Thrombolysis For Pulmonary Embolism Research Articles

In-Hospital Management and Follow-Up Treatment of Venous Thromboembolism: Focus on New and Emerging Treatments.

Venous thromboembolism (VTE), encompassing pulmonary embolism (PE) and deep venous thrombosis (DVT), is a major cause of morbidity and mortality of particular relevance for intensivists and hospitalists. Acute VTE is usually managed with parenteral unfractionated heparin or low-molecular-weight heparin, followed by an oral vitamin K antagonist. Data are lacking for optimal treatment of less common occurrences, such as upper extremity DVT, and for approaches such as thrombolysis for PE associated with early signs of hemodynamic compromise or inferior vena cava filters when anticoagulation is contraindicated. Direct oral anticoagulants (DOACs) including apixaban, dabigatran, edoxaban, and rivaroxaban are now added to the armamentarium of agents available for acute management of VTE and/or reducing the risk of recurrence. This review outlines an algorithmic approach to acute VTE treatment: from aggressive therapies when anticoagulation may be inadequate, to alternative choices when anticoagulation is contraindicated, to anticoagulant options in the majority of patients in whom anticoagulation is appropriate. Evidence-based guidelines and the most recent DOAC clinical trial data are discussed in the context of the standard of care. Situations and treatment approaches for which data are unavailable or insufficient are identified. VTE therapy in care transitions is discussed, as are choices for secondary prevention.

Practice patterns and complication rates of thrombolysis for pulmonary embolism.

Practice patterns, bleeding complication rates, and outcomes of thrombolytic use for pulmonary embolism (PE) outside of clinical trials are not well characterized. Retrospective cohort study of patients with PE, using an enhanced administrative database of approximately 20% of hospitalizations in the United States, 2008-2011. We used hierarchical logistic regression to identify patient- and hospital-level factors associated with thrombolytic use and quantified between-hospital variation in thrombolysis. We calculated rates of hemorrhagic complications and mortality in patients receiving thrombolytics stratified by vasopressor use. We identified 91,860 hospitalizations for PE; thrombolytics were utilized in 13.2% (578/4363) who received vasopressors and 1.6% (1320/82,997) who did not receive vasopressors. Patients who received thrombolytics were younger, more likely white, with private insurance, fewer comorbidities and more acute organ failures. Hospitals varied widely in thrombolysis rates for PE (0-100% of patients on vasopressors, 0-12.5% not on vasopressors) with 17% of variation unexplained by patient or hospital characteristics. Bleeding complication rates for patients receiving thrombolytics versus no thrombolytics, respectively, were: ICH (0.8 vs. 0.08%, p<0.01), major bleeding (13 vs. 3%, p<0.01), and major bleeding with transfusion (2.5 vs. 0.05%, p<0.01). Among patients given vasopressors, thrombolytics were not associated with hospital mortality (thrombolysis 41% vs. no thrombolysis 35% mortality; adjusted OR 0.97, 95% CI 0.93-1.01, p=0.15). There is wide variation in thrombolytic use for PE in the US. Patient characteristics and complications associated with real-world thrombolytic use were similar to published randomized trials.

3:54 PMAbstract No. 213 - Catheter-directed thrombolysis for submassive pulmonary embolism: technique and initial results

3:54 PMAbstract No. 213 - Catheter-directed thrombolysis for submassive pulmonary embolism: technique and initial results

4:03 PMAbstract No. 214 - Improvement of pulmonary hypertension and right ventricular dysfunction after ultrasound-accelerated catheter-directed thrombolysis for submassive pulmonary embolism

4:03 PMAbstract No. 214 - Improvement of pulmonary hypertension and right ventricular dysfunction after ultrasound-accelerated catheter-directed thrombolysis for submassive pulmonary embolism

Systemic Full Dose, Half Dose, and Catheter Directed Thrombolysis for Pulmonary Embolism. When to Use and How to Choose?

