Unilateral Pulmonary Edema During Transesophageal Echocardiography

Unilateral Pulmonary Edema During Transesophageal Echocardiography Shmuel Stienlauf, MD, Michaela Witzling, MD, Michael Herling, MD, and David Harpaz, MD, Holon and Tel-Aviv, Israel

Transesophageal echocardiography is considered to be a relatively safe procedure, the complications of which are well known and include probe-related and procedure-related complications. Congestive heart failure rarely occurs. Unilateral pulmonary edema is relatively uncommon and to the best of our knowl-

Transesophageal echocardiography (TEE) is considered to be a safe procedure, accompanied by a very low complication rate of less than 0.5%.1-3 The complications of this procedure are well known. Congestive heart failure rarely occurs except in patients with preexisting significant myocardial compromise. Unilateral pulmonary edema (ULPE) is relatively uncommon in heart failure. We describe an unusual case of ULPE that developed during the course of TEE.

CASE REPORT A 59-year-old man was referred for an elective TEE for investigation of the potential source of emboli after a documented cerebrovascular accident and multiple infarcts found on a computed tomography of the brain. The patient’s past history included hypertension, non– insulin-dependent diabetes mellitus, and an old myocardial infarction with mild left ventricular systolic dysfunction with a left ventricular ejection fraction (LVEF) of 43%, as was estimated by a previous multiple gated acquisition scan. A Thallium-201 perfusion scan was negative for inducible ischemia. The patient’s New York Heart Association functional capacity was class II. The patient was treated with nitrates, ACE inhibitors, and a low dose of diuretics. Transthoracic echocardiography was performed in the left lateral decubitus position, lasting for 20 minutes, during which he was relaxed and without any apparent distress. The transthoracic study revealed a mildly enlarged left ventricle (a diastolic dimension of 57 mm) and a reduced From the Department of Internal Medicine E, Department of Radiology and the Heart Institute, E. Wolfson Medical Center, Holon, and the Sackler Medical School, Tel-Aviv University. Reprint requests: David Harpaz, MD, The Heart Institute, E. Wolfson Medical Center, Holon, 58-100, Israel. Copyright © 1998 by the American Society of Echocardiography. 0894-7317/98 $5.00 1 0 27/4/89026

edge has never been reported in association with transesophageal echocardiography. Herein we describe an unusual case of unilateral pulmonary edema that developed during the course of transesophageal echocardiography. (J Am Soc Echocardiogr 1998; 11:491-3.)

left ventricular function caused by three vessels’ distribution of wall motion abnormalities. The LVEF was estimated to be 32%. A Doppler study did not reveal any significant valvular regurgitation. After 20 minutes, in which the patient was sitting, the pharynx was anesthetized with 10% lidocaine spray. Ten milliliters of lidocaine gel was then given to the patient to swallow. No intravenous medications were injected. The patient was placed again in the left lateral decubitus position and the esophagus was immediately intubated. Vital signs before inserting the TEE probe were blood pressure 190/100 mm Hg, heart rate 120 beats/min, and arterial oxygen blood saturation (measured by pulse oximetry) 95%. Within 1 minute after swallowing the probe and the beginning of the TEE examination, the patient developed progressive dyspnea and the arterial oxygen blood saturation dropped to 84% to 85%. Blood pressure was 190/110 mm Hg and heart rate was 145 beats/min. The arterial oxygen saturation remained low despite oxygen supplementation by nasal cannula. The patient denied any chest discomfort. No electrocardiographic changes, new wall motion abnormalities, or mitral regurgitation were detected by the TEE. The TEE probe was withdrawn because of progressive dyspnea 1 minute later. The patient was admitted to the Internal Medicine ward. On admission he was mildly dyspneic, the respiratory rate was 18 per minute, blood pressure was 140/95 mm Hg, heart rate was 80 beats/min, and the arterial oxygen saturation was 90% (with oxygen supplementation). Fine respiratory crackles and reduced inspiratory sounds over the left lung were noted. The electrocardiograph remained unchanged without any changes compatible with acute ischemia. Routine laboratory tests including cardiac enzyme levels were all within normal limits. Methhemoglobin and carboxyhemoglobin could not be detected in the blood. A chest radiograph, performed within 30 minutes of the acute event, revealed diffuse unilateral opacities over the left lung (Figure 1, A). The patient was treated only with oxygen supplementa491

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Figure 1 A, Chest radiograph performed within 30 minutes of the acute dyspneic event, revealing diffuse unilateral opacities over the dependent left lung. B, Follow-up chest radiograph performed 24 hours later, showing resolution of the opacities over the left lung. tion and resumption of his medications. The dyspnea resolved completely after a few hours. The opacities over the left lung cleared on a follow-up chest radiograph performed 24 hours after the initial event (Figure 1, B).

