difficult cases july . august 2005220

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D I F F I C U L T C A S E S I N H E A R T F A I L U R E

Mandeep R. Mehra, MD; Hector O. Ventura, MD Editors

Cardiac Unilateral Pulmonary Edema: Is It Really a Rare Presentation?

Unilateral pulmonary edema is a distinctly unusual clinical entity that presents interesting and confusing diagnostic chal-lenges. It is usually described as occurring with re-expansion of a collapsed lung after rapid thoracocentesis of pleural air or pleural fluid. Unilateral pulmonary edema as an initial presenting manifestation for heart failure is uncommon and can be confused with other more common causes of alveolar or interstitial infiltrate, which can lead to a significant delay in treatment.

(CHF. 2005;11:220–223) ©2005 CHF, Inc.

Walid Hassan, MD, FCCP;1 Fayez ElShaer, MD;1 Mohamed Eid Fawzy, MD, FRCP, FESC;1 Sumaya Al Helaly, MD;1 Hesham Hegazy, MD;1 Nathem Akhras, PharmD2

From the Department of Cardiovascular Diseases1 and Department of Pharmacy,2 King Faisal Specialist Hospital and Research Center, Riyadh, Saudi ArabiaAddress for correspondence: Walid Hassan, MD, FCCP, Department of Cardiovascular Diseases (MBC 16), King Faisal Specialist Hospital and Research Center, P.O. Box 3354, Riyadh 11211, Saudi ArabiaE-mail: hassanw@kfshrc.edu.sa

F ive cases of patients with unilateral pulmonary edema are presented.

The focal imbalance of Starling forces is the common denominator shared in the wide variety of etiologies.

Case Presentation 1A 30-year-old woman with rheumatic heart disease and severe mitral steno-sis underwent mitral balloon valvulo-plasty in 1992 and 1994. The patient remained well until February 2003, when she presented with progressive shortness of breath (SOB), orthop-nea, and paroxysmal nocturnal dys-pnea. Chest x-ray (CXR) showed a prominent left atrium, right pulmonary artery, and lobar vessels and unilat-eral (right-sided) alveolar process (infil-trate), mainly in the middle and lower lung fields (Figure 1A). The patient was 5 months pregnant; the CXR was taken with caution. Echocardiogram revealed mitral restenosis with a mitral

valve area of 0.6 cm2 and a gradient of 26/14 mm Hg. The patient underwent successful mitral balloon valvuloplas-ty using the Inoue-Balloon Catheter (Toray Group, Houston, TX) with an increase in mitral valve area to 1.6 cm2 and a significant drop in mean pressure gradient from 14 mm Hg to 4 mm Hg. The patient remained well and gave birth uneventfully. Repeat CXR (Figure 1B) showed complete resolution of her unilateral pulmonary edema.

Case Presentation 2A 36-year-old man with a history of rheumatic heart disease and tight mitral stenosis underwent successful mitral balloon valvuloplasty in March 1992. The patient was evaluated in March 2003 for umbilical hernia sur-gery. The patient was tachycardic and complained of SOB, orthopnea, and paroxysmal nocturnal dyspnea. CXR showed right pulmonary congestion,

peribronchial cuffing, left hyperlucent lung, and mitral valve contour (Figure 2A). There were no symptoms or signs of infection. Repeat echocardiogram revealed severe mitral stenosis (mitral valve area 0.6 cm2) and a gradient of 24/19 mm Hg with moderate mitral regurgitation. He was given diuretics and his condition stabilized and CXR cleared (Figure 2B). Later, he under-went mitral valve replacement and hernia repair.

Case Presentation 3A 19-year-old man who had cardiac transplantation and pacemaker inser-tion in 1996 presented with chest pain, SOB, orthopnea, and paroxys-mal nocturnal dyspnea. CXR showed significant right-sided pulmonary edema with minimal changes on the left side (Figure 3A). Complete blood count was normal; blood urea nitro-gen and serum creatinine were mildly

Congestive Heart Failure® (ISSN 1527-5299) is published bimonthly (Feb., April, June, Aug., Oct., Dec.) by CHF, Inc., Three Parklands Drive, Darien, CT 06820-3652. Copyright ©2005 by CHF, Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions and ideas expressed in Congestive Heart Failure® do not necessarily reflect those of the Editor and Publisher. For copies in excess of 25 or for commercial purposes, please contact Sarah Howell at showell@lejacq.com or 203.656.1711 x106.

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elevated. Echocardiogram revealed mild left ventricular (LV) dysfunction with elevated filling pressures. Cardiac catheterization revealed normal coro-naries. His condition stabilized with adjustment of therapy for heart failure. Repeat CXR showed complete resolu-tion of unilateral edema (Figure 3B).