Treatment of pulmonary embolism (PE) is variable amongst different and even the same institutions. With the introduction of different forms of thrombolysis, catheter based interventions, and new oral anticoagulants, the treatment and decision-making process has become more complex. The different forms of classification of PE into massive, submassive, severe, moderate, intermediate high risk, intermediate low risk, and low risk have only added to this complexity. The main two reasons for such classifications have been to aid in assessment of patient prognosis and in the intent to carefully select patients who are high risk and would benefit from thrombolysis. The literature supports the use of thrombolysis in high risk patients albeit at the risk of a higher bleeding rate. It has been suggested that survival can improve in both massive and submassive PE with thrombolysis. Studies have shown a reduced risk of bleeding with reduction of the doses of the thrombolytic and anticoagulant agents while imparting the same beneficial effects seen in full dose thrombolysis. The opinion of this author is that treatment of massive and submassive forms of PE can become standardized, safe, streamlined, and simplified by using a lower dose of systemic thrombolysis for both and an anticoagulation regimen without the necessity for expensive approaches such as invasive catheter placement in the pulmonary circulation.

Staged Ultrasound-Assisted Catheter-Directed Thrombolysis for Bilateral Pulmonary Embolism: “All with one Catheter-Technique”

A 70-year-old male presented with two days increasing dyspnea. His past medical history was notable for deep venous thrombosis with consecutive pulmonary embolism (PE). Diagnostic workup showed normal blood pressure (130/80mmHg), sinus tachycardia with SIQIII-pattern on electrocardiogram, and elevation of troponin (0.22ng/nl).

Potential role of systemic thrombolysis in acute submassive intermediate risk pulmonary embolism: review and future perspectives.

Submassive (intermediate risk) pulmonary embolism (PE) continues to be a significantly morbid disease process that remains unrecognized, inadequately risk stratified and suboptimally treated. Appropriate early clinical and imaging-based risk stratification represents the cornerstone for adequate therapeutic decision making, particularly for the selection of candidates who may benefit the most from systemic thrombolysis. The relevance of estimating clinical prognostic scores, in combination with imaging data, for accurate assessment of right ventricular function and laboratory biomarkers, indicative of myocardial injury for identification of normotensive patients at intermediate risk for an adverse short-term outcome are emphasized in this review. Recent clinical trials have demonstrated improvement in hemodynamics and mortality with the use of systemic thrombolysis among intermediate risk patients; however, it came at the cost of a significantly increased risk of major bleeding. Catheter-based therapies have garnered considerable clinical interest in recent years; of particular note is the ultrasound accelerated catheter-directed thrombolysis which has emerged as a novel and attractive alternative therapeutic modality with an increasing number of single center studies and ongoing randomized trials. Our review focuses on the major trials and studies involved in submassive PE in the recent literature including the role of thrombolytic therapy. We include major trials with reasonable sample size and extensive review of the potential side effects, such as major bleeding.

Случай успешного тромболизиса при массивной тромбоэмболии легочной артерии у беременной

We present a case of successful thrombolysis in massive pulmonary embolism in pregnancy. No severe haemorrhagic complications were observed. Thrombolysis was effective and did not affect the pregnancy and the fetus.

Thrombolysis for postoperative Submassive pulmonary Embolism

Pulmonary embolism (PE) is the most preventable cause of inhospital death. Although safe and effective, thrombolytic therapy is relatively contraindicated within 10 days of major surgery due to the risk of bleeding. Our patient developed submassive PE, within 48 h of surgery and had catheter-directed thrombolysis with Streptokinase (STK) injection successfully, without any bleeding complications. This case demonstrates that thrombolysis may be safely and effectively done in postoperative patients. In such scenarios, where the therapy is relatively contraindicated, the decision whether to thrombolyse or not, must be multidisciplinary, giving utmost importance to the patient's best interest and to ensure that no single individual is denied potentially life-saving therapy.

