Patient Factors But Not the Use of Novel Anticoagulants or Warfarin Are Associated With Internal Jugular Vein Access-Site Hematoma After Right Heart Catheterization

Abstract: Introduction. Right heart catheterization (RHC) is routinely performed to assess hemodynamics. Generally, anticoagulants are held prior to the procedure. At our center, anticoagulants are continued and ultrasound guidance is always used for internal jugular vein access. A micropuncture access kit is used to place a 5 or 6 Fr sheath using the modified Seldinger technique. Manual compression is applied for 10-15 min and the patient is observed for at least 2 hours after the procedure. In a retrospective analysis, we investigated the risk of bleeding complications associated with RHC via the internal jugular vein in patients with and without full anticoagulation. Methods and Results. Our catheterization laboratory database was searched for adult patients who underwent RHC by a single operator between January 2012 and December 2015. A total of 571 patients were included in the analysis. Baseline characteristics, labs, relevant invasive hemodynamics, co-morbid conditions, and incidence of access-site hematoma are presented. Multivariable binary logistic regression was performed using IBM SPSS v. 23.0 software. Statistically significant associations with access-site hematoma were observed with body mass index (P=.02; 95% confidence interval [CI], 1.0-1.1), right atrial pressure (P=.03; 95% CI, 0.7-0.9), and dialysis dependence (P<.01; 95% CI, 0.1-0.6). There was no association of access-site hematoma with the use of anticoagulants (P>.99). Conclusion. The incidence of internal jugular vein access-site hematoma is small when using careful access techniques for RHC even with the continued use of novel oral anticoagulants and warfarin. Patient characteristics and co-morbid conditions are related to bleeding complications. 

J INVASIVE CARDIOL 2017;29(12):401-403.

Key words: right heart catheterization, bleeding, anticoagulants, warfarin, novel oral anticoagulant, NOAC

Right heart catheterization (RHC) is a routinely performed procedure for the hemodynamic assessment of patients with cardiovascular disease.^1,2 Although the procedure-related complications are infrequent, they can include pneumothorax, arterial puncture, infection, hematoma, bleeding, and death.^3-5 Patients maintained on anticoagulant medications are at particularly high risk for procedure-related bleeding complications.^6,7 Limited data show that maintenance of international normalized ratio (INR) between 1.5 and 2.0 during the procedure can provide an appropriate balance between the bleeding complications and risk of thromboembolism.⁸ We performed a retrospective study to further explore the risk of bleeding complications associated with RHC via right internal jugular vein access in fully anticoagulated patients. 

Methods

At our center, ultrasound guidance for internal jugular vein access is the standard of care. Modified Seldinger technique with the use of micropuncture needle for access is used to place a 5 or 6 Fr sheath. Manual compression is applied for at least 10-15 min after sheath removal to achieve hemostasis. The patient is observed by a nurse for at least 2 hours after the procedure. Anticoagulation is not routinely discontinued.

Medical charts of adult patients (age >18 years) who underwent RHC via internal jugular vein access by a single operator between January 2012 and December 2015 were reviewed. Data collection included demographics, diagnosis, comorbidities, laboratory investigations (complete blood count, renal function, prothrombin time, and INR), medications, complications, and length of procedure. Patients with missing data regarding anticoagulant medications or laboratory investigations were excluded.

Statistical analysis. Data analysis was performed using IBM SPSS v. 23.0 software. Descriptive statistics were performed. Results were expressed as mean ± standard deviation for continuous variables and as number (percentage) for categorical variables. 

Multivariate binary logistic regression analysis was performed to identify independent predictors of bleeding in patients undergoing RHC on therapeutic anticoagulation. A two-tailed P-value of <.05 was considered statistically significant. 

Results

A total of 571 patients were included in the study; 185 patients were on warfarin and 36 patients were on a novel oral anticoagulant (NOAC). Patients on warfarin had an INR of 2.1 ± 0.7.

Mean patient age was 61 ± 14 years. Patients were predominantly obese (body mass index, 33.3 ± 8 kg/m²), white (72.9%), and male (54.3%). Relevant biochemical data are listed in Table 1. The most frequent indications for the procedure were dyspnea (39.3%) and decompensated heart failure (27.9%). 

Clinically detectable hematoma occurred in 10 patients (1.8%), of which 4 had end-stage renal disease (ESRD), 4 had moderate-severe pulmonary hypertension, and 9 were on antiplatelet therapy (aspirin, clopidogrel). All hematomas occurred in the early-observation period. There were no reports of delayed hematoma by the patients or on follow-up clinic visits. In patients with hematoma, only 2 were on anticoagulation therapy; 1 patient was on warfarin and 1 patient was on an NOAC. INR was <1.5 in all of these cases. There was no statistically significant difference between the two groups (on/off anticoagulation) (Figure 1). There were no procedure-related deaths. 

Multivariate logistic regression analysis demonstrated a statistically significant association between body mass index (95% CI, 1.0-1.1; P=.02), right atrial pressure (95% CI, 0.7-0.9; P=.03), and dialysis dependence (95% CI, 0.1-0.6; P<.01) and access-site hematoma.

Discussion

Internal jugular vein access is routinely used to perform RHC for hemodynamic assessment in critically ill patients.⁹ The current report of our experience with RHC via the internal jugular vein supports its safe use in patients on therapeutic anticoagulation. Our complication rate was low (1.8%) and was comparable to a larger, previously published series.³ 

Hoeper et al reviewed complications of RHC procedures in patients with pulmonary hypertension. The procedure was found to have low morbidity and mortality. Death was reported in 1 case secondary to massive thromboembolism after interrupting anticoagulation.³

At our institution, oral anticoagulation is not routinely discontinued prior to RHC. Our results did not show increased risk of hematoma in patients on therapeutic anticoagulation. All 10 patients who developed hematoma had INR <1.5, only 2 were on anticoagulants, one-half of the patients had end-stage renal disease (ESRD) and moderate-to-severe pulmonary hypertension, while one-third had chronic lung disease. 

