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Inferior vena cava thrombosis in patients undergoing extracorporeal membrane oxygenation: a case series and literature review

BMC Anesthesiology volume 24, Article number: 437 (2024) Cite this article

Abstract

Background

Extracorporeal membrane oxygenation (ECMO) is mainly used for support of patients with cardiopulmonary collapse. The increasing use of ECMO has shown promising outcomes; however, it still carries the risk of significant complications. Inferior vena cava (IVC) thrombosis is an underestimated complication.

Methods

We described a series of 5 ECMO patients diagnosed with IVC thrombosis in our institution. An electronic literature search of the PubMed, Cochrane Library and Web of Science databases. A total of 12 cases were identified.

Results

The occurrence of IVC thrombosis in ECMO patients is not uncommon. In our case series, elevated CRP and PCT levels and activated partial thromboplastin times (aPTT) of less than 50 s during ECMO operation were observed. In the literature review, a higher proportion of veno-arterial (VA) ECMO application (67%; 8/12) was presented in patients with IVC thrombosis. Eight patients (73%; 8/11) were monitored for anticoagulation using either aPTT or a combination of aPTT and ACT, with all aPTT measurements achieving the target range for anticoagulation. The mainstay of treatment for IVC thrombosis was anticoagulation alone (75%; 9/12). After the treatment, IVC thrombosis disappeared in the majority of patients (75%; 9/12) and there was no thrombosis-related mortality.

Conclusion

Factors such as elevated CRP and PCT levels, low aPTT levels, and the use of VA ECMO may contribute to the development of ECMO-related IVC thrombosis. Monitoring of anticoagulation with aPTT alone or in combination with ACT during ECMO may have inherent limitations. Anticoagulation alone may be an effective treatment for IVC thrombosis.

Peer Review reports

Introduction

Extracorporeal membrane oxygenation (ECMO) has been increasingly used for support of patients with cardiopulmonary collapse [1]. According to the Extracorporeal Life Support Organization (ELSO), more than 200,000 patients worldwide had received ECMO support and half of them had been discharged alive from ELSO centers [2]. Despite its increasing use and encouraging results, ECMO still carries the risk of a number of severe complications, such as bleeding, thrombosis, hemolysis and infection [3]. As a form of venous thromboembolism, more than 30% of cases of IVC thrombosis led to fatal pulmonary embolism (PE), while 20% of unresolved IVC thrombosis cases led to chronic venous insufficiency (CVI) and post-thrombotic syndrome (PTS) [4, 5]. In rare cases, IVC occlusion due to IVC thrombosis can lead to severe lumbar radicular pain, sciatica, and even cauda equina syndrome [6, 7]. However, limited individual case reports have described ECMO-related IVC thrombosis, and the management and prognosis of IVC thrombosis is still lacking.

In this study, we report a case series of 5 ECMO patients with IVC thrombosis in our intensive care unit (ICU) and provide a review of the available literature on similar cases. This review may provide some insight for the prevention and treatment of IVC thrombosis during ECMO.

Patients and methods

Patients

The study included 5 patients diagnosed with IVC thrombosis during ECMO at our institution from May 1, 2021 to October 1, 2023, out of a total of 103 patients who underwent ECMO treatment during the same period. Medical records were reviewed for patient characteristics, laboratory tests, ECMO parameters, and interventions for IVC thrombosis. The study was approved by the Institutional Research and Ethics Committee (IREC) of our institution and patient consent waived by the IREC due to its retrospective and observational nature. All patient data included in this study has been anonymized.

Methodology of literature review

Electronic searches

We conducted a review of the literature by searching the PubMed, Cochrane Library and Web of Science databases from January 1, 1997 to October 31, 2023. The following search terms were used and combined: “extracorporeal membrane oxygenation”, “ECMO”, “inferior vena cava thrombosis” and “IVC thrombosis”. Only articles in the English language were included. All published case reports and case series on ECMO with IVC thrombosis were considered relevant and selected for review.

