The authors sought, and received, written permission from the patient to report this case. A 62-year-old female (body surface area 1.9 m−2) was scheduled to undergo an elective mitral valve (MV) replacement. An intraoperative transesophageal echocardiography (TEE) examination revealed a bileaflet MV prolapse, mitral annular dilation, severe central mitral regurgitation, and enlarged left atrium. After separation from cardiopulmonary bypass (bicaval cannulation with 34 F cannulae), TEE showed well-seated mitral prosthesis with laminar flow across it and no paravalvular leak. The mean gradient across the prosthesis was 1.1 mm Hg. There was laminar flow in both cavae in the midesophageal bicaval view and absence of any pathological findings. The patient was transferred to the intensive care unit in stable hemodynamic condition. Over 6 postoperative hours, she became more acidotic despite increasing levels of inotropic support.
Differential diagnoses included mitral prosthesis dysfunction, left ventricular failure, right ventricular failure, hypovolemia, and cardiac tamponade. An emergent TEE revealed normal mitral prosthesis function, hyperdynamic underfilled ventricles, and a small pericardial effusion. Turbulent flow into a collapsed right atrium (RA) on color-flow Doppler (CFD) was noted in the midesophageal 4-chamber view. To ascertain the origin of this turbulence, we obtained a modified bicaval view that revealed that turbulence originated at the inferior vena cava (IVC)–RA junction (Fig. 1) (Video 1, see Supplemental Digital Content 1, http://links.lww.com/AA/A328). In this view, the diameter of the IVC–RA junction measured 7 mm. Pulsed-wave Doppler (PWD) at the IVC–RA junction showed peak velocity of 1.6 m · s−1 and a pressure gradient of 10 mm Hg (Fig. 2). The infradiaphragmatic IVC (caudal to the stenosis) was examined by obtaining the hepatic vein view, which has been previously described.1,2 The IVC measured 25 mm in diameter, had evidence of spontaneous echo contrast (Video 2, see Supplemental Digital Content 2, http://links.lww.com/AA/A329), and no flow in the hepatic vein on PWD was noted. Surgical re-exploration revealed a deep suture stricture and tissue swelling at the IVC–RA junction. Under deep hypothermic circulatory arrest, IVC–RA stenosis was repaired with use of pericardial patch. Postcardiopulmonary bypass TEE examination revealed an IVC–RA junction measuring 1.2 cm in diameter and some turbulence on CFD (Fig. 3). The turbulence could be attributed to the presence of residual swelling and sutures at the site of the patch repair. The patient's postoperative recovery was uneventful. She left the hospital 14 days later.
Surgical technique for MV intervention involves bicaval cannulation to provide optimal MV exposure and a bloodless surgical field. A similar technique is used for orthotopic heart transplantation. Any surgical procedure that involves instrumentation of the superior vena cava and IVC could result in an iatrogenic complication such as stenosis, which is rare but potentially fatal. IVC stenosis has been described after orthotopic heart, heart–lung, and liver transplantations.3 Difficulty in performing IVC anastomosis due to crowding of surgical field by cannulae and tourniquets, mismatch of the donor and recipient cavae, and deep hemostatic sutures have been implicated as risk factors.3 The clinical presentation of IVC stenosis is acute or chronic. Chronic obstruction may be asymptomatic or characterized by hepatic dysfunction, lower limb edema, and ascites. Acute IVC stenosis presents as a rapid, refractory hemodynamic deterioration associated with signs of hepatic and renal dysfunction (coagulopathy, oliguria) as seen in our case.3
In an emergent situation, several echocardiograhic views may provide diagnostic confirmation of IVC stenosis (Tables 1 and 2). Key echocardiography features of IVC stenosis include visualization of the site of stenosis, demonstration of a low-flow state proximal to the stenosis, and flow acceleration at the level of stenosis (Table 1). The acquisition of TEE images to diagnose IVC stenosis may involve the use of views such as the modified bicaval view and hepatic vein view, which are not a part of the routine intraoperative TEE examination recommended by the Society of Cardiovascular Anesthesiologists. Flow interrogation proximal and distal to stenosis can be performed using routine modalities of Doppler echocardiography such as PWD and CFD.
