Abstract
BACKGROUND:
This study aimed to investigate the impact of parenchymal infarction (PI) on the progression of pulmonary thromboembolism (PTE).
METHODS:
This retrospective, multicenter study evaluated patients diagnosed as having PTE via thoracic computed tomography angiography (CTA). Patients were divided into two groups, those with PI (Group 1) and those without PI (Group 2), based on CTA parenchymal windows. Clinical, demographic, radiologic, and laboratory characteristics, prognostic scores (Pulmonary embolism severity ındex [PESI]), early mortality evaluations, and 30-day mortality outcomes were recorded and compared between the groups, adhering to the European Society of Cardiology PTE guidelines.
RESULTS:
The study included 455 patients (mean age: 63.2 ± 16.8 years; 244 women [53.6%], 211 men [46.4%]). Group 1 consisted of 160 patients (35.2%), and Group 2 included 295 patients (64.8%). The mean age in Group 1 was 59 years, with a comorbidity rate of 70%. In Group 2, these were 65 years and 87%. Fever and C-reactive protein levels were significantly higher in Group 1 (P < 0.05). PESI scores and 30-day mortality rates were not statistically significant between the groups (P > 0.05). However, hemodynamic instability and high-risk PTE rates were significantly higher in Group 1 (P < 0.05).
CONCLUSION:
PI, observed in approximately one-third of PTE patients, may influence certain parameters affecting the prognosis of PTE.
KEYWORDS: Hemodynamic instability, pulmonary infarction, pulmonary thromboembolism
Background
Infarction refers to ischemic tissue necrosis in an organ caused by vascular pathologies. Infarction in vital organs (heart, kidneys, brain) can lead to severe clinical problems, but it can present with relatively milder symptoms in organs with collateral or dual blood supply systems, such as the lungs.[1]
Pulmonary infarction (PI) in pulmonary thromboembolism (PTE) arises from the occlusion of peripheral pulmonary arteries (PAs) by thrombus material, leading to tissue necrosis in the periphery of the occluded PAs. Studies report the prevalence of PI in PTE patients to range between 10% and 50%.[2] Uncertainty persists regarding which patients develop PI and its clinical implications. Historically, infarction has been considered a poor prognostic marker due to its association with impaired cardiac function. However, recent research suggests that healthier patients may be at greater risk of infarction due to a less robust collateral blood supply.[3]
PI is a condition observed in patients with PTE. However, PI is not included as a parameter in the PTE classification or mortality criteria in the European Society of Cardiology (ESC) guidelines.[4] This study aims to investigate the potential clinical effects of PI in PTE patients from a physician’s perspective.
Materials and Methods
This study, which was conducted in accordance with the International Declaration of Helsinki and received ethics committee approval (decision no: 353, date: November 27, 2024), was planned as a retrospective and multicenter study. The medical files of patients diagnosed as having definitive PTE through thoracic computed tomography angiography (CTA) between January 2021 and December 2023 in the Chest Diseases clinics of our centers were identified, and the records were documented. Based on the ESC guideline, the clinical, radiologic, demographic, and laboratory characteristics of the patients at the time of presentation were recorded. Patients with uncertain PTE diagnoses, patients diagnosed as having PTE through methods other than thorax CTA (ventilation perfusion (V/Q) scintigraphy and/or clinical diagnosis), patients diagnosed as having highly probable pneumonia before or together with PTE, patients with infiltrate density or nodules suggestive of interstitial lung disease (ILD) that could be confused with PI in thorax CTA parenchymal section, pregnant patients, and patients aged under 18 years were excluded from the study.
Study population
In all patients with PTE, age, sex, additional disease characteristics, fever, pulse, blood pressure, and apical heart rate (AHR) values at the time of diagnosis, oxygen saturation values at hospitalization, and partial pressure of oxygen values in arterial blood gas examinations were recorded. The thoracic CTAs of the patients were examined, and the presence of PI due to PTE and the lobar distribution of PI were recorded. In addition, the intravascular distribution of the detected thrombus (bilateral distribution within the pulmonary arterial system, presence of thrombus in the main PA root, right and left main PA, bilateral lobar, segmental, and subsegmental branches) and the presence of pleural effusion due to PTE were recorded. In addition, the presence of right ventricular strain findings on echocardiography (ECHO) and PA systolic pressures, and thrombus on Doppler ultrasonography (USG) were recorded. Routinely measured leukocytes (white blood cell), platelets, serum C-reactive protein (CRP), procalcitonin (PRC), alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, urea-creatinine, electrolytes, troponin, brain natriuretic peptide (BNP), and D-dimer levels during the diagnosis and treatment of PTE were recorded.