Criteria for considering publications

The criteria for the inclusion of publications in this review were (1) reported on relevant cases; (2) patients underwent ECMO; (3) IVC thrombosis was confirmed by imaging tests such as ultrasound, CT scan.

The criteria for the exclusion of publications in this review were (1) cases of IVC thrombosis during ECMO not reported in the full text; (2) patients with a history of IVC thrombosis before ECMO therapy; (3) cases that did not explicitly report the details of anticoagulation therapy during ECMO.

Data extraction and management

Two review authors independently extracted the data related to sex, age, the primary cause of ECMO (severe pneumonia, fulminant myocarditis, lung transplantation, etc.), catheter position, ECMO circuit, anticoagulants, anticoagulation assay methods, total duration of ECMO, IVC thrombosis and patient outcomes. Additional data related to the authors and year of publication were recorded, as well.

Statistical analysis

A narrative synthesis of the collected data was undertaken. Data on the parameters listed above were extracted, pooled, and re-analyzed. Continuous variables are presented as mean ± standard deviations, while categorical variables are represented by numbers and percentages. The collected data were analyzed using the SPSS 26.0 for Windows statistical analysis software (IBM Corporation., New York, NY; formerly SPSS Inc., Chicago, IL).

Results

Case 1

A 29-year-old female was admitted to the ICU with cardiogenic shock due to Takotsubo syndrome, and bedside ultrasound showed the severely weakened left ventricular systolic function. Despite the administration of a high dose of inotropic agents, the circulation was still difficult to maintain. The VA ECMO was introduced done through the right femoral artery cannula size 16 Fr and the left femoral vein cannula size 18 Fr. Considering the patient's recent brain surgery history and severe hepatic insufficiency, anticoagulation was not performed during ECMO. ECMO was weaned on day 5 and a thrombosis in the IVC was revealed by Ultrasound after decannulation. An IVC filter was placed to prevent the dislodgement of the thrombus. With enoxaparin anticoagulation for two weeks, ultrasound assessments found thrombosis in the IVC and right common femoral vein had disappeared. The IVC filter was removed after the thrombus disappeared. This patient's general condition gradually improved without other thrombus complications, and she was discharged smoothly.

Case 2

A 42-year-old female was admitted to our ICU with cardiogenic shock due to fulminant myocarditis. VA ECMO was initiated and continuous anticoagulation therapy was administered using Nafamostat mesylate and unfractionated heparin (UFH) during ECMO support. A 20F cannula was placed in the right femoral artery and an 18F cannula was placed in the right femoral vein. As the clinical status of patient improved, VA ECMO was discontinued after 9 days. After decannulation, an IVC thrombosis was discovered using bedside ultrasound. In spite of continuous anticoagulation with UFH and enoxaparin for 7 days and thrombolytic therapy with intravenous alteplase, the thrombus did not shrink obviously. Then, this patient underwent Catheter-Directed Thrombolysis (CDT) and sequential enoxaparin anticoagulation. No residual thrombotic material was detected by ultrasound after 3 days of CDT treatment.

Case 3

A 21-year-old male suffered multiple fractures following a fall from a height (sixth floor). He developed severe acute respiratory distress syndrome (ARDS) and was provided with a VV ECMO system. Cannulation was performed via femoro-jugular approach using a right femoral drainage cannula (21F) and a right jugular reinfusion cannula (19F). Intermittent anticoagulation was performed because the patient's thoracic and abdominal drains showed bloody fluid and the patient's hemoglobin and platelets were very low during anticoagulation. As the patient’s condition improved, ECMO was removed after 10 days. Bedside ultrasound revealed a thrombus measuring 4.38*1.30 cm in the IVC. With continuous UFH anticoagulation, no remaining thrombotic material was observed.