The IVC and hepatic veins are examined to estimate RA pressure and thus the intravascular volume status of a patient (Table 2). A normal IVC diameter is 12 to 17 mm, measured along its long axis just proximal to the junction of hepatic veins at end-expiration in a spontaneously breathing patient.4 A caveat to this is that respiratory variation in IVC diameter is not reliable in positive pressure ventilation. Hence a thorough TEE examination with additional views (Table 1) and clinical correlation is required to diagnose this extremely complex clinical scenario.
This case highlights the importance of emergent TEE in case of iatrogenic IVC stenosis presenting as intractable postoperative hypotension. We recommend examination of IVC and hepatic veins as a part of comprehensive perioperative TEE after bicaval cannulation.
Name: Vivek Sharma, MD.
Contribution: Video and imaging collection, manuscript preparation.
Attestation: Attests to the integrity of original data and analysis.
Name: Marcin Wasowicz, MD.
Contribution: Reviewer and intensive care unit clinical management.
Name: Stephanie Brister, MD.
Contribution: Reviewer and surgical aspects.
Name: Jacek Karski, MD.
Contribution: Collection of original clips.
Name: Massimiliano Meineri, MD.
Contribution: Senior supervising author.
Attestation: Attests to the integrity of original data and analysis.
This manuscript was handled by: Martin J. London, MD.
APPENDIX: VIDEO CAPTIONS
Video 1. Modified bicaval view, demonstrating turbulent flow in the right atrium (RA). The arrow indicates stenosis at the level of the inferior vena cava (IVC)–RA junction.
Video 2. Hepatic vein view showing spontaneous echo contrast in the inferior vena cava.
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3. Jacobsohn E, Avidan MS, Hantler CB, Rosemier F, De Wet CJ. Inferior vena-cava right atrial anastomotic stenosis after bicaval orthotopic heart transplantation. Can J Anaesth 2006;53:1039–43
4. Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, Picard MH, Roman MJ, Seward J, Shanewise JS, Solomon SD, Spencer KT, Sutton MS, Stewart WJ. Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005;18:1440–63
5. Brennan JM, Blair JE, Goonewardena S, Ronan A, Shah D, Vasaiwala S, Kirkpatrick JN, Spencer KT. Reappraisal of the use of inferior vena cava for estimating right atrial pressure. J Am Soc Echocariogr 2007;20:857–61
Clinician's Key Teaching Points By Martin M. Stechert M.D., Roman M. Sniecinski M.D., Martin J. London M.D.
- The inferior vena cava (IVC) is a large caliber vessel typically measuring 1.2 to 1.7 cm in diameter and is responsible for returning about 2/3 of the venous blood volume to the heart via its infero-posterior connection to the right atrium (RA). Although collateral pathways for venous return (azygos, intrathoracic and vertebral veins) can develop over time, acute IVC obstruction can result in low cardiac output, hepatic and renal dysfunction, and cardiovascular collapse if left untreated.
- After cardiac surgery and cardiopulmonary bypass (CPB), low cardiac output syndrome can be caused by tamponade, right or left ventricular dysfunction, hypovolemia, or valvular abnormalities. Additionally, the combination of under-filled cardiac chambers with hyperdynamic biventricular activity and plethoric hepatic veins should raise the suspicion of IVC stenosis, particularly if the IVC was cannulated as part of the surgical procedure. The bicaval view is a good starting point for investigation of the IVC and taking its measurement, which is done about 1 to 2 cm from the RA junction.
- In this case, a patient developed low cardiac output syndrome indicated by worsening metabolic acidosis several hours after mitral valve replacement. Transesophageal echocardiography demonstrated a narrowing at the IVC-RA junction with turbulent flow into the RA on color flow Doppler. Spectral Doppler was used to measure flow velocity past the narrowing and showed a gradient between the proximal IVC and RA which would not normally be present, suggesting a stenosis at that level.
- IVC stenosis after cardiac surgery, although rare, can occur after instrumentation of the IVC, particularly with bicaval cannulation. When low cardiac output syndrome cannot be otherwise explained after CPB, flow conditions in the caval veins should be investigated.