Assessment of prognostic status, early mortality outcomes, and definition of risk factors
The prognostic status and early mortality scores of all patients were recorded in accordance with the ESC guidelines.[4] Pulmonary embolism severity ındex (PESI) scoring was used for the prognostic assessment of PTE. The PESI scores of the patients were recorded [Appendix 1]. For the classification of the severity of PTE and the assessment of early mortality (EMA) (classification of pulmonary embolism severity and the risk of early (in-hospital or 30-day death), the patients were classified as low, moderate-high, moderate-low, and high risk [Appendix 2]. Again, according to the ESC guidelines, hemodynamic instability in PTE was defined as the presence of cardiac arrest, obstructive shock, and persistent hypotension[4] [Appendix 3]. For EMA (30 days), the numbers of low, moderate-high, moderate-low, and high risk patients and those with hemodynamic instability were recorded. The definition of risk factors for PTE in the patients was classified according to three subheadings as major risk factors for PTE, moderate risk factors for PTE, and weak risk factors for PTE, in accordance with the ESC guidelines [Appendix 4].
Definition of pulmonary ınfarction
The diagnosis of infarction was accepted as supportive of the diagnosis by the presence of a wedge-shaped consolidation in the lung parenchyma at the periphery of a segmental or subsegmental PA region occluded by thrombus material on thoracic CTA, and the presence of one or more of the following: central lucency and/or vessel signs and/or air bronchogram findings, as defined in previous studies on this subject[5] [Figure 1] The patients were divided into two groups, those with radiologic PE (Group 1) and those without (Group 2). The cases were divided into two groups as cases diagnosed with PE with radiologically detected PI (Group 1) and cases diagnosed with PE without radiologically detected PI (Group 2). Clinical, demographic, radiologic, laboratory data, EMAs, hemodynamic instability status, 30-day survival, Wells, and PESI scores of the two groups were compared.
Figure 1.
(a and b) Axial thoracic CT images showing pulmonary infarction in the lung parenchyma and thrombus in the pulmonary artery (Pulmonary infarction is shown in blue circles, thrombus in the pulmonary artery is shown with red arrows). (c and d) Coronal CT images showing peripheral pulmonary infarction in the right hemithorax (Pulmonary infarction is shown in blue circles, thrombus in the pulmonary artery is shown with red arrows).
Statistical analysis
Statistical analysis was performed using the SPSS 24.0 software package. Continuous variables are expressed as mean ± standard deviation, and categorical variables as percentages. Normal distribution was assessed using the Kolmogorov–Smirnov test. Comparisons were made using the Chi-square test, Student’s t-test, with P < 0.05 considered statistically significant.
Results
A total of 486 patients were examined for the study. Of these, seven were excluded because they were pregnant, 13 because their PTE diagnosis was made using V/Q scintigraphy, six because the PTE diagnosis was not definite (diagnosed with acute deep vein thrombosis and appropriate clinical picture), two because their PTE was diagnosed during pneumonia treatment, two because PI could not be distinguished from the radiologic findings of ILD and one because the retrospective screening revealed chronic thromboembolic hypertension (CTEPH).
Our study included 455 patients, 244 (53.6%) females and 211 (46.4%) males, with a mean age of 63.2 ± 16.8 years. PI was present on thorax CTA in 160 (35.2%) patients (Group 1), and not present on thorax CTA in 295 (64.8%) (Group 2). The mean number of lobes with PI was 1.8 ± 0.9. Three hundred seventy (81.3%) patients had an additional disease, and 85 (18.7%) had no additional disease. The most common additional disease detected was hypertension in 174 (38.2%) patients. The mean temperature, pulse rate, systolic-diastolic blood pressure, and oxygen saturation values of the patients at hospitalization were as follows: 36.5°C, 90.9 ± 18.2, 123.3 ± 21.6–73.8 ± 11.7 mmHg, and 92.6 ± 5.6, respectively. The only difference between the laboratory values of the two groups was detected in CRP values. CRP was statistically significantly higher in Group 1 (P < 0.001). The mean hospitalization period of the patients was 7.9 ± 5.8 days. The demographic characteristics, comorbidities, laboratory parameters, and clinical features (such as vital signs at presentation) of the two groups are presented in a comparative manner in Table 1. When the patients were evaluated according to the presence of risk factors for PTE, 119 (74.3%) patients in Group 1 and 223 (75.5%) patients in Group 2 had risk factors (P = 0.774). Fifty-three percent of the patients in Group 1 and 47% in Group 2 had a major risk factor (P = 0.024). A detailed comparison of the presence of risk factors in the two groups, as well as the distribution of existing risk factors by category (Major–Medium–Weak), is presented in Table 2.