Case Presentation 4A 71-year-old dyslipidemic man with coronary artery disease and a history of anterior myocardial infarction (1986) and percutaneous transluminal coronary angioplasty to the left anterior descend-

ing and left circumflex arteries, with severely impaired LV function (ejection fraction, 25%), presented with SOB and cough with clear expectoration for several days. CXR showed unilateral, right middle-field infiltrate (Figure 4A). We challenged the emergency depart-ment diagnosis of pneumonia, and the patient underwent Swan-Ganz catheter insertion. Hemodynamics were consis-tent with cardiogenic pulmonary edema secondary to severe LV dysfunction, with a pulmonary capillary wedge pres-sure of 29 mm Hg. The patient was

given therapy for heart failure, includ-ing inotropic agents. His condition sta-bilized and CXR findings normalized (Figure 4B).

Case Presentation 5A 60-year-old woman with a perforat-ed chronic duodenal ulcer presented in a state of shock. The patient had a history of hypertension with hyper-tensive heart disease, hypopituitarism (Sheehan syndrome), bilateral knee replacement, and spinal fusion. The patient was admitted for emergency

Figure 1. A) Anteroposterior radiograph of the chest at the time of hospital admis-sion. The right lung is consolidated with infiltrate in the middle and lower lobes; left heart with mitral valve configura-tion. B) Posteroanterior radiograph of the chest post-successful mitral balloon valvuloplasty with complete resolution of the right pulmonary edema.

Figure 2. A) Posteroanterior radiograph of the chest at the time of hospital admis-sion showing right pulmonary congestion, peribronchial cuffing, and a hyperlucent left upper field. B) Posteroanterior radiograph of the chest post-diuresis with an almost clear lung field.

Figure 3. A) Posteroanterior radiograph of the chest at the time of presentation with frank right pulmonary edema and pacer leads in right atrium and right ven-tricle. B) Posteroanterior radiograph of the chest post-antifailure treatment with complete clearing of edema.

Congestive Heart Failure® (ISSN 1527-5299) is published bimonthly (Feb., April, June, Aug., Oct., Dec.) by CHF, Inc., Three Parklands Drive, Darien, CT 06820-3652. Copyright ©2005 by CHF, Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions and ideas expressed in Congestive Heart Failure® do not necessarily reflect those of the Editor and Publisher. For copies in excess of 25 or for commercial purposes, please contact Sarah Howell at showell@lejacq.com or 203.656.1711 x106.

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minilaparotomy. Postoperatively, she developed SOB; CXR showed diffuse unilateral (left) pulmonary edema with an almost whited-out lung (Figure 5A). She responded well to afterload- and preload-reducing agents guided by hemodynamic monitoring. Her condi-tion stabilized and CXR returned back to baseline with a small, right-side discoid atelectasis (Figure 5B).

DiscussionUnilateral pulmonary edema is unusual in presentation and is mainly seen in the re-expansion phase after pneumothorax,

systemic-to-pulmonary shunt, paren-chymal lung disease, and unilateral sympathectomy. The mechanisms of unilateral pulmonary edema include an increase in capillary blood flow, reduced surfactant, rapid re-expansion of a col-lapsed lung, and disruption of venular post-capillary sphincter function after sympathectomy.1–3

One must learn the common pat-terns of acute pulmonary edema and be aware that many unusual pat-terns of pulmonary edema, such as nonhomogenous, focal, or asymmet-ric density, can be confusing—with

underlying chronic obstructive pulmo-nary disease, pneumonia, pulmonary embolism, neoplasm, and drug toxicity altering the radiographic pattern of pulmonary edema. Recently, B-type natriuretic peptide has shown promise in the diagnosis of cardiac etiology.4,5

Presence of Kerley’s lines, particu-larly Kerley’s B lines, almost always indicates cardiac or concomitant hydrostatic edema in the intensive care setting. Kerley’s lines are absent in increased-permeability pulmonary edema. Infrequently, one may see peri-bronchial cuffing, plural effusions, and the “bat’s wing” shadow.

Pulmonary edema can be localized to the right upper lung in mitral regurgita-tion and is related to the vector of blood flow across the incompetent mitral valve; this may be targeted preferen-tially at the pulmonary vein of the right upper lobe and cause a local increase in pulmonary venous pressure.6,7

The term “acute respiratory distress syndrome” is used to describe a hetero-geneous group of symptoms of respira-tory insufficiency that develops a char-acteristic clinical, pathophysiologic, and radiographic pattern, hours to days after a severe local or systemic insult. One usually needs serial CXRs, since findings are usually normal in the initial 12–24 hours. Abnormal CXR during the first 8–12 hours is usually due to complicat-ing factors such as aspiration pneumonia, volume overload, or congestive heart failure. Usually, acute respiratory distress syndrome appears about 24 hours after the initial insult, but the more fulminant the injury, the shorter the latent period. The radiography should be correlated with physiologic data such as central venous pressure or pulmonary capillary wedge pressure.

The Starling curve plots the develop-ment of pulmonary edema. Two principal determinants of the outward filtration of fluid at the level of pulmonary capillar-ies are the hydrostatic microvascular pressure (the permeability of the endo-thelial membrane) and protein osmotic pressure between the pulmonary micro-vasculature and the perimicrovascular interstitial space. In congestive heart

Figure 4. A) Posteroanterior radiograph of the chest at the time of presentation showing right middle-field infiltrate and Kerley’s lines. B) Posteroanterior radio-graph of the chest after antifailure treatment showing clear and complete resolution and normal lung field.

