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A 33-Year-Old Man With a History of Intravenous Drug Use and Fevers FREE TO VIEW

Gisela I. Banauch, MD; Michael Colancecco, DO
Author and Funding Information

Dr Colancecco is currently at Lahey Hospital & Medical Center (Burlington, MA).

CORRESPONDENCE TO: Gisela I. Banauch, MD, Department of Medicine, Division of Pulmonary Allergy Critical Care and Sleep Medicine, University of Massachusetts Medical Center, 55 Lake Ave N. Worcester, MA 01655


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(3):e75-e77. doi:10.1016/j.chest.2015.09.042
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Published online

A 33-year-old man with a history of IV drug use presented with a 2-week history of fatigue and malaise with accompanying fever and chills. After 1 week of symptoms, he had presented to an outside emergency department and had been discharged, with his complaints attributed to a viral infection. He subsequently developed a nonproductive cough, dyspnea with exertion, and pleuritic chest pain, and grew Staphylococcus aureus in blood cultures that had been obtained during his first visit to the emergency department. This prompted reevaluation and transfer from the emergency department of the outside hospital.

The patient’s medical history was notable only for a prior soft-tissue infection attributed to methicillin-resistant S. aureus several years prior. A detailed review of systems was also notable for decreased urine output.

Physical examination revealed a young male in moderate distress. Vital signs were: temperature, 39°C; BP, 140/95 mm Hg; heart rate, 110 beats/min; respiratory rate, 30 breaths/min; and pulse oximetric oxygen saturation, 99% while breathing room air. Neck examination revealed large-amplitude jugular venous pulsations to approximately 10 cm of water above the sternal angle with head of bed at 45°. Lung examination was clear to auscultation bilaterally. Cardiac examination was notable for a regular tachycardic rhythm without appreciable murmurs, rubs, or gallops. No stigmata of endocarditis were found on a detailed examination of the skin. Neurologic examination was unremarkable.

Laboratory and imaging data on admission was notable for leukocytosis with a WBC count of 18,000 cells/mm3, anemia with a hemoglobin of 10.9 g/dL, thrombocytopenia with platelets of 80,000 th/mm3, and acute kidney injury with a creatinine of 1.8 mmol/L. The admission chest radiograph demonstrated a normal-sized cardiac silhouette, bibasilar consolidations, moderate pulmonary edema, and small bilateral pleural effusions. An echocardiogram (Video 1) and lung ultrasound (Video 2) were performed by the ICU team.

Question: What are the diagnoses for this patient?

Answer: Tricuspid valve infective endocarditis with possible septic pulmonary emboli

Hospital course was complicated by bilateral pulmonary septic emboli as well as empyema, which necessitated bilateral surgical chest tube drainage. The acute kidney injury was found to be due to a combination of acute tubular necrosis and biopsy-proven glomerulonephritis. The acute lung injury imaged on initial lung ultrasound required low levels of supplemental oxygen only, but the patient remained markedly tachypneic for several days. For the first 10 days of his inpatient stay, the patient was closely observed in the ICU because of his sepsis-related hypermetabolic state and acute kidney injury. After initiation of antibacterial therapy, the patient’s blood cultures remained sterile. He was discharged in ambulatory condition to a rehabilitation facility to complete a 6-week course of intravenous nafcillin for methicillin-sensitive S. aureus. He has since re-presented with further complications related to IV drug use.

The clinical scenario suggests infective endocarditis in this patient. His history of injection drug use makes endocarditis of the right heart structures the most likely diagnosis. Goal-directed ECG confirms this diagnosis, with large vegetations involving the anterior and septal leaflets of the tricuspid valve evident in all views in which the tricuspid valve is imaged (Video 3). On two-dimensional (2D) imaging, valvular vegetation appears as an irregular mass that displays motion independent of the valve. Because the vegetation floats passively and frequently develops at sites of endothelial damage caused by high-velocity jets, the character of the motion is often oscillatory. For the same reason, at different phases of the cardiac cycle, the vegetation will appear in both the originating and the receiving chamber between which flow across the infected valve occurs.