The case of a successful cardiopulmonary resuscitation with using thrombolysis in massive pulmonary embolism in puerperant after cesarean section

Pulmonary embolism (PE) is a leading cause ofmaternalmortality in the developedworld.1 Today, there are few reports of the use of thrombolytic therapy in pregnant and postpartum women.2,3 We present here the case of a puerperant with massive PE who underwent successful thrombolysis during cardiopulmonary resuscitation. In 30-year-old puerperal woman after elective caesarean sectionoccurred suddenacute dyspnea anddecreasedblood pressure. An immediate electrocardiogram showed a typical S1-Q3 pattern. After 10min from the onset of clinical signs of pulmonary embolismwas fixed cardiac arrest. Intubation andmechanical ventilation and chest compressions were started immediately. There was pulseless electrical activity. Within 1h was intravenously administered 5mg epinephrine. Thrombolysis with streptokinase (250,000units) was administered 1h after the beginning of resuscitation. Immediately after administration of streptokinase restore blood pressure but developed a severe uterine bleeding. Hysterectomy and packing was performed for to stop bleeding. Floating thrombus in the right femoral vein was subsequently diagnosed. The operation thrombectomy was performed after 2 days. On the fifth day the patient was disconnected from the ventilator. The patientwasdischarged fromthehospital after 20dayswithoutneurological complications. The rescue thrombolysis on background CPR is a very important option in the treatment of massive pulmonary embolism with cardiac arrest.

Systemic Thrombolysis Compared to Catheter Directed Thrombolysis in Acute Pulmonary Embolism

Systemic Thrombolysis Compared to Catheter Directed Thrombolysis in Acute Pulmonary Embolism

Tromboembolismo pulmonar

Pulmonary embolism (PE) is a complication of deep vein thrombosis (DVT), from more than 90% of the lower limbs. They are different expressions of the same entity called venous thromboembolism (VTE). The diagnosis is based on a series of signs and symptoms, both nonspecific and common to other cardiac pathologies; D dimer is a degradation product of fibrin present in the thrombus, its presence in plasma indicates the existence of thrombosis and fibrinolysis, has a very high sensitivity to VTE, but low specificity, as may be associated with other clinical situations very diverse. The technique of choice remains the multidetector CT angiography. The prognostic stratification is useful for choosing the best treatment (anticoagulation, recanalization treatment) and the best place for treatment of these patients (home, hospital ward or ICU). The most important prognostic factor in PE is the hemodynamic status at the time of diagnosis. In the high-risk PE thrombolysis treatment it is recommended; in the low risk or intermediate-risk PE the treatment of choice is anticoagulation in all its forms depending on patient characteristics.

Pulmonary Embolism Response to Fragmentation, Embolectomy, and Catheter Thrombolysis (PERFECT): Initial Results From a Prospective Multicenter Registry

Systemic thrombolysis for acute pulmonary embolism (PE) carries up to a 20% risk of major bleeding, including a 2% to 5% risk of hemorrhagic stroke. We evaluated the safety and effectiveness of catheter-directed therapy (CDT) as an alternative treatment of acute PE. One hundred one consecutive patients receiving CDT for acute PE were prospectively enrolled in a multicenter registry. Massive PE (n = 28) and submassive PE (n = 73) were treated with immediate catheter-directed mechanical or pharmacomechanical thrombectomy and/or catheter-directed thrombolysis through low-dose hourly drug infusion with tissue plasminogen activator (tPA) or urokinase. Clinical success was defined as meeting all the following criteria: stabilization of hemodynamics; improvement in pulmonary hypertension, right-sided heart strain, or both; and survival to hospital discharge. Primary safety outcomes were major procedure-related complications and major bleeding events. Fifty-three men and 48 women (average age, 60 years [range, 22-86 years]; mean BMI, 31.03 ± 7.20 kg/m2) were included in the study. The average thrombolytic doses were 28.0 ± 11 mg tPA (n = 76) and 2,697,101 ± 936,287 International Units for urokinase (n = 23). Clinical success was achieved in 24 of 28 patients with massive PE (85.7%; 95% CI, 67.3%-96.0%) and 71 of 73 patients with submassive PE (97.3%; 95% CI, 90.5%-99.7%). The mean pulmonary artery pressure improved from 51.17 ± 14.06 to 37.23 ± 15.81 mm Hg (n = 92) (P < .0001). Among patients monitored with follow-up echocardiography, 57 of 64 (89.1%; 95% CI, 78.8%-95.5%; P < .0001) showed improvement in right-sided heart strain. There were no major procedure-related complications, major hemorrhages, or hemorrhagic strokes. CDT improves clinical outcomes in patients with acute PE while minimizing the risk of major bleeding. At experienced centers, CDT is a safe and effective treatment of both acute massive and submassive PE. ClinicalTrials.gov; No.: NCT01097928; URL: www.clinicaltrials.gov.