Case 4

A 67-year-old male was admitted to the ICU with severe pneumonia. VV ECMO was performed. The right internal jugular vein was cannulated for infusion (19 F), and the right femoral vein was cannulated for drainage (21 F). Continuous anticoagulation with argatroban was performed. On day 23, during postural changes, the patient developed sudden hypoxemia and low ECMO flow. Bedside ultrasound revealed a thrombus in the IVC near the right atrium inlet. Despite therapy with systemic argatroban anticoagulation and intravenous alteplase thrombolysis, the thrombus did not shrink apparently. This patient then underwent CDT therapy, and bedside ultrasound demonstrated an obvious shrunken thrombus.

Case 5

A 16-year-old boy was transferred to the ICU with severe pneumonia. After 16 h of continuous prone position ventilation and optimization of ventilation parameters, the arterial pH < 7.25 and PaCO2 > 60 mmHg for over 6 h, VV ECMO was then performed with Nafamostat mesylate continuous anticoagulation. A 21F cannula was placed in the right femoral vein and an 18F cannula was placed in the right jugular vein. As the patient’s condition improved, ECMO was taken off after 5 days. Bedside ultrasound showed a thrombus formation in the IVC after decannulation. Subcutaneous enoxaparin was administered and the thrombus gradually shrunk assessed by bedside ultrasound. The patient was then transferred to a specialized rehabilitation hospital on day 16.

Results of the case series

From May 1, 2021 to October 1, 2023, a total of 103 patients were treated with ECMO in the ICU of our institution, among whom five (4.9%; 5/103) developed IVC thrombosis. The detail characteristics of the five patients were described in Table 1. The ECMO details and intervention of IVC thrombosis were presented in Table 2. During the ECMO procedure, CRP and PCT levels were elevated in all five patients, and the aPTT values were less than 50 s in all patients.

Table 1 Baseline Characteristics of Patients
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Table 2 The ECMO details and intervention of IVC thrombosis
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Results of the literature review

We identified 11 references through an electronic search of the PubMed, Cochrane Library and Web of Science databases. The reference flow is summarized in the study flow chart (Fig. 1). Initially, 57 records were identified through database searching. After removing duplicates, 44 records remained. Then by carefully reading the full text, we excluded 24 irrelevant references that did not report ECMO-related IVC thrombosis. Of the remaining 20 records, we further excluded 3 references because of thrombosis occurring prior to ECMO. Finally, we excluded literature that did not explicitly report the details of the anticoagulation regimen during ECMO. Twelve patients who developed IVC thrombosis during ECMO were included (Table 3).

Fig. 1
figure 1

This flowchart details the process used to select studies for analysis in our review of inferior vena cava thrombosis (IVCT) in patients on extracorporeal membrane oxygenation (ECMO). Initially, 57 records were identified through database searches, reduced to 44 after duplicates were removed. Following screening, studies were excluded based on absence of IVCT cases, IVCT prior to ECMO, or unspecified anticoagulants used during ECMO, resulting in 11 studies being included for detailed analysis. This visual representation ensures clarity in our methodological approach, enhancing the transparency and replicability of our findings

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Table 3 Case Reports of Inferior Vena Cava Thrombosis During Extracorporeal Membrane Oxygenation
Full size table

One patient who underwent pneumorrhagia due to chest compressions during CPR did not receive any anticoagulant. The anticoagulation procedures during ECMO were given to 11 patients. The vast majority (82%; 9/11) chosed UFH alone as the anticoagulant. The remaining two patients switched UFH to fondaparinux and argatroban respectively, due to heparin-induced thrombocytopenia (HIT). Of the 11 patients who were definitively anticoagulated during ECMO, the most common monitoring method (64%; 7/11) was aPTT. Eight patients (73%; 8/11) were monitored for anticoagulation using either aPTT or a combination of aPTT and ACT.

Therapeutically, anticoagulation alone (75%; 9/12) was the mainstay of treatment for all twelve patients with IVC thrombosis. The anticoagulants included UFH (56%; 5/9), enoxaparin (22%; 2/9), fondaparinux (11%; 1/9) and low molecular weight heparin sodium (11%; 1/9). Of the remaining three patients, one (8%; 1/12) used an unspecified type of anticoagulant in combination with an IVC filter, one (8%; 1/12) used UFH in combination with surgical embolectomy, and one (8%; 1/12) used Warfarin, IVC filter, and suction thrombectomy.