Because of the anterior position of the tricuspid valve, transthoracic imaging will often suffice to detect vegetations of the native valve, and the transesophageal route has been recommended for special circumstances only (ie, suspected involvement of the pulmonic valve, suspected involvement of left-sided valves, and poor clinical course). When vegetation size exceeds 2 cm in right-sided endocarditis, patient mortality has been shown to approach the high mortality of left-sided endocarditis.

For a comprehensive characterization of the tricuspid valve, the examiner should aim for images in three orthogonal planes. These planes include the right ventricular long axis in the right ventricular inflow view (this view can be obtained either parasternally or subcostally), an orthogonally oriented long axis through the right ventricle that includes the left ventricular long axis as well (ie, apical and subcostal four-chamber views), and the right ventricular short axis (this view can again be obtained either parasternally or subcostally).

Once vegetation has been identified on 2D imaging, the hemodynamic effect can be further assessed with color Doppler imaging. The color Doppler images for this patient show severe tricuspid regurgitation, which is most evident in the subcostal short axis and can also be appreciated well in the apical four-chamber view and the subcostal view of the inferior vena cava (Video 4).

To avoid overestimating the severity of regurgitant flow, it is important to properly adjust gain on the color Doppler display before imaging. This is achieved in the following manner: before applying the transducer to the skin, the gain is increased slowly until the appearance of random color pixels is observed. From this gain setting that shows random color pixels, the gain is then decreased slightly to a setting in which the random color pixels have just disappeared from the display.

On color Doppler imaging with the gain setting adjusted properly, features that indicate that the regurgitant flow through the tricuspid valve is severe in nature for this patient include: (1) the jet fills more than 40% of the right atrium (or an area on the 2D image ≥10 cm2) and (2) systolic flow reversal in the hepatic veins can be observed. Because the tricuspid valve has a complex coaptation zone and vegetations impede the coaptation in a variable manner, it is important to carefully image the transvalvular flow from as many directions as possible to accurately assess the severity of regurgitation.

Activating the color Doppler option that includes a visual representation of flow velocity variances (often referred to as the variance map) can assist significantly in identifying regurgitant flows because regurgitant flows are turbulent and thus have a higher variance of flow velocities, and this variance is displayed visually in hues of green when the variance map is activated. Because regular intracardiac flows are displayed in hues of red and blue, encoding turbulent flows with green hue makes the regurgitant flow stand out visually.

Bilateral B lines on lung ultrasound suggest pulmonary edema. Clinically, this patient was euvolemic on presentation. It follows that this patient’s pulmonary edema is likely noncardiogenic and thus caused by sepsis-mediated acute lung injury. On further high-resolution imaging of the pleural line (achieved with the linear transducer), small subpleural consolidations were appreciated (Video 5). The presence of these consolidations may have been caused either by intense subpleural inflammation associated with ARDS or by small septic pulmonary emboli. The subpleural consolidations make a noncardiogenic etiology of the patient’s pulmonary edema even more likely.

Subpleural consolidations consist of small regions where the pleural line appears less distinct, with a hypoechoic appearance of the lung parenchyma deep to the indistinct pleural line. The hypoechoic region represents the consolidated parenchyma. Deep to the hypoechoic consolidation, better aerated lung is again evident. The depth at which better aerated lung is imaged varies at different points of the consolidation, producing a hyperechoic, irregular aspect of the deep border. At the deep border, vertical hyperechoic artifacts similar in appearance to B lines are often seen (and are especially evident in the clip from the left chest in this patient). The hyperechoic border indicates improved aeration of lung parenchyma deep to the area of subpleural consolidation. Because the vertical hyperechoic artifacts deep to the hypoechoic parenchyma do not originate from the pleural line, they are not B lines. Instead, the appearance of the deep border of a subpleural consolidation is termed “the shred sign” if vertical hyperechoic artifacts originate from it.