Safety and efficacy of ultrasound-accelerated catheter-directed lytic therapy in acute pulmonary embolism with and without hemodynamic instability.

The objective of this study was to evaluate the safety and effectiveness of ultrasound-accelerated thrombolysis in acute pulmonary embolism. A retrospective study of 45 patients was performed to evaluate treatment of acute pulmonary embolism at a single center from January 2011 to December 2013. All patients were diagnosed with computed tomography or ventilation-perfusion scan and had hemodynamic instability (systolic blood pressure <100 mm Hg) or right-sided heart strain evidenced by right ventricular dilation, septal deviation, or hypokinesis by echocardiography or computed tomography. EkoSonic catheters (EKOS Corporation, Bothell, Wash) were placed into the affected pulmonary arteries, and recombinant tissue plasminogen activator was infused through the catheters at 0.5 to 1.0 mg/h per catheter. Hypotension (systolic blood pressure <100 mm Hg) was present in 12 patients, with 100% resolution by treatment completion. Tachycardia (heart rate >100 beats/minute) was present in 26 patients and resolved in 92% by treatment completion; the average heart rate for all patients decreased from 109 to 77 beats/minute during the treatment period. Direct pulmonary artery pressure measurement showed average decrease of 21.5 mm Hg, representing a 40.2% reduction. Postprocedure echocardiography demonstrated complete resolution of cardiac dysfunction in 64%. Patients received a total dose of 30.5 mg (range, 14-66 mg) recombinant tissue plasminogen activator during an infusion time of 14.2 hours (range, 8-21 hours). There were no deaths through 90 days of follow-up and no major periprocedural bleeding events. This retrospective study demonstrates the safety and efficacy of current ultrasound-accelerated thrombolysis methods to treat acute pulmonary embolism.

Fluid Protocol for Acute Respiratory Distress Syndrome, Catheter Thrombolysis for Intermediate Risk Pulmonary Embolism, and Steroids for Community-acquired Pneumonia

Fluid Protocol for Acute Respiratory Distress Syndrome, Catheter Thrombolysis for Intermediate Risk Pulmonary Embolism, and Steroids for Community-acquired Pneumonia

Thrombolysis-related intracerebral hemorrhage and cerebral amyloid angiopathy: accumulating evidence.

