Article

Other causes of unilateral pulmonary edema

Correspondence 129

will generate artifact in different location, whereas a true dissection will be consistent. Reconstruction by a multi- detector row CT (helical CT) in a sagittal view will also give a more accurate assessment of aortic artifact [12,13]. Cardiac gating has been shown to reduce the artifact at the aortic root [14]. However, in emergency condition, its application has not yet been validated [12]. Transesophageal echocardiogram could also assist in proper diagnosis. The sensitivity and specificity of TEE have been reported to be as high as 98% and 63% to 96%, respectively [15]. The main limitation of TEE is its strong dependence on the experience of the investigator.

Missed diagnosis of aortic dissection leads to a poten- tially lethal outcome, whereas misjudgment of artificial images results in unnecessary thoracotomy. Familiarity with these diagnostic pitfalls of CT facilitates correct recognition of aortic dissection.

Wen-Chu Chiang MD, MPH

Pei-Chieh Kao MD Chan-Ping Su MD

Department of Emergency Medicine National Taiwan University Hospital, Yun-Lin Branch

Taipei 100, Taiwan E-mai address: [email protected]

Juan Hsu MD

Department of Cardiovascular Surgery National Taiwan University Hospital, Yun-Lin Branch

Taipei 100, Taiwan

doi: 10.1016/j.ajem.2006.04.011

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Other causes of unilateral pulmonary edema

To the Editor,

We read with interest the article bUnilateral pulmonary edema related to massive mitral insufficiencyQ wherein the authors describe the occurrence of unilateral pulmonary edema after mitral insufficiency [1]. We describe a case of unilateral pulmonary edema related to end-stage renal disease that improved rapidly with hemodialysis and review the literature for the causes of unilateral pulmonary edema. A 34-year-old man, with a known case of end-stage renal disease (secondary to chronic glomerulonephritis) requiring maintenance hemodialysis, presented in the emergency department with severe dyspnea. Over the previous 12 hours, he experienced progressive orthopnea and cough with mucoid expectoration. The last session of hemodialysis was administered 24 hours ago, and the patient denied any history of undue salt or water intake, hemoptysis, or fever. On examination, the patient was pale, in severe respiratory distress, and had to sit in an upright position as a result of orthopnea. Blood pressure was 160/90 mm Hg, pulse rate 110/min, respiratory rate 34/min, and oral temperature

37.28C. Auscultation revealed diminished breath sounds over the lower two thirds of the left lung and crackles in the lower one third of the right lung. Auscultation of the heart was normal. The progressive orthopnea led to the Initial diagnosis of pulmonary edema, and the patient was shifted to the respiratory intensive care unit where he was treated with oxygen, intravenous diuretics, and morphine. Preliminary investigations revealed a white blood cell count

of 12000/lL with 70% neutrophils, hemoglobin level of

9.3 g/dL, creatinine level of 8.2 mg/dL, sodium level of 141 mEq/L, potassium level of 5.8 mEq/L, and Creatine phosphokinase (MB isozyme) of 20 IU/L. Arterial blood gas analysis revealed a pH of 7.2, Pao2 of 62 mm Hg, Paco2 of 25 mm Hg, and HCO3 of 10 mEq/L, at Fio2 of 0.28. The electrocardiogram demonstrated sinus tachycardia. Chest x-ray revealed a unilateral homogenous pulmonary opacity occupying the right lower lobe and left pleural effusion (Fig. 1). Bedside echocardiography was normal with a left ventricular ejection fraction of 56%. Although the patient’s

130 Correspondence

temperature was normal, in the presence of a unilateral pulmonary infiltrate, as pneumonia could not be ruled out, treatment with intravenous cefpirome and azithromycin was initiated. In view of metabolic acidosis and hyperkalemia the patient underwent hemodialysis. After the dialysis, the patient’s disease course was characterized by rapid recov- ery: within a few hours, breathing improved dramatically and repeated arterial blood gas analysis revealed a pH of 7.32, Pao2 of 72 mm Hg, Paco2 of 35 mm Hg, and HCO3 of 18 mEq/L, at FiO2 0.21. Repeat chest x-ray obtained 12 hours after admission showed resolution of the pulmo- nary opacity with residual left pleural effusion (Fig. 2). These findings, together with the lack of fever, suggested that pneumonia was not a likely diagnosis. Moreover, sputum for culture and Gram stain was negative and we terminated the antibiotic treatment. The patient was inves- tigated for the left pleural effusion. Pleural biopsy showed caseous granulomas with acid-fast bacilli. The patient was started on antituberculous therapy and discharged unevent- fully after 7 days of hospitalization with advice for regular maintenance hemodialysis.

Unilateral pulmonary edema is an uncommon, if not rare,

entity that can be mistaken for other causes of unilateral alveolar and interstitial infiltrates, especially pneumonia. It has been described after congestive heart failure [2], prolonged rest on one side in a patient with cardiac decompensation or receiving large amounts of fluids [3], in patients with mitral valve insufficiency [1], in cases of rapid expansion of the lung after Pleural effusions and pneumothorax [4], in the normal lung in patients with

Fig. 1 Chest radiograph shows prominent right hila and dense homogenous opacity in the right lower lobe; also present are left pleural effusion and a central venous catheter for dialysis.

Fig. 2 Chest radiograph shows complete clearing of the opacities on the right side.

unilateral pulmonary disease such as MacLeod syndrome

[5] and unilateral pulmonary agenesis [6], after talc pleurodesis [7], trauma [8], epilepsy [9], upper airway obstruction [10], pulmonary artery compression from aortic dissection [11,12], pulmonary venous obstruction from mediastinal fibrosis [13] or postlobectomy [14], unilateral main stem intubation [15], Neurogenic pulmonary edema [16], nitrogen mustard [17], amiodarone-related [18] and heroin-related [19] pulmonary edema, pregnancy [20], and in cases of fluid overload [21-23].

Unilateral pulmonary edema can result from myriad of causes. Thus, even if the pulmonary opacities are unilateral, if the clinical manifestation is compatible with pulmonary edema and not with pneumonia, early and aggressive treatment should be initiated for pulmonary edema.

Ritesh Agarwal MD, DM Ashutosh N. Aggarwal MD, DM

Dheeraj Gupta

Department of Pulmonary Medicine Postgraduate Institute of Medical Education and Research

Chandigarh-160012, India

E-mail addresses: [email protected]

[email protected]

doi:10.1016/j.ajem.2006.05.025

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