Address of correspondence:
Alexandros Briasoulis
Section of Heart Failure and Transplant, Division of Cardiovascular Diseases
University of Iowa Hospitals and Clinics,
200 Hawkins Dr, Iowa City, IA 52242
Office: 319-678-8418
Fax: 319-353-6343
E-mail: alexbriasoulis@gmail.com
Abstract: Outflow cannula occlusion is an infrequent complication occurring among recipients of continuous flow left ventricular assist devices (LVAD). Hereby, we present a case of intrinsic and extrinsic outflow cannula obstruction resulting in cardiogenic shock and multiorgan failure.
Data availability : upon request by Editors
International Review Board approval : Waived, as this is a single case report
Informed consent : This is a case report, informed consent was not obtained as the patient did not survival to hospital discharge.
Case Description: A 66 year old Caucasian male with medical history of emphysema, ischemic cardiomyopathy and stage D heart failure status post HeartMate 3 LVAD implantation as destination therapy eighteen months before the index admission for fever and shortness of breath. His international normalized ratio was in therapeutic range between 2 and 3 on admission. Despite early symptomatic improvement of the respiratory symptoms with intravenous diuresis and antibiotics on the fifth day of this hospital stay he developed low flow alarms, decreased power but stable LVAD speed (5600 rpm) (Figure A). A bedside echo showed persistent aortic valve opening in spite of increasing speed to 6000rpm. Outflow cannula obstruction was suspected and a CT scan of the chest was performed which revealed an irregular circumferential hypodensity in the outflow cannula of the left ventricular assist device consistent with thrombus or extrinsic compression from material between the outflow and the bend relief material, without evidence of acute kinking of the outflow graft (Figures B-D). Of note, a previous CT angiography of abdomen did not reveal evidence of outflow graft occlusion (Figure E). The became became hypotensive and was intubated because of altered mentation and worsening respiratory distress. He was resuscitated with infusion of norepinephrine and dobutamine. The lactate dehydrogenase (LDH) and plasma free hemoglobin were not elevated. The patient was started intravenous anticoagulation with intravenous heparin in anticipation of surgical intervention. However, in the first 48 hours of initiation of intravenous anticoagulation, he developed diffuse alveolar hemorrhage diagnosed with a CT chest and confirmed by bronchoscopy. His overall condition progressed rapidly to multiorgan failure (acute kidney and liver injury). His hemodynamics at the time suggested cardiogenic shock with Fick and thermodiluation cardiac index of <1.8 l/minute/m2, mixed venous saturations <40%, and elevated pulmonary capillary wedge pressure over 20 mmHg and central venous pressure of 14mmHg. After meeting with family of the patient, the decision of the multi-disciplinary team was to proceed with comfort care measures and hospice on the basis of deteriorating multi-organ function, low likelihood of lung function recovery in the context of acute on chronic lung disease, and poor candidacy for cardiac surgery.
Autopsy exam revealed instrinsic and extrinsic outflow graft obstruction. The extrinsic obstruction consisted of fibrinous tissue between the woven polyester tube and the bend relief (Figures F-N).