The outcome of IVC thrombosis was explicitly reported in ten cases (83%; 10/12), and not reported in two cases (17%; 2/12). After appropriate treatment, one patient (10%; 1/10) had a recurrence of thrombosis [15], and the thrombus of other patients (90%; 9/10) disappeared. The mortality of these 12 patients was 17% (2/12), one was brain dead due to cardiac arrest [16] and the other one developed sepsis and subsequent death [14]. There was no thrombosis-related mortality.

Discussion

The significance of this study is as follows: (1) IVC thrombosis in ECMO patients has a certain incidence rate, which is often overlooked. With enhanced monitoring, the incidence may be higher. Given the poor cardiopulmonary compensatory function in ECMO patients and the potential for IVC thrombosis to cause severe complications, clinicians should pay close attention to the occurrence and prevention of IVC thrombosis; (2) The incidence of IVC thrombosis is higher in VA ECMO compared to VV ECMO. This suggests that separate anticoagulation targets may be formulated for VA and VV ECMO patients; (3) Inflammation may be a high-risk factor for IVC thrombosis in ECMO patients. Anticoagulation management in these patients should not solely rely on aPTT or other anticoagulation markers but should also take into account the patient’s inflammatory status; (4) The duration of ECMO therapy appears to have little correlation with the development of IVC thrombosis; (5) Anticoagulation therapy can be administered for IVC thrombosis, and no severe life-threatening complications have been reported thus far. However, due to the under-recognized incidence resulting from a lack of close monitoring, the clinical prognosis should still be approached with caution.

The inflammatory response in ECMO may regulate the coagulation function to promote IVC thrombosis. At the moment when the patient’s blood first comes into contact with the surface of the extracorporeal circuit, a cascade of coagulation and inflammatory reactions is triggered [19]. CRP and PCT are common biomarkers of systemic inflammation [20, 21]. A 4-year follow-up study showed that the systemic inflammatory response was likely to be actively involved in the pathogenesis of venous thromboembolism (VTE), rather than the outcome of VTE [22]. In our center, elevated levels of CRP and PCT were observed during ECMO in all five patients with IVC thrombosis. When monitoring inflammation in ECMO treated patients, it is important to assess not only CRP and PCT levels, but also pro-inflammatory cytokine levels [23]. These biomarkers may contribute to a broader understanding of the inflammatory response and its role in thrombosis. On the one hand, pro-inflammatory cytokines such as interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor α (TNFα) stimulated the release of tissue factor (TF), activating the TF-driven coagulation pathway [24]. TF binds with coagulation factor VII to form the TF/FVIIa complex, which activates factor IX and factor X, triggering a cascade that generates thrombin, fibrin and activates platelets, thereby promoting thrombosis [25, 26]. On the other hand, pro-inflammatory cytokines also decreased the concentration of natural hemostatic inhibitors such as antithrombin, protein S and thrombomodulin [27]. TNF-α and IL-1β can inhibit hepatic or increase consumption of these anticoagulant proteins, which shifts the hemostatic balance toward a procoagulant state [26]. Additionally, IL-6 and IL-8 contribute to platelet activation, aggregation and adhesion, which further increases the risk of thrombosis [28]. Moreover, in response to cytokines, endothelial cells release reactive oxygen species (ROS) as mediators, which increase vascular permeability, damage vessel wall integrity, and result in endothelial dysfunction, thereby facilitating thrombosis [29].

