Objective
To describe the clinical profiles of cardiac arrest due to fatal pulmonary embolism (FPE), and review the literature on FPE diagnosis and treatment.
Methods
The clinical profiles of two cases with cardiac arrest for FPE were presented. A systematic search of Medline (1950 - 2014) and EMbase (1980-2014) was conducted to identify studies that investigated the use of thrombolytic medications to treat cardiac arrest for FPE.
Results
The fatal event of two patients occurred after surgery. Both of them survived with cardiopulmonary resuscitation and administration of thrombolysis and anticoagulation, but one of them had major bleeding during anticoagulation. Six articles were found involving 72473 cases of cardiac arrest due to pulmonary embolism (PE) or unstable massive PE. The thrombolytic agents were recombinant tissue plasminogen activator or streptokinase, but the administration and dose of thrombolytic agents were unclear. Overall, administration of thrombolytics can shorten the time to return of spontaneous circulation and improve the survival rate. There was, however, an increased risk of bleeding events following administration of thrombolytics.
Conclusions
Because of the high mortality of cardiac arrest for FPE, the clinician should correctly identify patients with a high likelihood of FPE. Early use of thrombolytics is very important and can potentially improve patient outcomes.
To assess the efficacy and safety of thrombolytic therapy. Electronic search was applied to the Cochrane Airways Group register (MEDLINE, EMBASE, CINAHL standardized searches) with the date up to 2003 April. Hand searched respiratory journals and meeting abstracts. All randomized controlled trials comparing thrombolytic therapy with heparin alone or surgical intervention (eg. embolectomy) met the inclusion criteria. Two reviewers independently selected trials, assessed trial quality and extracted the data.
Objective To investigate the risk factors, clinical characteristics and prognostic factors of venous thrombosis (and pulmonary embolism) in patients with idiopathic hypereosinophilia (IHE) so as to provide a theoretical basis for clinical prevention of venous thrombosis and improve prognosis.Methods Thirty-nine patients with IHE admitted to West China Hospital of Sichuan University from January 2010 to January 2022 were collected in this retrospective case-control study to explore the risk factors of venous thrombosis (including pulmonary embolism) and thrombosis recurrence after treatment. Results There were 17 (43.5%) patients combined with venous thrombosis of 39 patients with IHE. In the patients with vascular involvement, pulmonary embolism was the initial expression of IHE accounted for 29% (5/17). patients of IHE with pulmonary embolism were younger [44 (24.5 - 51.0) vs. 56 (46.3 - 67.8) year, P=0.035] and had higher peak absolute eosinophil counts [11.7 (7.2 - 26.5)×109/L vs. 3.8 (2.9 - 6.7)×109/L, P=0.020] than those without pulmonary embolism. After a mean follow-up of 13 months (2 - 21 months), thrombosis recurred in 35.3% (6/17) of patients. Persistent increasing in eosinophils (>0.5×109/L) was an independent risk factor for thrombus recurrence (odds ratio 13.33, 95% confidential interval 1.069 - 166.374). Conclusions Thrombosis is a common vascular impaired complication in IHE , and increased eosinophilia is a risk factor for thrombosis and thrombus recurrence after therapy. Controlling and monitoring the eosinophilic cell levels in patients with IHE may avoid severe comorbidities.
ObjectiveTo investigate diagnostic and prognostic value of pulmonary embolism severity index (PESI), troponin I (cTnI) and brain natriuretic peptide (BNP) in patients with acute pulmonary embolism (APE).
MethodsA total of 96 patients confirmed with APE were collected from January 2010 to January 2013, and 50 cases of non-APE controls were also selected in the same period. According to the PESI scores, patients were divided into low-risk, mid-risk, and highrisk group. According to the results of cTnI and BNP, patients were divided into positive group and negative group. Then, we evaluated the diagnostic and prognostic value of the PESI score, cTnI and BNP for patients with APE.
ResultsFor the APE patients, the higher the risk was, the higher the constituent ratio of massive and sub-massive APE was (P<0.01). In the cTnI positive group, massive and sub-massive APE accounted for 82.9%, and in the cTnI negative group, non-massive APE was up to 81.9%; in the BNP positive group, massive and sub-massive APE accounted for 73.3%, and in the BNP negative group, non-massive APE was up to 86.3%. The patients with positive cTnI and BNP had a higher rate of right ventricular dysfunction, cardiogenic shock and mortality than the negative group (P<0.01).
ConclusionThe combined detection of cTnI, BNP and PESI score is important in the diagnosis and risk stratification in APE patients.
Objective
To explore the relationship between thrombocytosis and all-cause in-hospital mortality in patients with chronic obstructive pulmonary disease (COPD) and low-risk pulmonary embolism (PE).
Methods
In a multicenter retrospective study on clinical characteristics, COPD patients with proven acute PE between October 2005 and February 2017 were enrolled. The patients in risk classes III-V on the basis of the PESI score were excluded. The patients with COPD and low-risk PE were divided into two groups of those with thrombocytosis and without thrombocytosis after extracting platelet count on admission. The clinical characteristics and prognosis of the two groups were compared. Multivariate logistic regression was performed to reveal an association between thrombocytosis and all-cause in-hospital mortality after confounding variables were adjusted.
Results
A total of 874 consecutive patients with COPD and PE at low risk were enrolled in which 191 (21.9%) with thrombocytosis. Compared with those without thrombocytosis, the thrombocytopenic group had significantly lower body mass index [(20.9±3.3) kg/m2 vs. (25.1±3.8) kg/m2, P=0.01], lower levels of forced expiratory volume in one second (FEV1) [(0.9±0.4) L vs. (1.3±0.3) L, P=0.001] and lower partial pressure of oxygen in the arterial blood (PaO2) [(7.8±1.2) kPa vs. (9.7±2.3) kPa, P=0.003]. The COPD patients with thrombocytosis had a higher proportion of cardiovascular complications as well as higher level of systolic pulmonary arterial pressure (sPAP) [(46.5±20.6) mm Hg vs. (34.1±12.6) mm Hg, P=0.001]. Multivariate logistic regression analysis after adjustment for confounders revealed that thrombocytosis was associated with all-cause mortality in hospitalized patients with COPD and low-risk PE (adjusted OR=1.53, 95%CI 1.03–2.29), and oral antiplatelet treatment was a protective factor (adjusted OR=0.71, 95%CI 0.31–0.84).
Conclusions
Thrombocytosis is an independent risk factor for all-cause in-hospital mortality in COPD patients with PE at low risk. Antiplatelet therapy may play a protective role in the high-risk cohort.
