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Spontaneous Cerebral Hemorrhage and Sudden Biventricular Failure After Lung Transplantation | Pulmonary Medicine | JAMA Cardiology | ÌÇÐÄvlog

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JAMA Cardiology Clinical Challenge
±·´Ç±¹±ð³¾²ú±ð°ùÌý2016

Spontaneous Cerebral Hemorrhage and Sudden Biventricular Failure After Lung Transplantation

Author Affiliations
  • 1Division of Thoracic Surgery, Department of Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois
  • 2Division of Pulmonary and Critical Care Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois
JAMA Cardiol. 2016;1(8):963-964. doi:10.1001/jamacardio.2016.2568

A woman in her mid-60s with end-stage lung disease secondary to systemic sclerosis and pulmonary hypertension underwent bilateral sequential lung transplantation without cardiopulmonary bypass through a clamshell thoracotomy. The immediate postoperative course was uneventful, and she was weaned off oxygen support. On postoperative day 10, she developed seizures when walking and was immediately intubated. Brain imaging revealed a new intracerebral hemorrhage in the right frontal and left occipital lobes, with narrowing of the internal carotid, basilar, posterior cerebral, and right posterior communicating arteries, suggestive of vasospasm or vasculopathy. Subsequently, she developed hypoxemia and hypotension associated with acute pulmonary edema and new cardiomegaly (Figure 1A). An electrocardiogram showed nonspecific ST changes with T-wave inversion (Figure 1B), and serum levels of troponin and creatine phosphokinase were negative. Transesophageal echocardiography revealed new dilation of the left ventricle (LV), with an ejection fraction of 10%, functional mitral regurgitation, anterior and apical akinesis, and basal hypokinesis (Video 1, Video 2, and Video 3). The right ventricle (RV) was distended, with moderate tricuspid regurgitation. Recent pretransplantation coronary angiography did not reveal atherosclerosis. Her cardiopulmonary status rapidly worsened, with cardiogenic shock and refractory hypoxemia (arterial blood pH, 7.12; arterial partial pressure of oxygen, 43 mm Hg; and partial pressure of carbon dioxide, 56 mm Hg), despite mechanical ventilation (rate, 24/min; tidal volume, 6 mL/kg; fraction of inspired oxygen, 100%; and positive end-expiratory pressure, 15 cm H2O), neuromuscular blockade, and administration of inotropes.

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