Table 1.
Clinical, demographic and laboratory characteristics of patients with pulmonary thromboembolism with and without pulmonary infarction.
| Parameter | PI present (n=160) | PI absent (n=295) | P |
|---|---|---|---|
| Age (mean±SD) | 59.6±18 | 65.1±15.7 | 0.001 |
| Sex (female/male), n (%) | 82 (51.2)/78 (48.8) | 162 (54.9)/133 (45.1) | 0.454 |
| Comorbidities, n (%) | 112 (70) | 258 (87.5) | <0.001 |
| HT | 53 (33.1) | 121 (41) | 0.098 |
| Malignancy | 45 (28.1) | 79 (26.8) | 0.758 |
| DM | 29 (18.1) | 70 (23.7) | 0.167 |
| CHD | 29 (18.1) | 60 (20.3) | 0.570 |
| CRD | 19 (11.9) | 69 (23.4) | 0.003 |
| CND | 21 (13.1) | 2 (9) | 0.696 |
| CKD | 4 (5.3) | 35 (11.9) | 0.553 |
| Clinical features (mean±SD) | |||
| Body temperature (°C) | 36.6±0.4 | 36.5±0.4 | 0.033 |
| Pulse (/min) | 92.1±18.1 | 90.2±18.2 | 0.305 |
| Systolic blood pressure (mmHg) | 120.8±19.5 | 124.6±22.5 | 0.079 |
| Diastolic blood pressure (mmHg) | 72.7±10.9 | 74.5±12.1 | 0.111 |
| Hospitalization saturation (%) | 92.5±6.4 | 92.7±5.1 | 0.560 |
| Laboratory values (mean±SD) | |||
| WBC (103UL) | 8966±4838 | 8349±4426 | 0.171 |
| HB (g/dL) | 12.2±1.8 | 12.6±8 | 0.534 |
| PLT (103/uL) | 26,5721±115,174 | 25,0169±115,464 | 0.171 |
| MPV (fL) | 10±1 | 10.1±1.3 | 0.354 |
| LDH (U/L) | 273.7±148.2 | 282.6±148.1 | 0.584 |
| D-dimer (mg/L) | 8.5±8.9 | 8±11.2 | 0.720 |
| D-dimer quality | 6718±9309 | 3569.7±4583 | 0.072 |
| Urea (g/dL) | 35.3±18 | 39.4±33.8 | 0.149 |
| Creatinine (mg/dL) | 0.9±0.2 | 0.9±0.4 | 0.175 |
| ALT (U/L) | 30.4±30.5 | 27.5±27.4 | 0.315 |
| AST (U/L) | 29.1±27 | 30.2±30.5 | 0.693 |
| Albumin (g/L) | 36.7±6.6 | 38.1±19.4 | 0.385 |
| CRP (μg/L) | 86.5±86.8 | 58.6±72.1 | <0.001 |
| PRC (mg/dL) | 0.4±1.3 | 0.7±4 | 0.372 |
| BNP (ng/L) | 1860±3826 | 2380±4589.4 | 0.380 |
| Troponin (ng/L) | 42.4±74.4 | 56.3±112.1 | 0.238 |
| ABG-pO2 value (mmHg) | 65.3±18.7 | 62.2±18.5 | 0.410 |
| Day of hospitalization (mean±SD) | 8.5±6.6 | 7.6±5.3 | 0.113 |
ABG: Arterial blood gas, ALT: Alanine amino transferase, AST: Aspartate amino transferase, BNP: Brain natriuretic peptide, CRP: Serum reactive protein, DM: Diabetes mellitus, HB: Hemoglobin, HT: Hypertension, CRD: Chronic respiratory disease, CHD: Chronic heart disease, CND: Chronic neurological disease, CKD: Chronic kidney disease, AHR: Apical heart rate, female: LDH: Lactate dehydrogenase, MPV: Mean platelet volume, PI: Pulmonary infarction, PLT: Platelet, PRC: Procalcitonin, SD: Standard deviation, pO2: Oxygen partial pressure, WBC: White blood cell
Table 2.