Figure 5. A) Posteroanterior radiograph of the chest at presentation with diffuse left-sided pulmonary edema (whiteout) and effusion. B) Posteroanterior radiograph of the chest after unloading treatment with clearing of pulmonary edema and small, right basal atelectasis.

Congestive Heart Failure® (ISSN 1527-5299) is published bimonthly (Feb., April, June, Aug., Oct., Dec.) by CHF, Inc., Three Parklands Drive, Darien, CT 06820-3652. Copyright ©2005 by CHF, Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions and ideas expressed in Congestive Heart Failure® do not necessarily reflect those of the Editor and Publisher. For copies in excess of 25 or for commercial purposes, please contact Sarah Howell at showell@lejacq.com or 203.656.1711 x106.

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failure, microvascular hydrostatic pres-sure is increased and fluid may eventu-ally move into the alveolar spaces. To explain unilateral pulmonary edema, we must postualte the existence of a set of factors—extrapulmonary, pulmonary, or pleural—preventing the pressure modi-fication from being expressed bilaterally.3 Leeming8 found that in patients treated with positive pressure ventilation, there was a significant positive correlation between the position of the patient and the localization of edema. One of the effects of gravity is to cause variations in pulmonary venous pressure in the pres-ence of congestive heart failure or mitral stenosis. In the lateral decubitus posi-tion, it seems possible that in the lower lung, higher pulmonary venous pressure calls for higher capillary and arterial pressures, causing not only redistribu-tion of blood flow to the upper lung, but also alveolar edema in the lower lung when severe pulmonary venous hyper-tension exists.

It has been proposed that unilat-eral pulmonary edema may be due

to unilateral impairment of lymphat-ic drainage on a congenital basis or because of prior inflammatory scar-ring, uneven distribution of blood flow secondary to local emphysematous changes, or because lying on one’s side can interfere with lymphatic drainage. Pathologic studies have indicated that pulmonary edema fluid is usually more pronounced on the right side.9

Goodrich10 showed that the role of neurogenic control proves to be very important in some noncardiac causes of unilateral pulmonary edema, but neurogenic control is still speculative in heart failure. Pleural and pulmonary factors can produce unilateral pulmo-nary edema by damaging vasculature; indeed, it is obvious that hemodynamic edema cannot occur in a nonperfused or very poorly perfused area. Our patients were free from pleural pathol-ogy; likewise, there was no hypoplasia or congenital absence of a pulmonary artery, no evidence of aortic aneu-rysm compressing pulmonary vessels, no pulmonary edema or compensatory

emphysema due to previous lobectomy, and no signs of infection. In our second patient, the left hyperlucent lung prob-ably was the result of partial obstruc-tion of the left main bronchus by a large left atrium.11 The acute onset and signs of elevated filling pressures (LV end-diastolic and left atrial pressure) guided us to avoid unnecessary delay in diagnosis and management.

ConclusionCardiac unilateral pulmonary infil-trate with edema is a rare entity and may very well be underdiagnosed. Management of pulmonary edema sec-ondary to heart failure is the same whether the edema is radiographically unilateral or bilateral. The key is to recognize pulmonary edema and not to confuse it with other unilateral pro-cesses. Physicians and critical care per-sonnel should be aware of the varied features of unilateral pulmonary edema and should consider the diagnosis of cardiac failure in patients who present with unilateral pulmonary infiltrate.

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3 Gleason DC, Steiner RE. The lateral roentgen-ogram in pulmonary edema. Am J Roentgenol Radium Ther Nucl Med. 1966;98:279−290.

4 Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart

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6 Gurney JW, Goodman LR. Pulmonary edema localized in the right upper lobe accom-panying mitral regurgitation. Radiology. 1989;171:397−399.

7 Roach JM, Stajduhar KC, Torrington KG. Right upper lobe pulmonary edema caused by mitral

regurgitation. Diagnosis by transesophageal echo-cardiography. Chest. 1993;103:1286−1288.

8 Leeming BWA. Gravitational edema of the lungs observed during assisted respiration. Chest. 1973;64:719−722.

9 Tzivoni A, Kerren A, Stern S. Unilateral pulmo-nary edema. Primary Cardiol. 1983;9:163.

10 Goodrich WA. Pulmonary edema, a correla-tion of X-ray appearance and physiological changes. Radiology. 1948;51:58−65.

11 Mobeireek AF, Joharjy I, Mobeireek AF. Hyperlucent lung in a patient with mitral valve disease. Chest. 1998;114:1469−1471.

Congestive Heart Failure® (ISSN 1527-5299) is published bimonthly (Feb., April, June, Aug., Oct., Dec.) by CHF, Inc., Three Parklands Drive, Darien, CT 06820-3652. Copyright ©2005 by CHF, Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions and ideas expressed in Congestive Heart Failure® do not necessarily reflect those of the Editor and Publisher. For copies in excess of 25 or for commercial purposes, please contact Sarah Howell at showell@lejacq.com or 203.656.1711 x106.