ESRD patients on hemodialysis were independently associated with higher risk of access-site hematoma formation. Several factors may explain the increased risk of hematoma in association with ESRD and hemodialysis. Uremia-related platelet dysfunction contributes to bleeding diathesis in ESRD patients. Dysfunction of glycoprotein IIb/IIIa may contribute to reduced platelet aggregation and impaired platelet adhesion.¹⁰ The bleeding tendency may also be relatively higher in such patients due to their inherent risk for complications secondary to their relatively advanced age, multiple comorbidities, and frequent heparin used in dialysis access.

We found that elevated body mass index was associated with access-site hematoma. Possible explanations for the increased risk of this procedure in obese patients include the increased volume of adipose tissue to be crossed by the needle to reach the vein, the possible need for >1 attempt for successful access, the difficulty to achieve adequate manual compression after sheath pull, and possible delayed detection of hematoma. In addition, obese patients usually have more comorbidities that inherently add to their procedural risk.

The association between hemodynamic parameters and increased catheterization-related complications has been previously evaluated in pulmonary arterial hypertension patients by Zuckerman et al.¹¹ Only mean right atrial pressure was associated with increased complication rate, whereas other hemodynamic measures were unrelated. This is also consistent with our finding that only elevated right atrial pressure was associated with increased risk of hematoma (P=.03; 95% CI, 0.7-0.9). Elevated right atrial pressure leads to a higher hydrostatic pressure in the internal jugular vein, which makes hemostasis more difficult to achieve and maintain.

A single-operator experience was investigated because the complication rate of any invasive procedure is a function of the experience and skill of the operator. Our low rate of adverse events in this study might be related to the fact that the procedures were done in a high-volume center by an experienced operator. 

There are several limitations inherent to our study. First, this is a retrospective, single-center, single-operator experience. Second, only large hematomas are likely to be reported, whereas small hematomas might have been missed or not considered clinically significant enough to be reported. Third, selection bias is a possibility where those patients considered at high risk for procedural complications were not referred for the procedure. 

Conclusion

The present data reassure that RHC in adult patients maintained on anticoagulation is associated with a low risk of access-site bleeding complications when using careful access techniques and adequate manual hemostasis. Patient characteristics and comorbidities such as obesity, dependence on dialysis, and elevated right atrial pressures are associated with bleeding complications post RHC. This association should be explored in further studies.

References

1.     Barst RJ, McGoon M, Torbicki A, et al. Diagnosis and differential assessment of pulmonary arterial hypertension. J Am Coll Cardiol. 2004;43:40S-47S.

2.     Galie N, Torbicki A, Barst R, et al. Guidelines on diagnosis and treatment of pulmonary arterial hypertension. The task force on diagnosis and treatment of pulmonary arterial hypertension of the European Society of Cardiology. Eur Heart J. 2004;25:2243-2278.

3.     Hoeper MM, Lee SH, Voswinckel R, et al. Complications of right heart catheterization procedures in patients with pulmonary hypertension in experienced centers. J Am Coll Cardiol. 2006;48:2546-2552. Epub 2006 Nov 28.

4.     Caldini P, Gensini GG, Hoffman MS. Primary pulmonary hypertension with death during right heart catheterization. A case report and a survey of reported fatalities. Am J Cardiol. 1959;4:519-527.

5.     Snider GL. Primary pulmonary hypertension: a fatality during pulmonary angiography. Clinical conference from Boston University School of Medicine. Chest. 1973;64:628-635.

6.     Jaffer AK, Ahmed M, Brotman DJ, et al. Low-molecular-weight-heparin as periprocedural anticoagulation for patients on long-term warfarin therapy: a standardized bridging therapy protocol. J Thromb Thrombolysis. 2005;20:11-16.

7.     Douketis JD, Johnson JA, Turpie AG. Low-molecular-weight heparin as bridging anticoagulation during interruption of warfarin: assessment of a standarized periprocedural anticoagulation regimen. Perspect Vasc Surg Endovasc Ther. 2005;17:176.

8.     Larson BJ, Zumberg MS, Kitchens CS. A feasibility study of continu- ing dose-reduced warfarin for invasive procedures in patients with high thromboembolic risk. Chest. 2005;127:922-927. 

9.     Ranu H, Smith K, Nimako K, Sheth A, Madden BP. A retrospective review to evaluate the safety of right heart catheterization via the internal jugular vein in the assessment of pulmonary hypertension. Clin Cardiol. 2010;33:303-306. 

10.     Gawaz MP, Dobos G, Spath M, Schollmeyer P, Gurland HJ, Mujais SK. Impaired function of platelet membrane glycoprotein IIb-IIIa in end-stage renal disease. J Am Soc Nephrol. 1994;5:36-46.

11.     Zuckerman WA, Turner ME, Kerstein J, et al. Safety of cardiac catheterization at a center specializing in the care of patients with pulmonary arterial hypertension. Pulm Circ. 2013;3:831-839.

From the ¹Department of Internal Medicine, ²Division of Cardiovascular Medicine, University of Toledo Medical Center, Toledo, Ohio; and ³Mercy St. Vincent Medical Center, Department of Internal Medicine, Toledo, Ohio.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted March 20, 2017, provisional acceptance given April 4, 2017, final version accepted April 20, 2017.

Address for correspondence: George V. Moukarbel, MD, Associate Professor of Medicine, Division of Cardiovascular Medicine, The University of Toledo Medical Center, 3000 Arlington Avenue, Toledo, OH 43614. Email: george.moukarbel@utoledo.edu