Distribution of patients according to risk factors for pulmonary thromboembolism.
| Risk factors | PI present (n=160), n (%) | PI absent (n=295), n (%) | P |
|---|---|---|---|
| Risk factor present | 119 (74.3) | 223 (75.5) | 0.774 |
| Major risk factor present | 86 (53.7) | 126 (42.7) | 0.024 |
| Medium risk factor present | 15 (9.3) | 41 (13.8) | 0.161 |
| Weak risk factor present | 16 (10) | 56 (18.9) | 0.012 |
| Hereditary risk factor present | 2 (1.2) | - | 0.054 |
PI: Pulmonary infarction
When the radiologic features of both groups were examined, the presence of bilateral segments and subsegment PA branches and pleural fluid due to PTE was statistically significantly higher in Group 1 (P = 0.041, P = 0.002, and P < 0.001, respectively). On the other hand, the presence of thrombus in bilateral venous Doppler USG was higher in Group 2 (P = 0.027). The distribution of thrombi detected in the pulmonary arterial system on thoracic CTA, as well as the echocardiographic (ECHO) and bilateral lower extremity venous Doppler ultrasound (USG) findings of the two groups, are presented in detail in Table 3. When the prognostic status and early mortality data of both groups were examined, the mean Wells score of Groups 1 and 2 was 5 ± 2.3 and 4.2 ± 2.5, respectively (P = 0.002). The mean PESI scores of Groups 1 and 2 were 90.9 ± 37.6 and 94 ± 30.9, respectively (P = 0.341). The distribution and comparison of the PESI score classification (a scoring system to predict mortality, survival, and clinical outcomes) between the two groups are presented in detail in Table 4. In terms of EMA, the number of high-risk patients in Group 1 and Group 2 was 16 (10%) and 14 (4.8%), respectively (P = 0.034). The risk stratification table used to predict and assess early mortality in PTE cases, along with the statistical comparison of the distribution percentages of the parameters comprising this table between the two groups, is presented in detail in Table 5.
Table 3.
Radiologic characteristics of pulmonary thromboembolism patients with and without pulmonary infarction.
| Radiologic parameters | PI present (n=160), n (%) | PI absent (n=295), n (%) | P |
|---|---|---|---|
| Embolism in the main pulmonary artery on thorax CTA | 14 (8.7) | 37 (12.5) | 0.221 |
| Embolism in the left pulmonary artery on thorax CTA | 42 (26.2) | 40 (13.5) | 0.001 |
| Embolism in the right pulmonary artery on thorax CTA | 52 (32.5) | 79 (26.7) | 0.198 |
| Embolism in both PAs on thorax CTA | 48 (30) | 69 (23.3) | 0.123 |
| Embolism in unilateral segment branches on thorax CTA | 56 (35) | 95 (32.2) | 0.545 |
| Embolism in bilateral segment branches on thorax CTA | 100 (62.5) | 155 (52.5) | 0.041 |
| Unilateral subsegment branch embolism on thorax CTA | 44 (27.5) | 67 (22.7) | 0.256 |
| Bilateral subsegment branch embolism on thorax CTA | 90 (56.2) | 122 (41.3) | 0.002 |
| Presence of pleural fluid due to embolism on thorax CTA | 73 (45.6) | 35 (11.8) | <0.001 |
| Presence of thrombus on Doppler USG | 60 (24) | 81 (36.3) | 0.027 |
| Presence of right ventricular involvement on ECHO | 47 (29.3) | 74 (25) | 0.656 |
| Pulmonary artery systolic pressure value on ECHO (mean±SD) | 34.9±13.8 | 37.6±14.6 | 0.094 |
CTA: Computed tomography angiography, ECHO: Echocardiography, PI: Pulmonary infarction, USG: Ultrasonography, SD: Standrad deviation, PAs: Pulmonary arteries
Table 4.
