LAUSR

Hemolysis induced by occlude devices to repair the structural cardiac defects is not very infrequent in intervention cardiology. The unavoidable residual leaks, which are featured by high velocity, vortices, and rapid deceleration, impose significant shear on red blood cells leading to hemolysis [1, 2]. There are several cases that reported acute hemolysis after transcatheter closure of VSD or PDA in the literature [3, 4]. However, hemolysis due to intracardiac device for ASD closure is rather rare. Although in some cases surgical removal of the device or transcatheter occlusion of a residual shunt may be necessary, most hemolysis can be conservatively managed with fluids, sodium bicarbonate, and corticosteroids. A 51-year-old female weighing 54 kg was admitted to the catheter lab with the aim of performing a transcatheter device closure of ASD. She presented a 2-year history of exertional chest distress. The second heart sound was prominent, and a grade 3/6 systolic murmur was heard at the left midsternal border during physical examination. Any marked abnormality was not detected in the laboratory tests. Electrocardiogram showed complete right bundle branch block and echocardiography revealed the presence of a large secundum-type ASD with a diameter of 35 mm, as well as mild mitral valve regurgitation and severe tricuspid regurgitation. The pulmonary artery systolic pressure (PASP) gradient was 90 mm Hg as estimated by the Doppler method (Fig. 1a). After preoperational preparation, diagnostic catheterization revealed an elevated mean pulmonary artery pressure (mPAP) of 38 mm Hg, and a 50-mm SHSMATM (Shanghai Shape Memory Alloy Co., Ltd., Shanghai, China) ASD occluder was implanted via right femoral venous approach through a 14F delivery sheath (Fig. 1b). Intraoperative echocardiography showed the proper position of the occluder (Fig. 1c, d). After the procedure, the patient was treated with heparin and aspirin as well as continuous ECG monitoring during hospitalization. On the first day after the operation, the patient had developed intense hemolysis marked by dark coloured urine and her haemoglobin was 10.7 g/dL. Anticoagulation was ceased, while sodium bicarbonate for urinary alkalization and dexamethasone was immediately administered. On the second day, her haemoglobin dropped to 9.7 g/dL, but fortunately the vital signs were stable and the colour of urine turned lighter. Echo on day three showed minor residual shunt across the device which is common in large arial septal defect. Severe mitral and tricuspid valve regurgitation were observed and impinging on the left and right discs of the prosthesis, respectively (Fig. 1e). The patient was discharged when urine colour changed gradually from Coca Cola to normal on day 8, with Hb 95 g/L. Four months after the closure, the patient came to our hospital for a reexamination. Her haemoglobin increased to 11.6 g/dL and urine test was normal. Echo showed minor residual shunt across the device and severe tricuspid regurgitation with normal cardiac function. What was interesting was that her mitral valve regurgitation turned from severe to moderate. Device closure of septal defects may result in various complications such as endocarditis, device embolisation, cardiac rupture and arrhythmias. Haemolysis, a rare but potentially hazardous complication that can cause acute renal failure and even mortality, has been documented after transcatheter device closure of congenital heart diseases, including PDA, ASD and VSD. Although surgery or transcatheter intervention is required in some patients with severe intravascular haemolysis, this complication is generally managed conservatively. Manli Yu, Xinghua Shan and Yuan Bai have contributed equally.