Intracerebral hemorrhage (ICH) is the most feared risk of systemic thrombolysis for ST-elevated myocardial infarction, pulmonary embolism, or acute ischemic stroke. Clinical, radiological, and pathological evidence suggests that cerebral small vessel disease and, in particular, cerebral amyloid angiopathy (CAA) may contribute to or in some cases directly underpin thrombolysis-related intracerebral hemorrhage (TICH) (1). Further developments, particularly in neuroimaging, have strengthened this hypothesis, hinting at the prospect of identifying biomarkers to measure TICH risk for individual patient groups. Emerging biomarkers for CAA such as lobar cerebral microbleeds (2) may become increasingly useful for outcome endpoints in clinical trials and patient risk stratification for TICH (3). Thrombolysis-related intracerebral hemorrhage is a complex pathophysiological process. For ischemic stroke patients, a key issue is the location of TICH, i.e., hemorrhage into the area of ischemia vs. hemorrhage in a remote non-ischemic site (occurring in about 20% of patients with symptomatic TICH). Classification of TICH has traditionally focused on clinical and radiological features (4), with less emphasis on whether different mechanisms might be implicated in TICH in remote from or within the acute infarcted region (5) or whether pathological assessment has occurred. Coregistered Pittsburgh compound B positron emission tomography (PiB-PET) imaging has revealed that spontaneous hemorrhage hotspots preferentially occur at locations with increased amyloid β-protein burden (6). In patients treated with recombinant tissue plasminogen activator (rt-PA) for acute ischemic stroke, cerebral amyloid β-protein (as detected with PiB-PET) retention was higher in patients with parenchymal hemorrhage compared to patients without (7). Although PiB-PET has somewhat poor spatial resolution and cannot reliably resolve parenchymal and cerebrovascular amyloid β-protein, the finding is probably one of the strongest pieces of radiological evidence implicating CAA in TICH. Matrix metalloproteinase 9, a zinc-dependent endopeptidase and a marker of hemorrhagic transformation after ischemic stroke, is released from neutrophil granules by rt-PA in humans (8). Amyloid β-protein can also release and activate MMP-9 from mouse endothelial cells (9), suggesting that convergent risk factors may lead to hemorrhage. Cerebral microbleeds identified on MRI in a lobar distribution are considered a characteristic hemorrhagic marker of a vasculopathy related to CAA (2). It has slowly emerged that multiple microbleeds might increase the risk of symptomatic ICH following thrombolysis treatment, a relationship which increases with increasing numbers of microbleeds (10, 11). In more recent studies with larger groups of ischemic stroke patients receiving intravenous thrombolysis in both European and Chinese populations, multiple cerebral microbleeds were more clearly associated with symptomatic and parenchymal hemorrhage, respectively (12, 13). Future study may provide insights into potential mechanisms, and meta-analyses may highlight the relative importance of lobar and non-lobar cerebral microbleeds in stratifying the intracerebral hemorrhagic risk from thrombolysis. In a review in 2004 (1), we identified 10 patients with pathological investigation of TICH, 7 of whom had evidence of CAA. All of these patients had been treated for acute myocardial infarction and nine of the patients had multiple hemorrhages in a lobar distribution. With an increasing emphasis on primary percutaneous intervention for ST-elevated myocardial infarction, it may not be surprising that no further TICH cases following thrombolysis for acute myocardial infarction have been reported. However, although thrombolysis rates have increased for acute ischemic stroke patients, in an updated systematic literature search, only two further autopsy TICH cases (multiple and both hemispheres) have been reported in the stroke literature, both of whom had CAA (14). The relative lack of human pathological studies compared to neuroimaging studies hampers further developments in this area. A pathological register attached to a clinical register would enhance our understanding of TICH, particularly in the older population with acute ischemic stroke. The known predictors of clinically significant TICH currently include age, clinical stroke severity, high blood pressure, hyperglycemia, early CT ischemic changes, large baseline diffusion lesion volume, leukoaraiosis, and cerebral microbleeds on MRI; the evidence for a role of CAA in TICH continues to accumulate.

PCV17 - Effectiveness And Cost-Effectiveness Of Catheter-Directed Thrombolysis In Massive Pulmonary Embolism

PCV17 - Effectiveness And Cost-Effectiveness Of Catheter-Directed Thrombolysis In Massive Pulmonary Embolism