Distribution of patients according to pulmonary embolism severity index scores.
| PESI score distribution | PI present (n=160), n (%) | PI absent (n=295), n (%) | P |
|---|---|---|---|
| PESI-I | 39 (24.4) | 49 (16.6) | 0.045 |
| PESI-II | 41 (25.6) | 78 (26.4) | 0.850 |
| PESI-III | 30 (18.8) | 68 (23.1) | 0.287 |
| PESI-IV | 23 (14.4) | 61 (20.7) | 0.098 |
| PESI-V | 27 (16.9) | 39 (13.2) | 0.291 |
PESI: Pulmonary embolism severity index, PI: Pulmonary infarction
Table 5.
Risk distribution in early mortality evaluation.
| Risk level | PI present (n=160), n (%) | PI absent (n=295), n (%) | P |
|---|---|---|---|
| High risk | 16 (10) | 14 (4.7) | 0.034 |
| Intermediate-high risk | 23 (14.3) | 62 (21) | 0.076 |
| Intermediate-low risk | 46 (28.7) | 106 (35.9) | 0.804 |
| Low risk | 83 (51.8) | 123 (41.6) | 0.050 |
PI: Pulmonary infarction
The number of patients with hemodynamic instability was 17 (10.6%) in Group 1 and 16 (5.4%) in Group 2 (P = 0.041).
When the 30-day mortality results of both groups were evaluated, nine (5.6%) patients in Group 1 and 26 (8.8%) patients in Group 2 died within 30 days from the time of diagnosis (P = 0.223).
DISCUSSION
In this study, the characteristics of patients with PTE with radiologic PI detected in the lung parenchyma were investigated. Interestingly, hemodynamic instability and high-risk PTE incidence were statistically significantly higher in patients with PI detected in the PTE group. PI was more common in patients with major risk factors for PTE. In addition, our patients with PI detected had fewer comorbidities and were in a relatively younger age group. Fever and CRP values were higher in terms of clinical and laboratory features. Radiologically, bilateral PA segment and subsegment branch filling defects and pleural effusion due to PTE were higher in the PI group. There was no statistically significant difference between PESI scores and 30-day mortality values.
The hypothesis that PI is more common in older patients with more comorbidities is about to lose its validity with current studies.[6,7] Current studies suggest that younger, healthier patients are at greater risk for PI due to less collateral circulation compared with older patients with more comorbidities.[5,8] Although there are interesting studies on different radiologic imaging methods in the diagnosis of PI, thoracic CTA remains the gold standard method[9,10,11,12] In the majority of studies on patients with PTE with PI, more filling defects are detected in the segmental and subsegmental branches of the PAs and more pleural effusion is seen in patients with PI. This finding is an expected finding in accordance with the physiopathology of PI.[13]
CRP is a nonspecific laboratory method that can quantitatively evaluate the inflammatory process, which can be increased in noninfectious conditions that cause inflammation or tissue damage, as well as infections. It usually starts to increase in serum within a few hours after the onset of inflammation[14] because PI is an inflammatory cascade, and tissue necrosis, fever, and CRP elevation in patients with PI can be seen as a response of the immune system.[15,16] PRC levels, which are considered specific to bacterial infections, are not expected to significantly increase in necrosis, inflammation, and viral infections, unlike CRP.[17] We think that the possible reason for the significant difference in CRP values in the PI group and the lack of a significant difference between PRC values in our study is that PI is an inflammatory process.
Many of the results of our study were consistent with the literature. Notably, age, comorbidity, some radiologic features (segmental and subsegmental embolism), fever, and CRP elevation were consistent with the literature and the pathophysiology of the disease and were as expected. In a recent review on the subject, Gagno et al.[3] stated that there were nonspecific molecular methods such as D-dimer, troponin, and BNP that support the diagnosis of PTE, but there was no molecular method that supported the diagnosis of PI. In our opinion, moderate CRP elevation in patients with PTE that is not accompanied by PRC elevation and do not describe clinical signs of infection may be a candidate molecular aid to overcome this deficiency.
It is expected that PI will resolve over time, but because thorax CT cannot be performed repeatedly to monitor the situation, it is not clear how long it takes for resolution to occur. There is a need for studies to investigate the feasibility of using increasing CRP in monitoring resolution depending on the developing PI.
