported below. P -values were calculated using one-sided paired t test

Safety and Mortality Outcomes

Safety and mortality outcomes for the cohort are shown in Table  4 . There were 2 (0.7%) major bleeds consisting of 1 case of abdominal bleeding detected post-procedure likely due to rebleed of a retroperitoneal hematoma and 1 case resulting from intraprocedural laceration of the corona mortis which occurred during sheath insertion and was treated with coil embolization. Two (0.7%) pulmonary vascular injuries occurred: 1 case of contrast extravasation into the mediastinum observed on postprocedural angiogram and 1 pulmonary artery pseudoaneurysm. The pulmonary artery pseudoaneurysm was identified intraprocedurally when a 1-cm outpouching was noted along the main pulmonary artery immediately distal to the pulmonic valve. Immediate CTA of the chest confirmed the diagnosis, and no corrective procedure was performed. At 1-month follow-up the pseudoaneurysm was measured and documented stable, and at 1-year follow-up, the pseudoaneurysm was not appreciable on CTA. All four major bleeding or pulmonary vascular injury events observed in the study occurred in patients with intermediate-risk PE.

Table 4

Safety outcomes and mortality by risk classification

Values are n (%)

PE pulmonary embolism

a Both high-risk patients with intraprocedural cardiac arrest also had cardiac arrest prior to procedure. The intermediate-low-risk patient with intraprocedural cardiac arrest had multiple seizures prior to procedure, with an intraprocedural seizure requiring resuscitation

b Patient arrested, had impaired neurological exam, and CT suggestive of anoxic brain injury prior to the procedure and during further post-procedural assessments was found to have suffered a stroke. It is possible that the pre-existing neurologic insult was exacerbated by the procedure, though the relatedness is uncertain

c N  = 282 for full cohort and N  = 211 for intermediate-high-risk PE

d All PE-related deaths in the high-risk group occurred in patients who had cardiac arrest prior to the procedure

There were 4 (1.4%) procedure-associated decompensation events, consisting of 3 (1.0%) intraprocedural cardiac arrests and 1 (0.4%) stroke. These 4 events appeared to be exacerbations of ongoing decompensations and not new events that began during or after the procedure. Of the 3 intraprocedural cardiac arrests, 2 occurred in high-risk patients who also experienced cardiac arrest prior to the procedure (1 expired during the procedure and 1 expired in the ICU following the procedure). The remaining intraprocedural cardiac arrest occurred in an intermediate-low-risk patient who had multiple seizures prior to the procedure and an intraprocedural seizure requiring resuscitation; this patient survived to discharge. The stroke occurred in a high-risk patient with arrest, an impaired neurological exam, and CT suggestive of anoxic brain injury prior to the procedure. PE thrombectomy was performed expediently and thereafter, assessment revealed the patient had suffered a stroke. The stroke was considered procedure-associated because the occurrence of intraprocedural paradoxical embolism via a patent foramen ovale could not be ruled out. Twenty patients had clinical decompensation events not associated with the procedure: 5 additional high-risk patients experienced cardiac arrest prior to the procedure, 11 intermediate-risk patients experienced pre-procedural decompensation related to other conditions (cancer n  = 4, pneumonia n  = 4, congestive heart failure n  = 1, sepsis n  = 1, severe lactic acidosis n  = 1), and 4 intermediate-risk patients decompensated following the procedure for unrelated reasons (cardiac arrest in the setting of palliative care, hemorrhagic shock, stroke, and adrenal insufficiency; n  = 1 each). Pre-procedural decompensation in the 4 patients presenting with known cancer diagnosis was attributable to superimposed pneumonia, sepsis, metabolic acidosis, and hemorrhage.

At 7 days post-procedure, all-cause mortality for the full cohort was 2.4% ( n  = 7), including 21.7% ( n  = 5) for patients with high-risk PE, 0.9% ( n  = 2) with intermediate-high-risk PE, and 0% with intermediate-low- or low-risk PE. No deaths were attributed to the device, relationship to the procedure could not be ruled out. All 5 high-risk patients who expired within 7 days had experienced cardiac arrest prior to the procedure and expired while hospitalized. One additional high-risk patient died within 30 days after hospitalization while in hospice; this patient also experienced cardiac arrest prior to the procedure. At 30 days post-procedure, all-cause mortality for the full cohort was 6.7% ( n  = 19), including 26.1% ( n  = 6) for patients with high-risk PE, 4.7% ( n  = 10) with intermediate-high-risk PE, and 6.3% ( n  = 3) with intermediate-low- or low-risk PE. PE-related mortality at 30 days post-procedure was 3.5% ( n  = 10). These PE-related deaths through 30 days included all 6 deaths in high-risk patients, 3 deaths in intermediate-high-risk patients, and 1 death in an intermediate-low-risk patient.

This single-center analysis of LBAT treatment of PE in a large real-world population found that treatment with the FlowTriever System was associated with low 7-day (2.4%) and 30-day (6.7%) all-cause mortality and a favorable safety profile with no cardiac injuries, few pulmonary vascular injuries (0.7%), and minimal procedure-associated decompensations (1.4%). Rapid improvements in hemodynamic measurements were observed.