Among the patients with IVC thrombosis, VA ECMO application accounted for a higher proportion in our cases, compared to VV ECMO. A similar result was found in our literature review. In two meta-analyses previously, VTE occurred in 4.6% of VV and 10% of VA ECMO patients, respectively [30, 31]. The pathophysiology of IVC thrombosis in patients with VA ECMO could be explained as follows. Firstly, VA ECMO-supported patients have poorer cardiac function and lower cardiac output. Secondly, during VA ECMO, most of the blood from the right atrium is diverted to the ECMO circuit, resulting in a lower left ventricular preload and a further decrease in the patient's cardiac output [32], which leads to a decrease in the blood flow rate in the IVC and increases the probability of thrombosis. Thirdly, in our patients, the VA ECMO flow rate was lower compared with VV ECMO, and the slow blood flow rate may aggravate thrombus formation.

Anticoagulation monitoring strategies are a core component of an anticoagulation regimen, and the selection of appropriate anticoagulation monitoring strategies to balance coagulation and anticoagulation is essential to reduce ECMO thrombotic complications [33, 34]. UFH is the preferred anticoagulant during ECMO support [35]. Activated clotting time (ACT), activated partial thromboplastin time (aPTT), and anti-factor Xa (Anti-Xa) are the most commonly used monitoring tests of UFH anticoagulation [36]. Thromboelastography (TEG) and rotational thromboelastometry (ROTEM) which evolved from TEG technology, have also been used to monitor UFH use in ECMO patients [37]. However, the strategy for managing anticoagulation monitoring during ECMO varies in different medical centers. APTT is most commonly used as the preferred monitoring anticoagulation tool during ECMO [38]. Anticoagulation guidelines state that the aPTT for ECMO patients should be set at 1.5 to 2.5 times the patient's pre-treatment baseline aPTT [39]. However, in order to reduce the risk of bleeding, it is recommended that the aPTT should be maintained at around 50 s in most cases [40, 41]. This recommended value may be too low to prevent VTE [42]. A small single-center studies have shown that aPTT > 72 s is an independent risk factor for major bleeding in patients with peripheral ECMO [43]. According to previous studies, maintaining an aPTT between 50 and 70 s may maximize the avoidance of thrombosis and bleeding in ECMO patients [44]. Optimal aPTT recommendations remain to be explored by further clinical trials.

A series of studies have shown that anti-Xa and aPTT are superior to ACT for monitoring the efficacy and dose of UFH in patients with ECMO [36, 45,46,47,48]. One retrospective study further indicated that the anti-Xa assay better correlated with heparin dose than aPTT [49]. In several laboratory tests for heparin anticoagulation, only anti-Xa showed a strong correlation with heparin infusion dose in ECMO children [50]. In addition, anti-Xa levels have been demonstrated to predict DVT in both pediatric and adult patients on ECMO, with a sevenfold increase in DVT for each unit decrease in anti-Xa level [51,52,53]. Therefore, the anti-Xa assay may be the more suitable test to monitor UFH anticoagulation during ECMO. Target values of the anti-Xa assay during ECMO range from 0.3 to 0.7 IU/mL [54].

TEG provides information on R-time, kinetics time, α-angle, maximal amplitude (MA) and lysis index 30 min after MA, reflecting the whole process from coagulation to fibrinolysis [39]. Mauro et al. [55] found that the TEG protocol merely allowed for a lower heparin dose and had a tendency to reduce bleeding compared to the aPTT protocol, but did not reduce thrombotic complications. However, there still lacks of large, multicenter, prospective randomized trials comparing TEG with conventional coagulation measures and their effectiveness in guiding anticoagulation therapy.

At present, the optimal treatment method for IVC thrombosis remains unclear. The alternative options include anticoagulation alone, thrombolytic therapy, mechanical intervention, surgical removal and IVC filter placement [56]. Patients on ECMO are generally critically ill, and thus surgical removal of the thrombus is not considered an appropriate first-line treatment [57]. Systemic thrombolytic therapy does not mean a rapid clot resolution, but increases the risk of bleeding [58]. UFH or low molecular heparin (if not contraindicated) is considered to be the mainstay of treatment [5]. With anticoagulation alone, IVC thrombosis disappeared or was reduced in 3 patients at our center and in 8 patients in the literature review. However, there are no large sample statistics on the success of anticoagulation alone in treating IVC thrombosis. Currently, the application of vascular interventions for the treatment of IVC thrombosis is equally promising. The AngioVac (AngioDynamics, Latham, NY) system, an emerging mechanical thrombus retrieval product, has the advantage of a large-bore suction cannula, which allows suction of large amounts of thrombus. A single-center study showed a 100% success rate with the AngioVac device in 11 patients with IVC thrombosis [59]. Several small series also suggested a positive role for AngioVac in the treatment of IVC thrombosis, especially in patients with acute IVC thrombosis [6].

