Unilateral pulmonary edema in acute aortic regurgitation: A complication of infective endocarditis

Abstract

Cardiogenic unilateral pulmonary edema (UPE) is an uncommon clinical entity and it represents just 2% of cardiogenic pulmonary edema with inclination for the right upper lobe and it is most commonly associated with severe mitral regurgitation. In our review, the literature does not include any UPE cases that are associated with severe aortic regurgitation (AR). Herein, we present a case with UPE, that includes a patient diagnosed with infective endocarditis who presented with shortness of breath. Initial chest imaging revealed UPE. Severe acute AR was diagnosed clinically and confirmed by echocardiogram, caused by vegetations on the non-coronary cusp of the aortic valve. The patient was transferred for emergent surgical intervention. This case underscores the importance of emergently evaluating valvular pathology to reduce the mortality rate that is associated with this condition.

<Learning objective: In this study, we are highlighting the importance of having a high suspicion index to consider the diagnosis of unilateral pulmonary edema, as this condition is rare and hard to diagnose and carries a high mortality as well.>

Introduction

Left ventricular (LV) systolic or diastolic dysfunction increases hydrostatic pressure which causes cardiogenic pulmonary edema. Acute decompensated heart failure has been found to be the most common etiology for cardiogenic pulmonary edema [1,2]. Bilateral alveolar edema or ‘butterfly shadow’ is the typical chest radiography finding in cardiogenic pulmonary edema [1]. On the other hand, unilateral pulmonary edema is hard to diagnose because it is so rare. Often, it is confused with respiratory disease which leads to a higher mortality rate from delayed treatment of heart failure. Literature indicates that severe mitral regurgitation (MR) causes most cases of cardiogenic unilateral pulmonary edema (UPE) and these mostly occur in the right upper lobe [3,4]. No cases have been documented in the literature where acute aortic regurgitation (AR) was found to have caused cardiogenic UPE.

Case report

A 30-year-old male was brought from a short-term rehabilitation facility to the emergency department. He presented with a two-day history of fever, shortness of breath, and dry cough. His breathlessness had worsened in the previous 12 hours. One month previously, the patient had suffered an embolic stroke secondary to infective endocarditis. He was started on culture-targeted antibiotic therapy. He was on antibiotics at presentation to the emergency department. Surgical intervention for infective endocarditis was likely deferred initially due to acute ischemic stroke and high risk of intracranial bleeding in the acute phase.

Initial examination showed that the patient was hypoxemic with 85% SpO2 on room air, tachycardic at 112 beats/minute, temperature of 101.3 F, blood pressure of 107/71 mmHg, and respiratory rate of 18 breaths per minute. A venturimask at 40% helped improve his SpO2 to 94%. The patient was not in respiratory distress and he did not have accessory muscle use. Cardiac examination revealed a harsh diastolic murmur at the left sternal border. Crackles were heard throughout the right lung. Hemoglobin was 13.0 g/dL and the white cell count was elevated (18.3 k/ul). N-terminal prohormone of B-type natriuretic peptide was 23,607 pg/ml and troponin was elevated (9.29 ng/ml).

A chest radiograph revealed interstitial alveolar infiltrates limited to the right lung field (Fig. 1A). A computed tomography scan of the chest displayed ground-glass attenuation with superimposed interlobular septal thickening with right side predominance (Fig. 1C). After suspicion of hospital-associated pneumonia with possibility of being positive for COVID-19, the patient was admitted and started on broad spectrum antibiotics immediately.

Fig. 1.

Chest imaging. (A) Alveolar-interstitial infiltrates seen, limited to the right lung on a chest radiograph. (B) Post-intubation, diffuse bilateral alveolar-interstitial infiltrates were demonstrated on repeat X-ray with interval worsening. (C) Ground-glass attenuation with superimposed interlobular septal thickening was demonstrated by chest computed tomography scan with contrast and the lesions were found to be predominantly on the right side.

The patient developed acute cardiogenic shock and respiratory distress shortly after arrival to the intensive care unit requiring pressors and mechanical ventilatory support. Post-intubation, diffuse alveolar-interstitial infiltrates were now seen bilaterally on a repeat chest radiograph (Fig. 1B).

An echocardiogram revealed a large, highly mobile vegetation on the non-coronary cusp of the aortic valve with severe aortic regurgitation with possible destruction of the cusps. The LV ejection fraction was estimated to be 60–65% (Fig. 2). The patient was transferred to a tertiary facility for emergent surgical intervention. The patient was found to have a bicuspid valve, severe aortic regurgitation, a dilated left ventricle, and a healed abscess cavity in the right ventricle. The patient underwent reconstruction of the right ventricular abscess cavity with a bovine pericardial patch, homograft root replacement, and reimplantation of the coronaries (Fig. 3). Two days later, the patient was extubated, and his post-operative recovery was unremarkable.