Patients in this analysis were largely similar in characteristics to those in the all-comer FLASH registry ( N  = 799) [ 8 ]. They presented with similar ages (60.5 years in our analysis vs 61.2 years in FLASH), proportion with a history of cancer (18.9% vs 20.7%), proportion with concomitant deep vein thrombosis (62.9% vs 65%), and PE risk stratification (8.0% vs 7.9% high-risk and 90.9% vs 92.1% intermediate-risk). Our analysis also included 3 patients deemed low-risk by the PERT on presentation who were referred to LBAT after failing medical therapy. The concordance between outcomes in this analysis and FLASH suggests that the observation of infrequent major bleeding (0.7% vs 1.4%), common ICU avoidance (49.3% vs 62.6%), and reductions in mean PAP (–6.8 mmHg vs –7.6 mmHg), systolic PAP (–11.7 mmHg vs –12.8 mmHg), and heart rate (–13.5 bpm vs –12.0 bpm) are broadly generalizable. Median total procedure time (83 min vs. 66 min) and post-procedural hospital LOS (5 days vs. 3 days) were increased compared with the FLASH registry [ 8 ], but comparable to previously published retrospective analyses [ 11 , 14 , 17 ]. Varying operator experience profiles and study inclusion criteria may have contributed to these differences.

A marginally higher rate of short-term mortality was observed in this analysis than in the FLASH registry (2.4% at 7 days vs 0.3% at 48 h in FLASH) [ 8 ]. However, this 7-day all-cause mortality is comparable to the in-hospital mortality found in a recent meta-analysis of aspiration mechanical thrombectomy (3.6%) [ 18 ] and may be driven by the inclusion of all LBAT patients, as compared with registry enrollment with certain eligibility criteria. Another recently published, independently conducted retrospective single-center analysis of similar size ( n  = 257) evaluating LBAT with the FlowTriever System reported similar outcomes to those in this study [ 17 ]. The overall 30-day mortality rate in the aforementioned study was 3% compared to 6.7% in our analysis, with greater similarity observed in the rate of 30-day PE-attributable mortality (2% compared to 3.5% in this study).

In our analysis, the 7-day mortality rate in high-risk patients was 21.7%. This compares favorably to acute high-risk PE mortality rates in a recent administrative database analysis (39%) and a meta-analysis of high-risk patients (28%) [ 3 , 4 ]. However, the 7-day mortality rate in high-risk PE in our study appears higher than acute rates reported from the FLASH and FLAME registries (0%–1.9%) [ 10 , 19 ]. One reason for these differences may lie in the proportion of patients in our analysis who presented with so-called “catastrophic” high-risk PE, a term recently described in the literature [ 20 , 21 ] and defined as high-risk PE presentation with cardiac arrest or the need for high-dose vasopressors due to concern for impending cardiac arrest. In our analysis, 34.8% ( n  = 8) of high-risk patients experienced cardiac arrest prior to thrombectomy, which would classify them as having catastrophic high-risk PE. In the FLAME and FLASH registries, comparatively fewer high-risk patients experienced cardiac arrest prior to the procedure (20.8% and 6.3%, respectively) [ 10 , 19 ]. Kobayashi et al. reported that in-hospital mortality among patients with catastrophic high-risk PE was appreciably higher than in non-catastrophic high-risk PE (42.1% vs 17.2%, p  < 0.001) [ 21 ], so the greater prevalence of catastrophic high-risk PE in our analysis may contribute to the higher mortality rates with regard to the FLASH and FLAME registries.

Given our experience with a broad range of intermediate-risk patients, we have found LBAT to be a safe and effective procedure regardless of patient age or anatomy. Technical success can be more difficult to achieve in embolic cases involving chronic thrombus. The key to success is meticulous technique, particularly with guidewire selection and positioning which greatly improve the ability to advance the aspiration catheter to the target location. These same considerations are important to minimize catastrophic guidewire perforations. As our experience has grown, we have been able to carry this same approach to more critically ill, high-risk PE patients. Despite presenting in extremis with cardiac arrest, 25% ( n  = 2) of the “catastrophic” high-risk PE patients treated with LBAT survived through 30-day follow-up. We feel this justifies consideration of the procedure for this subgroup of patients as part of a collaborative PERT discussion.

This study is limited by its retrospective and single-center nature, as well as a lack of long-term outcomes. However, the findings from this large, non-industry-sponsored analysis with no exclusion criteria comprising both high- and intermediate-risk PE patients provide an informative comparison to other FlowTriever clinical studies performed to date.

This analysis confirms prior clinical study findings that the FlowTriever System is safe and effective for the treatment of high- and intermediate-risk PE in a diverse cohort of PE patients with various comorbidities encountered in the course of real-world clinical practice.

Acknowledgements

The author acknowledges editorial support from Kelly Koch, PharmD, and Van Willis, PhD, and statistical and analysis support from Yu-Hsiang Shu, PhD.

This study was not supported by any funding.

Declarations

SD Butty has received consultant fees from Inari Medical. AW Schmitz, T Pebror, A Gauger, and R Masterson declare no conflict.

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. For this type of study, formal consent is not required.

This research activity was granted exemption from full Institutional Review Board review and waived informed consent by a qualified staff member of the Human Research Protection Program of Indiana University in accordance with 45 CFR 164.512(i)(2)(ii).

For this type of study, consent for publication is not required.

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