There is an uncertain situation regarding the clinical effects and mortality of PI, which can be seen in approximately one-third of patients with PTE. A significant portion of studies conducted on the subject show that there is no significant mortality difference in the presence of PI.[5,8,15] A few studies have emphasized that even if there is no mortality difference, the presence of PI may cause some undesirable clinical conditions. Kaptein et al.[18] observed that patients with PTE with PI developed more functional limitations in their 3-month follow-up. Cha et al.[13] reported that there was no mortality difference between the two groups in their study, but thrombolytic agent use was higher in patients with PI (P = 0.07). Chengsupanimit et al.[19] documented 97% survival at discharge in their study with 74 patients with PI, with an average age of 55 years. It has been reported that there was a slight decrease in survival rates in the 3rd and 6th months after discharge of the same patients (93% and 88%, respectively). Apart from this, in some patients with PTE with PI, which were reported as case reports, it has been shown that the presence of PI may have a negative effect on survival due to secondary infections occurring in the PI region.[20,21]
In our study, 30-day mortality rates were similar between the two groups. Although the mortality indicators of our study are consistent with the literature, we would like to state that we have a different opinion on this point. Although PI groups consist of younger patients in most studies in the literature and in our study, and there is no statistically significant difference between the two groups in terms of serious comorbidities such as cancer/chronic heart disease; the fact that the mortality rates in the PI group were similar to the non-PI group is actually an important result that should be considered. One of the important results of our study was that the rate of hemodynamic instability and high-risk PTE was significantly higher in the PI group. We could not find a study in the English literature directly examining the relationship between PI and hemodynamic instability and high-risk PTE. However, a hypothesis proposed by Akhoundi et al.[22] in patients with PTE with PI is interesting. In their study,[22] the authors designed a new index (New Combined Qanadli Index) by adding “PI and increased right ventricle/left ventricle (RV/LV) ratio” to the Qanadli index in pulmonary CTAs of patients with PTE to predict short-term mortality in patients with PTE, considering that the status of the lung parenchyma (presence of PI) or the presence of increased RV/LV ratio could be quite effective in determining the prognosis of patients. They found this new index to be superior in predicting changes in cardiovascular parameters and short-term mortality in patients with PTE. This study supports, in one respect, that the presence of PI is a parameter that should be taken into consideration in patients with PTE.
There are several limitations of our study that should not be ignored when interpreting the study results or planning new studies on the subject. The first and most important is that it has a retrospective design, and in retrospective studies, there may be significant data losses that will affect the results. Although it is multicenter, the number of patients is relatively small. The small number of patients in subgroup analyses, such as hemodynamic instability and 30-day mortality, significantly affected the power of the study. Although we did not include clinically radiologically lung parenchymal infections, ILD, and peripheral nodules that could be confused with PI, our definition of PI was a radiologic-based diagnosis.
Conclusion
As a result, the vast majority of the results of this study are consistent with previous related studies in the literature. We observed more hemodynamic instability and high-risk embolism in patients in the presence of PI. We think that the fact that PI was observed in younger patients and that the groups were similar in terms of serious comorbidities, despite the fact that their 30-day mortality rates were similar, is a significant result, both in the studies conducted in the literature and in our study. Future studies on the subject will clarify whether these two data obtained in our study (hemodynamic instability and high-risk embolism PI relationship) are variables that affect the relation between PI in younger patients and comorbidity severity.
Author contributions
Conceptualization: Coşkun Doğan, Elif Torun Parmaksız; Data curation: Coşkun Doğan, Metin Karakaya, Sibel Karakaya, Ceren Çelik; Formal analysis: Coşkun Doğan, Samet Samancı, Ülkü Aka; Funding acquisition: Coşkun Doğan, Demet Turan, Sacit İçten; Investigation: Özlem Soğukpınar, Makbule Özlem Akbay; Methodology: Coşkun Doğan, Ferhan Karataş; Project administration: Ülkü Aka, Demet Turan, Elif Torun Parmaksız; Resources: Şükran Mutlu, Salih Küçük, Göksel Menek; Software: Şükran Mutlu, Salih Küçük, Metin Karakaya, Sibel Karakaya, Ceren çelik; Supervision: Coşkun Doğan, Ferhan Karataş, Göksel Menek; Validation: Coşkun Doğan, Samet Samancı; Visualization: Coşkun DOĞAN, Ülkü Aka, Demet Turan, Sacit İçten; Roles/Writing - original draft: and Writing - review and editing: Coşkun Doğan.