This study had several limitations. First, this was a single-center study, and the results may not be generalizable to all centers because patient backgrounds and ECMO management protocols vary across institutions and countries. Additionally, the retrospective nature of this analysis presents inherent limitations, notably the risk of selection bias and the presence of uncontrolled confounding factors. The relatively small sample size also limits statistical power, potentially impacting the precision and generalizability of our findings. Finally, due to limited data, we were unable to perform subgroup analyses—such as stratification by age, comorbidities, or ECMO duration—that might have offered valuable insights into the specific mechanisms and risk factors associated with ECMO-related IVC thrombosis. These limitations highlight the need for future multicenter, prospective studies with larger sample sizes to validate our findings and to explore the specific risk factors and underlying mechanisms of ECMO- related IVC thrombosis in greater detail.

Conclusion

The complication of IVC thrombosis in ECMO patients is not rare, thus warranting close attention. Factors such as elevated CRP and PCT levels, low aPTT levels, and the use of VA ECMO may contribute to the development of ECMO-related IVC thrombosis. The monitoring of anticoagulation with aPTT alone or in combination with ACT during ECMO may have inherent limitations. Anticoagulation alone may be an effective treatment for ECMO-related IVC thrombosis. However, this study is merely a case review with existing information gaps. Further research with a more comprehensive design is still needed to explore the mechanism of IVC thrombosis during ECMO.

Data availability

No datasets were generated or analysed during the current study.

Abbreviations

ECMO:

Extracorporeal membrane oxygenation

IVC:

Inferior vena cava

aPTT:

Activated partial thromboplastin time

CRP:

C-reactive protein

PCT:

Procalcitonin

VA:

Veno-arterial

VTE:

Venous thromboembolism

CVI:

Chronic venous insufficiency

PTS:

Post thrombotic Syndrome

IREC:

Institutional research and ethics committee

ELSO:

Extracorporeal life support organization

PE:

Pulmonary embolism

ARDS:

Acute respiratory distress syndrome

CDT:

Catheter-directed thrombolysis

UFH:

Unfractionated heparin

ACT:

Activated clotting time

ICU:

Intensive care unit

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Author notes

  1. Chengchao Peng and Su Wang contributed equally to this work.

Authors and Affiliations

  1. Department of Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan , Hubei, 430022, China

    Chengchao Peng, Su Wang, You Shang & Xiaojing Zou

  2. Department of Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan , Hubei, 430030, China

    Le Yang

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Contributions

CP and LY drafted the manuscript and performed the professional literature search and the literature screening. XZ organized the study as an overall supervisor. SW provided significant contributions to the data analysis and interpretation. CP and SW wrote the final manuscript with the supervision of LY, XZ, and YS.All authors met authorship criteria and participated in the study.

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Correspondence to You Shang, Le Yang or Xiaojing Zou.

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All procedures complied with the tenets of the Helsinki Declaration, and approved by the Institutional Review Boards of Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, with approval number 2024–0479. The requirement for written informed consent was waived, owing to the non-interventional and retrospective nature of the study.

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Peng, C., Wang, S., Shang, Y. et al. Inferior vena cava thrombosis in patients undergoing extracorporeal membrane oxygenation: a case series and literature review. BMC Anesthesiol 24, 437 (2024). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12871-024-02827-9

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  • DOI: https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12871-024-02827-9

Keywords

BMC Anesthesiology

ISSN: 1471-2253

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