Article Text

Download PDFPDF

Complete occlusion of the left pulmonary artery and paradoxical cerebral embolus from tricuspid valve endocarditis
Free
  1. Jean Michael Garcia Sabile1,
  2. Audrey Tran2 and
  3. Nattapron Tun1
  1. 1Internal Medicine, Oregon Health & Science University, Portland, Oregon, USA
  2. 2School of Medicine, Oregon Health & Science University, Portland, Oregon, USA
  1. Correspondence to Dr Jean Michael Garcia Sabile; jsabile1{at}gmail.com

Statistics from Altmetric.com

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Description

A woman in her early 20s with history of intravenous substance use disorder was admitted with sepsis. Transthoracic echocardiogram (TTE) demonstrated severe tricuspid valve (TV) regurgitation and multiple large vegetations encompassing all three leaflets. Blood cultures revealed Streptococcus mitis and S. gordonae. CT angiography (CTA) of the chest revealed a large right ventricular filling defect attached to the posterior TV leaflet measuring over 3 cm in length (figure 1A,B), consistent with a valvular vegetation.

Figure 1

Axial and sagittal images of CTA with contrast of the chest with demonstration of large vegetation most visible on the posterior leaflet of the TV (A, white arrow) and patent left PA (A, black arrow). Subsequent CTA obtained on following admission for acute hypoxaemic respiratory failure demonstrating marked decrease in size of previously visualised TV vegetation (B, white arrow) with new abrupt cut-off of contrast opacification in the left PA (B, black arrow) representing complete occlusion and new triangular subpleural consolidations noted in the lung periphery (B, right image). CTA, CT angiography; PA, pulmonary artery; TV, tricuspid valve.

Following treatment with intravenous ceftriaxone, sepsis resolved, and blood cultures cleared by day 2. She was discharged with plan for outpatient intravenous ceftriaxone and close follow-up. Three weeks later, she returned to the hospital with sudden onset of dyspnoea and was found to have hypoxaemic respiratory failure with stable blood pressure. Directly prior to the patient’s second admission, she was noted to be afebrile and with associated elevated C reactive protein of 11.7 mg/dL (ref 0–0.5 mg/dL) and leucocytosis to 21.98 K/cu mm (ref 3.5–10.8 K/cu mm). Physical exam and repeat TTE redemonstrated torrential TV regurgitation with smaller TV vegetations (figure 2A–D) and right to left atrial shunt with agitated saline contrast administration, consistent with patent foramen ovale. Repeat CTA redemonstrated known bilateral septic pulmonary emboli, now with abrupt cut-off of the left lower lobar pulmonary artery and associated triangular subpleural consolidations in the left upper and lower lobes. The previously visualised tricuspid posterior leaflet vegetation was markedly decreased in size compared with the patient’s previous admission.

Figure 2

Echocardiogram from the patient’s subsequent admission demonstrating parasternal long-axis view of RV inflow (A,B) and PSSA view of RV inflow (C,D). Parasternal RV inflow view demonstrates RV and RA with vegetation (A, black asterisk) involving anterior TV leaflet. Colour Doppler demonstrates torrential tricuspid regurgitation (B). PSSA redemonstrates vegetation of the tricuspid posterior (C, single white asterisk) and septal leaflets (C, double white asterisk). Colour Doppler of the PSSA (D) view redemonstrates torrential tricuspid regurgitation. PSSA, parasternal short axis; RA, right atrium; RV, right ventricular; TV, TV, tricuspid valve.

Given known endocarditis with large vegetations and the absence of deep vein thrombosis, the pulmonary embolus was favoured to represent dislodgement of vegetation.1 The patient was designated a Pulmonary Embolism Severity Index class I for the presence of tachycardia and low oxygen saturations. Intravenous heparin drip was administered without thrombolysis, given the patient’s risk stratification.2 Cardiothoracic surgery was consulted for TV replacement but ultimately deemed the patient to have high surgical risk in the context of poor nutritional status denoted by prealbumin 4.3 mg/dL (ref 17.0–42.0 mg/dL) and incomplete dental workup.3 The patient was clinically stable and proceeded with a planned course of 6 weeks of antibiotics, weekly chest CT for surveillance and transitioned from heparin to apixaban until hospital day 19, when she developed lethargy and right sided hemiparesis with CT evidence of a left-sided haemorrhagic stroke. Given isolated right-sided endocarditis and patent foramen ovale, the patient was felt to have experienced haemorrhagic conversion of an ischaemic stroke secondary to paradoxical embolus from the known TV vegetation.4 5 Repeat TTE demonstrated progression of right-to-left ventricular shunt with worsened TV regurgitation, progressive right atrial enlargement and widened PFO. She required external ventricular drain placement and was ultimately discharged to inpatient rehabilitation on hospital day 33.

Learning points

  • While use of the Pulmonary Embolism Severity Index score is a useful tool for estimated risk of mortality for patients with acute PE, it may not necessarily accurately reflect an individual’s risk of cardiovascular and neurological morbidity.

  • Paradoxical embolus is a rare complication of right-sided endocarditis with tricuspid vegetations and represents a potential source of significant morbidity, including thromboembolic stroke and subsequent haemorrhagic conversion.

  • There is equipoise regarding anticoagulation for embolic complications of endocarditis, particularly for isolated right-sided disease. In this context, particularly if risk of cerebral embolism is present, anticoagulation carries substantial risk.

Ethics statements

Patient consent for publication

References

Footnotes

  • Twitter @JeanSabile, @audreyamadean

  • Contributors JMGS, AT and NT contributed to the patient’s care during hospital admission, subsequent write-up of the body of the report, and detailed edits leading up to manuscript submission. JMGS generated the case figures and legends and fulfilled the role of corresponding author.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.