Ethical statement
The Declaration of Helsinki was complied with and ethics committee approval was obtained. Approval was obtained from the ethics committee of our hospital (decision no: 353, date: November 27, 2024).
Patient consent
The written informed consent was obtained from all patients for this study.
Data availability statement
Data are available if requested.
Conflicts of interest
There are no conflicts of interest.
Acknowledgments
None.
Appendix 1: Pulmonary Embolism Severity Index scoring.
| Variable | PESI |
|---|---|
| Age >80 years | Age/year |
| Male sex | +10 points |
| Presence of cancer | +30 points |
| History of heart failure | +10 points |
| History of chronic lung disease | +10 points |
| Heart rate ≥110/min | +20 points |
| Systolic blood pressure <100 mmHg | +30 points |
| Respiratory rate ≥30/min | +20 points |
| Body temperature <36°C | +20 points |
| Mental status change | +60 points |
| SpO2 <90% | +20 points |
| Low-risk | |
| Class I | ≤65 |
| Class II | 66–85 |
| High-risk | |
| Class III | 86–105 |
| Class IV | 106–125 |
| Class V | >125 |
PESI: Pulmonary Embolism Severity Index, SpO2: Oxygen saturation
Appendix 2: Classification of pulmonary embolism severity and the risk of early death.
| Risk indicators | ||||
|---|---|---|---|---|
| Early mortality risk | Hemodynamic instability | PESI class III–IV | Ventricular dysfunction on TTE or CTA | Increased cardiac troponin levels |
| High | + | + | + | + |
| Intermediate-high | − | + | + | + |
| Intermediate-low | − | + | One (+) or both (−) | |
| Low | − | − | − | − |
CTA: Computed tomography angiography, PESI: Pulmonary Embolism Severity index, TTE: Transthoracic echocardiography
Appendix 3: Definition of hemodynamic instability in pulmonary embolism.
| Cardiac arrest | Obstructive shock | Persistent hypotension |
|---|---|---|
| Presence of cardiac arrest requiring cardiopulmonary resuscitation | Systolic blood pressure <90 mmHg or Despite adequate fluid support, vasopressor requirement to maintain systolic blood pressure ≥90 mmHg and End-organ hypoperfusion (altered consciousness, cold-clammy skin, oliguria/anuria, increased serum lactate level) End organ hypoperfusion (altered mental status, cold and clammy skin, oliguria/anuria, increased serum lactate levels) |
Systolic blood pressure <90 mmHg or A decrease in systolic blood pressure of more than 40 mmHg (lasting longer than 15 min and not explained by new-onset arrhythmia, hypovolemia, or sepsis) |
Appendix 4: Classification of risk factors for pulmonary thromboembolism.
| Major risk factors for PTE |
| Lower extremity fracture, hospitalization for CHF/AF/flutter (in the last 3 months), hip or knee replacement, major trauma, MI in the last 3 months, previous VTE, presence of spinal cord injury |
| Moderate risk factors for PTE |
| Arthroscopic knee surgery, autoimmune disease, blood transfusion, CVP, IV catheters, CT therapy, CHF or RF, erythropoiesis stimulating agents, hormone replacement therapy, in vitro fertilization, OC therapy, postpartum therapy, infection, IBD, cancer, paralytic stroke, superficial vein thrombosis, presence of thrombophilia |
| Weak risk factors for PTE |
| Bed rest for more than 3 days, DM, arterial HT, sitting still for long periods, advanced age, laparoscopic surgery, obesity, pregnancy, varicose veins, presence of venous catheters |
AF: Atrial fibrillation, DM: Diabetes mellitus, CT: Chemotherapy, CHF: Congestive heart failure, HT: Hypertension, MI: Myocardial ınfarction, OC: Oral contraceptive, VTE: Venous thromboembolism, IBD: Inflammatory bowel disease, IV: Intravenous, RF: Respiratory failure, CVP: Central venous catheter, PTE: Pulmonary thromboembolism
Funding Statement
Nil.
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Associated Data
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Data Availability Statement
Data are available if requested.