  • 1.

    On 2D imaging, a valvular vegetation appears as an irregular mass whose motion has the following sonographic characteristics: (a) it is independent of the valve; (b) at different phases of the cardiac cycle, the mass appears in both the originating and the receiving chamber between which the affected valve is located; and (c) the character of the motion is often oscillatory.

  • 2.

    Subpleural consolidations occur in inflammatory pulmonary parenchymal diseases (embolic and nonembolic) and have the following sonographic characteristics: (a) a small region where the pleural line appears indistinct, (b) the pulmonary parenchyma deep to the indistinct pleural line appears hypoechoic, and (c) a shred sign is often evident deep to the hypoechoic subpleural parenchymal area.

  • 3.

    On color Doppler imaging, features that indicate that regurgitant flow through the tricuspid valve is severe in nature include: (a) the jet fills more than 40% of the right atrium (or an area ≥10 cm2on the two-dimensional image) and (b) systolic flow reversal in the hepatic veins can be observed.

Financial/nonfinancial disclosures: None declared.

Other contributions:CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.

Additional information: To analyze this case with the videos, see the online version of this article.

Feigenbaum H. .Armstrong W. .Ryan T. . Infective endocarditis.Feigenbaum H..Armstrong W..Ryan T.. Feigenbaum’s Echocardiography.  :375-398 [PubMed]journal
 
Albert San Román J. .Vilacosta I. .López J. .et al Role of transthoracic and transesophageal echocardiography in right-sided endocarditis: One echocardiographic modality does not fit all. J Am Soc Echocardiogr. 2012;25:807-814 [PubMed]journal. [CrossRef] [PubMed]
 
Martín-Dávila P. .Navas E. .Fortún J. .et al Analysis of mortality and risk factors associated with native valve endocarditis in drug users: the importance of vegetation size. Am Heart J. 2005;150:1099-1106 [PubMed]journal. [CrossRef] [PubMed]
 
Zoghbi W.A. .Enriquez-Sarano M. .Foster E. .et al Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003;16:777-802 [PubMed]journal. [CrossRef] [PubMed]
 
Kisslo J.A. .Adams D. . Creation of the color image.Kisslo J.A..Adams D..Belkin R.N.. Doppler Colour Flow Imaging.  :25-46 [PubMed]journal
 
Lichtenstein D. . Lung ultrasound in the critically ill. Ann Intens Care. 2014;4:1-12 [PubMed]journal. [CrossRef]
 

Figures

Tables

References

Feigenbaum H. .Armstrong W. .Ryan T. . Infective endocarditis.Feigenbaum H..Armstrong W..Ryan T.. Feigenbaum’s Echocardiography.  :375-398 [PubMed]journal
 
Albert San Román J. .Vilacosta I. .López J. .et al Role of transthoracic and transesophageal echocardiography in right-sided endocarditis: One echocardiographic modality does not fit all. J Am Soc Echocardiogr. 2012;25:807-814 [PubMed]journal. [CrossRef] [PubMed]
 
Martín-Dávila P. .Navas E. .Fortún J. .et al Analysis of mortality and risk factors associated with native valve endocarditis in drug users: the importance of vegetation size. Am Heart J. 2005;150:1099-1106 [PubMed]journal. [CrossRef] [PubMed]
 
Zoghbi W.A. .Enriquez-Sarano M. .Foster E. .et al Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003;16:777-802 [PubMed]journal. [CrossRef] [PubMed]
 
Kisslo J.A. .Adams D. . Creation of the color image.Kisslo J.A..Adams D..Belkin R.N.. Doppler Colour Flow Imaging.  :25-46 [PubMed]journal
 
Lichtenstein D. . Lung ultrasound in the critically ill. Ann Intens Care. 2014;4:1-12 [PubMed]journal. [CrossRef]
 
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