Refractory hypoxemia after mitral valve surgery: an unusual cause and its successful percutaneous treatment.
We describe the case of a patient who underwent elective mitral valve replacement and whose postoperative progress was complicated by a persistently high inspired oxygen requirement and consequent inability to wean from respiratory support. The reason for this was initially unclear, but transesophageal echocardiography identified the cause as a postoperative iatrogenic atrial septal defect (ASD). This complication was specifically related to the transseptal surgical approach that had been employed. The refractory arterial hypoxemia encountered postoperatively was due to an element of right-to-left shunting across the defect, in the absence of raised pulmonary artery pressures, likely related to a baffle-like effect of the residual atrial septal tissue. This postulated mechanism was supported both by Doppler color flow mapping across the defect at transesophageal echocardiography, and later by observing a rise in systemic arterial oxygen saturations immediately after device closure of the ASD. Once the iatrogenic ASD had been diagnosed, there was a consensus of opinion that the patient was too unwell to survive further open heart surgery. Hence, percutaneous closure of the defect was performed using an Amplatzer occluder device. This was technically successful and led to a marked improvement in the patient's clinical state, subsequent rapid weaning from ventilatory support and later hospital discharge. This case illustrates a rare presentation of an occasional complication of mitral valve surgery. Percutaneously delivered device closure of the ASD proved highly effective in this patient for whom no other options were felt to be feasible.