Flash pulmonary oedema and bilateral renal artery stenosis: the Pickering Syndrome

Abstract

In 1988 Pickering et al . reported in the Lancet a series of 11 hypertensive patients with bilateral atheromatous renovascular disease who presented with a history of multiple episodes of pulmonary oedema.1 Seven of these patients had stenosis of both renal arteries and in a subsequent series of 90 patients, pulmonary oedema was significantly more common in patients with bilateral than in those with unilateral renal artery stenosis (RAS).2 Successful revascularization of one or both renal arteries eliminated pulmonary oedema in 77% of patients with bilateral RAS.2 The authors concluded that ‘bilateral RAS may be a specific and treatable predisposing factor to pulmonary oedema in azotemic hypertensive patients'.1 Since the initial observation of this clinical entity 29 case reports,3–31 9 case series,1,32–39 and 10 clinical studies1–2,40–47 of flash pulmonary oedema (FPO) and RAS (both unilateral and bilateral) have been published of which 16 case reports, 2 case series, and 7 clinical studies comprising a total of 87 patients relate to bilateral RAS and FPO. The underlying pathophysiological mechanisms responsible for triggering FPO in patients with bilateral RAS have been delineated in several clinical and experimental studies. Since FPO and bilateral RAS seem to be a unique entity with distinct pathophysiological, clinical, and therapeutic features, we propose to name it Pickering Syndrome. In the following, we review incidence, pathophysiology, clinical findings, and treatment of the Pickering Syndrome. Flash pulmonary oedema is a general term used to describe a particularly dramatic form of acute decompensated heart failure. Regardless of its aetiology, an acute increase of left ventricular (LV) end diastolic pressure is the conditio sine qua non for the development of FPO and remains the common denominator of all clinical situations associated with …