Fig. 2.

Echocardiogram findings. The echocardiogram showed a large (greater than 1 cm) and highly mobile vegetation on the non-coronary aortic leaflet. Severe aortic regurgitation was also seen on the right coronary leaflet with reversal of diastolic descending aortic flow.

Fig. 3.

Aortic valve replacement. shows the bicuspid aortic valve, abscess cavity, and the ventricular defect from the abscess. Aortic valve replacement and homograft root prior to reimplantation of the coronary arteries was performed. Right and left coronary arteries have the purple marker on them.

Discussion

Acute cardiogenic pulmonary edema, a critical condition, has been associated with high mortality [5]. Patients with bilateral pulmonary edema present a lower risk of death as compared to UPE patients and the increased mortality in UPE cases can be explained by the delay in adequately treating this condition [4]. Bilateral symmetrical opacities have been found in the central zones of the lungs on the basis of the usual radiographic findings of acute cardiogenic pulmonary edema which result in the classic ‘butterfly shadow’. UPE can easily be mistaken in chest radiography for pneumonia and other causes of unilateral infiltrate because it is a rare entity. Cardiogenic UPE can be differentiated from acute pneumonia by obtaining helpful information such as perihilar unilateral ‘bat wing’ consolidation in the right lung field, elevated B-type natriuretic peptide plasma level in the absence of positive procalcitonin level, and sudden onset of other symptoms [5]. In this patient, however, infective endocarditis (IE) led to a high level of procalcitonin. As compared to C-reactive protein, procalcitonin has higher positive predictive value and high specificity which can be used to diagnose IE in addition to transesophageal echocardiogram, blood cultures, and Duke criteria for IE. Upon physical examination, a murmur can be useful [6]. The presence and severity of valvular abnormalities can be determined by echocardiography. In order to avoid delaying treatment that can affect prognosis, it is important to promptly recognize UPE.

It has been reported that 2.1% of cases with cardiogenic pulmonary edema are represented by UPE [4]. This was reported in patients with cardiac decompensation who rest for prolonged periods on one side, after receiving large amounts of fluids or after congestive heart failure and it is also seen in cases where a rapid lung expansion has occurred after pneumothorax and pleural effusion. UPE has also been noted in the normal lung of unilateral pulmonary disease patients in the form of MacLeod syndrome and agenesis or unilateral pulmonary artery hypoplasia, pulmonary artery compression from left ventricular pseudoaneurysm or aortic dissection, and pulmonary venous obstruction caused by mediastinal fibrosis. Mostly, it is reported in connection with severe MR [7]. In literature, UPE secondary to acute AR has not yet been documented.

In a majority of UPE cases that are associated with left heart failure, it is observed that the right lung is affected. This can be possibly explained by the fact that the small-caliber right broncho-mediastinal trunk carries out poorer lymphatic drainage of the right lung as compared to the large-caliber thoracic duct in case of the left lung. The left-sided cardiac enlargement can be another explanation which is observed in majority of heart failure patients and it may reduce capillary volume by physically impeding blood flow in the left pulmonary artery [8].

The LV pathologically fills during ventricular diastole in acute severe AR which prevents forward flow from the left atrium (LA). This helps reduce stroke volume greatly and the cardiac output is maintained by the compensatory tachycardia as a result. The AR is met by a relatively stiff LV in this acute setting and it leads to an increase in LV pressure. Flow from the LA is stifled by the increased pressure in the LV which can cause pulmonary congestion. Increased LV pressure in case of severe AR can cause mitral valve to close early prior to atrial systole. As the atria contract against a closed valve, pulmonary congestion is exaggerated [9]. Through our current research, we are unaware of any similar published reports documenting UPE from acute severe aortic insufficiency. The etiology of this presentation remains unclear and we need detailed studies and registries to further our knowledge in the pathophysiology of this presentation.

Conclusion

It is possible that cardiac UPE can be underdiagnosed because it is such a rare entity. Whether the edema is radiographically bilateral or unilateral, management of pulmonary edema secondary to heart failure does not change. It is important to recognize UPE without confusing it with other focal processes. Physicians should have knowledge of the various features of UPE as early recognition is vital for saving lives of patients because of the increased mortality risk that is associated with this condition. This case teaches us the importance of acknowledging the rare entity of UPE and its various potential causes. In addition to clinical suspicion multiple modalities may be helpful in identifying the underlying cause, such as laboratory abnormalities and echocardiography. Lastly, we present severe acute AR, a previously unrecognized etiology of UPE.

Declaration of Competing Interest

None.