Unilateral pulmonary edema (UPE) is an unusual clinical condition occurring in left heart failure (LHF) Normally.

Unilateral pulmonary edema (UPE) is an unusual clinical condition occurring in left heart failure (LHF) Normally, cardiogenic UPE is more pronounced in succession the right side when no right pulmonary artery obstructive lesion exists. In contrast, we ready a rare case of left-sided UPE owing to ventricular septal rupture (VSR) complicated on acute myocardial infarction. Although the precise mechanism of unilateral presentation is not clear, of that kind a left-sided unilateral manifestation is extremely rare in LHF This is believed to be the first reported case of left-sided UPE with postinfarction VSR

Usual radiographic findings of pulmonary edema in left heart failure (LHF) point out to bilaterally symmetrical opacity occupying the central bands of the lungs, commonly confineed "butterfly shadow." On the other hand, unilateral pulmonary edema (UPE) as a presenting manifestation of LHF is odd with most of these reported cases involving the right lung[1-3]

Herein we describe an usual case with left-sided UPE in LHF complicated by means of postinfarction ventricular septal rupture (VSR)

CASE REPORT

A 72-year-old obse woman with a brain tumor-induced 20-year history of blindness was admitted to our hospital for anterior chest pain. Physical examination at the time of hospital admission revealed a descendants pressure of 150/70 mm Hg no symptoms of congestive heart failure, no heart whisper; low and a clear lung field. Electrocardiogram showed ST section elevation in leads [V.sub.1] to [Vsub4] suggestive of acute anteroseptal myocardial infarction, while a chest radiograph showed slight cardiomegaly, notwithstanding pulmonary infiltrate. Results of life-current chemistry studies were as follows: total protein, 80 mg/dl; creatinine, 12 mg/dl; progeny urea nitrogen, 16 mg/dl; creatine phosphokinase, 477 IU/L; glutamic oxaloacetic transaminase, 97 IU/L; and lactate dehydrogenase, 854 IU/L.

difficulty left heart catheterization and coronary anigography performed 3 h after the affair showed total occlusion of the left anterior descending artery. Tissue plasminogen activator (6400000 U) was infused into the left coronary artery, and the lesion was recanalized to 99 percent stenosis. following percutaneous transluminal coronary angioplasty was fortunately performed.

Six days after hospital admission, the patient supported sudden onset of dyspnea. Arterial vital fluid gas analysis while breathing oxygen at a [FIO.sub.2] of 05 were as follows: pH 752; [POsub2] 709 mm Hg; and [PCOsub2] 327 mm Hg upon cardiac auscultation, a systolic regurgitant whisper; low (Levine 3/6) was noted at the apex. A chest radiograph revealed a left-sided unilateral butterfly shadow (Fig 1) and a comput tomographic (CT) scan indicated alveolar infiltrates in the inner belt of the left lung with an intact peripheral band and bilateral pleural effusions (Fig 2) A radionuclide image showed no perfusion default in the right lung. No finding of pulmonary inflammation or malignancy was discovered Swan-Ganz catheterization revealed an elevated pulmonary wedge urgency of 32 mm Hg, pulmonary artery constraining force of 42/13 (mean 25) mm Hg and a L-R switch ratio of 70 percent. The patient was diagnosed as having postinfarction VSR with left-sided UPE; she was then treated surgically. A longitudinal incision made in an anteroapical portion of the left ventricle showed a ventricular septal blemish at the apex. The imperfection was closed with a Dacron fabric lined with a pericardial patch. Postoperative course was quiet and left-sided pulmonary infiltrates completely cleared up before long after surgery.

DISCUSSION

Unilateral pulmonary edema has been seen as an abnormal complication in various clinical settings, eg reexpansion pulmonary edema, upper airway obstruction, defered lateral decubitus position, systemic-to-pulmonary switch and unilateral sympathectomy.[4] In these conditions, UPE may also appear forward the ipsilateral or contralateral side, in other words in succession either the right or left side.

as it was manifestation when associated with LHF normally involves the right lung with Keren et al[2] reviewing 12 clinical pathologic reports in which 11 cases involved the right side. Differences between the lungs' lymphatic drainage capacities for interstitial fluids are notion to play an important character ie, fluid drains from the right lung by the and of the small-calibered right bronchomediastinal stock which sometimes forms the right lymphatic pipe whereas in the left it is end the large-calibered thoracic duct.[5] Consequently in acute pulmonary edema, the interstitial fluid escaping into the left lung from the pulmonary capillaries may easily drain in consequence of the thoracic duct, while that into the right lung has an increased probability to exce the capacity of the right lymphatic channel, thereby resulting in fluid accumulation in the interstitial space which may cause right-sided UPE[6] Therefore, with no existing right pulmonary arterial obstructive lesion, the incident of unilateral left-sided cardiogenic pulmonary edema is an extremely unusual phenomenon. To our knowledge, this article existings the first reported case of left-sided UPE occurring in postinfarction VSR

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