Compression in acute stroke: nursing considerations

British Journal of Neuroscience NursingVol. 11, No. Sup2 CommentCompression in acute stroke: nursing considerationsEmma GeeEmma GeeSearch for more papers by this authorEmma GeePublished Online:27 Apr 2015https://doi.org/10.12968/bjnn.2015.11.Sup2.20AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References CLOTS trial collaboration (2009) Effectiveness of thigh-length graduated compression stockings to reduce the risk of deep vein thrombosis after stroke (CLOTS Trial 1): a multicentre, randomised controlled trial. Lancet 373(9679): 1958–65 Crossref, Google ScholarCLOTS trials collaboration (2010) Thigh-length versus below-knee stockings for DVT prophylaxis after stroke: a randomised trial. Ann Intern Med 153(9): 553–62 Crossref, Google ScholarCLOTS (Clots in Legs Or sTockings after Stroke) Trials Collaboration et al. (2013) Effectiveness of intermittent pneumatic compression in reduction of risk of deep vein thrombosis in patients who have had a stroke (CLOTS3): a multicentre randomised controlled trial. Lancet 382(9891): 516–24 Crossref, Google ScholarCLOTS (Clots in Legs Or sTockings after Stroke) Trials Collaboration (2014) Effect of intermittent pneumatic compression on disability, living circumstances, quality of life, and hospital costs after stroke: secondary analyses from CLOTS 3, a randomised trial. Lancet Neurol 13(12): 1186–92 Crossref, Google ScholarKearon C (2003) Natural History of Venous Thromboembolism. Circulation 107(23): 122–30 Google ScholarKelly J, Rudd A, Lewis RR, Coshall C et al. (2004) Venous Thromboembolism after acute ischaemic stroke; a prospective study using magnetic resonance direct thrombus imaging. Stroke 35: 2320–25 Crossref, Google ScholarKohro S, Yamakage M, Sato K et al. (2005) Intermittent pneumatic foot compression can activate blood fibrinolysis without changes in blood coagulability and platelet activation. Acta Anaesthesiologica Scandinavica 49: 660–4 Crossref, Google ScholarLankeit M, Konstantinides S (2011) Mortality risk assessment and the role of thrombolysis in pulmonary embolism. Critical Care Clinics 27(4): 953–67 Crossref, Google ScholarNational Institute for Health and Care Excellence (2010) NICE clinical guidance 92. Venous thromboembolism: reducing the risk: Reducing the risk of venous thromboembolism (deep vein thrombosis and pulmonary embolism) in patients admitted to hospital. https://www.nice.org.uk/guidance/cg92 (accessed 26 March 2015) Google ScholarNational Institute for Health and Care Excellence (2015) Addendum to NICE clinical guidance CG92. Reducing the risk of venous thromboembolism in patients admitted to hospital (Chapter 24-stroke patients). Draft for consultation. http://tinyurl.com/pdyk9xz (accessed 26 March 2015) Google ScholarStevens S, Woller S (2013) Intermittent pneumatic compression in patients with stroke. Lancet 382(9891): 484–6 Crossref, Google Scholar FiguresReferencesRelatedDetails 1 April 2015Volume 11Issue Sup2ISSN (print): 1747-0307ISSN (online): 2052-2800 Metrics History Published online 27 April 2015 Published in print 1 April 2015 Information© MA Healthcare LimitedPDF download

Transforming and simplifying the treatment of pulmonary embolism: "safe dose" thrombolysis plus new oral anticoagulants.

Administration of systemic thrombolysis in pulmonary embolism (PE) has been limited to severe forms due to the risk of intracerebral hemorrhage (ICH). There is growing evidence from small studies that low-dose systemic thrombolysis has equal efficacy to standard dose, while eliminating the risk of ICH. Little data exists on the combined use of low-dose systemic thrombolysis and new oral anticoagulants (NOAC). We evaluated the clinical and echocardiographic outcome of patients treated with low or "safe dose" thrombolysis (SDT) and NOAC at intermediate term. We retrospectively identified 159 patients with massive and submassive PE who were treated with SDT and NOAC over a 2-year period by our group. They were followed prospectively for PE-related mortality, recurrent PE, bleeding, change in right/left ventricle (RV/LV) size, pulmonary artery systolic pressure (PASP), and clinical improvement at a mean follow-up of 18 ± 3 months. At 6 months, the RV/LV size was reduced from 1.29 ± 0.28 to 0.89 ± 0.03 (p < 0.001). The PASP dropped from 53.12 ± 3.85 mmHg to 30.39 ± 3.93 mmHg (p < 0.001). There was no ICH or in-hospital major or minor bleeding. At 18 months, three patients died of cancer. Recurrent PE developed in one patient who had been later switched to warfarin. The duration of hospitalization was 1.8 ± 0.3 days. With combination of SDT and NOAC, treatment of massive and submassive PE becomes identical and is transformed from an "anticoagulation first" to a "thrombolysis first" approach, thereby making treatment streamlined, simple, safe and effective, accessible and inexpensive.

Systemic thrombolysis in pulmonary embolism - another paradigm falling?

From the societiesSymposium der Kuratoriumsmitglieder der DGA: Führung und Kommunikation - Ärztliche Tätigkeit im Spannungsfeld zwischen Patienten, Kollegen und eigenem IchPublished Online:February 19, 2015https://doi.org/10.1024/0301-1526/a000424PDF ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinkedInReddit SectionsMoreFiguresReferencesRelatedDetails Volume 44Issue 2March 2015ISSN: 0301-1526eISSN: 1664-2872 InformationVasa (2015), 44, pp. 157-160 https://doi.org/10.1024/0301-1526/a000424.© 2015Hogrefe AGPDF download