DISCUSSION The two most common forms of pulmonary edema are those initiated by an imbalance of Starling law and those initiated by disruption of one or more components of the alveolar-capillary membrane. ULPE, which is an uncommon disorder, categorized only in 1978,4 may occur when there is a combination or alteration of these factors on the affected side (ipsilateral pulmonary edema) or when there is a pulmonary perfusion defect on the opposite side (contralateral type). Gravity has been implicated as a major cause of ipsilateral pulmonary edema.5,6 Gravity raises the hydrostatic pressure in the dependent lung, impairing circulation and affecting the production of surfactant.4 The lateral decubitus position could compromise lung mechanisms. There is relative hyperperfusion and hypoventilation of the dependent lobes, and when volume overload or heart failure exists, it could result in pulmonary edema of the dependent lung. ULPE of the dependent lung usually develops in patients placed in the lateral decubitus position for a prolonged period of time, during medical procedures such as mechanical ventilation to promote bronchial drainage,7 and in patients immobilized because of neurologic deficits. Other cardiac causes of ULPE are systemic–to–pulmonary artery shunts (i.e., Water-

stone and Pott’s procedures, Blalock-Taussig anastomosis), impaired perfusion of a single pulmonary artery8,9 or impaired pulmonary venous drainage,10,11 and left ventricular failure.5,12 Acute exacerbation of heart failure rarely occurs during TEE. It occurs in patients with preexisting left ventricular dysfunction. In a large series of 5441 patients,1 only two developed overt heart failure. We believe this is the first report of ULPE developing during TEE. The patient developed ULPE just a few minutes after being repositioned in the lateral decubitus position. It is postulated that the combination of failure of the patient to take the prescribed medications during fasting before the procedure, his compromised left ventricular systolic function (LVEF approximately 30%), the endogenous catecholamine stimulation preceding the TEE, and the left lateral decubitus position in which he was placed earlier were reasons for this unusual event. As a policy, we usually elect not to routinely premedicate older patients unless they require it or in cases of preprocedural excessive hypertension, anxiety, or discomfort during intubation of the esophagus. Most of the elderly patients tolerate the procedure quite well with no premedication, which causes reduction of oxygen saturation and does not avoid the temporary rise in blood pressure at the moment of swallowing the probe. Because lateral decubitus is a risk factor for development of ULPE in patients with left ventricular dysfunction, the time the patient spends in such a position should be shortened; other possible triggers of acute heart failure, for example, hypertension and

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anxiety, should be recognized and treated promptly. Patients should be instructed to continue the essential medications even while fasting with minimal water intake. The physician should also include ULPE in the differential diagnosis of acute dyspnea developing during TEE. The authors would like to thank Ms. Lori Mandelzweig, MPH, for editorial assistance. REFERENCES 1. Khandheria BK, Tajik AJ, Freeman WK. Transesophageal echocardiographic examination: technique, training, and safety. In: Freeman WK, Seward JB, Khandheria BK, Tajik AJ, editors. Transesophageal echocardiography. Boston/New York/Toronto/London: Little, Brown & Company, 1994:49-51. 2. Khandheria BK, Oh J. Transesophageal echocardiography: state-of-the-art and future directions. Am J Cardiol 1992;69: 61H-75H. 3. Daniel WG, Erbel R, Kasper W, et al. Safety of transesophageal echocardiography: a multicenter survey of 10,419 examinations. Circulation 1991;83:817-21. 4. Calenoff L, Kruglik GD, Woodruff A. Unilateral pulmonary edema. Radiology 1978;126:19-24.

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5. Bahl OP, Oliver GC, Rockoff SD, et al. Localized unilateral pulmonary edema: an unusual presentation of heart failure. Chest 1971;60:277-80. 6. Leeming BW. Gravitational edema of the lungs observed during assisted respiration. Chest 1973;64:719-22. 7. Snoy FJ, Woodside JR. Unilateral pulmonary edema (down lung syndrome) following urological operation. J Urol 1984; 132:776-7. 8. Cocina EG, Rossas G, Ruiz F, et al. Left ventricular pseudoaneurysm: a cause of unilateral pulmonary edema by compressing the left pulmonary artery. Am Heart J 1996;132: 1306-7. 9. Takahasi M, Ikeda U, Shimada K, et al. Unilateral pulmonary edema related to pulmonary artery compression resulting from acute dissecting aortic aneurysm. Am Heart J 1993;126: 1225-7. 10. Premser C, Cajulis R, Glagov S. Pulmonary vein and superior vena cava obstruction due to expanding aneurysm of the pulmonary artery. Chest 1988;93:206-7. 11. Roach JM, Stajduhar KC, Torrington KG. Right upper lobe pulmonary edema caused by acute mitral regurgitation: diagnosis by trans esophageal echocardiography. Chest 1993;103: 1286-8. 12. Rusumi RK, Walker SS, Fulkerson PK, et al. Unilateral pulmonary edema associated with left ventricular failure. Heart Lung 1984;13:263-6.