Cerebral Venous Congestion Secondary to Jugular Venous Compression

Tuesday, March 7, 2023

4:12 PM – 4:21 PM

Location: Phoenix Convention Center, 222C

Presenting Author(s)

CH

Caleb Heiberger, MD

Radiology Resident
Johns Hopkins

Disclosure(s): No financial relationships to disclose

Author/Co-author(s)

TM

Tej I. Mehta, MD

Interventional Radiology Resident
Johns Hopkins Hospital
MK

Minsoo Kim, BS

Medical Student
The Johns Hopkins Hospital
WC

Won Kyu Choi, MD

Resident
The Johns Hopkins Hospital
MH

Matthew Hoyer, MD (he/him/his)

Resident
The Johns Hopkins Hospital
FH

Ferdinand Hui, MD

Physician
Queens Medical Center

Disclosure(s):

Caleb Heiberger, MD: No financial relationships to disclose

Tej I. Mehta, MD: No financial relationships to disclose

Matthew Hoyer, MD: No financial relationships to disclose

Purpose:

Cerebral venous congestion (CVC) is a disorder with deleterious effects, such as cognitive dysfunction, headaches and visual obscurations [1]. A risk factor for CVC is internal jugular vein (IJV) compression. We have previously reported on CVC pathophysiology [2]. Herein, we illustrate anomalies which may cause CVC secondary to IJV compression. We also have developed and will present dynamic, 3D printed models of select pathologies to further illustrate these anomalies. Finally, we describe a diagnostic concept for monitoring CVC, the “brain-heart gradient” (BHG).

Materials and Methods:

A retrospective review of patients evaluated for CVC at our facility between June 2019 and September 2022 was conducted. All patients with cross-sectional or angiographic data available were assessed for IJV compression. Venous pressures at the superior sagittal sinus (SSS), torcular herophili (TH) and trans-stenosis (TS) were obtained. The BHG was calculated as the difference between the TH pressure and the right atrial pressure. T-tests were used to compare pre and post therapy pressure measurements.

Results:

91 cases were reviewed. 29 cases were male, mean age at presentation was 41.3 years, mean body mass index was 26.6 kg/m².

6 categories of IJV compression were identified with the involved structures including: C1 transverse process and styloid process, isolated C1 transverse process, internal carotid artery (ICA), head and neck muscles, jugular foramen and iatrogenic causes. 53 cases were due to IJV impingement between the styloid process and the lateral mass of C1. 10 were due to isolated IJV impingement by the lateral masses of C1, 8 were due to muscular compression, 3 were due to ICA compression, 1 due to jugular foramen stenosis, 4 were due to extracorporeal membrane oxygenation cannulae and 1 was secondary to post-radiotherapy fibrosis. Most patients presented with chronic headaches, vertigo, vision abnormalities and “fullness” of the head and neck.

Mean pre-treatment SSS, TH, TS pressures and BHG were 16.1, 17.0, 8.3 and 9.5 mmHg respectively. Post-treatment SSS, TH, TS pressures and BHG were 13.3, 14.0, 3.0 and 4.4 mmHg respectively with significant reductions in post-treatment pressures (P < 0.05 for all). 33 patients were treated with endovascular or surgical management for IJV compression, the remainder were medically treated.

Conclusion:

IJV stenosis may result in CVC. We identified 6 categories for IJV compression, described pre and post treatment venous pressures and described the concept of the BHG. Familiarity with the mechanisms of IJV compression may inform CVC management choices.